Complex Regional Pain Flashcards

1
Q

What is complex regional pain syndrome (CRPS)?

A

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 even

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2
Q
A

RSD, causalgia, algodystrophy, Sudeck atrophy, and various other conditions are all grouped under CRP

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3
Q

What are the two types of CRPS?

A
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4
Q
A

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.

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5
Q
A

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.

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6
Q

What are the diagnostic criteria for CRPS? What is the incidence of this disease?

A

Orlando criteria or a modified version referred to as the Budapest criteria. Abnormal function of the sympathetic nervous system (vasomotor changes, skin color changes) Swelling Movement disorder Changes in tissue growth (dystrophy and atrophy) Sensory disturbances (hyperalgesia or allodynia)

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7
Q
A

The main features include pain that is continuous, burning in nature, independent of type and severity of injury, and not limited to a dermatomal distributionPatients 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.

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8
Q

Define allodynia

A
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9
Q

hyperalgesia

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10
Q

hyperesthesia

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11
Q

dysesthesia.

A
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12
Q

What are the stages of CRPS?

A
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13
Q

What are the possible etiologies of CRPS?

A

Inflammatory conditions (e.g., fasciitis, tendonitis, bursitis, and arthritis)
Immobilization as a result of injury or cast application
Inflammatory conditions (e.g., fasciitis, tendonitis, bursitis, and arthritis) Immobilization as a result of injury or cast application Peripheral nerve injury resulting from direct compression or ischemia (e.g., brachial plexopathy, postherpetic neuralgia, and nerve root injury
Peripheral nerve injury resulting from direct compression or ischemia (e.g., brachial plexopathy, postherpetic neuralgia, and nerve root injury

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14
Q

Explain the pathophysiology of the development of CRPS.

A

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.

  1. Abnormal discharges in sympathetic and nociceptive afferents produced by trauma
  2. Sensitization of peripheral sensory receptors produced by sympathetic hyperactivity Formation of ephapses (artificial synapses) after peripheral nerve injury
  3. Spontaneous neuronal ectopy at the site of demyelination or axonal injury Central reorganization of pain processing (central sensitization)
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15
Q

Define sympathetically maintained pain (SMP

A

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

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16
Q

sympathetically independent pain (SIP).

A

pain conditions that show features of sympathetic overactivity, yet fail to respond to sympathetic blocks, are described as SIP.

17
Q

How does CRPS differ from neuralgia?

A

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.

18
Q

What is central pain? How will you differentiate central pain from CRPS?

A

Central pain is regional pain initiated or caused by a primary lesion or dysfunction in the central nervous system; it is usually associated with abnormal sensitivity to temperature and to noxious stimulus. Central pain, also referred to as deafferentation pain, is a difficult pain syndrome to treat because the pathophysiology is not well understood. Regional pain not relieved by peripheral nerve blocks, either sympathetic or somatic, is more likely to be central pain. Central pain may be associated with various neurologic symptoms and signs such as monoparesis, hemiparesis, or paraparesis. Central pain conditions typically include partial or complete loss of sensation, involvement of spinothalamic functions, and development of hypersensitivity in body parts that have loss normal somatosensory feedback as a result of a central nevous system lesion.

19
Q

Is the social history of this patient relevant to the development of chronic pain syndrome?

A

Also noted is the fact that as the CRPS progresses, patients’ personality measures such as Minnesota Multiphasic Personality Inventory (MMPI) profiles tend to resemble those of patients experiencing chronic pain and psychological distress as evidenced by hypochondriasis, depression, and hysteria scales. Certainly, stress has been implicated in increasing sympathetic outflow. The literature suggests that the presence of psychological disorders,particularly anxiety and depression, may predispose the patient to the development of CRPS. However, a large case-control study reported no differences in psychological variables between those with CRPS and those without CRPS after controlling for age, sex, and trauma. Furthermore, anxiety and stress can augment nociception, and therefore, antidepressive treatments can be useful.

20
Q

How will you work up CRPS types I and II?

A

CRPS is diagnosed clinically
Objective signs are variable but almost universally include loss of function of the affected part due to pain. Allodynia and hyperalgesia are extremely common. Change in temperature and sweating may vary depending on the stage of the disease. Several diagnostic studies may aid in the diagnosis of CRPS but are seldom pathognomonic.
quantitative sweat test
Radiologic studies may reveal patchy osteoporosis in early stages. Triple-phase bone scintigraphy using technetium-99mmay show increased periarticular uptake in the affected extremity illustrated by unilateral hyperperfusion in the perfusion and blood pool phases. Negative triple-phase bone scan results do not rule out CRPS

21
Q

How will you treat this patient?

A
22
Q

What is stage i

A

Stage I
Onset of severe pain limited to the site of injury
Increased sensitivity of skin to touch and light pressure (hyperesthesia)
Localized swelling
Muscle cramps
Stiffness and limited mobility At the onset, the skin is usually warm, red, and dry; then it may change to blue (cyanotic) in appearance and become cold and sweaty. Increased sweating (hyperhidrosis)
Stage I Onset of severe pain limited to the site of injury Increased sensitivity of skin to touch and light pressure (hyperesthesia) Localized swelling Muscle cramps Stiffness and limited mobility At the onset, the skin is usually warm, red, and dry; then it may change to blue (cyanotic) in appearance and become cold and sweaty. Increased sweating (hyperhidrosis)

23
Q

Stage ii

A

Pain becomes even more severe and more diffuse.
Swelling tends to spread and it may change from a soft to hard (brawny) type.
Hair may become coarse then scant; nails may grow faster and become brittle, cracked, and heavily grooved.
Spotty wasting of bone (osteoporosis) occurs early but may become severe and diffuse.
Muscle wasting begins.

24
Q

Stage iii

A

Marked wasting of tissue (atrophic) eventually becomes irreversible.
For many patients, the pain becomes intractable and may involve the entire limb.
A small percentage of patients have developed generalized CRPS affecting the entire body.