This document discusses increased intracranial pressure. It can result from an increase in brain tissue, blood, or cerebrospinal fluid within the skull. Common causes include head injuries, brain tumors, strokes, and hydrocephalus. Symptoms include restlessness, changes in consciousness, changes in vital signs, headaches, nausea, vomiting, pupil changes, and decreased motor function. Treatment involves managing symptoms, monitoring intracranial pressure, administering medications to reduce pressure such as mannitol and diuretics, and surgical intervention if needed.

1. INCREASED INTRACRANIAL
PRESSURE

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

12. Complications
 Cerebral perfusion
 Cerebral herniation
 SIADH
 Diabetes Insipidus

13. Diagnostic Studies
 MRI
 CT Scan
 Cerebral angiography
 EEG
 ICP Measurement
 PET

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

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

25. Normal ICP Waveforms
P1 – percussion wave – represents arterial
pulsations
P2 – rebound wave – reflects intracranial
compliance
P3 – dicrotic wave – follows dicrotic notch;
represents venous pulsations

26. Normal ICP Waveform

27. Abnormal ICP waveform indicating
high pressure & noncompliant brain

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

36. THANK YOU!
Melania silva-banaticla,
rn,man

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

46. a. epidural hematoma
b. subdural hematoma

47. Types of Brain Injury
D. Compression of the Brain – results from
depressed fracture causing edema &
hemorrhage

48. ASSESSMENT
 S/Sx of increased ICP
 CSF leakage from ears & nose
 Battle’s sign ( hematoma at the mastoid
process) in basilar head trauma

49. Battle’s sign

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.

57. Thank you!