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Emergency Medicine > neck emergencies > Flashcards

neck emergencies Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

AVPU

A

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

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2
Q

head injury GCS ranges

A
  1. GCS 13-15: Mild Head Injury
  2. GCS 9-12: Moderate Head Injury
  3. GCS 3-8: Severe Head Injury
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3
Q

Standardized evaluation of neurological status

A

The Glasgow Coma Scale

Predictive of morbidity/mortality

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4
Q

AMPLE history

A

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..?)

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5
Q

Cushing’s Triad what is it and what is it used for

A

Increased ICP and impending Herniation – pt’s will die

Bradycardia

hypertensioN

irregular respiration

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6
Q

pupillary response to light mydriasis would indicate

A

Mydriasis ipsilateral to site of 3rd nerve injury in herniation events

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7
Q

Motor deficits usually ipsilateral or contralateral to the sight of injury?

A

Motor deficits usually contralateral to the sight of injury

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8
Q

typical sxs in head exam of injury (3)

A
  1. Battle sign, Racoon eyes, hematotympanum
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9
Q

labs

A

cbc, electrolytes, stat glucose, coags, tox screen, ETOH level

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10
Q

threshold for intubation

A

very low threshold

GCS<8), hypoxia, hypoventilation, need to sedate for trip to the scanner

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11
Q

treat presumptively for ICP if

A

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

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12
Q

leakage of blood from the MMA creates

A

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

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13
Q

lens shaped bleed

A

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

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14
Q

Associated with skull fracture in 40-85%

Laceration of dural vessels from skull fracture (91%), usually the middle meningeal artery

A

epidural hematoma

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15
Q

common sxs associated with epidural hematoma

A

Transient loss of consciousness; lucent interval

3rd nerve palsy (sign of cerebral herniation)

Somnolence 24-96 hrs after accident
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16
Q

course of EDH

A

Hematoma expands

Increased ICP, decreased CBF

Herniation, ipsilateral CN-3 dysfunction and contralateral paralysis or posturing

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17
Q

who get’s SDH

A

infants, elderly, drunk

Underlying brain injury (50%)
Worse long term prognosis than epidural hematoma

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18
Q

stages of SDH

A

Hyperdense (<1 week);

isodense (1-3 weeks);

hypodense (3-4 weeks)

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19
Q

course of acute SDH

A
  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
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20
Q

cause of SDH

A

Cause: damage to subdural veins (“bridging veins”)

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21
Q

Most common acute finding in child abuse (whiplash injury)

A
  1. Usually posterior

Interhemispheric Subdural Hematoma:

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22
Q

Chronic Subdural Hematoma MC seen in what population

A
  1. Following minor injury, rarely parenchymal injury, alcohol makes it more likely to occur
  2. Convex configuration
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23
Q

Bleeding from small vessels at site of coup or contrecoup injury

A

Sub-Arachnoid Hemorrhage

24
Q

if CT is negative and you suspect SAH

A

traumatic SAH should be ruled out from CT alone

for trivial trauma–> treat like atraumatic get a LP

25
Q

Separation of suture between temporal and occipital bones

A

Seldom fatal (except for race car drivers)

SAH

26
Q

battle sign

A

bruising from behind the ear

basal skull fracture

27
Q

basal skull fracture sxs

A

CSF otorrhea
, CSF rhinorrhea
(danger of meningitis!)

if you get two rings on the coffee filter paper then suspect CSF

28
Q

how do you get basal skull fractures

A

a. Caused by deceleration injury or occipital trauma

29
Q

other PE in basal skull fractures

A

h. Battle’s sign
i. Racoon eyes
j. Hematotympanum

30
Q

Hematotympanum

A

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).

31
Q

how do you treat basal skull fx

A

abx

need to make sure they do not get infected

32
Q

treatment of the seriously head injured patient how to prevent seizures

A

IV Phenytoin or Kepra*

33
Q

other than seizure med what do you do to treat injury initially

A

Prevent fever

Control bleeding, transfuse to HCT>30

Antibiotics for penetrating injury or basal skull fracture

34
Q

Treat hypotension in neck injury by

A

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

35
Q

Control excessive hypertension

A

Labetolol to reduce BP 20-30%

36
Q

treat ICP by

A

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)

37
Q

why is hyperventilation not a great solution

A

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

38
Q

find optic disc and look at the shadow it casts

A

> 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

39
Q

when can you discharge a patient

A

a. GCS of 15 with resolved symptoms:, dispo to home with vigilant family members and return preacautions

40
Q

mild injury (GCS14-15)

A

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

41
Q

GCS of 9-13 ( “moderate” injuries)

A

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

42
Q

protocol for GCS<8 Severe injuries

A

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

43
Q

what are the high risk indications for a head CT exam (5)

A

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

44
Q

Moderate risk indications for Head CT

A

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

45
Q

vi. Nexus II Rule states that all of these have to be absent in order to forgo a CT

A

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

46
Q

MC grade of concussion

A

a. Transient confusion without amnesia.
b. No loss of consciousness
c. Mental status abnormalities resolve within 15 minutes
d. Most common

47
Q

grade 2 concussion

A

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

48
Q

grade 3 concussion

A

a. Loss of consciousness for any amount of time

b. Mental status change and/or amnesia is not included in the definition

49
Q

ii. Risk factors for more severe injury

A
  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
50
Q

sciwora

A

spinal cord injury without radiographic abnormality seen in children likely related to high elasticity

51
Q

variable sensory loss seen in

A

central cord syndrome

52
Q

loss of distal motor function and pinprick as well as pain and temperature sense

A

anterior cord syndrome

53
Q

MOA in anterior cord syndrome *

A

forced hyperflexion disk herniation or fracture

54
Q

MOA of central cord syndrome *

A

forced hyperflextension injury

55
Q

MOA in brown squared syndrome *

A

penetrating trauma most common

56
Q

what would you expect to see in brown squared syndrome *

A

complete ipsilateral motor paralysis and loss of vibration
pressure and proprioception

contralateral loss of pinprick pain and temperature sense

Emergency Medicine (28 decks)

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