buat sayatan ”I”, dimulai dari incisura jugularis, ke arah bawah sampai ke symphisis pubis, potong rawan iga mulai dari iga ke-3 kiri dan kanan, pisahkan rawan iga dan tulang dada keatas sampai ke perbatasan antara iga ke-2 dan iga ke-3, potong tulang dada setinggi perbatasan antara tulang iga ke-2 dan ke-3, setelah kandung jantung tampak, buat insisi pada bagian depan kandung jantung dengan insisi ”I”, sepanjang kira-kira 5-7 sentimeter; kedua ujung sayatan tersebut dijepit dan diangkat dengan pinset (untuk mencegah air yang keluar), masukkan air ke dalam kandung jantung, melalui insisi yang telah dibuat tadi, sampai jantung terbenam; akan tetapi bila jantung tetap terapung, maka hal ini merupakan pertanda adanya udara dalam bilik jantung, tusuk dengan pisau organ yang runcing, tepat di daerah bilik jantung kanan, yang berbatasan dengan pangkal a. Pulmonalis, kemudian putar pisau itu 90 derajat; gelembung-gelembung udara yang keluar menandakan tes emboli hasilnya positif, bila tidak jelas atau ragu-ragu, lakukan pengurutan pada a. Pulmonalis, ke arah bilik jantung, untuk melihat keluarnya gelembung udara, bila kasus yang dihadapi adalah kasus abortus, maka pemeriksaan dengan prinsip yang sama, dilakukan mulai dari rahim dan berakhir pada jantung, semua yang disebut di atas adalah untuk melakukan tes emboli pulmoner, untuk tes emboli sistemik, pada prinsipnya sama, letak perbedaannya adalah : pada tes emboli sistemik tidak dilakukan penusukan ventrikel, tetapi sayatan melintang pada a. Coronaria sinistra ramus desenden, secara serial beberapa tempat, dan diadakan pengurutan atas nadi tersebut, agar tampak gelembung kecil yang keluar, dosis fatal untuk emboli udara pulmoner 150-130 ml, sedangkan untuk emboli sistemik hanya beberapa ml.
Emboli udara, baik yang sistemik maupun emboli udara pulmoner, tidak jarang terjadi. Pada emboli sistemik udara masuk melalui pembuluh vena yang ada di paru-paru, misalnya pada trauma dada dan trauma daerah mediastinum yang merobek paru-paru dan merobek pembuluh venanya. Emboli pulmoner adalah emboli yang tersering, udara masuk melalui pembuluh-pembuluh vena besar yang terfiksasi, misalnya pada daerah leher bagian bawah, lipat paha atau daerah sekitar rahim (yang sedang hamil); dapat pula pada daerah lain, misalnya pembuluh vena pergelangan tangan sewaktu diinfus, dan udara masuk melalui jarum infus tadi. Fiksasi ini penting, mengingat bahwa tekanan vena lebih kecil dari tekanan udara luar, sehingga jika ada robekan pada vena, vena tersebut akan menguncup, hal ini ditambah lagi dengan pergerakan pernapasan, yang ”menyedot”.
AUTOPSI PADA DUGAAN KEMATIAN AKIBAT EMBOLI UDARA
Terbukanya pembuluh darah akibat trauma, kadangkala dapat menyebabkan timbulnyaemboli udara. Dikenal 2 jenis emboli udara berdasarkan letak dari emboli tersebut, emboliudara vena (= emboli udara paru) dan emboli udara arterial (= emboli udara sistemik).Untuk membuktikan terdapatnya emboli udara, perlu dilakukan teknik autopsi yangkhusus, menyimpang dari teknik autopsi rutin. Pada dasarnya, pembuktian dilakukan denganmemperlihatkan adanya udara dalam system vena atau arteri dengan membuka arteri atauvena tersebut di bawah permukaan air.Pada pembukaan kulit leher dalam melakukan autopsi rutin, vena daerah ini mudahterpotong terutama vena jugularis. Bila ini terjadi, maka terdapat kemungkinan masuknya udara post mortal ke dalam pembuluh darah tersebut. Pada pengangkatan alat leher kemudian,terjadi manipulasi terhadap leher dan kepala sehingga udara yang masuk tadi berpindah danmasuk ke dalam jantung. Hal tersebut di atas akan menghasilkan pemeriksaan yang salah(false positive) dan karenanya harus dihindari, dengan jalan tidak membuka daerah leher sebelum dilakukan pemeriksaan emboli.Pemeriksaan emboli udara venaDengan mengingat kemungkinan terjadinya hasil false positive seperti yang diuraikandi atas, maka pembukaan kulit dimulai dari setinggi incisura jugularis ke bawah sepanjang g a r i s median. Kulit bagian leher dibiarkan utuh untuk sementara dan jangan g a n j a l b a h u mayat dengan malok. Kulit dan otot dinding dada serta rongga perut dibuka seperti biasa.Rawan iga dipotong mulai dari iga ke-3 ke arah kaudo-lateral. Insersi otot diafragma dipotonguntuk melepaskan bagian bawah stemum dan iga. Kemudian bagian depan dinding dada inidilepaskan dengan terlebih dahulu menggergaji tulang dada (stermum) melintang setinggi igake-3.T i n d a k a n m e m o t o n g t u l a n g d a d a s e t i n g g i i g a k e - 3 i n i d i l a k u k a n u n t u k m e n c e g a h terpotongnya pembuluh darah besar yang berjalan di belakng iga ke-2 dan tulang selangka.Kandung jantung dibuka dengan melakukan pengguntingan memanjang pada tempat y a n g l e t a k n y a p a l i n g t i n g g i ( d i p e r t e n g a h a n k a n d u n g j a n t u n g ) s e p a n j a n g 5 s a m p a i 7 sentimeter. Ke dalam kandung jantung kemudian diisikan air sehingga seluruh jantung terdapat di bawah permukaan air (terendam). Kadang-kadang jantung c e n d e r u n g u n t u k mengapung. Dalam hal ini tekanlah jantung dengan jari tangan kiri dan jagalah agar jantungtetap terendam. Dengan pisau organ, tusuklah ventrikel kanan dekat dengan permulaan a. pulmonalis sampai menembus ke dalam bilik kanan. Dengan melakukan pemutaran bidang pisau (knife blade) sebanyak 90 derajat, maka lubang tusukan diperlebar. Perhatikan apakahterdapat gelembung udara yang keluar dari lubang tersebut. Dengan cara yang sama, ventrikelkiri juga dilubangi dan perhatikan juga apakah terdapat gelembung udara yang keluar.Pada kasus dengan emboli udara vena, udara kan terkumpul dalam bilik kanan jantungdan karenanya, pada pemeriksaan akan ditemukan keluarnya gelembung udara dari lubangyang dibuat pada bilik kanan, sedangkan dari bilik jantung kiri tidak terdapat gelembung udara yang keluar.Bila pada pemeriksaan tidak keluar gelembung baik dari bilik kanan maupun kiri, maka kemungkinan terdapatnyaemboli udara vena dapat disingkirkan.Bila pada penusukkan bilik kanan dan kiri keduanya memberikan gelembung udara,maka hal ini dapat disebabkan oleh adanya emboli udara vena disertai defek septurn, atau diakibatkn oleh terbentuknya gas pembusukan dalam bilik jantung kanan maupun yang kiri.Dalam hal ini kemungkinan terdapatnya emboli udara vena tidak dapat dipastikan
maupundisingkirkanD i s a m p i n g d i l a k u k a n p e m e r i k s a a n s e p e r t i t e r s e b u t d i a t a s , b e b e r a p a h a l d a p a t menyokong akan adanya emboli udara vena. Antara lain adalah: distensi jantung sebelahkanan akibat tekanan udara. Vena cav a, bilik kanan a. pulmonalis dan v v. coronariae yang berisi darah yang berbuih dan berwarna merah terang. Vena cava inferior yang mengalami distensi, tetapi sangat sedikit atau sama sekali tidak terisi darah.Pemeriksaan emboli udara arterilUntuk membuktikan adanya emboli udara arterial, lakukan persiapan pemeriksaan seperti pada pemeriksaan emboli udara vena. Dengan jantung yang seluruhnya terdapat di b a w a h permukaan air, lakukan pemotongan permulaan a. coronaria kiri dengan j a l a n mengirisnya pada bagian arterior septum dan perhatikan apakah terdapat gelembung udarayang keluar. Bila perlu dapat dilakukan pengurutan sepanjang septum dari arah apex jantungkea rah tempat pengirisan. Dalam menilai hasil pemeriksaan emboli udara arterial ini perludiperhitungkan kemungkinan terbentuknya gas pembusukan dalam pembeluh itu sendiri
Air embolism Liza C O'Dowd, MD Mark A Kelley, MD
Mar 2, 2000
Air embolism is an uncommon but potentially catastrophic event which occurs as a consequence of the entry of air into the vasculature. A venous, or pulmonary air embolism occurs when air enters the systemic venous circulation and travels to the right ventricle and/or pulmonary circulation. An arterial air embolism results from introduction of air into the arterial system and can produce ischemia of any organ with poor collateral circulation [1,2,3]. This card will review the causes, pathophysiology, diagnosis, and treatment of air embolism. Issues related to the embolization of thrombi, amniotic fluid, fat, or tumor cells are discussed separately on designated cards. ETIOLOGY — Two conditions must be present for air embolism to occur: • A direct communication between a source of air and the vasculature must exist • A pressure gradient favoring the passage of air into the circulation (rather than bleeding from the vessel) must be present Patients in the intensive care unit (ICU) are at particular risk for air embolism because they are subjected to a number of procedures in which these two conditions are commonly met (show table 1). Examples include surgery, instrumentation of the central venous system, and positive
pressure ventilation [1,2]. Surgery — Venous air embolism most commonly complicates neurosurgical and otolaryngological interventions because the surgical incision is made at a level above the heart by a distance greater than the central venous pressure. This is a particular problem if the patient is placed in the Fowler's, or sitting position, which further increases negative venous pressure relative to the atmosphere. The estimated incidence of venous air embolism during neurosurgical procedures ranges from 10 percent (for surgical patients in the prone position) to 80 percent (for patients undergoing repair of cranial synostosis while in the Fowler's position) [1,4,5,6,7]. Most episodes are clinically silent or result in mild, transient hypotension. Penetrating chest injuries may produce a bronchopulmonary venous fistulae and arterial air emboli. The mortality rate in one series of 9 patients with this complication was 66 percent [8]. Air embolism has also been reported following Nd:YAG laser treatment of endobronchial lesions, likely due to coolant gas (which exits the bronchoscope under high flow/high pressure conditions to cool the laser probe) entering the pulmonary venules and gaining access to the systemic circulation [2,9]. (See "Bronchoscopic laser resection"). Other surgical procedures associated with air emboli are listed in Table 1 (show table 1). Central venous catheterization — Venous air embolism is a serious and often under-recognized complication of central venous catheterization. The incidence of line-associated air embolism has varied from 1 in 3000 to 1 in 47 in different reports [10,11,12]. Venous air emboli can occur at the time of central line or pulmonary artery catheter insertion, while the catheter is in place, or at the time of catheter removal. (See "Indications for and placement of central venous catheters"). The risk of catheter-related venous air embolism is increased by a number of factors [2,12,13]: • Fracture or detachment of catheter connections (which accounts for 63 to 93 percent of episodes) • Failure to occlude the needle hub and/or catheter during insertion or removal • Dysfunction of self-sealing valves in plastic introducer sheaths • Presence of a persistent catheter tract following the removal of a central venous catheter • Deep inspiration during insertion or removal, which increases the magnitude of negative pressure within the thorax • Hypovolemia, which reduces central venous pressure • Upright positioning of the patient, which reduces central venous pressure Barotrauma — Patients requiring positive pressure ventilation are at risk for barotrauma and, as a consequence, both arterial and venous air emboli. Gas may enter the circulation if violation of pulmonary vascular integrity occurs concomitantly with alveolar rupture caused by overdistension of the airspaces. This complication has been reported most frequently in adult patients with the acute respiratory distress syndrome and in premature neonates with respiratory distress syndrome (hyaline membrane disease), but also occurs in patients with other diagnoses [2,14,15,16,17]. Divers are also at risk for barotrauma, and one series estimated that barotrauma and air embolism
complicate approximately 7 of every 100,000 dives [18]. Rapid ascent without exhalation can result in expansion of gas in the lungs and consequent alveolar rupture. If pulmonary veins tear as the alveoli rupture, air can return to the left heart with oxygenated blood and can embolize within the arterial system to produce tissue ischemia [19,20]. (See "Complications of diving"). PATHOPHYSIOLOGY — Air introduced into the venous circulation travels to the right heart and then usually lodges in the pulmonary circulation, causing a venous air embolism. Arterial embolization can result from several mechanisms [1]: • The direct passage of air into the arterial system • Paradoxical embolization through a septal defect, patent foramen ovale, or pulmonary arterial-venous malformation • Incomplete filtering of a large air embolus by the pulmonary capillaries Patients with a left-to-right shunt may suffer paradoxical air emboli following initial emboli to the pulmonary circulation which raise right heart pressures and reverse the direction of the shunt. The effect of an air embolus depends both upon the rate and volume of air introduced into the circulation. The capacity of the lung to filter microbubbles of air from the venous circulation is exceeded when gas enters the circulatory system at a rate greater than 0.30 mL/kg per minute in a canine model; infusions at greater rates generally result in arterial emboli and tissue ischemia [21]. Large, rapid boluses of air are tolerated less well than slow infusions of small amounts of air. It is estimated that 300 to 500 mL of gas introduced at a rate of 100 mL/sec is a fatal dose for humans [2,12]. This flow rate can be attained through a 14 gauge catheter with a pressure gradient of only 5 cm H2O [22]. Upright positioning places the patient at particular risk for entraining air very rapidly into the venous circulation, since the venous pressure is below atmospheric pressure in this setting [2]. Hemodynamic complications of venous air embolism — Gas introduced into the venous circulation can cause cardiac dysfunction by obstruction of the pulmonary outflow tract, pulmonary arterioles, or pulmonary microcirculation. Obstruction of the pulmonary outflow tract ("air lock") diminishes blood flow from the right heart and results in increased central venous pressure and reductions in pulmonary and systemic arterial pressures [12]. Smaller bubbles within the pulmonary arterioles can impede blood flow directly and result in vasoconstriction [1,12]. As a result of these changes in the pulmonary vascular bed, the following hemodynamic effects may be observed [1,5,12]: • Increased pulmonary vascular resistance • Pulmonary artery hypertension • Increased right ventricular pressure • Initial brief increase (due to tachycardia) followed by a decrease in cardiac output and systemic arterial pressure
• Myocardial ischemia, (secondary to hypoxia, right ventricular overload, and/or air emboli to the coronary arterial circulation) Pulmonary complications of venous air embolism — Bubbles in the pulmonary microcirculation are associated with local endothelial damage and the accumulation of platelets, fibrin, neutrophils, and lipid droplets at the gas-fluid interface. Secondary injury to the endothelium occurs due to the activation of complement and the release of mediators and free radicals from neutrophils and other inflammatory cells; noncardiogenic pulmonary edema and bronchoconstriction may result [23,24,25,26,27]. A number of physiologic changes can ensue, including [1,5,12,26,27,28]: • Hypoxemia, due to alveolar flooding and ventilation-perfusion mismatching • Increased physiologic dead space, with a rise in PaCO2 if ventilation is held constant • Decreased lung compliance secondary to pulmonary edema • Increased airway resistance, postulated to be due to release of bronchoconstricting mediators such as serotonin and histamine from endothelium damaged by the air bubbles [5] Systemic complications of air embolism — Air bubbles in the microcirculation directly occlude blood flow and cause ischemic damage to end-organs, such as the brain, spinal cord, heart, and skin [2,12]. Secondary tissue damage from the release of inflammatory mediators and oxygen free radicals in response to air embolism has also been suggested by animal experiments [29]. CLINICAL FEATURES AND DIAGNOSIS — Minor cases of air embolism occur frequently and are minimally symptomatic. Severe cases are characterized by hemodynamic collapse and/or acute vascular insufficiency of specific organs such as the brain or spinal cord. Differentiation from pulmonary thromboemboli, acute myocardial infarction, or cerebrovascular accident may be difficult. Dyspnea is an almost universal finding, and may be accompanied by substernal chest pain and a subjective sense of doom. Common signs and symptoms of air embolism are listed in Table 2 (show table 2) [1,2,5,19]. Air embolism should be considered in the differential diagnosis of any patient who has the sudden onset of cardiopulmonary or neurologic decompensation in a clinical setting which puts the patient at risk for air embolism (show table 1). Disorders which should be considered in the differential diagnosis of air embolism are listed in Table 3 [12] (show table 3). Confirming the diagnosis of air embolism is difficult, and is complicated by the fact that air may be rapidly absorbed from the circulation while diagnostic tests are being arranged. Exclusion of other life-threatening processes is generally required. Some of the following techniques may be useful in supporting the clinical diagnosis of air embolism: Laboratory, hemodynamic, and chest x-ray findings — A summary of common laboratory, hemodynamic, and chest x-ray findings is shown in Table 4 (show table 4) [1,2,12,30]. One study documented significant elevations in serum creatine kinase activity in all of 22 divers with
arterial air embolism, but not in 22 control divers [31]. The sensitivity of elevated serum creatine kinase activity in other populations with arterial air emboli has not been reported. Echocardiography — Transthoracic and transesophageal echocardiography have been used to document the presence of air in the right ventricle and may show evidence of acute right ventricular dilation and pulmonary artery hypertension consistent with air embolism [3,32]. Continuous monitoring with echocardiography or transcranial Doppler techniques have been used during high-risk surgical procedures to detect air embolism in the preclinical phase [33,34,35]. End-tidal CO2 monitoring — The worsening of ventilation-perfusion matching and increase in physiologic dead space which occur with venous air embolism produce a fall in end-tidal CO2 and may raise intraoperative suspicion of the condition. However, this finding is nonspecific and also occurs with pulmonary embolism, massive blood loss, circulatory arrest, or disconnection from the anesthesia circuit [36]. The combination of intraoperative echocardiography and endtidal CO2 monitoring may increase intraoperative sensitivity in detecting preclinical air emboli in high-risk patients [5,34]. Pulmonary artery catheters — A rise in pulmonary artery pressure may be observed when venous air embolism occurs in a patient in whom a pulmonary artery catheter has been placed. However, this is a nonspecific finding, with an estimated sensitivity of only 45 percent [34]. Ventilation-perfusion scan — Ventilation-perfusion scan abnormalities which mimic those seen in pulmonary thromboembolism may be seen in the setting of massive air embolism. However, the perfusion defects due to air embolism resolve more rapidly, frequently within 24 hours [37]. Chest CT — Chest CT may detect air emboli in the central venous system (especially the axillary and subclavian veins), right ventricle, or pulmonary artery. The specificity of these findings is greatest when large defects are detected because small (<1 mL), asymptomatic air emboli occur during the performance of 10 to 25 percent of contrast-enhanced CT scans if carefully sought [38,39]. False positive studies may be more common when higher resolution or electron beam CT scanners are used. (See "Principles of conventional and helical CT scanning" and see "Electron beam (ultrafast) computed tomography for the evaluation of cardiac disease and function"). Pulmonary angiography — Pulmonary angiography may be normal in patients who have suffered air embolism because of rapid resorption of air between the time of presentation and the performance of the procedure. If positive, vascular occlusion and/or findings consistent with vasoconstriction may be seen, including "corkscrewing" of vessels, tapering of vessels, and delayed emptying of vessels in the affected versus the unaffected lung [1]. TREATMENT — The primary aims of treatment are identification of the source of air entry and prevention of further air embolization, removal of embolized gas, and restoration of the circulation. Supportive care (eg, the use of mechanical ventilation, vasopressors, volume resuscitation as indicated) is the cornerstone of management, but several active measures may also be helpful [1,2,12].
Nitrogen washout — High-flow supplemental oxygen increases the partial pressure of oxygen and decreases the partial pressure of nitrogen in blood [40]. This produces a positive pressure gradient for the diffusion of nitrogen from the air bubbles to the blood, accelerating bubble resorption. In contrast, nitrous oxide, when given during general anesthesia, can diffuse from blood to air emboli, causing clinical deterioration as gas bubbles enlarge [41]. Thus, nitrous oxide should be discontinued at the first suspicion of air embolism. Hyperbaric therapy — Patients with continued evidence of cardiopulmonary compromise or neurologic deficits generally should receive treatment with hyperbaric oxygen therapy (HBO) [42]. HBO reduces air bubble size, accelerates nitrogen resorption, and increases the oxygen content of arterial blood, potentially ameliorating ischemia. Although prompt initiation of HBO is preferred, it may improve outcome even if delayed up to 30 hours [43]. No randomized controlled trials of HBO in air embolism have been conducted in humans, and the potential benefits of HBO must be weighed against the potential risks of transport to the HBO facility [44]. (See "Hyperbaric oxygen therapy"). Patient positioning — Patients who develop an "air lock" from a large gas bubble obstructing the right ventricular outflow tract may benefit from maneuvers which float air emboli into other areas of the ventricle. Both the left lateral decubitus position (Durant's maneuver) and the Trendelenburg position can restore forward blood flow by placing the right ventricular outflow tract inferior to the right ventricular cavity, permitting air to migrate superiorly to a nonobstructing position [1,2,4,12]. Closed-chest cardiac massage — Closed-chest cardiac massage forces air out of the pulmonary outflow tract into smaller pulmonary vessels, thus improving forward blood flow [45,46]. This technique improved survival in dogs as effectively as positioning and intracardiac aspiration of air [45]. Aspiration of air from the venous circulation — Air has been successfully aspirated from the right ventricle via a percutaneously introduced needle or a central venous catheter in several experimental models and case reports [12,45]. In general, however, these maneuvers are of limited benefit because the volume of air recovered is less than 20 mL [34]. Most authors recommend attempting to aspirate air only if a central venous catheter is already in place [2,12]. PROGNOSIS — Mortality in untreated patients historically was reported to be in excess of 90 percent, but these figures may have been biased by selective reporting of catastrophic cases. With supportive therapy such as vasopressors, positioning, supplemental oxygen, and closedchest cardiac massage, mortality was reduced to approximately 30 percent in a series form the 1960s [46]. A later series of 16 patients with either arterial or venous air emboli treated with HBO in the early 1980s reported a mortality rate of 7 percent, with one-half of survivors experiencing complete recovery and the remaining one-half suffering some residual deficits [44]. PREVENTION — Efforts should be made to reduce the risk of air embolism during mechanical ventilation and central line placement. Measures towards this end include [1,5,12]:
• Minimization of airway pressures in mechanically ventilated patients to prevent barotrauma (see "Physiologic and pathophysiologic consequences of positive pressure ventilation") • Placing the patient in the Trendelenburg position during central venous catheter insertion and removal • Asking the patient to Valsalva or breath hold at the time of central venous catheter insertion and removal • Occluding the hub of the central venous catheter during insertion • Treating hypovolemia prior to catheter placement, if possible • Keeping all connections to a central line closed and locked when not in use 1. Dudney, TM, Elliott, CG. Pulmonary embolism from amniotic fluid, fat, and air. Prog Cardiovasc Dis 1994; 36:447. 2. King, MB, Harmon, KR. Unusual forms of pulmonary embolism. Clin Chest Med 1994; 15:561. 3. Muth, CM, Shank, ES. Gas embolism. N Engl J Med 2000; 342:476. 4. Raskin, JM, Benjamine, E, Iberti, TJ. Venous air embolism: Case report and review. Mt Sinai J Med 1985; 52:367. 5. O'Quin, RJ, Lakshminarayan, S. Venous air embolism. Arch Intern Med 1982; 142:2173. 6. Hybels, C. Venous air embolism in head and neck surgery. Laryngoscope 1980; 90:946. 7. Faberowski, LW, Black, S, Mickle, JP. Incidence of venous air embolism during craniectomy for craniosynostosis repair. Anesthesiology 2000; 92:20. 8. Estrera, AS, Pass, LJ, Platt, MR. Systemic arterial air embolism in penetrating lung injury. Ann Thorac Surg 1990; 50:257. 9. Tellides, G, Ugurlu, BS, Kim, RW, HAmmond, GL. Pathogenesis of systemic air embolism during bronchoscopic Nd:YAG laser operations. Ann Thorac Surg 1998; 65:930. 10. James, JM, Myers, RT. Central venous pressure monitoring. Ann Surg 1972; 175:693. 11. Doblar, DD, Hinkle, JC, Fay, ML, et al. Air embolism associated with pulmonary artery catheter introducer kit. Anesthesiology 1982; 56:307. 12. Orebaugh, SL. Venous air emboli: Clinical and experimental considerations. Crit Care Med 1992; 20:1169. 13. Kashuk, JL, Penn, I. Air embolism after central venous catheterization. Surg Gynecol Obstet 1984; 159:249. 14. Morris, WP, Butler, BD, Tonnesen, AS, Alen, SJ. Continuous venous air embolism in patients receiving positive end-expiratory pressure. Am Rev Respir Dis 1993; 147:1034. 15. Kane, G, Hewins, B, Grannis, FW. Massive air embolism in an adult following positive pressure ventilation. Chest 1988; 93:874. 16. Marini, JJ, Culver, BH. Systemic gas embolism complicating mechanical ventilation in the adult respiratory distress syndrome. Ann Intern Med 1989; 10:699. 17. Ulyatt, DB, Judson, JA, Trubuhovich, RV, Galler, LH. Cerebral arterial air embolism associated with coughing on a continuous positive airway pressure circuit. Crit Care Med 1991; 19:985. 18. Leitch, DR, Green, RD. Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism. Aviat Space Environ Med 1986; 57:931. 19. Melamed, Y, Shupak, A, Bitterman, H. Medical problems associated with underwater diving. N Engl J Med 1992; 326:30. 20. Wilmshurst P. ABC of oxygen: Diving and oxygen. BMJ 1998; 317:996. 21. Butler, BD, Hills, BA. Transpulmonary passage of venous air emboli. J Appl Physiol 1985; 59:543. 22. Ordway, CB. Air embolus via CVP catheter without positive pressure. Ann Surg 1974; 179:479. 23. Warren, BA, Philp, RB, Inwood, MJ. The ultrastructural morphology of air embolism: Platelet adhesion to the interface and endothelial damage. Br J Exp Pathol 1973; 54:163. 24. Hartveit, F, Lystad, H, Minken, A. The pathology of venous air embolism. Br J Exp Pathol 1968; 49:81. 25. Oyama, Y, Spencer, MP. Cardiopulmonary effects of intravenous gas embolism; with special reference of fate of intravascular gas bubbles. Jpn Circ J 1971; 35:1541. 26. Adornato, DC, et al. Pathophysiology of intravenous air embolism in dogs. Anesthesiology 1978; 49:120. 27. Lam, KK, Hutchinson, RC, Gin, T. Severe pulmonary oedema after venous air embolism. Can J Anaesth 1993; 40:964. 28. Clark, MC, Flick, MR. Permeability pulmonary edema caused by venous air embolism. Am Rev Respir Dis 1984; 129:633. 29. Dutka, AJ, Kochanek, PM, Hallenbeck, JM. Influence of granulocytopenia on canine cerebral ischemia induced by air embolism. Stroke 1989; 20:390. 30. Kizer, KW, Goodman, PC. Radiographic manifestations of venous air embolism. Radiology 1982; 144:35. 31. Smith, RM, Neuman, TS. Elevation of serum creatine kinase in divers with arterial gas embolization. N Engl J Med 1994; 330:19. 32. Marcus, RH, Weinert, L, Neumann, A, et al. Venous air embolism: Diagnosis by spontaneous right-sided contrast echocardiography. Chest 1991; 99:784. 33. Gottdiener, JS, et al. Incidence and cardiac effects of systemic venous air embolism: Echocardiographic
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