Patients may develop bradycardia after surgical procedure

Upper-Thoracic Sympathectomy; 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

Sympathetic denervation for 6 weeks resulted in increased choroidal thickness, vascular luminal area, numbers of large venules and large arterioles, and capillaries in the outer nuclear layer. Capsaicin pretreatment prevented sympathectomy-induced increases in choroidal thickness, vascular luminal area and large venules and large arterioles, whereas pterygopalatine ganglionectomy was without effect."
Biotech Week. Atlanta: Jan 21, 2004. pg. 396

83% of patients reported severe 'compensatory sweating'

Fully 83% of patients who underwent T2 sympathectomy reported severe compensatory sweating one year after surgery and the majority of those reported they regretted the decision to have the surgery.
Heather Ennis. Medical Post. Toronto: Feb 15, 2005. Vol. 41, Iss. 7; pg. 17, 2 pgs

sympathectomy increased the bacterial tissue burden

sympathectomy increased the bacterial tissue burden, which was caused by a reduction in corticosterone tonus, and decreased both interleukin-4 secretion from peritoneal cells and the influx of lymphocytes into the peritoneal cavity. In both models, the peritoneal wall was the critical border for systemic infection. These results show the dual role of the sympathetic nervous system in sepsis. It can be favorable or unfavorable, depending on the innate immune effector mechanisms necessary to overcome infection.
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

Following removal of the superior cervical ganglion (SCG), large molecular weight (MW) NGF species, including proNGF-A, were increased in distal intracranial SCG targets, such as pineal gland and extracerebral blood vessels (bv).

Brain Research; Research from Miami University provides new data about brain research

Science Letter. Atlanta: May 15, 2007. pg. 1746

Neuronal Source of Plasma Dopamine

Determinants of plasma norepinephrine (NE) and epinephrine concentrations are well known; those of the third endogenous catecholamine, dopamine (DA), remain poorly understood. We tested in humans whether DA enters the plasma after corelease with NE during exocytosis from sympathetic noradrenergic nerves. We reviewed plasma catecholamine data from patients referred for autonomic testing and control subjects under the following experimental conditions: during supine rest and in response to orthostasis; intravenous yohimbine (YOH), isoproterenol (ISO), or glucagon (GLU), which augment exocytotic release of NE from sympathetic nerves; intravenous trimethaphan (TRI) or pentolinium (PEN), which decrease exocytotic NE release; or intravenous tyramine (TYR), which releases NE by nonexocytotic means. We included groups of patients with pure autonomic failure (PAF), bilateral thoracic sympathectomies (SNS-x), or multiple system atrophy (MSA), since PAF and SNS-x are associated with noradrenergic denervation and MSA is not. Orthostasis, YOH, ISO, and TYR increased and TRI/PEN decreased plasma DA concentrations. Individual values for changes in plasma DA concentrations correlated positively with changes in NE in response to orthostasis (r = 0.72, P < 0.0001), YOH (r = 0.75, P < 0.0001), ISO (r = 0.71, P < 0.0001), GLU (r = 0.47, P = 0.01), and TYR (r = 0.67, P < 0.0001). PAF and SNS-x patients had low plasma DA concentrations. We estimated that DA constitutes 2%-4% of the catecholamine released by exocytosis from sympathetic nerves and that 50%-90% of plasma DA has a sympathoneural source. Plasma DA is derived substantially from sympathetic noradrenergic nerves.
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

Cardiac sympathetic innervation was visualized by means of a glyoxylic catecholaminergic histofluorescence method. Transient outward current (I-to) of ventricular myocytes was recorded with the whole-cell configuration of the patch clamp technique. We observed that sympathectomy (i) decreased cardiac sympathetic nerve density and norepinephrine level, (ii) reduced the protein expression of Kv4.2, Kv1.4, and Kv channel-interacting protein 2 (KChIP2), (iii) decreased current densities and delayed activation of I-to channels, (iv) reduced the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and cAMP response element-binding protein (CREB), and (v) increased the severity of ventricular fibrillation induced by rapid pacing.
Heart Disease Weekly. Atlanta: Dec 28, 2008. pg. 54

Pain following endoscopic sympathectomy

The mean postoperative follow-up period was 11.5 months (range, 3-25 months). The hands of all patients were warm and dry after operation. No conversion to open surgery was necessary, and no operative mortality was recorded in either group. The mean inpatient pain scores were significantly higher in the biportal group (1.2 +/- 0.6) than that in the uniportal group (0.89 +/- 0.5, P=0.025). For the first three weeks after operation, four out of 20 (20%) patients in the uniportal group constantly suffered from mild or moderate residual pain while eight out of 25 (32%) cases in the biportal group (P=0.366). Among them, two cases in the uniportal group and five cases in the biportal group need to take analgesics.
Medical Devices & Surgical Technology Week. Atlanta: Sep 6, 2009. pg. 203

Laparoscopic surgery is associated with an increased incidence of postoperative atelectasis

Atelectasis occurs regularly after induction of general anesthesia, persists postoperatively, and may contribute to significant postoperative morbidity and additional health care costs. Laparoscopic surgery has been reported to be 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 procedures^{6 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

Surgical Upper Thoracic Sympathectomy Reduces Arterial Oxygenation During One-Lung Ventilation

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Journal of Cardiothoracic and Vascular Anesthesia
Volume 19, Issue 5, October 2005, Pages 703-704

PATHOPHYSIOLOGY OF ONE-LUNG VENTILATION

In estimating the degree of shunt that is created by one-lung ventilation when it is performed in the lateral decubitus position, on average, 40% of cardiac output perfuses the nondependent lung and the remaining 60% perfuses the dependent lung (Fig. 1).¹⁵ Mechanisms that tend to decrease the percent of cardiac output perfusing the nondependent, nonventilated lung are passive (e.g., mechanical-like gravity, surgical manipulation, amount of pre-existing lung disease) or active (e.g., hypoxic pulmonary vasoconstriction).¹⁵ The normal response of the pulmonary vasculature to atelectasis is an increase in pulmonary vascular resistance (in the atelectatic lung), and the increase in atelectatic lung resistance is almost entirely caused by hypoxic pulmonary vasoconstriction. Hypoxic pulmonary vasoconstriction is a protective reflex mechanism that diverts blood flow away from the atelectatic lung. With an intact hypoxic pulmonary vasoconstriction response, the transpulmonary shunt through the nondependent lung decreases to approximately 23% of the cardiac output (see Fig. 1).
Anesthesiology Clinics of North America
Volume 19, Issue 3, 1 September 2001, Pages 435-453

sympathectomy will blunt the normal tachycardic response to hypovolemia.

Spinal or epidural analgesia may cause a sympathectomy that will blunt the normal tachycardic response to hypovolemia.
OBSTETRIC ANAESTHESIA OUR WAY
Royal Women's Hospital Melbourne
Author: Dr Philip Popham