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
Monday, October 10, 2011
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
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
Subscribe to:
Posts (Atom)