Fatal Acute Myocardial Infarction after Multiple Blunt Injuries Involving the Chest.

The patient was a 60-year-old male fell whose head and left chest hit the ground after falling from a height of 2 m. He complained of the left shoulder and chest pain after regaining consciousness. On arrival, he showed left bloody otorrhea, left chest tenderness, and a limited range of motion due to the left shoulder pain. Emergency chest roentgenography revealed multiple left rib fractures, left clavicular fracture with decreased radiolucency in the left lung field, suggesting lung contusion. When the patient was being transported for computed tomography, he suddenly displayed ventricular tachycardia with pulse and subsequently became VF storm, which required percutaneous cardiopulmonary support. The coronary angiogram showed complete obstruction of the branch of the anterior descending artery. Coronary angioplasty resulted in recanalization; however, massive hemorrhage from the left ear was recognized. Computed tomography revealed traumatic subarachnoid hemorrhage and left massive hemothorax requiring thoracostomy. Massive hemorrhage from the left ear and left thoracic cavity continued after the patient was transported to the coronary care unit. He underwent massive transfusion; however, he died on the same day.

INTRODUCTION

Blunt cardiac trauma encompasses a wide range of clinical entities, including myocardial contusion, cardiac rupture, valve avulsion, pericardial injuries, arrhythmia, and coronary artery injury leading to myocardial ischemia or infarction.[1] We herein reveal a case of fatal acute myocardial infarction (AMI) after multiple blunt injuries that involved the chest.

CASE REPORT

The patient was a 60-year-old male fell whose head and left chest hit the ground after falling from a height of 2 m while working. He was initially in an unconscious state but complained of the left shoulder and chest pain after regaining consciousness during transportation. The patient had hypertension, gastric ulcer, and previous appendectomy. On arrival, his Glasgow Coma Scale was E3V4M6, and his vital signs were as follows: blood pressure was 162/98 mmHg, heart rate was 84 beats/min with premature ventricular contraction, and SpO2 99% with 10 L/min by oxygen mask. He showed left bloody otorrhea, left chest tenderness, and limited range of motion due to the left shoulder pain. Emergency chest roentgenography revealed multiple left rib fractures, left clavicular fracture with decreased radiolucency in the left lung field, suggesting lung contusion [Figure 1]. Focus assessment with sonography for trauma (FAST) was negative. The main results of a blood biochemical analysis on arrival were as follows: white blood cells, 11,600/μL, creatine phosphokinase was 731 IU/L, and fibrin degradation product was 56.8 μg/mL. When the patient was being transported for computed tomography, he experienced sudden-onset ventricular tachycardia. At one point, he regained sinus rhythm spontaneously; however, this was followed by ventricular fibrillation (VF), which required electrical shock, chest compression, and tracheal intubation. A return of spontaneous circulation was initially obtained. However, he subsequently experienced VF storm, which did not respond to four applications of electrical shock or an infusion of amiodarone and lidocaine. He was transferred to the radioscopy room for the induction of percutaneous cardiopulmonary support (PCPS) and coronary angiography. In total, he underwent 30 min of chest compression. Spontaneous circulation was regained after the commencement of PCPS with an infusion of heparin in the 30 min after the initial VF attack. Antiplatelets were not administered. The electrocardiogram revealed ST elevation at the I, aVL, and precordial leads [Figure 2]. The coronary angiogram showed a normal right coronary and circumflex branch of left coronary artery but complete obstruction of the branch of the anterior descending artery [Figure 3]. After obtaining spontaneous circulation, his pupils regained light reflex, and he moved spontaneously, and hence, he underwent the infusion of midazolam for sedation. Coronary angioplasty induced fresh thrombus from the obstruction, resulting in the successful recanalization of the anterior descending artery. Intravascular ultrasound revealed plaque formation and no findings of dissection in the coronary artery. After finishing 75 min of coronary intervention with the insertion of PCPS and intra-aortic balloon pump, massive hemorrhagic otorrhea was confirmed around his head, and his systolic blood pressure did not reach 80 mmHg. Computed tomography revealed skull base fracture, cerebral contusion, traumatic subarachnoid hemorrhaging, and left massive hemothorax in addition to lung contusion and pneumothorax, requiring thoracostomy. Initial bleeding volume was over 1500 ml. Massive continuous fresh hemorrhaging from the left ear and left thoracic cavity continued over 3000 ml after the patient was transported to the coronary care unit. As he was in a severe hemorrhagic shock state and had an activated partial thromboplastin time exceeding 150 s, induced hypothermic therapy was not applied. He underwent massive transfusion; however, he died on the same day.

Figure 1

Emergency chest roentgenography on arrival. Emergency chest roentgenography revealed multiple left rib fractures, and left clavicular fracture with decreased radiolucency in the left lung field, suggesting lung contusion

Figure 2

An electrocardiogram after obtaining spontaneous circulation. The electrocardiogram demonstrated ST elevation at the I lead, aVL, and precordial leads

Figure 3

The coronary angiogram on arrival. The coronary angiogram showed a normal right coronary artery and circumflex branch of the left coronary artery but complete obstruction of the branch of anterior descending artery

DISCUSSION

We reported a case of AMI with VF storm, requiring PCPS, after multiple blunt injuries including chest injuries, which resulted in bleeding that led to death as a complication of PCPS.[2] As a trauma patient, his probability of survival based on the trauma injury severity score was 91%; thus, the likelihood of survival would have been high if the patient had not experienced AMI.[3] We could not determine when the AMI occurred, but his colleague was not aware of the patient complaining of chest pain before his fall; thus, the occurrence of AMI after blunt chest trauma was most likely. Based on the results of coronary intervention, the estimated mechanism of complication of AMI was that traumatic impact triggered plaque disruption, followed by platelet aggregation that grew in association with an increase in fibrin formation, leading to persistent coronary flow obstruction and blood coagulation.[4]

AMI is a rare complication after blunt chest trauma. Autopsy studies of blunt chest trauma cases have revealed that heart injuries were involved in 20% of cases, and that the coronary arteries were involved in <2%.[1] In a review of 77 published cases of coronary artery injury caused by blunt chest trauma, the mechanisms of trauma included traffic accident, followed by sports, fighting, and animal attack.[5] Only one case of the cases was caused by a fall; thus, this case represents the second report.[6] The other epidemiological characteristics of coronary artery injury due to blunt chest trauma, included a male predominance and age of <45 years. The most frequently injured vessel was the left anterior descending artery (71%) similar to the present case. This is because the left anterior descending artery run anterior of the heart; thus, they tend to be vulnerable to external impact.[5] Five of the 77 cases (6.5%) had a fatal outcome; thus, the mortality rate was not so high. However, we could not find any reports of patients who survived after cardiac arrest due to coronary artery injury caused by blunt chest trauma. The initial complaints of acute coronary syndrome were masked by the chest injury; thus, a prompt evaluation by 12-lead electrocardiography is necessary to detect life-threatening acute coronary syndrome in patients with blunt chest trauma.[7]

When acute coronary syndrome, which requires antithrombolytic therapy, complicates bleeding diseases such as gastroduodenal ulcer, the mortality rate increases.[7] In the present case, the patient was bleeding to death from traumatic lesions due to the use of heparin for PCPS.[28] While our patient had a negative FAST result initially, occult active bleeding from injured sites might have continued and deteriorated after he was administered heparin, as he was transported to our hospital due to the low sensitivity of FAST for detecting hemorrhaging.[8] In addition, bleeding from the traumatic lesions had also deteriorated after chest compression, as rib fracture, sternum fracture, and internal organ injury can occur as complications induced by the chest compression itself.[9]

Tseng et al. in their study reported eight cases involving patients with posttraumatic cardiac arrest who were treated with extracorporeal circulation without heparin infusion for at least 24 h.[10] Among them, three patients, who received damage control surgery, ultimately survived. If a patient with blunt chest trauma complicated cardiac arrest due to coronary artery injury requires PCPS to support circulation, heparin control, or heparin-free PCPS with damage control surgery may help achieve survival; even though it may increase the possibility of the obstruction of the PCPS circuit by thrombosis.[1112]

CONCLUSION

If a patient with blunt chest trauma complicated cardiac arrest due to coronary artery injury requires PCPS to support circulation, heparin control, or heparin-free PCPS with damage control surgery may help achieve survival.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Youichi Yanagawa receives a research fund from the Ministry of Education, Culture, Sports, and Science and Technology (MEXT)-Supported Program for the Strategic Research Foundation at Private Universities, 2015–2019, concerning (The constitution of total researching system for comprehensive disaster, medical management, corresponding to wide-scale disaster).

Conflicts of interest

There are no conflicts of interest.