1. Medical Nutrition Therapy in Pulmonary Disease

2. Malnutrition and the Pulmonary System
Malnutrition impairs
Respiratory muscle function
Ventilatory drive
Response to hypoxia
Pulmonary defense mechanisms

3. 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)
Aurora N, Rochester, D. Am Rev Respir Dis 126:5-8, 1982
Aurora N, Rochester D. J Appl Physiol: Respirat Environ Exercise physiol 52:64-70, 1982

4. 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

5. 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

7. Normal Lung Anatomy

8. Selected Airway Disorders

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

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

11. 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

12. Pulmonary Conditions w/ Nutritional Implications
Infection
Pneumonia
Tuberculosis (TB)
Respiratory Failure
Acute respiratory failure
Lung transplantation
Neuro-muscular Abnormalities
Muscular dystrophy
Paralysis

13. Pulmonary Conditions w/ Nutritional Implications
Skeletal
Osteoporosis
Scoliosis
Cardiovascular
Pulmonary edema
Endocrine
Severe obesity
Prader-Willi syndrome

14. 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

15. 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

16. 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

17. Chronic Lung Disease

18. 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

19. BPD: Signs and Symptoms
Hypercapnea (CO2 retention)
Tachypnea
Wheezing
Dyspnea
Recurrent respiratory infections
Cor pulmonale (right ventricular enlargement of the heart)

20. Growth Failure in BPD Increased energy needs Inadequate dietary intake
Gastroesophageal reflux
Emotional deprivation
Chronic hypoxia

21. Goals of Nutritional Management in BPD
Meet nutritional needs
Promote linear growth
Develop age-appropriate feeding skills
Maintain fluid balance

22. 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) kcals/kg
Energy needs in convalescence (oral feeds, activity, temperature regulation) as high as kcals/kg

23. Protein Needs in Babies with BPD
Protein: within advised range for infants of comparable post-conceptional 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. Feeding Strategies in Gastroesophageal Reflux
Thickened feedings (add rice cereal to formula)
Upright positioning
Medications like antacids or histamine H2 blockers
Surgical fundoplication

30. 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

31. 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

32. Cystic Fibrosis
Epithelial cells and exocrine glands secrete abnormal mucus (thick)
Affects respiratory tract, sweat, salivary, intestine, pancreas, liver, reproductive tract

34. 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

35. 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

36. 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

37. 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)

38. Nutritional Care Goals
Control malabsorption
Provide adequate nutrients for growth or maintain weight for height or pulmonary function
Prevent nutritional deficiencies

39. Common Treatments Pancreatic enzyme replacement
Adjust macronutrients for symptoms
Nutrients for growth
Meconium ileus equivalent: intestinal obstruction (enzymes, fiber, fluids, exercise, stool softeners)

40. 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

41. 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

42. 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

43. 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

44. 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

45. Disease Coefficient in CF
Normal lung function =
Moderate lung disease = 0.2
FEV % of that predicted
Severe lung disease = 0.3
FEV1 <40% of that predicted
FEV = forced expiratory volume

46. 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 ( )
TEE = [(15.3 (54) + 679] X 1.7
TEE = 2559 kcals

47. 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

48. 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

49. 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

50. 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

51. Symptoms of Fat Intolerance
Increased frequency of stools
Greasy stools
Abdominal cramping

52. Carbohydrate in CF
Eventually intake may need to be modified if glucose intolerance develops
Some patients develop lactose intolerance

53. 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)

54. 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)

55. Minerals in CF
Decreased bone mineralization, low iron stores, and low magnesium levels have all been described in CF

56. 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

57. 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

58. Nutritional Implications of Tuberculosis
TB is making a comeback
Many patients are developing drug-resistant TB

59. 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)

60. 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

61. Nutritional Needs in TB
Energy: kcals/kg of ideal body weight
Protein: grams/kg body weight, or 15% of energy or grams/day
Multivitamin-mineral supplement at % DRI

62. 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 5

63. 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

64. 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

65. Chronic Bronchitis

66. Emphysema

67. 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)

69. 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

70. 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

71. Nutrient Needs in Stable COPD
Protein: 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)

72. Nutrient Needs in Stable COPD
Vitamins: intakes should at least meet the DRI
Smokers may need more vitamin C ( mg) depending on cigarette use
Minerals: meet DRIs and monitor phosphorus and magnesium in patients at risk for refeeding during aggressive nutrition support

73. Treatments for COPD Bronchodilators—theophylline and aminophylline
Antibiotics—secondary infections
Respiratory therapy
Exercise to strengthen muscles 9

74. 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

75. 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

76. 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

77. MNT in COPD Oral supplements Nocturnal or supplemental tube feedings
Specialized pulmonary
products generally
not necessary

78. Food Drug Interactions
Aminoglycosides lower serum Mg++ —may need to replace
Prednisone—monitor nitrogen, Ca++, serum glucose, etc.

79. MNT in Respiratory Failure

80. 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

81. 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

82. 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

83. 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

84. Goals of Treatment of ALI and ARDS
Improve oxygen delivery and provide hemodynamic support
Reduce oxygen consumption
Optimize gas exchange
Individualize nutrition support

85. 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

86. 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.