Vascular spasm and gangrene during heparin–dihydro-ergotamine prophylaxis

Cunningham, Mark T.; Torrenté, Antoine de; Ekoé, Jean‐Marie; Ackermann, Johannes; Humair, L

doi:10.1002/bjs.1800711106

Cited by 25 publications

(6 citation statements)

References 3 publications

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“…In previous studies in patients with increased ICP after severe traumatic brain lesions, physiological variables have not indicated that DHE therapy causes cerebral ischemia (3). However, being a rather non-specific drug acting on various 5-HT, dopamine> aland a2adrenergic receptors (31, 36) DHE also constricts peripheral arteries and may cause ischemia in the distal parts of the extremities (10). A more specifically acting cerebral vasoconstrictor might consequently be preferred for the treatment of increased ICP.…”

Section: Discussionmentioning

confidence: 99%

Effects of dihydroergotamine and sumatriptan on isolated human cerebral and peripheral arteries and veins

Nilsson¹,

Nilsson²,

Edvinsson³

et al. 1997

Acta Anaesthesiol Scand

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Both DHE and sumatriptan cause contraction of isolated human cortical arteries and veins at very low concentrations. The differences observed between the two drugs may be explained by the fact that DHE is an alpha-adrenergic as well as a 5-HT agonist while sumatriptan acts specifically on 5-HT receptors. The study supports the hypothesis underlying the use of DHE for the treatment of increased ICP in patients with severe traumatic brain lesions.

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Section: Discussionmentioning

confidence: 99%

Effects of dihydroergotamine and sumatriptan on isolated human cerebral and peripheral arteries and veins

Nilsson¹,

Nilsson²,

Edvinsson³

et al. 1997

Acta Anaesthesiol Scand

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“…She subsequently required a below-knee amputation. Thirteen similar patients have been described in the literature [61 ], 9 of whom have had multiple trauma or serious conditions predisposing to hemodynamic instability. It therefore seems prudent to avoid the use of this drug for DVT prophylaxis in trauma patients.…”

Section: Patbopbysiologymentioning

confidence: 93%

Deep Venous Thrombosis and Pulmonary Embolism in Trauma Patients

Shackford

Moser

1988

J Intensive Care Med

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Trauma patients are at exceedingly high risk for the development of deep venous thrombosis and pulmonary embolism. The incidence, pathophysiology, diagnosis, prophylaxis, and therapy of deep venous thrombosis and pulmonary embolism in the trauma patient are reviewed. The type of injury, systemic pertubations, and enforced immobility are important factors in pathogenesis. Patients with lower extremity injuries and spine fractures with paraplegia appear to be at highest risk. Orthopedic devices used to treat these injuries often preclude the conventional noninvasive diagnostic modalities. Further, hemorrhagic risk often impacts the judgment regarding the use of prophylactic measures as well as the therapy once deep venous thrombosis is diagnosed. Better data regarding the incidence of venous thromboembolism and the applicability of existing diagnostic, prophylactic, and treatment approaches in this population are needed. Accidents are responsible for over 140,000 deaths and approximately 70 million nonfatal injuries annually in the United States [1]. Most of the fatalities occur within hours of injury as a result of exsanguination or a lethal head injury, but approximately 20% survive for days or weeks [2], usually in the intensive care unit. The primary causes of late death are sepsis and multiple-organ failure [2]. Increasing evidence, however, suggests that pulmonary embolism (PE) is now becoming a leading cause of late death, especially in some high-risk groups [3][4][5].The increase in the incidence of PE is due in part to improvements in trauma care, which have lowered the early mortality rate [6-8], leaving more patients at risk for late death. In addition, autopsy examinations, used more frequently to audit trauma care systems [6,9], have documented an increase in clinically unsuspected deep venous thrombosis (DVT) and PE.This review was prompted because of the apparent increase in DVT and PE in the trauma population, and because the trauma patient presents very difficult and unique problems compared with the nontrauma patient with regard to the diagnosis, prophylaxis, and treatment of these disorders. In this review, we address the incidence, pathophysiology, diagnosis, treatment, and prophylaxis of DVT and PE in the trauma patient. We do not consider the entities of fat embolism or pulmonary microemboli as a cause of late pulmonary failure.

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“…Because of their vasoconstrictive properties, both DHE and sumatriptan are contraindicated in patients with cardiovascular disease. This contraindication is based on studies in which small contractions to these drugs were observed in human proximal coronary arteries (7,10). Recently, we showed that the effect of sumatriptan is larger in distal coronary arteries than in proximal coronary arteries (11).…”

Section: Introductionmentioning

confidence: 99%

Dihydroergotamine and sumatriptan in isolated human coronary artery, middle meningeal artery and saphenous vein

et al. 2014

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Contractions to DHE in distal coronary arteries are smaller than those to sumatriptan, while at clinical concentrations they both induce only slight contractions. In meningeal arteries contractions to DHE and sumatriptan are significantly larger, showing their cranioselectivity. Contractions to DHE in the saphenous vein are higher than those in the arteries, confirming its venous contractile properties.

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Vascular spasm and gangrene during heparin–dihydro-ergotamine prophylaxis

Cited by 25 publications

References 3 publications

Effects of dihydroergotamine and sumatriptan on isolated human cerebral and peripheral arteries and veins

Effects of dihydroergotamine and sumatriptan on isolated human cerebral and peripheral arteries and veins

Deep Venous Thrombosis and Pulmonary Embolism in Trauma Patients

Dihydroergotamine and sumatriptan in isolated human coronary artery, middle meningeal artery and saphenous vein

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