Reactions Weekly | 2021
Caffeine
Abstract
Generalised tonic-clonic seizures: case report A 33-year-old woman developed generalised tonic-clonic seizures during treatment with caffeine for presumed postdural puncture headache. The primigravida woman, who was 39 weeks pregnant, was admitted with ruptured membranes. She was induced with oxytocin. On admission, she was normotensive with 1+ of proteinuria. Successful placement of a lumbar epidural catheter for labour analgesia occurred, but only following two dural punctures. Six hours afterwards, failure to progress necessitated an emergency caesarean section, which was performed after an epidural ‘top-up’; the epidural catheter was removed at the end of the operation. On the second day post-operation, she developed posturally-related symptoms of nausea, severe shoulder and neck pain and pressure across the temples. She had developed ankle oedema. Initial treatment for presumed postdural puncture headache with oxycodone, paracetamol and ibuprofen was not effective. Therefore, she was initiated on oral caffeine 100mg two times a day. On day 3, although her neck stiffness was ameliorating; she felt mildly confused. She developed two generalised tonic-clonic seizures, 30 minutes apart. Her BP was 102/52mm Hg. Following the second seizure, the woman was administered diazepam, clonazepam and magnesium sulphate. She was transferred to the network tertiary hospital, where her BP was found to be elevated, although laboratory screening for markers of eclampsia were negative. On day 6, magnetic resonance angiography and MRI excluded dural venous sinus thrombosis and acute infarction, but showed features indicative of both intracranial hypotension and cortical oedema in the posterior regions of the brain. An electroencephalograph performed on day 5 identified posterior slowing. Concurrently, the neck pain and postural headache continued to hamper her ability to ambulate such that, on day 7 post caesarean section (and dural puncture), an epidural blood patch was performed injecting 38mL of blood with no sequelae. On day 8, her headache had improved significantly although she had become unsteady on her feet, forgetful and disorientated in place and time. She displayed mild dyspraxia, inappropriate affect, dysarthria and right-sided neglect (sensory and visual) with brisk reflexes and mild right-sided weakness. Her BP was 150/100mm Hg. Repeat magnetic resonance angiography and MRI on day 9 now showed increased hyperintensity on T2 and fluidattenuated inversion recovery images, in the left posterior parietal lobe, congruous with a recent left middle cerebral artery infarct. Additionally, multiple focal areas of narrowing affecting bilateral anterior, posterior and middle cerebral arteries demonstrated possible vasculitis. The neurologists believed the clinical picture was congruous with a postpartum vasculopathy leading to an ischaemic cerebral infarct, despite her vasculitic screen being negative for double-stranded deoxyribonucleic acid, anti-nuclear, anticardiolipin and extractable nuclear antibodies, lupus anticoagulant and rheumatoid factor. Treatment with nimodipine and IV fluid was initiated for 1 week. Over the following 10 days, slow neurological amelioration occurred, and on day 19, she was discharged to rehabilitation. A repeat MRI performed 3 months later revealed a persisting left parietal infarct, but the absence of vessel narrowing. With the exception of some residual right-sided ‘clumsiness’, there had been almost complete resolution of her neurological deficits. This was congruous with the vasospasm resolution one sees in a posterior reversible encephalopathy syndrome (PRES).