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More than 100 patients (38 in the head and neck) have been treated by the insertion of tissue expanders since the technique was introduced six years ago. Our methods have been refined as we have learned more, and these improvements are described. Morbidity is high when untrained surgeons start to use the technique. The most important decision is the planning of the expander and filling port pockets, but above all the location of the incision(s): Incisions must be kept small and away from the defect, the pocket, and the future flap. Intraoperative filling of the expander reduces the need for drains by preventing haematoma and seroma formation, and reduces the formation of expander envelope folds. The optimal location of the valve is a "quiet" area above or lateral to (or both) the expander, and at least 7 cm away. Mathematical formulas are useless in predicting available flap length, as elasticity and contractility depend on individual factors. A good estimation of flap length is twice the height of the expander above the skin surface or the distance over the dome of the expander minus the corresponding measurement of its base. Overexpansion by 30-50% makes the procedure more predictable.

Forty-seven adults with urinary tract infection (UTI), 9 with recent acute pyelonephritis and 38 with previous renal infection, were investigated for the presence of autoantibodies to Tamm-Horsfall protein (THP). All patients except 6 had or had had vesicoureteric reflux (VUR). In patients with recent acute pyelonephritis, only IgA antibodies were significantly elevated. Among the patients with previous UTI, more than 6 months before the time of testing, a graded response was found for IgG and IgM specific antibodies, with the lowest value in those with renal damage and elevated serum creatinine and the highest in those with a normal X-ray. A negative correlation was found between IgG antibodies to THP and elevated serum creatinine (r = -0.76, P less than 0.02). No significant correlation was found between VUR itself and antibodies to THP. A low IgG antibody level to THP in patients with a history of previous UTI seems to be a useful indicator of renal scarring. Possible immunologic mechanisms behind the low antibody level and the renal damage are discussed.

No abstract

Twenty-four arteries of rabbit ears, divided into three groups of eight, were prepared and 32P-platelets injected. Arteriotomy (7 mm) and intimectomy (5 mm) were performed and in vivo platelet accumulation followed for 2 hours. Group A comprised untreated control animals, group B was treated with 17 ml saline/kg bw, and group C with 1 g dextran and 17 ml saline/kg bw (Macrodex). Significant differences in platelet accumulation were observed only between the control and Macrodex groups at 105 and 120 minutes. In the control and saline groups four of eight vessels showed poor or no patency. All Macrodex vessels showed good patency. Control and saline vessels had large amounts of red thrombotic material, except for three saline cases with small amounts. After Macrodex treatment five of eight vessels were apparently clean, while the other three showed only small amounts of red thrombotic material. Dextran seems not to influence platelet function but rather to inhibit fibrin stabilization and probably increases fibrinolysis. Vascular patency was only endangered by the formation of solid fibrin-containing red thrombi.