Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Emergency Medicine > Neurology/NeuroSx > Flashcards

Neurology/NeuroSx Flashcards

You may prefer our related Brainscape-certified flashcards:
Royal College: Emergency Medicine flashcards
1
Q

What are 7 signs of early ischemia secondary to stroke on CT?

A
  1. Hypodensity
  2. Hyperdense MCA sign (acute thrombus in vessel)
  3. Sulcus effacement (loss of definition of sulci due to edema)
  4. Disappearing basal ganglia (loss of definition between the basal ganglia)
  5. Loss of Insular ribbon sign (loss of definition in the insular cortex)
  6. Loss of grey-white differentiation
  7. Mass effect/ Ventricular compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define wernicke’s aphasia

A

Receptive aphasia

- person not able to comprehend but can talk fluently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define Broca’s aphasia

A

Expressive aphasia

- Person is able to comprehend but cannot fluently express it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a normal opening pressure for LP?

A

5-20 cm H2O

Obese: 25 cm H20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What would the expected CSF results be in bacterial meningitis?

A
  1. WBC - elevated, mostly neutrophils also lymphocytes (more with early bacterial and viral) >1000
  2. Gram stain - 80% will see organism
  3. Glucose: decreased (normal 0.6:1 CSF to serum glucose). also low in fungal.
  4. Protein: elevated
  5. Lactate: elevated (more in bacterial, non-specific)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the ddx for elevated protein in CSF? (6)

A
  1. Bacterial meningitis
  2. Fungal meningitis (cryptococcus)
  3. Vasculitis
  4. Demyelinating dz (MS)
  5. Syphilis
  6. Neoplasms
  7. TB meningitis
  8. Guillain barre syndrome (icr protein no wbc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What results in Xanthrochromia? breakdown of what substances?

A

Is breakdown of oxyhemoglobin, bilirubin and methemoglobin in the CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are 2 other causes of xanthochromia and RBC in LP other than SAH?

A
  1. Nonaneurysmal perimesencephalic subarachnoid hemorrhage (PMSAH) 5% of SAH
  2. Other non-aneurysmal bleeds
    Generally good prognosis, observation is all thats needed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the ddx Ring enhancing lesion on CT?

A 
'DRMAGICL'
Demyelinating disease
Resolving hematoma, Radiation necrosis.
Mets
Abscess
GBM
Infarct (subacute)
Contusion
Lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DDX blown pupil

A

Herniation
PComm aneurysm
CN III palsy
AntiCholinergics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the management of malignant spinal cord compression?

A
  1. Steroids indicated → loading dose of dex in ED 10-16mg
    AHS guidelines: 4 mg q4-6h after initial bolus.
  2. Immediate radiation therapy should be considered
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Stroke syndromes: Describe clinical findings for Anterior cerebral a. stroke territory

A
  • Apraxia, Altered mentation + insight
  • Bowel, bladder incontinence
  • Contralateral paralysis + hypoesthesia → Leg&raquo_space;arm
  • Primitive reflexes (grasp, suck) - ‘frontal release signs’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Stroke syndromes: Describe clinical findings for stroke in the Middle Cerebral Artery (MCA) territory.

A
  • Agnosia
  • Aphasia (if dominant hemisphere)
  • Marked contralateral motor +sensory findings
  • Face + Arm&raquo_space; Leg
  • Numbness in same distribution as weakness
  • Ipsilateral hemianopsia
  • Gaze towards lesion → disruption of cortical lateral gaze centres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stroke syndromes: Describe clinical findings for stroke in PCA territory

A
  • PCA: Portions of parietal + occipital lobes → vision, thought processing are impaired
  • Visual agnosia (inability to recognize seen objects)
  • Alexia (inability to understand writing)
  • CN III palsy
  • Homonymous hemianopsia +/- visual neglect
  • VF defecits
  • Nystagmus
  • Diplopia
  • Vertigo, syncope, weakness, paralysis, spasticity, ataxia,
  • dysarthria, dysphagia
  • Crossed deficits: motor and sensory deficits on opposite sides
  • Nausea, vomiting
  • Can present with coma!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List 2 strokes that can cause depression of consciousness:

A
  1. Stroke in unaffected hemisphere of a patient who has had a previous contralateral stroke. so will have bilateral cerebral hemisphere involvement.
  2. Posterior circulation stroke affecting brainstem → RAS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the gaze preference in seizure and stroke?

A
  • Seizure → look away form irritative focus

- Stroke → look towards catastrophe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List 10 stroke mimics

A

Other intracranial pathology:

  • SDH / EDH → in elderly, those at most risk for a fall and stroke!
  • Intracranial lesions → tumor, abscess
  • CVT (although really is a stroke syndrome itself)
  • Atherosclerotic dz - steal like syndrome

Other acute neurologic syndromes:

  • Seizure (distinguishing feature = amnesia)
  • Todd’s paralysis (post ictal paralysis)
  • Migraine with aura (evolves over 10-45min)

Metabolic abnormalities:

  • Hypoglycemia
  • Wernicke’s encephalopathy (ataxia, confusion, opthalmoplegia)

Peripheral nerve pathology:

  • Bell’s palsy
  • Peripheral nerve palsy
  • Demyelinating disease

Vestibular apparatus pathology:

  • Labrynthitis
  • Vestibular neuritis
  • Meniere’s (vertigo, hearing loss, tinnitus)
  • Peripheral vertigo → BPPV

Vasculitis / inflammatory:

  • Giant cell arteritis (Claudication, myalgias, H/A, visual disturbance)
  • Polyarteritis nodosa
  • SLE

Drug toxicity:

  • Lithium
  • Dilantin
  • Carbamazepine

Other:

  • Air embolism in right context (diving, medical procedures)
  • HTN encephalopathy (esp in DDx for ICH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the SN and SP of CTA to detect intracranial occlusions?

A

SN: 92-100%
SP 82-100%

Should be obtained, if available, in ischemic and hemorrhagic strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathophysiologically, what 3 mechanisms can result in NMJ dysfunction?

A
  1. Blockade of nicotinic receptors → myasthenia gravis
  2. Reduced ACh released → botulism
  3. Inactivation of acetylcholinesterase by irreversible binding, resulting initially in hyperstimulation followed by paralysis → organophosphate toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name 3 conditions that are myopathies (proximal > distal muscle weakness)

A
  1. Polymyositis
  2. Dermatomyositis
  3. Rhabdomyolysis
  4. PMR
  5. Metabolic (hypokalemia)
  6. Periodic paralysis (familial/thyrotoxic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Name 3 conditions that effect the NMJ?

A
  1. Myesthenia Gravis: block nicotinic ACh receptors
  2. Botulism: inhibit pre-synaptic Ach release
  3. Eaton-Lambert (rare - paraneoplastic syndrome)
  4. Tick paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is myasthenia Gravis (MG)?

A
  • Blockade of nicotinic ACh receptors at the NMJ
  • From autoantibodies against receptor or muscle specific tyrosine kinase
  • Result: destruction of nicotinic ACh receptors → reduced total # available
    Involves: ocular, bulbar, cervical, proximal limb, and respiratory muscles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do MG patients present ?

A
  • Progressive weakness and
  • Easy fatiguability with repeated activity
  • Occular muscle weakness first sign in ~40% → ptosis, diplopia, blurred vision worse at the end of the day
  • Bulbar muscles involved → dysphagia, dysarthria
  • 17% have involvement of muscles of respiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does an ice bag placed on the face do to the ptosis in MG?

A

Improves it!!
- Cold temporarily blocks acetylcholinesterase → increases ACh at synaptic cleft → improved ocular muscle strength
o Apply ice bag to more severely affected eye for 2 min.
o Improvement in ptosis of 2mm is diagnostic
o Sn: ~80%; Sp: ~100%
- Same response as with edroponium administration → short acting ACh-esterase blocker (will soon no longer be available)
o 1mg test dose, them 3 → 3 → 5mg doses (max 10mg) with atropine at bedside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is Lambert-Eaton myasthenic syndrome?

A
  • Rare. Paraneoplastic syndrome, 50% associated with lung SCC
  • Compared to MG: weakness improves with repeated stimulation → more ACh in synapse to bind receptors
  • Sx: improving weakness with use, hyporeflexia, autonomic dysfunction (dry mouth)
  • Rx: Treat cancer +/- IVIG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is a myasthenic crisis?

A

Respiratory crisis with respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List 5 conditions that can precipitate a myasthenic crisis?

A
  1. Pregnancy
  2. Infection
  3. Surgery
  4. Aspiration
  5. Cessation of anticholinesterases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List 10 drugs that can precipitate a myasthenic crisis?

A

Sedative / Anasthetics

  • Diazepam*
  • Ketamine*
  • Lidocaine*
  • NM blocking agents*

Cardiovascular:

  • BBs*
  • CCBs*
  • Quinidine
  • Lidocaine*
  • Procainamide

Antibiotics:

  • Aminoglycosides*
  • Tetracyclines
  • Clindamycin*
  • Polymxin B*
  • Colistin
  • Fluoroquinolones*

Other:

  • Phenytoin*
  • NM blockers*
  • Corticosteroids** this is a part of their treatment.
  • Thyroid replacement
  • Anticholinergics
  • Diuretics*
  • Statins*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Outline your approach to the patient in myasthenic crisis:

A
  1. Determine need for intubation:

Negative inspiratory force (NIF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is mestinon/ pyridostigmine ?

A

A parasympathomimetic and a reversible cholinesterase inhibitor.
- allows Ach to remain in the NMJ longer and thus prevent breakdown and improve strength.

31
Q

Describe the pathophysiology of botulism:

A
  • Botulism toxin binds irreversibly to the pre-synaptic neuron, inhibits the release of ACh from presynaptic membrace
  • Acts in peripheral nerves and cranial nerves
  • Blocks voluntary AND autonomic functions
  • As new receptors are regenerated, Sx improve
32
Q

What are the Sx of botulism?

A
  • Onset Sx 6-48 after injestion of botulism toxin +/- Sx gastroenteritis
  • CN & bulbar muscle dysfunction
    o First to be affected
    o Diploplia, dysarthria, dysphagia
  • NMJ dysfunction
    o Descending, symmetric, flaccid paralysis
  • Antimuscarinic Sx:
    o Urinary retention
    o Dry skin elevated temperature
    o Mydriasis
33
Q

What is the treatment of botulism?

A
  • Adult: HBAT → heptavalent botulinum antitoxin
  • Infant: BabyBIG → IV human botulism IG
  • Long turnaround time for botulism testing, if high index of suspicion administer
34
Q

Provide a list of 3 conditions that can cause ascending flaccid paralysis:

A
  • GBS
  • Myasthenia gravis
  • Eaton-Lambert syndrome
  • Tick paralysis
  • Poliomyelitis
  • Botulism
  • Diptheritic polyneuropathy
35
Q

What electrolyte abnormalities can cause muscle weakness?

A
  • Hypokalemia
  • Hyperkalemia
  • Hypocalcemia
  • Hypercalcemia
  • Hypermagnesemia
  • Hypophosphatemia
36
Q

What syndromes can cause periodic paralysis?

A
  • Familial periodic paralysis → hypokalemic or hyperkalemic
  • Thyrotoxic periodic paralysis
  • Asian men most commonly affected
  • AD disorders
37
Q

How is familial periodic paralysis (hypokalemic type) managed.

A

The paralysis is NOT due to systemic depletion but shifting, so first give fluids to redistribute K and can give small doses of PO K.

38
Q

Outline your approach to status epilepticus

A
  1. IV access, O2, monitors, C/S, GLUCOSE
  2. Airway management
    - Avoid long acting paralytics
    - Induction / sedation with propofol
    - EEG if unable to assess for ongoing Sz
  3. Ativan 2-4mg IV [0.1mg/kg] → repeat x 2, if no success
  4. Phenytoin / PE load 20mg/kg → over 20min for Phenytoin
  5. Second line agents if above fails:
    - Phenobarbital 20mg/kg
    - VPA (valproate) 20-40mg/kg IV infusion
    - Keppra a new favorite
    - Barbiturate coma → infusion 0.5-3mg/kg/hr
    - Volatile anesthetics
  6. Look for refractory etiologies of status!!!
    - INH → pyridoxine 5g [70mg/kg] or 1g per 1mg pyridoxine ingested
    - Hypoglycemia
    - Inadequate antiepileptic dosing
    - Toxicological cause
39
Q

List 2 situations where pyridoxine can be an antidote for refractory seizures?

A
  • INH toxicity

- Neonatal status → may have pyridoxine deficiency

40
Q

Outline Management of Eclampsia

A
  • Mg 6g IV bous then 2g/h infusion x 24 hrs
  • BP reduction: Labetolol 10-20mg IV bolus q 2-3 minutes, nicardipine
  • Benzos
  • Delivery
41
Q

What are 10 cannot miss causes of HA

A
  1. SAH
  2. Cervico-cranial artery dissections
  3. Temporal Arteritis
  4. Acute Angle Closure Glaucoma
  5. Trauma (EDH, SDH)
  6. Meningitis (bacterial)
  7. CO toxicity
  8. Cerebral/Dural venous sinus thrombosis
  9. Space Occupying lesion
  10. Cerebellar infarction
  11. Idiopathic intracranial hypertension
  12. Pituitary apoplexy
  13. Pre-eclampsia
42
Q

What are 3 causes of Xanthrochromia?

A
  1. SAH
  2. Nonaneurysmal perimesencephalic subarachnoid hemorrhage (PMSAH) 5% of SAH
  3. Other non-aneurysmal bleeds
    Generally good prognosis, observation is all thats needed.
  4. Jaundice
  5. Increased CSF protein
  6. Rifampin
  7. Excess carotenoids
43
Q

What is the management for acute angle closure glucoma?

A
  1. Block production of aqueous humor:
    - Topical BB: Timoptic 0.5% 1 drop q30min x 2
    - Carbonic anhydrase inhibitor: Acetazolamide 500mg IV/PO/IM, then 250 q6h
    - Alpha-2 agonist: Apraclonidine 1 drop q30min x 2
  2. Reduce volume of vitreous:
    - PO Osmotic agents: Glycerol 1mL/kg po, Isosorbide 100mg po
    - IV osmotic agents: Mannitol 1-1.5g/kg IV
  3. Facilitate outflow of aqueous humor:
    - Topical pilocarpine
    - Blue eyes 2% 1 drop q15min for 1-2 hrs
    - Brown eyes 4% 1 drop q15min for 1-2 hrs
  4. Definitive Care
    - Referral to ophthalmologist for iridotomy
44
Q

List 4 ways that post LP headache can be reduced:

A
  • Non-cutting needle
  • Bevel parallel to Dural fibers
  • Replace stylet before removal
  • Smaller needle
  • Lay on back post procedure
45
Q

What are the physical exam findings of CN 3 palsy?

A
  • Pupil down and out
  • ptosis
  • Mydriasis
  • May have pain
46
Q

Name 4 conditions that can cause CN 3 palsy?

A
  1. Traumatic (herniation)
  2. Tumor
  3. Vertebrobasilar ischemia
  4. Aneurysm
  5. Hemorrhage into brainstem
47
Q

What are 3 CT findings for Cerebral sinus thrombosis?

A
  1. Normal in 30% Sn:60-70%
  2. Delta sign (dense triangle from hyperacute thrombosed superior sagittal sinus)
  3. Cord sign (thrombosed cortical vein)
  4. Venous infarcts at grey white jxn
  5. Hemorrhage in non-arterial distribution (bilat grey white jxn)
  6. Edema
48
Q

What is another name for the wallenberg syndrome?

A

Posterior inferior cerebellar artery syndrome

49
Q

What are the clinical manifestations of Wallenberg syndrome (lateral medullary infarct)

A

My dad is very loving and honest (DAD VLH)

D - Dysphagia
A - Ataxia (limb) (wid tendency to fall to the involved side)
D - Dysphonia

V - Vertigo,Nausea, Vomiting

L - Loss of pain & temperature sensation on same side of face & contralateral side of trunk/limbs.

H - Horner’s syndrome (ptosis, miosis, anhydrosis)

50
Q

What diagnose(s) must be ruled out for new onset horner’s syndrome?

A
  1. Thalamus, brainstem, cord pathology (stroke, tumor)
  2. Lung apex pathology
  3. ICA dissection (Red flag neck pain)
  4. ICA aneurysm
  5. Cavernous sinus pathology
51
Q

What diagnoses must be ruled out for CN 3 palsy (mydriasis, ptosis, “down and out”, diplopia)

A
  1. Aneurysm :Pcomm, PCA, Basilar
  2. Tumor
  3. SAH
  4. Cavernous sinus pathology (esp with CN 4)
52
Q

In hemorrhagic stroke, what are the MAP BP goals?

in pt with incr ICP what is the goal CPP (MAP-ICP)?

A

Difficult question, there isnt great evidence for either question and is patient dependent. From Stroke guidelines
1) Maintain MAP ~125 ( CPP 70 mmHg) in pts with chronic HtN
No HtN: MAP 110 (160/90)

2) if incr ICP then CPP > 70mmHg

53
Q

What are some reason nitroprusside is cautioned against in HTN management in hemorrhagic stroke?

A
  1. risk of cyanide toxicity (as per doig, if not in renal failure and not using high dosing (>8mcg/kg/min) this is not an issue)
  2. Risk of incr. ICP (due to vasodilatory effect, increasing cerebral blood flow = incr ICP. This has not been demonstrated in a clinical study is a theoretical risk
54
Q

What is the definition of incr ICP?

A

> 20mmHg

55
Q

What are 5 main categories of treating incr ICP acutely?

A
  1. elevate HOB, neck midline, no constricting tape around neck (optimize jugular venous outflow)
  2. Hyperventilation goal pCO2 30-35 (cerebral vasoconstriction
  3. Diueresis: Mannitol, or hypertonic saline
  4. Deep sedation and paralysis (Propofol, benzodiazepine, suxx, roc)
  5. High dose barbiturate therapy (‘reduce swelling and volume’). Not standard therapy
  6. Surgical decompression
56
Q

Why is high BP a concern in hemorrhagic stroke? (non -aneursymal)

A

The thought is that high BP promotes hematoma expansion. There have been a few studies that did not show a correlation between hematomal expansion and BP..

57
Q

What is the argument against aggressive BP control in hemorragic stroke? (Non-aneursymal)

A
  • Concern #1: The thought is that there is a perihematomal ischemic zone and lowering BP may result in low blood flow around the hematoma.
  • Some studies have suggested that low blood flow around the hematoma may be a result of reduced cerebral metabolism rather than primary reduction of blood flow.
  • concern #2: Cerebral ischemia may result in chronic hypertensives (shift in autoregulatory curve, pts with incr ICP may have cerebral ischemia due to low CPP)
58
Q

In acute hemorragic stroke which anti-hypertensives are recommended?

A 
Rapid and short acting..
Labetolol
Hydralazine
Nitroprusside
Nicardipine
Esmolol
Enalipril
59
Q

What are BP goals in acute ischemic stroke?

A

No clear guidelines, would not actively treat HTN.

  • reason to lower if >180 sBP and giving or going to get tPA.
  • OR sBP>220 dBP >120 (goal no more than 15% reduction in first 24 hours)
60
Q

What is a complete spinal cord injury?

A

There is complete motor and sensory loss below the level of injury.
- Uncommonly is the cord transected by sx caused by contusion of cord.

61
Q

What is anterior cord syndrome?

A
  • Anterior spinal artery is disrupted..
  • Complete motor loss below level of SCI
  • Loss of pain and temperature. Preservation of light touch and proprioception, vibration and two point discrimination
  • Autonomic dysfunction may be present and can manifest as hypotension (either orthostatic or frank hypotension), sexual dysfunction, and/or bowel and bladder dysfunction
  • Areflexia, flaccid internal and external anal sphincter, urinary retention and intestinal obstruction may also be present in individuals with anterior cord syndrome
62
Q

What is central cord syndrome?

A
  • Paralysis and/or loss of fine motor control or hands >Legs
  • Sensory loss below level of SCI may occur in varying degrees
  • Loss of bladder control may occur
63
Q

What is Brown Sequard syndrome?

A
  • Rare spinal disorder, injury to half spinal cord
  • Ipsilateral: paralysis, loss of proprioception, light touch, vibration, two point discrimination
  • Contra-lateral loss of pain and temperature and crude touch
64
Q

What is the classic mechanism for central cord syndrome?

A

Forceful hyperextension neck injury with prior existence of degenerative ligamentous and osteophytic spinal column disease.
- Common in elderly that fall face first.

65
Q

In SCI patients what do you want to avoid?

A

Avoid:

  1. Hypotension, maintain MAP>85
  2. Hypoxia
  3. Hypercarbia
  4. Acidosis
  5. Hyperglycemia
66
Q

What are the brain stem reflexes?

A
  1. Pupils
  2. Corneal reflex
  3. Conjugate gaze (test for dolls eyes or cold caloric if c-spine)
  4. Gag reflex
  5. Respiration
67
Q

Senerio: Patient has ICH, is normally on BB or clonidine. Usually anti-hypertensives are held and short acting BP meds are used to achieve BP goals. What is the concern with holding BB and clonidine?

A

You can get BB withdrawal with BB and rebound HTN with clonidine.

68
Q

Whats the dose of mannitol for incr ICP?

A

0.25-1g/kg IV as needed

1g/kg is the usual dose..

69
Q

What is the dose for Hypertonic saline for incr ICP?

A

3% : 15-30 mL boluses PRN

70
Q

When do people with cerebral aneursyms typically get a sentinel bleed? (from the big SAH)

A

2-8 weeks before overt SAH

71
Q

What are the s/sx of a sentinel bleed?

A
  1. HA - usually not as severe SAH
  2. N/V
    Meningismus uncommon
72
Q

What is the sn of CTA for aneurysms?

A

Really depends on size and location

Size >5mm: sn:95-100%
Size

73
Q

What is the Hunt Hess classification for SAH?

A

1: Mild Headache, Alert and Oriented, Minimal (if any) Nuchal Rigidity
2: Full Nuchal Rigidity, Moderate-Severe Headache, Alert and Oriented, No Neuro Deficit (Besides CN Palsy)
3: Lethargy or Confusion, Mild Focal Neurological Deficits
4: Stuporous, More Severe Focal Deficit
5: Comatose, showing signs of severe neurological impairment (ex: posturing)

Use for prognosis: 1 point = 30% mortality, 5 points =90% morality

74
Q

What is your approach to myasthenic crisis

A

Determine need for intubation

  1. Clinical status
  2. NIF less than…

Emergency Medicine (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions