Electrocardiographic changes after head trauma

Journal of Electrocardiology 38 (2005) 77 – 81 Case Report Electrocardiographic changes after head trauma Xavier Wittebole, MDa, Philippe Hantson, MD, PhDa, Pierre-François Laterre, MDa, Ricardo Galvez, MDa, Thierry Duprez, MDb, Daniel Dejonghe, MDc, Jean Renkin, MD, PhDc, Bernhard L. Gerber, MD, PhDc, Christian R. Brohet, MD, PhDc,* a Department of Intensive Care, University Hospital Saint-Luc, Catholic University of Louvain, Brussels, Belgium B1200 Department of Radiology and Medical Imaging, University Hospital Saint-Luc, Catholic University of Louvain, Brussels, Belgium B1200 c Division of Cardiology, Department of Internal Medicine, University Hospital Saint-Luc, Catholic University of Louvain, Brussels, Belgium B1200 b Abstract We report the case of a patient who developed, a few days after a closed head injury, marked electrocardiographic changes mimicking an acute coronary event, in the absence of actual cardiac damage. The electrocardiographic changes were fully reversible, paralleling the neurologic status. Neuroimaging examinations excluded subarachnoid hemorrhage or space-occupying hematoma, but demonstrated diffuse axonal injury using susceptibility-weighted magnetic resonance techniques. This kind of traumatic brain injury thus may be responsible for a pseudo-acute myocardial ischemic syndrome. D 2005 Elsevier Inc. All rights reserved. Keywords: Head trauma; Diffuse axonal injury; ECG changes 1. Introduction Electrocardiographic (ECG) features in cerebrovascular events and central nervous system diseases are well documented [1-3], but those occurring after a head trauma have been less reported [4]. Most previous studies have dealt with ECG changes and other cardiac consequences of subarachnoid hemorrhage (SAH) [5], or other conditions, mostly increasing the intracranial pressure [6]. We report the case of a patient in whom dramatic ECG abnormalities occurred after a closed head injury without obvious structural brain damage on standard computed tomography (CT) imaging. 2. Case report A 32-year-old man without previous medical history was admitted to the emergency department after a head trauma due to a road accident. The patient was not the driver but the passenger, and the impact was lateral, on the driver side. The driver had a fracture of the humerus. The passenger wore no * Corresponding author. Cliniques Universitaires Saint-Luc, B1200 Brussels, Belgium. Tel.: +32 2 764 2881; fax: +32 2 764 55 36. E-mail address: [email protected] (C.R. Brohet). 0022-0736/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2004.09.004 safety belt but the airbags were inflated after the accident. The passenger was fully conscious but agitated. He was able to leave the car without help and just refused at first to be transferred to the hospital. He never lost consciousness before or during transfer to the hospital and the Glasgow Coma Score (GCS) at admission was 15/15. But shortly after admission, he became subcomatose, more agitated, and the GCS fell to 8/15. The patient was admitted to the intensive care unit and he was intubated. He had no evidence of thoracic contusion. The total body CT scan performed after admission showed no thoracic wall injury, nor any lung injury. A brain CT scan was normal, excluding, that is, a subdural or an epidural hematoma, an intracerebral hemorrhagic or ischemic injury, and a cerebral edema. The EEG failed to reveal any irritative area. A brain magnetic resonance examination confirmed the absence of freshly extravasated collected blood but demonstrated multiple hypointense artifactual areas on T2* images corresponding to microdeposits of deoxyhemoglobin featuring a diffuse axonal injury (DAI) (Fig. 1). The patient’s clinical status was stable the next 3 or 4 days with a GCS at 10/15 on day 5 after trauma and the patient was extubated. But the same day, the neurologic status suddenly worsened with a GCS falling to 7/15, requiring reintubation. Dramatic ECG changes appeared 78 X. Wittebole et al. / Journal of Electrocardiology 38 (2005) 77 – 81 Fig. 1. A, Transverse T2-weighted gradient-echo (T2*) magnetic resonance image using the echoplanar imaging technique reveals areas of deep hyposignal intensity at the white-gray matter interfaces in the supratentorial space. Hypointensity within damaged areas is due to deoxyhemoglobin-related susceptibility artifacts that feature axonal shearing injury. B, Coronal T2-weighted gradient-echo (T2*) magnetic resonance image reveals areas of deep hyposignal intensity at the white-gray matter interfaces in both the infra- and the supratentorial spaces. Hypointensity within damaged areas is also due to deoxyhemoglobin-related susceptibility artifacts. concomitantly. Whereas the 12-lead ECG at admission was within normal limits, the tracing recorded on the fifth day after admission showed a sinus tachycardia and a pattern of subepicardial injury with elevated ST segment especially marked in leads I, II, aVL, aVF, V5, V6, but also somewhat visible in leads V1 through V3, and a terminal T-wave negativity with prolonged QT interval (Fig. 2A). At the same time, there were numerous self-terminating salvos of polymorphous ventricular tachycardia (Fig. 2B). The patient was then treated by intravenous infusion of lidocain and by b-blockers, and a close cardiac follow-up was initiated. There was a rise of the plasma levels of cardiac enzyme creatine kinase with total creatine kinase at 18 000 UI/L (normal value, b 400 UI/L) and Troponin I at 2.5 ng/mL (normal value, b 0.06 ng/mL). The transthoracic echocardiogram was slightly abnormal showing only a slight hypokinesia of the inferior wall of the left ventricle. The transesophageal echocardiogram showed a mild mitral regurgitation. Because of the ECG changes mimicking a subepicardial injury in the inferoposterolateral region and the rise of cardiac enzymes, an acute coronary event was suspected and a coronary angiography was performed on day 6 after trauma. The coronary arteries were normal, wall motions were normal, and the left ventricular ejection fraction was 66%. Fig. 3 shows the ECG recorded concomitantly to the coronary angiography. There is a progressive resolution of the current of subepicardial injury in the inferoposterolateral leads, but the ST segment is now more elevated in the anterior chest leads V1 through V3, which also display a wide T wave and a prolonged QT interval. A follow-up cerebral CT scan performed on the same day was unremarkable. In the following days, the clinical course remained uneventful. The patient’s neurologic status steadily improved. He was discharged from the intensive care unit on the 16th day. At that time, the ECG only showed residual T-wave inversion in the inferior leads. Four months later, a cardiological outpatient visit failed to reveal any residual cardiac abnormality. The patient had no cardiac complaint, the physical examination was normal, no segmental wall abnormality was present on the echocardiogram, and the 12-lead ECG was normalized. Also, the neurologic status was normal. 3. Discussion This case illustrates the occurrence of severe evolving electrocardiographic abnormalities mimicking an acute cardiac event after a closed head trauma without obvious brain injury using standard brain CT imaging. Most of the ECG abnormalities described after an acute cerebral event were linked to SAH [5], but other causes have been reported, for example, cerebral venous thrombosis, acute cerebral infarction, neurosurgery, and cryohypophysectomy [1-3]. In SAH, the incidence of ECG abnormalities ranges from 49% to 100%, including T-wave changes (36%), ST segment changes (28%), U wave (24%), QT prolongation (23%), and pathological Q waves (3%) (5). The most typical feature is QT prolongation with giant negative T waves. Elevation or depression of the ST segment may also occur thereby simulating an acute myocardial injury. In some instances, the ST segment elevation is diffuse suggesting an acute pericarditis or pericardial effusion [2]. Various types of arrhythmias have also been described, including torsades de pointes [7]. The ECG in Fig. 1 showed ST elevation in the inferoposterolateral leads and raised the hypothesis of an acute coronary syndrome although a pericardial abnormality was X. Wittebole et al. / Journal of Electrocardiology 38 (2005) 77 – 81 79 Fig. 2. Electrocardiograms recorded on the fifth day after head trauma. A, There is sinus tachycardia (125 beats per minute). The ST segment is elevated, producing a pattern of subepicardial injury in leads I, II, III, aVL, aVF, and V5 through V6, corresponding to the infero-postero-lateral region. The ST segment is also somewhat elevated in the right precordial leads V1 through V3. There is QT prolongation, the T wave extending up to the next sinus P wave, and also T-wave alternans is best seen in lead II. B, In the context of marked repolarization abnormality with QT prolongation appeared bouts of polymorphous ventricular tachycardia (upper row, a triplet of premature ventricular contractions; lower row, a string of 8 wide QRS complexes). Fig. 3. Electrocardiogram recorded on the sixth day after head trauma. There is progressive resolution of the current of subepicardial injury in the inferopostero-lateral leads but now the ST segment elevation is more pronounced in the anterior chest leads V1 through V3, with wide T wave and prolongation of QT interval. 80 X. Wittebole et al. / Journal of Electrocardiology 38 (2005) 77 – 81 also possible. The echocardiogram did not reveal a pericardial effusion and the only abnormal finding was a mild hypokinesia of the left ventricular inferior wall. The hypothesis of a cardiac contusion was readily discarded for several reasons. First, there was no evidence of chest trauma at physical examination and on the thoracic CT scan. Although cardiac contusion can occur in the absence of chest bruising, up to 75% of cases of cardiac contusion are accompanied by chest injury. Second, there were no cardiac symptoms, for example, no chest pain, and there was no echocardiographic evidence of right ventricular damage, the most frequent abnormality in cardiac contusion. Finally, the increased Troponin I level with a peak value of 2.5 ng/mL might very well indicate a myocardial injury directly produced by the sympathetic stimulation secondary to the neurologic condition [5,8]. In support of this hypothesis was the remarkable synchronism between the neurologic status and the cardiac manifestations. Increased cardiac enzymes and multiple bouts of polymorphous ventricular tachycardia suggested a myocardial ischemia, but the coronary arteriography and the left ventriculography were normal and, on the following day, the signs of subepicardial injury had moved to the anterior chest leads. The occurrence of evolving ECG abnormalities in a patient with head trauma and DAI but a normal head CT, in the absence of cardiac injury, has not been reported previously. Diffuse axonal injury has been identified as the most important cause of significant morbidity in patients with traumatic brain injuries, leading some patients to persistent vegetative state. Diffuse axonal injury is uncommon in the absence of severe closed injury. Diffuse axonal injury is normally caused by axonal shear strain deformations induced by sudden acceleration/deceleration or rotational forces on the brain. The injuries are often diffuse, bilateral, and located in the lobar white matter, corpus callosum, and upper brain stem. Disruption of penetrating blood vessels is usual. The lesions are essentially diagnosed by microscopic examination. Patients with DAI have usually a normal admission CT scan [9,10]. The magnetic resonance appearance of DAI depends on the presence or absence of hemorrhage and age of lesions. Multifocal hypointense foci are usually seen at the gray-white interfaces at T2-weighted imaging [11]. Electrocardiographic abnormalities after head injury have so far been scarcely reported [4]. Greenspahn et al [6] described ECG changes with deep T wave inversion simulating subepicardial infarction in the presence of cerebral concussion without gross structural brain pathology. In a series of 22 acutely ill patients with deep T-wave inversion in precordial leads and reversible myocardial contraction abnormalities, there were 6 cases of central nervous system injury, but only a single case with closed head trauma [12]. This patient remained comatose for 1 month and, during each episode of decerebrate posturing, transient anterior ST segment elevation appeared, followed by T-wave inversion. The technetium Tc 99m sestamibi myocardial scintigraphy showed diffuse heterogeneous myocardial defects that did not correspond to a single vascular distribution and the coronary angiogram was normal. In our patient, we observed severe ECG changes with ST elevation corresponding to various vascular territories and nonsustained polymorphous ventricular tachycardia paralleling neurologic status worsening. The brain CT scan was unremarkable, excluding pericerebral or intraparenchymal macroscopic hemorrhage, but brain magnetic resonance imaging disclosed on susceptibility-weighted images (T2*) a specific pattern for DAI (Fig. 1). As far as we know, this kind of brain injury, which can have severe functional neurologic consequences, has not been described as a cause of posttraumatic ECG changes. In acute cerebrovascular events, and especially in SAH, the suggested mechanisms to explain the ECG changes include direct damage to the cardiac innervation or imbalance between the left and right sympathetic outflows to the heart [13], direct injury to the hypothalamic region [1,2], hormonal effect of the release of catecholamines producing a reversible myocardial injury, the so-called catecholaminergic storm [8,9]. The mechanism for DAI-related ECG changes remains speculative, but could involve one or more of these hypotheses. In the latter mechanism, a direct toxic effect by the overproduction of catecholamines has been advocated at the myocardial cellular level [5,8]. This type of catecholaminergic injury has also been suggested in the pheochromocytoma crisis and in the catecholamine-induced myocarditis and/or cardiomyopathy [14]. This was also probably the case in our patient who presented extreme agitation, tachycardia, and hypertension when sedative drugs were tapered off. 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