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34 Cards in this Set
- Front
- Back
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Primary vs Secondary traumatic brain injury
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Primary - moment of impact, Treatment - PREVENTION
Secondary Brain Injury - more neurological damage resulting from: a) cerebral edema and increased intracranial pressure b) hypotension & hypoxemia c) cerebral hypoperfusion Secondary brain injury is primary cause of death |
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Effects of secondary brain injury
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neuronal death due to cerebral ischemia
increased morbidity primary cause of hospital mortality if hospitalized |
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What anatomy contributes to secondary brain injury
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rigid nonexpansile skull filled with brain, CSF, blood
Cerebral blood flow is autoregulated and compensation can be disrupted in the injury Mass effect of the intracranial hemorrhage |
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How does body deal with increased mass in cranial cavity (through bleed, edema, etc.)
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Follows Monroe-Kellie Rule to deal with any 4th mass
Normal - just brain, csf, blood in arteries and veins Mild mass - compensation by lowering CSF and venous blood volume. Pressure DOES NOT increase Large mass - Pressure increases, dangerous levels of CSF and venous blood lost, then arterial blood (ischemia), then brain mass |
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Intracranial pressure normal, abnormal and severe.
Factors contributing to adverse outcome |
Normal - 10mmHg, Abnormal - >20mmHg, Severe - >40mmHg
Sustained high levels leads to decreased brain function and poor outcome Hypotension and low saturation adversely affect outcome |
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Monro-Kellie Volume Pressure Curve
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Body can deal with increasing mass via removing CSF and venous blood until POINT OF DECOMPOSITION. Then intracranial pressure begins to spike and herniation occurs
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Cerebral Perfusion Pressure
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MAP-ICP = CPP
It is not equal to cerebral blood flow |
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Autoregulation of brain, in brain injury changes, vulnerabilities
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maintains cerebral blood flow between a mean BP of 50-60mmHg
In moderate or severe brain injury, autoregulation is impaired so CBF varies with mean BP Injured brain more vulnerable to episodes of hypotension, causing secondary brain injury |
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Classifications of head injury by mechanism, morphology, brain injuries
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Mechanism:
Blunt - high and low velolcity Penetrating - gun shot wound and other Morphology - skull fractures Vault - depressed/nondepressed Open (HIGH meningitis risk)/closed Brain injuries Focal - epidural, subdural, intracerebral Basilar - with or w/o CSF leak or with and w/o cranial nerve palsy Diffuse - concussion, multiple contusions, hypoxia/ischemic |
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Clinical signs of skull fracture
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raccoon eyes, Battle's sign, otorrhea, rhinorrhea
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Epidural Hematoma Cause, Presentation, Treatment
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Cause: middle meningeal artery tear often due to skull fracture
Presentation: lenticular/biconvex on xray due to dura's adherence to skull, lucid interval (maybe), rapidly fatal Treatment: early evacuation can recover completely IPSILATERAL pupil dilation, CONTRALATERAL hemiparesis |
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Subdural Hematoma Cause, Presentation, Treatment
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Cause: venous tear/brain laceration
Presentation: blood covers cerebral surface Mortality/morbidity due to underlying injury Treatment: surgical evacuation esp. if >5mm shift of midline IPSILATERAL pupil dilation |
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Intracerebral Hematoma/Contusion Cause, Presentation, Treatment
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Cause: coup/contracoup injuries (impacted vs bounce off)
Presentation: frontal lobe or temporal lobe, use CT to watch progress Treatment: no operation, usually resolves |
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Concussion symptoms, dx
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transient loss of consciousness
retrograde or antegrade amnesia nausea, vomiting and headache may worsen before lessening Dx: symptomatically, can get CT but may or may not show edema, if symptoms worsen definitely get CT |
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GCS Score (mild, moderate, severe), how to approach/treat, what needed to discharge pt
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Categorizes head injuries into Mild, Moderate and Severe
MILD GCS score 13-15, get History, exclude systemic injuries, neuro exam, x-rays/CT (still probably get CT), alcohol/drug screen, admit if old and on coumadin b/c of bleed risk To be discharged - need to be alert and oriented to understand instructions and a companion for 24 hrs MODERATE GCS score 9-12 Initially same as mild, CT scan for ALL, admit and observe (frequent neuro exams, CT scans) if deteriorate manage as severe. Withold substance. Watch out for DTs to prevent death if alcoholic. Only 10% here. Of those 10-20% go to coma or neuro decline SEVERE GCS score 3-8 Evaluate and resuscitate and treat, intubate for airway protection, focuse neuro exam, frequent reevaluation, identify associated injuries. Hypotension and hypoxia related mortality severe |
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Resucitation in traumatic brain injury
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Inadequate fluids or narcotic, hypnotic or diuretic use can cause hypotension and hypovolemia contributing to ischemia
Use arterial line to monitor MABP, central venous line to monitor CVP Keep MABP >90 and CVP 4-10mm to prevent hypotension, stay away from LS and use normal saline. |
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Neurologic Exam Parts and Glasgow Coma Scale
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EYES
Opens spontaneously - 4 Opens to verbal command - 3 Opens to pain - 2 No response - 1 BEST VERBAL RESPONSE Oriented and converses - 5 Disoriented and converses - 4 Inappropriate words - 3 Incomprehensible Sounds - 2 No response - 1 BEST MOTOR RESPONSE Obeys command - 6 Localizes pain - 5 Flexion withdrawal - 4 Flexion abnormal - 3 Extension 2 NO response - 1 Ranges 3-15, MOTOR most important, if could only do one DO MOTOR, Braindead pt is GCS 3 |
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Pupil reactivity to light and asymmetry in neuro exam
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Reactivity to light - positive if >1mm constriction
Pupil asymmetry - >1mm is significant Need CN II and III |
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When to consider neurosurgical intervention for intracranial mass lesion
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1) Extra cerebral collection associated with >5mm midline shift
2) Cerebellar lesion with brain stem mass effect 3) Anterior temporal lobe hemorrhagic contusion with mass effect 4) Frontal/temporal mass lesion with intractable ICP>25mmHg For hematoma may not do surgery if on dominant hemisphere (speech risk) and do a conservative craniectomy to allow release of pressure) |
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When should intracranial pressure be monitored and how, other uses, when to remove
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If GCS < 8 due to traumatic brain injury
How: ventricular catheter connected to external strain gauge or indwelling strain gauge. Infection risk low, hemorrhage risk lower Other uses: CSF drainage to reduce ICP and maintain <15mmHg Get CSF protein/glucose, cell count, cultures DAILY If culture positive, remove and place contralateral ventriculostomy If ICP <15mmHg w/o drainage for 24hrs, then can remove Tank up and tighten up to raise BP and keep perfusion high with norepinephrine |
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ABC's
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Airway
Breathing Circulation ALWAYS EVALUATE FIRST FOR ANY TRAUMA Brain circulation critical |
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Most common sites of brain trauma/contusions
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Occipital and temporal poles (back of head) and inferior frontal lobe and anterior temporal pole
Then slightly toward midline and lateral of those Least common is directly on top and bottom of brain |
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Contre-coup contusions
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contusion that appears opposite side of impact from rebound
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Diffuse Axonal Injury Pathology, Histology, Gross Pathology
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Torsional injury to deep white matter structures (supratentorial and infratentorial) damages integrity of axon at nodes of Ranvier due to stretching (disrupts flow)
Results in accumulation of mitochondria, organelles, amyloid, alpha synuclein leading to AXONAL SWELLINGS (spheroids) seen with silver stain May or may not have actual impact with contusion Histology: axonal spheroids, microglial nodules, rarefaction of neuropil Gross Pathology: Hemorrhage to CORPUS CALLOSUM and Midbrain/PONS (SUPERIOR CERBRAL PEDUNCLES) chronically get white matter degeneration then gray matter degeneration |
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Shaken Baby Syndrome Triad, Histology
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Encephalopathy (diffuse axonal injury), poorly conscious
Subdural Hematomas Retinal Hemorrhages Histology: Diffuse axonal injury may show beta amyloid precursor protein (BAPP), optic nerve hemorrhages |
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Blood type epidural vs subdural hematoma
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Epidural - usually arterial from skull fracture (middle meningeal artery)
Subdural - venous blood, still attached to skull, rupture of bridging vein traversing subdural space to superior sagittal sinus. manifest within 48 hours of injury and BIL in 10%. Pressure causes headache and confusion |
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Evolution of chronic subdural hematoma
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clot lysis in about a week
fibroblast grow in from dura within 1-2 weeks loose fibrous membranes form in 3-4 weeks dense inner membrane forms in 4-6 weeks dense organization occurs in 3 months |
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Subarachnoid hemorrhage cause, Symptoms, consequences
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MOST FREQUENT TRAUMATIC BRAIN LESION
Cause: rupture of vessels in subarachnoid space due to contusion or aneurysm Sx: severe headache (WORST OF LIFE) due to hemoglobin release from RBCs that triggers vasospasm and ischemia Long term - fibrosis of subarachnoid space with hydrocephalus (impaired CSF reabsorption due to fibrosis of arachnoid granulations) |
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Chronic Traumatic Encephalopathy, Pathology, Histology
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long term sequelae of repetitive traumatic brain injuries (ex. boxers) aka "dementia pugilistica"
Seen in NFL, NHL players, contact sports Pathology: neurodegenerative features with mild atrophy and deposition of TAU and Beta AMYLOID NO senile plaques |
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Things that can elevate ICP
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HIE, stroke, meningitis, brain abscesses, brain tumor, hydrocephalus, epidural hematoma, subdural hematoma
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3 most common herniations in brain
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Subfalcine - cingulate gyrus to opposite hemisphere under falx
Transtentorial - uncus through tentorial notch Tonsillar - tonsil of cerebellum through foramen magnum |
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Argyle-Robinson pupil
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syphilis
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Ways to lower ICP
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Elevate head 30 degrees (fastest)
Hyperventilate (causes decreased blood flow to brain if used chronically) Mannitol push Craniatomy |
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Mild hypothermia use in brain injury
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Best within 1 hr
Reduces elevated ICP, unsure about outcome Complications: can induce coagulable state |
