Acute liver failure is defined as severe liver injury with impaired function and encephalopathy in a previously healthy liver or one with underlying disease. Common causes include acetaminophen overdose, idiosyncratic drug reactions, and viral hepatitis A and B. Prognosis depends on the grade of encephalopathy, with higher grades having lower recovery rates. Treatment involves treating complications like cerebral edema, infections, and managing precipitating factors of hepatic encephalopathy. Liver transplantation may be considered for patients with grade 3 or 4 encephalopathy.
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool.
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool.
The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena.
The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena.
Dr Neerav Goyal discusses the various aspects of acute liver failure that includes the criteria, pre transplant issues, critical care management, overall survival.
dr Mohammed Hussien ( assistant Lecturer of Gastroenterologist and Hepatology at Kaferelsheik University Egypy) illusterating one of Major complication of Cirrhosis --H.E
This is a practical pocket summary for acute liver cell failure which includes the etiology, clinical picture, investigations and management. It is based on the most recent guidelines.
3. rapid development of severe acute liver injury
with impaired function and encephalopathy
in previously normal liver or well compensated
liver disease
4. encephalopathy within 8 wks previous
healthy liver
encephalopathy within 2 wks of developing
jaundice with previous underlying liver
dysfunction
12. Hepatitis viruses
hepatitis A most common acute viral hepatitis but
rare for acute infection to progress to ALF
Hepatitis B most common viral cause ALF
18. Hepatic encephalopathy
Ages 10–60 years
Handwriting and hand coordination deteriorate in
stages 1 and 2
Asterixis prominent in stage 2
Reflexes symmetrically hyperactive in stage 3
Mental and neurologic signs change rapidly (over 6–12
hours)
19. Age >60
Signs of underlying liver disease diminish (25%)
Confusion more prominent
Precipitating GI hemorrhage or infection less often
identified
Remains in stage 1 or 2 for many days
Progression slower
20. Age <10
Signs of underlying liver disease prominent; usually
FHF or extremely advanced cirrhosis
Progression through the stages very rapid, often 6–12
hours
Wilson disease can imitate HE
26. Hepatic encephalopathy (HE)
ammonia within the gut lumen
Concept ammonia
precipitating factors IGSCALP
Restrict Protein diet = 40-70 g/day
non-absorbable disaccharides = lactulose
antibiotic = rifaximin, neomycin, metronidazole,
vancomycin
27. First Line
50% Lactulose syrup 30–60 mL PO 4 times daily when ≥3
bowel movements occur daily.
Lactulose enema 300 mL plus 700 mL tap water
If worsening or no improvement in 2 days, add antibiotics:
Rifaximin: 400 mg 3 times a day
Neomycin: 1–2 g per day divided q6–8h, if renal status is
good
Metronidazole and vancomycin are alternative antibiotics.
Antacids as needed
Second Line
Flumazenil (benzodiazepine antagonist)
28. Cerebral edema
astrocyte edema
IICP and brainstem herniation, most common causes
of death
classic signs IICP include Cushing's triad and
Neurologic manifestations hypertonic, hyperreflexia,
and altered pupillary responses
29. Treatment cerebral edema
Control ICP < mmHg and CPP > mmHg
Env. with minimal sensory stimulation
elevate head position
prevent overhydration
if ICP > mmHg Hyperventilation
PCO2 < mmHg if no response use
hyperosmotic agents
manitol 0.5 - 1 g/kg
If no response use pentobarbitone 3-5 mg/kg IV
30. 1. Liver transplant
Liver recovery
2.1 Grade encephalopathy(50)
Grade I-II recovery 65-70
Grade III 40-50
Grade IV < 20
Age
cause FHF acetaminophen >
idiosyncratic drug reactions > Wilson’s disease
31. Acute liver failure.
http://emedicine.medscape.com/article/186101-
overview#showall
http://www.sciencedirect.com/science/article/pii/S135
7272502003965
Eric Goldberg, Sanjiv Chopra. Acute liver failure:
Definition and etiology. Uptodate . Mar 2010
Eric Goldberg, Sanjiv Chopra. Acute liver failure:
Prognosis and management. Dec 2010
32. I = infection
G = GI bleeding
S = sedation
C = constipation
A = alkalosis
L = low K
P = protein high