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
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
