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Biomedical subjects

S Braude

Publications and source records attributed to S Braude.

At least 19 recordsLinked to original sources
PubMed2000

Persistent, progressive hypophosphataemia after voluntary hyperventilation.

Hyperventilation (HV) and respiratory alkalosis are associated with hypophosphataemia, although the extent and duration of HV required to produce changes in serum phosphate levels are not known. We sought to characterize the effects of HV, with or without dextrose loading, on serum phosphate levels and other biochemical parameters. HV was monitored by controlling the end-tidal partial pressure of carbon dioxide (PETCO(2)). The effect of dextrose was studied because infusion of a glucose load is known to promote a fall in serum phosphate via stimulation of glycolysis. Eight healthy volunteers were enrolled in four study protocols: (1) HV for 20 min to a PETCO(2) of 25-30 mmHg (mild); (2) HV for 20 min to a PETCO(2) of 15-20 mmHg (severe); (3) mild HV with intravenous dextrose loading, and (4) dextrose loading alone. Periodic measurements of serum phosphate, venous pH, serum 2,3-diphosphoglycerate (2,3-DPG) and other parameters were made. Serum phosphate fell during HV and continued to decline after cessation of HV. Dextrose loading alone caused a fall in serum phosphate that continued for at least 30 min after cessation of the infusion (P<0.0002). HV combined with dextrose resulted in a greater decline in serum phosphate than either variable alone (P=0.003). The maximal decline in serum phosphate occurred in severe HV, with a mean decrease of 0.38 mmol/l at 20 min after cessation of HV (P<0.0001). Serum phosphate was still significantly lowered compared with baseline at 90 min after cessation of HV (P=0.001). Other significant changes seen with HV included a decrease in serum glucose (P<0.01), a decrease in serum potassium (P<0.05) and an increase in venous pH (P<0.007). Serum 2, 3-DPG levels did not change significantly in any study protocol. Thus relatively mild acute HV produces significant changes in serum phosphate. In both mild and severe HV this effect is progressive after cessation of HV. This phenomenon has not been shown before, and may have significant clinical implications.

Adult↗
PubMed1999

Ruptured abdominal aortic aneurysm--outcome in a community teaching hospital intensive care unit.

Ruptured abdominal aortic aneurysm (RAAA) is a surgical emergency associated with a high mortality often requiring postoperative intensive care. Our objectives were to assess the outcome of RAAA management in a nontertiary community hospital intensive care unit (ICU) and to compare this with historical data from tertiary hospitals. We also sought to identify variables related to outcome and evaluate the potential of an organ failure score to identify patients at increased risk of death. The study was a retrospective chart review of patients with RAAA over 11 years (1986-1996 inclusive) at Manly District Hospital, a 210 bed community teaching hospital with eight intensive care beds. Forty patients were identified in the study period as having been admitted to ICU after RAAA surgery. There was an overall hospital mortality rate of 47.5% and intensive care mortality rate of 42.5% for successfully operated RAAA. Five variables were significantly different between survivors and non-survivors. These were age, total amount of blood products required, duration of operation, development of hypotension (systolic blood pressure < 90 mmHg) in ICU postoperatively, and APACHE II score at Day 1 ICU. A trend was also found between mortality rate and the number of failed systems after 48 hours intensive care stay. Mortality for a patient with zero failed systems was 38%, one failed system 42%, two 58% and three 67%. Based on these results, management of RAAA in a non-tertiary setting appears appropriate with postoperative care occurring in an ICU where there is adequate equipment and medical and nursing staff experienced in the care of complex critical illness.

Aged↗
PubMed1997

Acute respiratory distress syndrome in a community hospital ICU.

OBJECTIVE: To estimate the incidence of the acute respiratory distress syndrome (ARDS) in an Australian urban community, and to describe the pattern of disease and outcomes in a community hospital intensive care unit (ICU). SETTING: An eight-bed general ICU in a community hospital. DESIGN: Retrospective chart review. PATIENTS: 32 patients identified over a 4-year period as having ARDS. MEASUREMENTS AND RESULTS: The incidence of ARDS in an Australian urban community was estimated to be 7.3-9.3 cases/100,000 population per year. In-hospital mortality was 59%, while ICU mortality was 47%. Sepsis, pneumonia and aspiration were the main aetiological factors accounting for 94% of the patient population. There was no trauma. The Acute Physiology and Chronic Health Evaluation and Murray scores and values for the ratio of the partial pressure of oxygen in arterial blood and fractional inspired oxygen on admission to the ICU were similar between survivors and nonsurvivors, and none of these parameters were reliable predictors of outcome. Mean age, however, was different between survivors (56 +/- 16 years) and non-survivors (69 +/- 9 years) (p < or = 0.01). Mean daily fluid balance was also different between survivors (536 +/- 545 ml/day) and non-survivors (1576 +/- 1255 ml/day) (p < or = 0.02). Haemodynamic data were collected on 21 of the 32 patients within 72 h of the onset of ARDS. None of the haemodynamic parameters reached significance. There was, however, a trend for better cardiac function and oxygen consumption in the survivors. CONCLUSIONS: These data show that for ARDS, at least, mortality outcome can be comparable in a community ICU to a tertiary referral institution. The pattern of disease in an urban Australian community hospital is different to that often reported from tertiary centres. The incidence of ARDS in an Australian urban community is comparable to the reported incidence in North America and Western Europe.

Adult↗
PubMed1997

Tumour microembolism presenting as "primary pulmonary hypertension".

Pulmonary tumour microembolism is a rare cause of pulmonary hypertension. A case of rapidly progressive pulmonary hypertension in a patient with a past history of breast carcinoma is presented. Despite active consideration and investigation for malignancy as a cause, correct diagnosis was only made at necropsy.

Adenocarcinoma↗
PubMed1994

Pulmonary endothelial permeability in patients with severe lung injury. Clinical correlates and natural history.

STUDY OBJECTIVE: To establish the natural history of lung injury in adult respiratory distress syndrome (ARDS) in terms of increased pulmonary vascular permeability. Secondly, to relate such changes to the number of neutrophils in bronchoalveolar lavage (BAL) and a clinical score of the severity of lung injury. DESIGN: Prospective, open. SETTING: Adult intensive care unit of a tertiary (national) referral hospital. PATIENTS: Fourteen patients meeting accepted diagnostic criteria for ARDS. INTERVENTIONS: Mechanical ventilatory support. Conventional intensive care and support for other failed organ systems as appropriate. MEASUREMENTS AND RESULTS: Pulmonary vascular permeability was estimated using a dual isotope technique (protein accumulation index [PAI]), neutrophil numbers by BAL and the severity of ARDS by the lung injury score (LIS). The PAI and LIS were measured simultaneously on three occasions as far apart as possible during the course of the illness. A single BAL was performed immediately after one of the three PAI/LIS measurements, the precise timing being dictated by the clinical stability of each patient. Fourteen patients (8 male; age range, 19 to 69 years) were studied, 1.40 +/- 0.16, 11.36 +/- 1.79, and 20.90 +/- 2.30 days after the onset of ARDS (mean +/- SEM). Six patients died. The PAI (normal range, 0 to 1.0 x 10(-3)) was 2.81 +/- 0.39, 2.94 +/- 0.48, and 2.80 +/- 0.87; and LIS (severe injury > or = 2.5) was 2.18 +/- 0.25, 2.48 +/- 0.14, and 2.06 +/- 0.27, respectively. The BAL neutrophil content was 54.09 +/- 8.89. There were significant positive correlations between PAI and LIS (r = 0.73, p < 0.001) and PAI and BAL neutrophil content (r = 0.81, p < 0.001). CONCLUSIONS: These data suggest that increased pulmonary vascular permeability persists throughout the course of ARDS and is related to a clinical score of injury severity and BAL neutrophil content.

Adult↗
PubMed1992

Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass.

OBJECTIVE: To assess the possibility that changes in lung function following cardiopulmonary bypass are associated with increased pulmonary capillary permeability. DESIGN: A prospective, descriptive study. SETTING: Adult cardiothoracic ICU in a post-graduate teaching hospital. PATIENTS: Ten sequential patients undergoing cardiac surgery requiring cardiopulmonary bypass. MEASUREMENTS: Arterial blood gas tensions, helium dilution end-expiratory lung volume, and carbon monoxide transfer were measured by a rebreathing technique preoperatively and 2 hrs postoperatively. Lung extravascular protein accumulation index was measured by a double-isotope technique 2 hrs postoperatively and in a group of normal controls. RESULTS: Mean +/- SEM alveolar-arterial PO2 gradient increased from 77 +/- 14 torr (10.3 +/- 1.8 kPa) to 138 +/- 24 torr (18.5 +/- 3.2 kPa) (p less than .01). Functional residual capacity decreased by 20.2 +/- 5.6% (p less than .01). Carbon monoxide transfer decreased by 26.7 +/- 5.3% (p less than .01) for the lung as a whole and by 17.9 +/- 3.2% (p less than .01) per liter of accessible gas volume. Protein accumulation index ranged from 0.03 to 3.2 x 10(-3) (median 0.6) postoperatively (median for normal subjects 0.4; p less than .05), although only one patient had a value indicative of clinically important endothelial injury. CONCLUSIONS: Cardiac surgery involving cardiopulmonary bypass results in a deterioration in lung function characterized by a loss of lung volume, a reduction in carbon monoxide transfer, and an increase in the alveolar-arterial PO2 gradient. These changes do not appear to be mediated by an increase in pulmonary endothelial permeability.

Aged↗
PubMed1992

Refractory hypoxaemia after pneumonectomy: diagnosis by transoesophageal echocardiography.

A patient with normal oxygenation before operation became very breathless and hypoxaemic after a right pneumonectomy. Transoesophageal echocardiography showed right to left interatrial shunting due to a patent foramen ovale. Transoesophageal echocardiography should be included in the assessment of patients who became inappropriately dyspnoeic after pneumonectomy.

Cardiac Catheterization↗
PubMed1992

Serial assessment of pulmonary microvascular permeability in a patient developing the adult respiratory distress syndrome.

Serial measurements of lung extravascular accumulation of 113mIndium-transferrin were made in a patient with acute respiratory failure during the development of the adult respiratory distress syndrome (ARDS). Abnormality of this index of pulmonary microvascular permeability antedated radiological change and appeared to predict the onset of frank ARDS.

Capillary Permeability↗
PubMed1991

Lymphoedema/hypercalcaemia syndrome mediated by parathyroid-hormone-related protein.

A 24-year-old woman presented with a cryptogenic, hypercalcaemic syndrome with metastatic pulmonary calcification and leg and massive breast enlargement and bilateral chylous pleural effusions compatible with a generalised lymphatic abnormality. The patient's serum parathyroid hormone-related protein concentration was very high at a time when she was significantly hypercalcaemic, implying that the hypercalcaemia was mediated by this protein.

Adult↗
PubMed1987

Failure of aerosolised 99mTc DTPA clearance to predict outcome in patients with adult respiratory distress syndrome.

The rate of clearance of technetium-99m labelled diethylene triamine pentacetic acid (99mTc DTPA) was measured in 32 patients with adult respiratory distress syndrome to determine if a more rapid clearance rate, possibly reflecting a more severe abnormality of pulmonary function, was associated with a reduced likelihood of recovery from pulmonary failure. Although the mean rate of clearance from lung to blood (T1/2LB) of 99mTc DTPA was more rapid in the patients (T1/2LB = 29 (SEM 3.2) min than in 42 normal subjects (T1/2LB = 59 (1.8)min), there was no difference between the clearance rate in the 18 patients who recovered from respiratory failure (T1/2LB = 31 (5) min) and the 14 who died (T1/2LB = 27 (4) min). Additionally, not all patients studied had abnormally rapid clearance rates. In 12 of the 32 patients the T1/2 fell within the range for normal individuals; this was found more commonly in patients who were predisposed to develop adult respiratory distress syndrome by pancreatitis or massive blood transfusion. These data suggest that a single measurement of 99mTc DTPA clearance in patients with established respiratory failure and adult respiratory distress syndrome is of no value in assessing the likelihood of recovery from this condition.

Adolescent↗
PubMed1987

Epithelial and endothelial flux after bypass in dogs: effect of positive end-expiratory pressure.

Cardiopulmonary bypass (CPB) causes lung injury that occasionally progresses to the adult respiratory distress syndrome (ARDS). We measured the effect of 10 cmH2O of positive end-expiratory pressure (PEEP) on small solute and protein flux in dogs 1 wk before and 2 h after the completion of CPB. As an index of alveolar epithelial permeability, the clearance from lung to blood of inhaled technetium-99m-labeled diethylenetriaminepentaacetic acid (99mTc-DTPA) was measured. To assess microvascular endothelial integrity, the rate of accumulation in the lung interstitium of intravascular 113mIn-transferrin was measured. The clearance half time (t 1/2) for 99mTc-DTPA in the study dogs declined from 18.8 +/- 1.9 min (mean +/- SE) at base line to 9.4 +/- 2.0 min during PEEP (P less than 0.05). Two hours after CPB, the t 1/2 was 8.1 +/- 1.6 min at base line and unchanged during PEEP. The 113mIn-transferrin rate of accumulation was unchanged by PEEP before CPB. After CPB, the index was 3.25 +/- 0.95 slope/min X 10(-3) (P less than 0.05). Of the five dogs with a significant slope, four showed a decrease in microvascular flux during PEEP, although for the group the mean change in slope was not significant (P = 0.10). We conclude that the application of PEEP does not increase 99mTc-DTPA clearance in lungs already injured by CPB, and may actually decrease the apparent microvascular protein flux in some cases.

Animals↗
PubMed1987

A comparison of 99mTc-DTPA and 113mIn-DTPA aerosol clearances in humans. Effects of smoking, hyperinflation, and in vitro oxidation.

As an index of permeability of the alveolar epithelium, the clearance of an inhaled aerosol of 99mTc-DTPA is increased in several disease states. However, the usefulness of the test to assess the severity of disease is limited because healthy smokers also have abnormally rapid rates of clearance. Because the stability of the 99mTc-DTPA bond might be a contributory factor, we tested the affinity of 99mTc for DTPA in vitro, and in groups of healthy smokers (n = 13) and nonsmokers (n = 7) we measured the clearances of 99mTc-DTPA and 113mIn-DTPA, which have a similar molecular shape and charge. In vitro, sodium hypochlorite or hydrogen peroxide released as much as 98% of free 99mTc from the 99mTc-DTPA complex. When incubated with human neutrophils stimulated with phorbol myristate acetate, between 4 and 7% of free 99mTc-DTPA was released after 30 min, and 12% was released after 60 min. In vivo, the clearances of both 99mTc-DTPA and 113mIn-DTPA in the smokers (n = 13) were faster than in the nonsmokers (n = 7) (p less than 0.05). Within the smokers, the mean 99mTc-DTPA clearance (T1/2 25 +/- 4 min) was faster than the mean 113mIn-DTPA clearance (34 +/- 6 min), (p less than 0.05). For nonsmokers, the difference was smaller (T1/2 99mTc-DTPA, 56 +/- 6; T1/2 113mIn-DTPA, 62 +/- 6) and not significant. During hyperinflation, smokers (n = 8) and nonsmokers (n = 8) both demonstrated an increase in 113mIn-DTPA clearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Infused salbutamol accentuates acid-induced lung injury in the rat.

The effect in the rat of salbutamol infusion (1 microgram min-1 kg-1) on acid-induced lung injury has been determined. Severity of lung injury was assessed by two techniques: the pulmonary clearance of 99mTc-diethylenetriaminepenta-acetate (99mTc-DTPA) and the lung wet/dry weight ratio, giving indices of alveolar epithelial permeability and transendothelial water filtration respectively. Mean half-time of clearance of 99mTc-DTPA was increased significantly in rats who had intratracheal acid-induced injury and control (saline) intravenous infusion (19.4 +/- 2.6 min) compared with non-acid-treated rats (98.1 +/- 7.2) (P less than 0.0001). However, those animals who had intratracheal acid injury and subsequent salbutamol intravenous infusion had significantly faster clearance (11.5 +/- 1.9) than the acid and control infusion group (P less than 0.05). Gravimetric lung water in the acid-only rats (expressed as wet/dry weight ratio) was increased significantly (6.4 +/- 0.3) compared with the non-acid-treated controls (5.4 +/- 0.2) (P less than 0.01). Acid-treated rats who had salbutamol infused had dramatically increased lung water (10.0 +/- 0.6) (P less than 0.001 vs acid and control infusion). Intravenous salbutamol infusion itself produced no significant difference in the results for both techniques, compared with the non-acid-treated time-course controls. Infused salbutamol accentuates acid-induced lung injury in the rat. Possible factors responsible for these findings include beta 2-adrenergic agonist mediated inhibition of hypoxic pulmonary vasoconstriction (HPV) and a predominant beta 1-adrenergic agonist inotropic effect of salbutamol with resultant rise in pulmonary artery pressure.

Albuterol↗
PubMed1986

Comparison of lung vascular and epithelial permeability indices in the adult respiratory distress syndrome.

Measurements of pulmonary clearance of inhaled 99mTc-DTPA and transvascular 113mIntransferrin flux were made in 12 patients with established ARDS and 14 volunteer control subjects (7 smokers and 7 nonsmokers). Smokers had significantly increased 99mTc-DTPA clearance (clearance rate constant, 3.6 +/- 0.8; mean +/- SEM) compared with nonsmokers (1.2 +/- 0.1). All patients with ARDS had increased clearance of 99mTc-DTPA (5.2 +/- 0.9), but the finding was nonspecific in that increased clearance overlapped with the findings in normal smokers. Protein flux in smokers (protein flux units, 0.0 +/- 0.2) was similar to that in nonsmokers (0.3 +/- 0.2). In 9 of the 12 patients with ARDS, protein flux was increased, and as a group (3.2 +/- 1.0) they differed significantly (p less than 0.01) from the combined smoking and nonsmoking control subjects (0.2 +/- 0.1, n = 14). The parameters of DTPA clearance and transvascular protein flux correlated well in the patients with ARDS (Spearman's rank correlation = 0.71, p less than 0.01). Although 99mTc-DTPA clearance is a sensitive technique in ARDS, a single study in this context does not allow a diagnostic conclusion because of its non-specificity. Abnormal protein flux appears to be more specific for ARDS but was not a universal finding in the patients studied.

Adult↗