Fluid management in COVID-19
I read with interest the summary of NICE guidelines for the prevention and management of acute kidney injury (AKI) in COVID-19 patients (1). The authors highlight the role of hypovolemia in the development of AKI and the importance of fluid management. They mention that the aim should be to "achieve and maintain optimal fluid status" but do not provide clear guidance on how to achieve that goal, nor define what they mean by “optimal fluid status”. The authors suggest that clinical examination and the use of heart rate, blood pressure, and pulmonary edema may help to assess fluid status. I believe that the assessment of volume status may be much more complex in COVID-19 patients.
First, these patients are septic, and a high pulse rate or a low blood pressure may simply reflect fever and systemic vasodilation. Pulmonary edema, a major cause of mechanical ventilation and intensive care unit (ICU) admission, is rather due to pulmonary capillary leak than to fluid overload. Second, dynamic predictors of fluid responsiveness, often used in critically ill patients to guide fluid management, are difficult to interpret, when not impossible to use. For instance, in emergency departments and on hospital wards, the pleth variability index (a quantification of the respiratory variation in the pulse oximetry waveform), or the inferior vena cava collapsibility (estimated by ultrasound techniques), do not help to predict fluid responsiveness. Indeed, in spontaneously breathing patients with acute respiratory failure, they depend more on respiratory efforts than on the volume status (2). In the ICU, where most patients are mechanically ventilated and have a radial arterial catheter, the arterial pulse pressure variation (PPV), easy to measure, could be used to guide fluid management. However, in the context of protective mechanical ventilation with low tidal volume, although a high PPV (>13%) is highly suggestive of hypovolemia, a low PPV cannot exclude it (3).
So, what could be done to rationalize fluid administration? First, we can mimic the effects of a fluid challenge with a passive leg raising (PLR) maneuver (4). In hypovolemic patients, PLR induces significant changes in stroke volume (SV, measured by a cardiac output monitor), in the velocity time integral (VTI) of the left ventricular outflow tract (measured by echo-Doppler), in the peripheral perfusion index (PI, measured by pulse oximetry) and in PPV (measured from any arterial waveform) (5). In the context of pulmonary edema, the PLR has the major advantage to provide information without the need to administer a single drop of fluid (4). The alternative to the PLR maneuver is the mini-fluid challenge that consists in the quick administration of a small volume of fluid (100 ml in a few minutes). Both the PLR and the mini-fluid challenge can be used in mechanically ventilated and in spontaneously breathing patients. During mechanical ventilation, the end-expiratory occlusion test (transient interruption of mechanical ventilation), the tidal volume challenge (transient increase in tidal volume) and the lung recruitment maneuver (transient increase in airway pressure) can be used as well to detect changes in SV, VTI, PI and PPV and unmask an hypovolemic state (5).
In summary, I agree with Selby et al. (1) that detecting and correcting hypovolemic states is key to prevent AKI in COVID-19 patients. However, I believe that clinicians cannot simply rely on clinical examination to detect hypovolemia and need actionable guidelines to rationalize fluid therapy.
1. Selby et al. BMJ 2020; 369:m1963
2. Michard & Shelley. Should we monitor pulsus paradoxus via pulse oximetry in COVID-19 patients with acute respiratory failure? Am J Respir Crit Care Med, in press
3. Michard et al. Applicability of pulse pressure variation: how many shades of grey? Crit Care 2015; 19 :144
4. Monnet & Teboul. Passive leg raising: five rules, not a drop of fluid! Crit Care 2015; 19:18
5. Michard. Toward precision hemodynamic management. Crit Care Med 2017; 45:1421-23
Competing interests: No competing interests