neck emergencies Flashcards
AVPU
a. Alert, or responsive to
b. Verbal stimuli, or to
c. Painful stimuli, or
d. Unresponsive
head injury GCS ranges
- GCS 13-15: Mild Head Injury
- GCS 9-12: Moderate Head Injury
- GCS 3-8: Severe Head Injury
Standardized evaluation of neurological status
The Glasgow Coma Scale
Predictive of morbidity/mortality
AMPLE history
A -> Allergies
M -> Medications (especially anticoagulants/anti-platelets V IMPORTANT)
P -> Past medical history
L -> Last meal (especially if surgery is indicated emergently)
E -> Events (what happened just before..?)
Cushing’s Triad what is it and what is it used for
Increased ICP and impending Herniation – pt’s will die
Bradycardia
hypertensioN
irregular respiration
pupillary response to light mydriasis would indicate
Mydriasis ipsilateral to site of 3rd nerve injury in herniation events
Motor deficits usually ipsilateral or contralateral to the sight of injury?
Motor deficits usually contralateral to the sight of injury
typical sxs in head exam of injury (3)
- Battle sign, Racoon eyes, hematotympanum
labs
cbc, electrolytes, stat glucose, coags, tox screen, ETOH level
threshold for intubation
very low threshold
GCS<8), hypoxia, hypoventilation, need to sedate for trip to the scanner
treat presumptively for ICP if
seizure and ICP **
(GCS<8), fixed and dilated pupil(s), decorticate or decerebrate posturing, bradycardia, hypertension or respiratory depression
b. Initial treatment is HOB up 30degrees and Manitol 1g/kg iv
leakage of blood from the MMA creates
Dura –> glued on the inside of the cranium
b. When you have bleeding from the middle meningeal artery, it starts to tear that membrane but it’s a tough membrane so the dura bulges in towards the brain (epidural hematoma)
Arterial bleed so each beat of the heart squeezes more blood in, causing more of a bulge
lens shaped bleed
subdural hematoma
from venous source and accumulates MORE SLOWLY spreading out in a crescent shape
not always the case but this is what we see
most reliable way to distinguish is how quickly are there symptoms occurring
Associated with skull fracture in 40-85%
Laceration of dural vessels from skull fracture (91%), usually the middle meningeal artery
epidural hematoma
common sxs associated with epidural hematoma
Transient loss of consciousness; lucent interval
3rd nerve palsy (sign of cerebral herniation)
Somnolence 24-96 hrs after accident
course of EDH
Hematoma expands
Increased ICP, decreased CBF
Herniation, ipsilateral CN-3 dysfunction and contralateral paralysis or posturing
who get’s SDH
infants, elderly, drunk
Underlying brain injury (50%)
Worse long term prognosis than epidural hematoma
stages of SDH
Hyperdense (<1 week);
isodense (1-3 weeks);
hypodense (3-4 weeks)
course of acute SDH
- May be acute, like epidural hematoma
- May have delayed course, days to weeks
- Increased ICP, edema, herniation
- ETOH increases cerebral edema by increasing the permeability of the blood brain barrier
cause of SDH
Cause: damage to subdural veins (“bridging veins”)
Most common acute finding in child abuse (whiplash injury)
- Usually posterior
Interhemispheric Subdural Hematoma:
Chronic Subdural Hematoma MC seen in what population
- Following minor injury, rarely parenchymal injury, alcohol makes it more likely to occur
- Convex configuration
Bleeding from small vessels at site of coup or contrecoup injury
Sub-Arachnoid Hemorrhage
if CT is negative and you suspect SAH
traumatic SAH should be ruled out from CT alone
for trivial trauma–> treat like atraumatic get a LP
Separation of suture between temporal and occipital bones
Seldom fatal (except for race car drivers)
SAH
battle sign
bruising from behind the ear
basal skull fracture
basal skull fracture sxs
CSF otorrhea
, CSF rhinorrhea
(danger of meningitis!)
if you get two rings on the coffee filter paper then suspect CSF
how do you get basal skull fractures
a. Caused by deceleration injury or occipital trauma
other PE in basal skull fractures
h. Battle’s sign
i. Racoon eyes
j. Hematotympanum
Hematotympanum
A collection of blood in the tympanic cavity behind the tympanic membrane. Visible on otoscopy as a blue, intact eardrum. Occurs secondary to head trauma (e.g. basilar skull fracture).
how do you treat basal skull fx
abx
need to make sure they do not get infected
treatment of the seriously head injured patient how to prevent seizures
IV Phenytoin or Kepra*
other than seizure med what do you do to treat injury initially
Prevent fever
Control bleeding, transfuse to HCT>30
Antibiotics for penetrating injury or basal skull fracture
Treat hypotension in neck injury by
resucitate to MAP>90 (SBP 120-140 with NS. Pressors as needed. N.B. isolated head injury is unlikely to be hypotensive on initial presentation, so look for other injuries!
SBP of less than 180
Control excessive hypertension
Labetolol to reduce BP 20-30%
treat ICP by
target <20, cpp70-80)
Raise head of bed to 30 degrees
IV Mannitol boluses once euvolemic (serum osmolality 280-300)
Mannitol increases the volume of blood and makes it less viscous
(or 3% saline)
why is hyperventilation not a great solution
Hyperventilate PCO2 to 26-30?
Consider only if other measures ineffective
- If PCO2 is high, that means ICP is high as well so bringing it down is important
- PCO2 should be no lower than 25
Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP. This effect is mediated my pH changes in the extracellular fluid which cause cerebral vasoconstriction or vasodilation depending on the pH. can lead to quick rebound
find optic disc and look at the shadow it casts
> 5 correlates with increase ICP
this is the optic nerve sheath widening in response to increased pressure
or a nipple in the eyeball is ICP
can also see pappiladema
when can you discharge a patient
a. GCS of 15 with resolved symptoms:, dispo to home with vigilant family members and return preacautions
mild injury (GCS14-15)
Admit for observation. Neurological exams every 1-4 four hours. IV fluids, analgesia, anti-emetics.
Repeat head CT if worsening pain, vomiting or adverse change in level of consciousness
GCS of 9-13 ( “moderate” injuries)
Admit to ICU. Neurological exams every 1-2 hours.
NPO
Repeat head CT six hours after admission or promptly if pt worsens
If pt is immobile, DVT prevention may be warranted
protocol for GCS<8 Severe injuries
Admit to ICU with hourly neurological exams.
ii. NPO.
iii. Intracranial pressure monitor
iv. Analgesia and sedation.
Tight control of BP and intracranial pressure
vi. Seizure prophylaxis
vii. DVT prevention
what are the high risk indications for a head CT exam (5)
Glasgow Coma Scale <15 at 2 hours after injury
Open or depressed skull fracture
Vomiting (Two or more episodes)
Age 65 years or over (other studies suggest age 60)
Basal skull fracture signs:
Hemotympanum Periorbital Bruising (Raccoon Eyes)
Mastoid process Ecchymosis (Battle’s Sign)
Cerebrospinal fluid leakage from ear or nose
Moderate risk indications for Head CT
Pre-trauma amnesia lasting longer than 30 minutes
High risk mechanism of injury
Pedestrian in motor vehicle accident
Passenger ejected from vehicle
Fall from height over 3 feet or 5 stairs
vi. Nexus II Rule states that all of these have to be absent in order to forgo a CT
a. Age ≥ 65yr
b. Evidence of significant Skull Fracture
c. Scalp hematoma
d. Neurologic deficit
e. Altered Level of Alertness
f. Abnormal behavior
g. Coagulopathy
h. Recurrent or forceful vomiting
MC grade of concussion
a. Transient confusion without amnesia.
b. No loss of consciousness
c. Mental status abnormalities resolve within 15 minutes
d. Most common
grade 2 concussion
a. Transient confusion or amnesia lasting greater than 15 minutes.
b. No loss of consciousness
c. Patient may have retrograde amnesia of events preceding the injury
grade 3 concussion
a. Loss of consciousness for any amount of time
b. Mental status change and/or amnesia is not included in the definition
ii. Risk factors for more severe injury
- MVC, higher speeds, air bag deployment, intrusion into vehicle or car totaled
- Sports: diving, horseback riding, football, gymnastics, skiing, hang gliding
- Age over 65, arthritis, osteoporosis
sciwora
spinal cord injury without radiographic abnormality seen in children likely related to high elasticity
variable sensory loss seen in
central cord syndrome
loss of distal motor function and pinprick as well as pain and temperature sense
anterior cord syndrome
MOA in anterior cord syndrome *
forced hyperflexion disk herniation or fracture
MOA of central cord syndrome *
forced hyperflextension injury
MOA in brown squared syndrome *
penetrating trauma most common
what would you expect to see in brown squared syndrome *
complete ipsilateral motor paralysis and loss of vibration
pressure and proprioception
contralateral loss of pinprick pain and temperature sense
