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332

Shalimar and S.K. Acharya

 

 

Acute liver failure

Resuscitation: A, B, C Admit to ICU.

 

Rule out other causes of fever with

 

encephalopathy

 

Clinical evaluation and assessment of

 

grade of encephalopathy, cerebral edema

 

and prognostic indicators

 

Investigate CBC, electrolytes, BUN, creatinine, RBS

 

serum bilirubin, transaminases, PT, CXR, arterial blood

 

gases, arterial ammonia daily, blood culture endotracheal

 

aspirate in intubated patients, and urine culture

Liver transplant available: Early referral—if prognostic models support high mortality at admission

Liver transplant not available/contraindicated: Continue supportive measures

Maintenance of blood sugar, electrolytes, oxygen saturation temperature Cerebral edema: head end elevation, mannitol, intubation in grades 3–4 Prophylactic antibiotics: Third-generation cephalosporins, vancomycin, and fluconazole NAC

Improvement: Continue

No improvement: Control sepsis

supportive therapy

(antibiotics as per culture reports), supportive care

Fig. 41.1 A summary of approach to FHF

Suggested Reading

1.Bhatia V, Singhal A, Panda SK, Acharya SK. A 20-year single-center experience with acute liver failure during pregnancy: is the prognosis really worse? Hepatology. 2008;48:1577–85.

The mortality of pregnant patients with ALF is similar to that of nonpregnant women and is independent of the cause or trimester. Pregnancy per se should not be regarded as a poor prognostic factor for a patient with ALF

41 Acute Liver Failure

333

 

 

2.Acharya SK, Dasarathy S, Kumer TL, Sushma S, Prasanna KS, Tandon A, et al. Fulminant hepatitis in a tropical population: clinical course, cause and early predictors of outcome. Hepatology. 1996;23:1448–55.

The study was conducted prospectively, at a single tertiary care center in India, to document the demographic and clinical characteristics, natural course, and causative profile of patients with FHF as well as to define simple prognostic markers in these patients. The prognostic model developed in the current study is simple and can be performed at admission.

3.Riegler JL, Lake JR. Fulminant hepatic failure. Med Clin North Am. 1993;77:1057–83.

A comprehensive review of the management of fulminant hepatic failure

4.Trey C, Davidson CS. The management of fulminant hepatic failure. In: Popper H, Schaffner F, editors. Progress in liver failure. New York: Grune and Stratton; 1970. pp. 282–98.

Acute Decompensation in Chronic Liver

42

Failure

Deepak Amarapurkar

A 54-year-old male patient, diagnosed to have cryptogenic cirrhosis 3 years back, was brought to the hospital, with abnormal behavior, inability to walk, edema over the feet, and distention of the abdomen for 3 days. On examination, the patient was found conscious but disoriented, having flapping tremors, icteric with edematous feet, and moderate ascites.

Hepatic encephalopathy of any form is seen in 50–70% patients of cirrhosis. Mortality in patients of cirrhosis with encephalopathy ranges from 30% to 50% at the end of 1 year and 70% at the end of 3 years.

Step 1: Initiate resuscitation

All patients who have altered sensorium and cannot maintain their airway require immediate attention to airway. This assessment is done mainly by clinical means.

They should be put on high-flow oxygen to increase SpO2 to above 90%. Patients who are unable to maintain their oxygenation are put on assisted ventilation.

Circulation needs to be maintained by fluid infusion. If clinically there is evidence of cardiac impairment, fluids should be given cautiously.

Step 2: Take history to identify precipitating factors

In a patient of cirrhosis with acute worsening, take history to identify the precipitating factors. Usual precipitating factors in acute encephalopathy are shown in Table 42.1.

D. Amarapurkar, D.M, D.N.B. (*)

Department of Gastroenterology, Bombay Hospital & Medical Research Centre, Mumbai, India

e-mail: amarapurkar@gmail.com

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

335

DOI 10.1007/978-81-322-0535-7_42, © Springer India 2012

 

336

D. Amarapurkar

 

 

Table 42.1 Precipitating

Gastrointestinal bleeding

factors in portosystemic

Constipation

encephalopathy

Large protein meal

 

 

Psychoactive drugs

 

Electrolyte imbalance—hypokalemia and hyponatremia

 

Infections

 

Superimposed acute hepatic injury

 

Alkalosis

 

Sedation

Step 3: Send investigations

The following investigations should be sent:

Complete blood count

Liver function tests including prothrombin time

Blood glucose, urea, serum creatinine, serum electrolytes

Blood culture

Arterial ammonia level

Urine examination including culture

Chest X-ray posteroanterior view

Ultrasound examination of the whole abdomen including liver, spleen, portal vein, kidneys, ureter, and bladder (KUB) and ascites

Ascitic fluid examination including culture of the fluid, inoculated in the blood culture bottle at bedside

Step 4: Stage encephalopathy

Once hepatic encephalopathy is diagnosed, it should be staged as shown in Table 42.2.

Table 42.2 Clinical stages of hepatic encephalopathy

Stage

Mental status

Neuromuscular function

1

Impaired attention, irritability, depression

Tremor, incoordination, apraxia

2

Drowsiness, behavioral changes, memory

Asterixis, slowed or slurred speech, ataxia

 

impairment, sleep disturbances

 

3

Confusion, disorientation, somnolence,

Hypoactive reflexes, nystagmus, clonus,

 

amnesia

muscular rigidity

4

Stupor and coma

Dilated pupils and decerebrate posturing,

 

 

oculocephalic reflex

Step 5: Manage hepatic encephalopathy

(A)Standard Therapeutic Measure in Hepatic Encephalopathy

Nutritional management:

Normal protein diet for episodic hepatic encephalopathy

1–2 g of protein per kg/day

Zinc replacement

42 Acute Decompensation in Chronic Liver Failure

337

 

 

Reduction in nitrogenous load arising from the gut.

Bowel cleansing.

Nonabsorbable disaccharides—lactulose is a first-line pharmacological treatment for hepatic encephalopathy. Lactulose should be given to have two to three loose stools per day.

Antibiotics—a therapeutic alternative to nonabsorbable disaccharides for treatment in acute and chronic encephalopathy and cirrhosis. Rifaximin is equally effective as lactulose. Rifaximin is used up to 1,200 mg/day in divided doses.

Ornithine aspartate in oral or intravenous form is only useful for a short duration. It should be avoided in renal dysfunction.

Drugs that affect the neurotransmission—flumazenil and bromocriptine administration may have a therapeutic role in selected patients.

Manipulation of the splanchnic circulation—closure of large portosystemic shunts.

(B)Renal Failure in Cirrhosis

Step 1: Assess the renal function

Measuring renal function in cirrhosis:

Creatinine of more than 1.5 mg/dL is considered renal failure.

Fallacies of measuring creatinine:

Underestimation of severity of renal dysfunction due to poor muscle mass. Creatinine may be falsely low.

Small changes in creatinine (0.4–0.8) may signal significant declines in glomerular filtration rate.

Step 2: Assess the cause of renal dysfunction

• Important causes of renal failure are given in Table 42.3.

Table 42.3 Causes of renal dysfunction in cirrhosis

Acute

Chronic

Hypovolemia

Glomerulonephritis

Diuretics

Hepatitis B

Gastrointestinal bleed

Hepatitis C

Diarrhea (lactulose-induced)

IgA nephropathy (alcoholic)

Nephrotoxic drugs

Diabetic nephropathy

Aminoglycosides

 

Nonsteroidal anti-inflammatory drugs

 

Contrast agents

 

Sepsis

 

Acute kidney injury

 

Step 3: Workup of renal dysfunction in patients with cirrhosis

Evaluate to find the cause and severity of renal dysfunction in cirrhosis.

One of the very important investigations of such a patient is urine examination (Table 42.4).

338

 

 

 

 

D. Amarapurkar

 

 

 

 

 

Table 42.4 Typical urinalysis in renal dysfunction in cirrhosis

 

 

 

 

Osmolality

Urine sodium

 

Protein

Cause

(mOsm/kg)

(mmol/L)

Sediment

(mg/day)

Prerenal hypovolemia

500

<20

Normal

<500

Hepatorenal syndrome (HRS)

500

<20

Nil

<500

Intrinsic

 

 

 

 

 

ATN

<350

> 40

Granular casts

<500

Acute interstitial nephritis

<350

> 40

RBC and

500–2,000

(AIN)

 

 

 

eosinophils

 

Acute glomerulonephritis (AG)

Variable

Variable

WBCs, red cell

 

 

 

 

 

 

casts

 

 

 

 

 

 

 

 

 

Renal failure in patients of acute

 

 

 

 

 

 

decompensation in chronic liver disease

 

 

 

 

 

 

 

 

 

 

 

ECF fluid losses; rapid or excessive diuresis, vomiting, diarrhea, hemorrhage, recent LVP or hemodynamic changes due to use of NSAIDs or other drugs

No

Recent use of nephrotoxic medications (aminoglycosides, radiocontrast), hypotension (sepsis, hemorrhage)

No

Glomerular proteinuria and hematuria, i.e. dysmorphic RBC,s RBC casts

No

Imaging (ultrasound, CT scan) shows hydronephrosis or urinary retention

No

Yes

Yes

Yes

Yes

Hold diuretics or other offending medications, trial of intravascular volume expander (albumin); if renal function improves, diagnosis of prerenal state is made

Toxic or ischemic ATN

Suspect glomerular disease. Depending on clinical scenario, further workup may include cryoglobulins, C3, C4, and renal biopsy

Suggestive of obstructive uropathy. Unless long standing relief of obstruction should lead to improvement in renal function

Patient has evidence of portal hypertension

 

Yes

 

 

 

 

Hepatorenal Syndrome

(ascites). Cr > 1.5

 

 

 

 

 

 

 

 

 

 

 

 

Fig. 42.1 Evaluation and management of renal failure

Step 4: Diagnose and manage renal failure

Management depends on the type of injury. If there is an obvious precipitating factor like volume depletion, it should be corrected. Nephrotoxic drugs should be stopped, and diuretics should be withheld. If there is sepsis, appropriate antibiotics should be used (Fig. 42.1).

42 Acute Decompensation in Chronic Liver Failure

339

 

 

Step 5: Identify Hepatorenal syndrome

(HRS) HRS is a reversible functional renal impairment that occurs in patients with advanced liver cirrhosis or those with fulminant hepatic failure. It requires quick recognition of type of hepatorenal syndrome (Table 42.5) and aggressive management; otherwise outcomes are bad.

Table 42.5 Hepatorenal syndrome

 

Type 1

Type 2

Rapid reduction in renal function in less

Renal function slowly deteriorates over weeks

than 2 weeks

to months

Doubling of initial serum creatinine

Increase in serum creatinine to more than

to >2.5 mg/dL or 50% Reduction of the initial

1.5 mg/dl or creatinine clearance less

24-h creatinine clearance to <20 mL/min

than 40 ml/mt

 

Occurs in cirrhotic patients with refractory

 

ascites

Severely ill patients

Mild jaundice

Jaundice

Some degrees of coagulopathy

Coagulopathy

 

Step 6: Treat hepatorenal syndrome

Measure creatinine clearance in the patient with tense ascites.

Use diuretics judiciously if creatinine clearance is low.

Avoid nonsteroidal anti-inflammatory drugs.

Avoid aminoglycosides.

Treat volume depletion aggressively.

Treat infection and sepsis aggressively.

Restrict Na+ intake to 1 g/day.

• If serum Na+ is less than 125 mEq/L, restrict fluid intake.

Treat gastrointestinal bleeding.

Use intravenous plasma expanders and vasoconstrictors.

Consider liver transplant if the patient has refractory ascites or refractory hypotension.

Recommendations for the use of vasoconstrictors in patients with type 2 hepatorenal syndrome:

The goal of treatment is to reduce serum creatinine concentrations to £1.5 mg/ dL (130 mmol/L).

Terlipressin at a dose of 0.5 mg should be given intravenously every 4 h; the dose can be increased in a stepwise fashion (i.e., every 2 days) to 1 mg every 4 h and then up to 2 mg every 4 h in cases of where there is no reduction in the serum creatinine concentration.

Alternatively a continuous infusion of terlipressin at a dose of 2 mg/day can be given. When the serum creatinine concentration does not reduce by at least 30%, the dose can be increased every 2 days up to 12 mg/day.

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