SIMULTANEOUS BOTULISM IN TWO BROTHERS ADDICTED TO

ARCH SOC ESP OFTALMOL 2007; 82: 583-586
SHORT COMMUNICATION
SIMULTANEOUS BOTULISM IN TWO BROTHERS
ADDICTED TO COCAINE
BOTULISMO SIMULTÁNEO EN DOS HERMANOS
COCAINÓMANOS
AGUIRRE-BALSALOBRE F1, GONZÁLEZ-HERRERA M1, MENGUAL-VERDÚ E2,
GARCÍA-CONCA V1, HUESO-ABANCENS JR2
ABSTRACT
RESUMEN
Introduction: Botulism is currently an uncommon
disease in which the botulinum toxin causes a progressive muscular paralysis that can lead to the
death due to a failure of respiratory muscles.
Clinical case: Two brothers, both addicted to cocaine, came to the casualty department because of a
decrease of near visual acuity and bilateral mydriasis. Two days later, they developed eyelid ptosis,
asymmetric dysfunction of the extraocular muscles
and vomiting.
Discussion: The presence of a paralysis of accommodation, with bilateral mydriasis that reacts to
pilocarpine, makes it necessary to consider botulism as a possible cause (Arch Soc Esp Oftalmol
2007; 82: 583-586).
Introducción: El botulismo es poco frecuente en la
actualidad. La toxina botulínica produce una parálisis muscular progresiva que puede producir la
muerte del paciente por parada de los músculos respiratorios.
Caso clínico: Dos pacientes hermanos, adictos a la
cocaína, acudieron al Servicio de Urgencias por disminución de la agudeza visual cercana, con midriasis bilateral. A los dos días presentaban, además,
ptosis palpebral, disfunción asimétrica de la motilidad ocular extrínseca, y vómito.
Discusión: Ante la presencia de una parálisis de la
acomodación con una midriasis bilateral que responde a pilocarpina, se debe considerar el botulismo como una posible etiología.
Key words: Botulism, pupil disorders, pupillary
reflex, cocaine abuse, mydriasis.
Palabras clave: Botulismo, alteraciones pupilares,
reflejos pupilares, abuso de cocaína, midriasis.
Received: 31/5/06. Accepted: 25/7/07.
San Juan de Alicante University Hospital. Alicante. Spain.
1 Graduate in Medicine.
2 Ph.D. in Medicine.
Correspondence:
Fernando Aguirre Balsalobre
Servicio de Oftalmología
Hospital Universitario San Juan de Alicante
Ctra. Ncnal. 332 Alicante-Valencia, s/n
Apartado de correos, 41
03550 San Juan de Alicante (Alicante)
Spain
E-mail: [email protected]
AGUIRRE-BALSALOBRE F, et al.
INTRODUCTION
Botulism is a neuroparalytic disorder caused by
Clostridium botulinum’s exotoxins. It is a rare disease, diagnosing 10 to 50 cases per year in Spain (1).
The usual way for contracting this disease in
adult patients is through food poisoning, generally
caused by the intake of home-made food preserves
not previously cooked and manufactured at least
eight days before, or else induced by penetrating
cutaneous wounds.
Depending on the amount present in the body, the
first symptoms appear from twelve hours to eight
days later. This toxin blocks muscle contractions by
blocking the release of preganglionic acetylcholine
in the neuromuscular plate, which leads initially to
ocular alterations such as non-reactive mydriasis,
palpebral pthosis or oculomotor nerve palsy dyplopia. Subsequently, weakness due to muscular palsies expands, leading to respiratory failure and
death of the patient (1,2).
The diagnosis is made by detecting the toxin in
serum or other body fluids. Treatment consists of
eliminating the toxin from the digestive tract, administering an antitoxic serum, penicillin G and providing breathing support. Symptoms will revert in the
opposite order as they occurred (1,2).
CASE REPORT
Two brothers, aged 38 and 42, arrived in the
emergency room reporting blurry vision for the past
24 hours, and worse near vision. They did cocaine
regularly, and linked the current symptoms to it, since they had just changed providers the day before.
In both cases, far visual acuity had been preserved (0.8), but near visual acuity stood below 0.4.
Their bilateral non-reactive mydriasis (figs. 1 and 2)
returned in a few minutes after instilling 1% pilocarpine. Extrinsic ocular movements and convergence, just as the remaining exploration, were normal.
They arranged an appointment for check-up and
were diagnosed with possible mydriasis due to drug
tampering. Two days later, the symptoms included
bilateral palpebral pthosis and dyplopia. There was
limited abduction of both eyes, while the remaining
gaze cardinal positions were only partially restricted. Furthermore, both patients suffered from nauseas, vomits, dysphagia and micturition difficulties.
Deepening the anamnesis, the patients reported
they had eaten home-made cardoon preserves two
days before the onset of symptoms. The likelihood
of poisoning caused by Clostridium botulinum was
suggested.
The cranial image testing performed (computed
axial tomography) was normal. However, the electromyograms revealed blocking at the level of the
muscular motor plate, prompting the administration
of botulinum antitoxin.
The youngest brother required in-hospital care
during eighteen days, twenty-nine days for the
eldest, who required mechanical ventilation. Toxin
detection in the faeces was negative in both
patients.
Ocular pathologies remitted completely and in the
reverse order. Mydriasis did not fully disappear forty
days after the onset (figs. 1 and 2), and improvement
Fig. 1: Bilateral mydriasis in the eldest brother, in worse condition, three weeks after the onset of symptoms.
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Botulism in cocaine addicts
Fig. 2: Mydriasis in the younger brother three weeks after the onset of symptoms.
occurred earlier than in the youngest brother, who
suffered the less acute condition (figs. 3 y 4).
DISCUSSION
Faced with a fixed pupilary mydriasis without
prior trauma, we must first discard as the most frequent cause pupilary dilation by means of eye drops
or vegetal products, whether by accident or
willingly. It is also important to assess extrinsic and
palpebral ocular movements in case the cause was
palsy of the II cranial nerve. If the biomicroscopy
reveals an irregular pupil in the context of a mydriasis slowly reactive to light, the most probable diagnosis would be Adie’s pupil (3).
The instillation of topical pilocarpine facilitates
diagnosis. Any pupil subjected to the instillation of
a parasympathetic agent may react or react slightly
to 1% pilocarpine. Adie’s pupil contracts at low
doses of 0.125% pilocarpine, whereas the III nerve
palsy tends to react to higher doses. The two last
pathologies are more frequently unilateral than
pharmacological mydriasis (3).
Accommodation should be taken into consideration. A bilateral mydriasis cannot be attributed to
cocaine (sympathetic stimulation) when there is an
accommodation disorder because of parasympathetic blockers (4,5).
Even though botulism is extremely rare, when
faced with a bilateral mydriasis that reacts to pilocarpine one should question the patient regarding
any potential relevant food-related history. Whenever in doubt, the patient should be immediately
referred for electromyographic examination. The
botulum antitoxin should be administered early on,
Fig. 3: Palpebral pthosis and weak ocular movements in the eldest brother three weeks after the onset of symptoms.
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AGUIRRE-BALSALOBRE F, et al.
Fig. 4: Lesser degree pthosis and lower limitation of ocular movements in the youngest brother three weeks after the
onset of symptoms.
even if the presence of toxins in the body or food
has not been confirmed, which sometimes may be
the case.
In other words, early diagnosis of this pathology
is crucial for the vital prognosis of patients, thus the
significance of taking it into account in the differential diagnosis of bilateral mydriasis.
2.
3.
4.
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