NCC BOARDS CLINICAL PEARLS Flashcards
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?
Zosyn
- Cefepime lowers seizure threshold
When do you use different forms of valproic acid?
Difference between different anti epileptic meds
Which ICH/SAH/SDH locations increase seizures or predispose a patient to seizures?
Which medications lower seizure threshold?
Which seizure drugs affect anticoagulation? Or which anticoagulation drugs affect seizure medications?
Which antiepileptic meds require renal dosing?
Interactions between antipsychotics and seizure medications/thresholds?
Stepwise management of seizures inpatient and outpatient?
What is the Fisher Grading Scale of SAH?
Main difference between SIADH and Cerebral Salt Wasting?
Check intravascular volume -
- CSWS - hypovolemia (water problem)
- SIADH - euvolemia (salt problem)
- Both have Na <135, Serum Osm < 285, urine Na >25, urine osm >200
Medications associated with SIADH?
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
Treatment strategies for SIADH?
Fluid restriction of free water, supplement Na (PO «_space;IV - NS vs 3%), demeclocycline (takes >1 wk), vasopressin antagonists (prompt response over first 24 hours, causes diuresis)
What were the SALT 1 and 2 trials?
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
What is cerebral salt wasting? How is it treated?
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
How quickly should you correct hyponatremia? What happens if corrected too quickly?
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)
What is the Hunt and Hess SAH grading system?
How do the World Federation of Neurological Surgeons Scale, the Hunt and Hess Scale and the Modified Fisher Scale correlate?
Does initial GCS correlate without outcomes in SAH?
Yes a positive correlation with long term outcomes
What is the limitation of the HH grading system?
Margins between categories are ill-defined and has poor interobserver reliability and reproducibility (intensity of headache is subjective)
What is the limitation of the Fisher grading system?
Some literature has reported a low correlation between grade and incidence of vasospasm and it has interporsoal variability in assessing the estimated blood volme
What is the modified fisher scale?
What did Ko and Colleagues report about the Fischer Scale and Modified Fisher scale?
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)
What did Klimo and Schmidt report on relationship of CT findings in SAH and rate of developing cerebral vasospasm after aneurysmal SAH?
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.
