Cerebral Air Embolism Complicating Transbronchoscopic Lung Biopsy ALLAN D. ERICKSON, M.D.; RICHARD S. IRWIN, M.D.; CARL TEPLITZ, M.D.; WILLIAM M. CORRAO, M.D.; and JOSEPH T. TARPEY, M.D. Veterans Administration Medical Center, Rhode Island Hospital, and Brown University; Providence, Rhode Island A L T H O U G H transbronchoscopic lung biopsy generally causes little morbidity, life-threatening c o m p l i c a t i o n s have been noted (1). Cerebral air e m b o l i s m , not previously reported, is described here. A 48-year-old man with known alcoholic liver disease and chronic bronchitis was admitted with increasing weakness and shortness of breath of 2 weeks' duration. At physical examination, his oral temperature was 38.3 °C and respirations 24/min. Jaundice and scattered wheezes were noted bilaterally. Hematocrit was 33% and leukocyte count 5400/mm'. Arterial Po ; was 59 torr and Pco, 26 torr (room air). Chest roentgenogram showed diffuse, uniform, finely nodular infiltrates. Skin test with intermediate strength tuberculin (purified protein derivative) was negative at 48 h; skin test with streptokinase-streptodornase was positive. Routine blood and urine cultures were negative, as were acid-fast and cytologic smears of sputum. Bone marrow biopsy showed no granulomas, acid-fast organisms, or tumor. The patient was started on isoniazid, rifampin, and streptomycin therapy. Since no firm diagnosis had been established by the 10th hospital day and some observers thought the patient's condition was deteriorating, other causes of diffuse, nodular infiltration were considered in addition to tuberculosis. Platelet count and prothrombin and partial thromboplastin times were normal. With oxygen delivered by nasal cannula, Po 2 was 70 torr. The patient was sedated with 5 mg of intravenous diazepam. With electrocardiographic and fluoroscopic monitoring, flexible fiberoptic transbronchoscopic lung biopsy was done according to the method of Zavala (2). The biopsy forceps (2-mm Olympus # F B - 1 C ; Olympus Corporation of America, New Hyde Park, New York) were passed into the right lateral basilar segment. At the end of the patient's exhalation, with the bronchoscope wedged to control any potential hemorrhage (3), the forceps were closed and withdrawn. No more than 240 mg of lidocaine had been used to anesthetize the respiratory tract. At no time did the supine, spontaneously breathing patient cough, forcefully exhale, or perform a Valsalva maneuver. About 10 s after removal of the forceps, the patient had a grand mal seizure and a respiratory arrest. Heart rate fell to 50/min. The bronchoscope was immediately withdrawn and endotracheal intubation accomplished. Although spontaneous respirations resumed within minutes and the patient developed a tachycardia, he was noted to be comatose, flaccid, and to have bilateral Babinski reflexes. N o more than 50 mL of blood had been suctioned from the trachea; no pneumothorax had occurred. An ECG showed sinus tachycardia without an injury pattern. Within minutes the cause of the seizure and respiratory arrest became apparent on funduscopic examination: Multiple round, colorless, refractile bubbles consistent with air emboli were seen within retinal vessels by several physicians. These bubbles disappeared over the next several hours. N o other ocular abnormalities were noted. Despite supportive measures, the patient died on the 13th hospital day. The biopsy specimen confirmed the diagnosis of miliary tuberculosis and showed the source of the air emboli (Figure 1). Postmortem examination revealed findings consistent with air embolus. There was marked vascular congestion of the brain and multiple hemorrhages within the brain stem. Caseating granulomas as well as acid-fast bacilli were seen scattered throughout both lungs. The biopsy site could not be identified. Subsequent cultures of lung grew Mycobacterium tuberculosis.

With this report, cerebral air embolism must be added Brief Reports 937

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to the list of complications associated with transbronchoscopic lung biopsy (1, 4). The clinical setting was typical: A sudden central nervous system catastrophe occurred during lung trauma; the communication between the tracheobronchial tree and pulmonary vein (5) had been made with the biopsy forceps. Since intrabronchial or parenchymal pressure had to exceed pulmonary venous pressure for cerebral air embolism to occur, and since our patient did not cough, perform a Valsalva maneuver, or receive positive pressure ventilation, we can only speculate on how the necessary pressure differential occurred. If the bronchoscope became wedged just before the patient began to exhale, possibly air distal to the obstructing bronchoscope became trapped and compressed as exhalation continued, so that the intrabronchial pressure, locally, increased sufficiently to exceed pulmonary venous pressure. The patient's obstructive airways disease may have contributed to this trapped gas volume since the biopsy was taken at end exhalation and in a dependent lung segment. Also the perivenous tuberculous granuloma with resultant early phlebosclerosis may have been a contributing factor. It may have decreased venous pressure in the vascular segment distal to the contiguous pa-

thology, thereby causing pulmonary venous pressure to be less than intrabronchial pressure. Further, the transmural fibrosis obliterating medial smooth muscle may have prevented reactive vascular constriction that might normally have been protective. Since wedging of the bronchoscope at the beginning of exhalation may have played a role in causing bronchopulmonary venous air embolism, we recommend that the bronchoscope not be wedged until the lung biopsy has been taken at the end of exhalation. This represents a modification of the technique of Zavala (2, 3). REFERENCES 1. H E R F SM, S U R A T T PM, A R O R A NS: Deaths and complications associat-

ed with transbronchial lung biopsy. Am Rev Respir Dis 115:708-711, 1977 2. ZAVALA DC: Transbronchial biopsy in diffuse lung disease. Chest 73(suppl):727-733, 1978 3. ZAVALA DC: Pulmonary hemorrhage in fiberoptic transbronchial biopsy. Chest 70:584-588, 1976 4. P E R E I R A W J R , K O V N A T D M , SNIDER GL: A prospective cooperative

study of complications following flexible fiberoptic bronchoscopy. Chest 73:813-816, 1978 5. THOMAS AN: Air embolism following penetrating lung injuries. J Thorac Cardiovasc Surg 66:533-540, 1973 © 1 9 7 9 American College of Physicians

Figure 1 . Transbronchial biopsy specimen (low magnification). A large ( 3 mm) segment of pulmonary vein runs from the lower arrow where the vessel lumen (I/) can be seen to the upper arrow where the wall is tangentially oriented. Interalveolar septa (AS) on both sides of the adventitia and the venouslike arrangement of elastic fibers delineating a thin media confirm an interlobular septal location. A caseating granuloma (G) is seen adjacent to the vein in the pulmonary parenchyma (P). At higher magnification, medial and focal intimal fibrosis indicating phlebosclerosis was seen. The micrometre scale indicates 0 . 1 m m units. (Trichrome-elastic tissue stain; original magnification, x 2 5 . ) 9 3 8

June 1979 • Annals of Internal Medicine • Volume 90 • Number 6

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Cerebral air embolism complicating transbronchoscopic lung biopsy.

Cerebral Air Embolism Complicating Transbronchoscopic Lung Biopsy ALLAN D. ERICKSON, M.D.; RICHARD S. IRWIN, M.D.; CARL TEPLITZ, M.D.; WILLIAM M. CORR...
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