Slowly the surgeons admit to more and more side-effects
Go to Dr Reisfeld's web site to read his new comments about ETS: www.sweaty-palms.com/blushing.html
"Another clinical observation which will need more time for verification is the thought that the higher failure rate of sympathectomy when ETS is done only for facial blushing has to do with the fact that when the sympathectomies were done in the past for vascular problems the success rate was very minimal. At this time we know that higher failure rate was due to a clinical situation which we call denervation hypersensitivity. In essense the blood vessels become very sensitive to certain circulating hormones within the blood system. Dr. Reisfeld believes that the same phenomenon happens in this facial blushing presentation. More time and more clinical experience is needed before there can be a more definite conclusion."
Hopefully this may assist court cases but it sounds like Reisfeld is trying to cover his legal liability in his "at the time we thought..." comments.
Also see how the Australian site www.easternsurgical.com.au (click on blushing) have now admitted "some failures" and had to remove their biased comments about 500 consecutive successes.
Unfortunately the more people who have ETS side effects, the more the statistics become 'significant' to such doctors.
Madonna
"Another clinical observation which will need more time for verification is the thought that the higher failure rate of sympathectomy when ETS is done only for facial blushing has to do with the fact that when the sympathectomies were done in the past for vascular problems the success rate was very minimal. At this time we know that higher failure rate was due to a clinical situation which we call denervation hypersensitivity. In essense the blood vessels become very sensitive to certain circulating hormones within the blood system. Dr. Reisfeld believes that the same phenomenon happens in this facial blushing presentation. More time and more clinical experience is needed before there can be a more definite conclusion."
Hopefully this may assist court cases but it sounds like Reisfeld is trying to cover his legal liability in his "at the time we thought..." comments.
Also see how the Australian site www.easternsurgical.com.au (click on blushing) have now admitted "some failures" and had to remove their biased comments about 500 consecutive successes.
Unfortunately the more people who have ETS side effects, the more the statistics become 'significant' to such doctors.
Madonna
Australian Story1
ETS studies are not done in the Australian climate and resulting CS means ETS should never have been allowed here without a review. One conducted by Monash University concluded not enough evidence on ETS is available and that existing ETS studies are flawed.These boards are accountable.
.....Madonna Aussie
.....Madonna Aussie
Norepinephrine Turnover - increase in plasma NE=increase in brain NE
Norepinephrine Turnover Is Increased in Suprabulbar Subcortical Brain Regions and Is Related to Whole-Body Sympathetic Activity in Human Heart Failure
From the Baker Medical Research Institute, Melbourne, Australia.
© 2002 American Heart Association, Inc.
This study, for the first time, demonstrates elevated suprabulbar subcortical noradrenergic activity in human CHF and identifies a positive correlation between this and the level of whole-body NE spillover. The findings suggest that the activation of noradrenergic neurons projecting rostrally from the brain stem mediates sympathetic nervous stimulation in CHF.
cerebrovascular CO2 reactivity
- Acta Physiol Scand. 1977 Sep;101(1):122-5.
Effects of intraventricular 6-hydroxydopamine on cerebrovascular CO2 reactivity in anesthetized rats.
Regional cerebral blood flow was measured by the 14C-ethanol technique in anesthetized rats before and after intraventricular injection of 6-hydroxydopamine. This treatment reduced the fluorescence of the central noradrenaline and dopamine nerve terminals, as well as of the perivascular nerve terminals in cerebral vessels. The administration of 6-hydroxydopamine had no significant effect on cerebral blood flow at normocapnia. The cerebrovascular reactivity to hypercapnia was significantly increased in the 6-hydroxydopamine treated animals. The results indicate an involvement of central catecholamine pathways in the cerebrovascular reactivity to hypercapnia.
PMID: 906856 [PubMed - indexed for MEDLINE]
catecholamine neuron in cerebral circulation
J Neurosurg. 1986 Sep;65(3):370-5
A role of the central catecholamine neuron in cerebral circulation.
The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 +/- 2.8 ml/100 gm/min; control cortex 38.5 +/- 3.5 ml/100 gm/min; p less than 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10(-5) M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% +/- 0.6%/mm Hg; control cortex 3.53% +/- 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.
Why many patients who undergo SYMPATHECTOMY complain about stuffy nose/a cold for life...?!
AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 3
494-R500, Copyright © 1987 by American Physiological Society
Articles by Haxhiu, M. A.
Articles by Cherniack, N. S.
A role for the ventral surface of the medulla
in regulation of nasal resistance
M. A. Haxhiu, K. P. Strohl, M. P. Norcia, E. van Lunteren,
E. C. Deal Jr and N. S. Cherniack
Nasal resistance is known to be affected by changes in nasal blood volume
and hence to depend on sympathetic discharge to nasal blood vessels.
Structures located superficially near the ventrolateral surface of the medulla
significantly affect respiratory and sympathetic activity and the tone of the
trachea. To assess the importance of these structures on nasal patency, we
measured transnasal pressure at a constant flow and examined the change in
pressure produced by topically applied N-methyl-D-aspartic acid (NMDA).
Experiments were performed in chloralose-anesthetized, paralyzed, and
artificially ventilated cats. NMDA administered on the intermediate area of
the ventral surface of the medulla decreased transnasal pressure and increased phrenic nerve activity. The response to
NMDA could be diminished or abolished by application to the ventral medullary surface of the NMDA antagonist
2-amino-5-phosphonovalerate (2-APV) or the local anesthetic lidocaine. Carotid sinus denervation and
posthypothalamic decerebration did not alter the nasal and phrenic nerve responses to NMDA; however, cervical
sympathetic denervation decreased these responses, both in intact and in bilaterally adrenalectomized animals. Therefore,
activation of NMDA receptors on structures near the ventral surface of the medulla increases tone in the nasal
vasculature and leads to a response pattern that includes changes in not only phrenic nerve activity and blood pressure
but also nasal patency.
494-R500, Copyright © 1987 by American Physiological Society
Articles by Haxhiu, M. A.
Articles by Cherniack, N. S.
A role for the ventral surface of the medulla
in regulation of nasal resistance
M. A. Haxhiu, K. P. Strohl, M. P. Norcia, E. van Lunteren,
E. C. Deal Jr and N. S. Cherniack
Nasal resistance is known to be affected by changes in nasal blood volume
and hence to depend on sympathetic discharge to nasal blood vessels.
Structures located superficially near the ventrolateral surface of the medulla
significantly affect respiratory and sympathetic activity and the tone of the
trachea. To assess the importance of these structures on nasal patency, we
measured transnasal pressure at a constant flow and examined the change in
pressure produced by topically applied N-methyl-D-aspartic acid (NMDA).
Experiments were performed in chloralose-anesthetized, paralyzed, and
artificially ventilated cats. NMDA administered on the intermediate area of
the ventral surface of the medulla decreased transnasal pressure and increased phrenic nerve activity. The response to
NMDA could be diminished or abolished by application to the ventral medullary surface of the NMDA antagonist
2-amino-5-phosphonovalerate (2-APV) or the local anesthetic lidocaine. Carotid sinus denervation and
posthypothalamic decerebration did not alter the nasal and phrenic nerve responses to NMDA; however, cervical
sympathetic denervation decreased these responses, both in intact and in bilaterally adrenalectomized animals. Therefore,
activation of NMDA receptors on structures near the ventral surface of the medulla increases tone in the nasal
vasculature and leads to a response pattern that includes changes in not only phrenic nerve activity and blood pressure
but also nasal patency.
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related to brain homeostasis
Journal of Cerebral Blood Flow & Metabolism (1997) 17, 894–904;
doi:10.1097/00004647-199708000-00008
Astroglial and Vascular Interactions of Noradrenaline Terminals
in the Rat Cerebral Cortex
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related
to brain homeostasis, metabolism, local blood flow, and blood-brain barrier permeability.
In the current study, we investigate the possible associations that exist between
NA-immunoreactive nerve terminals and astrocytes and intraparenchymal blood vessels
in the rat frontoparietal cortex, both at the light and electron microscopic levels. As a
second step, we sought to determine whether the NA innervation around intracortical
microvessels arises from peripheral or central structures by means of injections of
N-(2-chloroethyl-N-ethyl-2-bromobenzylamine) (DSP-4), a neurotoxin that specifically
destroys NA neurons from the locus ceruleus. At the light microscopic level, 6.8% of all
NA-immunoreactive nerve terminals in the frontoparietal cortex were associated with
vascular walls, and this perivascular noradrenergic input, together with that of the cerebral
cortex, almost completely disappeared after DSP-4 administration. When analyzed at the
ultrastructural level in control rats, NA terminals in the neuropil had a mean surface area
of 0.53 0.03 m2 and were rarely junctional (synaptic incidence close to 7%). Perivascular
terminals (located within a 3-m perimeter from the vessel basal lamina) counted at the
electron microscopic level represented 8.8% of the total NA terminals in the cortical tissue.
They were smaller (0.29 0.01 m2, P < 0.05) than their neuronal counterparts and were
located, on average, 1.34 0.08 m away from intracortical blood vessels, which consisted
mostly of capillaries (65%). None of the perivascular NA terminals engaged in junctional
contacts with surrounding neuronal or vascular elements. The primary targets of both
neuronal and perivascular NA nerve terminals consisted of dendrites, nerve terminals,
astrocytes, and axons, whereas in the immediate vicinity (0.25 m or less) of the
microvessels, astrocytic processes represented the major target. The results of the current
study show that penetrating arteries and intracortical microvessels receive a central NA
input, albeit parasynaptic in its interaction, originating from the locus ceruleus.
Particularly, they point to frequent appositions between both neuronal and perivascular
NA terminals and astroglial cells and their processes. Such NA neuronal-glial and
neuronal-glial-vascular associations could be of significance in the regulation of local
metabolic and vascular functions under normal and pathologic situations.
doi:10.1097/00004647-199708000-00008
Astroglial and Vascular Interactions of Noradrenaline Terminals
in the Rat Cerebral Cortex
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related
to brain homeostasis, metabolism, local blood flow, and blood-brain barrier permeability.
In the current study, we investigate the possible associations that exist between
NA-immunoreactive nerve terminals and astrocytes and intraparenchymal blood vessels
in the rat frontoparietal cortex, both at the light and electron microscopic levels. As a
second step, we sought to determine whether the NA innervation around intracortical
microvessels arises from peripheral or central structures by means of injections of
N-(2-chloroethyl-N-ethyl-2-bromobenzylamine) (DSP-4), a neurotoxin that specifically
destroys NA neurons from the locus ceruleus. At the light microscopic level, 6.8% of all
NA-immunoreactive nerve terminals in the frontoparietal cortex were associated with
vascular walls, and this perivascular noradrenergic input, together with that of the cerebral
cortex, almost completely disappeared after DSP-4 administration. When analyzed at the
ultrastructural level in control rats, NA terminals in the neuropil had a mean surface area
of 0.53 0.03 m2 and were rarely junctional (synaptic incidence close to 7%). Perivascular
terminals (located within a 3-m perimeter from the vessel basal lamina) counted at the
electron microscopic level represented 8.8% of the total NA terminals in the cortical tissue.
They were smaller (0.29 0.01 m2, P < 0.05) than their neuronal counterparts and were
located, on average, 1.34 0.08 m away from intracortical blood vessels, which consisted
mostly of capillaries (65%). None of the perivascular NA terminals engaged in junctional
contacts with surrounding neuronal or vascular elements. The primary targets of both
neuronal and perivascular NA nerve terminals consisted of dendrites, nerve terminals,
astrocytes, and axons, whereas in the immediate vicinity (0.25 m or less) of the
microvessels, astrocytic processes represented the major target. The results of the current
study show that penetrating arteries and intracortical microvessels receive a central NA
input, albeit parasynaptic in its interaction, originating from the locus ceruleus.
Particularly, they point to frequent appositions between both neuronal and perivascular
NA terminals and astroglial cells and their processes. Such NA neuronal-glial and
neuronal-glial-vascular associations could be of significance in the regulation of local
metabolic and vascular functions under normal and pathologic situations.
redistribution of cerebral bloodflow following sympathectomy!
SM Mueller, DD Heistad and ML Marcus
Effect of sympathetic denervation in dogs.
Total and regional cerebral blood flow during hypotension, hypertension, and hypocapnia.
The major new findings in this study are,
first, that hypotension produces a redistribution of CBF which tends to preserve blood flow to brainstem and to
cerebral gray matter...
1977 American Heart Association
Effect of sympathetic denervation in dogs.
Total and regional cerebral blood flow during hypotension, hypertension, and hypocapnia.
The major new findings in this study are,
first, that hypotension produces a redistribution of CBF which tends to preserve blood flow to brainstem and to
cerebral gray matter...
1977 American Heart Association
the effect of sympathectomy on ventilation
Influence of cervical sympathetic nerves on ventilation and upper
airway resistance in the rat
K.D. O'Halloran*, A.K. Curran**, A. Bradford+
Influence of cervical sympathetic nerves on ventilation and upper airway resistance in the
rat. K.D. O'Halloran, A.K. Curran, A. Bradford. ©ERS Journals Ltd 1998.
ABSTRACT: The cervical sympathetic trunks innervate the carotid bodies, carotid
baroreceptors, thyroid gland and the upper airway mucosa, structures which can
influence breathing and upper airway resistance. (same in humans)
However, their role in the control of ventilation and upper airway patency
is poorly understood.
A constant airflow was applied to the upper airway through a high-cervical trache-
ostomy in anaesthetized rats breathing spontaneously through a low-cervical trache-
ostomy. The peripheral ends of the cut cervical sympathetic trunks were stimulated
electrically and airflow resistance and ventilation were measured. The effects of cervi-
cal sympathetic trunk section on ventilation were also measured in conscious rats.
In conscious rats, cutting the sympathetic trunks caused a decrease in ventilation
during normoxia but only slightly affected ventilatory responses to hypoxia and
hypercapnia. In anaesthetized rats, sympathetic trunk stimulation caused an inhibi-
tion of breathing which was sometimes followed by excitation. These responses were
unaffected by α- or β-adrenoceptor blockade but were abolished by cutting the
carotid sinus nerves. Sympathetic stimulation also caused a fall in upper airway
resistance which was reduced by bypassing the nose, unaffected by propranolol or
carotid sinus nerve section and abolished by phentolamine.
It was concluded that the cervical sympathetic nerves exert important influences
on ventilation and upper airway resistance.
Eur Respir J 1998; 12: 177–184.
airway resistance in the rat
K.D. O'Halloran*, A.K. Curran**, A. Bradford+
Influence of cervical sympathetic nerves on ventilation and upper airway resistance in the
rat. K.D. O'Halloran, A.K. Curran, A. Bradford. ©ERS Journals Ltd 1998.
ABSTRACT: The cervical sympathetic trunks innervate the carotid bodies, carotid
baroreceptors, thyroid gland and the upper airway mucosa, structures which can
influence breathing and upper airway resistance. (same in humans)
However, their role in the control of ventilation and upper airway patency
is poorly understood.
A constant airflow was applied to the upper airway through a high-cervical trache-
ostomy in anaesthetized rats breathing spontaneously through a low-cervical trache-
ostomy. The peripheral ends of the cut cervical sympathetic trunks were stimulated
electrically and airflow resistance and ventilation were measured. The effects of cervi-
cal sympathetic trunk section on ventilation were also measured in conscious rats.
In conscious rats, cutting the sympathetic trunks caused a decrease in ventilation
during normoxia but only slightly affected ventilatory responses to hypoxia and
hypercapnia. In anaesthetized rats, sympathetic trunk stimulation caused an inhibi-
tion of breathing which was sometimes followed by excitation. These responses were
unaffected by α- or β-adrenoceptor blockade but were abolished by cutting the
carotid sinus nerves. Sympathetic stimulation also caused a fall in upper airway
resistance which was reduced by bypassing the nose, unaffected by propranolol or
carotid sinus nerve section and abolished by phentolamine.
It was concluded that the cervical sympathetic nerves exert important influences
on ventilation and upper airway resistance.
Eur Respir J 1998; 12: 177–184.
75% PNEUMOTHORAX EXPECTED AFTER SYMPATHECTOMY
A small insignificant pneumothorax can be expected
after ETS in about 75% of cases [15], which gets spon-
taneously absorbed, usually within 24 h. limbs: a critical analysis and long-term results of 480 operations.
Comparing T2 and T2–T3 ablation in thoracoscopic
sympathectomy for palmar hyperhidrosis: a randomized
control trial
A. N. Katara, J. P. Domino, W.-K. Cheah, J. B. So, C. Ning, D. Lomanto
Minimally Invasive Surgical Centre, Department of General Surgery, National University Hospital, 5 Lower Kent Ridge Road, Singapore, 119074
Received: 13 October 2006/Accepted: 2 November 2006
after ETS in about 75% of cases [15], which gets spon-
taneously absorbed, usually within 24 h. limbs: a critical analysis and long-term results of 480 operations.
Comparing T2 and T2–T3 ablation in thoracoscopic
sympathectomy for palmar hyperhidrosis: a randomized
control trial
A. N. Katara, J. P. Domino, W.-K. Cheah, J. B. So, C. Ning, D. Lomanto
Minimally Invasive Surgical Centre, Department of General Surgery, National University Hospital, 5 Lower Kent Ridge Road, Singapore, 119074
Received: 13 October 2006/Accepted: 2 November 2006
Orthostatic hypotension after surgery, high mortality
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.
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.
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
