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Brain Injury Part II.

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Presentation on theme: "Brain Injury Part II."— Presentation transcript:

1 Brain Injury Part II

2 Concept Map: Selected Topics in Neurological Nursing
PATHOPHYSIOLOGY Traumatic Brain Injury Spinal Cord Injury Specific Disease Entities: Amyotropic Lateral Sclerosis Multiple Sclerosis Huntington’s Disease Alzheimer’s Disease Myasthenia Gravis Guillian-Barre’ Syndrome Meningitis Parkinson’s Disease ASSESSMENT Physical Assessment Inspection Palpation Percussion Auscultation ICP Monitoring “Neuro Checks” Lab Monitoring PHARMACOLOGY --Decrease ICP --Disease Specific Meds Care Planning Plan for client adl’s, Monitoring, med admin., Patient education, more…based On Nursing Process: A_D_P_I_E Nursing Interventions & Evaluation Execute the care plan, evaluate for Efficacy, revise as necessary

3 Objectives 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

4 Prevent Secondary Injury !!!
Meaningful recovery of function after head injury is possible IF secondary injuries are prevented or minimized

5 Secondary Brain Injury
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

6 Brain Injury Management
Frequent Re-assessments + Rapid Response

7 Be Vigilant for Increased ICP !
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

8 Glasgow Coma Score Q15 minutes
Monitor: Neuro Checks q 15 minutes Vital Signs Q15 minutes Glasgow Coma Score Q15 minutes

9 Expanded Neuro Assessment Tool

10 EARLY Signs of ↑ ICP Slight LOC changes ***MOST IMPORTANT****
2. Pupils sluggish / Impaired eye movement 3. Limb strength changes 4. Headache

11 Level Of Consciousness (LOC) ***MOST IMPORTANT**** + EARLIEST
Change in Level Of Consciousness (LOC) ***MOST IMPORTANT**** + EARLIEST Indicator of neurological deterioration

12 Cushing’s Triad: Signs of ↑ ICP
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)

13 TREND Re-Assessment Data to Baseline Assessment Data
+ COMPARE to Baseline Assessment Data Temp Pulse BP

14 LATE(R) Signs of ↑ ICP Further decreased LOC Cushing’s Triad / Reflex
Abnormal respiration patterns Pupils asymmetrical / Dilated Projectile vomiting Hemiplegia / decorticate or decerebrate posturing

15 Decerebrate Rigidity

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

17 Too Late Now! Tentorial (Brain) Herniation)

18 Tentorial (Brain) Herniation
Normal

19 ABI Nursing Interventions
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

20 ICP Monitoring IntraCranial Pressure

21 Neurosurgeon drilling prior to placing an intracranial pressure monitor

22 Normal ICP for adults: 10 to 15 mm Hg

23 ABI Priority Nursing GOALS
* Minimize cerebral edema * Maximize cerebral perfusion

24 ABI Nursing Interventions
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

25 ABI Nursing Interventions
Implement seizure precautions / Siderails Phenytoin (Dilantin) (prevent / treat Sz) Maintain head midline (neutral position) HOB > 30 degrees

26 ABI Nursing Interventions
Address all self-care deficits…BUT Avoid clustering activities Provide emotional support

27 ABI Nursing Interventions
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

28 Minimize Cerebral Edema
Mannitol (Osmitrol) + Urinary catheter Fluid restriction (I & O)…? Dexamethasone / Decadron (Know side effects!) Prevent / Treat fever Prevent Infections (closed STERILE monitoring system)

29 Burr Holes

30 Minimize Cerebral Edema
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

32 Optimize Cerebral Perfusion
Keep head position midline HOB elevated ( degrees ) Oxygen **** Sedate prior to activity Minimal ADL movement of client

33 Teach Client / Family 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)

34 Cerebral Concussion 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

35 Discharge …. 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

36 Cerebral Contusion More severe Brain bruised
Possible surface hemorrhage Initially appears like shock Can have B & B incontinence Can be aroused…briefly

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

38 IntraCranial Hemorrhage
Bleeding within the cranial vault

39 Intracranial Epidural / Extradural Hematoma
- Between skull and dura - Extreme emergency - Mostly arterial

40 Epidural / Extradural Hematoma

41 Subdural Hematoma Between dura and brain Mostly venous

42 Subdural Hematoma 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

43 Subdural Hematoma

44 Head trauma leading to subdural hematoma and intracranial hypertension

45 Subarachnoid Hemorrhage
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

46 Subarachnoid Hemorrhage

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49 IntraCerebral Hemorrhage
Bleeding within the tissue of the brain

50 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

51 Gunshot Wounds (GSW) 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

52 Head GSW Comparative visualization of the soft tissue damage along the bullet track within the cerebellum using MRI. Visualization of a gunshot wound through the cerebellum by showing the bony details using CT. Clearly visible is the typically funnel shaped exit wound.

53 Outcome 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

54 ALL Cranial Injury Tx 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

55 Surgical Outcomes Normal pupil reactivity prior to surgery is associated with a favorable outcome in % 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

56 Head Injury Recovery 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

57 Continued…. 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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59 Recovery can be a long process…


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