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1 Traumatic Brain Injury John Miller American Association of Neuroscience Nurses, http://www.aann.org/ Increased intracranial pressure Monroe-Kellie hypothesis o Because the rigid skull around the brain, when one of the three components (blood, CSF, brain tissue) expands, the other two will decrease to compensate by decreasing volume for ICP to remain constant. Normal ICP 5-15 mm Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) – intracranial pressure (ICP) For a BP of 120/60, the MAP = [(2 X diastolic) + systolic] /3 (example 2X60= 120, 120/3=40) Need CPP above 0 to perfuse the brain. Risk factors Tumor Infarction (stroke, trauma) CSF outflow obstruction (hydrocephalus) Abscess Toxic substances, metabolic toxins Decreased blood flow to and from brain Vasodilatation from increased pCO2 or low pO2 Systemic hypertension Increased thoracic pressure Edema from surgery or injury due to disruption of the blood brain barrier. National Institute of health: National institute for neurological disorders and stroke http://www.ninds.nih.gov/index.htm Pathophysiology Compliance o Compensation by brain to adapt to increasing pressure with increasing ICP (through the MonroeKellie mechanism). First: ICF movement out of brain Clinical manifestations of increased ICP develop when the maximum amount is removed. Second: blood flow reduction to brain Acidosis, hypoxia, ischemia develop when flow is reduced too much. Pathophysiology (cont.), Autoregulation Last: herniation (displacement) of brain tissue across tentorium or through the foramen magnum (fatal) o Supratentorial compartment Left and right hemispheres, o Infratentorial compartment Cerebellum Brainstem Intracranial blood vessels change diameter to maintain a constant blood flow when the cerebral perfusion pressure changes. This ability is lost in increased ICP 2 Causes of increased ICP Brain swelling o Increase in cerebral blood volume from dilated cerebral blood vessels. o Major mechanism for causing increased ICP. o Treated with hyperventilation using a ventilator to cause vasoconstriction. Brain (cerebral) edema o Increase in brain bulk because of blood-brain barrier disruption o Composed of electrolytes, proteins, blood o Maximum @ 48-72 hours after surgery or injury o Treated with osmotic diuretics Assessment Changes are subtle. o Any alteration in consciousness o Decrease in Glasgow coma scale score o Speech, pupillary reactivity, motor or sensory ability, cardiac rate or rhythm Headache, nausea, vomiting, diplopia, papilledema Late response (medulla pressure): Cushing's triad o Increased systolic, widened pulse pressure, bradycardia Respiratory pattern changes o Cheyne Stokes to central neurogenic hyperventilation Hyperthermia followed by hypothermia Early assessment of increased intracranial pressure Headache Decreasing level of consciousness o Alert to comatose o Assess with Glasgow coma scale rather than a label, such as comatose or confused. o Decreasing Glasgow Coma Scale (GCS) Consists of verbal response, eye opening, best motor response GCS of 15 = oriented, follows commands, opens eyes spontaneously GCS of 8 or less = coma Levels of consciousness Full consciousness: A&O x 3, understands spoken and written language Confusion: Unable to think quickly, poor memory, short attention, etc. Disorientation: Not A&O x 3 Obtundation: Lethargic, somnolent, responds to verbal and tactile stimuli but quickly falls asleep Stupor: Unresponsive except to repeated strong stimuli, arouses, localizes stimuli Semicomatose: Unresponsive except may stir, moan, or withdraw from strong stimuli, does not arouse Coma: Unresponsive to any stimuli Deep coma: Unresponsive to any stimuli and absence of DTRs, corneal, pharyngeal, and pupillary reflexes 3 Coma states Persistent vegetative state o Unawareness of self and environment o Cannot interact with the environment o Can chew and be awake Locked in syndrome o Intact cognitive abilities o Cannot communicate through speech or movement o Motor paralysis Brain death o Deep coma o Apnea o Pupils fixed and dilated o Absent dolls and caloric reflexes o Flat EEG and no cerebral circulation by angiography Diving Bell and the Butterfly https://youtu.be/G69Zh7YIg8c Glasgow Coma Scale at 40 | The new approach to Glasgow Coma Scale assessment https://youtu.be/v6qpEQxJQO4 Glasgow coma scale Verbal response o Examples What is your name? Where are you? What is the month, year, season, nearest holiday? What is your home address? Who is your employer? Changes in 2016 Incomprehensible words changed to just words. Incomprehensible sounds changed to just sounds. Determining Brain Death https://www.aan.com/Guidelines/home/GetGuidelineContent/432 Eye opening, GCS Observe without speaking to client. o Are his eyes open and does he look around? If eyes are closed, same client’s name. If no eye opening, raise your voice and try again. If not able to open eyes, use mildly painful central stimulus o Trapezius squeeze o Supraorbital pressure o Do not use sternal rub or finger pressure. Best motor response, GCS Assess the best extremity response. o Weaker side is not scored in Glasgow Have person squeeze your hand and then release. If not able to move, use mildly painful central stimulus. o Localizes (to where the stimulus is located). o Withdraws (generally without localizing, may do with more than one extremity). o Posturing o No response 4 Motor activity comparison -Not in GCS Assess all extremities. Compare tone. Compare muscle strength. o Arms On command, have grasp and then release hands. If cannot grasp, have raise against gravity. o Legs On command, have push with feet or raise legs against resistance. If cannot raise against resistance, have raise against gravity. o If cannot follow commands, check for posturing, decerebrate or decorticate (pons level). o If no posturing, check for flaccidity (medulla level). Assessment of moderate increased intracranial pressure Pupil size o Midsize to larger or small Pupil reactivity o Brisk to sluggish to no reaction Projectile vomiting Cheyne-Stokes respirations Limited to the same side as injury (ipsilateral), later expands. Central transtentorial herniation syndrome Medical emergency Injury in cerebrum pressing downward, eventually reaching brainstem. Respiration assessment o Cheyne-Stokes (first) o Central neurogenic hyperventilation o Ataxic (apneustic, Biots) o Apnea (last) Pupil assessment o Small but react, later fixed and dilated o Doll’s eyes and caloric testing positive until brain stem involvement. Treatment o Hyperventilation used as a temporary measure because it reduces blood flow. Vestibulo-ocular reflex 13/25 (Dolls Eyes) https://youtu.be/j_R0LcPnZ_w Respiratory Care (Patterns) of Neurosurgical Patients http://www.neuroanesthesia.info/respiratorycare.htm 5 Assessment of late stage increased intracranial pressure Cushing's Triad o Increased systolic BP o Widened pulse pressure Increasing difference of systolic and diastolic BP o Bradycardia Decorticate posturing o Abnormal flexion of arms and extension of legs to pain stimulus Decerebrate posturing o Abnormal extension of arms and extension of legs to pain stimulus Abnormal respiratory patterns o Ataxic o Central neurogenic hyperventilation o Cluster o Apnea Very late Hypothermia Circulatory collapse o Very late Diagnostic Tests MRI CT Serum osmolality (280-300), keep slightly elevated at 325 to draw fluid into vascular system ABGs: more acid pH and pCO2 vasodilate more than hypoxia Interventions: Airway, Breathing, Hyperthermia Maintain cerebral oxygenation o Maintain airway and ventilation with ET and ventilator if needed o Keep pO2 up near 100. Keep pCO2 near 35. o Mechanical ventilation: Hyperventilation only if herniation imminent Hyperthermia o Initiate treatment for fever over 38.5. o Ice packs, fans, IV fluids, spray bottle, rectal or bladder probe to constantly monitor temperature o Cooling blanket only if needed. o Medications to decrease shivering, which increases the temperature. o Acetaminophen to reset the hypothalamic regulatory mechanism. Interventions to decrease intracranial pressure Head of bed up 30 degrees Prevent obstruction of jugular veins o Neck not flexed o Head in neutral rotation o Not turned No hip flexion 6 More Interventions to decrease ICP o Prevent seizures o Administer IV fluids if needed to avoid hypotension: NS or 0.45 NaCL Use isotonic NaCl solution. Avoid hypotonic solutions, including D5W. Example of parameters for BP treatment: 100 – 150 mm systolic o Manual bagging or ventilator hyperventilation if herniating to reduce pCO2 o Osmotic diuretic, free radical scavenger: Mannitol Less used: Loop diuretic, furosemide o Hypertonic saline (3 or 7.5%) infusions: Remove fluid. Watch for dehydration and left heart CHF. o ICP shunt for chronic increased ICP, such as hydrocephaly o Bone flap, need helmet Osmotic diuretic: Mannitol Other classifications: Free radical scavenger, plasma expansion briefly. Used before surgery, rebound effect. Onset15 minutes, lasts up to six hours. Bolus doses Use filter because of sugar particles at higher concentrations. Pulls fluid out of cells Increases cerebral blood flow and oxygen delivery Monitor renal function and electrolytes o Monitor for dehydration with sodium and osmolarity labs Mannitol, Intravenous Guidelines, GlobalRPH, http://www.globalrph.com/mannitolhttp://www.aann.org/_dilution.htm Prevent complications Cerebral edema, acute hydrocephalus Neurogenic pulmonary edema Stress ulcers: PPIs or Histamine 2 Receptor Antagonists Seizures: Phenytoin Infections: antibiotics More complications Diabetes Insipidus Syndrome of inappropriate anti-diuretic hormone (SIADH) Cardiac dysrhythmias Subarachnoid hemorrhage / aneurysm Post-trauma response Malnutrition, hypoglycemia: enteral nutrition Monitor intracranial pressure Invasive measurement using catheter in ventricles, subarachnoid space, brain parenchyma Risk of infection, hemorrhage, obstruction Remove CSF to reduce pressure if needed Check compliance of brain with small volumes of fluid Other methods o Transcranial Doppler studies o Juglar bulb oxygen saturation in vein 7 Prevent intracranial hypertension CSF drainage Diuretics: Mannitol Hyperventilation Sedation, chemical paralysis Anticonvulsants: Phenytoin Barbiturates High dose pentobarbital Induces coma o Lowers ICP o Decreases mortality Used in uncontrollable ICP that is refractory to other treatments. ET, ventilator, pulmonary artery catheter Patient is completely dependent for all protective functions. Neuromuscular blockers (paralytics) Not given with barbiturates Sedatives and analgesics must be given with paralytics. Examples: pancuronium or succinylcholine Nursing Management: Assessment Level of consciousness: Glasgow coma scale Pupil size, equality, response, position (nystagmus), accommodation, eye movement o Change is usually on the same side as the injury (ipsilateral) o Use penlight, not flashlight o Check for consensual reaction also. o Check shape: oval is sign of increased ICP Vital Signs o Check every 15 minutes until stable. Temp every 2 hours. o Cushing's Response (late sign) Blink reflex Gag reflex Facial symmetry o Frown, smile Nursing Interventions Osmotics, anticonvulsants, stool softeners Position to avoid increases in ICP. Maintain patent airway. Maintain fluid balance. o Euvolemic o Fluid restriction for SIADH. Allow for periods of rest, but also avoid clustering of too many activities, which increase ICP. Surgical Management Remove cause of pressure. Ventriculoperitoneal shunt Remove some brain tissue to reduce pressure (decompression). Bone flap may not be immediately replaced or dura not closed to allow room for the swelling. Flap eventually replaced, but needs helmet until it is. 8 Traumatic Brain Injury Often have other injuries. Shock is rarely caused by head injury alone. Risk factors: alcohol, MVA, no seat belt Mechanisms of injury o Primary injuries o Skull fracture o Diffuse injury Coup-contrecoup injuries Penetrating trauma Neurotrauma Featured Images, Trauma.org, http://www.trauma.org/index.php/main/category/C9 Assessment: Contrecoup Initial injury to the brain Second injury on the opposite side of the brain o From the brain ricocheting off the skull Observe closely for increased intracranial pressure as seen in a hematoma. Assessment: Basilar Skull Fracture Base of skull is fractured by great force. CSF leaks o Nose (rhinorrhea) o Ears (otorrhea) o Show a positive glucose with a dextrostix Halo (ring) on paper Periorbital ecchymosis (raccoon eyes) Mastoidal ecchymosis (Battle’s sign) Basilar skull fracture and the halo sign http://www.cmaj.ca/content/185/5/416/F1.expansion.html Raccoon eyes ,a sign for basal skull fracture, Doctors Gates, http://doctorsgates.blogspot.com/2011/02/raccoon-eyes-sign-for-basal-skull.html Basilar Skull Fracture, Neurosurgery Student https://neurosurgerystudentblog.wordpress.com/2016/01/01/basilar-skull-fracture/ Assessment: Epidural hematoma Temporal skull fracture o Middle meningeal artery is lacerated. Initially, loss of consciousness from the concussion. Then, an awake period or lucid interval. Finally, a rapid return of unconsciousness due to increased intracranial pressure from the arterial bleeding. Must be taken to surgery quickly. Epidural Hematoma in Emergency Medicine Clinical Presentation, Emedicine, http://emedicine.medscape.com/article/824029-clinical 9 Assessment: Subdural hematoma Decreased levels of consciousness Hours, days, months after trauma from a lacerated vein Must be taken to surgery. Acute, chronic Subdural Hematoma, Emedicine, http://emedicine.medscape.com/article/1137207-overview Assessment: Concussion This is defined as a loss of consciousness after head trauma. Immediate loss of consciousness Amnesia Headache Drowsiness, confusion, dizziness Visual: Diplopia, blurred vision Brief seizures with apnea, bradycardia, hypotension, pallor Observe closely for increased intracranial pressure as seen in a hematoma. o In ED for 1-2 hours Post concussion syndrome o Persistent headache o Dizziness o Irritability, insomnia o Impaired memory and concentration Crossing the Blood Brain Barrier (animation https://youtu.be/IumJxRCqgw8 Assessment: Depressed skull fracture Skull fragments are impacted into brain. Surgical elevation is required. Medical management Initial Interventions ABCs Assess C-spine and for other injuries Treatment for increased ICP Cover open head injuries. Do not apply pressure to stop bleeding unless just a scalp wound. Leave objects in. Uncomplicated lacerations are sutured. Unconscious period duration o Mild: a few seconds o Classic: 6 hours or less, if severe, watch for seizures and respiratory arrest o Diffuse Axonal Injury Interventions Concussion: Admitted if LOC more than 2 minutes TBI o Keep MAP at least 90 with isotonic and hypertonic fluids o Other interventions to reduce ICP as previously mentioned 10 Diffuse Axonal Injury Half of all injuries and 1/3 of all deaths Acceleration deceleration Mild: Coma less than 24 hours Moderate and severe have permanent deficits Concussion https://youtu.be/tgChTeALF7g More Interventions Treat for increased ICP. Treat wounds. Avoid suctioning nasopharynx or putting an NG in until a basilar skull fracture is ruled out. Let CSF drain in basilar skull fracture, but put sterile cotton drip pad under nose. Concussion - Official Trailer #2 (ft Will Smith) https://youtu.be/tNCvaa-RogQ Surgical management Burr holes for epidural or subdural hematomas Craniotomy o Compound (depressed) skull fractures are elevated and cleaned (debrided). SDH Burr Holes OR HD, rjk2103, http://youtu.be/jD3JTOaS2-0 Craniotomy Preoperative interventions o May need ventriculostomy to drain CSF. Catheter inserted through a burr hole. o Assess neurological status o Remove hair at surgical site. Intraoperative craniotomy interventions o Positions o Head supporting frames Potential for skin pressure on head Edema of face Muscle soreness, especially neck Postoperative craniotomy interventions Ecchymosis and periorbital edema may be present but is temporary. Interventions for increased ICP (stroke, trauma) Avoid preventative coughing as it can cause valsalva and increased ICP. Anticonvulsant medications Notify neurosurgeon of any changes in assessment. Complications of craniotomy Increased ICP Motor or sensory deficits Seizures CSF leak Wound infection CNS infection Acute Subdural Hematoma https://youtu.be/Ji7fohBEPnM 11 Video Atlas of Neurosurgery 1e: Awake Craniotomy & Speech Mapping for Gliomas https://youtu.be/IgktH7woZ1k Brain Surgery https://youtu.be/rZcCClwSIYg?list=PLdVvae0BQcKz5ubhxWsTtjs21YtMPsK0i What to expect before, during and after pituitary surgery. https://youtu.be/ym6P-Rwq9OQ?list=PLdVvae0BQcKz5ubhxWsTtjs21YtMPsK0i Endoscopic Endonasal Pituitary Macroadenoma Surgery https://youtu.be/aih0kqd13Y8 Transphenoidal hypophysectomy Endoscopic incision with microsurgical instruments inside nostril Postoperative hypophysectomy interventions o Salt water nasal rinses or spray o No blowing nose. If need to cough or sneeze, do it gently. o Monitor for diabetes insipidus or SIADH. o Keep head up and elevated when sleeping. Complications of transphenoidal hypophysectomy and other craniotomies Diabetes insipidus (DI) Usually temporary May be permanent if stalk of pituitary is removed. Caused by decreased secretion of anti-diuretic hormone o Polyuria (2-15 liters of urine / day) o Specific gravity (SG) 1.005 or less (dilute) o Need to follow sodium and serum osmolality frequently. o Assess for shock and hypertonic encephalopathy. o Maintain hydration. o Administer IV vasopressin or inhalation desmopressin. Polydipsia Traumatic brain injury.org http://traumaticbraininjurysupport.org/ Brain Injury Resource Center (Seattle) http://www.headinjury.com/linktbisup.htm Brain injury association of America http://www.biausa.org/ Living with Traumatic Brain Injury: Personal Stories http://www.brainline.org/landing_pages/categories/livingwithtbi_results.php?feat=personal%20stories For People with TBI, brainline.org, http://www.brainline.org/landing_pages/TBI.html CNS Case Studies http://www.neuroskills.com/about-us/cns-case-studies.php