Halothane
·
Bromochlorotrifluoroethane.
·
Halothane is a non-flammable, volatile
liquid. It is colourless and has a sweetish odour. It is light-sensitive.
·
Halothane can be used in combination with oxygen, or
other gas mixtures such as nitrous oxide and oxygen for general anaes-thesia.
During such use, the arterial blood levels of halothane usually range from 80
to 260 mg/L.
·
Halothane is known for its abuse potential among hospital
personnel since inhalation of small amounts produces pleasur-able effects. A
popular method of halothane abuse is to drip the liquid onto a pad held over
the face.
·
Approximately 60 to 80% of absorbed
halothane is elimi- nated unchanged in the exhaled gas in the first 24 hours,
and smaller amounts continue to be exhaled over the subsequent days or even
weeks.
·
Of the non-exhaled fraction, 50%
undergoes biotransfor- mation by the hepatic P450 system, while the remaining
is eliminated unchanged by other routes, especially urine which contains
organic fluorine-containing compounds such as trifluoroacetic acid.
·
Metabolites include apart from
trifluoroacetie acid, bromide and chloride salts, chlorotrifluoroethane, and
chlorodif- luoroethylene.
·
Hypotension, cardiac rhythm
disturbances, malignant hyper-thermia. Malignant hyperthermia has been reported
in patients given halothane with and without suxam-ethonium (succinylcholine).
·
Concomitant administration of
adrenaline increases the risk of ventricular arrhythmias and acute pulmonary
oedema. Halothane potentiates the effect of neuromuscular blocking agents.
·
Chlorpromazine and morphine enhance
the respiratory depressant properties of halothane.
· The
most important
toxic effect is hepatitis. Two types of hepatitis have been observed.
o
The first is a mild dysfunction which develops in about 20%
of exposed patients, is characterised by moderate elevation of serum
aminotransferase level, and is associ-ated with complete recovery.
o
The second is a life-threatening hepatitis occurring in
about 1 in 10,000 exposed patients which can terminate in massive hepatic
necrosis in approximately 1 in 35,000 patients. Chills and fever are often
associated with the hepatitis reaction seen with halothane. The
histopathological findings in such a case are identical to those seen in viral
hepatitis.
o
Predisposing factors to halothane hepatitis include multiple
exposures, obesity, female sex, and old age. Genetic factors may also play a
role as some races (e.g. Mexican-Indian or Mexican-Spanish) are more
susceptible.
· Pulmonary oedema and seizures occur
if halothane is administered intravenously, while inhalation is not associ-ated
with such effects.
· On ingestion, there is vomiting,
depression of conscious-ness, hypotension, shallow breathing, bradycardia with
extrasystoles, and pulmonary oedema. Asystole has occurred with therapeutic
use.
· Sinus tachycardia occurs often in
early phases of halothane overdose.
· There is a characteristic fruity or
sweet odour to the breath.
· Full recovery is usual with
supportive care, endotracheal intubation, and gastric lavage. Ingestion of this
inhalational anaesthetic is unlikely, but has occurred. Absorption is rapid and
gastric lavage is not routinely recommended as it is unlikely to be useful
unless performed very soon after ingestion. Consider administration of
activated charcoal after a potentially toxic ingestion.
· For bradycardia, give 0.5 mg to 1 mg
of atropine intrave-nously; repeat every five minutes if bradycardia persists.
3 mg (0.04 mg/kg) intravenously is a fully vagolytic dose in most adults. Doses
less than 0.5 mg may cause paradoxical bradycardia in adults.
· Dantrolene may be used for malignant
hyperthermia. The dose is 1 mg/kg by rapid intravenous infusion until symp-toms
subside (maximum dose 10 mg/kg in a single dose).
· N-acetylcysteine has been an
effective pre-treatment in protecting against halothane-induced hepatotoxicity
in animals. The importance of this finding is unknown in human overdoses, as
hepatitis is not a commonly occurring effect with acute overdose.
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