Patients with sympathectomy are not suitable controls for sleep study. Why?

Exclusions:
Patients with permanent pacemaker, non-sinus cardiac arrhythmias, peripheral vasculopathy or neuropathy, severe lung disease, status postbilateral cervical or thoracic sympathectomy, finger deformity that precludes adequate sensor application, using a-adrenergic receptor blockers, or alcohol or drug abuse during the last 3 years.

Evaluation of a Portable Device Based on Peripheral Arterial Tone for Unattended Home Sleep Studies

 The clinic sleep laboratory of the Technion Sleep Medicine Centre, Israel
http://chestjournal.chestpubs.org/content/123/3/695.long
CHEST March 2003 vol. 123 no. 3 695-703

MSAC Application no 1130, Assessment Report

The amount of compensatory sweating depends the amount of cell body reorganization in the spinal cord after surgery

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

ETS considered psychiatric surgery - says Dr Nagy

"ETS (sympathectomy)  can alter many bodily functions, including sweating , heart rate , heart stroke volume , blood pressure , thyroid , baroreflex , lung volume , pupil dilation, skin temperature, goose bumps and other aspects of the autonomic nervous system . It can diminish the body's physical reaction to exercise and/or strong emotion, and thus is considered psychiatric surgery. In rare cases sexual function or digestion may be modified as well. "
http://www.lvhyperhidrosis.com/treatment.html

Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block

The cardiovascular responses to epidural anaesthesia are almost entirely due to the fact that the local anaesthetic injected into the epidural space not only blocks somatic, sensory and motor fibres, but also produces preganglionic sympathetic denervation.

Postganglionic sympathetic nerves play an important role in controlling cardiac function and vascular tone. The most important of the cardiovascular effects are related to blockade of vasoconstrictor fibres (below T4) with resulting dilatation of resistance and capacitance vessels and/or cardiac sympathetic fibres with loss of chronotropic and inotropic drive to the myocardium (T1-5) (Figure 1).

The cardiac sympathetic outflow emerges from C5 to T5 levels, with the main supply to the ventricles from T1 to T43. A significant part of the chronotropic and inotropic control of the heart is mediated through the upper four thoracic spinal segments.
Denervation of preganglionic cardiac accelerator fibres leaving the cord at T1-T5 results in minimal vasodilatory consequences. Changes however in heart rate, left ventricular function and myocardial oxygen demand may occur due to high thoracic epidural blockade and are discussed below.

The major determinant of heart rate is the balance between sympathetic and parasympathetic systems with the latter predominating. A high thoracic epidural anaesthesia (TEA) covering the cardiac segments (T1-T4) produces small but significant reductions in heart rate4-8. During cardiac sympathetic denervation, parasympathetic cardiovascular responses, including those involved in baroreflexes, may dominate.


It was suggested that the sympathetic control of heart rate modified the dominating parasympathetic tone, rather than functioning as an active cardiac accelerator. In this study there was no compensation for changes in preload;
therefore cardiopulmonary baroreceptors affected by changes in central volume secondary to peripheral vasodilatation or vasoconstriction might have altered arterial baroreceptor heart rate reflex as well.



High TEA added to general anaesthesia significantly decreased the cardiac acceleration in response to decreasing blood pressure, suggesting that baroreflex-mediated heart rate response to a decrease in arterial blood pressure depends on the integrity of the sympathetic nervous system. However general anaesthesia, in addition to high levels of epidural anaesthesia, may have modified the balance between sympathetic and parasympathetic tone as well.
By applying power spectral analysis, i.e., frequency analysis of electrocardiographic R-R interval, the individual components of the autonomic nervous system can be discerned and can be used as a sensitive indicator of sympathovagal interaction.


Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block.
Anaesth Intensive Care 2000; 28: 620-635
B. T. VEERING*, M. J. COUSINS†
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands and Department of Anaesthesia and
Pain Management, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales

diabetic autonomic neuropathy has already sympathectomized the patient

Although not specific, the symptoms suffered by diabetics from sweating disturbances are fairly typical [5]. Initially there is heat intolerance accompanied by hyperhidrosis of the upper half of the body, particularly affecting the face, neck, axillae and hands. It is of interest that these patients rarely perspire excessively below the umbilicus. This diabetic syndrome has been attributed to a lesion of the sympathetic nerve fibres which control sweat secretion [11] and follow the course of the peripheral nerves [12]. This affects the efferent branch of the reflex arch and is identical to that occurring distal to a surgical sympathectomy [13].

There was no difference found between the histological changes in the nerves of the spontaneous anhidrotic patients
(Fig. 1) and those of the two previously sympathectomized patients.

A number of papers have been published which stressed [22-24] the high failure rate of sympathectomy operations in diabetics. We believe that the failure of the operation is due to the fact that diabetic autonomic neuropathy has already sympathectomized the patient. The results of the present study are compatible with this idea.
http://www.springerlink.com/content/v21h52461037653k/

Production of neurogenic electrocardiographic changes by unilateral alteration of sympathetic tone

Circ Res 1966;18:416-428. 51.

sympathectomy will block the chronotropic response

Around 50% of patients have bradycardia in the following minutes of a bilateral surgery with mean and diastolic blood pressure significant reduction. Since the sympathectomy will block the chronotropic response, a significant increase of the ejection volume is observed when the patient moves in the erect position from dorsal decubitus [6]. Two cardiovascular complications were reported in the literature. First, an asystolic cardiac arrest in an 18-year-old woman during the second side (left) of bilateral sympathectomy for severe hyperhidrosis, requiring resuscitation maneuvers, with no chronic sequelae [7]. The second case was reported in a 23-year-old woman in whom a bilateral T₂ sympathectomy was performed for facial hyperhidrosis. Two years later, following electrophysiologic studies confirming unopposed vagotonic stimulation, she underwent permanent pacemaker insertion for symptomatic bradycardia [8].
http://icvts.ctsnetjournals.org/cgi/content/full/8/2/238

HAZARDS ASSOCIATED WITH CERVICO-THORACIC SYMPATHECTOMY

The need for a realistic appraisal of the potentialities for harm in Cervico-Thoracic sympathectomy is apparent on anatomic grounds alone (Orkin et al. ] 950). Fatalities occur from time to time, but only a few reports of such fatalities find their way into the literature (Adriani et al. 1952). Reported complications associated with Ccrvico-Thoracic sympathectomy, which is, in effect a permanent Stellate
Ganglion block (Moore 1954), include pneumothorax, Horner's syndrome, phrenic and recurrent laryngeal nerve damage, infection from oesophageal puncture, cardiac arrhythmias (Tochinai 1974), and very infrequently cardiac arrest (Moore 1954).
The following is a case report of a healthy 18-year-old woman who had bilateral Cervico-Thoracic sympathectomy done in two stages for severe hyperhidrosis in the palms of her hands.
Two episodes of asystolic arrest occurred during the 2nd stage left Cervico-Thoracic sympathectomy.
The cause of hyperhidrosis apparently originates from some poorly understood stimulation of the sympathetic nervous system (Cloward 1969), and in sensitive patients this may possibly lead to excessive vagal stimulation to counteract it,
as illustrated by the bradycardia and asystolic reaction to the sudden removal of the sympathetic control, and by the high doses of sympathomimetic drugs necessary to recommence cardiac activity. Anatomically the heart is innervated by the cardiac plexus which consists of the cardiac nerves derived from the cervical and upper thoracic ganglia of the
sympathetic trunk and branches of the vagus. The pacemaker of the heart, the sino-atrial node, is innervated by both the parasympathetic and sympathetic nerves (King and Coakley 1958). The ventricular muscle of the heart is
supplied solely by the sympathetic nerves, and the larger branches of the coronary arteries are also predominantly innervated by sympathetics (Woollard 1926). These factors may also have a bearing on the hazard of a bilateral cervico-thoracic sympathectomy, which leaves the heart solely under vagal control. Usually, following
denervation, the heart will initiate its own impulse, without recourse to external agencies, but there may be a place for transvenous electrode cardiac pacing, if spontaneous initiation of impulse is delayed, or bradycardia is severe.
Anaesthesia and Intensive Care, Vol. V, No. 1, February, 1977

R. F. Y. ZEE
Royal Perth Hospital, Perth

abnormalities of the autonomic nervous system are correlated with death risk

Michael Lauer: It's been known for a long time that abnormalities of the autonomic nervous system are correlated with death risk, but the problem is that the way in which these abnormalities are measured are very difficult. They require sophisticated equipment and they require the kind of tests which simply have not entered the realm of normal clinical practice. What we find is that these very, very simple measures that are obtained as part of regular routine exercise testing deflect what happens to the autonomic nervous system and provides us with just as powerful predictors of risk of death.
(Dr Michael Lauer, cardiologist, Cleveland Clinic in Cleveland, Ohio)
http://www.abc.net.au/rn/talks/8.30/helthrpt/stories/s63595.htm