Traumatic Brain Injury (TBI)

1 Adult Health II Traumatic Brain Injury—Part 2 Jerry Carley RN, MA, MSN, CNE Summer 2010

Concept Map: Selected Topics in Neurological Nursing ASSESSMENT

Physical Assessment

Inspection Palpation Percussion Auscultation

ICP Monitoring “Neuro Checks” Lab Monitoring

Care Planning Plan for client adl’s, Monitoring, med admin., Patient education, more…based On Nursing Process: A_D_P_I_E PATHOPHYSIOLOGY Traumatic Brain Injury Spinal 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 Nursing Interventions & Evaluation Execute the care plan, evaluate for Efficacy, revise as necessary

Objectives

3 

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

Prevent Secondary Injury !!!

4

Meaningful recovery of function after head injury is possible

IF

secondary injuries are prevented or minimized

Secondary Brain Injury

5 

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 bleeding, seizures Increased ICP caused by hypotension, hypoxia, intracranial

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. Foramen Magnum ICP Peaks 48 – 72 hours after injury

Monitor: Neuro Checks q 15 minutes

8 

Vital Signs Q15 minutes



Glasgow Coma Score Q15 minutes

Expanded Neuro Assessment Tool

9

EARLY Signs of

↑

ICP

10

1.

Slight LOC changes ***MOST IMPORTANT**** 2. Pupils sluggish / Impaired eye movement 3. Limb strength changes 4. Headache

11

Change in L evel O f C onsciousness (LOC) *** MOST IMPORTANT ****

+

EARLIEST Indicator of neurological deterioration

Cushing’s Triad: Signs of ↑ ICP

12    

Blood Pressure Systolic BP Increases Diastolic BP Decreases Pulse Decreases Widening Pulse Pressure Bradycardia *** You will also see listed in some resources: --Irregular Respirations (Cheyne-Stokes) --Elevated Temperature (Hyperpyrexia)

TREND Re-Assessment Data

13

+

COMPARE to Baseline Assessment Data

Temp Pulse BP

LATE(R) Signs of

↑

ICP

14

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 Rigidity

15

Brain Herniation occurs when a part downward inside the skull through the opening that leads into the neck (Foramen Magnum)

Too Late Now!

Tentorial (Brain ) Herniation)

17

Tentorial ( Brain ) Herniation

18 Normal

ABI Nursing Interventions

4) 5) 6) 7) 8) 1) 2) 3)

19

Continuous monitoring of Vitals, PERL and Glasgow Coma Score Report client condition changes ASAP Maintain airway patency (eg positioning, suctioning, etc) Minimize cerebral edema Maximize cerebral perfusion Implement seizure precautions / Siderails Provide emotional support Address all self-care deficits

ICP Monitoring I ntra C ranial P ressure

20

Neurosurgeon drilling prior to placing an intracranial pressure monitor

21

22

Normal ICP for adults:

10 to 15 mm Hg

ABI Priority Nursing GOALS

23

* Minimize cerebral edema * Maximize cerebral perfusion

ABI Nursing Interventions

24 

Continuous monitoring of Vitals, PERL and Glasgow Coma Score



Report client condition changes ASAP



Maintain airway patency BUT …



Avoid suctioning or with 100% Hyperventilate O2 FIRST

ABI Nursing Interventions

25 

Implement seizure precautions / Siderails



Phenytoin (Dilantin)

(prevent / treat Sz) 

Maintain head midline (neutral position)



HOB > 30 degrees

ABI Nursing Interventions

26 

Address all self-care deficits… BUT



Avoid clustering activities



Provide emotional support

ABI Nursing Interventions

27 

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 Edema

28 

Mannitol (Osmitrol) + Urinary catheter



Fluid restriction (I & O)…?



Dexamethasone / Decadron

(Know side effects!) 

Prevent / Treat fever



Prevent Infections

(closed STERILE monitoring system)

Burr Holes

29

Minimize Cerebral Edema

30

Maintain Cerebral perfusion pressure MAP of 50 – 70 mm Hg Prevents Hypoxia (Hypercarbia)

31

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

Optimize Cerebral Perfusion

32 

Keep head position midline



HOB elevated ( 30 - 60 degrees )



Oxygen ****



Sedate prior to activity



Minimal ADL movement of client

Teach Client / Family

33 •

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 Concussion

34 

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



No apparent structural damage



Usually involves unconsciousness minutes for a few seconds or



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 Contusion

36 

More severe



Brain bruised



Possible surface hemorrhage



Initially appears like shock



Can have B & B incontinence



Can be aroused…briefly

IntraCerebral Hemorrhage IntraCranial Hemorrhage Bleeding within the tissue of the brain Bleeding within the cranial vault

Intra Cranial

38

Hemorrhage

Bleeding within the cranial vault

Intracranial

Epidural / Extradural Hematoma

39 - Between skull and dura - Extreme emergency - Mostly

arterial

Epidural / Extradural Hematoma

40

Subdural Hematoma

41

Between dura and brain Mostly venous

Subdural Hematoma

42

3 Types: Acute Subacute Sx in 24 – 48 hours Sx in 48 hours – 2 weeks Chronic Sx in 3 weeks – months Common in elderly after even minor injury Often misdiagnosed as stroke

Subdural Hematoma

43

Head trauma leading to

subdural hematoma

and intracranial hypertension 44

Subarachnoid Hemorrhage

45  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 Neck pain & ridigity & loss of consciousness (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 Hemorrhage

46

47

Intra Cerebral Hemorrhage

Bleeding within the tissue of the brain

Intracerebral Hemorrhage / Hematoma area Causes: - Force is exerted to the head over a small (missile injuries, bullet wounds, etc) - Systemic hypertension causes degeneration and rupture of blood vessels - Tumors - Bleeding disorders

Gunshot Wounds (GSW)

51  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.

Outcomes

53  The predictors of poor neurological outcome or death after a gunshot wound to the head include: after - Initial Glasgow Coma Scale score - Older age - Presence of low blood pressure or inadequate oxygenation early injury - Dilated non-reactive pupils  Bullet traverse the brainstem, multiple lobes of the brain, or the ventricular system (chambers where cerebrospinal fluid is located) are particularly lethal trajectory through the brain has major significance. Bullets that  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 Outcomes

55 

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 Recovery

56  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 typically maximal by one year to 18 months

and is

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 changes

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  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

58

Recovery can be a long process…

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