a technique that is associated with a number of potential problems

Transthoracic endoscopic sympathectomy is now considered the treatment of choice for patients with upper limb hyperhidrosis requiring sympathetic ablation. This procedure requires the use of an endobronchial double lumen tube and subsequent one-lung anaesthesia, a technique that is associated with a number of potential problems. Full patient monitoring is thus required and includes pulse, ECG, non-invasive blood pressure measurement, pulse oximetry, end-tidal carbon dioxide concentration and peak inspiratory airway pressure.

Anaesthetic implications for transthoracic endoscopic sympathectomy.

PMID: 7524779 [PubMed - indexed for MEDLINE] Eur J Surg Suppl. 1994;(572):33-6.

Hypoxaemia is of a major concern during thorascopic sympathectomy

However the pathophysiology of hypoxaemia and consequent decrease in SpO2 differs between the two anaesthetic techniques.

The normal physiological response to massive atelectasis is an increase in pulmonary vascualr resistance (hypoxic pulmonary vasoconstriction) with re-routing of blood to well ventilated lung zones and consequent improvement of in PaO2. However, during endobronchial anaesthesia for thoracic sympathectomy there is an apparent failure of this compensatory mechanism. When more than 70% of the lung is atelectatic, compensation by hypoxic pulmonary vasonstriction appears to be ineffective. Furthermore, in in vitro and animal studies, inhalation anaesthetic agent have been shown to depress hypoxic pulmonary vasoconstriction.

In a study by Hartrey and colleagues, SpO2<95%>20 mm Hg in 21% of patients. Similarly, we have reported sudden hypotension and bradycardia after injudicious carbon dioxide insufflation.

In an interesting study of the delayed cardiac effects of T2-4 sympathectomy, Drott and colleagues demmonstrated significantly reduced heart rate at rest, and during both exercise and the recovery phase of the exercise.
Changes in the electrical axis and shortening of the QT interval have also been reported.
B. Fredman, D. Olsfanger, R. Jedeikin
British Journal of Anaesthesia 1997; 79: 113-119

Loss of coordinated autonomic responses to demands on heart rate and vascular tone

Autonomic dysreflexia - Spinal cord injuries (SCI) above T6 may be complicated by a phenomenon known as autonomic dysreflexia, a manifestation of the loss of coordinated autonomic responses to demands on heart rate and vascular tone [5,6]. Uninhibited or exaggerated sympathetic responses to noxious stimuli lead to diffuse vasoconstriction and hypertension. A compensatory parasympathetic response produces bradycardia and vasodilation above the level of the lesion, but this is not sufficient to reduce elevated blood pressure. SCI lesions lower than T6 do not produce this complication, because intact splanchnic innervation allows for compensatory dilatation of the splanchnic vascular bed.

The estimated frequency of this complication is quite variable, ranging from 20 to 70 percent of patients with SCI lesions above T6 [5,6]. Autonomic dysreflexia is unusual within the first month of SCI but usually appears within the first year [7,8].

Common clinical manifestations are headache, diaphoresis, and increased blood pressure [7]. Flushing, piloerection, blurred vision, nasal obstruction, anxiety, and nausea may also occur. Bradycardia is common; however, some patients have tachycardia instead. The severity of attacks ranges from asymptomatic hypertension to hypertensive crisis complicated by profound bradycardia and cardiac arrest or intracranial hemorrhage and seizures. The severity of the SCI influences both the frequency and severity of attacks.

CAD mortality also appears to be higher among SCI patients [4]. One contributing factor may be that SCI lesions above the T5 level may lead to atypical presentations for cardiac ischemia; manifestations may include autonomic dysreflexia or changes in spasticity rather than typical chest pain.

The autonomic nervous system dysfunction that results from SCI disrupts normal cardiovascular hemostasis. With SCI above the T6 level, baseline blood pressure is usually reduced, and baseline heart rate may be as low as 50 to 60 beats per minute [12,16]. This is generally not a clinical problem, but may contribute to hemodynamic instability and exercise intolerance.

Acute cervical SCI is associated with a risk of cardiac arrhythmia due to excess vagal tone, as well as complicating hypoxia, hypotension, and fluid and electrolyte imbalances.

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