A thickened gallbladder wall is often seen with ultrasound in alcoholic cirrhosis. Hypoalbuminaemia is thought to be the cause since there is a strong association between bowel wall thickening and low serum albumin. To determine the role of portal hypertension in producing gallbladder wall thickening we studied 40 consecutive stable patients-37 with cirrhosis and three with portal hypertension due to primary biliary cirrhosis. Ultrasound assessment of the gallbladder wall was made after an overnight fast using a Technicare autosector. Wall thickness 4 mm or greater was considered abnormal. Twenty-seven patients had a thickened gallbladder wall and all had evidence of portal hypertension. Hypoalbuminaemia was not an important factor since it was only present in six cases with thickened walls. In two cases reduction in portal pressure with oral propranolol was associated with a decrease in gallbladder wall thickness. These results suggest that portal hypertension, not hypoalbuminaemia, is the dominant factor causing gallbladder wall thickening in cirrhosis. Ultrasound demonstration of gallbladder wall thickening in chronic liver disease should suggest the presence of portal hypertension.

Hyponatremia developing some days after transsphenoidal pituitary adenectomy is a treacherous complication of uncertain cause. Of 19 patients monitored in a pilot study at the Wessex Neurological Centre, plasma sodium fell below 125 mmol/liter in three patients at times ranging from 6 to 9 days postoperatively. One patient had evidence of inappropriate secretion of arginine vasopressin (AVP), and the other two probably had steroid insufficiency despite apparently adequate steroid cover. In a more detailed study, the fluid and sodium balance of a further 16 patients was monitored for 7 to 11 days following transsphenoidal surgery together with plasma cortisol, renin, and AVP concentrations. No patient became severely hyponatremic. Three developed partial diabetes insipidus. Two patients with Cushing's disease had evidence of postoperative corticosteroid insufficiency despite normal steroid protection. An inappropriately low plasma cortisol concentration was recorded in both. Plasma AVP concentrations did not show a delayed surge postoperatively. Delayed hyponatremia appears to occur most often in patients with hypoadrenalism, as glucocorticoid cover is decreased. It results from water retention combined with natriuresis, and is reversed by glucocorticoid treatment.

This case is a rare adult type Tillaux fracture. This fracture should be diagnosed in the emergency department. The fracture requires careful evaluation with awareness of associated injury. Standard radiological views (antero-posterior and lateral) of the ankle may not clearly show the fracture displacement hence, an oblique view is required. The fracture should be managed by the emergency physician, if the displacement is less than 2 mm, by immobilising with a non-weight bearing cast or ankle braces for 6 weeks. If the fracture fragment is displaced more than 2 mm, it should be treated by closed reduction failing which open reduction and internal fixation is the standard practice.

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