The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Monday, July 20, 2009

Neuroma following nerve injury/surgery

When a nerve is cut, the piece of nerve that is beyond the cut point eventually dies, however, its Schwann cells, the cells that encircle the nerve fibers remain for a much longer time. These Schwann cells secrete a chemical messenger known as nerve growth factor that tells the cut end of nerve where to grow back. So the cut end of nerve will send out multiple sprouts in the direction of the nerve growth factor, however, these sprouts do not go out in an orderly manner, instead they grow out in all directions and eventually cluster and form a knot of nerve fibers. This eventually leads to the formation of a TRUE neuroma or a END BULB or STUMP neuroma.

 www.tarsaltunnelcenter.com/assets/recurrent.shtml

Risks during Thoracic Sympathectomy - Surgery not as safe as reported

Even epidural blockade limited only to the thoracic dermatomes is liable to cause complete sympathectomy, including cardiac sympathetic denervation. The ensuing vasodilation and bradycardia lead to hypotension, poor tolerance of mechanical interference with the heart, and inability to respond to acute changes in intravascular volume or body position. This symptom complex is especially troublesome to manage during intrathoracic operations when avoidance of hypervolemia is emphasized.
Thoracic sympathectomy has two other potenital consequences: effect on bronchomotor tone and effect on oxygenation.

During intrathoracic procedures using one-lung ventilation, a right-to-left intrapulmonary shunt is intentionally created (in the form of the nonventilated lung). The ensuing arterial oxygen tension (PaO2) is determined by a complex interaction involving cardiac output, mixed venous oxygen tension, the status of the ventilated lung, size of the shunt, and most significantly, hypoxic pulmonary vasoconstriction (HPV).
HPV diverts pulmonary blood flow away from the shunt by vavsoconstriction in the nonventilated lung, and is the principal adaptive defense mechanism against arterial hypoxemia during one-lung ventilation. The cellular mechanism and regulation of HPV, and the possible role of the autonomic nervous system are not completely understood.
The effect of thoracic sympathectomy of HPV is even less well understood. Since potent vasodilators such as nitroprusside antagonize HPV-induced vasoconstriction and lower the arterial oxygen tension, it is reasonable to assume that HPVwill become less effective with thoracic sympathectomy.
Clinical studies have produced conflicting conclusions, most probably because direct measurement of HPV is not possible in human studies, and the surrogate endpoing examined PaO2 is determined not only by HPV, but also by a host of interacting factors, some of which may be affected by the sympathectomy and can not be held constant.

Risk Factor for Neuraxial Anesthesia-Associated Bradycardia:
Block height higher than T5
Younger age


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Spinal and Epidural Anesthesia

By Cynthia Wong

  • Publication Date: 2007-01-01 Publisher: MCGRAW-HILL EDUCATION - EUROPE Country of origin: UNITED STATES

    • Alteration in Cerebral Blood Flow after sympathectomy

    Jeng and associates observed an increase in cerebral blood flow after T2 sympathectomy, and they suggested the possibility of using such a surgical approach to improve cerebral blood flow in patients with cerebral vascular insufficiency.

    Youmans Neurological Surgery, 5th Edition
    Publisher: Saunders
    Publication Date: 2003-10-10

    The angina-relieving effects of sympathetic blockade

    In the 1930's it was recognised by neurosurgeons performing destructive sympathectomies for angina pectoris that local anaesthetic infiltration around the stellate ganglion often resulted in pain relief outlasting the duration of action of the local anaesthetic drug13. This observation has been more recently confirmed14, and is currently (June 1999) the subject of a large scale randomised double-blind placebo-controlled trial funded by the British Heart Foundation.

    The pathogenesis of angina and myocardial infarction pain involves the activation of the afferent sympathetic pathway. A frequent and important consequence of pain (especially when severe) is the `flight or fight' response through activation of sympathetic efferents. The clinical image of the patient with an acute myocardial infarction (cold, clammy, sweaty, anxious, tachycardic) is secondary to this adrenergic activation. Therefore, angina might be regarded as the sensory component of a positive feedback loop, which cannot under these circumstances be conceived as resulting in benefit, and which may be considered to be a maladaption.

    The angina-relieving effects of sympathetic blockade might be due to interference with this maladaptive feedback loop, in a similar manner to the way in which adenosine interrupts a re-entrant tachycardia. If such a loop exists, it may partly explain chronic refractory angina and the fact that temporary interruption of this pathway has a prolonged effect on pain14. Beneficial amelioration of angina can be achieved with repeated blocks14. There does not appear to be any predictability in the length of time a patient remains pain-free after successive blocks.

    http://www.angina.org/source/pro/symp_block.htm

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