Rhabdomyolysis, Acute Renal Failure, and Disseminated Intravascular Coagulation in a Man With Sickle Cell Trait

Rf, Hynd; Bharadwaja, K; Ja, Mitas; Jt, Lord

doi:10.1097/00007611-198507000-00033

Cited by 17 publications

(8 citation statements)

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“…Such endothe lial damage is capable of triggering DIC with gen eralized systemic complications, including acute renal failure and a fatal outcome. [559][560][561]563 Hyper pyrexia, per se, is not a specific requirement for development of this syndrome. 560 Patients with sickle cell disease may also have multiple vaso-occlusive complications, including bone and joint injury (dactylitis, long bone and marrow infarction), splenic dysfunction, papillary necrosis, pulmonary emboli with infarctions and cor pulmonale, cerebrovascular events, including subarachnoid hemorrhage, stroke, spinal cord com promise, as well as peripheral deep vein thrombosis, portal vein thrombosis, and intestinal infarction.…”

Section: Sickle Cell Diseasementioning

confidence: 97%

“…[559][560][561]563 Hyper pyrexia, per se, is not a specific requirement for development of this syndrome. 560 Patients with sickle cell disease may also have multiple vaso-occlusive complications, including bone and joint injury (dactylitis, long bone and marrow infarction), splenic dysfunction, papillary necrosis, pulmonary emboli with infarctions and cor pulmonale, cerebrovascular events, including subarachnoid hemorrhage, stroke, spinal cord com promise, as well as peripheral deep vein thrombosis, portal vein thrombosis, and intestinal infarction. 562 DIC (which develops as an acute superimposed phenomenon) is to be considered in the patient who presents with signs such as upper gastrointestinal hemorrhage, hematuria, oozing from venipuncture sites, and respiratory failure and with laboratory ab normalities of low fibrinogen, positive protamine sulfate, high FDPs levels, prolongation of clotting times, and thrombocytopenia.…”

Section: Sickle Cell Diseasementioning

confidence: 97%

“…Persons who are vigorously active have been noted to develop an acute illness after severe physical stress characterized by exertional rhabdomyolysis, renal failure, and DIC. [559][560][561][562][563] With exer cise, hypoxia, acidosis, and hemoconcentration may predispose to sickling in patients with sickle cell trait. 560,564,565 Sickling may occlude the microvasculature, resulting in endothelial injury.…”

Section: Sickle Cell Diseasementioning

confidence: 99%

“…[559][560][561][562][563] With exer cise, hypoxia, acidosis, and hemoconcentration may predispose to sickling in patients with sickle cell trait. 560,564,565 Sickling may occlude the microvasculature, resulting in endothelial injury. Such endothe lial damage is capable of triggering DIC with gen eralized systemic complications, including acute renal failure and a fatal outcome.…”

Section: Sickle Cell Diseasementioning

confidence: 99%

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Clinical Aspects of Disseminated Intravascular Coagulation: A Clinician's Point of View

Baker¹

1989

Semin Thromb Hemost

151

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DIC is a disorder of coagulation that is demonstrated to occur in many settings. In view of the fulminant nature of the disorder once it is fully activated, the potential for considerable morbidity and mortality, and the difficulty in treating this syndrome, the necessity for a thorough understanding of the disorder is clear. A high index of suspicion is absolutely essential; however, this requires a thorough knowledge of the medical and surgical disorders in which DIC is likely to occur. The presenting manifestations of DIC, the time course of development of the fulminant syndrome, and the specific complications of the disorder may be intrinsically related to the specific clinical characteristics of the underlying disease. Clinical evaluation of the patient must be comprehensive and consider not only the laboratory and clinical manifestations of DIC but the triggering illness. Without the ability to treat the underlying primary illness, controlling or abating the DIC may be difficult or impossible. This comprehensive review of the disease entities in which DIC is likely to occur and the associated clinical manifestations will, it is hoped, guide a more precise definition of the overall clinical picture that confronts the clinician when evaluating a patient with possible DIC.

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Section: Sickle Cell Diseasementioning

confidence: 97%

Section: Sickle Cell Diseasementioning

confidence: 97%

Section: Sickle Cell Diseasementioning

confidence: 99%

Section: Sickle Cell Diseasementioning

confidence: 99%

See 2 more Smart Citations

Clinical Aspects of Disseminated Intravascular Coagulation: A Clinician's Point of View

Baker¹

1989

Semin Thromb Hemost

151

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“…Most of these cases have been associated with high ex treme exertion and exposure at high altitudes [1, 2,4 ,6,7]. Nonfatal complications include intravascular coagulation [4,8,9], splenic infarction [10][11][12], rhabdomyolysis and myoglobinuria which may lead to renal failure [4,[8][9][10][11], Values are mean ± SD (n = 11 for AA and n = 11 for SCT). See text for discussion of sta tistical tests.…”

Section: Introductionmentioning

confidence: 99%

Effects of Physical Stress on Complete Blood Count and Venous Blood Gas Profile of Individuals with Sickle Cell Trait

Hardy¹,

Mukherjee

Hinds³

et al. 1992

Acta Haematol

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The association between sickle cell trait (SCT) and adverse effects of exercise has been controversial. While individuals with SCT are at higher risk of sudden death, the mechanism for this outcome remains to be elucidated. In order to shed light on this controversy, we have monitored venous blood count and blood gas parameter values in normal and SCT subjects during treadmill exercise. White and red blood cell counts and hemoglobin changed significantly over time in both the SCT and normal groups, with peak exercise values different from pre-exercise or post-exercise values. Red blood cell counts showed significant group-time interaction; increase in count during exercise was accentuated in SCT subjects. All blood gas parameters showed significant changes over time in both groups. O₂ content was significantly higher in SCT than AA at all time intervals. O₂ saturation, pO₂ and CO binding to hemoglobin showed significant group-time interaction. Furthermore, O₂ saturation for the combined groups was significantly greater at peak exercise and at rest than before exercise. It is possible that treadmill exercise causes microvascular shunting in SCT subjects, leading to a decrease in the peripheral utilization of oxygen.

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The Morbid Anatomy of Sickle Cell Disease and Sickle Cell Trait

Lucas¹

2004

Practical Management of Haemoglobinopathies

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Rhabdomyolysis, Acute Renal Failure, and Disseminated Intravascular Coagulation in a Man With Sickle Cell Trait

Cited by 17 publications

References 0 publications

Clinical Aspects of Disseminated Intravascular Coagulation: A Clinician's Point of View

Clinical Aspects of Disseminated Intravascular Coagulation: A Clinician's Point of View

Effects of Physical Stress on Complete Blood Count and Venous Blood Gas Profile of Individuals with Sickle Cell Trait

The Morbid Anatomy of Sickle Cell Disease and Sickle Cell Trait

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