Massive air embolism during cardiopulmonary bypass

Massive air embolism during cardiopulmonary bypass

J THoRAc CARDIOVASC SURG 80:708-717, 1980 Massive air embolism during cardiopulmonary bypass Causes, prevention, and management Massive air embolis...

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J

THoRAc CARDIOVASC SURG

80:708-717, 1980

Massive air embolism during cardiopulmonary bypass Causes, prevention, and management Massive air embolism during cardiopulmonary bypass is a frightening complication requiring immediate response and carrying strong medicolegal implications. From July, 1971. to July. 1979. there were eight instances of massive air embolism during 3,620 cardiopulmonary bypass operations. Five such accidents from other institutions are included in this report. Causes were (I) inattention to reservoir level, (2) reversal of pump head tubing or direction of pump head rotation, (3) unexpected resumption of heartbeat, (4) inadequate steps to remove air after cardiotomy, (5) high-flow suction deep in a pulmonary artery, (6) defective oxygenator, (7) use of a pressurized cardiotomy reservoir, and (8) inadvertent detachment of oxygenator during bypass. Prevention includes a systematic check of pump suckers and perfusion lines before bypass, a sensing device on the oxygenator reservoir, secure fixation of the oxygenator and avoidance of traffic around pump equipment, immediate cessation of pump and inspection for abnormal noise, use of standard maneuvers to remove air from the heart, and carotid compression with resumption (if heartbeat. Immediate management of massive air embolism consists of placing the patient in a deep Trendelenburg position and making a large stab wound in the ascending aorta for retrograde drainage from the cerebrovascular bed. Temporary retrograde perfusion through the superior vena cava (SVC) may also be used. Subsequent steps are hypothermia with the resumption of cardiopulmonary bypass. elevation of blood pressure. steroids. ventilation with 100% oxygen, and deep barbiturate anesthesia. Among the 13 patients, there were four instantaneous deaths. Cerebral injury which resolved within a 2 month period occurred in three patients. The remainder had no neurologic sequelae. Nonfatal cerebral air injury may be associated with prolonged convalescence yet complete recovery, as compared to embolism from debris or clot, which offers a poorer prognosis.

Noel L. Mills, M.D., and John L. Ochsner, M.D., New Orleans, La.

For nearly one hundred years air embolism has been a cause of death in patients undergoing thoracic surgery. I The brain is the organ most vulnerable; only an immediate response by the surgical team can prevent death or permanent neurologic damage. Air embolism is especially regrettable because it is iatrogenic. With the recent surge in the number of coronary artery bypass operations, newly formed teams may suddenly be faced with this problem. It is our purpose here to discuss our experiences and those of others and to define procedures that can either prevent these problems or manage From the Department of Surgery, Ochsner Medical Institutions, New Orleans, La. Read at the Sixtieth Annual Meeting of The American Association for Thoracic Surgery, San Francisco, Calif., April 28 to 30, 1980. Address for reprints: Dr. Noel L. Mills, Ochsner Clinic, 1514 Jefferson Highway, New Orleans, La. 70121.

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them successfully. We will focus attention primarily on the causes, prevention, and management of massive air embolism involving relatively large amounts of gas released into the systemic arterial circuit. Patients

From July, 1971, to July, 1979, there were eight instances of massive air embolism among 3,620 cardiopulmonary bypass operations performed at the Ochsner Foundation Hospital. The patients included seven men, aged 24 to 72 years, and one 5-year-old girl. One of the men had a preoperative neurologic deficit, the result of cardiac arrest from a myocardial infarction. We included five additional cases of massive air embolism from other institutions which exemplify more of the possible causes of the problem. Four of these patients were men and one was a child.

0022-5223/80/110708+10$01.00/0 © 1980 The C. V. Mosby Co.

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Table I. Air embolism during cardiopulmonary bypass Medical center

Operation

Cause of embolism

OFH

1*

M

ACB

Inattention to blood level

OFH OFH OFH Other

2

3* 4* 5

M M M

ACB ACB ACB ACB

Inattention Inattention Inattention Inattention

Other OFH OFH

7* 8

ACB ACB Aortic valve replacement

Vent tubing reversal Vent tubing reversal Sudden resumption of heartbeat

Repair of tetralogy Pulmonary valvulotomy Repair of ventricular aneurysm ACB ACB

Oxygenator knocked over Suction wedged in pulmonary artery Inadvertent continued arterial perfusion Pressured cardiotomy reservoir Defective oxygenator

Other OFH Other Other OFH

6

M M

9 10 II

F

12

13*

M

to to to to

blood blood blood blood

level level level level

Outcome Bilateral transient radial nerve paresis Slow awakening only No sequelae No sequelae Slow awakening-no permanent sequelae Immediate death No sequelae Early-coma, dysarthria laterecovery Immediate death No sequelae Immediate death Immediate death No sequelae

Legend: OFH, Ochsner Foundation Hospital. ACB, Aona-coronary bypass.

• Retrograde pumping via the superior vena cava.

Five different types of oxygenators were used during the study period, and in only one instance was the air accident caused by a defective oxygenator. The gas mixture through all oxygenators was uniformly 100% oxygen. A blood level sensor device* has been used in more recent years, but it was in place in only two of the eight cases and in neither instance was it turned on. Flooding of the field with carbon dioxide was not used in any operation. All patients were fully heparinized when the accidents occurred.

Causes The most common cause of embolism (five cases) was a lapse in attention to the oxygenator blood level (Table I). The ventricular vent suction tubing was reversed in two patients (Fig. I). Deep cardiotomy suction tubing wedged into the pulmonary artery resulted in air being drawn into the left atrium in the 5-year-old child, who had pulmonary stenosis (Fig. 2). This patient had a nonpatent foramen ovale and an intact ventricular septum. In another patient sudden, unexpected resumption of heartbeat occurred during attempted aspiration of the left ventricle after aortic valve replacement. A defective defoarning chamber in an oxygenator resulted in loss of level with the pumping of foam into the ascending aorta in one patient. An oxygenator was inadvertently knocked off its attachment in another case and air was instantaneously pumped into the arterial circuit. *Lev-L-Sentry, Delta Medical Industries, Costa Mesa, Calif.

One patient had an uneventful repair of a ventricular aneurysm and, after supposed cessation of cardiopulmonary bypass, the arterial perfusion control knob was inadvertently left on a very low flow rate. This was not detected, and systemic air embolism resulted. One patient had a left ventricular vent inserted that was connected to a closed system reservoir. The cardiotomy return suckers from the nearly occlusive pump heads were at a high rate and caused pressurization of the reservoir. Air traversed the vent sucker line retrogradely past the slow-moving nonocclusive pump head to enter the left ventricle and systemic arterial circuit (Fig. 3). Treatment

Treatment varied among the patients and the institutions. In most of the patients at Ochsner Foundation Hospital treatment consisted of removal of the cannula in the ascending aorta with the patient in deep Trendelenburg position; purging of the perfusion lines; manual stripping of the coronary arteries to propel air through the coronary circuit; distal perforation of the coronary arteries with a 25 gauge needle; hypothermic cardiopulmonary bypass; administration of vasopressors and steroids; and ventilation with 100% oxygen. Retrograde perfusion through the superior vena cava (SVC) catheter after purging of the arterial line was used in five of our eight patients. Neither deep pentobarbiturate anesthesia nor use of a decompression chamber was employed in any of the patients in this report.

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Table II. Causes of air embolism I. Inattent ion to oxygenator blood level 2 . Unexpected resumpti on of heartbeat 3. Reversal of vent or perfusion lines in pump head 4. Pressurized cardiotomy reservoir 5. Opening a beating heart 6 . Clotted oxyge nator 7. Runaway pump head 8 . Kink in arterial line proximal to pump head 9 . Break in integrity of lines or oxygenator 10. Detachment of oxy gena tor dur ing perfusion II . Faulty technique dur ing circulatory arres t 12. Unnoticed rotation of arte rial pump head

Reversal of Tubing in P um p

Table III. Prevention of air embolism Fig. 1. In ad vertent re versal of left ve ntric u la r ve nt as a cause o f air embol ism . A ll ve nts a nd s uct io n sho u ld be tested w ith sa line be fore use .

I. Constant attention to oxygenator blood level 2. 3. 4. 5. 6. 7. 8. 9. 10. II. 12. 13. 14.

Fig. 2. Card iot omy s uc tio n wedged deep int o th e pulmonary a rtery may re sult in a ir ente rin g the pu lm on a ry ci rc u it. C ar d iot omy s uc tion sho uld be o n ly as high as ne cessa ry to e ffe ct a bl ood-fr ee o pe ra tiv e field.

Results There were no earl y or late sequelae in five of the pat ients (Table I). In four patients there was transient neurologic deficit with no permanent damage. The early deficit s varied from slow awakening to deep coma. One patient, who awoke with bilateral radial ner ve pal sy , had had the sa me temporary neurologic defe ct occur 8 yea rs earli er after a gastric operation . We have no ass urance that air embolism , treated with retrograde per fusion , was relev ant to the radial ner ve pare sis in this massively obe se patient. Four patients could not be resus citated immediatel y after the acci dent. Open aortotorny with Trendelenburg position or

Blood le vel sensor Arterial filter Air-activated ball valve in arterial line System atic check of integrity and direction of perfusion lines Immediate cessation of pump and inspection upon any abnormal noise Testing of vents and suckers in saline prior to bypass Avoid ance of traffic around perfu sion lines Tubing clamp count prior to bypass Secure fixation of oxygenator Adequate vent on reservoir to avoid pressurization Carotid comp ress ion with resu mption of heartbeat Immediate ability to fibrillate heart Standard mane uvers to remove air from the heart

retrograde pumping was not atte mpted in any of these four patients. None of the other patients with retro grade pumping via the S VC, used in the later years of the study period, had any neurologic deficit result. Hence there appears to be a relation between retrograde perfu sion and a successful outco me .

Discussion The incide nce of sys temic air embolism during cardiac operation s has ranged from 0 % to 11.7%. 2- 4 Clearl y , fro m our own inquiry, the vast majority of instances are unreported and quietly ignored , partly because of fear of litigation. Such accidents are decreased with incre ased cardiopulmonary bypass experience but are not unknown even in cent ers in which large numbers of cardi ac operations are performed . The fact that most patients are heparinized and often under some degree of hypothermia enh ances the possibility for a successful outcome. Experience . educational level, and professionali sm of extra corporeal pump techn icians are relat ive . The surgeon must depend on a number of personnel

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Oxygenator

Fig . 3. Pressurization of the cardiotomy reservoir may be carr ied out purp osefull y to drive blood through a filter or inadvertentl y by high suction of cardiotomy suckers with near-occlusion pump heads. Air can be inadvertently driven past the slow -mo ving nonocclusive pump head of the ventricular vent to enter the systemic circuit. Thi s may be avo ided if relief port s on the cardiotom y reservoir are opened to prev ent its pre ssurization .

over whom he does not have direct control. Few occasions in the experience of a cardiovascular surgeon are as stressful as the period of waiting for a patient to awaken after a systemic air emboli sm . The surgeon has the ultimate responsibility and, therefore, can allow only a limited degree of independent function by perfusionist s . Guidelines for emergency procedures should be set up and practiced technically by the pump team. Should an air embolism occur, and there is any hint of system malfunction , the extracorporeal equipment should not be taken down and the legal advisor should be contacted immediately (Alsobrook HE Jr, Adams & Reese Law Firm, New Orleans , La.) . Non-air emboli to the systemic circulation appear to have a much worse prognosis than gaseous emboli. During the same study period at the Ochsner Foundation Hospital, four patients experienced emboli from nongaseous sources. All patients with embolization of overt debris had localized neurologic signs and permanent neurologic deficit. There was one death in that group .

Causes and prevention Very little information is available in standard textbooks on the causes of air embolism (Table II). The control of air embolism lies in prevention (Table III) . Constant attention to the oxygenator blood level is

mandatory through the bypass procedure and instant access to the cutoff switch is imperative. Blood level alarm sensors * should be used , but they are not entirely safe and have the disad vantage of tlase alarms. Because of such false warnings, low-level pump cutoff switches are not popular. A weight-activated alarm on the oxygenator is available. t However, this device has the distinct disadvantage of giving false readings with extra circuit weight added. An infrared sensing device also may be used to detect air in the arterial line ,:j: but it has limitations because of interference from other electrical apparatuses. Despite the shortcomings associated with the use of sensing devices, we feel that use of at least one type of low-level alarm system is a mandatory part of the cardiopulmonary bypass system. An arterial filter (Fig. 4) distal to the arterial pump head has been shown to trap smaller bubbles effectively and will certainly "buy time" with massive embolism ..s. 6 Hemolysis was associated with the use of in-line arterial filtration in our early experience and for that reason was not used by us until more recent years . Use of a ball-valve device in the proximal arterial line may prevent a large surge of air into the system *Lev-L-Sentry, Delta Medical Industries, Costa Mesa, Calif. t Advanced Med-Science, Newton Upper Falls, Mass. :j:Sams, Inc., Ann Arbor. Mich.

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Fig. 5. Ventilation of the lungs and needle aspiration of the right superior pulmonary vein decreases the tendency for air to remain trapped in the superior pulmonary veins. To Oxygenator

To Patient

Fig. 4. An arterial filter in line on the arterial circuit may trap air that can be shunted to the cardiotomy reservoir or oxygenator. A bypass circuit as seen here is standard in the event of filter malfunction .

Table IV. Standard maneuvers to remove airfrom heart I . Bleeding aortotomy 2. Needle aspiration of cardiac chambers 3. Tilting and aspiration of cardiac apex 4 . Invagination of left atrial appendage 5. Closing left atrium under blood 6. Catheter or device across mitral valve to produce incompetence 7. Temporary change in bypass flow to fin heart 8. Ventilation of lungs to evacuate pulmonary venous air

circuit. * Detachment of the oxygenator is synonymous with instantaneous pumping of air. Detachment of the oxygenator during perfusion , especially at high flow rates, result s in immediate pumping of air into the arterial circuit when the arterial outlet reache s an air level. " Traffic " around perfusion lines should be prohibited. In two cases in this series , the vent tubing was mistakenly reversed and air resulted . Cardiotomy suckers and vents should be tested in a sterile solution at the operating table to assure suction and not pressure . A sucker tip should not be wedged deeply into a pulmonary artery while on a high suction rate . We have been able to reproduce that method of air embolism in the experimental laboratory in dog s. The integrity of the perfusion lines and the direction of flow should be checked at *Delta Medical Industries, Costa Mesa, Calif.

Table V. Management of air embolism I. 2. 3. 4. 5.

6. 7.

8. 9. 10.

Stop pump-deep Trendelenburg position Stab or exit wound in ascending aorta Temporary retrograde perfusion via superior vena cava Hypothermia Elevation of blood pressure Massage air from coronaries 100% oxygen ventilation Steroids Deep barbiturate anesthesia Decompression chamber

the pump before bypass. A clamp count prior to initiating bypass protects against inadvertently clamping the perfusion line . Although pressure has been used to drive blood through arteri al filters , we find that there is no need for a pressurized reservoir. The importance of immediate cessation of the pump in the event of any abnormal noise around the operative field cannot be overemphasized . This phenomenon alerted us to the presence of an air embolism in three patients. The unexpected resumption of the heartbeat may result in an immediate ejection of a large volume of air. The ability to fibrillate the heart immediately should be available during the course of removing air after open cardiotomy . With suspected debris or air emboli, the lower common carotid arteries may be compressed by the anesthesiologist for 30 to 45 seconds when the first pulsatile heartbeat is effected . We have found no ill effect from this maneuver, and we use it routinely when

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Retrograde

SVC Pumping

Fig. 6. A, Massive air embolism into the systemic circuit by way of the ascending aort ic cannula. B, After the aortic perfu sion line is purged of air. the arterial perfusion cannula is wedged into the divided superior vena cava (S VCj cannula. Retrograde perfu sion at 1,200 cc/ min at 20° C is carried out for 1 to 2 minutes . Air and foam ex it the aortic cannulati on site.

the ascending aorta is atherosclerotic in patients having coronary artery bypass . Although we have never had air pumped from a runaway pump head," we have had that type of pump malfunction on two occa sions . To manage this problem we unplugged the bypass machine and manually rotated the pump head. A kink in the arterial line near the pump head produces an in-line negative pressure sufficient to remove gas from solution. Likewise, a break in the integrity of the lines or of ports from the oxygenator itself may result in a large amount of air being produced . The clotted oxygenator may produce air in the arterial circuit before it is recognized by the perfu sionist. Monitoring of the clotting mechanism with the use of activated clotting time determinations has become standard procedure in most centers. Sudden pharmacologic vasodilatation during the course of the operative procedure may result in a drastic change in the level of the oxygenator, and unless the perfusionist is advised , a low level with vortexing or pumping of air, or both, may occur. Faulty techniques during circulatory arrest may allow air into the ascending aortic cannula or cerebral circuit, or both. An unnoticed arterial pump head with continued very slow rotation after cardiopulmonary

bypass has resulted in emptying of the oxygenator with perfusion of air into the arterial circuit. Routine clamping of the perfusion lines after cardiopulmonary bypass is advisable. Finall y, the old dictum "do not open a beating heart " remains true .

Removal of air from the heart The routine removal of air from the chambers of the heart should be conducted in a systematic fashion related to the flow of blood, beginning with the right atrium and ending with the aorta (Table IV). When the right side of the heart has been opened, the right atrial appendage and then the highest part of the right ventricle and main pulmonary artery are aspirated with a large-bore needle. The left side is cleared of air by ( I) aspiration of the right superior pulmonary vein while the lungs are being intermittently ventilated, (2) aspiration of the apex of the elevated left ventricle during continued insufflation of the lungs , and (3) inversion of the left atrial appendage . This approach minimizes the tendency for air to be trapped in the superior pulmonary veins (Fig . 5). The final step of removing air is through a bleeding aortotomy, 8. 9 which is used in every instance in which the heart has been opened . Adjunctive measures also include the closing of the left atriotomy

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Fig. 7. A. Deep Trendelenburg position of the patient facilitates removal of air from the cerebral circuit. B. Temporary pressure on the carotid arteries by the anesthesiologist will allow retrograde purging of the vertebral system.

under fluid and the use of a catheter or a device across the mitral valve to produce incompetency of the valve as the heart begins to beat. 10 One may also wish to decrease the bypass flow rate temporarily in order to fill the heart and pulmonary vessel s and thereby aid in the flow of blood and air through the chambers in sequence .

Management In the management of systemic air embolism (Table V), the pump is immediately stopped and the patient is put in deep Trendelenburg position . The ascending aortic cannula is removed, purged of air, and tern-

porarily wedged in the S VC cannula. If indicated , rapid infusion of fluid at 3 Llmin into the oxygenator is facilitated by a special tubing . * Should a single right atrial cannula be used, it may be directed into the SVC or the aortic cannula may be directed into the SVC, by way of a small incision at the site of the cavoatrial junction. Retrograde perfusion with hypothermia at 20° C and at a flow rate of I to 2 Llmin by way of the SVC is carried out for I to 2 minutes (Fig. 6). Air returning from the aortotomy has confirmed the effectiveness of this technique . Temporary pressure on the carotids by the anes *Rapid Fluid Addition Set, Cobe Laboratories, Inc., Lakewood, Colo.

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thesiologist will allow retrograde purging of air through the vertebral system (Fig. 7). With an extensive systemic air accident, the air may be forced into the abdominal, femoral, or other vessels and, in the extreme case, is seen in the peripheral arterial transducer monitoring system. In this event we recommend retrograde perfusion of the inferior vena cava until the distal aortic circuit is purged, during which the cerebral vessels are temporarily clamped to prevent the return of air into that system. Standard cardiopulmonary bypass is resumed with hypothermia, and if any air was introduced into the coronary arteries, attention is turned toward their evacuation of air. The heart is massaged, and the blood pressure is elevated by drugs. Small needle punctures aid in evacuating air from the distal coronary artery branches. Dexamethasone (Decadron), 10 mg (adult dose), is administered immediately, 11 operation is continued in the usual fashion, and after slow rewarming, cardiopulmonary bypass is discontinued. High-dose dexamethasone may offer some improvement in results." Inspired oxygen at 100% is maintained for the first 6 hours after operation. No nitrous oxide is used after the insult. Deep anesthesia by sodium pentobarbital (Pentothal) drip may be initiated for protection of the brain. Sodium pentobarbital is initially given in a dosage of 10 mg/kg and then infused at a rate of 1 to 3 mg/kg/hr. A blood level in the range of 10 uglcc is attempted. Ideally, intracranial pressure is monitored, and when it has been normal for 24 to 48 hours the drug is discontinued. The decompression chamber has appeared to be beneficial, especially if used early after injury. 13-17 At present the number of cases in which it has been used is too few to be certain of its efficacy: Years of clinical and experimental research have failed to definitely prove its benefit in the management of gas gangrene, however, and cases of air embolism have been reported in which permanent neurologic impairment resulted despite its use. There is a trend in the oxygenator industry to produce oxygenators with smaller priming volumes, and this factor, in addition to shorter periods of oxygenator response time to changes in volume, increases the hazard of air embolism. REFERENCES Davis lC, Hunt TH: Hyperoxygen therapy, Arterial Gas Embolism, Chap 11, GF Bond, ed., Bethesda, Md., 1977, Undersea Medical Society, pp 141-152

2 Nicks R: Arterial air embolism. Thorax 22:320-326, 1967 3 Silverstein A, Krieger HP: Neurologic complications of cardiac surgery. Arch NeuroI3:601-605, 1960 4 Allen P: Central nervous system emboli in open heart surgery. Can 1 Surg 6:332-337, 1963 5 Taylor HM, Devlin Bl, Mittra SM, Gillan JG, Brannan 11, McKenna 1M: Assessment of cerebral damage during open-heart surgery. A new experimental model. Scand J Thorac Cardiovasc Surg 14:197-203, 1980 6 Wellons HA Jr, Nolan SP: Prevention of air embolism due to trapped air in filters used in extracorporeal circuits. J THORAC CARDIOVASC SURG 65:476-478, 1973 7 Kurusz M, Shaffer CW, Christman EW, Tyers GFO: Runaway pump head. New cause of gas embolism during cardiopulmonary bypass. 1 THORAC CARDIOVASC SURG 77:792-795, 1979 8 Brenner WI, Wallsh E, Spencer FC: Aortic vent efficiency. A quantitative evaluation. J THORAC CARDIOVASC SURG 61:258-264, 1971 9 Groves LK, Effler DB: A needle-vent safeguard against systemic air embolus in open heart surgery. J THORAC CARDIOVASC SURG 47:349-355, 1964 10 Kantrowitz A, Haller JD: Gage device for preventing air embolism during open mitral valve surgery. Am J Surg 118:476-477, 1969 11 Safar P, Bleyaert A, Nemoto EM, Moossy 1, Snyder IV: Resuscitation after global brain ischemia-anoxia. Crit Care Med 6:215-227, 1978 12 Bruce DA, Gennarelli TA, Langfitt TW: Resuscitation from coma due to head injury. Crit Care Med 6:254-269, 1978 13 Stoney WS, Alford WC, Burrus GR, Glassford OM Jr, Thomas CS Jr: Air embolism and other accidents using pump oxygenators. Ann Thorac Surg 29:336-340, 1980 14 Takita H, Olszewski W, Schimert G, Lanphier EH: Hyperbaric treatment of cerebral air embolism as a result of open-heart surgery. J THORAC CARDIOVASC SURG 55: 682-685, 1968 15 Steward 0, Williams WG, Freedom R: Hypothermia in conjunction with hyperbaric oxygenation in the treatment of massive air embolism during cardiopulmonary bypass. Ann Thorac Surg 24:591-593, 1977 16 Kindwall EP: Massive surgical air embolism treated with brief recompression to six atmospheres followed by hyperbaric oxygen. Aerosp Med 44:663-666, 1973 17 Winter PM, Alvis JH, Gage AA: Hyperbaric treatment of cerebral air embolism during cardiopulmonary bypass. JAMA 215:1786-1788, 1971

Discussion DR. TORKEL ABERG Uppsala, Sweden

We have been interested in the subject of cerebral protection during the past 8 years and have prospectively used psychometric testing in well over 400 cases. The patients have

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been given a test battery before operation and about I week, 2 months, and I year after operation. We have been able to follow 2 cases of massive air embolism. Both patients had air embolism because of faulty de-airing at termination of bypass. Both were unconscious after the operation, one for 2 days and the other for 3 days. Neither had seizures. When they were able to communicate, they exhibited signs of slow cerebration, confusion, and hostility. Intellectual function was extremely impaired I week postoperatively. However, at 2 months and I year the intellectual function has returned to normal. This is corroborated by an analysis of their social situation and by an interview with their families, who state that there have been no personality changes. We therefore would agree with the authors' conclusion that the prognosis in patients with massive air embolism may be better than anticipated. So much for complicated cases. What about the normal uncomplicated cases? In 1974 we could show by psychometric tests that an open cardiac procedure was followed by intellectual impairment. Subsequent changes in our intraoperative routines have markedly improved the quality of bypass, and the psychometric methods can no longer pick up these changes. Therefore, we have turned to cerebral spinal fluid analysis. We assess adenylate kinase 24 hours after bypass. The level of this brain damage marker is significantly elevated even in uncomplicated cases. Open cardiac operations still put the patient's brain in jeopardy. Even in patients who are totally normal patients clinically there are signs of brain injury. We should be aware of this fact and continue our search for methods and routines that minimize the risks to the patient's brain.

the alarm system should be mandatory for all pumpoxygenator systems. DR. G. HUGH LAWRENCE Port/and. Ore.

I commend the authors for bringing to our attention this serious surgical misadventure which may happen in the best centers despite the most elaborate and sophisticated precautions and electronic safeguards. My discussion has been stimulated from three sources: (1) the five patients in their series who had a total recovery, without neurologic sequelae, without benefit of hyperbaric chamber; (2) a recent editorial in The Annals of Thoracic Surgery recommending hyperbaric therapy; and (3) our studies reported before this Association in Atlanta, Georgia, in 1971. There is a quantum difference between what we were talking about then and what Dr. Mills is talking about. We were analyzing small bubbles by Doppler technique. There was an extreme variability in the central nervous system response to air which was not necessarily quantitive. I would reinforce the authors' opinion about treatment in hyperbaric chambers. Having practiced in a hospital that had a decompression chamber, I can only be impressed by the logistics of placing an extremely ill patient and an attendant in the chamber for a prolonged period of time. The surgeon should complete the operation that he intended to perform even though he has noted air during its early phases. We have recently noted a complete recovery following reoperation for aortic valve replacement with a graft to the anterior descending coronary artery in a patient who had gross air embolus at the onset of the procedure owing to abrupt cessation of venous return.

DR. WILLIAM S. STONEY Nashville. Tenn.

DR. BENSON B. ROE

I would like to congratulate Dr. Mills on his excellent review of this problem, which has not received appropriate attention in the past. Following a similar serious air embolism accident 2 years ago, we conducted a survey to try to establish the frequency of accidents directly related to pump oxygenators. A total of 349 cardiac surgeons responded to our survey, which covered a 6 year period. There were 1,400 accidents including air embolism, disseminated intravascular coagulation, and mechanical failure of the pump or oxygenator. One hundred patients were injured and 264 deaths were directly related to pump accidents. The incidence, therefore, is one accident per 300 pump procedures. Injury or death occurs once per 1,000 procedures. Air embolism from the arterial line occurred 429 times. Sixty-one patients were permanently injured and 92 patient deaths were related to arterial line air embolism. At the time of this survey, which was in 1978, 42% of the respondents used a low-level alarm system and 58% of the respondents did not. Since prevention is the most important feature of this problem, I would like to ask Dr. Mills his opinion as to whether

San Francisco. Calif

Air is the bane of cardiac surgery. I think the authors are to be thanked for emphasizing the importance of this everpresent hazard. God is good to cardiac surgeons, because the heart cannot be opened without some air being left behind. However, it seldom causes any complication. Our own Doppler probe studies many years ago demonstrated escaping air bubbles as long as 15 minutes after discontinuing bypass. I rise primarily to call attention to another source of massive air embolism, namely, the anesthetist. I lost a patient once because he was lightly anesthetized and had a diaphragmatic contraction at the moment the atrial appendage was opened to insert a caval catheter. The expanded intrathoracic volume caused a rapid descent of the air-fluid level through the atrium and through an atrial septal defect, so that in two beats the aorta was full of air. Be sure the anesthetist is alert to the importance of maintaining positive intrapulmonary pressure during cannulation to keep positive hydraulic pressure in the atrium. Gravitational factors should also be emphasized. The left atrial appendage and the ascending aorta are sites of almost

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unavoidable air trapping. I believe that it is useful to put the patient's head down before removing the aortic clamp; thus any remaining intracardiac air will traverse the inside of the aortic arch and not go to the patient's head. DR. FRANK C. SPENCER New York, N. Y.

We are all most grateful to Dr. Mills for calling attention to this disaster which can occur with any seemingly uneventful bypass. When one recalls that between 80,000 and 100,000 bypasses are performed each year, the magnitude of this problem is clear. Several years ago we had a grim example about air embolism with a pump oxygenator. This occurred with two experienced technicians sitting in front of the oxygenator. Through an unfortunate combination of three or four circumstances occurring simultaneously, the pump went dry in about 15 seconds. The first warning was air in the aorta. In desperation, we employed retrograde perfusion through the inferior vena cava, which Dr. Mills described, and, at the time, aspirated foam from both carotid arteries with a catheter. The child recovered, probably because the temperature was 25° C at the time. He had convulsions for 4 days, but, fortunately, made a B+ in mathematics in school the following year! After that grim experience and the calculation that this could occur within 15 seconds, it was clear that this situation was beyond the capacity of human detection. Two electronic controls were designed: (I) an audible alarm that sounds when the level in the oxygenator falls below a certain level and (2) a "fail-safe device" that tums off the oxygenator when the blood level drops even lower. With these two devices, we went for 2 years without any

Massive air embolism during CPB

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problems, and then a more grim catastrophe occurred. After 3 hours of pumping, the arterial line suddenly filled with air. The cause was never found, despite repeated search. On reexamining the oxygenator, we found that the electronic control system was not functioning, although it had been checked at the start of bypass. The patient remained in a vegetative state for 15 months in the hospital until he died. Because of the obvious rapidity with which air embolism can occur, and the devastating complications that may happen with even the most uneventful case, I think that all oxygenators should be electronically controlled with a device that will not only sound an audible alarm but will turn off the pump head when the oxygenator level drops to a dangerous degree. DR. MIL L S (Closing) I would like to thank the discussers for their comments. Dr. Aberg, I did not have time to mention it in the course of the presentation, but during this study period we had four cases in which overt debris was released into the arterial circulation. Three of the patients had permanent neurologic defects and one died. We certainly agree that sequelae from air embolism are apparently much more reversible than those from embolic material. Dr. Stoney, we feel as you do that alarms should be mandatory . Dr. Lawrence, I thank you for your comments and thoughts on the chamber. I certainly agree with Dr. Roe, and I would like to thank you, Dr. Spencer, for calling our attention to the fact that electronic devices certainly can fail.