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Hemorrhagic Shock After Epicardial Pacing Wire Removal

A Case Report

Warner, Paul A., MD*; Warner, Lindsay L., MD*; Pochettino, Alberto, MD; Roy, Tuhin K., MD, PhD*

doi: 10.1213/XAA.0000000000000640
Case Reports
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Epicardial pacing wires are routinely used to avoid hemodynamic instability due to perioperative arrhythmias after cardiac surgery. In rare cases, pacing wires themselves can be associated with potentially life-threatening complications. Herein, we present a novel case of hemorrhagic shock and hemoperitoneum after temporary epicardial pacing wire removal.

From the Departments of *Anesthesiology and Perioperative Medicine and Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota.

Accepted for publication September 8, 2017.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Paul A. Warner, MD, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN. Address e-mail to warner.paul@mayo.edu.

Cardiac surgery is frequently complicated by postoperative arrhythmias, especially in patients with history of diabetes mellitus or preexisting dysrhythmias.1 Temporary epicardial pacing wires are routinely inserted to optimize cardiac output in the setting of significant bradyarrhythmias.2–4 Although rare, temporary epicardial pacing wire extraction can lead to potentially life-threatening complications that significantly contribute to the morbidity and mortality of critically ill patients.5

We present a very rare complication of hemoperitoneum with hemorrhagic shock after temporary epicardial pacing wire removal.

Written consent has been obtained.

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CASE

A frail, 69-year-old gentleman transferred from an outside hospital to the Mayo Clinic Cardiac Surgery intensive care unit (ICU) for management of acute aortic valve regurgitation with acute exacerbation of chronic left ventricular systolic congestive heart failure. His medical and surgical history included medically managed type B aortic dissection; type A ascending aortic dissection status post ascending 30 mm Hemashield aortic graft and aortic valve resuspension several years prior; renal artery stenosis status post renal artery stent; chronic kidney disease, stage 3; hypertension; and peripheral arterial disease status post iliac artery stenting.

He presented to his home hospital with a chief complaint of 1 week of worsening chest pain associated with the sudden onset of dyspnea. He was found to be in frank respiratory distress with evidence of significant pulmonary edema by examination and chest x-ray. Computed tomography (CT) angiography of the chest and transthoracic echocardiogram demonstrated moderately severe aortic regurgitation in the setting of an aneurysmal enlargement of the ascending aorta around his prosthesis. He immediately transferred to the Mayo Clinic for surgical consultation and critical care management. With diuresis, systemic vascular afterload reduction, and noninvasive positive pressure ventilation, his heart failure symptoms improved dramatically.

Ten days after hospital transfer and resultant medical optimization, he underwent definitive surgical repair of his ascending aortic aneurysm and aortic regurgitation. He underwent coronary artery bypass grafts times 4; total arch replacement with elephant trunk technique; revascularization of the left subclavian, left common carotid, and distal innominate artery; as well as aortic root replacement with a 29 mm porcine Freestyle Medtronic root utilizing deep hypothermic circulatory arrest.

Intraoperatively, 3 attempts to separate from cardiopulmonary bypass were unsuccessful due to severe left ventricular systolic dysfunction. He was started on epinephrine, norepinephrine, and milrinone infusions. Due to his complex aortic anatomy, intraaortic balloon pump was not an option for optimizing his cardiac function. On the fourth attempt, separation from cardiopulmonary bypass was successful. Given the complexity of the surgery and difficulty in weaning from bypass, temporary epicardial pacing wires were placed.

Both atrial and ventricular leads were secured due to the severe burden of his coronary dysfunction and the high likelihood for the development of significant postoperative arrhythmias. These were secured in standard fashion with sutures to the epicardium and then blindly tunneled to the skin at the caudal end of the midline sternal incision at the subcostal margin. Two grounding wires and 2 percutaneous epicardial pacing leads were placed in total. In spite of the fact that this was a revision of a prior cardiac surgery, there was no apparent difficulty in securing these pacing wires.

His postoperative course initially was complicated by cardiogenic and vasoplegic shock, which improved significantly over the following 3 days. He was successfully extubated on postoperative day 4 after elective bronchoscopy for clearance of mucous plugging of the left main stem bronchus with near-complete collapse of the left lung. He remained on a nicardipine infusion to control his blood pressure due to an unrepaired descending thoracic aortic aneurysm measuring greater than 6 cm.

He developed significant sinus node dysfunction with resultant labile bradycardia requiring atrial pacing at 80 beats per minute. During the course of his first week of recovery, the patient regained normal sinus activity without further requirement for atrial pacing. The temporary epicardial pacing wires were removed with gentle manual traction by a member of the surgical team on postoperative day 8 at the patient’s bedside in the surgical ICU.

Approximately 2 hours after removal of the pacing wires, the patient had an acute episode of altered mental status, decreased level of consciousness, and severe hypotension with a systolic blood pressure nadir of 60 mm Hg. Fluid resuscitation commenced immediately with the concomitant use of intermittent boluses of ephedrine and phenylephrine. A bedside point-of-care hemoglobin showed a hematocrit of 14%. A hemoglobin value of 8.0 had been drawn on routine laboratory monitoring 3.5 hours earlier, consistent with prior hemoglobin levels. Previous international normalized ratio, activated partial thromboplastin time, and platelet count were 0.9, 33, and 136, respectively. Chest tube drainage was unchanged. A left internal jugular introducer sheath was placed to facilitate blood product administration. The patient was emergently transfused 6 units packed red blood cells, 1 unit platelets, and 2 units fresh frozen plasma. He required endotracheal intubation for increased work of breathing and airway protection in the setting of altered mental status.

An emergent bedside transthoracic echocardiogram demonstrated a normally functioning left ventricle with no evidence of new pericardial effusion, tamponade physiology, or ischemic ventricular wall motion. The patient was resuscitated and stabilized in the ICU over the subsequent 2 hours. The patient was evaluated by the Cardiac and Vascular Surgery Services, and the decision was made to proceed with a CT angiogram of the chest to evaluate other potential bleeding sources, such as retroperitoneal bleed, splenic laceration, or aortic dissection. CT findings in the thoracic cavity were unchanged, demonstrating a stable, preexisting mediastinal fluid collection, as well as a similarly stable, resolving hemothorax within the left chest. It also demonstrated a duplicated left-sided superior vena cava with central venous cannulation (Figures 1 and 2). The most significant interval change per the interpretation of the radiologist was the development of a new collection of acute blood products in the peritoneum displacing the spleen inferiorly and extending further into the pelvic cavity. There was no evidence of active extravasation or splenic laceration at the time of imaging approximately 3 hours after the removal of the pacing wires and subsequent resuscitation.

Figure 1

Figure 1

Figure 2

Figure 2

The patient was taken to the operating room directly from the CT scanner in preparation for exploratory laparotomy; however, after discussion between the surgeons and anesthesiologists, no surgical intervention was performed, due to the lack of definitive bleeding source on imaging with stable hemodynamic indices and coagulation markers. Shortly after arrival to the operating room, he transitioned back to the surgical ICU for further hemodynamic monitoring, and did not ultimately require surgical or percutaneous intervention. He remained intubated and mechanically ventilated overnight and was extubated 1 day later with no evidence of cardiopulmonary compromise.

Review of the case among the surgeons, anesthesia intensivists, and radiologists yielded a consensus diagnosis of hemorrhagic shock likely following incidental laceration of a superior epigastric vessel or a mesenteric tear that acquired in situ hemostasis. Ultimately, the diagnosis was speculative and one of exclusion. The diagnosis was based on the timing of the pacing wire removal and the onset of symptoms; the radiologist’s interpretation of a peritoneal, not a retroperitoneal, hemorrhage; the lack of other sources of hemorrhage on both transthoracic echocardiography and CT angiogram; as well as the prior reports of superior epigastric vessel compromise on extraction of temporary epicardial pacing wires.5

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DISCUSSION AND MANAGEMENT CONSIDERATIONS

Temporary epicardial pacing wires are typically removed by gentle, percutaneous traction at the bedside in the postoperative setting. These are usually simple, uncomplicated procedures; however, the majority of complications associated with temporary epicardial pacing wires occur during the time of lead extraction. The overall frequency of major complications is estimated at 0.04%.6,7 Ventricular rhythm disturbances, including premature ventricular complexes and nonsustained runs of ventricular tachycardia, are the most commonly associated complication, although these are rarely clinically significant.8

Cardiac tamponade is the most cited cause of major morbidity, although saphenous vein graft laceration has also been described.2,9 Retained wires from failed extractions can similarly cause complications, most notably localized infection and wire migration into surrounding tissue beds.10–14

Close hemodynamic monitoring is warranted after pacing wire removal due to the potential for life-threatening development of arrhythmias or hemorrhage. Standard resuscitative methods should be utilized if hemorrhagic shock is unmasked with special concern for cardiac tamponade physiology in the setting of atrial or ventricular wall laceration. Emergent bedside transthoracic echocardiography should routinely be performed to assess for hemopericardium.5

The incidence of hemoperitoneum secondary to temporary epicardial pacing wire extraction is unspecified in current medical literature. The most likely etiology of hemorrhage in this particular case is the inadvertent laceration of a superior epigastric vessel or a tear of an intraabdominal mesentery in close approximation to the extracted leads. Fortunately, further surgical or interventional hemostasis was not required here, since hemostasis was likely accomplished by in situ tamponade of the culprit vessel; however, had hemodynamic instability continued, emergent surgical exploratory laparotomy would have been warranted.

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CONCLUSIONS

Temporary epicardial pacing wires have well-established safety profiles in cardiac surgery. They are routinely used to prevent and treat unstable arrhythmias in the perioperative setting. In rare instances, extraction of these devices can cause life-threatening hemorrhage or arrhythmia. Extraction, therefore, should only be performed in a monitored care setting. Occult bleeding should be ruled out by CT angiography in the setting of suspected hemorrhage when transthoracic echocardiography does not reveal evidence of hemopericardium or is otherwise nondiagnostic.

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DISCLOSURES

Name: Paul A. Warner, MD.

Contribution: This author helped care for the patient, and draft and edit the manuscript.

Name: Lindsay L. Warner, MD.

Contribution: This author helped collect the data and references, and draft the manuscript.

Name: Alberto Pochettino, MD.

Contribution: This author helped care for the patient, and edit the manuscript.

Name: Tuhin K. Roy, MD, PhD.

Contribution: This author helped care for the patient, and edit the manuscript.

This manuscript was handled by: Mark C. Phillips, MD.

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