Antifibrinolytic agents have been claimed to reduce the rebleed rate in patients with subarachnoid haemorrhage from intracranial aneurysms. However, these agents may in themselves increase the incidence of delayed cerebral ischaemia in these patients. We have used aspirin in an attempt to reduce the incidence of this complication. In a prospective, double-blind trial of aspirin against placebo, 53 patients with subarachnoid haemorrhage were all treated with the antifibrinolytic agent tranexamic acid. Twenty-seven patients received aspirin and 26 patients received placebo. The morbidity and mortality was similar in each group. A further breakdown into patients who had their aneurysms clipped at craniotomy (21 patients) similarly failed to show a more favourable outcome in either group. It is concluded that aspirin does not affect the outcome in patients with subarachnoid haemorrhage treated with tranexamic acid.
SUMMARY An unusually severe hypersensitivity reaction to carbamazepine is described, in which the patient presented with lymphadenopathy, hepatosplenomegaly, bone marrow suppression, immunosuppression and other features strongly suggestive of a lymphoma.Case history A 26 year old man with a three year history of severe depression had been treated as an inpatient by being given imipramine at his initial presentation. He had recently relapsed and had attempted to commit suicide. An electroencephalograph test after a blackout had shown a severely abnormal pattern following alcohol consumption. He was therefore given carbamazepine 200 mg twice a day for both its antidepressant as well as its antiepileptic effect. Within two weeks he started to complain of a severe sore throat and noticed that his neck had become swollen and tender. He developed drenching night sweats, anorexia, and general malaise. He was initially treated by his general practitioner with oral penicillin and then referred to the haematology department when his neck swelling deteriorated.On admission to hospital he was unwell with severe cervical lymphadenopathy combined with facial and neck oedema. He had a high fluctuating fever with temperatures of up to 41°C and a diffuse erythematous macular rash. Hepatosplenomegaly was noted together with a few small axillary lymph nodes.Initial investigations showed a haemoglobin con- Biopsy of the cervical lymph nodes showed partial preservation of nodal architecture with scattered Accepted for publication 21 May 1986 small lymphoid follicles widely separated by a polymorphous infiltrate. A striking feature was oedema affecting perinodal fat, the capsule, and the parenchyma. There were irregular zones of necrosis affecting not only the follicles but also the interfollicular regions. Small arteries showed fibrinoid necrosis of their walls and they contained fibrin thrombi. The cellular infiltrate in the T zones included large numbers of immunoblasts with oval vesicular nuclei and a single central nucleolus, together with small lymphocytes, plasma cells, and some macrophages. Occasional large cells with single or multiple somewhat lobed nuclei and prominent nucleoli in ill defined cytoplasm were present; these showed features indistinguishable from Reed-Sternberg cells. Eosinophils were sparse. Vascular channels lined by plump endothelial cells ramified through the stroma. Immunoperoxidase stains of the paraffin embedded tissue showed diffuse positivity for IgM, IgA, IgG, K and A light chains, indicating polyclonality. The overall features were in keeping with angioimmunoblastic lymphadenopathy.A computed tomography scan of the abdomen confirmed the presence of hepatosplenomegaly but showed no intra-abdominal lymphadenopathy. A lymphangiogram showed no lymphadenopathy or lymphamatous architecture within the abdomen, and a chest X-ray was within normal limits. The bone marrow aspirate and trephine showed reactive features only with no evidence of lymphamatous infiltrate. A throat swab and blood cultures grew ...
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