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J H de Bruyn

Publications and source records attributed to J H de Bruyn.

14 recordsLinked to original sources

Patients presenting with fresh trauma after interpersonal violence. Part I. Alcohol and substance abuse.

BACKGROUND: Patients presenting with fresh trauma frequently have evidence of substance abuse. Nevertheless, few South African studies have measured the levels of both alcohol and other substances in patients presenting with fresh trauma after interpersonal violence. METHODS: A representative sample of patients presenting with fresh trauma to the Trauma Unit of Tygerberg Hospital was selected for study. Subjects were questioned about the nature of the trauma and breath alcohol concentrations were determined. Blood and urine samples for analysis of alcohol and other substances were obtained from approximately half the subjects. RESULTS: Alcohol was found to be present in a majority of patients who presented after interpersonal violence, while other substances were present less commonly. There was a high correlation between clinical history of alcohol use, breath analysis of alcohol and blood alcohol measurement. CONCLUSIONS: Alcohol use plays a significant role in trauma due to interpersonal violence. It is essential to screen victims of interpersonal violence for a history of alcohol and other substances. Breath analysis for alcohol is a useful adjunct to clinical screening.

Adult↗

Patients presenting with fresh trauma after interpersonal violence. Part II. Assault history.

BACKGROUND: Patients presenting with fresh trauma are frequently victims of interpersonal violence. Nevertheless, few South African studies have documented the history surrounding such assaults and their management. METHODS: Patients presenting with fresh trauma to the Trauma Unit of Tygerberg Hospital were selected in order to provide a representative sample. Where patients were victims of interpersonal violence, a history of the current and previous assault(s) was taken. RESULTS: Victims of interpersonal violence often reported that they had been involved in such violence on previous occasions. Nevertheless, these patients had rarely received management from psychosocial services. Patients with a previous history of having been assaulted had a number of distinct characteristics, including female gender and increased substance use. CONCLUSIONS: Trauma has justifiably been described as a recurrent disease. There is an urgent need for effective psychosocial services for victims of interpersonal violence; ideally, this would prevent future multiple hospital admissions.

Adult↗

Splint renal function after captopril in unilateral renal artery stenosis.

The renal extraction ratios of 131I-sodium iodohippurate (131I-Hippuran) and 125I-thalamate were greatly reduced on the affected side by 50 mg captopril in seven out of 14 patients with unilateral renal artery stenosis. With long term captopril 150 mg daily the uptake of 99mTc-diethylenetriaminepenta-acetic acid by the affected kidney, which was determined by scintillation camera renography, became almost zero in these seven patients, indicating severe reduction of the glomerular filtration rate. Function of the affected kidney returned on discontinuing treatment. The reduced extraction of sodium iodohippurate probably reflected a shortened plasma transit time through the kidney due to intrarenal vasodilatation. The reduced extraction of thalamate reflected a low filtration fraction, suggesting that the vasodilatation was, at least in part, at the level of the postglomerular arterioles. Captopril had little effect on the contralateral kidney and on the kidneys of 17 patients with essential hypertension, and serum creatinine concentrations showed minor changes. Radioisotope renography should be performed after beginning captopril treatment in patients with renal artery stenosis. This is also recommended for patients given captopril as a third line drug when renal artery stenosis has not been excluded. Hypertension is these patients is often severe and difficult to control. Renal artery disease is not rare in this difficult group and finding seriously impaired renal function on one side during captopril treatment may be diagnostic.

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Haemodynamic profile of captopril treatment in various forms of hypertension.

The effects of captopril 450 mg/day for 4 weeks on blood pressure, heart rate, cardiac output and extracellular fluid volume were compared in severe, often drug-resistant hypertension (n = 23), mild to moderate hypertension associated with renal artery stenosis (n = 10) and mild to moderate essential hypertension (n = 20). Plasma renin in the three groups was 52 +/- 19, 58 +/- 17 and 20 +/- 4 microU/ml (mean +/- SEM), respectively. Blood pressure fell by 18 +/- 4%, 21 +/- 2% and 18 +/- 1%. The pressure drop was mainly due to a fall in peripheral vascular resistance. Addition of the diuretic hydrochlorothiazide (25-100 mg/day) caused a further fall in resistance. Despite the vasodilator effect of captopril, reflex cardiostimulation and reactive fluid retention were not observed. In severe hypertension, captopril alone was more effective in lowering blood pressure than combined diuretic-betablocker-vasodilator therapy. Moreover, cardiac output in these patients was higher and resistance was lower after captopril than during combined treatment. Thus, captopril was capable of normalising the abnormal haemodynamic state in patients with essential hypertension, and in hypertension associated with renal artery stenosis. Despite marked differences in pre-treatment plasma renin, the effects of captopril on systemic haemodynamics were similar in all the patients.

Adult↗

Effects of an angiotensin-converting enzyme inhibitor (captopril) on blood pressure in anephric subjects.

Randomised, double-blind cross-over trials were performed in seven anephric patients to determine the effect of the orally active angiotensin-converting enzyme inhibitor captopril on blood pressure in fluid-depleted and fluid-replete patients. Patients were given captopril, 100 mg orally, or placebo one hour after haemodialysis, when they were fluid depleted. Their mean (+/- SEM) supine blood pressure fell from 127 +/- 12/71 +/- 6 mm Hg before captopril to 106 +/- 13/54 +/- 4 mm Hg 24 hours after the drug, while on placebo it rose from 123 +/- 11/73 +/- 5 mm Hg to 134 +/- 10/82 +/- 8 mm Hg. All patients developed orthostatic hypotension after captopril. In the fluid-replete state, two days after haemodialysis, captopril had no effect on blood pressure. The plasma concentration of active renin was extremely low and did not rise after fluid withdrawal or captopril. Thus the hypotensive effect of captopril did not appear to depend on circulating renin concentrations. The concept of "renin-dependent" hypertension, which is responsive to captopril, as opposed to "volume-dependent" hypertension, which is not responsive to captopril, may therefore be invalid.

Adult↗

Captopril affects blood pressure equally in renovascular and essential hypertension and in the fluid-depleted anephric state.

1. The haemodynamic effects of 100 mg of captopril in renovascular hypertension (n = 11), essential hypertension (n = 12) and the anephric state (n = 7) were compared. Brachial artery pressure was measured in all patients, and changes in right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure and cardiac output were followed in renovascular and essential hypertension. Nephrectomized patients were studied before and after fluid withdrawal by ultrafiltration. 2. The pretreatment concentration of active renin in plasma was 100 +/- 24 mu-units/ml (mean +/- SEM) in renovascular hypertension, and 24 +/- 4 mu-units/ml in essential hypertension. In nephrectomized patients pretreatment renin was 1.7 +/- 0.3 mu-units/ml, and renin was unresponsive to withdrawal of 1.8 +/- 0.21 of body fluid. 3. The effects of captopril were maximal after 60-90 min. Mean arterial pressure after 90 min was lowered by 19 +/- 4% in renovascular hypertension, by 17 +/- 4% in essential hypertension and by 16 +/- 3% in fluid-depleted nephrectomized patients. These changes were not significantly different despite the marked differences in renin. Captopril had no effect on arterial pressure in the fluid-replete anephric state. 4. The effects of captopril on cardiac filling pressures and cardiac output in renovascular and essential hypertension were also not different. 5. It is concluded that the antihypertensive action of captopril may be largely independent of circulating renin.

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