NEURO 213: Intracranial Pressure, Head Injury, and Seizures
Intracranial Pressure (ICP)
Definition: The pressure exerted by the brain tissue, cerebrospinal fluid (CSF), and blood within the rigid confines of the skull.
Essential Components of the Skull: Brain tissue, blood, and cerebrospinal fluid (CSF).
Brain tissue: 78\% of intracranial volume.
Intravascular blood: 12\% of intracranial volume.
Cerebrospinal fluid (CSF): 10\% of intracranial volume.
Factors Influencing ICP:
Arterial pressure
Venous pressure
Intraabdominal and intrathoracic pressure
Posture
Temperature
Blood gases (especially CO_2 levels)
Regulation and Maintenance: Monro-Kellie Doctrine
Monro-Kellie Doctrine: Stated that if one of the three essential components (brain tissue, blood, CSF) increases in volume, another component must decrease to maintain a constant total intracranial volume and thus, maintain ICP.
Normal ICP: 5 to 15 mm Hg.
Elevated ICP: Considered elevated if sustained at >20 mm Hg.
Normal Compensatory Adaptations:
Changes in CSF volume (e.g., displacement of CSF into the spinal subarachnoid space, increased CSF absorption).
Changes in intracranial blood volume (e.g., compression of cerebral veins, vasoconstriction/vasodilation of cerebral blood vessels).
Changes in brain tissue volume (e.g., displacement of brain tissue).
Limitation of Compensation: The ability to compensate is limited. If the volume increase continues beyond the compensatory capacity, ICP will rise, leading to decompensation.
Cerebral Blood Flow (CBF)
Definition: The amount of blood in mL passing through 100 g of brain tissue in 1 minute.
About 50 mL/min per 100 g of brain tissue.
Autoregulation: The brain's ability to adjust the diameter of cerebral blood vessels to ensure consistent CBF, despite changes in systemic arterial pressure.
Autoregulation is only effective if the mean arterial pressure (MAP) is between 70 to 150 mm Hg.
Cerebral Perfusion Pressure (CPP):
Formula: CPP = MAP - ICP
Normal Range: 60 to 100 mm Hg.
Clinical Significance: A CPP of <50 mm Hg is associated with ischemia and neuronal death.
Effect of Cerebral Vascular Resistance:
CPP = Flow \times Resistance
Compliance: The expandability of brain tissue, which impacts the effect of volume change on pressure.
Formula: Compliance = \frac{Volume}{Pressure}
Intracranial Volume-Pressure Curve
Visually represents the relationship between intracranial volume and pressure.
High Compliance (Stages 1 & 2): Initial increases in volume cause minimal changes in ICP due to compensatory mechanisms. The brain can still accommodate volume.
Low Compliance (Stages 3 & 4): As compensatory mechanisms are exhausted, further increases in volume result in sharp, exponential increases in ICP.
Stages of Increased ICP
Stage 1: Total Compensation:
Compensatory mechanisms are fully active.
ICP remains within normal limits.
Stage 2: Decreased Compensation; Risk for Increased ICP:
Compensatory mechanisms are beginning to fail.
ICP may remain normal, but minor increases in volume will cause greater proportional increases in ICP.
Stage 3: Failing Compensation; Clinical Manifestations of Increased ICP (Cushing's Triad):
Compensatory mechanisms are largely depleted.
Small increases in volume significantly elevate ICP.
Clinical manifestations of increased ICP become evident, including Cushing's triad.
Stage 4: Herniation Imminent $\rightarrow$ Death:
Severe, uncontrolled ICP leads to devastating brain shift and herniation.
Compression of vital brain structures, ultimately leading to death.
Factors Affecting Cerebral Blood Vessel Tone
CO_2 (Carbon Dioxide):
Increased arterial PCO_2 causes cerebral vasodilation, increasing CBF.
Decreased arterial PCO_2 causes cerebral vasoconstriction, decreasing CBF.
O_2 (Oxygen):
Decreased arterial PO_2 (hypoxemia) causes cerebral vasodilation, increasing CBF (a compensatory response).
Hydrogen Ion Concentration:
Increased acidity (higher H^+ concentration) causes vasodilation.
Pathophysiology of Increased ICP
Life-threatening Condition: Occurs when any of the three components (brain tissue, blood, CSF) within the skull increase.
Sequence of Events:
Insult to brain (e.g., trauma, lesion).
Tissue edema in the brain.
Increased ICP due to increased tissue volume.
Compression of ventricles and compression of blood vessels.
Decreased cerebral blood flow (CBF).
Decreased O_2 with death of brain cells.
Edema around necrotic tissue develops.
Increased ICP with compression of brainstem and respiratory center.
Accumulation of CO_2 due to impaired perfusion and brainstem dysfunction.
Vasodilation in response to CO_2 accumulation, further increasing blood volume.
Increased ICP resulting from increased blood volume.
Death.
Herniation
Definition: The displacement of brain tissue from an area of higher pressure to an area of lower pressure, typically across rigid dural folds (falx cerebri, tentorium cerebelli) or through the foramen magnum.
Types of Herniation:
Falx cerebri: Herniation of the cingulate gyrus under the falx cerebri.
Tentorial Herniation: Downward displacement of the brainstem through the tentorial notch, or herniation of the temporal lobe into the tentorial notch. This can cause compression of the opposite cerebral peduncle against the unyielding tentorium.
Foramen Magnum: Final and most devastating form, where the brainstem is displaced downward through the foramen magnum.
Cerebral Edema
Definition: Increased extravascular fluid accumulation in the brain.
Causes: Variety of causes, including trauma, tumors, infection, ischemia, and metabolic disturbances.
Three Types of Cerebral Edema:
Vasogenic Cerebral Edema (Most Common):
Occurs mainly in white matter.
Fluid leaks from the intravascular space (blood vessels) to the extravascular space (around brain cells) due to disruption of the blood-brain barrier.
Variety of causes (e.g., brain tumors, abscesses, injury).
Leads to a continuum of symptoms, potentially progressing to coma.
Cytotoxic Cerebral Edema:
Disruption of cellular membrane integrity, often secondary to destructive lesions or trauma to brain tissue.
Fluid shifts from the extracellular space into the intracellular space, causing swelling of brain cells.
Occurs particularly in gray matter.
Causes include anoxia, trauma, and toxins.
Interstitial Cerebral Edema:
Usually a result of hydrocephalus.
Caused by excess CSF production, obstruction of CSF flow, or inability to reabsorb CSF.
Manifests as fluid accumulation in the periventricular white matter.
Treatment involves managing hydrocephalus, often with a ventriculostomy or shunt.
Clinical Manifestations of Increased ICP
Change in Level of Consciousness (LOC):
Often the most sensitive and earliest indicator.
Ranges from flattening of affect to coma.
Includes restlessness, confusion, lethargy, difficulty in arousal.
Change in Vital Signs:
Cushing's Triad: A classic late sign of increased ICP and brainstem compression.
Widened pulse pressure (increasing systolic BP, decreasing or stable diastolic BP).
Bradycardia (slow heart rate).
Irregular respirations (e.g., Cheyne-Stokes, central neurogenic hyperventilation).
Change in body temperature (may be due to hypothalamic compression).
Ocular Signs (Compression of Oculomotor Nerve, Cranial Nerve III):
Unilateral pupil dilation (ipsilateral to the lesion).
Sluggish or no response to light.
Inability to move the eye upward.
Eyelid ptosis (drooping eyelid).
Bilateral dilated, fixed pupils (ominous sign, indicates brainstem damage).
Pinpoint pupils (pons damage or drug effect).
Decreased in Motor Function:
Hemiparesis/Hemiplegia: Weakness or paralysis on one side of the body.
Posturing:
Decorticate posturing (flexor): Adduction and internal rotation of the arms, flexion of the elbows, wrists, and fingers, extension of the legs. Indicative of damage to the cerebral hemispheres or tracts above the midbrain.
Decerebrate posturing (extensor): Stiff extension and pronation of the arms, flexion of the wrists and fingers, extension of the legs, and plantar flexion of the feet. Indicates more serious damage, usually to the midbrain or pons.
Headache:
Often continuous and persistent.
Worse in the morning due to accumulation of CO_2 during sleep, causing vasodilation.
Vomiting:
Often not preceded by nausea.
Characteristically projectile.
Complications of Increased ICP
Inadequate Cerebral Perfusion:
Direct consequence of increased ICP, leading to ischemia and neuronal damage.
Cerebral Herniation:
Tentorial herniation: Displacement of brain tissue past the tentorium cerebelli.
Uncal herniation: Medial temporal lobe (uncus) herniates into the tentorial notch.
Cingulate herniation: Cingulate gyrus herniates under the falx cerebri (lateral displacement).
Diagnostic Studies for Increased ICP or Brain Injury
Imaging:
CT scan: Best initial diagnostic test to determine craniocerebral trauma, identify masses, edema, or hemorrhage.
MRI: Provides more detailed imaging of brain structures.
PET (Positron Emission Tomography): Measures brain metabolism and blood flow.
Physiological Monitoring:
EEG (Electroencephalogram): Measures electrical activity of the brain.
Cerebral angiography: Visualizes cerebral blood vessels.
ICP and brain tissue oxygenation measurement (e.g., LICOX catheter): Direct measurement of ICP and brain tissue oxygenation.
Doppler and evoked potential studies: Assess cerebral blood flow and neural pathway integrity.
Contraindicated Procedure: Lumbar Puncture (LP):
NO lumbar puncture if increased ICP is suspected, as it can cause a rapid decrease in pressure in the spinal canal, leading to brain herniation.
Measurement of ICP
Purpose: Guides clinical care and allows for early detection of changes.
Indications for ICP Monitoring:
Glasgow Coma Scale (GCS) of \le8 (indicating severe neurological impairment).
Abnormal CT scans or MRI findings (e.g., hematomas, contusions, edema).
Potential Placements of ICP Monitoring Devices:
Ventricular (Ventriculostomy): Catheter inserted into the lateral ventricle, most common and gold standard. Allows for CSF drainage.
Subarachnoid
Intraparenchymal
Epidural
Subdural
Ventriculostomy:
Catheter inserted into the lateral ventricle.
Coupled with an external transducer to measure pressure.
Allows for closed CSF drainage system, either intermittently or continuously.
Leveling: The transducer must be leveled properly (e.g., at the Tragus of the ear) to obtain accurate readings.
ICP Monitoring Principles:
Prevent and monitor for infection: Strict aseptic technique during insertion and dressing changes.
Measure as mean pressure.
Waveform should be recorded: Normal, elevated, and plateau waves indicate different pressure states.
Evaluate changes with patient condition: Correlate ICP readings with neurological assessments.
Causes of Inaccurate Readings:
CSF leaks
Obstruction in catheter/kinks in tubing
Differences in height of bolt/transducer
Incorrect height of drainage system
Bubbles/air in tubing
ICP Control with CSF Removal:
Ventricular catheters allow for removal of CSF to control ICP.
Intermittent or continuous drainage.
Careful monitoring of the volume of CSF drained is essential to prevent rapid or excessive drainage, which could lead to ventricular collapse or herniation.
Interprofessional Care for Increased ICP
Overall Goal: Treat the underlying cause of increased ICP.
Respiratory Management:
Adequate oxygenation: Maintain arterial PO_2 > 100 mm Hg.
Maintain arterial PCO2 between 35 to 45 mm Hg (to avoid vasodilation from high CO2 or critical vasoconstriction from low CO2).
Intubation and mechanical ventilation may be required to maintain airway and optimize blood gases.
Surgical Intervention: Depending on the cause (e.g., removal of hematoma, tumor resection).
Drug Therapy for Increased ICP
Mannitol (Osmitrol):
Mechanism: Plasma expansion (reduces blood viscosity, increasing CBF and O_2 delivery) and osmotic effect (moves fluid from brain tissue into blood vessels).
Monitoring: Fluid and electrolyte status (hyponatremia, hypokalemia) and kidney function.
Hypertonic Saline (e.g., 3\% NaCl):
Mechanism: Moves water out of brain cells and into the blood vessels (similar osmotic effect as mannitol but also expands plasma volume more effectively).
Monitoring: Blood pressure and serum sodium levels (risk of central pontine myelinolysis with rapid correction of hyponatremia).
Corticosteroids (e.g., Dexamethasone):
Indication: Primarily for vasogenic edema (as seen with brain tumors or abscesses).
Monitoring: Fluid intake, serum sodium and glucose levels (risk of hyperglycemia).
Concurrent Medications: Antacids, H2 receptor blockers, or proton pump inhibitors are often prescribed to prevent gastrointestinal ulcers (due to steroid use).
Other Medications:
Antiseizure medications: To prevent or treat seizures that can exacerbate ICP.
Antipyretics: To control fever, as hyperthermia increases cerebral metabolic rate and blood flow.
Sedatives (e.g., Dexmedetomidine, Propofol): To control agitation, decrease metabolic demands, and facilitate ventilation without masking neurological signs excessively.
Analgesics: To manage pain, which can increase ICP.
Barbiturates (e.g., Pentobarbital, Thiopental): Used in refractory increased ICP to induce a barbiturate coma, thereby suppressing brain activity, decreasing cerebral metabolic rate, and reducing CBF and ICP.
Nutritional Therapy for Increased ICP
Metabolic State: Patients with brain injury are often in a hypermetabolic and hypercatabolic state, leading to increased nutritional needs.
Glucose: Increased need for glucose as the primary fuel for the brain.
Feeding: Early feeding (within 3 days of injury) via enteral or parenteral routes is crucial to support brain healing and prevent secondary injury.
Fluid Management: Keep the patient normovolemic.
IV 0.9\% NaCl (normal saline) is generally preferred over D5W (dextrose 5\% in water) or 0.45\% NaCl (half-normal saline), as hypotonic solutions like D5W can cause cerebral edema.
Nursing Assessment for Increased ICP
Subjective Data
Level of Consciousness (LOC): Use the Glasgow Coma Scale (GCS) components:
Eye opening response (1-4)
Best verbal response (1-5)
Best motor response (1-6)
History: Mechanism of injury, medications (especially anticoagulants), alcohol/drug use, risk-taking behaviors, headache characteristics, mood/behavioral changes, mentation changes, impaired judgment, aphasia, dysphasia, fear, denial, anger, aggression, depression.
Objective Data
Altered Mental Status.
Pupillary Check: Size, shape, equality, and reaction to light (sluggish, brisk, fixed). PERRLA : Pupils are equal, round, reactive to light, and accommodation.
Pupils equal and react normally.
Sluggish or brisk reaction (slow response).
Dilated pupil (compressed cranial nerve III, ipsilateral).
Bilateral dilated, fixed pupils (ominous sign, brainstem damage).
Pinpoint pupils (pons damage or drug effect).
Cranial Nerves: Assess eye movements, corneal reflex, oculocephalic reflex (doll's eye reflex - contraindication if cervical spine injury), oculovestibular reflex (caloric stimulation).
Motor Function:
Motor Strength: Squeeze hands, pronator drift test (arm drifts outward and downward with eyes closed), raise foot off bed, bend knees.
Motor Response: Spontaneous movement or response to pain (e.g., localization, withdrawal, decorticate/decerebrate posturing).
Vital Signs: Monitor for Cushing's triad (widened pulse pressure, bradycardia, irregular respirations), changes in body temperature.
Abnormal Respiratory Patterns of Coma:
Cheyne-Stokes: Cycles of hyperventilation and apnea (bilateral hemispheric disease or metabolic dysfunction).
Central neurogenic hyperventilation: Sustained, regular, rapid, and deep breathing (brainstem between lower midbrain and upper pons).
Apneustic breathing: Prolonged inspiratory phase or pauses alternating with expiratory pauses (mid or lower pons).
Cluster breathing (Biot's respiration): Clusters of breaths followed by irregular pauses (medulla or lower pons).
Ataxic breathing: Completely irregular with random deep and shallow breaths, irregular pauses, and slow rate (reticular formation of the medulla).
Other Findings: Lacerations, contusions, abrasions, hematoma, Battle's sign (postauricular ecchymosis), Raccoon eyes (periorbital ecchymosis), otorrhea (CSF/blood from ears), rhinorrhea (CSF/blood from nose), exposed brain (in severe open injuries), impaired gag reflex, vomiting (projectile), bowel and bladder incontinence, uninhibited sexual expression, seizures.
Diagnostic Findings: Abnormal CT/MRI, abnormal EEG, positive toxicology screen or alcohol level, increased or decreased blood glucose, increased ICP.
Nursing Planning and Goals for Increased ICP
Overall Goals:
Maintain a patent airway.
Maintain ICP within normal limits (5-15 mm Hg).
Maintain normal fluid and electrolyte balance.
Prevent complications secondary to immobility and decreased LOC.
Acute Care for Increased ICP
Respiratory Function:
Maintain a patent airway (oral airway, endotracheal tube).
Elevate head of bed 30 degrees (with proper body alignment to facilitate venous drainage and lower ICP) unless contraindicated by spinal instability.
Address suctioning needs judiciously (can increase ICP; pre-oxygenate, limit passes).
Minimize abdominal distention (prevents upward pressure on diaphragm, which can increase intrathoracic pressure and impede venous return).
Monitor ABGs (arterial blood gases) to ensure adequate oxygenation and CO_2 control.
Maintain ventilatory support as prescribed.
Pain and Anxiety Management:
Use opioids (e.g., fentanyl) carefully to manage pain without excessive sedation.
Sedatives (e.g., Propofol, Dexmedetomidine) for agitation and to reduce metabolic demands.
Neuromuscular blocking agents (e.g., vecuronium) may be used for intubated patients to facilitate ventilation and reduce muscle activity that can increase ICP.
Benzodiazepines (e.g., lorazepam) for anxiety and to treat seizures, but use cautiously due to sedative effects.
Fluid and Electrolyte Balance:
Monitor IV fluids closely.
Daily electrolytes (sodium, potassium, etc.).
Monitor for Diabetes Insipidus (DI; high urine output, hypernatremia) or Syndrome of Inappropriate Antidiuretic Hormone (SIADH; low urine output, hyponatremia), both of which can complicate fluid balance and ICP.
Monitor and minimize increases in ICP (e.g., during nursing activities, prevent Valsalva).
Interventions to Optimize ICP and CPP:
HOB elevated appropriately (typically 30 degrees).
Prevent extreme neck flexion, which can impede venous drainage.
Turn slowly and gently to avoid sudden increases in ICP.
Avoid coughing, straining, and Valsalva maneuver.
Avoid hip flexion >90 degrees, which can increase intra-abdominal and intrathoracic pressure.
Minimize Complications of Immobility:
Protection from self-injury (e.g., side rails padded, close observation).
Judicious use of restraints (mechanical or chemical) as needed, but avoid overuse as agitation can increase ICP.
Seizure precautions (padding, airway management).
Maintain a quiet, non-stimulating environment.
Provide psychologic considerations and support for the patient and family.
Evaluation for Increased ICP
Expected Outcomes:
Maintain ICP and CPP within normal parameters.
No serious increases in ICP during or following care activities.
No complications of immobility (e.g., pressure injuries, contractures, pneumonia).
Head Injury
Definition: Any trauma to the skull, scalp, or brain.
Traumatic Brain Injury (TBI): A specific type of head injury involving direct damage to the brain.
Incidence: High incidence, with TBI being twice as common in males.
Most Common Causes:
Falls
Motor vehicle accidents (MVAs)
Other Causes: Firearm-related injuries, assaults, sports-related trauma, recreational injuries, war-related injuries.
Potential for Poor Outcome: High, with deaths occurring at three points in time after injury:
Immediately after the injury (due to direct trauma/hemorrhage).
Within 2 hours after the injury (due to worsening hematomas or edema).
3 weeks after the injury (due to multisystem organ failure, infection).
Scalp Lacerations
Description: External head trauma (cuts to the scalp).
Vascularity: The scalp is highly vascular, leading to profuse bleeding even from minor lacerations.
Major Complications: Significant blood loss (hypovolemic shock) and infection.
Skull Fractures
Classification by Type:
Linear or Depressed: Linear (break in bone without displacement), Depressed (inward indentation of the skull, can cause brain tissue damage).
Simple, Comminuted, or Compound: Simple (fracture without fragmentation or communicating skin lesion), Comminuted (multiple bone fragments), Compound (severe, bone fragments penetrate skin).
Closed or Open: Closed (dura intact), Open (dura torn, exposing brain).
Signs of Skull Fractures (especially basilar fractures):
Periorbital edema and ecchymosis (Raccoon Eyes): Bruising around the eyes, often due to blood entrapped by the orbital septum.
Postauricular ecchymosis (Battle's Sign): Bruising behind the ear.
Hemotympanum: Blood in the tympanic membrane (middle ear).
Rhinorrhea: CSF leakage from the nose.
Otorrhea: CSF leakage from the ear.
Halo Sign: A ring of CSF around a blood stain on gauze, indicating a CSF leak.
Decreased hearing and facial palsy may also occur with basilar fractures.
Types of Head Injuries (Brain Tissue Damage)
Diffuse (Generalized): Affects the entire brain (e.g., concussion, diffuse axonal injury).
Focal (Localized): Affects a specific area of the brain (e.g., lacerations, contusions, hematomas, cranial nerve injuries).
Severity (based on Glasgow Coma Scale - GCS):
Key GCS Components: Eye opening (1-4), Verbal response (1-5), Motor response (1-6).
Minor TBI: GCS 13-15
Moderate TBI: GCS 9-12
Severe TBI: GCS 3-8
Diffuse Injuries
Concussion:
Brief disruption in LOC.
Retrograde amnesia (loss of memory of events leading up to the trauma).
Headache.
Short duration.
May result in Post-Concussion Syndrome:
Persistent headache.
Lethargy.
Personality and behavior changes.
Shortened attention span, decreased short-term memory.
Changes in intellectual ability.
Diffuse Axonal Injury (DAI):
Widespread axonal damage (shearing and tearing of axons).
Results in decreased LOC (often prolonged coma).
Increased ICP.
Decortication or decerebration (posturing).
Global cerebral edema.
Focal Injuries
Lacerations:
Tearing of brain tissue, often associated with depressed and open fractures and penetrating injuries.
Can lead to significant hemorrhage:
Intracerebral hemorrhage (bleeding within the brain tissue).
Subarachnoid hemorrhage (bleeding into the subarachnoid space).
Intraventricular hemorrhage (bleeding into the ventricles).
Contusions:
Bruising of brain tissue, commonly associated with closed head injury.
Can cause hemorrhage, infarction, necrosis, and edema.
Coup-Contrecoup Injury: Impact at the site of injury (coup) and a secondary impact at the opposite side of the brain (contrecoup) due to the brain moving within the skull.
Can rebleed and worsen neurological outcome.
Focal and generalized manifestations.
Monitor for seizures.
Potential for increased hemorrhage if the patient is on anticoagulants.
Hematomas (Complications)
Epidural Hematoma:
Location: Bleeding between the dura mater and the inner surface of the skull.
Neurologic Emergency: Rapid accumulation can lead to brain compression.
Source: Venous origin (slower) or arterial origin (rapid, typically from middle meningeal artery tear - seen in 85-90\% of cases).
Clinical Presentation: Often involves an initial period of unconsciousness, followed by a brief lucid interval (conscious but deterioration is occurring), then a rapid decrease in LOC.
Other signs: Headache, nausea, vomiting, focal neurological findings (e.g., hemiparesis, fixed and dilated pupil on the affected side).
Treatment: Requires rapid surgical evacuation (craniotomy).
Subdural Hematoma:
Location: Bleeding between the dura mater and the arachnoid mater.
Source: Most common source is veins that drain the brain surface into the sagittal sinus (slower venous bleed), but can also be arterial.
Types based on onset:
Acute Subdural Hematoma:
Occurs within 24 to 48 hours of injury (usually severe trauma).
Symptoms are related to increased ICP: decreased LOC, headache.
If severe, ipsilateral pupil (on the same side as the injury) may be dilated and fixed.
Treatment: Craniotomy, evacuation, and decompression.
Subacute Subdural Hematoma:
Occurs within 48 hours to 2 weeks after severe trauma.
May appear to enlarge over time as clot liquefies.
Symptoms progress more gradually, typically alteration in mental status.
Treatment: Evacuation and decompression.
Chronic Subdural Hematoma:
Occurs weeks or months (usually >20 days) after injury.
Often results from seemingly trivial injuries or injuries forgotten by the patient, common in older adults (brain atrophy creates more space for blood accumulation).
Presents as nonspecific, nonlocalizing symptoms: progressive alteration in LOC, headache, memory loss, drowsiness, often mistaken for dementia or stroke.
Increased risk for misdiagnosis due to vague symptoms and delayed onset.
Treatment: Evacuation and decompression, membranectomy.
Intracerebral Hematoma:
Location: Bleeding within the brain tissue itself.
Common Locations: Usually within the frontal and temporal lobes.
Outcome: Size and location of the hematoma determine patient outcome; surgical removal is often difficult due to location.
Diagnostic Studies for Head Injury
CT scan: The best diagnostic test to determine craniocerebral trauma due to its speed and ability to identify acute bleeds, fractures, and edema.
MRI, PET, Evoked Potential Studies: Provide more detailed information on brain tissue, metabolism, and functional integrity.
Transcranial Doppler Studies: Assess cerebral blood flow velocity.
Cervical Spine X-ray: Essential to rule out associated cervical spine injury (as it often accompanies head trauma).
Nursing Assessment: Glasgow Coma Scale (GCS), assessing and monitoring neurological status frequently, assessing for CSF leak.
ICP Monitoring: Essential for patients with severe TBI.
Interprofessional Care - Emergency Care for Head Injury
Immediate Priorities:
Patent airway: Crucial for oxygenation and CO_2 removal.
Stabilize cervical spine: Assume neck injury until proven otherwise (use cervical collar, logroll).
Oxygen administration: To maintain adequate PO_2. A non-rebreather mask is common.
IV access: Two large-bore IVs for fluid administration (e.g., normal saline or hypertonic saline).
Intubation: If GCS is <8 (indicating inability to protect airway).
Control external bleeding: Apply direct pressure.
Remove patient's clothing: To assess for other injuries.
Maintain patient warmth: Prevent hypothermia.
Ongoing monitoring: Frequent neurological assessments, vital signs.
Administer fluids cautiously: Avoid fluid overload which can worsen cerebral edema.
Treatment Principles for Head Injury
Prevent secondary injury: Focus on managing ICP, maintaining CPP, and preventing hypoxia/hypotension.
Timely diagnosis: Critical for appropriate intervention.
Surgery: If necessary, depending on the type and severity of injury.
Concussion and contusion: Usually observation and management of ICP for contusions.
Skull fractures: Conservative treatment for linear, surgery if depressed (to elevate bone fragments and débride tissue).
Subdural and epidural hematomas: Surgical evacuation (craniotomy, burr-holes are often initial emergency access) or craniectomy in cases of extreme swelling (to allow brain expansion and reduce pressure).
Nursing Assessment for Head Injury
Subjective Data
Past Medical History: Mechanism of injury is crucial, any prior head injuries, existing medical conditions.
Medications: Especially anticoagulants, which increase the risk of hemorrhage.
Substance Use: Alcohol/drug use, risk-taking behaviors (impacts judgment, increases injury risk).
Symptoms: Headache, mood or behavioral changes, mentation changes (difficulty concentrating, impaired judgment), aphasia, dysphasia.
Emotional Responses: Fear, denial, anger, aggression, depression.
Objective Data
Altered Mental Status: From confusion to coma.
Scalp/Facial Injuries: Lacerations, contusions, abrasions, hematoma, Battle's sign, periorbital edema and ecchymosis (Raccoon eyes).
CSF Leaks: Otorrhea, rhinorrhea, exposed brain (with open fractures).
Neurological Deficits:
Impaired gag reflex.
Altered/irregular respirations (e.g., Cheyne-Stokes, central neurogenic hyperventilation).
Cushing’s triad.
Vomiting.
Bowel and bladder incontinence.
Peculiar behaviors (e.g., uninhibited sexual expression).
Seizures.
Pupil dysfunction (size, shape, reactivity).
Cranial nerve deficits (e.g., facial palsy, visual disturbances).
Motor deficits: Hemiparesis, hemiplegia, palmar drift, paralysis, spasticity, posturing (decortication, decerebration), rigidity or flaccidity, ataxia.
Diagnostic Findings: Abnormal CT scan or MRI, abnormal EEG, positive toxicology screen or alcohol level, increased or decreased blood glucose level, increased ICP.
Nursing Diagnoses and Goals for Head Injury
Nursing Diagnoses:
Risk for ineffective cerebral tissue perfusion.
Hyperthermia.
Impaired physical mobility.
Anxiety.
Potential complication: increased ICP.
Overall Goals:
Maintain cerebral oxygenation and perfusion.
Achieve normothermic status.
Control pain and discomfort.
Remain free of infection.
Achieve adequate nutrition.
Regain maximal cognitive, motor, and sensory function.
Nursing Implementation for Head Injury
Health Promotion
Prevention of Accidents: Promote safe driving practices (wear seat belts), wear safety helmets for sports and motorcycles, implement home safety measures to prevent falls (especially for older adults and children).
Acute Care
Maintain Cerebral Perfusion: Implement strategies to optimize ICP and CPP.
Prevent Secondary Cerebral Ischemia: Monitor for signs of worsening neurological status (e.g., changes in LOC, pupil changes, motor weakness).
Patient and Family Teaching: Provide ongoing education about the injury, treatment, and expected course.
Eye Problems: Due to periorbital edema or cranial nerve damage.
Eye drops to prevent corneal drying.
Compresses to reduce swelling.
Eye patch to protect the eye.
Hyperthermia: Common complication.
Goal temperature: 36^ ext{o} to 37^ ext{o} C (96.8^ ext{o} to 98.6^ ext{o} F).
Prevent shivering, which increases metabolic demand and can raise ICP.
Measures for Patients Leaking CSF:
Head of bed elevated to reduce pressure.
Loose collection pad under the nose (for rhinorrhea) or over the ear (for otorrhea) to absorb fluid and assess for halo sign.
NO sneezing or blowing nose to prevent increasing intracranial pressure.
NO NG tube placement (risk of entering the brain through the fracture).
NO nasotracheal suctioning (risk of introducing bacteria or catheter into brain).
Measures for Immobilized Patients:
Administer antiemetics (for vomiting), analgesics (for pain).
Provide pre-operative preparation, if surgery is needed.
Ambulatory Care (Rehabilitation)
Address Residual Deficits: Motor and sensory deficits, communication issues (aphasia, dysarthria), memory and intellectual functioning impairments.
Nutritional Support: Continue efforts to ensure adequate nutrition.
Bowel and Bladder Management: Strategies for incontinence or retention.
Seizure Disorders: Education and medication management for post-traumatic seizures.
Mental and Emotional Difficulties: Address anxiety, depression, personality changes, cognitive issues.
Progressive Recovery: Emphasize the long-term nature of recovery and the importance of continued therapy.
Family Participation and Education: Involve family in patient care and provide education on coping strategies and home modifications.
Nursing Evaluation for Head Injury
Expected Outcomes:
Maintain normal cerebral perfusion pressure.
Achieve maximal cognitive, motor, and sensory function possible.
Experience no infection or hyperthermia.
Seizures
Definition: Transient, uncontrolled electrical discharge of neurons in the brain, interrupting normal function.
May accompany other disorders or occur spontaneously without apparent cause.
Metabolic Disturbances Associated with Seizures (Not Considered Epilepsy if Reversible):
Acidosis
Electrolyte imbalances (e.g., hyponatremia, hypokalemia, hypomagnesemia)
Hypoglycemia
Hypoxemia
Alcohol or barbiturate withdrawal
Dehydration or water intoxication
Extracranial Disorders Associated with Seizures:
Hypertension
Systemic lupus erythematosus
Diabetes mellitus
Septicemia
Epilepsy
Definition: A disease with a continuing predisposition to seizures with neurobiologic, psychologic, and social consequences.
Affects 2.2 million Americans.
Etiology and Pathophysiology of Seizure Disorders
Causes Vary by Age:
First 6 months of life: Severe birth injury, congenital birth defects involving CNS, infections, inborn errors of metabolism.
Ages 2 to 20: Birth injury, infection, trauma, genetic factors.
Ages 20 and 30: Structural lesions (e.g., trauma, brain tumor, vascular disease).
After age 50: Stroke, metastatic brain tumors.
Idiopathic Generalized Epilepsy (IGE): About 1/3 of cases are idiopathic, meaning not attributable to a specific cause.
Abnormal Neurons: Undergo spontaneous firing, which spreads to adjacent or distant areas of the brain.
Cause of abnormal firing is unclear. Locating the seizure focus is critical for successful surgical intervention.
Gliosis (Scar Tissue): Often found in the area of the brain where seizure activity arises.
Thought to interfere with the normal chemical and structural environment of neurons, making them more likely to fire abnormally.
Role of Astrocytes: Changes in the function of astrocytes (glial cells) may play several key roles in recurring seizures.
Activation of astrocytes by hyperactive neurons is one of the crucial factors that predisposes nearby neurons to generate an epileptic discharge.
Genetic Link:
Genetic abnormalities may be the most important factor contributing to IGE.
Some types of epilepsy run in families, and other types of IGE are related to abnormalities in specific genes.
Difficult to determine the exact role of genetics due to the problem of separating genetic from environmental or acquired influences.
Clinical Manifestations of Seizures
Classification: Determined by the site of the electrical disturbance.
Two major classes: Generalized and Focal seizures.
Phases of a Seizure:
Prodromal phase: Sensations or behavior changes preceding a seizure (e.g., aura, mood changes) by hours or days.
Aural phase: A sensory warning that is part of the seizure (e.g., visual disturbances, dizziness, metallic taste).
Ictal phase: The actual seizure episode, from the first symptom to the end of seizure activity.
Postictal phase: The period of recovery following a seizure, characterized by changes in LOC, fatigue, muscle soreness.
Generalized Seizures
Affect both sides of the brain simultaneously. Consciousness is lost or impaired.
Tonic-Clonic Seizures (Grand Mal):
Characterized by loss of consciousness and falling.
Tonic phase: Body stiffens suddenly (often with a cry).
Clonic phase: Subsequent jerking of extremities.
Associated signs: Cyanosis, excessive salivation, tongue or cheek biting (risk of injury).
Postictal phase: Muscle soreness, fatigue, may sleep for hours, may not feel normal for hours to days, usually no memory of the seizure.
Typical Absence Seizures (Petit Mal):
Typical symptom is a staring spell, often described as “daydreaming.”
Lasts only a few seconds.
Often goes unnoticed, may occur up to 100 times/day when untreated.
EEG demonstrates a unique 3 Hz spike-and-wave pattern.
Usually occurs only in children and rarely beyond adolescence; may cease as the child matures or develop into another type of seizure.
Can be precipitated by flashing lights and hyperventilation.
Atypical Absence Seizures:
Characterized by a staring spell with other manifestations (e.g., eye blinking, jerking movements of the lips).
Lasts more than 10 seconds, usually continues into adulthood.
Myoclonic Seizure:
Characterized by sudden, excessive jerk or twitch of the body and extremities.
Can be forceful enough to cause a fall.
Brief (milliseconds).
May occur in clusters.
Atonic Seizure (Drop Attack):
Involves a tonic episode or paroxysmal loss of muscle tone (sudden-onset).
Person falls suddenly.
Typically lasts less than 15 seconds.
Person usually remains conscious.
Can resume normal activity immediately afterward.
Great risk for head injury.
Tonic Seizures:
Involve sudden onset of maintained increased tone in the extensor muscles (stiffening).
Often occur in sleep.
Affect both sides of the body.
Usually last less than 20 seconds.
Consciousness is usually preserved.
Clonic Seizures:
Begin with loss of consciousness and sudden loss of muscle tone.
Followed by rhythmic limb jerking that may or may not be symmetric.
Relatively rare.
Focal Seizures (Partial or Partial Focal Seizures)
Begin in a specific region of the cortex (one hemisphere of the brain).
Produce manifestations based on the function of the area of the brain involved.
Divided into:
Simple Focal Seizures:
Person remains conscious and alert.
Experiences unusual feelings or sensations (e.g., sudden joy, anger, sadness, nausea; or sensory phenomena: hearing, smelling, tasting, seeing, or feeling things that are not real).
Complex Focal Seizures:
Patients have loss of consciousness or alteration in awareness.
Eyes may remain open but cannot interact with the environment.
May display strange, repetitive, purposeless behaviors called automatisms (e.g., lip-smacking, picking at clothes, fumbling).
Do not remember an activity started before or continued during the seizure.
Secondary Generalized Seizure: Any tonic-clonic seizure preceded by an aura or warning is actually a focal seizure that secondarily generalizes.
May result in transient residual neurological deficit postictally, known as Todd’s paralysis (temporary weakness or paralysis on one side of the body).
Psychogenic Seizures (Pseudo-seizures):
Can be misdiagnosed as epilepsy.
Often have a history of emotional or physical abuse or a specific traumatic event.
Accurate diagnosis usually requires video-EEG monitoring to differentiate from true epileptic seizures.
Complications of Seizures
Status Epilepticus (SE):
A state of continuous seizure activity or a condition when seizures recur in rapid succession without return to consciousness between seizures.
Any seizure lasting >5 minutes should be considered SE.
Neurologic Emergency: Can occur with any type of seizure.
Causes the brain to use more energy than is supplied, leading to neurons becoming exhausted and ceasing to function; permanent brain damage can result.
Convulsive Status Epilepticus (Most Dangerous):
Can cause ventilatory insufficiency, hypoxemia, cardiac dysrhythmias, hyperthermia, and systemic acidosis.
Can be fatal.
Subclinical Seizures: Seizures that are not externally observable (e.g., subtle changes in LOC or continuous EEG discharge).
Injury and Death:
Severe injury and death can result from trauma during a seizure.
Patients who lose consciousness are at greatest risk.
Persons with epilepsy have a mortality rate 2-3 times the rate of the general population.
SUDEP (Sudden Unexpected Death in Epilepsy): A rare but serious complication, the cause of which is not fully understood.
Effect on Lifestyle (Most Common Complication):
Depression (common due to chronic illness).
Social stigma still exists.
Discrimination in employment and education.
Driving sanctions (loss of driver's license can impact independence).
Diagnostic Studies of Seizures
History: Accurate, comprehensive description of seizures (onset, duration, frequency, characteristics) and health history is crucial.
EEG (Electroencephalogram):
May help determine the type of seizure and pinpoint the seizure focus.
Important Note: Many patients do not have abnormal findings on a single EEG, especially if not conducted during a seizure.
Magnetoencephalography (MEG): Used in conjunction with EEG, provides greater sensitivity for detecting small magnetic fields generated by neuronal activity.
Blood Tests: CBC, serum chemistries, liver and kidney function tests, UA (urinalysis) to rule out metabolic disorders, glucose levels, electrolyte levels.
Imaging:
CT or MRI: For new-onset seizures, to rule out structural lesions (tumors, stroke, trauma).
Cerebral angiography, SPECT (Single-Photon Emission CT), MRS (Magnetic Resonance Spectroscopy), MRA (Magnetic Resonance Angiography), and PET: Used in selected situations for more detailed information, especially for surgical candidates.
Treatment: Diagnosing the seizure type is necessary to determine appropriate treatment.
Interprofessional Care for Seizures
Emergency Care: Most seizures do not require emergency medical care because they are self-limiting.
Immediate medical care is needed if:
Status epilepticus (SE) occurs.
Significant bodily harm occurs during a seizure.
The event is a first-time seizure.
Antiseizure Drug Therapy (AEDs):
Primary Treatment: Goal is preventing seizures with minimum toxic side effects from drugs.
Cure is not possible with AEDs, but control is achievable for many.
Mechanism: Drugs act by stabilizing nerve cell membranes and preventing the spread of the epileptic discharge.
Regimens: About 1/3 of patients require a combination regimen for adequate control.
Therapeutic Drug Ranges: Serve as guides for dosing; newer drugs may not require routine drug levels.
Patient Education: Emphasize importance of following the specific drug regimen regularly and continuously (often for a lifetime) and what to do if a dose is missed.
Drug Therapy for Seizure Disorders
Primary Drugs for Generalized Tonic-Clonic and Focal Seizures:
Phenytoin (Dilantin)
Carbamazepine (Tegretol)
Phenobarbital (Luminal)
Divalproex (Depakote)
Primidone (Mysoline)
Primary Drugs for Absence and Myoclonic Seizures:
Ethosuximide (Zarontin)
Divalproex (Depakote)
Clonazepam (Klonopin)
Broad-Spectrum Drugs (Effective for Multiple Seizure Types):
Gabapentin (Neurontin)
Topiramate (Topamax)
Lamotrigine (Lamictal)
Tiagabine (Gabitril)
Levetiracetam (Keppra)
Zonisamide (Zonegran)
Additional Treatment for Focal Seizures (Not Successfully Controlled with a Single Medication):
Pregabalin (Lyrica)
Status Epilepticus Treatment:
Initially, rapid-acting IV lorazepam (Ativan) or diazepam (Valium) to stop the seizure.
Followed by long-acting drugs (e.g., phenytoin, fosphenytoin, levetiracetam) once the acute seizure is controlled.
Drug Administration Considerations:
Many antiseizure drugs have a long half-life, allowing for once or twice daily dosing (improves compliance).
A simplified drug regimen can increase medication compliance.
Medications should be routinely reviewed and adjusted as needed.
Crucial Rule: Antiseizure drugs should not be discontinued abruptly, as this can precipitate seizures.
Common Side Effects: Involve the CNS and include diplopia (double vision), drowsiness, ataxia (impaired coordination), and mental slowing.
Neurologic Assessment for Toxicity: Regularly assess for:
Nystagmus (involuntary eye movements).
Hand and gait coordination.
Cognitive functioning.
General alertness.
Noncompliance: A significant concern contributing to treatment failure.
Gerontologic Considerations:
Many older adults experience a first single seizure (must be recurring for AED therapy).
More responsive to antiseizure drugs, but also more likely to experience side effects at lower doses.
Phenytoin may be problematic for older adults with compromised liver function.
Phenobarbital, Tegretol (carbamazepine), and Mysoline (primidone) can negatively affect cognitive function.
Newer antiseizure medications (e.g., gabapentin, lamotrigine, oxcarbazepine, levetiracetam) may be safer for older adults due to fewer effects on cognitive function and less drug interactions.
Alternative Treatments for Epilepsy (Medically Refractory)
Surgery: An option for many with uncontrolled epilepsy (especially focal seizures).
Anterior temporal lobe resection: About 70\%-80\% are seizure-free after this procedure, and 10\%-20\% have a marked reduction in seizure activity.
Vagal Nerve Stimulation (VNS):
Adjunct to medications when surgery is not feasible.
Exact mechanism is not entirely known; thought to interrupt synchronization of epileptic brain-wave activity and stop excessive discharge of neurons.
Ketogenic Diet:
Has been effective in controlling seizures in some patients, especially children.
High-fat, low-carbohydrate diet, which causes ketones to pass into the brain and replace glucose as an energy source.
Biofeedback: Teaches patients to maintain a certain brain wave frequency, aiming to gain control over seizure activity.
Nursing Assessment for Seizures
Health History
Risk Factors: Birth defects or injuries at birth, anoxic episodes, CNS trauma or infections, stroke, metabolic disorders, alcoholism, exposure to metals or carbon monoxide, hepatic or renal failure.
Medication Compliance: History of compliance with antiseizure medications, or history of barbiturate or alcohol withdrawal, cocaine/amphetamines use.
Pre-seizure Symptoms: Headaches, aura, mood or behavioral changes before seizure.
Psychosocial Factors: Anxiety, depression, loss of self-esteem, social isolation, decreased sexual drive, erectile dysfunction (impact of chronic illness).
Precipitating Factors
Metabolic acidosis or alkalosis, hyperkalemia, hypoglycemia, dehydration, water intoxication.
Objective Data (During and After Seizure)
Physical Signs: Bitten tongue, soft tissue damage, cyanosis.
Respiratory: Abnormal respiratory rate, apnea (ictal), absent or abnormal breath sounds, airway occlusion.
Cardiovascular: Hypertension, tachy/bradycardia.
Incontinence: Bowel/urinary incontinence, excessive salivation.
Postictal Neurological Deficits: Weakness, paralysis, ataxia.
Diagnostic Findings: Abnormal CT, MRI, EEG.
Clinical Manifestations by Seizure Type (Observed)
Tonic-Clonic: Loss of consciousness, muscle tightening (tonic) then jerking (clonic), dilated pupils, hyperventilation then apnea, postictal somnolence.
Absence: Altered consciousness (staring spell), minor facial motor activity.
Simple Focal: Aura, focal sensory, motor, cognitive, or emotional phenomena, unilateral “marching” motor seizure.
Complex Focal: Altered consciousness with inappropriate behaviors (automatisms), amnesia of the event.
Nursing Planning and Goals for Seizures
Overall Goals:
Patient will be free from injury during a seizure.
Patient will have optimal mental and physical functioning while taking antiseizure medications.
Patient will achieve satisfactory psychosocial functioning.
Nursing Implementation for Seizures
Health Promotion
Safety Measures: Wear a helmet if at risk for head injury, promote general health habits (diet, exercise).
Trigger Avoidance: Assist patients to identify events or situations precipitating seizures and avoid them if possible.
Lifestyle Modifications: Instruct to avoid excessive alcohol, fatigue, and loss of sleep (common triggers).
Acute Care (During and Immediately After a Seizure)
Observe, Treat, and Document Seizure: Detailed description of the event is crucial.
Safety Interventions:
Maintain a patent airway.
Support the head.
Turn the patient to their side (to prevent aspiration).
Loosen constrictive clothing.
Ease the patient to the floor if seated or standing.
DO NOT restrain the patient.
DO NOT place any objects in their mouth.
Post-Seizure Care: May require positioning, suctioning (if secretions present), or oxygen after the seizure.
Rescue Medication: May require rescue medication (e.g., IV lorazepam or diazepam) to break a prolonged seizure.
Ambulatory Care (Rehabilitation for Seizures)
Address Residual Issues: Motor and sensory deficits, communication issues, memory, and intellectual functioning.
Holistic Management: Nutrition, bowel and bladder management, management of seizure disorders, and mental and emotional difficulties.
Recovery and Support: Progressive recovery with family participation and education.