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Biomedical subjects

I J Sarfeh

Publications and source records attributed to I J Sarfeh.

At least 19 recordsLinked to original sources
PubMed1992

Surgical treatment of enteric 'bud' fistulas in contaminated wounds. A riskless extraperitoneal method using split-thickness skin grafts.

We describe methods and results of a local extraperitoneal method of repairing enterocutaneous "bud" fistulas in abdominal-wall defects. The method is performed with local anesthesia and involves an extraperitoneal closure with skin-graft coverage. Of the nine fistulas so treated, five healed. No patient's postoperative course was set back by the repairs that failed since the method precludes intraperitoneal entrance. Two of three high-output fistulas were successfully repaired with the extraperitoneal method, reversing an otherwise stormy clinical course. We conclude that for epithelialized enterocutaneous fistulas, little is lost if our method of repair fails and much is gained if it is successful in these critically ill patients.

Abdominal Muscles↗
PubMed1992

Increased expression of epidermal growth factor receptor during gastric ulcer healing in rats.

Expression of epidermal growth factor receptor (EGFR) was studied immunohistochemically in rat gastric mucosa during healing of acetic acid-induced ulcers. In normal control gastric oxyntic mucosa, EGFR was expressed in proliferative zone cells and in some parietal cells. In mucosa of the ulcer margin, at 3, 7, and 16 days after ulcer induction, there was a 75-fold increase (over controls) in the number of cells expressing EGFR. Seventy percent of ulcers healed by the 16th day, and all were healed by the 25th day. The mucosal scar that replaced the ulcer was composed of dilated glands lined with poorly or aberrantly differentiated cells showing persistence of increased EGFR expression. An increased EGFR expression indicates an important role of EGF in ulcer healing and scar formation.

Analysis of Variance↗
PubMed1992

Adaptation of gastric mucosa to chronic alcohol administration is associated with increased mucosal expression of growth factors and their receptor.

In our previous study we found that chronic, intragastric administration of ethanol to rats produces adaptation of the gastric mucosa to subsequent challenge with an acute dose of 50% ethanol. The mechanism of this mucosal tolerance remains unexplained. Epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) stimulate cells growth and proliferation in the gastric mucosa with noted trophic effect, protect the gastric mucosa against acute injury and accelerate healing of injured mucosa. Many of these effects are exerted through EGF and TGF alpha action on their common receptor (EGFR). The aim of the present study was to determine the effect of chronic alcohol administration on cell proliferation and gastric mucosal expression and distribution of EGF, TGF alpha and EGFR. Chronic administration of ethanol (1 ml, 50% ethanol, twice daily) significantly increased the extent of gastric mucosal mucous and proliferative cell zones, the number of proliferating (DNA synthesizing) cells and mucosal expression of EGF, TGF alpha and EGFR by 13, 6, and 20-fold, respectively. Thus, adaptation of gastric mucosa to chronic alcohol administration is associated with increased cell proliferation and increased expression of mucosal EGF, TGF alpha and EGFR.

Adaptation, Physiological↗
PubMed1992

Epidermal growth factor protects portal hypertensive gastric mucosa in ischemia/reperfusion: the role of capillary endothelia and prostaglandins.

BACKGROUND: Epidermal growth factor (EGF) protects gastric mucosa against a variety of injurious agents, but the mechanism is unclear. Because the abnormal microvasculature of portal hypertensive (PHT) gastric mucosa is a major target of ischemia/reperfusion (I/R) injury, we used this model to assess EGF's protective role at the microvascular level. METHODS: Rats with PHT (staged portal vein ligation) received either EGF, 20 micrograms/kg, or saline solution intravenously, with or without indomethacin pretreatment (20 mg/kg subcutaneously). I/R was produced by withdrawing blood to systemic pressures of 30 mm Hg for 20 minutes and reinfusing it. Stomachs were excised 20 minutes later and evaluated for gross and histologic necrosis, microvascular permeability, mucosal ultrastructure and vimentin, and cyclooxygenase immunofluorescence. RESULTS: In saline-treated rats, gross and histologic damage involved 46% +/- 3% of glandular mucosa and 23% +/- 3% of mucosal sections, respectively. Microvascular permeability was increased 43-fold over that of normal control rats. Vimentin immunofluorescence intensity was reduced to 36% +/- 4% that of normal control rats. EGF pretreatment reduced histologic necrosis to 2% +/- 1% (p less than 0.01). Microvascular permeability and vimentin intensity were almost normalized. Indomethacin partially reversed the mucosal protection induced by EGF. CONCLUSIONS: EGF significantly reduces I/R injury to PHT gastric mucosa. Microvascular endothelia of PHT gastric mucosa are the major target of I/R injury and the site of EGF's protective action. Prostaglandins in part mediate EGF's protective action.

Animals↗
PubMed1991

Increased susceptibility of the portal hypertensive gastric mucosa to damage.

Portal hypertensive gastropathy has recently been recognized as a unique entity distinct from other gastropathies involving the normotensive gastric mucosa. To delineate the pathophysiology of this disorder, we developed a rat model of portal hypertension using two-staged portal vein ligation. In this model, features of the portal hypertensive mucosa include increased luminal hydrogen ion loss, reduced electronegativity of potential difference, and increased submucosal edema. Ultrastructurally, the portal hypertensive gastric mucosa has marked endothelial hypertrophy of capillaries resulting in prominent compromise of microvascular lumina. Combined with the submucosal edema, the microvasculopathy results in reduced oxygenation of the surface gastric mucosa. This is associated with diminished prostaglandin production, which impairs gastric mucosal protection in portal hypertension. These observations are strengthened by experiments that demonstrated significantly increased gastric mucosal damage by alcohol, bile acids, aspirin, and shock/reperfusion in portal hypertensive rats compared to normotensive sham-operated controls. Many of our experimental findings have been confirmed clinically; however, much more research in this area is clearly needed.

Animals↗
PubMed1990

Portal hypertension predisposes the gastric mucosa to hemorrhagic shock/reperfusion injury.

We have previously demonstrated that the portal hypertensive (PHT) gastric mucosa has unique functional and morphologic features which predispose it to increased damage by noxious agents such as aspirin or alcohol. In this study we examine the PHT gastric mucosa following hemorrhagic shock and reperfusion. Portal hypertension was produced in 12 rats using staged portal vein occlusion, and seven animals (controls) underwent sham procedures. All rats received 2 ml 0.1 N HCl intragastrically. Shock was then induced by withdrawing blood to reduce systemic arterial pressures to approximately 30 mm Hg for 20 min. Blood was then reinfused and stomachs were excised 20 min later for gross and microscopic quantitation of injury. We found that gross damage to gastric glandular mucosa was more than doubled in PHT rats over sham-operated controls. In PHT gastric mucosa, deep histologic necrosis involved 22.5 +/- 3.8% of mucosal section lengths compared with 6.9 +/- 2.0% in control mucosa (P less than 0.005). Histologically, mucosal injury patterns were predominantly ischemic, with deep necrosis and disintegration of glands and microvessels, all prominently more extensive in PHT mucosa. We conclude that PHT gastric mucosa has significantly increased susceptibility to damage following hemorrhagic shock/reperfusion compared with portal normotensive mucosa. Since hemorrhagic shock is a frequent complication of portal hypertension, this study suggests clinical investigations of gastric mucosal function and pathophysiology in PHT patients following hemorrhage and resuscitation.

Animals↗
PubMed1990

Impaired generation of prostaglandins from isolated gastric surface epithelial cells in portal hypertensive rats.

We studied generation of prostaglandins E2 and 6-keto F1a by surface epithelial cell isolated from the gastric mucosa of portal hypertensive and sham-operated rats. Oxygenated cell suspensions containing 80 +/- 3% of surface epithelial cells were incubated for 30 min at 37 degrees C and the concentration of prostaglandin E2 and 6-keto-prostaglandin F1a in medium was measured by radioimmunoassay. Viability of the cells was assessed with Fast green exclusion at baseline and after 30-min and 60-min incubation. Within 30 minutes the surface epithelial cells obtained from portal hypertensive rats generated 22.0 +/- 1.6 (mean +/- SE) pg prostaglandin E2 and 40.7 +/- 4.7 pg 6-keto prostaglandin F1a, per 10(6) cells. These were significantly less than prostaglandin generation by cells obtained from sham-operated rats. The viability of the surface epithelial cells from portal hypertensive rats was also significantly reduced compared with sham-operated rats after 60 minute incubation. Reduced ability of the surface epithelial cells to generate prostaglandins may be one mechanism for increased susceptibility of portal hypertensive gastric mucosa to injury by noxious agents.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Three-phase study of phlebitis in patients receiving peripheral intravenous hyperalimentation.

We found clinical phlebitis in 57 of 88 patients with peripheral hyperalimentation (65%). To determine if this was a problem common to all intravenous fluid therapy at our hospital, we performed a point-prevalence study. The prevalence of phlebitis in nonhyperalimentation intravenous patients was 18% (84 of 456 patients). We then performed a randomized, prospective, double-blind trial of sham versus standard in-line filters to determine if bacteria or filterable particulate matter was responsible for phlebitis in the peripheral hyperalimentation group. The standard-filter group had a phlebitis rate of 74% compared with 64% in the sham-filter group. We then eliminated in-line filters and replaced the standard glucose-based solution with a glycerol-based peripheral hyperalimentation solution. The phlebitis rate decreased from 68% to 27% (p less than 0.001). In conclusion, phlebitis in peripheral hyperalimentation patients was probably due to chemical properties of the peripheral hyperalimentation solution rather than bacteria or particulates.

Amino Acids↗
PubMed1990

Diagnosis and hemodynamic assessment of portal hypertension.

Rational treatment of portal hypertensive complications requires a knowledge of the cause of portal hypertension and an assessment of the severity of liver disease. In the United States, chronic liver disease, usually due to alcohol, is the most common underlying cause. The history, physical examination, and laboratory analysis are usually sufficient to confirm the presence of underlying liver disease. If there is any question as to the etiology of portal hypertension, however, a more complete evaluation is required, whether the presenting complication is ascites, variceal bleeding, or hypersplenism. Usually, such an evaluation will require a liver biopsy, portal pressure measurement, and angiography. Occasionally, a noninvasive evaluation will be sufficient, but the value of these noninvasive parameters is still under investigation. Surgical mortality generally depends on the severity of the liver disease. Therefore, surgical intervention must be carefully considered in comparison to other therapeutic modalities depending on the patient's hepatic functional reserve. Secondary bacterial peritonitis due to perforation requires surgery regardless of the severity of the underlying liver disease.

Esophageal and Gastric Varices↗
PubMed1990

Small-diameter portacaval H-graft for variceal hemorrhage.

This report describes the steps in the development of the concept of partial shunting from its earliest stages to the 8-mm-diameter portacaval H-graft. Sequentially decreasing the diameter of the graft from 20 mm did not seem to affect hepatic hemodynamics until the 10-mm-diameter graft was used. At this point, we began to see some patients maintain prograde portal flow. Further reduction in diameter gave a higher rate of patients with prograde flow. Postoperative flow patterns correlate with lower encephalopathy rates and better long-term survival. Important nuances of the operative technique as well as pre- and postoperative management are described.

Blood Vessel Prosthesis↗
PubMed1989

Impaired oxygenation of gastric mucosa in portal hypertension. The basis for increased susceptibility to injury.

Increased susceptibility to mucosal damage is a prominent feature of portal hypertensive gastropathy. Since the portal hypertensive gastric mucosa has extensive microvascular changes, we postulated that the increased sensitivity to mucosal damage could have an ischemic basis. We measured distribution of gastric serosal and mucosal oxygenation in a group of portal hypertensive and sham-operated rats, and then studied the effects of intragastric aspirin. In the basal state, gastric mucosa of portal hypertensive rats had significantly reduced oxygenation compared to controls (24 +/- 5 vs 45 +/- 7 mm Hg PO2, P less than 0.02), while serosal oxygenation was similar between the two groups. Intragastric aspirin produced significantly greater mucosal damage to portal hypertensive rats and mucosal oxygenation was almost one third that of sham-operated controls. Systemic arterial pressures and oxygenation were similar between the two groups. We conclude that there is impairment of gastric mucosal oxygenation and increased mucosal damage by aspirin in portal hypertensive rats compared with sham-operated controls. These results support our hypothesis that the increased sensitivity of the portal hypertensive mucosa to damage is a consequence of impaired mucosal oxygenation.

Animals↗
PubMed1989

Acquired immune deficiency syndrome (AIDS). Indications for abdominal surgery, pathology, and outcome.

Thirty-six major abdominal operations were performed on 35 Acquired Immune Deficiency Syndrome (AIDS) patients (33 men, two women). Twenty-two elective operations were indicated for diagnosis of abdominal or retroperitoneal mass (6), incomplete bowel obstruction (5), intra-abdominal infection (4), biliary symptoms (3), thrombocytopenia (3), and toxic megacolon (1). Fourteen emergency operations were for perforated viscus or peritonitis (11), massive gastrointestinal bleeding (2), and cecal volvulus (1). In 5 of 22 (23%) elective operations AIDS was unknown to the treating physicians until diagnosed by the surgical pathology; in contrast, all 14 emergency operations were in patients who had a known diagnosis of AIDS. The operative findings were related to AIDS in 34 of 36 (94%) operations. Cytomegalovirus was the most common pathogen, isolated or identified microscopically in 11 patients (eight emergency and three elective operations). Mycobacterial infections presented as retroperitoneal adenopathy or splenic abscess in six patients. Non-Hodgkins lymphoma was the most common malignancy found, presenting as an abdominal mass (4), bowel obstruction (3), or with gastrointestinal bleeding (2). Kaposi's sarcoma was diagnosed at laparotomy in four patients. The 1-month operative mortality rate for elective operation was 9% (2 of 22) and 46% (6 of 13) in emergencies. Postoperative complications included 1 reoperation for sepsis caused by inadequately resected CMV colitis; 1 pancreatic fistula; 1 wound dehiscence, and 2 minor wound infections.

Abdomen↗
PubMed1989

Repair of incisional hernia.

Because wound infection is a major cause of incisional hernia, the question posed is whether or not repairs of incisional hernias are at a higher risk for wound infection also. To answer this, we analyzed the incidence of wound infection after repair of incisional hernias during a 30 month period and compared it with the infection rate in all other clean procedures performed during the same period. All repairs of incisional hernias were performed upon patients with completely healed incisions without clinical signs of infection. Patients undergoing concomitant procedures upon the gastrointestinal tract were excluded. During the 30 month period, 995 clean operations were performed. In the 80 repairs of incisional hernias, there were 13 infections proved by culture, yielding an over-all infection rate of 16 per cent. In the remaining 915 clean procedures, there were 14 wound infections (1.5 per cent, p less than 0.0001). Of these 915 clean operations, 241 were repairs of inguinal hernias. Two infections occurred in this subgroup (0.8 per cent, p less than 0.0001, compared with repairs of incisional hernias). In patients undergoing repairs of incisional hernias with previously documented wound infections, 41 per cent had infected repairs. By comparison, only 12 per cent of patients without a prior infection had infections develop in the hernial repair (p less than 0.05). The infection rate for patients not receiving prophylactic antibiotics (21 per cent) was almost twice the rate for those receiving antibiotics (11 per cent), p = 0.07. We concluded that repair of incisional hernias has a significantly higher rate of infection than do other clean general surgical procedures. Herniorrhaphy of a wound that was previously infected is at a higher risk for reinfection, despite complete healing of the skin and absence of clinical signs of infection. Perioperative antibiotic prophylaxis may be indicated, but randomized studies are needed. For reporting and surveillance purposes, repairs of incisional hernias should not be classified as clean surgical procedures.

Abdominal Muscles↗
PubMed1989

Modeling splanchnic hemodynamics after distal splenorenal shunt: a computer simulation and sensitivity analysis.

The distal splenorenal shunt operation was specifically designed to preserve portal flow and maintain elevated portal pressure. However, although this goal is met in the immediate postoperative period, flow decreases over time, and in as many as 75% of alcoholic patients, portal flow is lost in the first year. Various explanations have been offered for this observation, and modifications of the original operation have been proposed (splenopancreatic disconnection). Although other portacaval shunts have been successfully modeled as electrical circuits, this approach has never been described for the distal splenorenal shunt. In this study we developed a computer program that modeled the distal splenorenal shunt as an electrical circuit. We performed an analysis to determine the sensitivity of portal flow to changes in each resistance element and then performed a series of simulation experiments to critically examine the various explanations offered for the gradual changes in hepatic hemodynamics. We found that portal flow was most sensitive to resistance in the renal vein followed by resistance in the anastomosis. The simulation experiments suggested a new alternative to splenopancreatic disconnection--restricting the ability of the splenic vein, anastomosis, or renal vein to dilate. Additional clinical studies will be needed to test these predictions.

Collateral Circulation↗
PubMed1988

Computer-derived equations for predicting survival postoperatively. Their usefulness and limitations.

We used multivariate analysis to determine whether survival following perforations of the gastrointestinal tract could be accurately predicted from preoperative data. Of 12 variables tested, four were found to have predictive value. These were age, pulmonary disease, preoperative shock, and the attending surgeon. When these four variables were employed in a logistic regression equation on 42 patients, it correctly predicted which 21 patients died before leaving the hospital. To produce an equation useful for other hospitals, we recalculated it without the attending surgeon variable. Again, the equation was used to predict survival. The correlation of predicted vs observed outcome remained high, and, using a 2 x 2 chi 2 test, the correlation was significant. We then cross validated the three-variable model on data from a second hospital. The model accurately predicted the new data equally well. We believe that predictive models can identify risk factors in a variety of patient populations and can determine who is likely to benefit from specific treatment modalities.

Age Factors↗
PubMed1988

Protective effect of pentoxifylline on gastric mucosa.

Pentoxifylline (PF) has been shown to increase tissue oxygen tension. This study was performed to determine if PF has a protective effect on the gastric mucosa against alcohol (EtOH)-induced injury. Fasted Sprague-Dawley rats were pretreated with randomized test solution (control, normal saline, or PF, 75 mg/kg) intraperitoneally (ip). At 30 min, 100% EtOH (pH 8.5) was given intragastric. At 90 min, laparotomy was performed and gastric serosal stomach surface oxygen tensions (pO2) were measured. Stomachs were excised and opened and pH was measured. Photographs were taken and sections were obtained for histologic analysis to determine mucosal injury. The PF-pretreated rats had significantly higher serosal pO2 and significantly lower intragastric pH than control animals. There was significantly less gross and histologic mucosal injury in PF-treated animals. We conclude that PF is protective against EtOH gastric mucosal injury. This effect correlates with increased gastric serosal pO2 and is likely due to improved microcirculatory blood flow following PF administration.

Animals↗