Ann Thorac Surg 2002;74:239-241
© 2002 The Society of Thoracic Surgeons
Case report
Pericarditis after trauma resulting in delayed cardiac tamponade
Riyad Karmy-Jones, MD*a,
Tina Yen, MDa,
Carol Cornejo, MDa
a Department of Surgery, Harborview Medical Center, Seattle, Washington, USA
Accepted for publication January 22, 2002.
* Address reprint requests to Dr Karmy-Jones, Department of Surgery, Box 359796, 325 Ninth Ave, Harborview Medical Center, Seattle, WA 98104 USA
e-mail: karmy{at}u.washington.edu
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Abstract
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Pericarditis complicating cardiac trauma and resulting in tamponade is uncommon. Possible causes include an autoimmune reaction or an inflammatory response to blood entering the pericardium. We present two patients, one with effusive and one with constrictive pericarditis occurring within 2 weeks of a penetrating trauma close to but not directly involving the heart. These cases illustrate the importance of clinical suspicion and aggressive management in the diagnosis and management of such patients.
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Introduction
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Pericarditis leading to tamponade resulting from traumatic injury is an uncommon event. The cause appears to be an autoimmune phenomenon, similar to that described in postcardiac injury syndrome [1, 2]. Although the majority of delayed effusions are clinically insignificant, and can be treated by expectant management or antiinflammatory agents, a rare few can evolve into tamponade [3–5]. In addition, although constrictive complications typically occur months or years after the inciting event, rarely clinical compromise can occur within days [6]. We present 2 patients with pericarditis occurring within 2 weeks of a penetrating injury that required operative intervention. Both patients presented initially with symptoms consistent with pulmonary embolism. A high-degree of suspicion, including liberal use of echocardiography, should be maintained when patients present with signs and symptoms consistent with pericarditis in combination with deteriorating cardiopulmonary status.
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Case reports
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Patient 1
A 39-year-old man presented with a gunshot wound to the posterolateral left chest, with the bullet lodged in the right costal margin, in the midclavicular line. At laparotomy, injuries to the diaphragm, stomach, and left lobe of the liver were found. A pericardial window was negative, and the window closed. Eight days after operation he developed low-grade fevers (maximum temperature 39°C) and leukocytosis. Within 24 hours he complained of increasing left precordial and substernal chest pain. The pain was aggravated by recumbency, deep inspiration, and twisting of the torso. Chest radiograph was normal except for some left basilar collapse. The cardiac silhouette was within normal limits. A small pleural effusion was also noted. Electrocardiogram revealed diffuse ST-T changes. An abdominal computed tomographic scan, performed to rule out intraabdominal sepsis, revealed a thickened pericardium and a relatively large effusion with a "floating" heart (Fig 1).
Lung windows revealed atelectasis of the left lower lobe. A transthoracic echocardiogram documented a 2-cm pericardial effusion, without signs of tamponade. That evening, the patient developed severe left chest pain, exacerbated by inspiration, and shortness of breath. Physical examination was notable for muffled heart sounds, a pulsus paradoxus of 15 mm Hg, and distended jugular veins despite the patient sitting upright. A blood gas on 50% face mask revealed the following: arterial oxygen tension of 67 mm Hg and arterial carbon dioxide tension of 34 mm Hg. To rule-out a pulmonary embolus, an urgent pulmonary angiogram was obtained, which was negative. The patient was taken directly to the operating room where a limited (nonrib spreading) anterolateral left thoracotomy was performed. The pericardium was inflamed and thickened. A large section of the pericardium anterior to the phrenic nerve was excised and 350 mL of clear fluid drained. In addition, 600 mL of clear pleural fluid was evacuated. The patient’s systolic blood pressure increased acutely from 90 to 100 mm Hg to 130 to 140 mm Hg. Of note, the pericardium at the site of the previous window was completely healed. In addition, an area of contusion on the anterior surface of the left ventricle was clearly identified. All pericardial cultures were negative and pathology revealed acute inflammation and fibrosis of the pericardium. Subsequently, the patient made a complete recovery.
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Fig 1. Computed tomographic scan demonstrating thickened pericardium, effusion, and heart "floating" within the pericardial sac.
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Patient 2
A 25-year-old man underwent urgent laparotomy after a gunshot wound inferior to the xiphoid. Injuries included a laceration to the inferior vena cava and left lobe of the liver. The cava was repaired and a left lateral hepatic lobectomy performed. Bilateral chest tubes were placed, and a pericardial window performed. The window was negative and subsequently closed. After two subsequent operations for abdominal pack removal and washout, the patient was transferred to the ward on hospital day 10. A follow-up computed tomographic scan noted a clot in the inferior vena cava and iliac veins and he was started on heparin. On hospital day 13 he developed acute respiratory compromise and was intubated. After transfer to the intensive care unit, a pulmonary artery catheter was placed, which revealed elevated right-sided filling pressures. Shortly after he suffered a cardiac arrest. A bilateral thoracotomy was performed with the goal of either removing clot or, by open compression, breaking up the presumed clot. At thoracotomy, however, the pericardium was found to be significantly inflamed and diffusely adherent to the underlying myocardium. Resection of pericardium released 200 mL of clear fluid, and the heart bulged out of the surgical defect. Once the pericardium was released, spontaneous circulation resumed. An emergency transthoracic echocardiogram revealed a dilated hypokinetic right ventricle, with elevated pulmonary pressure, but no visible clot. The patient continued to require inotropic support, but it became apparent that he had suffered an extreme hypoxic insult. He was declared brain dead 2 days later.
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Comment
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Pericarditis has been noted to be as high as 2% to 4% after myocardial infarction, and 22% after penetrating cardiac injury in survivors [5, 7, 8]. Although rarely becoming clinically significant, exudative nonhemorrhagic pericardial effusions leading to tamponade have been reported after blunt chest trauma, myocardial infarction, and cardiac operations [3, 5, 8]. The etiology has been predominantly attributed to an autoimmune reaction with antibodies directed against myocardium or pericardium after injury [1]. In addition, the introduction of blood into the pericardium may also set up a vigorous inflammatory response [9].
As Dressler [2] noted, the predominant clinical features are recurrent fever and pleuropericardial pain. These symptoms usually occur days or months after injury. The fevers are low grade (38° to 40°C) and the pain tends to be predominantly precordial, although it may radiate to the shoulder, neck, or scapular area. In addition, the pain is aggravated by inspiration, recumbency, and twisting of the torso. A pericardial friction rub may be heard until the effusion is large enough to cause muffled heart sounds. Large pericardial effusions, with or without tamponade, may result in compression atelectasis of the left lower lobe lung base [10]. Echocardiography is the most specific diagnostic modality. Not only will it document the effusion but also it may demonstrate pericardial thickening, consistent with inflammation. Progressive tamponade can be demonstrated initially by collapse of the right atrium and then subsequently, the right ventricle during diastole. Both have a predictive accuracy for tamponade of 72% [10]. Accuracy is affected by volume status and the presence of pulmonary hypertension.
In most instances posttraumatic pericarditis is self-limiting, although recurrences are not uncommon. Initial treatment, in the absence of tamponade, includes antiinflammatory agents. Acetylsalicylic acid is often effective, but if relapses recur, steroids, particularly if a growing effusion is documented, may be required [3, 5]. Once the effusion causes cardiac decompensation, drainage, either by pericardiocentesis or by operative approaches, is required. Constrictive pericarditis is even more uncommon after trauma, and has been related more to the effect of blood in the pericardial cavity [5, 9]. Usually it occurs weeks, but more often, years after the event [11]. Rarely, it can present within days of injury [6]. In the more delayed cases, extensive calcification is the rule [5].
In the first patient, the acute decompensation and "normal" echocardiogram suggested the possibility of pulmonary embolism. When this was excluded, urgent operative drainage was performed. The anterolateral approach was taken to avoid the risk of possible contamination of the pericardium from abdominal sites of infection, to allow wide pericardial resection, and, if suppurative pericarditis was present, to allow maximal debridement without risking sternal infection. Given the finding of a left ventricular contusion and the path of the bullet, we presume that the patient developed pericardial inflammation as a consequence of the blast injury to the heart. In the second patient, we still suspect that pulmonary embolism was also present, although autopsy did not confirm this. However, the pericardial restriction also significantly contributed to cardiac decompensation, as evidenced by the spontaneous return of cardiac activity once the pericardium was opened. Again, the path of the bullet was just inferior to the cardiac structures. In both patients, the introduction of blood into the pericardial sac during pericardial window may have been either the cause or a contributing factor.
Both of these patients illustrate the need for a high degree of suspicion for pericarditis and effusion in patients with respiratory and hemodynamic changes, even in the absence of direct cardiac injury. In particular, this condition may coexist with other syndromes, including infection. Echocardiography is a relatively accurate noninvasive modality for the diagnosis of pericardial effusion. However, the diagnosis of tamponade remains a clinical one. If there are no echocardiographic findings suggestive of tamponade, but clinical findings are consistent with tamponade physiology, a drainage procedure should be performed.
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References
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- Dressler W. A post-myocardial infraction sysndrome. JAMA 1956;160:1379-1383.
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Abstract
Introduction
