Specialty Sections From CHEST® Physician

Nutrition support during adult critical illness


 

Many critically ill patients you care for cannot maintain volitional oral intake. Therefore, nutrition support, through enteral or parenteral routes, remains a cornerstone in ensuring our critically ill patients receive substrates like glucose and protein. To understand the supportive role of nutrition during critical illness, let’s identify and contextualize the different phases of critical illness.

Phases of critical illness

The European Society of Parenteral and Enteral Nutrition’s (ESPEN) 2018 critical care nutrition guideline incorporates stages of critical illness in making nutrition recommendations (Singer P et al. Clin Nutr. 2019;38:48-79). The first week of critical illness is the acute phase and hallmarked by catabolism and metabolic and hemodynamic instability. The late phase is thereafter and hallmarked by rehabilitation and anabolism or chronic critical illness. The acute phase is further divided into early (days 1-2) and late acute phase (days 3-7). The time-points are arbitrary and merely serve as placeholders. An objective marker to distinguish phases does not exist and transition periods will be different for each patient.

Acute phase

Critical illness defining conditions like circulatory shock, respiratory failure, and trauma are stressors and lead to two key acute phase perturbations that nutrition may have a role in altering:

The first is hypercatabolism. Critical illness defining conditions activate neuroendocrine, inflammatory/immune, adipokine, and GI tract hormone pathways that increase serum glucagon, cortisol, and catecholamines to promote glycogenolysis, gluconeogenesis, insulin resistance, protein catabolism, and restricted/impaired anabolism.

The second is gut dysfunction. During health, there is cross-talk signaling that occurs between commensal bacteria, epithelium, and the immune system, which maintains gut barrier functions, achieved, for example, by promoting tight junction protein production. Acute critical illness pathophysiology loosens epithelial tight junctions, and the gut barrier is breached, creating an opportunity for downstream migration of pancreatic enzymes and cytokines. Furthermore, the microbiome morphs into a virulent pathobiome, which induces gut-derived inflammation.

When, where, and how much should we feed critically ill patients?

Since the acute phase of critical illness begins a series of events leading to negative energy balance and gut dysfunction, you might find early nutrition provision intuitive. Indeed, the 2016 ASPEN/SCCM and 2018 ESPEN critical care nutrition guidelines recommend early (within 24-48 hours of ICU admission) enteral nutrition (EN), delivered into the stomach, for all critically ill patients unable to maintain volitional intake. Meta-analyses of randomized controlled trials (RCT) conducted between1979 and 2013 show early EN reduces both mortality and infectious complications, compared with no early nutrition (McClave SA et al. JPEN. 2016;40:159-211).

RCT level data do not show superiority of EN over parenteral nutrition (PN). Nonetheless, early EN is recommended over PN because it maintains epithelial barrier function and supports immunity.

What is the optimal nutrition dose? The 2016 ASPEN/SCCM guideline recommends getting to >80% estimated energy goal within 48-72 hours in patients with high nutrition risk while the 2018 ESPEN guideline suggests maintaining a hypocaloric, or not exceeding 70% of prescribed energy goal, during the early acute phase. The recommendation is based on meta-analyses of RCTs conducted between 2011 and 2017, which shows no mortality difference between hypocaloric and isocaloric nutrition.

Biologically plausible rationale for starting hypocaloric, as opposed to full dose nutrition, during the acute phase of critical illness includes: (a) the acute phase represents a period of hemodynamic instability and mitochondrial dysfunction, and full-dose EN may lead to feeding intolerance and lack of substrate utilization, respectively; (b) in those with risk factors (like pre-existing malnutrition), starting full dose nutrition may lead to refeeding syndrome; and (c) endogenous glucose production occurs during the acute phase, and full dose nutrition may worsen hyperglycemia.

Therefore, during the early acute phase of critical illness, hypocaloric feeding using an isosmotic formula, with a slow up-titration to goal rate thereafter, while monitoring for feeding intolerance and refeeding syndrome is a reasonable starting point.

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