Hemodynamic and Pathological Findings in Experimental Fat Embolism

Parker, Frederick B.; Wax, Stennis D.; Kusajima, Katsuyuki; Webb, Watts R.

doi:10.1001/archsurg.1974.01350250060017

Cited by 27 publications

(18 citation statements)

References 5 publications

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“…The latter have included injections of a variety of oily substances given by the carotid, intravenous, or intraperitoneal routes. Lipids used have included mayonnaise, 58 olive oil,*"-â nimal fat, 81 ' w Wesson oil,"…”

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confidence: 99%

Cerebral fat embolism: a neuropathological study of a microembolic state.

Kamenar

Burger²

1980

Stroke

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SUMMARY Multiple cerebral petechlae associated with intravascular globules of neutral fat and localized primarily within the white matter are distinctive lesions which secure the pathologic diagnosis of cerebral fat embolism. The abundance of these lesions in an unknown, but presumably small, percentage of cases of fat embolism, along with the even more widespread distribution of embolic fat droplets throughout both white and gray matter, suggest that these lesions and emboli must hare a profound effect on neurologic function. Nevertheless, respiratory insufficiency is by far a more common clinical manifestation of the fat embolism syndrome and the neurologic involvement of such patients is often attributed to the secondary effects of generalized hypoxia. The following patient with orert respiratory and neurologic symptoms re-emphasizes the direct primary effect of fat emboli within the central nervous system as a cause of white matter hemorrhages and neurologic deterioration. Explanations for the selectivity of the lesions for the cerebral white matter are explored. Stroke, Vol 11, No 5, 1980FOR OVER A CENTURY, fat embolization has been recognized as a potentially serious, but poorly understood, sequela of skeletal trauma. Relative to the frequent subclinical embolization of fat droplets following fractures, 1 ' 2 the "fat embolism syndrome" is less common and is unpredictable in the severity with which it affects the major target organs, the lungs and the brain. Because of its greater incidence, the pulmonary, rather than the cerebral, component has received primary attention in clinical and experimental studies which attempt to define the relationship between embolic intravascular fat and clinical disease.3 In contrast to the lung, however, the brain may present more distinctive, if not diagnostic, pathologic lesions in this syndrome. With the aid of an illustrative patient, this discussion reviews cerebral fat embolism from the perspective of the pathologist and surveys our incomplete understanding of its pathogenesis. Patient PresentationThe patient was a 45-year-old man who sustained in an automobile accident multiple right-sided rib fractures and a comminuted fracture of the right femur. He did not lose consciousness. After initial treatment for shock at an outside hospital, he was transferred to Duke University Medical Center where his blood pressure on admission was 120/80 mm Hg, pulse 120/min, and respiratory rate 28/min. He was dyspneic, but neurologically intact except for anisocoria (right 4 mm, left 2 mm). Arterial blood gases revealed a Po 2 of 51 mm Hg, O 2 saturation of 83%, pH of 7.31, HCO, of 14 mEq/1, and a Pco 2 of 28 mm Hg. Bilateral pneumothoraces were noted; he was intubated and chest tubes were placed. Alveolar densities were also seen throughout both lung fields. His right leg was splinted in traction.Four hours after arrival (12 hours after the accident), he became lethargic and responded to pain

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confidence: 99%

Cerebral fat embolism: a neuropathological study of a microembolic state.

Kamenar

Burger²

1980

Stroke

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“…31,32 In our study, pulmonary arterial pressure rose, even in the presence of a relatively minor embolic response, and it therefore seems likely that factors such as vasoconstriction, resulting from either hypoxia or the local release of vasoactive mediators, or as a reflex response from the sympathetic nervous system, may also be important in the genesis of this effect. 32,44,45 Despite the considerable increase in pulmonary artery pressure, this appeared to be self-limiting in most traumatic tibial and femoral fractures (groups I and II), with no evidence of right ventricular dysfunction or of an effect on gas exchange. In pathological fractures (group III), however, the nailing procedures produced hypoxic episodes (diminished PaO 2 /FiO 2 ratio) and an increase in alveolararterial oxygen difference, reflecting a degree of ventilation-perfusion inequality.…”

Section: Discussionmentioning

confidence: 97%

“…An increased alveolar-arterial oxygen difference can be caused by both abnormally low or abnormally high ventilation-perfusion ratios within the lung. From animal studies [44][45][46] it would appear that after embolisation the hypoxia is at least partially attributable to a reduced ventilation-perfusion ratio in the non-embolised regions of the lung, as a result of their increased blood flow (increased physiological shunt); blood is diverted from regions with reduced blood flow as a result of embolisation and there is also a compensatory reflex reduction in ventilation of the underperfused areas, as a result of reflex bronchoconstriction. 32 This view is supported by our finding of increased venous admixture during insertion of the guidewire and reaming in patients with pathological fractures.…”

Section: Discussionmentioning

confidence: 99%

The coagulative and cardiorespiratory responses to reamed intramedullary nailing of isolated fractures

Robinson

Ludlam

Ray

et al. 2001

The Journal of Bone and Joint Surgery. British volume

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We measured the changes during operation in seven markers of coagulation in a prospective series of 84 patients with fractures of the tibia or femur who were undergoing reamed intramedullary nailing. All patients were also continually monitored using transoesophageal echocardiography to assess marrow embolism. In a subset of 40 patients, intraoperative cardiopulmonary function was monitored, using pulmonary and systemic arterial catheterisation.The procedure produced a significant increase in prothrombin time, activated partial thromboplastin time, the level of prothrombin fragments F 1+2 and D-dimers, and a decrease in the fibrinogen level, suggesting activation of both the coagulation and fibrinolytic pathways. There was evidence of both platelet hyper-reactivity and depletion, as estimated by an increase in ␤-thromboglobulin levels and a decrease in the platelet count. In the patients who had invasive monitoring there was an incremental increase in mean pulmonary arterial pressure, with the changes being greatest during insertion of the guide-wire and reaming.The change in markers of coagulation, pulmonary artery pressure and arterial oxygen partial pressures correlated with the intraoperative embolic response. Greater changes in these parameters were observed during stabilisation of pathological fractures and in those patients in whom surgery had been delayed for more than 48 hours.Seven patients with pathological fractures developed more severe hypoxic episodes during reaming, which were associated with significantly greater arterial hypoxaemia, a fall in the right ventricular ejection fraction and an increase in the mean pulmonary artery pressure, pulmonary capillary wedge pressure, central venous pressure and the pulmonary vascular resistance index. These changes suggested that the patients had transient intraoperative right heart strain.Eight patients developed significant postoperative respiratory compromise. They all had severe intraoperative embolic responses and, in the three who had invasive monitoring, there was a significantly greater increase in pulmonary artery pressure and alveolar-arterial oxygen gradient, and a fall in the ratio of arterial partial pressure of oxygen to the inspired oxygen concentration. Operative delay, intraoperative paradoxical embolisation and the scores for the severity of the coagulative and embolic responses were predictive of the development of postoperative respiratory complications on univariate logistic regression analysis. On multivariate analysis, however, only the embolic and coagulative scores were significant independent predictors of respiratory complications.

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“…It has been postulated that decreased hepatic clearance as in shock, sepsis, or decreased plasma concentration of albumin also increase the risk of FES ( Mays, 1970;Moylan et al, 1976). FFAs have been shown in both animal and human studies to have the following systemic effects  Toxicity to lung parenchyma:  capillary leak  curtailed surfactant production  interstitial hemorrhage and pulmonary edema (Herndon, 1975;Parker et al, 1974;Szabo et al, 1977)  Cerebral cortical cell damage (Parisi et al, 2002)  Cardiac contractile dysfunction (Dedhia & Mushambi, 2007;Hulman, 1988b)  C-reactive protein which is elevated in these patients appears to interact with circulating chylomicrons to form fat globules de novo, which can explain non traumatic fat embolism (Hulman, 1988a). Coagulation cascade activation, disseminated intravascular coagulation (DIC), and antifibrinolytic pathways may further contribute to lung injury (E. G. King et al, 1971;Saldeen, 1970).The biochemical theory, could explain "latent period" and nontraumatic forms of FES (Schnaid et al, 1987).…”

Section: Biochemical Hypothesismentioning

confidence: 99%