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Two Cardiac Arrests Because of Venous Air Embolism During Endoscopic Retrograde Cholangiopancreatography: A Case Report

Sisk, Joseph M. MD; Choi, Monica D. MD; Casabianca, Andrew B. MD, DMD; Hassan, Ali M. MD

doi: 10.1213/XAA.0000000000000420
Case Reports: Case Report
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Venous air embolism is a rare but potentially catastrophic complication of endoscopic retrograde cholangiopancreatography. We report 2 cases of venous air embolism and subsequent cardiac arrests. During resuscitation efforts, a transesophageal echocardiogram was placed, which demonstrated significant air in the right heart. Although gastroenterologists seem to be more aware of this complication, it is underreported in the anesthesiology literature. As anesthesiologists continue to expand coverage to endoscopy suites, anesthesia providers must be aware of predisposing factors and maintain a high index of suspicion to recognize and treat in a timely manner to prevent serious adverse outcomes.

From the Department of Anesthesiology, The University of Toledo College of Medicine, Toledo, Ohio.

Accepted for publication August 1, 2016.

Funding: Departmental.

The authors declare no conflicts of interest.

Address correspondence to Monica D. Choi, MD, Department of Anesthesiology, The University of Toledo Medical Center, 3000 Arlington Ave, MS 1137, Toledo, OH 43614. Address e-mail to monica.choi@utoledo.edu.

The use of endoscopy as a diagnostic and therapeutic tool increasingly is prevalent in the United States. According to the Center for Medicare and Medicaid Services, the number of cases of endoscopic retrograde cholangiopancreatography (ERCP) performed has risen from 233 378 to 288 715 from the year 2000 to 2010, a 23.7% increase.1,2 It is estimated that currently more than 500 000 ERCP procedures are performed annually in the United States alone.3

Concurrent with this increase in volume, there has been a similar increase in demand for anesthesia services, especially for the more complex, high-risk endoscopic procedures. In 2003, only 13% of patients undergoing gastrointestinal (GI) endoscopy required the involvement of anesthesia. In 2009, it was 30% and continues to increase.2 As anesthesia practice continues to expand within the endoscopy suite, it becomes essential to be aware of potentially devastating complications. Venous air embolism (VAE) during ERCP is rare but potentially life-threatening. A literature review published in 2013 identified 41 cases of VAE after various endoscopic procedures.4 The majority of these cases were published in GI journals. We report 2 cases of VAE leading to cardiac arrest after common bile duct stent placement during ERCP. Risk factors, clinical presentation, diagnosis, and management of this phenomenon are discussed.

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CONSENT FOR PUBLICATION

The University of Toledo College of Medicine’s Office of Legal Affairs, Institutional Review Board, and Office of Compliance determined that (1) the signed general consent form, (2) the deidentified Protected Health Information (PHI), and (3) the case study used solely for research purposes are sufficiently in compliance with institutional guidelines per Health Insurance Portability and Accountability Act (HIPAA) regulations. The general consent authorizes use of the patient’s medication history and/or medical history electronically for scientific or educational purposes as long as the patient’s identity is not disclosed.

Per the HIPAA regulations: “A covered entity may always use or disclose for research purposes health information which has been de-identified (in accordance with 45 Code of Federal Regulations [CFR] 164.502(d), and 164.514(a)-(c) of the Rule)….”

In addition, according to CFR 45 §164.512 (iii) Research on decedent’s information, can be used if the covered entity obtains from the researcher. (A) Representation that the use or disclosure sought is solely for research on the protected health information of decedents; (B) Documentation, at the request of the covered entity, of the death of such individuals; and (C) Representation that the protected health information for which use or disclosure is sought is necessary for the research purposes.

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CASE DESCRIPTION

Patient 1 was a 37-year-old man, American Society of Anesthesiologists physical status III, with a medical history significant for recurrent pancreatitis because of common bile duct obstruction and end-stage renal disease, status postkidney transplant. He presented for ERCP with common bile duct stent placement under general endotracheal anesthesia. This patient had undergone unsuccessful biliary duct decompression via ERCP 3 days previously.

During placement of the biliary stent, the patient experienced significant hypertension, blood pressure 240/140 mm Hg, and narrow complex tachycardia, heart rate 140 bpm. This state initially was attributed to epinephrine lavaged into the stent placement site by the gastroenterologist for hemostasis. Soon thereafter, end-tidal CO2 (ETCO2) and oxygen saturation (SpO2) values dropped precipitously. Blood pressure and pulse were undetectable, and the patient quickly progressed from bradycardia to asystole. The gastroenterologist removed the endoscope, the patient was turned supine, and ACLS protocol was initiated. Chest compressions, multiple rounds of epinephrine, and atropine led to the return of electrical activity followed by spontaneous circulation. A transesophageal echocardiogram (TEE) probe was placed to determine whether a cardiac event was the cause of arrest. The TEE revealed the right heart had a “white-out” effect from entrapped air in both the atrium and the ventricle (Figure). The TEE also showed normal left ventricular function.

Figure

Figure

A magnetic resonance imaging of the brain on the sixth postoperative day was consistent with acute small watershed infarcts, possibly from air emboli. A postoperative TEE failed to demonstrate the presence of an intracardiac shunt, although it cannot be ruled out that during the arrest a right-to-left shunt may have occurred across a patent foramen ovale because of elevated right atrial pressures. Because the patient failed to show signs of neurologic recovery, support was withdrawn, and he died on the 14th postoperative day.

Patient 2 was a 79-year-old woman, American Society of Anesthesiologists physical status IVE, with medical history significant for ascending cholangitis status post-ERCP with biliary stent placement 2 years previously. During her hospitalization, she developed septic shock, and her workup for sepsis once again suggested ascending cholangitis. She was taken emergently to surgery for an ERCP with stone removal and biliary stent replacement under general endotracheal anesthesia.

In the operating room, the patient remained stable during placement of the endoscope, fluoroscopic examination, and initial ballooning of the biliary tree. Difficulty placing the biliary stent required multiple passes through the common bile duct. During placement of the stent, the patient’s SpO2 and ETCO2 both rapidly declined, and pulse oximeter waveform and arterial line tracing flat-lined. The ECG tracing rapidly progressed from normal sinus to bradycardia to asystole. The patient was turned supine, and ACLS was initiated. A TEE showed large amounts of air in the right heart. Resuscitation was unsuccessful.

Both procedures were performed with the patients in the prone position, making observation of abdominal/duodenal distention difficult, and operative reports do not mention whether these cavities were decompressed on removal of the endoscopes.

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DISCUSSION

VAE can have significant cardiovascular, pulmonary, and neurologic consequences. During ERCP or other endoscopic procedures, diagnosis may be difficult because presentation can mimic symptoms related to a patient’s comorbidities. Life-threatening processes generally are excluded first, leading to delays in treatment when early intervention is critical.

GI endoscopy involves insufflation of air at up to 2 L/min.5 Air escapes via natural body orifices; however, if a blood vessel is traumatized, air may be insufflated into the vascular system. Pressures up to 45 kPa or 6.5 psi can be reached during ERCP, creating a favorable pressure gradient leading to a VAE. For consideration, the average recommended tire inflation pressure is around 32 psi. The majority of cases of VAE during ERCP have been linked to mucosal trauma, either in the form of pre-existing ulceration6,7 or trauma at the time of sphincterotomy or stent placement.4,8–12 Other risk factors include previous instrumentation of the bile duct system, transhepatic portosystemic shunts, or trauma to the liver. Inflammation of the digestive system, postsurgical GI fistulas, or GI interventional techniques also have been implicated.

Air emboli may range from clinically silent to catastrophic severity, depending both on the volume and on the rate of air entry.4 Severe cases of VAE may result in cardiovascular collapse. It was thought an “air-lock” phenomenon from large amounts of air entrained into the right heart prevented blood from exiting the ventricle. It appears more likely that the acute increase in right ventricular pressure and decreased perfusion pressure leads to right ventricular ischemia, right heart failure, arrhythmias, and ultimately cardiovascular collapse.13

A patent foramen ovale has been demonstrated in 20% to 30% of the population, placing these patients at high risk for paradoxical air embolism. Air in the systemic circulation may manifest as myocardial infarction and/or cerebral vascular accident.8,11

Early diagnosis requires vigilance and a high index of suspicion. Although VAE is associated more commonly with ERCP, it may occur during any endoscopic procedure in which vasculature integrity is compromised.4 VAE may be identified with transesophageal or transthoracic echocardiography. Significant amounts of air can be visualized in the right heart. Right ventricular strain on electrocardiogram and pulmonary artery hypertension also can be seen. Auscultation or precordial Doppler may demonstrate the characteristic mill-wheel murmur of a VAE. Capnography reveals a decrease in ETCO2 because of a decrease in cardiac output. If air is being used for insufflation, nitrogen will be seen among the expired gases.4 Symptoms may occur suddenly, especially with change of the patient from the prone to supine position.

The most important step in management is to have a high index of suspicion. Prophylactic measures to minimize the potential for VAE and additional patient monitoring may help. Initial treatment should focus on the “ABCs” of resuscitation. The procedure should be terminated and the airway secured if the patient is not already intubated and placed on 100% oxygen. The gastroenterologist should decompress the stomach and duodenum on withdrawal of the endoscope to reduce the pressure gradient and stop additional air entrainment. Cardiopulmonary resuscitation should be performed to support the patient’s circulation, with a focus on improving right ventricular function. Resuscitation may be performed in either the supine or the prone position. There appears to be little benefit from positioning the patient in the left lateral decubitus position, although the Trendelenburg position may decrease the spread of air to the cerebral circulation.14 Volume expansion to increase central venous pressure may prevent further embolization. If systemic air embolism is suspected, a computed tomographic scan may identify air within the affected organs, namely the cardiac and/or cerebral circulation.12 Hyperbaric oxygen can be used during the recovery phase to decrease the size of air bubbles that may have spread to the systemic circulation, especially the cerebral vasculature. The use of a precordial Doppler probe may be beneficial for high-risk patients detecting air before symptoms appear.4,8,9,11 Carbon dioxide has been suggested for insufflation, being more soluble in blood and more rapidly absorbed than air.

Both cases share many commonalities with other cardiac arrests secondary to VAE during endoscopy. Predisposing factors, including difficult or previous instrumentation of the common bile duct, existed. We saw hemodynamic instability, decreasing ETCO2 values signifying decreased cardiac output, and a rapid progression to cardiac arrest. In both patients, alternate diagnoses were entertained during the resuscitation, including myocardial infarction, electrolyte abnormalities, and pulmonary embolism. A TEE examination found large quantities of residual air in the right heart, helping to aid our diagnosis. Although patient 1 initially became hypertensive and tachycardic, an uncommon initial presentation reported in the literature8,11 they rapidly progressed to hypotension, bradycardia, and eventually asystole. Patient 2 became hypotensive and bradycardic immediately before asystole, the more commonly reported presentation. Consistent with other case reports, VAE was not identified until well into the resuscitation.

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CONCLUSIONS

VAE is a potentially catastrophic complication of ERCP. The rarity of this complication leads to delayed diagnosis when early diagnosis is critical. The most crucial step in patient management is to understand risk factors and maintain a high index of suspicion. Arrhythmias, hypotension, along with a decrease in ETCO2 and SpO2 should warn of a potential VAE. Treatment should include cessation of the procedure, securing the airway, administering 100% oxygen, and preparing to support the patient hemodynamically, including volume expansion with the goal of improving right ventricular function. A TEE can be helpful in the diagnosis, and the initiation of hyperbaric oxygen can reduce the volume of gas bubbles, lessening the cardiovascular and neurologic sequelae. As anesthesiologists continue to expand coverage to endoscopy suites, providers must be aware of this disastrous complication.

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DISCLOSURES

Name: Joseph M. Sisk, MD.

Contribution: This author helped complete the manuscript.

Name: Monica D. Choi, MD.

Contribution: This author helped complete the manuscript.

Name: Andrew B. Casabianca, MD, DMD.

Contribution: This author helped complete the manuscript.

Name: Ali M. Hassan, MD.

Contribution: This author helped complete the manuscript.

This manuscript was handled by: Raymond C. Roy, MD.

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