ライフサイエンスコーパス: fluid resuscitation

1 inistration of normal saline solution (i.e., fluid resuscitation).

2 inistration of normal saline solution (i.e., fluid resuscitation).

3 inistration of normal saline solution (i.e., fluid resuscitation).

4 inistration of normal saline solution (i.e., fluid resuscitation).

5 olic blood pressure less than 90 mm Hg after fluid resuscitation.

6 d perioperative medicine as controversial as fluid resuscitation.

7 (0.2 units/kg) or placebo during the initial fluid resuscitation.

8 eived supportive standard intensive care and fluid resuscitation.

9 65 mm Hg, both during and following adequate fluid resuscitation.

10 nary circulation in the absence of immediate fluid resuscitation.

11 stinal barrier function after hemorrhage and fluid resuscitation.

12 (two times the shed blood volume) to provide fluid resuscitation.

13 Only two of 13 deaths occurred during fluid resuscitation.

14 e level greater than 2 mmol/L after adequate fluid resuscitation.

15 model of hemorrhagic shock in the absence of fluid resuscitation.

16 be as effective and efficient as intravenous fluid resuscitation.

17 icrocirculations during hemorrhage and after fluid resuscitation.

18 roximately 40 mm Hg for 90 mins) followed by fluid resuscitation.

19 minutes after injury before any significant fluid resuscitation.

20 e has been immediate, aggressive intravenous fluid resuscitation.

21 sure 35-40 mm Hg for 90 minutes) followed by fluid resuscitation.

22 hock (blood pressure, 35 mm Hg), followed by fluid resuscitation.

23 y PulseCO and LiDCO at 10 and 120 mins after fluid resuscitation.

24 inistration of either crystalloid or colloid fluid resuscitation (1B); fluid challenge to restore mea

25 ntricular (RV) infarct (1C), the efficacy of fluid resuscitation (1C) and inotropic therapy (2C), pre

26 Interventions included fluid resuscitation (35 cases), pleural drainage (three

27 1.4 [0.53--7.9] mmol/L, p<0.0001) and after fluid resuscitation (5.5 [1.3--18.6] vs 1.3 [0.26--3.2],

28 eutic interventions included median 80-mL/kg fluid resuscitation; 65% of patients required dopamine,

29 likely to require vasopressors after initial fluid resuscitation (68.5% vs. 52.5%, p < 0.01).

30 Acute fluid resuscitation after trauma-hemorrhage restores but

31 Fluid resuscitation after traumatic hemorrhage has histo

32 Early therapy of sepsis involving fluid resuscitation and antibiotic administration has be

33 After fluid resuscitation and antibiotic therapy, careful card

34 ligation and puncture and were treated with fluid resuscitation and antibiotics.

35 nts, and profound shock requiring aggressive fluid resuscitation and careful hemodynamic monitoring a

36 rapy when cardiac output remains low despite fluid resuscitation and combined inotropic/vasopressor t

37 Variability in fluid resuscitation and difficulty recognizing early sep

38 receive after 12 hours of fecal peritonitis fluid resuscitation and either norepinephrine (group NE;

39 urfactant, glucose, insulin, hydrocortisone, fluid resuscitation and fluid removal, superior vena cav

40 eading to hypoxemia and may be used to guide fluid resuscitation and optimize tissue oxygenation.

41 ssue hypoperfusion resulting from inadequate fluid resuscitation and the development of AKI after lun

42 We sought to review the evidence for rapid fluid resuscitation and to outline its clinical indicati

43 impact on the current clinical approach for fluid resuscitation and treatment of coagulopathy for tr

44 as important clinical implications regarding fluid resuscitation and treatment of coagulopathy.

45 yndrome and persistent hypotension following fluid resuscitation and vasopressor infusion.

46 e in adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to

47 in our institution of "poorly responsive to fluid resuscitation and vasopressor therapy" being the p

48 heir "blood pressure is poorly responsive to fluid resuscitation and vasopressor therapy." Because th

49 includes hypotensive hemostasis, minimizing fluid resuscitation, and allowing the systolic blood pre

50 Large bowel resection, large-volume fluid resuscitation, and an increasing number of abdomin

51 quivalent (IE) counts, estimated blood loss, fluid resuscitation, and blood transfusions.

52 tachycardia; and d) refractory shock despite fluid resuscitation, and vasoactive medications.

53 Adequate fluid resuscitation, appropriate inotropic support, atte

54 pportive treatment consisting of high-volume fluid resuscitation (approximately 10 liters per day in

55 Intravenous and enteral fluid resuscitation are frequently used therapies in the

56 ars that pharmacologic agents in addition to fluid resuscitation are needed to restore cardiovascular

57 ation of inhalation injury and its impact on fluid resuscitation, as well as on a protective lung str

58 tion facilitated the hemodynamic response to fluid resuscitation, attenuated tissue inflammatory inju

59 capacity, more difficult intravenous access, fluid resuscitation based on weight with 40-60 mL kg or

60 d with % TBSA burn, inhalation injury grade, fluid resuscitation, Baux score, revised Baux score, Den

61 Rapid fluid resuscitation benefits pediatric patients with sev

62 dentified patients who received large-volume fluid resuscitation, defined as greater than 60 mL/kg ov

63 in intracranial pathologies, as small volume fluid resuscitation during spinal shock, and as maintena

64 Fluid resuscitation during the first 24 to 48 hrs after

65 e been developed in an effort to standardize fluid resuscitation during this time.

66 Optimal sepsis management including fluid resuscitation, early antibiotic administration, an

67 critical care interventions, including rapid fluid resuscitation, early antibiotics, and patient moni

68 a dedicated study medical officer comprising fluid resuscitation, early antibiotics, and regular moni

69 re management components such as the initial fluid resuscitation, end-organ support, pain management,

70 rvention with broad-spectrum antibiotics and fluid resuscitation, even in the absence of hypotension,

71 Fluid resuscitation following hemorrhagic shock is often

72 ough most clinicians still generally support fluid resuscitation for multisystem blunt trauma, partic

73 tion, and in 60- to 120-min intervals during fluid resuscitation for up to 300 min.

74 shock (blood pressure 35 mmHg), followed by fluid resuscitation (four times the shed blood volume in

75 aCl adenosine, lidocaine, and Mg hypotensive fluid resuscitation from the rat to the pig.

76 ents might have therapeutic potential during fluid resuscitation from trauma.

77 eatitis, post-cardiopulmonary resuscitation, fluid resuscitation > 5 L/24 hr, vasoactive or inotropic

78 s. 12% of the survivors (p<.05), and delayed fluid resuscitation (>2 hrs after burn injury), identifi

79 level greater than 2 mmol/L (18 mg/dL) after fluid resuscitation had a significantly higher mortality

80 Rapid fluid resuscitation has gained increased recognition sin

81 Liberal fluid resuscitation has little effect on this sequestrat

82 n remain controversial, and the best form of fluid resuscitation has yet to be identified.

83 nd efficacy of hydroxyethyl starch (HES) for fluid resuscitation have not been fully evaluated, and a

84 eceived intravenous antibiotics and adequate fluid resuscitation, hemodynamic management according to

85 Among 4,710 patients receiving large-volume fluid resuscitation, hyperchloremic acidosis was documen

86 ith two lisofylline dosing regimens added to fluid resuscitation in a shock model.

87 asma levels of IL-6, we propose that chronic fluid resuscitation in addition to acute fluid replaceme

88 ecreases in cardiac output or the effects of fluid resuscitation in dogs.

89 O) during severe hemorrhagic shock and after fluid resuscitation in dogs.

90 ized that administration of AM/AMBP-1 during fluid resuscitation in hemorrhaged animals (i.e., posttr

91 starch (HES) [corrected] is widely used for fluid resuscitation in intensive care units (ICUs), but

92 esponded to notable changes in the volume of fluid resuscitation in patients with heart failure and/o

93 antly related to blood loss before and after fluid resuscitation in the 16 survivors.

94 omly assigned patients with severe sepsis to fluid resuscitation in the ICU with either 6% HES 130/0.

95 ebate about the safety and efficacy of rapid fluid resuscitation in the pediatric patient.

96 develops during abdominal surgery and after fluid resuscitation in trauma patients.

97 Hypotensive fluid resuscitation in uncontrolled hemorrhagic shock wi

98 5 +/- 5 (SEM) mm Hg for 90 mins, followed by fluid resuscitation) in male C3H/HeN mice and the animal

99 hibitor improved the hemodynamic response to fluid resuscitation, increased blood oxygen content, pre

100 Endotoxin administration with fluid resuscitation induced a distributive shock with a

101 mmon cause of acute kidney injury (AKI), and fluid resuscitation is a major part of therapy.

102 Fluid resuscitation is different in bleeding and septic

103 Rapid fluid resuscitation is most commonly used for children w

104 Fluid resuscitation is the cornerstone of sepsis treatme

105 Therefore, following the initial fluid resuscitation, it is important to identify which p

106 urring as a consequence of overly aggressive fluid resuscitation may adversely affect outcome in hemo

107 eplacement therapy, as well as goal-directed fluid resuscitation may lead to improved survival in cri

108 s and arterial catheterization, antibiotics, fluid resuscitation, mechanical ventilation, vasopressor

109 l blood lactate early (median 4 h) and after fluid resuscitation (median 12 h) in patients admitted t

110 In separate experiments, using a fluid resuscitation model we studied mitochondrial funct

111 the fluids they received during large-volume fluid resuscitation multiplied by the volume of fluids.

112 resuscitation: retransfusion of shed blood, fluid resuscitation, norepinephrine titrated to maintain

113 drated and need adequate vascular access for fluid resuscitation, nutrition, and phlebotomy for labor

114 ded by algorithms including upper limits for fluid resuscitation of extravascular lung water (<10 mL/

115 e, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic

116 associated with statistically more rigorous fluid resuscitation of patients, greater administration

117 Recent studies show that early, aggressive fluid resuscitation of up to 60 ml/kg within 1-2 h may b

118 n = 9) or sham burn receiving anesthesia and fluid resuscitation only (n = 8) and were killed 48 hrs

119 sing to IAH/ACS include sepsis, large volume fluid resuscitation, polytransfusion, mechanical ventila

120 mendations are to limit or delay intravenous fluid resuscitation preoperatively in those with uncontr

121 e evolving evidence suggests that aggressive fluid resuscitation prior to hemostasis leads to additio

122 ount of chloride received during intravenous fluid resuscitation (r = .44), with the base excess chan

123 rocardiography and echocardiography results, fluid resuscitation, radiography results, and laboratory

124 Fluid resuscitation remains the cornerstone of acute bur

125 ropriate use of loperamide, and knowledge of fluid resuscitation requirements of affected patients is

126 interest was first 24-hour blood product and fluid resuscitation requirements.

127 ted to hemorrhage and underwent a randomized fluid resuscitation scheme on separate visits 1) formula

128 trials from the past to the present include fluid resuscitation, sepsis, immune function, hypermetab

129 There were no sex differences in fluid resuscitation, shock index, coagulation, and base

130 This approach to fluid resuscitation should be abandoned.

131 Transfer patients were less likely to have fluid resuscitation started by 3 hours (54% vs 89%; p <

132 nalysis to compare liberal versus restricted fluid resuscitation strategies in trauma patients.

133 nal studies, odds for mortality with liberal fluid resuscitation strategies increased (odds ratio, 1.

134 rent evidence indicates that initial liberal fluid resuscitation strategies may be associated with hi

135 tment of hemorrhagic shock in the absence of fluid resuscitation; therefore DCA may be a good candida

136 In the absence of fluid resuscitation, these changes persisted and were ac

137 dentification of septic patients, aggressive fluid resuscitation, timely antibiotic administration, a

138 lowed by UHS via tail amputation and limited fluid resuscitation to maintain mean arterial pressure a

139 lterations that can be minimized by adequate fluid resuscitation to maintain tissue perfusion, early

140 to 135 mins) with hemostasis and aggressive fluid resuscitation to normalize hemodynamics; and obser

141 Acute bleeding management relies on fluid resuscitation to promote renal excretion of active

142 Rats were observed without fluid resuscitation until death (apnea and pulselessness

143 ide or 0.9% sodium chloride (saline) for all fluid resuscitation until ICU discharge, death, or 90 da

144 fs and combinations for blood pressure (BP), fluid resuscitation, vasopressors, serum lactate level,

145 injury characteristics that most influenced fluid resuscitation volumes received.

146 s was easily established in all animals, and fluid resuscitation was carried out effectively through

147 After 4 hours of hypotension, fluid resuscitation was initiated with a crystalloid sol

148 As fluid resuscitation was initiated, tumor necrosis factor

149 Fluid resuscitation was performed with saline alone or i

150 After randomization, fluid resuscitation was started 2 hours after severe acu

151 d hemorrhage with an extremely low volume of fluid resuscitation was used to mimic the combat situati

152 g values for a threshold of 3.0 mmol/L after fluid resuscitation were 76%, 97%, 30, and 0.24.

153 ne output < 0.5 mL/kg/hr for > 6 hrs despite fluid resuscitation when applicable) predicts meaningful

154 subdiaphragmatic blood loss and allow for IV fluid resuscitation when intrinsic cardiac activity is s

155 pressure less than 90 mm Hg after an initial fluid resuscitation, who lacked an obvious source of hyp

156 r conventional cooling methods consisting of fluid resuscitation with 0.9% sodium chloride solution,

157 Fluid resuscitation with acadesine produced no adverse h

158 hod within 12 hrs of diagnosis (1C); initial fluid resuscitation with crystalloid (1B) and considerat

159 Acidotic patients received fluid resuscitation with either dextran 70 or starch at

160 Patients with severe sepsis assigned to fluid resuscitation with HES 130/0.42 had an increased r

161 Numerous animal studies have suggested that fluid resuscitation with HS bolus after hemorrhagic shoc

162 g from normotensive to hypotensive (limited) fluid resuscitation with plasma substitutes.

163 ldly to moderately dehydrated child, enteral fluid resuscitation with the aid of an antiemetic such a

164 olloid, and electrolyte solution for limited fluid resuscitation with the smallest volume should cont

165 septic shock requiring vasopressors despite fluid resuscitation within a maximum of 6 hours after th