This week in Morning Report, our AACU resident presented the case of a patient with nausea and vomiting, initially felt to be secondary to a viral gastroenteritis. When seen in follow up (one of the big advantages of ambulatory care!), the patient’s symptoms were intractable – eventually leading to a diagnosis of a much more sinister cause of nausea.
‘This patient is nauseous, can you please order a prn’ is probably one of the most common pages you will see in your PGY1 year! When I was a junior trainee, I had a ‘blunt instrument’ approach to nausea and vomiting – Gravol if the patient was young, and if that didn’t work or if they were older, Ondansetron 4mg IV q4h prn. Raise your hand if you’re guilty of the same!
Spending a bit of time understanding the pathophysiology of nausea and vomiting will significantly improve your ability to treat it in a more nuanced and effective way.
1. How and where is the sensation of nausea created?
Nausea and vomiting are governed by key structures located in the brainstem.
- The Chemoreceptor Trigger Zone (CTZ): This is a zone located in the brainstem in the area postrema near the fourth ventricle, outside the blood brain barrier. The fact that it is outside the BBB is critically important – it means that emetogenic stimuli can reach this area through the bloodstream! This zone contains several important receptors: Histamine (H1), Muscarinic (M1), Dopamine (D2), Serotonin (5-HT3) and Neurokinin (NK-1) receptors.
- The Vomiting Centre: The vomiting centre (now sometimes called the Central Pattern Generator) is located in the medulla and is the effector/efferent pathway that activates vomiting. Individuals with severe brain damage and decortication can still vomit, because the Vomiting Centre does not depend on cortical input!
There are three important sources of inputs into the CTZ and Vomiting Centre that start the nausea-generation cascade:
- Cortex: Stimuli such as pain, anxiety, and stress
- Vestibular System: This is your inner ear/balance system, which is mediated by Histamine (H1) and Muscarinic (M1) receptor cascades
- GI Tract: The GI tract sends lots of feedback to the brain – in the form of visceral afferents, mechanoreceptors that are stimulated by gastric stretch, and chemoreceptors stimulated by luminal contents. These are primarily serotonin, or 5-HT3 mediated.
2. How do you approach a DDx in a patient with nausea/vomiting?
As always, remember that diagnosis = timecourse x localization. A vast majority of presenting nausea/vomiting concerns are self-limiting, of short duration, and attributable to various transient GI illnesses. However, many aren’t — and there are a lot of sinister causes of refractory or unrelenting nausea. For this reason, classifying N/V by GI vs. non-GI sources can be helpful. I’ve summarized our differential in the flowchart below:
3. How do you treat nausea and vomiting?
Our key takeaway from this Morning Report is this: Thou shalt not freely prescribe Gravol and Zofran without understanding where the problem is!
Take a moment to understand where the nausea is coming from, and which receptors might be involved. You can then use specific drugs to target those receptors. I’ve summarized this in the table below:
One more pearl in the treatment of nausea — have you tried inhaled isopropyl alcohol (aka an alcohol swab – readily available in most wards near you)? A small but well-performed single-centre study in 2018 found that sniffing alcohol swabs was superior to oral ondansetron in treating nausea. It’s my favourite trick and pretty cheap and easy to do!
I hope you found this morning report helpful – thank you to our AACU resident for bringing this case!