years 2000 - 2001:
Total: 1034
years 2001-2002:
Total: 1575
years 2002 - 2003
Total: 1228
years 2003 - 2004
Total: 1193
years 2004 - 2005
Total: 1483
years 2005 - 2006
Total:1358
years 2006 - 2007
Total: 972
years 2007 - 2008
Total: 850
years 2008 - 2009
Total: 891
years 2009 - 2010
Total: 1083
source: aihw.gov.au
"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding." Associate Professor Robert Boas, Faculty of Pain Medicine of the Australasian College of Anaesthetists and the Royal College of Anaesthetists, The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 258-260
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
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
Friday, May 11, 2012
Wednesday, May 9, 2012
Iatrogenic harlequin syndrome resulting from sympathectomy
Postgrad Med J 2003;79:278 doi:10.1136/pmj.79.931.278
A 29 year old man with severe facial hyperhidrosis underwent an uncomplicated right thoracoscopic sympathectomy. Before operating on his left side, a starch-iodine preparation was applied to his face in order to demarcate residual sudomotor function. The preparation becomes blue on exposure to moisture, thereby representing residual sweat gland activity.
Figure 1 demonstrates that sympathetic innervation to the face is strictly unilateral, and nerve fibres do not appear to cross the midline. This is essentially an iatrogenic variation of the harlequin syndrome,2 which usually results from interruption of post-ganglionic sympathetic fibres secondary to malignant invasion.
His facial hyperhidrosis was completely treated once the contralateral sympathectomy was performed.
Monday, May 7, 2012
T3 sympathectomy leads to subclinical pupillary dysfunction with a tendency for miosis
We found statistically significant differences (P < 0.001) between the preoperative P/I ratio [0.40 mm (standard deviation, SD 0.07 mm)] and the postoperative basal ratio [0.33 (SD 0.05)] at 24 h. The P/I ratio at 24 h increased from 0.33 to 0.36 (SD 0.09), a nonsignificant increase (P = 0.45), after instillation of medicated eye drops. No differences were observed between the preoperative [0.40 (SD 0.07)] and 1-month basal values [0.38 (SD 0.07)], and instillation of apraclonidine no longer induced a hypersensitivity response.
http://www.ncbi.nlm.nih.gov/pubmed/22044979
CONCLUSIONS:
T3 sympathectomy leads to subclinical pupillary dysfunction with a tendency for miosis, even though this impairment is not generally evident on standard physical examination or reported by patients. This subclinical dysfunction may be caused by injury to an undefined group of presympathetic nerve cell axons in caudocranial direction that communicate with the cervical sympathetic ganglia and whose function is mydriatic pupillary innervation.http://www.ncbi.nlm.nih.gov/pubmed/22044979
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