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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 PATHOPHYSIOLOGY PHARMACOLOGY 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 Care Planning Plan for client adl’s, Monitoring, med admin., Patient education, more…based On Nursing Process: A_D_P_I_E --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 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 Monitor: Neuro Checks q 15 minutes 8 Vital Signs Q15 minutes Glasgow Coma Score Q15 minutes 9 Expanded Neuro Assessment Tool 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 Level Of Consciousness (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 of the brain16pushes 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 19 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 20 ICP Monitoring IntraCranial Pressure 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 Hyperventilate with 100% 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 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 Contusion 36 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 IntraCranial38Hemorrhage 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 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 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 & 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 Hemorrhage 46 47 IntraCerebral Hemorrhage Bleeding within the tissue of the brain Intracerebral Hemorrhage / Hematoma Causes: area - 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: - 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 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 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 58 Recovery can be a long process… 59