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

Tsin Yeo, Daniel Lampah, Emiliana Tjitra, Enny Kenangalem, Ric Price, Nicholas Anstey

Research output: Contribution to journalArticleResearchpeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)528-536
Number of pages9
JournalJournal of Infectious Diseases
Volume207
Issue number3
DOIs
Publication statusPublished - 2012

Fingerprint

Falciparum Malaria
Oxygen Consumption
Malaria
Skeletal Muscle
Oxygen
Sepsis
Parasites
Indonesia
Near-Infrared Spectroscopy
Microvessels
ROC Curve
Biomass
Ischemia
Odds Ratio
Control Groups
Mortality

Cite this

@article{106e5768ff644bc6b3aaba62f05104e8,
title = "Impaired skeletal muscle microvascular function and increased skeletal muscle oxygen consumption in severe falciparum malaria",
abstract = "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.",
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Impaired skeletal muscle microvascular function and increased skeletal muscle oxygen consumption in severe falciparum malaria. / Yeo, Tsin; Lampah, Daniel; Tjitra, Emiliana; Kenangalem, Enny; Price, Ric; Anstey, Nicholas.

In: Journal of Infectious Diseases, Vol. 207, No. 3, 2012, p. 528-536.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Impaired skeletal muscle microvascular function and increased skeletal muscle oxygen consumption in severe falciparum malaria

AU - Yeo, Tsin

AU - Lampah, Daniel

AU - Tjitra, Emiliana

AU - Kenangalem, Enny

AU - Price, Ric

AU - Anstey, Nicholas

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

KW - ampicillin

KW - antibiotic agent

KW - artemisinin

KW - artesunate

KW - ceftriaxone

KW - gentamicin

KW - lactic acid

KW - oxygen

KW - adult

KW - area under the curve

KW - article

KW - controlled study

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KW - disease association

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KW - female

KW - human

KW - hypoxemia

KW - Indonesia

KW - lactate blood level

KW - major clinical study

KW - malaria falciparum

KW - male

KW - microbial biomass

KW - microvasculature

KW - mortality

KW - muscle metabolism

KW - near infrared resonance spectroscopy

KW - near infrared spectroscopy

KW - oxygen consumption

KW - predictive value

KW - priority journal

KW - protein blood level

KW - receiver operating characteristic

KW - septic shock

KW - skeletal muscle

KW - Article

KW - clinical article

KW - drug substitution

KW - hand function

KW - oxygen transport

KW - sepsis

KW - thenar

KW - Adolescent

KW - Adult

KW - Biological Markers

KW - Female

KW - Humans

KW - Malaria, Falciparum

KW - Male

KW - Microvessels

KW - Middle Aged

KW - Muscle, Skeletal

KW - Oxygen Consumption

KW - ROC Curve

KW - Severity of Illness Index

KW - Spectroscopy, Near-Infrared

KW - Young Adult

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DO - 10.1093/infdis/jis692

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EP - 536

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

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