Article, Emergency Medicine

Hyperacute cerebral fat embolism in a patient with femoral shaft fracture

Fat embolism in a pa”>American Journal of Emergency Medicine 31 (2013) 1420.e1-1420.e3

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Case Report

Hyperacute cerebral fat embolism in a patient with femoral shaft fracture

Abstract

Fat embolism syndrome is a potentially fatal complication and occurs most commonly after long bone fracture. In patients who sustained severe trauma, both cerebral fat embolism (CFE) and diffuse axonal injury (DAI) could be the cause of Altered consciousness in the absence of marked intracranial lesions in cranial computed tomogra- phy. However, distinguishing CFE and DAI can be difficult clinically. Generally, DAI develops immediately after the insult, whereas CFE occurs 48 to 72 hours after the trauma and even after internal fixation for the fractures. Fat embolism syndrome develops within an average of 48.5 hours after long bone fracture [1] but has never been reported to occur in less than 2 hours. Here, we present a patient who developed hyperacute CFE and eventually had poor neurological outcome, in contrast to previous reports stating that CFE usually has a long latent period and favorable outcomes.

A 31-year-old man was transferred to the emergency department (ED) because of car accident 20 minutes before arrival to the ED. His Glasgow Coma Scale score was 15 (E4M6V5), blood pressure was 157/59 mm Hg, heart rate was 101/min, respiratory rate was 30/ min, and oxygen saturation was 99%. A plain radiograph showed closed displaced fracture of the right femoral shaft and nondisplaced fracture of the right distal tibia and fibula. Result of a cranial computed tomography was unremarkable. One hour after the accident, his Glasgow Coma Scale declined to E1M4V1. Neurologic examination revealed tetraparesis, diminished deep tendon reflex, normal reaction of both pupils to light, and absence of Babinski sign. Episodic generalized tonic-clonic seizure with upward gaze was also noted. The results of blood gas analysis revealed metabolic acidosis. No hypotension or tachycardia was noted. Focus assessment sonography in trauma showed no internal bleeding. Repeated cranial CT showed absence of intracranial lesions, Brain edema, or punctate hemorrhages. brain magnetic resonance imaging (MRI)

was performed to differentiate diffuse axonal injury (DAI) from cerebral fat embolism (CFE). It demonstrateda starfield pattern and multiple punctate lesions on both deep cerebral white matter in all vascular territories (Fig. 1), a finding compatible with a micro- emboli-related CFE. Fat embolism syndrome (FES) was diagnosed according to the typical imaging findings accompanied by the fulfilled Lindeque criteria, including femur fracture, sustained pH less than 7.3, and increased work of breath. Transthoracic echocar- diogram revealed no right-to-left shunt. external fixation with skeletal traction was performed, and he was admitted to the intensive care unit. He was discharged with minimal neurologic improvement. On follow-up at 2 months, he remained in poor responsive status and required tube feeding.

Here we present a patient who developed hyperacute CFE and eventually had poor neurological outcome, in contrast to previous report stating that CFE usually has a latent period and favorable outcomes. Fat embolism syndrome can result in multiorgan systems manifestation including the lungs, brain, skin, heart, and eyes. The central nervous system is the second most commonly involved system [2], accounting for around 60% of patients with FES [3]. Fat embolism syndrome has been most commonly seen after long bone fracture. The incidence of FES in long bone fractures is 2% to 5% [4], and the mortality rate is about 5% to 15% [5]. The pathophysiology can be attributed to mechanical and biochemical theory. The mechanical theory suggests that fat particles enter the circulatory system from the medullary channel [6], whereas the biochemical theory argues that trauma-related hormonal changes induce mobilization of stored free fatty acids lodging in the capillary system [7]. The risk factors of FES are young age, multiple fractures, closed fractures, and Conservative therapy for long bone fractures [8]. Fat embolism syndrome consists of a triad of Respiratory insufficiency, cerebral decompensation, and skin petechiae [9-11]. The diagnosis can be made depending on the patient’s history, supported by clinical signs of FES triad and image finding and aided by the Lindeque criteria.

Fig. 1. brain MRI.

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Table 1

Summary of the reported CFE patients who had latent period less than 8 hours

No.

Age/sex

Latent period

Fractures

Neurological outcome

References

1

31/M

1 h

Femoral and distal tibiofibular fracture

Bedridden and required tube feeding

Present case

2

54/M

2 h, 53 min

Multiple fracture sites including rib, clavicle, and femur

brain death on the 5th hospital day

[14]

3

25/M

3 h

Femoral and tibiofibular fracture

Fair improvement with minimal memory impairment

[15]

4

21/M

8 h

femoral fracture

Minimal response with diffuse spasticity and needing tube feeding

[3]

Table 2

Comparison of CFE and DAI

CFE DAI

Mechanism Most patients with long bone fracture Shearing forces during acceleration, deceleration, and rotation of the head Latent period Typically 24 to 72 h after the insult Instantaneous loss of consciousness during impact

Pathology Fat particles or stored free fatty acids into the brain Shear force-related diffuse axons damage Neurologic examination Vary in severity Vary in severity

CT Invariably normal Punctate hemorrhages (b20%)

diffusion-weighted MRI 1. Diffuse punctuate hyperintense signal called starfield pattern

in cerebral white matter

2. No prognostic relevance

High signal intensity in the splenium of the corpus callosum, dorsolateral brainstem, and cerebral gray-white matter junction
  • Prognostic relevance
  • Treatment Supportive Supportive

    Prognosis Often favorable Less favorable

    Acutely deteriorated consciousness after injury suggested me- chanical theory in the patient. Frequently, these embolic particles cross an Intracardiac shunt to induce systemic FES. Microfat droplets that traverse the pulmonary circulation without sequestration [12] could be the possible mechanism for this patient.

    Fat embolism syndrome typically manifests 24 to 72 hours after the injury and rarely occurs as early as 12 hours after the inciting event [13]. We had found only 3 patient who had latent period of less than 8 hours (Table 1) [3,14,15]. On searching medical literatures, we had not identified any patient who had hyperacute CFE within 1 hour. Cerebral fat embolism should be considered in a patient who sustained long bone fracture and rapidly deteriorated consciousness. In contrast to previous reports stating that patients who sustained CFE had good neurological recovery [16], we subsequently found that only 1 of these 4 patients who had an early CFE had good Neurologic recovery with only minimal memory impairment. The remaining 3 patients had Poor neurologic outcome. We propose that acute onset of CFE might be a risk factor for poorer neurologic outcome.

    Cerebral fat embolism and DAI have mimic clinical presentations. A comparison between DAI and CFE is shown in Table 2. Many studies had proposed the role of MRI in the diagnosis of CFE [17] and in distinguishing CFE from DAI [15,16,18] in the ED. Diffusion-weighted MRI of the entire brain can be accomplished rapidly using echo-planar imaging technology [19]. We propose that MRI should be obtained to facilitate a Timely diagnosis. The clinical treatment strategies for FES are mainly supportive. Pharmacological intervention, including administration of heparin, dextran, aspirin, albumin, and steroids and glucose loading, proved to be ineffective [2,11] Although early detection of CFE does not alter the treatment options, early diagnosis and appropriate supportive care can reduce the complication and mortality rates [20,21].

    In conclusion, we highlight that CFE could develop within hours after long bone fractures. The diagnosis of CFE should not be excluded based on latent period. We propose that early onset of CFE portends a poorer neurologic outcome. Magnetic resonance imaging should be performed to facilitate early diagnosis of CFE.

    Po-Chuan Chen MD Department of Emergency Medicine Tri-Service General Hospital National Defense Medical Center

    Taipei 114, Taiwan

    Chin-Wang Hsu MD Department of Emergency and Critical Care Medicine Taipei Medical University-Wan Fang Hospital

    Taipei, Taiwan

    Wen-I Liao MD Yu-Long Chen MD Cheng-Hsuan Ho MD Shih-Hung Tsai MD

    Department of Emergency Medicine Tri-Service General Hospital National Defense Medical Center

    Taipei 114, Taiwan E-mail address: [email protected]

    http://dx.doi.org/10.1016/j.ajem.2013.05.003

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