Cerebrovascular Accident (CVA)

For Quick Review

Types of CVA

(Brigham and Women’s Hospital, 2022a, 2022b, 2022c; Britt & Agarwal, 2021; Hamby, 2017; Johns Hopkins Medicine, n.d.; Goodfriend, et al., 2021)

    • 87% of all strokes

    • Occurs when a blood clot blocks or narrows an artery leading to the brain. Clot’s can be categorized as:

      • Thrombotic: where the clot grows in size sufficiently to block an artery. Usually results from atherosclerosis

      • Embolic: where the clot originates in a different site and lodges in a vessel that’s too small, blocking arterial blood flow. Usually results from atrial fibrillation.

    • Sudden mortality: 8-12%

    • Treatments Include:

      • BP Regulation: check orders as parameters can change and be very high

      • Tissue Plasmingen Activator (tPA): Administered (via IV or IA) within 4.5 hours of symptom onset to break down clots. Transferred to ICU where blood pressure is monitored for 24 hours, anticoagulants are held, invasive procedures are avoided, and therapy is deferred for the first 8 hours

      • Intra-Arterial Thrombectomy (IAT): Clot retrieval via a catheter. Can be performed up to 24 hours post-stroke. Bed rest parameters based on location & procedure (i.e., femoral artery approach)

    • 13% of all strokes

    • Brain bleed occurring as a result of a head injury/trauma or spontaneously from a ruptured cerebral aneurysm—categorized as subarachnoid hemorrhage (SAH; bleeding in the subarachnoid space) and intracranial hemorrhage (ICH; bleeding between the brain tissue and skull or within the brain tissue itself)

    • Sudden mortality within 30 days: SAH: 33-50%; ICH: 50-67%

    Subarachnoid Hemorrhage (SAH)

    • Aneurysmal

      • Treatment: craniotomy for aneurysm clipping, endovascular embolization (coils, stent, or blood diversion), manage blood pressure (beta-blockers: do not increase ICP; hydralazine & Ca channel blockers: lower increase in ICP than nitro), hydrocephalus/ICP management (EVD/lumbar drain)

      • Vasospasm is a potential complication leading to longer LOS (up to 21+ days)

        • Window 5-10 days after SAH; can cause a secondary stroke (ischemic)

        • Treatment: manage BP, medications to dilate vessels via endo, daily TCDs, follow-up angiogram

      • Minute ventilation for pCO2 30-35; hyperventilation can potentiate vasospasm and ischemia

      • Therapy implications: variable anti-coagulation & activity restrictions per MD

    • Non-Aneurysmal: traumatic, occult aneurysm/cavernous malformation, AVM (intracranial/spinal), intracranial arterial dissection

      • Same medical management & monitoring

    Intracranial Hemorrhage (ICH)

    • This can lead to increased pressure on the brain and spasm of blood vessels

    • Treatment: reverse anticoagulation, BP management, & ICP management

    • Intraventricular Hemorrhage (IVH): extension of ICH, poor prognostic sign

      • IVH Treatment: EVD, BP management, fibrinolysis as appropriate.

    • Bulge in a blood vessel caused by a weakness in the blood vessel wall. This weakness in the artery can cause the aneurysm to rupture leading to bleeding in the brain. Risk of rupture is dependent on size, shape, and location upon other variables.

    • Symptoms: Many people are unaware they have an aneurysm and many small brain aneurysms go unnoticed. Often, even with larger aneurysms, there are no symptoms until it ruptures. Symptoms can include:

      • Large unruptured aneurysm: pupil dilation, double or blurred vision, numbness on one side of the face, or drooping eyelid

      • Leaking aneurysm: sudden and severe headache

      • Aneurysm rupture: sudden and severe headache, nausea, vomiting, neck stiffness, seizure, confusion, blurred vision, eye pain, dilated pupils, sensitivity to light, drooping eyelid, loss of balance, muscle weakness, speech impairment, or loss of consciousness

    • Treatment: depends on size of the aneurysm and if it has already ruptured. Small aneurysms typically have a low risk for rupture can be monitored regularly. But risk of rupture increases as the size increases. Goal of treatment is to reduce the risk of rupture or future rupture.

      • Endovascular Treatment: catheter is threaded through a blood vessel to “coiling” or “stenting

      • Surgical clipping: requiring bony window in the skull, craniotomy, to express the aneurysm. Following this, the neurosurgeon places a metal clip at the neck of the aneurysm to prevent blood flow to the aneurysm.

    For further reading/viewing: Brain Aneurysm Treatments

    • Abnormal, tangled connection between the arteries and veins. Can occur in the spinal cord or brain.

    • Normal circulation: blood flows from arteries > capillaries > veins. Blood goes from high pressure to low pressure gradually

      • In AVM’s: blood flows directly from arteries to veins through an abnormal passageway (fistula) rather than capillaries. Leads to effects such as increased flow and pressure. Over time these vessels fatigue and can rupture.

    • Symptoms: Most people are unaware they have an AVM and experience no symptoms. However, symptoms can include:

      • New onset seizure, muscle weakness/paralysis, impaired coordination, dizziness, headache, visual changes, language difficulties, cognitive changes (memory, attention, confusion), abnormal sensations (pain, numbness), and hallucinations.

    • Treatment: depends on the location and size of the AVM. Can be treated with:

      • Serial imaging & observation: observed in yearly imaging and clinical follow-up. These AVMs are typically best left “untreated” and monitored.

      • Endovascular embolization: inject material to block blood flow to the AVM

      • Surgical resection: remove AVM from spinal cord or brain

      • Stereotactic radiosurgery (SRS): direct highly focused beams at the AVM.

    • Damage occurs: 1) rupture of the AVM (considered a type of ICH, SAH, or SDH depending on location), 2-4% of all AVMs hemorrhage, 2) compressing or displacing parts of the brain or spinal cord, or 3) gradual deficits over time as blood flow and oxygen to the brain decreases.

    • Occurs when a blood clot forms in the brain’s venous sinuses. Clot keeps blood from draining out of the brain, resulting in pressure build-up in the blood vessels. The buildup of pressure can lead to swelling and hemorrhage in the brain.

    • Symptoms: headache, blurred vision, fainting/loss of consciousness, loss of control over movement in a part of the body, seizures, and coma.

    • Rare in the general population but one of the more common causes of stroke in patients <45 years old. Flap-like tear of the inner lining of the vertebral artery, which is located in the neck and supplies blood to the brain. After the tear, blood enters the arterial wall and forms a blood clot, thickening the artery wall and often impeding blood flow. May occur after physical trauma to the neck (i.e., blunt injury), strangulation, or after sudden neck movements. However, can occur spontaneously.

    • Symptoms: head/neck pain, intermittent or permanent stroke symptoms (i.e., difficulty speaking, impaired coordination, and visual loss.)

    • Treatment: antiplatelets or anticoagulation for 3-6 months, angioplasty (balloon), or stenting

    • Separation of the layers of the artery wall supplying oxygen-bearing blood to the head and brain. Most common cause of stroke in young adults. May occur after physical trauma to the neck (i.e., blunt injury), strangulation, or after sudden neck movements. However, can occur spontaneously.

    • Non-Ischemic symptoms: localized headache, neck pain, swollen tongue, decreased pupil size, or tinnitus

    • Ischemic symptoms: temporary vision loss, ischemic stroke

    • Treatment: antiplatelets or anticoagulation for 3-6 months, angioplasty (balloon), or stenting

Blood Pressure Parameters

Determined based on the type of stroke. The goal is cerebral autoregulation or maintaining a relatively stable blood flow. Below are some general guidelines, be sure to check is there is any variation at your hospital.

For further explanation

Precautions

(Hamby, 2017; Popovich, 2011)

    • 5-33% of all ischemic strokes convert to hemorrhagic strokes, but not all hemorrhages are large enough to cause symptoms

    • Hemorrhagic conversion can occur due to BP spike and/or weakened cerebral vessels from a stroke.

    • *Monitor changes and potential deterioration in the patient’s neurologic status

    • After stroke: risk for seizure within 24 hrs is 2%-23%

    • Blood flow is compromised when stenosis is 90-100% bilaterally, however therapy is typically allowed despite stenosis especially if the patient is awaiting carotid endarterectomy (CEA). Be sure to monitor vitals and patient symptoms during all activity.

    • Following SAH, blood in the subarachnoid space begins to break down and release hemoglobin and other toxins that can lead to a sustained pathologic inflammatory vasoconstriction of the cerebral arteries, often most severe in the proximal cerebral arteries—Vasospasm. This can result in ischemia due to decreased blood flow or hypoperfusion which can lead to tissue injury and death.

      • ~1/3 of patients with SAH or ruptured aneurysm are at high risk for vasospasm, especially 4-14 days after the initial episode.

    • Avoid all situations which may increase ICP, while the patient is in vasospasm or is at risk for vasospasm, such as putting head in a dependent position or doing any activities that may result in a Valsalva maneuver, including heavy lifting

    • Clinical signs that may suggest a patient is in vasospasm include: neurological decline in status; increased confusion; increased headache; weakness (LE>UE); decreased cognition, especially indecision, and decreased attention/initiation; aphasia; decrease in level of consciousness; seizure; new or increased focal neurological signs which could lead to coma or death.

    • Monitoring: Transcranial doppler (TCD) and long-term monitoring electroencephalography (LTM EEG)

    • Treatment: may include “triple-H therapy” which consists of 1) increasing blood volume (hypervolemia), 2) increasing blood pressure (hypertension), and 3) dilating the blood vessels (hemodilation) to improve perfusion in the areas of vasospasm. *If MD orders the patient’s BP to stay within elevated parameters, a concern for hypoperfusion is likely*

    • Activity orders: Per the medical team. Activity restrictions will depend on the degree of vasospasm.

References

Brigham and Women’s Hospital. (2022a). Stereotactic radiosurgery and radiotherapy. https://www.brighamandwomens.org/neurosurgery/brain-tumors/stereotactic-radiosurgery-radiotherapy

Brigham and Women’s Hospital. (2022b). What is a brain aneurysm? https://www.brighamandwomens.org/neurosurgery/brain-aneurysm

Brigham and Women’s Hospital. (2022c). What is arteriovenous malformation (AVM)? https://www.brighamandwomens.org/neurosurgery/arteriovenous-malformations

Britt, T. B., & Agarwal, S. (2021). Vertebral Artery Dissection. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK441827/

Goodfriend, S. D., Tadi, P., & Koury, R. (2021). Carotid Artery Dissection. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK430835/

Hamby, J. (2017). The Nervous System. In H. Smith-Gabai & S. E. Holm (Eds.), Occupational Therapy in Acute Care (2nd ed.). AOTA Press. https://library.aota.org/OT_in_Acute_Care_2e/134?highlightText=intensive%20care%20unit

Johns Hopkins Medicine. (n.d.). Cerebral venous sinus thrombosis (CVST). Retrieved November 24, 2021, from https://www.hopkinsmedicine.org/health/conditions-and-diseases/cerebral-venous-sinus-thrombosis

Popovich, K. (2011). The Intensive Care Unit. In H. Smith-Gabai (Ed.), Occupational Therapy in Acute Care (1st ed., pp. 41–73). AOTA Press.