Discussion
Postoperative Acute Mental Status Change
There are many causes of postoperative mental status change after intramedullary nailing. Change may be cardiogenic, infectious, pharmacologic, or neurologic in origin. Age should be considered in the work-up of postoperative mental status change, as common complications differ between older and younger patients, with geriatric patients at particularly high risk for delirium.
In addition, past medical history is important in determining causes of mental status change, as many conditions (eg, cardiac disease, hypercoagulable state, dementia, polypharmacy) can cause or exacerbate these changes. A systematic approach is recommended for evaluating any patient with an acute mental status change (Figure 3).1,5,7Next to be evaluated are vital signs—particularly hypoxia, as isolated tachycardia may simply be a manifestation of pain. The cardiac system is then assessed with EKG and cardiac-specific laboratory tests, including a troponin level test if there is suspicion of myocardial infarction. PE and FES are complications with a higher prevalence in intramedullary nailing, and pulmonary involvement can be ruled out with the CT with PE protocol. Skin examination is important as well, as FES presents with petechial rash in 60% of patients8 (rash was absent in our patient’s case). Narcotic overdose is easily ruled out with administration of naloxone. Infection and sepsis can cause mental changes, though more commonly in the elderly and seldom so soon after surgery. Evaluation for infection and sepsis involves urinalysis and culturing of blood, urine, and other bodily fluids. If there is concern about surgical site infection, the postoperative dressing should be immediately removed and the wound examined. Last, neurologic and embolic phenomena can be initially investigated with CT to rule out hemorrhagic stroke. If CT of the brain is negative, MRI should be performed. MRI is the gold standard for diagnosing ischemic stroke and CFE caused by FES.9
Prevalence of Fat Embolism Syndrome
Development of intramedullary fat release in patients with long-bone injuries is common. A prospective study found circulating fat globules in 95% of 43 patients with femur fractures.10 In another study, transesophageal EKG showed cardiac embolism in 62% of patients who had undergone intramedullary nail fixation.11 Despite this high rate, only 0.9% to 2.2% of patients developed symptomatic FES. Risk factors for FES include younger age, multiple fractures, closed fractures, and nonoperative or delayed management of long-bone fractures.2 As already mentioned, average time to FES presentation after long-bone fracture is about 48 hours. One study found that FES typically occurs within 24 to 72 hours after initial insult (average, 48.5 hours) and that the incidence of FES is 0.15% in tibia fractures, 0.78% in femur fractures, and 2.4% in multiple long-bone fractures.4 The timeline is consistent with the present case—our patient developed symptoms about 36 hours after injury. In addition, other studies have found a higher mortality rate (5%-15%) for patients with bilateral femur fractures than for patients with only one fracture.7,12,13 Patients with a floating knee injury (ipsilateral tibia and femur fractures) are at higher risk for FES and have higher overall morbidity and mortality rates in comparison with patients with an isolated femur or tibia fracture, though the increased risk has not been quantified.
Review of Case Literature: FES With CFE
Few cases of FES with symptomatic CFE in the setting of long-bone fracture or long-bone surgery have been reported in the literature. There is wide variation in the development of FES with respect to preoperative or postoperative status and mechanism of injury. Duran and colleagues14 described a 20-year-old man with ipsilateral tibia and femur fractures caused by gunshots. Twenty-four hours after presentation, he developed tonic-clonic seizures and the classic triad of rash, hypoxia, and altered mental status. MRI confirmed CFE secondary to FES. The patient was optimized neurologically before definitive fixation and was discharged with minimal neurologic deficits on POD-27. Chang and colleagues15 and Yeo and colleagues16 described CFE in patients who underwent bilateral total knee arthroplasty. Symptoms developed 9 hours and 2 days after surgery, respectively. Both patients had fat emboli in the lungs and brain, underwent intensive care treatment, and recovered from the initial insult. After discharge at 44 days and 2 weeks, respectively, they fully recovered.
Other patients with CFE have had less favorable outcomes. Chen and colleagues6 reported the case of a 31-year-old man who sustained closed femur and tibia fractures in an automobile collision and experienced an acute decline in neurologic status 1 hour after arrival in the emergency department. The patient was intubated, CFE was diagnosed on the basis of MRI findings, and the orthopedic injuries were treated with external fixation. After 2 weeks, the patient was discharged with persistent neurologic deficits and the need for long-term tube feeding. Walshe and colleagues17 reported the case of a 19-year-old woman who sustained multiple long-bone injuries and traumatic brain injury and showed fat emboli on MRI. The patient experienced brain herniation while in the intensive care unit and later was declared brain-dead. According to the literature, it is important to maintain high suspicion for FES and possible CFE in the setting of high-energy fracture but also to be aware that FES may develop even with nondisplaced fracture or with reaming of the intramedullary canal in elective total joint arthroplasty.18