Nutrition for Patients with Metabolic or Respiratory Stress

Nutrition for Patients with Metabolic or Respiratory Stress

Critical illness generally refers to any acute, life-threatening illness or injury, such as trauma (e.g., gunshot wounds, motor vehicle accidents, severe burns), certain diseases (e.g., pancreatitis, acute renal failure), extensive surgery, or infection. It is typically associated with a state of catabolic stress characterized by a systemic inflammatory response and carries the risk of increased infectious morbidity, multiple-organ dysfunction, prolonged hospitalization, and disproportionate mortality (McClave et al., 2016). Once considered adjunct therapy, nutrition support is now thought to help mitigate the metabolic response to stress, prevent oxidative cellular injury, and favorably dampen immune responses. Early enteral nutrition (EN), appropriate macro- and micronutrient delivery, and tight glycemic control may reduce the severity of the illness, reduce complications, decrease length of stay in the ICU, and improve outcomes (McClave et al., 2016).

This chapter discusses the stress response and nutrition therapy for critical illness. Nutrition therapy for burns and acute respiratory distress syndrome is presented.


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.


Nutrition therapy in critical illness largely means nutrition support. Oral intake is established as soon as possible, but anorexia is common and may preclude oral intake for days to months (Casaer & Van den Berghe, 2014). Nutrition support is used until the patient is able to orally consume 66% to 75% of estimated needs (Brantley & Mills, 2012). The goal of nutrition support is to improve outcomes, namely, infectious morbidity, ventilator-dependent days, and length of stay in ICU (McClave et al., 2016).

Nutrition Support the provision of nutrition via enteral feeding tubes or parenteral catheters.

Minimizing body protein catabolism is a secondary goal. Box 16.2 summarizes current guidelines for nutrition support in critically ill patients.

Nutrition Support

For most critically ill patients, EN is a safe and more practical feeding route than PN. EN is preferred because it helps maintain gut integrity, modulates stress and the systemic immune response, and lessens disease severity (McClave et al., 2016). It is recommended that EN be initiated as soon as fluid resuscitation is complete and the patient is hemodynamically stable, preferably within the first 24 to 48 hours (McClave et al., 2016). However, not all studies agree that early nutrition support through PN is more harmful than through EN (Harvey et al., 2014). Guidelines for when to use PN are outlined in Box 16.3.

Studies support the idea that bowel sounds and passing flatus or stool are not required before EN can begin in critically ill patients based on the rationale that bowel sounds are only indicative of contractility and do not necessarily relate to mucosal integrity, barrier function, or absorptive capacity (McClave et al., 2016). In most critically ill patients, delivery into the stomach is acceptable; however, lower gastrointestinal (GI) feedings are recommended for patients
at high risk for aspiration or those who are intolerant to gastric feedings. Volume-based feeding protocols that specify total amount per 24 hours provide more nutrition than hourly rates (McClave et al., 2016).

Regarding enteral formula selection,

  • For most patients, a standard polymeric (intact macronutrients) formula may be used to initiate nutrition support in the ICU.

  • For obese patients, a low-caloric density formula with a reduced nonprotein calorie-to-nitrogen ratio (NPC:N) is suggested (proportionately lower in calories from carbohydrates and fats than in protein content).

  • For patients in the surgical ICU or with severe trauma, an immune-modulating formula that provides arginine, fish oils, and/or glutamine may be considered.

  • No benefit has been shown for routine use of other specialty formulas and disease-specific formulas in the ICU, such as pulmonary formulas for acute respiratory failure and hepatic formulas for critically ill patients with acute or chronic liver disease.


Indirect calorimetry (IC) is considered the gold standard for determining calorie requirements, but it is not routinely performed because it is difficult and impractical (Peake et al., 2014). IC is not widely available and cannot be performed on all patients, such as on patients with a chest tube, those using supplemental oxygen, or patients who are uncooperative.

Indirect Calorimetry (IC) an indirect estimate of resting energy expenditure that measures the ratio of CO2 expired to the amount of oxygen inspired and uses those values in a mathematical equation.

When IC is not an option, calorie needs can be estimated by either a predictive equation or a simple weight-based equation (see Box 16.2). Although there are more than 200 predictive equations, their accuracy rates range from 40% to 75% when compared to IC and none stand out as being the most accurate for ICU patients (McClave et al., 2016). Regardless of the method used to estimate calorie requirements, calorie expenditure should be reevaluated more than once a week so that intake can be optimized (McClave et al., 2016).

EN during critical illness has consistently been shown to provide substantially less than the full-recommended calorie requirement, mostly because of GI dysmotility, especially delayed gastric emptying (Peake et al., 2014). Frequent interruption of EN delivery for procedures or surgery contributes to the typical provision of approximately 60% of estimated calorie needs. A study
by Peake et al. (2014) found that substituting routine formula that provides 1.0 cal/mL with a 1.5-cal/mL formula resulted in 46% greater delivery of calories without adverse effects when administered at the same rate. Studies are needed to determine if increasing the delivery of calories affects patient outcomes.

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Nov 8, 2018 | Posted by in NURSING | Comments Off on Nutrition for Patients with Metabolic or Respiratory Stress

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