My patient has received fluid. How to assess its efficacy and side effects?

Xavier Monnet, Jean-Louis Teboul, Xavier Monnet, Jean-Louis Teboul

Abstract

Many efforts have been made to predict, before giving fluid, whether it will increase cardiac output. Nevertheless, after fluid administration, it is also essential to assess the therapeutic efficacy and to look for possible adverse effects. Like for any drug, this step should not be missed. Basically, volume expansion is aimed at improving tissue oxygenation and organ function. To assess this final result, clinical signs are often unhelpful. The increase in urine output in case of acute kidney injury is a poor marker of the kidney perfusion improvement. Even if oxygen delivery has increased with fluid, the increase in oxygen consumption is not constant. Assessing this response needs to measure markers such as lactate, central/mixed venous oxygen saturation, or carbon dioxide-derived indices. If tissue oxygenation did not improve, one should check that cardiac output has actually increased with fluid administration. To assess this response, changes in arterial pressure are not reliable enough, and direct measurements of cardiac output are required. In cases where cardiac output did not increase with fluid, one should check that it was not due to an insufficient volume of fluid administered. For this purpose, volume markers of cardiac preload sometimes lack precision. The central venous pressure, in theory at least, should not augment to a large extent in fluid responders. The worst adverse effect of fluids is the increase in the cumulative fluid balance. In patients with acute respiratory distress syndrome (ARDS), the risk of aggravating pulmonary oedema should be systematically assessed by looking for increases in extravascular lung water, or, more indirectly, increases in central venous or pulmonary artery occlusion pressure. In ARDS patients receiving fluid, one should always keep in mind the risk of inducing/aggravating right ventricular dilation, which should be confirmed through echocardiography. The risk of increasing the intra-abdominal pressure should be carefully sought in patients at risk. Finally, fluid-induced haemodilution should not be neglected. Like for any drug which has inconsistent effectiveness and may exert significant harm, the correct fluid management should include a cautious and comprehensive assessment of fluid-induced benefits and side effects.

Keywords: Cardiac output; Extravascular lung water; Fluid challenge; Fluid responsiveness; Passive leg raising; Pulse pressure variation.

Figures

Fig. 1
Fig. 1
Schematic pathway through which fluid administration leads to organ function improvement, and the issues that may interrupt it
Fig. 2
Fig. 2
Summary of the criteria on which the benefits and risks of volume expansion might be assessed. CO cardiac output, CVP central venous pressure, FiO2 oxygen inspired fraction, IAP intra-abdominal pressure, LV left ventricular, PCO2 carbon dioxide partial pressure, PaO2 arterial oxygen partial pressure, RT refill time, SvO2/ScvO2 mixed/central venous oxygen saturation

References

    1. Aya HD, Rhodes A, Chis Ster I, Fletcher N, Grounds RM, Cecconi M. Hemodynamic effect of different doses of fluids for a fluid challenge: a quasi-randomized controlled study. Crit Care Med. 2017;45:e161–e168. doi: 10.1097/CCM.0000000000002067.
    1. Guerin L, Teboul JL, Persichini R, Dres M, Richard C, Monnet X. Effects of passive leg raising and volume expansion on mean systemic pressure and venous return in shock in humans. Crit Care. 2015;19:411. doi: 10.1186/s13054-015-1115-2.
    1. Monnet X, Julien F, Ait-Hamou N, Lequoy M, Gosset C, Jozwiak M, et al. Lactate and venoarterial carbon dioxide difference/arterial-venous oxygen difference ratio, but not central venous oxygen saturation, predict increase in oxygen consumption in fluid responders. Crit Care Med. 2013;41:1412–1420. doi: 10.1097/CCM.0b013e318275cece.
    1. Monnet X, Letierce A, Hamzaoui O, Chemla D, Anguel N, Osman D, et al. Arterial pressure allows monitoring the changes in cardiac output induced by volume expansion but not by norepinephrine. Crit Care Med. 2011;39:1394–1399. doi: 10.1097/CCM.0b013e31820edcf0.
    1. Ospina-Tascon G, Neves AP, Occhipinti G, Donadello K, Buchele G, Simion D, et al. Effects of fluids on microvascular perfusion in patients with severe sepsis. Intensive Care Med. 2010;36:949–955. doi: 10.1007/s00134-010-1843-3.
    1. Ronco JJ, Fenwick JC, Wiggs BR, Phang PT, Russell JA, Tweeddale MG. Oxygen consumption is independent of increases in oxygen delivery by dobutamine in septic patients who have normal or increased plasma lactate. Am Rev Respir Dis. 1993;147:25–31. doi: 10.1164/ajrccm/147.1.25.
    1. Gattinoni L, Brazzi L, Pelosi P, Latini R, Tognoni G, Pesenti A, et al. A trial of goal-oriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group. N Engl J Med. 1995;333:1025–1032. doi: 10.1056/NEJM199510193331601.
    1. Legrand M, Dupuis C, Simon C, Gayat E, Mateo J, Lukaszewicz AC, et al. Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study. Crit Care. 2013;17:R278. doi: 10.1186/cc13133.
    1. Moussa MD, Scolletta S, Fagnoul D, Pasquier P, Brasseur A, Taccone FS, et al. Effects of fluid administration on renal perfusion in critically ill patients. Crit Care. 2015;19:250. doi: 10.1186/s13054-015-0963-0.
    1. Giraud R, Siegenthaler N, Gayet-Ageron A, Combescure C, Romand JA, Bendjelid K. ScvO2 as a marker to define fluid responsiveness. J Trauma. 2011;70:802–807. doi: 10.1097/TA.0b013e3181e7d649.
    1. Kuiper AN, Trof RJ, Groeneveld AB. Mixed venous O2 saturation and fluid responsiveness after cardiac or major vascular surgery. J Cardiothorac Surg. 2013;8:189. doi: 10.1186/1749-8090-8-189.
    1. Mekontso-Dessap A, Castelain V, Anguel N, Bahloul M, Schauvliege F, Richard C, et al. Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients. Intensive Care Med. 2002;28:272–277. doi: 10.1007/s00134-002-1215-8.
    1. Monnet X, Marik PE, Teboul JL. Prediction of fluid responsiveness: an update. Ann Intensive Care. 2016;6:111. doi: 10.1186/s13613-016-0216-7.
    1. Ait-Oufella H, Bourcier S, Alves M, Galbois A, Baudel JL, Margetis D, et al. Alteration of skin perfusion in mottling area during septic shock. Ann Intensive Care. 2013;3:31. doi: 10.1186/2110-5820-3-31.
    1. Pierrakos C, Velissaris D, Scolletta S, Heenen S, De Backer D, Vincent JL. Can changes in arterial pressure be used to detect changes in cardiac index during fluid challenge in patients with septic shock? Intensive Care Med. 2012;38:422–428. doi: 10.1007/s00134-011-2457-0.
    1. Chemla D, Hebert JL, Coirault C, Zamani K, Suard I, Colin P, et al. Total arterial compliance estimated by stroke volume-to-aortic pulse pressure ratio in humans. Am J Physiol. 1998;274:H500–H505. doi: 10.1152/ajpcell.1998.274.2.C500.
    1. Monnet X, Teboul JL. Transpulmonary thermodilution: advantages and limits. Crit Care. 2017;21:147. doi: 10.1186/s13054-017-1739-5.
    1. Monnet X, Persichini R, Ktari M, Jozwiak M, Richard C, Teboul JL. Precision of the transpulmonary thermodilution measurements. Crit Care. 2011;15:R204. doi: 10.1186/cc10421.
    1. Jozwiak M, Silva S, Persichini R, Anguel N, Osman D, Richard C, et al. Extravascular lung water is an independent prognostic factor in patients with acute respiratory distress syndrome. Crit Care Med. 2013;41:472–480. doi: 10.1097/CCM.0b013e31826ab377.
    1. Vincent JL, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H, et al. Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006;34:344–353. doi: 10.1097/01.CCM.0000194725.48928.3A.
    1. Schuster DP, Stark T, Stephenson J, Royal H. Detecting lung injury in patients with pulmonary edema. Intensive Care Med. 2002;28:1246–1253. doi: 10.1007/s00134-002-1414-3.
    1. Jozwiak M, Teboul JL, Monnet X. Extravascular lung water in critical care: recent advances and clinical applications. Ann Intensive Care. 2015;5:38. doi: 10.1186/s13613-015-0081-9.
    1. Mitchell JP, Schuller D, Calandrino FS, Schuster DP. Improved outcome based on fluid management in critically ill patients requiring pulmonary artery catheterization. Am Rev Respir Dis. 1992;145:990–998. doi: 10.1164/ajrccm/145.5.990.
    1. Vieillard-Baron A, Matthay M, Teboul JL, Bein T, Schultz M, Magder S, et al. Experts’ opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation. Intensive Care Med. 2016;42:739–749. doi: 10.1007/s00134-016-4326-3.
    1. De Waele JJ, De Laet I, Malbrain ML. Understanding abdominal compartment syndrome. Intensive Care Med. 2016;42:1068–1070. doi: 10.1007/s00134-015-4089-2.
    1. Holodinsky JK, Roberts DJ, Ball CG, Blaser AR, Starkopf J, Zygun DA, et al. Risk factors for intra-abdominal hypertension and abdominal compartment syndrome among adult intensive care unit patients: a systematic review and meta-analysis. Crit Care. 2013;17:R249. doi: 10.1186/cc13075.
    1. Cordemans C, De Laet I, Van Regenmortel N, Schoonheydt K, Dits H, Huber W, et al. Fluid management in critically ill patients: the role of extravascular lung water, abdominal hypertension, capillary leak, and fluid balance. Ann Intensive Care. 2012;2:S1. doi: 10.1186/2110-5820-2-S1-S1.

Source: PubMed

Sponsors and Collaborators

Medical Conditions

Drug Interventions

3
Subscribe