Management of the lower gastrointestinal system in burn: A comprehensive review

Ng, J.; Cairns, S A; O’Boyle, Ciaran P.

doi:10.1016/j.burns.2015.08.007

Cited by 16 publications

(17 citation statements)

References 52 publications

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“…In stressor shock conditions, the systemic blood circulation will adjust to be redistributed to ensure the perfusion of vital organs, such as the brain and heart; however, perfusion of the gastrointestinal tract decreases significantly [ 19 ]. The result of a lower level of IL-6 in serum and gastric mucosa in the mild hypothermia-treated group demonstrates that mild hypothermia treatment may decrease the level of IL-6 and diminish the inflammatory reaction.…”

Section: Discussionmentioning

confidence: 99%

Mild Hypothermia Protects Pigs’ Gastric Mucosa After Cardiopulmonary Resuscitation via Inhibiting Interleukin 6 (IL-6) Production

et al. 2016

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BackgroundThe purpose of this study was to determine the effect of mild hypothermia therapy on gastric mucosa after cardiopulmonary resuscitation (CPR) and the underlying mechanism.Material/MethodsVentricular fibrillation was induced in pigs. After CPR, the surviving pigs were divided into mild hypothermia-treated and control groups. The changes in vital signs and hemodynamic parameters were monitored before cardiac arrest and at intervals of 0.5, 1, 2, 4, 6, 12, and 24 h after restoration of spontaneous circulation. Serum IL-6 was determined at the same time, and gastroscopy was performed. The pathologic changes were noted, and the expression of IL-6 was determined by hematoxylin and eosin (HE) staining and immunohistochemistry under light.ResultsThe heart rate, mean arterial blood pressure, and cardiac output in both groups did not differ significantly. The gastric mucosa ulcer index evaluated by gastroscopy 2 h and 24 h after restoration of spontaneous circulation (ROSC) in the mild hypothermic group was lower than that the control group (P<0.05). The inflammatory pathologic score of gastric mucosa in the mild hypothermic group 6–24 h after ROSC was lower than that in the control group (P<0.05). Serum and gastric mucosa IL-6 expression 0.5–4 h and 6, 12, and 24 h after ROSC was lower in the mild hypothermic group than in the control group (P<0.05).ConclusionsMild hypothermia treatment protects gastric mucosa after ROSC via inhibiting IL-6 production and relieving the inflammatory reaction.

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Section: Discussionmentioning

confidence: 99%

Mild Hypothermia Protects Pigs’ Gastric Mucosa After Cardiopulmonary Resuscitation via Inhibiting Interleukin 6 (IL-6) Production

et al. 2016

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“…Constipation is also extremely common from opioid use following burn, as pain from burn injury requires substantial amounts of analgesia. 18,21 Past studies have demonstrated decreased gastric motility and increased gastric emptying time following thermal injury. 22 Decreased splanchnic blood flow and hemodynamic instability sometimes requiring vasopressor support together present an increased risk for bowel ischemia when EN is initiated in the postburn setting.…”

Section: Risks Of Early Enteral Feedingmentioning

confidence: 99%

“…Additionally, thermal injury decreases splanchnic blood flow and, in so doing, raises the risk of ischemic bowel injury. Constipation is also extremely common from opioid use following burn, as pain from burn injury requires substantial amounts of analgesia . Past studies have demonstrated decreased gastric motility and increased gastric emptying time following thermal injury .…”

Section: Introductionmentioning

confidence: 99%

Feeding During Resuscitation After Burn Injury

2019

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Burn injury results in a sustained hypermetabolic state with resulting increased caloric and protein requirements to support the stress and immune responses; augmented protein, fat, and carbohydrate catabolism; oxidative stress; and exudative losses. Along with surgical debridement, nutrition and resuscitation are the foundations of patient management after severe burn injury. Recent literature has demonstrated a clear benefit to early enteral nutrition initiation during the resuscitation period. This review aims to examine recent literature discussing both physiologic impact of burn injury and approaches to feeding during resuscitation after burn injury; including methods of determining nutrition requirements, routes, timing, and monitoring response and the associated benefits and consequences thereof.

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“…Physiological barrier injury caused by intestinal damage after burn injury is an important factor for causing the mortality of burn patients (Grimes et al, 2016; Ng et al, 2016). Severe burn injury, increases intestinal microvascular permeability increases, damages intestinal cell necrosis, apoptosis and intestinal mucosal barrier function impair, lead to displacement of intestinal bacterial and toxin, induction of systemic inflammatory response syndrome and multiple organ dysfunction syndromes (Zhang et al, 2017a; Osuka et al, 2017) .…”

Section: Introductionmentioning

confidence: 99%

Edaravone reduces oxidative stress and intestinal cell apoptosis after burn through up-regulating miR-320 expression

Bian

Liu

et al. 2019

Mol Med

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BackgroundIntestinal mucosa barrier dysfunction after burn injury is an important factor for causing mortality of burn patients. The current study established a burn model in rats and used a free radical scavenger edaravone (ED) to treat the rats, so as to investigate the effect of edaravone on intestinal mucosa barrier after burn injury.MethodsAnesthetized rats were subjected to 40% total body surface area water burn immediately, followed by treatment with ED, scrambled antagomir, or antagomiR-320. Intestinal mucosa damage was observed by hematoxylin-eosin staining and graded by colon mucosal damage index (CMDI) score. The contents of total sulfhydryl (TSH), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were determined by spectrophotometry. Cell apoptosis, protein relative expression,and the in situ expressions of p-Akt and p-Bad were detected by flow cytometry, Western blotting and immunohistochemistry, respectively. The miR-320 expression was determined by quantitative real-time polymerase chain reaction.ResultsED alleviated intestinal mucosal damage caused by burn injury, down-regulated the levels of MDA, cytochrome C, cleaved caspase-9 and cleaved caspase-3, but up-regulated the levels of TSH, SOD, CAT and Bcl-2. We also found that ED could reduce oxidative stress, inhibit cell apoptosis, increase the expressions of p-Akt, p-Bad and miR-320, and decrease PTEN expression. PTEN was predicted to be the target gene for miR-320, and cell apoptosis could be promoted by inhibiting miR-320 expression.ConclusionED regulates Akt/Bad/Caspase signaling cascade to reduce apoptosis and oxidative stress through up-regulating miR-320 expression and down-regulating PTEN expression, thus protecting the intestinal mucosal barrier of rats from burn injury.

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Management of the lower gastrointestinal system in burn: A comprehensive review

Cited by 16 publications

References 52 publications

Mild Hypothermia Protects Pigs’ Gastric Mucosa After Cardiopulmonary Resuscitation via Inhibiting Interleukin 6 (IL-6) Production

Mild Hypothermia Protects Pigs’ Gastric Mucosa After Cardiopulmonary Resuscitation via Inhibiting Interleukin 6 (IL-6) Production

Feeding During Resuscitation After Burn Injury

Edaravone reduces oxidative stress and intestinal cell apoptosis after burn through up-regulating miR-320 expression

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