Datasets:

pdf2dataset

/

c2fb3c4b6fc771c00b9592ad8171fb24

like 0

Follow

PDF2Dataset 10

3. P revent exacerbations from infectious processes through common health promotion measures such as hand washing and crowd avoidance. 4. V accination: Both the pneumococcal polysaccharide vaccine (PPSV23) and the pneumococcal conjugate vaccine (PCV-13) are recommended (CDC, 2015b). Annual vaccination against the seasonal flu vaccine is also recommended. D. Monitoring and follow-up care 1. C ontinue to monitor exacerbations frequency/ severity, symptoms including responsiveness to pharmacotherapy; promote smoking cessation or maintenance of nonsmoking status; promote avoid-ance of smoke/fumes/toxins/pollution exposure; manage comorbidities; and evaluate disease progres-sion, when indicated, through spirometry. E. Management of exacerbations 1. B ackground information a. D efinition: “ An exacerbation of COPD is defined as an acute event characterized by worsening of the patient's respiratory symptoms that is beyond normal day-to-day variations and leads Table 49-5 Initial Pharmacologic Management of COPD* Patient Group r ecommended First Choice Alternative Choice o ther Possible tr eatments** A Short-acting anticholinergic prn Or Short-acting beta 2-agonist prn Long-acting anticholinergic Or Long-acting beta 2-agonist Or Short-acting beta 2-agonist and short-acting anticholinergic Theophylline B Long-acting anticholinergic prn Or Long-acting beta 2-agonist prn Long-acting anticholinergic and long-acting beta 2-agonist Short-acting beta2-agonist and/or Short-acting anticholinergic Theophylline C Inhaled corticosteroid + long-acting beta 2-agonist Or Long-acting anticholinergic Long-acting anticholinergicand long-acting beta 2-agonist or Long-acting anticholinergicand phosphodiesterase-4inhibitoror Long-acting beta 2-agonist and phosphodiesterase-4inhibitor Short-acting beta 2-agonist and/or Short-acting anticholinergic Theophylline D Inhaled corticosteroid + long-acting beta 2-agonist and/or Long-acting anticholinergic Inhaled corticosteroid +long-acting beta 2-agonist and long-acting anticholinergicor Inhaled corticosteroid +long-acting beta 2-agonist and phosphodiesterase-4 inhibitoror Long-acting anticholinergicand long-acting beta 2-agonist or Long-acting anticholinergic andphosphodiesterase-4 inhibitor Carbocysteine N-acetylcysteine Short-acting beta 2-agonist and/or Short-acting anticholinergic Theophylline *Medications in each box are mentioned in alphabetical order and therefore not necessarily in order of preference. **Medications in this column can be used alone or in combination with other options in the Recommended First Choice and Alternative Choice columns. Reproduced from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2015). Pocket guide to COPD diagnosis, management, and prevention. Available from http://www. goldcopd. org/. Used with permission. 472 CHAPTER 49 | Chronic Obstructive Pulmonary Disease

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 49-6 Formulations and T ypical Doses of COPD Medications* Drug Inhaler (mcg)s olution for n ebulizer (mg/m L) o ralv ials for Injection (mg)Duration of Action (hours) b eta2-agonists Short-acting Fenoterol 100-200 (MDI) 1 0. 05% (Syrup)   4-6 Levalbuterol 45-90 (MDI) 0. 21, 0. 42     6-8 Salbutamol (albuterol)100, 200 (MDI & DPI) 5 5 mg (Pill), 0. 024%(Syrup)0. 1, 0. 5 4-6 Terbutaline 400, 500 (DPI)   2. 5, 5 mg (Pill)   4-6 Long-acting Formoterol 4. 5-12 (MDI & DPI) 0. 01     12 Arformoterol   0. 0075     12 Indacaterol 75-300 (DPI)       24 Salmeterol 25-50 (MDI & DPI)       12 Tulobuterol     2 mg (transdermal)  24 a nticholinergics Short-acting Ipratropium bromide20, 40 (MDI) 0. 25-0. 5     6-8 Oxitropium bromide100 (MDI) 1. 5     7-9 Long-acting Aclidinium bromide  322 (DPI)     12 Glycopyrronium bromide  44 (DPI)       Tiotropium   18 (DPI), 5 (SMI)     24 Umeclidinium   62. 5 (DPI)     24 Combination short-acting beta 2-agonist plus anticholinergic in one inhaler Fenoterol/ipratropium200/80 (MDI) 1. 25/0. 5     6-8 Salbutamol/ipratropium100/20 (SMI)       6-8 Combination long-acting beta 2-agonist plus anticholinergic in one inhaler Formoterol/aclidinium12/340 (DPI)       12 Indacaterol/glycopyrronium85/43 (DPI)       24 Vilanterol/umeclidinium25/62. 5 (DPI)       24 Methylxanthines Aminophylline     200-600 mg (Pill) 240 Variable, up to 24 Theophylline (SR)     100-600 mg (Pill)   Variable, up to 24 (continues)473 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

to a change in medication” (GOLD, 2014, p. 40). Additionally, exacerbations are recognized to reduce physical function and objective pulmo-nary function, accelerate disease progression, have a negative impact on quality of life, and cause considerable morbidity and increased risk of mortality (GOLD, 2014). b. M ost exacerbations are caused by lower respiratory tract infection or air pollution. Symptoms may overlap with other illnesses such as pneumonia, pulmonary embolism, pleural effusion, pneumo-thorax dysrhythmia, and heart failure. c. E tiology can be viral or bacterial. Most common bacterial etiologies are Haemophilus Influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis. d. Key hi story: acute change in symptoms of COPD—dyspnea, fatigue, cough, and sputum production/sputum character including dura-tion of symptoms. Determine frequency/pattern of exacerbations. Individuals who have two or more exacerbations per year are considered “fre-quent exacerbators” (Hurst et al., 2010). Elicit if required hospitalizations in past and if required intubation. Consider comorbidities, especially in older adults. Review current medications (including adherence to regimen) as breaks in maintenance therapy has been associated with exacerbations. Severity of airflow limitation at baseline must be kept in consideration when in exacerbation (GOLD, 2014). (Continued) Table 49-6 Formulations and T ypical Doses of COPD Medications* Drug Inhaler (mcg)s olution for n ebulizer (mg/m L) o ralv ials for Injection (mg)Duration of Action (hours) Inhaled corticosteroids Beclomethasone 50-400 (MDI & DPI) 0. 2-0. 4       Budesonide 100, 200, 400 (DPI) 0. 20, 0. 25, 0. 5       Fluticasone 50-500 (MDI & DPI)         Combination long-acting beta2-agonists plus corticosteroids in one inhaler Formoterol/ beclometasone6/100 (MDI)         Formoterol/budesonide4. 5/160 (MDI)9/320 (DPI)        Formoterol/mometasone10/200, 10/400 (MDI)        Salmeterol/fluticasone50/100, 250, 500 (DPI)        Vilanterol/fluticasone furoate 25/100 (DPI)         Systemic corticosteroids Prednisone     5-60 mg (Pill)     Methyl-prednisolone    4, 8, 16 mg (Pill)     Phosphodiesterase-4 inhibitors Roflumilast     500 mcg (Pill)   24 MDI = metered dose inhaler; DPI = dry powder inhaler; SMI = soft mist inhaler *Not all formulations are available in all countries; in some countries, other formulations may be available. † Formoterol nebulized solution is based on the unit dose vial containing 20 mcg in a volume of 2. 0 m L. Reproduced from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2015). Pocket guide to COPD diagnosis, management, and prevention. Available from http://www. goldcopd. org/. Used with permission. 474 CHAPTER 49 | Chronic Obstructive Pulmonary Disease

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

e. P hysical examination: body temperature; tachy-pnea; tachycardia; blood pressure and pulse (hemodynamic instability is a serious sign); pulse oximetry; altered mental status (serious sign); increased work of breathing; use of acces-sory muscles, poor air entry; wheezing; rhonchi; new or worsening peripheral edema; progres-sive new or worsening cyanosis (serious sign). If possible, sputum should be observed by the clinician. f. Di agnostic studies i. A rterial blood gas: Pa O2 less than 60 or Spo2 less than 90%; moderate to severe acido-sis (p H < 7. 36) plus hypercapnia (Pa CO2 45-60) in the patient with respiratory failure indicates the need for mechanical ventilation. ii. C hest radiograph: identify alternative diag-nosis (pneumonia, heart failure). iii. Ele ctrocardiogram: look for right ventricu-lar hypertrophy, arrhythmias, and ischemia. Others: sputum culture, metabolic panel, and complete blood count (may not be nec-essary for outpatient treatment but should be considered). Spirometry is not consid-ered helpful in the midst of exacerbation. 2. E xacerbation treatment The discussion that follows here applies only to mild exacerbations that can be safely treated as an outpa-tient. The reader is directed to the GOLD Guidelines (GOLD, 2014) for detailed guidance and recommen-dations for management of exacerbations in moderate and severe cases and recommendations for emergen-cy department and hospital treatment. a. D etermine appropriate treatment site: Strongly consider hospitalization for the following: sud-den/significant increase in symptoms, severe airflow limitation at baseline, changes in men-tal status, new physical examination findings (edema, cyanosis), self-care/functional impair-ment, inadequate home support, uncertain diagnosis, inadequate outpatient response to treatment, inability to eat or sleep due to symp-toms, worsening hypoxemia and hypercapnia, high-risk comorbidity (pneumonia, dysrhyth-mias, heart failure, diabetes mellitus, or renal or liver failure) (GOLD, 2014) b. Out patient treatment of exacerbation: summary of GOLD Guidelines, Chapter 5: Management of Exacerbations (GOLD 2014). Limited to out-patient management. See GOLD Guidelines for management of urgently/severely/critically ill. i. I ncrease short-acting bronchodilator: Beta2-agonist and/or anticholinergic short-acting bronchodilators through a metered dose inhaler or via nebulizer are recommended; a spacer device is optional. ii. Or al corticosteroids: prednisone 40 mg PO for 5 days is recommended. Oral prednisolone is preferable; nebulized budesonide can also be used in place of oral prednisone. iii. A ntibiotic treatment: Controversial; in outpatient setting sputum culture not helpful. Antibiotics recommended when all three cardinal symptoms of infec-tion are present: increased dyspnea, increased sputum volume, and more purulent sputum. The following antibiotic are recommended, but antibiotic selec-tion should take into consideration local bacterial resistance patterns: aminopenicil-lin (with or without clavulanic acid), tetra-cycline, or macrolide. iv. P atient/family education and follow-up: smoking cessation (if actively smoking); medication side effects, dosing and dosing schedule; when to expect symptoms to improve; signs and symptoms of worsening; when to call provider or seek emergency evaluation. Provide written instructions. The patient should be reappointed to see the provider again in 2-3 days or sooner as needed. v. Car e from a population health perspective A. Smoking cessation Smoking cessation is by far the most important preventa-tive strategy; smokers should be counseled and supported in achieving and maintaining cessation at all clinical encounters. All adjuncts to cessation should be employed and care should support cessation indefinitely. B. Promotion and advocacy for disease awareness, screening, and access to spirometry for identification and clinical monitoring C. Risk reduction by working for clean air and environmental issues at a public health level D. Active management of comorbidities in addition to COPD symptoms, especially in older adults. 475 Care from a population health perspective

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

re Feren Ces American Thoracic Society. (1962). Chronic bronchitis, asthma and pul-monary emphysema: A statement by the Committee on Diagnostic Standards for Nontuberculous Respiratory Diseases. American Review of Respiratory Disease, 85, 762-768. American Thoracic Society-European Respiratory Society. (2004). Standards for the diagnosis and management of patients with COPD. Retrieved from www. thoracic. org/clinical/copd-guidelines /index. php. Balmes, J. R., & Speizer, F. E. (2015). Chapter 311: Occupational and envi-ronmental lung disease. In D. L. Kasper, A. S. Fauci, S. L. Hauser, D. L. Longo, J. L. Jameson, & J, Loscalzo (Eds. ), Harrison's principles of internal medicine [Electronic version]. Retrieved from http://accessmedicine . mhmedical. com. ucsf. idm. oclc. org/View Large. aspx?figid=79744941. Bestall, J. C, Paul, E. A., Garrod, R., Garnham, R., Jones, P. W., & Wedzicha, J. A. (1999). Usefulness of the Medical Research Council (MRC) dys-pnea scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax, 54, 581-586. Celli, B. R., Cote, C. G., Marin, J. M., Casanova, C., Montes de Oca, M., Mendez, R. A., et al. (2004). The body-mass index, airflow obstruction, dyspnea and exercise capacity index in chronic obstructive pulmonary disease. New England Journal of Medicine, 350, 1005-1012. Centers for Disease Control and Prevention. (2012). Chronic obstructive pulmonary disease among adults—United States, 2011. Morbidity and Mortality Weekly Report, 61(46), 938-943. Centers for Disease Control and Prevention. (2015a). COPD statistics. Retrieved from www. cdc. gov/copd/data. htm. Centers for Disease Control and Prevention. (2015b). Pneumococcal vaccination. Retrieved from www. cdc. gov/vaccines/vpd-vac/pneumo /default. htm. Decramer, M., De Benedetto, F., Del Ponte, A., & Marinari, S. (2005). Systemic effects of COPD. Respiratory Medicine, 99, S3-S10. Global Initiative for Asthma. (2014). Diagnosis of diseases of chronic air-flow limitation: Asthma, COPD and Asthma-COPD Overlap Syndrome (ACOS). Retrieved from www. goldcopd. org/asthma-copd-overlap. html. Global Initiative for Chronic Obstructive Lung Disease. (2015). Global strategy for the diagnosis, management, and prevention of chronic obstruc-tive pulmonary disease. Update 2015. Retrieved from www. goldcopd. org /guidelines-global-strategy-for-diagnosis-management. html. Hurst, J. R, Vestbo, J., Anzueto, A., Locantore, N., Mullerova, H., T al-Singer, R., et al. (2010). Susceptibility to exacerbation in chronic obstructive pulmonary disease. New England Journal of Medicine, 363, 1128-1138. Jones, P. W., Hardy, G., Berry, P., Wiklund, I., Chen, W. H., & Lines Leidy, N. (2009). Development of the first validation of the COPD Assessment T est. European Respiratory Journal, 34, 648-654. Maltais, F., Decramer, M., Casaburi, R., Barrioer, E., Burelle, Y., Debigare, R., et al. (2014). An official American Thoracic Society/European Respiratory Society statement: Update on limb muscle dysfunction in chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 189(9), e15-e62. Tilert, T., Paulose-Ram, R., & Brody, D. J. (2015). Lung obstruction among adults aged 40-79: United States, 2007-2012 (NCHS Data Brief No. 180). Hyattsville, MD: National Center for Health Statistics. Retrieved from www. cdc. gov/nchs/data/databriefs/db180. pdf. 476 CHAPTER 49 | Chronic Obstructive Pulmonary Disease

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

A. Definition and overview The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Pain is always subjective. Each individual learns the appli-cation of the word through experiences related to injury in early life” (IASP, 2012, para. 2). IASP further describes the subjective nature of pain as “Many people report[ing] pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons” (IASP, 2012, para 1). “If they regard their experience as pain and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This definition avoids tying pain to the stimulus” (IASP, 2012, para 2). Chronic pain is generally defined as “pain which persists beyond the normal tissue healing time” With nonmalignant pain, three months is the most convenient point of division between acute and chronic pain” (IASP, 2014, p. 4). Some authors, however, use 6 months as the duration needed to meet the definition of chronic pain (Barclay & Nghiem, 2008; Bedard, 1997; Chou et al., 2009). Chronic pain may occur in the context of numerous diseases and syndromes. For the purpose of this guideline, all chronic pain disorders outside of cancer pain are referred to as CNP. Chronic pain syndrome is a condition in which a client's pain “consumes and incapacitates his/her life to the point that the pain and suffering becomes his/her main focus” (Saxe et al., 2009, p. 1). Anxiety and depression are common comorbidities, and the client often has difficulty with work and personal life (Saxe, Smith, & Mc Nerney, 2013; Yalcin & Barrot, 2014). Examples of CNP include but are not limited to osteoarthritis, rheumatoid arthritis, trigeminal and postherpetic neuralgia, fibromyalgia, myofascial pain, low back pain, peripheral neuropathy, phantom limb pain, reflex sympathetic dystrophy, sickle cell disease, temporomandibular joint dysfunction, I. Intr oduction and general background In this chapter, the authors examine nonpharmacologic treatments, nonopioid medications, and the use of chronic opioid medication for the management of chronic nonma-lignant pain (CNP). If nonpharmacologic agents and nono-piates fail to relieve pain, the subsequent use of opioids may be indicated. According to the 2009 American Pain Society Guidelines, “evidence is limited, but chronic pain can be effectively treated with chronic opioid therapy” (Chou et al., 2009, p. 1). We also discuss patient selection concerns related to chronic opioid therapy; risk evaluation, a strategy to initiate and monitor chronic opioid therapy; and related informed consent and safety issues. One difficulty of managing opioid therapy for CNP patients is that clients may present with a history of risk behaviors or a potential for or history of substance abuse (Passik & Weinreb, 2000). Definitions of substance use, including dependence, addiction, pseudoaddiction, sub-stance abuse, physical dependence, and tolerance are impor-tant for review and are included in Figure 50-1 (Federation of State Medical Boards of the United States, 2004). Patients with substance abuse history do have chronic pain, perhaps at a higher prevalence than the general population, but there are few studies that document this (Rosenblum et al., 2003). This chapter provides guidelines based on the American Pain Society (Chou et al., 2009) and the Medical Board of California (2014) recommendations for chronic opioid therapy, so that patients in higher risk populations, including those with histories of substance abuse, can be safely treated. The goal of therapy for the clinician is to provide adequate management of CNP in a timely, safe, and effective manner for the patient. The goals of therapy for many individuals with CNP often includes maximizing self-care strategies for pain management and control, optimizing function, and preventing untoward outcomes related to chronic pain (Caudill, 2009; Saxe et al., 2009, Saxe, Smith, & Mc Nerney, 2013). Jo Anne M. Saxe, Nicole Una, and Kellie Mc Nerney Chro NIC No NMA l Ig NAN t PAIN M ANA ge M e N t© Eliks/Shutterstock; © donatas1205/Shutterstock 47750Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

chronic abdominal pain from such conditions as Crohn's disease or chronic pancreatitis, and headaches, including cluster, tension, and migraine. B. Prevalence and costs The prevalence of chronic pain in the general popula-tion of the United States has been estimated at between 10% and 35% or 70-105 million people (Rosenblum et al., 2003; Turk, 2006). Chronic pain affects about 100 million American adults, more than the total affected by heart disease, cancer and diabetes combined (Institute of Medicine [IOM], 2011). An international survey of chronic pain revealed an overall prevalence of chronic pain as 22% of the population (Rosenblum et al., 2003). Significant financial burden is attributed to this syndrome because of loss of productivity and disability and the direct cost of physician visits and medication treatment (Turk, 2006). Costs associated with chronic pain have been estimated to be $635 billion each year in medical treatment and lost productivity (IOM, 2011). II. Database (may include but is not limited to) A. Subjective 1. H istory of the presenting complaint The history of the presenting symptom should include the identification of pain: its source onset, location, radiation, duration, characteristics, allevi-ating factors, aggravating factors, treatments tried, and the response to treatments. The significance of FIg Ure 50-1 Definition of terms Addiction is “a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors. Addiction is char-acterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one's behaviors and interpersonal relationships, and a dysfunctional emotional response. Like other chronic diseases, addiction often involves cycles of relapse and remission. Without treatment or engage-ment in recovery activities, addiction is progressive and can result in disability or premature death” (American Society of Addiction Medicine, 2011). Pseudoaddiction is the “iatrogenic syndrome resulting from the misinterpretation of relief seeking behaviors as though they are drug-seeking behaviors that are commonly seen with substance use disorders. The relief seeking behaviors resolve upon institution of effective analgesic therapy” (Federation of State Medical Boards of the United States, 2004). Physical dependence “is a state of biologic adaptation that is evidenced by a class-specific withdrawal syndrome when the drug is abruptly discontinued or the dose rapidly reduced, and/or by the administration of an antagonist. ” Signs of substance abuse and dependence may include some or all of following: Manipulative or abusive behavior directed at caregivers, including intimidation or coercion and aimed at acquisition and continuance of the substance abuse Evidence of compulsive drug use, such as unsanctioned dose increases or unapproved uses despite side ef fects Chaotic psychosocial history Involvement with the law Diversion for sale or misuse of controlled substances Urine drug screening with aberrancies from prescribed medications (Medical Board of California, 2014) Signs of poor personal habits, activities of independent living, or social dysfunction Physical or emotional deterioration and deconditioning T olerance “is a state of physiologic adaptation in which exposure to a drug induces changes that result in diminution of one or more of the drug's effects over time. Tolerance is common in opioid treatment, has been demonstrated following a single dose of opioids, and is not the same as addiction. ” Data from Federation of State Medical Boards of the United States. (2004). 478 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

challenging to assess in nonverbal individuals, such as persons affected by advanced dementia, behav-ioral pain assessment tools or surrogate pain reports will need to be used (Herr et al., 2006). See the Objective section for additional details. pain (i. e., impact on work, relationships, and activi-ties of daily living) should also be assessed. Pain and functional scales can be helpful in measuring the subjective report of pain (Figure 50-2). Note: Because pain and related functional assessments are FIg Ure 50-2 CNP Client P ain Questionnaire 1. Please tell us about your pain: Where is your pain? When did it start? How often do you have this pain? What do you think caused your pain? How would you rate your pain on a scale of 1 to 10 (1 being mild pain and 10 being the worst pain ever)? Describe your pain (check all that apply):q Stabbing q Throbbing q Aching q Burning q Pins and needles q Other 2. What helps your pain? 3. Does your pain interfere with any of the following activities (check all that apply)? q W ork q Household chores q Exercising q Shopping q Self-care activities (bathing, dressing, preparing food) q Sex q Relationships with family and friends q Recreational activities q Other 4. Please check all of the activities below that are limited because of your pain: q Standing q W alking q Sitting q T urning/twisting q Raising your arms/legs q Repeated arm/hand use (using a computer, etc. ) q Other 5. Does your pain interfere with your energy level? q Y es q No 6. How many hours do you sleep at night? During the day? 7. What treatments have you received for your pain? 8. What medications have you taken for your pain, including ones you are taking now? 9. What tests have you had to find out the cause of your pain? Reproduced from Hockenberry, M. J., & Wilson, D. (2009). Wong's essentials of pediatric nursing (9th ed. ). St. Louis, MO: Mosby. Used with permission. Copyright Mosby. 479 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

2. P ast health history a. M edical and psychiatric illnesses, surgical history, hospitalizations, and physical and psychological trauma in relation to the pain syndrome b. M edications: current and history of medications c. M edication allergies and drug interactions 3. F amily history of chronic pain and mental health disorders. 4. O ccupational history: if pain occurred as a result of a job injury, note any related litigation issues, present ability to work, and goals for work in the future. 5. P sychosocial history: to include substance abuse screening. A tool, such as the CAGE-AID (Brown & Rounds, 1995) or equivalent tool, may be used. The CAGE-AID can be downloaded from www. cqaimh. org/pdf/tool_cageaid. pdf. 6. R eview of systems a. C onstitutional signs and symptoms: fatigue or weight gain b. S kin: scar tissue including trauma or surgical scars c. C ardiac: chest pain or arrhythmias (assessing risk for side effects or contraindication to medications including opiates) d. R espiratory: shortness of breath and sleep apnea (assessing risk for side effects or contraindica-tions to opiates) e. G astrointestinal: constipation f. M usculoskeletal: joint erythema, swelling and/ or warmth, pain, decreased range of motion, arthralgias, myalgias, stiffness, and muscle wasting g. N eurologic: paresthesias, dysthesias, abnormal gait, muscle strength, symmetry, mood disorders, depression, and anxiety B. Objective 1. The p hysical examination: focus on the areas affected, which typically includes the completion of musculoskeletal and neurologic examinations. The initial examination should also include a baseline cardiopulmonary examination, especially if opioids will be considered in the future. 2. Di agnostics a. P ain assessment includes behavioral, functional, mood, and substance use and abuse and opioid risk assessment tools. For example:i. P ain and function assessment: CNP Client Pain Questionnaire (see Figure 50-2) is especially useful during an initial evaluation. The PEG (pain intensity [P], interference with enjoyment of life [E], and interfer-ence with general activity [G]) Scale (Krebs et al., 2009) is valuable for repeated and brief pain assessments. All items are weighted on a scale of 0 (no pain or major interference, respectively) to 10 (severe to major interference, respec-tively). The PEG Scale can be accessed at https://openi. nlm. nih. gov/detailedresult . php?img=2686775_11606_2009_981 _Fig1_HTML&req=4. For elderly individuals who are nonver-bal, assessment tools have been developed to evaluate their pain (Herr et al., 2006). One such tool is the Pain Assessment Scale for Seniors with Severe Dementia that includes an assessment of facial expressions, social/personality/mood indicators, activity/body movement, and physiological indicators/eating/sleeping changes/vocal behaviors (Fuchs-Lacelle & Hadjistavropoulos, 2004). For depression screening, use the Patient Health Questionnaire-9 (Spitzer, Kroenke, & Williams, 1999) or equivalent resource. (The Patient Health Questionnaire-9 can be accessed at http://www. integration. samhsa . gov/images/res/PHQ%20-%20Questions . pdf. ) ii. S ubstance use and abuse risk: CAGE-AID (Can be accessed at www. cqaimh. org/pdf /tool_cageaid. pdf. ) iii. O pioid risk assessment: Opioid Risk T ool (Webster & Webster, 2005) (see Figure 50-3) b. Obt ain a baseline electrocardiogram for QT c interval measurement before methadone admin-istration (Cohen & Mao, 2009; Krantz, Martin, Stimmel, Metha, & Haigney, 2009). c. R eview pertinent laboratory studies and imaging or other radiologic examinations. d. R eview any other relevant past medical documents or diagnostic tests. III. Assessment A. Determine the diagnosis with appropriate International Classification of Diseases-10 codes (www. icd10data. com/) (e. g., chronic primary osteoarthritis of the right hip: M16. 11)480 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

IV. g oals of clinical management Focus on the patient's desired goals and expected outcomes, which may include but are not limited to: A. Improve and maximize functioning in relationships, at work, or at home B. Decrease related depression and anxiety C. Minimize pain and pain-related distress and disability B. Severity Assess severity of symptoms (e. g., “moderate pain with frequent episodes of severe pain related to activity inter-fering with sleep and ability to work”). C. Significance and motivation Assess significance of diagnosis in relation to functional capacity, mood, and support systems. Determine the client's strengths, ability to follow the treatment plan, and risk for nonadherence and/or substance misuse Date_________________________ Patient Name__________________________ OPIOID RISK TOOL 1. Family History of Substance Abuse 2. Pe rsonal History of Substance Abuse 3. Age (Mark box if age 16-45) 4. History of Preadolescent Sexual Abuse 5. Psyc hological Disease Alcohol Illegal Drugs Prescription Drugs Alcohol Illegal Drugs Prescription Drugs Attention Deficit Disorder,Obsessive Compulsive Disorder,Bipolar,Schizophrenia Depression Mark each box that applies Item Score If Female Item Score If Male 1 2 43 3 4 3 4 53 4 5 11 30 22 TOTA L11 Total Score Risk Category Low Risk 0-3 Moderate Risk 4-7 High Risk ≥ 8_____ _____ Figure 50-3 Opioid Risk T ool Reproduced from Webster, L. R., & Webster, R. (2005). Predicting aberrant behaviors in opioid-treated patients: preliminary validation of the Opioid Risk Tool. Pain Med 6(6):432. 481 Goals of clinical management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

D. Minimize adverse effects and/or associated risks from pain management strategies V. Plan (interventions and ongoing approach to care) A. Nonmedication strategies include but are not limited to: 1. C ognitive behavioral therapy a. S tress reduction b. R elaxation techniques c. A ttention diversion d. Go al setting e. P ain and symptom diary 2. P hysical activity and physical therapy 3. T ranscutaneous electrical nerve stimulation unit for neuropathic pain 4. H eat and cold therapies 5. P ain support group 6. Ac upuncture 7. Ma ssage 8. G uided imagery techniques 9. L augh therapy and laugh yoga (Barclay & Nghiem, 2008; Buckhardt et al., 2005; Caudill, 2009; Keefe, Somers, & Kothadia, 2009) B. Nonopiate medication strategies (Barclay & Nghiem, 2008; Caudill, 2009) 1. Ac etaminophen: for mild to moderate pain 325 mg one to two tablets, four times daily, not to exceed 3 g/day; 2g/day for the elderly. Caution with liver disease, alcohol use, hepatitis, and use of other medications metabolized by the liver. 2. N onsteroidal anti-inflammatory drugs (NSAIDs): for mild to moderate pain, may use in conjunction with acetaminophen. Examples include ibuprofen, 400-800 mg every 6-8 hours yet not to exceed a total of 2,400 mg per 24 hours; diflunisal, 500-1,000 mg twice daily; or naproxen, 250-500  mg twice daily. If one class fails, consider switching to another class of NSAIDs (e. g., switching from a nonselective cyclooxygenase inhibitor (e. g., ibuprofen) to a salicylic acid derivative (e. g., trilisate propionic acids) or a selective cyclooxygenase inhibitor (e. g., celecoxib). It is important to review the specific medication because dose and timing vary depending on the medication. Note the precautions associated with hypertension, coronary artery disease, diabetes, benign prostatic hypertrophy, and individuals older than 50 years of age. NSAIDs are contraindicated in patients with a history of gastrointestinal ulcer disease and chronic kidney disease. 3. T opical analgesic creams and patches: Appropriate for mild to moderate pain; may be used in conjunction with acetaminophen and NSAIDs. Dose varies and is dependent on analgesia desired and person's response. Examples include lidocaine 5% patches, up to three patches to the affected area at once for 12 hours within a 24-hour period; and lidocaine 4% cream or capsaicin cream 0. 025-0. 075%, applied to the affected area up to three to four times daily. 4. A ntidepressants: chronic pain can cause depression or may worsen depression. Additionally, depression can worsen with chronic pain. As such, antidepressants may be a useful adjunctive therapy. T ricyclic antidepressants are helpful for neuropathic pain disorders and associated sleep disturbances. A baseline electrocardiogram is indicated before initiating this classification of medication to assess for any conduction abnormalities because they may cause arrhythmias. Start with a low dose and titrate up over several weeks. Serotonin-norepinephrine reuptake inhibitors (SNRIs), e. g., duloxetine and venlafaxine, may also be effective in the management of pain and depres-sion. Because SNRIs may cause an increase in blood pressure, the person's blood pressure should be well controlled before initiating an SNRI. Additionally, duloxetine should not be used in persons with cur-rent liver impairment or risk of liver impairment, given reports of fatal hepatotoxicity (e Med Expert, 2007—2014). As with tricyclics, SNRIs should be titrated. They should not be abruptly discontinued given the risk for withdrawal signs and symptoms (may include but not limited to nausea, dizziness, irritability, and insomnia). Some antidepressants can change the potency of opiates. Be certain to check for medication interactions. 5. A nticonvulsants: These medications have been used for neuropathic pain, such as diabetic neuropathy and postherpetic neuralgias. Examples include gabapentin, 300-600 mg three times a day. Start at 300  mg at bedtime, titrate up by 300 mg weekly. Use with caution in renal insufficiency. Pregabalin (Lyrica®) can be started at 25-75 mg twice per day dependent on the severity of pain. Pregabalin may be titrated up to 450 mg/day in divided doses. Adjustments for renal impairment are indicated. Refer to reliable drug resources for dosing adjustment guidelines. 482 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

chronic, the provider obtains and completes the same pain questionnaire, depression, sub-stance abuse, and opioid risk screening required for adherence to the protocol (see Figures 50-2 and 50-3). d. E nrollment in a CNP protocol is indicated if the clinician deems that opioid therapy is appropriate for care. The following matters are discussed with the patient and family in depth, including a signed and agreed-upon CNP treatment agree-ment plan (see Figure 50-5): i. The pr escribed treatment plan, which includes a discussion about associated risks and benefits of opioid treatment, medica-tions to be used, nonopioid therapies to be pursued, and the follow-up interval. ii. P atient expectations and responsibilities including keeping appointments, adherence to treatment plans, obtaining medications from a single provider, single pharmacy, feedback to provider, and legal issues including diversion. iii. H ow to take the medication and impor-tance of dosing and timing of dose and interaction with other medications. iv. P otential adverse effects of treatment with opioid medication include safety and rec-ommending not driving or operating equip-ment until the patient is tolerant of the medication regime. Other adverse effects include the potential for altered mentation, respiratory depression, and arrhythmias, and the risk of death if used incorrectly or in conjunction with other substances. v. R isk of overdose, signs of overdose (see Figure 50-6), and a rapid response to an actual and potential overdose. vi. P rophylactic treatment for constipation caused by opiates, because untreated consti-pation can worsen back and abdominal pain. vii. R andom urine testing is required for all patients on opioid therapy (at initiation, randomly, or at least annually). Because the interpretation of urine tests is frequently misunderstood, providing interpreta-tion guides and training for all providers is strongly recommended. Gourlay, Heit, and Caplan (2010) have noted important details related to this matter at http://issuu. com/cafamilydocs/docs/udtmonograph. viii. The pr ocedure for CNP protocol treatment agreement, and minor and major agreement breaks, is reviewed including consequences of breaks (for example, evidence of drug 6. Othe r adjunctive medications: muscle relaxants. Examples include baclofen, 10-20 mg three times daily, or cyclobenzeprine, 5-10 mg three times daily. Avoid carisoprodol (Soma®) because of abuse potential and availability of other muscle relaxants. C. Opiates 1. S tandards for prescribing controlled substances The clinician follows the accepted standards for prescribing controlled substances. For example, in the state of California, nurse practitioners and nurse midwives are expected to follow Standardized Procedures for Controlled Substances (Figure 50-4). 2. S tarting opiates The following recommendations for starting opiates, if indicated, are based on the American Pain Society-American Academy of Pain Medicine's clinical guide-lines for the use of chronic opioid therapy in chronic noncancer pain (Chou et al., 2009) and the Medical Board of California's (2014) guidelines for prescrib-ing controlled substances for pain. a. N ew clients require sufficient visits to com-plete a full history and physical and to review all prior medical records, pain and functioning questionnaires, depression and substance abuse screenings with appropriate laboratory studies, imaging, and urine drug screen, and if available, a state prescription drug monitoring program (PMP) report. In the state of California, the Department of Justice compiles a record of all Schedule II through IV prescriptions so phar-macists and prescribers can access the database called Controlled Substance Utilization Review and Evaluation System (CURES) (California Department of Justice, 2014). PMPs are increas-ingly used nationally in pain management and frequently used by providers before initiating a controlled medication prescription. This report-ing is designed to prevent individuals from obtaining multiple controlled prescriptions in 1 month, prevent dangerous mixing of medica-tions, and decrease the potential for misuse. b. A me ntal health evaluation visit is recommended during the establishment of care. Opiates are not prescribed until these procedures are complete and 30 days have passed. Exceptions can be made if the provider has access to the patient's previous records and, ideally, have been approved by a chronic pain treatment team. c. E xisting patients receiving primary care may be given a trial of opioid therapy before enrolling in the CNP protocol if the primary care pro-vider deems the patient is a candidate for opioid therapy. If the provider believes therapy will be 483 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

FIg Ure 50-4 Furnishing and o rdering Controlled Substances from Schedule II-V at the UCSF DC h S Faculty Practices I. POLICY : A. Only approved nurse practitioners with current furnishing licenses and DEA registration for ordering schedule II-V CS may furnish these drugs and devices. B. The qualified nurse practitioner may initiate, alter, discontinue, and renew category II-V CS (see addendum) included in the UCSF DCHS Faculty Practices Formulary. C. As described in the Policies and in the “Furnishing/Ordering Drugs and Devices by Nurse Practitioners” Standardized Procedure. II. PROTOCOL A. Definition: This protocol covers the management of Schedule II-V CS for all adults and children seen in the UCSF DCHS Faculty Practices with the following conditions, illnesses, diseases: 1. Acute traumatic injuries, 2. Acute infections (e. g., pyelonephritis), 3. Acute and chronic musculoskeletal disorders, 4. Acute and chronic neurological disorders (e. g., migraines), 5. Chronic psychological disorders (e. g., ADHD), 6. Acute urological conditions (e. g., renal calculi), and/or 7. Post-surgical pain. B. Subjective Data: Subjective information will include but is not limited to:1. Relevant health history to warrant the use of the drug or device. 2. No allergic history to the drug or device. 3. No past health, family and/or personal-social history, which are an absolute and/or potential for contra-indication to the use of the drug or device. C. Objective: Objective information will include but is not limited to:1. A physical examination to indicate/contraindicate the use of the drug and/or device. 2. Diagnostics: Laboratory tests or procedures to determine the underlying etiology of pain and/or to indicate/contraindicate use of the drug and/or device, if needed. D. Assessment: Subjective and objective data supports the use of the drug and/or device. Contraindications, safety issues, and/or cost concerns have been adequately assessed and documented. E. Management: 1. Diagnostics: Ordering relevant laboratory/diagnostic studies. 2. T reatment: a. The following controlled substances may be used:i. Opioid agonists (For example but not limited to: Morphine, morphine controlled-release, hydromorphone, levorphanol, meperidine, methadone, oxymorphone, fentanyl, buprenor-phine, tramadol, codeine (with or without aspirin or acetaminophen), hydrocodone, oxycodone or oxycodone controlled-release): Use the guidelines noted in the current UCSF DCHS Faculty Practices Formulary Guidelines for drug dosage, frequency, route of administration. Schedule II opioid agonist analgesics should be reserved for severe, incapacitating pain. Schedule III opioid agonists should be used for moderate to severe pain. ii. Stimulants (For example but not limited to: Mixed salts of dextroamphetamine and amphet-amines, dextroamphetamine sulfate, atomoxetine, methylphenidate, and pemoline): Use the guidelines noted in the current UCSF DCHS Faculty Practices Formulary Guidelines. 3. Drug/device order: W rite a separate drug order for each Schedule II-V CS on anti-fraud prescription form. (Note: Telephone orders are acceptable for Schedule III through V CS. ) Each order needs to include: a. Name, age, telephone number, and the medical record number of the client, b. Name of the medication/device, c. Dosage, frequency, route, duration of the use, amount; and number of refills of the drug/device (Note: CS II may not be refilled. Schedule III CS may only be filled 5 times in a 6 month period),484 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

d. Brief statement regarding the reason for using the drug/device, and e. Printed name, furnishing number, DEA number and signature of the nurse practitioner 4. Supportive/Adjunctive Therapy: a. Consider using tricyclic antidepressants, sustained-release bupropion, or anticonvulsants for neuro-pathic pain since these medications may be more effective in managing the pain as compared to opioids. b. Recommend non-pharmacologic therapies (e. g., thermal therapy, massage, physical therapy, chiropractic, acupuncture, and meditation) as indicated since these modalities may be useful in pain management. 5. Client Education: a. Provide the client and/or the client' s caregiver with the information and counseling in regards to the action and use of the drug/device. Caution the client and/or the client's caregiver on the pertinent side effects and complications with the chosen drug/device. Advise on how to communicate with the Clinic staff should s/he have any questions/concerns/side effects/complications. 6. Physician Consultation/Referral: Consult or refer to physician if the client is: a. Unresponsive to the drug/device therapy, b. Demonstrating unusual or unexpected side ef fects, c. Known to have a history of CS and/or alcohol abuse; and as indicated in the general policy section. 7. Follow-up: In accordance with standard practice or with consulting physician' s recommendation. 8. Record keeping: As described in General Policies. Addendum Federal Contr olled Substance Law Federal Controlled Substance Law: The Federal Controlled Substances Act of 1970 recognized five schedules of drugs based upon their relative abuse potential (Note: California State regulatory requirements have been added. ) The lists of schedules for controlled substances are updated annually and can be accessed at http://www. deadiversion. usdoj. gov/21cfr/cfr/2108cfrt. htm Class I: Drugs with no current medical application and maximum abuse potential. Examples: Heroin, lysergic acid dieth-ylamide (LSD), marijuana, 3, 4 methylenedioxymethamphetamine (MDMA [Ecstasy]). Class II: Includes opioid analgesics (e. g., codeine, hydrocodone, morphine, methadone and oxycodone), stimulants (e. g., dextroamphetamine, cocaine, methylphenidate), and depressants (e. g., pentobarbital). Facsimile of Schedule II CS permitted under certain circumstances (e. g., hospice care). Facsimile for emergency dispensing must be followed up with a written and signed transmittal order within 7 days. Refills are prohibited. Class III: Buprenorphine; codeine (Not more than 1. 8 grams of codeine per 100 milliliters or not more than 90 milligrams per dosage unit) and other opioids in lower doses than class II controlled substances along with non-narcotic agents May communicate to pharmacist Schedule III-V CS prescriptions/transmittal orders either orally, in writing, or by facsimile. May refill Schedule III-IV's 5 times in 6 months; and refills of Schedule V's as noted by the practitioner. Class IV: Benzodiazepines (e. g., Valium®, Ativan®, Xanax®, Klonopin®), stimulants such as phentermine. Written prescription required, up to 5 refills allowed within 6 months of issuance for this class. In August 2014, Tramadol was classified as Schedule IV due to possible abuse potential. Class V: Low-dose controlled substances containing non-narcotic active medicinal ingredients (e. g., Cough medicines with codeine in low dose (Robitussin-AC®). May refill Schedule III-IV's 5 times in 6 months; and refills of Schedule V's as noted by the practitioner. IMPORTANT: Refills for schedule II medications or future dated prescriptions are not allowed by the Drug Enforcement Agency. Data from State of California Board of Registered Nursing, 1998, 2004a, 2004b; University of California San Francisco [UCSF], Department of Community Health Systems [DCHS], 2010, 2015; U. S. Department of Justice, Drug Enforcement Agency, 2014. FIg Ure 50-4 Furnishing and o rdering Controlled Substances from Schedule II-V at the UCSF DC h S Faculty Practices (Continued)485 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

FIg Ure 50-5 P ain Management Agreement Glide Health Services 330 Ellis Street San Francisco, CA 94102 The purpose of this agreement is to prevent misunderstandings about certain medicines you will be taking for pain management or other medical conditions. This agreement will help both you and your provider comply with laws regarding controlled pharmaceuticals. I. Client Name and Provider Name have decided together to use a controlled substance for management of pain or other medical condition. MEDICATION INSTRUCTIONS AMOUNT PER WEEK/MONTH ✓I agree that this medication will only be used by myself and as it is prescribed. ✓I will not share, sell or trade my medication with anyone. ✓I will safeguard my medication from loss or theft. Lost or stolen medicine may not be replaced. ✓If I run out of the medication, Glide Health Services may not refill the prescription early. ✓I will not seek controlled substances from other medical providers. ✓I understand that there will be no refills on my medications without a provider visit at Glide. ✓I agree to share my complete medications history in order to avoid adverse drug interactions. ✓ I will attend all my scheduled appointments, including any referral appointments my clinician has made for me, and follow up as designated in my plan of care. ✓I agree to bring all unused pain medication to every of fice visit. ✓I understand pharmacy records may be reviewed to confirm prescriptions. ✓ I understand I may be required to have random urine or blood testing completed. I agree to this testing, and understand that if I fail to do so, I will be safely tapered off the medication(s). ✓I understand if I break this agreement, my provider may stop prescribing these pain medicines. ✓ I understand that many pain medicines may cause drowsiness and impair my ability to drive and operate machin-ery and may impair my thinking and judgment. ✓ I understand that misuse of these drugs or use of these drugs in combination with alcohol, unauthorized prescrip-tion medications, or illicit drugs may have serious effects including death. ✓The prescribing provider has explained that the above medications have possible side ef fects and may be addictive. Comments: Client's Signature Date Provider Signature Date486 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

c. R efills of medications are documented in the electronic health record or paper chart to include date, name of opiate, dose, instructions for use, quantity prescribed, and number of refills. The patient brings all pain medication bottles to each and every visit at the request of the provider. d. One pr imary provider writes prescriptions. In their absence, an alternate or covering provider is determined. This arrangement is reviewed with the patient. e. R efills on controlled substances should be done during the visit with only enough medication to last until the next visit. f. R efills are not completed without an appoint-ment or over the telephone. g. L ost medications or stolen medications should not be replaced and recorded as a major agree-ment break. With rare exceptions, providers do not routinely refill lost or stolen medications. Exceptions by provider discretion require docu-mentation of the rationale, and the incident must be recorded as a minor agreement break. h. A tr eatment plan for addressing adverse effects is discussed and documented. 4. M edication considerations a. N ote contraindications to opioid therapy i. A bsolute contraindications a. A llergy to opiate agents b. C oadministration of drug capable of inducing life-threatening drug-drug interaction c. Act ive diversion of controlled substances d. U nwillingness or inability to comply with treatment plan e. U nwillingness to adjust at-risk activi-ties that may result in serious injury/re-injury ii. R elative contraindications (prescribe with caution and more intensive monitoring)a. M eets criteria for current substance use disorder (e. g., as noted by the Diagnostic and Statistical Manual of Mental Disorders-5 [American Psychological Association, 2013]) b. Ac ute psychiatric instability or high suicide risk c. H istory of intolerance, serious adverse effects, or lack of efficacy of opioid therapy d. I nability to manage opioid therapy responsibly (i. e., cognitive impair-ment; without stable and reliable care-giver or social support network)treatment completion or 6-month waiting period before being reconsidered to resume opiate management). 3. S ubsequent evaluations Subsequent visits are determined by the clinician but initially may be monthly. More frequent visits may be required at the provider's discretion. Exceptions may be made for low-risk clients with stable housing situ-ations. These low-risk patients should be seen every 2-3 months at a minimum. The provider makes this determination after at least 2 months of contact and assessment. a. A ll patients leave a urine sample on monthly or routine follow-up visits, but it is up to the pro-vider to determine if urine toxicology screens are done randomly on that visit (Chou et al., 2009; Saxe et al., 2009). b. C linical encounters include an assessment of: i. P ain: intensity and response to treatment plan (Figure 50-2) ii. Adv erse events and side effects of therapy iii. Act ivity and functioning level to evaluate efficacy of treatment plan iv. Ad herence to essential components of treatment agreement is documented with nonadherence to plan of care and docu-mentation of minor or major agreement break on the problem list. Specific plans for addressing agreement breaks should be discussed and documented. For example, a setting may consider adopting the follow-ing approach: any client with more than two major agreement breaks or three minor breaks will be referred for evaluation to a CNP team to determine appropriate action to follow. FIg Ure 50-6 Signs of o piate o verdose Extreme sleepiness with an inability to awaken the person verbally or with vigorous movement (e. g., sternal rubbing) Slow respirations (<12 respirations/minute) and/ or shallow breathing Vomiting Cyanosis of the digits and/or lips Constricted pupils Bradycardia and/or hypotension487 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

e. Severe social instability or inability to manage medications safely f. Client with sleep apnea not on contin-uous positive airway pressure machine g. Elderly clients particularly without stable and reliable caregiver or social support network b. Assess and address common adverse effects of opioid therapy: constipation, nausea and vomit-ing, itching, sweating, peripheral edema, urinary retention, myoclonus, hyperalgesia, dyspepsia, changes in cognition, perceptual or affective adverse effects, or sexual dysfunction. c. Short-acting opiates: Short-acting medications should generally not be the mainstay of chronic pain treatment. Short-acting medications are not recommended for chronic pain because of high-risk metabolites (e. g., meperidine/Demerol®); low efficacy (e. g., propoxyphene/Darvocet®); or risk of rebound headaches (e. g., butalbital/Fioricet®). Note: Potency varies considerably; see analgesic comparison tables at www. global-rph. com/narcoticonv. htm for assistance with converting from one opiate to another, and converting short-acting to long-acting opiates (Mc Auley, 2015). Cost varies considerably; many are now available as a generic. Types of short-acting opiates are noted on T able 50-1. However, short-acting medications for CNP may be appropriate in the following situations: i. T o manage pain until the correct dose of long-acting medications is determined, and then the short-acting medications can be discontinued. ii. T o assist with titrating the patient off of or down from longstanding opiate regimes. iii. T o manage predictable pain flares (long travel or before exercise, dental appoint-ments, and so forth) iv. T o manage chronic pain in patients who do not need high doses of medications (e. g., elderly patients may do well with hydroco-done/acetaminophen, 5/325 mg half a tab-let four times daily on a schedule, plus half a tablet as needed for additional pain) d. As noted by Dowell, Haagerich and Chou (2016), “clinicians should regularly evaluate the benefits and harms with patients within 1 to 4 weeks of starting opioid therapy for chronic pain or of dose escalation” especially in light of the questionable efficacy of long-term opioid therapy. e. Changing from short-acting to long-acting medi-cations: Changing from short-acting to long-acting medications is the standard of care for chronic pain, because short-acting medications have increased dependence, addiction poten-tial, and increased street value with an increased risk of diversion. Short-acting opiates also may not control baseline pain and require a greater total dose of medications to control pain (Chou et al., 2009). Equianalgesic tables provide help-ful guidelines with the conversion of dosing TABLE 50-1 Short-Acting Opiates Medication Strengths Comments Hydrocodone combined with acetaminophen or ibuprofen5-, 7. 5-, and 10-mg tablets Caution: keep acetaminophen dose at or under 3,000 mg daily, or 2,000 mg daily in the elderly Oxycodone combined with acetaminophen or aspirin2. 5-, 5-, 7. 5-, and 10-mg Also available in extended release. Caution: keep acetaminophen dose under 4,000 mg daily, or 2,000 mg in the elderly. Approximately 10% of patients do not metabolize oxycodone well and will not get effective pain relief; consider changing opiates if there is a poor response (Chou et al., 2009). Codeine combined with acetaminophen30/300 or 60/300 Caution: keep acetaminophen dose at or under 3,000 mg daily, or 2,000 mg daily in the elderly. Morphine 15 and 30 mg Also available in long-acting form. Hydromorphone 2, 4, and 8 mg Fentanyl transmucosal lozenge 100-, 200-, 400-, 600-, and 800-mcg buccal tablets Typically used for cancer pain because of rapid action, occasionally used for chronic pain. It is expensive. Oxymorphone 5 and 10 mg Also available as extended release TABLE 50-1 Short-Acting Opiates Medication Strengths Comments Hydrocodone combined with acetaminophen or ibuprofen5-, 7. 5-, and 10-mg tablets Caution: keep acetaminophen dose at or under 3,000 mg daily, or 2,000 mg daily in the elderly Oxycodone combined with acetaminophen or aspirin2. 5-, 5-, 7. 5-, and 10-mg Also available in extended release. Caution: keep acetaminophen dose under 4,000 mg daily, or 2,000 mg in the elderly. Approximately 10% of patients do not metabolize oxycodone well and will not get effective pain relief; consider changing opiates if there is a poor response (Chou et al., 2009). Codeine combined with acetaminophen30/300 or 60/300 Caution: keep acetaminophen dose at or under 3,000 mg daily, or 2,000 mg daily in the elderly. Morphine 15 and 30 mg Also available in long-acting form. Hydromorphone 2, 4, and 8 mg Fentanyl transmucosal lozenge 100-, 200-, 400-, 600-, and 800-mcg buccal tablets Typically used for cancer pain because of rapid action, occasionally used for chronic pain. It is expensive. Oxymorphone 5 and 10 mg Also available as extended release TABLE 50-1 Short-Acting Opiates Medication Strengths Comments Hydrocodone combined with acetaminophen or ibuprofen5-, 7. 5-, and 10-mg tablets Caution: keep acetaminophen dose at or under 3,000 mg daily, or 2,000 mg daily in the elderly Oxycodone combined with acetaminophen or aspirin2. 5-, 5-, 7. 5-, and 10-mg Also available in extended release. Caution: keep acetaminophen dose under 4,000 mg daily, or 2,000 mg in the elderly. Approximately 10% of patients do not metabolize oxycodone well and will not get effective pain relief; consider changing opiates if there is a poor response (Chou et al., 2009). Codeine combined with acetaminophen30/300 or 60/300 Caution: keep acetaminophen dose at or under 3,000 mg daily, or 2,000 mg daily in the elderly. Morphine 15 and 30 mg Also available in long-acting form. Hydromorphone 2, 4, and 8 mg Fentanyl transmucosal lozenge 100-, 200-, 400-, 600-, and 800-mcg buccal tablets Typically used for cancer pain because of rapid action, occasionally used for chronic pain. It is expensive. Oxymorphone 5 and 10 mg Also available as extended release488 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 50-2 Long-Acting Opiates Medication Strengths Comments Morphine sulfate (sustained/extended release): examples include Kadian ® and MS Contin®Kadian® (sustained-release pellets in capsules): 10-, 20-, 30-, 50-, 60-, 80-, 100, and 200-mg capsules; MS Contin ® (sustained-release tablets): 15-, 30-, 60-, 100, and 200-mg tablets Dose varies by product, generally daily to twice a day. Often preferred by providers because diversion potential is lower. Methadone 5-and 10-mg tablets Methadone is an appropriate medication for severe pain for patients with CNP, even in opioid-tolerant patients. Titrate up very slowly because methadone has a very long and “highly variable” half-life (Chou et al., 2009). Get a baseline ECG to measure QTc interval, recommend a repeat in 30 days and an ECG early or more frequently at doses over 100 mg daily, because fatal arrhythmias can occur if patients develop long QTc intervals (Krantz et al., 2009). Safe starting dose for opioid-naive patient is 2. 5 mg every 8 hours. Increase medication weekly, not more frequently. Use cautious titration and dosing (e. g., consider starting with half-tablets) in the elderly or patients with renal or hepatic dysfunction (Chou et al., 2009). Although withdrawal symptoms are prevented in daily dosing and the half-life is long, the pain relief is at most 8 hours; dosing must be at least every 8-12 hours when prescribing methadone for pain. Oxycodone controlled release10-, 15-, 20-, 30-, 40-, 60-, and 80-mg controlled-release tablets10% of people do not metabolize this drug well, so they do not feel effective relief (Chou et al., 2009). Consider transition to another opiate for patients who request escalation of dose because of inadequate pain control. Considered to have a high street value. Fentanyl patch 12, 25, 50, 75, and 100 mcg/h patch The fentanyl patch is not indicated for opiate-naive patients. Change the patch every 48-72 hours (some patients report difficulty with adherence and pain relief after 48 hours). Start at lower doses and start cautiously because of the long half-life. Initial fentanyl transdermal doses are based on daily total morphine requirements for individuals already on opiates. The total daily dosing is then moderately reduced, usually 25-50% (Chou et al., 2009). Considered to have a high street value. Hydromorphone Has numerous strengths with short-acting and extended-release formulations It is not commonly used in some community clinics. Buprenorphine/naloxone combo: Suboxone2-and 8-mg sublingual tablets This opiate agonist-antagonist is not approved by the Food and Drug Administration for pain, yet some patients with mixed addiction and chronic pain do well on this option. Although prescribed for addiction, it can offer some pain relief for patients with CNP. Requires special Food and Drug Administration license and training. 489 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

between different types of opiates, yet they do not play a role in individual patient factors that influence safe dosing (Vissers, Besse, Hans, Devulder, & Morlion, 2010). As such, it has been recommended by notable authorities to reduce dosing on these tables by one-third to two-thirds of the stated dosing (Vissers et al., 2010). A well-referenced web-based opiate conversion chart can be found at http://www. globalrph. com /narcoticonv. htm (Mc Auley, 2015). f. D ose Ceiling: Since 2010, several municipalities and clinics have implemented dose ceilings on opiates. These limits were a response to escalat-ing rates of accidental overdose deaths, increased hyperalgesia among individuals receiving chronic opiates, and data revealing limited improvement of functionality with high doses of opiates among treatment recipients during the previous years. There is no national consensus on a precise ceil-ing dose at which opiates are no longer safe. The Medical Board of California (2014) issued rec-ommendations that above 80 mg of morphine equivalents, a pain management specialist should be consulted before further dose escalation. g. I ndications to stop opiate therapy: Medication nonadherence or noncompliance with the pain agreementi. I nstitutions differ on the definition of agreement breaks and the consequences. At the authors' institution, the number of minor and major agreement breaks that require action is defined (Saxe et al., 2009). Examples of minor agreement breaks include missed appointments, early refill requests, seeking medications from another provider or different pharmacy, and not adhering to treatment agreement plans. ii. M ajor agreement breaks include refusal of urine toxicology screen, lost or stolen medications, drug screening (with high-sensitivity confirmation, such as gas chro-matography) indicating that the prescribed medication is absent despite client state-ments of recent ingestion, client is abusive to staff, pill count discrepancy, or request for pill count is refused. iii. The in stitution has in place consequences of agreement breaks; for example, two major agreement breaks may be grounds for review by a CNP team and consider-ation for addiction referral and discon-tinuation of opioid therapy. Unless there has been fraud or multiple prescribers, consider a standard policy of weaning as opposed to abrupt discontinuation. This increases the chance that the patient will continue to work with  the team on other options (complementary treatments, behav-ioral therapy, and addiction treatment) as opposed to just seeking another provider, and it decreases the likelihood of emergency department visits for withdrawal symptoms. Pharmacies can be instructed to dispense small supplies at a time (a 1-, 3-, or 7-day supply) to assist the weaning plan (Saxe et al., 2009). A recommended weaning strategy is to decrease opiate dose by 10% every 3 days (Medical Board of California, 2014). iv. I nappropriate use of alcohol or illicit drugs may be considered a major agreement break or cause for termination. Some institutional flexibility may be spelled out per chronic pain team. For example, rather than termi-nation, the client must agree to a mental health evaluation and commit to a drug treatment cessation program to continue treatment. v. O pioid therapy may be discontinued for patients with multiple minor agreement breaks or at the provider's discretion. Otherwise the patient is evaluated by the primary provider frequently until adher-ence problems have resolved. Final deter-mination to address repetitive agreement breaks is made by a CNP team or medical director (Saxe et al., 2009). vi. O pioid therapy is discontinued when the therapy or side effects of the therapy are a greater detriment than benefit as deter-mined by consultation with the client, family, and CNP team. vii. O pioid therapy is discontinued if evalua-tion demonstrates lack of efficacy, the client desires to discontinue therapy, or the cause of pain has resolved. viii. O pioid therapy is discontinued when there are serious safety issues as a result of treatment. ix. W hen opioid therapy is discontinued, opioid is tapered and weaned off, unless there is dangerous or illegal behavior. Strategies for tapering and weaning have been suggested by the Medical Board of California (2014). Opioid therapy should 490 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

VI. P atient education A. Assist the patient and family in understanding and coping with chronic pain, and steps of care in terms of CNP protocol 1. P rovide verbal and written information regarding chronic pain and nonpharmacologic and pharmaco-logic treatments. 2. A ssist the patient and family in obtaining all prior medical records and diagnostics, and facilitate the request for prior medical records. B. Provide self-care strategies as mentioned in nonpharmacologic management of chronic pain C. Discuss management rationale for: 1. N onpharmacologic and nonopiate strategies as first-line treatment and progression to opiates as indicated 2. R easons for a CNP team and protocol D. Review the individual treatment agreement if the patient proceeds to the CNP protocol 1. Di scuss medication(s): dose; schedule of dosing; side effects of medications; and safety of activity on medication (e. g., driving or swimming), including risk of death if medications are used incorrectly or combined with substances or dangerous activity. 2. P rovide an explanation that one provider prescribes and one pharmacy dispenses, patient responsibility for managing medications safely, keeping appointments, and random urine screening. 3. P rovide an overview of and the need for signing the individual treatment plan or pain agreement (Figure 50-5). 4. Di scuss overdose prevention that includes ready access to drug and alcohol treatment services and management strategies that include access to emergency medical services and the administration for naloxone. For additional information and educational resources, review the Substance Abuse and Mental Health Services Administration (2014) Opioid Overdose T oolkit at http://store. samhsa. gov/shin/content//SMA14 -4742/Overdose_T oolkit. pdf. 5. Di scuss the need for documenting the consequences of nonadherence to the treatment plan including discontinuation. E. Encourage chronic pain support groups F. Encourage mental health provider evaluation for ongoing supportbe immediately discontinued for unsafe use of medications, diversion of prescription of medication, or alteration or forgery of pre-scriptions. Provider should treat withdrawal symptoms with noncontrolled medications or refer for addiction counseling (Chou et al., 2009; Saxe et al., 2009). x. C lients that have been dismissed from opiate treatment for agreement breaks may not receive prescriptions for controlled substances from other providers at the same institution unless that client is first reviewed by a CNP team and approved for renewal of treatment, with a plan in place to address the previous cause of dismissal, for example, showing successful completion of substance treatment program or after a break of at least 6 months (Saxe et al., 2009). 5. R eferral to mental health and substance abuse services for further management is recommended for the following indications: a. P atients with a past or current history of behav-iors suggestive of substance abuse disorder. It is recommended to include this statement in the patient's treatment agreement. b. P atients with psychosocial problems that hinder treatment of pain. c. P atients with a diagnosis of depression, anxiety, or other mental health disorders. d. P rovider's discretion: all patients may benefit from learning cognitive behavioral techniques to improve self-care and function. 6. C onsultation with pain specialist or addiction specialist is indicated when: a. P atients have significant chronic, substantiated pain that develops addiction behaviors in the context of chronic opioid therapy (IASP, 2009; Saxe et al., 2009). b. The patient's pain is not well controlled on current pain treatment plan and/or exceeds the established dose ceiling limits c. The pr ovider determines the need for consultation. d. A ll consultation is documented as part of the patient record. Not all patients have access to pain management specialists because of finan-cial, insurance, location, availability, and trans-portation barriers. In these circumstances, review of the case with a CNP team or review of the case with pain specialists by email or telephone consultation may be appropriate (Saxe et al., 2009). 491 Patient education

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

VII. Chronic pain support resources and tools A. American Pain Society: www. ampainsoc. org B. International Association for Study of Pain: www. iasp. org C. Laughter Yoga International: www. laughteryoga. org D. Self-help book, Managing Pain Before It Manages You (Caudill, 2009) E. Kaiser Permanente Chronic Pain Program and Support Group re Fere NCe S American Pain Society (2009). Guideline for the use of chronic opioid therapy in chronic noncancer pain: Evidence review. Retrieved from http:// americanpainsociety. org/uploads/education/guidelines/chronic -opioid-therapy-cncp. pdf. American Psychological Association. (2013). Diagnostic and statistical manual of mental disorders-5 (5th ed. ). Arlington, VA: American Psychological Association. American Society of Addiction Medicine (2011). American Society of Addiction Medicine (ASAM). The definition of addiction. Chevy Chase, MD: The Society. Barclay, L., & Nghiem, H. T. (2008). Primary care management of nonma-lignant pain reviewed. Medscape Multispecialty. Retrieved from www. medscape. org/viewarticle/584508. Bedard, M. E. (1997). Fact sheet on chronic non-malignant pain (CNP). American Society for Action on Pain. Retrieved from www. druglibrary. org/schaffer/asap/factsheet. html. Brown, R. L., & Rounds, L. A. (1995). Conjoint screening questionnaires for alcohol and other drug abuse: Criterion validity in a primary care practice. Wisconsin Medical Journal, 94(3), 135-140. Buckhardt, C. S., Goldenberg, D., Crofford, L., Gerwin R, Gowens, S., Jackson, K., Kugel, P., Mc Carberg, W., Rudin, N., Schanberg, L., T aylor, A. G., T aylor, J., & Turk, D. (2005). Guideline for the management of fibromyalgia syndrome pain in adults and children. p. 109 (Clinical practice guideline; no. 4). Glenview, IL: American Pain Society. Caudill, M. A. (2009). Managing pain before it manages you (3rd ed. ). New Y ork, NY: Guilford Press. Chou, R., Fanciullo, G., Fine, P., Adler, J. A., Ballantyne, J. C., Davies, P., et al. (2009). Clinical guidelines for the use of chronic opioid therapy in chronic noncancer pain. Journal of Pain, 10(2), 113-130. Cohen, S. P., & Mao, J. (2009). Concerns about consensus guidelines for QT c interval screening in methadone treatment, letters. Annals of Internal Medicine, 151(3), 216-217. Retrieved from http://annals. org /article. aspx?articleid=744638. e Med Expert. (2007-2014). Antidepressants comparison: Effexor versus Cymbalta. Retrieved from www. emedexpert. com/compare /effexor-vs-cymbalta. shtml. Federation of State Medical Boards of the United States, Inc. (2004). Model policy for the use of controlled substances for the treatment of pain. Retrieved from www. painpolicy. wisc. edu/sites/www. painpolicy. wisc . edu/files/model04. pdf. Federation of State Medical Boards of the United States, Inc. (2013). Model policy for the use of controlled substances for the treatment of pain controlled substances for the treatment of pain. Retrieved from http://www. fsmb . org/Media/Default/PDF/FSMB/Advocacy/pain_policy_july2013 . pdf Fuchs-Lacelle, S., & Hadjistavropoulos, T. (2004). Development and preliminary validation of the pain assessment checklist for seniors with limited ability to communicate (PACSLAC). Pain Management in Nursing, 5(2), 37-49. Gourlay, D. L., Heit, H. A., & Caplan, Y. H. (2010). Urine drug testing in clinical practice (4th ed. ). Baltimore, MD: Johns Hopkins University School of Medicine. Retrieved from http://issuu. com/cafamilydocs /docs/udtmonograph. Herr, K., Coyne, P. J., Key, T., Manworren, R., Mc Caffery, M., Merkel, S., et al. (2006). Pain assessment in the nonverbal patient: Position statement with clinical practice recommendations. Pain Management Nursing, 7(2), 44-52. Retrieved from http://www. medscape. com/viewarticle/533939_4. Hockenberry, M. J., & Wilson, D. (2009). Wong's essentials of pediatric nursing (8th ed. ). St. Louis, MO: Mosby. International Association for the Study of Pain. (2009). Recommendations for pain treatment services. Retrieved from http://www. iasp-pain. org /Education/Content. aspx?Item Number=1381. International Association for the Study of Pain. (2012). IASP taxonomy. Retrieved from http://www. iasp-pain. org/T axonomy#Pain International Association for the Study of Pain. (2014). Classification of Chronic Pain, Second Edition (Revised), Introduction. Retrieved at http://www . iasp-pain. org/Publications News/Content. aspx?Item Number=1673 Institute of Medicine. (2011). Relieving pain in America: A blueprint for transforming prevention, care, education, and research. Washington, DC: Author. Retrieved from www. iom. edu/~/media/Files/Report% 20Files/2011/Relieving-Pain-in-America-A-Blueprint-for -T ransforming-Prevention-Care-Education-Research/Pain% 20Research%202011%20Report%20Brief. pdf. Keefe, F. J., Somers, T. J., & Kothadia, S. M. (2009). Coping with pain. Pain Clinical Update, 17(5), 1-6. Krantz, M. J., Martin, J., Stimmel, B., Metha, D., & Haigney, M. C. P. (2009). QT c interval screening in methadone treatment. Annals of Internal Medicine, 150(6), 387-399. Retrieved from http://annals. org/article . aspx?articleid=744382. Krebs, E. E., Lorenz, K. A., Bair, M. J., Damush, T. M., Wu, J., Sutherland, J. M., et al. (2009). Development and initial validation of the PEG, a three-item scale assessing pain intensity and interference. Journal of General Internal Medicine, 24(6), 733-738. Mc Auley, D. F. (2015). Opioid (narcotic) analgesic converter. Retrieved from http://www. globalrph. com/narcoticonv. htm Medical Board of California. (2014). Guidelines for prescribing controlled substances for pain. Retrieved from www. mbc. ca. gov/Licensees /Prescribing/Pain_Guidelines. pdf. Passik, S. D., & Weinreb, H. J. (2000). Managing chronic non-malignant pain: Overcoming obstacles to the use of opioids. Advances in Therapy, 17(2), 70-80. Rosenblum, A., Joseph, H., Fong, C., Kipnis, S., Cleland, C., & Portenoy, R. K. (2003). Prevalence and characteristics of chronic pain among chemically dependent patients in methadone maintenance and residen-tial treatment facilities. JAMA, 289(18), 2370-2378. Retrieved from http://jama. ama-assn. org/content/289/18/2370. full. 492 CHAPTER 50 | Chronic Nonmalignant Pain Management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Prescription Drug Monitoring Program (PDMP). Retrieved from http:// oag. ca. gov/cures-pdmp. Substance Abuse and Mental Health Services Administration. (2014). Opioid overdose prevention toolkit. Retrieved from http://store. samhsa. gov/product/Opioid-Overdose-Prevention-T oolkit-Updated-2014 /SMA14-4742. Turk, D. (2006). Pain hurts—individuals, significant others and society! American Pain Society Bulletin, 16(1). U. S. Department of Justice. (2014). List of controlled substances. Retrieved from www. deadiversion. usdoj. gov/schedules/index. html. University of California San Francisco (UCSF), Department of Community Health Systems. (2010; 2015). Standardized procedures, unpublished manuscript, San Francisco: UCSF. Vissers, K. C., Besse, K., Hans, G., Devulder, J., & Morlion, B. (2010). Opioid rotation in the management of chronic pain: Where is the evidence? Pain Practice, 10(2), 85-93. Webster, L. R., & Webster, R. (2005). Predicting aberrant behaviors in opioid-treated patients: Preliminary validation of the Opioid Risk T ool. Pain Medicine, 6(6), 432-442. Yalcin, I., & Barrot, M. (2014). The anxiodepressive comorbidity in chronic pain. Current Opinion in Anaesthesiology, 27(5), 520-527. Saxe, J. M., Smith, V. & Mc Nerney, K. (2013). A blueprint to managing multiple chronic conditions and pain. Journal of Family Practice, 62(12), S1-S25. Saxe, J. M., Smith, V., Ligon, E. D., Mc Nerney, K., Hill, K., & Nierman, J. (2009). Glide Health Services chronic nonmalignant pain management protocol (unpublished protocol). San Francisco, CA: Glide Health Services. Spitzer, R. L., Kroenke, K., & Williams, J. B. W. (1999). Validation and utility of a self-report version of PRIME-MD: The PHQ primary care study. JAMA, 282(18), 1737-1744. State of California Board of Registered Nursing. (1998). An explanation of standardized procedure requirements for nurse practitioner practice. Retrieved from www. rn. ca. gov/pdfs/regulations/npr-b-20. pdf. State of California Board of Registered Nursing. (2004a). Nurse practitioner expanded furnishing authority for schedule II controlled substances, BPC 2836. 1. Retrieved from www. rn. ca. gov/pdfs/regulations/npr-b-51. pdf. State of California Board of Registered Nursing. (2004b). Criteria for furnishing number utilization by nurse practitioners. Retrieved from www. rn. ca. gov/pdfs/regulations/npr-i-16. pdf. State of California Department of Justice. (2014). Controlled Substance Utilization Review and Evaluation System (CURES), California 493 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

the risk is 90% (without HBV vaccine and HBIG). Risk of acute HBV infection has been dramatically reduced by universal HBV vaccination. 3. H BV Natural History Natural history of HBV has stages—initially after infection, patients often have high HBV DNA and HBe Ag is present. In late childhood and early adult-hood, most patients with chronic infection develop inactive chronic HBV with low-level HBV DNA and normal alanine aminotransferase (ALT) and loss of HBe Ag, and later in life it can reactivate with elevated ALT and high-level HBV DNA and can have reactiva-tion of HBe Ag. Patients can move between active and inactive HBV, but typically antiviral treatment is used during active phases. High HBV DNA levels increase the risk of cirrhosis and HCC and HCC can develop in the absence of cirrhosis (Lok & Mc Mahon, 2009). 4. H BV Screening Screening for HBV with HBs Ag is recommended for many demographic groups including Alaskan natives; persons born in endemic areas; first-generation immi-grants from Southeast Asia; injection drug users; men who have sex with men; persons with HCV, HIV, and alcohol use; and long-term hemodialysis. B. Chronic hepatitis C 1. D efinition and Overview The hepatitis C virus (HCV) is a single-stranded, enveloped RNA virus from the flaviviridae family. Exposure to HCV results in chronic infection in 75-80% of the cases. Persistence of HCV RNA in the serum for 6 months or more after exposure results in chronic HCV infection. HCV replicates with a high mutation rate, thereby resulting in heterogeneity within the HCV genome. HCV has six major genotypes (1-6) with subtypes (1a, 1b, 2a, 2b, etc) within the genotypes. Genotype 1 is the most common genotype in the United States, accounting for approximately 70% of the population. I. Intr oduction and general background The liver is the largest solid organ in the body, weighing approx-imately 1-1. 5 kg. The majority of cells in the liver consist of hepatocytes. Hepatocytes are responsible for the synthesis of serum proteins (albumin, coagulation factors, many hormonal and growth factors), the production of bile, the regulation of nutrients, and metabolism and conjugation of lipophilic com-pounds for excretion in the bile or urine. Although there are many causes of liver diseases, one of the most common is viral hepatitis. Chronic viral hepatitis is defined by the persistence of viral infection for 6 months or more after initial exposure. The primary causes of chronic viral hepatitis are hepatitis B virus (HBV) and hepatitis C virus (HCV). Potential long-term complications of chronic viral hepatitis include cirrhosis, decompensated liver disease, and hepatocellular carcinoma (HCC) and are the leading indication for liver transplantation in the United States (Ghany & Hoofnagle, 2005). A. Chronic hepatitis B 1. D efinition and Overview Chronic HBV is defined as persons positive for hepatitis B surface antigen (HBs Ag) for more than 6  months. Worldwide, there are 350 million individuals with chronic HBV, and in the United States, there are approximately 1. 25 million. HBV is a DNA virus from the hepadnavirus family. It replicates by forming an RNA intermediate, which is copied using reverse transcriptase to generate DNA strands (Lavanchy, 2004; Mc Quillan et al., 1999). 2. H BV Prevalence/Incidence In the United States, the prevalence is approximately 1% of the population. The prevalence is greatest in Alaskan natives, first-generation immigrants from Southeast Asia, injection drug users, and men who have sex with men. After an acute HBV infection, the risk of developing chronic infection varies with age. In an adult, the risk is approximately 10%. In a newborn, Miranda Surjadi Chron IC VIral h epat I t IS© Eliks/Shutterstock; © donatas1205/Shutterstock 494 51Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

ii. Obs tetrical/gynecological history: Recent pregnancy may flare HBV; risk of transmission to fetus and efficacy of hepatitis B immunoglobulin (HBIG)/HBV vaccine will depend on level of maternal HBV DNA. iii. E xposure history: Born in endemic area, parents born in endemic area, healthcare worker, sexual exposure, injection drug use (IDU) iv. M edication history: a. M edications that can cause flare-up of HBV such as steroids, chemotherapy, biologic agents (TNF-alpha inhibitors) b. H epatotoxic medications, such as tuberculosis (TB) medications, meth-otrexate, statins, etc. b. F amily history i. C hronic hepatitis B ii. H epatocellular carcinoma c. O ccupational/environmental history i. W ork-related exposures: healthcare worker d. P ersonal/social history i. S exual history, illicit drug use, alcohol use ii. H ousehold contacts e. R eview of systems i. C onstitutional signs and symptoms: Fatigue, weight loss, fevers/chills (acute HBV) ii. S kin, hair, and nails: Itching, bruising iii. Ea r, nose, and throat: Jaundice iv. C hest: Gynecomastia v. C ardiac: Shortness of breath, chest pain, palpitations vi. A bdomen: Abdominal pain, nausea, vomit-ing, clay-colored stools vii. Ge nitourinary: Dark urine viii. M usculoskeletal: Joint pains ix. E xtremities: Pedal edema x. N eurological: Confusion, tremors, sleep/ wake cycle disturbances 2. C hronic Hepatitis C a. P ast health history i. M edical illnesses: HIV, coinfected with hepatitis B, NAFLD, other illnesses that may affect liver function/enzymes. Cardiopulmonary diseases (if ribavirin is to be used in treatment). ii. Obs tetrical/gynecological history: a. M other to child transmission is < 5% (except with HIV coinfection, then risk is 20%). b. B reastfeeding in HCV-infected mother is safe for the baby. iii. E xposure history: IDU, blood transfusions, sexual exposure, needlestick exposure Genotypes 2 and 3 account for 25% of the U. S. popu-lation. Genotypes 4, 5, and 6 are rare and account for the remainder. Genotypes do not influence progres-sion of liver disease, but genotype is a major determi-nant of treatment regimens. 2. HC V Prevalence/Incidence It is estimated that 180 million people are infected with hepatitis C worldwide. In the United States, it is estimated that there are 3. 9 million individuals infected with HCV. The prevalence is highest in people born between 1945 and 1965 and individuals with a history of injection drug use, blood transfu-sions before 1992, and HIV infection. Incidence has declined since screening for HCV in blood banks and use of needle exchange programs. 3. HC V Natural history Chronic HCV infection has variable rates of fibrosis progression. It is estimated that cirrhosis develops in 15-30% of cases. On average, cirrhosis will take 20-30 years to develop in immunocompetent adults. Alcohol, HIV, metabolic syndrome, and coinfection with other hepatitis viruses will increase the likeli-hood of developing cirrhosis and hasten the devel-opment of cirrhosis (Ghany et al., 2009). The  risk for hepatocellular carcinoma is 1-5% per year in persons with chronic HCV and cirrhosis (Ghany et al., 2009). 4. HC V Screening It is estimated that 50% of persons with HCV in the United States are unaware of their infection. New recommendations from the Centers for Disease Control and Prevention and the U. S. Preventive Services T ask Force are that all persons born between 1945 and 1965 have a one-time HCV antibody test, regardless of risk factor. Additionally, persons with risk factors (e. g., any history of injection drug use even once) should be tested for HCV Ab, and in persons with ongoing risk behaviors, periodic screening should be continuously performed. II. Database (may include but is not limited to) A. Subjective 1. C hronic Hepatitis B a. P ast health history i. M edical illnesses: HIV, coinfection with hepatitis C or D, hepatitis A, nonalcoholic fatty liver disease (NAFLD), diabetes mellitus, hyperlipid-emia, obesity, other illnesses which may affect liver enzymes or liver function495 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

iv. M edication history: Hepatotoxic medications such as TB medications, methotrexate, statins etc. b. F amily history i. Othe r viral hepatitis ii. H epatocellular carcinoma c. P ersonal/social history i. I DU, other illicit drugs, alcohol intake ii. H ousing, access to phone, refrigerator if needed iii. M ental health/psych history: suicidal/ homicidal ideation if pegylated interferon will be used as part of HCV treatment d. R eview of systems i. C onstitutional signs and symptoms: Fatigue, fevers/chills (acute HCV) ii. S kin: Jaundiced, itchy, bruising iii. Ea r, nose, and throat: Jaundiced iv. C ardiac: Shortness of breath, chest pain, palpitations v. A bdomen: Abdominal pain, nausea, vomit-ing, clay-colored stools vi. Ge nitourinary: Dark urine vii. M usculoskeletal: Joint pains viii. E xtremities: Pedal edema ix. N eurological: Confusion, tremors, sleep/ wake cycle disturbances B. Objective 1. P hysical exam findings (see T able 51-1) 2. S upporting data from relevant diagnostic tests (see T ables 51-2, 51-3, and 51-4)Table 51-1 Physical Examination Findings Condition Associated Findings (may or may not include): Chronic Hepatitis B and CAssess: 1. Vital Signs: temperature, heart rate 2. General Appearance: lethargy (hepatic encephalopathy) 3. Skin/hair: jaundiced, pruritus, bruising (cirrhosis) 4. Eyes: icteric sclerae (cirrhosis) 5. Chest/Lungs: spider nevi, gynecomastia, crackles (from right heart failure due to portal hypertension) 6. Cardiovascular: increased jugular venous pressure (due to right heart failure from portal hypertension) 7. Abdomen: ascites, fluid wave, caput medusae, hepatomegaly, splenomegaly (cirrhosis) 8. Extremities: palmar erythema, pedal edema (cirrhosis) 9. Neurological: asterixis, tremors, behavioral changes (hepatic encephalopathy) 10. Genitourinary: testicular atrophy, dark urine (cirrhosis) Table 51-2 HBV Serologic T ests Test Clinical Implications Comments Hepatitis B surface antigen (HBs Ag) If positive for 6 months or more, denotes chronic infection Hepatitis B core antibody Ig G (Ig G anti-HBc) Past exposure to HBV Hepatitis B core antibody Ig M (Ig M anti-HBc) Acute exposure to HBV Reactivation of chronic infection Hepatitis B surface antibody (HBs Ab) Immunity to HBV Vaccine induced immunity will not have positive anti-HBc Hepatitis B DNA (HBV DNA) Active viral replication May be present in inactive disease state, but usually < 2,000 IU/m L Hepatitis B E antigen (HBe Ag) Active viral replication May be negative in those with a precore mutant HBV Hepatitis B E antibody (HBe Ab) Low replicative state Hepatitis D virus RNA virus that needs HBs Ag to replicate Consider ordering if coinfection of HDV is suspected Hepatitis B genotype and resistance Quasispecies of HBV (genotype A responds well to pegylated interferon) Resistance to antiviral medications based on mutations of HBVConsider ordering if past resistance to antiviral therapy is suspected or when considering pegylated interferon therapy. 496 CHAPTER 51 | Chronic Viral Hepatitis

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 51-3 Common Liver T ests Function test Definition Clinical Implications Comments Marker of hepatocellular injury Aspartate amino-transferase (AST)Found mainly in hepatocytes. Released into bloodstream when there is liver injury Increased in viral hepatitis AST :ALT ratio 2:1 in alcoholic hepatitis Found in liver, heart skeletal muscle, brain Marker of hepatocellular injury Alanine amino-transferase (ALT)Found mainly in hepatocytes. Released into bloodstream when there is liver injury Increased in viral hepatitis ALT > AST in chronic viral hepatitis Found in liver Marker of cholestatic injury Alkaline phosphatase Canicular enzyme that plays a role in bile production Increased in hepatobiliary disease, bone disease, pregnancy, hyperparathyroidism Found in liver, bone, intestine, and placenta Marker of cholestatic injury Bilirubin Breakdown product of hemolysis. Taken up by liver cells and conjugated to water soluble product. Excreted in bile. Elevations may indicate hepatic or extrahepatic disorder Hepatitis and cirrhosis causes conjugated hyperbilirubinemia Marker of liver function Albumin Major component of plasma proteins. Liver synthesizes albumin Decreased in cirrhosis from chronic liver disease. Also decreased in nephrotic syndrome, malabsorption, protein losing enteropathy Indication of severity of liver disease Marker of liver function Prothrombin time Liver produces clotting factors I, II, V, VII, and X. Prothrombin time depends on the activity of these clotting factors. Increased in cirrhosis from chronic liver disease. Also increased with coumadin, vitamin K deficiency Vitamin K is needed to activate some of the clotting factors. Table 51-4 HCV Serologic tests test Definition Clinical Implications Comments Hepatitis C Antibody (HCV Ab)Detects antibodies to hepatitis C virus Positive in patients who have been exposed to hepatitis CWill stay positive even if HCV treatment is successful and sustained virologic response is achieved. HCV RNA Determines HCV viral load and determines if HCV RNA is undetectable Positive in patients with chronic hepatitis C. Useful in monitoring response to HCV therapy . HCV RNA values will fluctuate. Values do not correlate with liver disease progression. Hepatitis C genotype Genotype 1-6 and subtype a or b Necessary for determining appropriate HCV treatment regimen and duration497 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

III. a ssessment A. Determine the diagnosis 1. C hronic hepatitis B (see T ables 51-2 and 51-5) 2. C hronic hepatitis C (see T able 51-4) 3. Othe r conditions that may explain the patient's elevated liver function tests (LFT s) a. Aut oimmune hepatitis: antinuclear antibody (ANA)/antismooth muscle antibody positive; chronic necroinflammatory liver disease of unknown etiology b. N onalcoholic steatohepatitis (NASH)/ NAFLD: associated with diabetes mellitus, hyperlipid-emia, obesity c. P rimary biliary cirrhosis: antimitochondrial antibody positive in 95%; chronic cholestatic liver disease more common in women age 50 and older d. H emochromatosis: most common genetic dis-order in the Caucasian population. The extent of liver injury is associated with the accumulation of hepatic iron. e. W ilson's disease: autosomal recessive defect of cellular copper export; decreased ceruloplasmin f. A lpha-1 antitrypsin deficiency: genetic disorder that affects lungs and liver g. P rimary sclerosing cholangitis: chronic biliary duct inflammation; associated with inflamma-tory bowel disease B. Severity Assess the severity of the liver disease and deter-mine if patient has cirrhosis or intact liver function (normal platelets, albumin, total bilirubin, prothrombin time/international normalized ratio). Decompensated liver disease is manifested by history of ascites, pedal edema, encephalopathy, and/or variceal bleeding. These patients should be referred to a liver transplant center for evaluation and treatment. Calculate MELD (Model for End-Stage Liver Disease) score (United Network for Organ Sharing, 2015). Allocation calculators: https://www. unos. org/transplantation/allocation-calculators/). If MELD score is 10 or greater, refer to liver transplant center. C. Significance Assess the significance of the problem to the patient and significant others. Discuss transmission and vaccinate appropriately. D. Motivation and ability Determine the patient's willingness and ability to follow the treatment plan. IV. Goals of clinical management A. Hepatocellular carcinoma (HCC) screening/surveillance 1. C hoose a cost-effective approach for screening. B. Treatment goals 1. C hronic HBV: a. C onvert HBs Ag positive to HBs Ag negative (very rare) b. C onvert HBe Ag positive to negative with the development of anti-HBe. c. H BV DNA undetectable d. N ormalization of liver enzymes 2. C hronic HCV: a. Go al of hepatitis C therapy is elimination of the virus from the bloodstream, as defined by a sustained virologic response (SVR), consid-ered a virologic cure. SVR is defined by a HCV RNA that becomes undetectable during treat-ment and remains undetectable 3 months after completion of HCV therapy. Evidence supports that achieving an SVR will significantly reduce the likelihood of progression to cirrhosis, development of hepatocellular carcinoma, and development of end stage liver disease. Patients who achieve SVR will continue to have HCV antibodies but no longer have detectable HCV RNA in their serum, liver tissue, or mononucle-ar cells. HCV treatment should be considered for all HCV patients, weighing the benefits of potential SVR in light of other medical prob-lems and life expectancy. Table 51-5 Interpretation of Chronic HBV Serologies Chron IC hepat It IS B r eplicative p hasen onreplicative p hase HBs Ag + + HBs Ab--HBc Ab (total) + + HBe Ag +/--HBe Ab-+/-ALT normal or elevatednormal HBV DNA ≥ 2,000 IU/m L < 2,000 IU/m L498 CHAPTER 51 | Chronic Viral Hepatitis

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

b. Ge notype 1: SVR in 95-100% of patients with 12-24 weeks of HCV therapy. c. Ge notype 2: SVR 94-100% with 12-16 weeks of HCV therapy d. Ge notype 3: SVR 84-97% with 12-24 weeks of HCV therapy e. Ge notype 4: SVR 95-100% with 12-24 weeks of HCV therapy f. Ge notypes 5 and 6: SVR 96-100% with 12 weeks of HCV therapy. Genotypes 4, 5, and 6 are very rare in the United States. g. C irrhotic patients and previous nonresponders to HCV therapy tend to have decreased SVR rates. C. Patient adherence 1. S elect an approach that maximizes patient adherence (i. e., all-oral regimen and easy dosing instructions). V. p lan A. HCC Screening/ Surveillance The American Association for the Study of Liver Diseases (AASLD) guidelines recommends screening with abdominal ultrasound every 6 months. Measurement of alpha fetoprotein (AFP) is optional but not necessary for screening, and AFP alone is not recommended as a screen-ing tool, unless in rare cases where imaging is not available. Imaging is the necessary technique for HCC screening. Whom to screen: 1. A ll patients with cirrhosis 2. A ll patients with family history of HCC 3. I n chronic hepatitis B patients: a. A ll Asian men 40 years and older b. A ll Asian women 50 years and older c. A ll Africans 20 years and older d. P atients above 40 years with an elevated ALT and HBV DNA > 2,000 IU/m L should be considered for HCC surveillance. B. Diagnostic Tests 1. C hronic hepatitis B: The detection of HBs Ag at 6 months after time of infection defines chronic HBV. Most patients with HBs Ag will also have detectable HBV DNA at some level. Patients with normal ALT and low level HBV DNA (< 2,000 IU/m L) are considered inactive chronic HBV, whereas patients with elevated ALT and higher levels of HBV DNA are considered chronic HBV. a. C omplete blood count (CBC), complete meta-bolic panel, coagulation tests (PT/INR) b. H BV DNA, HBe Ag anti-HBe. c. H IV d. H epatitis serologies: Hepatitis C Ab, Hep A total Ab, Hepatitis D Ab (if coinfection is suspected) e. Othe r tests to rule out other types of liver diseases if etiology is not certain: ANA, iron studies, anti-mitochondrial antibody (AMA), antismooth muscle antibody, ceruloplasmin, lipids, glucose (gastroenterology [GI]/hepatology specialist may order these tests) f. I maging—see special populations who need HCC surveillance g. F ibrosis testing—newer and noninvasive tests for fibrosis testing are preferable to liver biopsy if available. Some blood test markers (e. g., Fibrosure) are becoming more widely available. T ransient elastography is a technique used to estimate liver stiffness (e. g., Fibroscan) but is not as widely available. Liver biopsy is still consid-ered the gold standard for staging fibrosis but is less often performed than in the past and is rarely required for treatment initiation. 2. C hronic hepatitis C: If HCV antibody is positive, then confirm chronic HCV infection with an HCV RNA test. Formerly, HCV RNA tests were categorized as quantitative or qualitative but as RNA testing has developed greater sensitivity, extremely low levels of RNA are detectable and most assays are able to determine quantitative measurements as well as low-level qualitative virus detection. a. I f HCV RNA negative, then recheck in 6 months to confirm resolved Hepatitis C. Two negative HCV RNA tests 6 or more months apart will confirm resolved hepatitis C. b. I f HCV RNA is positive, then you have con-firmed chronic HCV. There is no need to use HCV RNA as a monitoring tool for liver disease progression. HCV RNA, both qualitative and quantitative, is used primarily in the setting of HCV therapy. i. C BC, complete metabolic panel, coagula-tion studies ii. HC V genotype iii. H IV iv. A FP v. H epatitis serologies: Hep Bs Ag, Hep Bs Ab, Hep Bc Ab, Hep A total Ab (vaccinate for Hep A and Hep B if not immune) vi. Othe r tests to rule out other types of liver diseases if etiology is uncertain: ANA, iron studies, AMA, antismooth muscle antibody, ceruloplasmin, lipids, glucose (GI/hepatology specialist may order these) vii. B aseline imaging to look for cirrhosis499 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

is persistently > 2,000 IU/m L for 6 months or more. b. F ollow HCC surveillance guidelines for all chronic hepatitis B patients (both active and inactive) c. V accinate for hepatitis A if not immune 2. C hronic hepatitis C. See T able 51-7 for a list of medications for the treatment of chronic hepatitis C and T able 51-8 for an explanation of the classification system and level of evidence noted in T able 51-7. a. W ho and when to refer to specialist for HCV treatment: i. HC V treatment should be considered for all patients. Patients with an urgent need for treatment are those with:a. Adv anced fibrosis or cirrhosis (liver biopsy stage 3-4 fibrosis by Metavir staging) b. L iver transplant recipients c. S evere extrahepatic manifestations of HCVi. M ixed cryoglobulinemia with end organ manifestations (i. e., vasculitis) ii. P roteinuria, nephritic syndrome, or membranoproliferative glomer-ulonephritis ii. The fo llowing groups of patients should be considered high priority for HCV treatment:a. S tage 2 fibrosis b. H IV coinfection c. H BV coinfection d. Othe r coexistent liver disease condi-tions (i. e., NASH/NAFLD) e. D ebilitating fatigue iii. The fo llowing group of patients present an elevated risk of increased transmission of HCV and HCV treatment may result in decrease of transmission:a. M en who have sex with men with high-risk sexual practices (MSM) b. Act ive IDU c. I ncarcerated persons d. Thos e on long-term hemodialysis e. HC V-infected women of childbearing age b. C hronic HCV patients who are being followed by primary care providers (those who are not currently receiving treatment)i. C irrhotic patients: a. HC C surveillance b. M onitor MELD score every 3-6 months: INR, total bilirubin, albumin, creatinine, AST, ALT, plateletsviii. L iver biopsy for staging or diagnosing of liver disease if indicated to start treat-ment (usually this is ordered by the GI/hepatology specialist). C. Management 1. C hronic hepatitis B (see T able 51-6 for a list of medications for chronic HBV treatment)—Refer chronic HBV patients to specialists when they are in chronic active, replicative phase (see T able 51-5) If hepatitis B surface antigen is positive: a. H epatitis B E antigen positive i. A lanine aminotransferase (ALT) elevated ii. H BV DNA ≥ 20,000 IU/m L iii. R efer to specialist for treatment b. H epatitis B E antigen negative i. A LT elevated ii. H BV DNA ≥ 2,000 IU/m L iii. R efer to specialist for treatment c. C irrhotics—Refer all to specialist for treatment despite ALT or HBV DNA level d. C oinfection with hepatitis D—Refer to specialist for treatment despite ALT or HBV DNA level e. I nactive chronic hepatitis B or isolated positive hepatitis B core antibody who are about to undergo immunosuppressive therapy. Refer to specialist for treatment despite ALT or HBV DNA level f. I nactive chronic hepatitis B i. A LT normal ii. H BV DNA < 2,000 IU/m L iii. F ollowed by primary care provider every 6 months: ALT, HBV DNAa. R efer to specialist when ALT becomes abnormal or if HBV DNA Table 51-6 T reatment for Chronic HBV Patients Generic name Dose r esistance r ate Lamivudine 100 mg daily 14-32% in 1 year Adefovir 10 mg daily 29% in 5 yrs*Entecavir 0. 5 mg, 1 mg daily 1. 2% in 5 yrs 7. 8% in 2 years if lamivudine resistance is present Telbivudine 600 mg daily 25% in 2 yrs *Tenofovir 300 mg daily None*Pegylated interferon180 mcg SQ weekly x 48 weeks None *Considered first-line treatment. Entecavir 1 mg used for patients with past treatment experience to lamivudine and decompensated cirrhotic patients. 500 CHAPTER 51 | Chronic Viral Hepatitis

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

c. R efer to liver transplant/liver specialist when appropriate for evaluation and treatment (if MELD > 12). d. V accinate for hepatitis A and B. e. P atient education: avoid alcohol, low-salt diet, avoid raw fish/shellfish, avoid Table 51-7 Initial T reatment of Chronic Hepatitis C: Recommendations from the American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) (2015) Genotype 1a Ledipasvir 90 mg/sofosbuvir 400 mg 1 tablet daily for 12 weeks. SVR 97-99% (Class I, Level A). Paritaprevir 150 mg/ritonavir 100 mg/ombitasvir 25 mg daily plus dasabuvir 250 mg and weight-based ribavirin twice daily for 12 weeks (no cirrhosis, SVR 95%) or 24 weeks (cirrhosis, SVR 95%) (Class I, Level A). Simeprevir 150 mg daily plus sofosbuvir 400 mg daily with or without weight-based ribavirin for 12 weeks (no cirrhosis, SVR 95%) or 24 weeks (cirrhosis, SVR 100%) (Class IIa, Level B) Daclatasvir 60 mg plus sofosbuvir 400 mg daily for 12 weeks (no cirrhosis) and 24 weeks (with cirrhosis) with or without weight based ribavirin. SVR 96% Class I, Level B (no cirrhosis); Class IIa, Level B (cirrhosis) Genotype 1b Ledipasvir 90 mg/sofosbuvir 400 mg 1 tablet daily for 12 weeks. SVR 97-99% (Class I, Level A) Paritaprevir 150 mg/ritonavir 100 mg/ombitasvir 25 mg daily plus dasabuvir 250 mg for 12 weeks (no cirrhosis, SVR 99%). The addition of weight-based ribavirin is recommended for cirrhotic patients, SVR 98. 5% (Class I, Level A) Simeprevir 150 mg daily plus sofosbuvir 400 mg daily with or without weight-based ribavirin for 12 weeks (no cirrhosis, SVR 95%) or 24 weeks (cirrhosis, 100%) (Class IIa, Level B) Daclatasvir 60 mg plus sofosbuvir 400 mg daily for 12 weeks (no cirrhosis) and 24 weeks (with cirrhosis) with or without weight based ribavirin. SVR 96% Class I, Level B (no cirrhosis); Class IIa, Level B (cirrhosis) Genotype 2 Sofosbuvir 400 mg daily plus weight-based ribavirin for 12 weeks. SVR 94% (Class I, Level A). Sofosbuvir 400 mg daily plus weight-based ribavirin for 16 weeks is recommended in patients with cirrhosis (Class IIb, Level C) Daclatasvir 60 mg plus sofosbuvir 400 mg daily for 12 weeks is recommended for patients who cannot tolerate ribavirin. SVR 92%. (Class IIa, Level B) Genotype 3 Sofosbuvir 400 mg daily plus weight-based ribavirin for 24 weeks. SVR 84% (Class I, Level B). Sofosbuvir 400 mg daily plus weight-based ribavirin plus weekly pegylated interferon for 12 weeks. SVR 97% (Class IIa, Level A). Daclatasvir 60 mg plus sofosbuvir 400 mg daily for 12 weeks (no cirrhosis) and 24 weeks (with cirrhosis) with or without weight based ribavirin. SVR 90-97%. Class I, Level A (no cirrhosis); Class IIa, Level C (cirrhosis) Genotype 4 Ledipasvir 90 mg/sofosbuvir 400 mg 1 tablet daily for 12 weeks. SVR 95% (Class IIb, Level B). Paritaprevir 150 mg/Ritonavir 100 mg/ombitasvir 25 mg daily plus weight-based ribavirin for 12 weeks. SVR 100% (Class I, Level B). Sofosbuvir 400 mg plus weight-based ribavirin for 24 weeks. SVR 100% (Class IIa, Level B). Genotype 5 Sofosbuvir 400 mg daily plrus weight-based ribavirin plus weekly pegylated interferon for 12 weeks. SVR 100% (Class IIa, Level B). Genotype 6 Ledipasvir 90 mg/sofosbuvir 400 mg 1 tablet daily for 12 weeks. SVR 96% (Class IIa, Level B). Sofosbuvir 400 mg daily plus weight-based ribavirin plus weekly pegylated interferon for 12 weeks. SVR 100% (Class IIa, Level B). *HIV/HCV coinfected persons should be treated the same as persons without HIV infection after managing potential interactions with antiretroviral medications. nonsteroidal anti-inflammatories, and limit acetaminophen with a maximum of 2,000 mg daily 3. C hronic HCV—no evidence of cirrhosis a. M onitor ALT/AST every 6-12 months as needed501 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

b. HC V RNA monitoring is not necessary unless during treatment and in the 6 months after treatment c. V accinate for hepatitis A and B d. P atient education: avoid alcohol, support groups e. U pdate patients on future HCV therapies and refer when appropriate for treatment of chronic HCV D. Client education 1. C hronic hepatitis C treatment side effects a. A ll new oral agents for hepatitis C have very few if any side effects. See T able 51-9 if patients are taking pegylated interferon and/or ribavirin for a list of side effects. b. Adv ice for patients currently undergoing treat-ment with pegylated interferon and ribavirin:i. Dr ink plenty of clear liquids. T ry to drink between 8 and 10 glasses of water or another clear liquid every day. Increase this amount if you are vomiting. ii. A void drinks that have alcohol, caffeine (coffee, cola, and strong tea) or lots of sugar (most soft drinks). iii. T ry to get plenty of sleep at night. T ake short naps during the day. iv. Ea t small, nutritious meals. Crackers, clear sodas, and ginger ale can help settle your stomach. Greasy, high-fat foods (including most fast food) can make you feel worse. T ry to eat even if you are not very hungry. v. E xercise lightly. Walking and lifting light weights are good exercises while you are on treatment. Table 51-8 Classification System and Levels of Evidence Classification Description Class I Conditions for which there is evidence and/or general agreement that a given diagnostic evaluation, procedure, or treatment is beneficial, useful, and effective Class II Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness and efficacy of a diagnostic evaluation, procedure, or treatment Class IIa Weight of evidence and/or opinion is in favor of usefulness and efficacy Class IIb Usefulness and efficacy are less well established by evidence and/or opinion Class III Conditions for which there is evidence and/or general agreement that a diagnostic evaluation, procedure, or treatment is not useful and effective or if it in some cases may be harmful Level of Evidence Description Level A Data derived from multiple randomized clinical trials, meta-analyses, or equivalent Level B Data derived from a single randomized trial, nonrandomized studies, or equivalent Level C Consensus opinion of experts, case studies, or standard of care Table 51-9 Side Ef fects of Pegylated Interferon and Ribavirin Drug Side Effects Pegylated interferon Flulike symptoms Depression/anxiety/irritability Complete blood count abnormalities: neutropenia, thrombocytopenia Anorexia, nausea, diarrhea, vomiting (rare) Alopecia Skin irritation around shot Thyroid abnormalities (rare) Retinal disorders (rare) Ribavirin Anemia Insomnia Birth defects (need double contraception) Rash/pruritus Numbness/tingling in extremitiesvi. T ake your medicine before you go to bed, so that you can sleep through the side effects. vii. T ake any pain relievers recommended by your doctor. T aking a pain reliever about a half hour before your pegylated interferon injection can help make the side effects less severe. Do not take any pain reliever, how-ever, unless your doctor says it is okay. 502 CHAPTER 51 | Chronic Viral Hepatitis

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Feld, J. J., Kowdley, K. V., Coakley, E., Sigal, S., Nelson, D. R., Crawford, D., et al. (2014). T reatment of HCV with ABT-450/r-ombitasvir and dasabuvir with ribavirin. New England Journal of Medicine, 370(17), 1594-1603. Ghany, M., & Hoofnagle, J. H. (2005). Approach to the patient with liver disease. In D. L. Kasper, A. S. Fauci, D. L. Longo, E. Braunwald, S. L. Hauser, & J. L. Jameson, Harrison's principles of internal medicine (pp. 1808-1813). New Y ork: Mc Graw-Hill. Ghany, M. G., Strader, D. B., Thomas, D. L., & Seeff, L. B. (2009). Diagnosis, management, and treatment of hepatitis C: An update. Hepatology, 49(4), 1335-1374. Jacobson, I. M., Gordon, S. C, Kowdley, K. V., Y oshida, E. M., Rodriguez-T orres, M. Sulkowski, M. S., et al. (2013). Sofosbuvir for hepatitis C genotype 2 or 3 in patients without treatment options. New England Journal of Medicine, 368(20), 1867-1877. Kowdley, K. V., Gordon, S. C., Reddy, K. R., Rossaro, L., Bernstein, D. E., Lawitz, E., et al. (2014). Ledipasvir and sofosbuvir for 8 or 12 weeks for chronic HCV without cirrhosis. New England Journal of Medicine, 370(20), 1879-1888. Lavanchy, D. (2004). Hepatitis B virus epidemiology, disease burden, treat-ment, and current and emerging prevention and control measures. Journal of Viral Hepatitis, 11(2), 97-107. Lawitz, E., Mangia, A., Wyles, D., Rodriguez-T orres, M., Hassanein, T., Gordon, S. C., et al. (2013). Sofosbuvir for previously untreated chronic hepatitis C infection. New England Journal of Medicine, 368(20), 1878-1887. Lawitz, E., Poordad, F. F., Pang, P. S., Hyland, R. H., Ding, X., Mo, H., et al. (2014). Sofosbuvir and ledipasvir fixed dose combination with or with-out ribavirin in treatment naïve and previously treated patients with genotype 1 hepatitis C virus infection (LONESTAR): An open label randomized, phase 2 trial. Lancet, 383(9916), 515-523. Lawitz, E., Sulkowski, M. S., Ghalib, R., Rodriguez-T orres, M., Y ounossi, Z. M., Corregidor, A., et al. (2014). Simeprevir plus sofosbuvir, with or without ribavirin, to treat chronic infection of hepatitis C virus genotype 1 in non-responders to pegylated interferon and ribavirin and treatment naïve patients: The COSMOS randomized study. Lancet, 384(9956), 1756-1765. Lok, A. S., & Mc Mahon, B. J. (2009). Chronic hepatitis B: Update 2009. Hepatology, 50(3), 1-36. Mc Quillan, G. M., Coleman, P. J., Kurszon-Moran, D., Moyer, L. A., Lambert, S. B., & Margolis, H. S. (1999). Prevalence of hepatitis B virus infection in the United States: The National Health and Nutrition Examination Surveys. American Journal of Public Health, 89(1), 14-18. Shiffman, R. N., Shekelle, P., Overhage, J. M., Slutsky, J., Grimshaw, J., & Deshpande, A. M. (2003). Standardized reporting of clinical practice guidelines: A proposal from the Conference on Guideline Standardization. Annals of Internal Medicine, 139(6), 493-498. Swain, M. G., Lai, M. Y., Shiffman, M. L., Cooksley, W. G., Zeuzem, S., Dieterich, D. T., et al. (2010). A sustained virologic response is durable in patients with chronic hepatitis C treated with peginterferon alfa-2a and ribavirin. Gastroenterology, 139(5), 1593-1601. United Network for Organ Sharing. (2015). Allocation calculators. Retrieved at https://www. unos. org/transplantation/allocation-calculators/viii. A void situations or “triggers” that make you feel worse, such as loud noises, bright lights, strong odors, and/or skipped meals. ix. D o not color or perm your hair until after your treatment is finished. x. D o not use harsh detergents or soaps that might irritate your skin. xi. S imple, unscented lotions can help dry, itchy skin. If taking ribavirin gives you a rash, Benadryl lotion might help. c. F or patients who are having mood symptoms on pegylated interferon and ribavirin therapyi. T alk about your feelings with a family member, friend or someone else that you trust. ii. T ell people close to you when you are taking your HCV treatment. T ell them that it can affect your moods. iii. J oin a support group. iv. A void things that can make you feel stressed, like too much caffeine, sugar, or nicotine. v. L earn ways to relax. Meditate or breathe quietly. Go for a walk or do some other light exercise. vi. T ake care of your body. Eat healthy meals, get lots of sleep and drink plenty of water. vii. I f you are taking medicine because you are depressed, be sure not to skip a dose. Keep all of your appointments with your psychia-trist or therapist. VI. Self-management r esources and tools A. Patient/client education 1. A merican Association for the Study of Liver Diseases, www. aasld. org 2. N ational Institute of Diabetes and Digestive and Kidney Diseases, http://www2. niddk. nih. gov/ 3. A merican Liver Foundation, www. liverfoundation. org/ re Feren Ce S American Association for the Study of Liver Diseases & Infectious Diseases Society of America. (2015). HCV guidance: Recommendations for testing, managing, and treating hepatitis C. Retrieved from www. hcvguidelines. org/full-report/when-and-whom-initiate-hcv-therapy. 503 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

memory function), the disease eventually affects multiple regions of the brain. Neuronal death is caused by the overaccumulation of amyloid plaques and neurofibrillary tangles. The strongest risk factor for AD is advanced age, although prior head injury, family history of AD, and cardiovascular factors, such as hypertension, pose increased risk for development of AD. When AD occurs in a person younger than age 65, it is referred to as presenile, early age onset, younger onset, or early onset AD. Most cases of AD are not familial, although genetic risk increases in presenile AD when a first-degree relative has AD and in the presence of certain genetic mutations. 2. P revalence One in nine people age 65 and older have AD, whereas one in three people age 85 and older have AD. More women than men have AD largely because women typically live longer than men. It is estimated that a growing number of Americans will live into their 80s and 90s, resulting in even greater numbers of people with dementia. B. Vascular dementia 1. D efinition and overview Vascular dementia (also called multi-infarct dementia) is caused by cerebrovascular ischemia and lacunar infarcts in the brain (often referred to as white matter disease). Symptoms are similar to AD, although the onset may be more easily identified and the progres-sion of symptoms can be characterized by “stepwise” changes reflecting the occurrence of strokes. Risk factors include strokes, hypertension, hypercholes-teremia, and diabetes. Vascular dementia may coexist with AD or DLB. 2. P revalence Vascular dementia is considered the second most common cause for dementia, occurring in approxi-mately 20-30% of people with dementia (Plassman et al., 2007; Rizzi, Rosset, & Roriz-Cruz, 2014). I. Intr oduction and general background Dementia refers to diseases and conditions characterized by decline in cognitive function that negatively affects a person's abilities to perform daily activities (Alzheimer's Association, 2014). Dementia is typically a slowly progressive disease caused by damage and death of neurons in the brain. The definition of dementia has been recently categorized as a neurocogni-tive disorder that is either mild (cognitive impairment with no impact on daily function) or major (cognitive impairment that interferes with daily function). Presenting symptoms are varied and can include memory loss, executive dysfunction, speech and language changes, and/or behavioral and emotional symp-toms. Common causes of dementia include Alzheimer's disease (AD), vascular dementia, frontotemporal dementia (FTD), and dementia with Lewy bodies (DLB). Other disorders that may be associated with dementia are Huntington's disease, HIV/AIDS, Parkinson's disease, alcoholism, and head trauma. Rapidly progressive dementias are rare and may include Creutzfeldt-Jakob disease. For many individuals (especially those of older age), there are multiple types of pathology present. There is no cure for dementia, although current research aimed at the reversal or prevention of dementia is under way. There is no single test for dementia and the evaluation is directed at clarifying the nature of the impairment, ruling out reversible conditions, and specifying the likely cause for the dementia (see T able 52-1). Approximately 9% of patients have a potentially treatable cause for dementia (e. g., thyroid abnor-mality, vitamin deficiency, depression, delirium, medication side effects, and excessive use of alcohol). Thus, a comprehen-sive evaluation is critical to correctly identify and diagnose patients with dementia and to initiate appropriate management. A. Alzheimer's disease (AD) 1. D efinition and overview AD is the most common cause of dementia. Although the sites of earliest damage in AD are the hippo-campus and entorhinal cortex (areas important to Jennifer Merrilees De Ment Ia© Eliks/Shutterstock; © donatas1205/Shutterstock 504 52Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

are proteins involved in cellular dysfunction and death that occur with FTD. The average age at onset of FTD is between 50 and 60 years of age. 2. P revalence The prevalence of FTD is 81 per 100,000 cases of dementia among people under the age of 65 (Ratnavalli, Brayne, Dawson, & Hodges, 2002). E. Mixed dementia 1. D efinition and overview Mixed dementia occurs when more than one type of dementia is present. Common combinations include AD and vascular, AD with DLB, and AD with vascular and DLB. 2. P revalence Advances in research have shown that the presence of mixed pathologies is relatively common. About half of people with dementia have mixed pathology. II. Database (may include but is not limited to) A. Subjective (see Table 52-2 ) One of the most important steps in the evaluation of a person with suspected dementia is to obtain a description of the symptoms and associated features with the patient and an informant (someone who knows the patient well). It is critical to involve an informant to verify information: patients with dementia may have limited insight and may mask or downplay their deficits. The focus of the inter-view is aimed at onset and duration of symptoms and whether they represent a change from the patient's base-line abilities. T aking a careful history is critical to deter-mine how the symptoms have progressed and potential temporal relationships of related factors (for example, medical conditions, medications, stroke events). It is C. Dementia with Lewy bodies (DLB) 1. D efinition and overview The symptoms of DLB can be similar to AD with several important distinctions. Diagnostic criteria for DLB include the presence of visual hallucinations; Parkinsonian signs (stiffness, slowness of movement, shuffling gait); and fluctuations in alertness and atten-tion (Mc Keith, 2006). DLB is caused by the accumu-lation of Lewy bodies containing α-synuclein, which deposit within neurons and affect multiple brain regions. 2. P revalence DLB is considered the third most common cause for dementia. It occurs in 1 out of 25 cases of dementia (Vann Jones & O'Brien, 2014). D. Frontotemporal dementia (FTD) 1. D efinition and overview FTD refers to a heterogeneous group of syndromes caused by focal damage to the frontal and anterior temporal lobes of the brain. The focal damage results in behavioral disorders, executive dysfunction, and language deficits. FTD is divided into two major sub-types: behavioral variant frontotemporal dementia (bv FTD) and aphasia syndromes. The aphasia syn-dromes include a semantic variant and progressive nonfluent aphasia (PNFA). Behavioral variant FTD is the most common clinical subtype typically char-acterized by social disinhibition, impulsivity, apathy, loss of empathy, and executive dysfunction. Semantic variant is characterized by difficulty naming common objects, people, and words with progressive trouble in identifying the meaning of those items they are trying to name. Complaints about fluency or speech rhythm and pronunciation occur with PNFA. Other FTD-related movement disorders include corticobasal degeneration, progressive supranuclear palsy and motor neuron disease. T au, TDP-43, and progranulin Table 52-1 Possible Causes of Dementia (Partial List) Neurodegenerative Alzheimer's disease, Down syndrome, Parkinson's disease, dementia with Lewy bodies, frontotemporal dementia, multisystem atrophy, Huntington disease Cerebrovascular Vascular dementia, vasculitis Prion-associated Creutzfeldt-Jakob disease, Gerstmann-Straüssler-Scheinker syndrome, fatal familial insomnia Neurogenetic Spinocerebellar ataxias, mitochondrial encephalopathies, Wilson's disease Infectious Meningitis, encephalitis, leukoencephalopathy, neurosyphilis, Whipple's disease, HIV Toxic or metabolic Systemic: thyroid, parathyroid, adrenal, liver, kidney, sarcoidosis, vitamin deficiencies, hypoxia/ischemia, drugs, alcohol, heavy metals Other Multiple sclerosis, neoplastic, hydrocephalus505 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 52-2 Features of Dementia Syndrome Symptoms Onseta reas of Brain a ffected Biochemical/ Protein Possible a ssociated Symptoms Progression Alzheimer's disease Short-term memory loss, word-finding difficulty, visual-spatial difficulties (getting lost or disoriented)Gradual; more common after age 65, but can occur earlier Multiple areas; global atrophy on imaging Deficits in acetylcholine/beta amyloid and tau Apathy, depression, diminished insight over time Slowly progressive over 7-10 yrs (or longer) Dementia with Lewy bodies Recurrent and well-formed visual hallucinations, fluctuating cognition, parkinsonian symptoms, visual-spatial deficits, short-term memory loss Gradual Multiple areas; global atrophy on imaging Deficits in acetylcholine and dopamine/alpha synuclein Rapid eye movement sleep behavior disorder, falls, anxiety Slowly progressive Vascular dementia Dependent on the location of ischemia May be sudden with identifiable onset and proceed in a stepwise manner Cortical or subcortical changes on imaging Irritability, apathy Dependent on management of stroke risk factors Frontotemporal dementia Behavior and personality change: apathy, disinhibition, poor judgment, social misconduct, executive dysfunction Gradual; before age 60Frontal and anterior temporal lobes (anterior sections of the brain)Deficits in serotonin/tau, Pick bodies, or TDP-43Speech and language changes occur in the aphasic variant. Motor deficits occur in progressive supranuclear palsy and corticobasal degeneration, and amyotrophic lateral sclerosis (related disorders), diminished insight early in disease (behavioral variant frontotemporal dementia)Progressive over 6-8 yrs 506 CHAPTER 52 | Dementia

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

important to understand the pattern and character of the deficits. Patients and families can be encouraged to main-tain a log or journal to help in the evaluation of the person with suspected cognitive deficits. It can be helpful to start with general questions: “What are you concerned about?” moving to more specific questions, such as “What was the very first thing that was different or caused you concern?” and “How have the symptoms progressed: have they worsened, stayed the same, or improved?” Most dementia conditions have a slow progression and an onset that can be hard to identify. In contrast, the rapidly progressive dementias (RPDs) can manifest in a much shorter time, sometimes over weeks to months. If RPD is suspected, the evaluation should be completed with referral to a specialist made promptly. A careful review of medications (prescription and over-the-counter) should be conducted. It is important that the patient bring all medications to the evaluation in order to clarify dosages and expiration dates and the patient's understanding of the purpose, administration, and adherence for the medications. 1. A lzheimer's disease a. P atients or families often report deficits in short-term memory although memory loss is not always a primary cognitive deficit. First symptoms can also include nonamnestic symptoms such as problems with word finding, visual-spatial deficits (getting lost), or executive dysfunction (organization and planning). Statements may include: “s/he seems more forgetful,” “s/he takes longer to get things done,” “s/he is getting lost in familiar places,” “s/he repeats the same question multiple times,” “s/he cannot multitask as well as before,” “s/he cannot come up with the right word to use,” or “s/he is having trouble learning new things, such as the computer, cell phone, or television remote control”. b. R eport of personality or behavioral changes: apathy, depression, anger/aggression, or irrita-bility and mood swings. Common complaints may include: “s/he is quieter,” “s/he doesn't engage in activities as in the past,” or “s/he angers easily now. ” c. R eport of functional decline. Examples may include problems with completing tasks at work, paying bills late, forgetting appointments, misplacing personal items, diminished standards in personal hygiene and grooming (e. g., not showering as often, appearance that is unkempt, or wearing the same clothes over again), and problems with driving (e. g., running through stop signs, driving too fast or slow, getting lost, new traffic violations or car accidents, and/or new dents and scrapes on the car). d. R eport of risk factors for AD. Risk factors include advanced age, family history of AD, history of moderate and severe traumatic brain injury (with loss of consciousness or posttraumatic amnesia), cardiovascular disease risk factors, and mild cognitive impairment. 2. V ascular dementia a. P atient or family reports of deficits in short-term memory, finding the right word, navigation, or executive function (organization and planning). b. R eport of personality or behavioral changes: apathy, depression, irritability, or anxiety. c. R eport of functional decline. See examples in 1. Alzheimer's disease. d. R eport of a strokelike event that coincides with the previously mentioned cognitive, behavioral, and functional changes. It may be possible to identify a specific time point that symptoms presented. A medical review may reveal the presence of vascular risk factors (hypertension, hypercholesteremia, or diabetes). 3. D ementia with Lewy bodies (DLB) a. P atient or family reports of fluctuating deficits in visual-spatial abilities, navigation, executive function (organization and planning), short-term memory, or finding the right word. b. R eport of personality or behavioral changes. Visual hallucinations are common (for example, small people or animals, movement in one's peripheral vision) as well as misperceiving objects (for example, mistaking a tree for the figure of a person). Other examples of behavioral changes may include daytime sleepiness, anxiety, apathy, and depression. c. R eport of functional decline. See examples in 1. Alzheimer's disease. d. R eport of motor symptoms suggestive of Parkinsonism (shuffling gait or dragging feet more while walking, bradykinesia, stiffness, and falls caused by tripping). e. R eport of sleep changes suggestive of rapid eye movement behavior disorder. Symptoms may include new onset of thrashing and moving while sleeping, arm and leg movements as if warding off an attack, hitting the bed partner during sleep, or falling out of bed during sleep. 4. F rontotemporal dementia (FTD) a. R eport of executive dysfunction, poor judgment, speech and language changes that may include loss of object and word meaning, or dysarthria. Common complaints may include: “s/he has been making risky decisions,” “s/he cannot seem to organize tasks,” “s/he doesn't know what 507 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

c. E xamples of functional assessment instruments include the Functional Activities Questionnaire (Pfeffer, Kurosaki, Harrah, Chance, & Filos, 1982) and the Instrumental Activities of Daily Living Scale (Lawton & Brody, 1969). Both tools are easy to administer and have good reli-ability and validity. A disadvantage of both tools is the reliance on self-or informant report rather than direct observation of functional abilities. d. A n instrumental activities of daily living scale is available at http://consultgerirn. org. e. Dir ect observation of a person's function can be accomplished with tools such as the T exas Functional Living Scale or the Executive Function Performance T est. In addition, occupa-tional therapists can be helpful in the assessment of mobility, function, self-care, and swallowing. 3. A ssessment of mood a. E valuation should include an assessment for depression because mood disorders share similar features with neurodegenerative conditions. Depression can coexist with dementia, although its prevalence decreases with increased dementia severity. b. A c ommonly used screen is the Geriatric Depression Scale. Using a yes/no format, patients answer questions about their mood over the past week. A long version (30 items) and a short version (15 items) are available. Scoring guidelines are provided to rate the severity of depression. c. The Ge riatric Depression Scale is available at http://consultgerirn. org. d. The P atient Health Questionnaires (PHQ) are mental health screening tools designed for use in the office practice setting. They are available at www. phqscreeners. com. For additional details about the PHQ, see Chapter 53, Depression. 4. P hysical and neurologic examination a. The r outine physical examination should be completed to identify the presence of any medical problems (e. g., hypertension or atrial fibrillation). b. The ne urologic examination should include an assessment of motor abilities, reflexes, coordi-nation, gait and balance, and an assessment for focal neurologic signs. 5. R elevant diagnostic tests a. L aboratory screening routinely includes com-plete blood count (to rule out anemia and infection), serum chemistries, thyroid and liver function, and vitamin B 12 (to rule out metabolic conditions). Rapid plasma reagin test (RPR) certain words mean anymore,” or “speech is halting and it is hard to get words out. ” b. R eport of personality and behavioral changes: apathy, disinhibition, impulsivity, social or personal misconduct, unusual eating behaviors, compulsions, and diminished empathy. Common complaints: “s/he has become a different person,” “s/he has been yelling at people,” “s/he doesn't care about things, doesn't care about me,” “s/he  says she will do things, but doesn't,” “s/he makes suggestive comments to others,” “s/he talks to strangers more readily,” “s/he has become self-centered,” “eating behavior has changed (eats more, carbohydrate cravings, or engaging in food fads). ” c. R eport of functional decline. Examples may include trouble with task completion, trouble maintaining a job, diminished abilities in man-aging financial and legal matters (showing poor judgment, making risky investments, unusual purchases, or giving away money), and dimin-ished standards in hygiene and grooming. d. R eport of motor symptoms suggestive of amyo-trophic lateral sclerosis, corticobasal degen-eration, or progressive supranuclear palsy (falls, weakness, or diminished ability to control limb movements). e. R eport of a family history suggestive of FTD that may include dementia, behavioral disorders, or psychiatric disorders. B. Objective 1. M ental status screening and evaluation a. U se a reliable and valid instrument. The Montreal Cognitive Assessment (MOCA) provides brief screening of memory, language, executive func-tion, and visual-spatial abilities. It is available in multiple languages and is free of charge. b. The MO CA along with administration instruc-tions are available at www. mocatest. org. c. C omprehensive neuropsychological testing by a neuropsychologist may be necessary to accu-rately demonstrate the presence and character of deficits. 2. F unctional assessment a. A reliable and valid instrument that assists in comparing present with past performance in functional domains can be used in conjunction with the clinical interview. b. F unctional abilities can be assessed in multiple domains including occupational performance, finances, driving, use of computer, household tasks (e. g., housekeeping and cooking), and personal hygiene. 508 CHAPTER 52 | Dementia

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

and/or folate level or homocysteine and meth-ylmalonic acid may be warranted depending on clinical findings and history. See T able 52-3 for a summary of routine laboratory screening. b. Othe r tests may be indicated based on the his-tory or physical examination (e. g., electrocardi-ography or electroencephalography). c. Bi omarkers i. B rain imaging can help identify the degree and pattern of atrophy and may detect other causes for cognitive deficits (e. g., intracranial bleeding, space-occupying lesions, and hydrocephalus). The most common imaging techniques are magnetic resonance imaging (MRI) and computed tomography (CT). Functional brain imaging such as positron emission tomography (PET) provides infor-mation on metabolic activity in the brain, although the data can be difficult to inter-pret. The Food and Drug Administration has approved newer techniques in PET imaging using florbetapir (binds to beta-amyloid protein). This imaging is not covered by most insurance and current guidelines suggest its use be always in the context of an evaluation by a specialist as the results are difficult to interpret if not in conjunction with an appropriate work-up. ii. P roteins in cerebrospinal fluid (CSF): Specialty laboratories can provide analysis of levels of β-amyloid and phosphory-lated tau although these results can be inconclusive and difficult to interpret. d. Ge netic testing: may be pursued if there is a family history, a known gene, and a desire for confirmation. The different types of dementia carry varying familial risk. Referral to a genetic counselor is typically indicated in order to clarify the presence of genetic risk and to discuss the implications of genetic testing. III. a ssessment A. Determine the diagnosis 1. D ementia is diagnosed when there are cognitive or behavioral (neuropsychiatric) symptoms that interfere with usual function, represent a decline from previous levels of performance, and are not explained by delirium or major psychiatric disorder. The cognitive or behavioral impairment involves a minimum of two of the following domains: (a) impairment in ability to remember new information, (b) impaired reasoning and ability to manage complex tasks, (c) impaired visuospatial abilities, (d) impaired language functions, or (e) changes in behavior, personality, or comportment (American Psychiatric Association, 2013). 2. I f cognitive impairment is present, and there is no decline in functional abilities, consider a diagnosis of mild neurocognitive disorder or mild cognitive impairment (MCI), terms to describe a condition that may or may not precede the development of dementia. Schedule follow-up testing within 6 months to a year or as needed. IV. Goals of clinical management Desired outcomes for the patient with dementia are that (a) s/he remains as independent as possible in an environment that matches his or her functional abilities; and (b) the demen-tia and comorbid conditions are well managed. V. Plan A. Conduct further work-up or referral to specialist as needed. Referrals are indicated when symptoms are atypical, occurring in a younger patient, are suggestive of a rapidly progressive dementia, or confounded by difficult psychi-atric or behavioral disturbances. Referrals may be helpful when a second opinion is desired. Table 52-3 Common Laboratory Screening in Assessment of Dementia Laboratory tests Complete blood cell count Serum electrolytes, including magnesium Serum chemistry panel, including liver function Thyroid function Vitamin B 12 Folate acid level or homocysteine Methylmalonic acid Urinalysis Serologic tests for syphilis*Toxicology screening*Human immunodeficiency virus* * Based on clinical relevance. 509 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

C. Nonpharmacologic management 1. C onduct patient and family education a. Di scuss implications of diagnosis as it pertains to the patient's occupation and other responsibilities. b. P rovide education regarding dementia diagnosis, progression, and goals of care in a manner that is consistent with their values, culture, education, and abilities. c. S tress the importance of exercise: physical exercise has been linked to improvement of mood, maintenance of mobility, and decrease in the risk for falls, and may improve cognition. d. P rovide information regarding educational and supportive resources available in the community (see Resources and T ools at end of chapter for suggestions). e. P rovide information about advance directives and durable power of attorney while the patient is in the early stages of disease and able to articu-late his or her wishes. Make referrals for legal and financial advice, especially if there are concerns about the patient's judgment, decision making, or vulnerability. A formal evaluation for capacity may be warranted. f. Di scuss participation in research. The National Institutes of Health maintains a listing of all clinical trials at www. clinicaltrials. gov. 2. S afety management a. D etermine whether patient is residing in a setting that best meets his or her functional and cognitive abilities. Types of living situations range from living at home alone, living at home B. Pharmacologic management 1. The re are several classes of medications used to treat disease symptoms or improve cognitive function. Currently, there are no agents available to cure dementia. 2. C ommonly used medications are outlined in T able 52-4. Discuss possible side effects of the acetylcholinesterase inhibitors including gastrointes-tinal upset and vivid dreams. Slow titration of medica-tion, use of the patch, or administration of medication in the morning and not bedtime are common strate-gies to prevent these side effects. These medications are not indicated for patients with bradycardia: it may be necessary to obtain an electrocardiogram before initiation of therapy. 3. R eview expected and realistic goals of treatment (e. g., treatment is for symptomatic improvement and not a cure or reversal of disease). Expected benefits may be mild improvement in memory function, mood, and alertness. Higher doses are often indicated in DLB. It is recommended that 6-12 months of therapy are needed to adequately assess the benefit of therapy (California Workgroup on Guidelines for Alzheimer's Disease Management, 2008). 4. Die tary supplements and other medications: ginkgo biloba, vitamin E, and estrogen have been considered as treatment for AD, although research has not provided compelling evidence in favor of these medications. 5. I f the patient has vascular disease or mixed dementia, they should receive management and education regarding modification of cardiovascular risk factors. Table 52-4 Medications Used in the T reatment of Dementia Drug Indications Possible Side e ffects Other Considerations Cholinesterase inhibitors: Donepezil (Aricept®); Galantamine (Razadyne®, Reminyl®); Rivastigmine (Exelon®)Used primarily in AD and DLB to slow the breakdown of acetylcholine, a neurotransmitter important for memory. May be helpful in managing the hallucinations and fluctuating cognition of DLB. Gastrointestinal (nausea, vomiting, diarrhea). Contraindicated in patients with bradycardia. Obtain baseline electrocardiogram before initiation in patients with cardiovascular conditions. Rivastigmine available in patch form. N-methyl-D-aspartate antagonist: Memantine (Namenda ®)Used to reduce glutamate-mediated excitotoxicity that occurs with cell death. Approved for treatment of advanced AD (Mini-Mental Status Examination scores ≤ 15). Constipation, dizziness, and headache. Not effective in FTD. Selective serotonin reuptake inhibitors Used to treat mood disorders in dementia as well as the behavioral symptoms in FTDGastrointestinal (nausea and diarrhea), agitation. 510 CHAPTER 52 | Dementia

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

with supervision, board and care, assisted living, and memory care units. b. I f wandering or getting lost is a concern, discuss strategies for maintaining safety and refer the patient and family to the Medic Alert +Alzheimer's Association Safe Return program (operated by the Alzheimer's Association). Discuss strategies for ensuring safety concerns (e. g., door alarms and supervision). c. P atients with dementia and their caregivers are vulnerable to abuse. Refer to Adult Protective Services if there is concern for the well-being of the patient or the caregiver. d. Dr iving i. D epending on cognitive and motor find-ings, the patient can be requested to stop driving, complete test of driving abilities through the department of motor vehicles, or be referred to a driver's safety course that will assess driving ability. ii. R eporting to the department of motor vehicles of the diagnosis of dementia should be consistent with state laws: some states have mandatory reporting requirements. 3. M anagement of behavioral symptoms Behavioral symptoms occur commonly in dementia and contribute to caregiver distress. Behavioral symp-toms are caused by structural changes in the brain, a result of neurotransmitter depletion, by changes in how the patient perceives and responds to envi-ronmental stimuli, or a combination of all of these factors. a. The fir st step in managing these symptoms is to discuss the character, frequency, and severity of the symptoms with the patient and caregiver. Describe the behavior specifically (e. g., not just “sundowning,” but “behavior that changes in the evening and includes pacing, repetitive statements that this is not their house, pushes caregiver away, and tries to open front door to leave the house”). b. I dentify whether the symptoms are hazardous, annoying, or tolerable. Not all behaviors are problematic. For example, wandering is a ben-eficial form of exercise as long as the patient can engage in the activity safely. Other behaviors are hazardous, such as agitation and aggression that may be physically dangerous to the patient or the caregiver. c. D evelop an individualized plan of care for managing behavioral symptoms. Strategies for managing behavioral symptoms fall into five categories. In many cases, using a combination of interventions is necessary. i. E nvironmental refers to modifying the patient's environment. Examples include providing activities that are enjoyable for the patient and match his/her functional level without overwhelming. For patients vulner-able to sweepstakes offers in the mail, have mail diverted to a post office box where it can be screened before reaching the patient. If the patient is having disturbing visual illu-sions, remove the stimuli from the environ-ment. Environmental strategies also include the use of communication techniques that match the patient's level of comprehension and that do not provoke an argument. ii. B ehavioral refers to substituting for a behavior that is more tolerable or safer than the current/prior behavior(s). Examples include substitution of sugar-free candy or nonalcoholic beverages for patients with food cravings. iii. Ph armacologic refers to the use of a medi-cation targeted specifically for the behav-ior. Examples include a selective serotonin reuptake inhibitor to treat agitation. Antipsychotics can be used for delusions that are frightening and disabling for the patient. Their use is associated with increased risk of death and should be used only in cases of severe agitation, aggression, or psychosis and in conjunction with an assessment for potential medical reasons for the behavior. iv. Ph ysical refers to the use of a physical restraint or barrier to prevent patient's movement. These strategies should only be considered as a last resort. It may be neces-sary to move the patient to a more protected and supportive environment such as a memory care unit in which the patient can move about in a secured setting. v. I nternal to the caregiver refers to acknowl-edgement and acceptance by the caregiver for the behavior. Counseling and education regarding expected disease symptoms, iden-tification of strategies for effective behavior management, and obtaining respite and support from caregiving duties are examples of helpful interventions. 4. F ollow-up care a. F ollow-up assessment of the person with dementia is typically every 6 months to a year or sooner if needed and should include:i. A n assessment of daily function to assess progression of disease and to identify con-cerns of the patient or family. 511 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

care. Dementia family caregiving is associated with negative physical and emotional outcomes for the caregiver although many express satisfaction with their roles. Race, ethnicity, financial resources, supportive resources, and preparedness are only a few of the factors that affect the caregiver's experi-ence with this role. Children and teenagers often need support and education. Desired outcomes for family caregivers include the promotion of positive coping and emotional and physical well-being. A. Assess the caregiver's physical and emotional health concerns 1. A ssess their level of strain: The Modified Caregiver Strain Index (CSI) is a 13-item survey designed to measure strain for certain aspects of caregiving with higher scores indicative of greater strain. The CSI is available at http://consultgerirn. org. 2. A ssess for depression and anxiety. Consider tools such as the Geriatric Depression Scale or the Patient Health Questionnaires (PHQ) as previously noted. 3. A ssess the caregiver's coping strategies for managing the strain of caregiving and promote positive strategies (e. g., exercise, counseling, and so forth). 4. A ssist the caregiver in identifying activities that are pleasurable for them and methods for incorporating these activities into their lifestyle. 5. R efer to caregiver support groups, counseling, respite care, or other services B. Provide assistance for children and teenagers dealing with a family member's dementia 1. The re are educational and supportive resources for children and teenagers coping with a family member's dementia: a. w ww. alz. org/living_with_alzheimers_just_for _kids_and_teens. asp b. h ttp://www. alzheimers. org. uk/site/scripts /documents VIII. Resour ces and tools A. Resources for all 1. A lzheimer's Association is a national organization with local offices and can be a resource for all types of dementia (www. alz. org; 1-800-272-3900) 2. A lzheimer's Disease Education and Referral Center, a service sponsored by the National Institute on Aging (www. alzheimers. org; 1-800-438-4380) 3. l zheimers. gov: sponsored by the U. S. Department of Health and Human Servicesii. C ognitive status testing to assess progres-sion of disease. iii. R eview for comorbid physical or neuropsy-chiatric conditions. iv. R eview of current medications to assess for therapeutic effectiveness and potential negative side effects. v. P hysical examination as appropriate. vi. C ontinuation of patient and family educa-tion as needed and referrals for education and support as needed. 5. P reparation for end-of-life care. a. A ssess the patient's and family's cultural values and preferences (per advance directives if available). b. Di scuss goals for managing patient care regarding dementia and any comorbid conditions. c. E mphasize comfort measures (e. g., simplify medication regimen, maximize comfort for patient, and initiate referral for hospice care as indicated). VI. a ssessment and management of concomitant conditions There are factors that may negatively affect the status of the patient with dementia and their caregiver. For example, depres-sion has been shown to contribute to excess disability of the patient with dementia. The selective serotonin reuptake inhibi-tors are the ideal medication for treating depression (Swartz, Barak, Mirecki, Naor, & Weizman, 2000). Sudden changes in the patient's behavior may not be caused by advancing dis-ease but may be delirium, a result of underlying acute medical change, such as pneumonia or urinary tract infection, constipa-tion, or poorly controlled pain. Sudden changes warrant both a medical evaluation and a review of the patient's medications. VII. a ssessment of the status of the family caregiver Family caregivers provide the bulk of care to people with dementia. Survival of AD is typically 4 to 8 years following diagnosis, although some people live as long as 20 years with the disease. Over the disease trajectory, family caregivers provide an extensive range of assistance. Caregiving respon-sibilities may include a variety of tasks ranging from manage-ment of medications and appointments, decision making, money management, guarding the safety of the patient, locating and arranging for assistance via community resources and programs, hiring and supervising hired help, and assis-tance with walking, dressing, and other aspects of physical 512 CHAPTER 52 | Dementia

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

4. F amily Caregiver Alliance (https://www. caregiver. org) 5. Ge t Palliative Care: Palliative care directory (http:// getpalliativecare. org) B. Resources for providers 1. C osta, P., Williams, T., & Somerfield, M. (1996). Early identification of Alzheimer's disease and related dementias. Clinical practice guideline, Quick reference guide for clinicians (AHCPR Publication No. 97-0703). Rockville, MD: Author. 2. G uideline for Alzheimer's Disease Management: California Workgroup on Guidelines for Alzheimer's Disease Management. (www. alz. org/socal/images /professional_NATLguideline. pdf). 3. The H artford Institute for Geriatric Nursing, College of Nursing, New Y ork University. Contains best practice information on the care of older adults and multiple assessment tools with administration and scoring instructions (http://consultgerirn. org or www. hartfordign. org). Refe Ren Ce S Alzheimer's Association. (2014). 2014 Alzheimer's disease facts and figures. Alzheimer's & Dementia, 10(2). Retrieved from www. alz. org /downloads/facts_figures_2014. pdf. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Publishing. Lawton, M., & Brody, E., (1969). Assessment of older people: Self-maintaining and instrumental activities of daily living. Gerontologist, 9(3):179-186. Mc Keith, I. G. (2006). Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the consor-tium on DLB International Workshop. Journal of Alzheimer's Disease, 9(Suppl. 3), 417-423. Pfeffer, R., Kurosaki, T., Harrah, C., Chance, J., & Filos, S. (1982). Measurement of functional activities in older adults in the community. Journal of Gerontology, 37(3), 323-329. Plassman, B. L., Langa, K. M., Fisher, G. G., Heeringa, S. G., Weir, D. R., Ofstedal, M. B., et al. (2007). Prevalence of dementia in the United States: The aging, demographics, and memory study. Neuroepidemiology, 29(1-2), 125-132. Ratnavalli, E., Brayne, C., Dawson, K., & Hodges, J. R., (2002). The preva-lence of frontotemporal dementia. Neurology, 58(11), 1615-1621. Rizzi, L., Rosset, I., & Roriz-Cruz, M., (2014). Global epidemiology of dementia: Alzheimer's and vascular types. Bio Med Research International, 2014, 908915. Swartz, M., Barak, Y., Mirecki, I., Naor, S., & Weizman, A. (2000). T reating depression in Alzheimer's disease: Integration of differing guidelines. International Psychogeriatrics, 12(3), 353-358. Vann Jones, S., & O'Brien, J. (2014). The prevalence and incidence of dementia with Lewy bodies: A systematic review of population and clinical studies. Psychological Medicine, 44(4), 673-683. 513 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Zuithoff et al., 2009), so it is important for the primary care provider to screen for, assess, and treat depression. Although depression is comparable in prevalence to other disorders commonly seen in primary care, it remains underrecognized by primary care providers (Wittkampf et al., 2009). Depression is not only underdiagnosed, it is also undertreated; it is estimated that only about 20% of Americans with depression receive care consistent with treatment guidelines (Gonzalez et al., 2010). Fortunately, initiatives to improve quality of depression care in primary care settings have resulted in the development of a number of diagnostic and treatment planning tools (Mac Arthur Initiative on Depression & Primary Care, 2009). Depression is a significant public health problem; the Global Burden of Disease Study 2010 rates depression as the fifth leading cause of U. S. years of health lost to disability (U. S. Burden of Disease Collaborators, 2013). Depression has a significant impact on public health for multiple reasons: it is common and interferes with many aspects of functioning; the typical age of onset is in the teenage or young adult years; and the disorder can easily become chronic, particularly if treatment is not prompt and adequate. If depressive episodes are not adequately treated, the brain becomes sensitized to being in a depressed state, which is then more likely to recur in the future. This phenomenon, called “kindling,” may lead to depressive episodes that are more frequent, more severe, and of longer duration, with incomplete recovery between episodes. For this reason, it is important to prevent long-term morbidity through early diagnosis and aggressive treatment with the goal of complete remission. Inadequately treated depression is problematic not just in and of itself but also because it exacerbates other health problems. Persons with major depressive disorder seen in general medical settings have more pain and physical illness and more impairment in physical, social, and role functioning than other patients (American Psychiatric Association [APA], 2013). I. Intr oduction and general background A. Definition, overview, and epidemiology The term “depression” may be used to describe a mood state, a clinical syndrome, or a distinct mental disorder. In a clinical context, “depression” refers to conditions char-acterized by persistent depressed mood accompanied by additional symptoms (see Figure 53-1). Depression can be expressed as discrete major depressive episodes or as persistent depressive disorder (dysthymia), a condition characterized by depressive symptoms of varying severity that continue for at least 2 years. It can also occur as part of a bipolar mood disorder in which depressive episodes alternate with manic or hypomanic episodes or where both manic-hypomanic and depressive symptoms are manifested during the same period of time (mixed episode). Depression can appear similar to, or accompany, other psychiatric disorders, such as anxiety disorders, thought disorders, and substance abuse disorders. Thus, clini-cians should be familiar with the current version of the Diagnostic and Statistical Manual of Mental Disorders (DSM) to distinguish depression from other psychiatric illnesses. As with all psychiatric illness, medical causes of depressive symptoms must be ruled out before determin-ing a diagnosis of depression. Therefore, clinical evaluation should involve the assessment of biologic, psychological, and social factors. The 12-month prevalence of major depressive disorder for U. S. adults has been estimated at 6. 9% (see Figure 53-2; National Institute of Mental Health [NIMH], n. d. ). Lifetime prevalence of major depressive disorder has been estimated at 16. 6% (Kessler, Chiu, Demier, Merikangas, & Walters, 2005). The prevalence of depres-sion in primary care settings is estimated to be between 5% and 9% among adults (U. S. Department of Health and Human Services, Depression Guideline Panel, 1993; Matt Tierney and Beth Phoenix De Press Ion© Eliks/Shutterstock; © donatas1205/Shutterstock 514 53Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

In addition to the significant burden of depression-related disability, depression is also a significant cause of premature mortality from suicide. Many adults who died by suicide visited their primary care provider within 1 month of their deaths; thus, familiarity with suicide risk factors is strongly recommended (Luoma, Pearson, & Martin, 2002). The SAD PERSONS mnemonic (T able 53-1) summarizes major risk factors for suicide. The combination of severe depression and excessive alcohol consumption is implicated in a substantial majority of completed suicides in the United States, making substance use assessment a critical part of depression screening. The U. S. Preventive Services T ask Force (USPSTF) recommends depression screening for adults when support services, including the ability to provide follow-up, are in place to accurately diagnose and treat depression. Figure 53-1 Patient Health Questionnaire-9 (PHQ-9) Reproduced from Pfizer. (1999). Patient Health Questionnaire-9 (PHQ-9). Retrieved from www. phqscreeners. com. Scoring table reproduced from US Preventative Services Task Force. Retrieved from http://www. uspreventiveservices taskforce. org/Home/Get File By ID/218. Client Name: Chart No. Date: Over the last 2 weeks, how often have you been bothered by any of the following problems?Not at all Several days More than half the days Nearly every day 1. Little interest or pleasure in doing things 01 23 2. Feeling down, depressed, or hopeless 01 23 3. Trouble falling or staying asleep, or sleeping too much 01 23 4. Feeling tired or having little energy 01 23 5. Poor appetite or overeating 01 23 6. Feeling bad about yourself — or that you are afailure or have let yourself or your family down01 23 7. Trouble concentrating on things, such as reading thenewspaper or watching television 01 23 8. Moving or speaking so slowly that other people couldhave noticed? Or the opposite — being so fidgety or restlessthat you have been moving around a lot more than usual 01 23 9. Thoughts that you would be better off dead or of hurtingyourself in some way01 23 For office coding 0 +______+ ______+ ______ = Total Score:______ If you checked off any problems, how difficult have these problems made it for you to do your work, take care of things at home, or get along with other people?_ Not difficult at all _ Somewhat difficult _ Very difficult _Extremely difficult PHQ-9 Scoring For healthcare professional use Total Score Depression Severity 1-4 Minimal Depression5-9* Mild Depression10-14* Moderate Depression15-19* Moderately Severe Depression 20-27* Severe Depression * For any score 5 and above offer referral for Behavioral Health Services515 Introduction and general background

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

depressed, or hopeless?” and “'Over the past 2 weeks, have you felt little interest or pleasure in doing things?” A positive response to either of these questions warrants a more thorough screening for depression using diagnos-tic criteria from the DSM (Figure 53-1). The Geriatric Depression Scale may be used to screen for and monitor depressive symptoms in older adults (Greenberg, 2012). II. Database A. Subjective (Table 53-2 ) 1. P ast health history: depression; anxiety; other psychiatric illness; trauma history including head trauma; chronic medical illnesses (e. g., HIV/AIDS, hepatitis C); physical disability; new serious health diagnosis; obstetric history; medication history, including current medications, medications or supplements taken in the past, and effect on depression 2. F amily history: depression, including death by suicide; other psychiatric illness; alcoholism or other substance abuse USPSTF does not recommend a specific screening instru-ment. The following two questions, sometimes referred to as the Patient Health Questionnaire (PHQ)-2, are highly effective in identifying most cases of depression (Arroll et al., 2010): “Over the past 2 weeks, have you felt down, Percent Sex Overall Female Male 18-25 26-49 50+ Hispanic White Black Asian AI/AN* 2 or more Age gr oup Race *AI/AN = American Indian/Alaska Native6. 98. 4 5. 28. 9 7. 6 5. 57. 0 7. 1 6. 3 3. 210. 0 7. 7 024681012 Figure 53-2 12-month Prevalence of Major Depressive Episode Among U. S. Adults Reproduced from National Institute of Mental Health. (n. d. ). Major depression among adults. Retrieved from http:// www. nimh. nih. gov/health/statistics/prevalence/major-depression-among-adults. shtml Table 53-1 SAD PERSONS Mnemonic for Suicide Risk Factors Sex (male) Age (elderly or adolescent)Depression Previous suicide attempts Ethanol abuse Rational thinking loss (psychosis)Social supports lacking Organized plan to commit suicide No spouse (divorced > widowed > single)Sickness (physical illness) Modified from Patterson, W. M., Dohn, H. H., Bird, J., & Patterson, G. A. (1983). Evaluation of suicidal patients: The SAD PERSONS scale. Psychosomatics, 24(4), 343-349. 516 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

3. O ccupational history: presence or absence of rewarding and meaningful work, work stress 4. P ersonal and social history: support systems; substance use, including alcohol, nicotine, narcotics, and illicit drugs; relationship status; precipitating factors (stressors and losses) 5. R eview of systems: somatic complaints without focal findings, including headaches and other pain; anhedonia, depressed mood, hypersomnia or insomnia, psychomotor agitation or slowing; indecisiveness or decrease in concentration; fatigue or loss of energy; changes in appetite or weight; feeling guilty or poor self-esteem; suicidal thoughts or plans; irritability; pressured speech or thoughts; increase in goal-directed behaviors or risk-taking behaviors or in activities that have a high potential for negative consequences (e. g., buying sprees or sexual indiscretions); expansive or euphoric mood; psychosis including paranoia and auditory or visual hallucinations; and inability to care for activities of daily living. B. Objective 1. P hysical examination findings a. V ital signs, including weight b. Th yroid examination c. N eurologic examination if indicated. Clinical assessment sometimes reveals that depres-sive symptoms are caused by an organic brain illness. Many discrete neurologic disorders (e. g., Parkinson's disease, Alzheimer's disease, cerebral vascular accidents, multiple sclerosis, traumatic brain and spinal cord injuries, dementias, and epilepsy) are associated with increased risk of depression (Hellman-Regen et al., 2013). Thus, a neurologic examination is often indicated in the physical assessment of depression. d. M ental status examination i. A ppearance and behavior: patient may dem-onstrate poor hygiene, poor eye contact, and inability to engage with interviewer. ii. M otor function: may demonstrate motor slowing or agitation. iii. A ffect: can vary from anxious or irritable, to depressed with constricted affect. iv. M ood: use the patient's own description of mood. v. L anguage: assess flow and volume. Speech may be quiet with few words and slow or may exhibit some nervous pressure. vi. Thou ght process: may be slow, evidenced by increased latency of response. vii. Thou ght content: what are the patient's main concerns? Patient may have suicidal or homicidal thoughts with or without a plan to carry these out (these may indicate an emergency situation and must be care-fully evaluated). Depressive symptoms may include obsessions, perseverations, para-noid ideas, feelings of depersonalization or unreality, and morbid thoughts. Psychotic depression may include auditory or visual hallucinations, or delusions. viii. C ognition: assess possible changes in all areas, including orientation, concentration, and memory; visuospatial skills; ability to abstract; and executive functioning. ix. I nsight: rated good, fair, or poor based on the patient's awareness of their depres-sive symptoms. Patients who are unsure or unaware that symptoms may be caused by depression are rated fair or poor. x. J udgment: rated good, fair, or poor based on the patient's ability to gather and orga-nize information to make plans and func-tion well. 2. D ata from diagnostic tests. No single test is associated with a definitive diagnosis of depression; however, the following should be considered as part of a basic work-up of depressive symptoms from other causes or of medical problems associated with depression a. C omplete blood count to rule out anemia b. M etabolic panel to rule out possible medical causes of depressive symptoms c. Th yroid-stimulating hormone and free T4 to rule out thyroid dysregulation Table 53-2 Depression Risk Factors Other serious physical and mental health problems Concurrent substance abuse or dependence Family history of depression or suicide Childhood depression or physical, emotional, or sexual abuse Long-term use of certain medications Personality traits, such as having low self-esteem and being overly dependent, self-critical, or pessimistic Having recently given birth Unemployment or low socioeconomic group Female gender Poor social support Negative life events, such as bereavement, new onset of illness, institutionalization, financial strain, work-related distress, or experience of discrimination517 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

a. B ipolar disorder: if patient currently meets criteria for a depressive episode but also has a his-tory of manic or hypomanic episodes character-ized by sustained expansive, euphoric, or irritable mood with pressured speech or thoughts, with increase in goal-directed behaviors or risk-taking activities (e. g., gambling with money that is meant to be used to pay rent) or with reduced need for sleep without feeling fatigue. b. Thou ght disorder: presence of psychosis, disorganized thinking, or paranoia. c. A nxiety disorder: when patient does not meet all criteria for a depressive disorder but may have some of the symptoms accompanied by disabling worry about things that are out of the patient's control. d. S ubstance abuse disorder: if depressive symp-toms are better accounted for by substance intoxication or withdrawal. e. Othe r medical conditions that explain symptoms, including but not limited to thyroid or other endocrine disorders, dementia, anemia, and malnutrition. f. M edication side effects (T able 53-3) g. Be reavement: persistent feelings of grief associ-ated with loss of a loved one. d. S erum vitamin D, vitamin B12, and folic acid levels to rule out vitamin deficiencies e. Dr ug of abuse screen to rule out co-occurring substance use disorders f. H ormone levels (gender specific) to rule out endocrine dysregulation III. Assessment A. Determine the diagnosis (DSM-5) 1. M ajor depressive disorder: presence of five out of nine depressive symptoms, with one of the symptoms being depressed mood or anhedonia, occurring daily for at least 2 weeks. 2. P ersistent depressive disorder (dysthymia): presence of three depressive symptoms (including depressed mood) for a duration of at least 2 years, with symptoms present more days than not. 3. D ysthymia with intermittent major depressive episodes (“double depression”): persistent depression with periods of more severe depressive symptoms. 4. Othe r psychiatric conditions that may explain the patient's presentation Table 53-3 Medications That May Cause Depression Acyclovir Clonidine Metoclopramide Alcohol Cocaine (withdrawal) Metrizamide Amantadine Contraceptives Metronidazole α-Methyldopa Corticosteroids NSAIDs Amphetamines (withdrawal) Cycloserine Opiates Anabolic steroids Dapsone Pentazocine Anticonvulsants Digitalis Pergolide Antihistamines Disopyramide Phenylpropanolamine Antineoplastic agents Disulfiram Physostigmine Antipsychotic medications Estrogens Prazosin Baclofen Ethambutol Progestins, implanted Barbiturates Fluoroquinolone antibiotics Reserpine Benzodiazepines Guanethidine Statins β-Adrenergic blockers Interferon alfa Sulfonamides Bromocriptine Isotretinoin Thiazide diuretics Calcium channel blockers Levodopa Cimetidine Mefloquine Note. NSAIDs = nonsteroidal anti-inflammatory drugs. Reproduced from Schatzberg, A., & Nemeroff, C. (2009). The American Psychiatric Publishing textbook of psychopharmacology (4th ed. ). Washington, DC: APA. Reprinted with permission (Copyright 2009). American Psychiatric Publishing, Inc. 518 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

5. S pecifiers may be used if appropriate a. S everity: mild, moderate, or severe, based on the impact depression has on the patient's func-tional ability, the intensity of distress caused by symptoms of depression, and by the presence of suicidal thoughts b. C hronicity: single episode or recurrent c. W ith or without psychotic features, such as nihilistic delusions or ideas of reference d. W ith atypical features: presence of weight gain and hypersomnia. Although “typical depression” is characterized by insomnia and weight loss, “atypical depression” is characterized by hyper-somnia and weight gain. This specifier can be misleading, because both types of depression are commonly seen in the primary care setting. e. I n remission: partial (alleviation of some but not all symptoms) or full (complete alleviation of symptoms); early (< 6 months) or sustained (> 6 months) f. Othe r specifiers, including with anxious distress, with mixed features, with melancholic features, with catatonia, with peripartum onset, and with seasonal pattern. Note: The reader is encouraged to consult the DSM-5 for a description of these specifiers (APA, 2013, pp. 184-188). B. Significance and motivation Assess the significance of depression to the patient and significant others, including impact on work, relationships, and activities. Determine the patient's willingness and ability to follow the treatment plan. Assess for presence of social supports and other patient strengths that may influence the ability to recover from depression. IV. Goals of clinical management A. Screening and diagnosing depression Although there is no consensus on screening for depres-sion, the USPSTF notes that “recurrent screening may be most productive in patients with a history of depression, unexplained somatic symptoms, comorbid psychological conditions (e. g., panic disorder or generalized anxiety), substance abuse, or chronic pain. The optimal interval for screening is unknown” (U. S. Department of Health and Human Services, 2009, p. 125). B. Treatment Select a treatment plan that leads to sustained full remission of depressive symptoms. Approximately one-third of depressed patients achieve remission with their initial treatment regimen, and approximately another one-third requires several treatment regimens. Another one-third fail to respond to two or more adequate trials of antidepressant monotherapy, which is considered treatment-resistant depression (Gaynes et al., 2009). T reatment resistance is associated with a range of comor-bid physical and mental disorders, including substance abuse. Recovery is likely to begin within 3 months of onset for about 40% of individuals with major depression and about 80% will recover within a year. “Recency of onset is a strong determinant of the likelihood of near-term recovery, and many individuals who have been depressed only for several months can be expected to recovery spon-taneously” (APA, 2013, p. 165). Depression can remit without treatment; one model estimates that 23% of cases of untreated depression will remit by 3 months, 32% by 6  months and 53% by 12 months (Whiteford et al., 2013). All patients with depression need to be monitored for changes in condition, and treatment planning should involve not only a consideration of the severity and impact of depression but also the patient's health beliefs as well as adherence to the treatment plan and ability to access components of the care plan. 1. T reatment phases (see Figure 53-3) a. Ac ute phase: 0-16 weeks. Plan: initiate treat-ment and monitor weekly for first month and at least once a month thereafter. b. C ontinuation phase: 16-20 weeks after symp-tom remission. Plan: continue treatment, moni-tor every 2-3 months. c. M aintenance phase: 6 months symptom free. Plan: continue monitoring and treatment every 2-3 months. d. Di scontinuation: consider treatment discon-tinuation only after patient has been symptom free for 6-12 months. Because risk of relapse is highest in the initial 2-month period following discontinuation of treatment, patients should continue to be monitored for several months. Patient education should include a review of the early signs of depression, such as sleep disturbance and loss of interest in normal activities, and emphasize the importance of immediately resuming previously successful treatment in the event of a symptom relapse (APA, 2010). C. Patient adherence Select an approach that maximizes patient adherence, including but not limited to cost, frequency of treatment, tolerability of treatment, and patient health beliefs. 519 Goals of clinical management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Figure 53-3 Primary Care T reatment Algorithm for Depression Data from Fancher, T., Mc Carron, R. M., Kukoyi, O., & Bourgeois, J. A. (2009). Chapter 2: Mood disorders—Depression. In R. M. Mc Carron, G. L. Xiong, & J. A. Bourgeois (Eds. ), Lippincott's Primary Care Psychiatry, 31. Lippincott Williams & Wilkins. Mild to Moderate Depression: First line Antidepressant (Selective serotonin reuptake inhibitors, Serotonin norepinephrine reuptake inhibitors, Bupropion, Mirtazapine) and psychoeducation or Psychot herapy, such as Cognitive behavioral therapy or Interpersonal therapy, with psychoeducation Moderate to Severe Depression: First line Antidepressant (Selective serotonin reuptake inhibitors, Serotonin norepinephrine reuptake inhibitors, Bupropion, Mirtazapine) AND Psychotherapy, such as Co gnitive behavioral therapy or Interpersonal therapy, AND psychoeducation <25% improvement* >25% improvement* Evaluate for: Co-morbid anxiety or psychotic disorder Co-morbid substance abus e Psychosocial stressors Maximize dose of curren t Antidepressant Switch Antidepressant class (preferable ) OR maximize dose OR add augmentation therap y Continue current An tidepressant<25% improvement* >25% improvement* Switch Antidepressant class or maximize dose or add augmentation therapy and refer for psychiatric consultation. Monitor patients weekly for the first month, then at least monthly to week 16. Goal: Symptom remission (APA, 2010) At weekly or monthly follow-ups: reassess for suicidal ideation, access to firearms, treatment adherence and sympto m improvement (APA, 2010) Continuation phase 16-20 weeks after symptoms remission. Plan: Continue treatment, monitor every 2-3 months (APA, 2010) Maintenance Phase 6 months symptom-free. Plan: Continue monitoring and treatment every 2-3 months (APA, 2010) Discontinua tion Consider treatment discontinuation only after p atient has been symptom-free for 6-12 months. Since risk of relapse is highest in the initial 2-month period following discontinuation of treatment, patients should continue to be monitored for several months (APA, 2010) *Patient self-report or PHQ-9520 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

V. Plan A. Diagnostic tests to rule out other causes of depressive symptoms Complete blood count with differential; complete metabolic panel, vitamin B12, folate, thyroid-stimulating hormone, free T4; gamma-glutamyl transferase (GGT) or breathalyzer if alcohol use suspected; consider a drug of abuse screen and a more thorough toxicology screen (e. g., heavy metal screen) if indicated by history. HIV testing if indicated by history. B. Management (includes treatment, consultation, referral, and follow-up care) 1. M edication management. Medication treatment should always include consideration of the following: patient history of medication treatment for depression, cost and insurance coverage, past or anticipated side effects, and concurrent patient medications (T ables 53-4, 53-5, and 53-6) 2. P sychotherapy: for mild to moderate depression, psychotherapy has generally been found to be equal in efficacy to pharmacologic treatment (Wolf & Hopko, 2008), and the combination of medication and psychotherapy is more effective than either modality alone. Circumstances under which referral for psychotherapy should be considered as a first-line treatment option include patient preference and pregnancy and lactation. Even brief psychotherapy of 6 to 8 sessions, in particular cognitive behavioral therapy and problem-solving therapy, can be effective in treating depression (Nieuwsma et al., 2012). Behavioral activation, in which patients are encouraged to increase their participation in interesting and enjoyable activities, is easy to administer in primary care settings and has shown efficacy in decreasing depressive symptoms (Gros & Haren, 2011). 3. C ombined treatment with antidepressants and psychological treatment is recommended for: a. P artial response to either treatment alone b. P atients with personality disorders or complex psychosocial problems c. P atients with a history of chronic or severe depression4. C onsultation with physician: Confirmed or suspicion of concurrent medical illness and polypharmacy treatment. 5. R eferral to mental health or psychiatric specialty for evaluation or management: psychotic symptoms, suspicion of bipolar disorder or thought disorder, current or prior treatment-resistant depression, active suicidal ideation or plan and concurrent psychiatric or neurologic disorder. Additionally, the World Federation of Societies of Biological Psychiatry (WFSBP) recommends that mental health specialists should take responsibility for treating depression that is recurrent, that presents with atypical features or with special risks, or when the patient's dysfunction or risk for mortality is severe (Bauer et al., 2013, p. 342) C. Client education 1. I nformation: provide verbal and written information regarding: a. The disease process, including but not limited to signs and symptoms and possible causes and risks, including self-harm b. The impor tance of treatment, including non-pharmacologic treatment, with the goal of com-plete and sustained remission of depression; expected treatment duration; and community resources to manage psychiatric crises c. S election of written educational materials should consider:i. P atient educational and reading level ii. A vailability of materials in patient's preferred language iii. Ac curacy of information and freedom from commercial bias 2. C ounseling a. S upportive counseling, focusing on problem solving and use of coping strategies (Mac Arthur Initiative on Depression & Primary Care, 2009) b. Be havioral recommendations: regular exercise, especially aerobic exercise; balanced diet; presence of supportive relationships; increased engagement in pleasurable activities; and sleep hygiene521 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 53-4 Overview of Antidepressant Classes selective serotonin r euptake Inhibitors ( ssr I)Tricyclic Antidepressants (TCA)Monoamine o xidase Inhibitors (MA o I) Efficacy First-line treatment in MDD (FDA approved for all except fluvoxamine), dysthymia PD (FDA approved for fluoxetine, paroxetine, and sertraline) OCD (FDA approved for all except citalopram and escitalopram) PTSD (FDA approved for sertraline and paroxetine) Bulimia (FDA approved for fluoxetine) GAD (FDA approved for fluoxetine [Sarafem only], paroxetine [controlled release only], and sertraline)Second-or third-line agents for MDD (FDA approved for all) Panic disorder OCD (FDA approved for clomipramine) Pain syndromes, migraine prophylaxis Enuresis (FDA approved for imipramine)Third-line agents for MDD (FDA approved for resistant depression) Social anxiety Panic disorder Second-line agents for Parkinson's disease (selegiline has FDA approval) Side Effects GI side effects (nausea, diarrhea, heartburn) Sexual dysfunction ( libido, delayed orgasm) Headache Insomnia/somnolence Dry mouth, constipation, urinary retention, blurred vision, confusion Weight gain Sedation Sexual dysfunction Orthostasis Tachycardia Cardiac conduction abnormalities Weight gain Orthostasis Sexual dysfunction Dry mouth Insomnia/somnolence Headache Dosage and Administration Citalopram, paroxetine, fluoxetine: daily dosing, starting at 10-20 mg, increasing to a maximum of 40 mg (citalopram), 50 mg (paroxetine), and 80 mg (fluoxetine). Escitalopram: daily dosing, starting at 10 mg, increasing to 20 mg after minimum of 1 week. Sertraline: starts at 25-50 mg and is increased, as needed, to 200 mg maximum. Individualize with low bedtime dosing (25-50 mg) for imipramine and amitriptyline. Increase by 25-50 mg every 3-7 days to target dosage of 150-300 mg/day. (Nortriptyline should be started at 10-25 mg and increased, as needed, to a maximum dosage of 150 mg/day. ) Monitor levels and ECGs after dose stabilized. Phenelzine: start at 15 mg bid or tid and increase by 15 mg per week to target dosage of 60-90 mg/day. Tranylcypromine: start at 10 mg bid or tid and increase by 10 mg per week to target dosage of 40-60 mg/day. Isocarboxazid: start at 10 mg bid and increase dosage, if the drug is tolerated, by 10 mg every 2-4 days to 40 mg/day by end of first week. Maximum recommended dosage is 60 mg/day, administered in divided doses. Selegiline transdermal system (Emsam): start with 6-mg patch daily for 4 weeks and then increase to 9-mg patch for 2 weeks, and then 12-mg patch as needed. No dietary restrictions at 6 mg/day. 522 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

(Continued) Table 53-4 Overview of Antidepressant Classes selective serotonin r euptake Inhibitors ( ssr I)Tricyclic Antidepressants (TCA)Monoamine o xidase Inhibitors (MA o I) Discontinuation Paroxetine, fluvoxamine, sertraline: discontinuation associated with parasthesias, nausea, headaches, flulike symptoms, 1-7 days after sudden discontinuation Flulike and GI symptoms from cholinergic rebound. Reduce by 25-50 mg every 3 days. Flulike symptoms, hallucinations, hypomania, and dysphoria reported with sudden discontinuation. Taper dose by 25% per week. Drug Interactions MAOI (contraindicated): serotonin syndrome  TCA levels (paroxetine, fluoxetine)  Carbamazepine, phenobarbital, phenytoin levels  Haloperidol, clozapine levels (fluvoxamine)  Theophylline levels (fluvoxamine)  Encainide, flecainide levels (avoid)CNS depressants:  sedation, ataxia Anticoagulants:  warfarin levels Antipsychotics:  TCA and antipsychotic levels Cimetidine:  TCA levels Clonidine: hypertensive crisis (avoid) L-Dopa: TCAs  absorption MAOIs: serotonin syndrome (avoid clomipramine; imipramine and amitriptyline may be used with close monitoring) Stimulants:  TCA levels Oral contraceptives:  TCA levels Quinidine:  arrhythmias (avoid) SSRIs:  TCA levels Sympathomimetics:  arrhythmias, hypertension, tachycardia Food containing high levels of tyramine, such as aged cheeses or cured or pickled foods (contraindicated) hypertensive crisis β-Blockers:  hypotension, bradycardia Oral hypoglycemics:  hypoglycemic effects Bupropion (contraindicated): hypertensive crisis, seizure Carbamazepine (contraindicated): hypertensive crisis Meperidine (contraindicated): serotonin syndrome Nefazodone: possible serotonin syndrome Sympathomimetics: hypertensive crisis SSRIs (contraindicated): serotonin syndrome TCAs: clomipramine contraindicated Mirtazapine (contraindicated): hypertensive crisis SNRIs (contraindicated): serotonin syndrome Safety in Overdose Generally safe in overdose to 30-90 days' supply; manage with vital sign support, lavage Seizures/status epilepticus (rare)Lethal in overdose (induces arrhythmias). Lavage and monitor on a cardiac bed for QRS widening. Can be lethal in overdose. Hypertensive crisis, stroke, and myocardial infarction have been reported. Manage with lavage, emesis induction, and close management of blood pressure and airway. Notes: CNS = central nervous system; ECG = electrocardiogram; FDA = U. S. Food and Drug Administration; GAD = generalized anxiety disorder; GI = gastrointestinal; MAOI = monoamine oxidase inhibitor; MDD = major depressive disorder; SNRI = serotonin-norepinephrine reuptake inhibitor; OCD = obsessive-compulsive disorder; PD = panic disorder; PMDD = premenstrual dysphoric disorder; PTSD = posttraumatic stress disorder; SSRI = selective serotonin reuptake inhibitor; TCA = tricyclic antidepressant. Adapted from Schatzberg, A. F., & De Battista, C. (2015). Manual of clinical psychopharmacology (8th ed. ). Arlington, VA: American Psychiatric Publishing. 523 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 53-5 Antidepressant Names, Formulations and Strengths, and Dosages Generic name Br and n ame Formulations & s trengths Therapeutic Dosage r ange (mg/day)a Selective Serotonin Reuptake Inhibitors citalopram escitalopramfluoxetine fluvoxamine paroxetinesertraline Celexa ® Lexapro® Prozac® Luvox® Luvox CR® Paxil® Paxil-CR® (controlled-release) Zoloft®Tablets: 10, 20, 40 mg Oral solution: 10 mg/5 m L (240-m L bottle)Tablets: 5, 10, 20 mg Oral solution: 5 mg/5 m L (240-m L bottle)Capsules: 10, 20, 40 mg Capsule (weekly): 90 mg Oral solution: 20 mg/5 m L (120-m L bottle)Tablets: 10, 20 mg Tablets: 25, 50, 100 mg Tablets: 100, 150 mg Tablets: 10, 20, 30, 40 mg Oral suspension: 10 mg/5 m L (250-m L bottle)Tablets: 12. 5, 25, 37. 5 mg Tablets: 25, 50, 100 mg Oral concentrate: 20 mg/m L (60-m L bottle)20-40 20-60 100-200 20-50 50-200 Serotonin Norepinephrine Reuptake Inhibitors venlafaxine desvenlafaxine duloxetinelevomilnacipranmilnacipran b Effexor® Effexor-XR® (sustained-release) and generic Pristiq® Cymbalta® Fetzima® Savella®Tablets: 25, 37. 5, 50, 75, 100 mg Capsules: 37. 5, 75, 150 mg Tablets (extended release): 50, 100 mg Capsules: 20, 30, 60 mg Capsules: 20, 40, 80, 120 mg Tablets: 12. 5, 25, 50, 100 mg75-375 50-100 60-12040-120 100-200 5-HT 2 antagonists nefazodonetrazodone Generic only Generic only Oleptro (extended release)Tablets: 50, 100, 150, 200, 250 mg Tablets: 50, 100, 150, c 300c mg Tablets (scored): 150, 300 mg300-500150-300150-375 Tricyclics d amitriptylineclomipraminedesipraminedoxepin imipramine imipramine pamoatenortriptyline protriptyline trimipramine maleate Elavil ® Anafranil® Norpramin® Sinequan® Tofranil® Tofranil-PMe Aventyl®, Pamelor® Vivactil® Surmontil®Tablets: 10, 25, 50, 75, 100, 150 mg Capsules: 25, 50, 75 mg Tablets: 10, 25, 50, 75, 100, 150 mg Capsules: 10, 25, 50, 75, 100, 150 mg Oral solution: 10 mg/m L (120-m L bottle)Tablets: 10, 25, 50 mg Capsules: 75, 100, 125, 150 mg Capsules: 10, 25, 50, 75 mg Oral solution: 10 mg/5 m L (480-m L bottle)Tablets: 5, 10 mg Capsules: 25, 50, 100 mg150-300100-250150-300150-300 150-300 150-300 50-150 15-60 150-300524 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

(Continued) Table 53-5 Antidepressant Names, Formulations and Strengths, and Dosages Generic name Br and n ame Formulations & s trengths Therapeutic Dosage r ange (mg/day)a Tetracyclicse amoxapine maprotiline Asendin® Ludiomil®Tablets: 25, 50, 100, 150 mg Tablets: 25, 50, 75 mg150-400150-225 Monoamine Oxidase Inhibitors phenelzine selegiline tranylcypromine isocarboxazid Nardil ® Eldepryl® Carbex® Zelapar® Emsam® Parnate® Marplan®Tablet: 15 mg Capsule: 5 mg Tablet: 5 mg Orally disintegrating tablet: 1. 25 mg Patch: 6 mg/24 hr, 9 mg/24 hr, 12 mg/24 hr Tablet: 10 mg Tablet: 10 mg45-9020-50 30-60 30-60 Other Antidepressants bupropion mirtazapine vortioxetine vilazodone Wellbutrin ® and generic Wellbutrin SR® (sustained-release) Wellbutrin XL® (extended-release) Remeron® Brintellix® Viibryd®Tablets: 75, 100 mg Tablets: 100, 150, 200 mg Tablets: 150, 300 mg Tablets: 7. 5, 15, 30, 45 mg Soltabs: 15, 30, 45 mg Tablets: 5, 10, 20 mg Tablets: 10, 20, 40 mg200-450 15-45 10-20 40 Note. 5-HT2 = serotonin2 receptor. a Dosage ranges are approximate. Many patients respond at relatively low dosages (even dosages below those in the ranges given in table); others may require higher dosages. b Approved for fibromyalgia; doses given are those recommended for that use. c Trazodone also available in 150-and 300-mg divided-dose formulations. d All the tricyclic and tetracyclic antidepressants shown are available generically. Most of the brand name drugs listed have been discontinued. e Sustained release. Adapted from Schatzberg, A. F., & De Battista, C. (2015). Manual of clinical psychopharmacology (8th ed. ). Arlington, VA: American Psychiatric Publishing. (continues)Table 53-6 Antidepressant Side Ef fects Side effects account for as many as two-thirds of all premature discontinuations of antidepressants. Most side effects are early onset and time limited (e. g., SSRI decreased appetite, nausea, diarrhea, agitation, anxiety, headache). These can be managed by temporary aids to tolerance. Some side effects are early onset and persistent or late onset (e. g., SSRI apathy, fatigue, weight gain, sexual dysfunction) and may require additional medications or a switch in antidepressant. Strategies for Managing Antidepressant Side Effects: 1. Allow patient to verbalize his/her complaint about side ef fects. 2. W ait and support. Some side effects (i. e., GI distress) will subside over 1-2 weeks. 3. Lower the dose temporarily. 4. T reat the side effects (discussed next). 5. Change to a dif ferent antidepressant. 6. Discontinue medications and start psychological counseling. 525 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

(Continued) Table 53-6 Antidepressant Side Ef fects side effectssr Is & e ffexor Tricyclics (nortriptyline, amitriptyline, imipramine) Bupropion Mirtazapine Management s trategy Sedation ± ++-+ Give medication at bedtime. Increase Remeron dose. Try caffeine. Anticholinergic-like symptoms: Dry mouth/eyes, Constipation, Urinary retention, Tachycardia± +++-± Increase hydration. Sugarless gum/candy. Dietary fiber. Artificial tears. Consider switching medication. GI distress Nausea++-+ ± Often improves in 1-2 weeks. Take with meals. Consider antacids or H2 blockers. Restlessness Jitters/tremors+ ± ++-Start with small doses, especially with anxiety disorder. Reduce dose temporarily. Add beta-blocker (propranolol 10-20 mg bid/tid). Consider short trial of benzodiazepine. Headache +-+-Lower dose. Acetaminophen. Insomnia +-+-Trazodone 25-100 mg po qhs (can cause orthostatic hypotension and priapism). Take medication in A. M. Sexual dysfunction++---May be part of depression or medical disorders. Decrease dose. Consider a trial of Viagra. Try adding bupropion 100 mg qhs or bid. Try adding buspirone 10-20 mg bid/tid. Try adding cyproheptadine 4 mg 1-2 hrs before sex. Seizures--+ ± Discontinue antidepressant. Weight gain ± ± ± ++ Exercise. Diet. Consider changing medications. Agranulocytosis---± Monitor for signs of infection, flulike symptoms. Stop drug, check white blood count. Key:-Very unlikely; ± Uncommon/mild; + moderate Courtesy of Mac Arthur Foundation Initiative on Depression and Primary Care. Mac Arthur Toolkit—Copyright April 2009 3 CM LLC. Used with permission. Retrieved from http://www. dphhs. mt. gov/Portals/85/amdd/documents/AMDD%20Website%20Migration%20Documents/13macarthurtoolkit. pdf526 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

VI. s elf-management resources and tools Brief educational or self-management interventions, such as manualized or book-based therapies and the use of interactive web-based or other computer programs based on cognitive-behavioral approaches, have been shown to improve depres-sion outcomes for patients treated in primary care settings (Mc Naughton, 2009). A. Educational resources (books and websites) 1. P atient education brochures about depression in English and Spanish can be downloaded or ordered from the National Institutes for Mental Health (http://www. nimh. nih. gov/health/publications /depression/complete-index. shtml). The National Institutes for Mental Health also produced a brief video about depression (“www. nimh. nih. gov/health /publications/depression/complete-index. shtml). The National Institutes for Mental Health also produced a brief video about depression (https://www. youtube. com/watch?v=ml NCavst2EU). 2. The M ac Arthur Initiative on Depression and Primary Care (2009) developed patient education materials as part of its Depression Management T ool Kit. The toolkit can be accessed at www. dphhs. mt. gov/Portals/85/amdd /documents/AMDD%20Website%20Migration%20Documents/13macarthurtoolkit. pdf. 3. Bey ond Blue (www. beyondblue. org. au), an organization to address issues related to depression in Australia, has information about depression as well as online communities, a hotline, and online chat. Depression information in multiple languages including Spanish, Chinese, Arabic, and Vietnamese can be found at www . beyondblue. org. au/resources/for-me/multicultural -people. 4. The A ntidepressant Skills Workbook, a self-management manual for adults with depression, can be downloaded free from www. comh. ca /antidepressant-skills/adult/. 5. F eeling Good: The New Mood Therapy (Burns, 1980) describes a cognitive therapy approach to depression management. It is commonly used as self-guided treatment and in depression treatment programs. 6. A f ree interactive skills program based on cognitive-behavioral and interpersonal psychotherapy approaches can be found at http://moodgym. anu. edu. au. B. Community support groups 1. N ational Alliance on Mental Illness website (www . nami. org). This support, education, and advocacy organization offers a variety of educational materials about depression including fact sheets, podcasts, and video clips. 2. The D epression and Bipolar Support Alliance (www . dbsalliance. org) offers educational brochures about depression and other mood disorders and conducts in-person and online support groups and educational events. re Feren Ces American Psychiatric Association. (2010, October). Practice guideline for the treatment of patients with major depressive disorder (3rd ed. ). Retrieved from https://psychiatryonline. org/pb/assets/raw/sitewide/practice _guidelines/guidelines/mdd. pdf. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Washington, DC: Author. Arroll, B., Goodyear-Smith, F., Crengle, S., Gunn, J., Kerse, N., Fishman, T., et al. (2010). Validation of PHQ-2 and PHQ-9 to screen for major depression in the primary care population. Annals of Family Medicine, 8(4), 348-353. doi:10. 1370/afm. 1139. Bauer, M., Pfennig, A., Severus, E., Whybrow, P. C., Angst, J., & Moller, H-J. (2013). World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of unipolar depressive disorders, Part I: Update 2013 on the acute and continuation treatment of unipolar depressive disorders. World Journal of Biological Psychiatry, 14, 334-385. doi: 10. 3109/15622975. 2013. 804195 Burns, D. D. (1980). Feeling good: The new mood therapy. New Y ork: William Morrow. Fancher, T., Mc Carron, R. M., Kukoyi, O., & Bourgeois, J. A. (2009). Chapter 2: Mood disorders—Depression. In R. M. Mc Carron, G. L. Xiong, & J. A. Bourgeois (Eds. ), Lippincott's primary care psychiatry (pp. 17-39). Philadelphia, PA: Wolters Kluwer/Lippincott Williams and Wilkins. Gaynes, B. N., Warden, D., T rivedi, M. H., Wisniewski, S. R., Fava, M., & Rush, A. J. (2009). What did STAR*D teach us? Results from a large-scale, practical, clinical trial for patients with depression. Psychiatric Services, 60(11), 1439-1445. Gonzalez, H. M., Vega, W. A., Williams, D. R., T araf, W., West, B. T., & Neighbors, H. W. (2010). Depression care in the United States: T oo little for too few. Archives of General Psychiatry, 67(1), 37-46. Greenberg, S. A. (2012). The Geriatric Depression Scale (GDS). In Try this: Best practices in nursing care to older adults (No. 4). Retrieved from http://consultgerirn. org/uploads/File/trythis/try_this_4. pdf Gros, D. F., & Haren, W. B. (2011). Open trial of brief behavioral activa-tion psychotherapy for depression in an integrated Veterans Affairs primary care setting. Primary Care Companion to CNS Disorders, 13(4), PCC. 11m01136. doi:10. 4088/PCC. 11m01136527 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Schatzberg, A., & Nemeroff, C. (2009). The American Psychiatric Publishing textbook of psychopharmacology (4th ed. ). Washington, DC: APA. U. S. Burden of Disease Collaborators. (2013). The state of U. S. health, 1990-2010: Burden of diseases, injuries, and risk factors. JAMA, 310(6), 591-608. U. S. Department of Health and Human Services, Depression Guideline Panel. (1993). Clinical practice guideline No. 5, depression in primary care: Vol. 1. Detection and diagnosis. (AHCPR Publication No. 93-0550). Rockville, MD: Author. U. S. Department of Health and Human Services. (2009). Guide to clinical preventive services, 2009 recommendations of the U. S. Preventive Services T ask Force (pocket guide, Abridged version of the recommendations). Retrieved from www. ncbi. nlm. nih. gov/books/NBK37637/. Whiteford, H. A., Harris, M. G., Mc Keon, G., Baxter, A., Pennell, C., Barendregt, J. J., et al. (2013). Estimating remission from untreated major depression: a systematic review and meta-analysis. Psychological Medicine, 43(8):1569-1585. doi: 10. 1017/S0033291712001717. Wittkampf, K., van Ravesteijn, H., Baas, K., van de Hoogen, H., Schene, A., Bindels, P., et al. (2009). The accuracy of Patient Health Questionnaire-9 in detecting depression and measuring depression severity in high-risk groups in primary care. General Hospital Psychiatry, 31(5), 451-459. Wolf, N. J., & Hopko, D. R. (2008). Psychosocial and pharmacological interventions for depressed adults in primary care: A critical review. Clinical Psychology Review, 28, 131-161. Zuithoff, N. P., Vergouwe, Y., King, M., Nazareth, I., Hak, E., Moons, K. G., et al. (2009). A clinical prediction rule for detecting major depressive disorder in primary care: The PREDICT-NL study. Family Practice, 26(4), 241-250. Hellmann-Regen, J., Piber, D., Hinkelmann, K., Gold, S. M., Heesen, C., Spitzer, C., et al. (2013). Depressive syndromes in neurological disorders. European Archives of Psychiatry and Clinical Neuroscience, 263, (2, Suppl. ), 123-136. Kessler, R. C., Chiu, W. T., Demier, O., Merikangas, K. R., & Walters, E. E. (2005). Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62(6), 617-627. Luoma, J. B., Pearson, J. L., & Martin, C. E. (2002). Contact with mental health and primary care prior to suicide: A review of the evidence. American Journal of Psychiatry, 159, 909-916. Mac Arthur Initiative on Depression & Primary Care. (2009). Depression man-agement toolkit. Retrieved from http://www. dphhs. mt. gov/Portals/85 /amdd/documents/AMDD%20Website%20Migration%20Documents /13macarthurtoolkit. pdf. Mc Naughton, J. L. (2009). Brief interventions for depression in primary care: A systematic review. Canadian Family Physician, 55(8), 789-796. National Institute of Mental Health. (n. d. ). Major depression among adults. Retrieved from http://www. nimh. nih. gov/health/statistics /prevalence/major-depression-among-adults. shtml. Nieuwsma, J. A., T rivedi, R. B., Mc Duffie, J., Kronish, I., Benjamin, D., & Williams, J. W. (2012). Brief psychotherapy for depression: A systematic review and meta-analysis. International Journal of Psychiatry in Medicine, 43(2), 129-151. Patterson, W. M., Dohn, H. H., Bird, J., & Patterson, G. A. (1983). Evaluation of suicidal patients: The SAD PERSONS scale. Psychosomatics, 24(4), 343-349. Schatzberg, A. F., & De Battista, C. (2015). The manual of clinical psychophar-macology (8th ed. ). Arlington, VA: American Psychiatric Publishing. 528 CHAPTER 53 | Depression

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

insulin production. Risk factors for type 2 include age older than 45 years, obesity, sedentary lifestyle, family history of diabetes, history of gestational diabetes, delivery of a baby over 9 lb, and race or ethnicity (African Americans, Latinos, Native Americans, and Asian Americans/Pacific Islanders). Type 2 diabetes is becoming more common in children and adoles-cents. According to the SEARCH for Diabetes in Y outh Study (Dabelea et al., 2014), type 2 diabetes in youth represents 50% of new-onset diabetes in youth. Moreover, ethnic minority youth are at higher risk for type 2 diabetes when compared to their white peers. D. Gestational diabetes 1. D efinition and overview Gestational diabetes occurs in 3-12% of pregnancies. Pregnancy is an insulin-resistant state. Women with a history of gestational diabetes have a 40-60% chance of developing type 2 diabetes in the next 5-10 years after their pregnancy; therefore, they should have their blood sugar monitored periodically. For more in depth information, see Chapter 33 on gestational diabetes. II. Database (may include but is not limited to) A. Subjective 1. H istory of presenting illness a. A ge of onset b. P resenting signs and symptoms: Assess for classic signs or symptoms—weight gain or loss, polyuria, polydipsia, and/or polyphagia c. Gr owth and developmental history for children and youth d. H abits: including nutrition (food diary, meal planning), exercise (type and duration)I. Intr oduction and general background Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia that results from decreased insulin secretion, insulin resistance, or both. There are several types of diabetes. The most common types are type 1, type 2, and gestational diabetes. A. Prevalence and incidence Approximately 29. 1 million children and adults in the United States (9. 3% of the population) have diabetes. Of these, 21. 0 million are diagnosed and 8. 1 million are undi-agnosed (Centers for Disease Control and Prevention, 2014). Type 1 diabetes accounts for approximately 5-10% of diagnosed diabetes cases, whereas type 2 makes up the other 90-95% (American Diabetes Association [ADA], 2009b). This number is predicted to increase from 23. 6 million in 2009 to 44. 1 million in 2034 (Huang, Basu, O'Grady, & Capretta, 2009). B. Type 1 diabetes 1. D efinition and overview Type 1 diabetes (T1D) is caused by an autoimmune process that destroys the β cells in the pancreas, thereby resulting in little or no insulin production. Individuals with type 1 diabetes cannot live without administration of exogenous insulin. Whereas T1D is usually associated with youth, there is a form of T1D diagnosed in adulthood called latent autoimmune diabetes of the adult or LADA. The presentation of T1D is often acute and approximately 25% of new-onset T1D presents in diabetic ketoacidosis (DKA) (Dabelea et al., 2014). C. Type 2 diabetes 1. D efinition and overview Type 2 diabetes is usually the result of insulin resis-tance, although it can also be caused by decreased Carolina Noya and Maureen Mc Grath DIabetes Mell Itus© Eliks/Shutterstock; © donatas1205/Shutterstock 529 54Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

c. E xercise: type and duration d. C ultural history, living arrangements, housing, presence of food insecurity, and psychosocial supports and problems e. S exual history: partners and sexual activity; sexu-ally transmitted infection prevention/condom use 6. R eview of symptoms a. C onstitutional signs and symptoms: fatigue, weight loss, and polydipsia b. S kin, hair, and nails; slowed wound healing c. E ye, ear, nose, and throat; blurry vision; and gum infections or dental disease d. R espiratory: shortness of breath e. C ardiac: chest pain f. G astrointestinal: polyphagia and symptoms of gastroparesis g. Ge nitourinary: polyuria, recurrent vaginal yeast infections, sexual or erectile dysfunction h. N eurologic: decreased sensation or tingling and numbness in extremities i. P sychiatric: anxiety and/or depression B. Objective 1. P hysical examination findings a. H eight, weight, body mass index (BMI > 25 or > 23 in Asians) b. V ital signs, including orthostatic blood pressure if indicated c. S kin: acanthosis nigricans; fungal infections of feet or toenails; and cracks in skin or wounds, especially hands and feet; insulin injection sites d. H ead, eyes, ears, nose, and throat: fundoscopic exam to assess for retinopathy, cataracts, vision test for blurry vision, teeth or gum inflammation, and poor dentition e. Th yroid: thyromegaly f. L ungs: crackles consistent with cardiovascular sequela g. C ardiac: irregular heartbeat, cardiomegaly, and murmurs h. A bdomen: hepatomegaly i. V ascular: peripheral pulses, bruits, and edema j. N eurologic: sensory; motor strength; and deep tendon reflexes (patellar and Achilles) k. F oot examination: inspection (note calluses, lesions, edema, nail integrity, and any structural deformities); pulses in dorsalis pedis and pos-terior tibial, determination of proprioception, vibration, and monofilament sensatione. R eview of medication regimens, response to therapy, and adherence issues f. A ssessment of readiness for change, SMART (Specific-Measurable-Attainable-Realistic-Timely) goal attainment, and barriers to self-care g. S elf-glucose monitoring: assess trends of high and low values. h. H ypoglycemia: assess for awareness, frequency, and cause. 2. P ast health history a. M edical illnesses: hypertension, metabolic syn-drome, hyperlipidemia, pancreatitis, pancre-atic cancer, cystic fibrosis, hemochromatosis, Cushing's syndrome, acromegaly, glucagonoma, obesity, and pheochromocytoma. Diabetes-related complications: Microvascular disease (retinopathy, nephropathy, neuropathy, includ-ing sensory and autonomic). Macrovascular dis-ease: cardiovascular disease (CVD), peripheral artery disease, and cerebrovascular disease. b. S urgical history: pancreatic surgery and liver surgery c. T rauma history: pancreatic trauma d. Obs tetric and gynecological history: history of gestational diabetes or delivery of baby weighing more than 9 lb; contraception method e. M edication history: medications that increase blood glucose levels or interfere with the release of insulin (e. g., glucocorticoids, pentamidine, nicotinic acid, thyroid hormone, phenytoin, atypical antipsychotics, and thiazides). Any over-the-counter or herbal medication (e. g., sweetened cough preparations). 3. F amily history a. DM b. M etabolic syndrome c. Obe sity d. Aut oimmune disorders e. Othe r endocrine disorders 4. O ccupational and educational history a. E ducation and literacy level b. O ccupation: type, ability to control environment as it relates to food intake, self-monitoring of blood glucose, and rest c. D ays missed from school or work due to illness 5. P ersonal and social history a. T obacco, alcohol, and drug use b. Die t history and recall530 CHAPTER 54 | Diabetes Mellitus

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

islet cell autoantibodies and autoantibodies to insulin). Y et, their use in regard to diagnosis is limited because of variable predictive values, availability, and/or cost (ADA, 2015; Patel, & Macerollo, 2010). 2. Ge stational diabetes a. The re are two strategies, but no clinical evidence to support one or the other. i. One-step strategy: 2-hour, 75-g oral glucose tolerance test or ii. T wo-step approach: 1-hour, 50-g (nonfast-ing) screen followed by a 3-hour, 100-g oral glucose tolerance test for those who screen positive. b. Di agnosis of gestational diabetes mellitus (GDM) is made when values exceed:i. One step: Fasting ≥ 92 mg/d L 1h: ≥ 180 mg/d L 2h: ≥ 153 mg/d L ii. T wo step: 1h: ≥ 140 mg/d L, then proceed to step 2 3h: ≥ 140 mg/d L (ADA, 2015, p. S14) B. Severity Assess the severity of the disease via the presence or absence of end-organ complications and/or impact on basic and intermediate activities of daily living. C. Significance Assess the significance of the problem to the patient and significant others. D. Motivation and ability Determine patient's motivation for change, via motiva-tional interviewing techniques, and assess for support and barriers to achieve self-management goals. 2. S upporting data from relevant diagnostic tests (T able 54-1) III. a ssessment A. Type 1. T ype 1 and type 2 diabetes (See T able 54-1 for the criteria of diagnosis and T able 54-2 for the clinical interpretations of plasma glucose concentrations) a. S pecial tests for T1D may be obtained to assess for beta cell function (e. g., C-peptide) and immune-mediated beta cell destruction (e. g., Table 54-1 Diagnostic Criteria for Nongestional Diabetes 1. Hgb A1C ≥ 6. 5% 2. Fasting (minimum of 8 hours without food) plasma glucose ≥ 126 mg/d L 3. 2-hour plasma glucose ≥ 200 mg/d L following a 75-g oral glucose tolerance test 4. Random plasma glucose 200 mg/d L in patients presenting with signs & symptoms of hyperglycemia Repeat testing should be done unless test results are clearly unequivocal. Data from American Diabetes Association. (2015). Standards of medical care in diabetes—2015. Diabetes Care, 38(Suppl. 1), S9. Table 54-2 Clinical Interpretations of Plasma Glucose Concentrations Glucose Concentration (mg/d l ) Clinical Interpretation Fasting < 100 Within the reference range 100-125 Impaired fasting glucose/prediabetes≥ 126 Overt diabetes mellitus 2-hr postchallenge load (75-g oral glucose tolerance test)< 140 Within the reference range 140-199 Impaired glucose tolerance/prediabetes≥ 200 Overt diabetes mellitus Data from American Diabetes Association. (2015). Standards of medical care in diabetes—2015. Diabetes Care, 38(Suppl. 1), S1-S93. 531 Assessment

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

IV. Goals of clinical management A. Screening or diagnosing diabetes (see Tables 54-1, 54-2, and 54-3 ) Choose a cost-effective approach for screening and diagnosing diabetes. B. Treatment Select a treatment plan that controls glucose in a safe and effective manner, without causing hypoglycemia. T reatment goals should be adjusted and determined by multiple factors, including risk for hypoglycemia, disease duration, life expectancy, comorbidities, vascular compli-cations, and resources and support systems available to patient (ADA, 2015). For type 2 diabetes, current guidelines should be used to address dyslipidemia and hypertension therapy goals. Refer to current guidelines (Aronow, 2014; Eckel et al., 2014). C. Patient adherence Provide self-management education and support in order to maximize patient adherence. Providers should use motivational interviewing and problem-solving strate-gies to support patients and create collaborative goals. National standards for diabetes self-management educa-tion (DSME) clearly state that goals should be patient centered, personally relevant, and take into account the patient's lived experience (Haas et al., 2012). D. Prevention of complications For all types of diabetes, screening of kidney disease, retinopathy, and neuropathies is of primary importance, as glycemic control can reduce microvascular complica-tions. Additionally, for type 2 DM, primary and secondary prevention of cardiovascular risk factors is as important as glycemic control. V. Plan A. Primary prevention: criteria screening of high-risk groups (see Table 54-3) 1. T reatment guidelines for prediabetes: Individuals at high risk for developing type 2 diabetes (prediabetes), defined as impaired fasting glucose (IFG) of 100-125 mg/d L, impaired glucose tolerance (IGT) of 140-199 mg/d L 2 hours post glucose load, or an Hb A 1C of 5. 7-6. 4%, should be referred to structured programs that emphasize lifestyle changes, including moderate weight loss (7% body weight) and regular physical activity (150 min/wk, strength training 2x/wk) (ADA, 2015). In at-risk individuals with a BMI > 35 kg/m 2 and younger than 60 years old, metformin therapy should be considered for the prevention of type 2 diabetes. Ongoing monitoring for diabetes should be done at least annually. Modifiable CVD risk factors should be identified and appropriate interventions are recommended (ADA, 2015). Refer to T able 54-3 for criteria of high-risk groups. B. Diagnostics Care 1. Hg b A1C every 3-6 months (depending on control) 2. A nnual urine albumin:creatinine ratio 3. C reatinine, e GFR, potassium 4. A nnual lipid panel 5. L iver function tests if on thiazolidinedione medica-tions and/or statins C. Management (includes treatment, consultation, referral, and follow-up care) Providers must first investigate the cause of the diabetes, especially if it is related to infection or medication use, and treat the patient accordingly. Patients initially presenting with type 1 diabetes may be hospitalized depending on Table 54-3 Criteria for T esting for Diabetes or Prediabetes in Asymptomatic Adults 1. T esting should be considered in all adults who are overweight (BMI ≥ 25 kg/m2 or ≥ 23 kg/m2 in Asian Americans) and have additional risk factors: Physical inactivity First-degree relative with diabetes High-risk race/ethnicity (e. g., African American, Latino, Native American, Asian American, Pacific Islander) Women who delivered a baby weighing > 9 Ib or were diagnosed with GDM Hypertension (≥ 140/90 mm Hg or on therapy for hypertension) HDL cholesterol level < 35 mg/d L (0. 90 mmol/L) and/or a triglyceride level > 250 mg/d L (2. 82 mmol/L) Women with polycystic ovary syndrome A1C ≥ 5. 7%, IGT, or IFG on previous testing Other clinical conditions associated with insulin resistance (e. g., severe obesity, acanthosis nigricans) History of CVD 2. For all patients, particularly those who are overweight or obese, testing should begin at age 45 years. 3. If results are normal, testing should be repeated at a minimum of 3-year intervals, with consideration of more frequent testing depending on initial results (e. g., those with prediabetes should be tested yearly) and risk status. Reproduced from American Diabetes Association. (2015). Standards of medical care in diabetes—2015. Diabetes Care, 38(Suppl. 1), S10. 532 CHAPTER 54 | Diabetes Mellitus

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

disease, hypertension, smoking, dyslipid-emia, or albuminuria]) (Handelsman et al., 2015). ii. A ngiotensin-converting enzyme inhibi-tors or angiotensin receptor blockers for patients with hypertension or micro-albuminuria (ADA, 2015; Joslin Diabetes Center & Joslin Clinic, 2009b; Handelsman et al., 2015). b. T ype 1 DM For type 1 diabetes management, the main-stay of the treatment plan is insulin, prefer-ably a basal/bolus regimen via injection or insulin pump. Dosing of insulin for type 1 is often 0. 4-1. 0 units/kg (ADA, 2015). According to the Diabetes Control and Complications T rial (DCCT) and the follow-up Epidemiology of Diabetes Interventions and Complications (EDIC) (National Diabetes Information Clearinghouse, 2009), it is well established that patients with type 1 diabetes check their blood glucose level and base insulin dosing on the amount of carbohydrates eaten and the corre-sponding blood glucose level. Current therapy for patients with type 1 diabetes usually requires prandial injections of a rapid acting insulin and a once or twice per day long-acting basal insulin. This type of therapy is referred to as basal/bolus therapy and insulin pumps provide an alternate their symptoms and degree of illness (e. g., diabetic keto-acidosis). The goal of treatment is to achieve near-normal blood glucose levels without significant hypoglycemia, attain and maintain reasonable body weight, and normal-ize lipids and blood pressure as indicated. 1. M edical nutrition therapy (MNT) a. R eduction in energy intake is a cornerstone of treatment in type 2 diabetes and may be needed in type 1 diabetes. MNT for both types of diabetes  involves distribution of carbohydrates that takes into consideration an individual's pharmacological treatment as well as the person's activity pattern. b. O f the macronutrients, carbohydrates (CHO) have the most significant effect on blood glucose levels so patients need to learn to “carb count” or use “experience-based estimation. ” Recent evi-dence suggests that there are no ideal percent-ages for CHO, protein, and fat intake and that the individual MNT plan should be personalized and address current eating patterns as well as per-sonal preference inclusive of cultural traditions. It is advisable that patients obtain most of their carbohydrates from whole foods such as fruit, vegetables, whole grains, legumes, and other low glycemic index foods. Sucrose is allowable but if used on a regular basis will replace more nutrient-dense food. Sugar-containing beverages should be avoided as much as possible because of their immediate effect on blood glucose levels and contribution to nonnutritive calories and may worsen CVD risk profiles. c. F iber, saturated fat, and dietary cholesterol intake are as recommended for the general population. Newer studies show benefit from Mediterranean-style diets that are rich in MUFA—monounsatu-rated fatty acids (ADA, 2015). 2. E xercise a. A t least 150 minutes/week of moderate-intensity aerobic physical activity (50-70% of maximum heart rate). For exercise rules and precautions, refer to T able 54-4. b. P atients with type 2 diabetes without contrain-dications should perform resistance training at least two times per week (ADA, 2015). 3. P harmacological therapy a. P rophylactic medications i. A spirin, 75-162 mg/day for patients with type 1 or type 2 diabetes at increased car-diovascular risk (most men > 50 years of age and women > 60 years of age who have at least one additional major risk factor [i. e., family medical history of cardiovascular Table 54-4 Exercise Rules and Precautions Avoid vigorous exercise in the presence of ketosis. Wear properly fitted footwear. Before starting, screen for vascular or neurologic complications. Caution in patients with retinopathy, neuropathy, and peripheral vascular disease. High-risk patients should start slowly. Carry identification that includes diagnosis and medication list. If taking sulfonylureas, meglitinides, or insulin, check glucose before starting and carry carbohydrates. Check glucose before and after exercise. Avoid exercise in extreme temperatures and humidity. Use proper equipment. Complete proper warm-up and stretching exercises. Adequate hydration. Stop for any pain, lightheadedness, or shortness of breath. Data from American Diabetes Association. (2015). Standards of medical care in diabetes—2015. Diabetes Care, 38(Suppl. 1), S9. 533 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

delivery to the minimum of 4-6 injections required for this intensive regimen. c. T ype 2 DM Type 2 diabetes management usually begins with lifestyle modification, exercise, and then oral agents. This treatment plan is, however, usually guided by the patient's Hgb A 1C level, blood glucose levels, and their comorbidities. If the patient is grossly hyperglycemic at pre-sentation (e. g., Hgb A 1c > 9%), then insulin is recommended. There are several algorithms for the treatment of type 2 diabetes (American Diabetes Association, 2015; Joslin Diabetes Center & Joslin Clinic, 2009a; Rodbard et al., 2009) (Figure 54-1). d. Or al agents (T able 54-5)Figure 54-1 Algorithm for Management of T ype 2 Diabetes Mellitus Data from Inzucchi, S. E., Bergenstal, R. M., Buse, J. B., Diamant, M., Ferrannini, E., Nauck, M., et al. (2012). Management of hyperglycemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care, 35,1364-1379. STEP 1 Initial drug monotherapy IF INDIVIDUAL GOALS NOT REACHED AFTER 3 MONTHSIF INDIVIDUAL GOALS NOT REACHED AFTER 3 MONTHSIF INDIVIDUAL GOALS NOT REACHED AFTER 3-6 MONTHSEfficacy: High Hypoglycemia Risk: Low Weight: Neutral/loss Major SEs: GI/lactic acidosis Cost: Low To avoid GI side effects at initiation, consider starting at 500mg QD or BID andincreasing by 500mg/wk (Maximum to tal daily dose is 2,000-2,500 mg). Take with meals. Efficacy: Intermediate Hypoglycemia Risk: Low Weight: Neutral Major SEs: Rare Cost: High Efficacy: High Hypoglycemia Risk: Low Weight: Gain Major SEs: Edema, HF, Fx's Cost: High Efficacy: High Hypoglycemia Risk: Low Weight: Loss Major SEs: GICost: High Efficacy: Highest Hypoglycemia Risk: High Weight: Gain Major SEs: Hypoglyc emia Cost: Variable Efficacy: High Hypoglycemia Risk: Moderate Weight: Gain Major SEs: Hypoglyc emia Cost: Low Metformin STEP 2 Two-drug combinations Sulfonylurea (SU)Metformin + OR Thiazolidinedione (TZD) OR DPP-4 Inhibitor (DPP-4-i) OR GLP-1 Receptor agonist (GLP-1-RA) OR Insulin (usually basal)STEP 3 Three-drug combinations STEP 4 More complex insulin strategies Refer to Tables 54-06A and 54-06B fo r information on insulin preparations Insulin (multiple dai ly doses of ten in combination with one or tw o non-insulin agents)Sulfonylurea + OR TZD or DPP-4-i or GLP-1-RAor Insulin (usually basal) Thiazolidinedione + SU or DPP-4-i or GLP-1-RAor Insulin (usually basal) OR DPP-4 Inhibito r + SU or TZDor Insulin (usually basal) OR GLP-1 Receptor agonist + SUor TZDor Insulin (usually basal) OR Insulin (usually basal) + TZDor DPP-4-ior GLP-1-RA534 CHAPTER 54 | Diabetes Mellitus

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

4. S elf-blood glucose monitoring (SBGM) According to the Joslin Diabetes Center & Joslin Clinic (2009b), “the frequency of self glucose moni-toring is highly individualized and should be based on such factors as glucose goals, exercise, medication changes and patient motivation. Patients with type 1 diabetes should monitor at least three times a day. In patients with type 2 diabetes, the frequency of e. I njectable (other than insulin) i. E xenatide (Byetta): class-incretin mimetic; dose 5-10 mcg taken 60 minutes before a meal (type 2 only) ii. P ramlintide (Symlin): class-synthetic hor-mone; dose for type 1 is 15-60 mcg and for type 2 is 60-120 mcg taken before meals f. I nsulins (T able 54-6A and 54-6B)Table 54-5 Oral Agents* Generic b rand Name Daily Dose (Min-Max)Dosing (QD = Daily; b ID = twice a day; t ID = three times a day) Sulfonylureas Glipizide Glucotrol®2. 5-40 mg QD-BID Glipizide controlled release Glucotrol XL®2. 5-20 mg QD Glimepiride Amaryl®1-8 mg QD Glyburide Micronase®, Dia Beta®1. 25-20 mg QD-BID Micronized glyburide Glynase®0. 75-12 mg QD-BID Meglitinide analogs Repaglinide Prandin ®0. 5-16 mg BID before meals D-Phenylalanine derivative Nateglinide Starlix ®120-360 mg TID before meals Biguanides Metformin Glucophage ®500-2,000 mg QD-TID with meals Metformin extended-release Glucophage XR® Glumetza®500-2,000 mg QD with a meal Metformin Riomet® (oral solution) (5 cc = 500 mg) 500-550 mg QD-TID with meals Thiazolidinediones Pioglitazone Actos ®15-45 mg QD Rosiglitazone Avandia®4-8 mg QD-BID Alpha-glucosidase inhibitors Acarbose Precose ®25-300 mg TID with meals Miglitol Glyset®25-300 mg TID with meals DPP-4 inhibitors Sitagliptin Januvia ®100 mg QD Saxagliptin Onglyza®2. 5-5 mg QD SLGT-2 inhibitors Canagliflozin Invokana 100-300 mg QD Dapagliflozin Farxiga 5-10 mg Q am Empagliflozin Jardiance 10-25 mg QD * Note: There are several combinations of various oral agents that are often available. 535 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

monitoring is dependent upon such factors as mode of treatment and level of glycemic control” (p. 2). 5. S elf-management goals and clinical goals (T able 54-7) 6. H ealthcare maintenance a. I mmunizations i. A nnual influenza vaccine ii. P neumococcal 23-valent polysaccharide vaccine (> 2 years old) and pneumococcal 13-valent conjugate vaccine (> 65 years old)Table 54-6a Insulins* Generic Name b rand Name type Onset P eak Duration Aspart Novo Log®Rapid 10-20 min 1-3 hr 3-5 hr Lispro Humalog®Rapid 5-15 min 30-75 min 2-4 hr Glulisine Apidra®Rapid 5-15 min 30-75 min 2-4 hr Regular insulin Novolin® R Short acting 30-60 min 2-4 hr 5-8 hr Humulin® R Same Same Same Same NPH Novolin® N Intermediate 1-3 hr 6-10 hr 16-24 hr Humulin® N Same Same Same Same Glargine Lantus®Long acting 45 min-4 hr None 24 hr Detemir Levemir®Long acting 45 min-4 hr None 24 hr *Inhaled insulins (e. g., glargine u-300 [Toujeo®] and Humulin Regular u-500) are available yet less commonly used than the standard injectable insulins. Table 54-6b Combined Insulins Premixed b rand Name NPH/Regular Novolin® 70/30 Humulin® 70/30 Humulin® 50/50 Lispro protamine/lispro Humalog® Mix 75/25 Lispro protamine/lispro Humalog® Mix 50/50 Aspart protamine/aspart Novolog® Mix 70/30 Table 54-7 Clinical Goals american Diabetes a ssociationa merican a ssociation of Clinical e ndocrinologists Preprandial glucose 80-130 < 110 2-hour postprandial glucose < 180 < 140 Hb A1C< 7% with a less stringent goal of 8% for selected populations≤ 6. 5% for most. Less stringent for people with comorbidities and older adults. Blood pressure < 140/90 < 130/80: Individualized based on age, comorbidities, and duration of disease. Lipids ADA recommendations are in alignments with the American College of Cardiology (ACC) and American Heart Association (AHA) cholesterol treatment guidelines: The focus on statin therapy should be tailored for cardiovascular risk rather than LDL target therapy (Stone et al., 2014). See Chapter 63, Lipid Disorders, for additional information. Low-density lipoprotein (LDL) mg/d L: < 100, moderate risk; < 70, high risk Triglycerides: < 150 mg/d L Same Urine albumin/creatinine ratio < 30 mg /g alb/creat ratio Same Data from American Diabetes Association (2015). Standards of medical care in diabetes—2015. Diabetes Care, 38(Suppl. 1), S1-S93; Handelsman, Y., et al. (2015). American Association of Clinical Endocrinologists and American College of Endocrinology—Clinical practice guidelines for developing a diabetes mellitus comprehensive care plan. Endocrine Practice, 21(Suppl. 1), 1-87. 536 CHAPTER 54 | Diabetes Mellitus

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

b. E ducation: diabetes self-management education and support c. C oncerns and feelings Assist the patient and significant others in expressing and coping with concerns and feelings related to the diagnosis of diabetes, its potential complications, and the management of this disease. Assist the patient to develop strate-gies to promote behavior change. d. I nformation: provide verbal and written infor-mation regarding:i. The diabetes disease process, including signs and symptoms of hyperglycemia and hypoglycemia; pathophysiology of type 1 and type 2 diabetes; and complications of diabetes ii. Di agnostic tests, including what they mean, frequency, and importance of testing iii. M edical management iv. M eal planning and exercise: how to incor-porate these into the patient's lifestyle v. R ationale, action, use, side effects, and cost of therapeutic interventions, including medications vi. S elf-glucose monitoring: what the param-eters are and how to interpret the results for self-management decision making (American Diabetes Association, 2014) vii. Ad herence to long-term treatment plans viii. P revention of complications, self-management strategies ix. T ravel instructions, medical alert identi-fication, sick-day guidelines, and health maintenance VI. s elf-management resources and tools There are numerous educational opportunities for individuals with diabetes, either online, by mail, or by telephone. A. National Diabetes Education Program The National Diabetes Education Program has publica-tions available by mail or online that are geared toward different age groups (from teenagers to older adults) and ethnic backgrounds and are written in a variety of languages (http://ndep. nih. gov/) B. American Diabetes Association The American Diabetes Association's (2009a) website has extensive patient information online, brochures for iii. H epatitis B vaccine in adults 19-59 years old if unvaccinated, and consider if > 60  years old (ADA, 2015) iv. P ap and mammogram for women v. S moking cessation counseling at every visit 7. R eferrals and monitoring Patients should be educated about potential compli-cations from diabetes and how to prevent them. With this in mind, all people with diabetes should have the following referrals and monitoring. a. P atients with diabetes should be referred to an endocrinologist for the following reasons:i. S tarting an insulin pump ii. R ecurrent diabetic ketoacidosis iii. R ecurrent hypoglycemia iv. U nable to adequately control glucose or erratic blood glucose readings b. W omen of childbearing age should receive pre-conception counseling and care. Note: com-bined oral contraceptives should be avoided in patients with DM-related complications and who are over the age of 35 (American College of Obstetricians and Gynecologists, 2000). c. M ental health referrals should be made as needed: screen for depression, diabetes-related stress, anxiety, eating disorders, and cognitive impairment when self-management is poor. d. A ll patients with diabetes mellitus should be referred for diabetes self-management education and support services. e. Di lated eye examination by an ophthalmologist annually. For people with type 1 DM, first referral should occur after 5 years of disease onset and yearly thereafter. For people with type 2 DM referral should occur at initial visit, if exam is normal it can be followed up every 2 years. Women with GDM should be referred during the first trimester. f. F oot examination at every primary care provider visit (with 10 g monofilament) and by a podia-trist every 12 months (for patients without complications). g. D ental examination every 6 months with dentist 8. P atient education a. S ick-day guidelines i. P revent dehydration and ketosis ii. Ade quate fluid and calorie intake iii. A lert patient to signs and symptoms of hypoglycemia and hyperglycemia iv. I nclude patient's family and significant others in the plan537 Self-management resources and tools

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

purchase, and a hotline number for patients who want to speak with someone directly (www. diabetes. org). C. Joslin Diabetes Center The Joslin Diabetes Center has patient education online, brochures, and cookbooks for purchase, including some for children and teenagers, and has Spanish and Asian American websites (www. joslin. org). D. Juvenile Diabetes Research Foundation International The Juvenile Diabetes Research Foundation International provides online or printed information for adults, teenagers, and children and has links to Facebook, Twitter, and Y ou Tube. In addition, it has links to commu-nity events, local chapters, and affiliates around the globe (www. jdrf. org). E. Community support groups There are numerous support groups for individuals with diabetes, in addition to those listed previously. 1. D efeat Diabetes Foundation, Inc. Find local support groups (www. defeatdiabetes. org/). 2. A merican Diabetes Association Website has a link to community events and pro-grams, including those geared for specific ethnic groups (www. diabetes. org/). 3. Di abetes Health Website links to multiple community events (www. diabeteshealth. com/)d Life (www. dlife. com)GLU (https://myglu. org/)Tu Diabetes (www. tudiabetes. org/)Diabetes Mine (www. healthline. com/diabetesmine)TCOYD—T aking Control of Y our Diabetes (http://tcoyd. org/)Behavioral Diabetes Institute (www. behavioraldiabe-tesinstitute. org/)dia T ribe (http://diatribe. org/) Refe Re NCes American College of Obstetricians and Gynecologists. (2000). The use of hormonal contraception in women with coexisting medical conditions (ACOG Practice Bulletin No. 18). Washington, DC: American College of Obstetricians and Gynecologists. Retrieved from www. guideline. gov/content. aspx?id=10924. American Diabetes Association. (2009a). Community events. Retrieved from www. diabetes. org/in-my-community/. American Diabetes Association. (2009b). Diabetes statistics. Retrieved from www. diabetes. org/diabetes-basics/diabetes-statistics/. American Diabetes Association. (2014). Standards of medical care in diabetes—2014. Diabetes Care, 37(1), S14-S80. American Diabetes Association. (2015). Standards of medical care in diabetes—2015. Diabetes Care, 38 (Suppl. 1), S1-S93. Retrieved from care. diabetesjournals. org/content/38/Supplement_1/S4/suppl/DC1 Aronow, W. S. (2014). Eighth Joint National Committee guidelines. Future Cardiology, 10(4), 461-463. Centers for Disease Control and Prevention. (2014). National diabetes statistics report, 2014. Retrieved from www. cdc. gov/diabetes/pubs /statsreport14/national-diabetes-report-web. pdf. http://www. cdc. gov /diabetes/pubs/statsreport14/national-diabetes-report-web. pdf Dabelea, D., Rewers, A., Stafford, J. M., Standiford, D. A., Lawrence, J. M., Saydah, S., et al. (2014). T rends in the prevalence of ketoacidosis at dia-betes diagnosis: The SEARCH for Diabetes in Y outh Study. Pediatrics, 133(4). e938-e945. doi: 10. 1542/peds. 2013-2795 Eckel, R. H., Jakicic, J. M., Ard, J. D., de Jesus, J. M., Houston Miller, N., Hubbard, V. S., et al. (2014). 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: A report of the American College of Cardiology/American Heart Association T ask Force on Practice Guidelines. Journal of the American College of Cardiology, 63(25, Pt. B), 2960-2984. Haas, L., Maryniuk, M., Beck, J., Cox, C. E., Duker, P., Edwards, L., et al. (2012). National standards for diabetes self-management education and support. Diabetes Educator, 38(5), 619-629. Handelsman, Y., Bloomgarden, Z. T., Grunberger, G., Umpierrez, G., Zimmerman, R. S., Bailey, T. S. et al. (2015). American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for developing a diabetes mellitus compre-hensive care plan. Endocrine Practice, 21(Suppl. 1), 1-87. Huang, E. S., Basu, A., O'Grady, A., & Capretta, J. C. (2009). Projecting the future diabetes population size and related costs for the U. S. Diabetes Care, 32(12), 2225-2229. Inzucchi, S. E., Bergenstal, R. M., Buse, J. B., Diamant, M., Ferrannini, E., Nauck, M., et al. (2012). Management of hyperglycemia in type 2 dia-betes: A patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care, 35, 1364-1379. Joslin Diabetes Center & Joslin Clinic. (2009a). Clinical guideline for pharmacological management of type 2 diabetes. Retrieved from www. joslin. org/09_12_2014_Pharma_Guideline_emb_final. pdf Joslin Diabetes Center & Joslin Clinic. (2009b). Clinical guidelines for adults with diabetes. Retrieved from www. joslin. org/joslin_clinical_guidelines . html. National Diabetes Information Clearinghouse. (2009). DCCT and EDIC: The diabetes control and complications trial and follow-up study. Retrieved from http://diabetes. niddk. nih. gov/dm/pubs/control/. Patel, P., & Macerollo, A. (2010). Diabetes mellitus: Diagnosis and screening. American Family Physician, 81(7), 863-870. Rodbard, H. W., Jellinger, P. S., Davidson, J. A., Einhorn, D., Garber, A. J., Grunberger, G., et al. (2009). Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: An algorithm for glycemic control. Endocrine Practice, 15(6), 540-559. Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Merz, C. N. B., Blum, C. B., Eckel, R. H., et al. (2014). 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association T ask Force on Practice Guidelines. Circulation, 129(25, Suppl. 2), S1-S45. 538 CHAPTER 54 | Diabetes Mellitus

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Strawbridge, 2012). People of all ages, genders, and ethnici-ties are affected by epilepsy. As a group, people with epilepsy face both medical and psychosocial challenges (including employment and educational barriers). The lifetime risk of dying from a seizure-related cause is estimated to be as high as 20% (Hesdorffer & T omson, 2013). Successful treatment of epilepsy both prolongs life and improves quality of life (Galanopoulou et al., 2012). II. Database (may include, but is not limited to) A. Subjective 1. S eizure history a. A ge of onset b. D escription of seizures from patient and witnesses c. M ost recent seizures: characteristics and frequency d. A ny changes in seizure pattern (including characteristics and frequency) e. T riggering events (stress, fatigue, alcohol, sleep deprivation, and menstruation) f. I mpairment of consciousness g. A ny recent intervention including paramedics, emergency department visits, or benzodiaz-epine use h. A ny previous intervention, including surgery or medications changes i. P revious diagnostic work-up, including electro-encephalogram (EEG) and magnetic resonance imaging (MRI); last visit with neurologist 2. A ntiepileptic drugs (AEDs) and medications a. N ame, formulation, strength, and dosing schedule. Note recent change from brand to generic or between different generics and adherence to medication. I. Intr oduction and general background This chapter provides information to help the primary care provider evaluate a patient with previously diagnosed epilepsy. Epilepsy refers to a group of conditions that are character-ized by the recurrent risk of disturbances of cerebral func-tion (seizures) because of excessive neuronal discharges in the brain occurring in a paroxysmal manner (Fisher et al., 2014). An epileptic seizure occurs when the cerebral cortex is rendered hyperexcitable (because of an increase in excitatory neurotransmission, a decrease in inhibitory neurotransmis-sion, or a disturbance in brain circuitry) by any of a number of causes, including metabolic disturbances, injuries, strokes, tumors, and developmental abnormalities (Lowenstein, 2008). Depending on the site in the brain that is affected, the disturbance of function may result in a loss or impairment of consciousness, a disturbance of behavior, or an abnormality of motor or sensory function. When the cause of the disturbance is easily reversible (e. g., hyponatremia, hypoglycemia, alcohol withdrawal, medication toxicity, or fever), the seizure is said to be “provoked” and the patient's condition is not considered epilepsy. When the cause of the seizure is not readily reversible, and seizures have occurred on more than one occasion, the chance for further seizures is high and the patient is said to have epilepsy (Marks & Garcia, 1998). According to the International League Against Epilepsy (ILAE), epilepsy can be diagnosed when two or more unprovoked seizures recur after 24 hours; when a person has one unprovoked seizure but is at high risk of another; or, if the person is diagnosed with an epilepsy syndrome (Fisher et al., 2014). Epilepsy is a common condition in all medical practices, and almost all practitioners are called on to care for patients with epilepsy. In the United States, an estimated 2. 2 million people live with epilepsy and 150,000 new cases are diag-nosed each year. About 1 in 26 people will develop epilepsy in his or her lifetime (England, Liverman, Schultz, & Maritza Lopez, Paul Garcia, and M. Robin Taylor EPILEP sy© Eliks/Shutterstock; © donatas1205/Shutterstock 539 55Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

ii. C erebellar testing (special emphasis on gait disturbances and Romberg) iii. F ocal motor signs and mental status d. S kin: rashes, signs of neurocutaneous syndrome (hypo/hyperpigmented macules) 2. Di agnostic testing and work-up a. S ource (should be neurologist or epileptologist) b. S upporting documentation i. A bnormal electroencephalogram (EEG) (not always present) ii. MR I. Though not always revealing, MRI remains the best modality to identify subtle but dangerous structural causes of seizures (e. g., small tumors or vascular malforma-tions). A CT scan can be obtained quickly at most institutions and, thus, is useful for visualizing acute structural causes such as hemorrhages or trauma; however, if CT is unrevealing, MRI is still necessary to exclude subtle structural causes (Ramli, Rahmat, Lim, & T an, 2015). III. Assessment A. Determine the diagnosis: the following diagnoses should be considered for all patients presenting with seizures 1. E pilepsy (T able 55-1) 2. C erebrovascular disease 3. C ardiac arrhythmias with resulting cerebral hypoper-fusion 4. S yncope 5. N onepileptic (i. e., psychogenic) seizure 6. T ransient ischemic attack 7. M igraine 8. A lzheimer's and other neurodegenerative disorders (can cause seizures in the geriatric population) 9. I nfection, may exacerbate seizures 10. M ovement disorder 11. D iabetes B. Severity 1. D etermine if seizures are fully controlled. 2. I f seizures are not fully controlled, determine if the patient is at the maximum clinically tolerated dose of medication (regardless of serum levels) 3. A ssess for AED toxicity (T able 55-2)b. D ose changes: drugs tried in the past, responses (therapeutic and toxic), and tolerability c. S igns and symptoms of AED toxicity including blurred vision, diplopia, ataxia, somnolence or fatigue, confusion or mental slowing, and gastro-intestinal upset d. C oncomitant treatment for other conditions that may interact with AEDs (e. g., nonsteroidal anti-inflammatory drugs, antibiotics, oral contracep-tives, and anticoagulants, herbal supplements) e. U se of rescue medications, such as sublingual lorazepam, buccal midazolam, or rectal diazepam 3. P ast medical history a. H ead trauma, developmental and genetic disor-ders, and neurologic and psychiatric disorders b. R ecent minor illnesses, especially gastrointes-tinal disorders with vomiting or fever c. C hronic illnesses (e. g., HIV/AIDS, cerebrovas-cular disease, and cancer) 4. F amily history (query both sides of the family): epilepsy, Alzheimer's disease, neurodegenerative disorders, malignancy, and psychiatric disorders 5. P ersonal and social history a. O ccupational history b. H abits: alcohol or illicit drug use c. S leep patterns (change in sleep patterns may provoke seizures) d. S tress and coping: recent stressors (can provoke seizures), coping strategies, and social support e. R ecreational activities and safety: driving, swim-ming, climbing, other risky activities for patients with ongoing seizures, and use of helmets or other protective devices 6. R eview of systems a. S kin: rash or jaundice b. G astrointestinal: signs and symptoms of chemical hepatitis (e. g., nausea, vomiting, anorexia, abdominal pain, or malaise) c. N eurologic: full review of systems d. P sychiatric: note affect and symptoms of active psychiatric disease e. W eight gain or loss B. Objective 1. P hysical examination a. T emperature and blood pressure b. C ardiac (rule out cardiac origin) c. N eurologic examination i. C ranial nerves (special emphasis on nystagmus)540 CHAPTER 55 | Epilepsy

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

C. Significance Assess the significance of the symptoms and chronic nature of this disorder to the patient and significant others (i. e., burden, quality of life, eagerness for surgical intervention) D. Patient adherence Assess if the patient is able to adhere to the treatment plan (direct, open-ended inquiry; medication refill history). IV. Goals of clinical management A. Achieve seizure-free status with lowest side effect profile of AED therapy B. Attempt to arrive at AED monotherapy if possible Table 55-1 Epilepsy Syndromes Generalized Focal Seizures begin diffusely throughout the cerebral cortex Seizures arise from a discrete focus in cerebral cortex or limbic structures (hippocampus or amygdala) Idiopathic (primary, without clear cause)Seizure types: absence, myoclonic, tonic-clonic Neurologic examination: normal Neuroimaging: normal EEG: normal background with fast (3-6 Hz) generalized spike-and-wave discharges Common examples: childhood absence epilepsy, juvenile myoclonic epilepsy, epilepsy with generalized tonic-clonic seizures on awakening Treatment: valproate, ethosuximide (effective for absence seizures only), topiramate, lamotrigine, felbamate, levetiracetam, or zonisamide Seizure types: simple partial (focal without impairment of consciousness), complex partial (focal with impairment of consciousness), or secondarily generalized tonic-clonic Neurologic examination: normal Neuroimaging: normal EEG: normal background with focal epileptiform discharges Common examples: benign childhood epilepsy with centrotemporal spikes (Rolandic epilepsy); benign epilepsy with occipital paroxysms Treatment: often no medical treatment is necessary; all AEDs may be effective except ethosuximide Symptomatic (secondary; caused by an apparent or assumed brain lesion)Seizure types: atypical absence, myoclonic, tonic, atonic, tonic-clonic Neurologic examination: diffuse or multifocal abnormalities Neuroimaging: diffuse or multifocal abnormalities common EEG: abnormal background with slow (< 3 Hz) generalized or multifocal epileptiform discharges Common examples: Lennox-Gastaut syndrome, progressive myoclonus epilepsies Treatment: valproate, lamotrigine, levetiracetam, felbamate, rufinamide, topiramate, zonisamide, clobazam, ketogenic diet, or corpus callosotomy, vagus nerve stimulator Seizure types: focal without impairment of consciousness, focal with impairment of consciousness, secondarily generalized tonic-clonic Neurologic examination: focal abnormalities or normal Neuroimaging: focal abnormalities common EEG: normal or abnormal background with focal or multifocal epileptiform discharges Common examples: temporal lobe epilepsy, frontal lobe epilepsy Treatment: carbamazepine, phenytoin, valproate, gabapentin, pregabalin, lacosamide, lamotrigine, levetiracetam, oxcarbazepine, topiramate, zonisamide, (adjunct therapy— vigabatrin, pregabalin, ezogabine, perampanel, eslicarbazepine) or resective surgery Modified with permission from “Management of seizures and epilepsy,” 1998, American Family Physician. Copyright © 1998 American Academy of Family Physicians. All Rights Reserved; Modified from Marks, W. J., Jr., & Garcia, P. A. (1998). Seizures and epilepsy: Current management. American Family Physician, 57(7), 1589-1600. 541 Goals of clinical management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 55-2 Oral Antiepileptic Medications Generic Name Brand Names trengths Available1 (mg)Typical Adult s tarting Dose2Typical Increment and Rate of Ascension 3Most Common Dose-Related Adverse Effects Nondose-Related and Idiosyncratic Reactions Carbamazepine Tegretol® Tegretol-XR® Carbatrol®100, 200100, 200, 400 100, 200, 300200 mg BID 200 mg BID200 mg BID200 mg/wk (dose TID-QID) 200 mg/wk200 mg/wk Dizziness, somnolence, ataxia, nausea, vomiting, diplopia, blurred vision Hyponatremia, rash, Stevens-Johnson syndrome, leukopenia, aplastic anemia, agranulocytosis, transaminitis, hepatic failure Clobazam Onfi® 2. 5 mg/m L Tablet: 10 mg, 20 mg10 mg BID 10 mg BID on week 1 then to 20 mg BIDAtaxia, dysarthria, constipation, drooling, lethargy, somnolence, urinary tract infection, cough, fever, aggressive behavior Stevens-Johnson syndrome Eslicarbazepine Aptiom® 200, 400, 600, 800400 mg daily Increments of 400 mg/wk to 800-1,200 mg Nausea, vomiting, ataxia, dizziness, headache, somnolence, fatigue, blurred vision, diplopia Drug-induced eosinophilia, liver dysfunction, anaphylaxis, angioedema Ethosuximide Zarontin® 250 250 mg QD to 250 mg BID250 mg/wk Anorexia, nausea, vomiting, drowsiness, headache, dizziness Rash, Stevens-Johnson syndrome, hemopoietic complications, systemic lupus erythematosus (SLE) Ezogabine Potiga® 50, 200, 300, 400100 mg TID increase dosage by 50 mg or less 3 times daily (150 mg/day) every week to max 200-400 mg TIDConfusion, dizziness, decrease coordination, memory impairment, somnolence, tremor, vertigo, blurred vision, diplopia, fatigue Prolonged QT interval, syncope, amnesia, psychotic effects such as hallucinations, renal effects. Felbamate Felbatol® 400, 600 1,200 mg/ day in 3 to 4 divided doses600-mg increments every 2 weeks to 2,400 mg/day Photosensitivity, weight loss, abdominal pain, nausea/vomiting, dizziness, headache, insomnia Stevens-Johnson syndrome, hematologic abnormalities (i. e., aplastic anemia and leukopenia, hepatic failure Gabapentin Neurontin® 100, 300, 400, 600, 800300 mg TID 300 mg/wk Somnolence, dizziness, ataxia, fatigue Rash, weight gain, behavioral changes, extremity edema Lacosamide Vimpat® 50, 100, 150, 20050 mg BID 100 mg/wk to max 400 mg/d Dizziness, ataxia, vomiting, diplopia, nausea, vertigo PR interval lengthening 542 CHAPTER 55 | Epilepsy

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 55-2 Oral Antiepileptic Medications Generic Name Brand Names trengths Available1 (mg)Typical Adult s tarting Dose2Typical Increment and Rate of Ascension 3Most Common Dose-Related Adverse Effects Nondose-Related and Idiosyncratic Reactions Lamotrigine Lamictal® Lamictal-XR®25, 100, 150, 200 25, 50, 100, 20025 mg daily only for monotherapy (special considerations for polytherapy not addressed here)25-50 mg/ 2 wk only for monotherapy (special considerations for polytherapy not addressed here)Dizziness, ataxia, somnolence, headache, diplopia, blurred vision, nausea, vomiting, rash Rash, Stevens-Johnson syndrome, transaminitis Levetiracetam Keppra® Keppra-XR®250, 500, 750 500, 750500 mg BID 1,000 mg/d/ 2 wk to max 3,000 mg Somnolence, asthenia, infection, dizziness Depression, irritability Oxcarbazepine Trileptal® Oxtellar150, 300, 600300 mg BID 600 mg/d/wk to max 2,400 mg Dizziness, somnolence, diplopia, fatigue, nausea, vomiting, ataxia, abnormal vision, abdominal pain, tremor, dyspepsia, abnormal gait Stevens-Johnson syndrome, bone marrow suppression, hyponatremia Perampanel Fycompa® 2, 4, 6, 8, 10, 122 mg orally Increase by 2 mg daily per week. Max dose 12 mg qhs. Backache, unsteady gait, ataxia, dizziness, headache, somnolence, psychiatric effects, fatigue Psychiatric behavior, homicidal, suicidal thoughts Phenobarbital 15, 30, 60, 100100 mg QD 15-30 mg/wk Somnolence, cognitive and behavioral effects Rash, Stevens-Johnson syndrome, hematopoietic complications, transaminitis, hepatic failure Phenytoin Dilantin ® 30, 50, 100 300 mg daily 25-30 mg/wk Ataxia, diplopia, slurred speech, confusion Rash, Stevens-Johnson syndrome, hematopoietic complications, gingival hyperplasia, coarsening of facial features, transaminitis, hepatic failure Pregabalin Lyrica® 25, 50, 75, 100, 150, 200, 225, 30075 mg BID or 50 mg TID300 mg/wk to max 600 mg/day Dizziness, somnolence, dry mouth, peripheral edema, ataxia, confusion, asthenia, abnormal thinking, blurred vision, incoordination, weight gain Weight gain Skin rash (continues)(Continued)543 Goals of clinical management

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 55-2 Oral Antiepileptic Medications Generic Name Brand Names trengths Available1 (mg)Typical Adult s tarting Dose2Typical Increment and Rate of Ascension 3Most Common Dose-Related Adverse Effects Nondose-Related and Idiosyncratic Reactions Rufinamide Banzel® 200, 400 400-800 mg/d (BID doses)400-800 mg/day every 2 days to max 3,200 mg/day Somnolence, dizziness, ataxia, headache, fatigue, nausea Multiorgan hypersensitivity, QT interval shortening Tiagabine Gabitril® 4, 6, 8, 10, 12, 164 mg daily 4 mg/wk (dose BID-QID)Dizziness, nervousness, asthenia, confusion, tremor Topiramate Topamax 1® Trokendi XR25, 50, 100, 200 (same as above)25 mg BID 50 mg daily50 mg/wk(same as above)Somnolence, dizziness, ataxia, slurred speech, psychomotor slowing, cognitive problems, word-finding difficulty Weight loss, transaminitis, nephrolithiasis Valproate Depakote® Depakote-ER®125, 250, 500 250, 500250 mg TID500 mg daily250 mg/wk Same as above Nausea, vomiting, tremor, thrombocytopenia, weight gain Transaminitis, hepatic failure, pancreatitis, rash, Stevens-Johnson syndrome, hair damage or loss, Vigabatrin Sabril® 500 500 mg orally twice daily500-mg increments at weekly intervals, depending upon response, up to 1,500 mg twice daily Weight increase, confusion, decreased coordination, blurred vision, diplopia, infection of ear, aggressive behavior, fatigue Hepatic failure, visual field defect, psychiatric disorder, suicidal thoughts. Zonisamide Zonegran® 25, 50, 100 100 mg/day 200 mg/day for 2 wk to max 400 mg/day Somnolence, anorexia, dizziness, headache, nausea, agitation/irritability Stevens-Johnson syndrome, oligohydrosis/hyperthermia, nephrolithiasis 1Strengths listed are for tablet or capsule formulations of the brand name agents. 2Initiation doses for some agents vary, depending on concomitant medications, body weight, age of patient, and other factors; consult prescribing information for each drug. Doses are for nonurgent initiation of medication; clinical circumstances may necessitate higher initial doses and accelerated titration. See prescribing information for pediatric doses, which are based on body weight and often must be administered more frequently than in adults. 3Rate of ascension may need modification, depending on seizure frequency and occurrence of adverse effects. Note that phenytoin may be increased in 25-mg increments by using a halved 50-mg Dilantin® Infatab® tablet or by 30 mg using a 30-mg Dilantin Kapseal® capsule. 3For children and adults with swallowing impairments, check with your pharmacy to see whether tablets can be crushed or if oral solutions/ suspensions are available. Data from “Management of seizures and epilepsy,” 1998, American Family Physician. Copyright © 1998 American Academy of Family Physicians. All Rights Reserved; Marks, W. J., Jr., & Garcia, P. A. (1998). Seizures and epilepsy: Current management. American Family Physician, 57(7), 1589-1600. Additional medication information was obtained from: http://www. micromedexsolutions. com/micromedex2/librarian/ © 2015 Truven Health Analytics Inc Reviewed by Brian Alldredge, Pharm D UCSF Epilepsy Center. Acknowledgment: Robin Taylor, NP, authored prior edition. (Continued)544 CHAPTER 55 | Epilepsy

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

uncommonly clinically significant and usually does not require discontinuation of the AED. 4. C onsider other tests if diagnosis is in question (electrolytes, glucose, creatinine, rapid plasma reagin [RPR], EKG, tilt-table [to rule out syncope], video-EEG telemetry) C. Medication management (Tables 55-2 and 55-3 ) D. Referral guidelines Refer to neurologist or epileptologist when: 1. Di agnosis of epilepsy is in question 2. S eizures are uncontrolled on one AED at maximum tolerated dose 3. C omplete seizure control, but with bothersome or intolerable AED side effects 4. A ED withdrawal: Consider after 2-3 years of seizure control 5. P regnant woman with a seizure disorder E. Client education 1. P rovide verbal and written information about the etiology and treatment of epilepsy. 2. Di scuss the importance of adherence to medication regimes, emphasizing that the maximum tolerated dose is one increment below the dose at which the patient experiences side effects (Alldredge, 2013). 3. R eview the importance of lifestyle issues on seizure control: regular sleep-wake schedule, minimal or modest alcohol intake, maintaining hydration. C. Assist the patient to achieve optimal level of functioning with daily activities and quality of life while living with a chronic, often unpredictably relapsing disorder V. Plan A. Screening: There are no screening tests or preventive strategies for epilepsy. B. Diagnostic tests 1. B lood levels of AEDs: to assess for adherence or possible toxicity. Not all AEDs have defined “therapeutic ranges” (e. g., benzodiazepines and all AEDs released subsequent to valproic acid). Note that AED therapeutic ranges are only a rough guide; many patients require levels in the “toxic” range to achieve complete seizure control and tolerate these levels without significant clinical toxicity. Likewise, some patients may have their seizures controlled at blood levels below the usual therapeutic range. Routine blood level monitoring is not useful. 2. C omplete blood count: thrombocytopenia, anemia, and leukopenia secondary to AEDs. Obtain a baseline before initiating a new AED and in early phase of treatment or if patient is symptomatic. 3. L iver enzymes and liver function tests: obtain a baseline before initiating a new AED and in early phase of treatment or if patient is symptomatic. Some AEDs can cause elevated liver enzymes, but this is Table 55-3 Medication T reatment Strategies for Patients with Epilepsy Establish an epilepsy syndrome diagnosis for each patient (Table 55-1). Select medications appropriate for that epilepsy syndrome (Table 55-1). Among the syndrome-appropriate medications, choose the agent best suited for the particular patient, based on patient and medication characteristics (Table 55-2). Initiate and titrate the medication at doses, increments, and rates appropriate for that medication to enhance tolerability (Table 55-2). Ascend the medication, regardless of serum levels, until complete seizure control is achieved, or until persistent, unacceptable side effects occur. If satisfactory seizure control is not achieved, transition the patient to another agent appropriate for the epilepsy syndrome being treated. Attempt to arrive at antiepileptic drug monotherapy for each patient. If trials with one or two agents fail to achieve acceptable results, refer the patient to an epilepsy specialist for consultation. Modified with permission from “Management of seizures and epilepsy,” 1998, American Family Physician. Copyright © 1998 American Academy of Family Physicians. All Rights Reserved; Modified from Marks, W. J., Jr., & Garcia, P. A. (1998). Seizures and epilepsy: Current management. American Family Physician, 57(7), 1589-1600. 545 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

VI. s elf-management resources A. Epilepsy Foundation An excellent resource for patient and families can be found at: www. epilepsy. com/. This site is sponsored by the Epilepsy Therapy Project and the Epilepsy Foundation. The individuals involved with this site are among the top epilepsy experts in the country. A wide variety of resources is available on diagnosis, treatment, clinical trials, and support for family and caregivers. It is also a good resource for patients and families to identify local Epilepsy Foundation affiliates throughout the country. The local affiliates can help direct patients and families to local resources (advocacy, job training, support groups, etc). The site has a function called “My Epilepsy Diary,” which allows patients and families to enter seizures, medi-cations, side effects, and healthcare appointments. It can be used to set alerts so that patients remember to take their medications at the proper times. The site also has a section for healthcare professionals, with more sophisticated information that tends to be highly accurate and carefully reviewed: http://professionals. epilepsy. com/homepage /index. html. B. Seizure tracker Seizure T racker is a website that allows patients to enter data on medication dosages, seizure frequencies, use of res-cue medications, and so forth and then share this informa-tion with healthcare providers of their choosing. https://www. seizuretracker. com/. C. Citizens United for Research in Epilepsy (CURE) CURE is an organization that promotes awareness and education of epilepsy and raises funds for research in epilepsy. www. cureepilepsy. org/. REFERENCE s Alldredge, B. K. (2013). Seizure disorders. In Kimble, M., B. K. Alldredge, R. L. Corelli, M. E. Ernst, B. J. Guglielmo, P. A. Jacobson, W. A. Kradjan, & B. R. Williams (Eds. ), Koda-Kimble & Young's applied therapeutics: The clinical use of drugs. (10th ed. ). Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins. England, M. J., Liverman, C. T., Schultz, A. M., & Strawbridge, L. M. (2012). Epilepsy across the spectrum: Promoting health and understanding. A summary of the Institute of Medicine report. Epilepsy & Behavior, 25, 266-276. Fisher, R., Acevedo, C., Arzimanoglou, A., Bogacz, J., Cross, H., Elger, C. E., et al. (2014). A practical clinical definition of epilepsy. Epilepsia, 55(4), 415-482. Galanopoulou, A., Buckmaster, P. S., Staley, K., Moshé, S. L., Perucca, E., Engel J., Jr., et al. (2012). Identification of new epilepsy treatments: Issues in preclinical methodology. Epilepsia, 53(3), 571-582. Hesdorffer, D., & T omson, T. (2013). Sudden unexpected death in epilepsy. Potential role of antiepileptic drugs. CNS Drugs, 27(2), 113-119. Lowenstein, D. H. (2008). Seizures and epilepsy. In A. S. Fauci, E. Braunwald, D. L. Kasper, S. L. Hauser, D. L. Longo, J. L. Jameson, et al. (Eds. ), Harrison's principles of internal medicine online (17th ed. ). New Y ork: Mc Graw Hill. Marks, W. J., Jr., & Garcia, P. A. (1998). Management of seizures and epilepsy. American Family Physician, 57(7), 1589-1600. Ramli, N., Rahmat, K., Lim, K. S., & T an, C. T. (2015). Neuroimaging in refractory epilepsy. Current practice and evolving trends. European Journal of Radiology, 84(9), 1791-1800. doi:10. 1016 /j. ejrad. 2015. 03. 024546 CHAPTER 55 | Epilepsy

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

7 in the United States in the past 4 decades (Spechler & Souza, 2014). Additional complications associated with GERD include esophagitis, esophageal ulceration, and esophageal strictures. Respiratory manifestations, such as chronic cough, shortness of breath, and exacerbation of asthma, are also commonly seen. It is important to always consider the possibility of GERD in patients with respiratory symptoms (Galmiche, Zerbib, & Des Varannes, 2008). Reflux of gastric acid can also cause sore throats and tooth decay. Antisecretory therapy and other treatment modalities for GERD produce a huge economic burden. B. Pathophysiology and etiology of GERD Several factors can contribute to the development of GERD. In normal individuals (i. e., those who do not have GERD), four mechanisms protect the esophageal epithe-lium from being damaged by reflux of gastric contents (Hauser et al., 2008). 1. A c ompetent lower esophageal sphincter (LES), which acts as a barrier to reflux 2. Effe ctive movement of contents through the esophagus 3. S econdary peristalsis, which sweeps refluxed material back into the stomach and closes the LES 4. The a cid-neutralizing effect of swallowed saliva and mucous present in the upper GI (UGI) tract From a broad perspective, the final common path in the development of GERD is altered gastric motility or injury to the UGI tract. Esophageal dysmotility is associated with a great many illnesses, including rheumatologic and endocrine disorders. Altered gas-tric motility may be associated with a weak LES or transient LES relaxation, weak or disordered esopha-geal peristalsis, or delayed gastric emptying. GERD is sometimes the first symptom in young women with scleroderma, CREST syndrome, or mixed con-nective tissue disorders. Local esophageal damage can be caused by increased gastric acid secretion I. Definition and overview Gastroesophageal reflux disease (GERD) is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric acid into the esophagus, the oral cavity or the lung (Kahrilias, 2008). It is the most common gastrointestinal (GI) diagnosis recorded during outpatient clinic visits in the United States (Katz, Gerson, & Vela, 2013). GERD affects 19 million adults, accounting for 4,590,000 outpatient visits and 96,000 hospitalizations annually (Practice Parameters Committee of the American College of Gastroenterology, Wang, & Sampliner, 2008). Prevalence is estimated at 20-25% of adults (Practice Parameters Committee of the American College of Gastroenterology et al., 2008; T alley & Vakil, 2005). Studies show that 40% of adults in the United States report regular heartburn and regurgitation; 18% report it weekly. It is more common with increased age. It has become more preva-lent in China, Japan, and other Asian countries because of the increasing adoption of a Western diet (Hauser, Oxentanko, & Sanchez, 2014). A. Significance and complications Recognizing and treating GERD is important, not only for symptomatic management, but also to avoid the complication of Barrett's esophagus and esophageal carcinoma (Kahrilias, 2008). Approximately 5. 6% of the population in the United States has Barrett's esophagus (Spechler & Souza, 2014). Barrett's esophagus involves the replacement of normal squamous epithelium with columnar epithelium, which can occur when normal esophageal mucosa is exposed repeatedly to stomach acid. The columnar epithelium can transform into dysplasia, a precursor to cancer. The worldwide incidence of esopha-geal cancer is 65. 8 cases per 1,000 patient-years in those with high-grade dysplasia. The risk with low-grade dysplasia is 16. 98 cases per 1,000 patient-years compared to 5. 98 cases without dysplasia (Hauser et al., 2014). The mortality rate is high with adenocarcinoma. Esophageal adenocarcinoma has increased in frequency by a factor of Karen C. Bagatelos, Geraldine Collins-Bride, and Fran Dreier Gastroesopha G eal r e F lux D I sease© Eliks/Shutterstock; © donatas1205/Shutterstock 547 56Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

weight gain, even in an individual of normal BMI, is also thought to have this effect (Katz et al., 2013). c. G allbladder disease may cause symptoms similar to GERD d. P regnancy can exacerbate reflux because of hor-monal influences and increased pressure on the upper digestive tract e. N eurologic disease, such as a stroke or brain tumor, or any condition that affects neural path-ways, including neurologic medications f. Di abetes can cause gastroparesis, which in turn causes increased reflux g. C ollagen-vascular disease (scleroderma, mixed connective tissue disease, and systemic lupus erythematosis) can cause changes in the mucosa or the circulation in the UGI tract h. R ecurrent pulmonary infections (possible aspi-ration) and asthma i. C erebral palsy and other neurodevelopmental disabilities j. M edications: aspirin, nonsteroidal anti-inflam-matory drugs, hormones, vitamins, adrenergics, and anticholinergics 2. F amily history a. P eptic ulcer disease, GI cancer, gallbladder disease b. Di abetes, rheumatologic, and other endocrine disordersor the retrograde passage of bile and pancreatic juice. Mucosal injury further decreases the rate of passage of the bolus of food through the UGI tract. Additional factors that decrease the flow of acid and food through the UGI tract include reduced saliva, increased hydrochloric acid, and decreased mucosal blood flow. Specific structural or physiologic con-ditions, such as a hiatal hernia or obstructive sleep apnea (Hauser et al., 2008), also decrease the rate of passage of food through the UGI tract. Motility is further affected by factors that increase abdominal pressure (pregnancy, weight gain, obesity, and tight clothing) and by hormonal influences (progesterone, cholecystokinin, secretin, and low gastrin). Hormonal influences can cause transient LES relaxation, excess acid production, and decreased UGI tract motility (T able 56-1). II. Database (may include but is not limited to) A. Subjective 1. P ast medical history a. P eptic ulcer disease (associated with a hyperse-cretory state) b. Obe sity (body mass index [BMI] > 29) causes increased pressure on the stomach and lower esophagus causing more acid to reflux. A recent Table 56-1 GERD Common Etiologies Causative Factor Clinical e xamples Motility disorders Esophageal dysmotility caused by diminished peristalsis: rheumatologic and endocrine disorders, such as Sjögren syndrome, scleroderma, CREST syndrome, or mixed connective tissue disorders. Altered gastric motility including a weak lower esophageal sphincter or transient lower esophageal sphincter relaxation, weak or disordered esophageal peristalsis, and delayed gastric emptying seen with gastroparesis or gastric outlet obstruction. Local damage Increased gastric acid secretion or the retrograde passage of bile and pancreatic juices that cause damage to the esophageal mucosa. Change in resistance to gastric acid Factors that decrease the flow of acid and food through the upper gastrointestinal tract, such as reduced saliva (Sjögren syndrome, anticholinergic medications), increased hydrochloric acid (stress response or gastrinoma), or decreased mucosal blood flow (radiation therapy or ischemia). Structural and physiologic changes Associated with the following conditions: hiatal hernia, obstructive sleep apnea, weight gain, obesity, pregnancy, or wearing tight clothing. Hormonal influences Progesterone, cholecystokinin, secretin, and low gastrin. 548 CHAPTER 56 | Gastroesophageal Reflux Disease

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

B. Objective 1. P hysical examination a. Ge neral: appearance, development, nourish-ment; note tight clothing if present b. W eight, BMI c. Ea r, nose, and throat: dentition changes, tooth decay, and pharyngeal erythema d. C ardiac examination: should be normal in a patient with GERD e. C hest examination: wheezing, adventitious sounds f. A bdominal examination: obesity, epigastric ten-derness, distention, and tympanic bowel sounds g. R ectal examination: stool hemoccult III. a ssessment A. Determine the diagnosis GERD is most commonly diagnosed by history and presenting symptoms. The following diagnoses should be considered for all patients presenting with symptoms of GERD: 1. C ardiac disease or angina (should be excluded before beginning GI evaluation) (Katz et al., 2013) 2. Es ophageal stricture or mass 3. Es ophageal motility disorder 4. Es ophageal spasm 5. H elicobacter pylori infection. In contrast to previous practice, screening for H pylori is not recommended in the diagnostic evaluation of GERD according to the 2013 practice guidelines of the American College of Gastroenterology (Katz et al., 2013). 6. G astroparesis 7. P eptic ulcer disease 8. Z ollinger-Ellison syndrome B. Severity Assess the severity of the disease, including duration of symptoms and risk for complications of untreated or poorly treated GERD. The diagnosis of GERD is currently subdivided into: 1. ER D (erosive disease) 2. NER D (nonerosive disease) C. Significance and motivation Assess the significance of the symptoms to the patient and explain the often chronic nature of this disorder. Determine the motivation and ability of the patient to follow through with the treatment plan that can involve significant modification of weight, habits, food choices, and timing of meals. 3. P ersonal and social a. C urrent life stressors: stress can reduce the esophageal perception thresholds for pain (Mizyad, Fass, & Fass, 2009). b. Die t: i. A lthough it has been accepted in the past that alcohol, tobacco, caffeine (coffee, colas, and tea), spicy foods, fatty foods, acidic foods (tomatoes, oranges), carbonated beverages, mint, and chocolate can produce or worsen GERD, studies to date show conflicting evidence for the effect of these habits on the LES, and there are currently no published studies that document improve-ment in GERD symptoms or complica-tions with cessation of these habits. Current guidelines call for individual patients with GERD to avoid those foods and habits that worsen their symptoms (Katz et al., 2013). ii. L arge meals and late night eating are known provoking factors for GERD. 4. R eview of systems a. G astrointestinal i. P ain: the typical symptom is heartburn, a retrosternal burning sensation originating in the subxyphoid region and spreading upward into the chest occurring 30-60 min-utes after meals. In severe episodes, there are esophageal spasms or noncardiac chest pain. The pain can radiate into the neck, shoulders, and back. ii. D ysphagia, episodes of choking (can present as coughing with eating) iii. R egurgitation of gastric contents into the mouth iv. N ausea and vomiting (can be seen with GERD, although not a common associated symptom) v. A ggravating factors for these symptoms a. P osition (lying down, especially post-prandial reclining; bending over and lifting heavy objects) b. W earing tight clothing or belts c. I ndividual provoking factors (as noted previously, this may include tobacco, alcohol, caffeine, and certain foods) b. Ea r, nose, and throat: chronic sore throat, early morning hoarseness c. M outh: complaint of bad breath (halitosis) d. C ardiac: full cardiac review of systems is indicated e. P ulmonary: cough (especially nocturnal cough), wheezing (shortness of breath is not typically seen with GERD)549 Assessment

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

IV. Goals of clinical management A. Screening The American College of Gastroenterology recommends that patients with typical GERD symptoms of heartburn and/or regurgitation be managed pharmacologically. Patients with alarm symptoms or signs such as dysphagia or weight loss do require diagnostic studies such as esophago-gastroduodenoscopy (EGD). It has been reported that 50% of the patients who are screened with EGD have nonero-sive gastroesophageal reflux (NERD) (Hauser et al., 2014). B. Treatment 1. M edical management is designed to promote gastric emptying, augment the resting tone of the LES, and favorably alter the nature of refluxed material through nonpharmacologic and pharmacologic means. 2. T reatment aims to assist the patient in the management of GERD symptoms and enhance lifestyle modification to prevent recurrence of symptoms and disease. C. Prevention of complications These include the following: Barrett's esophagus, adeno-carcinoma, esophagitis, dysphagia caused by esophageal strictures, narrowing or spasm, ulcers, persistent pain, and bleeding. V. p lan A. Screening There are no screening tests available for the early detection or prevention of GERD. However, there are preventive measures that can be taken. These include maintaining normal body weight, reducing stress, and avoiding eating large fatty meals before bedtime. B. Diagnostic tests 1. L aboratory tests: complete blood count, stool for occult blood. In unrelenting cases, check serum gastrin to evaluate for Zollinger-Ellison syndrome. 2. Ele ctrocardiogram if chest pain is present. Perform or refer for additional cardiology diagnostic studies if angina is suspected. 3. UGI s eries: if dysphagia is present, consider UGI series to rule out a stricture or mass. 4. Ac cording to the 2013 Practice Guideline for the Diagnosis and Management of GERD (Katz et al., 2013), endoscopy is indicated in the following circumstances:a. A larm signs or symptoms, such as persistent vom-iting, hematemesis, evidence of GI blood loss, involuntary weight loss, progressive dysphagia, anemia, evidence of GI bleeding, chest pain proven to be of noncardiac etiology, or a mass, stricture, or ulcer found on imaging studies. b. W heezing, orthopnea, or atypical respiratory symptoms c. U nrelenting symptoms despite therapy, or family history of esophageal cancer d. P atients who have reflux of many years' dura-tion should receive an endoscopy to screen for Barrett's esophagus. If Barrett's esophagus is con-firmed, then surveillance endoscopy should be done every 6 months to 3 years, depending on pathologic findings and the endoscopist's recom-mendations (Practice Parameters Committee of the American College of Gastroenterology et al., 2008). Caucasian men over 50 have the highest risk for Barrett's esophagus. e. R ecurrent symptoms after antireflux surgery. 5. S pecial studies Additional evaluation includes tests to measure reflux and more precisely evaluate the motility of the esophagus and stomach (gastric emptying study, manometry with a 24-hour p H study, and endos-copy with biopsy). A gastric emptying study may reveal decreased gastric emptying, which can cause functional dyspepsia. A manometry with p H study can quantify the amount of reflux that a patient has in 24  hours and also measures the pressure in the upper and lower esophageal sphincters. These tests characterize GERD more precisely and also provide evidence for determining if the patient is an appropriate surgical candidate. C. Management Many patients with GERD respond to management with weight reduction, antacids or other medication, habit changes, elevation of the head of the bed, stress reduction, and other nonsurgical measures. For those who cannot be managed successfully with these measures but do respond to proton pump inhibitors (PPIs), and who do not want to take medication indefinitely, surgery is a viable option. 1. N onpharmacologic measures a. M echanical measures: raise the head of the bed 8-10 inches, and maintain an upright posture for a minimum of 30-60 minutes after eating. b. Die tary measures i. D o not eat within 3 hours of bedtime. ii. A void those foods that seem to aggravate symptoms. c. S moking cessation should be considered550 CHAPTER 56 | Gastroesophageal Reflux Disease

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

effectiveness over time (tachyphylaxis) within a relatively short time. See T able 56-2 for a list of side effects associat-ed with GERD medications. Serious side effects can be associated with H2RAs, but these are rare. Although PPIs have a good safety profile, there can be side effects associated with their use. Because PPIs affect calcium metabolism, they should be used with caution in patients at high risk for hip fracture (T argownik & Leung, 2010). PPIs are also associated with an increased risk of Clostridium difficile and other enteric infections, and may be contraindicated in patients at high risk for these infections. d. F or patients with slow gastric emptying, consid-er using prokinetics/antiemetics:i. M etoclopramide (Reglan®), 10 mg three to four times daily. This agent increases the rate of gastric and esophageal empty-ing by stimulating the smooth muscle of the intestine. The potential side effects of metoclopramide should be reviewed with the patient before initiating treatment. The most serious, although infrequent, side effects include tardive dyskinesia, agranulo-cytosis, supraventicular tachycardia, hyper-aldosteronism, and neuroleptic malignant syndrome. ii. C isapride (Propulsid®), 10 mg four times daily before meals and at bedtime. Given its risk for potentially life-threatening arrhyth-mias, this agent is now only available for limited access protocol use by gastroen-terologists. It is very effective in enhancing gastric emptying and generally has fewer side effects than metoclopramide. iii. F or nausea, one can use ondansetron (Zofran®) or promethazine (although the latter often produces drowsiness). iv. D omperidone has been found to be effec-tive but is not approved for GERD by the U. S. Food and Drug Administration. e. F or patients with gastroparesis who do not respond to medications, consider a referral to a tertiary medical center for a gastric stimulator. 3. S urgical options The most common surgical procedure performed for GERD is the Nissen fundoplication. This surgery may be indicated in a small number of patients with severe reflux who do respond to PPIs but who may have reasons, such as drug side effects, for prefer-ring surgical management. The patient must undergo detailed evaluation by a gastroenterologist before d. W eight loss when body mass index is greater than 29 or when there has been a recent weight gain e. S tress management 2. P harmacologic measures Initial pharmacologic treatment of GERD is influ-enced by the frequency and severity of symptoms, and whether the patient is thought to have ERD (erosive reflux disease) or NERD (nonerosive reflux disease). Excellent documentation exists showing that PPIs are more effective and relieve symptoms more rapidly than H2 receptor antagonists (H2RAs), although those patients with ERD seem to have a higher rate of symptom relief. a. F or mild symptoms : patients with infrequent symptoms often respond well to antacids. Liquid preparations can be used, 15 m L (double-strength preparations) and 30 m L (single-strength prepa-rations) 1 and 3 hours after meals and at bedtime until symptoms resolve. b. F or mild to moderate symptoms in NERD, H2RAs can be effective and are less expensive than PPIs. They work by blocking histamine-induced stim-ulation of gastric parietal cells. H2RAs are most effective when given as a divided dose twice daily. Clinicians who use a “step-down approach” to the treatment of GERD often begin treatment with PPIs rather than with H2RAs. Clinicians who prefer a “step-up” approach begin with H2RAs. c. F or moderate to severe symptoms or for the suspicion or diagnosis of ERD, treatment of choice is a PPI. PPIs are potent inhibitors of gastric acid secretion, working by turning off the pumps in parietal cells. All PPIs seem to be equally effective. Selection of a particular PPI is often determined by insurance company for-mularies. There are many preparations on the market and the reader is encouraged to consult information for each agent. Most PPIs are given once daily, 30-60 minutes before the first meal of the day. Dosage can be increased to twice daily if needed or given at bedtime if nighttime symptoms are an issue. PPI treatment should achieve resolution of symptoms and complete healing of the esophagus in 8 weeks. If symptoms recur within 6 months, chronic therapy may be needed with either daily or twice-daily dosing of a PPI (T able 56-2). Patients who do have reso-lution of symptoms can continue taking PPIs or H2RAs on as needed basis. H2RAs can be added to PPIs to control nighttime symptoms, but it should be noted that H2RAs can exhibit waning 551 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 56-2 Commonly Used GERD Medications* Medication Category with e xamples Initial Dose Maintenance Dose p recautions Antacids Use with caution in renal impairment. Many drug interactions, especially with higher doses (e. g., antipsychotics, anticonvulsants, and calcium channel blockers). Aluminum hydroxide and magnesium hydroxide (Alamag OTC, Maalox ®)5-10 ml or 2-4 tablets 1-3 hours after meals and bedtime HSPRN according to symptoms Calcium carbonate and magnesium hydroxide (Mylanta ® Gelcaps, Mylanta® Supreme, or Rolaids® Extra Strength)Same as above Same as above Constipation is a frequent side effect H2 receptor antagonists Many adverse reactions including cardiac arrhythmias, reversible confusional states, and increased prolactin levels. Use with caution in renal impairment (creatinine clearance < 50). Monitor for vitamin B 12 deficiency with long-term use. Ranitidine (Zantac®) 150 mg twice daily or 300 mg daily (taken in the evening or at bedtime if single dose)150 mg at bedtime Famotidine (Pepcid ®) 20 mg twice daily, take second dose in the evening or at bedtime20 mg at bedtime Nizatidine (Axid ®) 150 mg twice daily or 300 mg daily (taken in the evening or at bedtime if single dose)150 mg daily Proton pump inhibitors (PPIs)Usually prescribed for 6-8 weeks for initial treatment Check for drug interactions Good safety profile. Long-term safety use best studied with omeprazole, the first PPI on the market. Long-term use of PPIs: adjust to the lowest dose for symptom control (Kahrilias, Shaheen, & Vaezi, 2008). Take before breakfast. If twice daily dosing, take second dose before evening meal. No dose adjustment required for renal impairment Omeprazole (Prilosec ®) 20-40 mg daily 20-40 mg daily Take 30 minutes before a meal. Lansoprazole (Prevacid®) 15-30 mg daily 15-30 mg daily Take 30 minutes before a meal. Pantoprazole (Protonix®) 20-40 mg daily 20-40 mg daily Take at least 1 hour before a meal. Rabeprazole (Acip Hex®) 20 mg daily 20 mg daily Esomeprazole (Nexium®) 40 mg daily 40 mg daily * Reflects suggested dosages for GERD. Dosages for erosive esophagitis and other esophageal disorders may vary. 552 CHAPTER 56 | Gastroesophageal Reflux Disease

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

surgery can be considered. Presurgical evaluation includes endoscopy, UGI series, and esophageal manometry with a 24-hour p H study. The surgical treatment of choice for the obese patient is bariatric surgery. D. Follow-up 1. F ollow-up in approximately 4-6 weeks after initiating treatment or sooner if symptoms increase in severity. Assess adherence to treatment plan. 2. G astroenterology consult if symptoms worsen or complications occur. If no response to treatment, consider EGD, UGI series, or Cine esophagram. 3. A ssess for side effects of medications. E. Patient education 1. A ssist the patient and family to voice their concerns and develop coping strategies with respect to the disease process and its management. 2. P rovide verbal and written information about the pathophysiology of GERD and its treatment. The National Institutes of Health has a very good handout that is available for distribution. See the website below. 3. Di scuss what the patient can expect with diagnostic testing, including preparation and aftercare. 4. E xplain the therapeutic benefit and side effects of any prescribed treatment. 5. S tress that follow-up is recommended in person or by telephone to monitor treatment response and make appropriate treatment regimen changes. VI. s elf-management resources A. The National Institutes of Health The National Institutes of Health has multiple brochures for patients. Refer to their website: http://digestive. niddk. nih. gov/ddiseases/pubs/gerd/. B. The Mayo Clinic The Mayo Clinic also has excellent resources: www. mayoclinic. com/health/gerd/DS00967. re Feren Ces Galmiche, J. P., Zerbib, F., & Des Varannes, S. B. (2008). Review article: Respiratory manifestations of gastro-esophageal reflux disease. Alimentary Pharmacology & Therapeutics, 27(8), 449-464. Hauser, S. C., Oxentanko, A. S., & Sanchez, W. (2014). Mayo Clinic Gastroenterology and Hepatology Board Review. Rochester, MN: Mayo Clinic Scientific Press. Kahrilias, P. J. (2008). Gastroesophageal reflux disease. New England Journal of Medicine, 359(16), 1700-1707. Kahrilias, P. J., Shaheen, N. J., & Vaezi, M. F. (2008). American Gastroenterological Association medical position statement on man-agement of gastroesophageal reflux disease. Gastroenterology, 135(4), 1383-1391. Katz, P. O., Gerson, L. B., & Vela, M. F. (2013). Guidelines for the diagnosis and management of gastroesophageal reflux disease. American Journal of Gastroenterology, 108, 308-328; doi: 10. 1038/ajg. 2012. 444 Mizyad, I., Fass, S. S., & Fass, R. (2009). Gastro-oesophageal reflux disease and psychological comorbidity. Alimentary Pharmacology & Therapeutics, 29(4), 351-358. Practice Parameters Committee of the American College of Gastroenterology, Wang, K. K., & Sampliner, R. (2008). Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett's esophagus. American Journal of Gastroenterology, 103, 788-797. Spechler, S. J., & Souza, R. F. (2014). Barrett's esophagus. New England Journal of Medicine, 371, 836-845. T alley, N. J., & Vakil, N. (2005). Guidelines for the management of dyspepsia. American Journal of Gastroenterology, 100, 2324-2337. T argownik, L. E., & Leung, S. L. (2010). Proton-pump inhibitor use is not associated with osteoporosis or accelerated bone mineral density loss. Gastroenterology, 138(3), 896-904. 553 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

arrangements like moving or new caregivers, or recent hospitalization. B. Sensory impairment 1. D efinition and overview Both visual and hearing impairment greatly impact the quality of life for older adults. Other sensory impairments that are seen in advanced age include change of taste and smell. Along with sensory impair-ments comes social isolation, depression, anxiety, loss of independence, greater risk of falls, and functional decline. Visual impairment is defined as visual acuity less than 20/40. Blindness is defined as visual acuity less than 20/200 (Durso & Sullivan, 2013). There are many common eye conditions older adults are likely to develop as they age that result in worsening visual acuity. Those include but are not limited to cataracts, age-related macular degeneration, glaucoma, and diabetic retinopathy. Hearing impairment has a substantial negative impact on the way patients communicate. It has also been linked to increased incidence of cogni-tive deterioration, increased falls, and gait disorders. Presbycusis is defined as age-related hearing loss. There are many reasons why older adults suffer from hearing loss and it is important to recognize the dif-ferent types of hearing loss. The most common type in older adults is sensorineural hearing loss. Other types of hearing loss are classified as conductive or mixed. Various infections can also cause hearing loss as well in older adults and some individuals may have an autoimmune inner ear disease that can contribute to hearing loss such as systemic lupus erythematous, Crohn's disease, and ulcerative colitis to name a few. Diabetes mellitus can affect the vasculature of the cochlea leading to hearing loss. Ototoxic medica-tions like aminoglycoside antibiotics, antimalarial medications, platinum-based chemotherapy agents, I. Intr oduction and general background Geriatric syndromes are defined as common conditions seen in older adults that cannot be classified into a single disease but have a significant impact on well-being and quality of life. They are complex conditions more frequently seen among older adults that are multifactorial in etiology and require a multidisciplinary approach to management and treatment. The geriatric syndromes discussed in this chapter include many of the conditions commonly seen in primary care of older adults. Those syndromes are frailty, sensory impairment, falls, urinary incontinence, and delirium. A. Frailty 1. D efinition and overview Frailty is an increasingly recognized geriatric syn-drome that has a tremendous impact on the older individual, their family, and society as a whole (Theou et al., 2011). Frailty is a condition made up of many different components. Presenting com-plaints commonly include decreased energy, poor appetite and inability to consume adequate nutri-tion, weight loss, weakness, and decreased physical activity. It is a chronic syndrome which is progressive in nature developing along a continuum of severity. Frailty is associated with a high risk for poor clinical outcomes due to inability to recover from stressors. These adverse clinical outcomes often include falls, functional impairment, loss of independence, and mortality. The main goal is prevention of frailty by maintaining muscle mass and activity level in older adults as well as adequate nutritional intake. 2. P revalence Frailty tends to be more prevalent in the presence of any stressors to the body. Stressors in older adults can include factors such as infections, dehydration, new medications, depression, and any changes in living Courtney Gordon Ger Iatr IC Syndrome S© Eliks/Shutterstock; © donatas1205/Shutterstock 554 57Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Leading risk factors for urinary incontinence include female gender, cognitive impairment, abdominal surgery, obesity, impaired mobility, and increasing age. Incontinence has a substantial impact financially on the healthcare system as well as the individual's quality of life. An estimated 12 billion dollars is spent annually on incontinence supplies, medications, and caregiver time (Williams et al., 2014). The different types of urinary incontinence include functional incontinence, stress incontinence, urge incontinence, overflow incontinence, and mixed incontinence. Please refer to Chapter 25, Urinary Incontinence in Women, for more detailed information. 2. P revalence Urinary incontinence increases in incidence with age and is more common in women than men. Approximately 15-30% of healthy older adults expe-rience some urinary leakage. The prevalence is nearly 50% among frail community dwellers and between 50% and 75% among institutionalized older adults (Williams et al., 2014). Incontinence often goes unreported by patients due to embarrassment and social stigma. Urinary incontinence, like falls, is one of the main reasons persons are moved out of their homes into residential nursing facilities. It has a great burden on caregivers and negatively affects quality of life. Family members have difficulty helping their loved ones with their toileting and as a result need more help. Urinary incontinence is associated with a 30% increase in functional decline, and a 2-fold increased risk of falls, depressive symptoms, and nursing home placement (Goode, Burgio, Richter, & Markland, 2010). E. Delirium 1. D efinition and overview Like the previous syndromes, delirium is multifacto-rial and important to recognize in the geriatric popu-lation as individuals experiencing delirium are at an increased risk for poor clinical outcomes. Key features include an acute onset with a fluctuating course as well as waxing and waning of symptoms. Typically described as a transient syndrome some cases of delir-ium have been reported to last as long as a few weeks to months. Delirium often goes misdiagnosed as demen-tia especially in the acute care setting. It is important to remember most dementias typically present gradu-ally and progressively over many months to years, unlike delirium, which occurs suddenly and changes often over the course of 24 hours. However, a major predisposing factor for the development of delirium is underlying cognitive impairment, so often older adults can have both delirium and dementia. Other loop diuretics, and nonsteroidal anti-inflammatory drugs can all worsen hearing loss. Acoustic neuroma, Meniere disease, trauma, and radiation can all also contribute to hearing loss in the older adult. 2. P revalence Both visual and hearing impairments increase in incident as people age. These impairments have a substantial impact on the quality of life of the older adult as well as the medical system. Chronic eye conditions are one of the most common reasons for office visits among those 65 years and older (Durso & Sullivan, 2013). Hearing loss is one of the most common chron-ic conditions affecting people over the age of 65. The prevalence of hearing loss is 20-40% in adults aged 50 years or older and more than 80% for those aged 80 years or older (Chou, Dana, Bougatsos, Fleming, & Beil, 2011). C. Falls 1. D efinition and overview Significant morbidity and mortality are associated with falls in older adults. The prognosis worsens in people with repetitive and frequent falls. Falls and gait disorders, like all geriatric syndromes, play an important role in the quality of life for older adults. Depression and confusion are often seen in patients who suffer from falls. Family members also begin thinking of placing their loved ones in a residential facility due to falls, gait disorders, and resultant risk of injury to themselves in the home. The fear of fall-ing can also create stress to individuals and family. The fear of falling has been shown to increase over-all fall risk. One of the major consequences of fear of falling is the restriction and avoidance of activities (Delbaere, Crombez, Vanderstraeten, Willems, & Cambier, 2004). 2. P revalence Falls are the most common event that in turn causes loss of independence in older adults. More than one-third of community-living adults older than 65 years fall each year. Approximately 10% of falls result in a major injury such as a fracture, soft tissue injury, or traumatic brain injury (Tinetti & Kumar, 2010). The incidence increases for those individuals over the age of 80 and those who reside in residential facilities. D. Urinary incontinence 1. D efinition and overview Urinary incontinence is defined as any involun-tary leakage or loss of urine. Urinary incontinence is a syndrome that can result from different medi-cal conditions and the usage of certain medications. 555 Introduction and general background

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

to decipher what requires attention from an ophthal-mologist versus what can be handled in the outpa-tient setting. Questions to ask include: Do they now require reading glasses? Do they have associated pain? Is their vision blurred? What is the time frame for loss of vision? Hearing loss data are often reported from family members and caregivers who find the patient is not hearing as well as normal. Hearing loss that is asso-ciated with age is gradual and spans many years. Common complaints from patients are not being able to hear well in large crowds; for example, when dining out they have difficulty engaging in conver-sations due to inability to hear well. Hearing loss is often considered by patients and family members as a normal part of aging and not something that can be fixed. Often this is not the case. As a clinician it is important to about ask the nature of the hearing loss, the timing (days, months, years), and any associated symptoms like ear pain, ringing, drainage, or dizzi-ness. If they have already been examined and have hearing aids, are they wearing them appropriately? Do they know how to care for them? 3. Fa lls During the detailed history it is important to ask if the patient has had any previous falls, balance issues, or worsening in vision recently. What medications is the person taking? Are they depressed or suffer from dizziness, and do they have any associated pain? These factors all contribute to the increased risk for falls. By targeting risk factors, interventions can be made to decrease incidence of falls. 4. U rinary incontinence A thorough history of urinary incontinence must include gaining information from the patient, family member, or caregiver about frequency, duration, and severity of symptoms. Often an older adult is reluc-tant to discuss urinary incontinence due to embar-rassment. Questions should also include: Do you ever leak urine when you cough or sneeze? Do you have problems making it to the bathroom in time? If yes, why do you have difficulty? Do you find yourself getting up frequently during the night to urinate? 5. D elirium Clinical diagnosis is made after a detailed history, a cognitive assessment, and a physical and neuro-logical exam. Knowing a patient's cognitive status at baseline is important to determine any fluctuations or subtle changes. Obtaining a detailed history from family members and caregivers is vital to ascertain any recent changes in mental status. It is important predisposing factors for delirium include depression, coexisting medical conditions, drugs/medications, environmental changes, electrolyte disturbances, infection, injury, and change in functional status, poor appetite, and sensory impairment. Three different forms of delirium exist—hyperactive, hypoactive, and mixed. Hyperactive delirium is the individual who is very anxious and agitated, has difficulty sleep-ing, and can be aggressive with staff and caregivers. Hypoactive deliriums are often missed because the main symptoms are the patient is more lethargic and sleepy than their baseline. Mixed delirium is common and is a combination of the two (Wong, Holroyd-Leduc, Simel, & Straus, 2010). 2. P revalence Delirium is a common occurrence in older adults and is associated with high morbidity and mortality. Delirium is also associated with functional decline and immobility, which result in further complications of care. Delirium is the most common complication among hospitalized older adults (Witlox, Eurelings, de Jonghe, Kalisvaart, Eikelenboom, & van Gool, 2010). On admission to the hospital prevalence of delirium can range from 10% to 40% of older adults. Patients admitted to the ICU have an even higher inci-dence of 70-87% (Williams et al., 2014). The preva-lence of delirium at the end of life is also reported to be quite high as well, upwards of 80-85% (Durso & Sullivan, 2013). Delirium complicates hospital stays for at least 20% of the 12. 5 million patients 65 years of age or older who are hospitalized each year and increases hospital costs by $2,500 per patient, so that about $6. 9 billion of Medicare hospital expenditures are attributable to delirium (Inouye, 2006). II. d atabase A. Subjective 1. F railty Subjective data are obtained from a detailed history from the patient if they are able to provide informa-tion as well as from any family members or care-givers who are present. Family members typically complain that their loved one is slowing down. The individual seems weaker or more tired than usual. Patients often complain of having no energy and feeling as if everything is a burden. 2. S ensory impairment Patients with visual impairments will have various complaints. It is important to do a detailed history 556 CHAPTER 57 | Geriatric Syndromes

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

for clinicians to note the timing of the mental status change and the course thus far. Additionally, iden-tify any preceding factors such as new medications, change in physical environment, or injury. It is impor-tant to diagnose delirium as it can be a medical emer-gency and improve with treatment quickly. B. Objective: physical examination 1. F railty a. P ertinent physical exam findings may include: i. H ead, eyes, ears, nose, and throat (HEENT)—temporal wasting, dry mucous membranes ii. C ardiovascular—tachycardia or other arrhythmias iii. W eight loss and poorly fitting clothes 2. S ensory impairment a. M easure visual acuity using the Snellen chart. b. E xamine whether the older adult's pupils respond to light. c. A ssess visual fields via confrontation and extra-ocular motility. d. E xamine the outer parts of the eye (lids, lashes, and brows) e. W ith an ophthalmoscope assess the lens for opacities; the optic disc for increased cupping or pallor, arteriovenous narrowing, nicking and/or copper and silver wiring; and the maculae for hemorrhages, exudates, and drusen. f. W hen assessing hearing it is imperative to examine with an otoscope and observe the ear canal as well as the tympanic membrane. Cerumen can occlude the ear canal resulting in significant hearing loss as well as discom-fort and can be easily removed providing relief. When inspecting the ear canal look for any tumors, cysts, polyps, or foreign bodies that might impair hearing. It is important to look for any perforation of the tympanic membrane or significant thickening of the membrane, which can worsen hearing. g. W hen assessing hearing, clinicians can perform tuning fork tests with both the Weber and the Rinne to differentiate the type of hearing loss in the older adult. 3. Fa lls a. E xamine footwear and clothing, which can impede safety. b. Obt ain orthostatic vital signs. c. A ssess cognitive status with a validated tool like the ones included in this chapter (see Figures 57-1 and 57-2). d. C heck visual acuity (see previous section on sensory impairment). e. P ertinent physical exam findings can include: i. H EENT—Nystagmus and other ocular deficiencies contributing to the risk for falls. Ears impacted with cerumen contrib-uting to dizziness and falls. Examine mouth to look for moist mucous membranes. Dry membranes are an indicator for dehydra-tion, which can contribute to falls. ii. C ardiovascular—Assess for arrhythmias and other cardiac abnormalities that can cause syncope and falls. Assess both carotid arteries for bruits. iii. M usculoskeletal—Examine for strength and any movement disorders that can con-tribute to falls. f. The re are several validated tests that measure balance and mobility in the older adult but are often not practical to perform in a busy clinic setting. The Timed Up and Go test and the functional reach test however are fairly easy to use and take relatively little time. (See T able 57-1). 4. U rinary incontinence a. P atients or their caregivers can complete a void-ing or bladder diary, which the clinician can use to review episodes of incontinence regarding timing and frequency. Patients or their caregivers write down the time of urination, the amount, and any additional comments such as what they were doing, for example, coughing, sneezing, or sleeping. b. P hysical exam is less useful for initial assessment of urinary incontinence than the detailed history (Goode et al., 2010). However, a thorough physical exam should include:i. C ardiovascular—A thorough cardiovas-cular assessment looking for signs of fluid overload associated with congestive heart failure, which can contribute to inconti-nence. Elevated jugular venous pressure, arrhythmias, increased edema to extremi-ties, and shortness of breath. ii. A bdominal—Palpate the bladder for full-ness and if there is any associated pain or tenderness. Examine the abdomen for any constipation, which can contribute to incontinence. iii. A r ectal exam should be done in particu-lar for men to assess for enlarged prostate, masses, or fecal impaction. 557 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

The Confusion Assessment Method Instrument: 1. [Acute Onset] Is there evidence of an acute change in mental status from the patient's beseline? 2A. [Inattention] Did the patient have difficulty focusing attention, for example, being easily distractible, or having difficulty keeping track of what was being said? 2B. (If present or abnormal) Did this behavior fluctuate during the interview, that is, tend to come and go or increase and decrease in severity?3. [Disorganized thinking] Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?4. [Altered level of consciousness] Overall, how would you rate this patient's level of consciousness? (Alert [normal]; V igilant [hyperalert, overly sensitive to environmental stimuli, startled very easily], Lethargic [drows y, easily aroused]; Stupor [difficult to arouse]; Coma; [unarousable]; Uncertain)5. [Disorientation] Wa s the patient disoriented at any time during the interview, such as thinking that he or she was somewhere other than the hospital, using the wrong bed, or misjudging the time of day?6. [Memory impairment] Did the patient demonstrate any memory problems during the interview, such as inability to remember events in the hospital or difficulty remembering instructions? 7. [Perceptual disturbances] Did the patient have any evidence of perceptual disturbances, for example, hallucinations, illusions or misinterpretations (such as thinking something was moving when it was not)?8A. [Psychomotor agitation] At any time during the interview did the patient have an unusually increased level of motor activity such as restlessness, picking at bedclothes, tapping fingers or making frequent sudden changes of position?8B. [Psychomotor retardation] At any time during the interview did the patient have an unusually decreased level of motor activity such as sluggishness, staring into space, staying in one position for a long time or moving very slowly?9. [Altered sleep-wake cycle] Did the patient have evidence of disturbance of the sleep-wake cycle, such as excessive daytime sleepiness with insomnia at night? The Confusion Assessment Method (CAM) Diagnostic Algorithm Feature 1: Acute Onset or Fluctuating Course This feature is usually obtained from a family member or nurse and is shown by positive responses to the following questions: Is there evidence of an acute change in mental status from the patient's baseline? Did the (abnormal) behavior fluctuate during the day, that is, tend to come and go, or increase and decrease in severity? Feature 2: Inattention This feature is shown by a positive response to the following question: Did the patient have difficulty focusing attention, for example, being easily distractible, or having difficulty keeping track of what was being said? Feature 3: Disorganized thinking This feature is shown by a positive response to the following question: Was the patient's thinking disorganized or incoherent, sach as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject? Feature 4: Altered Level of consciousness This feature is shown by any answer other than “alert” to the following question: Overall, how would you rate this patient's level of consciousness? (alert [normal]), vigilant [hyperalert], lethargic [drowsy, easily aroused], stupor [difficult to arouse], or coma [unarousable]) The diagnosis of delirium by CAM requires the presence of features 1 and 2 and either 3 or 4. Figure 57-1 Confusion Assessment Method (CAM) Reproduced from Inouye, S., van Dyck, C., Alessi, C., Balkin, S., Siegal, A. & Horwitz, R. (1990). Clarifying confusion: The confusion assessment method. Annals of Internal Medicine, 113(12), 941-948. 558 CHAPTER 57 | Geriatric Syndromes

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Figure 57-2 Montreal Cognitive Assessment (MOCA) Copyright Z. Nasreddine, MD. Reproduced with permission. Copies are available at www. mocatest. org. 559 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

iii. N eurological—Focus attention on mental status, which might show hyperalertness or lethargy. Assess mood, which can be agitated, anxious, more confused. Assess grip strength and motor skills to rule out stroke. III. a ssessment A. Frailty Using a comprehensive geriatric assessment allows clinicians to care for frail older adults. This allows clini-cians to address the different components of frailty. A team-based approach including physicians, nurses, phar-macists, therapists, and dieticians has been shown to have positive effects when treating older adults. The focus of assessment in frailty is to eliminate or treat any underlying stressors that are contributing to frailty. According to the American Geriatric Society a person must have three or more characteristics in order to be classified with frailty (Durso & Sullivan, 2013). 1. W eight loss—more than 10 lbs unintentionally in the past year 2. E xhaustion—sensation that everything takes an enormous effort to complete 3. S lowness—time to walk 15 feet 4. L ow activity level—uses less than 270 kcal/weekiv. F or women, assess for prolapse or atrophy, which can contribute to incontinence, as well as any masses. 5. D elirium a. C linicians should use the Confusion Assessment Method (CAM) (see Figure 57-1), Minicog, MOCA (see Figure 57-2), or another validated tool to help determine cognitive status (Durso & Sullivan, 2013). These tests assess for cognitive changes, attention span, organization, and level of consciousness. b. The C AM is simple to use and also comes in an ICU format for patient's admitted to inten-sive care units. It is easily administered at the bedside. c. I t is important to perform MOCA at routine follow-up visits in the outpatient setting to assess baseline cognitive functioning and therefore be able to identify any changes. d. P ertinent physical exam findings may include: i. C ardiovascular—Assess for cardiac arrhyth-mias such as atrial fibrillation, bradycardia, tachycardia, congestive heart failure (CHF) exacerbation, which could be the source of the delirium. ii. A bdominal—Assess for distention, pain, and bowel sounds. Acute abdominal pain and constipation can cause delirium in the older adult. Table 57-1 Special Maneuvers Timed Up and Go Test The most frequently recommended screening test for mobility, takes less than 1 minute to administer Measure an older adult's strength and balance Patient should stand from a chair without using arms to push up Patient walks across the exam room and turns around Patient walks back to chair and sits down again without using arms Inability to do this test within 15 seconds indicates an increased fall risk Patient is also graded on a scale of 1 to 5 regarding muscle strength, balance, and gait abnormalities while performing test Functional Reach Test Performed with a leveled yardstick secured to the wall just above the patient's waist Patient being tested stands with shoulders perpendicular to the wall and he or she makes a fist and extends the arm as far forward as possible along the wall without losing balance or taking a step. Test should be done without shoes or socks The distance reached is measured using the yardstick Patient should accomplish 6 inches or greater Inability to do so is an indicator to pursue further testing and assessment for functional decline Data from Tinetti, M. E., & Kumar, C. (2010). The patient who falls. “It's always a trade-off. ” JAMA, 303(3), 258-266. 560 CHAPTER 57 | Geriatric Syndromes

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

5. W eakness—can calculate with grip strength measurement A clinician should be able to recognize any precipi-tating causes of frailty and address these to promote functional improvement and decrease decline in status. Important to assess nutritional status, and note any impairments in their instrumental activi-ties of daily living (IADLs) and activities of daily living (ADLs). ADLs are basic activities of daily living that persons do to function during the day: eating, bathing, toileting, transferring (walking), and continence. IADLs are things that are not con-sidered to be necessary for fundamental function-ing but do allow an individual to live independently in the community. IADLs include preparing meals, housework, managing medications, and taking medications. B. Sensory impairment It is important to recognize normal changes in the aging eye versus an acute or progressive visual problem. In all adults, presbyopia develops as a result of the lens becom-ing less flexible and losing the ability to accommodate. Older adults have the inability to focus their eyes on objects that are near. Most all older adults will require reading glasses in their lifetime in order to see objects that are near. Common ocular disorders to identify and/or to be suspicious of and refer to an ophthalmologist are dry eyes (keratoconjunctivitis sicca), cataracts, glaucoma, retinopathy, and macular degeneration. Some predisposing factors of hearing impairment cannot be changed like genetic predisposition, sex, and aging of the cochlea. Other factors can be modified like removal of cerumen impaction, reduction of exposure to noise and ototoxic medications. Clinicians must be able to differentiate the different types of hearing loss in older adults. C. Falls Often falls are not a result of one single action but rather a culmination of events leading up to the fall. Independent risk for factors for falling in the older adult population include balance impairment, previous falls, decreased muscle strength, visual impairment, more than four medications or the use of a psychoactive medication, gait impairment, depression, dizziness, functional limitations, age greater than 80 years, female, low body mass index, urinary incontinence, cognitive impairment, arthritis, diabetes, and pain (Tinetti & Kumar, 2010). D. Urinary incontinence Once the cause and type of urinary incontinence the older adult is suffering from are identified, steps can be made to treat and correct contributing factors. Management of urinary incontinence should focus on the individual's goals and issues that are most problematic to the older adult. E. Delirium The diagnosis of delirium is primarily clinical and based on careful observation of key features. Key clinical features include acute onset and fluctuating course, inattention, disorganized thinking, altered level of consciousness, disorientation, memory impairment, perceptual distur-bances, increased or decreased psychomotor activity, and disturbance of the sleep wake cycle (Wong et al., 2010). A useful mnemonic to help identify reversible causes of delirium is listed in T able 57-2. Table 57-2 Delirium Mnemonic D Drugs Any changes to prescription regimen. Any new medications, adjustments in dosage, and interactions with other medications and foods. E Electrolyte disturbances Dehydration, thyroid abnormalities, sodium and potassium deficiencies L Lack of drugs Withdrawal from medications, poor pain control due to inefficient prescribing and treatment, withdrawal from alcohol or other drugs I Infection Urinary tract and respiratory are the most commonly seen R Reduced sensory input Poor vision and inability to hear as well as changes in smell, taste, and touch I Intracranial Stroke, hemorrhage, brain injury, infectious process of the brain U Urinary Urinary retention, incontinence, and infection. Also includes fecal incontinence and impaction. M Myocardial Myocardial infarction, CHF, arrhythmias Data from Geriatric Review Syllabus. (2013). 561 Assessment

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

2. T reatment/patient and caregiver education a. B y identifying the visual condition affecting the older adult, steps can be taken to fix the problem or allow the patient to accommodate to new visual changes. For example, dry eyes tend to be a common complaint in older adults, especially women. The use of nonprescription artificial tears can help alleviate dry eyes. b. E ncourage patients to have an annual eye exam. c. P rovide education regarding a safe visual envi-ronment in the home, meaning making sure there is adequate lighting. Older adults lose the ability to see well in dim light. d. T reatments for common conditions like cataracts, age-related macular degeneration, glaucoma, and diabetic neuropathy vary on the diagnosis so recognizing the condition can then allow you to guide treatment. e. D epending on the cause of the hearing loss some conditions can be helped with medical and or surgical intervention. f. T o better assess hearing, refer to an audiologist for formal audiometric testing and assistance with obtaining hearing aids and other devices that can amplify hearing such as a pocket talkers if appropriate. There are many devices such as  amplified telephones, visual alarm systems, and vibrating alarm clocks available to help older adults who suffer with hearing loss adjust to their living environment. g. Ad aptive techniques, such as, teaching family members to speak directly in front of the patient and using low tones have been shown to be beneficial. Older adults lose the ability to hear high pitched tones. C. Falls 1. Di agnostic studies (see T able 57-3) 2. T reatment/patient and caregiver education a. F all prevention strategies are important. Working with families and institutions if the person is residing in a facility should be done to promote an environment that is safe and reduces risk of falls. b. N eed to individualize treatment plans for patients based on cause of falls. c. T reat any modifiable risk factors that can contribute to falls, for example, correcting visual impairment and ensuring the older adult has appropriate footwear. d. M edication reduction and physical therapy have been shown to be helpful in reducing further falls (Cameron et al., 2010). IV. Goals of clinical management A. Screening 1. Thor ough screening to determine geriatric syndrome 2. I t is important to choose screening and diagnostic tools that are cost effective and patient appropriate B. Treatment 1. S elect a safe and effective treatment plan based on diagnosis of geriatric syndrome as well as patient's goals of care. C. Patient adherence 1. S elect an approach that maximizes patient adherence and continue to monitor patient adherence throughout treatment. V. Plan A. Frailty 1. Di agnostic studies (See T able 57-3) 2. T reatment/patient and caregiver education a. P revention is key. b. C auses of frailty should be treated in order to prevent the human and economic burden associ-ated with this syndrome (Theou et al., 2010). c. I mmobility is often a precursor to worsening frailty so making sure the older adult remains physically active is important. Maintaining muscle mass and strength through routine exercises including stretching and weight resistance have been shown to be beneficial (Theou et al., 2010) d. C ounseling patients and caregivers on adequate nutrition and caloric intake is important. Depending on the case, supplemental protein might be used. e. C ounseling patients, family members, and care-givers on availability of community support systems. For example, meals on wheels or other home delivery food options. B. Sensory impairment 1. Di agnostic studies are sometimes needed in the assessment and treatment of sensory impairments. When pursuing diagnostic studies it is important to review goals of care and what will be done with results of studies obtained. Occasionally a CT scan/MRI of the brain might be used if there is concern for a stroke or head injury contributing to impairment. 562 CHAPTER 57 | Geriatric Syndromes

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Table 57-3 Geriatric Syndromes and Labs/Imaging Labs/Imaging to obtain Geriatric Syndr ome r ationale Complete blood count Frailty Falls Urinary incontinence Delirium Assess for anemia and/or elevated white count, which could indicate an infectious process contributing to these particular geriatric syndromes Serum electrolyte Frailty Falls Urinary incontinence Delirium Assess for hypo/hyperkalemia, hypo/hypernatremia, dehydration, which can contribute to these particular geriatric syndromes Renal panel Frailty Falls Urinary incontinence Delirium Assess kidney functioning to determine if kidney injury, failure, or disease is contributing to these particular geriatric syndromes Thyroid panel Frailty Delirium Assess for hyper/hypothyroidism. Hyperthyroidism can contribute to weight loss and frailty. Uncontrolled hyper/hypothyroidism can lead to delirium. Urinalysis, urine culture Frailty Falls Urinary incontinence Delirium If concern for infectious process that is treatable and contributes often to frailty, falls, increased urinary incontinence, and delirium. Especially helpful in patients with dementia who cannot express symptoms of infection. Albumin, prealbumin Frailty Indicator of protein intake and overall nutritional state Serum glucose Falls Delirium Assess for hypoglycemia, which can lead to falls and delirium in the older adult Vitamin B 12Falls Delirium Low levels are associated with proprioceptive problems contributing to falls and increased confusion resulting in delirium Vitamin D Falls High risk for fractures from fall if level is low Electrocardiogram Falls Delirium Evaluate for abnormal rhythm or cardiac pathology contributing to syncope resulting in a fall or delirium Computerized tomography (CT) scan/magnetic resonance imaging (MRI) brain Sensory impairment Falls Delirium If concern for stroke, bleed, or injury to the head, which can contribute to sensory impairment, falls, and/or delirium Ultrasound of bladder Urinary incontinence To assess volume of urine inside the bladder. A postvoid residual is often done in the hospital setting to examine for urinary retention. This test is rarely needed in the ambulatory setting. Renal ultrasound Urinary incontinence Evaluate for kidney disease and problems with the urinary tract CT abdomen/pelvis Urinary incontinence Evaluate for obstructions, tumors, cysts Arterial blood gas Delirium If concern for hypoxia, poor perfusion contributing to delirium Toxicology Falls Delirium Assess for presence of illegal substances contributing to falls and delirium Electroencephalogram Sensory impairment Falls Delirium If concern for seizure activity contributing to sensory impairment, falls, and/or delirium563 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

E. Delirium 1. Di agnostic studies (see T able 57-3) 2. T reatment/patient and caregiver education a. A fter accurate diagnosis of delirium, steps can be made to reduce complications and provide treatment. b. I mportant to identify and treat any reversible conditions contributing to delirium. c. A ttempt to prevent further complications and decline by reducing medications where appropriate. d. N onpharmacologic strategies include correcting any sensory impairment (see the section on sensory impairment for details), avoiding physi-cal restraints including foley catheters that keep patients from being mobile, sleep hygiene, reori-entation, and environment optimization. e. P harmacologic strategies are useful for severe cases of delirium where the person's safety and well-being are at risk. Pharmacologic treatment strategies include the use of an antipsychotic such as Haldol, atypical antipsychotics such as risperidone, olanzapine, or quetiapine, a benzo-diazepine such as lorazepam, and/or an antide-pressant such as trazodone (Inouye, 2006). The same geriatric principles apply when prescribing these medications: starting low and going slow, meaning start with a low dose and titrate up slowly if needed. f. I t is important to weigh goals of care for the indi-vidual being treated with invasiveness of proce-dure and tests. VI. o nline resources for clinicians, patients, and caregivers A. AARP (www. aarp. org) B. Alzheimer's Association (www. alz. org) C. American Geriatrics Society (www. americangeriatrics. org) D. American Geriatrics Society Beers Criteria (http://geriatricscareonline. org/Product Abstract /american-geriatrics-society-updated-beers -criteria-for-potentially-inappropriate-medication -use-in-older-adults/CL001) E. Family Caregiver Alliance (www. caregiver. org) F. Gerontological Advanced Practice Nurses Association (https://www. gapna. org)e. C linicians should work along with physical therapist colleagues to establish an exercise program for older adults. f. M anage postural hypotension by titrating medi-cations, optimizing fluid intake, and teaching behavioral strategies to reduce incidents. g. P rovide vitamin D supplement when appropriate to reduce risk of fractures from falls. D. Urinary incontinence 1. Di agnostic studies (see T able 57-3) 2. T reatment/patient and caregiver education a. I nitiate behavioral targeted therapies as well as medications or at times surgical interven-tion when appropriate based on type of urinary incontinence. Make referral to urology and/or urogynecology. b. I t is also important to recognize medications that contribute to worsening of urinary incontinence and remove those from the patient if this can be done safely. Common medications include alpha-blockers, antipsychotics, loop diuretics, narcotics, and tricyclic antidepressants. c. T reat comorbid conditions contributing to urinary incontinence such as diabetes mellitus and dementia. d. Be havioral modifications include timed voiding, for example, having the patient empty the bladder every 2 hours, and pelvic muscle training, which are Kegel exercises to strengthen the pelvic floor and surrounding muscles. e. M edications can be used to treat some types of urinary incontinence. Anticholinergic drugs are the most commonly prescribed medications for incontinence and it is important to recognize the side effects of these medications in older adults, which can be quite problematic. Some of these side effects include confusion, constipation, dry eyes and mouth, and falls. Other agents often prescribed are antimuscarinics such as oxybu-tynin, tolterodine, trospium, and fesoterodine. Alpha-blockers and tricyclic antidepressants have also been used. f. D evices such as pessaries can be trialed in women who suffer from organ prolapse result-ing in overflow incontinence. It is important to recognize pessaries do require some care from the individual so often they are not appropriate for older adults with cognitive impairment g. S everal different surgical interventions can also be used if patient is deemed a surgical candidate. Appropriate referrals are needed to specialists. Please refer to Chapter 25, Urinary Incontinence in Women, for more detailed treatment regimens. 564 CHAPTER 57 | Geriatric Syndromes

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

G. John A. Hartford Foundation (www. jhartfound. org) H. The Hartford Institute for Geriatric Nursing, College of Nursing, New York University (http:// consultgerirn. or/ or www. hartfordign. org) 1. The H artford Institute Assessment T ools T ry This (www. hartfordign. org/practice/try_this) I. The Hospital Elder Life Program (www. hospitalelderlifeprogram. org/about) J. Medicare (www. medicare. gov) K. National Institute on Aging (http://nia. nih. gov) L. U. S. Preventive Services Task Force: Falls Prevention in Older Adults: Counseling and Preventive Medication (www . uspreventiveservicestaskforce. org/Page/Topic /recommendation-summary/falls-prevention -in-older-adults-counseling-and-preventive -medication) referen Ce S Cameron, I. D., Murray, G. R., Gillespie, L. D., Robertson, M. C., Hill, K. D., Cumming, R. G., et al. (2010). Interventions for preventive falls in older people in nursing care facilities and hospitals. Cochrane Database of Systematic Reviews, 1. Chou, R., Dana, T., Bougatsos, C., Fleming, C., & Beil, T. (2011). Screening adults aged 50 years or older for hearing loss: A review of the evidence for the U. S. Preventive Services T ask Force. Annals of Internal Medicine, 154(5), 347-355. Delbaere, K., Crombez, G., Vanderstraeten, G., Willems, T., & Cambier, D. (2004). Fear-related avoidance of activities, falls, and physical frailty. A prospective community-based cohort study. Age and Ageing, 33(4), 368-373. Du Moulin, M. F., Hamers, J. P., Ambergen, A. W., Janssen, M. A., & Halfens, R. J. Prevalence of urinary incontinence among community-dwelling adults receiving home care. Research in Nursing & Health, 31(6), 604-612. Durso, S., & Sullivan, G. (Eds. ). (2013). Geriatrics review syllabus: A core curriculum in geriatric medicine (8th ed. ). New Y ork: American Geriatrics Society. Goode, P. S., Burgio, K. L., Richter, H. E., & Markland, A. D. (2010). Incontinence in older women. JAMA, 303(21), 2172-2181. Inouye, S. K. (2006). Delirium in older persons. New England Journal of Medicine, 354(11), 1157-1165. Inouye, S., van Dyck, C., Alessi, C., Balkin, S., Siegal, A., & Horwitz, R. (1990). Clarifying confusion: The confusion assessment method. Annals of Internal Medicine, 113(12), 941-948. Theou, O., Stathokostas, L., Roland, K. P., Jakobi, J. M., Patterson, C., Vandervoort, A. A., et al. (2011, April 4). The effectiveness of exercise interventions for the management of frailty: A systemic review. Journal of Aging Research, 1-19. Tinetti, M. E., & Kumar, C. (2010). The patient who falls. “It's always a trade-off. ” JAMA, 303(3), 258-266. Williams, B., Chang, A., Ahalt, C., Chen, H., Conant, R., Landefeld, S., et al. (Eds. ). (2014). Current diagnosis & treatment: geriatrics (2nd ed. ). New Y ork: Mc Graw-Hill Education. Witlox, J., Eurelings, L. S., de Jonghe, J. F. M., Kalisvaart, K. J., Eikelenboom, P., & van Gool, W. A. (2010). Delirium in elderly patients and the risk of postdischarge mortality, institutionalization, and dementia: A meta-analysis. JAMA, 304(4), 443-451. Wong, C. L., Holroyd-Leduc, J., Simel, D. L., & Straus, S. E. (2010). Does this patient have delirium? Value of bedside instruments. JAMA, 304(7), 779-786. 565 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

splenic congestion, predominantly arise from systemic venous fluid congestion. Two major clinical subsets of heart failure are systolic and diastolic. Systolic heart failure, often called heart fail-ure with reduced ejection fraction or HFr EF, occurs when the heart loses its ability to contract normally. As systolic heart failure progresses the ventricle may become dilated. Reduced contractile function causes increased end systolic and end diastolic volumes, dilating the ventricle. This con-dition is called dilated cardiomyopathy (DCM). DCM is largely categorized into two etiologies: ischemic or non-ischemic. Ischemic disease is the predominant cause of left ventricular systolic failure in the United States. There are multiple causes of nonischemic cardiomyopathy including but not limited to familial, alcohol induced, cardiotoxic-ity due to medications, infectious diseases, inflammatory diseases, rheumatologic disorders, thyroid disease, some muscular dystrophies, longstanding poorly controlled hypertension, and valvular heart disease. Diastolic heart failure is abnormal filling of the left or right ventricle caused by impaired myocardial relaxation or stiffness of the heart muscle. Common causes of dia-stolic heart failure are chronic hypertension with left ven-tricular hypertrophy as well as restrictive, infiltrative, and hypertrophic cardiomyopathies. Fifty percent of patients with heart failure have a preserved ejection fraction (EF) (Yancy et al., 2013). Heart failure with preserved EF is now commonly referred to as HFp EF. The New Y ork Heart Association (NYHA) and American College of Cardiology Foundation/American Heart Association (ACCF/AHA) have complimentary classifications and staging for defining the functional status and severity of heart failure. NYHA classifications are (Criteria Committee of the American Heart Association, 1994): 1. C lass I: no symptoms with or limitations in ordinary activities 2. C lass II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion I. Intr oduction and general background Heart failure is a common condition seen in the primary care setting. It is a clinical syndrome that can occur suddenly or over time and arises from cardiac derangements within the pericardium, myocardium, or endocardium, and/or structural abnormalities of the vessels or valves. A. Definition and overview Heart failure as defined by the American College of Cardiology and American Heart Association is a complex clinical syndrome that results from any structural or func-tional impairment of ventricular filling or ejection of the blood (Yancy et al., 2013). Heart failure is a clinical diag-nosis based on the presentation of symptoms, which typi-cally include dyspnea, fatigue, fluid retention, and exercise intolerance. Heart failure can involve the left ventricle, right ventri-cle, or both ventricles. Left ventricular heart failure occurs when the left ventricle is unable to pump sufficiently to meet the body's demands. The myocardial muscle may be too weak and thin to eject the blood from the ventricle or the myocardial muscle may be too thick and stiff causing inadequate ventricular filling. Both forms of heart failure cause elevated left ventricular filling pressures. The symptoms of left ventricular failure predominantly include dyspnea and fatigue. Dyspnea arises from pulmo-nary edema. Pulmonary edema occurs from the ineffective ejection of blood from the left ventricle, causing elevated left atrial pressures resulting in fluid back up in the lungs. Subsequently, the persistent increased pulmonary volume and pressure can begin to affect the right ventricle. Fatigue arises from the inability of the ventricles to eject enough blood to meet the needs of the body, causing decreased forward flow and ultimately decreased cardiac output. However, the symptom of fatigue occurs in both left and right ventricular failure. Signs of right ventricular failure, which include peripheral edema, ascites, and hepatic and Lisa Guertin and Barbara Boland Heart Fa ILure© Eliks/Shutterstock; © donatas1205/Shutterstock 566 58Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

anemia, thyroid disease, peripartum myopathy, other hormonal disorders, systemic lupus erythe-matosus, scleroderma, sarcoidosis, amyloidosis, infectious diseases including HIV, Chagas disease, viral endocarditis and myocarditis, and malignan-cies requiring medications such as anthracycline, trastuzumab (Herceptin), high-dose cyclophos-phamide, toxoids, mitomycin-C, 5-fluorouracil, and the interferons or other nonchemo cardio-toxic medications (Yancy et al., 2013). b. S urgical history: Cardiac surgeries, including valve replacements, myectomy, coronary artery bypass. Endovascular procedures such as stent placement, ethanol, or radiofrequency ablation. c. M edication history: Some categories of medica-tions used in heart failure may have an adverse effect. For example, calcium channel blockers (harmful) and beta-blockers are negative inotropes. However, beta-blockers should not be excluded from the treatment regimen, as they remain part of the primary treatment for systolic heart failure. Antiarrhythmic medications and ino-tropes may be proarrhythmic. Thiazolidinediones and nonsteroidal anti-inflammatories can cause fluid retention. Other cardiotoxic medications are previously mentioned. 2. F amily history: Atherosclerosis, MI, cerebrovascular accident (CVA), peripheral arterial disease, sudden cardiac death, arrhythmias, conduction disease (often requiring pacemakers or internal cardioverter defibrillators [ICDs]), heart failure, or cardiomyopathy 3. O ccupational and educational history a. E xposures to chemicals or toxins b. L evel of education c. A bility to work; days missed from work or school 4. P ersonal and social history a. A lcohol, cocaine, methamphetamine, and intra-venous drug use b. Die t: Adherence to a heart-healthy and low-sodium diet. c. E xercise: Assess the distance able to ambulate without stopping due to fatigue or shortness of breath, the ability to climb stairs, and participa-tion in routine exercise or sedentary lifestyle. d. Act ivities of daily living: Ability to perform routine tasks without fatigue or shortness of breath e. C ulture and cultural practices f. L iving situation 5. R eview of symptoms a. C onstitutional signs and symptoms: Recent hospitalizations, fever, chills, rigors, fatigue, 3. C lass III: marked limitation of any activity; the patient is comfortable only at rest 4. C lass IV: severe limitations; any physical activity causes discomfort and symptoms occur at rest The ACCF/AHA staging of heart failure are (Yancy et al., 2013): 1. S tage A: Patients at high risk for developing heart failure but without structural heart disease or symptoms of heart failure. 2. S tage B: Structural heart disease but without signs or symptoms of heart failure. 3. S tage C: Structural heart disease with prior or current symptoms of heart failure. 4. S tage D: Refractory heart failure requiring specialized interventions. B. Prevalence and incidence The American Heart Association estimates 5. 7 million Americans over the age of 20 have heart failure, occur-ring more frequently in men and in those over the age of 60 (Mozaffarian et al., 2015). The prevalence is expected to increase 46% by the year 2030, with 870,000 new cases diagnosed every year (Mozaffarian et al., 2015). Multiple risk factors contribute to heart failure includ-ing but not limited to coronary disease, obesity, insulin resistance, inflammation and elevated inflammatory markers, men with hypertension, and cigarette exposure (Go et al., 2014). It is important to note 75% of heart failure cases have an antecedent of hypertension (Go et al., 2014). Although survival after a heart failure diagnosis has improved, mortality remains at 50% within 5 years of diagnosis (Go et al., 2014). According to the AHA and Centers for Disease Control and Prevention (CDC), the estimated annual cost of heart failure to the nation is between $30  billion and $32 billion (Mozaffarian et al., 2015; National Center for Chronic Disease Prevention and Health Promotion, 2013). II. Database (may include but is not limited to) A. Subjective 1. P ast health history a. M edical history: hypertension, coronary artery disease (myocardial infarction [MI]), arrhythmia, valvular heart disease including aortic or pulmonic stenosis, mitral or tricuspid stenosis, or mitral or aortic regurgitation, congenital heart disease, obesity, peripheral vascular disease, diabetes, obstructive sleep apnea, hyperlipidemia, 567 Database

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

d. I nterstitial lung disease e. P neumonia f. S leep apnea g. P ulmonary artery hypertension h. M yocardial ischemia i. V alvular heart disease j. A trial fibrillation or other arrhythmia k. A nemia or other blood dyscrasias l. V enous insufficiency or thrombosis m. C irrhosis n. G astrointestinal disorders o. R enal disease or failure p. E ndocrine disorders such as thyroid disease q. D econditioning r. D epression s. Obe sity t. Adv erse effects from medications B. Severity 1. A ssess the severity of the disease based on the NYHA classifications and/or ACCF/AHA heart failure staging. C. Motivation and ability 1. D etermine the patient's willingness and ability to adhere to a treatment plan. IV. Goals of clinical management A. Select and implement a treatment plan that appropriately manages heart failure in a beneficial and cost-effective manner. B. Implement an appropriate treatment plan that enables patients' adherence. C. Relieve symptoms. D. Prevent/decrease admissions to an acute care facility. E. Improve survival. V. Plan A. Diagnostic tests 1. N oninvasive testing a. Ge neral laboratory studies: Complete blood count (CBC), metabolic panel, calcium, magne-sium, blood urea nitrogen, serum creatinine, liver function tests, fasting glucose, urinalysis, lipid panel, and thyroid-stimulating hormone. weight gain or loss. Weight loss is concerning as it is a poor prognostic indicator of heart failure. b. R espiratory: Dyspnea with or without exertion, shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and cough. c. C ardiac: Chest pain, palpitations, edema, syn-cope, and presyncope. d. G astrointestinal: Anorexia, nausea, increasing abdominal girth, and abdominal discomfort. e. Ge nitourinary: Sexual dysfunction, sexually transmitted disease exposure, and urination patterns. f. E ndocrine: Heat or cold intolerance g. N eurologic: Lightheadedness, dizziness, frequent naps or inability to stay awake, decreased con-centration, memory loss, and signs of transient ischemic attack (TIA) or CVA. h. P sychiatric: Anxiety and/or depression. B. Objective 1. P hysical examination findings a. H eight, weight, body mass index, body habitus, and general appearance b. V ital signs: orthostatic blood pressures c. P ulse: Assess strength and regularity through-out. Assess the character of the carotid upstroke d. S kin: Pallor, cyanosis, cool temperature e. Th yroid/neck: Goiter and/or bruits f. L ungs: T achypnea, rales, wheezing, ability to speak full sentences g. C ardiac: Arrhythmia, elevated jugular venous pressure, additional heart sounds such as S3 gal-lop, S4, or murmur, laterally displaced point of maximum intensity (PMI), heaves, lifts, thrills, and edema (abdominal, peripheral, or sacral) h. A bdomen: Increased abdominal girth, abdominal tenderness, hepatomegaly and hepatojugular reflux lasting longer than 10 seconds with sustained abdominal pressure. III. a ssessment A. Determine the diagnosis Heart failure is a clinical diagnosis that is largely based on findings from the history and physical examination. Diagnostic testing is important and useful in confirming the diagnosis, the underlying etiology, and the severity of the disease. 1. Di fferential diagnosis a. C hronic obstructive pulmonary disease b. A sthma c. P ulmonary embolism568 CHAPTER 58 | Heart Failure

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

b. C ardiac-specific laboratory studies: Natriuretic peptide: B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT pro-BNP) can be useful in patients with dyspnea and to assess severity of the disease (Yancy et al., 2013). It is important to consult the laboratory preforming the test to obtain their normal range of laboratory values. Additionally, there are multiple factors that may cause and elevated BNP and NT pro-BNP. c. Ele ctrocardiogram: Left ventricular hypertrophy, evidence of prior MI, arrhythmia, conduction problems, and axis deviation. d. C hest radiograph: Cardiomegaly, pulmonary congestion. e. E chocardiogram: Ventricular size, function, wall motion, atrial size, valvular function, and hemo-dynamic values. f. C ardiovascular magnetic resonance may be appropriate for the initial evaluation of heart failure and may be helpful in assessing myocardial perfusion, viability, and fibrosis imaging (Patel et al., 2013). 2. I nvasive testing a. H emodynamic monitoring with pulmonary artery catheter to guide treatment in patients who have respiratory distress and clinical evi-dence of impaired perfusion and intracardiac filling pressures cannot be determined from the clinical assessment (Yancy et al., 2013). b. C oronary angiogram is recommended if the etiology of heart failure is concerning for isch-emic heart disease and the patient is a candidate for revascularization (Patel et al., 2013). c. R ight heart catheterization may be useful in determining volume status, hemodynamic values, and intracardiac filling pressures to assess specific therapeutic questions (Yancy et al., 2013). d. E ndomyocardial biopsy (EMB) may be useful in diagnosis and management of acute onset unex-plained cardiomyopathy that does not respond to the usual standard of practice. Furthermore, EMB plays a role in suspected infiltrative disease that presents either as unexplained hypertro-phic cardiomyopathy or as restrictive disease (Bennett et al., 2013). B. Management (includes treatment, consultation, referral, and follow-up care) 1. Ac ute heart failure: Immediate intervention of oxygen; arrange hospital admission. Depending on the severity, emergency response may be required and therefore admitted via the emergency department. The patient may require ventilator support, intravenous diuretics, ultrafiltration, intravenous inotropes, vasopressors, vasodilators, or mechanical support (National Clinical Guideline Centre, 2014). 2. C hronic heart failure a. T reatment is often performed in a progressive stepwise approach. A referral to cardiology should be initiated upon diagnosis (see Figure 58-1). b. The foc us of stage A heart failure management is on risk modification including hypertension control, diabetes control and lipid management to control atherosclerosis and obesity. c. S tage B heart failure management includes stage A management plus intervention of structural heart disease. Special considerations should be given to patients with stage B heart failure patients with a history of MI and/or revascular-ization and structural heart disease. d. The de velopment of symptoms classifies patients as stage C. Stage C heart failure management is multifaceted and aims at reducing morbidity and mortality by self-care and pharmacologic strate-gies. ICD implantation may be appropriate for this group of patients for either primary or sec-ondary prevention. Additionally, cardiac resyn-chronization therapy (CRT) may be indicated for a subset of patients. e. S tage D heart failure patients are considered refractory and the disease progresses despite implementation of goal-directed therapy (strat-egies in stages A, B, and C). These patients may require intravenous inotropic support or other advanced therapies such as mechanical circula-tory support or heart transplantation. f. L ifestyle modification i. S moking cessation ii. A lcohol cessation or restriction iii. Il licit drug use cessation iv. E xercise: Regular exercise 20-30 minutes three to five times per week. Referral to cardiac rehabilitation. Lack of improvement after a training program portends a poor prognosis (T ang & Francis, 2010). v. Die t: Sodium restriction in patients who are symptomatic. Less than 3 g/daily should be effective in symptom relief; 1. 5 g/daily to aid in hypertension control in patients with stage A and B heart failure (Yancy et al., 2013). vi. F ree water: Restrict daily intake to 1. 5-2 L in patients with stage D heart failure and hyponatremia (Yancy et al., 2013). 569 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

STAGE A At high risk for HF but without structural heart disease or symptoms of HFSTAGE B Structural heart disease but without signs or symptoms of HFSTAGE C Structural heart disease with prior or current symptoms of HFSTAGE D Refractory HFAt Risk for Heart Failure e. g., Patients with:· HTN Atherosclerotic disease DM Obesity Metabolic syndrome or Patients Using cardiotoxins With family history of cardiomyopathy Structural heart disease THERAPY Goals Heart healthy lifestyle Prevent vascular, coronary disease Prevent LV structural abnormalities Drugs ACEI or ARB in appropriate patients for vascular disease or DM Statins as appropriate THERAPY Goals Prevent HF symptoms Prevent further cardiac remodeling Drugs ACEI or ARB as appropriate Beta blockers as appropriate In selected patients ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Prevent hospitalization Prevent mortality Strategies Identification of comorbidities Treatment Diuresis to relieve symptoms of congestion Follow guideline driven indications for comorbidities, e. g., HTN, AF, CAD, DM Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Patient education Prevent hospitalization Prevent mortality Drugs for routine use Diuretics for fluid retention ACEI or ARB Beta blockers Aldosterone antagonists Drugs for use in selected patients Hydralazine/isosorbide dinitrate ACEI and ARB Digoxin In selected patients CRT ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Reduce hospital readmissions Establish patient's end- of-life goals Options Advanced care measures Heart transplant Chronic inotropes Temporary or permanent MCS Experimental surgery or drugs Palliative care and hospice ICD deactivatione. g., Patients with: Previous MI LV remodeling including LVH and low EF Asymptomatic valvular diseasee. g., Patients with: Known structural heart disease and HF signs and symptomse. g., Patients with: Marked HF symptoms at rest Recurrent hospitalizations despite GDMTe Refractory symptomsof HF at rest, despite GDMTDevelopment ofsymptoms of HFHeart Failure HFp EF HFr EF Figure 58-1 Heart Failure Risk ACEI = angiotensin-converting enzyme inhibitor, CAD = coronary artery disease, DM = diabetes mellitus, GDMT = guideline-determined medical ther-apy, HRQOL= health-related quality of life, HTN = hypertension, MCS = mechanical circulatory support. Reproduced from Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Drazner, M. H., et al. (2013). 2013 ACCF/AHA guideline for the man-agement of heart failure: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Journal of the American College of Cardiology, 62(16), e147-e239. 570 CHAPTER 58 | Heart Failure

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

g. W eight and blood pressure monitoring: Document weight and blood pressure daily, at the same time every day; monitor trends. Provide parameters that indicate when the patient should contact the provider regarding weight gain, evidence of volume overload, and blood pressure. h. H ealthcare maintenance i. A nnual flu vaccine ii. P neumococcal vaccine iii. M edic alert information iv. D ental care i. T reatment of other illnesses/conditions that may be causative or contributory to heart failurei. Di abetes (see Chapter 54, Diabetes Mellitus)ii. H ypertension (see Chapter 60, Hypertension) iii. Obe sity (see Chapter 66, Obesity) iv. S leep apnea v. Th yroid disorders (see Chapter 69, Thyroid Disorders) vi. I nfection vii. I nflammation or inflammatory processes j. P harmacologic therapy for heart failure (systolic or diastolic), volume retention, heart rhythm and rate control, and hypertension. Start at a low dose and titrate up as patient tolerates until the maximum safe dosage allowable. See Box 58-1 for medication approaches for systolic heart fail-ure with low EF. Management for diastolic heart failure predominantly consists of controlling Box 58-1 Medication Management for Systolic Heart F ailure with Low e jection Fraction ( e F) 1. Angiotensin-converting enzyme inhibitor (ACE-I) (see Table 58-1) a. Provides left ventricular remodeling and survival benefit. ACE-I can be replaced with an aldosterone receptor blocker (ARB) if unable to tolerate ACE-I, typically due to a dry, irritating cough. Monitor electrolytes and renal function closely after initiation of treatment and dosage adjustments. 2. Hydralazine in conjunction with a nitrate (see T able 58-1) a. Can be utilized if the patient is unable to tolerate both ACE and ARB; it can also be used as adjunctive therapy in NYHA class III-IV heart failure. 3. Beta-blockers (see Table 58-1) a. Can provide improvement in EF as well as anti-ischemic properties and reduce mortality. 4. Diuretic therapy (see Table 58-2) a. Indicated for patients to control volume retention. b. Monitor electrolytes and renal function closely after initiation of treatment and dosage adjustments. 5. Aldosterone antagonists (see T able 58-1 and 58-2) a. Recommended for patients with persistent symptoms with NYHA class II-IV heart failure and EF < 35%. b. Monitor electrolytes and renal function closely after initiation of treatment and dosage adjustments. 6. Digoxin a. Remains controversial in the patient population with systolic heart failure. b. Digoxin can be used in patients as adjunctive therapy if they remain symptomatic despite guideline directed management. c. Digoxin should be avoided in patients with sinus node or atrioventricular node conduction disease (Y ancy et al., 2013). d. Monitor digoxin levels to ensure they remain in a therapeutic range and do not become toxic. 7. Amiodarone and dofetilide a. The only recommended antiarrhythmic medications to have neutral ef fects on mortality on patients with heart failure (Yancy et al., 2013). b. Prior to starting and after initiation of amiodarone, monitor thyroid-stimulating hormone. c. Monitor for signs of amiodarone induced pulmonary fibrosis, liver dysfunction, and thyroid toxicity. 8. Antithromboticsa. Use is based upon the CHA2DS2-VACs score for arrhythmia and dilated cardiomyopathy due to an increased risk of left ventricular thrombus (Yancy et al., 2013). b. Choose an appropriate, approved, and individualized antithrombotic agent for the patient. (continues)571 Plan

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf