Principles of the anaesthetic management of

patient with renal failure

AIms
Define chronic & acute renal failure
Calculation of glomeral filtration rate
Anaesthetic considerations:
Pre-operative
Intra-operative
Post-operative

Chronic Kidney Disease

Presence for at least three months of either of the following
Structural or functional abnormality of kidney with or without
fall in GFR
GFR <60ml/ml/1.73m2

Glomerular filtration rate

Normal level of GFR varies with age, sex & physiological state
GFR estimated from urinary clearance of a filtration marker:
Endogenous: urea, creatinine
Exogenous: inulin
Cockcroft-Gault Equation
Creatinine clearance = (140-Age) x weight( 0.85 if female)/
(72xPcr)
MDRD study equation
GFR (mL/min/1.73 m2) = 175 (Scr)-1.154 (Age)-0.203 (0.742 if female)
(1.212 if African American)

Stages of Chronic Kidney Disease

(NKF,2003)
Stage

Description

GFR

Kidney Damage with normal GFR

>/=90

Kidney Damage with mild fall in GFR

60-89

3a

Moderate fall in GFR

45-59

3b

Moderate fall in GFR

30-44

Severe fall in GFR

15-29

Kidney Failure

<15

Acute kidney injury

1.Rapid time course ( 48 hrs)
2.Reduction in Kidney functions:
a) Rise in Creatinine- Absolute in S.Creatinine of
0.3mg/dl ( 26.4 mol/l) or a percentage in
S.Creatinine of 50% (1.5 fold from baseline).
b)

Reduction in urine output (documented oliguria of 0.5

ml/kg/hr for more than six hrs).

(from Acute Kidney Injury Network - AKIN)

Etiology and Pathophysiology

Divided into three major categories:
1. Prerenal ARF (~55%)- Diseases that cause renal
hypoperfusion, resulting in function without frank
parenchymal damage,
2. Renal or Intrinsic ARF (~40%)- Diseases that directly involve
the renal parenchyma,
3. Postrenal ARF (~5%)- Diseases associated with urinary tract
obstruction.

Anaesthetic considerations
Pre-operative optimisation
Risk stratification
Optimising the patient
Medication review
Specialist input

Peri-operative risk of AKI

Effect on drug handling

Protein bound drugs have increase free fraction due to hypoalbuminaemia and acidosis.
Lipid insoluble drugs excreted by kidney.
Hepatic metabolites of lipid soluble drugs are excreted by
kidney.
Uremia and metabolic acidosis changes structure and
function of drugs.

Specific drugs
Opioids:
Morphine metabolites renal excretion
Fentanyl/Alfentanil/Remifentanil no change in clearance

Inhalational agents:
Isofluorane/Sevofluorane contain nephrotoxic fluorine

IV agents:
Most will require a reduced dose

Muscle relaxants
Most will have a prolonged block in renal disease

Opioids
Morphine

Conj. to M-3-G, M-6- Active metabolite has

G , active
renal elimination, 40%
metabolite, resp
conj occurs in kidney
depresion

Dose
adjustment
required

Meperidine
(Pethidine)

Normeperidine, CNS Active metabolite has

toxicity
renal elimination

Dose
adjustment
required

Fentanyl

Plasma protein
binding, free drug

Clearance not altered

safe

Sufentanil

Plasma protein
binding, free drug

Clearance not altered

safe

Alfentanil

Initial vol of
distribution, free
drug

Clearance not altered

safe

Clearance not altered

safe

Remifentan No change
il

Volatile agents
Halothane

Inorganic fluoride levels are less

No
Neprotoxicity

Isoflurane

Inorganic fluoride levels are less

No
Neprotoxicity

Desflurane

Inorganic fluoride levels are very less, highly No

stable & resists degradation by soda-lime &
Neprotoxicity
liver

Sevoflurane

Inorganic fluoride levels are less but not

stable , degraded by soda-lime to compound
A & undergoes liver metabolism

Compound A is
neprotoxic

Enflurane

Biotranformed to inorganic fluoride levels

after prolonged use (> 4hrs)

Nephrotoxic,aft
er prolonged
use

Methoxyflurane Biotranformed to high inorganic fluoride

levels

Highly
nephretoxic

IV 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

Metabolism
unchanged ,
excretion,

Propofol

Metabolised by liver

No adverse effect

Etomidate

Metabolised by liver, partial renal

excretion

No adverse effect

Benzodiazepine
s

Metabolised in liver & excreted

by kidney, longer acting BZD
accumulate, duration of action

Interval or
dose

Used in dose

Muscle relaxants
Succinylcholin
e

Metabolised 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 Mild effect

elimination
Vecuronium

30% renal elimination

Prolonged duration

Rocuronium

Vol of distribution, No change in

clearence

Prolonged duration

Pancuronium

40-50%renal excretion, partly via less

Prolonged duration

Intraoperative management
Aim to maintain adequate renal perfusion:
Appropriate IV fluid replacement
Avoid nephrotoxic drugs
Maintain adequate MAP
?increased monitoring
Anticipation of anaesthetic & surgically induced
haemodynamic instability both intra- and post-operatively
Reversal:
Neostigmine has 50% renal excretion
Glycopyrolate has 80% renal excretion

Increased duration of block

Post-operative Management
Remain at risk of AKI
Due to hypovolaemia
Medications (NSAIDS)
Residual effects of anaesthesia

Ensure adequate fluid therapy

May be requirements for RRT

SUmmary
Renal disease is common
Management involves:
Good preoperative assessment
Simple measures reduce risk