OVERDOSAGE
In all cases of suspected overdosage, call your regional Poison
Control Center to obtain the most up-to-date information about the treatment of
overdose. This recommendation is made because, in general, information regarding
the treatment of overdosage may change more rapidly than do package
inserts.
Initial consideration should be given to the management of the
CNS effects of propoxyphene overdosage. Resuscitative measures should be
initiated promptly.
Symptoms of Propoxyphene Overdosage
The manifestations of acute overdosage with propoxyphene are
those of narcotic overdosage. The patient is usually somnolent but may be
stuporous or comatose and convulsing. Respiratory depression is characteristic.
The ventilatory rate and/or tidal volume is decreased, which results in cyanosis
and hypoxia. Pupils, initially pinpoint, may become dilated as hypoxia
increases. Cheyne-Stokes respiration and apnea may occur. Blood pressure and
heart rate are usually normal initially, but blood pressure falls and cardiac
performance deteriorates, which ultimately results in pulmonary edema and
circulatory collapse, unless the respiratory depression is corrected and
adequate ventilation is restored promptly. Cardiac arrhythmias and conduction
delay may be present. A combined respiratory-metabolic acidosis occurs owing to
retained CO2 (hypercapnia) and to lactic acid formed during anaerobic
glycolysis. Acidosis may be severe if large amounts of salicylates have also
been ingested. Death may occur.
Treatment of Propoxyphene Overdosage
Attention should be directed first to establishing a patent
airway and to restoring ventilation. Mechanically assisted ventilation, with or
without oxygen, may be required, and positive pressure respiration may be
desirable if pulmonary edema is present. The narcotic antagonist naloxone will
markedly reduce the degree of respiratory depression, and 0.4 to 2 mg should be
administered promptly, preferably intravenously. If the desired degree of
counteraction with improvement in respiratory functions is not obtained,
naloxone should be repeated at 2- to 3-minute intervals. The duration of action
of the antagonist may be brief. If no response is observed after 10 mg of
naloxone have been administered, the diagnosis of propoxyphene toxicity should
be questioned. Naloxone may also be administered by continuous intravenous
infusion.
Treatment of Propoxyphene Overdosage in Pediatric
Patients
The usual initial dose of naloxone in pediatric patients is 0.01
mg/kg body weight given intravenously. If this dose does not result in the
desired degree of clinical improvement, a subsequent increased dose of 0.1 mg/kg
body weight may be administered. If an IV route of administration is not
available, naloxone may be administered IM or subcutaneously in divided doses.
If necessary, naloxone can be diluted with Sterile Water for
Injection.
Blood gases, pH, and electrolytes should be monitored in order
that acidosis and any electrolyte disturbance present may be corrected promptly.
Acidosis, hypoxia, and generalized CNS depression predispose to the development
of cardiac arrhythmias. Ventricular fibrillation or cardiac arrest may occur and
necessitate the full complement of cardiopulmonary resuscitation (CPR) measures.
Respiratory acidosis rapidly subsides as ventilation is restored and hypercapnia
eliminated, but lactic acidosis may require intravenous bicarbonate for prompt
correction.
Electrocardiographic monitoring is essential. Prompt
correction of hypoxia, acidosis, and electrolyte disturbance (when present) will
help prevent these cardiac complications and will increase the effectiveness of
agents administered to restore normal cardiac function.
In addition to
the use of a narcotic antagonist, the patient may require careful titration with
an anticonvulsant to control convulsions. Analeptic drugs (for example, caffeine
or amphetamine) should not be used because of their tendency to precipitate
convulsions.
General supportive measures, in addition to oxygen, include,
when necessary, intravenous fluids, vasopressor-inotropic compounds, and, when
infection is likely, anti-infective agents. Gastric lavage may be useful, and
activated charcoal can adsorb a significant amount of ingested propoxyphene.
Dialysis is of little value in poisoning due to propoxyphene. Efforts should be
made to determine whether other agents, such as alcohol, barbiturates,
tranquilizers, or other CNS depressants, were also ingested, since these
increase CNS depression as well as cause specific toxic effects.
Symptoms of Acetaminophen Overdosage
Shortly after oral ingestion or an overdose of acetaminophen and
for the next 24 hours, anorexia, nausea, vomiting, diaphoresis, general malaise,
and abdominal pain have been noted. The patient may then present no symptoms,
but evidence of liver dysfunction may become apparent up to 72 hours after
ingestion, with elevated serum transaminase and lactic dehydrogenase levels, an
increase in serum bilirubin concentrations, and a prolonged prothrombin time.
Death from hepatic failure may result 3 to 7 days after overdosage.
Acute
renal failure may accompany the hepatic dysfunction and has been noted in
patients who do not exhibit signs of fulminant hepatic failure. Typically, renal
impairment is more apparent 6 to 9 days after ingestion of the overdose.
Treatment of Acetaminophen Overdosage
Acetaminophen in massive overdosage may cause hepatic toxicity in
some patients. In all cases of suspected overdose,
immediately call your regional poison center or the Rocky Mountain Poison
Center’s toll-free number (800-525-6115) for assistance in diagnosis and
for directions in the use of N-acetylcysteine as an antidote.
In adults,
hepatic toxicity has rarely been reported with acute overdoses of less than 10 g
and fatalities with less than 15 g. Importantly, young children seem to be more
resistant than adults to the hepatotoxic effect of an acetaminophen overdose.
Despite this, the measures outlined below should be initiated in any adult or
pediatric patients suspected of having ingested an acetaminophen
overdose.
Because clinical and laboratory evidence of hepatic toxicity
may not be apparent until 48 to 72 hours postingestion, liver function studies
should be obtained initially and repeated at 24-hour intervals.
Consider
emptying the stomach promptly by lavage or by induction of emesis with syrup of
ipecac. Patients’ estimates of the quantity of a drug ingested are notoriously
unreliable. Therefore, if an acetaminophen overdose is suspected, a serum
acetaminophen assay should be obtained as early as possible, but no sooner than
4 hours following ingestion. The antidote, N-acetylcysteine, should be
administered as early as possible, and within 16 hours of the overdose ingestion
for optimal results. Following recovery, there are no residual, structural, or
functional hepatic abnormalities.
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