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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