Bringing up an old thread here - one that I missed before - I just wanted to add my experience that often, just around the time of a flair, I will have significant bruising around the site of the original injury that led to the RSD, and without any apparent stimulus whatsoever.
This has been going on since roughly a year after I first got RSD: and more than 3 years before I went on blood thinners following a mild heart attack. In fact, it's been with me big time over the last couple of days, hence the interest in the subject.
I'm convinced there must be some clinical significance to this, especially where it is known that the sympathetic nervous system triggers the release of vasal constrictors in response to bleeding, which could easily result in a flair, but I'm not sure what triggers the bleeds in the first place.
That said, there are some clues out there that may be worth noting. Check out the following PubMed [govt. source: not copywrited] abstract:
"Exaggerated vasoconstriction in complex regional pain syndrome-1 is associated with impaired resistance artery endothelial function and local vascular reflexes," Dayan L, Salman S, Norman D, Vatine JJ, Calif E, Jacob G.J., J. Rheumatology 2008 Jul; 35(7):1339-45. Epub 2008 May 1.
OBJECTIVE: Local regulatory mechanisms and microvascular function play a major role in the pathogenesis of hemodynamic and trophic changes in patients with complex regional pain syndrome-1 (CRPS). Venoarteriolar and venoarteriolar-myogenic reflexes (VAR, VMR, respectively) as well as endothelial-dependent vasodilatation are important contributors to local vasoregulation. We examined whether VAR and VMR as well as resistance artery endothelial function are damaged in affected limbs of patients with CRPS. METHODS: We measured reactive hyperemic response as an index of resistance artery endothelial function, VAR and VMR in extremity soft-tissue vasculature in patients with CRPS. RESULTS: Baseline blood flow values were not different between CRPS affected and unaffected upper and lower limbs. Resistance artery endothelial function indices, i.e., values of maximal flow after ischemia and the area under the flow-time curve (AUC), were significantly higher in the unaffected versus CRPS-affected upper limbs (19 +/- 3 vs 16 +/- 3 ml*min(-1)*dl(-1) and 373 +/- 71 vs 319 +/- 70 units, for maximal flow AUC, respectively) and lower limbs (9 +/- 2 vs 6 +/- 1.5 ml*min(-1)*dl(-1) and 160 +/- 51 vs 130 +/- 42 units, for maximal flow and AUC, respectively). Flow indices reflecting VAR were lower in the lower, but not upper CRPS-affected limbs compared with unaffected contralaterals (2 +/- 0.24 vs 1.55 +/- 0.3 ml*min(-1)*dl(-1); p = 0.027). Microvascular myogenic reflex-VMR indices, however, were not different in the upper or in the lower CRPS-affected limbs compared with their unaffected contralaterals. CONCLUSION: Impaired balance exists in CRPS-affected limbs between vascular regulation systems responsible for vasoconstriction and vasodilation.
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
Translation: perhaps the same mechanisms that are responsible for impaired vasoconstriction and vasodilatation in the RSD affected limb may have a pronounced effect at the site of the original injury, leading to subsequent hemorrhaging without any apparent cause.
Any thoughts?
Mike