Reply to Thomas et al
Note Potential conflicts of interest. Both authors: No reported conflicts.
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TO THE EDITOR—We agree with Thomas et al that classifying patients with dengue can be difficult [1]. However, dengue shock syndrome (DSS) is a unique clinical entity that follows a very typical course; after 4–5 days of general systemic symptoms, previously healthy children and young adults present around the time of defervescence with substantial plasma leakage and hypovolemic shock, sometimes accompanied by bleeding. Urgent intervention is crucial to prevent progression to profound or refractory shock, which is often complicated by severe hemorrhage, organ failure, and death [2]. We use the standard definition for DSS that is familiar to most physicians working in endemic areas—a history consistent with dengue, with hemodynamic compromise defined as either narrowing of the pulse pressure or hypotension for age together with evidence of impaired perfusion—with the caveat that the definition refers to hypovolemia due to vascular leakage rather than due to blood loss [3]. Although gastrointestinal losses may result in some degree of dehydration during the initial febrile phase, it is highly unlikely that “straightforward dehydration” could explain these clinical signs. First, patients presenting with DSS usually look surprisingly well. They do not exhibit any of the conventional signs of dehydration, such as dry lips, sunken eyes, or reduced skin turgor, and yet in our series the median percentage hemoconcentration at presentation was 35% (interquartile range, 27%–45%). This level of dehydration should be immediately obvious to the treating physician, and indeed it is partly because
most patients look tired but otherwise unremarkable that close attention to pulse pressure and general cardiovascular status are so strongly encouraged, to allow prompt identification during the early phase of compensated shock. Second, although pleural and peritoneal effusions are rarely present at onset of DSS, within 12–24 hours of commencing fluid resuscitation, approximately 30% of our subjects developed clinically detectable effusions [3], and >95% of those assessed radiologically had detectable effusions (unpublished data); this is not consistent with hypovolemia due to dehydration alone. Thomas et al also suggest addition of complex criteria to the diagnosis of DSS, including a number of laboratory investigations, use of intensive care unit severity scoring systems, and presence of “indisputable diagnostic features of plasma leakage.” However, the vast majority of DSS cases are managed in healthcare facilities without immediate access to blood gas analysis, coagulation screening, or urgent radiological investigations, and none of the scoring systems mentioned are relevant to children (the primary DSS population) or have been evaluated in dengue-endemic areas to assess their utility. Finally, “indisputable evidence of leakage” is rarely apparent until after resuscitation has commenced. We feel strongly that the diagnosis of DSS should remain practical and simple [2], designed to be immediately within the grasp of everyday clinicians working in environments where they are faced with identifying and treating hundreds of such cases annually. In our case series of direct admissions, patient outcomes were excellent, largely due to prompt diagnosis and skilled management by experienced personnel. Undoubtedly, mortality is higher in referred cases or those diagnosed late in the illness evolution [4–6].
Both authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed. Phung Khanh Lam1 and Bridget Wills1,2 1
Oxford University Clinical Research Unit, Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam; and 2 Centre for Tropical Medicine, Centre for Clinical Vaccinology and Tropical Medicine, University of Oxford, United Kingdom
References
Correspondence: Phung Khanh Lam, MD, Oxford University Clinical Research Unit, 764 Vo Van Kiet Street, Ward 1, District 5, Ho Chi Minh City, Vietnam ([email protected]). Clinical Infectious Diseases 2014;58(7):1039–40 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/ licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. DOI: 10.1093/cid/ciu017
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1. Thomas L, Cabié A, Teyssou R. Dengue shock syndrome or dehydration? The importance of considering clinical severity when classifying patients with dengue. Clin Infect Dis 2014; 58:1038–9. 2. World Health Organization. Dengue: guidelines for diagnosis, treatment, prevention and control. Geneva, Switzerland: WHO, 2009. 3. Lam PK, Tam DT, Diet TV, et al. Clinical characteristics of dengue shock syndrome in Vietnamese children: a 10-year prospective study in a single hospital. Clin Infect Dis 2013; 57:1577–86. 4. Trung DT, Thao Le TT, Dung NM, et al. Clinical features of dengue in a large Vietnamese cohort: intrinsically lower platelet counts and greater risk for bleeding in adults than children. Plos Negl Trop Dis 2012; 6:e1679. 5. Bunnag T, Kalayanarooj S. Dengue shock syndrome at the emergency room of Queen Sirikit National Institute of Child Health, Bangkok, Thailand. J Med Assoc Thai 2011; 94(suppl 3): S57–63. 6. Anders KL, Nguyet NM, Chau NVV, et al. Epidemiological factors associated with dengue shock syndrome and mortality in hospitalized dengue patients in Ho Chi Minh City, Vietnam. Am J Trop Med Hyg 2011; 84:127–34.
Note Potential conflicts of interest. Both authors: No reported conflicts.
CORRESPONDENCE
•
CID 2014:58 (1 April)
•
1039
Downloaded from http://cid.oxfordjournals.org/ at Eccles Health Sci Lib-Serials on December 1, 2014
TO THE EDITOR—We agree with Thomas et al that classifying patients with dengue can be difficult [1]. However, dengue shock syndrome (DSS) is a unique clinical entity that follows a very typical course; after 4–5 days of general systemic symptoms, previously healthy children and young adults present around the time of defervescence with substantial plasma leakage and hypovolemic shock, sometimes accompanied by bleeding. Urgent intervention is crucial to prevent progression to profound or refractory shock, which is often complicated by severe hemorrhage, organ failure, and death [2]. We use the standard definition for DSS that is familiar to most physicians working in endemic areas—a history consistent with dengue, with hemodynamic compromise defined as either narrowing of the pulse pressure or hypotension for age together with evidence of impaired perfusion—with the caveat that the definition refers to hypovolemia due to vascular leakage rather than due to blood loss [3]. Although gastrointestinal losses may result in some degree of dehydration during the initial febrile phase, it is highly unlikely that “straightforward dehydration” could explain these clinical signs. First, patients presenting with DSS usually look surprisingly well. They do not exhibit any of the conventional signs of dehydration, such as dry lips, sunken eyes, or reduced skin turgor, and yet in our series the median percentage hemoconcentration at presentation was 35% (interquartile range, 27%–45%). This level of dehydration should be immediately obvious to the treating physician, and indeed it is partly because
most patients look tired but otherwise unremarkable that close attention to pulse pressure and general cardiovascular status are so strongly encouraged, to allow prompt identification during the early phase of compensated shock. Second, although pleural and peritoneal effusions are rarely present at onset of DSS, within 12–24 hours of commencing fluid resuscitation, approximately 30% of our subjects developed clinically detectable effusions [3], and >95% of those assessed radiologically had detectable effusions (unpublished data); this is not consistent with hypovolemia due to dehydration alone. Thomas et al also suggest addition of complex criteria to the diagnosis of DSS, including a number of laboratory investigations, use of intensive care unit severity scoring systems, and presence of “indisputable diagnostic features of plasma leakage.” However, the vast majority of DSS cases are managed in healthcare facilities without immediate access to blood gas analysis, coagulation screening, or urgent radiological investigations, and none of the scoring systems mentioned are relevant to children (the primary DSS population) or have been evaluated in dengue-endemic areas to assess their utility. Finally, “indisputable evidence of leakage” is rarely apparent until after resuscitation has commenced. We feel strongly that the diagnosis of DSS should remain practical and simple [2], designed to be immediately within the grasp of everyday clinicians working in environments where they are faced with identifying and treating hundreds of such cases annually. In our case series of direct admissions, patient outcomes were excellent, largely due to prompt diagnosis and skilled management by experienced personnel. Undoubtedly, mortality is higher in referred cases or those diagnosed late in the illness evolution [4–6].
Both authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed. Phung Khanh Lam1 and Bridget Wills1,2 1
Oxford University Clinical Research Unit, Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam; and 2 Centre for Tropical Medicine, Centre for Clinical Vaccinology and Tropical Medicine, University of Oxford, United Kingdom
References
Correspondence: Phung Khanh Lam, MD, Oxford University Clinical Research Unit, 764 Vo Van Kiet Street, Ward 1, District 5, Ho Chi Minh City, Vietnam ([email protected]). Clinical Infectious Diseases 2014;58(7):1039–40 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/ licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. DOI: 10.1093/cid/ciu017
1040
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CID 2014:58 (1 April)
•
CORRESPONDENCE
Downloaded from http://cid.oxfordjournals.org/ at Eccles Health Sci Lib-Serials on December 1, 2014
1. Thomas L, Cabié A, Teyssou R. Dengue shock syndrome or dehydration? The importance of considering clinical severity when classifying patients with dengue. Clin Infect Dis 2014; 58:1038–9. 2. World Health Organization. Dengue: guidelines for diagnosis, treatment, prevention and control. Geneva, Switzerland: WHO, 2009. 3. Lam PK, Tam DT, Diet TV, et al. Clinical characteristics of dengue shock syndrome in Vietnamese children: a 10-year prospective study in a single hospital. Clin Infect Dis 2013; 57:1577–86. 4. Trung DT, Thao Le TT, Dung NM, et al. Clinical features of dengue in a large Vietnamese cohort: intrinsically lower platelet counts and greater risk for bleeding in adults than children. Plos Negl Trop Dis 2012; 6:e1679. 5. Bunnag T, Kalayanarooj S. Dengue shock syndrome at the emergency room of Queen Sirikit National Institute of Child Health, Bangkok, Thailand. J Med Assoc Thai 2011; 94(suppl 3): S57–63. 6. Anders KL, Nguyet NM, Chau NVV, et al. Epidemiological factors associated with dengue shock syndrome and mortality in hospitalized dengue patients in Ho Chi Minh City, Vietnam. Am J Trop Med Hyg 2011; 84:127–34.
