Dengue Fever: Clinical Features, Warning Signs, Diagnosis and Management
Clinical Medicine Year 3 • dengue illness, dengue with warning signs, severe dengue and dengue shock
Clinical safety note: Dengue can deteriorate rapidly when fever settles and the critical phase begins. Treatment is mainly careful fluid management and monitoring. Avoid aspirin, ibuprofen, diclofenac and intramuscular injections until significant bleeding risk has been excluded. Use current national/WHO/CDC guidance for fluid volumes, admission and paediatric care.
Why dengue matters
Dengue is an acute infection caused by one of four closely related dengue virus serotypes (DENV-1, DENV-2, DENV-3 and DENV-4). It is transmitted mainly by infected female Aedes aegypti mosquitoes. Most illness is self-limited, but plasma leakage, shock, severe bleeding, liver failure, myocarditis and encephalopathy can develop—often around the time the fever improves.
The key bedside skill is to classify the patient repeatedly. A patient who looks stable during the febrile phase may become critically ill during the 24–48-hour critical phase. Serial examination, haematocrit, urine output, pulse pressure and mental state are more useful than a single platelet count.
Learning outcomes
- Explain dengue serotypes, transmission, pathogenesis and the risk of secondary infection.
- Distinguish undifferentiated dengue, dengue with warning signs and severe dengue.
- Recognise the febrile, critical and recovery phases.
- Interpret CBC, haematocrit, liver tests, NS1/PCR and dengue serology.
- Manage hydration, shock, bleeding, organ dysfunction and safe discharge.
Definition, virology and epidemiology
Dengue virus is an enveloped, positive-sense single-stranded RNA flavivirus. Infection with one serotype usually gives long-lasting immunity to that serotype but only temporary and incomplete protection against the others. A later infection with a different serotype can be more severe in some patients because pre-existing non-neutralising antibodies may facilitate viral entry into Fc-receptor-bearing cells—an immunologic process called antibody-dependent enhancement.
Dengue is endemic in many tropical and subtropical regions. Risk increases with urban crowding, water storage, climate conditions that support mosquito breeding, population movement and low community immunity.
Transmission and incubation
- An infected female Aedes mosquito acquires virus while feeding on a viraemic person.
- After an extrinsic incubation period in the mosquito, it can transmit dengue during later bites.
- Mosquitoes commonly bite during daylight, especially in the early morning and late afternoon.
- Human incubation is usually about 4–10 days.
- Rare non-vector transmission can occur through blood products, organ transplantation or vertical transmission.
Pathophysiology: why severe dengue causes shock
- Virus replicates in dendritic cells, monocytes and macrophages and triggers innate immune responses.
- Cytokines, complement and endothelial mediators alter vascular permeability.
- In severe disease, plasma leaks from the intravascular space into the pleural and abdominal cavities while red cells remain intravascular.
- Intravascular volume falls even though the patient may appear oedematous. Haematocrit rises because plasma is lost but red cells are concentrated.
- If leakage is untreated, tissue perfusion fails, causing metabolic acidosis, organ injury and shock.
- Platelet destruction, marrow suppression and coagulopathy contribute to mucosal or gastrointestinal bleeding.
Interpretation principle: In a patient with warning signs, a rising haematocrit with a falling platelet count suggests ongoing plasma leakage. A falling haematocrit in a shocked patient may instead indicate bleeding or haemodilution after fluids.
Clinical phases
| Phase | Typical timing | What to look for |
|---|---|---|
| Febrile | Usually 2–7 days | High fever, headache, retro-orbital pain, myalgia, arthralgia, nausea, vomiting, rash, mild bleeding and leukopenia |
| Critical | Often around defervescence; about 24–48 hours | Capillary leakage, rising haematocrit, narrow pulse pressure, shock, fluid accumulation, severe bleeding or organ dysfunction |
| Recovery | After leakage stops | Reabsorption of fluid, improved appetite/urine, slowing pulse, convalescent rash and sometimes transient bradycardia |
Clinical manifestations
Uncomplicated dengue
- Sudden high fever, chills and severe headache.
- Retro-orbital pain, photophobia and marked muscle, bone or joint pains (“breakbone fever”).
- Nausea, vomiting, anorexia and abdominal discomfort.
- Macular or maculopapular rash, facial flushing and pruritus during recovery.
- Mild gum or nose bleeding, petechiae or a positive tourniquet test may occur.
- Leukopenia and thrombocytopenia are common; not every low platelet count means severe disease.
Warning signs
- Severe abdominal pain or abdominal tenderness.
- Persistent vomiting or inability to maintain oral fluids.
- Clinical fluid accumulation: ascites, pleural effusion or pericardial effusion.
- Mucosal bleeding, haematemesis, melaena, haematuria or heavy vaginal bleeding.
- Lethargy, restlessness, irritability, confusion or reduced Glasgow Coma Scale.
- Enlarged tender liver.
- Progressively rising haematocrit, especially with rapidly falling platelets.
- Reduced urine output, cold extremities, tachycardia or narrowing pulse pressure.
Severe dengue
Severe dengue is diagnosed when there is one or more of:
- Severe plasma leakage causing shock or respiratory distress from fluid accumulation.
- Severe bleeding judged clinically important, especially with haemodynamic compromise.
- Severe organ involvement: AST/ALT often very high, encephalitis/encephalopathy, myocarditis, arrhythmia, acute kidney injury or other organ failure.
History and examination
| Assess | Questions/examination | Clinical decision |
|---|---|---|
| Timing | Day of illness, day fever settled, prior dengue and travel/outbreak exposure | Predicts the transition into the critical phase |
| Hydration | Oral intake, vomiting, thirst, mucosa, capillary refill, urine volume | Determines oral versus IV fluids |
| Circulation | Pulse, systolic/diastolic BP, pulse pressure, extremity temperature, mental state | Detects compensated shock before hypotension |
| Leakage/bleeding | Abdominal tenderness, ascites, pleural signs, gums, stool, urine, menstrual loss | Guides admission and blood-product decisions |
| Organ function | Glucose, liver size, jaundice, neurologic state, chest findings, ECG | Identifies severe dengue and ICU needs |
| Special groups | Pregnancy, infancy, elderly age, obesity, renal/cardiac disease | Requires lower threshold for observation and careful fluid titration |
Investigations
Baseline and serial tests
- Full blood count: leukopenia, thrombocytopenia and serial haematocrit.
- Haematocrit should be interpreted with the fluid history and bleeding assessment.
- Urea, creatinine, electrolytes, glucose, AST/ALT, bilirubin and albumin.
- Coagulation profile when bleeding, liver failure or severe illness is suspected.
- Chest radiograph or ultrasound for pleural effusion, ascites and pulmonary oedema.
- ECG/troponin/echocardiography when myocarditis or arrhythmia is suspected.
- Malaria testing and cultures when clinically indicated; dengue and malaria can coexist.
Specific dengue tests
- RT-PCR: detects viral RNA early in illness and can identify serotype.
- NS1 antigen: useful in the early febrile period, although sensitivity varies by serotype and whether infection is primary or secondary.
- IgM: usually becomes detectable after approximately day 4–5 and remains detectable for weeks to months.
- IgG: a single positive result often indicates previous flavivirus exposure; paired sera or a fourfold rise is more informative.
Do not exclude dengue because one rapid test is negative. Interpret the test according to day of illness and repeat or use another method if the clinical picture is convincing.
Differential diagnosis
| Condition | Distinguishing points |
|---|---|
| Malaria | Parasitological confirmation; can cause fever, thrombocytopenia, anaemia, jaundice and coma. |
| Chikungunya | Often prominent persistent polyarthritis; thrombocytopenia and leakage usually less dominant. |
| Yellow fever | Jaundice, hepatic failure and outbreak/travel pattern; confirm with appropriate testing. |
| Leptospirosis | Water/animal exposure, conjunctival suffusion, renal failure and jaundice. |
| Typhoid, meningococcaemia and sepsis | Look for focal infection, altered sensorium, persistent shock and positive cultures. |
| Viral hepatitis or acute HIV | Exposure history and specific serology; does not explain every dengue-like presentation. |
Management by severity
Never treat dengue by the platelet count alone. The immediate danger is plasma leakage and shock. Use clinical perfusion, pulse pressure, urine output, mental state, respiratory findings and serial haematocrit to guide fluids.
Group A: outpatient dengue without warning signs
- Encourage frequent oral fluids containing water and electrolytes; continue breastfeeding.
- Give paracetamol for fever within safe dosing limits. Avoid aspirin and NSAIDs.
- Provide written warning signs and a clear return date, especially around days 3–7 or when fever settles.
- Review daily or according to local protocol while fever persists and during the critical window.
- Advise mosquito precautions so an infected patient does not infect local mosquitoes.
Group B: dengue with warning signs
- Admit for close observation, serial vital signs, urine output, haematocrit and platelet trends.
- Start oral fluids if tolerated; use carefully titrated isotonic crystalloid if oral intake is inadequate or perfusion is threatened.
- Reassess after each fluid intervention. Look for improving pulse pressure, capillary refill, mental state and urine output without pulmonary oedema.
- Investigate for occult bleeding, severe organ involvement and alternative diagnoses.
Group C: severe dengue or shock
- Move to a high-dependency or intensive-care area; obtain IV/IO access, blood group and cross-match.
- Give isotonic crystalloid boluses according to current protocol and patient age/weight, then reassess frequently. A common adult teaching approach is 10–20 mL/kg over 15–30 minutes for shock, but local protocols and cardiac/renal status take priority.
- If shock persists, repeat or adjust fluids based on pulse pressure, capillary refill, urine output, lactate, haematocrit and respiratory examination.
- A rising haematocrit with ongoing shock suggests continued leakage and need for more carefully titrated crystalloid/colloid decisions; a falling haematocrit with instability suggests bleeding and need for blood.
- Use packed red cells or whole blood for clinically significant bleeding or suspected occult haemorrhage. Do not give prophylactic platelet transfusions solely because the platelet count is low.
- Correct hypoglycaemia, acidosis, electrolytes, hypoxaemia and temperature abnormalities.
- Use vasopressors in refractory shock after adequate volume assessment and treat myocardial dysfunction when present.
- Manage acute liver failure, encephalopathy, renal failure, myocarditis and respiratory failure with specialist support.
Fluid-management cautions
- Both under-resuscitation and over-resuscitation are dangerous.
- When leakage stops in recovery, fluid is reabsorbed rapidly; continuing the same IV rate may cause pulmonary oedema.
- Reduce or stop IV fluids when perfusion and urine improve, haematocrit stabilises/falls appropriately and oral intake returns.
- Avoid unnecessary colloids, corticosteroids and routine antibiotics unless a separate indication exists.
Prevention and public health
- Remove stagnant water from tyres, containers, roof gutters and discarded objects.
- Cover water storage, use larvicides where appropriate and support municipal vector-control programmes.
- Use repellents, long clothing, window screens and bed nets during daytime rest.
- Patients with fever should avoid mosquito bites during the viraemic period.
- Community education should emphasise that danger can occur when fever improves.
- Vaccination policy depends on the licensed product, age, prior infection, national programme and local risk; consult current Uganda/WHO guidance rather than assuming every traveller or child has the same indication.
Discharge and follow-up
Discharge only when the patient is afebrile and clinically stable, has improving appetite and urine output, no respiratory distress or bleeding, stable haematocrit/platelet trend, and can drink reliably. Explain return precautions: recurrent fever, severe abdominal pain, persistent vomiting, bleeding, drowsiness, breathlessness, cold limbs, reduced urine or yellowing.
Exam-focused pearls
- Dengue has febrile, critical and recovery phases.
- The critical phase often begins around defervescence, not at the height of fever.
- Rising haematocrit with falling platelets suggests plasma leakage.
- Secondary infection with a different serotype can increase severe-disease risk.
- Use paracetamol, not aspirin or NSAIDs.
- Shock may be compensated: narrowing pulse pressure and delayed capillary refill can precede frank hypotension.
- Platelet transfusion is not a substitute for treating leakage or shock.
