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NEUROLOGICAL ASSESSMENT & FUNCTIONAL ANATOMY
Neurological Assessment
Neurological assessment identifies deficits, recognizes deterioration, and helps determine the underlying neurological problem.
Interpret neurological findings together rather than as isolated abnormalities.
New neurological deficits require:
Focused assessment.
Assessment for associated symptoms.
Timely reporting to the provider.
CLINICAL GEM: The location and pattern of neurological deficits can help identify the affected area of the brain.
Cerebral motor deficits commonly occur contralateral to the affected brain hemisphere.
Right cerebral injury → left-sided motor deficits.
Left cerebral injury → right-sided motor deficits.
Frontal Lobe
Functions include:
Personality.
Motor function.
Motor speech.
Judgment.
Injury may cause:
Emotional instability.
Agitation.
Restlessness.
Impaired judgment.
Personality or behavioral changes.
Behavioral and judgment changes can create significant safety concerns and may persist after acute stabilization.
Occipital Lobe
Primarily associated with vision.
Injury may cause:
Blurred vision.
Visual disturbances.
Abnormal colors.
Spots within the visual field.
Brainstem
Controls essential functions including:
Respirations.
Heart rate.
Severe increased ICP can compress the brainstem and compromise respiratory and cardiovascular function.
Hypothalamus & Pituitary
Compression may interfere with:
Temperature regulation.
Fluid regulation.
Electrolyte regulation.
Endocrine function.
Monitor for:
SIADH.
Diabetes insipidus.
Ventricles & CSF
The ventricular system contains and circulates CSF.
The brain contains four ventricles, including two lateral ventricles.
Clinical significance:
Ventricles can become compressed by increasing ICP.
Ventricles can be accessed for direct ICP monitoring.
CSF can be drained through a ventriculostomy.
TRAP: Detailed ventricular anatomy is not an exam focus.
KEY TAKEAWAYS
Neurological findings should be interpreted as a complete pattern rather than isolated abnormalities.
Cerebral motor deficits commonly occur contralateral to the affected brain hemisphere.
Frontal-lobe injury can cause behavioral, personality, judgment, and safety problems.
Occipital-lobe injury commonly produces visual disturbances.
Brainstem compression threatens respiratory and cardiovascular function.
Pituitary and hypothalamic compression can disrupt temperature, fluid, electrolyte, and endocrine regulation.
Detailed ventricular anatomy is not an exam focus.
INTRACRANIAL REGULATION & INCREASED INTRACRANIAL PRESSURE
Primary vs. Secondary Brain Injury
Primary injury
Direct injury caused by the original trauma or neurological insult.
Secondary injury
Additional damage developing as a consequence of the primary injury.
May include:
Cerebral edema.
Increased ICP.
Decreased cerebral perfusion.
Ischemia.
Additional neurological deficits.
Preventing and treating secondary brain injury is a major neurological-management goal.
Injury → inflammation → tissue swelling/fluid shifts → compression → decreased cerebral blood flow → ischemia → tissue death → possible herniation.
Intracranial Pressure
Normal ICP: 5–15 mm Hg.
Sustained ICP ≥20 mm Hg → clinically significant increased ICP with risk for:
Neurological deterioration.
Coma.
Death.
Trend ICP and neurological findings rather than relying on a single measurement.
Monro-Kellie Doctrine
The closed skull contains:
Brain tissue.
Blood.
CSF.
Increasing one component requires compensation by the others to prevent ICP from rising.
When compensation is exhausted:
ICP rises.
Cerebral vessels and brain tissue become compressed.
The doctrine assumes a closed skull.
It does not apply in the same manner with an open skull fracture.
TRAP: Focus on understanding the pressure-volume relationship rather than memorizing a formal definition.
Cerebral Blood Flow & Autoregulation
Normal cerebral blood flow: approximately 50 mL/min/100 g brain tissue.
Brain tissue requires continuous:
Oxygen.
Glucose.
Autoregulation adjusts vascular resistance to maintain cerebral blood flow.
Increased cerebral vascular resistance → vasoconstriction → decreased cerebral blood flow.
Cerebral blood flow is affected by:
CO₂.
O₂.
Hydrogen ion concentration.
Increased PaCO₂ causes cerebral vasodilation in a normally autoregulating brain.
Severe neurological injury may cause loss of autoregulation.
MAP & CPP
MAP = [SBP + 2(DBP)] ÷ 3
CPP = MAP − ICP
Normal CPP: 60–100 mm Hg.
Maintain CPP >60 mm Hg during ICP management.
Neurological patients require MAP approximately ≥70 mm Hg in this lecture framework.
MAP >150 mm Hg was identified as undesirable.
CLINICAL GEM: Increasing ICP can reduce CPP even when systemic blood pressure initially appears adequate.
Progression of Increased ICP
Neurological insult → cerebral edema → increased ICP.
Increased ICP compresses ventricles and cerebral vessels.
Cerebral blood flow decreases.
Brain oxygen delivery decreases.
Ischemia and brain-cell death occur.
Necrotic tissue produces additional edema.
Compression worsens.
Brainstem/respiratory centers become compromised.
CO₂ accumulates.
Acidosis develops.
Aututoregulation fails.
Herniation and death may occur.
Time is tissue.
Brain Herniation
Severe ICP can displace brain tissue downward.
Brainstem displacement through the tentorial opening is an ominous progression.
Herniation represents catastrophic neurological deterioration.
Cerebral Edema
Cerebral edema increases intracranial volume and ICP.
Vasogenic edema
Fluid moves from the vascular compartment into surrounding brain tissue.
Cytotoxic edema
Associated with cellular injury from cerebral hypoxia/anoxia.
Interstitial edema
Fluid accumulates within brain tissue and contributes to compression and tissue destruction.
Treatment focuses on:
Decreasing cerebral edema.
Moving excess fluid out of brain tissue.
Preserving cerebral perfusion.
Level of Consciousness
Change in LOC is one of the most sensitive and reliable manifestations of neurological deterioration.
LOC changes may be:
Gradual.
Sudden.
Neurological status should be assessed routinely and more frequently when deterioration is suspected.
Even subtle LOC or behavioral changes require attention.
Nursing staff, including the nurse or CNA, may be the first to recognize a subtle change.
CLINICAL GEM: The significance is the change from baseline, even when the abnormality initially appears subtle.
CLINICAL GEM: An initially negative CT does not eliminate the need for continued neurological assessment after head trauma.
A later LOC change may indicate evolving bleeding or secondary brain injury.
Glasgow Coma Scale
Evaluates:
Eye opening.
Verbal response.
Motor response.
Highest GCS: 15.
Lowest GCS: 3.
GCS ≤8 → anticipate airway protection/intubation.
Use GCS to objectively trend neurological status rather than relying only on orientation.
TRAP: Score the patient's actual response rather than a general impression of neurological status.
CLINICAL GEM: A substantial decline in GCS represents neurological deterioration even when individual component scoring is debated.
Cushing’s Triad
Cushing’s triad is a medical emergency associated with severe increased ICP.
Components:
Systolic hypertension with widening pulse pressure.
Bradycardia with a bounding pulse.
Irregular respirations.
Respiratory patterns may become increasingly irregular or paradoxical with severe deterioration/herniation.
Normal pulse pressure is approximately 40 mm Hg.
Approximately 30/35–45/50 mm Hg was discussed as the usual pulse-pressure range.
Pulse pressure ≥60 mm Hg is widened.
CLINICAL GEM: Declining LOC + new unequal pupils + rising systolic BP/widening pulse pressure + bradycardia + respiratory changes → severe increased ICP with impending neurological deterioration.
Temperature changes may occur with hypothalamic compression.
Major temperature-regulation changes in this setting indicate significant intracranial compression.
Pupillary Changes
CN III compression can alter pupillary response.
Unilateral pupillary changes associated with intracranial compression occur ipsilateral to the affected side in this lecture framework.
Bilaterally fixed and dilated pupils are an ominous finding associated with herniation.
Pinpoint pupils may indicate:
Pontine injury.
Drug effects.
Trend:
Pupil size.
Equality.
Reactivity.
Motor Changes
Increased ICP may produce:
Contralateral hemiparesis.
Contralateral hemiplegia.
Localized abnormal motor responses.
Bilateral posturing with severe injury.
Decorticate and decerebrate posturing
Abnormal neurological motor responses.
Opisthotonic posturing
Severe arching of the body.
May occur with severe neurological injury or neurotoxicity.
Ominous neurological finding.
Headache & Vomiting
Headache may accompany increased ICP.
TRAP: Headache alone does not establish increased ICP.
Interpret headache with:
Mechanism.
LOC.
Neurological findings.
Vital-sign trends.
Increased ICP may cause vomiting that is:
Sudden.
Unexpected.
Projectile.
Not preceded by nausea.
Neurological Diagnostics
CT
Rapidly evaluates intracranial structures and bleeding.
MRI
Provides more sensitive neurological imaging.
Less rapid than CT for emergency evaluation.
Angiography
Evaluates cerebral vasculature.
Transcranial Doppler
Evaluates cerebral blood flow and vasculature.
Infrascanner
May help identify cerebral hemorrhage contributing to compression.
Diagnostic planning must account for the entire patient.
CLINICAL GEM: Significant renal disease is important when contrast-based studies are considered.
Lumbar Puncture
May obtain CSF when an infectious neurological cause is suspected.
Assess:
Coagulation status.
Anticoagulant therapy.
Bleeding risk.
After LP:
Monitor the puncture site for bleeding.
Monitor for severe headache.
Keep the patient flat for approximately 30–60 minutes in this lecture framework.
Severe post-LP headache may require a blood patch.
Laboratory Assessment
May include:
CBC.
Chemistry panel.
Coagulation studies.
Electrolytes.
Ammonia.
Toxicology screening.
Electrolytes become particularly important when pituitary/hypothalamic compression affects fluid regulation.
Toxic substances may:
Mimic neurological abnormalities.
Mask neurological deterioration.
Complicate assessment.
Direct ICP Monitoring
Direct monitoring guides ongoing management.
Continue trending:
GCS.
Neurological status.
Vital signs.
Hemodynamics.
Oxygenation.
Critically ill patients may require:
Arterial line.
Central venous access.
ScvO₂ monitoring.
Cardiac-output monitoring.
Ventriculostomy
Ventriculostomy is the gold standard for ICP monitoring.
A catheter is inserted into a lateral ventricle and connected to a transducer.
Functions:
Measures ICP.
Allows CSF drainage.
Positioning
HOB approximately 30°.
Maintain neutral head/neck and body alignment.
Avoid neck flexion.
Proper positioning promotes cerebral venous drainage.
When ICP trends upward, assess the patient first.
Assess neurological status.
Check head/neck and body alignment.
Assess vital-sign trends.
Identify excessive stimulation.
ICP Management Targets
ICP: 5–15 mm Hg.
CPP: >60 mm Hg.
PaO₂: ≥100 mm Hg.
Systolic BP: 100–160 mm Hg.
Maintain adequate fluid balance.
Monitor for widening pulse pressure.
Maintain normothermia.
Slightly cooler temperatures may reduce cerebral metabolic demand.
Cerebral Oxygenation Monitoring
Licox
Measures brain-tissue oxygen pressure.
Target: 20–40 mm Hg.
SjvO₂
Reflects cerebral oxygen delivery/utilization.
Normal: 60–75%.
CSF Drainage
Ventriculostomy drainage may be:
Continuous.
Intermittent.
Drainage parameters are provider-prescribed.
Remove CSF slowly to reduce risk of ventricular collapse.
Monitor for:
Infection.
Herniation.
Neurological deterioration.
Maintain a closed drainage system.
Reducing Cerebral Metabolic Demand
Increased cerebral metabolism increases requirements for:
Oxygen.
Glucose.
Reduce:
Fever.
Agitation.
Excessive environmental stimulation.
Unnecessary movement.
Excessive visitors.
Sedation or paralysis may be required.
TRAP: Sedation and paralysis can mask clinical manifestations of neurological deterioration.
Direct ICP monitoring provides objective pressure information when the neurological examination is limited.
Mannitol (Osmitrol)
Osmotic diuretic.
Presented as the primary/gold-standard osmotic diuretic used to reduce cerebral edema in this lecture.
Pulls water from swollen brain tissue into the vascular compartment.
Fluid is then excreted through the kidneys.
Effective therapy requires adequate renal function.
Hypertonic Saline
Pulls water out of cells into the vascular compartment.
May be used with mannitol to decrease cerebral edema.
Monitor:
Electrolytes.
Fluid status.
Strict I&O.
Prescribed fluid restrictions.
Blood pressure.
Fluid removal must be balanced against maintaining adequate BP and CPP.
Corticosteroids
Dexamethasone may be considered for selected inflammatory causes of cerebral edema.
Whether corticosteroids are started depends on the clinical situation and provider treatment plan.
If used, therapy was discussed as generally beginning within the first 24 hours.
Monitor for:
Hyperglycemia.
Infection.
Peptic ulcer disease.
Protonix may be used for GI prophylaxis.
Prolonged acid suppression may contribute to:
Superinfection.
Diarrhea.
Antiseizure Therapy
Examples:
Phenytoin (Dilantin).
Phenobarbital.
Levetiracetam (Keppra).
Increased ICP places patients at heightened seizure risk.
During a seizure:
Protect the airway.
Protect the head and bony prominences.
Keep suction available.
Time the seizure.
Recurrent seizures → increased ICP → decreased cerebral blood flow/perfusion.
Fever Control
Fever increases cerebral metabolic demand.
Increased metabolic demand can worsen ICP.
Fever control is part of ICP management.
Nutrition
Begin nutritional support approximately 24–48 hours after injury.
Early feeding reduces catabolism associated with high metabolic demand.
Routes may include:
NG.
OG.
TPN.
NG/OG placement may be contraindicated with facial/skull trauma.
Monitor:
I&O.
Weight.
Protein/nutritional status.
Albumin.
Glucose.
Insulin requirements with TPN.
Infection.
Bowel sounds/gut motility.
IV Fluids
Normal saline is commonly used unless another solution is indicated.
NEVER DO: Avoid hypotonic solutions such as 0.45% saline during increased ICP because they promote fluid movement into tissue.
Lactated Ringer's was discussed as:
Closer to serum composition.
Potentially less acidifying than large amounts of normal saline.
Respiratory & Hemodynamic Support
Severe neurological injury may require:
Mechanical ventilation.
Oxygen therapy.
ABG monitoring.
Acid-base management.
Hemodynamic instability may require:
Fluid resuscitation.
Pressors.
Inotropes.
Fluid removal depending on condition.
Sedation & Analgesia
Examples:
Midazolam (Versed).
Fentanyl.
Propofol.
Dexmedetomidine (Precedex).
Sedation decreases:
Agitation.
Stimulation.
Metabolic demand.
Precedex was discussed as useful during ICP management.
Monitor Precedex for:
Hypotension.
Bradycardia.
TRAP: Medication-related hemodynamic changes must be distinguished from neurological deterioration.
Fluid & Endocrine Monitoring
Maintain strict I&O.
A urinary catheter may be required.
Urine output may be measured hourly.
Monitor pituitary/hypothalamic involvement for:
SIADH.
Diabetes insipidus.
Safety
Maintain seizure precautions.
Protect confused, agitated, or restless patients from injury.
Restraints may sometimes be required for safety.
During acute ICP management, restraints may increase agitation and ICP.
Sedation may be preferred when clinically appropriate.
KEY TAKEAWAYS
Normal ICP is 5–15 mm Hg; sustained ICP at or above 20 mm Hg indicates clinically significant increased ICP.
CPP = MAP − ICP.
MAP = [SBP + 2(DBP)] ÷ 3.
Normal CPP is 60–100 mm Hg, with a treatment target above 60 mm Hg.
Secondary brain injury is a major target of neurological treatment.
Change in LOC is one of the most sensitive and reliable indicators of neurological deterioration.
GCS ranges from 3–15; GCS at or below 8 requires anticipation of airway protection.
Cushing’s triad is systolic hypertension with widened pulse pressure, bradycardia, and irregular respirations.
Normal pulse pressure is approximately 40 mm Hg; pulse pressure at or above 60 mm Hg is widened.
Unilateral pupillary changes from compression occur ipsilateral to the affected side in the lecture framework.
Bilaterally fixed and dilated pupils are an ominous finding associated with herniation.
Ventriculostomy is the gold standard for direct ICP monitoring and can also drain CSF.
Maintain HOB at approximately 30° with neutral head and neck alignment.
When ICP rises, assess the patient first.
ICP management targets include PaO₂ at or above 100 mm Hg and systolic BP 100–160 mm Hg.
Licox brain-tissue oxygen target is 20–40 mm Hg.
SjvO₂ is normally 60–75%.
Mannitol is the primary/gold-standard osmotic diuretic discussed for reducing cerebral edema.
Mannitol requires adequate renal function for intended fluid removal.
Hypertonic saline moves water out of cells and into the vascular compartment.
Recurrent seizures increase ICP and decrease cerebral perfusion.
Fever and excessive stimulation increase cerebral metabolic demand and can worsen ICP.
Nutritional support is generally initiated within 24–48 hours after injury.
Avoid hypotonic fluids such as 0.45% saline during increased ICP.
Pituitary/hypothalamic compression requires monitoring for SIADH and diabetes insipidus.
TRAUMATIC BRAIN & HEAD INJURIES
Head Injury & TBI
Head injury may involve:
Scalp.
Skull.
Brain.
TBI is a more serious form involving brain injury.
Injury severity depends on:
Mechanism.
Severity.
Resulting intracranial injury.
A patient with concussion symptoms should be removed from activity and neurologically assessed.
TRAP: Do not dismiss a concussion as simply having one's “bell rung.”
TBI Severity
Brain-injury severity is classified using GCS.
Focus on:
What GCS assesses.
How the score is calculated.
How changes reflect neurological deterioration.
Skull Fractures
Types discussed:
Comminuted.
Compound.
Depressed.
Linear.
Simple.
TRAP: The exam focus is not diagnosing or defining individual skull-fracture types.
Focus on:
Location.
Assessment findings.
Neurological manifestations.
Complications.
Basilar/Skull-Fracture Findings
Raccoon eyes
Periorbital edema/ecchymosis.
Battle sign
Posterior/mastoid ecchymosis.
Otorrhea
CSF drainage from the ear.
Halo sign
Blood remains centrally located on gauze.
Clearer fluid separates outward around the blood.
Supports concern for CSF leakage.
CSF drainage may undergo laboratory testing.
Glucose testing can produce false-positive results.
A standard bedside glucometer is not used for this CSF glucose assessment.
NEVER DO: Avoid NG/OG placement when facial or basilar skull trauma makes the route unsafe.
Diffuse vs. Focal Injury
Diffuse
Generalized rather than localized.
Concussion is an example.
Severe diffuse injury may progress to DAI.
Focal
Localized to a specific area.
Contusion is an example.
Cerebral Contusion
Contusion = brain bruise.
Can contribute to:
Cerebral edema.
Increased ICP.
Intracranial bleeding.
Coup-Contrecoup Injury
Forward impact causes the frontal brain to strike the skull.
Rebound causes the posterior/occipital brain to strike the skull.
May cause:
Visual disturbances.
Blurred vision.
Dizziness.
Confusion.
Memory loss/amnesia.
Evaluate for:
Intracranial bleeding.
Increased ICP.
Diffuse Axonal Injury
DAI involves widespread damage to axonal nerve fibers.
Disrupts neuronal communication throughout the brain.
Patients may rapidly progress to:
Coma.
Death.
DAI carries high mortality.
Severe motor-vehicle trauma is a common mechanism discussed.
Chronic Traumatic Encephalopathy
Associated with repetitive head trauma and repeated concussions.
May cause chronic:
Agitation.
Memory loss.
Aggression.
Erratic behavior.
Definitive diagnosis occurs through autopsy after death.
CLINICAL GEM: Repeated head injuries can produce cumulative long-term neurological consequences even when individual injuries initially appear less severe.
Intracranial Hematomas
Epidural
Blood accumulates between the dura and inner skull.
Expanding blood compresses underlying brain tissue.
Subdural
Blood accumulates beneath the dura.
Expanding blood compresses brain structures.
Intracerebral
Bleeding occurs within brain tissue.
Expanding blood → brain compression → impaired cerebral perfusion → increased ICP → possible herniation.
Head-Injury Imaging
Rapid noncontrast CT head is the initial imaging emphasized when intracranial bleeding is suspected.
CT rapidly identifies:
Hemorrhage.
Mass effect.
MRI is more sensitive but less rapid for initial emergency evaluation.
CLINICAL GEM: A negative initial CT does not eliminate the possibility of an evolving intracranial bleed.
Continue serial:
LOC assessment.
Pupillary assessment.
Motor assessment.
GCS.
Vital-sign assessment.
Collaborative Management
Determine mechanism:
What happened?
Where was the impact?
Was an object involved?
Mechanism helps identify:
Primary injury.
Potential secondary injury.
Continue:
GCS.
Neurological assessment.
Physical assessment.
Vital signs.
Hemodynamic monitoring.
Treat:
Cerebral edema.
Increased ICP.
Impaired oxygenation.
Time is tissue.
Rapid deterioration may require operative intervention to:
Evacuate blood.
Decompress the brain.
Preoperative Management
Maintain prescribed NPO status.
Obtain baseline:
Vital signs.
Neurological status.
Ensure informed-consent requirements are addressed.
An unconscious or neurologically impaired patient may be unable to provide valid consent.
Emergency life-saving intervention may proceed through the appropriate emergency-consent process when delay threatens survival.
Neurosurgical Procedures
Burr hole
Creates an opening through the skull for drainage/decompression.
Craniectomy
Removes a portion/bone flap of the skull for decompression.
Craniotomy
Temporarily removes a bone flap for surgical access.
Bone flap is replaced.
Cranioplasty
Repairs/reconstructs the skull.
Shunt
Drains excess CSF.
May be used for hydrocephalus.
Stereotactic procedure
Additional neurosurgical approach discussed.
Postoperative Care
Protect the surgical/decompressed area.
Monitor for infection.
Continue neurological assessment.
Continue ICP monitoring when indicated.
Evaluate whether intervention reduced:
Swelling.
ICP.
Neurological deterioration.
Continue monitoring for secondary brain injury after surgery.
Long-Term Neurological Recovery
Recovery may require:
Rehabilitation.
Subacute care.
Short-term care.
Long-term residential care.
Interprofessional care may involve:
Nursing.
Case management.
Social work.
Rehabilitation.
Family/caregivers.
Bowel Management
Neurological injury and immobility can impair bowel function.
Routine care may include:
Stool softener.
Laxative.
TRAP: Stool softener alone does not adequately treat established constipation.
A laxative may be required.
Enema may be considered if constipation persists.
Bladder Management
Spastic bladder
Contracts but may not completely empty.
Residual urine increases UTI risk.
Antispasmodic therapy may help.
Flaccid bladder
Bladder muscle does not function effectively.
May require chronic bladder management/catheterization.
Swallowing
Neurological injury may impair swallowing.
Swallow evaluation is essential when dysphagia is suspected.
VTE Prevention
Immobility increases thromboembolic risk.
Pharmacological prophylaxis may include:
Enoxaparin.
Subcutaneous heparin.
Chronic Neurological Effects
Some patients develop chronic seizure disorders requiring long-term or lifelong antiseizure therapy.
Frontal-lobe injury may cause persistent:
Personality changes.
Mood changes.
Agitation.
Aggression.
Impaired judgment.
Psychological and emotional consequences may persist after physical stabilization.
Brain injury affects:
Patient.
Family/caregivers.
Social Determinants & Recovery
Recovery can be affected by:
Healthcare access.
Education.
Transportation.
Financial/resource limitations.
These factors influence access to:
Rehabilitation.
Medications.
Follow-up care.
Ongoing treatment.
KEY TAKEAWAYS
TBI severity is evaluated using the GCS and ongoing neurological assessment.
Concussions require assessment and should not be dismissed.
Raccoon eyes, Battle sign, and CSF otorrhea are concerning findings after skull trauma.
Avoid nasal tube placement when facial or basilar skull trauma makes the route unsafe.
Diffuse injury is generalized; focal injury affects a specific brain area.
Contusion is a focal brain bruise.
Coup-contrecoup injury involves primary and rebound impacts against the skull.
DAI causes widespread axonal injury and carries a high risk for coma and death.
Repetitive head trauma is associated with CTE; definitive diagnosis occurs through autopsy.
Epidural, subdural, and intracerebral hematomas can compress brain tissue and increase ICP.
Rapid noncontrast head CT is the initial imaging emphasized for suspected intracranial hemorrhage.
A negative initial CT does not eliminate the need for continued neurological assessment.
Head-injury management focuses on recognizing primary injury and preventing secondary injury.
Craniectomy removes a bone flap; craniotomy temporarily removes and replaces the bone flap.
A shunt drains excess CSF and may be used for hydrocephalus.
Swallow evaluation is essential when neurological injury causes suspected dysphagia.
Frontal-lobe injury can cause persistent personality and behavioral changes.
Long-term brain-injury management includes physical, psychological, family, social, and rehabilitation needs.
OTHER CAUSES OF INCREASED INTRACRANIAL PRESSURE
Brain Tumors
Intracranial tumors can cause:
Compression.
Increased ICP.
Neurological deficits.
Manifestations depend on the affected:
Brain lobe.
Cranial nerve.
Intracranial structure.
Neurological changes may initially be subtle.
CLINICAL GEM: A subtle new neurological or cranial-nerve deficit may be an early clue to a slowly developing intracranial tumor.
Tumors may be:
Benign.
Malignant.
The blood-brain barrier complicates delivery of some treatments to brain tissue.
Brain tumors can carry significant mortality.
Meningitis
Inflammation/infection of the meninges.
Causes include:
Bacterial.
Viral.
Identifying the underlying cause determines treatment.
May cause:
Nuchal rigidity.
Neurological changes.
Increased ICP.
SIRS/sepsis.
Management may require simultaneous treatment of:
Increased ICP.
Infection.
Systemic sepsis.
Encephalitis
Inflammation/swelling within brain tissue.
Causes discussed include:
Viral.
Bacterial.
Viral infection was emphasized.
West Nile virus
Mosquito-borne viral cause.
May produce:
Altered mental status.
Neurological deficits.
Increased ICP.
Severe disease may require:
Intubation.
Sedation.
Critical care.
Neurological deficits may persist after acute infection resolves.
Cognitive difficulties.
Word-finding difficulties.
Brain Abscess
Creates:
Localized compression.
Increased ICP.
Dental infection is an important potential source.
Include oral/dental assessment:
Inspect dentition and oral cavity.
Ask about tooth pain.
Identify possible dental abscess.
Ensure oral care.
Suspected dental infection should be reported because infection can spread and contribute to intracranial infection.
Lumbar Puncture for Infection
LP may obtain CSF when an infectious neurological process is suspected.
CSF is analyzed to identify the underlying infectious cause.
The primary purpose in this setting is diagnostic identification of infection, not simply removal of CSF.
KEY TAKEAWAYS
Brain tumors, meningitis, encephalitis, and brain abscesses can contribute to increased ICP.
Brain tumors may initially present with subtle neurological or cranial-nerve deficits.
The blood-brain barrier can complicate treatment of brain tumors.
Meningitis may require simultaneous management of increased ICP, infection, and sepsis.
Encephalitis can cause altered mental status, cerebral swelling, increased ICP, and persistent neurological deficits.
West Nile virus is a mosquito-borne cause of viral encephalitis discussed in the lecture.
Dental infection is an important potential source of brain abscess.
Oral and dental assessment can identify a potential source of intracranial infection.
Lumbar puncture can obtain CSF to identify the underlying cause of neurological infection.
CEREBROVASCULAR ACCIDENT & ACUTE STROKE MANAGEMENT
Stroke Recognition — BE FAST
BE FAST provides rapid recognition of stroke manifestations.
B — Balance
Assess for sudden loss of balance or coordination.
CLINICAL GEM: Balance disturbance may be an early stroke manifestation even when other findings remain subtle.
E — Eyes
Assess for sudden:
Visual changes.
Visual loss.
Eye-movement abnormalities.
F — Face
Assess for facial droop or asymmetry.
Ask the patient to smile.
A — Arms
Compare bilateral upper-extremity strength.
Assess for:
Weakness.
Asymmetry.
Arm drift.
Unequal hand grasps.
S — Speech
Assess:
Speech quality.
Ability to produce language.
Ability to understand language.
Appropriateness of responses.
T — Time
Determine symptom onset and last-known-well time.
Activate emergency stroke response immediately.
Focused Stroke Assessment
Assess:
Eye movement and tracking.
Pupillary response.
Facial symmetry.
Smile and mouth movement.
Tongue movement.
Bilateral upper- and lower-extremity strength.
Sensation.
Speech.
Language comprehension.
Any new focal neurological deficit requires rapid stroke evaluation.
Communication & Swallowing Deficits
Expressive aphasia
Difficulty producing meaningful language.
Receptive aphasia
Difficulty understanding language.
Dysarthria
Mechanical impairment of speech articulation.
Dysphagia
Difficulty swallowing.
Increases aspiration risk.
TRAP:
Aphasia → language-processing problem.
Dysarthria → articulation/mechanical speech problem.
Dysphagia → swallowing problem.
Generalized Hemisphere Patterns
Right-brain stroke
May cause:
Left-sided motor deficits.
Impulsivity.
Impaired judgment.
Impaired spatial awareness.
Depth-perception problems.
Impulsivity + impaired spatial awareness significantly increase fall and injury risk.
Left-brain stroke
May cause:
Right-sided motor deficits.
Aphasia.
Anxiety.
Depression.
TRAP: Hemisphere patterns are general patterns rather than absolute rules.
Evaluate the complete neurological presentation.
Acute Stroke Priorities
Time is tissue.
Rapid recognition and treatment are intended to:
Preserve cerebral perfusion.
Limit progression of cerebral injury.
Prevent secondary injury.
Immediate priorities include:
Establish last-known-well.
Perform focused neurological assessment.
Activate stroke response.
Obtain rapid diagnostic imaging.
Determine whether the stroke is ischemic or hemorrhagic.
Last-Known-Well
Determine last-known-well time as early as possible.
Reperfusion-treatment eligibility depends on the neurological timeline.
TRAP: Do not use hospital-arrival time as a substitute for last-known-well.
Communicate last-known-well during:
EMS handoff.
Stroke-alert activation.
Treatment evaluation.
Prehospital & Initial Stroke Management
Obtain:
Blood glucose.
Baseline ECG.
Relevant medical history.
Medication history.
Cardiovascular history.
Last-known-well.
Accurate weight.
Establish IV access.
Preferably two working IVs.
Continue:
Airway assessment.
Neurological assessment.
Cardiac monitoring.
Notify the receiving hospital before arrival to facilitate stroke-team preparation.
Avoid delaying definitive stroke evaluation for lower-priority testing.
Blood Glucose
Obtain during initial stroke evaluation.
Glucose abnormalities can:
Accompany neurological illness.
Complicate the neurological presentation.
TRAP: An isolated glucose value does not establish long-term diabetic control.
Hemoglobin A1C evaluates longer-term glucose control.
Atrial Fibrillation
Important risk factor for embolic ischemic stroke.
A thrombus may form and travel into cerebral circulation.
Continue cardiac monitoring.
TRAP: Atrial fibrillation increases concern for an embolic source but does not independently prove the stroke mechanism.
Stroke Alert — Interdisciplinary Care
Acute stroke management requires rapid coordination among:
Emergency provider.
RN/stroke nurse.
Neurology.
Pharmacy.
Charge nurse.
Technician.
CT/radiology.
Laboratory.
Cardiology when indicated.
RN responsibilities include:
Ongoing assessment.
Immediate nursing care.
Preparing ordered treatment.
Administering treatment within RN scope.
Monitoring response.
RN does not independently determine eligibility for:
Fibrinolytic therapy.
Mechanical thrombectomy.
Immediate Noncontrast CT
Obtain a noncontrast head CT within 20 minutes.
CT interpretation should occur within 45 minutes.
Primary immediate purpose:
Rule out intracranial hemorrhage.
TRAP: Initial noncontrast CT does not necessarily definitively identify every ischemic stroke.
NEVER DO: Do not administer fibrinolytic therapy when intracranial hemorrhage is present.
CLINICAL GEM: Ischemic and hemorrhagic stroke may initially produce similar neurological deficits, but their treatment pathways differ.
CLINICAL GEM: The immediate CT question is whether bleeding is present because hemorrhage changes the treatment pathway.
Initial Laboratory & Cardiovascular Evaluation
Relevant studies may include:
Troponin.
Coagulation studies.
Platelet count.
Chest X-ray may also be obtained.
Obtain baseline ECG.
Continue cardiovascular and neurological reassessment.
NIH Stroke Scale
NIHSS = National Institutes of Health Stroke Scale.
Objectively evaluates stroke-related neurological deficits.
Higher NIHSS score = greater neurological impairment.
Serial NIHSS assessments compare current status with baseline.
Improving score/findings → neurological improvement.
Persistent/worsening findings → continued impairment or deterioration.
Stroke assessment may identify:
Altered orientation.
Gaze deviation.
Visual-field loss.
Facial weakness.
Unilateral arm/leg weakness.
Sensory loss.
Aphasia.
Dysarthria.
Neglect.
CLINICAL GEM: The NIHSS establishes a standardized neurological baseline that can be trended over time.
CLINICAL GEM: Weakness that prevents coordination testing should not automatically be classified as ataxia.
Ataxia is identified when it is out of proportion to the patient's weakness.
Students are not expected to memorize the entire scoring table.
NIHSS uses standardized criteria.
TRAP: Do not score based on a general impression of how impaired the patient appears.
Assessment requires appropriate training.
Student nurses may participate with appropriate RN supervision.
Trend the individual neurological findings as well as the total score.
Stroke Risk-Factor Assessment
Assess:
Past medical history.
Allergies.
Medication history.
Medication adherence.
Access to medications.
Primary-care follow-up.
Cardiology follow-up.
Determine whether the patient takes anticoagulants because anticoagulation affects bleeding risk and acute treatment decisions.
Stroke Risk Factors
Nonmodifiable
Age.
Gender.
Ethnicity/race.
Family history.
Hereditary background.
Modifiable
Hypertension.
Previous TIA.
Atrial fibrillation.
Heart disease.
Diabetes.
Smoking.
Obesity.
Sleep apnea.
Metabolic syndrome.
Physical inactivity.
Diet.
Alcohol/substance use.
Hypertension is a major modifiable stroke risk factor.
Familial Hyperlipidemia
May have:
Heterozygous form.
Homozygous form.
Severe inherited hyperlipidemia can contribute to cardiovascular events at a young age.
Monitor:
Cholesterol.
Medication therapy.
Liver enzymes as indicated.
Social Determinants & Stroke Risk
TRAP: Do not assume poor disease control means the patient simply does not want to care for themselves.
Assess barriers involving:
Medication access.
Nutrition.
Transportation.
Follow-up care.
Financial resources.
Long-term risk-factor management.
Discharge planning must be realistic for the patient's circumstances.
Transient Ischemic Attack
TIA = transient ischemic attack.
Temporary neurological dysfunction.
Warning sign/risk factor for stroke.
Symptoms generally last <1 hour in this lecture.
TIA symptoms require medical evaluation even when they resolve.
TRAP: Resolution of symptoms does not mean the event should be ignored.
Major Stroke Categories
Ischemic
Inadequate cerebral blood flow caused by vascular occlusion.
Includes:
Thrombotic.
Embolic.
Cryptogenic.
Hemorrhagic
Bleeding into or around brain tissue.
Includes:
Intracerebral hemorrhage.
Subarachnoid hemorrhage.
Stroke type must be identified because treatment differs significantly.
NEVER DO: Do not begin fibrinolytic treatment until intracranial hemorrhage has been excluded.
Thrombotic Ischemic Stroke
Clot develops locally within the diseased vessel.
Vessel-wall disease/atherosclerotic plaque → local clot formation → narrowing/occlusion → decreased cerebral blood flow.
Associated risks include:
Diabetes.
Hypertension.
Atherosclerotic disease.
Ischemic stroke is the most common overall stroke category.
Embolic Ischemic Stroke
Embolic material originates elsewhere and travels until it obstructs a cerebral vessel.
Embolic material may include:
Blood clot.
Calcification.
Fat.
Air.
Associated conditions include:
Atrial fibrillation.
Endocarditis.
Rheumatic heart disease.
Valvular prosthesis.
Atrial septal defects.
CLINICAL GEM:
Thrombotic = forms there.
Embolic = travels there.
TRAP: An embolus can still be a blood clot.
The differentiator is where it formed and whether it traveled.
Cryptogenic Stroke
Stroke with no clearly identified source.
An embolic mechanism may be suspected even when the original source cannot be identified.
Cardiac Evaluation for Embolic Source
May include:
Echocardiogram.
ECG/cardiac monitoring.
Evaluation for atrial fibrillation.
Evaluation for PFO.
Bubble study
May identify an abnormal intracardiac opening such as a PFO.
PFO may permit a clot to enter arterial circulation and contribute to embolic stroke.
Intracerebral Hemorrhage
Cerebral vessel ruptures and bleeds directly into brain tissue.
Hypertension is a major cause discussed.
Blood-pressure control is a major treatment priority.
Basal ganglia was discussed as a common location.
Pattern may include:
Sudden onset.
Progressive worsening over minutes to hours.
Severe headache.
Nausea.
Vomiting.
Severe headache followed by nausea/vomiting is an important hemorrhagic-stroke pattern.
Expanding bleeding can cause:
Increased ICP.
Neurological deterioration.
Subarachnoid Hemorrhage & Aneurysm
Bleeding occurs into the space surrounding the brain.
Commonly associated with cerebral aneurysm rupture.
Aneurysms commonly develop within major cerebral vessels, including the Circle of Willis region.
Patients may have no warning symptoms before rupture.
Rupture can produce sudden catastrophic deterioration.
Family history of aneurysm is important.
Additional Stroke Imaging
MRI
May be obtained approximately 24–48 hours later.
More sensitive for further evaluation of cerebral injury.
Movement and claustrophobia may interfere with completion.
CTA
Evaluates cerebral vascular structures.
Requires contrast-related considerations.
Carotid duplex
Evaluates carotid arteries for abnormalities contributing to stroke risk.
Diagnostic-Test Safety
Before MRI:
Complete MRI safety screening.
Identify implanted/external devices.
Determine MRI compatibility.
Determine whether essential equipment can safely be removed.
Before contrast:
Assess kidney function.
Assess contrast tolerance.
Review medication history.
Metformin therapy requires consideration when contrast studies are planned.
Do not assume a patient is MRI-ready simply because the study has been ordered.
Acute Ischemic Stroke — Blood Pressure
Acute hypertension may represent cerebral autoregulation attempting to preserve perfusion.
Lower BP carefully.
NEVER DO: Do not rapidly or drastically decrease BP in acute ischemic stroke.
Excessive reduction can decrease cerebral perfusion and worsen ischemia.
Permissive hypertension
Elevated pressure may intentionally be tolerated to preserve cerebral perfusion.
TRAP: Do not automatically normalize every elevated BP in ischemic stroke.
BP Goals
Ischemic stroke receiving fibrinolytic therapy
BP must be <185/110 mm Hg before treatment.
Ischemic stroke not receiving fibrinolytic therapy
BP may be maintained <220/120 mm Hg.
Intracerebral hemorrhage
Target SBP <140 mm Hg.
Approximately 130–140 mm Hg was discussed as the desired range.
CLINICAL GEM:
Ischemic stroke → preserve cerebral perfusion while remaining within treatment parameters.
Intracerebral hemorrhage → tighter BP control to reduce continued bleeding.
Acute Stroke Antihypertensives
Labetalol
Adrenergic blocker/nonselective beta blocker.
Decreases BP through reduced cardiac output and vasodilation.
Monitor:
BP.
HR.
TRAP: Nonselective beta blockade creates concern with asthma/COPD.
Nicardipine
Continuous titratable IV infusion.
Requires close hemodynamic monitoring.
Clevidipine
Additional IV antihypertensive option.
Hydralazine
Vasodilator.
Monitor for excessive BP reduction.
Enalapril
ACE inhibitor.
Fibrinolytic Therapy
Fibrinolytics actively break down an existing clot.
Door-to-needle goal: <60 minutes.
Extended treatment window: 4.5 hours.
Treatment within 3 hours is preferred when possible.
CLINICAL GEM: “4.5 is great, but 3 is better.”
Last-known-well is critical for eligibility.
Provider determines whether treatment criteria are met.
RN responsibilities:
Preparation.
Administration after order.
Monitoring.
Recognition of complications.
Fibrinolytic Screening
Fibrinolytic therapy requires screening for bleeding risk and contraindications before administration.
Screening considerations include:
Coagulation abnormalities.
Recent GI bleeding.
Recent stroke or head trauma.
Recent major surgery.
Recent active internal bleeding.
Stroke or head trauma within the previous 3 months is a screening consideration.
Major surgery within the previous 14 days is a screening consideration.
Recent active internal bleeding within the previous 22 days is a screening consideration.
Extended 3–4.5-Hour Window Considerations
The 3–4.5-hour treatment window requires additional patient-specific screening.
Additional considerations discussed include:
Advanced age.
Oral anticoagulant use.
Previous ischemic stroke combined with diabetes.
High baseline NIHSS.
LECTURE INCONSISTENCY
Version A:
Verbal lecture referenced a high NIHSS threshold of >5.
Version B:
Course slide referenced NIHSS >25.
Fibrinolytic vs. Anticoagulant
Fibrinolytic
Breaks down an existing thrombus.
Anticoagulant
Helps prevent additional clot formation/propagation.
Heparin was discussed as an example.
TRAP: Fibrinolytics and anticoagulants are not the same therapy.
TRAP: Anticoagulation used for long-term stroke prevention is not the same as acute fibrinolytic reperfusion therapy.
Accurate Weight
Fibrinolytic dosing is weight-based.
Obtain an accurate weight immediately.
Standing weight is preferred when safely possible.
If using a bed scale:
Zero the bed correctly.
TRAP: An inaccurate weight can produce an inaccurate fibrinolytic dose.
Alteplase
Also referred to as rtPA.
Dose: 0.9 mg/kg.
Maximum: 90 mg.
10% of total dose over the first 1 minute.
Remaining 90% infused over 60 minutes.
NEVER DO: Do not administer the remaining alteplase dose as a rapid IV push.
Worked application
86.4 kg × 0.9 mg/kg = 77.76 mg total.
10% = approximately 7.78 mg over the first minute.
Remaining dose = approximately 69.98 mg over 60 minutes.
CLINICAL GEM: The case calculation demonstrates application of the dosing formula; the formula, maximum dose, 10% bolus, and 60-minute infusion are the information to retain.
Tenecteplase
Also referred to as TNK/TNKase.
Acute-stroke dose taught: 0.25 mg/kg IV.
Maximum: 25 mg.
Administered rapidly rather than through the prolonged alteplase infusion.
Worked application
86.4 kg × 0.25 mg/kg = 21.6 mg.
TRAP:
Alteplase → 10% bolus + remaining dose by infusion.
Tenecteplase → rapid IV administration.
Fibrinolytic Medication Safety
Requires an independent two-RN double-check.
Verify:
Patient.
Weight.
Dose calculation.
Reconstitution.
Preparation.
Administration.
Pump settings when applicable.
CLINICAL GEM: Accurate weight + accurate calculation + independent verification are major fibrinolytic safety anchors.
Mechanical Thrombectomy
May be considered for eligible large-vessel occlusion.
May be considered within a 24-hour window.
Last-known-well remains important.
RN does not determine eligibility.
Nursing responsibilities include:
Preparing for procedure/transport.
Preprocedure management.
Postprocedure neurocritical care.
Post-Fibrinolytic Monitoring
Continue frequent neurological reassessment.
Compare findings with established baseline.
Monitor for:
Improvement.
Persistent deficits.
Neurological deterioration.
Bleeding.
New/worsening severe headache.
Continue frequent BP monitoring and BP control during and after fibrinolytic administration.
New neurological deterioration or severe headache after fibrinolysis requires immediate evaluation for intracranial hemorrhage.
Obtain as indicated:
STAT CT.
STAT coagulation studies.
STAT fibrinogen.
STAT CBC.
Type and crossmatch.
Blood products/cryoprecipitate may be required when bleeding occurs.
CLINICAL GEM: A negative initial CT does not protect the patient from developing intracranial hemorrhage after treatment.
Apply increased-ICP assessment principles when neurological deterioration occurs.
Serial Reassessment
Compare every neurological assessment with baseline.
Determine:
Improvement.
Persistence.
Deterioration.
Depending on acuity, reassessment may occur minute by minute.
Continually:
Assess.
Identify the problem.
Intervene.
Evaluate response.
Reassess.
Document neurological findings and changes.
CLINICAL GEM: Improvement in vital signs does not establish neurological improvement when focal neurological deficits remain unchanged.
Whole-Patient Stabilization
TRAP: Do not focus on neurological findings while ignoring other physiological systems.
Maintain:
Hemodynamic stability.
Cerebral perfusion.
Oxygenation.
Homeostasis.
Acid-base balance.
Swallow & Aspiration Safety
Swallow evaluation is a primary safety assessment after stroke.
Primary concern = aspiration.
Establishes the swallowing baseline.
May need repetition as neurological status changes.
Speech-language pathology may perform formal evaluation.
A trained RN may perform a facility-approved bedside swallow screen.
Coughing after swallowing is concerning.
A wet cough after swallowing suggests impaired swallowing/aspiration.
TRAP: Being awake and able to communicate does not prove swallowing is safe.
Keep the patient NPO until the swallow evaluation is passed.
CLINICAL GEM: Neurological function can improve; an initial swallowing deficit is not necessarily permanent.
Modified Barium Swallow
Evaluates:
Swallowing mechanics.
Aspiration.
Contrast-containing material is swallowed while imaging evaluates movement.
Post-Stroke Nutrition
Nutritional support is important during the first 24–48 hours.
If gag/swallow function does not return:
Enteral feeding may be required.
Feeding tube may be necessary during recovery.
Goals:
Adequate nutrition.
Aspiration prevention.
Visual Dysfunction
Assess:
Pupillary response.
Eye movement.
Tracking.
Visual fields.
Homonymous hemianopia
Loss of the same visual field involving both eyes.
Immediate safety:
Initially approach from the side the patient can see.
Rehabilitation:
Teach intentional head turning.
Teach scanning toward the affected visual field.
Neglect & Spatial-Perceptual Dysfunction
Patient may:
Ignore the affected side.
Misinterpret surroundings.
Misjudge depth/distance.
Spatial-perceptual deficits increase fall risk.
Communication Support
Determine whether impairment involves:
Language production.
Language comprehension.
Mechanical articulation.
Adapt communication to the deficit.
Verify patient/family understanding.
Fall & Bleeding Safety
Stroke patients with sensory-perceptual deficits are high fall risk.
Bleeding consequences are greater when receiving:
Anticoagulants.
Antiplatelets.
Fibrinolytics.
NEVER DO: Allow a high-risk post-stroke patient receiving bleeding-risk medication to ambulate without appropriate safety precautions.
Prevent head injury because a fall can cause serious intracranial bleeding.
Critical Post-Stroke Period
First 12–24 hours are particularly critical.
Goals:
Prevent progression.
Recognize deterioration.
Prevent secondary complications.
Requires frequent:
Neurological assessment.
Hemodynamic monitoring.
Previous Stroke & Baseline
Determine:
When previous stroke occurred.
Which deficits remained.
TRAP: Do not automatically interpret a chronic neurological deficit as a new stroke finding.
Compare current findings with established baseline.
Secondary Stroke Prevention
May include:
Anticoagulants.
Antiplatelets.
Antihypertensives.
Lipid-lowering medications.
Before discharge, verify that appropriate secondary-prevention medications have been addressed.
If an expected medication is absent:
Determine whether a contraindication exists.
Communicate with the provider.
Medication education includes:
Purpose.
Expected effect.
Adverse effects.
TRAP: Medication adverse effects may contribute to nonadherence.
Assess the reason for nonadherence rather than assuming unwillingness.
Anticoagulation & Antiplatelet Therapy
Anticoagulation may be prescribed for secondary prevention when indicated.
Warfarin regimens may involve different doses on different days.
Complex regimens require clear education.
Alternatives discussed:
Dabigatran.
Apixaban.
Antiplatelet examples:
Aspirin.
Clopidogrel.
Appropriate antithrombotic therapy should be addressed before discharge unless contraindicated.
Procedural Secondary Prevention
Left atrial appendage intervention
May reduce thromboembolic risk when the appendage is the source.
PFO closure
May be considered when an abnormal intracardiac opening contributes to embolic risk.
Carotid endarterectomy
Removes carotid plaque.
Angioplasty
Balloon dilation improves flow through a narrowed vessel.
Stenting
Supports the vessel and maintains patency.
Secondary prevention should address the mechanism responsible for the stroke whenever possible.
Hemorrhagic Stroke Procedures
Surgical treatment depends on:
Location.
Severity.
Surgical accessibility.
May include evacuation of:
Hematoma.
Aneurysm-related bleeding.
Some lesions may not be surgically accessible.
IV seizure prophylaxis may be used.
Aneurysm Clipping & Coiling
Clipping
Clip isolates the aneurysm to prevent continued/recurrent bleeding.
Coiling
Coil is placed within the aneurysm to stop blood flow into it.
Nursing care includes:
Preprocedure management.
Postprocedure management.
Neurological monitoring.
Monitoring for complications.
Previous aneurysm clipping/device must be identified during MRI screening and compatibility verified.
Stroke Core Measures
Major care areas discussed:
VTE prophylaxis.
Antithrombotic therapy.
Anticoagulation with atrial fibrillation/flutter.
Thrombolytic therapy when indicated.
Statin therapy.
Stroke education.
Rehabilitation assessment.
Identify missing elements of expected care and advocate for the patient.
Nutrition & Risk-Factor Management
Interdisciplinary resources may include:
Diabetes educator.
Dietitian/nutritionist.
Cardiac rehabilitation nurse.
Assess normal dietary patterns before recommending changes.
Teaching should involve realistic changes the patient can maintain.
Goals include:
Lipid management.
Cardiovascular risk reduction.
Diabetes management.
Warfarin & Nutrition
TRAP: Do not teach patients taking warfarin to completely eliminate vitamin K-containing foods.
Emphasize:
Moderation.
Consistency.
Matching medication management with realistic dietary patterns.
Dramatic dietary changes can destabilize anticoagulation.
Culturally Appropriate Nutrition
Do not simply tell patients to eliminate traditional foods.
Recommendations should fit:
Culture.
Lifestyle.
Normal dietary practices.
Teach realistic modifications and nutrition-label reading.
CLINICAL GEM: A theoretically ideal diet is ineffective if the patient cannot realistically follow it.
Patient Self-Management
Teach patients to evaluate whether treatment is working.
Home monitoring may include:
BP.
HR.
Patient journals can document trends for follow-up visits.
If monitoring equipment is inaccessible:
Identify the barrier.
Communicate the need.
Explore resources.
Successful discharge requires realistic tools for safe self-management.
Rehabilitation
Focuses on recovering:
Strength.
Mobility.
Communication.
Functional independence.
Specialized rehabilitation may be required for aphasia or other persistent deficits.
Connect patients with:
Stroke survivorship resources.
Community networks.
Rehabilitation services.
Discharge & Post-Acute Care
Discharge planning includes:
Durable medical equipment.
Functional limitations.
Barriers to discharge.
Appropriate post-acute level of care.
Short-term rehabilitation may be appropriate when:
Skilled care remains necessary.
Acute hospital-level care is no longer required.
Placement should match the patient's functional and rehabilitation needs.
Psychological, Family & Community Recovery
Stroke recovery includes psychological care for:
Patient.
Family.
Communication deficits may interfere with education.
Adapt teaching.
Verify understanding.
Sexual function/dysfunction should be assessed during recovery.
Medication-related sexual dysfunction may contribute to nonadherence.
Long-term goals include:
Rehabilitation.
Functional recovery.
Self-management.
Community reintegration.
Prevention of recurrent stroke.
KEY TAKEAWAYS
BE FAST assesses balance, eyes, face, arms, speech, and time.
Aphasia is a language deficit; dysarthria is an articulation deficit; dysphagia is a swallowing deficit.
Right-brain stroke may produce left-sided weakness, impulsivity, and spatial-perceptual deficits; left-brain stroke may produce right-sided weakness and aphasia.
Time is tissue in suspected stroke.
Last-known-well time is essential for reperfusion-treatment decisions.
Initial stroke evaluation includes neurological assessment, glucose, ECG, medication history, cardiovascular history, accurate weight, and IV access.
Atrial fibrillation is an important risk factor for embolic ischemic stroke.
Obtain noncontrast head CT within 20 minutes with interpretation within 45 minutes.
The immediate purpose of noncontrast CT is to rule out intracranial hemorrhage.
Never administer fibrinolytic therapy when intracranial hemorrhage is present.
NIHSS provides a standardized neurological baseline and should be trended over time.
Thrombotic stroke forms locally; embolic material travels from another location.
TIA symptoms generally last less than 1 hour and still require evaluation.
BP must be below 185/110 mm Hg before fibrinolytic therapy.
Ischemic stroke without fibrinolytic therapy may allow BP below 220/120 mm Hg.
Intracerebral hemorrhage requires tighter systolic BP control below 140 mm Hg.
Avoid drastic BP reduction during acute ischemic stroke because cerebral perfusion can decrease.
Door-to-needle time for fibrinolytic therapy should be less than 60 minutes.
The fibrinolytic treatment window may extend to 4.5 hours, with treatment within 3 hours preferred.
Additional 3–4.5-hour screening considerations include advanced age, oral anticoagulant use, previous ischemic stroke with diabetes, and high baseline NIHSS.
Alteplase is dosed at 0.9 mg/kg to a maximum of 90 mg.
Alteplase is administered as a 10% bolus over 1 minute followed by the remaining 90% over 60 minutes.
Tenecteplase is dosed at 0.25 mg/kg to a maximum of 25 mg in the acute-stroke dosing taught.
Fibrinolytic preparation and administration require an independent two-RN safety check.
Mechanical thrombectomy may be considered for eligible large-vessel occlusion within a 24-hour window.
New neurological deterioration or severe headache after fibrinolysis requires immediate evaluation for intracranial hemorrhage.
Swallow evaluation is a major post-stroke safety priority because of aspiration risk.
Keep the patient NPO until swallowing safety has been established.
A wet cough after swallowing is concerning for aspiration.
Homonymous hemianopia and neglect require immediate safety adaptations and rehabilitation strategies.
The first 12–24 hours after stroke are particularly critical for recognizing progression and deterioration.
Previous neurological deficits must be established as baseline so chronic findings are not mistaken for new deterioration.
Secondary stroke prevention should address the underlying mechanism and modifiable risk factors.
Warfarin teaching emphasizes consistent rather than complete elimination of vitamin K-containing foods.
Stroke recovery continues through acute care, rehabilitation, secondary prevention, self-management, and community reintegration.