Search PubMed⌕ Search

Biomedical subjects

B N Datta

Publications and source records attributed to B N Datta.

At least 73 records · Page 4Linked to original sources
PubMed1977

Acute renal failure following copper sulphate intoxication.

Eleven out of a series of twenty-nine patients (37-9%) with acute copper sulphate poisoning developed acute renal failure. Intravascular haemolysis appeared to be the chief factor responsible for renal lesions in these patients. Histological lesions observed in the kidney varied from those of mild shock to well established acute tubular necrosis. In one case, granulomatous lesions were seen in response to tubulorrhexis. Renal failure was the chief indication for dialysis in ten patients, whereas one patient was dialysed primarily for removal of copper. Notwithstanding the adequate control of uraemia by dialysis, only six of the eleven patients recovered. Septicaemia was responsible for death in three, hepatic failure in one and methaemoglobinaemia in another. It is postulated that release of copper from haemolysed red cells during acute haemolytic episodes may initiate, or contribute to, the development of renal damage.

Acute Kidney Injury↗
PubMed1977

Endomyocardial fibrosis in Chandigarh area, India. A study of nine autopsies.

The clinical and autopsy data of nine cases of endomyocardial fibrosis encountered over a period of 11 years are presented. These account for nearly 24% of primary cardiomyopathies and 0.8% of cardiac diseases seen at autopsy. There were four cases with biventricular endomyocardial fibrosis, three with a predominantly left and two with a predominantly right ventricular affection. There was no correlation between the clinical data and the autopsy pattern of endomyocardial fibrosis; all of them presented as congestive cardiac failure.

Adolescent↗
PubMed1976

Acute renal failure of obstetric origin.

Acute renal failure of obstetric origin is common among North Indian patients and comprised 72 (22.1%) of 325 patients undergoing dialysis over an 11-year period. Of these, 46 gravidas had developed renal failure following abortion, and 29 cases were due to complications of late pregnancy. The most striking feature of this study was a high incidence of irreversible renal lesions of bilateral diffuse cortical necrosis in early (18.6%) as well as late pregnancy (37.8%). Overall incidence of diffuse cortical necrosis was 25%. In the remainder, acute tubular necrosis was seen in 52 (72.2%), patchy cortical necrosis in 1 (1.4%), and tubular necrosis along with glomerular involvement in 1 patient (1.4%). Pathogenetic factors which contributed to the development of renal failure, either singly or in combination, were loss of blood failure, either singly or in combination, were loss of blood (79.1%), septicemia (31.9%), hypotension due th hemorrhagic and septicemic shock (51.4%), eclamptic toxemia (11.1%), and disseminated intravascular coagulation in 12.5% patients. Infrequent occurrence of disseminated intravascular coagulation in the septic anc eclamptic patients who developed diffuse cortical necrosis was an interesting finding, as was the fact that coagulopathy was more frequently observed in acute tubular necrosis. Late referral, frequent sepsis, and high incidence of bilateral diffuse cortical necrosis contributed significantly to a high mortality (55.3%).

Abortion, Induced↗
PubMed1975

Portal hypertension in chronic leukaemia.

Portal haemodynamic studies were carried out in 11 subjects, seven with chronic myeloid leukaemia and four with chronic lymphatic leukaemia, and results compared with those obtained in five patients with 'idiopathic' splenomegaly and with control subjects. All 11 patients with chronic leukaemia had intrasplenic pressures above 11 mmHg and of these four had pressures above 20 mmHg. Portosystemic collaterals were seen on splenovenography in four of these patients. Hepatic vein wedge pressure was above 7 mmHg in nine patients and these high levels were a result of increased free hepatic vein pressure. The corrected sinusoidal pressure and post sinusoidal resistance were essentially normal in all patients. Evidence of increased pre-sinusoidal resistance was seen in six patients. Estimated hepatic blood flow above 1500 ml/min was seen in six patients and all had evidence of histological portal or sinusoidal infilatration. Patients with 'idiopathic' splenomegaly regardless of increased liver blood flow did not have a significant increase in intrasplenic pressure and no alteration in other haemodynamic parameters. It appears that increased liver blood flow alone in a normal liver can only minimally elevate intrasplenic pressure but can play a significant part in the pathogenesis of portal hypertension when liver structure is altered.

Chronic Disease↗