Acute renal failure short review with anaesthetic management

1. Dr Riyas A
Acute Renal failure Patho
physiology & anaesthetic
management

2. Definition
“Acute renal failure (ARF) or Acute kidney injury
(AKI) is characterised by deterioration of renal
functions over a period of hours to few days,
resulting in failure of the kidneys to excrete
nitrogenous waste product and to maintain fluid,
electrolytes and acid-base homeostasis”.
Harrison's Manual of Medicine,

3. Diagnostic Criteria's of ARF
Introduced by Acute Kidney Injury Network (AKIN)
1. Rapid time course (≤ 48 hrs)
2. Reduction in Kidney functions:
a) Rise in S.Creatinine- Absolute ↑ in S.Creatinine of
≥0.3mg/dl (≥ 26.4 μmol/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).
Harrison's Manual of Medicine,

4. Staging System of Acute Kidney Injury
Stage Serum Creatinine criteria Urine output criteria
1 Increase in s.creatinine of ≥0.3 mg/dl (≥26.4
μmol/l) or
increase to ≥150% to 200% (1.5- to 2fold) from
baseline
Less than 0.5 ml/kg/hr
for more than 6 hours
2 Increase in s.creatinine to more than 200% to
300% (> 2 to 3 fold) from baseline
Less than 0.5 ml/kg/hr
for more than 12
hours
3 Increase in s.creatinine to more than 300% (> 3
fold) from baseline (or s.creatinine of ≥4 mg/dl [≥
354 μmol/l] with an acute increase of at least 0.5
mg/dl [44 μmol/l])
Less than 0.3 ml/kg/hr
for 24 hours or anuria
for 12 hours

5. classification
 According to urine flow rates
 oliguric
 non oliguric
 Poly uric renal failure
 Major problem inability to maintain dynamic
balance b/w dietary intake of essential substance
and production of waste products

6. 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.

8. Prerenal Azotemia Renal Azotemia (Intrinsic) Postrenal (Obstructive)
Acute hemorrhage Acute glomerulonephritis
Upper urinary tract
obstruction (ureteral)
Gastrointestinal fluid
loss
Interstitial nephritis (drugs,
sepsis)
Lower urinary tract
obstruction (bladder outlet)
Trauma and Surgery Acute tubular necrosis
Burns Ischemia
Low output syndrome
Nephrotoxic drugs
(antibiotics)
Renal artery stenosis
Solvents (carbon
tetrachloride, ethylene
glycol)
Relative decrease Radiographic contrast dyes
Sepsis Myoglobinuria
Hepatic failure
Allergic reaction

9. Pre Renal Azotemia
 Most common type
 Designation for a rise in S.Cr, BUNdue to
inadequate renal plasma flow and hydrostatic
pressure

14. Intrinsic AKI
 Sepsis
 Ischemia

15. ischemia
 Post operative AKI
 Burns & acute pancreatitis
 d/s of micro vasculature leading to ischemia
 Nephrotoxin associated AKI

17. Nephrotoxin
 Contrast agents:m/c clinical course ,increase in
s.cr 24-48hrs,peaking with in 3-5 dys, resolving
with in 1 week
 Antibiotids
 Chemotherapeutic
 toxic ingestions
 Endogenous toxins

18. Contrast agents
 (1) hypoxia in the renal outer medulla due to
perturbations in renal microcirculation and
occlusion of small vessels;
 (2) cytotoxic damage to the tubules directly or via
the generation of oxygen free radicals, especially
since the concentration of the agent within the
tubule is markedly increased; and
 (3) transient tubule obstruction with precipitated
contrast material

19. contrast
 Prevention of radiocontrast nephropathy
depends on adequate hydration (e.g., 1 mL/kg
normal saline initiated at least 4 hours before
and continued for 12 hours after radiocontrast
administration)
 Elective surgical procedures should be
deferred until the effects of the dye have been
evaluated and treated.
 Nonionic, low-, or iso-osmolar radiocontrast
media are less nephrotoxic but are expensive
and offer optimal cost-benefit ratio when used
in high-risk situations only

20. Prevention of CONTRAST
 N acetyl cystein
 fendolopam

21. Antibiotics & chemotherapy
 Aminoglycosides andamphotericin B both cause
tubular necrosis
 Cisplatin and carboplatin are accumulated by
proximal tubular cells and cause necrosis and
apoptosis
 Ifosfamide may cause hemorrhagic cystitis and
tubular toxicity
 Antiangiogenesis agents such as bevacizumab,
can cause proteinuria and hypertension via injury
to the glomerular microvasculature (thrombotic
microangiopathy).

23. Intrinsic AKI

24. Post renal

26. Pre operative evaluation
 Most patient with ARF requiring surgery are
critically ill
 Optimal perioperative management
dependent on preoperative dialysis
 Preoperative dialysis on the day or previous
day of surgery
 Physial and lab examination depend up on
cardiac and pulmonary function
 Physical signs of fluid overload ,hypovolemia

27. Pre operative evaluation
 Pre ,current and post dialysis weight
 pre operative red blood cell transfusion
 Drug therapy should be carefully reviewed

28. Investigations & Diagnostic Tools
 CBC - Anemia
 BUN (10-20 mg/dl)
 S.Creatinine (0.6-1.3 mg/dl)
 Creatinine clearence (110-150 ml/min)
 Serum Electrolytes- HyperK⁺
 Urinalysis
 CXR
 ECG & ECHO
 ABG- Metabolic acidosis, hypoxemia,
 Imaging modalities

29. Urinary Indices
Index Pre-renal Causes Renal Causes
Urinary sodium concentration
(mEq/L)
<20 >40
Fractional excretion of sodium (%) <1 >1
Urine osmolarity (mOsm/L) >400 250–300
Urine creatinine/plasma
creatinine
>40 <20
Urine/plasma osmolarity >1.5 <1.1

30. Pre Anaesthetic Optimisation
 No specific treatment
 Symptomatic and supportive treatment- hypotension,
hypovolemia, low cardiac output state- maintenance of BP
 Treat underlying cause
 Correct fluids
 Diuretics
 Electrolytes and acid-base derangements
 Mannitol ??- pre ischemic insult, ↑PG-renal vasodilatation,
free radical scavenging, osmotic diuresis
 Low dose Dopamine??
 N-acetylcysteine- free radical scavenger, (600 mg orally
BD)
 Dialysis

31. Indication for dialysis
 Fluid overload
 Refractory GI symptoms
 Hyperkalemia
 Drug toxicity
 Severe acidosis
 Mb encephalopathy
 Pericarditis
 Coiagulopathy

32. Anaesthetic
Considerations

33. Anaesthetic Problems & Concerns
 Fluid homeostasis -Hypotension, hypovolemia, CHF, HTN,
pulmonary edema, hypoalbuminemia
 Electrolyte disturbances - Hyperkalemia, hypocalcemia
 Acid-base disturbances - Metabolic acidosis, hypoxemia
 Delayed gastric emptying - ↑Aspiration
 Arrhythmias, conduction blocks
 Neurological complications
 Dilutional Anemia
 Infections
 Effect on drug handling

34. Opioids
Morphine Conj. to M-3-G, M-6-G
, active metabolite, resp
depresion
Active metabolite has renal
elimination, 40% conj
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 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 Clearance not altered safe

35. Inhalation 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
stable & resists degradation by soda-lime & liver
No Neprotoxicity
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,after
prolonged use
Methoxyflurane Biotranformed to high inorganic fluoride levels Highly
nephretoxic

36. 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
Metabolism unchanged ,
↓ excretion,
Used in ↓ dose
Propofol Metabolised by liver No adverse effect
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

37. Local anaesthetics
 Dose reduction needed
 Respiratory or metabolic acidosis increases the
risks for CNS toxicity from local anesthetics
 Elevated PaCO2 enhances cerebral blood flow and
thus the anesthetic is delivered more rapidly to
the brain. In addition, diffusion of carbon dioxide
into neuronal cells decreases intracellular pH,
which facilitates conversion of the base form of
the drugs to the cationic form. The cationic form
does not diffuse well across the nerve membrane,
so ion trapping will occur, which will increase the
apparent CNS toxicity of local anesthetics

38. 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

39. Pre-Medication
 Reduced doses of an opioid or BZD,
 H2 blocker - Aspiration prophylaxis,
 Metoclopramide -10 mg for accelerating gastric
emptying, prevent vomiting, ↓risk of aspiration,
 Antihypertensive agents should be continued until the
time of surgery.

40. Induction
Patients are at increased risk of aspiration: rapid-sequence
induction with 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

41. Maintenance
 Ideal maintenance - control hypertension with minimal
effects on cardiac output,
 Controlled ventilation with cuffed endo-trachial tube should
be considered for patients with renal failure,
 Fluid therapy: D5W, isotonic crystalloids (lactated Ringer’s?,
NS), colloids, pRBC,
 Anaesthesia can be maintained with inhalation agents or
propofol with muscle relaxants ↓NM monitoring.

42. 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.

43. Post Operative
• Monitoring of fluid overload or hypovolemia titrated fluids,
• Residual neuromuscular blockade,
• Monitoring of urea and electrolytes,
• ECG monitoring for detecting cardiac dysrhythmias.
• Continue oxygen supplementation in post operative period,
• Analgesia with regional,
• Carefully titrated opioids, ↑CNS depression, respiratory depression
– naloxone.

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

45. summary
 Patients presenting for surgery with renal
insufficiency or failure present a significant
challenge for the anesthesiologis
 It is imperative that the anesthesiologist not only
understands the management of these complex
patients but also intervenes to prevent further
renal injury during the perioperative period.
 Judicious fluid management,the maintenance of
normovolemia, and avoidance of hypotension are
priorities for the successful prevention of further
renal injury

46. References
• Miller RD. Anesthesia. 7th ed. NY: Churchill
Livingstone Inc.; 2010. Anesthesia and the Renal and
Genitourinary Systems, 2105-2134.
• G.Edward morgan 4h edition,746-751
• Stoelting’s Anesthesia & Co-existing Disease, 5th ed.
Renal Disease,358-384.
• Harrison’s Principles of internal medicine, 18th ed.
Approach to a Patient with Renal Disease and Renal
Failure,2293-2299

47. Thank
you..