Making Good Choices: Sparky
Article by Elana Rybak, DVM, cVMA
On Friday March 1, 2024, we had Sparky, a 6 year-old male neutered Shih Tzu that presented to us through the Pet+E.R. for evaluation of progressive non-ambulatory tetraparesis with obtundation and possible seizure.
After assessing Sparky, Dr. Mannix, our neurologist, decided that she needed an MRI of his brain to see what was going on, with high suspicion of an inflammatory process but also to rule out a space-occupying lesion, or other causes.
Anesthesia considerations:
Due to Sparky's compromised state, I elected to use small doses of reversible and/or short acting medications to anesthetize Sparky for his MRI. I chose the following protocol for him:
Fentanyl 2mcg/kg: This medication is short-acting, has some sedative properties, minimal cardiovascular effects, lowers the volume of induction drug needed for intubation, and is fully reversible.
Midazolam 0.1mg/kg: Sparky had a history of seizure activity - this medication is used as a treatment for seizures. It also has minimal cardiovascular effects, is fully reversible, and is an excellent 'co-induction' drug to allow lower doses of induction medication needed for intubation. This dose was lowered (I usually use 0.2mg/kg) due to Sparky's fragile state.
Propofol to effect: Sparky needed only a very small dose (15mg) for intubation.
Sparky was then maintained on Isoflurane (between 1.4 - 1.6%) for the duration of his anesthesia. He did not require manual ventilation.
During anesthesia, we noted that Sparky's End Tidal CO2 was staying around 26mmHg, and we were not able to correct this.
Sparky's blood pressure during anesthesia started out good (MAP=80), dropped a bit mid-MRI (MAP=60), Iso was decreased and then BP came back up (MAP=100).
When it was time to recover Sparky, we did give him a dose of Naloxone to reverse any residual effects of the Fentanyl. We did not reverse the Midazolam since there was possible risk of seizure activity. Sparky was able to be extubated within ~10-15 minutes.
Some things to think about with this case:
Sparky's ASA Status:
Sparky was a pretty high anesthetic risk case. I categorized him as an ASA Class 4 (High risk, significantly compromised by disease). I put him in Class 4 because he was starting to slightly improve after his HTS and Mannitol. You could certainly argue he was ASA Class 5 (A moribund patient who is not expected to survive without the procedure).
(ASA Classes and examples: https://www.thinkanesthesia.education/sites/default/files/2021-03/US%20-%20ASA%20physical%20Status%20Classification%20Chart%20-%20%20V2.pdf)
Sparky's Premedication:
I chose Fentanyl as my opioid. Another potential option could have been Butorphanol, however it is longer-acting with heavier sedation properties which we didn't necessarily need or want in this case. I also did not want Hydromorphone or Methadone in this case because those are more likely to cause panting and/or vomiting. Panting and vomiting can increase intracranial pressure (ICP), and Sparky already had increased ICP which we did not want to exacerbate further.
Why didn't I just give Sparky a big dose of Propofol? This would have very likely caused apnea as well as a big swing in his BP, which was already at high risk of being unstable due to his high intracranial pressure.
Why not Alfaxalone? Alfaxalone would have been completely OK to use here.
I would just keep in mind that Alfaxalone can sometimes cause paddling, tremoring and twitching behaviors, which may be confused with seizure in this type of patient. Propofol can also cause some twitching but generally not as profound in my experience, especially in recovery. Personally, I prefer to use Propofol in these types of 'brain' cases but use what you are more comfortable with!
Sparky's Blood Pressure:
In cases where we have brain swelling and therefore increased Intracranial Pressure, we see something called a 'Cushing Reflex'. The Cushing Reflex is often seen as a 'triad' consisting of
hypertension (often with widened pulse pressure - increasing systolic, decreasing diastolic),
bradycardia, and
irregular respirations.
During anesthesia, in my experience, these patients will often do one of two things: Beautifully maintain their BP during the entire anesthetic time, OR their BP will be all over the place and VERY difficult to manage.
Luckily for us, Sparky's blood pressure stayed within normal parameters with minimal intervention.
Sparky's End Tidal CO2:
One of the big things we worry about when anesthetizing patients with brain lesions is their EtCO2. This is because ELEVATED EtCO2 causes cerebral vasodilation which in turn can increase intracranial pressure. So, when we anesthetize patients with suspected increased ICP, we often will hyperventilate them to achieve an EtCO2 of approximately 35mmHg.
In Sparky's case, his EtCO2 was already quite low. His RR was mostly in the low to mid 20's - mildly tachypneic for an anesthetized patient. To check if this was real and/or if we could manage it better, we tried a few things: We re-zero'd the EtCO2 monitor - no change. We tried slower manual ventilation to see if that helped normalize his EtCO2 - this didn't help. We did not think we had an endobronchial intubation, but if we were concerned we could have tried backing out the ETT a bit (before you ask - I have seen endobronchial intubation cause hi, low, or normal EtCO2!).
Since Sparky was otherwise doing OK, we just allowed him to continue to breathe on his own and not intervene further with his respiration.
So why was his EtCO2 so low? Possible causes in Sparky's case could have been an acid/base imbalance (metabolic acidosis can occur from hypertonic saline administration) and/or lactic acidosis. Sparky also had such an altered respiratory drive from his brain swelling that this was likely contributing to the low EtCO2.
In general, Respiratory Alkalosis (where the body’s pH is elevated to greater than 7.45 due to a respiratory process, usually hyperventilation - which we can see as low EtCO2), is not itself life-threatening, however the systemic cause for it can be.