Recent Updates on Acute Liver failure.pptx

This slide summarizes Acute liver failure

1. Acute Liver Failure

2. INTRODUCTION AND DEFINITION Acute liver failure refers to the development of severe acute liver injury with impaired synthetic function (INR of ≥1.5) and altered mental status in a patient without cirrhosis or preexisting liver disease. A commonly used cutoff to define acute liver failure is an illness duration of <26 weeks. Patients with acute severe alcoholic hepatitis, even if recognized for <26 weeks, are considered to have acute-on-chronic liver failure.

3. Acute liver failure may also be diagnosed in patients with previously undiagnosed Wilson disease Vertically acquired or reactivation of hepatitis B virus Autoimmune hepatitis In whom underlying cirrhosis may be present, provided the disease has been recognized for <26 weeks.

4. Cerebral edema and intracranial hypertension may complicate encephalopathy and is associated with a high mortality rate. Overall survival rate of over 70%. Etiology may be drug-induced, viral, immunologic, ischemic, toxic, or unknown.

5. ETIOLOGY AND EPIDEMIOLOGY Main identified viruses that cause ALF are HAV, HBV, HDV, and HEV. Acetaminophen overdose is the most common cause of ALF in the United Kingdom and the USA. A cause for acute liver failure can be established in approximately 60 to 80 percent of patients No data from Ethiopia.

6. CLINICAL FEATURES Encephalopathy Mandatory for a diagnosis of ALF. Intracranial Hypertension and Cerebral Edema. Papilledema is rarely observed Hemodynamic Changes and Circulatory Failure Similar to those observed in systemic inflammatory response syndrome (SIRS) or septic shock. Infection Patients with ALF are highly prone to infection.

7. ACUTE KIDNEY INJURY May occur in 40% to 80% of cases. Coagulopathy Little clinical evidence of bleeding. Risk of bleeding is linked to the platelet count. Coombs-negative hemolytic anemia is characteristic of Wilson disease. Coombs-positive hemolytic anemia may be seen in ALF associated with autoimmune hepatitis.

8. DIFFERENTIAL DIAGNOSIS The primary entity in the differential diagnosis of acute liver failure is severe acute hepatitis. Patients with severe acute hepatitis have jaundice and coagulopathy but lack signs of hepatic encephalopathy. Features that suggest neurologic Wilson disease rather than hepatic encephalopathy include the presence of dysarthria, dystonia, tremors, or parkinsonism.

9. DIAGNOSIS Acute liver failure should be in the differential diagnosis of patients with the recent onset (<26 weeks) of mental status changes, jaundice, or right upper quadrant pain. Diagnosis of ALF is clinical and based on the presence of: Altered mental status (hepatic encephalopathy) Prolonged prothrombin time (INR ≥1.5)

10. APPROACH TO MANAGEMENT Should be managed in centers with an active liver transplantation program. Manage in the intensive care unit (ICU). Patients’ rooms should be quiet, without audible monitors or alarms in the room, and dimly lit. Initial priorities are adequate fluid resuscitation and protection of the airway in patients with encephalopathy.

11. N-Acetylcysteine - for acetaminophen overdose. Antiviral drugs effective against HBV. Penicillin, and possibly silymarin , may be beneficial in patients with Amanita phalloides toxicity. Patients should be monitored and treated for hypoglycemia, hypokalemia, hypomagnesemia, and hypophosphatemia.

12. Patients who are hypotensive should be resuscitated with normal saline. Dextrose should be added to crystalloid solutions in patients with hypoglycemia. The goal is to maintain a mean arterial pressure of at least 75 mmHg. Avoid overhydration. Vasopressor support for unresponsive patient. Norepinephrine is often preferred.

13. N-acetylcysteine for those: Who are not candidates for liver transplantation In whom acetaminophen toxicity may be contributing to the liver failure ( eg , a patient with acute hepatitis B who was taking acetaminophen). With an indeterminate cause for the acute liver failure. Taking medications that induce cytochrome P450 activity Patients with chronic liver disease.

14. TREATMENT OF COMPLICATIONS ENCEPHALOPATHY Few treatments are directed specifically to its management. Endotracheal intubation and mechanical ventilation are indicated once grade 3 encephalopathy develops. Mannitol has been the mainstay of treatment of increased intracranial pressure. INFECTION Encephalopathy at the time of admission and the presence of SIRS are significant predictors of bacteremia. Detection of infection relies on a high level of clinical suspicion and close microbiological surveillance.

15. ACUTE KIDNEY INJURY Early fluid challenge is indicated in patients with oliguria or biochemical evidence of renal dysfunction. Minimize secondary insults. Early intervention with renal replacement therapy should be considered. COAGULOPATHY Administration of fresh frozen plasma interferes with the use of coagulation studies in assessing prognosis. Stress ulcer prophylaxis with an H2 blocker or proton pump inhibitor.

16. Hyponatremia -responds to administration of IV saline. Metabolic acidosis Fluid resuscitation is first-line therapy, but persistence of acidosis may be an indication to initiate hemofiltration. Nutrition Enteral nutrition is desirable to help maintain the integrity of the small intestinal mucosa. Feeding is normally commenced within 24 hours of admission to an ICU.

17. PROGNOSIS Three important determinants of outcome: Underlying etiology of ALF Age of the patient Grade of encephalopathy. Only 40% of patients with acute liver failure recover spontaneously.

18. LIVER TRANSPLANTATION Two fundamental approaches are used to select patients with ALF for LT First is to use indicators of a poor prognosis To list all eligible patients and make the decision to transplant when a suitable donor organ becomes available. Objective evidence of brainstem injury with established fixed and fully dilated pupils should preclude LT. Confirmed systemic fungal infection should contraindicate LT.