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Sudden hypoxia during knee surgery

Cleveland Clinic Journal of Medicine. 2012 June;79(6):401-409 | 10.3949/ccjm.79a.09129
June 1, 2012|Cleveland Clinic Journal of Medicine
Uusula A. Galway, MD;David Gugliotti, MD, FACP, SFHM
Author and Disclosure Information

Uusula A. Galway, MD
Department of General Anesthesiology, Cleveland Clinic, and Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

David Gugliotti, MD, FACP, SFHM
Department of Hospital Medicine, Cleveland Clinic

Address: Ursula A. Galway, MD, Department of General Anesthesiology, E31, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail galwayu@ccf.org

FAT EMBOLI AFFECT THE LUNGS, SKIN, AND BRAIN

3. Where on the body is the rash associated with fat embolism syndrome usually seen?

  • Face
  • Near a site of fracture or surgery
  • Chest, axilla, conjunctiva
  • Distal extremities

Petechiae are part of the classic presenting triad of fat embolism syndrome, which also includes pulmonary and cerebral dysfunction.

Petechiae usually appear on the 2nd to 4th day after injury.26 They are usually found across the chest, the anterior axillary folds, and the neck, as well as on the oral mucosa and the conjunctiva. The rash is caused by occlusion of dermal capillaries by fat, which increases their fragility.10

Pulmonary changes usually begin with tachypnea, dyspnea, and a drop in oxygen saturation, leading to generalized hypoxia. Respiratory symptoms are present in 100% of cases.2 Respiratory symptoms can acutely develop with the sudden manipulation of a fracture, reaming of bone, or release of a limb tourniquet.27

Cerebral dysfunction can be variable, from anxiety and confusion to seizures and coma. The neurologic signs are typically diffuse; however, focal symptoms such as hemiplegia or aphasia can occasionally occur. Neurologic signs are present in 80% of cases.2,28

Body systems affected by fat embolism syndrome are summarized in Table 2.

4. How many hours after injury does fat embolism syndrome typically manifest?

  • 1 to 2 hours
  • 6 to 12 hours
  • 12 to 20 hours
  • 24 to 48 hours
  • 72 to 84 hours

Most patients develop signs and symptoms 24 to 48 hours after injury. Patients presenting earlier than 12 hours usually have a more fulminant course.29

The time between fat embolization and the development of fat embolism syndrome is thought to be related to the time required for the metabolic conversion of fat to free fatty acids.30 We suspect that the early desaturation seen in our patient was the result of a heavy showering of fat intraoperatively. However, this could only be concluded after we had ruled out other causes of acute hypoxia and hypotension.

Fat embolism syndrome is a diagnosis of exclusion and is based on clinical criteria. No specific sign, symptom, or test is pathognomonic. It may often be confused with other conditions such as systemic inflammatory response syndrome or sepsis. However, the triad of respiratory and neurologic symptoms and petechiae coupled with the clinical picture of recent trauma or orthopedic surgery almost assures the diagnosis.

Fat embolism syndrome can range from subclinical to fulminating, with the more fulminating course attributable to a huge load of fat emboli, which leads to acute cor pulmonale.

The diagnostic criteria established by Gurd and Wilson13 are widely accepted and include major, minor, and laboratory criteria (Table 3). According to their criteria, the diagnosis of fat embolism syndrome requires the presence of one major feature plus four minor features plus fat macroglobulinemia. Major signs appear in 60% of patients within 24 hours and in 85% of patients within 48 hours.13

Variations on these diagnostic guidelines require two major criteria, one major and three minor criteria, two major and two minor criteria, and one major and two minor criteria.31 Other authors, perceiving these criteria to be insensitive, have focused on other factors, including hypoxemia by arterial blood gas monitoring.12,32 Lindeque at al12 thus included arterial blood gas analysis in their criteria (Table 4). However, their criteria have been criticized for focusing only on the pulmonary system, and many of these features may be present in patients with ARDS with a cause other than fat embolization, such as burns, septicemia, aspiration, and multiple transfusions.

Schonfeld et al32 created a fat embolism index to diagnose fat embolism syndrome; a score greater than 5 indicates that the syndrome is likely (Table 5).32

Regardless of the criteria used, one must have a high index of suspicion for fat embolization syndrome in patients undergoing orthopedic procedures, particularly hip and knee surgery, and in patients with fractures, especially fractures of the femur, tibia, or pelvis and multiple, concomitant fractures.

CASE CONTINUED

Our patient was given furosemide (Lasix) empirically for diuresis and to improve oxygenation. However, his oxygen saturation remained low.

Chest radiography 4 hours after surgery showed bilateral pulmonary infiltrates. Serial electrocardiography showed no acute changes. Levels of cardiac enzymes and troponins were normal. Transthoracic echocardiography showed no left ventricular dysfunction, a normal right ventricle, and no evidence of valvular lesions. Urine and blood fat stains were negative, but the sputum stain was positive for copious extracellular fat. The patient became comatose 5 hours postoperatively. Computed tomography of the brain was normal. He was transferred to the surgical intensive care unit.

The clinical course was marked by hemodynamic instability requiring norepinephrine (Levophed) and vasopressin (Pitressin) for hypotension. Right ventricular filling pressures via central venous pressure monitoring showed no evidence of hypovolemia. The hemoglobin concentration and the hematocrit were stable, with no evidence of acute or ongoing bleeding. Blood, urine, and sputum cultures remained negative. Acute myocardial infarction was ruled out by serial electrocardiography, cardiac enzyme testing, and troponin testing.

Figure 1. Magnetic resonance imaging on postoperative day 2 showed multiple hyperintense areas, consistent with emboli.

Magnetic resonance imaging (MRI) of the brain on postoperative day 2 showed foci of acute ischemia suggestive of embolic phenomena consistent with fat embolism syndrome (Figure  1). Transthoracic echocardiography was repeated but again showed no evidence of a patent foramen ovale. Electroencephalography on postoperative day 4 showed severe, diffuse encephalopathy. There was no petechial skin rash. Other laboratory studies showed progressive thrombocytopenia with a platelet count of 53 × 199/L on postoperative day 3.

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