Effect of age on progression through temporary prostheses after below-knee amputation.

Forty six patients that underwent below knee amputation for diabetes, trauma/osteomyelitis or peripheral vascular disease were studied. Healing was estimated by the rate of progression through temporary prostheses as determined weekly by the amputee rehabilitation team (physiatrist, orthopedist, physical therapist, nurse, and prosthetist). For all groups combined, mean days +/- standard error from amputation to above knee cast with pylon and foot (AKPy) were 22.9 +/- 1.9, to below knee cast with pylon and foot (BKPy) 41.6 +/- 2.8 and to laminated temporary prostheses 66.5 +/- 4.5. A regression analysis of these variables on age (range: 29 to 84 yr) showed significant positive correlations for AKPy (r = 0.34, P = 0.0214) and BKPy (r = 0.40, P = 0.0056). An analysis of variance with contrasts (Tukey's protected t) showed significant lower values (P < 0.05) for amputation to BKPy in the trauma/osteomyelitis group when compared to diabetes or peripheral vascular disease and no difference among the last two groups. However, when variables were adjusted for age (analysis of covariance with age as a covariate), the differences among groups disappeared (covariance F(2,44) = 0.9, P > 0.4). In conclusion, age, not the cause of the amputation, correlated with healing after below knee amputation as estimated by the rate of progression through temporary prostheses.

Are transient pulmonary solitary nodules a common event in human dirofilariosis?

Infection by Dirofilaria immitis is a rare cause of solitary pulmonary nodule. We describe the second case of transitory pulmonary nodule found by us in the course of a case-finding study, the third one reported in the literature. The detection of cases of transient pulmonary dirofilariotic nodules suggests that human infection is more prevalent than usually thought, and that this kind of manifestation is frequent in human dirofilariosis. Greater awareness is warranted in endemic areas.

Comparison of different methods for endoscopic hemostasis of bleeding canine esophageal varices.

Despite advances in the therapy of acute esophageal variceal hemorrhage, morbidity and mortality remain high. Continued severe variceal hemorrhage remains a major clinical problem in poor risk patients who cannot tolerate emergency surgery for hemostasis. Several endoscopic hemostatic methods might be effective for variceal hemostasis, but they have not been systematically evaluated. Using a reproducible canine model of esophageal varices, several hemostatic modalities were tested and compared to determine which were most effective in stopping variceal bleeding. Methods tested were endoscopic sclerotherapy, organ laser, neodymium-yttrium-aluminum-garnet laser, monopolar electro-coagulation, bipolar electrocoagulation, ferromagnetic tamponade, and endoscopic heater probe. Both neodymium-yttrium-aluminum-garnet laser and endoscopic sclerotherapy provided reliable hemostasis in acutely bleeding canine varices. Large heater probe controlled bleeding 50% of the time, and all the other methods stopped bleeding in less than half the trials. Rebleeding after balloon inflation proximal to the coagulated bleeding site did not occur with neodymium-yttrium-aluminum-garnet laser or endoscopic sclerotherapy-treated varices but did occur with the other methods. The principal differences between neodymium-yttrium-aluminum-garnet laser and endoscopic sclerotherapy were the ease of application of neodymium-yttrium-aluminum-garnet laser, the higher frequency of esophageal ulcers or erosions with neodymium-yttrium-aluminum-garnet laser, and the lack of variceal obliteration with neodymium-yttrium-aluminum-garnet laser.

A reproducible canine model of esophageal varices.

One of the most promising nonoperative techniques for control of variceal hemorrhage is sclerosis via the fiberoptic endoscope. Many questions remain, however, about sclerosing agents, guidelines for effective use, and limitations of endoscopic techniques. A reproducible large animal model of esophageal varices would facilitate the critical evaluation of techniques for variceal hemostasis or sclerosis. Our purpose was to develop a large animal model of esophageal varices. Studies in pigs and dogs are described which led to the development of a reproducible canine model of esophageal varices. For the final model, mongrel dogs had laparotomy, side-to-side portacaval shunt, inferior vena cava ligation, placement of an ameroid constrictor around the portal vein, and liver biopsy. The mean (+/- SE) pre- and postshunt portal pressure increased significantly from 12 +/- 0.4 to 23 +/- 1 cm saline. Weekly endoscopies were performed to grade the varix size. Two-thirds of animals developed medium or large sized esophageal varices after the first operation. Three to six weeks later, a second laparotomy with complete ligation of the portal vein and liver biopsy were performed in animals with varices (one-third of the animals). All dogs developed esophageal varices and abdominal wall collateral veins of variable size 3-6 wk after the first operation. After the second operation, the varices became larger. Shunting of blood through esophageal varices via splenic and gastric veins was demonstrated by angiography. Sequential liver biopsies were normal. There was no morbidity or mortality. Ascites, encephalopathy, or spontaneous variceal bleeding did not occur. We have documented the lack of size change and the persistence of medium to large esophageal varices and abdominal collateral veins in all animals followed for more than 6 mo. Variceal bleeding could be induced by venipuncture for testing endoscopic hemostatic and sclerosis methods. We suggest other potential uses of this reproducible canine model of esophageal varices.