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Biomedical subjects

J E Bredfeldt

Publications and source records attributed to J E Bredfeldt.

At least 19 recordsLinked to original sources
PubMed2001

Reusable biopsy forceps: a prospective evaluation of cleaning, function, adequacy of tissue specimen, and durability.

BACKGROUND: Recent studies have indicated that reusable biopsy forceps remain contaminated after reprocessing and can only be used a mean of 12 to 25 times without malfunction. Because this contradicts traditional endoscopic practice, our study investigated the ability to sterilize a type of commercially available biopsy forceps and prospectively evaluated their function in vivo until malfunction and/or breakage. METHODS: Thirty reusable biopsy forceps were studied, 15 of which were contaminated for 5 trials each with 10(6) Bacillus stearothermophilus, and 15 of which were prospectively evaluated clinically over an 18-month period (9/98-3/00). Contaminated forceps were reprocessed by using a standard protocol and placed in a sterile bag containing soy broth. The latter was passed through a 0.2 micron filter and was subsequently cultured. In vivo data included biopsy site, size, adequacy, problems obtaining a biopsy specimen, and reasons for ultimate forceps failure. RESULTS: After contamination, all biopsy forceps yielded a heavy growth of B stearothermophilus. No forceps, including 5 that were piecemeal dismantled with a wire cutter, had residual bacteria after reprocessing. In the in vivo study, 1507 biopsy sessions were undertaken in 1339 procedures. Forceps were categorized as new or like-new in 1259 of 1339 (94%) procedures, some loss of function but usable in 72 of 1339 (5.4%), and inadequate function or broken at use in 8 of 1339 (0.6%). Histologically, 1501 specimen sets were adequate (99.6%) and mean specimen size was 2.7 +/- 0.1 mm. Mechanical problems were noted in only 38 of 1507 (3%) sessions to include such things as sticky forceps, and the mean number of uses to malfunction or breakage was 91 +/- 15 (SEM) (range 19-132). CONCLUSIONS: This reusable biopsy forceps can be sterilized and used a mean of 91 times with adequate tissue sampling. Mechanical problems were minor to time of breakage. Contingent on acquisition and reprocessing costs as well as the number of procedures performed, this reusable forceps has the potential for significant cost savings.

Biopsy, Needle↗
PubMed1995

Esophageal dilation can be done safely using selective fluoroscopy and single dilating sessions.

Maxims for safe esophageal dilation have included recommendations to use fluoroscopy in all instances and to limit dilation sessions to 2-mm increments. We reviewed a 34-month experience of all esophageal dilations undertaken at a large multispecialty clinic to define adherence to these recommendations and to delineate whether deviation was associated with significant complications. Four hundred thirty-two patients underwent 716 courses of esophageal dilation during this time, 92% of whom had benign disease. Eighty-nine percent of patients were dilated with polyvinyl dilators (Savary/American) and only 8% of these patients required fluoroscopic monitoring for the bougienage. Seventy-eight percent of the dilating sessions for patients without achalasia were undertaken using either a single large dilator (> or = 45 Fr) or employed incremental dilator sizes > 2 mm (6 Fr) in a single session. There was a single perforation in 662 nonachalasia dilations and this was a consequence of attempted placement of an esophageal endoprosthesis. We conclude that use of guide wire technology and newer dilating techniques do away with the need for routine fluoroscopic control. Moreover, single large dilators or dilator increments > 2 mm may be safely used, contingent on endoscopic stricture assessment.

Dilatation↗
PubMed1991

Portal colopathy: prospective study of colonoscopy in patients with portal hypertension.

Twenty patients with portal hypertension related to a variety of causes prospectively underwent colonoscopy for hematochezia (n = 10), hemoccult positive stool and anemia (n = 9), or polyp found with screening flexible sigmoidoscopy (n = 2) (includes 1 patient with anemia/heme-positive stool). Twelve patients (60%) had previously undergone a course of sclerotherapy, and 10 (50%) had endoscopic evidence of congestive gastropathy. Colonoscopic findings included mucosal abnormalities resembling multiple vascular ectasias in 14 (70%), 4 of whom also had endoscopic features suggesting a mild, chronic colitis. Neither signs of chronic liver disease nor stigmata suggestive of more severe portal hypertension correlated with the colonoscopic findings. Two patients required heater probe therapy for actively oozing lesions resembling vascular ectasias and an additional two patients sclerotherapy for bleeding midrectal varices. Although likely an overestimate of the frequency, this study suggests that portal colopathy can occur in portal hypertension. Vascular ectasialike lesions in such settings may be associated with acute as well as chronic gastrointestinal bleeding and may require pharmacological, directed endoscopic, or portal decompressive therapy. Additional studies are required to determine not only the pathophysiology but also the true frequency of this entity.

Capillaries↗
PubMed1989

Sinusoidal lymphocytosis of the liver in Felty's syndrome with a review of the liver involvement in Felty's syndrome.

A 68-year-old woman with Felty's syndrome had massive hepatomegaly. Liver biopsy showed diffuse infiltration of the sinusoids with mature lymphocytes (sinusoidal lymphocytosis of the liver). Nodular regenerative hyperplasia of the liver and portal fibrosis were not found. Although liver involvement is frequent in association with Felty's syndrome, sinusoidal lymphocytosis of the liver is unusual.

Aged↗
PubMed1989

Autoimmune chronic active hepatitis masquerading as acute hepatitis.

An unusual clinical presentation of chronic active hepatitis is the abrupt onset of symptoms and jaundice, suggesting acute viral hepatitis. In this report, six patients had the acute onset of a severe liver disease. Five of the patients were female and ranged in age from 13 to 64 years. Marked elevations in the total bilirubin (17.1 +/- 11.4 mg/dl), AST (1,346 +/- 352 mIU/ml), and ALT (1,043 +/- 213 mIU/ml) were present (mean +/- SD). Negative serologies for hepatitis A and B were found. Liver histology showed severe hepatocellular injury. A diagnosis of autoimmune chronic active hepatitis with acute features was made on the basis of high titers of antinuclear antibody and smooth muscle antibody and the presence of hypergammaglobulinemia. As immunosuppressive therapy is a beneficial treatment of autoimmune chronic active hepatitis, an acute presentation of this liver disease should be considered as an alternative diagnosis to acute non-A, non-B hepatitis in patients with these clinical characteristics.

Acute Disease↗
PubMed1985

Hepatitis B virus. Update on the spectrum of clinical infections and on prophylaxis.

Knowledge about hepatitis B virus (HBV) has expanded vastly over the past 20 years, elucidating not only the spectrum of clinical illnesses it causes but also its biologic characteristics. HBV is an important cause of both acute and chronic liver disease in the United States. The most serious outcome of hepatitis B infection is chronic liver disease, which can range from chronic hepatitis eventuating in cirrhosis to primary hepatocellular carcinoma. Molecular biologic studies have shown that HBV-DNA can be integrated into the genome of hepatocytes. This integration may be part of the natural history of chronic hepatitis B infection and may transform normal hepatocytes into neoplastic cells. Immunization with hepatitis B vaccine (Heptavax-B) of persons at high or intermediate risk is an essential means for preventing transmission of hepatitis B. Use of the vaccine after recent exposure to hepatitis B breaks the chain of transmission--an exciting capability. Postexposure immunization of neonates born of HBsAg-positive mothers is particularly important in preventing vertical, or perinatal, transmission of infection.

Carrier State↗
PubMed1985

Compensatory mechanisms in response to an elevated hepatic oxygen consumption in chronically ethanol-fed rats.

During conditions that elevate hepatic oxygen consumption (VLO2), oxygen delivery, or oxygen extraction may also increase, acting as compensatory mechanisms. VLO2 was quantitated by an in vivo method in chronically ethanol-fed rats to establish whether VLO2 was increased and what compensatory mechanisms might ensue. VLO2 was increased 45% (0.32 +/- 0.02 ml O2 X min-1 X 100 g body wt-1; P less than 0.001) in rats chronically fed ethanol for 8 wk, while VLO2 (0.28 +/- 0.04; P = NS) was not increased in chronically ethanol-fed rats withdrawn from ethanol 20 h before study compared with control rats (0.22 +/- 0.01). Oxygen delivery was increased 31% (P less than 0.05) in ethanol-fed rats and adequately compensated for the increased VLO2. Hepatic artery blood flow did not increase in ethanol-fed rats, indicating a lack of hepatic artery vasodilation in response to the elevated VLO2. As a result, a greater percentage of oxygen delivery was supplied via portal venous blood flow that has a reduced oxygen content. These observations might suggest that ethanol-fed rats may have a decreased reserve for maintaining an adequate oxygen supply to the liver and may be at an increased liability for developing hepatic hypoxia if oxygen delivery and/or extraction were compromised.

Alcoholism↗
PubMed1984

Increased blood flow through the portal system in cirrhotic rats.

Portal venous pressure is the result of the interplay between portal venous blood flow and the vascular resistance offered to that flow. Whether portal hypertension is maintained only by an increased portal venous resistance or also by an increased blood flow within the portal venous system is still open to speculation. To resolve these differences, splanchnic and systemic hemodynamics were evaluated in cirrhotic rats, induced by CCl4. Blood flow and portal-systemic shunting were measured by radioactive microsphere techniques. All cirrhotic rats had portal hypertension (portal venous pressure 13.5 +/- 1.1 vs. 9.0 +/- 0.5 mmHg, in normal control rats; p less than 0.01), but portal-systemic shunting in cirrhosis (31% +/- 13% vs. 0.2% +/- 0.02%; p less than 0.05) was variable, ranging from 1% to 97%. Portal venous inflow, the total blood flow within the portal system, was increased in cirrhotic rats (5.75 +/- 0.04 vs. 4.52 +/- 0.36 ml/min per 100 g; p less than 0.05). Total splanchnic arterial resistance was reduced in cirrhotic rats (3.3 +/- 0.2 vs. 5.8 +/- 0.5 dyn X s X cm-5 X 10(5); p less than 0.01). Portal venous resistance, however, was not abnormally elevated in cirrhotic rats (4.6 +/- 0.5 vs. 4.7 +/- 0.5 dyn X s X cm-5 X 10(4), p = NS). Splanchnic hemodynamics in cirrhotic rats demonstrate that portal hypertension is maintained, at least in part, by a hyperdynamic portal venous inflow. The hemodynamic data in cirrhotic rats provided evidence that supports the role of an increased portal blood flow in portal hypertension and gives a quantitative definition of splanchnic hemodynamics in intrahepatic portal hypertension.

Animals↗
PubMed1983

Hepatic oxygen consumption, in vivo, in the rat.

A method is described that quantitates hepatic oxygen consumption, in vivo, in the rat. This method can evaluate hepatic oxygen consumption resulting from chronic conditions that may alter it.

Animals↗
PubMed1983

Hyperdynamic circulation in portal-hypertensive rat model: a primary factor for maintenance of chronic portal hypertension.

Two dissimilar hemodynamic hypotheses, the "backward flow" theory and the "forward flow" theory, have been advanced to define splanchnic hemodynamics in portal hypertension. An animal model with portal hypertension and high-grade portal-systemic shunting, the portal vein-stenotic rat, was studied to determine whether a hemodynamic picture compatible with either theory would develop. Splanchnic and systemic hemodynamics and portal-systemic shunting were measured by radioactive microsphere techniques. The portal-hypertensive rats (portal pressure, 12.8 +/- 0.5 vs. 8.3 +/- 0.4 mmHg) with greater than 95% portal-systemic shunting had a 60% increase in portal venous inflow (23.46 +/- 2.54 vs. 14.97 +/- 1.61 ml/min; P less than 0.01) with a concomitant 50% decrease in splanchnic arteriolar resistance (3.86 +/- 0.43 vs. 7.60 +/- 0.80 dyn . s . cm-5 . 10(5); P less than 0.001) compared with control rats. Cardiac index (391 +/- 17 vs. 250 +/- 20 ml . min-1 . kg-1) was elevated 50% (P less than 0.001), and total peripheral resistance (7.1 +/- 0.4 vs. 11.7 +/- 0.8 dyn . s . cm-5 . 10(4)) was decreased 60% (P less than 0.001). The resistance to portal blood flow in portal vein-stenotic rats (4.77 +/- 0.57 dyn . s . cm-5 . 10(4)) was similar to the resistance to portal blood flow in control rats (4.82 +/- 0.43 dyn . s . cm-5 . 10(4)), indicating that the hyperdynamic portal venous inflow, not resistance, provided the main impetus for maintaining the elevated portal venous pressure. The splanchnic hemodynamic observations directly support the forward flow theory of portal hypertension. The relation between splanchnic arteriolar resistance and total peripheral resistance (r = 0.67; P less than 0.01) indicated that the systemic hemodynamic parameters were secondarily altered by the splanchnic hemodynamic changes. This animal model of chronic portal hypertension gave evidence for a generalized splanchnic arteriolar vasodilation occurring in the presence of high-grade portal-systemic shunting.

Animals↗
PubMed1982

Idiopathic portal hypertension in a renal transplant recipient.

A renal transplant recipient developed a noncirrhotic form of portal hypertension, idiopathic portal hypertension, several years after the transplantation. The liver histology by light microscopy disclosed only chronic portal inflammation and portal fibrosis; however, a prominent collagen deposition with the space of Disse seen only by electron microscopy evolved during the course of the liver disease. This report, in association with other reports of the same disorder in renal transplant recipients, suggests that idiopathic portal hypertension may occur as a direct consequence of renal transplantation.

Adult↗
PubMed1980

Hypertonic upper esophageal sphincter in the oculopharyngeal syndrome.

The oculopharyngeal syndrome (OPS) is a rare variant of muscular dystrophy characterized by progressive ptosis and dysphagia. Previous esophageal motility studies in OPS have yielded conflicting results because of low-fidelity esophageal recording systems. Although cricopharyngeal myotomy improves symptoms, accurate postoperative manometric findings have not been reported. Using a low-compliance, high-fidelity system and a radially oriented esophageal motility catheter in an OPS patient we found a hypertonic upper esophageal sphincter (UES), a hypotonic proximal esophagus, and elevated pressures in the distal two-thirds with prolonged duration of contraction. Clinical improvement followed myotomy. We also found a similar manometric pattern but a normotensive UES in an asymptomatic sibling.

Blepharoptosis↗