Ann Thorac Surg 2007;84:1025-1027
© 2007 The Society of Thoracic Surgeons
Case Reports
Is Previous Thoracic Sympathectomy a Risk Factor for Exertional Heat Stroke?
Alan D.L. Sihoe, FRCSEd(CTh)a,*,
Raymond W.T. Liu, MRCPb,
Alex K.L. Lee, MRCPb,
Chak-Wah Lam, FHKAMb,
Lik-Cheung Cheng, FRCSa
a Division of Cardiothoracic Surgery, Department of Surgery, The University of Hong Kong, Grantham Hospital, Hong Kong SAR, China
b Department of Medicine, Ruttonjee Hospital, Hong Kong SAR, China
Accepted for publication April 17, 2007.
* Address correspondence to Dr Sihoe, Division of Cardiothoracic Surgery, Department of Surgery, The University of Hong Kong, Grantham Hospital, Aberdeen, Hong Kong SAR, China (Email: adls1{at}excite.com).
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Abstract
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We report the case of a physically fit young man who presented with severe, life-threatening heat stroke after running a 10 km road race. He had previously received bilateral thoracic sympathectomy for axillary hyperhidrosis at another hospital, and was known to have upper body and limb anhidrosis. Thoracic sympathectomy can result in reduced sweating and disturbed peripheral vascular and heart rate responses. Patients should be warned that these mechanisms may play a role in the development of exertional heat stroke.
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Introduction
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Although thoracic sympathectomy is commonly used to reduce upper limb sweating, it may also lead to facial anhidrosis and disturbed cardiovascular responses to temperature. The resultant effect on overall body heat loss has not been documented. We present a case of a young patient with previous thoracic sympathectomy who suffered severe heat stroke after heavy exercise.
A 28-year-old man presented with heat stroke and syncope after running a 10 km road race. The temperature on the day of the race was between 21°C and 26°C, and the relative humidity was between 75% and 95%. On arrival his body temperature was 41.8°C and his Glasgow coma score was E4V2M4. He was in shock with a systolic blood pressure of 55 mm Hg, requiring aggressive fluid resuscitation. A computed tomographic scan of the brain showed no intracranial pathology, and initial blood tests revealed no significant biochemical or hematologic abnormality. However, the pyrexia persisted for 10 hours despite passive cooling measures, during which time his creatine phosphokinase level rose sharply to > 20,000 IU/L and his creatinine level rose to 254 µmol/L, indicating significant rhabdomyolysis. He had multiple organ dysfunction syndrome develop, with severe renal and hepatic failure, grade II hepatic encephalopathy, and disseminated intravascular coagulation. He responded remarkably well to aggressive supportive measures including forced alkaline diuresis, and he was eventually discharged home after 1 month.
The patient was previously a healthy, physically fit, nonsmoker. He worked as a body building trainer and led an active, sporty lifestyle. The only significant medical history was that he had received thoracic sympathectomy for axillary hyperhidrosis 4 years ago at another hospital. According to the operation records from that hospital, bilateral video-assisted thoracic surgery (VATS) was performed, and the sympathetic trunks from the lower border of the second rib to the lower border of the fifth rib were excised from both sides. After surgery he was said to have had anhidrosis in both axillae, both upper limbs, the upper chest, and the head and neck. He had severe compensatory sweating over his abdomen and back, but no Horner’s syndrome, gustatory sweating, or other symptomatic post-sympathectomy complication. No specific mention of postoperative bradycardia was noted in the records from the hospital performing the sympathectomy.
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Comment
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Thoracic sympathectomy has been established to be a safe and effective treatment for palmar hyperhidrosis, facial blushing, selected cases of upper limb ischemic syndromes, and occasionally axillary hyperhidrosis. The most commonly used surgical approach is VATS, with needlescopic VATS using 2-mm to 3-mm instruments now becoming increasingly popular [1, 2]. The most common complication after sympathectomy is compensatory hyperhidrosis, which can occur in 30% to 100% of all patients. Limiting the extent of sympathetic resection has been suggested to reduce the incidence of some of these complications. Resection of the sympathetic trunk between the second to fifth rib levels as performed by the other hospital in this patient would be regarded as very extensive by many surgeons. Other, often reported sequelae include Horner’s syndrome, gustatory sweating, and chest wall pain and paresthesia [2, 3].
It is impossible to prove definitively that the heat stroke in this patient was related to the previous sympathectomy. He was running a strenuous road race in hot and humid conditions. Nonetheless, for an athletic young man who regularly exercised and who had no other known risk factors, the severity of heat stroke in this case is striking. As the only notable feature in his past medical history, the sympathectomy may have played a significant role in the heat stroke in several ways.
First, the abolition of sweating from the upper body as well as the axillae and both upper limbs may have significantly reduced the capacity of the patient to lose heat through sweating during exercise. Anhidrosis in the head and neck after sympathectomy affects a proportion of patients, but is often neglected in most reports of post-sympathectomy complications [3]. The loss of head and neck sweating in this patient may have further impaired overall heat loss. However we would also note that the degree of heat loss impairment after sympathectomy has never been quantified, and its effect on body temperature during exercise remains to be established.
Second, thoracic sympathectomy has been demonstrated to abolish or alter sympathetic vasoconstrictive responses in the skin, and this may contribute to abnormal peripheral vascular responses to temperature [4]. Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy [5]. It is not impossible that such atypical peripheral vascular responses to rising body temperature may have contributed to impaired heat loss during exercise or to an inappropriate response to shock on the development of the heat stroke.
Third, it has been shown that thoracic sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise [6]. Although absolute tachycardia is not eliminated, given the endocrine and paracrine stimuli during exercise, the maximum heart rate reached during exercise has been shown to be significantly reduced after sympathectomy. Thus for a given workload during exercise, there will be a relative bradycardia. This may possibly affect the circulatory system’s ability to convey heat from the body core to the extremities for heat loss.
During the development of heat stroke, great stress is placed in the cardiovascular system. Dehydration, translocation of blood from the central circulation to the peripheries, increased nitric oxide production, and other factors can all contribute to circulatory collapse [7, 8]. An already impaired cardiovascular system is recognized to be a significant risk factor for development of heat stroke. In the post-sympathectomy patient, the abnormal sympathetic skin response may lead to peripheral vascular failure or the reduced cardiac chronotropic response may impair the body’s capacity to compensate for shock. These may have contributed to the rapid development of shock and severe multiple organ dysfunction syndrome in this patient.
Although a direct causal relationship between the sympathectomy and the heat stroke can not be verified here, the previously mentioned pathophysiologic effects of sympathectomy have all been individually well documented in the literature. Until further information becomes available, our experience with this case suggests that patients undergoing thoracic sympathectomy should be cautioned about the possible increased risk of exertional heat stroke.
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References
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- Grogan H, Hopkins PM. Heat stroke: implications for critical care and anaesthesia Br J Anaesth 2002;88:700-707.[Abstract/Free Full Text]
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Abstract
Introduction
