NURS 471 Week 8: Cerebral Vascular Disorder and Stroke

Stroke

is a time‑critical neuro emergency; you need rapid assessment plus evidence‑based reperfusion strategies for ischemic stroke, and a solid grasp of intracranial pressure (ICP) physiology and neuro infection/seizure presentations to guide timely interventions.

Stroke: Emergent Management

Goal: Apply evidence‑based practice (EBP) for emergent management of patients with ischemic stroke by integrating rapid assessment and intervention.

Ischemic stroke is caused by a blockage of blood flow to part of the brain, leading to tissue ischemia and potential infarction.

Emergent management focuses on rapid recognition, rapid assessment, and rapid reperfusion to limit brain damage (“time is brain”).

Use rapid stroke assessment tools and neuro checks to quickly identify symptoms and severity.

Integrate rapid interventions (e.g., activating stroke protocols, preparing for reperfusion therapies) to restore blood flow as soon as possible.

Intracranial Dysfunction and ICP Dynamics

Goal: Analyze normal and abnormal intracranial pressure (ICP) dynamics and relate these to patient outcomes.

Normal ICP is low and stable; abnormal ICP (intracranial hypertension) occurs when pressure inside the skull rises and cannot be compensated.

Increased ICP reduces cerebral perfusion, can cause brain herniation, and leads to poor neurologic outcomes or death if untreated.

Understand how changes in ICP (e.g., edema, bleeding) affect blood flow and oxygen delivery to the brain.

Link abnormal ICP to clinical deterioration (↓ LOC, neurologic deficits) and long‑term disability.

Meningitis vs Seizure Disorders

Goal: Differentiate clinical presentations of meningitis and seizure disorders to guide timely, appropriate interventions.

Meningitis: infection/inflammation of the meninges, commonly presenting with fever, severe headache, neck stiffness, and altered mental status.

Seizure disorders: abnormal electrical activity in the brain, presenting as episodic events (e.g., tonic‑clonic movements, staring spells, changes in awareness).

Why this matters for you:

-You must recognize when a patient’s symptoms suggest infection with possible increased ICP (meningitis) versus primary seizure activity.

-Correct differentiation guides your next steps (e.g., antibiotics and isolation vs seizure precautions and anticonvulsants).

Stroke Epidemiology: Burden and Disability

Leading cause of long‑term disability

Is a leading cause of serious long‑term disability in adults.

In the U.S., more than 7 million stroke survivors are living, and about two‑thirds are currently disabled.

Frequency and Mortality

Every 40 seconds, someone in the United States has a stroke, and every about 3-4 minutes someone dies of stroke.

Ischemic Stroke

Accounts for 87% of all strokes. Remaining percentage is hemorrhagic.

Caused by a blocked cerebral artery and reduced blood flow to brain tissue.

Thrombus or embolus occludes a vessel → decreased perfusion → infarct core and surrounding ischemic penumbra.

Clinical takeaway

-Because these strokes are the vast majority, most emergent stroke protocols and EBP strategies you apply will focus on this type of stroke.

-However, you must always rule out hemorrhage (e.g., via CT) before certain interventions (like thrombolytics), as treatment differs substantially.

Ischemic Stroke Subtypes

Thrombotic and Embolic

Thrombotic Stroke

Blood clot forms in an artery supplying the brain, usually on a vessel already narrowed by atherosclerotic plaque.

The clot gradually narrows then blocks the artery → decreased blood flow → ischemia/infarction.

Embolic Stroke

Clot or other debris forms elsewhere (often heart or large arteries) and travels (“emboli”) to the brain, lodging in a cerebral artery.

Suddenly blocks a previously normal or only mildly narrowed artery, causing abrupt onset of symptoms.

Debris travels and blocks the artery.

Hemorrhagic Stroke

A burst blood vessel allows blood to leak into or around brain tissue, increasing ICP and damaging brain cells until clotting stops the bleed.

Subtypes:

Intracerebral hemorrhage (ICH): bleeding directly into brain tissue.

Subarachnoid hemorrhage (SAH): bleeding into the subarachnoid space (often from ruptured aneurysm).

Transient Ischemic Attack (TIA)

Has stroke‑like symptoms caused by a brief blockage, but no permanent brain damage.

Is often called a “mini‑stroke” or “warning stroke”; it is managed as an emergency because you cannot tell it from a full stroke at onset.

= temporary interruption of blood flow, no infarct

Difference Between this and a Stroke:

stroke = prolonged interruption with infarct and persistent deficits.

Stroke Recognition: BEFAST

B – Balance: sudden loss of balance, dizziness, unsteady gait.

E – Eyes: sudden vision changes, blurred or loss of vision in one or both eyes.

F – Face: facial droop or uneven smile.

A – Arms: arm (or leg) weakness or drift on one side.

S – Speech: slurred speech, word‑finding difficulty, or confusion.

T – Time: time is brain → call 911 immediately; note time of symptom onset.

Initial Stroke Evaluation (ED/Code Stroke flow)

History and focused neuro exam

Rapid history: stroke risk factors, medications (especially anticoagulants), onset and progression of symptoms.

Neuro exam: assess level of consciousness, cranial nerves, motor/sensory deficits, speech, and coordination (often via NIHSS).

Last Known Well (LKW)

Document the last time the patient was seen at baseline; this determines eligibility for time‑dependent reperfusion therapies (e.g., thrombolytics).

NIHSS (National Institutes of Health Stroke Scale)

Standardized stroke scale to quantify neurologic deficit.

Higher score = worse stroke severity; lower score = milder deficits.

Diagnostics in Acute Stroke

Stat non‑contrast head CT

ECG (EKG)

Key labs: CBC, Glucose, Pt/PTT, Troponin

Assess for thrombolytic treatment

Stat non‑contrast head CT

Done immediately to rule out hemorrhage.

For thrombolytic treatment: CT negative (no bleed) supports ischemic stroke and potential eligibility for IV thrombolytic therapy.

ECG (EKG)

Looks for rhythm problems (e.g., atrial fibrillation) that can cause embolic stroke.

Glucose

rule out hypoglycemia/hyperglycemia as mimics and manage metabolic abnormalities.

CBC

evaluate hemoglobin, platelets.

PT/PTT (coagulation studies)

check clotting status and safety for thrombolytics.

Troponin

assess for concurrent cardiac ischemia or damage.

Assess for thrombolytic treatment

Use history, exam, imaging, and labs to decide whether the patient meets criteria and has no contraindications for IV thrombolytics (e.g., alteplase).

Pons and Medulla

are critical brainstem regions.

They regulate automatic functions such as breathing, heart rate, blood pressure, and aspects of temperature control.

Stroke or hemorrhage in these areas can be rapidly fatal or cause profound neurologic deficits.

Head CT (CAT scan)

midline shift

Midline shift on CT suggests significant mass effect from bleeding, tumor, or edema, indicating increased ICP and risk of herniation.

ePET Scan

Perfusion/metabolic imaging

In stroke imaging, color differences often represent tissue state:

Red area = infarcted (dead) tissue, not salvageable.

Green area = ischemic penumbra, still at risk but potentially salvageable with timely reperfusion.

IV Thrombolytic Inclusion Criteria (ischemic stroke)

Patients who should receive IV thrombolytic (facility protocol may vary):

Diagnosis of acute ischemic stroke with a measurable and disabling neurological deficit.

Last known well (LKW) time: able to initiate treatment within 4.5 hours of symptom onset (many textbooks emphasize the original 3‑hour window, but guidelines now commonly use up to 4.5 hours).

Age ≥ 18 years.

For mechanical thrombectomy, selected patients with large‑vessel occlusion may be treated up to about 24 hours from LKW if advanced imaging shows salvageable tissue (penumbra).

IV Thrombolytic Exclusion Criteria

Absolute/major exclusions (do NOT give thrombolytic):

Severe hypertension not controllable despite treatment: BP remains > 185/110 mmHg.

Significant head trauma, prior stroke, or intracranial/spinal surgery within the last 3 months.

Evidence of intracranial hemorrhage or subarachnoid hemorrhage on initial CT.

Known history of intracranial aneurysm, arteriovenous malformation (AVM), or brain neoplasm (especially those with higher bleeding risk).

Non‑compressible arterial puncture site (e.g., recent femoral arterial catheterization) that would be difficult to control if bleeding occurs.

Relative exclusions (risk–benefit decision):

Current anticoagulant use with elevated labs, such as INR > 1.7 or PT > 15 seconds.

Major surgery or significant trauma within the last 2 weeks.

GI or GU bleeding within the last 21 days.

Example "Code Stroke" process (TIME IS BRAIN)

Activation:

Dial 2299 and report: “Code Stroke,” room number, and location.

Emphasize time of symptom onset / last known well; “time is brain.”

Stroke team response (your facility example):

ICU Charge RN

ICU Resident

Respiratory Therapist (RT)

Hospitalist/Intensivist

Phlebotomist

Nursing Supervisor

Radiology Tech

Chaplain

Thrombolytic medication: Tenecteplase

Key points listed:

Tenecteplase is the primary thrombolytic your facility uses now.

It has replaced alteplase in many protocols because it is simpler and faster to administer (single bolus rather than bolus + 1‑hour infusion).

Nursing Actions During Code Stroke / Thrombolysis

Assessment & monitoring:

-Perform NIHSS to quantify stroke severity (higher score = worse; lower score = better).

-Place patient on continuous cardiac monitoring (ECG telemetry).

Obtain IV access (2 lines) for meds, fluids, and thrombolytic.

Blood pressure management:

-If thrombolytic candidate treat BP before & after thrombolytic

-Clinical caution: lower BP enough to meet targets, but avoid dropping too low, to preserve cerebral perfusion pressure.

Other key nursing measures:

-Keep patient normothermic (avoid fever); fever increases metabolic demand and free radical release, which can worsen brain injury.

-Maintain glucose 140–180 mg/dL (avoid hypoglycemia or severe hyperglycemia).

-Use actual weight to dose tenecteplase accurately.

-Keep patient NPO until a swallow screen is completed to prevent aspiration.

-Administer thrombolytic safely but quickly, following your facility protocol and double‑check processes.

Nursing BP Management During Code Stroke / Thrombolysis

If candidate for thrombolytic, treat BP before and after:

-Before thrombolytic: maintain BP < 185/110 mmHg to meet inclusion criteria.

-After thrombolytic: maintain BP ≤ 195/105 mmHg (your facility target; some guidelines use ≤ 180/105).

Recommended BP Medication During Code Stroke/Thrombolysis

Labetalol 10–20 mg IV over 1–2 minutes.

Clevidipine or nicardipine IV infusions, titrated to desired BP (both calcium channel blockers with vasodilating effects).

Tenecteplase

is the primary thrombolytic your facility uses now.

It has replaced alteplase in many protocols because it is simpler and faster to administer (single bolus rather than bolus + 1‑hour infusion).

Relationship to alteplase:

-is a genetically modified form of alteplase (rt‑PA) with a longer half‑life and higher fibrin specificity.

-Alteplase stroke dosing is more complex (0.9 mg/kg, IV bolus then 60‑minute infusion), so tenecteplase is often preferred for simplicity.

Tenecteplase Dose

0.25 mg/kg, maximum 25 mg.

Reconstitute to 5 mg/mL; push over about 5 seconds, then flush with 10 mL normal saline.

Risk: intracranial (brain) hemorrhage — monitor closely.

Post‑Thrombolytic Nursing Checklist

First 24 hours after IV thrombolytic (rt‑PA or tenecteplase):

No anticoagulants or antiplatelets for 24 hours (e.g., no heparin, warfarin, DOACs, aspirin) until follow‑up imaging confirms no bleed.

Avoid invasive procedures for 24 hours when possible:

-No nasogastric tube (NGT),

-Avoid blood draws from non‑compressible sites,

-Avoid new invasive lines or arterial punctures unless absolutely necessary.

Repeat head CT or MRI at 24 hours post‑thrombolytic to evaluate for hemorrhage and further ischemia.

Rehab consult (PT/OT/SLP) early to plan for recovery and long‑term function.

ICU admission for code stroke patients who receive thrombolytic, for close neuro and hemodynamic monitoring.

Worst thing that can happen (in the case of a Ischemic Stroke!)

Decreased level of consciousness (LOC) – patient becomes drowsy, difficult to arouse, or unresponsive.

New or worsening headache – often severe, can be described as “worst headache of life.”

Increased blood pressure – sudden, significant elevation (e.g., 200/100) can accompany bleeding or rising ICP.

Nausea and vomiting – especially sudden onset and repeated episodes, often linked to increased ICP or hemorrhage.

When these appear in an ischemic stroke patient (particularly post‑thrombolytic), think: possible brain bleed or rapidly worsening edema.

Immediate orders when you suspect hemorrhage

STAT non‑contrast head CT

Goal: quickly determine if intracranial or subarachnoid hemorrhage has occurred and assess for mass effect/midline shift.

STAT labs

PT, PTT, fibrinogen, type and crossmatch

These support decisions about reversing coagulopathy and preparing for potential blood product administration (e.g., FFP, cryoprecipitate, platelets).

“May have to reverse since they bled”

If imaging confirms hemorrhage and the patient received thrombolytic or is on anticoagulants, the team may initiate reversal strategies (per protocol and medication type).

Ongoing Inpatient Stroke Care Items

After the acute phase and once stabilized:

NIHSS by 2 RNs at any handoff

Dual scoring at handoff helps ensure consistency and catches subtle changes in neuro status.

Bedside swallow evaluation

Screen for dysphagia before PO intake to reduce aspiration risk.

VTE prophylaxis by day #2

Implement venous thromboembolism prophylaxis (mechanical and/or pharmacologic) by hospital day 2, unless contraindicated (e.g., hemorrhage).

Antithrombotic therapy by day #2 (ischemic stroke)

For ischemic strokes, start antiplatelet therapy (e.g., aspirin) by day 2, unless contraindicated.

Blood pressure management

Continue careful BP control tailored to stroke type and treatment received (ischemic vs hemorrhagic; thrombolytic vs thrombectomy).

Activity → OOB (out of bed)

Early mobilization as tolerated (with PT/OT guidance) to prevent deconditioning and complications.

Nursing interventions

Ongoing neuro checks, skin integrity, fall prevention, education, and psychosocial support.

Discharge checklist

Ensure medications, follow‑up appointments, risk factor modification (BP, diabetes, cholesterol, smoking), and rehab services are arranged before discharge.

Mobile Stroke Unit

is a specialized ambulance equipped with a CT scanner, telehealth capabilities, and stroke‑trained staff.

Purpose: bring the “hospital to the patient” – imaging, decision‑making, and even thrombolytic treatment can start in the field, shortening time to treatment.

In the San Francisco Bay Area, Sutter Health’s Mills‑Peninsula program operates a mobile stroke unit in partnership with local EMS.

Intracerebral Hemorrhage (ICH)

accounts for a substantial portion of hemorrhagic strokes 41% (often cited around 10–20% of all strokes overall).

Limited primary therapies; management focuses on preventing hematoma expansion, controlling BP, correcting coagulopathy, and managing ICP.

Intracerebral Hemorrhage (ICH): Common Complications

Increased intracranial pressure (ICP)

Cerebral hypoxia

Decreased cerebral blood flow

Risk of further bleeding

Hydrocephalus from blood blocking CSF pathways.

Subarachnoid Hemorrhage (SAH)

Common cause: rupture of an aneurysm or arteriovenous malformation (AVM).

Classic symptom: “worst headache of my life” → treat as emergency and get a CT scan immediately.

ICH and SAH: anticipated treatments

General approach (Code Stroke + hemorrhage‑focused care):

Activate Code Stroke.

Establish blood pressure goals:

You noted: ICH SBP 130–150 (modest reduction without losing CPP).

SAH SBP < 160 to reduce risk of rebleeding.

Reverse antiplatelet/anticoagulation as appropriate (e.g., platelets for antiplatelets, PCC/FFP/vitamin K for warfarin, specific reversal agents for DOACs).

ICP management (osmotic therapy, CSF drainage, head elevation, etc.).

Maintain normoglycemia – avoid significant hypo/hyperglycemia.

Use non‑sedating pain control as much as possible to preserve neuro exam quality.

Seizure precautions/management (pads, airway safety, anticonvulsants when indicated).

Transfer to facility with appropriate neuro capabilities (neurosurgery, neuro ICU) as needed.

Collaborative Care Post Stroke

Key interdisciplinary focus areas:

Ongoing neuro assessments (LOC, focal deficits).

Dysphagia screening and management.

Nutrition support and safe routes (PO/NG/PEG).

Comfort measures (pain, anxiety).

Communication strategies for receptive and expressive aphasia.

Engagement of PT/OT/Speech therapy.

Focus on rehab and recovery (functional goals).

Prevention of complications (aspiration, VTE, skin breakdown, depression).

Technology in Stroke Rehabilitation

Video games (e.g., Shark Showdown) – task‑oriented, engaging motor and cognitive rehab.

Virtual reality (VR) – immersive environments that encourage movement and cognitive tasks.

Motor therapy – repeatedly cueing movements (“move your left arm”) even when the limb cannot move, to reinforce brain‑body connection and motor pathways.

Mirror therapy – patient watches their intact limb move in a mirror, tricking the brain into perceiving movement on the affected side, promoting cortical reorganization.

Metabolic Activity and Autoregulation

The brain requires continuous oxygen and glucose for energy and metabolism; it cannot store them in meaningful amounts.

Autoregulation: the brain’s ability to maintain constant perfusion despite changes in systemic blood pressure.

-When BP is too low, cerebral vessels dilate to increase blood flow.

-When BP is too high, cerebral vessels constrict to protect the brain from hyperperfusion and edema.

Monro‑Kellie Hypothesis

Total intracranial volume (VIC) is the sum of brain tissue + blood + CSF in a closed, rigid system.

Compensatory mechanisms (shifting CSF, venous blood) allow small increases in one component without major ICP change.

Any significant disturbance (e.g., tumor, edema, large bleed) overwhelms compensation and raises ICP, compromising brain function.

Cerebral Perfusion Pressure (CPP)

CPP formula: CPP=MAP−ICP

Normal CPP range: approximately 60–80 mm Hg.

CPP < 40–50 mm Hg often leads to loss of autoregulation and cerebral hypoxia, causing decreased perfusion and ischemia.

Increased Intracranial Pressure (IICP)

is a higher than normal pressure within the cranial cavity.

Normal ICP: about 5–15 mm Hg in adults.ncbi.nlm.nih+1

ICP > 20 mm Hg sustained for 5–10 minutes is serious and associated with reduced CPP and risk of herniation.

Elevated ICP → decreased CPP, impaired autoregulation, and is a medical emergency.

Normal ICP

about 5–15 mm Hg in adults.

Increased Intracranial Pressure: Primary Causes

(intracranial):

brain tumor or space‑occupying lesion

spontaneous cerebral hemorrhage

trauma (TBI)

ischemic stroke with edema

hydrocephalus

post‑operative cerebral edema

meningitis.

Increased Intracranial Pressure: Secondary Causes

(systemic):

airway obstruction

hypoxia or hypercarbia from hypoventilation

hypertension/hypotension

hyperthermia

seizures, metabolic disorders (e.g., hyponatremia).

These secondary problems can increase ICP and further decrease perfusion, worsening brain injury.

Neurological Assessment: General Principles

Ongoing and accurate neuro assessment is one of the most important aspects of caring for neuro patients.

“Wax and wane” pattern: status may be good at one time and worse at another — frequent checks establish baseline and detect changes.

Hourly "Neuro Checks"

Vital signs.

Glasgow Coma Scale (GCS)

Glasgow Coma Scale (GCS)

Eye opening (spontaneous vs to stimulation).

Motor response (obeys commands vs abnormal posturing – decorticate/decerebrate).

Verbal response (oriented vs incomprehensible sounds).

On a ventilator, verbal score is 1.

Total score range: 3–15.

-13–15: mild/no brain injury.

-9–12: moderate injury.

-8 or less: severe injury.

Pain stimulation examples from lecture included sternal rub and nail-bed pressure to assess response.

Motor response should be assessed carefully for localization, withdrawal, abnormal flexion, abnormal extension, or no response.

Pupillary Function

Assess size, shape, and reaction to light:

Normal Neurological Pupil Index: 3-4.9mm

Small pupils: can be due to bright light, certain medications (e.g., glaucoma drops, opioids), or neurologic damage in the pons. <3 is concerning.

Dilated pupils: can reflect fear/anxiety or certain drugs (e.g., cocaine), but neurologically may indicate brainstem compression.

A markedly dilated, non‑reactive pupil (> 4 mm) is often called a “blown pupil”, suggesting serious brain herniation.

Pupillometer may be used for objective measurement.

Motor Assessment

Graded from best to worst movement:

Patient lifts and holds extremity against resistance.

Patient lifts and holds extremity against gravity.

Patient lifts extremity but it falls back.

Patient moves extremity but cannot overcome gravity.

Muscle shows only a trace of movement.

No movement.

Posturing (decorticate/decerebrate) indicates significant brain damage.

Cranial Nerve Assessment: Pupillary Response

CN II (optic) and CN III (oculomotor).

Cranial Nerve Assessment: Corneal Reflexes

CN V (trigeminal) and CN VII (facial).

Cranial Nerve Assessment: Hearing, Tinnitus, Dizziness

CN VIII (acoustic/vestibulocochlear).

Cranial Nerve Assessment: Cough and Gag

CN IX (glossopharyngeal) and CN X (vagus).

Brainstem Reflexes: Oculocephalic (doll’s eyes)

absent reflex usually indicates damage to pons and/or medulla.

Brainstem Reflexes: Oculovestibular (cold calorics)

absent reflex suggests lesion in pons or medulla.

Brainstem Reflexes: Cough and gag

absent responses indicate impaired brainstem function.

Intracranial Pressure Monitoring

device inserted into the cranial cavity that records pressure and is connected to a monitor that shows a picture of the pressure waveforms

EVD/Intraventricular Catheter and other Probes.

Can be linked to a waveform and drainage system.

EVD: System leveling/zeroing is done at the Tragus.

EVD (External Ventricular Drain)

“brain drain”

Used to monitor ICP and drain CSF to lower pressure.

You cannot simultaneously get accurate pressure readings and drain large volumes continuously; drainage patterns affect ICP readings.

Waveform monitoring helps interpret ICP trends.

ICP Waveform

produces three waves, numbered P1, P2, and P3; in cases of decreased intracranial compliance, the P2 wave is elevated above the P1 and P3 waves

P1 (percussion): Systolic peak pressure transmitted to CSF

P2 (rebound or tidal): Brain compliance

P3 (dicrotic): aortic valve closure

the waveform is interpreted similarly to other hemodynamic waveforms, but the system must never be flushed into the brain.

Indications for ICP Monitoring

Indications include:

Severe head injury with GCS 3-8

SAH

Hydrocephalus

Brain tumors

Stroke

Meningitis.

EVD drains CSF or blood to lower pressure and also allows ICP measurement.

Risks discussed include infection, misplacement, hemorrhage, clot obstruction, excess drainage, and dislodgment.

Nursing Responsibilities: External Ventricular Drain

Setup and calibration.

Record initial pressures and hourly pressures, waveforms, and neuro status.

Record hourly ICP, waveforms, MAP, CPP, and neuro status.

Maintain aseptic technique and dress insertion site.

Monitor for CSF leakage (e.g., halo sign – yellowish fluid forming a halo on dressing).

Watch for complications: infection, headache, hemorrhage during insertion/removal.

Lecture pearl: some systems cannot measure and drain at the exact same time; staff may have to switch modes intentionally.

Early Signs of Increased ICP

(often subtle):

Change in LOC – earliest and most sensitive sign.

N/V

Headache.

Motor changes (weakness, drift) on side opposite lesion.

Late Signs of Increased ICP

Pupil changes (fixed, dilated).

Profound shallow/irregular respirations.

Cushing’s triad (classic late sign):

Hypertension with widened pulse pressure.

Bradycardia.

Irregular or shallow respirations.

These are signs of impending herniation → require STAT CT and emergent interventions.

Cushing's triad

(classic late sign)

Hypertension with widened pulse pressure.

Bradycardia.

Irregular or shallow respirations.

Nursing Management of Elevated ICP

Focus areas:

Monitor:

Neuro status – frequent checks.

ICP monitoring – via EVD or other device.

Oxygenation/ventilation – avoid hypoxia and hypercarbia.

Maintain normothermia (avoid fever).

Interventions to reduce ICP:

-Head elevation (about 30°).

-Keep neck aligned, avoid flexion or rotation.

-Minimize environmental and procedural stimuli.

-Administer medications as ordered.

Ventilation Goal: Keep PaC02 at 35-40

Nursing Assessment for Increased ICP

The most important nursing priority is ongoing, accurate neurological assessment to establish baseline and detect change.

Neuro patients "wax and wane," meaning status can change quickly from one assessment to the next.

Medication Management of Elevated ICP

Hypertonic solutions (e.g., hypertonic saline): draw fluid out of brain tissue into vasculature, lowering ICP. Osmotic Diuretics: Mannitol, Hypertonic Saline.

Mannitol reduces cerebral edema but requires monitoring for hypotension/dehydration and renal effects; hypertonic saline requires sodium/fluid monitoring.

Steroids (for certain tumors) to reduce inflammation and edema around the lesion.

BP control: Labetalol, Nicardipine to lower BP and prevent further ICP rise — but avoid dropping BP too much, because that would reduce CPP and worsen ischemia.

Pain meds.

Sedation

PRIMARY CAUSES OF INCREASED ICP: MENINGITIS

Risk Factors:

Circumstances that promote exposure to infectious organisms (close living quarters, sharing drinks, etc.).

Presence of ear, sinus, or oral infections (otitis media, sinusitis, mastoiditis, dental infections) that can spread to meninges.

Neurologic injury, surgery, or invasive procedures that breach protective barriers (skull fractures, neurosurgery).

IV drug use – increases risk of bacteremia and CNS seeding.

Immunocompromise and alcohol misuse – impaired immune response (AIDS, diabetes, alcohol use disorder, steroids).

These factors make meningitis more likely and increase risk for severe disease and elevated ICP.

Meningitis Pathophysiology

Organisms gain access to the CNS via the bloodstream or by direct spread from adjacent structures (ear, sinus, skull).

Once in the CSF, infectious agents survive and flourish because immune defenses there are limited.

Inflammatory exudate extends throughout the CSF spaces and meninges.

ICP rises as exudate, edema, and altered CSF flow increase intracranial volume.

Brain edema progresses; cerebral autoregulation is impaired, and blood flow falls.

Septic shock may develop, further decreasing cerebral perfusion.

Patient can die from systemic complications (shock, multiorgan failure) or from diffuse CNS ischemic injury due to severe ICP and hypoperfusion.

Meningitis: Manifestations

Classic triad: headache, stiff neck, and fever.

Limb pain and cold hands and feet with mottled/pale skin – early septicemia signs.

Symptoms of meningeal irritation:

-Photophobia (light sensitivity).

-Positive Kernig/Brudzinski (depending on exam).

Seizures – can occur from cortical irritation or elevated ICP.

Symptoms of increased ICP:

Decreased LOC, vomiting, worsening headache, possible Cushing‑type changes.

These findings make meningitis a time‑sensitive emergency requiring rapid antibiotics and ICP‑conscious care.

Lecture story reinforced that agitation/altered behavior may be misread as intoxication or drugs when meningitis is actually present.

Meningitis: Treatment and Nursing Care

Lumbar puncture (LP)

Confirms meningitis via CSF analysis (cells, glucose, protein, culture).

Often done after CT in patients with suspected elevated ICP or focal deficits to reduce herniation risk.

Antibiotics

Broad‑spectrum IV antibiotics started as soon as meningitis is suspected, then tailored to culture results.

Droplet precautions

Maintain droplet isolation until 24 hours after appropriate IV antibiotics are given, then adjust based on organism and policy.

Comfort and fever management

Short‑acting analgesics (e.g., acetaminophen, opioids with caution) for severe headache.

Maintain normothermia (avoid hyperthermia that increases metabolic demand and ICP).

Nursing priorities: airway, breathing, circulation, neuro checks, ICP monitoring/precautions, early recognition of sepsis and shock.

Seizures: Basic Concept

Seizures occur when the electrical system of the brain malfunctions.

Brain cells fire repeatedly and haphazardly, producing abnormal synchronous activity.

Seizures: Clinical Features

-Change in LOC (confusion, unresponsiveness).

-Inability to speak or respond appropriately.

-Uncontrolled motor movements – tonic stiffening, clonic jerking, automatisms.

Different seizure types have different patterns, but your summary captures the general idea.

Important pearl: not all seizures are obvious generalized tonic-clonic events; some are subtle or nonconvulsive.

Eye deviation/twitching in a neuro ICU patient raised concern for seizure even without full-body movement.

Seizures: Treatment and Nursing Care

Protect airway and prevent aspiration

Turn patient to side, maintain open airway; suction when safe.

Protect from injury

Pad bed rails, clear environment, do not restrain or put objects in mouth.

Maintain airway and oxygenation

Provide supplemental oxygen; prepare for possible intubation in status epilepticus.

Medicate with anticonvulsants: lorazepam, phenytoin, or levetiracetam

Benzodiazepines for acute control; scheduled anti‑epileptic drugs to prevent recurrence, per provider orders.

Nursing goals: stop ongoing seizure activity, support ABCs, identify cause (e.g., meningitis, metabolic disturbance), and prevent complications (hypoxia, trauma).

Cerebel rapid EEG headband can help detect seizure activity, including nonconvulsive seizures, described as allowing non-experts to identify seizure patterns more effectively.

EEG and Seizure Monitoring

EEG (electroencephalogram) measures electrical brain activity and is used to:

-Confirm presence of seizures, including non‑convulsive events.

-Monitor seizure control after treatment, especially in status epilepticus.

“Cerebel → 2 hours and no artifact”

Conceptually: prolonged or high‑quality EEG recording without artifact helps accurately detect subtle seizure activity and confirms resolution after therapy.