Traumatic brain injury and subsequent decompressive hemicraniectomy in a 53-year-old woman resulted in transient and recurrent complete heart block with severe bradycardia to 15 bpm.
Case Report (n=1)
Complete heart block following severe neurologic injury may represent a transient, reversible neurogenic dysfunction rather than primary cardiac pathology, warranting conservative management before considering permanent pacemaker implantation.
Abstract Introduction Complete heart block (CHB), or third-degree atrioventricular block (AVB), represents failure of impulse conduction between the atria and ventricles. In adults, most cases are acquired and associated with ischemic, infiltrative, or inflammatory cardiac disease. Beyond these cardiac causes, acute neurological injury has been linked to diverse cardiac manifestations, including arrhythmias and myocardial dysfunction. However, CHB in this context is exceedingly rare, with only isolated reports following traumatic brain injury (TBI). We report a case of transient and recurrent CHB after decompressive hemicraniectomy for traumatic subdural hematoma, illustrating the reversible neurogenic mechanisms underlying this phenomenon. Case Description A 53-year-old woman with alcohol-related cirrhosis presented after a ground-level fall with obtundation. Head CT revealed a subdural hematoma with midline shift, prompting emergent right decompressive hemicraniectomy and hematoma evacuation. Her postoperative course was complicated by intraparenchymal hemorrhage requiring temporal lobectomy.On hospital day 8, she developed severe bradycardia to 15 bpm refractory to atropine. ECG demonstrated complete heart block (Figure 1a). Transcutaneous pacing (40 bpm) and dobutamine were initiated. Echocardiography revealed moderate left ventricular hypertrophy and moderately elevated pulmonary artery systolic pressure. Over 48 hours she required intermittent pacing, then spontaneously reverted to normal sinus rhythm (Fig 1b). Six days later, she again developed intermittent CHB with a ventricular rate in the 40s. During this time, she remained poorly responsive with continued brain hemorrhage and midline shift (Fig 1c). Given her poor neurologic prognosis, care transitioned to comfort measures, and she passed away. Discussion This case highlights a rare manifestation of neurogenic atrioventricular conduction disturbance following TBI. The transient resolution and recurrence of CHB suggests a functional autonomic mechanism rather than irreversible damage to the conduction system. Parasympathetic discharge and sympathetic withdrawal related to elevated intracranial pressure or abrupt decompression may underlie the phenomenon.These neurocardiac interactions underscore the complexity of the brain-heart axis, in which severe neurologic injury can alter cardiac rhythm independent of structural heart disease. Recognizing neurogenic CHB is crucial because conduction may recover with stabilization of intracranial dynamics. Awareness of this may prevent premature pacemaker implantation and support conservative management until neurologic recovery or goals-of-care decisions are clarified. Conclusions This case emphasizes that AVB after neurologic injury may represent transient neurogenic dysfunction rather than primary cardiac pathology. Clinicians should consider reversible autonomic causes of bradyarrhythmia before committing to permanent pacing, particularly in neurotrauma patients. This abstract is funded by: None
Roche et al. (Fri,) conducted a case report in Complete heart block after traumatic brain injury (n=1). Decompressive hemicraniectomy was evaluated. Traumatic brain injury and subsequent decompressive hemicraniectomy in a 53-year-old woman resulted in transient and recurrent complete heart block with severe bradycardia to 15 bpm.