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Dr. Cheng neuro review Qs > neuro critical care > Flashcards

neuro critical care Flashcards

1
Q

What are three types of cerebral edema?

A
  1. vasogenic 2. cytotoxic 3. interstitial
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2
Q

What is interstitial edema associated with?

A

seen in acute obstructive hydrocephalus; as the CSF is forced by hydrostatic pressure to move from the ventricular spaces to the interstitium of the parenchyma

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3
Q

What is vasogenic edema?

A

an extracellular accumulation of fluid that is usually associated with a disruption in the BBB

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4
Q

What is cytotoxic edema?

A

intracellular accumulation of fluid due to hypoxic-ischemic insult leading to depletion of ATP and subsequent failure of the Na+K+ ATPase, causing an alteration in the selective permeability of cellular membranes. This leads to intracellular edema

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5
Q

What is the goal target for therapeutic hypothermia and how long do you maintain it for?

A

32 to 34 degrees Celsius and for 12 to 24 hours

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6
Q

The evidence supports hypothermic therapy in cardiac arrest associated with what particular arrhythmias?

A

cardiac arrest from VF; limited evidence in the setting of non-VF rhythms, including PEA or asystole

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7
Q

What are potential complications for hypothermic therapy? (4)

A
  1. coagulopathy 2. arrhythmias 3. electrolyte abnormalities 4. risk of infections
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8
Q

Uncal herniation presents with what 3 findings caused by compression of what 3 structures?

A
  1. compresses parasympathetic fibers that mediate miosis resulting mydriasis (fixed dilated pupil localizes the side of the uncal herniation) 2. if uncus compresses ipsilateral cerebral peduncle - contralateral hemiparesis 3. compression of PCA - infarction
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9
Q

What is the normal ICP range?

A

5-15 mmHg

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10
Q

general txt of ICP (6)? specific txt of ICP (9)?

A

General txt: 1. head of the bed at 30 degrees 2. maintain normothermia 3. glucose control 4. BP control 5. adequate nutrition 6. prevention of complications specific txt: 1. hyperventilation 2. osmotic agents (ie mannitol) 3. hypertonic solutions 4. corticosteroids in select cases (ie brain tumor) 5. CSF drainage 6. surgical decompression in select cases 7. barbiturate coma 8. pharmacologic ppx 9. hypothermia

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11
Q

How long does the effect of hyperventilation on ICP last for?

A

10 - 20 hours and subsequently a rebound phase with increased ICP may be seen

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12
Q

How does hyperventilation work to decrease ICP?

A

hyperventilation –> reduction in partial pressure of CO2 –> hypocapnia –> cerebral vasoconstriction –> decrease cerebral blood vol –> reduction in ICP

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13
Q

What is the target pCO2 in hyperventilation?

A

a reduction of pCO2 by 10 mmHg and or to a target of 30mm Hg

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14
Q

How does mannitol work? What is the dose and the target serum osmolarity?

A

-raises the serum osmolarity producing an osmotic gradient that drives water from the interstitium to the intravascular compartment -boluses of 0.5 to 1.5g/kg -target level no higher than 320 mOsm/L

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15
Q

Prolonged infusion of sodium nitroprusside can lead to what kind of toxicity? What is the treatment?

A

-cyanide and thiocynate toxicity (metabolites toxicity) txt: -sodium thiosulfate transform cyanide into thiocynate -although thiocynate is still toxic, it can be excreted by the kidneys -thus can also be treated with dialysis

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16
Q

What is the appearance of SDH on head CT?

A

crescent or concave shape

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17
Q

What causes SDH?

A

trauma that produces an acceleration force that causing tearing/rupture of the surface bridging veins

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18
Q

When is surgical evacuation indicated for SDH?

A

if the SDH is more than 1 cm or if there is midline shift

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19
Q

What is the appearance of epidural hematoma on head CT?

A

lenticular shaped or biconvex

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20
Q

What causes epidural hematomas?

A

rupture of the middle meningeal artery (usually associated with a skull fracture)

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21
Q

Describe Lundberg A, B waves, anc C waves in ICP monitoring. What is the significance of these waves, duration, and amplitude?

A
  • Lundberg A waves are pathological; associated with decrease intracranial compliance, intracranial hypertension, with risk of ischemia. Also known as plateau waves. Duration 5 to 20 minutes. Amplitude ranges from 50 mmHg to 100 mmHg.
  • B waves are normal; duration 1 -2 minutes; amplitude 20 to 50 mmHg
  • C waves are normal; duration 4 to 5 minutes; amplitude < 20 mmHg
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22
Q

What is the initial management of SAH? (5)

A
  1. if cannot protect airway - intubate 2. avoid hypertension/control BP (one aneurysm is secured then you can be more liberal with BP) 3. aggressive isotonic fluids 4. ppx AED 5. mild sedation/optimize pain control
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23
Q

What is the CCB of choice that has been shown to improve outcomes from vasospasm? What is the dose and duration of therapy?

A

Nimodipine; 60mg Q 4hours for 21 days

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24
Q

What is triple H therapy?

A

hypervolemia, hypertension, hemodilution Recommended for treatment of vasospasm

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25
Q

What are the risks of triple H therapy?

A
  1. rebleeding from unsecured aneurysm 2. pulmonary edema 3. congestive heart failure 4. cerebral edema
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26
Q

What is apneusis and where does it localize to?

A

respiratory pause at full inspiration and occurs from bilateral pontine lesions

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27
Q

What is Cheyne-Stoke respiration? Where does it localize to?

A

hyperpnea alternates with apnea and depth of breathing increases and decreases gradually -poorly localizing; can be seen with forebrain impairment in the setting of intact brainstem respiratory reflexes, but also present in severe cardiopulmonary disease

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28
Q

What is ataxic breathing and where does it localize to?

A

irregular respiratory pattern (gasping respiration) seen with lesion damaging the respiratory rhythm generator in the upper medulla

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29
Q
A
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30
Q

What is the treating of ICH in the setting of Warfarin with an INR of 6?

A
  1. withhold warfarin
  2. give vitamin K dependent factors (FFP or prothrombin complex concentrates)
  3. IV Vitamin K
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31
Q

What is the treatment of ICH for pt who is on a NOAC?

A

some patients are on newer oral anticoagulants including factor Xa inhibitors and direct thrombin inhibitor.

  • Dabigatran is a direct thrombin inhibitor with reversal agent idarucizumab
  • no available reversal agents for Rivaroxaban and Apixaban
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32
Q

What are risk factors for critical illness polyneuropathy and myopathy?

A
  1. sepsis
  2. SIRS
  3. use of neuromuscular blocking agents
  4. use of steroids
  5. poor nutrition
  6. abnormal glucose levels
  7. low albumin levels
33
Q

What are the EMG findings for critical illness polyneuropathy? Histopathology findings?

A
  • nerve conduction studies with reduction in CMAPs and SNAPs
  • normal or mildly reduced conduction velocities

Histo: axonal degeneration of motor and sensory fibers and denervation atrophy

34
Q

What are the EMG findings in critical illness myopathy? Histology findings?

A
  • SNAP > 80% of the lower limit of normal
  • low amp CMAPs

fibrillation potentials and positive sharp waves

Histo: loss of thick myosin filaments and varying degrees of necrosis

35
Q

Requirements for the diagosis of brain death (6)

A
  1. castrophic CNS condition leading to irreversible damage
  2. absent brainstem reflexes
  3. positive apnea test
  4. absence of intoxication, neuromuscular blockade, pharmacologic sedation, or a medical condition that may obscure the clinical pic
  5. normal or near normal core body temp ( >36 degrees C)
  6. SBP > 90, or MAP > 60
36
Q

How is apnea test performed?

A
  1. preoxygenate for 10 miniunutes for FiO2 100%
  2. baseline abg and pCO2 btwn 35 - 40
  3. d/c ventilator but maintain O2 at 6L/min; observe for 10 minutes, look for chest or abdominal rise
  4. check abg if pCO2 has risen to 60 or greater and there were no inspiratory attempt, it is consistent with brain death
37
Q

If there are doubts regarding the brain death testing, what other tests can be performed?

A
  1. EEG showing electrocerebral silence for at least 30 mins
  2. transcranial doppler with no flow signals or abnormal flow signals
  3. nuclear medicine showing no isotope uptake in the brain parenchyma or no intracranial flow
  4. angiography demonstrating no flow in the circle of Willis
38
Q

Where is the lesion in decorticate rigidity?

A

-decorticate: lesion above the red nucleus –> resulting in disinhibition of the red nuclei with facilitation of the rubrospinal tracts (which enhances flexor tone in the upper extremities)

39
Q

where is the lesion in decerebrate posturing?

A
  • lesion in the brainstem at or below the superior colliculi and the red nuclei, but above the vestibular nuclei
  • since the vestibular n are intact, enhances extensor tone without influence from the red nuclei.
40
Q

What is the Monroe-Kellie Doctrine state?

What is the relationship between ICV and ICP?

A

the volume in the intracranial cavity is constant, and an increase in the volume of a ny of the components of this cavity will produce a displacement of other components

-intially system is compliant with only small increases in ICP as volume increases. This compliance is limited, and as volume increases, pressure will rise exponentially

41
Q

What is normal CPP? What is the equation for CPP?

A

Cerebral perfusion pressure > 70 mmHg is normal; CPP = MAP - ICP

42
Q

Factors that affect cerebral blood flow?

A
  1. MAP
  2. ICP
  3. vascular autoregulation
  4. pC02 (increases in pCO2 causes vasodilation)
  5. lower hematocrit –> increase cerebral blood flow
43
Q

What is the rate of correction of hyponatremia that is safe to reduce risk of central pontine myelinolysis?

A

12 mEq/L per day or

0.5 mEq/L per hour

44
Q

What are exam findings that are predictive of poor outcomes after cardiac arrest? (3)

A
  1. no pupillary response at 24 to 72 hours
  2. no corneal reflexes at 72 hours
  3. no eye movements at 72 hours
45
Q

What ancillary tests are predictive of poor outcomes after cardiac arrest?

A
  1. EEG showing burst suppression or generalized suppression
  2. somatosenosry-evoked potentials with median nerve stim showing bilaterally absent N20 responses at day 1 to 3
  3. neuron-specific enolase elevation
46
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48
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49
Q

Action of muscle:

deltoid

A

shoulder abduction

50
Q

Action of muscle:

biceps

A

elbow flexion, palm up

51
Q

Action of muscle:

triceps

A

elbow extension

52
Q

Action of muscle:

extensor carpi radialis

A

wrist extension

53
Q

Action of muscle:

extensor digitorum

A

Finger extension

54
Q

Action of muscle:

dorsal interossei

A

finger abduction

55
Q

Action of muscle:

abductor pollicis brevis

A

thumb abduction

56
Q

Action of muscle:

Ilipsoas

A

hip flexion

57
Q

Action of muscle:

quadriceps

A

knee extension

58
Q

Action of muscle:

hamstrings

A

knee flexion

59
Q
A
60
Q

Action of muscle:

tibialis anterior

A

ankle dorsiflexion

61
Q

Action of muscle:

gastrocnemius

A

ankle plantarflexion

62
Q

Action of muscle:

extensor hallucis longus

A

Great toe extension

63
Q

Action of muscle:

rhomboids

when to test?

A

retraction of the scapula; test by pressing the palm backwards from the small of the back;

suspect lesion of C5

64
Q

Action of muscle:

serratus anterior

when to test?

A

scapular fixation (look for scapular winging);

suspect lesion of long thoracic nerve

65
Q

Action of muscle:

infraspinatus

when to test?

A

shoulder external rotation;

suspect lesion of C5, C6, trunk, suprascapular nerve

66
Q

muscle action:

brachioradialis

when to test?

A

elbow flexion with thumb up;

suspect lesion of radial nerve

67
Q

Muscle action:

pronator teres

when to test?

A

forearm pronation; test C6, C7

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Dr. Cheng neuro review Qs (9 decks)

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