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Internal Medicine›Condition·Updated Apr 17, 2026·v1

Dengue Fever

Dengue fever is a major global health threat characterized by a three-phase clinical course. Management hinges on early identification of warning signs and careful fluid resuscitation, as no specific antiviral therapy exists.

High Evidence101 references·454 words·2 min read·v1
Infectious DiseaseTropical MedicineArbovirusFlavivirus

Quick Reference

RxDrug of choiceAcetaminophen (Paracetamol) for analgesia/antipyresis
AltAlternativesIsotonic crystalloids (Lactated Ringer's) for volume expansion
⊘AvoidNSAIDs (Ibuprofen, Naproxen), Aspirin, and prophylactic platelet transfusions
DxTest of choiceNS1 Antigen or RT-PCR (Days 1-5); IgM/IgG ELISA (>Day 5)
ScKey scoreWHO 2009 Dengue Classification (Warning Signs vs. Severe Dengue)
→When to referPresence of any warning signs (abdominal pain, persistent vomiting, mucosal bleed) or signs of shock
Dengue is a dynamic illness where the transition from fever to the critical phase (days 3-7) requires vigilant monitoring for plasma leakage and strict avoidance of NSAIDs.
Dengue fever is a mosquito-borne viral illness caused by the dengue virus (DENV-1 to DENV-4), a member of the Flaviviridae family. Transmitted primarily by Aedes aegypti and Aedes albopictus, it has become the most rapidly spreading mosquito-borne viral disease globally, driven by urbanization and climate change. The clinical course is notoriously dynamic, progressing through febrile, critical, and recovery phases.

Overview and Recommendations

Background

  • •Recognize dengue as a systemic viral infection caused by four distinct serotypes (DENV-1, 2, 3, and 4), where DENV-2 is frequently associated with the highest virulence and risk of severe outbreaks.
  • •Understand the transmission cycle involving female Aedes mosquitoes, which acquire the virus from viremic humans and can also transmit the virus vertically to their larvae, allowing environmental persistence during dry seasons.
  • •Identify the primary risk factor for severe disease as secondary infection with a different serotype; this triggers antibody-dependent enhancement (ADE), where non-neutralizing antibodies facilitate viral entry into macrophages, causing a massive cytokine release.
  • •Note the expanding geographic range of the vectors, with Aedes albopictus facilitating transmission in temperate regions like Southern Europe, while Aedes aegypti remains the dominant urban vector in tropical hyperendemic zones.
  • •Consider the impact of comorbidities such as , , and , which significantly increase the risk of symptomatic presentation and progression to severe organ involvement.

Evaluation

  • •Suspect dengue in any patient with acute high-grade fever (≥38°C) who has lived in or traveled to an endemic region (e.g., Southeast Asia, Puerto Rico, Mexico) within the last 14 days.
  • •Ask about the classic triad of "breakbone fever": severe frontal headache, retro-orbital pain, and intense myalgias or arthralgias, often following a biphasic or "saddleback" fever pattern.
  • •Examine the skin for the pathognomonic "isles of white in a sea of red" rash—a confluent erythematous exanthema with small circular areas of skin sparing—and check for petechiae on the extremities.
  • •Perform the Tourniquet Test (TT) to assess capillary fragility: inflate a blood pressure cuff to the mean arterial pressure [(Systolic + Diastolic) / 2] for 5 minutes; a count of ≥10–20 petechiae per square inch on the ventral forearm is positive.
  • •Monitor for "Warning Signs" during the transition from the febrile to the critical phase (typically days 3–7), including abdominal pain or tenderness, persistent vomiting, mucosal bleeding, and lethargy.
  • •Order a (CBC) daily to track the characteristic progression of leukopenia (WBC <5,000 cells/mm³), followed by a rapid drop in platelet count and a rising hematocrit indicating plasma leakage.
  • •Obtain NS1 antigen and/or RT-PCR for definitive diagnosis if the patient presents within the first 5 days of symptom onset (the viremic phase).
  • •Order IgM and IgG serology if the patient presents after day 5 of illness; note that a four-fold rise in IgG titers in paired sera is diagnostic of recent infection.
  • •Utilize bedside ultrasonography to detect subclinical plasma leakage, specifically looking for gallbladder wall thickening, , and pleural effusions (often appearing first on the right side).
  • •Rule out co-infections such as , , and , particularly in regions where these pathogens overlap, as co-infection can exacerbate anemia and organ dysfunction.
  • •Assess for neurological complications, including cerebellar , , or signs of if the patient exhibits motor weakness or altered consciousness.
  • •Monitor respiratory mechanics closely if plasma leakage is suspected; an FVC < 15 mL/kg should prompt consideration for mechanical ventilation due to massive effusions or pulmonary edema.

Management

  • •Administer Acetaminophen (Paracetamol) for fever and pain control, maintaining a maximum dose of 4g/day in adults; strictly avoid Aspirin and NSAIDs (e.g., Ibuprofen) due to the risk of gastritis and platelet dysfunction.
  • •Encourage aggressive oral hydration in the ambulatory setting, aiming for approximately 2 liters of fluid per day (e.g., oral rehydration salts, fruit juices) to reduce the risk of hospitalization.
  • •Initiate IV fluid therapy with isotonic crystalloids (e.g., Lactated Ringer's or Normal Saline) at 5–7 mL/kg/hour for patients with warning signs who cannot maintain oral intake.
  • •Manage (DSS) with an immediate IV bolus of isotonic crystalloid at 10–20 mL/kg over 15–30 minutes, followed by reassessment of hemodynamic status.
  • •Consider colloid boluses (e.g., 5% albumin) in patients with refractory shock or those with massive where crystalloids may worsen extravascular fluid accumulation.
  • •Monitor hematocrit every 6–12 hours during the critical phase; a rising hematocrit despite fluid resuscitation suggests ongoing plasma leakage and requires an increase in fluid rate.
  • •Avoid prophylactic platelet transfusions even in cases of severe thrombocytopenia; reserve transfusions for patients with clinically significant, life-threatening hemorrhage.
  • •Delay elective surgeries or delivery in pregnant patients until the critical phase has passed to minimize the risk of massive maternal hemorrhage.
  • •Administer IVIG 2 g/kg as a single infusion in pediatric patients who develop -like features (e.g., coronary artery aneurysms) post-dengue.
  • •Refer patients to intensive care if they exhibit severe plasma leakage leading to respiratory distress, severe organ impairment (AST/ALT ≥1000 U/L), or impaired consciousness.
  • •Monitor for fluid overload during the recovery phase; as third-spaced fluid is reabsorbed, decrease IV fluids and watch for signs of pulmonary edema or heart failure.
  • •Discharge patients only when they have been afebrile for 48 hours without antipyretics, show a rising platelet count, and have stable hematocrit levels with improving clinical symptoms.
  • •Counsel patients on the use of the Dengvaxia vaccine only if they have laboratory-confirmed prior dengue infection, as it may increase the risk of severe disease in seronegative individuals.

Board Review — High Yield

  • •Breakbone fever — Common name for dengue due to severe myalgia and arthralgia.
  • •Isles of white in a sea of red — Classic description of the confluent erythematous rash with skin sparing.
  • •Antibody-Dependent Enhancement (ADE) — Mechanism where secondary infection with a different serotype leads to more severe disease.
  • •Tourniquet Test — Bedside marker for capillary fragility; positive if ≥10-20 petechiae per square inch.
  • •Critical Phase — Occurs at the time of defervescence (fever drop), which is when plasma leakage and shock are most likely.
  • •NS1 Antigen — Viral protein detectable in the blood from day 1 of symptoms, used for early rapid diagnosis.
  • •Hematocrit/Platelet Divergence — A rising hematocrit with a falling platelet count is a hallmark of the critical phase.
  • •Dengvaxia — Vaccine only recommended for those with evidence of prior dengue infection to prevent ADE-like reactions.

Deep Dive — Evidence Details

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