Sudden hypoxia during knee surgery
CASE CONTINUED
On arrival at the PACU, our patient’s oxygen saturation was 94% while he was breathing oxygen via a simple face mask at a flow rate of 10 L/min. His heart rate was 60 bpm, blood pressure 110/60 mm Hg, and temperature 37.5°C (96.3°F). Chest sounds were normal on auscultation.
However, 3 hours later, his mental status rapidly deteriorated. He was oriented only to person, and he was drowsy. He had escalating respiratory distress with a rapid respiratory rate and decreasing oxygen saturation. At this point, auscultation of his chest wall revealed bilateral crackles and rales.
He was promptly intubated. Profuse fluid and secretions were noted to be coming from his lungs, filling the endotracheal tube. Arterial blood gas measurement showed a pH of 7.22, Pao2 64 mm Hg, and Paco2 56 mm Hg on 100% fraction of inspired oxygen, with no increased anion gap.
2. Which consequence of fat embolism is most likely at this time in this patient?
- Coexisting sepsis
- Fat embolism syndrome
- Acute cardioembolic stroke
- Anaphylaxis
Fat embolism syndrome should be highly suspected in this patient. As mentioned, it can affect many different organs. It is the most serious condition resulting from fat embolization after surgery or trauma.
Sepsis was unlikely in our patient, since he presented for his surgery in good health and with no preexisting signs or symptoms of infection. Acute cardioembolic stroke could have caused the neurologic signs, but this would not necessarily explain the coexisting hypoxia. An anaphylactic reaction to drugs or surgical cement would most likely present intraoperatively, shortly after exposure occurred, rather than several hours after surgery.
How common is fat embolism syndrome?
The occurrence rate of fat embolism syndrome has been reported to be 0.25% to 30% after multiple fractures and 0.1% to 12% after knee and hip joint surgery, with a mortality rate of 13% to 36%.2,9–14 The rate of occurrence after unilateral total knee joint replacement has been reported to be 1.8% to 5%, and 4% to 12% after bilateral total knee replacement.15–19
The syndrome is relatively more common with traumatic fractures of the lower extremities. However, it has also been reported with liposuction, total parenteral nutrition, bone marrow harvest and transplantation, burns, and acute pancreatitis, to mention a few.10
The broad range of reported incidence rates can be attributed to the fact that many studies were in patients with multiple trauma, whose concomitant injuries may have made it difficult to clearly define the contribution of fat embolism syndrome to the overall rates of morbidity and mortality. Also, different studies used different criteria to define the syndrome.
How does fat embolism syndrome occur?
Two hypotheses for how this syndrome occurs were proposed nearly a century ago.20,21
The “mechanical” theory is that fat emboli are formed as a result of trauma and disruption of adipose tissue and other cells in the bone marrow. Increases in intramedullary pressure force the fat emboli through damaged medullary venous channels in the bone and into the circulation of the lower extremities. This embolization of fat causes an initial mechanical pulmonary obstruction. Mechanical obstruction by fat emboli in the pulmonary system leads to increased pulmonary pressures and an increase in right heart outflow pressure. The right heart becomes strained, leading to a decreased right-sided cardiac output. As a result, the left heart filling pressures diminish and hypotension ensues.20
The “biochemical” theory, on the other hand, is that chylomicrons within the vascular system are modified and their stability is compromised as a result of stress. These traumatized chylomicrons then coalesce to form droplets of fat that accumulate in the pulmonary circulation and produce a mechanical obstruction. This would explain why nontraumatic, nonorthopedic insults can produce this syndrome.
Autopsy studies show that there is little correlation between the presence and quantity of intravascular fat and the severity of clinical symptoms, thus implying that the syndrome is caused by more than just mechanical obstruction. The biochemical theory postulates that fat globules within the circulatory system then cause the release of lipase from the pulmonary alveolar cells, which then hydrolyses the fat into free fatty acids. These free fatty acids cause an inflammatory reaction, complementmediated leukocyte aggregation, chemotoxin release, and subsequently endothelial damage. These vasoactive substances damage type 2 pneumocytes and lead to an increased permeability of the pulmonary capillary beds. Acute respiratory distress syndrome (ARDS) may ensue. Disseminated intravascular coagulation may occur as a result of the formation of microthrombi involving lipids, platelets, and fibrin.21,22
Embolization of fat to the central nervous system can occur as fat globules cross into the systemic circulation via a patent foramen ovale, an atrioventricular shunt, or the pulmonary capillaries. This can then result in cerebral ischemia.23
Although patent foramen ovale may seem the most direct route for cerebral embolization, the neurologic impairment and signs of cerebral emboli in fat embolism syndrome may occur in the absence of patent foramen ovale.24,25 The fat globules may actually go through the lung capillaries, being flexible and forced through by increased pulmonary pressure.
But whether the cause of fat embolism syndrome is occlusion by globules, the release of biochemical mediators, or a combination of both is unknown. Both mechanisms are likely responsible. We can only suspect that the degree of fat load and intrinsic metabolic differences between individuals account for the variation in susceptibility.
