Sudden hypoxia during knee surgery

A 75-year-old man with type 2 diabetes and hypothyroidism underwent bilateral total knee replacement at our hospital.

His functional capacity had been moderately limited by knee pain, but he could easily climb one flight of stairs without symptoms. His medications at that time included levothyroxine (Synthroid) and metformin (Glucophage). He had no known cardiac or pulmonary disease. The preoperative evaluation, including laboratory tests and electrocardiography, was within normal limits.

Spinal anesthesia was used for surgery, and he was given 2 mg of midazolam (Versed) intravenously for sedation. No additional sedation was given. He was given oxygen via nasal cannula at 2 L/min.

All vital signs were stable at the start of the procedure. However, about halfway through, when the thigh tourniquet was released, his oxygen saturation dropped abruptly from 100% to 92%. All other vital signs remained stable, and he was asymptomatic, was oriented to person, time, and place, was conversing freely, and was in no distress. The oxygen flow was increased to 6 L/min, his oxygen saturation improved, and the procedure was then completed as planned.

At the conclusion of the surgery, before the patient was transported to the postanesthesia care unit (PACU) and while his oxygen flow rate was still 6 L/min, his oxygen saturation again dropped to 92%. A simple face mask was placed, and the oxygen flow rate was increased to 10 L/min. His oxygen saturation stayed low, near 90%.

Bleeding during surgery had been nominal. He had received 2 L of lactated Ringer’s solution and 500 mL of hetastarch (Hextend) during surgery. He continued to be asymptomatic in the PACU.

1. What is the most likely cause of oxygen desaturation during bilateral total knee arthroplasty?

• Fat embolism
• Intraoperative pneumonia
• Venous thromboembolism with pulmonary embolism
• Acute myocardial infarction
• Acute pulmonary edema
• Excessive sedation

The differential diagnosis of oxygen desaturation during orthopedic procedures is listed in Table 1.

Fat embolism is the most likely cause, particularly given the greater fatty embolic load that occurs with bilateral total knee arthroplasty than with unilateral total knee arthroplasty.

At what point the maximal showering of fat emboli occurs is not known. Fat may be released into the circulation with pressurization of the medullary canal during surgery or with manipulation of a fracture. The emboli may collect in the leg veins and then be released in a shower when the thigh tourniquet is released. Vasoactive mediators and methylmethacrylate cement released into the circulatory system after tourniquet deflation may also cause vasodilation, hypotension, and increased dead-space ventilation, resulting in hypoxia and a drop in end-tidal CO₂.

Pneumonia during surgery is rare without an apparent aspiration event.

Venous thromboembolism is possible but is more likely later in the postoperative period after major orthopedic surgery.

Acute myocardial infarction could present with hypoxia, particularly in a diabetic patient, who may not experience chest pain. However, intraoperative electrocardiographic changes would likely be seen. If myocardial infarction is suspected, postoperative serial electrocardiograms and measuring troponin and cardiac enzyme levels aid in the diagnosis.

Acute pulmonary edema is possible but not as highly suspected, as the patient had no history of congestive heart failure and received an appropriate amount of fluid for this type of surgery.

Excessive sedation could cause hypoventilation and, thus, oxygen desaturatation. However, this patient’s oxygen desaturatation began more than an hour after the midazolam was given. Midazolam is a short-acting benzodiazepine. It is unlikely that the patient would show signs of hypoventilation and oversedation an hour after the drug was given. Our patient also did not show any signs of excessive sedation, as he was awake and conversing during the surgery.

Fat emboli vs fat embolism syndrome

Fat embolism is the presence of fat drops within the systemic and pulmonary microcirculation, with or without clinical sequelae.¹ Fat embolism syndrome, on the other hand, is defined as injury to and dysfunction of one or more organs as a result of the embolization of fat, usually within 24 hours of injury or orthopedic surgery.²

Fat embolism syndrome is an unpredictable condition with a varied presentation. Fat droplets are thought to embolize via the venous circulation into the pulmonary arteries, occluding small blood vessels in the lung. However, they also get into the arterial circulation and occlude arteries in the brain, kidney, heart, and liver (more on this phenomenon below).

Fat embolism is reported to originate primarily from fractures of the femur, tibia, and pelvis.^2,3 As many as 90% of trauma patients have been shown to have evidence of fat embolism on autopsy.⁴ However, only a small number of patients develop the classic fat embolism syndrome,^2,3,5 Why some develop the syndrome and others do not is still unknown.

Orthopedic procedures associated with fat embolization include knee arthroplasty and hip arthroplasty, particularly if it involves intramedullary manipulation or medullary fixation.⁶ It has also been reported during spinal procedures in which pedicular screws are used.⁷ The syndrome occurs in 0.25% to 30% of patients following multiple fractures and in 0.1% to 12% of patients during or following knee or hip arthroplasty.

One study⁸ showed evidence of fat on transesophageal echocardiography in 88% of patients undergoing medullary reaming of lower-extremity fractures and hip hemiarthroplasty. Blood sampling from the right atrium confirmed that fat was responsible for the echocardiographic abnormalities. The study also showed that the severity of the embolic showering correlated with the severity of hypoxia and the decrease in end-tidal CO₂.⁸