Enteral Nutri on Copd Patient

7/30/2019 Enteral Nutri on Copd Patient

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Eur Respir J, 1996, 9, 364370DOI: 10.1183/09031936.96.09020364Printed in UK - all rights reserved

Copyright ERS Journals Ltd 1996European Respiratory Journal

ISSN 0903 - 1936

Enteral nutrition in patients with respiratory disease

S.K. Pingleton

Enteral nutrition in patients with respiratory disease. S.K. Pingleton. ERS JournalsLtd 1996.ABSTRACT: Nutritional assessment and management is an important therapeuticmodality in patients with respiratory disease. Malnutrition adversely affects res-piratory function. Nutritional therapy for the spontaneously breathing patientshould include an appropriate diet plus the consideration of nutritional supplements.Complete nutritional support should be undertaken with enteral nutrition in criti-cally ill patients with respiratory failure. Nutritional complications occur. Overfeed-ing can lead to nutritionally associated hypercapnia.Eur Respir J., 1996, 9, 364370.

Division of Pulmonary Diseases and CriticalCare Medicine, University of Kansas MedicalCenter, Kansas City, Kansas, USA.

Correspondence: S.K. Pingleton, Divisionof Pulmonary Diseases and Critical CareMedicine, University of Kansas MedicalCenter, 39th and Rainbow Blvd, KansasCity, Kansas 66160, USA

Keywords: Enteral nutrition, malnutrition,respiratory disease

Received: April 6 1995Accepted for publication November 7, 1995

Nutrition is an important aspect of patient care in anypatient with respiratory disease. Malnutrition adverselyeffects lung function by diminishing respiratory musclestrength, altering ventilatory capacity, and impairingimmune function. Repletion of altered nutritional statusor refeeding results in improvement of altered functionand may be important in improving outcome. Whenspontaneous oral intake is inadequate, enteral feeding ispreferred over parenteral feeding in all but those withnonfunctional gastrointestinal tracts. Unfortunately, aswith any therapy, complications of nutritional supportexist. Those complications presenting special problemsto the patient with respiratory disease are nutritionally-related hypercapnia and aspiration of enteral feedings.This article considers the association of respiratory dis-ease and malnutrition, the determinants of appropriatenutritional support in respiratory disease, the use of ente-ral nutritional support to reverse malnutrition, and thecomplications associated with enteral feeding. Althoughpatients with a variety of respiratory diagnoses are appro-priate targets for this discussion, the article will deal

largely with patients with chronic obstructive pulmonarydisease (COPD), as this is the respiratory disease mostcommonly studied. General principles involved in thenutritional care of the COPD patient can be applied topatients with other respiratory diagnoses.

Adverse effects of malnutrition

A substantial proportion of patients with COPD aremalnourished. The incidence depends largely upon dis-ease severity. As many as 25% of out-patients withCOPD may be malnourished while almost 50% of patientsadmitted to hospital have evidence of malnutrition [1,2]. Critically ill COPD patients with acute respiratory

failure (ARF) have a 60% incidence of malnutrition [3].Disease severity can be assessed by the degree of pulmo-nary function and gas exchange abnormalities. Malnutri-tion occurs in 50% of patients with chronic hypoxaemiaand normoxaemic patients with severe airflow obstruc-tion (forced expiratory volume in one second (FEV1)


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muscle weakness when other mechanical abnormalitiesare present that increase the work of breathing. Thus,malnutrition may further compromise an already com-promised lung function. Dyspnoea may worsen in thespontaneously breathing COPD patient. Hypercapnic res-piratory failure and/or difficulty in weaning from mech-

anical ventilation may be more easily precipitated in themalnourished patient with COPD than in the normallynourished patient with COPD.

In simple starvation or undernutrition, fat and proteinare lost, but the loss of protein is minimized by reduc-ing the need to use it as a source of energy [9]. Nitrogenloss is modified by mobilization of fat, and enhanced fatoxidation is the principal source of energy in the starv-ing individual. Some protein wasting does occur, despitethe availability of fat as a source of energy, and it becomesmarkedly accelerated when fat stores are used up. Whenbody weight drops to less than 80% of ideal body weight,protein catabolism occurs in the spontaneously breath-

ing COPD patient. In critical illness, protein catabolismoccurs to provide energy. With inadequate caloric intakein critically ill patients, energy sources are derived fromprotein breakdown and glyconeogenesis. Of various pro-tein "pools" available, the muscle protein pool is sus-ceptible to catabolism to provide fuel [10]. Inspiratoryand expiratory muscles, primarily the diaphragm andintercostals, are skeletal muscles and therefore suscep-tible to this catabolic effect. Because the diaphragm isthe principal respiratory muscle, the following discus-sion will focus on it, although these considerations aregenerally valid for all respiratory muscles. It is impor-tant to note that little, if any, data exist directly exami-ning respiratory muscle function and malnutrition in

critically ill, mechanically-ventilated patients with COPD.Malnutrition reduces diaphragmatic muscle mass in

health and disease [11, 12]. In necropsy studies, bodyweight and diaphragmatic muscle mass were reduced,respectively, to 70 and 60% of normal in underweightpatients dying of a variety of diseases [12]. Animal stud-ies confirm the loss of diaphragmatic strength in prolong-ed and acute nutritional deprivation [13, 14]. Respiratorymuscle function is also impaired in poorly nourishedhumans. When malnourished patients without lung dis-ease were studied, respiratory muscle strength, maximumvoluntary ventilation and vital capacity were reduced by37, 41 and 63%, respectively [15]. Respiratory muscle

strength in patients without a systemic disease is alsodecreased. Maximal inspiratory pressures were lower inmalnourished postoperative patients compared to nor-mally nourished patients [16]. Recently, similar datahave also been described in anorexia nervosa patients, arelatively pure model of malnutrition without systemicdisease [17]. Transdiaphragmatic pressures elicited byphrenic nerve stimulation, were markedly diminished inanorexia patients before institution of enteral nutritionalsupport.

The effect of nutritional status on respiratory musclefunction in patients with COPD is controversial. In COPD,primary abnormalities of decreased inspiratory pressureand increased work of breathing are found. Inspiratory

muscle weakness, as assessed by maximal inspiratory

pressure, results from mechanical disadvantage to inspi-ratory muscles consequent to hyperinflation and perhapsgeneralized muscle weakness [18]. Controversy exists asto the additive role of denutrition in the aetiology of themeasured inspiratory muscle weakness. Cystic fibrosis(CF) patients with hyperinflation and malnutrition were

compared to asthmatics with hyperinflation but no mal-nutrition and to anorexia nervosa patients with malnutri-tion but no hyperinflation, as well as control patients withneither [19]. Peak inspiratory pressures in CF with hyper-inflation were decreased as were pressures in anorexianervosa patients. With volume correction, however, thedifference in inspiratory strength in the CF group disap-peared. These data suggest that hyperinflation may be amajor cause of diminished respiratory muscle weaknessin COPD. In contrast to these data, renutrition studies inCOPD as well as CF patients documenting improved mus-cle strength suggest that malnutrition is an important causeof diminished muscle strength [20, 21].

Malnutrition also affects ventilatory drive [22]. Theinteraction of nutrition and ventilatory drive appearsto be a direct function of the influence of nutrition onmetabolic rate [23]. In general, conditions which reducemetabolic rate reduce ventilatory drive. A decrease inmetabolic rate occurs with starvation. A parallel fall inmetabolic rate and hypoxic ventilatory response has beendocumented in humans [23]. A 58% reduction in theventilatory response to hypoxia was found in volunteersplaced on a balanced 550 kcalday-1 diet for 10 days.The ventilatory response returned to normal with refeed-ing. Ventilatory response is also affected by constituentsof the diet. After a 7 day protein-free diet, a bluntedventilatory response to carbon dioxide was noted [24].

Consequences of decreased respiratory strength anddecreased ventilatory drive could include decreased coughand, thus, increased likelihood for atelectasis and subse-quent pneumonia in spontaneously breathing patients withany type of respiratory disease. A decrease in respira-tory muscle strength and drive may also possibly pro-long the duration of mechanical ventilation in patientswho are otherwise candidates for weaning. Thus, thepotential for adverse outcomes is present in patients whoare initially malnourished from their disease as well asin patients with respiratory disease who develop mal-nutrition as a consequence of other intercurrent diseases.

Malnutrition has also been shown to alter immune func-

tion. Protein calorie malnutrition is the most frequentcause of acquired immunodeficiency in humans [25].Polymorphonuclear leucocytes are normal in number, andchemotaxis, opsonic function and phagocytic functionusually remain or are mildly depressed, whilst intracel-lular killing is reduced [26]. Thymus, spleen and lymphnodes become markedly atrophic, and lymphocytes maydecrease. Whilst immunoglobulins remain normal or slig-htly increased, antibody response may be depressed [26].

Effect of renutrition on malnutrition

Nutritional repletion can improve diminished respira-tory muscle strength in some patients. A 37% increase

in maximal inspiratory pressure and a 12% increase in

E NT ER AL N UT RI TI ON I N PAT IE NT S W IT H R ES PI RAT ORY D IS EA SE 365


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body cell mass was found in 21 of 29 hospitalized patientsgiven parenteral nutrition for 24 weeks [16]. Short-term oral refeeding in malnourished COPD patients canalso improve respiratory muscle function, although it app-ears to depend on the presence of weight gain [20]. Whensix ambulatory patients with COPD were given oral nut-

ritional repletion for 2 weeks, body weight increased by6% and transdiaphragmatic pressures increased by 41%[20]. In contrast, when 8 weeks of nutritional supple-mentation in 21 malnourished COPD patients producedno change in weight, no change in respiratory musclefunction was found [27]. Intensive, nocturnal, nasoen-terally-administered nutrition in COPD and cystic fibro-sis can result in weight gain and improved respiratorymuscle and pulmonary function [28]. Renutrition hasalso been found to improve diaphragmatic contractilityin a more "pure" model of malnutrition, that of anorex-ia nervosa [17]. After 1 month of enteral nutrition (weightgain 15%), stimulated transdiaphragmatic pressure (Pdi)

was increased from 165 to 237 cmH2O, documentingimproved diaphragmatic function with renutrition. Withlong-term nocturnal enteral feeding, CF patients werefound to have improved pulmonary function in con-junction with significant weight gain [21].

The mechanisms of improved muscle performance withrenutrition is not known with certainty. In animal andhuman studies, chronic hypocaloric dieting produceschanges in skeletal muscle that may be important in thegenesis of muscle dysfunction. In addition to proteincatabolism, these changes include depletion of glycoly-tic and oxidative enzymes, reduction in high-energy phos-phate stores and increases in intracellular calcium [29,30]. The electrophysiological properties of the muscle

can also be altered by modification of the cell membraneproperties, which decrease the sodium potassium pumpactivity, alter ionic permeability and, thus, lead to animbalance in the intercellular electrolyte composition[29]. These data suggest that alterations in muscle con-tractility and endurance properties are not simply orsolely due to changes in lean tissue. Indeed, renutritionstudies in hypocaloric dieting and fasting and in the severestarvation of anorexia nervosa patients document improve-ment in muscle performance at a time when significantchanges in body composition could not be detected [31].Changes in intracellular electrolytes may be responsiblefor early improvement in muscle contractility and endur-

ance properties.

Nutritional support

The optimum mode of nutrition in any patient is oral,spontaneous intake of an appropriate balanced diet. Un-fortunately, patients with respiratory disease may requiresupplementation or even complete nutritional support, de-pending on the severity and intensity of illness. However,the principles of nutritional support are independent ofthe type of respiratory disease, the mode of nutritional ad-ministration, or the severity of respiratory illness. Whe-ther nutritional support requires either supplementation

or total support, the following discussion will focus on

enteral nutrition, as the enteral route is preferred when-ever nutritional support is indicated.

Energy needs

Several methods exist for estimating caloric require-ments of patients with respiratory disease. Levels of ener-gy expenditure can be estimated, calculated with formulaeor nomograms, or determined by using measurements ofenergy expenditure (table 2). In mechanically-ventilatedpatients with respiratory disease, guidelines of 25 kcalkg-1

daily have been suggested [32]. Estimates of basal meta-bolic rate (BMR) via a resting energy expenditure (REE)can be obtained from the Harris-Benedict equation, whichrelates energy expenditure to sex, weight in kilograms(W), height in centimetres (H), and age in years (A).

BMR (males) = 66.47 + 13.75 (W) + 5.0 (H) - 6.76 (A)BMR (females) = 655.1 + 9.65 (W) + 1.85 (H) - 4.68 (A)

A "stress factor" or percentage increase in energyrequirement is then added to this determination, basedon the severity of the patient's illness. Stress factors arebased on estimated metabolic needs over and above rest-ing needs, and will vary with respect to body tempera-ture, degree of physical activity, or extent of injury [33].Most critically ill patients with respiratory disease requirea stress factor of 1.2. The utility of the Harris-Benedictequation in clinical practice is controversial. Caloricneeds may be inaccurate, with overestimation of caloricrequirements [34]. It is, however, a relatively simplemethod of estimating caloric requirements, especially in

critically ill patients.The most accurate method of determination of energyrequirements is indirect measurement of actual energyexpenditure with a metabolic cart. In this case, caloricrequirements can be indirectly determined by measuringthe rate of oxygen consumption, each litre representingapproximately 45 kcal. Metabolic carts can be usedto measure oxygen consumption both in mechanically-ventilated and spontaneously breathing patients but areexpensive and require technical expertise. Unfortunately,the stringent conditions that must be imposed during thesestudy periods are not the ordinary conditions of clini-cal care. Also, it should be noted that while indirectcalorimetry may accurately reflect the energy require-

ments over the 3060 min time-period of measurements,it is difficult to know how to extrapolate this measure toa 24 h time-period.

S.K. PINGLETON366

Table 2. Determination of daily expenditure in patientswith respiratory disease

Estimation25 kcalkg-1 daily for respiratory failure

CalculationResting energy expenditureHarris-benedict plus "stress" factor

MeasurementIndirect calorimetryPulmonary artery catheter measurements


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Energy requirements in COPD patients follow generalguidelines, with several caveats. Malnourished sponta-neously breathing COPD patients have increased restingenergy requirements, approximately 15% above valuespredicted by Harris-Benedict equations, resulting in fargreater expected energy requirement [35]. The "relative

hypermetabolism" is explained by the increased energyneeds of the ventilatory muscles [36]. The energy costof respiratory muscles can be approximated from theseverity of lung hyperinflation. Assessment of thesepoints should be made in the perspective of whether theCOPD patient is spontaneously breathing or being mech-anically-ventilated. Nutritional support in the spontane-ously breathing COPD patient should also take in accountthe limitations that COPD patients have in augmentationof caloric intake, such as early satiety, anorexia, bloat-ing and fatigue.

When calculating, estimating, or measuring total dailyenergy needs, it is important to remember that the nutri-

tional goal is appropriate total daily calories, i.e. neitherunderfeeding nor overfeeding the patient. Whether theintake is spontaneous, supplemented or completely con-trolled, physicians caring for the patient with respiratorydisease should determine appropriate daily calories. Un-derfeeding the patient over a long period of time or dur-ing hypermetabolic states, such as critical illness, risksthe adverse effects of malnutrition on thoracopulmonaryfunction. Overfeeding the patient risks metabolic com-plications, especially nutritionally related hypercapnia.

Substrate mix

Once total energy requirements are determined, thenext question relates to the most appropriate substratemix, that is the percentage of total calories that are car-bohydrate, fat and protein. Protein (nitrogen) require-ments in the patient with pulmonary disease are notsignificantly different from that in other patients. Optimalsupport would establish neutral or positive nitrogen bal-ance, depending on the need for repletion. In the criti-cally ill patient with ARF, this can be accomplished bygiving 13 g of proteinkg-1 daily [32]. Generally, thisamounts to approximately 20% of total calories beingadministered as protein.

The most appropriate carbohydrate/fat substrate mix

for COPD patients is complicated and controversial. Theprecise substrate mix is largely an issue for respiratorydisease patients in the Intensive Care Unit, where nutri-tional support is totally controlled and adverse sequelaeare theoretically more likely. Spontaneous oral intakeis less problematical, except for those occasions whenthe intake is supplemented by prepared oral formula-tions.

Although the critically ill patient with respiratory fail-ure does use lipid preferentially as a fuel source, glucoseoxidation is not impaired, and lipid infusion probablydoes not change patterns of fuel oxidation [37]. Thus,there is no theoretical metabolic reason to choose onefuel over the other. There is also no benefit of glucoseover lipids and vice versa in the "sparing" effect of proteins.

Clear disadvantages of carbohydrate administration exist.Hyperglycaemia, especially in diabetics or patients receiv-ing corticosteroid therapy, can be exacerbated by highdextrose concentrations. Elevated blood glucose can neg-atively affect humoral immune function and potentiatethe growth of Candida albicans [38]. Excess glucose

administration is not oxidized but stored as body fat.Clinically, this can result in increased fatty deposition inthe liver, as well as nutritionally associated hypercap-nia.

Fat calories are required in total nutritional support toprovide essential fatty acids. Intravenous lipids, evenduring slow administration, may cause pulmonary haemo-dynamic changes in injured lungs [39]. The clinical sig-nificance of these changes may be small. Lipids, especiallylong-chain triglycerides, can impair reticuloendothelialclearance functions, even when hypertriglyceridaemia isabsent [40]. Hepatic steatosis is significantly influencedby the proportion of fat calories as well as glucose calo-

ries in excess of caloric needs [41]. Despite many dis-advantages of intravenous lipids, fats in enteral feedingformation are well-tolerated with few adverse effects.

While recommendations for an appropriate substratemix of carbohydrates and fats vary, generally 6070%carbohydrates are given with 2030% fats (table 3).

Complications of nutritional support

Multiple complications are associated with enteral nutri-tion and are of importance to the patient with respiratorydisease (table 4). Complications can be generally clas-sified into mechanical, infectious, gastrointestinal and

metabolic types. Whilst of concern to all patients requir-ing enteral nutrition, patients with respiratory disease areparticularly susceptible to adverse sequelae of pulmonary


Table 3. Nutritional recommendations for patients withrespiratory disease

Determination of daily energy requirements (total calories)Substrate mixProtein

20% of total calories12 gmkg-1 daily

Carbohydrates6070%

Fats

2030%

Table 4. Complications of enteral nutritional support

MechanicalInadvertent tracheal intubationClogging or obstruction of tubeAspiration of enteral feeding

GastrointestinalVomitingAbdominal distensionDiarrhoea

MetabolicHyperglycaemiaHypophosphataemia

Hypercapnia


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aspiration and the metabolic complication of nutritionally-related hypercapnia.

Pulmonary aspiration of enteral feeding has the poten-tial for significant adverse sequelae in patients with res-piratory disease. Large volume aspiration of enteralfeeding can precipitate or worsen respiratory failure,

small volume aspiration can cause nosocomial pneu-monia with the potential for sepsis. The frequency ofpulmonary aspiration is difficult to determine as the inci-dence of pulmonary aspiration reported with gastric intu-bation by feeding tubes varies widely, ranging 0.877%[4244]. In a review of 253 hospitalized patients treat-ed with enteral nutritional support, only two patients(0.8%) were diagnosed as suffering aspiration pneumo-nia [42]. When detected by glucose-positive endotra-cheal secretions, aspiration was diagnosed in 21% ofmechanically-ventilated patients [43]. Likewise, 77% oftracheally-intubated patients were found to aspirate asdetermined by the presence of methylene blue in tra-

cheal secretions [44]. It is difficult to draw general con-clusions about the effect of feeding tubes from thesestudies because all differ in the population studied, studydesign, method of diagnosing aspiration, and size ofenteral feeding tube.

Multiple factors can affect the frequency and severityof aspiration. Clearly, the presence of an endotrachealtube and the type of endotracheal tube influences theincidence of aspiration [45]. Other risk factors for aspi-ration include a reduced level of consciousness, with con-sequent compromise in glottic closure, the presence ofan artificial airway, and ileus or gastroparesis [46].

Small bore feeding tubes are generally recommendedas a means of reducing gastro-oesophageal reflux and,

ultimately, pulmonary aspiration. Data supporting this re-commendation are controversial. No aspiration of me-thylene blue dyed tube feeding was found in 30 ventilatedpatients with small bore (8 F) feeding tubes [42]. Incontrast, bore size was not a significant variable in wit-nessed aspiration or aspiration pneumonia in hospitali-zed patients [47]. Recent data suggest that feeding tubesize may not be an important variable in reflux. Whenreflux was assessed by gastro-oesophageal scintiscan-ning in normals, no difference was found in reflux bet-ween large bore (14 F) and small bore (8 F) nasogastricfeeding tubes [48]. These data suggest that additionalfactors may be more important in reflux. One of these

is clearly the position of the patient. In early work, nor-mal volunteers with nasogastric tubes were studied inthe supine, 10, 30 and 45 degree position, as well as sit-ting upright. After a large volume of acid had beeninstilled into the stomach, aspiration, as detected by afall in oesophageal pH, occurred only in the supineposition [49]. More recent data confirm the importanceof patient position, with studies of pulmonary aspirationby scintiscanning of tracheal secretions after isotopiclabelling of enteral nutrition [50]. Radioactive countsand, therefore, aspiration were four times higher in thesupine position than in the semirecumbent position.Duration of supine position is also important. Aspirationincreased 650% 16 h after placement in the supine posi-

tion.

These data confirm the presence of aspiration withenteral feeding, but documentation of aspiration is diffi-cult. Recent data suggest that detection of aspiration byglucose determinations of tracheal secretions may be mis-leading [51]. Prevention of aspiration of gastric contentshould be directed at minimizing the mechanical factors

contributing to regurgitation, such as patient elevationand improper tube placement. Gastric residuals shouldbe frequently checked, especially in patients at risk forslow gastric emptying.

Nutritionally associated hypercapnia is a notable meta-bolic complication of nutritional support in patients withrespiratory disease. Nutritionally associated increasesin carbon dioxide production (V'CO2) can produce hyper-capnia [52]. Clinical sequelae include worsening of dysp-noea and exercise tolerance, precipitation of ARF, anddelayed weaning from mechanical ventilation [53, 54]. Hy-percapnia results from increased V'CO2 for two reasons.Glucose combustion causes a greater V'CO2 than combus-

tion of lipid, in that an isocaloric substitution of all lipidfor all glucose calories results in a 22% reduction in V'CO2[52]. More importantly, excess glucose calories result inlipogenesis and markedly increased respiratory quotient(RQ). The RQ of glucose is 1.0 and of fat is 0.7; how-ever, the RQ of lipogenesis or fat production is approxi-mately 8.0, reflecting the proportionally greater V'CO2relative to oxygen consumption (V'O2) with lipogenesis.In normal subjects, hypercapnia is avoided by increasedventilation. Patients with compromised ventilatory sta-tus, such as COPD, or those with fixed minute ventila-tion due to weak respiratory muscles may not be able toincrease ventilation appropriately. Hypercapnia can resultand precipitate respiratory distress, ARF and difficulty

in weaning from mechanical ventilation [53, 54].The cause of nutritionally related hypercapnia is gener-

ally thought to be excess carbohydrate or glucose calories.Some confusion has existed, however, as to whether thoseexcess glucose calories relate to an excess proportion ofcarbohydrate in a nutritional regimen or simple excessof total glucose calories. Prior data suggest that the causeof elevated V'CO2 and hypercapnia is simple excess totalcalories. A 62% increase in V'CO2 in surgical patientswas found to precipitate respiratory distress [55]. Totaldaily calories were 2.25 REE. ARF was precipitatedafter the onset of total parenteral nutrition (TPN) in threeelderly patients with COPD [53]. Total calories were in

excess of 2,200 caloriesday-1

in all. More recent dataconfirm increased V'CO2 with stepwise increases in totalcalories [56]. V'CO2 increased in 10 mechanically-venti-lated patients receiving nutritional regimens at 1.0, 1.5and 2.0 REE with 60% carbohydrate and 20% fat. TheV'CO2 was significantly increased at 1.5 and 2.0 REEcompared to baseline. In contrast, when 10 additionalpatients were given isocaloric regimens that varied thepercentage carbohydrate from 4060 to 75% of total cal-ories, V'CO2 was not different. These data suggest thattotal calories more clearly influence V'CO2 production thanpercentage of carbohydrate calories when total caloriesare not excessive.

Quantitation ofV'CO2 is accomplished by indirect calo-

rimetry or by analysing a timed collection of expired air.

S.K. PINGLETON368


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This problem can be avoided by identifying patients atrisk, especially the patient with respiratory disease, andavoiding excessive total calories.

Enteral formulations with altered carbohydrate/fat ratioshave been developed and promoted, especially for patientswith COPD. These formulations commonly have lower

concentrations of carbohydrate calories with resultanthigher fat concentrations. Data evaluating V'CO2 fol-lowing administration of isocaloric nutritional regimensin COPD are limited. Eight postoperative patients receiv-ed isocaloric nutritional regimens (1.5 REE) of either100% glucose or 50% glucose and 50% fat [57]. TheV'CO2 increased in both nutritional regimens as comparedto basal values, although it was 11% higher with glu-cose alone compared with glucose and lipid. In a studyof exercise gas exchange in normals, V'CO2 decreasedfrom 290 to 240 mLmin-1 with a low carbohydrate (10%)concentration [58]. However, despite this decrease, meanminute ventilation was not different during rest or exer-

cise, suggesting that numerical decreases in V'CO2 fromvery low percentage carbohydrate calories may not havea practical significance in decreasing minute ventilation.These data suggest there is little value for special enteralformulations in COPD that decrease carbohydrate calo-ries when total calories are appropriate.

Summary

In summary, malnutrition adversely affects the patientwith respiratory disease by impairing respiratory func-tion, increasing symptoms and worsening outcome.Physicians should evaluate nutritional status and intake

in all patients with respiratory disease. When spontane-ous oral intake is judged inadequate, consideration shouldbe given to supplementing oral intake with enteral nut-ritional formulations or, in cases of critical illness, pro-viding complete nutritional support with enteral feeding.Estimation or calculation of total energy needs is of vitalimportance in the patient with respiratory disease to pre-vent under- or overfeeding. Reduction of carbohydratecalories, especially in supplemental nutritional formula-tions, appears to be of little value and not necessary whenappropriate nutritional support is provided.

References

1. Braun ST, Keim NL, Dixon RM, et al. The prevalenceand determinants of nutritional changes in chronic obstruc-tive pulmonary disease. Chest1984; 86: 558563.

2. Hunter ABM, Carey MA, Larsh HW. The nutritionalstatus of patients with chronic obstructive pulmonary dis-ease. Am Rev Respir Dis 1981; 124: 376381.

3. Driver AG, McAlevy MT, Smith JL. Nutritional ass-essment of patients with chronic obstructive pulmonarydisease and respiratory failure. Chest1982; 82: 568571.

4. Rochester DF, Esau SA. Malnutrition and the respira-tory system. Chest1984; 85: 411415.

5. Braun NMT, Arora NS, Rochester DF. Respiratory mus-cle and pulmonary function in proximal myopathies.

Thorax1983; 38: 616623.

6. Lands L, Desmond KJ, Demizio D, Pavilanis A, CoatesAL. The effects of nutritional status and hyperinflationon respiratory muscle strength in children and youngadults. Am Rev Respir Dis 1990; 141: 15061509.

7. Braun NMT, Arora NS, Rochester DF. Respiratory mus-cle and pulmonary function in proximal myopathies.

Thorax1983; 38: 616623.8. Rochester DF, Braun NMT. Determinants of maximalinspiratory pressure in chronic obstructive pulmonary dis-ease. Am Rev Respir Dis 1985; 132: 4247.

9. Cahill G. Starvation in man. N Engl J Med 1970; 282:668675.

10. Long CL, Birkham RH, Geiger JW. Contribution ofskeletal muscle protein in elevated rates of whole bodyprotein catabolism in trauma patients. Am J Clin Nutr1981; 34: 10871093.

11. Thurlbeck WM. Diaphragm and body weight in emphy-sema. Thorax1978; 33: 483487.

12. Arora NS, Rochester DF. Effect of body weight andmuscularity on human diaphragm muscle mass, thick-ness and area. J Appl Physiol: Respirat Environ Exercise

Physiol 1982; 52: 6470.13. Kelsen SG, Ference M, Kapoor S. Effects of prolongedundernutrition on structure and function of the diaphragm.J Appl Physiol 1985; 58: 13541359.

14. Lewis MI, Sieck GC, Fournier M, Belman MT. Effectof nutritional deprivation on diaphragm contractilityand muscle fiber size. J Appl Physiol 1986; 60: 596603.

15. Arora NS, Rochester DF. Respiratory muscle strengthand maximal voluntary ventilation in undernourishedpatients. Am Rev Respir Dis 1982; 126: 58.

16. Kelly SM, Rosa A, Field S, Coughlin M, Shizgal HM,Macklem PT. Inspiratory muscle strength and body com-position in patients receiving total parenteral nutritiontherapy. Am Rev Respir Dis 1984; 130: 3337.

17. Murciano D, Rigaud D, Pingleton S, Armengaud MH,

Melchior JC, Aubier M. Diaphragmatic function in seve-rely malnourished patients with anorexia nervosa. Am JRespir Crit Care Med1994; 150: 15691574.

18. Gibson GJ, Pride NB, Newson DJ. Pulmonary mechan-ics in patients with respiratory muscle weakness. AmRev Respir Dis 1978; 118: 373376.

19. Weiner P, Suo J, Fernandez E, Cherniack RM. The effectof hyperinflation on respiratory muscle strength and effi-ciency in healthy subjects and patients with asthma. AmRev Respir Dis 1990; 141: 15011505.

20. Wilson DO, Rogers RM, Sander MH, et al. Nutritionalintervention in malnourished patients with emphysema.Am Rev Respir Dis 1986; 134: 672677.

21. Steinkamp G, von der Hardt H. Improvement of nutri-tional status and lung function after long-term nocturnal

gastrostomy feeding in cystic fibrosis. J Pediatr1994;124: 244249.

22. Doekel RC Jr, Zwillich CW, Scoggin CH. Clinical semi-starvation: depression of hypoxic ventilatory response.N Engl J Med1976; 295: 358361.

23. Askanazi J, Rosenbaum SH, Hyman AI, et al. Effectsof parenteral nutrition on ventilatory drive. Anesthesiol1980; 53 (Suppl. 1): 185.

24. Askanazi J, Weissman C, La Sala PA, et al. Effect ofprotein intake on ventilatory drive. Anesthesiol 1984;60: 106110.

25. Chandra RK. Malnutrition. In: Chandra RK, ed. Primaryand Secondary Immunodeficiency Disorders. New York,Churchill Livingstone, 1983; p. 187.

26. Shizgal HM. Nutrition and immune function. Surg Ann

1981; 12: 1229.



7/7

27. Lewis MI, Belman MJ, Dorr-Uyemural L. Nutritionalsupplementation in ambulatory patients with COPD. AmRev Respir Dis 1987; 125: 10621068.

28. Whittaker JS, Ryan CF, Buckley PA, Rood JD. Theeffects of refeeding on peripheral and respiratory mus-cle function in malnourished COPD patients. Am Rev

Respir Dis 1990; 142: 283288.29. Pichard C, Vaughn C, Struk R, Armstrong RL, JeejeebhoyKN. Effect of dietary manipulation (fasting, hypocaloricfeeding and subsequent refeeding) on rat muscles ener-getics as assessed by nuclear magnetic resonance spec-troscope. J Clin Invest1988; 82: 895901.

30. Sieck GC, Lewis ML, Banco CE. Effects of undernu-trition on diaphragm fiber size, SDH activity and fatigueresistance. J Appl Physiol 1989; 66: 21962205.

31. McRussel DR, Pendergast PJ, Daily PL, Garfinkel PE,Whitwell J, Jeejeebhoy KN. A comparison between mus-cle function and body composition in anorexia nervosa:the effect of refeeding. Am J Clin Nutr1983; 38: 2937.

32. DeBiasse MA, Wilmore DW. What is optimal nutri-tional support? New Horizons 1994; 2: 122130.

33. Long CL, Schaffel N, Geiger JW, et al. Metabolicresponse to injury and illness: estimates of energy andprotein needs from indirect calorimetry and nitrogen bal-ance. J Parent Ent Nutr1979; 3: 452456.

34. Daly JM, Heymsfield SB, Head CA, et al. Human energyrequirements: overestimation by widely used predictionequations. Am J Clin Nutr 1985; 42: 11701174.

35. Wilson DO, Rogers RM, Pennock B. Metabolic rate andweight loss in obstructive lung disease. J Parent EntNutr1990; 14: 711.

36. Donahoe M, Rogers RM, Wilson DO, et al. Oxygenconsumption of the respiratory muscles in normal andmalnourished patients with chronic obstructive pulmonarydisease. Am Rev Respir Dis 1989; 149: 385391.

37. Cohen FJ. Glucose vs lipid calories. In: Zaloga GP,

ed. Nutrition in Critical Care. St. Louis, Mosby-YearBook Inc., 1994; pp. 169183.

38. Goldmann DA, Martin WT, Worthington JW. Growthof bacteria and fungi in total parenteral nutrition solu-tions. Am J Surg 1973; 126: 314318.

39. Venus B, Smith RA, Patel C, et al. Hemodynamic andgas exchange alterations during intralipid infusion inpatients with adult respiratory distress syndrome. Chest1989; 95: 12781281.

40. Seidner DL, Mascioli EA, Isfan NW, et al. Effects oflong-chain triglyceride emulsions in reticuloendothelialsystem function in humans.J Parent Ent Nutr1989; 13:614619.

41. Baker AL, Rosenberg IH. Hepatic complications of totalparenteral nutrition. Am J Med1987; 82: 489497.

42. Cataldi-Betcher EL, Seltzer MH, et al. Complicationsoccurring during enteral nutrition support: a prospectivestudy. J Parent Ent Nutr 1983; 7: 546552.

43. Kingston GW, Phang PT, Leathley MJ. Increased inci-dence of nosocomial pneumonia in mechanically-venti-lated patients with subclinical aspiration. Am J Surg1991; 161: 589592.

44. Elpern EH, Jacobs ER, Bone RC. Incidence of aspira-tion in tracheally-intubated adults. Heart Lung 1987; 16:

527531.45. Andrews MJ, Pearson FG. Incidence and pathogenesisof tracheal injury following cuffed tube tracheostomywith assisted ventilation. Ann Surg 1971; 173: 249263.

46. Mullan H, Robenoff RA, Robenoff R. Risk of pulmonaryaspiration among patients receiving enteral nutrition sup-port. J Parent Ent Nutr1992; 16: 160164.

47. Metheny NA, Eisenberg P, Spies M. Aspiration pneu-monia in patients fed through nasoenteral tubes. HeartLung 1986; 15: 256261.

48. Dotson R, Robinson R, Pingleton SK. The effect ofnasogastric tube size on gastroesophageal reflux. Am JRespir Crit Care Med 1994; 149: 16591662.

49. Nagler R, Spiro HM. Persistent gastroesophageal refluxinduced during prolonged gastric intubation. N Engl J

Med1963; 269: 495503.50. Torres A, Serra-Batlles J, Rose E, et al. Pulmonary aspi-ration of gastric contents in patients receiving mechani-cal ventilation: the effect of body position. Ann InternMed1992; 116: 540543.

51. Kinsey GC, Murray MJ, Swensen SJ, Miles JM. Glucosecontent of tracheal aspirates: implications for the detec-tion of tube feeding aspiration. Crit Care Med 1994;22: 15571562.

52. Silberman H, Silberman AW. Parenteral nutrition, bio-chemistry, and respiratory gas exchange. J Parent EntNutr1986; 10: 151154.

53. Covelli HD, Black JW, Olsen MS, Bechman JF. Respiratoryfailure precipitated by high carbohydrate loads. AnnIntern Med1981; 95: 579581.

54. Dark DS, Pingleton SK, Kerby GR. Hypercapnia dur-ing weaning: a complication of nutritional support. Chest1985; 88: 141143.

55. Askanazi J, Rosenbaum SH, Hyman AL, et al. Respiratorychanges induced by the large glucose loads of total par-enteral nutrition. J Am Med Assoc 1980; 243: 14441447

56. Talpers SS, Romberger DJ, Bunce SB, Pingleton SK.Nutritionally associated increased carbon dioxide pro-duction: excess total calories vs high proportion of car-bohydrate calories. Chest1992; 102: 551555.

57. Delafosse B, Bouffard Y, Viale JP, Annat G, Bertrand O,Motin J. Respiratory changes induced by parenteral nutri-tion in postoperative patients undergoing inspiratory pres-sure support ventilation. Anesthesiol 1987; 66: 393396.

58. Sue DY, Chung MM, Gsosvenor M, Wasserman K. Effect

of altering the proportions of dietary fat and carbohy-drate on exercise gas exchange in normal subjects. AmRev Respir Dis 1989; 139: 14301434.

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