Dear Cricket –

If the orthopedist is saying the change if spread is “very high” that should be your first clue to have a good pain management doctor involved now!

If you don’t have a good pain specialist, I would suggest going to the search engine maintained by the American Board of Pain Management, the group which accredits all pain management fellowships in the U.S., and in contrast to another certification program only certifies doctors who have completed a fellowship in pain management (along with some grandfathering in of unquestioned experts in the field who came up before pain management fellowships were in place) and sat for and passed an 8-hour written exam. http://www.association-office.com/ab...dir/search.cfm The search engine allows you to search by “specialty of origin,” e.g., the area in which the doctors completes their residency. For CRPS/RSD I would stay away from physiatrists, with my first choice being neurology and anesthesiology a close second. Psychiatry is okay too. But the physiatrists (who may be great for lower back pain, etc.) did not in my admittedly small sample have a handle on CRPS.

You say that you are in a “walking boot” for four weeks. Is this a cast or an actual boot you can take off when you bathe or even sleep? The reason I ask is that my CRPS set in both ankles when they were cast to allowing my peroneus brevis tendons to “rest” after they were chewed up pretty badly through the repeated use of a machine at the gym. (On which I had been placed and supervised by a personal trainer.) And we all know that immobilization and CRPS are not a good combination. See, The Natural History of Complex Regional Pain Syndrome, Schwartzman RJ, Erwin KL, Alexander GM, Clin J Pain.2009;25: 273-280, at 274, FULL TEXT @ http://www.rsds.org/2/library/articl...lexanderGM.pdf (in a sample of 656 adult patients with CRPS of at least 1-year duration 77.6% listed an injury as the precipitating cause of their CTPS, and of those 50% had their extremity immobilized after the injury); [and] Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients, Allen G, Galer BS, Schwartz L, Pain 1999 Apr; 80(3):539-44 at p. 541, FULL TEXT @ http://www.rsds.org/2/library/articl...r_schwartz.pdf (47% of patient charts mentioned a history of physician imposed immobilization by cast or splint, having a mean duration of immobilization of 3 weeks and a range of 1 -24 weeks).

Accordingly, if you are immobilized 24/7, I would “run not walk” back to the orthopedist to consider what would be literally more flexible alternatives.

That said, there is good news in the picture. Which is that, quite simply, RSC/CRPS cannot spread to a cite of a new injury without neuro-inflammation at that point, on account of which a recent study while seeking individuals with “long-standing, refractory CRPS” was nevertheless restricted to persons who had either had stable RSD for a period of 6 – 30 months or seen spread to a non-contiguous area within the preceding 30 months. Intravenous Immunoglobulin Treatment of the Complex Regional Pain Syndrome: A Randomized Trial, Goebel A, Baranowski A, Maurer K, Ghial A, McCabe C, Ambler G, Ann Intern Med. 2010;152:152-158 at 156, FULL TEXT @ http://www.rsds.org/2/library/articl...rnMed_2010.pdf

Our results suggest that immune mechanisms play an important role in sustaining long-standing CRPS, but the precise nature of the immune contribution or how it might relate to the putative central drive is unknown. Experimental models suggest that both peripheral and central glia-mediated neuroimmune activation temporarily sustain posttraumatic pain and an analogous augmented immune activation may play a role in CRPS. Intravenous immunoglobulin treatment may reduce this immune activation. [Citations omitted.]

So if the problem at hand is immediate immune suppression in your foot or ankle, at the very least, you should be speaking to a pain specialist about getting an IMMEDIATE, frequent and heavy duty series of lumbar sympathetic blocks, each packed with a good dose of cortisone – or its equivalent - along with the local anesthetic. Because even if blocks stopped working for you in the past there is - you may be certain - a brand new site of neuro-inflammation in your foot and ankle, on account of which an immediate course of steroid laden blocks may be of considerable value.

Of course it would be better if you could arrange for continuous regional anesthesia, where the brew would be pumped continuously into your foot and ankle, presumably on an in-patient basis. But outside of Walter Reed, I'm not aware of that currently being offered in North America, as much as I hope to be proven wrong. See, A Unique Presentation of Complex Regional Pain Syndrome Type I Treated with a Continuous Sciatic Peripheral Nerve Block and Parenteral Ketamine Infusion: A Case Report, Everett A, Mclean B, Plunkett A, Buckenmaier C, Pain Medicine 2009 Sep;10(6):1136-9. Epub 2009 Sep 9, FULL TEXT @ http://www.rsds.org/2/library/articl...n_Plunkett.pdf

Walter Reed Army Medical Center-Army Regional Anesthesia & Pain Medicine, Washington, DC 20307, USA.

Abstract
OBJECTIVE: To successfully treat a patient with complex regional pain syndrome, refractory to standard therapy, to enable a rapid and full return to professional duties. SETTING: This case report describes the rapid resolution of an unusual presentation of complex regional pain syndrome type I after four days of treatment with a continuous sciatic peripheral nerve block and a concomitant parenteral ketamine infusion. The patient was initially diagnosed with complex regional pain syndrome (CRPS) I of the right lower extremity following an ankle inversion injury. Oral medication with naproxen and gabapentin, as well as desensitization therapy, failed to provide any relief of her symptoms. She was referred to the interventional pain management clinic. A lumbar sympathetic block failed to provide any relief. The patient was diagnosed with CRPS I and was admitted for treatment with a continuous peripheral nerve block and parenteral ketamine. CONCLUSION: This case suggests therapeutic benefit from aggressive treatment of both the peripheral and central components of CRPS.

PMID: 19744217 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19744217

AND

Glucocorticoid inhibition of neuropathic limb edema and cutaneous neurogenic extravasation, Kingery WS, Guo T, Agashe GS, Davies MF, Clark JD, Maze M, Brain Res. 2001 Sep 21;913(2):140-8:

Department of Functional Restoration, Stanford University School of Medicine, Stanford, CA, USA. wkingery@stanford.edu

Abstract
Sciatic nerve section in rats evokes chronic limb edema, pain behavior, and hindpaw hyperalgesia, a syndrome resembling the complex regional pain syndrome type II (CRPS II or causalgia) in man. Glucocorticoids such as methylprednisolone (MP) have been used as analgesic and anti-edematous agents in patients suffering from CRPS, and interestingly these therapeutic effects appear to persist in some patients after stopping the medication. Similar to the CRPS clinical response to glucocorticoids, we now demonstrate that chronic hindpaw edema in the sciatic transection CRPS model is reversed by a continuous infusion of MP (3 mg/kg/day over 21 days), and this anti-edematous effect persists for at least 1 week after discontinuing MP. Furthermore, there is a chronic increase in spontaneous protein extravasation in the hindpaw skin of rats after sciatic transection, similar to the increased protein extravasation observed in the edematous hands of CRPS patients. A 2-week infusion of MP (3 mg/kg/day) reduced spontaneous protein extravasation in the hindpaw skin by 80%. We postulated that increased spontaneous neurogenic extravasation resulted in development of limb edema in both the animal model and the CRPS patient, and that the anti-edematous effects of MP are due to an inhibition of spontaneous extravasation. Additional experiments examined the inhibitory effects of MP infusion on electrically-evoked neurogenic extravasation in the hindpaw skin of normal rats. MP inhibition was dose- and time-dependent, with an ED(50) of 1.2 mg/kg/day for a 14-day continuous infusion of MP, and a maximum inhibitory effect requiring 17 days of MP infusion (3 mg/kg/day). MP (3 mg/kg/day for 14 days) also blocked both capsaicin- and SP-evoked neurogenic extravasation, indicating a post-junctional inhibitory effect. Our interpretation is that increased spontaneous neurogenic extravasation in this CRPS model contributed to the development and maintenance of hindpaw edema, and that chronic MP administration dose- and time-dependently blocked neurogenic extravasation at a post-junctional level, thus reversing spontaneous extravasation and limb edema in this model.

PMID: 11549377 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/11549377

[To be continued . . . .]