2/ RN lets you know that the patient just completed their TEE....
O2 is beeping, 88% ➡️87%➡️ 86%
3/ Time to quickly go over your checklist
✅Auscultate breath sounds?
Normal.
✅Change sensor on O2 sat probe?
Still 86%.
✅Check ETT placement?
Unchanged from the day prior.
✅Compliance/Plugging issue?
Normal Peak and Plateau pressure. Nothing clogged.
4/ Fine…time to jack up the FiO2 to 100%
.
.
.
Still satting at 86%. 🤔 Is this a PTX?
U/S shows the following
5/Patient looking more and more uncomfortable. He's becoming less interactive. What’s going on?!
6/ Time to 📞 a friend (& attending extraordinaire @CajalButterfly ), who calmly assesses the situation.
“Send a blood gas”
7/ So what’s going on??
8/ Yes! It’s methemoglobinemia!
A brief review,
In normal Hgb, Iron is in the ferrous state (Fe2+), which allows binding and release of oxygen. In methemoglobin, the altered Hgb has its Iron oxidized in its ferric state (Fe3+), which does not bind to oxygen at all!
9/ This causes normal heme to have an increased affinity to oxygen ➡️less oxygen gets to the tissues ➡️ produces a left shift on the oxygen-hemoglobin dissociation curve
10/ Symptoms range from being asymptomatic to having cyanosis, dyspnea, headache, seizures, fatigue, shock, and respiratory failure.
It can be hereditary or acquired.
From the acquired group, the MCC are medication including dapsone, chloroquine, inhaled nitric oxide….
11/ And a topical inhalants commonly used to do things like anesthetize a patient’s pharynx for TEE
.
.
.
Benzocaine spray.
Sure enough, a look back through our patient’s chart confirms our suspicion!
12/ Treatment includes discontinuing the offending agent and increasing oxygen to help oxygen delivery.
For mild cases, you can use Vitamin C IV 1-10g (although it can take a while to work).
13/ For moderate/severe cases where methemoglobin is >20%, or in patients with significant symptoms, you can use methylene blue IV at 1-2mg/kg aka Smuff’s Blood (though caution in patients with G6PD deficiency).
14/ So why does the pulse ox sensor show an oxygen saturation at 85% even if PaO2 is high? It’s the way the pulse ox uses the ratio of light being absorbed at two different wavelengths to calculate the results.
15/ Oxygenated🩸absorbs more light at the 940nm, whereas deoxygenated🩸absorbs light more at 660nm.
Methemoglobin absorbs light equally at 940nm and 660nm thereby “confusing” the pulse ox into thinking oxygen saturation is ~85% when it may actually be much lower
Back to our case.
Reading from right to left, you can see the SpO2 go from 90% at 1700 ➡️ 86% at 1800 [given methylene blue about 30-45 minutes later] ➡️ 88% at 1900 ➡️ 97% at 1935…all cured!
17/ Now you know that the next time you get pulled into a desatting patient’s room, your first question should always be, “did this person just have a TEE?” #justkidding#nobutreally
2/ The transfer 📞 you got was a 28 yo with no other history. They were concerned about her being in status epilepticus.
You turn off all sedation. They're still unresponsive.
3/ Clinically, they're intubated and have fixed and dilated 👀. No corneal or cough and not breathing over the vent. No motor response w/ painful stimuli 🤕
You scan their labs - ✅ no significant abnormalities You check their vitals - ✅ looks all good
1/ There’s a lot of AEDs that work great together to tx szs! Unfortunately, Valproic acid (VPA) and Phenytoin (PHT) are two that didn’t get that memo.
Get ready for a fun and educational two-part #tweetorial on the do not miss VPA and PHT interactions w/ @theABofPharmaC
2/ Let’s go back in time.
Valproic acid was first synthesized in 1882 by Burton. It wasn’t until 1963 when its anticonvulsant properties were discovered by Eymard.
Phenytoin was first synthesized in 1908 by Biltz and discovered to have anticonvulsant properties in 1936
3/ VPA works by ⬆️ GABA lvls and blocking Na and Ca channels. It’s broad-spectrum permits its use for various szs types: partial, tonic clonic, myoclonic, and absence.
PHT works solely by inhibiting Na channels and has a narrower spectrum of use: partial and tonic clonic szs
2/ On quick review, patient was admitted 5 days earlier at the OSH. Initially admitted for encephalopathy that was then c/b seizures the following day. Initial ammonia was normal. CT/CTA unremarkable. MRI brain w/ contrast shows the following abnormality over the R frontal area
3/ Further hx significant for excessive EtOH (~2-3 glasses of wine/day). Recently in the mountains drinking homemade moon shine. He had nausea and vomited ~24-48 hrs later before becoming encephalopathic. Eventually admitted ~4 days later.