Risks during Thoracic Sympathectomy - Surgery not as safe as reported

T(2)-T(3) ganglionectomy significantly decreases pulse rate and systolic blood pressure, reduces myocardial oxygen demand, increases left ventricular ejection fraction and prolongs Q-T interval. A certain loss of lung volume and decrease of pulmonary diffusion capacity for CO result from sympathectomy. Histomorphological muscle changes and neuro-histochemical and biochemical effects have also been observed.

http://www.ncbi.nlm.nih.gov/pubmed/14673672

 

a significant impairment of the heart rate to workload relationship was consistently observed following sympathectomy

Several reports also demonstrate significantly lower heart rate increases during exercise in subjects who have undergone bilateral ISS [9–12] compared to pre-surgical levels. In spite of this high occurrence, recent reviews on the usual collateral effects of thoracic sympathectomy still do not include these possible cardiac consequences [6].
The aim of the present prospective study was to confirm that a significant impairment of the heart rate to workload relationship was consistently observed following unilateral and/or bilateral surgery.
Eur J Cardiothorac Surg 2001;20:1095-1100
http://ejcts.ctsnetjourna...i/content/full/20/6/1095

 

disturbed peripheral vascular and heart rate responses after sympathectomy

Thoracic sympathectomy can result in reduced sweating and disturbed peripheral vascular and heart rate responses. Patients should be warned that these mechanisms may play a role in the development of exertional heat stroke.

Alan D.L. Sihoe, FRCSEd(CTh)^a,_*, Raymond W.T. Liu, MRCP^b, Alex K.L. Lee, MRCP^b, Chak-Wah Lam, FHKAM^b, Lik-Cheung Cheng, FRCS

 

Even epidural blockade limited only to the thoracic dermatomes is liable to cause complete sympathectomy, including cardiac sympathetic denervation. The ensuing vasodilation and bradycardia lead to hypotension, poor tolerance of mechanical interference with the heart, and inability to respond to acute changes in intravascular volume or body position. This symptom complex is especially troublesome to manage during intrathoracic operations when avoidance of hypervolemia is emphasized.

Thoracic sympathectomy has two other potenital consequences: effect on bronchomotor tone and effect on oxygenation.

During intrathoracic procedures using one-lung ventilation, a right-to-left intrapulmonary shunt is intentionally created (in the form of the nonventilated lung). The ensuing arterial oxygen tension (PaO2) is determined by a complex interaction involving cardiac output, mixed venous oxygen tension, the status of the ventilated lung, size of the shunt, and most significantly, hypoxic pulmonary vasoconstriction (HPV).
HPV diverts pulmonary blood flow away from the shunt by vavsoconstriction in the nonventilated lung, and is the principal adaptive defense mechanism against arterial hypoxemia during one-lung ventilation. The cellular mechanism and regulation of HPV, and the possible role of the autonomic nervous system are not completely understood.
The effect of thoracic sympathectomy of HPV is even less well understood. Since potent vasodilators such as nitroprusside antagonize HPV-induced vasoconstriction and lower the arterial oxygen tension, it is reasonable to assume that HPV will become less effective with thoracic sympathectomy.
Clinical studies have produced conflicting conclusions, most probably because direct measurement of HPV is not possible in human studies, and the surrogate endpoing examined PaO2 is determined not only by HPV, but also by a host of interacting factors, some of which may be affected by the sympathectomy and can not be held constant.

Risk Factor for Neuraxial Anesthesia-Associated Bradycardia:
Block height higher than T5
Younger age

Spinal and Epidural Anesthesia By Cynthia Wong

Publication Date: 2007-01-01 Publisher: MCGRAW-HILL EDUCATION - EUROPE Country of origin: UNITED STATES

After thoracoscopic sympathectomy for hyperhidrosis, very severe discomfort and hyperhidrosis in the neighboring non-sympathectomized regions occurred with alarming frequency and intensity. (p.879)

Alteration in Cerebral Blood Flow after sympathectomy

Jeng and associates observed an increase in cerebral blood flow after T2 sympathectomy, and they suggested the possibility of using such a surgical approach to improve cerebral blood flow in patients with cerebral vascular insufficiency.

Youmans Neurological Surgery, 5th Edition
Publisher: Saunders
Publication Date: 2003-10-10

Sympathetic nerves protect against blood-brain barrier disruption

 http://www.ncbi.nlm.nih.gov/pubmed/7064183?holding=ukpmc

Effect of adrenalectomy or sympathectomy on spinal cord blood flow

After sympathectomy, RSCBF (regional spinal cord blood flow) was unchanged during hypothermia. In the cauda equina, flow fell in all hypothermic rats. The hypothermia-associated increases in RSCBF were not related to changes in mean arterial blood pressure. We conclude that adrenalectomy near-totally ablates the hypothermia-associated increase in RSCBF measured in intact rats and that abdominal sympathectomy totally ablates it. This evidence complements morphological evidence for adrenergic innervation of the spinal cord vasculature.Am J Physiol. 1991 Mar;260(3 Pt 2):H827-31. 

Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy
http://www.ncbi.nlm.nih.gov/pubmed/5498231?holding=ukpmc

The angina-relieving effects of sympathetic blockade

In the 1930's it was recognised by neurosurgeons performing destructive sympathectomies for angina pectoris that local anaesthetic infiltration around the stellate ganglion often resulted in pain relief outlasting the duration of action of the local anaesthetic drug^13. This observation has been more recently confirmed¹⁴, and is currently (June 1999) the subject of a large scale randomised double-blind placebo-controlled trial funded by the British Heart Foundation.

The pathogenesis of angina and myocardial infarction pain involves the activation of the afferent sympathetic pathway. A frequent and important consequence of pain (especially when severe) is the `flight or fight' response through activation of sympathetic efferents. The clinical image of the patient with an acute myocardial infarction (cold, clammy, sweaty, anxious, tachycardic) is secondary to this adrenergic activation. Therefore, angina might be regarded as the sensory component of a positive feedback loop, which cannot under these circumstances be conceived as resulting in benefit, and which may be considered to be a maladaption.

The angina-relieving effects of sympathetic blockade might be due to interference with this maladaptive feedback loop, in a similar manner to the way in which adenosine interrupts a re-entrant tachycardia. If such a loop exists, it may partly explain chronic refractory angina and the fact that temporary interruption of this pathway has a prolonged effect on pain¹⁴. Beneficial amelioration of angina can be achieved with repeated blocks¹⁴. There does not appear to be any predictability in the length of time a patient remains pain-free after successive blocks.

http://www.angina.org/source/pro/symp_block.htm

pain states associated with the loss of sympathetic fibres

Postsympathectomy limb pain, postsympathectomy parotid pain, and Raeder's paratrigeminal syndrome are pain states associated with the loss of sympathetic fibres and in particular with postganglionic sympathetic lesions. There is a characteristic interval of about 10 days between surgical sympathectomy and onset of pain. It is proposed that this pain in man is correlated with the delayed rise in sensory neuropeptides seen in rodents after sympathectomy. These chemical changes probably reflect the sprouting of sensory fibres and may result from the greater availability of nerve growth factor after sympathectomy. The balance between the sensory and sympathetic innervations of a
peripheral organ may be determined by competition for a limited supply of nerve growth factor.
Lancet. 1985 Nov 23;2(8465):1158-60. 

Behavioral changes after sympathectomy

Six experiments are reported on the effects of 2,4,5-trihydroxyphenylethyl-amine (6-hydroxydopamine) on two-way escape and avoidance learning. Rats were tested on either escape or avoidance learning at 80 days of age after chemical sympathectomy at birth or 40 or 80 days of age. Neonatal and chronic sympathectomy (at 40 days), but not acute sympathectomy (at 80 days), resulted in depressed escape learning. Avoidance learning was affected by neonatal sympathectomy and partially by acute sympathectomy. The results have implications for the role of the autonomic nervous system in escape-avoidance learning.
J Comp Physiol Psychol 1976; 90:303-16.

normal forearm vasodilator response to mental stress was absent months or years after surgical sympathectomy

Additional indirect evidence on this topic in humans comes from a study conducted in the 1950s (3). In this study, the normal forearm vasodilator response to mental stress was absent months or years after surgical sympathectomy.
J Appl PhysiolVol. 92, Issue 5, 2019-2025, May 2002

Haematological changes during stress abolished by sympathectomy

To study haematological effects of emotional stress, blood samples were obtained from 29 healthy, normotensive, non-smoking males aged 20–34 years before, during and after 10 min of mental arithmetic. There were significant increases in pheripheral blood cell count, haemoglobin concentration, and haematocrit in response to mental stress. Parallel to these changes significant increases in heart rate, and systolic and diastolic blood pressure were observed. The relative increments of leucocyte (8%) and platelet (3·5%) count were significantly higher than the increase in haemoglobin concentration (2%). There was a significant positive correlation between the blood pressure increase and the mobilization of leucocytes, whereas the increase in erythrocyte count, haemoglobin concentration, and haematocrit showed significant positive correlations with heart rate reactivity. It is concluded that mental stress causes an increase in leucocyte and platelet count that could not solely be accounted for by the concurrent haemoconcentration.

The emotional leucocytosis observed in dogs has been claimed to be neurogenic in origin, since sympathectomy abolished the rise in leucocyte count (Garrey & Bryan, 19 3 5).
http://www3.interscience.wiley.com/journal/120731423/abstract 

sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise

it has been shown that thoracic sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise [6]. Although absolute tachycardia is not eliminated, given the endocrine and paracrine stimuli during exercise, the maximum heart rate reached during exercise has been shown to be significantly reduced after sympathectomy. Thus for a given workload during exercise, there will be a relative bradycardia. This may possibly affect the circulatory system’s ability to convey heat from the body core to the extremities for heat loss.
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025 

thoracic sympathectomy has been demonstrated to abolish or alter sympathetic vasoconstrictive responses in the skin, and this may contribute to abnormal peripheral vascular responses to temperature [4]. Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy [5]. It is not impossible that such atypical peripheral vascular responses to rising body temperature may have contributed to impaired heat loss during exercise or to an inappropriate response to shock on the development of the heat stroke.
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025 

the abolition of sweating from the upper body as well as the axillae and both upper limbs may have significantly reduced the capacity of the patient to lose heat through sweating during exercise. Anhidrosis in the head and neck after sympathectomy affects a proportion of patients, but is often neglected in most reports of post-sympathectomy complications [3]. The loss of head and neck sweating in this patient may have further impaired overall heat loss. However we would also note that the degree of heat loss impairment after sympathectomy has never been quantified, and its effect on body temperature during exercise remains to be established.
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

"Although thoracic sympathectomy is commonly used to reduce upper limb sweating, it may also lead to facial anhidrosis and disturbed cardiovascular responses to temperature. The resultant effect on overall body heat loss has not been documented. We present a case of a young patient with previous thoracic sympathectomy who suffered severe heat stroke after heavy exercise.

An already impaired cardiovascular system is recognized to be a significant risk factor for development of heat stroke. In the post-sympathectomy patient, the abnormal sympathetic skin response may lead to peripheral vascular failure or the reduced cardiac chronotropic response may impair the body’s capacity to compensate for shock. These may have contributed to the rapid development of shock and severe multiple organ dysfunction syndrome in this patient.
He had multiple organ dysfunction syndrome develop, with severe renal and hepatic failure, grade II hepatic encephalopathy, and disseminated intravascular coagulation. He responded remarkably well to aggressive supportive measures including forced alkaline diuresis, and he was eventually discharged home after 1 month. The patient was previously a healthy, physically fit, nonsmoker. He worked as a body building trainer and led an active, sporty lifestyle. The only significant medical history was that he had received thoracic sympathectomy for axillary hyperhidrosis 4 years ago at another hospital.

http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

Glycogen accumulation in Reissner's membrane following chemical sympathectomy

Acta Otolaryngol. 1978 Nov-Dec;86(5-6):314-30.
PMID: 213930 [PubMed - indexed for MEDLINE]

Role of the ANS in cerebral circulation

It is proposed that the autonomic innervation of brain vessels participates in the control not only of the cerebral circulation but also of associated intracranial pressure phenomena.
Blood Vessels 1974;11:2-31

Sympathectomy alters cranial nerves and cerebral blood flow

Moya-Moya Syndrome

Moya Moya syndrome is a vasculopathy of the cranial arteries, usually the carotids, leading to progressive intracranial occlusion with distal collateral vessels. This is a very frequent cause of pediatric stroke in India(10,11). Children usually present with an acute focal deficit such as hemiplegia, whereas in later years sub-arachnoid hemorrhage is a common presenta-tion. Due to bilateral carotid involvement sometimes alternating hemiplegia is seen. The outcome varies widely without treatment. Moya Moya disease is usually idiopathic, although same radiographic pattern is seen in some patients with sickle cell disease, neuro-fibromatosis, postcranial irradiation and in various other conditions(15). There is no proven treatment of Moya Moya disease. Medical management involves use of aspirin but needs further testing. Surgical treatment involves cervical sympathectomy, intracranial graft of omentum or temporalis muscle and bypass of superficial temporal artery to the middle cerebral artery(34).

http://indianpediatrics.net/feb2000/personal.htm

sympathectomy greatly reduces ventilation

In conscious animals, cervical sympathectomy greatly reduces ventilation in normoxia and slightly affects ventilatory responses to hypoxia and hypercapnia, also suggesting an important role for these nerves in the control of breathing.
Eur Respir J 1998; 12: 177–184

reduces the amount of adrenaline

Cervical sympathectomy
A form of surgery that is useful for some people with LQTS. It reduces the amount of adrenaline and its by-products produced and delivered to the heart by certain nerves (the left cervical ganglia). It involves operating on the left neck and removing or blocking these nerves

http://www.sads.org.uk/technical_terms.htm

sympathectomy totally ablates regional spinal cord blood flow

We conclude that adrenalectomy near-totally ablates the hypothermia-associated increase in RSCBF measured in intact rats and that abdominal sympathectomy totally ablates it. This evidence complements morphological evidence for adrenergic innervation of the spinal cord vasculature.

http://ajpheart.physiology.org/cgi/content/abstract/260/3/H827

Transverse myelitis

Transverse myelitis is a neurological disorder caused by an inflammatory process of the grey and white matter of the spinal cord, and can cause axonal demyelination.
In some cases, the disease is presumed to be caused by viral infections or vaccinations and has also been associated with spinal cord injuries, immune reactions, schistosomiasis and insufficient blood flow through spinal cord vessels. Acute myelitis accounts for 4 to 5 percent of all cases of neuroborreliosis.^[1] Symptoms include weakness and numbness of the limbs as well as motor, sensory, and sphincter deficits. Severe backpain may occur in some patients at the onset of the disease.

http://en.wikipedia.org/wiki/Transverse_myelitis

One patient with documented transection of the cord above T5 behaved like subjects after surgical sympathectomy 

 

Increase in blood flow is generally followed by a rise in skin temperature but decrease in blood flow in response to the Gibbon-Landis procedure after sympathectomy is not necessarily accompanied by a fall in surface temperature. This poor correlation between skin temperature and blood flow confirms the previous report of Hoobler and co-workers and helps define the limits of usefulness of measurements
of skin temperature as an index of blood flow to the extremity.

The vasomotor responses to the Gibbon-Landis procedure (reflex response to warming) were studied in hemiplegic patients, subjects with "high transection" of the cord, and in sympathectomized patients.

One patient with documented transection of the cord above T5 behaved like subjects after surgical sympathectomy.
Of 11 sympathectomized limbs tested for vasodilatation in response to the Gibbon-Landis procedure, 4
showed no response, while 7 responded with decrease in blood flow (vasoconstriction).

Vasomotor Responses in the Extremities of Subjects with Various Neurologic Lesions
I. Reflex Responses to Warming
By WALTER REDISCH, M.D., FRANCISCO T. TANGCO, M.D., LOTHAR WERTHEIMER, M.D.,
ARTHUR J. LEWIS, M.D., J. MURRAY STEELE, M.D.
1957;15;518-524 Circulation

inhibition of sympathetic activity and a possible impairment of endothelial function

Alterations in skin microcirculation induced by brachial plexus block can be evaluated by wavelet transform of the laser Doppler flowmetry signal. Brachial plexus block reduces the oscillatory components within the 0.0095- to 0.021- and 0.021- to 0.052-Hz intervals of the perfusion signal. These alterations are related to inhibition of sympathetic activity and a possible impairment of endothelial function.

Anesthesiology:

September 2006 - Volume 105 - Issue 3 - pp 478-484

Clinical Investigations

Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and often leads to atherosclerosis.
http://en.wikipedia.org/wiki/Endothelium

'Emotional' sweating regulated by neocortex and limbic cortex

Careful observations showed that the forearm sweating responded diversely to various mental stimuli, unlike the palmar sweating whose response was always an increase. Mental arithmetic, mental testing and physical exercise caused an immediate increase in the palmar sweating but often elicited a transient decrease in the forearm sweating, whereas pain, noise, and emotional stimuli consistently provoked an increase of sweating on the forearm as well as on the palm. These observations suggest that the activities of higher centers, presumably involving neocortex and limbic cortex, exert various influences on the central mechanisms of palmar and generalized sweating.
Jpn J Physiol. 1975;25(4):525-36.
http://www.ncbi.nlm.nih.gov/pubmed/1206808 

90% may experience Gustatory sweating after surgery for Hyperhidrosis

Some individuals (up to 90%) may experience another type of sweating that is increased while eating or smelling certain foods (gustatory sweating) (Hornberger).Source: Medical Disability Advisor

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