Continuous arteriovenous ultrafiltration versus continuous arteriovenous hemofiltration.
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Biomedical subjects
Publications and source records attributed to T S Ing.
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In a retrospective study of total hip replacement (THR) arthroplasty in patients with renal transplants, femoral head avascular necrosis (AVN) was found in 19 of 138 (15%) patients. Nine THRs in eight of these 19 patients (average age, 47 years) were studied. Preoperatively, all patients had hip pain due to AVN and a history of long-term treatment with systemic corticosteroids. Six of the eight patients had been treated with parenteral pulsed steroids on three occasions, and the other two patients on one occasion, for rejection episodes. All patients showed some degree of femoral head collapse roentgenographically. There were no major surgical complications. All patients had markedly improved functional capacities and relief of pain. With follow-up averaging three years, there has been no evidence of component loosening.
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Seventeen moderately hypertensive patients, whose blood pressure was previously controlled with hydrochlorothiazide and oral clonidine (blood pressure 129 +/- 8/85 +/- 5 mmHg during therapy), were treated with a transdermal system involving application of one or more clonidine-containing patches (3 mg per patch) to the skin once a week. The patients continued to take 50 mg of oral hydrochlorothiazide daily. By four to eight weeks, 15 of 17 patients using the transdermal system had achieved baseline blood pressure levels (130 +/- 10/84 +/- 6 mmHg, NS). During the maintenance phase of transdermal therapy, plasma clonidine levels measured four hours (0.78 +/- 0.43 ng/ml), four days (0.89 +/- 0.48 ng/ml), and seven days (0.78 +/- 0.41 ng/ml) after patch application did not differ significantly from one another or from trough plasma clonidine levels (0.86 +/- 0.54 ng/ml) measured during oral clonidine therapy. The results suggest that, in moderately hypertensive patients, blood pressure can be controlled with a once-weekly application of clonidine-containing skin patches as effectively as with oral clonidine.
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Five severe reactions occurred in four maintenance hemodialysis patients 1 to 5 minutes after initiating dialysis with Cuprophan capillary dialyzers. All reactions were life-threatening and one resulted in death. Inadequate rinsing of the dialyzers was probably the cause of the reactions. The severe reactions were managed by immediate discontinuation of dialysis and the institution of supportive treatment. Antianaphylactic measures were also attempted, but their therapeutic effectiveness remains to be determined.
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To study the disposition of amantadine hydrochloride in patients with impaired renal function, 100 mg was administered orally to 13 patients with creatinine clearances ranging from 48 to 10 ml/min/1.73 m2 body surface area. Six adults with normal renal function served as controls. Plasma half-life averaged 68.5 +/- 9.5 SEM hours in the renal patients (range: 27 to 144), versus 12.6 +/- 1.7 hours in controls. Plasma half-life correlated significantly with serum creatinine (r = 0.8476, P less than 0.001) and serum urea nitrogen levels (r = 0.8791, P less than o.001). Similarly, plasma elimination constant correlated with creatinine clearance/1.73 m2 body surface area (r = 09201, P less than 0.001). Renal amantadine clearance also correlated with creatinine clearance/1.73 m2 body surface area (r = 0.8217, P less than 0.001). However, renal amantadine clearance regularly exceeded creatinine clearance, suggesting that tubular secretion plays a role in the elimination of this drug. Amantadine excretion is decreased in patients with impaired renal function. The amount by which dosage must be reduced can be estimated based on creatinine clearance.
In 12 diabetic patients who were being treated with maintenance hemodialysis or maintenance peritoneal dialysis, coma and other neurologic deficits did not occur in spite of extremely elevated serum glucose levels. The mean serum values of these patients were: glucose 1,174 +/- 248 (SD) mg/100 ml, sodium 125 +/- 5 mEq/l, calculated total osmolality 342 +/- 13 mOsm/kg water and calculated effective osmolality (without urea) 316 +/- 13 mOsm/kg water. It is suggested that the absence of osmotic diuresis and the lack of substantial osmotic ultrafiltration prevented the development of hypernatremia and marked hyperosmolality. The osmolar effect of glucose alone at these serum concentrations apparently was not sufficient to induce neurologic impairment.