Traumatic Brain Injury PDF

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Summary

Warning: TT: more functions defined than expected Traumatic Brain InjuryHead Injury  Includes any trauma to the scalp, skull or brain.  Term used primarily to signify craniocerebral trauma Epidemiology  40% of traumatic injuries include the brain  1 million persons are treated and released with ...

Description

Traumatic Brain Injury Head Injury  Includes any trauma to the scalp, skull or brain.  Term used primarily to signify craniocerebral trauma Epidemiology  40% of traumatic injuries include the brain  1.4 million persons are treated and released with TBI (Traumatic Brain Injury)  50,000 people die  235,000 people are hospitalized with TBI Etiology  Mild concussion to coma and death  Most serious form (TBI)  Falls: 28%  MVC: 20%  Assaults: 11%  Highest risk: 15-19 yrs.  Males> females Pathophysiology  Not all damage occurs at moment of impact  Two forms  Primary injury  Initial damage to the brain  Contusion, laceration, torn blood vessels  Secondary injury  Evolves over hours or days  Results from inadequate delivery of nutrients and oxygen Cranial Vault Contents  Brain  Blood  Cerebrospinal fluid (CSF) Monro-Kellie Doctrine  Cranial vault is closed system  If one system increases in volume→two others must decrease in volume

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CSF (75 mL:10%) Blood (75 ml:10%) Brain Mass (1400 gms: 80%)

Normal ICP = 5 - 15 mmHg 3 constant volumes in skull (chg. in one leads to shift in other) Brain mass (tissue) 80% Vascular (blood) 10% CSF 10% Central Nervous Sys. Peripheral Nervous Sys. Autonomic Nervous Sys Brain (Sympathetic) 12 pr. Cranial nerves Spinal Cord (Parasympathetic) 31 pr. Spinal nerves Region & Functions Cerebrum- Interpret sensory input; control skeletal muscle activity; process intellect & emotions; contain skills memory Diencephalon - Conduct sensory & motor impulses; regulate autonomic nervous system; regulate & produce hormones; mediate emotional response Brain Stem - Conduction pathway; site of decussating of tracts; contains resp. nuclei; helps regulate skeletal muscles Cerebellum - Processes inf.; provides info necessary for balance, posture & coordinated muscle movement

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Pathophysiology

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Skull & Scalp Injuries Skull Fractures  Linear  Depressed  Simple, Comminuted  Open or Closed Scalp Lacerations  Scalp is very vascular with poor constrictive abilities  Profuse bleeding can occur  Complication: Infection Clinical Manifestations  Depends on severity and anatomic location  Hemorrhage from nose, pharynx or ears  Ecchymosis over mastoid (battle’s sign)  CSF otorrhea (basilar skull fracture)  CSF rhinorrhea (basilar skull fracture)

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Neuro Assessment  Battle’s sign  Raccoon's Eyes/Periorbital Ecchymosis  Glasgow Coma Scale

Medical Management  Non-depressed skull fractures generally do not require surgical treatment  Close observation  Home vs. hospitalization  Depressed skull fractures require elevation of skull and debridement  Associated brain injury  Cervical collar Important Points!  Brain can’t store oxygen or glucose  Cell death/irreversible brain damage occurs if blood supply is interrupted for even a few minutes  Closed head injury  Open head injury

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Review of Anatomy

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Location of Hematomas

Head Injuries Concussion  Temporary loss of neurologic function  +/- LOC  Close observation overnight  Post-concussive syndrome Contusion  Brain is bruised  Most common: anterior portions of frontal and temporal lobes  Confusion/stupor  Patient outcomes based on area and severity of injury  Hemorrhage and edema peaks at 18-36 hours  Diffuse Axonal Injury  Widespread axonal damage  Occurs after mild, moderate or severe TBI (12-24 hours to develop)  Axon swelling occurs 7

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Diffuse, no identifiable lesions Prolonged traumatic coma Poor prognosis S/S:  Decreased LOC  Increased ICP  Global Cerebral

Edema  DAI   Intracranial Hemorrhage  Hematomas: collection of blood in brain 1. Epidural: above the dura 2. Subdural: below the dura 3. Intracerebral: within the brain  Epidural Hematoma  Bleeding between the skull and the dura  Neurologic emergency 1. Linear skull fracture 2. Laceration of middle meningeal artery 3. Temporal bone  Brief LOC→ lucid interval→ increasing restlessness, agitation→ coma  Epidural Hematoma  Brain attempts to compensate by rapid absorption of CSF to maintain normal intracranial pressure  Epidural Hematoma Treatment  Burr holes  Clot removal  Bleeding control  Craniotomy may be required  Drain placement to prevent re-accumulation of blood  Epidural Hematoma  Subdural Hematoma  Occurs from bleeding between the dura mater and the brain  Usually venous in origin Etiology  Trauma, coagulopathy or ruptured aneurysm  Usually venous in origin 8

 Acute and Chronic in nature  Acute Subdural Hematoma Acute  Associated with major head injury  Clinical symptoms develop 24-48 hours  Change in LOC  Pupillary changes  Hemiparesis  ↑BP/↑RR/↓HR  Treatment: Emergent craniotomy/evacuation  Chronic Subdural Hematoma Chronic  Frequent in elderly  Minor injury’s can cause symptoms weeks to months down the line  HA, personality changes, focal seizures  Mistaken for psychiatric condition  Treatment: Burr holes, craniotomy Intracerebral Hematoma  Bleeding occurs within the parenchyma  Force exerted within a small area causing hemorrhage  Other causes  Systemic hypertension  Rupture of aneurysm or vessel (Subarachnoid Hemorrhage)  Intracranial tumors  Bleeding disorders (leukemia, hemophilia, thrombocytopenia)  Complications of anticoagulant therapy  Vascular anomalies Intracerebral Hemorrhage  Treatment  Supportive care  Management of ICP  Management of fluid/electrolytes  Management of hypertension  Surgical intervention: craniotomy

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Penetrating Head Trauma  Clinical Manifestations and Physical Assessment (p. 1861, p. 1927)  Altered level of consciousness (ALOC)  Confusion  Pupillary abnormalities  Altered or absent gag reflex  Absent corneal reflex  Sudden onset of neurologic deficits  Changes in vital signs  Altered respiratory pattern  Widened pulse pressure  Bradycardia  Tachycardia  Hypo or hyperthermia  Vision/hearing impairment  Sensory dysfunction  Headache  Seizures Pupillary Changes Neuro Assessment: Abnormal Posturing  Decorticate Rigidity (Flexion)  leg extension and internal rotation. Internal rotation and adduction of the arms.  Decerebrate Rigidity (Extension)  Hyperpronation of the arms. Plantar flexion of the feet.  Glasgow Coma Scale o Eye Opening response o Verbal Response o Motor Response

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Diagnostic Measures  CT scan of head/brain and neck  Presence, nature, location and extent of acute lesions  Helpful in ongoing management (cerebral edema, late changes)  MRI  More accurate picture of anatomic nature of injury  When stable  Positron emission tomography (PET)  Determines brain function  Plain x-ray films  Cerebral angiography Management of Brain Injuries  Physical examination  Neurologic examination  Diagnostics  CT or MRI  Any patient with a head injury is presumed to have a cervical spine injury until proven otherwise 11

 Head and neck in alignment  Cervical collar and long-spine board  Prevention of secondary injury  Stabilization of cardiovascular and respiratory function to maintain adequate cerebral perfusion Therapy is directed towards→  Preserving brain homeostasis  Preventing secondary injury  Causes of secondary injury  Cerebral edema  Hypotension  Respiratory depression  Hypoxemia  Electrolyte disturbance Increased Intracranial Pressure associated with TBI  Remember the Monro-Kellie Hypothesis  Limited space for expansion  Increase in any one of the components causes a change in the volume of others  Displaces or shifts CSF  Increases the absorption or diminishes production of CSF  Decreasing cerebral blood volume  Intracranial Pressure Factors that influence intracranial pressure: 1. Arterial pressure 2. Venous pressure 3. Intraabdominal and intrathoracic pressure 4. Posture 5. Temperature 6. Blood gases (C02 levels/02 levels) Other causes of Increased ICP  Brain tumors  Subarachnoid hemorrhage  Toxic or vial encephalopathy's

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In order to understand what influences ICP; you must understand cerebral blood flow (CBF) and cerebral perfusion pressure (CPP) Normals MAP= 50-150 mm Hg CPP= 70-100 mm Hg ICP= 0-15 (10) mm Hg

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 Purpose of cerebral auto regulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits Increased ICP results in decreased CBF  Increased ICP= ↓cerebral blood flow→ ischemia and cell death  Compensation evidenced by: Slow, bounding pulse, irregular RR  CBF regulated by concentration of carbon dioxide in the blood and in the brain tissue  Increased PaC02: Vasodilation=↑ CBF and ICP  Decreased PaC02: Vasoconstriction=↓ CBF Cerebral Edema causes Increased Intracranial Pressure What is cerebral edema?  Abnormal accumulation of water or fluid in the intracellular space, extracellular space or both  As brain tissue swell, brain attempts to compensate Cerebral Response to IICP: CPP  Compensatory mechanisms in brain  Steady CBF if arterial SBP 50-150 mm Hg and ICP is < 40 mm Hg  Changes in ICP closely linked to cerebral perfusion pressure (CPP) How do you calculate CPP?  Normal cerebral perfusion pressure (CPP)  70-100 mm Hg  CPP= ICP -MAP  CPP < 50 mm Hg→ irreversible brain damage  Goal: CPP 70-80 mm Hg  If ICP=MAP: cerebral circulation ceases Cerebral Perfusion Calculation  CPP=MAP-ICP Example: SBP: 122/84 MAP: 97 mm Hg ICP: 12 mm Hg 14

CPP: 97-12= 85 mm Hg Cerebral Response to IICP: Vital Signs  Cushing’s Reflex  Increased arterial pressure with widening of pulse pressure  Vasomotor center triggers increase in arterial pressure in an effort to overcome the increased ICP  Bradycardia  Late sign!  Cushing’s Triad  Bradycardia  Hypertension  Bradypnea  Risk of herniation if not treated Complication of IICP: Herniation  Shifting of brain tissues from an area of high pressure to an area of lower pressure  Interferes with blood supply in area  Cessation of cerebral blood flow results in  Cerebral ischemia  Infarction  Brain death Complications of IICP: SIADH & DI  Diabetes Insipidus  Decreased ADH  Excessive urine output  Decreased urine osmolality  Serum hyperosmolarity  Therapy  Fluids  Electrolyte replacement  Vasopressin (DDAVP)  SIADH  Increased secretion of ADH  Volume overload  Urine output diminishes  Serum sodium concentration becomes dilute 15

 Therapy  Fluid restriction (< 800 mL/day with no free water)  3% hypertonic saline solution Nursing : Monitoring  Earliest sign of ALOC: confusion  s/s ICP elevation  Calculation of CPP  Antiseizure med blood levels  Skin integrity  Oral mucosa  ROM  Abdominal assessment  I/O  Fluid/electrolytes  Weigh  Laboratory results  ABG results  Diagnostic results  VS/ 02 saturation  Functional level prior to injury  Full neurologic assessment Specific Neuro Assessment  GCS  Vital signs  ↑Temperature  Indicates brain stem damage  Poor prognosis  Increased metabolic demands  Motor assessment  Abnormal responses  Pupil assessment  Unilateral dilation and poorly responding pupil  developing hematoma  Bilateral fixed/dilated  overwhelming injury  Damage to upper brain]  Eye movement abnormalities 16

Monitoring ICP & Cerebral Oxygenation

Medical Management of IICP  Decrease cerebral edema  Limiting overall fluid intake  Avoid overhydrating  Maintain normothermia or hypothermia  Maintain cerebral perfusion  Improve cardiac output (Keep CPP> 70 mm Hg)  Reducing CSF: ventriculostomy  Reducing intracranial blood volume  Maintain PaC02 >30 mm Hg  Maintain oxygenation  Reduce metabolic demands  Barbiturate coma  Sedation Pharmacologic Management of IICP  Osmotic Diuretics (Mannitol)  draws water across intact membranes, reducing volume of the brain and extracellular fluid  Loop Diuretics (Lasix)  Maintain negative fluid balance 17

Antiseizure meds (Dilantin) Corticosteroids (Decadron) Histamine H2 receptor antagonist (Tagamet) Proton Pump Inhibitor (Prilosec) Levophed or Dobutamine  Maintains CPP  Tylenol  Maintain normothermia

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Nursing Actions that Increase ICP  Suctioning  PEEP  Coughing  Positioning  Environmental Stimuli  Clustering nursing care Nursing Diagnosis for the patient with Head Injury and IICP  Ineffective airway clearance r/t diminished protective reflexes  Ineffective breathing patterns r/t neurologic dysfunction  Ineffective cerebral tissue perfusion r/t IICP  Deficient fluid volume r/t fluid restriction  Risk for infection r/t ICP monitoring system Nursing Interventions  Maintain patent airway  Achieve adequate breathing pattern  Optimize cerebral tissue perfusion  Maintain negative fluid balance  Prevent infection  Monitor and manage potential complications  Monitor and manage secondary complications (SIADH, DI)  Monitoring ICP Expected Outcomes  Maintains patent airway  Attains optimal breathing pattern  Demonstrates optimal cerebral tissue perfusion  Attains desired fluid balance  Has no signs or symptoms of infection  Absence of complications 18

Brain Death Criteria O Irreversible coma; irreversible brain damage as manifested by absolute unresponsiveness to all stimuli, absence of all spontaneous muscle activity, and an isoelectric electroencephalogram for 30 minutes, all in the absence of hypothermia or intoxication by central nervous system depressants O Unanswered Questions O No true standardization of brain death criteria exists O P&P vary widely among facilities O Who is qualified to perform a brain death assessment? O What is the appropriate timing between clinical assessment? O Are clinical assessments enough to determine brain death? O What confirmatory test are acceptable? O Guidelines O Uniform Determination of Death Act (1980) O An individual who has sustained either O Irreversible cessation of circulatory and respiratory functions O OR O Irreversible cessation of all functions of the entire brain, including the brainstem O Diagnosing Brain Death 1. Coma of known cause as established by history, clinical exam, lab testing, and neuroimaging O CT, MRI O Complicating conditions must be ruled out first O Hypotension O Hypothermia O Hypoxemia 2. Normal or near-normal core body temperature (> 36º) 3. Normal systolic BP (> or = to 100 mm Hg 4. At least one neurologic exam (some states and hospital protocols require two) O Patient must be observed for a period to exclude the possibility of recovery O Ruling out Complicating Conditions O Paralytics, sedatives or other drugs used in rapid sequence induction in order to facilitate intubation by EMS in the field O Ingested drugs 19

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O Opioids, barbiturates, benzodiazepines, tricyclic antidepressants, aminoglycosides, anticholinergics, antiepileptic drugs, chemotherapy agents, alcohol, antipsychotics, stimulants and many cardiac medications Acid-base abnormalities Determining antidote for overdose O If ingestion is unknown: waiting period of 2 days is recommended Severe facial trauma that impacts pupillary assessment O Acute metabolic or endocrine crises O Results in cerebral edema, anoxia or demyelination O Fulminant liver failure O Ketoacidosis O Hyperglycemia O Hyponatremia O Hypernatremia Brain Death Exam Requires complex neurologic examination Usually performed by: O Neurologist O Neurosurgeon O Critical Care intensivist Brain Death Exam Head-to-toe approach O Pupillary response O Oculocephalic reflex (doll’s eye reflex) O Oculovestibular reflex O Facial sensory and motor responses O Corneal reflexes O Pharyngeal and tracheal reflexes (gag) O Response to painful stimuli Apnea Test Confirms loss of spontaneous respirations Can only be reliably performed by disconnecting patient from ventilator O Taken off vent for > 10 minutes O Performed last O Baseline PaC02 obtained via ABG O Eucapnia must be achieved first 20

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O Pre-oxygenated with 100% FI02 for at least 10 minutes prior to apnea test Target Pa02: > 200 mg Hg Disconnect from vent: NC 6 L/minute via ETT Chest and abdomen observed for movement If no movement: ABG repeated and patient placed back on ventilator O Rise in paC02 of 20 mm Hg over baseline or > 60 mm Hg is considered positive test Confirmatory Testing Not mandatory but is desirable in patients whom specific components of the clinical assessment cannot be reliably performed or evaluated O Cerebral angiography O EEG O Transcranial Doppler's O CTA Nursing Interventions Complete physical assessment Monitoring of vital signs and pulse oximetry during apnea test Family support O Case management O Palliative care team Lab value monitoring

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