| TOXIC HEPATITIS AND DRUG-INDUCED HEPATITIS
Certain chemicals have toxic effects on the liver and when taken by mouth
or injected parenterally produce acute liver cell necrosis, or toxic hepatitis.
The chemicals most commonly implicated in this disease are carbon tetrachloride,
phosphorus, chloroform, and gold compounds. These substances are true
hepatotoxins. Many medications may induce hepatitis but and sensitizing
rather than toxic. The result, drug-induced hepatitis, is similar to acute
viral hepatitis; however, parenchymal destruction tends to be more extensive.
Some examples of medications that can lead to hepatitis are isoniazid,
halothane, acetaminophen, and certain antibiotics, antimetabolites, and
anesthetic agents.
TOXIC HEPATITIS: MANIFESTATIONS AND MANAGEMENT
Toxic hepatitis resembles viral hepatitis in onset. Obtaining a history
of exposure to hepatotoxic chemicals, medications, or other agents assists
in early initiation of treatment and removal of the offending agent. Anorexia,
nausea, and vomiting are the usual symptoms; jaundice and hepatomegaly
are noted on physical assessment. Symptoms are more intense for the more
severely toxic patient. Recovery from acute toxic hepatitis is rapid if
the hepatotoxin is identified early and removed or if exposure to the
agent has been limited. Recovery, however, is unlikely if there is a prolonged
period between exposure and onset of symptoms. There are no effective
antidotes. The fever rises; the patient becomes very toxic and prostrated.
Vomiting may be persistent, with the emesis containing blood. Clotting
abnormalities may be severe, and hemorrhages may appear under the skin.
The severe gastrointestinal symptoms may lead to vascular collapse. Delirium,
coma, and convulsions develop, and within a few days the patient usually
dies of fulminant hepatic failure. Short of liver transplantation, few
treatment options are available.
Therapy is directed toward restoring and maintaining fluid and electrolyte
balance, blood replacement, and provision of comfort and supportive measures.
A few patients recover from acute toxic hepatitis only to develop chronic
liver disease. In the event that the liver heals, there may be scarring,
followed by postnecrotic cirrhosis.
DRUG-INDUCED HEPATITIS: MANIFESTATIONS AND MANAGEMENT
Medication-induced hepatitis is responsible for up to 25% of cases of
fulminant hepatic failure in the United States. Manifestations of sensitivity
to a medication may occur on the first day of its use or not until several
months later, depending on the medication. Usually, the onset is abrupt,
with chills, fever, rash, pruritis, arthralgia, anorexia, and nausea.
Later, there may be jaundice and dark urine and an enlarged and tender
liver. When the offending medication is withdrawn, symptoms may gradually
subside. Reactions may be severe, however, and even fatal, even though
the medication is stopped. If fever, rash, or pruritis occurs from any
medication, its use should be stopped immediately.
Although any medication can affect liver function, those most commonly
associated with liver injury include but are not limited to anesthetic
agents, medications used to trat rheumatic and musculoskeletal disease,
antidepressants, psychotropic medications, anticonvulsants, and antituberculosis
agents.
Halothane (Fluothane), a commonly used nonexplosive inhalation anesthetic,
may cause serious, and sometimes fatal, liver damage; therefore, its use
is contraindicated in (1) patients with known liver disease; (2) repeated
instances, particularly in patients who have had a fever of unknown cause
after the first administration of halothane; and (3) patients with evidence
of prior sensitization. Such sensitization would have been evident during
the second postoperative week, with such manifestations as fever, rash,
eosinophilia, arthralgia, or jaundice.
Source: Brunner and Suddharth's Textbook of Medical-Surgical Nursing
(Eight Edition), by Suzanne C. Smeltzer and Brenda G. Bare. 1996 Lippincott-Raven
Publishers, Pittsburg (p.984)
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