Analysis of altered capillary pressure and permeability after thermal injury

Pitt, R. M.; Parker, James C.; Jurkovich, Gregory J.; Taylor, Aubrey E.; Curreri, P. William

doi:10.1016/0022-4804(87)90013-8

Cited by 81 publications

(36 citation statements)

References 7 publications

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“…One may wish on this basis to initiate fluid resuscitation at a higher rate than that predicted by the formula. However, edema formation during the early postburn hours is particularly sensitive to hydrostatic pressure, 18 such that early largevolume resuscitation may worsen edema with no permanent effect on plasma volume.…”

Section: Discussionmentioning

confidence: 98%

Predicting Increased Fluid Requirements During the Resuscitation of Thermally Injured Patients

Cancio

Chávez

Alvarado-Ortega

et al. 2004

The Journal of Trauma: Injury, Infection, and Critical Care

127

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Section: Discussionmentioning

confidence: 98%

Predicting Increased Fluid Requirements During the Resuscitation of Thermally Injured Patients

Cancio

Chávez

Alvarado-Ortega

et al. 2004

The Journal of Trauma: Injury, Infection, and Critical Care

127

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“…Several mechanisms were implicated in the pathophysiology of burn edema, such as increased filtration pressure, decreased lymphatic clearance, microvascular barrier dysfunction, and increased interstitial osmotic activity due to degraded matrices (2,4,5,25,26). Huang et al (27) showed that the myosin light chain kinase inhibitor ML-7 decreases capillary leakage, indicating that endothelial contraction may lead to microvascular barrier dysfunction.…”

Section: Introductionmentioning

confidence: 97%

Burn Plasma Transfer Induces Burn Edema in Healthy Rats

Kremer

Abé²,

Weihrauch³

et al. 2008

Shock

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Thermal injuries greater than 20% body surface area (BSA) result in systemic shock with generalized edema in addition to local tissue destruction. Burn shock is induced by a variety of mediators, mainly immunomodulative cytokines. This experimental study evaluates if burn shock can be induced in healthy rats by transfer of burn plasma (BP) with mediators. Thermal injury was induced by hot water (100 degrees C water, 12 s, 30% BSA) in male syngenic Wistar rats. Donor rats were killed 4 h posttrauma, and BP was harvested. Burn plasma was transferred to healthy animals by continuous intravenous infusion in three types of dilution (100%, 10%, and 1%). Positive controls were directly examined 4 h after thermal injury, and negative control rats had a continuous infusion done with sham burn (SB) plasma (37 degrees C water, 12 s, 30% BSA). Afterwards, intravital fluorescence microscopy was performed in postcapillary mesenteric venules at 0, 60, and 120 min. Edema formation was assessed by relative changes over time in fluorescence intensity of fluorescein isothiocyanate-albumin in the intravascular versus the extravascular space. The interactions of leucocytes and endothelium were evaluated by quantification of leukocyte sticking. Additionally, microhemodynamic (volumetric blood flow, erythrocyte velocity, venular wall shear rate, venular diameters) and macrohemodynamic parameters (blood pressure, heart frequency, temperature) were assessed online (arterial catheter). For statistics, an ANOVA was performed with Bonferroni adjustment procedure. Differences were considered significant when P < 0.05. There are no statistically significant differences in microhemodynamics or macrohemodynamics between study groups. Burn plasma infusion and thermal injury lead to significant increases in fluorescein isothiocyanate-albumin extravasation, whereas SB plasma shows no significant changes. Even BP diluted in 0.9% saline (10% and 1%) results in a similar transvascular flux of plasma proteins as direct thermal injury. Differences between positive controls and BP infusion are not significant, whereas all groups are statistically different from the SB group (P<0.05). Leukocyte sticking is significantly increased in all groups except the SB group, and the number of adherent leukocytes is dose dependent. The present study demonstrates that as early as 4 h after thermal injury, there are sufficient factors (e.g., cytokines) in BP to induce systemic burn shock in healthy rats even in diluted plasma (1%). However, the "key" cytokines are not identified at this point. The burned tissue is no longer required for burn shock induction, and the pathophysiologic process seems to be self-perpetuating as early as 4 h posttrauma. Leukocytes are activated by thermal injury and BP infusion. The role of leukocyte-endothelium interactions for edema formation remains uncertain and requires further investigation.

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“…Multiple pathophysiological changes characterize the early post-traumatic phase. Massive systemic inflammation comparable to severe sepsis leads by the release of numerous mediators such as leukotrienes, prostaglandins, and particularly histamine, in combination with complement activation products, to an extensive capillary leak [1,2]. Intravascular molecule and fluid shifts into the extravascular space cause severe hypovolemia and shock [3].…”

Section: Introductionmentioning

confidence: 99%

Early fluid resuscitation with hydroxyethyl starch 130/0.4 (6%) in severe burn injury: a randomized, controlled, double-blind clinical trial

et al. 2013

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IntroductionThere are limited data on the efficacy of early fluid resuscitation with third-generation hydroxyethyl starch (HES 130) in burn injury. Adverse effects of HES on survival and organ function have been reported.MethodsIn this randomized, controlled, double-blind trial, 48 patients with severe burn injury were assigned to receive either lactated Ringer’s solution plus 6% HES 130/0.4 in a ratio of 2:1 or lactated Ringer’s solution with no colloid supplement for the first 72 hours. Primary outcome parameter was the group difference of administered total fluid from intensive care unit (ICU) admission up to day 3. Secondary outcomes included kidney and lung injury and failure, length of stay, and mortality.ResultsThree-day totals of administered resuscitation fluid (medians) were 21,190 mL in the lactated Ringer’s group and 19,535 mL in the HES group (HES: −1,213 mL; P = 0.39). Creatinine levels from day 1 to 3 (HES: +0.4 μmol/L; 95% confidence interval (CI) −18.7 to 19.5; P = 0.97) and urinary outputs from day 1 to 3 (HES: −58 mL; 95% CI −400 to 283; P = 0.90) were not different. Six patients in each group developed acute respiratory distress syndrome (ARDS) (risk ratio 0.96; 95% CI 0.35 to 2.64; P = 0.95). Length of ICU stay (HES vs. lactated Ringer’s: 28 vs. 24 days; P = 0.80) and length of hospital stay (31 vs. 29 days; P = 0.57) were similar. Twenty-eight-day mortality was 4 patients in each group (risk ratio 0.96; 95% CI 0.27 to 4.45; P = 0.95), and in-hospital mortality was 8 in the HES group vs. 5 patients in the lactated Ringer’s group (hazard ratio 1.86; 95% CI 0.56 to 6.19; P = 0.31).ConclusionsThere was no evidence that early fluid resuscitation with balanced HES 130/0.4 (6%) in addition to lactated Ringer’s solution would lead to a volume-sparing effect in severe burn injury. Together with the findings that early renal function, incidence of ARDS, length of stay, and mortality were not negatively influenced by HES in this setting, balanced HES 130/0.4 (6%) plus lactated Ringer’s solution could not be considered superior to lactated Ringer’s solution alone.Trial registrationClinicalTrials.gov NCT01012648

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Analysis of altered capillary pressure and permeability after thermal injury

Cited by 81 publications

References 7 publications

Predicting Increased Fluid Requirements During the Resuscitation of Thermally Injured Patients

Predicting Increased Fluid Requirements During the Resuscitation of Thermally Injured Patients

Burn Plasma Transfer Induces Burn Edema in Healthy Rats

Early fluid resuscitation with hydroxyethyl starch 130/0.4 (6%) in severe burn injury: a randomized, controlled, double-blind clinical trial

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