LOC and Coma Flashcards
Another name for a concussion?
What is it caused by?
What does it result in?
- 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
Eye opening - Glasgow scale?
- spontaneous 4
- response to verbal command 3
- response to pain 2
- no eye opening 1
Best verbal response - glasgow scale?
- oriented 5
- confused 4
- inappropriate words 3
- incomprehensible sounds 2
- no verbal response 1
Best motor response - glasgow scale?
- 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
What is a TBI? pts at highest risk?
Rating on GCS?
- 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
Etiologies of TBI?
- MVAs (20-45%)
- falls (30-38%, increasing in older pt)
- occupational accidents (10%)
- assaults (5-17% - increasing)
- contact sports
- soldiers in combat
Primary injury phase - cortical contusion (direct trauma)
- 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
Secondary brain injury pathophys?
- 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
Clinical features of TBI?
Assoc sxs?
- or - LOC, confusion, stupor, amnesia: impt to know presence and length of any of these sxs
- assoc sxs:
HA, dizziness, disorientation, N/V
TBI signs?
- vacant stare
- inabilty to focus
- gross incoordination
- memory difficulties
- delayed verbal expression
- slurred or incoherent speech
- emotionality out of proportion to events
Complicated TBI? assoc signs and sxs?
- 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?)
Management of TBI?
- 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
What are the guidelines for CT scan in ER?
- 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)
What are signs of a basilar skull fracture?
- raccoon eyes
- hematoma behind ears (battle sign)
- hemotympani
- CSF draining out of ears or nose
- fracture is hard to detect on CT - do MRI
CT scan abnormalities?
- subdural hematoma
- intracranial bleeding
- cerebral edema
- skull fracture
What TBI pts should be hospitalized?
- hospitalization for those at risk: GCS less than 15 or deteriorating abnorm CT seizures abnormal bleeding parameters
Criteria for TBI pts who can be observed as outpt?
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
Sequela from TBI?
- 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
Sxs of post-concussion syndrome (PCS)?
RFs?
- HA
- dizziness
- neuropyschiatric
- cog impairment including noise sensitivity
- PP: direct brain injury, psychogenic
- female gender and increasing age: RFs
Dx and Tx of PCS?
- 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
How can we prevent TBIs?
- 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!!
Definition of coma? common etiologies?
- unarousable and unresponsive (lasts longer than 1 hr)
- common etiologies:
TBI
hypoxic ischemic encephalopathy (HIE)
drug overdose
intracranial hemorrhage
CNS infections
brain tumors
etiologies of coma? Systematically?
- primary cerebral: bilateral, unilateral - brain stem disorders (pons, midbrain) - systemic (toxins: meds, drug overdoses) - endocrine
What is the ARAS?
- 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
What information do you want from the pt’s hx?
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?
What should you focus on during PE?
- 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
Coma posturing and meaning?
- 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
Different respiratory patterns seen with coma?
- 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
Dx goal in coma?
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
Labs to order in coma pts?
- CBC
- CMP (w/ Ca and magnesium)
- TSH
- Tox screenings
- UA
- adrenal fxn tests
- carboxy hemoglobin
- specific drug concentrations
Management of coma pt?
- ID tx causes
- supportive: protect airway, hydrate, monitor blood glucose and electrolytes