ICP & Acute Head Injury

- ICP
o Skull has 3 essential components:
 Brain tissue
 Blood
 Cerebrospinal fluid (CSF)
- Components of the Brain:
o Cerebrum: heavy thinking
o medulla, pons, brain stem = midbrain (early brain development) = CNS,
basic center of control
o Cerebellum: balance, coordination
o Hypothalamus: autoregulation homeostasis
o Pituitary gland: secretion of hormones
o Ventricles: CSF held
- Factors that Influence ICP
o Arterial pressure
o Venous pressure
o Intraabdominal and intrathoracic pressure
o Posture
 Keep patients in a neutral point: 35-40 degrees and neck aligned;
head propped
o Temperature
o Blood gases (CO2 levels)
- Regulation & Maintenance
o Monro-Kellie doctrine
 If one component increases, another must decrease to maintain ICP.
o Normal ICP 5 to 15 mm Hg
 Elevated if >20 mm Hg sustained
o Normal fluctuations occur but this is if there is SUSTAINED increased ICP
o Normal compensatory adaptations
 Changes in CSF volume
 Changes in intracranial blood volume
 Changes in tissue brain volume
o Ability to compensate is limited.
 If volume increase continues, ICP rises → decompensation
o Decreasing amount of blood = decreasing oxygen supply to brain
o Patients often don’t know they have something until they are unable to compensate
 People don’t know they have the tumor bc it grows so slowly and the body is able to compensate
 If rapid growing tumor = start seeing symptoms quickly
- Cerebral Blood Flow
o Definition
 The amount of blood in milliliters passing through 100 g of brain tissue in 1 minute
 About 50 mL/min per 100 g of brain tissue
 What it takes for the brain to be maintained
 Brain extracts 20-25% of glucose from blood
o Autoregulation
 Adjusts diameter of blood vessels
 Ensures consistent CBF
 Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg
 BP increase = arterioles in brain constrict bc they want to prevent tissues from getting hit with insult
 Preventing downstream neurons in head from getting hit with insult
 If BP is low = arterioles in the brain will dilate to get more blood = get oxygen and glucose to cells
 Hypertensive crisis: don’t drop blood pressure right away
 If we drop too quickly = brain will have decreased perfusion = lower slowly to gradually open vessels
 If systolic BP is too high = arterioles will CONSTRICT
 If systolic BP is too low = arterioles will DILATE
o Cerebral perfusion pressure (CPP)
 CPP = MAP – ICP
 Normal CPP is 60 to 100 mm Hg.
 Goal in treatment is 70-80
 If out of this range = interventions are necessary
  <50 mm Hg is associated with ischemia and neuronal death.
o Effect of cerebral vascular resistance
 CPP = Flow x Resistance
o Body will NOT OVERCOMPENSATE for a situation; SLOW to respond to
compensate
o Pressure changes
 Compliance is the expandability of the brain.
 Impacts effect of volume change on pressure
 Compliance = Volume/Pressure
 Amount of volume increases = dramatic increase in pressure
o Stages of increase ICP:
 Stage 1: total compensation
 Stage 2: ↓compensation; risk for ↑ICP
 Stage 3: failing compensation; clinical manifestations of ↑ICP (Cushing’s
triad)
 Stage 4: Herniation imminent → death
o Factors affecting cerebral blood vessel tone
 CO2
 O2
 Hydrogen ion concentration
 NEVER HYPERVENTILATE A PATIENT; want them to be maintaining
a normal CO2 and pH
 In general:
 Increase in CO2 = arteriole bed will DILATE to get more oxygen to
cells around those cells (not enough exchange going on)
o Hydrogen concentration increase = increase acid = decrease
pH
o Acidosis, hyercarbia, low O2 = cause vasoDILATION
 Low CO2: vasoconstriction
o High O2, alkalosis = vasoconstriction
o Increase ICP
 Life-threatening
 Increase in any of three components
 Brain tissue (swelling)
 Blood
 CSF
 ↑ cerebral edema
- Herniation (image on the left)
- Cerebral Edema
o ↑ Extravascular fluid in brain
o Variety of causes
 Mass lesions
 Head injuries- bleeding
 Cerebral infections
 Vascular insult
 Toxic or metabolic encephalopathy
o Clinical Manifestations
 Change in level of consciousness
 Change in vital signs (stage 3)
 Cushing’s triad
o Widened pulse pressure (diastolic drops)
o Bradycardia
o Irregular respirations
 Ocular signs
 Pressure on at least 1 cranial nerve
 REVIEW CRANIAL NERVES
 Change in level of consciousness
 Flattening of affect → coma
 Change in vital signs
 Cushing’s triad (widened pulse pressure, bradycardia, irregular respirations)
 Change in body temperature
 o Often see hyperthermia
o Temp elevation: increases metabolic demand (do NOT want this during injury bc creating more
byproducts of breaking down ATP)
 Cushing’s Triad and Cushing’s Reflex:
 Cushing’s Reflex:
o a hypothalamic response to brain ischemia wherein the sympathetic nervous system is activated which
causes increased peripheral vascular resistance with a subsequent increase in BP.
o The increased BP then activates the parasympathetic nervous system via carotid artery baroreceptors,
resulting in vagal-induced bradycardia.
o The brain ischemia that leads to cushings reflex is usually due to the poor perfusion that results from
increased ICP due to head bleeds or mass lesions.
 Cushing’s Reflex  clinical manifestation of Cushing’s triad:
o Systolic Hypertension
o Bradycardia
o Irregular respirations (Cheyne-Stokes breathing
o Cushings triad signals impending danger of brain herniation, and thus, the need for decompression.
Consider administering mannitol, hyperventilation, and elevation of the head of bed as temporizing
measures.
 No hyperventilation unless extreme emergency to prevent herniation
 Sustained hyperventilation will decrease oxygen to the brain
 Very likely they will move into stage 4 if Cushing’s reflex
 Blow off CO2 when hyperventilating = vasoconstrict = decrease blood to brain = decreasing oxygen to brain
 Compression of oculomotor nerve
 Unilateral pupil dilation
 Sluggish or no response to light
 Inability to move eye upward
 Eyelid ptosis
 Other cranial nerves
 Diploplia, blurred vision, EOM changes
 ↓ In motor function
 Hemiparesis/hemiplegia
 Decerebrate posturing (extensor)
o Indicates more serious damage
o Aware from core
o Arms stiffly extended, adducted, and
hyperpronated with hyperextension of the legs
with plantar flexion of the feet
o Results from disruption of motor fibers in
midbrain and brainstem
 Decorticate posturing (flexor)
o Knees come together
o Arms to core
o Flexion of arms, wrists, and finger
with adduction in upper
extremities. Extension, internal
rotation, and plantar flexion in
lower extremities
 Headache
 Often continuous
 Worse in the morning
 Vomiting
 Not preceded by nausea
 Projectile
- Major Complications:
o Inadequate cerebral perfusion
o Cerebral herniation
 Tentorial/ Tonsillar
o Herniation
 Uncal herniation
 Cingulate herniation
- Diagnostic Studies
o CT scan / MRI / PET
o EEG
o Cerebral angiography
o ICP and brain tissue oxygenation measurement (LICOX catheter)
o Doppler and evoked potential studies
o NO lumbar puncture
 no needle because pressure will come out = risk for cerebral
herniation d/t sudden release of pressure
o First sign of increased ICP: decrease LOC
- Measurement of ICP
o Guides clinical care
o Indications
 Glasgow Coma Scale of ≤8
 Abnormal CT scans or MRI
- Potential Placements of ICP Monitoring Devices
o Ventricular: only one that can drain fluid AND monitor pressure
- Measurement of ICP
o Ventriculostomy
 Catheter inserted into lateral ventricle
 Coupled with an external transducer
 Leveling = make sure not too much leaks out
 In this system, the transducer is external.
 It is important to make sure that the transducer of the
ventriculostomy is level to the foramen of Monro
(interventricular foramen) and that the ventriculostomy
system is at the ideal height.
 A reference point for this foramen is the tragus of the ear.
When the patient is repositioned, the system needs to be re-
zeroed.
 What are the current recommendations for when to place
ICP? Must know!
 GCS <8 who have abnormal CT….or
 Patients with evidence of altered cerebral tissue perfusion ,
have a normal CT but have 2 of the following:
o Age> 40
o Unilateral or bilateral motor posturing
o SBP < 90mm hg
o Fiberoptic catheter
 Sensor transducer located within the catheter tip
 an alternative technology, uses a sensor transducer located within
the catheter tip. The sensor tip is placed within the ventricle or the
brain tissue and provides a direct measurement of brain pressure
o Subarachnoid bolt or screw
 Between arachnoid membrane and cerebral cortex
 another method of monitoring ICP. It is placed just through the skull
between the arachnoid membrane and the cerebral cortex. It does not
allow for CSF drainage but is ideal for patients with mild or moderate head injury. It can easily be converted into a
ventriculostomy if the patient decompensates.
o Prevent and monitor for infection.
o Measure as mean pressure.
o Waveform should be recorded.
 Normal, elevated, and plateau waves
o Infection is a serious complication with ICP monitoring.
 Factors that contribute to the development of infection include ICP monitoring more than 5 days, use of a
ventriculostomy, the presence of a CSF leak, and a concurrent systemic infection.
 Routine assessment of the insertion site, the use of aseptic technique, and monitoring the CSF for a change in drainage
color or clarity are important nursing interventions.
o ICP should be measured as a mean pressure.
 If a CSF drainage device is in place, the drain must be closed for at least 6 minutes to ensure an accurate reading.
o Intracranial pressure monitoring can be used to continuously measure ICP. The ICP tracing shows normal, elevated, and
plateau waves.
 o Record the waveform strip along with other pressure monitoring waveforms.
o Evaluate changes with patient condition.
o Inaccurate readings caused by
 CSF leaks
 Obstruction in catheter/ kinks in tubing
 Differences in height of bolt/transducer
 Incorrect height of drainage system
 Bubbles/air in tubing
o Can control ICP by removing CSF (with ventricular catheter).
o Intermittent or continuous drainage
o Careful monitoring of the volume of CSF drained is essential.
o Prevent infection and other complications.
o With the ventricular catheter, it is possible to control ICP by removing CSF.
o The physician will typically order a specific level to initiate drainage (e.g., if ICP is greater than 20 mm Hg) as well as the
frequency of drainage (intermittent or continuously).
o When the ICP is above the indicated level, the ventriculostomy system is opened by turning a stopcock and allowing the
drainage of CSF, thus relieving the pressure inside the cranial vault .
o There are two options for CSF drainage: intermittent and continuous. If intermittent drainage is ordered, open the
ventriculostomy system at the indicated ICP and allow CSF to drain for 2 to 3 minutes. Then the stopcock is closed to return
the ventriculostomy to a closed system. If continuous ICP drainage is ordered, careful monitoring of the volume of CSF
drained is essential, keeping in mind that normal CSF production is about 20 to 30 mL/hr, with a total CSF volume of 90 to
150 mL within the ventricles and subarachnoid space.
o It is also recommended that a sign be posted above the patient’s bed to notify anyone before turning, moving, or suctioning
the patient to prevent the removal of too much CSF, which can result in other complications.
o Strict aseptic technique during dressing changes or sampling of CSF is imperative to prevent infection. The system must
remain intact to ensure that the ICP readings are accurate because treatment is initiated based on the pressures.
o Complications of this type of drainage system include ventricular collapse, infection, and herniation or subdural hematoma
formation from rapid decompression.
- Measurement of Cerebral Oxygenation and Perfusion
o LICOX catheter
 Measures brain oxygenation (PbtO2) and temperature; will give us ICP
 Placed in healthy white brain matter.
 Technology is available to measure cerebral oxygenation and assess perfusion. Two such devices used in ICU care
settings are the LICOX brain tissue oxygenation catheter and the jugular venous bulb catheter.
 The LICOX catheter, which measures brain oxygenation and temperature, is placed in viable (healthy) white matter of
the brain.
 The LICOX system provides continuous monitoring of the pressure of oxygen in brain tissue (PbtO 2). The
normal range for PbtO2 is 20 to 40 mm Hg. A lower than normal PbtO2 level is indicative of ischemia.
 Another advantage of the LICOX catheter is the ability to measure brain temperature. A cooler brain temperature
(96.8°F [36°C]) may produce better outcomes
o Jugular venous bulb catheter
 Measures jugular venous oxygen saturation (SjvO2).
 Not true ICP but telling us about O2 in brain
 The jugular venous bulb catheter is placed in the internal jugular vein and positioned so that the catheter tip is located
in the jugular bulb.
 Placement is verified by an x-ray.
 This catheter provides a measurement of jugular venous oxygen saturation (SjvO2), which indicates total venous
brain tissue extraction of oxygen.
 This is a measure of cerebral oxygen supply and demand. The normal SjvO 2 range is 55% to 75%. Values less
than 50% demonstrate impaired cerebral oxygenation.
- Collaborative Care
o Treat underlying cause.
o Adequate oxygenation
 PaO2 > 100 mm Hg
 PaCO2 35-45 mm Hg
 Intubation
 Mechanical ventilation
o Surgery
o Drug Therapy
 Mannitol (Osmitrol)
 Plasma expansion
 Osmotic effect
  Monitor fluid and electrolyte status.
 Hypertonic saline
 Moves water out of cells and into blood.
 Monitor BP and serum sodium levels.
 Corticosteroids
 Vasogenic edema
 Monitor fluid intake, serum sodium and glucose levels.
 Concurrent antacids, H2 receptor blockers, proton pump inhibitors
o Protect gut
 Antiseizure medications
 Usually started but if no seizure w/in 3-4 days = taper and d/c entirely
 Antipyretics
 Elevated temp = prevent fever
 Sedatives
 Reduce metabolic demand
 Analgesics - pain
 Barbiturates
o Nutritional Therapy
 Hypermetabolic and
hypercatabolic state ↑ need for
glucose
 Enteral or parenteral nutrition
 Early feeding (within 3 days of
injury)
 Keep patient normovolemic.
 IV 0.9% NaCl preferred over
D5W or 0.45% NaCl
 Within 24hrs of stabilization =
start nutritional therapy
 Make sure gut is perfused =
villi will die within 3 days
- Nursing Assessment
o Subjective data
o Level of consciousness (LOC)
o Glasgow Coma Scale
 Eye opening
 Best verbal response
 Best motor response
o Pupillary Check for Size and
Response
 Compare the pupils with one another for size, shape,
movement, and reactivity.
 If the oculomotor nerve [CN III] is compressed, the pupil on
the affected side (ipsilateral) becomes larger until it fully
dilates. If ICP continues to increase, both pupils dilate.
 Test pupillary reaction with a penlight. The normal reaction
is brisk constriction when the light is shone directly into the
eye. Also note a consensual response (a slight constriction
in the opposite pupil) at the same time. A sluggish reaction
can indicate early pressure on CN III (oculomotor nerve).
 A fixed pupil unresponsive to light stimulus usually
indicates increased ICP. However, it is important to note
that there are other causes of a fixed pupil, including direct
injury to CN III, previous eye surgery, administration of
atropine, and use of mydriatic eyedrops.
o Cranial Nerves
 Eye movements
 Eye movements controlled by cranial nerves III, IV, and VI can be examined in the patient who is awake and
able to follow commands and can be used to assess the function of the brainstem.
 Corneal reflex
  Testing the corneal reflex gives information about the functioning of cranial nerves V and VII. If this reflex is
absent, initiate routine eye care to prevent corneal abrasion
 Oculomotor:
 Eye movements of the uncooperative or unconscious patient can be elicited by reflex with the use of head
movements (oculocephalic) and caloric stimulation (oculovestibular).
 Oculocephalic reflex (doll’s eye reflex)
o turn the patient’s head briskly to the left or right while holding the eyelids open. A normal response is
movement of the eyes across the midline in the direction opposite that of the turning. Next, quickly flex
and then extend the neck. Eye movement should be opposite to the direction of head movement—up
when the neck is flexed and down when it is extended. Abnormal responses can help locate the
intracranial lesion. This test should not be attempted if a cervical spine problem is suspected.
 Oculovestibular (caloric stimulation)
o Insert cold water into ear canal then eyes turn towards it
 Test motor strength by asking the awake and cooperative patient to squeeze your hands to compare strength in
the hands. The palmar drift test is an excellent measure of strength in the upper extremities. The patient raises the
arms in front of the body with the palmar surface facing upward. If there is any weakness in the upper extremity,
the palmar surface turns downward, and the arm drifts downward. Asking the patient to raise the foot from the
bed or to bend the knees up in bed is a good assessment of lower extremity strength. Test all four extremities for
strength and evaluate for any asymmetry in strength or movement.
 Assess the motor response of the unconscious or uncooperative patient by observation of spontaneous
movement. If no spontaneous movement is possible, apply a pain stimulus to the patient and note the response.
Resistance to movement during passive range-of-motion exercises is another measure of strength. Do not include
hand squeezing as part of the assessment of motor movement in the unconscious or uncooperative patient, as this
is a reflex action and can provide a misrepresentation of the patient’s status.
 Also record the vital signs, including BP, pulse, respiratory rate, and temperature. Be aware of Cushing’s triad
because this indicates severely increased ICP. Besides recording respiratory rate, also note the respiratory pattern
o Motor strength
 Squeeze hands
 Palmar drift test
 measure of strength in the upper extremities. The patient raises the arms in front of the body with the palmar
surface facing upward. If there is any weakness in the upper extremity, the palmar surface turns downward, and
the arm drifts downward.
 Raise foot off bed or bend knees
 Asking the patient to raise the foot from the bed or to bend the knees up in bed is a good assessment of lower
extremity strength. Test all four extremities for strength and evaluate for any asymmetry in strength or
movement.
o Motor response
 Spontaneous or to pain
 Assess the motor response of the unconscious or uncooperative patient by observation of spontaneous movement. If no
spontaneous movement is possible, apply a pain stimulus to the patient and note the response. Resistance to movement
during passive range-of-motion exercises is another measure
of strength. Do not include hand squeezing as part of the
assessment of motor movement in the unconscious or
uncooperative patient, as this is a reflex action and can
provide a misrepresentation of the patient’s status.
o Vital signs
 including BP, pulse, respiratory rate, and temperature. Be
aware of Cushing’s triad because this indicates severely
increased ICP.
 Besides recording respiratory rate, also note the respiratory
pattern.
- Nursing Diagnosis
o Decreased intracranial adaptive capacity
o Risk for ineffective cerebral tissue perfusion
o Risk for disuse syndrome
o Nursing diagnoses for the patient with increased ICP include, but
are not limited to, the following:
 Decreased intracranial adaptive capacity related to decreased
cerebral perfusion or increased ICP
 Risk for ineffective cerebral tissue perfusion related to
reduction of venous and/or arterial blood flow and cerebral
edema
  Risk for disuse syndrome related to altered level of consciousness, immobility, and altered nutritional intake
- Nursing Planning
o Overall Goals
 Maintain a patent airway.
 ICP within normal limits
 Normal fluid and electrolyte balance
 Prevent complications secondary to immobility and decreased LOC
- Nursing Implementation
o Respiratory function
 Maintain patent airway.
 critical in the patient with increased ICP and is a primary nursing responsibility. As the LOC decreases, the
patient is at an increased risk of airway obstruction from the tongue dropping back and occluding the airway or
from accumulation of secretion.
 In general, any patient with a GCS less than or equal to 8 or an altered LOC who is unable to maintain a patent
airway or effective ventilation needs intubation and mechanical ventilation.
 Prevent hypoxia and hypercapnia in order to minimize secondary injur
 Elevate head of bed 30 degrees.
 Proper positioning of the head is important. Elevation of the head of the bed to 30 degrees enhances respiratory
exchange and aids in decreasing cerebral edema.
 Suctioning needs
 Remove accumulated secretions by suctioning as needed. An oral airway facilitates breathing and provides an
easier suctioning route in the comatose patient.
 Suctioning and coughing will cause transient decreases in the PaO2 and increases in the ICP.
 Keep suctioning to a minimum and less than 10 seconds in duration, with administration of 100% oxygen before
and after to prevent decreases in the PaO2.
 To avoid cumulative increases in the ICP with suctioning, limit suctioning to two passes per suction procedure, if
possible.
 Minimize abdominal distention.
 Try to prevent abdominal distention as it can interfere with respiratory function. Insertion of a nasogastric tube to
aspirate the stomach contents can prevent distention, vomiting, and possible aspiration. However, in patients with
facial and skull fractures, a nasogastric tube is contraindicated unless a basal skull fracture has been ruled out,
and oral insertion of a gastric tube is preferred.
 Monitor ABGs.
 ABGs should be measured and evaluated regularly. Frequently monitor the ABG values and take measures to
maintain the levels within prescribed or acceptable parameters. The appropriate ventilatory support can be
ordered on the basis of the PaO2 and PaCO2 values.
 Maintain ventilatory support.
o Pain and anxiety management
 Pain, anxiety, and fear from the primary injury, therapeutic procedures, or noxious stimuli can increase ICP and BP,
thus complicating the management and recovery of the brain-injured patient.
 The appropriate choice or combination of sedatives, paralytics, and analgesics for symptom management presents a
challenge to the ICU team. Administration of these agents may alter the neurologic state, thus masking true neurologic
changes. It may be necessary to temporarily suspend drug therapy to appropriately assess neurologic status. The
choice, dose, and combination of agents may vary depending on the patient’s history, neurologic state, and overall
clinical presentation.
 Opioids
 morphine sulfate and fentanyl (Sublimaze), are rapid-onset analgesics with minimal effect on CBF or oxygen
metabolism.
 Propofol (Diprivan)
 The IV anesthetic sedative propofol (Diprivan) has gained popularity in the management of anxiety and agitation
in the ICU because of its rapid onset and short half-life. An accurate neurologic assessment can be performed
very soon after turning off the infusion of propofol. A side effect of this drug is hypotension.
 Dexmedetomidine (Precedex)
 Dexmedetomidine (Precedex), an alpha-2 adrenergic agonist, is used for continuous IV sedation of intubated and
mechanically ventilated patients in the ICU setting for up to 24 hours. It is another ideal agent for neurologic
patients because of the ease in obtaining a neurologic assessment without altering the dose due to its anxiolytic
properties. When using continuous IV sedatives, be aware of the side effects of these drugs, especially
hypotension, as this can result in a lower CPP value.
 Neuromuscular blocking agents
 Nondepolarizing neuromuscular blocking agents (e.g., vecuronium [Norcuron], cisatracurium besylate
[Nimbex]) are useful for achieving complete ventilatory control in the treatment of refractory intracranial
 hypertension. Because these agents paralyze muscles without blocking pain or noxious stimuli, they are used in
combination with sedatives, analgesics, or benzodiazepines.
 Benzodiazepines
 although useful for sedation, are usually avoided in the management of the patient with increased ICP because of
the hypotensive effect and long half-life, unless they are used as an adjunct to neuromuscular blocking agents.
o Fluid and electrolyte balance
 Monitor IV fluids.
 Closely monitor IV fluids with the use of an accurate IV infusion control device or pump.
 Intake and output, with insensible losses and daily weights taken into account, are important parameters in the
assessment of fluid balance.
 Daily electrolytes
 Electrolyte determinations should be made daily, and any abnormal values should be discussed with the
physician. It is especially important to monitor serum glucose, sodium, potassium, magnesium, and osmolality.
 Monitor for DI or SIADH.
 Monitor urinary output to detect problems related to diabetes insipidus and syndrome of inappropriate
antidiuretic hormone (SIADH). Diabetes insipidus is caused by a decrease in antidiuretic hormone (ADH). It
results in increased urinary output and hypernatremia. The usual treatment of diabetes insipidus is fluid
replacement, vasopressin (Pitressin), or desmopressin acetate (DDAVP) (see Chapter 50). If not treated, severe
dehydration will occur. SIADH is caused by an excess secretion of ADH. SIADH results in decreased urinary
output and dilutional hyponatremia. It may result in cerebral edema, changes in LOC, seizures, and coma.
 Monitor and minimize increases in ICP.
 ICP monitoring is used in combination with other physiologic parameters to guide the care of the patient and
assess the patient’s response to treatment. Valsalva maneuver, coughing, sneezing, suctioning, hypoxemia, and
arousal from sleep are factors that can increase ICP. Be alert to these factors and attempt to minimize them.
o Interventions to optimize ICP and CPP
 HOB elevated appropriately
 Elevation of the head of the bed promotes drainage from the head and decreases the vascular congestion that can
produce cerebral edema. However, raising the head of the bed above 30 degrees may decrease the CPP by
lowering systemic BP
 Careful evaluation of the effects of elevation of the head of the bed on both the ICP and the CPP is required.
Position the bed so that it lowers the ICP while optimizing the CPP and other indices of cerebral oxygenation.
 Prevent extreme neck flexion.
 can cause venous obstruction and contribute to elevated ICP.
 Turn slowly.
 Adjust the body position to decrease the ICP maximally and to improve the CPP.
 Take care to turn the patient with slow, gentle movements because rapid changes in position may increase the
ICP.
 Prevent discomfort in turning and positioning the patient because pain or agitation also increases pressure.
 Avoid coughing, straining, Valsalva.
 Increased intrathoracic pressure contributes to increased ICP by impeding the venous return. Thus coughing,
straining, and the Valsalva maneuver should be avoided.
 Avoid hip flexion.
 Avoid extreme hip flexion to decrease the risk of raising the intra-abdominal pressure, which increases ICP.
o Minimize complications of immobility such as atelectasis and contractures.
o Protection from self-injury
 Judicious use of restraints; sedatives
 Seizure precautions
 Quiet, nonstimulating environment
o Psychologic considerations
- Evaluation
o Expected Outcomes
 Maintain ICP and CPP within normal parameters.
 No serious increases in ICP during or following care activities
 No complications of immobility
 Head Injury

- HEAD INJURY
o Any trauma to the
 Skull
 Scalp
 Brain
o Traumatic brain injury (TBI)
o High incidence
o Causes
 Motor vehicle collisions
 Falls
 Firearm-related injuries
 Assaults
 Sports-related injuries
 Recreational accidents
 War-related injuries
o High potential for poor outcome
o Deaths occur at three points in time after injury:
 Immediately after the injury
 Within 2 hours after the injury
 3 weeks after the injury.
 Multisystem failure or untreated
- Types of Head Injuries
o Scalp Lacerations
 External head trauma
 Scalp is highly vascular → Profuse bleeding
 Major complications – blood loss and infection
o Skull Fractures
 Linear or depressed
 Simple, comminuted, or compound
 Closed or open
 Location determines manifestations.
 Complications
 Infections
 Hematoma
 Tissue damage
- Raccoon Eyes and Battle’s Sign
o A basilar skull fracture is a specialized type of linear fracture that occurs when the fracture involves the base of the skull.
Manifestations can evolve over the course of several hours, vary with the location and severity of fracture, and may include
cranial nerve deficits, Battle’s sign (postauricular ecchymosis), and periorbital ecchymosis (raccoon eyes).
o This fracture generally is associated with a tear in the dura and subsequent leakage of CSF.
 Rhinorrhea (CSF leakage from the nose) or otorrhea (CSF leakage from the ear) generally confirms that the fracture
has traversed the dura. Rhinorrhea may also manifest as postnasal sinus drainage. The significance of rhinorrhea may
be overlooked unless the patient is specifically assessed for this finding. The risk of meningitis is high with a CSF
leak, and antibiotics should be administered to prevent the development of meningitis.
o Two methods of testing can be used to determine whether the fluid leaking from the nose or ear is CSF. The first method is to
test the leaking fluid with a Dextrostix or Tes-Tape strip to determine whether glucose is present. CSF gives a positive
reading for glucose.
o If blood is present in the fluid, testing for the presence of glucose is unreliable because blood also contains glucose. In this
event, look for the halo or ring sign. To perform this test, allow the leaking fluid to drip onto a white gauze pad (4 × 4) or
towel, and then observe the drainage. Within a few minutes, the blood coalesces into the center, and a yellowish ring
encircles the blood if CSF is present.
o Note the color, appearance, and amount of leaking fluid because both tests can give false-positive results.
o
o Diffuse (generalized; e.g. concussion)
 Concussion
 Brief disruption in LOC
 Retrograde amnesia
 Headache
 Short duration
 May result in postconcussion syndrome:
o Persistent headache
o Lethargy
o Personality and behavior changes
o Shortened attention span, decreased
short-term memory
o Changes in intellectual ability
 Diffuse Axonal Injury:
 Widespread axonal damage
 Decreased LOC
 Increased ICP
 Decortication, decerebration
 Global cerebral edema
 The damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal
ganglia, thalamus, and brainstem.
 Initially, DAI was believed to occur from the tensile forces of trauma that sheared axons, resulting in axonal
disconnection.
 There is increasing evidence that axonal damage is not preceded by an immediate tearing of the axon from the
traumatic impact, but rather the trauma changes the function of the axon, resulting in axon swelling and
disconnection.
 This process takes approximately 12 to 24 hours to develop and may persist longer.
 The clinical signs of DAI are varied but may include a decreased LOC, increased ICP, decortication or
decerebration, and global cerebral edema.
 Approximately 90% of patients with DAI remain in a persistent vegetative state.
 Patients with DAI who survive the initial event are rapidly triaged to an ICU where they will be vigilantly
watched for signs of increased ICP and treated for increased ICP.
o Focal (localized)
 Lacerations
 Tearing of brain tissue
 With depressed and open fractures and penetrating injuries
 Tissue damage is severe, and surgical repair of the laceration is impossible due to the nature of brain tissue.
 Medical management consists of antibiotics until meningitis is ruled out, and preventing secondary injury related
to increased ICP.
 If bleeding is deep into the brain tissue, focal and generalized signs develop.
 Intracerebral hemorrhage
o generally associated with cerebral laceration.
o This hemorrhage manifests as a space-occupying lesion accompanied by unconsciousness, hemiplegia on
the contralateral side, and a dilated pupil on the ipsilateral side.
 Subarachnoid hemorrhage
 Intraventricular hemorrhage
 Contusions
 Bruising of brain tissue within a focal area
 Associated with closed head injury
 Can cause hemorrhage, infarction, necrosis, edema
 Can rebleed
 Focal and generalized manifestations
 Monitor for seizures
 Potential for increased hemorrhage if on anticoagulants
 Hematomas
 Cranial nerve injuries
 Focal injury can be minor to severe and can be localized to an area of injury.
 Focal injury consists of lacerations, contusions, hematomas, and cranial nerve injuries.
o Minor (GCS 13-15)
 o Moderate (GCS 9-12)
o Severe (GCS 3-8)
- Coup-Countrecoup Injury
o With contusion, the phenomenon of coup-contrecoup
injury is often noted and can range from minor to
severe.
o Damage from coup-contrecoup injury occurs when the
brain moves inside the skull due to high-energy or high-
impact injury mechanisms.
o Contusions or lacerations occur both at the site of the
direct impact of the brain on the skull (coup) and at a
secondary area of damage on the opposite side away
from injury (contrecoup), leading to multiple contused
areas.
o Contrecoup injuries tend to be more severe, and overall patient prognosis depends on the amount of bleeding around the
contusion site.
- Complications
o Epidural Hematoma
 Bleeding between the dura and the inner surface of the skull
 Neurologic emergency
 Venous origin slow
 Arterial origin rapid
 Think ARTERY bleed that are RAPID
 LOC then regain then decline = hallmark of epidural
hematoma
 Initial period of unconsciousness
 Brief lucid interval followed by decrease in LOC
 Headache, nausea, vomiting
 Focal findings
 Requires rapid evacuation
o Subdural Hematoma
 Bleeding between the dura mater and the arachnoid
 Most common source is the veins that drain the brain surface
into the sagittal sinus.
 Can also be arterial
 More likely to be a VENOUS bleed
o Acute Subdural Hematoma
 Within 24 to 48 hours of the injury
 Symptoms related to increased ICP
 ↓ LOC, headache
 Ipsilateral pupil dilated and fixed if severe
o Subacute Subdural Hematoma
 Within 2 to 14 days of the injury
 May appear to enlarge over time
o Chronic Subdural Hematoma
 Weeks or months after injury
 More common in older adults
 Presents as focal symptoms
 ↑ Risk for misdiagnosis
 Common in old person who fell at home
o Intracerebral Hematoma
 Bleeding within the brain tissue
 Usually within frontal and temporal lobes
 Size and location of hematoma determine patient outcome.
- Diagnostic Studies
o CT scan
 Best diagnostic test to determine craniocerebral trauma
o MRI, PET, evoked potential studies
o Transcranial Doppler studies
o Cervical spine x-ray
o Glasgow Coma Scale (GCS)
- Collaborative Care
 o Emergency Tx:
 Patent airway
 Stabilize cervical spine.
 Oxygen
 IV access
 Intubate if GCS <8.
 Control external bleeding.
 Remove patient’s clothing.
 Maintain patient warmth.
 Ongoing monitoring
 Anticipate possible intubation.
 Assume neck injury.
 Administer fluids cautiously.
o Treatment principles
 Prevent secondary injury
 Timely diagnosis
 Surgery if necessary
o Concussion and contusion
 Observation and management of ICP
o Skull fractures
 Conservative treatment
 Surgery if depressed
o Subdural and epidural hematomas
 Surgical evacuation
 Craniotomy, burr-holes
 Craniectomy if extreme swelling
- Nursing Assessment
o Objective Data o Subjective Data
 Altered mental status  Past medical history
 Lacerations, contusions, abrasions  Mechanism of injury
 Hematoma  Medications
 Battle’s sign  Anticoagulants
 Periorbital edema and ecchymosis  Alcohol/drug use; risk-taking
 Otorrhea behaviors
 Exposed brain  Headache
 Rhinorrhea  Mood or behavioral changes
 Impaired gag reflex  Mentation changes; impaired
 Altered/irregular respirations judgment
 Cushing’s triad  Aphasia, dysphasia
 Vomiting  Fear, denial, anger, aggression,
 Bowel and bladder incontinence depression
 Uninhibited sexual expression
 Altered LOC
 Seizures
 Pupil dysfunction
 Cranial nerve deficit(s)
 Motor deficit
 Palmar drift
 Paralysis
 Spasticity
 Posturing
 Rigidity or flaccidity
 Ataxia
 Abnormal CT scan or MRI
 Abnormal EEG
 Positive toxicology screen or alcohol level
 ↑ or ↓Blood glucose level
 ↑ ICP
- Nursing Diagnosis
o Risk for ineffective cerebral tissue perfusion related to interruption of CBF associated with cerebral hemorrhage, hematoma,
and edema
o Hyperthermia related to increased metabolism, infection, and hypothalamic injury
 o Impaired physical mobility related to decreased LOC
o Anxiety related to abrupt change in health status, hospital environment, and uncertain future
o Potential complication: increased ICP related to cerebral edema and hemorrhage
- Nursing Planning
o Overall Goals
 Cerebral oxygenation & perfusion
 Normothermic
 Control pain and discomfort
 Free of infection
 Adequate nutrition
 Maximal cognitive, motor, and sensory function
- Nursing Implementation
o Health Promotion
 Prevent car and motorcycle accidents.
 Wear safety helmets.
 Use seat belts and child car seats.
 Home safety to prevent falls
o Acute Intervention
 Maintain cerebral perfusion.
 Prevent secondary cerebral ischemia.
 Monitor for changes in neurologic status.
 Patient and family teaching
 Major focus of nursing care relates to increased ICP.
 Eye problems
 Eye drops, compresses, patch
 Eye problems may include loss of the corneal reflex, periorbital ecchymosis and edema, and diplopia. Loss of the
corneal reflex may necessitate administering lubricating eye drops or taping the eyes shut to prevent abrasion.
Periorbital ecchymosis and edema decrease with time, but cold and, later, warm compresses provide comfort and
hasten the process. Diplopia can be relieved by use of an eye patch. A consult with an ophthalmologist should be
considered.
 Hyperthermia
 Goal 36°to 37° C
 Prevent shivering
 may occur from injury to or inflammation of the hypothalamus. Elevations in body temperature can result in
increased CBF, cerebral blood volume, and ICP. Increased metabolism secondary to hyperthermia increases
metabolic waste, which in turn produces further cerebral vasodilation. Avoid hyperthermia with a goal of 36°to
37°C as the standard of care. Use interventions to reduce temperature in conjunction with sedation as necessary
to prevent shivering.
 Measures for patients leaking CSF
 Head of bed elevated
 Loose collection pad may be placed under the nose or over the ear. Do not place a dressing in the nasal or ear
cavities
 No sneezing or blowing nose
 No NG tube
 No nasotracheal suctioning
 Measures for immobilized patients
 bladder and bowel function, skin care, and infection, are also indicated.
 Antiemetics
 Nausea and vomiting may be a problem and can be alleviated by antiemetic drugs. Headache can usually be
controlled with acetaminophen or small doses of codeine.
 Analgesics
 Pre-op preparation, if needed
 A burr-hole opening or craniotomy may be indicated, depending on the underlying injury that is causing the
symptoms. The emergency nature of the surgery may hasten the usual preoperative preparation. Consult with the
neurosurgeon to determine specific preoperative nursing measures.
 The patient is often unconscious before surgery, making it necessary for a family member to sign the consent
form for surgery. This is a difficult and frightening time for the patient’s caregiver and family and requires
sensitive nursing management. The suddenness of the situation makes it especially difficult for the family to
cope.
o Ambulatory and Home Care
 Acute rehabilitation
  Motor and sensory deficits
 Communication issues
 Memory and intellectual functioning
 Nutrition
 Bowel and bladder management
 Seizure disorders
 Mental and emotional difficulties
 Progressive recovery
 Family participation and education
- Expected Outcomes
o Maintain normal cerebral perfusion pressure.
o Achieve maximal cognitive, motor, and sensory function.
o Experience no infection or hyperthermia.
o Achieve pain control.
- Acute Spinal Cord Injury
o Epidemiology
 Motor vehicle accidents: 47 percent
 Falls: 23 percent
 Violence (especially gunshot wounds): 14 percent
 Sports accidents: 9 percent
 Other: 7 percent
o Types of SCI
 Complete
 Incomplete
o Cervical Cord
 C3 through C5 innervate the diaphragm, the chief muscle of
inspiration, via the phrenic nerve
 May have respiratory issues
 C4 through C7 innervate the shoulder and arm musculature
 May be able to move shoulders
 C6 through C8 innervate the forearm extensors and flexors
 C8 through T1 innervate the hand musculature
o Thoracic
 The spinal roots form the intercostal nerves that run along the
inferior rib margin and innervate the associated dermatomes
 contains sympathetic nerves that innervate the heart and
abdominal organs
o Lumbar
 L2 and L3 mediate hip
flexion
 L3 and L4 mediate knee
extension
 L4 and L5 mediate ankle
dorsiflexion and hip
extension
 L5 and S1 mediate knee
flexion
 S1 and S2 mediate ankle
plantar flexion
- Syndromes Associated with Incomplete SCI
o Central Cord Syndrome
 Disproportionately greater motor impairment in
upper > lower extremities
 Bladder dysfunction
 Sensory loss below level of injury
o Anterior Cord Syndrome
 Lesion affecting anterior or ventral 2/3 of spinal
cord
 Direct injury to anterior cord by disc or bone
fragments
o Brown-Sequard Syndrome
 Weakness, loss of vibration, and loss of
proprioception ipsilateral to the lesion
 No bladder symptoms
 Most common mechanism: knife/bullet injuries
 CONTRALATERAL LOSS OF PAIN !!
 Loss of movement on the same side of injury;
 Loss of sensation on the opposite side
o Posterior Cord Syndrome
 Loss of deep touch sensation
 Preserved motor, however difficult to rehab secondary to loss of proprioception
 Loss of ability to feel where their feet are
- What to Monitor for Acute SCI
o Priorities
 Pulmonary Status: airway
 Neurogenic Shock
 Spine precautions: Aspen collar or log rolling
 Goal is to maintain a MAP of 85-90
- Clinical Manifestations
o Respiratory System
 Closely correspond to level of injury
 Above level of C4
 Total loss of respiratory muscle function →
mechanical ventilation
 Below level of C4
 Diaphragmatic breathing → respiratory
insufficiency
 Cervical and thoracic injuries
 Paralysis of abdominal and intercostal
muscles → ineffective cough → atelectasis or
pneumonia
 ↑Risk for infection
 Risk for neurogenic pulmonary edema
 Blood shunted to lungs
o Cardiovascular System
 Injury above level T6 ↓influence of sympathetic
nervous system
 Bradycardia
 Peripheral vasodilation → hypotension
 Relative hypovolemia because of ↑ in venous capacitance
 Any cord injury above the level of T6 greatly decreases the affect of the sympathetic nervous system.
 Bradycardia occurs.
 Peripheral vasodilation results in hypotension.
 A relative hypovolemia exists because of the increase in the capacity of the dilated veins.
 LOW preload
 NEUROGENIC SHOCK
 Cardiac monitoring necessary
 Atropine to ↑ heart rate
 Blocks parasympathetic vagus nerve allowing HR to come up to normal
 Peripheral vasodilation
 ↓ Venous return of blood to heart
  ↓ Cardiac output
 IV fluids or vasopressor drugs to ↑ BP
- SPINAL SHOCK
o *Due to acute spinal cord injury
o *Absence all voluntary and reflex neurologic activity below level of injury
 Decreased reflexes
 Loss of sensation
 Flaccid paralysis below injury
o Lasts days to months
o *Spinal shock & neurogenic shock can in same patient-BUT not same disorder (some sources may group both together)
o not a true form of shock. It refers to the flaccid areflexia that may occur after spinal cord injury, and may last hours to weeks.
It may be thought of as ‘concussion’ of the spinal cord and resolves as soft tissue swelling improves. Priapism may be
present.
- NEUROGENIC SHOCK
o *Hemodynamic phenomenon-
 * Loss of vasomotor tone & Loss of sympathetic nervous system tone > inpaired cellular metabolism
o *Critical features-
 Hypotension (due to massive vasodilation
 Bradycardia- due to unopposed paraynmpathetic stimulation
 Poikilothermia; *Unable to regulate temperature-
o Occurs
 Within 30 min cord injury level T5 or above; last up to 6 weeks; also due to effect some drugs that effect vasomotor
center of medulla as opioids, benzodiazedines
o Management (*Determine underlying cause)
 Airway support
 Fluids as needed- Typically 0.9 NS , rate depends upon need
 Atropine for bradycardia
 Vasopressors as phenylelphrine for BP support
o classically characterised by hypotension, bradycardia and peripheral vasodilatation. Neurogenic shock is due to loss of
sympathetic vascular tone and happens only after a significant proportion of the sympathetic nervous system has been
damaged – as may occur with lesions at the T6 level or higher.
o The patient’s vital signs are consistent with neurogenic shock.
- Clinical Manifestations
o Urinary System
 Acute phase
 Urinary retention
 Bladder atonic and overdistended
 Indwelling catheter
 Postacute phase
 Bladder may become hyperirritable.
 Loss of inhibition from brain
 Reflex emptying
o Autonomic Dysreflexia
 Patient may experience headache/warmth/ “strange sensation”
 Medical emergency!!
 Requires immediate attention to the stimulus
 What are some nursing Interventions?
 Acute HTN as a result of this stimulus but can’t figure out what it is
 Goal: remove stimulus
o GI System
 Above T5→ hypomotility
 Paralytic ileus
 Gastric distention
o Nasogastric tube
o Metoclopramide (Reglan)
 Stress ulcers
 Intra-abdominal bleeding
 Neurogenic bowel
 Injury level of T12 or below
o Bowel initially areflexic with ↓ sphincter tone
 When reflexes return
  Sphincter tone is enhanced.
 Reflex emptying occurs.
 Regular bowel program
 Coordinate with gastrocolic reflex
o Integumentary System
 Potential for skin breakdown
 Poikilothermism
 Interruption of SNS
 ↓Ability to sweat or shiver
 More common with high cervical injury
 A major consequence of lack of movement is the potential for skin breakdown over bony prominences in areas of
decreased or absent sensation. Pressure ulcers can occur quickly and can lead to major infection and sepsis.
 Examining skin at least twice daily
 Avoid excess moisture in susceptible regions
 “Weight shifts” Use of pressure-relieving wheelchairs, cushions, and other devices
 Maintaining good nutrition and weight
 Poikilothermism is the adjustment of the body temperature to the room temperature. This occurs in SCIs because the
interruption of the sympathetic nervous system prevents peripheral temperature sensations from reaching the
hypothalamus.
 With spinal cord disruption there is also decreased ability to sweat or shiver below the level of the injury, which also
affects the ability to regulate body temperature.
 The degree of poikilothermism depends on the level of injury.
 Patients with high cervical injuries have a greater loss of the ability to regulate temperature than do those with
thoracic or lumbar injuries.
o Metabolic Needs
 NG suctioning → metabolic alkalosis
 ↓Tissue perfusion → acidosis
 Electrolyte imbalances
 ↑Nutritional needs
 High protein diet
o Peripheral Vascular Problems
 Deep vein thrombosis (DVT)
 Difficult to detect
 Pulmonary embolism
 Leading cause of death
- HALO Device
o Metal ring attached to skull with screw pins
o Weight of head is diverted through the brace
o Reduces movement of neck
o Safety -PRIORITY
o If no halo device, then traction
- TLSO “Clam”: provides means of trunk control
- SCI – Rehab
o DVT prophylaxis with Lovenox
o Nexium
o Pain Control - Percocet
o Orthostatic Hypotension – Midodrine
 Midodrine (brand names Amatine, ProAmatine, Gutron) is
a vasopressor/antihypotensive agent. Midodrine was approved in
the United States by the Food and Drug Administration (FDA) in
1996 for the treatment of dysautonomiaand orthostatic
hypotension.
o Skin care – weight shifts
o Bowel regimens
o SMOKING CESSATION
o