Author: Hassan Jafri, Sundas Sajid / Editor: Stephen Sheridan / Codes: ELP10, RP1, SLO3 / Published: 21/01/2026
A 48-year-old man presents to the Emergency Department (ED) with acute vomiting, blurred vision, tremor, and unsteady gait. His symptoms began two days after starting clarithromycin for cellulitis.
He reports receiving a vitamin B12 injection one week earlier, after which cellulitis develops at the injection site. Because of a penicillin allergy, his GP prescribes clarithromycin on Thursday. By Saturday, he develops neurological symptoms including tremor, vomiting, blurred vision, and ataxia. On Sunday, his symptoms worsen, prompting ED attendance.
His past medical history includes epilepsy (on carbamazepine), hypertension, colon cancer in remission, and previous DVTs on lifelong rivaroxaban.
On examination he is flushed, agitated, but oriented. Vital signs are stable. Neurological examination reveals dysdiadochokinesia, impaired heel-to-shin coordination, and horizontal nystagmus. Pupils are sluggishly reactive. The right upper arm shows cellulitis without abscess formation.
Investigations show sinus rhythm on ECG, a normal chest X-ray, and a normal CT brain. Serum carbamazepine is 26.5 µg/mL (therapeutic 4–12).
Clarithromycin and carbamazepine are immediately discontinued, supportive care provided, and doxycycline commenced. Toxicology advice is sought. Within 48 hours, his neurological symptoms resolve. Plans are made to recheck levels and cautiously restart carbamazepine.
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Question 1 of 3
1. Question
Which of the following clinical features is most characteristic of carbamazepine toxicity?
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Question 2 of 3
2. Question
Which of the following best explains the mechanism of this interaction?
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3. Question
From a systems perspective, which measure would be most effective in preventing such drug–drug interactions in the Emergency Department?
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7 responses
Great
Great clinical case
Thank you Great Insight
good case to discuss
Fantastic one.
nice
great insight.