- CRPS
- Manifested as triad
- Pain
- Trophic changes
- Vasomotor/sudomotor disturbances
- CRPS 1
- Absence of nerve injury
- Follows initiating noxious event
- Pain or allodynia beyond the territory of a single nerve and disproportionate
- Sudomotor activity at some time
- Absence of existing medical conditions which could explain pain
- CRPS 2
- Following major nerve injury
- Both CRPS 1 & 2 can be subdivided into sympathetically mediated pain (SMP) and sympathetically independent pain (SIP)
- The pathogenesis is unknown with central mechanisms predominant. In CRPS 2, axotomy causes upregulation of α-2 receptors rendering them sensitive to circulating catecholamines. The peripheral mechanisms lead to central hyper excitability and sensitisation. Nerves sprout sympathetic ipsilateral sympathetic axons around the DRG and also NMDA receptor mediated hyperexcitability occurs
- Causes
- Trauma
- Accidental
- Sprains, cuts, contusions, dislocations, crush injuries
- Surgical
- Tight casts, tissue or nerve damage from surgical procedures
- Occupational
- Diseases
- Visceral
- Neurological
- Vascular
- Diagnosis
- Presence of initiating noxious event
- Continuing pain/allodynia or hyperalgesia
- Sudomotor signs
- Lack of alternative diagnosis
- Treatments
- Sensory
- Neuropathic drugs, WHO ladder, TENS, Accupuncture, psychology
- Vasomotor
- Sudomotor
- Motor/trophic
- Clinical signs/symptoms
- Sensory
- Pain
- Usually continuous, burning, shooting, allodynia, often non-dermatomal
- Commoner in CRPS 2
- Hyperalgesia
- Deep somatic hyperalgesia
- Vascular
- Vasodilatation
- Vasoconstriction
- Skin temp abnormalities
- Skin colour changes
- Oedema, sweating
- Swelling
- Hyperhidrosis
- Hypohidrosis
- Motor, trophic changes
- Weakness
- Tremor
- Dystonia
- Hair/nail changes
- Skin atrophy
- Joint stiffness
- Osteoporosis
- CEACCP
Link:ceaccp.oxfordjournals.org/content/early/2013/09/03/bjaceaccp.mkt043.full.pdf