Role of Early Fluid Resuscitation in Pediatric Septic Shock

JAMA ◽  
1991 ◽  
Vol 266 (9) ◽  
pp. 1242 ◽  
Author(s):  
Joseph A. Carcillo
Keyword(s):  
Septic Shock ◽  
Fluid Resuscitation ◽  
Early Fluid

Role of early fluid resuscitation in pediatric septic shock

JAMA ◽  
1991 ◽  
Vol 266 (9) ◽  
pp. 1242-1245 ◽  
Author(s):  
J. A. Carcillo
Keyword(s):  
Septic Shock ◽  
Fluid Resuscitation ◽  
Early Fluid

Postoperative Vasodilatory Shock

2020 ◽  
pp. 333-342
Author(s):  
Fiona Roberts ◽  
Alan Gaffney
Keyword(s):  
Septic Shock ◽  
Cardiac Output ◽  
Fluid Resuscitation ◽  
Antimicrobial Therapy ◽  
Pulse Pressure ◽  
Vasodilatory Shock ◽  
First Line ◽  
Treatment Interventions ◽  
Common Cause ◽  
Early Fluid

This chapter discusses vasodilatory shock. The hallmark of vasodilatory shock is hypotension with normal or increased cardiac output. The hyperdynamic circulatory state of vasodilatory shock results in a tachycardia and an increased pulse pressure. Radiological and biochemical investigations can assist with determining the diagnosis of shock. The causes of vasodilatory shock are diverse; they include sepsis, surgical insult, anaphylaxis, and others such as trauma, burns, and pancreatitis. However, sepsis is by far the most common cause of vasodilatory shock. The pathophysiology of vasodilatory shock is also complex and multifactorial. Although still not fully understood, it is widely accepted that it includes activation of several intrinsic vasodilatory pathways and a vascular hyporesponsiveness to vasopressors. Early fluid resuscitation and appropriate antimicrobial therapy are the most crucial treatment interventions in septic shock. Meanwhile, noradrenaline is the first-line vasopressor of choice in septic shock.

The Role of IL-1, IL-6, TNF-α and MIF in Relative Adrenal Insufficiency in Septic Shock: A Study in Piglet Model

2018 ◽  
Author(s):  
Bina Akura ◽  
Jose Batubara ◽  
Zakiudin Munasir ◽  
Gunati unknown ◽  
Joedo Prihartono ◽  
...  
Keyword(s):  
Septic Shock ◽  
Adrenal Insufficiency ◽  
Relative Adrenal Insufficiency ◽  
Tnf Α

The Role of Histones and Heparin in Sepsis: A Review

2021 ◽  
pp. 088506662199232
Author(s):  
Xiaojuan Zhang ◽  
Xin Li
Keyword(s):  
Septic Shock ◽  
Multiple Organ ◽  
Clinical Settings ◽  
The Past ◽  
Life Saving ◽  
Extracellular Histones ◽  
Sepsis And Septic Shock ◽  
Development And Management ◽  
Made In

Septic shock with multiple organ failure is a devastating situation in clinical settings. Through the past decades, much progress has been made in the management of sepsis and its underlying pathogenesis, but a highly effective therapeutic has not been developed. Recently, macromolecules such as histones have been targeted in the treatment of sepsis. Histones primarily function as chromosomal organizers to pack DNA and regulate its transcription through epigenetic mechanisms. However, a growing body of research has shown that histone family members can also exert cellular toxicity once they relocate from the nucleus into the extracellular space. Heparin, a commonly used anti-coagulant, has been shown to possess life-saving capabilities for septic patients, but the potential interplay between heparin and extracellular histones has not been investigated. In this review, we summarize the pathogenic roles of extracellular histones and the therapeutic roles of heparin in the development and management of sepsis and septic shock.

scholarly journals Peroxynitrite decomposition catalyst reduces vasopressin requirement in ovine MRSA sepsis

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Osamu Fujiwara ◽  
Satoshi Fukuda ◽  
Ernesto Lopez ◽  
Yaping Zeng ◽  
Yosuke Niimi ◽  
...  
Keyword(s):  
Septic Shock ◽  
Fluid Resuscitation ◽  
Conscious State ◽  
Smoke Inhalation ◽  
Post Injury ◽  
Adjunct Treatment ◽  
Aggressive Fluid Resuscitation ◽  
Severe Hypotension ◽  
Bolus Intravenous Injection

Abstract Background Sepsis is one of the most frequent causes of death in the intensive care unit. Host vascular hypo-responsiveness to vasopressors during septic shock is one of the challenging problems. This study tested the hypothesis that adjunct therapy with peroxynitrite decomposition catalyst (WW-85) would reduce arginine vasopressin (AVP) requirements during sepsis resuscitation, using ovine sepsis model. Methods Thirteen adult female Merino sheep, previously instrumented with multiple vascular catheters, were subjected to “two-hit” (cotton smoke inhalation and intrapulmonary instillation of live methicillin-resistant Staphylococcus aureus; 3.5 × 1011 colony-forming units) injury. Post injury, animals were awakened and randomly allocated to the following groups: (1) AVP: injured, fluid resuscitated, and titrated with AVP, n = 6 or (2) WW-85 + AVP: injured, fluid resuscitated, treated with WW-85, and titrated with AVP, n = 7. One-hour post injury, a bolus intravenous injection of WW-85 (0.1 mg/kg) was followed by a 23-h continuous infusion (0.02 mg/kg/h). Titration of AVP started at a dose of 0.01 unit/min, when mean arterial pressure (MAP) decreased by 10 mmHg from baseline, despite aggressive fluid resuscitation, and the rate was further adjusted to maintain MAP. After the injury, all animals were placed on a mechanical ventilator and monitored in the conscious state for 24 h. Results The injury induced severe hypotension refractory to aggressive fluid resuscitation. High doses of AVP were required to partially attenuate the sepsis-induced hypotension. However, the cumulative AVP requirement was significantly reduced by adjunct treatment with WW-85 at 17–24 h after the injury (p < 0.05). Total AVP dose and the highest AVP rate were significantly lower in the WW-85 + AVP group compared to the AVP group (p = 0.02 and 0.04, respectively). Treatment with WW-85 had no adverse effects. In addition, the in vitro effects of AVP on isolated artery diameter changes were abolished with peroxynitrite co-incubation. Conclusions The modulation of reactive nitrogen species, such as peroxynitrite, may be considered as a novel adjunct treatment option for septic shock associated with vascular hypo-responsiveness to vasopressors.

scholarly journals Effects of capillary refill time-vs. lactate-targeted fluid resuscitation on regional, microcirculatory and hypoxia-related perfusion parameters in septic shock: a randomized controlled trial

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ricardo Castro ◽  
Eduardo Kattan ◽  
Giorgio Ferri ◽  
Ronald Pairumani ◽  
Emilio Daniel Valenzuela ◽  
...  
Keyword(s):  
Septic Shock ◽  
Randomized Controlled Trial ◽  
Fluid Resuscitation ◽  
Controlled Trial ◽  
Tissue Perfusion ◽  
Capillary Refill Time ◽  
Capillary Refill ◽  
Randomized Controlled ◽  
Microcirculatory Flow ◽  
The Impact

Abstract Background Persistent hyperlactatemia has been considered as a signal of tissue hypoperfusion in septic shock patients, but multiple non-hypoperfusion-related pathogenic mechanisms could be involved. Therefore, pursuing lactate normalization may lead to the risk of fluid overload. Peripheral perfusion, assessed by the capillary refill time (CRT), could be an effective alternative resuscitation target as recently demonstrated by the ANDROMEDA-SHOCK trial. We designed the present randomized controlled trial to address the impact of a CRT-targeted (CRT-T) vs. a lactate-targeted (LAC-T) fluid resuscitation strategy on fluid balances within 24 h of septic shock diagnosis. In addition, we compared the effects of both strategies on organ dysfunction, regional and microcirculatory flow, and tissue hypoxia surrogates. Results Forty-two fluid-responsive septic shock patients were randomized into CRT-T or LAC-T groups. Fluids were administered until target achievement during the 6 h intervention period, or until safety criteria were met. CRT-T was aimed at CRT normalization (≤ 3 s), whereas in LAC-T the goal was lactate normalization (≤ 2 mmol/L) or a 20% decrease every 2 h. Multimodal perfusion monitoring included sublingual microcirculatory assessment; plasma-disappearance rate of indocyanine green; muscle oxygen saturation; central venous-arterial pCO2 gradient/ arterial-venous O2 content difference ratio; and lactate/pyruvate ratio. There was no difference between CRT-T vs. LAC-T in 6 h-fluid boluses (875 [375–2625] vs. 1500 [1000–2000], p = 0.3), or balances (982[249–2833] vs. 15,800 [740–6587, p = 0.2]). CRT-T was associated with a higher achievement of the predefined perfusion target (62 vs. 24, p = 0.03). No significant differences in perfusion-related variables or hypoxia surrogates were observed. Conclusions CRT-targeted fluid resuscitation was not superior to a lactate-targeted one on fluid administration or balances. However, it was associated with comparable effects on regional and microcirculatory flow parameters and hypoxia surrogates, and a faster achievement of the predefined resuscitation target. Our data suggest that stopping fluids in patients with CRT ≤ 3 s appears as safe in terms of tissue perfusion. Clinical Trials: ClinicalTrials.gov Identifier: NCT03762005 (Retrospectively registered on December 3rd 2018)

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