EARLY TREATMENT AND ACUTE STROKE MANAGEMENT

Early treatment with drug administration, if appropriate, is the next link in the chain of survival. If the patient is not a candidate for drug therapy, endovascular therapy may be the treatment of choice.

Ischemic Stroke Treatment

For ischemic strokes, the goal is to preserve tissue in the penumbra, where perfusion, although decreased, remains sufficient to prevent further infarction. Attempts to establish revascularization includes fibrinolysis by the administration of intravenous recombinant tissue-type plasminogen activator (rtPA) and intra-arterial approaches.

FIBRINOLYSIS WITH rtPA (ALTEPLASE)

It is recommended to treat carefully selected ischemic stroke patients with the fibrinolytic drug rtPA (alteplase), the only fibrinolytic agent with FDA approval for use in such patients. Initially, the drug was to be given within 3 hours of the onset of clearly defined stroke symptoms and only after CT scanning had ruled out hemorrhagic stroke. Subsequently, the AHA/ASA revised the guidelines and expanded the window of treatment from 3 hours to 4.5 hours after the onset of symptoms.

The chief benefit of thrombolysis is improved final functional outcome, and the chief risk is intracerebral hemorrhage. Three months post tPA therapy, approximately 30% of patients are neurologically normal or near normal, and approximately 50% of patients are completely or almost complete independent in activities of daily living (Saver, 2021).

Tenecteplase is a variant of alteplase with modifications that allow for the convenience of a single bolus administration. While tenecteplase is not approved by the FDA as of 2022 for the treatment of acute ischemic stroke, there is strong evidence suggesting that it has similar safety and efficacy outcomes compared with alteplase, and AHA guidelines recommend considering its use over alteplase (Mathew & Kile, 2022).

Eligibility for rtPA

The following table indicates inclusion criteria guidelines for administration of rtPA in patients whose onset of symptoms is known to be under 3 hours.

INCLUSION CRITERIA GUIDELINES FOR rtPA ADMINISTRATION

(Saver, 2021)
By stroke status:	Diagnosis of ischemic stroke causing measurable neurologic deficit Neurologic signs not clearing spontaneously to baseline Neurologic signs not minor and isolate. Symptoms not suggestive of subarachnoid hemorrhage Onset of symptoms is <3 hours prior to beginning treatment No seizure with postictal residual neurologic impairments CT does not show a multilobar infarction (hypodensity >1/3 of cerebral hemisphere)
By blood vessel status:	No head trauma or prior stroke in the previous 3 months No myocardial infarction in the previous 3 months No known arteriovenous malformation No gastrointestinal or urinary tract hemorrhage in the previous 21 days No major surgery in the past 3 months No arterial puncture at a noncompressible site in the previous 7 days No history of previous intracranial hemorrhage Systolic blood pressure <185 mmHg and diastolic pressure <110 mmHg No evidence of active bleeding or acute trauma (e.g., a fracture) on examination
By thrombotic status:	Not taking an oral anticoagulant, or If anticoagulant is being taken, INR <1.7 If patient received heparin in previous 48 hours, aPTT (activated partial thromboplastin time) must be within a normal range Platelet count >100,000 mm3
Other criteria:	Blood glucose >50 mg/dL
Understanding of risks/benefits:	Patient or family understands the potential risks and benefits of treatment

Eligibility criteria for rtPA at 3 hours to 4.5 hours from onset are similar but more stringent, with any one of the following being an additional exclusion criterion:

• Over 80 years of age
• Use of oral anticoagulants, regardless of the INR
• Baseline NIHSS score >25
• Combination of both previous ischemic stroke and diabetes mellitus
  (Oliveira-Filho & Samuels, 2022)

Administration of rtPA

The protocol for administering rtPA should be written and approved by members of the stroke team and should be reviewed prior to administration. Treating an ischemic stroke with rtPA must be done promptly. Therefore, stroke EDs need electronic standing orders for the drug and an established procedure for quickly dispensing the drug from the pharmacy at any hour.

The dosage is calculated based on the patient’s weight, with a maximum total of 90 mg over 60 minutes. Ten percent of the dose is given as an IV bolus over 1 minute, followed by an IV infusion of the remainder of the dose over 1 hour. It may be administered intravenously or intra-arterially (an off-label route).

Prior to administration, a registered nurse ensures that:

• Blood pressure has been carefully lowered to maintain systolic BP <185 mmHg and diastolic BP <110 mmHg before initiating fibrinolytic therapy
• Due to an increased risk of intracranial bleeding, INR, aPTT, and blood glucose have been completed
• For patients who are hemodynamically unstable, any prior anticoagulant therapy is discontinued before and during the thrombolytic infusion to minimize risk of bleeding
• Vital signs and neurologic assessment have been completed
• CT scan has been completed and interpreted
• Inclusion/exclusion criteria have been met and stroke scale is completed
• Continuous ECG and SpO₂ monitoring are in place
• Appropriate lab studies are completed
• Patient’s identity has been verified according to institutional protocol
• rtPA dose is verified to the order with a second RN or physician
• All procedures that might cause bleeding (indwelling urinary catheters, nasogastric tubes) are completed
• At least two large-bore IVs are in place

Initiating the infusion: The nurse makes certain that the rtPA is infused with no other drugs.

During administration, the nurse:

• Maintains the patient on strict bedrest during treatment
• Completes a neurologic assessment and takes vital signs every 15 minutes during infusion for 2 hours, then every 30 minutes for 6 hours, then hourly until 24 hours after treatment
• Increases frequency of BP monitoring if systolic BP >180 mmHg or if diastolic BP >105 mmHg; administers antihypertensive as needed to maintain these levels
• Monitors the patient and notifies the physician for adverse allergic reactions
• Discontinues infusion and obtains an emergency CT scan and appropriate laboratory work if the following signs of intracranial bleeding occur:
• Acute hypertension
• Severe headache
• Nausea and/or vomiting
• Worsening neurologic exam
• Avoids invasive procedures and IM injections, and performs venipunctures carefully and only as required, avoiding internal jugular and subclavian venous punctures
• Frequently assesses all punctures for bleeding; if bleeding occurs, stops the infusion immediately
• If extravasation occurs, stops the infusion and applies local therapy

Post administration:

• Checks vital signs and neurologic status:
• Every 15 minutes for 2 hours, then
• Every 30 minutes for 6 hours, then
• Every 60 minutes until 24 hours after rtPA treatment
• Maintains BP <180/105 mmHg for at least 24 hours post treatment
• Withholds antiplatelet or anticoagulant therapy and invasive procedures for 24 hours following treatment
• Monitors for serious adverse events, such as bleeding and angioedema:
• Concomitant use of angiotensin-converting enzyme (ACE) inhibitors may increase the risk of orolingual angioedema.
• Concomitant use of anticoagulants and drugs that inhibit platelet function increase the risk of bleeding.
• Delays insertion of nasogastric tubes, indwelling catheters, or intra-arterial pressure catheters if patient can be managed without them
• Obtains follow-up CT or MRI scan 24 hours after treatment and before starting anticoagulants or antiplatelet agents
  (LNC, 2021a)

Management of bleeding within 24 hours after administration of alteplase, the nurse:

• Stops alteplase infusion
• Obtains complete blood count (CBC), prothrombin time (PT) test (INR), aPTT, fibrinogen level, type, and cross-match
• Obtains emergent nonenhanced head CT
• Per order, administer cryoprecipitate (includes factor VIII): 10 U infused over 10–30 minutes (onset in 1 hour, peaks in 12 hours); administer additional dose for fibrinogen level <150 mg/dL
• Per order, administers tranexamic acid 1 gram (or 10 to 15 mg/kg) once; administers at a rate not to exceed 100 mg/minute (over 10 to 20 minutes) OR ε-aminocaproic acid 4–5 g over 1 hour, followed by 1 g per hour IV for 8 hours or until bleeding is controlled
• Obtains hematology and neurosurgery consult
• Manages BP, intracranial pressure (ICP), cerebral perfusion pressure (CPP), mean arterial pressure (MAP), temperature, and glucose

Management of orolingual angioedema requires the nurse to:

• Maintain airway:
• Intubation may not be needed if edema is limited to anterior tongue and lips.
• Edema involving larynx, palate, floor of mouth, oropharynx with rapid progression (within 30 minutes) poses higher risk of respiratory compromise requiring intubation.
• Awake fiberoptic intubation is preferred.
• As ordered, perform the following:
• Discontinue IV alteplase infusion and hold ACE inhibitors
• Administer IV methylprednisolone 125 mg
• Administer IV diphenhydramine 50 mg
• Administer ranitidine 50 mg IV or famotidine 20 mg IV
• If there is an increase in angioedema, administer epinephrine (0.1%) 0.3 mL subcutaneously or by nebulizer 0.5 mL
• Administer icatibant (selective bradykinin B2 receptor antagonist), 3 mL (30 mg) subcutaneously in abdomen. Additional 30 mg doses may be given at 6-hour intervals not to exceed 3 injections in 24 hours.
  (Powers et al., 2019)

Complications

Symptomatic intracranial hemorrhage (ICH) after IV rtPA for ischemic stroke occurs in 2%–7% of patients. Approximately half of symptomatic intracranial hemorrhages occur by 10 hours after treatment, with the rest occurring by 36 hours. Intracranial hemorrhage occurring after 36 hours is not likely due to rtPA.

ICH may be signaled by acute hypertension, headache, neurologic deterioration, and nausea or vomiting. If ICH is suspected, an emergent head CT scan and labs, including PT, aPTT, platelet count, and fibrinogen, are done. If ICH is present on CT scan, lab results are evaluated and, if necessary, 6 to 8 units of cryoprecipitate containing fibrinogen and factor VIII, 6 to 8 units of platelets, and/or fresh frozen plasma are administered. Use of recombinant factor VII may also be considered but carries a risk of inducing thrombotic events.

Certain patients are more susceptible to ICH following rtPA administration. These include patients with:

• Older age
• Higher baseline glucose
• Greater stroke severity
• Prior hypertension
• Congestive heart failure
• Renal impairment
• Hyperglycemia and diabetes mellitus
• Ischemic heart disease
• Atrial fibrillation
• Baseline antiplatelet use
• Smoking
• Higher baseline neutrophil count and neutrophil-to-lymphocyte ratio
  (Maier et al., 2020; Saver, 2021)

TREATMENT WITH OTHER ANTITHROMBOTIC DRUGS

Following clinical trials, tenecteplase (TNKASE), a single-bolus thrombolytic approved by the FDA for use in mortality reduction associated with acute myocardial infarction, may be chosen over IV alteplase in patients without contraindications for IV fibrinolysis who are also eligible to undergo mechanical thrombectomy. Tenecteplase has not been proven to be superior or noninferior to alteplase but might be considered as an alternative in patients with minor neurologic impairment and no major intracranial occlusion.

Antiplatelet treatment with aspirin is recommended in patients with AIS within 24–48 hours after onset. For those treated with IV alteplase, aspirin administration is commonly delayed until 24 hours later. Aspirin, however, is not recommended as a substitute for acute stroke treatment in patients who are otherwise eligible for IV alteplase or mechanical thrombectomy.

In patients presenting with noncardioembolic ischemic stroke (NIHSS score ≤3) who did not receive IV alteplase, treatment with dual antiplatelet therapy (aspirin and clopidogrel) started within 24 hours after symptom onset and continued for 21 days is effective in reducing recurrent ischemic stroke for a period of up to 90 days from symptom onset (Powers et al., 2019).

Anticoagulant treatment is seldom given for treatment of acute ischemic stroke because of the risk of excessive bleeding. Full-dose anticoagulant therapy with heparin or low–molecular weight heparin is used by some clinicians for certain types of strokes, such as those caused by cardioembolism or dissection.

Low-dose anticoagulant therapy with heparin or low molecular weight heparin is sometimes used for people with ischemic stroke who are paralyzed from the stroke in order to help prevent thrombi from forming in the legs or other veins, which could cause pulmonary embolism (Caplan, 2021).

ENDOVASCULAR TREATMENT

Mechanical Thrombectomy

Thrombectomy is a mechanical interventional procedure by which a blood clot is removed under image guidance using endovascular devices. The use of mechanical thrombectomy is considered the standard of care for a large vessel occlusion. Early intra-arterial treatment with mechanical thrombectomy is safe and effective for reducing disability and is superior to standard treatment with intravenous thrombolysis alone for ischemic stroke caused by a documented large artery occlusion in the proximal anterior circulation.

Thrombectomy utilizes various techniques, most commonly stent-retrieval, direct aspiration, or a combination of both. The primary purpose of mechanical thrombectomy in ischemic stroke is to rescue the ischemic penumbra.

AHA/ASA guidelines for the early management of AIS recommend the following criteria for endovascular mechanical thrombectomy therapy:

• Pre-stroke modified Rankin scale <2
• Alberta Stroke Program Early CT Score (ASPECTS) of ≥6 within 6 hours of symptom onset.
• NIH stroke scale score ≥6.
• Start of procedure within 6 hours of symptom onset.
• Causative occlusion of the internal carotid artery or the proximal middle cerebral artery
• Age 18 years or older

Mechanical thrombectomy has been shown to improve clinical outcomes versus standard care alone in select patients with large vessel ischemic stroke presenting up to 24 hours after the start of symptoms. Current indications for its use have extended the time of thrombectomy to 24 hours post symptom onset.

Contraindications for its use include:

• Intracranial hemorrhage
• Large infarct core with minimal penumbra
• Small vessel occlusion
• Coagulopathies that cannot be corrected
• Elevated blood pressure (systolic >185 mmHg or diastolic >110 mmHg) that cannot be corrected
  (Mathews & De Jesus, 2021; Oliveira-Filho & Samuels, 2022)

Both second-generation stent retrievers and catheter aspiration devices can be used for mechanical thrombectomy. The choice depends on local expertise and availability. In some cases, the stent retriever and aspiration techniques may be used in combination. Catheterization is performed via a femoral artery puncture under general anesthesia or conscious sedation. The catheter is guided to the internal carotid artery and from there to the site of the occlusion. The tiny net-like stent retriever is then inserted into the catheter and guided to the occlusion. The stent is then pushed directly through the clot, after which it expands to the size of the artery wall. At this point, the retriever has captured the clot, and it is removed as the device is pulled back.

Mechanical thrombectomy devices can remove a clot in a matter of minutes, whereas pharmaceutical thrombolytics, even those delivered intra-arterially, may take as long as two hours to dissolve a thrombus. AHA/ASA guidelines state that patients eligible for IV alteplase should receive it even if mechanical thrombectomy is being considered, and that patients under consideration for the procedure should not wait for observation to assess for clinical response following the IV (Powers, et al., 2019).

Symptomatic intracerebral hemorrhage is a potential adverse event of mechanical thrombectomy, resulting from instrument manipulation. Despite this complication, the risk of symptomatic intracerebral bleeding is not significantly different from the medical standard of care. Complications can include:

• Dislodging of embolic material distal to the occlusion
• Stenosis at the thrombectomy site
• Vessel perforation and dissection
• Groin and retroperitoneal hematomas at the puncture site
• Reocclusion secondary to a high platelet count on admission, pre-existing stenosis, or embolic material around the thrombectomy site

Although these acute complications are not common, they indicate a poor prognosis (Mathews & De Jesus, 2021).

Emergency CEA/Carotid Angioplasty

A carotid endarterectomy (CEA) is a surgical procedure done to open and clean a carotid artery. AHA/ASA 2019 guideline recommendations state that the usefulness of emergent or urgent CEA/carotid angioplasty and stenting when clinical indicators or brain imaging suggests a small infarct core with large territory at risk, compromised by inadequate flow from a critical carotid stenosis or occlusion, or in the case of acute neurologic deficit after CEA, in which acute thrombosis of the surgical site is suspected, is not well established.

In patients with unstable neurologic status (e.g., stroke-in-evolution), the efficacy of emergency or urgent CEA/angioplasty and stenting is not well established (Powers et al., 2019).

BLOOD PRESSURE CONTROL IN ISCHEMIC STROKE

Treating hypertension in the acute setting is controversial, since both high and low blood pressures are associated with poor outcomes. The rationale for lowering blood pressure is to reduce cerebral edema and limit hemorrhagic transformation. However, rapid lowering of blood pressure worsens cerebral hypoperfusion, exacerbates stroke symptoms, expands ischemic core, increases the size of infarction, and is not associated with greater therapeutic benefit (Haidar et al., 2021).

AHA/ASA guidelines indicate that in patients who do not qualify for either intravenous alteplase or mechanical thrombectomy, blood pressure should not be lowered unless it exceeds 220/120 mmHg. However, patients with AIS presenting with symptoms of other severe acute comorbidities, (e.g., acute coronary event, acute heart failure, aortic dissection, preeclampsia/eclampsia) may require an emergency blood pressure reduction. Blood pressure reduction should be individualized since an exaggerated drop can result in complications, including stroke progression or acute kidney injury. To date, no blood pressure reduction strategy has been shown to be superior.

Patients who are eligible for treatment with IV thrombolysis should have their blood pressure carefully lowered so it is <185/110 mmHg and with a blood pressure goal <180/105 mmHg for the first 24 hours following thrombolytic administration.

In patients undergoing mechanical thrombectomy, and who have not received IV thrombolysis, it is recommended that blood pressure be maintained at ≤185/110 mmHg before the procedure, ≤180/105 mmHg during and for the 14 hours post procedure, regardless of whether the recanalization has been achieved.

In patients with blood pressure ≥220/120 mmHg who did not receive IV alteplase or mechanical thrombectomy and have no comorbid condition requiring urgent antihypertensive treatment, the benefit of initiating or reinitiating treatment of hypertension within the first 48–72 hours is uncertain. It might be reasonable to lower blood pressure by 15% during the first 24 hours after stroke onset.

Low blood pressure may be triggered by conditions such as hypovolemia, cardiac arrhythmia, or blood loss due to periprocedural hemorrhage during mechanical thrombectomy. Guidelines recommend hypotension and hypovolemia be corrected to maintain a systemic perfusion level necessary to support organ function. It is not indicated at what blood pressure level should be initiated, how long it should be maintained, or which blood pressure level should be a treatment goal (Powers, 2019; Aziz & Mistry, 2022; Gasecki et al., 2021).

SUPPORTIVE CARE

Meticulous attention to the care of the stroke patient during treatment for ischemic stroke can prevent further neurologic injury and minimize common complications, optimizing the chance of functional recovery. Supportive care for patients during treatment for ischemic stroke includes:

• Bed rest for the first 12–24 hours
• Routine placement on aspiration, deep venous thrombosis, fall, and seizure precautions
• Head of bed lowered if perfusion limitation is suspected but raised in those suspected of having cerebral edema or elevated intracranial pressure
• Airway and ventilation maintenance
• Continuous hemodynamic monitoring
• Strict glucose control regardless of whether the patient has a known history of diabetes
• Close monitoring for signs of neurologic worsening
• Nothing by mouth (NPO) until dysphagia screening is completed within 4–24 hours
• Minimizing skin friction and pressure
  (Green et al., 2021; Chawla, 2021)

Intracranial Hemorrhagic (ICH) Stroke Treatment

Intracranial hemorrhage includes four broad types of hemorrhage, including:

• Epidural: Bleeding between the skull and the dura mater
• Subdural: Bleeding between the dura mater and the arachnoid membrane
• Subarachnoid: Bleeding between the arachnoid membrane and pia mater
• Intracerebral or intraparenchymal: Bleeding within the brain tissue

Each type involves different causes and variable clinical findings, prognosis, and outcomes. Most ICHs are due to head injury. Others may be the result of an aneurysm or an arteriovenous malformation.

Although intracerebral hemorrhage is the second most common cause of stroke, it accounts for an inordinate amount of morbidity and mortality. Bleeding occurs within the brain quickly, without warning signs, and severely enough to result in coma or death.

Management and treatment depend on whether the stroke is within the brain (intracerebral) or on the surface between the brain and skull (subarachnoid). The goal is to stop the bleeding, repair the cause, relieve symptoms, and prevent complications. Treatment may be a combination of surgery and medications as well as:

• Advanced trauma life support
• Control of bleeding
• Seizure control
• Blood pressure control
• Intracranial pressure control
  (Rordorf & McDonald, 2022; Tenny & Thorell, 2022)

ADVANCED TRAUMA LIFE SUPPORT MEASURES

Management begins with ensuring adequate airway, breathing, and circulation; the acquisition of an emergent CT scan; and rapid stabilization of vital signs. Intubation should be considered if the patient has a deteriorating Glasgow coma, a Glasgow coma score of ≤8, or worsening neurologic status. Patients with elevated intracranial pressure should be intubated and hyperventilated (Tenny & Thorell, 2022).

CONTROL OF BLEEDING

Anticoagulation-associated intracranial hemorrhage has a high morbidity and mortality rate. Patients on warfarin have an increased incidence of hemorrhagic stroke. The necessity of reversing anticoagulation is a medical emergency, and reversals must be accomplished as quickly as possible to prevent further expansion of the hematoma. All anticoagulant and antiplatelet drugs should be stopped immediately, and medication-specific reversal agents should be administered.

• Warfarin: Four-factor prothrombin complete concentrate (4F-PCC) or, if unavailable, three-factor prothrombin plex with recombinant activated factor VII or fresh frozen plasma may be given. IV Vitamin K should also be given to sustain the short-acting effect of 4F-PCC or FFP
• Direct oral anticoagulants: Two specific reversal agents for direct oral anticoagulants have FDA approval: idarucizumab for dabigatran, and andexanet alfa for apixaban and rivaroxaban.
• Heparin and low–molecular weight heparin: Protamine sulfate for heparin, and andexanet alfa for low molecular weight heparin.

Patients with severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement or platelet transfusion (Rordorf & McDonald, 2022).

SEIZURE CONTROL

For those with acute ICH who have a seizure, immediate intravenous antiseizure medication should be initiated to reduce risk of recurrent seizure. These drugs, however, have not been shown to improve functional outcome or reduce the rate of poststroke epilepsy. There are many antiseizure medications, which may include:

• Brivaracetam
• Cannabidiol
• Carbamazepine
• Gabapentin
• Phenobarbital
• Phenytoin
• Valproate

For patients who have an early seizure (<14 days from onset), continue treatment for several days and then wean when clinically stable if seizures do not recur.

For patients who have later seizures (>14 days from onset), continue with long-term seizure therapy.

For patients with acute ICH who do not have a seizure, antiseizure medication prophylaxis should not be administered (Rorfdorf & McDonald, 2022).

BLOOD PRESSURE CONTROL

Elevated blood pressure is common in patients with acute ICH. Uncontrolled elevations in blood pressure and blood pressure variability are risk factors for hemorrhage expansion and poor outcome. Lowering blood pressure has been shown to reduce the risk of recurrent stroke by up to 30%.

In patients with spontaneous ICH requiring acute BP lowering, titrate to ensure continuous smooth and sustained control of BP. Avoiding peaks and large variability can be beneficial for functional outcomes. Initiating treatment within 2 hours of ICH onset and reaching target BP can be beneficial and also improve functional outcomes. In patients with moderate to severe ICH with systolic BP (SBP) of 150–220 mmHg, acute lowering of SBP to a target of 140 mmHg with the goal of maintaining in the range of 130–150 mmHg is safe and may be reasonable for improving functional outcomes

For patients with large or severe ICH or those requiring surgical decompression, the safety and efficacy of intensive BP lowering are not well established.

In patients with ICH of mild to moderate severity presenting with SBP >150 mmHg, acute lowering of SBP to <130 mmHg is potentially harmful (Greenberg et al., 2022).

For systolic BP >220 mmHg, rapidly lower to <220 mmHg. For SBP of 150–220 mmHg, lower to a target of 130 mmHg. Recommended medications include:

• Nicardipine for patients with a systolic BP ≥160 mmHg
• Labetalol for patients with systolic BP <160 mmHg

Other intravenous medications that may be used include:

• Clevidipine
• Esmolol
• Enalaprilat
• Fenoldopam

Nitroprusside is typically avoided because it may increase intracranial pressure (Rordorf & McDonald, 2022).

INTRACRANIAL PRESSURE CONTROL

Acute ICH may lead to increased intracranial pressure due to several mechanisms, including:

• Mass effect of the initial hematoma
• Expansion or rebleeding of the ICH
• Cerebral edema surrounding the hemorrhage
• Hydrocephalus from ventricular outflow obstruction

To improve jugular venous outflow and lower intracranial pressure, the head of the bed should be elevated to 30 degrees, and the head should be maintained at midline and not turned to either side. The patient may require analgesia (morphine or alfentanil [Afentna]) and sedation (propofol) to assist with this recommendation (Kitagawa, 2022).

Mannitol 20% is given at a dose of 1.0–1.5 g/kg. Corticosteroids should not be administered for treatment of elevated ICP.

Hyperventilation after intubation and sedation to a pCO of 28–32 mmHg will be necessary if the ICP increases further.

Recommendations are to monitor ICP with a parenchymal or ventricular catheter for all patients with a Glasgow coma scale <8 or those with evidence of transtentorial herniation or hydrocephalus. Transtentorial herniation is life-threatening, involving the movement of brain tissue from one intracranial compartment to another. It is a time-critical pathology that may be reversed with emergent surgical intervention and medical management.

The ventricular catheter has the advantage of draining of CSF in the event of hydrocephalus. The aim of management is to maintain cerebral perfusion pressure of 50–70 mmHg (Unnithan et al., 2022).

SURGICAL INTERVENTIONS

Despite much progress in the acute management of ICH, the ideal surgical management is still to be determined. Minimally invasive surgery, however, does seem to be more effective than conservative treatment in patients with ICH in reducing both morbidity and mortality.

Indications for surgical intervention depend on the ICH size and location, the time since onset, and the clinical status of the patient. Patients presenting acutely with a cerebellar hemorrhage greater than 3 cm in diameter and brainstem compression will most likely require urgent surgical decompression.

Decompression surgery relieves pressure on the brain, allowing pooled blood to be removed and repair to be done to damaged blood vessels, thereby reducing secondary damage to the brain resulting from increased intracranial pressure. There are four surgical methods to accomplish this:

• Craniotomy with open surgery is performed when a hematoma is very large or when it is compressing the brainstem. It involves removal of a portion of the skull to drain the hematoma and repair blood vessels.
• Simple aspiration involves drilling a small hole in the skull and draining the hematoma using a tube or catheter. This is a relatively noninvasive procedure but does not always allow for complete drainage of the hematoma.
• Endoscopic evacuation is similar to simple aspiration in that it involves drilling a hole in the skull, but instead of using traditional surgical instruments, the hematoma can be reached and drained using a tiny camera-guided instrument.
• Stereotactic aspiration uses CT scanning to locate the hematoma and a specially developed suction tool to drain it. The patient is immobilized in a stereotactic head frame that allows for a greater degree of precision and accuracy than otherwise would be possible.
  (Stieg, 2021)

TREATMENT OF ANEURYSMS

There are two types of treatment for aneurysm: surgical clipping and endovascular coiling.

Surgical clipping is a procedure done to close off an aneurysm to prevent rebleeding. A portion of the skull is removed to access the aneurysm, and a metal clip is placed on the neck of the aneurysm to stop blood flow to it. This clamp can keep the aneurysm from bursting, or it can keep an aneurysm that has recently hemorrhaged from bleeding again. Following clamping, the skull portion is replaced.

Endovascular coiling is a less-invasive procedure than clipping and has been used increasingly in recent years with excellent success. During this procedure, a tiny detachable coil is advanced through an artery in the groin into the aneurysm, filling it with the coil. A blood clot forms within the coil, blocking blood flow to the aneurysm and preventing it from rupturing again. Endovascular treatment may be preferred over surgical clipping when:

• An aneurysm is in a difficult location to access surgically
• The aneurysm is small-necked and located in the posterior fossa
• The patient is elderly
• The patient has a poor clinical grade
  (Brown, 2022)

ARTERIOVENOUS MALFORMATION (AVM) TREATMENT

An AVM causes blood to flow directly from the arteries to the veins without supplying blood to vital tissues, resulting in brain tissue that starts to die off. Three surgical options are used: conventional surgery, endovascular embolization, and radiosurgery. Endovascular embolization and radiosurgery are less invasive than conventional surgery and offer safer treatment options for AVMs located deep inside the brain. An AVM grading system can help estimate the risk of surgery based on the size of the AVM, location in the brain, surrounding tissue involvement, and any leakage.

Surgical resection. If an AVM has bled and/or is in an area that can be easily accessed, then conventional brain surgery is recommended. AVMs may be approached via a craniotomy over the cerebral convexity, via the base of the skull, or via the ventricular system. Arterial feeders are isolated and ligated, and the tangle of abnormal blood vessels is resected. Postsurgical angiography is performed to ensure that no residual AVM remains. There have, however, been instances of reappearance of AVMs years following a negative postresection angiogram.

Endovascular embolization. This procedure involves the insertion of a long, thin catheter through a groin artery then threaded through blood vessels to the brain using X-ray imaging. The catheter is positioned into one of the arteries feeding the AVM, and a substance is injected, such as fast-drying glue-like materials, fibered titanium coils, and tiny balloons that will travel through blood vessels and create an artificial blood clot in the center of an AVM. This is repeated for each vessel that feeds the AVM. This procedure is less invasive than surgical resection and is frequently used prior to it to make the procedure safer by reducing the size of the AVM or the likelihood of bleeding. Endovascular embolization by itself does not typically eliminate the AVM and, therefore, is almost always used as a preliminary step in preparation for either microsurgical resection or stereotactic radiotherapy.

Stereotactic radiosurgery (SRS). SRS is an even less-invasive therapeutic approach often used to treat a small AVM that has not ruptured but is in an area difficult to reach by regular surgery. This treatment uses proton beam, linear accelerator, or gamma knife methods to precisely deliver a high dose of radiation to destroy the AVM. SRS directs many highly targeted radiation beams at the AVM to damage the blood vessels and cause scarring. Over the next several months, the irradiated vessels gradually degenerate and eventually close, leading to resolution of the AVM.

(Sen, 2021; NINDS, 2022c)

SUBARACHNOID HEMORRHAGE (SAH) TREATMENT

Treatments for SAH include surgical intervention with clipping or endovascular coiling. Subarachnoid hemorrhage has a poor prognosis due to the wide array of associated complications that can develop. Only about one third of patients with SAH have a “good” result after treatment (Pressman, 2021).

Delayed Cerebral Ischemia (DCI)

Delayed cerebral ischemia continues to be a major complication and source of morbidity following SAH. Current agreement is that the origin and development of DCI is a multifactorial and complex process that includes vasospasm, but also neuroinflammation as well as microthrombosis, disturbance in neuronal electrophysiology, and breakdown of the blood-brain barrier (Goursaud et al., 2021).

Induced hypertension has long been the choice of therapy for cerebral vasospasm and DCI, and was originally part of the triple-H therapy (hypertension, hypervolemia, and hemodilution). This therapy, however, has been found to lack a clinical effect on patient outcomes and remains controversial.

The only treatment shown to prevent DCI is the oral vasodilator nimodipine. This is the only FDA-approved drug shown to reduce ischemic neurologic deficit from DCI, and it is the only recommendation in current clinical guidelines. Even with nimodipine, however, DCI remains a common complication (Sadan & Akbik, 2022).

Hydrocephalus

Hydrocephalus can lead to cognitive decline and neurologic deterioration, even when the primary cause of SAH has been treated successfully. Hydrocephalus results from a blood clot from the SAH becoming lodged in one of the CSF drainage sites. CSF is produced in the ventricles of the brain and travels out through small openings know as foramina. If these openings are clogged, the CSF is still produced but has nowhere to go. This allows for pressure buildup that spreads to the brain and skull.

Acute hydrocephalus can be managed with a closed external ventricular drainage (EVD) system for a few days until the CSF dynamics stabilize. When the patient becomes continuously dependent on EVD, the decision to convert to a permanent CSF diversion is required, with a ventriculoperitoneal shunt as the first treatment of choice.

The prolonged use of an EVD may increase the risks of meningitis and/or ventriculitis, which can impact outcome, and also increases the risk of the patient becoming shunt-dependent (Bhattacharjee et al., 2021; Kuo & Huang, 2021).

SUPPORTIVE CARE

Supportive preventive measures should be taken for all patients, including:

• Keeping the head of the bed elevated >30 degrees
• Providing sedation for comfort
• Administering antipyretics for temperature >100.4 °F
  (Rordorf & McDonald, 2022)

Patients being treated for hemorrhagic stroke require:

• Constant hemodynamic monitoring in an ICU
• Frequent neurologic assessment
• Bed rest with sedation and head of bed elevated to 30 degrees; strict bed rest until etiology of hemorrhage is determined
• Cautious use of sedatives and analgesics due to potential to mask neurologic findings
• Pain control for headache
• Temperature control (elevated temperature can increase the degree of ischemic damage; maintain normal temperature using acetaminophen PO/PR; consider cooling devices)
• Maintaining hydration with intravenous IV normal saline
• Maintaining NPO status until swallowing function is evaluated
• Avoiding hypoglycemia
• Correcting hyperglycemia to 140–180 mg/dL
• Correcting metabolic acidosis
• Continuous ICP using direct measurement
• Hypertension treatment with IV medication
  (Rordorf & McDonald, 2022)