Abstract:BACKGROUND-Adjunctive direct peritoneal resuscitation (DPR) from hemorrhagic shock (HS) improves intestinal blood flow and abrogates postresuscitation edema. HS causes water shifts as a result of sodium redistribution and changes in transcapillary Starling forces. Conventional resuscitation (CR) with crystalloid aggravates water sequestration. We examined the compartment pattern of organ tissue water after HS and CR, and modulation of tissue edema by adjunctive DPR.
“…The benefits reported in this animal modelbased research included instantaneous and sustained increases in mesenteric microvascular perfusion (arterioles and capillaries alike) [4,5]. In addition, they demonstrate restoration of premucosal A3 arteriolar endothelial cell receptor-dependent dilator function [4], avoidance of endothelial cellular edema [4] and tissue edema [6], decreases in resuscitation gut lymph flow and gut lymph concentrations of inflammatory cytokines and hyaluronic acid (a structural glycoprotein involved in regulation of tissue hydration) [7], and decreases in rat mortality [8]. They call this technique "direct peritoneal resuscitation" and have done considerable work toward delineating the vascular response mechanisms involved.…”
Section: Discussionmentioning
confidence: 83%
“…Over the past decade, Garrison and colleagues have reported local and systemic benefits and the mechanisms involved after the serosal exposure of the intestines to 2.5% dextrose clinical dialysis solution (Delflex, Fresenius Medical Care, Walthum, MA, USA) used as adjunctive treatment with conventional resuscitation after hemorrhagic shock [4][5][6][7][8][9]. The benefits reported in this animal modelbased research included instantaneous and sustained increases in mesenteric microvascular perfusion (arterioles and capillaries alike) [4,5].…”
Section: Discussionmentioning
confidence: 88%
“…We present observations from 2 cases of perforated NEC resuscitated by repeated pre-and postoperative intraperitoneal infusions of 2.5% dextrose solution. We discuss our observations and the recent research reports using a similar 2.5% dextrose infusion in an animal model of hemorrhagic shock [4][5][6][7][8][9]. We believe we witnessed 2 examples of benefit outside the hemorrhagic shock arena of the technique called "direct peritoneal resuscitation.…”
“…The benefits reported in this animal modelbased research included instantaneous and sustained increases in mesenteric microvascular perfusion (arterioles and capillaries alike) [4,5]. In addition, they demonstrate restoration of premucosal A3 arteriolar endothelial cell receptor-dependent dilator function [4], avoidance of endothelial cellular edema [4] and tissue edema [6], decreases in resuscitation gut lymph flow and gut lymph concentrations of inflammatory cytokines and hyaluronic acid (a structural glycoprotein involved in regulation of tissue hydration) [7], and decreases in rat mortality [8]. They call this technique "direct peritoneal resuscitation" and have done considerable work toward delineating the vascular response mechanisms involved.…”
Section: Discussionmentioning
confidence: 83%
“…Over the past decade, Garrison and colleagues have reported local and systemic benefits and the mechanisms involved after the serosal exposure of the intestines to 2.5% dextrose clinical dialysis solution (Delflex, Fresenius Medical Care, Walthum, MA, USA) used as adjunctive treatment with conventional resuscitation after hemorrhagic shock [4][5][6][7][8][9]. The benefits reported in this animal modelbased research included instantaneous and sustained increases in mesenteric microvascular perfusion (arterioles and capillaries alike) [4,5].…”
Section: Discussionmentioning
confidence: 88%
“…We present observations from 2 cases of perforated NEC resuscitated by repeated pre-and postoperative intraperitoneal infusions of 2.5% dextrose solution. We discuss our observations and the recent research reports using a similar 2.5% dextrose infusion in an animal model of hemorrhagic shock [4][5][6][7][8][9]. We believe we witnessed 2 examples of benefit outside the hemorrhagic shock arena of the technique called "direct peritoneal resuscitation.…”
“…Previous studies demonstrated that endorgan injury and subsequent MODS result from a cause-effect relationship between three pathophysiologic events, which likely interact in a time-dependent, tissue-specific fashion. First, a persistent and progressive splanchnic vasoconstriction and hypoperfusion leading to relative ischemia/hypoxia [26,27]; Second, a gut-derived systemic inflamematory response generated by the ischemic gut [28]; and third, inevitable fluid shifts at both the cellular level due to ionic-disequilibrium and at the capillary level due to alteration of the trans-capillary Starling forces that govern fluid exchange [29,30].…”
Multiple organ dysfunction syndrome (MODS) is a systemic, dysfunctional inflammatory response that requires long intensive care unit (ICU) stay. It is characterized with high mortality rate depending on the number of organs involved. It has been recognized that organ failure does not occur as an all-or-none rule, but rather a range of organ dysfunction exists resulting in clinical organ failure. In the absence of a gold standard scoring or tool for early diagnosis or prediction of MODS, a novel bio-clinical scoring is mandatory. Moreover, understanding the pathophysiology of MODS in medical, surgical and trauma, ICUs should take a priority to achieve a favorable outcome. Herein we reviewed the literatures published in English language through the research engines (MEDLINE, Scopus, and EBASE) from 1982 to 2011 using key words: "multiorgan dysfunction", "organ failure", "intensive care units" to highlight the definition, mechanism, diagnosis and prediction of MODS particularly at its earliest stages. Bring up new bio-clinical scoring to a stage where it is ready for field trials will pave the way for implementing new risk-stratification strategy in the intensive care to reduce the morbidity and mortality and save resources. Prospective studies are needed to answer our question and to shift MODS from an inevitable to a preventable disorder.
“…This splanchnic and distant organ hyperperfusion was associated with downregulation of the systemic inflammatory response and an increase in survival compared with conventional resuscitation therapies. 16,18 Recent studies [19][20][21] have noted that postresuscitation tissue neutrophils infiltration, which is tissue and time dependent, cellular edema, and capillary perfusion regulated by hydrogen and potassium membrane transport and water compartment distribution are all normalized by DPR with hypertonic peritoneal dialysis fluid.…”
Section: E S P I T E a D V A N C E S I Nmentioning
Hemorrhagic shock and resuscitation increased lymph flow by altering capillary water transport and expanding interstitial volume. Increased lymph hyaluronic acid and inflammatory cytokines with traditional resuscitation were modulated to sham levels by DPR. In addition, DPR reduces these patterns presumably via an osmotic effect on capillary water transport. Adjunctive DPR might offer novel protection from systemic inflammatory response syndrome after hemorrhagic shock and resuscitation.
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