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Treating Massive Air

Albert J. Valk, Richard A. Kanten, Mark Oosterheert Dept. Extracorporeal Circulation Butterworth Hospital Grand Rapids, Mich.

Abstract ______Pathophysiology ______

The purpose of this paper is to present concepts re­ The clinical picture of cerebral air embolism presents garding the physiology and treatment of massive air itself in three basic forms. First is the patient who does embolism resulting from cardiac surgery and cardio­ not fully regain consciousness following surgery. The pulmonary bypass. This includes physical, pharma­ second is that of the patient who regains consciousness cological, transport, and hyperbaric measures. The in the early post-operative period but within 12 to 24 concepts and review of the literature are presented to hours displays a decrease in sensorium, often accom­ aid the cardiovascular surgical team in formulating a panied by convulsions. Focal neurological deficits such protocol for handling and treating air embolism. as hemiplegia, aphasia, blindness, etc. constitute the third type of clinical picture. 1 Introduction ______The pathology of cerebral air embolism is a result of mechanical obstruction to the flow of , the Of the many potential complications of cardiac air-blood interface, and the air-vessel wall interface. surgery, one of the most dangerous and life-threatening bubbles that enter systemic circulation may remain is massive cerebral air embolism. Air emboli may be lodged in the arterial circulation causing sludging of introduced into systemic arterial circulation either from blood beyond the obstruction, or may be passed into the the pump-oxygenator system or from the left heart venous circulation. 2 The air-blood interface is char­ following cardiotomy. In some cases the occurrence of acterized by the development of a protein layer on an air embolism may be immediately evident, but it which adhesions of platelets and droplets form. 3 should also be suspected in a patient who demonstrates This layer is often capable of separating from the post-operative neurological deficits. The purpose of this original surface producing further emboli. The paper is to serve as a review and summary of the blood also reacts to the bubble as a foreign substance available literature dealing with the pathophysiology triggering the reaction of leukocytes and changes in and treatment of air embolism secondary to cardiac circulating platelets. The air-vessel wall interface surgery. produces a local vasospasm which may last for several minutes and increase the degree of mechanical ob­ struction. 3 The presence of pressurized air in the vessel Address Communications to: Albert J. Valk RN CCRN, Dept. of Extracorporeal Circ., Butterworth Hospital, 100 Michigan NE, Grand may produce damage to the walls, and may Rapids, Mich 49503 act as a chemical irritant producing endothelial damage Presented at The Nineteenth International AmSECT Conference, San Francisco, California, March 2-5, 198!. and subsequent fibrin formation. 3 The results of these

Volume 14, Number I, 1982 The Journal of Extra-Corporeal Technology 325 mechanisms are cerebral , , inflamma­ hyperbaric chamber was developed in the 1930's for use tion, and thrombus formation. in submarine escape training to treat ruptures and sickness. In 1945 the Navy developed tables for regulating 9ecompression time, but the table Treatment______used for patients with central involve­ ment required the patient and attending personnel to The treatment of air embolism is aimed at mini­ remain in the chamber for 38 hours. This amount of mizing the travel of the air to the cerebral circulation, time was impractical for the post-surgical patient as relieving the obstruction, reducing cerebral edema, much of the necessary care could not be carried out improving oxygenation of the affected area, and except in very large and sophisticated chambers. Also eliminating the nitrogen from the blood. Stoney et. al. the amount of time was very taxing on the attending presents several mechanical measures that can be taken personnel in the chamber. Therefore, the tables were to remove air should a massive embolism occur in the modified in 1966 to a protocol for treating air embolism ascending aorta. These include aortotomy, massage of that requires only 5 to 6 hours in the chamber. 5 the heart and great vessels, and gentle retrograde Hyperbaric treatment should be considered in any into the superior vena cava.4 Once cardio­ case of evident or suspected air embolism, even if there pulmonary bypass can be initiated, moderate to pro­ would be a delay of several hours before treatment is found should be induced to reduce the initiated.2 The cardiac team should become aware of effects of cerebral edema and hypoxia. 1 Steroids should the location of a hyperbaric chamber nearest them that be administered to reduce cerebral edema. However, is large enough to handle a surgical patient and can be some authors have suggested that if hyperbaric treat­ pressurized to a depth of 165 feet (6 ATA). When in­ ment is to be used, the administration of the steroids vestigating various modes of transportation to a should be delayed until the patient reaches a decom­ chamber, it should be remembered that travel in an pression level of 1.9 atmospheres (ATA) as steroids are unpressurized aircraft is particularly hazardous to a known to potentiate toxicity. 5 Heparinization patient with air embolism. Prior to entering the is useful in decreasing both the platelet adhesion to the chamber, the patient should be evaluated by a physi­ bubble surfaces and the coagulation of stagnant blood. cian familiar with hyperbaric treatment to establish Once embolization has occurred however, the admin­ baseline parameters and detect possible contraindica­ istration of heparin probably will not be helpful since tions. it will not reach the blocked microcirculation.6 Osmotic After the patient enters the chamber it is rapidly diuretics, such as urea or Mannitol should be used to pressurized to six atmospheres which applies Boyle's reduce cerebral edema by decreasing total body water. 1 law (gas volume is inversely proportional to pressure) The patient should be placed in Trendelenburg's po­ and compresses the bubbles to approximately 17% of sition to mechanically reduce bubble embolization to their original volume. 5 Compression above six atmo­ the cerebral circulation. If nitrous oxide anesthesia is spheres offers no advantage in that it results in only a being used, it should be immediately discontinued as small change in bubble volume and may potentiate the it may diffuse into the bubbles increasing their size or development of in chamber personnel. pressure. The patient should be ventilated with an Fi02 The pressure of 6 AT A is maintained for 30 minutes of 1 to aide in elimination of nitrogen from the blood. and then a very controlled decompression is initiated If the patient is not anesthetized sedation may be nec­ (generally over a 4 or 5 hour period). essary to reduce convulsions and prevent shivering Because mechanical compression of the bubbles during induction of hypothermia. 1 cannot totally resolve emboli, 100% oxygen at hyper­ The aspect of treatment that has made the greatest baric is used for three important effects. impact on the mortality of massive air embolism is Fick's law is applied, providing an increased concen­ hyperbaric oxygenation. The use of this modality of tration gradient to promote the denitrogenation of the treatment in the post-cardiac surgery patient was first blood. Hyperbaric oxygen also has a vasoconstrictive reported by Takita in 1968.7 Basically, the patient is effect which aides in reducing intra-cranial pressure. placed in a chamber which is pressurized, maintained The third effect is the preservation of the viability of at that pressure for a short period of time, and then is affected . At 3 AT A on I 00% oxygen, the

depressurized at a controlled rate. The concept of the patient's Pa02 may exceed 2000 torr producing a large

326 The Journal of Extra-Corporeal Technology Volume 14, Number I, 1982 blood-tissue gradient and enhancing and plan for the often complicated transportation and distance. 8 treatment of the air embolism patient. If an embolism There are certain potential dangers to hyperbaric event does occur, the chamber team should be con­ oxygenation. One is additional nitrogen bubbles in the tacted as early as possible so that chamber preparations blood which may cause if the can be started. With a concerted effort, even this dan­ patient or chamber personnel are air. This gerous of cardiac surgery can be treated may be reduced by following strict decompression effectively and efficiently to give the patient the best protocols and some centers use a -oxygen chance at recovering with little or no neurological breathing mixture when at high pressures. Another deficit. potential danger is with its neurological and pulmonary reactions, although this can be avoided References by not administering pure oxygen above 3 ATA of pressure. 8 Hypoventilation caused by decreased volume I. Allen, P.: 'Emboli in Open Heart Surgery, Canadian Journal of Surgery. 6:334, .1963. of gas required for oxygenation and the increased 2. Calverley, R. K., Dodds, W. A., Trapp, W. G., Jenkins, L. C.: Hy­ workload of breathing (due to the denser gas) should perbaric Treatment Of Cerebral Air Embolism: A Report of a Case Following Cardiac Catheterization, Canad. Anaesth. Soc. J. 18: be corrected to prevent and atelectasis. 666-6 72, 1971. 3. Warren, B. A., Philp, R. B., Inwood, M. J.: The Ultrastructural Morphology of Air Embolism: Platelet Adhesion to the Interface and Summary ______Endothelial Damage. Br. J. Exp. Path. 54:163, 1973. 4. Stoney, W. S., Alford, W. C., Burrus, G. R., Glassford, D. M., The treatment of massive air embolism consists of Thomas, C. S.: Air Embolism and Other Accidents Using Pump Oxygenators, The Annals of Thoracic Surgery. 29( 4), 1980. hypothermia, steroids, heparinization, sedation, di­ 5. Kindwall, E. P.: Massive Surgical Air Embolism Treated with Brief uretics, positioning, and hyperbaric oxygenation. The Recompression to Six Atmospheres Followed by Hyperbaric Oxygen, goals of treatment are to restore circulation, reduce Aerospace Med. pp 664-666, 1973. 6. Steward, D., Williams, W. G., Freedom, R.: Hypothermia in Con­ edema, reduce disturbances of clotting, protect viable junction with Hyperbaric Oxygenation in the Treatment of Massive tissue, and eliminate the nitrogen from the blood. With Air Embolism During , The Annals of Thoracic Surgery. 24:592, 1977. the cardiac surgical patient there is a great potential 7. Takita, H., Olszewski, W., Schimert, G., Lanphier, E. H.: Hyperbaric for air embolism, therefore the surgical team should be Treatment of Cerebral Air Embolism as a Result of Open-Heart Surgery, J. Thorac. Cardiovasc. Surg. 55:684, 1968. aware of the various aspects of treatment. Regarding 8. Norkool, D. M.: Concepts of Hyperbaric Oxygenation in hyperbaric treatment, the team should contact a facility Critical Care, Heart and Lung. 8(4), 1979.

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