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Biomedical subjects

M J Kleinfeld

Publications and source records attributed to M J Kleinfeld.

9 recordsLinked to original sources
PubMed1980

Arsine poisoning.

A 31-year-old patient was admitted to the hospital because of dark red urine which on examination was found to be due to extracellular hemoglobin. The cause of the hemoglobinuria was exposure to arsine gas from a cylinder thought to be empty. The worker's exposure time was approximately one to two minutes. The degree of hemolytic anemia required only one unit of packed red cells. The patient was hydrated intravenously to avoid acute tubular necrosis. The arsenic content in the urine taken was 0.72 mg/L on the day of admission and dropped to 0.1 mg/L on the fourth day of hospitalization. The patient was discharged eight days after admission, when clinical and hematological status had improved sufficiently. Occupational history revealed that protective procedures employed in the handling of the cylinders containing the arsine gas were inadequate. It was found that the valve on one of the cylinders was half-opened and leaking and that the dust caps, which were attached to the outside of the valves of the cylinders, were present on some and not on others and, where present, had been hand-tightened and not wrench-tightened. Moreover, the cylinders although specified to be empty, were not, according to regulations requiring pressure to be less than 25 pounds gauge or 45 absolute.

Adult↗
PubMed1980

Bilateral renal artery occlusion in a patient with progressive systemic sclerosis.

A patient with renal failure due to progressive systemic sclerosis showed bilateral renal artery occlusion on renal angiography. The mechanism for the involvement of the main renal arteries is unknown, but it is postulated that the involvement of the main stem renal arteries was an extension of the pre-existing occlusive process in the interlobular arteries. This was hastened by the severe reduction in renal blood flow due to the hemorrhage and sepsis complicating the course. Another possible mechanism is a reduction of the fibrinolytic activity in the region of the intimal narrowing of the renal artery, coupled with reduction of the blood flow. The kidney biopsy showed intimal thickening and almost complete occlusion of interlobar arteries. Similar changes were observed in the smaller arteries. These findings are consistent with scleroderma of the kidney.

Adult↗
PubMed1978

Symptomatic improvement in a patient with sick sinus syndrome after the onset of stable atrial flutter.

A patient with sick sinus syndrome (SSS) presented with episodic lightheadedness and weakness. The electrocardiographic features were marked supraventricular bradyarrhythmias and paroxysmal atrial flutter. The symptoms lasted for four years and disappeared with the onset of stable atrial flutter which has persisted for the past seven years. Over the 11-year period of observation, there has been progressive involvement of the His-Purkinje system manifested by the development of left anterior fascicular block, right bundle-branch block, and prolongation of the HV conduction time. The patient has refused pacemaker implantation. In the absence of angina and in the presence of a normal heart size, the etiology of his SSS is postulated to be idiopathic fibrosis of his conduction system.

Atrial Flutter↗
PubMed1978

Junctional escape rhythm in the sick sinus syndrome.

In 21 patients with and 31 without junctional escape beats, a comparison of the symptoms, revealed that there were no significant differences (p greater than 0.05) in the symptoms between these two groups manifesting a sick sinus syndrome. Thus, the occurrence of junctional escape beats did not provide the anticipated shortening of the asystolic pauses to prevent the occurrence of symptoms related to the period of electrical silence. In 7 patients with an escape junctional rhythm, the long pause was interrupted by the occurrence of a regular junctional rhythm. The pause was not preceded by a supraventricular tachycardia, ruling out physiologic overdrive suppression of the junctional pacemaker. The period of asystole preceding the junctional rhythm was not multiple of the R-R interval of the junctional rhythm. 4 additional patients demonstrated long periods of asystole, uninterrupted by junctional escape beats and at other times exhibited shorter pauses which were terminated by junctional escape beats. These findings can be explained by the presence of a 'junctional arrest' which is analogous to sinoatrial arrest. The phenomenon of 'junctional arrest' may be one tenable explanation to account for the lack of protection by junctional escape activity against the symptoms associated with the sick sinus syndrome.

Aged↗
PubMed1977

Alternans of the ST segment in Prinzmetal's angina.

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.

Adult↗