types
What is ONE SPECIFIC THING that can cause a tbi?
A brain abscess (commonly caused by strep and/or immunosuppression/AIDS)
primary brain injury : open vs. closed?
open: skull is fractured or pierced by a penetrating object and exposed to environmental contaminants
closed: skull intact but damage to brain tissue as a result of increased intracranial pressure
Epidural hematoma: what kind of bleed?
ARTERIAL
Why do we only suction when absolutely necessary?
Suctioning increases icp as well as induces cough, which increases icp too.
whats the main med we would use for increased icp? hint: molly asks for this all the time
what do we monitor every 6 hrs when we have a patient on this med? what do we want the range at?
MANNITOL <3
osmolality q6hrs, we want it to range 310-320 mOm/L
Direct vs. Indirect injury
direct- injury occurs as a result of a blow, jolt, or penetration to head
indirect- force applied to another body part with a rebound effect to brain
secondary brain injury....
-results from?
-most commonly have increased ICP. from what?
-Primary cause???
results from brain injury (duh), neurologic damage that occurs after the primary injury
increased icp r/t edema, hemorrhage, hematoma, impaired auto-regulation
primary cause is HYPOXIA, HYPOTENSION
VENOUS
ANY PATIENT W/ A TBI SHOULD BE TREATED AS IF THEY HAVE A _______?
SCI. CERVICAL COLLAR AND LOG ROLL THEM PEOPLE!!!
What do we use for ventilated patients?
what should we have NEARBY when we use these meds?
Fentanyl or morphine.
HAVE DAT NARCAN READY.
MILD TBI : GCS? LOC? S/S?
If a minor head injury, what medication can we give for headache? What do we instruct the patient to NOT DO?
gcs of 13-15 and a loc of up to 30 mins. Headaches, n/v, dizziness, memory issues.
Acetaminophen for headache. Do not blow nose, clean ears, or do any strenuous activity for 48 HRS.
Hypotension and Hypoxia r/t secondary brain injury
MAP?
Hypoxemia #?
map < 70 mmhg
PAO2 < 80 mmhg
What hematoma has the highest mortality rate? why?
signs and symptoms?
Subdural hematoma - goes unrecognized until patient presents with severe neurological compromise
s/s: confusion, worsening headaches, seizures, decreased loc, coma
Neuro assessment: a change in how many points in GCS indicates the patient is deteriorating?
most important to assess?
2 or more points
assess loc. a decrease or change in loc is the first sign!
What can we use to decrease anxiety and promote rest?
Lorazepam (ativan) and midazolam (versed)
MODERATE TBI : GCS? LOC? WHAT IS DIFFICULT FOR THESE PATIENTS?
gcs of 9-12, loc 30 min to 6 hrs, will have difficulty resuming normal daily activites
Normal icp range?
what maintenance number do we want icp @? THIS IS THE GOAL OF TX!
FOR AN EXTRA 250 POINTS... NAME SOME EARLY AND LATE SIGNS OF INCREASED ICP!!!
normal- 10-15 mmHg
maintenance- 60-70 mmHg
early: headache, nausea, vomiting, amnesic to event, altered loc, restless, drowsiness, changes in speech, loss of judgement
Late: dilated non reactive pupil, unresponsive to verbal/painful stimuli, cushings triad, halo sign
Brain Herniation: what is it?
clinical manifestations?
do they recover?
TX??
Downward shift of brain tissue r/t cerebral edema; FATAL CONSEQUENCE OF UNTREATED INCREASING ICP!!
manifestations: non reactive dilated pupils, deteriorating loc, cheyne stokes resps, hemodynamic instability, abnormal posturing, ptosis(eyelid dropping)
Recovery likelihood: ZERO. THEY DEAD.
TX: mannitol or surgery
Cardiac monitoring for moderate/severe tbi patient: what might we see?
Specific ST/T wave changes
therapeutic hypothermia does what?
cool to ...? for how long after injury?
decreases metabolic demands of the brain and edema
cool to 89.6 f - 93.2 f FOR 24-48 HRS AFTER INJURY
SEVERE TBI: GCS? LOC? WHAT DO WE MONITOR?
gcs 3-8, loc longer than 6 hrs, monitor cardiac and icp
Define Cushings Triad; a classic, yet late sign of increased ICP.
(HINT: as icp increased, perfusion decreases)
Severe hypertension, widened pulse pressure, bradycardia
-hypotension
-hypoxemia
-hypercapnia (paco2 greater than 40-45)
-hypocapnia (paco2 less than 40-45)
What can an EEG tell us?
measures electrical signals to brain generated by hearing, touch, sight, auditory, visual, etc
Brain death: who declares it?
what do they do to declare it?
Neuro and critical care declare it.
We do: cerebral angiography, EEG, cerebral CTA, transcranial doppler