Orthopedics

Case Reports 

Post-traumatic Cerebral Fat Embolism Prior to Operative Repair of Femoral and Tibial Fractures

Kyung-Cheon Kim, MD; Deuk-Soo Hwang, MD; Hyun-Dae Shin, MD

Abstract

Most cases of fat embolism syndrome reported in the literature have developed after the instrumentation of fractures. Unequivocal cases of fat embolism in the setting of trauma before operative repair are rare because concomitant injuries may distort the clinical scenario.1 Cases of primary cerebral fat embolism as a postoperative complication and without right to left shunt also are rare.

This article presents a case of post-traumatic cerebral fat embolism that occurred prior to operative repair of femoral and tibial fractures in a patient without right to left shunt.

Figure 1: Plain radiographs showing the left tibial shaft and right segmental femoral shaft fractures.

A 25-year-old man was brought to the hospital immediately after a traffic accident. He sustained a right segmental femoral shaft fracture and a left tibial shaft fracture (Figure 1). The patient was alert, and his admission Glasgow coma scale score was 15, with no neurological deficits.

Immediate temporary immobilization was performed with skeletal traction on the tibial tuberosity for the segmental femoral fracture and on the calcaneus for the tibial shaft fracture.

Approximately 13 hours postinjury, the patient’s mental status deteriorated, and he developed dyspnea. An arterial blood gas analysis performed with the patient breathing room air revealed hypoxia with an oxygen partial pressure of 44 mm Hg, and his oxygen saturation was 81%.

Figure 3: Suction drainage of the tibia medullary cavity was performed via a 6.5-mm cannulated screw (A, B). After a tourniquet was applied on the thigh, open decompression of a hematoma containing a large number of lipid droplets and open reduction was performed via a small incision at the fracture sites in the femoral shaft fracture (C, D).

In addition, his platelet count dropped to 125,000 µL. There was no decrease in erythrocytes or leukocytes. A petechial rash also developed on his chest, axillary folds, and abdomen. The patient was intubated to protect his airway because of his declining mental state.

One day postinjury, magnetic resonance imaging (MRI) of the brain revealed extensive multifocal infarction owing to embolic showering throughout the brain parenchyma (Figure 3). Computed tomography (CT) with intravenous contrast revealed no evidence of embolism in the lungs, abdomen, or pelvis. Transthoracic and transesophageal echocardiogram revealed no circulating embolic particles or intracardiac shunt. Three days postinjury, CT scan of the lung revealed air space consolidation in the posterobasal segment of the lower lobe in the left lung and pleural effusion in both lower lungs.

Figure 2: MRI of the brain shows extensive multifocal lesions owing to embolic showering throughout nearly the entire parenchyma of the brain (black arrow). T2-weighted (A) and diffused-weighted (B) MRI at the same level 1 day postinjury showing multiple high signal intensity lesions in the basal ganglia, thalamus, and frontoparieto-occipital lobe bilaterally. T2-weighted MRI 4 days postinjury showing multiple high signal intensity lesions in the thalamus, splenium, and frontoparietal lobe bilaterally (C, D).

Five days postinjury, decompression of a hematoma containing a large number of lipid droplets was performed via a small incision at the fracture sites in the femur shaft fracture. Suction drainage of the tibia medullary cavity was established via a 6.5-mm cannulated screw, and a tourniquet was applied to the thigh in the tibia shaft fracture (Figure 2). The patient underwent closed reduction and internal fixation with a reamed intramedullary nail in the tibia, and open reduction and internal fixation with a reamed nail in the femur (Figure 4). Supportive medical treatment included endotracheal ventilatory support and tracheostomy, which precluded the use of either preoperative or postoperative corticosteroid therapy.

Thirteen days postinjury, the patient’s mental status slowly began to improve. He was discharged from the…

Most cases of fat embolism syndrome reported in the literature have developed after the instrumentation of fractures. Unequivocal cases of fat embolism in the setting of trauma before operative repair are rare because concomitant injuries may distort the clinical scenario.1 Cases of primary cerebral fat embolism as a postoperative complication and without right to left shunt also are rare.

This article presents a case of post-traumatic cerebral fat embolism that occurred prior to operative repair of femoral and tibial fractures in a patient without right to left shunt.

Figure 1: Plain radiographs showing the left tibial shaft and right segmental femoral shaft fractures

Figure 1: Plain radiographs showing the left tibial shaft and right segmental femoral shaft fractures.

Case Report

A 25-year-old man was brought to the hospital immediately after a traffic accident. He sustained a right segmental femoral shaft fracture and a left tibial shaft fracture (Figure 1). The patient was alert, and his admission Glasgow coma scale score was 15, with no neurological deficits.

Immediate temporary immobilization was performed with skeletal traction on the tibial tuberosity for the segmental femoral fracture and on the calcaneus for the tibial shaft fracture.

Approximately 13 hours postinjury, the patient’s mental status deteriorated, and he developed dyspnea. An arterial blood gas analysis performed with the patient breathing room air revealed hypoxia with an oxygen partial pressure of 44 mm Hg, and his oxygen saturation was 81%.

Figure 3: Suction drainage of the tibia medullary cavity was performed via a 6.5-mm cannulated screw

Figure 3: Suction drainage of the tibia medullary cavity was performed via a 6.5-mm cannulated screw (A, B). After a tourniquet was applied on the thigh, open decompression of a hematoma containing a large number of lipid droplets and open reduction was performed via a small incision at the fracture sites in the femoral shaft fracture (C, D).

In addition, his platelet count dropped to 125,000 µL. There was no decrease in erythrocytes or leukocytes. A petechial rash also developed on his chest, axillary folds, and abdomen. The patient was intubated to protect his airway because of his declining mental state.

One day postinjury, magnetic resonance imaging (MRI) of the brain revealed extensive multifocal infarction owing to embolic showering throughout the brain parenchyma (Figure 3). Computed tomography (CT) with intravenous contrast revealed no evidence of embolism in the lungs, abdomen, or pelvis. Transthoracic and transesophageal echocardiogram revealed no circulating embolic particles or intracardiac shunt. Three days postinjury, CT scan of the lung revealed air space consolidation in the posterobasal segment of the lower lobe in the left lung and pleural effusion in both lower lungs.

Figure 2: MRI of the brain shows extensive multifocal lesions owing to embolic showering throughout nearly the entire parenchyma of the brain

Figure 2: MRI of the brain shows extensive multifocal lesions owing to embolic showering throughout nearly the entire parenchyma of the brain (black arrow). T2-weighted (A) and diffused-weighted (B) MRI at the same level 1 day postinjury showing multiple high signal intensity lesions in the basal ganglia, thalamus, and frontoparieto-occipital lobe bilaterally. T2-weighted MRI 4 days postinjury showing multiple high signal intensity lesions in the thalamus, splenium, and frontoparietal lobe bilaterally (C, D).

Five days postinjury, decompression of a hematoma containing a large number of lipid droplets was performed via a small incision at the fracture sites in the femur shaft fracture. Suction drainage of the tibia medullary cavity was established via a 6.5-mm cannulated screw, and a tourniquet was applied to the thigh in the tibia shaft fracture (Figure 2). The patient underwent closed reduction and internal fixation with a reamed intramedullary nail in the tibia, and open reduction and internal fixation with a reamed nail in the femur (Figure 4). Supportive medical treatment included endotracheal ventilatory support and tracheostomy, which precluded the use of either preoperative or postoperative corticosteroid therapy.

Thirteen days postinjury, the patient’s mental status slowly began to improve. He was discharged from the hospital 50 days after admission. Two months later, he had resumed activities of daily living, but a speech disturbance remained.

Figure 4: Postoperative radiographs showing the reduced tibial and femoral fractures

Figure 4: Postoperative radiographs showing the reduced tibial and femoral fractures.

Discussion

Cerebral fat embolism is a potentially serious complication following long bone fractures. Paradoxical emboli are defined as emboli that originate in the systemic venous circulation and access the systemic arterial circulation.

Nastanski et al1 developed two theories to explain the pathophysiology of paradoxical fat embolism. Their first theory is a mechanical explanation hinging on the concept that intramedullary fat percolates into the traumatized venous system and floods the pulmonary vasculature. However, this model did not account for the neurological manifestations, so it was proposed microfat emboli are small enough to escape the sieve of the pulmonary capillary bed and cause systemic manifestations.

Fat emboli also can cross intracardiac shunts directly, resulting in neurological symptoms. Possible causes of this phenomenon include a patent foramen ovale, ventricular septal defect, pulmonary arteriovascular malformation, and persistent truncus arteriosus. Of these anomalies, the most common pathway is through a patent foramen ovale. Della Valle et al2 reported 2 cases of paradoxical cerebral embolism with foramen ovale after total hip arthroplasty and surgery for idiopathic scoliosis.

Peltier3 identified the toxic effects of neutral fat in the lung, introducing the concept of local alteration of chemical physiology. The results suggest fat globules activate chemical mediators that alter capillary permeability. The free fatty acids potentiate the release of prostaglandins, leukotrienes, and thromboxanes, which enhance capillary permeability and exacerbate tissue edema.

In recent years, the debate on the relative merits of reamed and unreamed nails has intensified, and there is still disagreement regarding the surgical treatment of femoral shaft fractures in polytrauma patients. Several authors have reported complications following reamed intramedullary nailing, which can lead to fat embolism syndrome, particularly in patients with multiple injuries and lung contusion.1-6

However, in their study using a pig model, Buttaro et al4 reported pulmonary changes and fat embolization during intramedullary nailing occurred to the same degree in reamed and unreamed femurs. Similarly, Schemitsch et al,5 using a canine model, reported the amount of intravascular fat persisting in the lungs, kidneys, and brain 24 hours after pressurization of the intramedullary canal was not affected by the fracture fixation method (plating or intramedullary nailing). They concluded the method of fracture fixation had little influence on the outcome of treatment.

Although there are some reports on the management of fat embolism syndrome occurring after surgery and the prophylaxis of fat embolism, reports of the surgical management of fat embolism syndrome occurring before operative repair are rare.1,2 Nastanski et al1 reported a case of post-traumatic paradoxical fat embolism to the brain prior to the surgical repair of nondisplaced bilateral tibia fractures, as well as right pneumothorax with associated rib fractures. The patient underwent uneventful unreamed placement of intramedullary rods in both tibias the following day.

A clinical investigation indicated the use of a tourniquet is of value in the prophylaxis of fat embolism.3 The intravasation of fat droplets to the circulation is retarded or reduced by rigid immobilization or by early opening of the fracture site with decompression of the fracture hematoma.6 Therefore, the use of a tourniquet and early immobilization with decompression in patients with preoperative fat embolism syndrome will reduce the amount of fat reaching the general circulation, as well as subsequent fat emboli.

References

  1. Nastanski F, Gordon WI, Lekawa ME. Posttraumatic paradoxical fat embolism to the brain: a case report. J Trauma. 2005; 58(2):372-374.
  2. Della Valle CJ, Jazrawi LM, Di Cesare PE, Steiger DJ. Paradoxical cerebral embolism complicating a major orthopaedic operation: a report of two cases. J Bone Joint Surg Am. 1999; 81(1):108-110.
  3. Peltier LF. Fat embolism: the prophylactic value of a tourniquet. J Bone Joint Surg Am. 1956; 38(4):835-840.
  4. Buttaro M, Mocetti E, Alfie V, Paniego G, Pineiro L. Fat embolism and related effects during reamed and unreamed intramedullary nailing in a pig model. J Orthop Trauma. 2002; 16(4):239-244.
  5. Schemitsch EH, Jain R, Turchin DC, et al. Pulmonary effects of fixation of a fracture with a plate compared with intramedullary nailing. A canine model of fat embolism and fracture fixation. J Bone Joint Surg Am. 1997; 79(7):984-996.
  6. Peltier LF. Fat embolism: a perspective. Clin Orthop Relat Res. 1988; (232):263-270.

Authors

Drs Kim (K.-Y.), Rhee, Lee, Hwang, Shin, Yang, and Kim (Y.-M.), are from the Department of Orthopedic Surgery, College of Medicine, Chungnam National University, Daejeon, South Korea.

Drs Kim (K.-Y.), Rhee, Lee, Hwang, Shin, Yang, and Kim (Y.-M.) have no relevant financial relationships to disclose.

Correspondence should be addressed to: Kyung-Cheon Kim, MD, Department of Orthopedic Surgery, College of Medicine, Chungnam National University, #640 Daesa-Dong, Jung-Gu, Daejeon 301-040, South Korea.

10.3928/01477447-20080201-15

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