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INCREASED INTRACRANIAL
PRESSURE
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
CAUSES
 Head injury
 Brain tumor
 CVA (cerebrovascular accident)
 Hydrocephalus
 Cerebral edema
 Bleeding post surgery
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).
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)
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
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.
 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
Complications
 Cerebral perfusion
 Cerebral herniation
 SIADH
 Diabetes Insipidus
Diagnostic Studies
 MRI
 CT Scan
 Cerebral angiography
 EEG
 ICP Measurement
 PET
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
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
Planning
 Have ICP within normal limits
 Maintain a patent airway
 Demonstrate normal fluid & electrolyte
balance
 Have no complications secondary to
immobility & decreased LOC
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
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)
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.
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
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
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
Normal ICP Waveforms
P1 – percussion wave – represents arterial
pulsations
P2 – rebound wave – reflects intracranial
compliance
P3 – dicrotic wave – follows dicrotic notch;
represents venous pulsations
Normal ICP Waveform
Abnormal ICP waveform indicating
high pressure & noncompliant brain
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
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
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
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
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
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
 Phenobarbital (Na Luminal)
 Side effects:
 Sedation in adults
 Paradoxical active reaction in children
 Habituation
 Tegretol (Carbamazepine)
 Side effects: rash, ataxia, drowsiness
 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
THANK YOU!
Melania silva-banaticla,
rn,man
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.
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
Etiology
A. Blunt
 Motor vehicle collision
 Pedestrian event
 Fall
 Assault
 Sports injury
B. Penetrating
 Gunshot wound
 arrow
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
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.
Major potential complication of skull
fracture
 Intracranial infections
 Hematoma
 Meningeal & brain tissue damage
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
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
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
a. epidural hematoma
b. subdural hematoma
Types of Brain Injury
D. Compression of the Brain – results from
depressed fracture causing edema &
hemorrhage
ASSESSMENT
 S/Sx of increased ICP
 CSF leakage from ears & nose
 Battle’s sign ( hematoma at the mastoid
process) in basilar head trauma
Battle’s sign
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
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
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
Planning
 Maintain adequate cerebral perfusion
 Remain normothermic
 Be free from pain, discomfort & infection
 Attain maximal cognitive, motor & sensory
function
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
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.
Thank you!

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ICP-Head-injury.ppt

  • 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
  • 9.
  • 10.
  • 11.
  • 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
  • 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
  • 24.
  • 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
  • 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
  • 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
  • 50.
  • 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.