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Enteral Nutrition in Patients with Respiratory Disease

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Enteral Nutrition in Patients with Respiratory Disease 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 malnourished. The incidence depends largely upon dis- Table 1. – Adverse effects of malnutrition on thoraco- ease severity. As many as 25% of out-patients with pulmonary function in patients with respiratory disease 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
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