Block 3 Neuro Flashcards
Sx of HTN ICH? Diagnosis?
Patients usually have focal deficits
Headache and vomiting common
Diagnosis confirmed with head CT w/o contrast or MRI
RF for SAH?
Cigarette smoking and hypertension are the largest risk factors
Hallmark Sx of SAH?
Almost always caused by saccular aneurysm
“Worst headache of my life”/thunderclap headache
Sentinel headache 6-20 days prior
What is Cushing’s Reflex? What condition is it found in?
Found in Herniation
Cushing’s Reflex:
Increased pulse pressure (elevated SBP)
Bradycardia
Irregular breathing
Normal CPP and how do you calculate it?
60-70
𝑪𝑷𝑷=𝑴𝑨𝑷−𝑰𝑪𝑷
SBP goal of Hypertensive ICH + Aneurysmal SAH?
HTN ICH <140
Aneurysmal SAH <160
What are the agents used for acute BP reduction?
Hydralazine
Labetalol
Nicardipine
Clevidipine
Pearls of:
Hydralazine
Labetalol
Nicardipine
Clevidipine
Nicardipine = titratable, but large amounts of fluid/hr
Clevidipine = titratable (fastest), but solution is in a lipid emulsion
Hydralazine = unpredictable onset
Labetalol = caution in patients with bradycardia or history of reactive airway disease
If antifibrinolytic therapy is started, how long should you use it for aneurysmal SAH?
Dont go beyond 72hrs, but typically its not recommended to use at all
_________ is a major contributor to death and complications related to aneurysmal SAH
Vasospams
Vasospasms can be detected using ________ or directly with endovascular approaches
Transcranial dopplers
What is the only FDA-approved medication to reduce DCI associated with aSAH?
Nimodipine
Dosing: 60 mg orally or per tube every 4 hours for 21 days
When is VTE prophylaxis started after HTN ICH or Aneurysmal SAH is stable?
After 24 hrs
What are the 2 types of TBI injury?
Focal
Caused by penetrating or closed impact
Evidenced by hematomas and contusions on CT scan
Diffuse
Caused by rapid acceleration/deceleration
No impact required for this type of injury (MRI works better)
What does the Glasgow Coma Scale (GCS) look at?
Eyes
Motor Response
Verbal Response
3-8 = severe
13-15 = minor
Complications of TBI?
Nosocomial Infection
Deep Vein Thrombosis
Post-traumatic seizures (PTS)
Post-traumatic epilepsy (PTE)
SBP goal of TBI?
Age 50-69 → SBP > 100 mmHg
Age 15-49, 70+ → SBP > 110 mmHg
IC Pressure goal of TBI?
<20
Tx if >22
Non pharm Tx for TBI?
Craniectomy
Therapeutic or prophylactic hypothermia (not recommended)
CSF drainage
Ventilation therapies
What rx are used for TBI?
Mannitol (diuretic) careful in AKI pt
Hypertonic saline; anything above 900 osmolarity (3%NaCl) needs to be given in central line
Analgesics, anesthetics, and Sedatives; they dont lower ICP pressure except propofol
Seizure prophylaxis; phenytoin or keppra can be used for EARLY post-traumatic seizure
Dont give steroids
Albuterol Theophylline Pseudoephedrine Midodrine Fludrocortisone
Which ones increase HR/BP?
HR only:
Albuterol
Theophylline
BP only:
Midodrine
Fludrocortisone
Both:
Pseudoephedrine
Albuterol Theophylline Pseudoephedrine Midodrine Fludrocortisone
Which one has a narrow concentration level?
Theophylline
10-20
What kind of diet works well with fludrocortisone to increase BP?
High salt diet
What are the different GSCE stages?
1 - 0 to 30 min (impeding)
2 - 30 to 60 min (established)
3 - >120 min (refractory); continuous after 2-3 Tx
4 - >24 hrs (super refractory)
What are the main excitatory and inhibitory NT? What receptors?
Excitatory - glutamate on NMDA
Inhibitory - GABA
Epilepsy + Glutamate
Causes opening of (calcium/potassium/sodium/magnesium/chloride) channels leading to (depolarization/hyperpolarization/repolarization)
Calcium + sodium
Depolarization
Epilepsy + GABA
Causes opening of (calcium/potassium/sodium/magnesium/chloride) channels leading to (depolarization/hyperpolarization/repolarization)
Chloride
Hyperpolarization
The reason it goes away is GABA receptors experience endocytosis, decreasing their concentrations in prolonged seizures
Seizure patho Part 1
during the first ________ of seizure
30 minutes
Phase 2 is immediately after
What is happening in your body during part 1 of seizures?
Epinephrine, norepinephrine, and steroid concentrations increase significantly
Glycogenolysis
Lactic acid buildup
Airway obstruction, increase in secretions
What is happening in your body during part 2 of seizures?
Patients may stop convulsing but seizures may still be evident on EEG
Converted to NCSE
Everything in part 1 is basically depleted
________ is a big marker of a true seizure
Incontinence
Prehospital Care of SE?
PR diazepam if available; otherwise:
IN midazolam or IM midazolam
Initial Hospital Care of SE
Consider thiamine 100 mg (adult), pyridoxine 50-100 mg (infants)
Glucose (D50W or D10W) if hypoglycemic
Naloxone for suspected narcotic overdose
Antibiotics if infection suspected
Treatment of hyperthermia
GSCE (0-30 min) Treatment?
IV lorazepam
Consider IN midazolam or IM midazolam
GSCE (30-60 min) Treatment?
First line
Phenytoin (IV) or fosphenytoin (IV or IM)
Second line
Phenobarbital (IV)
Valproate (IV)
Third line
Lacosamide (IV)
Levetiracetam (IV)
GSCE (>120 min) Treatment?
Midazolam, propofol, or pentobarbital infusions
If on propofol, continuous ECG monitoring
Assure cerebral perfusion pressure is > 70 mmHg
Achieve MAP > 120 mmHg
GSCE (>24 hours) Treatment?
Ketamine, lidocaine, topiramate
Hypothermia
Inhaled anesthetics
Immunomodulating therapies
Assure cerebral perfusion pressure is > 70 mmHg
Achieve MAP > 120 mmHg
Dose and rate of phenytoin and fosphenytoin for SE?
Phenytoin 15-20 mg/kg IVPB (rate < 50 mg/min)
Fosphenytoin 15-20 mg PE/kg IVPB (rate < 150 mg PE/min)
(Phenytoin/Fosphenytoin) is mixed in diluent (propylene glycol) that can cause hypotension and cardiac arrhythmias
Phenytoin
How do you check the free level of phenytoin?
If no lab exists use equation:
PHT level / (0.2 or 0.1 if CrCl<20 x albumin + 0.1)
Should be 10-20
Phenobarbital dosing and AE?
Phenobarbital (IV) 15-20 mg/kg
Hypotension, respiratory and CNS depression
Contains propylene glycol
Goal levels of valproate?
50-100
If valproate + phenytoin are given together, what do you do?
Increase valproate dose
What happens if valproate + aspirin are given together?
Valproate concentrations go up
Valproate AE?
LFT elevation + edema
Lacosamide AE?
Dizziness, loss of balance, memory problems
Keppra AE?
Somnolence, headache, mood swings
How are meds for refractory GCSE given?
Bolus, then drip
alpha 1 antagonism
muscarinic antagonism
sodium blockade
potassium blockade
QRS widening - myocardial depression
QT widening - torsades
hypotension
anticholinergic effects
Match antipysch effects!
alpha - hypotension
muscarinic - anticholinergic
sodium - QRS widening - myocardial depression
potassium - QT widening - torsades
NMS general signs?
Rigidity, fever
NMS treatment?
BZD
Bromocriptine
Dantrolene
Antipsych + hypotension or QRS widening, what do you do?
Hypotension - fluids with vasopressors
QRS widening - sodium bicarb
Acute and chronic lithium toxicity symptoms? How do you treat it?
Acute - N/V, dizziness
Chronic - tremors, more kidney damage, diabetes
Fluid resuscitation
Avoid enhancing elimination with loop diuretics
Hemodialysis if poor eGFR
MAOI overdose symptoms and treatment?
Hyperthermia - cooling bath/blankets
Hyperreflexia - BZD
HTN - Titratable calcium channel blocker (nicardipine, clevidipine), sodium nitroprusside
CNS effects (seizures) - BZD
TCA overdose symptoms and treatment?
Arrhythmia - sodium bicarb
Hypotension - fluids + vasopressors
Seizure - BZD, barbiturates
Refractory sx - IV fat emulsion
Serotonin syndrome general signs?
Hyperreflexia
Hot + sweaty
Confusion, tremors
Serotonin syndrome treatment?
- BZD
If refractory, give Cyproheptadine (serotonin antagonist)
What is the concern of taking flumazenil for chronic and acute BZD users?
Chronic - Causes abrupt withdrawal from BZD which could result in neuronal hyperexcitation
Acute - withdrawal should not happen, so no issues
