Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside

Lévy, Bruno; Collin, Solène; Sennoun, N.; Ducrocq, Nicolas; Kimmoun, Antoine; Asfar, Pierre; Perez, Pierre; Meziani, Ferhat

doi:10.1007/s00134-010-2045-8

Cited by 172 publications

(94 citation statements)

References 78 publications

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“…These results may suggest that progression of AKI is more likely when higher doses of norepinephrine are required to maintain targeted blood pressure levels in more severely ill patients with severe sepsis, plausibly by causing excess constriction of regional vascular beds [29]. It may also reflect the impact of more severe illness and more profound vascular hyporesponsiveness on the progression of AKI [30]. …”

Section: Discussionmentioning

confidence: 99%

Hemodynamic variables and progression of acute kidney injury in critically ill patients with severe sepsis: data from the prospective observational FINNAKI study

et al. 2013

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IntroductionKnowledge of the association of hemodynamics with progression of septic acute kidney injury (AKI) is limited. However, some recent data suggest that mean arterial pressure (MAP) exceeding current guidelines (60–65 mmHg) may be needed to prevent AKI. We hypothesized that higher MAP during the first 24 hours in the intensive care unit (ICU), would be associated with a lower risk of progression of AKI in patients with severe sepsis.MethodsWe identified 423 patients with severe sepsis and electronically recorded continuous hemodynamic data in the prospective observational FINNAKI study. The primary endpoint was progression of AKI within the first 5 days of ICU admission defined as new onset or worsening of AKI by the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. We evaluated the association of hemodynamic variables with this endpoint. We included 53724 10-minute medians of MAP in the analysis. We analysed the ability of time-adjusted MAP to predict progression of AKI by receiver operating characteristic (ROC) analysis.ResultsOf 423 patients, 153 (36.2%) had progression of AKI. Patients with progression of AKI had significantly lower time-adjusted MAP, 74.4 mmHg [68.3-80.8], than those without progression, 78.6 mmHg [72.9-85.4], P < 0.001. A cut-off value of 73 mmHg for time-adjusted MAP best predicted the progression of AKI. Chronic kidney disease, higher lactate, higher dose of furosemide, use of dobutamine and time-adjusted MAP below 73 mmHg were independent predictors of progression of AKI.ConclusionsThe findings of this large prospective multicenter observational study suggest that hypotensive episodes (MAP under 73 mmHg) are associated with progression of AKI in critically ill patients with severe sepsis.

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Section: Discussionmentioning

confidence: 99%

Hemodynamic variables and progression of acute kidney injury in critically ill patients with severe sepsis: data from the prospective observational FINNAKI study

et al. 2013

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“…Other clinical studies have shown that hyperchloremic acidosis resulting from saline infusion is associated with reduced gastric blood flow and mucosal pH in elderly surgical patients (Wilkes et al, 2001), delayed recovery of gut function, increased complications, prolonged hospital stay in patients undergoing colonic surgery (Lobo et al, 2002a;Brandstrup et al, 2003), and impairment in cardiac contractility as well as diminished response to inotrope causing hypotension (Mitchell et al, 1972;Levy et al, 2010;Schotola et al, 2012). Saline resuscitation for patients with gastrointestinal hemorrhage exacerbated bleeding resulting in more transfusions compared to balanced fluid resuscitation (Barak et al, 2004).…”

Section: Saline-induced Pathological Effects In Humansmentioning

confidence: 99%

0.9% saline is neither normal nor physiological

Sun

Yap

et al. 2016

J. Zhejiang Univ. Sci. B

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Abstract:The purpose of this review is to objectively evaluate the biochemical and pathophysiological properties of 0.9% saline (henceforth: saline) and to discuss the impact of saline infusion, specifically on systemic acid-base balance and renal hemodynamics. Studies have shown that electrolyte balance, including effects of saline infusion on serum electrolytes, is often poorly understood among practicing physicians and inappropriate saline prescribing can cause increased morbidity and mortality. Large-volume (>2 L) saline infusion in healthy adults induces hyperchloremia which is associated with metabolic acidosis, hyperkalemia, and negative protein balance. Saline overload (80 ml/kg) in rodents can cause intestinal edema and contractile dysfunction associated with activation of sodium-proton exchanger (NHE) and decrease in myosin light chain phosphorylation. Saline infusion can also adversely affect renal hemodynamics. Microperfusion experiments and real-time imaging studies have demonstrated a reduction in renal perfusion and an expansion in kidney volume, compromising O 2 delivery to the renal parenchyma following saline infusion. Clinically, saline infusion for patients post abdominal and cardiovascular surgery is associated with a greater number of adverse effects including more frequent blood product transfusion and bicarbonate therapy, reduced gastric blood flow, delayed recovery of gut function, impaired cardiac contractility in response to inotropes, prolonged hospital stay, and possibly increased mortality. In critically ill patients, saline infusion, compared to balanced fluid infusions, increases the occurrence of acute kidney injury. In summary, saline is a highly acidic fluid. With the exception of saline infusion for patients with hypochloremic metabolic alkalosis and volume depletion due to vomiting or upper gastrointestinal suction, indiscriminate use, especially for acutely ill patients, may cause unnecessary complications and should be avoided. More education regarding saline-related effects and adequate electrolyte management is needed.

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“…The pharmacodynamic effects of catecholamines are characterized by a linear increase in effect which is dependent on the logarithmic increase of the concentration [12]. Consequently, high doses of norepinephrine may be necessary to maintain mean arterial pressure (MAP) above 65 mmHg [13]. …”

Section: Introductionmentioning

confidence: 99%

Outcome of patients with septic shock and high-dose vasopressor therapy

Auchet

Régnier

Girerd

et al. 2017

Ann. Intensive Care

118

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BackgroundDespite the dissemination of international guidelines, mortality from septic shock remains high. Norepinephrine is recommended as first-line vasopressor therapy with a target mean arterial pressure of 65 mmHg. High-dose vasopressor (HDV) may also be required. This study aimed to assess survival in patients with septic shock requiring HDV. We conducted a retrospective study of patients admitted between January 2008 and December 2013 to a 13-bed ICU for septic shock and receiving high-dose vasopressor therapy (defined by a dose >1 µg/kg/min). Primary outcome was 28-day mortality (D28). Secondary outcomes were 90-day mortality (D90), organ failure score (SOFA), duration of organ failure, duration and dosage of vasopressor agent and ischemic complications.ResultsIn our cohort of 106 patients, mortality reached 60.4% at D28 and 66.3% at D90. One in two patients died before D10. The weight-based mean dose of vasopressor (WMD) represented the best prognostic factor. Using a cutoff of 0.75 µg/kg/min, WMD was associated with mortality with a sensitivity of 73% and specificity of 74%. The mortality rate reached 86.4% when WMD was above the cutoff value and associated with a SOFA score >10. Digital or limb necrosis was documented in 6 patients (5.7%).ConclusionsIn total, 40% of septic shock patients receiving high-dose vasopressor therapy survived at day 28 after admission. A WMD cutoff value of 0.75 µg/kg/min, associated with a >10 SOFA score, was a strong predictor of death. These results provide insights into outcome of refractory septic shock, showing that administration of high-dose vasopressor may indeed be useful in these patients.

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Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside

Cited by 172 publications

References 78 publications

Hemodynamic variables and progression of acute kidney injury in critically ill patients with severe sepsis: data from the prospective observational FINNAKI study

Hemodynamic variables and progression of acute kidney injury in critically ill patients with severe sepsis: data from the prospective observational FINNAKI study

0.9% saline is neither normal nor physiological

Outcome of patients with septic shock and high-dose vasopressor therapy

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