Impaired skeletal muscle microvascular function and increased skeletal muscle oxygen consumption in severe falciparum malaria

Background: Organ dysfunction and tissue hypoxia in severe falciparummalaria result from an imbalance between oxygen delivery and demand. In severemalaria, microvascular obstruction from parasite sequestration decreases oxygendelivery. However, host microvascular function (defined as the capacity toincrease oxygen delivery in response to ischemia) and oxygen consumption havenot been assessed.

Methods: Weused near-infrared resonance spectroscopy to measure thenar musclemicrovascular function (StO₂recov) and oxygen consumption (VO₂) in 36 adults in Papua, Indonesia, withsevere malaria, 33 with moderately severe malaria (MSM), 24 with severe sepsis,and 36 healthy controls.

Results: Inthe severe malaria group, the StO₂recov of 2.7%/second was 16% and 22%lower than that in the MSM group (3.1%/second) and control group (3.5%/second),respectively (P < .001), and comparable to thatin the severe sepsis group (2.5%/second). In the severe malaria group, StO₂recov was inversely correlated withlactate level (r = −0.63; P < .001) and predicted death(area under the receiver operating characteristic curve, 0.71 [95% confidenceinterval {CI}, .51–.92]), with each percentage decrease associated with anincreased odds of mortality (odds ratio, 2.49 [95% CI, 1.05–6.2]). Conversely,VO₂ increasedin the severe malaria group by 18%, compared with levels in the control andsevere sepsis groups (P <.001), and was associated with parasite biomass (r =0.49; P = .04).

 

Conclusions: Impaired microvascular function is associated with increasedmortality among individuals with severe malaria, while oxygen consumption isincreased. Tissue hypoxia may result not only from microvascular obstruction,but also from impaired ability of the microvasculature to match oxygen deliveryto increased oxygen demand.