Medical Nutrition

Therapy in Pulmonary
Disease

Malnutrition and the

Pulmonary System
Malnutrition impairs
Respiratory muscle function
Ventilatory drive
Response to hypoxia
Pulmonary defense mechanisms

Effects of Malnutrition
in Pts without Lung
Disease
Respiratory muscle strength by 37%

Maximum voluntary ventilation by

41% (1)

Vital capacity (lung volume) 63% (1)

Diaphragmatic muscle mass to 60%

of normal in underweight patients who
died of other ailments (2)

1.

Aurora N, Rochester, D. Am Rev Respir Dis 126:5-8, 1982

2.

Aurora N, Rochester D. J Appl Physiol: Respirat Environ Exercise physiol 52:64-70, 1982

Effects of Malnutrition in
Pts with Pulmonary
Disease

Decreased cough and inability to

mobilize secretions
Atelectasis and pneumonia
Prolonged mechanical ventilation
and difficulty weaning with
prolonged ICU stay

Effects of Malnutrition in
Pts with Pulmonary
Disease

Altered host immune response and

cell-mediated immunity
Contributes to chronic or repeated
pulmonary infections
Decreased surfactant production
Decreased lung elasticity
Decreased ability to repair injured
lung tissue

Normal Lung
Anatomy

Selected Airway
Disorders

Chronic Pulmonary
Disorders
Bronchopulmonary displasia
Cystic fibrosis
Tuberculosis
Bronchial asthma
Chronic obstructive
pulmonary disease (COPD)

Acute Pulmonary
Disorders
Pulmonary aspiration
Pneumonia
Tuberculosis
Cancer of the lung
Acute respiratory distress
syndrome
Pulmonary failure

Pulmonary Conditions
w/ Nutritional
Neonate
Bronchopulmonary displasia
Implications
(BPD)

Obstructio Cystic fibrosis (CF)

n
Chronic obstructive
pulmonary disease (COPD)
Emphysema
Chronic bronchitis
Asthma
Tumor

Lung cancer

Pulmonary Conditions
w/ Nutritional
Implications
Infection
Pneumonia
Tuberculosis (TB)
Respiratory Acute respiratory failure
Failure
Lung transplantation
NeuroMuscular dystrophy
muscular
Paralysis
Abnormaliti
es

Pulmonary Conditions w/
Nutritional Implications
Skeletal

Osteoporosis
Scoliosis

Cardiovascula Pulmonary edema

r
Endocrine

Severe obesity
Prader-Willi syndrome

Adverse Effects of Lung

Disease on Nutritional
Status

Increased energy expenditure

Increased work of breathing
Chronic infection
Medical treatments (e.g.
bronchodilators, chest physical
therapy

Adverse Effects of Lung

Disease on Nutritional
Status

Reduced intake
Fluid restriction
Shortness of breath
Decreased oxygen saturation when
eating
Anorexia due to chronic disease
Gastrointestinal distress and vomiting

Adverse Effects of Lung

Disease on Nutritional
Status

Additional limitations
Difficulty preparing food due to
fatigue
Lack of financial resources
Impaired feeding skills (for infants
and children)
Altered metabolism

Chronic Lung Disease

Bronchopulmonary
Dysplasia:
Pathophysiology

Chronic lung condition in newborns

that often follows respiratory distress
syndrome (RDS) and treatment with
oxygen
Characterized by broncheolar
metaplasia and interstitial fibrosis
Occurs most frequently in infants who
are premature or low birth weight

BPD: Signs and

Symptoms

Hypercapnea (CO2 retention)

Tachypnea
Wheezing
Dyspnea
Recurrent respiratory infections
Cor pulmonale (right ventricular
enlargement of the heart)

Growth Failure in BPD

Increased energy needs

Inadequate dietary intake
Gastroesophageal reflux
Emotional deprivation
Chronic hypoxia

Goals of Nutritional
Management in BPD

Meet nutritional needs

Promote linear growth
Develop age-appropriate feeding
skills
Maintain fluid balance

Energy Needs in BPD

REE in infants with BPD is 25-50%

higher than in age-matched controls
Babies with growth failure may have
needs 50% higher
Energy needs in acute phase (PN,
controlled temperature) 50-85 kcals/kg
Energy needs in convalescence (oral
feeds, activity, temperature regulation)
as high as 120-130 kcals/kg

Protein Needs in
Babies with BPD

Protein: within advised range for

infants of comparable postconceptional age
As energy density of the diet is
increased by the addition of fat
and carbohydrate, protein should
still provide 7% or more of total
kcals

Macronutrient Mix in
BPD

Fat and carbohydrate should be

added to formula only after it has
been concentrated to 24 kcals/oz
to keep protein high enough
Fat provides EFA and energy when
tolerance for fluid and
carbohydrate is limited
Excess CHO increases RQ and CO2
output

Fluid in BPD

Infants with BPD may require fluid

restriction, sodium restriction, and
long term treatment with diuretics
Use of parenteral lipids or
calorically dense enteral feeds
may help the infant meet energy
needs

Mineral Needs in BPD

Often driven by the babys premature status

Lack of mineral stores as a result of
prematurity (iron, zinc, calcium)
Growth delay
Medications: diuretics, bronchodilators,
antibiotics, cardiac antiarrhythmics,
corticosteroids associated with loss of
minerals including chloride, potassium,
calcium

Vitamin Needs in BPD

Interest in antioxidants, including

vitamin A for role in developing
epithelial cells of the respiratory
tract
Provide intake based on the DRI,
including total energy, to promote
catchup growth

Feeding Strategies in
BPD

Calorically dense formulas or

boosted breast milk (monitor fluid
status and urinary output)
Small, frequent feedings
Use of a soft nipple
Nasogastric or gastrostomy tube
feedings

Feeding Strategies in
Gastroesophageal
Reflux
Thickened feedings (add rice

cereal to formula)
Upright positioning
Medications like antacids or
histamine H2 blockers
Surgical fundoplication

Long Term Feeding

Problems in BPD

History of unpleasant oral experiences

(intubation, frequent suctioning,
recurrent vomiting)
History of non-oral feedings
Delayed introduction of solids
Discomfort or choking associated with
eating solids
Infants may tire easily while breastfeeding or bottle feeding
May require intervention of
interdisciplinary feeding team

Cystic Fibrosis

Inherited autosomal recessive disorder

2-5% of the white population are
heterozygous
CF incidence of 1:2500 live births
30,000 people treated at CF centers in
the U.S.
Survival is improving; median age of
patients has exceeded 30 years

Cystic Fibrosis

Epithelial cells and exocrine glands

secrete abnormal mucus (thick)
Affects respiratory tract, sweat,
salivary, intestine, pancreas, liver,
reproductive tract

Diagnosis of Cystic
Fibrosis

Neonatal screening provides

opportunity to prevent
malnutrition in CF infants
Sweat test (Na and Cl >60 mEq/L)
Chronic lung disease
Failure to thrive
Malabsorption
Family history

Nutritional
Implications of CF

Infants born with meconium ileus

are highly likely to have CF
85% of persons with CF have
pancreatic insufficiency
Plugs of mucus reduce the digestive
enzymes released from the
pancreas causing maldigestion of
food and malabsorption of nutrients

Nutritional
Implications of CF

Decreased bicarbonate secretion

reduces digestive enzyme activity
Decreased bile acid reabsorption
contributes to fat malabsorption
Excessive mucus lining the GI
tract prevents nutrient absorption
by the microvilli

Gastrointestinal
Complications of CF

Bulky, foul-smelling stools

Cramping and intestinal obstruction
Rectal prolapse
Liver involvement
Pancreatic damage causes impaired
glucose tolerance (50% of adults
with CF) and development of
diabetes (15% of adults with CF)

Nutritional Care Goals

Control malabsorption
Provide adequate nutrients for
growth
or maintain weight for height or
pulmonary function
Prevent nutritional deficiencies

Common Treatments

Pancreatic enzyme replacement

Adjust macronutrients for
symptoms
Nutrients for growth
Meconium ileus equivalent:
intestinal obstruction (enzymes,
fiber, fluids, exercise, stool
softeners)

Pancreatic Enzyme
Replacement

Introduced in the early 1980s

Enteric-coated enzyme
microspheres withstand acidic
environment of the stomach
Release enzymes in the
duodenum, where they digest
protein, fat and carbohydrate

Pancreatic Enzyme
Replacement
Dosage depends on
Degree of pancreatic insufficiency
Quantity of food eaten
Fat, protein, and carbohydrate
content of food eaten
Type of enzymes used

Pancreatic Enzyme
Replacement

Enzyme dosage limited to 2500 lipase

units per kilogram of body weight per
meal
Adjusted empirically to control
gastrointestinal symptoms, including
steatorrhea, and promote growth
Fecal fat or nitrogen balance studies
may help to evaluate the adequacy of
enzyme supplementation

Distal Intestinal
Obstruction Syndrome

AKA recurrent intestinal impaction

Occurs in children and adults
Prevention includes adequate
enzymes, fluids, dietary fiber, and
regular exercise
Treatment involves stool softeners,
laxatives, hyperosmolar enemas,
intestinal lavage

Estimation of Energy
Needs in CF

Use WHO equations to estimate

BMR
Multiply by activity coefficient +
disease coefficient
TEE BMR X (AC + DC)
Disease coefficient is based on
lung function

Disease Coefficient in
CF

Normal lung function =

Moderate lung disease =

0.0
0.2

FEV1 40-79% of that predicted

Severe lung disease

= 0.3

FEV1 <40% of that predicted

FEV = forced expiratory volume

Example Equation TEE

in CF

Male patient 22 years old, weight

54 kg, relatively sedentary
FEV1 is 60% of predicted
(moderate lung disease)
TEE = BMR X (1.5 + 0.2)
TEE = [(15.3 (54) + 679] X 1.7
TEE = 2559 kcals

Calculate the Daily

Energy Requirement
(DER)

Takes into account steatorrhea

Pancreatic sufficiency: TEE = DER
Pancreatic sufficiency is Coefficient
of fat absorption >93% of intake

Pancreatic insufficiency: DER =

TEE (0.93/CFA)
CFA is a fraction of fat intake based
on stool collections

Calculation of DER in
CF

72-hour fecal fat collections

reveals that CFA is 78% of intake
DER = TEE X (.93/CFA)
= 2559 X (0.93/.78)
= 2559 X 1.19
DER = 3045 kcals/day

Protein in CF

Protein needs are increased in CF

due to malabsorption
If energy needs are met, protein
needs are usually met by
following typical American diet
(15-20% protein) or use RDA

Fat Intake in CF

Fat intake 35-40% of calories, as

tolerated
Helps provide required energy, essential
fatty acids and fat-soluble vitamins
Limits volume of food needed to meet
energy demands and improves
palatability of the diet
EFA deficiency sometimes occurs in CF
patients despite intake and pancreatic
enzymes

Symptoms of Fat
Intolerance

Increased frequency of stools

Greasy stools
Abdominal cramping

Carbohydrate in CF

Eventually intake may need to be

modified if glucose intolerance
develops
Some patients develop lactose
intolerance

Vitamins in CF

With pancreatic enzymes, water

soluble vitamins usually
adequately absorbed with daily
multivitamin
Will need high potency
supplementation of fat soluble
vitamins (A, D, K, E)

Minerals in CF

Intake of minerals should meet

DRI for age and sex
Sodium requirements increased
due to loss in sweat
North American diet usually provides
enough
Infants need supplementation (1/41/2 teaspoon/day)

Minerals in CF

Decreased bone mineralization,

low iron stores, and low
magnesium levels have all been
described in CF

Feeding Strategies in
CF: Infants

Breast feeding with supplements

of high-calorie formulas and
pancreatic enzymes
Calorie dense infant formulas (2027 kcals/oz) with enzymes
Protein hydrolysate formulas with
MCT oil if needed

Feeding Strategies in
CF: children and adults

Regular mealtimes
Large portions
Extra snacks
Nutrient-dense foods
Nocturnal enteral feedings
Intact or hydrolyzed formulas
Add enzyme powder to feeding or take
before and during

Nutritional
Implications of
Tuberculosis
TB is making a

comeback
Many patients
are developing
drug-resistant TB

Nutritional Factors
that Increase Risk of
TB
Protein-energy malnutrition:

affects the immune system;

debate whether it is a cause or
consequence of the disease
Micronutrient deficiencies that
affect immune function (vitamin
D, A, C, iron, zinc)

Nutritional
Consequences of TB

Increased energy expenditure

Loss of appetite and body weight
Increase in protein catabolism
leading to muscle breakdown
Malabsorption causing diarrhea,
loss of fluids, electrolytes

Nutritional Needs in TB

Energy: 35-40 kcals/kg of ideal

body weight
Protein: 1.2-1.5 grams/kg body
weight, or 15% of energy or 75100 grams/day
Multivitamin-mineral supplement
at 100-150% DRI

Chronic Obstructive
Pulmonary Disease
(COPD)
Characterized by airway obstruction

Characterized by airway obstruction

Emphysema: abnormal, permanent
enlargement of alveoli,
accompanied by destruction of their
walls without obvious fibrosis
Chronic bronchitis: chronic,
productive cough with inflammation
of one or more of the bronchi and
secondary changes in lung tissue

Chronic Obstructive
Pulmonary Disease
(COPD)

Emphysema: patients are thin,

often cachectic; older, mild
hypoxia, normal hematocrits
Chronic bronchitis: of normal
weight; often overweight;
hypoxia; high hematocrit

Chronic Obstructive
Pulmonary Disease
(COPD)

Bronchospasm: asthma
Cor pumonale: heart condition
characterized by right ventricular
enlargement and failure that
results from resistance to passage
of blood through the lungs

Chronic Bronchitis

Emphysema

Bronchial Asthma

Food sensitivities may be triggers

for asthmatic episodes (sulfites,
shrimp, herbs) but not the most
common causes
Provide healthy diet and maintain
healthy weight
Be aware of drug nutrient
interactions (steroids)

MNT Assessment in
COPD

Fluid balance and requirements

Energy needs
Food intake (decreased intake
common)
Morning headache and confusion
from hypercapnia (excessive CO2 in
the blood)
Fat free mass

MNT Assessment in
COPD

Food drug interactions

Fatigue
Anorexia
Difficulty chewing/swallowing because of
dyspnea
Impaired peristalsis secondary to lack of
oxygen to the GI tract
Underweight patients have the highest
morbidity/mortality

Nutrient Needs in
Stable COPD

Protein: 1.2-1.7 grams/kg (15-20% of

calories) to restore lung and muscle
strength and promote immune function
Fat: 30-45% of calories
Carbohydrate: 40-55% of calories
Maintain appropriate RQ
Address other underlying diseases
(diabetes, heart disease)

Nutrient Needs in
Stable COPD

Vitamins: intakes should at least meet

the DRI
Smokers may need more vitamin C
(+16-32 mg) depending on cigarette
use
Minerals: meet DRIs and monitor
phosphorus and magnesium in patients
at risk for refeeding during aggressive
nutrition support

Treatments for COPD

Bronchodilatorstheophylline and
aminophylline
Antibioticssecondary infections
Respiratory therapy
Exercise to strengthen muscles

MNT in COPD Based on

Weight/Height

Routine care
Anticipatory guidance: 90% IBW
Supportive intervention: 85% to 90% IBW
Resuscitative/palliative: below 75% IBW
Rehabilitative care: consistently below
85% IBW
JADA1997

MNT in COPD

GI motility: adequate exercise,

fluids, dietary fiber
Abdominal bloating: limit foods
associated with gas formation
Fatigue: resting before meals,
eating nutrient-dense foods,
arrange assistance with shopping
and meal preparation

MNT in COPD
Suggest that patient

Use oxygen at mealtimes

Eat slowly
Chew foods well
Engage in social interaction at mealtime
Coordinate swallowing with breathing
Use upright posture to reduce risk of
aspiration

MNT in COPD

Oral supplements
Nocturnal or supplemental tube
feedings
Specialized pulmonary
products generally
not necessary

Food Drug Interactions

Aminoglycosides lower serum

Mg++
may need to replace
Prednisonemonitor nitrogen,
Ca++, serum glucose, etc.

MNT in Respiratory
Failure

Causes of Acute Lung

Injury (ALI)

Aspiration of gastric contents or

inhalation of toxic substances
High inspired oxygen
Drugs
Pneumonitis, pulmonary contusions,
radiation
Sepsis syndrome, multisystem trauma,
shock, ,pancreatitis, pulmonary
embolism

Aspiration

Movement of food or fluid into the

lungs
Can result in pneumonia or even
death
Increased risk for infants, toddlers,
older adults, persons with oral,
upper gastrointestinal, neurologic,
or muscular abnormalities

Aspiration

Reported incidence of aspiration in

tubefed patients varies from .8% to 95%.
Clinically significant aspiration 1-4%
Many aspiration events are silent and
often involve oropharyngeal secretions
Symptoms include dyspnea, tachycardia,
wheezing, rales, anxiety, agitation,
cyanosis
May lead to aspiration pneumonia

Acute Respiratory
Distress Syndrome
(ARDS)

Most severe form of acute lung injury

Sepsis usually the underlying cause
Increasing pulmonary capillary
permeability
Pulmonary edema
Increased pulmonary vascular
resistance
Progressive hypoxemia

Goals of Treatment of
ALI and ARDS

Improve oxygen delivery and

provide hemodynamic support
Reduce oxygen consumption
Optimize gas exchange
Individualize nutrition support

Nutrition Assessment
in ALI and ARDS

Indirect calorimetry best tool to

determine energy needs in critically ill
patients
In absence of calorimetry, use
predictive equations with stress factors
Avoid overfeeding
Patients may need high calorie density
feedings to achieve fluid balance

Nutrition Support in
ARDS

In one randomized, controlled trial in 146

patients with ARDS, enteral nutrition with omega3 fatty acids (eicosapentaenoic acid) gammalinonenic acid, and antioxidants appeared to
reduce days on mechanical ventilation, new
organ failure, and ICU length of stay
This study was sponsored by Ross Laboratories,
makers of Oxepa
Have been unable to locate further studies since
then
Gadek JE et al. Effect of enteral feeding with eicosapentaenoic acid, gammalinolenic acid, and antioxidants in patients with acute respiratory distress syndrome.
Enteral Nutrition in ARDS Study Group. Crit Care Med 1999;27:1409.