Complications of severe falciparum malaria

Complications of severe falciparum malaria • Morbidity and mortality of P. falciparum species is greatest among the malaria species because of its increased parasetemia and its ability to cytoadhere • Mortality rises once vital organ dysfunction occurs or proportion of erythrocytes infected increases to >3% • P. falciparum is also known for developing drug resistance to chloroquine, quinine and tetracycline

Complications • Cerebral malaria • Hypoglycemia • Lactic acidosis • Noncardiogenic pulmonary edema • Renal impairment • Hematologic abnormalities • Liver dysfunction

Cerebral malaria • Coma: characteristic & ominous feature of falciparum malaria; mortality rate of ~0.1%, but if there is vital-organ dysfunction, mortality rises steeply • Manifests as diffuse symmetric encephalopathy • Eyes may be divergent • Muscle tone increase or decrease • ~15% have retinal hemorrhages • Convulsions: generalized; occur up to 50% of children with cerebral malaria

Cerebral malaria • ~15% of children with cerebral malaria have been reported to suffer neurologic deficit when they regain consciousness: • Hemiplegia • Cerebral palsy • Cortical blindness • Deafness • Impaired cognition and learning

Hypoglycemia • Common complication of severe malaria • Associated with poor prognosis • Particularly problematic in children and pregnant women • Results from a failure of hepatic gluconeogenesis & an ↑ in the consumption of glucose both by host & the malaria parasites • Quinine & quinidine are powerful stimulants of pancreatic insulin secretion

Lactic acidosis • Commonly coexists with hypoglycemia • Caused by combination of: • Anaerobic glycolysis in tissues where sequestered parasites interfere with microcirculatory flow • Hypovolemia • Lactate production by the parasites • Failure of hepatic and renal lactate clearance • Coexisting renal impairment compounds acidosis • Acidotic breathing: sign of poor prognosis • Plasma concentrations of bicarbonate or lactate: best biochemical prognosticators in severe malaria

Noncardiogenic pulmonary edema • Mortality rate: >80% • Aggravated by overly vigorous administration of IV fluid • Can also develop in otherwise- uncomplicated vivax malaria (recovery is usual)

Renal impairment • Rare among children • May be related to RBC sequestration interfering with renal microcirculatory flow & metabolism • Manifests as acute tubular necrosis • Early dialysis or hemofiltration enhances the likelihood of a patient’s survival, particularly in acute hypercatabolic renal failure

Hematologic Abnormalities • Anemia • results from accelerated RBC destruction & removal by the spleen in conjunction with ineffective erythropoiesis • both infected & uninfected RBCs show reduced deformability • ↑ splenic clearance of RBCs • Slight coagulation abnormalities & mild thrombocytopenia

Liver Dysfunction • Severe jaundice – more common among adults than children • Results from hemolysis, hepatocyte injury, and cholestasis • Hepatic dysfunction contributes to hypoglycemia, lactic acidosis, and impaired drug metabolism

Complications of severe falciparum malaria