Pediatric emergency medicine trisk 4553 4553
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arsenal in the 1950s and 1960s, and was weaponized by Iraq in the 1980s. The
Aum Shinrikyo cult in Japan tried unsuccessfully to disseminate botulinum toxin
before deciding to release sarin in the Tokyo subway system.
Pathophysiology. Botulinum toxins are produced by certain strains of
Clostridium botulinum, a strictly anaerobic spore-forming gram-positive rod
commonly found in soil. Most cases of naturally occurring botulism result from
ingestion of preformed toxin (food poisoning) or intestinal toxin formation (infant
form). Infant botulism has additional unique epidemiologic considerations; more
extensive discussion of this disease, and of botulism in general, may be found
elsewhere in this text (see Chapters 82 Weakness and 97 Neurologic Emergencies
). The botulinum neurotoxins are the most toxic substances known to man. These
toxins function at the peripheral cholinergic presynaptic nerve terminals,
principally the neuromuscular junction, by preventing the release of acetylcholine
and thereby leading to a generalized flaccid paralysis and autonomic symptoms.
In keeping with the fact that toxins are chemical poisons produced by biologic
organisms, it is important to keep in mind that cases of botulism arising from a
terrorist attack represent intoxication rather than infection caused by replicating
C. botulinum organisms.
Clinical Manifestations. Following a latent period ranging from 24 hours to
several days, victims begin to experience cranial nerve dysfunction, manifesting
as bulbar palsy, ptosis, photophobia, and blurred vision owing to difficulty in
accommodation. Symptoms progress to include dysarthria, dysphonia, and
dysphagia. Ultimately, a descending, symmetric, flaccid paralysis ensues,
although sensorium and sensation are not affected primarily. The mucous
membranes are dry; this fact, along with mydriasis, the nature of the paralysis
(lack of initial fasciculations), and the latent period, all differentiate botulism
from nerve-agent intoxication. A solitary case of botulism must also be
differentiated from myasthenia gravis, Guillain–Barré syndrome, tick paralysis,
and a few other uncommon neurologic disorders. The presence of multiple
casualties with similar symptoms should raise the concern for botulism.
Management. Supportive care, with meticulous attention to ventilatory support,
remains the mainstay of botulism management. Patients may require such support
for several months, making the management of a large-scale botulism outbreak
especially problematic in terms of medical resources. A heptavalent (types A to
G) despeciated (Fab2) equine botulinum antitoxin was licensed in 2013 for the
management of noninfant botulism and is available through the CDC. Although
