8. Head Injury
• High potential for poor outcome
• Deaths occur at three points in time after
injury:
– Immediately after the injury
– Within 2 hours after injury
– 3 weeks after injury
9. Classification
• By Nature of insult; penetrating or blunt.
• Concomitant injuries; isolated head injury or
multiple trauma.
• Timing of the injury; Primary or Secondary.
10. Classification
• Primary injury is that occurring at the scene and is
usually outside the control of the intensivist.
• Secondary injury is anything that occurs to augment
the primary injury; the prevention of this is
predominantly where intensive therapy is aimed.
11. Types of Head Injuries
• Scalp lacerations
– The most minor type of
head trauma
– Scalp is highly
vascular → profuse
bleeding
– Major complication is
infection Cephal Hematoma
12. Minor Head Trauma
Manifestation
– Concussion
• A sudden transient mechanical head injury
with disruption of neural activity and a
change in LOC
• Brief disruption in LOC
• Amnesia
• Headache
• Short duration
13. Minor Head Trauma
Manifestation
– Postconcussion syndrome
• 2 weeks to 2 months
• Persistent headache
• Lethargy
• Personality and behavior changes
14. Types of Head Injuries
• Skull fractures
– Linear or depressed
– Simple,
comminuted, or
compound
– Closed or open
– Direct & Indirect
15. Types of Head Injuries
• Skull fractures
– Location of fracture alters the
presentation of the manifestations
– Facial paralysis
– Deviation of gaze
– Battle’s sign
16. Types of Head Injuries
• Basal Skull fractures
– CSF leak (extravasation) into ear (Otorrhea) or
nose (Rhinorrhea)
– High risk infection or meningitis
– “HALO Sign (Battle Sign)”
– Possible injury to Internal carotid artery
– Permanent CSF leaks possible
17. Basilar :
with/with out CSF leak
with/with out seventh-nerve palsy
Raccoon eyes
Battle sign CSF rhinorrhea
20. Manifestation of Major Head
Trauma
– Includes cerebral contusions and
lacerations
– Both injuries represent severe trauma to
the brain
21. Manifestation of Major Head
Trauma
– Contusion (“brain bruises” )
• bruising’ within the brain with relatively
localised cellular damage, haemorrhage and
oedema or The bruising of brain tissue
within a focal area that maintains the
integrity of the pia mater and arachnoid
layers
– Lacerations
• Involve actual tearing of the brain tissue
• Intracerebral hemorrhage is generally
associated with cerebral laceration
22. Pathophysiology
• Diffuse axonal injury (DAI)
– Widespread axonal damage occurring
after a mild, moderate, or severe TBI
– Process takes approximately 12-24 hours
23. Pathophysiology
• Diffuse axonal injury (DAI)
– Clinical signs:
∀↓ LOC
∀↑ ICP
• Decerebration or decortication
• Global cerebral edema
24. Approach to a Patient With Head
Injury
• History
• Initial Assessment
Primary Survey
Secondary Survey
25. Diagnostic Studies and
Collaborative Care
• CT scan considered the best diagnostic test to
determine craniocerebral trauma
• MRI
• Cervical spine x-ray
• Glasgow Coma Scale (GCS)
26. Management of Traumatic Head
Injury
• Maximize oxygenation and ventilation
• Support circulation / maximize cerebral perfusion
pressure
• Decrease intracranial pressure
• Decrease cerebral metabolic rate
27. Nursing Management
Nursing Assessment
– GCS score
– Neurologic status (GCS)
– Presence of CSF leak
31. Nursing Management
Intubation with Cervical inline stabilization
• Breathing and ventilation : Intubation precautions
Pre-medicate with Lidocaine, 1mg/kg IV 2
minutes prior to attemptICP Spike
• Laryngoscopy produces an
34. Decreasing Intracranial Pressure
Diuretic Therapy
Osmotic Diuretic Loop Diuretic
• Mannitol (0.25-1 gm / kg) • Furosemide
• Increases serum osmolarity • Decreased CSF formation
• Vasoconstriction • Decreased systemic and
(adenosine) / less effect if cerebral blood volume
autoregulation is impaired (impairs sodium and water
and if CPP is < 70 movement across blood
• Initial increase in blood brain barrier)
volume, BP and ICP • May have best affect in
followed by decrease conjunction with mannitol
• Questionable mechanism of
lowering ICP
35. Nursing Management of Skull
Fractures
• Minimize CSF leak
– Bed flat
– Never suction orally; never insert NG tube; never use Q-Tips
in nose/ears; caution patient not to blow nose
• Place sterile gauze/cotton ball around area
• Verify CSK leak:
– DEXTROSTIX: positive for glucose
• Monitor closely: Respiratory status+++
36. Nursing Management
Nursing implementation
Health Promotion
• Prevent car and motorcycle accidents
• Wear safety helmets
37. Nursing Management
Nursing implementation
Acute Intervention
• Maintain cerebral perfusion and prevent
secondary cerebral ischemia
• Monitor for changes in neurologic status
38. Nursing Management
Nursing implementation
Ambulatory and Home Care
• Nutrition
• Bowel and bladder management
• Spasticity
• Dysphagia
• Seizure disorders
• Family participation and education
39. Nursing Management
Evaluation
Expected Outcomes
• Maintain normal cerebral perfusion
pressure
• Achieve maximal cognitive, motor, and
sensory function
• Experience no infection, hyperthermia, or
pain
40. Summary of Recommended Practices
• Decrease intracranial pressure
– Evacuate mass occupying hemorrhages
– Consider draining CSF with ventriculostomy when possible
– Hyperosmolar therapy, +/- diuresis (cautious use to avoid
hypovolemia and decreased BP)
– Mid-line neck, elevated head of bead (some research supports
elevation not > 30 degrees)
– Treat pain and agitation - consider pre-medication for nursing
activities, +/- neuromuscular blockade (only when needed)
– Careful monitoring of ICP during nursing care, cluster nursing
activities and limit handling when possible
– Suction only as needed, limit passes, pre-oxygenate / +/- pre-
hyperventilate (PaCo2 not < 30) / use lidocaine IV or IT when
possible
A&E(VMH)
– After careful preparation of visitors, allow calm contact
41. Complications
• Epidural hematoma
– Results from bleeding between the dura
and the inner surface of the skull
– A neurologic emergency
– Venous or arterial origin
42. Complications
• Subdural hematoma
– Occurs from bleeding between the dura
mater and arachnoid layer of the
meningeal covering of the brain
43. Complications
• Subdural hematoma
– Usually venous in origin
– Much slower to develop into a mass large
enough to produce symptoms
– May be caused by an arterial hemorrhage
44. Complications
• Subdural hematoma
– Acute subdural hematoma
• High mortality
• Signs within 48 hours of the injury
• Associated with major trauma (Shearing
Forces)
• Patient appears drowsy and confused
• Pupils dilate and become fixed
45. Complications
• Subdural hematoma
– Subacute subdural hematoma
• Occurs within 2-14 days of the injury
• Failure to regain consciousness may be
an indicator
Subgaleal_hemorrhage Subgaleal hemorrhage or hematoma is bleeding in the potential space between the skull periosteum and the scalp galea aponeurosis. Causes Majority (90%) result from vac Cephalhematoma is a hemorrhage of blood between the skull and the periosteum of a newborn baby secondary to ru ...
Battles's Sign- Periauricular ecchymosis Periauricular - around the external ear Ecchymoisis - bleeding under the skin
Raccoon Eyes - Ecchymosis in the periorbital area, resulting from bleeding from a fracture site in the anterior portion of the skull base
Subdural hemorrhage is bleeding due to trauma that occurs between the outer and middle membranes (meninges) covering the brain. The outer membrane is called the dura, the middle is called the arachnoid, and the inner membrane is known as the pia mater. Subdural hemorrhage, therefore, is bleeding beneath (below) the dura and above the arachnoid. This type of hemorrhage can result from blunt head trauma as minimal as a mild bump.
Cerebral contusions are “brain bruises” which occur from acceleration and de-acceleration of the head. Head trauma can also produce microscopic changes that are scattered throughout the brain. This category of injury is called diffuse axonal injury (DAI) and refers to the microscopic severing of axons (fibers which allow brain neurons to communicate with each other). If enough axons are injured in this way, then the ability of nerve cells to integrate and function may be lost or greatly impaired