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

Spinal cord infarction occurring during thoraco-lumbar sympathectomy
J Neurol Neurosurg Psychiatry 1963;26:418-421 doi:10.1136/jnnp.26.5.418

Saturday, July 23, 2011

The indications for neurolytic or surgical sympathectomy are uncertain

The indications for neurolytic or surgical sympathectomy are uncertain. There is no clear correlation between the degree or duration of pain relief and the actual period of sympathetic blockade and the same patient may show variable responses on different occasionsv (Loh et al 1980). Some patients demonstrate unexpected responses such as contralateral or delayed blocks and some are made worse (Purcell-Jones &Justins 1988, Evans et al 1980, Kleiman 1954)
http://www.springerlink.com/content/7013w45630522h6k/

Friday, July 22, 2011

Sympathectomy causes depigmentation of the skin

In this article, 2 patients were submitted to video-assisted thoracoscopic sympathectomy, and after approximately 8 months they noticed depigmentation of the region corresponding to the blockage of sympathetic stimulus. This fact could be explained by the possible effect of the nervous system on the melanocytes of human skin. 

Sympathectomy? 
Skin Depigmentation: Could it Be a Complication Caused by Thoracic 
 2009;88:42-43 Ann Thorac Surg 
http://ats.ctsnetjournals.org/cgi/reprint/88/4/e42.pdf 

platelet aggregation significantly lower after sympathectomy

It was shown that platelet aggregation in partially (with stellate ganglia containing 25% neurons of normal amount) and completely (0,5% neurons) sympathectomized rats was significantly lower than in intact animals. Concurrently the blood coagulation system of sympathectomized rats was hyperactive. The reasons for sympathectomy-induced changes seems likely to be elevated adrenalin blood concentration in such rats.
http://www.ncbi.nlm.nih.gov/pubmed/7388153

platelet aggregation significantly lower after sympathectomy

It was shown that platelet aggregation in partially (with stellate ganglia containing 25% neurons of normal amount) and completely (0,5% neurons) sympathectomized rats was significantly lower than in intact animals. Concurrently the blood coagulation system of sympathectomized rats was hyperactive. The reasons for sympathectomy-induced changes seems likely to be elevated adrenalin blood concentration in such rats.
http://www.ncbi.nlm.nih.gov/pubmed/7388153

Hyperhidrosis is not caused by 'overactivity' of the sympathetic nervous system

At the high-frequency band (0.15-0.5 Hz), which represents parasympathetic cardiac innervation, an interaction of type and position influencing spectral power was detected. Our highly interesting findings indicate that primary focal hyperhidrosis is based on a much more complex autonomic dysfunction than generalised sympathetic overactivity and seems to involve the parasympathetic nervous system as well.
Eur Neurol 2000;44:112-116 (DOI: 10.1159/000008207)

the sympathetic block, regularly extends six or more spinal segments above the level of sensory block

Chamberlain et al, using a very sensible technique with thermographic imaging, showed that the sympathetic block, at least partial, regularly extends six or more spinal segments above the level of sensory block [8].

Therefore, it seems that a partial sympathetic blockage exists on substantial area over and under of the level of somatic block. In fact, preganglionic sympathetic fibers, once they quit the dura, enter the paravertebral sympathetic chain. From there, these fibers can ascend or descend, synapsing with up to 18 postganglionic fibers, which may project to dermatomes well above and below the spinal segment from which they originated [9].

Bradycardia associated with spinal block is usually light, and contributes modestly to the drop of blood pressure. Rarely, bradycardia is associated with cardiac collapse. Traditional explanation of this bradycardia originating from a spinal anesthesia is the blockage of cardiac accelerator sympathetic nerves (T1-4). Many studies showed than the incidence and the severity of bradycardia is not related to the height of the sensory block.
Onset time of the bradycardia has poor relation with the timing of the spinal block [10]. Carpenter, in a prospective study on 1000 patients under spinal block., showed that bradycardia occured in 13% (heart rate < 50/min) with an onset time of 47 min (range from1 to 204).
There is a pulse rate paradoxical response to movement of the operation table. Under a spinal or epidural anesthesia, when one lift patient head, blood pressure decreases caused by pooling of the venous blood. But in place of a reflex tachycardia mediated by baroreceptors, there is a paradoxical bradycardia. Interestingly, in situation associated with severe reduction of venous return, paradoxical bradycardia can be seen even in the absence of sympathetic block.
There is similarities between hypotension related to bradycardia of the spinal anesthesia and vasovagal reaction. Vasovagal shock is characterized by hypotension and bradycardia, and can progress to syncope. It has a central or a peripheral etiology.
Because of their rare occurrence, almost all studies on cardiac arrest during spinal anesthesia are retrospective, therefore limited in their ability to identify variables and incidents of such events.
Caplan [14] in 1988 has identified 14 cases of sudden cardiac arrest on patients in good health and undergoing minor surgical procedures. None of these patients had unusually high block, nor received badly inadequate resuscitative care. Despite all this, only 8 of 14 patients survived, and only one survivors had acceptable neurological functions Retrospectively, respiratory insufficiency was suspected, secondary to a strong sedation, as the main etiology of the cardiac arrest. Even a complete sympathectomy leaves a good arterial vascular tone, but in presence of hypoxia and acidosis can lead to a fall in arterial tone, to an exaggerated decrease in blood pressure and cardiac collapse. Early sympathetic responses to hypoxia, which are tachycardia and vasoconstriction, are almost severely blunt by spinal anesthesia [15].
Mackey reported 3 cases of severe bradycardia during spinal anesthesia in the absence of hypoxia and strong sedation [16]. He concludes that severe bradycardya was caused by a drop in venous return triggering Bezold-Jarisch reflex which in presence of sympathetic block led to exaggerated bradycardia, hypotension and arrest.
http://www.esra-learning.com/site/generalites/pathology/b_haemodynamic.htm

Gustatory sweating is a frequent side effect of sympathectomy

The Annals of Thoracic Surgery
Volume 81, Issue 3, March 2006, Pages 1043-1047

http://www.sciencedirect.com/science/article/pii/S0003497505017571

Tuesday, July 19, 2011

Post-sympathectomy neuralgia

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome.

Pain.
 1996 Jan;64(1):1-9

http://www.ncbi.nlm.nih.gov/pubmed/8867242?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Neuroma following Sympathectomy

The authors conclude recomemnding the application of clips and if the syndrome nevertheless appears novocaine infiltration of the upper end of the sympathetic chain. The authors are convinced that the theory of Hermann and Cooley about neuroma formation at the ends of the sympathetic chain after resection of a segment is true.
http://www.revangiol.com/sec/resumen.php?or=web&i=e&id=227082.
Traumatic neuroma follows different forms of nerve injury (often as a result of surgery). They occur at the end of injured nerve fibres as a form of ineffective, unregulated nerve regeneration; it occurs most commonly near a scar, either superficially (skin, subcutaneous fat) or deep (e.g., after acholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

bone atrophy on the side of the sympathectomy

localized alopecia, corneal ulceration, keratitis, strabismus, enophthalmos, ocular atrophy, hemifacial atrophy and slight bone atrophy on the side of the sympathectomy were observed

http://www.ncbi.nlm.nih.gov/pubmed/1962072