Indirect: 0.2–0.7 mg/dL
Direct: <0.5 mg/dL Increased; jaundice seen with plasma bilirubin levels >3 mg/dL Serum glutamic oxaloacetic transaminase (aspartate aminotransferase) 10–40 units/L Increased Serum glutamic-pyruvic transaminase (alanine aminotransferase*) 5–35 units/L Increased Lactate dehydrogenase (LD-5*) 5.3%–13.4% Increased Alkaline phosphatase 87–250 units/L Normal; used to differentiate biliary obstruction Albumin 3.3–4.5 g/dL Decreased; levels <2.5 g/dL are precarious Ammonia <50 g/dL Increased ammonia converted to urea by the normal liver Blood urea nitrogen 7–20 mg/dL Normal or decreased by impaired excretion of sodium and retention of water; increased in hepatorenal syndrome Creatinine 0.6–1.3 mg/dL Increased in hepatorenal syndrome Sodium 135–145 mEq/L Usually decreased; increased sodium may result after the administration of lactulose or if replacement of free water is inadequate Potassium 3.6–5 mEq/L Decreased; related to the secondary effects of hyperaldosteronism, vomiting, diuretic use, or inadequate replacement; increased potassium may result from the use of blood products Magnesium 1.6–3 mEq/L Decreased Calcium 8.8–10.4 mg/dL Decreased Phosphorus 2.5–4.5 mg/dL Decreased Glucose 70–110 mg/dL Decreased; related to impaired gluconeogenesis and decreased insulin clearance

^*Specific for liver damage.

Clinical manifestations

No matter the exact cause of the patient’s liver failure, it inevitably affects the entire physiologic makeup. Physical examination is important for the approximation of liver and spleen size, evidence of bleeding abnormalities, identification of extravascular fluid shifts, and any other organ dysfunction. Listed in the table below are common clinical features of hepatic failure and their associated causes.

Clinical Features of Hepatic Failure and Associated Causes

Clinical Feature	Cause
Anemia	Iron, vitamin B12, or folate deficiency; hypersplenism; bone marrow suppression
Ascites	Portal hypertension; hypoalbuminemia; sodium and water retention
Fetor hepaticus (pungent sour odor detected in exhaled breath)	Inability to metabolize methionine
Gynecomastia	Increased circulating estrogen
Hepatic encephalopathy (hepatic coma)	Inability to metabolize ammonia; increased cerebral sensitivity to toxins; hypoglycemia
Hepatorenal syndrome	Decreased renal blood flow, particularly to the cortex; vasoconstriction; decreased glomerular filtration rate; renal retention of sodium
Increased bleeding tendencies, nosebleeds, gingival bleeding, menstrual bleeding, easy bruising	Anemia; thrombocytopenia; decreased production of clotting factors; decreased adherence of circulating platelets
Increased risk of infection	Endotracheal intubation with impaired cough reflex; intravenous catheters; central lines; urinary catheters; leukopenia; decreased neutrophil adherence; complement deficiencies
Increased skin pigmentation	Increased activity of melanocyte-stimulating hormone
Jaundice	Increased circulating bilirubin
Leukopenia	Hypersplenism; bone marrow suppression
Palmar erythema	Increased circulating estrogen
Pectoral and axillary alopecia	Increased circulating estrogen
Peripheral edema	Hypoalbuminemia; failure of the liver to inactivate aldosterone and antidiuretic hormone, with subsequent sodium and water retention
Spider angiomas, “nevi”	Increased circulating estrogen
Testicular atrophy	Increased circulating estrogen
Thrombocytopenia	Hypersplenism; bone marrow suppression
Weight loss and muscle wasting	Nausea and vomiting; anorexia; impaired gluconeogenesis; impaired insulin functioning; hypoproteinemia

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