Vol. 19, No. 7 thrombosis and not readily explained by pannus ingrowth. In a series of surgically removed prosthetic heart valves, Schoen (6) reported that tissue in- growth was not a cause of valve failure in any of 112 bioprosthetic valves, but accounted for 20% of the failures in 45 mechanical prosthetic valves. Nonethe- less, tissue ingrowth is a differential diagnostic consideration. Prosthetic mitral valves, particularly mechanical valves, have a high rate of thrombotic complications. Current practice is to anticoagulate all mechanical and most mitral bioprosthesis patients (7). Patients with thrombosis ofa mitral prosthesis generally have 1 to 3 days of orthopnea followed by congestive heart failure (8). Rapid clinical deterioration requires ur- gent valve debridement and atrial thrombectomy (9). Fibrinolytic therapy can be effective for treatment of late thromboses of prosthetic valves, but risk of systemic embolization is reportedly as high as 18% (10). The superior ability of transesophageal echocardiography to clarify prosthetic morphologic changes and to detect thrombus in the left atrial appendage may ultimately allow safer use of such therapy. However, a clinical element to the echo diagnosis of prosthetic thrombus is necessary. Transesophageal echocardiography should be used early in the assessment of suspected prosthetic valve CatHeTer-AssociaTeD Ain EMBOLISM 981 abnormalities to identify the cause and allow possible intervention directed toward prevention of additional sequelae. REFERENCES 1. Pearson AC, Castello R, Labovitz AJ: Safety and utility of transesophageal echocardiography in the critically ill patient. Am Heart J 1990; 119:1083 2. Daniel WG, Nellessen U, Schréder E, et al: Left atrial sponta- neous echo contrast in mitral valve disease: An indicator for an increased thromboembolicrisk. / Am Coll Cardiol 1988; 11:1204 3. Alam M, Rosman HS, Lakier JB, et al: Doppler and echocardiographic features of normal and dysfunctioning pros- thetic valves. J Am Coll Cardiol 1987; 10:851 4. Goldman ME, Mindich BP: Intraoperative two-dimensional echocardiography: New application of an old technique. J Am Coli Cardiol 1986; 7:374 5. Seward JB, Khandheria BK, Oh JK, et al: Transesophageal echocardiography: Technique, anatomical correlations, imple- mentations, and clinical applications. Mayo Clin Proc 1983; 63:649 6. Schoen FJ: Surgical pathology of removed natural and pros- thetic heart valves. Hum Pathol 1987; 18:555 7. Stein B, Fuster V, Halperin JL, et al: Anti-thrombotic therapy in cardiac disease: An emerging approach based on pathogen- esis and risk. Circulation 1989; 80:1501 8. Copans H, Lakier JB, Kinsely RH, et al: Thrombosed Bjork- Shiley prostheses. Circulation 1980; 61:169 9. Alvarez A, Ayuso L, Juffe A, et al: Thrombectomy: Surgical treatment of the thrombosed Bjork-Shiley prosthesis. J Thorac Cardiovasc Surg 1982; 84:906 10. Graver LM, Gelber PM, Tyras DH: The risks and benefits of thrombolytic therapy in acute aortic and mitral prosthetic valve dysfunction: Report ofa case and review of the literature. Ann Thorac Surg 1988; 48:85 Cerebral air embolism during removal of a pulmonary artery catheter SREENIVASA S. MOORTHY, MD, FCCM; KAREN A. TISINAI, MD; BERNADETTE S. SPEISER, BSN, CCRN; DOLORES F. CIKRIT, MD; STEPHEN F. DIERDORF, MD Monitoring of cardiovascular function by pulmo- nary artery catheter provides an important source of information to assist in the proper management of critically ill patients (1). There are a number of reported complications, both immediate and late, associated with the use of the pulmonary artery catheter (2). The most important complications are From the Department of Anesthesiology, Richard L. Roudebush VA Medical Center, Indianapolis, IN. Address requests for reprints to: Dr. S. S. Moorthy, Department of Anesthesiology, Richard L. Roudebush VA Medical Center, 1481 West Tenth Street, Indianapolis, IN 46202. Key Words: embolism; catheterization, pulmonary artery; foramen ovale; ventilation, mechanical; tachycardia; hemiplegia; air embolism; echocardiography; critical care; cerebrovascular accident venous air embolism, carotid artery puncture, cardiac dysrhythmias, pulmonary artery rupture, pulmonary infarction, and infection. Complications can occur during removal of the pulmonary artery catheter. These complications include: inability to remove the catheter, cardiac dysrhythmias, and ve- nous air embolism. The following case illustrates the occurrence of venous air embolism leading to paradoxical air embolism during the removal of a pulmonary artery catheter. CASE REPORT A 66-yr-old, 65-kg male with diabetes mellitus, occlusive peripheral vascular disease, coronary artery disease, left renal artery stenosis, hypertension, and cre- scendo claudication of the lower extremities underwent a 982 Critica Care MEbIcINE left femoral to posterior tibial artery saphenous vein bypass graft procedure. A general anesthetic was per- formed with the administration of isoflurane, nitrous oxide, and fentanyl. Intraoperative monitors included a continuous ECG, radial arterial catheter, capnograph, pulse oximeter, and pulmonary artery catheter inserted via the right internal jugular vein. Anesthesia and surgery were uneventful. After surgery, the patient was mechani- cally ventilated in the surgical ICU. Over the next 48 hrs, the patient was weaned from mechanical ventilation and the endotracheal tube was removed after it was deter- mined that normal arterial blood gas values could be maintained with room air. After extubation, the patient was alert with normal neurologic function. The pulmonary artery catheter was removed with the patient ina 15° head- up position. During obturator placement after catheter removal from the insertion sheath, there was bleeding from the junction of the side-port valve and the sheath. In an attempt to seal the leak, the port assembly was tight- ened and an obturator inserted into the sheath. During this procedure the patient became agitated, confused, hypertensive, and developed ventricular tachycardia that resolved within 1 min. The patient became unresponsive with conjugate movement of the eyes to the right and seizures involving the left side of the body. Diazepam (5 mg) iv, supplemental oxygen, and an iv nitroprusside infusion were administered. Fifty minutes after this event, a CT scan of the brain showed air bubbles in the cerebral circulation (Fig. 1), The patient improved over the next 48 hrs with increased responsiveness and a more alert sensorium, including proper verbal response. However, he continued to have periods of confusion and a persistent left hemiplegia. A contrast echocardiogram was performed, but no right-to-left intracardiac shunt could be demon- strated. Although he continued to improve clinically, he still has residual left hemiparesis. Four months after the episode, the patient is able to talk and walk with support. Figure 1. CT scan of the brain showing multiple air bubbles in the cerebral circulation (arrows) 50 mins after removal of the pulmonary artery catheter and development of acute neurologic signs. duty, 1991 DISCUSSION We are reporting this case because of the neuro- logic symptoms associated with the radiologically proved cerebral air embolism that occurred after removal of the pulmonary artery catheter, despite the lack of demonstrable intracardiac shunt. Venous air embolism has been reported to occur via a mal- functioning valve on the side-port assembly (3). Ve- nous air embolism is a potentially important compli- cation during central venous cannulation. The signs and symptoms of venous air embolism depend on the amount of air entering the circulation. Small quan- tities of air may produce no signs while large quanti- ties of air may produce increased central venous and pulmonary artery pressures, right ventricular fail- ure, hypotension, and death. Paradoxical air embolism can occur from venous air embolism, although there is usually an intracar- diac defect or a patent foramen ovale. A probe patent foramen ovale can be present in nearly 25% to 30% of the population with no history of cardiac disease (4). A patent foramen ovale can open or close depending on the pressure differential between right and left atria. When the right atrial pressure exceeds the left atrial pressure, as in pulmonary embolism, pulmo- nary hypertension, and right ventricular failure, a right-to-left shunt can result through a patent fora- men ovale. Consequently, demonstration of a patent foramen ovale will depend on the dynamic conditions present at the time of the study. The absence of a demonstrable shunt in our patient does not exclude the possibility of a patent foramen ovale. The transesophageal echocardiogram can also help detect paradoxical air embolism (5). Paradoxical air embo- lism can occur without an intracardiac shunt (6, 7). The air can pass through the pulmonary arterial system to the systemic arterial system through con- genital (8) or acquired (e.g., hepatic disease) (9, 10) arteriovenous communications in the lungs. How- ever, in most of these reports, the air bubbles associ- ated with the neurologic signs were not seen, but autopsy studies concluded that the pathologic changes were secondary to air embolism. Generally, pulmo- nary arteriovenous communications produce hypox- emia with resultant cyanosis and finger clubbing. Our patient did not show any evidence of pulmonary arteriovenous communication or hepatic disease. The amount of time required for clearance of air bubbles from the cerebral circulation is not known. Air bubbles were seen within 50 mins of the event in our patient. Autopsy studies in a report (9) demon- strated air in the cerebral vessels 2 days after occur- rence ina patient after liver transplantation. Air can also localize in the pulmonary circulation and serve Vol. 19, No. 7 as a reservoir for repeated systemic air embolism over a long period of time. The ventricular tachycardia in our patient could have been secondary to coronary artery air embo- lism, although there were no detectable ST-T wave changes. In conclusion, we report a patient who developed paradoxical air embolism with neurologic dysfunc- tion during removal of a pulmonary artery catheter. We were able to demonstrate air in the cerebral circulation by CT scan. We recommend meticulous care when removing pulmonary artery catheters, including checking for duckbill valve competence, loose connection of the side port to the sheath, and open ports. The head-up position should be avoided when removing pulmonary artery catheters. REFERENCES 1. Swan HJC, Ganz W, Forrester JS, et al: Catheterization of the heart in a man with the use of a flow directed balloon tipped catheter. N Engl J Med 1970; 283:447 AMINOPHYLLINE AND NEUROMUSCULAR BLOCKADE 983 2. Grum CM, Reynolds, AC: Perils and pitfalls of pulmonary artery catheters. Anesth Rev 1985; 12:46 3. Conahan TJ, Barberii JK, Calkins JM: Valve competence in pulmonary artery catheter introducers. Anesthesiology 1983; 58:189 4. Hagen PT, Scholz DG, Edwards WD: Incidence and size of patent foramen ovale during the first ten decades of life: An autopsy study of 965 hearts. Mayo Clin Proc 1984; 59:17 5. Black S, Muzzi DA, Nishimura RA, et al: Preoperative and intraoperative echocardiography to detect right to left shunts in patients undergoing neurosurgical procedures in the sitting position. Anesthesiology 1990; 72:436 6. Marquez J, Sladen A, Grendell H, et al: Paradoxical cerebral air embolism without an intracardiac septal defect. J Neurosurg 1981; 55:997 7. Gottdiener JS, Papademetriou V, Natargiocomo A, et al: Inci- dence and cardiac effects of systemic venous air embolism. Arch Intern Med 1988; 148:795 8. Nadas AS, Fyler DC: Pediatric Cardiology. Third Edition. Philadelphia, WB Saunders, 1972, p 413 9. Mazzoni G, Koep L, Starzl T: Air embolus in liver transplan- tation. Transplant Proc 1979; 11:267 10. Krowka MJ, Tajik J, Dickson ER, et al: Intrapulmonary vascular dilatations (IPVD) in liver transplant candidates. Chest 1990; 97:1165 Aminophylline antagonizes the neuromuscular blockade of pancuronium but not vecuronium JOHN A. DALLER, MD; BRIAN ERSTAD, PuarmD; LUIS ROSADO, MD; CHARLES OTTO, MD; CHARLES W. PUTNAM, MD Theophylline antagonizes nondepolarizing neuro- muscular blockade in animals (1, 2) and has been anecdotally noted to do so in man (3, 4). However, the two patients reported (3, 4) had both received hydro- cortisone, which has also been implicated in the antagonism of neuromuscular blockade (5). Herein, we report a patient not receiving other potentially antagonistic drugs in whom aminophylline caused resistance to neuromuscular blockade by pancuronium. Subsequently, successful blockade was achieved with the administration of vecuronium. From the Departments of Surgery (Drs. Daller, Rosado, and Putnam), Anesthesiology (Dr. Otto), and Pharmacy (Dr. Erstad), University of Arizona, Tucson, AZ. This study was supported, in part, by Veterans Administration merit review grant 003 (Dr. Putnam). Address requests for reprints to: John A. Daller, MD, Department of Surgery, College of Medicine, University of Arizona Health Science Center, 1501 N. Campbell Avenue, Tucson, AZ 85724. Key Words: aminophylline; pancuronium; vecuronium; antagonists; neuromuscular blocking agents; critical care; phosphodiesterase inhibitors; paralysis; theophylline CASE REPORT A 48-year-old white male weighing 82.3 kg was admit- ted for exploratory thoracotomy and pneumonectomy after the discovery of a mediastinal mass on a routine chest radiograph in July 1989. Before admission, a biopsy taken at mediastinoscopy demonstrated undifferentiated large- cell cancer. A metastatic “work-up” was negative. Two months before hospitalization, the patient received chemo- therapy consisting of cisplatin and VP-16 with chest and brain irradiation (45 Gy in 25 treatments over 35 days). Throughout his treatment course, the patient did not have any constitutional symptoms. Past medical history was not contributory. Family history was important only for several family members with other types of cancer. The patient was a 30 “pack-yr” cigarette smoker but had stopped for several years. He had no allergies and was taking no medications at the time of admission. Physical examination was exceptional only fora BP of 98/80 mm Hg. Preoperative laboratory studies showed a hematocrit of 34% and room air arterial blood gases of pH 7.42, Paco, 40.5 torr (5.4 kPa), Pao, 77.0 torr (10.2 kPa), ionized bicarbon- ate 26.5 mmol/L, and a hemoglobin saturation of 93.8%. The patient underwent a right posterolateral thoracotomy and pneumonectomy with mediastinal node