LOC and Coma Flashcards

1
Q

Another name for a concussion?
What is it caused by?
What does it result in?

A
  • TBI
    trauma induced alteration in mental status may or may not involve loss of consciousness
  • caused by direct blow to head, face, neck or body
  • result in neuropathological changes: fxnl not structural
  • resolution of clinical and cognitive sx follows a sequential course
  • assoc with grossly normal neuroimaging studies
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2
Q

Eye opening - Glasgow scale?

A
  • spontaneous 4
  • response to verbal command 3
  • response to pain 2
  • no eye opening 1
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3
Q

Best verbal response - glasgow scale?

A
  • oriented 5
  • confused 4
  • inappropriate words 3
  • incomprehensible sounds 2
  • no verbal response 1
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4
Q

Best motor response - glasgow scale?

A
  • obeys commands 6
  • localizing response to pain 5
  • withdrawal response to pain 4
  • flexion to pain 3
  • extension to pain 2
  • no motor response 1
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5
Q

What is a TBI? pts at highest risk?

Rating on GCS?

A
  • head injury due to contact and/or acceleration and/or deceleration forces
  • 1.5 mill reported incidents/yr in US
  • TBI leading cause of death for persons age 1-45 in north america, males greater than females, 5 mill people suffer TBI disability
  • pts at higher risk: less than 5 and older than 60 (fall prone)
  • mild: GCS 13-15 measured 30 min after injury
  • moderate: GCS 9-12
  • severe: GCS less than 8
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6
Q

Etiologies of TBI?

A
  • MVAs (20-45%)
  • falls (30-38%, increasing in older pt)
  • occupational accidents (10%)
  • assaults (5-17% - increasing)
  • contact sports
  • soldiers in combat
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7
Q

Primary injury phase - cortical contusion (direct trauma)

A
  • coup-direct blow to brain
  • contrecoup injury to brain on opp side of head
  • severe: axonal rupture
  • mild: diffuse axonal injury: disruption of axonal neurofilament organization, impairs axonal transport and leads to axonal swelling
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8
Q

Secondary brain injury pathophys?

A
  • begins quickly after primary phase
  • continues for hours to days
  • cascade of molecular injury mechanisms:
  • NT mediated excitotoxicity causing glutamate, free radical injury to cell membranes
  • electrolyte imbalances
  • mitochondria dysfxn
  • apoptosis
  • secondary ischemia from vasospasm, focal microvascular occlusion and vascular injury
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9
Q

Clinical features of TBI?

Assoc sxs?

A
    • or - LOC, confusion, stupor, amnesia: impt to know presence and length of any of these sxs
  • assoc sxs:
    HA, dizziness, disorientation, N/V
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10
Q

TBI signs?

A
  • vacant stare
  • inabilty to focus
  • gross incoordination
  • memory difficulties
  • delayed verbal expression
  • slurred or incoherent speech
  • emotionality out of proportion to events
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11
Q

Complicated TBI? assoc signs and sxs?

A
  • indicates more serious brain injury or rising ICP:
    seizures
    focal neuro signs
    worsening HA, confusion, lethargy
    protracted N/V
    other injuries to head/neck
    decreasing GCS (keep on repeating GCS - is it deteriorating?)
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12
Q

Management of TBI?

A
  • examine - look at pupils, do neuro exam: CNs, reflexes, strength, touch, movements
  • amnesia almost always involves loss of memory of traumatic event and frequently includes loss of recall for events immediately before and after trauma
  • longer the frame of amnesia - more serious the injury
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13
Q

What are the guidelines for CT scan in ER?

A
  • GCS less than 15
  • open or depressed skull fracture
  • any sign of basilar skull fracture: CSF leak
  • 2 or more episodes of vomiting
  • 65 yo or older
  • amnesia b/f impact of 3 or more minutes
  • dangerous mech (ejected from vehicle, fall from more than 3 ft)
  • bleeding diathesis or an oral anticoagulant (increased chance of brain bleed)
  • seizure or focal neuro sign
  • intoxication (drunk or brain injury - have to rule it out)
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14
Q

What are signs of a basilar skull fracture?

A
  • raccoon eyes
  • hematoma behind ears (battle sign)
  • hemotympani
  • CSF draining out of ears or nose
  • fracture is hard to detect on CT - do MRI
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15
Q

CT scan abnormalities?

A
  • subdural hematoma
  • intracranial bleeding
  • cerebral edema
  • skull fracture
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16
Q

What TBI pts should be hospitalized?

A
- hospitalization for those at risk:
GCS less than 15 or deteriorating
abnorm CT
seizures 
abnormal bleeding parameters
17
Q

Criteria for TBI pts who can be observed as outpt?

A

GCS=13-15, normal CT scan

outpt: must have responsible companion!!!
- somnolence or confusion
- diff w/ vision, severe or worsening HA
- urinary or bowel incont.
- weakness or numbness involving any body part
- unsteadiness or seizures
- N/V more than 2 episodes
- allow the pt to rest as needed but check on pt if any of the above occur return to ED

18
Q

Sequela from TBI?

A
  • post-concussion syndrome
  • post-traumatic HAs
  • post-traumatic seizures/epilepsy
  • post-traumatic vertigo
  • other CN injuries
  • second impact syndrome
  • cumulative neuropsych impairment: boxers - dementia pugilistica (20%),, football players - CTE
19
Q

Sxs of post-concussion syndrome (PCS)?

RFs?

A
  • HA
  • dizziness
  • neuropyschiatric
  • cog impairment including noise sensitivity
  • PP: direct brain injury, psychogenic
  • female gender and increasing age: RFs
20
Q

Dx and Tx of PCS?

A
  • Dx: clinically and w/ hx
  • if severe sx and pt hasn’t had MRI - get one!
  • Tx:
    education!!!!
    minimize meds, but use appropriately, low dose
  • typically resolves by 3 months 90% of the time
  • may need more extensive neurocognitive rehab
21
Q

How can we prevent TBIs?

A
  • sport-specific helmets: used in baseball, hockey, alpine sports found to reduce injuries
  • helmets used in soccer haven’t been found to reduce rate of head injury
  • in some cases use of protective equipment may encourage risky behavior
  • Bicycle and motorcycle helmets do reduce accident related head injuries!!
22
Q

Definition of coma? common etiologies?

A
  • unarousable and unresponsive (lasts longer than 1 hr)
  • common etiologies:
    TBI
    hypoxic ischemic encephalopathy (HIE)
    drug overdose
    intracranial hemorrhage
    CNS infections
    brain tumors
23
Q

etiologies of coma? Systematically?

A
- primary cerebral:
bilateral, unilateral 
- brain stem disorders (pons, midbrain) 
- systemic (toxins: meds, drug overdoses)
- endocrine
24
Q

What is the ARAS?

A
  • ascending reticular activating system (ARAS):
    originates upper pons and midbrain, the neurons project to thalamus and hypothalamus then to cerebral cortex
  • focal lesions to upper brainstem can alter alertness by damaging ARAS
  • in coma with toxic, metabolic and infectious etiologies mecahnism less well understood
25
Q

What information do you want from the pt’s hx?

A

obtained from family, witnesses, medical personnel:

  • time course of LOC
  • focal signs or sxs precede?
  • pt have previous neuro episode?
  • recent illness, fever, HA, falls, confusion?
  • Rx drugs, illicit drugs or alcohol?
26
Q

What should you focus on during PE?

A
  • complete with special attention to:
    LOC
    brainstem reflexes
    pupillary light, EOM and corneal reflexes
  • motor exam: assess muscle tone, spontaneous and elicited movements - note if asymmetric, reflexes
27
Q

Coma posturing and meaning?

A
  • decorticate: UE adduction with LE extension - dysfxn of cerebral cortex or thalamic damage (has better prognosis)
  • decerebrate posturing: UE extension, adduction and pronation with LE extension - injury to caudal diencephalon, midbrain or pons
28
Q

Different respiratory patterns seen with coma?

A
  • cheyne-stokes: cyclic pattern, hypernea, apnea: seen in pts with bilateral hemispheric or diencephalic insults
  • hyperventilation - injury to pontine or midbrain tegmentum
  • apneustic breathing: prolonged pause end of inspiration- indicates lesion to mid- and caudal pons
  • ataxic breathing: irregular in rate and tidal volume- damge to medulla
29
Q

Dx goal in coma?

A

ID tx causes:

  • infection, metabolic abnorm, seizures, intoxications/overdoses, surgical lesions
  • give O2, thiamin, fluids, narcan, glucose
  • papilledema/focal neuro findings suggest structural etiology - urgent brain CT
  • neuorimaging and coag test BEFORE lumbar puncture - IICP
  • LP: don’t delay tx if LP is delayed, get blood cultures
  • EEG: used primarily to detect seizures
30
Q

Labs to order in coma pts?

A
  • CBC
  • CMP (w/ Ca and magnesium)
  • TSH
  • Tox screenings
  • UA
  • adrenal fxn tests
  • carboxy hemoglobin
  • specific drug concentrations
31
Q

Management of coma pt?

A
  • ID tx causes

- supportive: protect airway, hydrate, monitor blood glucose and electrolytes