Global brain water increases after experimental focal cerebral ischemia: effect of hypertonic saline

OBJECTIVE: Isolated experiments suggest that global cerebral edema is a sequela of large hemispheric ischemic lesions, presumably as an extension of the initial ischemic insult into areas of vital, noninjured tissue. Diuretics and osmotic agents are controversial and poorly defined therapeutic modalities after large infarction. By using a rat model of middle cerebral artery occlusion (MCAO), we tested the hypothesis that significant edema occurs in the contralateral uninjured hemisphere and that this postischemic complication can be manipulated by hypertonic saline therapy. DESIGN: Prospective laboratory animal study. SETTING: Research laboratory in a teaching hospital. SUBJECTS: Halothane-anesthetized, male Wistar rats. INTERVENTIONS: Under controlled conditions of normoxia, normocarbia, and normothermia, rats were subjected to 2 hrs of MCAO. MEASUREMENTS AND MAIN RESULTS: Adequacy of MCAO and reperfusion was assessed by laser Doppler flowmetry. All animals except naive rats received continuous infusion of 0.9% saline at 0.5 mL/hr throughout the experiment. Brains were harvested, and tissue water content was estimated by comparing the wet-to-dry weight ratios of ipsilateral and contralateral cerebral hemispheres at 12 hrs, 24 hrs, or 2, 3, or 7 days postischemia. Naive and sham-operated rats served as control cohorts. In a second series of randomized experiments, wet-to-dry weight ratios were determined in rats treated with continuous intravenous infusion of 7.5% hypertonic saline (0.5 mL/hr; acetate/chloride, 50:50) and were compared with well-studied antiedema therapy: 20% mannitol (2.5 g/kg bolus every 6 hrs) or furosemide (2.5 mg/kg bolus every 6 hrs). Treatments were started at 24 hrs of reperfusion, and brain water was assessed at 2 days of reperfusion. In a third series of experiments, wet-to-dry ratios were determined in brains harvested at 2 days of reperfusion from rats that were subjected to 2 hrs of MCAO and did not receive any intravenous fluids. All values are mean +/- SEM. There were no differences between sham-operated and naive control cohorts. At 24 hrs of reperfusion, water content was higher in both ipsilateral ischemic (82.80 +/- 0.86%) and contralateral hemispheres (80.53 +/- 0.29%), compared with naive animals (ipsilateral, 79.62 +/- 0.12%; contralateral, 79.53 +/- 0.13%). Maximal cerebral edema was measured at 2 days in both hemispheres (ipsilateral, 83.94 +/- 0.47%; contralateral, 80.63 +/- 0.13%). Edema was present for up to 3 days in contralateral tissue (80.27 +/- 0.26%) and persisted to 7 days in the injured hemisphere (81.07 +/- 0.34%). Maximal edema (as assessed at 2 days postocclusion) was robustly attenuated with hypertonic saline therapy (ipsilateral, 81.59 +/- 0.52%; contralateral, 78.44 +/- 0.22%). The efficacy of hypertonic saline was equivalent to furosemide (ipsilateral, 82.09 +/- 0.50%; contralateral, 79.13 +/- 0.17%) but less robust than mannitol (ipsilateral, 79.89 +/- 0.36%; contralateral, 78.73 +/- 0.17%). CONCLUSIONS: These data demonstrate that cerebral edema persists in both injured and contralateral hemispheres for days after MCAO. The global, maximal increase in brain water is responsive to continuous 7.5% hypertonic saline treatment begun at 24 hrs postischemia and to standard diuretic/osmotic agents. These results may have implications for diuretic and osmotic therapy in clinical ischemic stroke.     

The effect of hypertonic saline and mannitol on coagulation in moderate traumatic brain injury patients

Background

Hyperosmolar therapy, using either hypertonic saline (HTS) or mannitol (MT), is considered the treatment of choice for intracranial hypertension, a disorder characterized by high intracranial pressure (ICP). However, hyperosmolar agents have been postulated to impair coagulation and platelet function. The aim of this study was to identify whether HTS and MT could affect coagulation in moderate traumatic brain injury (TBI) patients.

Effect of mannitol plus hypertonic saline combination versus hypertonic saline monotherapy on acute kidney injury after traumatic brain injury

PurposeTo compare the effect of mannitol plus hypertonic saline combination (MHS) versus hypertonic saline monotherapy (HS) on renal function in patients with traumatic brain injury (TBI).Materials and methodsThis was a secondary analysis of data from the Resuscitation Outcomes Consortium Hypertonic Saline Trial Shock Study and Traumatic Brain Injury Study. The study cohort included a propensity matched subset of patients with TBI who received MHS or HS. The primary outcome measure was the maximum serum creatinine value during critical illness.ResultsThe cohort consisted of 163 patients in the MHS group and 163 patients in the HS group (n = 326). The maximum serum creatinine value during hospitalization was 82 ± 47 μmol/L (0.86 ± 0.26 mg/dL) in the MHS group and 76 ± 23 μmol/L (0.92 ± 0.53 mg/dL) in the HS group (difference −6 μmol/L, 95% CI −14 to 2 μmol/L, p = .151). The lowest eGFR during hospitalization was 108 ± 25 mL/min in the MHS group and 112 ± 24 mL/min in the HS group (difference −4 mL/min, 95% CI −1 to 9 mLmin, p = .150).ConclusionsThe addition of mannitol to HS did not increase the risk of renal dysfunction compared to HS alone in patients with TBI.     

Osmotherapy with hypertonic saline attenuates water content in brain and extracerebral organs

OBJECTIVE: Because of their beneficial effects in patients with hemorrhagic shock and multiple-system trauma, hypertonic saline solutions are increasingly being used perioperatively for volume resuscitation. Although the anti-edema effects of hypertonic saline on brain are well documented in a variety of brain injury paradigms, its effects on the water content on other organs has not been studied rigorously. In this study, we tested the hypothesis that a) hypertonic saline when given as an intravenous bolus and continuous infusion attenuates water content of small bowel, lung, and brain in rats without neuro-injury; and b) attenuation of stroke-associated increases in lung water is dependent on achieving a target serum osmolality. DESIGN: Prospective laboratory animal study. SETTING: Research laboratory in a teaching hospital. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: In the first series of experiments, under controlled conditions of normoxia, normocarbia, and normothermia, spontaneously breathing, halothane-anesthetized (1.0-1.5%) adult male Wistar rats (280-320 g) were treated in a blinded randomized fashion with 7.5% hypertonic saline or 0.9% normal saline in a 8-mL/kg intravenous infusion for 3 hrs followed by a continuous intravenous infusion (1 mL/kg/hr) of 5% hypertonic saline or normal saline, respectively (n=10 each), for 48 hrs. A second group of rats were treated with continuous infusion only for 48 hrs of either 7.5% hypertonic saline or normal saline (1 mL/kg/hr) (n=10 each) without an intravenous bolus. Na?ve rats served as controls (n=10). Tissue water content of small bowel, lung, and brain was determined by comparing the wet-to-dry ratios at the end of the experiment. In a second series of experiments, rats (n=94) were subjected to 2 hrs of transient middle cerebral artery occlusion by the intraluminal occlusion technique. At 6 hrs following middle cerebral artery occlusion, rats were treated in a blinded randomized fashion with a continuous intravenous infusion of normal saline, 3% hypertonic saline, or 7.5% hypertonic saline for 24, 48, 72, and 96 hrs. Surgical shams served as controls (n=7). Hypertonic saline was instituted as chloride/acetate mixture (50:50) in all experiments. Serum osmolality was determined at the end of the experiment in all animals. MEASUREMENTS AND MAIN RESULTS: In rats without neuro-injury that received intravenous bolus followed by a continuous infusion, lung water content was significantly reduced with hypertonic saline (73.9+/-1.1%; 359+/-10 mOsm/L) (mean+/-sd) compared with normal saline treatment (76.1+/-0.53%; 298+/-4 mOsm/L) as was water content of small bowel (hypertonic saline, 69.1+/-5.8%; normal saline, 74.7+/-0.71%) and brain (hypertonic saline, 78.1+/-0.87%; normal saline, 79.2+/-0.38%) at 48 hrs. Stroke-associated increases in lung water content were attenuated with 7.5% hypertonic saline at all time points. There was a strong correlation between serum osmolality and attenuation of stroke-associated increases in lung water content (r=-.647) CONCLUSIONS: Bowel, lung, and brain water content is attenuated with hypertonic saline when serum osmolality is >350 mOsm/L without adverse effect on mortality in animals with and without neuro-injury. Attenuation of water content of extracerebral organs with hypertonic saline treatment may have therapeutic implications in perioperative fluid management in patients with and without brain injury.     

Regional intraparenchymal pressure differences in experimental intracerebral hemorrhage: effect of hypertonic saline

OBJECTIVE: To study regional intraparenchymal pressures within the cranial cavity during and after formation of intracerebral hemorrhage. We also assessed the effect of hypertonic saline on intraparenchymal pressure in different brain regions and on regional brain distribution of sodium within the brain. DESIGN: Prospective, controlled, laboratory trial. SETTINGS: Animal research laboratory. SUBJECTS: Eight mongrel dogs, weighing 15-25 kg. INTERVENTION: We introduced an intracerebral hematoma in eight mongrel dogs by infusing 6 mL of autologous arterial blood in the deep white matter adjacent to the basal ganglia. Sodium chloride (23.4%, 1.4 mL/kg) then was administered intravenously 6 hrs after introduction of hematoma. MEASUREMENTS AND MAIN RESULTS: Parenchymal pressure monitors were placed in the perihematoma region, both frontal lobes, and the cerebellum to record intraparenchymal pressure during and 6 hrs after intracerebral hematoma formation. Intraparenchymal pressure measurements were recorded for 3 more hours after administration of 23.4% sodium chloride. Regional cerebral perfusion pressure was calculated for each intraparenchymal pressure measurement. Regional sodium distribution was measured in extracts from brain regions by using ion selective electrode technique. A higher elevation in intraparenchymal pressure was recorded in the perihematoma region during the introduction of the hematoma compared with other compartments. After 5 mL of autologous blood was introduced, intraparenchymal pressure (mm Hg +/- SE) was significantly higher in the perihematoma region (42.1 +/- 3.5) than in the ipsilateral (30.0 +/- 4.6, p <.05) and contralateral (27.1 +/- 5.5, p <.01) frontal lobes and cerebellum (29.1 +/- 4.5, p <.05). Four hours after introduction of the hematoma, the cerebral perfusion pressure recorded in the perihematoma region (43.6 +/- 9.7) remained significantly lower than in the ipsilateral (58.6 +/- 9.3, p <.05) but not the contralateral frontal lobes (54.7 +/- 10.1) and cerebellum (51.0 +/- 11.1). Administration of 23.4% sodium chloride immediately reduced intraparenchymal pressure in each compartment. This effect was still observed at 3 hrs in each compartment. Sodium concentration was higher in the perihematoma region than in the frontal lobes, cerebellum, or brain stem. CONCLUSIONS: Prominent differences were observed in intraparenchymal pressure and cerebral perfusion pressure in the perihematoma region and frontal lobes during and after intracerebral hematoma. We speculate that the potential importance of regional intraparenchymal pressure differences in the clinical settings may be under appreciated. In this canine model of intracerebral hematoma, a single dose of hypertonic saline effectively reduces the intraparenchymal pressure in all regions of the brain.     

Hyperosmolar therapy in the treatment of severe head injury in children: mannitol and hypertonic saline

Traumatic brain injury is the result of a primary, acute injury and is complicated by the development of secondary injury due to hypotension and hypoxia. Cerebral edema due to brain injury compromises the delivery of essential nutrients and alters normal intracranial pressure. The Monroe-Kellie Doctrine defines the principles of intracranial pressure homeostasis. Treatment for intracranial hypertension is aimed at reducing the volume of 1 of the 3 intracranial compartments, brain tissue, blood, and cerebrospinal fluid. Hyperosmolar therapy is one treatment intervention in the care of patients with severe head injury resulting in cerebral edema and intracranial hypertension. The effect of hyperosmolar solutions on brain tissue was first studied nearly 90 years ago. Since that time, mannitol has become the most widely used hyperosmolar solution to treat elevated intracranial pressure. Increasingly, hypertonic saline solutions are being used as an adjunct to mannitol in basic science research and clinical studies. Hyperosmolar solutions are effective in reducing elevated intracranial pressure through 2 distinct mechanisms: plasma expansion with a resultant decrease in blood hematocrit, reduced blood viscosity, and decreased cerebral blood volume; and the creation of an osmotic gradient that draws cerebral edema fluid from brain tissue into the circulation. The pediatric section of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies adapted previously published guidelines for the treatment of adult brain injury into guidelines for the treatment of children with traumatic brain injury. These guidelines offer recommendations for the management of children with severe head injury, including the use of mannitol and hypertonic saline to treat intracranial hypertension. Acute and critical care pediatric advanced practice nurses caring for children with severe head injury should be familiar with management guidelines and the use of hyperosmolar solutions. The purpose of this article is to assist the advanced practice nurse in understanding the role of hyperosmolar therapy in the treatment of pediatric traumatic brain injury and review current guidelines for the use of mannitol and hypertonic saline.     

口服高渗甘露醇盐水多层螺旋CT小肠造影的临床应用价值

目的 评价口服高渗甘露醇盐水对比剂行多层螺旋CT小肠造影（MSCTE）的可行性和临床价值.方法 81例消化道病变和有小肠疾患症状的病例纳入研究（男47例,女34例,年龄26～81岁）,在90 min内口服约1500～3000 ml 高渗甘露醇盐水（2.5%甘露醇,1.5% NaCl）后,肌注20 mg山莨菪碱20 min后行CT三期扫描,并在工作站行冠状面、矢状面及任意斜面重组、多平面重组（MPR）、最大密度投影（MIP）和容积重建（VR）.将胃、小肠和结肠充盈程度分为满意、较好、不满意;按小肠长短和重叠分布程度分为密集型、均匀型和离散型.测量十二指肠、空肠和回肠各段小肠的最大管外径和肠壁强化程度,在动、静脉期将肠壁强化分为明显强化（＞90 HU）、中度强化（60～89 HU）和轻度强化（＜60 HU）.分析不同小肠病变的MSCTE表现.结果 除5例检查完成后出现腹泻外,其余患者均能顺利完成检查,未发现相关并发症.胃、小肠和结肠充盈满意46例,较好23例,不满意12例,十二指肠、空肠及回肠的充盈度经统计分析分别为（24±4.5）mm、（24±3.9）mm、（23±3.3）mm;小肠分布：小肠分布密集型7例,均匀型58例,离散型16例.小肠壁明显强化9例（动脉期明显强化有3例）,中度强化60例（动脉期明显强化17例）,轻度强化11例（动脉期明显强化3例）.MSCTE清楚地显示了肿瘤、Crohn病、粘连性肠梗阻等多种消化道疾患的肠内、肠壁、肠外血管、系膜及腹内脏器情况.结论 高渗甘露醇盐水MSCTE是一种简便、全方位显示小肠疾病的方法.     

高渗盐液治疗ICU重度脑外伤并休克患者的临床效果分析

目的 分析高渗盐液对ICU重度脑外伤并休克患者临床治疗效果情况.方法 选取我院2019年8月至2020年8月收治的ICU重度脑外伤并休克患者64例的临床资料,随机分为两组,各32例.对照组给予甘露醇溶液治疗,研究组给予高渗盐液进行治疗,观察两组临床效果及平均动脉压、心率情况.结果 治疗后,研究组总有效率比对照组高(P＜...     

Resuscitation from hemorrhagic shock: experimental model comparing normal saline,dextran, and hypertonic saline solutions

OBJECTIVE: To compare the effectiveness of normal saline, dextran, hypertonic, and hypertonic-hyperoncotic solutions in hemorrhagic shock. DESIGN: Laboratory investigation. SETTING: University hospital, Emergency Surgery and Intensive Care staff. SUBJECTS: Thirty-two large white female pigs. INTERVENTIONS: Routine care included: anesthesia and sedation (ketamine 10 mg/kg, droperidol 0.25 mg/kg, diazepam 0.7 mg/kg, fentanyl 0.006 mg/kg, 2% enflurane, 20% nitrous oxide, pancuronium bromide 0.13 mg/kg); volume-controlled ventilation (Paco(2) 35-40 torr; 4.7-5.4 kPa); cannulation of right carotid artery and pulmonary artery. Three flow probes (subdiaphragmatic aorta, superior mesenteric artery, right renal artery) and regional venous catheters (superior mesenteric vein, right renal vein) were positioned. Animals were bled to 45 mm Hg for 1 hr and resuscitated with four different fluids and blood to normal aortic blood flow and hemoglobin. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure and blood flow through abdominal aorta ([OV0312](aor)), mesenteric artery ([OV0312](mes)), and renal artery ([OV0312](ren)) were continuously monitored. Cardiac output, systemic and regional oxygen delivery ([U1E0A]o(2), [U1E0A]o(2mes), [U1E0A]o(2ren)), and consumption ([OV0312]o(2), [OV0312]o(2mes), [OV0312]o(2ren)) were recorded every 30 mins. Baseline [OV0312](aor) was restored with different amounts of fluids in the four groups: normal saline (91.35 +/- 22.18 mL/kg); dextran (16.24 +/- 4.42 mL/kg); hypertonic (13.70 +/- 1.44 mL/kg); and hypertonic-hyperoncotic (9.11 +/- 1.20 mL/kg). The amount of sodium load was less using dextran and hypertonic-hyperoncotic and sodium levels were only transiently increased after hypertonic infusion. Mean arterial pressure and cardiac output were normalized in all groups. Animals resuscitated with normal saline and dextran showed increased pulmonary artery pressures. [U1E0A]o(2) was significantly higher after hypertonic-hyperoncotic infusion, because of reduced hemodilution. Hypertonic and hypertonic-hyperoncotic normalized [OV0312](mes), [U1E0A]o(2mes), [OV0312]o(2mes), [OV0312](ren), and [U1E0A]o(2ren), whereas normal saline and dextran did not achieve this result. At the end of the experiment, hypertonic-hyperoncotic maintained mean arterial pressure, cardiac output, and [U1E0A]o(2) until the end of observation in contrast to normal saline, dextran, and hypertonic. CONCLUSIONS: Resuscitation with a small volume of hypertonic-hyperoncotic solution allows systemic and splanchnic hemodynamic and oxygen transport recovery, without an increase in pulmonary artery pressure. It only transiently increased sodium concentration.     

Higher-volume hypertonic saline and increased thrombotic risk in pediatric traumatic brain injury

PurposeHyperosmolar therapy is a mainstay in the acute medical management of traumatic brain injury (TBI). Emerging literature suggests that a hyperosmolar state may lead to thrombotic complications. The primary objective of this study was to investigate associations between hypertonic saline (HTS) and the outcome of deep venous thrombosis (DVT) in pediatric patients with severe TBI.Materials and methodsThis is a single-center retrospective cohort study of 58 patients admitted to the intensive care unit at a Level 1 pediatric trauma center between January 2010 and June 2013. Main measurements included volume of HTS administration, serum sodium levels, DVT confirmed with ultrasonography, survival at 30 days postinjury, and Glasgow Outcome Scale.ResultsThe cumulative total bolus volume of HTS (mL/kg) given to each subject was associated with DVT (P = .01). Peak sodium level and 72-hour sustained sodium levels were associated with DVT (P = .05). A sustained sodium level of at least 160 mmol/L was associated with DVT (P = .02).ConclusionIn children with severe TBI, the total bolus volume of 3% HTS and sustained sodium levels greater than 160 mmol/L are independently associated with DVT.     

Comparison of the protoscolocidal effectiveness of hypertonic saline, povidone-iodine and albendazole solutions in an experimental lung hydatid cyst model

Secondary hydatidosis is an important problem encountered during the surgical treatment of hydatid cysts. This study describes an experimental model of secondary hydatidosis by cyst inoculation, used to explore whether simultaneous inoculation of protoscolocidal agents could prevent secondary hydatidosis. Fertile cyst fluid was injected into the pleural space of rabbits alone (group 1, n = 8), and in combination with 2% albendazole solution (group 2, n = 8), 20% hypertonic saline (group 3, n = 8) or 10% povidone-iodine (group 4, n = 8). Computed tomography imaging of the thorax, indirect haemagglutination (IHA) titres and eosinophil counts were used to determine cyst development. After 16 months, three control rabbits had pneumothorax, seven had cysts and four had parenchymal nodules. Histopathological investigation of nodules revealed 87.5% cyst formation. Pleural thickening was observed in rabbits from all groups. Cyst formation rates, IHA titres and eosinophilia counts were higher in group 1 than in groups 2-4. This study demonstrated the experimental formation of secondary hydatidosis and found that topical protoscolocidal agents were beneficial in preventing cyst recurrence.     

高渗盐水对大鼠脑水肿及脑损伤标志物的影响

目的 探讨高渗盐水(HS)对大鼠脑缺血致脑水肿及脑损伤标志物的影响.方法 线栓法制作大鼠永久性右侧大脑中动脉闭塞脑缺血模型,随机分为3%HS组、10%HS组、生理盐水(NS)组,每组18只.于缺血6 h起,三组大鼠分别静注3%HS、10%HS或NS,均为0.3 mL/h,持续24 h.干预结束后测定缺血侧大脑含水量(BWC),干预前、后测定血神经元特异性烯醇化酶(NSE)、S-100蛋白(S-100)、血生化及血浆晶体渗透压等.结果 与NS组比较,干预后3%HS组、10%HS组BWC、NSE、S-100明显下降(P均＜0.05),血钠、氯浓度和血浆晶体渗透压明显升高(P均＜0.05);3%HS组与10%HS组BWC、血生化、血浆晶体渗透压、NSE及S-100比较差异无统计学意义(P均＞0.05).结论 3%HS和10%HS均可有效减轻脑缺血大鼠脑水肿,减轻脑损伤.     

Superiority of hypertonic saline/dextran over hypertonic saline during the first 30 min of resuscitation following hemorrhagic hypotension in conscious swine.

We compared the effectiveness of intravenously administering hypertonic saline/dextran (HSD; 7.5% NaCl in 6% Dextran-70, n = 6) to hypertonic saline (HS) alone (7.5% NaCl, n = 8) in rectifying detrimental effects of hemorrhage on cardiovascular function. Chronically instrumented conscious swine were hemorrhaged 37.5 ml/kg over 60 min. If untreated, this model is 100% lethal within 60 min. Swine received HSD or HS at 4 ml/kg. Functional variables were measured before and at 5, 15, and 30 min following treatment. HSD produced a significantly greater plasma volume expansion than HS alone (13.6 compared to 9.9 ml/kg). Over 30 min expansion was sustained in pigs receiving HSD but pigs receiving HS regressed. Cardiac index (CI) increased for both treatments, being greater with HSD, 104 ml/kg/min, compared to HS alone, 46 ml/kg/min. Neither group fully sustained these elevated values post-treatment, but remained consistently greater than values after hemorrhage; however, the difference in CI between treatments was maintained. Oxygen delivery showed a trend similar to that of CI. We conclude that resuscitation with HSD is superior to HS in improving cardiovascular function over the first 30 min after hemorrhage.     

高渗氯化钠溶液对创伤性休克大鼠的治疗作用

目的　探讨高渗氯化钠溶液复苏在创伤失血性休克治疗中的意义及其机制。方法　建立创伤性休克动物模型 ,随机分为对照组、处理组 ,处理组给予 7 5 %的高渗氯化钠溶液复苏 ,于休克末及给液后 1、3h测定骨骼肌、肝、小肠的组织氧分压 ,并测定给液后 2h后肺含水量变化 ,监测生命体征 ,记录存活时间。结果　复苏后处理组平均动脉压及肝脏、小肠的组织氧分压较对照组高 ,差异有显著性 (P <0 0 5 ) ,给液后 2h处理组大鼠肺含水量较对照组明显下降 ,差异有显著性 (P <0 0 5 ) ,处理组大鼠 1 2、2 4h存活率同对照组相比均有显著性差异。结论　高渗氯化钠溶液复苏可改善内脏器官的组织氧分压 ,减轻肺水肿 ,从而改善创伤性休克大鼠的预后     

The effect of hypertonic saline dextran on whole blood coagulation

Hypertonic saline dextran (RescueFlow) is being promoted for resuscitation from hypovolaemia following injury. We studied the in vitro effect on coagulation of serial dilutions of blood with this fluid. There was a mild procoagulant effect up to a dilution of 11% and an anticoagulant effect above this level, which rapidly increased so that coagulation was grossly deranged at a 15% dilution. Although the clinical significance of these findings is not yet known, it may suggest that for hypertonic saline dextran there is little to separate the top of the therapeutic window from the threshold of potentially serious adverse effects.     

Comparison of normal saline, hypertonic saline and hypertonic saline colloid resuscitation fluids in an infant animal model of hypovolemic shock

PurposeIncorrect resuscitation after hypovolemic shock is a major contributor to preventable pediatric death. Several studies have demonstrated that small volumes of hypertonic or hypertonic–hyperoncotic saline can be an effective initial resuscitation solution. However, there are no pediatric studies to recommend their use. The aim of this study is to determine if in an infant animal model of hemorrhagic shock, the use of hypertonic fluids, as opposed to isotonic crystalloids, would improve global hemodynamic and perfusion parameters.MethodsExperimental, randomized animal study including thirty-four 2-to-3-month-old piglets. 30 min after controlled 30 mL kg^?1 bleed, pigs were randomized to receive either normal saline (NS) 30 mL kg^?1 (n = 11), 3% hypertonic saline (HS) 15 mL kg^?1 (n = 12), or 5% albumin plus 3% hypertonic saline (AHS) 15 mL kg^?1 (n = 11).ResultsHigh baseline heart rate (HR) and low mean arterial pressure (MAP), cardiac index (CI), brain tissue oxygenation index (bTOI), and lactate were recorded 30 min after volume withdrawal, with no significant differences between groups. Thirty minutes after volume replacement there were no significant differences between groups for HR (NS, 188 ± 14; HS, 184 ± 14; AHS, 151 ± 14 bpm); MAP (NS, 80 ± 7; HS, 86 ± 7; AHS, 87 ± 7 mmHg); CI (NS, 4.1 ± 0.4; HS, 3.9 ± 0.4; AHS, 5.1 ± 0.4 mL min^?1 m^?2); lactate (NS, 2.8 ± 0.7; HS, 2.3 ± 0.6; AHS, 2.4 ± 0.6 mmol L^?1); bTOI (NS, 43.9 ± 2.2; HS, 40.1 ± 2.5; AHS, 46.1 ± 2.3%).ConclusionsIn this model of hypovolemic shock, hypertonic fluids achieved similar end-points as twice the volume of NS. Animals treated with albumin plus hypertonic saline presented prolonged increase in blood volume parameters and recovery of the oxygen debt.