Post-op opioid use s/p TKA/THA.

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An elevated PCS predicts it better than anything else. So, let's say you get it and it's >30. If no contra-indications do you beta block preop? Interestingly, beta blockers have a down regulating effect in the
amygdala.

http://onlinelibrary.wiley.com/doi/10.1002/acr.23091/full

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An elevated PCS predicts it better than anything else. So, let's say you get it and it's >30. If no contra-indications do you beta block preop? Interestingly, beta blockers have a down regulating effect in the
amygdala.

http://onlinelibrary.wiley.com/doi/10.1002/acr.23091/full


People who get beta blockers during joint surgery are older and sicker than those who do not, hence less opiate given/needed. Though I do agree with the general idea that beta blockers (and anti sympathomimetics like precedex/clonidine) do help with pain on some deep level. I give beta blocker for CV hemodynamics only not pain. If you start giving BB preop empirically get ready for intraop hypotension and possibly bad outcomes in the older folks who need to keep their presssure UP during anesthesia and blood loss.
 
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you cant make the presumption that beta blocker initiation preop would lead to decreased opioid use postoperatively based on that review. and there is no definitive cause/effect with beta blockers.

fyi, just look at the history of preoperative beta blockers, having gone from a Class 1 to a 11a or even "needing further research" status.

http://circ.ahajournals.org/content/130/24/2246

(please note that preoperative initiation of beta blockers has been associated previously with reduced risk of nonfatal MI, but also associated with increased risk of all cause mortality, including stroke, death...)
 

"These findings suggest that many FMS and TMD patients have dysregulated activity of the SNS that may directly contribute to their clinical myalgic pain as well as to alterations in their cardiovascular and catecholamine responses at rest and during stressors. Our results also indicate that some aspects of this SNS dysregulation, including pain symptoms, can be temporarily improved through use of low doses of the nonselective beta-antagonist, propranolol."

These findings, if substantiated, argue against FMS and CS being caused by characterological deficits and bad child rearing practices...
 
Equating BFI traits with 'characterological deficits' is your thesis, not mine and not in the BFI literature. I view your trolling my posts as arc de cercle reflex to my opposition to your view of all pain as a result of a nociceptor firing in the periphery:)
 
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...your view of all pain as a result of a nociceptor firing in the periphery:)

Which I don't believe at all...

Semin Arthritis Rheum. 2012 Feb;41(4):556-67. doi: 10.1016/j.semarthrit.2011.08.001. Epub 2011 Oct 28.
Central sensitization in patients with rheumatoid arthritis: a systematic literature review.
Meeus M1, Vervisch S, De Clerck LS, Moorkens G, Hans G, Nijs J.
Author information

Abstract
OBJECTIVE:
The goal of the present study is to systematically review the scientific literature addressing central sensitization and central nociceptive processing in patients with rheumatoid arthritis (RA).

METHODS:
To identify relevant articles, we searched PubMed and Web of Science. The search strategy was a combination of terms of the following groups: "Rheumatoid arthritis," inflammatory joint pain, or arthritis; AND (central) sensitization, (central) hypersensitivity, central hyperexcitability, pain modulation, pain processing, neural inhibition, or pain physiopathology; AND pain, nociception, hyperalgesia, pain threshold, or algometry. Articles fulfilling the inclusion criteria were screened for methodologic quality with specific checklists to evaluate different study designs (2 independent raters).

RESULTS:
Twenty-four full-text articles were included, of which the majority were case-control studies, followed by nonsystematic reviews, cross-sectional studies, and case reports. Methodologic quality was very heterogeneous. Preliminary evidence for generalized hyperalgesia in RA is available. In addition, the mechanism behind impaired central nociceptive processing remains rather obscure. The role of cytokines and neuropeptides especially remains to be elucidated. Windup appears to develop more easily in RA, but evidence in support of impaired nociceptive inhibition and cognitive emotional sensitization (sensitization due to cognitive bias) is scarce.

CONCLUSIONS:
The symmetrical manifestation of the disease, the poor relation between disease activity and symptoms, and the generalized hyperalgesia at both articular and nonarticular sites for different kinds of stimuli are indicative of the presence of central sensitization in RA patients. Further research is required to provide firm evidence in support of various aspects of central sensitization in humans with RA.
 
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