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Table 1 Analogy between the 4 Ds of antibiotic and fluid therapy Stewardship.

From: Intravenous fluid therapy in the perioperative and critical care setting: Executive summary of the International Fluid Academy (IFA)

  Description Antibiotics Fluids
Drug Inappropriate therapy More organ failure, longer ICU/hospital length of stay, longer duration mechanical ventilation (MV) Hyperchloremic metabolic acidosis, more acute kidney injury, more need for renal replacement therapy, increased mortality
Appropriate therapy Key factor in empiric AB choice is consideration of patient risk factors (prior AB use, duration of mechanical ventilation, corticosteroids, recent hospitalization, residence in nursing home, etc.) Key factor in empiric fluid therapy is consideration of patient risk factors (fluid balance, fluid overload, capillary leak, source control, kidney function, organ function). Do not use glucose as a resuscitation fluid
Combination therapy Possible benefits: broader spectrum, synergy, avoidance of emergency of resistance, less toxicity Possible benefits: specific fluids for different indications (replacement vs maintenance vs resuscitation), less toxicity
Appropriate timing Survival decreases with 7% per hour delay. Needs discipline and practical organization In refractory shock early goal-directed therapy (EGDT) has proven beneficial. The longer the delay, the more microcirculatory hypoperfusion
Dosing Pharmacokinetics Depends on distribution volume, clearance (kidney and liver function), albumin level, tissue penetration Depends on type of fluid: glucose remains 10% intravascular, crystalloids 25%, vs colloids 100% after 1 h, and other factors (distribution volume, osmolality, oncoticity, kidney function)
Pharmacodynamics Reflected by the minimal inhibitory concentration. Reflected by “kill” characteristics, time (T > MIC) vs concentration (Cmax/MIC) dependent Depends on type of fluid and where you want them to go: intravascular (resuscitation), interstitial vs intracellular (cellular dehydration)
Toxicity Some ABs are toxic for kidneys, advice on dose adjustment needed. However, not getting infection under control is not helping the kidneys either Some fluids (HES—starches) are toxic for the kidneys. However, not getting shock under control is not helping the kidneys either
Duration Appropriate duration No strong evidence but trend toward shorter duration. Do not use ABs to treat fever, CRP, infiltrates, but use ABs to treat infections No strong evidence but trend toward shorter duration. Do not use fluids to treat low central venous or mean arterial pressure, urine output, but use fluids to treat hypovolemia
Treat to response Stop ABs when signs and symptoms of active infection resolve. Future role for biomarkers (PCT) Fluids can be stopped when shock is resolved (normal lactate). Future role for biomarkers (NGAL, cystatin C, citrullin, L-FABP)
De-escalation Monitoring Take cultures first and have the guts to change a winning team After stabilization with early adequate fluid management (normal PPV, normal cardiac output, normal lactate), stop ongoing resuscitation and move to conservative late fluid management and late goal-directed fluid removal (= deresuscitation)
  1. AB antibiotic, Cmax maximal peak concentration, CRP C reactive protein, EGDT early goal-directed therapy, HES hydroxyl-ethyl starch, L-FABP L-type fatty acid-binding protein, MIC mean inhibitory concentration, MV mechanical ventilation, NGAL neutrophil gelatinase-associated lipocalin, PCT procalcitonin, PPV pulse pressure variation