NUR 265 Exam 3 Study Guide (2026) | Medical-Surgical Nursing | Galen

NUR 265
EXAM 3 STUDY GUIDE
Medical-Surgical Nursing
Galen College of Nursing

,NUR 265- EXAM THREE STUDY GUIDE

UNIT 7

INCREASED INTRACRANIAL PRESSURE (increased ICP)
 Normal range 10-15 mmHg
o 20mmHg and higher, if sustained, causes brain neurons to die
 Caused by:
o Bearing down, coughing, lying flat, any type of tissue hypoxia, fluid and
electrolyte imbalance, increase in CO2,
 Usually occurs 24-48 hours after initial injury
 Hydrocephalus leads to increased ICP if left untreated
 Any personality change/decline in LOC is the first sign of increased ICP!
o Agitation, restlessness, irritability, disorientation!
 Key Features of ICP:
o Cushing’s triad
 Severe Hypertension
 Bradycardia
 Widened pulse pressure
o Signs/symptoms of increase ICP
 Change in LOC
 Hypertension or hypotension
 change in size of pupils (“blown pupils”)
 cranial nerve dysfunction
 ataxia
 nausea/vomiting
 Cushing’s triad
 irregular respiratory rate
 changes in pupils  unequal, fixed, dilated
 severe headaches
 projectile vomiting
 seizures
 posturing
 decerebrate
o arms extended straight, legs straight, toes pointed
downward
 decorticate
o arms flexed inward; feet turned inward
 be constantly assessing your patient! They can go downhill quickly!
 Interventions of ICP
o Sit up HOB at least 30 degrees or as recommended by PHCP
o ABCs first!

,  Airway I most important!
 Upper cervical nerves innervate the diaphragm and if injury to the
brainstem. Monitor for hypoxia, hypocapnia, etc. report any
respiratory distress signs to the PHCP!
o Mechanical ventilation!
 No PEEP! - increase ICP
 PaCO2 35-38 mmHg because acidosis increases ICP
 Hyper oxygenate prior to and after suctioning
 Don’t hyperventilate!
o Keep O2 sat above 94 and provide O2 if lower than that.
o Keep head midline and neutral position
o Minimize hip and neck flexion when repositioning- logroll the patient to avoid
this
o Space out activities with patient. Allow patient’s ICP to recover before doing
more activity – AVOID CLUSTER CARE
o Keep room quiet and dark
o Mannitol- osmotic diuretic that allows for reverse fluid shift in the brain
 Use filter needle!  crystalizes
o Loop diuretics
 Used with mannitol
 Once fluid shifts back into vascular system, loop diuretics eliminate
the fluid.
o Don’t give glucocorticoids!
 Elevates glucose, wont treat the ICP and has higher mortality rate
o Barbiturate coma- to rest the brain
 Phenobarbital
o Opioids- vented patients for pain and agitation
o Antiepileptic- patient will seize
o Cooling baths of temps are above 101.5
 Tylenol won’t affect neuro temp!
 Three types of edema contributing to ^ICP
o Vasogenic edema
 Caused by abnormal permeability of the walls of the cerebral vessels,
allowing protein-rich plasma to leak into extracellular space of the
brain
o Cytotoxic edema
 Occurs as a result to a hypoxic insult, causes disturbance in cell
metabolism
 Brain quickly depleted of oxygen, glucose, glycogen
 Damage results in cell death
 May lead to vasogenic edema and worsening ^ICP
o Interstitial edema
 Occurs with fluid accumulation between cells of the brain

,  Associated with elevated BP and CSF pressure

TRAUMATIC BRAIN INJURY (TBI)
 TBI is damage to the brain from an external mechanical force and not caused by
neurodegenerative or congenital conditions.
 Open brain injury- occurs when the skull is fractured or when it is pierced by a
penetrating object. – could get meningitis because the skull is open
 Closed traumatic brain injury- the integrity of the skull and brain is intact from external
forces, but brain is damaged
o Concussion- mild traumatic brain injury
o Contusion- localized
 Coup- bruising found at the site of the bruise
 Contra-coup- or in line of opposite site of impact
 Primary- same as SCI- occurs at the time of the injury and results from the physical stress
(force) within tissue caused by blunt force
 Secondary injury- what happens because of the injury- hemorrhage, increased ICP,
hydrocephalus, brainstem herniation.
 Complications of TBI
o Epidural hematoma- atrial bleeding (active bleed- not a clot) into the space
between the dura and the inner skull- caused by fracture of the temporal bone
 Lucid intervals- patient is awake and talking followed by intervals of
unconsciousness
 Occurs minutes after injury
o Subdural hematoma- results from venous bleeding (active bleeding not a clot)
into the space beneath the dura and above the arachnoid. Occurs most often
from tearing of the bridging veins within cerebral hemisphere or from a
laceration of brain tissue.
 Bleeding from this injury occurs more slowly than from an epidural
hematoma
 Acute SDH – presents within 48hrs after impact
 Subacute SDH- presents within 48hrs to 2 weeks
 Chronic SDH- 2 weeks to several months
 Highest mortality rate because they are often unrecognized until
patient presents with severe neurologic compromise
o Intracerebral hematoma- acts as a tumor and can be potentially devastating,
depending on location.
 May also produce significant brain edema and ^ICP.
 Results from blow to the back of the head, fractures, torsion injuries to
brainstem
 Brainstem injuries have very poor prognosis.
o Hydrocephalus- CSF accumulation on the brain. ^ICP
 Communicating hydrocephalus – impaired reabsorption of CSF – from
subarachnoid hemorrhage or meningitis