Pediatric emergency medicine trisk 2084 2084
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Clinical Assessment. Patients may initially complain of fatigue, nausea,
vomiting, fever, and diffuse abdominal pain. Occasionally, right upper
quadrant pain is severe. Commonly, a history of a prodromal viral illness can
be elicited. The presence of jaundice usually initiates the first visit to the
physician. As liver failure progresses, patients become more jaundiced and
lethargic, and may report easy bruising or bleeding. History should include
any infectious and medication exposures including prescription and
nonprescription medications and herbal and other alternative remedies. ED
physicians should be cognizant of chronic acetaminophen exposure in addition
to acute toxicity. Family history should be assessed for Wilson disease, α1
antitrypsin deficiency, autoimmune conditions, infant deaths, metabolic or
mitochondria disorders, or liver failure of unknown etiology.
Physical examination findings may include small size, poor nutritional
status, jaundice, bruising, or petechiae. Hepatomegaly is common and some
patients may have splenomegaly. Findings associated with chronic liver
disease and portal hypertension would suggest an alternative diagnosis.
Encephalopathy is graded on a scale from I to IV from drowsiness, poor
concentration, and irritability to aggressive behavior or unresponsiveness.
Those with severe encephalopathy can develop cerebral edema and increased
intracranial pressure (ICP). Cerebral edema is a major cause of death in
patients with liver failure and requires aggressive supportive management.
Because it may be difficult to diagnose patients clinically, biochemical
evidence of liver failure is necessary. PT is a helpful measure of synthetic
function. Other laboratory markers suggestive of severe liver failure include
evidence of increasing cholestasis manifested by a rising serum bilirubin level,
hypoalbuminemia, and hypoglycemia.
It is also important to monitor serum transaminase levels. Falling
transaminase levels usually indicate resolving liver disease, although in the
setting of increasing jaundice and coagulopathy, this trend may indicate
excessive hepatocyte loss rather than hepatocyte recovery. Serum fibrinogen is
usually decreased in patients with liver failure. In cases in which the patient
has splenomegaly, thrombocytopenia and leukocytopenia may be present.
Hypoglycemia almost always accompanies ALF because the liver is the
primary organ for gluconeogenesis and glycogen storage is often depleted.
This may complicate the signs of encephalopathy. Hepatorenal syndrome
occurs in approximately 75% of patients who reach severe encephalopathy.
The cause of hepatorenal syndrome is unclear; however, the result is oliguria
