A splanchnic nerve lumbar sympathectomy was a surgical gamble used in about
10% of patients with advanced hypertension. Dramatic benefit was occasionally produced
at the cost of 0.5%–8.8% mortality, impotence and unpleasant orthostatic hypotension (3).
A view from the millennium: the
practice of cardiology circa 1950
and thereafter
Mark E. Silverman, MD, FACCa
Division of Cardiology, Department of Medicine,
Emory University School of Medicine and Chief of
Cardiology, Piedmont Hospital, Atlanta, Georgia,
USA
Manuscript received August 28, 1998; revised
manuscript received November 24, 1998, accepted
January 5, 1999.
Tuesday, January 22, 2008
Mortality in sympathectomised mice was significantly higher
Results: Mortality in sympathectomised mice was significantly
higher than that in sham operated mice following administration
of Jo-2. This result was also supported by apoptosis data in
which sympathectomised livers exhibited a significant elevation
in the number of apoptotic hepatocytes and caspase-3 activity
after Jo-2 treatment compared with sham operated livers.
Moreover, pretreatment with norepinephrine dose dependently
inhibited the hepatic sympathectomy induced increase in
mortality after Jo-2 injection. Antiapoptotic protein levels of
FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were
significantly lower in sympathectomised mice at one and two
hours following Jo-2 treatment than in sham operated animals.
In addition, interleukin 6 supplementation dose dependently
suppressed the hepatic sympathectomy induced increase in
mortality after Jo-2 treatment.
Conclusions: These results suggest that norepinephrine released
from the hepatic sympathetic nerve plays a critical role in
protecting the liver from Fas mediated fulminant hepatitis,
possibly via mechanisms including antiapoptotic proteins and
interleukin 6.
Chida, Y. and Sudo, N. and Takaki, A. and Kubo, C. (2005)
The hepatic sympathetic nerve plays a critical role in preventing
Fas induced liver injury in mice. Gut, 54 (7). pp. 994-1002.
ISSN 00175749
higher than that in sham operated mice following administration
of Jo-2. This result was also supported by apoptosis data in
which sympathectomised livers exhibited a significant elevation
in the number of apoptotic hepatocytes and caspase-3 activity
after Jo-2 treatment compared with sham operated livers.
Moreover, pretreatment with norepinephrine dose dependently
inhibited the hepatic sympathectomy induced increase in
mortality after Jo-2 injection. Antiapoptotic protein levels of
FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were
significantly lower in sympathectomised mice at one and two
hours following Jo-2 treatment than in sham operated animals.
In addition, interleukin 6 supplementation dose dependently
suppressed the hepatic sympathectomy induced increase in
mortality after Jo-2 treatment.
Conclusions: These results suggest that norepinephrine released
from the hepatic sympathetic nerve plays a critical role in
protecting the liver from Fas mediated fulminant hepatitis,
possibly via mechanisms including antiapoptotic proteins and
interleukin 6.
Chida, Y. and Sudo, N. and Takaki, A. and Kubo, C. (2005)
The hepatic sympathetic nerve plays a critical role in preventing
Fas induced liver injury in mice. Gut, 54 (7). pp. 994-1002.
ISSN 00175749
Cerebral ischemia may increase extracellular choline concentration by interfering with its removal by the circulation and by enhancing its net production from phospholipids.
Mia: these changes are present in post-sympathectomy patients as well, providing further proof on cerebral ischemia (Brain MRI) that causes the cognitive function changes in many patients who undergo the surgery.
Focal ischemia enhances choline output and decreases acetylcholine output from rat cerebral cortex
OU Scremin and DJ Jenden
Veterans Administration Medical Center, Albuquerque, New Mexico 87108.
Mia: these changes are present in post-sympathectomy patients as well, providing further proof on cerebral ischemia (Brain MRI) that causes the cognitive function changes in many patients who undergo the surgery.
Sympathectomy complications
26.3% or one quarter of patients with compensatory hyperhidro-
sis considered the complication major and disabling. The average time between surgical sympathectomy
and the appearance of compensatory hyperhidrosis was 4 months (range 1-6 months). The inci-
dence of compensatory hyperhidrosis did not seem to be different after open or endoscopic approach.
Irrespective of approach, two or more levels of denervation and removal of the stellate ganglion produced
noticeably higher incidence. Finally, the incidence of this complication seemed to be 3 times higher when
the surgery was performed for primary hyperhidrosis than neuropathic pain.
The weighted mean incidence of gustatory sweating after upper extremity surgical sympathectomy was
32.3% (range 0-79) (information retrieved from 44 papers and 5,142 patients)
The phenomenon appeared on average 5 months
after surgery. The weighted means appeared substantially greater when the open approach was used, two
or more levels were denervated, the chain was electrocoagulated but left in situ and primary hyperhidrosis
was the indication for the intervention.
The weighted mean incidence of phantom sweating was 38.6 %
The weighted mean incidence of neuropathic pain complications was 11.9% .
Several issues regarding sympathectomy remain open, as the objectives of this review were limited and
specific. This review is geared exclusively around late complications and does not address efficacy or
effectiveness of the procedure. While the vast majority of patients were operated for palmar hyperhidrosis,
the procedure is obviously used for other indications, most importantly ischemia and neuropathic pain.
However, questions around satisfaction of patients with the procedure for a given indication or which
approach is the best for the same indication were not asked. Similarly, we are unable to answer questions
regarding completeness or permanency of the sympathetic denervation..
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001
sis considered the complication major and disabling. The average time between surgical sympathectomy
and the appearance of compensatory hyperhidrosis was 4 months (range 1-6 months). The inci-
dence of compensatory hyperhidrosis did not seem to be different after open or endoscopic approach.
Irrespective of approach, two or more levels of denervation and removal of the stellate ganglion produced
noticeably higher incidence. Finally, the incidence of this complication seemed to be 3 times higher when
the surgery was performed for primary hyperhidrosis than neuropathic pain.
The weighted mean incidence of gustatory sweating after upper extremity surgical sympathectomy was
32.3% (range 0-79) (information retrieved from 44 papers and 5,142 patients)
The phenomenon appeared on average 5 months
after surgery. The weighted means appeared substantially greater when the open approach was used, two
or more levels were denervated, the chain was electrocoagulated but left in situ and primary hyperhidrosis
was the indication for the intervention.
The weighted mean incidence of phantom sweating was 38.6 %
The weighted mean incidence of neuropathic pain complications was 11.9% .
Several issues regarding sympathectomy remain open, as the objectives of this review were limited and
specific. This review is geared exclusively around late complications and does not address efficacy or
effectiveness of the procedure. While the vast majority of patients were operated for palmar hyperhidrosis,
the procedure is obviously used for other indications, most importantly ischemia and neuropathic pain.
However, questions around satisfaction of patients with the procedure for a given indication or which
approach is the best for the same indication were not asked. Similarly, we are unable to answer questions
regarding completeness or permanency of the sympathetic denervation..
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001
ARE WE PAYING A HIGH PRICE FOR SYMPATHECTOMY? 2
Nevertheless, immediate (perioperative and postoperative) complications (primarily for the open but also
the endoscopic approach) include: fever, hematoma, transient Horner’s syndrome, bleeding, pneumotho-
rax, infection, wound pain, lymphatic leak, chylothorax, arterial injury, brachial plexus injury, etc.17. Late
complications include: permanent Horner’s syndrome, neuralgic pains, unsightly wound appearance, com-
pensatory hyperhidrosis, gustatory sweating and phantom sweating, and in the case of bilateral lumbar
sympathectomy erectile dysfunction in the male and lack of clitoral tumescence in the female18.
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001
the endoscopic approach) include: fever, hematoma, transient Horner’s syndrome, bleeding, pneumotho-
rax, infection, wound pain, lymphatic leak, chylothorax, arterial injury, brachial plexus injury, etc.17. Late
complications include: permanent Horner’s syndrome, neuralgic pains, unsightly wound appearance, com-
pensatory hyperhidrosis, gustatory sweating and phantom sweating, and in the case of bilateral lumbar
sympathectomy erectile dysfunction in the male and lack of clitoral tumescence in the female18.
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001
ARE WE PAYING A HIGH PRICE FOR SYMPATHECTOMY?
ARE WE PAYING A HIGH PRICE FOR
SURGICAL SYMPATHECTOMY?
Andrea Furlana,c MD, Angela Mailisa,b MD, MSc, FRCPC (PhysMed) and
Marios Papagapioua MSc
Conclusions: Surgical sympathectomy irrespective of approach is accompanied by several potentially
disabling complications.
Surgical sympathectomy is performed in thousands of patients around the world primarily for the treatment
of bothersome palmar hyperhidrosis.1-7 Much less frequent indications are: neuropathic pain syndromes
(like Reflex Sympathetic Dystrophy and Causalgia)2;8;9 , ischaemic conditions including peripheral vascular
disease and Raynaud’s phenomena2 and rarely facial blushing10, Prinzmetal’s angina11, as well as migraine,
dysmenorrhea and pancreatitis2;12
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001
SURGICAL SYMPATHECTOMY?
Andrea Furlana,c MD, Angela Mailisa,b MD, MSc, FRCPC (PhysMed) and
Marios Papagapioua MSc
Conclusions: Surgical sympathectomy irrespective of approach is accompanied by several potentially
disabling complications.
Surgical sympathectomy is performed in thousands of patients around the world primarily for the treatment
of bothersome palmar hyperhidrosis.1-7 Much less frequent indications are: neuropathic pain syndromes
(like Reflex Sympathetic Dystrophy and Causalgia)2;8;9 , ischaemic conditions including peripheral vascular
disease and Raynaud’s phenomena2 and rarely facial blushing10, Prinzmetal’s angina11, as well as migraine,
dysmenorrhea and pancreatitis2;12
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001
Nerves regenerate after surgery and cause the abnormal sweating - among other symptoms
Regeneration after cervicothoracic sympathectomy producing gustatory responses.
Treatment for Gustatory Sweating? Avoid food.
9 months later, within one minute of eating a sour apple, the patient developed severe sweating over the left half of the face and the left chest. The reaction was confirmed by infra-red thermography which proved that the skin temperature in the sweating region had fallen to 3 degrees C. The likely cause of localized gustatory sweating is intra-operative damage of the stellate ganglion or its preganglionic nerve connections. Treatment is limited to avoidance of the precipitating gustatory stimulus.
Dtsch Med Wochenschr. 1992 Oct 9;117(41):1556-60.
Plendl H, Paulus W, Witt TN.
Dtsch Med Wochenschr. 1992 Oct 9;117(41):1556-60.
Plendl H, Paulus W, Witt TN.
Neurologische Klinik, Klinikum Grosshadern, Universität München.
injury=sympathectomy
Blackwell Synergy - Br J Dermatol, Volume 142 Issue 1 Page 194-195 ...
Pathological gustatory sweating and flushing can develop after injury to preganglionic cervicothoracic sympathetic fibres, an unavoidable consequence of ...www.blackwell-synergy.com/
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