Cerebrovascular Accident	26

V. Dedeepiya Devaprasad and Nagarajan Ramakrishnan

A 60-year-old male with diabetes presented with weakness of the left arm and leg. He was conscious, alert, oriented and denied any headache or vomiting. Clinical examination suggested a left-sided hemiparesis.

Acute stroke (cerebral infarct or intracerebral hemorrhage) is the most frequent cause of admission in neurocritical care units. Time is brain in these situations, and prompt attention and intervention may salvage some patients from this catastrophic problem.

Step 1: Initiate resuscitation and exclude common stroke mimics such as hypoglycemia

•Initiate resuscitation as mentioned in Chap. 78.

•Intubation is done routinely when the Glasgow coma scale (GCS) is less than

or equal to 8, when there is insufficient ventilation (PO2 < 60 mmHg or PCO2 > 50 mmHg), obvious signs of pupillary asymmetry, and depressed consciousness that threatens the airway.

•The patient should be intubated after maximal preoxygenation and administration of drugs to avoid reflex arrhythmias, blood pressure derangements, and fluctuations in ICP (intracranial pressure).

Step 2: Perform urgent noncontrast CT scan of the brain

•CT scan can reveal either a normal study, a hyperdense lesion (white) suggestive of hemorrhage, or a hypodense lesion (black) suggestive of ischemia.

V.D. Devaprasad, M.D., I.D.C.C.M. (*)

Department of Critical Care Medicine, Apollo Hospitals, Chennai, India e-mail: [e-mail]

N. Ramakrishnan, A.B.(I.M.), F.A.C.P.

Department of Critical Care Medicine, Apollo Hospitals, Chennai, India

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,	213
DOI 10.1007/978-81-322-0535-7_26, © Springer India 2012

214	V.D. Devaprasad and N. Ramakrishnan

•Normal CT scan excludes intracerebral hemorrhage (ICH), but it is possible that the patient may have an ischemic stroke.

•MRI of the brain, especially with diffusion-weighted image/perfusion-weighted image (DWI/PWI) (bright lesion), may be a superior tool in identifying early ischemic stroke when a CT scan is reported as normal. In these patients, a diffu- sion–perfusion mismatch will help in identifying early ischemia.

•However, for all practical considerations including cost, easy availability, and time taken to perform the test, a non-contrast CT scan of the brain is preferable as the initial investigation in the management of stroke.

Step 3: Ascertain the duration of stroke

•It is sometimes difficult to determine the time when stroke occurred. Time of stroke onset is not the time when deficit was first noticed, but the time when the patient was last seen normal.

Management of Ischemic Stroke

Step 4: Urgently thrombolyze if indicated in ischemic stroke

•Restoration of perfusion is one of the most important measures to achieve in an ischemic stroke. This is usually accomplished by using thrombolytic agents.

•The National Institute of Neurological Disorders and Stroke (NINDS) study group trial showed that thrombolysis was safe and effective if performed within 3 h of stroke onset.

•There is increasing evidence that this time window may be extended to 4.5 h in selected patients (age less than 80 years, nondiabetics, no previous stroke).

•The only approved agent is recombinant tissue plasminogen activator (tPA) given at a dose of 0.9 mg/Kg up to a maximum of 90 mg (10% of dose given as a bolus over 1 min and the remainder infused over 1 h).

•Appropriate informed consent should be taken from the patient or surrogate.

•The most important considerations in the use of thrombolytic therapy are:

–Appropriate inclusion and exclusion criteria (Table 26.1).

–To get the exact time window of 3–4.5 hours from stroke onset

•Anticoagulant and antithrombotic agents, such as warfarin, heparin, or antiplatelet drugs, should not be administered for at least 24 h after the tPA infusion is completed.

•Invasive procedures, such as vascular puncture, urinary catheter placement, and nasogastric tube insertion, should be avoided for at least 24 h.

•Hemodynamic and close neurologic monitoring with half hourly GCS scoring should be charted.

•A follow-up noncontrast head CT scan should be obtained at 24 h particularly if treatment with antithrombotic agents, such as aspirin or heparin, is planned.

•Although thrombolysis has been shown to result in good functional outcome, it is still not widely used because of late presentation, fear of complications, and cost factors.

26 Cerebrovascular Accident	215

Table 26.1 Eligibility criteria for thrombolysis of acute stroke

Inclusion criteria

Clinical diagnosis of ischemic stroke

With measurable neurological deficit consistent with ischemic stroke

Within 3–4.5 h of onset of symptoms (if exact time of stroke onset is unclear, it is defined as the time when the patient was last noted to be normal)

Exclusion criteria

History

Stroke or head trauma within the prior 3 months Any prior history of intracranial hemorrhage Major surgery in the previous 14 days

Gastrointestinal or genitourinary bleeding within the previous 21 days Myocardial infarction (MI) within the prior 3 months

Arterial puncture at a noncompressible site within 7 days Lumbar puncture within 7 days

Clinical

Rapidly improving stroke symptoms

Only minor and isolated neurological signs

Seizure at the onset of stroke with postictal residual neurological impairments Symptoms suggestive of subarachnoid hemorrhage, even if the CT scan is normal Clinical presentation consistent with acute MI or post-MI pericarditis

Persistent SBP > 185 mmHg, DBP > 110 mmHg, or requiring aggressive therapy to control BP Pregnancy or lactation

Active bleeding or acute trauma (fracture) Laboratory

Platelets <100,000/mm3

Serum glucose <50 mg/dL (2.8 mmol/L) or >400 mg/dL (22.2 mmol/L)

International normalized ratio >1.7 if the patient is on warfarin and increased activated partial thromboplastin time if on heparin

Head CT scan

Evidence of hemorrhage

Evidence of early major infarct such as diffuse swelling of the affected hemisphere, parenchymal hypodensity, and/or effacement of >33% of the middle cerebral artery territory

•Consider intracerebral hemorrhage (ICH) to be the likely cause of neurological worsening after the use of a thrombolytic drug until a brain scan confirms or refutes hemorrhage.

•Immediately discontinue ongoing infusion of the thrombolytic drug if intracerebral bleed is suspected.

•Obtain emergent head CT scan.

•Obtain blood samples for type and crossmatch, prothrombin time, activated partial thromboplastin time (APTT), platelet count, and fibrinogen assay.

•If ICH is confirmed by imaging:

–Give 10 units of cryoprecipitate to increase the levels of fibrinogen and factor VIII.

–Give 6–8 units of random donor or equivalent single donor platelets.

216	V.D. Devaprasad and N. Ramakrishnan

–In patients receiving unfractionated heparin (UFH), consider giving 1 mg of protamine for every 100 units of UFH received in the preceding 4 h.

–Obtain neurosurgical consultation, and consider evacuation of the hematoma if feasible.

Step 5: Maintain hemodynamics

•In ischemic stroke, it is recommended that if the patient is to undergo thrombolysis, the patient’s blood pressure (BP) should be kept below 185/110 mmHg prior to thrombolysis and for 24 h after.

•If the patient is not eligible for thrombolysis, BP need not be treated unless it is more than 220/120 mmHg or the patient has heart failure, acute coronary syndrome, aortic dissection, or worsening renal function.

•The BP can be lowered by 15% during the first 24 h, ensuring that the patient is neurologically stable. A slower reduction to baseline may then be attempted over the next 7–10 days after stroke.

•Intravenous (IV) labetalol is the drug of choice, preferably by IV infusion.

•Initial bolus dose of 10 mg IV should be followed by infusion of 2–8 mg/min, or intermittent boluses of 10 mg every half an hour. Maximum daily dose of IV labetalol is 300 mg/day. Switch to oral labetalol once patient is stable.

•Monitor the heart rate and hold infusion if it is less than 60/min.

•Other agents that are recommended for treating hypertension in ischemic stroke are sodium nitroprusside, nicardipine, angiotensin-converting enzyme inhibitor, and hydralazine. Nitrates should be avoided because they tend to increase intracranial pressure (ICP) (refer to Chap. 24).

Step 6: Start antiplatelet therapy

•Because ICH is an anticipated side effect of thrombolysis, antiplatelets should not be initiated for 24 h until a repeat CT scan is performed to rule out significant bleed.

•If for any reason thrombolysis is not given, it is imperative to start antiplatelet therapy (aspirin, clopidogrel, aspirin in combination with extended release dipyridamole) without delay.

•In contrast to the patients with coronary artery disease where dual antiplatelet therapy is the rule, only a single antiplatelet therapy is recommended in patients with ischemic stroke.

•Aspirin is the preferred drug and is recommended to be initiated at a loading dose of 325 mg then 150–325 mg/day within 48 h of stroke onset. If the patient has documented aspirin allergy or has peptic ulcer disease, then clopidogrel 75 mg is recommended.

Step 7: Consider other adjunctive measures

•Anticoagulants are recommended in prophylactic doses in an attempt to prevent deep vein thrombosis after 24 h of stroke.

•Full-dose anticoagulation is not recommended even in patients with atrial fibrillation until about 3 weeks after a stroke because of the low risk of recurrent re-embolization.

26 Cerebrovascular Accident	217

•However, if the risk of re-embolization is high (e.g., mechanical valve prosthesis), full-dose anticoagulation may be initiated within a week.

•Other adjunctive treatment would include statins, for example, atorvastatin 40 mg/day or equivalent.

•There should be appropriate glycemic control, hypoglycemia should be avoided, and serum glucose level should be kept below 150 mg/dL.

•Treat fever aggressively.

•Maintain proper hydration and normovolemia particularly in patients on mannitol therapy.

Step 8: Anticipate complications in the first week of stroke

•If the patient has worsening sensorium, perform an urgent CT brain scan.

•Three common complications to watch for include infarct expansion, infarctrelated edema, and hemorrhagic transformation.

•Infarct expansion

–Infarct expansion can be suspected if there is worsening of sensorium or appearance of new neurological deficits.

–In such patients, hypertension should not be aggressively corrected; if necessary, antihypertensive drugs should be withheld.

–A cautious trial of induced hypertension may be tried. With an increase in mean arterial pressure (MAP), if the neurological deficits improve, it is reasonable to assume that it was due to infarct expansion, and in such patients an elevated MAP needs to be maintained.

•Infarct-related edema

–Infarct-related edema usually starts at day 2 of stroke and lasts until day 7, but may rarely persist until day 14.

–Pupillary asymmetry and deepening coma are clinical pointers to edema occurrence and worsening.

–It may lead to secondary infarction and loss of more brain tissue due to ischemia. It also leads to subfalcine herniation and tentorial herniation that can result in brain death.

–It is treated with bolus therapy of 10–20% mannitol (1 g/Kg IV) given over 10–20 min repeated as frequently as needed, or hypertonic saline, and head of bed elevation to 30°.

–Infarct-related edema can be prevented by avoiding hypoxemia, hypoventilation, hypovolemia, hypotonic solution, dehydration, seizures, and fluctuations in serum glucose levels.

–Fever should be suppressed by physical (surface cooling) or chemical methods (antipyretic drugs) because it can also lead to infarct-related edema.

•Hemorrhagic transformation

–Hemorrhagic transformation is suspected clinically by a decrease in sensorium and confirmed by a CT scan.

–It should be managed by withholding antiplatelets and anticoagulants.

218	V.D. Devaprasad and N. Ramakrishnan

Step 9: Consider investigating the risk factor for stroke

–Lipid profile.

–Echocardiogram—for cardioembolic source.

–Carotid Doppler study—for critical carotid stenosis.

–HbA1c—for glycemic control.

–Holter monitoring to detect paroxysmal atrial fibrillation.

–In a young stroke patient, vasculitis profile and thrombophilia profile should be performed.

A 60-year-old hypertensive male was admitted with sudden-onset slurring of speech, vomiting, headache, and rapidly progressive drowsiness. His blood pressure was measured as 190/100 mmHg. An urgent noncontrast CT brain scan suggested the occurrence of a hemorrhagic stroke.

Step 1: Maintain airway

As mentioned above in Step 1.

Step 2: Reduce BP judiciously

•Current guidelines for managing BP in spontaneous ICH

–If systolic blood pressure (SBP) is 200 mmHg or MAP (SBP + 2 × DBP)/3 is 150 mmHg, then consider aggressive reduction of BP with continuous IV infusion and frequent BP monitoring.

–If SBP is 180 mmHg or MAP is 130 mmHg and there is a possibility of elevated ICP, then consider reducing BP using intermittent or continuous IV medications.

–If SBP is 180 mmHg or MAP is 130 mmHg and there is no evidence of elevated ICP, then consider a modest reduction of BP (e.g., MAP of 110 mmHg or target BP of 160/90 mmHg) using intermittent or continuous IV medications to control BP and examine the patient frequently.

–IV labetalol is the drug of choice, preferably by IV infusion.

–Initial bolus dose of 10 mg IV followed by infusion of 2–8 mg/min, or intermittent boluses of 10 mg every half an hour. Maximum daily dose of IV labetalol is 300 mg/day.

–Monitor heart rate, and hold infusion if it is less than 60/min.

–Other agents that are recommended for treating hypertension in hemorrhagic stroke are nicardipine, angiotensin-converting enzyme inhibitor, and hydralazine. Nitrates should be avoided because they tend to increase ICP (refer to Chap. 24).

•Addressing pain may also help to reduce hypertension.

26 Cerebrovascular Accident	219

Step 3: Consider management of raised ICP

•Raised ICP is expected to follow ICH and is defined as ICP ³20 mmHg for >3 min, with the therapeutic goal being decrease of ICP to <20 mmHg or maintaining the cerebral perfusion pressure between 50 and 70 mmHg.

•Generally, it is recommended that a patient with GCS £8 or with rapidly deteriorating GCS that is attributable to raised ICP or features of transtentorial herniation may benefit from an ICP monitor.

•Patients with intraventricular hemorrhage and hydrocephalus may also benefit from ICP measurement.

•This is not usually done in many centers for fear of infection risk and lack of outcome studies showing reduction in mortality (see Chap. 31).

•Raised ICP is treated with bolus therapy of 20% mannitol (1mg/kg) IV given over 10–20 minutes repeated as frequently as needed or hypertonic saline and head of bed elevation to 30°.

Step 4: Cautious use of fresh frozen plasma (FFP), platelet transfusion, or aFVII (activated factor VII)

•Current recommendations are against the use of aFVII in unselected patients.

•This can be considered for patients who are coagulopathic and require urgent surgical evacuation and at risk for volume overload with FFP infusion and do not have the potential for thrombogenic complication such as active coronary artery disease.

•The usefulness of platelet transfusion in patients who have received antiplatelets earlier is investigational and unclear.

•However, if the patient has severe thrombocytopenia, they should receive platelet transfusion.

•Routine use of FFP is not recommended.

•However, if the patient has severe coagulation abnormalities or has been on oral anticoagulants, FFP should be administered.

•In addition to FFP, patients on oral anticoagulation should also receive vitamin K and have further doses of oral anticoagulation withheld.

•In patients with urgent need for anticoagulation (such as mechanical valve prosthesis), continuous infusion of UFH with APTT monitoring with lower than the usual therapeutic goal may be instituted.

•It is preferable to use unfractionated heparin because it can be easily reversed.

Step 5: Selected use of antiepileptics

•There is no role for prophylactic anticonvulsants, and hence they should not be used.

•In selected cases of lobar hemorrhage, they can be used for 1 month.

•However, if the patient has clinical seizures, they should receive antiepileptics.

•If the patient has deterioration in mental status, that is, out of proportion to the degree of brain injury, a continuous electroencephalogram (EEG) monitor is indicated to exclude non-convulsive seizures, and should these patients have any evidence of seizures on EEG, they should receive anticonvulsants.

•In the absence of continuous EEG monitoring, introduction of antiepileptics in the presence of disproportionate mental status changes may be considered with closed neurological monitoring.