Syndromes
Related to Intoxication
An
accurate diagnosis is of fundamental importance in the assess-ment of a
patients who may be intoxicated. A full history must be obtained in the
awareness that progression to potentially fatal over-dose or withdrawal
syndromes may occur. The focuse of physical examination should be the acute
effects of intoxication (such as vital and neurologic signs) and chronic signs
and symptoms asso-ciated with drug dependence (size of liver, evidence of
venipunc-ture). Drug use within the previous 4–12 hours can be determined by
analysis of blood and breath samples wheareas urinalysis is use-ful for
assessing substance use within the preceding 24–72 hours. With the exception of
alcohol testing, urine is generally the body fluid of choice for toxicologic
analysis. Urine testing systems for drugs of abuse providing immediate results
(e.g. dipsticks) are in-creasingly available and are handy for rapid office or
clinic-based assessment. Saliva testing is also increasingly available.
The rate
at which blood alcohol levels decline averages 15 mg/dL/hour. Overall,
nonpharmacological management is preferred because it avoids the risk of
interactions between drugs and alcohol. Lorazepam 1–2 mg orally may be
effective in bel-ligerent patients who cannot be managed by supportive limit
set-ting. If, despite these measures, the patient’s condition worsens over the
next 1–2 hours, an intramuscular injection of haloperidol 5 mg can be safely
given.
In
patients with significant mental status changes or alterations in sensorium,
clinicians should be alert to the possi-bility of other causes such head trauma
or metabolic disturbance (e.g. thiamine deficiency). Further, intoxicated
patients with a re-cent history of regular heavy use and likely physiologic
depend-ence on alcohol, may be at risk for serious alcohol withdrawal (seizures
or delirium) as the blood level clears, particularly if there is a past history
of such complications. In that case, cli-nicians should consider starting
tapering doses of a long-acting benzodiazepine (e.g. chlordiazepoxide) as acute
intoxication be-gins to clear.
Suspected
benzodiazepine overdosage can be reversed with the benzodiazepine antagonist flumazenil,
which should be admin-istered intravenously, beginning with 0.2 mg slow push
over 30 seconds, followed by increments of 0.3 mg or 0.5 mg if no response,
with total dose not to exceed 3 mg to 5 mg. If no re-sponse is obtained at
those total doses, then another cause stupor or coma should be considered.
As with
alcohol, clinicians should be alert to other causes of mental status changes,
and for patients with recent regular use and phsysiologic dependence on
sedative-hypnotics, particularly short-acting agents (e.g. alprazolam,
lorazepam), serious withdrawal can ensure, and prophylactic treatment with
taper of a long-acting agent considered.
Severe
opiate intoxication is a life-threatening condition because of the high likelihood
of respiratory depression or arrest. Opiate overdose is a common cause of
death, especially among teenag-ers and young adults, and is particularly likely
among individu-als with low levels of tolerance, including inexperienced users,
or patients who have recently detoxified or been abstinent for a period of
time. Death from opiate overdose is an underappreci-ated risk, and just as one
would assess risk of suicide in depressed patients, clinicians evaluating a
patient presenting with opiate in-toxication should evaluate the risk of
overdose, including level of tolerance and past history of overdose episodes.
The
presence of miosis and respiratory depression at pres-entation is an indication
for immediate treatment. An intrave-nous dose of the pure opiate antagonist
naloxone HCl 0.4–0.8 mg usually reverses opiate-induced respiratory and CNS
depression in 2 minutes. The dose may be repeated every 2–3 min if the
pre-vious dose was not effective.
Cocaine
and other stimulant use may be associated with serious physical consequences so
the cardiac and neurologic status of patients with this type of intoxication
must always be evaluated. A management plan for medical emergencies includ-ing
arrhythmias, hypertension and seizures should be prepared.
The
adverse behavioral and psychologic effects of stimu-lant intoxication should be
treated in a quiet environment and in a straightforward and reassuring way. If
drug treatment is indi-cated, lorazepam 2 mg is usually effective.
Benzodiazepines are also preferable for treating psychosis because
antipsychotic drugs may worsen cardiovascular complications such as tachycardia
or neurologic effects such as seizures and hyperthermia. However, a
high-potency antipsychotic such as haloperidol 5 mg may be used with caution if
treatment with a benzodiazepine does not control behavioral escalation. The
clearance of amphetamine may be in-creased by urinary acidification but this is
not recommended in cases of cocaine intoxication.
The usual
treatment option is the oral administration of 20 mg of diazepam; this should
attenuate the LSD experience and alleviate any associated panic to a halt
within 20 minutes and is consid-ered a superior treatment option than the
once-common “talking down” method.
Phencyclidine
undergoes entherohepatic recirculation and this is associated with
inter-individual variability in the time over which symptoms resolve. As a
result, symptoms may re-emerge after a period of apparent quiescence and
patients with phencyclidine intoxication should therefore be observed for 12
hours before being discharged.
There is
no specific antagonist for the effects of phencylid-ine and the aim of drug
treatment for phencyclidine intoxication is to produce sedation or relieve
psychosis. A benzodiazepine like lorazepam (orally or by intramuscular
injection) may be adminis-tered for general sedation; if this does not control
psychotic agi-tation, haloperidol is a reasonable choice of antipyschotic
agent. Antipsychotics with anticholinergic properties may exacerbate the
anticholinergic effects of phencyclidine and others may ad-ditively enhance
phencyclidine-induced muscle rigidity and dys-tonias. Although urinary acidification
has been suggested as a means to promote the clearance of phencyclidine, there
is a risk that it may exacerbate incipient metabolic acidosis and increase the
risk of renal failure secondary to rhabdomyolysis.
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