Fat Embolism

Tj, Berrigan; Ew, Carsky; Er, Heitzman

doi:10.2214/ajr.96.4.967

Cited by 23 publications

(2 citation statements)

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“…According to the various available scientific literature, bone marrow embolism is seen only following trauma to the bones. [5][6][7][8] Though anti-psychotic drugs especially atypical antipsychotics are known to cause cardiovascular side effects e.g., thromboembolism on long term use; it is not known to cause fat and marrow embolism according to available literature. 9,10 Therefore, this unique findings of this case, gives us a new perspective regarding investigation of cause of death in the cases of sudden death.…”

Section: Discussionmentioning

confidence: 99%

A case of sudden death due to pulmonary embolism of bone marrow origin, masked as acute drug toxicity: A rare case in a bewildering clinical scenario

Bandyopadhyay

Nandi²,

Mukherjee³

2023

SAJCRR

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Sudden death is unexpected death within 24 hours from the onset of symptoms with or without known preexisting conditions. Respiratory pathologies are the second most common cause of such deaths. 39 years old male patient with a history of mental illness for the last 10 years and on regular treatment with antipsychotic medications, suffered sudden deterioration of higher functions and was admitted to the Medical College, and Hospital, Kolkata with a provisional diagnosis of drug toxicity. He succumbed to his condition within 24 hours of admission and the dead body was referred to Kolkata Police Morgue for a medicolegal autopsy.Shows multi-system involvement in the form of Pulmonary Oedema, consolidation, broncho-pneumonic changes and subpleural petechiae, Cardiomegaly due to biventricular hypertrophy, Cerebral Oedema, Enlarged kidneys with loss of cortico-medullary differentiation and streaky cortico-medullary haemorrhages. Stomach findings were unremarkable.1) Toxicological Examination of blood, bile, vitreous and routine viscera was negative for any poison or pharmacological agents.2)Histopathological examination with routine H&E staining showed Pulmonary oedema with lymphocytic infiltration and the presence of fat and hematopoietic precursor cells in pulmonary vessels, Interstitial Oedema and focal glomerulosclerosis and Periportal inflammation in the liver.

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Section: Discussionmentioning

confidence: 99%

A case of sudden death due to pulmonary embolism of bone marrow origin, masked as acute drug toxicity: A rare case in a bewildering clinical scenario

Bandyopadhyay

Nandi²,

Mukherjee³

2023

SAJCRR

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“…Necropsy was carried out on the patients who died. Minor Fat Embolism (a) Fat globules in sputum (b) Haemoptysis (c) Signs of central pulmonary oedem i (d) Chest radiographic change of mizone mottling, patchy consolidation-which must be bilateral (e) Fat globules found in end samples Of urine Though the florid syndrome of fat embolism is easy to diagnose, many subclinical cases occur, with few if any of the classical signs, and may be diagnosed only by chest radiography (Berrigan et al, 1966). We have therefore classified our patients into two groups (Table II).…”

Section: Clinical Examinationmentioning

confidence: 99%

Injury, serum lipids, fat embolism, and clofibrate.

O’Driscoll¹,

Powell²

1967

BMJ

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The mechanism of fat embolism following injury has excited much controversy since it was first described by Zenker in 1862. Two theories seek to explain it-the classical mechanical theory, which is supported by Sevitt (1962), and the metabolic theory, which is supported by Evarts (1965) In this study, firstly, an attempt was made to try to establish whether there was any change in the serum non-cholesterol lipids after trauma; secondly, the incidence of all degrees of the syndrome of fat embolism was investigated; and, thirdly, the effect of Atromid (clofibrate) on the serum lipids and the incidence of fat embolism was studied. Clofibrate was used because it has an effect on the lipids of the hyperlipaemic patient and has also been found to depress postprandial lipaemia. Material and MethodsThe patients were inmates of the orthopaedic unit at St. James's Hospital, Leeds, either as a result of injury serious enough to warrant admission or because they were undergoing orthopaedic surgery. They were divided into two groups (Table I). One group received standard therapy, and the other received clofibrate as well, as soon as they were able to take capsules. The dosage of clofibrate used was 750 mg. by mouth followed by 500 mg. six-hourly for two days, then 250 mg. six-hourly for three days, then 250 mg. twice daily for two days, and finally 250 mg. daily for two days. The dose was tailed off to prevent any rebound effects. Eight patients who had had operations on non-bony structures also received clofibrate. Laboratory EstimationsPlasma total lipids were estimated by the rapid turbimetric method of Kunkel et al. (1948), giving normal ranges between 340 and 640 mg./l00 ml. and a 5% error against standard sera. Cholesterol levels were measured by the method of Carr and Drekter (1956) on the first 30 samples and subsequently by direct estimation on an autoanalyser (Kenny and Jamieson, 1963). Cholesterol levels were then subtracted from the total levels to give the non-cholesterol lipid levels.Sputum was examined for fat globules by adding scharlach R and then by direct microscopy. Urine (end samples) were examined by centrifugation for five minutes, adding scharlach R to the deposit, and then by direct microscopy.

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Non-infectious Parenchymal Lung Disease

Dalpiaz

2016

Emergency Radiology of the Chest and Cardiovascular System

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Fat Embolism

Cited by 23 publications

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A case of sudden death due to pulmonary embolism of bone marrow origin, masked as acute drug toxicity: A rare case in a bewildering clinical scenario

A case of sudden death due to pulmonary embolism of bone marrow origin, masked as acute drug toxicity: A rare case in a bewildering clinical scenario

Injury, serum lipids, fat embolism, and clofibrate.

Non-infectious Parenchymal Lung Disease

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