Acute Liver Failure - Etzion Flashcards
Definition of Acute Liver Failure aka Fulminant Hepatitis (FHF)
The clinical manifestation of sudden and severe hepatic injury. Rare.
Abrupt loss of immunologic and metabolic liver functions that lead to jaundice, encephalopathy , coagulopathy and in many cases progressive multiorgan failure
Potential reversibility is dependent on:
- etiology
- early identification and treatment
ABC causes of acute liver failure
A: acetaminophen (paracetamol, but not in developing countries), heptatis A, autoimmune hepatitis
B: Hepatitis B
C: Cryptogenic, hepatitis C
D: Hepatitis D, drugs (NSAIDs, Statins, Antibiotics, Antiepileptics, AntiTB)
E: Esoteric: Wilson’s disease, Budd-Chiari syndrome
F: Fatty infiltration: acute fatty liver of pregnancy, Reye’s syndrome
Hepatitis A and B most common in Africa and SE Asia
Signs that predict FHF development
Bilirubin> 20 mg%
Changes in consciousness
Hyperventilation (to blow off acid)
Hypoglycemia
Decrease in albumin
INR prolongation, decrease in coagulation factors 5,7 <40%
Decrease in liver span along with decline in transaminases and increase of bilirubin. Necroinflammation.
Encephalopathy Grades
I Minor disturbances of consciousness or motor function
II Drowsy but responsive to commands
III Stuporous but responsive to pain
IV Unresponsive to pain
Seizures may appear at any grade
Nitrates enter CNS from systemic
Mechanisms and Aggravating Factors of Encephalopathy
Nitrates travel to CNS from systemic:
Accumulation of nitrous metabolites
Accumulation of toxic substances
Hypoglycemia
Brain edema
False neurotransmitters
Electrolyte changes
Acidosis
Hypo or hypernatremia
Gastrointestinal hemorrhage (coagulopathy)
Hypovolemia (renal failure)
Potassium depletion
Hypoglycemia
Uremia
Infection
Constipation (from loss of GI function, leads to more nitrous material being absorbed)
Sedatives and anaesthetics
High protein intake (toxic metabolites)
Prognosis of FHF
Hyperacute best prognosis > Acute > subacute (poor)
Hyperacute develops quick (from paracetamol most commonly and Hep A/E)
Acute: 1-4 wks
Subacute: 4-12 wks
Most common cause of death: cerebral edema, brain presses on respiratory center. CT not useful in most patients, confirm by measuring cerebral pressure.
Hepatorenal syndrome characteristics
Cause unknown
Characterized by oliguria, anuria in later stages
ATN or functional renal failure may occur.
Essential to correct hypovolemia to maintain renal perfusion
Dopamine, furosemide, mannitol-hyperosmotic agents used to reduce brain edema
Hemodialysis or hemofiltration
Complications of FHF
Infection:
Increased susceptibility to infection, due to defect of opsonization, low complement,impaired PMN function, need if invasive monitoring
May not be associated with fever
May aggravate encephalopathy
Endotoxemia may increase liver injury
Gram negative organisms or Staph Aureus
The only sign of infection may be deterioration of liver function or encephalopathy
Hemodynamic instability
Hypoxia
Acid-base and electrolyte disturbances (=respiratory and metabolic alkalosis)
Treatment of acute liver failure
Standard intensive care treatment-transfer to tertiary care hospital
Additional specific measures- identification & removal of the insult causing FHF
Organ system support- maximizing liver regeneration
Prevention of complications
Early identification of patients eligible for liver transplantation
Hemodynamic support
Respiratory assistance
Correction of fluid and electrolytes abnormalities
Nutritional support- enteral NG low protein feeding-no bowel rest
Autoimmune hepatitis- steroids
Herpes simplex virus- acyclovir
HBV- nucleoside/nucleotide analogues
Paracetamol- N-acetyl-cysteine given within 24hrs of ingestion
Liver can regenerate by itself if young and healthy (and in a transplant unit just in case)
If nothing else works:
OLT remains the backbone of Rx for ALF
When appropriate candidates are carefully selected-80% 1 year survival
The million dollar question:
Who is the best candidate for OLT ?
The patient who is unlikely to recover with supportive measures alone
Systemic complications have not progressed beyond treatment
Biological (Prometheus-columns of hepatocytes) and nonbiological (MARS-dialysis) devices
Treatment of complications of acute liver failure
Cerebral edema:
Minimal sensory stimulation
Head elevation- 300
ICP monitoring
hyperventilation
Hyperosmotic agents (manitol-to reduce pressure)
Induced hypothermia-reduction of cerebral edema-experimental
Acute renal failure:
Maintaining renal perfusion pressure
Early identification and treatment of infections
Avoiding use of nephrotoxic drugs-especially antibiotics
Continuous renal replacement therapy
Infection:
Empiric broad spectrum antibioitics :
rapid progression to G-III-IV encephalopathy
Refractory hypotension
Presence of SIRS
Coagulopathy:
Stress ulcer prophylaxic PPI
Avoid FFP (volume overload)
rFVIIa – in patients requiring invasive procedures
