Histopathologic Features of Fat Embolism in Fulminant Fat Embolism Syndrome

Arai, Fumio; Nakai, Takeshi; Hori, Tomohide; Maki, Naritoshi; Kakiuchi, Masaaki; Sasaki, Shigeta

doi:10.1097/01.anes.0000278898.62036.5f

Cited by 20 publications

(9 citation statements)

References 3 publications

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“…97 A histopathological analysis of FES in a living body revealed intravascular thrombus formation consisting of fibrin, as well as erythrocytes and leukocytes with lipid granules. 98 The abovementioned studies suggest that FES is one of the main causes of DIC after trauma.…”

Section: Fat Embolism Syndromementioning

confidence: 99%

Hemostasis and Thrombosis in Trauma Patients

Gando

2015

Semin Thromb Hemost

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Hemostasis and thrombosis in trauma patients consist of physiological hemostasis for wound healing and the pathological reaction of disseminated intravascular coagulation (DIC). Whole body trauma, isolated brain injury, and fat embolism syndrome, if extremely severe, can cause DIC and affect a patient's prognosis. Shock-induced hyperfibrinolysis causes DIC with the fibrinolytic phenotype, contributing to oozing-type severe bleeding. If uncontrolled, this phenotype progresses to thrombotic phenotype at the late stage of trauma, followed by microvascular thrombosis, leading to organ dysfunction. Another type of pathological hemostatic change is acute coagulopathy of trauma shock (ACOTS), which gives rise to activated protein C-mediated systemic hypocoagulation, resulting in bleeding. ACOTS occurs only in trauma associated with shock-induced hypoperfusion and there is nothing to suggest DIC in this phenomenon. This review will provide information about the recent advances in hemostasis and thrombosis in trauma and will clarify the pathogeneses of the pathological processes observed in trauma patients.

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Section: Fat Embolism Syndromementioning

confidence: 99%

Hemostasis and Thrombosis in Trauma Patients

Gando

2015

Semin Thromb Hemost

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“…The most accepted cause of death in cases of pulmonary FE is an acute cor pulmonale with subsequent right ventricular failure [23,24]. In cases of massive fat embolism, the fat droplets occupy the pulmonary circle rapidly, which determines increasing pulmonary pressure directly by obstruction [7,25] and indirectly due to reactive vasoconstriction following hypoxemia [26,27]. A transitory increase of the pulmonary pressure is well tolerated by the heart that reacts with a double inotropic compensative mechanism: from one side an acute dilatation of the right ventricle occurs (Anrep's effect) [28,29], while from the other side, a better perfusion of the myocytes is determined by increased coronary flow [7].…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical identification of prevalent right ventricular ischemia causing right heart failure in cases of pulmonary fat embolism

et al. 2009

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Pulmonary fat embolism is a life-threatening event that may result to potentially determining right ventricular failure. Even if the pathophysiology of this phenomenon has been widely investigated, no immunohistochemical demonstration of right ventricular failure following pulmonary fat embolism has been reported till now. We performed an immunohistochemical investigation with the markers fibronectin and C5b-9 in 21 cases of polytrauma with bone fractures (study group-nine females and 12 males; mean age 64.6 years) compared to a control group of 21 forensic cases with various causes of death (nine females and 12 males; mean age 68.6 years). In each case at least one tissue slide from both cardiac ventricles (free wall of the right ventricle, anterior and/or posterior wall of the left ventricle) was available. The reactions were semi-quantitatively classified, and the two groups were compared. In the study group, the occurrence of ischemic changes at the right ventricle was significantly higher than in controls. The determining aspect, however, seems to be the prevalent ischemic lesion at the right ventricle compared to the left one. This may indicate the primary involvement of the right ventricle, thus, demonstrating a right ventricular failure.

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“…6 In our study, it was clear the shower of emboli was greatest when FloSeal was injected, especially when it was pressurized. In 2003, Hagio et al 5 noted severe emboli on TEE with cementless stem insertion during THA with PaO(2), systolic blood pressure, and arterial oxygen saturation decreasing signifi cantly during these embolic events.…”

Section: Discussionmentioning

confidence: 53%