Traumatic Brain Injury (TBI) 1

Adult Health IITraumatic Brain Injury—Part 2

Jerry Carley RN, MA, MSN, CNESummer 2010

Concept Map: Selected Topics in Neurological Nursing

PATHOPHYSIOLOGY

Traumatic Brain InjurySpinal Cord Injury

Specific Disease Entities: Amyotropic Lateral Sclerosis Multiple Sclerosis Huntington’s Disease Alzheimer’s Disease Huntington’s Disease Myasthenia Gravis Guillian-Barre’ Syndrome Meningitis Parkinson’s Disease

PHARMACOLOGY

--Decrease ICP--Disease Specific Meds

ASSESSMENTPhysical Assessment Inspection Palpation Percussion Auscultation

ICP Monitoring“Neuro Checks” Lab Monitoring

Care PlanningPlan for client adl’s, Monitoring, med admin.,Patient education, more…basedOn Nursing Process: A_D_P_I_E

Nursing Interventions & EvaluationExecute the care plan, evaluate for Efficacy, revise as necessary

Objectives3

Recall anatomy and physiology of the brain & cranial nerves

Explain pathophysiology of various brain (head) injuries

Detail signs, symptoms and prevention of Increased Intracranial Pressure (ICP)

Demonstrate effective use of Glasgow Coma Scale

Discuss medical & nursing management of brain injuries

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Prevent Secondary Injury !!!

Meaningful recovery of function after head injury is possible IF

secondary injuries are prevented or minimized

Secondary Brain Injury5

Any physiological event that can occur within minutes, hours, or days after the initial injury and leads to further damage of nervous tissue

Secondary Injury is mostly due to Increased ICP caused by hypotension, hypoxia, intracranial bleeding, seizures

Brain Injury Management 6

Frequent Re-assessments

+Rapid Response

Be Vigilant for Increased ICP !7

To understand intracranial pressure, think of the skull as a rigid box. After brain injury, the skull may become overfilled with swollen brain tissue, blood, or CSF.

The skull will not stretch like

skin to deal with these changes. The skull may become too full and increase the pressure on the brain tissue. This is called increased intracranial pressure.

ICP Peaks 48 – 72 hours after injury

Foramen Magnum

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Vital Signs Q15 minutes

Glasgow Coma Score Q15 minutes

Monitor: Neuro Checks q 15 minutes

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Expanded Neuro

Assessment Tool

EARLY Signs of ↑ ICP

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1. Slight LOC changes ***MOST IMPORTANT****

2. Pupils sluggish / Impaired eye movement

3. Limb strength changes

4. Headache

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Change in

Level Of Consciousness (LOC)

***MOST IMPORTANT**** +

EARLIEST

Indicator of neurological deterioration

Cushing’s Triad: Signs of ↑ ICP

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Blood Pressure Systolic BP

Increases Diastolic BP

Decreases Pulse Decreases

WideningPulsePressure

Bradycardia

*** You will also see listed in some resources:--Irregular Respirations (Cheyne-Stokes)--Elevated Temperature (Hyperpyrexia)

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TREND Re-Assessment Data

+

COMPARE

to Baseline Assessment Data

Temp

BP

Pulse

LATE(R) Signs of ↑ ICP

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1. Further decreased LOC

2. Cushing’s Triad / Reflex

3. Abnormal respiration patterns

4. Pupils asymmetrical / Dilated

5. Projectile vomiting

6. Hemiplegia / decorticate or decerebrate posturing

Decerebrate Rigidity15

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Brain Herniation occurs when a part of the brain pushes downward inside the skull through the opening that leads into the neck

(Foramen Magnum)

Too Late Now! Tentorial (Brain) Herniation)

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Tentorial (Brain) Herniation18

Normal

ABI Nursing Interventions19

1) Continuous monitoring of Vitals, PERL and Glasgow Coma Score

2) Report client condition changes ASAP

3) Maintain airway patency (eg positioning, suctioning, etc)

4) Minimize cerebral edema

5) Maximize cerebral perfusion

6) Implement seizure precautions / Siderails

7) Provide emotional support

8) Address all self-care deficits

ICP MonitoringIntraCranial Pressure

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Neurosurgeon drilling prior to placing an intracranial pressure monitor

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Normal ICP for adults:

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10 to 15 mm Hg

ABI Priority Nursing GOALS 23

* Minimize cerebral edema

* Maximize cerebral perfusion

ABI Nursing Interventions24

Continuous monitoring of Vitals, PERL and Glasgow Coma Score

Report client condition changes ASAP

Maintain airway patency BUT…

Avoid suctioning or Hyperventilate with 100% O2 FIRST

ABI Nursing Interventions25

Implement seizure precautions / Siderails

Phenytoin (Dilantin) (prevent / treat Sz)

Maintain head midline (neutral position)

HOB > 30 degrees

ABI Nursing Interventions26

Address all self-care deficits…BUT

Avoid clustering activities

Provide emotional support

ABI Nursing Interventions27

High dose barbituates > induced coma *decreases metabolic demands*

Pharmacological paralysis

Avoid overstimulation:

- Dark quiet room- Limit visitors appropriately- Speak softly- Limit dialogue – keep topics

light hearted

Minimize Cerebral Edema28

Mannitol (Osmitrol) + Urinary catheter

Fluid restriction (I & O)…?

Dexamethasone / Decadron (Know side effects!)

Prevent / Treat fever

Prevent Infections (closed STERILE monitoring system)

Burr Holes29

Minimize Cerebral Edema30

Maintain

Cerebral perfusion pressure MAP of 50 – 70 mm Hg

Prevents Hypoxia (Hypercarbia)

If BP too low…then O2 perfusion is poor…and Brain Can’t Function

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Optimize Cerebral Perfusion32

Keep head position midline

HOB elevated ( 30 - 60 degrees )

Oxygen ****

Sedate prior to activity

Minimal ADL movement of client

Teach Client / Family33

• Minimal stimulation environment

• No coughing, no straining, no hard laughing

• Head midline + Bedrest + HOB elevated

• S & S to report to nurse ASAP (Headache, drainage, etc)

• Purpose + frequency of neuro checks

• Medication regime (Narcotics, diuretics, stool softeners, etc)

• Medical interventions (Tests, traction, logrolling, surgery, etc)

Cerebral Concussion34

A ‘concussion’ is a relatively mild form of traumatic brain injury that results in temporary neurological changes

No apparent structural damage

Usually involves unconsciousness for a few seconds or minutes

Frontal lobe = bizarre irrational behavior

Temporal lobe = amnesia or disorientation

Discharge ….35

Mild concussion & neurological stability = usually will not require hospital admission

However !!! Must be observed by a reliable companion for at least 12 hours

No alcohol for several days

No pain medications stronger than Tylenol

Cerebral Contusion36

More severe

Brain bruised

Possible surface hemorrhage

Initially appears like shock

Can have B & B incontinence

Can be aroused…briefly

IntraCerebral Hemorrhage

Bleeding within the tissue of the brain

IntraCranial Hemorrhage

Bleeding within the cranial vault

IntraCranial Hemorrhage38

Bleeding within the cranial vault

Intracranial Epidural / Extradural Hematoma

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- Between skull and dura- Extreme emergency- Mostly arterial

Epidural / Extradural Hematoma 40

Subdural Hematoma41

Between dura and brain

Mostly venous

Subdural Hematoma42

3 Types:

Acute Sx in 24 – 48 hours

Subacute Sx in 48 hours – 2 weeks

Chronic Sx in 3 weeks – months Common in elderly after even

minor injury Often misdiagnosed as stroke

Subdural Hematoma43

Head trauma leading to subdural hematoma and intracranial hypertension

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Subarachnoid Hemorrhage45

Subarachnoid space is brain surface where blood vessels that supply the brain are located

Common causes of subarachnoid hemorrhage are trauma to “Circle of Willis” aneurysms and congenital arteriovenous malformations (AVM)

Unique S & Ss: - Sudden & unusually severe headache & loss of

consciousness- Neck pain & ridigity (nuchal rigidity) d/t meningeal

irritation

Untreated, the blood supply to a given area of the brain may fall so low that the brain tissue dies resulting in a stroke

Subarachnoid Hemorrhage46

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IntraCerebral Hemorrhage

Bleeding within the tissue of the brain

Intracerebral Hemorrhage / Hematoma

Causes:

- Force is exerted to the head over a small area

(missile injuries, bullet wounds, etc)

- Systemic hypertension causes degeneration and rupture of blood

vessels

- Tumors

- Bleeding disorders

Gunshot Wounds (GSW)

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Suicides, homicides or accidental shootings

GSWs to the head are the most lethal of all firearm injuries

Estimated that greater than 90% fatality rate and at least two thirds of the victims die before ever reaching a hospital

Because of the high mortality associated with gunshot wounds to the head, they account for only approximately 10% of all traumatic brain injury patients who survive

GSW to the Head 52

Visualization of a gunshot wound through the cerebellum by showing the bony details using CT. Clearly visible is the typically funnel shaped exit wound.

Comparative visualization of the soft tissue damage along the bullet track within the cerebellum using MRI.

Outcomes53

The predictors of poor neurological outcome or death after a gunshot wound to the head include:

- Initial Glasgow Coma Scale score- Older age- Presence of low blood pressure or inadequate oxygenation

early after injury- Dilated non-reactive pupils

Bullet trajectory through the brain has major significance. Bullets that traverse the brainstem, multiple lobes of the brain, or the ventricular system (chambers where cerebrospinal fluid is located) are particularly lethal

Many initial survivors develop uncontrollable intracranial pressure and subsequently succumb

 

ALL Cranial Injury Tx 54

ATLS evaluation & intervention (ABCs / Foley / NG / oxygen / Maintain traction)

Constant Monitoring

Diagnosis:

- CT scan (FAST!)- MRI - PET Scan (brain function assessment)

Medical interventions depend on severity:

- Endotracheal intubation / hyperventilation- Sedation- Diuresis- Rapid surgical evacuation

Surgical Outcomes55

Normal pupil reactivity prior to surgery is associated with a favorable outcome in 84 -100% of patients

When both pupils are dilated a poor outcome or death occurs in the great majority of individuals

Postoperative seizures are relatively common in these patients

In general, a favorable (functional) outcome is more likely in those patients who are treated very soon after injury, those who are younger adults, those with a higher GCS (above GCS of 6 or 7), those with reactive pupils, those without multiple cerebral contusions and those who do not develop difficult to control raised intracranial pressure

Head Injury Recovery56

Despite very severe initial injuries, some patients make dramatic recoveries within several months to a year after injury

Despite intensive intervention, long-term disability occurs in a large portion of the survivors

Patients with significant neuro-cognitive impairment are best managed at a comprehensive rehabilitation unit for several weeks or months after they leave the hospital

Recovery of function from the time of discharge to 6 months post-injury can be dramatic, even in some deeply comatose individuals

Improvement generally begins to plateau at 6 months post-injury and is typically maximal by one year to 18 months

Continued….57

Every brain injury is unique.  Severity and types of impairments depend on the area and extent of the damage to the brain

Rehabilitation and support provided to a person who has received an injury has a major impact on the person’s recovery

ABI is known as an Invisible Disability due to the invisible nature of changes that may occur following an injury to the brain, such as memory loss, cognitive impairments, challenging behaviours and personality changes

People with ABI usually retain previous IQ, past memories, skills and interests.  Their ability to use this knowledge can be lost to varying degrees

ABI is not an Intellectual or Psychiatric disability and therefore the needs of a person with an ABI are different from the needs of people with an intellectual or psychiatric disability

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Recovery can be a long process…59