Malaria

Severe malaria is a physiologic emergency - Treated mortality for severe malaria runs 10% to 20%, and roughly 50% in pregnancy. Elective anesthesia waits for treatment; only the genuinely urgent case goes ahead, and it goes ahead in a monitored setting.

Grade the severity before you induce - The two variables that track outcome in both adults and children are level of consciousness on a coma scale and the degree of metabolic acidosis. Get a blood gas with bicarbonate and base deficit, and a plasma lactate — not just a temperature and a parasitemia number.

Anemia comes from three directions at once - Parasites lyse erythrocytes as they replicate and exit, the spleen clears antibody-marked cells, and TNF-alpha suppresses marrow production and iron incorporation. Anemia is present in about 29% of adults and 78% of children with malaria and is worse with P. falciparum, which invades erythrocytes of all ages.

Check the platelet count and coagulation panel before neuraxial - Thrombocytopenia shows up in 60% to 70% of all cases, and severe thrombocytopenia or liver dysfunction extends the coagulation panel into real bleeding risk. Draw a CBC and coags rather than assuming a normal count in a febrile traveler.

Hypoglycemia is expected, not incidental - Severe malaria produces hypoglycemia, and children and second- and third-trimester patients are the highest-risk groups. Check point-of-care glucose at induction and periodically through the case; a general anesthetic hides every symptom of it.

Cerebral malaria is intracranial hypertension - It accounts for 80% of fatal malaria and presents as slow-onset altered mental status, agitation, headache, and fever up to 42 degrees C, followed by coma, acidosis, hypoglycemia, and seizures. Cerebral sequestration, blood-brain barrier failure, and cerebral edema raise brain volume, and increased brain volume is the main contributor to death — manage it as you would any other raised ICP, and treat new-onset seizures as part of the disease.

Dark urine is hemoglobinuria until proven otherwise - Blackwater fever is severe anemia with hemoglobinuria and renal failure from massive intravascular hemolysis, described with repeat P. falciparum infection treated with chronic quinine and associated with G6PD deficiency. Send a urinalysis rather than calling it concentrated urine.

Know the G6PD status before adding an oxidant - Primaquine clears the hepatic hypnozoite phase of P. vivax and P. ovale, and FDA labeling lists severe G6PD deficiency and pregnancy among its contraindications because of hemolytic anemia and fetal hemolysis. If primaquine is on the med list, a G6PD result exists — find it before you add another oxidant drug.

Renal and hepatic involvement changes drug handling - Expect indirect hyperbilirubinemia from hemolysis, hepatocellular injury from parasitic invasion, electrolyte derangement from released intracellular contents, and kidney injury from glomerular damage plus dehydration. Nephrotic-range proteinuria occurs, most commonly with P. malariae and P. knowlesi. Look at the metabolic panel and dose renally cleared drugs to the measured creatinine.

Keep the ECG up on an antimalarial infusion - When IV quinidine is used for severe malaria, continuous cardiac monitoring is required because of arrhythmia risk. A rhythm change in that patient belongs to the drug until you have ruled it out.

Resuscitate to endpoints, not to a volume - Higher initial parasitemia and a poor downtrend correlate with fluid imbalance, renal dysfunction, and respiratory distress syndrome. These patients are dehydrated and acidotic but also prone to pulmonary edema, so titrate to lactate, urine output, and gas exchange.

Splenomegaly changes positioning and retraction - The liver and spleen enlarge and can become massive. Be deliberate about left upper quadrant pressure, abdominal retraction, and positioning; splenic rupture is rare but carries mortality up to 80%.

Pregnancy is the high-risk group - Second- and third-trimester patients develop severe malaria with hypoglycemia and pulmonary edema more often than non-pregnant adults, and malaria in pregnancy raises the risk of prematurity, miscarriage, low birth weight, and stillbirth. Plan for a possible urgent delivery alongside the maternal resuscitation.

Malaria is a protozoal infection with one of five Plasmodium species, transmitted by the female Anopheles mosquito. Sporozoites reach the liver within about an hour, mature into merozoites, then re-enter the blood and invade erythrocytes, consuming hemoglobin and rupturing the cell. That erythrocytic cycle produces the classic paroxysmal fevers and, more importantly at the board, continuous intravascular hemolysis. P. falciparum carries the highest mortality because it invades erythrocytes of every age and makes them cytoadherent, so parasitized cells sequester in capillary beds; free heme plus a TNF-alpha and IFN-gamma driven response activates the endothelium and suppresses hematopoiesis.

Severe disease generally appears around 5% parasitemia and declares itself as cerebral malaria, severe anemia, metabolic acidosis, hypoglycemia, and kidney injury. P. vivax and P. ovale leave dormant hepatic hypnozoites and relapse months to years later.