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

Sunday, January 25, 2009

Sympathectomy impairs temperature homeostasis, decreases Cardiac output and myocardial work

The decrease in body temperature associated with the onset of central neuraxial block has three reported mechanism: loss of the patient's thermorgulatory capability, with impaired shivering and loss of the ablility to sense cold temperatures; sympathectomy induced peripheral vasodilation, resulting in admixing of peripheral (cool) with core (warm) blood (this mixing results in a 1C to 2C decrease in core temperature and is proporitonal to the extent of sympathetic block and patient's age, and loss of tissue heat below the level of sympathectomy due to vasodilation.

Neuraxial anesthesia decreases afterload by producing arterial vasodilation. This vasodilation however is not equivalent in all vascular beds. For instance, muscle and skin blood flow may be decreased by sympathectomy, whereas the total blood flow to the same extremity may be quadrupled. Additionally, the extent to which afterload is decreased by sympathetic denervation varies considerably from one patient to another.

The effectiveness of this reflex vasoconstriction in maintaining normotension is a function of the extent of the sympathetic block. If, for instance, sympathetic block reaches the fourth thoracic dermatome (T4) or higher, the intact upper limb vasculature may contribute only 5% of the total cardiac output. Even maximal vasoconstriction will be insuffiecient to compensate for the profound arterial vasodilation in the rest of the body.

Cardiac Function
Importantly, bradycardia during high (thoracic) levels of spinal or epidural anesthesia is due to two main factors: denervation of preganglionic cardiac accelerator fibers (T1-4) and diminished venous return to the right ventricle because of decreases in preload.

Cardiac Output
The extent of CO decrease is also a function of the degree of sympathetic denervation.
Conversely, assumption of an even slight head-up position during neuraxial anesthesia with high levels of sympathetic denervation (..) may have catastrophic consequences such as profound bradycardia, cerebral hypoperfusion and cardiac arrest. Reports of severe complications related to improper positioning of patients during high levels of spinal or epidural anesthesia have spanned the last six decades.

Myocardial Work
The significant decrease in myocardial work is due primarily to threee factors: Decrease in HR (heart rate), decrease in arterial/total peripheral resistance (afterload), and decrease in stroke volume of the left ventricle secondary to the decreased preload.

Supplemental Oxygen
The purpose of the supplemental oxygen is to assure that tissue oxygenation is maintained , despite decreases in CO and periperal blood low.

Complications in Anesthesiology
By Emilio B. Lobato, Nikolaus Gravenstein, Robert R. Kirby
Contributor Emilio B. Lobato, Nikolaus Gravenstein, Robert R. Kirby
Edition: 3, illustrated
Published by Lippincott Williams & Wilkins, 2007
ISBN 0781782635, 9780781782630