Fever with thrombocytopenia: suspect dengue, but assess for severe infection urgently

Emergency referral now for fainting, cold/clammy extremities, confusion, breathing difficulty, severe abdominal pain, persistent vomiting, bleeding, very low urine output, inability to drink, pregnancy, or rapidly worsening condition.

Dengue

1. Typical illness phases

2. Symptoms and signs

Common symptoms

• Sudden high fever
• Severe headache and pain behind the eyes
• Marked muscle, joint, and bone pain
• Fatigue, malaise, anorexia
• Nausea and vomiting
• Diffuse erythematous or maculopapular rash
• Minor mucosal bleeding, petechiae, easy bruising
• Positive tourniquet test may support the diagnosis

Common examination and laboratory findings

• Leukopenia
• Thrombocytopenia
• Mild to moderate AST/ALT elevation, often AST greater than ALT
• Hemoconcentration or rising hematocrit if plasma leakage occurs
• Hepatomegaly
• Pleural effusion or ascites in plasma leakage
• Coagulopathy in severe illness

3. Dengue warning signs

• Severe or persistent abdominal pain/tenderness
• Persistent vomiting
• Clinical fluid accumulation: ascites, pleural effusion
• Mucosal bleeding: gum bleeding, epistaxis, hematemesis, melena, heavy vaginal bleeding
• Lethargy, irritability, restlessness, altered sensorium
• Liver enlargement, especially painful hepatomegaly
• Postural dizziness, poor perfusion, decreasing urine output
• Rapid platelet decline with rising hematocrit

4. Severe dengue / dengue shock

• Narrow pulse pressure, tachycardia, hypotension as a late sign
• Cold extremities, delayed capillary refill, weak pulse
• Restlessness or confusion
• Oliguria
• Metabolic acidosis and rising lactate
• Significant bleeding
• Severe hepatitis, encephalopathy, myocarditis, acute kidney injury
• Respiratory distress due to plasma leakage or fluid overload

Evaluation

History

• Day of illness and whether fever has begun to fall
• Residence or travel in dengue-endemic area in the past 2 weeks
• Mosquito exposure and local outbreak
• Previous dengue infection
• Vomiting, abdominal pain, bleeding, urine output, oral intake
• Pregnancy, infancy/older age, diabetes, kidney/liver/heart disease
• Anticoagulants, antiplatelets, NSAIDs, aspirin, herbal products
• Malaria exposure
• VHF risk: travel to an outbreak/endemic area; contact with blood/body fluids of a sick person; healthcare exposure; tick exposure; animal, bat, rodent, or bushmeat exposure

Examination and monitoring

• Frequent vital signs, pulse pressure, capillary refill, peripheral temperature, mental status
• Accurate intake-output chart and urine output
• Weight, fluid balance, chest examination for crackles/effusions
• Assess skin/mucosal bleeding, hepatomegaly, abdominal tenderness, ascites
• Repeat assessment frequently during the critical phase

Initial tests

• CBC with hematocrit and platelet trend, not a single value alone
• Blood group and crossmatch if bleeding or severe disease
• Liver and renal profile, glucose, electrolytes
• PT/INR, aPTT, fibrinogen if bleeding, shock, liver dysfunction, or suspected DIC
• Venous/arterial blood gas and lactate if severe illness/shock
• Urinalysis and pregnancy test where appropriate
• Chest ultrasound/X-ray or bedside ultrasound if suspected effusion/ascites
• Blood cultures and sepsis work-up if clinically indicated
• Malaria smear/rapid test in endemic or returning travellers

Dengue-specific testing

• Days 0-7: dengue NAAT/RT-PCR or NS1 antigen, with IgM often added
• After day 7: dengue IgM serology, with confirmatory testing as appropriate

Management

General principles

Do

• Use paracetamol/acetaminophen for fever and pain
• Encourage oral fluids if able to drink and not vomiting
• Give clear return precautions and arrange daily reassessment during the risk period
• Monitor serial hematocrit, platelet count, vital signs, perfusion, and urine output
• Use isotonic crystalloid fluids when IV fluids are required
• Refer/admit when warning signs, inability to tolerate fluids, significant comorbidity, pregnancy, unreliable follow-up, or social barriers are present

Avoid

• Aspirin, ibuprofen, diclofenac, naproxen, and other NSAIDs
• Intramuscular injections and unnecessary invasive procedures
• Empiric platelet transfusion solely because the platelet count is low
• Excessive IV fluid administration, especially after the leak phase ends

A. Dengue without warning signs

• Is hemodynamically stable
• Can drink and maintain urine output
• Has no bleeding or warning signs
• Has reliable follow-up and access to urgent care

• Oral rehydration
• Paracetamol only
• Daily clinical review and CBC/hematocrit trend during the febrile-to-critical transition
• Return immediately if warning signs occur

B. Dengue with warning signs, but no shock

• Obtain hematocrit before fluids if this does not delay treatment.
• Start isotonic crystalloid fluid therapy and reassess frequently.
• A commonly used initial approach is 5-7 mL/kg/hour for 1-2 hours, then step down if perfusion and oral intake improve.
• Reassess pulse, blood pressure/pulse pressure, capillary refill, respiratory status, urine output, hematocrit, and fluid balance after each intervention.
• If hematocrit rises with ongoing poor perfusion, continued plasma leakage is likely and fluid escalation may be needed.
• If hematocrit falls with instability, suspect occult bleeding and arrange urgent blood-product evaluation.

C. Severe dengue or shock

• ABCDE approach, oxygen if hypoxemic or in respiratory distress
• Two IV lines if feasible, blood samples and crossmatch
• Prompt isotonic crystalloid bolus, usually weight-based, followed by reassessment after each bolus
• Monitor continuously and measure urine output, ideally with catheterization in shock
• Escalate to senior clinician/ICU early
• If shock persists, use hematocrit trend and clinical assessment to distinguish persistent leakage from hemorrhage
• Give packed red cells or whole blood for major bleeding or suspected bleeding with hemodynamic compromise, according to local protocol
• Avoid fluid overload. Pulmonary edema/respiratory distress can result from excessive fluids, particularly during recovery.

When to suspect a non-dengue viral hemorrhagic fever

• Contact with blood/body fluids of a person with a suspected VHF
• Healthcare exposure without appropriate PPE
• Exposure to bats, rodents, livestock, animal carcasses, or bushmeat in a relevant region
• Tick bite or livestock slaughter exposure in CCHF-risk regions
• Recent travel to a known outbreak area

Immediate action if VHF is plausible

1. Isolate immediately and avoid unnecessary procedures.
2. Use appropriate PPE and follow local infection-control protocols.
3. Notify hospital infection prevention, infectious diseases, and public-health authorities urgently.
4. Coordinate diagnostic testing with public health. Do not send samples casually or without laboratory notification.
5. Provide supportive resuscitation while maintaining infection-control precautions.

Practical take-home point

What is motor aphasia?

• Speech is sparse, effortful, slow, and “telegraphic”
• Naming and repetition are impaired
• Comprehension is relatively preserved, especially for simple commands
• Writing may also be impaired
• The patient is often aware of the deficit and frustrated

Most likely site of infarct

• Broca area in the posterior inferior frontal gyrus
  • Pars opercularis, Brodmann area 44
  • Pars triangularis, Brodmann area 45
• Adjacent frontal operculum, insula, and subcortical white matter can be involved.
• Vascular territory: superior division of the left middle cerebral artery (MCA), often an M2 superior-division branch.

Acute infarct in the dominant left frontal lobe, supplied by the superior division of the left MCA.

Important differential localization

Possible causes of the infarct

1. Cardioembolism
   • Atrial fibrillation
   • Recent myocardial infarction or ventricular thrombus
   • Valvular disease or infective endocarditis
   • Cardiomyopathy
   • Patent foramen ovale in selected younger patients
2. Large-artery atherosclerosis
   • Left internal carotid artery stenosis/occlusion
   • Carotid plaque embolism
   • Intracranial left MCA atherosclerotic stenosis
3. Small-vessel disease
   • Less likely to cause a classical cortical Broca aphasia in isolation, but can contribute through subcortical infarcts.
4. Arterial dissection
   • Especially carotid dissection in younger patients, after neck trauma/manipulation, or with neck pain and Horner syndrome.
5. Other causes
   • Hypercoagulable state, malignancy, vasculitis, antiphospholipid syndrome
   • Cocaine/amphetamine-related vasospasm
   • Septic embolus

Immediate evaluation

• Establish last-known-well time
• Check glucose immediately, as hypoglycemia can mimic stroke
• NIH Stroke Scale and focused neurological examination
• Non-contrast CT head urgently to exclude hemorrhage
• CT angiography of head and neck to detect left ICA/MCA occlusion
• CT perfusion or MRI diffusion/perfusion where available and appropriate
• ECG/telemetry for atrial fibrillation
• CBC, electrolytes/renal function, coagulation profile, troponin, glucose
• Echocardiography and vascular imaging for stroke mechanism

Practical one-line answer

Sudden motor aphasia most commonly indicates an acute ischemic infarct of Broca area in the dominant, usually left, inferior frontal gyrus, due to occlusion of the superior division of the left MCA. Common mechanisms are cardioembolism, carotid/MCA atherosclerotic embolism, and less commonly carotid dissection or hypercoagulability.