Questions
- 1.
Define complex regional pain syndrome type 1 and type 2.
- 2.
What are the pathophysiologic theories regarding the etiology of complex regional pain syndrome?
- 3.
Delineate the different stages of complex regional pain syndrome.
- 4.
What are the signs and symptoms of complex regional pain syndrome?
- 5.
How is complex regional pain syndrome diagnosed?
- 6.
What nerve blocks can be used for diagnosis and treatment of complex regional pain syndrome?
- 7.
What other modalities can be used to treat complex regional pain syndrome?
A 39-year-old secretary was healthy until 1 year ago when she tripped and fell onto her right arm while at work. She awoke 10 days later with severe burning pain from the palm to the midforearm. The arm began to swell and intermittently turned pale and red. When the patient presented, the arm was exquisitely tender to touch and the patient was unable to wear long-sleeved shirts. She was unable to use the arm and had become depressed.
1
Define complex regional pain syndrome type 1 and type 2.
Complex regional pain syndrome (CRPS) is a disease process that consists of continuous pain, often burning in nature, usually consequent to an injury or a noxious stimulus. CRPS usually manifests with varying degrees of autonomic and trophic changes along with sensory and motor dysfunction.
CRPS type 1 was previously known as reflex sympathetic dystrophy, and CRPS type 2 was previously known as causalgia. The nomenclature has been changed to dispel some of the old theories regarding the possible etiologies for these diseases.
CRPS types 1 and 2 have similar signs and symptoms. In CRPS type 2, a history is commonly elicited describing a macroscopic nerve injury, such as a traumatic amputation, whereas with CRPS type 1, the inciting event may be a minor injury or may never be determined.
2
What are the pathophysiologic theories regarding the etiology of complex regional pain syndrome?
Understanding of CRPS has increased substantially over the past decade. Three major pathophysiologic pathways have been identified: aberrant inflammatory mechanisms, vasomotor dysfunction, and maladaptive neuroplasticity. The clinical heterogeneity of CRPS is indicative of patient-to-patient variability in the activation of these pathways after noxious stimuli.
Even minor tissue trauma can be sufficient to amplify signaling in traumatized tissue and result in long-term peripheral sensitization. However, the way in which the immune system and nervous system interact, particularly in bones, muscle, and connective tissue, is not fully understood.
Vasomotor dysfunction is common in CRPS. The affected limb is usually warmer than the healthy limb early on and cooler than the healthy limb later on. This shift in temperature suggests that the activity in vasoconstrictor neurons changes over time in CRPS.
The central nervous system undergoes functional and structural changes in people with persistent pain, and these changes are thought to be especially important in people with CRPS. A potentially important mechanism is hyperalgesic priming. According to this theory, a transient insult triggers long-lasting changes in primary afferent nociceptors that cause them to become hyperresponsive to future mild insults that would not normally provoke pain.
Other theories include the existence of ephapses, or neurologic short circuits between the somatic and sympathetic nervous systems, possibly caused by trauma. It is unclear whether these connections are actual structural connections or “chemical” connections caused by the release of neurotransmitters. These ephapses could explain the clinical findings in CRPS. Stimuli that are usually mediated by the autonomic nervous system, such as responses to emotion, temperature, and weather, are rerouted through the somatic nervous system and cause pain. Stimuli that are usually mediated by the somatic nervous system, such as light touch, are rerouted through the autonomic nervous system and cause an uncoordinated sympathetic response .
3
Delineate the different stages of complex regional pain syndrome.
CRPS is usually described in three different stages ( Table 71-1 ).
| Stage | Name | Time | Findings |
|---|---|---|---|
| 1 | Acute or hyperemic | Days to weeks | Severe burning or lancinating pain |
| Skin is red, warm, and dry | |||
| Hyperesthesia | |||
| Allodynia | |||
| 2 | Dystrophic | Weeks to months | Skin is pale, cyanotic, and cool |
| Hyperesthesia | |||
| Allodynia | |||
| 3 | Atrophic | Months to years | Smooth glassy skin |
| Loss of hair | |||
| Brittle nails | |||
| Muscle atrophy | |||
| Demineralized bone (Sudek atrophy) |
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