The air in the right atrium and ventricle cleared within 20 min (Fig. 2B). The patient's clinical condition improved during this period. The left external jugular line was removed. A left internal jugular 7F triple-lumen catheter was placed for access. The patient was transferred to the intensive care unit (ICU) in stable condition.
Initial assessment in the ICU included arterial blood gas analysis and chest radiograph. The patient's clinical picture was consistent with adult respiratory distress syndrome (ARDS). The patient required urgent cardioversion for atrial fibrillation with a rapid ventricular response within 4 h of arrival in the ICU. Subsequent electrocardiogram and troponin and creatine phosphokinase-MB levels were consistent with subendocardial myocardial infarction. Transthoracic echocardiogram was notable for the absence of regional wall motion abnormalities and preserved left ventricular systolic function. The patient's respiratory status required mechanical ventilation with positive end-expiratory pressure (no more than 10 cm H2O) but improved over a 72-h interval. He was tracheally extubated on postoperative Day 3. Neurologic examination was normal.
The patient was discharged from the hospital on postoperative Day 7 without functional impairment. He was voiding without difficulty 1 yr after discharge and has had no long-term sequelae as result of the air embolism.
Passive VAE has been described in various clinical scenarios in the operating room (OR). VAE can occur whenever the heart is below the level of the surgical field. Air can be passively drawn into an open, noncollapsible vein by the negative intrathoracic venous pressure (4). Use of the low lithotomy position with the head positioned below the level of the prostate, bladder, or bladder neck is sufficient to create the required gradient to increase the risk of passive VAE.
In addition to passive movement of air into an open venous system, active VAE can occur when air is forced into an open venous channel (2,5). Use of the Ellik evacuator to rinse the bladder or irrigation of a three-way Foley catheter with an air/fluid filled syringe (1,2) can introduce air under pressure into the open venous sinuses of the prostate. There are no published reports of VAE in transurethral surgery associated with the use of an irrigation pump system. In the present case, an unknown quantity of air was pumped into the bladder over a period of 15–30 seconds. This occurred because the waste and patient lines were reversed during reassembly of the resectoscope circuit and drainage equipment once bleeding from the prostatic fossa was suspected.
The manufacturer labels the pump assembly with (a) arrows indicating the correct direction of flow and (b) warnings to “Follow flow path” and “Do not pump into patient.” The irrigation system is designed to drain fluid from the resectoscope via a continuous roller pump system. This pump system is calibrated to drain 750–800 mL/min at the setting used during transurethral surgery. The waste line is connected from the resectoscope to either a central drain in the floor of the OR or to a large container. If the lines are connected incorrectly, as occurred in the present case, air can be pumped from the drain or container through the resectoscope and into the patient. We have since modified the irrigation pump so that the inflow and waste portions of the pump are fitted with connections of different sizes. These size differences prevent improper connection of the inflow and outflow tubing. In addition, we have placed photo enlargements of the proper assembly in the appropriate locations in the ORs dedicated to urology. The use of color-coded inflow and outflow pump connections and tubing is an alternative solution.
The factors that influence morbidity and mortality of VAE include rate of entrainment, volume of air entrained, position of patient during the event, and cardiac status of the patient (6). The lethal volume of IV air in humans is estimated to be between 200 and 300 mL (7). There is no way to quantify the amount of air that our patient received. However, as calibrated, the irrigation system could have rapidly delivered as much as 200–400 mL during the 15- to 30-second episode. Air was present on the right side of the heart for approximately 20 minutes. The air was probably reabsorbed at the alveolar-capillary interface (8). We did not detect air in the left heart, suggesting that the patient had neither a patent foramen ovale nor transpulmonary passage of air.
The patient developed a clinical picture consistent with ARDS. This is a known complication of VAE (9). The shock state caused by acute right ventricular outflow tract obstruction and obstruction of the pulmonary arterioles by the air microemboli may cause activation of polymorphonuclear leukocytes, liberation of chemical mediators, and capillary injury, leading to ARDS (9).
In conclusion, we present a case of nonfatal VAE during TURP under combined spinal-general anesthesia. The source of the air was an improperly assembled irrigation system. This incorrect assembly caused air to be pumped from an open drain through the resectoscope into the bladder. Anesthesiologists and urologists should be aware of this potential complication.
1. Hofsess DW. Fatal air embolism during transurethral resection. J Urol 1984;131:355.
2. Vacanti CA, Lodhia KL. Fatal massive air embolism during transurethral resection of the prostate. Anesthesiology 1991;74:186–7.
3. Tsou MY, Teng YH, Chow LH, et al. Fatal gas embolism during transurethral incision of the bladder neck under spinal anesthesia. Anesth Analg 2003;97:1833–4.
4. Faberowski LW, Black S, Mickle JP. Incidence of venous air embolism during craniectomy for craniosynostosis repair. Anesthesiology 2000;92:20–3.
5. Nowitz A, ArtRu AA. Air embolism during radical cystectomy with ileal conduit urinary diversion. Anesthesiology 2002;96:506–8.
6. Durant TM, Long J, Oppenheimer MJ. Pulmonary (venous) air embolism. Am Heart J 1947;33:269–81.
7. Toung TJK, Rossberg MI, Hutchins GM. Volume of air in a lethal venous air embolism. Anesthesiology 2001;94:360–1.
8. Presson RG, Kirk KR, Haselby KA, et al. Fate of air emboli in the pulmonary circulation. J Appl Physiol 1989;67:1898–902.
© 2004 International Anesthesia Research Society
9. Verstappen FT, Bernards JA, Kreuzer F. Effects of pulmonary gas embolism on circulation and respiration in the dog. IV. Origin of arterial hypoxemia during pulmonary gas embolism. Pflugers Arch 1977;370:71–5.