Aging nutritional physiology predisposes elderly individuals to malnutrition syndromes.
Impaired intake and energy regulation and fuel metabolism derangements underscore the etiology of malnutrition in the elderly.
Malnourished elderly patients have a higher morbidity and mortality when hospitalized than their nourished counterparts.
Protein-energy malnutrition is the only reversible condition responsive to nutritional interventions.
A chronic inflammatory state exists in both sarcopenic and cachectic patients, leading to skeletal muscle mass loss and atrophy.
Nutritional screening is necessary in all elderly hospitalized patients in order to identify those at higher nutritional risk.
Feeding goals should be achieved within 48 hours in elderly intensive care unit patients with high nutritional risk factors.
Enteral nutrition via gastric feeding should be the first-line choice for feeding. Consider small bowel feeding in those at high risk for aspiration or those who can have an enteral feeding tube placed in the small bowel.
Obstacles that promote cessation of feeding must be identified and minimized on a daily basis.
Nutritional and metabolic derangements are common in elderly patients in the intensive care unit (ICU) and are important to recognize due to the many complications that arise on admission and throughout the course of hospitalization. They are often present before ICU admission in many elderly patients. These nutritional and metabolic derangements are primary determinants of frailty. Medical, psychiatric, and socioeconomic factors influence the nutritional status of the elderly. Malnutrition is an independent factor for ICU morbidity and mortality . This chapter explores the general malnutrition syndromes, including starvation, cachexia, and sarcopenia, that lead to frailty and its impact on the elderly ICU population (Figure 7.1). The physiologic derangements behind these processes, as well as assessments of their severity and potential interventions to treat them during ICU admission, will also be discussed. Current areas pertaining to specific nutritional interventions that may be helpful in critically ill patients will also be discussed. This chapter highlights the challenges of nutritional repletion in elderly ICU patients, which often falls below set goals and in and of itself is insufficient to reverse many of the nutritional and metabolic derangements that are present in the elderly.
Aging is associated with changes in nutritional physiology, promoting weight loss (Figure 7.2). The underlying mechanisms include impaired nutritional intake and alterations in energy expenditure and fuel processing. Decreased nutritional intake with aging has been attributed to reduced hunger and early satiety, as well as decreased senses of smell and taste. Delayed gastric emptying, insulin resistance, and decreased sensitivity to several digestive hormones are potentially responsible for these changes. Insulin resistance plays a central role in the overall process that leads to what has been termed the anorexia of aging, resulting in increasing satiation and promotion of skeletal muscle mass loss . Longitudinal studies examining body composition and energy expenditures (including daily, activity, and basal), performed over the life span of healthy elderly subjects, have shown overall decreases in both body composition and energy expenditure with age. Of note, these studies also found that the greatest decline is in energy expenditure related to activity compared with the other components. The consequence of lower overall energy expenditure is associated with an increase in functional limitations, thus predisposing the elderly to the increased risk of morbidities . Based on these findings, the elderly are at an increased risk of malnutrition and frailty regardless of their current health status.
The term frailty is commonly used to describe the ailing elderly, and its definition continues to evolve as more studies are performed that improve our understanding. Currently, frailty describes a state of vulnerability that is responsible for an inability to maintain normal physiological balance and response to stress . Frailty represents a physiologic trait that is independently associated with an increased risk of morbidity and mortality rather than a reflection of underlying comorbidities. The main signs heralding the presence of frailty are related to activity and nutrition. These include an unintentional weight loss of greater than 5 percent in a calendar year, decreased muscle strength, and a decrease in physical activity. Malnutrition, in combination with loss of muscle mass loss (sarcopenia), ultimately determines the degree of frailty present in a particular patient .
Sarcopenia represents a state involving muscle mass loss with its associated functional decline. The causes are multifactorial, including disuse, nutritional deficiencies, impaired response of skeletal muscle to nutrients, and endocrine dysregulation . Hormonal imbalances are important because they lead to muscle catabolism; these hormonal imbalances include insulin resistance as well as decreases in both estrogen and testosterone, and they promote a disparity between muscle protein synthesis and muscle protein breakdown with resulting muscle catabolism . As a person ages, there are associated alterations in muscle homeostasis and composition, including a decrease in muscle type II fibers, that are characterized by fast and powerful contractions with greater fatigue. The inability to generate power and the slowed rate of power development are hallmarks of both sarcopenia and frailty. These age-associated losses are further accelerated by malnutrition. Other derangements observed include an accumulation of damaged mitochondria and an increase in muscle apoptosis from excessive production of oxidative radicals. In sarcopenic patients, there exists some degree of chronic inflammation. This results in the presence of elevated protein markers, including tumor necrosis factor alpha (TNF-α), C-reactive protein, and interleukin 6 (IL-6). When TNF-α is elevated, an unregulated catabolic state is promoted that specifically targets skeletal muscle .
Starvation, more scientifically termed protein-energy malnutrition (PEM), is strictly caused by decreased intake. The prevalence of this state varies depending on the setting. For the community-dwelling elderly population, reported rates range from 5 to 10 percent, whereas in the elderly population in nursing homes and rehabilitation settings, the rates can be up to 70 percent. In the acute care setting, between 23 and 60 percent of elderly patients are malnourished . Risk factors attributed to PEM are often referred to as the nine d’s (dysphagia, dyspepsia, dementia, diarrhea, depression, disease, poor dentition, drugs, and dysfunction). These apply to all disorders of malnutrition and frailty, but the difference between PEM and the other disorders is that adequate feeding can reverse the negative effects of PEM.
Cachexia is defined as a “complex metabolic syndrome associated with underlying illness and characterized by loss of muscle, with or without loss of fat mass” . Nutritional derangements include anorexia, insulin resistance, and increased muscle protein breakdown. In the elderly, there are multiple dysregulated nutritional pathways that lead to an imbalance between catabolism and anabolism, with the complications of this syndrome not responsive to nutritional interventions. Common disease processes responsible for cachexia are cancer, chronic obstructive pulmonary disease, end-stage renal disease, rheumatoid arthritis, and congestive heart failure. A key distinction between sarcopenia and cachexia is that most cachectic patients are sarcopenic, whereas the reverse is not true; that is, not all sarcopenic patients are cachectic. The difference relates to the malnutrition caused directly by the underlying illness in cachexia, although both sarcopenia and cachexia share a common pathway that leads to anabolism resistance mediated by chronic inflammatory processes .
One of the challenges in the elderly ICU patient population is that most elderly ICU patients will have an interplay of all three syndromes – starvation, cachexia, and sarcopenia. Clinical distinction is not always possible among the three because these states are not mutually exclusive. The key is to identify the patients who present with nutritional derangements in order to formulate a multidisciplinary approach to restore a degree of the nutritional status with the goal of improving patient outcomes.
Many of the same mechanisms underlying malnutrition syndromes are present and amplified in the myopathy of critical illness. Sepsis, respiratory insufficiency, surgery, and trauma trigger a similar and common acute inflammatory pathway that leads to profound muscle wasting via TNF-α-mediated catabolism. One salient example is the effect of prolonged mechanical ventilation on sarcopenic elderly patients. The combination of decreased diaphragmatic muscular mass due to sarcopenia and disuse atrophy from mechanical ventilation leads to a vicious cycle of increased ventilator dependence. Emerging epidemiologic data suggest that frail elderly individuals have worse outcomes than their nonfrail counterparts. Even more alarming is that more than one-third of elderly patients meet the criteria for frailty. This figure will only continue to increase as the proportion of elderly population increases, with the effects of malnutrition superimposed on the high prevalence of chronic comorbidities. Interestingly, age alone is not consistently a predictor of mortality compared with frailty .
Furthermore, malnutrition syndromes are a major risk factor for persistent inflammatory immunosuppressed catabolic syndrome (PICS), a new phenotype of multiple-organ failure describing the underlying pathophysiology of chronic critical illness (defined as an ICU stay > 14 days) that is mostly associated with the elderly and has a high mortality rate. Similar to sarcopenia and cachexia, patients with PICS are refractory to nutritional supplementation. The underlying molecular pathophysiology shares a continuum with both sarcopenia and cachexia. The distinguishing features of PICS are the clinical setting and enhanced deterioration caused by the underlying illness and ensuing inflammatory insult .
All patients admitted to the ICU require an immediate nutritional screening. Unlike the complexity of diagnosing sarcopenia and frailty, determining baseline nutritional risk is relatively simple. Current guidelines endorse the Nutritional Risk Screening (NRS) 2002 and the Nutrition Risk in Critically Ill (NUTRIC) scoring systems over others . In contrast to other systems, both of these systems determine nutrition status and disease severity. Recent data support the use of assessment over screening tools in ICU patients because they indicate relevant outcomes (i.e., mortality, length of stay) independently. These assessments include Subjective Global Assessment and Mini Nutritional Assessment . Regardless of the tool used for assessment, each has its shortcomings. The key is to have a standardized and consistent approach for identification of baseline nutritional status. Current data indicate that appropriate and early nutritional interventions for patients at higher risk can lead to improved outcomes, including reduced infection, total complications, and mortality, compared with patients at low nutritional risk .
Traditional serum protein markers, including albumin, prealbumin, and transferrin, among others, merely reflect the acute-phase response and do not accurately represent the nutrition status of the patient in the ICU (Table 7.1). Interestingly, the albumin levels of sarcopenic patients have been shown to correlate with all-cause mortality in the elderly . Neither anthropometrics nor bioelectric impedance serves as a reliable assessment tool for sarcopenic status, nor do they assess the adequacy of nutritional therapy . To date, markers of inflammation, including TNF-α, C-reactive protein, and others, are still being investigated and are discouraged from being used as surrogate markers . Ultrasound and CT scan are emerging tools for muscle mass and body composition assessments. However, validation and reliability studies in ICU patients at the time of writing remain to be studied .
|C-reactive protein||2 days||Acute-phase reactant.|
|Levels influenced by underlying inflammation, infections, and cytokines.|
|Albumin||14–20 days||Long half-life limits usage in acute setting.|
|Potential marker for long-term outcome in sarcopenic patients.|
|Levels influenced by liver and renal disease, vascular permeability, and inflammation.|
|Prealbumin||12 hours||Negative acute-phase protein.|
|Levels influenced by the inflammatory cascade, renal and liver disease.|
|Transferrin||8–9 days||Levels influenced by inflammation, iron content, malabsorption, and liver and renal disease.|
Nutritional experts opine that accurate estimation of energy expenditure is required to help guide an effective nutritional strategy. Indirect calorimetry remains the gold standard for determining energy requirements, yet there are no data suggesting that accurately measuring resting energy expenditure to determine nutritional requirements improves outcome . A more practical recommendation is to use published predictive equations (e.g., Harris-Benedict, Penn State, etc.) or a simplistic weight-based equation (25–30 kcal/kg per day) to guide energy requirements. However, one of the shortcomings when using predictive equations is that they are less accurate in patients at the extremes of weight, that is, obese and underweight patients . One advantage of using weight-based equations is the simplicity of their application. An important caveat when using weight-based calculations in the critically ill ICU patient is that with dynamic fluid shifts (e.g., fluid resuscitation, edema), dry weight should be used instead of actual weight . Regardless of the approach used, nutritional evaluations should be dynamic and ideally occur more than once per week.