Transcript Nutrition Therapy in Pulmonary Disease

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 Implications
Neonate
Bronchopulmonary displasia
(BPD)
Obstruction Cystic fibrosis (CF)
Chronic obstructive pulmonary
disease (COPD)
Emphysema
Chronic bronchitis
Asthma
Tumor
Lung cancer
Pulmonary Conditions w/
Nutritional Implications
Infection
Pneumonia
Tuberculosis (TB)
Respiratory
Failure
Acute respiratory failure
Lung transplantation
NeuroMuscular dystrophy
muscular
Paralysis
Abnormalities
Pulmonary Conditions w/
Nutritional Implications
Skeletal
Osteoporosis
Scoliosis
Cardiovascular
Pulmonary edema
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 baby’s 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 breast-feeding
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 = 0.0
Moderate lung disease = 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 (1/4-1/2
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 (20-27
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 drugresistant 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 75-100
grams/day
Multivitamin-mineral supplement at
100-150% DRI
Chronic Obstructive
Pulmonary Disease (COPD)
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




Bronchodilators—theophylline and
aminophylline
Antibiotics—secondary 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
JADA—1997
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
Prednisone—monitor 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 omega-3 fatty
acids (eicosapentaenoic acid) gamma-linonenic
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, gamma-linolenic
acid, and antioxidants in patients with acute respiratory distress syndrome. Enteral
Nutrition in ARDS Study Group. Crit Care Med 1999;27:1409.