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Biomedical subjects

S J Bhatia

Publications and source records attributed to S J Bhatia.

At least 37 records · Page 2Linked to original sources
PubMed1993

Detection of rectal and pararectal varices in patients with portal hypertension: efficacy of transvaginal sonography.

OBJECTIVE: The appearance and frequency of pararectal varices in patients with portal hypertension have not been studied. Accordingly, we used transvaginal sonography to detect pararectal varices and to compare their appearance and frequency with those of rectal varices in patients with portal hypertension. SUBJECTS AND METHODS: Transvaginal sonography was performed in 21 women with portal hypertension of different causes. The frequency and appearance of pararectal varices were determined and compared with those of rectal varices detected either in the same sonographic study or by sigmoidoscopy. RESULTS: Pararectal varices were detected in 17 (81%) of 21 patients. The varices varied in diameter from 2.1 to 5.5 mm (median, 3.5 mm). Seven of the patients with pararectal varices did not have rectal varices. Rectal varices were detected in 10 of 21 patients by transvaginal sonography and in nine patients by sigmoidoscopy; the two methods together showed rectal varices in 13 patients. CONCLUSION: Transvaginal sonography is useful for detecting pararectal and rectal varices in patients with portal hypertension. Pararectal varices are more common than rectal varices in these patients.

Adult↗
PubMed1993

Intrapulmonary vascular dilatations with hypoxemia in extrahepatic portal vein obstruction.

Several mechanisms have been suggested for the development of hypoxemia in cirrhosis. A few patients of portal hypertension due to non cirrhotic liver disease with cyanosis have also been reported earlier. We report probably the first documented case of portal hypertension with portal cavernoma and a normal liver, who had intrapulmonary vascular dilatations leading to hypoxemia and cyanosis. Our case suggests that changes leading to hypoxemia can occur due to portal hypertension alone, in the presence of a normal liver.

Dilatation, Pathologic↗
PubMed1993

Pulmonary function tests in cirrhotic and non-cirrhotic portal hypertension.

OBJECTIVE: To determine pulmonary functions in portal hypertension of different etiologies and with various grades of ascites. SETTING: Gastrointestinal clinic in a large community based and secondary referral hospital. PATIENTS AND METHODS: Forty five patients with portal hypertension, including 19 cirrhotics with tense ascites, 8 with moderate ascites, 6 with no ascites and 12 patients with non-cirrhotic portal hypertension. All patients underwent basal pulmonary function testing by spirometry and helium dilution technique, and arterial blood gas estimation and measurement of ascitic fluid pressure. Patients with tense ascites underwent paracentesis of up to 2 liters following which ascitic fluid pressure and pulmonary functions were estimated again. MAIN RESULTS: In cirrhotic patients without ascites, FVC (forced vital capacity), RV (residual volume), TLC (total lung capacity) and FRC (functional residual capacity) were lower than predicted values. In patients with ascites, FVC, FEV1 (forced expired volume in one second) and FEF25-75 (forced expired volume in one second) and FEF25-75 (forced expiratory flow rate between 25% and 75% of forced vital capacity) were significantly lower as compared to predicted values. FVC, FEV1, FEF25-75, pO2, pCO2 and SaO2% decreased significantly with increasing ascites. Paracentesis in patients with tense ascites led to clinical improvement and significantly improved lung volumes. CONCLUSIONS: Pulmonary functions are impaired in patients with cirrhosis, and ascites causes further deterioration. Patients with non-cirrhotic portal hypertension have normal pulmonary functions.

Adult↗
PubMed1992

Oxygen desaturation and tachycardia during upper gastrointestinal endoscopy are transient and benign.

We continuously monitored the arterial oxygen saturation (SaO2) and pulse rate by pulse oximetry in 46 patients undergoing upper gastrointestinal endoscopy for diagnosis (21 cases) or variceal sclerotherapy (25). No premedication or prior topical anaesthesia was used. Significant hypoxaemia (percent drop in SaO2 > 2) occurred in 24 (52%) patients during the procedure; in 16 of these it occurred during introduction of the endoscope. Twenty seven (59%) patients had hypoxaemia during recovery, 25 of these immediately after withdrawal of the endoscope. All these episodes were short-lived and were probably due to gagging; basal levels were reached within 1 to 5 min. Tachycardia (> 100 beats/min) occurred in 41 (89%) patients. Sclerotherapy and history of smoking did not affect the incidence and magnitude of hypoxaemia and tachycardia. Transient cardio-respiratory changes occur during and immediately after endoscopy, but these appear to be clinically benign.

Adolescent↗
PubMed1991

A scoring system to differentiate cirrhotic from non-cirrhotic portal hypertension.

When it is not possible to perform a liver biopsy in cirrhosis, one has to rely on suggestive clinical and biochemical parameters and imaging procedures to arrive at a presumptive diagnosis. Based on the statistical method described by Spiegelhalter and Knill-Jones, we have devised a scoring system to reliably differentiate cirrhotic from non-cirrhotic portal hypertension without a liver biopsy. Age, presence of ascites, liver scan result and serum albumin, taken together, could confirm or rule out the diagnosis of cirrhosis in two-thirds of patients with portal hypertension. A score of 5 or more suggested cirrhosis (sensitivity 78%), and of 5 or more suggested cirrhosis (sensitivity 78%), and a score of -6 or less suggested a non-cirrhotic cause (sensitivity 64%) for portal hypertension, both with 100% specificity. Eliminating liver scan result reduced both sensitivity and specificity, suggesting that liver scan is an important component of the score. This score may be useful not only in the management of individual patients but also to classify them in clinical trials.

Adult↗
PubMed1990

Changes in placental blood flow in the normal human fetus with gestational age.

We assessed fetoplacental blood volume flow and placental resistance prospectively with Doppler sonography in 74 normal human fetuses of 19 to 42 wk gestation to determine the changes in placental perfusion with gestational age. Placental blood volume flow was assessed from the umbilical vein as the product of the mean flow velocity integral and the cross-sectional area of the umbilical vein. Placental resistance was assessed as the ratio of maximum systolic and minimum diastolic blood flow velocities from an umbilical artery. Umbilical vein blood volume flow increased exponentially (r = 0.86) with gestational age from 19 wk to term, and did not decrease in postdate fetuses. Umbilical vein blood volume flow increased linearly with fetal weight (r = 0.77), although volume flow per unit body weight changed little with gestational age. Umbilical artery velocity ratio decreased progressively, indicating diminishing placental resistance with gestational age, but did not correlate closely with umbilical vein blood volume flow. We submit that fetoplacental blood volume flow can be readily calculated directly from the umbilical vein with Doppler ultrasound and may provide a better index of placental perfusion than the umbilical artery velocity ratio.

Female↗
PubMed1990

Effect of sublingual isosorbide dinitrate in portal hypertension.

Nitrates decrease portal pressure by decreasing portal venous inflow and resistance. We studied over 20 minutes the effect of 10 mg isosorbide dinitrate sublingual on intrasplenic pulp pressure, mean arterial pressure and heart rate, in 13 patients with cirrhotic or non-cirrhotic portal hypertension. The pulp pressure fell progressively over 20 minutes, from mean 43.6 +/- 2.4 (SEM) to 35.6 +/- 1.8 cm H2O (p less than 0.001). This was accompanied initially by a significant fall in mean arterial pressure (85.8 +/- 1.9 to 80.4 +/- 2.7 mmHg at 4 minutes; p less than 0.01) and rise in heart rate (92.5 +/- 5.0 to 102.6 +/- 5.9 per minute at 6 minutes; p less than 0.02), following which these parameters remained stable. One patient developed giddiness due to hypotension at 15 minutes. We conclude that sublingual isosorbide dinitrate decreases pulp pressure in cirrhotic and non-cirrhotic portal hypertensives, but this is initially accompanied by significant hemodynamic changes.

Administration, Sublingual↗
PubMed1990

Evaluation of a modified medium for the one hour urease test for Helicobacter pylori infection.

The biopsy urease test is a simple and rapid method for the diagnosis of Helicobacter pylori infection; results are obtained within 4 h to 24 h. Various modifications of the media used in this test have been tried, to improve the accuracy and speed of the test. We compared the yield obtained with two media: the standard Christensen's urea medium and a modified plain urea medium (without the nutrients glucose and peptone); the result was read upto 1 h. In the first 53 cases, culture was obtained when either of the media gave a negative result. There was no difference in false positives in the two media, while there were more false negatives with the plain urea medium (4) compared to the Christensen's medium (1). In the latter 69 patients, we determined the accuracy of the two media by obtaining culture in all cases. The Christensen's medium had a sensitivity of 100% and a specificity of 92.1%, while the plain urea medium had a sensitivity of 96.7% and a specificity of 92.1%. The speed of reaction in both media was similar. We conclude that the Christensen's urea medium gives accurate results even when read at 1 h; the plain urea medium gives similar results.

Biopsy↗
PubMed1989

Assessment of valvular heart disease with Doppler echocardiography.

The addition of Doppler principles to two-dimensional echocardiography has revolutionized the noninvasive evaluation of valvular heart disease. Doppler techniques allow precise measurements of blood flow velocity at different locations in the heart and great vessels, so that many aspects of hemodynamics can now be measured noninvasively. These techniques are particularly useful for the quantitative assessment of valvular stenosis; both valve areas and transvalvular gradients may be determined. Doppler echocardiography (particularly with color flow mapping) is also useful for the qualitative assessment of valvular regurgitation. By understanding the uses and limitations of Doppler echocardiography, physicians may now confidently follow up patients with mild or moderate valvular disease with serial noninvasive studies, avoiding the risks of cardiac catheterization in many patients.

Blood Flow Velocity↗
PubMed1989

Left ventricular tamponade: echocardiographic and hemodynamic manifestations.

A patient with progressive systemic sclerosis was evaluated for dyspnea. Echocardiography revealed enlarged right heart chambers, a moderate pericardial effusion, and diastolic collapse of the left ventricle. Hemodynamic studies before and after removal of pericardial fluid were consistent with compromise of left, but not right, heart filling by the pericardial fluid.

Cardiac Tamponade↗
PubMed1989

Peak left ventricular pressure during percutaneous aortic balloon valvuloplasty: clinical and echocardiographic correlations.

Peak left ventricular pressure during balloon inflation was measured in 20 patients who underwent balloon valvuloplasty for severe aortic stenosis to define the determinants of ventricular pressure development in response to increased loading conditions. The peak left ventricular pressure ranged from 150 +/- 5 to 386 +/- 22 mm Hg (mean +/- SD), was reproducible in each patient with each balloon inflation (mean coefficient of variation 7.8%) and correlated with concurrent echocardiographic measurements of ejection fraction (r = 0.89, p = 0.0001) and mass/volume ratio in systole (r = 0.91, p = 0.0001) or diastole (r = 0.88, p = 0.0001). Thirteen patients with class II or more severe congestive heart failure had lower values for peak left ventricular pressure than did those without failure (225 +/- 46 versus 305 +/- 45 mm Hg, p = 0.002), whereas no difference in rest left ventricular systolic pressure was seen between the two groups. The measurement of peak left ventricular pressure was inversely related to rest mean circumferential end-systolic wall stress (r = 0.52, p = 0.046). Thus, peak left ventricular systolic pressure measured during aortic valvuloplasty in humans correlates closely with traditional measures of left ventricular function. This measurement, which previously has been obtained only in experimental animal studies, is a simple and reproducible hemodynamic index that may provide new insights in studies of ventricular function and congestive heart failure in aortic stenosis.

Adult↗
PubMed1989

Lactobacillus acidophilus inhibits growth of Campylobacter pylori in vitro.

Campylobacter pylori has been implicated as a causative factor in acid-peptic disease. Lactobacillus acidophilus is known to inhibit the growth of pathogens in the human gastrointestinal tract. We recovered C. pylori from gastric antral biopsies of seven patients with acid-peptic disease; the isolates were then cultured in brucella broth. The effect of L. acidophilus (cultured in DeMan-Rogosa-Sharpe broth) on the growth of C. pylori was tested by a mixed culture technique. L. acidophilus inhibited the growth of all seven isolates of C. pylori in vitro. All these isolates were also inhibited by the L. acidophilus culture supernatant (brucella blood agar cup technique) obtained at or after 48 h of incubation. Inhibition of C. pylori growth was also observed with 1 and 3% lactic acid but not with 0.5 and 1% hydrogen peroxide, the L. acidophilus sonic extract, or a citrate-phosphate buffer (pH 4.0). We conclude that the inhibitory action of L. acidophilus on C. pylori is dependent on an extracellular secretory product, probably lactic acid. This inhibitory effect may be of therapeutic relevance in patients with C. pylori-positive acid-peptic disease.

Campylobacter↗
PubMed1989

Suppression of silent ischemia by metoprolol without alteration of morning increase of platelet aggregability in patients with stable coronary artery disease.

To determine the effect of metoprolol on silent ischemia and platelet aggregability, 10 patients with coronary artery disease were studied with a randomized, double-blind, placebo-controlled, crossover trial. Patients were treated with metoprolol (200 mg b.i.d.) or placebo for 1 week and then received the alternate therapy. Two days before the end of each treatment period, platelet aggregability was studied for 24 hours, and a 48-hour ambulatory electrocardiogram was obtained. Compared with placebo, metoprolol significantly decreased the total number (from 26 to 4, p less than 0.1) and duration (from 735 to 84 minutes, p less than 0.01) of silent ischemic episodes. This decrease was accompanied by a decrease in the mean blood pressure (from 127/81 to 118/71 mm Hg, p less than 0.01) and the mean heart rate (from 70 to 54 beats/min, p less than 0.01). The incidence of silent ischemic episodes in the morning was significantly higher in untreated patients than in treated patients. The few episodes observed during metoprolol treatment occurred at the same time as the peak incidence observed during placebo treatment. During placebo treatment, platelet aggregability increased from 6:00 to 9:00 AM as reflected by a decrease in the threshold concentrations of ADP and epinephrine required to induce biphasic platelet aggregation (from 4.8 +/- 0.8 to 2.6 +/- 0.4 microM, p less than 0.02; and from 7.3 +/- 2.3 to 1.8 +/- 0.9 microM, respectively, p less than 0.02). Metoprolol did not alter the basal level nor blunt the morning increase of platelet aggregability.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Doppler echocardiographic study of the frequency and severity of aortic regurgitation in hypertrophic cardiomyopathy.

Aortic regurgitation (AR) has been reported sporadically in hypertrophic cardiomyopathy (HC) but neither its frequency nor severity has been determined. Thirty-one consecutive patients with HC were evaluated by Doppler echocardiography over a 2-year period. Twenty-nine had echocardiographically normal aortic cusps and participated in the study; 2 had calcified aortic valves and were excluded. AR of grade I to grade II severity was demonstrated in 9 of 29 (31%) patients. Patients were divided into 2 groups: group 1 (n = 9) with AR and group 2 (n = 20) without AR. Group 1 patients were significantly older than group 2 patients (73 +/- 7 vs 60 +/- 17 years, p less than 0.05) and had larger end-diastolic (4.5 +/- 0.5 vs 4.0 +/- 0.7 cm, p less than 0.01) and end-systolic (2.7 +/- 0.4 vs 2.3 +/- 0.4, p less than 0.02) left ventricular dimensions. Left ventricular wall thickness, degree of asymmetric septal hypertrophy and left ventricular fractional shortening were similar in the 2 groups. Mitral regurgitation was more common in group 1 (100% vs 35%, p less than 0.005), although there were no differences in left atrial size between the 2 groups. The HC patients were compared with a control group of 23 normal subjects of similar age. There was no mitral regurgitation or AR in the normal subjects. Thus, nearly one-third of patients with HC had mild AR by Doppler. The AR most probably results from high-velocity systolic blood flow causing microscopic damage to the valve cusps.

Adult↗