Cardiac arrhythmia associated with isolated head trauma in a dog

Authors


MADAM

The authors wish to report a case of cardiac arrhythmia associated with head trauma in a dog.

A 5-year-old, 5.1 kg intact male Chihuahua was referred to the University of Georgia Veterinary Teaching Hospital (UGA-VTH) 16 hours after being struck on the head by a golf club.

Clinical examination findings upon initial presentation to an emergency clinic included normal heart and respiratory rates, normal blood pressure, depressed to disoriented mentation, non-ambulatory tetraparesis, and left-sided exophthalmus and strabismus (direction not indicated). Mentation declined and the dog remained stuporous for 12 hours at the emergency hospital. Temperature, heart rate, and respiratory rate were within normal limits throughout the same time period. Systolic blood pressure was measured twice using a Doppler technique and both measurements were 130 mmHg.

At presentation to the UGA-VTH, the dog was mildly tachypneic (41 breaths per minute) with otherwise normal vital signs. There was scleral haemorrhage of the right eye and swelling of the subcutis over the rostral calvaria. The dog was responsive but mentation was depressed. The dog exhibited non-ambulatory tetraparesis, absent postural reactions and reduced withdrawal reflexes in all four limbs. The cranial nerve examination revealed spontaneous vertical nystagmus, a decreased menace response bilaterally (more marked in the right eye), and a general reduction in facial sensation, more notable on the right side.

On the basis of neurological findings, a lesion was localized to the left cerebrum or thalamus with probable involvement of the rostral medulla due to the vestibular signs and recumbency. The decreased withdrawal reflexes may be explained by trauma to the pons and medulla (Sukhotinsky and others 2005) or may be indicative of multifocal disease. Differential diagnoses included intra- and extra-axial haemorrhage, contusions, and depressed skull fractures. No clinically significant abnormalities on the complete blood count or chemistry profile were identified.

Radiographs of the cervical and thoracic vertebral column were normal. Skull radiographs revealed linear non-depressed fractures of the left temporal bone just rostral to the caudal aspect of the zygomatic arch (Fig 1).

Figure 1.

A dorsoventral radiograph of the skull revealing linear, non-displaced fractures of the left temporal bone just rostral to the caudal aspect of the zygomatic process (arrow).

Continuous electrocardiography (ECG) was maintained during hospitalization. On the second day of hospitalization, the dog had intermittent periods of bradycardia (rates as low as 50 beats per minute) with normal blood pressure. On the third day of hospitalization, four episodes of nonsustained atrial tachycardia were documented, an example of which is shown in Figure 2. This arrhythmia resolved without treatment within 24 hours. Serum electrolytes were normal at this time. On the fifth day of hospitalization, an echocardiogram was performed and disclosed normal myocardial function with no structural abnormalities.

Figure 2.

Lead II ECG tracing (25 mm/s, 1 mV/cm). Following initial and underlying sinus bradycardia with sinus arrhythmia (heart rate approximately 60 beats per minute), a short non-sustained run (6 complexes) of atrial tachycardia begins with an atrial premature complex (premature P wave marked by arrowhead). Heart rate during the last 5 atrial ectopic complexes (marked by solid line) is approximately 170 beats per minute.

The dog’s mentation improved over the course of two days; however, he remained tetraparetic. Magnetic resonance imaging (MRI) with a 3.0 Tesla magnet (GE Healthcare) was performed. Pre-contrast sequences included transverse T1-weighted fluid-attenuated inversion recovery (TIW FLAIR), T2-weighted (T2W), T2*-weighted, T2W FLAIR, short tau inversion recovery (STIR), 3 dimensional fast spoiled gradient recalled echo sequence (3D-FSPGR), sagittal T2W, and dorsal T2W. Post-contrast (0.1 mmol/kg iv gadopentate dimeglumine, Magnevist, Berlex) sequences included transverse and sagittal T1W FLAIR sequences. These sequences revealed regions of subdural and intraparenchymal haemorrhage with associated oedema in the rostral aspect of the frontal lobes, with the left side more severely affected. These lesions extended caudally along the left lateral aspect to the left parietal lobe (Fig 3). Linear fractures of the left frontal bone and palatine/sphenoid bone were also noted.

Figure 3.

Magnetic resonance transverse T2* gradient echo image at the level of the caudate nuclei. There is a lesion on the left side in the region of the parietal and temporal lobes. The lesion is poorly demarcated, characterized by a rim of hyperintense parenchyma (compared to the surrounding white matter) and a hypointense area adjacent to the calvaria. There is hyperintense signal in the white matter (dorsal internal capsule, centrum semiovale, left corpus callosum, left corona radiata) suggestive of vasogenic edema. Mass effect is causing a midline shift to the right. There is a non-displaced linear fracture in the ventral aspect of the left temporal bone (arrow). There is hyperintensity of the soft tissue surrounding this fracture. The lesion in the left parietal and temporal lobes appears markedly hypointense compared to the surrounding brain parenchyma suggesting hemorrhage. (TR: 500ms; TE: 26ms)

Re-evaluation of the patient three months after the trauma revealed a normal general physical examination including normal cardiac rhythm during prolonged ausculation. Neurological examination was normal other than a mild proprioceptive deficit in the left thoracic limb.

In humans, transient atrial fibrillation has been reported after head trauma, with structural cardiac disease found in 70% of cases reported (Muthu and others 2003). Electrocardiographic abnormalities following head trauma are classified broadly into two groups: arrhythmias (true rhythm disturbances) and altered repolarization. Repolarization abnormalities, evidenced by changes in the ST segment or T waves on the ECG, may themselves result in life-threatening arrhythmias such as ventricular tachycardia and/or ventricular fibrillation (Samuels 2007).

Head trauma is thought to result in depolarization of neurons with release of predominantly excitatory neurotransmitters and catecholamines resulting in cardiac lesions (Muthu and others 2003). Clinical studies in rats suggest that catecholamines released directly into the heart via neural connections are more detrimental than blood-borne catecholamines (Rabb and others 1961). The catecholamines result in an increased intracellular calcium concentration. This overload of calcium reduces myocardial contractility causing impaired cardiac function and perfusion disturbances (Masuda and others 2002). Elevated intracellular calcium levels also lead to arrhythmias.

Experimentally, intra-cranial subarachnoid haemorrhage results in ECG abnormalities. The animals in these studies had histopathologic changes of cardiac structures consistent with myofibrillar degeneration (also known as coagulative myocytolysis and contraction band necrosis) (Samuels 2007). These pathologic changes were reduced by pretreatment adrenalectomy, administration of atropine or reserpine suggesting an autonomic nervous system role in the pathogenesis (Hawkins and Clower 1971, Jacob and others 1972). Myocardial necrosis associated with lesions in the nervous system has been reported in veterinary medicine (King and others 1982). The histopathological changes described by King differ from those lesions described in humans in that actual degeneration of the myocardial cell was reported in this study. Neurogenic myocytolysis as described in the human literature includes preserved sarcolemma stroma and muscle nuclei. Both the human and veterinary histopathological lesions describe mineralization of the tissue, which may link the subcellullar mechanism of altered calcium entry to the myocardial damage seen (Samuels 2007).

Current theories suggest that a brain-heart connection creates an autonomic storm in response to stress or injury. Sympathetic activity is seen early, followed by parasympathetic activation (Samuels 2007). There is also a dominance of the cerebral hemispheres, with the left hemisphere causing predominately parasympathetic signs and the right sympathetic (Samuels 2007). Vagal and sympathetic activity may have been induced secondary to head trauma in the patient presented here. Vagal stimulation results in a shortening of the refractory period in atrial cardiomyocytes predisposing to atrial ectopy (Marshall 1976).

To the author’s knowledge, this is the first case reported in veterinary medicine documenting an arrhythmia following isolated head trauma. The prevalence and clinical impact of arrhythmia after head trauma in veterinary medicine is unknown, however given the presence and significant clinical impact of this association in human medicine, close cardiac monitoring is warranted in the veterinary patient with head trauma.

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