NRSG 3420 Adult Health 2
M ODU L E 3 R E V IEW
S U M M ER 2 0 2 3
P ROF. JA M ES
Neurological
Conditions
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Decorticate Posturing
Decerebrate Posturing
ICP and CPP
CPP (cerebral perfusion pressure) is closely linked to ICP
CPP = MAP (mean arterial pressure) – ICP
Normal CPP is 60 to 80
ICP & CPP
A CPP of less than 50 results in permanent neurologic damage
Example: MAP is 62 and ICP is 7, CPP = 55 (62-7). With a CPP of 55 is
dangerous and results in immediate action. Focus on prioritizing
interventions that increase CPP
Cerebral Perfusion Pressure (CPP)
Maintaining an adequate cerebral perfusion pressure is achieved by lowering the intracranial
pressure and supporting the mean arterial blood pressure through fluid resuscitation and directacting vasoconstrictors.
If ICP is increased, elevate head of bed 30 to 45 degrees to promote venous outflow from brain
and help reduce pressure.
Avoid measures that may trigger increased ICP such as coughing, vomiting, straining at stool,
neck in flexion, head flat, or bearing down which further reduce cerebral blood flow.
Increased
Intracranial
Pressure
Monro–Kellie hypothesis: because of limited space in the skull,
an increase in any one of components of the skull (brain tissue,
blood, CSF) will cause a change in the volume of the others
Compensation to maintain a normal ICP of 10 to 20 mm Hg is
normally accomplished by shifting or displacing CSF
ICP > 20 mmHg requires intervention
With disease or injury, ICP may increase
Increased ICP decreases cerebral perfusion & causes ischemia,
cell death, & (further) edema
Brain tissues may shift through the dura & result in herniation
Autoregulation: refers to the brain’s ability to change the
diameter of blood vessels to maintain cerebral blood flow
CO2 plays a role; decreased CO2 results in vasoconstriction, &
increased CO2 results in vasodilatation
Lumbar punctures contraindicated
Manifestations of Increased ICP
EARLY
LATE
Changes in LOC
Respiratory & vasomotor changes
Any change in condition
VS: Increase in SBP, widening of pulse pressure, & slowing of the
HR; pulse may fluctuate rapidly from tachycardia to bradycardia;
temperature increase
◦ Restlessness, disorientation/confusion, increasing drowsiness,
increased respiratory effort, purposeless movements
Pupillary changes & impaired ocular movements
Cushing triad: bradycardia, HTN, bradypnea
Weakness in one extremity or one side
Projectile vomiting
Headache: constant, increasing in intensity, or aggravated by
movement or straining
Further deterioration of LOC; lethargy & stupor to coma (serious
impairment)
Hemiplegia, decortication, decerebration, or flaccidity
Respiratory pattern alterations including Cheyne–Stokes breathing
& arrest, crackles in bases
Loss of brainstem reflexes: pupil, gag, corneal, & swallowing
Nursing Interventions for ICP
Elevating the head
of the bed to thirty
degrees
Keeping the neck in
a neutral position
Maintaining a
normal body
temperature
Preventing volume
overload/fluid
balance
Administer
benzodiazepines
PRN
Encourage patient
to exhale during
repositioning
Pathophysiology of Brain Damage
Primary injury:
• Consequence of direct contact
to head/brain during the instant
of initial injury
• Contusions, lacerations,
external hematomas, skull
fractures, subdural hematomas,
concussion, diffuse axonal
Secondary injury:
• Damage evolves over ensuing
days & hours after the initial
injury
• Caused by cerebral edema,
ischemia, or chemical changes
associated with the trauma
Subdural, Intracerebral, & Epidural
Hemorrhages
Blood collection in the space between the skull & the dura
Patient may have a brief loss of consciousness with return of
lucid state; then as hematoma expands, increased ICP will
often suddenly reduce LOC
Epidural
Hematoma
An emergency situation!
Treatment includes measures to reduce ICP, remove the clot,
& stop bleeding (burr holes or craniotomy)
Patient will need monitoring & support of vital body
functions; respiratory support
Collection of blood between the dura & the brain
Acute or subacute
Subdural
Hematoma
◦ Acute: symptoms develop over 24 to 48 hours
◦ Subacute: symptoms develop over 48 hours to 2 weeks
◦ Requires immediate craniotomy & control of ICP
Chronic
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Develops over weeks to months
Causative injury may be minor & forgotten
Clinical signs & symptoms may fluctuate
Treatment is evacuation of the clot
Hemorrhage occurs into the substance of the brain
May be caused by trauma or a nontraumatic cause
Intracerebral
Hemorrhage
Treatment
◦ Supportive care
◦ Control of ICP
◦ Administration of fluids, electrolytes, & antihypertensive
medications
◦ Craniotomy or craniectomy to remove clot & control
hemorrhage; this may not be possible because of the location or
lack of circumscribed area of hemorrhage
Diagnostic Evaluation
Physical & neurologic exam
Skull & spinal radiography
CT scan
MRI
PET
Spinal Cord Injury
GOALS
NURSING DIAGNOSIS
Maximize respiratory function
Risk for Ineffective Breathing Pattern
Prevent injury to the spinal cord
Impaired Physical Mobility
Promote mobility and/or independence – ROM early to
prevent contractures
Disturbed Sensory Perception
Prevent or minimize complications
Support psychological adjustment of patient and/or SO
Provide information about the injury, prognosis, and
treatment
Acute Pain
Anticipatory Grieving
Constipation
Impaired Urinary Elimination
Risk for Autonomic Dysreflexia
Risk for Impaired Skin Integrity
Spinal Cord Injury
294,000 persons in the United States live with disability from SCI
Causes include MVAs, falls, violence (gunshot wounds), and sports-related injuries
Males account for 78% of SCIs
Average age of injury is 43
Risk factors include young age, male gender, alcohol and drug use
Major causes of death are pneumonia, pulmonary embolism (PE), and sepsis
Pathophysiology of SCI:
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Result of concussion, contusion, laceration, or compression of spinal cord
Primary injury is the result of the initial trauma and usually permanent
Secondary injury resulting from SCI include edema and hemorrhage
Major concern for critical care nurses
Treatment is needed to prevent partial injury from developing into more extensive, permanent damage
Spinal and Neurogenic Shock
Spinal shock
◦ A sudden depression of reflex activity below the level of spinal injury
◦ Muscular flaccidity, lack of sensation and reflexes (flaccid = does not respond to stimuli)
Neurogenic shock
◦ Caused by the loss of function of the autonomic nervous system
◦ Blood pressure, heart rate, and cardiac output decrease
◦ Venous pooling occurs because of peripheral vasodilation
◦ Paralyzed portions of the body do not perspire
Care of the Patient with SCI
ASSESSMENT
PLANNING
Monitor respirations and breathing pattern
Major goals may include:
◦ Improved breathing pattern and airway clearance
◦ Improved mobility
◦ Prevention of injury due to sensory impairment
◦ Maintenance of skin integrity
◦ Relief of urinary retention
◦ Improved bowel function
◦ Decreasing pain
◦ Recognition of autonomic dysreflexia and absence
of complications
◦ Prevention of DVT
Lung sounds and cough
Monitor for changes in motor or sensory function;
report immediately
Assess for spinal shock
Monitor for bladder retention or distention, gastric
dilation, and ileus
Temperature; potential hyperthermia
Monitor for orthostatic hypotension
SCI Nursing Interventions
Promoting effective breathing and airway clearance
◦ Monitor carefully to detect potential respiratory failure
◦ Pulse Ox and ABGs, Lung sounds
◦ Early and vigorous pulmonary care to prevent and remove
secretions
◦ Suctioning with caution
◦ Breathing exercises
◦ Assisted coughing
◦ Humidification and hydration
Improving mobility
◦ Maintain proper body alignment
◦ If not on a specialized rotating bed, turn only if spine is
stable and as indicated by physician
◦ Monitor blood pressure with position changes
◦ PROM at least four times a day
◦ Use neck brace or collar, as prescribed, when patient is
mobilized
◦ Move gradually to erect position
Strategies to compensate for sensory and perceptual
alterations
Measures to maintain skin integrity
Temporary indwelling catheterization or intermittent
catheterization
NG tube to alleviate gastric distention
High-calorie, high-protein, high-fiber diet
Bowel program and use of stool softeners
Traction pin care
Hygiene and skin care related to traction devices
Autonomic
Dysreflexia
Acute emergency!
Occurs after spinal shock has resolved and may occur years
after the injury
Occurs in persons with SC lesions above T6
Autonomic nervous system responses are exaggerated
Symptoms include severe pounding headache, sudden
increase in blood pressure, profuse diaphoresis, nausea,
nasal congestion, red blotches below level of injury,
cold/clammy skin below level of injury, and bradycardia
Triggering stimuli include distended bladder (most common
cause), distention or contraction of visceral organs (e.g.,
constipation), or stimulation of the skin
Nursing Interventions for
Autonomic Dysreflexia
Place patient in seated position to lower BP
Rapid assessment to identify and eliminate cause
◦ Empty the bladder using a urinary catheter or irrigate or change indwelling catheter
◦ Examine rectum for fecal mass
◦ Examine skin
◦ Examine for any other stimulus
Administer ganglionic blocking agent such as hydralazine hydrochloride (Apresoline) IV
Label chart or medical record that patient is at risk for autonomic dysreflexia
Instruct patient in prevention and management
Seizures
Abnormal episodes of motor, sensory,
autonomic, or psychic activity (or a combination
of these) resulting from a sudden, abnormal,
uncontrolled electrical discharge from cerebral
neurons
Classification of seizures
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Focal: originates in one hemisphere
Generalized: occur and engage bilaterally
Unknown: epilepsy spasms
“Provoked” related to acute, reversible condition
Specific Causes of Seizures
Cerebrovascular
disease
Hypoxemia
Fever
(childhood)
Head injury
Hypertension
Central nervous
system
infections
Metabolic and
toxic conditions
Brain tumor
Drug and
alcohol
withdrawal
Allergies
Observation and documentation of
patient signs and symptoms before,
during, and after seizure
Plan of Care for
a Patient
Experiencing a
Seizure
Nursing actions during seizure for
patient safety and protection
After seizure care to prevent
complications
Scalp Wounds and
Skull Fractures
Manifestations depend on the severity and
location of the injury
Scalp wounds
◦ Tend to bleed heavily and are portals for infection
Skull fractures
◦ Usually have localized, persistent pain
◦ Fractures of the base of the skull
◦ Bleeding from nose pharynx or ears
◦ Battle sign—ecchymosis behind the ear
◦ CSF leak: halo sign—ring of fluid around the blood stain from
drainage
Other Neurologic Impacts
Decreased or altered mental status due to chemical or medication
overdose
◦ Priority is ABC
◦ if patient is nonresponsive, but has a HR, then securing the
patient’s airway is #1
◦ If patient is nonresponsive and no pulse (which means they are
not breathing either) then starting CPR is #1