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While endoscopically placed gastrostomy tubes are routinely simple, they are not always feasible. Endoscopic technique also does not uniformly secure the tube to the abdominal wall, which presents possible complications, including leakage, accidental early tube removal, intraperitoneal catheter migration and necrosis of the stomach or abdominal wall because of excessive traction. Presented herein is a technique that is rapid, simple and eliminates some of these potential complications. The technique is easily combined with other operative procedures, such as tracheostomy, is done under direct vision, can be performed quickly with intravenous sedation and local anesthetic and is a safe method of tube placement for enteral feeding or gastric decompression.

In a canine model of acute hemorrhagic pancreatitis, crystalloid resuscitation with a balanced salt solution adequately restored plasma volume, supported tissue perfusion and prevented excessive hemodilution without detrimental effects on pulmonary pressures or oxygenation. No advantages in using colloid resuscitation were apparent in our study.

Doppler ultrasound was used to determine whether or not colonic anastomoses have sufficient blood supply for healing to occur. Experimental anastomoses placed at, or 1 centimeter from, the last audible arterial signal healed; those placed 2 or 3 centimeters distally had a high incidence of disruption. Results were statistically significant by chi-square analysis, p less than 0.05. Clinical parameters of intestinal viability would not have predicted anastomotic failure.

The onset of experimental hemorrhagic pancreatitis in dogs was rapidly followed by a deterioration of CO, blood pressure, LVSW and RVSW, along with significant elevations of Hct, SVR and PVR. These alterations could all be reversed by the administration of Ringer's lactate. These findings support the concept that the major physiopathologic characteristic of severe acute pancreatitis is a loss of effective plasma and extracellular fluid volumes and that the replacement of fluid losses corrects the hemodynamic alterations. In neither of the experimental groups did pulmonary hypertension develop. We found no evidence in this model of hemorrhagic pancreatitis for a circulating pulmonary vasoactive substance.

Thyrocalcitonin release mediated by glucagon secreted from the acutely inflamed pancreas has been postulated as a possible mechanism for hypocalcemia in acute pancreatitis. To test this hypothesis, hemorrhagic pancreatitis was induced in a group of thyroidectomized pigs. No source of thyrocalcitonin other than the thyroid has been described in the pig. Their subsequent serum calcium concentrations were compared with those in a group of thyroid intact pigs also given hemorrhagic pancreatitis. The results indicate that the hypocalcemia observed during the first 24 hours following induction of pancreatitis is not related to the presence of an intact thyroid. Differences observed in the degree of hypocalcemia between the two groups 30 to 48 hours after pancreatitis developed may be of significance but could be explained by dilutional differences alone. Thyrocalcitonin apparently has little if any role in the hypocalcemia observed during the course of acute pancreatitis.