ANAESTHETIC MANAGEMENT OF THE PATIENT WITH ACUTE RENAL FAILURE FOR NON-RENAL SURGERY OF URGENT NATURE

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ANAESTHETIC MANAGEMENT OF THE PATIENT WITH ACUTE
RENAL FAILURE FOR NON-RENAL SURGERY OF URGENT
NATURE
University College of Medical Sciences GTB
Hospital, Delhi
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Clinical Scenario

• A 22yrs Male presented to ED with P/C of
• Fever from past 8 days
• Vomiting for 4 days
• Pain in abdomen for 4 days
• Distension of abdomen for 4 days
• No passage of flatus and feces 4 days
• O/E
• PR - 130 bpm,
• BP - 100/68 mmHg,
• Chest CVS WNL,
• Abdo Distended abdomen with generalised
  tenderness and absent bowel sounds.

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Cont..

• Investigations
• Hb- 12gm, RBS- 98 mg/dl,
• TLC- 14,000, BU- 85 mg/dl,
• Plt- 90,000, S.Creat- 2.2
  mg/dl,
• S.E- 135/3.5 mEq/L,
• Urine Output- 700 ml in last 24 hrs out of this
  only 200ml in last 12 hrs.
• Diagnosis Acute Peritonitis
• Plan Exploratory Laparotomy on emergency basis

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Defination

• 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, Approach to a
  patient with renal disease, page 785

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Diagnostic Criteria's of ARF

• Introduced by Acute Kidney Injury Network (AKIN)
• Rapid time course ( 48 hrs)
• Reduction in Kidney functions
• 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).
• Reduction in urine output (documented oliguria of
  0.5 ml/kg/hr for more than six hrs).
• Harrison's Manual of Medicine, 17 ed., Renal
  Failure, chapter 146, page 789

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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 (gt 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 (gt 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
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Etiology and Pathophysiology

• Divided into three major categories
• Prerenal ARF (55)- Diseases that cause renal
  hypoperfusion, resulting in ? function without
  frank parenchymal damage,
• Renal or Intrinsic ARF (40)- Diseases that
  directly involve the renal parenchyma,
• Postrenal ARF (5)- Diseases associated with
  urinary tract obstruction.
• Klahr S, Miller SB Acute oliguria. N Engl J Med
  1998338671675
• Thadhani R, Pascual M, Bonventre JV Acute renal
  failure. N Engl J Med 199633411481169.

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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
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Clinical Presentation Complications

• GIT Anorexia, nausea, vomiting, adynamic ileus,
  peptic ulcer, hemorrhage, delayed gastric
  emptying (due to autonomic neuropathy)
  aspiration,
• CVS CHF and pulm edema, HTN,LVH, conduction
  blocks, arrhythmias, pericarditis. (Sodium
  retention, fluid overload),
• Pulmonary Hyperventilation, interstitial edema,
  hypoxemia,
• Hematological Anemia, platelet and leukocyte
  dysfunction,

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Cont..

• CNS Uremic encephalopathy, autonomic and
  peripheral neuropathies,
• Endocrine Abnormal glucose tolerance, secondary
  hyperparathyroidism,
• Metabolic Hyperkalemia, hyperphosphatemia,
  hypocalcemia, hypermagnesemia, hyperuricemia,hypoa
  lbuminemia, metabolic acidosis.

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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

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Urinary Indices
Index Pre-renal Causes Renal Causes
Urinary sodium concentration (mEq/L) lt20 gt40
Fractional excretion of sodium () lt1 gt1
Urine osmolarity (mOsm/L) gt400 250300
Urine creatinine/plasma creatinine gt40 lt20
Urine/plasma osmolarity gt1.5 lt1.1
Klahr S, Miller SB Acute
oliguria. N Engl J Med 1998338671-675
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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
• Dialysis

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Anaesthetic Considerations
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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

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Effect on drug handling

• Protein bound drugs have increase free fraction
  due to hypo-albunemia 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.

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Opioids Opioids Opioids 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
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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.

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Inhalation Agents Inhalation Agents 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 (gt 4hrs) Nephrotoxic,after prolonged use
Methoxyflurane Biotranformed to high inorganic fluoride levels Highly nephretoxic
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Intravenous Agents Intravenous Agents 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
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Muscle Relaxants Muscle Relaxants 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, No change in clearence Prolonged duration
Pancuronium 40-50renal excretion, partly via less active 3hydroxy pancuronium renal excreation Prolonged duration
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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

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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.

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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
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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 Ringers?, NS), colloids, pRBC,
• Anaesthesia can be maintained with inhalation
  agents or propofol with muscle relaxants ?NM
  monitoring.

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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.

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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.

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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
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References

• Miller RD. Anesthesia. 7th ed. NY Churchill
  Livingstone Inc. 2010. Anesthesia and the Renal
  and Genitourinary Systems, 2105-2134.
• Clinical Anaesthesia, Barash, Cullen Stoelting,
  5thed. The Renal System and Anesthesia For
  Urologic Surgery,2098-2168.
• Stoeltings Anesthesia Co-existing Disease, 5th
  ed. Renal Disease,358-384.
• Harrisons Principles of internal medicine, 17th
  ed. Approach to a Patient with Renal Disease and
  Renal Failure,785-822.

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Thank you..