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Disabling orthostatic hypotension caused by sympathectomies performed for hyperhidrosis: Difference between revisions
Disabling orthostatic hypotension caused by sympathectomies performed for hyperhidrosis (view source)
Revision as of 17:23, 6 July 2014
, 6 July 2014no edit summary
(Created page with "''J.J. van Lieshout, W. Wieling''<br /> ''Department of Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam (The Netherlands)''<br /><br /> {{case_present...") |
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B = celiac and superior mesenteric ganglia | B = celiac and superior mesenteric ganglia | ||
C = lower abdominal sympathetic ganglia]] | C = lower abdominal sympathetic ganglia]] | ||
On physical examination at the dorsal thoracic and lumbar regions small scars of the surgical procedures were visible. Neurological examination showed no abnormalities. | |||
Supine blood pressure was normal. Upon standing, systolic and diastolic blood pressures dropped markedly (Fig. 2) and dizziness ensued. Heart rate increased from 50 to 85 beats/min in 15 s and to 100 beats/min after 35 s. In spite of the progressive fall in blood pressure heart rate did not increase further but slightly decreased to 95 beats/min after 2 min of standing. | |||
[[File:OrthostaticHypotension_Fig2.jpg | thumb | 400px | Fig. 2 Blood pressure and heart rate responses upon standing. A progressive blood pressure drop is accompanied by an instantaneous heart rate increment indicating sympathetic vasomotor lesions and intact vagal heart rate control. ]] | |||
Supine values of plasma noradrenaline and adrenaline were abnormally low and there was virtually no increase upon standing. | |||
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== Editor's comments == | |||
Hyperhidrosis is a pathological condition of excessive sweating of unknown origin. In patients with hyperhidrosis various non-surgical therapies have been considered. Although anticholinergic drugs seem to be effective, their use has been limited because of side effects [2]. Therefore, in selected cases of hyperhidrosis, destruction of the sympathetic ganglia by thoracoscopic sympathectomy is held as the reference treatment for severe palmar hyperhidrosisis [3]. | |||
Notwithstanding thoraco-lumbar sympathectomies cardiovascular control remained sufficient even to meet the needs of prolonged and intermittently vigorous exercise of competitive field hockey. However, after the final surgical procedure that resulted in an almost complete sympathetic denervation of the splanchnic area (Fig 1), symptoms of postural hypotension became manifest. The critical importance of the splanchnic area for the control of blood pressure is well known [4-10]; sympathectomies have little influence on postural blood pressure control until the major part of the sympathetic outflow to the splanchnic area is destroyed [5-7]. | |||
Sympathetic nerve supply to the heart is derived from the segments Th I - Th IV (V), synapsing in all cervical and the upper four (five) thoracic ganglia [2]. In view of the pattern of sympathectomies carried out, therefore, sympathetic innervation of the heart was expected to be at least partially intact (Fig 1) and functional integrity was present upon testing. An abnormally large increase in heart rate (45 bpm) was observed. Thus this patient is a rare example of a hypoadrenergic orthostatic response with intact heart rate control (Fig. 2). The opposite pattern i.e. intact vasomotor control and complete cardiac denervation is observed in patients with a cardiac transplant. In these patients orthostatic blood pressure control is normal despite no increase in heart rate. Figure 3 shows an example of the heart rate and blood pressure response upon active standing and passive head-up tilting in a 38-year-old fit patient with a cardiac transplant. | |||
[[File:OrthostaticHypotension_Fig3.jpg | thumb | 400px | Figure 3. Finger blood pressure and heart rate responses upn active standing and passive head-up tilting in a 38-year old male with a cardiac transplant. Note marked difference in blood pressure adjustment in the first 15 s.]] | |||
Patients with circumscribed anatomical lesions on the arterial baroreflex arc provide unique opportunity to study cardiovascular control in otherwise intact humans. Figure 4 provides a schematic drawing of the baroreceptor afferent and autonomic efferent pathways of the baroreflex arc with possible mechanisms of failure of cardiovascular resulting in a tendency to orthostatic hypotension and syncope. | |||
[[File:OrthostaticHypotension_Fig4.jpg | thumb | 400px | Figure 4. Schematic drawing of the arterial baroreceptor afferents and the efferent autonomic pathways. VMC indicates vasomotor centra. Mechanism that can cause failurte in the baroreflex arc are indicated: 1) lesion in the sinus caroticus/aortic baroreceptors, 2) lesion in the sinus caroticus/aortic afferents, 3) lesion in the medulla, 4) spinal cord lesion, 5) preganglionic/ganglionic lesion, 6) postganglionic lesion ]] | |||
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