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

University College of Medical Sciences & GTB Hospital, Delhi

Clinical Scenario• A 22yrs Male presented to ED with P/C of:

a. Fever from past 8 daysb. Vomiting for 4 days c. Pain in abdomen for 4 daysd. Distension of abdomen for 4 dayse. 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.

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

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

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, 17 ed., Renal Failure, chapter 146, page 789

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

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.

Klahr S, Miller SB: Acute oliguria. N Engl J Med 1998;338:671–675; Thadhani R, Pascual M, Bonventre JV: Acute renal failure. N Engl J

Med 1996;334:1148–1169.

Prerenal AzotemiaRenal 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

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,

Cont..

• CNS: Uremic encephalopathy, autonomic and peripheral neuropathies,

• Endocrine: Abnormal glucose tolerance, secondary hyperparathyroidism,

• Metabolic: Hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, hyperuricemia,hypoalbuminemia, metabolic acidosis.

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

Urinary IndicesIndex 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

Klahr S, Miller SB: Acute oliguria. N Engl J Med 1998;338:671-675

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

Anaesthetic Anaesthetic ConsiderationsConsiderations

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

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.

OpioidsMorphine 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

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.

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

Intravenous AgentsThiopentone 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

Muscle RelaxantsSuccinylcholine

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 40-50%renal excretion, partly via less active 3hydroxy pancuronium renal excreation

Prolonged duration

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

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.

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

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.

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.

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.

Drugs Drugs safe Drugs safe inlimited or

reduced doses

Drugs contraindicate

d

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

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.

• Stoelting’s Anesthesia & Co-existing Disease, 5th ed. Renal Disease,358-384.

• Harrison’s Principles of internal medicine, 17th ed. Approach to a Patient with Renal Disease and Renal Failure,785-822.

Thank you..