17.1 Acute Ischemic Stroke & Intracranial Hemorrhage

Emergency Triage & The "Time Is Brain" Paradigm

Acute stroke is a hyperacute medical emergency wherein approximately 1.9 million neurons, 14 billion synapses, and 12 km (7.5 miles) of myelinated axonal fibers are destroyed each minute that a large vessel occlusion remains untreated. Rapid emergency triage and streamlined multidisciplinary protocols are critical to salvage the ischemic penumbra—the rim of structurally intact, hypoperfused neural tissue surrounding the irreversibly infarcted core.

Prehospital Stroke Screening Tools

Prehospital identification by emergency medical services (EMS) activates hospital "Code Stroke" teams prior to patient arrival, dramatically reducing door-to-needle (DTN) and door-to-puncture times.

• FAST Screen: Face drooping, Arm weakness, Speech difficulty, Time to call emergency services. Widely utilized, highly sensitive (~85%) for anterior circulation hemispheric strokes.
• BE-FAST Screen: Adds Balance (acute ataxia, gait unsteadiness) and Eyes (sudden loss of vision, diplopia, conjugate gaze deviation). Increases sensitivity for posterior circulation strokes (vertebrobasilar territory) from 85% to >95%.
• Cincinnati Prehospital Stroke Scale (CPSS): Evaluates 3 findings: facial droop (have patient smile/show teeth), motor arm drift (eyes closed, arms extended 10 seconds), and abnormal speech ("The sky is blue in Cincinnati"). If any 1 of the 3 parameters is abnormal, the probability of an acute ischemic stroke is 72%; if all 3 are present, the probability exceeds 85%.

American Heart Association / American Stroke Association (AHA/ASA) Target Metrics

Immediate Bedside Resuscitation & Triage Rules

1. Airway, Breathing, Circulation (ABCs): Support ventilation and oxygenation; administer supplemental oxygen only if oxygen saturation (SpO2) falls <94%. Hyperoxia induces reactive oxygen species and cerebral vasoconstriction.
2. Point-of-Care Capillary Blood Glucose (STAT): The single mandatory lab test that must not delay thrombolysis. Hypoglycemia (<50 mg/dL) is the most frequent stroke mimic and can produce focal hemiplegia, aphasia, and altered sensorium. If hypoglycemia is present, treat immediately with 25 to 50 mL of 50% dextrose (D50W) IV and reassess neurological status. Hyperglycemia (>180 mg/dL) also worsens ischemic neuronal injury and must be treated with subcutaneous or IV regular insulin.
3. Peripheral Venous Access & STAT Laboratory Panels: Place two large-bore peripheral IV lines (avoid central lines or arterial punctures that preclude thrombolytic administration). Draw CBC with platelets, PT/INR, aPTT, troponin, and type and screen. Crucial Rule: In patients without a known history of thrombocytopenia, hepatic failure, or anticoagulant therapy, intravenous thrombolysis must NOT be delayed while awaiting laboratory results.

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The National Institutes of Health Stroke Scale (NIHSS)

The NIHSS is a validated, 11-domain quantitative neurological scoring tool ranging from 0 to 42 points that objectively measures acute neurological deficit severity, monitors clinical trajectory, predicts vascular occlusion sites, and stratifies outcomes.

NIHSS Structural Components (11 Domains)

1. 1a. Level of Consciousness (LOC): 0 = Alert; 1 = Not alert, arousable by minor stimulation; 2 = Not alert, requires repeated/painful stimulation; 3 = Comatose/unresponsive. 1b. LOC Questions: Ask patient their current month and age (0 = Both correct; 1 = One correct; 2 = Neither correct). 1c. LOC Commands: Ask patient to open/close eyes and grip/release non-paretic hand (0 = Both correct; 1 = One correct; 2 = Neither correct).
2. Best Gaze: Horizontal eye movements (0 = Normal; 1 = Partial gaze palsy; 2 = Forced deviation or total gaze paresis).
3. Visual Fields: Confrontation testing in all 4 quadrants (0 = No visual loss; 1 = Partial hemianopia; 2 = Complete hemianopia; 3 = Bilateral hemianopia / cortical blindness).
4. Facial Palsy: Symmetry of smile, eyebrow elevation, and eye closure (0 = Normal; 1 = Minor asymmetry; 2 = Partial lower facial palsy; 3 = Complete unilateral facial paralysis).
5. Motor Arm (Left & Right tested separately): Limb held at 90° seated or 45° supine for 10 seconds (0 = No drift; 1 = Drift before 10s; 2 = Some effort against gravity; 3 = No effort against gravity; 4 = No movement; UN = Amputation/joint fusion).
6. Motor Leg (Left & Right tested separately): Limb held at 30° supine for 5 seconds (0 = No drift; 1 = Drift before 5s; 2 = Some effort against gravity; 3 = No effort against gravity; 4 = No movement).
7. Limb Ataxia: Finger-to-nose and heel-to-shin testing out of proportion to weakness (0 = Absent; 1 = Present in one limb; 2 = Present in two limbs).
8. Sensory: Pinprick response compared bilaterally (0 = Normal; 1 = Mild-to-moderate partial sensory loss; 2 = Severe/total sensory loss).
9. Best Language: Describe the Cookie Theft picture, name common objects, and read standard sentences (0 = No aphasia; 1 = Mild-to-moderate aphasia; 2 = Severe receptive/expressive aphasia; 3 = Mute / global aphasia).
10. Dysarthria: Articulation of words like "mama," "tip-top," "fifty-fifty," "baseball player" (0 = Normal; 1 = Mild-to-moderate slurring; 2 = Severe dysarthria / anarthria; UN = Intubated).
11. Extinction & Inattention (Neglect): Double simultaneous visual and cutaneous sensory stimulation (0 = No neglect; 1 = Visual, tactile, auditory, or spatial hemi-inattention; 2 = Profound hemi-inattention in >1 modality).

Clinical Interpretation & Large Vessel Occlusion (LVO) Correlation

• Score 0: Normal neurological examination.
• Score 1–4: Minor / mild stroke (often eligible for thrombolysis if deficits are functionally disabling, e.g., isolated hemianopia, aphasia, or distal hand weakness).
• Score 5–15: Moderate stroke.
• Score 16–20: Moderate-to-severe stroke.
• Score 21–42: Severe stroke (approaches >70% risk of severe disability or in-hospital mortality).
• High-Yield Exam Pearl: An NIHSS score ≥ 6 (or presence of cortical signs: gaze deviation, aphasia, hemineglect) strongly predicts an anterior circulation Large Vessel Occlusion (LVO) involving the internal carotid artery terminus or proximal middle cerebral artery (MCA M1 segment), mandating emergent vascular imaging for mechanical thrombectomy.

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Emergent Neuroimaging: Non-Contrast CT, CTA, and Perfusion Mismatch

Emergency neuroimaging must be initiated within 20 minutes of hospital arrival. The primary objective is to differentiate acute ischemic stroke from intracranial hemorrhage and identify large vessel occlusions amenable to catheter-directed intervention.

1. Non-Contrast Head CT (NCCT)

• Primary Role: The immediate gold standard to definitively exclude acute intracranial hemorrhage (ICH), which presents as bright, hyperdense parenchymal, intraventricular, or subarachnoid blood.
• Early Ischemic Changes (EIC): In acute infarction, cytotoxic edema causes water influx into neurons and glial cells, decreasing tissue X-ray attenuation (hypoattenuation):
  • Hyperdense Middle Cerebral Artery Sign: Increased radiodensity within the M1 segment of the MCA, reflecting acute intraluminal thromboembolism.
  • Insular Ribbon Sign: Loss of gray-white matter differentiation in the insular cortex.
  • Obscuration of the Lentiform Nucleus: Blurring of the putamen and globus pallidus borders.
  • Cortical Sulcal Effacement: Localized effacement of cortical sulci secondary to gyral swelling.
• Alberta Stroke Program Early CT Score (ASPECTS):
  • A 10-point topographic quantitative scoring system of the MCA territory on axial NCCT at two standardized levels (ganglionic and supraganglionic).
  • The territory is partitioned into 10 regions: Caudate, Lentiform, Internal capsule, Insular cortex, and 6 cortical MCA territories (M1 to M6).
  • 1 point is subtracted for each region demonstrating early ischemic hypoattenuation. A normal CT scores 10. An ASPECTS < 6 correlates with a large, established ischemic core (>70 mL), predicting poor functional recovery and a high risk of hemorrhagic transformation.

2. CT Angiography (CTA) of Head and Neck

• Performed immediately following NCCT (single-session multiphase CTA) from the aortic arch to the vertex of the skull.
• Rapidly identifies high-grade arterial stenosis, cervical dissection (intimal flap, flame-shaped occlusion), and anterior or posterior circulation Large Vessel Occlusions (carotid siphon/terminus, MCA M1/M2 bifurcation, basilar artery, vertebral arteries).

3. Advanced Perfusion Imaging (CT Perfusion & MRI DWI-PWI)

• Utilizes automated deconvolution software (e.g., RAPID) to quantitatively distinguish irreversibly dead brain tissue from salvageable penumbra:
  • Ischemic Core: Irreversibly infarcted tissue defined on CT Perfusion as cerebral blood flow (CBF < 30% of normal contralateral tissue) or on MRI as high-signal restricted diffusion on Diffusion-Weighted Imaging (DWI) with corresponding low Apparent Diffusion Coefficient (ADC).
  • Ischemic Penumbra: Hypoperfused tissue at risk of infarction defined as time-to-maximum (Tmax > 6 seconds).
  • Mismatch Volume & Ratio: Mismatch Volume = Volume(Tmax > 6s) - Volume(CBF < 30%). A mismatch ratio ≥ 1.8 and absolute mismatch volume ≥ 15 mL identifies patients who benefit dramatically from reperfusion therapy up to 24 hours after onset.

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Intravenous Thrombolytic Therapy (Alteplase & Tenecteplase)

Intravenous thrombolysis degrades fibrin within occlusive thrombi by converting plasminogen to active plasmin, re-establishing microvascular and macrovascular perfusion.

Pharmacological Regimens

1. Alteplase (Recombinant Tissue Plasminogen Activator, rtPA):
   • Dosing: 0.9 mg/kg IV (maximum cumulative dose 90 mg).
   • Administration Protocol: Infuse 10% of the total calculated dose as an intravenous bolus over 1 minute; infuse the remaining 90% continuously over 60 minutes via an infusion pump.
2. Tenecteplase (TNK-tPA):
   • Dosing: 0.25 mg/kg IV (maximum dose 25 mg), administered as a single intravenous bolus over 5 to 10 seconds.
   • Guideline Status: Now recognized as an evidence-based alternative to alteplase. Tenecteplase possesses higher fibrin specificity, an 80-fold resistance to plasminogen activator inhibitor-1 (PAI-1), and a longer elimination half-life. Single-bolus administration significantly accelerates workflow and facilitates inter-facility transfers for mechanical thrombectomy.

Therapeutic Eligibility Windows

• Standard Window (<3 Hours): Established by the landmark 1995 NINDS trial; demonstrated a >30% relative increase in patients achieving minimal or no disability (modified Rankin Scale 0–1) at 3 months.
• Extended Window (3 to 4.5 Hours): Established by the European ECASS-III trial; expands eligibility to select patients presenting between 3 and 4.5 hours from last known well.
• "Wake-Up Stroke" & Unknown Onset Time: In patients who awaken with stroke symptoms or have unwitnessed onset >4.5 hours from last known well, intravenous thrombolysis is indicated if an MRI demonstrates a DWI-FLAIR mismatch (positive restricted diffusion on DWI representing acute ischemia, with absence of parenchymal hyperintensity on FLAIR, proving that the stroke is <4.5 hours old; WAKE-UP trial).

Inclusion & Exclusion Criteria for Intravenous Thrombolysis

               INTRAVENOUS THROMBOLYSIS ELIGIBILITY SCREENING
               
    ┌────────────────────────────────────────────────────────────────────────┐
    │ CLINICAL INCLUSION CRITERIA:                                           │
    │ 1. Diagnosis of acute ischemic stroke causing measurable neurologic   │
    │    deficit (NIHSS ≥4 or disabling deficit)                             │
    │ 2. Time from Last Known Well <4.5 hours (or MRI DWI-FLAIR mismatch)   │
    │ 3. Age ≥18 years                                                       │
    └───────────────────────────────────┬────────────────────────────────────┘
                                        │
                                        ▼
    ┌────────────────────────────────────────────────────────────────────────┐
    │ ABSOLUTE CONTRAINDICATIONS (DO NOT ADMINISTER):                        │
    │ • Non-contrast CT demonstrates acute intracranial hemorrhage or        │
    │   frank hypodensity involving >1/3 of the MCA territory               │
    │ • Previous history of ANY intracranial hemorrhage (ICH, SAH, AVM)     │
    │ • Severe head trauma or acute ischemic stroke within preceding 3 MONTHS│
    │ • Intracranial or intraspinal surgery within preceding 3 MONTHS        │
    │ • Active internal bleeding (e.g., acute GI ulcer hemorrhage, hematuria)│
    │ • Suspected aortic arch dissection or infective endocarditis           │
    │ • Platelet count <100,000/µL                                           │
    │ • Coagulopathy: INR >1.7, PT >15 seconds, or aPTT >40 seconds          │
    │ • Therapeutic Direct Oral Anticoagulant (DOAC) ingestion within 48h    │
    │ • Blood pressure >185 mm Hg systolic or >110 mm Hg diastolic refractory│
    │   to emergency intravenous antihypertensive therapy                    │
    │ • Blood glucose <50 mg/dL (unless deficit persists post-correction)    │
    └───────────────────────────────────┬────────────────────────────────────┘
                                        │
                                        ▼
    ┌────────────────────────────────────────────────────────────────────────┐
    │ RELATIVE CONTRAINDICATIONS & EXTENDED 3–4.5h CAUTIONS (ECASS-III):     │
    │ • Age >80 years (guidelines permit treatment with shared decision)     │
    │ • Severe baseline stroke severity (NIHSS >25)                          │
    │ • Concomitant history of prior ischemic stroke AND diabetes mellitus   │
    │ • Current treatment with oral anticoagulants (regardless of INR)       │
    │ • Major surgery or serious non-head trauma within preceding 14 days    │
    │ • Gastrointestinal or urinary tract hemorrhage within prior 21 days    │
    │ • Arterial puncture at non-compressible site within prior 7 days       │
    └────────────────────────────────────────────────────────────────────────┘

Post-Thrombolysis Management & Critical Complications

• Monitoring: Frequent vital signs and neurological assessments (every 15 minutes for 2 hours, every 30 minutes for 6 hours, then hourly for 16 hours).
• Blood Pressure Target: Maintain BP <180/105 mm Hg continuously for at least 24 hours post-thrombolysis.
• Antithrombotic Hold: Withhold all antiplatelet agents (aspirin, clopidogrel) and parenteral/oral anticoagulants for 24 hours. Obtain a follow-up non-contrast head CT or MRI at 24 hours to rule out asymptomatic or symptomatic hemorrhage before initiating antiplatelet therapy.
• Emergency Management of Complications:
  1. Symptomatic Intracranial Hemorrhage (sICH): Occurs in ~6% of alteplase patients (NINDS). Suspect immediately if acute headache, acute hypertension, nausea/vomiting, or sudden drop in NIHSS score (≥ 2 points) occurs.
     • Protocol: Stop thrombolytic infusion immediately! Obtain STAT non-contrast head CT. Draw STAT type and screen, PT/INR, aPTT, fibrinogen, and platelets.
     • Medical Reversal: Administer Cryoprecipitate 10 units IV (infuse over 10–20 minutes; replenishes fibrinogen; target fibrinogen >150 mg/dL; repeat if necessary). Administer Tranexamic Acid (TXA) 1000 mg IV over 10 minutes (or aminocaproic acid 4–5 g IV). Consult neurosurgery emergently.
  2. Orolingual Angioedema: Occurs in 1–5% of patients due to bradykinin accumulation, especially those taking concurrent ACE inhibitors. Characterized by unilateral or bilateral tongue, lip, and oropharyngeal swelling.
     • Protocol: Stop thrombolysis infusion immediately. Administer IV Methylprednisolone 125 mg, IV Diphenhydramine 50 mg, and IV Famotidine 20 mg. For rapidly progressive airway compromise, administer subcutaneous/IM epinephrine 0.3 mg (0.3 mL of 1:1000) and prepare for emergent awake fiberoptic endotracheal intubation or surgical cricothyroidotomy.

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Endovascular Thrombectomy (EVT) for Large Vessel Occlusion

Mechanical thrombectomy utilizes intra-arterial microcatheters, stent retrievers (e.g., Solitaire, Trevo), and direct contact aspiration catheters to mechanically extract large occlusive emboli from proximal intracranial arteries.

Standard 0 to 6 Hour Window (HERMES Meta-Analysis)

Class I, Level A indication for patients meeting all of the following criteria:

1. Age ≥ 18 years;
2. Pre-stroke modified Rankin Scale (mRS) score 0 or 1 (functionally independent);
3. Causative occlusion of the Internal Carotid Artery (ICA) or proximal Middle Cerebral Artery M1 segment;
4. Baseline NIHSS score ≥ 6;
5. Initial ASPECTS score ≥ 6 on NCCT;
6. Treatment can be initiated (groin puncture) within 6 hours of symptom onset. Bridging Paradigm: Eligible patients presenting <4.5 hours should receive intravenous thrombolysis immediately; do not wait to observe the clinical effect of IV thrombolysis before transferring to the catheterization laboratory.

Extended 6 to 24 Hour Window (DAWN & DEFUSE 3 Trials)

Patients presenting between 6 and 24 hours from last known well (including wake-up strokes and unwitnessed onsets) who have an anterior circulation LVO qualify for EVT based on automated CT perfusion or diffusion MRI tissue mismatch criteria:

• DAWN Trial Criteria (Up to 24 Hours): Based on clinical-core mismatch:
  • Group A: Age ≥ 80 years, NIHSS ≥ 10, and ischemic core volume <21 mL.
  • Group B: Age <80 years, NIHSS ≥ 10, and ischemic core volume <31 mL.
  • Group C: Age <80 years, NIHSS ≥ 20, and ischemic core volume 31 to 51 mL.
  • Result: Number needed to treat (NNT) of 2.8 to achieve functional independence (mRS 0–2) at 90 days.
• DEFUSE 3 Trial Criteria (Up to 16 Hours): Based on perfusion-core mismatch:
  • Ischemic core volume <70 mL;
  • Mismatch ratio (penumbra volume / core volume) ≥ 1.8;
  • Absolute penumbral volume ≥ 15 mL.
  • Result: Significant reduction in 90-day mortality and functional disability (NNT = 2.0 for improved functional score).

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Hemodynamic & Blood Pressure Management in Acute Ischemic Stroke

Cerebral autoregulation is profoundly impaired in ischemic brain tissue. The cerebral perfusion pressure (CPP = MAP - ICP) within the ischemic penumbra depends linearly on systemic mean arterial pressure (MAP). Precipitous blood pressure drops collapse collateral leptomeningeal flow and convert salvageable penumbra into necrotic core.

Blood Pressure Algorithms in Acute Ischemic Stroke

               BLOOD PRESSURE TARGETS IN ACUTE ISCHEMIC STROKE
               
    ┌────────────────────────────────────────────────────────────────────────┐
    │ PATIENTS NOT RECEIVING REPERFUSION (NO THROMBOLYSIS OR EVT):           │
    │ • PERMISSIVE HYPERTENSION: Allow BP up to 220/120 mm Hg                │
    │ • Do NOT treat unless SBP >220 mm Hg or DBP >120 mm Hg                 │
    │ • If BP >220/120 mm Hg: Lower BP by a cautious 15% over the first 24h  │
    │ • EXCEPTION: Treat BP immediately if concurrent acute aortic           │
    │   dissection, acute MI, pulmonary edema, or hypertensive encephalopathy│
    └────────────────────────────────────────────────────────────────────────┘
                                        
    ┌────────────────────────────────────────────────────────────────────────┐
    │ PATIENTS CANDIDATES FOR IV THROMBOLYSIS OR EVT:                        │
    │ • BEFORE THROMBOLYSIS: BP must be lowered to <185/110 mm Hg            │
    │ • DURING & FOR 24 HOURS POST-THROMBOLYSIS: Maintain BP <180/105 mm Hg  │
    │ • POST-SUCCESSFUL EVT (TICI 2b/3): Target SBP <140–160 mm Hg to prevent│
    │   reperfusion injury and hyperperfusion syndrome                       │
    └────────────────────────────────────────────────────────────────────────┘

Preferred Intravenous Antihypertensive Pharmacotherapy

1. IV Labetalol:
   • Dose: 10 to 20 mg IV bolus over 1 to 2 minutes; may repeat once or double the dose every 10 minutes (e.g., 20 mg, 40 mg, 80 mg) up to a cumulative maximum dose of 300 mg.
   • Mechanism: Combined competitive antagonist at alpha-1 and beta-adrenergic receptors (beta-to-alpha ratio 7:1 IV), lowering systemic vascular resistance without inducing reflex tachycardia.
2. IV Nicardipine:
   • Dose: Continuous intravenous infusion initiated at 5 mg/hour; titrate upward by 2.5 mg/hour every 5 to 15 minutes until desired target is reached (maximum infusion rate 15 mg/hour). Once blood pressure stabilizes, down-titrate to 3 mg/hour.
   • Mechanism: Dihydropyridine L-type calcium channel blocker; selective arterial vasodilator with rapid titration kinetics.
3. IV Clevidipine:
   • Dose: Continuous infusion initiated at 1 to 2 mg/hour; double the dose every 90 seconds until blood pressure approaches target; titrate by smaller increments every 5 to 10 minutes (maximum dose 32 mg/hour).
   • Mechanism: Third-generation ultra-short-acting dihydropyridine CCB rapidly metabolized by blood and tissue esterases (t1/2 ≈ 1 minute), eliminating dependency on renal or hepatic clearance.

• STRICTLY CONTRAINDICATED: Sublingual or immediate-release oral nifedipine (causes erratic, uncontrollable precipitous hypotension, reflex sympathetic stimulation, and watershed cerebral infarction).

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Spontaneous Intracerebral Hemorrhage (ICH)

Spontaneous non-traumatic intracerebral hemorrhage accounts for 10% to 15% of all strokes and carries a 30-day mortality approaching 40% to 50%. Up to 35% of hematomas expand significantly within the first 6 hours, making hyperacute hemostatic and blood pressure stabilization vital.

Etiological Subtypes & Anatomical Distribution

1. Hypertensive Microangiopathy (Arteriolosclerosis, ~60–70% of ICH):
   • Longstanding systemic hypertension produces fibrinoid necrosis, lipohyalinosis, and microaneurysmal dilatation (Charcot-Bouchard microaneurysms) of small, deep penetrating parenchymal arteries (50–150 µm diameter).
   • Predilection Sites: Putamen and basal ganglia (50%), thalamus (15%), pons (10%), and deep cerebellar hemispheres (10%).
2. Cerebral Amyloid Angiopathy (CAA, ~20–30% of ICH):
   • Progressive deposition of beta-amyloid peptide (Aβ40) within the media and adventitia of small-to-medium cortical and leptomeningeal arteries, weakening vessel architecture.
   • Predilection Sites: Exclusively lobar cortical and subcortical regions (frontal, parietal, temporal, occipital lobes) in elderly individuals (>65 years); strictly spares the deep basal ganglia and brainstem.
   • High propensity for recurrent lobar hemorrhages and cognitive decline.
3. Secondary Etiologies: Arteriovenous malformations (AVMs), cavernous hemangiomas, dural arteriovenous fistulas, ruptured saccular aneurysms, hemorrhagic conversion of ischemic stroke, cerebral venous sinus thrombosis, intracranial neoplasms (choriocarcinoma, melanoma, renal cell carcinoma, glioblastoma), and sympathomimetic illicit drug toxicity (cocaine, methamphetamine).

Non-Contrast CT Findings in ICH

• Hyperdense Intraparenchymal Hematoma: Bright white parenchymal attenuation (60–80 Hounsfield Units) with distinct margins.
• Perihematomal Vasogenic Edema: Surrounding dark, hypodense rim reflecting secondary inflammatory capillary breakdown.
• Mass Effect: Compression of adjacent brain parenchyma, effacement of the ipsilateral lateral ventricle, and midline shift of the septum pellucidum across the falx cerebri.
• Intraventricular Extension (IVH): Blood breaking into the ventricular system; dramatically increases mortality and risks acute obstructive hydrocephalus requiring an external ventricular drain (EVD).
• The CT Angiography "Spot Sign": Multifocal foci of contrast enhancement within the hematoma during CTA; represents active extravasation and strongly predicts rapid hematoma expansion.

Acute Blood Pressure Control in Intracerebral Hemorrhage

Elevated systolic blood pressure drives active ongoing bleeding and hematoma expansion. However, excessive reduction risks renal injury and cerebral hypoperfusion.

• Guideline Blood Pressure Target: Rapidly lower systolic blood pressure to a target of 130 to 140 mm Hg within 1 to 2 hours of arrival.
• Landmark Clinical Trial Evidence:
  • INTERACT-2 Trial: Early intensive blood pressure lowering (target SBP <140 mm Hg within 1 hour) compared to standard lowering (<180 mm Hg) was safe, reduced hematoma growth, and showed significant improvements in functional recovery (better mRS scores).
  • ATACH-2 Trial: Compared target SBP 110–139 mm Hg against 140–179 mm Hg using IV nicardipine. Demonstrated that targeting SBP <120 mm Hg provided no additional clinical benefit and caused a significantly higher incidence of acute kidney injury and cardiac events.
  • Clinical Bottom Line: Target SBP 130–140 mm Hg with continuous IV nicardipine or clevidipine; strictly avoid dropping SBP <120 mm Hg.

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Emergency Anticoagulant Reversal Protocols in ICH

Patients taking therapeutic anticoagulants who suffer an ICH experience catastrophic hematoma enlargement. Coagulopathy reversal must be initiated immediately upon CT confirmation of hemorrhage.

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Management of Increased Intracranial Pressure (ICP) & Impending Herniation

Pathophysiology & Monro-Kellie Doctrine

The cranial vault is an inelastic, rigid box with a fixed total internal volume composed of three compartments: brain parenchyma (80%), cerebrospinal fluid (10%), and intravascular blood (10%). An acute pathological mass (e.g., intraparenchymal hematoma or massive hemispheric ischemic edema) initially triggers compensatory spatial displacement of CSF into the lumbar spinal subarachnoid space and venous blood into the jugular system. Once compensatory mechanisms are exhausted, intracranial pressure (ICP) rises exponentially.

• Normal ICP: 5 to 15 mm Hg.
• Pathological Intracranial Hypertension: ICP > 20 mm Hg.
• Cerebral Perfusion Pressure (CPP): CPP = MAP - ICP. Target CPP is 60 to 70 mm Hg. If ICP surges or MAP plunges, CPP drops below 50 mm Hg, inducing global secondary cerebral ischemia.
• Cushing's Triad (ominous sign of impending brainstem herniation): Severe hypertension with widened pulse pressure, bradycardia, and irregular respirations (Cheyne-Stokes or ataxic).

Stepwise Medical Management of Increased ICP

                      STEPWISE ICP MANAGEMENT CASCADE
                      
    ┌────────────────────────────────────────────────────────────────────────┐
    │ TIER 1: GENERAL PHYSIOLOGICAL & POSITIONING MEASURES                   │
    │ • Elevate Head of Bed to 30 DEGREES with neck in neutral midline       │
    │   position (unimpeded jugular venous return)                           │
    │ • Loosen endotracheal tube ties and cervical collars                   │
    │ • Aggressive Normothermia: Scheduled acetaminophen; target <37.5°C     │
    │ • Analgesia & Mild Sedation: IV fentanyl/propofol to prevent shivering,│
    │   coughing, and posturing spikes in ICP                                │
    │ • Avoid Hypotonic IV fluids (use ONLY isotonic 0.9% saline)            │
    └───────────────────────────────────┬────────────────────────────────────┘
                                        │
                                        ▼
    ┌────────────────────────────────────────────────────────────────────────┐
    │ TIER 2: OSMOTIC THERAPY (TARGET SERUM OSMOLALITY <320 mOsm/kg)         │
    │ • HYPERTONIC 3% SALINE: 250 mL IV bolus over 15–30 min, or continuous  │
    │   infusion targeting serum Na+ 145–155 mEq/L (expands intravascular    │
    │   volume; preferred in hemodynamically unstable patients)              │
    │ • 20% MANNITOL: 0.5 to 1.0 g/kg IV bolus over 20 min (causes osmotic   │
    │   diuresis; monitor volume status; contraindicated in hypotension)     │
    └───────────────────────────────────┬────────────────────────────────────┘
                                        │
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    ┌────────────────────────────────────────────────────────────────────────┐
    │ TIER 3: TEMPORIZING EMERGENCY RESCUE INTERVENTIONS                     │
    │ • BRIEF CONTROLLED HYPERVENTILATION: Target PaCO2 30–35 mm Hg          │
    │   - Induces cerebral vasoconstriction; decreases cerebral blood volume │
    │   - STRICT RULE: Use ONLY as a temporary rescue bridge (15–30 min)     │
    │     while mobilizing neurosurgery; prolonged hyperventilation causes   │
    │     severe rebound cerebral ischemia                                   │
    │ • High-Dose Barbiturates (Pentobarbital coma) for refractory ICP       │
    └───────────────────────────────────┬────────────────────────────────────┘
                                        │
                                        ▼
    ┌────────────────────────────────────────────────────────────────────────┐
    │ SURGICAL DECOMPRESSION (DEFINITIVE RESCUE):                            │
    │ • Cerebellar Hemorrhage (≥3 cm or brainstem compression/hydrocephalus): │
    │   EMERGENT Suboccipital Craniectomy & Hematoma Evacuation              │
    │ • Malignant MCA Infarction (age ≤60, large volume): Decompressive     │
    │   Hemicraniectomy within 48 hours (reduces mortality from 70% to 20%)  │
    └────────────────────────────────────────────────────────────────────────┘

• STRICT CONTRAINDICATION TO CORTICOSTEROIDS: High-dose dexamethasone or methylprednisolone is effective for vasogenic edema surrounding brain neoplasms and CNS infections, but is strictly contraindicated in acute ischemic stroke and intracerebral hemorrhage. Randomized trials demonstrate no reduction in ICP, no improvement in outcomes, and significantly higher rates of lethal infections, hyperglycemia, and mortality.