Thorax 1992;47:141-143 141

THORAX
Editorial

Nutritional support in chronic obstructive lung disease

Why? however, total energy expenditure was found to be normai

In the last decade increasing attention has been focused on in patients" as measured during 24 hours in a metabolic
nutritional problems in respiratory disorders, and particu- chamber.26 Spontaneously reduced physical activity could
larly in chronic obstructive lung disease. This stems from save energy in these patients and compensate for their
an awareness that malnutrition is an important clinical resting hypermetabolism. Thus weight loss probably
problem in a subpopulation of patients with chronic results primarily from inadequate energy intake in relation
ob-structive lung disease. The picture of the emaciated to energy needs, which is lilely to occur curing many
emphysematous patient, or pink puffer, is known to every exacerbation the disease.
clinician. his common perception is substantiated by How much support is necessary also depends on the
several reports.1-12 In a study from the United States metabolic response to nutritional supplementation. Hyper-
Natlonal Institutes of Health on the effects of intermittent metabolism causec by stress, bums, or injuries commonly
positive pressure breathing nearly a quarter of 779 men requires a very hgh energy and nitrogen intake to stabilise
with stable chronic obstructive lung disease welghed less nitrogen retention. Although hypermetabolic at rest, mar-
than 90% of their ideal body weight, a simple albeit nourished patients with chronic obstructive lung disease
imper?j'of malnutritlon." The prevalence of achieve a positive nitrogen balance when enerx intake-is
malnutritionlincreases with the severity of airways obstruc- adequate for expenditure.'u Thus they react like
tion 2411 an _ _ _ _ f nutritionally depleted individuals and should theoretisally
WTtients WSA.- oVUCVJ, 1Otde benefit from nutritional support.
in the 1960s showed that malnutrition in itself contributed Several co6iBrolled studies have assessed the effect of
to mortality.35" The more recent National Institutes of nutritional support in chronic obstructive lung disease,
Health trial also showed that mortality was higher in either in outpatients27"' or in inpatients." In addition to
malnourished patients, independently ot hMe severity of changes in nutrition, the peripheral and respiratory muscle
airways obstruction." Reduced respiratory muscle mass performance and exercise capacity have been evaluated.
anctGfunctian,!- as well as increased susceptibility to The outcome of these studies was directly related to the
infectioe' are recognised as deleterious consequence& of actual increment in energy intake. Weight gain could be
malnutrition. achieved only by sLLlly increasing energy intake, by
Because malnutrition appears to be common and life more than 30% aboVe me usua intake, amounting to more
threatening in patients with chronic obstructive ljng than 45 rcal (0 19 MJ)/kg per day. Moreover, improve-
disease, it;da uf providing them with nurniLiai ouplvort ment in muscle fr_erance occurred
has logically emerged. Several questions need to be only wit `conc=nitan weight gain.
answered, however, before nutritional support can be In one of these controlled studies oral supplementation
efficiently implemented. was given for three months to ambulatory malnourished
patients with chronic obstructive lung diease. Daily
energy intake ae usual intake and
How much? corresponded to 47 kcal (0- 196 MJ)/kg on average. The
The question of how much energy needs to be provided authors reported a mean weight gain of 4-2 kg, an incrase in
perhaps depends on the mechanism of weight loss in maximal respiratory pressures and in handgrip and
chronic obstructive lung disease: is this due to reduced sternomastoid strength, and a decrease in sternomastoid
energy intake or to increased energy output? Earlier muscle fatigability; similar improvements were not
studies, based on dietary histories, showed that the energy observed in a control group. Unfortunately these
intake of malnourished patients with chronic obstructivc improvements waned or disappeared once the patients had
lung disease was either adequate in relation to the recom- returned to their usual iet. In another study six mal-
mended daily allowances or at least sim-ilar to that of wel nourished patients with chronic obstructive luisease
nourished patents. I0 Using indirect calorimetry, received noctural supplemental feeding via a nas
however, several groups have recently reported a Q.9-/Ao tube for 16 days-.Energy intake increased by 75 % above the
increase in resting energy expenditure in patients with usual and c?rresponded to 49-5 kcal (0207 MJ)/kg a day on
stable chronlc obstructive iung disease.">' This excessive average. Body weight increased by 2-4 kg and was accom-
energy expenditure with the reduced metalic
contrasts panied by an improvement in respiratory muscle strength
rate uaall, ul-vvd ill iLL itiuLi anzl has een and endurance. None of these changes occurred in four
attributed to the increnstd cnet bQ:eathing.22
if According to similar patients receiving sham supplementation.3' In
these findings, weight loss would seem to be the con- contrast, no change in weight or muscle performance was
sequence of increased energy output rather than of reduced observed in patients whose increment in energy intake was
intake. Despite a higher resting energy expenditure, smaller.27 3
142 Editorial

What? will be essential to define selection criteria to recognise

The composition of nutritional supplementation for those patients likely to benefit from nutritional support.
patients with lung disease has received some attention. Because of the labour and cost required this intervention
Carbon dioxide production ((Co2) is higher when carbo- should not be applied indiscriminately. These questions
hydrates are the m;ainenergy sources and ower Wena s need to be answered and a cost-benefit analysis must be
mainly oxidised. Thu mie respiratory quotient performed before nutritional support can be recommended
(RQ = Vco2/Vo2) tends towards 10 with rhohydrate on a wide scale in chronic obstructive lung disease.
based diets and towards 07 with fat based diets. For JEAN-WILLIAM FITTING
arterial carbon dio*ide tension (Paco2) to remain constant Division de Pneumologie,
Centre Hospitalier Universitaire Vaudois,
an incregsea vc-2 IS iepen3en? on an increase m alveolar 1011 Lausanne,
ventilatilon.Thus carbohydrate loads could induce or Switzerland
worsen hypercapnia in patients with severe ventilatory
limitation. This has been observed with high energy Reprint requests to: Dr Fitting
supplements administered to patients during mechanical
ventilation or weaning.3233 Mitchell RS, Filley GF. Chronic obstructive bronchopulmonary disease. I.
Patients with chronic obstructive lung disease who are in Clinical features. Am Rev Respir Dis 1964;89:360-71.
2 Burrows B, Niden AH, Barclay WR, Kasik JE. Chronic obstructive lung
a stable clinical state, however, usually appear to tolerate disease. II. Relationship of clinical and physiologic findings to the severity
carbohydrates without diffnilty. At rest both normocapnic of airways obstruction. Am Rev Respir Dis 1964;91:665-78.
3 Sukumalchantra Y, Williams MH. Serial studies of pulmonary function in
and hypercapnic patients were able to maintain a constant patients with chronic obstructive pulmonary disease. Am J Med
Paco2 after a 920 kcal (3-85 J) carbohydrate load.3 No 1965;39:941-5.
clinicallyisignihicant difference could be noted with low or 4 Renzetti AD, McClement JH, Litt BD. The veterans administration
cooperative study of pulmonary function. III. Mortality in relation to
high carbohydrate' diets in a grop o p s respiratory function in chronic obstructive pulmonary disease. Am J Med
with chronic obltrucuive_ung disease.' Furthermore, 5
1966;41:1 15-29.
Vandenbergh E, Van de Woestijne KP, Gyselen A. Weight changes in the
respiratory failure was not reported in stable patients while terminal stages of chronic obstructive pulmonary disease. Am Rev Respir
they were-r- ci Dis 1967;95:556-65.
formulas con u to 54% carboh drates. 36 6 Hunter AMB, Carey MA, Larsh HW. The nutritional status of patients with
chronic obstructive pulmonary disease. Am Rev Respir Dis 1981;i24:
Thus low carbonydrate, high fat formulas do not seem 376-81.
necessary for nutritional support in patients with stable 7 Driver AG, McAlevy MT, Smith JL. Nutritional assessment of patients
with chronic obstructive pulmonary disease and acute respiratory failure.
chronic obstructive lung disease. Chest 1982;82:568-71.
8 Openbrier DR, Irwin MM, Rogers RM, Gottlieb GP, Dauber JH, Van
Thiel DH, et al. Nutritional status and lung function in patients with
emphysema and chronic bronchitis. Chest 1983;83:17-22.
How? 9 Braun SR, Keim NL, Dixon RM, Clagnaz P, Anderegg A, Shrago ES. The
The failure of nutritional support that was observed in prevalence and determinants of nutritional changes in chronic obstructive
pulmonary disease. Chest 1984;86:558-63.
some trials conducted in patients with chronic obstructive 10 Fiaccadori E, Del Canale S, Coffrini E, Vitali P, Antonucci C, Cacciani G, et
lung disease seems mainly due to the inability of the al. Hypercapnic-hypoxemic chronic obstructive pulmonary disease
patients to increas' their energy intake sufficiently.27' ' (COPD): influence of severity of COPD on nutritional status. Am J Clin
Nutr 1988;48:680-5.
Spontan re n in the usual energy intake and 11 Wilson DO, Rogers RM, Wright EC, Anthonisen NR. Body weight in
intolerance of supplemental formulas were frequently chronic obstructive pulmonary disease. The National Institutes of Health
intermittent positive-pressure breathing trial. Am Rev Respir Dis
encountered. Nocturnal supplemental feeding via a 1989;139:1435-8.
nasoenteric tube may obviate these difficulties and proved 12 Schols A, Mostert R, Soeters P, Greve LH, Wouters EFM. Inventory of
to be effective in inpatients."l When oral supplements are nutritional status in patients with COPD. Chest 1989;96:247-9.
13 Boushy SF, Adhikari PK, Sakamoto A, Lewis BM. Factors affecting
used they should be given at the end of meals or between prognosis in emphysema. Dis Chest 1964;45:402-1 1.
meals so that the usual dietary intake is maintained. Both 14 Thurlbeck WM. Diaphragm and body weight in emphysema. Thorax
1978;33:483-7.
inpatients and outpatients must have close monitoring and 15 Arora NS, Rochester DF. Effect of body weight and muscularity on human
counselling if they are to Min tl gyTrgo Md diaphragm muscle mass, thickness, and area. J Appi Physiol 1982;52:
64-70.
learn vaiiiiu- st s forcopig With mea related 16 Rochester DF, Braun NMT. Determinants of maxlunal inspiratory pressure
complaints such as anorexia, early satiety, bloating, and in chronic obstructive pulmonary disease. Am Rev Respir Dis 1985;
dyspnoefa 3' From oarl r-
17
132:42-7.
Gray-Donald K, Gibbons L, Shapiro SH, Martin JG. Effect of nutritional
vention Aap ears to be feasible but difficult inchrpic status on exercise performance in patients with chronic obstructive
obstructive ease, requiring dedicated and special- pulmonary disease. Am Rev Respir Dis 1989;140:1544-8.
ised personnel. 18 Niedermann MS, Merrill WW, Ferranti RD, Pagano KM, Palmer LB,
Reynolds HY. Nutritional status and bacterial binding in the lower
respiratory tract in patients with chronic tracheostomy. Ann Intern Med
1984;100:795-800.
19 Openbrier DR, Irwin MM, Dauber JH, Owens G, Rogers RM. Factors
For whom? affecting nutritional status and the impact of nutritional support in patients
At the moment we know several things about nutritional with emphysema. Chest 1984;85:67-9S.
deficiency in chronic obstructive lung disease. Firstly, 20 Goldstein SA, Thomashow BM, Kvetan V, Askanazi J, Kinney JM, Elwyn
DH. Nitrogen and energy relationships in malnourished patients with
malnutrition is known to represent an important clinical emphysema. Am Rev Respir Dis 1988;138:636-44.
problem, with its high prevalence and its aggravating 21 Fitting JW, Frascarolo Ph, Jequier E, Leuenberger Ph. Energy expenditure
and rib cage-abdominal motion in chronic obstructive pulmonary disease.
influence on mortality. Secondly, we are beginning to Eur Respir J 1989;2:840-5.
understand the disruption of energy balance that leads to 22 Donahoe M, Rogers RM, Wilson DO, Pennock BE. Oxygen consumption of
weight loss in these patients. Thirdly, malnutrition has the respiratory muscles in normal and in malnourished patients with
chronic obstructive pulmonary disease. Am Rev Respir Dis 1989;140:
been shown to be improved by nutritional intervention. 385-91.
Finally, we know how nutritional support should be 23 Wilson DO, Donahoe M, Rogers RM, Pennock BE. Metabolic rate and
weight loss in chronic obstructive lung disease. Journal of Parenteral and
provided in chronic obstructive lung disease, and also that Enteral Nutrition 1990;14:7-1 1.
it represents a major undertaking. 24 Lanigan C, Moxham J, Ponte J. Effect ofchronic airflow limitation on resting
We still lack some important information, however. oxygen consumption. Thorax 1990;45:388-90.
25 Schols AMWJ, Soeters PB, Mostert R, Saris WHM, Wouters EFM. Energy
Firstly, ifnutritional support appears intuitively logical for balance in chronic obstructive pulmonary disease. Am Rev Respir Dis
patients with chronic obstructive lung disease its impact on 1991;143:1248-52.
26 Hugli 0, Schutz Y, Leuenberger Ph, Fitting JW. The daily energy
morbidity, quality of life, number of hospital admissions, expenditure of COPD patients in confined and free-living conditions
and mortality has yet to be seen. Once this has been done it [abstract]. Am Rev Respir Dis 1991;143:A453.
Editorial 143

27 Lewis MI, Belman MJ, Door-Uyemura L. Nutritional supplementation in 32 Covelli HD, Waylon Black J, Olsen MS, Beekman JF. Respiratory failure
ambulatory patients with chronic obstructive pulmonary disease. Am Rev precipitated by high carbohydrate loads. Ann Intern Med 1981;95:579-81.
Respir Dis 1987;135:1062-8. 33 Dark DS, Pingleton SK, Kerby GR. Hypercapnia during weaning. A
28 Knowles JB, Fairbarn MS, Wiggs BJ, Chan-Yan C, Pardy RL. Dietary complication of nutritional support. Chest 1985;88:141-3.
supplementation and respiratory muscle performance in patients with 34 Gieseke T, Gurushanthaiah G, Glauser FL. Effects of carbohydrates on
COPD. Chest 1988;93:977-83. carbon dioxide excretion in patients with airway disease. Chest
29 Efthimiou J, Fleming J, Gomes C, Spiro SG. The effect of supplementary 1977;71:55-8.
oral nutrition in poorly nourished patients with chronic obstructive 35 Angelillo VA, Bedi S, Durfee D, Dahl J, Patterson AJ, O'Donohue WJ.
pulmonary disease. Am Rev Respir Dis 1988;137:1075-82. Effects of low and high carbohydrate feedings in ambulatory patients with
30 Otte KE, Ahlburg P, D'Amore F, Stellfeld M. Nutritional repletion in chronic obstructive pulmonary disease and chronic hypercapnia. Ann
malnourished patients with emphysema. Journal of Parenteral and Enteral Intern Med 1985;103:883-5.
Nutrition 1989;13:152-6. 36 Wilson DO, Rogers RM, Sanders MH, Pennock BE, Reilly JJ. Nutritional
31 Whittaker JS, Ryan CF, Buckley PA, Road JR. The effects of refeeding on intervention in malnourished patients with emphysema. Am Rev Respir
peripheral and respiratory muscle function in malnourished chronic Dis 1986;134:672-7.
obstructive pulmonary disease patients. Am Rev Respir Dis 1990;142: 37 Donahoe M, Rogers RM. Nutritional assessment and support in chronic
283-8. obstructive pulmonary disease. Clin Chest Med 1990;11:487-504.

Thorax 1992;47:143

Editorial note

Supplements for Thorax

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