Ann Thorac Surg 2002;73:1314-1315
© 2002 The Society of Thoracic Surgeons
Case report
Delayed cardiac tamponade after coronary artery laceration
John Bozinovski, MD, MSa,
Shaohua Wang, MD*a,
Someshewar Nakai, MDa
a Department of Cardiovascular and Thoracic Surgery, University of Alberta, Edmonton, Alberta, Canada
Accepted for publication July 30, 2001.
* Address reprint requests to Dr Wang, Department of Cardiovascular and Thoracic Surgery, Room 2H2.34, Walter Mackenzie Health Sciences Centre, 8440-112 St, Edmonton, Alberta, Canada, T6G 2B7
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Abstract
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Delayed cardiac tamponade after laceration of a coronary artery is unusual and uncommonly reported in the literature. We describe a patient in whom this potentially fatal complication developed 8 days after a stab wound to his chest. In our review of the English language literature we identified only one other report of delayed tamponade after coronary artery laceration.
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Introduction
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Pericardial effusion causing tamponade results from numerous etiologies including direct penetrating trauma to the heart. In the case of acute tamponade it can be expeditiously identified and treated. Fortunately, the occurrence of delayed tamponade following penetrating cardiac injury is not common but can remove the patient from the acute care setting and timely resuscitation. We report the case of a patient who developed delayed cardiac tamponade following penetrating cardiac trauma.
An intoxicated 18-year-old man was brought to a community hospital by ambulance after stab wounds to the chest, head, and back. Initially, he complained of no chest pain. The head and back wounds were superficial; two stab wounds to the left anterior chest measuring 1 cm and 2.5 cm appeared to be deeper but were not digitally explored. His blood pressure was 100/70 mm Hg, his heart rate was 92 beats per minute, and his respiratory rate was 20 breaths per minute. There were no postural changes to his vital signs. Mild hypoxemia improved with supplemental oxygen. Chest roentgenogram demonstrated left basilar contusion and a small amount of subphrenic free air. Electrocardiography demonstrated diffuse ST-segment elevations consistent with pericarditis. He was admitted to the hospital at that time and over the following 3 days he began to experience left-side pleuritic type chest pain.
Three days after initial admission he was transferred to a tertiary hospital for further investigation and treatment. On arrival his pleuritic chest pain persisted and vital signs continued to be stable with blood pressure measuring 110/70 mm Hg, normal sinus rhythm, heart rate of 84 beats per minute, and no postural changes. Jugular venous pulse was not elevated. Auscultation revealed normal heart sounds, no pericardial friction rub, and except for bilateral basal crepitations, normal breath sounds. Peripheral pulses were palpable in all four limbs. Arterial blood gases on room air were as follows: pO2 61 mm Hg, pCO2 42 mm Hg, SaO2 91%, HCO3 25 mmol/L, and pH 7.39. Hemoglobin measured 10.5 g/dL. Electrolytes, prothrombin time, and partial thromboplastin times were normal. Creatine kinase was elevated mildly but the myocardial fraction was normal. The patient was admitted and given an antiinflammatory medication for his pain. Echocardiography demonstrated normal chamber sizes with no collapsed chambers, normal wall thickness, and an ejection fraction of 0.70 and no pericardial effusion. Electrocardiography showed a high ST segment takeoff in leads I, II and V2 through V6. This was interpreted as being a normal variant with early repolarization. Serial chest roentgenography was unchanged over the 5 days the patient was at our institution and he was discharged home in stable condition.
That evening he returned to the original hospital after collapsing and gave a history of epigastric pain, dyspnea, and fatigue over the previous 5 hours. On admission his blood pressure was 70/50 mm Hg, his respiratory rate was 40 breaths per minute, he had a weak pulse and sinus tachycardia at 140 beats per minute. After establishing an airway and volume resuscitating the patient, he was transferred by air ambulance to our center. The patient had a brief stop in the emergency department and was found to be in shock with a blood pressure of 80/50 mm Hg and a weak pulse of 130 beats per minute; hemoglobin level was 10.8 g/dL. He was tachypnic with bilaterally equal breath sounds, with no deviation of his trachea and had muffled heart sounds. Electrocardiography demonstrated diffuse ST-segment elevation and PR depression. Chest roentgenogram revealed a widened mediastinum and a globular cardiac silhouette consistent with a pericardial effusion.
The patient was taken to the operating room immediately where a midline sternotomy was performed and 600 mL of clotted blood was evacuated from the pericardium. His systolic blood pressure immediately improved from 80 to 120 mm Hg. Exploration revealed no injury to the myocardium itself; however, the left anterior descending coronary artery was lacerated in the middle third segment and actively bleeding although the injury did not extend through to the back wall of the vessel. It was repaired with interrupted 6-0 Prolene suture, using a Doppler probe to ensure satisfactory distal flow. He had an otherwise uneventful hospital stay and was discharged 7 days later in stable condition.
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Comment
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Delayed cardiac tamponade can be a devastating complication after penetrating injury to coronary vessels. This complication is compounded for patients who are no longer hospitalized as they are further removed from timely resuscitation in the event of significant cardiopulmonary failure. Recommendations regarding treatment and duration of observation and follow-up of such injuries lack the influence afforded by numbers, as isolated coronary artery injuries are very uncommon and delayed tamponade after coronary vessel injury is even less common. As a result the optimal approach to treating these patients has not yet been determined. Additionally, injured vessels may not be actively bleeding when the patient is first seen. Our patient had penetrating trauma to the chest and was stable on discharge, 8 days after the injury, only to return with a delayed tamponade. The delay in presentation is attributed to lack of bleeding initially from the injured artery. The vessel likely went into spasm at the time of injury and very shortly thereafter formed a clot to facilitate hemostasis. At some point after the patient’s discharge from hospital the clot either released or was resorbed so that hemostasis was lost.
In general, survival is poor after penetrating trauma to the chest. It is estimated that a significant majority of patients with penetrating cardiac injuries do not reach the hospital alive [1]. Another study of 100 patients hospitalized with acute penetrating cardiac injuries demonstrated a survival of only 31% [2]. Seventy-seven percent of these patients had an acute tamponade but the authors did not mention the incidence of delayed tamponade.
Coronary artery perforations after percutaneous transluminal coronary interventions have been reported in the literature quite frequently [3–6]. In addition, the complication of delayed cardiac tamponade after percutaneous coronary intervention has also been reported [6]. However, there are few reports of delayed tamponade after penetrating injury to the chest. A review of the literature using Medline 1966 to 2000 to search English language articles identified only one such report [7].
It is clear that the dangers of penetrating chest trauma are mainly acute in nature. However, after the acuity of the situation has been managed risks to the patient remain, as demonstrated in the previous report and in this case report. The optimal management of these patients remains to be elucidated and some have recommended surgical management despite the absence of hemodynamic indications. They argue that late complications such as delayed tamponade, heart failure, and coronary artery fistula justify early surgical correction. Delayed tamponade occurred in both of these patients after being discharged from the hospital and both occurred within 8 days of the initial injury. Early surgical exploration could have prevented our patient from having delayed cardiac tamponade; however, surgical exploration is hard to justify in a hemodynamically stable patient with no pericardial effusion demonstrated by echocardiography.
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References
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Heller R.F., Rahimtoola S.H., Ehsani A., et al. Cardiac complications: results of penetrating chest wounds involving the heart. Arch Intern Med 1974;135:491-496.
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Ellis S.G., Ajluni S., Arnold A.Z., et al. Increased coronary perforation in the new device era. Incidence, classification, management and outcome. Circulation 1994;90:2725-2730.[Abstract/Free Full Text]
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Altman F., Yazdanfar S., Wertheimer J., Ghosh S., Kotler M. Cardiac tamponade following perforation of the left anterior descending coronary system during percutaneous transluminal coronary angioplasty: successful treatment by pericardial drainage. Am Heart J 1986;111:1196-1197.[Medline]
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Tseng C.D., Chen C.Y., Chiang F.T., et al. Coronary artery perforation and delayed cardiac tamponade following balloon coronary angioplasty. J Formos Med Assoc 1996;95:789-792.[Medline]
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Abstract
Introduction
