Acute liver failure Flashcards
What is acute liver failure?
Damage to normally functioning liver that causes coagulation abnormalities (INR >1.5), hepatocytes (liver cells) are destroyed, protein synthesis is disrupted, unable to produce clotting factors, and increased bilirubin levels
What is cirrhosis?
Scarring of liver caused by chronic rxn to hepatic inflammation and necrosis. It is irreversible/progressive and it ends in end stage liver disease
What can ALF be caused by?
- Drug induced- dose dependent (tylenol, tetracycline, wild mushrooms), NSAIDs, phenytoin, statins, herbal (skullcap, comfrey), chronic alcohol use
- Viral infections- hepatitis C virus (most common), hepatitis a/b/c/d/e, HSV, cytomegalovirus, epstein barr virus
- Metabolic- HELLP, reye’s syndrome, wilson’s disease
- Vascular- sepsis, heart failure
High bilirubin in ALF?
Liver bile production is decreased in ALF and liver cells aren’t able to excrete bilirubin. This causes jaundices skin, decreased Vit K, and itchiness
Dx for ALF?
CT scan, ultrasound, blood work (INR, PT, ALT/AST/GGT, bilirubin, bile ducts, ammonia)
What is acetaminophen toxicity? and who’s at risk
Having more than 4g in 24 hrs and it can cause ALF because tylenol is absorbed through GI tract and metabolized in the liver. Tylenol is present in many meds and sometimes we don’t know that.
At risk- undernourished, anorexic, hx of alcohol abuse
Treatment for acetaminophen toxicity?
Decontaminate GI system using gastric lavage (clean out stomach content using tube) and then activated charcoal. Give acetylcysteine afterwards to prevent/lessen liver damage
Complications of ALF? 5 of them
Portal HTN, ascites, esophageal varices, biliary obstruction, and hepatic encephalopathy
What is portal HTN?
Persistent increase in portal vein pressure from normal 3 mmHg to 10. Caused by increased resistance to blood flow through the liver and blockage of blood flow through portal vein
What is ascites? and what causes it
Accumulation of free fluid in the peritoneal cavity d/t increased hydrostatic pressure from portal HTN
What is esophageal varices?
Esophageal veins become fragile and distended because of increased pressure. This can potentially lead to bleeding which is life threatening
What is biliary obstruction?
Liver bile production is decreased which prevents absorption of fat soluble vitamins like Vit K which led to abnormalities in coagulation levels (susceptible to bleeding and bruising)
What is hepatic encephalopathy? what causes it
Cognitive syndrome caused by liver failure and decreased ability to convert ammonia to urea for excretion. Develops quickly in acute liver dysfunction and most likely result of shunting portal venous blood into central circulation so the liver is bypassed (ammonia and GABA can build up by crossing the BBB),
Precipitating factors of HE?
Infection, worsening hepatic function, high protein diet, constipation, certain drugs, increased BUN/creatinine, GI bleeding, and hypovolemia
S+S of HE? early vs late
Early- speech problems, sleep/mood disturbances, mental status changes
Late- neuromuscular problems, altered LOC, impaired thinking
What is asterixis?
It’s a flapping tremor and neurological disorder that causes brief irregular lapses in sustained muscle contraction (have sudden loss of muscle tone). This is a red flag in HE and usually occurs before mental changes
How to treat HE?
Treat precipitating factors (infection..), ammonia reducing agents (reduces ammonia producing bacteria in the bowel), ammonia detoxicants (promotes movement of ammonia toxins from bowel), prevent hypoglycemia, prevent GI hemorrhage (give extra Vit K)
Is hypoglycemia common in ALF? and treatment
Yes because the liver stores glucose, so if function is impaired, glucose levels will decrease. Give IV infusion of 10% dextrose and replace electrolytes (like potassium)
What is hepatitis C?
Blood borne illness that causes chronic disease and compromises immunity. Causes inflammation that leads to scarring of the liver over time
S+S of ALF early vs late?
E- fatigue, change in weight, GI symptoms (anorexia, vomiting), pain in abdomen area, liver tenderness
L- GI bleeding, jaundice, ascites, bruising, dry/itchy skin, rashes, petechiae, warm/bright pigmentation of hands, peripheral edema, vit deficiency (ADEK)
Expected labs for ALF?
AST/ALT/LDH elevated because they are released into blood during inflammation (mean livery damage). High ALP indicates insufficient bile/bilirubin. Elevated GGT because of biliary obstruction. Elevated bilirubin and proteins. Increased creatinine (dehydration) and ammonia. Prolonged prothrombin time (decreased because it’s made in the liver), high INR (decreased blood clotting) and WBC decreased. Decrease platelet and decrease albumin (made in liver)
Signs of ammonia build up?
Tremor, disorientation, lethargy, and confusion
Cerebral edema in ALF? treatment
Most common cause of death in ALF. Need to monitor ICP. Give IV mannitol to decrease edema and elevate HOB
Goals for treatment for ALF?
Determine and correct underlying caused of ALF, prevent declining liver function, avoid complications, support organ function, monitor hemodynamics and ventilation status
Diet used for HE?
Small frequent meals
Recommended nutrition for ALF?
Low sodium diet and vitamins needed b/c of deficiencies
