Trace elements: Clinical perspectives in the critically ill

Abstract

Trace elements are required in minute quantities in the diet but play a vital role in a wide variety of functions, such as co-factors in antioxidant reactions and normal immune function to DNA and protein synthesis and skeletal and tissue remodelling and repair. Critically ill patients are at risk of trace element deficiency or excess, due to changes in intake, absorption, metabolism or excretion. Deficiency or excess can lead to a wide range of cellular and organ dysfunction that may be seen in patients with an acute or critical illness, including cardiomyopathy, impaired glucose tolerance and reduced oxygen delivery. In addition, various diseases, such as systemic inflammation and renal and intestinal failure, and intensive care treatments, such as parenteral nutrition, renal replacement therapy and diuretics, can increase the likelihood of deficient or excessive amounts of micronutrient levels. This narrative review discusses sources and normal physiology of trace element handling and how this may be impaired in critically ill patients. It then discusses various conditions seen in critically ill patients that may be caused or exacerbated by abnormal trace element status and the current evidence around whether supplementation is of benefit in particular critical illnesses.

Keywords: Micronutrient; critical illness; enteral nutrition; parenteral nutrition; trace elements.

Figure 1.

Commonest sites of absorption, storage and elimination of selected trace elements. See text for details.

Figure 2.

Suggested mechanisms of absorption of trace elements from the gastrointestinal tract through luminal cells into the circulation.

Figure 3.

Elimination graph of manganese in a critically ill patient with acute hepatobiliary failure^, (circles; terminal elimination half-life 153.3 days) compared with normal (continuous line, terminal elimination half-life 48 days.

Figure 4.

Proposed mechanism of action of intracellular chromium, copper and manganese. Binding of insulin to its receptor in response to glucose in the circulation allows chromium (Cr) to bind to inactive apochromodulin (a). Activated chromodulin binds to the insulin receptor (b), amplifying its effects of activating the glucose transporter Glut4 to transport glucose into the cell (c).^, Copper is thought to inhibit the breakdown of insulin, increase the activation of insulin receptors to increase glucose transport into cells, and increase the expression of glucose transporter type 1 (Glut1). Manganese is thought to increase insulin production and secretion, and increase the activation of insulin receptors to increase glucose transport into cells.

Figure 5.

Putative roles and sites of action of selected trace elements in cellular function.

Figure 6.

Conditions that may be due to or exacerbated by deficiency of selected trace elements. COPD: chronic obstructive pulmonary disease.

Figure 7.

Conditions that may be due to or exacerbated by excess of selected trace elements.