Disruptions to homeostasis elicit a body-wide stress response characterized by physical and hormonal changes to promote healing and resolve inflammation. The intensity of the stress response depends to some extent on the cause and/or severity of the initial injury; for instance, the larger the body surface area burned, the greater is the intensity of the stress response that follows. Hormonal and inflammatory responses account for the changes in metabolic rate, heart rate, blood pressure, and nutrient metabolism that characterize metabolic stress.
Hormonal Response to Stress
The stress response has three phases: the ebb phase, the flow phase, and the recovery or resolution phase. The ebb phase typically lasts for 12 to 24 hours postinjury. It is characterized by shock with hypovolemia and diminished tissue oxygenation. Cardiac output, oxygen consumption, urinary output, and body temperature fall, and glucagon and catecholamine levels rise. Treatment goals are to restore blood flow to organs, maintain adequate oxygenation to all tissues, and stop bleeding. This initial phase ends when the patient is hemodynamically stable.
Stress Response a complex series of hormonal and metabolic changes that occur to enable the body to adapt to stressors.
Hypercatabolism higher than normal breakdown of large molecules into smaller ones, such as muscle protein into amino acids.
Hypermetabolism higher than normal metabolism.
The flow phase follows and is marked by metabolic abnormalities. A spike in circulating levels of hormones that direct the “fight or flight response” (e.g., glucagon, catecholamines, cortisol) promotes the breakdown of stored nutrients (e.g., glucose from glycogen, amino acids from skeletal muscle tissue, fatty acids from adipose) to meet immediate energy needs. As stored nutrients and tissues are catabolized, energy expenditure and metabolic rate increase. Hypercatabolism and hypermetabolism cause oxygen consumption, cardiac output, carbon dioxide (CO2) production, and body temperature to increase. The length of this phase depends on the severity of injury or infection and the development of complications.
Resolution of the stress leads to the recovery phase, which is marked by anabolism and a return to normal metabolic rate.
Acute-Phase Response trauma- or inflammation-induced release of inflammatory mediators that cause changes in the levels of plasma proteins and clinical symptoms of inflammation.
C-reactive Protein an acute-phase protein that is produced by the liver and released into circulation during acute inflammation.
Cytokines a group name for more than 100 different proteins involved in immune responses. Prolonged production of proinflammatory cytokines promotes hypercatabolism.
Inflammatory Response to Stress
In reaction to infection or tissue injury, the immune system mounts a quick,
acutephase response to destroy infections agents, prevent further tissue damage, and promote healing. Inflammation causes positive acute-phase proteins, such as
C-reactive protein, to increase in concentration. Negative acute-phase proteins, such as albumin, prealbumin, and transferrin, decrease in response to inflammation.
Cytokines and
other immune system molecules are responsible for regulating acute-phase proteins; they also produce changes in other cells that cause systemic symptoms of inflammation, such as anorexia, fever, lethargy, and weight loss. Clinical and laboratory findings used to identify the presence of inflammation are listed in
Box 16.1.
The inflammatory response is a desired reaction and is generally self-limiting. However, when the response is exaggerated and prolonged the beneficial response becomes damaging.
Sepsis is a life-threatening syndrome where an abnormal systemic response to infection causes organ dysfunction (
Singer et al., 2016). Sepsis is the primary cause of death from infection (
Singer et al., 2016). Septic shock differs from sepsis in the severity of complications and the heightened risk of death.
Sepsis an abnormal systemic host response to infection that causes life-threatening organ dysfunction.
It is now well understood that inflammation related to critical illness is a potent contributor to malnutrition (
Malone & Hamilton, 2013). Malnutrition is associated with impaired immune function, weakened respiratory muscles, prolonged ventilator dependence, and increased infectious complications in critically ill patients (
Charles et al., 2014). However, it is difficult to actually define malnutrition in critically ill people. For instance, albumin and prealbumin have been used as diagnostic markers of malnutrition, but these negative acute phase proteins decrease in response to inflammation and physiologic stress and do not accurately reflect nutrition status in the ICU setting (
Davis, Sowa, Keim, Kinnare, & Peterson, 2012). Proposed guideline for diagnosing moderate malnutrition in acutely ill or injured patients is the presence of two or more of the following characteristics (
Malone & Hamilton, 2013):
Weight loss, such as 1% to 2% of usual body weight in 1 week
Calorie intake of <75% for >7 days
Mild depletion of body fat
Mild depletion of muscle mass
Mild fluid accumulation
The same characteristics are used to identify severe malnutrition, but the thresholds are more severe, such as calorie intake of ≤50% for ≥5 days and moderate to severe fluid accumulation.