Early Use of Regional and Local Anesthesia in a Combat Environment May Prevent the Development of Complex Regional Pain Syndrome in Wounded Combatants

Military Medicine, May 2006 by Jenson, Michael G, Sorensen, Raymond F

Complex regional pain syndrome (CRPS) is a relatively common disabling disorder of unknown pathophysiology. CRPS is a variable symptom complex that probably results from multiple causes through different pathophysiological mechanisms. Changes in peripheral, central, somatosensory, autonomic, and motor processing, accompanied by pathological interactions of sympathetic and afferent systems, are observed as underlying mechanisms. Standardized early interventions for patients with extremity wounds may prevent the onset of CRPS or at least reduce the severity or duration of the condition.

Introduction

Complex regional pain syndrome (CRPS) may develop as a disproportionate consequence of trauma affecting the limbs, without nerve injury (CRPS I or reflex sympathetic dystrophy) or with obvious nerve injury (CRPS II or causalgia). In the 17th century, Ambroise Pare1 presented the earliest description of CRPS, with severe burning pain following peripheral nerve injury, and Mitchell termed the condition causalgia (which means burning pain) in describing persistent symptoms following gunshot wounds to peripheral nerves in the U.S. Civil War in 1864.2 A significant number of extremity injuries are being seen in association with Operation Iraqi Freedom and Operation Enduring Freedom, which may lead to an increased number of patients with CRPS.

As of November 16, 2004, a total of 10,726 service members had suffered war injuries in Operation Iraqi Freedom. Of these, 1,361 died (1,004 were killed in action), 5,174 were wounded in action and could not return to duty, and 4,191 were less severely wounded and returned to duty within 72 hours.3 Blast injuries from improvised explosive devices are producing an unprecedented number of mangled extremities, with severe soft tissue, bone, and often vascular injuries.4 Since CRPS was first described in the 17th century, the medical community has attempted to understand and to treat this complex condition. The preponderance of early descriptions of the condition involved extremity wounds. The pathophysiology of the CRPS remains elusive, but most recent studies have shown a central mechanism for both the sensory features and the autonomie features. Peripheral mechanisms include tissue acidosis and neurogenic inflammation. Involvement of the immune system could imply the subsequent release of neuropeptides and proinflammatory cytokines, leading to complex cross-communication among primary and secondary mediators of inflammation.5

Sources report the incidence of causalgia (CRPS II) after injury to a peripheral nerve as 1 to 5%. The incidence of reflex sympathetic dystrophy (RSD) (CRPS I) is 1 to 2% after various fractures and 2 to 5% after peripheral nerve injury.6 It is difficult to estimate, however, because the literature contains studies in which clinical criteria for the diagnosis of CRPS vary dramatically. For example, upper-extremity CRPS, as understood and treated by hand surgeons, is described differently than lowerextremity CRPS diagnosed by rheumatologists or hip CRPS described by obstetricians. Some authors suggest that 8 to 10% of patients with fractures develop CRPS, but the frequency is much lower in studies.7 The occurrence of CRPS with gunshot and projectile wounds is well documented and is a reality of war.2

Symptoms

In 1994,8 the International Association for the Study of Pain (IASP), after development of consensus by a group of pain medicine experts, suggested that the term CRPS should replace RSD and causalgia, i.e., CRPS I for RSD and CRPS II for causalgia. The symptoms of CRPS are as follows.5

Pain

Pain is reported by >90% of patients. Most patients describe worsening of pain or other symptoms after exercising the affected limb.

Edema

Vascular abnormalities, often abnormal vasodilation and skin warming in the early phase and vasoconstriction in later stages, are characteristic symptoms of RSD/CRPS I. Typically, patients with CRPS I exhibit a warm, vasodilated, affected extremity in the early stages and cold pale skin in the later stages.

Alterations in Motor Function

Although the IASP did not include motor dysfunction in the formal criteria for diagnosing CRPS (because it is not universal), it acknowledged that such dysfunction is common. The abnormal motor symptoms that are reported most classically in CRPS include an inability to initiate movement, weakness, tremor, muscle spasms, and dystonia of the affected limb. In one study, weakness was reported for 95% of patients, tremor of the affected limb for 49%, and muscular uncoordination for 54%. In chronic CRPS, severe spasms were present for 25% of patients.

Alterations in Sensory Function

Although the IASP decided not to include sensory dysfunction in the formal criteria for diagnosing CRPS (because of variability), such symptoms, including hypoesthesia, hyperesthesia, and allodynia, may occur.

Psychological Dysfunction

The IASP also decided not to include psychological dysfunction in the formal criteria for diagnosing CRPS, because of ongoing debate regarding whether psychological dysfunction increases the risk of CRPS or the psychological dysfunction often seen among these patients is actually a result of CRPS. Psychological disturbances may include anxiety, hopelessness, and/or depression.