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Intensive Care Clerkship > Neuroscience ICU > Flashcards

Neuroscience ICU Flashcards

1
Q

HINTS exam

A

Stands for “head impulse, nystagmus, test for skew”

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2
Q

Dix-Hallpike is performed when ___.

HINTS is performed when ___.

A

Dix-Hallpike is performed when the patient is completely asymptomatic with no signs on exam.

HINTS is performed when nystagmus is present on exam (to differentiate central vs peripheral etiology)

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3
Q

TICI score

A

Evaluates post-thrombolysis/thrombectomy reperfusion.

0 - no reperfusion

1- little reperfusion

2a - < 2/3 reperfusion

2b - complete reperfusion, but slow

3 - brisk, complete reperfusion

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4
Q

Critical illness myopathy/neuropathy/neuromyopathy

A

Most common cause of neuromuscular weakness in the intensive care setting. Contribute to failed ventilator weaning in critically ill patients.

  • CIM: Proximal myopathy with atrophy if protracted, sensation intact.
  • CIPN: Distal weakness with sensory changes, limited atrophy.
  • CIPNM: Proximal and distal weakness with sensory changes and variable atrophy.

Characterized by slow or blocked conduction along muscle fibers (myopathy) and axonal loss with preserved myelination (neuropathy).

Dx: Eletrphysiologic studies (NCS-EMG). Direct muscle stimulation (DMS) can help differentiate between CIPN or CIM if there is uncertainty.

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5
Q

Tau-opathies that may cause parkinsonian symptoms

A

Progressive supranuclear palsy

Corticobasal syndrome/degeneration

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6
Q

PSP type Steele-Richardson

A

Whipple’s disease should always be on the ddx!!!

Characterized by:

  • Parkinsonism
  • Loss/slowing of vertical saccades
  • Lid retraction
  • Cognitive changes (pseudobulbar affect, abulia, aphasia)
  • Profound instability with early falls and significant injuries (“out of the blue”)
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7
Q

Why do we call it “corticobasal syndrome”?

A

Because it is a syndrome that can be caused by numerous neurodegenerative diseases, including prion disease and tau-opathy.

Imaging shows profound and somewhat selective atrophy of the primary motor cortex.

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8
Q

Alien limb in corticobasal syndrome

A

Very classic, but also quite rare

Lateralized cortical limb ataxia with asymmetric pyraidal signs is the core of the syndrome.

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9
Q

Syndromes assoiated with GIST

A

Carney’s triad

NF type 1

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10
Q

Carney’s triad

A
  • GIST
  • Pulmonary chondroma
  • Paraganglioma

Occurs primarily in young women. Rare tumors that tend to occur together in groups of 2 or 3.

Believed to be genetic, but no genetic etiology has yet been found.

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11
Q

Calculating the ELF concentration of drug

(for determining pulmonary penetration of antibiotics)

A

This is done by BAL. First, we use the plasma urea concentration and the urea concentration of the BAL fluid to estimate the original ELF volume (Equation 1).

Then, we use this volume and the measured BAL drug concentration to determine the ELF concentration (Equation 2).

Finally, we compare this to the plasma concentration of the drug.

“Penetration of Anti-Infective Agents into Pulmonary Epithelial Lining Fluid”

This measurement is not perfect, as cell lysis and other volume confounds may affect the volume.

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12
Q

Beta lactam penetration into pulmonary space

A

The availability of most beta lactams in the ELF is approximately 20% that of the serum availability. This includes most cephalosporins and cabapenems.

Cefaclor (2nd generation cephalosporin) and cefepime (4th generation cephaopsorin) are exceptions with decent pulmonary penetration.

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13
Q

Macrolide penetration into pulmonary space

A

Generally quite good (ELF/plasma > 1) with the exception of erythromycin.

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14
Q

Fluoroquinolone penetration into pulmonary space

A

Generally good, with an ELF:Serum ratio >1

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15
Q

Aminoglycoside penetration into pulmonary space

A

Relatively poor, with ELF > 1

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16
Q

Reasons to place an external ventricular drain (EVD)

A
  • Relieve elevated ICP
  • Drain infected CSF
  • Drain bloody CSF following hemorrhage
  • Monitor rate of flow of CSF
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17
Q

Acute SAH care

A

1 goal is to prevent rebleeding and vasospasm

  • Blood pressure control with non-nitrate medications (preferred agents: labetalol, nicardipine, clevidipine, enalapril).
  • Nimodipine (to prevent vasospasm)
  • DVT prophylaxis
  • Maintain euvolemia – but do no hypoperfuse or give extra fluid
  • ICP-reducing procedures (EVD placement)
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18
Q

Nitrates and ICP

A

Nitrates are preferrentially vasodilatory, and as such raise the ICP and reduce CPP.

Thus, alternative fast-acting antihypertensives should be used in the acute setting: Labetalol and dihydropyridine CCBs are preferred.

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19
Q

Furosemide and the ICP

A

Furosemide is a fast-acting venodilator, resulting in venodilation within ~5 minutes.

In contrast, the diuresis effect takes ~30 minutes to begin.

The result is a brief increase in ICP followed by a drop in ICP.

20
Q

Aneurysm repair in aneurysmal SAH

A

After aneurysmal SAH, patients are at risk for rebleeding – especially within the first 24 hours. Aneurysm repair with surgical clipping or endovsacular coiling is the only effective treatment to prevent recurrence.

If the patient is not a surgical candidate or aneurysm repair is otherwise impossible, patients may benefit from antifibrinolytic therapy starting at the 72 hour mark.

21
Q

Cerebral salt wasting

A

Inappropriate brain-derived BNP-mediated natriuresis in the setting of brain injury. Should always be on the ddx for SIADH. The exact etiology leading to BNP release is unclear – it may be injury-mediated or regulatory in mechanism.

Importantly, the treatments for SIADH and CSW are opposite. SIADH requires restriction of free water, CSW requires salt supplementation with a mineralocorticoid.

22
Q

Kocher’s point

A

Entry point through the frontal bone for an intraventricular catheter to drain CSF from the anterior horn of the lateral ventricle.

Found at the midpupillary line 2 cm anterior of the coronal suture.

Catheter is inserted angled towards the anterior midline at pupillary level.

23
Q

High-risk features suggestive of SAH

A
  • Age > 40 years
  • Meningismus
  • Witnessed loss of consciousness
  • Onset during exertion
  • Thunderclap headache (max intensity within 1 minute of onset)
  • Limited neck flexion on exam
24
Q

Neurogenic myocardial injury/stunning

A

Form of myocardial dysfunction that occurs in SAH, stroke, or seizures.

Thought to be seondary to the sudden catecholamine surge following cerebral aneurysm rupture, which leads to myocardial cell contraction band necrosis. Deeply inverted T waves with QTc prolongation, called cerebral T waves, are often present.

Classically has the appearance of Takatsubo cardiomyopathy – with ventricle apical akinesis leading to ballooning of the apex during systole, the shape of which resembles a Japanese octopus trap.

25
Q

Hyperacute aneurysmal SAH complications

A
  • Inability to protect airway/respiratory insufficiency
  • Neurogenic myocardial stunning
  • Acute hydrocephalus
  • Aneurysm rebleed (highest risk w/in 72 hours)
  • Global cerebral edema/ICP elevation
26
Q

Signs of acute hydrocephalus

A

Decreased level of consciousness

6th nerve palsy

Cushing’s reflex

27
Q

“Malignant MCA” syndrome

A

Basically just means cerebral edema following MCA infarct/stroke

28
Q

Nimodipine in SAH

A

Previously, it was thought that nimodipine prevented vasospasm following SAH.

Now we know that, while nimodipine does not prevent vasospasm, it does reduce mortality by some unknown mechanism. So, it is still given for 21 days following SAH.

29
Q

Post-SAH tertiary prevention

A

Any patient that has SAH will receive:

Kepra for 7 days

Nimodipine or Nicardipine for 21 days

30
Q

Cerebral salt wasting vs SIADH

A

Both can occur in patients with nonspecific neurologic injuries. Both present with low serum sodium and serum Osm, high urine sodium and urine Osm. You tell them apart by volume status.

CSW is BNP-mediated, patient will be hypovolemic, and is managed with salt tabs and fludricortisone.

SIADH is ADH-mediated, patient will be hypervolemic, nad is managed with fluid restriction +/- vaptans.

31
Q

Emergent measures for diffuse cerebral edema on presentation

A
  • HOB to 45 degrees or higher
  • Hyperventilate by ventilator or bag/mask prior to intubation with goal PCO2 of 25
  • Place, open, and /or drop EVD to drain ~ 5 mL CSF
  • Optimize sedation
  • Administer osmotherapy
  • STAT CT if immediate cause is unknown
  • Surgery as soon as able if surgically amenable lesion
32
Q

Bolus dosing of mannitol

A

1 gram / kg IV

33
Q

Theories of why mannitol works

A
  1. Immediate plasma-expanding effect
  2. Rheological effect (hemodilution, reducing blood viscosity, increasing RBC deformability)
  3. Delayed osmotic effect (drawing free water out of brain into vasculature)
34
Q

Hydralazine’s effects are primarily. . .

A

. . . arterial

Not so much venous

35
Q

Osm gap

A

Calculated serum Osm: Na x 2 + BUN / 2.8 + Glucose / 18

Osm gap = Actual Osm - Calculated Osm

Normal = 10-15 mmHg

36
Q

If mannitol fails to reduce ICP, __ is the next option

A

If mannitol fails to reduce ICP, 23.4% hypertonic saline 30 mL bolus is the next option

Techically they are equivalent from an evidence-based perspective at this time, but mannitol is usually used first.

37
Q

If a patient is critically ill and immobilized, extra dietary protein may manifest as. . .

A

. . . positive nitrogen balance with excess nitrogenous waste and uremia.

If they don’t need the protein, don’t give it to them.

38
Q

Post-SAH risk windows

A

Rebleed window (aneurysmal): 6h-72h

Vasospasm window: 3d - 21d (peak 3d - 7d)

39
Q

Hoover’s sign

A

For a suspected functional neurologic disorder

Ask the patient to try and raise the affected extremity. If the disorder os organic, the contralateral limb will subtly drop. If the disorder is functional, it will not.

40
Q

If cerebral edema is suspected, what are the target ventilator settings and respiratory markers?

A

30-35 mmHg pCO2

Avoid PEEP (can raise ICP)

Propofol for sedation (mildly reduces ICP)

41
Q

Primary goals in treating a patient with intracranial hypertension

A
  1. Aggressive euvolemia
  2. Maintain adequate CPP
  3. Avoid hypoxia
42
Q

When should you treat intracranial hypertension?

A

Once the ICP is above 20-25 cm water

43
Q

Indications for ventriculostomy

A
  • Acute symptomatic hydrocephalus
  • Adjunct management for ventriculoperitoneal shunts
  • Need for intracranial pressure monitoring
44
Q

Indications for intracranial pressure monitoring

A
  1. CT confirmed intracranial hemorrhage
  2. GCS of 8 or less
  3. Receiving sedation

All three must be met.

45
Q

Meningitis or SAH is suspected. What is the next best step?

If this does not yield results, what is the next best step after that?

A

The next best step is non-con CT to assess the intracranial anatomy and for hemorrhage. This is also to rule out obvious space-occupying lesions.

If this fails to yield an etiology, lumbar puncture is the next best step.

46
Q

Permissive hypertension goal

A

SBP < 180

Used in the setting of stroke and some other vascular brain injuries. Maintains perfusion without allowing pressure to be so high as to enable hemorrhagic conversion.

Intensive Care Clerkship (32 decks)

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