Medical Legal Implications of Cardiac Contusion – Case Report

Medical legal implications of cardiac contusion – case report

Dan Dermengiu1*, Mihai Ceauşu2, Mugurel Rusu3, Corneliu Căpăţînă1, Sorin Hostiuc1, George Cristian Curcă4

______Abstract: Cardiac contusions (contusio cordis) usually appear in penetrating thoracic trauma or high energy blunt trauma and only rarely in thoracic blunt trauma in homicidal context. The diagnosis could be easy if a traumatic context is/can be proven; if not the differential diagnosis with myocardial infarction, other causes of cardiac hemorrhages or post resuscitation cardiac trauma can be very difficult, as there are no specific tests for contusio cordis. We describe in this article a case of contusio cordis in a 31 year old male, caused by thoracic blunt trauma (hit with a wooden object) and discuss some particularities of this illness and its differential diagnosis. Key words: cardiac contusion, non-penetrating thoracic trauma, cardiac trauma

igh energy blunt trauma (fall from heights, traffic accidents) can lead to different types of H cardiac injuries, from valve or myocardial contusions to cardiac rupture. These lesions are usually associated with a high mortality rate by either hemorrhagic or arrhythmic complications. Sometimes though a lower energy thoracic blunt trauma can be associated with the development of cardiac trauma – there are a few cited cases in which a baseball or a hockey puck hitting the thoracic cage lead to lethal cardiac trauma [1]. Cardiac contusion is the most common traumatic injury of the heart due to thoracic blunt trauma [2] (See Figure 1 for details).. Clinically, cardiac contusions can lead to hypotension, hypoxia, and arrhythmia, symptoms which can be overlooked in severely traumatized patients with blood loss determined by other vascular, neurological, renal or orthopedic lesions. ECG and trans-esophageal echography were found to be the most sensitive methods to diagnose cardiac contusion in a meta-study by Sybrandy and Cramer.[2] (Figure 2) but their specificity were quite low (see Table 1 for details). As cardiac contusion lesions are similar to those from acute myocardial infarction, cardiac enzymes are often used as first screening tools for thoracic trauma patients. CK value is extremely limited as most trauma patients have skeletal or multi-organ lesions which are also associated with CK increase. CK-MB has a high sensitivity but a very low specificity, often giving false positive results, especially in multitrauma patients. Nowadays CK-MB is only used for detecting cardiac lesions in mild trauma cases. Serum troponins (T and I) are highly cardiac specific being able to detect with high accuracy myocardial lesions. Moreover, being cardiac specific, normal values have excellent negative predictive value.

______*1) Corresponding author; Professor, MD, PhD, National Institute of Legal Medicine “Mina Minovici”, Sos. Vitan Birzesti 9, Sector 4, 042122 – Bucharest, Bucharest, Romania, e-mail: [email protected] 2) MD, PhD, Chair of Pathology, University of Medicine and Pharmacy “Carol Davila” 3) MD, PhD, PI, Senior Lecturer, Chair of Anatomy, University of Medicine and Pharmacy “Carol Davila” 4) Associate Professor, MD, PhD, Chair of Legal Medicine, University of Medicine and Pharmacy “Carol Davila”

83 Dermengiu D et al Medical legal implications of cardiac contusion – case report

Other diagnostic methods, like cardiac scintigraphy, CT, MRI are less often use as diagnostic tools in blunt cardiac trauma. Myocardial contusions can be classified in five stages using clinical, imaging, biochemical markers, complication and sequelae rates [3]. (see Table 2 for details).

Method Signs Usability ECG non-specific ST-T wave changes Sometimes right derivations are needed (RV is Right bundle branch block more often involved in thoracic blunt trauma) Fascicular block negative predictive value of 80-90%[26] ST elevation, depression, new Q wave heart block (1,2,3 AV Block) dysrhythmias (sinus tachycardia, sinus bradycardia, atrial and ventricular extra-systoles, atrial tachycardia, atrial fibrillation, ventricular tachycardia, ventricular fibrillation) Pericarditis-like ST segment elevation or ST depression Prolonged QT interval Echography Wall motion abnormality (TTE, TEE) TEE is superior to ECG and cardiac enzymes in Pericardium effusion (TEE) the diagnosis of cardiac contusions Increased echo brightness (TTE,TEE) TEE use is limited by the need of experienced Increased end diastolic wall thickness of the contused myocardial area operators and the difficulty of image acquisition (TTE, TEE) in cases of chest wall injuries.[28] Acute valvular dysfunction[27] (TTE, TEE) Cardiac aneurysms (TEE) Intracardiac shunts (TEE) CK/ Parameter [27] Value (>) Sb Sp PPV NPV Non-specific, especially if skeletal muscle, CK-MB CK 100 IU/L 92 21 31 87.5 intestinal, liver or diaphragm lesions are present CK 1000 IU/L 15,5 85 28,5 72 Not-predictive for death, inotrope requirement, CK-MB activity 25 IU/L 77 49,5 37 84,5 arrhythmia or need for drug therapy[29] CK-MB activity 45 IU/L 19 91 45,5 74,5 CK-MB mass 5 ug/L 81 35,5 32,5 82,5 CK-MB mass 40 ug/L 27 91 54 76,5 CK-MB activity/CK ratio 6,00% 42,5 64 31,5 74 Troponins Parameter [27] Value (>) Sb Sp PPV NPV Cardiac specific (except for troponin C); can diagnose cTn-I 0.1 ug/L 23 97 75 76,5 a cardiac lesion but cannot differentiate between cTn-T 0.1 ug/L 12 100 100 74 cardiac contusion and acute myocardial infarction.

Table 1. Clinical diagnosis of cardiac contusions (TTE = trans-thoracic echography, TEE = trans-esophageal echography, Sb = sensitivity, Sp = specificity, PPV = positive predictive value, NPV = negative predictive value

Classification 0 (Suspect) 1 (Mild) 2 (Moderate) 3 (Severe) 4 (Catastrophic) Clinical - Angina-like Significant or protracted Severe intermittent or persistent Severe systemic signs and or atypical cardiac chest pain cardiac chest pain symptoms (cardiac, chest pain, pulmonary, vascular) palpitations Acute, severe valvular ECG +/- ST ST, AE, VE Marked ST, premature Marked, persistent ST, dysfunction requiring immediate transitory ST AE and VE, selflimited SVTA requiring aggressive medical or surgical intervention or T waves SVTA’s , significant/ therapy, VA, protracted, (papillary muscle, changes persistent ST-T wave significant ST - T wave multiple chordae, severe valve abnormalities abnormalities disruption) Herniation of heart through pericardial laceration with Enzymes -/borderline Mild Moderate-significant Markedly elevated or signs and symptoms of major elevation elevation elevation moderately elevated for longer vascular obstruction periods of time requiring immediate intervention Echography Normal Normal Mild, temporary Marked hypokinesia, Pericardial tamponade hypokinesia/ dyskinesia; dyskinesia, akinesia, pericardial Acute, severe congestive heart minimal pericardial effusion failure requiring effusion immediate, highly aggressive Scintigraphy Normal Normal Abnormal Easily discernible, grossly intervention abnormal scintigprahic study Ventricular or atrial septal X-Ray Normal Normal +/- fractures ribs, pleural effusion, pulmonary rupture sternum contusion, mild pulmonary Great vessel laceration vascular congestion Myocardial aneurysm Myocardial pseudoaneurysm Complications none none No permanent sequelae AMI (primary due to muscle Myocardial rupture / injury or secondary to coronary Permanent sequelae or death Associated arterial injury), arteriovenous highly probable lesions fistulas, pericardial laceration Death highly probable valvular disruption

Table 2. Classification of myocardial contusion [3]; ST = sinus tachycardia, AE = atrial extrasystoles, VE = ventricular extrasystoles, SVTA = supraventricular tachyarrhythmia, VA = ventricular arrhythmia, IMA = acute myocardial infarction.

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Sensitivity of various clinical diagnostic methods

for cardiac contusion in thoracic blunt trauma Fig. 1 Incidence of cardiac contusions in patients with blunt thoracic trauma as found with various clinical ECG 56 44 investigative methods. Highest frequency of positive TEE 56 44 results is reached by using ECG or trans-esophageal echography as the preferred diagnostic method. TTE = TTE 26 74 Trans-thoracic echography, TEE = Trans-esophageal CK‐MB 19 91 echography [2]

Troponins 24 76 Cardiac lesions secondary to thoracic blunt trauma

Papillary muscle Coronary artery lesions Case report lesions 2% 4% Valvular lesions A 31 year old RV Rupture 4% male was hit by a 10% neighbour during a fight Pericardial lesions RA Rupture 10% ,with an elongated, 6% wooden object. A few seconds after the fight, he LV Rupture felt sick and immediately 9% lost his consciousness. At Contusion the scene the ambulance 20% workers (which arrived in LA Rupture about five minutes) found 4% the victim unconsciouss, IAS Rupture 8% with a weak, irregular IVS Rupture Multiple Chamber pulse, and a BP of 80/40 6% Ruptures 17% mmHg. It was taken to Fig. 2 Cardiac lesions in thoracic blunt trauma (after [6]); LV = left ventricle, RV = right the county hospital where ventricle, LA = left atria, RA = right atria, IVS = interventricular septum, IAS = interatrial he arrived with GCS 4 septum. coma and hemopericardium was suspected after 3 hours of hospitalization. In the hospital he suffered a cardiac arrest (successfully defibrillated) and his hemopericardium was drained before being sent to Bucharest Clinical Emergency Hospital, with a preliminary diagnosis hypoxic encephalopathy. In BCEH he was found to have clinical and laboratory signs of acute ischemic damage in multiple organs - brain, kidneys, liver, heart (Table 3).

Criteria Commotio Cordis Contusio Cordis Hemorrhages or other Absent Present pathological findings Impact site Heart projection Presternal Energy Low; lesion severity is independent on the High; lesional severity is dependent on the impact force impact force Thoracic structure Elastic (most cases occur in children with Not dependent deformable thoracic cage) Association with cardiac cycle Dependent, the hit must occur within the 15 Independent ms repolarization period (immediately before T wave) Timing of the arrhythmic Immediately after the traumatic event Immediately after or with the presence of a event free interval (sec-hours) Arrhythmic trigger Premature beat induced by mechanical stretch Electrical silent areas favoring reentrant mechanisms

Table 3. Differential diagnosis between comotio cordis and contusion cordis.

85 Dermengiu D et al Medical legal implications of cardiac contusion – case report

As personal history and clinical signs suggested a cardiac trauma the heart was extensively studied: at admission he had high values for troponin, myoglobin, and creatin-kinase (see Table 3), which, associated with abnormal ECG findings (ST depression in inferior left areas), external examination (transversal bruise over the anterior thoracic cage at C4-C5 levels) and CT scans were highly suggestive for cardiac trauma.

Fig. 3 Anterior thoracic bruise. Fig. 4 Traumatic agent (rectangular shaped wooden stick

Fig. 5 Force direction and main contusive cardiac areas Fig. 6 Subepicardial hemorrhagic areas on the anterior side of the right ventricle; small hemorrhage at the basis of a papillary muscle (white arrow).

Fig. 7 Mural hemorrhagic lesion within the left ventricle Fig. 8 Arterial wall rupture on the first diagonal from left descending coronary artery

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Cardiac ultrasonography couldn’t find structural or functional abnornalities (except for the initial pericardial bleeding) until day four when diffuse wall movement abnormalities (left ventricle and interventricular septum) and decreased heart pump function (Ef = 35%) were diagnosed. He died four days later. External examination during the autopsy found numerous external bruises and ecchymoses whose shape suggested that he was beaten with an elongated, rough object (Figure 4); of a special interest was a horizontal bruise in the anterior thoracic area, between levels C4 and C5 (Figure 3). Corresponding, a horizontal sternum fracture was found during internal examination. The heart had nine hemorrhagic areas, most of them on the direction of the force: RV- anteroseptal, at the base of a papillary muscle, anterior wall near the apex and LV - anteroseptal, diaphragmatic side near the apex, anterior-inferior near the apex, inferior wall near the mitral valve, arterial cone (Figures 6, 7). A small arterial wall rupture was found on the first diagonal from left descending coronary artery (Figure 8).

Pathology investigation Material and methods Tissue samples of brain, lung, heart, liver and kidney were taken for histopathology investigation. For further detailed study, 11 samples of myocardial tissue from different areas of the heart were taken as follows: anterior wall of the left ventricle, inferior wall (paraseptal superior, apical and basal), the apex, the left edge of the left ventricle, lateral papillary muscle, the interventricular septum, anterior wall of the right ventricle, the apex of the right ventricle and the diagonal branch of the left anterior descendent artery (6 sections). The selected speci- mens were formalin-fixed and paraffin-embedded. Sections were cut at 5 microns and stained using the standard H&E stain and van Gieson. Special stains such as Lie, PTAH and Masson’s trichrome have also been carried out for myocardial tissue. Immunohisto-chemistry (IHC) was done for the following antibodies: troponin (muscle contraction protein, producer: Novocastra, clone T1/61, dilution 1:10), myoglobin (regulator muscle protein, producer: Santa Cruz / FL-154, polyclonal, dilution 1:50). An indirect bistadial technique was used, with hydro soluble polymerized dextran, accor-ding to manufacturer specifications (Dako EnVision Systems). To ensure the

Fig. 9 Diagonal branch of the left anterior descendent artery with double rupture: of reliability of the experimental the intima (inset, down right, HE, 20x) and of the media and intima (inset, up left, HE, study, internal quality control 10x); overview picture, HE, 5x of histopathological techni- ques was performed as a part of an implemented and certified quality assurance system (ISO 9001/2008). All slides were examined and photographed on a Zeiss AxioImager microscope. Digital images acquired with Zeiss Axio Vision program have been processed and analyzed with ACDSee Pro Photo Manager 3.0, running under Windows XP Professional.

87 Dermengiu D et al Medical legal implications of cardiac contusion – case report

Fig. 10 Interstitial, perivascular and perifibrilar hemorrhagic microfoci, associated with necrotic cardiomyocytic areas of the left ventricle (HE, 20x): a – lateral papillary muscle, b – interventricular septum, c – anterior wall, d – inferior wall

Fig. 11 Interstitial micro-hemorrhages in the wall of the right ventricle (HE, 20x): left – anterior wall, right – the apex

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Fig. 12 Histochemistry of the myocytic necrosis in the anterior wall of the left ventricle, emphasized by Lie stain (small fuchsinophilic areas), PTAH stain (absence of the periodic structure of the myofibrils and focal homogeneity of the cardiomyocytes), Masson’s trichrome (large area of cardiomyocytic necrosis)

Fig. 13 Immunohistochemical reaction for myoglobin: focally negative in necrotic cardiomyocytes and positive in rezidual perilesional cardiomyocytes (intern control), 40x

89 Dermengiu D et al Medical legal implications of cardiac contusion – case report

Fig. 14 IHC reaction for troponin: a) negative in large area of cardiomyocytic necrosis, b) difuselly positive in residual cardiomyocytes (intern control), 40x

Results The microscopic assessment of the serial sections from the diagonal branch of the left anterior descendent artery has revealed a double rupture of the wall with subsequent hemorrhage (Figure 9). The classic histopathology investigation of the anterior and inferior wall of the left ventricle, together with the lateral papillary muscle and the interventricular septum has shown interstitial, perivascular and perifibrilar hemorrhagic microfoci, associated with necrotic cardiomyocytic areas (Figure 10). Also, it was noticed interstitial micro-hemorrhages in the anterior wall and the apex of the right ventricle (Figure 11). The myocytic necrosis of the anterior wall of the left ventricle was observed better with Lie stain as small fuchsinophilic areas. PTAH stain showed the absence of the periodic structure of the myofibrils and focal homogeneity of the cardiomyocytes. Large areas of cardiomyocytic necrosis were also visible with Masson’s trichrome. The histochemistry of the damaged myocardium is shown in Figure 12. The aforementioned data were sustained by the immunohistochemical reaction for myoglobin, which was focally negative in necrotic cardiomyocytes, but positive in rezidual perilesional cardiomyocytes (intern control) and for troponin, which was negative in large area of cardiomyocytic necrosis, but difuselly positive in residual cardiomyocytes (intern control) (Figure 13 and 14). These results were compatible with a myocardial contusion of mixt type (necrotic and hemorrhagic), secondary to a blunt trauma of the chest. The cause of death in this case seems to be a cardiac contusion which led to cardiac pump deficiency associated with cerebral hypoperfusion, hypoxic encephalopathy and MSOF.

Discussions Depending on the impact velocity and the elasticity of the anterior-posterior diameter of the thoracic cage, this increased intrathoracic pressure could involve the heart in different degrees, with or without lesions, leading to commotio cordis or heart failure due to myocardial rupture. Cardiac

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contusions are usually due to acute heart elastic compression between sternum and spine secondary to an increased intrathoracic pressure. Other potentially involved mechanisms are: (1) direct injury from a fractured sternum [4], (2) “water hammer effect” – an abrupt increase in blood pressure within the cardiac chambers after chest/abdominal compression/crushing which can lead to heart distension, shearing or rupture [5]. There are seven types of forces able to determine cardiac contusions [6]: direct, indirect, bidirectional (compressive), decelerative, blast, concussive and combined, of which three are primary (direct, indirect, blast) and the other are secondary [7]. Usually lesions which are found on the direction of the force are produced by direct mechanisms and are more severe than the lesions produced by the “water hammer effect”, the latter being usually found in perivascular areas; this topography is respected by our case in which the most severe lesions, with bigger contusive areas and necrosis, are found on a straight line (on the direction of the force); we’ve also found a few other contusions, less severe, without necrosis, which are not located on the abovementioned line. Major causes for cardiac contusions are falls, traffic accidents (especially in drivers not wearing a seat-belt and in motorcycle accidents), fist blows, kicks, crushing, explosions, etc. [8] Cardiac contusion due to blunt trauma in homicidal context has only been cited several times in the scientific literature [5, 9-15], usually being associated with penetrating thoracic trauma. Due to its position the right heart is more susceptible to myocardial contusions[6, 16]. For example, in a study made on 546 autopsy cases with cardiac lesions due to thoracic blunt trauma, right heart ruptures were present in 16% whilst left heart ruptures were only present in 13% of the cases [6]. In a recent study published by Turan [17] in 109 autopsies cases with cardiac lesions were noted 115 right heart lesions (49 atrial and 66 ventricular) and only 96 left heart lesions (35 atrial and 61 ventricular).Valve contusive lesions though are more frequent on left valves although tricuspid valve involvement had been cited [6, 18]. Our case fits this pattern with cardiac contusive areas corresponding to the area where the sternum was fractured. As frequent associated lesions are cited intra-pericardial bleedings and arterial lesions, especially within the LAD’s branches, lesions present in our case also. Main complications of isolated cardiac contusions are acute cardiac insufficiency and arrhythmias. Acute cardiac insufficiency is determined to the ill-function of heart muscle pump, by a mechanism similar to the one associated with myocardial infarction.. A study on rabbit hearts [19] revealed that arrhythmogenesis occurs usually within the first 15 minutes after trauma, is usually due to reentrant mechanisms and its intensity is proportionate with the kinetic energy. The fact that arrhythmic events can occur to a later time is very useful for making the differential diagnosis with commotio cordis, where they are always appearing immediately after trauma. In order for a trauma to determine VF with subsequent commotio cordis the impact area must be over the center of the left ventricle, timed within the 20 ms window occurring before the T wave peak (representing about 4% of the cardiac cycle at a heart rate of 120 bpm), not preceded by other arrhythmic abnormalities (ischemic T changes, conduction abnormalities, ventricular tachycardia, etc), impact area shouldn’t be very large (most cited cases were associated with baseball-sized impact areas) and the force shouldn’t be extremely powerful (as they can lead to associated morphological abnormalities) [20-21]. See also Table 3. Cardiac contusion morphology is similar to that found in acute myocardial infarction, but usually the hemorrhage is more prominent and the affected area is better individualized. Microscopically cardiac contusion associates contraction band necrosis, segmentation of the myocardial cells, the presence of bundles of contracted myocardium alternating with bundles of distended myocardium, widening of the intercalated discs, granular disruption of the myocites, local and far away foci of perivascular hemorrhage, myofibril eosinophilia, sacomeres and nuclei elongation, troponin I, C and myoglobin depletion [22]. Troponins are very sensible markers for myocardial lesions but they cannot be used in identifying the cause of myocardial damage. Some authors suggested troponin C to have a higher specificity for cardiac contusion [23], but an agreement hasn’t yet been reached [24]. The most sensible in identifying myocardial damage associated with

91 Dermengiu D et al Medical legal implications of cardiac contusion – case report

contusio cordis seems to be however troponin I [24]. Troponin value for identifying myocardial lesions is, however, dependent on autolysis time, only being reliable up until 40 hours after death; after 50 hours troponin depletions is also present in control cases. As our case was resuscitated we had to make a differential diagnosis with post CPR cardiac lesions. Sometimes cardiac contusions may appear after cardiopulmonary resuscitation, although their incidence is very low. In a study made by Krisher et co [25] on 709 autopsies of resuscitated patients about 10% had cardiac complications (72 cases) from which only nine had myocardial contusions. It has been suggested that severe post CPR cardiac complications usually appear in hearts with preexisting ischemic pathologies.[9] Spatial correspondence of thoracic lesions and the absence of other specific post CPR lesions lead us to conclude that contusio cordis was indeed associated with the initial traumatic event. Other possible differential diagnoses include (after Stephan Seidl):

- Catecholamine excess – similar electrocardiographic changes and cardiac degeneration. - Traumatic head injuries, intracranial bleedings (either traumatic or non-traumatic) can produce cardiac arrhythmias, cardiac insufficiency, heart block and/or myocardial necrosis - Shock – cardiac degeneration probably associated with the initial cause and/or catecholamine discharges. - Substance abuse associated with sympathetic hyperactivity (cocaine, amphetamines, acetaminophen, etc) – can lead to cardiac arrhythmias and myocardial necrosis - Acute arsenic poisoning – can lead to severe subendocardial hemorrhages [1] (raised blood- filled blisters under the endocardium. - Viper bites – myocardial hemorrhages determined by intravascular disseminated coagulation. - Infective causes: viral (influenza, echo, etc.), bacterial (E. coli) - High-acceleration (8-9 G) – airplane crash, rocket pilots, etc.; cardiac hemorrhages incidence is directly correlated with the level and duration of the exposure, heart rate and catecholamine activity.

Therefore, not any myocardial hemorrhage found in a traumatic context can be diagnosed as myocardial contusion, additional data being needed for a correct diagnosis. In order for us to diagnose it, we had the following information: the proof of a traumatic event (witnesses), the traumatic object, tegumentary traumatic mark, a fractured sternum corresponding to the tegumentary traumatic mark, cardiac hemorrhages, most of them being on a the direction of the traumatic force, positive biochemistry, EKG, pathology and immuno- histochemistry, and a rupture on a diagonal artery from LAD, a positive traumatic marker, also found by other studies to be associated with cardiac contusions. Another particularity of this case is that the patient was successfully defibrillated and returned to normal sinus rhythm only after the development of hypoxic encephalopathy and, subsequent, multiple hypoxic organ dysfunctions.

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Cardiac trauma wasn’t so extended to be able led to another life threatening arrhythmic events after the initial defibrillation; in the first three days cardiac echography was normal and the only cardiac anomalies were slightly modified ECG patterns (probably associated with the arterial wall rupture of the first LAD diagonal, as they have spatial correspondence), a small intra-pericardial bleeding and elevated cardiac enzymes (Table 4). On the day he died however more severe cardiac lesions were noted with cardiac echography (wall motion abnormalities, decreased ejection fraction), but these lesions were, more probably, terminal events in MOSF. Therefore if the cardiac lesions weren’t associated with the development of multi organ system failure the chances of survival would probably have been much higher.

Acknowledgements

This work was supported by CNCSIS –UEFISCSU, project number PNII – IDEI 2642/2008

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