Retrieval of spilled stones during laparoscopic cholecystectomy.

Laparoscopic cholecystectomy is now widely practised in the Western world. One of the more common and often neglected complications is perforation of the gallbladder and spillage of bile and stones. With careful attention to technique this should be a rare complication. The effect of bile and stone spillage may depend on the presence or absence of biliary infection at the time of operation. When stone spillage occurs a number of options are available for the retrieval of stones and these are highlighted in this paper.

Laparoscopic general surgery.

Laparoscopic cholecystectomy has become the treatment of choice for symptomatic gallstones. The success of this procedure has prompted surgeons to explore the possibility of performing other procedures laparoscopically. This article describes some of these new techniques and discusses the merits of a minimally.

Pancreatic duct pressure, duct permeability and acute pancreatitis.

The relationship between pancreatic duct pressure, duct permeability to macromolecules and the development of acute pancreatitis was studied in a cat model. Perfusion of the pancreatic duct with 15 mM glycodeoxycholic acid, ethanol administration, or secretagogue-stimulated pancreatic secretion against greater than 50 per cent duct obstruction resulted in an increase in peak pancreatic duct pressure in all animals. Duct permeability to 20,000 molecular weight dextran molecules was increased in 22 of 29 experimental animals compared with two of 22 control animals (P less than 0.01). Perfusion of the pancreatic duct with activated pancreatic enzymes resulted in acute pancreatitis in 24 of 29 experimental animals compared with three of 22 control animals (P less than 0.01). These results suggest that pancreatic ductal hypertension, resulting in increased ductal permeability to large molecules, may be a common early event in gallstone and alcoholic pancreatitis.

Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats.

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.

Possible mechanisms of acute pancreatitis induced by ethanol.

We investigated the effect of intravenous and intragastric ethanol on pancreatic duct pressure, duct permeability to dextran molecules (20,000 molecular weight), and on the development of acute pancreatitis in an experimental model of the disease. Intragastric ethanol caused a small increase in pancreatic duct pressure (6 to 7 mm Hg) and an increase in duct permeability to dextran. Intravenous ethanol with exclusion of the sphincter of Oddi did not increase pancreatic duct pressure or permeability. Intravenous ethanol and intragastric normal saline solution altered neither pressure nor permeability. Artificial elevation of pancreatic duct pressure alone with no ethanol had no effect on duct permeability. However, when intravenous ethanol was given to produce similar systemic concentrations as achieved in the intragastric experiments (250 mg/dl) and duct pressure was artificially raised, duct permeability was increased. Ethanol concentrations similar to those found in peripheral blood were detected in secretin-stimulated pancreatic juice. Perfusion of the pancreatic duct with activated pancreatic enzymes after intragastric but not intravenous ethanol (that is, only in animals with increased duct permeability) caused acute edematous pancreatitis. Our results confirmed that increased duct permeability was necessary to produce acute pancreatitis in this model, and that this increase in permeability resulted from both a small increase in duct pressure and probably from the toxic metabolic effects of ethanol.

Vasoactive drugs, microvascular permeability, and hemorrhagic pancreatitis in cats.

We investigated the mechanisms by which 16,16-dimethyl prostaglandin E2 and histamine induced pancreatic hemorrhage in an experimental model of acute pancreatitis in cats. In normal animals, when large molecular weight dextran molecules were infused into the systematic circulation, they were recovered in secretin-stimulated pancreatic juice in low concentrations. Both 16,16-dimethyl prostaglandin E2 (in a dose that increased splenic artery blood flow and microvascular permeability) and histamine (in a dose that increased permeability only) increased the amount of dextran recovered in pancreatic juice. Isoproterenol, in a dose that produced the same increase in blood flow as 16,16-dimethyl prostaglandin E2 but which did not increase microvascular permeability, did not alter the amount of dextran recovered. This suggested that the increase in dextran output after 16,16-dimethyl prostaglandin E2 was primarily due to the increase in microvascular permeability caused by the drug. In other experiments, a combination of H1- and H2-receptor antagonists (mepyramine and cimetidine) protected against the development of pancreatic hemorrhage in both the prostaglandin- and histamine-treated animals. Indomethacin (a cyclooxygenase inhibitor) protected against the development of hemorrhage in the histamine-treated animals. Our results support the hypothesis that changes in microvascular permeability may be important in the pathogenesis of parenchymal hemorrhage in this model.

Treatment of acute pancreatitis with beta-adrenergic agonist drugs.

An increase in microvascular permeability may be important in the pathogenesis of acute pancreatitis. beta-adrenergic receptor agonist drugs are known to inhibit the increase in microvascular permeability induced by histamine and related vasoactive substances. These inflammatory mediators have been shown to be released during the course of experimental and human pancreatitis. We investigated the effect of isoproterenol and terbutaline sulfate on the development of acute edematous (AEP) and acute hemorrhagic (AHP) pancreatitis in a feline model of biliary pancreatitis. When given at the time of pancreatic insult, isoproterenol prevented the development of both AEP and AHP. Both isoproterenol and terbutaline sulfate reduced the severity of pancreatic inflammation, even when given up to 12 hours after the onset of AEP. Although neither drug was effective in treating established AHP, our findings suggest that, if given early in the course of the disease, they may be useful in preventing the progression of AEP to AHP.

Antibiotic prophylaxis and secondary haemorrhage following transurethral resection of the prostate: a prospective trial.

One hundred and sixty-two patients were studied in a random double-blind controlled trial of co-trimoxazole to prevent secondary haemorrhage following transurethral resection of the prostate (TURP). There was a significant correlation between the incidence of post-operative urinary infection and secondary haemorrhage (P less than 0.05) but no difference between the incidence of bleeding in the treatment and placebo groups. Although infection may play a role in the development of secondary haemorrhage, co-trimoxazole for 10 days does not decrease the incidence of this complication.

Potato steroidal alkaloids and neural tube defects: serum concentrations fail to demonstrate a causal relation.

Spoiled potatoes and, in particular, steroidal alkaloids have been proposed as an aetiological factor in the pathogenesis of neural tube defect (NTD). The present study involves the measurement of potato (solanum) steroidal alkaloid concentrations in serum by radioimmunoassay. Serum solanidine and total potato alkaloid concentrations were measured in two groups of women: one group pregnant with a fetus, subsequently shown to be affected by a NTD, the other with a healthy fetus. Serum alkaloid concentrations were, contrary to expectations, lower in the NTD group. They lend no weight therefore to the theory that potato alkaloids are responsible for NTD, but are consistent with the opinion that some water-soluble vitamins lessen the risk.

Measurement of potato steroidal alkaloids in human serum and saliva by radioimmunoassay.

Radioimmunoassay methods are described for measuring potentially toxic potato glycoalkaloids and the aglycone solanidine in human serum and saliva. Solanidine and total alkaloid concentrations in serum and saliva during the summer are given for a group of subjects from the UK and a group from Sweden. Serum concentrations ranged from 3.2 to greater than 125 nmol/l for total alkaloid and 2.5 to 92.5 nmol/l for solanidine and were comparable in the two populations. Salivary total alkaloid concentrations were only about 10% of serum values. Salivary solanidine concentrations did not exceed 20% of the serum levels. Good correlation was found between serum and salivary alkaloid concentrations (r = 0.734, for solanidine; r = 0.892 for total alkaloid). Serum and salivary alkaloid concentrations were significantly raised in a group of Swedish subjects eating potatoes containing unusually high concentrations of alkaloids when compared with those in a group of subjects eating their normal diets.

Inguinal herniotomy in children: a five year survey.

This retrospective review covers our experience over 5 years of 436 hernia repairs in 392 children upto the age of 15 years. The number of emergency presentations was 71 (18.1 per cent) and 66.2 per cent of these were under the age of 12 months. Most cases were initially treated conservatively and only 18 children required operation on the day of admission. There were 11 recurrences (7 elective and 4 emergency cases) giving a recurrence rate of 2.5 per cent. In all eleven cases the original operation was performed by a junior surgeon. The complication rate (excluding recurrences) was 2.8 per cent but may be an underestimate because of the limitations of a retrospective study. We suspect our results are typical of those to be found in any large British hospital and that with careful training and supervision of junior staff in the technique of inguinal herniotomy the results could be improved and approach those found in specialist paediatric units in America.

Technetium labelled red blood cell scintigraphy in the diagnosis of intestinal haemorrhage.

99m-Technetium labelled red blood cell scintigraphy was used in the investigation of 15 adult patients with suspected small or large bowel bleeding requiring at least five units of blood (mean 14.3 units) and one neonate with rectal bleeding. Scintigraphy was found to be an accurate method of detecting the site of haemorrhage and was superior to angiography. This technique may be of particular value in patients with profuse colonic haemorrhage when the view at colonoscopy is poor.

Solanidine is present in sera of healthy individuals and in amounts dependent on their dietary potato consumption.

Solanidine, a steroidal alkaloid, and its glycosides have been reported to have caused poisoning in man and animals. These alkaloids are normally present in small amounts in potatoes. Measurement of solanidine in body fluid would be expected to establish the real incidence of acute toxicity and help to resolve the question of any chronic toxicity including teratogenicity. We report the detection of solanidine in the serum of 57 normal healthy volunteer subjects in whom it measured 4.0-56.3 nmol/l (1.6-22.5 ng/ml) before the midday meal. There was a significant correlation between serum solanidine concentration and normal dietary intake of potato by the individual concerned. When two subjects abstained from potato and its products serum solanidine fell markedly and became minimal after the second week onwards.