Early prediction of norepinephrine dependency and refractory septic shock with a multimodal approach of vascular failure

Conrad, Marie; Perez, Pierre; Thivilier, Carine; Lévy, Bruno

doi:10.1016/j.jcrc.2015.03.029

Cited by 17 publications

(39 citation statements)

References 15 publications

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“…Other definitions are (a) worsening circulatory failure despite aggressive use of vasopressors and (b) increasing lactic acidosis despite 6 h of extrarenal replacement therapy (ERRT) [ 11 ]. In a study of 51 consecutive patients with septic shock [ 12 ], an overall 45% mortality was observed. Sixteen patients presented with refractory septic shock and death (31% of the enrolled patients).…”

Section: Septic Shockmentioning

confidence: 99%

“…Sixteen patients presented with refractory septic shock and death (31% of the enrolled patients). The definition of refractory septic shock of this group [ 12 ] was no reversal of shock (i.e., an inability to sustain SBP >90 mmHg for >24 h without NA): In the refractory septic shock group, the mortality over 48 h was 19%, given the whole 51 patients: ten patients (62% of the patients in refractory septic shock) died within 48 h of circulatory failure. The mortality over 28 d (early circulatory failure and late multiple organ failure) in the refractory septic shock patients was 100%.…”

Section: Septic Shockmentioning

confidence: 99%

“… In nonrefractory septic shock, the mortality over 28 d was 20%. The NA requirements were ≈1 μ g-1·kg-1·min-1, that is, ≈4 mg·h-1 [ 12 ]. …”

Section: Septic Shockmentioning

confidence: 99%

“…The second line of therapy is the use of vasopressors, usually NA, to achieve a MAP ≥65 mmHg. The dose of NA required varies from ≈1 μ g-1·kg-1·min-1 to ≈2.6 μ g-1·kg-1·min-1, respectively, in nonrefractory versus refractory septic shock (4 to 11 mg·h-1) [ 12 ]. However, the same established group [ 14 ] uses NA as high as 50–100 mg·h-1 to treat refractory septic shock.…”

Section: Septic Shockmentioning

confidence: 99%

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Pressor Response to Noradrenaline in the Setting of Septic Shock: Anything New under the Sun—Dexmedetomidine, Clonidine? A Minireview

Géloën

Pichot

Leroy

et al. 2015

BioMed Research International

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Progress over the last 50 years has led to a decline in mortality from ≈70% to ≈20% in the best series of patients with septic shock. Nevertheless, refractory septic shock still carries a mortality close to 100%. In the best series, the mortality appears related to multiple organ failure linked to comorbidities and/or an intense inflammatory response: shortening the period that the subject is exposed to circulatory instability may further lower mortality. Treatment aims at reestablishing circulation within a “central” compartment (i.e., brain, heart, and lung) but fails to reestablish a disorganized microcirculation or an adequate response to noradrenaline, the most widely used vasopressor. Indeed, steroids, nitric oxide synthase inhibitors, or donors have not achieved overwhelming acceptance in the setting of septic shock. Counterintuitively, α 2-adrenoceptor agonists were shown to reduce noradrenaline requirements in two cases of human septic shock. This has been replicated in rat and sheep models of sepsis. In addition, some data show that α 2-adrenoceptor agonists lead to an improvement in the microcirculation. Evidence-based documentation of the effects of alpha-2 agonists is needed in the setting of human septic shock.

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Section: Septic Shockmentioning

confidence: 99%

Section: Septic Shockmentioning

confidence: 99%

“… In nonrefractory septic shock, the mortality over 28 d was 20%. The NA requirements were ≈1 μ g-1·kg-1·min-1, that is, ≈4 mg·h-1 [ 12 ]. …”

Section: Septic Shockmentioning

confidence: 99%

Section: Septic Shockmentioning

confidence: 99%

See 2 more Smart Citations

Pressor Response to Noradrenaline in the Setting of Septic Shock: Anything New under the Sun—Dexmedetomidine, Clonidine? A Minireview

Géloën

Pichot

Leroy

et al. 2015

BioMed Research International

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“…In septic shock, intertwined pro-and anti-inflammatory mechanisms lead to immunoparalysis [222]. Extreme pro-inflammatory activity is associated with a cytokine "storm", hypotension refractory to high doses of noradrenaline and early death [88][89][90]. Extreme anti-inflammatory response is associated with a dysfunctional innate immune system and death (Figures 5 and 6; figure 1B in [223]; figure 2 in [224]).…”

Section: Iv) Perspectivesmentioning

confidence: 99%

Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?

et al. 2018

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During severe septic shock and/or severe acute respiratory distress syndrome (ARDS) patients present with a limited cardio-ventilatory reserve (low cardiac output and blood pressure, low mixed venous saturation, increased lactate, low PaO2/FiO2 ratio, etc.), especially when elderly patients or co-morbidities are considered. Rescue therapies (low dose steroids, adding vasopressin to noradrenaline, proning, almitrine, NO, extracorporeal membrane oxygenation, etc.) are complex. Fever, above 38.5-39.5 C, increases both the ventilatory (high respiratory drive: large tidal volume, high respiratory rate) and the metabolic (increased O2 consumption) demands, further limiting the cardio-ventilatory reserve. Some data (case reports, uncontrolled trial, small randomized prospective trials) suggest that control of elevated body temperature ("fever control") leading to normothermia (35.5-37 C) will lower both the ventilatory and metabolic demands: fever control should simplify critical care management when limited cardio-ventilatory reserve is at stake. Usually fever control is generated by a combination of general anesthesia ("analgo-sedation", light total intravenous anesthesia), antipyretics and cooling. However general anesthesia suppresses spontaneous ventilation, making the management more complex. At variance, alpha-2 agonists (clonidine, dexmedetomidine) administered immediately following tracheal intubation and controlled mandatory ventilation, with prior optimization of volemia and atrio-ventricular conduction, will reduce metabolic demand and facilitate normothermia. Furthermore, after a rigorous control of systemic acidosis, alpha-2 agonists will allow for accelerated emergence without delirium, early spontaneous ventilation, improved cardiac output and micro-circulation, lowered vasopressor requirements and inflammation. Rigorous prospective randomized trials are needed in subsets of patients with a high fever and spiraling toward refractory septic shock and/or presenting with severe ARDS.

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Optical Monitoring

Lima¹,

Backer²

2018

Monitoring Tissue Perfusion in Shock

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Early prediction of norepinephrine dependency and refractory septic shock with a multimodal approach of vascular failure

Cited by 17 publications

References 15 publications

Pressor Response to Noradrenaline in the Setting of Septic Shock: Anything New under the Sun—Dexmedetomidine, Clonidine? A Minireview

Pressor Response to Noradrenaline in the Setting of Septic Shock: Anything New under the Sun—Dexmedetomidine, Clonidine? A Minireview

Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?

Optical Monitoring

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