Polypharmacy and Dysphagia Issues

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Information about Polypharmacy and Dysphagia Issues

Published on October 14, 2008

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Medically Fragile Patients’ Polypharmacy and Dysphagia Issues : Medically Fragile Patients’ Polypharmacy and Dysphagia Issues ASHA November 14, 2003 Jo Puntil-Sheltman M.S. CCC. BRS-S sheltmanpub@earthlink.net Definition of Medically Fragile Patients : Definition of Medically Fragile Patients Doctors: a fragile patient is one who is hemodynamically labile. Nurses: a fragile patient is one who has two or more co-morbidities that accelerates the disease process or increases risks for complications to the patient. Speech Pathologists: one whose medical condition could become life threatening if they weren’t on various life support systems; IV hydration/ventilation Definition of Medically Fragile Patient : Definition of Medically Fragile Patient “At risk” population with chronic diseases who suffer from one or more chronic medical conditions or one that is terminal”. (Strumberg, 2002) An adult whose medical condition could become life threatening if there is a service, power or communications disruption; those on an apnea monitor, ventilator, respirator, dialysis, oxygen dependent, seizure prone. (Oklahoma Dept. of Human Services 2000) Key Changes of Normal Aging : Key Changes of Normal Aging Decreased Composition such as loss in height, increase in body fat, decrease in lean muscle tissue and aging of tissues Impaired senses such as decreased hearing, taste, vision, perception of viscosity Aging of the Mouth: decreased salivary function, loss of teeth, changes in jaw/gums, decreased lingual suction pressure, thickness, and mobility, reduced tone in the pharynx Changes of Normal Aging: Continued : Changes of Normal Aging: Continued Aging Alimentary Tract: food held longer in stomach, constipation, absorption takes longer, reduced esophageal motility Aging Lung: reserve is decreased, loss of elasticity Aging Nervous System: loss of neurons, action potential speed decreases, prolonged reaction times or slowed motor responses Decreased Functional Reserve Capacity: decreased ability to adapt to stress Shadden, 1998, Robbins J, Sonies B, et.al.1995 Interdisciplinary Team to Evaluate and Treat Medically Fragile Patients : Interdisciplinary Team to Evaluate and Treat Medically Fragile Patients Physicians Nurses Respiratory Therapists Dietitians Dysphagia Clinicians Physical Therapists Occupational Therapists Social Workers It is essential to understand normal nutrition/hydration, pulmonary, and gastroesophageal functions and their common diseases/disorders in order to evaluate/treat the medically fragile patient Common characteristics of the Medically Fragile Adult : Common characteristics of the Medically Fragile Adult Malnutrition Dementia Depression (mod/severe) Incontinence Decreased ability to perform 1 or more ADL’s Difficulty with Ambulation/Coordination History of falls (>1 in 3 months) One or more diseases processes (Winograd et al 1991) Nutrition and Hydration : Nutrition and Hydration Patients need adequate hydration and nutrition administered safely to survive and fight diseases or infection (lab values can determine levels, comprehensive Chem panel and pre-albumin levels) How much fluid does the average person need on a daily basis? What processes change the amounts of fluids and nutrition a patient needs? Normal Lab Values for a Chem Panel : Normal Lab Values for a Chem Panel Na 135-145 mEq/L (sodium) K 3.5-5.3 mEq/L (potassium) Cl 95-108 mEq/L (chloride) CO2 24-32 mEq/L (carbon dioxide) BUN 5-30 mg/DL Creatinine 0.5-1.4 mg/DL Glucose 70-120 mg/DL Pulmonary Considerations : Pulmonary Considerations Normal Respiratory/Swallowing Patterns Obstructive Airway Diseases Restrictive/Infectious Airway Diseases Cervical and Chest Auscultation Polypharmacy Normal Respiratory/Swallowing Patterns (young adults to older adults) : Normal Respiratory/Swallowing Patterns (young adults to older adults) Predominant pattern of exhalation-swallow-exhalation, secondarily one will see inhalation-swallow-exhalation Pattern is demonstrated regardless of bolus sizes or viscosity During fluid or food intake systemic blood oxygenation saturation(SaO2) remained fairly stable. Martin B., Logemann J. et.al. 1994 Chronic Obstructive Pulmonary Disease (COPD) : Chronic Obstructive Pulmonary Disease (COPD) COPD is defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema. The airflow obstruction generally is progressive, may be accompanied by airway hyper-reactivity, and may be partially reversible. Chronic Obstructive Pulmonary Diseases : Chronic Obstructive Pulmonary Diseases Chronic Bronchitis Emphysema Chronic Asthma COPD : COPD Frequency: In the U.S. approximately 14.2 million people have COPD, approximately 12.5 million have chronic bronchitis, and 1.7 million have emphysema. Since 1982, the patients diagnosed with COPD increased by 41.5%. S. Sharma M.D. 2003 Chronic Bronchitis : Chronic Bronchitis Definition: an inflammation/edema of the bronchial tubes. Causes: Viruses, bacteria, parasites, smoking, inhalation of chemical pollutants or dust. This is associated with excessive tracheobronchial mucus production sufficient to cause a cough with expectoration for at least 3 months during a period of 2 consecutive years. Chronic Bronchitis : Chronic Bronchitis Clinical Signs: Excessive sputum production usually associated with a cough Mucus is viscous, sticky, and thick Emphysema : Emphysema Defined as abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of the walls or collapsed airways. The destruction of the alveolar walls leads to loss of their elastic recoil properties. The patient has difficulty exhaling air because of collapsing airways and loss of passive relaxation forces Emphysema: Clinical Signs : Emphysema: Clinical Signs Shortness of breath, loss of weight, cough with little sputum production, quiet breath sounds and wheezing may occur with exercise Respiratory rate increases in proportion to disease severity In advanced disease, cyanosis, elevated jugular venous pressure (JVP), and peripheral edema Patient has a thin barrel-chested appearance and overuse of accessory musculature. Chronic Asthma : Chronic Asthma Considered a disorder of airway smooth muscle mediators and anatomic elements of the airway mucosa. Hypertrophied smooth muscle, which contracts during an attack causing bronchoconstriction. Chronic Asthma : Chronic Asthma Separated into allergic and non-allergic. Manifested by a sudden or prolonged onset of airway narrowing, which accounts for the varying degrees of airway obstruction and accompanying sensation of an inability to breathe in, and more importantly, to breathe out; these symptoms herald hyperinflation Chronic Asthma: Clinical Signs : Chronic Asthma: Clinical Signs Hyper-reactivity of the airways usually from irritants. Common to begin in childhood (usually from a virus) but may occur at any age. Breathlessness, anxiety, cough, chest tightness wheezing Mucus is thick tenacious and slow moving Prevalence: 17.7 million patients are affected Asthma Research Center of the American Lung Assoc. 2003 Polypharmacy for COPD : Polypharmacy for COPD Anti-inflammatory agents: inhaled and oral steroids such as flovent, pulmicort turbuhaler, prednisone, Bronchodialators: (decreases smooth muscle tone) Albuterol (proventil,Ventolin), Metaproterenol (alupent), Ipratropium (Atrovent), Theophylline (theo-24, Theo-Dur, Slo-bid) Polypharmacy for COPD : Polypharmacy for COPD Antibiotics: first-line treatment includes; ammoxicillin, cefaclor, second-line more expensive includes; azithromycin, clarithromycin, and fluoroquinolones. Mucolytic Agents: these reduce sputum viscosity and improve secretion clearance Oxygen Therapy: long term, low flow Surgical Care: bullectomy, Lung volume reduction, and lung transplantation Restrictive and Infectious Pulmonary Diseases : Restrictive and Infectious Pulmonary Diseases Pulmonary Fibrosis Pleural Effusion Pneumonia This is when the expansion of the lung is restricted because of alterations in the lung parenchyma (alveolar tissue), or because of disease of the pleura, chest wall, or neuromuscular apparatus. Reduced lung volumes and decreased lung compliance are noted. Pulmonary Fibrosis : Pulmonary Fibrosis Features: Thickening of the interstitium of the alveolar wall. Eventually the alveolar architecture is destroyed and the scarring results in multiple air filled cystic spaces “honeycomb lung” Clinical Features: dyspnea with rapid shallow breathing which increases with exercise. An irritating unproductive cough is noted Pleural Effusion : Pleural Effusion Definition: An abnormal accumulation of fluid rather than air in the pleural space. Clinical Signs: Dyspnea (most common) Chest pain (mild/severe) reduced movement of the chest on the affected side absence of breath sounds and possibly increasing lower extremity edema, fever, and night sweats Pleural Effusion : Pleural Effusion Pathophysiology: Pleural Effusion is an indicator of a pathologic process that may be of primary pulmonary origin or of an origin related to another organ system or to systemic disease Frequency: 1.3 million individuals each year based on underlying disease processes: CHF, bacterial pneumonia, malignancy, pulmonary embolus, pancreatitis, TB Pneumonia : Pneumonia Definition: is an inflammation and consolidation of the lung tissue typically accompanied by a buildup of fluid that can plug the alveoli usually due to an infectious agent. Types: Community Acquired (bacteria, typical and atypical) Nosocomial Acquired (hospital acquired), aspiration, bacterial, viral, lobular, lobar, and bronchial Aspiration Pneumonia : Aspiration Pneumonia Chemical Pneumonia: aspiration of gastric contents Bacterial Pneumonia: aspiration of bacteria from oral and pharyngeal areas Foreign Body Aspiration: can predispose the patient to bacterial pneumonia Pneumonia: Frequency : Pneumonia: Frequency In the U.S. 4.5 million cases of Community-acquired occur annually, 20% require hospitalization Nosocomial pneumonia range from 4-7 episodes per 1000 hospitalizations Approximately 25% of patients in ICU develop pneumonia Pneumonia is the 6th leading cause of death in the U.S S. Sharma MD 2003 Polypharmacy for Restrictive/Infectious Diseases : Polypharmacy for Restrictive/Infectious Diseases Critical to stabilize the respiratory and circulatory systems Antibiotics (if infectious pneumonia) Clindamycin (Cleocin), Amoxicillin (Augmentin), Azithromycin (Zithromax), Clarithromycin (Biaxin) Diuretics: such as Lasix Chest Tube placement (for pleural effusion) Anti-inflammatory Agents Cervical/Chest Auscultation : Cervical/Chest Auscultation Listen for: Amplitude (loudness) Quality (one or more sounds) Pitch (high, medium, low) Duration (length of inhalation and exhalation) Cervical/Chest Auscultation : Cervical/Chest Auscultation Normal Breath Sounds Bronchial/Tracheal (loud, high pitched, hollow/tubular) 2:3 ratio Bronchovesicular (mod/loud, med/high, hollow/breezy) 1:1 I=E Vesicular (mod/loud, low pitch, breezy) 3:1 I>E Decreased (soft, low, breezy) 3:1 I>E Absent Cervical/Chest Auscultation : Cervical/Chest Auscultation Adventitious Breath Sounds (abnormal breath sounds superimposed on baseline Rales (crackles) peripheral airways, popping sounds, discontinuous, Rhonchi- large airways, coarse, low-pitched sonorous sounds, continuous Wheeze-large/small airways, high pitched sometimes low, continuous Stridor-large airways, audible without stethoscope, loud, continuous and discontinuous sounds Cervical Auscultation for Swallowing : Cervical Auscultation for Swallowing Can be thought of as having 3 stages or distinguishable sounds that occur during a swallow. The swallow sounds may arise from the bolus flowing into the pyriform sinus. The most prominent acoustic feature is the movement of the bolus through the UES Cervical/Abdominal Auscultation : Cervical/Abdominal Auscultation Normal Sounds: as a burst and double click It is normal to have a “crispness” or sharp, crackling, or brilliant sounds It is important to listen to tracheal breath sounds post swallow In abdominal auscultation, one can sometimes hear and time when the bolus reaches/passes the LES Esophageal Diseases and Motility Disorders : Esophageal Diseases and Motility Disorders Bi-directional Flow Reversed Peristalsis Tertiary Contractions Diffuse Esophageal Spasms Achalasia GERD Structural Esophageal Disorders : Structural Esophageal Disorders Schatzki’s Ring Strictures Diverticulas Webs Esophagitis Tumors Pharmaceutical Intervention to aide in Mentation/Emotion : Pharmaceutical Intervention to aide in Mentation/Emotion Psychostimulants Cholinergics Antipsychotic and Anti-Anxiety “Sleepers” Psychostimulants: Modafinil (provigil)methylphenidate (ritalin) : Psychostimulants: Modafinil (provigil)methylphenidate (ritalin) Therapeutic Effects Improves symptoms of inattention, distraction, disorganization, apathy, impulsiveness, hyperactivity, emotional lability, hypoarousal. Improves fine motor speed, accuracy, steadiness. Side Effects May cause hypertension, headache, anorexia, anxiousness, fearfulness, anxiety, nausea, dry mouth With high doses: may cause choreic or athetoid dyskinesias Cholinergic Exelon, Aricept, Reminyl : Cholinergic Exelon, Aricept, Reminyl Therapeutic Effects Correlated with recovery or maintenance of cortical function. Usually used in the treatment of mild/mod Alzheimer’s disease by boosting levels of acetylcholine (chemical receptors) Side Effects Nausea, bradycardia, dizziness, increased sweating, vomiting, loss of appetite, sleepiness, UTI, weight loss Antipsychotic/Anti-Anxiety : Antipsychotic/Anti-Anxiety Risperidone: (Risperdal) antipsychotic Quetiapine Fumarate (Seroquel) Buspirone hydrochloride (BuSpar) anti-anxiety Lorazepam (Ativan) Antipsychotic/Anti-Anxiety : Antipsychotic/Anti-Anxiety Therapeutic Effects: Decreases agitation, restlessness, anxiety, Works by diminishing the action of dopamine and serotonin, two of the brains chief chemical messengers. Side Effects: Abdominal pain, fatigue, dry mouth, dizziness, constipation, neck rigidity, tremor, weakness, lack of coordination Antidepressants SSRI : Antidepressants SSRI Citalopram hydrobromide (Celexa) Escitalopram oxalate (Lexapro) pure form of celexa Paroxetine hydrochloride (Paxil) Fluoxetine hydrochloride (Prozac) Sertraline (Zoloft) Antidepressants : Antidepressants Therapeutic Effects: Decreases clinical depression, agitation, aggression, increases attention span (with frontal lobe injuries), helps to control lability, Works by boosting levels of serotonin Side Effects: Drowsiness, dry mouth, fatigue, constipation, heartburn, decreased sex drive, diarrhea, headache, decreased appetite, abdominal pain, tingling, tremor Antidepressants SNRB (serotonin norepinephrine receptor blocker : Antidepressants SNRB (serotonin norepinephrine receptor blocker Mirtazapine: (Remeron) Treatment for major depression. It adjusts the balance of the brain’s natural chemical messengers, especially norepinephrine and serotonin Side Effects: Most common in increased appetite!, sleepiness, weight gain, abnormal dreams and thinking Less common: confusion, labored breathing, fluid retention, peripheral edema Insomnia : Insomnia Zolpidem Tartrate: (Ambien) Triazolam: (Halcion) Used for difficulty falling asleep, staying asleep, or early awakening Side Effects: drowsiness, dizziness, headache, Rare Side Effects: aggressiveness, behavioral problems, constipation, delusions, chest pain, confusion, coughing, difficulty swallowing Slide 48: BIBLIOGRAPHY Buchholz D, Bosma J, Donner M: (1985) Adaptation, Compensation and Decompensation of the Pharyngeal Swallow. Gastrointest Radiolo, 10:235-239. Christensen J. (1976) Effects of drugs on Esophageal Motility. Arch Intern Med; 136: 532-537. Christianson R, Lufkin R, Hanafee W: (1987) Normal Magnetic Resonance Imaging Anatomy of the Tongue, Oropharynx, Hypopharynx, and Larynx. Dysphagia; 1:119-127. Cunningham E Jr, Sawchenko P: (1990) Central Neural Control of Esophageal Motility: A Review. Dysphagia, 5:35-51. Dodds, WJ, (1988) “The Physiology of Swallowing”, Dysphagia 3, 171-178. Dodds, WJ, Logemann, J, Stewart E, (1990) “Physiology and Radiology of Normal Oral and Pharyngeal Phases of Swallowing”, American Journal of Radiology, 154, 953-963. Dodds W, Man D, Cook I, Kahrilas P, Stewart T, Kern M: (1988) Influence of Bolus Volume on Swallow-Induced Hyoid Movement in Normal Subjects. AJR, 150: 1307-1309. Doty R., Richmond W., & Storey A., “Effect of Medullary Lesions on Coordination of Deglutition”. Experimental Neurology, 17 91-106. Feinberg M.J., Knebl J., & Tully J, (1996) Prandial aspiration and pneumonia in an elderly population followed over 3 years. Dysphagia, 11, 104-109. Fiaterone M.A., & Evans W.J.,(1993). The etiology and reversibility of muscle dysfunction in the aged. Journal of Gerontology, 48 (Spec. No.) 77-83. Franssen, F., (2003) The influence of comorbid factors on muscle function, morphology and metabolism in COPD, European Respiratory Monograph, 8, 99-112. Hiss S., Treole K., & Stuart A., (2001) Effects of age, gender, bolus volume, and trial on swallowing apnea duration and swallow/respiratory phase relationships of normal adults Dysphagia, 16, 128-135. Hugli O., Fitting J.W., (2003) Alterations in metabolism and body composition in chronic respiratory diseases, European Respiratory Monograph, 8, 11-22. Klahn M.S., & Perlaman A.L., (1999) Temporal and durational patterns associating respiration and swallowing. Dysphagia, 14, 131-138. Langmore S., Terpenning M., Curtis J., Murray J., (1994) Risk Factors for Aspiration Pneumonia in the Elderly, ASHA Larson C, (1985) “Neurophysiology of Speech and Swallowing”, Seminars in Speech and Language, 6, 337-348. Levine R, Robbins J, Maser A,(1992) “Periventricular White Matter Changes and Oropharyngeal Swallowing in Normal Individuals”. Dysphagia, 142-147. Logemann J: (1988) Swallowing physiology and pathophysiology. Otolaryngol Clin North Am, 21:613-623. Martin B.J.W., Logemann J.A., Shaker R., & Dodds W., (1994) Coordination between respiration and swallowing: Respiratory phase relationships and temporal integration. Journal of Applied Physiology, 76, 714-723. Slide 49: Martin B., & Sessle B., (1993) The Role of the Cerebral Cortex in Swallowing. Dysphagia, 8 195-203. McConnel F., Cerenko D, Mendelsohn M,(1988) “Manofluorographic Analysis of Swallowing”, Otolayn Clinics of North America, .21 Miller, A, (1982)“Deglutition., Physiological Review, 62, 129-184. Miller A, (1986) “Neurophysiological Basis of Swallowing”,Dysphagia 1, 91-100. Miller A: Swallowing: (1987) Neurophysiologic control of the esophageal phase, Dysphagia, 2, 72-82. Palmer J, Rudin N, Lara G, Crompton A, (1992) “Coordination of mastication and Swallowing”, Dysphagia 7, 187-201. Pendergast DD.R., Fisher N.M., & Calkins E. (1993). Cardiovascular, neuromuscular and metabolic alterations with age leading to frailty. Journal of Gerontology, 48, 61-67. Robbins J, Hamiliton J, Kempster G, (1992), Oropharyngeal swallowing in normal adults of different ages., Gastroenterology, 103, 823-829. Robbins, J.A., Levine, R., Wood, J., et al. (1995). Age effects on lingual pressure generation as a risk factor for dysphagia. Journal of Gerontology, 50, M257-M262. Robbins J.A., Carnes, M, Prefer, B., Singaram C., (1995), Aging and Eating: An Interdisciplinary Approach to Optimizing Swallowing, AHSA Shadden, B.B., (1998), A Primer on Aging, ASHA Shaw D.W., Cook I.J., Dent J., et al. (1990). Age influences Oropharyngeal and upper esophageal sphincter function during swallowing. Gastroenterology, 98, A390 Sonies B.C. (1991). The aging Oropharyngeal system. Handbook of Communication Disorders (pp. 187-203). Austin, Tx Sturmberg J.P. (2002) Health assessments of an “at risk” population in general practice. Australian Family Physician, 34 (4), 384-387. Tracy F., Logemann J.A., Kahrilas P.J., et al. (1989) Preliminary observation on the effects of age on Oropharyngeal deglutition. Dysphagia, 4, 90-94. Westerterp K.R., (2003), Energy metabolism and Body composition: general principles, European Respiratory Monograph, 8 ,1-10. Wilkins R.L., Hodgkin J.E., Lopez B., (1996) Lung Sounds: A Practical Guide 2nd Edition, Mosby

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