Esophageal atresia with double tracheoesophageal fistula.
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Biomedical subjects
Publications and source records attributed to S Mehta.
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Feeding of vitamin A-deficient diet to male weanling rats for 10 weeks caused significant increase in the activities of Phase I enzyme system, i.e., cytochrome P-450, cytochrome b5 and arylhydrocarbon hydroxylase in the proximal, middle and distal segments of the intestine. Of the Phase II enzymes studied, UDP-glucuronyltransferase showed significant decrease whereas glutathione S-transferase showed significant increase. Treatment with benzo(a)pyrene caused greater induction in the levels of Phase I enzymes in deficient animals as compared to controls. In contrast to this, benzo(a)pyrene treatment induced the level of UDP-glucuronyltransferase in control rats more than in deficient rats. Intestinal NADPH cytochrome C-reductase and glutathione S-transferase remained insensitive to benzo(a)pyrene induction.
Two hundred and three laryngectomized patients have been evaluated for the possible causes of post operative complications. 58 out of 203 patients (28.5%) developed pharyngocutaneous fistula. Wound infection was present in 57 cases (28%). Two patients had flap necrosis and 12 patients developed dysphagia after surgery due to pharyngeal stenosis. The possible causes attributed to high occurrence of pharyngocutaneous fistula are, advanced nature of disease, preoperative radio therapy and wound sepsis. Prior to 1980, the incidence of pharyngocutaneous fistula in our series (Arora et al. 1983) was 41.6 percent. But it decreased to 13.7 percent between January 1981 to June 1987. The important factors which led to the decreased incidence of pharyngocutaneous fistula were thought to be the change of suture material for pharyngeal repair from chromic catgut to Vicryl, use of vacuum suction as a replacement of corrugated rubber drain and aseptic syringe drainage and postoperative coverage with broad spectrum antibiotics.
We report the use of ketoconazole to control disseminated intravascular coagulation due to prostatic carcinoma. Clinical improvement in the condition of the patient was noted in 48 hours and coagulation profile became normal in 10 days.
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Real time sonography followed by splenoportography was performed in 38 cases with non-cirrhotic portal hypertension. Eleven of these cases, in whom porto-systemic shunt surgery was done, were also evaluated by real time sonography post-operatively. The ultrasound findings correlated well in 37 cases (98%) with splenoportography. All the post-operative cases also revealed a patent portosystemic shunt on sonography. Ultrasonography, a valuable, non-invasive, initial investigation of portal hypertension, may thus be used as the only investigation to distinguish intra- from extra-hepatic obstruction and to evaluate patency of surgically created porto-systemic shunts. Invasive portography may be performed only if surgical treatment is anticipated.
This study compares some physical characteristics of a selection of cuffed endotracheal tubes with large-volume, low-pressure cuffs currently used in the United Kingdom. Six types of endotracheal tubes of Sizes 7, 8 and 9 were studied. There was considerable variation in physical characteristics of endotracheal tubes and cuffs from different manufacturers and even from the same manufacturer.
We have prospectively evaluated 41 patients who ingested acid for location, extent, severity, and outcome of the injury to the upper gastrointestinal tract. The injury was assessed within 36 h of acid intake by endoscopy or surgery, or at autopsy. Symptoms and signs were unreliable in predicting the extent and severity of injury. The degree of burns was classified as follows: grade 0 in 2 patients, grade 1 in 3, grade 2 in 16, and grade 3 in 20. Esophageal injury was seen in 87.8% of the patients, gastric injury in 85.4%, and duodenal injury in 34.1%. All patients with grade 0, 1, and 2a injury recovered without sequelae. Acute complications occurred in 39.1% of the cases, and death in 12.2%. It is significant that all such patients had grade 3 burns. Five of the 8 patients with grade 2b injury and all survivors of grade 3 injury developed esophageal or gastric cicatrization, or both, which subsequently needed endoscopic or surgical treatment. We find that endoscopy is not only the tool of choice for diagnosis in such cases but also aids in deciding upon treatment and prognosis. We conclude that acid injury of the upper gastrointestinal tract is a very serious condition that affects the esophagus and stomach equally and results in high morbidity and mortality.
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A ten year old child with extrahepatic portal venous obstruction had recurrent upper gastrointestinal bleeding after endoscopic variceal sclerotherapy. Sclerotherapy-induced esophageal ulcer complicated by candidiasis was found to be the source of bleeding. This as yet unrecognised complication of sclerotherapy requires prompt diagnosis and early antifungal therapy.
Fibreoptic endoscopy is a highly efficient diagnostic tool which is now being increasingly used in pediatric age group also. However, certain special considerations like the use of special instruments, use of general anesthesia in younger children and various indications of diagnostic and therapeutic endoscopy need to be clearly emphasized. Over a period of 24 months, 132 children underwent upper gastrointestinal endoscopic examination in our section. Diagnostic endoscopy was carried out on 102 occasions and therapeutic on 162 occasions. Most of the children below 3 years of age required general anesthesia for the procedure. Children above 3 years of age could be managed by intravenous diazepam and pentazocine. The commonest cause of upper gastrointestinal bleed in children was variceal (60.6%) followed by erosive gastritis (27.2%). In children with recurrent abdominal pain no underlying cause was detected at endoscopy. Injection sclerotherapy was found to be a safe and effective mean for control of variceal bleed and most of the foreign bodies ingested by children and still lying proximal to 2nd part of duodenum could be successfully retrieved endoscopically.
Feeding of vitamin A-deficient diet to male weanling rats for 10 weeks resulted in significant decrease in the body weight and marked reduction in the hepatic vitamin A content. The levels of hepatic phase I microsomal enzymes cytochrome P-450, cytochrome b5, aminopyrine N-demethylase and arylhydrocarbon hydroxylase were found to be substantially reduced by vitamin A-deficiency. Also, the activity of phase II microsomal UDP - glucuronyl transferase enzyme was significantly decreased in deficient animals. Following repeated oral administration of DDT (15 mg/kg/body wt/day) for 21 days, the phase I microsomal enzymes were induced to a greater extent in controls as compared to deficient animals. UDP - glucuronyltransferase remained insensitive to DDT induction. The results imply that the capacity for induction of the hepatic mixed-function oxidase enzyme system is impaired in deficient animals concurrently exposed to DDT.
NMRI mice immunosuppressed with dexamethasone followed by challenge intraesophageally with axenic Giardia lamblia (Portland I) trophozoites had severe infection in terms of the trophozoite counts in the jejunum. Although the immunosuppressive treatment with cortisone itself resulted in a deleterious effect on brush border membrane enzymes, the decline in disaccharidases (sucrase, maltase, and lactase) and alkaline phosphatase was highly significant (P less than 0.001) following G. lamblia infection. The alterations in enzymatic activity in immune intact but infected animals demonstrated the potential of the parasite itself to cause damage to the brush border membrane. We believe that individuals with underlying immunodeficiency, upon infection with G. lamblia, may have increased damage of the brush border membrane, leading to severe malabsorption.
Plasma membrane isolated from axenically grown Giardia lamblia (Portland 1 strain) by treatment with a membrane stabilizing agent followed by osmotic stress and manual sheer showed a significant enrichment of the membrane bound marker enzymes CA++ATPase/Mg++ATPase. Crossed immunoelectrophoresis (CIE) was used to identify membrane antigens. 11 major peaks were detected in CIE profiles of the whole trophozoites. 6 major peaks were detected in CIE profiles of the membrane preparation. 2 surface membrane peaks with relative mobilities of 0.10 (peak 2) and 0.70 (peak 6) were identified by absorption studies. Peak 2 had a molecular mass of 82 kDa whereas peak 6 had a molecular mass of 56 kDa. The monospecific antiserum raised against the surface antigens of strain Portland 1 with molecular masses of 82 kDa and 56 kDa revealed the existence of identical antigens on 2 other isolates (Isr & WB) of G. lamblia.
The specific anti-plasma membrane- or surface-specific serum antibodies to Mr 82,000 antigen of Giardia lamblia trophozoites in cases of persistent and nonpersistent giardiasis in a pediatric population indicated significantly low concentrations of these antibodies in patients with persistent giardiasis. There was an insignificant difference in the amount of antibodies to whole trophozoite extract in persistent and nonpersistent giardiasis or asymptomatic carriers. The acute/nonpersistent cases had predominantly IgM class antigiardial antibodies, whereas persistent and asymptomatic carriers had antigiardial antibodies of the IgG class. The inability of persistent cases of giardiasis to clear infection appears to be related to low concentrations of antiplasma membrane/anti-Mr 82,000 antigiardial antibodies.
The development and validation of a coated bead immunoassay for amniotic fluid acetylcholinesterase is outlined. The assay has good precision (between assay CV of 6.8% within the normal range), and is linear up to 250 arbitrary units/L. The clinical validity of this assay has been assessed using a panel of amniotic fluid samples from normal and abnormal pregnancies. At an assay cut off level of 200 arbitrary units/L, all cases of neural tube defect-affected pregnancies were identified and the number of false positives was very small. False positives resulted from severe blood staining of the amniotic fluid. Since the monoclonal antibody used recognises red cell membrane acetylcholinesterase and the stored amniotic fluids had been frozen and thawed a number of times, the extent of this problem needs to be further assessed using freshly collected samples. The performance of this assay was found to be superior to the differential inhibitor colorimetric method and close to that of the electrophoretic procedure. The quantitative nature of the assay and the independence from operator technique makes it a useful adjunct to the measurement of amniotic fluid AFP in the prenatal diagnosis of neural tube defects.