Still worsening after stroke?
800,000. That is the number of strokes that occur in the US every year. In approximately one-third of these cases, the patient’s symptoms will continue to deteriorate several days after onset. And the risk of neurologic deterioration directly correlates with the severity of the symptoms at onset, older age, stroke location, and pre-existing medical disease. Unfortunately, early neurologic worsening is associated with significant morbidity and mortality for these patients. But, why does it happen? Can we prevent it? Is it reversible? And how can we manage it? In this BrainWaves episode of Teaching through Clinical Cases, we review some of the most common mechanisms for neurologic deterioration and some of the concepts regarding management.
Why does it happen? In the most simplest explanation, ischemic strokes produce irreversible injury to a core region of brain tissue, with impaired perfusion of neighboring tissue (ischemic penumbra). With collateral vessel failure and glutamatergic neurotoxicity from cell lysis, the penumbra becomes progressively more ischemic, with resultant worsening neurologic deficits. Systemic hypotension, hyperthermia, abnormally high or low glucose levels, and even hyperemia (or hemorrhage) can contribute to penumbral compromise. Therefore, patients with acute stroke often require frequent neurologic monitoring and providers are encouraged to abide by strict guidelines to prevent deterioration.
Is it reversible? Yes, and no. Many causes of deterioration after stroke can be reversed. Early in the hospitalization, progressive infarction, focal cerebral edema account for the majority of cases of neurologic deterioration, with hemorrhagic transformation occurring in a small proportion (~5%). Later, infectious and metabolic processes may account for worsening. Consider a few examples: If a patient demonstrates postural symptoms (e.g., worsening with upright posture), reclining to a supine position may improve symptoms while cerebral autoregulation normalizes. If a patient becomes hemodynamically unstable (e.g., atrial fibrillation with rapid ventricular rate), rate control with improved cardiac output should improve cerebral perfusion and neurologic symptoms. That being said, many therapeutics have failed for the empiric prophylaxis of neurologic deterioration. The use of heparin, dual antiplatelet therapy, magnesium, steroids, and other pharmacologics have all been attempted to prevent neurologic deterioration, but these have limited efficacy or are contraindicated.
How do you manage a deteriorating patient? Obviously, we are not providing advice on medical management–only summarizing the available literature. Obviously, the patient’s airway and circulation come first. But after this is addressed, the causative mechanism should be targeted. The reader would be referred to current AHA guidelines on the management of medical and neurologic complications of stroke. To briefly summarize this 87-page document, the evaluation of ND starts with the basic concept of “is the deterioration focal” or is it global? A focal worsening (e.g., worsening right arm strength) implies evolution of the focal lesion–perhaps related to progressive infarction, focal cerebral edema, or hemorrhagic transformation. A global worsening, as in reduced level of consciousness or encephalopathy, implies a bilateral hemispheric, thalamic, or brainstem process–such as massive hemispheric edema with herniation, metabolic or infectious encephalopathy, etc. Often, repeat head imaging cannot be avoided, in order to exclude the possibility of hemorrhage. Certain immediate clues like low serum glucose or fever should raise your suspicion for more obvious etiologies of neurologic deterioration, but in a third of cases of post-stroke worsening, no cause is found.
To make sure you are adequately prepared, check out our podcast on neurologic deterioration.
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