Postsympathectomy pain of such severity that parenteral narcotics afforded no relief

Fifty-six consecutive patients who subsequently underwent ninety-six lumbar sympathectomies were studied prospectively with regard to the development of postoperative pain. Pain after operation was observed in thirty-four extremities by twenty-five of the patients (35 per cent). It began abruptly an average of twelve days after operation and was often accentuated nocturnally. The pain was almost always described as a deep, dull ache and persisted two to three weeks before spontaneously remitting. Postsympathectomy pain of such severity that parenteral narcotics afforded no relief developed in two of these fifty-six patients and in nine additional patients. Treatment with carbamazepine produced dramatic reduction in the intensity of pain in seven of these nine patients within twenty-four hours after the institution of therapy. Two patients were given intravenous diphenylhydantoin and both experienced immediate relief of pain. The mechanisms of the syndrome and of the action of these drugs are uncertain.

http://www.sciencedirect.com/science/article/pii/0002961074902384

Pain in the form of intercostal neuralgia with dysesthesia at the site of trocar insertion is rarely documented but more frequent than generally recognized

Pain in the form of intercostal neuralgia with dysesthesia at the site of trocar insertion is rarely documented but more frequent than generally recognized. Many centres perform short-stay surgery that may lead to underestimation of pain results. In most series pain resolves within months, but Walles and colleagues could detect a persistence for years (Walles et al., 2008).

http://www.intechopen.com/books/topics-in-thoracic-surgery/surgical-management-of-primary-upper-limb-hyperhidrosis-a-review

Patients with surgical sympathectomies have low plasma levels of DA and NE [49], whereas EPI:NE ratios are increased

Patients with surgical sympathectomies have low plasma levels of DA and NE [49], whereas EPI:NE ratios are increased (unpublished observations), suggesting decreased sympathetically mediated exocytosis and compensatory adrenomedullary activation.

Catecholamines 101, David S. Goldstein
Clin Auton Res (2010) 20:331–352

The mechanisms by which sympathectomy leads to increased local bone loss is unknown

In vivo effects of surgical sympathectomy on intra... [Am J Otol. 1996] - PubMed - NCBI: "Am J Otol. 1996 Mar;17(2):343-6.

In vivo effects of surgical sympathectomy on intramembranous bone resorption.
Sherman BE1, Chole RA.
Author information
1Department of Otolaryngology--Head and Neck Surgery, School of Medicine, University of California, Davis, USA.
Abstract
Bone modeling and remodeling are highly regulated processes in the mammalian skeleton. The exact mechanism by which bone can be modeled at a local site with little or no effect at adjacent anatomic sites is unknown. Disruption of the control of modeling within the temporal bone may lead to various bone disease such as otosclerosis, osteogenesis imperfecta, Paget's disease of bone, fibrous dysplasia, or the erosion of bone associated with chronic otitis media. One possible mechanism for such delicate control may be related to the ubiquitous and rich sympathetic innervation of all periosteal surfaces. Previous studies have indicated that regional sympathectomy leads to qualitative alterations in localized bone modeling and remodeling. In this study, unilateral cervical sympathectomy resulted in significant increases in osteoclast surface and osteoclast number within the ipsilateral bulla of experimental animals. The mechanisms by which sympathectomy leads to increased local bone loss is unknown. Potential mechanisms include disinhibition of resorption, secondary to the elimination of periosteal sympathetics, as well as indirect vascular effects."

Because of the anaesthetic implications and possible surgical complications, many surgeons are reluctant to perform transthoracic sympathectomy

Hypoxaemia is of a major concern during thorascopic sympathectomy. However, the pathophysiology of hypoxaemia and consequent decrease in SpO2 differs between the two anaesthetic techniques.

The normal physiological response to massive atelectasis is an increase in pulmonary vascular resistance (hypoxic pulmonary vasoconstriction) with re-routing of blood to well ventilated lung zones and consequent improvement in PaO2. HOWEVER, DURING ENDOBRONCHIAL ANAESTHESIA FOR THORACIC SYMPATHECTOMY THERE IS AN APPARENT FAILURE OF THIS COMPENSATORY MECHANISM. When more then 70% of the lung is atelectatic, compensation by hypoxic pulmonary vasoconstriction appears ineffective.

During carbon dioxide insufflation using endobronchial intubation, Hartrey and colleagues reported a decrease in systolic arterial pressure of >20mm Hg in 21% of patients. Similarly we have reported sudden hypotension and bradycardia after injudicious carbon dioxide insufflation.

Although extremely rare, sudden cardiac arrest has been reported after left T2-3 sympathetic nerve transection. While the exact pathophysiology of this occurence is unclear, it is postulated that before complete transection of the sympathetic trunk, continuous sympathetic stimulation to the stellate ganglions results in a reduction in the ventricular finrillation threshold, arrhythmia and cosequent cardiac arrest.
In an iteresting study of the delayed cardiac effects of T2-$ symtpathectomy, Drott and colleagues demonstrated significantly reduced heart rate at rest, and during both exercise and the recovery phase of exercise. Changes is the electrical axis and shortening of the QT interval have also been reported.

Irrespective of the technique used the reported incidence of postoperative pneumpthorax is variable, occuring in 2-15% of cases.
In a study by Gothberg, Drott and Claes, postoperative chest x-ray after 1274 procedures, in 602 patients demonstrated that a small apical pneumothroax was a usual occurence.

Conclusion: Because of the anaesthetic implications and possible surgical complications, many surgeons are reluctant to perform transthoracic sympathectomy.

British Journal of Anaesthesia 1997; 79: 113-119
B. Fredman, D. Olsfanger and R. Jedeikin