Imaging Studies:
Radiography may show periarticular demineralization in spots 3-6weeks after onset. Extension of osteoporosis is more extensivethan by immobilization.
Measuring skin temperature-simple but important. It is donethrough perception tactile surface thermometers and infraredthermometers. Vascular phases include regional pain syndrome-hyperemia on the skin temperature rises and the onsetof cold-member temperature drops late in the disease.Thermography is a test that demonstrates quantitative differencestenperatura skin.
Sudomotorii function testing: sweat-test evaluates the reflexresponse of the skin sympathetic sudomotor, sudomotor axonalreflex quantitative sweat test chemical.
Electrodiagnostics studies: results of electromyography and nerveare normal driving. Quantitative sensory testing assesses theperception of pain. Use stimuli accurate, reproducible allowingcomparison of symptomatic areas with asymptomatic toward sexand age and changes during treatment.
Laser Doppler imaging is an immediate test, noninvasive andpainless for the study of segmental autonomous function. Stimulisuch as cold pressure and inspiration are used to quantify skinvasoconstrictive reflexes.
The differential diagnosis is made with the following conditions:tendonitis, adhesive sealed, Neural brachial, brachial plexopatianeoplastic, postpolio syndrome, plexopatie radioatii induced,chronic pain syndrome, compartment syndrome, diabeticneuropathy, ischemic neuropathy monomelica, spasticity, spinal and neurological claudication .
Wednesday, June 1, 2011
Regional Pain
Regional pain syndrome may develop as a consequence of limb trauma without nerve damage or reflex sympathetic dystrophy or without obvious nerve injury-cauzalgia. This syndrome is relatively common in the population. Has an unknown disease. Complex Regional Pain is a variable that is determined probably symptomatic of multiple causes through different pathophysiological mechanisms. Changes in peripheral and central somatosensory, motor and autonomous interaction and associated pathological sympathetic systems are described as basic mechanisms.The condition can occur at any age, but the average diagnosis is 42 years. It affects men and women, but is three times more common in women.
Regional affected patient experience pain, tremors and muscle weakness, trophic changes of skin coloration and the affected segment, limb movement disorders, depression, anxiety, chronic edema, recurrent infection of the limb, hipoestezii. 20-70% of patients with hemiplegia will suffer from this syndrome.
Hospitalization is usually necessary for patients with regional pain syndrome, but it depends on the invasiveness of treatment for pain and severity of the case. Sometimes a short period of hospitalization is required for persons who require continuous nerve blocks. These patients may be controlled by other conditions orthopedic surgery.Physical therapy in combination with the Occupational play an important role in restoring function. It aims to increase strength and flexibility gradually. These patients have co miofasciala pain can be treated with relaxation techniques and massage miofasciala.
Strategies include improving the pharmacological treatment of pain, sympatholytic interventions and rehabilitation.Evolution of patients can be good if treatment is begun early, ideally within the first 3 months after onset. If treatment is delayed condition is rapidly expanding to the entire member and changes in bone, skin and nerves become irreversible. Member may suffer muscle atrophy, loss of function and amputation.
For patients who can not be treated with narcotic analgesia practice of neural blockade, although neuropathic pain can be very resistant to standard analgesics. All treatments have to follow the restoration of function. The use of drugs, sympathetic blocks, and psychotherapy help to control pain. Early medical intervention is important for its success. The duration between the onset of treatment and clinical improvement varies from several days to several years.
Pathogenesis
There are several hypotheses to the mechanism of sympathetic mediated pain and describes the central and peripheral components. It was demonstrated early loss of peripheral vasoconstrictor activity-autonomous dysfunction deriving from the central nervous system. Case vadculare abnormalities is unknown.The old concept of regional peripheral exaggerated inflammatory response is supported by new data indicating the accumulation of immunoglobulin G region.Electronic Studies of skeletal muscle biopsies showed reduced mitochondrial enzyme activity, mitochondrial veziculizarea, miofibrilelor decay, abnormal deposits lipofuscina, swelling and thickening of basement membrane layers encoteliale-signs of oxidative stress. Oxygen consumption is reduced in the affected limbs and regional pain syndrome has been described to reduce pain after taking oral avasodilatatoare.After a partial nerve injury, excessive activation of C fibers antidromica unaffected and the release of neuropeptides lead to active vasodilation in the territory innervated by the nerve affected.
Regional pain syndrome is divided into two types depending on the presence of nerve injury after injury:I-type known as reflex sympathetic dystrophy, Sudeck atrophy, reflex neurovascular dystrophy without evidence of nerve damageCauzalgia-type II or with nerve damage.
Causes and risk factors:Various injuries can lead to regional pain syndrome:-Trauma, dislocations, fractures, surgery, burns, bruises-Neurological disorders, stroke, tumor, siringomelieHerpes-zoster infection-Myocardial infarction, musculoskeletal disorders-Neoplasia, causes spontaneous / idiopathic.
Regional affected patient experience pain, tremors and muscle weakness, trophic changes of skin coloration and the affected segment, limb movement disorders, depression, anxiety, chronic edema, recurrent infection of the limb, hipoestezii. 20-70% of patients with hemiplegia will suffer from this syndrome.
Hospitalization is usually necessary for patients with regional pain syndrome, but it depends on the invasiveness of treatment for pain and severity of the case. Sometimes a short period of hospitalization is required for persons who require continuous nerve blocks. These patients may be controlled by other conditions orthopedic surgery.Physical therapy in combination with the Occupational play an important role in restoring function. It aims to increase strength and flexibility gradually. These patients have co miofasciala pain can be treated with relaxation techniques and massage miofasciala.
Strategies include improving the pharmacological treatment of pain, sympatholytic interventions and rehabilitation.Evolution of patients can be good if treatment is begun early, ideally within the first 3 months after onset. If treatment is delayed condition is rapidly expanding to the entire member and changes in bone, skin and nerves become irreversible. Member may suffer muscle atrophy, loss of function and amputation.
For patients who can not be treated with narcotic analgesia practice of neural blockade, although neuropathic pain can be very resistant to standard analgesics. All treatments have to follow the restoration of function. The use of drugs, sympathetic blocks, and psychotherapy help to control pain. Early medical intervention is important for its success. The duration between the onset of treatment and clinical improvement varies from several days to several years.
Pathogenesis
There are several hypotheses to the mechanism of sympathetic mediated pain and describes the central and peripheral components. It was demonstrated early loss of peripheral vasoconstrictor activity-autonomous dysfunction deriving from the central nervous system. Case vadculare abnormalities is unknown.The old concept of regional peripheral exaggerated inflammatory response is supported by new data indicating the accumulation of immunoglobulin G region.Electronic Studies of skeletal muscle biopsies showed reduced mitochondrial enzyme activity, mitochondrial veziculizarea, miofibrilelor decay, abnormal deposits lipofuscina, swelling and thickening of basement membrane layers encoteliale-signs of oxidative stress. Oxygen consumption is reduced in the affected limbs and regional pain syndrome has been described to reduce pain after taking oral avasodilatatoare.After a partial nerve injury, excessive activation of C fibers antidromica unaffected and the release of neuropeptides lead to active vasodilation in the territory innervated by the nerve affected.
Regional pain syndrome is divided into two types depending on the presence of nerve injury after injury:I-type known as reflex sympathetic dystrophy, Sudeck atrophy, reflex neurovascular dystrophy without evidence of nerve damageCauzalgia-type II or with nerve damage.
Causes and risk factors:Various injuries can lead to regional pain syndrome:-Trauma, dislocations, fractures, surgery, burns, bruises-Neurological disorders, stroke, tumor, siringomelieHerpes-zoster infection-Myocardial infarction, musculoskeletal disorders-Neoplasia, causes spontaneous / idiopathic.
Reflex Sympathetic Dystrophy - Treatment
Evolution of reflex sympathetic dystrophy is variable and unpredictable. Treatment is uncertain because there are few known pathogenesis and therapeutic procedures performed.Clinical experience shows that early recognition and treatment are necessary to avoid permanent disability, and limited efficacy once the patient has reached the chronic fibrotic phase. The incidence and severity of disease can be reduced by initiating prevention measures known as trigger situations: stroke, hemiplegia, fractures. These include the immediate mobilization of the affected extremity with active and passive exercises.There are two major therapeutic surgical approaches in the early stages of the disease: anti-inflammatory therapy and sympathetic blockade.
Sympathetic Blockade:It involves injecting a local anesthetic stellate ganglion and upper dorsal sympathetic efferent sympathetic impulses to block the affected extremity. Lidocaine and bupivacaine with or without epinephrine are used. This procedure heats the skin, inhibit sweating and cause hot flashes. A successful blockade is indicated by the development of ipsilateral Horner's syndrome: ptosis, miosis and enophtalmia. Reduce symptoms in 30 minutes, confirming the diagnosis. Once the patient is properly locked will ensure its participation in physical therapy. Although interruption lasts a few hours a few days the benefits are maintained. Use 1-2 per week blockade. Sympathectomy is performed for persistent symptoms or interventional catheter is placed subcutaneously for the blockade continues.
Sympatholytic medications:Simpaticolitice drugs may be effective when used alone in early stage disease. They are useful in combination with sympathetic blockade or sympathectomy in late stages. Peripheral regional sympathetic blockade with drugs simpaticolitice, as fenoxibenzamina has variable results. It is most useful in the early stages.
Anti-inflammatory medications:Although NSAIDs may bring pain relief are not effective in improving skin changes or evolution bloii. Corticosteroids in high doses can dramatically reduce pain, swelling and stiffness. They are useful in the early stages of the disease. Calcitonin is an anti-inflammatory but does not cause changes of reversibility of inflammation and pain. Subcutaneous injections are administered daily for 4-8 weeks.
Surgical therapy:Lumbar or upper thoracic sympathectomy:Indicate whether the procedure and anti-inflammatory improvement with sympathetic blockade do not appear constantly and relapsing disease despite treatment. These procedures are reserved for patients who have an initial response to sympathetic blockade.Indications include disease longer than 6 months and no permanent resolution 5 blockades made soup. The most significant improvement after the procedure is to reduce pain, although the circulation, movement and function are less affected. It opted for the procedure in early stage disease, after he installed fibrosis is minimal functional soothe joints.Chemical sympathectomy by phenol injection in precupune sympathetic chain. Spinal cord stimulation has been investigated and the relief of pain and function.
Physical Therapy:It is essential for control of reflex sympathetic dystrophy. It is a system that gradually improved after sympathetic blockade or sympathectomy, with passive exercise and active later. Massage the affected extremity is an important step in therapy.Thermotherapy relaxes muscles, improves movement and pain.
Amputation:It is very rarely recommended treatment. Risk of regional pain in the stump.
Therapies research:Vitamin C is useful due to its antioxidant properties. Medicines that may be helpful in some patients, still experimental include: antiepileptics, antidepressants, local anetstezicele creams with lidocaine or mexiletine, local analgesics, capsaicin, clonidine topical.
Prognosis:Approximately 80% of patients with this disease shows complete relief of pain and associated symptoms in 18 months, still not established any criteria to predict evolution. Some patients do not regress spontaneously and are cured by treatment. 50-80% of patients experience pain or disability limit secondary movements.Long duration of symptoms, this trophic changes associated with adverse prognosis and disability.Disease is associated with negligible mortality, although morbidity is extremely high. Despite good results after sympathetic blockade, and mobilization techniques, limb weakness is seen in 50% of patients. Achieving a normal mobility is observed only in 60% of patients.
Sympathetic Blockade:It involves injecting a local anesthetic stellate ganglion and upper dorsal sympathetic efferent sympathetic impulses to block the affected extremity. Lidocaine and bupivacaine with or without epinephrine are used. This procedure heats the skin, inhibit sweating and cause hot flashes. A successful blockade is indicated by the development of ipsilateral Horner's syndrome: ptosis, miosis and enophtalmia. Reduce symptoms in 30 minutes, confirming the diagnosis. Once the patient is properly locked will ensure its participation in physical therapy. Although interruption lasts a few hours a few days the benefits are maintained. Use 1-2 per week blockade. Sympathectomy is performed for persistent symptoms or interventional catheter is placed subcutaneously for the blockade continues.
Sympatholytic medications:Simpaticolitice drugs may be effective when used alone in early stage disease. They are useful in combination with sympathetic blockade or sympathectomy in late stages. Peripheral regional sympathetic blockade with drugs simpaticolitice, as fenoxibenzamina has variable results. It is most useful in the early stages.
Anti-inflammatory medications:Although NSAIDs may bring pain relief are not effective in improving skin changes or evolution bloii. Corticosteroids in high doses can dramatically reduce pain, swelling and stiffness. They are useful in the early stages of the disease. Calcitonin is an anti-inflammatory but does not cause changes of reversibility of inflammation and pain. Subcutaneous injections are administered daily for 4-8 weeks.
Surgical therapy:Lumbar or upper thoracic sympathectomy:Indicate whether the procedure and anti-inflammatory improvement with sympathetic blockade do not appear constantly and relapsing disease despite treatment. These procedures are reserved for patients who have an initial response to sympathetic blockade.Indications include disease longer than 6 months and no permanent resolution 5 blockades made soup. The most significant improvement after the procedure is to reduce pain, although the circulation, movement and function are less affected. It opted for the procedure in early stage disease, after he installed fibrosis is minimal functional soothe joints.Chemical sympathectomy by phenol injection in precupune sympathetic chain. Spinal cord stimulation has been investigated and the relief of pain and function.
Physical Therapy:It is essential for control of reflex sympathetic dystrophy. It is a system that gradually improved after sympathetic blockade or sympathectomy, with passive exercise and active later. Massage the affected extremity is an important step in therapy.Thermotherapy relaxes muscles, improves movement and pain.
Amputation:It is very rarely recommended treatment. Risk of regional pain in the stump.
Therapies research:Vitamin C is useful due to its antioxidant properties. Medicines that may be helpful in some patients, still experimental include: antiepileptics, antidepressants, local anetstezicele creams with lidocaine or mexiletine, local analgesics, capsaicin, clonidine topical.
Prognosis:Approximately 80% of patients with this disease shows complete relief of pain and associated symptoms in 18 months, still not established any criteria to predict evolution. Some patients do not regress spontaneously and are cured by treatment. 50-80% of patients experience pain or disability limit secondary movements.Long duration of symptoms, this trophic changes associated with adverse prognosis and disability.Disease is associated with negligible mortality, although morbidity is extremely high. Despite good results after sympathetic blockade, and mobilization techniques, limb weakness is seen in 50% of patients. Achieving a normal mobility is observed only in 60% of patients.
Reflex Sympathetic Dystrophy - Diagnosis
Imaging Studies:
Simple radiography showed pronounced demineralization of the skeleton MEMBER who becomes severely affected with diseaseprogression. Articular erosions are not present. Demineralizationbegins at the ends of bones and progresses until it becomessmooth.
Scanning scintigraphy is positive in 50% of patients. The study isuseful in the early stages of the disease. Items are abnormal latestages, with increased joint and periarticular capture. This findingis not specific reflex sympathetic dystrophy but cause suspicion.
The differential diagnosis is made with the following conditions:acute nerve injury, cellulitis, septic arthritis, upper limb occlusivedisease, median neuropathy, neurosarcoidoza, diabeticneuropathy, alcoholic neuropathy, toxic neuropathy, cauzalgia,insuficeinta pressure chronic peripheral nerve compression,plexopatii, flebotromboza, rheumatologic diseases.
Simple radiography showed pronounced demineralization of the skeleton MEMBER who becomes severely affected with diseaseprogression. Articular erosions are not present. Demineralizationbegins at the ends of bones and progresses until it becomessmooth.
Scanning scintigraphy is positive in 50% of patients. The study isuseful in the early stages of the disease. Items are abnormal latestages, with increased joint and periarticular capture. This findingis not specific reflex sympathetic dystrophy but cause suspicion.
The differential diagnosis is made with the following conditions:acute nerve injury, cellulitis, septic arthritis, upper limb occlusivedisease, median neuropathy, neurosarcoidoza, diabeticneuropathy, alcoholic neuropathy, toxic neuropathy, cauzalgia,insuficeinta pressure chronic peripheral nerve compression,plexopatii, flebotromboza, rheumatologic diseases.
Reflex Sympathetic Dystrophy
Reflex sympathetic dystrophy or complex regional pain syndrome is a clinical syndrome with variable and unknown causes evolution characterized by pain, swelling and vasomotor dysfunction of the extremities. The condition is often the result of trauma or surgery.
It is estimated that 5% of the population that has suffered trauma to the upper extremity reflex sympathetic dystrophy develops.Extremity immobilization can trigger disease. Without prophylactic measures, active physical therapy, reflex sympathetic dystrophy develops in 20% of people with stroke hemiplegia. The disease does not cause mortality.
The disease affects mainly women of 25-55 years. It is precipitated by trauma or surgery and affects the upper and lower extremities. The pain is accompanied by edema, vasomotor changes, sudomotorii, motor and trophic. It extends to other areas of the body. Multiple pharmacological and pharmacological interventions fail many times. Interfere with the profession, sleeping, moblitatea and personal care. Remissions and relapses are frequent.
80% of patients with this disease shows complete relief of pain and associated symptoms in 18 months. Some patients do not regress spontaneously and are cured by treatment. 50-80% of patients experience pain or disability limit secondary movements.Long duration of symptoms, this trophic changes associated with adverse prognosis and disability.Disease is associated with negligible mortality, although morbidity is extremely high. Despite good results after sympathetic blockade, and mobilization techniques, limb weakness is seen in 50% of patients.
Pathogenesis of reflex sympathetic dystrophyIt is not known. Three conditions are considered important in its development, including persistent painful lesions, succeptibilitatea predisposition to develop disease and an abnormal sympathetic reflex. Succeptibilitate factors are unknown and may include genetic predisposition in some patients a tendency towards increased sympathetic activity. This includes cold hands, hyperhidrosis, or history of seizures.
Healthy individuals presents a sympathetic response to injury, the vasoconstriction to prevent blood loss and swelling. This initial response is rapidly replaced by vasodilation and increased capillary permeability, allowing tissue repair.In patients with reflex sympathetic dystrophy, this sympathetic response continues. The reasons for maintaining sympathetic reflex are unknown but are related to dysfunction of the central regulation painful stimuli. This lack of control is mediated by neurons in the spinal cord. Prolonged ischemia caused by vasoconstriction causes pain setting that promotes the release of a sympathetic reflex arc and vasospasm. This is accompanied by local response to trauma with the release of substantial amounts of proinflammatory mediators such as histamine, serotonin and bradykinin. End result is a swollen, painful nonfunctionala.
Causes and risk factors:Reflex sympathetic dystrophy is posttraumatic or postsurgical and can occur on previously healthy end without known trigger.
Traumatic causes:-Laceration, abrasion, venipunctie, intramuscular injections-Gunshot wounds, neck and shoulder injuries-Traumatic acute carpal tunnel syndrome-Thoracic trauma, fracture or dislocation of the spine.
Postsurgical cases:Carpal-tunnel release, tooth extraction-Rib resection and repair of fractures-Postartroscopie.
Local and general diseases:-Nerve compression syndromes, arthritis, tissue ischemia-Stenosing tenosynovitis, myocardial infarction-Stroke, Pancoast tumorPancreatic-cancer, herpes zoster.
Possible risk factors:-Persistent mechanical irritation of peripheral nervesIncomplete regeneration of peripheral nerves-Abnormal neurotransmitter-activityNutritional deprivation secondary-abnormal arteriovenous shuntsGenetic predisposition or family-Cigarette-smoking, schizophrenia or depression.
Signs and symptomsThe three clinical stages of reflex sympathetic dystrophy are: acute, subacute and chronic. Acute form evolves around three months.Burning pain is one of the first symptoms initially limited function.Swelling, redness, vasomotor instability that worsens with cold extremities, hyperhidrosis are common. Demineralization of the skeleton is determined by the lack of limb use. If the process is not stopped or reversed in the acute phase, the condition can progress to the subacute stage, evolving nine months. The patient developed persistent pain and swelling fixed end, which was reversible during the acute phase. Redness acute stage is replaced by the pallor and cyanosis, or hyperhidrosis, or dry skin.Progressive loss of function, cause pain and fibrosis with chronic inflammation of joints. Lead to distortion from the cameraman finger flexion. The skin and subcutaneous tissues begin to atrophy.Bone demineralization is pronounced.
If the process continues, chronic phase develops in a year after onset. This stage may develop several years or may be permanent. The pain is more variable during this period. Continue undiminished or decreasing. Edema tends to resolve over time, leaving fibrosis around the joints. The skin is dry, pale, cold and bright. Flexion and extension are absent. Marked loss of function and stiffness, and osteoporosis is extreme. The upper extremity is manifested by frozen shoulder and hand in paw.
Reflex sympathetic dystrophy affecting the hands, wrist, shoulder, ankle and foot. Symptomatic disease is a condition of the extremities. Dystrophy is recognized and accepted best if the regional distribution affects the upper extremity involving the distal forearm, wrist, hands and occasionally the arm and shoulder. At the lower end are particularly affected foot and ankle.
Physical examination:Reflex sympathetic dystrophy usually affects only one extremity. It is bilateral in 25% of cases, but more prominent on one side.
Pain:-Constant and disproportionate to the injury-May be exacerbated by environmental factors such as noise and stress, bright lights, touch, active movement, passive-Is described as burning, like a knife as a pressure or sfisiietoare-Starts locally but can progress to the entire extremity.
Increased sympathetic activity:-Hyperhidrosis-Cold hands, pale-History of frequent seizures.
Edema:-Is the most frequently detected and the physical element is always disproportionate to the severity of the lesion-Pain, swelling and color changes may be more prominent in the early stages of addiction-Edema worsen than improve and extend beyond the region initially affectedGrows as a swelling-brown, which progresses to fibrosis nepruriginos intense joint.
Stiffness is severe and debilitating for the patient.
Skin discoloration:-Stage of the disease varies-May be cyanotic, dusty, pale or red skin can lead to hypopigmentation-Starts as redness or interphalangeal metacarpofalangiana and increases the whole deal.
Abnormal skin hydration:Wet-skin-hyperhidrosisLate-dry-skin.
Sensitivity is located initially but progressed to generalized form.Sensitivity is articular and periarticular. Patients and shows allodinia hiperpatie (mild pain on pressure).Skin and subcutaneous fat atrophy is overdue.
It is estimated that 5% of the population that has suffered trauma to the upper extremity reflex sympathetic dystrophy develops.Extremity immobilization can trigger disease. Without prophylactic measures, active physical therapy, reflex sympathetic dystrophy develops in 20% of people with stroke hemiplegia. The disease does not cause mortality.
The disease affects mainly women of 25-55 years. It is precipitated by trauma or surgery and affects the upper and lower extremities. The pain is accompanied by edema, vasomotor changes, sudomotorii, motor and trophic. It extends to other areas of the body. Multiple pharmacological and pharmacological interventions fail many times. Interfere with the profession, sleeping, moblitatea and personal care. Remissions and relapses are frequent.
80% of patients with this disease shows complete relief of pain and associated symptoms in 18 months. Some patients do not regress spontaneously and are cured by treatment. 50-80% of patients experience pain or disability limit secondary movements.Long duration of symptoms, this trophic changes associated with adverse prognosis and disability.Disease is associated with negligible mortality, although morbidity is extremely high. Despite good results after sympathetic blockade, and mobilization techniques, limb weakness is seen in 50% of patients.
Pathogenesis of reflex sympathetic dystrophyIt is not known. Three conditions are considered important in its development, including persistent painful lesions, succeptibilitatea predisposition to develop disease and an abnormal sympathetic reflex. Succeptibilitate factors are unknown and may include genetic predisposition in some patients a tendency towards increased sympathetic activity. This includes cold hands, hyperhidrosis, or history of seizures.
Healthy individuals presents a sympathetic response to injury, the vasoconstriction to prevent blood loss and swelling. This initial response is rapidly replaced by vasodilation and increased capillary permeability, allowing tissue repair.In patients with reflex sympathetic dystrophy, this sympathetic response continues. The reasons for maintaining sympathetic reflex are unknown but are related to dysfunction of the central regulation painful stimuli. This lack of control is mediated by neurons in the spinal cord. Prolonged ischemia caused by vasoconstriction causes pain setting that promotes the release of a sympathetic reflex arc and vasospasm. This is accompanied by local response to trauma with the release of substantial amounts of proinflammatory mediators such as histamine, serotonin and bradykinin. End result is a swollen, painful nonfunctionala.
Causes and risk factors:Reflex sympathetic dystrophy is posttraumatic or postsurgical and can occur on previously healthy end without known trigger.
Traumatic causes:-Laceration, abrasion, venipunctie, intramuscular injections-Gunshot wounds, neck and shoulder injuries-Traumatic acute carpal tunnel syndrome-Thoracic trauma, fracture or dislocation of the spine.
Postsurgical cases:Carpal-tunnel release, tooth extraction-Rib resection and repair of fractures-Postartroscopie.
Local and general diseases:-Nerve compression syndromes, arthritis, tissue ischemia-Stenosing tenosynovitis, myocardial infarction-Stroke, Pancoast tumorPancreatic-cancer, herpes zoster.
Possible risk factors:-Persistent mechanical irritation of peripheral nervesIncomplete regeneration of peripheral nerves-Abnormal neurotransmitter-activityNutritional deprivation secondary-abnormal arteriovenous shuntsGenetic predisposition or family-Cigarette-smoking, schizophrenia or depression.
Signs and symptomsThe three clinical stages of reflex sympathetic dystrophy are: acute, subacute and chronic. Acute form evolves around three months.Burning pain is one of the first symptoms initially limited function.Swelling, redness, vasomotor instability that worsens with cold extremities, hyperhidrosis are common. Demineralization of the skeleton is determined by the lack of limb use. If the process is not stopped or reversed in the acute phase, the condition can progress to the subacute stage, evolving nine months. The patient developed persistent pain and swelling fixed end, which was reversible during the acute phase. Redness acute stage is replaced by the pallor and cyanosis, or hyperhidrosis, or dry skin.Progressive loss of function, cause pain and fibrosis with chronic inflammation of joints. Lead to distortion from the cameraman finger flexion. The skin and subcutaneous tissues begin to atrophy.Bone demineralization is pronounced.
If the process continues, chronic phase develops in a year after onset. This stage may develop several years or may be permanent. The pain is more variable during this period. Continue undiminished or decreasing. Edema tends to resolve over time, leaving fibrosis around the joints. The skin is dry, pale, cold and bright. Flexion and extension are absent. Marked loss of function and stiffness, and osteoporosis is extreme. The upper extremity is manifested by frozen shoulder and hand in paw.
Reflex sympathetic dystrophy affecting the hands, wrist, shoulder, ankle and foot. Symptomatic disease is a condition of the extremities. Dystrophy is recognized and accepted best if the regional distribution affects the upper extremity involving the distal forearm, wrist, hands and occasionally the arm and shoulder. At the lower end are particularly affected foot and ankle.
Physical examination:Reflex sympathetic dystrophy usually affects only one extremity. It is bilateral in 25% of cases, but more prominent on one side.
Pain:-Constant and disproportionate to the injury-May be exacerbated by environmental factors such as noise and stress, bright lights, touch, active movement, passive-Is described as burning, like a knife as a pressure or sfisiietoare-Starts locally but can progress to the entire extremity.
Increased sympathetic activity:-Hyperhidrosis-Cold hands, pale-History of frequent seizures.
Edema:-Is the most frequently detected and the physical element is always disproportionate to the severity of the lesion-Pain, swelling and color changes may be more prominent in the early stages of addiction-Edema worsen than improve and extend beyond the region initially affectedGrows as a swelling-brown, which progresses to fibrosis nepruriginos intense joint.
Stiffness is severe and debilitating for the patient.
Skin discoloration:-Stage of the disease varies-May be cyanotic, dusty, pale or red skin can lead to hypopigmentation-Starts as redness or interphalangeal metacarpofalangiana and increases the whole deal.
Abnormal skin hydration:Wet-skin-hyperhidrosisLate-dry-skin.
Sensitivity is located initially but progressed to generalized form.Sensitivity is articular and periarticular. Patients and shows allodinia hiperpatie (mild pain on pressure).Skin and subcutaneous fat atrophy is overdue.
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