Table 1 Analogy between the four D’s of antibiotic and fluid therapy.
Description | Terminology | Antibiotics | Fluids |
|---|---|---|---|
Drug | Inappropriate therapy | More organ failure, longer ICU LOS, longer hospital LOS, longer MV | Hyperchloremic metabolic acidosis, more AKI, more RRT, increased mortality |
Appropriate therapy | Key factor in empiric AB selection is consideration of patient risk factors (e.g. prior AB, duration MV, corticosteroids, recent hospitalization, residence in nursing home) | Key factor in empiric fluid therapy is consideration of patient risk factors (e.g. fluid balance, fluid overload, capillary leak, kidney and other organ function). Do not use glucose as resuscitation fluid | |
Combination therapy | Possible benefits: e.g. broader spectrum, synergy, avoidance of emergency of resistance, less toxicity | Possible benefits: e.g. specific fluids for different indications (replacement vs. maintenance vs. resuscitation), less toxicity | |
Class | Broad-spectrum or specific, beta-lactam or glycopeptide, additional compounds as tazobactam. The choice has a real impact on efficacy and toxicity | Hypo- or hypertonic, high or low chloride and sodium level, lactate or bicarbonate buffer, glucose containing or not. This will impact directly acid–base equilibrium, cellular hydration and electrolyte regulation | |
Appropriate timing | Survival decreases with 7% per hour delay. Needs discipline and practical organization | In refractory shock, 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 10%, crystalloids 25%, versus colloids 100% IV after 1 h, distribution volume, osmolality, oncoticity, kidney function |
Pharmacodynamics | Reflected by the minimal inhibitory concentration. Reflected by “kill” characteristics, time (T > MIC) versus concentration (Cmax/MIC) dependent | Depends on type of fluid and desired location: IV (resuscitation), IS versus IC (cellular dehydration) | |
Toxicity | Some ABs are toxic to kidneys, advice on dose adjustment needed. However, not getting infection under control is not helping the kidney either | Some fluids (HES) are toxic for the kidneys. However, not getting shock under control is not helping the kidney either | |
Duration | Appropriate duration | No strong evidence but trend towards shorter duration. Do not use AB to treat fever, CRP or chest X-ray infiltrates but use AB to treat infections | No strong evidence but trend towards shorter duration. Do not use fluids to treat low CVP, MAP or UO, but use fluids to treat shock |
Treat to response | Stop AB when signs and symptoms of active infection resolves. 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 EAFM (normal PPV, normal CO, normal lactate) stop ongoing resuscitation and move to LCFM and LGFR (= de-resuscitation) |