Intracranial Regulation
Chapters 38, 39, & 41
OBJECTIVES
Define and describe the concept of intracranial regulation.
Notice risk factors that place individuals at risk for intracranial regulation problems.
Recognize when an individual has problems with intracranial regulation.
Provide appropriate nursing and collaborative interventions to optimize intracranial regulation.
ANATOMY OF THE SKULL
Parietal bone
Squamous suture
Occipital bone
Temporal bone (squamous portion)
Mastoid process of temporal bone
External auditory meatus
Styloid process
Condyloid process
Pterygoid process
Coronoid process
Frontal bone
Frontal lobe (emotion, cognition, behavior)
Sphenoid bone
Temporal lobe (hearing, learning, feelings)
Nasal bone
Malar (zygomatic) bone
Maxilla
Mandible
Brainstem (breathing, heart rate, temperature)
Parietal lobe (language, touch)
Occipital lobe (sight)
Cerebellum (balance, coordination)
INTRACRANIAL PRESSURE (ICP)
Defined by three components:
Brain Tissue
Blood
Cerebral Spinal Fluid (CSF)
Normal ICP: 10-15 mmHg
Abnormal ICP:
If ICP > 20 mmHg, requires immediate treatment.
CEREBROSPINAL FLUID (CSF)
Functions:
Shock absorber
Nutrient delivery (primarily glucose)
Formed in the ventricles.
Composition: Similar to plasma but minus proteins.
Implications of glucose levels:
Hypoglycemia: Can lead to widespread neuronal injury.
Hyperglycemia: Can worsen ischemia/injury, increase blood-brain barrier permeability.
CEREBRAL BLOOD FLOW (CBF)
Normal CBF rate: 750 mL/min or 15-20% of cardiac output.
Cerebral Perfusion Pressure (CPP):
Formula: ext{CPP} = ext{MAP} - ext{ICP}
CPP indicates the blood pressure required for brain perfusion.
A CPP of 70 mmHg is generally accepted as optimal.
If CPP < 60 mmHg, cerebral blood flow is compromised.
If CPP > 70 mmHg, indicates increased intracranial pressure.
MAP Calculation:
Formula: ext{MAP} = rac{(2 imes ext{Diastolic BP}) + ext{Systolic BP}}{3}
THE CONCEPT OF INTRACRANIAL REGULATION
Normal state: Expected intracranial regulation.
Impaired state: Issues arise impacting normal function.
AUTOREGULATION
Volume considerations:
Fixed volume within the skull; any change in one component necessitates a change in another (Monro-Kellie doctrine).
Normal state: ICP normal, generally at 75 mL.
Compensated state: ICP remains normal despite changes in individual component volumes.
Decompensated state: ICP elevated when autoregulation fails.
MONRO-KELLIE HYPOTHESIS
The hypothesis states that:
The sum of the intracranial volumes (blood, brain, CSF) is constant.
The skull is an enclosed, inelastic container.
An increase in one component's volume must be offset by decreases in others or will result in an increase in ICP.
Adaptation of blood and CSF volumes allows for some compensatory responses.
Once compensatory mechanisms are exhausted, increased volumes lead to significant rises in ICP.
INTRACRANIAL REGULATION MECHANISMS
Perfusion issues: Must ensure continued blood supply.
Potential problems include blockage, hypotension, loss of vessel integrity, or hydrocephalus (impaired CSF reabsorption or outflow).
Neurotransmission requirements: Optimal functioning depends on intact neuronal mechanisms.
Issues can arise from drugs, toxins, or seizures.
Pathological conditions: Tumors, degenerative diseases, and inflammatory processes disrupt brain function and regulation.
FACTORS AFFECTING ICP
Anything that increases intra-abdominal or thoracic pressure can increase ICP, such as:
Vomiting
Bearing down
Other influences on ICP fluctuations include:
Body temperature
Body position
Carbon Dioxide (CO2) and Oxygen (O2) levels
Arterial and venous pressures.
Widened pulse pressure is indicative of increased ICP.
If concerning signs arise (dropping pulse, widening pulse pressure, respiratory irregularities), notify the provider or rapid response team.
ASSESSMENT OF NEUROLOGICAL STATUS
Conduct the following tests:
Mental status testing
Cranial nerve testing
Glasgow Coma Scale (GCS)
National Institutes of Health Stroke Scale (NIHSS)
Monitor pupil responses for dilation (one or both sides).
Assess for abnormal posturing:
Decorticate posturing: arms toward body.
Decerebrate posturing: arms away from body (more ominous).
Monitor ICP levels and notify MD for any abnormalities or changes.
SYMPTOMS OF INCREASED ICP
Symptoms include:
Headache
Nausea
Vomiting
Increased blood pressure
Decreased mental abilities and confusion (time, location, people)
Double vision
Non-responsive pupils to light changes (one or both sides).
INDICATORS OF INCREASED ICP
Changes in LOC (Level of Consciousness):
Eyes/ Pupillary changes
Papilledema
Impaired eye movement
Various forms of posturing (specifically, decerebrate and decorticate).
Changes in speech
Infants:
Bulging fontanels
Increased head circumference
High-pitched cry.
POSTURING TYPES
Decorticate Posturing:
Characteristics:
Rigid, extended legs
Pointed and turned-in toes
Arms bent toward the center, curled wrists, and balled hands against the chest.
Decerebrate Posturing:
Characteristics:
Rigid, extended legs
Pointed and turned-in toes
Arms straight, tense wrists.
GLASGOW COMA SCALE
Behavior Response Assessment:
Eye Opening Response:
Spontaneously (4)
To speech (3)
To pain (2)
No response (1)
Best Verbal Response:
Oriented (5)
Confused (4)
Inappropriate words (3)
Incomprehensible sounds (2)
No response (1)
Best Motor Response:
Obeys commands (6)
Moves to localized pain (5)
Flexion withdrawal from pain (4)
Abnormal flexion (decorticate) (3)
Abnormal extension (decerebrate) (2)
No response (1)
Total Score:
Best response possible is 15.
Comatose < 8, unresponsive < 3.
ICP MONITORING METHODS
Types of ICP monitoring devices:
Subarachnoid
Intraparenchymal
Epidural
Ventricular
Subdural
Infection control is critical during ICP monitoring:
Emphasize handwashing.
Fever signals potential infection increasing ICP.
ICP MONITORING FUNCTIONALITY
ICP devices can drain CSF and monitor pressures.
Nursing interventions can affect ICP positively or negatively; goal is to prevent secondary brain injury.
INTERVENTIONS TO LOWER ICP
P-POSITIONING: Maintain appropriate positioning.
R-RESPIRATORY: Prevent hypoxia or hypercapnia.
E-ELEVATED TEMP: Monitor and manage elevated temperatures.
S-SYSTEM TO MONITOR: Implement neurological assessments (GCS and others).
S-STRAINING ACTIVITIES: Avoid activities that can induce strain.
U-UNCONSCIOUS PATIENT CARE: Avoid oversedation; ensure skin and mouth care.
R-RX:
Barbiturates to decrease metabolism
Use vasopressors to maintain SBP (at least 150 mmHg, not exceeding).
Administer anticonvulsants if necessary.
E-EDEMA MANAGEMENT: Use mannitol to draw water into blood.
Monitor for fluid and electrolyte depletion from treatment.
COMMON DIAGNOSTIC METHODS
Neuroimaging Techniques:
Magnetic Resonance Imaging (MRI)
Computed Tomography (CT) Scan
Skull Radiograph
Electroencephalogram (EEG)
Brain Biopsy
Lumbar Puncture
MANAGEMENT STRATEGIES
Treatment strategies depend on underlying conditions, focusing on:**
Preventing secondary brain injury.
Improving/maintaining cerebral perfusion by:
Reducing cerebral edema
Reducing ICP
Minimizing risk of brain herniation.
Increased ICP can be associated with brain tumors; implement precautions against potential seizures (e.g., antiepileptic medications).
CUSHING’S TRIAD
Key Indicators of Increased ICP:
Increased Systolic BP with widened pulse pressure
Decreased Heart Rate
Irregular/slower respirations
Represents a terminal response by the body to maintain brain perfusion, often indicative of impending death.
AUTOREGULATION FAILURE
Injured Brain: Treat hypotension quickly to ensure adequate blood flow.
If MAP decreases and ICP increases, cerebral perfusion pressure ceases when MAP equals ICP, leading to death.
Watch for signs of hypernatremia in post-craniotomy patients; prioritize serum sodium level assessment.
BRAIN DEATH CRITERIA
Patient must meet four criteria:
Coma from a known cause.
Normal or near-normal core temperature.
Normal systolic blood pressure.
At least one neurologic examination.
SEIZURES
Definition: Seizure is an uncontrolled electrical discharge of neurons resulting in changes in:
Level of consciousness
Motor or sensory ability
Behavior
Types of Seizures:
Generalized (tonic-clonic, myoclonic, atonic)
Partial (complex partial, simple partial)
Idiopathic and Secondary.
Potential Causes of Seizures:
Traumatic brain injury
Metabolic disorders
Acute alcohol withdrawal
Electrolyte disturbances
Heart disease
High fever
Stroke
Substance abuse.
SEIZURE PRECAUTIONS
Ensure availability of the following:
Oxygen
Suction equipment
Airway management tools
IV access
Ensure side rails are up for safety
Protect the patient from injury during seizures.
SEIZURE MANAGEMENT
Varies by type of seizure; includes:
Observation and documentation
Maintain patient safety (side-lying position and no restraints)
Avoid putting anything in the patient’s mouth.
Vagus Nerve Stimulation (VNS):
A surgical intervention involving tunneling the device under the skin.
Complications can include hoarseness, dysphasia, neck pain, and dyspnea.
ACUTE SEIZURE MANAGEMENT
Medications Used:
Lorazepam (Ativan)
Diazepam (Valium)
Phenytoin (Dilantin)
Chart 39.2 lists common examples of drug therapy.
Evaluate recent blood levels of the medications as required.
Be cognizant of drug-drug and drug-food interactions.
Ensure maintenance of therapeutic blood levels for efficacy and report side/adverse effects.
PATIENT AND FAMILY EDUCATION
Focus on independence and compliance with anticonvulsants (AEDs).
Introduction of social service resources to assist with medication costs.
Evaluate employment safety to reduce seizure risks.
Vocational rehabilitation may receive subsidies.
Important Teaching Points:
Do not stop medications when seizure control is reached.
Do not cease medication due to side effects (e.g., nausea).
Discuss pregnancy planning with healthcare provider before making changes to medications.