MODUL R3

CKD
CKD
 Incidence of ESRD (aka CRF) increasing worldwide – in USA
prevalence of ESRD more than doubled between 1990 and 2001
 4 –Year survival for ESRD patients in UK only 48%
 Approximately 26 million Americans have some form of CKD
(pre-dialysis kidney disease) and many remain undiagnosed
 The CKD patient population fits the “2nd hit injury” paradigm
because they have some stable chronic baseline organ dysfunction
that is disproportionately worsened when exposed to acute
physiologic stress such as hypotension, hypovolaemia, or drug
toxicity
Definition 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
RIFLE criteria
Aetiology of CKD

Diabetic Hypertensive Glomerular

Nephropathy Nephrosclerosis Disease

Interstitial Vascular Inherited

Diseases of the Diseases of the Kidney
Kidney Kidney Diseases
Pathophysiology of CRF
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
 Basic outline of the “Premed”
 History & Physical Examination
 CVS & Respiratory system evaluation ?? Fluid overload
 diabetic patients
 Basic bloods
 (Hb), 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 Anaesthetic Technique
Cardiorenal Syndrome

 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
 Classified into 5 types
 Cardiovascular Risk
 High prevalence of cardiovascular disease and increased perioperative
morbidity
 Cardiovascular risk assessment according to ACC/AHA guidelines
 Surgical risk for noncardiac procedures
 Major risk factors (before elective surgery)
 Risk profile for surgery
 Risk with intended procedure
 Decompensated HF or unstable coronary syndromes  postpone procedure until
medical management optimised
 Intermediate/Minor risk factors (before elective noncardiac surgery)
 Functional capacity (METs- metabolic equivalents or tasks)
 Self-reported/treadmill testing
 6 METs – better prognosis; good functional capacity – proceed to surgery
 Poor functional capacity – investigate and optimise prior surgery
 Type of surgery
 Intraoperative considerations:
Kidney Failure
 Monitoring
 Risk thrombosis – BP cuff not on arm with AV fistula
 Continuous intraarterial BP in uncontrolled HPT
 Induction
 RSI in patient GI bleed
 Induction dose adjustment
 Anaesthesia maintenance
 Control BP with minimal deleterious effect on CO
 Volatile agents, propofol & opioids (NB morphine effect prolonged)
 Ventilation control to avoid respiratory acidosis and alkalosis
 Hypercarbia may exacerbate existing acidaemia  circulatory depression & increase in
serum potassium
 Fluid therapy
 Replace insensible losses in superficial operations involving minimal tissue trauma
 Procedures associated with major fluid losses
 Isotonic crystalloids, colloids or both
 Ringers Lactate contains potassium  NB Hyperkalaemic patients
 Bloodtransfusions only as indicated
Postoperative Considerations
 Emergency surgery
 Postoperative cardiac assesssment
 Lack preoperative evaluation
 Diagnosis of postoperative MI should be based on combination of clinical,
laboratory & ECG evidence
 Environment
 Normal ward
 High Care/ICU
 Analgesia
 Regional anaesthesia reduces requirement for systemic analgesic drugs
 Epidurals potentially reduced incidence of postop respiratory complications and
VTE events
 Systemic anaglesia
 WHO pain ladder
 PO vs IMI vs PCA (IV)
 Immune Suppression with transplants – postoperative sepsis risk increase
 Pharmacological Considerations
 INTRAVENOUS AGENTS
 Induction Agents
 Muscle Relaxants
 Reversal Agents
 Benzodiazepines
 Opioids
 INHALATION AGENTS
 Volatile Agents
 Nitrous Oxide
 OTHER
 Induction Agents
PROPOFOL & Pharmacokinetics minimally affected and
ETOMIDATE pharmacodynamics unchanged
Changes in volume distribution and mental state
Decreased induction dose required

BARBITURATES Pharmacokinetics unchanged but

Increased sensitivity dt increased free circulating barbiturates
(decreased protein binding) and acidosis increases entry into brain
by increasing nonionised fraction

KETAMINE Pharmacokinetics minimally changed

Hepatic metabolites may depend on renal excretion and can
potentially accumulate
Muscle Relaxants
SUCCINYLCHOLINE Safe if HYPERKALAEMIA absent
CISATRACURIUM & DRUG OF CHOICE; plasma ester hydrolysis, nonenzymatic
ATRACURIUM Hoffman elimination
VECURONIUM Primary hepatic metabolism, 20% eliminated by kidneys. If use
>0,1mg/kg dose prolonged effect
ROCURONIUM Hepatic elimination but prolonged action in kidney disease
reported. Can be used if appropriate NM monitoring available
PANCURONIUM 60 – 90% dependant on renal excretion

Reversal Agents
NEOSTIGMINE Renal excretion. Halflife prolonged. Inadequate reversal
often related to other effects (“recurarizaton’)
ATROPINE & Safe for use.
GLYCOPYROLLATE Repeated doses potential for accumulation (50% drug excreted in
urine)
 Opioids
MORPHINE Active metabolites (morphine-6-glucoronide) may have
greater activity than parent drug and may accumulate
Start at lower suggested dosage and titrate dosage
upwards slowly and increase dose intervals
FENTANYL Inactivated by liver and excreted by urine
REMIFENTANYL Significant accumulation does not occur
ALFENTANYL No active metabolites

Benzodiazepines
MIDAZOLAM & Hepatic metabolism with urine elimination
DIAZEPAM Active metabolites accumulate
Protein bound ; increased sensitivity in
hypoalbuminaemic patients
Dose reduction 30 – 50%
Inhalation Agents

 Not dependent on renal function

 Sevoflurane and Enflurane may produce nephrotoxic fluoride
ions
 Some physicians avoid use in lengthy procedures
 Other
PHENOTHIAZINES Pharmacokinetics minimally altered but potentiation of
central depressant effect can occur
H2 RECEPTOR Depend on renal excretion
BLOCKERS Dose reduction required
PPI Dose adjustment not required
METOCLOPRAMIDE Accumulates in kidney failure
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
Renal Protection: Pharmacological
Interventions
 Dopamine
 Volume management by increasingUO
 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
TERIMA KASIH