Treatment of cutaneous leishmaniasis by curettage.
Authors: M A Currie
Journal: BMJ (1983)

Peptic ulcer in Reye's syndromeThe clinical and pathological features of Reye's syndrome are well known,' but to our knowledge neither gastric nor duodenal ulcers have been reported as a complication.In two recent cases of the syndrome at this hospital a perforated gastric and a perforated duo- denal ulcer were found at necropsy.The ulcers were not suspected and may have contributed to the deaths of both children. Case reportsCase 1-A 6 six month old baby girl presented with tachypnoea after a flu-like illness lasting five days that had been treated with salicylates.On admission she was fully conscious and had a generalised purpuric rash.Meningococcal septicaemia was suspected initially, but 19 hours after admission she developed generalised convulsions with episodes of decere- brate rigidity.Reye's syndrome was suspected and this was confirmed by results of investigations.She had raised serum transaminase activities (alanine transaminase 300 IU/1, aspartate transaminase 104 IU/1, and creatine phosphokinase 600 IU/1) and raised blood ammonia concentration (158 HUmol/l (927 pg/100 ml).Blood and cerebrospinal fluid glucose concentrations were low (1-6 mmol/l (29 mg/100 ml) and 0-6 mmol/l (11 mg/100 ml) respectively).Haemoglobin concentration was 12-4 g/dl with 538 v 109/1 platelets.Pro- thrombin time was raised at 1-7 seconds (control 1 second) as was cephalin- kaolin time at 120 seconds (normal range 38-48 seconds).Computed tomography showed cerebral oedema.She was treated with dexamethasone, mannitol, intermittent positive pressure ventilation, and high doses of phenobarbitone.She had frank bleeding from both upper and lower gastro- intestinal tract and oozing from venepuncture sites.She needed repeated administrations of clotting factors concentrate.Renal failure was treated by continuous peritoneal dialysis.She died from cardiac arrest after nine days in coma.At necropsy she had enlarged fatty liver, cerebral oedema, broncho- pneumonia, perforated gastric ulcer, and renal vein thrombosis.Histological examination showed widespread microvesicular fatty change of the liver and acute mucosal erosion of the stomach with inflammatory debris and blood forming the floor; adjacent submucosal blood vessels were dilated.Appearances were in keeping with acute stress erosion of gastric mucosa.Case 2-A 9 year old boy presented to another hospital with severe abdo- minal pain, weakness, and lethargy after a flu-like illness lasting three days.He was treated with intravenous fluids, salicylate suppositories, and intra- muscular diazepam.He was transferred the following day as results of investigations suggested Reye's syndrome.Blood ammonia concentration was raised (288 Hmol/l (1690 pg/100 ml)), haemoglobin concentration was 13-4 g/dl with 370x 109/1 platelets.Glucose concentration was 1-5 mmol/l (27 mg/100 ml) in blood, and 1-8 mmol/l (32-4 mg/100 ml) in cerebrospinal fluid.Prothrombin time was raised (2.3 seconds) as was cephalin-kaolin time (60 seconds).On admission to this hospital he was drowsy, confused, and irritable.He did not have any gastrointestinal bleeding.Computed tomography confirmed cerebral oedema and an intracranial pressure monitor was inserted.He was treated with intravenous Mannitol and intermittent positive pressure ventilation was started to induce hypocapnia.Clinical brain death occurred 14 hours after admission when intracranial pressure siuddenly spiked from 10 to 40 cm of water pressure.He died from cardiac arrest 36 hours after admission.Necropsy showed an enlarged pale fatty liver, left sided lobar pneumonia, cerebral oedema, large perforated ulcer in the first part of the duodenum anteriorly with secondary peritonitis.Histological examination showed hepatic appearances in keeping with Reye's syndrome, and examination of sections of the duodenum confirmed acute peptic ulceration. 2