This document discusses traumatic head injuries, including causes, risk factors, pathophysiology, assessment, complications, and nursing management. It describes different types of brain injuries such as concussions, hematomas, herniations, and diffuse axonal injury. Key points include identifying high risk groups for TBI, assessing neurological status using the Glasgow Coma Scale, monitoring for increased intracranial pressure, and treating complications like diabetes insipidus and SIADH. Nursing focuses on maintaining cerebral perfusion, minimizing stimuli, and addressing psychosocial needs through education and support.

1. TRAUMATIC HEAD
INJURIES
Linda H.Warren
EdD RN MSN CCRN
NUR 335

2. OBJECTIVES
■ Identify mechanisms of injury associated with brain trauma.
■ Describe the pathophysiologic changes as a basis for signs and symptoms.
■ Discuss the nursing assessment of patients with brain injuries.
■ Identify appropriate nursing diagnosis and expected outcomes for the brain injured
patient.
■ Plan appropriate interventions for patients with brain injuries.
■ Evaluate the effectiveness of nursing interventions for patients with brain injuries.

3. Traumatic Head Injury
• The CDC reports approximately 1.4 million people sustainTBI annually.
• 50,000 die
• 235,000 are hospitalized
• 1.1 million are treated and released from hospital EDs

4. Traumatic Brain Injury Among Children
Among children ages 0-14,TBI is responsible for:
 2,685 deaths
 37,000 hospitalizations
 435,000 emergency department visits

5. Living withTBI
• The CDC reports at least 5.3 millionAmericans living withTBI have…
long term or lifelong need for assistance with ADL’s.
• TBI may cause a wide range of functional changes affecting cognition,
sensation, language or emotions.
• Thinking: memory & reasoning
• Sensation: touch, taste & smell

7. High Risk Groups
• Males 2x more likely than females
• Young children: 0-5 years old
• Elderly >75 years old
• Military Personnel
• African Americans
• 15-19 years of age

8. Which one is most likely to sustain aTBI
leading to hospitalization and/or death?

9. Elderly:

10. Causes & Risk Factors:
• Falls
• Struck by or against an object
(includes intentional self-harm)
• MVC’s
• Assaults – firearms
• Low Socioeconomic
• ETOH use
• Rural (MVC, lightening, chemical
exposure)
• Urban (poisonings and homicide)

11. Pre-Hospital Care of theTrauma Patient
• TRIAGE: involves correct
identification of the injuries-
nature and extent.
• Treatment utilizing ATLS
• Levels ofTrauma Care
• Transport to the nearest available
Level I trauma center.

12. The Trauma Patient
• Traumatic injuries: induced suddenly without warning.
• Injuries are often subtle, lead to longer time to DX and treat effectively.
• Co-morbidities, drugs, and alcohol influence outcome.
• Involvement of bystanders can be difficult to manage:
• people need be interviewed, police involvement is necessary.
• Trauma Coordinators:
• Useful in crowd control.
• Identify those who need emotional support.
• Liaison to hospital support-clergy, psychiatry, grief counselors.

13. Mechanism of Injury (MOI):
• Kinetic Energy: injury
results when the body
can’t tolerate exposure
to excessive force.
• MVA: Acceleration /
Deceleration injuries
• Gunshot wounds
• Thermal (hot or cold-
temperature &
duration)
• Chemical
• Electrical
• Drowning

16. Skull Anatomy Review
 Scalp: five layers of tissue, protective cover, vascular
• Skin
• ConnectiveTissue
• Aponeurotic Galea
• Loose AreolarTissue
• Pericranium
 Skull: Formed by cranium and facial bones.
• Cranium: double layer of solid bone surrounds a spongy middle layer.
• Bones: Frontal,Temporal, Parietal, Occipital and Mastoid
• Vasculature: Middle Meningeal Artery

18. Brain Anatomy
• Cerebrum
• Diencephalon
• Cerebellum
• Brain stem

19. CEREBRUM:
Frontal Lobe:
Abstract thinking, Judgment
Broca’s Area: Speech
Parietal Lobe:
Sensory perception
Occipital Lobe:
Visual reception
Temporal Lobe:
Auditory
Basal Ganglia:
Gray matter, Motor control

22. BRAIN STEM:
• Midbrain
• Pons
• Medulla Oblongata
• Cranial Nerves
• Reticular Activating System
• Meninges
o Pia Mater
o Arachnoid Membrane
o Dura Mater

24. ASSESSINGTHE
CRANIAL NERVES:

25. Cerebrospinal Fluid
• Clear, colorless fluid
• SG of 1.007
• Produced in the ventricles  circulates
around the brain & spinal cord.
• Provides cushion & protection.
Ventricles:
• Center of the brain
• Secretes CSF by filtering blood
• Forms part the blood brain barrier
(BBB)

26. Metabolism & Perfusion: Cerebral Blood
Flow
• High metabolic rate
• Consumes 20% of the body’s oxygen!!
• Largest user of glucose
• Unable to store nutrients
Blood supplied by vertebral and internal
carotid arteries:
 Vertebral - supplies posterior brain,
cerebellum, & brain stem
 Carotid Arteries: supply the cerebrum

27. Cerebral Perfusion:
Cerebral Blood Flow (CBF)
 Dependent upon CPP
 Flow requires a pressure gradient.
Cerebral Perfusion Pressure (CPP)
 Pressure moving the blood
through the cranium
 Autoregulation allows BP changes
to maintain CPP
 CPP = MAP - ICP

29. Mean Arterial Pressure (MAP):
• Dependent on SVR
• MAP = Diastolic + 1/3 Pulse Pressure
• Need a MAP >60 to perfuse the brain!!!
Intracranial Pressure (ICP):
• Pressure exerted by the volume of the
intracranial contents within the cranial vault.
• Influenced by edema & hemorrhage
Cerebral Perfusion:

30. INTRACRANIAL PRESSURE (ICP):
IntracranialVault:
• Rigid – closed container
• Volume relatively stable
Contents:
• Brain (80%)
• Cerebral blood volume (10%)
• CSF (10%)

31. Monroe – Kelly Hypothesis:
 Change in volume of one component
must have reciprocal change in one or
both of the other components.
 If reciprocal change not
accomplished, the result is an
increase in ICP.
Cushing’sTriad: LATE SIGN OF ↑ ICP
 Increased systolic BP
 Widened pulse pressure
 Reflexive bradycardia
INTRACRANIAL PRESSURE (ICP):

33. CEREBRAL BLOOD FLOW &VOLUME
Increased CBF & CBV:
• Systemic hypotension
• ↑ metabolic rate (fever/pain)
• Systemic acidosis
(hypercapnia, ischemia)
• Cerebral vasodilation
Decreased CBF & CBV:
• Systemic HTN
• ↓ metabolic rate: sedation,
paralysis hypothermia
• Systemic alkalosis (hypocapnia)
• Cerebral edema
• ↓ CO
• Cerebral vasoconstriction

34. ↑ ICP: MANAGEMENT
• Adequate Oxygenation
• Management of CO2
• Diuretics:
Osmotic Diuretics: Mannitol
Loop Diuretics: Lasix
• Hemodynamics
• Reduce Metabolic Demands:
• Neuromuscular Blockade
• Barbiturates

36. ICP Waveform:
• Intraventricular Catheter (Ventriculostomy) or
Fiberoptic Transducer
• Subarachnoid Bolt or Screw
• Epidural Sensor or Transducer
• Parenchymal Fiberoptic Catheter
• Hemodynamic Monitoring
• Cerebral Oxygenation Monitoring
• Respiratory Monitoring
• Bedside EEG Monitoring
ICP MONITORING:

37. Measuring Cerebral Oxygenation
• Normal levels: 60-80%
• Cardiac pts may have levels btwn. 55-60%

38. CEREBRAL ISCHEMIA
↑ ICP = ↓ CPP
• Auto-regulation
• Hypoxemia:
 N/V/HA
 Altered LOC
 Amnesia of events
 Restlessness, drowsiness,
change in speech, loss of
judgment
• Secondary Brain Insult

40. CATEGORIES of BRAIN INJURY

45. PRIMARY BRAIN INJURY:
 Concussion
 Coup Injury:
 Direct point of impact, trauma to
the brain.
 Shearing of subdural vessels.
 Trauma to the base of the brain.
 Contre-coup Injury:
 Site of impact when brain hits
opposite side of skull.
 Shearing forces occur throughout
the brain.

46. EPIDURAL HEMATOMA
• RAPIDLY accumulating hematoma:
occurs between dura mater & cranium.
• Usually occurs from a laceration in the
middle meningeal artery.
• Associated with a skull fracture…
 May have HX of head trauma with loss
OC.
Immediate Surgical Intervention!!

47. SUBDURAL HEMATOMA
• Clot formation underneath dura.
• Tearing of the bridging vein
between the cerebral cortex & a
draining venous sinus.
• Venous in origin
• Elderly at risk.
• History may show loss OC with
recovery and NO relapse.

48. ASSESSMENT OF HEMATOMA:
***Determined by rate of accumulation.
Acute: HA, confusion, slowed thinking, agitation.
Subacute: May not appear for days or weeks.
Chronic:
• Vague, attributed to other conditions.
• HA, lethargy, absent mindedness, vomiting.
• Severe symptoms: Seizures, stiff neck, pupil changes, hemiparesis.

50. MANAGEMENT of HEMATOMAS:
• Surgical Evacuation
• Placement of subdural drain - J
• Remains in place for a few days.
• Monitor LOC
• Focused neuro. assessment

51. SUBARACHNOID HEMATOMA (SAH)
• Accumulation of blood btwn.
arachnoid layer of meninges & brain.
• Results in blood leakage into CSF.
• Nuchal Rigidity:
-Irritation of blood in arachnoid space.
-Neck stiffness
-Inability to passively flex & extend the head
normally.

52. MANAGEMENT OF SAH:
• Intraventricular Catheter:
Ventriculostomy
• Drainage of bloody CSF.
• ICP monitoring.
• Monitor Neuro. Status
• Monitor Quantity & Color
of CSF Drainage

54. INTRACEREBRAL HEMATOMA (ICH)
Accumulation of blood in the Parenchyma of brain
tissue.
• Uncontrolled HTN
• Ruptured Aneurysm
• Trauma w. high impact blow to the head
Clinical Manifestations: Vary r/t location of hematoma
Management:
• Management of ICP and CPP
• Surgical evacuation usually not possible

56. DIFFUSE AXONAL
INJURY
• Shearing or tearing of nerve fibers.
• Result of rapid acceleration /
deceleration motion, NOT
necessarily impact.
• Common in whiplash injuries or
amusement park rides.
• Severe brain injury, leads to coma.
Focal Injury:
• Involves a limited and
identifiable site of injury
• Localized damage

57. Categories of Brain Injury
CEREBRAL CONTUSION:
 Bruising of brain tissue.
 Frontal & temporal lobes.
 Complications: cerebral edema &
transtentorial herniation.
 Goal ofTX: Reduce ICP
 Prognosis: guarded

59. SKULL FRACTURES:
Linear Skull Fracture: most common!
• May be a simple non-displaced fracture
• May involve nicking of underlying blood
vessels.
Depressed Skull Fracture:
• Bone fragments embedded in brain tissue
• Brain tissue compression
• Dural laceration
• Associated with scalp laceration.
• Requires debridement and surgery

60. Comminuted (open) Skull Fracture:
• Open fracture with communication
btwn. brain & environment.
• Dura is interrupted
• Risk of infection
• Egg shell Fracture
• Result of a fall or blunt force.
SKULL FRACTURES:

61. Basilar Skull Fracture:
• Linear fracture at base of the brain.
• Associated with dural tear.
• Assess for S&S of meningitis / encephalitis.
S&S:
• Rhinorrhea
• Otorrhea (CSF leak from ears)
• Check drainage for glucose level…
>200mg/dL = CSF
• Filter paper: halo or ring sign (not
conclusive)
• Battle sign (bruising over mastoid process)
• Raccoon Eyes
SKULL FRACTURES:

62. HERNIATION
• Catastrophic Event
Herniation Syndromes:
• Cinigulate
• Central (transtentorial)
• Uncal or lateral transtentorial
• Tonsillar

63. HERNIATION: S&S
• Deterioration in LOC
• Pupillary abnormality
• Motor abnormality
• Brainstem dysfunction
• Alteration in vitals
Cushing’s Triad:
• Increased systolic pressure
• Widening pulse pressure
• Reflexive Bradycardia

64. HEAD INJURY: Nursing
Management
• Assess neuro. status
• Monitor ICP
• Assess for CSF leak
• Maintain airway
• Hyperventilation
• Minimize stimuli
• Elevate HOB (semi-fowlers)
• Fluid & electrolyte / Hypertonic solutions (Mannitol)
• Temp. regulation
• Pharmacological agents
• Implement early nutrition
• Provide emotional support
• Education

67. PHARMACOLOGICAL
AGENTS:
Dexamethasone (Decadron):
• Steroid
• Decreases cerebral edema
Mannitol:
• Osmotic diuretic
• Decreases cerebral edema
• May cause hypovolemia
• Changes in serum and urine osmolality
Furosemide (Lasix)

68. Neurological Assessment
 Review Medical History
 Allergies
 Mechanism of Injury

69. Neurological Assessment
• Onset
• Character
• Severity
• Location
• Duration
• Frequency of S&S
• Associated complications
• Relieving factors

70. Neurological Assessment
• Loss of consciousness (LOC)
• Drowsiness
• Confusion
• Headache
• N/V
• Seizures
• Personality changes

71. GLASGOW COMA SCALE (GCS)
 Best Eye Opening
 BestVerbal Response
 Best Motor Function

72. BEST EYE OPENING:
 Spontaneous--open with blinking
at baseline (4 points)
 Open to verbal stimuli,
command, speech (3 points)
 Open to pain only--not applied to
face (2 points)
 No response (1 point)

73. BEST VERBAL RESPONSE:
 Oriented (5 points)
 Confused conversation, but able
to answer questions (4 points)
 Inappropriate words (3 points)
 Incomprehensible speech (2
points)
 No response (1 point)

74. BEST MOTOR RESPONSE:
 Obeys commands for movement (6 points)
 Purposeful movement to painful stimulus
(5 points)
 Withdraws in response to pain (4 points)
 Decorticate posturing: Flexion in response
to pain (3 points)
 Decerebrate posturing: Extension response
in response to pain (2 points)
 No response (1 point)

75. COMPLICATIONS:
■ Diabetes insipidus (DI)
■ SIADH

76. o Abrupt onset of Polyuria
o High serum osmolarity
(concentrated)
o Low urine osmolarity
(dilute)
o Low urine S.G. (<1.010)
Diabetes Insipidus (DI):

77. DI: Management
Treat Hypovolemia!!!
Desmopressin (DDVAP)
• Most common drug used in
tx: DDAVP (vasopressin)
• When giving DDAVP
monitor patient for S&S of
water intoxication:
• Nausea, HA, HTN,
hyponatremia

78. • Excessive ADH production
• FVO: Increase of total body
water…
- Dilutional hyponatremia 
HA, seizures!
- Hypo-osmolarity
- Concentrated urine
o Low serum osmolarity (dilute)
o High urine osmolarity
(concentrated)
o High urine S.G. (<1.030)
SIADH:

79. ■ #1 FLUID RESTRICTION!!!
– Prevent worsening dilutional hyponatremia
SIADH: Management

80. NURSING DIAGNOSIS
• Ineffective cerebral tissue perfusion
• Risk for Injury
• Fluid Volume Deficit
• Risk for Imbalanced Body Temperature
• Potential for Disturbed Seep Pattern

81. TBI: NURSING INT.
• Seizure precautions
• Education
• Emotional support
• Family support
• Support groups
• National Head Injury Foundation