Malaria in Children: Clinical Case and Viva Q&A

1. Clinical Case of Malaria in Children

Case: Severe Malaria in a 4-year-old Child

A 4-year-old boy is brought to the emergency department by his parents with a 3-day history of high fever, lethargy, and decreased appetite. The family had recently returned from a 2-week vacation in sub-Saharan Africa.

Clinical Presentation:

• Temperature: 39.8°C (103.6°F)
• Heart rate: 130 bpm
• Respiratory rate: 32 breaths/min
• Blood pressure: 85/50 mmHg
• Oxygen saturation: 94% on room air

Physical examination reveals:

• Pallor
• Mild jaundice
• Hepatosplenomegaly
• Decreased level of consciousness (Glasgow Coma Scale: 12)

Laboratory Findings:

• Complete blood count: Hemoglobin 7.2 g/dL, Platelets 45,000/µL
• Blood smear: P. falciparum parasitemia (8% of RBCs infected)
• Blood glucose: 54 mg/dL
• Serum creatinine: 1.2 mg/dL
• Total bilirubin: 3.5 mg/dL

Diagnosis:

Severe malaria caused by Plasmodium falciparum

Management:

1. Admission to pediatric intensive care unit
2. Intravenous artesunate: 2.4 mg/kg at 0, 12, and 24 hours, then daily
3. Fluid resuscitation and maintenance
4. Glucose monitoring and correction of hypoglycemia
5. Blood transfusion (packed red blood cells)
6. Close monitoring of vital signs, urine output, and neurological status
7. Supportive care as needed

Outcome:

With prompt treatment, the child's condition improved over the next 72 hours. Parasitemia cleared, fever resolved, and consciousness returned to normal. The patient was discharged after 7 days with oral antimalarial medication to complete the course.

2. Clinical Presentations of Malaria in Children

Varieties of Clinical Presentations of Malaria in Children

1. Uncomplicated Malaria

   • Fever (may be intermittent or continuous)
   • Chills and rigors
   • Headache
   • Myalgia
   • Fatigue
   • Nausea and vomiting
   • Abdominal pain
   • Mild anemia
   • Splenomegaly

2. Cerebral Malaria

   • Impaired consciousness or coma
   • Seizures
   • Focal neurological deficits
   • Retinal changes (retinal whitening, vessel changes, hemorrhages)
   • Abnormal posturing

3. Severe Malarial Anemia

   • Severe pallor
   • Tachycardia
   • Tachypnea
   • Lethargy
   • Hemoglobin <5 g/dL or hematocrit <15%

4. Respiratory Distress Syndrome

   • Deep breathing
   • Intercostal retractions
   • Use of accessory muscles
   • Nasal flaring
   • Pulmonary edema

5. Metabolic Acidosis

   • Deep, labored breathing (Kussmaul respiration)
   • Lethargy
   • Vomiting
   • Altered mental status

6. Hypoglycemia

   • Altered consciousness
   • Sweating
   • Tachycardia
   • Seizures

7. Acute Kidney Injury

   • Oliguria or anuria
   • Edema
   • Elevated serum creatinine

8. Jaundice and Hepatic Dysfunction

   • Yellow discoloration of sclera and skin
   • Right upper quadrant tenderness
   • Hepatomegaly
   • Elevated liver enzymes and bilirubin

9. Disseminated Intravascular Coagulation (DIC)

   • Bleeding from multiple sites
   • Petechiae
   • Purpura
   • Prolonged clotting times

10. Algid Malaria (Shock)

    • Hypotension
    • Cold, clammy skin
    • Weak pulse
    • Decreased urine output

3. Viva Questions and Answers on Malaria in Children

Viva Questions and Answers on Malaria in Children

1. Q: What are the four main species of Plasmodium that cause malaria in humans, and which is the most severe in children?

   A: The four main species are Plasmodium falciparum, P. vivax, P. ovale, and P. malariae. P. falciparum is the most severe and life-threatening, especially in children.

2. Q: What is the incubation period for P. falciparum malaria?

   A: The incubation period for P. falciparum is typically 9-14 days, but can range from 7 to 30 days.

3. Q: Define severe malaria according to WHO criteria in children.

   A: WHO defines severe malaria in children as the presence of P. falciparum asexual parasitemia and one or more of the following: impaired consciousness, prostration, multiple convulsions, acidosis, hypoglycemia, severe malarial anemia, renal impairment, jaundice, pulmonary edema, significant bleeding, shock, or hyperparasitemia.

4. Q: What is the gold standard for diagnosing malaria?

   A: The gold standard for malaria diagnosis is microscopic examination of Giemsa-stained thick and thin blood smears.

5. Q: What are the advantages of Rapid Diagnostic Tests (RDTs) in malaria diagnosis?

   A: RDTs are quick (results in 15-20 minutes), easy to use, don't require electricity or special equipment, and can be performed by healthcare workers with minimal training.

6. Q: What is the first-line treatment for uncomplicated P. falciparum malaria in most endemic areas?

   A: The first-line treatment is Artemisinin-based Combination Therapy (ACT), such as artemether-lumefantrine or artesunate-amodiaquine, as recommended by WHO.

7. Q: What is the recommended treatment for severe malaria in children?

   A: Intravenous artesunate is the recommended first-line treatment for severe malaria in children, given at 2.4 mg/kg at 0, 12, and 24 hours, then daily until oral therapy can be tolerated.

8. Q: How is cerebral malaria defined in children?

   A: Cerebral malaria in children is defined as unarousable coma (Blantyre Coma Score ≤2 in young children or Glasgow Coma Score ≤9 in older children) persisting for more than 1 hour after a seizure, with asexual forms of P. falciparum in peripheral blood, and no other obvious cause of coma.

9. Q: What are the potential long-term neurological sequelae of cerebral malaria in children?

   A: Long-term sequelae may include cognitive impairment, epilepsy, behavioral disorders, motor deficits, visual impairment, and speech and language disorders.

10. Q: How is severe malarial anemia defined in children?

    A: Severe malarial anemia is defined as a hemoglobin concentration <5 g/dL or a hematocrit <15% in the presence of P. falciparum parasitemia >10,000/μL.

11. Q: What is the management of severe malarial anemia?

    A: Management includes blood transfusion (packed red blood cells or whole blood), intravenous artesunate, and supportive care. The WHO recommends transfusion for Hb <4 g/dL, or Hb <6 g/dL with signs of distress.

12. Q: What causes hypoglycemia in severe malaria, and how is it managed?

    A: Hypoglycemia is caused by impaired gluconeogenesis, increased glucose consumption by the parasite, and quinine-induced hyperinsulinemia. It's managed with IV glucose (2-4 mL/kg of 10% dextrose) followed by continuous glucose infusion and frequent monitoring.

13. Q: What is blackwater fever in malaria?

    A: Blackwater fever is a complication of severe malaria characterized by massive intravascular hemolysis, hemoglobinuria, and acute kidney injury. It's associated with G6PD deficiency and certain antimalarial drugs.

14. Q: How does P. falciparum cause severe malaria?

    A: P. falciparum causes severe malaria through cytoadherence of infected RBCs to endothelial cells, leading to microvascular obstruction, tissue hypoxia, and inflammatory responses. It also induces rosetting and sequestration in various organs.

15. Q: What is the role of exchange transfusion in severe malaria?

    A: Exchange transfusion is rarely used now but was historically considered for hyperparasitemia (>10%). Current WHO guidelines do not recommend routine use of exchange transfusion.

16. Q: How does acquired immunity to malaria develop in children living in endemic areas?

    A: Immunity develops gradually with repeated exposures. Children first develop immunity to severe disease, then to symptomatic infection, and finally to parasitemia. However, sterile immunity is rarely achieved.

17. Q: What is tropical splenomegaly syndrome (hyperreactive malarial splenomegaly)?

    A: It's a chronic complication of malaria characterized by massive splenomegaly, hepatomegaly, and hypersplenism. It's associated with overproduction of IgM and is seen in areas with intense P. falciparum transmission.

18. Q: How does placental malaria affect the newborn?

    A: Placental malaria can lead to low birth weight, preterm delivery, intrauterine growth restriction, and increased susceptibility to malaria in infancy.

19. Q: What is the recommended chemoprophylaxis for children traveling to malaria-endemic areas?

    A: Options include atovaquone-proguanil, mefloquine, or doxycycline (for children >8 years). The choice depends on the destination, duration of stay, and local resistance patterns.

20. Q: How does malaria affect the immune system in children?

    A: Malaria causes immunosuppression by impairing T-cell function, altering cytokine profiles, and inducing regulatory T-cells. This can increase susceptibility to other infections, particularly invasive bacterial infections.

21. Q: What is artemisinin resistance, and how does it impact malaria treatment in children?

    A: Artemisinin resistance is characterized by delayed parasite clearance after treatment with artemisinin-based therapies. It necessitates longer treatment courses, alternative drug combinations, and poses a significant threat to malaria control efforts.

22. Q: How does congenital malaria present, and how is it managed?

    A: Congenital malaria typically presents 2-6 weeks after birth with fever, irritability, poor feeding, and anemia. Diagnosis is by blood smear, and treatment is with oral ACT, adjusting doses for the infant's weight.

23. Q: What is the role of primaquine in treating malaria in children?

    A: Primaquine is used to eliminate hypnozoites in P. vivax and P. ovale infections, preventing relapses. It's also used as a gametocytocidal agent in P. falciparum malaria to reduce transmission. However, it's contraindicated in G6PD-deficient individuals and typically not given to children under 6 months.

24. Q: How does malnutrition affect the clinical course of malaria in children?

    A: Malnutrition can mask the typical signs of malaria, alter drug metabolism, and increase the risk of severe malaria and death. Malnourished children may have atypical presentations and require careful monitoring during treatment.

25. Q: What is the significance of retinopathy in cerebral malaria?

    A: Malarial retinopathy (characterized by retinal whitening, vessel changes, and hemorrhages) is highly specific for cerebral malaria. Its presence helps differentiate true cerebral malaria from coma due to other causes in endemic areas.

26. Q: How does sickle cell trait affect malaria in children?

    A: Sickle cell trait (HbAS) provides protection against severe P. falciparum malaria. Children with sickle cell trait have a reduced risk of severe malaria and death compared to those with normal hemoglobin (HbAA).

27. Q: What is the rationale behind Seasonal Malaria Chemoprevention (SMC) in children?

    A: SMC involves administering antimalarial drugs (usually sulfadoxine-pyrimethamine plus amodiaquine) to children monthly during the high transmission season. It's recommended in areas with highly seasonal malaria transmission to reduce morbidity and mortality in children under 5 years.

28. Q: How does malaria affect the growth and development of children in endemic areas?

    A: Chronic or recurrent malaria can lead to growth stunting, cognitive impairment, and reduced school performance. It can also cause chronic anemia, which further impacts physical and cognitive development.

29. Q: What is post-artesunate delayed hemolysis, and how is it managed in children?

    A: Post-artesunate delayed hemolysis is a complication occurring 1-3 weeks after treatment with artesunate for severe malaria. It's managed with close monitoring of hemoglobin levels and blood transfusion if necessary. The benefits of artesunate still outweigh this risk in severe malaria.