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Biomedical subjects

G Schulman

Publications and source records attributed to G Schulman.

68 records · Page 4Linked to original sources
PubMed1986

Pneumatosis intestinalis in cystic fibrosis.

We retrospectively reviewed the clinical and radiographic findings in patients with pneumatosis intestinalis (PI), who were identified among 441 patients with cystic fibrosis. Since 1944, the age at onset and the incidence of PI have increased. Pneumomediastinum, pneumothorax, or pulmonary interstitial emphysema was found in 95% of patients with PI compared with 62% of patients without PI. The type, distribution, and severity of PI often changed with time. PI is correlated with the development of obstructive pulmonary disease, which facilitates air dissection into interstitial spaces. Dissection of air is often clinically silent and tends to be self-perpetuating.

Adolescent↗
PubMed1985

Successful management of thrombocytopenia, microangiopathic anemia, and acute renal failure by plasmapheresis.

We report on the outcome of six consecutive adult patients who presented with microangiopathic anemia and thrombocytopenia. Clinical parameters on admission included platelet counts less than 45,000/mm3, microangiopathic red blood cell morphology, mental status abnormalities, and in three, rapidly progressive azotemia requiring dialysis. All patients underwent plasma exchange therapy as part of their treatments. Patients with renal failure underwent plasma exchange with a hollow fiber plasma separator, while those without renal failure were treated with a cytocentrifuge. All received fresh frozen plasma as replacement solution and were treated with glucocorticoids as well. For all six patients, plasmapheresis and conventional drug therapy resulted in remission that has lasted for 16 +/- 5 months (range 8 to 24 months). Early cessation of plasmapheresis in two patients resulted in rapid relapse. Patients who required dialysis now have a mean creatinine of 2.0 +/- 0.9 mg/dL (range 1.2 to 3.5). With similar volumes of exchange, and the same number of treatments, less fresh frozen plasma was used in the three patients treated with the hollow fiber separator than in patients treated with the cytocentrifuge (6.3 +/- 3.7 v 14.8 +/- 4.3 U/exchange, P less than 0.05). We conclude that plasmapheresis is a useful therapeutic modality for the treatment of thrombocytopenia and microangiopathic hemolytic anemia. In addition the use of a hollow fiber plasma separator for plasmapheresis is safe and efficient, particularly when concurrent dialysis is required.

Acute Kidney Injury↗
PubMed1985

Comparison of the response of the renal blood supply to acetylcholine and to a calcium channel blocking agent, diltiazem, in the dog.

Several vasodilators, including acetylcholine, are capable of inducing maximal renal vasodilatation when infused into the renal artery. Despite substantial interest in the renal vascular response to calcium channel blocking agents, there has been no systematic comparison of any of these agents to an index vasodilator, such as acetylcholine. We compared the renal vascular angiographic response to acetylcholine and diltiazem, infused into the renal artery in graded dosage, in 14 dogs. In eight of the dogs renal blood flow was measured with an electromagnetic flowmeter. At peak, the acetylcholine-induced increase in renal blood flow (155 +/- 25 to 309 +/- 55 ml/min) slightly exceeded that induced by diltiazem (143 +/- 13 to 257 +/- 58 ml/min). A close correlation was found between the maximal blood flow increase induced by acetylcholine and by diltiazem (R = .95). Dilatation of the intrarenal arterial tree evident on the renal arteriogram was substantially less striking with diltiazem than with acetylcholine in these eight dogs. To ascertain the possible contributing role of the surgery required for blood flow measurement, the two agents were assessed in six additional dogs without blood flow measurement. In these six dogs diltiazem and acetylcholine induced essentially identical degrees of renal arterial vasodilatation. It is concluded that diltiazem, the calcium channel blocking agent, produces near maximal renal vasodilatation at the arteriolar level and that responses of more proximal elements of the renal arterial tree, visible during renal arteriography, are sensitive to the conditions of the experiment.

Acetylcholine↗
PubMed1983

Reactions to intravenous contrast media. Part I: Severe and fatal cardiovascular reactions in a canine dehydration model.

Investigations into the nature of severe and fatal reactions to contrast media have been severely limited by their unpredictable occurrence in the clinical setting and the absence of suitable laboratory models. The authors report their experience with a canine dehydration model. Intravenous administration of 2 ml/kg of 76% sodium methylglucamine diatrizoate resulted in vomiting, shock, inappropriate slowing of the heart rate, and death. ECG findings indicated suppression of sinoatrial node automaticity, a decrease in the rate of atrioventricular conduction, and depression of myocardial contractility. These results suggest two possible mechanisms: (a) enhanced vagal tone as the result of stimulation of the vasomotor center of the medulla or (b) accentuation of direct contrast-induced myocardial toxicity.

Animals↗
PubMed1983

Reactions to intravenous contrast media. Part II: Acute renal response in euvolemic and dehydrated dogs.

Growing concern about acute renal failure as the result of contrast agents prompted an investigation into the renal effects of intravenous contrast materials in euvolemic and dehydrated dogs. Bolus injection of hypertonic agents induced marked reductions in filtration fraction and glomerular filtration rate in both groups of animals; however, these changes were transient, returning to near-base-line values within 30 minutes after injection. The most striking differences between euvolemic and dehydrated animals appeared to be related to prerenal factors such as hypovolemia and contrast-induced hypotension.

Animals↗
PubMed1983

Respiratory illness and hypophosphatemia.

We retrospectively reviewed the charts of 308 admissions to a pulmonary disease ward and 100 admissions to the general medical service over one year to find the prevalence, sequelae, and etiology of hypophosphatemia. The overall prevalence of low serum phosphate levels (less than 2.4 mg/dl) occurring at least once during hospitalization in chest patients was 17 percent, but was higher in patients with respiratory infections (28 percent). Moreover, the prevalence of hypophosphatemia on admission (before institution of intravenous fluid or drug therapy) was ten times higher in patients with respiratory infections than in patients with noninfectious respiratory illness or general medical patients (21 vs 2 percent, p less than 0.001). Serum phosphate less than 2.0 mg/dl occurred in 4 percent of patients. Twenty-seven percent of the patients (including two with ventilatory failure) with abnormally low serum phosphate levels had symptoms or signs of uncertain etiology later explicable by the presence of hypophosphatemia. The most common additional laboratory finding associated with hypophosphatemia was elevation of muscle enzymes. Although mortality was no higher in hypophosphatemic patients, hospital stay was twice as long as that of patients with normal levels of serum phosphate. No correlation was found between simultaneous arterial blood gases and serum phosphate levels. Two patients given antacids had severe hypophosphatemia and worsened ventilatory function; phosphate-binding antacids should be used judiciously in patients with severe respiratory disease, since they may lead to the development or worsening of hypophosphatemia and diminished ventilatory function.

Female↗
PubMed1982

Contrast medium-induced renal vasoconstriction and endogenous vasoconstrictor hormones.

Hypertonic solutions, such as contrast media (meglumine/sodium diatrizoate-76%; Renografin-76), induce vasoconstriction in the renal vascular bed via an unknown mechanism. We assessed a possible role of two vasoconstrictor hormones known to be released by the kidney, angiotensin II (AII) and the prostaglandin, thromboxane. Specific inhibition of AII at the smooth muscle receptor level by saralasin (0.33-0.75 microgram/kg/min, IA) did not attenuate the response. Inhibition of prostaglandin formation by indomethacin (4 mg/kg, IV), likewise, did not prevent the decrease in renal perfusion. We conclude that neither AII nor the prostaglandin system mediate the contrast medium-induced renal vasoconstriction.

Animals↗
PubMed1981

Loss of the glomerular contractile response to angiotensin in rats following myohemoglobinuric acute renal failure.

To examine the state of the glomerulus in rats protected from acute renal failure (ARF) by prior insult, we measured the contractile responses of isolated glomeruli to angiotensin II (AII) and dibutyryl cyclic AMP (DBcAMP). In healthy rats, both agents induced a dose-related fall in glomerular diameter (P less than 0.001). Saralasin, the angiotensin antagonist, blocked the glomerular response to AII totally and to DBcAMP partially. Two weeks following ARF induced with 50% glycerol (10 ml/kg, im), azotemia had reversed and the nephrotoxic effect of mercuric chloride (4.7 mg/kg, sc) was blunted, as anticipated. AII did not reduce glomerular size, but the response to DBcAMP was sustained at this time. To determine the specificity of the loss of the glomerular response to AII, we also assessed the effects of an AII infusion (1 microgram/kg/min) on blood pressure and renal blood flow. There was a substantial rise in blood pressure (control, 104 +/- 11.8 mm Hg; AI, 131.0 +/- 5.3 mm HG; P less than 0.001) and fall in renal blood flow (control, 2.45 ml/g per min; AII, 0.81 +/- 0.10 ml/g per min; P less than 0.025). Vascular responsiveness to AII was preserved at a time when glomeruli were totally unresponsive and rats were resistant to ARF. The loss of glomerular contractility may, in part, account for the protection from ARF seen in this model: if so, glomerular abnormalities may play a pathogenetic role.

Acute Kidney Injury↗
PubMed1978

Waldenström's macroglobulinaemia in South African Negroes.

Waldenström's or primary macroglobulinaemia has rarely been documented in Black Africans. Six South African Negro patients with Waldenströms macroglobulinaemia were assessed and followed during a 10-year period from 1966 to 1976. The hyperviscosity syndrome was the presenting feature in four patients and one patient each presented with the nephrotic syndrome and a lacrimal mass respectively. On initial evaluation of the six patients, the serum IgM varied from 1.3 to 4.8 g% and in two patients cryoglobulinaemia was found. The patients received supportive treatment, chemotherapy, and when necessary, plasmaphoresis. One patient was lost to follow-up, one patient died 7 years after the onset of his illness, but the remaining four patients are alive 18 months to 5 years after presenting with their disease. Although the disease occurred in a younger age group (mean age 43 years) than in Caucasians it did not differ in clinical features or response to treatment from other parts of the world.

Adult↗
PubMedDate not supplied

Indications for vancomycin in dialysis patients.

Resistance to vancomycin has emerged among Staphylococcus aureus, coagulase-negative staphylococci (CNS), and enterococci, and this emergence has particular prevalence in dialysis units. It has therefore become imperative that physicians use vancomycin judiciously. General recommendations regarding the appropriate use of vancomycin have been developed. Although in theory implementation of these guidelines should not be difficult, the medical community may be unable or unwilling to make the necessary adjustments in practice. The onslaught of cost constraints and bureaucratic encumbrance has occurred simultaneously with the increase in vancomycin resistance among pathogens commonly isolated among the dialysis population. When a patient responds to empiric antibiotic therapy and susceptibility data indicate that an antibiotic other than vancomycin would be appropriate, the clinician far too often does not make the change to this alternative. Previously there was no biological imperative to change the antibiotic. That complacency has infected an entire generation of physicians, and especially nephrologists. Furthermore, there is an active movement against change, driven by concerns such as malpractice accusations and frank errors in the interpretation of medical facts.

Anti-Bacterial Agents↗
PubMedDate not supplied

Mechanism of the renal response to contrast medium in dogs. Decrease in renal function due to hypertonicity.

Radiographic contrast media (CM) (meglumine/sodium diatrizoate-76%; 1650 mOsm/kg) and other hypertonic solutions induce renal vasoconstriction by an unknown mechanism. In anesthetized dogs, renal blood flow (RBF) was measured with an electromagnetic flowmeter and filtration fraction (FF) and glomerular filtration rate (GFR) by the renal extraction of technetium-99m tin chelate. Ureteral pressure (UP) and wedged renal venous pressure (VP) were measured as indices of intrarenal pressure. Measurements of renal length (L), along with pressures, made it possible to examine the compliance of the system. A 4-cc intrarenal bolus of CM caused a 59% reduction in GFR (control: 0.63 +/- 0.04 to 0.26 +/- 0.04 ml/min X g, mean +/- SEM), in association with a 23% reduction in RBF (control: 3.10 +/- 0.11 to 2.39 +/- 0.26 ml/min X g) and a 44% decrease in FF (control: 0.32 +/- 0.01 to 0.18 +/- 0.03). These responses were compared with a 3-microgram intrarenal bolus of norepinephrine (NOREPI) which resulted in a 79.0 +/- 7.5% reduction in RBF, 68.3 +/- 7.3% reduction in GFR and 42.6 +/- 15.6% increase in FF. The NOREPI-induced vasoconstriction caused transient decreases in renal L, UP, and VP, whereas the CM-induced decrease in renal blood flow was associated with increases in these parameters. In studies employing ureteral occlusion to elevate intrarenal pressure, the magnitude (area, cm2) of the CM-induced decrease in renal perfusion was accentuated with increased UP (r = 0.79, n = 24, P less than 0.001). The CM-induced increase in renal L, UP, and VP must reflect osmotic forces and an increase in intrarenal pressure. The decreases in FF and GFR probably reflect Starling forces in the glomerular capillaries, with osmotic transients dominating. The results suggest a mechanical mechanism for the CM-induced decrease in RBF.

Acetylcholine↗