PATIENTS WITH MULTIPLE INJURIES—Management in Office Practice

In the emergency treatment of a patient with multiple severe injuries who is brought to a physician''s office from the scene of an accident, the physician must make sure that a way for air to reach the lungs is open, must treat or prevent shock, stop hemorrhage and apply temporary splints to fractures of the extremity.The possibility that the tip of the tongue is blocking the pharynx and that blood or other fluid is clogging the airway must be considered. Fluids should be administered intravenously to prevent shock and gauze pads should be held firmly in place to control bleeding.     

Intra-abdominal injuries

With the increase in mechanization, the incidence of intra-abdominal injury is increasing. Bleeding, contamination or impairment of function of an intra-abdominal organ must be diagnosed early and dealt with immediately. Serial determination of hemoglobin and cell volume of the blood are useful diagnostic procedures. The older teachings of waiting for a patient to recover from shock before operating are to be decried. Immediate operative intervention to close a ruptured stomach, bowel or bladder, or to suture or remove may be necessary to save the life of the patient.     

INTRA-ABDOMINAL INJURIES

With the increase in mechanization, the incidence of intra-abdominal injury is increasing. Bleeding, contamination or impairment of function of an intra-abdominal organ must be diagnosed early and dealt with immediately. Serial determination of hemoglobin and cell volume of the blood are useful diagnostic procedures.The older teachings of waiting for a patient to recover from shock before operating are to be decried. Immediate operative intervention to close a ruptured stomach, bowel or bladder, or to suture or remove may be necessary to save the life of the patient.     

Microvascular experimental evidence on the relative significance of restoring oxygen carrying capacity vs. blood viscosity in shock resuscitation

The development of volume replacement fluids for resuscitation in hemorrhagic shock comprises oxygen carrying and non carrying fluids. Non oxygen carrying fluids or plasma expanders are used up to the transfusion trigger, and upon reaching this landmark either blood, and possibly in the near future oxygen carrying blood substitutes, are used. An experimental program in hemorrhagic shock using the hamster chamber window model allowed to compare the relative performance of most fluids proposed for shock resuscitation. This model allows investigating simultaneously the microcirculation and systemic reactions, in the awake condition, in a tissue isolated from the environment. Results from this program show that in general plasma expanders such as Ringer's lactate and dextran 70 kDa do not sufficiently restore blood viscosity upon reaching the transfusion trigger, causing microvascular collapse. This is in part restored by a blood transfusion, independently of the oxygen carrying capacity of red blood cells. These results lead to the proposal that effective blood substitutes must be designed to prevent microvascular collapse, manifested in the decrease of functional capillary density. Achievement of this goal, in combination with the increase of oxygen affinity, significantly postpones the need for a blood transfusion, and lowers the total requirement of restoration of intrinsic oxygen carrying capacity.     

微量失血对左肝外叶切除＋定容失血性休克大鼠生存率的影响

目的：观察在大鼠左肝外叶切除＋定容失血性休克模型制作过程中微量失血对最终大鼠生存率的影响。方法：45只SD大鼠按不同的放血比例分为三组,以Wigger改良法建立左肝外叶切除＋定容失血性休克模型,严格标化放血前的各项手术操作和观测指标,比较三组大鼠最终生存率的差异。结果：在分别按2．4ml／100g（A组）、2．5ml／100g（B组）、2．6ml／100g（C组）比例定容失血的大鼠模型中,各组大鼠生存率分别为：A组66．67％,B组42．86％,C组7．69％,A、B两组与C组大鼠的生存率相比较存在明显差异（P〈0．05）。结论：即使是0．1ml／100g的微量失血对于该模型大鼠的生存率也是有显著影响的,这一点在大鼠的定容失血性休克模型实验中是不应被忽视的。     

Renovascular reactivity measured by near-infrared spectroscopy

Hypotension and shock are risk factors for death, renal insufficiency, and stroke in preterm neonates. Goal-directed neonatal hemodynamic management lacks end-organ monitoring strategies to assess the adequacy of perfusion. Our aim is to develop a clinically viable, continuous metric of renovascular reactivity to gauge renal perfusion during shock. We present the renovascular reactivity index (RVx), which quantifies passivity of renal blood volume to spontaneous changes in arterial blood pressure. We tested the ability of the RVx to detect reductions in renal blood flow. Hemorrhagic shock was induced in 10 piglets. The RVx was monitored as a correlation between slow waves of arterial blood pressure and relative total hemoglobin (rTHb) obtained with reflectance near-infrared spectroscopy (NIRS) over the kidney. The RVx was compared with laser-Doppler measurements of red blood cell flux, and renal laser-Doppler measurements were compared with cerebral laser-Doppler measurements. Renal blood flow decreased to 75%, 50%, and 25% of baseline at perfusion pressures of 60, 45, and 40 mmHg, respectively, whereas in the brain these decrements occurred at pressures of 30, 25, and 15 mmHg, respectively. The RVx compared favorably to the renal laser-Doppler data. Areas under the receiver operator characteristic curves using renal blood flow thresholds of 50% and 25% of baseline were 0.85 (95% CI, 0.83-0.87) and 0.90 (95% CI, 0.88-0.92). Renovascular autoregulation can be monitored and is impaired in advance of cerebrovascular autoregulation during hemorrhagic shock.     

Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans.

Hemorrhage is a leading cause of death in both civilian and battlefield trauma. Survival rates increase when victims requiring immediate intervention are correctly identified in a mass-casualty situation, but methods of prioritizing casualties based on current triage algorithms are severely limited. Development of effective procedures to predict the magnitude of hemorrhage and the likelihood for progression to hemorrhagic shock must necessarily be based on carefully controlled human experimentation, but controlled study of severe hemorrhage in humans is not possible. It may be possible to simulate hemorrhage, as many of the physiological compensations to acute hemorrhage can be mimicked in the laboratory by applying negative pressure to the lower extremities. Lower body negative pressure (LBNP) sequesters blood from the thorax into dependent regions of the pelvis and legs, effectively decreasing central blood volume in a similar fashion as acute hemorrhage. In this review, we compare physiological responses to hemorrhage and LBNP with particular emphasis on cardiovascular compensations that both share in common. Through evaluation of animal and human data, we present evidence that supports the hypothesis that LBNP, and resulting volume sequestration, is an effective technique to study physiological responses and mechanisms associated with acute hemorrhage in humans. Such experiments could lead to clinical algorithms that identify bleeding victims who will likely progress to hemorrhagic shock and require lifesaving intervention(s).     

Novel method for early signs of clinical shock detection by monitoring blood capillary/vessel spatial pattern

The ability to monitor capillary/vessel spatial patterns and local blood volume fractions is critical in clinical shock detection and its prevention in Intensive Care Units (ICU). Although the causes of shock might be different, the basic abnormalities in pathophysiological changes are the same. To detect these changes, we have developed a novel method based on both spectrally and spatially resolved diffuse reflectance spectra. The preliminary study has shown that this method can monitor the spatial distribution of capillary/vessel spatial patterns through local blood volume fractions of reduced hemoglobin and oxyhemoglobin. This method can be used as a real‐time and non‐invasive tool for the monitoring of shock development and feedback on the therapeutic intervention. (© 2014 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)     

Cardiopulmonary effects of hemorrhagic shock in splenic autotransplanted pigs: a new surgical model

The spleen is an important organ for hemodynamic compensation during hemorrhagic shock. The aim of the study was to compare the hemodynamic and metabolic responses of sham-operated pigs with intact spleen, splenectomized pigs, and splenic autotransplanted pigs during hemorrhagic shock. Hemorrhagic shock was induced by 30% total blood volume bleed in sham-operated, splenectomized and splenic autotransplanted pigs (n = 20). Cardiopulmonary and metabolic variables were measured before, immediately after, and at 20, 60 and 100 minutes after hemorrhage. Upon hemorrhagic shock induction, body temperature, mean arterial pressure, mean pulmonary arterial pressure, cardiac output, cardiac index and oxygen delivery decreased, while lactate and shock index increased. Hemoglobin and hematocrit were significantly lower in the splenectomized and splenic autotransplant groups as compared with the control group at 60 and 100 minutes after hemorrhage (p < 0.05). Unlike intact spleen, splenic autotransplant could not improve hemodynamic parameters in hemorrhagic shock in pigs. In comparison to mice, rats or dogs, this species could be an interesting investigation model to test new surgical procedures during splenic related hemorrhagic shock, with potential applications in human medicine.     

限制性液体复苏对多发性骨折合并创伤失血性休克患者凝血功能、心肌损害指标及预后的影响

目的:探讨限制性液体复苏对多发性骨折合并创伤失血性休克患者凝血功能、心肌损害指标及预后的影响。方法:选取我院收治的多发性骨折合并创伤失血性休克患者77例,分为研究组(n=39)、对照组(n=38),对照组给予常规液体复苏,研究组给予限制性液体复苏,比较两组患者凝血功能、心肌损害指标、输液量、失血量、输血量、并发症发生率及病死率。结果:研究组的输液量、失血量、输血量均少于对照组(P0.05)。与复苏前相比,两组患者复苏1 h后凝血酶原时间(PT)、凝血活酶时间(APTT)、凝血酶时间(TT)均延长,且研究组长于对照组(P0.05);两组患者复苏1 h后肌酸激酶(CK)、肌酸激酶-同工酶(CK-MB)、肌钙蛋白T(CTnT)水平均下降,且研究组低于对照组(P0.05)。研究组复苏期间并发症发生率、病死率均低于对照组(P0.05)。结论:限制性液体复苏治疗多发性骨折合并创伤失血性休克患者,可改善患者凝血功能和预后,降低并发症发生率,同时还可减轻心肌损害。     

The physiological changes of cumulative hemorrhagic shock in conscious rats

Summary Hemorrhagic shock is a common cause of death in emergency rooms. Current animal models of hemorrhage encounter a major problem that the volume and the rate of blood loss cannot be controlled. In addition, the use of anesthesia obscures physiological responses. Our experiments were designed to establish an animal model based on the clinical situation for studying hemorrhagic shock. Hemorrhagic shock was induced by withdrawing blood from a femoral arterial catheter. The blood volume withdrawn was 40% of the total blood volume for group 1 and 30% for group 2 and 3. Group 3 was anesthetized with sodium pentobarbital (25 mg/kg, i.v.) at the beginning of blood withdrawal. Our data showed that the survival rate was 87.5% at 48 h in the conscious group and 0% at 9 h in anesthetic group after hemorrhage. The levels of mean arterial pressure, heart rate, white blood count, TNF-, IL1-, CPK, and LDH after blood withdrawal in the anesthetic group were generally lower than those in conscious groups. These results indicated that anesthetics significantly affected the physiology of experimental animals. The conscious, unrestrained and cumulative volume-controlled hemorrhagic shock model was a good experimental model to investigate the physical phenomenon without anesthetic interfernce.     

Pathophysiology of hemorrhagic shock. A model for studying the effects of acute blood loss in the rat

A model of acute blood loss in rats with a reproducible mortality rate over a wide range of body weights was developed by withdrawing various amounts of fixed blood volume per 100 g body weight via the left common carotid artery and observing the survival of the animals. Younger (lighter) animals survived the bleeding longer than older (heavier) animals. As early as 70 min following the shock episode there was evidence of acute tubular necrosis in kidney proximal tubules and focal centrilobular necrosis in the liver. The 84%, 50%, or 16% body weight - mortality line was: V84 = -0.17 BW + 3.25; V50 = -0.18 BW + 3.16; or V16 = -0.18 BW + 3.01 in animals ranging from 250 to 400 g body weight (where V = bleeding volume ml/100 g body weight, BW = body weight in grams X 10(-2). To produce the same mortality rate, the bleeding volume per unit body weight decreased with increased body weight. On the other hand, the bleeding volume per total blood volume or per unit body surface area increased with increased body weight. The body weight-mortality line is a useful method to calculate the bleeding volume to produce predetermined mortality rate. This method can be easily applied to various pathophysiological and metabolic studies on the nature of acute blood loss as well as in the treatment of acute blood loss.     

Septic Shock

Septic shock may be defined as hypotension caused by bacteremia and accompanied by decreased peripheral blood flow, evidenced by oliguria. Clinically, a shaking chill is the warning signal. The immediate cause of hypotension is pooling of blood in the periphery, leading to decreased venous return: later, peripheral resistance falls and cardiac failure may occur. Irreversible shock is comparable to massive reactive hyperemia. Reticuloendothelial failure, histamine release, and toxic hypersensitivity may be factors in the pathogenesis of septic shock. Adrenal failure does not usually occur, but large doses of corticosteroid are employed therapeutically to counteract the effect of histamine release or hypersensitivity to endotoxin. The keys to successful therapy are time, antibiotics, vasopressors, cortisone and correction of acidosis.     

Shock Caused by Continuous Infusion of Metaraminol Bitartrate (Aramine)

Increasing doses of metaraminol bitartrate (Aramine) in a continuous intravenous infusion were used to support the blood pressure in four patients. Under such treatment a state of shock developed, characterized by intense peripheral vasoconstriction, hypotension and anuria. In spite of an adequate fluid intake all patients showed severe hemoconcentration, and a critically low plasma volume could be demonstrated in two. While metaraminol (Aramine) was ineffective, noradrenaline still caused a moderate blood pressure response. Treatment with plasma expanders (Intradex) and small doses of noradrenaline (Levophed) resulted in transient improvement in one patient and complete recovery from shock in three. The peripheral vasoconstriction persisted up to 12 hours and renal function improved on the second day after the withdrawal of metaraminol. The etiology of this shock syndrome is believed to be similar to that of experimental shock produced with adrenaline and noradrenaline.     

淋浆对内毒素休克大鼠微循环障碍的干预作用

目的：探讨淋浆对内毒素休克的干预作用及其机制。方法：Wistar雄性大鼠60只,随机分为对照组、模型组和淋浆组,以颈静脉注射LPS（15 mg/kg）复制内毒素休克模型,造模15 min后,淋浆组自颈静脉注射正常淋浆（占全血量1/15）,观察对平均动脉血压（MAP）、回肠下段肠系膜微循环、细静脉壁白细胞粘附数、血浆P-选择素和细胞间粘附分子（ICAM-1）含量的影响。结果：正常淋浆可防止内毒素休克的MAP进行性下降,解除肠系膜微血管的病理性缩窄,减少白细胞在细静脉壁的粘附,改善微循环的流态,降低血浆P-选择素和ICAM-1的水平。结论：小量正常淋浆对LPS攻击导致内毒素休克的微循环障碍和低血压均有良好的干预作用,其机制与减少细胞粘附分子生成有关。     

Central histamine-induced reversal of critical haemorrhagic hypotension in rats--haemodynamic studies.

Volume-controlled irreversible haemorrhagic shock in rats produced by blood withdrawal until stabilisation of critical mean arterial pressure (MAP) 20-25 mmHg is associated with an extreme decrease in cardiac index (CI) and an increase in total peripheral resistance index (TPRI), with reductions in renal (RBF), hindquarters (HBF) and mesenteric blood flow (MBF), and leads to the death of all control animals within 30 min. Histamine (100 nmol) injected intracerebroventricularly (i.c.v.) in the early phase of critical hypotension produces a prompt and long-lasting increase in MAP and heart rate, with a 100% survival for 2 h after treatment. The effects are associated with the rise in the circulating blood volume and CI, and the decrease in TPRI, with the increase in RBF and HBF, and persistently lowered MBF. Both splenectomy and ligation of the suprahepatic veins inhibit histamine-induced increase in circulating blood volume as well as cardiac and regional haemodynamic effects. It can be concluded that histamine administered icv activates central endogenous compensatory mechanisms, which leads to the reversal of haemorrhagic shock conditions due to the mobilisation of blood from venous reservoirs, the increase in circulating blood volume and its redistribution. Moreover, histamine evokes the rises in Cl and perfusion of the renal and skeletal muscle vascular regions.     

The effects of heat shock and acclimation temperature on hsp70 and hsp30 mRNA expression in rainbow trout: in vivo and in vitro comparisons

Heat shock (25° C) of 10° C-acclimated rainbow trout Oncorhynchus mykiss led to increases in heat shock protein 70 (hsp70) mRNA in blood, brain, heart, liver, red and white muscle, with levels in blood being amongst the highest. Hsp30 mRNA also increased with heat shock in all tissues with the exception of blood. When rainbow trout blood was heat shocked in vitro , both hsp70 and hsp30 mRNA increased significantly. In addition, these in vitro experiments demonstrated that blood from fish acclimated to 17° C water had a lower hsp70 mRNA heat shock induction temperature than did 5° C acclimated fish (20 v. 25° C). The hsp30 mRNA induction temperature (25° C), however, was unaffected by thermal acclimation. While increases in hsp70 mRNA levels in blood may serve as an early indicator of temperature stress in fish, tissue type, thermal history and the particular family of hsp must be considered when evaluating stress by these molecular means.     

肠淋巴液引流对失血性休克大鼠红细胞流变性的影响

目的:观察肠淋巴液引流对失血性休克大鼠红细胞流变性指标以及血液黏度的作用。方法:Wistar雄性大鼠均分为假休克组、休克组(复制失血性休克模型)、引流组(复制失血性休克模型,自低血压1 h引流休克肠淋巴液)。在低血压3 h或相应时间,经腹主动脉取血,检测红细胞参数、红细胞电泳、红细胞沉降率(ESR)以及血液黏度,计算红细胞聚集指数、红细胞变形指数。结果:与假休克组比较,休克组红细胞数量、红细胞比积(HCT)、血红蛋白(Hb)、平均红细胞血红蛋白浓度(MCHC)、红细胞电泳率与迁移率、红细胞变形指数、全血黏度、全血低切与高切相对黏度和还原黏度显著降低,休克组平均红细胞体积、红细胞电泳时间、ESR、血沉方程K值与校正K值、红细胞聚集性指数、血浆黏度显著升高;引流组MCHC、红细胞电泳率与迁移率、全血黏度、全血低切与高切还原黏度均显著降低,引流组红细胞体积分布宽度(RDW-SD)显著增加。同时,引流组HCT、RDW-SD、红细胞变形指数、全血黏度、全血低切与高切相对黏度显著高于休克组;ESR、血沉方程K值与校正K值、红细胞聚集性指数、血浆黏度显著低于休克组。结论:休克肠淋巴液引流可改善失血性休克大鼠红细胞流变行为,从而改善血液流变性。     

Hepatic origin of hyperammonemia induced by shock in normal rats.

This study was undertaken in order to see whether instability in blood ammonia levels frequently observed in the anaesthesized rat could be explained by variations in blood pressure. In normal Wistar rats, anaesthesized with sodium pentobarbital, a bleeding of 1 ml/100 g body weigth produced in a few minutes a significant decrease in blood pressure and a significant increase in arterial blood ammonia level. With the blood pressure normalization following the blood reinfusion this hyperammonemia decreased but reappeared at high levels after a second and a third bleeding. The shock produced by an occlusion of the inferior vena cava above the renal veins gave similar results. The arterial hyperammonemia induced by shock did not result from muscle or renal ammonia production but is related to impaired hepatic uptake of portal ammonia. These results indicate that in the rat the blood pressure stability is a necessary precondition in any experiment on ammonia metabolism.     

The Blood Sinus System of Hagfish: Its Significance in a Low-pressure Circulation

The subcutaneous sinus (SCS) of hagfish is a large and seemingly expansible compartment. Hagfish have a high blood volume and more than 30% of this volume is contained within the sinus system. The rate of return of SCS blood to the central circulation is slow in animals at rest. Blood enters the branchial sinus system at papillae on the branchial vessels, but the routes of entry into the SCS are not fully understood.Hagfish have the lowest blood pressures with the Vertebrata. The low power requirement of the hagfish heart must contribute to the animal's low rate of energy consumption. However, this may be an incidental benefit associated with the need to prevent blood pressures from rising and thus forcing more blood into the sinus system. Low blood pressures appear to be essential for the functioning of the gill pouches. Bolus injections of saline into central blood vessels affect pressures for some time. This suggests that cardiac output is sensitive to venous filling pressures and that there must be mechanisms for controlling the partitioning of blood between the central circulation and the sinus system. It may not be correct to consider the low blood pressures of hagfish as a “primitive” character.