Aspiration Pneumonia Factors Beyond Just Laryngeal Aspiration[1]

Aspiration Pneumonia: Factors Beyond Just Laryngeal Aspiration John R. Ashford, Ph.D., CCC-SP VA Tennessee Valley Health Care Medical Center, Nashville Vanderbilt University Medical School Tennessee State University THE Question Why Do Some Dysphagic Patients Develop Pneumonia and Others Do Not? ? What about those who had pneumonia, left the hospital and 90+ days later had not had recurrence? Pneumonia: Definition  An acute inflammatory reaction in the lung parenchyma with an outpouring of inflammatory exudate into the alveoli.  Parenchyma: alveoli pulmonis, or pits  Originates in respiratory bronchioles Cole & MacKay, 1990; Skerrett, 1994; Siegel, 2003 Acute Inflammatory Reaction  aka “Inflammatory Response”    When resident immune defenses are insufficient to meet a microbial challenge Special immune cells & proteins are brought from the blood to the site of infection Can occur at any site in the body Skerrett, 1994 Pneumonia  Develops as a result of bacterial or viral pathogens entering the lower respiratory system     Airborne/aerosol ingestion Blood transmission from distant body site Translocation from gastrointestinal tract Upper airway flora aspirates CDC, 1996; Skerrett et al., 1989; Scannapieco & Mylotte, 1996 Nosocomial Pneumonia: Definition  A subcategory of pneumonia  A lower respiratory infection that develops in hospitalized patients in whom the infection is neither present nor incubated at the time of admission  Sanford & Pierce, 1979  Develops after 3 days  Siegel, 2003; Tobin & Grenvik, 1984 “Aspiration” Pneumonia: Definition  Subcategory of nosocomial pneumonia  Direct consequence of ingestion of foreign material into the airway or distal lung  Siegel, 2003  Represents 8% to 33% of all nosocomial infections  Tobin & Grenvik, 1984 “Aspiration” Pneumonia: An Overlooked Fact Serious Illness (CVA) Pneumonia Aspiration pneumonia is an “opportunistic” disease, developing in patients who are already seriously ill -Bartlett & Gorbach, 1975; Niederman, 1993 Serious Illnesses: “Aspiration” Pneumonia Risk Factors  Increased age  Mental status change  Dysphagia  CVA  Anesthesia  Nasogastric feeding  GERD  Alcoholism  Seizures  Drug addiction  Guillain-Barre Syn.  Myasthenia gravis  Diabetes  Heart Disease  Malignancy  Head Trauma  Malnutrition  Congestive Heart Failure  COPD  Decreased consciousness/coma Khawaja, Buffa, & Brandsetter (1992); Marrin (2000); Feldman (2001); Others Aspiration Pneumonia: Contributing Factors Serious Illness Hematological, Electrolytic Factors Pneumonia Neurological/ Structural Factors Side Note: Hematological Factors Transport Oxygen & carbon dioxide Waste to kidneys & liver Immune components Hormones & clotting agents Glucose Absorb nutrients from GI tract Blood Functions Circulate & cool body’s core Wildman & Medeiros, 2000, p. 29-30 Side Note: Hematological Factors  Glucose & Oxygen  Needed by slow twitch & fast twitch muscle fibers to power muscle cell functions  Chi-Fishman & Pfalzer (Yesterday!)  Reduced levels occur during serious illness result in muscle weakness, etc.  Weak muscles may cause dysphagia   May Hudson et al. 2000 Side Note: Hematological Factors  Iron  Necessary to attach oxygen molecule to red blood cell for transport to cells Affects cell functions including muscles Weakened muscles  May  Iron deficiency/anemia   result in dysphagia and prevent adequate nutrition intake. Carreim-Lewandowski, 1996 Side Note: Electrolytic Factors  Sodium, Potassium, Chloride  Remember your neuroscience class? never use this stuff!”  “I’m back” in your professional life!  “I’ll  Necessary for action potentials  Not just neurons “general debilitation”  Low RBC  Low Hemoglobin (iron)  Low Hematocrit (low RBC in whole blood)  Elevated immune system values  Imbalance of electrolytes  Result: Weakness, lethargy, lack of energy Aspiration Pneumonia: Contributing Factors Serious Illness Hematological, Electrolytic Factors Pneumonia Neurological/ Structural Factors Aspiration Pneumonia: Neurological/Structural Factors  Laryngeal valve    Gatekeeper of the lower airway Primary Protective Function: Cough Compromise  Inability to close efficiently  Inability to sense & clear airway  Compromise result: Aspiration Neurological/Structural Factors: SLP Intervention Diet Manipulation Bed Elevation Mendelsohn Maneuver Supraglottic Swallow Laryngeal Aspiration (Undefined motor exercises) Super Supraglottic Swallow Volitional Cough Head Rotation (Undefined sensory stimulation exercises) Aspiration Pneumonia: Neurological/Structural Factors  Tracheobronchial Tree Integrity  Primary protective function:Trap & clear  Mucociliary escalator  Protective function: Cough Inability to clear invaders/debris  Compromise   Compromise result: Aspiration/Pneumonia Neurological/Structural Integrity: SLP Intervention Tracheobronchial Aspiration & Pneumonia ? Volitional Cough ? Aspiration Pneumonia Serious Illness Pneumonia Neurological/ Structural Factors Immune System Factors Immune System: Overview  Function  To protect an organism from infection by distinguishing foreign molecules from self molecules and initiate destruction and elimination of invading organisms and any toxic molecules Alberts, et al, 1994 Components of the immune system  Phagocytic macrophages: surface receptors recognize bacteria & engulf them & secrete proteins attracting other immune elements     Astrocytes: nervous system Neutrophils: blood Monocytes: blood Lymphocytes: blood & lymphatics Components of the immune system  Neutrophils:   Specific phagocytes against bacteria Predominant leukocyte in blood  70-80% of white blood cells   1st in inflammatory response 3+ days Components of the immune system  Monocytes   Develop into macrophages & devour May initiate tissue repair processes Specific Types: T- & BActivated by macrophages Attracted to antigens draining into lymph system from infection sites  Lymphocytes    Immune System: Overview  Basic Subsystems  Innate Immunity System  1st defense  Antibody response  Injury or infection induces local inflammatory response  Local immune cells active immediately Janeway et al., 2001; Alberts et al., 1994 Local Inflammatory Response in the Brain - CVA Border Zone Cytokines: “Stressors” ; proteins released by cells that affect the behavior of other cells that bear receptors for them. Release initiates inflammatory response Cytokines Local Adaptive Stress Response CVA Astrocytes Microglia Immune System: Overview  Basic Subsystems (cont.)  Adaptive Immunity System 2nd defense  Activated by innate immunity system  Systemic immune system response  Specialized cells activated & brought in to react to specific pathogens  Clinical Point 96 hours for Adaptive Immune System to reach Optimum effect CVA patient develops nosocomial pneumonia 3 to 4 days AFTER entering the hospital, or after onset of new serious illness = Systemic Immune System Response Plasma Border Zone N CVA … ….… . .…. . T N N Blood Vessel (Dilates) N = Neutrophil T = T-cells N T Cytokines N T T T N T = PRO-inflammatory Cytokine Astrocytes Microglia = ANTI-inflammatory Cytokine De Simoni et al., 2002; Tarkowski, 2001; Janeway et al., 2001 Clinical Application Aspiration Pneumonia Serious Illness Physiological Stress Physiological Stress Pneumonia Neurological/ Structural Factors Immune System Factors Serious Illness “The greater the degree of serious illness in a given patient, the more likely he or she is to have gramnegative colonization of the oropharynx, and such colonization has been identified as a harbinger of pneumonia.” •Skerrett et al., 1989, p.470 Serious Illness “…the depression in the immune function (is) caused by severe stress during the course of (the) disease. Impairment of the immune function may increase susceptibility to infection.” • Czlonkowska, Cyrta, & Korlak, 1979 Stressors Healthy Stressors Unhealthy Unhealthy “Life exists by maintaining a complex dynamic equilibrium, or homeostasis, that is constantly challenged by intrinsic or extrinsic adverse forces or stressors.” - Chrousos, 1998 (Remember those cytokines??) Stress: Definition  “…the state in which the brain interprets the quantity of stimulation as excessive or its quality as threatening, thus responding in a generalized way.”  “…a state of threatened homeostasis…”  “…reestablished by a complex repertoire of physiologic and behavioral adaptive responses…” Chrousos, 1998; Habib et al, 2001 Stress: Adaptive Response  Counteracts against stressor forces to maintains internal homeostasis of the organism Adaptive Forces Stressor Forces Chrousos, 2000 Stress System Activation  CNS Response     Peripheral Response    Inc. arousal Inc. motor reflexes Better attention span/cognition Dec. feeding, digestion, growth & sexual reproduction Inc. pain tolerance     Altered cardiovascular function Metabolism changes Immune & inflammatory reaction modulation Inc. oxygen intake Inc. muscle fuel use Chrousos, 2000 Stress Physiology Cytokines Release Glucose (Liver) & fatty acids (Blood) Hypothalamus (CRH) (Feedback) Adrenaline 1st 2nd Pituitary Replenish Energy Stores (ACTH) Activates Sympathetic Nervous System Heart rate increase Oxygen intake increase Constricts blood vessels Adrenal Glands Cortisol Reduces glandular output*** Activates Adaptive Immune System Response Stress Physiology  Hypothalamic-Pituitary-Adrenal Axis:   2nd Stress Response Cornerstone of homeostasis  Connects neuro, endocrine, immune systems   Stimulated by Adrenaline & cytokines Adjusts homeostatic response Bear, Connors, & Paradiso, 2001 Cortisol Cortisol Stress  Cortisone (a glucocorticoid hormone)  One of 4 secreted from adrenal glands  Final hormone product of the HPA axis  Plays key role in regulating basal control of HPA axis via feedback loops  Inhibitory function  Helps terminate stress response Schteingart, 2003; McEwen, 2002 Cortisol: In Excess Cortisol  Alters    Protein & carbohydrate metabolism  Skin breakdown, muscle atrophy, osteoporosis     Distribution of adipose tissue Electrolytes The immune system  Inflammation suppression Gastric secretion Brain function Erythropoiesis Schteingart, 2003 Cortisol and CVA  Olsson et al. (1992)   Compared cortisol levels in CVA & normal subjects Results  Hypercortisolism common  among CVA Associated with higher mortality & poorer functional outcomes  Elevated cortisol levels correlated with acute confusion & extensive motor impairment Immunosuppression  Excessive HPA response to inflammation or continued stress increases susceptibility to infection  Severe illness, surgery, trauma, burns,  Hypercorticolism suppresses immune system function     Reduces antigen processing by phagocytes Reduces release of lymphocytes Reduces antibody production Reduces inflammatory response Stress and the Immune System Promotes movement of immune cells to sites where they are needed Enhances immunity Increasing amounts of Stress Suppresses movement of cells to sites where they are needed Suppresses Immunity Taken from McEwen, 2002 Adrenals Sympathetic Nervous System SNS Constricts blood vessels Reduces saliva/mucus output Reduces oral immune properties Increases colonization of oral pathogens “Aspiration” Pneumonia: Source “…patient’s own oropharynx.” Tobin & Grenvik, 1984 Normal Oral Flora Bacteroides Fusobacterium Streptococci sanguis mutans salivarius mitis Staphylococci Haemophilus Neisseria Moraxella catarrhalis Corynebacteria Lactobacilli Candida (fungus) 1ml (1cm3) 100,000,000 bacteria Saliva Pseudomonas aeruginosa Klebsiella Escherichia coli Enterobacter Proteus Skerrett, 1994 Bacteria Infectivity  Objective   “…to multiple rather than to cause disease, it is in the best interest of the bacteria not to kill the host.” Most do not invade cells but live off extracellular fluids  Compete for transferrin-bound IRON found in plasma necessary for life Peterson, 1996 Oropharyngeal Bacteria  Gram-negative bacteria  P. aeruginosa, S. aureus, Pseudomonas “…bacteria pooled from the tongue, gingiva, buccal mucosa, and pharynx.” Poor oral hygiene cultures: 1011/ml  Approaching numerical  Source of inoculants   limits of bacteria which can occupy this given mass Barlett & Gorbach, 1975; Gibson & Barrett, 1992; Scannapieco & Mylotte, 1996 Oral Pathogen Colonization  To penetrate & adhere to the epithelium & multiply before mucus & epithelial cells are swept away  Teeth   Plaque Clean surface  Mucosa Epithelium Peterson, 1996 Saliva & Mucus Immune Products  Prevents attachment   Fibronectin IgA Lactoferrin Lysozyme Mucins  Inhibits growth by withholding iron   Destroys pathogens   Surface coating  Gingival Crevicular Fluid  Very thin, plasma-like fluid that circulates at the base of the teeth between the teeth and epithelium  Function: fight periodontal disease  Secreted by alveolar capillaries  Very saturated with Immunoglobulin A Lower Respiratory Tract Immunity  Altered systemically with serious illness  Continuation of immune properties found in the oral cavity  Phagocytes, etc. Ends at the respiratory bronchioles IgA, fibronectin, etc.  Mucociliary escalator   Mucin  Relationship between pulmonary infection and oral diseases  12 studies since 1985 indicate      Oral cavity reservoir for bacteria in cystic fibrosis patients Topical antibiotics reduce oral bacteria in ICU patients Resp. pathogens colonize dental plaque & oral mucosa 0.12% chlorhexidine rinse reduces RTI in heart surgery patients Poor oral health assoc. with chronic dis. Mojon, 2002; Lindemann et al., 1985; Pugin et al., 1991; Scannapieco et al., 1992, 1998 Relationship between pulmonary infection and oral diseases  12 studies (cont.)      RTIs assoc. with greater plaque accumulation, specific oral health disorders, & presence of teeth Resp. plaque assoc. w/ N. Pneumonia Resp. path. found in 14% chronic care patients Oral care dec. pneum. risk in frail elderly Caries, cariogenic & peridontal pathogens sign. Risk factors DeRiso et al., 1996; Mojon et al., 1997; Fourrier et al., 1998; Russell et al., 1999 Stress Factors & Pneumonia: SLP Intervention  Recognize fact patient is not physiologically stable at the time of admission  First week post-CVA most critical  Use laboratory values to assist with understanding of patient’s status  Immune status  Elevate patient 45o at all times  Clean the mouth! Stress Factors & Pneumonia Laboratory Values  Becoming necessary part of dysphagia assessment     Mirrors patient’s stressed physiological status—generally Gives insight into whether current immune system reflects physiological stress, even with antibiotic infusion Provides insight into nutrition status Good review of status of other systems: oxygen, electrolytes, waste removal Pull It All Together CVA Stress Response Impaired Neuromotor/ Sensory System Altered Systemic Immune Response Altered Endocrine System Biomechanical Compromised Oropharynx/larynx Immune Compromised Oropharynx Laryngeal Aspiration HPA SNS Biomechanical Compromised Respiratory System Immune Compromised Respiratory System Pneumonia Possibilities To Ponder Senario #1 No Aspiration Senario #2 Aspiration Senario #3 No Aspiration Senario #4 Aspiration Nml Immune Response Nml Immune Response Impaired Immune Response No Pneumonia Impaired Immune Response Pneumonia No Pneumonia No Pneumonia