Management of dengue hemorrhagic fever. Management of dengue hemorrhagic fever.
"dengue hemorrhagic fever" AND management
dengue hemorrhagic fever management fluid resuscitation

This diagnostic comparison presents two anterior-posterior (AP) chest X-rays (labeled A and B) tracking the progression of pulmonary findings in a patient with dengue hemorrhagic fever (DHF) and iatrogenic fluid overload. Image A shows significant bilateral perihilar haze and increased pulmonary vascular markings, consistent with hilar congestion and early pulmonary edema following aggressive fluid resuscitation. The heart silhouette is visible, and the peripheral lung fields remain relatively clear. Image B, taken after the reduction of intravenous fluids and management toward a negative fluid balance, demonstrates a marked resolution of the bilateral hilar congestion. The central lung fields appear clearer with more distinct bronchial markings. Both images show metallic ECG leads overlying the thorax and a central venous catheter. This comparison illustrates the clinical relevance of radiographic monitoring in managing plasma leakage and fluid therapy in DHF patients to prevent and resolve pulmonary congestion.

This diagnostic image is an anteroposterior (AP) chest X-ray demonstrating severe pulmonary edema and pleural effusion in a 19-year-old female patient with Dengue Shock Syndrome. The lung fields show bilateral, diffuse, fluffy opacities and increased interstitial markings, characteristic of pulmonary edema. There is significant blunting of the right costophrenic angle, indicating a right-sided pleural effusion. The cardiac silhouette appears moderately enlarged, and the normal clear visualization of pulmonary vasculature is obscured by interstitial and alveolar infiltrates. ECG electrodes and leads are visible on the chest wall, reflecting an acute clinical monitoring setting. This imaging serves as a critical educational example of 'third space' fluid accumulation and capillary leak syndrome secondary to viral hemorrhagic fever, illustrating the rapid progression of respiratory distress during fluid resuscitation in Dengue Shock Syndrome.

Clinical photograph presenting cutaneous manifestations of Dengue Virus 2 (DV2) infection in a rhesus macaque animal model, serving as a surrogate for human hemorrhagic fever pathology. The image is divided into two primary panels illustrating hematomas and ecchymoses. Panel A displays localized skin lesions on Indian rhesus macaques (labeled RNe11 and RYc11) at Day 7 post-infection. These lesions appear as dark reddish-purple, irregular patches (ecchymoses) and deeper, raised areas of blood accumulation (hematomas). The morphology ranges from diffuse, blotchy purpura to elongated, streak-like hemorrhagic patterns. Panel B shows a Chinese rhesus macaque (GT49) at Day 6 post-infection, highlighting localized hemorrhaging in the perineal region. This area exhibits a patchy distribution of erythema and subcutaneous bleeding against a background of light-colored fur. The visual data demonstrates the clinical spectrum of vasculopathy and coagulopathy associated with acute flavivirus infection, specifically modeling the capillary leak and hemorrhagic tendencies observed in human Dengue Hemorrhagic Fever (DHF).

This clinical photograph displays a diffuse, erythematous maculopapular rash on the abdomen of a patient, characteristic of Dengue fever. The image is presented in a two-part sequence to demonstrate clinical blanching. On the left, a clinician's hand is shown applying direct pressure to the right side of the patient's abdomen. On the right, after the hand is removed, a clear, pale handprint-shaped outline remains where the pressure was applied, indicating that the redness fades (blanches) as blood is temporarily displaced from the superficial vessels. This finding confirms the rash is inflammatory rather than hemorrhagic (petechial/purpuric). The rash is widespread across the torso but typically spares the palms and soles in this clinical presentation. This image serves as a teaching tool for medical students and clinicians to distinguish between vascular inflammatory rashes and non-blanching hemorrhagic lesions in the context of viral hemorrhagic fevers and infectious diseases.
WHO dengue hemorrhagic fever management guidelines 2024 fluid therapy
| Grade | Clinical Features | Lab |
|---|---|---|
| I | Fever + positive tourniquet test, evidence of plasma leakage | Platelets <100,000/mm³, Hct rise ≥20% |
| II | Grade I + spontaneous bleeding (epistaxis, black stools, gum bleeding) | Same |
| III | Grade II + circulatory failure (weak rapid pulse, pulse pressure ≤20 mmHg, hypotension, cold clammy skin, restlessness) | Same |
| IV | Grade III + profound shock - undetectable BP/pulse | Same |


| Principle | Detail |
|---|---|
| Preferred fluids | Isotonic crystalloids: Normal saline or Ringer's lactate |
| Avoid | Hypotonic fluids (risk of hyponatremia and worsening plasma leakage) |
| Colloids (Dextran 40) | Use when crystalloids fail and Hct remains elevated |
| Guide therapy by | Serial hematocrit trends + urine output (target >0.5 ml/kg/h) |
| Discontinue IV when | Patient enters convalescent phase, plasma leakage resolves |
| Watch for fluid overload | During reabsorption phase - falling Hct from dilution, pulmonary edema, ascites |
| High-volume IV | Associated with increased risk of severe dengue progression in recent studies |
| Parameter | Frequency |
|---|---|
| Vital signs (BP, pulse, pulse pressure) | Every 1 hour in critical phase |
| Hematocrit | Every 4-6 hours (or more frequently in shock) |
| Urine output | Every 1-2 hours |
| Platelet count | Daily (or more often if declining rapidly) |
| Blood glucose | Regularly (tight glycemic control) |
| Coagulogram | If bleeding or refractory shock |
| Chest X-ray | If pleural effusion or respiratory distress suspected |
| Complication | Management |
|---|---|
| Severe bleeding/hemorrhage | Blood/blood product transfusion; identify source |
| Acute liver failure | Similar to ALF from other causes |
| Acute kidney injury | Judicious fluid management (target urine >0.5 ml/kg/h); early RRT if needed; CVVH preferred modality |
| ARDS/pulmonary edema | Reduce IV fluids; target negative fluid balance; oxygen/ventilatory support |
| Encephalopathy | Supportive; tight glycemic control; manage cerebral edema |
| Myocarditis | Inotropic support; avoid fluid overload |
| Electrolyte imbalance | Correct acidosis, hyponatremia, hypocalcemia, hypoglycemia |
| Step | Action |
|---|---|
| 1 | Rapid IV isotonic crystalloid 10-20 ml/kg/h for 1 hour + oxygen |
| 2 | Reassess VS and Hct after 1 hour |
| 3 | If improved: stepwise reduction of IV fluid rate |
| 4 | If not improved + Hct high: colloid/crystalloid bolus |
| 5 | If not improved + Hct falling: suspect bleeding → transfuse |
| 6 | Refractory shock: correct ABCS; consider inotropes |
| 7 | Once convalescent: reduce and stop fluids to prevent overload |