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Iowa Orthop J. 2010; 30: 211–214.
PMCID: PMC2958300



Fat embolus has been known to occur during major orthopedic surgery. In many cases, fat embolus syndrome is a postoperative complication of long bone orthopedic surgery, particularly femoral fractures occurring after trauma. Changes in intraoperative cardiopulmonary function have been reported in a subset of these patients, and they are associated with the degree of emboliza-tion occurring with manipulation or cementing of prostheses in the fractured femur. Intraoperative cardiovascular collapse has been reported, and this cardiac event is temporally associated with intramedullary manipulations such as reaming or cementing. We present a rare case of fatal intraoperative fat embolization diagnosed with trans-esophageal echocardiography.


Fat embolism syndrome (FES) may occur during long bone orthopedic surgery,1 particularly femoral fracture surgery.1,2 Reported changes in intraoperative cardiopulmonary function are associated with the extent of embolization after fracture manipulation or cementation of proximal femoral prosthetic devices.3 Complete intraoperative cardiovascular collapse has been reported during intramedullary reaming or cementing.4,5 We report a case of fatal intraoperative fat embolization that was diagnosed with transesophageal echocardiography.


An 83-year-old woman with a subcapital hip fracture underwent arthroplasty with placement of a cemented, bipolar hip prosthesis. The patient's cardiac history included coronary bypass surgery with valve replacement and placement of an automatic internal cardiac defibrillator. The patient had a history of asthma, although she had not had any recent exacerbations. She also had a history of dementia. She did not receive treatment with anticoagulation medication or anti-platelet aggregation medication. The preoperative platelet count was 280xl09/L, the prothrombin time was 15.2 seconds, and the international normalized ratio was 1.2.

After anesthetic options were reviewed with the patient, a spinal anesthetic with moderate sedation was planned for the surgical procedure. Standard monitoring procedure, including electrocardiography, pulse oxim-etry, and noninvasive blood pressure monitoring, was applied. Adequate sedation and analgesia (propofol, 30 mg; fentanyl, 50 meg) were administered intravenously with supplemental oxygen (4 L/min via nasal cannulae).

A hyperbaric spinal anesthetic was administered through a 25 gauge whiticare needle with 15 mg of mar-caine. After adequate spinal anesthesia was established, the patient was placed in the right, lateral, decubitus position. The patient was sedated with propofol and the incision was made without incident. The patient remained comfortable and communicative during removal of the fractured left femoral head. Blood pressure, oxygenation, and cardiac function monitoring showed that all vital signs were in the normal range.

The intramedullary femoral canal was reamed to prepare it for cementing of the bipolar hip prosthesis. Approximately three minutes after the reaming was complete, the patient had bradyarrhythmia (heart rate, 27 beats/min) and gradually worsening peripheral oxygen saturation levels. The patient quickly became unresponsive, and her peripheral blood pressure, measured tonometrically from the right humeral region, decreased to 80/37 mm Hg.

The patient was ventilated immediately by mask with positive pressure. Subsequently, intubation was necessary and was accomplished without incident. End-tidal carbon dioxide pressure was undetectable with mask assisted ventilation, but measured between 6 and 8 torr in the first minute after intubation. Equal bilateral breath sounds also were present after intubation. Volume-controlled ventilation with 100% oxygen was established. The heart rate remained slower than 30 beats/min, therefore atropine (0.4 mg) and epinephrine (1 mg) were injected intravenously. No heart rate response was noted immediately after atropine and epinephrine injections. More epinephrine (1 mg) was administered through the tracheal tube with no effect. Chest compression was initiated after the carotid pulse could not be palpated. Carotid and femoral pulses were present during chest compressions. Central venous access was established through the right subclavian vein, and additional epinephrine (1 mg), atropine (1 mg), calcium chloride (1 g), and sodium bicarbonate (50 mEq) were administered intravenously, approximately ten minutes after the initial bradyarrhythmic event.

With the patient's complex cardiac history and the temporal relation between the intramedullary reaming and the apparent cardiac event, a transesophageal echo-cardiographic probe was placed to establish the cause of the patient's sudden cardiovascular collapse. Upon insertion of the probe, a large mass was noted in the right atrium (Figure 1). Further examination showed that the mass was mobile and effectively obliterated the tricuspid valve inlet. No right ventricular cavity could be visualized.

Figures 1A
B. Midesophageal transesophageal echocardiogram shows a large embolus obstruction of the right atrium and tricuspid valve.

The patient had a bioprosthetic mitral valve, which was stable and appeared normal (without vegetations); it opened occasionally with cardiac compressions. The left ventricle did not appear dilated or distended, but biventricular global cardiac dysfunction was evident. Further transesophageal echocardiographic examination of the right atrium in the bicaval view showed a poorly differentiated, well demarcated, untethered mass that extended from the inferior vena cava into the right atrium (Figure 2). The mass was mobile and oscillated with external cardiac compressions. Further views of the mass in the right atrium showed that it was echodense in some areas and echolucent in others.

Figures 2A
B. Midesophageal transesophageal echocardiogram (bicaval view) shows a large, embolic mass that traversed the inferior vena cava at the right atrial junction.

With no forward flow evident in the right ventricle, the absence of ventricular contractility on echocardiog-raphy, and the large thrombus in the heart (Figure 3), external chest compressions were discontinued. The patient died. Postmortem examination was deferred by the patient's family.

Figures 3A
B. Transesophageal echocardiogram shows a large mass obstructing the tricuspid valve and protruding into the right ventricle.


This case describes the complication of a fatal, in-traoperative embolus that developed during hip arthro-plasty. Images taken following femoral intramedullary manipulation show a large embolus obstruction of the right atrium and bicuspid valve traversing the inferior vena cava at the right atrial junction. Transesophageal echocardiography can be used to detect propagation of large emboli during femoral fracture surgery. In this case, it was used to establish an early diagnosis by imaging a massive embolus obliterating the tricuspid valve inflow and extending beyond the right atrium into the inferior vena cava, which had not responded to standard resuscitative measures.

Previous reports have described fatal cardiopulmo-nary events associated with intramedullary reaming, long bone fracture manipulation, or cementing during hip arthroplasty.4,6 In these reports, hypotension and hypoxemia or the absence of end-tidal carbon dioxide pressure indicated minimal or absent pulmonary flow. A large retrospective series reported a mortality rate of 0.05% that was associated with primary hip arthroplasty; patient deaths presumably were due to fulminant fat embolism syndrome.7 However, these reports relied on postmortem examinations to confirm the fat emboliza-tion.

Transesophageal echocardiography, performed during femur or tibia surgery, has shown showering of small emboli to the right atrium and right ventricle.8,9 Gradations of embolic severity were associated with severity of symptoms, and longer or larger showers of emboli were associated with greater deterioration of pulmonary function.9 Extremely large emboli, up to 8 cm in length, were noted in some patients. The authors suggested that these larger emboli were caused by venous hypercoagulability during major marrow embolization. Measurement of our patient's echocardiographic image showed that the embolus was 7 cm in length.

The embolus that we observed in our patient prevented right ventricular filling. It extended several centimeters into the inferior vena cava and was a single mass (not a coalescence of smaller emboli). The size of the embolus was suggestive of a venous thrombus. However, the mass had a smooth capsule, particularly in the right atrial portion, and was echogenically heterogeneous, which suggested that bone marrow, rather than thrombus, was the source of the embolus. Highly ech-odense areas, which may represent large bone marrow emboli,8,9 were noted within the capsule of the right atrial embolic mass; this strongly suggested that the embolus was made primarily of bone marrow fat.

Intravasation of bone marrow into the venous circulation may occur as a result of increased intramedullary pressure.10 With severe osteoporosis, as observed in this patient, loss of trabecular bone may result in the increased venous migration of marrow because medullary fat lacks bony support.5 The piston effect of reaming and cementing of the femur may result in intramedullary pressures as high as 800 mm Hg in the distal femur (normal intramedullary pressures range from 30-50 mm Hg)2. This high intramedullary pressure is the probable main cause of fatty marrow release into the venous circulation, resulting in pulmonary emboli


We report the use of transesophageal echocardiography to detect propagation of a large embolus during prosthetic hip fracture surgery. In this case, the outcome was fatal. The immediate availability of personnel trained in transesophageal echocardiography allowed us to document the embolus that blocked blood flow into the right side of the heart, resulting in cardiovascular collapse and death. These compelling images that capture an end of life event are rarely seen.


Editing, proofreading, and reference verification were provided by the Section of Scientific Publications and the Department of Academic and Research Support, Mayo Clinic.


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Articles from The Iowa Orthopaedic Journal are provided here courtesy of The University of Iowa