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
where do most skull base fractures result from ? (impact to the skull where?)
from impact to the skull around its base (e.g. occiput, temporal region, frontal region – the so-called "hat band" distribution.
26
what meds may you give someone for skull base fx? (kinda weeds)
Antibiotic prophylaxis is often started in setting of CSF leak but should be discussed with a neurosurgeon (b/c possiblity of selecting resistant organisms)
27
raccoon eyes, battles sign and hemotymp are all signs of what type of fracture? what other sign may be present?
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
28
hematoma: epidural vs subdural vs subarachnoid
epidural hematoma- rapid expansion (arterial - bleeds hard and fast), lucid interval subdural - venous blood (bleeds slow), progressive consciousness decline subarachnoid- thunderclap HA, very dangerous
29
what artery is usually ruptured with epidural hematoma?
middle meningeal (blunt trauma to temperoparietal region)
30
CT w/out: epidural hematoma
Lens-shaped (or lemon-shaped), biconvex
31
how do you differentiate a epidural from subdural hematoma on CT?
Blood along the inside of the skull will not cross the sutures.
32
what can we do in the ER for an epidural hematoma ?
Medical care to decrease ICP: 1. Mannitol/hypertonic saline 2. Hyperventilation 3. Steroids/ventricular shunt 4. ICU admission
33
subdural hematomas are more common in what two patient populations?
 elderly and alcoholics (those with cerebral atrophy)
34
prognosis epidural vs subdural hematoma?
subdural worse than epidurals due to concurrent brain damage.
35
CT w/out: subdural hematoma
crescent moon shape
36
what can we do for a subdural hematoma in the ED?
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
intraparenchymal hemorrhage: S+S , PE
lethargy headache obtundation physical exam: focal motor and sensory deficits
38
intraparenchymal hemorrhage: imaging
Imaging: head CT/MRI without contrast hypodensity: look for mass effect or focal edema that may predict a herniation
39
intraparenchymal hemorrhage: txt - prevention of ICP, reversal of ICP
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
Diffuse Axonal Injury: DAI: what is it? what is the major cause?
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
typical clinical picture of DAI
comatose patient with no or minimal signs of injury on the initial CT. MR will detect the extent of injury *txt is supportive
42
major cause of atraumatic SAH
ruptured aneurysm @ Bifurcation of the circle of Willis
43
hematoma vs hemorrhage
A hematoma usually describes bleeding which has more or less clotted, whereas a hemorrhage signifies active, ongoing bleeding.
44
what size aneurysm are more likley to rupture?
>5-10 mm
45
classic symptom of SAH?
"Thunderclap" headache
46
what scoring system is used for SAH? (kinda weeds)
``` 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
Dx for SAH?
``` CT w/out Lumbar puncture (xanthochromia-yellow color- enzyme breakdown of blood releasing bilirubin, RBC count) ```
48
3 part medical mgmt of SAH?
Blood pressure Pain medications Antiemetics
49
SAH- risk of rebleeding is highest when? what meds do you give to prevent this?
Risk of rebleeding greatest in first 2-12 hours | Reduced by BP control: Labetalol or nicardipine
50
SAH- risk of vasospasm lasts how long? what do you give to prevent this?
Vasospasm 2-3 weeks post SAH | Nimodipine
51
CVA: what is it? S+S?
intracranial hemorrhage | S+S: Headache (more insidious than in SAH), n/v, dizziness, truncal, ataxia,  gaze palsies, decreased LOC. 
52
3 ways to dx CVA
history, *CT w/out, MRI
53
ED txt of CVA
Antipyretics, antiepileptic meds, BP, reverse coagulopathy | Elevate head of bed to 30 degrees (ICP), analgesia and sedation
54
goal of txt of major head trauma (ED)
prevent secondary injury to the brain, primarily through avoidance of hypotension and hypoxia
55
general txt of major head trauma (ED) (4)
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
when do we hyperventilate a pt for major head trauma ? why do we have to be careful with this?
ONLY to reduce ICP in impending herniation and death | - Causes cerebral vasoconstriction and exacerbates brain ischemia
57
what is the most common injury in the spine? why? what about the second most common? causes of each?
cervical spine- inherent inflexbility (C2, C5-7) usually from MVAs *second is T11-L2 from falls
58
primary vs secondary spinal cord injury
Primary injury: Mechanical forces that directly traumatize the spinal cord and vasculature Secondary injury: Vascular and chemical processes that result from initial insult
59
5 phases of spinal cord injury
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
what spinal nerves control the diaphragm? (breathing) what does this mean for who you will intubate?
C3,4,5 “keeps the diaphragm alive” | * intubate anyone with C5 or above
61
______ ________is not completely lost unless there is damage to both the spinothalamic tracts and the dorsal columns.
 light touch
62
spinal cord: two parts to the ascending tracts | one part of the descending tract
ascending: spinothalamic + dorsal (posterior) columns descending: corticospinal
63
ascending tracts transmit what? (spinothalamic and posterior columns)
spinothalamic: pain and temp | posterior columns: vibration and proprioception
64
descending tract transmit what? (corticospinal)
descending motor pathway
65
preservation of anogenital reflexes (i.e. anal wink, cremasteric reflex, no priapism) means what?
incomplete spinal cord level injury (
66
spinal cord lesion: complete vs incomplete
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
spinal shock
Temporary loss or depression of spinal reflex activity that occurs below a complete or incomplete spinal cord injury.  -lose all reflex activities below the area of injury, and lesions cannot be deemed truly complete until spinal shock has resolved.
68
how long does spinal shock last?
usually days - weeks, but can be up to 6 months
69
neurogenic shock
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
S+S of neurogenic shock
warm, peripherally vasodilated, and hypotensive with a relative bradycardia. 
71
Dx of neurogenic shock
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
who will you consider surgical intervention for (spina cord injury) ? (2)
1. Progressive neurologic deficits | 2. Unstable spine fractures