Questions asked throughout the episode
Can you describe pathophysiology of elevated ICP or cerebral edema?
“I always teach trainees that as long as you understand the pathophysiology behind a problem and the mechanisms behind the drugs we have available, we can find out where these 2 areas overlap and come to a rationale thought process”Tweet
- Important to understand that elevated ICP and CE can happen together, or they can happen independently of each other, or one can happen and lead to the other
- Certain neurologic injuries may cause one specific type of CE during the early phase of injury, and another type of CE during the later phases
- 5 primary types of CE, but I’ll focus on the 2 most common: vasogenic and cellular/cytotoxic -Briefly Describe vasogenic edema & cellular / cytotoxic edema
Can you tell me about what pharmacologic options we have for treating elevated ICP / cerebral edema?
- Broad summary – sedation, fever control, dexamethasone, osmotic diuretics, hypertonic sodium
Can you describe the mechanism of action of hypertonic Saline and mannitol?
- -Discuss mannitol and the straight forward mechanism
- -Discuss how mechanism with HTS isn’t fully understood and compare the two primary thought processes
- -Discuss how we aren’t just talking hypertonic sodium and the breadth of hypertonic sodium solutions that have been studied and can be used
Can you discuss any controversies you think exist about mannitol administration?
- -Pre-hospital administration
- -Dosing – discuss Cruz data & how this has been removed from TBI and CE guidelines
- -Dosing interval
- -Acute ICH administration
- -Rate of administration -Monitoring and AKI
Can you discuss any controversies you think exist about hypertonic saline administration?
- Na Goals
- -Bolus vs Infusion
- -Does it work when patient already has high Na?
- -Central vs peripheral
- -Rate of administration -Monitoring and other adverse effects