"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
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
Friday, January 18, 2008
SAMPLE OF THE SALES PITCH - THIS IS HOW IT'S DONE
Endoscopic sympathectomy is a highly-effective treatment for patients with palmar or facial hyperhydrosis. ETS allows simultaneous treatment of both sides with a very low risk of complications. Attention to surgical detail is important to achieve excellent long-term results. We continue to lead the New York metropolitan area in minimally invasive thoracoscopic procedures, and especially ETS.
THE SYMPATHECTOMY FAILURE
9780849386671
Chronic Pain: Reflex Sympathetic Dystrophy Prevention and Management
Hooshang Hooshmand
ISBN 13: 9780849386671
Publisher: CRC Pr I Llc
Publication Date: 1993
Binding: Hardcover
Melbourne Surgeon's definition of a very safe procedure
Not being able to sweat and cool of through the head is more than annoying. 40% of the body heat is released through the top of the head. This will be eliminated. The will be no sweating from the head, neck and shoulders.
The the skin's natural cleaning mechanism, sweating will be eliminated. The skin will become dehydrated, clogged up and more prone to acne. Sympathectomy also lowers the denervated skin's immune responses, it will be more prone to infections. Sympathectomy alters the skin's healing process. People undergoing the opearation will have scar tissue after the operation and from future cutaneous trauma.
Sympathetic denervation impairs epidermal healing in cutaneous wounds
LINCOLN R. KIM, BSCaI KEITH WHELPDALE, MSCb; MA TEUSZ ZUROWSKI, MSCb; BRUCE POMERANZ, MD, PhD°, b
INTRAOCULAR PRESSURE AND DENERVATION
MANY PATIENTS COMPLAIN ABOUT VISUAL DISTURBANCES, BLURRY VISION AFTER THE SURGERY. THERE IS THE CASE OF ORTHOSTATIC HYPOTENSION CAUSED BY THE SURGERY BY DISABLING REGULATION OF THE BLOODPRESSURE, SO THAT BLOOD POOLS INTO THE LEGS WHEN PATIENTS STAND UP. THIS CAN CAUSE BLURRY VISION. THE SYMPATHETIC NERVES ALSO INNERVATE THE SMOOTH MUSCLE THAT IS INVOLVED IN EYEMOVEMENTS. AND NOW THIS ARTICLE TALKING ABOUT THE CONNECTION BETWEEN INNERVATION AND INTRAOCULAR PRESSURE.
IT IS A WELL-DOCUMENTED FACT THAT THE OPERATION CAN CAUSE HORNER SYNDROME, CAUSING A DROOPY EYELID AND AFFECTING THE PUPILS.
b. Cervical sympathectomy causes photoreceptor-specific cell death in the
rat retina
Jena J. Steinle , , Naarah L. Lindsay and Bethany L. Lashbrook
There was a significant reduction (30%) in photoreceptor numbers in the sympathectomized eye. This loss was due to apoptosis, as there was over a doubling in apoptotic cell numbers after sympathectomy. This loss of photoreceptors in the sympathectomized eye resulted in a significantly reduced width of the outer nuclear layer of the retina when compared to the contralateral eye. Increased glial fibrillary acidic protein (GFAP) staining was also noted after sympathectomy in the ganglion cell layer with streaking toward the bipolar cell layer. These results suggest that loss of sympathetic innervation may cause significant changes to the physiology of the choroid.
Journal of Medical Colleges of PLA
AUTOIMMUNE DISEASE AND INNERVATION
Autoimmune disease and innervation.
Rainer H Straub
In the decades before 1987, most of the research devoted to neuronal innervation was carried
out in primary and secondary lymphoid organs at very different locations. This was an important period in order to understand hard-wiring of immune organs in physiology. Between 1988 and 1997, with the appearance of specific antibodies against neuronal markers, innervation was studied in inflamed tissue of patients and of animals with autoimmune diseases. This period clearly revealed that nerve fibers of, both, the sympathetic and sensory nervous system are altered, but only small amounts of tissue have been investigated by qualitative but not quantitative techniques. Between 1998 and 2007, with the understanding that sympathetic and sensory neurotransmitters might play opposite roles in inflammation, nerve fibers of the different nervous systems have been studied in parallel using quantitative techniques. These studies have been carried out in a large number of patients with long-standing autoimmune diseases. It turned out that sympathetic nerve fibers are lost in chronically inflamed tissue, while substance P-positive nerve fibers sprout into the inflamed area. This might be important because high concentrations of sympathetic neurotransmitters are antiinflammatory whereas substance P has a proinflammatory role. The first challenge for future research is the determination of innervation in the early human autoimmune disease. The second challenge is the identification of reasons for the differential loss of sympathetic in relation to sensory nerve fibers. It might well be that nerve repellent factors specific for the sympathetic nerve fiber might play an important role for the observed differential loss. Whether, or not, a therapy can be based on these findings remains to be established.
[Pubmed] [Scholar] [EndNote] [BibTex] [Doi]
THIS IS WHAT THERMOREGULATORY DYSFUNCTION LOOKS LIKE
CONSIDERABLE HYPERTHERMIA THROUGHOUT THE FACE AND NECK, WHICH IS CONSISTENT WITH AUTONOMIC DYSFUNCTION.
A SURGICALLY INDUCED AUTONOMIC DYSFUNCTION, THAT IS CONSISTENT WITH T2 SYMPATHECTOMY.
A SIGNIFICANT PATERN OF HYPOTHERMIA EXTENDING FROM THE RIGHT ARM INTO THE RIGHT AXILLA, THIS ALSO CORRELATES WITH THERMOREGULATORY DYSFUNCTION.
MORE ON BRAIN COOLING
“The efficiency of SBC (Selective Brain Cooling) is increased by evaporation of sweat on the head and by ventilation through the nose.” (Nagasaka et al. 1998)
“A necessary condition for SBC is a high heat loss capacity from the head itself, without such a heat loss SBC is not possible.” (Cabanac 1993)
“Because the human head sweats more than the rest of the body, heat loss from the head skin could amount to 125-175 Watts under conditions of moderate hyperthermia.” (http://www.editthis.info/corposcindosis/Changes_to_Systemic_Function%2C_part_1Cabanac 1993)
SELECTIVE BRAIN COOLING...IF THERE IS NO SWEATING FROM THE FACE...?
Selective Brain Cooling
Besides the general “heat intolerance”, ETS patients have anecdotally reported what they consider to be a “hot brain” syndrome. In particular, Taiwanese ETS patient and robotics engineer “Hpymaker” has made frequent references in the oral history to this hot brain phenomenon. Songboy1234 has also reported a very disturbing sensation like a fever that occurs when exercise is attempted.
Is there any scientific reason to suppose that ETS surgery could interfere with brain cooling, separate from the general thermoregulatory difficulties already shown? This would depend upon whether the normal human has any mechanism to selectively cool the brain; and if so, whether that mechanism is damaged by sympathectomy. The answers are yes we do; and yes it is.
Studies from decades ago began to confirm Selective Brain Cooling. “Cooling of the head skin . . .produces a significant improvement in the performance of heat-stressed humans.” (Kenney, see Williams & Shitzer, 1974).
The ability to selectively cool the brain during hyperthermia (overheating) has long been an accepted fact in many mammals, such as dogs. Dogs have a network of blood vessels in the head called the “carotid rete” which allows heat exchange between warm blood in arteries and cooler blood in veins. The excess heat escapes through the mouth during panting. Humans do not have a carotid rete, so for some time the notion of selective brain cooling in humans was controversial.
However, it has been shown that at 65.8˚ F (18.8˚ C) ambient temperature the deep trunk temperature of a marathon runner may rise to 107.4˚ F (41.9˚ C) with no clinical sign of heat illness (Cabanac et al. 1979; see Maron, Wagner & Horvath, 1977). Michel Cabanac at the Department of Physiology, Laval University, Quebec has been studying Selective Brain Cooling in Humans since the 1970’s, and has evidently discovered the mechanism by which humans accomplish this.
It turns out that certain veins in the face, such as the ophthalmic veins, will actually reverse the direction of blood flow when the body begins to overheat. The blood in these veins is cooled by evaporation of facial sweat, then flows backwards into the sinus and intercranuim area, cooling the carotid artery and the brain.
“The selective influence of facial fanning on human brain temperature can be attributed, therefore, to cool venous blood perfusing the cavernous sinus and possibly cooling the blood of the internal carotid artery.” (Cabanac et al. 1979)
A group of Japanese physiologists at Kanazawa University have been confirming and expanding upon Cabanac’s findings. Their studies subject people to heat stress and exercise, and measure variables such as skin temperature, core temperature, forehead sweating, and blood flow in the ophthalmic vein. They found “that there are elements within the brain that control the mechanisms for switching the direction of venous flow through the emissary veins to keep the brain cool during hyperthermia.” (Hirashita et al. 1992)
Given that this direction-reversing mechanism requires vascular control in the face, we already have strong reason to suspect that ETS would disturb if not destroy selective brain cooling. Is head sweating also important to this process?
“The efficiency of SBC (Selective Brain Cooling) is increased by evaporation of sweat on the head and by ventilation through the nose.” (Nagasaka et al. 1998)http://www.editthis.info/corposcindosis/Changes_to_Systemic_Function%2C_part_1
ETS SURGEON ADMITS OPERATION CAUSES HEAT INTOLERANCE
Nielson Website
Additional confirmation of thermoregulatory difficulties comes from ETS surgeon David Nielson, whose advertising website has, since 2003, listed “heat intolerance” among the “side effects” produced by the surgery.http://www.hyperhidrosis-usa.com/sideeffects.html
ANHIDROSIS AFTER SYMPATHETOMY
Prediction: Thoracic sympathectomy will cause anhidrosis in the denerved area.
Empirical Status: Confirmed.Anhidrosis
Sweat glands are controlled almost entirely via the sympathetic nervous system, and do not have parasympathetic innervation at all. Unlike most other sympathetic nerve terminals, the receptors in sweat glands are activated by acetylcholine, not norepinephrine. It is possible that sweat glands can be activated locally to a small degree by catecholamines in the blood, but for practical purposes sympathectomy renders sweat glands permanently non-functional in the denerved area. This dysfunction is called "anhidrosis".
Anhidrosis is considered dangerous, as we learn from the WebMD dictionary:
Anhidrosis: Not sweating. From the Greek an- meaning a lack of + hidros meaning sweat = lack of sweat. The inability to sweat may seem a blessing but it is not, since to sweat is to be able to stay cool. Anhidrosis creates a dangerous inability to tolerate heat. (WebMD dictionary)
In one clinical trial, ETS patients subjectively described the sensation of anhidrosis as “disturbing”.“Patients undergoing T2-T4 resection often experience anhidrosis from the nipple line upwards which has been disturbing for several individuals.” (Fischel et al. 2003)
http://www.editthis.info/corposcindosis/Changes_to_Individual_Effectors,_part_2
TREATMENT NEEDED AFTER THE TREATMENT ENDED UP NOT BEING A TREATMENT ...
COMMUNICATIONS AND BRIEF REPORTS
Treatment of Unilateral Compensatory Sweating after Endoscopical Thoracic Sympathectomy for General Hyperhidrosis with Botulinum Toxin A
- FALK GEORGES BECHARA, MD * * Department of Dermatology and Allergology, Ruhr-University Bochum, Bochum, Germany; ,
- MICHAEL SAND, MD * * Department of Dermatology and Allergology, Ruhr-University Bochum, Bochum, Germany; ,
- GEORG MOUSSA, MD * * Department of Dermatology and Allergology, Ruhr-University Bochum, Bochum, Germany; ,
- DANIEL SAND, BS † † Department of Physiological Science, University of California Los Angeles (UCLA), Los Angeles, California; ,
- PETER ALTMEYER, MD * * Department of Dermatology and Allergology, Ruhr-University Bochum, Bochum, Germany; ,
- KLAUS HOFFMANN, MD * * Department of Dermatology and Allergology, Ruhr-University Bochum, Bochum, Germany; and
- JOHANNES SCHMIDT, MD ‡ ‡ Department of Visceral Surgery, Lutherhaus Essen, University of Witten-Herdecke, Essen, Germany
- * Department of Dermatology and Allergology, Ruhr-University Bochum, Bochum, Germany; † Department of Physiological Science, University of California Los Angeles (UCLA), Los Angeles, California; ‡ Department of Visceral Surgery, Lutherhaus Essen, University of Witten-Herdecke, Essen, Germany
BODY WEIGHT
During Prolonged ICV Leptin Infusion
Robert L. Dobbins1, Lidia S. Szczepaniak1, Weiguo Zhang1 and J. Denis McGarry1,2
ABOUT LIPOLYSIS FOLLOWING SYMPATHECTOMY
Hormones in Muscular Activity
by Atko Viru - 1985 - Medical 121 ± 13 min).44 Consequently, following chemical sympathectomy the adrenal medulla is unable to ensure adequate lipolysis. ...
Limited preview - books.google.com/books?isbn=0849354943...
Monckeberg's sclerosis after sympathetic denervation
Medial arterial calcification is frequently seen in diabetic patients with severe diabetic
neuropathy. Sixty patients (19 diabetic and 41 non-diabetic) were examined
radiologically for typical Monckeberg's sclerosis of feet arteries 6-8 years after uni- or
bilateral lumbar sympathectomy. Fifty-five out of 60 patients (92%) revealed medial
calcification. This calcification was observed in both feet of 93% of patients, who had
undergone bilateral operation. After unilateral sympathectomy the incidence of calcified
arteries on the side of operation was significantly higher than that on the contralateral
side (88% versus 18%, p less than 0.01). Although diabetic patients showed longer
stretches of calcification than non-diabetic subjects, the difference was not significant in
terms of incidence and length. Of 20 patients who had no evidence of calcinosis
pre-operatively, 11 developed medial calcification after unilateral operation exclusively
on the side of sympathectomy. In seven patients calcinosis was detected in both feet after
bilateral operation. In conclusion, sympathetic denervation is one of the causes of
Monckeberg's sclerosis regardless of diabetes mellitus.
Reduced baroreflex sensitivity is associated with increased vascular calcification and arterial stiffness
Introduction. Vascular calcification is a critical determinant of cardiovascular morbidity and mortality in chronic haemodialysis (HD) patients. The pathophysiology underlying this observation remains obscure. Baroreceptor sensitivity (BRS) is important in the maintenance of an appropriate cardiovascular status both at rest and under the physiological stress of HD. BRS is determined by both the mechanical properties of the vascular wall, mediating the transfer of transmural pressure, and afferent and efferent autonomic function. We aimed to study the association between arterial structure, function and BRS in chronic HD patients.
Conclusion. The reduction in BRS and the resulting aberrant blood pressure response to the physiological stress and volume changes of HD may be important in the further understanding of the pathophysiology of the increased mortality in HD patients with vascular calcification.
Lindsay J. Chesterton1, Mhairi K. Sigrist1, Terence Bennett2, Maarten W. Taal1 and Christopher W. McIntyre
In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent
8. Describe the reflex compensations when someone suddenly stands up from a supine position. What would happen in a patient who just had a sympathectomy?
Sudden standing causes pooling of blood in the leg veins. This results in decreased venous return to the heart, which leads to decreased cardiac output (Frank-Starling mechanism), which leads to decreased MAP. This decrease in MAP is detected by the carotid sinus baroreceptors, which relay a message to the medullary cardiovascular control center, which increases sympathetic outflow and decreases parasympathetic outflow, this causes:
* An increase in HR and myocardial contractility, tending to restore cardiac output.
* Vasoconstriction in skeletal musculature, skin, kidneys and gut, reducing blood flow to these organs and increasing TPR.
* Venoconstriction decreasing capacitance and increasing venous return
A patient with a sympathectomy would experience what's referred to as orthostatic hypotension (which might lead to syncope). Orthostatic hypotension is a decrease in arterial pressure when going from supine to a standing position. A person with a normal baroreceptor mechanism will try to restore MAP. In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent.
Heart Physiology II
M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
Date Revised: Jan 16, 2002
Revised by: Gordon Li and Carolyn Nguyen
reflex vasoconstriction induced by mild central hypovolemia includes a significant reduction of jejunal mucosal perfusion in supine resting humans
J Auton Nerv Syst. 1998 Feb 5;68(3):157-63.
Baroreceptor-mediated reduction of jejunal mucosal perfusion, evaluated with endoluminal laser Doppler flowmetry in conscious humans.
Author information
Abstract
Reduction of central blood volume elicits a peripheral vasoconstrictor reflex in various tissues including skin, skeletal muscle and the hepatomesenteric region. The aim of the present study was to investigate whether this reaction includes a decreased perfusion of the jejunal mucosa in man. Laser Doppler flowmetry (LDF) was used to monitor jejunal mucosal and skin perfusion simultaneously in eleven healthy volunteers. LDF recordings were performed during quiescent (phase 1) periods of the migrating motor complex. Seven subjects demonstrated cycling changes of jejunal mucosal perfusion (vasomotion). The average minimum jejunal flux value was 72 +/- 6 perfusion units. The average intraindividual coefficient of variation was 18 +/- 2%. Lower body negative pressure (LBNP) was used to elicit controlled reductions of central blood volume. LBNP of 10 mm Hg induced a 12 +/- 4% (P < 0.05) decrease in jejunal perfusion and a 43 +/- 11 (P < 0.001) decrease in cutaneous perfusion. Corresponding responses to LBNP of 20 mm Hg were 17 +/- 5% (P < 0.01) and 37 +/- 10% (P < 0.01) reductions in jejunal mucosal and skin perfusion, respectively. Cardiac index was significantly reduced by the LBNP procedure, whereas heart rate remained unchanged and blood pressure changes were minor and inconsistent. These findings indicate that the reflex vasoconstriction induced by mild central hypovolemia includes a significant reduction of jejunal mucosal perfusion in supine resting humans. This reflex may provide one mechanism for the intestinal ischemia often occurring in critically ill patients.
Predicting CS?
Some surgeons tell their patients that it happens mostly to men, who are overweight and had a heavy sweating prior to surgery.
This has never been proven, and my experience with people who underwent the surgery and have the debilitating CS does not indicate any group that would be more likely to be affected.
Also: these statistics are unreliable. There has been no independent study the examine the severity or extent of the CS. Many questions are not asked, so that they will not tarnish the results. These statistics are collected and questions formulated by the surgeons who offer the surgery. It would be reasonable to assume that they will look for a confirmation of the effectiveness of the operation....otherwise they would not do the surgery....
15% regretted the operation.
Evaluation of compensatory sweating after bilateral thoracoscopic sympathectomy for palmar hyperhidrosis.
Department of Surgery "A," Faculty of Health Sciences, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
The study is a retrospective review of 60 patients undergoing bilateral T2-T3 thoracoscopic sympathectomy for palmar hyperhidrosis in our department between 1997 and 2003. The study was based on a telephone questionnaire and medical chart review. Forty patients (67%) replied to the questionnaire and were included in the study. Postoperative complications, therapeutic results, patient satisfaction, and the severity of compensatory sweating (CS) were assessed. In all patients both palms were dry at the end of surgery. Postoperative complications included permanent unilateral Horner syndrome, wound infection, and residual pneumothorax resolving after thoracal drainage, in one patient each. CS with different severity occurred in 35 patients (87.5%). Six patients (15%) regretted undergoing the operation due to the extent and severity of the CS seriously affecting their quality of life. Thoracoscopic sympathectomy is a simple procedure with a high success rate. However, CS is a serious complication and a significant number of patients may regret undergoing the operation; a careful selection of patients and comprehensive explanation are advisable.
Sympathectomy potentiates the vasoconstrictor response to nitric oxide synthase
METHODS:
RESULTS:
CONCLUSIONS:
http://www.ncbi.nlm.nih.gov/pubmed/10690345
Melatonin changes after sympathectomy
Sequential cerebrospinal fluid and plasma sampling in
humans: 24-hour melatonin measurements in normal
subjects and after peripheral sympathectomy. English.
72. 1991:819-23.
Brismar K, Mogensen L, Wetterberg L.
Depressed
melatonin secretion in patients with nightmares due to
beta-adrenoceptor blocking drugs. English. 221.
1987:155-8.
Evidence suggests a link between endogenous melatonin and the sleep cycle
• There is evidence of a link between endogenous melatonin and the temperature rhythm.
nerve blocks as a treatment for Herpes Zoster...
The Cancer Patient with Chronic Pain Due To Herpes Zoster
... were mild and tolerable and consisted primarily of somnolence and dizziness. ... Peripheral neurectomy, cordotomy, dorsal rhizotomy, sympathectomy, ...www.current-reports.com/
Insulin hypersensitivity produced by sympathectomy
hypersensitivity has been undeniably
produced by hypophysectomy, by ad-
renalectomy, by sympathectomy, by
spinal cord lesions, and by hypothalam-
ic lesions.
THE HYPOTHALAMUS: A REVIEW OF THE
EXPERIMENTAL DATA
W. R. Ingram
treatment of choice??!!
(internet ad for a surgeon from the US)
My comment: That is brilliant achievement! However the operation, no matter how many holes it requires, it will have the same effects on the patient.
Surely the definition of the surgery needs some rephrasing?! The operation disrupts more than the impulses to the sweat glands. It disrupts signaling between the body and the brain, partial autonomic dysfunction, disables thermoregulation, causes revascularization of the brain, reduces heart rate and blood pressure, abolishes homeostasis...a long list really.
All these effects have been proven.
The antihypertensive effects of the drug may be enhanced in the post-sympathectomy patient.
Diovan HCT Tablets
http://www.drugs.com/pro/hydrochlorothiazide.html
http://www.drugs.com/ppa/atenolol-chlorthalidone.html
http://www.drugs.com/pro/renese.html
Drug and SYMPATHECTOMY interaction
Tell your doctor if you have any of
the following medical conditions:
* kidney problems
* liver problems
* heart problems
* diabetes
* recent excessive vomiting or
diarrhoea
* Systemic Lupus Erythematosus
(SLE), a disease affecting the
skin, joints and kidneys
* a salt restricted diet
* a past operation known as
sympathectomy
If you have not told your doctor
about any of the above, tell
him/her before you start taking
Atacand Plus 16/12.5.
What Atacand Plus
16/12.5 is for
Atacand Plus 16/12.5 is used to treat
high blood pressure.