Abstract
During septic shock, fluid therapy is aimed at increasing cardiac output and improving tissue oxygenation, but it poses two problems: it has inconsistent and transient efficacy, and it has many well-documented deleterious effects. We suggest that there is a place for its personalization according to the patient characteristics and the clinical situation, at all stages of circulatory failure. Regarding the choice of fluid for volume expansion, isotonic saline induces hyperchloremic acidosis, but only for very large volumes administered. We suggest that balanced solutions should be reserved for patients who have already received large volumes and in whom the chloremia is rising. The initial volume expansion, intended to compensate for the constant hypovolaemia in the initial phase of septic shock, cannot be adapted to the patient’s weight only, as suggested by the Surviving Sepsis Campaign, but should also consider potential absolute hypovolemia induced by fluid losses. After the initial fluid infusion, preload responsiveness may rapidly disappear, and it should be assessed. The choice between tests used for this purpose depends on the presence or absence of mechanical ventilation, the monitoring in place and the risk of fluid accumulation. In non-intubated patients, the passive leg raising test and the mini-fluid challenge are suitable. In patients without cardiac output monitoring, tests like the tidal volume challenge, the passive leg raising test and the mini-fluid challenge can be used as they can be performed by measuring changes in pulse pressure variation, assessed through an arterial line. The mini-fluid challenge should not be repeated in patients who already received large volumes of fluids. The variables to assess fluid accumulation depend on the clinical condition. In acute respiratory distress syndrome, pulmonary arterial occlusion pressure, extravascular lung water and pulmonary vascular permeability index assess the risk of worsening alveolar oedema better than arterial oxygenation. In case of abdominal problems, the intra-abdominal pressure should be taken into account. Finally, fluid depletion in the de-escalation phase is considered in patients with significant fluid accumulation. Fluid removal can be guided by preload responsiveness testing, since haemodynamic deterioration is likely to occur in patients with a preload dependent state.
Key Points
- Personalizing Fluid Type Selection: Crystalloids remain the first-line fluids, with balanced crystalloids preferred over normal saline to prevent hyperchloremic acidosis. However, normal saline may still be appropriate for patients with traumatic brain injury or hypochloremia. The choice should be guided by patient-specific needs, including electrolyte balance and total fluid volume administered.
- Balancing Fluid Administration and Avoiding Overload: While excessive fluid administration is associated with worse outcomes, clinical trials on fluid restriction have not consistently demonstrated mortality benefits. The cumulative fluid balance should be carefully monitored, especially in patients at risk for organ dysfunction.
- Customizing Initial Fluid Volume: The recommendation of 30 mL/kg of crystalloid within the first three hours is arbitrary and may lead to over- or under-resuscitation. A more individualized approach considers the severity of vasodilation, absolute hypovolemia from fluid losses, and cardiac function.
- Assessing Preload Responsiveness: Fluid responsiveness should be evaluated before administering additional fluids, particularly after the initial resuscitation phase. Passive leg raising (PLR), mini-fluid challenge, and pulse pressure variation (PPV) can be used to assess responsiveness, with the choice of test depending on ventilation status and monitoring availability.
- Early Use of Vasopressors: Norepinephrine is typically introduced when fluid resuscitation alone fails to restore blood pressure. However, early initiation may reduce total fluid requirements and improve hemodynamic stability, particularly in patients with profound vasodilation.
- Monitoring for Fluid Overload: In ARDS patients, fluid therapy should be guided by pulmonary artery occlusion pressure (PAOP), extravascular lung water (EVLW), and pulmonary vascular permeability index (PVPI) rather than oxygenation alone. For patients with intra-abdominal hypertension, intra-abdominal pressure (IAP) should be considered to prevent visceral and renal hypoperfusion.
- Recognizing When to Stop Fluid Infusion: Once preload responsiveness disappears, further fluid administration is unlikely to benefit the patient and may increase the risk of edema and organ dysfunction. Central venous pressure (CVP) should not be used alone but can help assess the risk of venous congestion.
- Personalizing Therapeutic Targets: In non-ICU settings, capillary refill time, skin mottling, and urine output may be used as indicators of perfusion improvement, though these are less reliable than direct cardiac output monitoring. In ICU patients, stroke volume variation, venous oxygen saturation, and lactate clearance provide more accurate assessments of fluid effectiveness.
- Individualizing Fluid De-escalation Strategies: Fluid removal should be considered in patients with significant fluid accumulation, guided by preload responsiveness and hemodynamic stability. Diuretics are the first-line option, while ultrafiltration may be necessary in cases of renal dysfunction.
- Future Directions in Fluid Therapy: Advances in hemodynamic monitoring, machine learning, and individualized resuscitation strategies hold promise for refining fluid management in septic shock. A one-size-fits-all approach is insufficient, and personalization is key to optimizing outcomes.
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