失血性休克后液体复苏的研究进展

背景 失血性休克是外伤死亡的主要原因.在重危病例的急救和围手术期的处理中,液体复苏起着关键性的治疗作用. 目的 就重度失血性休克后液体治疗方案的研究进展作一综述. 内容 除了传统的晶体液,近年来开发了诸多新品种的液体用于复苏,如丙酮酸钠溶液等.复苏方式的研究也在静脉复苏的基础上拓展到了腹腔复苏. 趋向 丙酮酸钠溶液以及腹腔复苏是近年来研究提出的新的复苏液体和复苏方案,通过已有的研究已经证实其积极的治疗作用.其应用于失血性休克的方法、时间、疗效等仍需更进一步研究.     

Initial resuscitation of hemorrhagic shock

The primary treatment of hemorrhagic shock is control of the source of bleeding as soon as possible and fluid replacement. In controlled hemorrhagic shock (CHS) where the source of bleeding has been occluded fluid replacement is aimed toward normalization of hemodynamic parameters. In uncontrolled hemorrhagic shock (UCHS) in which bleeding has temporarily stopped because of hypotension, vasoconstriction, and clot formation, fluid treatment is aimed at restoration of radial pulse, or restoration of sensorium or obtaining a blood pressure of 80 mmHg by aliquots of 250 ml of lactated Ringer's solution (hypotensive resuscitation). When evacuation time is shorter than one hour (usually urban trauma) immediate evacuation to a surgical facility is indicated after airway and breathing (A, B) have been secured ("scoop and run"). Precious time is not wasted by introducing an intravenous line. When expected evacuation time exceeds one hour an intravenous line is introduced and fluid treatment started before evacuation.     

Effect of methylene blue on resuscitation after haemorrhagic shock.

OBJECTIVE: To compare prehospital hypotensive resuscitation with volume resuscitation, and find out whether reagents that inhibit free-oxygen radical formation, such as methylene blue, can improve resuscitation and survival. DESIGN: Randomised controlled trial. SETTING: Animal laboratory, Israel. ANIMALS: 48 adult male Wistar rats. INTERVENTIONS: After 30 minutes of controlled haemorrhage, rats were subjected to 60 minutes of uncontrolled haemorrhage with simultaneous resuscitation. Hartmann's solution alone, or with blood or with a bolus of methylene blue were infused to maintain the mean arterial pressure (MAP) at 80 or 40 mm Hg. Then haemorrhage was stopped and Hartmann's solution plus whole blood were infused to obtain a MAP that was within normal limits. MAIN OUTCOME MEASURES: Volumes of shed blood and resuscitation fluids, MAP, packed cell volume, blood pH and base deficit, and survival. RESULTS: During uncontrolled haemorrhage. a MAP of 80 mm Hg could not be reached in animals resuscitated with Hartmann's solution alone, and all died. All the rats given Hartmann's solution with a bolus of methylene blue or with whole blood achieved a higher MAP. MAP of 40 mm Hg was attained in all animals regardless of the resuscitation fluid. Only 15 of 24 animals resuscitated to a MAP of 80 mm Hg survived, compared with 22 survivors of the 24 rats resuscitated to a MAP of 40 mm Hg (p <0.04). Methylene blue or whole blood drastically reduced the volumes of shed blood and of fluids required, and moderated the reduction in packed cell volume, particularly during hypotensive resuscitation. CONCLUSION: Hypotensive protocols should be used to improve survival. Methylene blue given with the electrolyte solutions could negate their detrimental effects during resuscitation.     

消化道大出血并发休克的液体疗法

消化道大出血并发休克是普外科医生常见的紧急情况。出血性休克的治疗包括维持血压和组织灌注、直到出血被控制。具体治疗方法是止血、输血和输液。对休克的输液治疗又被称为输液复苏或液体复苏。然而 ,临床医师常遇到的情况是 :在病人出血被控制之前 ,输液复苏治疗虽能维持血压 ,防止休克 ,但由于应用不同的输液 ,也可加重出血或诱发心衰。因此 ,本文结合近年来的研究结果 ,对出血并发休克的病人如何进行有效合理的输液复苏进行探讨。一、动物实验研究尽管近来的研究对早期输液复苏的益处有所置疑 ,但有关早期输液复苏的动物实验研究证明 ,…     

Complement activation mediates intestinal injury after resuscitation from hemorrhagic shock

BACKGROUND: Endothelial cell injury after hemorrhage and resuscitation (HEM/RES) might contribute to intestinal hypoperfusion and mucosal ischemia. Our recent work suggests that the injury might be the result of complement activation. We hypothesized that HEM/RES causes complement-mediated endothelial cell dysfunction in the small intestine. METHODS: Male Sprague-Dawley rats (195-230 g) were anesthetized and HEM to 50% of baseline mean arterial pressure for 60 minutes. Just before RES, animals received either soluble complement receptor-1 (sCR1, 15 mg/kg) to inhibit complement activation or saline vehicle. Resuscitation was with shed blood and an equal volume of saline. Two hours after RES, the small bowel was harvested to evaluate intestinal nitric oxide synthase activity (NOS), neutrophil influx, histology, and oxidant injury. RESULTS: HEM/RES induced tissue injury, increased neutrophil influx, and reduced NOS activity by 50% (vs. SHAM), all of which were completely prevented by sCR1 administration. There were no observed differences in oxidant injury between the groups. CONCLUSION: Histologic tissue injury, increased neutrophil influx, and impaired NOS activity after HEM/RES were all prevented by complement inhibition. Direct oxidant injury did not seem to be a major contributor to these alterations. Complement inhibition after HEM might ameliorate reperfusion injury in the small intestine by protecting the endothelial cell, reducing neutrophil influx and preserving NOS function.     

Controlled resuscitation for uncontrolled hemorrhagic shock

OBJECTIVE: To test the hypothesis that controlled resuscitation can lead to improved survival in otherwise fatal uncontrolled hemorrhage. METHODS: Uncontrolled hemorrhage was induced in 86 rats with a 25-gauge needle puncture to the infrarenal aorta. Resuscitation 5 minutes after injury was continued for 2 hours with lactated Ringer's solution (LR), 7.3% hypertonic saline in 6% hetastarch (HH), or no fluid (NF). Fluids infused at 2 mL x kg(-1) x min(-1) were turned on or off to maintain a mean arterial pressure (MAP) of 40, 80, or 100 mm Hg in six groups: NF, LR 40, LR 80, LR 100, HH 40, and HH 80. Blood loss was measured before and after 1 hour of resuscitation. RESULTS: Survival was improved with fluids. Preresuscitation blood loss was similar in all groups. NF rats did not survive 4 hours. After 72 hours, LR 80 rats (80%) and HH 40 rats (67%) showed improved survival over NF rats (0%) (p < 0.05). Rebleeding increased with MAP. Attempts to restore normal MAP (LR 100) led to increased blood loss and mortality. CONCLUSION: Controlled resuscitation leads to increased survival compared with no fluids or standard resuscitation. Fluid type affects results. Controlled fluid use should be considered when surgical care is not readily available.     

Hypertonic/hyperoncotic fluid resuscitation after hemorrhagic shock in dogs.

We compared canine systemic and cerebral hemodynamics after resuscitation from hemorrhagic shock with 4 mL/kg (a volume approximating 12% of shed blood volume) of 7.2% saline (HS; 1233 mEq/L sodium), 20% hydroxyethyl starch (HES) in 0.8% saline, or a combination fluid consisting of 20% hydroxyethyl starch in 7.2% saline (HS/HES). Eighteen endotracheally intubated mongrel dogs (18-24 kg) were ventilated to maintain normocarbia with 0.5% halothane in nitrous oxide and oxygen (60:40). After a 30-min period of hemorrhagic shock (mean arterial blood pressure = 40 mm Hg), extending from time T0 to T30, animals received one of three randomly assigned intravenous resuscitation fluids: HS, HES, or HS/HES. Data were collected at baseline, at the beginning and end of the shock period (T0 and T30), immediately after fluid infusion (T35), and at 60-min intervals for 2 h (T95, T155). After resuscitation, mean arterial blood pressure and cardiac output increased similarly in all groups, but failed to return to baseline. Intracranial pressure decreased during shock and increased slightly, immediately after resuscitation in all groups. During shock, cerebral blood flow (cerebral venous outflow method) declined in all groups. After resuscitation, cerebral blood flow increased, exceeding baseline in the HS and HS/HES groups but remaining low in the HES group (P less than 0.05 HS vs HES at T35). We conclude that small-volume resuscitation (4 mL/kg) with HS, HS/HES, or HES does not effectively restore or sustain systemic hemodynamics in hemorrhaged dogs. In dogs without intracranial pathology, the effects on cerebral hemodynamics are also comparable, except for transiently greater cerebral blood flow in the HS group in comparison with the HES group.     

A novel method of peritoneal resuscitation improves organ perfusion after hemorrhagic shock

BACKGROUND: After resuscitation from hemorrhagic shock, intestinal microvessels constrict leading to impairment of blood flow. This occurs despite restoration and maintenance of central hemodynamics. Our recent studies have demonstrated that topical and continuous exposure of the gut microvasculature to a clinical solution (Delflex; Fresenius Medical Care), as a technique of direct peritoneal resuscitation (DPR), reverses the postresuscitation vasoconstriction and hypoperfusion to a sustained dilation and hyperperfusion. We hypothesize that initiation of DPR simultaneously with resuscitation from hemorrhagic shock enhance organ blood flow to all tissues surrounding the peritoneal cavity as well as distant organs. METHODS: Male Sprague-Dawley rats were anesthetized, intubated and cannulated for monitoring of hemodynamics and for withdrawal of blood. Rats were hemorrhaged to 50% of mean blood pressure for 60 minutes prior to resuscitation with shed blood plus 2 volumes of saline. Animals were randomized for intraperitoneal therapy with 30 mL saline (group 1, n = 9), or Delflex (group 2, n = 9). Whole organ blood flow was measured by colorimetric microsphere technique with phantom organ at baseline, after completion of resuscitation, and at 120 minutes postresuscitation. Replenishment of the dwelling intraperitoneal saline or Delflex was performed in (group 3, n = 8), and (group 4, n = 8), respectively at 90 minutes postresuscitation, and a single whole organ blood flow was performed at 120 minutes postresuscitation. RESULTS: Direct peritoneal resuscitation caused a significant increase in blood flow to the jejunum (35%), ileum (33%), spleen (48%), and pancreas (57%), whereas a marked increase in blood flow was detected in the lung (111%), psoas major muscle (115%), and diaphragm (132%), as compared with the saline treated animals in group 1. At 120 minutes postresuscitation, organ blood flow returned to the prehemorrhagic shock baseline level in all organs irrespective of peritoneal therapy. Replenishment of the intraperitoneal solution in group 3 and 4, enhanced blood flow to the liver, kidneys, and diaphragm. CONCLUSIONS: Direct peritoneal resuscitation enhanced blood flow to organs incited in the pathogenesis of multiple organ failure that follows hemorrhagic shock.     

Advances in fluid resuscitation of hemorrhagic shock.

The optimal fluid for resuscitation in hemorrhagic shock would combine the volume expansion and oxygen-carrying capacity of blood without the need for cross-matching or the risk of disease transmission. Although the ideal fluid has yet to be discovered, current options are discussed in this review, including crystalloids, colloids, blood and blood substitutes. The future role of blood substitutes is not yet defined, but the potential advantages in trauma or elective surgery may prove to be enormous.     

限制性液体复苏治疗失血性休克的临床研究

目的 探讨失血性休克早期限制性液体复苏的临床意义.方法 分析我院60例未控制失血性休克的液体复苏方法,比较常规液体组(n=30)与限制性液体复苏组(n=30)两种方法的治愈率、病死率及实验室指标血红蛋白(HBG)、红细胞压积(HCT)、血小板(PLT)、凝血酶原时间(PT)的结果.结果 常规组输液量(2 980±564)ml,治愈率66.7%、病死率33.3%,限制性组输液量(1980±302)ml,治愈率90.0%、病死率10.0%,两组间差异有统计学意义(P＜0.05),HBG、HCT、PLT、PT的比较,两组间差异有统计学意义(P＜0.01).结论 高渗液早期限制性液体复苏可提高治愈率,降低病死率,与常规复苏组比较不致于扰乱机体代偿机制及内环境.     

Methylene blue treatment for resistant shock following renal transplantation

We report a case of a 19‐year‐old female with a history of hyperoxaluria type 1 and renal failure. The patient presented for a second renal transplantation 17 years after her first combined liver and kidney transplantation. Postoperative shock was highly resistant to fluids and required massive pharmacologic hemodynamic support. Vasoplegic shock was the presumed diagnosis, and methylene blue was utilized as a rescue therapy, with a rapid hemodynamic response and no apparent side effects.     

Hypertonic saline solution resuscitation in hemorrhagic shock dogs

Objective: To find out the optimal concentration,infusion rate and dosage of saline for resuscitation. Methods: Forty-five dogs were used to establish hypovolemic shock models. The dogs were resuscitated with saline of different concentrations and different dosages under different infusion rates, and the resuscitation results were compared. Results: The best concentration was 7.5%, the best rate of infusion 20 ml/min ( a volume equivalent to 15 % of the shed blood ) and the best dosage 5.71 ml/kg. The method was effective for resuscitation, the mean arterial pressure (MAP) could be elevated to 89 % of the baseline,and this MAP could be kept for more than one hour. Conclusions： Using 7.5% sodium chloride solution equivalent to 15% of the shed blood at an infusion rate of 20 ml/min can achieve a best resuscitation result.     

Cardiac function during hemorrhagic shock and crystalloid resuscitation

It is concluded that (1) myocardial failure develops during hypovolemic shock; (2) inadequate coronary perfusion contributes to the decrease in myocardial function; (3) inadequate resuscitation prolongs myocardial dysfunction and decreased coronary blood flow and may lead to terminal arrhythmias; (4) crystalloid resuscitation relieves heart failure and corrects myocardial ischemia; and (5) no evidence exists for cardiac overload with use of large volumes of crystalloid.