Here’s a hint. The eyes have it.
A 47-year-old man was found dyspnoeic in his car and brought to the emergency department.
On arrival, he was hypertensive (139/102 mmHg), tachycardic (104 beats per minute) and mildly hypoxic with an oxygen saturation of 91% on room air. He was afebrile but diaphoretic.
He was awake but intermittently inattentive, with slurred, muffled speech. Despite reporting a sensation of tongue swelling and difficulty breathing, there was no visible facial or airway swelling. His lungs were clear, his abdomen was soft and nontender, and he was able to speak in full sentences.
He had a history of heavy alcohol use, consuming four to six drinks daily, and had been drinking in the hours before presentation.
During the previous two hours, he experienced the sensation of tongue swelling and difficulty breathing, but no headache, sore throat, odynophagia, nausea, vomiting, rash, itching or swelling of the face or limbs.
He reported no recent use of medications, no consumption of new foods or insect bites. Paramedics had administered epinephrine, antihistamines and glucocorticoids en route, but his symptoms persisted.
So, what are we thinking?
Anaphylaxis seems unlikely. There was no urticaria, hypotension, gastrointestinal involvement or visible angioedema, and the lack of response to epinephrine further argued against it. Infectious causes such as epiglottitis or deep neck space infections were also improbable in the absence of fever, sore throat or odynophagia.
Initial investigations showed mild leukopenia (3.8 × 10⁹/L), thrombocytopenia (58 × 10⁹/L) and a transaminitis with AST 297 U/L and ALT 168 U/L. His blood alcohol level was 0.209%, and toxicology screening was otherwise negative.
The key clue emerged on neurological examination.
The patient was found to have complete ophthalmoplegia – he could not move either eye in any direction. Pupils were equal and reactive, and other cranial nerve reflexes were initially preserved.
Central causes such as stroke, tumour and inflammatory conditions were effectively ruled out by normal CT and MRI imaging. The patient has no headache, fever or stiffness of the neck that would suggest meningitis.
Wernicke’s encephalopathy was considered given his alcohol history, but the absence of ataxia or confusion – and subsequent lack of response to thiamine – made this less likely.
Bickerstaff’s brain-stem encephalitis, an inflammatory disorder that may be manifested by ataxia, headache, seizures, altered mentation and various cranial-nerve deficits (including ophthalmoplegia), was another possible cause.
Attention turned to peripheral causes, including myasthenia gravis, Lambert–Eaton myasthenic syndrome, Guillain–Barré syndrome and botulism. Of these, only Guillain–Barré syndrome is typically associated with transaminitis, which is usually mild, so the aminotransferase levels of this patient were ruled more consistent with alcohol associated disease or cirrhosis.
Over the next 48 hours, the patient deteriorated.
He developed progressive descending paralysis, losing pupillary, corneal, cough and gag reflexes, and became areflexic. He required intubation for worsening respiratory failure. A lumbar puncture showed near-normal cerebrospinal fluid, without the elevated protein typically seen in Guillain–Barré syndrome.
At this point, one diagnosis moved to the top of the list.
Botulism.
The patient’s history provided a critical clue: he reported frequently consuming perishable foods left at room temperature for prolonged periods. Public health authorities were contacted, and botulinum antitoxin was administered approximately 90 hours after presentation.
Laboratory confirmation followed. Serum testing detected botulinum neurotoxin type A, confirming the diagnosis of foodborne botulism.
Botulism is a rare but life-threatening neuroparalytic illness caused by toxins produced by Clostridium botulinum. The toxin blocks acetylcholine release at the neuromuscular junction, leading to symmetrical descending paralysis, often beginning with cranial nerve involvement – including ophthalmoplegia, dysarthria and dysphagia.
This case highlighted how early features can mimic more common conditions. The patient’s initial complaint of “tongue swelling” and dyspnoea led to treatment for anaphylaxis, delaying recognition of a neurological cause.
The eyes, however, told the real story.
Despite treatment, recovery was prolonged. The patient required tracheostomy and long-term rehabilitation, with minimal neurological improvement after several months, underscoring the importance of early recognition and prompt antitoxin administration.
