EM: neuro Flashcards

1
Q

what is confusion? delirium vs dementia?

A

Confusion- alteration in content
Delirium—ACUTE alteration in content
Dementia—CHRONIC alteration in content

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2
Q

levels of consciousness (arousal)

A

Sleepy -> lethargic->obtunded->unconscious/coma

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3
Q

Glascow Coma Score (GCS): what is it? what scores correlate with mild, moderate and severe?

A
Sum defines TBI severity classification:
Severe 3-8
Moderate 9-13
Mild 14-15
**can be used for measuring recovery or response to treatment over time
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4
Q

GCS: ________ correlates independent of outcome

A

*Motor score independently correlates with outcome

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5
Q

altered mental status Ddx

A
AEIOU TIPS
A-Alcohol/acidosis
E- Endocrine/Epilepsy/Electrolyte/Encephalopathy
I- Infection
O- Opiates/Overdose
U-Uremia/Underdose

T-Trauma/Toxin
I-Insulin
P-Poison/Psychosis
S-Stroke/Seizure/Syncope

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6
Q

what 3 vital signs are important to get for mental status workup?

A

Cardiac Monitor/pulse ox
Blood glucose
Rectal temp (e.g. uti, sepsis, infection)

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7
Q

what routine labs do we do for altered mental status? (imaging, blood, urine)

A

Imaging: CT head WO, CXR
Blood: CBC/Chem8/Calcium/Mg/ (seizure or bleed)blood cultures
Urine: drug screen, UA with reflex (aka immediate culture if something is off)

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8
Q

what age and gender have the most TBIs?

A

Men, >75 yo

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9
Q

TBI: primary vs secondary

A

Primary: the immediate and permanent damage to brain tissue by the traumatic event.

Secondarybrain injury: response to initial mechanical trauma-Potentially preventable and reversible
-Impaired blood flow, edema, release of excitatory neurotransmitters and neurotoxins.

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10
Q

two types of primary TBI

A

Focal: hematomas, contusions, lacerations, intraventricular
Diffuse: axonal shearing, concussion

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11
Q

cerebral perfusion pressure: how do you calculate it? how does increase in ICP affect MAP and CPP?

A

Cerebral Perfusion Pressure (CPP)
CPP=MAP-ICP
If ICP increases, CPP decreases
if ICP increases, MAP (aka BP) - tries to go up to compensate and maintain CPP (“cushing’s reflex”)

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12
Q

autoregulation: what is it and what is it like for TBI pts?

A

**Autoregulationallows the body to control the cerebral blood flow. Mechanism is damaged in most TBI patients.

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13
Q

what is the monro-kellie doctrine?

A

An increase in the volume of any one of the intracranial contents (parenchyma, CSF, blood) must beoffset by a decrease in one or more of theothers OR be associated with a rise in ICP.

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14
Q

TBI: cushing’s triad

A

a pt with increased ICP –>progressive deterioration/impending herniation
signs of this: hypotension, bradycardia, respiratory irregularity

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15
Q

Dx of head trauma

A

Head CT WO contrast (b/c contrast would mask the bleed)- acute bleed would naturally show white

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16
Q

Canadian CT head injury/trauma rule

A

Age <16yo?
Pt on blood thinners?
Seizure after injury?
Neurologic deficit
… any of these apply with head trauma= NEED HEAD CT
Overall: have a low threshold for CT with head injury

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17
Q

what is the “Nexus II”?

A

a second evaluation criteria to determine if you need a head CT following head trauma

  • “head CT not required if none of these are present”
  • includes evidence of skull fracture, altered MS, abnormal coag
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18
Q

head trauma txt/mgmt: initial & airway/breathing &ventilation

A

initial: resuscitation (ABCs) and avoidance of hypoxia and hypotension. IMAGING asap!
airway: intubation, w/ neuro exam before sedation

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19
Q

head trauma txt/mgmt: ventilation and circulation goals

A

ventilation:Goal maintain normal PaCO2 (35-45 mmHg) circualtion: keep MAP above systolic of 100-110mmHg for adequate CPP

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20
Q

head trauma txt/mgmt: 2 medication changes

A

Reversal of Anticoagulation

Seizure prophylaxis: Keppra

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21
Q

head trauma txt/mgmt: immediate actions to lower ICP

A
  1. Elevate head of bed (30 degrees/reverse Trendelenburg)
    Keep head and neck in neural position, improving cerebral venous drainage
  2. hyperosmolar therapy: osmotic diuersis, mannitol or hypertonic saline
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22
Q

when can you discharge a linear skull fracture?

A

If no intracranial bleed or other injuries, observe for 4-6 hrs and discharge

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23
Q

how does a depressed skull fracture present? what does this indicate?

A

Depression/crepitus on exam

Result in bone of skull vault being folded/depressed inward into the cerebral parenchyma

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24
Q

in addition to neuro consult, what can you give someone with a depressed skull fracture (meds) ?

A

Antibiotics, seizure prophylaxis (e.g.Keppra),

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25
Q

where do most skull base fractures result from ? (impact to the skull where?)

A

from impact to the skullaround its base (e.g. occiput, temporalregion, frontal region – the so-called”hat band” distribution.

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26
Q

what meds may you give someone for skull base fx? (kinda weeds)

A

Antibioticprophylaxis is often started in setting of CSF leak but should be discussed with a neurosurgeon (b/c possiblity of selecting resistant organisms)

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27
Q

raccoon eyes, battles sign and hemotymp are all signs of what type of fracture? what other sign may be present?

A

skull base fracture
raccoon eyes- periorbital ecchymosis
battles sign- bruising over the mastoid
hemotymp- blood behind tympanic membrane
*CSF “halo” sign when dropped onto paper with blood

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28
Q

hematoma: epidural vs subdural vs subarachnoid

A

epidural hematoma- rapid expansion (arterial - bleeds hard and fast), lucid interval
subdural - venous blood (bleeds slow), progressive consciousness decline
subarachnoid- thunderclap HA, very dangerous

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29
Q

what artery is usually ruptured with epidural hematoma?

A

middle meningeal (blunt trauma to temperoparietal region)

30
Q

CT w/out: epidural hematoma

A

Lens-shaped (or lemon-shaped),biconvex

31
Q

how do you differentiate a epidural from subdural hematoma on CT?

A

Bloodalong the inside of the skull will not cross the sutures.

32
Q

what can we do in the ER for an epidural hematoma ?

A

Medical care to decrease ICP:

  1. Mannitol/hypertonic saline
  2. Hyperventilation
  3. Steroids/ventricular shunt
  4. ICU admission
33
Q

subdural hematomas are more common in what two patient populations?

A

elderlyandalcoholics (those with cerebral atrophy)

34
Q

prognosis epidural vs subdural hematoma?

A

subdural worse than epiduralsdue to concurrent brain damage.

35
Q

CT w/out: subdural hematoma

A

crescent moon shape

36
Q

what can we do for a subdural hematoma in the ED?

A

ICP Management:
1. Elevate head of bed
2. Short-term hyperventilation
3. Hyperosmolar agents (Mannitol, 3% Saline)
Reversal of anticoagulation
Treat and prevent hypotension and hypoxia

37
Q

intraparenchymal hemorrhage: S+S , PE

A

lethargy
headache
obtundation
physical exam: focal motor and sensory deficits

38
Q

intraparenchymal hemorrhage: imaging

A

Imaging: head CT/MRI without contrast
hypodensity: look for mass effect orfocal edemathat may predict a herniation

39
Q

intraparenchymal hemorrhage: txt - prevention of ICP, reversal of ICP

A

prevent elevation of ICP

  1. raise head of bed
  2. limit IV fluids
  3. treat HTN
  4. give calcium channel blockers (Nimodipine)

if ICP increased: 1. mannitol 2. hyperventilate 3. steroids 4. ventricular shunt

40
Q

Diffuse Axonal Injury: DAI: what is it? what is the major cause?

A

DAI is a primary brain injury caused by the shearing of axons in the deep white matter at the instant of the traumatic deceleration.
* “shaken baby syndrome”

41
Q

typical clinical picture of DAI

A

comatose patient with no or minimal signs of injury on the initial CT. MR will detect the extent of injury
*txt is supportive

42
Q

major cause of atraumatic SAH

A

ruptured aneurysm @ Bifurcation of the circle of Willis

43
Q

hematoma vs hemorrhage

A

A hematoma usually describes bleeding which has more or less clotted, whereas a hemorrhage signifies active, ongoing bleeding.

44
Q

what size aneurysm are more likley to rupture?

A

> 5-10 mm

45
Q

classic symptom of SAH?

A

“Thunderclap” headache

46
Q

what scoring system is used for SAH? (kinda weeds)

A
ottowa SAH rule for headache eval. (to rule out SAH) 
<40 years old
Without neck pain/stiffness
Without witnessed LOC
Without onset during exertion
Without thunderclap HA
Without limited neck flexion
47
Q

Dx for SAH?

A
CT w/out
Lumbar puncture (xanthochromia-yellow color- enzyme breakdown of blood releasing bilirubin, RBC count)
48
Q

3 part medical mgmt of SAH?

A

Blood pressure
Pain medications
Antiemetics

49
Q

SAH- risk of rebleeding is highest when? what meds do you give to prevent this?

A

Risk of rebleeding greatest in first 2-12 hours

Reduced by BP control: Labetalol ornicardipine

50
Q

SAH- risk of vasospasm lasts how long? what do you give to prevent this?

A

Vasospasm 2-3 weeks post SAH

Nimodipine

51
Q

CVA: what is it? S+S?

A

intracranial hemorrhage

S+S: Headache (more insidious than in SAH), n/v, dizziness, truncal, ataxia, gaze palsies, decreased LOC.

52
Q

3 ways to dx CVA

A

history, *CT w/out, MRI

53
Q

ED txt of CVA

A

Antipyretics, antiepileptic meds, BP, reverse coagulopathy

Elevate head of bed to 30 degrees (ICP),analgesia and sedation

54
Q

goal of txt of major head trauma (ED)

A

prevent secondary injury to the brain, primarily through avoidance of hypotension and hypoxia

55
Q

general txt of major head trauma (ED) (4)

A
  1. initial airway management and resuscitation
  2. ID injuries amenable to surgical therapy (EDH, SDH, traumatic hydrocephalus)
  3. Elevate head of bed
  4. Hyperventilation? (maybe)
56
Q

when do we hyperventilate a pt for major head trauma ? why do we have to be careful with this?

A

ONLY to reduce ICP in impending herniation and death

- Causes cerebral vasoconstriction and exacerbates brain ischemia

57
Q

what is the most common injury in the spine? why? what about the second most common? causes of each?

A

cervical spine- inherent inflexbility (C2, C5-7)
usually from MVAs
*second is T11-L2 from falls

58
Q

primary vs secondary spinal cord injury

A

Primary injury: Mechanical forces that directly traumatize the spinal cord and vasculature
Secondary injury: Vascular and chemical processes that result from initial insult

59
Q

5 phases of spinal cord injury

A
  1. Hemorrhage into the cord and edema at injured site and surrounding region
  2. Local ischemia secondary to vasospasm and thrombosis of small arterioles wihin grey/white matter.
  3. Edema ->compromises blood flow and increases ischemia
  4. Neural membrane dysfunction
  5. Cell death from electrolyte imbalances, cell edema, formation and release of oxidative substances
60
Q

what spinal nerves control the diaphragm? (breathing) what does this mean for who you will intubate?

A

C3,4,5 “keeps the diaphragm alive”

* intubate anyone with C5 or above

61
Q

______ ________is not completely lost unless there is damage to both the spinothalamic tracts and the dorsal columns.

A

light touch

62
Q

spinal cord: two parts to the ascending tracts

one part of the descending tract

A

ascending: spinothalamic + dorsal (posterior) columns
descending: corticospinal

63
Q

ascending tracts transmit what? (spinothalamic and posterior columns)

A

spinothalamic: pain and temp

posterior columns: vibration and proprioception

64
Q

descending tract transmit what? (corticospinal)

A

descending motor pathway

65
Q

preservation of anogenital reflexes (i.e. anal wink, cremasteric reflex, no priapism) means what?

A

incomplete spinal cord level injury (

66
Q

spinal cord lesion: complete vs incomplete

A

Complete: absence of sensory and motor function below the level of injury = Worse prognosis

Incomplete: if sensory, motor, or both functions are partially present below neurologic level of injury= Potential for some recovery

67
Q

spinal shock

A

Temporary loss ordepression of spinal reflex activity that occurs below a complete or incompletespinal cord injury.
-lose all reflex activities below the area of injury, and lesions cannot be deemed truly complete until spinal shock has resolved.

68
Q

how long does spinal shock last?

A

usually days - weeks, but can be up to 6 months

69
Q

neurogenic shock

A

type of distributive shock w/ CNS or spinal cord injury

  • Loss of peripheral sympathetic innervation->extreme vasodilation secondary to loss of sympathetic arterial tone.
  • > blood pooling in distal circulation-> hypotension
70
Q

S+S of neurogenic shock

A

warm, peripherally vasodilated, and hypotensive with a relative bradycardia.

71
Q

Dx of neurogenic shock

A

Dx of EXCLUSION: Hypotension in the trauma patient can never be presumed to be caused by neurogenic shock until other possible sources of hypotension are excluded

72
Q

who will you consider surgical intervention for (spina cord injury) ? (2)

A
  1. Progressive neurologic deficits

2. Unstable spine fractures