Neuroscience ICU Flashcards
HINTS exam
Stands for “head impulse, nystagmus, test for skew”
Dix-Hallpike is performed when ___.
HINTS is performed when ___.
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)
TICI score
Evaluates post-thrombolysis/thrombectomy reperfusion.
0 - no reperfusion
1- little reperfusion
2a - < 2/3 reperfusion
2b - complete reperfusion, but slow
3 - brisk, complete reperfusion
Critical illness myopathy/neuropathy/neuromyopathy
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.
Tau-opathies that may cause parkinsonian symptoms
Progressive supranuclear palsy
Corticobasal syndrome/degeneration
PSP type Steele-Richardson
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”)
Why do we call it “corticobasal syndrome”?
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.
Alien limb in corticobasal syndrome
Very classic, but also quite rare
Lateralized cortical limb ataxia with asymmetric pyraidal signs is the core of the syndrome.
Syndromes assoiated with GIST
Carney’s triad
NF type 1
Carney’s triad
- 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.
Calculating the ELF concentration of drug
(for determining pulmonary penetration of antibiotics)
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.
Beta lactam penetration into pulmonary space
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.
Macrolide penetration into pulmonary space
Generally quite good (ELF/plasma > 1) with the exception of erythromycin.
Fluoroquinolone penetration into pulmonary space
Generally good, with an ELF:Serum ratio >1
Aminoglycoside penetration into pulmonary space
Relatively poor, with ELF > 1
Reasons to place an external ventricular drain (EVD)
- Relieve elevated ICP
- Drain infected CSF
- Drain bloody CSF following hemorrhage
- Monitor rate of flow of CSF
Acute SAH care
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)
Nitrates and ICP
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.
Furosemide and the ICP
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.
Aneurysm repair in aneurysmal SAH
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.
Cerebral salt wasting
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.
Kocher’s point
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.
High-risk features suggestive of SAH
- 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
Neurogenic myocardial injury/stunning
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.
