Hip injection

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epidural man

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i haven't been around for ever but I don't think I'm such a newbie either. I think I do an ok job at keeping up on concepts and new articles.

However, I heard something today that was a completely new concept to me. I'm a little embarrassed to admit it.....but my colleague mentioned how intra-articulate steroid injections in the hip have been shown to be an independent risk factor for post op infection with hip replacement regardless of time course. wow!

I was leaning toward RF of obturator and articulating branch from femoral anyway, this totally pushes me over.
ThoughtS?
 
depends on the study....

Increased risk studies:
http://www.ncbi.nlm.nih.gov/pubmed/25250699
Arthritis Rheumatol. 2015 Jan;67(1):162-8. doi: 10.1002/art.38886.
Intraarticular hip injection and early revision surgery following total hip arthroplasty: a retrospective cohort study.
Ravi B1, Escott BG, Wasserstein D, Croxford R, Hollands S, Paterson JM, Kreder HJ, Hawker GA.
Author information
Abstract

OBJECTIVE:
Therapeutic intraarticular injections are used in the management of hip osteoarthritis (OA). Some studies suggest that their use increases the risk of infection and subsequent revision surgery after primary total hip arthroplasty (THA), while others do not. We undertook this study to clarify the relationship between prior intraarticular injection and the risk of complication in a subsequent primary THA.

METHODS:
In a cohort of patients with hip OA who underwent a primary elective THA between 2002 and 2009, we identified those who received ≥1 intraarticular injection performed by a radiologist in the 5 years preceding their THA. Multivariable Cox proportional hazards models were used to determine the relationship between receipt of a presurgical injection (no injection, 1-5 years prior to THA, or <1 year prior to THA) and the occurrence of postsurgical joint infection and revision THA in the following 2 years, while controlling for confounders.

RESULTS:
Of 37,881 eligible THA recipients, 2,468 (6.5%) received an intraarticular injection performed by a radiologist within 5 years of their THA (1,691 at <1 year, 777 at 1-5 years). Controlling for age, sex, comorbidity, frailty, income, and provider volume, those who had an injection in the year preceding surgery were at increased risk of infection (adjusted hazard ratio
1.37, P = 0.03) and revision THA (adjusted HR 1.53, P = 0.03) within 2 years of the primary THA, relative to patients who did not. The association between prior injection and revision arthroplasty was attenuated and became nonsignificant (adjusted HR 1.41, P = 0.13) after occurrence of postoperative infection was controlled for in the regression model. No effect was found for injection 1-5 years prior to surgery.

CONCLUSION:
Intraarticular injection in the year preceding THA independently predicted increased risk of infection leading to early revision surgery. Further studies are warranted to elucidate explanations for these findings.


http://www.ncbi.nlm.nih.gov/pubmed/25391629

J Orthop Surg Res. 2014 Nov 13;9:107. doi: 10.1186/s13018-014-0107-2.
Dose intraarticular steroid injection increase the rate of infection in subsequent arthroplasty: grading the evidence through a meta-analysis.
Xing D1, Yang Y2, Ma X3, Ma J4, Ma B5, Chen Y6.
Author information
Abstract

BACKGROUND:
Intraarticular steroid injections are widely used in joint arthritis. However, the data regarding an association between an increased risk for arthroplasty infection after an intraarticular steroid injection are still conflicting. We conducted a meta-analysis to evaluate the evidence from relevant studies that examine the relation between intraarticular steroid injections and infection rates in subsequent joint arthroplasty and to develop GRADE based recommendations for using the steroid before arthroplasty.

METHODS:
A systematic search of all studies published through August 2014 was conducted using the MEDLINE, EMBASE, OVID, ScienceDirect and Cochrane CENTRAL databases. The relevant studies that examined the relation between intraarticular steroid injections and infection rates in subsequent joint arthroplasty were identified. Demographic characteristics, infection rates and clinical outcomes were manually extracted from all of the selected studies. The evidence quality levels and recommendations were assessed using the GRADE system.

RESULTS:
Eight studies looking at hip and knee arthroplasties were included. Meta-analysis showed that patients with steroid injection before arthroplasty had a higher deep infection rate than patients without steroid injection (OR = 2.13, 95% CI 1.02-4.45), but no significant effect on superficial infection rate (OR = 1.75, 95% CI 0.74-4.16). The overall GRADE system evidence quality was very low, which lowers our confidence in their recommendations.

CONCLUSIONS:
Intraarticular steroid injections may lead to increased deep infection rates of subsequent joint arthroplasty but not the superficial infection rates. Due to the poor quality of the evidence currently available, further studies are still required.

Maybe Not:
http://www.ncbi.nlm.nih.gov/pubmed/25298367


Send to:


Med Sci Monit. 2014 Oct 9;20:1878-83. doi: 10.12659/MSM.890750.
Does previous intra-articular steroid injection increase the risk of joint infection following total hip arthroplasty or total knee arthroplasty? A meta-analysis.
Wang Q1, Jiang X2, Tian W3.
Author information
Abstract

BACKGROUND:
Joint infection might be one of the rare but serious complications following a total knee or hip arthroplasty (TKA, THA). A previous intra-articular steroid injection was considered as a risk factor. The purpose of present study was to access the effects of ipsilateral intra-articular steroid injection followed by TKA or THA on the incidence of infections later.

MATERIAL AND METHODS:
Clinical studies reporting infection in THA or TKA after previous injection of intra-articular steroid were identified from the online database of PubMed, Embase, the Cochrane Library, and additional manual searches until July 2013. The pooled effects were measured by risk difference (RD), together with 95% confidence intervals (CIs).

RESULTS:
A total of 11 related studies met our inclusion criteria. The final meta-analysis investigated 6 clinical studies designed as retrospectively created cohort studies with control groups, involving 1474 participants reporting 14 deep infections and 72 superficial infections. Compared with the control group, there was no significantly increased rate of infection among the participant with steroid injection prior to THA or TKA, with corresponding RD (95% CIs) of 0.01 (-0.01, 0.02) for deep infection, 0.01 (-0.02, 0.03) for superficial infection, and 0.02 (-0.02, 0.07) for total infection. The data from 3 prospective studies without control groups and 2 case-control studies were consistent with the results of our meta-analysis.

CONCLUSIONS:
No increased risk of infection among patients who received steroid injections prior to the surgery was identified from the present evidence. A multicenter prospective study with more defined variables is needed further investigate this issue.
 
dont do a shot within 3 months of a planned hip replacement.

some surgeons are sticklers, who dont want a shot within a year, or ever for that matter. however, i think they do this mainly to increase their surgery rate.
 
in that respect, the studies suggesting there is no relationship are of similar quality...

careful and thorough patient counselling is the best course of action, and using an injection is to prevent surgical intervention, imho.
 
Just wanted a quick opinion. You all would consider this a good arthrogram correct?
 

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Excellent arthrogram.
 
Yup.....i tend to place some close to the area of worse djd as well....usually superolateral
 
Yup.....i tend to place some close to the area of worse djd as well....usually superolateral
Thanks... and how do you place the medication superolaterally? I always land my needle on the neck/head junction or a little higher of the head.
 
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It helps to cover the capsule as well as get in the joint. The capsule is what gives the joint its ROM. The earliest sign of OA is ROM reduction and biopsies show inflammatory mediators in the capsule prior to OA changes.
 
It helps to cover the capsule as well as get in the joint. The capsule is what gives the joint its ROM. The earliest sign of OA is ROM reduction and biopsies show inflammatory mediators in the capsule prior to OA changes.

So getting in the joint and having the medicine in total contact with the internal component of the capsule isn't good enough? GO on....
 
So getting in the joint and having the medicine in total contact with the internal component of the capsule isn't good enough? GO on....

No it isn't. You are free to do your own research project on it. Do you really perform only IA injections on everybody with a joint pain? smh
 
No it isn't. You are free to do your own research project on it. Do you really perform only IA injections on everybody with a joint pain? smh

Xray with moderate to severe OA, + hip scour and FABER on exam. Then inject. Literature proves PT useless for hip oA. I can sometimes get visco approved. Alternative is fem/obt block and RF or THA.

But I have never heard of spraying the hip capsule as a procedure for anything.
 
How do you get visco approved? Sometimes I attempt to inject the knee and I miss and it lands in the hip by accident.

So what are you going to do when someone has hip pain, radiographs don't show OA changes yet, but there is diminished ER or IR? I don't waste anyone's time with P.T. either, agree. RF seems a little aggressive. A capsule injection is like prolo without the nonsense of laxity.
 
How do you get visco approved? Sometimes I attempt to inject the knee and I miss and it lands in the hip by accident.

So what are you going to do when someone has hip pain, radiographs don't show OA changes yet, but there is diminished ER or IR? I don't waste anyone's time with P.T. either, agree. RF seems a little aggressive. A capsule injection is like prolo without the nonsense of laxity.

the limited ROM MIGHT be due to capsular tightness, but that certainly is not the only factor. bony block from osteophystes, tight adductors, etc can contribute. how do you
"inject" the capsule if it a 360 degree structure thats 5 inches long? does not compute
 
The topic is hip pain from joints that don't have OA changes on imaging, meaning no osteophytes. Tight adductors aren't causing diminished IR with pain laterally. So you're 0/2. You can put medication on the capsular insertion on one side of the joint and not the other. It can be done under US because you can see it. You can see the acetabulum under fluoro as well. So you guys only inject joint spaces?
 
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The topic is hip pain from joints that don't have OA changes on imaging, meaning no osteophytes. Tight adductors aren't causing diminished IR with pain laterally. So you're 0/2. You can put medication on the capsular insertion on one side of the joint and not the other. It can be done under US because you can see it. You can see the acetabulum under fluoro as well. So you guys only inject joint spaces?

Hip area: IA, GTB, IB, GM tendon, pudendal nerve.

Never heard of splashing the capsule.
 
Okay. Does capsulitis only mean the person who can't move their shoulder?

You must recognize the hole in your practice pattern though right? Someone without
Xray with moderate to severe OA, + hip scour and FABER on exam. Then inject.
gets an RF? Please. It wouldn't be my hip or any of my family members that I actually talk to. All I can gather is if someone has pain without OA changes you guys presume its from other places than the joint even with diminished ROM and joint tenderness. Mid-40s patient, normal ER, painful IR, normal HF, not appreciably tender over the GT but tender just superior to it. This isn't a rare species.
 
Okay. Does capsulitis only mean the person who can't move their shoulder?

You must recognize the hole in your practice pattern though right? Someone without gets an RF? Please. It wouldn't be my hip or any of my family members that I actually talk to. All I can gather is if someone has pain without OA changes you guys presume its from other places than the joint even with diminished ROM and joint tenderness. Mid-40s patient, normal ER, painful IR, normal HF, not appreciably tender over the GT but tender just superior to it. This isn't a rare species.


it looks like you are trying to suggest that there is an entity called "frozen hip" -- akin to adhesive capulitis in the shoulder or frozen shoulder.

interstesting, but ive never heard of it.

even if there is capsular tightness, i still dont see how you inject "the capsule as it attaches on the lateral hip joint/(femur)". this is still a 360 degree attachment. in the frozen shoulder, you just inject the shoudler -- maybe put in more volume to distend the capsule and break up the adhesions. you cant inject a piece of paper -- it is a 2 dimensional structure.
 
I'm saying the capsule gives a joint its range, I think we can agree on that. If a capsule was made of steel there would be ROM of zero. A capsule made of a Slinky there would be no end range. A capsulitis has a range of severity from severe and "adhesive" with ROM greatly reduced to mild with milder symptoms. I think we can also agree the capsule of any joint can be a pain generator, even a facet. How many times have we heard the facet capsule is "richly innervated"?

The capsule is discrete under US. You can put the medication right on top of it and avoid exposing cartilage to steroid.
 
I'm saying the capsule gives a joint its range, I think we can agree on that. If a capsule was made of steel there would be ROM of zero. A capsule made of a Slinky there would be no end range. A capsulitis has a range of severity from severe and "adhesive" with ROM greatly reduced to mild with milder symptoms. I think we can also agree the capsule of any joint can be a pain generator, even a facet. How many times have we heard the facet capsule is "richly innervated"?

The capsule is discrete under US. You can put the medication right on top of it and avoid exposing cartilage to steroid.

fair enough, but i would think that both the inside and outside of the capsule are symmetrically innervated, so one would need to coat both sides. sounds like you could get a 20610 as well as a 20551 out of it. the only difference is that medication injected inside the joint capsule stays there, but medication injected outside of it would just float away.
 
My texts and pubmeds do not show me what you are talking about.

What, that a capsule causes pain or putting medication to it can help? Saw it in an old ortho book years ago. So what. The regenerative medicine course in San Diego mentioned OA beginning as capsular tightness also. Makes complete sense in the right circumstances.
 
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These guidelines suggest that physical therapy can be helpful for select patients with hip pain caused by hip OA. http://www.orthopt.org/uploads/cont...eficits___Hip_Osteoarthritis___April_2009.pdf

Anectdotally I will say that I can be helpful to a person in designing a "prehab" program (i.e. in preparation for upcoming THA, or one that is likely in the future IMO), and in sizing and training in the proper use of an appropriate assistive device (i.e. walking stick vs cane vs FWW vs 4WW).

Further, there's little to no evidence to support or negate what I do for people with non OA hip pain, yet anectdotally I would bet it's a lot more helpful (i.e. Post-lat hip muscle insertion tendinitis). A lack of evidence is not evidence of a lack of benefit however. http://www.orthopt.org/uploads/cont...._Nonarthritic_Hip_Joint_Pain___June_2014.pdf

I always wonder what you guys base your opinions on physical therapy with regard to this or that. Patient report? Likely to be skewed with imaging and interventions at the ready ("if 'the PT' isn't working") on f/u's with you guys.

Not to mention the uselessness of the diagnosis of Hip OA based on imaging and then assuming this is the cause of the person's pain/problem.
 
Effect of Physical Therapy on Pain and Function in Patients With Hip OsteoarthritisA Randomized Clinical Trial FREE
Kim L. Bennell, PhD1; Thorlene Egerton, PhD1; Joel Martin, BAppSc1; J. Haxby Abbott, PhD2; Ben Metcalf, BSci1; Fiona McManus, BPhysio1; Kevin Sims, PhD3; Yong-Hao Pua, PhD4; Tim V. Wrigley, MSc1; Andrew Forbes, PhD5; Catherine Smith, MSc (Applied Statistics)5; Anthony Harris, MSc6; Rachelle Buchbinder, PhD7,8

JAMA. 2014;311(19):1987-1997. doi:10.1001/jama.2014.4591.


Importance There is limited evidence supporting use of physical therapy for hip osteoarthritis.

Objective To determine efficacy of physical therapy on pain and physical function in patients with hip osteoarthritis.

Design, Setting, and Participants Randomized, placebo-controlled, participant- and assessor-blinded trial involving 102 community volunteers with hip pain levels of 40 or higher on a visual analog scale of 100 mm (range, 0-100 mm; 100 indicates worst pain possible) and hip osteoarthritis confirmed by radiograph. Forty-nine patients in the active group and 53 in the sham group underwent 12 weeks of intervention and 24 weeks of follow-up (May 2010-February 2013)

Interventions Participants attended 10 treatment sessions over 12 weeks. Active treatment included education and advice, manual therapy, home exercise, and gait aid if appropriate. Sham treatment included inactive ultrasound and inert gel. For 24 weeks after treatment, the active group continued unsupervised home exercise while the sham group self-applied gel 3 times weekly.

Main Outcomes and Measures Primary outcomes were average pain (0 mm, no pain; 100 mm, worst pain possible) and physical function (Western Ontario and McMaster Universities Osteoarthritis Index, 0 no difficulty to 68 extreme difficulty) at week 13. Secondary outcomes were these measures at week 36 and impairments, physical performance, global change, psychological status, and quality of life at weeks 13 and 36.

Results Ninety-six patients (94%) completed week 13 measurements and 83 (81%) completed week 36 measurements. The between-group differences for improvements in pain were not significant. For the active group, the baseline mean (SD) visual analog scale score was 58.8 mm (13.3) and the week-13 score was 40.1 mm (24.6); for the sham group, the baseline score was 58.0 mm (11.6) and the week-13 score was 35.2 mm (21.4). The mean difference was 6.9 mm favoring sham treatment (95% CI, −3.9 to 17.7). The function scores were not significantly different between groups. The baseline mean (SD) physical function score for the active group was 32.3 (9.2) and the week-13 score was 27.5 (12.9) units, whereas the baseline score for the sham treatment group was 32.4 (8.4) units and the week-13 score was 26.4 (11.3) units, for a mean difference of 1.4 units favoring sham (95% CI, −3.8 to 6.5) at week 13. There were no between-group differences in secondary outcomes (except greater week-13 improvement in the balance step test in the active group). Nineteen of 46 patients (41%) in the active group reported 26 mild adverse effects and 7 of 49 (14%) in the sham group reported 9 mild adverse events (P = .003).

Conclusions and Relevance Among adults with painful hip osteoarthritis, physical therapy did not result in greater improvement in pain or function compared with sham treatment, raising questions about its value for these patients.
 
Effect of Physical Therapy on Pain and Function in Patients With Hip OsteoarthritisA Randomized Clinical Trial FREE
Kim L. Bennell, PhD1; Thorlene Egerton, PhD1; Joel Martin, BAppSc1; J. Haxby Abbott, PhD2; Ben Metcalf, BSci1; Fiona McManus, BPhysio1; Kevin Sims, PhD3; Yong-Hao Pua, PhD4; Tim V. Wrigley, MSc1; Andrew Forbes, PhD5; Catherine Smith, MSc (Applied Statistics)5; Anthony Harris, MSc6; Rachelle Buchbinder, PhD7,8

JAMA. 2014;311(19):1987-1997. doi:10.1001/jama.2014.4591.


Importance There is limited evidence supporting use of physical therapy for hip osteoarthritis.

Objective To determine efficacy of physical therapy on pain and physical function in patients with hip osteoarthritis.

Design, Setting, and Participants Randomized, placebo-controlled, participant- and assessor-blinded trial involving 102 community volunteers with hip pain levels of 40 or higher on a visual analog scale of 100 mm (range, 0-100 mm; 100 indicates worst pain possible) and hip osteoarthritis confirmed by radiograph. Forty-nine patients in the active group and 53 in the sham group underwent 12 weeks of intervention and 24 weeks of follow-up (May 2010-February 2013)

Interventions Participants attended 10 treatment sessions over 12 weeks. Active treatment included education and advice, manual therapy, home exercise, and gait aid if appropriate. Sham treatment included inactive ultrasound and inert gel. For 24 weeks after treatment, the active group continued unsupervised home exercise while the sham group self-applied gel 3 times weekly.

Main Outcomes and Measures Primary outcomes were average pain (0 mm, no pain; 100 mm, worst pain possible) and physical function (Western Ontario and McMaster Universities Osteoarthritis Index, 0 no difficulty to 68 extreme difficulty) at week 13. Secondary outcomes were these measures at week 36 and impairments, physical performance, global change, psychological status, and quality of life at weeks 13 and 36.

Results Ninety-six patients (94%) completed week 13 measurements and 83 (81%) completed week 36 measurements. The between-group differences for improvements in pain were not significant. For the active group, the baseline mean (SD) visual analog scale score was 58.8 mm (13.3) and the week-13 score was 40.1 mm (24.6); for the sham group, the baseline score was 58.0 mm (11.6) and the week-13 score was 35.2 mm (21.4). The mean difference was 6.9 mm favoring sham treatment (95% CI, −3.9 to 17.7). The function scores were not significantly different between groups. The baseline mean (SD) physical function score for the active group was 32.3 (9.2) and the week-13 score was 27.5 (12.9) units, whereas the baseline score for the sham treatment group was 32.4 (8.4) units and the week-13 score was 26.4 (11.3) units, for a mean difference of 1.4 units favoring sham (95% CI, −3.8 to 6.5) at week 13. There were no between-group differences in secondary outcomes (except greater week-13 improvement in the balance step test in the active group). Nineteen of 46 patients (41%) in the active group reported 26 mild adverse effects and 7 of 49 (14%) in the sham group reported 9 mild adverse events (P = .003).

Conclusions and Relevance Among adults with painful hip osteoarthritis, physical therapy did not result in greater improvement in pain or function compared with sham treatment, raising questions about its value for these patients.
10 treatment sessions in 12 weeks, when does that happen besides never? Try 10 in 4 weeks and it would be a lot more representative of what actually takes place in real life. How did these people determine if the hip OA was actually the factor or a large factor in the patient symptoms? Did these people study for significance with patients being sub grouped (i.e. Less vs more severe on imaging? Less vs more severe pain? Patients with strong preconceived ideas about the effectiveness of physical therapy versus those without?). In my experience I don't know of a more difficult person to treat than someone who "knows" that "this isn't going to help me" because how is this going to "fix" the hip OA? The sham treatment isn't a sham at all IMO given the strong placebo effect that ultrasound and other such magic can have on people (BTW patients cannot tell if an ultrasound machine is on or off). Did they sham it on the treatment group as well?

I favor guidelines written about and by physical therapists based on all the evidence. The above study is flawed. What study is next? Injections for OA at 1/3 the medication dosage and then say that means practice patterns at 3x the dosage are ineffective?
 
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10 treatment sessions in 12 weeks, when does that happen besides never? Try 10 in 4 weeks and it would be a lot more representative of what actually takes place in real life. How did these people determine if the hip OA was actually the factor or a large factor in the patient symptoms? Did these people study for significance with patients being sub grouped (i.e. Less vs more severe on imaging? Less vs more severe pain? Patients with strong preconceived ideas about the effectiveness of physical therapy versus those without?). In my experience I don't know of a more difficult person to treat than someone who "knows" that "this isn't going to help me" because how is this going to "fix" the hip OA? The sham treatment isn't a sham at all IMO given the strong placebo effect that ultrasound and other such magic can have on people (BTW patients cannot tell if an ultrasound machine is on or off). Did they sham it on the treatment group as well?

I favor guidelines written about and by physical therapists based on all the evidence. The above study is flawed. What study is next? Injections for OA at 1/3 the medication dosage and then say that means practice patterns at 3x the dosage are ineffective?

ive never had a patient with moderate to severe OA of the hip get any pain relief or functional benefit with PT. N=300 or so
 
10 treatment sessions in 12 weeks, when does that happen besides never? Try 10 in 4 weeks and it would be a lot more representative of what actually takes place in real life. How did these people determine if the hip OA was actually the factor or a large factor in the patient symptoms? Did these people study for significance with patients being sub grouped (i.e. Less vs more severe on imaging? Less vs more severe pain? Patients with strong preconceived ideas about the effectiveness of physical therapy versus those without?). In my experience I don't know of a more difficult person to treat than someone who "knows" that "this isn't going to help me" because how is this going to "fix" the hip OA? The sham treatment isn't a sham at all IMO given the strong placebo effect that ultrasound and other such magic can have on people (BTW patients cannot tell if an ultrasound machine is on or off). Did they sham it on the treatment group as well?

I favor guidelines written about and by physical therapists based on all the evidence. The above study is flawed. What study is next? Injections for OA at 1/3 the medication dosage and then say that means practice patterns at 3x the dosage are ineffective?

please share your preferred literature justifying your argument.
 
please share your preferred literature justifying your argument.
The study itself that I was talking about justifies my arguments. I've already posted other literature above that justifies my argument that physical therapy is not useless for hip OA induced hip pain in all cases. Here that is again, the references that justify the guidelines are on pages 20-25 (? 216 studies, vs one flawed "study" probably funded by some orthopedic surgeon association that you guys cited). http://www.orthopt.org/uploads/cont...eficits___Hip_Osteoarthritis___April_2009.pdf

Here's another reference regarding variables that predict success of physical therapy for hip OA http://m.ptjournal.apta.org/content/91/4/510.short
 
I've always thought - without real proof besides a few things I've seen studied on the subject - that peri-articular injections are just as effective as intra-articular injections.

Does the joint make a difference? Who knows...SI joint and facet joint - most likely doesn't matter. Hip or knee or shoulder? Hmmm.....perhaps.

I will say that what we think is a mechanism of action - that seems really intuitive often turns out to be completely false when a mechanism if finally elicudated.

I heard from a pain physicain who heard from a ortho guy that thought that the reason RF of the hip innervation helps - not because of nerve destruction, but because the RF energy burns the capsule - causing it to shrink - tightning up the capsule which presumably was stretched and causing pain. Interesting theory - but what if it actually was true?
 
I've always thought - without real proof besides a few things I've seen studied on the subject - that peri-articular injections are just as effective as intra-articular injections.

Does the joint make a difference? Who knows...SI joint and facet joint - most likely doesn't matter. Hip or knee or shoulder? Hmmm.....perhaps.

I will say that what we think is a mechanism of action - that seems really intuitive often turns out to be completely false when a mechanism if finally elicudated.

I heard from a pain physicain who heard from a ortho guy that thought that the reason RF of the hip innervation helps - not because of nerve destruction, but because the RF energy burns the capsule - causing it to shrink - tightning up the capsule which presumably was stretched and causing pain. Interesting theory - but what if it actually was true?
I know you're just using that as an example to highlight your point re: mechanism of action, but why/how would a hip capsule ever get stretched out in the first place? It's not like it's a shoulder and is moved through a huge arc of motion and put in extreme positions.
 
I know you're just using that as an example to highlight your point re: mechanism of action, but why/how would a hip capsule ever get stretched out in the first place? It's not like it's a shoulder and is moved through a huge arc of motion and put in extreme positions.
If you're a gymnast it does 😉
 
The usual examination does not support capsular laxity. People with OA/joint pain have decreased motion.
Yes. My point exactly. The ortho mentioned in the previous post sounds like they are clinging to an analogy they were making about shoulder multi-directional instability which was treated with thermal capsuloraphy about 15-20 years ago.
 
If you're a gymnast it does 😉
True - but gymnasts are not the patients who are typically coming to me with a diagnosis of OA, or with physical exam findings consistent with hip pain due to degenerative processes. Of if they are, they're coming to the clinic several decades after they stopped gymnastics at which point they actually have decreased ROM into IR, AB, FLEX
 
i've been stretching out hip capsules up and down the east coast for years, if you know what i mean. especially in external rotation. hey-oooooooooooooooooooooooooooooh!!!!!!!!!

sorry. i feel ashamed.
 
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I know you're just using that as an example to highlight your point re: mechanism of action, but why/how would a hip capsule ever get stretched out in the first place? It's not like it's a shoulder and is moved through a huge arc of motion and put in extreme positions.
Most common reason is damage to labrum, whether it be labral tear or significant labral degeneration which accompanies mild/moderate degeneration of articular cartilage. This increases micromotion through the hip capsule and increases hip joint laxity, and can occur at relatively young age if missing large portion of labrum from tear.

This phenomenon is not recognized/well understood by 80% of the orthopedic surgeons or physical therapists in the country.
 
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