A novel animal model to study delayed resuscitation following traumatic hemorrhage.

A focus of combat casualty care research is to develop treatments for when full resuscitation after hemorrhage is delayed. However, few animal models exist to investigate such treatments. Given the kidney's susceptibility to ischemia, we determined how delayed resuscitation affects renal function in a model of traumatic shock. Rats were randomized into three groups: resuscitation after 1 h (ETH-1) or 2 h (ETH-2) of extremity trauma and hemorrhagic shock, and sham control. ETH was induced in anesthetized rats with muscle injury and fibula fracture, followed by pressure-controlled hemorrhage [mean arterial pressure (MAP) = 55 mmHg] for 1 or 2 h. Rats were then resuscitated with whole blood until MAP stabilized between 90 and 100 mmHg for 30 min. MAP, glomerular filtration rate (GFR), creatinine, blood gases, and fractional excretion of sodium (nFENa+) were measured for 3 days. Compared with control, ETH-1 and ETH-2 exhibited decreases in GFR and nFENa+, and increases in circulating lactate, creatinine, and blood urea nitrogen (BUN) before and within 30 min after resuscitation. The increases in creatinine, BUN, and potassium were greater in ETH-2 than in ETH-1, whereas lactate levels were similar between ETH-1 and ETH-2 before and after resuscitation. All measurements were normalized in ETH-1 within 2 days after resuscitation, with 22% mortality. However, ETH-2 exhibited a prolonged impairment of GFR, increased nFENa+, and a 66% mortality. Resuscitation 1 h after injury therefore preserves renal function, whereas further delay of resuscitation irreversibly impairs renal function and increases mortality. This animal model can be used to explore treatments for prolonged prehospital care following traumatic hemorrhage.NEW & NOTEWORTHY A focus of combat casualty care research is to develop treatment where full resuscitation after hemorrhage is delayed. However, animal models of combat-related hemorrhagic shock in which to determine physiological outcomes of such delays and explore potential treatment for golden hour extension are lacking. In this study, we filled this knowledge gap by establishing a traumatic shock model with reproducible development of AKI and shock-related complications determined by the time of resuscitation.

[Value of renal injury marker protein in early diagnosis of acute kidney injury in burn patients with delayed resuscitation].

Objective: To explore the value of renal injury marker protein in early diagnosis of acute kidney injury (AKI) in burn patients with delayed resuscitation. Methods: The retrospective case-control research was conducted. Forty-three burn patients with delayed resuscitation (27 males and 16 females, with age of 18-75 (35±3) years)who were admitted to Zhengzhou First People's Hospital from May 2018 to May 2020 met the inclusion criteria. The patients were divided into AKI group with 23 patients and non-AKI group with 20 patients according to whether AKI occurred within 7 days after burns. The gender, age, deep partial-thickness burn area, full-thickness burn area, and acute physiology and chronic health evaluation Ⅱ of patients were compared between the two groups.The fluid supplement volume and serum creatinine at 12, 24, and 48 h after burn, serum albumin/fibrinogen ratio (AFR), urinary heat shock protein 70 (HSP70), tissue inhibitor of metalloproteinase-2 (TIMP-2)×insulin-like growth factor binding protein 7 (IGFBP-7), and neutrophil gelatinase associated lipocalin (NGAL)at 12, 24, 48, 72, 120, and 168 h after burn were detected.Data were statistically analyzed with Mann-Whitney U test, analysis of variance for repeated measurement, independent-samples t test, chi-square test and Bonferroni correction. The independent variable to predict the occurrence of AKI was screened by multi-factor logistic regression analysis. The receiver's operating characteristic curve was drawn for predicting the occurrence of AKI in burn delayed resuscitation patients, and the area under the curve (AUC), the best threshold, and the sensitivity and specificity under the best threshold were calculated. Results: The gender, age, deep partial-thickness burn area, full-thickness burn area, acute physiology and chronic health evaluation Ⅱ of patients in two groups were similar (χ(2)=1.98, t=1.98, 1.99, 1.99, 1.99, P>0.05). The fluid supplement volume of patients in AKI group at 24 and 48 h after burn was significantly less than that in non-AKI group (t=15.37, 6.51, P<0.01). The serum creatinine of patients in AKI group at 12, 24, and 48 h after burn was significantly higher than that in non-AKI group (Z=2.16, 5.62, 6.72, P<0.01). The serum AFR of patients in AKI group at 12, 24, 48, 72, 120, and 168 h after burn was significantly lower than that in non-AKI group (t=16.14, 35.35, 19.60, 20.47, 30.20, 20.17, P<0.01). The levels of urinary HSP70 of patients in AKI group at 12, 24, 48, 72, 120, and 168 h after burn were (6.89±0.87), (6.42±0.73), (5.81±0.72), (5.17±0.56), (4.63±0.51), (3.89±0.51) µg/L, which were significantly higher than (3.89±0.75), (3.57±0.63), (2.66±0.41), (1.83±0.35), (1.48±0.19), (1.28±0.19) µg/L in non-AKI group (t=12.00, 13.61, 17.39, 22.98, 26.34, 21.59, P<0.01). Urinary TIMP-2×IGFBP-7 and NGAL of patients in AKI group at 12, 24, 48, 72, 120, 168 h after burn were significantly higher than those in non-AKI group (t=26.94, 101.11, 35.50, 66.89, 17.34, 14.30, 14.00, 13.78, 12.32, 14.80, 21.36, 22.62, P<0.01). Urinary HSP70 and serum AFR at 12 h after burn, urinary TIMP-2×IGFBP-7 and NGAL at 24 h after burn were included into multi-factor logistic regression analysis (odds ratio=2.42, 3.47, 7.52, 5.61, 95% confidence interval=1.99-2.95, 1.86-3.92, 2.87-9.68, 2.14-14.69, P<0.01). For 43 patients with burn delayed resuscitation, the AUC of receiver's operating characteristic curve of serum AFR at 12 h after burn for predicting AKI was 0.739 (95% confidence interval=0.576-0.903), the optimal threshold was 9.90, the sensitivity was 82%, and the specificity was 90%. The AUC of urinary HSP70 at 12 h after burn was 0.990 (95% confidence interval=0.920-1.000), the optimal threshold was 1.40 µg/L, the sensitivity was 98%, and the specificity was 96%. The AUC of urinary TIMP-2×IGFBP-7 at 24 h after burn was 0.715 (95% confidence interval=0.512-0.890), the optimal threshold was 114.20 µg(2)/L(2), the sensitivity was 91%, and the specificity was 95%. The AUC of urinary NGAL at 24 h after burn was 0.972 (95% confidence interval=0.860-1.000), the optimal threshold was 78 µg/L, the sensitivity was 95%, and the specificity was 96%. Conclusions: Urinary HSP70 and NGAL have higher value in early diagnosis of AKI in burn patients with delayed resuscitation.

Fluid resuscitation in trauma: what are the best strategies and fluids?

BACKGROUND: Traumatic injuries pose a global health problem and account for about 10% global burden of disease. Among injured patients, the major cause of potentially preventable death is uncontrolled post-traumatic hemorrhage. MAIN BODY: This review discusses the role of prehospital trauma care in low-resource/remote settings, goals, principles and evolving strategies of fluid resuscitation, ideal resuscitation fluid, and post-resuscitation fluid management. Management of fluid resuscitation in few special groups is also discussed. CONCLUSIONS: Prehospital trauma care systems reduce mortality in low-resource/remote settings. Delayed resuscitation seems a better option when transport time to definitive care is shorter whereas goal-directed resuscitation with low-volume crystalloid seems a better option if transport time is longer. Few general recommendations regarding the choice of fluid are provided. Adhering to evidence-based clinical practice guidelines and local modifications based on patient population, available resources, and expertise will improve patient outcomes.

Sodium butyrate inhibits the production of HMGB1 and attenuates severe burn plus delayed resuscitation-induced intestine injury via the p38 signaling pathway.

BACKGROUND: Inflammatory response triggered by high mobility group box-1 (HMGB1) protein and oxidative stress play critical roles in the intestinal injury after severe burn. Sodium butyrate, a histone deacetylase inhibitor, has potential anti-inflammatory properties, inhibiting the expression of inflammatory mediators such as HMGB1 in diverse diseases. This study was designed to investigate the effects of sodium butyrate on severe burn plus delayed resuscitation-induced intestine injury, intestinal expressions of HMGB1 and intracellular adhesion molecule-1 (ICAM-1), oxidative stress, and signal transduction pathway changes in rats. MATERIALS AND METHODS: Fifty-six Sprague-Dawley rats were divided into 3 groups randomly: (1) sham group, animals underwent sham burn; (2) burn group, rats subjected to full-thickness burns of 30% total body surface area (TBSA) and received 2ml/kg/TBSA lactated Ringer solution for resuscitation at 6, 12, and 36h after burn injury; (3) burn plus sodium butyrate (burn+SB) group, animals received burn injury and lactated Ringer solution with sodium butyrate inside for resuscitation in the same manner. Diamine oxidase (DAO) concentration in plasma was measured by enzyme-linked immunosorbent assay. Intestinal fatty acid binding protein (I-FABP) and ICAM-1 expressions in the intestine were analyzed by immunohistochemical method. HMGB1 and p38 mitogen-activated protein kinase (MAPK) expressions in the intestine tissues were examined by Western blot. The intestinal concentration of malondialdehyde (MDA) was also determined. RESULTS: Intestinal HMGB1 expression was significantly increased in burn group compared with sham group. Sodium butyrate administration significantly inhibited the HMGB1 expression in the intestine, decreased the DAO concentration in plasma, reduced the intestinal I-FABP expression, and improved the intestinal histologic changes induced by burn injury plus delayed resuscitation. Sodium butyrate treatment also markedly reduced the increase of intestinal ICAM-1 expression and MDA content, and inhibited p38 MAPK activity in the intestine of severely burned rats with delayed resuscitation. CONCLUSIONS: Sodium butyrate inhibits HMGB1 expression which could be attributed to p38 MAPK signal transduction pathway and decreases intestinal inflammatory responses and oxidative stress, thus attenuates burn plus delayed resuscitation-induced intestine injury.

[Effects of cardiac support on delayed resuscitation in extensively burned patients with shock].

Objective: To explore the effects of cardiac support on delayed resuscitation in extensively burned patients with shock. Methods: Clinical data of 62 extensively burned patients with shock on admission, admitted to the 159th Hospital of PLA (hereinafter referred to as our hospital) from January 2012 to January 2017, were retrospectively analyzed. They were divided into cardiac support group (n=35) and control group (n=27) according to the use of deslanoside and ulinastatin. All patients were treated with routine fluid resuscitation based on the formula of the Third Military Medical University till post injury hour (PIH) 48. Patients in cardiac support group were given slow intravenous injection of deslanoside which was added in 20 mL 100 g/L glucose injection with first dose of 0.4 to 0.6 mg, 0.2 to 0.4 mg per 6 to 8 h, no more than 1.6 mg daily, and slow intravenous injection of 1×10(5)U ulinastatin which was added in 100 mL 50 g/L glucose injection, once per 12 h. Other treatments of patients in the two groups followed the same conventional procedures of our hospital. The following data of the two groups of patients were collected. (1) The data of urine volume per hour within PIH 48, heart rate, mean arterial pressure (MAP), central venous pressure (CVP), blood lactic acid, base excess, hematocrit, and albumin at PIH 48 were recorded. (2) The input volumes of electrolyte, colloid within the first and second 24 hours post burn and the total fluid input volumes within PIH 48 were recorded. (3) The data of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, ß(2)-microglobulin, urea nitrogen, and creatinine at PIH 48 were recorded. (4) The complications including cardiac failure, pulmonary edema, pleural effusion, seroperitoneum, renal failure, sepsis, and death were also recorded. Data were processed with independent sample ttest, Fisher's exact test, Pearson chi-square test, or continuous correction chi-square test. Results: (1) There were no statistically significant differences in urine volume within PIH 48, heart rate, MAP, CVP, hematocrit, or albumin at PIH 48 between the patients of two groups (t=0.150, 0.488, 0.805, 0.562, 1.742, 0.696, P>0.05). While the levels of blood lactic acid and base excess were respectively (4.2±2.2) and (-4.3±2.0) mmol/L in patients of cardiac support group, which were significantly better than (5.9±1.7) and (-6.0±3.1) mmol/L in patients of control group (t=3.249, 2.480, P<0.05 or P<0.01). (2) There was no statistically significant difference in input volume of colloid within the first 24 hours post burn between the patients of two groups (t=0.642, P>0.05). The input volume of electrolyte within the first 24 hours post burn, the input volumes of electrolyte and colloid within the second 24 hours post burn, and the total fluid input volume within PIH 48 of patients in cardiac support group were significantly less than those in control group (t=2.703, 4.223, 3.437, 2.515, P<0.05 or P<0.01). (3) The levels of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, ß(2)-microglobulin, urea nitrogen, and creatinine of patients in cardiac support group at PIH 48 were significantly lower than those in control group (t=3.066, 3.963, 3.225, 2.943, 2.431, 3.084, 4.052, 2.915, 3.353, P<0.05 or P<0.01). (4) The occurrences of pleural effusion and seroperitoneum and mortality of patients in cardiac support group were significantly lower than those in control group (χ(2)=5.514, 6.984, 4.798, P<0.05 or P<0.01). There were no statistically significant differences in cardiac failure, pulmonary edema, renal failure, and sepsis between the patients of two groups [χ(2)=1.314 (sepsis), P>0.05]. Conclusions: The cardiotonic and cardiac protection treatments in delayed resuscitation of extensively burned patients with shock contribute to improving the cellular anonic metabolism, reducing the volume of fluid resuscitation, and mitigating the ischemic and hypoxic damage to organs, so as to lay foundation for decreasing further complication incidences and mortality.

Effects of cardiac support on delayed resuscitation in extensively burned patients with shock / 中华烧伤杂志

Objective@#To explore the effects of cardiac support on delayed resuscitation in extensively burned patients with shock.@*Methods@#Clinical data of 62 extensively burned patients with shock on admission, admitted to the 159th Hospital of PLA (hereinafter referred to as our hospital) from January 2012 to January 2017, were retrospectively analyzed. They were divided into cardiac support group (n=35) and control group (n=27) according to the use of deslanoside and ulinastatin. All patients were treated with routine fluid resuscitation based on the formula of the Third Military Medical University till post injury hour (PIH) 48. Patients in cardiac support group were given slow intravenous injection of deslanoside which was added in 20 mL 100 g/L glucose injection with first dose of 0.4 to 0.6 mg, 0.2 to 0.4 mg per 6 to 8 h, no more than 1.6 mg daily, and slow intravenous injection of 1×105U ulinastatin which was added in 100 mL 50 g/L glucose injection, once per 12 h. Other treatments of patients in the two groups followed the same conventional procedures of our hospital. The following data of the two groups of patients were collected. (1) The data of urine volume per hour within PIH 48, heart rate, mean arterial pressure (MAP), central venous pressure (CVP), blood lactic acid, base excess, hematocrit, and albumin at PIH 48 were recorded. (2) The input volumes of electrolyte, colloid within the first and second 24 hours post burn and the total fluid input volumes within PIH 48 were recorded. (3) The data of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, β2-microglobulin, urea nitrogen, and creatinine at PIH 48 were recorded. (4) The complications including cardiac failure, pulmonary edema, pleural effusion, seroperitoneum, renal failure, sepsis, and death were also recorded. Data were processed with independent sample ttest, Fisher′s exact test, Pearson chi-square test, or continuous correction chi-square test.@*Results@#(1) There were no statistically significant differences in urine volume within PIH 48, heart rate, MAP, CVP, hematocrit, or albumin at PIH 48 between the patients of two groups (t=0.150, 0.488, 0.805, 0.562, 1.742, 0.696, P>0.05). While the levels of blood lactic acid and base excess were respectively (4.2±2.2) and (-4.3±2.0) mmol/L in patients of cardiac support group, which were significantly better than (5.9±1.7) and (-6.0±3.1) mmol/L in patients of control group (t=3.249, 2.480, P<0.05 or P<0.01). (2) There was no statistically significant difference in input volume of colloid within the first 24 hours post burn between the patients of two groups (t=0.642, P>0.05). The input volume of electrolyte within the first 24 hours post burn, the input volumes of electrolyte and colloid within the second 24 hours post burn, and the total fluid input volume within PIH 48 of patients in cardiac support group were significantly less than those in control group (t=2.703, 4.223, 3.437, 2.515, P<0.05 or P<0.01). (3) The levels of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, β2-microglobulin, urea nitrogen, and creatinine of patients in cardiac support group at PIH 48 were significantly lower than those in control group (t=3.066, 3.963, 3.225, 2.943, 2.431, 3.084, 4.052, 2.915, 3.353, P<0.05 or P<0.01). (4) The occurrences of pleural effusion and seroperitoneum and mortality of patients in cardiac support group were significantly lower than those in control group (χ2=5.514, 6.984, 4.798, P<0.05 or P<0.01). There were no statistically significant differences in cardiac failure, pulmonary edema, renal failure, and sepsis between the patients of two groups [χ2=1.314 (sepsis), P>0.05].@*Conclusions@#The cardiotonic and cardiac protection treatments in delayed resuscitation of extensively burned patients with shock contribute to improving the cellular anonic metabolism, reducing the volume of fluid resuscitation, and mitigating the ischemic and hypoxic damage to organs, so as to lay foundation for decreasing further complication incidences and mortality.

Comparative observation of the clinical effect of immediate recovery of fluid resuscitation in traumatic shock and delayed resuscitation / 中国综合临床

Objective To investigate the clinical value of immediate fluid resuscitation and delayed resuscitation in patients with traumatic shock. Methods The patients with traumatic shock treated in the Critical Care Medicine Department of People's Hospital of Wenjiang District from March 2014 to March 2017 were selected. According to the number of admission cases,one hundred and twenty patients with traumatic shock were randomly divided into two groups,60 cases in each group. The control group was given early immediate fluid resuscitation,the observation group was given delayed resuscitation,and the blood coagulation and blood routine indexes of the two groups were compared before and after the fluid resuscitation in the two groups,and the amount of fluid rehydration and the fatality rate in the two groups of patients with 1 h shock were observed,and the incidence rate of acute respiratory distress syndrome ( ARDS) and multiple organ dysfunction syndrome (MODS) were compared. Results After treatment,the blood clotting and blood routine indexes of the two groups were improved (P<0. 05),of which the thromboplastin time (PT) ((11. 04±1. 17) s),activated partial thromboplastin time (APTT) ((28. 12±5. 93) s) in the observation group in the observation group were lower than those of the control group( (15. 12±1. 26) s,(36. 17±9. 05) s) (t = -15. 37,-9. 81,P<0. 05),platelet countPLT) ((146. 92±16. 85)×109 / L) was higher than that of the control group ((114. 18±10. 69)×109 / L ) (t= -9. 77,P<0. 05),and the blood routine hemoglobin (Hb) ((112. 21±9. 46) g/ L),and the base surplus (BE)((-5. 30 ± 2. 45) mmol/ L ) were all higher than those of the control group ((92. 95 ± 11. 20) g/ L, (-8. 27±3. 53) mmol/ L ) (t= -11. 46,-8. 99,P<0. 05),blood lactic acid (BL) ((2. 79±1. 12) mmol/ L ) was lower than that of the control group ((3. 54±1. 37) mmol/ L) (t = -8. 99,P<0. 05). The volume of 1 h infusion of shock in the observation group ((569. 96±187. 34) ml ) was lower than that of the control group((1957. 35±204. 14) ml) (t = 8. 725,P<0. 05). The incidence of ARDS (3. 33% (2/ 60)),MOD(3. 33%(2/ 60)) and fatality(1. 67%(1/ 60)) were lower than those of the control group(8. 33%(5/ 60),6. 67%(4/60),6. 67%(4/ 60) ( χ2 = 2. 725,3. 214,2. 985,P< 0. 05) . Conclusion The early stage of traumatic shock delayed fluid resuscitation is conducive to the protection of the blood coagulation function of patients,to improve blood indicators,to reduce the amount of 1 h infusion and to reduce the incidence of ARDS and MODS.

Permissive hypotension/hypotensive resuscitation and restricted/controlled resuscitation in patients with severe trauma.

Achieving a balance between organ perfusion and hemostasis is critical for optimal fluid resuscitation in patients with severe trauma. The concept of "permissive hypotension" refers to managing trauma patients by restricting the amount of resuscitation fluid and maintaining blood pressure in the lower than normal range if there is continuing bleeding during the acute period of injury. This treatment approach may avoid the adverse effects of early, high-dose fluid resuscitation, such as dilutional coagulopathy and acceleration of hemorrhage, but does carry the potential risk of tissue hypoperfusion. Current clinical guidelines recommend the use of permissive hypotension and controlled resuscitation. However, it is not mentioned which subjects would receive most benefit from this approach, when considering factors such as age, injury mechanism, setting, or the presence or absence of hypotension. Recently, two randomized clinical trials examined the efficacy of titrating blood pressure in younger patients with shock secondary to either penetrating or blunt injury; in both trials, overall mortality was not improved. Another two major clinical trials suggest that controlled resuscitation may be safe in patients with blunt injury in the pre-hospital setting and possibly lead to improved outcomes, especially in patients with pre-hospital hypotension. Some animal studies suggest that hypotensive resuscitation may improve outcomes in subjects with penetrating injury where bleeding occurs from only one site. On the other hand, hypotensive resuscitation in blunt trauma may worsen outcomes due to tissue hypoperfusion. The influence of these approaches on coagulation has not been sufficiently examined, even in animal studies. The effectiveness of permissive hypotension/hypotensive resuscitation and restricted/controlled resuscitation is still inconclusive, even when examining systematic reviews and meta-analyses. Further investigation is needed to elucidate the effectiveness of these approaches, so as to develop improved treatment strategies which take into account coagulopathy in the pathophysiology of trauma.

Hydrogen-rich saline resuscitation alleviates inflammation induced by severe burn with delayed resuscitation.

Severe burns with delayed resuscitation are associated with high morbidity which is attributed to ischemia-reperfusion injury. This study was undertaken to investigate the effect of hydrogen-rich saline known as a significant selective antioxidant on the inflammatory reaction induced by severe burns with delayed resuscitation. By establishing the model of severe burns with delayed resuscitation in rats, we recorded improvement on the mortality, secretion of cytokines and reaction of oxidative stress of rats treated with hydrogen-rich saline. We found that resuscitation by hydrogen-rich saline alleviated inflammation significantly. We further detected the change of the key nuclear factor NF-κB contributed to inflammation. The expression of both NF-κB and phosphorylated NF-κB in rats having severe burns with delayed resuscitation by hydrogen-rich saline was lower than that in rats with delayed resuscitation with Ringers' solution. Our data imply that hydrogen-rich saline significantly improves the inflammatory reaction in rats with severe burns with delayed resuscitation, possibly by inhibiting activation of NF-κB.

Clinical study on anesthesia method of surgical operation in severe traumatic shock patient / 重庆医学

Objective To investigate the application of anesthesia methods and clinical experience in treatment of severe traumat-ic shock .Methods 48 severe traumatic shock patients were randomly divided into two groups by different anesthesia treatment ,in-cluding delayed resuscitation group (A group) and routine group (B group) ,24 cases in each group .Results Patients completed operation as expected with stable vital signs in the operation .Patients completely awaked and recovered the spontaneous respiration after 3~4 hours .4 cases in group A (16 .6% ) and 12 cases in group B (50% ) were died .The mortality of group A was significant-ly lower than that of group B (P<0 .05) .Conclusion The appropriate anesthetic managements for the severe traumatic shock pa-tients could maintain the function of each organ ,create favorable conditions for operation ,and improve the survival rate of critical patients .

Protective effect of hydrogen-lactated Ringer's solution against extensive burn-induced intestine injury in rats after delayed fluid resuscitation / 第二军医大学学报

Objective: To investigate the protective effect of hydrogen-rich lactated Ringer's solution (HRS) against intestine injury induced by extensive burn in Sprague-Dewley (SD) rat model after delayed fluid resuscitation. Methods: Thirty-six male SD rats were randomly divided into three groups (n=12): sham-burn group(S group), burn plus normal lactated Ringer's solution(NRS) group (BR group) and burn plus hydrogen-rich lactated Ringer's solution(HRS) group (BH group). Rats in the S group were immersed into 37°C water without fluid replacement; those in BR group and BH group were subjected to 30% total body surface area (TBSA) m degree full-thickness scald. At first, a total of 2 ml · (1% TBSA)-1 · kg-1 of HRS or NRS were replaced at7h post-burn and half volume of the total solution was replaced at the 9 h and 17 h. All rats were sacrificed at 24 h. Small intestine tissues were removed forH-E staining and determination of MDA content, MPO and SOD activity; and the levels of the IL-1ß and TNF-α were determined by ELISA. Results: The intestinal injury was relieved in BH group compared with BR group. The intestinal MDA content (P<0. 05) and activities of MPO and SOD (P<0. 01) were all decreased in BH group. IL-1ß and TNF-α levels in BH group were significantly lower than those in the BR group (P < 0. 01). Conclusion: HRS can attenuate intestine injury induced by extensive burn after delayed fluid resuscitation. It can decrease the oxidative injury following extensive burn and delay fluid resuscitation, and it can also suppress the generation of proinflammatory cytokine IL-1ß and TNF-α.

The effects of delayed fluid resuscitation on hemodynamics and visceral perfusion in dogs with hemorrhagic shock / 中华急诊医学杂志

Objective To investigate the effects of delayed fluid resuscitation on hemodynamics and visceral perfusion in dogs with hemorrhagic shock. Methods Fourteen Beagle dogs were prepared for cannulation of carotid artery and jugular vein, and 24 hours later they were subjected to hemorrhagic shock with about 42% of total blood volume exsanguinated. Animals were divided into delayed resuscitation group ( DR group, n = 8) and immediate resuscitation group ( IR group, n = 6) . In the first 24 hours after hemorrhage, dogs in Dr group were given no fluid resuscitation, while those in IR group were immediately given resuscitation with intra-venous glucose-electrolyte solution, of which the volume was three times that of blood loss. In the second 24 hours, all animals had intra-venous fluid resuscitation. The variables of hemodynamics and visceral perfusion were determined before hemorrhage and 2, 4, 8, 24, 48 and 72 hours after hemorrhage under conscious state of dogs. Results After hemorrhage, the mean arterial pressure,cardiac output index, max of left ventricular contractility, blood flow of intestinal mucosa and urinary output greatly decreased and systemic vascular resistance obviously increased in each group compared with those before hemorrhage ( P ＜ 0.05 ) . From 4 hours after hemorrhage, the above measurements of dogs in IR group gradually resumed and reach Oh levels in 72 hours after hemorrhage except systemic vascular resistance index and intestinal blood flow. Whereas those measurements in dogs of DR group kept on worsening, and the levels of mean arterial pressure, cardiac output index, intestinal blood flow and urinary output were significantly lower than those in dogs of IR group ( P ＜ 0. 05 ) . Over 72 hours, five of eight dogs died with anuria in DR, and no animals died in IR group. Conclusion The findings indicate that delayed fluid resuscitation deteriorates hemodynamics, handicapping the restoration of visceral perfusion and increasing mortality in dogs with hemorrhagic shock.

A Clinical Study on the Delayed Rapid Fluid Resuscitation in Burn Patients with Shock / 中国医师杂志

Objective To explore a suitable plan for the delayed rapid fluid resuscitation in burn patients with shock. Methods 20 patients with total body surface area (TBSA) burned over 40% admitted 4～8h after postburn were enrolled in this study. The patients were randomly divided into plasma and gelofusin groups. Rapid fluid replacement was given immediately after admission under close hemodynamic monitoring. Hemodynamic (PAP, PAWP, CO, PVR, SVR) and hemorrheological parameters, tissue oxygenation (DO 2, VO 2, O 2ext , lactic acid, base deficit) as well as indices reflecting the main visceral functions and damage were investigated. Results The amount of rapid fluid infusion within 2h after admission accounted for 38 8?6 1% of the amount calculated with the formula for the first 24h. When the infusion amount of pre-hospitalization was added, the amount would be (48 3?5 0)% of the amount for the first 24h. The real amount of the infusion for the first 24h was (31 4?14 3)% more than that of the amount calculated with the Evans formula. The real infused fluid amount for the second 24h was almost equal to the amount calculated with the formula. After fast fluid replacement therapy, all the parameters determined were markedly improved. Conclusions It is proposed that the formula for the delayed rapid fluid resuscitation in burn patients with shock should be: the amount infused for the first 24h (ml) =TBSA (%)?body weight (kg)?2 6,the ratio of colloid to electrolytes is 1:1, water=2000ml. Half of the total amount should be infused in the first 2h after admission under close hemodynamic monitoring. The amount infused for the second 24h (ml)=TBSA (%)?body weight (kg)?1,the ratio of colloid to electrolytes is 1:1, water=2000m1.