Compare conditions

Put any two — or three — conditions side by side, adult or pediatric, to spot the look-alike differences fast, row by row.

Acute Liver Failure

—

In one line

·Acute liver failure means most of your liver cells suddenly die within 26 weeks, stopping the liver from making clotting proteins (so you bleed easily) and clearing ammonia (so your brain becomes confused)—in someone whose liver was healthy before.

—

Normal physiology

·Your liver makes clotting factors (proteins II, V, VII, IX, and X that stop bleeding) and albumin (a protein that holds fluid inside your blood vessels). It detoxifies ammonia into urea, a safer waste your kidneys can remove. It breaks down medications and toxins. It stores glycogen (chains of sugar) and releases glucose (blood sugar) between meals to keep your brain fed. In health, these jobs keep your blood clotting normal, your brain ammonia low, and your energy supply steady.

—

What goes wrong

·Massive sudden death of liver cells from a toxin, virus, or immune attack stops the liver from making clotting factors and clearing ammonia, so blood clotting fails and the brain becomes confused.

—

Hallmark signs

·Yellowing of the skin and eyes (Jaundice) (yellow skin, eyes, and under the tongue)
·Confusion, sleepiness, or coma (hepatic encephalopathy)
·Easy bruising, tiny red spots on the skin, bleeding gums, nosebleeds, or blood in vomit or stool
·Pain or tenderness below the right rib cage
·Nausea, vomiting, and complete loss of appetite
·Flapping hand tremor when arms are held out (asterixis)
·Fast heart rate (over 100 beats per minute) and low blood pressure (top number under 90 or mean arterial pressure under 65 mmHg)
·Very little urine (less than 400 mL in 24 hours or less than 0.5 mL per kilogram of body weight per hour for six hours or more)

—

Red flags · escalate now

·Stupor (arousable only to painful stimuli) or coma (no response to pain)—this is grade III or IV hepatic encephalopathy and signals high risk of brain swelling (cerebral swelling (edema)), pressure inside the skull rising above 20 mmHg, and the brain herniating (getting squeezed through the skull base). The person needs a breathing tube placed immediately, transfer to the ICU, and (in transplant centers) a device to monitor brain pressure.
·INR above 4.0 or active bleeding from the gut (vomiting blood, black tarry stool, or bright red blood from the rectum)—this means the blood has almost no clotting ability and bleeding can be deadly. Fresh frozen plasma, prothrombin complex concentrate, or recombinant factor VIIa must be given, and if bleeding is ongoing, a camera scope (endoscopy) must look inside the gut to find and stop the source.
·Blood sugar below 60 mg/dL despite continuous IV dextrose (sugar solution)—this means the liver has lost almost all ability to make new glucose (gluconeogenesis) or release stored glucose (glycogenolysis). Less than 10 percent of liver cells are still working. Without an emergency liver transplant, death is imminent.
·Creatinine above 2.0 mg/dL or climbing more than 0.3 mg/dL per day, plus very little urine—this strongly suggests hepatorenal syndrome type 1 or death of kidney tubule cells (acute tubular tissue death (necrosis)). Both mean multiple organs are failing. Without a liver transplant, 70 to 80 percent of patients will die.
·Blood pressure so low that it requires vasopressor drugs (norepinephrine or vasopressin) through an IV to keep mean arterial pressure at or above 65 mmHg—this is distributive shock and multiorgan dysfunction syndrome. The person must go to the ICU immediately for close monitoring and be evaluated urgently for emergency liver transplant. Without transplant, fewer than 20 out of 100 patients survive.

—

Workup

·INR (international normalized ratio) and PT (prothrombin time)
·Total and direct bilirubin
·ALT (alanine aminotransferase) and AST (aspartate aminotransferase)
·Arterial blood gas with lactate
·Serum ammonia
·Blood glucose
·Acetaminophen level
·Hepatitis A IgM, hepatitis B surface antigen and core IgM, hepatitis E IgM; HSV and CMV PCR

—

Treatment

·N-acetylcysteine (NAC) intravenous infusion
·Fresh frozen plasma, prothrombin complex concentrate, or cryoprecipitate — only for active bleeding or before procedures
·Hyperosmolar therapy: mannitol 0.5–1 g/kg IV or 3% saline bolus for brain swelling
·Urgent liver specialist consultation and transplant evaluation (King's College Criteria or MELD score)
·Continuous IV dextrose (D10 or D20) to keep blood glucose above 70 mg/dL
·ICU monitoring and organ support: infection surveillance, antibiotics for sepsis, dialysis for kidney failure, breathing tube for airway protection in grade III–IV brain dysfunction
·Cause-specific therapy: acyclovir for herpes virus hepatitis, chelation (penicillamine or trientine) for Wilson disease, delivery for HELLP syndrome or acute fatty liver of pregnancy

—

NCLEX trap

·In acute liver failure (sudden death of most liver cells within 8 weeks in a person with no prior liver disease), yellowing of the skin and eyes (jaundice) is only a visible sign—like yellow paint on a broken car. The real killers are brain swelling (cerebral swelling (edema)) and inability to clot blood (coagulopathy). Treat brain swelling with mannitol 20% or hypertonic saline 3% IV—these pull water out of the swollen brain like a sponge soaking up a puddle. Give blood products (fresh frozen plasma, platelets) ONLY when the patient is actively bleeding—not to fix a lab number. Yellowing of the skin and eyes fades only when dying liver cells stop releasing bilirubin and new liver cells grow back. No medicine directly lowers bilirubin in acute liver failure.
·In acute liver failure, confusion (hepatic encephalopathy) comes mainly from brain swelling, not just ammonia buildup. Lactulose and rifaximin work poorly when liver cells are dying by the millions. Give mannitol 20% (0.5–1 g/kg IV) or hypertonic saline 3% to lower the pressure inside the skull (intracranial pressure). The confusion here is a life-or-death emergency needing ICU monitoring for brain swelling and immediate transplant evaluation—not a stable long-term problem you manage at home with lactulose.
·In acute liver failure, brain swelling and multi-organ failure can kill the patient within hours to days. Call the liver transplant team the moment the patient meets King's College Criteria: for acetaminophen poisoning (blood pH below 7.3 after giving fluids, OR INR over 6.5 plus creatinine over 3.4 mg/dL plus grade III–IV encephalopathy); for other causes (INR over 6.5, OR any three of these: age under 10 or over 40 years, non-A non-B hepatitis or drug reaction or Wilson disease, yellowing of the skin and eyes (jaundice) for over 7 days before confusion starts, INR over 3.5, bilirubin over 17.5 mg/dL). Waiting for the liver to heal on its own can lead to the brain herniating (brain tissue shifts down and crushes the brainstem) or death. Liver transplant (replacing the failed liver with a donor liver) is the only cure for severe acute liver failure.
·In acute liver failure, clotting problems come from the liver no longer making clotting proteins—not from using them up. Giving FFP or platelets 'just in case' can overload the bloodstream with fluid, worsen brain swelling, and hide the INR trend that doctors use to judge how sick the patient is and whether transplant is urgent. Transfuse FFP, platelets, or cryoprecipitate ONLY for active bleeding (vomiting blood, black tarry stool, bleeding in the brain) or right before an invasive procedure (placing a central line, inserting a brain pressure monitor). Treat the dying liver—not the lab number alone.
·Fever in acute liver failure can come from millions of dying liver cells releasing inflammatory chemicals—not only from infection. But patients with acute liver failure have a very weak immune system (the liver makes proteins needed to fight germs), and infection (sepsis) speeds up multi-organ failure. Start broad-spectrum antibiotics (covering gram-positive, gram-negative, and fungi per your hospital's patterns) for ANY sign of infection—fever, low blood pressure, rising white count, new shadow on chest X-ray—even without positive cultures. AND keep managing the liver failure itself with transplant evaluation and ICU support. Antibiotics alone do not stop liver cell death or restore the liver's ability to make vital proteins.
·If acute liver failure is from acetaminophen poisoning (more than 4 grams per day in adults, or toxic levels on the Rumack-Matthew nomogram), stopping further doses prevents new damage—but liver cell death has already happened. Give N-acetylcysteine (NAC) immediately as a 21-hour IV protocol (loading dose 150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours). NAC restocks glutathione (an antioxidant that detoxifies the harmful metabolite NAPQI), and studies show it helps even when started beyond 24 hours after ingestion. Even with NAC, if the patient develops confusion, brain swelling, or multi-organ failure, transplant evaluation is required. Removing the toxin stops new injury—but the already-dead liver tissue must either grow back (takes weeks and may not happen in severe cases) or be replaced with surgery.

—

Install Maldek by Hill as an app — studies work even offline