Glossopharyngeal neuralgia associated with cardiac syncope developed in a 53 year old man. Symptoms were controlled with temporary and permanent transvenous pacing and carbamazepine. pacemaker (fig 2).Further examination of his throat showed congestion of the posterior pharyngeal wall with oedema of the uvula and tonsillar fauces. The left upper molars were loose and carious. During the dental examination the patient developed typical pain, followed by asystole which was interrupted by pacemaker intervention. A trigger zone was noted around the left peritonsillar and paramolar region, which when touched with cotton wool or ethyl chloride spray induced an attack. There was no evidence of hypersensitivity of the carotid sinus-carotid massage on either side did not produce significant bradycardia, hypotension, or asystole.' Somatic pain produced by squeezing the achilles tendon failed to induce an attack.

We describe a case of severe traumatic brain injury with multiple facial and skull fractures where CT angiogram (CTA) failed to yield a definite result of brain death as an ancillary test. A 28-year-old man was admitted following a road traffic accident with a Glasgow Coma Score (GCS) of 3/15 and fixed pupils. CT brain revealed uncal herniation and diffuse cerebral oedema with associated multiple facial and skull fractures. 72 h later, his clinical condition remained the same with high intracranial pressure refractory to medical management. Clinical confirmation on brain death was not feasible owing to facial injuries. A CTA, performed to determine brain perfusion, yielded a ‘false-negative’ result. Skull fractures have possibly led to venous prominence in the cortical and deep venous drainage system. This point needs to be borne in mind while considering CTA as an ancillary test to confirm brain death.

A 42 year old woman presented with a 5-hour history of acute severe generalized abdominal pain, with no associated symptoms. During the preceding 4 days she had complained of dull intermittent right upper quadrant pain. On examination she was pale, clammy and hypotensive, with generalized abdominal tenderness, rebound tenderness and guarding. Resuscitation was instituted with intravenous fluids, blood sent for full blood count, urea and electrolytes, blood sugar, amylase and crossmatching, urinary catheterization performed, and radiographs taken of the chest and abdomen. Haemoglobin estimation was 8.6 g/dl, and a provisional diagnosis of spontaneous intraperitoneal haemorrhage was made. The patient was immediately transferred to the operating theatre where a long midline laparotomy was performed. The peritoneal cavity was full of fresh blood and clot, confirming the suspected diagnosis. The haemorrhaging lesion was a suspicious-looking 4 x 3 cm nodule on the dome of the right lobe of the liver, which had ruptured and stripped the capsule off a large area. Numerous such lesions were seen in both lobes of the liver; they looked like tumour nodules, but there was no evidence of a primary intra-abdominal neoplasm.After unsuccessful attempts to control the haemorrhage by ligation, deep hepatic sutures and hepatic arterial clamping, the liver was packed off with large swabs, the abdomen closed, and arrangements made for subsequent transfer of the patient to a nearby centre with a specialist hepatic surgeon. However, the patient became hypotensive despite rapid infusion of large volumes of intravenous fluids and blood. A second laparotomy revealed gross haemoperitoneum, and both hepatic lobes were literally disintegrating, precluding any possibility of resection.At post-mortem, in addition to the lesions described in the liver, two similar tumour nodules 1 cm in diameter were identified in the apex of the left lung. The absence of an obvious primary tumour was confirmed. Histological examination showed the nodules to be deposits of melanocarcinoma. On closer questioning of relatives, it was disclosed that the patient had undergone excision of a malignant melanoma, 0.9 mm thick, from the skin of the back, 5 years previously.In the absence of a known hepatic lesion the diagnosis of spontaneous rupture may be difficult. A thorough history may provide important clues. The combination of peritoneal irritation and hypovolaemic shock, with a short duration of symptoms, may suggest intraperitoneal haemorrhage. Successful surgical management has been claimed for resection ofthe affected lobe,'-3 hepatic artery ligation,4 or direct injection of ethanol into the bleeding lesion.5 However, despite early diagnosis and prompt surgery, the mortality of this condition is considerable. Retroperitoneal haemorrhage from a renal carcinoma in association with streptokinase therapy Sir, We wish to report an unusual complication of treatment with intravenous streptokinase for suspected myocardial infarction, which we believe has not previous...

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