crf

1. Anaesthetic consideration in a
patient with chronic renal
failure
MODERATOR – DR. NISHANT SOOD
PRESENTER- DR.JAVED

2. Why this is important…….
Unique Pathophysiology relating to both CRF and its underlying cause
Considerable advances in renal replacement therapy (RRT) and renal
transplantation mean that a greater number of these patients are
presenting for anaesthesia to assist vascular access procedures and renal
transplantation
As their survival increases they also present more frequently for surgery
unrelated to their renal disease
The aim of this presentation is to present the features of CRF that
influence the conduct of anaesthesia and to introduce some of the
anaesthetic techniques used for this group of patients

3. Renal blood flow ⸟20-25% of
CO 80% cortical nephrons,
20% medullary
Autoregulation of RBF @
MAP of 80-180 mm Hg
Physiological peculiarities

4. Physiology & Vulnerability
Kidneys exquisitely sensitive to hypoxic injury
medullary thick ascending limb have the highest O2
extraction ratio (80%)!
Intrinsic vasodilating Prostaglandin synthesis, imp.
mechanism during hypotension/ischemia
Reversible ↓ in RBF, GFR, urinary flow & Na+ excretion
occur with GA (& RA)

6. CRF
Chronic kidney disease is defined as kidney disease that has been
present for months to years.
CRF is the progressive, irreversible deterioration of renal function that
results from a wide variety of diseases.
Chronic renal disease (CRD/CKD), Chronic renal failure (CRF), and
Chronic renal insufficiency refer to the same condition.

8. ANAESTHESIA FOR PATIENTS
WITH CHRONIC RENAL FAILURE
CKD
Preoperative Evaluation
Pharmacologic
Considerations
Intra-operative
Considerations
Post-operative
Considerations

9. Definition of CKD
2002 National Kidney Foundation Kidney Disease
Outcomes Quality Initiative (K/DOQI) guidelines
proposed a 5 stage classification for CKD based on GFR
GFR < 60mL/min/1.73m2 for > 3 months where there is
evidence of kidney damage, or
Evidence of kidney damage for > 3 months based on
pathologic specimen, imaging or laboratory tests (e.g
proteinuria) irrespective of GFR

10. Chronic Kidney Disease-Stages
Stage Description GFR
(ml/min/1.73m2)
I CKD with normal GFR but other renal damage
(e.g. haematuria, proteinuria)
> 90
II Mild CKD and other kidney damage 60-89
III Moderate CKD 30-59
IV Severe CKD 15-29
V Established ESRF < 15 or on RRT

12. RIFLE criteria(Risk, Injury, Failure, Loss of kidney function, and ESKD)

13. Diabetesmellitusistheleadingcauseofend-stagerenal
disease(ESRD)followedcloselybysystemichypertension
Aetiology of CKD

14. Pathophysiology of CRF

15. Uraemia
Refers to the multitude of (uncorrected) effects resulting from
The inability to excrete products of metabolism of proteins and
amino acids
Impaired wide range of metabolic & endocrine functions of the
kidney
Usually seen when GFR <25mL/min
GFR <10mL/min is dependent on RTT for survival

16. CARDIOVASCULAR
SYSTEM
SYSTEMIC HYPERTENSION
•SODIUM AND WATERRETENSION
• ALTERED RENIN-
ANGIOTENSIN SECREATION
CHF
•PRIMARY: UREMIC CARDIOMYOPATHY
•SECONDARY: FLUID OVERLOAD
CAD
• ACELERATED ATHEROSCLEROSIS
UREMIC PERICARDITIS
CARDIAC TEMPONADE
CARDIAC DYSARRYTHEMIAS
•HYPERKALEMIA
•HYPOCALCEMIA

18. ANAEMIA(Hb: 6 – 8g/dL)
• Decreased EPO production
• GITblood loss
• Haemodilution
•BMsuppression (reccur. infxn)
PLA
TELETDYSFUNCTION
• Increasedbleeding time
• Consider when choosing
regional anaesthesia
LEUCOCYTEDYSFUNCTION
• Increasedsusceptibility infection
HYPERVENTILA
TION
•Mayrequire increased MVto
compensate for metabolic acidosis
INTERSTITIALOEDEMA
•Increasedalveolarto arterial
gradient  risk hypoxemia
ALVEOLAROEDEMA
•Permeability alv-capmembrane
PLEURALEFFUSION

19. CRF
NEURO
LOGICAL
ENDOC
RINE
META
BOLIC
GASTRO
INTESTINAL
GLUCOSEINTOLERANCE
•Peripheralinsulin resistance
SECONDARY
HYPERPARA
THYROIDISM
• Metabolicbone disease
•Osteopeniapredispose to #
HYPERTRIGL
YCERIDAEMIA
•Acceleratedatherosclerosis
PERIPHERALNEUROPA
THY&
AUTONOMICNEUROPA
THY
• Delayedgastric emptying
• Postural hypotension
•Silent MyocardialIschaemia
DIAL
YSISPA
TIENTS
• Dialysisdementia
• Dysequilibrium syndrome
ANOREXIA&N/V (malnutrition)
DELA
YEDGASTRICEMPTYING(RSI)
HYPERACIDITY(PPI)
MUCOSALULCERA
TIONS
(urea mucosalirritant)
HAEMORRHAGE
ADYNAMICILEUS
ACIDOSIS
• Lessclearance H+ andHighAG-MA
FLUID&ELECTROLYTE abn.
• Hyperkalaemia–acidosis(avoid
hypercarbiain GA)
• Sodiumbalance–diuretic use
andcardiac function
Ca2+ &PO42- Derangement

20. DIALYSIS RELATED
PROBLEMS
DIALYSIS DEMENTIA
DIALYSIS DISEQUILIBRIUM
SYNDROME
HYPOVOLEMIA
PERITONITIS
SYSTEMIC ANTICOUGULATION

21. Anaemia
Platelet dysfunction
Coronary artery disease
Metabolic acidosis
Hypervolemia/CHF
Electrolyte imbalance
Hypertension
Neuropathy
Gastroparesis
Key Peri-operative issues

22. Anaemia
CAUSES:
• Chronic blood loss
• Hemolysis
• Marrow supression by uremic
factors
• Reduced erythropoetin
production
• Chronic infection
• Bone marrow fibrosis due to
hyperparathyroidism
Anaesthetic Implications:
•Decreased oxygen delivery
•Increased cardiac output
•Cardiac enlargement
•Angina
•CHF
•Impaired mental acquity
•Impaired host defense against
infection
Erythropoetin therapy – target
hematocrit 36 –40%
Intraoperative transfusion –
packed cells, for hypotension, hct
< 18%
Patients with ESRD on
hemodialysis require Hb levels
11-12 g/dl

23. Hypertension
> 100
Threshold for initializing treatment for  BP
 SBP ≥ 140, DBP ≥ 90 or both
 SBP ≥130, DBP ≥80 or both if urine protein to Creatinine ratio is
mg/mmol and diabetic patient
BP of <130/80 mm Hg is required for optimal control
In patients with proteinuria ≥ 1gm/24 hrs, target of <125/75 mmHg is
needed

24. Coagulation abnormality
CAUSES:
•Decreased platelet factor III
•Abnormal platelet aggregation &
adhesion
•Impaired prothrombin consumption
Anaesthetic Implications:
•Regional anaesthesia:
Weigh the risk vs benefit of
epidural placement in
uremic patients
Thromboembolic complications
CAUSES:
•Urinary loss of antithrombin
•Decreased levels of protein C and S
•Hyperfibrinogenemia
•Impaired fibrinolysis
•Increased platelet aggregability
Seen in patients with
nephrotic syndrome

25. Hyperkalemia
Serum potassium > 5.5 mEq/L
Impaired renal excretion in CRF
Peri-operative aggravating factors:
• Hemolysis
• Hemorrhage
• Massive blood transfusion
• Metabolic acidosis (every 0.1 unit change in blood pH  increase K+
by 0.6 mEq/L
• Rhabdomyolysis
• Succinylcholine
• Beta blockers, ACE inhibitors

26. Treatment of Hyperkalemia
Antagonism of membrane effects ofhyperkalemia
Calcium gluconate –
- 10 ml of10%solution over5-10 min
- Dosecanbe repeated ifno changeinECG after 5-10 min
- decreasesmembrane excitability
- Canexacerbate digitalisinducedarrythmia  calciumgluconategiven
in 100 ml D5%over20-30 min.
Potassium movement into thecells
Insulin and glucose –
- 25 to 50 gramglucosewith 10-20 units ofregular insulin@ 100 ml/hr
- Insulinshiftspotassiuminto the cells
- Onset in 15 min, peakin 60 min, duration 4-6 hr.
- Decreasespotassiumlevelsby0.5 to 1.5mEq/L

27. Potassium movement into thecells
Beta adrenergic agonists
- 20 mgin 4ml salinenebulisationover10 min/ 0.5 mgiv
- shiftspotassiuminto the cells
- Onset in30-60 min, duration 2-4 hr.
- Decreasespotassiumlevelsby0.5 to 1.5mEq/L
Others
Loop diuretics
- Furosemide20-40 mg iv
Sodium bicarbonate infusion-
- Mostusefulin metabolicacidosiswith hyperkalemia
- Watchfor sodiumoverloadandvolumeexpansionin CRF

28. Preoperative Evaluation

29. Preoperative Evaluation
Multidisciplinary approach involving anaesthetists, surgeons and
renal physicians
Optimise medical condition & address potentially reversible
manifestations of uraemia
Cardiorenal syndrome* & Cardiovascular Risk
Renal Risk Assessment and Interventions
Dialysis and Renal Transplant Patients
* Pathophysiological disorder of the heart and kidneys wherein the acute or chronic
deterioration of one organ results in acute or chronic deterioration of the other.
• Cardiovascular risk assessment according to ACC/AHAguidelines

30. Clinical History
History related to
present surgical
condition
History related to kidney
disease:
Cause
Duration
Treatment
Dialysis/ICU or hospital
admission

31. Signs + Symptoms
•Nausea
•Vomiting
•Loss of appetite and weight loss
•Fatigue and weakness
•Insomnia
•Changes in urine output
(polyuria  oliguria)
•Decreased mental sharpness
•Seizures
•Muscle twitches and cramps
•Peripheral oedema
•Persistent itching/Jaundice
•Hiccups
•Chest pain
•Shortness of breath
•High blood pressure
•Increased blood urea nitrogen
(BUN) and Creatinine
•Anaemia
•Neuropathy
•Erectile dysfunction (in men)
•Abnormal hemostasis

32. • Past History-
H/o Co-morbid conditions :
Hypertension , Diabetes, HIV, Polycystic kidney
disease, obstructive uropathy
Onset
Progression
Treatment – drugs, compliance, control
Complications
• Time since last dialysis :
 last dialysis :12-24 hrs prior
 Post dialysis status
 Dialysis related complications

33. Basic outline of the“PreOp”
History & Physical Examination
-CVS & Respiratory system evaluation (?? Fluid overload)
Sugar Charting
Basic bloods
-FBC (Hb), BU/SE (postdialysis), INR/PTT (platelet dysfunction
in uraemia – count may be normal)
CXR (clinical impression)
ABG
-Acid-Base status (Resp. distress);oxygenation; ventilation
ECG/Echo
Blood transfusion – only in severe (symptomatic) anaemia
Consider AnaestheticTechnique

34. Renal Risk Assessment &Interventions
(non-dialysis pt)
Detailed Background History
Co-morbidities
Duration CKD
Usual fluid intake
Usual daily urine output
Renal function (baseline & current)
Urea & Creatinine
GFR
Electrolyte concentrations
Na
K

35. Renal Risk Assessment and
Interventions cont….
• Euvolaemic,
• Responsive to diuretic therapy with,
• No significant electrolyte abnormalities and
• No bleeding tendencies
Uncomplicated
cases
• Oedema, CHF, Pulmonary congestion ± responsive to
diuretic therapy  cardiovascular evaluation
• If Cardiovascular evaluation OPTIMAL – fluid
overload can be attributed to CKD
• Consider combination diuretics to achieve euvolaemia
prior to surgery
Complicated
cases
• Poorly controlled Diabetes – greater
tendency to volume overload or
cardiovascular disease
• Advanced CKD with diuretic resistance and
progressive oedema
Consider
preoperative
dialysis

36. Indication of dialysis
Worsening clinical state
Overhydrated state (CHF, HTN, wt. )
Neurological s/s – uremic encephalopathy
Pericarditis
Bleeding tendency
Biochemical
rising trends
↑ K+ > 0.5 meq / l / day
↑ creatinine > 1 mg % / day
↑ BUN > 20 mg % / day
Blood urea > 200 mg%, Creat > 10 mg %, K+ > 7 meq /l

37. Dialysis and Renal TransplantPatients
Extra Considerations
1. Dialysis adequacy
2. Preoperative dialysis needs
last dialysis should finish atleast 12-24 hrs prior to Surgery
within 24 hrs of surgery-
Fluid depletion & redistribution, electrolyte disturbances & residual
anticoagulation from heparinisation
Post dialysis BU/SE prior surgery –intraoperative cardiac dysrythmias
Postoperative dialysis timing
Dosage requirements for all medications

38. Pharmacology
In patients with CKD, the effect of altered clearance,
the production and accumulation of active metabolites,
and the risk of aggravating pre-existing kidney disease
on drug administration must be considered.
Dose adjustment is not usually necessary until the GFR
is <50 ml/min/1.73 m2

39. Pharmacokinetics
Absorption - affected by delayed gastric emptying
Distribution – volume of distribution is increased or
decreased depending on total body water,
protein binding & time since last dialysis
Elimination – prolonged half life for drugs with renal
elimination. eg. Vecuronium

40. Local Anaesthetics
 L.A. have two plasma protein binding sites: a high affinity,
low capacity site on AAG (α1-acid glycoprotein) and a low
affinity, high capacity site on albumin.
 The albumin binding site becomes increasingly important as
the plasma concentration of the local anaesthetic increases.
 Metabolic acidosis increases the percentage of unbound drug
and this effect is more pronounced with bupivacaine.
 Dose to be decreased by 25% to compensate for decreased
protein binding.

41. Inhalation Agents
“All inhalation agents bio-transformed to non-volatile
products of metabolism which are eliminated by kidney ,
but reversal of CNS effect depends upon pulmonary
excretion”.
All inhalation agents causes transient reversible ↓ of GFR,
RBF, U/O, renal auto regulation.
Miller RD. Anesthesia. 7th ed., Anesthesia and the renal and
genitourinary systems, page 2113.

42. Inhalation Agents
Halothane Inorganic fluoride levels are less:1-2 μM/L No Nephrotoxicity
Isoflurane Inorganic fluoride levels are less: 3-5 μM/L No Nephrotoxicity
Desflurane Inorganic fluoride levels are very less, <1 μM/L
after 1MAC-hr; highly stable & resists
degradation by soda-lime & liver
No Nephrotoxicity
Sevoflurane Inorganic fluoride levels are less but not stable ,
50 μM/L prolonged use; degraded by soda-
lime to compound A & undergoes liver
metabolism
Compound A is
nephrotoxic
Enflurane Biotransformed to inorganic fluoride levels after
prolonged use (> 4hrs)
Nephrotoxic after
prolonged use
Methoxyflurane Biotransformed to high inorganic fluoride levels Highly nephrotoxic

43. Intravenous Agents
Thiopentone CNS effect reversed by redistribution &
hepatic metabolism, also 80% protein bound,
↓albumin in uremia ↑ free drug, more free
un-ionised drug in acidosis, also ↑ Vd
•Metabol. unchanged ,
•Rate of admin.
should be slow
•Used in ↓ dose
(↓ protein binding)
Propofol ↑ Vd but clearance & t1/2 unaltered,
Metabolized by liver
No adverse effect, time
taken to awake after
infusion ↓
Etomidate Metabolised by liver, partial renal excretion No adverse effect
Benzodiazepines Metabolised in liver & excreted by kidney,
Longer acting BZD accumulate,
↑ duration of action
↑ Interval or ↓ dose
Ketamine Pharmacokinetics minimally changed
Hepatic metabolites may depend on
renal excretion and can potentially
accumulate
Used in↓ dose

44. Muscle Relaxants
Succinylcholine Metabolised by psedocholinesterase to non toxic
products which are excreted by kidney,
↑ duration in ESRD, also ↓ psedocholinesterase
in uremia, Associated with rapid transient ↑K⁺
(0.5mEq/L)
Longer block in ESRD
& uremia,
Cautiously used in
hyperkalemia
Atracurium Degraded by enzymatic ester hydrolysis & non
enzymatic alkaline degradation (Hoffmann
elimination) to inactive products
Not dependent on renal
elimination
Mivacurium Metabolised by plasma psedocholinesterase Longer block in ESRD
Cis-atracurium 77% hoffmann elimination & 16% renal
elimination
Mild effect
Vecuronium 30% renal elimination Prolonged duration
Rocuronium ↑Vol of distribution,
30% renal elimination ,No change in clearance
Prolonged duration
Pancuronium 40-50% renal excretion, partly via less active
3-OH pancuronium- renal excretion
Prolonged duration

45. CLINICAL IMPLICATIONS IN CRFPATIENTS
IncreasedVolume
of distribution
Larger initial dose to
produce NM blockade
Reduced metabolism
and
Excretion of drugs
Reduce
maintenance dose
Avoid long acting
NMBs
Neuro-muscular
monitoring
In general, the initial dose required to produce neuromuscular block is larger in patients
with CKD than in normal subjects.
But, with the exception of atracurium and cisatracurium, the dose required to maintain
block is reduced

46. Reversal Agents
Neostigmine clearance is reduced (50% renal) and its T1/2 is
prolonged (80 min. in normal vs. 180 min in CKD)
This may result in a para-sympathomimetic response, including
bradycardia and AV block, especially when used in combination
with atropine rather than the longer-acting glycopyrrolate.
Prolonged duration of action prevents recurarisation
Sugammadex is helpful in preventing PORC .
It has got fewer side effects.

47. Analgesic agents
In administering analgesic agents, the anaesthetist
needs to consider:
The impact of renal impairment on the distribution
and elimination of the parent compound and hence
the need for adjusting the dose or dose interval;
The formation of active metabolites; And the risk of
compromising residual renal function.
Analgesic nephropathy is mainly associated with
prolonged use of compound analgesics containing
two antipyretic agents with caffeine or codeine.

48. Prolonged use of Acetaminophen (≥40 mg/kg/day) is
associated with analgesic nephropathy, but occasional or
moderate use is safe and does not require dose adjustment
even in perioperative period.
NSAIDS: They exacerbate hypertension and precipitate
oedema, hyponatraemia, and hyperkalaemia. There is an
increased risk of GI bleeding, cardiovascular complications
in this at risk population. They precipitate an acute decrease
in GFR and may also cause acute interstitial nephritis .
The renal effects of the COX-2 inhibitors (rofecoxib) are
similar to those of the non-selective NSAIDs and hence
outweigh any potential benefit in perioperative period.

50. Opioids
Opioids have no direct toxic effects on the kidney.
They do, however, have an antidiuretic effect, and they may
cause urinary retention.
1. Tramadol: 30 % of tramadol is excreted unchanged in the
urine. O-Demethyl tramadol is an active metabolite which is
excreted by the kidneys. Uraemia is associated with a
lowered seizure threshold, and tramadol may be
epileptogenic in these circumstances.
2. Codeine and dihydrocodeine are also best avoided as their
elimination half-life is significantly prolonged, and
conventional doses have resulted in central nervous system
depression.

51. Opioids
Morphine Conj. to M-3-G, M-6-G ,
active metabolite, resp
depresion
Active metabolite has renal
elimination, 40% conjugat
occurs in kidney
Dose adjustment
required
Meperidine
(Pethidine)
Normeperidine, CNS
toxicity
Active metabolite has renal
elimination
Dose adjustment
required
Fentanyl ↓ Plasma protein
binding,↑ free drug
Clearance not altered (7%
renal metabolism)
safe
Sufentanil ↓ Plasma protein
binding,↑ free drug
Clearance not altered safe
Alfentanil ↓ Initial vol of
distribution,↑ free drug
Clearance not altered safe
Remifentanil No change
(ester hydrolysis )
Clearance not altered safe

52. Others
PHENOTHIAZINES
(chlorpromazine)
Pharmacokinetics minimally altered but potentiation of
central depressant effect can occur
H2 RECEPTOR
BLOCKERS
Depend on renal excretion
Dose reduction required
PPI Dose adjustment not required
METOCLOPRAMIDE Accumulates in kidney failure
ONDANSETRON
/DOLASETRON
Dose adjustment not required
NSAIDS Avoid in kidney disease
LOCAL
ANAESTHETICS
Decreased duration of action
Maximum dose to be decreased by 25% due to decreased
protein binding and lower CNS seizure threshold

53. Drugs Drugs safe Drugs safe in
limited or
reduced doses
Drugs
contraindicated
Premedication
Midazolam, Temazepam Diazepam
Induction Thiopental, Propofol,
Ethiomedate
Ketamine
Maintenance
Isoflurane, Desofluarne,
Halothane, Propofol Sevoflurane
Enflurane,
Methoxyflurane
Muscle Relaxants Sch*,Atracurium,
Cistracurim
Vecuronium,
Rocuronium Pancuronium
Opioids Alfentanil, Remifentanil,
Sufentanil
Fentanyl, Morphine
Pethidine, Tramadol
Local Anaesthetic Bupivicaine, Lidocaine
Analgesic
Paracetamol
Opioids
NSAIDS

54. Choice of Anaesthesia
Regional anesthesia : Neuraxial anesthesia may be considered in CKD patients
A sympathetic blockade of T4 to T10 levels may theoretically improverenal
perfusion by attenuating catecholamine induced renal vasoconstriction and
suppressing the surgical stress response.
Adequacy of coagulation should be considered and the presence of uremic
neuropathies must be excluded before regional anesthesia.
Onset of sensory block faster:
 Acidosis increased free fraction;&
 Reduced volume of epidural space due to distension of epidural and spinal veins by hyper
dynamic circulation
Duration of sensory & motor blocks shorter by 20%:
 Increased cardiac output causes faster washout of local anesthetic from its site of
action

55. Choice of Anaesthesia
Platelet dysfunction and the effects of residual heparin in patients receiving
hemodialysis must also be considered.
PT/INR >1.4 is a contraindication
Brachial plexus blockade is useful for placing the vascular shunts necessary
for long-term hemodialysis.
 In addition to providing analgesia, this form of regional anesthesia abolishes
vasospasm and produces vasodilation that facilitates the surgical procedure.
Intra-operative Blocks:
 TAPblock
 Quadratus Lumboram Block
Latest interest: Buprenorphine patch
Co-existing metabolic acidosis may decrease the threshold for
seizure in response to local anesthetics

56. Intra-operative considerations: CKD
• Risk thrombosis – BP cuff not on arm withAV
fistula
• Continuous intra-arterial BP in uncontrolled HT
Monitoring
• RSI in patient with N&V or GI bleed
• Induction dose adjustment
Induction
• Control BP with minimal deleterious effect on CO
• Ventilation control to avoid respiratory acidosis and
alkalosis
• Hypercarbia may exacerbate existing acidaemia 
circulatory depression & increase in serum potassium
Anaesthesia
maintenance
• Replace insensible losses in superficial/minor operations
• Procedures associated with major fluid losses
• Isotonic crystalloids, colloids or both
• Ringers Lactate contains potassium  Hyperkalaemic patients
• Blood transfusions only as indicated
Fluid therapy

57. Monitoring
All routine monitoring – ECG, NIBP, SpO₂, EtCO₂, NM
monitoring
Monitoring urinary output and intravascular volume
(desirable urinary output: 0.5 ml/kg/hr)
Intra-arterial, central venous, pulmonary artery monitoring
are often indicated
Intra-arterial blood pressure monitoring in poorly
controlled hypertensive patients

58. Associated Concerns
Patients are at increased risk of aspiration: rapid-sequence
induction with cricoid pressure.
Attention to patient positioning on the operating room table is
important.
Poor nutritional status renders the skin particularly prone to
bruising and sloughing, and extra padding is required to protect
vulnerable nerves around the elbows, knees, and ankles.

59. Associated Concerns
Fistulas must be protected at all costs and be well
padded to prevent pressure injury.
Blood pressure cuffs should not be applied to the
arm with the fistula.
If at all possible, the arm with the fistula should
not be tucked but should be positioned so that the
fistula thrill can be checked periodically
throughout surgery.

60. Induction
Patients are at increased risk of aspiration: Rapid-sequence
inductionwith cricoid pressure.
Drugs Normal Dosages Altered Dosages
Thiopental 3-5 mg/kg 2-3 mg/kg
Propofol 1-2 mg/kg 1-2 mg/kg
Etomidate 0.2-0.4 mg/kg 0.2-0.4 mg/kg
Succinylcholine 1-2 mg/kg 0.5-1.5 mg/kg
Atracurium 0.6 mg/kg 0.6 mg/kg
Cisatracurium 0.15 mg/kg 0.15 mg/kg

61. Maintenance
Ideal maintenance - control hypertension with minimal
effects on cardiac output,
Controlled ventilation with cuffed endo-tracheal tube
should be considered for patients with renal failure,
Anaesthesia can be maintained with inhalation agents
or propofol with muscle relaxants ↓ NM monitoring.

62. Fluid Management
Appropriate fluid resuscitation must be given to any patients with signs of dehydration
pre-operatively to avoid excessive hypotension at induction of anaesthesia.
Avoid high molecular weight and/or highly substituted HES
Medium molecular weight starches (HES 200/0.5, 130/0.4) are easily renally excreted
Maintain Urine output to 0.5ml/kg/hr
RL to be avoided in hyperkalemic Patients (RL = k+ 4 mEq/L)
0.9% saline causes: (Potura etal. 2015 A &A)
– Hyperchloremia
– More patient required catcholamine
Ideal fluid: Mixture of saline & RL
SuperficialOp, minimumtissueTrauma 5%Dextrose inwater
Maintenance 30%ofthe calculated fluid rate
3rd spaceloss BalancedSalt Solution
Bloodloss replace with colloidor PRBC

63. Reversal
Neuro-muscular blockage is reversed with Neostigmine or
pyridostgmine in combination with anticholenergic.
Neostigmine and pyridostgmine has 50% & 70% renal elimination
respectively.
Glycopyrolate has 80% renal excretion so should be used cautiously.
Atropine undergoes 25% renal elimination and rest hepatic
metabolism to form metabolite noratropine which has renal excretion.
Extubation should be done after complete reversal of NM blockage.

64. Postoperative management
Admission to ICU may be suitable for patients with
significant comorbidities and after major surgeries
Post op cardiac assessment must be performed and continued
for 3-5 days with daily ECGs and screening of cardiac
enzymes to detect and treat perioperative MI which most
frequently occurs within 72 hrs and are often silent yet quite
fatal.
HD should be ideally delayed till the risk of fluid shifts and
hemorrhage has fallen ( some suggest at least 24 hrs )
Avoid nephrotoxic drugs
Consider maintaining tight glycemic control in all patients

65. Postoperative management
Close attention to fluid electrolyte balance. CVP to be kept
between 10-12 cm of H2O
Multimodal analgesia : PCM is safe and effective . Intraoperative
LA infiltration is simplest and easiest but often inadequate and
with finite duration.
Medications for HTN, IHD etc should be re established to pre
operative normalcy as soon as possible.
For abdominal surgery patients placing feeding tubes facilitate
drug administration even in presence of reduced gastric emptying
Continuation of supplemental O2 into the postoperative period
(anemia)
Immune Suppression with transplants – postoperative sepsis
risk increase

66. Renal Protection:Pharmacological
Interventions
Dopamine
Volume management by increasing UO
Evidence does not support “renal protective effect”
Loop Diuretics – Furosemide
Used to preserve intraoperative UO – high doses in ARF reduce need for dialysis (no improvement in mortality)
“Protective effect” only demonstrated in rodent models
Osmotic Diuretic Mannitol
Old data in kidney transplants – impaired renal perfusion with goal of renal protection and maintenance of
adequate UO
Recent randomised trial failed to show protective benefit patients undergoing major vascular surgery
ACE inhibitors
No data to support benefit
CCB’s
Data insufficient to support benefit
N -Acetyl Cysteine
Prevention of contrast nephropathy (high risk in CKD)
Combination with adequate hydration
Data fails to show benefit when used as renoprotective agent during major surgery

70. Optimisation of patient’s other co-morbidities in the
preoperative period, closeintra-op monitoring, optimal
fluid status as well as appropriate use of anaesthetic
agents are the key to successfulanaesthetic management
of CKD patients.