Nutrition in Critical Illness

Abstract

Appropriate feeding has become an integral part of the management of critically ill patients [1–5]. Moreover, Wischmeyer has postulated a key role for nutrition in survival after critical illness that extends for months or even years [6]. Disease-related malnutrition in critically ill patients is associated with increased morbidity and mortality [4, 7–12]. Compromised immune function, blunted respiratory drive and respiratory muscle weakness due to energy deficit may predispose the patients to further complications, the so-called second hit of nosocomial infections, and prolonged dependence on respiratory support with its inherent complications [13–16]. Associated with the inflammatory response triggered in critical illness, there is hypermetabolism due to metabolic stress and bed rest, all of which may promote protein catabolism [4, 17]. Thus, the critically ill may quickly develop malnutrition [12]. Malnutrition is common in acutely severely ill patients with a reported occurrence of 30–50 % [14, 18, 19]. In the critically ill, this overall weakness is termed ICU-acquired critical illness weakness and is the result of substantial loss of lean body mass, inadequate physical activity and marked catabolic metabolism [20–22]. Feeding patients has been shown to be beneficial, improving wound healing, mitigating the catabolic response, maintaining gastrointestinal barrier function preventing bacterial translocation, attenuating disease severity, modulating the immune system, enhancing insulin sensitivity and improving the overall outcome [2, 23]. However, feeding may result in harmful side effects such as gastric volume retention (gastroparesis) due to disturbed gut motility, bacterial colonization of the stomach and potentially an increased risk of aspiration and nosocomial pneumonia [24, 25]. Overfeeding can also result in significant metabolic stress aggravating the metabolic response to stress [26, 27] and is associated with harmful effects such as disturbed glycaemic control, deranged liver function, increased infections and even poor outcomes [28–31]. Furthermore, some authors argue that enteral feeding is contraindicated in unstable patients in shock requiring vasoactive medications [32, 33] as pyloric dysfunction is common in cardiogenic shock [34] and often combined with intestinal atony [35]. As such, after cardiac surgery, acute mesenteric ischaemia resulting from hypoperfusion – often related to hypotension – is seen in 0.5 % [36] to 1.4 % [37] of patients and associated with substantial mortality rates ranging between 11 and 27 % [36, 37]. Enteral feeding is shown to enhance the local mesenteric oxygen demand at the expense of vital organs [35]. Publications have suggested that enteral feeding may be generally deleterious in the critically ill unstable patient resulting in disturbed gastrointestinal motility, poor glycaemic control and worsened clinical outcome [26, 29, 38]. However, other studies show that enteral feeding may be beneficial even in haemodynamically compromised critically ill patients if applied with caution [39–43], and malnutrition is found to be associated with reduced LV systolic function, lower contractility and compliance [44]. There are ongoing controversies as to the amount of enteral feed and which formulation should be offered [4–6, 28]. The timing is not conclusively answered yet, and the role of parenteral nutrition, particularly in the case of compromised enteral function, is not determined [3, 12, 45, 46] though recent evidence has helped to clarify some of these issues.