Acute Liver Failure-1

ACUTE LIVER FAILURE
Dr OKANGA
• Development of jaundice, coagulopathy, and
encephalopathy within 8 weeks of onset of
hepatocellular injury;
• subclassified into hyperacute (day 0–7), acute (day 8–
28) and subacute (day >28)
• Causes – Viral hepatitis, paracetamol, other drugs,
pregnancy, Amanita phalloides (mushroom) poisoning,
Wilson’s disease, shock, cyrptogenic and, rarely, in
extensive malignant disease of the liver.
• Clinical presentation -
Clinical presentation -
• Encephalopathy
• Cerebral edema - unequal or abnormally reacting pupils,
fixed pupils, hypertensive episodes, bradycardia,
hyperventilation, profuse sweating, local or general
myoclonus, focal fits or decerebrate posturing
• Initially increased cardiac output, and reduced systemic
peripheral vascular resistance, Later -circulatory failure.
• Patients are prone to infections
• Renal failure.
Hepatic encephalopathy grades
Investigations
1. Toxicology screen of blood and urine
2. HBsAg, IgM anti-HBc
3. IgM anti-HAV
4. Anti-HEV, HCV, CMV, HSV, EBV
5. Caeruloplasmin, serum copper, urinary copper, slit-
lamp eye examination
6. Autoantibodies: ANA, ASMA, LKM, SLA
7. Immunoglobulins
8. Ultrasound of liver and Doppler of hepatic veins
Adverse prognostic criteria in acute liver failure*
* Predict a mortality rate of ≥ 90% and are an indication for referral for
possible liver transplantation
Management.
• Patients with coagulopathy/Hepatic
encephalopathy should be treated in ICU/HDU
• N-acetylcysteine therapy may improve
outcome, particularly in patients with acute
liver failure due to paracetamol poisoning.
• Liver transplant.
COMPLICATIONS OF HEPATIC FAILURE
★ SCREAM ★
1. S epsis
2. C oagulopathy
3. R enal failure
4. E ncephalopathy
5. A scites
6. M etabolic changes (hypoglycemia,
electrolyte abnormalities, acidosis)
Liver cirrhosis
• Defined histopathologically as diffuse hepatic
fibrosis with the replacement of the normal
liver architecture by nodules.
Pathophysiology
• Following liver injury, stellate cells in the space
of Disse are activated by cytokines produced
by Kupffer cells and hepatocytes.
• This transforms the stellate cell into a
myofibroblast-like cell, capable of producing
collagen, pro-inflammatory cytokines and
other mediators that promote hepatocyte
damage and tissue fibrosis.
Causes of cirrhosis
Clinical features
• May asymptomatic - diagnosis is made incidentally at
ultrasound or at surgery.
• Isolated hepatomegaly,
• Splenomegaly and collateral vessel formation, ascites in portal
hypertension,
• Florid spider telangiectasia, gynaecomastia and parotid
enlargement are most common in alcoholic cirrhosis.
• Pigmentation - haemochromatosis and in any cirrhosis
associated with prolonged cholestasis
• loss of male hair distribution and testicular atrophy.
• Hepatic encephalopathy, edema, Jaundice, renal failure
Management
• Treat underlying cause,
• Maintain nutrition
• Treat complications (ascites, hepatic
encephalopathy, portal hypertension and
varices)
• Surveillance for hepatocellular carcinoma
• 2yrly endoscopy to screen for varices
Child–Pugh classification of prognosis
in cirrhosis
Portal hypertension
• Elevation of the hepatic venous pressure gradient
(HVPG) to >5 mmHg.
• The normal hepatic venous pressure gradient
(difference between the wedged hepatic venous
pressure (WHVP) and free hepatic venous pressure;
is 5–6 mmHg.
• Clinically significant portal hypertension is present
when the gradient exceeds 10 mmHg and risk of
variceal bleeding increases beyond a gradient of 12
mmHg.
Hepatic venous pressure gradient (HVPG). A, Transjugular wedge balloon
for measuring HVPG. B, HVPG is calculated as the difference between free
hepatic vein pressure (FHVP) and wedged hepatic vein pressure (WHVP),
which is a surrogate for portal vein pressure in sinusoidal causes of portal
hypertensio
Clinical features
• Splenomegaly
• Collateral vessels may be visible on the anterior
abdominal wall and occasionally several radiate from
the umbilicus to form a ‘caput medusae’
• Esophageal, gastric and rectal collaterals (Varices) –
Rupture may cause catastrophic bleeding.
• Fetor hepaticus results from portosystemic shunting of
blood, which allows mercaptans to pass directly to the
lungs.
• Ascites occurs as a result of renal sodium retention
Pathophysiology
• ↑ portal vascular resistance leads to a↓ in the flow of
portal blood to the liver and development of collateral
vessels, allowing portal blood to bypass the liver and
enter the systemic circulation directly.
• Portosystemic shunting occurs in the distal
oesophagus, stomach and rectum, in the anterior
abdominal wall, renal, lumbar, ovarian and testicular
vasculature.
• Eventually more than half of the portal blood flow
may be shunted directly to the systemic circulation.
Investigations
• Diagnosis – clinical, portal venous pressure rarely
measured.
• FHG – may show thrombocytopenia and leucopenia due to
hypersplenism.
• Endoscopy to confirm varices.
• U/s – Shows splenomegaly, collateral vessels, may reveal
cause of portal HTN e.g cirrhosis or portal vein thrombosis,
• CT and magnetic resonance angiography can identify the
extent of portal vein clot and are used to identify hepatic
vein patency.
Management of Portal HTN
• Largely focused on the prevention and/or
control of variceal haemorrhage.
• Large varices have a 30% risk of bleeding
compared to 7% for small varices in 2yrs in the
presence of portal HTN.
• Mortality from bleeding is up to 45% for
patients with poor liver function (Child Pugh
C). Overall mortality 15%.
Primary prevention of variceal bleeding
• Propranolol 80 – 160 mg od or Nadolol 40 –

240mg od or carvedilol 6.25 – 12.5mg od
• Aim to reduce HR by 25% or 50 – 55beats per
minute.
• Beta blockade effectiveness is similar to
prophylactic banding of varices.
• Variceal bleeding reduced by 47%.
Management of acute bleeding from oesophageal varices.
Variceal banding
• Stops variceal bleeding in 80%
of patients and can be repeated if bleeding recurs.
• Varices are sucked into a cap placed on the end of the
endoscope, allowing them to be occluded with a tight
rubber band.
• The occluded varix subsequently sloughs with variceal
obliteration.
• Banding is repeated every 2–4 weeks until all varices are
obliterated.
• Has fewer side effects than sclerotherapy.
Balloon tamponade
A stent is placed between the portal vein and the hepatic vein within the liver to
provide a portosystemic shunt and therefore reduce portal pressure. It stops and
prevents further variceal bleeding. Hepatic encephalopathy is a common
complication – reduced by decreasing shunt diameter.
Secondary prevention of variceal bleeding
• Beta blockers
• oesophageal banding programme with
repeated sessions of therapy at 12–24-week
intervals until the varices are obliterated.
• TIPSS.
HEPATIC ENCEPHALOPATHY
HE …
• Alteration in mental status and cognitive
function occurring in the presence of liver
failure.
• Pathophysiology – Portosystemic shunting and
reduced liver mass results in accumulation of
Gut-derived neurotoxins in systemic circulation.
• These toxins cross BBB and cause symptoms of
HE.
Precipitants of HE
1. NH 4 —↑ protein intake, constipation, GI
bleed, transfusion, infection (spontaneous
bacterial peritonitis), azotemia, hypokalemia
2. ↑ Diffusion across BBB- alkalosis
3. ↓ Metabolism —dehydration, hypotension,
hypoxemia, anemia, portosystemic shunt,
hepatoma, progressive liver damage
DDX
• Intracranial bleed (subdural/extradural haematoma,
• Drug or alcohol intoxication.
• Delirium tremens/alcohol withdrawal.
• Wernicke’s encephalopathy.
• Primary psychiatric disorders.
• Hypoglycaemia.
• Neurological Wilson’s disease.
• Post-ictal state.
GRADING OF HEPATIC ENCEPHALOPATHY
1 —reversed sleep cycle, mild confusion, tremor,

incoordination
2 —lethargy or irritability, disoriented to time,
asterixis, ataxia
3 —somnolence or agitation, disoriented to
place, asterixis, hyperreflexia, positive
Babinski
4 —coma, decerebrate
Investigations
• Diagnosis - clinical;
• EEG - shows diffuse slowing of the normal
alpha waves with eventual development of
delta waves.
Management Acute HE
• Treat or remove precipitating causes and suppress the production of
neurotoxins by bacteria in the bowel.
• Work up for sepsis
• correct hypokalemia, if present.
• Lactulose 30 g PO BID–QID PRN titrate to 2–4 bowel
movements/day; if patient obtunded and NPO, consider lactulose
300 mL (mixed with 700 mL of H 2 O or NS) PR via rectal balloon
catheter QID until awake.
• Consider sedation ( haloperidol 1–2 mg PO/IV/ SC q6h and q1h PRN)
and ventilation,
• mannitol 1 g/kg 20% solution,
• Treat underlying cause —liver transplant
Management chronic HE
• Lactulose 30 g PO BID–QID PRN titrate to 2–4
bowel movements/day
• Prophylaxis with metronidazole 800 mg PO
daily (associated peripheral neuropathy),
neomycin 500–2000 mg PO TID (associated
ototoxicity and nephrotoxicity), or rifaximin
550 mg PO BID
• Treat underlying cause —liver transplant.

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ACUTE LIVER FAILURE

• Propranolol 80 – 160 mg od or Nadolol 40 –

1 —reversed sleep cycle, mild confusion, tremor,

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