Cardiac arrest (CA) is one of the leading causes of death worldwide. During the follow-up of these patients, the most frequently recorded heart rate, in 25%–75% of cases, is ventricular fibrillation (VF). The treatment of a witnessed CA is the immediate initiation of resuscitation maneuvers, whether basic or advanced, to ensure adequate perfusion of the brain and other organs in order to minimize subsequent sequelae.1
In this paper we present the case of a 56-year-old man, who was a former injecting and smoking drug addict with a history of hepatitis C infection (under treatment with glecaprevir/pibrentasvir), moderate to severe mitral valve regurgitation, heart failure, and chronic obstructive pulmonary disease (COPD) with a Global Initiative for Chronic Obstructive Lung Disease (GOLD) grade A.
Due to a four-day history of dyspnea, he visited his Primary Care clinic, where a rapid severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) detection test yielded a negative result. During the consultation, he went into CA, with VF and a subsequent “torsade de pointes” being recorded. Advanced resuscitation maneuvers were consequently initiated, including up to 24 defibrillations, the administration of 5 mg of adrenaline and 900 mg of amiodarone, as well as orotracheal intubation. He subsequently recovered a normal heart rate, with a sinus rhythm and no repolarization defects.
However, during his subsequent transfer, he experienced a new episode of VF, which was reversed with two defibrillations, and he required a dopamine perfusion due to developing hemodynamic instability.
Upon his arrival to the Intensive Care Unit, a coronary angiography was performed, viewing lesion-free coronary arteries. A transthoracic echocardiogram showed an ejection fraction of 56% without segmental asymmetries, as well as the known moderate-severe/severe mitral valve regurgitation secondary to a mitral valve prolapse (P2).
Twenty-four hours after his admission, once hemodynamic stabilization had been achieved, both sedation and analgesia were discontinued, and the patient was extubated prematurely. A thorough neurological examination was carried out to assess potential sequelae of the CA, detecting a Glasgow Coma Scale score of 15 and paraplegia, with significant motor and thermoalgesic sensory impairment, although with preserved superficial tactile sensation and proprioception. A magnetic resonance imaging (MRI) scan showed an area of L1–L3 diffusion restriction compatible with an ischemic spinal cord injury (Fig. 1 ).
Fig. 1.
MRI diffusion sequences. Hyperintense focus in the dorsolumbar spinal cord (arrow), from D8 to the L1–L2 medullary cone, exhibiting clear diffusion restriction suggestive of a vascular disorder (medullary infarction).
Seventy-two hours later, he experienced a new arrhythmic storm and passed away despite the implementation of advanced cardiopulmonary resuscitation maneuvers.
Acute spinal cord ischemia is a rare syndrome that accounts for 1%–2% of neurological vascular disorders and is usually associated with a poor functional and vital prognosis. Nowadays, successful cardiopulmonary resuscitations after a CA are more common, owing to which ischemic complications are being diagnosed more frequently within the first few hours following the episode.2, 3
Although post-CA cerebral ischemic features have been widely described, the effects and location of an ischemic spinal cord injury have not been extensively studied. The mid-thoracic region (T4–T6) has traditionally been identified as the most susceptible area due to its poor vascularization characteristics; however, clinicopathological studies suggest that ischemia may have a greater impact on the lower lumbar spinal cord due to hyperfusion of the Adamkiewicz artery. The degree of the injury depends, among other factors, on the intensity of the hypoperfusion, the duration of the episode of cardiac arrest, and the subsequent survival.3
Although spinal cord ischemia after a cardiac arrest results from the main damage caused to the anterior horn of the gray matter, somatosensory pathways usually retain their integrity, which translates into preservation of superficial tactile sensation and proprioception.4
The diagnosis is reached after performing an MRI in patients in which this condition is suspected.5
In conclusion, spinal cord ischemia after an episode of cardiac arrest is a rare disease, albeit with devastating consequences for the patient. Hence, the study of neuroprotection strategies in generalized hypoperfusion processes is of significant interest given the vulnerability of the spinal cord to ischemia.3
Funding
The authors declare that they received no financial support for the conduct of this study.
Acknowledgments
We would like to thank the Intensive Care Unit of University Clinical Hospital Lozano Blesa of Zaragoza, Spain.
Footnotes
Please cite this article as: Lozano Gómez H, Isern de Val I, Zalba Etayo B. Isquemia medular tras parada cardiaca. Med Clin (Barc). 2021;157:e331–e332.
References
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