autonomic neuropathy in which the sympathetic nerve function has been divided into two distinct regions
A severe form of CS is the split-body syndrome, corposcindosis, which is defined as an
autonomic neuropathy in which the sympathetic nerve function has been divided into two distinct
regions, one dead and the other hyperactive. In these cases, the patient feels like he or she is living
in two separate bodies.
The rates of CS in some series from the past 10 years are summarized in Table 4, with rates of mild CS varying from 14% to 90% and severe CS from 1.2% to 30.9%.
Some investigators only report on patients who have severe CS because they believe that almost all patients develop mild CS after sympathectomy.
Pascal DUMONT Thorac Surg Clin 18 (2008) 193–207
produces the equivalent of a sympathectomy, preventing noradrenaline release
Class III
Mode of action
- increases action potential duration and refractory period of cardiac cells
- antifibrillatory effect on ventricular muscle - may be more important than class III effects in emergency treatment of malignant ventricular arrhythmias
- initially causes noradrenaline release and then produces the equivalent of a
sympathectomy, preventing noradrenaline release (class II effect)
Clinical use
- useful adjunct to DC shock in managing life-threatening ventricular
arrhythmias, especially refractory VF
- theoretical advantages of lignocaine but no advantage has been demonstrated clinically
alterations in the relative abundance of TH mRNA mediate changes in TH activity induced by chronic stress or sympathectomy
Journal of Neuroscience Research
Published Online: 11 Oct 2004
Cardiac hypertrophy accelerated by left cervical sympathectomy
Biomedical and Life Sciences | |
SpringerLink Date | Tuesday, August 02, 2005 |
The HPA axis regulates the secretion of glucocorticoids (GCs), which play important roles in diverse brain functions, including cognition, emotion
The Journal of Neuroscience, March 1, 2000, 20(5):2064-2071
peripheral sympathetic denervation may modulate immune function via activation of the hypothalamic-pituitary-adrenal (HPA) axis
Ann N Y Acad Sci. 2000;917:923-34.
Increasing evidence suggests that the detrimental effects of glucocorticoid (GC) hypersecretion occur by activation of the hypothalamic-pituitary-adrenal (HPA) axis in several human pathologies, including obesity, Alzheimer's disease, AIDS dementia, and depression. The different patterns of response by the HPA axis during chronic activation are an important consideration in selecting an animal model to assess HPA axis function in a particular disorder.
Detrimental effects of chronic hypothalamic-pituitary-adrenal axis activation. From obesity to memory deficits
Raber J Mol Neurobiol 1998 Aug; 18(1): 1-22
Renin-Angiotensin activation following sympathectomy
We should note that baroreflex response for maintaining cardiovascular stability is
suppressed in the patients who received the ETS.
Anesthesiology 2001; 95:A160
“cervical sympathectomy isolates all these sympathetic ganglion cells from the central nervous system and prevents them from responding to reflex or emotional changes in the central nervous system." Cunningham's Manual of Practical Anatomy: Volume III: Head, Neck and Brain, 1986
The renin-angiotensin system (RAS) is a major regulatory system of cardiovascular and renal function. Many new aspects of this system have been revealed in recent years, leading to new therapeutic approaches. It's well known that RAS blocking agents have potent antiatherosclerotic effects, which are mediated by their antihypertensive, anti-inflammatory, antiproliferative, and oxidative stress lowering properties. Inhibitors of RAS are now first-line treatments for hypertensive target organ damage. Their effects are greater than expected by their ability to lower blood pressure. Angiotensin receptor blockers reduce the frequency of atrial fibrillation and stroke, are also able to prevent cardiovascular and renal events in diabetic patients. Thus, blockade of RAS represents one of the most important strategies in order to reduce cardiovascular risk.
Neurol Sci. 2008 Sep;29 Suppl 2:S277-8.
Renin-angiotensin system and stroke.
Patients may develop bradycardia after surgical procedure
Heart Disease Weekly. Atlanta: Feb 23, 2003. pg. 71
sympathectomy-induced increases in choroidal thickness, vascular luminal area and large venules and large arterioles
Biotech Week. Atlanta: Jan 21, 2004. pg. 396
83% of patients reported severe 'compensatory sweating'
Heather Ennis. Medical Post. Toronto: Feb 15, 2005. Vol. 41, Iss. 7; pg. 17, 2 pgs
sympathectomy increased the bacterial tissue burden
The Journal of Infectious Diseases. Chicago: Aug 15, 2005. Vol. 192, Iss. 4; pg. 560, 13 pgs
pineal gland and extracerebral blood vessels folowing sympathectomy
Neuronal Source of Plasma Dopamine
David S Goldstein, Courtney Holmes. Clinical Chemistry. Washington: Nov 2008. Vol. 54, Iss. 11; pg. 1864, 8 pgs
sympathectomy decreased cardiac sympathetic nerve density and norepinephrine level
Heart Disease Weekly. Atlanta: Dec 28, 2008. pg. 54
Pain following endoscopic sympathectomy
Medical Devices & Surgical Technology Week. Atlanta: Sep 6, 2009. pg. 203
Laparoscopic surgery is associated with an increased incidence of postoperative atelectasis
Anesth Analg 2009; 109:1511-1516
© 2009 International Anesthesia Research Society
significant adverse effects on cardiopulmonary physiology
Because of technologic advances and improved postoperative recovery, endoscopic surgery has become the technique of choice for many thoracic surgical procedures6 and 25; however, endoscopic visualization of intrathoracic structures requires retraction or collapse of the ipsilateral lung, which can have significant adverse effects on cardiopulmonary physiology. These cardiopulmonary changes can be further affected by the pathophysiologic changes associated with the disease process requiring the surgical procedure.
Because acute changes in cardiopulmonary function can compromise patient safety severely, a clear understanding of the dynamic interaction between the anesthetic–surgical technique and patient physiology is essential. This article discusses the effect of thoracoscopic surgery and the impact of various anesthetic interventions on cardiovascular and pulmonary physiology. In addition, some recommendations for “damage control” are made.
Anesthesiology Clinics of North America
Volume 19, Issue 1, 1 March 2001, Pages 141-152
PATHOPHYSIOLOGY OF ONE-LUNG VENTILATION
Anesthesiology Clinics of North America
Volume 19, Issue 3, 1 September 2001, Pages 435-453
sympathectomy will blunt the normal tachycardic response to hypovolemia.
OBSTETRIC ANAESTHESIA OUR WAY
Royal Women's Hospital Melbourne
Author: Dr Philip Popham
Influence of thoracic sympathectomy on cardiac induced oscillations in tissue blood volume
http://cat.inist.fr/?aModele=afficheN&cpsidt=14106877
low heart rate variability is associated with an increased risk for sudden cardiac death
http://www.annals.org/content/118/6/436.abstract
Thursday, November 12, 2009
Isointegral mapping revealed that ETS altered electroactivity on the heart
Eur J Cardiothorac Surg 1999;15:194-198
Obviously, it is not simply a compensatory hyperhidrosis transposition
Ann Thorac Surg 2001;72:667-668
collateral effects of thoracic sympathectomy not disclosed to patients
Eur J Cardiothorac Surg 2001;20:1095-1100
similar to beta-blocker therapy
JNS - March 2004 Volume 100, Number 3
http://www.springerlink.com/content/xe7g2w72617phl0e/
Volume 13, Number 4 / August, 2003
Clinical conditions that cervico-thoracic sympathetic blockade may benefit
Amblyopia due to quinine poisining (also causes retinal artery spasm and thrombosis)
Edition: 4 - 2008
Acquired cardiovascular disease following Sympathectomy
We found statistically significant differences (P < .05) in both time and frequency domains. Parameters that evaluate global cardiac autonomic activity (total power, SD of normal R-R intervals, SD of average normal R-R intervals) and vagal activity (rhythm corresponding to percentage of normal R-R intervals with cycle greater than 50 ms relative to previous interval, square root of mean squared differences of successive normal R-R intervals, high-frequency power, high-frequency power in normalized units) were statistically significantly increased after sympathectomy. Low-frequency power in normalized units, reflecting sympathetic activity, was statistically significantly decreased after sympathectomy. Low-/high-frequency power ratio also showed a significant decrease, indicating relative decrease in sympathetic activity and increase in vagal activity.
The Journal of Thoracic and Cardiovascular Surgery
Volume 137, Issue 3, March 2009, Pages 664-669
sympathectomy leads to peripheral vasodilation, reduced preload, and subsequently decreased cardiac output
Table 42-1
Classification of percutaneous neural destructive procedures:
Anatomy
1. Peripheral neurotomy (such as destruction of intercostal, ilioinguinal nerves)
2. Rhizotomy (spinal dorsal root rhizotomy, trigeminal rhizotomy)
3. Destruction of sensory pathways in the spinal cord (midline punctuate myelotomy, cordotomy)
4. destruction of brain sensory centers (hypophysectomy)
5. Sympathectomy
(p.992)
The authors found that the incidence of hypotension was a function of the level of sympathetic denervation, occurring in 60% of patients with a T7 sympathectomy, and in 100% of patient with a T4 or higher level of sympathectomy.
(p 226)
After thoracoscopic sympathectomy for hyperhidrosis, very severe discomfort and hyperhidrosis in the neighboring non-sympathectomized regions occurred with alarming frequency and intensity.
(p.879)
Cardiovascular effects of epidural blockade
"Central" Sympathetic block (T1-T4) - Blockade of
Cardiac sympathetic outflow from vasomotor center
Cardiac sympathetic reflexes at segmental level
Vasoconstrictor fibers to head, neck, and arms
Effect:
HR ↓ CO ↓
Vasodilation in upper limbs
"Inappropriate bradycardia"; "sudden bradycardia"; vagal arrest (p. 247)
↓↓Venous return may result in sudden parasympathetic tone ("faint response")
↓ ↓ HR → cardiac arrest
"Inappropriate" bradycardia (i.e. "normal" HR in face of ↓MAP with sensory level T3-T4)
Peripheral vasodilation should evoke an ↑ HR. But ↓ venous return → ↑vagal tone, so HR remains at preblock rate but is "inappropriately" slow.
↓HR with visceral traction in presence of blockade to T1.
Total sympathetic block
Unopposed vagus
Changes in vagal tone → profound changes in HR; may → transient asystole (p. 248)
Thermoregulation and Shivering
Hypothermia (a decrease in core temperature) is common in patients undergoing surgery with epidural anesthesia and is thought to result from heat loss to the cold environment due to sympathectomy-induced vasodilation. The normal process by which thermoregulation usually minimizes intraoperative core temperature is prevented, since epidural anesthesia directly inhibits vasoconstriction in the analgesic dermatomes. (p.253)
Central neuraxial anesthesia-induced sympathectomy leads to peripheral vasodilation, reduced preload, and subsequently decreased cardiac output. The incidence and extent of hypotension depends on the height of the block, the patient's position, and whether appropriate measures were instituted prophylactically to minimize hypotension.
Edition: 4 - 2008
Perioperative risks are low, but complications can be devastating
- Endoscopic thoracic sympathectomy (ETS) involves division of the thoracic sympathetic chain between T2 and T4.
- The main indication for ETS is the treatment of palmar hyperhidrosis.
- The most common method of anaesthesia for ETS uses intermittent positive pressure ventilation via a standard tracheal tube.
- Perioperative risks are low, but complications can be devastating.
- Postoperative compensatory sweating occurs in almost 50% of patients.
hypoxic pulmonary vasoconstriction may be impaired after Sympathectomy
Mean arterial blood pressure was decreased from 81.9+/-2.89 to 73.2+/-2.49 mmHg after thoracic sympathectomy and heart rate was decreased from 104.4+/-3.12 to 88.2+/-2.31beats/min. Arterial oxygen tension was decressed from 570.5+/-17.9 to 521.4+/-23.2mmHg after position change, and decreased to 271.1+/-28.1 mmHg under one-lung ventilation, and finally decreased to 217.0+/-18.3 mmHg after thoracic sympathectomy. With the above results, we can conclude that patients for TES should be carefully observed during and after the procedure, and hypoxic pulmonary vasoconstriction may be impaired after TES.
Korean J Anesthesiol. 1993 Aug;26(4):695-699.
profound decrease of arterial oxygen partial pressure during sympathectomy
Pulse oximetry and repeated blood gas measurements are needed during endoscopic transthoracic sympathectomy in order to detect and treat hypoxemic events, which may jeopardize the patient's life.
Journal of Cardiothoracic and Vascular Anesthesia
Volume 10, Issue 2, February 1996, Pages 207-209
Spinal cord infarction occurring during thoraco-lumbar sympathectomy
Spinal cord infarction, because of interference with an important radicular tributary, is a rare complication of thoraco-lumbar sympathectomy.In a brief survey of the literature we found only 12 previously recorded cases in which this complication
was presumed to have occurred.
J. Neurol. Neurosurg. Psychiat., 1963, 26, 418