The complications and side effects are very significant, such as irreversible compensatory sweating (20% to 50%), low satisfaction with results, Claude-Bernard-Horner syndrome, pneumothorax, hemothorax, asymmetry of results, intercostal neuralgia, causalgia, incomplete results, and anesthetic complications11-13.
Retroperitoneoscopic lumbar sympathectomy (video-assisted): this technique is effective in the treatment of isolated or persistent plantar hyperhidrosis (compensatory after thoracic sympathectomy). The treatment consists of removing the nerves of the sympathetic chain located in the abdomen, in the anterolateral portion of the lumbar vertebrae. It requires hospitalization and is carried out under general anesthesia. It may lead to complications such as lesions of structures adjacent to the sympathetic chain, light abdominal distension, neuralgia, and causalgia as well as hypoesthesia in the thighs and groin, limitation of leg movement,
paresthesia in the anterolateral abdominal wall, change in libido, dyspareunia, pulmonary thromboembolism, hemorrhages, arrhythmias, and cardiac decompensation, amongst others. It definitively eliminates plantar hyperhidrosis14,15.
http://www.scielo.br/scielo.php?pid=S1983-51752011000400008&script=sci_arttext&tlng=en#end
Sunday, June 10, 2012
limited understanding of the role of the sympathetic nervous system in mediating pain
The role of sympathetic blocks in herpes zoster (HZ) and postherpetic neuralgia (PHN) remains controversial due to methodologic shortcomings in published studies and limited understanding of the role of the sympathetic nervous system in
mediating pain.
Local anaesthetic block of the sympathetic chain can be used to produce transient increase in blood flow to a limb (stellate ganglion block for arm, lumbar sympathetic block for leg).
Neurolytic (phenol) lumbar sympathectomy can increase lower limb blood flow for up to 6 months. Neurolytic stellate ganglion block carries high risk of injury to adjacent nerves and is rarely used.
SCS can improve tissue perfusion in ischaemic heart disease and peripheral vascular disease.
What is the evidence?
Neurolytic lumbar sympathectomy increases popliteal artery flow and perfusion of leg muscles in peripheral vascular disease42. A prospective series has shown total relief of pain and healing of ulcers in 58.7% of cases of non-operable peripheral vascular disease43.
Both retrospective44 and prospective45 case series support a role for SCS in the management of refractory angina pectoris. Use of SCS resulted in reduced anginal symptoms and medication use.
Information for Health Professionals
Hunter Integrated Pain Service
Updated January 2010
Procedural Intervention Guideline
mediating pain.
Local anaesthetic block of the sympathetic chain can be used to produce transient increase in blood flow to a limb (stellate ganglion block for arm, lumbar sympathetic block for leg).
Neurolytic (phenol) lumbar sympathectomy can increase lower limb blood flow for up to 6 months. Neurolytic stellate ganglion block carries high risk of injury to adjacent nerves and is rarely used.
SCS can improve tissue perfusion in ischaemic heart disease and peripheral vascular disease.
What is the evidence?
Neurolytic lumbar sympathectomy increases popliteal artery flow and perfusion of leg muscles in peripheral vascular disease42. A prospective series has shown total relief of pain and healing of ulcers in 58.7% of cases of non-operable peripheral vascular disease43.
Both retrospective44 and prospective45 case series support a role for SCS in the management of refractory angina pectoris. Use of SCS resulted in reduced anginal symptoms and medication use.
Information for Health Professionals
Hunter Integrated Pain Service
Updated January 2010
Procedural Intervention Guideline
Vasodilation; Vasomotor Disturbances
Complex regional pain syndromes (CRPS) are characterized by vascular disturbances primary affecting the microcirculation in the distal part of the involved extremity. In the acute stage inhibited sympathetic vasoconstriction and exaggerated neurogenic inflammation driven by central and peripheral mechanisms, respectively, seem to be the major pathophysiological mechanisms inducing vasodilation. During the chronic course of the disease as well as early in some patients vasoconstriction dominates the clinical picture induced by changes in the microcirculation itself such as endothelial dysfunction or vascular hyperreactivity, whereas sympathetic vasoconstrictor activity returns and neurogenic inflammation is less severe. It can be suggested that the interaction between different mechanisms underlying vasomotor disturbances as well as the severity of each single mechanism in the individual patient have a great impact on the variety of the overall clinical picture in CRPS. Irrespective of the underlying pathophysiology, measurements of skin temperature differences between the affected and the contralateral extremity can serve as a diagnostic tool in CRPS, in particular when sensitivity and specificity is increased by considering dynamic alterations in skin temperature asymmetries.
http://onlinelibrary.wiley.com/doi/10.1111/j.1526-4637.2010.00914.x/abstract
- After traumatic injury (65%)
- Infection (4%)
- Prior inflammation (2%)
- No clear cause (10%)
A review stated that women are predominantly affected, by a factor of 3,5 and a genetic predisposition has also been theorized.
The disease affects all ages, though most cases are between 50 and 70 years old, and it is generally believed to occur mainly in caucasian and Japanese people.[4]
- Autonomic and trophic disorders:
http://onlinelibrary.wiley.com/doi/10.1111/j.1526-4637.2010.00914.x/abstract
Epidemiology /Etiology
CRPS is found to result:[1]- After traumatic injury (65%)
- 1-2% of all fractures result in CRPS
- Largest risk of CRPS for fractures of the wrist
- Infection (4%)
- Prior inflammation (2%)
- No clear cause (10%)
A review stated that women are predominantly affected, by a factor of 3,5 and a genetic predisposition has also been theorized.
The disease affects all ages, though most cases are between 50 and 70 years old, and it is generally believed to occur mainly in caucasian and Japanese people.[4]
Characteristics/Clinical Presentation
The following symptoms have been found in literature:[5]- Autonomic and trophic disorders:
- Distal Edema in 80% of the patients
- Skin temperature changes at the affected body part in 80% of the patients, initially warmer and in 40% of patients gradually cools down until colder in comparison to the rest of the body as the disease progresses. Another review mentioned that 30% of the patients start off from the primarily cold stage.3
- In 40% of the patients skin at the affected body part starts showing redness, but becomes pale or livid in later stages
- In 55% altered sweating takes place, with hyperhydrosis being more common than hypohydrosis.
- Hair and nail growth possibly increase in early stages
- Atrophy of skin and muscles in later stages, as well as contractures may severely restrict movement
- Spontaneous pain occurs in 75%, usually burning dragging or stinging
- 68% felt in deep structures
- 32% felt in skin
- In 77% pain shows fluctuating intensity, lesser proportion shows shooting pain
- Pain can be increased by orthostasis, anxiety, exercise or temperature changes.
- In many cases, pain is more pronounced at night
- Sensory gain (Mechanical hyperalgesia, allodynia, ...) or sensory loss (hypaesthesia, hypalgesia, …) may be present.
- Motor weakness
- Severe impairment of complex movements
- Impairment of range of motion, initially by concomitant edema, later by contractures and fibroses
- Neglect like symptoms have been found in some patiƫnts, described as the body part in question feeling foreign.
- Enhanced physiological tremor in around 50%
- Myoclonus or dystonia, especially in type II CRPS
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