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EM VivasSeizures and first fit

EM Vivas · Seizures and first fit

First seizure that did not recover — the viva

A data viva on two traps in the first seizure: non-convulsive status epilepticus in the patient who does not wake, and the long-QT cardiac cause masquerading as a seizure.

data2 min readSource-verified ·

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Prompt
A 65-year-old man is brought to the emergency department after a generalised tonic-clonic seizure at home. Thirty minutes after arrival he has not regained consciousness, although the overt convulsive movements stopped. His capillary glucose is 6.2 mmol/L and his observations are stable. His ECG shows a corrected QT of 520 ms. Discuss the differential of the non-recovering 'post-ictal' patient and your management.

Interpretation

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The key finding is the failure to recover consciousness, not the ECG. A patient who has not regained consciousness 20 to 30 minutes after the overt convulsive movements have stopped is in non-convulsive status epilepticus until proven otherwise — the seizure has continued electrically beneath the suppressed motor activity (subtle eyelid or facial twitching, nystagmoid eye movements, or simply a vacant unresponsive state). The bedside glucose is normal, so hypoglycaemia is excluded. The diagnosis is confirmed with an urgent EEG; in interim patient is treated empirically with a benzodiazepine and a second-line antiepileptic (the status ladder — lorazepam 4 mg IV, then levetiracetam 60 mg/kg, fosphenytoin 20 mg PE/kg, or valproate 40 mg/kg), the airway is protected, and the intensive-care and neurology teams are involved early. This bridges directly to the status epilepticus topic.

[1]

The long QT (520 ms) is the second trap and changes the differential. A markedly prolonged QT interval in a patient presenting with a "seizure" raises the possibility that the convulsion was a cardiac arrhythmia (torsades de pointes or ventricular tachycardia) with secondary cerebral hypoperfusion, not an epileptic seizure. The QT is prolonged by congenital long-QT syndrome, electrolyte disturbance (hypokalaemia, hypocalcaemia, hypomagnesaemia), and drugs (antiarrhythmics, antipsychotics, macrolides, fluoroquinolones, methadone, ondansetron). I check the potassium, calcium and magnesium and correct any abnormality, review the drug history for QT-prolonging agents, place the patient on continuous cardiac monitoring, and involve cardiology — a congenital or drug-induced long-QT syndrome presenting as a "first seizure" is easily missed and is a cause of sudden death. The lesson: perform an ECG on every patient with a suspected first seizure, and read it for the QT and the inherited channelopathies — a "seizure" with a long QT is a cardiac event until proven otherwise.[1][2]

Management in parallel. Airway, breathing, circulation; IV access; continuous monitoring and a 12-lead ECG; treat as non-convulsive status empirically with the benzodiazepine ladder; arrange an urgent EEG; correct the electrolytes (potassium, calcium, magnesium) and stop any QT-prolonging drug; non-contrast CT to seek a structural cause; involve ICU, neurology and cardiology; admit to a monitored bed. The two diagnoses are not mutually exclusive — a primary cardiac arrhythmia can produce both a convulsion and a prolonged post-ictal state, and non-convulsive status can coexist with a cardiac cause.[1]

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References2ShowHide
  1. [1]Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-based guideline: Management of an unprovoked first seizure in adults: Report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology, 2015.PMID 26503589
  2. [2]Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia, 2014.PMID 24730690
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