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1/5. Caudal epidural blood patch for treating intractable vomiting in a child after placement of a permanent intrathecal catheter.

    Postdural puncture cerebral spinal fluid (CSF) leak most often manifests as a postdural puncture headache (PDPH). The reported frequency in young children varies (1-4). Persistent CSF leak may also be present without PDPH. We present a case of postoperative nausea and vomiting resulting from a presumed lumbar CSF leak in a nonverbal child after surgical placement of a permanent intrathecal catheter. Treatment with an epidural blood patch (EBP) via the caudal approach resulted in complete relief of symptoms.
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2/5. Idiopathic "benign" intracranial hypertension: case series and review.

    Idiopathic "benign" intracranial hypertension is an uncommon but important cause of headache that can lead to visual loss. This study was undertaken to review our experience in the diagnosis and management of idiopathic intracranial hypertension, giving special attention to treatments used. A retrospective chart review was conducted on 32 patients diagnosed with idiopathic intracranial hypertension between 1984 and 1995. Subjects included 23 females and ranged in age from 2 to 17.5 years. headache was the most common symptom, followed by nausea and vomiting, double vision, and visual loss. papilledema was the most common sign. Others were VIth cranial nerve palsy and compromised visual acuity at or within 3 months of presentation. Management included administration of acetazolamide or corticosteroids, lumboperitoneal shunt, optic nerve fenestration, and repeat lumbar puncture. Treatment combinations were used in 40% of cases. During follow-up, headache, papilledema, and decreased visual acuity persisted for longer than 10 months in a significant number of patients. We conclude that idiopathic intracranial hypertension causes significant short- and long-term morbidity with no proven effective treatment available. A prospective study is needed to establish the indications for treatment and the efficacy of the treatments used.
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3/5. The role of the biochemistry department in the diagnosis of pituitary apoplexy.

    A 47-year-old man presented with severe clinical hypoglycaemia. He had long-standing insulin-dependent diabetes with previously good glycaemic control. Intense headaches and vomiting initiated hospitalization. A brain computed tomography (CT) scan was normal, and a lumbar puncture showed elevated cerebrospinal fluid (CSF) protein [0.67 g/L; normal range (NR) 0.15-0.45 g/L], suggesting resolving viral meningitis. Routine thyroid function tests were abnormal (free thyroxine 10.6 pmol/L, NR 9-22.5 pmol/L; thyroid-stimulating hormone 0.16 mU/L, NR 0.35-5 mU/L). In the absence of evident thyroid therapy, the laboratory policy required an urgent cortisol assay to be added; this was very abnormal (42 nmol/L), suggesting hypopituitarism. Later analysis showed that concentrations of gonadotrophins and adrenocorticotrophin were low. An urgent pituitary magnetic resonance imaging scan revealed an unsuspected pituitary tumour with recent haemorrhage (pituitary apoplexy). The patient was given intravenous hydrocortisone and then stabilized on oral hydrocortisone, thyroxine and mesterolone. He made a full recovery and the hypoglycaemia resolved. The normal brain CT scan was falsely reassuring and the CSF protein was not due to viral meningitis but to haemorrhage into the pituitary tumour. If laboratory policy had not required the urgent cortisol assay be added, the diagnosis of hypopituitarism would have been delayed or even missed altogether. This could have led to the death of the patient.
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4/5. An unusual case of chronic meningitis.

    BACKGROUND: Chronic meningitis is defined as symptoms and signs of meningeal inflammation and persisting cerebrospinal fluid abnormalities such as elevated protein level and pleocytosis for at least one month. CASE PRESENTATION: A 62-year-old woman, of unremarkable past medical history, was admitted to hospital for investigation of a four-week history of vomiting, malaise an associated hyponatraemia. She had a low-grade pyrexia with normal inflammatory markers. A CT brain was unremarkable and a contrast MRI brain revealed sub-acute infarction of the right frontal cortex but with no evidence of meningeal enhancement. Due to increasing confusion and patient clinical deterioration a lumbar puncture was performed at 17 days post admission. This revealed gram-negative coccobacilli in the CSF, which was identified as neisseria meningitidis group B. The patient made a dramatic recovery with high-dose intravenous ceftriaxone antibiotic therapy for meningococcal meningitis. CONCLUSIONS: 1) Chronic bacterial meningitis may present highly atypically, particularly in the older adult. 2) There may be an absent or reduced febrile response, without a rise in inflammatory markers, despite a very unwell patient. 3) Early lumbar puncture is to be encouraged as it is essential to confirm the diagnosis.4) Despite a delayed diagnosis appropriate antibiotic therapy can still lead to a good outcome.
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5/5. pneumocephalus following the treatment of a postdural puncture headache with an epidural saline infusion.

    We report a case of pneumocephalus following the attempted treatment of a postdural puncture headache by a continuous epidural saline infusion. Within 1 hour of infusion, symptoms of a severe headache, nausea, and vomiting prompted a computerized tomographic scan of the head that showed 12 to 15 ml of air in the cranium. The epidural space was located easily with the loss-of-resistance technique using 3 ml of air. A saline bolus and infusion were initiated after confirmation of correct placement of the epidural catheter. We suggest that air passed from the negative-pressure epidural space through the dural puncture created by the diagnostic spinal tap, producing a pneumocephalus.
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