Life is Pain, Highness

Noon conference this week was about safe opiate prescribing. I hope that some of you were there and enjoyed it.  As I was making the talk, I felt that I also wanted to learn/teach more about chronic pain and how to treat it.

Most of this information comes from a great TMS (no really) course on Complex Chronic Pain.  If you are interested in the topic, I recommend the course. TMS is here, and you can find the course by searching for V07 Complex Chronic Pain Course. Of course you have to be a VA employee to access TMS.

Do you have patients in your clinic that carry a diagnosis of “Chronic Pain.” Not chronic back pain, or osteoarthritis, or fibromyalgia, but just “chronic pain.” It has been a pet peeve of mine, to label the pain but not the etiology, but turns out that it is a real thing, and our traditional biomedical model just doesn’t do a great job at addressing the issue. We start out with the right things: history and physical, careful testing, conservative treatment. When that doesn’t work, we might refer to a specialist, or PT, or send the patient for injections. Slowly we tread into unproven, non-evidence based therapies, which often don’t work either. Or, the patient feels a little better; often because they felt that they were heard and they believe in the treatment plan, not because the therapy worked.  We keep doing the same things and expecting a different result. the patient feels that their life is on hold while their doctor gets their pain under control. Eventually, the patient gets frustrated with us, we get frustrated with the patient, and the relationship becomes strained.  Often, the patient finds a new doctor and the cycle starts over again.  We are all frustrated and unsatisfied, and we resolve not to do that again.  But we do, because the tools we have are insufficient for the problem

.Components of Chronic Pain

A new way to think about this is from a biopsychosocial model. The root cause of the pain is as much psychosocial and emotional as it is biological, and emotional and social stressors make it worse, just as lifting a refrigerator would. In this model, the doctor has to give up some control, it is really up to the patient to get better. We become the coach, the therapist, rather than the omniscient expert with the prescription pad.  The goal shifts from relieving pain to restoring function and improving health.  Patients move away from a focus on ending pain and minimizing symptoms to “expecting pain” and living their life in spite of that.  The office visit is less about pain control and more about setting and achieving functional goals.  Your job is to teach patients that you hear their frustration and believe that they have pain, but there isn’t a medical solution to this problem, and the two of you are going to work together to help them move on with their life.

there are no magic pills

Chronic pain is aggravated by a variety of things. If you can identify these in your patient, you may be able to help them move forward in recovery. The first is deconditioning: think like an athlete in spring training, they don’t expect to come in at mid-season form. Second is poor coping skills and ineffective stress managment techniques. We should teach that pain is not necessarily leading to more damage, but represents a bump in the road that they will move past.  Pain is inevitable, but misery is optional. Finally, outright mood disorders can aggravate pain. It is reasonable to aggresively seek out and treat these, but in such a way so that the patient doesn’t come away feeling that you don’t believe their pain.

How to help the patient set goals. These need to come from the patient, not you.  Ask about what they want to do, but can’t now.  Listen carefully and pick up on anything that the patient identifies, then try and troubleshoot the barriers.  If they want to exercise, but always have increasing pain, then try and reduce the intensity back to a level that they can acheive. Set goals that seem too easy, too simple, so that you can build on successes- first you have to have successes.  If the patient is not even getting dressed every day, make that a first step. Later they can work toward the gym membership, but if you try and do it all at once, they will end up hurting and less likely to try again.

Goals need to be acheivable, almost easy for the patient. Then build on success.

If you have access, pain psychology or mental health providers can help with cognitive behavioral therapy around coping mechanisms, goal setting, and stress managment techniques.  You can also teach your patient some simple stress managment. Deep breathing and meditation is a simple concept to understand and provides a coping strategy for the patient to deal with pain.  There is an app “Breathe 2 Relax” that teaches deep breathing and website calm.com that does guided imagery relaxation.

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The trick for all of this is getting patients to buy in. They are doing all of the work and the motivation has to come from within. So long as you really listen to their pain story, and have done an adequate evaluation, you don’t necessarily change the treatment plan because of resistance. However, don’t become confrontational, don’t fight.  Pushing hard for patient self managment strategies will often backfire.  Use your best Motivational Interviewing jujitsu to roll with resistance and put the onus to change back onthe patient. They can certainly stay the same, but you might point out that isn’t getting them anywhere.

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Chronic Kidney Disease for the Generalist

 

Protect those nephrons!  From AMR this week, a handy primer on CKD for your continuity clinic.  

When do your patients have CKD? Decline in GFR for >3 months PLUS Evidence of Kidney Disease (evidenced by one of the following)

  • ›Albuminuria
  • ›Urine sediment abnormalities
  • ›Electrolyte and other abnormalities due to tubular disorders
  • ›Abnormalities detected by histology
  • ›Structural abnormalities detected by imaging
  • ›History of kidney transplantation

Figure out what caused it: 75% are HTN and/or Diabetes

  • Glomerular disease
  • Obstructive uropathy
  • Vascular diseases
  • Hepatorenal/cardiorenal syndromes
  • Congenital disease: PKD

Do the workup:

  • GET THE UA  Active sediment/proteinuria vs a bland UA will be a major branch point in your evaluation, so you have to get a UA.  Spot urine protein and creatinine are also useful.
  • US Looking for cystic kidneys, hydronephrosis, asymmetry, or even symmetric evidence of “medical renal disease” is useful.
  • Based on historical clues, you can also check: HIV, hepatitis serologies, SPEP/UPEP, ANA, ANCAs

Stage it: based on GFR. VGFR- MDRD and CKD-EPI are most commonly used formulas. Here’s a handy calculator that gives you both, plus the stage.

Stage Description GFR
1 Kidney damage with nl GFR >90
2 Kidney damage with increased GFR 89-60
3a Moderately decreased GFR 59-45
3b 44-30
4 Severely decreased GFR 29-15
5 Kidney failure <14 or on dialysis

 

Call for Backup: Nephrology Referral

  • You don’t know why the patient has kidney disease
  • It is progressing quickly (loss of 50% of their GFR within one year)
  • Nephrosis: Lots of proteinuria (>3g/day)
  • Nephritis: active urine sediment with blood, protein, casts
  • Dialysis planning: sometime during stage3b is probably ideal, certainly by the time patient has GFR <30
    • Mortality benefit for patients that see nephrology earlier.

OK, now what?  Manage it:

  • Fix reversible causes: remove nephrotoxins, relieve obstruction, treat CHF/Cirrhosis/HIV/Hepatitis
  • Slow progression
    • HTN: JNC8 guidelines recommend goal 140/90
    • DM: ACCORD trial showed benefit with treatment to HbA1c <7.5
    • Add an ACE-inhibitor or ARB if there is proteinuria
  • Aggressive cardiovascular risk reduction (Cardiovascular disease is going to kill these patients before the renal disease does- see graph below)
  • Deal with the complications

CV mortality in CKD

Sarnak M J et al. Circulation. 2003;108:2154-2169

What Complications?

  • Hyperkalemia: Lasix helps
  • Anemia: Replace Iron, consider EPO if Hgb <10
  • Acidosis: consider when serum bicarb <22
  • Volume Overload: Lasix helps
  • Mineral Bone Disease: replace Vitamin D, bind PO4

Great posts by our own Dr.Centor on CKD here (don’t miss the comments) and here.

2012 KDIGO Guidelines for the evaluation and management of CKD.

Unicorn Sighting

Happy guideline season!

I’ve been hearing about JNC 8 for so long, that I thought it didn’t really exist.  Thanks to some persistent hypertension experts, it is here at long last.  Here’s a quick review of the major points. I’m sure that we will see some commentary in the days and weeks to come, I’ll try to keep you updated on that as well.   I’d love to hear what you think- start the conversation in the comments below.

Higher BP targets

We are used to aiming for 140/90 for most people, and 130/80 for those with CKD, diabetes, CAD, and other comorbidities.  But new evidence  has emerged that these may not be so great, particularly for elderly patients.  So JNC 8 says- Adults 18-60 (even with DM or CKD) should aim for BP <140/90.  We can be a little more relaxed with patients over 60, and aim at 150/90 for them, so long as they don’t have CKD or DM.  Most of this change comes because there really was no outcome data for our prior target, and it seems that getting people to the 140s systolic provides just as much benefit as the 130s range.

Relaxed first line medicine choices

We’ve known that this was coming for a while.  JNC 7 recommended thiazides as first line for all, but there was never any real data to back that up.  So JNC 8 says that we can use thiazides, ACE-I/ARBs, or calcium channel blockers as a first choice for most patients.  They do acknowledge the racial difference in response to ACE inhibition, and recommend that we DON’T use ACE/ARB as first line for our black patients. EXCEPT (there’s always an exception) that for patients with chronic kidney disease (but not necessarily diabetes without ckd), use ACE-I first, no matter the race.

Second, and third, and fourth line medicines

Really not much different here, except there are not really recommendations about when to start two medicines at first visit.  JNC 8 says we can pick a variety of treatment strategies– maximize one medicine at a time, add a second agent before maximizing the first, or start two medicines at once.  When you add agents; pick from that first line list (thiazides, ACE/ARB, CCB) until you’ve used them all, then use aldosterone antagonists, beta blockers, central agents, or other vasodilators.  They do recommend avoiding ACE-I and ARB combos for most patients.

What’s Missing

JNC 7 discussed prehypertension, secondary hypertension, resistant hypertension, adherence, how to measure blood pressure, and lots of other related issues. The JNC 8 group just picked 3 questions that they felt were most important: does starting treatment at a particular threshold improve outcomes, does a particular treatment goal improve outcomes, do various drugs have important differences in risk/benefit calculation and outcomes.  Very evidence based and outcome oriented, which is kind of refreshing.

What about my patients now?

For all of us who have been trying to follow JNC 7 (and the subsequent performance measures created from that guideline), should we go adjusting therapy on our patients to meet new targets?  No, say these experts.  If your patient has a blood pressure of <150/90 on their current therapy, and is doing well, no need to change. Stay tuned to see if any of our performance targets change.

A great big picture algorithm from the JNC 8 group is here, and the link to the guidelines themselves is here (on the JAMA website subscription may be needed).

Here’s a great, plain language summary from the NYT Well blog.