This document provides guidance on intensive care medicine topics that may be covered in the FRCA exam, with a focus on acute liver failure and cardiogenic shock. It discusses 20 specific ICU questions that may appear in the MCQ section and advises candidates to focus on structure in their answers. Example cases are presented on acute liver failure and a postoperative patient with cardiogenic shock, with discussion points provided for each. Key topics in the management of these conditions like encephalopathy, fluid balance and inotropes are reviewed. Candidates are encouraged to answer just the question asked and not provide irrelevant extra details.
new technique for pain management ,described by dr forero ,it can replace epidural anesthesia,paravertebral anesthesia and other regional blocks.it can be used for both acute and chronic painful conditions
The transversus abdominis plane, more commonly referred to as the TAP block,
Places local anesthetic in the lateral abdominal wall in a plane between the internal oblique and the transversus abdominis muscles.
Here, the local anesthetic block can block many of the abdominal nerves as they pass to the abdominal structures.
Erector spinae plane block is a relatively novel approach to pain management for a variety of surgical procedures. ESP block is a challenging anesthesia and analgesia technique that needs more research.
new technique for pain management ,described by dr forero ,it can replace epidural anesthesia,paravertebral anesthesia and other regional blocks.it can be used for both acute and chronic painful conditions
The transversus abdominis plane, more commonly referred to as the TAP block,
Places local anesthetic in the lateral abdominal wall in a plane between the internal oblique and the transversus abdominis muscles.
Here, the local anesthetic block can block many of the abdominal nerves as they pass to the abdominal structures.
Erector spinae plane block is a relatively novel approach to pain management for a variety of surgical procedures. ESP block is a challenging anesthesia and analgesia technique that needs more research.
Brigadas para ayuda a damnificados por el Huracán Alex, entre los socios y amistades se recaudaron y entregaron:
- 550 despensas
- 698 lts. de agua en diferentes presentaciones.
Gracias a la intervención de uno de nuestros socios, es que se pudo conseguir un helicóptero para poder llegar a comunidades que estaban prácticamente incomunicadas
David Anderson gives an entertaining and informative talk about Acute Liver Failure at BCC4. He covers thinking about diagnosis, management and prognosis of acute liver failure. The podcast for this presentation is found at www.intensivecarenetwork.com
Definition, classification, epidemiology, etiology, diagnosis, prognosis of DCM, HOCM, LVNC
Also review of acute myocarditis in children
R/v of heart failure management
Dr Ashling Lillis, National Director's Clinical Fellow Macmillan Support, final year trainee in Acute Oncology
Dr Clare Philliskirk, Trainee in Acute Medicine, West Midlands
Dr Sarbit Clare, Acute Medical Consultant, Sandwell and West Birmingham Hospitals
Dr Neerav Goyal discusses the various aspects of acute liver failure that includes the criteria, pre transplant issues, critical care management, overall survival.
Pulmonary Arterial Hypertension in Rural Communities: Early Diagnosis and Int...HorizonCME
Pulmonary Arterial Hypertension in Rural Communities: Early Diagnosis and Intervention to Improve Outcomes
Learning Objectives
-Identify the signs, symptoms, and risk factors associated with PAH to facilitate timely referral of patients to specialized pulmonary hypertension centers for early diagnosis and treatment
-Explain the WHO PH Groups and functional status classifications for PAH and their impact on treatment selection
-Outline the diagnostic tests that may be used to identify patients with PAH
-Identify the indications and contraindications for currently available therapies used in the treatment of patients with PAH
-Describe the role of PCPs in managing PAH patients
Is life worth living? It depends on the liver by Dr Stephen WarrillowSMACC Conference
Management of the patient with decompensated liver disease is clearly more straightforward in specialist centres with multi-disciplinary input, access to liver transplantation teams and advanced technology. Bioartificial extra-corporeal liver support systems are undergoing evaluation and include the extra-corporeal liver assist device (ELAD developed by Vital Technologies).
ELAD is an investigational, extra-corporeal, human cell-based system. The human liver-derived cells (VTL C3A) may mimic certain functions of in vivo human liver cells. The principles of operation of the ELAD system are as follows: plasma ultrafiltrate is passed through hollow fibre cartridges containing human liver-derived cells (VTL C3A cells) and allowing two-way transfer of toxins, metabolites and nutrients, mimicking liver function. Toxins, such as bilirubin, glucose and oxygen pass from the ultrafiltrate to the VTL C3A cells. Treated plasma ultrafiltrate is then reconstituted with blood cells and returned to the patient. Data evaluating this system shows trends indicating a potential for ELAD to increase survival rates in selected patients with decompensated liver failure.
Issues in the management of liver failure include cardiorespiratory support, and the management of cerebral oedema. The principles for haemodynamic support are as for most critically ill patients, with early restoration of organ perfusion and use of vasopressors if hypotension persists despite restoration of volume. For the patient with liver failure, lactate-containing solutions and fluid overload should be avoided. New monitoring techniques for encephalopathy have been developed, including brain tissue oxygen tension, continuous EEG, transcranial Doppler and cerebral microdialysis.
Key issues for regional centres are basic management principles, liaison with specialist centres and timing of transfer. Who and when to refer is a difficult problem for the regional Australasian unit, given the tyranny of distance and issues relating to retrieval and transfer of the critically ill patient. Early liaison with the regional liver unit is key.
2. Why ICU matters for the FRCA…
20 specific questions in MCQ
Helps with medicine/surgery MCQs
SAQs - 1 or 2 questions for sure…maybe more
SOE 1 - potential topic/part of topic
SOE 2 - 10 minutes of pure fun!
3. Be calm…
The examiners are human (honestly!!!)
The questions are (mostly) mainstream
You will have seen many of the cases
Guillain-Barre / Myasthenic crisis / weakness
Brainstem death
Status epilepticus and asthmaticus
Trauma
Septic shock
ARDS
Acute pancreatitis
Burns
Some questions just won’t lie down and die e.g. PAC
4. But don’t be complacent…
People still fail the exam! 10/17 passed in 2008
Don’t assume you know enough…make sure you do
Structure…structure…structure!
Don’t waffle - answer the actual question, not the one you
wanted to be asked!!
5. Other potentials…
• Acute hepatic failure
• Sedation
• Fluid balance and outcome
• Nutritional therapy
• Tissue oxygenation and oxygen delivery
• Abdominal compartment syndrome
• Cardiogenic shock
• Clostridium difficile
• Scoring systems
6. Examples…
In the question on the brain-stem dead patient, too many candidates
included detail of brain stem testing in their answers, which was not
required. Candidates are reminded to answer the question as written; no
credit will be given for irrelevant information
It cannot be emphasised enough that the answer provided to the examiners
is less than a page and is focused completely to the question.
7.
8.
9. Case scenario 1
49 year old female, history of depression & anxiety found
unconscious in apartment having failed to turn up for work
On arrival A&E GCS 5-6, BM = 0.4
After 50ml 50% glucose BM = 14.5 and GCS 12-14
Bruising left buttock and thigh
Tender abdomen, jaundiced, BP 75/45, HR 104, Temp 34.1
CT brain NAD, CT abdo - mild hepatomegaly, ? fatty
Labs: Lactate 10.2, Bili 27, AST 4465, ALT 1945, INR 4,
Paracetamol 25, tox negative, K 1.9, Ca 0.8, PO4 0.4, Hb 10.4, WBC
15.9, Plts 102, CK 595
10. Questions for discussion
What are the main differential diagnoses?
What other information/tests would you like?
Why is the GCS abnormal?
How do you assess fluid status and responsiveness?
What does the lactate level tell you?
Why is the B low and how will you tackle it?
How do you assess the adequacy of oxygen delivery?
Does this patient need antibiotics?
What problems are likely in the next 24-48 hours?
11. Acute hepatic failure
Early death despite support
Survival with supportive therapy (liver regeneration)
Unlikely to survive with supportive therapy alone
candidate for emergency transplant
NOT candidate for emergency transplant
INFO
“Life-threatening multi-system illness resulting from massive liver
injury. The defining clinical symptoms are coagulopathy and
encephalopathy occurring within days or weeks of the primary
insult in patients without pre-existing liver injury”
Auzinger G, Wendon J. Curr Opin Crit Care 2008; 14: 179-188
12. Aetiology based therapy
INFO
Aetiology Therapy Comments
Paracetamol N-Acetylcysteine (NAC)
Early non-paracetamol
ALF
N-Acetylcysteine (NAC) Lee WM, Rossaro L, Fontana
RJ et al. Hepatology 2007;
46(Suppl 1); 268A.
? increased infection risk due to
reduced neutrophil burst
? antiplatelet action
Fatty liver of pregnancy or
HELLP
Delivery! Usually reverses before
need for transplant
Acute hepatitis B Lamivudine
Amanita Phalloides Penicillin G
13. Paracetamol toxicity
INFO
Enhanced risk
1.Excess alcohol
2.Enzyme-inducing drugs
carbamazepine
phenytoin,
phenobarbitone
St John's Wort
rifampicin
3. Glutathione depletion
malnutrition
eating disorders
malabsorption
HIV
NAPQI
Major paths
Minor path
14. N-acetylcysteine
INFO
(1) Initially 150mg/kg in 200mL glucose 5% given over 15 minutes, then
(2) 50mg/kg in 500mL glucose 5% given over 4 hours, then
(3) 100mg/kg in 1000mL glucose 5% given over 16 hours
15. Referral criteria
INFO
Day 2 Day 3 Day 4
Arterial pH < 7.3 Arterial pH < 7.3 INR > 4.4 or PT > 75s
INR > 3 or PT > 50s INR > 4.4 or PT > 75s Progressive rise in PT
Oliguria Oliguria Oliguria
Creatinine > 200 Creatinine > 200 Creatinine > 300
Hypoglycaemia Encephalopathy Encephalopathy
Severe thrombocytopaenia Severe thrombocytopaenia
Hyperacute Acute Subacute
Encephalopathy Encephalopathy Encephalopathy
INR > 2 or PT > 30s INR > 2 or PT > 30s INR > 1.5 or PT > 20s
Renal failure Renal failure Renal failure
Hypoglycaemia Hypoglycaemia Hypoglycaemia (rare)
Hyperpyrexia Hyponatraemia
Shrinking liver on CT
Non-paracetamol
Paracetamol
16. Referral criteria - Kings College Hospital
INFO
Paracetamol Non-paracetamol
Arterial pH < 7.3 after resuscitation
OR
Grade III/IV encephalopathy
PT > 100s (INR > 6.5)
OR
any 3 of the following
Creatinine > 300
Aetiology = seronegative hepatitis or
drug-induced liver failure
PT > 100s (INR > 6.5) Age < 10 or > 40
Lactate > 3.5 @ 4hrs or > 3 @ 12 hrs Jaundice to encephalopathy > 7 d
Hypoglycaemia Bilirubin > 300
PT > 50s (INR > 3.5)
Paracetamol Non-paracetamol
18. Clinical Issues in ALF
Renal
Oliguria
Acute renal impairment - drugs, hepatorenal, pre-
renal, ATN, intra-abdominal hypertension
Haematological
Thrombocytopaenia and coagulopathy
Procedural bleeding possible
Spontaneous bleeding rare
Infection
Monocyte (HLA-DR), complement, Kupffer cell failure
Responsible for most deaths!
INFO
19. Useful references
INFO
Kramer DJ, Canabal JM, Arasi LC. Application of Intensive Care
Medicine Principles in the Management of the Acute Liver Failure
Patient. Liver Transplantation 2008; 14: S85-89.
Auzinger G, Wendon J. Intensive Care Management of Acute Liver
Failure. Current Opinion in Critical Care 2008; 14: 179-188.
Stravitz T. Critical Management Decisions in Patients with Acute Liver
Failure. Chest 2008; 134: 1092-1102.
20. Case scenario 2
56 year old male, history of IHD/PVD/smoker/MI/EF 35%
Admitted to ICU following emergent leaking AAA repair…complicated by
intraoperative ST depression and hypotension
On arrival ICU BP = 90/45, HR 121 SR, NA @ 0.5 mg/kg/min, lactate 5
CVP 14, pO2 11 on 70% O2 with PEEP 5, creps bilaterally
ECG: infero-lateral ST depression
In theatre 4 L crystalloid, 2 L tetraspan, 6 packed cells, 2 FFP
Abdomen distended and tense, skin clammy
Over next 4 hours: NA increasing, lactate 8, U/O poor
Labs: Hb 9.5, Plts 85, WBC 7.9, Na 141, K 5.3, U 10.5 Creat 168, APTT 47,
PT 18, fibrinogen 0.95
21. Questions for discussion
List the main clinical issues in this case
How would you approach the respiratory failure?
What factors contribute to the hypotension/malperfusion?
What is your strategy to improve haemodynamics?
What is your target for fluid balance in the next 24 hours?
How does PPV assist the left ventricle?
What other monitors/investigations might assist you?
When would you involve the surgeons?
22. Cardiogenic Shock
• Definition
• Incidence
• Aetiology
• Pathophysiology
• Therapy
Clinical:
• Hypotension i.e. SBP below 90 mmHg
• Impaired tissue perfusion
• After correction of non-cardiac factors
Haemodynamic:
• Cardiac index < 2.2 litres/min/m2
• Systolic blood pressure < 90 mm Hg
• LAP/RAP > 18 mm Hg or PCWP > 16
• Urine output < 20 ml/hr
• SVR > 2100 dynes-sec·cm–5
INFO
23. Incidence & Mortality
Study Incidence Mortality Patient group Country
CREATE-ECLA [1] 6.5% 68% STEMI China, India, Pakistan
NRMI [2] 8.6% 47.9% STEMI USA
COMMIT [3] 4.4% 68% AMI (93% STEMI) China
5.0% 68% Metoprolol
3.9% 72% Plcaebo
SHOCK [4] 20% 75% CS on admission USA/Belgium
80% 56% Delayed CS
[1] The CREATE-ECLA Trial Group. Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-
segment elevation myocardial infarction: the CREATE-ECLA Randomized Controlled Trial. JAMA 2005; 293: 437–446.
[2] Babaev A, Frederick PD, Pasta DJ, et al. Trends in management and outcomes of patients with acute myocardial
infarction complicated by cardiogenic shock. JAMA 2005; 294:448–454.
[3] Jeger RV, Harkness SM, Ramanathan K, et al. Emergency revascularization in patients with cardiogenic shock on
admission: a report from the SHOCK trial and registry. Eur Heart J 2006; 27:664–670.
[4] Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial
infarction: randomized placebo controlled trial. Lancet 2005; 366:1622–1632.
INFO
28. Therapy - Reducing iNOS
“Excessive NOS results in high levels of nitric oxide that, in turn, lead to inappropriate
systemic vasodilatation, progressive systemic and coronary hypoperfusion, and
myocardial depression”
Effect of Tilarginine Acetate in Patients With Acute Myocardial Infarction and
Cardiogenic Shock - The TRIUMPH Randomized Controlled Trial. JAMA 2007; 297: 1657-1666
INFO
29. Cardiogenic Shock: Therapy
• Optimise volume / oxygenation / rhythm
• Inotropic agents & vasopressors
b agonists
a agonists
PDE III inhibitors
LEVOSIMENDAN
• sensitizes myocardial contractile proteins to calcium
• independent of sympathetic NS and so NO increase in MVO2
• Prolonged action beyond infusion duration
• IABP
• PCI
INFO
30. Abdominal compartment syndrome
Increasingly recognised problem
LOOK for it! - don’t forget “medical” ICU patients
Thinks about screening if
Large volume resuscitation > 3.5 L in 24 hours
Abdominal Surgery/Primary Fascial Closure
Coagulopathy or polytransfusion
Pulmonary, renal or hepatic dysfunction
Acidosis
Hypothermia
Ileus
Physical exam is NOT accurate
INFO
31. Intra-abdominal pressure
INFO
Patient Intra-abdominal pressure
Normal adult 0-5 mmHg
Typical ICU patient 5-7 mmHg
Post-laparotomy patient 10-15 mmHg
Septic shock patient 15-25 mmHg
Acute abdomen 25-40 mmHg
Grade of IAH Pressure
Grade I 12-15 mmHg
Grade II 16-20 mmHg
Grade III 21-25 mmHg
Grade IV > 25 mmHg
Abdominal perfusion pressure = MAP - IAP (aim > 60 mmHg)
32. Abdominal Compartment
Syndrome
INFO
ACS = sustained IAP > 20 mmHg (with or without APP < 60
mmHg) that is associated with new organ dysfunction/failure
World Society of the Abdominal Compartment Syndrome (www.wsacs.org)
35. Case scenario 3
25 year old female, “fit and well”
Admitted to ICU after 6 day prodromal illness (fever, aches) followed by
confusion, shortness of breath and now fluid-resistant hypotension
Intubated in A&E as hypoxic and combative, received 3 L saline
On arrival ICU BP = 75/40, HR 135 SR, NA @ 0.7 mg/kg/min, lactate 7,
CVP 9, pO2 9 on 100% O2 with PEEP 7, creps bilaterally
Temperature 39.7, flushed
Over next 2 hours: NA increasing, lactate 9, U/O poor
Labs: Hb 10.5, Plts 65, WBC 27.9, Na 137, K 3.3, U 12.5 Creat 138,
APTT 47, PT 19, fibrinogen 1.0, CK 290
37. What is the differential diagnosis?
What are the possible sources?
What are the principles of management?
Describe your haemodynamic targets and approach
How do you make the diagnosis of ARDS?
What ventilator settings will you choose?
What principles guide your ventilation strategy?
What are your ventilator targets?
Questions for discussion
38. Sepsis: Know what you mean…
SIRS - 2 or more of the following
Temperature > 38 or < 36 o
C
Heart rate > 90 bpm
Respiratory rate > 20/min or pCO2 < 4.2 kPa
WBC > 12000/mm3 or < 4000/mm3 or > 10% bands
Sepsis
Systemic response to infection
SIRS + infection
Severe sepsis
Sepsis + organ dysfunction, hypotension or hypoperfusion
May be oliguria, encephalopathy or lactate rise
Septic shock
Sepsis induced SBP < 90 mmHg or SBP fall > 40 mmHg
PLUS hypoperfusion despite adequate fluid resuscitation
i.e. sepsis-induced hypotension requiring vasopressors
INFO
39. Principles of septic shock management
Initial resuscitation
Fluid resuscitation - ? EGDT (Rivers)
Diagnosis
Antibiotic therapy
Source identification and control
Haemodynamic and adjunctive therapy
Vasopressors and/or inotropes (know characteristics & pros and cons)
Steroids (know relative adrenal insufficiency principles)
rhAPC (know trials and controversies)
Other support
Blood products
Safe ventilation in ALI/ARDS (know ARDSNet etc.)
Sedation (know sedation breaks)
Glucose control (know controversies medical v surgical pts)
RRT
DVT prophylaxis
Stress ulcer prophylaxis (relationship to Cdiff?)
Limitation of therapy?
INFO
40. When septic shock isn’t just septic…
TOXIC SHOCK SYNDROME
Toxins act as “superantigens”
Activate up to 30% of neutrophils (normal <0.1%)
Cytokine storm => MSOF
Differences in treatment from “simple” septic shock
Prodromal illness…source can be subtle => LOOK HARD
Remember vaginal infections
Predominant organisms
S. aureus (often blood culture negative)
Menstrual and non-menstrual forms
May not have protective antibodies
Group A strep (majority blood culture positive)
Therapeutic principles
As for septic shock BUT
Toxin suppressing antimicrobial: clindamycin or linezolid
Immunoglobulin 1g/kg then 0.5 g/kg for 4-5 days
INFO
41. Q: Nutrition - how and why?
Your patient stabilises over the next 18-24 hours
She weighs 60 kg at baseline
She hasn’t eaten at home for 5 days
How are you going to support her nutrition?
What are her requirements?
How much do you give her today?
How do you manage “intolerance”
Why is nutrition important?
42. Nutrition Support/Therapy
INFO
When to feed = EARLY (< 36 hours) if possible
Support EN with TPN but EN preferred
Early nutrition decreases infection, hospital LOS and may
decrease mortality
CUMULATIVE ENERGY DEFICIT KILLS!!!!
> 10000 kcal deficit correlates with poor outcome
= 5 days off food in sepsis!!
every day in ICU without feeding is a day closer to death!
43. Nutrition Support/Therapy
INFO
Nutrition modulates stress response
Nutrition modulates systemic immunity
Gut surface area = tennis court!!
Exposure to and in harmony with trillions of organisms
GALT = gut associated lymphoid tissue - appropriate
exposure enhances systemic immunity
44. Nutrition Support/Therapy
INFO
No feeding + systemic illness = leaky gut (BAD)
Antibiotics = higher pH and less anaerobic flora (BAD)
Anaerobes produce substances which enhance immune
response (GOOD)
Fewer anaerobes = poor WBC function and more systemic
infection (BAD)
Leaky gut = bugs and cytokines (BAD)
GUT-LUNG conduit: bugs/cytokines via thoracic duct and
heart to pulmonary capillary bed => lung inflammation (BAD)
45. Nutrition Support/Therapy
INFO
Anaerobe levels Mortality Bacteraemia
Maintained 16% 6%
Low then recover 25% 50%
Persistently low 81% 75%
Short-chain fatty acids related to anaerobe levels
Short-chain fatty acids are colonocyte fuel
WBCs have receptors for SCFA = imprived function!
Attention to nutrition/antibiotics and pre/probiotics
46. What and how much?
INFO
Energy (kcal)
generally 25 kcal, up to 35 kcal/kg
start at 25-35% of requirement if refeeding syndrome risk
Protein
generally 1.25 g/kg
no need for < 1g/kg in acute liver disease
Lipids
? omega-3 FA’s in ARDS (favour anti-inflammatory eicosanoids)
Trace elements
selenium in sepsis?
Amino acids
arginine (vasodilatory)
glutamine (enterocyte fuel and ? better WBC function in trauma)