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10/12/2015 Dengue Clinical Presentation: History, Physical Examination http://emedicine.medscape.com/article/215840clinical 1/6 Dengue Clinical Presentation Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM; Chief Editor: Michael Stuart Bronze, MD more... Updated: Oct 05, 2015 History Patients with dengue will have a history of living in, or recent travel to, a region where the disease is endemic. The incubation period is 314 days (average, 47 days); symptoms that begin more than 2 weeks after a person departs from an endemic area are probably not due to dengue. Many patients experience a prodrome of chills, erythematous mottling of the skin, and facial flushing (a sensitive and specific indicator of dengue fever). The prodrome may last for 23 days. Children younger than 15 years usually have a nonspecific febrile syndrome, which may be accompanied by a maculopapular rash. Classic dengue fever begins with sudden onset of fever, chills, and severe (termed breakbone) aching of the head, back, and extremities, as well as other symptoms. The fever lasts 27 days and may reach 41°C. Fever that lasts longer than 10 days is probably not due to dengue. Pain and other accompanying symptoms may include any of the following: Headache Retroorbital pain General body pain (arthralgias, myalgias) Nausea and vomiting (however, diarrhea is rare) Rash Weakness Altered taste sensation Anorexia Sore throat Mild hemorrhagic manifestations (eg, petechiae, bleeding gums, epistaxis, menorrhagia, hematuria) Lymphadenopathy Rash in dengue fever is a maculopapular or macular confluent rash over the face, thorax, and flexor surfaces, with islands of skin sparing. The rash typically begins on day 3 and persists 23 days. Fever typically abates with the cessation of viremia. Occasionally, and more commonly in children, the fever abates for a day and then returns, a pattern that has been called saddleback fever. A second rash may occur within 12 days of defervescence, lasting 15 days; it is morbilliform, is maculopapular, spares the palms and soles, and occasionally desquamates. Recovery is complete but slow, with fatigue and exhaustion often persisting after the fever has subsided. The convalescent phase may last for 2 weeks. Patients are at risk for development of dengue hemorrhagic fever or dengue shock syndrome at approximately the time of defervescence. Abdominal pain in conjunction with restlessness, change in mental status, hypothermia, and a drop in the platelet count presages the development of dengue hemorrhagic fever. Of patients with dengue hemorrhagic fever, 90% are younger than 15 years. The initial phase of dengue hemorrhagic fever is similar to that of dengue fever and other febrile viral illnesses. Shortly after the fever breaks (or sometimes within 24 hours before), signs of plasma leakage appear, along with the development of hemorrhagic symptoms such as bleeding from sites of trauma, gastrointestinal bleeding, and hematuria. Patients may also present with abdominal pain, vomiting, febrile seizures (in children), and a decreased level of consciousness. If left untreated, dengue hemorrhagic fever most likely progresses to dengue shock syndrome. Common symptoms in impending shock include abdominal pain, vomiting, and restlessness. Patients also may have symptoms related to circulatory failure. Physical Examination Dengue fever presents in a nonspecific manner and may not be distinguishable from other viral or bacterial illness. According to the Pan American Health Organization (PAHO), the clinical description of dengue fever is an acute febrile illness of 27 days duration associated with 2 or more of the following: Severe and generalized headache Retroorbital pain Severe myalgias, especially of the lower back, arms, and legs Arthralgias, usually of the knees and shoulders Characteristic rash Hemorrhagic manifestations Leukopenia Additional findings may include the following: Injected conjunctivae Facial flushing, a sensitive and specific predictor of dengue infection Inflamed pharynx

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Page 1: Dengue Clinical Presentation_ History, Physical Examination

10/12/2015 Dengue Clinical Presentation: History, Physical Examination

http://emedicine.medscape.com/article/215840clinical 1/6

Dengue Clinical PresentationAuthor: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM; Chief Editor: Michael StuartBronze, MD more...

Updated: Oct 05, 2015

HistoryPatients with dengue will have a history of living in, or recent travel to, a regionwhere the disease is endemic. The incubation period is 314 days (average, 47days); symptoms that begin more than 2 weeks after a person departs from anendemic area are probably not due to dengue.

Many patients experience a prodrome of chills, erythematous mottling of the skin,and facial flushing (a sensitive and specific indicator of dengue fever). Theprodrome may last for 23 days. Children younger than 15 years usually have anonspecific febrile syndrome, which may be accompanied by a maculopapular rash.Classic dengue fever begins with sudden onset of fever, chills, and severe (termedbreakbone) aching of the head, back, and extremities, as well as other symptoms.The fever lasts 27 days and may reach 41°C. Fever that lasts longer than 10 daysis probably not due to dengue.

Pain and other accompanying symptoms may include any of the following:

HeadacheRetroorbital painGeneral body pain (arthralgias, myalgias)Nausea and vomiting (however, diarrhea is rare)RashWeaknessAltered taste sensationAnorexiaSore throatMild hemorrhagic manifestations (eg, petechiae, bleeding gums, epistaxis,menorrhagia, hematuria)Lymphadenopathy

Rash in dengue fever is a maculopapular or macular confluent rash over the face,thorax, and flexor surfaces, with islands of skin sparing. The rash typically begins onday 3 and persists 23 days.

Fever typically abates with the cessation of viremia. Occasionally, and morecommonly in children, the fever abates for a day and then returns, a pattern thathas been called saddleback fever. A second rash may occur within 12 days ofdefervescence, lasting 15 days; it is morbilliform, is maculopapular, spares thepalms and soles, and occasionally desquamates.

Recovery is complete but slow, with fatigue and exhaustion often persisting afterthe fever has subsided. The convalescent phase may last for 2 weeks.

Patients are at risk for development of dengue hemorrhagic fever or dengue shocksyndrome at approximately the time of defervescence. Abdominal pain inconjunction with restlessness, change in mental status, hypothermia, and a drop inthe platelet count presages the development of dengue hemorrhagic fever.

Of patients with dengue hemorrhagic fever, 90% are younger than 15 years. Theinitial phase of dengue hemorrhagic fever is similar to that of dengue fever andother febrile viral illnesses. Shortly after the fever breaks (or sometimes within 24hours before), signs of plasma leakage appear, along with the development ofhemorrhagic symptoms such as bleeding from sites of trauma, gastrointestinalbleeding, and hematuria. Patients may also present with abdominal pain, vomiting,febrile seizures (in children), and a decreased level of consciousness.

If left untreated, dengue hemorrhagic fever most likely progresses to dengue shocksyndrome. Common symptoms in impending shock include abdominal pain,vomiting, and restlessness. Patients also may have symptoms related to circulatoryfailure.

Physical ExaminationDengue fever presents in a nonspecific manner and may not be distinguishable fromother viral or bacterial illness. According to the Pan American Health Organization(PAHO), the clinical description of dengue fever is an acute febrile illness of 27days duration associated with 2 or more of the following:

Severe and generalized headacheRetroorbital painSevere myalgias, especially of the lower back, arms, and legsArthralgias, usually of the knees and shouldersCharacteristic rashHemorrhagic manifestationsLeukopenia

Additional findings may include the following:

Injected conjunctivaeFacial flushing, a sensitive and specific predictor of dengue infectionInflamed pharynx

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LymphadenopathyNausea and vomitingNonproductive coughTachycardia, bradycardia, and conduction defects

Up to half of patients with dengue fever develop a characteristic rash. The rash isvariable and may be maculopapular or macular. Petechiae and purpura maydevelop as hemorrhagic manifestations. Hemorrhagic manifestations mostcommonly include petechiae and bleeding at venipuncture sites.

A tourniquet test is often positive. This test is performed by inflating a bloodpressure cuff on the upper arm to midway between diastolic and systolic bloodpressures for 5 minutes. The results are considered to be positive if more than 20petechiae per square inch are observed on the skin in the area that was underpressure. Other hemorrhagic manifestations include nasal or gingival bleeding,melena, hematemesis, and menorrhagia.

Neurologic manifestations such as seizures and encephalitis/encephalopathy havebeen reported in rare cases of dengue infection. Some of these cases did notdisplay other typical features of dengue infection. Other neurologic complicationsassociated with dengue infection include neuropathies, GuillainBarré syndrome,and transverse myelitis.

Dengue hemorrhagic fever

Findings for dengue hemorrhagic fever are similar to those for dengue fever andinclude the following:

Biphasic fever curveHemorrhagic findings more pronounced than in dengue feverSigns of peritoneal effusion, pleural effusion, or both

Minimal criteria for the diagnosis of dengue hemorrhagic fever, according to theWorld Health Organization (WHO), are as follows[45] :

FeverHemorrhagic manifestations (eg, hemoconcentration, thrombocytopenia,positive tourniquet test)Circulatory failure, such as signs of vascular permeability (eg,hypoproteinemia, effusions)Hepatomegaly

In addition, conjunctival injection develops in approximately one third of patientswith dengue hemorrhagic fever. Optic neuropathy has been reported andoccasionally results in permanent and significant visual impairment.[46] Pharyngealinjection develops in almost 97% of patients with dengue hemorrhagic fever.Generalized lymphadenopathy is observed.

Hepatomegaly is present more often in dengue shock syndrome than in mildercases. Hepatic transaminase levels may be mildly to moderately elevated.Encephalopathy is a rare complication that may result from a combination ofcerebral edema, intracranial hemorrhage, anoxia, hyponatremia, and hepatic injury.

Dengue shock syndrome

Findings of dengue shock syndrome include the following:

HypotensionBradycardia (paradoxical) or tachycardia associated with hypovolemic shockHepatomegalyHypothermiaNarrow pulse pressure (< 20 mm Hg)Signs of decreased peripheral perfusion

Differential Diagnoses

Contributor Information and DisclosuresAuthorSuzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Professor of Emergency Medicine, EducationOfficer, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Educationand Research, PENN Travel Medicine; Medical Director, Fast Track, Department of Emergency Medicine

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies:Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine andHygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, WildernessMedical Society

Disclosure: Nothing to disclose.

Coauthor(s)Patrick B Hinfey, MD Emergency Medicine Residency Director, Department of Emergency Medicine, NewarkBeth Israel Medical Center; Clinical Assistant Professor of Emergency Medicine, New York College ofOsteopathic Medicine

Patrick B Hinfey, MD is a member of the following medical societies: American Academy of EmergencyMedicine, Wilderness Medical Society, American College of Emergency Physicians, Society for AcademicEmergency Medicine

Disclosure: Nothing to disclose.

William H Shoff, MD, DTM&H Director, PENN Travel Medicine; Associate Professor, Department of EmergencyMedicine, Hospital of the University of Pennsylvania, University of Pennsylvania School of Medicine

William H Shoff, MD, DTM&H is a member of the following medical societies: American College of Physicians,American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society forAcademic Emergency Medicine, Wilderness Medical Society

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Disclosure: Nothing to disclose.

Chief EditorMichael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart GWolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health ScienceCenter; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, AmericanMedical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation,Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

AcknowledgementsJoseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics,Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, AmericanAcademy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, PediatricInfectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Hagop A Isnar, MD, FACEP Department of Emergency Medicine, Crouse Hospital

Hagop A Isnar, MD, FACEP is a member of the following medical societies: American College of EmergencyPhysicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech, Carilion School of Medicine, Roanoke,Virginia

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, AmericanCollege of Physicians, American Public Health Association, American Society for Microbiology, American Societyof Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, andWilderness Medical Society

Disclosure: Nothing to disclose.

Deborah Sentochnik, MD Consulting Staff, Department of Internal Medicine, Division of Infectious Disease,The Mary Imogene Bassett Hospital

Deborah Sentochnik, MD is a member of the following medical societies: American College of Physicians,Infectious Diseases Society of America, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center;Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics,American Association of Immunologists, American Pediatric Society, American Society for Microbiology,Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society,Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical CenterCollege of Pharmacy; EditorinChief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College ofPharmacy; EditorinChief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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