Post-Cardiac Arrest Syndrome
OBJECTIVES
To present a survivor with postanoxic encephalopathy after out-of-hospital cardiac arrest due to ventricular fibrillation.
To describe the neurological aftermath of postanoxic encephalopathy at greater than 6 months’ follow-up.
To describe the functional status and long-term neurological outcome post-cardiac arrest.
VIGNETTE
A 45-year-old-man with hypertension, dyslipidemia, and diabetes mellitus, complicated by diabetic retinopathy and prior left foot fourth and fifth digit amputation, had ventricular fibrillation cardiac arrest while working out at a fitness center. Advanced cardiac life support (ACLS) was initiated within 1 to 2 minutes. An automatic external defibrillator (AED) was applied, and the patient was shocked. Cardiopulmonary resuscitation (CPR) continued. An ambulance was present at the scene within 10 minutes. He remained unresponsive and was taken to a local hospital, where he had endotracheal intubation in the emergency department and taken to the cardiac catheterization laboratory where he was revascularized with a coronary artery stent to a 99% stenosed left anterior descending (LAD) artery. He remained intubated and was admitted to the intensive care unit (ICU). A therapeutic hypothermia protocol was promptly initiated. He received a beta-blocker and angiotensin-converting enzyme (ACE) inhibitor. He was extubated 3 days after admission. A recommendation for an internal cardiac defibrillator (ICD) depending on resolution of neurologic status was made.
The patient continued to have altered mental status attributed to anoxic brain injury with resulting post-cardiac arrest encephalopathy. Electroencephalogram (EEG) showed diffuse background slowing. Head computed tomography (CT) without contrast was unremarkable. There was normal gray-white matter differentiation throughout. Magnetic resonance imaging (MRI) of the brain demonstrated some scattered foci of increased signal on T2 and FLAIR images in the periventricular and subcortical white matter bilaterally.
During his hospitalization, his level of alertness began to improve with some purposeful movements and “nonsensical” speech according to family members. He was started on nasogastric feeds. He became febrile due to aspiration pneumonia. He also had renal insufficiency, likely due to contrast administration as well as sudden cardiac arrest with resulting kidney hypoperfusion.
At his family’s request, he was transferred to our institution, where he had four additional coronary artery stents. Following cardiac stabilization, he was transferred for inpatient rehabilitation. Ongoing behavioral issues, cognitive impairment, apathy, and bladder and bowel incontinence delayed his evaluation by a few months after his cardiac arrest. A repeat EEG showed mild to moderate slowing of the background. There were no epileptiform discharges, EEG seizures, or focal abnormalities at any point during the recording.
