What are the complications of dengue fever and how are they managed?

Complications of Dengue Fever and Their Management

Major Complications

The most serious complications of dengue fever are dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), which are characterized by plasma leakage, hemorrhage, and potentially fatal shock, with mortality rates of 1-5% when severe. 1, 2

Dengue Hemorrhagic Fever (DHF)

• DHF is defined by minor or major bleeding phenomena, thrombocytopenia (low platelet count), and evidence of plasma leakage from blood vessels into tissues 1
• Plasma leakage manifests as pleural effusion, fluid accumulation in the abdominal cavity, or hemoconcentration (rising hematocrit levels) 3
• This leakage typically lasts only 48 hours and resolves spontaneously if properly managed 3

Dengue Shock Syndrome (DSS)

• DSS includes all DHF criteria plus hypotension or narrow pulse pressure (≤10 mmHg) 1
• Shock results from increased vascular permeability and low intravascular volume, with endothelial dysfunction occurring abruptly 3
• Colloids should be immediately administered to children presenting with pulse pressure at or below 10 mmHg 4

Warning Signs Requiring Immediate Attention

The following danger signs indicate potential progression to severe dengue and warrant immediate hospitalization: 5

• Persistent vomiting 5
• Severe abdominal pain or tenderness (particularly right upper quadrant due to liver involvement) 5
• Clinical fluid accumulation (pleural effusion, ascites) 5
• Mucosal bleeding 5
• Lethargy or restlessness 5
• Hepatomegaly (liver enlargement) 5
• Hematocrit rise with concurrent rapid platelet drop 5

These warning signs typically appear around days 3-7 of illness, coinciding with defervescence (when fever subsides) 5

Hemorrhagic Complications

• Bleeding in dengue is most likely caused by activated platelets resulting from damaged capillary endothelium, not simply from low platelet counts 4
• A critical pitfall: platelet or blood transfusions should NOT be administered based on platelet count alone 4
• Low platelet counts do not predict clinically significant bleeding 4
• DHF and DSS cases frequently have compensated consumptive coagulopathy that seldom requires treatment 4
• Blood transfusion is only necessary for significant active bleeding with hemodynamic compromise 1

Management of Complications

Fluid Resuscitation for Shock

• For DSS, administer an initial fluid bolus of 20 mL/kg with careful reassessment afterward 1
• Normal saline alone can safely treat DHF and DSS 4
• Consider colloid solutions for severe shock when available, particularly for persistent tissue hypoperfusion despite adequate crystalloid resuscitation 1
• Vasopressors such as dopamine or epinephrine may be required for persistent hypoperfusion despite adequate fluid resuscitation 1

Monitoring Requirements

• Daily complete blood count monitoring is essential to track platelet counts and hematocrit levels 1
• Continuous cardiac telemetry and pulse oximetry monitoring for patients with DSS 1
• Mean arterial blood pressure (MAP) monitoring can detect plasma leakage earlier than hematocrit values alone 3
• Ultrasonographic measurement (such as gallbladder wall thickening) can detect plasma leakage in the early phase with positive likelihood ratio 2.14 3

Secondary Infections

• Obtain blood and urine cultures and chest radiograph if fever persists beyond 5 days of treatment 1
• Broaden management to include coverage for potential secondary bacterial infections in hemodynamically unstable patients 1
• Avoid the pitfall of changing antibiotics based solely on persistent fever pattern without clinical deterioration or new findings 1

Critical Pitfalls to Avoid

• Never use aspirin or NSAIDs under any circumstances due to high bleeding risk 1
• Do not delay fluid resuscitation in patients showing signs of shock 1
• Do not transfuse platelets or blood products based on laboratory values alone without active bleeding 4
• Most fatal cases relate to late detection of illness with massive hemorrhage and severe intravascular volume depletion 3

Underlying Mechanisms

• Severe dengue involves immune-mediated cytokine storm with activation of both innate and adaptive immune systems 6
• The transient period of vascular leakage suggests effects of short-lived biological mediators 6
• Non-neutralizing cross-reactive antibodies from prior dengue infections can increase virus uptake and viral replication, contributing to severity 3
• Higher NS1 protein levels correlate with more severe disease 3

Risk Factors for Severe Disease

• Females, infants, elderly patients, and those with concomitant diseases are prone to more severe infection 3
• Secondary infection with a different dengue serotype increases risk of severe disease 3, 4
• Human leukocyte antigen alleles correlate with both protection and susceptibility to DHF and DSS 4