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EM Head Trauma

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Question
Answer
Suspect head trauma?   CT  
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Monro-Kellie doctrine   vol. fixed, if vol changes, change must be accomodated for  
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Avg. Intracranial volume   about 1500ml. brain is 85-90%, cerebral blood is 10%, remainder is CSF  
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CPP   Cerebral perfusion Pressure. Net pressure of blood delivered to the brain. CPP=MAP-ICP. (MAP=mean arterial pressure, ICP=intracranial pressure)  
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CBF constant in range of   50-150mmHg b/c of autoregulation.  
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When MAP is less than 50mmHg, be concerned about   ischemia from insufficient blood flow. When MAP is greater than 150mmHg (excess CBF can increase the ICP)  
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Glasgow Coma Scale   motor (1-6), Eye opening (1-4), Verbal (1-5). Best score = 15  
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Mild Severity   GCS: 14-15.  
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Moderate Severity   GCS of 9-13  
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Severe head injury   GCS: 3-8  
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Types of skull fxs   basilar, closed, open, depressed (seen in babies b/c their skull bones are not completely set). Skull fxs increase chances of intracranial hematoma  
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Raccoon eyes   periorbital ecchymosis. Head injury causes increased pressure, must go somewhere.  
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Battle's sign   Retroauricular ecchymosis  
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CSF leakage   from nose or ear.  
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Clinical findings in a skull fracture   periorbital ecchymosis, retroauricular ecchymosis, CSF leakage, VII or VIII nerve injury  
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Communited   multiple fractures  
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Simple skull fx skull management   observation, neurovascular intact  
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Operative repair skull fx management   dural evaluation, ICP management (don't want it to further push out skull pieces), wire repair  
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Epidural hematomas more commonly seen in   the temporal or temporoparietal areas. Usually the result of direct mechanical force resulting in a skull fx. Usually from arterial injury, but can also occur from venous injury  
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Epidural hematoma notes   More common in younger patients, rare in the elderly and in those under 2 years because the dura is closely attached in those populations. Classic lucid interval seem only 30% of the time.  
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Simple skull fx skull management   observation, neurovascular intact  
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Operative repair skull fx management   dural evaluation, ICP management (don't want it to further push out skull pieces), wire repair  
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Epidural hematomas more commonly seen in   the temporal or temporoparietal areas. Usually the result of direct mechanical force resulting in a skull fx. Usually from arterial injury, but can also occur from venous injury  
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Epidural hematoma notes   More common in younger patients, rare in the elderly and in those under 2 years because the dura is closely attached in those populations. Classic lucid interval seem only 30% of the time.  
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Subdural Hematomas   More common than epidural hematomas. Usually occur from the tearing of small cerebral cortex surface vessels. Cover the entire surface of the hemisphere. More severe underlying brain injury than that of an epidural hematoma  
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Subdural hematomas contd   Seen with acceleration deceleration injuries (MVA, fall)More common in the elderlyBlood clot forms between the dura mater and the brain with extensive parenchymal injury at the site of the clot. on CT-hyperdense lesion that hugs convexity of brain.  
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Initial Management of head trauma   ABCs, Maintain C-spine immobolization, second survey and hx (numbness, tingling, etc), tx hypotension (bleeding, shock), pCO2 range of 30-35mmHg is goal, reduce ICP with cerebral vasoconstriction (can dec. ICP by 25% in most pts), consider osmotic agents  
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Initial Management of head trauma contd   seizure prophylaxis, non-contrast head CT (not worried about allergies or kidneys, just worried about a bleed that is pushing on head parenchyma at this time)  
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Concussions   Trauma-induced alteration in mental status that may or may not involve a loss of consciousness. Mild traumatic brain injury that is caused by an impact or jolt to the head or as an immediate and transient impairment of neural function from mechan. force  
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Common presentation of Concussions   usual complaints are headache, confusion, amnesia. PE: neuro exam is nonfocal.  
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pathophysiology of Concussion   Shearing or stretching of white matter fibers. Temporary neuronal dysfunction. Transient alterations in neurotransmitter levels. Temp. changes in cerebral blood flow and oxygen use  
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Grade I concussion   No loss of consciousness, Transient confusion.Concussion symptoms or mental status changes resolving in less than 15 minutes  
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Grade II concussion   No LOC, transient confusion. concussion sx or mental status changes lasting more than 15 minutes  
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Grade III concussion   LOC of any duration.  
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Return to Play Paramenters in Grade I   remove from event, examine for mental status changes every 5 min., if no sx for 15 min can return to play, a second Grade I will eliminate the player from competition with a return in 1 week if asyx  
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RTP Parameters in Grade II   Remove from event with no return. On site eval with repeat eval NEXT DAY. If sx free at rest and with exertion for 1 week then do neuro exam for clearance. If still sx >1wk do a repeat CT or MRI. 2 wks before RTP  
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RTP Parameters in Grade III   If not stable, transport to nearest facility. complete neuro exam. Brief? No RTP until asx 1 wk. Prolonged? withhold RTP 2 wks, 2nd Grade III? withhold 1 month min. CT abnl? end season  
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Post concussive syndrome   seen in many pts after mild traumatic brain injury. Key elements are somatic, cognitive and affective sx  
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Somatic Sx in post concussive sx:   Headache, sleep disturbance, dizziness/vertigo, nausea, fatigue, hypersensitivity to light/sound  
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Cognitive Sx in post concussive sx:   attention/concentration difficulty, memory problems  
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Affective Sx in post concussive sx:   irritability, anxiety, depression, emotional lability  
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Discharge? Low risk   no LOC, No postraumatic amnesia, no mod or high risk factors  
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Discharge? Mod or High risk:   LOC, Posttraumatic amnesia, alteration of level of consciousness, severe or increasing HA, persistent N/V, intoxication, seizures, <2 yo, use of warfarin, hx of hemophilia or marrow suppression  
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