Pathogenesis of Non-Traumatic Fat Embolism

Hulman, Geoffrey

doi:10.1016/s0140-6736(88)92182-4

Cited by 56 publications

(27 citation statements)

References 13 publications

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“…The released marrow material, including fat, may cause an inflammatory response, which raises serum levels of acutephase proteins, especially C-reactive protein (CRP). Hulman [42] has hypothesized that raised levels of CRP, which is often high in sepsis, trauma, neoplasia, myocardial infarction, and inflammatory disorders, can lead to agglutination of chylomicrons and VLDL. In addition, free fatty acids liberated either from marrow-derived depot fat or chylomicrons and VLDL have been shown to directly cause lung injury [43].…”

Section: Review Of Literaturementioning

confidence: 99%

Bone marrow embolism in sickle cell disease: A review

et al. 2005

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The fat embolism syndrome is an important complication of patients with sickle cell hemoglobinopathies because of severe morbidity and mortality. Our recent experience with three cases that survived with intensive supportive care and prompt use of transfusion stimulates this review. A high index of suspicion, prompt use of diagnostic tools, and aggressive clinical management are the keys to a successful outcome. Am.

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Section: Review Of Literaturementioning

confidence: 99%

Bone marrow embolism in sickle cell disease: A review

et al. 2005

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“…IL 6may be increased due to increased production of tumor necrosis factor α and IL 1β, possibly related to soft tissue injury [10]. CRP level in FES is increased and is related to lipid agglutination (chylomicrons and LDL), which may obstruct blood flow in the microvasculature [12].…”

Section: Discussionmentioning

confidence: 99%

Fat Embolism Syndrome – A Case Report with Literature Review

Gomez¹,

IshaVerma²,

L³

et al. 2015

MOJCR

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Background: The fat embolism syndrome (FES) has been considered a diagnostic enigma since its first description over a century ago. Varying degree of presentation along with absence of specific diagnostic criteria or a scoring system makes it difficult to be diagnosed. Simple fat embolism may be a pathologic finding with variable clinical significance; patients with the FES have fat emboli in multiple organs, causing extensive organ dysfunction. While most patients with FES fully recover, there is an estimated 5to15percent mortality rate. There is no wide accepted specific treatment beyond aggressive supportive care.Case Report: A 72 year old Caucasian female presented with dyspnea, hypoxia and altered mental status within 24 hours of admission for an inferior pubic rami fracture secondary to fall. Patient required intubation and mechanical ventilation for respiratory failure. An Echocardiogram revealed Right Ventricular strain and MRI of the brain showed multiple acute/subacute infarcts, which supported a diagnosis of FES, especially as pulmonary embolism was deemed less likely with a negative CT Chest Angiogram and US Doppler of Legs. The patient gradually recovered with supportive care, successfully extubated with eventually discharged after thirty days of hospitalization. Conclusion:Fat emboli syndrome has a variable degree of presentation, ranging from mild symptoms to severe multi organ involvement that can ultimately be fatal. It can also be associated with long term morbidity which emphasizes the need for rapid precise diagnosis and management.

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“…18 Serum levels of sPLA2 initially were shown to be uniformly elevated in a small group of patients with ACS, with more striking elevations in those with more severe episodes 19 ; in a follow-up study elevation was detected 24-48 hours before clinical onset. 20 In a multicenter trial, 21 80% of subjects with ACS had sPLA2 elevation.…”

Section: Nothing Happens Without a Cause (Voltaire)mentioning

confidence: 93%

How I treat acute chest syndrome in children with sickle cell disease

Miller

2011

Blood

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IntroductionAcute chest syndrome is (ACS) the second most common cause of hospitalization and challenges infection 1 as the leading cause of sickle cell-related mortality 2 in children. Still, management is largely determined by the experience of individual practitioners, and there are no conclusive randomized controlled clinical trials to guide therapy. What follows is a review of treatment options and related issues to assist in management; it will likely be especially useful to those who do not regularly encounter children with this potentially life-threatening complication.What is in a name? That which we call a rose by any other name would smell as sweet. (William Shakespeare)ACS is the term used to describe a new pulmonary infiltrate with respiratory findings in a person with sickle cell disease. 3 The etiology of these episodes is often multifactorial and difficult to discern. Although children may be more likely to have infectious etiologies for their chest syndrome and adults more likely sickle cell-related causes, 4,5 infection and inflammation may well induce sickling, and embolism/infarction may lead to superimposed infection. This is perhaps best illustrated by the fact that 2 common causes of ACS, Chlamydia pneumoniae and Mycoplasma pneumoniae, are associated with a severe clinical course in children with sickle cell disease 6-9 rather than the "walking pneumonia" that typifies infection in others. It thus makes no sense to try to differentiate between "pneumonia" and ACS.Chance is a word that does not make sense. Nothing happens without a cause. (Voltaire)The investigators of a multicenter National Acute Chest Syndrome Study (NACSS) 4 published in 2000 made aggressive attempts to identify etiology, including the performance of bronchoalveolar lavage (BAL) on consenting study enrollees; 72% of the 671 enrolled in the study had a lavage or sputum sample available. Despite these efforts, the authors only established potential causation in 38% overall and 70% of those with a complete assessment.The most common identifiable cause of ACS in this study was pulmonary fat embolism (PFE). 4 Originally described in trauma victims, PFE is a frequent complication of bone fracture and may progress to involve the lungs and CNS with multiorgan failure and death. 10,11 The NACSS made the diagnosis by using BAL to identify fat-laden macrophages; less-invasive means of making the diagnosis are not well established, and even the specificity of fat-laden macrophages in BAL specimens has been questioned. 12 Vichinsky et al, 13 in the first systematic, prospective search for PFE in sickle cell disease, found that 44% of patients with moderate-tosevere ACS had PFE as a probable etiology. These patients had longer, more severe hospital courses and a greater decrease in hemoglobin concentration and platelet count than those without fat emboli. Fat from bone marrow, which is typically infarcted during acute pain episodes, 14 embolizes to the lungs and, in its most extreme form, fat embolism syndrome may involve the brain, k...

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Pathogenesis of Non-Traumatic Fat Embolism

Cited by 56 publications

References 13 publications

Bone marrow embolism in sickle cell disease: A review

Bone marrow embolism in sickle cell disease: A review

Fat Embolism Syndrome – A Case Report with Literature Review

How I treat acute chest syndrome in children with sickle cell disease

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