in the presence of near-normal intravascular pressures Metabolic acidosis occurs in approximately 30% of patients who have liver failure, and the risk of sepsis is increased secondary to the patient’s compromised immune function Management All patients suspected of having liver failure should undergo a complete physical examination, including a thorough and serial neurologic evaluation Laboratory testing should include serum glucose, transaminases, total and direct bilirubin, albumin, PT, GGT, CBC count with differential, electrolytes, blood culture, and fibrinogen Infection can be both the cause and a complication of ALF and is a major cause of morbidity and mortality Infection may be the cause of death in up to 20% of patients Patients with ALF may not present with an elevated WBC count and fever, so the ED clinician should have a very low threshold for empiric broad-spectrum antibiotics Patients with hypoglycemia should receive IV fluids with 10% dextrose, with additional dextrose boluses as necessary, and should undergo frequent blood glucose monitoring (every hour) until their blood glucose level stabilizes Metabolic acidosis should be corrected; however, correction of hyponatremia should be gradual in patients with ascites Patients who have a life-threatening coagulopathy should be given IV vitamin K (2.5 mg in infants; mg in older children and adolescents) In the case of non–life-threatening coagulopathy, vitamin K should be given subcutaneously because of the risk of infusion reactions A repeat PT should be performed to hours after administration An uncorrectable PT is suggestive of severe hepatocyte damage Clinicians should be cautious about aggressive management of coagulopathies in patients without active bleeding, as this may quickly lead to difficulties with patient volume status without significant improvement in the patient’s coagulopathy Recombinant factor VII may help correct a coagulopathy without the need for significant volume, however the data of its efficacy in children is lacking In addition, there is a decrease in both procoagulant and anticoagulant factors, so an elevated PT and INR may not accurately reflect a patient’s risk of bleeding Patients also often exhibit thrombocytopenia secondary to decreased production and increased consumption Platelet dysfunction is also seen in liver failure Therapeutic management of ascites should occur only in the face of respiratory distress or renal failure In these cases, IV 25% albumin (1 g/kg) followed by IV furosemide can be used Otherwise, the introduction of a