Endoftalmitis post quirúrgica: análisis de 30 casos tratados en Fundación Oftalmológica Los Andes: 1997-2000 / Post Surgical Endophthalmitis: analysis of 30 cases treated in Fundacion Oftalmológica Los Andes: 1997-2000

Objetivos: 1) Evaluar la presentación clínica, espectro microbiológico y evolución visual de pacientes con diagnóstico de endoftalmitis post quirúrgica. 2) Establecer factores predictores de mal pronóstico visual final. Métodos: Revisión de 30 casos con diagnóstico de endoftalmitis post quirúrgica con un seguimiento mínimo de 6 meses. Se consideraron edad, sexo, signos y síntomas, tipo de cirugía y lapso desde cirugía hasta el momento del diagnóstico. Resultados: 30 pacientes (30 ojos) divididos en 2 grupos según tiempo desde cirugía al momento del diagnóstico. : Endoftalmitis aguda (< 14 días) y Endoftalmitis Lenta (>14 días). La cirugía de catarata fue la más frecuentemente asociada a Endoftalmitis. Los principales signos y síntomas fueron baja de AV, dolor, hipopion, ojo rojo y fibrina en cámara anterior. Un 53 por ciento de los cultivos fue positivo, con predominio de Staphylococcus Epidermidis (62,5 por ciento). Todos recibieron antibióticos intravítreos, un 56 por ciento corticoides intravítreos y un 40 por ciento vitrectomía por pars plana. Se obtuvo un mejor resultado visual en los que consultaron durante la primera semana post operatoria. Los pacientes con Diabetes Mellitus tuvieron un peor resultado visual. Conclusiones: La endoftalmitis post quirúrgica se presentó usualmente durante las 2 primeras semanas después de la cirugía de catarata, a diferencia de otros tipos de cirugía ocular. Un mejor resultado visual se observó en los pacientes que recibieron tratamiento en forma precoz. Los pacientes con antecedentes de Diabetes Mellitus tuvieron un peor resultado visual final.

Elevated levels of opioid growth factor in the plasma of patients with pancreatic cancer.

Opioid growth factor (OGF, [Met5]-enkephalin) is an endogenous peptide that regulates the growth of human pancreatic cancer. To evaluate whether human subjects with pancreatic cancer have alterations in plasma levels of OGF, fasting blood samples were obtained from 15 patients with histologically confirmed pancreatic adenocarcinoma. Forty-five subjects with other malignancies, 20 patients with acute pancreatitis, and 30 aged-matched patients without cancer served as control populations. Individuals with pancreatic cancer had OGF values, as determined by radioimmunoassay, that were up to 7.3-fold greater than control subjects. No differences were found between OGF values obtained from patients with other malignancies, acute pancreatitis, or subjects without cancer. The sensitivity and specificity of OGF for pancreatic cancer were greater than either CA 19-9 or CEA. These data indicate that pancreatic cancer is associated with a marked increase in plasma OGF levels and suggest that this peptide may serve as a useful diagnostic tool in the screening for this disease.

Identification and characterization of opioid growth factor receptor in human pancreatic adenocarcinoma.

Pancreatic cancer is the fourth most common cancer-related mortality in the United States, and the ninth most common cause of death from cancer worldwide. The opioid growth factor (OGF), [Met5]-enkephalin, inhibits the growth of human pancreatic adenocarcinoma in vitro and in vivo, and acts in a receptor-mediated fashion. Ligand binding assays using PANC-1 human pancreatic tumor cells and [3H]-[Met5]-enkephalin were performed to identify and characterize the receptor responsible for the growth-regulatory effects of OGF in pancreatic cancer. Specific and saturable binding was detected, and a Scatchard analysis revealed that the data were consistent for a single binding site with a binding affinity of 1.2+/-0.3 nM and a binding capacity of 36.4+/-4.1 fmol/mg protein. Subcellular fractionation studies showed that binding was restricted to the nuclear fraction. Competition experiments revealed that cold [Met5]-enkephalin was the most effective ligand at displacing [3H]-[Met5]-enkephalin; ligands for mu, delta, and kappa opioid receptors exhibited little or no competition. Binding was detected in 3 other human pancreatic tumor cell lines. Receptor number in xenografts of Capan-1 was decreased 8.6-fold compared to the same cells grown in tissue culture. Binding to radiolabeled [Met5]-enkephalin was detected in pancreatic cancers obtained from surgical resections. Binding capacity, but not binding affinity, was 7.1-fold greater in normal pancreatic tissues than in pancreatic neoplasia. The function, pharmacological and biochemical characteristics, distribution, and subcellular location of OGF binding in human pancreatic cancer were consistent with the OGF receptor (OGFr). In addition, human pancreatic cancer appears to have a low number of receptors for OGF, having the net effect of diminishing control of cellular replicative events.

Acute right-lower-quadrant mass presenting after laparoscopic cholecystectomy.

Hernia formation at trocar sites has been reported following laparoscopic surgical procedures. We present a case, however, of a healthy woman with signs, symptoms, and physical findings consistent with an incarcerated inguinal hernia 3 days after an uneventful laparoscopic cholecystectomy. Exploratory laparotomy revealed a small bile leak from an accessory duct of Luschka but did not identify an intra-abdominal process responsible for the patient's symptoms. Following the exploration, it was felt that the patient's presentation was likely due to tracking of carbon dioxide and bile-stained irrigation fluid to the right lower quadrant from the lateral laparoscopic trocar sites.

Endoscopic management of a bronchobiliary fistula.

A bronchobiliary fistula is a rare entity that manifests as bilioptysis. We report a 73-year-old woman with a hepato-cellular carcinoma who developed a bronchobiliary fistula. Endoscopic biliary sphincterotomy and insertion of a prosthesis led to successful resolution of symptoms and restoration of normal bile flow. We review the pertinent literature and the basis for management.

Intracerebroventricular secretin enhances pancreatic volume and bicarbonate response in rats.

BACKGROUND: Although secretin has been found within the brain, its central role in pancreatic exocrine function has not been previously addressed. The hypothesis that intracerebroventricular secretin enhances pancreatic volume and bicarbonate output at doses that have no effect when given intravenously was tested. METHODS: Sprague-Dawley rats had a cannula stereotactically placed into the left lateral cerebral ventricle 24 hours before study. At laparotomy the bile and pancreatic ducts were separately cannulated and excluded for tared collections and bicarbonate assay. RESULTS: Increasing doses of intracerebroventricular secretin (0.005, 0.05, and 0.5 microgram/1.0 microliter) induced a significant dose-related increase in bicarbonate output (2.95, 3.32, and 4.02 microEq/30 min, respectively) above basal (2.62 microEq/30 min) compared with control or intracerebroventricular saline treated animals. Pancreatic volume increased to 59.7 microliters at the lowest intracerebroventricular dose and increased (p < 0.025) to 65.8 microliters at the 0.05 intracerebroventricular secretin dose when compared with basal (59.4 microliters). To show that this was not a systemic effect of secretin, intravenous infusion of secretin at 0.005 and 0.05 microgram/kg/hr failed to stimulate either volume or bicarbonate output compared with that observed with intracerebroventricular secretin over the same dose range. CONCLUSIONS: These observations indicate that intracerebroventricular secretin stimulates pancreatic volume and bicarbonate output and suggest that central secretin may play a role in the regulation of exocrine pancreatic secretion.

Epidermal growth factor enhances intestinal mitotic activity and DNA content after acute abdominal radiation.

BACKGROUND: Mediators of radiation-induced enteritis and colitis remain undefined. Epidermal growth factor (EGF) is an endogenous peptide that is trophic to the gastrointestinal tract. We tested the hypothesis that EGF enhances DNA synthesis and mitotic activity and prevents acute radiation enteritis after total abdominal radiation. METHODS: Four equal groups (n = 6) of Sprague-Dawley rats were studied: I (control), II (radiation), III (EGF), and IV (radiation + EGF). Animals in groups III and IV received EGF (10 micrograms/kg) every 8 hours for 48 hours before radiation exposure and for 72 hours after radiation, and the remaining animals were given an equal volume of vehicle. Animals in groups II and IV were administered a single dose of abdominal radiation (1000 cGy) 48 hours after the start of either vehicle or EGF. Distal ileum and colon were harvested 72 hours after radiation, examined histologically, and assayed for total DNA content. RESULTS: Group II or radiated animals had diarrhea, significant weight loss (p < 0.05), and decreased food consumption consistent with acute clinical radiation enteritis. Mitotic activity and total DNA content were significantly reduced (p < 0.05) when compared with group I (nonradiated controls). Group IV animals treated with EGF and exposed to radiation did not suffer the acute clinical manifestations of radiation enteritis. In addition, total DNA content and mitotic activity of the terminal ileum increased significantly (p < 0.05), and a significant increase in mitotic activity occurred in the distal colon when compared with radiated controls. CONCLUSIONS: The results of this study suggest that (1) a decrease in mitotic activity and total DNA content occurs early and persists for at least 72 hours after acute radiation, (2) EGF treatment significantly increases small and large bowel mitogenicity in acutely radiated animals, and (3) EGF significantly decrease the acute clinical manifestations of radiation enteritis.

Pyeloduodenal fistula: a previously undescribed complication of Stamm gastrostomy.

A variety of complications have been described after placement of a Stamm gastrostomy in infants and children, including gastric volvulus, pancreatitis, jaundice, gastroduodenal mucosal intussusception with gastric outlet obstruction, and even aortogastric fistula. However, this is the first report of pyeloduodenal fistula after Stamm gastrostomy in a 4 1/2-month-old boy. The child successfully underwent nonoperative therapy; he was treated by withdrawing the gastrostomy tube (Foley catheter) from the renal pelvis, bowel rest, and total parenteral nutrition. After the case presentation is a brief review of this rare entity, with its clinical presentation and pathophysiological differences between adult and pediatric cases. Various treatment options, both operative and nonoperative, are also described.

Stimulated pancreatic exocrine secretion does not require pancreatic hyperemia in rats. Potential cholinergic role.

Although blood flow and cholinergic tone influence gastric and salivary gland secretion, their role in pancreatic secretion is poorly defined. The purpose of the present study was: (1) to test the hypothesis that an increase in pancreatic blood flow accompanies stimulated pancreatic exocrine secretion, and (2) to examine the effects of cholinergic agents on basal and stimulated blood flow using hydrogen gas clearance. Stimulated pancreatic exocrine secretion (secretin 0.4, 0.8, 1.6 micrograms/kg/hr) resulted in a significant (P < 0.005) increase in secretory volume; however, pancreatic blood flow was not significantly changed, and a negative correlation between blood flow and secretion was observed. A pharmacologic dose of secretin (5.0 micrograms/kg/hr) resulted in a significant (P < 0.05) increase in pancreatic blood flow, which was inhibited by atropine (5.0 micrograms/kg/hr) infusion. Although 2-deoxyglucose caused a significant decrease (P < 0.03) in basal pancreatic blood flow, atropine had no effect on basal blood flow levels. These observations suggest that: (1) under physiologic conditions, secretin- or 2-deoxyglucose-stimulated pancreatic secretion does not require pancreatic hyperemia; (2) a pharmacologic dose of secretin does produce pancreatic hyperemia, perhaps through a local cholinergic mechanism; (3) peripheral cholinergic tone does not contribute significantly to basal pancreatic blood flow; and (4) basal pancreatic blood flow may be influenced by central mechanisms.

Gallbladder mucosal blood flow increases during early cholesterol gallstone formation.

Gallbladder absorption increases during early cholesterol gallstone formation and is influenced by the intraluminal presence of lithogenic bile. The effect of lithogenic bile on gallbladder mucosal blood flow is unknown. The current study tested the hypothesis that the presence of lithogenic gallbladder and hepatic bile enhances gallbladder mucosal blood flow in cholesterol-fed (0.4%) prairie dogs, as determined by hydrogen gas clearance. Gallbladder mucosal blood flow in control animals was 35.57 +/- 3.9 mL.min-1.100 g-1. In contrast, basal gallbladder mucosal blood flow in cholesterol-fed animals was significantly (P less than 0.01) increased to 64.94 +/- 8.7 mL.min-1.100 g-1. In crossover studies, the addition of lithogenic gallbladder bile to control animals (n = 6) resulted in a significant (P less than 0.025) 26% increase in gallbladder mucosal blood flow, whereas the addition of nonlithogenic gallbladder bile into gallbladders of cholesterol-fed prairie dogs resulted in a significant (P less than 0.025) 58% decrease in gallbladder mucosal blood flow. Similarly, hepatic bile crossover studies showed that the addition of lithogenic hepatic bile to control gallbladders significantly increased (P less than 0.025) gallbladder blood flow by 30%, whereas instillation of nonlithogenic hepatic bile in gallbladders of cholesterol-fed animals significantly (P less than 0.025) decreased gallbladder mucosal blood flow by 29%. These results suggest that alterations in gallbladder mucosal blood flow, influenced by the presence and absence of lithogenic bile, may play a role in cholesterol gallstone formation.

Localization of central prostaglandin E2 antisecretory effects.

Intracerebroventricular prostaglandin E2 (PGE2) inhibits stimulated gastric acid secretion; however, the central site of action is unknown. Specific PGE2 binding sites have been localized to the ventromedial hypothalamic nucleus and central amygdala (A). The nuclear accumbens has been shown to play a role in central neurotensin-induced antisecretory effects. These studies tested the hypothesis that microinjections of PGE2 into the ventromedial hypothalamic nucleus, central amygdala, and nuclear accumbens inhibit stimulated gastric acid secretion. The hippocampus served as a cerebral control region. Two days before the experiments, metal cannulas were stereotaxically positioned bilaterally into specific areas of the brain, and metal gastric cannulas were operatively implanted, under nembutal anesthesia, in male 250-g Sprague-Dawley rats. On the experimental day, the rats, fasted for 14 hours, were given saline or PGE2 (0.1-1.0 micrograms in 0.2 microL/side) through the central cannulas 10 minutes before administering pentagastrin (40 micrograms/kg SC). Gastric secretion was measured at 30-minute intervals and expressed as acid output, micromoles per hour. Acid output (mean +/- SE) in control animals was 161 +/- 14 mumol/h. Prostaglandin E2 administration at doses of 0.10, 0.50, and 1.0 micrograms/side (a) into ventromedial hypothalamic nucleus reduced acid output to 53 +/- 11,* 36 +/- 10,* and 27 +/- 11* mumol/h regularly; (b) into NACB reduced acid output to 157 +/- 36, 60 +/- 12,* and 38 +/- 12* mumol/h; and (c) into A reduced acid output to 144 +/- 31, 141 +/- 26, and 90 +/- 19* mumol/h, respectively (*P less than 0.05 by Neuman-Keuls test). Prostaglandin E2 (0.50 micrograms/side) administration into hippocampus had no significant effect on acid output (134 +/- 28 mumol/h). Although central PGE2 administration was associated with hyperthermia, this occurred at lower doses than those required to inhibit acid secretion. Prostaglandin E2 administration into specific brain areas known to have PGE2 receptors, the central amygdala and ventromedial hypothalamic nucleus, and into nuclear accumbens inhibits stimulated gastric acid secretion. These observations suggest that PGE2 may have a physiological role in the central control of gastric acid secretion.

Afferent loop obstruction presenting as acute pancreatitis and pseudocyst: case reports and review of the literature.

Afferent loop obstruction after gastrectomy and Billroth II reconstruction is an uncommon problem. Complete acute obstruction requires emergent laparotomy. However, chronic obstruction may begin insidiously and its symptoms may reflect other gastrointestinal diseases. Two patients are described who developed acute abdominal pain, marked hyperamylasemia, and palpable abdominal masses 5 and 15 years after Billroth II gastrectomy. The masses were initially interpreted as pancreatic pseudocysts. Both patients were found to have chronically obstructed afferent limbs, and in one the obstruction was associated with hundreds of stasis stones within the afferent limb. Surgical decompression was accomplished in each patient. Patients who have undergone Billroth II reconstruction have signs, symptoms, and laboratory findings consistent with acute pancreatitis. A history of previous gastrectomy, recurrent or severe abdominal pain, hyperamylasemia with characteristic tomography, and endoscopic findings will establish the diagnosis and necessitate surgical evaluation and intervention.

Delayed reconstructive surgery for complex enterocutaneous fistulae.

A retrospective analysis was performed of 51 consecutive patients with complex enterocutaneous fistulae who underwent delayed reconstructive surgery. In this group of seriously ill patients, gastrointestinal continuity was restored in 94 per cent and the mortality rate was 4 per cent. The authors believe that patients with multiple or recurrent fistulae, or those associated with large abdominal wall defects can be managed through a staged multi-disciplined approach in which definitive surgery is deferred beyond the usually recommended period of six weeks.

Postoperative wound infection associated with Vibrio parahaemolyticus in a patient without exposure to seawater.

This report describes a case of wound infection associated with Vibrio parahaemolyticus. The patient had ingested steamed crabs 7 days before admission for surgical treatment of intestinal obstruction due to colon carcinoma. The Vibrio sp. was isolated from postoperative wound drainage as well as from stool. Recovery was uneventful.

Recurrent hepatic hemangiomas. Possible association with estrogen therapy.

Hemangiomas are the most common benign tumors occurring in the liver. However, the natural history of hepatic hemangiomas has not been well defined. Four patients (3 women, 1 man) with recurrent giant liver hemangiomas underwent either surgical or radiation therapy as initial treatment for the primary tumor. The average time until recurrence was 14 years, and each tumor weighed more than 600 g. Each of the female patients had been given chronic estrogen (Premarin) replacement therapy. Three of the four patients underwent surgical resection for intractable symptoms or progressive enlargement. It is believed that estrogen replacement therapy may play a role in the pathogenesis of these tumors. Furthermore, operative intervention should be considered in patients with recurrent giant liver hemangioma.

Influence of motilin and cholecystokinin on sphincter of Oddi and duodenal mobility.

The sphincter of Oddi and the duodenum exhibit cyclical activity in phase with the migrating myoelectric complex. Both motilin and cholecystokinin have been shown to modulate gastrointestinal and sphincter of Oddi motility. However, previous studies have not monitored the effects of these hormones on simultaneously recorded sphincter of Oddi and duodenum pressures. The present investigation was undertaken, therefore, to determine the influence of both motilin and cholecystokinin on simultaneously recorded sphincter of Oddi and duodenal motility. In seven anesthetized prairie dogs, a triple-lumen, side-hole, pressure-monitored perfusion catheter was positioned with the proximal port in the sphincter of Oddi and the distal port in the duodenal lumen. Sphincter of Oddi and duodenal motility was recorded before and during 20-min infusions of motilin and cholecystokinin octapeptide (CCK-8) at 1, 10, and 100 ng.kg-1.min-1. Both hormones produced dose-related increases in sphincter of Oddi and duodenal motility. No response was observed with either hormone at 1 ng.kg-1.min-1. At 10 ng.kg-1.min-1, the duodenum was slightly more sensitive to motilin than to CCK-8, while the sphincter of Oddi was equally affected by both hormones. At 100 ng.kg-1.min-1, both hormones stimulated the sphincter of Oddi and the duodenum equally. These data indicate that in the prairie dog, both motilin and cholecystokinin stimulate sphincter of Oddi and duodenal motility.

The role of dietary iron in pigment gallstone formation.

Recent studies suggest that dietary factors may be responsible for the increasing incidence of pigment gallstones. Although iron deficiency alters the activities of several hepatic enzymes, its effects on biliary lipid metabolism are not known. The aim of this study was to define the role of dietary iron in pigment gallstone formation. Three groups of prairie dogs were maintained for 2 months on either a control chow (iron-198 ppm), a high-carbohydrate diet with normal iron levels (CHO group; iron-220 ppm), or a high-carbohydrate, iron-deficient (iron-56 ppm) diet (CHO-FeD group). Serum analysis confirmed iron deficiency in the CHO-FeD group. The CHO animals had a significant (p less than 0.01) increase in hepatic bile phospholipids, while CHO-FeD animals had increased (p less than 0.01) concentrations of phospholipids and cholesterol as compared with controls. Similar findings were noted in gallbladder bile with the addition of increased calcium levels in both carbohydrate groups. Calcium bilirubinate crystals and stones were found in only 17% of CHO animals, as compared with 67% of CHO-FeD animals. These data indicate that consumption of diets rich in carbohydrates but deficient in iron alters hepatic metabolism of cholesterol and may be an important etiologic factor in pigment gallstone formation. Iron supplementation may prevent pigment gallstones in certain high-risk groups.

Altered gallbladder concentration of biliary lipids during early cholesterol gallstone formation.

Whether gallbladder absorptive function is altered during formation of cholesterol gallstones is unclear. We tested the hypothesis that alterations in biliary lipid composition present during early cholesterol gallstone formation enhance gallbladder absorption, as manifested by an increase in the ratio of gallbladder to hepatic bile lipid concentrations. Prairie dogs received either control or a 0.4% cholesterol-enriched chow for two or six weeks. The bile acid pool of each animal was labeled with [14C]cholic acid. Gallbladder and hepatic bile were analyzed for lipid composition with calculation of indices for cholesterol saturation, gallbladder stasis, and gallbladder absorption. Animals maintained on cholesterol-enriched chow for two weeks had a significant increase, as compared to controls, in the ratio of gallbladder to hepatic bile concentrations of cholesterol (8.66 +/- 1.09 vs 5.76 +/- 0.48), phospholipids (4.76 +/- 0.42 vs 3.21 +/- 0.34), bile acids (6.42 +/- 2.20 vs 3.54 +/- 0.46), and total lipid content (6.22 +/- 0.94 vs 3.64 +/- 0.43). These changes occurred at a time when gallbladder stasis is present and cholesterol crystals are forming, but prior to stone formation. Similar findings were noted in six-week cholesterol-fed prairie dogs. We propose the uniformly increased ratios of biliary lipids result from enhanced gallbladder absorption of water and sodium. The resulting increase in solute concentration may promote nucleation and, therefore, may be an important etiologic factor in cholesterol gallstone formation.