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Flashcards in neck emergencies Deck (56)


a. Alert, or responsive to
b. Verbal stimuli, or to
c. Painful stimuli, or
d. Unresponsive


head injury GCS ranges

1. GCS 13-15: Mild Head Injury
2. GCS 9-12: Moderate Head Injury
3. 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



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)

1. Battle sign, Racoon eyes, hematotympanum



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

1. May be acute, like epidural hematoma

2. May have delayed course, days to weeks

3. Increased ICP, edema, herniation

4. 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)

1. Usually posterior

Interhemispheric Subdural Hematoma:


Chronic Subdural Hematoma MC seen in what population

1. Following minor injury, rarely parenchymal injury, alcohol makes it more likely to occur
2. 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)



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



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


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
1. If PCO2 is high, that means ICP is high as well so bringing it down is important
2. 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.
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

1. MVC, higher speeds, air bag deployment, intrusion into vehicle or car totaled
2. Sports: diving, horseback riding, football, gymnastics, skiing, hang gliding
3. Age over 65, arthritis, osteoporosis



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