2. Increased Intracranial Pressure
A life threatening situation that results from an
increase in any or all of the three components
(brain tissue, blood, CSF) of the skull.
Brain tissues (space-occupying lesions) e.g. tumor,
abscess, edema
Blood supply – e.g. thrombosis, embolism, aneurysm,
A-V malformation
CSF – e.g obstruction to the flow caused by a brain
tumor, overproduction of the CSF due to tumor in the
choroid plexus.
Above the threshold of 20 mm Hg
3. CAUSES
Head injury
Brain tumor
CVA (cerebrovascular accident)
Hydrocephalus
Cerebral edema
Bleeding post surgery
4. Clinical Manifestations
1. Restlessness – initial sign of Increased ICP
2. Change in Level of consciousness
Unconsciousness – abnormal state of complete or
partial unawareness of self or environment.
Lethargic
Drowsy
Stupor
Motor/sensory change
Due to the affectation of ascending reticular activating
system (ARAS).
5. Clinical Manifestations
3. Changes in vital signs – caused by
increasing pressure on the thalamus,
hypothalamus, pons, & medulla.
irregular respirations
bradycardia with full & bounding pulse
widening pulse pressure
( CUSHING’S TRIAD)
6. Clinical Manifestations
4. Headache & irritability
5. Nausea & vomiting (projectile)
6. Pupillary Changes (Ocular signs)
brisk constriction – normal reaction
Anisocoria (inequality in the size of the pupil) due to CN
III compression. There is ipsilateral pupil dilatation.
Sluggish reaction - indicates early pressure on cranial
nerve III.
Fixed pupil – no response to light stimulus, indicates
uncal herniation. This causes compression of the
brainstem that results to respiratory arrest.
Pinpoint pupils – indicate pons involvement
7. Clinical Manifestations
6. Decrease in motor function
Hemiparesis or hemiplegia
Decorticate & decerebrate posturing
•Inability to move the eye upward
•Ptosis of the eyelid
•Papilledema – (choked disk) swelling &
protrusion of the blind spot of the eye caused
by edema & compression of the optic nerve.
8. A. Decorticate response –
flexion of arms,wrists,& fingers
with adduction in upper
extremities. Extension, internal
rotation, & plantar flexion in
lower extremities.
B. Decerebrate response – all
four extremities in rigid
extension, with hyperpronation
of forearms & plantar flexion of
feet.
C. Decorticate response on
right side of the body &
decerebrate response on the
left
D. Opisthotonic posturing
14. Nursing Diagnosis
Ineffective airway clearance r/t ↓ LOC,
immobility, & inability to mobilize
secretions as manifested by ineffective
cough, inability to clear secretions,
crackles on auscultation, thick secretions
Ineffective tissue perfusion (cerebral) r/t
cerebral edema as manifested by GCS <8,
agitation, systolic BP, bradycardia, &
widened pulse pressure, ICP >20mmHg
15. Nursing Diagnosis
Self-care deficit r/t altered LOC as
manifested by inability to follow commands
or move purposively, inability to perform
ADLs.
Interrupted family processes
16. Planning
Have ICP within normal limits
Maintain a patent airway
Demonstrate normal fluid & electrolyte
balance
Have no complications secondary to
immobility & decreased LOC
17. Nursing Management
Monitor v/s / “Neuro-checks”
Maintain patent airway ( lying on one side with
frequent position changes, suctioning, oral
airway)
Control HTN ( it reduces cerebral tissue
perfusion
Keep head of bed elevated 30-45 degrees
It promotes drainage of CSF from the subarachnoid
space of the brain
It also promote maximum lung expansion
18. Nursing Management
Avoid factors that increase ICP
Nausea & vomiting
Sneezing & coughing
Valsalva maneuver, e.g. straining at stool
Over suctioning
Restraints
Rectal examination
Enema
Flexion of waist, hip neck ( bending or stooping)
Abdominal distention (NGT)
19. Nursing Management
ABG monitoring
Fluid & electrolyte balance
IVF monitoring, restrict fluid intake 1,200 to 1,500
ml/day to reduce CSF production
Electrolyte determinations (serum glucose, sodium,
potassium & osmolality)
Urinary output is monitored to detect problems
related to diabetes insipidus ( uo related to ↓ in
antidiuretic hormone secretion.
SIADH (syndrome of inappropriate antidiuretic
hormone), which results in ↓ in urinary output.
20. Nursing Management
Monitoring intracranial pressure
Ventriculostomy – the “gold standard” for
monitoring ICP whereby a catheter is inserted
into the lateral ventricle & coupled to an
external transducer.
Consider infection
21.
22. Special Consideration
ICP should be measured as a mean
pressure at the end of expiration.
If a CSF drainage device is in place, the
drain must be closed for at least 6
minutes to ensure an accurate reading
The waveform strip should be recorded
along with other pressure monitoring
waveforms
23. Factors Affecting ICP readings
CSF leaks around the monitoring device
Obstruction of the intraventricular catheter
or bolt (from tissue or blood clot)
Difference between the height of the bolt &
the transducer
Kinks in the tubing
In fluid coupled systems, bubbles or air in
the tubing also dampens the waveform
28. Pathologic ICP waveforms
A (plateau) waves indicate sharp increase in ICP, B waves
often precede A waves & C waves are related to normal
fluctuations in resp. & BP
29. Drug Therapy
Mannitol – osmotic diuretics, most widely used
agent & is given IV.
Decrease ICP in two ways:
1. Plasma expansion- there is an immediate plasma-
expanding effect that reduces the hematocrit & blood
viscosity, thereby increasing CBF (cerebral blood
flow) & cerebral oxygen delivery.
2. Osmotic effect – fluid moves from the tissues into the
blood vessels, therefore the ICP is reduced by a
decrease in the total brain fluid content
• Contraindicated if renal disease is present & if serum
osmolality is elevated.
• Check hourly urine output & BP
30. Loop diuretics
Furosemide (Lasix), Bumetanide (Bumex),
Ethacrynic acid (Edecrin)
Inhibit sodium & chloride reabsorption in the
ascending limb of the loop of Henle & thus
reduce blood volume & ultimately tissue volume.
Also cause a reduction in the rate of CSF
production.
Normal CSF production (adult) 20 to 30ml/hour
Total CSF volume 90 to 150ml within the ventricles &
subarachnoid space
31. Corticosteroids
E.g Dexamethasone (decadron)
Thought to control the vasogenic edema
surrounding tumors & abscesses but appear to
have limited value in management of head-
injured patients.
It reduces cerebral edema by its anti-
inflammatory effect.
The only corticosteroid that can pass through the
blood-brain barriers.
S/E: hyperglycemia, increased incidence of
infections, gastrointestinal (GI) bleeding &
hyponatremia
32. Barbiturates
Pentobarbital (Nembutol, Thiopental
(Penthotal)
Produce a decrease in cerebral
metabolism & subsequent decrease in ICP
Secondary effect is a reduction in cerebral
edema & production of a more uniform
blood supply to the brain
33. Antiseizure drugs
Valium (Diazepam)
Phenytoin Sodium (Dilantin)
Administer after meals if given p.o. to prevent GI upset
Prepare 10 ml NSS to flush the IV line before & after
administration, it crystallizes in the vein
Side effects:
Gum hyperplasia – provide good oral care, use soft-bristled
toothbrush, massage the gums
Sedation
Hirsutism
Ataxia
Nystagmus
GI upset
aplastic anemia
Reddish urine
34. Phenobarbital (Na Luminal)
Side effects:
Sedation in adults
Paradoxical active reaction in children
Habituation
Tegretol (Carbamazepine)
Side effects: rash, ataxia, drowsiness
35. Antacids to prevent GI irritation which may
be induced by dexamethasone
Histamine-H2 receptor antagonists to
prevent stress ulcer
Anticoagulants to prevent
thromboembolism
NOTE: Opiates & sedatives are
contraindicated because they cause
respiratory depression & acidosis
37. HEAD INJURY
includes any trauma to the scalp, skull, or
brain.
The term “Head Trauma” is used primarily to
signify craniocerebral trauma, which includes an
alteration in consciousness, no matter how brief.
Has high potential for poor outcome
Deaths occur at 3 time points after injury:
immediately after injury, 2 hours after injury &
approximately 3 weeks after injury.
38. Factors that predict poor outcome
Presence of intracranial hematoma
Increasing age of the patient
Abnormal motor responses
Impaired or absent eye movements or pupil light
reflexes
Early sustained hypotension
Hypoxemia or hypercapnia (presence of high
CO2 in the blood)
ICP levels higher than 20mmHg
39. Etiology
A. Blunt
Motor vehicle collision
Pedestrian event
Fall
Assault
Sports injury
B. Penetrating
Gunshot wound
arrow
40. Types of head injuries
1. Scalp Lacerations – most minor type of
head trauma.
Associated with profuse bleeding
because the scalp contains many blood
vessels with poor constrictive abilities
Infection is the major complication
41. Types of head injuries
2. Skull Fractures
linear or depressed
Simple, comminuted or compound
Closed or open
Type & severity depend on the velocity,
momentum, the direction of injuring agent, &
the site of impact.
42. Major potential complication of skull
fracture
Intracranial infections
Hematoma
Meningeal & brain tissue damage
43. Types of Brain Injury
A. Concussion – injury is a temporary loss
of neurologic function with no apparent
structural damage
- May have period of unconsciousness
lasting for a few seconds or minutes
- Observe patient for headache, dizziness
, lethargy, irritability and anxiety
44. Types of Brain Injury
B. Contusion – bruising of the brain tissue
within a focal area that maintains the
integrity of the pia mater & arachnoid
layers.
A structural alteration characterized by
extravasation of blood cells.
Seizures are a common complication
45. Types of Brain Injury
C. Laceration – tearing of tissues caused by
a sharp fragment or object or a shearing
force.
Hemorrhage is a serious complication, that
may cause:
Epidural hematoma – bleeding between the dura & the
inner surface of the skull.
Subdural hematoma – bleeding between the dura matter
& the arachnoid layer of the meningeal covering of the
brain.
Intracerebral or subarachnoid hemorrhage
51. Collaborative Management
Care of the client with increased ICP
Monitor for s/sx of meningitis, atelectasis,
pneumonia, UTI
Monitor drainage from ears & nose.
Two methods of testing:
1. test the leaking fluid with a Dextrostix or Tes-
Tape to determine the presence of glucose, CSF
gives a positive reading for glucose.
2. “halo” or “ring” sign
52. Nursing Diagnosis
Ineffective Tissue Perfusion (cerebral) r/t
interruption of CBF associated with
cerebral hemorrhage, hematoma, &
edema.
Hyperthermia r/t metabolism, infection, &
loss of cerebral integrative function
secondary to possible hypothalamic injury.
Acute pain (headache) r/t trauma &
cerebral edema
53. Nursing Diagnosis
Impaired physical mobility r/t ↓ LOC &
treatment-imposed bed rest.
Anxiety r/t abrupt change in health status,
hospital environment, & uncertain future
Potential complication: ICP r/t cerebral
edema & hemorrhage
54. Planning
Maintain adequate cerebral perfusion
Remain normothermic
Be free from pain, discomfort & infection
Attain maximal cognitive, motor & sensory
function
55. Interventions (emergency
management)
Initial
Ensure patent airway
Stabilize cervical spine
Administer O2 via nasal cannula
Establish IV access
Control external bleeding with sterile pressure
dressing
Assess for rhinorrhea, otorrhea, scalp wounds
Remove patient’s clothing
56. Interventions (emergency
management)
Ongoing Monitoring
Maintain patient warmth using blankets, lights,
warm IV fluids, warm humidified O2
Monitor v/s, LOC, O2 Sat, cardiac rhythm,
GCS score, pupil size & reactivity.
Anticipate need for intubation if gag reflex is
absent
Assume neck injury with head injury
Administer fluids cautiously to prevent fluid
overload & ICP.