Biomedical subjects
Publications and source records attributed to K J Miloszewski.
Dysphagia in a 79 year old lady was caused by a giant polypoid tumour in mid-oesophagus. Surgery was not appropriate. Shrinkage of the tumour and its eventual detachment were achieved by stopping its blood supply by YAG laser photocoagulation of the tumour stalk. Good, temporary palliation of the dysphagia was achieved.
In 277 consecutive episodes of suspected upper gastrointestinal bleeding, lesions bearing stigmata of recent haemorrhage (stigmata) were found by endoscopy in 110 (47%) out of 233 patients who were judged to have bled; 78 (33%) had lesions without stigmata, and in 45 (19%) no lesion was seen. Results in 176 entirely unselected admissions for upper gastrointestinal bleeding were similar.Forty-eight chronic duodenal and 41 chronic gastric ulcers were identified by endoscopy. Stigmata were found in 27 (56%) and 33 (80%) of these cases respectively. Sixteen patients had multiple lesions, and in 12 (75%) the presence of stigmata permitted diagnosis of the source of the haemorrhage. Stigmata were more likely to be seen in cases of duodenal ulcer, Mallory-Weiss lesions, and oesophageal varices when endoscopy was performed within 12 hours of bleeding, but were as common in cases of gastric ulcer after longer intervals.In the absence of stigmata one out of 21 patients with duodenal ulcer had further haemorrhage and one other needed emergency surgery; no patient with gastric ulcer had further haemorrhage or needed emergency surgery. In contrast, when stigmata were present 15 of the 27 patients with duodenal ulcer (56%) had further haemorrhage and 17 (63%) needed emergency surgery; of the 33 patients with gastric ulcer, 10 (30%) had further haemorrhage and 15 (45%) required emergency surgery. Superficial mucosal lesions may have been the source of haemorrhage when an ulcer unmarked by stigmata was seen at endoscopy. Stigmata were superior to any other single factor or combination of factors in predicting rebleeding and the need for emergency surgery.
A variety of indirect techniques has been claimed to provide evidence of spontaneous reversal of portal blood flow in hepatic cirrhosis but the existence of the phenomenon has been doubted by some who do not accept the validity of the indirect evidence. There are few reports of the demonstration of hepatofugal portal flow by selective hepatic arteriography, which is the only acceptable technique. We report three patients with histologically confirmed cirrhosis in whom hepatofugal portal blood flow was unequivocally demonstrated by arteriography, in whom no surgical portosystemic shunt had been performed and in whom there was no evidence of the Budd-Chiari Syndrome or hepatoma, situations accepted as associated with reversed portal blood flow. Theoretical considerations suggest that shunt surgery for bleeding esophageal varices should not be ruled out on the grounds of hepatofugal portal flow. However, end-to-side portacaval anastomosis and distal splenorenal shunt might predispose to the early redevelopment of esophageal varices when reversed portal flow is present. Side-to-side portacaval and conventional splenorenal shunts might be preferable in having less effect on hepatic parenchyma perfusion than when orthograde portal flow in the case.