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Epidemiology, Pathophysiology, and Management of Complex Regional Pain Syndrome

Epidemiology, Pathophysiology, and Management of Complex Regional Pain Syndrome
Epidemiology, Pathophysiology, and Management of Complex Regional Pain Syndrome

Pain Practice, Volume 1, Number 1, 2001 11–20

Epidemiology, Pathophysiology,

and Management of Complex Marco Pappagallo, MD*; Andrew D. Rosenberg, MD?

*Comprehensive Pain Treatment Center and ?Department of Anesthesiology, Hospital for Joint

Diseases, Mt. Sinai/NYU Health, New York, New York

I

n order to further the understanding of the 2 clinical entities known as reflex sympathetic dystrophy (RSD)and causalgia, the International Association for the Study of Pain (IASP) decided to reclassify their terminol-ogy. Thus, in 1994 the IASP renamed the 2 disorders re-spectively CRPS type 1 (formerly referred to as RSD)and CRPS type 2 (the disorder previously known as causalgia, associated with a definable nerve lesion. 1 As described by Stanton-Hicks, 2 the term CRPS implies the presence of regional pain and sensory findings after a noxious event with additional abnormalities including edema and changes in skin color, temperature, and su-domotor activity. These changes all appear to be out of proportion with the physical damage from the noxious event. It must be noted that the IASP diagnostic criteria for CRPS type 1 and type 2 still await full clinical and scientific validation. 3–5

Moreover, numerous practitio-ners have questioned the usefulness of these new terms.One major problem is that the diagnostic criteria for CRPS type 1 and type 2 remain too vague. This might result in overdiagnosing the 2 entities and in causing dif-ficulties with analyzing treatment outcome data.

Undoubtedly, these disorders are complex and diffi-cult to understand. Pain medicine experts continue to struggle for the development of satisfactory treatment

? Abstract: Complex regional pain syndromes (CRPS) are challenging neuropathic pain states quite difficult to compre-hend and treat. Although not yet fully understood, advances are being made in the knowledge of the mechanisms in-volved with CRPS. Patients often present with incapacitating pain and loss of function. Patients suffering from these disor-ders need to have treatment plans tailored to their individual problems. A comprehensive diagnostic evaluation and early and aggressive therapeutic interventions are imperative. The therapeutic approach often calls for a combination of treat-ments. Medications such as antiepileptics, opioids, antidepres-sants, and topical agents along with a rehabilitation medicine program can help a major portion of patients suffering from these disorders. Implantable devices can aid those patients with CRPS. While progress is being made in treating patients with CRPS, it is important to remember that the goals of care are always to: 1) perform a comprehensive diagnostic evalua-tion, 2) be prompt and aggressive in treatment interventions,3) assess and reassess the patient’s clinical and psychological status, 4) be consistently supportive, and 5) strive for the max-imal amount of pain relief and functional improvement. In this review article, the current knowledge of the epidemiol-ogy, pathophysiology, diagnostic, and treatment methodolo-gies of CRPS are discussed to provide the pain practitioner with essential and up-to-date guidelines for the management of CRPS. ?

Key Words: CRPS, comprehensive evaluation, aggressive therapeutic regimen, psychological support, prolonged re-habilitation

Address correspondence and reprint requests to: Marco Pappagallo,MD, Director, Comprehensive Pain Treatment Center, Hospital for Joint Diseases, 301 East 17th Street, New York, NY 10003. U.S.A

algorithms. CRPS is a formidable challenge for pain medicine specialists as well as for affected patients. This remains true despite all the recent scientific advances in the fields of pain neurophysiology and pharmacology.

In this review, we will present the most updated and relevant information on the epidemiology and patho-physiology of CRPS. We will also discuss the assessment of patients with CRPS, and the use of diagnostic tech-niques as well as propose new treatment options in its management.

THE ROLE OF SYMPATHETICALLY

MAINTAINED PAIN IN CRPS

In contradistinction to CRPS, sympathetically main-tained pain (SMP) is a pathogenetic mechanism and not a clinical entity. In the past, it was often misunderstood that all patients with RSD had abnormal sympathetic nervous system involvement. On the contrary, it is now understood that the majority of patients with CRPS do not have SMP. A neuropathic pain state can be main-tained by several peripheral and central nervous system (PNS, CNS) mechanisms. SMP appears to represent 1 of the PNS mechanisms (see below, Pathogenesis). SMP may be present, perhaps only temporarily, and compli-cate CRPS as well as other painful disorders including shingles, neuralgia, and metabolic or autoimmune neu-ropathies. Pain not responsive to sympathetic blockade is referred to as sympathetically independent pain (SIP). It is possible that over time a patient may present to the same physician with SMP, then SMP and SIP, and there-after SIP alone.2,6 Therefore, it should be reasserted that the diagnosis of CRPS no longer rests on the response to a sympathetic block alone.

EPIDEMIOLOGY AND

PATHOPHYSIOLOGY OF CRPS

Knowledge of the epidemiology of CRPS suffers from a lack of adequate prospective studies. Retrospective study on the subject by Allen, Galer, and Schwartz that includes 134 patients indicates an average age of onset at 38 years.7 In their study, patients with CRPS type 1 presented to a multidisciplinary center with an average disease dura-tion of 2.5 years. Females are affected more commonly than males (2:1). A small percentage (5%) of patients could not recall any traumatic insult precipitating their symptoms. It appears that there may be a genetic predis-position to the development of CRPS type 1, with a higher incidence in certain HLA types. Kelmer demon-strated an increased incidence of CRPS type 1 in patients with HLA DQ 1.8 Mailis and Wade noted an increased incidence of HLA A3, B7, and DR215 in patients with CRPS. A poor response to standard treatments was noted in the DR215 group.6,9

A clear understanding of the pathophysiology of CRPS remains to be elucidated. It is unclear as to what ignites the disease process after the traumatic event and how an injury causes the PNS and CNS to react in an abnormal, exaggerated manner. Hypotheses include the development of ectopic nociceptive activity (occasion-ally driven by an SMP mechanism), an abnormal re-sponse to the local release of neurotrophic factors, and the occurrence of a local neuro-immunological inflam-matory process. These peripheral events can be compli-cated by temporary or long-term CNS changes such as central sensitization and then reorganization of the pain pathways at the dorsal horn level. Pathological studies in 8 patients affected by intractable CRPS type 1 demon-strated a microangiopathic process and on electron mi-croscopy the presence of C fiber axonal sprouts in at least four of the affected patients. These findings sug-gested the occurrence of a small fiber neuropathy.10 CRPS, however, is likely the expression of neurophysio-logical abnormalities affecting both the peripheral and central nervous system.11,12 A trauma may result in ec-topic repetitive discharges from the nociceptors inner-vating the injured area. Damaged A-delta and C-noci-ceptors can produce such ectopic discharges. The axons of the injured fibers develop an abnormal mechano-sen-sitivity, and, at times, an alpha-adrenoreceptor excit-ability.13,14 If a component of SMP is present it proba-bly has its origin at this point as injured nociceptors acquire alpha-adrenoreceptor excitability. Of interest, not only abnormal changes are noted in the dorsal root ganglion (DRG) cells of the injured afferent axons, but also in the cell bodies of uninjured axons within the same DRG. A state of CNS hyperexcitability occurs as af-fected afferent C-fibers release large amounts of glutamate, substance P, and other neuropeptides. This results in a cen-tral sensitization state with its clinical correlates of allo-dynia and hyperalgesia.15

The release of neurotrophic factors from damaged tissue may play a role in CRPS.16,17 Neurotrophic fac-tors, including nerve growth factor, induce the develop-ment of miniature axon sprouts from the endings of small nerve afferent fibers as well as from the sympa-thetic efferent nerves, and this may favor a coupling be-tween the 2 types of nerve fibers.18 If the affected noci-ceptors have begun to express alpha-adrenoreceptor excitability, the coupling may indeed favor the SMP state. Bennett has proposed that CRPS may also be asso-

ciated with an abnormal neuro-immunological inflam-matory process.19 If an abnormal immune response oc-curs after an injury, inflammatory cytokines such as tumor necrosis factor alpha, interleukin 1-beta, IL-6, and IL-8 are released locally. These cytokines are known to induce significant changes in nociceptors, including sensitization, activation, and even axonal damage.19 An outgrowth of the concept that immunological changes may result in the occurrence of CRPS is the number of observations addressing the role of macrophages and macrophage-released cytokines in contributing to hyper-algesia and Wallerian degeneration, as well as the role of biphosphonates as a nerve treatment option for CRPS (see below).20–23

In summary, while the multiple pathogeneses of CRPS have not been defined, it appears that a traumatic injury to the distal extremity of genetically predisposed individuals may initiate a process that results in a neuro-pathic “stalemate” state in the affected limb. Of interest is that in several instances CRPS appear to be main-tained by “plastic” mechanisms that can be switched off by early and aggressive therapeutic interventions. It is conceivable that these mechanisms are centered on a complex interplay of both physiological (eg, PNS and CNS sensitization of pain pathways, tissue-released neu-rotrophic factors) and pathological states (eg, neuro-immunological inflammation, expression of abnormal receptors and channels in the nociceptors membrane of the affected limbs) that can be more easily and likely rec-tified by therapeutic interventions employed early in the course of these painful states.

EVALUATION OF THE PATIENT WITH CRPS

Patients suffering from CRPS need to undergo a thor-ough and comprehensive evaluation so that an individu-alized treatment plan can be initiated. Treatment usually involves a long-term patient-physician relationship, re-quiring initiating a medical plan, reevaluation, and likely repeated adjustments of the treatment plan. It is important to keep the referring physician in the “loop”of medical management decision-making so that a conti-nuity of care can be guaranteed. Treatment goals in-clude satisfactory pain relief and improvement in psy-chological and physical well being.

In obtaining the patient’s history, the pain medicine specialist has to determine the nature of the initiating event, and the onset and features of symptoms. While CRPS usually involves a single distal extremity, there are reports of spread to other extremities. The physician has to assess the degree and qualities of spontaneous pain and bring forth the features of allodynia and hyperalge-sia, necessary to the diagnosis of CRPS. At the time of the evaluation, the affected limb may or may not show classic CRPS changes. However, at some point in time from the disease onset, abnormalities such as skin color and temperature changes, edema, and sweating should be elicited. Patients with SMP typically present with cold hyperalgesia in the affected limb.15

CRPS is likely dependent on a variety of pathogenetic mechanisms (as discussed under the section Epidemiol-ogy and Pathophysiology), and the clinical experience suggests that multiple treatment modalities are often necessary for the majority of cases. Although there is a paucity of controlled trials in the field of CRPS manage-ment, established clinical experience indicates that a few treatment modalities have some usefulness. However, in the majority of the affected patients, combinations of treatments are often needed to achieve a satisfactory treatment outcome, such as a sympatholytic procedure for SMP, a combination of pharmacological agents, phys-ical therapy and rehabilitation medicine, and for intracta-ble cases, utilization of implantable devices.

THE DIAGNOSIS OF SMP

Useful diagnostic tests include regional sympathetic blocks, such as the stellate ganglion block for the arm and the lumbar sympathetic block for the leg, and intra-venous sympatholytic blocks, such as the phentolamine or the bretylium blocks. Hereafter, we will describe the techniques for blocking the stellate ganglion and the lumbar sympathetic chain.

Stellate Ganglion Block

The stellate ganglion carries the sympathetic fibers to the upper extremity. It is formed from the inferior cervi-cal and the first thoracic sympathetic ganglia. The stel-late ganglion is located behind the carotid artery and in-ternal jugular vein, anterior to the longus colli muscle and approximately 2.5 cm ? 1 cm ? 0.5 cm in size. Technique. The patient is placed on the stretcher in the supine position. A folded sheet or towel is placed behind the shoulders, and the neck is extended. This maneuver places the esophagus in a direct line posterior to the tra-chea. The neck is prepped and draped, and the middle and index fingers are placed on the neck above the stern-oclavicular junction in the immediate paratracheal area. This can be done at the C7 level. Some physicians like to perform this maneuver at C6. Pulsations of the carotid artery can be appreciated. While using enough pressure

to feel the deep structures of the neck, the carotid sheath and the sternocleidomastoid muscle are retracted later-ally, away from the midline. The fingers are then sepa-rated and a skin wheal is raised between the fingers. A 22-gauge 3.5 needle is advanced perpendicular to the neck until the advancing needle meets the transverse process of C7. The needle is then withdrawn by 1 mm to bring it proximal to the longus colli fascia, stabilized,and then aspirated for any blood or cerebrospinal fluid (CSF). If aspiration is negative for blood or CSF, a short acting local anesthetic, eg, lidocaine, 5 mL of 1%, and a long acting anesthetic, eg, bupivacaine 10 mL of 0.25%are administered with intermittent aspiration. After fin-ishing the injection of local anesthetic, the needle is re-moved and the head of the bed is raised. See Figure 1. 24 With blockade of the stellate ganglion, ipsilateral Hor-ner’s signs occur. However, the ipsilateral upper extremity should be examined for an increase in temperature of at least 2 ? C when compared to the temperature of the con-tralateral limb, the presence of cutaneous vasodilatation,and the absence of any signs of sensory somatic blockade (in particular along the C6, C7, and C8 dermatomes) be-fore a stellate ganglion procedure can be called specific and adequate for the diagnosis of upper limb SMP. When performing this block appropriate resuscitation equip-ment must be available. The patient may complain of some hoarseness and the sensation of a lump in the https://www.doczj.com/doc/023711420.html,plications can include injection into the vertebral ar-tery, subarachnoid injection, pneumothorax, or brachial plexus lesion. 25

Lumbar Sympathetic Block

The sympathetic chain lies on the anterolateral aspect of the L2 vertebra. Therefore, an anesthetic injection at

this level is sufficient to obtain a sympathetic blockade of the ipsilateral lower extremity of the patient. Usually,the sympathetic trunk is located 1.5–2 inches deep to the transverse process. The major variable in performing this block is the distance from the skin to the transverse pro-cess and this depends on the body habitus of the patient. 25

Technique. In performing this block, the patient is placed on the stretcher in the prone position with a pillow placed under the abdomen. Counting cephalad from the L4-5 in-terspace the L2 spinous process is identified. Alterna-tively, this site can be verified by fluoroscopy. The back is prepped and draped. A skin wheal is raised 4 cm lateral to the L2 spinous process. A needle is passed perpendic-ular to the skin until it encounters the transverse process of L2. The needle is then withdrawn and passed caudal to the transverse process of L2 in a slightly medial direc-tion. The needle can be felt to pass the vertebrae. At this point the needle tip is close to the anterolateral aspect of the L2 vertebrae. A syringe is attached to the needle and 5 mL of 1% lidocaine and 10 mL of 0.25% bupivacaine are injected after aspiration is negative for blood or CSF.Aspiration is performed intermittently. 25 Another method of performing the block requires the physician to start more laterally, approximately 7–8 cm laterally, and ad-vance the needle to encounter the anterolateral aspect of the L2 vertebrae. The procedure is performed under fluo-roscopic guidance. 26 If the patient has SMP, relief should be obtained shortly after the procedure has been per-formed. An increase in skin temperature of at least 2 ?

C,increased cutaneous vasodilatation, and no signs of so-matic blockade should be noted in the ipsilateral lower limb before calling the sympatholytic procedure ade-

quate for the diagnosis of SMP (Figure 2).

Figure 1. (a) When performing a stellate ganglion block the carotid sheath is retracted and the neddle advanced. (b)This view demonstrates how the fingers retract the carotid sheath as the needle is ad-vanced to the stellate gan-glion.

TREATMENTS

Physical Therapy and Rehabilitation Medicine Immobilization appears to be an important predis-posing factor to the development of CRPS. Therefore,once this diagnosis is entertained, the patient should be started on an aggressive program of physical and occupa-tional therapy. Early treatment seems to be very advanta-geous. 27 The goal is to make the extremity as functional as possible. If the patient is receiving a series of sympa-

thetic blocks as a treatment for CRPS/SMP, it is impor-tant to employ physical therapy while the patient is ben-efiting from the sympatholytic effects of the block. In fashioning an individual treatment plan, the combina-tion of relaxation techniques, biofeedback, and cogni-tive behavioral therapy may be considered as adjuvant therapy for some patients.

Pharmacological Therapies

Antiepileptic drugs (AEDs). Some AEDs have been used successfully in the treatment of neuropathic pain, and,as such, they have also been frequently used as a treat-ment modality for CRPS. Controlled clinical trials have shown efficacy of gabapentin in the treatment of pos-therpetic neuralgia and painful diabetic neuropathy. 28,29 Overall clinical experience with gabapentin in the man-agement of CRPS has also been encouraging. Of note,gabapentin act on neither GABA receptors nor sodium channels, and its analgesic mechanism of action is unclear.Trigeminal neuralgia responds well to carbamazepine,while another AED, lamotrigine, has shown some efficacy for carbamazepine-resistant trigeminal neuralgia. 30 Car-bamazepine and lamotrigine are known to block voltage-gated neuronal membrane sodium channels. An overex-pression of these channels at the site of nerve injury (ie,neuroma) or an up-regulation of a nociceptor-specific so-dium channel subtype of the affected limb may play a pathological role in the case of CRPS, in particular per-haps, in CRPS type 2. Lastly, topiramate has been anecdot-ally used with benefit in the treatment of CRPS type 1. 31

Opioids, NMDA antagonists, and cannabinoids. Opi-oids are currently the most potent and effective analge-sics utilized to treat acute and chronic painful states, and as such they have been prescribed to patients suffering from intractable CRPS. Efficacy of opioid analgesics for neuropathic pain of noncancer origin has recently been established. 32,33,34 Unlike anti-inflammatory drugs, opi-oid agonists have no analgesic “ceiling dose” and do not cause direct organ damage. Except for constipation, tol-erance occurs for most of the opioid related side effects (eg, nausea, vomiting, respiratory depression, and drows-iness). Of note, studies indicate that patients on a stable opioid analgesic regimen do not report significant im-pairment in their driving ability, attention, mood, and general cognitive functioning. 35,36 Addiction (ie, a pat-tern of abnormal drug-seeking and drug-taking behav-iors for nontherapeutic purposes) and clinically relevant analgesic tolerance 36,37

are rarely seen in patients who

Figure 2. The lumbar sympathetic block can be performed (a) 4cm lateral to the spinous process of L2. The needle is advanced until it encounters the transverse process fL2 and then redi-rected caudally onto the anterolateral aspect of the body of L2.Alternatively (b) starting from a point more laterally, 7–8 cm, a needle is advanced under flouroscopic guidance until the ante-rolateral aspect of L2 is encountered.

receive these medications for pain control. Among the available opioid agents, methadone has unique proper-ties. It is a potent long acting mu opioid agonist with an intrinsic NMDA antagonistic effect. There is evidence gleaned from animal experiments and clinical observa-tions that NMDA receptors play an important role in the central mechanisms of hyperalgesia and chronic pain.34 Ketamine and the oral agent dextromethorphan are NMDA antagonists that may be used in conjunction with opioids in the management of severe neuropathic states characterized by allodynia and hyperalgesia. H owever, these agents, in particular ketamine, have a very narrow therapeutic window. Ketamine can easily cause intolera-ble side effects, such as hallucinations and memory im-pairment. Also of interest is the possibility that NMDA antagonists may prevent or counteract tolerance to opi-oid analgesia. These agents may be used at subclinical, and therefore safe, dosages in order to block the pro-gression of opioid tolerance.34

Several lines of evidence from experimental animal studies and clinical observations indicate that cannab-inoids, including the currently available antiemetic dronab-inol, have analgesic properties. Interestingly, the coadmin-istration of inactive doses of cannabinoids in combination with inactive doses of mu opioid agonists can produce an-tinociception. Moreover, cannabinoids appear to have a predominant antiallodynic/antihyperalgesic effect. This may be quite advantageous in the treatment of some in-capacitating neuropathic pain states.38 Antidepressants. Tricyclic antidepressants (TCAs) and selective serotonin uptake inhibitors (SSRIs) have often been utilized in the management of chronic pain. Post-herpetic neuralgia and painful diabetic neuropathy may respond to TCAs, such as amitriptyline, nortriptyline, or desipramine.39 Despite the fact that TCAs have been frequently used for more than 30 years in the manage-ment of chronic painful states, their role as primary an-algesics in the treatment of CRPS has been quite limited and unsatisfactory. Side effects of the TCAs, such as orthostatic hypotension, confusion, cardiotoxicity, uri-nary retention, weight gain, dry mouth, and nightmares may be common and persistent, causing serious difficul-ties to patients taking these medications.5 A new antide-pressant, venlafaxine, seems to possess the analgesic prop-erties of TCAs with the advantage of having fewer side effects. While being also used for neuropathic pain, SSRIs, such as paroxetine and fluoxetine, are not as efficacious as the TCAs.5,39 Antidepressants have an important role as adjuvants in the treatment of chronic pain. While not the mainstay medications for CRPS, these agents may be very useful in the management of several comorbidities frequently affecting the CRPS patient population such as anxiety, depression, and insomnia.5

Local anesthetics. Local anesthetics, eg, intravenous lidocaine or oral mexiletine, have been utilized in pa-tients with neuropathic pain.40 Mexiletine is a local an-esthetic with antiarrhytmic properties. The putative mech-anism of its analgesic action relies on the blockade of the neuronal membrane sodium channels,41,42 and in this, mexiletine is similar to some AEDs, such as carbamazepine or lamotrigine. If a cardiac conduction defect such as a 2nd or 3rd degree heart block is present, mexiletine may not be administered. In addition, if the patient is taking any anti-arrhytmic medications, a cardiology consultation should be obtained.5

Topical analgesics. Capsaicin, lidocaine, and clonidine are 3 agents that can be administered topically to pro-vide pain relief in patients suffering from CRPS and neu-ropathic pain.43,44 Capsaicin, the pungent substance found in the hot chili peppers is a C-fiber/nociceptor specific neu-rotoxin. Indeed, after prolonged use of topical capsaicin, a significant decrease in cutaneous density of C-fibers occurs. Capsaicin is known to activate the vanilloid receptor, which allows calcium and sodium to enter the nerve fi-ber.45,46 Following a brief period of depolarization (cor-responding to the initial burning pain elicited by capsai-cin application), desensitization of the nociceptor fibers occurs. The duration and the degree of the desensitizing effect on the nociceptors are dose-dependent. Unfortu-nately, poor patient compliance is common with the use of capsaicin creams at low concentrations (ie, over-the-counter preparations) since application is painful and a few weeks of multiple daily applications are needed to obtain some benefit.5 The clinical experience with low-dose capsaicin creams has given overall unimpressive re-sults. H owever, the administration of a large dose of capsaicin (compounded at ?1%), when given at the ap-propriate site (ie, at the presumed location of the pain generator) and under regional anesthesia, does appear to be efficacious.46 This novel method of capsaicin ad-ministration may provide a long-lasting benefit after a single application and may facilitate physical therapy and functional recovery of the affected limb. In patients suffering from SMP, transdermal clonidine has been shown to relieve allodynia in the area of patch application. Lidocaine patches have also been used in patients suffer-ing from CRPS, with some reports of benefit.47 Of note,

efficacy of transdermal lidocaine has been demonstrated for postherpetic neuralgia.43

Biphosphonates. It has been hypothesized that in CRPS type 1 regional osteoporosis (which has been observed to develop over time in the affected limb) as well as sen-sitization of nociceptors may be related, to some extent, to the pathological activation of osteoclasts and mac-rophages with consequent release of proinflammatory cytokinines, eg, tumor necrosis factor alpha, interleukin (IL) 1-beta, IL-6, and IL-8. Biphosphonates are com-monly used in the treatment of osteoporosis. Some of these agents when given intravenously and at a relatively high dose can also relieve bone pain secondary to meta-static disease. Biphosphonates such as clodronate, alen-dronate, and pamidronate may not only inhibit osteo-clastic and macrophagic activity, but also block or interfere with the macrophagic and osteoclastic release of proin-flammatory cytokinins. Of note, in the neuropathic pain model of sciatic nerve ligature, thermal hyperalgesia was significantly decreased by a biphosphonate.20 While the mechanism of action has not been totally elucidated, it has been suggested that the analgesic effect of intrave-nous biphosphonates may be mediated through the de-pletion of macrophages in the area of injury and20 the decreased release of proinflammatory cytokines.21,22,23 More recently intravenous biphosphonates have been noted to be efficacious in the treatment of CRPS. Intra-venous pamidronate was used in 10 women and 13 men with recalcitrant CRPS. A significant decrease in pain was observed.22 In a recently conducted randomized trial, Varennna et al. utilized clodronate as a 10-day intrave-nous treatment for CRPS type 1. Significant pain relief was obtained when compared to placebo controls.21 The following case report reflects a very recent anecdotal ex-perience from our institution, the Hospital for Joint Dis-eases (HJD) in New York City. It points out not only the potential useful role of intravenous biphosphonate ther-apy in the management of CRPS type 1, but also the im-portance of performing combinations of pharmacologi-cal trials according to our current understanding of CRPS pathophysiology.

Case Study

A 38-year-old female sustained a traumatic injury to her right arm after a fall, which resulted in significant wrist and arm pain. The patient underwent carpal tun-nel release after the diagnosis of posttraumatic carpal tunnel syndrome was made by electrodiagnostic studies;the arm was immobilized after the procedure. A few days later, the patient began to experience a new type of pain, which she described as a severe throbbing, burning pain associated with marked skin sensitivity to light touch and air movement. Swelling of the arm and skin color changes were noted. The cast was removed and the patient was diagnosed as having CRPS type 1. She underwent multiple stellate ganglion blocks (?10 blocks), which provided a few hours of pain relief with a decrease in allodynia after each block. An MRI of the right shoul-der was unremarkable, while a MRI of the cervical spine showed a narrow left C3-C4 foramen.

At the time of her presentation to the Comprehensive Pain Treatment Center at HJD (1 year after the onset of her symptoms), she was taking tramadol 100 mg PO QID, propoxyphene 60 mg PO TID PRN, amitriptyline 50 mg PO QHS, gabapentin 900 mg PO TID, Lidoderm patch QD, and ibuprofen 400-800 mg PO TID PRN. She was also applying 0.1 mg clonidine patch to the right deltoid region Q3-4 days. The patient rated her overall pain at 8 on the numerical scale 0–10 (where 0 ?no pain and 10 ? the worst pain imaginable). Her neu-rological examination revealed normal cranial nerves I-XII, full strength in the nonsymptomatic limbs (strength in the right arm was formally untestable due to excruciating pain elicited by minimal movements and tactile stimuli), normal coordination on finger to nose and heel/knee/shin testing bi-laterally, 1? DTRs in the asymptomatic limbs with down-going plantar responses (DTRs of the right arm were un-testable because of pain), normal gait, and a sensory examination remarkable for mechanical allodynia (prima-rily along the radial aspect of her right hand and along the lateral aspect of her forearm).

Three days after her initial consultation, the patient was hospitalized for more advanced pharmacological trials and diagnostic work-up. On day #1, propoxyphene, tramadol, amitriptyline and ibuprofen were discontinued. The patient was maintained on gabapentin at the dose of 600 mg QID. She was also started on a patient controlled analgesia (PCA) titration trial of intravenous (IV) fentanyl, intravenous pamidronate 90 mg infusion QD, tizanidine 2 mg BID PRN and dextromethorphan 30 mg PO TID.

On hospital day #2, the patient was still symptomatic of her allodynia. She rated her ongoing arm pain at 7 out of 10. She continued to use the IV PCA fentanyl. A transdermal fentanyl patch of 25 mcg/hour was added to her medication regimen. She complained of moderate drowsiness and moderate to severe nausea. For nausea and as analgesic adjuvant, the patient was started on dronabinol 10 mg PO BID, while for drowsiness the pa-

tient was given methylphenidate 5 mg PO Q6am and 5 mg PO Qnoon. The clonidine patch was moved from the patient’s shoulder to her right wrist. Tizanidine was withheld due to drowsiness. An MRI of the brachial plexus was unrevealing. On the morning of day #2, the patient underwent an EMG-NCV study. Because of pain, the patient was unable to tolerate the completion of the study. The preliminary report, however, indicated no evidence of entrapment neuropathy, brachial plexop-athy, or cervical radiculopathy. Of note, the patient re-ported a worsening of her pain following the EMG study. On the evening of day #2, the patient was in se-vere distress with worsening of her allodynia and was complaining of severe nausea. She received her second intravenous dose of pamidronate. The patient was noted to use the IV PCA fentanyl extensively. The dose of the fentanyl patch was increased to 50 mcg/h. A consulta-tion was also called for a spinal cord stimulation trial.

In the late morning of her hospital day #3, the patient began to experience pain relief, reporting a significant improvement in allodynia. The intensity of her ongoing pain decreased to 3 out of 10. The use of the IV PCA fentanyl decreased progressively throughout the day. The patient also reported a substantial improvement in drowsiness and nausea. She received her third infusion of pamidronate. By the evening of day #3, the patient rated her pain at 1 out of 10. Her mood was much im-proved. On hospital day #4, the patient reported resolu-tion of her allodynia and no ongoing pain except for brief and intermittent sharp mild pains in her right arm. The patient rated her pain at 0–1 out of 10. No allo-dynia or hyperalgesia was present in her right arm. The patient was discharged from the hospital in excellent conditions on the evening of day #4. She was given pre-scriptions for gabapentin 600 mg PO QID, dronabinol 10 mg PO BID, dextromethorphan 30 mg PO TID, fent-anyl patch 25 mcg/hour Q 3 days, clonidine patch 0.2 mg Q 3 days. The patient was discharged with remark-able pain relief. Ten days later, the patient returned to the HJD Comprehensive Pain Treatment Center for fol-low-up evaluation (follow-up visit #1). She stated that when she left the hospital she could not fill out her hos-pital prescriptions. She could not afford paying in ad-vance for the fentanyl patches, dronabinol, and dex-tromethorphan, since the overall cost amounted to more than $1000.00. However, the patient felt so great that she thought she had been cured. According to the pa-tient, her right hand had regained its normal shape and size after being shiny, swollen, and darker. At that point the patient’s medications included only gabapentin and the clonidine patch. At her follow-up visit, the patient was reporting 80% improvement in her condition when compared to her prehospitalization state. The swelling of her arm and the allodynia had vanished. Her baseline pain intensity level was 1 out of 10. She was still com-plaining of brief attacks of sharp pains. However, the patient reported that the frequency of the brief pains was at least 50% less when compared to the frequency of the attacks she had prior to the hospitalization.

At the time of her most recent follow-up (follow-up visit #2), 4 weeks following her hospital discharge, the patient was taking gabapentin 900 mg TID, clonidine 0.2 mg patches applied to the right wrist Q 3 days, and tizanidine 2 mg PO BID PRN. She continued to experi-ence good to excellent pain relief. The patient wrote a thank you letter:

“. . . I’d like to take this time to express my sincere gratitude for being able to participate in your treat-ment for my RSD. I have had surgery, been on count-less medications, and have endured at least 12 stellate ganglion blocks, which were painful . . . with results that almost ended me up on a respirator due to com-plications. Being a woman and a registered nurse, this disease has taken tolls on me that have been un-imaginable. I am right-handed and it has affected the extremity that is involved. My hand has been black and swollen for over a year. No other treatment that

I have ever received has done what you have accom-

plished in three days. I cried all weekend staring at my normal-sized hand. . . . This disease is so compli-cated, misunderstood, and unknown (even to the medical profession). . . . There are so many people af-fected by this condition that could benefit from these new therapies that you have to get the word out in any way. Thank you.” Signed by the patient.

Invasive Treatment Interventions

Implantable devices have become more popular in treating patients with intractable pain. Implantable de-vices include spinal cord stimulators and pumps. Spinal cord stimulators have been successfully used in patients with intractable pain that is not treatable by conven-tional methods. A recent randomized trial48 showed ef-ficacy of spinal cord stimulation for CRPS. Thirty-six patients were randomly assigned to receive spinal cord stimulation. After trial test stimulation, only 24 patients received permanent spinal cord stimulators. Patients who received spinal cord stimulation (SCS) and physical ther-

apy demonstrated a significant decrease in pain intensity when compared to those receiving physical therapy alone.

H owever, while significant pain relief was obtained, no significant improvement in the functional status was ob-served in the treated patients with SCS.52

Implantable pumps are used to deliver opioids, such as clonidine, local anesthetics, baclofen, and other emerg-ing analgesic agents (eg, SNX-111, adenosine), directly into the cerebral spinal fluid. Intrathecal morphine is cur-rently the most common medication administered by pump. However, prior to implanting an intrathecal mor-phine pump, opioid trials need to be performed to demon-strate that the patient’s pain is opioid responsive. Pumps can be implanted in a permanent fashion once trials are successful. In some patients who suffer from intractable dystonia associated with CRPS, intrathecal baclofen has been effective in decreasing the severity of dystonia.49

CONCLUSIONS

The medical conditions CRPS type 1 and CRPS type 2 are difficult disorders to understand and treat. Al-though not yet fully understood, advances are being made in the treatment of CRPS. Patients suffering from these disorders need to have individual treatment plans. They often require a series of diagnostic tests and phar-macological trials. As indicated, sympathetic blocks or medications such as antiepileptics, opioids, biphospho-nates, and topical agents often given in combination along with aggressive physical therapy can help patients suffering from these disorders. Implantable devices can aid the patient with chronic intractable disease. While progress is being made in treating patients with CRPS, it is important to remember that the goal of therapy is to obtain the maximal degree of pain relief and improve-ment in quality of life that will hopefully bring patients back to the most functional life-style possible.

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精神病学章节练习题 第六章 躯体疾病所致精神障碍

第六章躯体疾病所致精神障碍 【选择题】 (一)A型题 1.心脏病伴发的精神障碍,最多见的表现为 A.幻觉 B.妄想 C.抑郁发作 D. 焦虑情绪 E.行为迟缓 2.甲状腺功能减退伴发的精神障碍,禁用何种药物 A.氯丙嗪 B.奋乃静 C.地西泮 D. 氟哌啶醇 E.舒必利 3.垂体前叶功能减退伴发的精神障碍,治疗时禁用 A.氯丙嗪 B.奋乃静 C.地西泮 D. 肾上腺皮质激素 E.甲状腺素 4.严重的一氧化碳中毒可以出现假愈期,假愈期最长可达 A.10周 B.4周 C.6周 D. 1周 E.12周 5.肾上腺皮质激素引起的精神障碍,常发生于用药后 A.数分钟 B.数小时 C.数天到一周 D.数天或2个月内 E.半年以上 6.肾上腺皮质激素所致的精神障碍与哪种因素无关 A.用药剂量与持续的时间 B.病前性格 C.个体的机能状况 D.以上都是 E.以上都不是 7.某女性病人,分娩时大出血,产后体弱,表现乏力,消瘦,乳房萎缩,全身毛发脱落。一年后出现疑人害,吵闹,不认识自己的亲人,外出不知归家。此病人最可能的诊断是A.红斑狼疮所致的精神障碍 B.多发性硬化 C.白塞病所致精神障碍D. 席汉病所致精神障碍E.阿狄森病所致精神障碍 8.男性患者,36岁。入院诊断乙肝后肝硬化。患者妻子向你报告他有些反常,如刷过牙又找牙刷,说要去刷牙,东西放置比平时凌乱。情绪不稳,有时显得很高兴,有时又流泪。检查时发现患者一般对答尚切题,对刷牙一事,不好意思地说“忘了”。这时你的判断和首先需要做的是 A.在病历上记录患者家属反映的情况和你的检查结果,继续观察 B.安慰家属,告诉她病人反应正常,不必过分担心 C.向护士或同病室的病友了解情况 D.注意检查患者的认知功能,提防肝性脑病的发生 E.复查肝功能 9.糖尿病伴发的精神障碍治疗时下列哪种药物需要慎用或禁用 A.氯丙嗪 B.氟哌啶醇 C.地西泮 D. 阿普唑伦 E.多塞平 10.躯体感染性疾病所致精神障碍以下哪条不对 A.起病较急,病程发展常起伏不定 B.精神症状通常与感染性躯体疾病消长平行 C.大多预后不良 D.及时发现原发感染性疾病是正确诊断的关键 E.处理上最重要的是治疗原发疾病 11.躯体疾病所致的精神障碍的处理原则以下哪项不对 A.首先必须治疗引起精神障碍的原发躯体疾病 B.支持疗法包括维持水电解质平衡、充足的营养供应等 C.护理包括安静、安全的环境和防止意外发生等

二、分析天平的基本操作

模块二滴定分析基本操作任务一分析天平的基本操作 一、分析天平的分类 分析天平是定量分析中最常用的准确称量物质的仪器。分析天平分类:等臂(双盘)分析天平、不等臂(单盘)分析天平、电子天平。 二、电子天平的介绍 1、工作原理:电磁平衡原理,秤盘通过支架连杆支架作用于线圈上,重力方向向下。线圈内有电流通过时,根据电磁基本理论,通电的导线在磁场中将产生一个向上作用的电磁力,与秤盘重力方向相反大小相同,与之相平衡,而通过导线的电流与被称物体的质量成正比。 2、性能特点:a.使用寿命长,性能稳定,灵敏度高,体积小,操作方便 b.称 量速度快、精度高 c.具有自动校准、累计称量、超载显示、自动去皮等功能 3、称量的一般程序 水平调节——打扫——预热——开启显示器——校准——称量——结束工作 ①水平调节检查水平仪,调节水平调节脚,使水泡位于水平仪中心。 ②打扫打扫天平秤盘 ③预热通电预热30min以上 ④开启显示器按ON键,显示器亮,显示屏出现0.0000g ⑤校准按“校准”键 ⑥称量被称物置于秤盘中间进行称量 ⑦称量结束工作取下被称物,核对零点,关闭天平,进行使用登记 4、基本称量方法 ①直接称量法将称量物直接放在天平盘上直接称量物体的质量。例如,称量 小烧杯的质量,容量器皿校正中称量某容量瓶的质量,重量分析实验中称量某坩埚的质量等,都使用这种称量法。 ②固定质量称量法

用于称量某一固定质量的试剂(如基准物质)或试样。适于称量不易吸潮、在空气中能稳定存在的粉末状或小颗粒样品。 A、去皮将干燥的容器置于秤盘上,待显示平衡后按“去皮”键扣除皮重并显示零点 B、加样打开天平门,用药匙将试样抖入容器内,使之达到所需质量。 固定质量称量法注意:若不慎加入试剂超过指定质量,用牛角匙取出多余试剂,直至试剂质量符合指定要求为止。严格要求时,取出的多余试剂应弃去,不要放回原试剂瓶中。操作时不能将试剂散落于天平盘等容器以外的地方,称好的试剂必须定量地由表面皿等容器直接转入接受容器,此即所谓“定量转移”。 ③递减称量法(减量法) 用于称量一定质量范围的样品或试剂。样品易吸水、易氧化或易与二氧化碳等反应时,可选择此法。。 称量步骤:试样的保存——取出盛试样的称量瓶——称出称量瓶质量——敲样——再称出其质量——样品质量——连续称样——称量工作结束 A、试样保存待称样品放于洁净的干燥容器(称量瓶)中,置于干燥器中保存 B、取出称量瓶左手戴手套取出称量瓶或者用折叠成约1cm的纸取出 C、称出称量瓶质量称出称量瓶质量,记录数据 D、敲样将称量瓶取出,在接收容器的上方倾斜瓶身,用称量瓶盖轻敲瓶口上部使试样慢慢落入容器中,瓶盖始终不要离开接受器上方。当倾出的试样接近所需量时,一边继续用瓶盖轻敲瓶口,一边逐渐将瓶身竖直,使粘附在瓶口上的试样落回称量瓶,然后盖好瓶盖,准确称其质量。两次质量之差,即为试样的质量。按上述方法连续递减,可称量多份试样。

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