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Eur Respir J, 1996, 9, 364–370 Copyright ERS Journals Ltd 1996
DOI: 10.1183/09031936.96.09020364 European Respiratory Journal
Printed in UK - all rights reserved ISSN 0903 - 1936
SERIES 'CLINICAL PHYSIOLOGY IN RESPIRATORY INTENSIVE CARE'
Edited by A. Rossi and C. Roussos
Enteral nutrition in patients with respiratory disease
S.K. Pingleton
Enteral nutrition in patients with respiratory disease. S.K. Pingleton. ©ERS Journals Division of Pulmonary Diseases and Critical
Ltd 1996. Care Medicine, University of Kansas Medical
ABSTRACT: Nutritional assessment and management is an important therapeutic Center, Kansas City, Kansas, USA.
modality in patients with respiratory disease. Malnutrition adversely affects res- Correspondence: S.K. Pingleton, Division
piratory function. Nutritional therapy for the spontaneously breathing patient of Pulmonary Diseases and Critical Care
should include an appropriate diet plus the consideration of nutritional supplements. Medicine, University of Kansas Medical
Complete nutritional support should be undertaken with enteral nutrition in criti- Center, 39th and Rainbow Blvd, Kansas
cally ill patients with respiratory failure. Nutritional complications occur. Overfeed- City, Kansas 66160, USA
ing can lead to nutritionally associated hypercapnia. Keywords: Enteral nutrition, malnutrition,
Eur Respir J., 1996, 9, 364–370. respiratory disease
Received: April 6 1995
Accepted for publication November 7, 1995
Nutrition is an important aspect of patient care in any failure (ARF) have a 60% incidence of malnutrition [3].
patient with respiratory disease. Malnutrition adversely Disease severity can be assessed by the degree of pulmo-
effects lung function by diminishing respiratory muscle nary function and gas exchange abnormalities. Malnutri-
strength, altering ventilatory capacity, and impairing tion occurs in 50% of patients with chronic hypoxaemia
immune function. Repletion of altered nutritional status and normoxaemic patients with severe airflow obstruc-
or refeeding results in improvement of altered function tion (forced expiratory volume in one second (FEV1) <35%
and may be important in improving outcome. When of predicted); however, it is also present in 25% of patients
spontaneous oral intake is inadequate, enteral feeding is with moderate airflow obstruction [4].
preferred over parenteral feeding in all but those with Poor nutritional status can adversely affect thoraco-pul-
nonfunctional gastrointestinal tracts. Unfortunately, as monary function in spontaneously breathing as well
with any therapy, complications of nutritional support as mechanically-ventilated patients with respiratory dis-
exist. Those complications presenting special problems ease by impairment of respiratory muscle function, ven-
to the patient with respiratory disease are nutritionally- tilatory drive, and pulmonary defence mechanisms [5]
related hypercapnia and aspiration of enteral feedings. (table 1). The adverse effects of malnutrition occur inde-
This article considers the association of respiratory dis- pendently of the presence or absence of primary lung
ease and malnutrition, the determinants of appropriate disease; however, they can be additive in some patients
nutritional support in respiratory disease, the use of ente- with ARF, such as those with respiratory failure due to
ral nutritional support to reverse malnutrition, and the COPD. In COPD, primary abnormalities of decreased
complications associated with enteral feeding. Although inspiratory pressure and increased work of breathing
patients with a variety of respiratory diagnoses are appro- are found. Inspiratory muscle weakness, as assessed by
priate targets for this discussion, the article will deal maximal inspiratory pressure, results both from mechan-
largely with patients with chronic obstructive pulmonary ical disadvantage to inspiratory muscles consequent to
disease (COPD), as this is the respiratory disease most hyperinflation and generalized muscle weakness [6, 7].
commonly studied. General principles involved in the In COPD, inspiratory muscle weakness must be severe
nutritional care of the COPD patient can be applied to for hypercapnia to occur. In patients with myopathy,
patients with other respiratory diagnoses. hypercapnia occurs when inspiratory pressures are less
than one third [7]. However, hypercapnia is found in
the majority of COPD patients when inspiratory pres-
Adverse effects of malnutrition sures are only less than half normal [8]. Thus, hyper-
capnia occurs with a much lower level of respiratory
A substantial proportion of patients with COPD are Table 1. – Adverse effects of malnutrition on thoraco-
malnourished. The incidence depends largely upon dis- pulmonary function in patients with respiratory disease
ease severity. As many as 25% of out-patients with
COPD may be malnourished while almost 50% of patients Decreased respiratory muscle strength
admitted to hospital have evidence of malnutrition [1, Altered ventilatory drive
2]. Critically ill COPD patients with acute respiratory Impaired immunological function
ENTERAL NUTRITION IN PATIENTS WITH RESPIRATORY DISEASE 365
muscle weakness when other mechanical abnormalities pressure, results from mechanical disadvantage to inspi-
are present that increase the work of breathing. Thus, ratory muscles consequent to hyperinflation and perhaps
malnutrition may further compromise an already com- generalized muscle weakness [18]. Controversy exists as
promised lung function. Dyspnoea may worsen in the to the additive role of denutrition in the aetiology of the
spontaneously breathing COPD patient. Hypercapnic res- measured inspiratory muscle weakness. Cystic fibrosis
piratory failure and/or difficulty in weaning from mech- (CF) patients with hyperinflation and malnutrition were
anical ventilation may be more easily precipitated in the compared to asthmatics with hyperinflation but no mal-
malnourished patient with COPD than in the normally nutrition and to anorexia nervosa patients with malnutri-
nourished patient with COPD. tion but no hyperinflation, as well as control patients with
In simple starvation or undernutrition, fat and protein neither [19]. Peak inspiratory pressures in CF with hyper-
are lost, but the loss of protein is minimized by reduc- inflation were decreased as were pressures in anorexia
ing the need to use it as a source of energy [9]. Nitrogen nervosa patients. With volume correction, however, the
loss is modified by mobilization of fat, and enhanced fat difference in inspiratory strength in the CF group disap-
oxidation is the principal source of energy in the starv- peared. These data suggest that hyperinflation may be a
ing individual. Some protein wasting does occur, despite major cause of diminished respiratory muscle weakness
the availability of fat as a source of energy, and it becomes in COPD. In contrast to these data, renutrition studies in
markedly accelerated when fat stores are used up. When COPD as well as CF patients documenting improved mus-
body weight drops to less than 80% of ideal body weight, cle strength suggest that malnutrition is an important cause
protein catabolism occurs in the spontaneously breath- of diminished muscle strength [20, 21].
ing COPD patient. In critical illness, protein catabolism Malnutrition also affects ventilatory drive [22]. The
occurs to provide energy. With inadequate caloric intake interaction of nutrition and ventilatory drive appears
in critically ill patients, energy sources are derived from to be a direct function of the influence of nutrition on
protein breakdown and glyconeogenesis. Of various pro- metabolic rate [23]. In general, conditions which reduce
tein "pools" available, the muscle protein pool is sus- metabolic rate reduce ventilatory drive. A decrease in
ceptible to catabolism to provide fuel [10]. Inspiratory metabolic rate occurs with starvation. A parallel fall in
and expiratory muscles, primarily the diaphragm and metabolic rate and hypoxic ventilatory response has been
intercostals, are skeletal muscles and therefore suscep- documented in humans [23]. A 58% reduction in the
tible to this catabolic effect. Because the diaphragm is ventilatory response to hypoxia was found in volunteers
the principal respiratory muscle, the following discus- placed on a balanced 550 kcal·day-1 diet for 10 days.
sion will focus on it, although these considerations are The ventilatory response returned to normal with refeed-
generally valid for all respiratory muscles. It is impor- ing. Ventilatory response is also affected by constituents
tant to note that little, if any, data exist directly exami- of the diet. After a 7 day protein-free diet, a blunted
ning respiratory muscle function and malnutrition in ventilatory response to carbon dioxide was noted [24].
critically ill, mechanically-ventilated patients with COPD. Consequences of decreased respiratory strength and
Malnutrition reduces diaphragmatic muscle mass in decreased ventilatory drive could include decreased cough
health and disease [11, 12]. In necropsy studies, body and, thus, increased likelihood for atelectasis and subse-
weight and diaphragmatic muscle mass were reduced, quent pneumonia in spontaneously breathing patients with
respectively, to 70 and 60% of normal in underweight any type of respiratory disease. A decrease in respira-
patients dying of a variety of diseases [12]. Animal stud- tory muscle strength and drive may also possibly pro-
ies confirm the loss of diaphragmatic strength in prolong- long the duration of mechanical ventilation in patients
ed and acute nutritional deprivation [13, 14]. Respiratory who are otherwise candidates for weaning. Thus, the
muscle function is also impaired in poorly nourished potential for adverse outcomes is present in patients who
humans. When malnourished patients without lung dis- are initially malnourished from their disease as well as
ease were studied, respiratory muscle strength, maximum in patients with respiratory disease who develop mal-
voluntary ventilation and vital capacity were reduced by nutrition as a consequence of other intercurrent diseases.
37, 41 and 63%, respectively [15]. Respiratory muscle Malnutrition has also been shown to alter immune func-
strength in patients without a systemic disease is also tion. Protein calorie malnutrition is the most frequent
decreased. Maximal inspiratory pressures were lower in cause of acquired immunodeficiency in humans [25].
malnourished postoperative patients compared to nor- Polymorphonuclear leucocytes are normal in number, and
mally nourished patients [16]. Recently, similar data chemotaxis, opsonic function and phagocytic function
have also been described in anorexia nervosa patients, a usually remain or are mildly depressed, whilst intracel-
relatively pure model of malnutrition without systemic lular killing is reduced [26]. Thymus, spleen and lymph
disease [17]. Transdiaphragmatic pressures elicited by nodes become markedly atrophic, and lymphocytes may
phrenic nerve stimulation, were markedly diminished in decrease. Whilst immunoglobulins remain normal or slig-
anorexia patients before institution of enteral nutritional htly increased, antibody response may be depressed [26].
support.
The effect of nutritional status on respiratory muscle Effect of renutrition on malnutrition
function in patients with COPD is controversial. In COPD,
primary abnormalities of decreased inspiratory pressure Nutritional repletion can improve diminished respira-
and increased work of breathing are found. Inspiratory tory muscle strength in some patients. A 37% increase
muscle weakness, as assessed by maximal inspiratory in maximal inspiratory pressure and a 12% increase in
366 S.K. PINGLETON
body cell mass was found in 21 of 29 hospitalized patients enteral nutrition, as the enteral route is preferred when-
given parenteral nutrition for 2–4 weeks [16]. Short- ever nutritional support is indicated.
term oral refeeding in malnourished COPD patients can
also improve respiratory muscle function, although it app-
ears to depend on the presence of weight gain [20]. When Energy needs
six ambulatory patients with COPD were given oral nut- Several methods exist for estimating caloric require-
ritional repletion for 2 weeks, body weight increased by ments of patients with respiratory disease. Levels of ener-
6% and transdiaphragmatic pressures increased by 41% gy expenditure can be estimated, calculated with formulae
[20]. In contrast, when 8 weeks of nutritional supple- or nomograms, or determined by using measurements of
mentation in 21 malnourished COPD patients produced energy expenditure (table 2). In mechanically-ventilated
no change in weight, no change in respiratory muscle -1
function was found [27]. Intensive, nocturnal, nasoen- patients with respiratory disease, guidelines of 25 kcal·kg
terally-administered nutrition in COPD and cystic fibro- daily have been suggested [32]. Estimates of basal meta-
sis can result in weight gain and improved respiratory bolic rate (BMR) via a resting energy expenditure (REE)
muscle and pulmonary function [28]. Renutrition has can be obtained from the Harris-Benedict equation, which
also been found to improve diaphragmatic contractility relates energy expenditure to sex, weight in kilograms
in a more "pure" model of malnutrition, that of anorex- (W), height in centimetres (H), and age in years (A).
ia nervosa [17]. After 1 month of enteral nutrition (weight BMR (males) = 66.47 + 13.75 (W) + 5.0 (H) - 6.76 (A)
gain 15%), stimulated transdiaphragmatic pressure (Pdi) BMR (females) = 655.1 + 9.65 (W) + 1.85 (H) - 4.68 (A)
was increased from 16±5 to 23±7 cmH O, documenting
2
improved diaphragmatic function with renutrition. With A "stress factor" or percentage increase in energy
long-term nocturnal enteral feeding, CF patients were requirement is then added to this determination, based
found to have improved pulmonary function in con- on the severity of the patient's illness. Stress factors are
junction with significant weight gain [21]. based on estimated metabolic needs over and above rest-
The mechanisms of improved muscle performance with ing needs, and will vary with respect to body tempera-
renutrition is not known with certainty. In animal and ture, degree of physical activity, or extent of injury [33].
human studies, chronic hypocaloric dieting produces Most critically ill patients with respiratory disease require
changes in skeletal muscle that may be important in the a stress factor of 1.2. The utility of the Harris-Benedict
genesis of muscle dysfunction. In addition to protein equation in clinical practice is controversial. Caloric
catabolism, these changes include depletion of glycoly- needs may be inaccurate, with overestimation of caloric
tic and oxidative enzymes, reduction in high-energy phos- requirements [34]. It is, however, a relatively simple
phate stores and increases in intracellular calcium [29, method of estimating caloric requirements, especially in
30]. The electrophysiological properties of the muscle critically ill patients.
can also be altered by modification of the cell membrane The most accurate method of determination of energy
properties, which decrease the sodium potassium pump requirements is indirect measurement of actual energy
activity, alter ionic permeability and, thus, lead to an expenditure with a metabolic cart. In this case, caloric
imbalance in the intercellular electrolyte composition requirements can be indirectly determined by measuring
[29]. These data suggest that alterations in muscle con- the rate of oxygen consumption, each litre representing
tractility and endurance properties are not simply or approximately 4–5 kcal. Metabolic carts can be used
solely due to changes in lean tissue. Indeed, renutrition to measure oxygen consumption both in mechanically-
studies in hypocaloric dieting and fasting and in the severe ventilated and spontaneously breathing patients but are
starvation of anorexia nervosa patients document improve- expensive and require technical expertise. Unfortunately,
ment in muscle performance at a time when significant the stringent conditions that must be imposed during these
changes in body composition could not be detected [31]. study periods are not the ordinary conditions of clini-
Changes in intracellular electrolytes may be responsible cal care. Also, it should be noted that while indirect
for early improvement in muscle contractility and endur- calorimetry may accurately reflect the energy require-
ance properties. ments over the 30–60 min time-period of measurements,
it is difficult to know how to extrapolate this measure to
Nutritional support a 24 h time-period.
The optimum mode of nutrition in any patient is oral, Table 2. – Determination of daily expenditure in patients
spontaneous intake of an appropriate balanced diet. Un- with respiratory disease
fortunately, patients with respiratory disease may require Estimation
-1
supplementation or even complete nutritional support, de- 25 kcal·kg daily for respiratory failure
pending on the severity and intensity of illness. However, Calculation
the principles of nutritional support are independent of Resting energy expenditure
the type of respiratory disease, the mode of nutritional ad- Harris-benedict plus "stress" factor
ministration, or the severity of respiratory illness. Whe- Measurement
ther nutritional support requires either supplementation Indirect calorimetry
or total support, the following discussion will focus on Pulmonary artery catheter measurements
ENTERAL NUTRITION IN PATIENTS WITH RESPIRATORY DISEASE 367
Energy requirements in COPD patients follow general Clear disadvantages of carbohydrate administration exist.
guidelines, with several caveats. Malnourished sponta- Hyperglycaemia, especially in diabetics or patients receiv-
neously breathing COPD patients have increased resting ing corticosteroid therapy, can be exacerbated by high
energy requirements, approximately 15% above values dextrose concentrations. Elevated blood glucose can neg-
predicted by Harris-Benedict equations, resulting in far atively affect humoral immune function and potentiate
greater expected energy requirement [35]. The "relative the growth of Candida albicans [38]. Excess glucose
hypermetabolism" is explained by the increased energy administration is not oxidized but stored as body fat.
needs of the ventilatory muscles [36]. The energy cost Clinically, this can result in increased fatty deposition in
of respiratory muscles can be approximated from the the liver, as well as nutritionally associated hypercap-
severity of lung hyperinflation. Assessment of these nia.
points should be made in the perspective of whether the Fat calories are required in total nutritional support to
COPD patient is spontaneously breathing or being mech- provide essential fatty acids. Intravenous lipids, even
anically-ventilated. Nutritional support in the spontane- during slow administration, may cause pulmonary haemo-
ously breathing COPD patient should also take in account dynamic changes in injured lungs [39]. The clinical sig-
the limitations that COPD patients have in augmentation nificance of these changes may be small. Lipids, especially
of caloric intake, such as early satiety, anorexia, bloat- long-chain triglycerides, can impair reticuloendothelial
ing and fatigue. clearance functions, even when hypertriglyceridaemia is
When calculating, estimating, or measuring total daily absent [40]. Hepatic steatosis is significantly influenced
energy needs, it is important to remember that the nutri- by the proportion of fat calories as well as glucose calo-
tional goal is appropriate total daily calories, i.e. neither ries in excess of caloric needs [41]. Despite many dis-
underfeeding nor overfeeding the patient. Whether the advantages of intravenous lipids, fats in enteral feeding
intake is spontaneous, supplemented or completely con- formation are well-tolerated with few adverse effects.
trolled, physicians caring for the patient with respiratory While recommendations for an appropriate substrate
disease should determine appropriate daily calories. Un- mix of carbohydrates and fats vary, generally 60–70%
derfeeding the patient over a long period of time or dur- carbohydrates are given with 20–30% fats (table 3).
ing hypermetabolic states, such as critical illness, risks
the adverse effects of malnutrition on thoracopulmonary Complications of nutritional support
function. Overfeeding the patient risks metabolic com-
plications, especially nutritionally related hypercapnia. Multiple complications are associated with enteral nutri-
tion and are of importance to the patient with respiratory
Substrate mix disease (table 4). Complications can be generally clas-
sified into mechanical, infectious, gastrointestinal and
Once total energy requirements are determined, the metabolic types. Whilst of concern to all patients requir-
next question relates to the most appropriate substrate ing enteral nutrition, patients with respiratory disease are
mix, that is the percentage of total calories that are car- particularly susceptible to adverse sequelae of pulmonary
bohydrate, fat and protein. Protein (nitrogen) require- Table 3. – Nutritional recommendations for patients with
ments in the patient with pulmonary disease are not respiratory disease
significantly different from that in other patients. Optimal Determination of daily energy requirements (total calories)
support would establish neutral or positive nitrogen bal- Substrate mix
ance, depending on the need for repletion. In the criti- Protein
cally ill patient with ARF, this can be accomplished by 20% of total calories
-1 -1
giving 1–3 g of protein·kg daily [32]. Generally, this 1–2 gm·kg daily
amounts to approximately 20% of total calories being Carbohydrates
administered as protein. 60–70%
The most appropriate carbohydrate/fat substrate mix Fats
for COPD patients is complicated and controversial. The 20–30%
precise substrate mix is largely an issue for respiratory
disease patients in the Intensive Care Unit, where nutri- Table 4. – Complications of enteral nutritional support
tional support is totally controlled and adverse sequelae Mechanical
are theoretically more likely. Spontaneous oral intake Inadvertent tracheal intubation
is less problematical, except for those occasions when Clogging or obstruction of tube
the intake is supplemented by prepared oral formula- Aspiration of enteral feeding
tions. Gastrointestinal
Although the critically ill patient with respiratory fail- Vomiting
ure does use lipid preferentially as a fuel source, glucose Abdominal distension
oxidation is not impaired, and lipid infusion probably Diarrhoea
does not change patterns of fuel oxidation [37]. Thus, Metabolic
there is no theoretical metabolic reason to choose one Hyperglycaemia
fuel over the other. There is also no benefit of glucose Hypophosphataemia
over lipids and vice versa in the "sparing" effect of proteins. Hypercapnia
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