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CHEST SEEK Library > Neurologic Disorders > Flashcards

Neurologic Disorders Flashcards

1
Q

stroke syndromes;

  • motor/sensory = upper body, facial droop
  • visual = eyes deviate TOWARDS lesion
  • other = receptive or expressive aphasia
A

MCA (anterior circulation)

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2
Q

stroke syndromes;

  • motor/sensory = lower body
  • visual = n/a
  • other = urinary incontinence, personality change
A

ACA (anterior circulation)

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3
Q

stroke syndromes;

  • motor/sensory = n/a
  • visual = CONTRAlateral homonymous hemianopsia
  • other = visual hallucinations
A

PCA (posterior circulation)

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4
Q

stroke syndromes;

  • motor/sensory = contralateral hemiplegia
  • visual = IPSilateral CN 3 palsy (“down and out”), ipsilateral Horner’s syndrome
  • other = mild contralateral gait disturbance
A

Weber’s (posterior circulation)

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5
Q

stroke syndromes;

  • motor/sensory = contralateral hemiplegia
  • visual = IPSilateral CN 3 palsy (“down and out”), ipsilateral Horner’s syndrome
  • other = severe contralateral gait disturbance
A

Benedikt’s (posterior circulation)

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6
Q

stroke syndromes;

  • motor/sensory = IPSilateral FACIAL sensory loss (CN 5), CONTRAlateral BODY sensory loss
  • visual = ipsilateral Horner’s syndrome
  • other = vertigo, ataxia, dysarthria, dysphagia
A

PICA (Wallenberg’s) (posterior circulation)

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7
Q

in a patient w/ a previous stroke, what are the 2 most likely processes if there’s an abrupt worsening of symptoms?

A
  • new stroke
  • seizure from the stroke scar
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8
Q

in acute ischemic stroke, the eyes tend to move in which direction?

A

TOWARD the stroke lesion

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9
Q

in seizures, the eyes tend to move in which direction?

A

AWAY from the focus of the seizure

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10
Q

which neurological condition could lead to the eyes deviating TOWARDS the seizure focus?

A

Todd’s paralysis

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11
Q

what is the dosing for tPA for acute ischemic stroke?

A

0.9 mg/kg (up to a total dose of 90 mg) IV; divided into 10% bolus followed by 90% of the remaining dose infused over 60 minutes

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12
Q

what are the 2 important points to d/w a patient about tPA for stroke?

A
  1. doesn’t change mortality, but increases likelihood of recovery to independence
  2. hemorrhage risk is slightly higher in patients who get tPA (< 7%) than those who don’t
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13
Q

contraindications for tPA in acute ischemic stroke

A
  • recent major surgery
  • AC w/ INR > 1.7
  • thrombocytopenia
  • recent stroke or head trauma w/i 3 months
  • GIB w/i 3 weeks
  • uncontrollable HTN before administration
  • h/o intracranial hemorrhage
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14
Q

contraindications for tPA in acute ischemic stroke

A
  • recent major surgery
  • AC w/ INR > 1.7
  • thrombocytopenia
  • recent stroke or head trauma w/i 3 months
  • GIB w/i 3 weeks
  • uncontrollable HTN before administration
  • h/o intracranial hemorrhage
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15
Q

how to calculate NIH stroke scale

A
  • level of consciousness
  • ask month and age
  • can blink eyes and squeeze hands
  • horizontal EOM
  • visual fields
  • facial palsy
  • UE motor drift
  • LE motor drift
  • limb ataxia
  • sensation
  • language/aphasia
  • dysarthria
  • extinction/inattention
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16
Q

NIH stroke scale score range

A

0 to 42

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17
Q

time window for tPA administration for acute ischemic stroke

A

w/i 3-4.5 hours from LSW

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18
Q

SAH diagnosis

A
  • acute-onset severe headache
  • neck stiffness
  • noncontrast CT scan
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19
Q

when is LP done to diagnose SAH?

A

if CTH is negative but high clinical suspicion based on patient history

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20
Q

most important early consideration in a patient diagnosed w/ SAH

A

identifying a vascular abnormality that could rebleed

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21
Q

in a patient w/ SAH and a cerebral angiogram negative for aneurysm, what other imaging study should be performed?

A

MRI of the spine to check for spinal AVMs

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22
Q

spinal AVMs can lead to neurological disability in what 2 ways?

A
  • bleeding causing damage to the spinal cord or brainstem
  • venous HTN from arterialization of the spinal draining veins which leads to spinal infarction
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23
Q

what intervention has the best evidence of improving outcome in severe traumatic brain injury (TBI)?

A

prevention of hypotension

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24
Q

what are some triggers of enzymatic dysfunction of urea cycle metabolism leading to hyperammonemia?

A
  • infection
  • severe exercise
  • seizures
  • dietary protein loading
  • TPN
  • drugs (abx, valproate, anti-TB meds)
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25
Q

what is the most common inborn error of metabolism affecting the urea cycle?

A

ornithine transcarbamylase deficiency

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26
Q
  • evidence of cirrhosis at an early age
  • Kayser-Fleisher rings
  • disrupted copper metabolism leading to cirrhosis and neurologic injury
A

Wilson’s disease

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27
Q

what AED can cause decompensation in patients w/ urea cycle enzymatic dysfunction and CI?

A

valproate

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28
Q

medication and dose that is MOST successful at both stopping convulsions in the first 20 minutes and preventing the recurrence of status epilepticus?

A

lorazepam 0.1 mg/kg iv

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29
Q

what paralytic is contraindicated in patients w/ chronic hemiplegia or chronically bed-bound patients and why?

A
  • succinylcholine
  • potential for massive hyperkalemia and arrhythmias
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30
Q

depolarizing paralytic agents

A

succinylcholine

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31
Q
  • fast-acting
  • nondepolarizing paralytic
  • relatively long half-life; approximately 45 minutes
A

rocuronium

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32
Q

what is a common feature in the first 72 hours in patients w/ ICH, and is more frequent in patients w/ ICH who have intraventricular extension?

A

fever

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33
Q

what is the cause of fever in approximately half of the patients in the neurological ICU?

A

noninfectious

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34
Q

what lab test might assist in the diagnosis of infection and deescalation or discontinuation of abx w/ suspected infection, especially PNA?

A

procalcitonin, however, brain injury is a/w elevated procalcitonin levels which may complicate its application

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35
Q

autoimmune paraneoplastic syndrome often lead to what?

A
  • severe encephalopathy
  • seizures
  • eventually death
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36
Q

the most common precipitating illness for autoimmune paraneoplastic syndrome is

A

small cell lung cancer (SCLC)

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37
Q

benign ovarian and testicular teratomas are a/w what syndrome?

A

anti-NMDA receptor encephalitis syndrome

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38
Q

opsoclonus-myoclonus is most commonly a/w

A

SCLC in older patients

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39
Q

retinal blindness is typically a/w

A

breast cancer

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40
Q

Lambert-Eaton myasthenic syndrome (LEMS) is often a/w

A

SCLC but can be a/w breast cancer and lymphosarcoma

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41
Q

anti-NMDA receptor encephalitis syndrome is a unique paraneoplastic syndrome for what reasons?

A
  • atypical presentation
  • initially manifest w/ paranoia and psychosis followed by progressive encephalopathy and seizures until 1 of 3 things happens:
  • patient is treated
  • syndrome resolves spontaneously
  • patient succumbs
  • most commonly seen in young adults
  • majority of patients are found to have nonmalignant disease
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42
Q

treatment for all paraneoplastic syndromes

A
  • plasmapheresis or IVIG
  • followed by suppression of immune response w/ immunomodulatory medications
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43
Q

what is the most common neurological syndrome found in the critical care setting?

A

delirium

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44
Q

delirium, by definition, is what type of encephalopathy?

A
  • not a/w an identifiable cause, and
  • is a diagnosis of exclusion
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45
Q

what are patient-inherent factors that are significant risk factors for delirium?

A
  • age
  • dementia
  • previous episodes of delirium
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46
Q

what are extrinsic risk factors for delirium?

A
  • lack of sleep-wake cycle regulation
  • medications (including γ-aminobutyric acid agonists such as benzodiazepines)
  • immobility
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47
Q

delirium is defined as

A
  • confusion
  • waxing and waning course
  • periods of agitation or withdrawal
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48
Q

clinical trials and quality initiatives have attempted to address preventing delirium in susceptible patients w/ what interventions?

A
  • early mobility
  • sleep hygiene
  • activities
  • limiting benzodiazepines
  • limiting sleep-disrupting interventions
  • are only marginally successful
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49
Q

what pharmacological interventions have been shown to improve patients w/ delirium?

A

none

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50
Q

treatment for delirium w/ agitation

A

behavior control

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51
Q

treatment for delirium w/ withdrawal

A

??? (few interventions tested)

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52
Q

what does the term “completed stroke” mean?

A
  • old term that shouldn’t really be used anymore
  • usually signifies a focal neurological disability that came on abruptly and has become stabilized; 18-24 hours if the lesion is in the carotid system, and up to 72 hours if in vertebral-basilar system
  • others use the term to mean that all the deficit that is to occur has already accrued
  • others have used the term to imply that all the deficit possible in a given vascular territory is already present
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53
Q

based on the DAWN and DIFUSE-3 trials, if a patient has a LVO in the IC or MCA, and little evidence of a “completed stroke,” patients outside the 3 and 4.5 hour windows for tPa should be evaluated for what?

A

mechanical thrombectomy

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54
Q

how are stroke patients evaluated for thrombectomy?

A

proprietary software (RAPID) that calculates the percentage of the entire affected vessel occlusion field that is involved BUT not yet infarcted (brain at risk)

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55
Q

in both the DAWN and DIFUSE-3 trials, both MR and CT angiography were accepted, and required LVO for enrollment; patients need to have what on CT perfusion scan or MR diffusion scan before thrombectomy?

A

significant mismatch between occluded vessel territory and brain infarction

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56
Q

the INTERACT 2 trial found what regarding patients w/ ICH w/ ventricular extension?

A

target SBP < 140 mm Hg was a/w lower rate of hematoma expansion and modestly improved neurologic outcomes, but no improvement in the primary outcome of combined mortality and major disability

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57
Q

the ATACH 2 trial demonstrated what regarding patients w/ ICH w/ ventricular extension?

A

no improvement in neurologic outcome w/ more aggressive treatment of SBP < 120 mm Hg, but a/w 2x worsening renal function

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58
Q

what did the PATCH trial demonstrate regarding patient on an antiplatelet medication that p/w supratentorial ICH?

A
  • platelet transfusion did not improve neurological outcomes at 3 months
  • higher odds of death or dependency in platelet transfusion group
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59
Q

ICH w/ intraventricular blood is a/w a high mortality rate and severe disability d/t what mechanisms?

A
  • excitatory neurotoxicity
  • acute hydrocephalus
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60
Q

in the CLEAR III trial, intraventricular alteplase or saline administered through a previously inserted EVD in patients w/ ICH and ventricular blood w/ 3rd or 4th ventricle obstruction showed what?

A

no improvement in survival

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61
Q

autoimmune syndrome that attacks the myelin covering the neurons of the peripheral nervous system

A

Guillain-Barré syndrome (GBS)

62
Q

Guillain-Barré syndrome (GBS) is often preceded by what?

A
  • prodromal viral infection, or
  • prodromal Campylobacter infection
63
Q

what are the 2 variants of Guillain-Barré syndrome (GBS)?

A
  • AXONAL variant that manifests w/ a similar progression as a typical demyelinating disease
  • Miller Fisher variant is a/w early CRANIAL nerve dysfunction and respiratory failure
64
Q

which variant of Guillain-Barré syndrome (GBS) is more amenable to treatment?

A

the demyelinating syndrome

65
Q

how does the axonal variant w/ demyelinating disease typically present?

A
  • ascending paralysis
  • sensory loss
  • affects the most distal nerve territories first then progresses more proximally
66
Q

in the worst cases, Guillain-Barré syndrome (GBS) can lead to

A

complete paralysis, including all of the cranial nerves

67
Q

what are the typical treatments for Guillain-Barré syndrome (GBS)?

A
  • IVIG
  • plasmapheresis
68
Q

what happens when you treat Guillain-Barré syndrome (GBS)?

A

typically stops progression of damage, but recovery is limited by the speed at which nerves can remyelinate or grow depending on the mechanism

69
Q

in the axonal variant of Guillain-Barré syndrome (GBS), how long can recovery take?

A

can be as long as 2-4 years; the time it takes to regrow peripheral nerves

70
Q

mortality in Guillain-Barré syndrome (GBS) is almost entirely d/t medical complications a/w severe paralysis; what is one complication that is directly related to the disease?

A

autonomic insufficiency

71
Q

in severe cases of Guillain-Barré syndrome (GBS), the autonomic nerves can be denervated (particularly but not exclusively in patients w/ the axonal variant); this manifests how clinically?

A
  • hypotension
  • bradycardia
  • hypothermia
  • constipation
72
Q

in Guillain-Barré syndrome (GBS), the presence of dysautonomia has what effect on mortality?

A

3x motality

73
Q

what are the most likely causes of death in patients w/ Guillain-Barré syndrome (GBS)?

A
  • arrhythmias
  • profound hypotension
  • infections
74
Q

what treatments may be used for hypotension d/t dysautonomia from Guillain-Barré syndrome (GBS)?

A
  • mineralocorticoid = fludrocortisone
  • α-agonist = midodrine
75
Q

if nerve dysfunction from Guillain-Barré syndrome (GBS) is severe enough to functionally denervate the heart, what medication will not help w/ bradycardia?

76
Q

some patients w/ Guillain-Barré syndrome (GBS) develop a forme fruste of autonomic denervation that leads to what?

A

wild shifts in BP and HR as autonomic nerves intermittently respond to stimuli

77
Q

in patients w/ aneurysmal SAH and AMS most likely d/t hyponatremia, what is the next best step?

A

hypertonic saline

78
Q

in patients w/ hyponatremia in the period of delayed cerebral ischemia (DCI or vasospasm), even in patients thought to have SIADH, what should be avoided and why?

A
  • fluid restriction
  • worsens outcomes
79
Q

should albumin infusion be given in patients w/ delayed cerebral ischemia (DCI or vasospasm)?

A

no, no clear evidence of benefit

80
Q

patients w/ aneurysmal SAH classically p/w

A
  • headache
  • LOC
  • stroke symptoms
81
Q

what 2 grading systems are used to stratify patients w/ SAH?

A
  • Hunt/Hess grade
  • modified Fisher scale
82
Q

the Hunt/Hess grades predicts what?

A

outcome after SAH

83
Q

the modified Fisher scale predicts what and how?

A

uses the amount of hemorrhage and the presence of intraventricular blood to predict which patients will develop DCI (vasospasm)

84
Q

management of SAH after securing the aneurysm

A

largely reactive

85
Q

what is the ddx of AMS in a patient w/ SAH after securing the aneurysm?

A
  • rebleeding from the aneurysm (less likely after successful coiling)
  • hydrocephalus
  • seizures
  • fever
  • meningitis (for patients w/ an EVD or who have surgical clipping)
  • hyponatremia
  • DCI (vasospasm)
86
Q

DCI (vasospasm) after SAH can lead to stroke or long-term cognitive deficits and usually occurs w/i what timeline?

A

5 to 14 days after hemorrhage

87
Q

in a patient w/ SAH, does successful vasodilation of arteries in spasm improve outcomes?

A

no, suggesting spasm isn’t the only mechanism of damage

88
Q

what is known to lead to stroke in the setting of DCI (vasospasm)?

A

volume depletion

89
Q

what is the only therapy that treats hyponatremia from both cerebral salt wasting and SIADH in the setting of post-SAH?

A

hypertonic saline solutions

90
Q

what is the most severe consequence of cerebral edema after brain injury?

A

brain herniation

91
Q

in large ischemic strokes that occupy > 50% of the territory of a hemisphere, herniation in the first 48-72 hours is likely d/t what?

A

cerebral edema in the damaged brain

92
Q

why does cerebral edema lead to herniation syndromes?

A

the calvarium is a fixed structure that limits the amount of volume that can be accomodated (Monro-Kellie principle)

93
Q

there is only room in the calvarium for what compartments?

A
  • brain
  • blood
  • CSF
94
Q

treatments to alleviate herniation syndromes have the goal of decreasing ≥ 1 compartments; what 2 treatments are used to decrease blood flow to the brain?

A
  • induced hyperventilation –> alkalosis –> alkalization of CSF –> smooth muscle contraction and vasoconstriction by neurovascular unit modulation (brain control of blood vessels)
  • systemic cooling –> decreases metabolic demand of the brain –> decreases blood flow (through the neurovascular unit)
95
Q

can hyperventilation lead to brain ischemia and how?

A
  • yes, it’s a potential side effect
  • blood flow by this mechanism is not paired to decreased metabolism
96
Q

when is ischemia d/t hyperventilation most commonly seen?

A

when PCO2 levels are < 20 mm Hg

97
Q

can systemic cooling lead to brain ischemia?

A

no, because metabolic demand drives blood flow

98
Q

how do mannitol and hypertonic saline act to reduce cerebral edema?

A

increases tonicity of blood –> drives water from the lower tonic environment of the brain to the blood –> excess volume can then be transported out of the brain

99
Q

can brain water removal w/ mannitol or hypertonic saline cause ischemia?

A

no, does not impair O2 delivery

100
Q

what is the only treatment used acutely to decrease CSF in a patient w/ cerebral edema?

A

EVD or lumbar drain

101
Q

can ischemia occur in a patient w/ cerebral edema that has an EVD or lumbar drain?

A

no, they do not impede blood flow or substrate delivery

102
Q

what is the pathophysiology of SDH?

A

rupture of bridging veins that traverse the subdural space as they drain the cerebral and/or cerebellar cortex to veins in the skull; as people get older and their brains atrophy, the length of the bridging veins increases and are more prone to damage

103
Q

what is the most common cause of SDH?

A

mild trauma w/ or w/o coagulopathy

104
Q

can spontaneous SDH occur in patients w/ coagulopathies?

A

yes, w/ warfarin being the most common

105
Q

because SDH is a venous bleeding syndrome, the collection of blood can occur over what time period?

106
Q

symptoms from SDH occur because of 3 separate processes; what are they?

A
  • blood in the subdural space can irritate the brain leading to cognitive decline and delirium
  • as the blood collection occupies more space, it compresses adjacent brain regions leading to focal neurologic symptoms
  • SDH can lead to seizures
107
Q

the presentation of subdural blood on CT scan changes over time; what are these changes?

A
  • initially, bright (because of [Ca++] in blood collection)
  • transition period, from bright to dark, isodense w/ brain parenchyma
  • over time, hypodense as blood degrades (same density as CSF)
108
Q

treatment of small SDH w/o significant mass effect

A

conservatively w/o surgery

109
Q

treatment of larger SDH and more symptomatic hemorrhages

A

surgery

  • if fresh clot that forms a solid rind = open neurosurgery
  • if chronic SDH which liquifies = burr hole and catheter-based drainage
110
Q

treatment for symptomatic SDH w/ large mass effect

111
Q

patients w/ severe traumatic brain injury (defined as GCS of ≤ 8) should receive what ppx?

A

phenytoin x 7 days posttrauma to reduce the incidence of early posttraumatic seizures

112
Q

what is a/w worse neurologic outcomes at 3 and 6 months and why?

A
  • prophylactic hyperventilation
  • hyperventilation-induced reduction in brain blood flow worsening cerebral ischemic injury
113
Q

in patients w/ severe TBI and elevated ICP, what intervention is a/w worse neurologic outcome at 6 months?

A

cooling to 32°C to 35°C

114
Q

the CRASH trial showed what in patients w/ severe TBI?

A
  • risk of death at 2 weeks was higher in the methylprednisolone group
  • risk of death and death or severe severe disability at 6 months was higher in the methylprednisolone group
115
Q

what are some myths regarding critically ill patients in a coma in the ICU?

A
  • patients in coma do not sense anything in
    the environment; some patients likely have
    no environmental awareness, but predicting
    which patients is not reliably possible
  • patients in a coma remember events from
    the time when they are unconscious; most
    patients w/ altered consciousness claim not
    to remember anything of their ICU stay; there
    are very few cases of patients under sedation
    or anesthesia who are awake and aware of
    what is going on around them, but this is rare
    and relegated to patients w/o brain injury
  • patients in a coma proceed to brain death;
    not all patients in a coma proceed to brain
    death
116
Q

what is the most common cause of poor responsiveness in the ICU?

A

oversedation

117
Q

what 2 syndromes are occasionally confused w/ coma?

A
  • locked-in state
  • catatonia
118
Q

locked-in state is characterized as

A
  • patient is fully awake and aware
  • cannot respond to environment d/t dysfunction of ventral brainstem (not the reticular activating system but the motor output of the brainstem)
119
Q

typically, how can patients w/ locked-in state show that they can follow commands?

A

eye movement (often upward gaze)

120
Q

catatonia is characterized as

A
  • patients are unable to respond to the environment
  • might have abnormal postures
  • oscillates w/ other behaviors
121
Q

what is one of the most common methods for assessing delirium in the ICU in conscious patients?

A

Confusion Assessment Method ICU (CAM-ICU) test

122
Q

the CAM-ICU test cannot be performed on which patients?

A

unconscious patients

123
Q

the MIND-USA trial showed what regarding
all patients w/ delirium?

A

neither haloperidol nor ziprasidone was
better than placebo for the treatment of
delirium in the ICU

124
Q

multiple studies of dexmedetomidine vs benzodiazepines have suggested what for patients in the ICU?

A
  • possibility of briefer duration of MV
  • no improvement in cognitive impairment or survival
125
Q

studies of daily awakening trials have suggested what for patients in the ICU?

A

improve duration of MV and survival

126
Q

do daily awakening trials lead to increased incidence of airway injury or unplanned extubation?

127
Q

if no CIs, what is the time cutoff for tPa in a patient that p/w ischemic stroke?

A
  • 4.5 hours
  • 3 hours if > 80 yoa
128
Q

intracytoplasmic protein that can abnormally aggregate in various cells in the CNS

A

α-synuclein

129
Q

clinical entity resulting from accumulation of α-synuclein in the substantia nigra and striatonigral tract

A

Parkinson’s disease

130
Q

clinical entity resulting from diffuse accumulation of α-synuclein at onset

A

dementia w/ Lewy bodies

131
Q

what clinical entities fall w/i the spectrum of multiple system atrophy (MSA) as a result of deposition of α-synuclein?

A
  • olivopontocerebellar atrophy
  • striatonigral degeneration
  • Shy-Drager syndrome
132
Q

the clinical spectrum of disease caused by accumulation of α-synuclein includes

A
  • hypokinetic movement d/o’s
  • dementia
  • dysautonomia
133
Q
  • classically reported in elderly patients
  • elevated BP
  • hyperthermia
A

apathetic thyrotoxicosis

134
Q
  • chromaffin cells of the sympathetic nervous system in the urinary bladder
  • micturition syncope from release of catecholamines by bladder contraction
A

pheochromocytoma in the urinary bladder

135
Q

in patients w/ pheochromocytoma, what are the 2 ways that can result in loss of vasoconstriction leading to postural or orthostatic hypotension?

A
  • desensitization to norepinephrine
  • loss of blood vessel norepinephrine receptors
136
Q

how does hyperthermia occur in patients w/ pheochromocytoma?

A
  • peripheral vasoconstriction
  • excess production of IL-1
137
Q

recent studies have demonstrated that bedside US assessment of the diaphragm in patients undergoing MV can provide what valuable pronostic information?

A

patients w/ either thickening or thinning of the diaphragm over the first week of MV have longer weaning times, longer ICU stays, and more complications of MV

138
Q

in one study of serial measurements of diaphragm thickness over the first week of MV, which patients had significantly longer weaning periods, longer ICU stays, and more complications of MV, including need for tracheostomy?

A

patients w/ either a 10% increase OR decrease in diaphragm thickness

139
Q

thinning of the diaphragm in a MV patient suggests what?

A

marked reduction in diaphragm activation (signaled by atrophy and thinning)

140
Q

thickening of the diaphragm in a MV patient suggests what?

A

excessive loading of the diaphragm (d/t inadequate ventilatory support or dyssynchrony w/ the ventilator and signaled by diaphragm injury, edema, and thickening)

141
Q

what are the mechanisms proposed for diaphragm injury?

A
  • overassistance
  • underassistance
  • eccentric contraction
  • excessive end-expiratory shortening
142
Q

what 2 entities should be carefully considered in MV patients regarding diaphragmatic injury?

A
  • critical illness-associated diaphragm weakness
  • ventilator-induced diaphragm dysfunction
143
Q

how can fat embolism syndrome occur?

A
  • long-bone fracture
  • orthopedic surgery
  • sickle cell crisis
  • cosmetic surgery that involves withdrawal or injection of fat
144
Q

fat embolism syndrome is a/w

A
  • direct endothelial injury
  • microvascular occlusion
  • systemic inflammatory changes
145
Q

clinically, fat embolism syndrome manifests w/

A
  • hypotension
  • neurological dysfunction
  • rash
146
Q

what happens in severe cases of fat embolism syndrome?

A

pulmonary vascular resistance increases, which may lead to right ventricular cardiogenic shock

147
Q

in most cases of fat embolism syndrome, what will the CTH show?

148
Q

in most cases of fat embolism syndrome, what will the CTH show?

149
Q

neurological dysfunction is commonly seen in fat embolism syndrome, but what about coma?

A

rarely a/w coma

150
Q

in a patient w/ fat embolism syndrome that has disproportionate encephalopathy w/ coma, what should be further evaluated?

A

nonconvulsive status epilepticus w/ EEG

151
Q

can hemodialysis remove bone marrow particles in a patient w/ fat embolism syndrome?

CHEST SEEK Library (11 decks)

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