Mortality After Burn Injury in Children: A 33-year Population-Based Study

Duke, Janine M.; Rea, Suzanne; Boyd, James H.; Randall, Sean; Wood, Fiona

doi:10.1542/peds.2014-3140

Cited by 71 publications

(35 citation statements)

References 47 publications

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“…based on differential responsive burn treatments and is the standard classification used in Western Australia Population-based Burn Injury Project studies. 24,33,34 Baseline comorbidity (yes/no) was assessed with a 5-year lookback period 35 using the Charlson comorbidity index 36 and the principal and additional diagnoses data in the hospital morbidity records. Congenital anomaly was identified using principal and additional diagnoses (ICD-10-AM: Q00-G99).…”

Section: Methodsmentioning

confidence: 99%

Respiratory Morbidity After Childhood Burns: A 10-Year Follow-up Study

et al. 2016

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Section: Methodsmentioning

confidence: 99%

Respiratory Morbidity After Childhood Burns: A 10-Year Follow-up Study

et al. 2016

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“…11,12 Recent analysis of population-based health administrative data identified increased long-term mortality after both severe and minor burn injury in children. 13 Given the potential of burn injury to have longer-term impacts on the heart and circulatory system, the aim of this study was to use population-based linked health data to assess whether children who are hospitalized for a burn injury when younger than 15 years of age have increased longer-term hospital use for circulatory diseases, after adjustment for demographic factors and preexisting comorbidities.…”

Section: What's Known On This Subjectmentioning

confidence: 99%

“…8,13 Despite the absence of a hypermetabolic response, minor burns elicit a substantial acute inflammatory response. 9 It may be that this response in part mediates the profound long-term changes observed after minor burn injuries.…”

Section: Figurementioning

confidence: 99%

Long-term Effects of Pediatric Burns on the Circulatory System

et al. 2015

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The systemic responses to burns (in particular, elevated levels of catecholamines and stress hormones) have been shown to have an impact on cardiac function for at least 3 years in children with burns. However, it is not clear if these changes lead to long-term effects on the heart. The aim of this study was to assess whether pediatric burn injury is associated with increased long-term hospital use for circulatory diseases.

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“…Burn-induced cardiodynamic derangements contribute to multiple organ system failure, sepsis, and death [4,5]. Higher total body surface area (TBSA) results in higher mortality in both human patients [6] and animals [7] due to cardiac dysfunction post burn [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway

Wen

Cummins

Radhakrishnan

2020

IJMS

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Burn-induced heart dysfunction is a key factor for patient mortality. However, the molecular mechanisms are not yet fully elucidated. This study sought to understand whether burn-induced heart dysfunction is associated with cardiac mitochondrial dysfunction and interruption of the PDE5A-cGMP-PKG pathway. Sixty percent total body surface area (TBSA) scald burned rats (±sildenafil) were used in this study. A transmission electron microscope (TEM), real-time qPCR, O2K-respirometer, and electron transport chain assays were used to characterized molecular function. Cardiac mitochondrial morphological shapes were disfigured with a decline in mitochondrial number, area, and size, resulting in deficiency of cardiac mitochondrial replication. Burn induced a decrease in all mitDNA encoded genes. State 3 oxygen consumption was significantly decreased. Mitochondrial complex I substrate-energized or complex II substrate-energized and both of respiratory control ratio (RCRs) were decreased after burn. All mitochondrial complex activity except complex II were decreased in the burn group, correlating with decreases in mitochondrial ATP and MnSOD activity. Sildenafil, a inhibitor of the PDE5A-cGMP-PKG pathway, preserved the mitochondrial structure, respiratory chain efficiency and energy status in cardiac tissue. Furthermore, sildenafil treatment significantly restored ADP-conjugated respiration in burned groups. In conclusion, cardiac mitochondrial damage contributes to burn-induced heart dysfunction via the PDE5A-cGMP-PKG pathway.

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Mortality After Burn Injury in Children: A 33-year Population-Based Study

Abstract: To assess the impact of burn injury sustained during childhood on long-term mortality and to quantify any increased risk of death attributable to burn injury.

Cited by 71 publications

References 47 publications

Respiratory Morbidity After Childhood Burns: A 10-Year Follow-up Study

Respiratory Morbidity After Childhood Burns: A 10-Year Follow-up Study

Long-term Effects of Pediatric Burns on the Circulatory System

Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway

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