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L. Weaning Guidelines
1. Commencement of weaning is a medical decision.
2. Weaning is contraindicated with any of the following:
a) Unstable ICP (abort weaning if ICP increases)
b) Need for heavy sedation (e.g. upper airway obstruction)
c) Haemodynamic instability
d) Significant bronchospasm
e) High work of breathing.
3. Trial pressure support daily if the patient meets both the following criteria:
a) PaO2/FiO2 ratio > 150
b) Patient can take spontaneous breaths if SIMV resp-rate reduced.
4. Weaning protocol:
a) See the flow diagram following page.
b) Set initial pressure support to maintain adequate VT
i) Start at 10 cmH2O and adjust to:
VT ≤ 6 ml/kg IBW for patients recovering from ARDS.
VT ≤ 8 ml/kg IBW for all others.
IBW Males = 0.91 × (height [cm] – 152.4) + 50
IBW Females = 0.91 × (height [cm] – 152.4) + 45.5
ii) Alternatively, use target VT = 80-100% of set SIMV VT
iii) Allowable PS range = 5-25 cmH2O
If VT cannot be achieved with 25cmH2O, cease trial
c) Assess at 15 and 30 minutes for “weaning success criteria”
d) Assess each hour for suitability to wean PS
e) Once PS has reached minimum (5cmH2O) then wean PEEP to 5cmH2O
f) If PS & PEEP = 5cmH2O then assess for extubation.
5. Weaning Success Criteria:
i) RR < 30/min
ii) SpO2 > 90%
May be set lower with COPD, e.g. >86-88%
iii) FIO2 ≤ 0.5
iv) No respiratory distress as shown by 2 or more of the following:
HR > 120% baseline
Accessory muscle use
Diaphoresis
Paradoxical abdominal movements
Marked dyspnoea](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-49-2048.jpg)
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c) Insertion procedure:
i) Local anaesthesia in awake patients
ii) Scrubbed assistant recommended
iii) Select size (by patient’s height)
< 152cm 25ml balloon
152 – 162cm 34ml balloon
162 – 183cm 40ml balloon
>183cm 50ml balloon
iv) Femoral artery insertion of a 12F introducer, Seldinger technique.
v) Check the length for balloon catheter insertion, using the angle of Louis
(level of T4) as the surface landmark, prior to insertion.
vi) Insert the balloon to the level of T4.
The double black marker on the balloon catheter must be visible
This indicates that the balloon has fully exited the sheath.
vii) Connect to pressure transducer and pump.
viii) Press the [IAB Fill] button to fill the balloon & wait for completion.
ix) Press the [Assist/Standby] button to start the pump.
x) Start on minimal augmentation and increase to maximum.
NB: subsequent augmentation should not be set below 50%
xi) Suture in place and cover with an occlusive dressing.
xii) Set timing:
Check balloon inflation against pressure wave:
set to peak of dicrotic notch.
Check balloon deflation against ECG:
prior to QRS complex and
observe decrease in end diastolic pressure.
Check diastolic augmentation on pressure wave.
Select augmentation ratio: *standard = 1:1
d) Maintenance
i) Check CXR post insertion:
tip of IABP below T4 (carina) & origin of the left subclavian artery
ii) Neurovascular obs of insertion site, lower limbs and left arm hourly.
iii) Nurse at < 30° elevation.
iv) Document pump timing (ratio) and adequacy of augmentation.
v) Assess haemodynamic response: CI, MAP, SVR, filling pressures, CXR.
vi) Ensure clear balloon tubing is exposed:
Monitor condensation (due to rapid helium shuttling), or
Blood in tubing (balloon rupture).
e) Timing during arrhythmias
i) Ectopics: keep on ECG trigger, system will automatically deflate on
ectopic
ii) Tachycardia > 160/min :
Reduce augmentation (equal to patient systole)
Decrease ratio to 1:2 if reducing augmentation is not adequate](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-62-2048.jpg)
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Amlodipine 5-10mg oral bd Long acting oral Ca++ antagonist.
Caution in renal impairment
Captopril Start low dose ~ 5-6.25mg Treatment of hypertension
up to 50mg orally 8 hrly Left ventricular dysfunction, esp post-MI
Syrup: 5mg/ml or tablets Left ventricular failure
Acute hypertension: 5-25mg Diabetic nephropathy
sublingually prn Caution in renovascular disease and renal failure
Perindopril Start 2.5mg daily
up to 10mg daily orally
Phenoxybenzamine Oral : 10mg/day and increase Long acting, non-competitive -blocker
until postural hypotension Preoperative preparation of phaeochromcytoma
IV : 1mg/kg/day Idiosyncratic hypotension may occur
dilute to 200-500ml
1/3 dose over 1/24
2/3 dose over 1/24
Prazosin Start with 0.5mg, and -blocker
increase up to 5mg tds orally Potent antihypertensive agent
Prominent first dose effect
Metoprolol Oral: 25-100mg bd High sympathetic drive states: neurogenic BP
IV: 1-2mg bolus every 2-3 All grades of hypertension, inc renovascular
minutes up to 10 mg. Cardiac ischaemia
Control of reflex tachycardia with vasodilators
Thyroid crisis
Caution in poor LV function, asthma
Mainly eliminated by hepatic metabolism
Esmolol Loading dose 0.5 mg/kg Ultra-short acting -blocker
Infuse 100mg/10ml and titrate Useful as trial for patients with poor LV function.
Adjunct to vasodilators post cardiac surgery
Clonidine 25µg boluses of up to Acute, centrally mediated hypertension
150µg/24hrs Useful post cardiac surgery
Oral: 75µg bd Withdrawal states
up to 150-300µg tds. Care with hepatic or renal dysfunction
Rebound hypertension with chronic use
Sedation, especially 1st dose
Dexmedetomidine 400 µg in 40mls Selective alpha-2-agonist
load 1µg/kg over 20min Acute, centrally mediated hypertension
infuse 1-5ml/hr Not a first line drug.
Selected use by senior medical staff only
Sedation
MgS04 5-10 mmol loading Pre-eclampsia / eclampsia
Infuse at 4-12 mmol/hr Phaeochromocytoma
Target plasma [Mg] ~ 1.5-2 Sympathetic overdrive in tetanus
mmol/L
Propanalol Portal hypertension](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-72-2048.jpg)
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H. Endocrine Drugs
1. Insulin
a) Indications:
i) Diabetic emergencies – DKA and hyperosmolar coma
ii) Treatment of hyperkalaemia
50% dextrose 50ml, plus Actrapid 10U
iii) Perioperative diabetic patients (both insulin and non-insulin dependent)
iv) General ICU patients
Hyperglycaemia 10 mmol/l or glycosuria in acute illness:
a. Maintaining BGL 6-10mmol/l is recommended for all critically ill
patients
b. Majority of ICU patients will require insulin using this protocol.
c. NB: This protocol is not designed for patients with diabetic
ketoacidosis and is a guideline only.
d. Some patients will require individual manipulation of dose.
Subcutaneous sliding scale insulin:
a. Is inadequate for most critically ill patients and should be avoided.
b. May be used in a small number of less critically ill patients, who
have a limited requirement for exogenous insulin.
c. A regular dose of subcutaneous intermediate/long-acting insulin,
adjusted according to BGL may be suitable in some ICU patients.
b) ICU Insulin Protocol – see following page.
i) Target BGL = 6-10mmol/l.
ii) Blood for testing should ideally be:
Sampled from the arterial line rather than capillary (finger prick), as the
former is more accurate in the critically ill.
Measured via the blood gas analyser, c.f. bedside glucometer.
iii) Protocol Precautions:
If insulin rate ≥ 8 U/hr and the BGL remains high, measurement may
be erroneous take a sample from another site and measure in the
blood gas analyser.
Consider holding the infusion if feed or glucose infusions are stopped.
Potassium level
a. Administration of insulin reduces K+ levels.
b. Check K+ on ABG specimen at least twice daily and more often if
the insulin infusion rate is high or changing acutely.
c. If [K+] < 3.5 mmol/l
KCl ~ 30 mmol over 1h via a pump.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-96-2048.jpg)
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C. Blood Component Therapy
1. Indications
a) Blood component therapy should only be given if benefit outweighs the risk
b) The decision to transfuse should be based on clinical assessment, disease course
and response to previous transfusion as well as [Hb] levels.
c) Potential risks including
i) Mis-identification / acute transfusion reaction
ii) Bacterial / viral infection
iii) Transfusion associated acute lung injury (TRALI)
iv) Transfusion associated circulatory overload (TACO)
v) Immune modulation (this and TRALI are probably the most significant)
d) The best way to reduce the risk of blood component therapy is to reduce
requirements
i) Minimise unnecessary blood sampling
ii) Minimise blood loss during procedures
iii) Consider nutritional and iron stores state
2. Red Blood Cells
a) Elective *as per NHMRC / ASBT guidelines.
i) Use of RBCs at Hb > 100g/L is likely to be inappropriate
ii) Use of RBCs at Hb < 70g/L is likely to be appropriate but in some
asymptomatic patients a lower threshold may be acceptable
iii) At Hb 70-100g/L clinical assessment of risk versus benefit is required.
iv) The following criteria may indicate RBC transfusion is indicated
Significant ongoing bleeding present or anticipated.
Clinical signs of impaired oxygen transport such as dyspnoea,
tiredness/weakness, angina, syncope.
Cardiac ischaemia or cardiac failure due to anaemia.
v) Order as “Red cells” or RBCs on the ICU or ward fluid chart
vi) “Type & Screen” specimens are held for 10 days for compatibility testing.
vii) For transfusion, a new specimen is needed for cross-match every 72 hours.
b) Resuscitation
i) Abnormal bleeding is usually surgical and requires urgent surgical and/or
radiological intervention.
ii) A full cross-match takes 30 minutes if marked urgent (not including the
time for transfer of blood); this should be performed if possible while
volume is replaced with crystalloid or colloid.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-122-2048.jpg)
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+
2. Hyponatraemia: Na < 130 mmol/l
a) Aetiology / classification
i) Misleading result
Isotonic - Hyperlipidaemia
- Hyperproteinaemia
Hypertonic - Hyperglcaemia
- Mannitol, glycerol, glycine or sorbitol excess
ii) Water Retention
Renal Failure
Hepatic Failure
Cardiac Failure
SIADH
Drugs
Psychogenic polydipsia
iii) Water retention / Salt depletion
Post-operative, post-trauma
Patients with excess fluid losses given inappropriate replacement
Cerebral salt-wasting syndrome
Adrenocortical failure
Diuretic excess
b) Diagnosis & Management:
i) Factitious: ignore and manage underlying condition then recheck Na+
ii) Misleading:
Hyperglycaemia: BGL 10 mmol/l [Na+] 3 mmol/l
a. Hyponatraemia per se is real, but treatment is directed at the
underlying cause, where correction of the hyperglycaemia will
correct the plasma [Na+]
b. NB: Total body Na+ deficit may co-exist with diuresis in DKA
Mannitol:
a. [Na+] early, then diuresis & late [Na+] are more problematic
b. Maintain adequate plasma volume with N.saline initially
Alcohols: permeate solutes, [Na+] less problematic
iii) Hypovolaemic states:
Restore volume with colloid or normal saline according to clinical
markers: urine output, plasma [Na+], RAP
Aim for slow Na+ correction: 2 mmol/l/hr, unless seizures.
Urine Na+ is uninterpretable after diuretics or catecholamines for 24hrs](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-137-2048.jpg)
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iv) Hypervolaemic states: *most common clinically
Fluid restriction < 15 ml/kg/day
a. “Water Excess” ~ (140 - Na+ )/140 × (Wt × 0.6)
e.g., 70kg patient with plasma [Na+] = 120 mmol/l:
= (140 - 120)/140 × (70kg × 0.6)
= 6 litres
b. Will slowly correct excess - ADH group & “reset osmostat”
c. Treat the underlying cause - CCF, nephrotic synd., ascites
v) SIADH
Causes
a. Ectopic ADH production by tumours
e.g. small cell bronchogenic tumour
b. CNS disorders
e.g. tumour, abscess, trauma, SAH etc
c. Pulmonary diseases
e.g. TB, pneumonia, abscess etc
Diagnosis
a. Hypo-osmolar hyponatraemia
b. Urine osmo > plasma osmo
c. Urine Na+ > 40 mosm/l
d. Normal endocrine, renal, hepatic, cardiac function
e. No diuretics or drugs affecting ADH secretion
f. Corrected by water restriction alone
Management: fluid restriction
vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness
Resuscitation / ABC
Consider anticonvulsants - phenytoin, benzodiazepines
Hypertonic saline (3%) may be indicated
a. Always discuss use with the Duty Consultant
b. Correct [Na+] rapidly only to ~ 120mmol/l
Thereafter, slow correction with N.saline over 24-36hrs ( 2 mmol/l/hr)
Treat the underlying cause.
3. Hypernatraemia: Na+ > 145 mmol/l
a) Hypernatraemia is always a hyperosmolar state
+
b) Most body fluids have a [Na ] < plasma net water loss
c) Aetiology / classification:
i) Water depletion / inadequate replacement
Renal
a. Diuretics, glycosuria
b. ARF/CRF, partial obstruction
c. Central diabetes insipidus
i. Post traumatic head injury or surgery
ii. CNS infection, tumour, granulomatous disease, GBS](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-138-2048.jpg)
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d. Nephrogenic diabetes insipidus:
i. 1° : congenital renal resistance to ADH
ii. 2° : hypokalaemia, hypercalcaemia, lithium, multiple
myeloma, sickle cell anaemia, nephrocalcinosis, amyloid
GIT losses - diarrhoea, vomiting, fistulae, SBO
Respiratory - IPPV with dry gases
Skin losses
a. Fever, high ambient temperature
b. Vasodilatory states
c. Exfoliative skin disorders, burns
d. Thyrotoxicosis
Unconsciousness
“Reset osmostat”
ii) Salt gain - Na+ gain > H2O gain
Iatrogenic
a. Most common cause
b. Excess “normal saline” ~ 150 mmol/l [Na+]
c. NaHCO3, feeding formulae, TPN
Mineralocorticoid excess:
a. Conn's, Cushing's syndromes
b. Steroid excess
d) Management
i) Hypovolaemic states
Restore volume according to clinical markers:
BP, HR, urine output, RAP
a. Hartmann’s solution - slightly hypo-osmolar
b. Colloid: initial resuscitation, severe hypovolaemic states
ii) Slow Na+ correction: 2 mmol/l/hr
Water deficit: ~ (Na+ - 140)/140 × (B.Wt × 0.6)
e.g. 70 kg patient, with plasma [Na+] = 160 mmol/l
~ (160-140)/140 × (70 × 0.6)
~ 6.0 litres
1 litre water replacement will reduce [Na+] ~ 3-4 mmol/l
In addition to basal fluid requirements & ongoing losses
Replace over a 24-48 hr period with 5% dextrose
Monitor [Na+] regularly
Manage aetiological causes
Cease causal drugs and inappropriate IVT
DDAVP for central DI only ~ 1-2 µg s.c.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-139-2048.jpg)
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+
4. Hypokalaemia: K < 3.0 mmol/l plasma
K+ < 3.5 mmol/l serum
a) Aetiology / classification:
i) Compartmental / transcellular shift
Alkalaemia pH ~ 0.1 [K+]pl ~ 0.5 mmol/l
Catecholamines / salbutamol
Insulin / anabolism - refeeding effect
Hypomagnesaemia - ICF K+ depletion
Toxic / poisoning - barium, toluene
Familial periodic paralysis
Hypothermia
ii) Reduced intake - urine [K+] < 20 mmol/L
Starvation
TPN
iii) Increased clearance/losses
Renal - urine [K+] > 20 mmol/L
a. Diuretics distal tubular flow
i. Loop agents - frusemide, bumetanide
ii. PT agents - acetazolamide, mannitol
iii. Early DT - thiazides
b. Steroids / Mineralocorticoid excess
i. Conn’s, Cushing’s, Bartter’s syndrome
ii. Ectopic ACTH - Small cell Ca lung
- Pancreatic, thymus carcinoma
iii. Exogenous steroids
c. Drugs
i. Anionic drugs - antibiotics (penicillins, amphotericin)
ii. High dose gentamicin
iii. Lithium
d. Hypomagnesaemia, Hypocalcaemia
e. RTA I, II
GIT losses
a. Villous adenoma
b. Ureterosigmoidostomy
c. Fistulae, malabsorption syndromes
d. Diarrhoea, Laxatives
Skin losses
b) Management:
i) Treat underlying cause
ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis
and hypokalaemia
iii) Always add Mg++
normomagnesaemia is essential for correction of hypokalaemia
iv) Look for and treat concurrent hypophosphataemia](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-140-2048.jpg)
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v) Potassium preparations
KCl: 10 ml = 10 mmol/l
KH2PO4: 10 ml = 10 mmol/l
K-acetate: 5 ml at 5 mmol/ml
25 mmol K+ + 25 mmol acetate (bicarbonate)
5. Hyperkalaemia: K+ > 5.0 mmol/l serum
K+ > 4.5 mmol/l plasma
a) Aetiology / classification:
i) Artefactual
Drip arm specimen
Tourniquet / Haemolysed specimen (extravascular)
Thrombocytosis > 750,000
Leukocytosis > 50,000
ii) Compartmental / transcellular shift
Acidosis pH ~ 0.1 [K+] ~ 0.5 mmol/l
Insulin deficiency: DKA
NB: normo- or hypo-kalaemia in the presence of severe DKA is
associated with a marked total body K+ deficit, which must be
addressed prior to correction of the acidaemia.
Familial periodic paralysis
Suxamethonium
Digoxin, -blocker overdose
Fluoride poisoning
ECF tonicity
a. Water moves from cells → [K+]ICF and passive diffusion
b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg)
c. Hyperkalaemia of DKA is due to this in addition to the acidaemia
& insulin deficiency
iii) Cellular disruption / death
Tissue breakdown
Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion
Severe burns
Tumour lysis syndrome, leukaemia
iv) Increased intake - rarely a problem unless impaired renal function
Massive transfusion
Direct IV/oral
Drugs (penicillins)](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-141-2048.jpg)
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7. “Rules of thumb” *these are approximations only
a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO2
i) Met Acid to min 7.10 e.g. pH 7.25 PaCO2 25 mmHg
ii) Met alkalosis to max 7.60 e.g. pH 7.57 PaCO2 57 mmHg
b) Primary respiratory acidosis:
i) HCO3 ~ 1mmol/l per 10mmHg PaCO2 above 40 to max 30
c) Primary respiratory alkalosis
i) HCO3 ~ 2.5mmol/l per 10mmHg PaCO2 below 40 to min 18
d) Chronic respiratory acidosis
i) HCO3 ~ 4mmol/l per 10mmHg PaCO2 above 40 to max 36
8. Metabolic acidosis
a) Assessment of metabolic acidosis must include the anion gap:
Anion Gap = [Na+ + K+] - [Cl- + HCO3-] ~ 12-17 mmol/l
Unmeasured cations Unmeasured anions
Mg++ ~ 1.2 mmol/l Albumin ~ 15 mEq/l
Ca++ ~ 2.2 mmol/l H2PO4- ~2 mmol/l
IgG Small HSO4- ~1 mmol/l
Organic ~5 mEq/l
~ 7.0 mEq/l ~ 23 mEq/l
b) This allows sub-classification of metabolic acidosis into raised or normal anion
gap acidoses.
i) Beware a low [Alb] in critically ill lowering the measured AG
ii) Measurement of chloride in the lab is highly variable
iii) Assessment of the AG must be viewed within the clinical context.
c) Aetiology of raised anion gap:
i) Renal failure - H2PO4- , HSO4- (rarely AG > 23)
ii) Lactic acidosis - types A&B
* normal AG does not exclude a lactic acidosis
iii) Ketoacids - -OH-butyrate, acetoacetate
- diabetes mellitus, starvation, alcohol
iv) Rhabdomyolysis - organic acids
v) Drugs / poisons:
Aspirin - salicylate, lactate, ketones
Paracetamol - lactate, pyroglutamate
Ethanol - acetoacetate, lactate
Methanol - formate (formaldehyde), lactate
Paraldehyde - formate, acetate, lactate, pyruvate
Ethylene glycol - oxalate
Xylitol, Sorbitol - lactate
Fructose - lactate](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-143-2048.jpg)
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Table: Classification of Lactic Acidosis
Type A Type B Drug induced Hereditary
Severe exercise Thiamine deficiency Phenformin G6PD deficiency
Seizures Diabetes Metformin Fructose-1,6-DP-
Cardiac arrest Hepatic failure Ethanol deficiency
Shock Renal failure Methanol
Hypoxia Infection Salicylates
Anaemia Leukaemia, lymphoma IV fructose
Pancreatitis Xylitol
Short bowel syndrome Sorbitol
d) Aetiology of low or normal anion gap:
i) Hyperchloraemic metabolic acidosis
Resolving renal failure
Resolving DKA
Renal tubular acidosis / carbonic anhydrase inhibitors
Mineralocorticoid deficiency
Pancreatic, enteric fistulae
Ureterosigmoidostomy
IV HCl, NH4Cl, Arginine
ii) Metabolic alkalosis due to HCO3- gain
iii) Hypoalbuminaemia
iv) Myeloma - IgG has positive charge, 's AG
v) Increased Mg++ or Ca++ (rarely)
vi) Artefactually elevated Cl-
vii) ? Hyperlipidaemia
e) Management
i) High anion gap
Treat the underlying cause
No indication for NaHCO3
ii) Normal anion gap
Treat the underlying cause.
Replace HCO3 serum level and losses
a. Approx. deficit = (24 - [HCO3]) × (Wt. × 0.6) mmol/l
e.g. for a 70kg patient with a [HCO3] = 4 mmol/l
deficit = (24 - 4) × (70 × 0.6)
= 840 mmol (= ml of standard bicarb solution)
b. Replace 1/3-1/2 of this amount then remeasure blood gases.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-144-2048.jpg)
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d) Prerequisites
i) Adequate glottic reflexes should be present to protect from aspiration -
moribund patients require intubation where appropriate.
ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B.
iii) Selected patients may be managed in Unit C.
e) Complications
i) Inadequate ventilation.
ii) Mask leaks.
iii) Aerophagia, gastric distension, vomiting, aspiration.
iv) Claustrophobia and mask intolerance.
v) Pressure necrosis of nasal bridge.
vi) Dry secretions.
vii) Barotrauma.
viii) Reduced preload and hypotension.
ix) Raised intracranial and intraocular pressure.
7. Non-Invasive Ventilators
a) BiPAP® Vision
i) Microprocessor controlled.
ii) Nasal, face & full head masks can be used.
iii) IPAP = Inspiratory positive airway pressure.
iv) EPAP = Expiratory positive airway pressure (PEEP).
v) Pressure support = IPAP - EPA
vi) Monitors machine pressure against proximal airway (mask pressure) to
ensure effective delivery of pressure despite circuit leaks.
vii) Need to calibrate for tubing and mask.
viii) Uses internal algorithm for respiratory cycling and leak adjustment.
ix) Liquid crystal displays:
IPAP, EPAP, Rate, FiO2.
VT, Vmin, PIP, Insp. time/total cycle time.
Leak (patient & total), % patient triggered breaths.
Graphical display of pressure, volume & flow.
x) Operation:
Machine starts up in mode previously used.
Press [Mode] hard key to display CPAP or S/T mode
Press [Activate New Mode] soft key to select the new mode.
Select soft key parameters displayed & turn adjustment knob
accordingly.
CPAP Mode - Default settings
a. CPAP 5cmH2O, FiO2 1.0
S/T Mode - Default settings
a. IPAP 15cmH2O, EPAP 5cmH2O
b. FiO2 1.0, Rate 12, TInsp 1 sec, IPAP rise time 0.1 sec](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-157-2048.jpg)
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g) Pressure Support (PS) + PEEP
i) Total inspiratory pressure, when using PS on the Evita, is the dialed value
plus dialled PEEP value
ii) Mode = CPAP
iii) Rise time = 0.2 secs
iv) PS = 10 cmH2O
v) PEEP = 5 cmH2O
vi) FiO2 = 1.0
h) I:E Ratio
i) Alteration of the I:E ratio is potentially hazardous and should only be done
following discussion with the duty consultant.
i) Measurement of auto-PEEP
i) Not accurate if patient effort, patients should be well sedated / paralysed.
ii) Measurement of intrinsic PEEP at end expiration + closed airway.
iii) Press the [Special Procedure] button & select [PEEPi].
iv) Press [Start] to begin the automatic 7sec manoeuvre.
v) Read off the PEEPi and trapped gas volume (VTrap)
vi) The value displayed includes applied PEEP, so:
vii) auto-PEEP = PEEPi - applied PEEP
j) Measurement of occlusion pressure (P0.1)
i) Measurement of the negative airway pressure generated in the first
100msec of inspiration against an occluded airway.
ii) Reflects diaphragmatic effort and neuromuscular drive.
iii) Normal value 3-4 mbar.
iv) Press [Special Procedure] button.
v) Select P0.1 and press [Start] to measure value.
k) Always examine the flow, pressure and volume vs time loops
i) Upper/lower airway obstruction.
ii) Recruitable lung.
iii) Increased airway resistance.
iv) Dynamic hyperinflation
e.g. flow does not return to baseline before the next breath
v) Sudden reversal of flow / pressure which does not trigger a breath may
indicate wasted patient effort.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-161-2048.jpg)
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14. RAH – ARDS Ventilation
a) Initial Ventilator Set-up and Adjustments (Dräger)
i) Mode: SIMV + PS
ii) Resp. Rate: 18 bpm
iii) Insp. Flow Rate: Autoflow
iv) Tidal Volume: 6 ml/kg IBW
b) Tidal Volume Settings are determined by calculated Ideal Body Weight
i) Males = 0.91 × (height [cm] – 152.4) + 50
ii) Females = 0.91 × (height [cm] – 152.4) + 45.5
iii) Calculate IBW and VT = 6 x IBW
c) Adjust RR to achieve the pH goals according to ABG’s.
i) After any RR change, check the I:E ratio and TInsp.
ii) Target I:E Ratio 1:1 – 1:3
iii) Maintain TInsp 0.8 sec.
d) Adjust VT according to inspiratory plateau pressure (PPlat) goals.
i) Target PPlat < 30cmH2O
ii) Check PPlat with a 2 sec inspiratory pause every 4 hrs and after each change
in PEEP or VT.
iii) Method (Dräger): [Measurements] + press [Insp Hold] for 0.5sec
PPlat will appear on the screen for 1 sec.
iv) PPlat > 30cmH2O
VT by 1 ml/kg IBW steps (min VT = 4ml/kg IBW).
v) PPlat < 25cmH2O and VT < 6ml/kg IBW
VT by 1ml/kg IBW.
vi) NB: Observe spontaneous tidal volumes and adjust PS downwards if
volumes generated are higher than the calculated goal VT.
e) Adjust FiO2 & PEEP according to SpO2 and PaO2.
i) Goal PaO2 = 55-80mmHg
or SpO2 = 88-95%.
ii) Use the table (right) to adjust FiO2 / PEEP combinations FiO2 PEEP
for the target PaO2 range required, e.g. 0.3 5
If FiO2 = 0.4 / PEEP = 5 and the PaO2 = 54, 0.4 5
PEEP to 8 cmH2O 0.4 8
If FiO2 = 0.9 / PEEP = 14 and the SpO2 = 99% 0.5 8
FiO2 to 0.8 0.5 10
0.6 10
f) Other therapies that may improve oxygenation. 0.7 10
i) Recruitment Manoeuvres 0.7 12
ii) Prone Ventilation 0.7 14
iii) Nitric Oxide / Nebulised prostacylcin. 0.8 14
iv) ECMO 0.9 14
0.9 16
None proven – see over.
1.0 16](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-162-2048.jpg)
![166
D. Management of Cardiothoracic Patients
1. General Principles
a) The following guidelines apply to elective post-cardiac surgical patients.
b) These are only guidelines and each individual consultant will manage the
patients as is clinically indicated.
2. Respiratory:
a) Following surgery use the following default ventilator settings:
i) FIO2 =1.0
ii) SIMV 12 × 600, PS 10cmH2O, PEEP 5cmH2O.
b) After the first ABG, adjust the FIO2 to maintain a PaO2 > 80mmHg
c) Wean from ventilation according to past history, surgery performed and current
clinical status
d) Suggested extubation criteria:
i) Temperature > 36C
ii) Awake, able to obey commands
iii) Adequate analgesia
iv) Cardiovascular stability on minimal inotropes
(< 10µg/min noradrenaline or adrenaline)
v) Adequate gaseous exchange:
PaO2 > 80 mmHg on FIO2 0.5, PEEP 5cm
vi) Bleeding: drain losses < 100 ml/hr
e) Respiratory failure post-extubation secondary to collapse / consolidation is
common.
i) Ensure good analgesia and frequent, effective physiotherapy
ii) CPAP may be required in the first 48 hours.
f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to
extubation failure and may benefit from the use of ACE inhibitors or inodilators
prior to extubation.
3. Post-operative bloods:
a) Check CBE, U&E, Mg, ACT, APPT, INR and ABGs on all patients.
b) Maintain [K+] > 4.0 mmol/l
4. Hypotension
± increasing inotrope requirements may occur for a variety of reasons:
a) Hypovolaemia
i) Return any remaining pump blood as soon as possible.
ii) Correct fluid/blood losses as appropriate
iii) Check ECG
b) Low cardiac output states
i) Noradrenaline is the first choice vasopressor.
ii) Low dose dobutamine (to improve regional blood flow to splanchnic/renal
vascular beds), may also be considered.
iii) Adrenaline can be used for severely impaired ventricles.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-166-2048.jpg)
![178
8. CVVHDF Equipment
a) Dialysis catheters
i) Priority of site placement and optimal catheter length:
R.IJ R.SC L.IJ L.SC Femoral
15cm 15cm 20cm 20cm 25cm
ii) Use Dolphin Protect® high flow catheter guided as above
iii) Heparin lock all catheter lumens 8 hourly when not in use
5000U in 3 mls, divided equally into both lumens.
b) Filters
i) Older filters were made from cellulose and would often initiate an
inflammatory response (i.e. “membrane reaction”).
ii) Membranes are now synthetic (polycarbonate, polyacrylonitrile)
iii) These are more permeable and biocompatible
iv) Standard filter = Prisma® AN69:
Membrane = acrylonitrile
Membrane thickness = 50m.
Surface area = 1m2 /1.5m2 (RT-150)
(larger filters 1.2–2m allow blood flow and clearance)
2
Blood volume in set = 150ml
c) Dialysis machine settings
i) The PrismaFlex® is the standard dialysis machine at the RAH
ii) Older “Prisma” machines are still in use but are being phased out.
d) For patients on ECMO
i) CVVHDF can be performed via the ECMO circuit without additional Vas-
Cath placement.
ii) Must be discussed with ICU consultant supervising ECMO
9. Prescribing CVVHDF
a) Orders for the PrismaFlex or Prisma® should be written on a standard sticker.
b) The following variables require assessment/prescription for CVVHDF.
c) Haemofiltration solution (“replacement”).
i) Standard solution = Gambro Phoxilium.
ii) Hemosol B-Zero will remain available when required for:
A [K+] < 4 mmol/l (e.g. severe hyperkalaemia), or
A phosphate free solution (e.g. tumour lysis syndrome)](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-178-2048.jpg)
![180
vi) Regional anticoagulation
Citrate (see citrate protocol)
Heparin
a. Utilised when:
Maintenance of filter life is problematic.
Systemic anticoagulation and citrate are contraindicated
No contraindication to heparin administration.
b. The circuit still needs to be primed with heparin
c. Heparin is administered pre-filter as above
d. Protamine 5-10 mg/hr post-filter
e. Check APTT 6 hourly after any dose changes.
vii) For patients with heparin induced thrombocytopenia (HIT) consider
Danaparoid or lepirudin (systemically, not into circuit – see protocol)
Prostacyclin 5 ng/kg/min (see protocol)
g) Fluid removal
i) Determine how much fluid should be removed from the patient.
ii) Consider its effects on patient haemodynamics
iii) The amount of fluid removed is the difference between the effluent and the
dialysate plus replacement fluid volumes
h) Potassium
i) Gambro® Phoxilium contains 4 mmol/l potassium and will not require
additional potassium
ii) Haemosol B-zero solution contains no potassium.
Supplementary K+:
a. Required for all patients, except in the initial management phase
of marked hyperkalaemia
b. Should to be added to both the replacement & dialysate bags
Plasma K+ < 4.0 mmol/l = 20 mmol / bag
Plasma K+ 4.1 – 4.8 mmol/l = 15 mmol / bag
Plasma K+ 4.9 - 5.5 mmol/l = 10 mmol / bag
Plasma K+ 5.5 – 6.0mmol/l = 5 mmol / bag
Plasma K+ > 6.0 = 0 mmol / bag
c. K-Acetate can be used in severe acidosis:
Acetate is effectively metabolised to HCO3- via the liver
Vial = 25mmol/5ml, dose = 3-4mls per 5L bag
iii) Target plasma [K+] = 3-4mmol/L
i) Drug prescription
i) Consult Antibiotic Guidelines / Pharmacy regarding antibiotic dosing
e.g. meropenem, ciprofloxacin, fluconazole
ii) Monitor drugs that are renally cleared and potentially toxic
e.g. gentamicin, vancomycin, digoxin](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-180-2048.jpg)
![182
v) Ionized calcium should be checked 30 min post-commencement, both
Post-filter (blue port)
a. Target ionized calcium: 0.3-0.5mmol/l
b. If > 0.5mmol/l [citrate] by 0.3-0.5mmol/l
c. If < 0.3mmol/l [citrate] by 0.3-0.5mmol/l
d. The usual citrate concentration range is 1.5-4.0mmol/l
Arterial
a. Target ionized calcium: 0.9-1.1 mmol/l.
b. Calcium replacement should be commenced with dialysis.
c. If [Ca2+] < 0.9 or there is a strong downward trend
commence infusion via CVC: CaCl 10% 4ml/hr.
d. After calcium is commenced arterial levels should be checked
hourly until stable.
e. Infusion rates should be adjusted by 1ml/hr until arterial calcium
is in the target range
f. If dialysis is ceased the calcium infusion should be stopped.
g. The Prismaflex will display an alert to this effect
(software v6.1 will automatically cease calcium infusion)
vi) Post-filter and arterial calcium should be monitored 2 hourly until stable
then checked 8 hourly
vii) With Prismaflex software v6.1 (due 2012)
Calcium replacement occurs via the ‘heparin syringe’ on the
Prismaflex using a Gambro algorithm.
Separate replacement is unlikely to be necessary.
Check Ca2+ via arterial analysis 8 hourly.
e) Complications
i) Hypocalcaemia:
Calcium is removed via:
a. Clearance of citrate:Ca2+ complexes during haemofiltration
b. Dialysis against calcium free dialysate
In the presence of citrate bound calcium fraction falls and may be as
low as 20%.
The systemic binding of calcium to citrate contributes to a small
degree, however this component reverts as citrate is metabolised.
Unless using Prismaflex software v6.1, separate replacement of
calcium via a CVC is recommended – see above.
ii) Hypercalcaemia:
May occur due to excess calcium replacement.
Corrected by monitoring and appropriate titration of CaCl.
iii) Acidosis:
Possible in advanced liver failure due to accumulation of citric acid.
Citrate anticoagulation is relatively contraindicated in liver disease.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-182-2048.jpg)
![191
e) Prevention and treatment of vasospasm
i) Specific drug therapy:
Nimodipine:
a. Indications
i. CT proven SAH
ii. IV preferably through central line (2 mg/hr)
*may be given through a peripheral IV
iii. Change to oral as soon as possible (60mg 4hrly)
b. Complications: hypotension (may require cessation of nimodipine)
Statins (simvastatin 80mg daily) may reduce the incidence of
radiological vasospasm and improve outcomes following SAH.
ii) Triple H therapy (hypertension / hypervolaemia / haemodilution):
Has no role in the prevention of vasospasm
prophylactic HHH therapy may be harmful
It is imperative to avoid hypotension and hypovolaemia.
Patients should have fluid therapy targeted at maintaining euvolaemia.
iii) Euvolaemic hypertension
May be indicated in selected patients with proven vasospasm post-
aneurysmal clipping / coiling.
Induced hypertension must be titrated to a mean arterial pressure:
systolic BP is not an accurate indicator of cerebral perfusion pressure.
Principles:
a. Discuss with ICU consultant prior to initiating therapy
b. Intra-arterial pressure monitoring is mandatory
c. Maintain IV volume
i. Continue IV filling until clinically euvolaemic
ii. Avoid volume overload (pulmonary congestion/oedema)
iii. Monitor electrolytes 8 hrly normal osmolality and [K+].
d. Commence noradrenaline titrated to:
i. MAP > 90mmHg, or
ii. MAP > 10mmHg above premorbid baseline
(for known hypertensive patients), or
iii. MAP 5-10mmHg > “defined MAP”
On occasions there may be neurological improvement at a
certain MAP titrate therapy 5-10mmHg above this
iv. Reset target MAP if high doses (> 10g/min) are required, or
if polyuria, arrhythmias or other complications ensue.
Complications:
a. Pulmonary oedema, hypoxia
b. Cardiac arrhythmias, myocardial ischaemia
c. Polyuria, electrolyte disturbances
iv) Chemical (papaverine / verapamil) or balloon angioplasty
Limited role in angiographically proven vasospasm
Requires transport for angiography and may be performed on
consecutive days.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-191-2048.jpg)
![206
iii) May be potentially useful following:
Iron overdose > 60mg/kg
Slow release potassium chloride > 2.5mmol/kg
Major slow release verapamil or diltiazem ingestion
Symptomatic arsenic trioxide ingestion
Lead ingestion
Body packers (heroine)
iv) Contraindications
Good outcome expected with standard care
Uncooperative patient
Uncontrollable vomiting
Reduced GCS or seizures expected in subsequent 4 hours
Ileus or bowel obstruction
Intubated patients (relative)
v) Technique
Polyethylene glycol solution (standard endoscopy bowel prep.)
Administer via correctly placed nasogastric tube at 2L/hour
(25ml/kg/hr in children)
To minimize vomiting start at a slower rate & titrate up as tolerated
Administer metoclopramide to enhance gastric emptying
Be prepared for explosive diarrhoea
- sit on commode or place effluent tube for example
Continue until rectal effluent is clear or an ileus/abdominal distension
occurs.
3. Osmolal Gap
a) OG = Measured – calculated osmolality
b) Calculated Osmo = 2×[Na + K] + Gluc + Urea + ethanol
c) Baseline osmolar gaps are highly variable in the normal population.
d) Evaluation of potential toxic alcohol ingestion requires serial assessments over
time looking for a characteristic pattern with worsening acidaemia, increasing
anion gap and decreasing osmolar gap.
e) Single measurements may confirm an ingestion but are not reliable in excluding
it.](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-206-2048.jpg)
![215
g) Toxic alcohols
i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are
used as industrial solvents, cleaning agents and reactants.
ii) Accidental ingestions are rarely of sufficient volume to cause toxicity
iii) Deliberate ingestion is associated with severe metabolic acidosis,
multiorgan dysfunction and potentially death.
iv) Cause an initial “ethanol like” intoxication followed by a progressive
metabolic acidosis and compound specific end-organ toxicities, e.g.
Retinal toxicity/blindness (methanol)
Acute renal failure (multiple agents)
Seizures (multiple agents)
Refractory hypotension (multiple agents)
Delayed neurological sequelae (diethylene glycol)
v) Diagnosis is based upon a history suggestive of ingestion and a
characteristic evolution of metabolic acidosis
Initially: osmolar gap (OG) + normal pH and anion gap (AG)
Evolution of acidosis with pH, OG and AG
Variability in osmolar gap amongst the normal population is such that
a single assessment of acid-base, AG and OG is insufficient to
exclude significant exposure (although it may confirm it)
vi) Specific treatment
Ethanol
a. Commence ASAP, regardless of symptomatology, in all with:
i. Acidosis, or
ii. An elevated OG (with or without acidosis),
b. Check baseline BAL, if > 0.1g/dl a loading dose is not required
c. Titrate to BAL 0.1-0.2g/dL while on dialysis
d. May be given orally (via NGT) or by IV infusion
e. Oral protocol *avoid in ICU if possible
i. Loading dose of 1.8ml/kg of 43% ethanol
(4 x 30ml vodka shots for a 70 kg adult)
ii. Maintenance infusion of 0.2-0.4 ml/kg/hr
(1 x 40ml vodka shot per hour)
f. Intravenous protocol
i. Loading dose: 8ml/kg of 10% ethanol
ii. Maintenance: 1-2ml/kg/hr of 10% ethanol
g. Actual requirements vary widely between individuals, and serial
blood alcohol assessments are required to ensure a level within the
target range
h. If on CVVHDF, then safer to dialyse against desired [ETOH]
i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement)
ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag](https://image.slidesharecdn.com/manualicu-130407013333-phpapp02/75/Manual-icu-215-2048.jpg)
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Manual icu
This document is a medical manual for the Royal Adelaide Hospital Intensive Care Unit from 2012. It provides information on administration, clinical procedures, drugs and infusions for ICU staff. The manual aims to standardize patient management through protocols and guidelines derived from evidence and experience. It contains sections on staffing, admission/discharge policies, documentation, consent, ward rounds, clinical duties, procedures, cardiovascular and respiratory drugs, sedation, and more. The director notes that while aiming for accuracy, errors may exist and staff should notify the duty consultant of any issues.
Manual icu
- 1. 1 Royal Adelaide Hospital IntensiveCare Unit Medical Manual 2012 Edition http://icuadelaide.com.au/
- 2. 2 FOREWORD Welcome to Intensive Care. This manual has been written to facilitate the daily running of the RAH Intensive Care Unit. It is by no means the definitive answer to all intensive care protocols and procedures, nor is it designed to be a textbook. A standardised approach to management is desirable for optimal patient care and safety, improving communication and understanding between members of the ICU team and associated specialties. This approach provides a common platform for staff who come from different countries and training backgrounds. The manual outlines various Protocols, which represent a standard approach to practice within the Unit. These have been derived from the available literature, clinical experience and where appropriate, cost-effectiveness. Guidelines designed to assist in clinical management are included but patient management will ultimately depend upon the clinical situation. Consultants may modify these guidelines on consideration of the nuances of a particular clinical case. Registrars wishing to go outside the guidelines should discuss this with the Duty Consultant before proceeding. Assistance is always available from the Duty Consultant and senior nursing staff. Use your time in the Unit to get the most out of the large clinical caseload. Ask questions about clinical problems, equipment and procedures with which you are unfamiliar. There are numerous textbooks, journals and references available in the Unit. This manual has undergone numerous changes, with contributions from many of the ICU staff and from other specialty services within the hospital. The contents of this manual are produced from the consensus views of the senior medical staff. We aim to make the information in this manual as accurate and consistent with the available evidence as possible at the time of publication. However no guarantee can be provided that errors do not exist – please notify the Duty Consultant if you identify any errors of fact. A/Prof Robert Young Director 2012 12th Edition
- 3. 3 CONTENTS FOREWORD ....................................................................................................................... 2 CONTENTS......................................................................................................................... 3 PART 1 - ADMINISTRATION .............................................................................................. 6 A. Staffing - Royal Adelaide Hospital ICU ............................................................... 6 B. Rostering and Job Descriptions ............................................................................. 8 Table: Team Duties .............................................................................................. 8 Table: Registrar Shifts ....................................................................................... 10 C. Orientation .......................................................................................................... 11 D. Weekly Programme............................................................................................. 12 Table: Weekly Unit Programme ........................................................................ 12 E. Admission and Discharge Policies ...................................................................... 13 F. Care for Patients Discharged from ICU for Terminal Care. ............................... 15 G. Clinical Duties in the ICU ................................................................................... 16 H. Documentation .................................................................................................... 19 I. Consent in ICU ................................................................................................... 21 J. ICU Ward Rounds............................................................................................... 22 K. Clinical Duties Outside of the Intensive Care Unit ............................................. 23 L. Hospital Emergencies ......................................................................................... 28 M. Research in ICU .................................................................................................. 29 N. Information Technology in ICU.......................................................................... 30 PART 2 - CLINICAL PROCEDURES .................................................................................. 31 A. Introduction ......................................................................................................... 31 B. Procedures ........................................................................................................... 31 C. Peripheral IV Catheters ....................................................................................... 32 D. Arterial Cannulation ............................................................................................ 33 E. Central Venous Catheters.................................................................................... 34 F. Urinary Catheters ................................................................................................ 36 G. Epidural Catheters ............................................................................................... 37 H. PICCO Catheters ................................................................................................. 37 Table: PiCCO Values and Decision Tree ........................................................... 38 I. Pulmonary Artery Catheters ................................................................................ 39 Table: Standard Haemodynamic Variables ........................................................ 41 J. Pleural Drainage.................................................................................................. 42 K. Endotracheal Intubation ...................................................................................... 44 L. Weaning Guidelines ............................................................................................ 49 Flowchart: Ventilation Weaning Protocol.......................................................... 50 M. Extubation ........................................................................................................... 50 N. Emergency Surgical Airway Access ................................................................... 52 O. Fibreoptic Bronchoscopy .................................................................................... 53 P. Tracheostomy ...................................................................................................... 54 Q. Cardiac Pacing .................................................................................................... 57 R. Pericardiocentesis................................................................................................ 60 S. Intra-Aortic Balloon Counterpulsation................................................................ 61 T. Gastric / Oesophageal Tamponade Tubes ........................................................... 64
- 4. 4 U.Extracorporeal Membrane Oxygenation.............................................................. 65 PART 3 - DRUGS AND INFUSIONS.....................................................................................66 A. Policy ................................................................................................................... 66 B. Principles of Drug Prescription in Intensive Care ............................................... 67 C. Cardiovascular Drugs .......................................................................................... 67 Table: Cardiovascular Effects of Catecholamines .............................................. 68 Table: Inotropic Agents Used in ICU ................................................................. 69 Table: Vasopressors............................................................................................ 70 Table: Antihypertensive & Vasodilator Agents.................................................. 71 Table: Antiarrhythmic Agents ............................................................................ 74 Table: Thrombolytics ......................................................................................... 77 Table: Antiplatelet Agents .................................................................................. 78 D. Respiratory Drugs................................................................................................ 79 Table: Bronchodilators ....................................................................................... 80 E. Sedation, Analgesia and Delirium ....................................................................... 81 Table: Nurse Controlled Sedation Protocol ........................................................ 82 Table: Modified Richmond Agitation Sedation Scale (RASS) .......................... 82 Table: Drugs Associated with Increased Delirium ............................................. 84 Flowchart: Confusion Assessment Method for ICU (CAM-ICU) ..................... 85 Table: Sedatives / Analgesics ............................................................................. 86 F. Muscle relaxants .................................................................................................. 88 Table: Muscle Relaxants .................................................................................... 88 G. Anticoagulation ................................................................................................... 89 Table: HITS Probability Score – ‘4T Score’ ...................................................... 92 Table: Anticoagulants ......................................................................................... 93 Table: Heparin Infusion Protocol ........................................................................ 94 Table: Lepirudin Infusion Protocol ..................................................................... 94 H. Endocrine Drugs .................................................................................................. 96 Flowchart: Blood Glucose Management in ICU ................................................ 97 Table: Insulin Infusion Protocol ......................................................................... 97 Table: Steroid Doses / Relative Potencies .......................................................... 99 I. Renal Drugs - Diuretics ................................................................................... 100 Table: Diuretics ................................................................................................ 101 J. Gastrointestinal Drugs ....................................................................................... 102 Table: GI Drugs ................................................................................................ 103 K. Antibiotics ......................................................................................................... 104 Table: Vancomycin Dosing Schedule .............................................................. 106 Table: Antibiotic Infusion Schedules ............................................................... 107 Table: Peri-operative Antibiotic Prophylaxis ................................................... 109 Table: Perioperative Endocarditis Prophylaxis................................................. 110 Table: Empiric Antibiotics ............................................................................... 111 Table: Antibiotics for Specific Organisms ....................................................... 113 PART 4 - FLUIDS AND ELECTROLYTES .........................................................................114 A. Principles of Fluid Management in Intensive Care............................................ 114 Table: Common IV Solutions ........................................................................... 115 B. Nutrition ............................................................................................................ 116
- 5. 5 Flowchart: Nutritional Therapy Protocol ......................................................... 117 Table: Average Daily Requirements ................................................................ 120 Table: Baxter TPN Solution Options ............................................................... 121 C. Blood Component Therapy ............................................................................... 122 Table: Critical Bleeding (Massive Transfusion) .............................................. 124 Table: Guidelines for the Management of an Elevated INR ............................ 128 Table: Pre-operative Dabigatran Management................................................. 131 Flowchart: Management of Bleeding Patient on Dabigatran ........................... 132 Table: Blood Transfusion Reactions ................................................................ 135 D. Guidelines for the Management of Electrolytes ................................................ 136 Table: Classification of Lactic Acidosis .......................................................... 144 PART 5 - CLINICAL MANAGEMENT .............................................................................. 147 A. Cardiopulmonary Resuscitation ........................................................................ 148 Flowchart: Basic Life Support ......................................................................... 148 Flowchart: Advanced Life Support .................................................................. 149 Flowchart: Paediatric Cardiorespiratory Arrest ............................................... 150 Induced Hypothermia Post Cardiac Arrest........................................................ 151 B. Failed Intubation Drill ....................................................................................... 152 Flowchart: Failed Intubation Drill ................................................................... 153 C. Respiratory Therapy .......................................................................................... 154 Table: Oxygen Delivery Devices ...................................................................... 154 Table: Oxygen Delivery Percentage - Nasal High Flow .................................. 156 D. Management of Cardiothoracic Patients ........................................................... 166 Flowchart: Arrest Post Cardiac Surgery........................................................... 168 Flowchart: Bleeding Post Cardiac Surgery ...................................................... 169 Table: Antibiotic Prophylaxis for Cardiac Surgery .......................................... 170 E. Renal Failure ..................................................................................................... 171 Table: Haemodialysis Solutions ....................................................................... 179 Prismaflex – ST 150 Circuit .............................................................................. 184 Form: Dialysis Data for Drug Overdose .......................................................... 185 F. Neurosurgical protocols .................................................................................... 186 Flowchart: Cerebral Perfusion Pressure Algorithm .......................................... 189 Table: World Federation of Neurosurgeons Classification .............................. 190 G. Microbiology Protocols..................................................................................... 195 Flowchart: Antifungal Treatment in Immunosuppressed Patients ................... 201 H. Drug Overdose .................................................................................................. 204 Flowchart: The Unconscious, Undetermined Overdose .................................... 207 Graph: Modified Rumack-Matthew Nomogram .............................................. 209 Flowchart: Acute Paracetamol OD - Known Time of Ingestion ...................... 210 Flowchart: Repeated Supratherapeutic Paracetamol Ingestion ........................ 211 Table: N-Acetylcysteine Administration ......................................................... 211 I. Bites and Envenomation ................................................................................... 220 J. Limitation of Therapy ....................................................................................... 221 K. Brain Death and Organ Donation ...................................................................... 221 L. Donation After Cardiac Death (DCD) .............................................................. 226 Table: Contact Phone Numbers ....................................................................... 229
- 6. 6 PART 1 - ADMINISTRATION A. Staffing - Royal Adelaide Hospital ICU 1. Consultant Medical Staff Director A/Prof Rob Young Deputy Director Dr Peter Sharley Director of Research A/Prof Marianne Chapman Supervisor of Training Dr Nick Edwards Consultants Dr Mike Anderson Dr Stuart Baker Dr David Clayton Dr Adam Deane Dr David Evans Dr Mark Finnis A/Prof Arthas Flabouris Dr Ken Lee Dr Matt Maiden Dr Stuart Moodie Dr Richard Newman Dr Ben Reddi Dr Richard Strickland Dr Krishnaswamy Sundararajan A/Prof Mary White Dr Alex Wurm 2. Senior Nursing Staff Nursing Director: Mr Ian Blight Clinical Services Coordinators: Ms Deb Herewane Ms Ros Acott Ms Tracey Cramey Mr Michael Schwarz Mr Steve Wills Nurse Managers: Ms Ali Coventry Ms Heather Pile
- 7. 7 3. Administrative Staff Administrative Manager Ms Melissa Filleti Resource Accountant Ms Tammy Moffat Team Leader / Roster Manager Ms Sherridan Clark Unit Secretary Ms Kristina Gabell Ward Clerks Ms Ali Fraser Ms Lisa Migliaccio Mr Gavin Sain 4. Registrars a) Three levels of registrars are rostered in the unit: i) Senior Registrars (SR): Advanced trainees in the College of Intensive Care Medicine (CICM) (or equivalent training program) Have completed or near completed specialist training. Take “first on-call” at night and experience responsibility at a consultant level. The SRs help manage the registrar roster, coordinate registrar presentations, simulator training and contribute to teaching activities. ii) Senior Trainees: Usually CICM trainees (or equivalent) Rostered according to seniority and experience. iii) Junior Trainees/RMOs: Vocational trainees, trainees in other specialist programs e.g. surgical, physician training, etc Residents in general rotations. b) Portfolios are determined by experience and rostering requirements. c) All registrars, except SRs, will rotate through Units A, B and C. d) Training positions at Royal Adelaide Hospital: i) Intensive Care Positions The College of Intensive Care Medicine has accredited the RAH as a C24 Unit for training for the fellowship in intensive care (FCICM). Registered CICM trainees may undertake their full 24 months of core ICU training at the RAH. Non-CICM-trainee registrars wishing to gain further postgraduate experience in intensive care may apply for these positions. Applications including a current c.v. should be forwarded to: Dr Alex Wurm. (alex.wurm@health.sa.gov.au) Trainees in formal training programs are given appointment priority.
- 8. 8 ii) Positions for non-intensive care trainees Rotations of registrars in these positions are made from the respective specialty based training programs at the RAH. Anaesthesia trainees: 1 position (3 or 6 month term). Physician trainees: 1 position (3 or 6 month term). Surgical trainees: 1 position (3 or 6 month term). Emergency Medicine trainees: 2 positions (3 or 6 month term). iii) Supervisors of Training at Royal Adelaide Hospital: Intensive Care: Drs Nick Edwards & Peter Sharley Medicine: Dr S M Guha Anaesthesia: Dr I Banks Surgery: Mr P G Devitt Emergency Medicine: Dr R Dunn B. Rostering and Job Descriptions Table: Team Duties 0800 - 1900 Consultant Team A Manages Unit A ICU Team A Senior Registrar A Manages Unit A, TPN Beds 1-12 Registrar A1 (D1) Beds 1-6. Registrar A2 (D2) Beds 7-12. Consultant Team B Manages Unit B ICU Team B Senior Registrar B Manages Unit B Beds 12-24 Registrar B1 (D3) Beds 13-18 Registrar B2 (D4) Beds 19-24 Consultant Team C Manages Unit C ICU Team C Registrar C1 (D5) Beds 25-34 Unit C, Beds 25-34. Registrar C2 (D6) Duty Intensivist Bed management, Ward consults Speed Dial 1650 D7 registrar Consults, Code blue, TPN CICU Consultant Cardiothoracic ICU Consultant Teaching Consultant Undergraduate and postgraduate teaching
- 9. 9 1830 -0830 ICU 1st On-Call Attends evening handover round. Consultant / Senior Registrar On-call for any problems overnight. ICU 2nd On-Call Consultant Backs-up ICU 1st on-call when required. Night Registrar 1 (N1) Beds 1-12 Night Registrar 2 (N2) Beds 13-24 Night Registrar 3 (N3) Beds 25-34 Consults, Code blue calls. Night Senior (NS) Oversees beds 1-34, allocates workload Senior Registrar 1 First Consultant call Wednesday and Saturday Senior Registrar 2 First Consultant call Thursday and Sunday NB: The allocation of responsibilities overnight is at the discretion of the registrars present and should be established by mutual agreement between the registrars and consultant on call. It is assumed that all registrars will maintain an awareness of all patients in ICU and will provide assistance in other areas of the ICU if required. Hence the workload should be spread evenly and all registrars should be allowed to have their required (and reasonable) rest periods. 1. Roster Guidelines a) Rosters are primarily designed to meet training and patient care requirements, taking into account overall staff numbers and skill-mix. b) In addition, award requirements, occupational health & safety considerations, and individuals’ preferences and requests are taken into account. c) The system is not infallible – if there is a problem with any aspect of the roster, please notify the ICU secretary as soon as possible. d) Each roster covers a 4 week period, with the working week commencing on a Wednesday. e) Rosters are usually posted two weeks in advance. f) Where possible you will be rostered two or more days-off following night duty. g) When rostered to night duty, you are not expected to attend weekly teaching sessions, as this would result in unsafe work hours. h) The rostering system utilises a wide variety of different codes as set out in the following table:
- 10. 10 Table: Registrar Shifts Abbr Shift Description Times & Meal Breaks Hrs SR Senior Registrar 08:00-18:00 9.5 D8 Day shift: report to DI 1x 30min meal break D1,2 Day shift Unit A D3,4 Day shift Unit B 08:00-19:00 10.5 D5,6 Day shift Unit C 1x 30min meal break D7 Day shift: consults & Code blue N1 Night shift Unit A N2 Night shift Unit B 18:30-08:30 13 N3 Night shift Unit C 2x 30min meal breaks N4 Night shift: consults & Code blue A Annual, Study, Exam, Conference leave @ Request 2. Requesting Shifts a) Particular shifts or days-off can be entered on a ‘request roster sheet’ that is posted on the pin-up board opposite the medical staff pigeon holes. b) The request sheet is collected on the date indicated on the top of the sheet. c) Requests should also be discussed with the ICU secretary. (Ph: 8222 5325 or email: sherridan.clark@health.sa.gov.au). d) Factors to consider when requesting shifts: i) Requests can significantly complicate the roster and you should therefore exercise some restraint and not request your entire roster. ii) If you need to request several shifts please indicate in red, which two are the most important and priority will be given to these requests. iii) Requests cannot be granted if they disadvantage other staff, compromise skill-mix, or overall staffing numbers necessary for the shift.
- 11. 11 3. Changing/Swapping Shifts a) If you wish to change a shift after the roster has been posted, you may do so with the following guidelines: i) Once the roster is posted, the onus is on the individual to arrange any shift swaps and these must occur within the same roster period. ii) You should first endeavour to swap the shift with someone in the same skill group so that the skill-mix is maintained for the shift. iii) You must speak to the ICU Secretary for approval (T: 8222 5325 or email: sherridan.clark@health.sa.gov.au) and then note changes on the rosters posted in the ward and on the medical pin-up board. 4. Annual Leave a) Annual leave for medical staff is on a “first come - first served” basis, so book leave as soon as possible. b) Only 3 registrars can be on leave at any one time, so before filling in an application form check that leave is available with the ICU secretary. c) Please contact the ICU Secretary if you have any questions or concerns about your roster at anytime. d) Leave is in accordance with the SA Salaried Medical Officers’ Award (5 weeks annual and 1 week study leave) and registrars are required to forward a signed copy of leave requests to the Senior Registrar for rostering purposes. 5. Sick Leave a) If you are sick and unable to attend work, please contact both: i) The Duty Intensivist by day, or Senior Registrar at night (SD: 1650), and ii) The Roster Manager - Mon-Fri (09:00-16:00) b) If you can, predict an expected day or night of return to work. c) Annotate your pay sheet as “sick leave” accordingly. C. Orientation 1. Registrars commencing duty within the unit at the main RMO changeover dates will undergo a half-day orientation program. 2. This will include sessions from: a) The Director of ICU (or delegate) b) The Director of Research c) Infectious Diseases / Clinical Microbiology d) The Acute Pain Service
- 12. 12 D. Weekly Programme Table: Weekly Unit Programme Monday Tuesday Wednesday Thursday Friday 08:00 Handover round Handover round Handover round Handover round Handover round 09:00 Bedside round Bedside round 10:00 Bedside round Bedside round Bedside round 11:00 ICU Grand Round ICU Grand Round 12:00 ICU X-ray meeting Consultant meeting 13:00 Bedside round Primary Exam 14:00 Tutorial Simulator Training Simulator Training (1y trainees) 15:00 Audit Journal Club BICMed Course Clinical Teaching Trainee Tutorial junior registrar 16:00 Registrar tutorial (trainees) tutorial (all registrars) 17:00 18:30 Handover round Handover round Handover round Handover round Handover round
- 13. 13 E. Admission and Discharge Policies 1. Admissions Policy a) Patients are managed by the ICU staff during their stay in ICU. b) Admission is reserved for patients with actual or potential vital organ system failures, which appear reversible with the provision of ICU support. c) All admissions, including transfers and retrievals, must be approved by the Duty Intensivist (SD: 1650). d) Resuscitation or admission must not be delayed in imminently life threatening cases, unless specific advanced directives exist and are clearly documented. e) Such admissions should be discussed with the Duty Intensivist ASAP. f) Patients are admitted to ICU under the ‘bed-card’ of the original or taking clinic. g) MedStar Retrievals i) Require admission under a parent clinic, who should be aware prior to patient transfer and notified of the patient’s arrival in the ICU. ii) Must be discussed with the Consultant when the SR is on 1st call. h) Clinics requesting elective postoperative surgical beds should book the bed at least one day in advance and must confirm bed availability with the Duty Intensivist on the day of surgery, prior to anaesthesia commencing. i) Admission disputes must be referred to the Duty Intensivist. 2. Discharge Policy: a) All discharges should be: i) Approved by the responsible ICU consultant. ii) Discussed with the parent clinic prior to patient transfer including discussion of any ongoing or potential problems. iii) Transferred “In hours” i.e. prior to 18:00 - unless specifically approved by a consultant. b) A discharge summary must be completed and a copy filed in the case-notes. c) All patients on insulin protocols should be referred to the Endocrine Unit prior to discharge (preferably the day before) d) Patients discharged on TPN must be entered in the TPN folder in Unit A. e) Notify the Acute Pain Service of patients discharged under their care. f) Withdrawal or limitation of therapy is a consultant responsibility. g) Treatment limitation/non-escalation directives must be discussed with the patient or patient’s family, the parent clinic and clearly documented prior to discharge. h) Referral to the Palliative Care should occur pre-discharge where indicated. 3. Deaths Policy: a) The duty ICU consultant must be informed of all unexpected deaths. b) The duty ICU registrar must ensure: i) A death certificate is completed or the Coroner notified ii) The parent clinic or duty intern is notified iii) Referring doctors (i.e. GP’s, other specialists / hospitals) are notified.
- 14. 14 c) Where indicated,consent for a post-mortem should be obtained from relatives as soon as possible. d) The Coroner must be notified in all cases where death is: i) A death in custody, e.g. police, corrections, mental health detention. ii) A death by unusual, unexpected, unnatural, violent or unknown cause. iii) A death during, as a result of or within 24 hours of a surgical, invasive or diagnostic procedure, including the administration of an anaesthetic for the carrying out of the procedure. iv) The term ‘anaesthetic’ means a local or general anaesthetic and includes a sedative or analgesic. The following procedures are excluded: The giving of an intravenous injection The giving of an intramuscular injection Intravenous therapy The insertion of a line or cannula Artificial ventilation Cardio-pulmonary resuscitation Urethral catheterisation The insertion of a naso-gastric tube Intra-arterial blood gas collection Venipuncture for blood collection for testing Subcutaneous injection or infusion v) A death within 24 hours of being discharged from a hospital or having sought emergency treatment at a hospital. vi) A death of a person under a ‘protected person’ order under the Aged or Infirm Persons’ Property Act 1940 or the Guardianship and Administration act 1993. vii) A death in the course or as a result or within 24 hours of a person receiving medical treatment to which consent for that treatment has been given under Part 5 of the Guardianship and Administration act, 1993. viii) A death of a child subject to a custody or guardianship order under the Children’s Protection Act 1993. ix) A death on an aircraft or vessel with a place in South Australia as its place of disembarkation. x) A patient death in an approved treatment centre under the Mental Health Act 1993. xi) Death of a resident of some (but not all) supported residential facilities licensed under the Supported Residential Facilities Act. A list of the relevant facilities is provided in the “Coroner’s Folder” in the nursing bay stations. xii) A death in a hospital or treatment facility for the treatment for a drug addiction. xiii) If no certificate as to the cause of death has been given to the Registrar of Births, Deaths and Marriages.
- 15. 15 F. Care for Patients Discharged from ICU for Terminal Care. 1. Preparation for discharge. a) For the families of dying patients, moving from a familiar environment will add a level of anxiety and uncertainty, even if it will be to a quieter setting. b) Handover to the ward treating team should be as comprehensive as possible, including a social as well as medical history. c) Families should be supported to accept that there may still be uncertainty about the patient’s course and the timing of death. d) Families should be reassured that the focus will be on maintaining comfort. e) Levels of ongoing active support for the patient, e.g. IV or subcutaneous fluids should be clarified between ICU staff, the Ward team and family members. 2. Symptom management in terminal care. a) Physical symptoms that should be considered in planning ongoing care are: i) Pain – either spontaneous or on movement ii) Agitation, restlessness iii) Respiratory tract secretions iv) In a conscious patient there may be other symptoms e.g. nausea and vomiting, dyspnoea v) Prevention of seizures may be a relevant issue b) If the patient is requiring either analgesia or sedation in ICU, these should be continued on discharge to the ward. i) Opioid infusions can be continued as subcutaneous infusions via a pump (e.g. Graseby® or equivalent) ii) If sedation is required, midazolam can be administered via subcutaneous route as a continuous infusion, with an opioid if already in use. c) If the patient has not required regular opioid or sedation in ICU, the following PRN orders should be in place prior to discharge: i) For pain: Opioid naïve patient - e.g. morphine 2.5-5mg s.c. 2 hrly prn Opioid tolerant - dose guided by background usage ii) For agitation, restlessness: Midazolam 2.5mg - 5mg s.c. 1 hrly prn iii) For management of secretions: Hyoscine hydrobromide 400 µg s.c. 3-4 hourly prn Atropine 600 µg s.c. 3-4 hourly prn 3. Where appropriate, formal consult and involvement of the Palliative Care Service is encouraged.
- 16. 16 G. Clinical Dutiesin the ICU 1. Infection Control in ICU a) Prevention and containment of nosocomial infection is a fundamental principle of effective medical practice. b) The critically ill patient is highly vulnerable to nosocomial infection, which results in significant morbidity, prolonged length of hospital stay, increased cost and attributable mortality. c) It is the responsibility of every member of the health care team to ensure compliance with Hospital and Unit infection control policies. This may include reminding senior colleagues or visiting teams to conform to basic issues such as hand-washing or additional precautions. d) Hand-hygiene remains an established method of effective infection control and must be strictly performed by all members of the health care team: i) Aqium hand gel must be used by all staff: Every time they enter or exit a patient’s cubicle (defined as the line of the door or curtain of bed space.) Before wearing gloves Before and after patient contact Before and after contact with a patient’s environment ii) Hand wash with soap where: Contact with blood or body fluids Hands are visibly soiled After removing gloves iii) Hand wash with chlorhexidine: Prior to clinical procedures After contact with patients with multi-resistant organisms e) Gloves i) Disposable gloves must be worn for all contact with patient’s bodily fluids, dressings and wounds. ii) Gloves must be disposed of within the patient cubicle on leaving f) Plastic aprons are to be worn: i) With gross physical contact with the patient (e.g. patient turns) ii) For “additional precautions” (see below) g) Additional precautions: i) The following patients require additional precautions: Infection or colonisation with: a. Methicillin Resistant Staph. Aureus b. Vancomycin Resistant Enterococcus c. Multiresistant gram negatives d. Clostridium difficile Burns Febrile neutropenia Immunosuppressed patients as directed by Infection Control
- 17. 17 ii) These patients will normally be managed in either Units A or B. iii) An “Additional Precautions” sign is placed outside cubicles of patients identified as infective risks: Red sign = patient has multi-resistant organism Blue sign = patient is immunocompromised iv) New disposable gowns and gloves must be used for each person entering the cubicle and disposed of within the cubicle upon leaving. v) Consumable stock within the cubicle should be kept to a minimum. vi) Notify appropriate staff if patients are transported to theatre, for diagnostic procedures, or for ambulance transport. vii) Once the patient has been transferred or discharged, the area should remain vacant until “terminally cleaned” in accordance with RAH policy. viii) Environmental swabbing in Intensive Care is conducted as required by Infection Control staff. h) Aseptic technique i) Aseptic technique is to be used for all patients undergoing major invasive procedures (refer to procedures section). ii) This includes: Hand disinfection: surgical scrub with chlorhexidine for >1 minute Sterile barrier: full gown, mask, hat, gloves and sterile drapes. Skin preparation with chlorhexidine 2% in 70% alcohol. i) Sharps disposal i) The person performing the procedure is responsible for disposal of all sharps (needles, blades) using the sharp disposal containers. ii) The nursing staff are not responsible for sharps disposal. j) “Traffic control” i) Movement of people through the unit should be kept to a minimum. ii) This applies equally to visiting clinics and large numbers of relatives. iii) All visitors are expected to conform to the above infection control measures and should be tactfully reminded or instructed when necessary. k) Nominated isolation/quarantine rooms for highly contagious patients: i) Rooms 3, 4, 5 & 6 - shared air-conditioning ii) Rooms 21 & 22 - sealed, independent, negative pressure A/C units. 2. Guidelines for admission of a new patient to ICU a) Handover from the referring doctor. Obtain as much information as possible. b) Primary survey: i) Ensure adequate airway, breathing and place the patient on a FiO2 = 1.0 until a blood gas is done. ii) Check circulation and venous access. c) Notify the duty consultant. d) Secondary survey: fully examine the patient.
- 18. 18 e) Document essential orders: i) Ventilation ii) Sedation / analgesia iii) Drugs, infusions iv) Fluids f) Outline the management plan to the nursing staff. g) Secure appropriate basic monitoring/procedures: i) SpO2 ii) ECG iii) Arterial line iv) IDC, nasogastric tube v) CVC for the majority h) Basic investigations as indicated: i) Routine biochemistry, blood picture and coagulation studies ii) Group and screen. iii) Septic screen / microbiology. iv) Arterial blood gas v) ECG vi) CXR (after placement of appropriate lines) i) Advanced investigations: CT, angiography, MRI, etc j) Advanced monitoring where indicated: e.g. PA catheter, ICP, PiCCO. k) Document in case notes. (See below) l) Notify the parent clinics of patients admitted directly to ICU NB: this applies particularly to patients who have been retrieved. m) Clinic Interns and RMOs should clerk hospital admissions direct to ICU. n) Inform and counsel relatives. 3. Daily management in ICU. a) Daily investigations: i) Routine blood tests (U&E, LFT, Mg, Hb, WCC, Plts, ABG) are ordered on the daily flow chart and signed for on the 11:00 am fluid round. ii) Coagulation studies, drug levels or other tests are requested as required and may also be requested on the daily flow chart. iii) The night duty nurses take the bloods at 06:00 and complete the request form, which must be signed by the night registrar. iv) Registrars are responsible for taking blood specimens: When nursing staff request assistance. For blood transfusion - the requesting MO must ensure that the labelling of the request form and specimen matches the patient’s wristband.
- 19. 19 v) Chest x-rays are ordered after the morning handover round via OACIS. Routine daily chest x-rays are not performed in ICU Chest x-rays are performed a. On admission to ICU (beds 1-24) b. Following invasive procedures: i. Endotracheal intubation ii. Complicated percutaneous tracheostomy iii. CVC placement (subclavian or jugular) iv. Nasogastric or IABP placement c. Suspected pneumothorax d. At the discretion of the attending doctor b) Handover ward rounds are at 08:00 and 18:30. These are brief business rounds to handover essential information to the next team (either day or night) and are attended by the duty consultant, team registrars and senior nursing staff. c) Liaison with parent clinics is essential to ensure continuity of management. Clinics must be informed of significant changes in a patient’s condition or the requirement for specialist investigations or interventions. d) Complex investigations (e.g. CT, MRI scans) and procedures should be authorised by the duty consultant and discussed with the parent clinic where appropriate. H. Documentation The following guidelines are designed to facilitate the recording of clear, relevant information that is essential for continuity of care, audit and medico-legal review. Entries should establish a balance, being concise but still accurately recording all relevant information and events. Specific documentation expected from ICU registrars includes: 1. Admission note for all patients admitted to ICU (Units A, B & C) 2. Daily entry in case notes during admission. 3. Handover summary 4. Discharge summary 5. Death certificates. 1. Admission Notes a) All patients admitted to Units A & B must have a detailed admission summary. i) The admitting clinic must be notified by the admitting registrar and invited to record an admission summary for patients admitted directly to ICU. This is to ensure that clinics are aware when a patient has been admitted under their bedcard. ii) The admission note should incorporate all relevant aspects of the patient’s medical history, clinical examination and investigation results.
- 20. 20 b) Complicated Unit C patients require the same detail as Unit A & B patients. c) Routine postoperative, short stay patients in Unit C do not need detailed admission notes. In these patients record: i) Relevant operative & anaesthetic details ii) Significant comorbidities and history iii) Anticipated problems iv) Procedures e.g. epidural, invasive monitoring, TPN 2. Daily case-note entries a) A daily entry must be made in the case notes. i) Notes are most efficiently recorded after the 11:00 ward round so that current results and management plans are recorded b) Additional notes must be made for the following: i) Significant changes in physical condition necessitating changes in management, e.g. renal failure requiring dialysis. ii) Invasive procedures, e.g. laparotomy, tracheostomy, PAC/CVC insertion iii) Results of specific investigations or tests, e.g. CT scans, endocrine tests iv) Changes in policy, e.g. non-escalation of treatment, advance directives. 3. Handover summary a) Due to the large number of complex patients, an ongoing handover summary should be established for each patient b) This facilitates ease of handover between day and night resident staff and for the duty consultant staff. c) This is not a formal casenote, nor does it take the place of a thorough review of each patient and their casenotes. This is meant to be an aide-mémoire to be updated each shift. d) This is stored in a specific ICU database available on the PCs in the ICU. 4. Discharge summary a) All patients transferred from ICU (Units A/B/C) require a Medical Transfer Summary (MR 42) form completed. b) This is a single page document outlining all relevant transfer information. c) The original should be filed in the case notes and a photocopy placed in the marked box in the Unit B station for filing by the secretary. d) The duty registrar on the day of transfer is responsible for completing the form. e) Incomplete or missing summaries will be forwarded to the responsible registrar for completion. f) Short term Unit C patients do not require detailed discharge summaries, only pertinent information relating to their stay.
- 21. 21 5. Death certificates a) The following forms need to be completed: i) RAH Notification and Certification of Death (MR 150.2) all patients including those reported to the Coroner ii) Death Certificate ("the yellow form") do not complete this for deaths reported to the Coroner iii) First Medical Certificate do not complete this for deaths reported to the Coroner b) Deaths notifiable to the Coroner: i) Contact the Coroner’s office and provide preliminary demographic details of the deceased. ii) The Coroner’s office will then fax the Medical Practitioner’s Deposition form for you to complete and return by fax. iii) File the original deposition in the patient’s case-notes. I. Consent in ICU 1. Competent patients: a) All competent patients undergoing invasive procedures should have a standard RAH consent form (MR: 60.16) completed and signed by the patient. 2. Incompetent patients (sedation, coma or encephalopathy): a) Third party consent is not necessary for routine ICU procedures: i) endotracheal intubation ii) arterial lines iii) central venous lines iv) pulmonary artery catheters v) transvenous pacing wires vi) underwater seal drains vii) jugular bulb catheters viii) intra-aortic balloon counterpulsation ix) oesophageal tamponade tubes x) bronchoscopy b) However, relatives should be informed prior to the procedure if present. c) The indications, conduct and complications of the procedure should be documented in the casenotes. d) Major invasive procedures such as percutaneous tracheostomy, coronary angiography, permanent pacemaker insertion or major surgical procedures require completion of a consent form: i) Emergency procedures signed by two doctors ii) Non-urgent procedures by third party consent (next-of-kin). e) Responsibility for consent lies with the operator performing the procedure.
- 22. 22 f) ICU staff are not responsible for consent for procedures performed outside of ICU, e.g. surgical tracheostomy, or PICC lines placed in radiology g) A person, not necessarily next-of-kin, who has been nominated by the patient as a medical power of attorney may sign or refuse consent on behalf of the patient. h) Relatives should always be informed of any non-routine procedures and the consent issue explained, irrespective of the presence or absence of a medical or legal power of attorney. i) If relatives cannot be contacted, emergency life saving treatment should proceed immediately, with discussion with the Duty Consultant. J. ICU Ward Rounds 1. Grand rounds a) Held on Mondays and Fridays are an integral feature of the running of the unit. b) These are open, multi-disciplinary meetings to discuss management issues and are a valuable teaching forum. c) Current x-rays and investigation results are displayed via computer projection. d) The ward round is attended by: i) Team A, B, C and Duty ICU consultants and all floor registrars ii) An infectious diseases consultant iii) Senior nursing staff iv) Physiotherapists v) A pharmacist vi) A dietician vii) Invited clinics when appropriate viii) Medical students e) Registrars are expected to present their allocated patients and to actively participate in management discussion. f) Presentations should be of a standard suitable for a fellowship examination: i) Should take no more than 5-8 minutes. ii) Emphasise the relevant and pertinent issues only: Patient details and demographics. State day of ICU admission (e.g. Day 6 ICU). Diagnosis or major problems. Relevant pre-morbid history pertinent to this admission. Relevant progress and events in ICU (deterioration/improvement, procedures, investigations). Current clinical status (system by system). Outline features on daily pathology and radiology. Current plan of management: a. Medications b. Further investigations / procedures c. Discharge planning & prognosis
- 23. 23 2. Bedside patientrounds a) Are held daily, including grand-round days. b) Team consultants and registrars review each patient’s condition. c) Unit A&B flowcharts are re-written daily and include orders for ventilation, procedures, medications, infusions and fluid therapy. i) To ensure all aspects of patient care have been considered, the “FATDOGS” algorithm should be considered in all patients: F - Feeding & fluids A - Analgesia & sedation T - Thromboprophylaxis D - Drugs – therapeutic & usual O - Oxygen & ventilation G - Glucose control S - Sit out of bed ii) You need to either write up each one of these each day or have a reason why you have not. d) Printed stickers should be used for routine medications and infusions. e) All orders must be signed by a doctor. f) Requests for routine blood tests are made on the chart. g) Patients transferred to the general ward or Unit C i) Should have the hospital “blue folder” completed. ii) All medication orders should be re-written iii) Fluid or nutrition orders for the next 24 hours are prescribed. iv) Patients started on TPN should have their details entered in the “TPN folder” kept in Unit A. h) Similarly, Unit C patients have their charts reviewed, however all medications and fluids are recorded on the hospital blue treatment folders. K. Clinical Duties Outside of the Intensive Care Unit 1. Policy regarding outside consults: a) NB: The Unit must not be left unattended at any time to attend outside calls. (i.e. at least one registrar must remain on the floor) b) The consults and code-blue/trauma pagers are carried by the Consults Registrar (D7) during the day and Night Senior overnight (this may be modified at the discretion of the 1st on-call consultant / senior registrar). c) All consults should be addressed as soon as possible. d) If the ICU workload is heavy, refer ward consults to the DI, who will delegate appropriately. e) Notify the senior nurse and fellow registrar(s) when leaving the floor. f) The following duties accompany the Consults pager (pager no #89 22888*): i) Ward consults ii) Requests for Total Parenteral Nutrition (refer to Team A SR) iii) Requests for retrieval (refer to MedStar)
- 24. 24 g) The following duties accompany the Emergency pager (#33) i) Code blue calls | ii) Escalated MET calls | *see (4) below. iii) Trauma (P1) resuscitation Trauma pages are subdivided into levels Attendance by the ICU registrar is only required for Level 1 calls. h) All consults/MET calls potentially requiring admission to ICU must be discussed with the Duty Intensivist (DI). 2. Ward Calls a) Consults regarding potential admissions from the general wards, theatre or ED. b) Pre-operative consults for potential or booked surgical patients. c) Advice regarding fluid and electrolyte management, oxygen therapy, sedation and analgesia (usually referred to APS). d) Review as requested patients in the: i) Spinal Injuries Unit with potential respiratory failure. ii) Burns Unit for airway / breathing assessment, IV access or resuscitation. e) Requests for venous access: i) Requests must come from registrar level or above and after reasonable attempts have been made to obtain IV access. ii) Radiology provide a PICC line service in working hours. iii) CVCs are not to be inserted on ward patients. iv) Should be attended to in a timeframe appropriate to the patient’s condition. f) Requests for TPN. 3. Total Parenteral Nutrition (TPN) a) ICU provides a TPN service for the hospital. b) Requests for TPN are elective (i.e. Mon to Fri: 0800-1800) and should be made according to recommended indications. c) Requests are made via the DI or consults registrar. d) The ‘TPN Folder’ is kept in the Unit A ward station. e) The Team A Senior Registrar and Consultant will manage: i) Initial consultation with the requesting clinic. ii) Recording TPN patients in the “TPN Folder”. iii) Insertion of a PICC catheter. iv) Daily: Review of electrolytes and fluid balance, Review of the central venous catheter/PICC, Prescription of TPN orders ± vitamins / trace elements, Issue a request form for serum electrolytes. Use pink labels from ICU & leave a spare for labelling of specimen tubes - this ensures priority in the lab f) Refer to the section on nutrition in the clinical protocols for indications & complications.
- 25. 25 4. Code Blue& MET Calls a) The RAH medical emergency code is “33#”. i) Upon dialling 33#, switchboard automatically page the following people: ICU registrar ICU equipment nurse Medical registrar b) These calls are divided into: i) Code Blue *all calls must be attended immediately Cardiac &/or respiratory arrest (actual or impending) Threatened airway Major haemorrhage ii) MET calls Significant clinical deterioration (see MET criteria) MET calls are not routinely attended by ICU Registrars. The ICU Registrar should remain immediately available if a MET call has been activated, so that assistance can be provided to the MET team if required (e.g. avoid starting procedures such as CVC insertions if the MET pager has activated). c) When “33” is displayed on the pager: i) Dial “33#” on an internal phone. ii) Switchboard will then state the location of the arrest. iii) Clearly state who you are (i.e. ICU registrar) and go to the location. d) Ensure that the ICU staff know where you are going and that the Unit is not left unattended. e) At the emergency: i) This hospital follows the Australian Resuscitation Council guidelines for cardiopulmonary resuscitation. ii) The ICU/resuscitation registrar is responsible for initial assessment, securing the airway and establishing effective ventilation. iii) Basic life support is done by attending nursing and medical staff and may be directed by either ICU or medical registrar. iv) Advanced life support is directed by the more senior registrar present. This is usually the ICU registrar. v) Depending on the outcome of the Code Blue, the patient may be admitted to ICU, CCU or remain on the ward according to standard admission policies. vi) As a general rule, it is better to admit a patient if previous details are not immediately available than to prematurely abandon resuscitation. vii) Document your involvement with the resuscitation in the casenotes. viii) The home team should be involved or at least informed of their patient’s condition, including when resuscitation is unsuccessful.
- 26. 26 5. Trauma Calls a) As in cardiac arrest, a “33#” call is activated for trauma patients who meet specified trauma criteria. (Refer to trauma directives.) b) Trauma pages will appear as 2 Levels: i) Level 1: major trauma requiring immediate attendance / airway support ii) Level 2: trauma requiring full assessment in ED/Resus. c) The following people are paged and the level response detailed on the pager: i) ICU/resuscitation registrar ii) Trauma Service registrar iii) Accident and emergency registrar d) On receiving a Level 1 call the ICU registrar should proceed directly to Resus in the Emergency Department (ED) e) Ensure that ICU staff know where you are going and that the Unit is not left unattended. f) At the trauma resuscitation: i) This hospital follows the Early Management of Severe Trauma (RACS) guidelines. ii) The team leader is designated by the current Trauma Service Directive (found on the wall in Resus). iii) Role of the ICU registrar: Primarily as a backup for acute life threatening situations in the event that sufficiently experienced personnel are not available in Resus. If anaesthetic staff are present in Resus, there is no requirement for ICU registrars to attend the resuscitation unless specifically requested by these personnel or the Trauma Director. If anaesthetic staff are not immediately available, the following role is indicated until appropriate personnel arrive: a. Initial airway assessment and management. b. Establishing effective ventilation c. Assistance with vascular access and restoration of circulation. d. Other acute interventions (e.g. UWSD) as required Once anaesthetic & trauma team members are present and the situation is under control, return to ICU - do not leave ICU unattended for lengthy periods of time. If prolonged resuscitation is anticipated, call in the ICU or Trauma Consultant and/or delegate to the anaesthetic/resuscitation registrars. Transportation of trauma patients to CT scan, angiography etc. is the responsibility of the emergency anaesthetic staff. ICU registrars must not do prolonged intra-hospital transports for trauma patients without approval by the duty ICU consultant.
- 27. 27 iv) General principles: Document your involvement with the resuscitation in the casenotes Once the primary survey is completed, proceed to the secondary survey and order appropriate investigations as per the Trauma team leader. In critically ill patients, ensure that a suitably qualified person (in terms of resuscitative skills) remains with the patient at all times. This is mandatory if the patient is transported from Resus (e.g. to radiology, ICU, theatre). Notify ICU staff of pending admissions. Demarcation disputes are referred to the duty Trauma Consultant. 6. Retrieval Requests a) Requests for consultation may originate from a number of sources. Namely, i) The DI phone (SD: 1650) ii) Other ICU telephones iii) ICU registrar pager iv) Other clinics who have been consulted by outside medical officers. b) All retrieval requests should be referred immediately to the state retrieval service, MedStar on 82224222. c) All requests from MedStar for the transfer of patients to the RAH must be referred to the on-call ICU consultant. 7. Intrahospital transportation of Intensive Care patients a) All transports must be authorised by the duty ICU consultant. b) The transport/investigation must be considered in the best interests of the patient. c) All ventilated and potentially unstable transports need a medical escort. d) Stable, self-ventilating patients may be transported by an ICU RN e) If ICU nursing staff are concerned, then a medical escort is required. f) At no stage must the unit be left uncovered. g) If the Unit is busy, or transports clash with ward rounds, other personnel may be deployed to do the transport. This is coordinated by the duty ICU consultant. h) As a general rule, ICU staff are responsible for transportation of ICU patients. i) Anaesthesia is responsible for transport of the following ICU patients: i) Trauma resuscitation patients ii) Patients to and from theatre iii) Patients to and from hyperbaric medicine. j) The transport of patients undergoing prolonged investigations or treatments, (e.g. MRI, angiographic embolisation, invasive radiological procedures, TIPS) should be discussed with the Duty ICU consultant and Duty Anaesthetist (SD 1175)
- 28. 28 k) Guidelines i) Registrars must familiarise themselves with transport monitors, portable ventilators and infusion pumps. ii) Inform and discuss the transport with the nursing staff as soon as possible. iii) Patients must be appropriately monitored during the transport and observations recorded on the flow chart. iv) Document any problems which may occur during transport. v) Ensure that the results of investigations performed (e.g. CT scans etc) are recorded in the case notes by the appropriate person. L. Hospital Emergencies 1. The emergency number is 33# : state the nature and location of emergency 2. Fire a) A copy of the hospital emergency procedures (fire, smoke, bomb-threat) is kept in the P4A and P4C nursing stations. b) The chief fire and emergency officer is the overall controller during a fire or smoke emergency (Code Red). c) Become familiar with the location of fire exits, extinguishers and blankets in ICU i) Unless small and easily contained do not attempt to fight a fire yourself. ii) Remove yourself from the immediate vicinity of the fire, alerting other staff members as indicated, and position yourself behind the automatic fire doors. iii) The MFS has a 3 minute response time to the RAH. iv) Wait for the arrival of the Fire Chief and assist in any patient movement/evacuation only as indicated by the Fire Chief. d) Role of medical staff: i) There is no place for “heroic” action - ensure your own safety first! ii) Wait for the arrival of the MFS. iii) Assist in patient assessment/management under the coordination of the Fire Chief. iv) In the event of a significant fire / smoke hazard, staff will only re-enter the danger zone in the immediate company of a MFS fire-fighter, with appropriate breathing apparatus.
- 29. 29 M. Research inICU 1. Background: There is a prolific research programme at the RAH ICU. This research is world leading in the areas of gastrointestinal motility, nutrient absorption and incretin hormones in the critically ill. 2. Personnel: a) Director of Research - A/Prof. Marianne Chapman b) Research Fellow - Dr Adam Deane c) Research Manager - Ms Stephanie O’Connor d) Research Nurses - Ms Justine Rivett - Mr Luke Chester - Ms. Alison Ankor e) Research Scientists - Mr Matthew Summers - Mr Antony Zaknic 3. There are students studying toward their higher degrees frequently working in the ICU. These students are strongly supported by the ICU Research Unit. Trainees interested in undertaking a higher degree are always well received. 4. There are broadly 3 types of research studies occurring in the unit: a) Locally initiated studies b) Drug company sponsored studies c) Studies performed with the ANZICS Clinical Trials Group (see below). 5. Medical and nursing staff are encouraged to become involved in research: a) Registrars are expected to assist in obtaining consent for ongoing studies. b) Knowledge of these studies can be obtained from any of the research staff. c) Further involvement is encouraged and there are supports within the unit to facilitate research to occur. d) Because the ICU is a world-leader in several areas, it is advised to leverage on the expertise and availability of sophisticated methodologies within the group. However, independent projects, driven by highly committed individuals, will always be supported. 6. The CICM formal project takes, at a minimum, 12 months to complete. a) Trainees interested in undertaking a study for their formal project are advised to approach potential supervisors with sufficient time to complete their project. b) Potential projects (and initial contact persons) are: i) Retrospective observational studies (A/Prof Flabouris and Dr Finnis) ii) Prospective observational studies (Dr Sundarajarajan) iii) Experimental work using a sheep model (Dr Maiden) iv) Laboratory based work (Dr Reddi) and v) Prospective clinical research (A/Prof Chapman and Dr Deane).
- 30. 30 7. Most projectsrequire prior RAH Research Ethics Committee approval. Your supervisor will be able to provide details. 8. Completed research projects should be presented at either a local or interstate scientific meeting. a) Partial funding is available for staff who present work at approved meetings. b) Applications should be made to the Coordinator of Research. c) Eligible meetings include, but are not limited to: i) ANZICS / ACCCN Annual Scientific Meeting - October. ii) CICM Annual Scientific Meeting – May/June. iii) ACCCN (Institute of Continuing Education), Conference. Annual – May. 9. ANZICS Clinical Trials Group (CTG). a) A national clinical trials group to facilitate multicentre trials in Australia & NZ. b) World-leading in critical care research and is open to all interested parties. c) CTG meetings are held once per season, with the main meeting in March. d) Resource person: A/Prof. Marianne Chapman. 10. If you are unsure of what to do about a patient enrolled in a study, please contact the relevant staff member regardless of the time of day. a) Queries about drug company sponsored studies should be directed to the ICU Research Nurse on-call (SD 1520) b) Queries relating to a local investigator studies should be directed to the primary investigator. N. Information Technology in ICU a) All consultant and registrar offices and the Registrar Teaching Room are equipped with PCs, connected to the RAH local area network (LAN). b) Facilities available through the LAN include: i) Intranet e-mail accounts ii) WWW browsing facilities (available on application). iii) Intranet resources, which are being continuously expanded: UpToDate®, eMIMS, Medline, Toxnet, etc. An extensive range of electronic text books ICU Handover Database iv) On application registrars will be allocated a username, which will carry with it an ‘Internet’ e-mail account for the duration of their stay. c) In addition, many of the consultants have access to the University of Adelaide, including Barr-Smith Library resources. d) The Unit has an internet presence at http://www.icuadelaide.com.au/ e) NB: Use of hospital computers to access inappropriate material is not tolerated. RAH guidelines detail appropriate use.
- 31. 31 PART 2 - CLINICAL PROCEDURES A. Introduction 1. Registrars are encouraged to become proficient in all Intensive Care procedures. 2. Invasive procedures should be authorised by a senior registrar or the duty ICU consultant. 3. Adequate familiarisation and supervision with unfamiliar procedures is essential: there is always someone available to help. 4. The relative risk vs. benefit of all procedures must be carefully considered. 5. Do not persist if you are having difficulty with the procedure - call for help. 6. Consent for procedures: *refer to Administration / Consent a) Competent patients undergoing invasive procedures should have a standard RAH Consent Form (MR:60.16) completed and signed by the patient b) Third party consent is not necessary for incompetent patients undergoing routine ICU procedures. c) Major ICU procedures, such as percutaneous tracheostomy or enterogastrostomy, require third party or two-doctor consent. 7. The indications, conduct and any complications of the procedure should be clearly documented in the case notes, in addition to a consent form if this is completed. 8. Discuss the planned procedure with the nursing staff and allow sufficient time for setting up of trays and equipment. 9. Remember: the nursing staff have extensive experience with these procedures. 10. It is the responsibility of the operator to discard all sharps used in the procedure and to ensure that they are placed in a sharps disposal container. B. Procedures 1. Registrars are expected to become proficient in all routine procedures. 2. Where appropriate trainees are expected to learn to place lines both a) Via surface anatomical landmark, and b) With ultrasound guidance 3. Whilst ultrasound may aid in delineating the relevant anatomy: a) Trainees will find themselves in environments where U/S is unavailable b) The time delay involved in the use of U/S may be clinically deleterious, and c) There are insufficient data that the use of U/S actually reduces complications. 4. Specialised procedures are done either by the Duty Consultant or strictly under consultant supervision. 5. Guidelines for the listed routine and specialised procedures are outlined in the following sections.
- 32. 32 Routine ICU procedures Endotracheal intubation Peripheral venous catheterisation Arterial cannulation Central venous catheterisation / PICC line insertion Urinary catheterisation Lumbar puncture Epidural catheterisation PiCCO Catheter Pulmonary artery catheterisation Pleural Drainage Underwater seal drain insertion Pleurocentesis Peritoneocentesis Nasogastric tube insertion Specialised ICU procedures Fibreoptic bronchoscopy Percutaneous tracheostomy Cardiac (transvenous) pacing Pericardiocentesis Intra-aortic balloon counterpulsation Oesophageal tamponade tube insertion Extracorporeal Membrane Oxygenation C. Peripheral IV Catheters 1. Indications: a) First line IV access for resuscitation, especially blood transfusion b) Stable patients where a CVC is no longer necessary 2. Management protocol: a) Remove/replace all resuscitation lines inserted in unsterile conditions. b) Generally avoid peripheral IV use in ICU patients and remove if not in use. c) Use local anaesthesia in awake patients. d) Aseptic technique: i) Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%) + gloves ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) iii) Dressing: Opsite® or equivalent occlusive dressing e) Change / remove all peripheral lines after 48 hours. f) Avoid lower-limb placement in patients with vascular disease.
- 33. 33 3. Complications a) Infection - local and systemic b) Thrombosis c) Extravasation in tissues D. Arterial Cannulation 1. Indications: a) Routine measurement of systemic blood pressure in ICU b) Multiple blood gas and laboratory analysis c) Measurement of BP during transport of patients in hostile environments 2. Management protocol: a) Remove and replace lines inserted in unsterile conditions as soon as possible. b) Brachial and femoral arterial lines should be changed as soon as radial or dorsalis pedis arteries are available. c) Aseptic technique: i) Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%) + sterile gloves ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) d) Local anaesthesia in awake patients. e) Cannulae: i) Arrow® radial or femoral kits (Seldinger technique). ii) 20G Insyte®. iii) Single lumen 20G CVC (paediatric) for femoral arterial lines. f) Insertion sites – in order of preference: radial > dorsalis pedis > femoral > brachial g) The femoral artery may be the sole option in the acutely shocked patient. h) Secure with a StatLock® device. i) There is no optimal time for an arterial line to be removed or changed. j) IA cannulae are changed/removed in the following settings: i) Invasive IA line is no longer necessary. ii) Distal ischaemia iii) Mechanical failure (overdamped waveform, inability to aspirate blood) iv) Evidence of local or unexplained systemic infection k) Measurement of pressure: i) Transducers should be ‘zeroed’ each nursing shift ii) Zero reference = the mid-axillary line, 5th intercostal space l) Maintenance of lumen patency i) Continuous pressurised (Intraflo®) saline flush at 3ml/hr. 3. Complications a) Infection b) Thrombosis / digital ischaemia c) Vessel damage / aneurysm d) Haemorrhage / disconnection
- 34. 34 E. Central Venous Catheters NB: Registrars should be familiar with the interpretation and limitations of haemodynamic variables derived from central catheters (CVC, PICCO and PAC) in critically ill patients. 1. Indications: a) Standard IV access in ICU patients: i) Vasoactive infusions ii) Fluid administration (including elective transfusion) iii) Hypertonic solutions (TPN, amiodarone, nimodipine, etc.) b) Monitoring of right atrial pressure (CVP) c) Venous access for: i) Pulmonary artery catheterisation (PAC) ii) Continuous renal replacement therapy (CVVHDF) iii) Plasmapheresis. iv) Transvenous pacing. v) Jugular bulb oximetry. d) Resuscitation i) Large bore peripheral IV line(s) are 1st line. ii) Standard lumen CVCs are not appropriate for acute volume resuscitation. iii) Consider using a PAC sheath or Vascath if central access is required and adequate peripheral access is unobtainable. 2. Management protocol: (applies to all types of CVC): a) Types: i) The default CVC for all ICU patients is a Cook antimicrobial impregnated (rifampicin/minocycline) 7F 15 or 20cm 3-lumen catheter. ii) Non-impregnated catheters inserted outside the ICU should be changed to an impregnated catheter according to clinical indication. iii) Dolphin Protect® catheters are used for CVVHDF and plasmapheresis iv) Pulmonary artery catheter sheath (part of the PAC kit) v) Dress non-impregnated catheters with a BioPatch® b) Sites: i) Preferred site for routine stable patients → SCV > IJV. ii) Femoral v. access is preferable where: Dolphin Protect® / CVVHDF Limited IV access (burns, multiple previous CVC’s), A thoracic approach is considered hazardous with: a. Severe respiratory failure from any cause (PaO2/FiO2 < 150) b. Hyper-expanded lung fields (severe asthma, bullous disease) c. Coagulopathy (see below) Inexperienced staff requiring urgent access, where supervision is not immediately available.
- 35. 35 c) Coagulopathic patients: i) INR > 2.0 or APTT > 50s correct with FFP and/or prothrombinex ii) INR 1.5-2.0 or APTT 40-50s correct with FFP, or use IJ or femoral approach iii) Platelets < 50,000 transfuse 1 pack (5U) platelets Failure to increment femoral approach or PICC iv) Uncontrolled coagulopathy femoral approach or PICC Including recent therapy with Dabigatran v) Insertion under ultrasound guidance may be preferred. d) Technique policy i) Use local anaesthesia in awake patients. ii) Strict aseptic technique at insertion: Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%) Sterile barrier: gown, sterile gloves, mask, hat sterile drapes (CVC - Patient Cover) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) iii) Seldinger technique or ultrasound guided insertion – Sonosite® iv) U/sound guided insertion may be preferred where: There is an increased complication risk (e.g. bleeding, pneumothorax) Large bore catheter insertion. Distorted patient anatomy. v) CVC Catheter lengths: 15cm - right subclavian or internal jugular 20cm - left subclavian or internal jugular, either side femoral vi) Secure all lines with a StatLock® device or securely suture vii) Dressing: non-occlusive dressing viii) Flush all lumens with saline. ix) Transduce pressure ASAP post-insertion to exclude arterial placement. x) Check CXR prior to use (SCV, IJV), except in urgent circumstances e) Maintenance i) Routine IV administration set change at 7 days. ii) Daily assessment for infection irrespective of insertion duration. iii) Catheters remain as long as clinically indicated and are changed when: Evidence of systemic infection a. New, unexplained fever or WCC b. Deterioration in organ function c. Positive blood culture by venipuncture with likely organisms (S. epidermidis, candida spp.), and/or Evidence of local infection - inflammation or pus at insertion site. iv) Guidewire exchanges are actively discouraged. They may be indicated in the following situations, only after discussion with a consultant: Mechanical problems in a new catheter (leaks or kinks) Difficult or limited central access (e.g. burns).
- 36. 36 v) Maintenance of lumen patency Central venous catheters (pre-printed on the patient flowsheet) a. Flush unused lumens with 1ml normal saline 8 hourly Vascath: into each lumen 8 hourly (printed sticker) a. Withdraw 2ml and discard. b. Flush with 2ml normal saline. c. Flush 1.5ml solution (5000U heparin/3ml = 2500U/lumen). d. NB: Each lumen has it’s internal volume printed on it. 3. Complications: a) At insertion i) Arterial puncture – haematoma, thrombosis, embolism ii) Pneumothorax, haemothorax, chylothorax iii) Neural injury (phrenic, brachial plexus, femoral nn.) b) Passage of wire/catheter i) Arrhythmias ii) Wire embolism *if this occurs, notify senior staff immediately iii) Perforation of SVC / RA - tamponade c) Presence of catheter i) Catheter infection: rates increase under the following conditions: Size of catheter - thicker catheters (PAC, Vascaths) Site of catheter - femoral > internal jugular > subclavian sites Number of lumens Nature of fluid through catheters - TPN or dextrose solutions ii) Thrombosis, HITS secondary to heparin iii) Catheter / Air embolism iv) Knotting of catheters (esp. PAC) v) Pulmonary infarct / arterial rupture (PAC) NB: Where CVC insertion presents a “significant risk” in a non-urgent situation, consider insertion of a PICC line as an alternative. F. Urinary Catheters 1. Standard in all ICU patients 2. Management protocol: a) Aseptic technique at insertion. i) Hand disinfection: surgical scrub with chlorhexidine for >1 minute ii) Sterile barrier: gloves and sterile drapes. iii) Skin prep: chlorhexidene 1% b) Local anaesthesic gel in all patients. c) Only BiocathTM catheters should be inserted in ICU & changed 6 weekly. d) Standard Foley catheters should be changed to a BiocathTM after 14 days. e) Silastic catheters should be changed after 1 month. f) Remove catheters in anuric patients and perform intermittent catheterisation weekly, or as indicated.
- 37. 37 G. Epidural Catheters 1.Indications a) Post-operative pain relief (usually placed in theatre) b) Analgesia in chest trauma. 2. Management protocol: a) Notify the Acute Pain Service of any epidural placed in ICU. b) Epidural cocktails should follow the Acute Pain Service protocols c) Strict aseptic technique at insertion. d) Daily inspection of the insertion site. The catheter should not be routinely redressed, except under the advice of the APS. e) Leave in for a maximum of 5 days and then remove. f) Remove if: i) Not in use for > 24 hours, or ii) Clinical evidence of unexplained sepsis, or iii) Positive blood culture by venipuncture with likely organisms (S. epidermidis, candida). iv) Heparin/Warfarin Protocol *also see ‘Acute Pain Service Guidelines for Anaesthetists’ 3. Complications a) Hypotension from sympathetic blockade / relative hypovolaemia i) This usually responds to adequate intravascular volume replacement ii) Occasionally, a low-dose vasopressor infusion is required iii) If this is considered, occult bleeding must be excluded. b) Pruritis, nausea & vomiting, or urinary retention (opioid effects) c) Post-dural puncture headache d) Infection: epidural abscess e) Pneumothorax (rarely) 4. NB: Further guidelines for the management of epidural catheters can be obtained from “The Acute Pain Service Guidelines for Anaesthetists”. Manuals are stored in each ICU station. H. PICCO Catheters 1. Introduction a) PiCCO uses a combination of thermodilution and pulse waveform analysis to provide an estimate of cardiovascular status. b) Trainees should become familiar with the theory of insertion, indications, interpretation and complications of PiCCO catheters. c) Indicated in the assessment & response to therapy in shock states.
- 38. 38 2. Technique a) A normal CVC line can be used. b) The peripheral arterial catheter is inserted into a femoral, brachial or axillary artery using an aseptic Seldinger technique. c) The pulse waveform analysis of continuous cardiac output is calibrated by thermodilution according to the device instructions. d) Calibration should be repeated once per nursing shift and as indicated. e) Additional measurements of Global End-diastolic Volume Index (GEDI) and Extravascular Lung Water Index (ELWI) can be made via thermodilution. 3. Below are the normal values and a suggested decision tree from the manufacturer which should be used as a guide only: Table: PiCCO Values and Decision Tree Variable Abbr. Normal Units Cardiac Index CI 3.0-5.0 l/min/m2 Global End-diastolic Blood Volume Index GEDI 680-800 ml/m2 Intrathoracic Blood Volume Index ITBI 850-1000 ml/m2 Stroke Volume Variation SVV 10 % Extravascular Lung Water Index* ELWI* 3.0-7.0 ml/kg
- 39. 39 I. Pulmonary Artery Catheters 1. Policy a) Insertion of PA catheters must be authorised by the duty consultant. b) Trainees should become familiar with the theory of insertion, indications, interpretation and complications of PACs. c) Insertion of a PAC must never delay resuscitation of a shocked patient. d) Allow sufficient time for nursing staff to set up insertion trays and transducers. e) Remove catheters once they are not being routinely used. f) They may be left in situ for up to 7 days. 2. Indications: a) Haemodynamic measurements (CO/I, SV/I, SVR/I) i) Aid to diagnosis and response to therapy of shock states, e.g. cardiogenic, septic or hypovolaemic b) Measurement of right heart pressures (RAP, PAP): i) Acute pulmonary hypertension ii) Pulmonary embolism iii) Cardiac tamponade c) Estimation of preload / left heart filling (PAOP) i) Intravascular volume status & response to fluid loading ii) LVF d) Measurement of intracardiac shunt: (Acute VSD) e) Derivation of oxygen delivery & utilization variables (VO2, DO2) 3. Management protocol: a) Insertion protocol as per CVC, with the following features: i) Sheath introducer (8.5Fr) with side port, haemostatic valve and plastic contamination shield. ii) Shared transducer for RAP (proximal) and PAP (distal) lumens iii) Check competence of balloon and concentric position iv) Ensure all lumens are flushed with heparinised-saline prior to insertion. v) Ensure the system is zeroed and an appropriate scale (0-40mmHg) on the monitor prior to insertion. vi) Insert the catheter observing changing waveforms (RARVPA) on the monitor, with the balloon inflated and locked, until catheter displays pulmonary artery occlusion tracing Subclavian and left IJ ~ 50cm Right IJ ~ 40cm vii) Deflate the balloon and ensure an adequate PA trace reappears. viii) Adjust the catheter depth until a PAOP trace appears consistently with 1-1.5ml balloon inflation. ix) Suture introducer and attach the contamination shield to the hub. x) Apply a BioPatch® and non-occlusive dressing. b) Ensure an adequate PA tracing is on the monitor at all times
- 40. 40 c) “Wedged” tracings must be corrected as soon as possible: i) Flush distal lumen with 2ml N.Saline ii) Withdraw the catheter until a PA trace is visible d) Measurement of pressures: i) Reference pressures to the mid-axillary line ii) Measure at end-expiration of the respiratory cycle iii) Do not disconnect ventilated patients to measure pressures. iv) Measurement of PAOP: End expiration: lowest point in ventilated patients, highest point in spontaneously ventilating patients Use the “electronic cursor” on monitors after 2-3 respiratory cycles. Do not use the electronic average of the wedge tracing. e) Haemodynamic measurements i) These are routinely performed by the nursing staff, however registrars should become familiar with the procedure. ii) Record all measurements in the flow chart in the results folder. iii) Cardiac outputs: Injectate: 10ml 5% dextrose @ room temperature Inject at random times in the respiratory cycle Take > 3 measurements and ignore values > 10% from average. iv) Derived variables: CO/CI and SVR are routinely charted (8 hrly or as indicated). Other variables including PVR(I), SV(I), L(R)VSWI are recorded in the haemodynamics flowsheet. Mixed venous oxygen levels should be measured on a sample taken from the distal (yellow) port. Oxygen saturation should be directly measured with co-oximetry. Derived haemodynamic variables (see table), should be used in conjunction with clinical assessment. 4. Complications a) Related to CVC cannulation (see CVC section) b) Related to insertion/use of a PAC i) Cardiac perforation ii) Thromboembolism iii) Pulmonary infarction ~ 0-1.4% (2 persistent wedging) iv) Pulmonary artery rupture ~ 0.06-0.2% (mortality 50%) v) Catheter related sepsis vi) Endocarditis vii) Pulmonary valve insufficiency viii) Catheter knotting ix) Balloon fragmentation / embolism x) Tachyarrhythmias xi) RBBB
- 41. 41 Table: Standard HaemodynamicVariables Variable Formula Normal range Cardiac index CI CO/BSA 2.5-5 l/min/m2 Systemic vascular MAP RAP 750-1500 SVR 79.9 resistance CO dyn.sec/cm5/m2 Systemic vascular MAP RAP 1400-2400 SVRI 79.9 resistance index CI dyn.sec/cm5/m2 Pulmonary vascular mPAP PAOP 150-250 PVRI 79.9 resistance index CI dyn.sec/cm5/m2 Stroke volume index SVI CI 33- 47 ml/beat/m2 HR LV stroke work index LVSWI MAP PAOP SVI 0.0136 50-120 g/m2 / beat RV stroke work index RVSWI mPAP PAOP SVI 0.0136 25-55 g/m2 / beat Arterial oxygen content CaO2 Hb 134 SaO2 PaO2 0.003 . 17-20 ml/100ml Venous oxygen content CvO 2 Hb 134 SvO 2 PvO 2 0.003 . 12-15 ml/100ml Oxygen delivery index DO2 I CI CaO2 10 550-750 ml/min/m2 Oxygen consumption index VO2I CI CaO2 CvO2 10 115-160 ml/min/m2 VO 2 I Oxygen extraction ratio O 2 ER 0.24-0.4 DO 2 I Qs CcO 2 CaO 2 Shunt equation 100 5-15% Qt CcO 2 CvO 2 End capillary oxygen CcO 2 Hb 1.34 1.0 PAO2 0.003 80-100 ml/100ml content Alveolar gas equation PAO2 FiO2 760 47 PaCO2 125 . 100-650 mmHg
- 42. 42 J. Pleural Drainage 1. Indications: a) Pneumothorax b) Tension pneumothorax may require urgent needle thoracostomy c) Haemothorax d) Large symptomatic pleural effusion 2. Management protocol: a) Needle thoracostomy (tension pneumothorax): i) 14 or 16G cannula placed in mid-clavicular line, 2nd intercostal space ii) Always place an UWSD following this procedure b) Pleurocentesis: (pleural effusion) i) Prior to commencement, ultrasound the chest to confirm the presence of fluid and indentify/mark an appropriate insertion site. ii) Strict aseptic technique at insertion: Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%) Sterile barrier: gown, sterile gloves, mask, hat & drape(s) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) iii) Local anaesthesia in conscious patients. iv) Seldinger technique: Pigtail catheter or ThalQuick® 12F kit. Insert guidewire through needle into pleural space Insert catheter into pleural space over the wire Aspirate intermittently with closed system or attach to an UWSD. v) Record volume removed and send for MC&S, cytology & biochemistry. vi) Check CXR post-procedure. c) Underwater seal drainage: i) Local anaesthesia in awake patients. ii) Aseptic insertion technique - as above. iii) Site: Mid-axillary line, 3-5th intercostal space Mid-clavicular line, 2nd intercostal space ( air only) Do not insert drains through old wounds iv) ICU patients need large drains: 28F catheter or larger v) Use soft Mallinkrodt tubes in preference to the stiffer Argyle tubes vi) Remove the trochar from catheter: do not use the trochar for insertion vii) For the usual lateral ICD, go for the anterior or mid-axillary lines, avoid the posterior sites as the chest wall is too thick, and there is a danger to neurovascular structures viii) Make a 2-3cm skin incision parallel to the ribs (#10 or #15 scalpel)
- 43. 43 ix) Instruments & technique: Blunt dissect using short artery forceps, avoid long forceps. Do not “plunge” into the chest with either instrument. Access to the intercostal space is by careful blunt dissection of the intercostal muscles above the rib below. The chest wall hole must be 2-3 cm wide in order that a finger can be inserted into the pleural space to identify possible adhesions. The soft tube should be guided by the intrapleural finger so that the tube goes in between the finger and chest wall x) Connect to an underwater seal drain apparatus xi) Insert 2 purse string sutures: 1 to fasten the tube 1 (‘Z’ or purse-string) to close the skin incision on drain removal. xii) Insert additional sutures as required to close the external wound. xiii) Dressing: occlusive dressing (Hypafix) xiv) Check CXR. xv) Maintenance Remove or replace drains inserted in unsterile conditions ASAP. Leave the drain in situ until: a. Radiological resolution of pleural collection (air/fluid) b. No ongoing air-leak (no drain bubbling) c. Minimal drainage (< 150 ml/24 hrs). In ventilated patients, consider clamping the drain for 4 hours prior to removal, providing the patient remains stable and/or post CXR. Surgically placed drains are the responsibility of the surgeon and should only be removed in consultation. 3. Complications a) NB: minimised using the blunt technique b) Incorrect placement - extrapleural, intrapulmonary, subdiaphragmatic c) Pulmonary laceration - haemorrhage, fistula d) Pneumothorax e) Bleeding i) local incision, intercostal vessels ii) lung iii) IMA (with anterior placement) iv) Great vessels (rare) f) Infection i) Soft tissue ii) Empyema g) Mechanical (kinking, luminal obstruction)
- 44. 44 K. Endotracheal Intubation 1.Policy: a) Endotracheal intubation in ICU patients is a high risk but vital procedure: i) Usually an emergency procedure, with limited time. ii) Usually indicated for acute respiratory failure, or associated with limited respiratory reserve iii) Patients may have cardiovascular instability and significant co-morbidities iv) Patients may have cervical spine or oropharyngeal trauma / surgery v) Patients are at risk of vomiting and aspirating vi) Positioning is difficult. b) Familiarisation with the intubation trolleys, equipment and drugs is essential. c) Intubation should ideally not be done as a sole operator procedure. Skilled assistance should always be sought. d) If you are alone (i.e. after hours): call for help! i) Expertise in intubation is always available. ii) Remember emergency anaesthesia staff. e) The majority of ICU patients mandate rapid sequence induction. 2. Indications a) Institution of mechanical ventilation b) To maintain an airway i) Upper airway obstruction Potential e.g. early burns Real e.g. epiglottitis, trauma ii) Patient transportation c) To protect an airway i) Patients at risk of aspiration ii) Altered conscious state iii) Loss of glottic reflexes d) Tracheal toilet 3. Techniques a) Orotracheal intubation is the standard method of intubation in this unit. b) Nasotracheal intubation may be indicated where: i) Patients require short-term ventilation and are intolerant of oral ET tubes. ii) Nasal Fibreoptic intubation may be indicated for: Oro-maxillary surgery and pathology Inability to open the mouth: e.g. intermaxillary fixation, TMJ trauma, rheumatoid arthritis. Upper airway obstruction and nasal route preferred iii) Contraindicated in base of skull & LeForte facial fractures c) Methods: i) Direct laryngoscopy, C-MAC after rapid sequence induction ii) Fibreoptic bronchoscopic awake intubation (oral or nasal) iii) Intubating laryngeal mask – LMA – Fastrac®
- 45. 45 4. Endotracheal Tubes a) Standard tube: i) Low pressure, high volume cuff. ii) Males: 8-9 mm secure at 21-23cm to incisors iii) Females: 7-8 mm secure at 19-21cm to incisors iv) Do not cut tubes to less than 26 cm length b) Double lumen tubes: *rarely indicated in ICU: i) Lung isolation for broncho-pulmonary fistula, abscess or haemorrhage ii) Inserted as a temporary manoeuvre prior to definitive therapy iii) Allow differential lung ventilation iv) Males: Left 41F v) Females: Left 39F vi) NB: right bronchial tubes are harder to correctly site. vii) Position should be checked with bronchoscope. c) Intubated patients from theatre may have the following tubes that are not recommended for prolonged intubation. These tubes must be changed if intubation is anticipated > 48 hrs and exchange is safe and feasible. i) Plain PVC tubes - no above cuff suction port ii) Armoured tubes - risk kinking & obstruction iii) RAE tubes - difficulty with suction & malposition 5. Protocol for endotracheal intubation in ICU a) Personnel: i) Intubation is a 3-4 person procedure - skilled assistance is mandatory ii) The “top end” intubator coordinates the procedure iii) One person to administer drugs iv) One person to apply cricoid pressure (CP) post-induction: This is routine for all emergency intubations CP is considered safe in the presence of suspected spinal injury. CP must be correctly applied - distortion of the larynx and difficulty in intubation may occur if poorly applied. v) One person to provide in-line cervical spine immobilisation (trauma and spinal patients only). b) Secure adequate IV access c) Equipment (kept in difficult airway & intubation trolleys in P4-A,B&C). Ensure the following equipment is available and functional: i) Adequate light ii) Oropharyngeal airways iii) Working suction with a rigid (Yankauer) sucker iv) Self-inflating hand ventilating assembly and mask v) 100% oxygen, i.e. working flowmeter at 15 l/min vi) 2 working laryngoscopes (standard & long blades) vii) Magill forceps viii) Malleable introducer and gum-elastic bougie
- 46. 46 ix) 2 Endotracheal tubes Normal size + 1 size smaller Check cuff competence x) Access to difficult intubation equipment and be aware of the difficult airway trolley location and its contents. Be aware of the Failed Intubation Drill. Airtrach, C-MAC, Heine Flex tip Intubating Fastrach LMA Cricothyroidotomy equipment a. Percutaneous kit or b. #15 scalpel & #6.0 cuffed ETT d) Monitoring (on all patients) : i) SpO2, ETCO2, ECG ii) Invasive BP *desirable but not essential and must not delay intubation if urgent e) Drugs i) Induction agent - propofol, fentanyl, ketamine, midazolam ii) Suxamethonium - 1-2mg/kg is the muscle relaxant of choice. Contraindicated in: a. Burns > 3 days b. Chronic spinal injuries (i.e. spastic plegia) c. Chronic neuromuscular disease (e.g. GBS, motor neurone disease) d. Hyperkalaemic states. (K+ > 5.5) Consider Rocuronium (1-2 mg/kg) if Sux. contraindicated iii) Atropine - 0.6-1.2mg available iv) Adrenaline - 10ml 1:10000 solution available f) Procedure: Rapid sequence induction and orotracheal intubation i) Pre-oxygenate with 100% oxygen for 3-4 minutes. ii) For patients on mask CPAP/NIV, pre-O2 with the NIV mask iii) Preload with 250-500ml IV crystalloid iv) Inotropes may be necessary after induction/intubation v) Induction agent + suxamethonium Induction doses in the critically ill must be modified from routine doses used in general anaesthesia vi) Cricoid pressure applied (ensure correct positioning) vii) Direct visualisation of vocal cords and tracheal intubation viii) Inflation of cuff until airway sealed ix) Confirmation of ETCO2 x) Chest and gastric auscultation with manual ventilation xi) Cricoid pressure released xii) Secure tube at correct length xiii) Connect patient to ventilator (see default ventilator parameters) xiv) Ensure adequate sedation ± muscle relaxant
- 47. 47 xv) Consider insertion of a naso/oro-gastric tube. Required by the majority of ICU patients. Insertion will avoid repeating the CXR. xvi) Chest X-ray xvii) Confirm blood gas analysis and adjust FIO2 accordingly. g) Sedation post-intubation: i) None if comatose or haemodynamically unstable ii) Propofol ± fentanyl infusions as clinically indicated. 6. Maintenance of endotracheal tubes a) Securing to face i) Secure ETT with white tape after insertion. ii) Ensure that the loop of tape is snug around back of neck but not too tight to occlude venous drainage should allow 2 fingers under tape. iii) Re-secure with adhesive tape once CXR check done. b) Cuff checks i) Volumetric tests are done following insertion and whenever a leak is detected: sufficient air to obtain a seal + 1ml ii) Seal is assessed by auscultation over trachea during normal ventilation. iii) Manometric tests are inaccurate and do not correlate with mucosal pressure. These are an adjunct only if cuff malfunction is suspected. c) Persistent cuff leaks i) Tubes requiring more than 8ml of air to obtain a seal or if there is a persistent cuff leak must be examined by direct laryngoscopy as soon as possible: Even if taped at the correct distance at the teeth. Ensure that the cuff has not herniated above the cords Tube has not ballooned inside the oral cavity and “pulled’ the cuff above the cords. ii) Patients at high risk for cuff leaks: Nasal RAE’s - prone to outward migration Cut tubes - do not cut tubes < 26 cm Facial swelling - burns, facial trauma Patients requiring high airway pressures during ventilation
- 48. 48 7. Endotracheal tubechange protocol a) Ensure adequate skilled assistance, equipment, drugs and monitoring as for de novo intubation. b) Procedure i) Set the FIO2 = 1.0 and change SV modes to SIMV. ii) Ensure sufficient anaesthesia and muscle relaxation (fentanyl / propofol + neuromuscular blockade) iii) Perform laryngoscopy and carefully identify: Patency of upper airway after suction Anatomy of larynx Degree of laryngeal exposure and swelling. iv) IF clear view of larynx and no or minimal laryngeal swelling: Application of cricoid pressure by assistant and careful, graded extubation under direct laryngoscopic vision. Maintain laryngoscopy and replace tube under direct vision. v) IF impaired visualisation of larynx: Re-evaluate the need to change ETT Use gum elastic or ventilating bougie Place bougie through tube under direct vision and insert to a length that would be just distal to the end of the ETT (approximately 30cm from end of tube) Have an assistant control the bougie so that it does not move during movement of the endotracheal tube Application of cricoid pressure by assistant and careful, graded extubation Maintain laryngoscopy and ensure bougie is through the cords on extubation Replace tube over bougie and guide through larynx under available vision. Inflate cuff, check ETCO2, auscultation and expired tidal volume Release cricoid pressure. Secure tube with tape.
- 49. 49 L. Weaning Guidelines 1. Commencement of weaning is a medical decision. 2. Weaning is contraindicated with any of the following: a) Unstable ICP (abort weaning if ICP increases) b) Need for heavy sedation (e.g. upper airway obstruction) c) Haemodynamic instability d) Significant bronchospasm e) High work of breathing. 3. Trial pressure support daily if the patient meets both the following criteria: a) PaO2/FiO2 ratio > 150 b) Patient can take spontaneous breaths if SIMV resp-rate reduced. 4. Weaning protocol: a) See the flow diagram following page. b) Set initial pressure support to maintain adequate VT i) Start at 10 cmH2O and adjust to: VT ≤ 6 ml/kg IBW for patients recovering from ARDS. VT ≤ 8 ml/kg IBW for all others. IBW Males = 0.91 × (height [cm] – 152.4) + 50 IBW Females = 0.91 × (height [cm] – 152.4) + 45.5 ii) Alternatively, use target VT = 80-100% of set SIMV VT iii) Allowable PS range = 5-25 cmH2O If VT cannot be achieved with 25cmH2O, cease trial c) Assess at 15 and 30 minutes for “weaning success criteria” d) Assess each hour for suitability to wean PS e) Once PS has reached minimum (5cmH2O) then wean PEEP to 5cmH2O f) If PS & PEEP = 5cmH2O then assess for extubation. 5. Weaning Success Criteria: i) RR < 30/min ii) SpO2 > 90% May be set lower with COPD, e.g. >86-88% iii) FIO2 ≤ 0.5 iv) No respiratory distress as shown by 2 or more of the following: HR > 120% baseline Accessory muscle use Diaphoresis Paradoxical abdominal movements Marked dyspnoea
- 50. 50 Flowchart: Ventilation WeaningProtocol NO Weaning Contraindication: PaO2/FiO2 > 150 Unstable ICP & AND Need for heavy sedation PEEP < 10 cmH2O Haemodynamic instability Significant bronchospasm. Check each 15 minutes - Weaning Success Criteria: “Start Weaning” Settings: RR < 30/min Reduce patient sedation SpO2 > 90% (*lower in COPD) Reduce SIMV-Rate to 8bpm FIO2 ≤ 0.5 Adjust initial PS to target VT No respiratory distress as shown 8ml/kg IBW, or by 2 or more of the following: 6ml/kg IBW if ARDS HR > 120% baseline Allowed PS range (5-25 cmH2O) Accessory muscle use PEEP remains on previous setting. Diaphoresis Paradoxical muscle movements Marked dyspnoea Weaning Failure: IF post PS decrease return to previous settings *note change to PS decrease rate Fail Pass IF post return to settings set PS to max = 25 cmH2O IF on maximum PS return to SIMV settings IF PSMax or SIMV, patient should Assess After Each Hour - be reviewed by SR or Consultant Set Pressure Support Level: If weaning successful after 1st Hour cease SIMV If successful on subsequent hours decrease PS, as per … If no previous weaning failure Weaning Complete: decrease PS by 4 cmH2O If PS = 5 & PEEP = 5 cmH2O If previous episode of failure Check ABG decrease PS 1-2 cmH2O Assess for Extubation – see over. If at minimum PS = 5 cmH2O decrease PEEP by 1-2 cmH2O
- 51. 51 M. Extubation 1. Thedecision to extubate is made by medical staff, in consultation with either the senior registrar, fellow or duty consultant. 2. Extubation is to be performed by medical or senior nursing staff, with airway competent medical staff immediately available. 3. Criteria to predict successful extubation are helpful, however, ongoing success should never be assumed: a) FiO2 < 0.5 with PEEP ≤ 5 cmH2O b) PaO2 > 70 mmHg ** lower values may be appropriate in SpO2 > 90% chronically hypoxaemic patients c) RR < 30 with PS ≤ 5cmH2O (Dräger) d) pH > 7.2 e) No respiratory distress (see over) f) Patient able to obey commands g) Patient able to protect airway and cough h) Patient able to cope with amount of secretions i) Reason for intubation resolved. *this may include checking for an air leak with the cuff deflated 4. Early extubation to NIV may be considered for some patients who present with hypercapnic exacerbation of COPD or pulmonary oedema: a) Performed with close supervision by senior medical staff. b) If no improvement after 1-2 hrs, the patient should be considered for reintubation. 5. Extubation protocol: a) Ensure equipment, monitoring and adequate assistance is available, as for intubation b) Plastic surgical and ENT patients with intermaxillary fixation/wiring require consultation with the Parent Clinic. i) A wire cutter must be present in the room at all times. ii) The parent clinic should be given opportunity to be present during extubation if the jaws are wired. c) All patients should receive supplemental oxygen pre/post-extubation.
- 52. 52 N. Emergency Surgical Airway Access 1. Policy a) Call for skilled assistance then proceed without delay. b) Difficult airway & failed intubation trolleys are in areas A, B & C c) Cricothyroidotomy, percutaneous or surgical, is the recommended procedure for urgent surgical airway access and emergency oxygenation. d) Standard percutaneous tracheostomy is not an emergency procedure. e) Cricothyroidotomy is a temporary airway - arrange a definitive surgical airway (ENT surgeons) as soon as possible. 2. Indications: a) Refer to the failed intubation drill in the clinical protocols section. b) Inability to establish an effective airway following failed laryngoscopy despite: i) Basic manoeuvres - jaw thrust / chin lift / oral-nasal airways ii) Attempted LMA insertion c) Inability to ventilate. 3. Cricothyroidotomy a) Percutaneous technique i) Equipment Cook Melker Emergency Cricothyrotomy Catheter kit (cuffed) ii) Procedure Palpate cricothyroid membrane with neck well extended 1cm horizontal incision through skin Locate tracheal lumen with fluid-filled syringe & needle/cannula Insert wire through cannula, then remove the cannula over the wire. Insert dilator/introducer & tube assembly over wire in single motion Remove wire & introducer leaving the cuffed tube. Inflate cuff & suction prior to ventilation. Confirm endotracheal placement with ETCO2 & CXR. b) Surgical technique i) Equipment Size 15 scalpel + handle Size 6.0 cuffed endotracheal tube Straight forceps Oxygen delivery circuit: Laerdal bag ii) Procedure Palpate cricothyroid membrane. 2cm horizontal incision through skin and cricothyroid membrane Insert forceps into wound and open to enlarge the wound Consider insertion of long blue ventilating bougie into trachea Insert endotracheal tube, directly into the trachea or over bougie Remove bougie and connect oxygen circuit Confirm placement with ETCO2, auscultation and CXR Perform catheter suction ASAP after adequate oxygenation
- 53. 53 O. Fibreoptic Bronchoscopy 1.Policy: a) This is only to be used by skilled personnel and authorised by the duty consultant. b) Under no circumstances may the bronchoscope be loaned to other clinics. c) Expertise with bronchoscopy takes time. Registrars are encouraged to approach the Department of Thoracic Medicine to attend bronchoscopy clinics to become familiar with the anatomy of the tracheobronchial tree and use of the flexible fibrescope. 2. Indications: a) Semi-elective difficult intubation: not used as an aid to failed intubation b) Luminal obstruction i) Sputum retention - persistent collapse refractory to physiotherapy ii) Foreign bodies iii) Luminal pathology - diagnostic c) Diagnostic bronchoalveolar lavage (BAL) 3. Protocol for fibreoptic intubation a) Indication as per endotracheal intubation b) Procedure i) All equipment, drugs and monitoring c.f. routine endotracheal intubation ii) Supplemental oxygen must be given Routinely via a mask – this may need to be cut to facilitate intubation May also be given via the suction channel of the bronchoscope iii) Can be via oral (with bite protection mandatory) or via nasal route iv) Local anaesthesia / preparation of the airway: Nasal mucosa - topical 10% lignocaine or 2% amethocaine spray. Pharynx - viscous lignocaine gargle Larynx - choice according to operator experience a. Transtracheal injection and/or direct application through the scope b. Nebulised - 5 mls 4% lignocaine c. Superior laryngeal nerve blockade (2-3ml 1-2% lignocaine). v) Check ET tube cuff vi) Place a warmed appropriately sized ETT (7mm tube for either sex) into posterior nasal space. vii) Insert the scope through the tube under direct vision. viii) Identify the vocal cords and advance the scope into the trachea. ix) Advance the ETT over scope into trachea, maintaining view of the tracheal rings or carina, then remove the scope. x) Confirm ETT placement by ETCO2, auscultation and CXR. xi) Administer additional sedation/analgesia to the patient as required. xii) NB: Suction at least 500ml water through scope immediately following use and notify the equipment nurse for cleaning ASAP.
- 54. 54 4. Protocol forBAL a) Diagnosis of nosocomial pneumonia (colonization vs. infection) b) Other indications – alveolar proteinosis, eosinophilic lung disease, etc. c) Sufficient reserve to tolerate procedure: i) Ideally PaO2 > 70 and FiO2 < 0.7 ii) BAL will commonly result in a 10% reduction in PaO2 for up to 24 hours after procedure d) Procedure i) Ensure sufficient sedation & place patient on 100% oxygen ii) Select lobe to be lavaged from recent CXR iii) Local anaesthetic gel is contra-indicated (interferes with culture media) iv) If possible, do not suction through scope prior to lavage (upper airway bacterial contamination) v) Pass the scope directly into the selected lobe vi) Wedge the scope as far as possible – ideally to 3rd generation bronchi vii) Lavage with 4-6 x 20-40 ml aliquots of sterile normal saline viii) Aspirate between aliquots and label aliquots accordingly ix) Send aspirates for quantitative culture and atypical pneumonia screen. NB: label specimens “Immunocompromised protocol” as indicated. P. Tracheostomy 1. Policy: a) Percutaneous tracheostomy (PCT) is the preferred procedure in suitable patients. b) To be performed only by consultant staff or advanced ICU trainees. c) Patients must have the option of surgical tracheostomy cleared by the parent clinic (either medical or surgical). This is a courtesy. d) The decision to perform a PCT is at the discretion of the ICU consultant. e) PCT is an elective procedure and has no place in urgent airway access. 2. Indications : a) The indications for PCT are the same as surgical tracheostomy: b) Airway maintenance i) Prolonged intubation, e.g. > 10 days ii) Laryngeal pathology – this may also be a contraindication to PCT c) Airway protection i) Delayed return of glottic reflexes ii) Tracheal toilet 3. Relative Contraindications to PCT a) Lack of consent - absolute b) Coagulopathy i) Platelets: < 100,000 ii) APTT: > 40 iii) INR: > 1.5
- 55. 55 c) Difficult anatomy - e.g. previous neck surgery, short fat neck d) Unstable cervical spine injury e) Grade III or IV intubation (relative – consider use of Glidescope / C-MAC) f) FIO2 0.6 / PEEP 10cmH2O 4. Procedure: a) Ensure consent has been obtained and documented. b) Equipment, monitoring and drugs as per endotracheal intubation c) Coagulation screen prior to procedure. d) Bedside procedure light essential. e) General anaesthesia - the airway operator must be appropriately experienced. f) Ventilate the patient on 100% oxygen. g) Tracheostomy equipment: i) Standard technique: modified Cook Ciaglia kit using the “Blue Rhino” ii) Tracheostomy tubes EVAC® aspirating tubes are standard for all tracheostomies. a. Includes patients having surgical tracheostomies b. Ensure that an EVAC tube goes with the patient to theatre. Patients who have non-aspirating tracheostomy tubes in place (e.g. from CTSU or other hospitals) must have these tubes changed to an EVAC tube as soon as safe and feasible. This is usually 4-5 days post- tracheostomy. Other tubes: a. Foam cuffed tubes - patients with tracheomalacia or persistent air leaks b. Uncuffed tube (usually #6.0) used in weaning c. Fenestrated tube: these are either cuffed or un-cuffed with a fenestration to allow patients to talk. d. XLT – extended length tubes: useful for patients with marked neck or soft tissue swelling. h) Insertion technique: i) Aseptic technique. ii) Goggles are essential for both the operator and anaesthetist iii) Local anaesthetic infiltration (2% lignocaine + 1:200000 adrenaline) over the pretracheal rings. iv) Check the tube cuff, lubricate and insert the dilator into the tube. v) 1.5-2cm horizontal incision over 1st or 2nd tracheal ring vi) Pretracheal tissue blunt dissection down to fascia *look for anterior jugular vein and ligate if identified. vii) Insert a 14G IV cannula mounted on a syringe with saline into trachea and aspirate through saline/water to confirm intratracheal placement. viii) Removal the stylet and reconfirm intratracheal placement by aspirating air via the IV cannula ix) Insert the guide-wire through the IV cannula and remove the cannula.
- 56. 56 x) Insert the small pre-dilator over the wire into the trachea and make a hole large enough to accommodate the main dilating instrument. xi) Blue Rhino® graduated 1-step dilator: Lubricate with water, not gel Place the dilator and guide cannula (white) over the wire, noting: a. The black marker on the guide at the proximal end of the Rhino b. The silver marker on the wire at the proximal end of the guide Slowly insert to the required ETT size, ensuring that both markers (wire and guide) remain in alignment at the proximal end. xii) Remove the dilator leaving the white guide cannula on the wire and insert the tracheostomy tube & dilator over the wire/guide into the trachea xiii) Remove the dilator and wire, inflate the cuff and suction the trachea xiv) Ventilate and confirm ETCO2 - self-inflating bag or ventilator xv) Secure tracheostomy tube with tapes. xvi) Obtain a CXR post procedure. xvii) Document the procedure in the case notes and complete a separate operation note. 5. Complications (of tracheostomy) a) Loss of the airway *immediately re-intubate the patient orally b) Bleeding c) False passage d) Pneumothorax e) Cricoid cartilage fracture f) Laryngeal dysfunction g) Tracheal stenosis h) Infection 6. Prolonged care of tracheostomy a) Cuff checks i) Volumetric (sufficient air to obtain a seal) tests are done following insertion and whenever a leak is detected with a manual hyperinflation once per nursing shift. ii) Manometric tests are inaccurate and do not correlate with mucosal pressure. These are an adjunct only if cuff malfunction is suspected. b) Tube changes - routine change at 28 days. c) Aspirate EVAC tube 2 hourly or more frequently if > 10ml supraglottic secretion per hour.
- 57. 57 Q. Cardiac Pacing 1.Policy: a) If inserted by ICU staff, the procedure is only to be performed by consultant staff or advanced vocational trainees under supervision. b) Become familiar with the theory of insertion, indications, interpretation and complications of TVP. 2. Indications: a) Medical pacing with adrenaline or transthoracic pacing may be adequate to treat some symptomatic bradycardias and has obviated the need for prophylactic pacing in high-risk patients. NB: particularly for retrievals. b) Any sustained symptomatic bradycardia which does not respond to medical treatment, or predisposes to a malignant ventricular arrhythmia. Note: pacing is indicated by the haemodynamic consequences of the rhythm, not the arrhythmia per se. c) Ventricular tachycardias (especially polyphasic) may respond to overdrive suppression pacing. d) Following cardiac surgery in high-risk patients (epicardial leads): i) Valve replacement / repair (especially mitral). ii) VSD repair / papillary muscle rupture. iii) Acute myocardial infarction. 3. Types: a) Semi-rigid, bipolar pacing lead (VVI) inserted under image intensification (standard TVP at RAH) b) Epicardial leads i) Placed during cardiac surgery in high risk patients ii) Usually unipolar ventricular, but may be bipolar, atrial or ventricular: check the operative note and liaise with the surgeon. c) Balloon flotation leads - ECG or pressure guided catheters d) Paceport PA catheters 4. Paceport PA protocol a) VVI mode only b) Ensure a ventricular demand pacemaker box is available c) Insert the Paceport PA catheter using standard technique (see PAC section) d) A pressure transducer should be attached to the RV as well as the distal port e) The RV port should be 1-2cm distal to the tricuspid valve i) In some patients the catheter may wedge before the RV port is in the RV in these cases an alternate technique should be used f) Attach the adapter to the RV port g) Insert probe to the reference mark h) Connect distal electrode to V lead of ECG and advance until ST elevation indicates contact with the endocardium (usually 4-5cm) i) Secure the probe and connect side port to a saline flush
- 58. 58 j) Commence pacing k)Check adequate capture and sensing (see next section)
- 59. 59 5. Semi-rigid Wireprotocol: (VVI lead) a) Strict aseptic technique b) Image intensification c) Local anaesthesia where appropriate d) Insertion protocol: i) 6F peel away sheath or PAC introducer ii) Right IJ vein is the preferred route, then left subclavian. NB: if permanent pacing is likely then avoid subclavian placement. iii) Under I-I control, feed the wire until the tip just stops on the RV wall iv) Connect to the control box (switched off) v) Set output and sense to their minimum value, and rate 20bpm faster than the patient's own rate (or 70bpm, whichever is greater). vi) Turn the generator on and gradually increase the output while watching the ECG for capture. vii) If there is no capture or a high output is required: Place on demand mode Turn output right down, advance or reposition the wire slightly Try to capture again. An ideal capture setting is ~ 2 mA Ensure wires are not exposed and tape both sides viii) Suture the wire and apply an occlusive dressing ix) Arrange a post-insertion CXR. x) Always be aware of the risk of tamponade even when pacing has been unsuccessful. e) Daily check: i) Battery strength ii) Capture: set the output 2x higher than threshold for safety. 6. Flotation Catheter Insertion a) These may be inserted either “blind”, under ECG guidance (standard recommendation), or via pressure guidance for catheters having an infusion lumen (c.f. PA catheter insertion). b) Aseptic technique & local anaesthesia where appropriate c) Insertion protocol: i) 6F peel away sheath, do not use a PAC introducer as these will leak ii) Attach V5 lead of an ECG to the distal electrode of catheter & monitor iii) Note P then QRS wave-form changes as the catheter advances to the RV iv) Advance catheter another 2cm, deflate the balloon & advance 1cm v) Connect to the pulse generator (switched off) vi) Set output and sense to their minimum value, and rate 20 bpm faster than the patient's own rate. vii) Turn the generator on and gradually increase output while watching the ECG for capture. viii) If there is no capture or a high output is required - see (5.d.vii) above ix) Suture the wire and apply an occlusive dressing x) Arrange a post-insertion CXR.
- 60. 60 R. Pericardiocentesis 1. Policy a) This procedure must be authorised by an ICU consultant and performed by consultant staff, trainees under supervision, or cardiology. b) Confirmation of pericardial effusion or tamponade with echocardiography is required prior to the procedure, except in peri-arrest situations. c) Liaison with cardiology is essential. 2. Indications a) Symptomatic pericardial effusion (tamponade). b) Although advocated in EMST (ATLS), this procedure has limited utility in traumatic pericardial tamponade. 3. Procedure a) Strict aseptic technique. b) Local anaesthetic infiltration in an awake patient. c) This procedure should be performed under ultrasound guidance. d) Technique: Seldinger technique and insertion of a pigtail catheter i) Insert needle on syringe at 45° from the horizontal axis and aim for tip of left shoulder ii) Advance slowly and aspirate until confirmation by aspirating blood or serous fluid iii) Insert catheter using Seldinger technique over guidewire. iv) Confirm placement by aspiration and/or echocardiography v) Check CXR (pneumothorax) vi) Suture and occlusive dressing if leaving for > 24 hours. 4. Complications a) Cardiac tamponade! b) Arrhythmias c) Myocardial laceration d) Pneumothorax, pneumopericardium e) Liver laceration
- 61. 61 S. Intra-Aortic Balloon Counterpulsation 1. Policy: a) The ICU consultant should be involved in the decision to insert an IABP b) Only to be performed by a consultant or advanced vocational trainee under supervision. c) Become familiar with the theory of insertion, indications, interpretation and complications of IABP. 2. Indications : a) As a mechanical bridge prior to, and/or following myocardial revascularization or transplantation: b) Ischaemic heart disease i) Low cardiac output states following cardiac surgery ii) Cardiogenic shock: in association with angiography and revascularization (PTCA, stent or CAVG) iii) Acute mitral incompetence (papillary muscle rupture) or VSD following AMI pending operative repair. c) Myocardial disease i) Severe myocardial contusion ii) Severe myocarditis iii) Cardiomyopathy iv) Severe -blocker overdose. 3. Contra-indications: a) Aortic regurgitation b) Aortic dissection c) Severe peripheral vascular disease d) Tachyarrhythmias (relative) e) Coagulopathy (relative) 4. Procedure protocol a) Strict aseptic technique b) Check IABP function prior to insertion: i) Adequate helium cylinder volume ii) Arterial pressure manifold: referenced & zeroed to mid-axillary line iii) Dedicated 5 lead ECG connected to IABP iv) Turn on and leave in standby mode v) Initial settings: ECG sense: 1:3 ratio Augmentation: minimum (pre-insertion only) Inflate and deflate times: zero
- 62. 62 c) Insertion procedure: i) Local anaesthesia in awake patients ii) Scrubbed assistant recommended iii) Select size (by patient’s height) < 152cm 25ml balloon 152 – 162cm 34ml balloon 162 – 183cm 40ml balloon >183cm 50ml balloon iv) Femoral artery insertion of a 12F introducer, Seldinger technique. v) Check the length for balloon catheter insertion, using the angle of Louis (level of T4) as the surface landmark, prior to insertion. vi) Insert the balloon to the level of T4. The double black marker on the balloon catheter must be visible This indicates that the balloon has fully exited the sheath. vii) Connect to pressure transducer and pump. viii) Press the [IAB Fill] button to fill the balloon & wait for completion. ix) Press the [Assist/Standby] button to start the pump. x) Start on minimal augmentation and increase to maximum. NB: subsequent augmentation should not be set below 50% xi) Suture in place and cover with an occlusive dressing. xii) Set timing: Check balloon inflation against pressure wave: set to peak of dicrotic notch. Check balloon deflation against ECG: prior to QRS complex and observe decrease in end diastolic pressure. Check diastolic augmentation on pressure wave. Select augmentation ratio: *standard = 1:1 d) Maintenance i) Check CXR post insertion: tip of IABP below T4 (carina) & origin of the left subclavian artery ii) Neurovascular obs of insertion site, lower limbs and left arm hourly. iii) Nurse at < 30° elevation. iv) Document pump timing (ratio) and adequacy of augmentation. v) Assess haemodynamic response: CI, MAP, SVR, filling pressures, CXR. vi) Ensure clear balloon tubing is exposed: Monitor condensation (due to rapid helium shuttling), or Blood in tubing (balloon rupture). e) Timing during arrhythmias i) Ectopics: keep on ECG trigger, system will automatically deflate on ectopic ii) Tachycardia > 160/min : Reduce augmentation (equal to patient systole) Decrease ratio to 1:2 if reducing augmentation is not adequate
- 63. 63 iii) Atrial fibrillation: move deflate slide to extreme right to deflate on R wave (not required on newer pumps) iv) VT or VF: defibrillate or cardiovert as required, the IABP is isolated v) Cardiac arrest (no output) start ECM Effective output: set on pressure trigger to synchronise balloon inflation with ECM No output: set internal mode for a fixed rate of 40 bpm + 20ml augmentation f) Weaning: i) Commence when patient’s haemodynamics have improved. ii) Methods: Reducing ratio from 1:1 to 1:2 to 1:3 and / or Reduce augmentation. NB: minimum balloon inflation 50% g) Removal of catheter i) Notify cardiac / vascular surgeons ii) Cease heparin infusion 3 hours prior to removal iii) Disconnect IABP tubing: do not aspirate the balloon iv) Withdraw balloon up to (but not into) the introducer sheath. Even empty the used balloon will not fit into the sheath, and may rupture if attempted. v) Remove the sheath and balloon as single unit, applying pressure immediately. vi) Use Femostop® local pressure during catheter removal: Remove IABP catheter with Femostop at 60-80mmHg Inflate dome to 20mmHg above systolic as catheter is fully withdrawn Reduce pressure by 15mmHg at 10-15 min intervals If bleeding occurs, reinflate the Femostop to the previously effective pressure and recommence cyclic pressure reduction Remove Femostop and apply a firm dressing vii) 10-20% may require surgical repair to the artery. 5. Complications: a) Limb ischaemia – thrombotic or embolic b) Bleeding at the insertion site or systemically c) Infection d) Aortic dissection e) Occlusion of origins of aortic arch vessels if too high f) Occlusion of renal/splanchnic vessels if too low g) Thrombocytopaenia h) Balloon rupture: gas embolism i) Femoral artery aneurysm
- 64. 64 T. Gastric / Oesophageal Tamponade Tubes 1. Policy: a) Ensure the Gastroenterology Unit are informed. b) The ICU consultant must be involved in the decision to insert an oesophageal tamponade tube. c) All patients should be intubated prior to insertion and managed in ICU. i) High risk torrential regurgitation of blood into the airway ii) Should only be undertaken by an experienced operator. d) Major complications following insertion of tamponade tubes have been reported to occur in 15%, particularly if inserted by inexperienced clinicians. 2. Indications: a) Upper gastro-intenstinal variceal haemorrhage. i) Temporising measure while awaiting endoscopy, TIPSS and / or surgery. ii) The tamponade tubes are used in conjunction with an octreotide infusion. 3. Types of tubes: a) Minnesota: oesophageal and gastric balloons and 2x aspirating ports b) Sengstaken: oesophageal and gastric balloons and gastric aspirating port c) Linton: gastric balloon and aspirating port 4. Procedure: a) Preferably use a bulk & frame bed to allow application of traction. b) Prior to insertion: i) Check both balloons for leaks. ii) Inflate the gastric balloon with 300ml of air and record pressure reading with a manometer. iii) Deflate all balloons completely and lubricate the tube. c) Estimate insertion length = bridge of nose to earlobe + nose to xiphoid process. d) Insert via nose or mouth, under direct vision using a laryngoscope. e) Must ensure gastric balloon is not in the oesophagus. i) Perform urgent x-ray to tube is adequately in the stomach. ii) NB: inflating the gastric balloon in the oesophagus is virtually 100% fatal! f) Inflate the gastric balloon in 50ml increments up to 300ml while monitoring the balloon pressure. i) If the balloon pressure ≥ 5mmHg above the pre-insertion pressure then incorrect (oesophageal) placement is probable ii) This mandates deflation of the balloon and reinsertion of the tube. g) Pull back until resistance is felt as the balloon rests against the gastric fundus. h) Note the measurement at the lips and apply gentle traction with 500ml bag of fluid on a rope and pulley system.
- 65. 65 i) Inflation of the oesophageal balloon is usually not required. i) If bleeding continues despite adequate placement of the gastric balloon and optimizing medical therapy, consider inflating oesophageal balloon. ii) It should only be inflated after discussion with the ICU consultant. iii) Inflate oesophageal balloon to 40 mmHg and reduce pressure by 5mmHg once bleeding is controlled. j) Recheck position on x-ray once balloons inflated and traction applied. k) After 12-24 hours, the balloons should be deflated to check for ongoing bleeding. U. Extracorporeal Membrane Oxygenation 1. Extra Corporeal Membrane Oxygenation (ECMO) is a method of oxygenating blood in cases of overwhelming respiratory failure (veno-venous ECMO) or temporary circulatory support in reversible cases of refractory cardio-respiratory failure (veno-arterial ECMO). 2. ECMO policies and protocols are a separate document to this ICU manual and can be accessed on the RAH ICU website (www.icuadelaide.com.au). 3. Any requests for ECMO support must be immediately directed to the ICU consultant. 4. ECMO circuit and equipment must not be altered without ICU consultant and/or perfusionist supervision.
- 66. 66 PART 3 - DRUGS AND INFUSIONS A. Policy 1. Patients admitted to the ICU must have a complete drug history documented: a) Premorbid and current medications *see pharmacy’s drug listing within the patient’s medical records. b) Previous adverse drug reactions and allergies *if known the basis for that allergy. c) Note potential drug interactions. 2. Charting of drugs and infusions is to be done by ICU medical staff. a) Parent clinics must not write on the ICU flowchart. b) Therapeutic changes suggested by the home team must be communicated to the appropriate ICU medical staff for consideration prior to charting. 3. All changes to drug and fluid orders must be written and signed for on the flowchart. a) Nursing staff must be notified of such changes. b) Verbal orders alone are neither sufficient nor legal. 4. All drugs, infusions and fluids are reviewed and transcribed at least daily. 5. Printed labels for commonly used infusions and drugs should be used where possible. 6. Standardisation of infusion concentrations is essential for the prevention of drug errors. Infusion concentrations should not be changed (e.g. ‘double strength’) from the protocols outlined below. 7. Vasoactive or hypertonic infusions (e.g. TPN) must be administered through a dedicated lumen of a CVC or PICC. 8. Vasoactive infusions must not be used in the general wards, other than for patients en route to ICU and who are being continuously monitored. 9. All antibiotics written on the ICU flowchart must also have an indication of either: a) Date started and due date for review/completion, or b) Duration and position in course, e.g. “Day 4/7”. 10. Patients cleared for discharge from ICU must have all appropriate drugs, infusions and fluids prescribed on the standard hospital forms, prior to discharge. Where appropriate, old drug charts should be re-written. 11. Patients discharged on TPN must have their details entered in the TPN folder (stored in the Unit A office area). 12. Any changes to acute pain drug regimens in patients under the care of the Acute Pain Service should be done in consultation with the Acute Pain Service. 13. Any proposed changes to specialty type drugs, e.g. immunosuppressives, anticoagulants, antiplatelet agents, etc should be discussed with home teams.
- 67. 67 B. Principles of Drug Prescription in Intensive Care 1. Drugs should be prescribed according to Unit protocols and guidelines. 2. Critically ill patients have altered pharmacokinetics and pharmacodynamics, with the potential for toxicity and drug interactions. 3. Where possible: a) Use drugs that can be titrated or prescribed to an easily measured endpoint. b) Use drugs that can be measured to monitor therapeutic drug levels. c) Avoid drugs with narrow therapeutic indices (e.g. digoxin, theophylline), particularly in patients with associated hepatic or renal dysfunction. d) Cease a drug if there is no apparent benefit. e) If two drugs are of equal efficacy, choose the cheaper drug as the cost of drugs in ICU is significant. 4. Prescribe using generic drug names only. 5. When there is a medication change (e.g. replacing an antibiotic for another, alteration in drug dose, ceasing a drug) then some indication as to the reason behind doing so should be made within the patient’s medical records or drug chart. 6. A Clinical Pharmacist conducts a daily review (Mon-Fri) of ICU drug charting, attends grand ward-rounds and is available for consultation. This is an invaluable service and should be utilized accordingly. C. Cardiovascular Drugs 1. Inotropes Inotropes (specifically catecholamines) are frequently used in ICU. There are varied prescription practices and preferences for these drugs, mostly based upon the reported pharmacological effects of the different agents. a) General principles: i) Defence of BP in the critically ill forms the basis of haemodynamic resuscitation and organ perfusion. Must be interpreted in the context of the patient’s pre-morbid BP Particularly in renovascular hypertension or cerebrovascular disease. ii) Hypovolaemia is the most common cause of hypotension and low cardiac output in ICU and must be assiduously monitored and corrected. iii) The main indications for the use of inotropes are to increase myocardial contractility, heart rate and/or vascular tone. iv) The use of inotropes requires regular haemodynamic monitoring: Arterial line and CVC are mandatory Where indicated - PAC, PiCCO, Vigileo CO or ultrasound. v) No single inotrope (or mixture) has been shown to be superior to another. vi) There is marked inter-individual variation in the response to inotropes: Pre-existing chronic illness, genetic variation Co-administration of other drugs Qualitative and quantitative changes in adrenergic receptor kinetics.
- 68. 68 vii) Prolonged exposure to catecholamine infusions can produce adrenergic receptor down-regulation and tachyphylaxis. b) Catecholamines i) Receptor effects may be unpredictable, however, in general: -adrenergic effects predominate at low doses, and -adrenergic effects at higher doses. ii) It is impossible to predict the dose range for an individual patient. iii) Prescription on a body weight basis (µg/kg/min) is of little clinical utility. iv) Infusions should be started at a low rate (3-5 µg/min) and titrated to a set clinical response, e.g. MAP (not systolic) v) There is no well established maximal dose. vi) Regular assessment should be made of both global (pH, lactate) and regional effects (urine output/creatinine clearance, limb perfusion). c) Phosphodiesterase inhibitors (milrinone) i) Inhibition of PDE3 increases intracellular cAMP and calcium, causing: an increase in myocardial contractility systemic and pulmonary vasodilatation, and improved diastolic relaxation (lusitropy) ii) Any resultant hypotension (due to systemic vasodilatation) usually responds with the addition of a vasopressor (e.g. noradrenaline). iii) Phosphodiesterase inhibitors have longer half-lives than catecholamines, are less titratable and their half-life is prolonged with renal failure. Table: Cardiovascular Effects of Catecholamines 1 effects 2 effects 1 effects 2 effects Chronotropy Inotropy Inotropy Inotropy Agent Dromotropy Vasodilatation Inotropy Bronchodilatation Vasoconstriction Vasoconstriction glucose/lactate Adrenaline Noradrenaline effects predominate at low dose effects predominate at high dose Dopamine Dobutamine + + (+) - Isoprenaline + (+) - - + = strong effect (+) mild effect - = no effect
- 69. 69 Table: InotropicAgents Used in ICU Agent Standard Infusion Uses Noradrenaline 6 mg / 100 ml 5% dextrose First line drug in septic shock (ml/hr = µg/min) Maintenance of blood pressure Adrenaline 6 mg / 100 ml 5% dextrose Cardiopulmonary resuscitation (ml/hr = µg/min) Acute severe asthma Anaphylaxis Cardiogenic shock Maintenance of blood pressure Medical pacing Dobutamine 500 mg / 100 ml 5% dextrose Primarily a vasodilator, weak inotropic action (ml/hr approx µg/kg/min) Traditionally used in cardiogenic shock or low output, high afterload states or when filling pressures high Often used in combination with noradrenaline Dopamine 400 mg / 100ml 5% dextrose Maintenance of blood pressure (ml/hr approx µg/kg/min) No advantage over adrenaline/noradrenaline “Renal dose” dopamine is not used Endocrine side effects Isoprenaline 6 mg / 100 ml 5% dextrose Vasodilator, chronotrope (rarely used) (ml/hr = µg/min) Symptomatic bradycardia Levosimendan 12.5 mg / 250 mL 5% dextrose Calcium sensitizer Loading dose: 6-12µg/kg/10min Increases myocardial contractility in an oxygen Infusion: 0.05-0.2 µg/kg/min efficient manner and dilates coronary and systemic vessels NB: Loading dose may cause Role in Intensive Care not established marked hypotension, may be omitted or reduced. Milrinone 10mg / 100 ml 5% dextrose Cardiogenic shock due to diastolic failure Loading dose: 50µg/kg/20 min Pulmonary hypertension following valve Infusion: 0.5 µg/kg/min* replacement Catecholamine induced down regulation *Standard milrinone prescription for 70 kg patient: Loading dose: 3500 µg = 35 ml over 20 minutes Maintenance: 2100 µg/hr = 20 ml/hr. 2. Vasopressor agents a) General principles i) Vasopressors usually act directly on the peripheral vasculature and are primarily used to acutely elevate BP ii) The most common cause of hypotension in ICU patients is hypovolaemia. iii) Pressor agents should not be used as an alternative to fluid resuscitation.
- 70. 70 b) Indications (in ICU) i) Tissue infiltration with local anaesthesia ii) Topically prior to nasal intubation iii) Hypotension following sympathetic block (e.g. epidural anaesthesia) iv) Hypotension refractory to large doses of catecholamines (vasoplegia): Consider relative hypoadrenalism Consider use of vasopressin c) Complications i) Rebound hypertension ii) Vagal reflex bradycardia iii) Tachyphylaxis Table: Vasopressors Agent Standard Infusion / Dose Uses Metaraminol 10mg / 10ml 5% dex: titrate Potent short acting vasoconstrictor Ephedrine 30mg / 10ml 5% dex: titrate Synthetic indirect sympathomimetic. Commonly used in anaesthesia, little benefit over adrenaline. Vasopressin 20units/20ml 5%dex: Noradrenaline resistant hypotension. 1.8mls/hrs (0.03u/min) May be useful in septic shock and post cardiac bypass for catecholamine resistant hypotension 3. Antihypertensive agents a) General principles i) The most common cause of hypertension in ICU patients is sympathetic drive due to pain, agitation, drug withdrawal or delirium. These should be treated with adequate sedation, anxiolytics and/or analgesia. ii) Patients in the recovery phase of acute renal failure are often hypertensive. This usually represents the resetting of endogenous neurohumoral mechanisms and as such does not routinely require treatment. iii) Hypertension following an intracranial event (haemorrhagic or ischaemic) is common and the underlying mechanism dictates therapy. A high BP may be tolerated in ischaemic stroke, c.f. the setting of SAH with an unclipped aneurysm, where treatment would be paramount. iv) Target therapy should be titrated against the patient’s premorbid BP. v) In the absence of adverse effects, the maximal therapeutic dose of a selected agent should be used prior to commencing a second or third agent.
- 71. 71 b) Indications i) Acute Perioperative control of BP in “at risk” patients. Hypertensive crisis (malignant hypertension) Pre-eclampsia / eclampsia Phaeochromocytoma Untreated aneurysm or vascular injury, e.g. intracranial aneurysm, ruptured/dissected aorta ii) Other indications for vasodilators Reduction of afterload in CCF or valvular disease Adjunct to passive warming in hypothermia iii) Chronic Sustained essential hypertension Ischaemic heart disease Cerebrovascular disease c) Complications – are many, but in relation to ICU patients: i) Hypotension First-dose effect / especially in hypovolaemia ii) Reflex tachycardia iii) Tachyphylaxis iv) Pulmonary vasodilatation shunt and hypoxaemia v) Cyanide toxicity (SNP) vi) Angioedema – especially ACEI vii) Deterioration in renal function viii) Electrolyte disturbances Table: Antihypertensive & Vasodilator Agents Agent Infusion & Dose Uses Glyceryl 30mg / 100ml 5%D Mainly venodilation: trinitrate (GTN) (non PVC bottle and giving set) Useful in cardiac ischaemia Range 2-25 ml/hr Less predictable control of BP than SNP First line drug in RAH ICU Tachyphylaxis develops within 24-48hr Can be given topically. will need additional agents for persistent BP Sodium 50mg / 250 ml 5%D Rapid control of hypertensive crises. nitroprusside Range 3-40 ml/hr Tachyphylaxis and metabolic acidosis may imply (SNP) cyanide toxicity (total dose > 1.5mg/kg/24 hrs) Phentolamine 10mg / 10ml 5%D: titrate Pure -blockade, short acting antihypertensive Hydralazine 5-10 mg as bolus Short to medium term IV agent. 20-40 mg 6-8 hourly Often use with -blockers to control reflex tachycardia Useful in renovascular hypertension
- 72. 72 Amlodipine 5-10mg oral bd Long acting oral Ca++ antagonist. Caution in renal impairment Captopril Start low dose ~ 5-6.25mg Treatment of hypertension up to 50mg orally 8 hrly Left ventricular dysfunction, esp post-MI Syrup: 5mg/ml or tablets Left ventricular failure Acute hypertension: 5-25mg Diabetic nephropathy sublingually prn Caution in renovascular disease and renal failure Perindopril Start 2.5mg daily up to 10mg daily orally Phenoxybenzamine Oral : 10mg/day and increase Long acting, non-competitive -blocker until postural hypotension Preoperative preparation of phaeochromcytoma IV : 1mg/kg/day Idiosyncratic hypotension may occur dilute to 200-500ml 1/3 dose over 1/24 2/3 dose over 1/24 Prazosin Start with 0.5mg, and -blocker increase up to 5mg tds orally Potent antihypertensive agent Prominent first dose effect Metoprolol Oral: 25-100mg bd High sympathetic drive states: neurogenic BP IV: 1-2mg bolus every 2-3 All grades of hypertension, inc renovascular minutes up to 10 mg. Cardiac ischaemia Control of reflex tachycardia with vasodilators Thyroid crisis Caution in poor LV function, asthma Mainly eliminated by hepatic metabolism Esmolol Loading dose 0.5 mg/kg Ultra-short acting -blocker Infuse 100mg/10ml and titrate Useful as trial for patients with poor LV function. Adjunct to vasodilators post cardiac surgery Clonidine 25µg boluses of up to Acute, centrally mediated hypertension 150µg/24hrs Useful post cardiac surgery Oral: 75µg bd Withdrawal states up to 150-300µg tds. Care with hepatic or renal dysfunction Rebound hypertension with chronic use Sedation, especially 1st dose Dexmedetomidine 400 µg in 40mls Selective alpha-2-agonist load 1µg/kg over 20min Acute, centrally mediated hypertension infuse 1-5ml/hr Not a first line drug. Selected use by senior medical staff only Sedation MgS04 5-10 mmol loading Pre-eclampsia / eclampsia Infuse at 4-12 mmol/hr Phaeochromocytoma Target plasma [Mg] ~ 1.5-2 Sympathetic overdrive in tetanus mmol/L Propanalol Portal hypertension
- 73. 73 4. Antiarrhythmics a) General principles i) Prior to administration of antiarrhythmic agents, optimise correction of the following: Hypovolaemia Metabolic abnormalities a. K+, Mg++, Ca++, HPO4= b. Hypoxaemia, hypo/hyper-carbia, alkalosis/acidosis Myocardial ischaemia or cardiac failure (especially post-cardiac surgery) Pain and agitation. ii) All antiarrhythmic drugs are potentially arrhythmogenic. iii) Virtually all depress myocardial contractility. iv) Antiarrhythmics drugs are indicated with: Actual or potential haemodynamic compromise, or Susceptible patients with myocardial ischaemia. v) Consider anticoagulation if AF > 48 hours vi) More than one antiarrythmic may be required b) Indications i) Termination of an acute arrhythmia ii) Prophylaxis against recurrence iii) Rate control iv) Enhance efficacy of cardioversion
- 74. 74 Table: Antiarrhythmic Agents Agent Infusion & Dose Uses Amiodarone Acute use: Rapid AF / flutter or MAT 900mg / 250ml 5%D: Monomorphic ventricular tachycardia Generally does not suppress contractility Load 100ml / 1 hr (5mg/kg) Can cause acute hypotension if given too rapidly Infuse 10 ml/h for 24-48 hrs Less proarrhythmic than most other drugs (15mg/kg/day) Causes QTc, but rarely Torsade de pointes Renal excretion is minimal – no need to change dose Bolus Dose 150-300mg in renal failure Long term side-effects rare in short-term use. Chronic: Interference with digoxin kinetics and assay. 200-400 mg IV/oral daily Interference with thyroid function tests. Magnesium 5-10 mmol IV slow bolus Acts principally as a calcium blocker Infuse at 2-5 mmol/hr. 2.4g MgSO4 Useful in SVT and Torsade de pointes = 10 mmol Mg++ Verapamil 5-10 mg IV slow bolus Conversion atrial flutter SR SVT Digoxin Loading dose: 0.5-1 mg IV. Ventricular rate control in rapid AF (usually 2nd line to Maintenance: 62.5-250 µg IV/day amiodarone in critically ill) Narrow therapeutic index esp in renal failure and Levels: 0.6–1.0 mmol/l metabolic abnormalities ( K+, Mg, PO4, alkalosis) Proarrhythmic potential high in critically ill patients Minimal inotropic effect in critically ill patients Hypokalaemia potentiates effects Metoprolol 1-2 mg IV bolus (up to 10 mg) Used in high sympathetic drive states : neurogenic 25-100 mg oral bd hypertension, hyperthyroidism Control of reflex tachycardia with vasodilators Caution in poor LV function, asthma Mainly hepatic metabolism Sotolol 10-80 mg IV slow bolus Class III and -blocking actions (10-15 min) Supraventricular tachyarrhythmias Conversion AF/flutter SR Low pro-arrhythmic potential Adenosine 6-12 mg IV push Diagnosis / conversion of SVT Lignocaine 0.4% solution = 4mg/ml : 2nd line drug after amiodarone 60 ml/hr (4mg/min) for 1-2 hrs Sustained, recurrent VT 45 ml/hr for 2-4 hrs No longer routinely used for prophylaxis for VT 30 ml/hr for 2-4 hrs VF resistant to defibrillation (now questioned) Potent negative inotrope, pro-convulsant Flecanaide 1 mg/kg slow IV push SVT 100 mg oral BD (max of 300 AV nodal re-entrant tachycardia mg/day) WPW Ventricular dysrythmias Phenytoin 15 mg/kg loading / 1 hr Digoxin toxicity 300 mg/day Tricyclic induced malignant arrhythmias (level 40-80 mmol/l)
- 75. 75 5. Thrombolytic Therapy a) All patients with acute MI are potential candidates for primary angioplasty: i) Cardiology must be notified as early as possible. ii) The duty cardiologist will decide between primary angioplasty, thrombolysis and medical management. b) Indications i) Acute myocardial infarction Thrombolysis is standard in the management of AMI unless primary angioplasty is performed. a. No specific age limit b. Onset within 12hrs (potentially 24hrs) of presentation i. Benefit is inversely proportional to delay in thrombolysis, therapy should be considered a “medical emergency” ii. Late therapy may be inappropriate for “small” infarcts. c. ECG evidence of acute infarction: i. ST segment 2mm in 2 adjacent chest leads, or ii. ST segment 1mm in 2 adjacent limb leads, or iii. New LBBB iv. Posterior infarction (R in V1 + ST in V2) d. No benefit has been demonstrated for patients with ST-depression, T-wave inversion, or a normal ECG. The patient should be advised of the potential risks and benefits. ii) Haemodynamically unstable pulmonary embolism. An unequivocal diagnosis is necessary (spiral CT or angiogram). Tenecteplase is preferred in life threatening pulmonary embolism. iii) Ischaemic Cerebrovascular Accident Within 4.5 hrs of onset of symptoms CT head: confirming CVA and excluding intracranial haemorrhage Oedema on initial CT head is associated with a higher incidence of bleeding In consultation with a neurologist according to RAH protocol. c) Contraindications: i) Absolute: Active internal bleeding or bleeding diathesis. Recent head/facial trauma, major trauma or surgery within 3 months. Previous intracerebral haemorrhage. Known structural cerebral vascular lesion or malignant intracranial neoplasm CVA within 3 months.
- 76. 76 ii) Relative: Lack of verbal informed consent. Prolonged CPR (> 10 mins) and/or traumatic resuscitation History of poorly controlled hypertension Uncontrolled hypertension at presentation: systolic >180mmHg and/or diastolic >110mmHg CVA greater than 3 months Other intracranial disease, including dementia Diabetic proliferative retinopathy. For streptokinase or anistreplase - a prior exposure (>5 days previously) or allergic reaction to these drugs Major Surgery within 3 weeks. Active peptic ulceration or other GI bleeding within 2-4 weeks Non-compressible vascular puncture/injury. Pregnancy. d) Complications i) Reperfusion arrhythmias ii) Bleeding (cerebral haemorrhage 0.5%) iii) Anaphylaxis/anaphylactoid reactions: hypotension, rash, bronchospasm e) Routine follow-up i) ECG at 1 and 4 hours post TNK ii) Cardiac enzymes 6, 12 and 24 hours post infusion iii) If ST-elevation persists ≥ 1 hr post-TNK, contact cardiology regarding “rescue angioplasty”.
- 77. 77 Table: Thrombolytics Drug Dose Protocol Tenecteplase Single dose: Aspirin 150mg pre-Rx, then daily TNK 1. 0.5 mg/kg over 10 sec Enoxaparin 30mg IV prior to TNK 2. non-glucose containing line Enoxaparin 1mg/kg sc bd 3. flush line with N.Sal pre & post (if renal function normal) If renal impairment consider heparin IV Maximum dose = 50mg (=10,000U) instead of enoxaparin. Alteplase Bolus Dose = 15 mg. Observe vital signs and neurological Infusion (1) = 0.75 mg/kg over 30 min observations every 30 minutes for the first (max of 50mg), then 6 hours post infusion then hourly for the Infusion (2) = 0.5 mg/kg over 60 min next 16 hours (max of 35mg) Repeat BP more frequently if elevated Therapeutic Heparin Infusion Keep BP <180/105 - per RAH protocol. Alteplase in 0.9 mg/kg intravenously (max 90mg) Heparin 5000U IV pre-TNK Pulmonary 10% as a bolus, then Heparin infusion: APTT > 50-80 secs Embolus remainder over 60 min Bleeding Monitor: Apply local pressure (if possible) protocol: APTT Reverse heparin with protamine PT / INR Cryoprecipitate 10 units + FFP 2 units Fibrinogen level Defibrination or intracranial bleed: Euglobulin clot lysis time tranexamic acid 10 mg/kg over 20 minutes then 1mg/kg/hr infusion
- 78. 78 6. Antiplatelet Agents Table: Antiplatelet Agents Agent Usual dose Indications/Comments Aspirin 75-150 mg Post acute coronary syndrome Other thrombotic cardiac event Post TIA / stroke Clopidogrel 75mg orally daily Irreversibly modifies platelet ADP receptor, inhibiting aggregation 300mg oral loading dose pre-PTCA Uses: prevention of vascular ischaemic events (then 75mg daily) e.g. MI, CVA, PTCA ReoPro Bolus: 0.25mg/kg IV over 1 min, Only to be ordered by Cardiology (abciximab) 10mins before PTCA Binds to platelet glycoprotein IIb/IIIa receptor, inhibiting platelet aggregation and thrombus Infusion: formation 0.125µg/kg/min IV for 12hrs. Primarily used with PTCA (max rate = 10µg/min) Used with aspirin and heparin (target ACT >200sec) Increased risk of major bleeding and thrombocytopaenia Tirofiban Bolus: Only to be ordered by Cardiology (aggrastat) 0.4 µg/kg/min Blocks glycoprotein IIb/IIIa receptor for 30 mins Short half-life (1.4-1.8 hrs) Uses: unstable angina, non-Q wave MI Maintenance: Use with heparin and aspirin 0.1 µg /kg/min Continue through angiography, and for 12-24hrs for at least 48hrs post-PTCA Check platelet count 6hrs post-bolus, then at NB: reduce doses by 50% with least daily. If <90,000 cease and contact severe renal insuff. (e.g. creat cardiology clearance <30ml/min) SEs: bleeding (major 1.4%), thrombocytopenia, fever
- 79. 79 D. Respiratory Drugs 1. Inhaled bronchodilators a) General Principles: i) Relieve bronchoconstriction. ii) They are not routinely used in all ventilated patients. iii) Not all wheeze is bronchoconstriction – consider other pathology such as upper airway obstruction, pulmonary oedema, consolidation. iv) Regularly review: Patients symptoms. Work of breathing (i.e. respiratory rate, accessory muscle use). Wheeze. Airway pressures. End-tidal CO2. Blood gases. b) Indications: i) Asthma. ii) Chronic obstructive pulmonary disease (COPD). iii) Bronchospasm 2° to infection, aspiration or during mechanical ventilation, not primarily due to airway secretions. iv) For the treatment of hyperkalaemia (nebulised salbutamol only). c) Metered dose inhalers: i) MDIs are the default therapy for ICU patients. ii) Can be administered via a MDI adaptor on the ventilator circuit. d) Nebulised medication: i) Nebulsied medications are best avoided due to the risk of aerosolising airway secretions and suboptimal delivery of drug to smaller airways. ii) Nebulisers are used only if inadequate response to 10 puffs of MDI. iii) Continuous nebulised bronchodilators can be administered in status asthmaticus. 2. Parenteral therapy a) Indications: i) Adjunctive therapy for patients with acute severe asthma or COPD not responding to maximum dose inhaled bronchodilators. b) Complications i) Tachyarrhythmias. ii) Hypokalaemia. iii) Hyperglycaemia. iv) Lactic acidosis.
- 80. 80 Table: Bronchodilators Drug Infusion / dose Clinical uses Salbutamol MDI Usual Dose - 2 puffs 4 hrly. First line bronchodilator. Max Dose - 10 puffs every 15 Default method of administration. minutes. Salbutamol (nebulised) Usual Dose - 5mg every 1-4 hours. Bronchospasm refractory to MDI. Max Dose - 20mg every hour Severe hyperkalaemia. (i.e. continuous nebs). Ipratropium MDI Usual Dose – 2 puffs 6hrly Max Dose - 4 puffs hrly as required. Acute Asthma. Chronic obstructive pulmonary disease. Ipratroprium Usual Dose - 500ug 8 hrly. Bronchorrhoea. (nebulised) Max Dose - 500ug hrly as required. Adrenaline (nebulised) Max Dose – 1mg every 15 minutes. Severe bronchospasm unresponsive to continuous salbutamol nebs. Salbutamol (IV) 6 mg / 100 ml 5%D Acute severe asthma (ml/hr = µg/min) Acute severe asthma unresponsive to Load = 200ug over 1 minute. continuous inhaled bronchodilators + systemic Infusion = 5-20ug/min steroids. Adrenaline (IV) 6 mg / 100 ml 5%D Acute severe asthma unresponsive to (ml/hr = µg/min) continuous inhaled bronchodilators + systemic Infusion = 1-20 ug/min steroids. Titrate until blood pressure rises.. Aminophylline 1000mg / 100ml 5%D Unproven efficacy in acute asthma / COAD. Loading 5-7mg/kg, Narrow therapeutic index. Infuse 2-4ml/hr (1gm/day) Levels: 55-110 mol/l
- 81. 81 E. Sedation, Analgesia and Delirium 1. Sedation and Analgesia a) Adequate analgesia and anxiolysis are primary management goals in ICU. b) Pain and anxiety are associated with significant adverse effects: i) Hypertension, tachycardia ii) Increased myocardial and cerebral oxygen consumption iii) Gastric erosions iv) Intracranial hypertension v) Increased catabolism vi) Delirium c) Sedatives and analgesics are also associated with adverse effects: i) Respiratory depression ii) Prolonged ventilation and complications (e.g. nosocomial infections) iii) Delirium iv) Hypotension v) Gastroparesis, ileus and resultant feed intolerance vi) Increased cost & ventilator days d) Sedation protocol for ICU patients: i) Important to obtain a reasonable balance between the awake, distressed patient and the patient that is oversedated. ii) Sedation should be given by infusion ± boluses to maintain constant levels rather than peaks and troughs iii) Titrate infusions to clinical effect: there is marked inter-individual variability and absolute doses are of little value iv) Sequential increases in infusion rate, without the use of a bolus dose, increases the risk of over-sedation as steady-state is reached (5 half-lives) v) The half-life for fentanyl increases with the duration of infusion (context- sensitive half-time), so time to steady-state may be greatly prolonged. vi) Grimacing alone is not a reliable sign and may only indicate awareness or reflex activity. vii) Patients with an encephalopathy, renal or hepatic impairment are likely to require significantly less or no sedation. viii) Prescribe the desired sedation level (RASS = 0 to -5) in the box on the ICU flow chart. ix) In the absence of a contraindication, sedation should be held daily from 0800 for all patients, except those prescribed a sedation score of - 4 or -5. e) PCA or epidurals are considered when the patients are awake, in cooirdination with the Acute Pain Service.
- 82. 82 Table: Nurse Controlled Sedation Protocol Hold the infusion until the patient reaches the prescribed level Over-sedated If ongoing sedation is required, recommence at half the previous infusion rate. Use a bolus of sedation/analgesia and increase rate according to Under-sedated dose range prescribed. If insufficient repeat until a satisfactory sedation level is attained. Infusions should not be titrated to responses during high-intensity stimuli, e.g. suction. In these situations, bolus sedation should be provided. Table: Modified Richmond Agitation Sedation Scale (RASS) Score Term Description Overtly combative / violent +4 Immediate danger to staff Very agitated, pulls or removes tube(s) or catheter(s) +3 Aggressive Agitated, frequent non-purposeful movement +2 Fights ventilator Restless, anxious +1 Movements not aggressive or vigorous Alert and calm 0 Eyes open spontaneously Not fully alert but responds easily to voice or light touch. -1 Sustained awakening & eye contact >10 seconds Responds easily to voice or light touch. -2 Difficulty staying awake & eye contact <10 seconds Difficult to rouse, responds to voice or touch with movement or brief eye opening -3 No eye contact No response to voice or touch. -4 Movement or eye opening to physical stimulation (discomfort / tracheal suction) No response to voice or physical stimulation -5 Weak or absent cough on tracheal suction 2. Delirium a) Delirium: “an acute, reversible organic mental syndrome with disorders of attention and cognitive function, increased or decreased psychomotor activity and a disordered sleep wake cycle”. b) An independent predictor of longer ICU stay and increased mortality. c) Three forms characterised: i) Hyperactive - agitated, paranoid ii) Hypoactive - withdrawn, quiet, paranoid iii) Mixed - combination of above
- 83. 83 d) Hypoactive deliriumis under recognised, especially without specific screening. e) Patients with a modified RASS score ≥ -3 will be screened for delirium by nursing staff using the CAM-ICU (see below): i) Adaptation of the ‘Confusion Assessment Method’ for non-verbal patients. ii) Sensitive and specific tool and if positive the patient likely has delirium. iii) Should be assessed and a management plan formulated daily. f) Prevention: i) Provide appropriate analgesia and anxiolysis, avoiding oversedation ii) Hold sedation daily until the patient wakes RASS > -1, unless contraindicated, i.e. patients prescribed RASS -4 / -5 iii) When possible correct physiological disturbances Hypoxia, acidosis, electrolyte imbalance Drug withdrawal (nicotine, alcohol, opiates, benzodiazepines) iv) After prolonged infusion opiates may require weaning rather than abrupt cessation v) Provide psychological support and orientation Encourage patient participation in treatment Repeatedly orientate the patient in time, place and person Involve relatives in reassuring patient if possible Consider papers, television etc. to help orientate patient during the day vi) Provide an unambiguous environment vii) Allow an environment for sleep (minimal noise, light etc. at night) If possible do not performing invasive procedures at night Minimise nocturnal interventions when clinically safe. Perform RASS concurrent with GCS assessment. Use nocturnal sedation as a last resort viii) Maintain competence Maintain activity levels and promote early mobilisation Make sure glasses, hearing aids etc. available for use Consider interpreters for non English speaking patient ix) Minimise use of drugs associated with delirium. (see table below) If appropriate consider sedation with a central α-2 agonist g) Management of Delirium i) Identify and treat predisposing factors: Pain Metabolic and haemodynamic instability Infection Drug interactions and withdrawal CNS disorders (stroke, abscesses, seizures, tumours) Renal, cardiac, hepatic, GI failure Myocardial ischaemia Ventilator dysynchrony Immobilisation Frustration / Anxiety
- 84. 84 ii) Minimise use of drugs associated with delirium: Table: Drugs Associated with Increased Delirium Analgesics Codeine Morphine Fentanyl Antiemetics Prochlorperazine Corticosteroids Dexamethasone Hydrocortisone Prednisolone Antidepressants Amitriptyline Paroxetine Antimuscarinic Atropine Hyoscine Hypnotics Diazepam Midazolam Thiopentone Anticonvulsants Phenytoin Phenobarbital Cardiovascular Atenolol Digoxin Dopamine Lignocaine Antihistamines Chlorphenamine Promethazine Antipsychotics Chlorpromazine Misc. Furosemide Ranitidine iii) Pharmacotherapy Limited evidence pharmacotherapy shortens duration of established delirium however may be necessary for behavioural control Drug choice should be individualized and therapy short term. Recommended agents (see table below) include: a. Haloperidol b. Olanzapine c. Dexmedetomidine /clonidine d. Quetiapine, Chlorpromazine Benzodiazepines are best avoided unless indicated for rapid sedation or treatment of GABA withdrawal syndromes, e.g. delirium tremens. One agent should be titrated to maximal safe dose (or onset of adverse effect) before introduction of a second agent. iv) Physical Restraint – see following. 3. Physical Restraint – for emergency medical treatment a) The use of restraints can be humane and effective while facilitating diagnosis and treatment and preventing injury to the patient and medical staff. b) Restraint may be indicated when a professional and proper approach, including verbal techniques are unsuccessful. c) Patients may be restrained under either: i) The Mental Health Act (1993): when a patient requires immediate treatment for a mental illness including drug and alcohol induced delirium ii) The Consent to Medical Treatment and Palliative Care Act (1995): when a patient over 16 years of age requires treatment for an immediate risk to life or health and is incapable of giving consent
- 85. 85 d) The process requires: i) Examination by two doctors (when available) to confirm the patient is incapable of giving consent. A person can be deemed incapable when they are unable to comprehend, retain and judge information relating to the consequences of having or not having treatment ii) This can be demonstrated by positive CAM-ICU iii) Documentation in the case-notes of the patient’s incapability and a treatment plan for the condition, detailing the need for temporary restraint. e) Identification and treatment of the illness precipitating the mental incapability f) The doctor to be acting in good faith and in accordance with professional standards in order to preserve or improve quality of life g) Regular reassessment of the need for physical restrain is required and restraints must be removed if a patient regains mental competence (ie the delirium resolves, which may be evidenced by a negative CAM-ICU) h) If the patient has a guardian they should be notified of the need for restraint as soon as possible. i) A Form 1 need only be completed if the patient is detained under The Mental Health Act (1993). In this instance it is necessary to inform the Psychiatry team. j) A patient with the capacity to make reasonable decisions and who poses no threat to himself or others cannot be confined or restrained without their permission. Doing so is illegal. If patient deemed to be competent poses a significant threat security and the police should be called k) On ICU discharge ensure a plan regards cessation of agents used to manage delirium is documented and communicated verbally to the home team. Flowchart: Confusion Assessment Method for ICU (CAM-ICU)
- 86. 86 Table: Sedatives /Analgesics Drug Infusion/dose Clinical uses Propofol 10mg/ml (neat solution) First line sedation in combination with fentanyl Initial rate 3-5ml/hr Anaesthesia for minor procedures where prompt return of Titrate against effect consciousness is required (e.g. tracheostomy, CVC) Potent myocardial depressant/vasodilator No analgesic effect. Maximum 4mg/kg*/hr (*estimate lean weight) Fentanyl 100-200 µg IV bolus First line analgesic Infusion: 20-200 µg/hr Potent medium acting narcotic with relative (neat solution) haemodynamic stability Combined with propofol for sedation Useful for ICU procedures. Morphine and morphine 60mg + Second line sedation - consider if propofol Midazolam midazolam 30mg contraindicated or causing adverse effects (eg per 50ml 5% dextrose hypotension) Review rate/sedation at least daily Rate: 1-10 ml/hr Effects prolonged in renal failure Morphine 1-5 mg IV, sc prn, or Alternative analgesic to fentanyl PCA per protocol Caution in renal failure Diazepam IV: 2-10 mg prn First line in acute alcohol or benzodiazepine withdrawal Orally: 5-20mg bd-qid* Larger doses may be required esp. delirium tremens Avoid in delirium not related to alcohol/benzo withdrawal Epidural cocktail Fentanyl 5µg/ml and Standard epidural analgesic regimen (APS protocol) Bupivacaine 0.1% or Plain bupivacaine may be used (0.25%) Ropivacaine Maximal duration 4 days unless indicated Rate: age related doses (per APS) Dexmedetomidine 400 µg in 40mls Selective central alpha-2-agonist load 1µg/kg over 20min Short term sedation / weaning from ventilation / delirium / infuse 0.2-0.7 ug/kg/hr withdrawal states Selected use by senior medical staff only Agents Primarily Used in Agitation/Delirium Haloperidol 0.5-2.5 mg IV prn First line major tranquilliser Delirium, agitation Max dose: 10mg Esp. in opioid / benzodiazepine withdrawal. blocker : may cause hypotension QTc, seizures, extrapyramidal ettects Chlorpromazine 2.5-5 mg IV prn 2nd / 3rd line agent for delirium More sedating, unpredictable & longer acting Vasodilator Olanzapine 5-10mg SL or orally Increase delirium (central cholinergic effect) (off-label) (2.5-5mg in the elderly) QTc prolongation Maximum dose 10mg BD Reduced seizure threshold Extrapyramidal effects Metabolism (CYP-1A2) is reduced by Ciprofloxacin Quetiapine 50-100mg enterally BD QTc prolongation (off-label) Reduced seizure threshold. Metabolism (CYP-3A4) with fluconazole, erythromycin
- 87. 87 4. Analgesia inAwake Patients – See APS Intranet Guidelines ACUTE PAIN SERVICE SC AND ORAL OPIOIDS – INITIAL DOSES SC morphine/oxycodone Oral oxycodone* Age (yrs) (mg) (mg) 15 – 39 7.5 – 12.5 15.0 – 25.0 40 – 59 5.0 – 10.0 10.0 – 20.0 60 – 69 2.5 – 7.5 5.0 – 15.0 70 – 85 2.5 – 5.0 5.0 – 10.0 > 85 2.0 – 3.0 2.5 – 5.0 Recommended dose interval: 2 hourly prn * ↓ if pain not severe Acute Pain Service (APS) contact numbers Mon-Fri: 0830-1730 pager 22556 After 1730 hrs SD 1175 W/E & Pub Hol via Switch Notes: ▪ Suggest start in middle of dose range; upper limit of dose range can be increased if analgesia is inadequate, sedation score is less than -2 and resp rate > 8 /min (first check that doses are correct/ have been given as ordered) ▪ Sedation score - 2 = responds easily to voice or light touch but difficulty staying awake, eye contact maintained < 10 seconds Dose equiv. SC (mg) Oral (mg) Morphine 10 30 Oxycodone 10 20 Fentanyl 150 microgram - Buprenorphine 400 microgram (patch) 800 microgram (SL) Simple analgesia: ▪ Unless contraindicated, paracetamol is best ordered for all patients and on a regular rather than prn basis
- 88. 88 F. Muscle relaxants 1. General principles a) These agents have a limited role in ICU and must not be used unless the patient is adequately sedated (modified RASS -4 / -5). b) Non-depolarising agents (except rocuronium) should not be used for emergency (rapid sequence induction) endotracheal intubation. 2. Indications a) Depolarising: suxamethonium i) First line agent for emergency endotracheal intubation b) Non-depolarising: rocuronium, vecuronium, atracurium i) Acute control of ventilation post-intubation ii) Patient transport / retrieval on Oxylog ventilator who cannot be managed by other means iii) Selected patients with poor lung compliance who are difficult to ventilate following “heavy” sedation iv) With anaesthesia for procedures: tracheostomy, bronchoscopy 3. Complications a) Hyperkalaemia, bradycardia (suxamethonium) b) Sympathetic overdrive, particularly in under-sedated patients c) Adverse outcome in head injury when used as a measure to control ICP d) Use of non-depolarising relaxants may be associated with increased risk of critical illness polyneuropathy, especially with concomitant use of steroids. Table: Muscle Relaxants Relaxant Dose Comment Suxamethonium 100-200 mg or 1st line agent in Rapid Sequence Induction (RSI) 1-2 mg/kg Consider pre-treatment with atropine (0.6-1.2mg) if potential bradycardia Contraindicated in burns (>3 days), chronic spinal and neuromuscular disease, hyperkalaemic states (K+ > 5.5) Caution in any patient with any central or peripheral muscle weakness including critical illness related weakness Rocuronium 0.6 mg/kg First line non-depolarising agent in ICU Rapid onset (60secs) 1.0 mg/kg 2nd line agent in RSI = alternative to suxamethonium for RSI Duration of action : 30-40 minutes Vecuronium 4-10mg IV prn 2nd line non-depolarising agent in ICU Duration similar to rocuronium Cardiostable, low incidence of allergy
- 89. 89 G. Anticoagulation 1. Generalprinciples a) All patients on systemic anticoagulation must have an APTT, INR and CBP performed daily. 2. Indications a) Acute systemic anticoagulation: i) As a general rule, heparin infusions are used in critically ill patients: Allows monitoring/titration to a therapeutic APTT. Provision for reversal if indicated (e.g. procedures, bleeding). ii) Enoxaparin is effective but more difficult to use in critically ill patients: Inability to monitor activity Dose variation in renal disease and Inability to reverse effect. iii) Indications: Proven venous or arterial thromboembolism Acute coronary syndromes Prosthetic heart valves: a. Prior to commencement of oral anticoagulants b. During an acute illness, where oral anticoagulation is relatively contraindicated. AF in patients complicated by emboli < 70 years. AF for more than 48 hours, in which cardioversion is being considered Extracorporeal circuits e.g. CVVHDF, ECMO iv) RAH Heparin Protocol – see below b) Partial anticoagulation i) low dose IV heparin (500 u/hr) ii) IV prostacyclin c) Warfarin i) The kinetics of warfarin are highly variable in the critically ill. ii) Normally only used in stable long term patients iii) Prosthetic valves (mitral > aortic valves) iv) Previous thromboembolism v) Maintenance of thromboprophylaxis in high risk patients (# pelvis)
- 90. 90 3. Protocol forDVT/VTE prophylaxis All patients must have a documented plan for DVT prophylaxis a) Mechanical prophylaxis i) TED stockings All patients except those with: a. Significant PVD b. Significant lower limb trauma, cellulitis, dermatitis or oedema c. Peripheral venous or arterial access on lower limb(s) d. For most of the above patients, a single TED should be used on the unaffected limb TED stockings can be used in patients with proven DVT to decrease the incidence of post DVT thrombophlebitis Continue until the patient can mobilise effectively ii) Sequential calf compression devices SCCD’s have an additive effect to other forms of DVT prophylaxis. Patients unable to use chemoprophylaxis or at high risk are given priority. In patients without DVT prophylaxis > 24 hrs consider a lower limb ultrasound to exclude DVT prior to application of SCCD’s b) Chemoprophylaxis i) Enoxaparin or heparin should be charted for all patients unless contraindicated and continued throughout their ICU stay ii) For patients with a high risk of bleeding, communication with the relevant surgical teams (neurosurgery, spinal, ophthalmology, etc) is essential. iii) Enoxaparin 40 mg s/c daily is the default agent. Start on day 1 or as early as possible especially in high risk patients. Potential accumulation in renal failure Not routinely monitored (anti-Xa level). iv) Unfractionated (UF) Heparin 5000U s/c b.d.-t.d.s Used in patients with a high risk of bleeding or renal failure Shorter duration of action and ease of reversal. v) Enoxaparin 60 mg s/c daily (20mg mane + 40mg nocte) Considered for high risk patients: a. Pelvic or long bone fractures b. Significant spinal injury or paralysis c. Previous PTE/DVT Routine monitoring is not necessary. vi) No other DVT protocols are to be used except post-pelvic surgery Adjusted dose heparin protocol may be used See “VTE Prophylaxis in Orthopaedics” on the RAH Intranet vii) Cease prophylaxis for significant bleeding or suspected HITS - see below
- 91. 91 viii) Absolute and relative contraindications for heparins: Significant active haemorrhage High risk of bleeding a. Coagulopathy - DIC, thrombocytopenia, liver failure, etc. b. Post-surgical - neuro, spinal, eyes c. Major trauma - TBI with parenchymal lesions, liver/spleen Known or suspected adverse reaction to heparin a. Documented or suspected HITS, known heparin allergy Patients already on therapeutic anticoagulation c) IVC filter i) In high risk patients with ongoing contraindications to chemoprophylaxis, an IVC filter can be considered. 4. Perioperative anticoagulation in patients on Warfarin a) Heparin infusion i) First choice in ICU ii) Effect is more readily monitored and reversed. b) Where heparin is contraindicated, consider danaparoid or consult haematology. 5. Protocol for Heparin Induced Thrombocytopaenia Syndrome (HITS) a) General principles i) HITS is a prothrombotic disorder caused by platelet-activating antibodies ii) An intense hypercoagulable state often complicated by venous and arterial thrombosis iii) Risk factors Duration of therapy *see 4T table Type of Heparin UFH > LMWH Type of patient postsurgical > medical > pregnancy b) Diagnosis i) The 4T Score ‘pre-test probability’ of HITS Points - 0, 1, or 2 for each of 4 categories (see table) Maximum possible score = 8 a. High risk 6-8 points b. Intermediate risk 4-5 points c. Low risk 0-3 points If probability is intermediate or high do a HIT screen for antibodies. If high probability cease heparin immediately pending test results ii) HIT Screen ELISA detects antibodies against heparin and PF4. Also detects other non-HIT heparin-Ab, therefore lower specificity If ELISA positive then test further with a "functional assay", serotonin release assay (SRA) iii) Lower limb doppler U/S
- 92. 92 Table: HITS ProbabilityScore – ‘4T Score’ Risk Factor 2 Points 1 Point 0 Points Thrombocytopenia Platelet fall >50% Platelet fall 30-50% Platelet fall <30% Nadir >20 or >50% fall due to surgery Nadir <10 or nadir 10-19 Timing of onset of Day 5-10 > Day 10 or timing unclear < Day 4 platelet fall (or other or or No recent heparin sequelae of HITS) Day 1 with heparin < Day 1 with heparin in last 30 days in last 31-100 days Thrombosis or Proven new thrombosis, Progressive or recurrent None other sequelae skin necrosis thrombosis, or erythematous skin lesions, Anaphylactoid reaction after suspected thrombosis, IV heparin bolus asymptomatic upper limb DVT OTher cause None Possible Definite of platelet fall Pre-test probability score: High (6-8) | Intermediate (4-5) | Low (0-3) a) Treatment principles i) Two Do’s Do stop all heparin (including flushes, LMWH, etc ) Do start an alternative non-heparin anticoagulant in therapeutic doses. a. Lepirudin - difficult to use, or b. Danaproid - may cross react c. Discuss with haematology ii) Two Don’ts Don’t administer warfarin acutely and if warfarin has already been administered, give vitamin K Don’t give prophylactic platelet transfusions iii) Two Diagnostics Test for HIT antibodies Investigate for lower limb DVT
- 93. 93 6. Anticoagulants Table: Anticoagulants Drug Infusion / Dose Variable dose Daily INR See age-adjusted Warfarin loading protocol on the RAH intranet. Warfarin NB. This is meant only as a guide, and was developed for non- critically ill patients, whose pharmacodynamics may differ significantly from the intensive care population. 25000u/50ml = 500u/ml Heparin (infusion) See below: titrate against APTT: Cease 4-6 hours prior to surgical procedures 5000 u subcut bd <70 kg Heparin (subcut) 5000 u subcut 8 hrly >70 kg or high risk DVT Prophylaxis: 40mg subcut daily 20mg subcut daily if Creat clearance < 30ml/min Enoxaparin (Clexane®) “High risk” 20mg mane 40mg nocte Treatment: 1mg/kg subcut bd - lean body mass 1mg/kg subcut once daily if CrCl < 30ml/min Dose: 0.2-0.6 µg/kg/hr 500µg (+10ml diluent): add to 40ml NSal = 10µg/ml solution Prostacyclin (infusion) Start at 2ml/hr and monitor platelet count May cause hypotension IV loading dose: < 60kg 1500 U 60-75 kg 2250 U 75-90 kg 3000 U > 90 kg 3750 U Danaparoid sodium Infusion: 2250U of danaparoid in 250ml 5% dextrose: (Orgaran®) 44 ml/hr (400 U/hr) x 4 hours Infusion 33 ml/hr (300 U/hr) x 4 hours 22 ml/hr (200 U/hr) Adjust dose to anti-Xa levels (target 0.5-0.8 anti-Xa U/ml) Long half life (25 hrs): cease early if changing to oral anticoagulants Danaparoid (subcut) 750 U 8-12 hourly Lepirudin Complex see below Dabigatran See below
- 94. 94 Table: Heparin InfusionProtocol Weight (kg) 45-55 56-65 66-75 76-85 86-95 >95 Bolus (U) 3,500 4,200 4,900 5,600 6,300 7,000 Infusion (U/hr) 900 1,100 1,250 1,400 1,600 1,800 Infusion adjustment APTT IV bolus Stop Infusion Rate Change Repeat APTT < 37 5,000 units 400u/hr 6 hrs 38-64 200u/hr 6 hrs 65-110 No change Daily 111-130 50u/hr 6 hrs 131-140 30 min 100u/hr 6 hrs 141-150 60 min 150u/hr 6 hrs 120 min or > 150 200u/hr 2 hrs APTT <150 Note: Infusion: 25,000 units in 50ml syringe = 500U/ml Check first APTT 6 hrs after bolus dose Table: Lepirudin Infusion Protocol Maintenance Infusion CrCl (ml/min) Bolus Dose mg/kg/hr % original dose 0.4 mg/kg > 60 0.1 (max 11mg/hr) 100% (max 44mg) 45-60 0.2 mg/kg 0.05 50% 30-44 0.025 25% 15-29 0.01 10% None < 15 0.005 5% CVVHDF 0.01 10%
- 95. 95 7. Lepirudin a) Recombinant direct thrombin inhibitor b) Dose range varies by a factor of 20x i) Care must be used in determining the precise dose ii) Renally excreted and must be carefully monitored in the critically ill c) NB: a bolus dose is only used if patient has life threatening thrombus 8. Dabigatran a) Competitive direct thrombin inhibitor. b) Used as an oral alternative to warfarin. c) Current indications include: i) Atrial fibrillation ii) VTE prophylaxis following major orthopaedic surgery. d) Renally cleared with a half-life 12-14 hrs. e) Monitoring i) INR cannot be used to monitor efficacy or toxicity. ii) APTT provides an approximate indication of the level of anticoagulation iii) A normal APTT suggests that drug is unlikely to be present in significant concentration. iv) APTT of > 80 seconds suggests that drug is present in excess. f) No specific antidote is available to reverse effect. i) For severe bleeding, supportive strategies are recommended, including transfusion of fresh whole blood, or fresh frozen plasma. ii) Dialysis may be indicated in patients with prolonged APTT particularly if renal function is impaired. iii) The role of prothrombinex and rFVIIa is unclear. iv) For advice under these circumstances contact the on-call Haemostasis Service through Transfusion on 8222 5430 or 8222 5431.
- 96. 96 H. Endocrine Drugs 1.Insulin a) Indications: i) Diabetic emergencies – DKA and hyperosmolar coma ii) Treatment of hyperkalaemia 50% dextrose 50ml, plus Actrapid 10U iii) Perioperative diabetic patients (both insulin and non-insulin dependent) iv) General ICU patients Hyperglycaemia 10 mmol/l or glycosuria in acute illness: a. Maintaining BGL 6-10mmol/l is recommended for all critically ill patients b. Majority of ICU patients will require insulin using this protocol. c. NB: This protocol is not designed for patients with diabetic ketoacidosis and is a guideline only. d. Some patients will require individual manipulation of dose. Subcutaneous sliding scale insulin: a. Is inadequate for most critically ill patients and should be avoided. b. May be used in a small number of less critically ill patients, who have a limited requirement for exogenous insulin. c. A regular dose of subcutaneous intermediate/long-acting insulin, adjusted according to BGL may be suitable in some ICU patients. b) ICU Insulin Protocol – see following page. i) Target BGL = 6-10mmol/l. ii) Blood for testing should ideally be: Sampled from the arterial line rather than capillary (finger prick), as the former is more accurate in the critically ill. Measured via the blood gas analyser, c.f. bedside glucometer. iii) Protocol Precautions: If insulin rate ≥ 8 U/hr and the BGL remains high, measurement may be erroneous take a sample from another site and measure in the blood gas analyser. Consider holding the infusion if feed or glucose infusions are stopped. Potassium level a. Administration of insulin reduces K+ levels. b. Check K+ on ABG specimen at least twice daily and more often if the insulin infusion rate is high or changing acutely. c. If [K+] < 3.5 mmol/l KCl ~ 30 mmol over 1h via a pump.
- 97. 97 Flowchart: Blood GlucoseManagement in ICU Target BGL = 6-10mmol/l Perform BGL on Admission BGL = 6-10mmol/l BGL > 10 mmol/l Perform BGL 4hrly Commence Protocol Table: Insulin Infusion Protocol Starting BGL Bolus Subsequent infusion Repeat BGL infusion mmol/l Units IV Units/hr Units/hour Hours >15 2 2 Increase by 1 1 10.1-14.9 1 1 Increase by 1 1 If BGL dropping continue current rate. 8-10 0 0 1 If static or rising increase by 0.5 Continue current rate 1 (2hrly if 5-7.9 0 0 If BGL dropping for 2 consecutive hrs BGL stable decrease rate by 0.5. for 6 hrs) 1 (4hrly if off 3.5-4.9 0 0 Cease insulin>6hrs) <3.5 Call MO 0 Cease 1 c) Discharge Management: i) Pre-discharge, cease insulin infusion for at least 4 hours and check BGL ii) Order BGL to be checked 8 hourly on the ward iii) Refer to the RAH intranet documents: Insulin Protocol for Patients Discharged from ICU. Diabetes Management Guidelines. iv) Liaise with Endocrinology as indicated.
- 98. 98 2. Diabetes insipidus:protocol for DDAVP a) Diabetes insipidus may occur in the following situations: i) Post ablative pituitary surgery ii) Severe head injury, esp. anterior cranial fossa #, trauma iii) Evolving brain death iv) Lithium administration b) Indications for DDAVP i) Acute perioperative management (24-48hrs) of DI following pituitary surgery is usually fluid based – the use of DDAVP is rarely indicated. ii) Persistent polyuria in the absence of diuretics > 300ml/hr for > 3hrs iii) Altered conscious state, inability to detect thirst or take oral fluids iv) Low urine osmolality in the presence of high plasma osmolality v) Pre-existing hyperosmolar state or predisposition to pre-renal failure where persistent polyuria may exacerbate this. c) DDAVP Prescription i) Dose 1-2µg s.c. bd as required. (4µg is excessive) ii) Adjust maintenance fluids according to the response d) Maintenance fluids should be prescribed in the usual manner, according to volume status, renal function and osmolality. e) Presumptive or proven brain death: i) DI should be treated early (i.e. as soon as polyuria occurs) ii) Delayed administration of DDAVP can result in significant electrolyte abnormalities, which may influence the organ donation process. 3. Steroids a) Indications i) Pre-existing steroid therapy: Wide variety of indications, doses and durations of therapy. The need to continue steroids, with or without dose adjustment, should be assessed. ii) ICU conditions where steroid therapy may be beneficial. : Addisonian crisis Anaphylaxis Asthma, Chronic obstructive pulmonary disease Bacterial meningitis - esp. pneumococcal prior to antibiotics Croup, post-extubation laryngeal oedema Fulminant vasculitis Hypercalcaemia Idiopathic thrombocytopenic purpura Myasthenic crisis Myxoedema coma / Thyroid storm. Organ transplantation Pneumocystis jurovecii pneumonia
- 99. 99 iii) Conditions where supporting data are variable and the decision to administer steroids should be made on a case-by-case basis Sepsis ARDS b) Contra-indications / non-indications Active infection Acute head injury Guillain-Barré syndrome Fat embolism syndrome c) Relative drug potencies Table: Steroid Doses / Relative Potencies Equivalent Glucocorticoid Mineralocorticoid Drug dose (mg) activity activity Hydrocortisone 100 1 1 Prednisone 25 4 0.3 Methylprednisolone 20 4 0 Dexamethasone 4 30 0 Cortisone acetate 125 0.8 0.8 Fludrocortisone 1 10 250 d) Limitations of a random cortisol i) Marked fluctuation in plasma cortisol in the critically ill. ii) The ‘normal’ range in critical illness is not defined. iii) There is no consensus ‘cut-off’ value below which insufficiency is present. e) Limitations of total cortisol i) Free cortisol is the bioactive fraction of cortisol ii) Large variation in total cortisol assay results when the same specimen is tested in different laboratories and using different assays iii) Peripheral tissue-specific glucocorticoid resistance is not tested f) Conventional (high-dose) short synacthen test (HDSST) i) Synacthen concentrations are supraphysiological ii) Published data likely overestimate the incidence of adrenal insufficiency, as most studies did not excluded patients on etomidate. iii) The low-dose SST may be more a better predictor of outcome. iv) Insufficient data to support the routine use in patients with septic shock. v) Should only be performed if there is suspicion of hypoadrenalism Hyperkalaemia/hyponatraemia Hypoglycaemia Refractory acidosis Catecholamine resistance
- 100. 100 I. Renal Drugs - Diuretics 1. General principles a) Oliguria in acutely ill patients is frequently a manifestation of: i) Hypovolaemia – relative or absolute ii) Decreased cardiac output iii) Direct renal toxicity, or iv) A combination of these factors. b) Therapy should be directed toward causative factors and not maintenance of urine output by the administration of a diuretic agent. c) Urine output, in the absence of diuretic use, represents one of the best markers of end-organ perfusion and is a useful guide to clinical management. d) Diuretics should never be used to treat oligo/anuria, they are only a treatment for fluid overload 2. Indications a) Symptomatic fluid overload i) Pulmonary oedema / CCF ii) Cor pulmonale b) Hyperaldosterone states: ascites c) Chronic renal failure 3. Contraindications a) Hypovolaemic and/or Na+-depleted states b) Known drug hypersensitivity (esp. sulphonamide group) 4. Complications a) Hypovolaemia b) Hyperosmolar states c) Potentiation of renal failure - 2° to hypovolaemia d) Electrolyte disturbance especially K+, Mg, PO4, metabolic alkalosis e) Natriuresis and kaliuresis will alter urine electrolytes and osmolality for 24-48 hrs post dose.
- 101. 101 Table: Diuretics Drug Infusion/dose Clinical uses Frusemide 40-250 mg/day First line, potent loop diuretic IV / oral Doses may be increased in diuretic dependence K+, Mg, PO4, metabolic alkalosis common Acetazolamide 250-500 mg IV tds Carbonic anhydrase inhibitor Alkaline diuresis with HCO3- excretion Used for severe metabolic alkalosis after correction of hypovolaemia: K+, Mg++, PO4= Post-hypercapnic alkalosis Spironolactone 25-100 mg oral bd Potassium sparring diuretic Often given with loop and thiazide diuretics Indicated as part of a chronic treatment regimen for left ventricular failure Use in acute LVF is less certain May be of use in patients with ascites, particularly if secondary hyperaldosteronism is a feature. Careful administration is required in patients with impaired renal function. Mannitol 20% solution / Potent osmotic diuretic 200 mg/ml May cause - initial hypervolaemia - late hypovolaemia Dose 100 ml prn - hyperosmolal state (20g) - osmolal gap. Maintain measured osmolality < 300 mosmol/l (0.5g/kg is Limited role in suspected acute life-threatening too much!!) intracranial hypertension as a bridge to definitive surgical therapy. Limited (unproven) roles in rhabdomyolysis, transfusion reactions, myoglobinuria for renal protection
- 102. 102 J. Gastrointestinal Drugs 1. Stress ulcer prophylaxis a) Routine ‘stress ulcer prophylaxis’ is not indicated: i) Low prevalence of clinically significant bleeding due to stress ulceration ii) No evidence of survival benefit with use of stress ulcer prophylaxis iii) Possible increased incidence of VAP and/or clostridium difficile infection b) Pantoprazole may be considered in patients at high risk. c) Patients on pre-existing therapy (with PPIs or H2-blockers) should be continued d) Patients with clinically suspected GI bleeding should commence on a PPI e) Enteral feeding should be commenced as soon as possible. 2. Acute GI bleeding a) Definition i) Overt bleeding Blood in the NGT Haematemesis or malaena ii) Plus either: MAP > 20 mmHg Hb 20 g/L in 24 hours Required 2 units blood transfusion in 24 hrs iii) Blood in the NG tube is frequently due to local erosion and by itself does not constitute clinically significant GI bleeding. b) Management i) Resuscitation - ABC ii) Correct coagulopathy iii) Cease heparin / anticoagulants iv) Commence PPI - pantoprazole 40 mg bd/tds. v) Endoscopy sclerotherapy vi) If the source is not identified and with ongoing bleeding, consider: Labelled red cell scan Angiography (+/-embolisation), or Colonoscopy.
- 103. 103 3. GI drugs Table: GI Drugs Drug Dose Clinical uses Metoclopromide 10 mg IV 6 hrly, prn Persistent vomiting, nausea Large gastric aspirates (in combination with erythromycin) Erythromycin 100-200 mg IV bd Large gastric aspirates (in combination with metoclopramide) Droperidol 0.625 mg IV prn Potent, effective antiemetic Minimal side effects Tropisetron 2 mg IV / oral daily Use if anticholinergic side effects are to be avoided. Ondansetron 4 mg IV prn / 12 hrly Second line, antiemetic (not available at RAH) Ranitidine 50 mg 8hrly IV Stress ulcer prophylaxis 150-300 mg daily po Peptic ulcer disease Does not prevent acute rebleeding Reduce dose in renal failure. Pantoprazole Acute RX: First line RX for peptic ulceration 40 mg IV bd/tds Refractory peptic ulcer, ulcerative oesophagitis Maint. RX: Z-E syndrome 40 mg daily Upper GI bleeding Octreotide Bolus: 50 g IV Variceal bleeding Varices: 50 g / hr (as effective as sclerotherapy) Fistulae: 100-200 g Enteric, pancreatic fistulae sc 8-hrly Sulphonylurea overdose Severe secretory diarrhoea, e.g. post-chemo
- 104. 104 K. Antibiotics 1. Policy a) Prescription of antibiotics must conform to RAH guidelines. b) The over-prescription and irrational use of antibiotics is associated with the development of bacterial resistance, nosocomial infection and drug related morbidity c) All antibiotics must be reviewed daily and where appropriate, discussed with Infectious Diseases or Clinical Microbiology. d) Record the day and expected course of antibiotics in the left-hand margin of the drug chart, e.g. ‘D4/7’ = day 4 of a 7 day course. e) Record date, test and results (including sensitivities) in the “results folder”. 2. Principles of antibiotic prescription a) The treatment of infection consists of (in order of priority) i) Adequate resuscitation ii) Source control drainage of infected collections, etc. iii) Relevant samples for microbiological and/or histological analysis iv) Routine cultures: Blood - 2 sets at different times from venous stabs Urine Sputum Any other suspicious site v) Prompt administration of Rational empiric antibiotics Culture-directed antibiotics NB: time to effective ABx treatment affects outcome. b) General indications for antibiotics: i) Prophylaxis for invasive procedures and operations Proven indications a. Abdominal surgery which involves a breach of the colonic mucosa (traumatic or elective), or draining an infected cavity b. Selected obstetrical and gynaecological procedures: i. Caesarean section with ruptured foetal membranes ii. Vaginal hysterectomy c. Insertion of a prosthetic device d. Compound fractures e. Amputation of gangrenous limb Unproven but recommended a. Lacerations penetrating into periosteum or into joint cavities b. Crush injuries c. Insertion of a neurosurgical shunt d. Cardiac valve replacement e. Arterial prosthesis
- 105. 105 ii) Empirical antibiotics Obtain as many cultures as possible before antibiotics commenced. Should be commenced early in critically ill patients Should be rationalised according to gram stain & culture results. iii) Specific infections where the organisms is known c) Complications of antibiotics i) Antibiotic effect related Bacterial resistance Nosocomial infection Pseudomembranous colitis ii) Systemic reactions Skin rashes Anaphylactoid / anaphylactic reactions iii) Specific organ toxicities, e.g. Interstitial nephritis, ATN Seizures Marrow suppression, thrombocytopaenia QT prolongation iv) Cost d) Gentamicin / Tobramycin i) Where possible, the aminoglycosides should be used for a limited duration and therapy changed to a suitable alternative when possible. ii) Pharmacodynamic properties Concentration-dependent killing peak:MIC ~ 10:1 Significant post-antibiotic effect iii) Toxicity Nephrotoxicity - non-oliguric renal failure Ototoxicity - permanent, vestibular or auditory iv) Dosing All dosing is by estimated Lean Body Weight (LBW): a. Male: kg 50 + 0.9×(height - 150cm) b. Female: kg 45 + 0.9×(height - 150cm) Initial Dose: 5-7 mg/kg *irrespective of renal function a. Measure level 6-10 hrs post-dose b. Liaise with ICU Pharmacist (Pg: 22916), or Drug Information (Ext: 25546) re further dose requirements. c. Do not use the standard dosing normogram in ICU patients. Synergistic gentamicin, e.g. tds dosing in endocarditis a. Measure pre-dose trough levels b. Aim for < 1.0 mg/L to avoid toxicity.
- 106. 106 e) Vancomycin i) Pharmacology Time-dependent killing max 24h-AUC:MIC ratio Moderate post-antibiotic effect Renally cleared Plasma t½ 4-6 hrs ii) Toxicity Ototoxicity < 2% Nephrotoxicity - very rare (20 case reports 1956-84) *probably non-existent with current preparations ‘Red-man’ synd. rate of IV administration. iii) Preference in ICU is for continuous infusion, c.f. interval dosing. More constant plasma levels & efficacy Reduced ‘red-man’ syndrome Irritant to veins, dilute to 250ml Daily drug levels until stable *assessment of CrCl in critical illness is sub-optimal. iv) For patients on CRRT or CrCl < 20ml/min Intermittent Dose = 1.0g slow IV when levels < 15mg/l v) For patients transferring to the ward, see RAH intranet guidelines. Table: Vancomycin Dosing Schedule CrCl CrCl CrCl < 20 ml/min Renal Function > 60 ml/min 20-60ml/min CRRT 25 mg/kg (max 2.0g) | Slow infusion (1/24) Initial Dosing Loading dose IV in All Patients Infusion Rate 2.0-4.0g / 24 hrs 1.0g / 24 hrs Not indicated Vanc Level *Daily levels until stable < 15mg/L§ Dose 1.0g/day§ Dose 0.5g/day§ Infusion Dose Adjustment 15-20mg/L Dose 500mg/day Dose 250mg/day Target Level = 20-25mg/L Cont Current Infusion Rate Not indicated Hold 12 hrs Hold 12 hrs > 30mg/L Recheck Level Recheck Level §In critically unwell patients with low levels, consider giving a further bolus dose 0.5-1.0g in addition to increasing the rate.
- 107. 107 Table: Antibiotic InfusionSchedules IV Loading Max Hrs 1 Standard Infusion Dose (per 24 hrs) Renal Function Antibiotic All Patients Stability CrCl > 60 ml/min CrCl ~ 20-60ml/min CrCl < 20 ml/min CRRT Vancomycin2 1.0-2.0g 24 1.0-4.0g/day – Per Levels Not indicated Penicillin G 1.2-1.8g 12 4.8-14.4g 4.8-9.6g 2.4g 4.8-9.6g Amoxycillin 1.0-2.0g 6 4.0-12.0g 4.0-6.0g 2.0g 4.0-12.0g Flucloxacillin 1.0-2.0g 24 4.0-12.0g 4.0g 4.0-12.0g Piperacillin 4.0g 24 12.0-16.0g 8.0g 12.0-16.0g Tazocin 4.5g 24 13.5g 9.0g 13.5g Ceftriaxone 1.0g 24 1.0-4.0g Ceftazidime 1.0-2.0g 24 3.0-6.0g 2.0-4.0g 1.0-2.0g 2.0-4.0g Meropenem 1.0-2.0g 8 3.0-6.0g 1.0-2.0g 0.5g 2.0g 1 StandardInfusion Orders: 24 Hrs Dose in 100ml {N.Saline | 5%Dext.} @ 4ml/hr (per Max Hrs Stability) 12 Hrs (Dose / 2) in 100ml {N.Saline | 5%Dext.} @ 8ml/hr 8 Hrs (Dose / 3) in 100ml {N.Saline | 5%Dext.} @ 12ml/hr 6 Hrs (Dose / 4) in 100ml {N.Saline | 5%Dext.} @ 16ml/hr 2 Vancomycin should be diluted into 250mls if given via a peripheral line. Loading dose over at least 60 mins, or 10mg/min. *NB: Add the reconstituted solutions to a 100mL bag of compatible fluid, having first removed an equivalent volume of solution, i.e. so the final total volume of the bag remains 100ml, then administer over the required interval.
- 108. 108 3. Ventilator associatedpneumonia (VAP) a) Significant cause of mortality and morbidity in ICU b) Clinical diagnosis based upon the presence of a number of the following: i) New CXR infiltrates (hard to see in patients with ARDS) ii) New clinical chest signs iii) Increasing oxygen requirement iv) Increased purulent sputum v) Indications of systemic sepsis: Increased/decreased WCC Fever Hypotension c) Treatment i) Sputum culture ii) Commence antibiotics immediately Tazocin 13.5g/24hrs & Gentamicin 5mg/kg on day 1, then as per levels If gentamicin contraindicated, ciprofloxacin 200-400mg b.d. In patients with known MRSA or ICU stay > 5days a. Add vancomycin b. Stop if no gram positive organisms seen on micro iii) Review sputum culture If no organism and not on ABx consider another diagnosis De-escalate to narrow spectrum therapy ASAP Normal treatment 5-7 days except pseudomonas sp. then 10-14 days 4. Antibiotic prophylaxis a) Peri-operative (Table) i) Ongoing prophylactic therapy is required for selected post-operative patients in ICU. ii) Refer to individual protocols for recommendations on pre-operative antibiotic prophylaxis.
- 109. 109 Table: Peri-operative AntibioticProphylaxis Specialty Procedure Antibiotics Orthopaedics Elective cases Cefazolin 1g IV 8h x 3 doses Traumatic wounds Cefazolin 1g IV 8h x 2 days Involving bone or joint compound fractures + severe tissue damage Cefazolin 1g IV 8h x 2 days + myonecrosis + Gentamicin 5 mg/kg IV daily x 2 days + vascular injury + Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days Abdominal Surgery Colorectal Cefazolin 1 gm ± gentamicin 3 mg/kg + Metronidazole 500mg IV single doses Biliary surgery Gentamicin 3 mg/kg x 1 dose, or cefazolin 1g x 1 dose Vascular surgery Elective cases Cefazolin 1g IV 8h x 3 doses + severe bowel injury + Gentamicin 5 mg/kg LBW IV daily x 2 days + myonecrosis or + Metronidazole 500 mg IV bd x 2 days vascular injury + Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days Amputation Cefazolin 1g IV 8h x 3 doses + Metronidazole 500 mg IV bd x 2 doses Neurosurgery CSF leak / # Skull base None: treat only if signs of meningitis Craniotomy / ICP insertion Cefazolin 1g IV at induction Head & neck, Craniofacial with breach of Cefazolin 1g IV 8h x 3 doses thoracic nasal or oral mucosa + Metronidazole 500 mg IV bd x 2 doses Cardiac Surgery See Section “Management of Cardiothoracic Patients”
- 110. 110 Table: Perioperative EndocarditisProphylaxis
- 111. 111 Table: Empiric Antibiotics Infection Type / Comment Antibiotics Community acquired Azithromycin 500mg IV daily, plus Immunocompetent *Ceftriaxone 1 IV daily Admitted to ICU / HDU For treatment failure, consider Moxifloxacin (i.e. respiratory failure) 400mg IV daily ± Flucloxacillin 1g 6h (if high suspicion of S.aureus) *Default ICU therapy differs from the RAH standard protocol (penicillin + gentamicin) due to Pneumonia the wide variability in renal function in ICU patients and the inability to use baseline creatinine as a marker of renal function. Ventilator associated Tazocin 4.5g IV 8 hrly or 13.5g/day Hospital acquired + Gentamicin 5 mg/kg IV daily Consider Vancomycin 1g b.d. IV See above Immunocompromised host Contact ID No antibiotics without evidence of proven infection. Aspiration Benzyl penicillin 1.2g IV 6 hrly, plus With proven infection metronidazole 500 mg IV 12 hrly Exacerbation of No clinical signs of pneumonia Treat as community acquired pneumonia COPD Epiglottitis Usually H. influenzae Ceftriaxone 1 g IV daily Suspected bacterial Ceftriaxone 2g IV 12 hrly, plus Usually: meningococcus Penicillin 1.8g to 2.4g IV 4 hrly Meningitis/ pneumococcus, or Dexamethazone 10mg IV encephalitis H. influenzae before or with the first dose of antibiotic then 6hrly for 4 days Not definitely bacterial Consider Acyclovir 10mg/kg IV 8hrly Without systemic sepsis in patients No treatment. with a urinary catheter Remove / change catheter Urinary tract infection With systemic sepsis Amoxycillin 2g IV 6 hrly, plus gentamicin 5mg/kg IV daily, or Ceftriaxone 1gm IV daily if unable to tolerate gentamicin Faecal peritonitis Amoxycillin 2 gm IV 6 hrly Perforated viscus + Gentamicin 5 mg/kg IV daily Intra-abdominal + Metronidazole 500 mg IV bd x 7 days sepsis Recurring intra-abdominal sepsis or Consult ID/Clinical Microbiology failed Rx with above No CT evidence of necrosis No antibiotics Pancreatitis Significant CT necrosis Tazocin 4.5g IV 8 hrly Acute cholecystitis Amoxycillin 1 g IV 6 h + Gentamicin 5 mg/kg/d IV x 7 days Biliary sepsis Ascending cholangitis Amoxycillin 2 gm IV 6 h + Gentamicin 5 mg/kg/d IV Previous biliary tract surgery or add Metronidazole 500mg IV BD x 7 days known biliary obstruction
- 112. 112 Septicaemia secondary to PID Amoxycillin 2g IV 6 h + Gentamicin 5 mg/kg IV dly Gynae sepsis + Metronidazole 500 mg IV bd x 5 days Suspected S. aureus infection Lincomycin 1.2g IV bd + Gentamicin 5 mg/kg IV dly x 7 days Community acquired Benzyl penicillin 1.8 g IV 4 h + Gentamicin 1 mg/kg IV tds ± Flucloxacillin 2g IV qid Suspected Bacterial Hospital acquired Vancomycin 1g IV bd Endocarditis Prosthetic valve, or + Gentamicin 1 mg/kg IV tds Penicillin allergic 3 sets of blood cultures, and review at 48 hrs Manage pre-dose trough levels for gentamicin <1 mg/L to avoid toxicity Suspected candidiasis Amphotericin 0.5-1 mg/kg/day, or Fluconazole 400 mg IV daily (in non-neutropaenic patients) Suspected aspergillosis Voriconazole IV/oral 6mg/kg BD loading for 24 hours, then 4mg/kg BD or Caspofungin 70mg IV daily loading for 24 Fungal hours, then 50mg daily Septicaemia 1. Consult ID for all proven fungaemias 2. Remove all potential sources of infection (lines, catheters, etc) 3. Monitor renal / hepatic function during the course of antifungal therapy. 4. Adjust the amphotericin dose in renal insufficiency, or consider the use of fluconazole if appropriate 5. Voriconazole levels can be monitored for toxicity and clinical responses. 6. IV voriconazole is contraindicated in patients with CrCl < 30mL/min due to accumulation of the excipient Burns No antibiotics without evidence of bacterial infection Wound infection Benzylpenicillin 1.8 g IV 4 h + signs of systemic sepsis + Flucloxacillin 1-2 g IV 6 h or Cefazolin 1g IV 8h Synergistic gangrene Meropenem Cutaneous Necrotising fasciitis plus infections Lincomycin 600 mg IV 8 hrly, or In addition to surgery Clindamycin 600 mg IV 8 hrly ± hyperbaric oxygen Consider IV-Ig 2.0g/kg total dose (3 days) Severe oral infections Penicillin 1.2 g IV 4-6 hourly + Metronidazole 500 mg IV bd Patient not overtly septic Remove unnecessary, old or clinically suspect lines & send for culture. Blood cultures by venipuncture Line sepsis No antibiotics Patient overtly septic Vancomycin 1 g IV BD until blood culture Prosthetic valve / arterial graft results available High risk patient
- 113. 113 Table: Antibiotics forSpecific Organisms Organism 1st choice 2nd choice Pneumococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1 IV dly Vancomycin 1gm IV bd or Staphylococcus aureus Flucloxacillin 2 gm IV 6 h Cefazolin 1-2g IV 8h Meningococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1g IV dly Meningococcus contacts Ciprofloxacin 500mg po x 1dose Rifampicin 600mg po bd x 2 days MRSA Vancomycin 1g IV bd Consult ID Amoxycillin 1-2 g IV 6 h Vancomycin 1g IV dly Enterococcus (+ Gentamicin 5 mg/kg if SBE) (+ Gentamicin 5mg/kg if SBE) Benzylpenicillin 1.8g 4 hrly IV Consult ID Gp A Strep. + Lincomycin 1.2g IV bd With Shock + Intragam 2.0g/kg total dose (3 days) Cease IG when pt. improves Amoxycillin 1-2 g IV 6 h Haemophilus influenzae Ceftriaxone 1g IV daily (if sensitive) H. influenzae contacts Rifampicin 600 mg oral bd x 4 days Ceftriaxone 1g IM dly x 2 doses (meningitis) E. Coli Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly Enterobacter Gentamicin 5 mg/kg IV dly Meropenem 500mg IV 8h Klebsiella Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly Pseudomonas aeruginosa Piperacillin 4 g IV 8 hrly Choice based on sensitivity results: + Gentamicin 5-7 mg/kg IV dly Ceftazidime 2g IV 8hrly or Tazocin 4.5g IV 8hrly PLUS Gentamicin 5-7 mg/kg IV daily or Ciprofloxacin 400mg IV bd Legionella spp. Moxifloxacin 400mg IV daily Azithromycin 500mg IV daily Mycoplasma pneumoniae Erythromycin 1g IV 6h Pneumocystis jurovecii Co-trimoxazole 15-20 ml IV 6 h Pentamidine isethionate + methylpred 40mg bd x 5d, 4 mg/kg/day IV methylpred 40mg die x 5d, + methylprednisolone methylpred 20mg die x 11d, 40mg 6 hrly x 7days Clostridium difficile: Cease antibiotics Consult ID or Clinical Micro. 1. Mild / moderate 1. Metronidazole 400 mg o tds Treatment options are: (or 500mg IV if npo) Bacitracin 25,000U 6hrly 7-10d x 7-10 days or 2. Severe, or relapse post RX 2. Repeat above Vancomycin 125mg po 6hrly 7-10d Clostridial infection Benzylpenicillin 1.8g IV 4 hrly Lincomycin 600 mg IV 8 hrly + Gentamicin 5 mg/kg IV dly + Gentamicin 5 mg/kg IV daily (Polymicrobial Infection) + Metronidazole 500 mg IV bd + surgical debridement hyperbaric oxygen
- 114. 114 PART 4 - FLUIDS AND ELECTROLYTES A. Principles of Fluid Management in Intensive Care 1. All fluids, infusions are reviewed daily and rewritten: a) On the ICU flowchart (Units A & B), or b) In the IV Fluid chart in the ward folder (Unit C). 2. Assessment of volume status and fluid balance: a) Clinical markers i) Skin turgor, mucous membranes, capillary refill, peripheral perfusion ii) HR, BP, Urine output iii) CVP, PAOP iv) PiCCO catheter - GEDI, ELWI, stroke volume variability. v) CXR, interstitial oedema vi) Echo – IVC distensibility index, LVOT-VTI variability b) Biochemical markers i) Serum Na+, Cl-, osmolality ii) Urea / creatinine (± ratio) iii) Bicarbonate iv) Haematocrit c) Charted fluid balance (notoriously inaccurate!) i) Total intake including drug & infusion volumes ii) Total output including urine output, drains, NG losses, blood loss iii) Insensible losses due to pyrexia, transcellular shifts, etc. (NB: usually impossible to quantify accurately) 3. Fluids should be considered in two components: a) Maintenance fluids i) Usually crystalloids - 5% dextrose, 4% dextrose + 1/5 N.Saline - N.Saline - Hartmann’s, CSL ii) Usual volumes: 25-30 ml/kg/day 80-120 ml/hr iii) TPN (refer to guidelines) b) Replacement / resuscitation fluids i) N.saline should be used for most fluid resuscitation. Equivalent to 4% albumin for resuscitation Better for patients with head trauma. ii) Colloid - 4% albumin, gelofusine May be considered for fluid resuscitation in selected patients. Greater cost, no demonstrable advantage. Should be avoided in patients with traumatic brain injury. iii) Blood and components as indicated according to NH&MRC guidelines. iv) Crystalloid replacement is usually used for excessive renal, enteric and burns losses (see below). v) Hyperchloraemia may be harmful so consider the use of fluids with other anions, e.g. Hartmann’s.
- 115. 115 4. Composition ofcommonly used fluids (1000ml solution): Table: Common IV Solutions Solution Na+ K+ Cl- Ca++ Lact. Gluc. Osm. Prot. N Saline 150 150 300 N/2 Saline 75 75 150 N/5 Sal. + 4% Dex. 30 30 40 g 282 5% Dextrose 50 g 278 Hartmann’s 131 5.0 111 2 29 280 Gelofusine (500ml) 77 60 274 20g Albumex 4% (500ml) 70 62.5 25g 5. Fluid management in burns patients a) The RAH Burns Unit uses the modified Parkland regimen. b) This is a guide - other clinical markers such as urine output, heart rate, blood pressure, CVP, serum sodium and osmolality, and haematocrit must be taken into account. c) As a result, both solution composition and administration rate may have to be modified in order to maintain the above parameters within normal ranges. d) Protocol: i) Assess the patient’s % burn surface area (%BSA) using an accurate chart. ii) Assess patient weight (kg). iii) Formula: First 24 hours = total fluid (as Hartmann’s solution): Wt. x %BSA burn x 4.0 ml a. give ½ the total fluid during first 8 hours post-burn b. give ½ the total during the subsequent 16 hours Second 24 hours fluid is given as Albumex 4% Wt x %BSA burn x 0.5 ml Other maintenance fluid is given according to the above physiological parameters The primary endpoint of fluid resuscitation is generally accepted to be a urine output 0.5-1 ml/kg/hr Catecholamines: a. Should be commenced only when adequate volume replacement is unable to maintain a satisfactory urine output, or there is associated myocardial failure. b. The duty consultant or SR should be consulted prior to use. iv) Commence enteral feeding as soon as possible.
- 116. 116 B. Nutrition 1. Enteral nutrition a) Enteric feeding is the preferred mode of nutritional support and should be considered in all patients as soon as possible after admission. b) Advantages i) Early EN in trauma patients has been associated with improved outcome. ii) Use of the gut decreases mucosal atrophy, which may reduce bacterial translocation thereby reducing the incidence and duration of sepsis. iii) The incidence and severity of gastric erosions and stress ulceration may be reduced. iv) Cheaper than TPN v) CVC complications (especially infection) are reduced or avoided. c) Disadvantages i) Regurgitation / aspiration ii) Nosocomial pneumonia iii) Diarrhoea (other causes are more likely than enteral feeding) d) Indications i) As soon as possible in all intubated / tracheostomised patients, where admission and duration of intubation is expected to be > 24-48 hours. ii) Patients with an operative jejunostomy may commence feeding within 6 hours of placement. e) Contraindications i) Gastrointestinal (including oesophageal) perforation, gastrointestinal fistulae, bowel obstruction, ileus. ii) Recent bowel anastomosis is not a contraindication – however, discussion with the surgical team is essential. iii) Absent bowel sounds are not a contraindication. f) Protocol (see feeding protocol at bedside) i) Liaise with the dietician (who will order feeds) during the fluid round. ii) Outline any problems: e.g. hyperkalaemia, renal failure, osmolality iii) Place a 12F or larger nasogastric tube (to allow reliable aspiration) iv) Use orogastric tubes in patients with anterior and middle cranial fossa # v) Check the position of the feeding tube with x-ray prior to use. Attach label to NG tube, and Document in notes that the position of the tube has been checked. vi) Nurse the patient at 30-45° head up. vii) Commence feed at 80 ml/hr continuously according to the protocol. viii) Aspirate all NG and PEG tubes 6 hrly ix) Do not aspirate jejunostomies, naso-duodenal/jejunal tubes or PEJs
- 117. 117 x) Flush jejunostomy/gastrostomy tubes with 20ml N.saline 6hrly. Aspirate < 250 ml: a. Return aspirate to stomach b. If {rate < max} then increase rate by 20 ml/hr c. Repeat aspiration at 6hrs and If {aspirate < 250 ml} then rate to max (usually 80-100 ml/hr) Aspirate > 250 ml: a. Return 250 ml b. Halve the feed rate (not less than 20 ml/hr) c. Continue to aspirate 6 hrly d. Consider prokinetics: i. Metoclopramide 10 mg IV 6 hrly, plus Erythromycin 100-200 mg IV bd ii. Continue until tolerating feed for > 72hrs, then cease and observe iii. Recommence as needed e. Reduce narcotic administration if possible. Aspirates > 250 ml while receiving prokinetics, consider: a. Post-pyloric feeding tube i. Using the Cortrak® device, or ii. Endoscopically placed by the GI Unit b. Feeding jejunostomy c. Nasogastric naloxone 4-8mg tds d. TPN. xi) Consider a PEG, PEJ or feeding jejunostomy in long term patients e.g. Guillain Barré or severe head injury xii) Cease feeds 4 hrs prior to extubation, tracheostomy, ET tube change. xiii) There is no requirement to cease feeds until immediately prior to going to theatre, unless: Surgical procedure on the GIT Planned for tracheostomy or ETT change. xiv) Remember to modify insulin dose when feeds are reduced or ceased. 2. Enteral Protocol - See over page. Flowchart: Nutritional Therapy Protocol
- 118. 118 Patients expected to be mechanically ventilated for > 48h should have enteral nutrition (EN) commenced within 24 h of admission to ICU Insert NET, confirm position by XR and confirm Pts unsuitable suitability for commencement of feeds Feeding interruptions for EN should • Do not hold feeds for be considered routine nursing care, for TPN if EN bedside procedures unlikely for > 5 Commence feeds Osmolite 1 ml/kg/h or diagnostic tests days. Include; (1 kcal/ml @ max 80 ml/h) unless specified. short gut, GI • No need to fast prior (unless pt fluid restricted) fistulae, to surgery unless contraindication ETT to be removed, to placing NET, i/o tracheostomy, GIT perforation. tracheostomy change Refer Pt to Dietitian for Nutritional Ax or GIT surgery. • If fasting for theatre, commence fast when pt called to theatre. Jejunostomy Or fast for 4 hr prior feeds should Check Gastric residual volume (GRV) every 6 h to r/o ETT, i/o commence at for ALL gastric tubes, document on chart. tracheostomy, rate of 1 ml/kg/h Do NOT aspirate post pyloric tubes. tracheostomy change or as or surgery on gut recommended lumen. by Dietitian and • EN and insulin to flushed 20 ml N cease during time in GRV < 250 ml saline QID. GRV ≥ 250 ml OT and restart at return aspirate, same rate as when return 250 ml, continue feed discontinued. halve feed rate, regimen (if not at • Cease feeds 4hr prior commence to planned goal increase rate prokinetics extubation. by 20 ml/h) Do NOT aspirate post pyloric feeding tubes. If GRV remains high (i.e. 2 Monitor pt for signs of intolerance including abdominal distension, constipation, aspirates ≥ 250 ml within diarrhoea or vomiting. Notify physician of concerns. 12 h) consider post-pyloric feeding Prokinetics Both Metoclopramide 10mg QID IV and Erythromycin 100 - 200mg BD IV Consider TPN if unable to Metoclopramide not recommended for use in head injury pts. place post pyloric tube Referral to Dietitian for Nutritional Ax Weekdays - ICU Dietitian will review ICU / SDU pts daily and chart max recommended feeding rate on daily obs chart. Contact ICU Dietitian on Pg 1342 if any concerns / queries. Weekends - Nursing T/L should be advised of new NET / changes to existing regimens. On call Dietitian should be contacted (SD 1156 / 0401711460) and advised of - new ICU / SDU NET feeds; changes to existing regimens; pt transfers. Cover (when ICU Dietitian on leave) - Clinical Dietetics should be contacted (Pg 1342) and advised of all NEW ICU / SDU NET feeds and changes to existing regimens.
- 119. 119 3. Post-pyloric feedingprotocol: a) Commence feed at 1ml/kg/hr, up to a maximum 80 ml/h. b) No need to cease feed for any procedures, other than GI surgery. c) Consider placement of a NG tube to aspirate and ensure an empty stomach. 4. Parenteral Nutrition a) General principles i) TPN may be harmful in critically ill patients. ii) Enteral nutrition is preferred and TPN should only be considered for patients in whom this is not possible. iii) Supplementing EN with TPN is not beneficial and should be avoided. iv) Refer to ‘Clinical Duties Outside ICU’, regarding the responsibilities and management of ward patients receiving TPN. v) TPN is usually ordered by the Unit A Senior Registrar, under the supervision of Dr Adam Deane. vi) IV access may be via a CVC or PICC line, with the latter being preferred. vii) TPN for ICU patients is prescribed during the midday fluid round. viii) Patient being discharged from ICU on TPN must be entered into the TPN folder in Unit A. b) Indications for TPN in the patient who cannot be fed enterally are: i) GIT Failure > 7-10 days and expected duration of support > 5-7 days. Prolonged post-operative ileus Enteric fistulae ii) Short GIT syndrome following major intestinal resection. c) Complications of TPN: i) Depression of immune function, esp. in cancer patients ii) Intestinal villous atrophy iii) Metabolic imbalance Electrolyte disturbances ( K+, HPO4=, Mg++) Glucose intolerance: hyperglycaemia and glycosuria Hyperosmolar dehydration syndrome Rebound hypoglycaemia on cessation of TPN Hyperbilirubinaemia CO2 production, esp. in COPD patients iv) Central venous access complications
- 120. 120 d) Protocol i) On commencement: Add the following orders to the patient's drug folder: a. Cernevit MV 1 ampoule IV daily. b. Trace elements 1 ampoule daily c. Vitamin K 10 mg IV weekly d. Commence insulin: i. Initial dose = 5U s.c. qid *hold if BGL < 10 ii. Check BGL qid iii. Adjust the dose on subsequent days guided by BGLs iv. “Sliding Scale” regimens are no longer used. Commence TPN solution at a lower rate (40ml/hr) in “starved” patients a. Potential movement of K+ / HPO4= into cells with re-feeding b. May cause acute severe hypokalemia and hypophosphataemia. Slowly increase to desired rate, usually 60-80 ml/hr. Dietician will provide a calculated energy requirement as a guide ii) Daily: Review the patient, CVC site, biochem, BGL chart and fluid balance. Prescribe TPN selecting the most appropriate “option” from the table below. These bags are pre-prepared and must not be altered, i.e. no further additives. Patients requiring K+, PO4 and fluids etc. above the quantities provided must receive these in a separate line/infusion. iii) Intralipid Commence TPN with lipid-free solutions (#3, #4) Lipid is indicated if the period of malnutrition > 4 weeks or if the patient is hyperglycaemic. Table: Average Daily Requirements Water 30-40 ml/kg/day 1. Glucose: 2g/kg/day @ 4.1 kcal/g Calories 25-30 kcal/kg/day 2. Fat: 2g/kg/day @ 9 kcal/g 1. 2:5 essential:total amino acids Protein 0.5-2.0 g/kg/day 2. 150:1 kcal:g N2 (non-nitrogen kcal) Sodium 1.0 mmol/kg/day Potassium 1.0 mmol/kg/day Dependent on renal function Phosphate 0.2 mmol/kg/day Dependent on renal function B groups daily Vitamins Trace elements as required. B12, Folate, A, D, E, K weekly 1. Urine 1. ½ Normal saline ± KCl 10 ml/L Replacement 2. Nasogastric/ileostomy 2. ½ Normal saline ± KCl 10 ml/L solutions 3. Pancreatic/biliary fistulae 3. Hartmann’s solution
- 121. 121 Table: Baxter TPNSolution Options Baxter Option 1 Baxter Option 2 Baxter Option 3 Baxter Option 4 Composition With Lipid With Lipid No lipid No Lipid With Potassium No Potassium With Potassium No Potassium Total Volume (ml) 2000 2100 2000 2100 Glucose (gm) 250 250 500 500 Lipids (gm) 100 100 0 0 Energy (kcal) 2270 2270 2300 2300 Protein (gm) 100 100 100 100 Nitrogen (gm) 16.5 16.5 16.5 16.5 Na + (mmol) 73 73 73 73 K+ (mmol) 60 0 60 0 Mg++ (mmol) 5 5 5 5 HPO4 = (mmol) 37.5 7.5 30 0 Cl- (mmol) 70 110 70 110 Acetate (mmol) 150 82 150 82 Solution shelf life 12 mths room T 6 mths room T 12 mths room T 6 mths room T 1. Lipid source is Clinoleic 20% which comprises olive oil 80% and soya oil 20%. 2. Multivitamin and trace elements to be given separately from TPN. 3. Nothing may be added to TPN bags. 4. All solutions come in triple phase bag and have light protection cover. NB: Specialised prescription TPN can be ordered via pharmacy, e.g. when large daily potassium requirements are not feasibly administered by 10mmol/100ml bags and the standard 60mmol/2L TPN.
- 122. 122 C. Blood Component Therapy 1. Indications a) Blood component therapy should only be given if benefit outweighs the risk b) The decision to transfuse should be based on clinical assessment, disease course and response to previous transfusion as well as [Hb] levels. c) Potential risks including i) Mis-identification / acute transfusion reaction ii) Bacterial / viral infection iii) Transfusion associated acute lung injury (TRALI) iv) Transfusion associated circulatory overload (TACO) v) Immune modulation (this and TRALI are probably the most significant) d) The best way to reduce the risk of blood component therapy is to reduce requirements i) Minimise unnecessary blood sampling ii) Minimise blood loss during procedures iii) Consider nutritional and iron stores state 2. Red Blood Cells a) Elective *as per NHMRC / ASBT guidelines. i) Use of RBCs at Hb > 100g/L is likely to be inappropriate ii) Use of RBCs at Hb < 70g/L is likely to be appropriate but in some asymptomatic patients a lower threshold may be acceptable iii) At Hb 70-100g/L clinical assessment of risk versus benefit is required. iv) The following criteria may indicate RBC transfusion is indicated Significant ongoing bleeding present or anticipated. Clinical signs of impaired oxygen transport such as dyspnoea, tiredness/weakness, angina, syncope. Cardiac ischaemia or cardiac failure due to anaemia. v) Order as “Red cells” or RBCs on the ICU or ward fluid chart vi) “Type & Screen” specimens are held for 10 days for compatibility testing. vii) For transfusion, a new specimen is needed for cross-match every 72 hours. b) Resuscitation i) Abnormal bleeding is usually surgical and requires urgent surgical and/or radiological intervention. ii) A full cross-match takes 30 minutes if marked urgent (not including the time for transfer of blood); this should be performed if possible while volume is replaced with crystalloid or colloid.
- 123. 123 iii) If blood is required faster than this, the request “Time Required” box should be marked: “Desperate” *group O Rh(D)-ve blood is issued immediately (see massive transfusion protocol) “10 minutes” *group-specific (ABO/Rh-D) but without full compatibility testing “30 minutes” urgently processed, fully crossmatched blood NB: The requesting MO accepts full responsibility for these (*) iv) Blood replacement should start immediately in the setting of: Rapid blood loss leading to hypovolaemia and shock. Blood loss estimated or anticipated to exceed 20-25% of blood volume, i.e. 1000-1500 ml in a normal adult. 3. Massive Transfusion Protocol a) Definition: i) Loss of one blood volume within a 24 hr period. ii) Alternative, more practical definitions: ≥ 50% blood volume loss within 3 hr, or ≥ 150 ml/min rate of loss. b) The RAH massive transfusion protocol should be activated as soon as the need is identified c) Correction of critical bleeding requires simultaneous approach to: i) Control the source of bleeding ii) Contact key personnel required for haemorrhage control iii) Maintain blood volume iv) Prevent hypothermia and acidosis d) Principles i) Trauma patients with critical bleeding are coagulopathic on presentation ii) Prevention of further coagulopathy with aggressive management is much more effective than delayed treatment iii) Acidosis and hypothermia worsen coagulopathy e) On identification: i) Take blood and place in red bags for: CBE, Group and match Extended Coags ii) Notify transfusion medicine on 47* iii) Dispatch blood samples ASAP iv) Transfusion will provide products in “Massive Transfusion Packs” v) Notify transfusion when bleeding controlled f) Tranexamic acid i) Routinely used in trauma only as per CRASH2 ii) Triggers modified for local use (see Chart) iii) Dose 1g over 10 minutes then 1g over 8 hours iv) Delivered with first MTP pack
- 124. 124 Table: Critical Bleeding(Massive Transfusion) Procedure Comments Laboratory Samples to Blood Bank for T&S Take samples at earliest opportunity as investigations CBE, INR, APTT, fibrinogen results may be affected by colloid Biochemical profile, blood gases etc. infusion. Mis-identification is commonest Repeat CBE, INR, APTT, Fib transfusion risk. after blood component infusion, or May need to give components before every 4 hrs until stable. results available. Use “Massive Transfusion–Priority Processing” labels with ‘Red bag’ to alert lab for speedy processing. Suitable RBC Un-crossmatched group O Rh(D) Rh(D) positive is acceptable if patient is negative in extreme emergency until male or post-menopausal female. blood group known, then group-specific. Laboratory will complete compatibility Then fully crossmatched blood when testing after issue. time permits. Further compatibility test not required To prevent hypothermia by the use of after replacement of 1 blood volume (8– blood warmer and/or rapid infusion 10 units). device. Blood-warmer indicated if flow rate >50 Employ intra-op blood salvage if ml/kg/hr in adult. available and appropriate. Salvage contraindicated if wound heavily contaminated. Platelets Anticipate platelet count <50x109/L after Target platelet count: >100x109/L for 2 x blood volume replacement. multiple/CNS trauma or if platelet function abnormal. Target >50x109/L for other situations. FFP Aim for INR <1.5 and APTT <40 secs. INR >1.5 and APTT >40 secs correlates (10-15 ml/kg – 1 litre Allow for 30 min thawing time. with increased surgical bleeding. or 4 units for an adult) Consider extended life plasma Keep Ca++>1.13mmol/L Cryoprecipitate Replace fibrinogen. Fibrinogen <0.5 strongly associated with (2-4 units) Aim for fibrinogen >1.0 g/L. microvascular bleeding. Allow for 30 min thawing time. Fresh whole blood Request hospital Blood Bank to contact Anticipated major blood loss in elective ARCBS on-call MO. patients with platelet or coagulation abnormalities. Continued significant bleeding even after use of conventional component therapy. Role in haemostasis controversial. Recombinant FVIIa Obtain approval from consultation with May be considered when the patient’s (Novoseven) senior Surgeons / Anaesthetists / condition continues to deteriorate to Intensivists and Haematologists / likely haemorrhagic death Dose ~ 90 μg/Kg ARCBS on-call MO. Usually as a desperate effort after other measures fail. See Massive Transfusion Protocol
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- 127. 127 4. Platelets a) Standard dose is “Platelets - 1 Adult Pack” b) Prophylactic transfusion before surgery or other “at risk” procedures: i) Platelet count < 50 × 109/L or ii) Platelet count > 50 × 109/L with evidence of inherited or acquired (drug-induced) platelet dysfunction c) Prophylactic transfusion in marrow failure: i) Platelet count < 10 × 109/L, or ii) Higher levels with clinical evidence of bleeding or other risk factor d) Therapeutic transfusion for uncontrolled haemorrhage: i) As per the massive transfusion protocol ii) Platelet count < 50 × 109/L iii) Platelet count < 100 × 109/L with microvascular bleeding iv) Irrespective of platelet count with evidence of platelet dysfunction. e) Platelet dysfunction can contribute to bleeding with a normal platelet count f) ITP: Only if life-threatening bleeding is present. 5. Fresh Frozen Plasma (FFP) a) Prophylactic transfusion before surgery or other invasive procedure that could result in significant bleeding: i) Urgent correction of prolonged INR or APTT in warfarin overdose or vitamin K deficiency (see below) ii) Correction of prolonged INR or APTT in liver disease iii) Correction of inherited coagulation factor deficiencies where specific coagulation factor concentrates are not available b) Therapeutic transfusion for uncontrolled haemorrhage in: i) Warfarin overdose ii) Liver disease iii) Vitamin K deficiency iv) Inherited coagulation factor deficiencies where specific coagulation factor concentrates are not available v) DIC c) Plasma exchange in TTP & related syndromes d) As per the massive transfusion protocol e) Post massive transfusion with coagulopathy: i) INR > 1.5, or ii) APTT > 40 seconds 6. Extended Life Plasma a) Recent regulatory changes allow transfusion laboratories to used thawed FFP for up to 5 days. b) By using thawed FFP the product can now be provided immediately, c.f. the standard 20-30 minute delay normally involved in thawing. c) Five day thawed FFP will be labelled ‘Extended Life Plasma’
- 128. 128 Table: Guidelines forthe Management of an Elevated INR Clinical Setting Action INR < 5.0 Lower the dose or omit the next dose of warfarin. Bleeding absent Resume therapy at a lower dose when the INR approaches therapeutic range. If the INR is only minimally above therapeutic range (up to 10%), dose reduction may not be necessary. INR ~ 5.0–9.0* Cease warfarin; consider reasons for INR and patient-specific factors. Bleeding absent If bleeding risk is high, give vitamin K1 (1.0–2.0mg orally or 0.5–1.0mg IV) †. Measure INR within 24 hrs, resume warfarin at a reduced dose once INR is in therapeutic range. INR > 9.0 Where there is a low risk of bleeding Bleeding absent Cease warfarin, give 2.5–5.0mg vitamin K1 orally or 1.0mg IV Measure INR in 6-12 hrs & resume warfarin at a reduced dose once INR < 5.0. Where there is high risk of bleeding‡ Cease warfarin, give 1.0mg vitamin K1 IV. Consider Prothrombinex-HT (25–50 IU/kg) and FFP (150–300mL) Measure INR in 6-12 hrs, resume warfarin at a reduced dose once INR < 5.0. Any clinically Cease warfarin therapy, give 5.0–10.0mg vitamin K1 intravenously, as well as significant Prothrombinex-HT (25–50 IU/kg) and fresh frozen plasma (150–300mL), assess bleeding where patient continuously until INR < 5.0, and bleeding stops.§ warfarin induced or coagulopathy is If fresh frozen plasma is unavailable, cease warfarin therapy, give 5.0–10.0mg considered a vitamin K1 intravenously, and Prothrombinex-HT (25–50 IU/kg), assess patient contributing factor continuously until INR < 5.0, and bleeding stops.§ or If Prothrombinex-HT is unavailable, cease warfarin therapy, give 5.0–10.0mg vitamin K1 intravenously, and 10–15mL/kg of fresh frozen plasma, assess patient continuously until INR < 5.0, and bleeding stops.§ * Bleeding risk increases exponentially from INR 5 to 9, INR ≥ 6 should be monitored closely. † Vitamin K effect on INR can be expected within 6-12 hours. ‡ Examples of patients with a high bleeding risk: active gastrointestinal disorders (such as peptic ulcer or inflammatory bowel disease) those receiving concomitant antiplatelet therapy those who underwent a major surgical procedure within the preceding two weeks, and those with a low platelet count. § In all situations carefully reassess the need for ongoing warfarin therapy. From consensus guidelines Australian Society of Thrombosis and Haemostasis 2004
- 129. 129 7. Cryoprecipitate a) Bleeding and fibrinogen < 1.0 g/L in: i) DIC. ii) Massive transfusion. iii) Hereditary hypofibrinogenaemia. b) 10U of cryoprecipitate will plasma fibrinogen by ~ 1.0g/l c) Standard dose = 8U for hypofibrinogenaemia. 8. DDAVP a) Standard dose = 0.3-0.4µg/kg intravenously over 30 mins b) Increases factors VIII:C, VIII:vWF and platelet adhesion. c) Indications: actual, or significant risk of bleeding with, i) Haemophilia A ii) type I von Willebrand's disease iii) Post cardio-pulmonary bypass (check with surgeon) iv) Clinical scenarios where platelet dysfunction is likely Uraemia Drugs - aspirin, clopidogrel 9. Recombinant activated factor VII (rFVIIa, NovoSeven) a) TGA approved indications i) Haemophilia patients with antibodies to factor VIII ii) Glanzmann's thrombasthenia with antibodies to GPIIb-IIIa and/or HLA, and who have past or present refractoriness to platelet transfusions iii) Patients with congenital factor VII deficiency b) Effective in improving coagulopathies associated with trauma, major surgery, and organ transplantation = ‘off-label’ indications. c) No risk of virus transmission and contains no human protein d) Binds to tissue factor (TF) activating both factors IX and X. i) High doses activate factor X on the surface of activated platelets ii) Has both TF-dependent and TF-independent effects e) Recommended dose for the treatment of a severe coagulopathy 90µg/kg f) Acts within a few minutes and has a half-life of about 2.5 hours. g) Requires consultant/haematology approval because of high cost and absence of current TGA approval for these indications.
- 130. 130 10. Dabigatran ClinicalGuidelines a) General Information i) Dabigatran etexilate (Pradaxa) is a pro-drug of dabigatran ii) Reversible direct thrombin inhibitor iii) Onset of anticoagulant effect within 30 minutes after oral administration iv) Peak plasma concentration and effect within 2-3hrs. v) Usual half-life: 12-14 hrs vi) Renally cleared, ClCr < 30 ml/min t½ > 24 hrs. b) Effect on Laboratory Coagulation Parameters i) Monitoring is not routinely required ii) No direct relationship between coagulation tests and therapeutic effect. iii) Thrombin time (TT) Particularly sensitive to dabigatran A normal TT excludes clinically significant dabigatran levels. iv) Activated partial thromboplastin time (APTT) Shows best correlation with plasma levels Increasing APTT occurs with dabigatran concentration. a. Usual peak concentration APTT ~ 2x control b. Trough levels (12 hrs post dose) ~ 1.5x A normal APTT suggests that minimal drug is present A significantly prolonged APTT suggests drug excess: a. APTT > 65s at trough (12 hrs post-dose) or b. APTT > 80s at any time. v) Prothrombin time (PT) At therapeutic concentrations (50-200 ug/L) dabigatran has little effect on PT and therefore INR. INR results therefore do not reflect anticoagulant activity. At supra-therapeutic concentrations the INR may be 2.0. c) Dabigatran Assay i) Haemoclot dabigatran assay has been established by SA Pathology ii) A “dabigatran level” should be requested on the pathology form and the timing of the last dabigatran dose given. iii) A single citrate tube is required. For further information ring 8222 3918. d) Dabigatran and other anticoagulants i) When converting patients from warfarin do not commence dabigatran until the INR is < 2.0. ii) For patients on dabigatran commencing parenteral anticoagulation, wait 12 hours (CrCl ≥ 30 mL/min) or 24 hours (CrCl < 30 mL/min) after the last dose. iii) For patients receiving a parenteral anticoagulant commencing dabigatran LMWH (b.d.) commence dabigatran 0-2 hours before the next dose of LMWH was to have been administered Heparin infusion - commence dabigatran on cessation of infusion.
- 131. 131 e) Peri-operative dabigatranmanagement i) The requirement to cease anticoagulation should be assessed ii) If cessation is required, the timing will be dependent upon renal function and the bleeding risk associated with the procedure. Table: Pre-operative Dabigatran Management Renal Function Half-life Timing of discontinuation prior to surgery (CrCl ml/min) dabigatran (hrs) Standard bleeding risk High bleeding risk > 80 13.4 24 hrs 2-4 days > 50 to 80 15.3 24 hrs 2-4 days > 30 to 50 18.4 At least 2 days 4 days 30* 27.2 2-5 days > 5 days NB: *Ongoing treatment with dabigatran should be reviewed as use in patients with a CrCl < 30ml/min is contra-indicated. f) Bridging therapy with parenteral anticoagulation i) Pre-operative bridging is not required in the majority of patients. ii) Post-operative bridging The onset of therapeutic anticoagulation after administration of dabigatran is rapid (within 1-2 hrs) Caution should be exercised in restarting within 48-72 hrs following high bleeding risk procedures Alternative parenteral prophylactic anticoagulation may be warranted (eg subcutaneous enoxaparin) in the time period prior to resuming dabigatran, depending on the procedure performed. g) Epidural and other regional anaesthesia/analgesia and dabigatran i) LP, spinal, epidural and some forms of major regional block should not be performed within 24 hrs post-dabigatran, longer with renal dysfunction. ii) Dabigatran should not be administered to patients with an epidural catheter in-situ (and some regional analgesia catheters – discuss with anaesthetist). iii) Dabigatran should be delayed 4 hrs following performance of an epidural, spinal, LP, regional block or after catheter removal. h) Emergency procedures i) Surgery or invasive procedures should be delayed at least 12 hrs post-dose ii) An urgent APTT +/- dabigatran level can be requested and bleeding risks are small providing: normal APTT or dabigatran level < 50 ug/L. iii) See guideline for management of bleeding in patients receiving dabigatran for details regarding the treatment of surgical bleeding.
- 132. 132 Flowchart: Management ofBleeding Patient on Dabigatran Bleeding Patient on Dabigatran Initiate Standard Resuscitation Procedures as Required Urgent bloods: FBC, APTT, PT, TT and dabigatran level* E, C&U, Creatinine *2 x citrate tubes + time of last dose of dabigatran. STOP DABIGATRAN THERAPY Severe Bleeding Moderate Bleeding - Consult critical bleeding on-call - Consult critical bleeding on-call haematologist via transfusion. haematologist via transfusion. (25430/25431) (25430/25431) Mild Bleeding - Consider oral charcoal administration if - Consult ICU or if necessary other - Local haemostatic measures. dabigatran ingestion < 2 hrs prior. appropriate facility. - Delay next dose of dabigatran - Local haemostatic measures - Institute measures as for moderate to or discontinue if felt severe bleeding. appropriate by prescribing o Mechanical compression physician. o Consider seeking an opinion regarding - Administer rVIIa 90 ug /kg surgical intervention (rounded up to nearest mg), and - Maintain adequate hydration to aid drug consider repeat dose at 30 clearance. minutes, if no response.* - Transfusion support - Consider dialysis particularly indicated if o Packed cell transfusion as indicated by Hb high drug level as indicated by excessively and ongoing bleeding prolonged aPTT > 80 secs or o Consider platelet transfusion if platelets < dabigatran level > 200 ug/L and/or impaired 70 x 109/L or if taking antiplatelet therapy. renal function. o Consider 25U/kg prothrombinex if INR > Consider dose of rVIIa immediately prior to 1.5. vascular access if significantly prolonged aPTT. o If ongoing bleeding resulting in clinical 4 hrs of haemodialysis will reduce instability despite above measures consider drug level by approx. 60%. rVIIa* +/- dialysis as described as for severe bleeding. - Neither rVIIa nor dialysis is likely to improve outcome in patients with a normal aPTT or a dabigatran level of < 50 ug/L Moderate bleeding – reduction in Hb ≥ 20g/L, transfusion of ≥ 2 units of red cells Severe bleeding – bleeding in critical area or organ (intraocular, intracranial, intraspinal, compartment syndrome, retroperitoneal or pericardial), hypotension not responding to resuscitation. * This is an off license use of rVIIa (NovoSeven) and the risk of thrombotic complications when rVIIa is used for this indication is unclear. The use of rVIIa is supported by laboratory data however clinical evidence supporting an improvement in clinical outcomes is still lacking.
- 133. 133 11. Disseminated intravascularcoagulation (DIC) a) Definition i) DIC occurs when the balance of the haemostatic and fibrinolytic systems becomes disordered. It occurs in response to severe pathophysiological stimuli and is a part of multisystem organ dysfunction (often associated with ARDS and acute renal failure). It is characterised by: Microthrombi formation causing microvascular obstruction Consumption of platelets and clotting factors Abnormal fibrinolysis b) DIC screen: i) Complete blood picture microangiopathic haemolytic anaemia with red cell fragmentation haemolysis thrombocytopenia ii) Extended coagulation screen: prolongation of TCT, APTT, PT hypofibrinogenaemia low factor VIII excess fibrinolysis with elevated FDPs iii) Liver and renal function tests c) Treatment i) Treatment of the underlying cause ii) Replacement of blood components in the bleeding patient FFP - based on INR/APTT cryoprecipitate - for marked fibrinogen deficiency iii) Controversial therapies (following consultant approval only) heparin, fibrinolytics (tPA) anti-fibrinolytics (EACA) 11. Blood transfusion reaction protocol a) Plasma can cause reactions ranging from mild pruritus, erythema and urticaria through to severe flushing, hypotension, fever, angioedema, bronchospasm and fulminant anaphylaxis. b) Suspected Reaction Protocol i) Stop the transfusion immediately – do not disconnect the IV line. ii) Recheck the patient identification on the blood product pack label against the patient’s wristband and verbally with the patient if possible. iii) If there is an unexplained discrepancy, discontinue the transfusion and treat as per (iv, v below) iv) Mild Reactions Temp. < 1.5º C Mild or no hives or rash. Action - slow the rate and continue transfusing the same unit of blood.
- 134. 134 v) Severe Reactions Severe hives and/or a rash. Temp. > 1.5°C and is the only clinical sign or symptom Action a. Consider an antihistamine and antipyretic b. Cease and then restart transfusing the same unit of blood after approximately 20 minutes. If there are further signs & symptoms of a reaction discontinue & order a transfusion reaction investigation If there is a sudden and acute change in the patient’s condition, e.g. cyanosis, bad headache, backache, or significant change in pulse or blood pressure for no apparent clinical reason discontinue & order a transfusion reaction investigation vi) Investigation of a transfusion reaction: A transfusion reaction investigation form (IMVS 224) should be completed and sent to Transfusion Medical Unit (TMU) with: a. A description of the relevant clinical findings and vital signs b. A post-reaction 10ml EDTA blood specimen, preferably from a vein other than that used for transfusion c. Any used or unused blood packs and the attached IV set(s). If there is a major reaction, it is also recommended that the first urine specimen voided after reaction is saved, and patient’s urine output over the next few hours is recorded. Further blood samples for biochemical assays, coagulation tests, and cultures will be needed. Administration of incompatible blood constitutes a Sentinel Event. vii) Haemovigilance The IMVS and RAH are participating in the ‘Blood Safe’ haemovigilance scheme, an adverse incident reporting system aimed at the quality and safety improvement of transfusion practices. Contact the Transfusion Safety RN (Pager: 1575, Tel: 22975)
- 135. 135 Table: Blood TransfusionReactions Type Signs & Symptoms Treatment Prevention Febrile non-haemolytic Pyrexia (> 1°C rise) Withhold transfusion. Consider use of transfusion reaction Rigors/chills Mild fever without other leucodepleted red cells or Anxiety symptoms may be treated platelets if a recurrent (FNHTR) by slowing infusion. problem. An antipyretic may be helpful. Investigate as for suspected HTR if the reaction is significant. Circulatory Overload Distended cervical veins. Discontinue. Give all fluids slowly to Pulmonary oedema Institute treatment for fluid patients with compromised Dyspnoea. Headache. overload, cardiac or renal status. Heaviness in limbs. e.g. diuretic Use red cell concentrates. If anticipated, give diuretic. Allergic Flushing Slow rate of flow. When anticipated, Urticaria, itchy hives Consider anti-histamine. use prophylactic Facial oedema Watch for laryngeal antihistamines. oedema and development of anaphylaxis. Anaphylaxis Dyspnoea from laryngeal Discontinue transfusion Use of Medi-Alert oedema or bronchospasm, immediately. wristband in proven sometimes cyanosis and Institute treatment for IgA deficient patients. collapse anaphylaxis, e.g. Adrenalin, steroids Acute Haemolytic Pyrexia Discontinue transfusion Extreme care in Transfusion Reaction Rigors/chills immediately. collecting the correct Lumbar pain Get expert advice blood sample for T&S. (HTR) Pain along vein immediately. Careful compatibility Jaundice Save all used packs, blood testing by laboratory. Haemoglobinuria samples. Careful method for storing Oliguria – later uraemia Save all urine. & labelling blood. Collect fresh blood Careful identification samples. of the correct recipient. Infected blood Bacterial sepsis with Discontinue transfusion Storage at correct temp. hyperpyrexia immediately. Do not remove from Pain in limb & chest Acute medical emergency refrigerator until Headache – get advice immediately. immediately before Pallor Save used packs, all blood transfusion Burning pain along vein samples, with labels. Low blood pressure Save all urine. Rapid pulse Anti-shock treatment and Profound collapse & shock antibiotics. Non-cardiogenic Dyspnoea Maintain blood pressure & Difficult, usually in the pulmonary oedema. ARDS picture within 6 cardiac output with fluid setting of multiparous blood Transfusion related acute hours after transfusion. support. May require donor with anti-recipient- lung injury (TRALI): rare ventilatory support. WBC antibodies. NB: See RAH Intranet, Transfusion Medicine (http://rahadm05v.had.sa.gov.au/)
- 136. 136 D. Guidelines for the Management of Electrolytes 1. General principles a) Total body water (60% total body weight): i) intracellular fluid : predominant ions : K+, PO42- ii) extracellular fluid: 75% interstitial fluid: predominant ions : Na+, Cl- 25% plasma volume (PV) b) Osmotic equilibrium is maintained by Na+/K+ pump i) ECF ions therefore reflect total osmolality: Calculated osmolality 2×Na+ + urea + glucose ii) Magnesium is a cofactor for this pump c) Most electrolyte disturbances in critically ill patients relate to changes in the distribution and concentrations of the predominant ECF and ICF ions. d) As a general rule, changes in one ion will be reflected in the associated cation or anion. e) Electrolyte disturbances should be considered in terms of the following groups: i) Erroneous results Lab error Bloods taken from a drip arm Haemolysed specimen - traumatic (old IA lines), delayed samples Osmolar agents ii) Decreased or increased losses: usually Renal Extra renal: GIT, skin losses iii) Transcellular shifts. iv) Decreased or increased intake f) Treatment should be directed at the underlying cause. g) Rapid correction of electrolyte disturbances may be deleterious. h) One electrolyte disturbance may be predictive of another electrolyte disturbance e.g. K+ often associated with Mg+ i) The following paragraphs outline the common electrolyte disturbances.
- 137. 137 + 2. Hyponatraemia: Na < 130 mmol/l a) Aetiology / classification i) Misleading result Isotonic - Hyperlipidaemia - Hyperproteinaemia Hypertonic - Hyperglcaemia - Mannitol, glycerol, glycine or sorbitol excess ii) Water Retention Renal Failure Hepatic Failure Cardiac Failure SIADH Drugs Psychogenic polydipsia iii) Water retention / Salt depletion Post-operative, post-trauma Patients with excess fluid losses given inappropriate replacement Cerebral salt-wasting syndrome Adrenocortical failure Diuretic excess b) Diagnosis & Management: i) Factitious: ignore and manage underlying condition then recheck Na+ ii) Misleading: Hyperglycaemia: BGL 10 mmol/l [Na+] 3 mmol/l a. Hyponatraemia per se is real, but treatment is directed at the underlying cause, where correction of the hyperglycaemia will correct the plasma [Na+] b. NB: Total body Na+ deficit may co-exist with diuresis in DKA Mannitol: a. [Na+] early, then diuresis & late [Na+] are more problematic b. Maintain adequate plasma volume with N.saline initially Alcohols: permeate solutes, [Na+] less problematic iii) Hypovolaemic states: Restore volume with colloid or normal saline according to clinical markers: urine output, plasma [Na+], RAP Aim for slow Na+ correction: 2 mmol/l/hr, unless seizures. Urine Na+ is uninterpretable after diuretics or catecholamines for 24hrs
- 138. 138 iv) Hypervolaemic states: *most common clinically Fluid restriction < 15 ml/kg/day a. “Water Excess” ~ (140 - Na+ )/140 × (Wt × 0.6) e.g., 70kg patient with plasma [Na+] = 120 mmol/l: = (140 - 120)/140 × (70kg × 0.6) = 6 litres b. Will slowly correct excess - ADH group & “reset osmostat” c. Treat the underlying cause - CCF, nephrotic synd., ascites v) SIADH Causes a. Ectopic ADH production by tumours e.g. small cell bronchogenic tumour b. CNS disorders e.g. tumour, abscess, trauma, SAH etc c. Pulmonary diseases e.g. TB, pneumonia, abscess etc Diagnosis a. Hypo-osmolar hyponatraemia b. Urine osmo > plasma osmo c. Urine Na+ > 40 mosm/l d. Normal endocrine, renal, hepatic, cardiac function e. No diuretics or drugs affecting ADH secretion f. Corrected by water restriction alone Management: fluid restriction vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness Resuscitation / ABC Consider anticonvulsants - phenytoin, benzodiazepines Hypertonic saline (3%) may be indicated a. Always discuss use with the Duty Consultant b. Correct [Na+] rapidly only to ~ 120mmol/l Thereafter, slow correction with N.saline over 24-36hrs ( 2 mmol/l/hr) Treat the underlying cause. 3. Hypernatraemia: Na+ > 145 mmol/l a) Hypernatraemia is always a hyperosmolar state + b) Most body fluids have a [Na ] < plasma net water loss c) Aetiology / classification: i) Water depletion / inadequate replacement Renal a. Diuretics, glycosuria b. ARF/CRF, partial obstruction c. Central diabetes insipidus i. Post traumatic head injury or surgery ii. CNS infection, tumour, granulomatous disease, GBS
- 139. 139 d. Nephrogenic diabetes insipidus: i. 1° : congenital renal resistance to ADH ii. 2° : hypokalaemia, hypercalcaemia, lithium, multiple myeloma, sickle cell anaemia, nephrocalcinosis, amyloid GIT losses - diarrhoea, vomiting, fistulae, SBO Respiratory - IPPV with dry gases Skin losses a. Fever, high ambient temperature b. Vasodilatory states c. Exfoliative skin disorders, burns d. Thyrotoxicosis Unconsciousness “Reset osmostat” ii) Salt gain - Na+ gain > H2O gain Iatrogenic a. Most common cause b. Excess “normal saline” ~ 150 mmol/l [Na+] c. NaHCO3, feeding formulae, TPN Mineralocorticoid excess: a. Conn's, Cushing's syndromes b. Steroid excess d) Management i) Hypovolaemic states Restore volume according to clinical markers: BP, HR, urine output, RAP a. Hartmann’s solution - slightly hypo-osmolar b. Colloid: initial resuscitation, severe hypovolaemic states ii) Slow Na+ correction: 2 mmol/l/hr Water deficit: ~ (Na+ - 140)/140 × (B.Wt × 0.6) e.g. 70 kg patient, with plasma [Na+] = 160 mmol/l ~ (160-140)/140 × (70 × 0.6) ~ 6.0 litres 1 litre water replacement will reduce [Na+] ~ 3-4 mmol/l In addition to basal fluid requirements & ongoing losses Replace over a 24-48 hr period with 5% dextrose Monitor [Na+] regularly Manage aetiological causes Cease causal drugs and inappropriate IVT DDAVP for central DI only ~ 1-2 µg s.c.
- 140. 140 + 4. Hypokalaemia: K < 3.0 mmol/l plasma K+ < 3.5 mmol/l serum a) Aetiology / classification: i) Compartmental / transcellular shift Alkalaemia pH ~ 0.1 [K+]pl ~ 0.5 mmol/l Catecholamines / salbutamol Insulin / anabolism - refeeding effect Hypomagnesaemia - ICF K+ depletion Toxic / poisoning - barium, toluene Familial periodic paralysis Hypothermia ii) Reduced intake - urine [K+] < 20 mmol/L Starvation TPN iii) Increased clearance/losses Renal - urine [K+] > 20 mmol/L a. Diuretics distal tubular flow i. Loop agents - frusemide, bumetanide ii. PT agents - acetazolamide, mannitol iii. Early DT - thiazides b. Steroids / Mineralocorticoid excess i. Conn’s, Cushing’s, Bartter’s syndrome ii. Ectopic ACTH - Small cell Ca lung - Pancreatic, thymus carcinoma iii. Exogenous steroids c. Drugs i. Anionic drugs - antibiotics (penicillins, amphotericin) ii. High dose gentamicin iii. Lithium d. Hypomagnesaemia, Hypocalcaemia e. RTA I, II GIT losses a. Villous adenoma b. Ureterosigmoidostomy c. Fistulae, malabsorption syndromes d. Diarrhoea, Laxatives Skin losses b) Management: i) Treat underlying cause ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis and hypokalaemia iii) Always add Mg++ normomagnesaemia is essential for correction of hypokalaemia iv) Look for and treat concurrent hypophosphataemia
- 141. 141 v) Potassium preparations KCl: 10 ml = 10 mmol/l KH2PO4: 10 ml = 10 mmol/l K-acetate: 5 ml at 5 mmol/ml 25 mmol K+ + 25 mmol acetate (bicarbonate) 5. Hyperkalaemia: K+ > 5.0 mmol/l serum K+ > 4.5 mmol/l plasma a) Aetiology / classification: i) Artefactual Drip arm specimen Tourniquet / Haemolysed specimen (extravascular) Thrombocytosis > 750,000 Leukocytosis > 50,000 ii) Compartmental / transcellular shift Acidosis pH ~ 0.1 [K+] ~ 0.5 mmol/l Insulin deficiency: DKA NB: normo- or hypo-kalaemia in the presence of severe DKA is associated with a marked total body K+ deficit, which must be addressed prior to correction of the acidaemia. Familial periodic paralysis Suxamethonium Digoxin, -blocker overdose Fluoride poisoning ECF tonicity a. Water moves from cells → [K+]ICF and passive diffusion b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg) c. Hyperkalaemia of DKA is due to this in addition to the acidaemia & insulin deficiency iii) Cellular disruption / death Tissue breakdown Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion Severe burns Tumour lysis syndrome, leukaemia iv) Increased intake - rarely a problem unless impaired renal function Massive transfusion Direct IV/oral Drugs (penicillins)
- 142. 142 v) Reduced clearance Acute renal failure a. Any cause for distal tubular flow, or distal NaCl delivery b. Hypoaldosteronism i. Mineralocorticoid deficiency, Addison’s ii. K+ is multifactorial - K+ICF K+ECF - distal tubular flow - DT aldosterone effect Type IV RTA ACE Inhibitors Potassium sparing diuretics a. aldosterone antagonists - spironolactone b. distal Na+ channel inhibitors - amiloride, triamterene b) Management: i) The clinical scenario will dictate treatment ii) Acute K+ > 6.0 mmol/l is a medical emergency iii) Associated with acute ECG changes, or haemodynamic compromise: In following order (not mixed together), CaCl2 10 ml IV stat NaHCO3 50-100 ml IV stat Glucose 50% 50g + Insulin 20 units Salbutamol nebs continuously iv) Refractory or persistent: CVVHDF intermittent dialysis v) Chronic K+ or slow rate of rise or no ECG changes: Resonium 30g oral / PR 8 hourly vi) Address aetiological factors vii) Normalise renal function / volume status 6. Acid base disturbances a) Acid base disturbances in ICU are frequently mixed disorders b) Correction of these should be directed at the underlying cause and maintenance of cardiopulmonary homeostasis. c) Primary correction of an acid base disturbance with acid or alkali is seldom required.
- 143. 143 7. “Rules ofthumb” *these are approximations only a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO2 i) Met Acid to min 7.10 e.g. pH 7.25 PaCO2 25 mmHg ii) Met alkalosis to max 7.60 e.g. pH 7.57 PaCO2 57 mmHg b) Primary respiratory acidosis: i) HCO3 ~ 1mmol/l per 10mmHg PaCO2 above 40 to max 30 c) Primary respiratory alkalosis i) HCO3 ~ 2.5mmol/l per 10mmHg PaCO2 below 40 to min 18 d) Chronic respiratory acidosis i) HCO3 ~ 4mmol/l per 10mmHg PaCO2 above 40 to max 36 8. Metabolic acidosis a) Assessment of metabolic acidosis must include the anion gap: Anion Gap = [Na+ + K+] - [Cl- + HCO3-] ~ 12-17 mmol/l Unmeasured cations Unmeasured anions Mg++ ~ 1.2 mmol/l Albumin ~ 15 mEq/l Ca++ ~ 2.2 mmol/l H2PO4- ~2 mmol/l IgG Small HSO4- ~1 mmol/l Organic ~5 mEq/l ~ 7.0 mEq/l ~ 23 mEq/l b) This allows sub-classification of metabolic acidosis into raised or normal anion gap acidoses. i) Beware a low [Alb] in critically ill lowering the measured AG ii) Measurement of chloride in the lab is highly variable iii) Assessment of the AG must be viewed within the clinical context. c) Aetiology of raised anion gap: i) Renal failure - H2PO4- , HSO4- (rarely AG > 23) ii) Lactic acidosis - types A&B * normal AG does not exclude a lactic acidosis iii) Ketoacids - -OH-butyrate, acetoacetate - diabetes mellitus, starvation, alcohol iv) Rhabdomyolysis - organic acids v) Drugs / poisons: Aspirin - salicylate, lactate, ketones Paracetamol - lactate, pyroglutamate Ethanol - acetoacetate, lactate Methanol - formate (formaldehyde), lactate Paraldehyde - formate, acetate, lactate, pyruvate Ethylene glycol - oxalate Xylitol, Sorbitol - lactate Fructose - lactate
- 144. 144 Table: Classification of Lactic Acidosis Type A Type B Drug induced Hereditary Severe exercise Thiamine deficiency Phenformin G6PD deficiency Seizures Diabetes Metformin Fructose-1,6-DP- Cardiac arrest Hepatic failure Ethanol deficiency Shock Renal failure Methanol Hypoxia Infection Salicylates Anaemia Leukaemia, lymphoma IV fructose Pancreatitis Xylitol Short bowel syndrome Sorbitol d) Aetiology of low or normal anion gap: i) Hyperchloraemic metabolic acidosis Resolving renal failure Resolving DKA Renal tubular acidosis / carbonic anhydrase inhibitors Mineralocorticoid deficiency Pancreatic, enteric fistulae Ureterosigmoidostomy IV HCl, NH4Cl, Arginine ii) Metabolic alkalosis due to HCO3- gain iii) Hypoalbuminaemia iv) Myeloma - IgG has positive charge, 's AG v) Increased Mg++ or Ca++ (rarely) vi) Artefactually elevated Cl- vii) ? Hyperlipidaemia e) Management i) High anion gap Treat the underlying cause No indication for NaHCO3 ii) Normal anion gap Treat the underlying cause. Replace HCO3 serum level and losses a. Approx. deficit = (24 - [HCO3]) × (Wt. × 0.6) mmol/l e.g. for a 70kg patient with a [HCO3] = 4 mmol/l deficit = (24 - 4) × (70 × 0.6) = 840 mmol (= ml of standard bicarb solution) b. Replace 1/3-1/2 of this amount then remeasure blood gases.
- 145. 145 9. Metabolic alkalosis a) Aetiology / classification i) Common causes: Diuretics Vomiting Post-hypercapnia > 48 hours Commonly associated with hypovolaemia and/or hypokalaemia however, actual causation by these is debated ii) Increased proton losses: acid loss is either renal or GIT Renal a. Na+ reabsorption (hypovolaemia, dehydration, etc.) b. Cushing's syndrome, exogenous steroids c. Hyperaldosteronism 1° / 2° d. Bartter's syndrome (JGA hyperplasia) e. Liddle's syndrome f. Hypercalcaemia / hypomagnesaemia nephrogenic DI g. Drugs: steroids, diuretics, carbenoxolone GIT a. N/G suctioning, protracted vomiting b. Diarrhoea iii) Increased bases Administration of NaHCO3 Metabolism of exogenous acid anions - citrate, lactate, acetate Milk/alkali syndrome Renal conservation of HCO3- - acidosis, hypercarbia iv) Factors tending to maintain an alkalosis Any fluid loss replaced with insufficient Na+ ↑ H+ excretion (contraction alkalosis) Hypovolaemia Hypokalaemia, hypochloraemia, hypomagnesaemia Chronic hypercapnia Mild chronic renal failure b) Management i) Correct hypovolaemia *normal ECF volume is essential for the correction of alkalosis ii) Inotropic support of cardiac output and GFR iii) Correct K+, Mg++, HPO4= iv) Consider acetazolamide if the alkalosis is persistent - provided the above are corrected.
- 146. 146 10. Respiratory acidosis a) Aetiology i) Any cause of hypoventilation respiratory failure (see diag.) A. Respiratory centre / CNS B. Upper motor neuron / spinal cord C. Anterior horn cell D. Lower motor neuron E. Neuro-muscular junction F. Respiratory muscles G. Elasticity/compliance of lungs/chest wall H. Structural integrity of chest wall & pleural cavity I. Increased airways resistance – intra/extrathoracic ii) May be acute or chronic b) Management i) Restore ventilation / manage underlying cause(s) ii) No indication for HCO3 2. Respiratory alkalosis b) Aetiology i) Early hypoxia, shock or hypotension ii) Anxiety, hysteria, neurogenic hyperventilation iii) PTE iv) Hepatic failure v) Prescribed hyperventilation (rarely indicated) c) Management i) Treat underlying cause ii) Neurogenic hyperventilation is a marker of severity of head injury
- 147. 147 PART 5 - CLINICAL MANAGEMENT The following protocols are designed to facilitate clinical management of patients in the Intensive Care. These protocols may vary from other ICUs and do not represent the sole approach to patient management. However, they do represent a standardised approach which has evolved in this ICU over the years. Each clinical scenario is managed according to the particular situation and individual patient - it is neither practical nor appropriate to apply rigid policies to clinical situations. However, as clinical medicine is at times more art than a science, these protocols are designed to assist in areas that are unfamiliar and to standardise approaches by all staff members of the Unit. The following protocols are outlined. A. Cardiopulmonary resuscitation B. Failed intubation drill C. Respiratory therapy D. Management of cardiothoracic patients E. Renal failure F. Neurosurgical protocols G. Microbiology protocols H. Drug overdose I. Bites and Envenomation J. Withdrawal of therapy K. Organ donation and brain death
- 148. 148 A. Cardiopulmonary Resuscitation Flowchart:Basic Life Support
- 149. 149 Flowchart: Advanced LifeSupport
- 150.
- 151. 151 Induced Hypothermia PostCardiac Arrest 1. Aim: To improve CNS outcome by actively cooling to a TCore 32-34°C 2. Inclusion Criteria a) Non-traumatic cardiac arrest with return of spontaneous circulation a) Unconscious, intubated and ventilated b) Absence of an immediately correctable cause for coma c) TC > 34.5°C 4. Exclusion Criteria a) Cardiac arrest related to trauma or intracranial injury b) Ongoing CPR and/or persistent cardiovascular instability c) Cardiology consultation need for acute intervention d) Criteria that preclude 40mls/kg of cold Hartmann’s solution, e.g. acute pulmonary oedema, TC < 34.5°C e) Time from cardiac arrest to ED > 12 hrs f) Pregnancy – relative C/I 5. Procedure - Initial Treatment Protocol a) ECG and routine blood tests as indicated b) Record core temperature (TC): rectal, oesophageal or bladder catheter c) Ensure adequate IV access (1x 16G) d) Document neurological function, specifically: i) Pupillary responses to light ii) Response to painful stimuli (all limbs), vocalization iii) Reflexes – gag, conjunctival, lash, tendon & plantar e) Hartmann’s (Temp. 4°C) / Bolus 40mls/kg. / Infuse @ 100ml/min. f) Maintain MAP 80-100mmHg (relative to premorbid BP) g) Maintain K+ 4-5mmol/L and Mg++ 0.8-1.2mmol/L h) If TC > 35°C after 1 hour, add surface cooling (cooling blanket / packs) i) If patient is shivering and/or goal TC not achieved: i) Midazolam (0.05mg/kg bolus, repeat every 5 min as required) ii) Midazolam (1-5mg/hr) or Propofol infusion as clinically indicated. iii) If sedation ineffective, consider a non-depolarizing muscle relaxant 6. Observations a) Maintain TC 32-34°C for 12-24 hrs from the time of achieving goal temp. b) To increase temp. (T < 31.5°C), use heated air blanket until 33°C c) To decrease temp. (T > 34.5°C), use cold packs, cooling blanket, sedation and then consider using non-depolarizing muscle relaxants 7. Complications a) Arrythmia b) Reduced cardiac index / increased peripheral resistance. c) Ongoing cardiac instability may necessitate stopping the hypothermia protocol. d) Hyperglycaemia 8. Aftercare a) At 24 hrs cease all active cooling and allow passive rewarming. b) If temp increases < 1°C per 4 hours then rewarm actively to temp > 36°C c) Once TC > 35°C, cease sedation and muscle relaxants
- 152. 152 B. Failed Intubation Drill 1. Following rapid sequence induction in ICU we are generally committed to securing the airway by some means. Allowing the patient to wake-up in the event of a failed intubation is rarely practical. 2. Risk of failed intubation in ICU is higher than in the operating theatre. 3. Before intubating, you MUST have a contingency plan for a difficult airway/failed intubation. 4. After hours, remember the anaesthesic staff may be available to assist. 5. Ensure all equipment is working and that the ETCO2 monitor provides a reliable waveform. 6. Ensure adequate IV access with running intravenous fluids. 7. Ensure ready access to vasopressors and resuscitation drugs. 8. Always have the difficult intubation trolley at hand. 9. Visually confirm that each individual piece of airway equipment is immediately available and operational. 10. ICU patients have limited O2 reserves and desaturate quickly. a) If initial intubation attempts fail, or the patient desaturates significantly, ensure you can manually ventilate the patient. b) Failure to achieve manual ventilation is an absolute emergency “can’t intubate + can’t ventilate” 11. If an intubation technique fails, move on quickly to an alternative. 12. There are a range of airway devices available to help secure the airway. a) Guedel airway / Nasopharyngeal airway b) Bougie c) C-Mac d) Laryngeal Mask / Intubating Laryngeal Mask e) Cricothyroidotomy f) Jet insufflation g) Bronchoscopy (for anticipated difficult intubations) 13. You must be familiar with the devices you plan to use in the case of a failed intubation. 14. Airway equipment and intubating manikins are available for practice in the registrar’s room.
- 153. 153 Flowchart: Failed IntubationDrill Committed to Intubation FURTHER Best Attempt ATTEMPTS USING Intubate Laryngoscopy ADVANCED DEVICE McCoy / Flextip C-MAC Airtraq Failure or SpO2 < 88% Call for help Yes Oxygenate/ventilate CALL No EMERGENCY ILMA +/- Intubate Bronchoscope Failure to Ventilate Crico- Thyroidotomy
- 154. 154 C. Respiratory Therapy 1. Respiratory Failure a) Definition = failure of efficient gaseous exchange and/or effective ventilation. i) Type 1 Respiratory Failure Hypoxaemia, PaO2:FiO2 < 300 mmHg i.e. failure to oxygenate ii) Type 2 Respiratory Failure Hypercapnoea, PaCO2 > 50 mmHg, with a pH < 7.35 i.e. failure to ventilate 2. Oxygen Delivery Capacity Table: Oxygen Delivery Devices Apparatus/Device Oxygen Flow (l/min) Approx. FIO2 (%) Nasal catheters 2-6 25-40% 5 35 6 50 Semi - rigid masks 8 55 (e.g. Hudson, CIG) 10 60 12 65 Venturi type mask 2-8 24 - 50 (e.g. Ventimask, Accurox) Nasal High Flow 30-50 l/min 21 - 95 (humidified circuit) Reservoir plastic masks 6 - 15 FiO2 = 21% + 4% per l/min (Non-rebreathing mask) Closed Circuits Variable 21 - 100 e.g. IPPV, NIV Oxylog 1000 and 2000 Variable Airmix : 60 No airmix : 100 Oxylog 3000 Variable 40 - 100 a) The FiO2 delivered to the patient by an “open circuit” will depend on the patient’s peak inspiratory flow rate (PIFR). b) The higher the PIFR, the higher the O2 flow required to provide a given FiO2.
- 155. 155 3. Humidification a) All ventilated patients must have adequate humidification of inspired gases for optimal mucociliary function and conservation of temperature. b) Optimal humidification requires: i) Delivery of gas to the trachea at a constant temperature (32-36ºC). ii) Relative humidity 75-100%. iii) No increase in circuit resistance. iv) No increase in circuit dead space. v) Applicable to spontaneous and controlled ventilation. vi) Sterile inspired gas c) Types of humidifiers available i) Heat/moisture exchangers (HME) First line humidification. Effective for most patients. Incorporates a bacterial and viral filter. Cannot be used with nebulised drugs. Secretions increase resistance and reduce HME efficacy. Change to wet circuit (FP) in patients with bronchorrhoea or mucous inspissation. Single use & change every 48 hrs, or as required. ii) Fisher Paykel (FP) evaporative humidifier (wet circuit) Bronchorrhoea or mucous inspissation. Hypothermic or heat-loss susceptible patients (e.g. burns). Ventilation anticipated for more than 48 hrs. Set chamber to 40°C. iii) Inspiron (aerosolised T-piece). Relatively inefficient humidification. Allows variable FiO2 : 0.21-0.7 4. Nasal High-Flow Oxygen a) NHF delivers high gas flows through a unique Optiflow™ nasal cannula. b) Critical to NHF is the delivery of optimal humidity to allow delivery of high flows directly into the nares. c) This provides greater patient comfort while optimising mucociliary clearance. d) Main benefits of NHF: i) Delivery of up to 100% oxygen. Actual FiO2 will depend upon the patient’s breathing pattern ii) Anatomical dead space flushed. iii) Positive airway pressure (2-5cmH2O) throughout the respiratory cycle. iv) Improved mucociliary clearance.
- 156. 156 Table: Oxygen Delivery Percentage - Nasal High Flow O2 % 30 LPM 40 LPM 50 LPM O2 Air O2 Air O2 Air 30 4 26 5 35 6 44 40 7 23 10 30 12 38 50 11 19 15 25 18 32 60 15 15 20 20 25 25 70 19 11 25 15 32 18 80 22 8 30 10 38 12 90 26 4 35 5 44 6 100 30 0 40 0 50 0 5. Mechanical Ventilation a) Mechanical ventilation is one of the mainstays of intensive care medicine. b) There are 2 main types of mechanical ventilation: i) Non-invasive ventilation. ii) Invasive ventilation. c) An understanding of the types of mechanical ventilation, indications, complications, practical aspects of mechanical ventilators and their use in respiratory failure is essential. d) Registrars should familiarise themselves with the ventilators, understand the default settings and common modes of ventilation. e) All changes to ventilation orders must be recorded on the flowchart and conveyed to the bedside nurse. f) All ventilator alarms must be addressed immediately. g) Any changes to alarm settings must be relayed to the bed-side nurse. 6. Non-Invasive Ventilation a) Definition: Mechanical positive pressure respiratory support in the absence of tracheal intubation (e.g. via a face mask, nasal mask, head piece/box) b) Modes i) Continuous positive airway pressure (CPAP) ii) Bi-level positive airway pressure (BiPAP). c) Indications i) As an adjunct to weaning from ventilation (e.g. extubation to NIV). ii) Acute exacerbation of COAD. iii) Cardiogenic pulmonary oedema. iv) Obstructive sleep apnoea / obesity hypoventilation syndrome. v) Post-extubation hypoxia due to pulmonary oedema or atelectasis. vi) Febrile neutropaenia with pulmonary infiltrates.
- 157. 157 d) Prerequisites i) Adequate glottic reflexes should be present to protect from aspiration - moribund patients require intubation where appropriate. ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B. iii) Selected patients may be managed in Unit C. e) Complications i) Inadequate ventilation. ii) Mask leaks. iii) Aerophagia, gastric distension, vomiting, aspiration. iv) Claustrophobia and mask intolerance. v) Pressure necrosis of nasal bridge. vi) Dry secretions. vii) Barotrauma. viii) Reduced preload and hypotension. ix) Raised intracranial and intraocular pressure. 7. Non-Invasive Ventilators a) BiPAP® Vision i) Microprocessor controlled. ii) Nasal, face & full head masks can be used. iii) IPAP = Inspiratory positive airway pressure. iv) EPAP = Expiratory positive airway pressure (PEEP). v) Pressure support = IPAP - EPA vi) Monitors machine pressure against proximal airway (mask pressure) to ensure effective delivery of pressure despite circuit leaks. vii) Need to calibrate for tubing and mask. viii) Uses internal algorithm for respiratory cycling and leak adjustment. ix) Liquid crystal displays: IPAP, EPAP, Rate, FiO2. VT, Vmin, PIP, Insp. time/total cycle time. Leak (patient & total), % patient triggered breaths. Graphical display of pressure, volume & flow. x) Operation: Machine starts up in mode previously used. Press [Mode] hard key to display CPAP or S/T mode Press [Activate New Mode] soft key to select the new mode. Select soft key parameters displayed & turn adjustment knob accordingly. CPAP Mode - Default settings a. CPAP 5cmH2O, FiO2 1.0 S/T Mode - Default settings a. IPAP 15cmH2O, EPAP 5cmH2O b. FiO2 1.0, Rate 12, TInsp 1 sec, IPAP rise time 0.1 sec
- 158. 158 ® b) CPAP via Dräger EVITA i) Operation: Select “Non-Invasive” Mode Default settings: a. Pressure support 10 cmH2O (above PEEP) b. PEEP 5 cmH2O c. Inspiratory time 4 sec d. Trigger 5 L/min Adjust Press Support and Rise Time to provide the assisted breaths. 8. Indications for Invasive Ventilation a) Respiratory Failure. b) Intubated for airway protection. c) Severe metabolic disturbance with altered conscious state. 9. When to institute invasive ventilation a) Clinical assessment is the most sensitive assessment of respiratory failure. b) Do not delay the initiation of ventilatory support pending results, blood gases or mechanical measurements in the following settings: i) Threatened airway. ii) Fatigue / exhaustion. iii) Failure of secretion clearance. iv) Overt respiratory failure. v) Speech impairment due to dyspnoea. vi) Reduced GCS in the absence of other causes. c) Objective measurements are adjuncts to clinical assessment: i) RR > 35 bpm ii) VC < 15 ml/kg iii) SpO2 < 90% on 15L O2 iv) PaCO2 > 60 mmHg (with pH < 7.2) 10. Modes of Ventilation in ICU a) Synchronised intermittent mandatory ventilation (SIMV). i) Default ventilation setting at RAH. ii) Prescribed tidal volume. iii) Airway pressure is variable. b) Pressure control ventilation (PCV). i) Prescribed peak pressure. ii) Tidal volume is variable. iii) High sedation requirements, occasional use of muscle relaxants. c) Pressure Support Ventilation (PSV) + PEEP i) Spontaneous ventilation mode for patients with adequate respiratory drive, respiratory mechanics and strength. ii) Commonly used when weaning from ventilation. iii) Requires patient effort to initiate ventilatory assistance.
- 159. 159 11. Optimising Ventilation a) Optimise oxygenation: i) Use the lowest FiO2 to achieve an ‘adequate’ SpO2 or PaO2. e.g. SpO2 > 95% and/or PaO2 > 80 mmHg. ii) Lower values may be appropriate with chronic lung disease. b) Optimise PaCO2: i) Adjust relative to pre-morbid PaCO2. ii) Consider permissive hypercapnia in patients with poor lung compliance. c) Optimise patient-ventilator interface: i) Reduce work of breathing through the ETT and ventilator circuit. ii) Pressure support. iii) Automatic Tube Compensation (ATC). iv) Appropriate trigger threshold. v) Adequate expiratory time. vi) Prevent gas trapping: measurement and manipulation of auto-PEEP vii) Patient positioning. d) Optimise sedation and analgesia. i) Review the need for sedation daily. ii) Calculate the RASS score for each patient daily. iii) Order depth of sedation on the ICU obs chart. iv) Always assess suitability for ceasing sedation. e) Minimise volutrauma (barotrauma) 12. Complications of Mechanical Ventilation a) Haemodynamic. i) Reduced preload. ii) Increased RV afterload unmasked hypovolaemia. b) Respiratory. i) Ventilator Associated Pneumonia (VAP). ii) Volutrauma / Barotrauma Ventilator associated lung injury. iii) Patient ventilator dys-synchrony. c) Metabolic. i) Post-hypercapnoeic metabolic alkalosis. ii) SIADH. d) Raised intracranial and intraocular pressure. e) Need for sedation i) Reduced patient mobility DVT, pressure sores, weakness ii) Reduced joint movement. f) Local pressure effects from intubation, tracheostomy or face masks.
- 160. 160 13. Drager EVITA2 Ventilator a) The Evita 2 are the default ventilator at the RAH. b) Modes: SIMV, PCV, Pressure Support, CPAP, APRV. c) Non-invasive ventilation modes are also available. d) Specific features: i) Auto flow: automated adjusted inspiratory flow according to lung mechanics during controlled ventilation. ii) Rise time: manual adjustment in all modes. iii) 100% O2 suction button: delivers 100% oxygen for 3 minutes. iv) Programmable default parameters. v) Flow and Pressure-Volume loops. vi) Preset emergency and apnoea ventilation parameters. vii) Automatic tube compensation to assist weaning. viii) Automated respiratory mechanics: Static and dynamic compliance. Automated estimation of auto-PEEP and occlusion pressure (P0.1). Inspiratory airway resistance. Negative inspiratory pressure. Vital capacity. e) SIMV i) Default settings: SIMV: 600×12, PS = 5 / PEEP = 5, FiO2 = 1.0 ii) Select mode: SIMV. iii) FiO2 = 1.0 iv) VT = 0.6 L v) Rate = 12 bpm vi) PS = 5 cmH2O vii) PEEP = 5 cmH2O viii) Rise time = 0.2 secs ix) Adjust TInsp I:E ratio 1:2 (default 1.7 secs) x) “Extra settings” mode Flow trigger = 5 l/min Backup ventilation (CMV) : Off f) PC (Pressure control) i) Default settings PInsp = 30×12, PEEP = 5, FiO2 = 1.0, I:E=1:2 ii) Select mode: PCV+ iii) Select total inspired level of pressure (PInsp) = 30 cmH2O iv) Rate = 12 v) Rise time = 0.2 secs vi) PS = 5 cmH2O vii) PEEP = 5 cmH2O viii) FiO2 = 1.0 ix) Adjust TInsp I:E ratio 1:2 (default 1.7 secs) x) Do not exceed total inspired pressure > 40 cmH2O xi) Tidal volume is determined by respiratory compliance.
- 161. 161 g) Pressure Support(PS) + PEEP i) Total inspiratory pressure, when using PS on the Evita, is the dialed value plus dialled PEEP value ii) Mode = CPAP iii) Rise time = 0.2 secs iv) PS = 10 cmH2O v) PEEP = 5 cmH2O vi) FiO2 = 1.0 h) I:E Ratio i) Alteration of the I:E ratio is potentially hazardous and should only be done following discussion with the duty consultant. i) Measurement of auto-PEEP i) Not accurate if patient effort, patients should be well sedated / paralysed. ii) Measurement of intrinsic PEEP at end expiration + closed airway. iii) Press the [Special Procedure] button & select [PEEPi]. iv) Press [Start] to begin the automatic 7sec manoeuvre. v) Read off the PEEPi and trapped gas volume (VTrap) vi) The value displayed includes applied PEEP, so: vii) auto-PEEP = PEEPi - applied PEEP j) Measurement of occlusion pressure (P0.1) i) Measurement of the negative airway pressure generated in the first 100msec of inspiration against an occluded airway. ii) Reflects diaphragmatic effort and neuromuscular drive. iii) Normal value 3-4 mbar. iv) Press [Special Procedure] button. v) Select P0.1 and press [Start] to measure value. k) Always examine the flow, pressure and volume vs time loops i) Upper/lower airway obstruction. ii) Recruitable lung. iii) Increased airway resistance. iv) Dynamic hyperinflation e.g. flow does not return to baseline before the next breath v) Sudden reversal of flow / pressure which does not trigger a breath may indicate wasted patient effort.
- 162. 162 14. RAH –ARDS Ventilation a) Initial Ventilator Set-up and Adjustments (Dräger) i) Mode: SIMV + PS ii) Resp. Rate: 18 bpm iii) Insp. Flow Rate: Autoflow iv) Tidal Volume: 6 ml/kg IBW b) Tidal Volume Settings are determined by calculated Ideal Body Weight i) Males = 0.91 × (height [cm] – 152.4) + 50 ii) Females = 0.91 × (height [cm] – 152.4) + 45.5 iii) Calculate IBW and VT = 6 x IBW c) Adjust RR to achieve the pH goals according to ABG’s. i) After any RR change, check the I:E ratio and TInsp. ii) Target I:E Ratio 1:1 – 1:3 iii) Maintain TInsp 0.8 sec. d) Adjust VT according to inspiratory plateau pressure (PPlat) goals. i) Target PPlat < 30cmH2O ii) Check PPlat with a 2 sec inspiratory pause every 4 hrs and after each change in PEEP or VT. iii) Method (Dräger): [Measurements] + press [Insp Hold] for 0.5sec PPlat will appear on the screen for 1 sec. iv) PPlat > 30cmH2O VT by 1 ml/kg IBW steps (min VT = 4ml/kg IBW). v) PPlat < 25cmH2O and VT < 6ml/kg IBW VT by 1ml/kg IBW. vi) NB: Observe spontaneous tidal volumes and adjust PS downwards if volumes generated are higher than the calculated goal VT. e) Adjust FiO2 & PEEP according to SpO2 and PaO2. i) Goal PaO2 = 55-80mmHg or SpO2 = 88-95%. ii) Use the table (right) to adjust FiO2 / PEEP combinations FiO2 PEEP for the target PaO2 range required, e.g. 0.3 5 If FiO2 = 0.4 / PEEP = 5 and the PaO2 = 54, 0.4 5 PEEP to 8 cmH2O 0.4 8 If FiO2 = 0.9 / PEEP = 14 and the SpO2 = 99% 0.5 8 FiO2 to 0.8 0.5 10 0.6 10 f) Other therapies that may improve oxygenation. 0.7 10 i) Recruitment Manoeuvres 0.7 12 ii) Prone Ventilation 0.7 14 iii) Nitric Oxide / Nebulised prostacylcin. 0.8 14 iv) ECMO 0.9 14 0.9 16 None proven – see over. 1.0 16
- 163. 163 15. Recruitment Manoeuvres a) Recruitment of under-ventilated alveoli may be achieved by prolonged inspiration with higher inspiratory pressures and higher PEEP. b) There are a variety of strategies employed. c) These should only be performed following discussion with the consultant. d) Contraindications to a LRM include the following: i) Mean BP < 60mmHg despite fluids/vasopressors ii) Active air leak through thoracostomy tube, i.e. broncho-pleural fistula iii) Pneumatoceles, subpleural cysts, or pericardial or mediastinal emphysema iv) Subcutaneous emphysema not related to trauma, surgical or ICU procedures e) Early termination of a LRM is mandatory if any of the following develop: i) SpO2 < 85% ii) HR < 60 or > 140 iii) New arrhythmia - except isolated supraventricular extrasystoles iv) New air leak through thoracostomy tube v) Fall in mean BP < 60 mmHg 16. Prone Ventilation. a) May improve oxygenation b) Has never been shown to improve ICU survival from ARDS c) Risky and labour intensive intervention. d) Should only be considered and undertaken under direct consultant supervision. 17. Nitric Oxide / Nebulised Prostacylcin. a) Both can improve oxygenation but do not improve survival from ARDS b) Nitric Oxide is not currently provided in ICU at RAH c) Nebulized prostacylcin should only be commenced per the duty consultant. 18. Extra-Corporeal Membrane Oxygenation (ECMO) a) ECMO can be used to provide either: i) Oxygenation in cases of overwhelming respiratory failure (veno-venous ECMO) ii) Circulatory support in reversible cases of refractory overwhelming cardio- respiratory failure (veno-arterial ECMO). b) ECMO services commenced at the RAH in 2009, and continue to evolve. c) Any cases for potential ECMO support will be discussed in detail prior to initiation, and will be supervised closely by duty ICU consultant. d) The ECMO circuit and equipment must not be altered without ICU consultant and/or perfusionist supervision. e) The policies, protocols and procedures for ECMO are contained in a manual that is attached to the ECMO machine and available online.
- 164. 164 19. Weaning FromVentilation a) General principles i) No mode of weaning has been demonstrated to be superior to another. ii) Short-term patients with acute resolution of respiratory failure (e.g. post- operative, drug overdose, trauma) may be rapidly weaned and extubated. iii) Long-term patients with multiple intercurrent problems take longer and effectively “go at their own pace”. iv) See – Flowchart: Ventilation Weaning Protocol (p50) b) Clinically important determinants for weaning from ventilation i) Resolution of the process requiring ventilation. ii) No new CXR abnormality. iii) Completion of therapeutic options that require ventilation e.g. debridements, operations. iv) Appropriate conscious state - cooperative patient. v) Appropriate peripheral motor function. vi) Adequate analgesia. vii) Haemodynamic stability. viii) Metabolic, acid-base stability. c) Methods i) Spontaneous effort is required for the patient to be weaned. ii) SIMV with reducing RR and VT in conjunction with PSV and PEEP. iii) Use PSV + PEEP alone once the patient’s spontaneous rate is sufficient to prevent a respiratory acidosis. iv) T-piece weaning: intermittent T-piece and positive pressure support. v) Non-invasive bi-level ventilation. d) “Objective” measurements i) Adjuncts to the assessment of weaning success. ii) Respiratory rate and tidal volume are the most sensitive: Rate ( f ) < 30/min VT > 5 ml/kg f /VT < 100 (rapid shallow breathing index) PaO2/FiO2 > 200 and PEEP < 10 cmH2O PaCO2 < 60 mmHg pH > 7.3
- 165. 165 20. Extubation Protocol a) The duty consultant or SR must be involved in all decisions to extubate. b) In case of urgent re-intubation, ensure equipment, monitoring and adequate assistance is immediately available. c) Extubation is preferentially done during daytime working hours and is a medical responsibility. d) Extubation criteria: i) Return of adequate conscious state to maintain adequate protective laryngeal reflexes and secretion clearance. ii) Adequate pulmonary reserve. iii) Adequate cuff leak if upper airway surgery or airway swelling. iv) Ability to be re-intubated. v) Resolution of reason why patient was intubated. e) Beware of patients with inter-maxillary fixation and wiring. i) Home team must be aware of planned extubation. ii) Wire cutters must be present during extubation. f) All patients must receive supplemental oxygen post extubation.
- 166. 166 D. Management of Cardiothoracic Patients 1. General Principles a) The following guidelines apply to elective post-cardiac surgical patients. b) These are only guidelines and each individual consultant will manage the patients as is clinically indicated. 2. Respiratory: a) Following surgery use the following default ventilator settings: i) FIO2 =1.0 ii) SIMV 12 × 600, PS 10cmH2O, PEEP 5cmH2O. b) After the first ABG, adjust the FIO2 to maintain a PaO2 > 80mmHg c) Wean from ventilation according to past history, surgery performed and current clinical status d) Suggested extubation criteria: i) Temperature > 36C ii) Awake, able to obey commands iii) Adequate analgesia iv) Cardiovascular stability on minimal inotropes (< 10µg/min noradrenaline or adrenaline) v) Adequate gaseous exchange: PaO2 > 80 mmHg on FIO2 0.5, PEEP 5cm vi) Bleeding: drain losses < 100 ml/hr e) Respiratory failure post-extubation secondary to collapse / consolidation is common. i) Ensure good analgesia and frequent, effective physiotherapy ii) CPAP may be required in the first 48 hours. f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to extubation failure and may benefit from the use of ACE inhibitors or inodilators prior to extubation. 3. Post-operative bloods: a) Check CBE, U&E, Mg, ACT, APPT, INR and ABGs on all patients. b) Maintain [K+] > 4.0 mmol/l 4. Hypotension ± increasing inotrope requirements may occur for a variety of reasons: a) Hypovolaemia i) Return any remaining pump blood as soon as possible. ii) Correct fluid/blood losses as appropriate iii) Check ECG b) Low cardiac output states i) Noradrenaline is the first choice vasopressor. ii) Low dose dobutamine (to improve regional blood flow to splanchnic/renal vascular beds), may also be considered. iii) Adrenaline can be used for severely impaired ventricles.
- 167. 167 iv) If required vasoactive agent > 20µg/min and increasing, and the patient is euvolaemic, consider: Echo to exclude tamponade, AMI, papillary muscle rupture, or VSD. PA catheter insertion or pulse contour CO measurement, e.g. Vigileo. v) Consider pacing (either epicardial or transvenous) if hypotension is rate related (HR < 60). A-V sequential pacing is the ideal mode (DDD) vi) Consider IABP if hypotension persists despite inotropes. vii) Consider milrinone or dobutamine for patients with predominantly diastolic cardiac failure or pulmonary hypertension. c) Tamponade i) This is a medical emergency. ii) If suspected, the cardiothoracic surgeon must be notified immediately. iii) Diagnosis: Refractory hypotension despite adequate volume replacement and inotropic support Cessation / reduction of blood coming from drains Perform urgent CXR if time available. Globular heart shadow on CXR and muffled heart sounds may be present but are unreliable signs Diastolic equalisation of right-sided pressures on PA catheter insertion Echocardiographic evidence of tamponade. iv) Treatment Support MAP with aggressive volume and inotropic support. Ensure sufficient blood is cross-matched ( 6 units) If stable, reopening in theatre is the preferred treatment In emergency situations the chest may need to be opened in ICU. d) Tension pneumothorax i) This is a medical emergency. ii) If a pleural drain is already present, quickly exclude obstruction/kinking. iii) Otherwise, needle decompression followed by insertion of an underwater seal drain. e) Cardiac arrest i) This is a medical emergency. ii) The resuscitation guidelines are different from standard BLS/ALS. iii) A major and important difference is that in patients who arrest following cardiac surgery, chest compressions should only be commenced if the sternotomy cannot be performed within 3 minutes. iv) See guidelines below.
- 168. 168 Flowchart: Arrest PostCardiac Surgery Resuscitation of a Patient Who Arrests Post Cardiac Surgery Assess rhythm Hand ventilate (Administer FiO2 100% with Bag mask/ETT turn OFF PEEP. Auscultate chest to exclude tension pneumothorax) Ventricular Fibrillation Asystole Pulsless Electrical Ventricular Tachycardia Profound Bradycardia Activity HR < 30 Commence Advanced Life Support If an IABP in situ change to pressure trigger No CPR or Precordial thump DC shock Atropine 3 mg IV If paced turn OFF to exclude (3 attempts) Pace : Invasively (If Wires Present) Ventricular Fibrillation +/- Amiodarone Noninvasively Activate 4 Key Roles in Emergency Resternotomy CPR if Resternotomy expected to take longer than 3 minutes Perform Resternotomy - Internal Defibrillation - Internal Cardiac Massage - Internal Cardiac Massage - Internal Cardiac Massage - Relieve Tamponade (If present) - Relieve Tamponade (If present) - Relieve Tamponade (If Present) Adapted From: Dunning J, et al. Guideline for resuscitation in cardiac arrest after cardiac surgery. European Journal of Cardiothoracic Surgery, 2009 5. Hypertension a) MAP should be kept at approximately 70 mmHg for the first 24-36 hrs. b) This may vary according to the patient’s pre-morbid BP. c) Management: i) Ensure adequate analgesia ii) Nitroprusside or GTN: titrate to maintain MAP ~ 70 mmHg. iii) If nitroprusside infusion > 40-50 ml/hr (2 µg/kg/min), consider: Metoprolol: 1-2 mg IV, (if no contraindication) Clonidine: 25-50 µg IV (up to 300µg/24 hrs) Hydralazine: 10-20 mg IV Captopril: 6.25-12.5mg 2 hourly PRN (up to 150mg/24 hrs)
- 169. 169 6. Management ofBleeding Flowchart: Bleeding Post Cardiac Surgery Excessive bleeding post-op: > 200 mL/hr for 3-4 hrs, or > 1500 mL total loss Or, as per Surgeon’s advice If ACT = 145-159s 25mg protamine once only ACT > 160s 50mg protamine once only Transfuse RC to maintain Hb > 80g/L INR > 1.5 or APTT > 45 sec give 3-4 units FFP Fib < 1.0g/L give 5 bags (apheresed) of cryoprecipitate Platelet <100 x 109/L or prolonged by pass time or pre-op clopidogrel give 1 bag of platelet (pooled/apheresed) Treat acidosis, hypocalcaemia, hypothermia Resend CBP/coag screen IF Bleeding Continues + Discuss with haematologist or activate MTP Consider DDAVP (0.3 mcg/kg) but must discuss with surgeon 7. Sedation/Analgesia: a) Propofol if required b) Fentanyl IV boluses PRN while on ventilator c) Morphine or fentanyl subcutaneously post-extubation d) Paracetamol IV or po 4/24 PRN for first day then 6/24 if no contraindication e) Oxycodone po 4/24 PRN in appropriate dose from second post-op day
- 170. 170 8. Anticoagulation /DVT prophylaxis: a) Heparin 5000U s/c 8 hrly - all patients. i) Start 6-12 hours post-op in the absence of excessive bleeding. b) Aspirin 300mg daily - following coronary artery grafts. i) Start at the same time as the heparin. ii) Give via NG/OGT or S/L if the patient remains intubated. c) Commence patients with mechanical valve replacements on warfarin (5mg nocte) from the second post-operative day if extubated. d) Discuss anticoagulation requirements for tissue valves with the surgeon. e) Patients with a mitral valve replacement ventilated > 48hrs may require heparinisation as will patients in AF for > 48hrs. 9. Antibiotic prophylaxis: Table: Antibiotic Prophylaxis for Cardiac Surgery Cardiac Non-allergic, or Cefazolin 2g IV Surgery Type 3 Penicllin allergy – + Gentamicin 240mg 30min pre-incision, then - CABG delayed rash only Cefazolin 1g IV post-onset-bypass, then Cefazolin 1g IV 8 hourly for 24 hours Gentamicin 240mg day 1 post-op (omit if CrCl < 60 ml/min) Penicillin allergy – Type 1 Vancomycin 1g (1.5g > 80kg) + Gentamicin 240mg 30min pre-incision, then Vancomycin 500mg, 6hrs post bypass Gentamicin 240mg day 1 post-op (omit if CrCl < 60 ml/min) Cardiac valve surgery Vancomycin 1g (1.5g > 80kg) + Gentamicin 240mg 30min pre-incision, then Vancomycin 500mg, 6hrs post bypass Gentamicin 240mg day 1 post-op (omit if CrCl < 60 ml/min) 10. Other Drugs a) Calcium Channel Blockers. Following radial artery grafts, diltiazem (30mg po tds) may be required from first postoperative day. Discuss with surgeon. b) Stress ulcer prophylaxis not routinely indicated unless the patient has pre- existing peptic ulcer disease. c) Insulin is managed as per the general ICU protocol. 11. Minimally Invasive Mitral Valve Repairs a) These are performed through a right sided mini-thoracotomy with the patient on femoro-femoral bypass b) Patients may have a “pain buster” placed perioperatively for analgesia c) Management is as for other cardiothoracic patients. d) Clarify with surgeon if warfarin is to be given postop. This may vary with exact type of repair, use of annuloplasty ring, heart rhythm etc.
- 171. 171 E. Renal Failure 1. Background a) The mortality from acute renal failure remains high: i) 8% in isolation ii) ≤ 70% when associated with other organ or system failures. b) Patients who die with acute renal failure, usually die from the underlying cause rather than ARF itself. c) There is a spectrum of renal dysfunction with variable definitions of what constitutes “Renal Failure”. d) Bellomo has proposed the following definitions: Creat Creat Urea Urea UO / d Normal 15-70 2-6 >800 Acute Renal Impairment > 120 > +60 >8 > +4 <800 Acute Renal Failure > 240 > +120 > 12 > +8 <400 e) Approx. 30% of ICU patients have pre-existing renal impairment. f) Patients at high risk of developing ARF are those with: i) Pre-existing renal impairment (creatinine > 120). ii) Severe sepsis iii) Hypertension iv) Diabetes v) Arteriovascular disease vi) Heart failure vii) Large contrast media loads g) The minimum urine output required to excrete the obligatory solute load 0.5 ml/kg/hr. h) ARF can be “oliguric” or “non-oliguric”. i) Non-oliguric renal failure has a better prognosis. j) Duration of ARF is variable and depends upon resolution of the underlying injury, severity of the injury and pre-morbid renal function. k) Consequences of ARF: i) Fluid overload. ii) Uraemia – encephalopathy, platelet dysfunction, pericardial effusions. iii) Acidaemia. iv) Electrolyte derangements – K+, PO4=, HCO3- v) Accumulation of pro-inflammatory cytokines (theoretical)
- 172. 172 2. Pathogenesis –ARF in critically ill patients is usually multifactorial. a) Pre-Renal i) The most common cause of renal failure in ICU. ii) Aetiologies: Low cardiac output states Hypovolaemia. Vasodilation - sepsis, vasodilators Renal vasoconstriction - NSAIDs Renal artery obstruction - stenosis, embolus, post-surgical iii) Reduced renal blood flow GFR and renal function angiotensin-II and glomerular efferent arteriolar constriction blood flow to the renal medulla If maintained, then ischaemic renal injury occurs (e.g. ATN). b) Renal i) Acute Tubular Necrosis. Ischaemic - see above Nephrotoxic - drugs, contrast, myoglobin, sepsis ii) Interstitial Nephritis - infections, drugs iii) Vascular disease - renal vein occlusion, HUS, vasculitis iv) Glomerulonephritis c) Post-Renal i) Obstruction of the renal collecting system leads to GFR. ii) Must be considered in unexplained renal failure. iii) Cannot be reliably ruled out clinically and hence requires imaging. iv) Ensure a bladder catheter is inserted and draining freely. v) Aetiologies: Drugs - opiates, anticholinergics Pelvic neoplasms. Retroperitoneal collections (e.g. blood, pus, fibrosis). Pregnancy. Prostatic Obstruction Renal calculi d) Specific Renal Failure Syndromes i) Increased intra-abdominal pressure (IAP) Effects at all levels - pre-renal, renal and post-renal May consider decompression when IAP > 20 mmHg with ARF. ii) Hepato-Renal Syndrome - predominantly pre-renal albumin, vasodilatation, splanchnic shunting diuretics for oedema, lactulose, diarrhoea, intra-abdo pressure iii) Rhabdomyolysis - pre-renal, renal and post-renal iv) Ineffective plasma volume e.g. nephrotic syndrome, liver failure, cardiac failure.
- 173. 173 3. Renal Investigations a) Blood tests i) Creatinine Logarithmic (inverse) relationship with GFR. Can lose up to 60% renal function and maintain a “normal” creatinine. Conversely in severe renal failure, a small decrease in renal function can cause large rises in serum creatinine. Lags behind the evolution of renal injury. Insensitive where muscle mass is low – elderly, wasting diseases ii) Creatinine clearance (ClCr) ClCr slightly overestimates GFR due to tubular secretion Estimated on IMVS biochemistry (eGFR) from single specimen creatinine, thus has same inaccuracies as creatinine Measured ClCr requires min 8 hour urine collection iii) Urea Less accurate indicator of GFR than creatinine Modified by diet, catabolic state, GIT blood, liver disease iv) Electrolytes - Na+, K+, HPO4=, ABGs. v) GN screen - ESR, C3, C4, ANA, RhF, ANCA, anti-GBM. vi) Haemolysis screen - RBC frags, LDH, haptoglobins, bilirubinaemia. b) Urine i) M, C&S - infection must always be excluded ii) Myoglobin iii) Urinary electrolytes impossible to interpret with diuretic or natriuretic agents (CAs). iv) Urinary sediment Epithelial cell casts - ATN RBC / WBC casts - GN Eosinophils - interstitial nephritis Crystals - oxalate (e.g. ethylene glycol) - urate (e.g. tumour lysis) c) Imaging i) Ultrasound Exclude urinary tract obstruction. Doppler studies can assess renal artery and venous flows ii) CT Renal Tract (non-contrast) – highlights renal stones and masses. iii) IVP - rarely required given availability of U/S and CT. iv) DMSA scan - a static radionuclide scan to reveal kidney structure. v) MAG3 scan - a dynamic radionuclide scan - renal function, collecting system obstruction, ATN. d) Biopsy i) Glomerulonephritis ii) Interstitial nephritis iii) Infiltration
- 174. 174 4. Renal protection a) Established renal protection strategies i) Fluid resuscitation to maintain circulating blood volume. ii) Haemodynamic support of MAP and CO using inotropes adrenaline, noradrenaline, dobutamine iii) Exclusion of post-renal obstruction check IDUC, renal tract U/S, nephrostomy iv) Avoidance / close monitoring of nephrotoxic drugs aminoglycosides, amphotericin contrast agents ACE inhibitors NSAIDs v) Prompt detection & treatment of urinary infection. b) Unproven strategies for renal protection i) N-acetyl cysteine ii) Frusemide infusion / high dose iii) Mannitol infusion / intermittent iv) HCO3- for rhabdomyolysis. v) Aminophylline infusion vi) Calcium channel blockers vii) Clonidine c) Contrast Prophylaxis i) Best evidence is to use HCO3- ii) Add 150ml 8.4% NaHCO3 to 850ml 5% Dextrose. iii) Run at 3ml/kg the hour prior to contrast administration, then continue at 1ml/kg/hr for 6 hours d) Low Dose Dopamine i) May temporarily increase urine output ii) Does not reduce the incidence of dialysis dependent renal failure or mortality. (ANZICS CTG).
- 175. 175 5. Indications forrenal replacement therapy a) Symptomatic or refractory: i) Acidosis ii) Hyperkalaemia iii) Fluid overload - e.g. pulmonary oedema iv) Uraemia - urea > 35 mmol/l or symptomatic b) Severe sepsis / developing oliguric renal failure c) Diuretic resistant pulmonary oedema. d) Drug removal (see Dialysis in Overdose) e) The decision to commence RRT should be discussed with the duty consultant. f) RRT is generally initiated early before serious complications develop. g) The choice of RRT modality depends on patient’s type and severity of illness, equipment availability and local expertise. h) The renal unit should be notified “early” of patients who are potential long-term dialysis candidates. 6. Renal Replacement Therapy Principles a) Haemofiltration. i) Convective solute and fluid removal down a hydrostatic pressure gradient to form an ultrafiltrate (UF). ii) Clears middle molecules (> 500D) and fluid. iii) UF formation is dependent on the pressure gradient and membrane characteristics (effective pore size & surface area). iv) Predilution replacement of ultrafiltrate with balanced salt solution increases the availability of urea for convective transfer by favouring its movement from red cells. b) Haemodialysis. i) Diffusion of solute down a concentration gradient across a semi-permeable membrane, running dialysate fluid counter-current to blood flow ii) Clears urea, creatinine, electrolytes (i.e. small molecules). iii) Solute clearance is adjusted by changing the dialysate fluid solute concentration, blood and dialysate flow rates. iv) Intermittent HD (IHD) Utilised if the patient is stable and requires longer-term dialysis. Takes 3-5 hours using higher blood flows of 300 ml/min Fluid removal occurs quickly, not tolerated in unstable patients. Performed by the Renal Unit. v) Sustained Low Efficiency Dialysis (SLED) Similar to standard IHD but occurs over 8-12 hours Lower blood and dialysate flow rates. Well tolerated by the critically ill. Used in some ICUs (not the RAH) for nursing and cost reasons. Although better tolerated than IHD in the critically ill, there is little evidence to confirm equipoise with CVVHD/F in terms of outcomes.
- 176. 176 c) Continuous veno-venous haemodiafiltration (CVVHDF). i) Standard form of continuous renal replacement therapy in this Unit. ii) The combination of ultrafiltration and dialysis improves solute clearance. iii) Advantages of CVVHDF over conventional intermittent haemodialysis: Effective and more flexible control over fluid balance. Greater cardiovascular stability. Does not require attendance of Renal Unit staff. May have a role in modification of the septic response. Some trials suggest improved patient mortality (not proven). Allows patients to receive continuous protein rich diet. 7. Complications of CVVHDF a) Hypothermia. b) Prolonged exposure to heparin: incidence of HITS, bleeding c) Prolonged venous access: infection, thrombosis, vascular injury d) Prolonged exposure to extracorporeal membrane: thrombocytopenia e) Air embolism. f) Increased nursing workload. g) Electrolyte imbalance: hypomagnasemia, hypophosphataemia
- 177. 177 Diagram: CVVHDF Circuit To Patient Ultrafiltrate Replacement Deaeration Chamber Heparin Effluent Dialysate Solution
- 178. 178 8. CVVHDF Equipment a) Dialysis catheters i) Priority of site placement and optimal catheter length: R.IJ R.SC L.IJ L.SC Femoral 15cm 15cm 20cm 20cm 25cm ii) Use Dolphin Protect® high flow catheter guided as above iii) Heparin lock all catheter lumens 8 hourly when not in use 5000U in 3 mls, divided equally into both lumens. b) Filters i) Older filters were made from cellulose and would often initiate an inflammatory response (i.e. “membrane reaction”). ii) Membranes are now synthetic (polycarbonate, polyacrylonitrile) iii) These are more permeable and biocompatible iv) Standard filter = Prisma® AN69: Membrane = acrylonitrile Membrane thickness = 50m. Surface area = 1m2 /1.5m2 (RT-150) (larger filters 1.2–2m allow blood flow and clearance) 2 Blood volume in set = 150ml c) Dialysis machine settings i) The PrismaFlex® is the standard dialysis machine at the RAH ii) Older “Prisma” machines are still in use but are being phased out. d) For patients on ECMO i) CVVHDF can be performed via the ECMO circuit without additional Vas- Cath placement. ii) Must be discussed with ICU consultant supervising ECMO 9. Prescribing CVVHDF a) Orders for the PrismaFlex or Prisma® should be written on a standard sticker. b) The following variables require assessment/prescription for CVVHDF. c) Haemofiltration solution (“replacement”). i) Standard solution = Gambro Phoxilium. ii) Hemosol B-Zero will remain available when required for: A [K+] < 4 mmol/l (e.g. severe hyperkalaemia), or A phosphate free solution (e.g. tumour lysis syndrome)
- 179. 179 Table: Haemodialysis Solutions Phoxilium Haemosol B-zero Volume 5L 5L HCO3- mmol/l 30 32 K+ mmol/l 4 - Na+ mmol/l 140 140 Cl- mmol/l 115.9 109.5 HPO4= mmol/l 1.2 - Mg++ mmol/l 0.6 0.5 Ca++ mmol/l 1.25 1.75 Lactate mmol/l - 3 iii) Flow rate 1000-2000 ml/hr (higher rates in catabolic patients) iv) Ultrafiltration rate target 25 ml/kg/hr (averaged over 24hrs) v) Standard is to deliver replacement pre-filter (termed pre-blood pump fluid), but may be given post-filter if required (e.g: some toxidromes) vi) When given pre-filter on the PrismaFlex®, still require at least 100ml/hr replacement post-filter for the deaeration chamber to function properly. d) Dialysis solution i) Gambro® Phoxilium (or Hemosol B-zero if indicated) ii) Rate = 500-2000 ml/hr (higher rates if marked electrolyte abnormalities) e) Blood flow rate i) On commencing CVVHDF, gradually increase blood flow as tolerated by patient haemodynamics ii) Target rate: 250ml/min *limited by machine/access pressures. f) Anticoagulation i) Blood passing through the filter activates the clotting cascade. ii) Anticoagulation is often required to prolong “filter life” iii) Circuit is primed with heparin 5,000U iv) No ongoing anticoagulation is required for patients with coagulopathy v) Systemic anticoagulation (if no contra-indications exist) Heparin 5000 units stat, then continue at 500-1000 units/hr Heparin is infused into the circuit pre-filter Check APTT after 6 hrs and then daily if stable End-point is “filter life” rather than a therapeutic APTT (i.e. if filter is working and APTT < 45sec, there is no need to increase heparin dose)
- 180. 180 vi) Regional anticoagulation Citrate (see citrate protocol) Heparin a. Utilised when: Maintenance of filter life is problematic. Systemic anticoagulation and citrate are contraindicated No contraindication to heparin administration. b. The circuit still needs to be primed with heparin c. Heparin is administered pre-filter as above d. Protamine 5-10 mg/hr post-filter e. Check APTT 6 hourly after any dose changes. vii) For patients with heparin induced thrombocytopenia (HIT) consider Danaparoid or lepirudin (systemically, not into circuit – see protocol) Prostacyclin 5 ng/kg/min (see protocol) g) Fluid removal i) Determine how much fluid should be removed from the patient. ii) Consider its effects on patient haemodynamics iii) The amount of fluid removed is the difference between the effluent and the dialysate plus replacement fluid volumes h) Potassium i) Gambro® Phoxilium contains 4 mmol/l potassium and will not require additional potassium ii) Haemosol B-zero solution contains no potassium. Supplementary K+: a. Required for all patients, except in the initial management phase of marked hyperkalaemia b. Should to be added to both the replacement & dialysate bags Plasma K+ < 4.0 mmol/l = 20 mmol / bag Plasma K+ 4.1 – 4.8 mmol/l = 15 mmol / bag Plasma K+ 4.9 - 5.5 mmol/l = 10 mmol / bag Plasma K+ 5.5 – 6.0mmol/l = 5 mmol / bag Plasma K+ > 6.0 = 0 mmol / bag c. K-Acetate can be used in severe acidosis: Acetate is effectively metabolised to HCO3- via the liver Vial = 25mmol/5ml, dose = 3-4mls per 5L bag iii) Target plasma [K+] = 3-4mmol/L i) Drug prescription i) Consult Antibiotic Guidelines / Pharmacy regarding antibiotic dosing e.g. meropenem, ciprofloxacin, fluconazole ii) Monitor drugs that are renally cleared and potentially toxic e.g. gentamicin, vancomycin, digoxin
- 181. 181 10. Citrate Anticoagulationfor Renal Replacement Therapy a) Rationale: i) Anticoagulation of the extracorporeal circuit improves life of dialysis filters resulting in improved ‘dose’ of dialysis, less patient blood loss and probable cost efficiency. ii) When systemic anticoagulants are contraindicated it is possible to use citrate to provide regional anticoagulation of the dialysis circuit without altering patients coagulation b) Indication: i) CRRT is indicated ii) Systemic anticoagulation is contraindicated and filter life is inadequate c) Requirements i) Appropriate high flow vascular access ii) Gambro Prismaflex dialysis machine iii) Gambro dialysis fluids Dialysate: Prism0cal PBP fluid: Prismocitrate 10/2 Post filter replacement: 0.9% saline iv) Dedicated central access for calcium infusion (not required if using Prismaflex software v6.1 – see below) d) Process i) Prior to priming the mode of anticoagulation is set to Citrate. ii) The Prismaflex software will display the steps necessary to prime the circuit Pre-blood pump (PBP) fluid (coded white) is Prismocitrate 10/2 Dialysate (coded green) is Prism0cal, a zero calcium, zero potassium, bicarbonate (32mmol/l) buffered dialysate. Post filter replacement (coded purple) is normal saline, a 1 liter bag can be hung on the central hook iii) At completion of the priming process the Prismaflex displays: Flow rates: a. Reduce dialysate to 1000ml/hr b. Reduce replacement to 100ml/hr c. Confirm “post replacement” is set The commencement citrate concentration should be set at 2.5mmol/l (current default 3.0mmol/l) Confirm final prescription and dialysis dose iv) Commence calcium infusion and dialysis simultaneously
- 182. 182 v) Ionized calcium should be checked 30 min post-commencement, both Post-filter (blue port) a. Target ionized calcium: 0.3-0.5mmol/l b. If > 0.5mmol/l [citrate] by 0.3-0.5mmol/l c. If < 0.3mmol/l [citrate] by 0.3-0.5mmol/l d. The usual citrate concentration range is 1.5-4.0mmol/l Arterial a. Target ionized calcium: 0.9-1.1 mmol/l. b. Calcium replacement should be commenced with dialysis. c. If [Ca2+] < 0.9 or there is a strong downward trend commence infusion via CVC: CaCl 10% 4ml/hr. d. After calcium is commenced arterial levels should be checked hourly until stable. e. Infusion rates should be adjusted by 1ml/hr until arterial calcium is in the target range f. If dialysis is ceased the calcium infusion should be stopped. g. The Prismaflex will display an alert to this effect (software v6.1 will automatically cease calcium infusion) vi) Post-filter and arterial calcium should be monitored 2 hourly until stable then checked 8 hourly vii) With Prismaflex software v6.1 (due 2012) Calcium replacement occurs via the ‘heparin syringe’ on the Prismaflex using a Gambro algorithm. Separate replacement is unlikely to be necessary. Check Ca2+ via arterial analysis 8 hourly. e) Complications i) Hypocalcaemia: Calcium is removed via: a. Clearance of citrate:Ca2+ complexes during haemofiltration b. Dialysis against calcium free dialysate In the presence of citrate bound calcium fraction falls and may be as low as 20%. The systemic binding of calcium to citrate contributes to a small degree, however this component reverts as citrate is metabolised. Unless using Prismaflex software v6.1, separate replacement of calcium via a CVC is recommended – see above. ii) Hypercalcaemia: May occur due to excess calcium replacement. Corrected by monitoring and appropriate titration of CaCl. iii) Acidosis: Possible in advanced liver failure due to accumulation of citric acid. Citrate anticoagulation is relatively contraindicated in liver disease.
- 183. 183 iv) Alkalosis: Citrate enters the citric acid cycle and end products of metabolism are CO2 and bicarbonate. A small increase in bicarbonate and pH is expected over days. Citrate overdose may result in metabolic alkalosis. Estimated 40-70% of citrate is cleared via a high flux dialyser, hence does not enter the systemic circulation. Significant alkalosis requires a reduction in citrate dose or cessation of citrate. This is uncommon. v) Hypophosphataemia Prolonged filter life and high pre-dilution flow rates may result in a high dose of dialysis being delivered. Associated with an increased risk of hypophosphataemia. Phosphate should be checked twice daily and replaced appropriately. Once stable daily monitoring is acceptable. vi) Hypomagnasaemia Mg2+ may be chelated by citrate and hypomagnasaemia is common. Mg2+ should be checked twice daily (with phosphate) and replaced appropriately 11. Dialysis in Overdose a) Institution of dialysis for a life-threatening overdose is a consultant decision. All cases are to be discussed with the ICU Consultant on call b) There are a number of drugs effectively cleared by extracorporeal techniques i) These agents are generally small, hydrophillic molecules with low protein binding and volume of distribution ii) The kinetics of many agents change in overdose (eg valproate) and therefore discussion with the ICU Consultant and Toxicologist is required iii) Common agents cleared by dialysis include: Lithium Toxic alcohols Sodium Valproate Carbamazepine Atenolol / Sotalolol Salicylates iv) There are a number of other less common agents potentially amenable to clearance via dialysis but requiring special consideration eg. paraquat, procanamide, methotrexate, chloral hydrate c) Institution of dialysis is more likely to be effective in the absorption phase when a drug is concentrated in plasma than after distribution to tissue. d) Standard ICU dialysis guidelines (ie. dialysis stickers) are designed for gradual clearance of uraemic toxins and are not ideal for use in overdose
- 184. 184 e) The aimof diafiltration in overdose is to optimize clearance by maximizing extracorporeal blood flow, dialysate gradient and occasionally transmembrane pressure gradient. i) For this reason all patients should be treated with the Prismaflex, not the older Prisma machines, with an ST-150 circuit ii) An appropriate size femoral dialysis catheter should be inserted to allow blood flow rates > 250ml/min (ideally 300ml/min) f) Diafiltration of life threatening overdose should commence as follows: Prismaflex – ST 150 Circuit Mode CVVHDF Blood Flow Rate *increase as tolerated 300 ml/min Dialysate Phoxilium or Hemosol BO 4000 ml/hr Pre-blood pump Replacement Phoxilium or Hemosol BO 100 ml/h Post Filter Replacement Phoxilium or Hemosol BO 2000 ml/hr Anticoagulation Heparin 500u/ml 1-2 ml/hr g) Potassium should be added to both dialysate and replacement when using Hemosol BO unless overdose is associated with severe hyperkalaemia. h) At high dialysis doses it must be remembered that i) Hypomagnasaemia and hypophosphataemia (if using Hemosol BO) are common and occur rapidly. Levels should be checked twice daily and replaced as indicated ii) Clearance of many therapeutic drugs is increased and dose adjustment may be necessary iii) Levels of other antidotes may be altered (e.g. ethanol) and where possible need regular monitoring i) Conventional intermittent haemodialysis may be preferable: i) Dialysate flow rates and early clearance of small molecules are greater. ii) If not readily available, institution of CVVHDF is indicated even though extraction ratios are generally lower, total body clearance is often greater on CVVHDF. j) Data on clearance of toxins using CVVHDF and modern membranes is sparse. For this reason samples should be taken for drug levels as per the form below:
- 185. 185 Form: Dialysis Datafor Drug Overdose Estimated Time of Overdose: Drug/s & Estimated Dose: Blood Flow Rate: Dialysis Flow Rate: Replacement Flow Rate: Fluid Balance: Haematocrit: Arterial Pre-filter Post-filter Effluent Urine 0 hrs (Pre-dialysis) 2 hours 4 hours 8 hours 12 hours
- 186. 186 F. Neurosurgical protocols 1. Neurotrauma in ICU a) Close liaison and communication with the neurosurgeons is essential for the coordinated management of acute head injuries. b) ICU management of the neurotrauma patient includes: i) Acute trauma resuscitation ii) Liaison and coordination with other clinics in the multi-trauma patient. iii) Cardiopulmonary / renal / metabolic homeostasis. iv) Maintenance of cerebral homeostasis – see CPP algorithm v) Transport for imaging c) Principles of ICU management: i) Ventilation Maintain normoxia: PaO2 > 80 mmHg Ventilation to normocapnia: PaCO2 35-40 mmHg ii) Haemodynamics: Fluid maintenance a. Maintain euvolaemia b. Crystalloid depending upon Na+ and measured osmolality c. Avoid dehydration if patients become polyuric (DI / mannitol) Maintain cerebral perfusion pressure: a. CPP 60–70 mmHg i. A lower threshold may be tolerable in some patients ii. Must be discussed with the ICU Consultant b. MAP 80 mmHg in the absence of ICP measurement c. NB: use inotropes if required once euvolaemic Avoid interference with cerebral venous return a. Nurse patients at 30° head-up elevation b. Neutral head position c. Avoid circumferential ETT ties, etc. iii) Osmotherapy Should be discussed with the ICU Consultant Indications for osmotherapy prior to ICP monitoring are: a. Unequivocal signs of intracranial hypertension prior to imaging or evacuation of an intracranial mass lesion b. Threatened transtentorial/brainstem herniation, or c. Progressive CNS deterioration not due to systemic pathology. Hypertonic saline a. Fewer complications c.f. mannitol. b. Standard dose: 20ml of 20%NaCl c. Slow IV push through a CVC d. Osmolality should not exceed 320mosmol/l
- 187. 187 Mannitol a. Patient must be euvolaemic and normotensive (relative to pre- morbid BP) before the administration of mannitol b. Osmolality (measured) should not exceed 320mosmol/l i. Mannitol and alcohol cause an osmolal gap ii. calculated measured osmolality c. Standard dose = 0.25g/kg i. 1.25ml/kg of 20% mannitol ii. Duration of action is variable (90min – 6hrs) d. A urinary catheter is essential. iv) Seizure prophylaxis - indications: Closed head injury with structural damage (intracerebral or paraxial haematomas) Penetrating head injuries Depressed skull fracture Pre-existing epilepsy Phenytoin prescription: a. 15 mg/kg loading over 30 minutes b. 300 mg iv daily or 400mg NG x 7 days only c. Monitor levels: therapeutic 40-80mol/l v) Antibiotics - indications: Insertion of ICP monitoring catheters: cefazolin 1g stat Base of skull fractures: antibiotics are not indicated in the absence of signs of meningitis Nosocomial infections: as per infectious diseases guidelines. vi) Sedation: Consider the use of propofol in patients where regular review of CNS status is required (majority of patients) Control large sympathetic swings with fentanyl (100-200µg IV) Many opioids have been demonstrated to increase ICP and should not be used as sole therapy to control intracranial hypertension. The use of muscle relaxants is relatively contraindicated and must be discussed with the ICU Consultant. Consider -blockade or clonidine in labile neurogenic hypertension. vii) Nutrition: Establish enteral feeding as soon as feasible Maintain BGL in the normal range by insulin infusions if necessary. Hyperglycaemia is common in the acute phase and may precipitate a hyperosmolar state with resultant polyuria. viii) Stress ulcer prophylaxis is not routinely indicated (see protocol)
- 188. 188 ix) Thromboprophylaxis: All patients should have TED stockings and SCCDs applied within 8hrs of admission unless contra-indicated. Pharmacological thromboprophylaxis is relatively contraindicated in the first 72 hrs after injury or surgery or if there is ongoing bleeding. Thromboprophylaxis may be commenced when indicated following discussion with Neurosurgery In patients at high risk of VTE or with contra-indications to mechanical prophylaxis, consideration should be given to early insertion of a caval filter x) Avoid hyperthermia. d) Monitoring of head injured patients: i) Cardiorespiratory: In addition to routine ICU monitoring ETCO2 is recommended a. Interpret with caution & calibrate with PaCO2 when, i. Change in ventilation ii. Sudden rise in ICP b. Adjust ETCO2 to PaCO2 35-40 mmHg ii) Neurological: ICP monitoring a. At the RAH ICP monitors are inserted by neurosurgeons b. Indications: i. Severe CHI (GCS < 8) and an abnormal CT scan, or ii. GCS < 8 and two of Age > 40 yrs Focal motor signs Hypotension after volume resuscitation iii. Brain swelling following evacuation of intracranial haematoma iv. Intracerebral haematomas where the decision to operate will depend on ICP v. Polytrauma patients in whom cerebral status cannot be adequately assessed (e.g. patients requiring ventilation) vi. Rarely in non-traumatic raised ICP Meningitis / encephalitis Hepatic failure. Ventricular drain and external pressure monitor: a. Closed system b. CSF for M,C&S as clinically indicated c. Set height for drainage according to neurosurgical consultation. d. Preferred for ICP monitoring in CHI
- 189. 189 Flowchart: Cerebral PerfusionPressure Algorithm Initial Therapy to Optimise CPP 1. Maintain euvolaemia with IV fluids 2. Ensure appropriate sedation 3. Commence inotropes to maintain CPP 60-70 mmHg (MAP-ICP) 4. Maintain normocarbia, PaCO2 35-40 mmHg THERAPY FAILURE: ICP > 20 mmHg for > 10min or CPP < 60 mmHg 1. Ensure accurate MAP, ICP and where relevant, SjO2 readings 2. Immediately correct hypovolaemia and hypoxia 3. Ensure normocarbia: PaCO2 35-40 mmHg 4. Ensure adequate sedation 5. Consider drainage 2-5ml CSF if intraventricular catheter in situ 6. Exclude contributing factors Neck position / venous obstruction 30º head-up position Fever, Seizures 7. Commence osmotherapy with hypertonic saline or mannitol and notify ICU Consultant 8. Consider short-term hyperventilation whilst arranging urgent CT 9. Consider neuromuscular blockade 10. Notify neurosurgeon on-call Surgical Lesion URGENT Immediate Neurosurgical CT Head Consultation Scan Non-Surgical Lesion 1. Attempt to maintain CPP > 60 mmHg with fluids / inotropes 2. Consider additional therapies after discussion with Duty ICU Consultant: Propofol / barbiturate coma Hypothermia Neurosurgical referral for decompressive crainectomy
- 190. 190 2. Aneurysmal Subarachnoid Haemorrhage Table: World Federation of Neurosurgeons Classification Grade GCS Motor Deficit I 15 Absent II 13-14 Absent III 13-14 Present IV 7-12 Present or absent V 3-6 Present or absent a) Principles of ICU management: i) Priorities: Monitoring of airway and adequacy of ventilation Maintenance of adequate cerebral perfusion maintain appropriate MAP (relative to premorbid BP) Monitoring of conscious state (GCS) Early diagnosis and treatment of causes of reduced GCS a. Rebleed from aneurysm (notify neurosurgeon) b. Hydrocephalus (notify neurosurgeon) c. Vasospasm d. Seizure ii) Monitoring: ECG, SpO2, Invasive BP ICP in patients with a ventricular drain in situ: a. May be set at a level (usually 10 cm) above head and/or b. Connected to monitor transducer c. CSF culture as clinically indicated b) Anticonvulsants: as clinically indicated c) Angiographic Coiling i) Prefered approach for selected, amenable aneurysms: Less invasive procedure Better outcomes at 12 months c.f. clipping ii) Performed in radiology under sedation (provided by anaesthesia) iii) May still require insertion of an EVD for hydrocephalus. iv) Post-procedure management in P4-C as for operative patients. d) Operative therapy: i) Early (within 48 hrs): usual practice at RAH Advantages (proposed): prevention of rebleeding, reduction of vasospasm, prevention of ischaemia Disadvantages: high risk of rupture, difficult dissection ii) Late (after 11 days) Advantages: easier procedure, opportunity to monitor. Disadvantages: re-rupture, prolonged risk of vasospasm
- 191. 191 e) Prevention andtreatment of vasospasm i) Specific drug therapy: Nimodipine: a. Indications i. CT proven SAH ii. IV preferably through central line (2 mg/hr) *may be given through a peripheral IV iii. Change to oral as soon as possible (60mg 4hrly) b. Complications: hypotension (may require cessation of nimodipine) Statins (simvastatin 80mg daily) may reduce the incidence of radiological vasospasm and improve outcomes following SAH. ii) Triple H therapy (hypertension / hypervolaemia / haemodilution): Has no role in the prevention of vasospasm prophylactic HHH therapy may be harmful It is imperative to avoid hypotension and hypovolaemia. Patients should have fluid therapy targeted at maintaining euvolaemia. iii) Euvolaemic hypertension May be indicated in selected patients with proven vasospasm post- aneurysmal clipping / coiling. Induced hypertension must be titrated to a mean arterial pressure: systolic BP is not an accurate indicator of cerebral perfusion pressure. Principles: a. Discuss with ICU consultant prior to initiating therapy b. Intra-arterial pressure monitoring is mandatory c. Maintain IV volume i. Continue IV filling until clinically euvolaemic ii. Avoid volume overload (pulmonary congestion/oedema) iii. Monitor electrolytes 8 hrly normal osmolality and [K+]. d. Commence noradrenaline titrated to: i. MAP > 90mmHg, or ii. MAP > 10mmHg above premorbid baseline (for known hypertensive patients), or iii. MAP 5-10mmHg > “defined MAP” On occasions there may be neurological improvement at a certain MAP titrate therapy 5-10mmHg above this iv. Reset target MAP if high doses (> 10g/min) are required, or if polyuria, arrhythmias or other complications ensue. Complications: a. Pulmonary oedema, hypoxia b. Cardiac arrhythmias, myocardial ischaemia c. Polyuria, electrolyte disturbances iv) Chemical (papaverine / verapamil) or balloon angioplasty Limited role in angiographically proven vasospasm Requires transport for angiography and may be performed on consecutive days.
- 192. 192 2. Status epilepticus a) Definition: i) Continuous seizure activity > 30 minutes duration, or ii) Sequential seizures (≥ 2) without recovery of consciousness. b) Principles of ICU management i) Assessment of airway and adequacy of ventilation Intubate and ventilate if appropriate Avoid muscle relaxants after intubation ii) IV access iii) Control of seizures: Midazolam: 1-10 mg/hr via infusion, or Diazepam: 10-20 mg IV prn Phenytoin: 18 mg/kg load, then 300 mg daily check for previous administration therapeutic levels 40-80mol/l If refractory, liaise with neurologists and consider: a. Clonazepam 1-2 mg IV prn or by infusion 0.5-2 mg/hr b. Valproate 200-500mg NG/IV 8 hrly c. Levetiracetam (Kepra) 500mg NG 8 hrly d. Thiopentone infusion i. Loading dose: 5mg/kg of 25mg/ml solution (2500mg / 100ml N.sal) ii. Infusion: 1-3 mg/kg/hr (~ 150 mg/hr or 6 ml/hr) e. Obtain EEG and consider EEG monitoring iv) Look for a cause and treat appropriately: CT scan with contrast if unclear Previous epilepsy / poor compliance Intracranial pathology: a. Vascular (haemorrhage, thrombosis), spasm b. Infection (consider LP if no evidence of raised ICP on CT) c. Tumour Extracranial pathology: a. Check electrolytes: especially Na+, Ca++, Mg++, K+, PO4= b. Metabolic: exclude hypoglycaemia, thiamine deficiency c. Toxic ingestion. Infection Severe hypertension c) Maintenance of homeostasis / seek and treat complications i) Ensure adequate hydration: maintenance fluids according to creatinine/urea, Na+ and osmolality ii) Ensure adequate urine output: prolonged seizures may be associated with rhabdomyolysis iii) Evaluate for joint dislocations and occult fractures
- 193. 193 4. Exclusion ofTraumatic Cervical Spinal Injury a) Safe practices are vital to prevent secondary damage to the cord b) Spinal immobilisation should be practiced in all patients with; i) significant distracting injury or injury above the clavicles ii) altered conscious state for any reason (head injury, alcohol, drugs etc) iii) neck pain or tenderness iv) abnormal neurological signs or symptoms v) NB: Hard collars allow up to 73% of normal flexion and extension – and so still need appropriate spinal care even if in place. Soft collars do not provide effective C-spine immobilisation. c) Clinically clearing the C-spine requires all of the following criteria to be fulfilled; i) normal conscious state, with no drugs or alcohol onboard ii) no neck pain or tenderness iii) no abnormal neurological signs or symptoms iv) no significant distracting injury, or significant injury above the clavicles and then, v) normal head control (unassisted) vi) pain-free movement d) If all of these are confirmed, the hard-collar can be removed, and the C-spine cleared. e) If the C-spine cannot be clinically cleared for any reason, radiology needs to be performed (the majority of patients seen in Trauma Resus) f) Virtually all patients presenting to Trauma Resus require a trauma series of adequate AP, lateral, and odontoid C-spine plain views g) A complete series of 3 plain views will still miss up to 7% of C-spine injuries – hence the importance of clinically clearing (if possible) the C-spine even if the Xrays appear normal. h) If the C-spine cannot be clinically cleared following normal plain films, maintain spinal precautions and liaise with the Trauma Registrar. i) Clearing the C-spine in the patient with altered conscious state: i) If drugs, alcohol or minor closed head injury are the problem, they are often resolved within 12 hours – maintain spinal precautions until that stage, and then assess clinically ii) If the patient is unlikely to become clinically assessable and clearable within 12-24 hours (most intubated ICU patients): Perform a complete plain Xray series in ED, and: Perform a limited CT; a. C0-2 in all, during first visit to scanner b. CT any suspicious areas on the plain films c. CT may be required to visualise cervicothoracic junction or d. CT entire cervical spine with 3-D reconstructions (the current recommendation)
- 194. 194 If these films are all documented normal, the collar may be removed and the C-spine cleared ‘as per RAH protocol’. Any ongoing concerns are referred to the Trauma and/or Spinal Registrar j) Flexion-extension views of the C-spine must not be performed, unless ordered by the Spinal Unit, with the Spinal Fellow in attendance k) As with the C-spine, the thoracolumbar spine should be imaged in all patients in whom it can not be clinically assessed. This should be done prior to arriving in ICU. If CT chest and abdomen have been performed, these images can be used to assess and clear the thoracic and lumbar spines. l) 25% with a spinal injury at one level will have a second non-contiguous injury. Therefore, if a fracture is found anywhere in the spine, the entire spine should be Xrayed m) Spinal Xrays should ideally be performed in an Xray area (Trauma Resus Room or Xray Dept) prior to ICU admission. n) The quality of spinal Xrays performed in ICU is usually very poor o) The Trauma Registrar must document the status of spinal clearance on the Trauma Form p) Steroid use in acute spinal cord injury is not currently recommended by the Spinal Injuries Unit. q) The RAH Trauma Service Procedures, Practices and Guidelines (TSPPG) on ‘Acute Spinal Injury Management’ is available on the RAH Intranet and contains more detail.
- 195. 195 G. Microbiology Protocols 1.Policy a) Sepsis is the most common cause of death in critically ill patients. b) The prompt diagnosis and treatment of infection in critically ill patients is both important and difficult. c) Sepaia must be aggressively sought and promptly treated with source control (where indicated) and appropriate antibiotics. d) Simple preventative measures are the most important factors in the containment of nosocomial infection and minimisation of bacterial resistance: i) Compulsory hand washing and/or use of alcohol hand-gel by all staff ii) Attention to aseptic technique for invasive procedures iii) Attention to invasive procedure protocols as outlined in this manual iv) Avoidance of over-prescription of antibiotics e) Regular routine microbiological examination in critical care patients is not cost effective. Investigations should only be ordered on specific indications. f) Septic screens must follow the guidelines below. 2. Definitions a) Systemic Inflammatory Response Syndrome (SIRS) i) Describes the inflammatory process that occurs in response to a variety of clinical insults resulting in a clinical picture suggestive of “sepsis” ii) The syndrome includes at least 2 of the following: temperature > 38° or < 36° C heart rate > 90 bpm respiratory rate > 20 bpm, or PaCO2 < 32 mmHg WCC > 12,000/mm3, or < 4,000/mm3, or > 10% immature (banded) neutrophils iii) SIRS is non-specific and may be due to non-infectious causes: Trauma, Post-operatively after major surgery Haemorrhagic shock, post blood transfusion Pancreatitis Burns Drug reactions Intracranial pathology, esp. intraventricular or thalamic blood b) Sepsis: the presence of SIRS 2° to infection c) Septic shock: decreased vital organ perfusion/function 2° to sepsis d) Nosocomial infection is defined as infection that occurs during hospitalisation that was neither present, nor incubating on admission. e) Colonisation is defined as the presence of microorganisms that do not elicit an inflammatory response.
- 196. 196 3. Septic screen a) Routine, performed only on the clinical suspicion of sepsis: i) New pyrexia ii) WCC, WCC, or Platelets iii) Deterioration in gaseous exchange or pH iv) Cardiovascular instability Hypotension / relative hypovolaemia Increased or new inotrope requirement v) Oliguria or increased creatinine b) Screen: i) Urine - C&S ii) Tracheal aspirate - urgent gram stain, C&S iii) Blood culture x2 iv) Any other drainage fluid as indicated, e.g. wound, pleural etc. c) Other i) Fungal cultures ii) Pleural fluid, CSF iii) Sinus x-rays iv) Bronchoscopy specimens (BAL) d) Urine: i) UTI in a catheterised patient is defined as: > 105 bacteria + positive culture of organisms, plus > 500 WBC/HPF. ii) Bacteria and white cells are a normal finding in a catheterised patient iii) Treatment with antibiotics will not result in clearance of colonisation and is only indicated for systemic involvement. iv) The only effective treatment is catheter removal. v) Bladder wash-out may reduce bacterial load / infective risk. e) Tracheal aspirate: i) Cultures often grow mixed colonising oral flora: Gram positive cocci - S. aureus and S. pnuemoniae Gram negative bacilli - H. influenzae Yeast - Candida sp. ii) Antibiotics will not result in a clearance of colonisation and are only indicated for invasive (local or systemic) infection. f) Blood cultures: i) Esily contaminated by skin organisms, careful technique required: Clean the skin with an alcohol or betadine swab Clean the top of culture medium bottle with an alcohol swab and allow to completely dry before injecting. Use a sterile needle and aseptic technique during venipuncture Inject blood immediately into bottle with same needle - do not touch the needle. ii) Blood cultures are best taken by clean venipuncture. iii) Skin organisms grown from a single bottle are usually a contaminant but must be interpreted in the context of the patient.
- 197. 197 4. Investigation ofpneumonia a) Community acquired pneumonia: i) Usual organisms: S. pneumoniae, H. influenzae ii) Less commonly: Bacterial: Legionella sp., Gram neg bacilli, S. aureus Viral: Influenza A, B, Parainfluenza, Adenovirus, RSV Other : Mycoplasma pneumoniae, Chlamydia psittaci (birds), Coxiella burnetti (sheep or cattle), TB, Chlamydia pneumoniae iii) Investigations Haematology - High (> 15000) or Low (< 3000) WCC - coagulopathy Biochemistry - note renal function and LFTs CXR ABGs Microbiology: * prior to antibiotic Rx where possible a. Blood cultures x 2 b. Endotracheal aspirate i. M,C&S + urgent gram stain ii. Legionella culture iii. Respiratory viral Ag (PCR) & culture NB: If not intubated, then collect a nasopharyngeal aspirate for respiratory viruses c. Urine - L. pneumoniae 1 Ag * only where high index of suspicion or outbreak d. Pleural fluid - M,C&S b) Healthcare associated pneumonia – Immunosuppressed Host: i) Possible organisms As above plus a. Bacterial: Nocardia b. Viral: CMV, HSV, varicella zoster c. Fungal: candida, cryptococcus, aspergillus d. Protozoal: pneumocystis jirovecii (PCP) Consider non-infective causes of a similar picture e.g. ARDS ii) Investigations: * As per above, plus Label request “Immunosuppressed Protocol” Sputum or tracheal aspirate of limited value Consider BAL if initial cultures negative HIV serology iii) Treatment prior to microbiological diagnosis: refer to antibiotic guidelines & discuss with ID.
- 198. 198 c) Nosocomial pneumoniain ICU i) Principles: Accurate diagnosis and treatment are important but difficult. Incidence: 20% of all ICU patients 70% of patients with ARDS major cause of death in patients with ARDS Clinically indistinguishable from pulmonary fibrosis, alveolar haemorrhage, atelectasis and other causes of lung infiltrates Clinical diagnosis, including use of tracheal aspirate, has poor sensitivity and specificity Appropriate antibiotics do improve outcome Empiric broad-spectrum antibiotics are potentially harmful. ii) Consider nosocomial pneumonia when: New and persistent CXR changes Tachycardia, tachypnoea Fever or hypothermia - temperature >37.5 or <35.5 Leucocytosis or leucopaenia - WCC: >10 or < 4 x 109/l Purulent sputum Deterioration in lung function iii) Confirmation of pulmonary infection: Tracheal aspirate → MC&S Preliminary results to direct therapy may be obtained on gram stain Consideration should be given to obtaining pulmonary samples by bronchoalveolar lavage (or open lung biopsy) for patients with: a. Persistent signs of pneumonia b. Inadequate response to antibiotics c. Inabililty to obtain adequate tracheal aspirates, or d. To exclude non-infectious causes of respiratory failure e.g. interstitial fibrosis or alveolar haemorrhage Septic screen including blood cultures should also be performed.
- 199. 199 5. Vascular cathetersepsis a) Refer to the invasive procedures section b) Suspect line sepsis when: i) Evidence of systemic infection New, unexplained fever Unexplained or in WCC Deterioration in organ function Positive blood culture by venipuncture with likely organisms (coagulase negative staph, candida), and/or ii) Evidence of local infection - inflammation or pus at the insertion site iii) The following patients are more susceptible to line infections: Prolonged vascular access (> 7-10 days) → exponential increase in line infection after 4 days. Endovascular infection (SBE, prosthetic graft infection) Cutaneous infection Burns Severe intra-abdominal infection (pancreatitis) Deep-seated infections (empyema / abscess) iv) The incidence of line sepsis with the antibiotic impregnated lines is around 1% and most of these are due to Candida spp. c) Protocol i) Take blood cultures from a peripheral vein ii) Positive blood cultures from the line may only indicate colonisation so blood culture bottles must be carefully labelled as to site of sampling Common organisms in line sepsis are normal skin flora e.g. Staph spp., C. albicans In ICU gram negative organisms can also be involved iii) On suspicion of line sepsis the line should be removed iv) The tip of the catheter should be sent for culture Avoid contamination of the catheter tip with skin organisms Skin should be cleaned thoroughly with alcohol, allowing at least one minute drying time, before removing the catheter v) Catheter related bloodstream infection is defined as infection where the same organism is grown from the blood and from the catheter tip d) Treatment i) Removal of the line will usually clear low-virulence organism bacteraemias, e.g. S. epidermidis ii) Antibiotics are indicated, even if blood culture negative, when: The patient is high risk - e.g. joint or endovascular prosthesis Infection with a virulent organism, e.g. S. aureus Signs of sepsis continue after catheter removal iii) If ongoing sepsis occurs, additional blood cultures should be taken prior to starting antibiotics iv) Refer to antibiotic guidelines.
- 200. 200 e) Further venous access: i) Reassess the need for ongoing central access, consider PICC line ii) Whenever possible: Wait 24 hours before reinsertion Select a different insertion site iii) Guidewire exchanges are not performed unless: Mechanical problems in a new catheter (leaks/kink & < 4 days old) Difficult or limited central access (e.g. burns) 6. Bacterial Meningitis a) Steroids should be started before antibiotics in all patients with a high probability of bacterial meningitis. i) No demonstrated benefit given post-antibiotics. ii) Should occur in A&E / pre-retrieval - check on admission b) Dose: dexamethasone 10mg 6 hrly for 4 days c) Antibiotics are as per ID guidelines 7. Fungal infections a) General principles i) The incidence of systemic fungal infections in ICU patients has increased: Increased numbers of immunosuppressed patients admitted to ICU The use of broad-spectrum antibiotics, and Prolonged use of intravascular catheters ii) Fungaemia is an indication to commence antifungal therapy. iii) Whilst candidaemia is associated with significant mortality, systemic infections can occur with negative blood cultures. b) Risk factors for candidaemia and disseminated candidiasis: i) Neutopaenia ii) Long term CVC use iii) Candida colonization iv) Broad spectrum antibiotics v) Haemodialysis vi) Immunosuppressants c) Antifungal prophylaxis i) Systemic prophylaxis is not recommended for general ICU patients ii) Solid organ transplant patients do not require prophylaxis iii) Posaconazole prophylaxis is effective and tolerated in bone marrow transplant and neutropaenic cancer patients d) Prophylaxis and treatment are as per the RAH guidelines – see flowchart in following page, or RAH intranet
- 201. 201 Flowchart: Antifungal Treatmentin Immunosuppressed Patients
- 202. 202 8. Necrotising softtissue infections a) General principles i) This is a generic group of patients with life threatening infections involving combinations of mucocutaneous, fascial and myofascial planes ii) These infections represent a medical emergency: patients may present with severe septic shock and rapidly developing multiple organ failure iii) In rapidly progressive infections, local signs of inflammation may underestimate the degree of underlying tissue necrosis iv) Usually due to one or more of the following organisms: Anaerobes - clostridium spp, bacteroides Gram positives - group A streptococcus, staphylococcus Gram negatives - enteric organisms b) Management protocol: i) Appropriately trained personnel, familiar with the severity of the patient's condition and with appropriate resuscitative equipment, must accompany these patients during all phases of their management ii) The hallmarks of management involve a detailed multidisciplinary approach coordinated by the duty Intensive Care consultant and involving the following: The duty ID consultant must be notified as soon as possible. Prompt and effective resuscitation, restoration of vital organ perfusion and control of metabolic emergencies (e.g. hyperkalaemia, hypoglycaemia, coagulopathy). This is coordinated by the Intensive Care team and must not significantly delay surgery. Early, aggressive and repeated surgical debridement. a. Patients with necrotising soft tissue infections must be reviewed by a plastic surgical consultant (not trainee) ASAP. b. The Duty Anaesthetist must be notified as soon as surgery is planned. Prompt identification of organisms with early prescription of appropriate empirical, then specific antibiotics as required (refer empirical and specific antibiotics section). Immune Globulin (IV-Ig) a. Clearest evidence in Gp A Strep infections. b. Should be used in conjunction with clindamycin c. Liaise with ID in all cases & confirm if to be used d. Standard regimen over 3 days: i. 1.0g/kg Day1 ii. 0.5g/kg Days 2&3 e. “Rescue Therapy” i. May be considered in cases where surgery would prove devastating, or where surgery is unduly delayed ii. Dose: 2.0g/kg as single bolus over 3-6hrs. NB: This may be > 3000ml IV-Ig
- 203. 203 Hyperbaric oxygenis an adjunctive therapy in selected patients: a. HBO must not delay debridement and resuscitation must be maintained during treatments. b. Indications for hyperbaric oxygen: i. Progressive bacterial (clostridial) gas gangrene. ii. Selected patients with severe multisystemic disease not responding to resuscitation, antibiotics and surgery. c. The number of HBO treatments on a given day will depend on the stability of the patient, availability of staff and timing of surgery. d. As a general rule, patients undergoing surgical debridement will return to ICU following surgery for stabilisation and assessment prior to subsequent transfers for HBO. This will be co-ordinated by the duty Intensive Care and hyperbaric medicine consultants.
- 204. 204 H. Drug Overdose 1.General principles a) The majority of drug overdoses are poly-pharmaceutical and respond to general supportive measures. b) Overall, early mortality is low and usually relates to cardiorespiratory arrest. c) Following admission, morbidity relates primarily to aspiration pneumonitis, or a delay in definitive respiratory care. d) There is a poor correlation between depth of coma and preservation of glottic reflexes. Accordingly, if there is any doubt the patient should be intubated. e) Antidotes such as naloxone or flumazenil: i) Should generally not be used as alternatives to supportive measures ii) Are not to be used to facilitate gastric lavage or charcoal administration iii) The main utility is in aiding diagnosis of the underlying cause of coma - small doses only are required iv) Usefulness in treatment is limited by their short half-lives v) Continuous infusion is required where ongoing therapy is contemplated vi) Both agents may initiate a withdrawal syndrome or unmask to the toxicity of co-ingestants. vii) In the case of flumazenil these effects may be life threatening. f) ICU/HDU admission criteria following an overdose may include: i) Intubated patients ii) Reduced GCS with potential airway compromise iii) Uncontrolled seizures iv) Persistent hypotension v) ECG criteria: Ventricular or supraventricular tachyarrhythmias Sinus tachycardia > 140/min with tricyclics or thyroxine AV block 2nd or 3rd degree QTC interval > 0.5s QRS interval 0.12s Acute RBBB vi) Metabolic disturbance requiring HDU-level of care vii) Requirement for extracorporeal elimination 2. Gastrointestinal Decontamination a) A variety of approaches have been used historically in an attempt to reduce the dose absorbed following an oral ingestion. b) There is minimal evidence for improved survival or shortened duration of toxicity, particularly when applied to unselected patients. c) The decision to use decontamination requires individual patient risk-benefit analysis. Appropriate patients and modalities should be selected, and gastrointestinal decontamination should never proceed to the detriment of resuscitative and supportive care.
- 205. 205 d) Gastric lavage i) Largely historical ii) Formal lavage (large bore tube placement, water instillation and aspiration) should not be performed. iii) For intubated patients, an orogastric or nasogastric tube of appropriate (standard) size should be inserted, and any gastric content aspirated iv) No additional fluid should be instilled via the tube. e) Charcoal i) Charcoal aspiration has a high morbidity and mortality: Adequate airway reflexes must be present, or If there is any doubt the patient should be intubated ii) For appropriate ingestions administer: 1g/kg body weight (to a maximum of 100g) stat 25g 4 hourly x 3 doses - slow release medications - drugs with enterohepatic circulation Cease administration should an ileus develop. iii) Indications: Presentation < 1hr from ingestion a. Compound bound by charcoal b. Ingestion expected to cause significant morbidity or mortality. Presentation > 1hr, consider administration for: a. Salicylates b. Slow release or enteric coated preparations c. Agents which delay gastric emptying, and d. Drugs with enterohepatic circulation. iv) Charcoal is ineffective for: Elemental metals and their salts Hydrocarbons and alcohols Acids or alkalis v) With multiple dose charcoal administration, constipation is likely and the addition of sorbitol may be considered. (NB. Sorbitol may interfere with the adsorptive capacity of charcoal.) f) Whole bowel irrigation i) Use of polyethylene glycol solution to decontaminate the bowel. ii) Use restricted to life threatening overdoses where: The agent is a slow release or enteric coated preparation The agent is not expected to be bound by charcoal. A good outcome is not expected with supportive care and antidote administration alone. The patient presents before the advent of severe toxicity
- 206. 206 iii) May be potentially useful following: Iron overdose > 60mg/kg Slow release potassium chloride > 2.5mmol/kg Major slow release verapamil or diltiazem ingestion Symptomatic arsenic trioxide ingestion Lead ingestion Body packers (heroine) iv) Contraindications Good outcome expected with standard care Uncooperative patient Uncontrollable vomiting Reduced GCS or seizures expected in subsequent 4 hours Ileus or bowel obstruction Intubated patients (relative) v) Technique Polyethylene glycol solution (standard endoscopy bowel prep.) Administer via correctly placed nasogastric tube at 2L/hour (25ml/kg/hr in children) To minimize vomiting start at a slower rate & titrate up as tolerated Administer metoclopramide to enhance gastric emptying Be prepared for explosive diarrhoea - sit on commode or place effluent tube for example Continue until rectal effluent is clear or an ileus/abdominal distension occurs. 3. Osmolal Gap a) OG = Measured – calculated osmolality b) Calculated Osmo = 2×[Na + K] + Gluc + Urea + ethanol c) Baseline osmolar gaps are highly variable in the normal population. d) Evaluation of potential toxic alcohol ingestion requires serial assessments over time looking for a characteristic pattern with worsening acidaemia, increasing anion gap and decreasing osmolar gap. e) Single measurements may confirm an ingestion but are not reliable in excluding it.
- 207. 207 Flowchart: The Unconscious,Undetermined Overdose RESUSCITATION (ABCDEFG) Consider: 1. Airway 1. Glucose 50% 2. Breathing 2. Naloxone 3. Circulation 3. Thiamine 4. Don’t Ever Forget Glucose History: Examination: Investigation: 1. Patient 1. Clinical toxidromes Blood Urine 2. Relatives 2. Trauma Biochem: Urine drug 3. SAAS Crew 3. Nerve palsies Electrolytes screens rarely 4. Pressure areas Glucose influence 5. Preganacy? Renal management and LFTs should be used Coags sparingly Drug levels: Other NO Metabolic Acidosis Paracetamol ECG routinely ABG 1. Sedatives Others as Measured 2. Hypnotics indicated osmolality 3. Paracetamol only 4. Theoplylline 5. Anticholinergics 6. Antihistamines 7. Antipsychotics 8. Antidepressants 9. Anticonvulsants 10. Lithium 11. Organophosphates Arterial Blood Gas Metabolic Acidosis Normal Anion Gap Raised Anion Gap 1. Acid ingestion + 2. Toluene sniffing Osmolal Gap§ 3. Bicarbonate loss OG < 10 OG > 10 Salicylates Methanol Cyanide Other alcohols Carbon monoxide Lactic acidosis Iron Isoniazid Metformin
- 208. 208 4. Specific therapies/ protocols a) Paracetamol: Acute overdose i) Defined as a single ingestion, or staggered ingestion occurring over 8 hours or less. ii) If the time of ingestion can be defined risk assessment and the decision to treat may be based upon the modified Rumack-Matthew nomogram (use the initial ingestion time as the assumed total ingestion time when plotting staggered ingestions occurring over < 8hrs). iii) Potentially hepatotoxic dose in a fit adult is > 200 mg/kg (or > 10g) iv) Markedly less in high risk individuals: Chronic alcoholics and the malnourished Pre-existing liver disease Those taking cytochrome P450 inducing medications v) The risk of hepatic injury without NAC (N-acetylcysteine) is predicted by plotting a level taken 4-15 post ingestion on the Rumack-Matthew nomogram. vi) The probability, with a 4hr drug level, is: 1-2% < 1320 µmol/L (200mg/L) 30% ~ 1320-1980 µmol/L (200-300mg/L) 90% > 1980 µmol/L (> 300mg/L) vii) The risk of hepatic impairment with NAC is determined primarily by the time from overdose to commencement of NAC: Survival is 100% where NAC is commenced within 8 hours Benefit is reduced if NAC commenced at 8-24 hours Benefit is not confirmed if commenced beyond 24 hours, except in the setting of hepatic failure. viii) The administration of NAC is indicated in the following settings (refer to flowcharts on following pages): Patients who present within 8 hours of ingestion and have a 4-8 hour level falling above the treatment line All patients presenting 8-24 hours post-ingestion *may be ceased if the subsequent level is non-toxic and transaminases are normal Patients presenting beyond 24 hours post-ingestion with detectable paracetamol and elevated transaminases Unknown time of ingestion (follow the >8 hour scenario in Box 3) Late presenters with clinical or biochemical evidence of hepatic injury ix) For repeated supra-therapeutic ingestions see “Flowchart: Repeated Supratherapeutic Paracetamol Ingestion” for management guidelines.
- 209. 209 x) For sustained released paracetamol preparations: Start NAC if > 200mg/kg or 10gm (whichever is less) ingested. Use paracetamol levels to determine the need for NAC. a. Check serum levels at 4 hours and repeated 4 hours later. b. If either level > nomogram line, continue or commence NAC. c. NAC may be discontinued if both levels < nomogram line xi) NAC may be ceased in the following settings: Patients in whom NAC was commenced < 8 hrs post-ingestion who are clinically well and without hepatic tenderness at the completion of the 20 hour infusion (no further investigation required) Patients in whom NAC was commenced > 8 hrs post-ingestion who are clinically well and have normal transaminases at the completion of the 20 hour infusion. Those whose transaminases are abnormal at this time should continue an infusion at 100mg/kg/16 hrs until transaminases and INR (tested 12-24 hourly) are falling. xii) Consultation with liver transplant services (FMC) for consideration of transplant should commence with any of the following high risk criteria: INR > 3.0 at 48 hours or > 4.5 at any time Oliguria or creatinine > 200 µmol/L Acidosis with pH < 7.3 after resuscitation Ongoing hypotension with systolic BP < 80mmHg Hypoglycaemia Severe thrombocytopenia Encephalopathy (any degree) xiii) The default position, if in doubt, should be to treat with NAC. xiv) Toxicological advice should be sought if there are any uncertainties. Graph: Modified Rumack-Matthew Nomogram
- 210. 210 Flowchart: Acute ParacetamolOD - Known Time of Ingestion *from Daly FFS, Fountain JS, Murray L, Graudins A, Buckley NA. Guidelines for the management of paracetamol poisoning in Australia and New Zealand – explanation and elaboration (Consensus Statement). MJA 2008; 188: 296-301.
- 211. 211 Flowchart: Repeated SupratherapeuticParacetamol Ingestion Table: N-Acetylcysteine Administration NAC 150mg/kg in 200mls of 5% dextrose over 30 minutes NAC 50 mg/kg in 500mls of 5% dextrose over 4 hours NAC 100mg/kg in 1000mls of 5% dextrose over 16 hours
- 212. 212 b) Lithium -Acute overdose i) Generally produces significant GIT symptoms with nausea, vomiting, abdominal pain and diarrhoea. ii) Ingestion < 25g in the setting of normal renal function is benign iii) Ingestion > 25g may cause more significant GIT toxicity iv) Neurotoxicity is rare with good supportive care and hydration v) Renal impairment, dehydration and sodium depletion cause a reduction in renal lithium excretion and increase the risk of delayed neurotoxicity vi) Patients presenting late with established neurotoxicity should be managed as for chronic toxicity, and have similar long term morbidity vii) Lithium levels > 5mmol/L 4-8 hrs post ingestion are not uncommon viii) Treatment Normal saline rehydration Maintenance of urine output > 1ml/kg/hr ix) Haemodialysis is reserved for: Those with established or worsening renal failure, and Those presenting late with established neurotoxicity c) Lithium - Chronic poisoning: i) The clinical features of chronic toxicity are primarily neurological ii) Develops when renal lithium excretion is impaired for any reason iii) Serum lithium levels correlate poorly with clinical toxicity iv) Neurotoxicity may persist well after lithium levels return to normal. v) The Hansen-Amdisen classification may be used to grade severity: Grade 1 (mild): tremor, weakness, ataxia, hyperreflexia Grade 2 (moderate): stupor, rigidity, hypertonia, hypotension Grade 3 (severe): myoclonus, convulsions, coma vi) Cardiac effects can occur in late toxicity following the establishment of neurological features, which includes rhythm disturbances, A-V delay, heart block and non-specific ST segment and T wave abnormalities vii) Lithium levels Confirm a diagnosis but should not be used to grade severity Are useful serially to monitor response to therapy viii) Principles of therapy Careful correction of fluid and sodium balance Cease lithium and any medications that may impair excretion Monitor urine output, renal function, electrolytes and lithium levels ix) Indications for haemodialysis Neurotoxicity and a serum level > 2.5 mmol/L Grade 3 neurotoxicity regardless of level Pre-existing renal or cardiac disease preventing the achievement of an adequate urine output with hydration alone Repeated haemodialysis treatments may be required
- 213. 213 d) Opioids i) Produce CNS and respiratory depression, often just above analgesic doses ii) Death is usually due to respiratory failure, either primary effect or compounded by aspiration, and good supportive care ensures survival iii) Some opioids may possess additional cardiac and neurologic toxicity - e.g. dextropropoxyphene, tramadol, pethidine iv) Controlled release preparations may cause delayed and prolonged toxicity v) Treatment is generally supportive vi) Naloxone (50 to 100µg IV repeated as needed) Useful for diagnostic purposes Can assist in the management of airway and breathing May result in a withdrawal syndrome vii) If repeated naloxone boluses are required to ensure a protected airway, intubation is the preferred method of ongoing management viii) If a naloxone infusion is established: Initial hourly requirement is generally half the effective dose used over the preceding hour, i.e. that required to achieve airway protection and adequate tidal volumes Infusions require constant observation/assessment Hospital deaths have occurred due to inadequate observation e) Carbon monoxide i) CO is a common cause of poisoning death ii) Most deaths occur pre-hospital. iii) Acute effects are due to tissue hypoxia iv) Those that arrive at hospital alive should survive. v) In-hospital management involves supportive care and identification of those at risk of long term neuropsychiatric sequelae vi) Delayed neurological effects are secondary to unrelated and incompletely understood mechanisms vii) HbF binds CO more avidly than HbA, and the foetus is at particular risk viii) Self poisonings involve high concentration, short term exposures, and are associated with fewer long-term sequelae than industrial and domestic exposures (low concentration, prolonged exposures) ix) High risk features for delayed neurological sequelae: Loss of consciousness or coma Persisting neurological deficit (e.g. confusion) Cerebellar signs Metabolic acidosis Myocardial ischaemia Age > 55yrs
- 214. 214 x) Treatment options Normobaric oxygen at high flow via non rebreather mask a. Continue until all symptoms resolve b. Pregnant women to continue for 24 hours with concomitant foetal assessment Hyperbaric oxygen a. May be indicated in patients with 1 or more high risk factors b. Indications and effectiveness are controversial f) Cyanide i) Acute cyanide poisoning is rare, dramatic and lethal ii) Removal from the source of exposure, good resuscitative care and selective antidote use provide the best chances of survival iii) Most deaths will occur pre-hospital, and those who arrive alive in hospital post-inhalational exposure are likely to survive with supportive care. iv) Risks to those involved in care delivery are negligible. v) Decontamination should involve removal of clothes and washing of skin with soap and water. vi) Cyanide levels are not available in a timely manner and do not aid management vii) Serum lactate levels parallel cyanide levels and may be used as a proxy marker of exposure viii) A lactate level > 10 mmol/L correlates with a toxic cyanide level (in the absence of an alternative cause for elevation) ix) Management should proceed along normal resuscitative lines with the delivery of 100% oxygen x) Consider using an antidote in the following settings: Altered mental state Seizures Hypotension Significant and persisting metabolic acidosis (lactic) xi) Antidote choice and administration 100% oxygen in all cases Hydroxocobalamin (1st line) a. 5g in 200mls of 5% dextrose over 30 minutes b. Repeat in 15 minutes if no improvement Sodium thiosulphate (adjunct to Hydroxocobalamin, or 2nd line) a. 12.5g IV b. Repeat dose at 30 minutes if acidosis persists Sodium nitrite a. 300mg IV over 3 minutes b. Follow immediately with sodium thiosulphate c. Half dose may be repeated in 30 minutes if required d. Monitor methaemoglobin (must not exceed 40%)
- 215. 215 g) Toxic alcohols i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are used as industrial solvents, cleaning agents and reactants. ii) Accidental ingestions are rarely of sufficient volume to cause toxicity iii) Deliberate ingestion is associated with severe metabolic acidosis, multiorgan dysfunction and potentially death. iv) Cause an initial “ethanol like” intoxication followed by a progressive metabolic acidosis and compound specific end-organ toxicities, e.g. Retinal toxicity/blindness (methanol) Acute renal failure (multiple agents) Seizures (multiple agents) Refractory hypotension (multiple agents) Delayed neurological sequelae (diethylene glycol) v) Diagnosis is based upon a history suggestive of ingestion and a characteristic evolution of metabolic acidosis Initially: osmolar gap (OG) + normal pH and anion gap (AG) Evolution of acidosis with pH, OG and AG Variability in osmolar gap amongst the normal population is such that a single assessment of acid-base, AG and OG is insufficient to exclude significant exposure (although it may confirm it) vi) Specific treatment Ethanol a. Commence ASAP, regardless of symptomatology, in all with: i. Acidosis, or ii. An elevated OG (with or without acidosis), b. Check baseline BAL, if > 0.1g/dl a loading dose is not required c. Titrate to BAL 0.1-0.2g/dL while on dialysis d. May be given orally (via NGT) or by IV infusion e. Oral protocol *avoid in ICU if possible i. Loading dose of 1.8ml/kg of 43% ethanol (4 x 30ml vodka shots for a 70 kg adult) ii. Maintenance infusion of 0.2-0.4 ml/kg/hr (1 x 40ml vodka shot per hour) f. Intravenous protocol i. Loading dose: 8ml/kg of 10% ethanol ii. Maintenance: 1-2ml/kg/hr of 10% ethanol g. Actual requirements vary widely between individuals, and serial blood alcohol assessments are required to ensure a level within the target range h. If on CVVHDF, then safer to dialyse against desired [ETOH] i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement) ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag
- 216. 216 Haemodialysis (HD) a. Significantly more efficient at clearing alcohols than CVVHD b. Indications i. Serum pH < 7.3 ii. Serum bicarb < 20 mEq/L iii. Worsening acidosis or vital signs despite supportive care and ethanol infusion Folate 50mg IV QID or folinic acid Thiamine 300mg IV daily & pyridoxine 50mg QID for ethylene glycol poisoning Correct hypocalcaemia (if symptomatic) & hypomagnesaemia h) Organophosphorous agents i) Includes the organophosphates (OP) and carbamates (CM) ii) Similar initial presentation iii) Most deaths occur as a consequence of respiratory failure iv) OPs as a group have greater lethality Form a covalent bond with serine esterase enzymes In contrast to the competitive bond formed by CM. v) There is great variability amongst the OPs in terms of enzyme aging, toxicity profiles, and pralidoxime responsiveness vi) High quality supportive care and aggressive use of antidotes is necessary to ensure survival. vii) The diagnosis is essentially clinical: Muscarinic features - diarrhoea, emesis, urination - miosis, lacrimation, salivation - bronchorrhoea, bronchospasm - bradycardia, hypotension Nicotinic features - fasciculation, tremor, weakness - respiratory muscle paralysis - tachycardia, hypertension CNS features - agitation, seizures, coma - delayed neuropsychiatric effects viii) Cholinesterase levels: Plasma cholinesterase levels fall more rapidly and recover more quickly than RBC cholinesterase levels, they are useful in confirming exposure but do not correlate with toxicity. RBC cholinesterase levels correlate better with toxicity and response to therapy, but take longer to perform (limiting their clinical utility) ix) Decontamination Resuscitation must not be delayed by external decontamination procedures These agents do not vapourise at atmospheric pressure There is no risk to care providers from inhalational exposure The characteristic odour is due to a hydrocarbon solvent, which may cause headaches & eye irritation, but is otherwise harmless
- 217. 217 Staff should wear impermeable gowns, gloves, glasses and facemasks Care should be delivered in a well ventilated setting The patient’s clothing should be removed and the skin washed with soap and water x) Treatment Ventilatory and CVS support as indicated Atropine a. Reverses muscarinic effects only – it will not reverse paralysis! b. Titrate 1.2 mg at 5 min intervals (doubling the dose every 5 min) until signs of successful atropinisation are noted i. Drying of secretions ii. Resolution of bradycardia iii. Clear chest c. Over 10-20mg, or infusions of up to 5 mg/hr may be required in severe poisoning. d. Typically commenced at 10-20% of loading dose per hour. e. NB: HR and pupil size are not useful for clinical monitoring after nerve agent exposure Diazepam IV a. Treatment of seizures b. Reduces the incidence of neuropsychiatric sequelae c. Regular dosing is recommended. Pralidoxime Iodide a. Efficacy is unclear and is likely to be compound specific b. Default is to give ASAP c. Not required for documented carbamate ingestion (although not contraindicated) i. 1g IV over 30 minutes ii. 500 mg/hr for 24 hours iii. May be ceased at 24 hours in the absence of nicotinic or muscarinic features. The benefit of continuing beyond 24 hours is unclear and warrants specialist consultation. i) Calcium Channel Blockers i) Of the common slow release formulations, verapamil and diltiazem frequently cause profound CVS collapse 4-16 hrs post-ingestion. ii) Other agents within the class rarely cause major toxicity iii) Onset of toxicity may be delayed: Up to 2 hours post-ingestion of the standard preparation, and Up to 16 hours after ingestion of the SR formulation iv) Ingestion of >10 tablets of verapamil SR or diltiazem SR may cause serious toxicity
- 218. 218 v) The key issues in management are: Identification of patients at risk Judicious use of the pre-toxicity window of stability Consideration of GIT decontamination options (including whole bowel irrigation), and A graduated approach to developing or established toxicity vi) Risk of serious toxicity is significantly increased by: Co-ingestion of other cardiac medications, and Underlying cardiac disease or advancing age vii) Graduated response to hypotension: failure to achieve stability at each step should prompt immediate initiation of the next Fluid load with 10-20 ml/kg isotonic crystalloid (avoid overload) Calcium load a. Calcium gluconate - 60ml of 10% solution, or b. Calcium chloride - 20ml of 10% solution c. Commence an infusion to keep calcium levels > 2.0mEq/L Atropine to a total of 1.8mg Catecholamine infusion effects are variable in terms of: a. Central - negative inotropic & chrontropic effects - Adrenaline is an appropriate 1st line agent b. Peripheral - reduced vascular tone -Noradrenaline 1st line agent c. Do not persist with escalating inotrope doses in the setting of continued instability High dose insulin & dextrose / euglycaemia a. Most effective when used early. b. Glucose i. Bolus 25g (50 mL of 50% solution) unless hyperglycaemia (BGL > 22 mmol/L) present ii. Infusion 25 g/h IV titrated to maintain euglycaemia c. Actrapid insulin i. 1 IU/kg bolus ii. Infusion 0.5 IU/kg/h titrated every 30 min to a maximum of 5-10 IU/kg/h d. Monitor: i. Glucose - every 20 min for first hour, then every 1 h ii. Potassium - replace only if < 2.5 mmol/L and there is a source of potassium loss e. Therapeutic end points: i. BP > 90mmHg, HR > 60, resolution of acidaemia ii. Adequate urine output (1-2 mL/kg/h) iii. QRS interval < 120 ms iv. Improved mentation
- 219. 219 viii) Seek guidance from Clinical Toxicologist (via switchboard or Poisons Information Centre) or ICU consultant staff regarding protocol ix) Cardiopulmonary bypass, ECMO, cardiac pacing and intra-aortic balloon pumps have been used successfully as extraordinary manoeuvres j) Beta Blockers i) Usually minimal toxicity and require only simple supportive care. ii) By contrast overdoses of sotalol or propranolol may be life threatening iii) In addition to class 1 and 2 effects (bradycardia, conduction blocks and hypotension) Propranolol a. Na+ channel blocking effects wide complex arrhythmias b. Highly lipid soluble enters the CNS (coma and seizures) Sotalol a. Blocks cardiac K+-channels b. Causing QT prolongation and torsades de pointes iv) The clinical response to overdose is highly variable, but the threshold for severe toxicity from propranolol may be as low as 1g v) With the exception of sotalol and slow release preparations, toxicity is usually apparent within a few hours post-ingestion vi) PR prolongation in the absence of bradycardia is an early marker of toxicity vii) Approach to immediate life threatening symptoms: Bradycardia and hypotension a. Atropine b. Adrenaline c. Noradrenaline d. Glucagon 5-10mg bolus & 1-5mg/hr infusion (cumbersome), or e. High dose insulin dextrose euglycaemia (targeting impaired contractility) Wide QRS a. Sodium bicarbonate bolus 1-2 mEq/kg b. Repeat as required c. Intubate and hyperventilate targeting serum pH 7.5 to 7.55 Torsades de pointes a. Isoprenaline b. Magnesium c. Overdrive pacing
- 220. 220 k) Tricyclic Antidepressants (TCAs) i) Tricyclic antidepressant use has escalated after an initial reduction secondary to SSRI introduction ii) TCAs remain a significant cause of toxicological morbidity and mortality iii) Poisoning rapid onset CNS and CVS toxicity peak between 4-6 hrs post ingestion Dose > 10mg/kg is potentially life threatening Dose > 30mg/kg is expected to cause severe cardiotoxicity and coma. Prompt intubation, hyperventilation and sodium bicarb administration at the onset of major toxicity is life saving. iv) The investigation of choice is the 12 lead ECG, with diagnostic and prognostic features including: Prolongation of the PR and QRS intervals Terminal R wave in aVR Increased R/S ratio (>0.7) in aVR QRS > 100 ms is predictive of seizures QRS > 160 ms is predictive of ventricular tachycardia v) The approach to resuscitative management includes the following: Prompt intubation and hyperventilation (to serum pH 7.5-7.55) at the onset of CNS depression Ventricular arrhythmias are unlikely to respond to defibrillation: a. NaHCO3 ~ 2 mmol/kg IV every 2 minutes until perfusing rhythm restored. (Most effective when used in combination with hyperventilation) b. Lignocaine is a 2nd line agent if arrhythmias persist despite pH. Hypotension is managed with crystalloid and alkalinisation followed by noradrenaline Seizures are managed with benzodiazepines (*avoid phenytoin) I. Bites and Envenomation 1. Up to date and detailed information on envenomation may be found at the toxinology website http://www.toxinology.com/ managed by the Women’s & Children’s Hospital 2. Medical advice for doctors can be sought by contacting the clinical toxinologist, A/Prof Julian White via the WCH switchboard (Ph: 81617000) 3. Emergency cases are seen through the Emergency Departments of major hospitals, while less urgent cases are seen after discussion with the treating doctor.
- 221. 221 J. Limitation of Therapy a) Limitation may involve either withholding and/or withdrawal of life supporting therapies. b) There is no ethical or legal distinction between these processes. c) Limitation may involve challenging ethical and legal issues; however, in patients with no realistic chance of meaningful recovery, decisions to limit life-sustaining therapies are both clinically and ethically indicated. d) Assisted suicide and euthanasia are medically and ethically distinct from limitation of therapy, are illegal in SA and should never occur. e) The administration of medication to relieve the suffering of a dying patient is imperative, even though a side-effect may be to hasten the onset of the patient’s death. Such therapy is legally distinct from euthanasia. f) Approximately 70% of all RAH-ICU deaths involve some limitation of therapy. g) Absolute requirements for limitation of therapy are: i) Medical consensus, including the treating ICU and admitting clinical teams ii) Clear and open discussion with the patient, family or next of kin regarding this consensus medical opinion; and, an ‘absence of objection’ to this proposed management direction. iii) Clear documentation in the patient’s medical record, along with a description of the process by which the decision was made. h) Counselling patients and families in limitation of therapy requires clarity and sensitivity to ensure that all parties understand and accept the plan of management. i) The concerns and wishes of the patient and family are important considerations. j) The overriding goal is to provide the best care possible for the patient. This may be to concentrate on palliation, rather than life sustaining therapies. k) The decision to limit treatment is a consultant responsibility. l) Refer to the CICM Policy Document IC-14 http://www.cicm.org.au/policydocs.php K. Brain Death and Organ Donation 1. Reference: ANZICS Statement on Death and Organ Donation http://www.anzics.com.au/death-and-organ-donation 2. For further information, trainees should liaise with the ‘Organ Donation Hospital Medical Directors’: a) Dr David Evans b) Dr Stewart Moodie c) Dr Peter Sharley d) Dr Alex Wurm
- 222. 222 3. Declaration ofbrain death a) This is an absolute requirement prior to ‘beating-heart’ organ donation b) Declaration must be made by two members of the ICU staff: i) The Duty ICU consultant, and ii) Another ICU doctor (more than 5yrs qualified with appropriate experience). c) The declaration of brain death may be by either clinical or imaging certification. 4. Clinical certification of brain death a) The procedure is completed on a Certification of Brain Death form (MR150.0) and documented in the case notes. b) Record the time of onset of coma i) Last time the patient showed response such as breathing, pupil reaction or coughed on suction. ii) This can be determined from the nursing observations c) Pre-conditions: i) A recognised irreversible cause of coma must be identified. ii) Potentially reversible causes of coma have been excluded: Hypotension Hypothermia *core temp must be > 35ºC Drugs or poisons. Neuromuscular blocking drugs Metabolic or endocrine disturbance including: a. Deranged renal or hepatic function b. Hyperglycaemia, hypoglycaemia, thyroid function c. Electrolyte disturbances iii) Ability to perform examination of: Cranial nerves Apnoea testing (e.g. not severely hypoxaemia or high cervical injury) d) Clinical confirmation of absent brain stem function i) Performed separately by 2 doctors, with the first test at least 4 hours after the onset of coma (longer in the case of hypoxaemic/ischaemic injuries). ii) Absent pupillary responses to light, both direct and consensual iii) Absent corneal reflexes iv) Absent vestibulo-ocular reflex No nystagmus on injection of 20ml iced water into the ear Check tympanic membranes prior to this procedure Occulo-cephalic reflexes are often tested, but are not formally required v) Absent gag / cough reflex. vi) Absent response to pain in the cranial nerve distribution. vii) Apnoea following disconnection from the ventilator: Pre-oxygenate patient with 100% oxygen Disconnect ventilator and connect to bag with 100% O2 at 1-2 l/min Confirm PaCO2 > 60mmHg and pH < 7.30 (with PaO2 > 60mmHg) Continuously look for apnoea clinically
- 223. 223 e) The following are compatible with Brain Death i) Spinal reflexes ii) Sweating, blushing and tachycardia iii) Normal BP without pharmacological support iv) Absence of Diabetes Insipidus f) The 2 practitioners may choose to be present at each examination, however, each must perform and be responsible for one of the 2 examinations g) From the onset of coma until the second set of testing, there should be a continuous period of observation by nursing staff h) Families may benefit from witnessing the clinical testing for brain death i) The time of death is the time when certification of brain death is completed – i.e. on completion of the second examination and documentation in the case notes. j) There is no legal requirement for certification of persons not considered for organ donation, however this is encouraged as it can assist in counselling relatives and the subsequent cessation of inappropriate medical intervention. 5. Imaging (Non-clinical) certification of brain death a) Consider when clinical examination is “consistent with” brain death, however, the preconditions (2c) for clinical certification cannot be met. b) Demonstrated absence of cerebral blood flow is therefore required. c) Ideally there should be a period of observation of 4 hours to increase the likelihood that no flow will be demonstrated. d) Absence of cerebral blood flow may be established by either: i) Radionuclide cerebral perfusion scan (Tc99 HMPAO). ii) 4 vessel cerebral angiography (rarely performed at the RAH) e) Certification of brain death is by 2 clinicians, (not including the doctor who performed the imaging investigation) who have considered the onset and cause of coma, the clinical examination and the results of the investigation performed. 6. Organ donation a) General principles i) Any patient who is, or may become brain dead is a potential donor. There are no automatic exclusion criteria. ii) All potential donors should be offered the opportunity to donate iii) Notify the Donor Coordinator from Donate Life, SA (Ph: 82077117) when a potential donor is identified. b) Criteria for brain dead organ donation i) The patient has been declared brain dead *for donation after cardiac death see below. ii) Usually, no patient history of: HIV, untreated bacterial, fungal or viral infection. IV drug abuse Malignancies other than primary brain tumours and minor skin lesions. Treatment with hormones of human pituitary origin. Dementia (or family history of dementia). Disease of the donor organ
- 224. 224 iii) All brain dead patients should be discussed with the Donor Coordinator, regardless of relative contraindications. c) Procedure: i) Organ donation should not be discussed with the family until brain death has been certified and the family informed. ii) Family approaches regarding donation prior to the patients death should be referred to the consultant iii) Counselling families with regard to brain death and organ donation requires considerable compassion, knowledge, skill and time. While this is primarily a consultant responsibility, advanced trainees are encouraged to participate in the process under supervision. iv) The wishes of the patient and family are paramount. v) A “donor kit” is kept in the cupboard in P4A which contains a check-list, plus all the forms and specimen bottles required. vi) Following consent for organ donation, blood should be sent for: HTLV-1, HIV 1 + 2 HBsAg, HBsAb, HBcAb, HCV CMV-IgG, EBV, RPR Group and X-match Tissue typing – volume of blood varies according to blood group Mark the request forms: “Urgent – Organ Donor, cc: Donate Life” vii) Coronial approval will be sought by the Donor Coordinator where required. viii) The RAH Designated Officer may give permission for donation if all efforts to find relatives have failed. ix) It is the responsibility of ICU medical staff to provide either a death certificate or report to the coroner. Time of death is the time of second certification. x) Notification of the recipient and procuring teams (which may come from interstate) and coordination of operating theatre time, collation of results and investigations are dealt with by the Donor Coordinator(s) xi) Donor coordinators may seek assistance from ICU staff with ordering investigations. xii) The following investigations are normally required: Recent ECG Recent CXR Echocardiography ABG d) Management of the organ donor: i) The situation is time critical as it is not possible to stabilise a brain dead patient indefinitely. ii) Aim to ensure perfusion and protection of all organs for donation to achieve the optimal outcome for all recipients iii) Avoid focused management strategies aimed at single organ systems
- 225. 225 iv) Ventilation: Adequate oxygenation: PaO2 > 60 mmHg | FIO2 < 0.5 Adequate ventilation: PaCO2 35-45 mmHg Prevention of atelectasis and lung recruitment is important. v) Cardiovascular instability: Common around the time of cerebral herniation (coning). Hypertensive episodes should be treated with short acting agents. Maintain MAP > 70 mmHg: a. Adequate volume loading prior to using inotropes. b. If CVC present: CVP 8-14mmHg c. High dose inotropic support may reduce organ viability. vi) Aim for a urine output > 0.5ml/kg/hr vii) Maintain normothermia: Established hypothermia can be difficult to manage. Prevention is preferred, using active warming devices if necessary. viii) Check biochemistry and maintain normal electrolytes. ix) Diabetes insipidus Common but not universal in the setting of brain death Treatment should commence on clinical suspicion and not be delayed for confirmatory results. Hypernatraemia adversely affects liver transplant outcomes. DDAVP 1-2 µg IV bd x) Evidence for hormonal resuscitation is conflicting. Steroids and vasopressin should be considered if hypotension is refractory. xi) Consider non-depolarising muscle relaxants if spinal reflexes persist, as these may be disconcerting for relatives and attending carers. 7. Tissue Donation a) All patients who die in the ICU may become tissue donors. b) Tissues donated include: i) Corneas ii) Heart valves iii) Bones
- 226. 226 L. Donation After Cardiac Death (DCD) 1. Introduction a) DCD provides an option where there is a strong desire for organ/tissue donation; however, the patient is unlikely to progress to brain death. b) In all circumstances, the decision to withdraw life sustaining therapy is made independent & prior to any consideration of organ donation. c) DCD may be considered when: i) A patient is planned for withdrawal of active therapy. ii) The patient and/or their representative(s) support organ/tissue donation. iii) Preferably age ≤ 65 (c.f. donation after brain death) iv) Cardiac standstill is probable within 90 minutes of withdrawal: Liver and Pancreas 30 minutes Kidneys 60 minutes Lungs 90 minutes. v) There is good underlying organ function vi) Normal contraindications to donation are absent e.g. malignancy, active infection etc. (consult donor coordinator) d) If a patient is likely to progress to brain death - this is preferred to DCD. 2. Determining the patient’s wishes a) As for all organ donations, the pre-morbid wishes of the patient are paramount. b) The Australian Organ Donor Register may assist with decision making. c) DCD can be difficult for families, relevant issues include but are not limited to: i) The discussion of donation prior to patient death ii) Families may change their mind at any time without reason or question. iii) Logistic requirements which inevitably delay the withdrawal process. iv) Reasonable escalation of supports may occur, however if the patient becomes too unstable donation may not occur. v) The requirement for ante-mortem testing and interventions. vi) Consent should be sought and rationale provided for ante mortem therapies intended solely to aid donation. vii) The immediate transfer of the deceased following death for organ procurement and effective “removal” from the family. viii) Difficulty in predicting the time of death. ix) A significant risk of donation not proceeding, depending upon timing. x) If the patient does not die within the organ suitability times, then palliative care will continue in ICU and possibly the ward. xi) There may be unknown medical reasons why donation cannot occur. d) Under some circumstances (such as complex difficult decisions to withdraw therapy) it may not be appropriate to include discussion about DCD. e) A plain language statement on DCD is available from the Donate Life website.
- 227. 227 3. Process ofDCD a) The process will be governed by the duty ICU consultant, in conjunction with the Organ and Tissue Donor Coordinator (OTDC - pager 83781671) and Organ Donation Hospital Medical Director as required. b) If “reportable” under the Coroner’s Act: i) The treating ICU team should complete the required documentation. ii) The OTDC will seek “in principle” approval for donation and notify the Coroner’s representative between death and donation. c) Withdrawal is best done as planned event in working hours. d) The organ retrieval teams must not be involved in direct patient care before death. 4. Ante-Mortem Interventions a) Ongoing supportive care prior to donation is rational and accepted. b) Escalation of care, for the sole purpose of facilitating donation, is less clear. c) The following may be considered excessive in most circumstances: i) CPR ii) Massive use of blood products iii) Escalating organ support in the setting of deteriorating physiology d) For invasive interventions, such as bronchoscopy or biopsy, discussion/consensus with the next of kin is recommended . e) Interventions directly aimed at the organ donation process i.e. of benefit to the recipient but not the patient, may be considered when unlikely to cause harm e.g. antibiotics or steroids. f) High dose heparin with intra-cerebral pathology or ante-mortem cannulation for organ perfusion are not considered acceptable. g) Advice can be sought from the Organ Donation Hospital Medical Director 5. Care of the dying patient a) Use of sedative and analgesic drugs should be in accordance with the standard practice of good palliative care. b) Locality i) There is no suitable location in the current theatre suite so withdrawal should occur in ICU with transport to theatre after death. ii) An appropriate route should be pre-identified and kept clear. iii) Normally there will be an OTDC with both the theatre and ICU teams. iv) Withdrawal should not occur until there is direct communication from the ODTC that theatre is ready. c) Monitoring i) HR, BP (IA), SpO2 and respiratory rate ii) Alarms should be disabled. iii) Remote monitoring may be preferable. iv) Warm ischaemic time is considered to be from when SBP ≤ 50 mmHg. v) All timing is recorded by the OTDC in the ICU.
- 228. 228 d) Determination of Death i) Death is considered “irreversible” in the context of DCD when 5 minutes have passed since circulation ceased. Best determined by loss of a pulsatile waveform on IABP. ECG monitoring may be used along with clinical signs. ii) A note including the time of death should be documented in the patient’s case notes declaring death prior to organ procurement surgery. iii) Should death not occur in the required time the family and organ retrieval teams should be informed and standard comfort care continued. iv) The family may wish to view their relative following organ procurement; this can be facilitated by the OTDC. See the 2010 Organ and Tissue Donation and Transplant Authority (AOTDTA) http://www.donatelife.gov.au/the-authority/national-protocol-for-donation-after-cardiac-death
- 229. 229 Table: Contact PhoneNumbers ICU Secretary Ph: 8222 5325 MedStar Ph: 8222 4222 F: 8222 2826 Organ Donor Coord T: 8207 7117 SD: 1650 Pg: 8378 1671 Duty Intensivist M: 0434 605 903 Transfusion IMVS Ext: 25430 / 25431 Consults Pager Pg: #89 22888 Pg: #89 1575 Transfusion RN Emergency Pg: #33 Ext: 22975 Massive Transfusion 47* Duty Anaesthetist SD: 1175 APS Pg: #89 22556 WCH Toxicology T: 8161 7000 ICU Research RN SD: 1520 SD: 1156 ICU Dietician M: 0401 711 460 Pg: 1342