Study of retinal changes in leukaemia.
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Biomedical subjects
Publications and source records attributed to V K Saini.
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The records of ninety-two patients treated between 1965 and 1976 at the Boston City Hospital for penetrating wounds of the heart were reviewed and the results were compared with a previous series of twenty-five patients admitted to the same institution between 1956 and 1964. The annual incidence rose from 2.8 cases during the first period to 8.0 during the more recent years. Gunshot wounds increased in frequency in the second period. The overall mortality was similar in the two series. However, there were more complex wounds and agonal patients subjected to immediate emergency room thoracotomy during the second phase of this experience. The salvage rate in the latter group of patients gradually improved and averaged 24% between 1965 and 1976. These data indicate that an aggressive approach, including the use of immediate thoracotomy, to the agonal patient with a heart wound will be rewarded with salvage of some patients.
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Two series of patients were studied by serial measurements of blood gas exchange and pulmonarmonary dysfunction and to evaluate the dangers of respiratory failure in post traumatic patients. There were 27 patients who had sustained profound hemorrhagic shock and massive blood replacement averaging 9.7 liters and 38 patients who suffered general peritonitis or other forms of fulminating nonthoracic sepsis. All were supported by endotrachael intubation and volume controlled ventilators. The overall mortality for the post shock patients without sepsis was 12% while in the septic patients it was 35%. The maximal pulmonary arteriovenous shunt encountered in the post hemorrhagic shock patients at 36 hours averaged 20 plus or minus 8% and was accompanied by high cardiac indices (average 5.1 plus or minus 1.3 L/M-2/min) but no significant rise of pulmonary arterial pressure or peak inspiratory pressure (PIP). Severe pulmonary dysfunction subsequently occurred only in those patients who later became septic. The studies on the septic patients were divided according to the magnitude of the cardiac indices (the high indices averaged 4.8 plus or minus 1.6L/M-2/min) and thelow indices averaged 1.9 plus or minus 1.0 L/M-2/min. In the former, the average maximal shunt of 30 plus or minus 6% was sustained for 4 or more days, accompanied by an elevation of PIP to 36 plus or minus 6 cm H2O and by Pa pressure of 28 plus or minus 5 mm Hg. The patients in low output septic shock usually had an associated bronchopneumonia and had an average venous admixture of 34 plus or minus 8% and PIP values of 41 plus or minus 8 cm H2O. The mean Pa pressure in this group was 29 plus or minus 6 mm Hg.
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.
This experimental study was designed to evaluate the effect of intraaortic balloon pumping (IABP) upon nutrient myocardial blood flow (NMBF) following acute myocardial ischemia in dogs, but also to determine whether IABP improves NMBF following revascularization. Localized myocardial ischemia was produced by ligation of one or two small branches of the circumflex coronary artery combined with a three hour snare occlusion of the left anterior descending coronary artery distal to the first septal branch. NMBF was measured by NaI131 washout at three points corresponding to the peripheral, intermediate, and central zones of the infarct. Occlusion of the coronary arteries reduced NMBF. Release of occlusion after three hours, or the equivalent of coronary artery revascularization, increased NMBF but did not restore it to control levels. The increase in flow was more marked in the peripheral zones of ischemia. IABP increased NMBF significantly both during and after release of occlusion. The effect was sustained after cessation of IABP only when the latter was maintained during the period of reperfusion. The results indicate that NMBF, defined by washout of a locally injected tracer, was improved by both IABP and reperfusion. The beneficial effect was maximal when the two techniques were combined.
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Lymph dynamics in idiopathic portal hypertension has been studied in two phases. In the first phase thoracic duct lymph transport was studied in 11 patients with idiopathic portal hypertension by cannulating the duct. This revealed altered lymph transport in the form of a distended thoracic duct, raised pressure in the duct, and haemorrhagic lymph with an increased flow rate. The lymph flow rate was analysed in relation to various hepatic haemodynamic and biochemical parameters. In the second phase of the study hepatic lymphatics were studied by percutaneous hepatography in 16 patients with idiopathic portal hypertension. By this technique hepatic lymphatics were opacified in patients with idiopathic portal hypertension and cirrhosis with equal frequency. The significance of this finding in relation to the altered hepatic haemodynamics and thoracic duct lymph transport is discussed.
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The thoracic duct was cannulated in six patients who were actively bleeding from varices and had not responded to conservative treatment but draining lymph from the thoracic duct did not control bleeding in five patients. There was no drop in intrasplenic pulp pressure following this procedure when recorded in three of these patients. Bleeding stopped in one patient after lymph had been drained for nine and a half hours, and there was only a modest change in intrasplenic pressure. The therapeutic use of this technique to control oesophageal varices could not be substantiated.