Severe intravascular hemolysis following surgical repair of endocardial cushion defects

Sigler, Arnold T.; Forman, Edwin N.; Zinkham, William H.; Neill, Catherine A.

doi:10.1016/0002-9343(63)90146-3

Cited by 89 publications

(12 citation statements)

References 26 publications

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“…This is in contrast to other chronic hemolytic anemias which have abnormally increased hepatic and splenic iron deposition, due to reticuloendothelial (i.e., extravascular) red cell destruction [23,25]. It is therefore unlikely that the decreased hepatic signal in three patients was caused by iron deposition resulting from the intravascular hemolysis in PNH.…”

Section: Discussionmentioning

confidence: 74%

“…disease, autoimmune hemolytic anemia, or hereditary spherocytosis, are characterized by extravascular hemolysis (i.e., reticuloendothelial degradation of damaged or defective red cells) resulting in iron deposition in the liver and spleen [22,23]. In contrast, intravascular hemolysis which occurs in either PNH or in mechanical hemolysis due to prosthetic cardiac valves, results in direct hemoglobin release into the plasma [24,25]. At very low rates of intravascular hemolysis, the hemoglobin attaches to the plasma protein haptoglobin and is removed by the hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

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MR of the kidneys, liver, and spleen in paroxysmal nocturnal hemoglobinuria

Roubidoux

1994

Abdom Imaging

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The magnetic resonance (MR) findings in the liver, kidneys, and spleen in eight patients with paroxysmal nocturnal hemoglobinuria (PNH) were retrospectively reviewed to determine whether characteristic features could be demonstrated. Eight patients underwent abdominal MR examinations by gradient echo sequences (seven patients), spin-echo sequences (seven patients), and inversion recovery (one patient). Signal intensities of the kidneys, liver, and spleen were visually evaluated. Autopsy and liver biopsy correlation were available in one case each. Renal signal intensity was decreased in all eight patients by either gradient-echo or T2-weighted sequences and in the single inversion recovery sequence. Hepatic signal intensity was decreased in three of eight patients on spin- and gradient-echo images. Splenic signal intensity was decreased in three of eight patients on spin- and gradient-echo images, and in two of these was manifest as focal low signal spots (Gamna-Gandy bodies). While the signal intensity in the renal cortex is typically decreased in patients with PNH, signal intensities in the liver and spleen are variable. Low signal intensity in the kidneys is due to hemosiderin deposition resulting from intravascular hemolysis, whereas low signal intensity in the liver or spleen may be due to either transfusion siderosis, or as a consequence of hepatic or portal venous thrombosis.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

MR of the kidneys, liver, and spleen in paroxysmal nocturnal hemoglobinuria

Roubidoux

1994

Abdom Imaging

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“…This finding is not specific for PNW, however, and may be expected in any other condition in which there is chronic or recurrent intravascular haemolysis. Roberts & Morrow (1966, 1969 found renal haemosiderosis at post-mortem in patients with prosthetic heart valves, and it has been reported after other cardiac operations (Sigler, Forman, Zinkham & Neill, 1963;Liddy & Roberts, 1970) and in . z $ g. unoperated calcific aortic valve disease (Roberts, 1966).…”

Section: Discussionmentioning

confidence: 90%

Renal Function in Chronic Intravascular Haemolysis Associated with Prosthetic Cardiac Valves

1973

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1. Glomerular filtration, wate rconcentration and acid load tests, measurement of urinary protein and cell excretion rates, bacteriological examination of the urine, and analysis of the urinary amino acid content were carried out in eight patients with chronic intravascular haemolysis due to aortic valve replacement.2. All results were normal except for a slight reduction in creatinine clearance rate in two patients and a slight elevation of urinary protein in a third; these abnormalities were considered of doubtful significance.3. It is concluded that chronic intravascular haemolysis with its consequent renal haemosiderosis appears not to interfere with renal function.

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“…T/2 = red cell half-life, i.e., time required for At/A, to reach 0. 5 There was no correlation demonstrated between the red blood cell survival and the severity of the valvular disease as determined by the magnitude of the transvalvular aortic systolic pressure gradient, the calculated valve area, the cardiac output, the stroke volume, or the presence or absence Five patients were studied preoperatively; and then restudied after insertion of valve prostheses. In four the aortic valve was replaced; in the fifth both the aortic and mitral valves were replaced.…”

mentioning

confidence: 99%

Red Blood Cell Survival in Patients with Aortic Valvular Disease and Ball-Valve Prostheses

et al. 1965

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Red blood cell survival was determined in patients with aortic valvular disease, postoperative patients with aortic valvular ball-valve prostheses and postoperative patients with multiple ball-valve prostheses. The red blood cell survival was reduced in the majority of patients in each group when compared with the red blood cell survival from a normal control group. A detailed analysis of the survival curves suggested that in many patients there was more than one population of red blood cells. The first population displayed rapid random destruction. This population was not present in normal persons in the control group. The second population showed the usual decline in radioactivity due to random destruction and loss of the red cell label due to elution. The shortened red blood cell survival in some patients was due to a large percentage of the first population of randomly destroyed red blood cells, in other patients to an accelerated rate of destruction of the usual single population of cells while others had a combination of the two mechanisms. A mechanism of mechanical hemolysis due to increased intracardiac turbulence was suggested as a cause for the shortened survival. When the turbulence was increased by a leak around the aortic or mitral valve prosthesis the red blood cell survival was found to be further decreased. In some cases this reduction in survival was enough to produce hemolytic anemia. The Coombs antiglobulin test was positive in three patients. The suggestion was made that the development of autoantibodies to red blood cells was secondary to increased destruction of red blood cells.

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Severe intravascular hemolysis following surgical repair of endocardial cushion defects

Cited by 89 publications

References 26 publications

MR of the kidneys, liver, and spleen in paroxysmal nocturnal hemoglobinuria

MR of the kidneys, liver, and spleen in paroxysmal nocturnal hemoglobinuria

Renal Function in Chronic Intravascular Haemolysis Associated with Prosthetic Cardiac Valves

Red Blood Cell Survival in Patients with Aortic Valvular Disease and Ball-Valve Prostheses

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