Complications
May occur with anterior circulation stroke affecting the pons or thalamus. One meta-analysis reported that the rate of early seizures after ischemic stroke was 3.3%, and the incidence of late seizures or epilepsy was 18 per 1,000 person-years.[262]
Orolingual edema can rarely complicate use of alteplase and can sometimes require intubation for airway protection.
Patients with large infarctions affecting the cerebellum or middle cerebral artery are at risk of developing edema and elevated intracranial pressure. If left unchecked, the edema compromises blood flow and causes brain herniation, which is frequently fatal.
Cerebellar swelling from edema may cause rapid elevations in pressure in the posterior fossa, pressure on the brainstem anteriorly, upward or downward cerebellar herniation, or acute hydrocephalus from compression of the fourth ventricle. Symptoms include obtundation, quadriparesis, oculomotor abnormalities, or new facial palsy. Placement of an external ventricular drain or decompressive surgery can be lifesaving.[263] Transfer of patients with large cerebellar infarction to a hospital with 24-hour availability of emergency neurosurgical consultation is indicated.
Decompressive hemicraniectomy should be considered for large hemispheric strokes causing deterioration from mass effect.[8] Consider decompressive hemicraniectomy in patients with large middle cerebral artery (MCA) infarction covering all or a significant MCA territory (also recognized as malignant MCA ischemic infarct), and declining consciousness within 45 hours after stroke onset.[264][265] In all patients with large ischemic infarcts with potential of brain swelling and herniation, neurosurgical consultation with focus on decompressive hemicraniectomy should be secured. Neurosurgical intervention reduces mortality, but survivors are frequently left with severe disability and poor quality of life. Surrogate decision-makers should be made aware of this and the decision to undertake surgery should be made on a case-by-case basis.
Post-stroke fatigue is common. At least half of all stroke survivors experience fatigue.[266] The intensity of fatigue does not relate to the size of the stroke.[267] Post-stroke fatigue affects quality of life and exerts a negative impact on a patient’s daily activities, such as decreased participation in physical activities and rehabilitation.[266] The exact cause is unclear. Depression, anxiety, effort adapting to post-stroke living, and disturbed sleep may all contribute. There is insufficient evidence on the efficacy of any intervention to treat or prevent fatigue after stroke.[268]
Modifiable factors such as depression and anxiety, sleeping or eating disturbances, pain, and fatigue-provoking drugs should be identified and appropriately managed.[266] Setting an attainable goal in rehabilitation, maintaining a healthy diet, and performing a tolerable level of exercise routinely may help improve post-stroke fatigue.[268][269]
Post-stroke cognitive impairment is very common. It has been reported to have a prevalence of over 50% in patients 6 months post‐stroke, with 38% of stroke survivors exhibiting a level of cognitive impairment 1 year after stroke that does not meet the criteria for dementia.[270][271][272] Post-stroke cognitive impairment is common even after successful clinical recovery; 70% patients with excellent clinical recovery from stroke at 3 months may still have some form of cognitive impairment.[273] Cognitive impairments include aphasia, executive dysfunction (including impaired abstracting or reasoning or difficulties with problem-solving), agnosia, acalculia, visuospatial difficulties (including issues relating to visual fields and neglect), and memory impairment. Development of post-stroke cognitive impairment is associated with the severity of stroke (high NIHSS scores), recurrent stroke, and increased age.[274] Many stroke patients may have more than one cognitive domain impairment. Tools such as the Mini-mental status examination (MMSE) and Montreal Cognitive Assessment (MoCA) can be considered for screening of cognition, but these measures should not be substitutes for comprehensive clinical assessment since they may not detect deficits in all cognitive domains.[275] A formal neuropsychologic exam (including assessment of language, neglect, praxis, memory, emotional responses, and specific cognitive syndromes) may be helpful after the detection of cognitive impairment with a screening instrument.[231]
Depression is common after stroke, and may warrant treatment with psychotherapy or antidepressant medications.[261]
Stroke-related dysphagia results in aspiration and subsequent pneumonia. A dysphagia screen should be performed in stroke patients prior to oral intake.[119] When aspiration pneumonia occurs, the pneumonia should be treated with antibiotics and consideration given to whether enteral feeding is indicated.[119]
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