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Primary brain injury occurs |
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damage throughout many areas of the brain |
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skull is fractured/pierced by a penetrating object and exposed to the environment |
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skull integrity is not violated |
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Simple clean break. bones bend inward, area around bends outward.
Most common type |
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Bone is pressed inward into the brain tissue to at least the thickness of skull |
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Scalp/dura lacerated, direct opening to brain tissue |
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fragmented bone with depression into the brain tissue |
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Occurs at base of skull. Can cause CSF leakage. May damage CNs |
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Bruising of the brain tissue |
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Tearing
Leads to secondary hemorrhage, edema and inflammation |
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Usually related to high speed acceleration/deceleration Widespread injury to the white matter of brain. Impaired cognition
Shearing causes nerves to die. Brain swells. |
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AKA concussion
Blow to head followed by a feeling of confusion, dazed or. disorientation |
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lasts for up to 30 minutes but not always present |
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Loss for events immediately before and after accident |
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No evidence of brain damage on scan
Seconday injury possible |
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Moderate TBI requirements |
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LOS from 30 min - 6 hours
GCS of 9-12 |
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Brain damage might be seen, but not always. |
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may last up to 24 hours after accident |
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Damage can be detected on scans |
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For secondary injury is high. Critical care pts. |
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Hypotension and hypoxemia #’s? |
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MAP < 70 mmHG Pao2 <80 mmHg |
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Leading cause of death for brain injuries that come to the hospital alive? |
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Caused by abnormal permeability of the walls of the cerebral vessels which allows protein rich plasma infiltrate to leak into the extra cellular space of brand.
Collects primarily in white matter |
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A result of hypoxia insult, which causes a disturbance in cellular metabolism and active ion transport.
Brain depleted of o2, glucose and glycogen. Converts to anaerobic metabolism Results in cell edema, dysfunction and death |
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Occurs with fluid accumulation between the cells of the brain |
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Intersticial edema associated with |
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elevated BP or increased CSF pressure |
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Cerebral perfusion pressure (CPP) equasion |
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Results from arterial bleeding into the space between the dura and inner skull. |
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Lucid intervals associated with |
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Results from venous bleeding into the space beneath the dura and above the arachnoid. |
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Subdural hematoma occurs..... |
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slowly. high mortality. Generally unrecognized |
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Accumulation of blood within the brain tissue caused by the tearing of small arteries/veins within the subcortical white matter
Blood vessel within brain bursts |
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Abnormally high CSF volume |
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Brain tissue shifts down in the presence of increased ICP |
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Shift of one or more areas of the temporal lobe
Creates pressure on CN III |
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Dialated and non reactive pupils, ptosis, rapid deteriorating LOC |
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Downward shift of brain stem/diencephalon from a supratenorial lesiond |
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SSX of central herniation |
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Cheyenne-stokes, non reactive and pin point pupils, and potential hemodynamics instability. |
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Loss of mobility/sensory perception Tenderness along spine Abnormal head tilt |
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Spinal cord precautions Positioning |
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Pt placed supine, and align spinal column in a neutral position.
No neck flexion with pillow or roll No thoracic/lumbar flexion with HOB controls |
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Spinal cord precautions activity |
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Spinal cord precautions repositioning |
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Use log roll procedure. Multiple people involved. Assess neurological function after every position change |
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Assess for Cushing triad
Hypotension/tacycardia suggest hypovolemic shock |
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Widened pulse pressure and bradycardia |
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GCS change: when to notify provider |
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1st sign in deteriorating neuro status |
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Pinpoint/non-responsive pupils indicates |
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brainstem dysfunction at pons |
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Midstage between normal pupil size and dilated |
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Fixed/dilated pupils is... |
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Risk for increased ICP decreases in TBI PT after what time |
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Fluids with halo sx
Clear/yellow ring surrounding blood |
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