Fluid therapy in critical illness

Abstract

Major surgery and critical illnesses such as sepsis and trauma all disturb normal physiological fluid handling. Intravenous fluid therapy for resuscitation and fluid maintenance is a central part of medical care during these conditions, yet the evidence base supporting practice in this area lacks answers to a number of important questions. Recent research developments include a refinement of our knowledge of the endothelial barrier structure and function and a focus on the potential harm that may be associated with intravenous fluid therapy. Here, we briefly describe the contemporary view of fluid physiology and how this may be disrupted by pathological processes. The important themes in critical illness fluid research are discussed, with a particular focus on two emerging ideas: firstly, that individualising fluid treatment to the patient, their underlying disease state and the phase of that illness may be key to improving clinical outcomes using fluid interventions and, secondly, that fluids should be considered to be drugs, with specific indications and contraindications, dose ranges and potential toxicities.

Keywords: Critical illness; Glycocalyx; Goal-directed therapy; Intravenous fluid; Surgery.

Figure 1

The revised Starling principle and equation. Hydrostatic pressures are higher within the vascular lumen (P_v) than within the interstitium (P_i), favouring outward fluid filtration. The endothelial surface layer (ESL) is formed by the endothelial glycocalyx (EG), which binds plasma proteins and excludes them from the subglycocalyx layer (S). This forms an oncotic gradient from the low protein concentration of the subglycocalyx (IIs) to the intravascular space (IIv). This gradient opposes outward fluid filtration. Net transcapillary flow (J_v)—dashed arrows—can be expressed using the revised Starling equation: J_v = K_f([P_v − P_i] − σ[π_v − π_s]), where K_f is the filtration coefficient and σ is the reflection coefficient (the degree to which the tendency of a macromolecule to cross the endothelial barrier is resisted). EC, endothelial cell. NB: Reproduced with permission from reference [2].