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Compensatory Hyperhidrosis After Sympathectomy: Level of Resection Versus Location of Hyperhidrosis
CORRESPONDENCE
Compensatory Hyperhidrosis After Sympathectomy: Level of Resection Versus Location of Hyperhidrosis To the Editor:
MISCELLANEOUS
Dewey and colleagues [1] and Reisfeld [2] suggested that including T2 in the sympathectomy level increases the incidence of severe compensatory hyperhidrosis (CH) and dissatisfaction rates. But in Dewey and colleagues’ [1] report and Reisfeld’s [2] letter, T2 sympathectomy was done for facial sweating and blushing. Because the level of sympathectomy was always decided by the location of the primary hyperhidrosis, the latter may well explain the risk of increased CH and patient dissatisfaction. Dewey and colleagues [1] noted increased dissatisfaction and severe CH in patients undergoing T2 sympathectomy, except those T2 sympathectomy patients who also underwent the procedure for palmar hyperhidrosis. In our experience [3], T2-3 sympathectomy led to a low incidence of severe CH, but the vast majority of our patients had palmar hyperhidrosis, and none had primarily facial hyperhidrosis or blushing. Several criteria seem to reliably predict which patients will have good results after T2-3 sympathectomy [4] (ie, massive palmar sweating approximating plantar sweating with onset either in early childhood or puberty, and exacerbation with ordinary hand lotion). Reisfeld [2] commented that the rates of dissatisfaction and severe CH for patients with only facial or axillary hyperhidrosis or blushing are too high and suggests that sympathectomy not be done for these patients. All these issues together suggest that patient dissatisfaction is less related to T2 sympathectomy than it is to the facial and axillary location of the primary hyperhidrosis. If the results of sympathectomy for palmar hyperhidrosis are excellent and for other locations they are less, then should sympathectomies even be done for axillary or facial hyperhidrosis and blushing? There are many patients with severe symptoms limited to the face and axilla whose lives have been significantly improved with surgical sympathectomy. What needs to be taken seriously, however, is that surgery for facial and axillary blushing and hyperhidrosis is trickier than for typical palmoplantar hyperhidrosis and has an increased rate of patient dissatisfaction. An extensive discussion of risks is crucial, as is an estimate of the patient’s psychological stability. The patient’s perception of the sweating problem before and after the operation is even more likely to be important than the quantitative level of compensatory sweating. Proper patient selection is the key. Confounding variables with regard to surgical sympathectomy (ie, location of hyperhidrosis, sympathectomy level, clamp vs cut vs resect, and role of medical management) lead to divergent conclusions from different studies, not all of which are well thought out. The importance of prospective, randomized trials to scientifically address these issues is apparent. However it also remains apparent that sympathectomy for severe palmar hyperhidrosis (whether at the T2 or T3 level) results in excellent outcomes and satisfaction in the overwhelming majority of patients. Fritz Baumgartner, MD Jiri Konecny, DO Surgery Associates 3791 Katella Ave, #201 Los Alamitos, CA 90720 e-mail: [email protected] © 2007 by The Society of Thoracic Surgeons Published by Elsevier Inc
References 1. Dewey TM, Hebert MA, Hill SL, Prince SL, Mack MJ. Oneyear follow-up after thoracoscopic sympathectomy for hyperhidrosis. Ann Thorac Surg 2006;81:1227–33. 2. Reisfeld R. One-year follow-up after thoracoscopic sympathectomy for hyperhidrosis (letter). Ann Thorac Surg 2007;83: 358 –9. 3. Baumgartner FJ, Toh Y. Severe hyperhidrosis: clinical features and current thoracoscopic surgical management. Ann Thorac Surg 2003;76:1878 – 83. 4. Baumgartner F. Compensatory hyperhidrosis after thoracoscopic sympathectomy (letter). Ann Thorac Surg 2005;80:1161; author reply 1161.
HIT in VAD Patients: Considerations To the Editor: We read with great interest the contribution by Koster and colleagues [1]. Unfortunately we found several aspects of the analysis to be rather misleading. Currently an increased incidence of clinical cases of heparininduced thrombocytopenia (HIT) has been observed; however the actual incidence has not been documented. There are considerable differences in diagnostic specificity among various laboratory assays to detect HIT antibodies. In their editorial, Warkentin and Crowther [2] criticized Koster and colleagues [1] for their usage of particle gel immunoassay (PaGIA) due to its intermediate specificity (ie, potential over-diagnosis) compared with serotonin-release assay (ie, the gold standard). The magnitude of the positive tests has not been described; we know a weak result is less likely to cause a clinically evident HIT. Moreover, in this study the patients who are positive for HIT antibodies have not been further studied to detect antibodies against thyroglobulin and peroxidase enzyme. Our laboratory has observed a cross-reaction between these antibodies and PF (Platelet Fraction)4/heparin complexes, producing false positive results (unpublished observations). We doubt whether the reported incidence of HIT (ie, 7.8% during ventricular assist device [VAD] implantation) is verified or not. Were all the patients affected by HIT? Once diagnosis of HIT has been confirmed, it is mandatory to suspend all heparin administrations. Three months after HIT diagnosis and after negative test results, heparin may be readministered in 1 single dose during the bypass pump time. Koster and co-workers [1] used two different protocols for cardiopulmonary bypass (ie, heparin plus tirofiban and heparin plus prostaglandin for patients affected by pulmonary hypertension). Both protocols are considered to be second choice according to the evidence-based guidelines for HIT management [3]. Moreover the time span between HIT diagnosis and surgery has never been specified. The authors used lepirudin with both the preoperative and postoperative times. However it is not clear why the same lepirudin has not been used intraoperatively. The type of monitoring and dosage of the drug have never been described. Therefore their protocol is difficult to be followed. Finally, we do not understand why they started lepirudin anticoagulation immediately after transferring the patient to the intensive care unit. Although we have limited experience about patients affected by HIT, we are aware that it is essential to conduct tight quantitative control of hourly bleeding and coagulation patterns before beginning any anticoagulant drug. We know that the anticoagulation protocols during postoperative time change according to the different implanted VADs. Ann Thorac Surg 2007;84:1422–7 • 0003-4975/07/$32.00 doi:10.1016/j.athoracsur.2007.04.091
Compensatory Hyperhidrosis After Sympathectomy: Level of Resection Versus Location of Hyperhidrosis To the Editor:
MISCELLANEOUS
Dewey and colleagues [1] and Reisfeld [2] suggested that including T2 in the sympathectomy level increases the incidence of severe compensatory hyperhidrosis (CH) and dissatisfaction rates. But in Dewey and colleagues’ [1] report and Reisfeld’s [2] letter, T2 sympathectomy was done for facial sweating and blushing. Because the level of sympathectomy was always decided by the location of the primary hyperhidrosis, the latter may well explain the risk of increased CH and patient dissatisfaction. Dewey and colleagues [1] noted increased dissatisfaction and severe CH in patients undergoing T2 sympathectomy, except those T2 sympathectomy patients who also underwent the procedure for palmar hyperhidrosis. In our experience [3], T2-3 sympathectomy led to a low incidence of severe CH, but the vast majority of our patients had palmar hyperhidrosis, and none had primarily facial hyperhidrosis or blushing. Several criteria seem to reliably predict which patients will have good results after T2-3 sympathectomy [4] (ie, massive palmar sweating approximating plantar sweating with onset either in early childhood or puberty, and exacerbation with ordinary hand lotion). Reisfeld [2] commented that the rates of dissatisfaction and severe CH for patients with only facial or axillary hyperhidrosis or blushing are too high and suggests that sympathectomy not be done for these patients. All these issues together suggest that patient dissatisfaction is less related to T2 sympathectomy than it is to the facial and axillary location of the primary hyperhidrosis. If the results of sympathectomy for palmar hyperhidrosis are excellent and for other locations they are less, then should sympathectomies even be done for axillary or facial hyperhidrosis and blushing? There are many patients with severe symptoms limited to the face and axilla whose lives have been significantly improved with surgical sympathectomy. What needs to be taken seriously, however, is that surgery for facial and axillary blushing and hyperhidrosis is trickier than for typical palmoplantar hyperhidrosis and has an increased rate of patient dissatisfaction. An extensive discussion of risks is crucial, as is an estimate of the patient’s psychological stability. The patient’s perception of the sweating problem before and after the operation is even more likely to be important than the quantitative level of compensatory sweating. Proper patient selection is the key. Confounding variables with regard to surgical sympathectomy (ie, location of hyperhidrosis, sympathectomy level, clamp vs cut vs resect, and role of medical management) lead to divergent conclusions from different studies, not all of which are well thought out. The importance of prospective, randomized trials to scientifically address these issues is apparent. However it also remains apparent that sympathectomy for severe palmar hyperhidrosis (whether at the T2 or T3 level) results in excellent outcomes and satisfaction in the overwhelming majority of patients. Fritz Baumgartner, MD Jiri Konecny, DO Surgery Associates 3791 Katella Ave, #201 Los Alamitos, CA 90720 e-mail: [email protected] © 2007 by The Society of Thoracic Surgeons Published by Elsevier Inc
References 1. Dewey TM, Hebert MA, Hill SL, Prince SL, Mack MJ. Oneyear follow-up after thoracoscopic sympathectomy for hyperhidrosis. Ann Thorac Surg 2006;81:1227–33. 2. Reisfeld R. One-year follow-up after thoracoscopic sympathectomy for hyperhidrosis (letter). Ann Thorac Surg 2007;83: 358 –9. 3. Baumgartner FJ, Toh Y. Severe hyperhidrosis: clinical features and current thoracoscopic surgical management. Ann Thorac Surg 2003;76:1878 – 83. 4. Baumgartner F. Compensatory hyperhidrosis after thoracoscopic sympathectomy (letter). Ann Thorac Surg 2005;80:1161; author reply 1161.
HIT in VAD Patients: Considerations To the Editor: We read with great interest the contribution by Koster and colleagues [1]. Unfortunately we found several aspects of the analysis to be rather misleading. Currently an increased incidence of clinical cases of heparininduced thrombocytopenia (HIT) has been observed; however the actual incidence has not been documented. There are considerable differences in diagnostic specificity among various laboratory assays to detect HIT antibodies. In their editorial, Warkentin and Crowther [2] criticized Koster and colleagues [1] for their usage of particle gel immunoassay (PaGIA) due to its intermediate specificity (ie, potential over-diagnosis) compared with serotonin-release assay (ie, the gold standard). The magnitude of the positive tests has not been described; we know a weak result is less likely to cause a clinically evident HIT. Moreover, in this study the patients who are positive for HIT antibodies have not been further studied to detect antibodies against thyroglobulin and peroxidase enzyme. Our laboratory has observed a cross-reaction between these antibodies and PF (Platelet Fraction)4/heparin complexes, producing false positive results (unpublished observations). We doubt whether the reported incidence of HIT (ie, 7.8% during ventricular assist device [VAD] implantation) is verified or not. Were all the patients affected by HIT? Once diagnosis of HIT has been confirmed, it is mandatory to suspend all heparin administrations. Three months after HIT diagnosis and after negative test results, heparin may be readministered in 1 single dose during the bypass pump time. Koster and co-workers [1] used two different protocols for cardiopulmonary bypass (ie, heparin plus tirofiban and heparin plus prostaglandin for patients affected by pulmonary hypertension). Both protocols are considered to be second choice according to the evidence-based guidelines for HIT management [3]. Moreover the time span between HIT diagnosis and surgery has never been specified. The authors used lepirudin with both the preoperative and postoperative times. However it is not clear why the same lepirudin has not been used intraoperatively. The type of monitoring and dosage of the drug have never been described. Therefore their protocol is difficult to be followed. Finally, we do not understand why they started lepirudin anticoagulation immediately after transferring the patient to the intensive care unit. Although we have limited experience about patients affected by HIT, we are aware that it is essential to conduct tight quantitative control of hourly bleeding and coagulation patterns before beginning any anticoagulant drug. We know that the anticoagulation protocols during postoperative time change according to the different implanted VADs. Ann Thorac Surg 2007;84:1422–7 • 0003-4975/07/$32.00 doi:10.1016/j.athoracsur.2007.04.091