Pain accompanied by burning and temperature change in this patient is most likely due to CRPS. The differential diagnosis may also include the following:

Over the years, CRPS has been referred to as reflex sympathetic dystrophy (RSD), causalgia, SMP, and chronic peripheral pain syndrome. The term CRPS was introduced in 1994 by the International Association for the Study of Pain subcommittee on taxonomy. It is subdivided into CRPS type I (formerly described as RSD) and CRPS type II (formerly described as causalgia).

CRPS is characterized by pain associated with sensory, autonomic, trophic, and motor abnormalities. CRPS is triggered by noxious stimuli (type I) or by nerve injury (type II). It is not limited to the distribution of a single peripheral nerve and is disproportionate to the inciting event.

RSD, causalgia, algodystrophy, Sudeck atrophy, and various other conditions are all grouped under CRPS. This diagnosis better describes the wide range of clinical signs and symptoms and the complexity of the pathophysiology responsible for the clinical picture.

CRPS-I is defined as a clinical syndrome triggered by a noxious stimulus that is not limited to the distribution of a single peripheral nerve; no nerve lesion can be identified. CRPS-II is defined as a clinical syndrome that is due to a nerve injury and is mostly limited to the distribution of the injured nerve. The diagnostic criteria are the same for CRPS-I and II.

The diagnosis of CRPS can be made in the following context: a history of trauma to the affected area associated with pain that is disproportionate to the inciting event plus one or more of the following as defined by either the Orlando criteria or a modified version referred to as the Budapest criteria.

The main features include pain that is continuous, burning in nature, independent of type and severity of injury, and not limited to a dermatomal distribution. Patients may complain of allodynia, dysesthesia, or hyperalgesia. Movement or stress exacerbates pain. Edema is usually present. Abnormal sudomotor activity, limb discoloration, and local temperature changes are common but inconsistent.

It affects between 200,000 and 1.2 million Americans. This syndrome may follow as many as 5% of all traumatic injuries with the arms being affected in approximately 60% of cases and the legs about 40%.

CRPS may follow relatively minor trauma with or without nerve injury. Causes leading to CRPS include the following:

Several hypotheses have been postulated, but none can explain all the findings and the varying responses to treatment in these patients. These hypotheses include the following:

More than one sequence of events likely take place in a patient, giving rise to a mixed clinical picture. A dynamic change in the physiology and structure of central pain projecting neurons mediated through the N-methyl-D-aspartate (NMDA) receptor. Injury initiates and maintains a state of central sensitization in the central pain pathways, resulting in a lower threshold to fire pain transmission neurons and an increase in their receptive fields. This may involve disinhibition of spinal and trigeminal nociceptive neurons. This often
precedes thermal and mechanical allodynia and spontaneous pain. Finally, the psychological component and neuromodulation cannot be discernibly separated.

The pain that is maintained by sympathetic innervation or circulating catecholamines is defined as SMP. It describes a pain mechanism, not a clinical syndrome. Therefore, by definition, patients with CRPS who report pain relief after a sympathetic block (e.g., stellate ganglion block) have SMP. Conversely, pain conditions that show features of sympathetic overactivity, yet fail to respond to sympathetic blocks, are described as SIP.

The chronic pain seen in neuralgia is usually paroxysmal in nature and follows the distribution of nerve. The pain is sharp and shooting without associated vasomotor or sudomotor changes. The chronic pain syndrome of CRPS is a sustained, diffuse, burning pain that is independent of nerve distribution and is associated with vasomotor and sudomotor changes, edema, allodynia or hyperalgesia, and changes in skin color.