Introduction

Blunt cardiac injuries are the leading causes of fatalities following motor-vehicle accidents(₁). Myocardial injury caused by blunt chest trauma has been recognized with increased frequency over the past 2 decades(₂). Increased awareness by physicians and the increased use of various clinical and laboratory diagnostic modalities have contributed to this recognition. Injuries range from inconsequential to catastrophic and can affect any or all areas of the heart: pericardium, myocardium, coronary arteries and veins, chordae, papillary muscles, valves, and great vessels(₂). Although many of the patients with anatomic cardiac injuries die at the scene, with improved prehospital care these patients have more likelihood of surviving the first hour and presenting to an emergency room alive for definitive treatment. Prompt recognition of the injury based on the mechanism and a high index of suspicion must lead to immediate surgical intervention in order for these patients to survive(₃).In addition to the medical importance of the diagnosis, substantial forensic implications have been known to arise(₂).

Case Presentation

Our case was a 27-year-old male who had experienced polytrauma due to a traffic accident happened two hours before the admittance to our hospital. He was referred to our Emergency Service from another health institution. His past medical history revealed excision of a tumor from the 3rd ventricle of his brain 10 years ago and a cerebrovascular accident related to this. Transthoracic echocardiography done at the other institution showed limited amount of pericardial fluid. Abdominal ultrasound and computed tomography (CT) pointed out no intraabdominal collection of fluid. Cerebral CT had suspicious findings of hydrocephalus of normal pressure. This case was referred then to our center.On arrival to our emergency unit, his blood pressure was 80/44 mmHg and his pulse rate was 115/min and regular but it was faint.He responded to the volume replacement. Chest X-ray revealed cardiomegaly but there was no pleural effusion or bone fracture. Echocardiogram revealed cardiac tamponade and he was diagnosed as cardiac rupture due to non penetrating trauma. According to echocardiogram, the thickness of the collected fluid was 11 millimeters at the anterior of the right ventricle, 20 millimeters at the apex of left ventricle and 16 millimeters at the lateral wall, pointing at the diagnosis of cardiac tamponade. Moreover, an image of fresh coagulum surrounding the heart was present (Figures 1 and 2).

Figure 1

Figure 1: Acute cardiac tamponade view in TTE.

Figure 2

Figure 2: Image corresponding with fresh coagulum surrounding the heart.

Our patient underwent operation urgently with a median sternotomy approach without using cardiopulmonary bypass. Coagulum materials was cleaned for exploration and localization of the injury was determined. Tear of the atrium was seen superior to the vena cava inferior localization(Figure 3).

Figure 3

Figure 3

Hemorrhage was controlled with digital compression. This simple myocardial injury was repaired primarily with teflon-felt and polypropylene sutures (Figure 4).

Figure 4

Figure 4

Afterwards, pleural spaces were entered bilaterally and all of the intrathoracic structures were explored. No major pathological finding was recognized (Figure 5).

Figure 5

Figure 5

The postoperative course was uneventful. We used double parenteral antibiotherapy prophylaxis and postoperative follow-up period was 8 days. He was discharged without any neurophysiological disturbance.

Discussion

Blunt cardiac trauma is the leading cause of fatalities following motor vehicle accidents(₃). Injury to the heart is involved in 20% of road traffic deaths(₁). Cardiac injuries were present in 16% of the patients in Glinz et al. series,suffering from blunt chest trauma. 25% of these cases had no concomitant rib fractures(₄).Structural cardiac injuries (chamber rupture or perforation) carry a high mortality rate and patients rarely survive long enough to reach hospital(₁). Chamber rupture is present at autopsy in 36-65% of death from blunt cardiac trauma, whereas in clinical series it is present in 0.3-0.9% of cases and is an uncommon clinical finding. Patients with large ruptures or perforations usually die at the scene or during transportation;the rupture of a cardiac cavity, coronary artery or intrapericardial portion of a major vein or artery is usually instantly fatal because of acute tamponade(₁). The small, rare, remaining group of patients who survive to hospital presentation usually have tears in a cavity under low pressure and prompt diagnosis and surgery can now lead to a survival rate of 70-80% in experienced trauma centres(₁). Two distinct syndromes are apparent--haemorrhagic shock and cardiac tamponade. Any patient with severe chest trauma, hypotension disproportionate to estimated loss of blood or with an inadequate response to fluid administration should be suspected of having a cardiac cause of shock(₁).

Sonography is extremely important for evaluation(₄). The main pathophysiologic determinant for most survivors is acute pericardial tamponade(₁). Early use of echocardiography to detect the presence of hemopericardium and cardiac tamponade in patients with suspected atrial rupture following blunt chest trauma is advocated(₅).

Heart wall rupture and luxation of the heart require operative treatment(₄). Cardiac tamponade can become fatal in minutes(₆). Decreasing cardiac output and following shock table develop because of depressed myocardial contractility and insufficient, atrial contractility (₇,₈). In this condition widespread reflex compensotary mechanisms, peripheral arterial and venous vasoconstruction and prevention of intravascular volume, and increased chronotropism maintain the cardiovasculary stability. General anesthesia can inhibit these reflexes and cardiac arrest can develop. Successful results have three basic elements and these are; replacing the blood volume, control of hemorrhagy and emergently relieving the tamponade(₆). In most reported cases, the cardiac tear has been repaired without using cardiopulmonary bypass. However, it is difficult to diagnose location of the tear, therefore, the repair became safer using cardiopulmonary bypass for the patients with cardiogenic shock(₉).

Correspondence to

Doç. Dr. Ufuk YETKIN, 1379 Sok. No: 9,Burç Apt. D: 13 - 35220, Alsancak – IZMIR / TURKEY Tel: +90 505 3124906 , Fax: +90 232 2434848 e-mail: ufuk_yetkin@yahoo.fr