Paradoxical Air Embolus During Endoscopic Retrograde Cholangiopancreatography: An Uncommon Fatal Complication Nicholas W. Markin, MD, and Candice R. Montzingo, MD, FASE Air embolism during endoscopic retrograde cholangiopancreatography is a rare but potentially fatal complication. A 66-year-old man underwent endoscopic retrograde cholangiopancreatography and remained stable until the end of the procedure, when he was found to have mottling on his right side and became hypoxic and unresponsive. Transesophageal echocardiography showed air within the left ventricle, consistent with systemic air embolism. Mortality resulted from significant cardiac and cerebral ischemia. The literature suggests that capnography is helpful in early diagnosis of air embolus, but it could not be used in this case because the patient’s trachea was not intubated. (A&A Case Reports. 2015;4:87–90.)
S
ystemic air embolism is a rare and potentially fatal complication of endoscopic retrograde cholangiopancreatography (ERCP), which is performed to evaluate the biliary and the pancreatic duct systems for the presence of strictures, stones, or tumors. A few reports in the literature describe venous air emboli entering from the inferior vena cava and travelling into the pulmonary vascular bed, leading to pulmonary hypertension and cardiovascular collapse.1 To date, there are 10 case reports published that describe fatal cerebral air embolism; only 1 of these cases also involved myocardial ischemia secondary to coronary air embolism.2,3 We describe a case in which loss of consciousness and evidence of myocardial ischemia after ERCP prompted a postoperative transesophageal echocardiogram that revealed systemic air emboli. The agent of the patient’s legal power of attorney provided permission for the publication of this case report.
CASE DESCRIPTION
A 66-year-old man with a history of recurrent pancreatitis secondary to choledocholithiasis presented for ERCP to evaluate a previously placed stent in the common bile duct. His medical history included human immunodeficiency virus infection, hypertension, and portal vein thrombosis. Prior echocardiographic evaluation revealed normal biventricular function. He was given midazolam 5 mg IV premedication as he had received with all previous ERCPs, was taken to the endoscopy suite, and was placed in a left lateral decubitus position while receiving oxygen through a nasal cannula.
Monitoring included noninvasive arterial blood pressure monitoring by cuff, pulse oximetry, and 5-lead electrocardiography. End-tidal carbon dioxide (EtCO2) monitoring was not used because the patient was not breathing through a mask, endotracheal tube, or laryngeal mask airway, and an EtCO2 sampling nasal cannula was not available. The patient was given a propofol infusion of 75 to 80 mcg/kg/min, resulting in deep sedation throughout the ERCP. The stent in the common bile duct was occluded and was subsequently removed and replaced by the gastroenterologist. The patient was spontaneously breathing, had oxyhemoglobin saturations >94%, and remained normotensive without electrocardiographic changes while in the endoscopy suite. On completion of the procedure, the room lights were turned on, and our patient was placed supine. Within 1 minute after turning supine, he became hypoxic and unresponsive, and it was noted that he had mottling on the right side of his body, extending from his scalp to his waist (Fig. 1). His oxyhemoglobin saturations decreased to the mid-70% during nonrebreather oxygen administration; his heart rate increased from 64 to 82 bpm; and his arterial blood pressure remained unchanged at 128/66 mm Hg. The patient was unresponsive to pain and had bilateral miosis and deviation of both eyes to the left. An endotracheal tube was placed without the administration of any medications, and arterial
From the Department of Anesthesiology, University of Nebraska Medical Center, Omaha, Nebraska. Candice R. Montzingo, MD, FASE, is currently affiliated with Department of Anesthesiology, University of Utah, Salt Lake City, Utah. Accepted for publication September 1, 2014. Funding: None. The authors declare no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.cases-anesthesia-analgesia.org). Address correspondence to Nicholas W. Markin, MD, Department of Anesthesiology, University of Nebraska Medical Center, 984455 Nebraska Medical Center, Omaha, NE 68198. Address e-mail to [email protected]. Copyright © 2015 International Anesthesia Research Society DOI: 10.1213/XAA.0000000000000121
April 1, 2015 • Volume 4 • Number 7
Figure 1. Photograph taken from the head of the bed, showing unilateral mottling secondary to systemic air embolization while the patient was in the left lateral decubitus position. cases-anesthesia-analgesia.org
87
Figure 2. A, Midesophageal 4-chamber transesophageal echocardiography view at 0° showing air emboli in the left atrium (LA) and the left ventricle (LV) but no air in the right atrium (RA) or the right ventricle (RV). B, Midesophageal bicaval view showing blood shunting left-to-right (indicated by arrow) through a patent foramen ovale in the interatrial septum (IAS).
Video 1. A, Transesophageal echocardiogram (TEE) in a midesophageal 4-chamber view showing air embolus in the left atrium (LA) and the left ventricle (LV) and no air in either the right atrium (RA) or right ventricle (RV). B, TEE of the LV in a midesophageal long-axis view showing air within the LA and LV and severely reduced LV systolic function. C, TEE of the patient’s patent foramen ovale (PFO) in a midesophageal bicaval view showing left-to-right shunting through the interatrial septum (IAS). D, Transthoracic echocardiogram in an apical 4-chamber view showing improved LV systolic function and the absence of intracardiac air.
blood gas analysis showed pH 7.2, Paco2 66 mm Hg, Pao2 80 mm Hg, bicarbonate 25 mmol/L, and a base deficit of 2.1. Noncontrast computed tomography of the head revealed air in multiple intracranial vascular structures and areas consistent with ischemia. The patient was transported to the postanesthesia care unit for placement of an arterial line and a central venous catheter and for further resuscitation. Upon return to the postanesthesia care unit, the patient developed significant ST segment elevation on the electrocardiogram and became hypertensive (204/100 mm Hg). Infusions of nitroglycerin and, subsequently, nitroprusside were initiated to control the hypertension. Transesophageal echocardiography revealed air in the left atrium, left ventricle, and ascending aorta, as well as severely reduced systolic function (Fig. 2A; Supplmental Digital Content, Video 1A and 1B, http://links.lww.com/AACR/A14). A relatively small amount of air was present in the right atrium
88 cases-anesthesia-analgesia.org
and right ventricle. A left-to-right shunt through a patent foramen ovale (PFO) was evident (Fig. 2B; Supplemental Digital Content, Video 1C, http://links.lww.com/AACR/ A14). The entry of air from the pulmonary veins into the left atrium ceased when positive-pressure ventilation was held during transition from a self-inflating manual ventilation bag to a mechanical ventilator. When ventilation resumed, air could be seen entering the left atrium from the right upper and lower pulmonary veins. Agitated saline bubble studies were performed through bilateral peripheral IV catheters to exclude anomalous venous drainage into the left atrium through an unroofed coronary sinus atrial septal defect as a source of the systemic air emboli. A 37-F, left-sided, double-lumen endotracheal tube was placed to investigate the association between positive-pressure ventilation and further influx of air into the left atrium. Ventilating both lungs resulted in air embolization into the left atrium (Fig. 3A). During 1-lung ventilation induced by left-lung isolation and positive-pressure ventilation, no air was seen entering the heart (Fig. 3B). Bronchoscopy showed no blood, lacerations, or injury to airway structures in either lung. One-lung ventilation of the left lung was continued for approximately 3 hours in the intensive care unit. A transthoracic echocardiogram performed when 2-lung ventilation was resumed showed no air emboli in either the right or the left side of the heart, as well as improved global left ventricular function (Supplemental Digital Content, Video 1D, http://links.lww.com/AACR/A14). The patient remained hemodynamically stable; however, he did not regain consciousness at any time after the ERCP. Subsequent magnetic resonance imaging and computed tomography revealed extensive ischemic changes in the brain, and his cardiac troponin level increased to 29.57 ng/mL. Nine days after the ERCP, the patient was declared brain dead.
DISCUSSION
Cases of systemic air embolization as a complication of endoscopic or laparoscopic procedures have been reported since 1978, when the first reported death from “air trapping” in the portal circulation occurred.1 Six reported fatalities due to air emboli have been reported since ERCP became
A & A case reports
Figure 3. A, Midesophageal left ventricular long-axis transesophageal echocardiography view at 113° showing air in the left atrium (LA) and left ventricle (LV) during 2-lung ventilation. B, Midesophageal left ventricular long-axis view showing no air in the LA or LV when only the left lung is ventilated. PA = pulmonary artery; RV = right ventricle.
a standard tool for the diagnosis and treatment of hepatobiliary disease.4–7 The mechanism of air embolism has not been identified in all cases; 2 reports suggest that air can enter the systemic circulation through either the injury and insufflation of duodenal portal venous radicals at the site of sphincterotomy and crossover within the liver or that gas in the biliary tree might crossover within the liver where the intrahepatic veins are injured from chronic biliary disease.4,8 Root et al.1 experimentally demonstrated in a canine model that CO2 entered into the portal system would cross into the systemic circulation through hepatic sinusoids at levels sufficient to cause hemodynamic changes and fatal air embolus. Air embolus has been associated with procedures such as liver biopsy,6 percutaneous transhepatic biliary drainage,4 and sphincterotomy and the manipulation of stents during ERCP.5,7,9 Air traversing the right side of the heart may result in increased pulmonary vascular resistance, which leads to increased dead space, an acute reduction in EtCO2, elevated pulmonary pressures, acute right heart failure, and subsequent increase in the right ventricular and right atrial pressures.9 As well, air emboli and the resultant air–blood interface cause platelet activation and lead to aggregation, further reducing transpulmonary blood flow.1 Autopsy reports of arterial air embolization in patients with and without a PFO hypothesized that when a significant quantity of air is introduced and right-sided pressures increase, the air can cross over at the level of the PFO if present or the air may traverse the lung via a transpulmonary shunt and allow for sufficient quantities of systemic arterial air emboli to cause end-organ damage.1,4,8 In the present case, no injury to the vasculature was seen on direct visualization by the gastroenterologist, and no abnormal bleeding was observed. However, it is presumed that a large amount of air entered the portal vein and passed through the hepatic sinusoids and onto the right heart and into the pulmonary circulation. The increase in pulmonary arterial resistance may have resulted in reversal of the PFO shunt and allowed air emboli to transition into the systemic circulation. Significant cyanosis secondary to the shunt was unlikely because of its small size. In addition, it is possible that some of the air preferentially went to the nondependent
April 1, 2015 • Volume 4 • Number 7
right lung, where it remained in the pulmonary veins until the patient was turned supine. At that point, the air could have passed from the right-sided pulmonary veins through the left atrium and into the systemic circulation. Finally, venous air may have become trapped in the right atrium throughout the case, and then, when the patient was turned from left lateral decubitus position to supine, the emboli exited into the pulmonary circulation, as well as through the PFO and into the systemic circulation. Total IV anesthesia in spontaneously breathing patients who are laterally positioned for ERCP makes the detection of air emboli difficult. A sudden decrease in EtCO2 alerts the anesthesiologist to a sudden increase in dead space, which may be useful in detecting pulmonary emboli more immediately. The importance of early detection is supported by the fact that 9 of the 10 reported fatalities occurred with systemic embolization.3 Although EtCO2 is not as sensitive as transesophageal echocardiography or precordial Doppler in the detection of air emboli, EtCO2 may aid in early detection of this complication. Quantitative EtCO2 measurements are difficult to obtain in spontaneously breathing patients who do not have a laryngeal mask airway or endotracheal tube in place. Patients with a nasal cannula with EtCO2 sampling may be helpful in identifying a qualitative decrease. Case reports of right-sided air embolism during ERCP have shown patient survival without permanent morbidity in 3 of 4 cases with monitoring and in none of 5 patients without EtCO2 monitoring or any other form of capnography.9 If air emboli are suspected, echocardiography and thoracic and cerebral computed tomography should be performed to confirm the diagnosis. In our case, the patient’s trachea was not intubated, and a nasal cannula with EtCO2 monitoring was not available. Furthermore, the patient’s hemodynamic stability and normal oxyhemoglobin saturation during the procedure did not elicit suspicion of a catastrophic complication during the ERCP. Finally, poor light in the endoscopy suite delayed the detection of the discoloration of the patient’s right side. Therapeutic measures are guided by the severity of symptoms. Embolization of air to the heart or brain requires immediate attention, including institution of 100% oxygen
cases-anesthesia-analgesia.org
89
administration, left lateral decubitus and Trendelenburg positioning, volume expansion, aspiration of air through a multiorifice central venous catheter when possible, and hyperbaric oxygen therapy when available.3 Although it was not done in this case, placing the patient in a hyperbaric oxygen chamber with a pressure of 2.5 atmospheres for >2 hours has been shown to be effective in treating air emboli from multiple sources and potentially increases a patient’s chance of survival.10 Providers should have a high index of suspicion for pulmonary and systemic air embolism if hemodynamic instability occurs during or immediately after ERCP. Review of the current literature suggests that securing the patient’s airway with an endotracheal tube may be a simple yet very useful aid the in rapid diagnosis of pulmonary air emboli because it permits accurate EtCO2 measurement. E REFERENCES 1. Root B, Levy MN, Pollack S, Lubert M, Pathak K. Gas embolism death after laparoscopy delayed by “trapping” in portal circulation. Anesth Analg 1978;57:232–7 2. van Boxel GI, Hommers CE, Dash I, Goodman AJ, Green J, Orme RM. Myocardial and cerebral infarction due to massive air embolism following endoscopic retrograde
90 cases-anesthesia-analgesia.org
cholangiopancreatography (ERCP). Endoscopy 2010;42 Suppl 2:E80–1 3. Finsterer J, Stöllberger C, Bastovansky A. Cardiac and cerebral air embolism from endoscopic retrograde cholangio-pancreatography. Eur J Gastroenterol Hepatol 2010;22:1157–62 4. Stabile L, Cigada M, Stillittano D, Morandi E, Zaffroni M, Rossi G, Lapichino G. Fatal cerebral air embolism after endoscopic retrograde cholangiopancreatography. Acta Anaesthesiol Scand 2006;50:648–9 5. Kennedy C, Larvin M, Linsell J. Fatal hepatic air embolism following ERCP. Gastrointest Endosc 1997;45:187–8 6. Siddiqui J, Jaffe PE, Aziz K, Forouhar F, Sheppard R, Covault J, Bonkovsky HL. Fatal air and bile embolism after percutaneous liver biopsy and ERCP. Gastrointest Endosc 2005;61:153–7 7. Nayagam J, Ho KM, Liang J. Fatal systemic air embolism during endoscopic retrograde cholangio-pancreatography. Anaesth Intensive Care 2004;32:260–4 8. Bisceglia M, Simeone A, Forlano R, Andriulli A, Pilotto A. Fatal systemic venous air embolism during endoscopic retrograde cholangiopancreatography. Adv Anat Pathol 2009;16:255–62 9. Romberg C. Systemic air embolism after ERCP: a case report and review of the literature (with video). Gastrointest Endosc 2009;70:1043–5 10. Mohammedi I, Ber C, Peguet O, Ould-Aoudia T, Duperret S, Petit P. Cardiac air embolism after endoscopic retrograde cholangiopancreatography in a patient with blunt hepatic trauma. J Trauma 2002;53:1170–2
A & A case reports
S
ystemic air embolism is a rare and potentially fatal complication of endoscopic retrograde cholangiopancreatography (ERCP), which is performed to evaluate the biliary and the pancreatic duct systems for the presence of strictures, stones, or tumors. A few reports in the literature describe venous air emboli entering from the inferior vena cava and travelling into the pulmonary vascular bed, leading to pulmonary hypertension and cardiovascular collapse.1 To date, there are 10 case reports published that describe fatal cerebral air embolism; only 1 of these cases also involved myocardial ischemia secondary to coronary air embolism.2,3 We describe a case in which loss of consciousness and evidence of myocardial ischemia after ERCP prompted a postoperative transesophageal echocardiogram that revealed systemic air emboli. The agent of the patient’s legal power of attorney provided permission for the publication of this case report.
CASE DESCRIPTION
A 66-year-old man with a history of recurrent pancreatitis secondary to choledocholithiasis presented for ERCP to evaluate a previously placed stent in the common bile duct. His medical history included human immunodeficiency virus infection, hypertension, and portal vein thrombosis. Prior echocardiographic evaluation revealed normal biventricular function. He was given midazolam 5 mg IV premedication as he had received with all previous ERCPs, was taken to the endoscopy suite, and was placed in a left lateral decubitus position while receiving oxygen through a nasal cannula.
Monitoring included noninvasive arterial blood pressure monitoring by cuff, pulse oximetry, and 5-lead electrocardiography. End-tidal carbon dioxide (EtCO2) monitoring was not used because the patient was not breathing through a mask, endotracheal tube, or laryngeal mask airway, and an EtCO2 sampling nasal cannula was not available. The patient was given a propofol infusion of 75 to 80 mcg/kg/min, resulting in deep sedation throughout the ERCP. The stent in the common bile duct was occluded and was subsequently removed and replaced by the gastroenterologist. The patient was spontaneously breathing, had oxyhemoglobin saturations >94%, and remained normotensive without electrocardiographic changes while in the endoscopy suite. On completion of the procedure, the room lights were turned on, and our patient was placed supine. Within 1 minute after turning supine, he became hypoxic and unresponsive, and it was noted that he had mottling on the right side of his body, extending from his scalp to his waist (Fig. 1). His oxyhemoglobin saturations decreased to the mid-70% during nonrebreather oxygen administration; his heart rate increased from 64 to 82 bpm; and his arterial blood pressure remained unchanged at 128/66 mm Hg. The patient was unresponsive to pain and had bilateral miosis and deviation of both eyes to the left. An endotracheal tube was placed without the administration of any medications, and arterial
From the Department of Anesthesiology, University of Nebraska Medical Center, Omaha, Nebraska. Candice R. Montzingo, MD, FASE, is currently affiliated with Department of Anesthesiology, University of Utah, Salt Lake City, Utah. Accepted for publication September 1, 2014. Funding: None. The authors declare no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.cases-anesthesia-analgesia.org). Address correspondence to Nicholas W. Markin, MD, Department of Anesthesiology, University of Nebraska Medical Center, 984455 Nebraska Medical Center, Omaha, NE 68198. Address e-mail to [email protected]. Copyright © 2015 International Anesthesia Research Society DOI: 10.1213/XAA.0000000000000121
April 1, 2015 • Volume 4 • Number 7
Figure 1. Photograph taken from the head of the bed, showing unilateral mottling secondary to systemic air embolization while the patient was in the left lateral decubitus position. cases-anesthesia-analgesia.org
87
Figure 2. A, Midesophageal 4-chamber transesophageal echocardiography view at 0° showing air emboli in the left atrium (LA) and the left ventricle (LV) but no air in the right atrium (RA) or the right ventricle (RV). B, Midesophageal bicaval view showing blood shunting left-to-right (indicated by arrow) through a patent foramen ovale in the interatrial septum (IAS).
Video 1. A, Transesophageal echocardiogram (TEE) in a midesophageal 4-chamber view showing air embolus in the left atrium (LA) and the left ventricle (LV) and no air in either the right atrium (RA) or right ventricle (RV). B, TEE of the LV in a midesophageal long-axis view showing air within the LA and LV and severely reduced LV systolic function. C, TEE of the patient’s patent foramen ovale (PFO) in a midesophageal bicaval view showing left-to-right shunting through the interatrial septum (IAS). D, Transthoracic echocardiogram in an apical 4-chamber view showing improved LV systolic function and the absence of intracardiac air.
blood gas analysis showed pH 7.2, Paco2 66 mm Hg, Pao2 80 mm Hg, bicarbonate 25 mmol/L, and a base deficit of 2.1. Noncontrast computed tomography of the head revealed air in multiple intracranial vascular structures and areas consistent with ischemia. The patient was transported to the postanesthesia care unit for placement of an arterial line and a central venous catheter and for further resuscitation. Upon return to the postanesthesia care unit, the patient developed significant ST segment elevation on the electrocardiogram and became hypertensive (204/100 mm Hg). Infusions of nitroglycerin and, subsequently, nitroprusside were initiated to control the hypertension. Transesophageal echocardiography revealed air in the left atrium, left ventricle, and ascending aorta, as well as severely reduced systolic function (Fig. 2A; Supplmental Digital Content, Video 1A and 1B, http://links.lww.com/AACR/A14). A relatively small amount of air was present in the right atrium
88 cases-anesthesia-analgesia.org
and right ventricle. A left-to-right shunt through a patent foramen ovale (PFO) was evident (Fig. 2B; Supplemental Digital Content, Video 1C, http://links.lww.com/AACR/ A14). The entry of air from the pulmonary veins into the left atrium ceased when positive-pressure ventilation was held during transition from a self-inflating manual ventilation bag to a mechanical ventilator. When ventilation resumed, air could be seen entering the left atrium from the right upper and lower pulmonary veins. Agitated saline bubble studies were performed through bilateral peripheral IV catheters to exclude anomalous venous drainage into the left atrium through an unroofed coronary sinus atrial septal defect as a source of the systemic air emboli. A 37-F, left-sided, double-lumen endotracheal tube was placed to investigate the association between positive-pressure ventilation and further influx of air into the left atrium. Ventilating both lungs resulted in air embolization into the left atrium (Fig. 3A). During 1-lung ventilation induced by left-lung isolation and positive-pressure ventilation, no air was seen entering the heart (Fig. 3B). Bronchoscopy showed no blood, lacerations, or injury to airway structures in either lung. One-lung ventilation of the left lung was continued for approximately 3 hours in the intensive care unit. A transthoracic echocardiogram performed when 2-lung ventilation was resumed showed no air emboli in either the right or the left side of the heart, as well as improved global left ventricular function (Supplemental Digital Content, Video 1D, http://links.lww.com/AACR/A14). The patient remained hemodynamically stable; however, he did not regain consciousness at any time after the ERCP. Subsequent magnetic resonance imaging and computed tomography revealed extensive ischemic changes in the brain, and his cardiac troponin level increased to 29.57 ng/mL. Nine days after the ERCP, the patient was declared brain dead.
DISCUSSION
Cases of systemic air embolization as a complication of endoscopic or laparoscopic procedures have been reported since 1978, when the first reported death from “air trapping” in the portal circulation occurred.1 Six reported fatalities due to air emboli have been reported since ERCP became
A & A case reports
Figure 3. A, Midesophageal left ventricular long-axis transesophageal echocardiography view at 113° showing air in the left atrium (LA) and left ventricle (LV) during 2-lung ventilation. B, Midesophageal left ventricular long-axis view showing no air in the LA or LV when only the left lung is ventilated. PA = pulmonary artery; RV = right ventricle.
a standard tool for the diagnosis and treatment of hepatobiliary disease.4–7 The mechanism of air embolism has not been identified in all cases; 2 reports suggest that air can enter the systemic circulation through either the injury and insufflation of duodenal portal venous radicals at the site of sphincterotomy and crossover within the liver or that gas in the biliary tree might crossover within the liver where the intrahepatic veins are injured from chronic biliary disease.4,8 Root et al.1 experimentally demonstrated in a canine model that CO2 entered into the portal system would cross into the systemic circulation through hepatic sinusoids at levels sufficient to cause hemodynamic changes and fatal air embolus. Air embolus has been associated with procedures such as liver biopsy,6 percutaneous transhepatic biliary drainage,4 and sphincterotomy and the manipulation of stents during ERCP.5,7,9 Air traversing the right side of the heart may result in increased pulmonary vascular resistance, which leads to increased dead space, an acute reduction in EtCO2, elevated pulmonary pressures, acute right heart failure, and subsequent increase in the right ventricular and right atrial pressures.9 As well, air emboli and the resultant air–blood interface cause platelet activation and lead to aggregation, further reducing transpulmonary blood flow.1 Autopsy reports of arterial air embolization in patients with and without a PFO hypothesized that when a significant quantity of air is introduced and right-sided pressures increase, the air can cross over at the level of the PFO if present or the air may traverse the lung via a transpulmonary shunt and allow for sufficient quantities of systemic arterial air emboli to cause end-organ damage.1,4,8 In the present case, no injury to the vasculature was seen on direct visualization by the gastroenterologist, and no abnormal bleeding was observed. However, it is presumed that a large amount of air entered the portal vein and passed through the hepatic sinusoids and onto the right heart and into the pulmonary circulation. The increase in pulmonary arterial resistance may have resulted in reversal of the PFO shunt and allowed air emboli to transition into the systemic circulation. Significant cyanosis secondary to the shunt was unlikely because of its small size. In addition, it is possible that some of the air preferentially went to the nondependent
April 1, 2015 • Volume 4 • Number 7
right lung, where it remained in the pulmonary veins until the patient was turned supine. At that point, the air could have passed from the right-sided pulmonary veins through the left atrium and into the systemic circulation. Finally, venous air may have become trapped in the right atrium throughout the case, and then, when the patient was turned from left lateral decubitus position to supine, the emboli exited into the pulmonary circulation, as well as through the PFO and into the systemic circulation. Total IV anesthesia in spontaneously breathing patients who are laterally positioned for ERCP makes the detection of air emboli difficult. A sudden decrease in EtCO2 alerts the anesthesiologist to a sudden increase in dead space, which may be useful in detecting pulmonary emboli more immediately. The importance of early detection is supported by the fact that 9 of the 10 reported fatalities occurred with systemic embolization.3 Although EtCO2 is not as sensitive as transesophageal echocardiography or precordial Doppler in the detection of air emboli, EtCO2 may aid in early detection of this complication. Quantitative EtCO2 measurements are difficult to obtain in spontaneously breathing patients who do not have a laryngeal mask airway or endotracheal tube in place. Patients with a nasal cannula with EtCO2 sampling may be helpful in identifying a qualitative decrease. Case reports of right-sided air embolism during ERCP have shown patient survival without permanent morbidity in 3 of 4 cases with monitoring and in none of 5 patients without EtCO2 monitoring or any other form of capnography.9 If air emboli are suspected, echocardiography and thoracic and cerebral computed tomography should be performed to confirm the diagnosis. In our case, the patient’s trachea was not intubated, and a nasal cannula with EtCO2 monitoring was not available. Furthermore, the patient’s hemodynamic stability and normal oxyhemoglobin saturation during the procedure did not elicit suspicion of a catastrophic complication during the ERCP. Finally, poor light in the endoscopy suite delayed the detection of the discoloration of the patient’s right side. Therapeutic measures are guided by the severity of symptoms. Embolization of air to the heart or brain requires immediate attention, including institution of 100% oxygen
cases-anesthesia-analgesia.org
89
administration, left lateral decubitus and Trendelenburg positioning, volume expansion, aspiration of air through a multiorifice central venous catheter when possible, and hyperbaric oxygen therapy when available.3 Although it was not done in this case, placing the patient in a hyperbaric oxygen chamber with a pressure of 2.5 atmospheres for >2 hours has been shown to be effective in treating air emboli from multiple sources and potentially increases a patient’s chance of survival.10 Providers should have a high index of suspicion for pulmonary and systemic air embolism if hemodynamic instability occurs during or immediately after ERCP. Review of the current literature suggests that securing the patient’s airway with an endotracheal tube may be a simple yet very useful aid the in rapid diagnosis of pulmonary air emboli because it permits accurate EtCO2 measurement. E REFERENCES 1. Root B, Levy MN, Pollack S, Lubert M, Pathak K. Gas embolism death after laparoscopy delayed by “trapping” in portal circulation. Anesth Analg 1978;57:232–7 2. van Boxel GI, Hommers CE, Dash I, Goodman AJ, Green J, Orme RM. Myocardial and cerebral infarction due to massive air embolism following endoscopic retrograde
90 cases-anesthesia-analgesia.org
cholangiopancreatography (ERCP). Endoscopy 2010;42 Suppl 2:E80–1 3. Finsterer J, Stöllberger C, Bastovansky A. Cardiac and cerebral air embolism from endoscopic retrograde cholangio-pancreatography. Eur J Gastroenterol Hepatol 2010;22:1157–62 4. Stabile L, Cigada M, Stillittano D, Morandi E, Zaffroni M, Rossi G, Lapichino G. Fatal cerebral air embolism after endoscopic retrograde cholangiopancreatography. Acta Anaesthesiol Scand 2006;50:648–9 5. Kennedy C, Larvin M, Linsell J. Fatal hepatic air embolism following ERCP. Gastrointest Endosc 1997;45:187–8 6. Siddiqui J, Jaffe PE, Aziz K, Forouhar F, Sheppard R, Covault J, Bonkovsky HL. Fatal air and bile embolism after percutaneous liver biopsy and ERCP. Gastrointest Endosc 2005;61:153–7 7. Nayagam J, Ho KM, Liang J. Fatal systemic air embolism during endoscopic retrograde cholangio-pancreatography. Anaesth Intensive Care 2004;32:260–4 8. Bisceglia M, Simeone A, Forlano R, Andriulli A, Pilotto A. Fatal systemic venous air embolism during endoscopic retrograde cholangiopancreatography. Adv Anat Pathol 2009;16:255–62 9. Romberg C. Systemic air embolism after ERCP: a case report and review of the literature (with video). Gastrointest Endosc 2009;70:1043–5 10. Mohammedi I, Ber C, Peguet O, Ould-Aoudia T, Duperret S, Petit P. Cardiac air embolism after endoscopic retrograde cholangiopancreatography in a patient with blunt hepatic trauma. J Trauma 2002;53:1170–2
A & A case reports
