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Weight-lifting: more of a headache than it's worth? Timothy Martin Ulster Hospital Dundonald Karen Adams Case Report Intracranial hypotension most commonly occurs following lumbar puncture, with spontaneous cases often misdiagnosed, leading to treatment delays. 1 The classic orthostatic headache may be accompanied by various neurological symptoms and signs. We describe the case of a 46 year old fireman who presented with such a headache two weeks following minor cervical discomfort while weight lifting. MRI confirmed intracranial hypotension with slumping of the mid brain, bilateral extra-axial collections, foramen magnum crowding and smooth dural Gadolinium enhancement. He improved with bed rest and hydration, and was discharged with lifestyle advice. Four weeks later he re-presented with worsening headache, facial dyskinesia, restless limbs and unusually gregarious behaviour. Repeat MRI confirmed progression of intracranial hypotension, with bilateral subdural haematomas compressing his cerebral hemispheres, distortion of midbrain and pons, and bilateral uncal herniation (figures 1&2). Interestingly, he had none of the clinical features typically associated with herniation due to raised intracranial pressure. A thirty degree head down tilt caused marked symptomatic improvement over two days, provided he remained recumbent. MR myelogram could not identify the source of his CSF leak and he was treated with two non-targeted lumbar epidural blood patches, eight days apart. The second resulted in sustained symptomatic resolution, with repeat MRI showing an epidural haematoma but relatively little change intracranially. Intracranial hypotension due to spontaneous CSF leak should be considered in patients presenting with orthostatic headache. Associated movement disorders are uncommon, and facial dyskinesia has not been previously reported. Diagnosis relies on clinical suspicion and cranial MRI, given CSF pressures and CT may be normal. 2 Symptoms can resolve with conservative management: bed rest, hydration, simple analgesia and caffeine. 3 If unsuccessful, epidural blood patching is indicated, though with a success rate of 33-57% multiple patches are often needed. 4,5 Failing this, epidural fibrin glue, continuous epidural infusion or surgical repair may be considered. 3 References 1. Schievink WI. Misdiagnosis of spontaneous intracranial hypotension. Arch Neurol. 2003;60(12):1713- 1718 2. Sun-Edelstein C, Lay CL. Headache attributed to spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis. Uptodate. Updated Jan 12 th Accessed 26/2/15. Available at www.uptodate.com.abc.cardiff.ac.uk/contents/headache-attributed-to-spontaneousintracranial-hypotension-pathophysiology-clinical-features-and-diagnosis 3. Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA. 2006;295(19):2286 4. Berroir S et al. Early epidural blood patch in spontaneous intracranial hypotension. Neurology. 2004;63(10):1950 5. Sencakova D, Mokri B, McClelland RL. The efficacy of epidural blood patch in spontaneous CSF leaks. Neurology. 2001;57(10):1921
You take my breath away- another cause of hyperlactaemia Nerys Conway University Hospitals Bristol Nick Suarez Background A 22-year-old lady was admitted to the Emergency Department complaining predominantly of dyspnoea. An arterial blood gas demonstrated a high lactate. Initially she was treated for sepsis. We discuss another cause of hyperlactatemia and the importance of ruling out other causes. Case Presentation She presented with dyspnoea and pleuritic chest pain. An arterial blood gas demonstrated a hyperlactaemia (5mmol/L) and respiratory alkalosis. A CXR and CTPA were unremarkable. Her ECG showed sinus tachycardia. She was referred to the Acute Medical Unit (AMU) with “sepsis- ?source”. On arrival to AMU she hyperventilated and had a panic attack. Her observations demonstrated a pulse of 125 bpm and a respiratory rate of 38. She described a similar episode at home which subsequently led to her admission. Her phosphate was 0.3mmol/l. Her inflammatory markers and other electrolytes were normal. The hypophosphataemia caused hyperventilation leading to a panic attack. She was given IV and oral phosphate replacement. Discussion Insufficient dietary intake or absorption; raised renal losses or redistribution of body phosphate stores can cause hypophosphataemia (
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