Asian Cardiovasc Thorac Ann 2004;12:139-142
© 2004 Asia Publishing EXchange Ltd
Delayed Cardiac Tamponade after Penetrating Thoracic Trauma
Felipe Rendón, MD,
Luis H Gómez Danés, MD,
Mario Castro, MD
Division of Cardiac Surgery, Hospital Universitario "José E. González", Nuevo León, México
For reprint information contact: Felipe Rendón, MD Tel: 52 81 8348 8305 Fax: 52 81 833 9077 Email: drfrendon{at}yahoo.com.mx Division of Cardiac Surgery, Hospital Universitario "José E. González", Madero y Gonzalitos S/N CP. 64460, Nuevo León, México.
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ABSTRACT
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Acute cardiac tamponade is very common after penetrating injuries to the chest. However, delayed cardiac tamponade is a rare phenomenon that may appear several days after injury. This paper presents three cases of delayed cardiac tamponade diagnosed weeks after ice pick wounds to the back. These experiences and a review of the literature on the subject are discussed.
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INTRODUCTION
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Penetrating cardiac injuries continue to increase in proportion to the steady rise in violence in our society. Most penetrating cardiac trauma presents dramatically and often with a fatal outcome even with early surgical intervention. Cardiac tamponade is not an infrequent occurrence with penetrating injuries to the chest, back, and upper abdomen. However, delayed cardiac tamponade is a rare phenomenon that may appear several days or weeks after injury. The following presents three cases of delayed cardiac tamponade diagnosed weeks after an ice pick wound to the back. These experiences and a review of the literature on the subject are discussed.
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CASE REPORT
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The first case concerned a 22 year-old male patient that was presented to our emergency department with 48 hours of chest pain and progressive shortness of breath. He had been discharged from another hospital 25 days earlier after sustaining an ice pick wound to the left posterior hemithorax, 3 cm lateral to the third dorsal vertebra. At that time, the patient presented a mild cough, epigastric abdominal pain, normal chest X-ray, no abnormal findings in laboratory tests and was discharged after 2 days. He was subsequently well until this presentation. He had no other medical history and was not taking medication. Physical examination demonstrated an anxious man with an alternans pulse of 95 bpm, blood pressure of 120/70 mmHg, respiratory rate of 28 breaths·min1, and temperature of 37.5°C. The neck veins were distended to 6 cm above the Louiss angle. A pulsus paradoxus of 18 mmHg was detected. Heart sound was normal. No pericardial rub was noted and the heart apex could not be palpated. The lung fields were normal to auscultation. He had a hemoglobin level of 9 g·L1, and a total leukocyte count of 15,000·mm3 with 81% neutrophils and 12% lymphocytes. Other biochemical tests showed a normal glucose level and mild liver enzyme elevation. The chest X-ray showed a moderate enlarged cardiac silhouette (bottle water sign) and normal lung fields. Electrocardiogram revealed a sinus rhythm, electrical alternans and negative T wave from V3 to V6. Echocardiography disclosed a 3 cm pericardial effusion and right atrium and ventricular diastolic collapse. Under local anesthesia and mild sedation a subxiphoid pericardial window was performed with findings of 1400 mL of serosanguineous fluid. Cell count revealed many red blood cells, 100 nucleated cells with 40% neutrophils, 48% lymphocytes, 6% monocytes and 4% eosinophils. Gram stain revealed no organism. The pericardial biopsy did not disclose any abnormality. The pericardial tube drained another 380 mL in the next 48 hours and was removed on hospital day 4 after an echocardiogram showed no effusion. Blood and pericardial fluid cultures remained negative throughout the hospitalization. The patient was discharged home on postoperative day 6 with anti-inflammatory agents for 1 week. At the 6 month follow-up the patient was doing well with no complaints and an unremarkable physical examination.
The second case involved a 28 year-old male patient who was transferred from another clinical center to the emergency department of our hospital with complaints of dyspnea and fever that had lasted for three days. Fifteen days before he had been stabbed with an ice pick in the left posterior hemithorax, 2 cm lateral to the fourth dorsal vertebra. Following observation in the emergency room and after all studies were reported normal, he was discharged after 24 hours and remained well until this presentation. Physical examination demonstrated a regular pulse of 105 bpm, blood pressure of 100/70 mmHg, respiratory rate of 30 breaths·min1, and a temperature of 38°C. The neck veins were distended 5 cm above the Louiss angle and a pulsus paradoxus of 15 mmHg was detected. Lung fields were clear bilaterally and the heart exam was normal. All blood and biochemical tests were normal. The chest X-ray showed a moderately enlarged cardiac silhouette. Electrocardiogram revealed a sinus rhythm with no other abnormalities. Echocardiography disclosed a 2 cm pericardial effusion and right atrium diastolic collapse. A subxiphoid pericardial window under local anesthesia and sedation was performed and 800 mL of serosanguineous fluid was found. Cell count revealed many red blood cells, 250 nucleated cells with 43% neutrophils, 45% lymphocytes, 7% monocytes and 4% eosinophils. Gram stain revealed no organism. The pericardial biopsy was normal. The pericardial tube drained another 150 mL in the next 48 hours and was removed on hospital day 3 after echocardiogram showed no effusion. Blood and pericardial fluid culture remained negative throughout the hospitalization. The patient was discharged home on postoperative day 9 with analgesics and anti-inflammatory agents. At the 9 month follow-up point the patient was doing well with no complaints and normal physical examination.
The final case concerned a 29 year-old male patient who was seen in the emergency department complaining of chest pain, progressive dyspnea, cough and fever for 24 hours. He had been discharged from the hospital 20 days earlier after sustaining an ice pick wound to the epigastrium and to the left posterior hemithorax, 4 cm lateral to the third dorsal vertebra. A diagnostic peritoneal lavage performed was normal. The chest X-ray, echocardiography and other studies were negative. The patient was discharged 48 hours later completely stable. He remained asymptomatic until this presentation. Physical examination revealed a patient who appeared ill, with an alternans pulse of 110 bpm, blood pressure of 105/60 mmHg, respiratory rate of 30 breaths·min1, and a temperature of 38.5°C. The neck exam was normal. A paradoxic pulse of 20 mmHg was seen. Heart sounds were muffled. The right lung field was clear and the left lung field disclosed a crepitant rales at the base. Complete blood count revealed a white blood cell count of 20000 mU·L1, with 85% neutrophils, 8% lymphocytes, 6% monocytes and 1% eosinophils. The chest X-ray showed an enlarged cardiac silhouette and left pleural effusion. The electrocardiogram was normal. The echocardiogram disclosed a 2.2 cm pericardial effusion and right atrium diastolic collapse. A diagnostic thoracocentesis was performed obtaining exudative pleural fluid. The patient was taken to the surgery room and under local anesthesia and mild sedation a 30 French chest tube was inserted and a subxiphoid pericardial window was performed. 1100 cc of serosanguineous fluid was removed. Cell count revealed many red blood cells, 800 nucleated cells with 52% neutrophils, 40% lymphocytes, 6% monocytes and 2% eosinophils. Gram stain from the pleural and pericardial fluid revealed no organism. The pericardial biopsy was normal. The pericardial tube drained another 280 mL in the next 3 days and was removed on hospital day 5 after echocardiogram showed no effusion. Blood, pleural and pericardial fluid culture remained negative throughout the hospitalization. The patient was discharged home on postoperative day 10 with anti-inflammatory agents. At the 12 month follow-up point, the patient was asymptomatic and had an unremarkable physical examination.
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DISCUSSION
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Penetrating trauma is a frequent presentation to urban emergency departments and these have shown a progressive increase over the past two decades. Although the literature indicates the increase is mostly due to gunshot wounds,1 stab wounds still remain a very frequent cause of penetrating cardiac injuries and in our experience they are the most frequent cause of penetrating trauma. Stab wounds produce a small tear in the pericardium that seals off, resulting in about 80 to 90% of acute cardiac tamponade.2 Delayed cardiac tamponade from such injuries are very rare. The first reports of delayed tamponade from cardiac injury were by MacQuot and Constantini in 1920.3 A survey based on a Medline search discovered only 12 patients with the diagnosis of delayed cardiac tamponade after penetrating trauma in the last 52 years (Table 1
). All these reported cases were lesions to the chest in the precordial area but one had a lesion in the epigastrium. Another, reported by Hasegawa et al4, resulted from an acupuncture needle inserted in the neck, that over time migrated to the heart and lacerated the pulmonary artery. No reported cases described lesion to the back as in our cases.
The mechanism of delayed cardiac tamponade is speculative. Pastor and Betts6 suggested it may be the result of the displacement of thrombus that temporarily closes the cardiac wound, or it may be due to the adhesion that forms at the time of the injury had been torn, mentioned by Mason et al.5 Another theory attributed to the presentation of pericarditis with effusion is due to postcardiac injury syndrome,7 which is characterized by fever, pleurocardial pain, pericarditis, and pulmonary involvement. It can present in as many as 22% of patients with penetrating cardiac injury8 and few of these patients will have cardiac tamponade. Postcardiac injury syndrome is attributed to auto-antibodies against the pericardium or myocardium.9
Cardiac tamponade is a clinical and hemodynamic syndrome that is well described in the literature. The classic physical findings are often not evident, making them less sensitive for ruling out cardiac tamponade. The electrocardiogram2 and the chest radiographs11 give some information to suggest the diagnosis but echocardiography is now the primary means of diagnosing cardiac tamponade and it must be performed in all cases of suspected penetrating cardiac injury.
The options currently available for the treatment of delayed cardiac tamponade are: pericardiocentesis, subxiphoid pericardial window and median sternotomy or thoracotomy. Excellent results are achievable with all of these methods and the selection of one of these depends on the clinical and hemodynamic status of the patient, the characteristics of the pericardial effusion, the etiology of the effusion and the experience of the surgical team. Pericardiocentesis is the least invasive means of draining a pericardial effusion. It may be performed at bedside or in the cardiac catheterization laboratory under electrocardiography or two-dimensional echocardiographic guidance. Markiewicz et al11 and Wong et al12 reported 83% and 32% incidences of recurrent tamponade, respectively, and a 15% rate of serious complications (1 death, 1 cardiac arrest, and 5 ventricular puncture) using this technique in medical patients. A subxiphoid pericardial window is an excellent therapeutic choice with excellent results and low morbidity. It can be performed under local or general anesthesia. It is recommended when the echocardiogram suggests that the fluid collection will not be approachable percutaneously and with confirmation of a cardiac injury, the incision can be extended as a median sternotomy for a cardiorrhaphy.
It is difficult to determine the exact cause of tamponade in these cases, but in accordance with the mechanism of the injury, the clinical presentation and the findings during surgical procedure, it appears that pericarditis (postcardiac injury syndrome) is the suggestive diagnosis. The taking of a pericardial biopsy is routine in all subxiphoid pericardial windows performed in our service, and in our experience it has a low sensitivity (around 25%) to help to make the etiologic diagnosis of the pericardial effusion. In these cases, it did not provide any more information. Although our patients lacked the complete Becks triad to make the clinical diagnosis of tamponade, the presence of the pulsus paradoxus in all patients, as well as the distended neck veins, the water bottle sign in chest X-ray, the pulsus alternans in one patient, and electrical alternans in another suggested the diagnosis of cardiac tamponade. Echocardiography is our gold standard diagnostic tool in the detection of cardiac tamponade. The use of computed tomography or magnetic nuclear resonance should be considered just when the doubt of another associated pathology exists.
Because of the suspicion of pericarditis with effusion, we tried as an initial treatment modality the subxiphoid pericardial window. If the patients had not improved, we would have promptly proceeded to a median sternotomy. However, this was unnecessary.
These cases emphasize the need for the physicians to be aware of the possibility of delayed cardiac tamponade in order to intervene in a timely fashion. We would recommend performing echocardiography in all patients with penetrating chest trauma as soon as the patient arrives at the emergency department, with follow-up six months after injury to detect such delayed sequelae and to educate and instruct the patients to return for symptoms of chest pain or dyspnea in order to promptly rule out complications.
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