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I'm currently dealing with a CRPS patient who is Type 1 Diabetic, with peripheral neuropathy, but good vasculature.
Had a fusion of the 1st mtpjt ages ago (10 years at least) and has now developed CRPS over the last 6 months dorsally to the 2nd ray, focused around the met-cuneiform joint.
The pain is not associated with activity, but classic signs of mottling, temperature changes and hypersensitivity.
X-rays were unremarkable other then the fusion.
MRI is requested.
Bone scan has been declined on basis of cost.
We have no pain clinic in this area of the NHS (whoppeeee)!
We've tried NSAIDs topical and oral, para-codeine combinations, gabapentin, amitriptyline and have exluded Charcot and osteomyelitis.
Can anyone suggest any intervention that may help?
Have you tried any of the newer agents for DPNP, lyrica or cymbalta, some pain doc's have been using these off label (singularly and in combination) for CRPS.
Tricky one. Autonomic neuropathy plays a role in CRPS and diabetes .... hmmmm?? - what abot neurological referal for sympathetic blocks (maybe problematic because of diabetes).
As this has potential to be, or already is, a chronic pain problem, then psychological counselling from a pain clinic may be needed.
__________________
Craig Payne
Department of Podiatry
La Trobe University
Melbourne, Australia http://www.latrobe.edu.au/podiatry
__________________________________________________ ___________________________________ God put me on this earth to accomplish a certain number of things - right now I am so far behind, I will never die.
The views expressed above are those of the author and not that of La Trobe University This is where I am, where are you?
I haven't tried any of the agents mentioned but will discuss with the Endocrinologist I'm working with regarding that.
Craig, I've no pain clinic to refer to, hence why we're still dealing with it, but counselling may be an avenue. We've sent him to an anaesthetist who does the nerve block stuff in the hospital in isolation of a pain clinic and are awaiting the results of the consultation.
What's really worrying is that none of the interventions we've tried have made the slightest difference and his wife's a Pharmacist, so she'd been expermenting with him before he got to us to no effect!
I read the thread on Laser therapy and painful peripheral neuropathy and I'm qualified in LLLT, but would be extremely uncomfortable doing this given the potential to make it worse, but wondered if anyone knew of anything else such as accupuncture etc that might help?
Any thoughts appreciated!
__________________ nicpod1
Last edited by Admin : 25th May 2006 at 04:46 PM.
Reason: added link to other thread
Debilitating syndrome characterised by severe pain out of proportion to initial injury that is associated with local autonomic dysregulation that usually occurs after trauma or surgery.
Many different diagnostic names given to this condition - causalgia; Sudeck’s atrophy; post-traumatic dystrophy; shoulder-hand syndrome; algodystrophy; post-traumatic pain syndrome; traumatic vasospasm; acute atrophy of bone; sympathetically maintained pain (the different and confusing terminology probably arose from the emphasis placed on the different and variable clinical manifestations of the syndrome).
Currently accepted terminology/nomenclature is that of the International Association for the Study of Pain:
1) Complex regional pain syndrome, Type 1 (reflex sympathetic dystrophy; not associated with a nerve injury)
2) Complex regional pain syndrome, Type 2 (causalgia; similar clinical picture to RSD, but are associated with injury to a peripheral nerve)
Appears to be a sympathetic nervous system disorder – pain is disproportionate to injury.
Aetiology:
Often follows trauma (fractures, lacerations, crush injuries, contusions, sprains); surgery; cast immobilisations; chemical and electrical burns; subcutaneous injections; malignancies; peripheral nerve disorders; strokes; myocardial infarction
Pathogenesis:
Several hypotheses/mechanisms have been proposed:
• May be related to early release of a sympathotropic factor following injury
• a vicious pain cycle is set up by abnormal firing of sympathetic neurons
• peripheral mechanoreceptors or central neurones may be more sensitive
Clinical Features:
Characteristically a burning superficial pain and a deep aching pain; occurs from days to 6 months after initial injury; localised to site of injury initially, but later spreads; pain out of proportion to injury; swelling; worse on movement; muscle spasm; hyperaesthesia; oedema; decreased motor function; trophic skin changes; vasodilation; colour changes (mottling of skin, purple discolouration from venous stasis); hyperhidrosis; feet feel cold; F>M; ABI may be increased relative to unaffected side.
Bone scan will show increased uptake; x-rays will show periarticular soft tissue swelling, regional and patchy demineralisation/osteoporosis; nerve conduction studies will show abnormalities (may not show changes in early stages). Thermograms can document subtle temperature differences
Diagnostic sympathetic nerve blocks will be effective if pain is ‘sympathetically mediated pain’ but not if it is ‘sympathetically independent pain’.
Differential diagnosis – high index of suspicion is needed; pain is regional and not in dermatome distribution; other painful polyneuropathies; lumbar radiculopathy; sciatica; tarsal tunnel syndrome;
Early diagnosis is important as the condition is much more treatable if detected early, but diagnosis is often missed early due to :
1) General lack of awareness of the existence of the condition
2) Difficulty in differentiating between the pain, swelling and colour changes associated with the condition from those of the precipitating injury
3) Limited understanding that the c0ndition may develop early after an injury, with features of pain that are put of proportion to the injury sustained
4) Limited acceptance of the regional rather than the nerve root or peripheral nerve distribution of the pain
5) Overstatement of the psychologic factors (eg reactive depression) as a cause of the condition/complaint rather than an effect of the condition.
6) A sense that the patients are non-compliant when they fail to continue with movement therapy because the pain is worsened with movement
7) Lack of a definitive diagnostic test for the condition – need to rely on ‘vague’ clinical criteria.
Clinical Stages:
Often difficult to place individuals in overlapping stages – can fluctuate between stages 1 and 2 or can progress through stages rapidly or over many years.
Stage 1 – Acute Hyperaemic Stage:
Occurs immediately or up to a few days post injury; usually lasts 1-3 months; localised severe burning pain that is out of proportion to the original injury; hyperaesthesia, allodynia, hyperalgesia, hyperpathia; localised oedema/swelling; pain on movement; muscle spasm; decreased joint range of motion; vasospasm – skin is initially warm, red and dry - then becomes cyanotic, cold, and sweaty; hyperhidrosis
Stage 2 – Dystrophic Ischaemic Phase
Lasts 3-6+ months; brawny appearing oedema spreads; pain is more severe and not as localised (spreads); skin is moist, cold and cyanotic; subcutaneous tissue and muscle wasting and atrophy; patchy osteoporosis;
Stage 3 – Atrophic Phase
Often irreversible; pain can be intractable, but may diminish; significant trophic changes; skin is smooth, shiny and tight; brittle nails; joint stiffness; muscle atrophy; generalised osteoporosis - risk for pathological fractures; pain exacerbated by cold.
Stage 4 – Psychological Phase
Untreated or poorly treated - depression and other psychopathology
International Association of the Study of Pain diagnostic criteria:
1) The presence of an initiating noxious event or cause of immobilisation
2) Continuing pain, allodynia or hyperalgesia with which the pain in disproportionate to any inciting event
3) Evidence at some time of oedema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain
4) This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction
However, these criteria are not very sensitive .
Treatment:
Early mobilisation following initial injury – may be painful as even slight movement may trigger spasm. Condition seems to progress if kept immobilised.
Avoidance of alcohol and stop smoking
Stimulation of inhibitory neurons (massage, counterirritants, TENS, spinal cord stimulator)
NSAID’s; analgesics; tricyclic antidepressants
In an uncontrolled study, pamidronate (bisposphonate) appeared to be effective in treatment of 29 refractory cases
Sympathetic blocks
Counselling in pain management techniques; emotional support; biofeedback; relaxation training
Physiotherapy – movement; aqua therapy (movement in water) - especially prevention of disuse atrophy
Later – chemical or surgical sympathectomy; morphine pump
__________________
Craig Payne
Department of Podiatry
La Trobe University
Melbourne, Australia http://www.latrobe.edu.au/podiatry
__________________________________________________ ___________________________________ God put me on this earth to accomplish a certain number of things - right now I am so far behind, I will never die.
The views expressed above are those of the author and not that of La Trobe University This is where I am, where are you?
Is it true that surgery,even nail procedures are absolutely contraindicated on people with CRPS?That would seem logical but I am not 100% sure.
As for the first post,lyrica or cymbalta may help.
John;
from what I've read you really need to be careful doing surgery on these patient's. They are so overly sensitive that it could start an RSD reaction over again. Seems similar to frostbite at times, in that these patients never seem to go without reactoin in that area from any cold exposure.
Sincerely;
Bruce Williams, D.P.M.
You might find that ipsilateral costo-vertebral (and/or lumbar) palpation will reproduce foot symptoms. Whether this helps is another thing.
If you know a gentle osteo/physio/chiro, 1 session may do something, even psychologically.
Like Craig said, sometimes I have referred to a local vascular surgeon for a block. I am sure they hit the major vessels rather than the minor ones.
BTW, I have never seen a driven athlete with this condition...never. It only seems to affect certain types (introverted etc.) Sorry for generalising, but that is my take on it.
I have had great success with CRPS. For whatever reason, I seem to catch this on many patient's per year and treat them with good to excellent success. Most repsond to injection thereapy, 1-1.5cc's of 2% carbocaine/marcaine, and 1-1/5 cc's of celstone or kenalog mixed. I ususally get 30-50% resolution from the intial injection and equal improvement with repeat injections. I have them do their own physio under wamr running water wiht ROM exercises. Once the motion returns then they are half way their. I will often send them to a neurologist but they like neurotin too much. I find that an anesthesiologidt / pain specialist can do a better regional block in the worst caess.
Bruce
After reading the first post I question the diagnosis. It seems that this pain is focal and not diffuse. CRPS typically involves a much larger area after 6 months. The skin changes could be a red herring. Could this be an entrapment of the SPN??? The entrapment site can be anywhere put typically occurs at the crural hiatus approx 9-13 cm above the ankle. If this area is sypmtomatic (tenderness or + tinel) you could do a cocktail block there a see what happens. In my practice, anyone with unexplained focal pain to the anterior ankle or dorsal midfoot that is not activity related and occurs hs is SPN until proven otherwise. This has rarely failed me. Tx- injection, nerve glides,Lidocaine patches,sometimes counter-irritants,sometimes TENS.
(Not to be picky, but the term is COMPLEX regional pain syndrome and not "Chronic". I made this mistake several times since the name change from RSD to CRPS.)
After reading the first post I question the diagnosis. It seems that this pain is focal and not diffuse. CRPS typically involves a much larger area after 6 months. The skin changes could be a red herring. Could this be an entrapment of the SPN??? The entrapment site can be anywhere put typically occurs at the crural hiatus approx 9-13 cm above the ankle. If this area is sypmtomatic (tenderness or + tinel) you could do a cocktail block there a see what happens. In my practice, anyone with unexplained focal pain to the anterior ankle or dorsal midfoot that is not activity related and occurs hs is SPN until proven otherwise. This has rarely failed me. Tx- injection, nerve glides,Lidocaine patches,sometimes counter-irritants,sometimes TENS.
(Not to be picky, but the term is COMPLEX regional pain syndrome and not "Chronic". I made this mistake several times since the name change from RSD to CRPS.)
In a chronic situation Scorpio, the entrapment point may be thick and hence may also respond to massage. You may even expect P/F to be slightly reduced.
With CRPS, what is the difference between CRPS1 and 2 etc?
Why would you not give an antiinflammatory to someone with this entrapment?
You certainly could but I would not on the first visit for two reasons- First, I do only local treatments specific for the entrapment to confirm the diagnosis. If they improve while on a systemic antiinflammatory(medrol,nsaid) it tells me nothing. Second, isn't the injection the most potent anti-inflammatory? If lasting improvement is seen, it tells me the site of pathology.
The objective of this paper is to investigate the effect of gabapentin in the earlier stage of reflex sympathetic dystrophy syndrome (RSD). Twenty-two patients diagnosed with RSD were enrolled. Initial gabapentin dosage was 600 mg/day. This dosage is increased gradually until a satisfactory pain level was reached. After this level, this dosage was maintained throughout the study. An exercise program was also applied to the patients. Provoked and static pain scores of the patients were obtained initially, at 3-day intervals for maintenance dosage determining, and at 6 weeks after the discharge. Functional improvement parameters were volumetric measurement; dynamometric measurement and third finger pulp-distal palmar crease distance measurement for hands; and metric circumferential measurement and range of motion for elbow, knee, and foot initially, at baseline, on the tenth day, upon discharge, and 6 weeks after the discharge. The mean maintenance dose of gabapentin was 1,145.46+/-377.6 mg/day (range, 900-1,800 mg/day). Improvements in spontaneous and provoked pain intensities were statistically significant. No statistically significant difference was obtained in functional improvement parameters. Dizziness in three patients, headache in two patients, and mild burning feeling in the tongue in one patient were the reported side effects. These symptoms resolved spontaneously in few days. Gabapentin cannot be recommended as the drug of choice, but it may be considered as one of the therapeutic alternatives in the management of pain due to RSD. We suggest that it is effective only for the pain and not for other symptoms of RSD. Serious side effects that will cause the patient to stop using the drug are rare
Chronic Regional Pain Syndrome / Sudecks
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