Adaptive Capacity Decreased: Intracranial - Increased Intracranial
Pressure; Altered Level of Consciousness
RN, MSN, CNRN
Michele Knoll Puzas, RNC, MHPE
NANDA: A clinical state in which intracranial fluid dynamic
mechanisms that normally compensate for increases in intracranial volumes are
compromised, resulting in repeated disproportionate increases in intracranial
pressure in response to a variety of noxious and non-noxious stimuli
Intracranial pressure (ICP) reflects the pressure exerted by the
intracranial components of blood, brain, and cerebrospinal fluid (CSF), each
ordinarily remaining at a constant volume within the rigid skull structure. Any
additional fluid or mass (subdural hematoma, tumor, abscess, or others)
increases the pressure within the cranial vault. Because the total volume
cannot change (Monro-Kellie doctrine), blood, CSF, and ultimately brain tissue
is forced out of the vault. The normal range of ICP is up to 15 mm Hg;
excursions above that level occur normally but readily return to baseline
parameters as a result of the adaptive capacity or compensatory mechanisms of
the brain and body, such as vasoconstriction and increased venous outflow. In
the event of disease, trauma, or a pathological condition, a disturbance in
autoregulation occurs, and ICP is increased and sustained. Exceptions include
persons with unfused skull fractures (the skull is no longer rigid at the
fracture site), infants whose suture lines are not yet fused (this is normal to
accommodate growth), and the elderly whose brain tissues have shrunk, taking up
less volume in the skull (allowing for abnormal tissue growth or intracranial
bleeding to occur for a longer period before symptoms appear).
- Increased cerebral blood flow (hypercapnea,
- Injury with cerebral edema
- Intracranial mass
- Systemic hypotension
- Decreased level of consciousness (LOC): confusion,
disorientation, somnolence, lethargy, and coma
- Pupil asymmetry
- Decreased pupil reactivity
- Impaired memory, judgment, thought processes
- Glasgow Coma Scale (GCS) score less than 13
- Unilateral or bilateral VI nerve palsy
- Repeated increases in ICP greater than 10 mm Hg for more than 5
- Elevated ICP waveforms
- Baseline ICP>10 mm Hg
- Wide amplitude ICP waveform
- Volume pressure response test variation
- Decreased cerebral blood flow (CBF)
- Decreased cerebral perfusion pressure (CPP)
- Increased or decreased heart rate with arrhythmias
- Widening pulse pressure
Patient maintains optimal cerebral tissue perfusion, as evidenced
by ICP<10 mm Hg, CGS>13, and CPP from 60 mm Hg to 90 mm Hg.
Ongoing Assessment Actions/Interventions/Rationale
- (i) independent
- (i) Assess neurologic status as follows: LOC per
Glasgow Coma Scale--pupil size, symmetry, and reaction to light; extraocular
movement (EOM); gaze preference; speech and thought processes; memory;
motor-sensory signs and drift; increased tone; increased reflexes; Babinski
- Deteriorating neurological signs indicate increased cerebral
- (i) Evaluate presence or absence of
protective reflexes (e.g., swallowing, gagging, blinking, coughing, and
- (i) Monitor vital signs.
- Continually increasing ICP results in life-threatening
hemodynamic changes; early recognition is essential to survival.
- (c) Monitor arterial blood gases (ABGs)
and/or pulse oximetry. Recommended parameters of PaO2>80 mm Hg and PaCO2<35 mm Hg with normal ICP. If patient's
lungs are being hyperventilated to decrease ICP, PaCO2 should be between 25 and 30 mm Hg.
- A PaCO2<20 mm Hg may decrease CBF because of
profound vasoconstriction that produces hypoxia. PaCO2>45 mm Hg induces vasodilation with
increase in CBF, which may trigger increase in ICP.
- (i) Monitor input and output with
urine-specific gravity. Report urine-specific gravity >1.025 or urine output
- May indicate decreased renal perfusion and possible
associated decrease in CPP.
- (i) Monitor ICP if measurement device is in
place. Report ICP>15 mm Hg for 5 minutes.
- (i) Calculate cerebral perfusion pressure
Calculate CPP by subtracting ICP from the mean systemic arterial
Determine MSAP using the following
Systolic BP - Diastolic BP + Diastolic BP
- Should be approximately 90 mm Hg to 100 mm Hg and not <50
mm Hg to ensure blood flow to brain.
- (c) Monitor serum electrolytes, blood urea
nitrogen (BUN), creatinine, glucose, osmolality, hemoglobin (HGB), and
hematocrit (HCT) as indicated.
- To detect treatment complications such as
- (c) Monitor closely when treatment of
increased ICP begins to taper.
- ICP may increase as treatment is tapered.
- (c) Serially monitor ICP pressure and
- Sustained ICP>15 mm Hg causes transtentorial herniation
and brain stem compression/herniation with resultant compression of the
respiratory center, apnea, and cardiac arrest. Presence of A and B waves
indicates neurological deterioration; the physician should be immediately
- Types of ICP waveforms:
- Lundberg A waves (plateau waves) are increased ICP>50 mm Hg
sustained for more than 5 minutes.
- These waves indicate a neurological emergency
necessitating immediate intervention to avoid brain damage.
- B waves are increased ICP, usually between 20 mm Hg to 40 mm Hg
and may precede an A wave.
- These can be seen with changes in respiratory pattern and
must be watched as a possible prelude to A waves.
- C waves are nonpathological and often correlate with heart rate
and respiratory rate.
- These waves are typically <20 mm Hg and occur every 4
to 8 minutes.
- (i) independent
- (i) Elevate head of bed 30 degrees, and keep
head in neutral alignment.
- To prevent decrease in venous outflow with increase in ICP.
Exceptions include shock and cervical spine injuries.
- (i) Avoid Valsalva's maneuver.
- Which increases intrathoracic pressure and CBF, thereby
- (c) If ICP increases and fails to respond
to repositioning of head in neutral alignment and head elevation, recheck
equipment. If ICP is increased, one or more of the following may be prescribed
by the physician:
- Hyperventilate the patient
- To decrease PaCO2 to between 25 mm Hg and 30 mm Hg; this
induces vasoconstriction and a decrease in CBF.
- Administer mannitol 0.25 to 1.0 g per kg given over 30 to 60
- This is a hyperosmotic agent and needs to be given with
caution. It is contraindicated with hypovolemic symptoms (e.g., hypotension,
tachycardia, CHF, renal failure, hypernatremia). A diuretic response can be
anticipated within 30 to 60 minutes. A Foley catheter should be in place. An
intravenous (IV) filter should be used when mannitol is infused. Electrolytes,
osmolality, and serum glucose must be monitored during mannitol
- Administer barbiturates and additional diuretics such as
furosemide (Lasix) if ICP is refractory to hyperventilation and mannitol
- If patient is intubated, administer neuromuscular blocking agent.
- To reduce shivering, coughing, bucking, Valsalva's
maneuver. Remember, however, that neuromuscular blocking agents have no effect
on cerebration; therefore, the patient should receive short-acting sedation
before noxious stimulation.
- Administer a short-acting pain reliever (e.g., morphine [Demerol]
or midazolam [Versed]), before painful stimulation or stress-related care such
as suctioning or IV line changes.
- Pain response includes increased blood
- Administer corticosteroids.
- To reduce the inflammatory response seen in acute brain
- (i) If ICP is elevated to 12 mm Hg to 15 mm Hg,
reduce nursing and medical procedures to those absolutely necessary.
- Counteract noxious stimulation with preoxygenation,
hyperventilation, and analgesia.
- (c) Maintain normothermia with
antipyretics, antibiotics and cooling blanket.
- Fever increases cerebral metabolic demand; may increase
cerebral blood flow and increase intracranial pressure.
- (c) Drain CSF at ordered rate and
- Removal of a small amount of CSF can significantly lower ICP.
This can be accomplished intermittently or, as in patients with hydrocephalus,
Education/Continuity of Care
- (i) independent
- (i) Assess knowledge of disorder, causes,
treatment, and expected outcome.
- (i) Define increased ICP (e.g., increased
pressure within the skull compressing brain tissues).
- (i) Discuss cause if known.
- (i) Reinforce discussions related to
treatment (e.g., head of bed elevated, medication, intubation, and
- (i) Offer family frequent feedback
regarding patient's status.
- (i) Encourage family presence and
participation in comfort measures.
- This occasionally calms the patient and decreases
- (i) Provide social service, community,
and/or support group information as appropriate to primary diagnosis.
- The primary diagnosis (e.g., a resolving head trauma versus
repeated stroke) necessitates different levels of postdischarge care
ICP Monitoring; Neurologic Monitoring; Cerebral Edema Management;
Teaching: Disease Process; Medication Administration: Parenteral
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