Value of a conventional approach to the diagnosis of traumatic cardiac contusion after chest injury

We wanted to evaluate whether current screening techniques effectively determine a patient's need for hospital admission and intensive care monitoring after blunt chest trauma. Consequently, we reviewed 104 consecutive admissions for "blunt chest trauma; rule out cardiac contusion." Neither clinical findings, cardiac enzyme levels, chest x-rays, nor ECGs predicted the high-risk patients who would subsequently develop complications related to myocardial contusion. Since only 23% of the study patients developed such complications, the plurality of study patients did not require admission and monitoring. There is, therefore, a definite need to develop new, accurate screening tests for patients at risk for myocardial contusion complications.     

Intra-aortic balloon counterpulsation for cardiogenic shock due to cardiac contusion in an elderly trauma patient

Blunt thoracic trauma may cause cardiac contusion and cardiogenic shock resistant to inotropic support. The use of intra-aortic balloon counterpulsation (IABCP) as a mechanical means of augmenting cardiac function following cardiac contusion is rare with case reports largely limited to its use in young trauma patients. We describe the case of a frail, 80-year-old woman who suffered cardiac contusion in a motor vehicle crash. She developed cardiogenic shock with electrocardiograph changes, elevated troponin T and severe global dysfunction on echocardiography. She was successfully managed with invasive monitoring, inotropic support and IABCP. This case provides support for aggressive resuscitation even in the very elderly as recovery from severe cardiac contusion may be possible.     

Electrocardiographic ST-segment elevation in the trauma patient: acute myocardial infarction vs myocardial contusion

The diagnosis of myocardial contusion in the setting of blunt trauma engenders much discussion and controversy-partly because of the lack of a gold standard for its identification other than histologic findings at autopsy. Furthermore, blunt cardiac trauma represents a spectrum of disorders ranging from transient electrocardiographic change to sudden death from myocardial rupture; hence, no single terminology exists to define such a wide range of scenarios. Here, we present 2 cases of electrocardiographic ST-segment elevation after high-speed motor vehicle crashes resulting in numerous injuries, including blunt chest trauma. Both patients demonstrated electrocardiographic ST-segment elevation, resulting from myocardial contusion and acute myocardial infarction.     

Diagnosis of traumatic cardiac contusion utilizing single photon-emission computed tomography

One hundred twenty-five consecutive patients with a diagnosis of blunt chest trauma underwent T1-201 thallous chloride single photon-emission computed tomography (SPECT) scan, as well as physical examination, serial ECG and cardiac enzymes. A subset of patients had 24-h Holter monitoring. SPECT scan was performed within 24 h of injury. Seventy-five patients had positive scans and 48 had negative. Two studies could not be completed. Eleven patients with positive studies developed serious arrhythmias (multiple premature ventricular beats or atrial fibrillation). None of these patients had a prior history of cardiac disease. While three patients with negative SPECT scans had arrhythmias, each had a prior history of cardiac disease and two were on chronic antiarrhythmia therapy. Neither ECG findings, creatinine phosphokinase (CPK), nor CPK-isoenzymes distinguished between those patients who did and did not develop arrhythmias. We conclude that SPECT scan is useful in screening patients at risk of developing arrhythmias from cardiac contusion. Utilization of SPECT scan allows early discharge of a significant number of patients with blunt chest trauma who would otherwise require hospitalization for arrhythmia monitoring.     

Complete Atrioventricular Block Associated with Non-penetrating Cardiac Trauma in a 40-year-old Man

Background

Myocardial contusion is a rare complication of blunt chest trauma. Transient conduction and rhythm problems, right ventricular dysfunction, or pulmonary embolism may occur after chest trauma, but these complications almost always occur early in the post-operative period.

Objectives

The objective is to describe a case illustrating that trauma may induce high-grade atrioventricular block.

Case Report

We report the case of a patient who developed delayed onset of complete atrioventricular block after transient complete atrioventricular block and alternating bundle branch block secondary to blunt chest trauma.

Conclusion

Even with an injury that does not seem to be caused by direct penetrating trauma to the heart, maybe every trauma patient needs an electrocardiographic evaluation. It is important to note that myocardial healing is a continuous process after trauma, and additional pathology may be revealed later in the course of healing from myocardial contusion.     

Blunt cardiac trauma

The incidence of cardiac injury after blunt chest trauma is difficult to determine and ranges from 8% to 76%. Moreover, the clinical presentation varies tremendously without a real gold standard to exclude or document cardiac involvement. Electrocardiogram as a single test is not sensitive or specific for diagnosing cardiac contusion. Furthermore, creatine kinase MB is non-reliable in the setting of severe trauma involving the liver, intestines or diaphragm. Although troponins T and I are highly specific for cardiac injury, their sensitivity in the setting of trauma is poor. The echocardiogram is very useful in the evaluation of trauma patients with suspected cardiac involvement. However, poor windows in the setting of chest and lung injuries and in intubated patients might be a major problem limiting the accuracy of transthoracic echocardiogram. On the other hand, transesophageal echocardiogram seems to be more sensitive and specific in trauma patients and should be the test of choice in patients with high clinical suspicion for blunt cardiac trauma.     

ECG findings in nonpenetrating chest trauma: a review

Significant ECG findings frequently accompany blunt chest trauma. Surface ECG in conjunction with creatinine phosphokinase (CPK) isoenzyme assay, has been an accepted standard for diagnosis of posttraumatic cardiac dysfunction, or "cardiac contusion." Studies employing recently developed noninvasive cardiac imaging techniques have called this practice into question and have shed new light on the pathophysiology of this clinical entity. As a result, it is appropriate to review the ECG manifestations of blunt chest trauma and to reappraise the utility of the ECG in its evaluation. This article will concern itself solely with nonpenetrating cardiac injuries not requiring initial surgical management, since clinical presentation, course, and prognosis differ when operative therapy is indicated.     

川芎嗪干预钝性肺挫伤急性期大鼠肺组织细胞的凋亡

背景：急性胸部撞击后所致的肺挫伤（钝性肺挫伤）常引起呼吸功能异常和继发性炎性反应,并参与全身炎性反应综合征和多器官功能障碍综合征,其发病原因及致病机制亟待明确。目的：观察胸部撞击所致钝性肺挫伤急性期细胞凋亡的变化及其川芎嗪对其的影响。方法：健康雄性SD大鼠随机分为正常对照组、模型组、川芎嗪治疗组,后两组制备胸部撞击伤模型,川芎嗪治疗组建模后立即腹腔注射川芎嗪80mg／kg1次。在创伤发生后1,2,3h观察肺组织病理形态学及细胞凋亡的改变、检测肺水肿程度和肺血管通透性改变,免疫组织化学检测肺组织Bcl-2、Bax和Caspase-3的表达及血液中肿瘤坏死因子α水平变化。结果与结论：模型组肿瘤坏死因子α水平在创伤后1h即显著增加,创伤后2h及3h间急剧增加（P〈0．05）;创伤后2h及3h肺组织细胞凋亡指数及肺组织损伤程度显著增高（均P〈0．05）;肺血管通透性及肺水肿程度增加（P〈0．05）;Caspase-3表达显著增高（P〈0．05）,Bcl-2／Bax比值显著降低（P〈0．05）。川芎嗪治疗组在相应时间点相对于模型组肿瘤坏死因子α水平显著降低（P〈0．05）,肺组织内细胞凋亡指数及肺组织损伤程度降低（P〈0．05）,肺血管通透性及肺水肿程度减轻（P〈0．05）;Caspase-3表达下降（P〈0．05）,Bcl-2／Bax比值增加（P〈0．01）。结果提示,川芎嗪可通过抑制肿瘤坏死因子CI表达,下调Caspase-3的表达并提高Bcl-2／Bax的比值,以降低胸部撞击所致肺组织急性期的异常凋亡并减轻胸部撞击所致急性期肺挫伤。     

Myocardial contusion. Using the index of suspicion for assessing blunt chest trauma

The body of literature devoted to the diagnosis and treatment of the patient with myocardial contusion (MC) frequently references the "index of suspicion" to qualify those patients at risk for cardiac embarrassment. Absent from this literature, however, is discussion of the importance of diligent nursing assessment and monitoring of these patients. This article shows the relevance of the index of suspicion to the nursing assessment of patients suspected of myocardial injury from blunt chest trauma.     

Late cardiac arrhythmias after blunt chest trauma

Objective: Case reports of two patients who developed fatal cardiac arrhythmias several days after blunt chest trauma.¶Design: Case reports.¶Setting: Surgical intensive care unit of a university hospital.¶Patients: A 23-year-old man and a 9-year-old girl with blunt chest trauma and multiple further injuries following car crashes were transferred to our institution. Although ECG on admission was normal, both patients developed fatal cardiac arrhythmias after 6 and 4 days, respectively. In both patients, post-mortem analysis confirmed myocardial contusion without coronary artery lesions. Histological findings included severe interstitial oedema, haemorrhages and infiltration of lymphocytes and neutrophils, fresh myocardial necrosis and fatty degeneration.¶Conclusion: Blunt chest trauma with myocardial contusion may lead to fatal cardiac arrhythmias even after several days, particularly when other severe injuries are present. Thus, a normal ECG on admission and absence of cardiac arrhythmias during the first 24 h of intensive care treatment do not necessarily exclude the occurrence of life-threatening arrhythmias in the further course.     

严重多发伤患者心脏肌钙蛋白Ι与创伤评分、多脏器功能障碍综合征之间的关系

目的观察严重多发伤患者心脏肌钙蛋白Ι(cTnI),探讨其与创伤评分、多脏器功能障碍综合征之间的关系.方法将116例严重多发伤患者,根据有无合并胸部创伤分为两组:合并胸部创伤80例,无合并胸部创伤36例,进行ISS评分和胸部损伤定级(IS).用微粒子免疫发光法采集血样检测cTnI浓度. 结果观察116例多发伤患者中,cTnI升高37例,其中合并胸部创伤30例,无合并胸部创伤7例;cTnI峰值随ISS值升高明显前移且绝对值增高;严重多发伤合并胸部创伤患者cTnI值升高例数比例,随AIS值升高而升高,血清cTnI峰值比较,差异有显著性意义(p<0.05);伴有MODS患者的血清,cTnI水平为(8.48±5.22)ng/ml,且持续时间较长,并与MODS的严重程度呈正相关. 结论严重多发伤患者出现心肌损伤以合并胸部创伤者为主,但严重多发伤患者无论胸部创伤与否均可出现心肌损伤,心肌损伤程度与MODS的发生率密切相关.     

Blunt chest trauma: a challenge to accident and emergency nurses

The incidence of myocardial contusion as a result of blunt chest trauma remains difficult to assess. As such the potentially lethal consequences are often difficult to mitigate against. The true incidence of myocardial contusion is not known and various authors have ascribed percentages in the very broad range of 8-71% of those having suffered blunt chest trauma. The extremely wide variation in presenting signs and symptoms further complicates the clinical picture creating a complicated and complex challenge for the assessing team. In the absence of clear guidelines to date a number of potential options are discussed exploring their efficacy and appropriateness in the management of those patients suffering from blunt chest trauma.     

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge

OBJECTIVE AND DESIGN: Pulmonary contusion is frequently followed by acute respiratory distress syndrome, pneumonia, and sepsis. However, immunologic alterations of circulating and resident immune cell populations contributing to the posttraumatic immunosuppression are poorly understood. We therefore characterized the influence of pulmonary contusion on peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages. To address the significance of the immunosuppression associated with lung contusion, we investigated how the consecutive addition of moderate or severe sepsis affected survival after blunt chest trauma. SUBJECTS: Male C3H/HeN mice (n = 10 per group) were anesthetized and subjected to chest trauma or sham procedure. MEASUREMENTS: The cytokine release of cultured peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages and plasma levels of tumor necrosis factor-alpha and interleukin-6 from those animals were quantified. Sepsis was induced via cecal ligation and puncture 24 hrs after lung contusion. MAIN RESULTS: Two hours after blunt chest trauma, plasma tumor necrosis factor-alpha and interleukin-6 were markedly increased, as was peripheral blood mononuclear cell cytokine production, lung myeloperoxidase activity, and lung chemokine concentrations. At 24 hrs and, in part, already at 2 hrs, cytokine release from peritoneal macrophages, splenic macrophages, and splenocytes was significantly suppressed. Furthermore, pulmonary contusion when followed by moderate sepsis significantly diminished survival rate when compared with chest trauma or moderate sepsis alone. CONCLUSIONS: These results indicate that pulmonary contusion causes severe immunodysfunction of splenocytes, macrophages, and monocytes in different local compartments and systemically. Moreover, this immunosuppression is associated with an increased susceptibility to infectious complications, which results in a decreased survival rate if blunt chest trauma is followed by a septic insult.     

Definitive management of acute cardiac tamponade secondary to blunt trauma

Blunt cardiac injuries are a leading cause of fatalities following motor-vehicle accidents. Injury to the heart is involved in 20% of road traffic deaths. Structural cardiac injuries (i.e. chamber rupture or perforation) carry a high mortality rate and patients rarely survive long enough to reach hospital. 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 in transit--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. 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. As regional trauma systems evolve, patients with severe, but potentially survivable cardiac injury are surviving to ED. 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. For patients with severe hypotension or in extremis, the treatment of choice is resuscitative thoracotomy with pericardotomy. Closed chest cardiopulmonary resuscitation is ineffective in these circumstances. Blunt traumatic cardiac injury presenting with shock is associated with a poor prognosis. The majority of survivors of blunt or penetrating cardiac injury present to the ED/trauma centre with vital signs. The main pathophysiologic determinant for most survivors is acute pericardial tamponade. The presence of normal clinical signs or normal ECG studies does not exclude tamponade. In recent years the widespread availability and use of ultrasound for the initial assessment of severely injured patients has facilitated the early diagnosis of cardiac tamponade and associated cardiac injuries. Two cases of survival from blunt traumatic cardiac trauma are described in the present paper to demonstrate survivability in the context of rapid assessment and intervention.     

Cardiac contusion: two case vignettes.

When patients with blunt chest trauma and suspected cardiac contusion are brought to the emergency department, focus on detecting subtle signs of myocardial dysfunction. Obtain the important first EKG, monitor for arrhythmia development, and assess for signs of failure of the right side of the heart.     

血清肌钙蛋白I在多发伤患者中的应用探讨

目的观察严重多发伤患者肌钙蛋白Ι(cTnI)水平变化,并探讨其与创伤评分、多脏器功能障碍综合征之间的关系。方法将116例严重多发伤患者,根据有无合并胸部创伤分为两组:合并胸部创伤组80例,无合并胸部创伤组36例,进行ISS评分和胸部损伤定级(AIS)。用微粒子免疫发光法采集血样检测cTnI水平。结果116例多发伤患者中,cTnI升高37例,其中合并胸部创伤30例,无合并胸部创伤7例;cTnI峰值随ISS值升高明显前移且绝对值增高;严重多发伤合并胸部创伤患者cTnI值升高例数比例,随AIS值升高而升高,血清cTnI峰值比较,差异有显著性意义(P<0.05);伴有MODS患者的血清,cTnI水平为8.48±5.22ng/ml,且持续时间较长,并与MODS的严重程度呈正相关。结论严重多发伤患者出现心肌损伤以合并胸部创伤者为主,但严重多发伤患者无论胸部创伤与否均可出现心肌损伤,心肌损伤程度与MODS的发生率密切相关。     

血清NT-proBNP和h-FABP在胸部创伤患者的临床检测价值

目的：通过检测胸部创伤患者治疗前后血清N末端B型钠尿肽原（NT-proBNP）和心脏型脂肪酸结合蛋白（h-FABP）水平变化,探讨血清NT-proBNP和h-FABP在其合并心功能及心肌细胞损害的早期检测价值。方法：选择82例胸部创伤合并心肌挫伤患者（挫伤组）和50例健康对照组为研究对象,挫伤组采用rhGH治疗。血清NT-proBNP检测采用电化学发光免疫分析（ECLIA）法,血清h-FABP检测采用双抗体夹心酶联免疫（ELISA）一步法。结果：①治疗前血清h-FABP阳性率（41.4%）显著高于NT-proBNP（29.8%）及ECG（17.7%）（P＜0.01）。②治疗前,胸部创伤合并心肌挫伤患者血清NT-proBNP 和h-FABP水平分别显著高于对照组（P＜0.01）;治疗后,两者水平均显著低于治疗前（P＜0.01）,与对照组差异无统计学意义（P＞0.05）。③胸部创伤合并心肌挫伤患者血清NT-proBNP与h-FABP呈显著正相关（r=0.719,P＜0.01）,相关性良好。④胸部创伤合并心肌挫伤的82例患者经rhGH治疗后,血清NT-proBNP 和h-FABP水平达正常,ECG也无异常表现,无1例死亡病例。结论：rhGH对胸部创伤合并心肌挫伤具有临床治疗作用,血清NT-proBNP和h-FABP的联合检测可早期诊断胸部创伤合并心功能及心肌细胞损害,也可观察临床疗效。     

Unusual cardiac injury following blunt chest trauma.

Cardiac injury following blunt chest trauma is known to occur, but traumatic rupture of ventricular septum is a rare injury, especially following blunt chest trauma. A case of a 20-year-old male is presented who fell on his back from a 9th-floor window and was resuscitated for 3 hours to no avail. Post-mortem examination confirmed a fracture of the pelvis, pulmonary contusion and rupture of ventricular septum of the heart.     

The use of inotropic drugs in myocardial contusion 2 case reports

Myocardial contusion is a common complication of blunt chest injury. Severe heart failure and shock may result. The haemodynamic consequences of myocardial contusion in two patients are described; both received inotropic agents. In the first patient dobutamine was successful in improving myocardial function; dopamine had similar effects on the heart. In the second patient dopamine, preferred for its renal effects, produced a short-term improvement in myocardial function. The rational use of pharmacological agents in this condition demands precise understanding of the underlying haemodynamic disturbances.     

Blunt chest trauma induces delayed splenic immunosuppression

Severe blunt chest trauma is frequently associated with multiple organ failure and sepsis. Posttraumatic immunosuppression seems to play a major role in their development. However, the immunologic alterations following pulmonary contusion are insufficiently elucidated. Specifically, it remains unknown whether immunocompetent cells located distant from the site of the impact are affected. We therefore aimed to characterize the influence of pulmonary contusion on lymphocytes and splenic macrophages. Male C3H/HeN mice (n = 8-10/group) were anesthetized and subjected to trauma or sham procedure. Blunt chest trauma was induced by a blast wave focused on the thorax. Two or 24 h later, splenocytes and splenic macrophages were isolated and stimulated for 48 h. The cytokine release (IFN-gamma, IL-2, IL-3, IL-10, IL-12, IL-18) from splenocytes as well as from splenic macrophages (TNF-alpha, IL-10, IL-12, IL-18) and plasma levels of TNF-alpha and IL-6 were quantified by ELISA. The results indicate that at 2 h after blunt chest trauma, plasma TNF-alpha and IL-6 were markedly increased. At the same time, no differences in splenocyte cytokine production were detectable. However, at 24 h a significantly depressed cytokine release was observed in trauma animals. Furthermore, splenic macrophages showed a significantly decreased production of TNF-alpha, IL-10, and IL-12 at 24 h and markedly increased release of IL-18 at 2 h after trauma. These results indicate that blunt chest trauma causes severe immunodysfunction of lymphocytes and splenic macrophages. Thus, lung contusion as a localized type of trauma causes dysfunction of immunocompetent cell populations, which are located distant from the site of injury.