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Emergency and Acute Medicine – Malaria
Basics description
Malaria is a protozoan infection transmitted through the bite of an infected female Anopheles mosquito. The incubation period is typically 8–16 days, although symptoms may be delayed for months depending on the species. The periodic nature of malaria symptoms reflects the parasite life cycle, which includes an exoerythrocytic phase in the liver followed by an erythrocytic phase in red blood cells. Fever corresponds to synchronous red blood cell lysis and release of merozoites into the circulation.
Pathophysiology and species differences
In the exoerythrocytic phase, sporozoites migrate to the liver and multiply into merozoites. These then enter the bloodstream and invade red blood cells, where replication leads to cell rupture every 48–72 hours. Plasmodium falciparum causes most severe disease and nearly all malaria-related deaths. It infects red blood cells of all ages, leading to profound hemolysis, anemia, and capillary obstruction with resultant end-organ hypoxia. Plasmodium vivax and Plasmodium ovale may cause relapsing disease due to dormant liver forms (hypnozoites), while Plasmodium malariae can persist at low levels in the bloodstream for decades.
Etiology and transmission
Transmission usually occurs via mosquito bite but may also result from blood transfusions or shared needles. Rare autochthonous transmission has been reported in North America due to the presence of Anopheles mosquitoes. Post-traumatic immunosuppression may precipitate relapse in individuals previously exposed in endemic regions. Children with sickle cell trait have partial protection, while pregnant patients—especially primigravidas—are at higher risk for severe disease.
Diagnosis signs and symptoms
Most patients become symptomatic within one year of exposure. Common symptoms include malaise, chills, fever greater than 38°C, myalgias, arthralgias, and orthostatic hypotension. The classic malaria paroxysm consists of chills followed by high fever and subsequent diaphoresis, although this pattern is uncommon in clinical practice. Hemolysis may lead to jaundice, dark urine (blackwater fever), anemia, and splenomegaly. Severe manifestations include cerebral malaria with headache, altered mental status, seizures, or coma; pulmonary edema; renal failure; abnormal bleeding; and circulatory collapse.
Essential workup and diagnostic testing
Diagnosis relies on oil immersion light microscopy of thick and thin Giemsa-stained blood smears, which demonstrate intraerythrocytic parasites. At least three negative smears over 48 hours are required to exclude malaria. Laboratory findings commonly include anemia, thrombocytopenia, leukocytopenia, elevated bilirubin and lactate dehydrogenase, electrolyte abnormalities, and evidence of renal or hepatic dysfunction. Chest radiography may reveal pulmonary edema. Advanced testing such as antigen detection assays or PCR can identify Plasmodium species and mixed infections. Lumbar puncture may be necessary to distinguish cerebral malaria from meningitis.
Differential diagnosis
The differential includes meningitis, encephalitis, sepsis, acute renal failure, viral hepatitis, acute hemolytic anemia, hypoglycemic coma, and heat stroke. In travelers or immigrants from endemic areas, malaria must be considered in any febrile illness.
Treatment and emergency management
Initial stabilization includes airway, breathing, and circulation management, isotonic fluid resuscitation for hypotension, active cooling for hyperthermia, and treatment of hypoglycemia or seizures as indicated. Antimalarial therapy depends on species, severity, and geographic resistance patterns, with artemisinin-based combination therapies recommended as first-line treatment worldwide. Severe P. falciparum infection requires intravenous artesunate. Supportive care for complications such as anemia, renal failure, and cerebral edema is critical.
Disposition and follow-up
ICU admission is indicated for severe P. falciparum malaria, high parasitemia, neurologic involvement, or inability to tolerate oral therapy. Patients with non–P. falciparum malaria who are clinically stable and able to take oral medications may be treated as outpatients with close follow-up.
Pearls and pitfalls
Malaria should always be considered in patients with fever and compatible exposure history, even months after travel. Fever patterns are unreliable, and early recognition is essential, as delays in treatment—especially with P. falciparum—are associated with high mortality.
Basics description
Malaria is a protozoan infection transmitted through the bite of an infected female Anopheles mosquito. The incubation period is typically 8–16 days, although symptoms may be delayed for months depending on the species. The periodic nature of malaria symptoms reflects the parasite life cycle, which includes an exoerythrocytic phase in the liver followed by an erythrocytic phase in red blood cells. Fever corresponds to synchronous red blood cell lysis and release of merozoites into the circulation.
Pathophysiology and species differences
In the exoerythrocytic phase, sporozoites migrate to the liver and multiply into merozoites. These then enter the bloodstream and invade red blood cells, where replication leads to cell rupture every 48–72 hours. Plasmodium falciparum causes most severe disease and nearly all malaria-related deaths. It infects red blood cells of all ages, leading to profound hemolysis, anemia, and capillary obstruction with resultant end-organ hypoxia. Plasmodium vivax and Plasmodium ovale may cause relapsing disease due to dormant liver forms (hypnozoites), while Plasmodium malariae can persist at low levels in the bloodstream for decades.
Etiology and transmission
Transmission usually occurs via mosquito bite but may also result from blood transfusions or shared needles. Rare autochthonous transmission has been reported in North America due to the presence of Anopheles mosquitoes. Post-traumatic immunosuppression may precipitate relapse in individuals previously exposed in endemic regions. Children with sickle cell trait have partial protection, while pregnant patients—especially primigravidas—are at higher risk for severe disease.
Diagnosis signs and symptoms
Most patients become symptomatic within one year of exposure. Common symptoms include malaise, chills, fever greater than 38°C, myalgias, arthralgias, and orthostatic hypotension. The classic malaria paroxysm consists of chills followed by high fever and subsequent diaphoresis, although this pattern is uncommon in clinical practice. Hemolysis may lead to jaundice, dark urine (blackwater fever), anemia, and splenomegaly. Severe manifestations include cerebral malaria with headache, altered mental status, seizures, or coma; pulmonary edema; renal failure; abnormal bleeding; and circulatory collapse.
Essential workup and diagnostic testing
Diagnosis relies on oil immersion light microscopy of thick and thin Giemsa-stained blood smears, which demonstrate intraerythrocytic parasites. At least three negative smears over 48 hours are required to exclude malaria. Laboratory findings commonly include anemia, thrombocytopenia, leukocytopenia, elevated bilirubin and lactate dehydrogenase, electrolyte abnormalities, and evidence of renal or hepatic dysfunction. Chest radiography may reveal pulmonary edema. Advanced testing such as antigen detection assays or PCR can identify Plasmodium species and mixed infections. Lumbar puncture may be necessary to distinguish cerebral malaria from meningitis.
Differential diagnosis
The differential includes meningitis, encephalitis, sepsis, acute renal failure, viral hepatitis, acute hemolytic anemia, hypoglycemic coma, and heat stroke. In travelers or immigrants from endemic areas, malaria must be considered in any febrile illness.
Treatment and emergency management
Initial stabilization includes airway, breathing, and circulation management, isotonic fluid resuscitation for hypotension, active cooling for hyperthermia, and treatment of hypoglycemia or seizures as indicated. Antimalarial therapy depends on species, severity, and geographic resistance patterns, with artemisinin-based combination therapies recommended as first-line treatment worldwide. Severe P. falciparum infection requires intravenous artesunate. Supportive care for complications such as anemia, renal failure, and cerebral edema is critical.
Disposition and follow-up
ICU admission is indicated for severe P. falciparum malaria, high parasitemia, neurologic involvement, or inability to tolerate oral therapy. Patients with non–P. falciparum malaria who are clinically stable and able to take oral medications may be treated as outpatients with close follow-up.
Pearls and pitfalls
Malaria should always be considered in patients with fever and compatible exposure history, even months after travel. Fever patterns are unreliable, and early recognition is essential, as delays in treatment—especially with P. falciparum—are associated with high mortality.
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