NCC BOARDS CLINICAL PEARLS

Question 1

45 M with possible seizure history presents after seizure activity resulting in a ground level fall. In the ED he has a witnessed seizure. CT head demonstrates temporal SAH. He has an anaphylactic reaction to contrast and a skull fracture overlying the dural sinus. Imaging is required to rule out a dural sinus thrombosis. He requires intubation to allow for adequate sedation for MRV to evaluate the sinus. On hospital day 3 he develops hypoxia and new thick secretions with fevers. Which broad spectrum antibiotic should be started given his history of seizures and current epileptiform activity on continuous EEG?

Answer 1

Zosyn

• Cefepime lowers seizure threshold

Question 2

When do you use different forms of valproic acid?

Question 3

Difference between different anti epileptic meds

Question 4

Which ICH/SAH/SDH locations increase seizures or predispose a patient to seizures?

Question 5

Which medications lower seizure threshold?

Answer 5

Question 6

Which seizure drugs affect anticoagulation? Or which anticoagulation drugs affect seizure medications?

Question 7

Which antiepileptic meds require renal dosing?

Question 8

Interactions between antipsychotics and seizure medications/thresholds?

Question 9

Stepwise management of seizures inpatient and outpatient?

Question 10

What is the Fisher Grading Scale of SAH?

Answer 10

Question 11

Main difference between SIADH and Cerebral Salt Wasting?

Answer 11

Check intravascular volume -
- CSWS - hypovolemia (water problem)
- SIADH - euvolemia (salt problem)
- Both have Na <135, Serum Osm < 285, urine Na >25, urine osm >200

Question 12

Medications associated with SIADH?

Answer 12

TBI, brain tumor, CVA, brain infection, SAH, ICH, pneumonia/TB, lung cancer, meds, SSRI, TCA, cabamazepine, oxcarbazepine, chlorpropamide, nicotine, opioids, antipsychotics, NSAIDS
- SCANT COON - SSRI, chlorpropamide, antipsychotics, NSIADS, TCAs, carbemapezine, oxcrbazepine, opioids, nicotine

Question 13

Treatment strategies for SIADH?

Answer 13

Fluid restriction of free water, supplement Na (PO &laquo_space;IV - NS vs 3%), demeclocycline (takes >1 wk), vasopressin antagonists (prompt response over first 24 hours, causes diuresis)

Question 14

What were the SALT 1 and 2 trials?

Answer 14

SALT-1 patients with tolvaptan had change in serum sodium to day 4 of 3.6 versus 0.25 in placebo. SALT-2 was 4.33 vs 0.42
Two multicenter randomized double blind placebo-controlled trials in patients with hyponatremia from CHF, cirrhosis and SIADH (SALT-1 US and SALT-2 international) - PO placebo versus tolvaptan (vasopressin antagonist) - serum sodium returned to placebo level when stopped

Question 15

What is cerebral salt wasting? How is it treated?

Answer 15

Etiology unknown but typically caused by increased secretion of natriuretic peptides causing loss of Na at the renal distal tubules
Tx: Na containing fluid (NS versus 3%)
Fludrocortisone 0.1-0.4 mg/day may be helpful in reducing Na loss in CSWS

Question 16

How quickly should you correct hyponatremia? What happens if corrected too quickly?

Answer 16

0.5 mEq/L/hr (chronic but if acute can correct more quickly)
More rapid - up to 1-2 mEq/L/hr can lead to cerebral pontine myelinolysis (limit Na to 12 mEq/L in the first 24 hours)

Question 17

What is the Hunt and Hess SAH grading system?

Answer 17

Question 18

How do the World Federation of Neurological Surgeons Scale, the Hunt and Hess Scale and the Modified Fisher Scale correlate?

Question 19

Does initial GCS correlate without outcomes in SAH?

Answer 19

Yes a positive correlation with long term outcomes

Question 20

What is the limitation of the HH grading system?

Answer 20

Margins between categories are ill-defined and has poor interobserver reliability and reproducibility (intensity of headache is subjective)

Question 21

What is the limitation of the Fisher grading system?

Answer 21

Some literature has reported a low correlation between grade and incidence of vasospasm and it has interporsoal variability in assessing the estimated blood volme

Question 22

What is the modified fisher scale?

Answer 22

Question 23

What did Ko and Colleagues report about the Fischer Scale and Modified Fisher scale?

Answer 23

Quantitative blood volume in contact with cisternal space (directly in cisternal SAH or IVH space) acts as cumulative blood burden and associated with increased risk of DCI (delayed cerebral edema)

Question 24

What did Klimo and Schmidt report on relationship of CT findings in SAH and rate of developing cerebral vasospasm after aneurysmal SAH?

Answer 24

The most consistent predictor of vasospasm is the amount of SAH seen on postictal CT scan. The greater the amount of blood within the basal cistern, the greater the risk of vasospasm. IVH, although not supported as strongly as cisternal SAH, has also been shown to be a risk factor for vasospasm.

Question 25

What are the initial steps in management of a high-grade acute aneurysmal SAH with poor mental status and IVH?

Answer 25

ABC and EVD
Ventric, ventric, ventric

Question 26

What do you check for when evaluating if an EVD is working?

Answer 26

Draining bloody CSF adequately when opened and maintains good waveforms when closed.

Question 27

What is IVH associated with in acute aneurysmal SAH? What symptoms does it cause and why?

Answer 27

Development of acute obstructive hydrocephalus which can cause vertical eye movement impairment and depressed level of arousal from mass effect on thalamus and midbrain.

Question 28

Is IVH an independent risk factor for development of symptomatic vasospasm in acute aneurysmal SAH?

Answer 28

Yes

Question 29

An EVD is placed for an acute high-grade aneurysmal SAH with IVH and the patient has improved and prolonged improvement in GCS. Does this affect the patients prognosis?

Answer 29

Yes - if patient has improved neurologic status that persists and goes from behaving like a high-grade SAH to a low-grade SAH, they possibly have a favorable outlook

Question 30

Frequency of alpha waves? Amplitude? Synchronized or dysynchronized? When does this occur? What happens with an alpha block?

Answer 30

F - 8-12 w/sec, A - 50, synchronized, inattentive brain, drowsiness or light sleep, parked in parietoocipital area, affected by eyes opening (visual stimuli or mental effort), alpha block - synchronized to desynchronized when eyes open or concentration

Question 31

Frequency of beta waves? Amplitude? Synchronized or dysynchronized? When do these occur? Affected by eye opening?

Answer 31

F - 15-60 w/sec, 5-10 mv, desynchronized, mental activity, mental tension, arousal state, not affected by eyes opening

Question 32

What are gamma waves?

Answer 32

30-100 w/sec - controvertial

Question 33

Frequency of delta waves? Amplitude? When are these seen? Affected by eye opening?

Answer 33

F - low (1-5/sec), amplitude - high (20-200 mV), early childhood waking and adults sleep, presence when adults awake suggest tumor, epilepsy, increaed ICP, mental defficiency or depression, not affected by opening eyes

Question 34

Theta wave frequency and amplitude? When are these seen?

Answer 34

Children <5 years old, low frequency (4-8), amplitude 10 mV