Anesth Analg 1999;88:1427
© 1999 International Anesthesia Research Society
LETTERS TO THE EDITOR
Fat Embolism and Neurological Dysfunction
Robert J. Byrick, MD, FRCPC
Department of Anaesthesia University of Toronto Toronto, Ontario M5B 1W8, Canada
The recent case report of delayed neurological deficits after total hip arthroplasty by Ozelsel et al. (1) was instructive. Their experience is strikingly similar to the delayed onset of coma hours after traumatic injury (2,3). They suggest that the "gradual development of cerebral edema" or "release of free-fatty acids and glycerin from the fat cells" may have been responsible for the delay in clinical presentation. There is little evidence that embolic fat, by itself, causes a primary, delayed "toxic effect on brain cells." Even when embolic fat persists for 72 h, there is no evidence of an inflammatory cellular reaction (4). The delayed presentation is more likely due to the time required for transpulmonary passage of emboli (5) and resulting perivascular edema (3).
An important clinical point is illustrated by Case 2. The authors report that an early computed tomographic scan showed no intracranial lesion, whereas characteristic lesions were noted on the magnetic resonance imaging (2,3). The investigation of altered consciousness in the perioperative period cannot exclude fat microembolism without using magnetic resonance imaging. The widespread, hyperintense spots are especially prominent on T2-weighted images and are predominantly distributed in the subcortical white matter of the cerebral hemispheres (2,3). Their case emphasizes that patients who fail to awaken or who have neuropsychiatric dysfunction after orthopedic or trauma surgery should be investigated with magnetic resonance imaging when cerebral fat embolism is suspected.
References
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Ozelsel TJP, Hein T, Marcel RJ, et al. Delayed neurological deficit after total hip arthroplasty. Anesth Analg 1998;87:1209–10.[Free Full Text]
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Yoshida A, Okada Y, Nagata Y, et al. Assessment of cerebral fat embolism by magnetic resonance imaging in the acute stage. J Trauma 1996;40:437–40.[Web of Science][Medline]
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Satoh H, Kurisu K, Ohtani M, Arita K, et al. Cerebral fat embolism studied by magnetic resonance imaging, transcranial Doppler sonography and single photon emission computer tomography: case report. J Trauma 1997;43:345–8.[Web of Science][Medline]
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Schemitsch EH, Turchin DC, Anderson GI, et al. Pulmonary and systemic fat embolization after medullary canal pressurization: a hemodynamic and histologic investigation in the dog. Trauma 1998;45:738–42.[Web of Science][Medline]
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Byrick RJ, Mullen JB, Mazer CD, Guest CB. Transpulmonary systemic fat embolism: studies in mongrel dogs after cemented arthroplasty. Care Med 1994;150:1416–22.
Response
Michael A. E. Ramsay, MD
Department of Anesthesiology and Pain Management Baylor University Medical Center Dallas, TX 75246
Dr. Byrick's comments are well received. The importance of magnetic resonance imaging in determining the cause of a neurological deficit after orthopedic surgery is also important in differentiating microembolic events from hypotensive or hypoxic-induced pathology. The latter produces lesions in watershed areas of the brain, as opposed to the subcortical white matter of the cerebral hemispheres, as described by Dr. Byrick. This can have considerable medicolegal and outcome significance.
During major bilateral joint replacement procedures, in which a significant embolic load may be expected, using the transesophageal echocardiogram intraoperatively may detect whether a large embolic shower occurs (1). If this is seen, then perhaps consideration may be given not to performing surgery on the second side.
The investigative work of Dr. Byrick in the animal laboratory on the transpulmonary passage of fat emboli has directly led to an understanding of how fat microemboli can reach the brain in patients with no intracardiac shunts (2). With supportive care, these patients may survive, as the fat emboli may slowly pass through the brain circulation as they did the pulmonary circulation, perhaps as demonstrated by the second patient in our report (3).
References
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Murphy P, Edelist G, Byrick RJ, et al. Relationship of fat embolism to haemodynamic and echocardiographic changes during cemented arthroplasty. Can J Anaesth 1997;44:1293–300.[Web of Science][Medline]
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Byrick RJ, Mullen JB, Mazer CD, Guest CB. Transpulmonary systemic fat embolism: studies in mongrel dogs after cemented arthroplasty. Med 1994;69:822–32.
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Ozelsel TJ, Hein HAT, Marcel RJ, et al. Delayed neurological deficit after total hip arthroplasty. Anesth Anal 1998;87:1209–10.
This article has been cited by other articles:
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R. J. Byrick
Fat Embolism: A Central Nervous System Problem
Seminars in Cardiothoracic and Vascular Anesthesia,
March 1, 2002;
6(1):
39 - 42.
[Abstract]
[PDF]
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