Published in:
Open Access 01-12-2016 | Editorial
Decatecholaminisation during sepsis
Published in: Critical Care | Issue 1/2016
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Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection [1]. The syndrome is characterised by autonomic dysfunction and increased plasma levels of noradrenaline and adrenaline [2]. These catecholamines originate mainly from the activated sympathetic nervous system, but also originate from the adrenal gland, gut, and immune cells [3]. While necessary and life-saving in the early fight or flight reaction to any insult, prolonged adrenergic stress is detrimental and contributes to organ dysfunction [4]. Strategies to reduce adrenergic stress have been proposed (Table 1) under the umbrella term decatecholaminisation.
Table 1
Decatecholaminisation strategies for patients with septic shock
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Strategy
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Recommendations
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|---|---|---|
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Blunt endogenous catecholamine release; avoid compensatory adrenergic stimulation
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Optimize cardiac preload and vascular filling
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Assess fluid status by leg-raise test
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Perform repetitive fluid challenges to a target (e.g. stroke volume)
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Use cardiac output monitoring and/or echocardiography
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Treat hypoxia and severe anaemia
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Target oxygen saturation between 92–96 %
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Transfuse red blood cells if haemoglobin falls below 70 g/l
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Optimize sedation and analgesia
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Avoid over-sedation; use sedation targets
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Interrupt sedation daily, especially if long-lasting sedatives (e.g. midazolam) are used
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Use dexmedetomidine (see text for details)
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Reduce exogenous catecholamine administration
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Avoid excessive beta-mimetic stimulation
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Use cardiac output monitoring and/or echocardiography Avoid supra-normal physiological targets
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Only use inotropes if contractility is impaired
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Use cardiac output monitoring and/or echocardiography
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Consider alternative drugs
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Consider alternative inotropes (e.g. levosimendan) and vasopressors (e.g. vasopressin)
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Accept abnormal physiological values
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Adjust therapeutic targets
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Consider beta-blockers if tachycardia persists
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Prefer short-acting drugs (e.g esmolol, see text) that can be stopped if adverse effects occur
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Blunt inflammatory response (to reduce cardiac depression and microvascular dysfunction)
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Treat underlying infection
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Use intravenous antibiotics (after sampling for microbiology)
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Push for urgent surgical/interventional source control
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Reduce cytokine load
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Consider low-dose steroids
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Consider extra-corporeal cytokine removal
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