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How long do you think that the saturation of the NMDA receptors lasts? What about multiple intra-operative painful episodes?

These questions were generated by one of my list's recipients, Alan Cohen, a friend and thoughtful anesthesiologist colleague, who may have expressed a sentiment that many others, who either read my blog or receive my list, also had.

Consider, for a moment, what's the largest organ in the body? The skin.

So, what organ also has the largest cortical representation of the homunculus? The skin.

What surgical 'specialty' performs most of its procedures on the skin? Plastic surgeons, ENT cosmetic surgeons, dermatologic surgeons, etc.

For whom have I been giving anesthesia exclusively these past 17 years and providing only PK MAC? Plastic surgeons, cosmetic surgeons, dermatologic surgeons, etc.

Are you beginning to suspect the next question might be, what organ has the most sensory nerves invested in it? You would be right again: the skin.

If I have had no contract (and I have not), what has secured my economic viability? The quality of the outcomes of my PK MAC.

IF the primary stimulus for the cascade of negative neuropeptides and G-d-knows-what-else happens within the brain chemistry is the 'violation' of the outer membrane (the skin) of the body (my belief),

and the blockade of the NMDA receptors for that stimulus only occurs by saturating them with 50 mg ketamine 3 minutes prior to stimulation @ BIS <75 (my belief validated by 17 years clinical experience with 5,000 patients and my personal surgical experience),

then, it may matter little what happens within the body's envelope during the surgery
relative to the actual duration of the NMDA blockade of the 50 mg ketamine.

The bonus, of course, is the postoperative continuation of the blockade of the skin sensory nerves by pre-closure wound instillation of bupivicaine.

FWIW, the duration of the dissociative period of the 50 mg ketamine for injection of local anesthesia varies between 10-20 minutes.

Clearly, that duration is insufficient to explain the postoperative course of either my THR or my 5,000 patients' experiences.

Bottom line: Only by clinical trial with your own patients can you decide 'Is it nifty to give fifty?'
You have virtually nothing to lose* (under GA, all of your patients will be BIS <60 and most will likely be <45 anyway) and everything to gain for your patients by trying.

    *Friedberg BL: Hypnotic doses of propofol block ketamine induced hallucinations.
Plast Reconstr Surg 91:196, 1993.

In my answer, I hope you understand that I make no claim of 'science,' only that which I have clinically observed professionally and personally over the past 17 years, as well as that which I have published in peer-reviewed journals and in my Cambridge University Press published anesthesia textbook, 'Anesthesia in Cosmetic Surgery.'

As Christian Apfel said about the 0.6% PONV outcomes reported in my 1999 5 year review of PK MAC* in his PONV chapter in the 2010 Millers 'Anesthesia:'

    "However, the lack of a control group in this study* necessitates a cautious interpretation. Nevertheless, this result is in accordance with small scale, high quality randomized controlled trials, such as the comparison of anesthetic techniques by White and colleagues."

Any time PK MAC gets favorably compared by Dr. Apfel to the legendary Paul White's work, and my non-emetogenic technique's (NO anti-emetics) PONV rate is 10X better than White's 'multi-modal' anti-emetic PONV protocol on the pages of Miller's 'Anesthesia, I can only say,

'PK MAC doesn't really need any greater validation.'
 

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