VENOUS air embolism (VAE) has been reported in a wide variety of procedures. In most cases, signs of clinically significant VAE are present soon after the entry of air into the circulation. We present a case of urologic surgery in which no signs of VAE were recognized during surgery, but circulatory collapse occurred when the patient was transferred from the operating room bed to the transport stretcher. The presumptive diagnosis of VAE as the cause of circulatory collapse was made on aspiration of frothy blood from the central venous pressure (CVP) catheter and was confirmed with the immediate placement of a transesophageal echocardiography (TEE) probe.

A 72-yr-old man was diagnosed with high-grade transitional cell carcinoma of the bladder after a radical prostatectomy in 1993 for prostate carcinoma. He was scheduled to undergo radical cystectomy and formation of ileal conduits. The patient had a history of hypertension but was not taking medication. He had no history of coronary artery disease. Although he had a 22–pack/year history of smoking, he had ceased smoking 28 yr previously. He had undergone an uneventful right inguinal herniorrhaphy 9 months previously.

Intravenous, arterial, and lumbar epidural catheters were placed preoperatively. Standard monitoring was used, including continuous end-tidal carbon dioxide monitoring and an esophageal stethoscope. A CVP catheter was inserted into the right internal jugular vein after induction of general anesthesia. The patient was positioned supine in the low lithotomy position with a slight Trendelenburg tilt.

Anesthesia was maintained with sevoflurane and nitrous oxide in 42% oxygen, and continuous infusion of 0.0625% bupivacaine with 40 μg/ml morphine into the epidural catheter. Vecuronium was used for muscle relaxation, and the lungs were mechanically ventilated. Surgical dissection was tedious and difficult because of dense adhesions from previous extensive surgery. The total estimated blood loss was 3.2 l, with a brief period of brisk blood loss associated with inadvertent division of the right external iliac vein at 2.5–3 h after the start of surgery. During this time, there were no notable changes in end tidal carbon dioxide, CVP, cardiac rhythm, or heart sounds, and a decrease in blood pressure was minimized by administration of blood and crystalloid. Peak airway pressures were constant throughout the procedure at 25 cm H2O. Total fluid replacement was 6.7 l, which included 4 units of erythrocytes, resulting in a hematocrit of 37% and a CVP of 9 mmHg at the end of surgery. The duration of surgery was 7 h.

At the conclusion of surgery, the patient was responsive to commands and breathing spontaneously through the endotracheal tube. Blood pressure was stable at 100/60 (mean 75) mmHg, and heart rate was 62 beats/min. The monitors were temporarily disconnected to move the patient to a stretcher for transfer to the postanesthesia care unit. After the patient was moved, he was noted to be unresponsive and pulseless. The monitors were reconnected. Blood pressure was not recordable, and electrocardiogram rhythm was documented as showing ventricular fibrillation.

Cardiopulmonary resuscitation was commenced immediately with 100% oxygen and manual ventilation via  the endotracheal tube. Circulatory support was achieved with chest compressions and epinephrine. Although sinus rhythm was restored within 4 min, ongoing treatment with epinephrine, bicarbonate, and calcium chloride was required.

The differential diagnosis included VAE, pulmonary embolism, a primary cardiac event, tension pneumothorax, respiratory insufficiency, or intraabdominal hemorrhage. Breath sounds were audible bilaterally. The electrocardiogram monitor showed sinus tachycardia and did not suggest acute myocardial infarction. Aspiration of the CVP catheter within the first few minutes of resuscitation yielded 10–20 ml frothy blood. A working diagnosis of VAE was made. A TEE probe inserted 15 min after resuscitation revealed a stream of bubbles in all four chambers of the heart. Repeated attempts to aspirate additional air from the CVP catheter were unsuccessful.

Heart rate, rhythm, and blood pressure normalized 25 min after resuscitation began, and epinephrine was discontinued. Continued TEE monitoring showed gradual resolution of the bubble stream over the same interval. Chest radiograph and fiberoptic bronchoscopy performed during the stabilization period were unremarkable. The patient was transferred to the intensive care unit 45 min after onset of cardiovascular collapse.

The patient required interim ventilatory and inotropic support for adult respiratory distress syndrome. A primary cardiac event was ruled out with further evaluation. A computed tomograph of the head on the second postoperative day revealed no abnormality, and there was no clinical evidence of neurologic deficit after sedation was discontinued. The patient improved and was discharged home 10 days after the event.

Venous air embolism has been documented in association with several urologic procedures. These include transvesical, 1transurethral, 2,3radical retropubic, 4and radical perineal 5prostatectomies. Venous air embolism has also occurred during retrograde pyelography, 6the use of lasers for urethral surgery, 7and percutaneous ultrasonic lithotripsy. 8We report a patient undergoing radical cystectomy with ileal conduit urinary diversion urologic surgery in which no signs of VAE were recognized during surgery, but circulatory collapse occurred when the patient was transferred from the operating room bed to the transport stretcher.

Venous air embolism occurs when air enters the right side of the heart by entrainment from negative intrathoracic venous pressure or by being pushed into an open venous channel by positive pressure. The patient was positioned supine in the low lithotomy position with slight Trendelenburg tilt. Extensive previous surgery caused dense adhesions and difficulty for the surgeon in identifying normal tissue planes and in performing the required dissection for the current procedure. The total blood loss for the procedure was approximately 3 l. Most of this occurred during the first 4 h of the procedure. This correlates temporally with the dissection. The patient's position, volume status, and open pelvic veins were favorable conditions for air to enter the venous system, which most likely occurred at 2.5–3 h after the start of surgery. The use of nitrous oxide may have contributed to the size of the bubbles that accumulated in the pelvic veins.

The mechanism of air entrainment into the right side of the heart manifested by circulatory collapse of this patient occurred at 4.5 h subsequent to the presumed time of entry of air into the venous system. We propose that accumulated air in the pelvic venous system may have been entrained into the right side of the heart during spontaneous ventilation when the patient was taken out of the lithotomy position for transfer to the stretcher. The possible formation of an air lock in the right side of the heart may have resulted in obstruction to cardiac output. A similarly delayed, but fatal presentation of air embolism has been described during transurethral resection of the prostate under spinal anesthetic. 3In that case, although the mechanism for the presence of intravenous air was different, the patient's cardiac arrest occurred only after his legs were lowered from the lithotomy position at the completion of the surgical procedure. A report of fatal air embolism during radical retropubic prostatectomy 4also describes the onset of hemodynamic instability consistent with VAE after the pelvic dissection had been completed and during the relatively quiescent period of bladder neck reconstruction.

The presence of air in all four chambers of the heart as seen with TEE in this patient is consistent with transpulmonary passage of air emboli. The differential diagnosis includes patent foramen ovale, which clearly cannot be ruled out during resuscitation. The continuing presence of air emboli in the left-sided cardiac chambers from transpulmonary passage has been demonstrated to persist for 15 min after the cessation of venous air entrainment and clearing of the right atrium and ventricle of any air in the absence of intracardiac shunt. 9,10TEE is the most sensitive method for detection of intracardiac air and can detect bubbles of 5–10 μm in diameter. However, it is not possible to quantify the amount of air seen, and the clinical significance of such small bubbles is not known. 10 

In the current case, a computed tomograph of the head obtained on the second postoperative day did not reveal any intracranial air. Had air been present, treatment with hyperbaric oxygen could have been considered. However, it is unlikely that such treatment begun on the second postoperative day would improve the quality of neurologic outcome.

It is a concern that the risk of VAE is present in urologic surgery when a gravitational gradient is introduced with lithotomy positions and a degree of Trendelenburg tilt. Procedures requiring these positions include transvesical, transurethral, radical retropubic, and radical perineal prostatectomies and radical cystectomy. All these procedures are also associated with blood loss from vascular surgical fields, resulting in an increased risk for VAE. Anesthesiologists should be aware of the range in temporal association of surgical events and the manifestation of signs of VAE and should monitor patients accordingly. In particular, monitoring should continue during repositioning of the patient at the end of surgery and should only be briefly interrupted, if at all, during transfer of the patient from the operating table to the transport stretcher.

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