Fat Embolism Syndrome in a Surgical Patient

James L. Glazer, MD, and Daniel K. Onion, MD, MPH
Fat embolism syndrome, a condition characterizedby hypoxia, bilateral pulmonary infiltrates, andmental status change, is commonly thought of inassociation with long-bone trauma. Fat embolizationcan frequently take place, however, within thesetting of elective and semiacute orthopedic procedures.1 In particular, there is a high incidence of fatembolization during placement of hip prostheses.Although studies suggest that embolization eventsinfrequently result in a clinically apparent fat embolismsyndrome,1,2 clinicians should be vigilant inconsidering fat embolism syndrome as a causativeagent of postoperative respiratory distress.Case ReportAn 80-year-old woman with a history of hip fractureand prosthesis placement of the left hip cameto the emergency department after a fall. A displacedfemoral neck fracture of the right hip wasdiagnosed based on clinical examination and radiologicfindings. The patient was admitted to thehospital by the orthopedics service.The patient was scheduled for operative placementof a bipolar prosthesis of her right hip on theday following admission. Her preoperative coursewas uneventful. An electrocardiogram (ECG)showed Q waves in leads III, aVF, and V3, whichwere interpreted as an old inferior infarction. Shewas afebrile, her blood pressure was 160/82 mmHg, and her oxygen saturations were 93% on roomair. In the operating room, she was sedated withmidazolam and fentanyl and received spinal anesthesia.Placement of a cemented hip stem (Johnson &Johnson Ultima) and femoral head component(Johnson & Johnson), bipolar shell, and bipolarliner was uneventful. The procedure lasted 96 minutes,during which the patient maintained oxygensaturations of 98% to 100% on 10 L of oxygen.Her blood pressure ranged between 90 and 135mm Hg systolic, and her pulse was less than 100beats per minute. Approximately 10 minutes postoperatively,the patient abruptly developed a sinustachycardia with a pulse of 135 beats per minute.Her blood pressure was 122/88 mm Hg and heroxygen saturations were 85% to 86% on room airat a respiratory rate of 36/min. At this point, consultationby the family practice service was requestedby the orthopedic surgeon.An ECG, complete blood count, and cardiacprofile were all obtained. The ECG showed sinustachycardia without acute ST or T wave changes.Her hematocrit was stable, cardiac enzyme levelswere negative, and a thyroid-stimulating hormonelevel was within normal limits. The patient’s tachycardiaand tachypnea continued, with her pulseranging from 135 to 140 beats per minute andrespirations between 24 and 36/min. Two hourspostoperatively, she developed a fever of 101.7° Fand systolic hypertension of 165 mm Hg.A diagnosis of pulmonary embolus was considered,and arterial blood gas readings and a chestradiograph were obtained. Arterial blood gas on 4L of inspired oxygen showed a pH of 7.41, carbondioxide 36 mm Hg, and oxygen 81 mm Hg, with97% saturation calculated. A chest radiographshowed bilateral perihilar fullness but a lack ofinfiltrate. Based on the patient’s persistent oxygenrequirement and her continued tachycardia andtachypnea, a d-dimer assay and ventilation-perfusionscan were obtained. Four hours postoperativelythe patient had oxygen saturations of 78% onroom air and 91% on 4 L of inspired oxygen.The d-dimer assay results were between 1,500and 2,000 mg/L, a positive result. The ventilationperfusionscan was read as intermediate probabilitywith matched segmental and subsegmental defectsbilaterally, predominately at the lung bases andworse on the left. The patient was given heparin.Approximately 1 hour before her initial bolus of saturations suddenly began to improve, from 89%to 95% on 4 L of oxygen. Her pulse returned to100 beats per minute, and her systolic blood pressurestabilized in the range of 125 to 135 mm Hg.During the next 24 hours, she was weaned fromoxygen, her low-grade temperature resolved, andher blood pressure remained stable. Several newpetechiae were noted on the patient’s anterior chestwall. A skin biopsy of the petechial lesions revealedintravascular fat, and a diagnosis of fat embolismsyndrome was made. A review of her symptomsfrom the previous night indicated the patient metfive of Gurd and Wilson’s criteria for fat embolismsyndrome, including petechiae, hypoxemia, pyrexia,tachycardia, and relative thrombocytopenia.3The heparin was discontinued.The patient did suffer some bleeding from herwound site and required a transfusion of 2 U ofpacked red blood cells. She had no hematoma andbegan to make excellent progress with physicaltherapy. She was released from the hospital 8 dayspostoperatively.At her 6-month follow-up, the patient was doingwell. She had suffered no complications of theprosthesis itself and was progressing well in physicaltherapy, with good return of function to heraffected hip. She had no long-term sequelae of herembolization event.DiscussionThe workup of a patient with acute onset of shortnessof breath after an orthopedic operative procedureshould include consideration of pulmonarythromboembolism and fat embolism as possiblecauses. Fat embolus is a common occurrence inmany orthopedic procedures. Although it has beendescribed extensively in the setting of long-bonefractures and multiple trauma, fat embolism syndromehas not been widely reported as a complicationof total hip arthroplasty.1,3–5In the patient described above, the diagnosis offat embolism syndrome was entertained after thepossibility of pulmonary thromboembolism wasruled out. The fat embolism syndrome was firstdescribed clinically by Von Bergmann,6 who caredfor a man with a broken femur and symptoms of thesyndrome in 1873. The prevalence of fat embolismsyndrome among all fracture patients is reported tobe between 0.25% and 1.25%.7 Among patientswith multiple bone fractures, the prevalence canreach 5% to 10%.8,9The pathophysiology of fat embolism syndromehas not yet been definitively characterized. A mechanicaltheory holds that the embolization eventresults from a transient rise in pressure in a fatcontainingcavity in association with torn bloodvessels, allowing escape of marrow or adipose fatcells into the circulation.10 Two alternative biochemicaltheories posit explanations for fat embolismsyndrome, both of which could account for theobservation of the syndrome in nontraumatic settings.In one, fat droplets already in the circulationare broken down at distal sites to free fatty acids,which then exert a local toxic effect on the tissues.This theory explains the appearance of petechiaeand the histologic changes in pneumocytes in associationwith fat-embolism–induced acute respiratorydistress syndrome (ARDS).11 The obstructiveexplanation for fat embolism syndrome proposesthat free fatty acids are mobilized by circulatingcatecholamines. Fat droplets in the circulationeventually coalesce and embolize, causing destructiveeffects.12Fat embolism syndrome can occur in immediateconjunction with a precipitating factor or it can bedelayed for up to 3 days, although 85% of cases areapparent within 48 hours.13 The diagnostic workupof a patient suspected of having fat embolism syndromeshould include serial arterial blood gas measurements,as hypoxemia is one of the cardinalfeatures. Serial chest radiographs can be used toobserve the progression of ARDS infiltrates in thelungs, although it should be noted that chest radiographicchanges are often not apparent in the initialstages of the syndrome. An ECG might show a newright bundle-branch block or nonspecific T-wavechanges. A late laboratory marker of fat embolismsyndrome is serum lipase, which becomes elevated3 to 5 days after embolization and peaks at 5 to 8days.Gurd and Wilson3 proposed the most widelyaccepted guidelines for the diagnosis of fat embolismsyndrome, which require at least one sign fromthe major and at least four signs from the minorcriteria (Table 1). An alternative set of standardswas later proposed by Lindeque et al,14 who believedthat the criteria of Gurd and Wilson weretoo restrictive. The criteria of Lindeque et al areseldom used among clinicians, in part because of
they are unable to distinguish fat embolism syndrome
from other causes of respiratory distress.15
The histologic diagnosis of fat embolism syndrome
relies on observing fat globules in vascular
spaces. This finding is most reliably obtained by a
biopsy of superficial cutaneous petechial lesions.
Fat globules can also be found in sputum and urine,
although this evidence is made more elusive by the
fact that fat must be actively circulating at the time
the sample is collected.
The treatment of fat embolism syndrome is primarily
supportive. As with other causes of ARDS,
maintaining adequate tissue oxygenation and an
arterial oxygen saturation of more than 90% should
be the clinician’s goal. The patient’s lung disease
might necessitate the use of positive airway pressure
or even mechanical ventilation. Because many
patients suffer fat embolism syndrome in conjunction
with multiple trauma, general supportive measures,
including hemodynamic stabilization, maintenance
of normal electrolyte values, and prompt
attention to orthopedic and soft-tissue injury
should be maintained.
The effects of steroids on patients with fat embolism
syndrome have long been debated in the
literature. The theoretical basis for using corticosteroids
is sound; they are thought to stabilize granulocyte
membranes, reduce catecholamine levels,
retard platelet aggregation, inhibit the activation of
complement system, and protect the capillary endothelium.
Corticosteroids have been shown to reduce
the incidence of fat embolism syndrome when
given prophylactically in the emergency department,
16 although data showing a therapeutic role
for them once clinically apparent fat embolism syndrome
has developed have remained elusive.
Orthopedic surgeons might be able to reduce
their patients’ risk of fat embolism syndrome. Early
fracture fixation has decreased the incidence of pulmonary
complications17 and fat embolism syndrome18
related to long-bone trauma. Using a distal
drain hole or a proximal and distal vacuum
during the cementing stage of total hip arthroplasty
has been associated with markedly reduced embolization.
Recent studies using ultrasound have detected
embolic events in routine total hip replacement
operations in 94% and 100% of patients
studied.1,19 No patients in either group, however,
showed clinically observable symptoms, underscoring
the complexity of the factors that contribute to
the genesis of the fat embolism syndrome.
It is thought that the technique used to cement
the intramedullary component of the prosthesis
causes embolic events during total hip arthroplasty.
5,20,21 In the traditional method, the femoral
canal is first reamed out. Next, glue is inserted into
the intramedullary canal, then the stem of the prosthesis.
This technique generates tremendous pressures
in the canal, which might cause the extravasation
of marrow or cement into the vasculature.
Use of a distal drain hole or vacuum greatly reduces
the intermedullary pressures during total hip arthroplasty.
Although such new approaches seem to
reduce a patient’s risk of fat embolism syndrome,
surgeons caution that operative techniques which
use a distal port might be associated with increased
incidence of cement failure and femoral shaft fracture.
Long thought to be a problem unique to trauma
patients, the fat embolism syndrome is common in
other settings as well (Table 2). In particular, it
should be considered in the differential diagnosis of
shortness of breath that occurs after any orthopedic
surgical procedure. It can be encountered in old
patients as well as young, and by family physicians
as well as surgeons and intensivists.

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