THE INFLAMMATORY RESPONSE OF DIFFERENT SEGMENTS OF THE GUT FOUR HOURS AFTER THERMAL INJURY.

ObjectivesComplete cytoreduction of ovarian cancer often requires excision or ablation of bowel serosa implants. Both argon beam coagulator (ABC) and thermal plasma energy (TPE) (PlasmaJet; PlasmaSurgical, Roswell, Ga) have been used to ablate bowel serosa implants. Our objective was to identify comparable power settings as well as determine the rate of bowel perforation, depth of thermal injury, and extent of inflammatory response with ABC versus TPE in a porcine model.Materials and MethodsNine pigs underwent vaporization of small bowel and colon serosa according to assigned treatment group (TPE vs ABC) and settings (ABC: 30, 50, and 70 W; TPE: Cut 10U, 20U, and 30U and Coagulation 10U, 20U, and 30U). Animals underwent necropsy with blinded histomorphologic evaluation on days 0, 3, and 10 postprocedure to assess for presence of bowel perforation, depth of thermal injury, and extent of inflammatory response.ResultsAt necropsy, bowel perforation was not identified in any animals. Depth of treatment with ABC in the porcine colon was variable and unrelated to power settings whereas TPE was associated with a consistent treatment depth of 1.0 mm regardless of location or power. Treatment with ABC resulted in greater tissue coagulation and desiccation as well as increased rates of mucosal necrosis, especially at higher settings (>50 W). Treatment with TPE primarily resulted in tissue ablation and minimal mucosal necrosis at low settings (Coag 10U–20U). The inflammatory response associated with TPE treatments was interpreted as biologically benign, and less than that observed with the ABC regardless of treatment settings.ConclusionsBoth ABC and TPE effectively ablate bowel serosa in a porcine model. The TPE seems to result in a more predictable tissue effect with less inflammatory response, especially when used at low power settings such as Coag 10U or 20U. These characteristics are appealing for ablation of bowel serosa implants during ovarian cancer surgery and warrant further investigation.

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Naturally existing CD11clowCD45RBhigh dendritic cells protect mice from acute severe inflammatory response induced by thermal injury

Immunobiology ◽

10.1016/j.imbio.2010.03.005 ◽

2011 ◽

Vol 216 (1-2) ◽

pp. 47-53 ◽

Cited By ~ 11

Author(s):

Qing-yang Liu ◽

Yong-ming Yao ◽

Shu-wen Zhang ◽

Yong-hong Yan ◽

Xu Wu

Keyword(s):

Dendritic Cells ◽

Inflammatory Response ◽

Thermal Injury

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Impact of Thermal Injury on Wound Infiltration and the Dermal Inflammatory Response

Journal of Surgical Research ◽

10.1016/j.jss.2008.07.034 ◽

2010 ◽

Vol 158 (1) ◽

pp. 112-120 ◽

Cited By ~ 35

Author(s):

Martin G. Schwacha ◽

Bjoern M. Thobe ◽

TanJanika Daniel ◽

William J. Hubbard

Keyword(s):

Inflammatory Response ◽

Thermal Injury ◽

Wound Infiltration

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Effect of a bradykinin antagonist on the local inflammatory response following thermal injury

Burns ◽

10.1016/0305-4179(95)00130-1 ◽

1996 ◽

Vol 22 (4) ◽

pp. 324-327 ◽

Cited By ~ 25

Author(s):

F.E. Nwariaku ◽

P.J. Sikes ◽

E. Lightfoot ◽

W.J. Mileski ◽

C. Baxter

Keyword(s):

Inflammatory Response ◽

Thermal Injury ◽

Local Inflammatory Response ◽

Bradykinin Antagonist

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Effect of systemic inflammatory response in the development of encephalopathy in severe thermal injury.

Medicni perspektivi (Medical perspectives) ◽

10.26641/2307-0404.2015.4.56136 ◽

2015 ◽

Vol 20 (4) ◽

pp. 50-56

Author(s):

O. Y. Sorokina ◽

T. O. Buryak

Keyword(s):

Inflammatory Response ◽

Thermal Injury ◽

Systemic Inflammatory Response

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Dynamics of hemostasis parameters and endothelial dysfunction markers in patients with thermal injury

Bulletin of Russian State Medical University ◽

10.24075/brsmu.2019.021 ◽

2019 ◽

pp. 65-69

Author(s):

VV Morrison ◽

AYu Bozhedomov

Keyword(s):

Endothelial Dysfunction ◽

Inflammatory Response ◽

Thermal Injury ◽

Systemic Inflammatory Response ◽

Burn Injuries ◽

Circulating Endothelial Cells ◽

Blood Concentrations ◽

Inflammation Mediators ◽

Thermal Burns ◽

Reactive Protein

Burn injuries kill thousands of people. The aim of this study was to investigate the dynamics of systemic inflammatory response parameters, endothelial dysfunction markers and hemostasis impairment in patients with thermal burn injuries. The study was conducted in 51 patients aged 16 to 80 years presenting with moderate to severe thermal burns. The systemic inflammatory response was assessed based on the levels of tumor necrosis factor α (TNFα), a number of interleukins (IL6, IL12), the С-reactive protein, and the monocyte chemoattractant protein 1 (MCP-1). Hemostatic impairments were inferred from the results of coagulation tests that measured the activated partial thromboplastin time (APTT), the prothrombin index (PI), the prothrombin time (PT) and the platelet count. Endothelial dysfunction was analyzed based on the levels of vascular endothelial growth factor (VEGF), total endothelin (TE) and circulating endothelial cells. The dynamics of the listed parameters were studied over 45 days following the injury. Endothelial dysfunction markers peaked on days 3–15 (VEGF 828.9 ± 993.2 pg/mL, TE 3.0 ± 1.7 fmol/mL, CEC 6.4 ± 6.0 • 104/l, IL6 264.4 ± 131.2 pg/mL, TNFα 41.4 ± 111.9 pg/ml, C-reactive protein 128.3 ± 52.4 nmol/mL). Coagulation was significantly impaired during the same period (APTT 41.4 ± 17.7 s, PI 83.6 ± 15.4%, PT 22.3 ± 10.0 s). By day 30–35, blood concentrations of proinflammatory cytokines and inflammation mediators had declined (TNFα 3.9 ± 9.6 pg/mL, IL6 49.0 ± 35.9 pg/mL, С-reactive protein 81.9 ± 341 nmol/ml); in that phase, the coagulation potential was continuing to decrease (APTT 51.8 ± 34.1 s, PI 82.9 ± 19.4%, PT 24.9 ± 21.4 s). The study demonstrates that damage to the endothelium results from both injured tissue breakdown and inflammation mediators. The risk of thromboembolic and hemorrhagic complications is the highest on days 7 through 15 following thermal injury. Further research is needed to study the mechanisms of endothelial damage in patients with thermal burns.

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