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6. P roject Health focuses on advocacy, education, and leadership for transgender health. They host a national online trans medical consultation service for healthcare providers (http://project-health. org). 7. T rans Bodies, Trans Selves (Erickson-Schroth, 2014) is a comprehensive book written by and for the transgender community. T rans patients and healthcare providers can benefit from the personal essays and practical overview of trans people's medical and psychosocial needs. references Centers for Disease Control and Prevention. (2015). HIV among transgender people. Retrieved from www. cdc. gov/hiv/risk/transgender /index. html. Center for Gender Sanity. (2009). Diagram of sex and gender. Retrieved from www. gendersanity. com/diagram. html. Center of Excellence for T ransgender Health. (2014). General prevention and screening. Retrieved from http://transhealth. ucsf. edu/trans?page =protocol-screening. Davidson, A., Francivich, J., Freeman, M., Lin, R., Martinez, L., Monihan, M., et al. (2013). T om Waddell Health Center protocols for hormonal reassignment of gender. Retrieved from https://www. sfdph. org/dph /comupg/oservices/med Svs/hlth Ctrs/T rans Gendprotocols122006. pdf. Erickson-Schroth, L. (Ed. ). (2014). Trans bodies, trans selves: A resource for the transgender community. New Y ork: Oxford University Press. Feldman, J., & Bockting, W. (2003). T ransgender health. Minnesota Medicine, 86(7), 25-32. Feldman, J., & Goldberg, J. (2006). Transgender primary medical care: Suggested guidelines for physicians in British Columbia. Retrieved from http://lgbtqpn. ca/wp-content/uploads/woocommerce_uploads /2014/08/Guidelines-primarycare. pdf. Feldman, J. L., & Goldberg, J. M. (2007). T ransgender primary medical care. International Journal of Transgenderism, 9(3/4), 3-34. Gates, G. J. (2014). LGB/T demographics: Comparisons among population-based surveys. Los Angeles, CA: Williams Institute, UCLA School of Law. Gender Neutral Pronouns. (n. d. ). Retrieved from http://forge-forward. org. Gooren, L. J., & T angpricha, V. (2015). T reatment of transsexualism. Up T o Date. Retrieved from www. uptodate. com/contents/treatment-of-transsexualism. Hembree, W., Cohen-Kettenis, P., Delemarre-van de Waal, H., Gooren, L., Meyer, W., Spack, N., et al. (2009, January 1). Endocrine treatment of transsexual persons: An Endocrine Society clinical practice guideline. Retrieved from https://www. endocrine. org/~/media/endosociety /Files/Publications/Clinical Practice Guidelines/Endocrine-T reatment-of-T ranssexual-Persons. pdf. Herbst, J. H., Jacobs, E. D., Finlayson, T. J., Mc Kleroy, V. S., Neumann, M. S., & Crepaz, N. (2008). Estimating HIV prevalence and risk behaviors of transgender persons in the United States: A systematic review. AIDS and Behavior, 12(1), 1-17. Kenagy, G. P. (2005). T ransgender health: Findings from two needs assessment studies in Philadelphia. Health & Social Work, 30(1), 19-26. Lombardi, E. (2001). Enhancing transgender health care. American Journal of Public Health, 91(6), 869-872. 2. The primary care provider can adequately manage hormone therapy and medications during the postoperative periods for patients who have under-gone transition surgery (either in United States or abroad). Follow-up surgical care is managed by the surgeon. 3. C ollaborate with mental health providers and other specialists to support patient during surgical process. 4. Adv ocate for patients seeking insurance approval for surger y. D. Patient education 1. P rimary focus should be on developing a trusting relationship with the patient and assisting the patient to overcome previous negative experiences with healthcare providers. 2. P rovide health counseling with particular attention to HIV prevention. 3. H arm reduction as needed based on findings of subjective and objective assessments 4. P rovide information on community resources, such as legal advice, housing assistance, and mental health counseling. 5. P eriodic health counseling as outlined in the chapter Healthcare Maintenance of the Adult and Older Adult. E. Self-management resources and tools 1. U niversity of California, San Francisco's Center of Excellence for T ransgender Health provides education, advocacy, and current research around transgender health needs for both trans individuals and providers (http://transhealth. ucsf. edu/). 2. V ancouver Coastal Health Clinic has excellent resources for both providers and patients on a variety of topics related to transgender health promotion, mental health, and other topics (www. transhealth. vch. ca) 3. W orld Professional Association for T ransgender Health conducts academic research and development of evidence-based medicine for transsexual, transgender, and gender nonconforming individuals (www. wpath. org/). 4. T ransgender Law Center advocates for individuals who have faced discrimination based on their gender identity of expression (http://transgenderlawcenter. org/). 5. N ational Center for T ransgender Equality is an advocacy organization working to advance equality of transgender individuals (http://transequality. org/). 372 CHAPTER 39 | Healthcare Maintenance for Transgender Individuals
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Sanchez, N. F., Sanchez, J. P., & Danoff, A. (2009). Health care utilization, barriers to care, and hormone usage among male-to-female transgender persons in New Y ork City. American Journal of Public Health, 99(4), 713-719. Sobralske, M. (2005). Primary care needs of patients who have under-gone gender reassignment. Journal of the American Academy of Nurse Practitioners, 17(4), 133-138. Minter, S., & Daley, C. (2003). Trans realities: A legal needs assessment of San Francisco's transgender communities. San Francisco, CA: T ransgender Law Center and National Center for Lesbian Rights. National Gay and Lesbian T askforce. (2009). National transgender discrimi-nation survey: Preliminary findings. Retrieved from www. thetaskforce . org/downloads/reports/fact_sheets/transsurvey_prelim_findings. pdf. San Francisco Department of Public Health. (n. d. ). T ransgender health services. Retrieved from https://www. sfdph. org/dph/comupg /oprograms/THS/procedures. asp. 373 References
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a PPend Ix a: a g u I de to c o MM on g ender-n eutral Pronoun c H o I ces a M ong t H e t rans c o MM un I ty subjective o bjective Possessive a djective Possessive Pronoun r eflexive s he Her Her Hers Herself He Him His His Himself Ze Zim Zir Zirs Zirself s ie/Zie Hir Hir Hirs Hirself Zie Zir Zir Zirs Zirself e y e m e ir e irs e irself Per Per Pers Pers Persself They Them Their Theirs Themself Modified from Gender Neutral Pronouns (n. d. ). Retrieved from http://forge-forward. org. 374 CHAPTER 39 | Healthcare Maintenance for Transgender Individuals
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A. When should PEP be considered? Best evidence suggests that the riskiest exposures to HIV occur when large amounts of infectious fluids (T able 40-1) are injected directly into the body or contacted by nonintact skin or mucous membranes. T able 40-2 shows the risks of contracting HIV infec-tion through various routes of exposure. The most recent guidelines from the United States Public Health Service (USPHS) eliminate the necessity to establish the level of risk in order to determine the number of drugs to use for PEP (Kuhar et al., 2013). The guidelines agree that any exposure of open skin or mucous membranes to probable HIV-infected blood, bloody body fluid, or other poten-tially infected materials warrants the initiation of three drug PEP. The testing of the source patient, recommended PEP regimen, and testing schedule for the infected health worker differ slightly between guidelines. T able 40-3 is a summary of the differences between the USPHS and the New Y ork State Department of Health (NYSDOH) AIDS Institute guidelines. The drugs recommended for PEP and n PEP have been chosen due to their proven effectiveness in HIV infection, ease of administration (most are once daily dosing), and lower incidence of and milder side effects. All HIV medications, however, have side effect risks and warrant strict adherence because of the danger of developing resistance if doses are skipped. Special attention must be paid to the source patient's viral load and history of antiretroviral use. If the source has a high viral load and/or has taken or is on antiretrovi-rals, it is prudent to use HIV medications that the source has never taken for PEP. However, not all HIV medications are appropriate for PEP (T able 40-4). As such, all cases where PEP is recommended require expert consultation (see end of chapter for resources). The guidelines agree that the timing of PEP is crucial. It must be started as soon as possible after exposure and within 72 hours in order to give the best chance for I. Intr oduction and general background Postexposure prophylaxis (PEP) for human immunodefi-ciency virus (HIV) infection is the use of antiretroviral (ARV) medications after an exposure to HIV has occurred in order to prevent infection with HIV. PEP is the term used when the exposure is occupational (occurs while a person is working at a job). When the exposure occurs at any other time (away from work), the prophylaxis is called nonoccupational postex-posure prophylaxis (n PEP). The advent of HIV infection in the 1980s brought with it widespread anxiety about the risks of infection in health care and other settings. As soon as antiretroviral medications were approved for use in HIV-infected individuals in the 1990s, the concept of using them in people with known exposures arose (PEP). There are an estimated 400,000 occupational exposures to HIV per year in the United States. By 2001, there were 57 confirmed and 138 possible HIV seroconversions caused by occupational exposures (Henderson, 2001). Antiretrovirals have been used for occupational (PEP) and increasingly for nonoccupational exposures (n PEP). Empiric evidence about the effectiveness of PEP, however, is in short supply. The first attempted randomized trial of zidovudine monotherapy for PEP was closed early because of enroll-ment difficulties. The best evidence for efficacy is a Centers for Disease Control and Prevention case-control study that suggests 81% reduction in risk of HIV infection with use of zidovudine only (Cardo et al., 1997). Randomized controlled trials of PEP are not feasible, but experts agree that the concept of giving antiretroviral medication to arrest infection before it is able to take hold makes sense and that PEP should be offered to individuals with high-risk expo-sures to HIV. As such, organizations have developed com-prehensive guidelines for the use of PEP (New Y ork State Department of Health AIDS Institute, 2014; World Health Organization, 2005). Barbara Newlin and Brooke Finkmoore Postex Posure Pro Phylax Is F or h IV I NF ect I o N© Eliks/Shutterstock; © donatas1205/Shutterstock 37540Chapt Er
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Table 40-1 HIV Infectious Fluids Body fluids infectious for HIV Blood and plasma Semen Amniotic fluid Vaginal secretions Cerebrospinal fluid Synovial fluid Pleural fluid Peritoneal fluid Pericardial fluid Body fluids noninfectious for HIVSaliva Tears Sweat Nonbloody urine or feces Data from Medical Care Criteria Committee, New York State Department of Health AIDS Institute. (2008). HIV prophylaxis following occupational exposure. Retrieved from www. hivguidelnes. org. Table 40-2 Risk of HIV T ransmission by Exposure Route exposure router isk Per 10,000 e xposures to an Infected s ource Blood transfusion 9,250 Needle-sharing injection-drug use 63 Receptive anal intercourse 138 Percutaneous needle stick 23 Receptive penile-vaginal intercourse8 Insertive anal intercourse 11 Insertive penile-vaginal intercourse4 Receptive oral intercourse low Insertive oral intercourse low Modified from Centers for Disease Control and Prevention. (2015). HIV risk behaviors. Retrieved from http://www. cdc. gov/hiv/risk/estimates /riskbehaviors. html Table 40-3 Occupational Exposure to HIV : Comparison of NYSDOH and USPHS Nys Doh a I r ecommendations (2014)* us P hs r ecommendations (2013)† Indication for PEP Percutaneous or mucocutaneous exposure with blood or visibly bloody fluid or other potentially infectious material. Indication for PEP Percutaneous injury or contact of mucous membrane or nonintact skin with blood, tissue, or potentially infectious body fluids, such as semen, vaginal secretions, and visibly bloody fluids and reasonable suspicion that the source patient is HIV infected. HIV Testing of the Source Patient If HIV serostatus of the source is unknown, voluntary HIV testing of the source should be sought. Rapid testing is strongly recommended for the source patient, and for those organizations subject to Occupational Safety and Health Administration regulations, rapid testing of the source patient is mandated for occupational exposures. When the source patient's rapid test result is negative, and the clinician has ascertained that the source patient could have possibly been exposed to HIV in the previous 6 weeks, a plasma HIV RNA assay should be used in conjunction with the rapid HIV antibody test. In these situations, PEP should be initiated and continued until results of the plasma HIV RNA assay are available. In New York State, when the source patient has the capacity to consent to HIV testing, specific informed consent is required. HIV Testing of the Source Patient Although concerns have been expressed regarding HIV-negative sources being in the window period for seroconversion, no case of transmission involving an exposure source during the window period has been reported in the United States. Rapid HIV testing of source patients can facilitate making timely decisions regarding use of HIV PEP after occupational exposures to sources of unknown HIV status. 376 CHAPTER 40 | Postexposure Prophylaxis for HIV Infection
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infection to be halted before becoming established (Kuhar et al., 2013). The New Y ork state guidelines encourage pro-viders to seek expert advice before starting PEP if more than 36 hours have passed since the exposure (New Y ork State Department of Health AIDS Institute, 2012). There is agreement that PEP should be continued for 28 days to maximize effectiveness (Kuhar et al., 2013; New Y ork State Department of Health AIDS Institute, 2014; World Health Organization, 2005). The steps for evaluating and manag-ing an occupational exposure to HIV are summarized by the New Y ork Department of Health in Figure 40-1. Nonoccupational postexposure prophylaxis (n PEP) for HIV has been used increasingly. Figure 40-2 summarizes the evaluation and management of n PEP. Table 40-3 Occupational Exposure to HIV : Comparison of NYSDOH and USPHS Nys Doh a I r ecommendations (2014)* us P hs r ecommendations (2013)† Recommendations for Number of Drugs in PEP Regimen A three-drug PEP regimen is the preferred option for all significant-risk occupational exposures. Recommendations for Number of Drugs in PEP Regimen A regimen containing three (or more) antiretroviral drugs is recommended for all occupational exposures. Clinicians facing challenges associated with a three-drug regimen might consider a two-drug regimen in consultation with an expert. Recommended PEP Regimen Tenofovir 300 mg PO daily +Emtricitabine 200 mg PO daily or Lamivudine 300 mg PO dailyplus Either Raltegravir 400 mg PO twice daily or Dolutegravir 50 mg PO daily Recommended PEP Regimen Tenofovir 300 mg PO daily + Emtricitabine 200 mg PO daily plus Raltegravir 400 mg PO twice daily Duration of PEP: 4 weeks Duration of PEP: 4 weeks HIV Antibody Testing of Healthcare Worker Baseline 1 month postexposure 3 months postexposure HIV Antibody Testing of Healthcare Worker Baseline 6 weeks postexposure 12 weeks postexposure 6 months postexposure Alternatively, if the clinician is certain that a fourth-generation antibody/antigen combination assay is being used, then HIV testing could be performed at baseline, 6 weeks, and concluded at 4 months post exposure. Timing of Initiation of PEP When a potential occupational exposure to HIV occurs, every effort should be made to initiate PEP as soon as possible, ideally within 2 hours. A first dose of PEP should be offered to the exposed worker while the evaluation is under way. In addition, PEP should not be delayed while awaiting information about the source or results of the exposed individual's baseline HIV test. Decisions regarding initiation of PEP beyond 36 hours post exposure should be made on a case-by-case basis with the understanding of diminished efficacy when timing of initiation is prolonged. Timing of Initiation of PEP PEP should be initiated as soon as possible, preferably within hours of exposure. Initiation of PEP should not be delayed while awaiting the results of a source patient's HIV test, nor should it be delayed during consultation with experts to determine ideal PEP regimens. *Reproduced from New York State Department of Health AIDS Institute. (2014). UPDATE: HIV Prophylaxis Following Occupational Exposure. Retrieved from www. hivguidelines. org. †Kuhar, D. T., Henderson, D. K., Struble, K. A., Heneine, W., Thomas, V., Cheever, L. W., et al. (2013). Updated U. S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis. Infection Control and Hospital Epidemiology, 34, 875-892. Retrieved from http://stacks. cdc. gov/view/cdc/20711. (Continued)377 Introduction and general background
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Table 40-4 Antiretroviral Drugs to A void as PEP Components Drug(s) to avoid r ationale Efavirenz (EFV) Poor adherence anticipated due to central nervous system (CNS) side effects, which are common CNS side effects may impair work after the initial and subsequent doses EFV should be avoided in first 6 weeks of pregnancy and in women of childbearing potential who are not using effective contraception Substantial EFV resistance in community HIV isolates Nevirapine Contraindicated for use in PEP due to potential for severe hepatotoxicity Abacavir Potential for hypersensitivity reactions Stavudine, didanosine Possibility of toxicities Nelfinavir, indinavir Poorly tolerated CCR5 coreceptor antagonists Lack of activity against potential CXCR4 tropic virus Figure 40-1 Steps for PEP Following Occupational HIV Exposure Modified from New York State Department of Health AIDS Institute. (2015). UPDATE: HIV Prophylaxis Following Occupational Exposure. Retrieved from www. hivguidelines. org. Source tests positive Sour ce pa tient refuses HIV testing Sourc e patient do es not have capacity to consent Obtain consent for rapid HIV testing of sourc e patient Sour ce pa tient HIV status unknown Sour ce test s nega tive Has the source patient been at risk for HIV exposure in the previous 6 we eks? NO YESStop PEP. not indicated Consider Consider Obtain HIV RNA Assay from source pt, contin ue PEP until res ults kn own HIV RNA Positive HIV RNA Negative Stop PEP Sourc e patient KNO WN TO BE HIV INFE CTED BY MEDI CAL RECO RDOffer worker first dose of PEP while evalua tion is underway Complete 28-day Recommended PEP Regimen: Tenofovir 300 mg PO daily and Emtricitabine 200 mg PO daily Raltegravir 400 mg PO twice daily OR Dolutegravir 50 mg PO daily Perform baseline confidential HIV testing of the exposed worker and refer to experienced HIV clinician within 3 days of initiating PEP Alternative regimens are available 378 CHAPTER 40 | Postexposure Prophylaxis for HIV Infection
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Figure 40-2 Steps for Evaluating and Managing Nonoccupational Exposures to HIV Reproduced from New York State Department of Health AIDS Institute. (2015). UPDATE: HIV prophylaxis following non-occupational exposure. Retrieved from www. hivguidelines. org. LOWER-RISK EXPOSURES: Oral-vaginal contact (receptive and insertive) Oral-anal contact (receptive and insertive) Receptive penile-oral contact with or without ejaculation Insertive penile-oral contact with or without ejaculation See Table 1 for factors thatmay increase risk. If PEP isindicated, go to Step 2. EXPOSURES THAT DO NOT WARRANTn PEP: Oral-to-oral contact without mucosal damage (kissing or mouth-to-mouth resuscitation) Human bites not involving blood Exposure to solid-bore needles or sharps not in recent contact with blood Mutual masturbation without skin breakdown or blood exposure Provide risk-reductioncounseling and offer HIV test. STOP. n PEP notindicated. STOP. n PEP notindicated. HIGHER-RISK EXPOSURES: Receptive and insertive vaginal or anal intercourse with HIV+ or unknown source Needle sharing with HIV+ or unknown source Injuries with exposure to blood or other potentially infected fluids from HIV+ or unknown source (including needlesticks with a hollow-bore needle, human bites, accidents)STEP 1: Evaluation of exposure: Is n PEP indicated? STEP 2: Is patient presenting within 36 hours? STEP 3: Initiate first dose of n PEP regimen STEP 5: Provide risk-reduction counseling STEP 4: Baseline testing BASELINE TESTING OF EXPOSED PERSON: HIV test* Pregnancy test for women GC/CT NAAT (based on site of exposure) RPR for syphilis *n PEP should not be continued in those who decline baseline HIV testing See Section IX for hepatitis B and C post-exposure management. SOURCE TESTING, if source is available: Obtain consent for HIV testing Obtain HIV test with turnaround time < 1 hour If the test results are not immediately available, continue exposed person's n PEP while awaiting results If the source person's HIV screening test result is negative but there may have been exposure to HIV in the previous 6 weeks, obtain plasma HIV RNA assay Continue exposed person's n PEP until results of the plasma HIV RNA assay are available YESa 28-DAY REGIMEN — Recommended PEP Regimen:b, c Tenofovir 300 mg PO qd + Emtricitabined 200 mg PO qd plus Raltegravire 400 mg PO bid or Dolutegravire 50 mg PO qd See Tables 4 and 5 for alternative regimens Provide risk-reduction and primary prevention counseling Refer for mental health and/or substance use programs when indicated; consider need for intensive risk-reduction counseling services Discuss future use of Pr EP with persons with ongoing risk behavior (see Appendix C for Al-funded referral sources) a Decisions to initiate n PEP beyond 36 hours post-exposure should be individualized, with the realization of diminished efficacy when timing of initiation is prolonged; assess for hepatitis B and C; recommend serial HIV testing at 0, 4, and 12 weeks; provide risk-reduction counseling. b If the source is known to be HIV-infected, information about his/her viral load, ART medication history, and history of antiretroviral drug resistance should be obtained when possible to assist in selection of a PEP regimen. 67 Initiation of the first dose of PEP should not be delayed while awaiting this information and/or results of resistance testing. When this information becomes available, the PEP regimen may be changed if needed in consultation with an experienced provider. c See Appendix A for dosing recommendations in patients with renal impairment. d Lamivudine 300 mg PO qd may be substituted for emtricitabine. A fixed-dose combination is available when tenofovir is used with emtricitabine (Truvada 1 PO qd). e See Appendix A for drug-drug interactions, dosing adjustments, and contraindications associated with raltegravir and dolutegravir. 379 Introduction and general background
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Table 40-5 PEP Drugs to A void During Pregnancy Drug(s) to avoid to xicity Efavirenz Teratogenicity Combination of stavudine and didanosine Mitochondrial toxicity Nevirapine Hepatotoxicity Unboosted indinavir in the second or third trimester Substantially lower antepartum indinavir plasma concentrations; risk for nephrolithiasis B. Weighing the risks and benefits of PEP and n PEP The clinician must decide what to recommend to poten-tially exposed clients. Because of the lack of empiric data, a cost/benefit analysis of PEP is impossible. Factors to weigh include route of exposure; amount of infectious fluid involved; HIV serostatus and stage of disease of the source (including viral load); overall health and preg-nancy status of the recipient; mental state of the recipient; and possibility of adverse reactions to the antiretrovirals. After carefully reviewing all the information, the clinician and the client can together make a decision about whether or not PEP will be initiated. Pregnancy and breastfeeding status of the patient are especially important considerations. Given the fact that acute HIV infection during pregnancy or breastfeeding greatly increases the risk of infection in the baby (due to very high viral loads during this time) and that the major-ity of recommended PEP drugs are considered safe in preg-nancy and breastfeeding (see exceptions in T able 40-5), PEP is highly recommended for pregnant and breast-feeding women with risky exposures. Both HIV and PEP drugs will be present in breast milk. It may be recom-mended that breastfeeding women stop breastfeeding while on PEP and/or when risk for primary infection is present (Antiretroviral Pregnancy Registry, 2015; Kuhar et al., 2013 New Y ork State Department of Health AIDS Institute, 2014). 1. D epending on the test used, the window period may be shorter than 6 weeks. Clinicians should contact appropriate laboratory authorities to determine the window period for the test that is being used. 2. I f the source is known to be HIV infected, information about his/her viral load, ART medication history, and history of antiretroviral drug resistance should be obtained when possible to assist in selection of a PEP regimen. Initiation of the first dose of PEP should not be delayed while awaiting this information and/or results of resistance testing. When this information becomes available, the PEP regimen may be changed if needed in consultation with an experienced provider. Be sure to adjust dosages for renally impaired patients. a. D ecisions to initiate n PEP beyond 36 hours post-exposure should be individualized, with the realization of diminished efficacy when timing of initiation is prolonged; assess for hepatitis B and C; recommend serial HIV testing at 0, 4, and 12 weeks; provide risk-reduction counseling. b. I f the source is known to be HIV-infected, infor-mation about his/her viral load, ART medication history, and history of antiretroviral drug resis-tance should be obtained when possible to assist in selection of a PEP regimen. Initiation of the first dose of PEP should not be delayed while awaiting this information and/or results of resistance testing. When this information becomes available, the PEP regimen may be changed if needed in con-sultation with an experienced provider. c. S ee www. hivguidelines. org for dosing recom-mendations in patients with renal impairment. d. L amivudine 300 mg PO qd may be substituted for emtricitabine. A fixed-dose combination is available when tenofovir is used with emtric-itabine (T ruvada 1 PO qd). e. S ee www. hivguidelines. org for drug toxicities. Interactions and alternative regimens. II. Database (may include but is not limited to) A. Subjective 1. H istory of exposure a. W hen did the exposure occur (exact time and date) b. W hat type of exposure (skin, mucous membrane, percutaneous, or sexual; route of exposure if sexual [vaginal, anal, or oral]) c. Othe r details about exposure: trauma involved, deep or shallow, and amount and type of fluid involved d. I nformation about the exposure source i. Kno wn HIV positive? Able to document? Stage of illness? Type of antiretrovirals 380 CHAPTER 40 | Postexposure Prophylaxis for HIV Infection
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Table 40-6 Signs and Symptoms of HIV Primary Infection (Acute Retroviral Syndrome) symptom/ sign P ercentage of Patients with s ymptom/ s ign Fever 96% Lymphadenopathy 74% Pharyngitis 70% Rash Erythematous maculopapular with lesions on face, trunk, and sometimes extremities, including palms and soles; mucocutaneous ulceration involving mouth, esophagus, or genitals70% Myalgia or arthralgia 54% Diarrhea 32% Headache 32% Nausea and vomiting 27% Hepatosplenomegaly 14% Weight loss 13% Thrush 12% Neurologic symptoms Meningoencephalitis or aseptic meningitis, peripheral neuropathy or radiculopathy, facial palsy, Guillain-Barré syndrome, brachial neuritis, or cognitive impairment or psychosis12% Data from Centers for Disease Control and Prevention. Antiretroviral postexposure prophylaxis after sexual, injection-drug use, or other nonoccupational exposure to HIV in the United States: recommendations from the U. S. Department of Health and Human Services. Morbidity and Mortality Weekly Report 2005; 54 (No. RR-2); Smith et al., 2005. taken now and in the past? Viral load (HIV RNA) at present time? ii. I f HIV status is unknown or documented negative, are there risk factors for HIV infection present? Does the source have signs or symptoms of primary HIV infec-tion (fever, rash, or flulike symptoms) (T able 40-6)? Can the source be located and can a rapid HIV test be obtained?2. P atient history, including but not limited to: a. A ny history of HIV infection or use of antiretro-virals, previous exposures to HIV, previous PEP, previous HIV testing, other HIV risk factors; liver or kidney disease (especially hepatitis A, B, or C); allergies or adverse reactions to medica-tions; previous sexually transmitted infections; surgeries b. Ge neral health history: any chronic disease c. S ocial history: sexual history, pregnancy, relation-ships, social support, living circumstances, and health habits 3. R eview of systems Complete review of systems is appropriate with emphasis on mouth, skin, liver, gastrointestinal, kidney, genitalia, neurologic (especially headache and peripheral neuropathy history), and psychiatric symptoms. B. Objective 1. P hysical examination a. E xamine area of exposure and assess for trauma, lesions, bruising excoriations, or other breaks in the integrity of skin or mucous membranes, and cleanliness. b. S kin: baseline to identify existing lesions or rashes c. H ead: baseline for headaches or sinus tenderness d. M outh: baseline for lesions or periodontal disease e. A bdomen: baseline liver and spleen size and tenderness, general state of abdomen f. N eurologic: baseline general neurology (especially deep tendon reflexes and sensory examination) g. Ge nital and anal examination for sexual exposures 2. Di agnostic testing Figures 40-1 and 40-2 delineate the basic initial testing needed before initiation of PEP or n PEP. The clinician may want to add more testing for individual patients, depending on the health state and problems. See T ables 40-7 and 40-8 for recommendations for initial and follow-up testing of patients on PEP and n PEP. An additional crucial consideration is the testing of the source patient (see Figures 40-1 and 40-2). Remember that hepatitis B and C testing and sexually transmitted infection (STI) testing may also be important in patients with exposures risky for HIV infection. 381 Database
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Table 40-7 Monitoring Recommendations After Initiation of PEP Regimens Following Occupational Exposurea   Baseline Week 1 Week 2 Week 3 Week 4 Week 12 Clinic Visit √ √ Or by telephone√ Or by telephone√ Or by telephone√   Pregnancy Test √           Serum liver enzymes, BUN, creatinine, CBC b√   √   √   HIV testc√       √ √ a For postexposure management for hepatitis B and C, see Section XI: Occupational Exposures to Hepatitis B and C. b Complete blood count (CBC) should be obtained for all exposed workers at baseline. Follow-up CBC is indicated only for those r eceiving regimen containing zidovudine. c Recommended even if PEP is declined. Reproduced from New York State Department of Health AIDS Institute. (2014). UPDATE: HIV prophylaxis following occupational exposure. Retrieved from www. hivguidelines. org. Table 40-8 Monitoring Recommendations After Initiation of PEP Regimens Following Nonoccupational Exposures   Baseline Week 1 Week 2 Week 3 Week 4 Week 12 Clinic Visit √ √ Or by telephone√ Or by telephone√ Or by telephone√   Pregnancy Test √           Serum liver enzymes, blood urea nitrogen (BUN), creatinine, CBC a√   √   √   HIV testb√       √ √ STI Screening (for exposures unrelated to sexual assault) b: Nucleic Acid Amplification Testing for Gonorrhea and Chlamydia (GC/CT NAAT) (based on site of exposure) Rapid Plasma Reagin (RPR) See HIV Prophylaxis for Victims of Sexual Assault for recommendations in cases of sexual assault. √   √ (consider)      Hepatitis B and C a For postexposure management for hepatitis B and C, see Section IX: Nonoccupational Exposures to Hepatitis B and C a CBC should be obtained for all exposed persons at baseline. Follow-up CBC is indicated only for those receiving a zidovudine-containing regimen. b Recommended even if PEP is declined. Reproduced from New York State Department of Health AIDS Institute. (2014). UPDATE: HIV prophylaxis following non-occupational exposure. Retrieved from www. hivguidelines. org. 382 CHAPTER 40 | Postexposure Prophylaxis for HIV Infection
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3. PEP or n PEP not r ecommended a. I f significant exposure has not occurred, counsel patient on why PEP is not recommended and how to avoid further exposures. b. Adv ise patient to follow up if experiencing any problems, especially symptoms of HIV primary infection (T able 40-6). C. Patient education Mechanism of HIV infection, possible medication tox-icities, strict adherence to medications regimen, mech-anism of resistance development, strategies for not infecting others, and signs and symptoms of primary infection (T able 40-6). D. Reporting requirements Remember to follow the requirements of your institution and your state on reporting and data keeping for occupa-tional exposures and injuries, including requirements for worker's compensation reporting. V. c linician and patient resources A. HIV Warmline: 800-933-3413 B. PEP Line: 888-HIV-4911Table 40-9 Counseling for Any Person Having Experienced Exposure to HIV is recommended (whether taking PEP or n PEP or not) Exposed person should be advised to use precautions (e. g., avoid blood or tissue donations, breastfeeding, or pregnancy) to prevent secondary transmission, especially during the first 6-12 weeks postexposure. For exposures for which PEP or n PEP is prescribed, patient should be informed regarding possible drug toxicities and the need for monitoring, possible drug interactions, and the need for adherence to PEP regimens. Consider reevaluation of exposed person 72 hours post-exposure, especially after additional information about the exposure or source person becomes available. Data from Centers for Disease Control and Prevention. Updated U. S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for Postexposure Prophylaxis. Morbidity and Mortality Weekly Report 2005; 54 (No. RR-9); Panlilio et al., 2005. III. a ssessment A. Determine the diagnosis and its significance 1. D etermine the level of risk for HIV exposure and weigh the benefits of treatment. 2. D etermine the significance of possible exposure to the patient and significant others, noting the amount of psychologic distress present. 3. A ssess the motivation and ability of the patient to follow through with the treatment plan. 4. N ote the amount of social support to help with coping during this stressful time. IV. Plan A. Diagnostic tests (See Figures 40-1 and 40-2, and Tables 40-7 and 40-8) B. Management 1. The a rea of exposure should be washed gently with soap and water (for skin) or rinsed liberally with clean water or saline solution (for mucous membranes). Genitals and anal area may be gently bathed with mild soapy water, but douching is not recommended. Any trauma should be appropriately treated. Avoid squeezing, scrubbing, or otherwise traumatizing the area of exposure. 2. PEP r ecommended a. I f PEP or n PEP is recommended, follow the algorithms and testing schedules (see Figures 40-1 and 40-2, and T ables 40-7 and 40-8). b. F ollow-up should ideally be referred to an HIV specialist, and when no specialist is avail-able, expert consultation should be sought. Every case should be discussed with an expert (see resources listed at end of chapter—immediate phone consultation is always avail-able). The client should be seen in follow-up at least after the first 3 weeks, or earlier if they are experiencing any problems (drug side effects), especially symptoms of HIV primary infection (see T ables 40-6, 40-7, and 40-8). c. S upportive counseling to ensure adherence to the medication regimen and alleviate anxiety is highly recommended (T able 40-9). 383 Clinician and patient resources
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Kuhar, D. T., Henderson, D. K., Struble, K. A., Heneine, W., Thomas, V., Cheever, L. W., et al. (2013). Updated U. S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis. Infection Control and Hospital Epidemiology, 34, 875-892. Medical Care Criteria Committee. (2008). HIV prophylaxis following occupational exposure. New Y ork: New Y ork State Department of Health AIDS Institute. Retrieved from www. hivguidelines. org. New Y ork State Department of Health AIDS Institute. (2014). Update: HIV prophylaxis following occupational exposure. Retrieved from www. hivguidelines. org/clinical-guidelines/post-exposure-prophylaxis /hiv-prophylaxis-following-occupational-exposure/. Smith, D. K., Grohskopf, L. A., Black, R. J., Auerbach, J. D., Veronese, F., Struble, K. A., et al. (2005). Antiretroviral postexposure prophylaxis after sexual, injection-drug use, or other nonoccupational exposure to HIV in the United States: Recommendations from the U. S. Department of Health and Human Services. Morbidity and Mortality Weekly Report, 54(RR-2), 1-20. World Health Organization. (2005). Post-exposure prophylaxis to prevent HIV infection: Joint WHO/ILO guidelines on post-exposure prophylaxis (PEP) to prevent HIV infection. Retrieved from http://www. who. int/hiv/pub /guidelines/PEP/en/C. National HIV/AIDS Clinicians' Consulting Center: www. nccc. ucsf. edu. A comprehensive website including links to many HIV-related guidelines, including PEP. It is advisable to check frequently for updates to these guidelines. re Fere Nces Antiretroviral Pregnancy Registry Steering Committee. (2015). Antiretroviral pregnancy registry international interim report for 1 January 1989 through 31 July 2015. Wilmington, NC: Registry Coordinating Center. Retrieved at www. APRegistry. comhttp://www. apregistry. com/forms /interim_report. pdf Cardo, D. M., Culver, D. H., Ciesielski, C. A., Srivastava, P. U., Marcus, R., Abiteboul, D., et al. (1997). A case-control study of HIV seroconversion in healthcare workers after percutaneous exposure. Centers for Disease Control and Prevention Needlestick Surveillance Group. New England Journal of Medicine, 337(21), 1485-1490. Centers for Disease Control and Prevention (2014). HIV risk behaviors. Retrieved at http://www. cdc. gov/hiv/risk/estimates/riskbehaviors. html Henderson, D. K. (2001). HIV postexposure prophylaxis in the 21st century. Emerging Infectious Diseases, 7(2), 254-258384 CHAPTER 40 | Postexposure Prophylaxis for HIV Infection
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Pr EP. The information included in this chapter reflects the USPHS recommendations. A. Evidence for Pr EP 1. Effica cy and effectiveness Randomized controlled trials investigating the efficacy of Pr EP have been conducted among vari-ous high-risk populations and in a number of settings. Among four Pr EP trials published as of August 2013, a 74% and 92% reduction in HIV risk was found among HIV-uninfected men and women who consistently used Pr EP; the reduction in HIV risk was lower and more variable, between 40% and 80%, for those who did not consistently use Pr EP (Baeten et al., 2012; Choopanya et al., 2013; Grant et al., 2010; Thigpen et al., 2012). Analyses of Pr EP trial data found that par-ticipants who took Pr EP 7 days a week were 99% pro-tected against infection, whereas those who took the pill 4 days a week were 96% protected and those who took the pill 2 days a week were 76% protected (U. S. Public Health Service, 2014a). Overall, these data demonstrate that Pr EP provides protection against HIV acquisition and that daily adherence is needed to achieve maximal prophylactic benefit. Studies on the effectiveness of Pr EP in real-life clinical practice have favorable results. For example, a study that randomized 545 high-risk men who have sex with men (MSM) to either immediate initia-tion of Pr EP or delayed initiation, found a 86% rela-tive reduction in HIV acquisition among those who immediately initiated Pr EP compared with those delayed Pr EP for 1 year and there was not an increase in STIs among immediate Pr EP users (Mc Cormack & Dunn, 2015). The optimal number of drugs for Pr EP is unknown. TDF alone was found to reduce the risk of HIV acqui-sition among IDUs, and the protective effects of TDF/FTC and TDF alone were similar among serodis-cordant heterosexual couples (Baeten et al., 2012; I. Intr oduction and general background Preexposure prophylaxis (Pr EP) is the daily use of antiretro-viral (ARV) drugs by HIV-uninfected persons to prevent the acquisition of HIV from nonoccupational exposures. In July 2012, the Food and Drug Administration approved the use of T ruvada as Pr EP (Food and Drug Administration, 2012). T ruvada is a fixed-dose combination pill of two ARV drugs, tenofovir disoproxil fumarate (TDF) and emtricitabine (FTC), that has been used as a part of combination antiretro-viral therapy (ART) for HIV-infected individuals since 2004 (Gilead Sciences, 2013). Pr EP is indicated for adult men and women who have a substantial risk of acquiring HIV either through sex or and intravenous drug use (IDU) (U. S. Public Health Service, 2014a). The presence of Pr EP in the blood-stream and other tissues can stop HIV from establishing infec-tion because it blocks important pathways for viral replication (U. S. Public Health Service, 2014a). If Pr EP is taken every day, it reaches its maximum protection in blood at 20 days, in rectal tissue at about 7 days, and in vaginal tissues at about 20 days (U. S. Public Health Service, 2014a). Clinicians are encouraged to offer Pr EP to at-risk patients as part of a comprehensive prevention strategy that also includes sexual-risk reduction counseling, condom provision, treatment of sexually trans-mitted infections (STIs), ART for HIV-infected partners, and referrals to drug treatment and mental health services when indicated. In 2014, the United States Public Health Service (USPHS) published a clinical practice guideline and a clinical provider supplement on Pr EP (U. S. Public Health Service, 2014a, 2014b). Increasing the use of and adherence to HIV prevention strategies is a public health priority because there are approxi-mately 50,000 new cases of HIV infection diagnosed annually in the United States (Centers for Disease Control and Prevention, 2012). These documents orient clinicians to an evidence-based HIV risk assessment, clinical eligibility for Pr EP, and safe management practices for patients who are on Barbara Newlin and Brooke Finkmoore Preex Posure Pro Phylax Is F or h IV 38541Chapter© eliks/Shutt erstock; © donatas1205/Shutterstock
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1. I ndividuals at substantial risk of acquiring HIV a. M en who have sex with men who have any of the following: an HIV-infected sexual partner, a recent bacterial STI, a high number of sex part-ners, a history of inconsistent or no condom use, current participation in commercial sex work. b. H eterosexual men and women who have any of the following: an HIV-infected sexual partner, a recent bacterial STI, a high number of sex part-ners, a history of inconsistent or no condom use, current participation in commercial sex work in high-prevalence area or network. c. I njection drug users who have any of the follow-ing: an HIV-infected injecting partner, a prac-tice of sharing injection equipment, recent drug treatment (but currently injecting). 2. C linical eligibility for Pr EP a. I ndividuals at substantial risk of acquiring HIV are clinically eligible for Pr EP if they have a negative HIV test at the time they start Pr EP, do not have signs or symptoms suggesting acute (primary) HIV infection (see Figure 41-1: Documenting HIV Status) and they have normal renal function (estimated creatinine clearance [e Cr Cl] ≥ 60 m L/min). b. P atients are not clinically eligible for Pr EP if they have signs or symptoms suggestive of acute HIV even if their HIV antibody test is negative because the administration of T ruvada alone in the setting of unrecognized HIV infection can select for drug-resistant virus. c. A ny person with an e Cr Cl < 60 m L/min should not be prescribed Pr EP with TDF/FTC. TDF is associated with acute and chronic kidney disease and there are no safety data on TDF in individuals with an e Cr Cl < 60 m L/min. There are no approved Pr EP regimens for individuals with baseline renal insufficiency. d. A ge is also a consideration: Pr EP is currently approved only for adults because there are insuf-ficient data on the safety and efficacy of Pr EP for those under 18 years of age. II. Database (may include but is not limited to) A. Subjective 1. P atient history Obtaining a thorough history of sexual and drug use behaviors is necessary to determine whether a patient is at substantial risk of acquiring HIV infection. Choopanya et al., 2013). Currently, the USPHS recommends daily oral Pr EP with TDF/FTC or TDF alone for IDUs at substantial risk and TDF/FTC for all other populations (U. S. Public Health Service, 2014a). 2. Sa fety TDF/FTC has an excellent safety profile and is well tolerated by HIV-infected individuals (Gallant, De Jesus, Arribas, et al., 2006; Gallant, Staszewski, Pozniak, et al., 2004). The Pr EP trials found TDF alone or in combination with FTC to be safe and well tolerated when used by HIV-uninfected individuals (Grant et al., 2010; Grohskopf et al., 2013). The ini-tiation of TDF/FTC is associated with self-limited start-up symptoms including nausea, vomiting, and dizziness (U. S. Public Health Service, 2014a). In one Pr EP trial, study subjects randomly assigned to the TDF/FTC group had greater declines in bone mass density compared with those in the placebo group but not a difference in the rate of fractures (Thigpen et al., 2012). In the i Prex study, TDF/FTC use was associated with mild but significant decrease in kidney function but not proximal tubular dysfunction (Solomon et al., 2014). The majority of elevations in serum creatinine occurred by the fourth week of TDF/FTC use and elevations were self-limited; all elevations resolved with discontinuation of TDF/FTC (Solomon et al., 2014). Routine monitoring of serum creatinine is recommended to manage the development of renal insufficiency in individuals on TDF or TDF/FTC for Pr EP (U. S. Public Health Service, 2014a). Although there have been concerns about the selection of viral mutations that confer resistance to TDF or FTC if Pr EP fails, instances of seroconversion with resistant virus were extremely rare in the Pr EP trials. TDF or FTC resistant virus was not detect-ed among study participants who seroconverted after study enrollment except in one study that was stopped early due to low adherence (Van Damme et al., 2012). Otherwise, viral resistance to TDF or FTC was found only in patients with existing and unrecog-nized HIV at the time of Pr EP initiation (U. S. Public Health Service, 2014a). None of the Pr EP trials studied the effects of Pr EP on a developing fetus. TDF/FTC, pregnancy cat-egory B, is recommended for serodiscordant couples trying to conceive in combination with ART in the infected partner (Panel on T reatment of HIV-Infected Pregnant Women and Prevention of Perinatal T ransmission, 2014). B. Indications for Pr EP Pr EP is indicated for individuals at a substantial risk of acquiring HIV who meet the clinical eligibility criteria. 386 CHAPTER 41 | Preexposure Prophylaxis for HIV
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(see Appendix 41-2: Screening T ool for MSM). Clinicians may consider STIs or pregnancy in the past 6 months as evidence of unprotected sex and poten-tial exposure to HIV. If a patient reports a sexual or parenteral exposure to HIV in the previous 72 hours, evaluation for postexposure prophylaxis (PEP) should be started without delay (see Chapter 40, Postexposure Prophylaxis for HIV Infection). The USPHS guidelines contain a set of behavioral risk assessment questions for MSM, heterosexual men and women, and IDU (see Appendix 41-1: Behavioral Risk Assessment Questions). The questions assess key sexual and drug use practices identified in epidemiologic studies and Pr EP trials that are associated with a high risk of HIV acquisition. A clini-cal screening tool for MSM has also been developed Figure 41-1 Documenting HIV Status Reproduced from U. S. Public Health Service. (2014). Preexposure prophylaxis for the prevention of HIV infection in the United States—2014 Clinical Practice Guideline. Signs/symptoms of acute HIV infection anytime in prior 4 weeks Retest antibody in one month; defer Pr EP decision Send blood for HIV antibody/antigen assay*Send blood for HIV-1 viral load (VL) assay VL < level of detection no signs/symptoms on day of blood draw VL < level of detection with signs/symptoms on day of blood draw Retest in one month Defer Pr EP decision HIV-Option 1 Positive Negative HIV-Eligible for Pr EP HIV+ Not Eligible for Pr EP HIV Status Unclear Defer Pr EP decision HIV+ HIV+ VL ≥ 50,000 copies/m L Retest VL; defer Pr EP decision VL < 50,000 copies/m L HIV-HIV-Option 2 Option 3No Yes *Use only HIV antigen/antibody tests that are approved by FDA for diagnostic purposes Indeterminate Positive Negative Consider HIV+ (pendingconfirmatorytesting)HIV immunoassay blood test (rapid test if available)387 Database
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2. R eview of systems Signs and symptoms of acute (primary) HIV infec-tion should be assessed in all patients considering Pr EP. Signs and symptoms of acute HIV include fever, fatigue, malaise, skin rash, headache, pharyn-gitis, cervical adenopathy, arthralgia, night sweats, and diarrhea. B. Objective 1. P hysical examination a. S kin: baseline inspection to identify existing lesions or rashes b. M outh: baseline inspection for lesions c. H ead, neck, throat: assess for lymphadenopathy d. A bdomen: baseline liver and spleen size and tenderness e. N eurologic: baseline general neurology f. Ge nital and anal examination for STIs 2. Di agnostic test results for clinical eligibility Prior to initiating Pr EP patients must have the fol-lowing tests to determine clinical eligibility: an HIV test (preferably with a fourth-generation antigen/antibody test); a serum creatinine test (and calculate e Cr Cl); hepatitis B virus (HBV) serology (hepatitis B surface antigen, hepatitis B surface antibody, and hep-atitis B core antibody). III. a ssessment A. Determine whether the patient is at substantial risk of HIV acquisition and is clinically eligible See Appendix 41-3: Summary of Guidance for Pr EP Use. B. Assess the patient's understanding of the treatment plan and motivation and ability to follow through with the plan If a patient meets clinical eligibility criteria but has significant barriers to daily medication adherence or if the provider is unable to develop an appropriate follow-up plan with the patient, the provider should consider delaying Pr EP initiation. C. Weigh the risks and benefits of Pr EP with the patient This should take into account the patient's level of HIV risk, kidney function, and HBV status. If the patient is pregnant or planning to conceive, refer the patient to an obstetrician and/or HIV specialist to discuss risks and benefits of Pr EP in pregnancy. IV. Goals of clinical management The goal of Pr EP is to prevent the acquisition of HIV. The goal of monitoring patients throughout the duration of Pr EP use is to ensure that the risks of Pr EP do not outweigh the benefits. V. Plan A. Diagnostic tests 1. H IV: clinicians should document a negative HIV antibody test the week before initiating Pr EP. a. A n immunoassay that detects both antibody to human immunodeficiency virus and HIV p24 antigen (i. e., a fourth-generation antigen/antibody test) is preferred as it increases the likelihood of diagnosing acute HIV infection (Pandori et al., 2009). 2. R enal function: obtain a serum creatinine test and calculate e Cr Cl. 3. H epatitis B virus serology: obtain hepatitis B surface antigen, hepatitis B surface antibody, and hepatitis B core antibody. a. P atients susceptible to HBV should be vaccinated. b. I f a patient has chronic HBV infection, the pro-vider and patient should be aware that a flare-up may occur if Pr EP is discontinued because both TDF and FTC have anti-HBV activity. It is pru-dent to consult with a hepatologist or a clinician who is experienced in HBV treatment when starting a patient with chronic HBV on Pr EP. 4. P atients should also have bacterial STI testing at baseline. 5. W omen should submit urine for a pregnancy test at baseline. B. Management 1. P rescribing Pr EP a. P atients who are initiating Pr EP should be given a prescription for a 300 mg TDF coformulated with 200 mg of FTC (T ruvada), or 300 mg of TDF alone for IDUs opting for one-drug Pr EP. b. P rescriptions should be written as oral, daily, and continuous. c. A 90-day supply or less is recommended to encourage patients to return for the recommended monitoring. 388 CHAPTER 41 | Preexposure Prophylaxis for HIV
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2. M onitoring patients on Pr EP a. P atients on Pr EP should be seen by their provider at least every 3 months for repeat HIV testing, medication adherence counseling, behavioral risk reduction support, and assess-ment of side effects of Pr EP. b. The pr egnancy intent and status of women on Pr EP should be assessed every 3 months. c. A r enal panel should be checked 3 months after Pr EP initiation and then again every 6 months (providers can consider monitoring renal func-tion more closely in patients with other risk fac-tors for renal disease including hypertension or diabetes). d. T esting for bacterial STIs should be conducted every 6 months or more frequently as needed. 3. Di scontinuing Pr EP a. P r EP should be discontinued if a patient's Cr Cl drops below 60 m L/min. However, Pr EP should not be discontinued if the serum creatinine rises above that patient's baseline and the Cr Cl remains ≥ 60 m L/min. Y et, a referral to a nephrologist should be made for any patient with a Cr Cl that is steadily declining even if it remains ≥ 60 m L/min. b. P r EP should be discontinued if a patient tests positive for HIV during follow-up. c. P atients may choose to discontinue Pr EP for other reasons including personal choice, cessation of HIV risk behaviors, and intolerable side effects. d. U pon discontinuation for any reason, the provid-er should document the following: HIV status, reason for Pr EP discontinuation, recent medica-tion adherence, and reported sexual risk behavior. C. Patient Education TDF/FTC is associated with self-limited start-up symp-toms including nausea, vomiting, and dizziness. Providing anticipatory guidance that these symptoms are common and typically resolve in 1 month may prevent patients from discontinuing Pr EP. Encourage patients to take Pr EP with food and use over-the-counter headache medicines or a prescription antiemetic to reduce symptoms. The Pr EP Clinical Provider's Supplement contains a template of a patient and provider checklist for initiat-ing Pr EP (see Appendix 41-4: Provider Checklist). Following this checklist and reviewing it closely with patients will ensure that they have been educated about the following key points: daily adherence is needed to achieve maximal efficacy of Pr EP; frequent monitoring is needed to maximize safety of Pr EP; and Pr EP does not completely eliminate the possibility of acquiring HIV and thus con-dom use is still highly recommended. VI. r esources for clinicians A. Pr EPline Clinicians may call the Pr EPline at 1-855-Pr EP for expert advice on Pr EP initiation or management from the Clinicians' Consultation Center (www. nccc. ucsf. edu). B. Updates to the USPHS guidelines As new data become available, recommendations may change. Revised recommendations may be posted on the CDC website (www. cdc. gov/hiv/pdf/guidelines /Pr EPguidelines2014. pdf). Revised recommendations may also be found at the AIDS Info website (www. aidsinfo. nih . gov). re Fere Nces Baeten, J. M., Donnell, D., Ndase, P., Mugo, N. R., Campbell, J. D., Wangisi, J., et al. (2012). Antiretroviral prophylaxis for HIV prevention in het-erosexual men and women. New England Journal of Medicine, 367(5), 399-410. doi: 10. 1056/NEJMoa1108524 Centers for Disease Control and Prevention. (2012). Estimated HIV inci-dence in the United States, 2007-2010 (HIV Surveillance Supplemental Report 2012, Vol. 17, No. 4). Atlanta, GA: Author. Retrieved from www. cdc. gov/hiv/pdf/statistics_hssr_vol_17_no_4. pdf. Choopanya, K., Martin, M., Suntharasamai, P., Sangkum, U., Mock, P. A., Leethochawalit, M., et al. (2013). Antiretroviral prophylaxis for HIV infection among people who inject drugs in Bangkok, Thailand (the Bangkok T enofovir Study): A randomised, double-blind, placebo-controlled phase 3 trial. Lancet, 381(9883), 2083-2090. doi: 10. 1016 /S0140-6736(13)61127-7. Food and Drug Administration (2012). FDA approves first medication to reduce HIV risk. Retrieved from www. fda. gov/For Consumers /Consumer Updates/ucm311821. htm. Gallant, J. E., De Jesus, E., Arribas, J. R., Pozniak, A. L., Gazzard, B., Campo, R. E., et al. (2006). T enofovir DF, emtricitabine, and efavirenz vs. zid-ovudine, lamivudine, and efavirenz for HIV. New England Journal of Medicine, 354(3), 251-260. Gallant, J. E., Staszewski, S., Pozniak, A. L., De Jesus, E., Suleiman, J. M., et al. (2004). Efficacy and safety of tenofovir DF vs. stavudine in combina-tion therapy in antiretroviral-naïve patients: A 3-year randomized trial. JAMA, 292(2), 191-201. Gilead Sciences. (2013). T ruvada [package insert]. Retrieved from www . gilead. com/pdf/truvada_pi. pdf. Grant, R. M., Lama, J. R., Anderson, P. L., Mc Mahan, V., Liu, A. Y., Vargas, L., et al. (2010). Preexposure chemoprophylaxis for HIV prevention in men who have sex with men. New England Journal Medicine, 363(27), 2587-2599. doi:10. 1056/NEJMoa1011205 Grohskopf, L. A., Chillag, K. L., Gvetadze, R., Liu, A. Y., Thompson, M., Mayer, K. H., et al. (2013). Randomized trial of clinical safety of daily oral tenofovir disoproxil fumarate among HIV-uninfected men who have sex with men in the United States. Journal of Acquired Immune Deficiency Syndromes, 64(1), 79-86. doi: 10. 1097/QAI. 0b013e31828ece33. 389 References
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Jenness, S. M., Neaigus, A., Murrill, C. S., Wendel, T., Forgione, L., & Hagan, H. (2007). Estimated HIV incidence among high-risk heterosexuals in New Y ork City. Journal of Acquired Immune Deficiency Syndromes, 56(2), 193-197. doi: 10. 1097/QAI. 0b013e318202a9c4. La Lota, M., Beck, D., Metsch, L., Brewer, T. H., Forrest, D. W., Cardenas, G. A., et al. (2011). HIV seropositivity and correlates of infection among heterosexually active adults in high-risk areas in South Florida. AIDS Behavior, 15(6), 1259-1263. doi: 10. 1007/s10461-010-9856-z Mc Cormack, S., & Dunn, D. (2015). Pragmatic pen-label Randomised T rial of Preexposure Prophylaxis: The PROUD Study. Retrieved from www. croiconference. org/sessions/pragmatic-open-label-randomised-trial -preexposure-prophylaxis-proud-study. Neaigus, A., Miller, M., Gyarmathy, V. A., & Friedman, S. R. (2011). HIV heterosexual sexual risk from injecting drug users among HIV-seronegative noninjecting heroin users. Substance Use and Misuse, 46 (2-3), 208-217. doi: 10. 3109/10826084. 2011. 521473 Pandori, M. W., Hackett, J., Jr., Louie, B., Vallari, A., Dowling, T., Liska, S., et al. (2009). Assessment of the ability of a fourth-generation immu-noassay for human immunodeficiency virus (HIV) antibody and p24 antigen to detect both acute and recent HIV infections in a high-risk set-ting. Journal of Clinical Microbiology, 47(8), 2639-2642. Panel on T reatment of HIV-Infected Pregnant Women and Prevention of Perinatal T ransmission. (2014). Recommendations for use of antiretro-viral drugs in pregnant HIV-1-infected women for maternal health and interventions to reduce perinatal HIV transmission in the United States. Retrieved from http://aidsinfo. nih. gov/contentfiles/lvguidelines /Perinatal GL. pdf. Peterson, L., T aylor, D., Roddy, R., Belai, G., Phillips, P., Nanda, K., et al. (2007). T enofovir disoproxil fumarate for prevention of HIV infection in women: A phase 2, double-blind, randomized, placebo-controlled trial. PLo S Clinical Trials, 2(5), e27. doi: 10. 1371/journal. pctr. 0020027 Smith, D. K., Pals, S. L., Herbst, J. H., Shinde, S., & Carey, J. W. (2012). Development of a clinical screening index predictive of incident HIV infection among men who have sex with men in the United States. Journal of Acquired Immune Deficiency Syndromes, 60(4), 421-427. doi: 10. 1097/QAI. 0b013e318256b2f6. Solomon, M. M., Lama, J. R., Glidden, D. V., Mulligan, K., Mc Mahan, V., Liu, A. Y., et al. (2014). Changes in renal function associated with oral emtric-itabine/tenofovir disoproxil fumarate use for HIV pre-exposure prophylaxis. AIDS, 28(6), 851-859. doi: 10. 1097/QAD. 0000000000000156 Thigpen, M. C., Kebaabetswe, P. M., Paxton, L. A., Smith, D. K., Rose, C. E., Segolodi, T. M., et al. (2012). Antiretroviral preexposure prophylaxis for heterosexual HIV transmission in Botswana. New England Journal of Medicine, 367(5), 423-434. doi: 10. 1056/NEJMoa1110711 U. S. Public Health Service (2014a). Preexposure prophylaxis for the preven-tion of HIV infection in the United States—2014 clinical practice guideline. Retrieved from www. cdc. gov/hiv/pdf/prepguidelines2014. pdf. U. S. Public Health Service (2014b). Preexposure prophylaxis for the prevention of HIV infection in the United States—2014 provider supplement. Retrieved from www. cdc. gov/hiv/pdf/prepprovidersupplement 2014. pdf. Van Damme, L., Corneli, A., Ahmed, K., Agot, K., Lombaard, J., Kapiga, S., et al. (2012). Preexposure prophylaxis for HIV infection among African women. New England Journal of Medicine, 367(5), 411-422. doi: 10. 1056/NEJMoa1202614390 CHAPTER 41 | Preexposure Prophylaxis for HIV
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a PPe NDIx 41-1: Beha VI oral r I sk a ssessme N t Quest I o N s RISK BEHAVIOR ASSESSMENT FOR MSM In the past 6 months: Have you had sex with men, women, or both? ( if men or both sexes) How many men have you had sex with? How many times did you have receptive anal sex (you were the bottom) with a man who was not wearing a condom? How many of your male sex partners were HIV-infected? (if any positive) W ith these HIV-infected male partners, how many times did you have insertive anal sex (you wer e the top) without you wearing a condom? Have you used methamphetamines (such as crystal or speed)? RISK BEHAVIOR ASSESSMENT FOR HETEROSEXUAL MEN AND WOMEN In the past 6 months: Have you had sex with men, women, or both? ( if opposite sex or both sexes) How many men/women have you had sex with? How many times did you have vaginal or anal sex when neither you nor your partner wore a condom? How many of your sex partners were HIV-infected? (if any positive) With these HIV-infected partners, how many times did you have vaginal or anal sex without a condom? Reproduced from U. S. Public Health Service. (2014). Preexposure prophylaxis for the prevention of HIV infection in the United States—2014 clinical practice guideline. 391 Appendix
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a PPe NDIx 41-2: s cree NING tool F or msm Reproduced from Smith, D. K., Pals, S. L., Herbst, J. H., Shinde, S., & Carey, J. W. (2012). Development of a clini-cal screening index predictive of incident HIV infection among men who have sex with men in the United States. Journal of Acquired Immune Deficiency Syndromes, 60(4), 421-427. doi: 10. 1097/QAI. 0b013e318256b2f6. MSM Risk Index25 1 How old are you today? Add down entries in right column to calculate total score * If score is 10 or greater, evaluate for intensive HIV prevention services including Pr EP. If score is below I0, provide indicated standard HIV prevention services. TOTAL SCORE*2 In the last 6 months, how many men have you had sex with? 3 In the last 6 months, how many times did you have receptive anal sex (you were the bottom) with a man without a condom? 4 In the last 6 months, how many of your male sex partners were HIV- positive? 6 In the last 6 months, have you used methamphetamines such as crystal or speed?5 In the last 6 months, how many times did you have insertive anal sex (you were the top) without a condom with a man who was HIV-positive?If <18 years, score 0If 18-28 years, score 8If 29-40 years, score 5If 41-48 years, score 2If 49 years or more, score 0 If 1 or more times, score 10 If 0 times, score 0 If >1 positive partner, score 8 If 1 positive partner, score 4If <1 positive partner, score 0 If 5 or more times, score 6 If 0 times, score 0 If yes, score 6 If no, score 0If >10 male partners, score 7 If 6-10 male partners. score 4If 0-5 male partners, score 0392 CHAPTER 41 | Preexposure Prophylaxis for HIV
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a PPe NDIx 41-3: s ummary o F Gu IDa N ce F or Pr e P u se Table 41-1 Summary of Guidance for P r EP Use men Who have sex with m en h eterosexual Women and m en Injection Drug u sers Detecting substantial risk of acquiring HIV infection HIV-positive sexual partner Recent bacterial STI High number of sex partners History of inconsistent or no condom use C ommercial sex work HIV-positive sexual partner Recent bacterial STI High number of sex partners History of inconsistent or no condom use Commercial sex work In high-prevalence area or network HIV-positive injection partner Sharing injection equipment. Recent drug treatment (but currently injecting) Clinically eligible Document negative HIV test result before prescribing P r EP No signs/symptoms of acute HIV infection Normal renal function; no contraindicated medications Documented hepatitis B virus infection and vaccination status Prescription Daily, continuing oral doses of TDF/FTC (Truvada), <90-day supply other services Follow-up visits at least every 3 months to provide the following: HIV test, medication adherence counseling, behavioral risk reduction support, side effect assessment, STI symptom assessment At 3 months and every 6 months thereafter, assess renal function Every 6 months, test for bacterial STIs Do oral/rectal STI testing Assess pregnancy intent Pregnancy test every 3 months Access to clean needles/ syringes and drug treatment services STI, sexually transmitted infection. Repr oduced from U. S. Public Health Service. (2014). Preexposure prophylaxis for the prevention of HIV infection in the United States—2014 clinical practice guideline. 393 Appendix
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a PPe NDIx 41-4: Pro VID er c heckl I st Section 1 Patient/Provider Checklist Organization/Clinic Name CHECKLIST FOR INITIATING PREEXPOSURE PROPHYLAXIS (Pr EP) Print name of provider Print name of patient Provider Section I have provided this patient with the following: (check all as completed): Assessment for possible acute HIV infection Indicated laboratory screening to determine indications for these medications An HIV risk assessment to determine whether Pr EP is indicated for this patient A medication fact sheet listing dosing instructions and side effects Counseling or a referral for counseling on condom use and any other HIV risk-reduction methods this patient may need Advice on methods to help the patient to take medication daily as prescribed Information about Pr EP use during conception and pregnancy (when indicated)A prescription for Truvada (300 mg tenofovir disoproxil fumarate, 200 mg emtricitabine) A follow-up appointment date Today's date (month/day/year) Limit refill periods to recommended intervals for repeat HIV testing (at least every 3 months)Conduct follow-up visits at least every 3 months that include the following:As the provider, I will: Assessment of HIV status (including signs or symptoms of acute HIV infection)Assessment of side effects and advice on how to manage them Assessment of medication adherence and counseling to support adherence Assessment of STI symptoms, HIV risk behavior and counseling support for risk-reduction practices Inform the patient of any new information about Pr EP and respond to questions Patient Section It has been explained to me that: Taking a dose of Pr EP medication every day may lower my risk of getting HIV infection This medicine does not completely eliminate my risk of getting HIV infection, so I need to use condoms during sex This medicine may cause side effects so I should contact my provider for advice by calling if I have any health problems It is important for my health to find out quickly if I get HIV infection while I'm taking thismedication, so I will contact my provider right away if I have symptoms of possible HIV infection (fever with sore throat, rash, headache, or swollen glands)My provider will test for HIV infection at least once every 3 months Therefore, I will: Give one copy to patient Try my best to take the medication my provider has prescribed every day Talk to my provider about any problems I have in taking the medication every day Not share the medication with any other person Attend all my scheduled appointments Call to reschedule any appointments I cannot attend Reproduced from U. S. Public Health Service. (2014). Preexposure prophylaxis for the prevention of HIV infection in the United States—2014 provider supplement. 394 CHAPTER 41 | Preexposure Prophylaxis for HIV
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Section V ii co MMon co MPL e X ADUL t G e R onto L o GY PR e S ent Ation Sweakened immune systems is at risk of developing abscesses of increased frequency and/or severity due to a decreased ability to fight infection. II. Database (may include but is not limited to) A. Subjective 1. R isk factors for MRSA a. I njection drug use b. I mmunosuppression c. I ncarceration in prison d. S haring sports equipment e. R ecent hospitalization or antibiotic therapy f. M en having sex with men (Gorwitz, Jernigan, Powers, & Jernigan, 2006) 2. P recipitating factors a. R ecent minor skin trauma b. I nsect stings c. M echanical manipulation of ingrown hairs or comedones (blackheads or whiteheads) d. Othe r foreign bodies, such as splinters or sutures 3. P ast health history a. S creen for history of abscesses or soft tissue infections b. M edical illnesses: immunosuppression, valvular heart disease, diabetes mellitus, or cancer c. M edication history: steroid use or recent antibi-otic therapy d. V accination history: Date of last tetanus vaccination 4. F amily or relative history of abscesses or soft tissue infections 5. P ersonal and social history: health-related behaviors, recent travel, and injection drug use I. Intr oduction and general background Cutaneous abscesses are a subcategory of skin and soft tissue infections (SSTIs) that involve the dermis and subcutaneous skin tissue (Stevens et al., 2014). They are inflamed, local-ized soft tissue masses that are encapsulated collections of pus (Baddour, 2014; Rogers & Perkins, 2006; Stevens et al., 2005). Furuncles and carbuncles are also purulent SSTIs that involve the hair follicles and form small abscesses in the surrounding tissues. Carbuncles are a collection of furuncles that become an inflamed, confluent purulent mass (Baddour, 2014). The etiology of purulent SSTIs is usually bacterial infection, of which methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S. aureus are the most common causative organisms (Frazee et al., 2005; Moran et al., 2006). Bacteria enter the dermis and deeper subcutaneous tissues as a result of a break in the integrity of the skin surface. These minor skin traumas may occur from shaving, abrasions, insect bites, splinters, or other foreign bodies. Abscesses may also occur spontaneously in healthy individuals without predis-posing conditions. They begin as localized erythema and ten-derness on the skin, and as they develop they enlarge and may become firm and indurated. The center of the abscess softens and is filled with purulent exudate or pus consisting of leu-kocytes, protein, and bacteria. A pustular point or head may develop. This softened area is known as the area of fluctuance. Characteristically, abscesses are painful, warm, well circum-scribed, indurated, and erythematous. They are often located on the buttocks, axillae, or the extremities but they may occur anywhere on the skin. T reatment of an abscess is directed at evacuating the collection of pus by incision and drainage. An abscess may have surrounding cellulitis where the adjacent sub-cutaneous tissue is inflamed, warm, and tender. The presence of cellulitis in the setting of an abscess presents added complex-ity and may require antibiotic therapy in addition to incision and drainage (Fitch, Manthey, Mc Ginnis, Nicks, & Pariyadath, 2007; Rogers & Perkins, 2006). The subset of patients with Rosalie D. Bravo ABscess M An Age M ent© Eliks/Shutterstock; © donatas1205/Shutterstock 39542Chapt Er
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cancer, because comorbid conditions may also change the treatment plan to include antibiotic therapy and hospital admission. Determine the need for specialty consultation by considering the location of the purulent SSTI and the underlying structures such as veins, arteries, and nerves. B. Differential diagnosis 1. S imple cutaneous abscess without surrounding cellulitis 2. C utaneous abscess with surrounding cellulitis 3. C utaneous abscess in the setting of patients at risk for bacteremia 4. F uruncle, an abscess involving a hair follicle and the adjacent soft tissue 5. C arbuncle, a larger abscess involving a group of hair follicles 6. A rteriovenous malformation 7. H idradenitis suppurativa, abscesses that involve the apocrine sweat glands located in the axillary or groin area 8. E pidermoid cyst C. Complications 1. Bac teremia 2. E ndocarditis 3. O steomyelitis 4. T enosynovitis 5. S eptic thrombophlebitis IV. g oals of clinical management A. Implement an appropriate, safe, and cost-effective treatment plan that enables patients' compliance. B. Relieve symptoms. C. Prevent systemic infection. D. Prevent recurrence and disfigurement. 6. R eview of systems a. C onstitutional systemic symptoms: fevers, chills, regional adenopathy, malaise b. S kin: Localized skin symptoms of pain, erythe-ma, warmth, induration, purulent drainage, his-tory of trauma or foreign body c. G astrointestinal: Nausea, vomiting, anorexia B. Objective 1. Ge neral appearance: Body habitus (e. g., obese, cachetic, or temporal wasting) and/or general level of distress 2. V ital signs: temperature, pulse, respiratory rate, and blood pressure 3. C areful skin examination a. N ote location and dimensions of erythema; dimensions of induration; visible abrasions or puncture wounds; presence of central fluctu-ance; and purulent, serous, or sanguineous drainage. b. Obs erve for erythematous streaking from the primary abscess site 4. E xamine proximal lymph nodes for adenopathy 5. C ardiac: auscultation for murmurs because patients with valvular heart disease or prosthetic valves are at risk for bacteremia (Rogers & Perkins, 2006) III. Assessment A. Determine the diagnosis Diagnosis in the ambulatory care setting is a clinical deci-sion based on the history and the physical examination findings. Differentiate between abscesses requiring inci-sion and drainage alone versus incision and drainage with antibiotics (e. g., abscess with evidence of cellulitis and/or sepsis). Determine if there is evidence of systemic involvement by considering abnormal vital signs that meet systemic inflammatory response syndrome criteria (see T able 42-1). It is important to consider host factors, such as diabetes, immunosuppression, valvular heart disease, or Table 42-1 The Systemic Inflammatory Response Syndrome (SIRS) Two or more of the following: Temperature > 38 degrees Celsius or < 36 degrees Celsius Heart rate > 90 beats/minute Respiratory rate > 20 breaths/minute or Pa CO2 < 32 torr White blood cell count > 12,000 cell/mm3, < 4,000 cells/mm3, or > 10% immature (band) forms Reproduced from American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. (1992). Critical Care Medicine, 20(6), 864-874. 396 CHAPTER 42 | Abscess Management
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c. C lindamycin 300-450 mg orally every 6 hours d. G ive prophylactic antibiotics 60 minutes before incision and drainage only for high-risk patients with prosthetic heart valves, unre-paired congenital heart defects, implantable cardiac devices, or prior history of infective endocarditis (Rogers & Perkins, 2006). Antibiotic prophylaxis can be delivered with a single dose of a cephalosporin. For severe peni-cillin allergies, give a single dose of intravenous vancomycin 1 g. 5. A nalgesic therapy—local anesthetic and drainage of pus will reduce pain. Over-the-counter pain medications may be recommended for the first 48 hours and prior to repacking the wound. C. Incision and drainage procedure 1. D escription: incision and drainage is a surgical procedure in which an incision is made into the fluctuant area of an abscess to drain the purulent contents of an abscess. The incision is then left open to promote further drainage. 2. I ndication: the presence of a cutaneous abscess where there is evidence of a collection of purulent exudate or pus. 3. C ontraindications to incision and drainage in the outpatient setting a. C ellulitis without an underlying abscess. b. The loca tion of the abscess is such that the inci-sion may cause a disfiguring defect. c. A bscesses in locations that pose a risk for com-plications or those requiring specialty consulta-tion such as those located on the hands or plantar surfaces; those located over arteries or large blood vessels such as those on the neck or over the antecubital fossa; and those on or around the nasolabial folds or orbital region of the face. d. F or large or deep abscesses that require more pain management than a local anesthetic and/or if the patient requires conscious sedation or gen-eral anesthesia to tolerate the procedure. 4. P reprocedure a. C ounsel the patient about risks of the potential for discomfort, bleeding, scarring, damage to surrounding structures, systemic spread of infec-tion, and incomplete or unsuccessful drainage. b. Di scuss the benefits and risks of undergoing inci-sion and drainage versus the benefits and risks of watchful waiting and conservative management. c. Obt ain informed consent from the patient or proxy if the patient is unable to give consent. V. Plan A. Diagnostics 1. U ltrasound if readily available may determine the presence of a fluid collection and the size and depth of the abscess. 2. F or mild or moderate purulent SSTIs aerobic and anaerobic wound cultures can be obtained from spontaneous wound drainage or obtained during the incision and drainage procedure (Stevens et al., 2014). 3. Add itional testing based on the severity of systemic signs and symptoms, such as fevers, rigors, and malaise, may include complete blood count with differential, metabolic panel, and blood cultures. Blood tests are not necessary for a healthy patient with a simple abscess. B. Management (includes treatment, consultation, referral, and follow-up care) T reatment is based on the Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infection Disease Society of America (see Figure 42-1). 1. W arm moist compresses if the furuncle or abscess is small and firm without fluctuance (Stevens et al., 2005). 2. T etanus prophylaxis if the patient has not had a tetanus vaccination within 10 years. 3. I ncision and drainage for fluctuant abscesses and all carbuncles. 4. A ntimicrobial therapy in addition to incision and drainage if there is a surrounding cellulitis. Antibiotics are unnecessary for immunocompetent patients who have a simple cutaneous abscess without surrounding cellulitis (Hankin & Everett, 2007; Rajendran et al., 2007; Stevens et al., 2014). Prescribe antibiotics for patients who have abscesses with surrounding cellulitis and for patients who are diabetic, immunocompromised, have valvular heart disease, or who have other comorbid conditions that increase the risk of bacteremia. Select antibiotics that are effective in treating MRSA and group A streptococcus. Be familiar with regional guidelines for MRSA treatment. Duration of antibiotic therapy should be based on the resolution of symptoms (Baddour, 2014; Hepburn et al., 2004). a. T rimethoprim-sulfamethoxazole, 160 mg/800 mg DS (double strength) (one to two tablets based on weight) every 12 hours b. D oxycycline, 100 mg twice daily397 Plan
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5. P rocedure a. M aterials i. Go wn, gloves, face shield, and one pair of sterile gloves ii. One bottle of povidine iodine or chlorhexi-dine solution iii. E ight to 10 packs of sterile 4 × 4s and alco-hol wipes iv. One #11 or #15 blade scalpel v. One s mall curved hemostat for blunt dissection vi. One 10-cc syringe vii. One 22-gauge needle for drawing up the local anesthetic viii. One 25-gauge needle for infiltrating lidocaine ix. L idocaine 1% or bupivacaine 0. 5% x. One ir rigation kit or a 30-to 60-m L syringe and splash guardxi. One 1-L bottle of sterile water or normal saline solution xii. S wabs for bacterial culture and sterile basin xiii. 0. 25-or 0. 50-in p lain or iodoform coated wound packing material, top dressings, and tape xiv. C otton-tip swabs or blunt-edged forceps b. I ncision and drainage procedure i. W ash your hands and observe universal precautions. ii. I dentify the patient by asking his or her name and assess the patient's allergy history. iii. C onsider premedication with an anxiolytic or analgesic medication. iv. P osition the patient so that the abscess is easily accessible. v. P ut on gloves and a face shield. vi. C leanse the skin with povidine iodine or chlorhexidine in a circular motion starting Severe Emergent Surgical Inspection/Debridement * Rule out necrotizing process Empiric Rx ° Vancom ycin PLUS Piperacillin/Tazobactam Defined Rx (Necrotizing Infections) Monomicrobial Streptococcuspyogenes Penicillin PLUS Clindam ycin Clostridial sp. Penicillin PLUS Clindam ycin Vibrio vulnificus Doxycycline PLUS Ce ftazidime Aeromonas hy drophila Doxycycline PLUS Ciproflo xacin Polymicrobial Vancom ycin PLUS Piperacillin/Tazobactam Intravenous Rx Penicillin or Ceftriaxone or Cefazolin or Clindam ycin Oral Rx Penicillin VK or Cephalosporin or Diclo xacillin or Clindam ycin Empiric Rx 1 Vancom ycin or Daptom ycin or Linezolid or T elevancin or Ceftaroline Empiric Rx TMP/SMX or Do xycycline I & DC & SI & DC & SI & D C & S Defined Rx MRSA See Empiric MSS A Nafcillin or Ce fazolin or Clindam ycin Defined Rx MRSA TMP/SMXMSS A Diclo xacillin or Cephalexin Moderate Mild Severe Moderate Mild Management of SSTls Purulent Furuncle/Carbuncle/Abscess Nonpurulent Necrotizing Infection/Cellulitis/Er ysipelas 1Since daptom ycin and t elevancin are not appr oved for use in children, vancom ycin is recommended; clindam ycin may be used if clindam ycin resistance is <1 0-15% at the institution. Figure 42-1 Management of SSTIs Reproduced from Stevens, D. L., Bisno, A. L., Chambers, H. F., Dellinger, E. P., Goldstein, E. J., Gorbach, S. L., et al. (2014). Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America, 59(2), e10-52. 398 CHAPTER 42 | Abscess Management
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xi. C ollect a culture of the wound using aerobic and anaerobic culture medium. Cultures are beneficial if it is a first abscess, if the abscess worsens after incision and drainage, or if there has been a history of antibiotic treat-ment failure. xii. I rrigate the incised abscess with normal saline solution using the large syringe and splash guard. An 18-gauge angiocatheter may be attached without the needle to the syringe. Irrigate until the drainage is clear or slightly serous. xiii. I nsert the 0. 25-or 0. 50-in packing gauze into the abscess taking care to loosely pack into the entire wound cavity. The goal is to keep the wound open to promote drain-age and prevent closure of the wound. Closure of the wound without adequate drainage may lead to reformation of the abscess. xiv. C over the wound with a sterile top dressing and paper tape. For additional information and a streaming video of the incision and drainage procedure, visit www. nejm. org (Fitch et al., 2007). 6. F ollow-up a. The p atient should return within 48-72 hours for a wound check. b. R emove the packing and assess the amount of drainage. If the drainage is minimal, then warm soaks should be initiated and continued until the wound is healed. If the wound continues to have purulent drainage, then the wound should be irrigated with normal saline, explored again to assess for any unbroken loculations, and then repacked with new gauze. The patient should return again in 48 hours (Fitch et al., 2007; Kronfol, 2009). 7. C riteria for hospital admission or referral for specialty consultation either at the time of initial evaluation or at follow up a. P atients with signs of systemic toxicity, such as fevers, rigors, or unstable vital signs, should be admitted for parenteral antibiotics. b. P atients who have failed appropriate initial treatment. c. The loca tion of the abscess is such that the incision may cause a disfiguring defect. Refer immediately to a dermatologist or plastic surgeon. d. A bscesses located on the hands or plantar surfaces should be immediately referred to an orthopedic or plastic surgeon. from the center of the abscess and working outward. Allow the cleaning solution to dry. vii. C over the surrounding area with sterile drapes so that the abscess is exposed. viii. I nfiltrate the intradermal tissue under the surface of the wound with a local anesthetic agent, such as lidocaine or bupivacaine, using a 22-or 25-gauge needle. The maxi-mum dose of lidocaine 1% solution with-out epinephrine is 4 mg/kg (Hsu, 2014). Bupivacaine without epinephrine should not exceed a dose of 1-2 mg/kg (Hsu). Neither bupivacaine or lidocaine with epi-nephrine is indicated for the incision and drainage procedure because local vasocon-striction is not necessary. Plain bupivacaine and lidocaine both provide a minimum duration of anesthesia for 30 minutes, which is sufficient to complete the proce-dure. If the patient is allergic to lidocaine, then conscious sedation should be consid-ered. Inject parallel to the skin surface. Do not inject perpendicular to the skin sur-face (i. e., into the deeper tissues) because this may spread the infection. An alterna-tive method is to inject in a field block pat-tern where the anesthetic agent is injected around the entire peripheral field surround-ing the abscess but not directly over the site to be incised. ix. P ut on sterile gloves. x. P alpate for the most fluctuant part of the abscess and make a small incision with a #11 blade scalpel over the center, then extend the incision to form a line. The depth and length of the incision are variable and should be based on the size and location of the abscess. If possible make the incision along the Langer's lines or skin-tension lines to promote optimal cosmetic results. The inci-sion should not puncture the back wall of the abscess capsule. The goal of the incision is to provide an opening large enough to allow for drainage of the abscess and insertion of packing material. In addition, the incision should be large enough to insert the curved hemostat into the incision to break up locu-lations. This is called blunt dissection, which allows for further drainage of pus. Gently compress the outer sides of the abscess to express more drainage. Insert the curved hemostats and explore the abscess cavity, and open the hemostats to break up loculations. 399 Plan
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Gorwitz, R. J., Jernigan, D. B., Powers, J. H., Jernigan, J. A., & Participants in the CDC-Convened Experts' Meeting on Management of MRSA in the Community. (2006). Strategies for clinical management of MRSA in the community: Summary of an experts' meeting convened by the centers for disease control and prevention. Retrieved from www. cdc. gov/mrsa/pdf /MRSA-Strategies-Exp Mtg Summary-2006. pdf. Hankin, A., & Everett, W. W. (2007). Are antibiotics necessary after incision and drainage of a cutaneous abscess? Annals of Emergency Medicine, 50, 48. Hepburn, M. J., Dooley, D. P., Skidmore, P. J., Ellis, M. W., Starnes, W. F., & Hasewinkle, W. C. (2004). Comparison of short-course (5 days) and standard (10 days) treatment for uncomplicated cellulitis. Archives of Internal Medicine, 164(15), 1669-1674. Hsu, D. (2014). Infiltrative anesthetics. Retrieved from www. uptodate . com/contents/infiltration-of-local-anesthetics. Kronfol, R. (2014). Retrieved from www-uptodate-com. ucsf. idm . oclc. org/contents/technique-of-incision-and-drainage-for-skin -abscess?source=search_result&search=technique+of+incision+and+drainage&selected Title=1%7E150 Moran, G. J., Krishnadasan, A., Gorwitz, R. J., Fosheim, G. E., Mc Dougal, L. K., Carey, R. B., et al. (2006). Methicillin-resistant S. aureus infections among patients in the emergency department. New England Journal of Medicine, 355(7), 666-674. Rajendran, P. M., Y oung, D., Maurer, T., Chambers, H., Perdreau-Remington, F., Ro, P., et al. (2007). Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncompli-cated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection. Antimicrobial Agents Chemotherapy, 51(11), 4044. Rogers, R. L., & Perkins, J. (2006). Skin and soft tissue infections. Primary Care: Clinics in Office Practice, 33, 697. Stevens, D. L., Bisno, A. L., Chambers, H. F., Dellinger, E. P., Goldstein, E. J., Gorbach, S. L., et al. (2014). Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clinical Infectious Diseases, 59(2), e10-e52. Stevens, D. L., Bisno, A. L., Chambers, H. F., Everett, E. D., Dellinger, P., Goldstein, E. J., et al. (2005). Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clinical Infectious Diseases, 41(10), 1373-1406. e. A bscesses located over arteries or large blood vessels on the neck or over the antecubital fossa or inquinal areas should be immediately referred to an otolaryngologist or vascular surgeon. f. A bscesses on or around the nasolabial folds may pose the risk of septic cavernous venous throm-bosis and the patient should be immediately referred to an otolaryngologist. D. Patient education 1. I nstruct the patient in the signs and symptoms of worsening infection (fevers or chills, increasing pain, redness or swelling, and increasing purulent drainage or recurrent abscess). 2. I nstruct the patient to be rechecked right away if these symptoms develop. Inform the patient of expected outcomes. The wound will likely heal in 7-10 days but may take longer. There will likely be a scar from the incision. This may be minimized by limiting direct sun exposure and wearing sun block if the scar is in an exposed area. Re Fe Rences American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. (1992). Critical Care Medicine, 20(6), 864-874. Baddour, L. M. (2014). Skin abscesses, furuncles, and carbuncles. Retrieved from www. uptodate. com/contents/skin-abscesses-furuncles-and-carbuncles. Fitch, M. T., Manthey, D. E., Mc Ginnis, H. D., Nicks, B. A., & Pariyadath, M. (2007). Videos in clinical medicine: Abscess incision and drainage. Retrieved from www. nejm. org/doi/full/10. 1056/NEJMvcm071319. Frazee, B. W., Lynn, J., Charlebois, E. D., Lambert, L., Lowery, D., & Perdreau-Remington, F. (2005). High prevalence of methicillin-resistant staphylococcus aureus in emergency department skin and soft tissue infections. Annals of Emergency Medicine, 45(3), 311-320. 400 CHAPTER 42 | Abscess Management
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This increase in intravascular volume starts at 6 weeks, peaks at about 28-34 weeks, and levels off during the last 6 weeks of pregnancy. Because plasma volume expansion is faster and greater than red blood cell production, there is a lowering of the Hgb and hematocrit referred to as “physiologic anemia. ” If there is no significant blood loss during the intrapartal period, the Hgb and hematocrit typically return to normal at about 6 weeks postpartum. Severe anemia in pregnancy is associ-ated with an increased risk of spontaneous abortion, low birth weight, preterm birth, and fetal death (Brabin, Hakimi, & Pelletier, 2001). Persistent severe anemia increases the risk of maternal mortality (Sifakis & Pharmakides, 2000). Otherwise, anemia is a sign and consequence of disease or treatments. It can be caused by a variety of systemic disorders and diseases and by a primary hematologic disorder. As a result, most individuals' physical symptoms and signs reflect the underlying illness rather than the anemia itself. Correct identification of the underlying disease is essential for appro-priately directed treatment. Anemia classification is based on (1) excessive RBC loss, (2) inadequate or ineffective RBC production, (3) abnormal RBC destruction, or (4) morphologic characteristics. These characteristics of cell size are microcytic, normocytic, and macrocytic (T able 43-1). Common microcytic anemias are iron deficiency, thalassemia, lead poisoning, and sideroblas-tic anemia. The most common causes of normocytic anemias include anemia of chronic disease, hemolytic anemia (may see elevated mean cell volume [MCV] due to reticulocytosis), bone marrow failure or infiltration, endocrine disorders, and renal disease. Common macrocytic anemias are vitamin B 12 and folate deficiencies. Multiple etiologies of anemia can coexist together requiring a stepwise diagnostic approach critical to not missing a treatable cause. Outside of the usual categories of anemia lies a unique group of poorly diagnosed anemias that occurs in the geriatric population, accounting for 43% of hypoproliferative anemia (Makipour, Kanapuru, & Ershler, 2008) (T able 43-2). I. Intr oduction and general background Anemia is defined as a decrease in the red blood cell (RBC) number, hemoglobin (Hgb) concentration, or the volume of packed red blood cells (hematocrit) in the blood. The World Health Organization defines anemia by laboratory definition as hemoglobin of less than 13 g/d L for adults, less than 12 g/d L for menstruating females, and less than 11 g/d L for pregnant females (Beutler & Waalen, 2006). However, data from the Scripps-Kaiser and National Health and Nutrition Examination Survey study recommend that lower limits of hemoglobin be stratified based on gender and race (black men ages 20-59: 12. 9 g/d L; black men > 60 years: 12. 7 g/d L; black women ages 20-49: 11. 5 g/d L; black women > 50 years: 11. 5 g/d L; white men ages 20-59: 13. 7 g/d L; white men > 60 years: 13. 2 g/d L; white women ages 20-49: 12. 2 g/d L; white women > 60 years: 12. 2 g/d L) (Beutler & Waalen, 2006). Erythropoiesis is the regulated process of RBC production through a series of steps (National Anemia Action Council, 2002). In adults, this process occurs in the bone marrow of the sternum, ribs, vertebrae, and pelvis. The process begins when pluripotent stem cells are dedicated and the hematopoi-etic precursor cells mature with growth factors and hormones. The key to erythropoietin production is the availability of oxygen, which is carried to the tissues bound to the hemo-globin. When oxygen is low, then erythropoietin (90% from the kidney) triggers the red cell production to meet tissue demand. This production feedback system can occur only when all the needed substrates are in place: normal renal pro-duction of erythropoietin, a functioning bone marrow, and an adequate support of substrates of hemoglobin synthesis (National Anemia Action Council, 2002). Normally, anemia is seen during pregnancy, because the blood volume increases by about 50% to meet the demands of increased circulation of the placenta and maternal fetal tissue. Michelle M. Marin and Laurie Jurkiewicz Ane MIA© Eliks/Shutterstock; © donatas1205/Shutterstock 401 43Chapt Er
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Table 43-2 Dif ferentiating Anemias MCV RDW Retics Iron TIBC % Sat Ferritin Iron deficiency D I D D I D D Iron depletion N N N N I D D β-Thalassemia DQ D I N N N N Sideroblastic D H I NII NID NII N Chronic disease D or N N NID D N/D N/I/D N Lead poisoning D N I N N N N I, increased; D, decreased; DQ, decreased greater than expected in iron deficiency; N, normal; II, increased significantly. pregnancy because of the increased red cell mass and the demands of the growing fetus ii. L ow-iron diets caused by inadequate intake or rapid growth during prolonged growth. iii. P oor absorption seen with gastric atrophy, achlorhydria iv. B lood loss caused by menstrual bleeding, large intra-abdominal or joint bleeding, or occult gastrointestinal and genitourinary bleeding. Of note, it takes 20 m L/day of blood for the usual stool hemoccult test to become positive (Umbreit, 2005). One mil-liliter of blood loss is equivalent to the loss of 0. 5 mg of iron (T ables 43-1 and 43-2). b. P revalence and incidence: Iron deficiency ane-mia is the most common nutritional deficiency (Umbreit, 2005). It affects more than 3 million people according to the National Heart, Lung, A. Microcytic anemias 1. I ron deficiency anemia a. D efinition and overview: Iron deficiency is a microcytic and hypochromic (decrease in hemo-globin concentration) anemia. It occurs when the bone marrow iron stores are less than what is needed to produce RBCs. Common causes of iron deficiency are:i. P regnancy accounts for about 75% of non-physiologic anemia in the childbearing woman (American College of Obstetricians and Gynecologists [ACOG], 2008). The physiology is described by an increased demand on iron stores during pregnancy not only for Hgb synthesis but also for fetal liver storage to meet the needs of the infant in the first 6 months of life. The demand for iron increases in the second half of the Table 43-1 Separating Anemia by MCV Hypochromic Microcytic MCV < 80 f LIron deficiency Thalassemia Sideroblastic Hemoglobinopathies Lead poisoning Normochromic/ Normocytic MCV 80-100 f LAcute hemorrhage Acute hemolysis Early iron deficiency, folate, and vitamin B 12 deficiency Anemia of chronic disease Chronic inflammation Acute and chronic infections Cancer Kidney disease Myelodysplastic syndromes: bone marrow failure, pregnancy Macrocytic MCV > 100 f LMegaloblastic: vitamin B 12 and folate deficiencies and drug induced Reticulocytosis: intense red blood cell stimulation caused by acute hemolysis or hemorrhage (reticulocytes are large and young red blood cells)Chronic liver disease Myelodysplastic syndromes: bone marrow failure or infiltration Endocrinopathies Postsplenectomy Reproduced from Collins-Bride, G., & Saxe, J. (Eds. ). (1998). Nurse practitioner/physician collaborative practice: Clinical guidelines for ambulatory care. San Francisco, CA: UCSF Nursing Press. Used with permission from the UCSF Nursing Press. 402 CHAPTER 43 | Anemia
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ii. α-Thalassemia minor: loss of two genes of α globin, hematocrit is low and MCV is 60-75 f L. iii. H emoglobin H: loss of three α genes, moderate microcytic anemia. iv. β-Thalassemia minor: mild microcytic anemia, asymptomatic. v. β-Thalassemia intermedia: severe anemia often requiring RBC transfusion. vi. β-Thalassemia major: condition is life threat-ening requiring chronic transfusions and possibly hematopoietic cell transplantation. vii. H g E/β-Thalassemia: combined (Yaish, 2013). b. P revalence and incidence: Thalassemias are the most common single genetic disorders known. They are encountered in every ethnic group and geographic location, although they are most common in the Mediterranean basin and tropic and subtropic areas of Asia and Africa. Thalassemia in these regions ranges from 2. 5 to 15%. In the United States, 15% of African-Americans are silent carriers of α-thalassemia, with 3% carrying the trait; 1-15% of those of Mediterraneans origin carry the trait. For β-thalassemia, 10-15% of Mediterraneans and 0. 8% of African-Americans in the United States are affected (Hoffman et al., 2008). In a world of immigration and intermarriage, new patterns of thalassemia have emerged. In southeastern Asians, Hb E and β-thalassemia combined, making this combination most common in many parts of the world (Yaish, 2013). 3. S ideroblastic anemia a. D efinition and overview: Sideroblastic anemias are a group of disorders with ringed iron-laden and Blood Institute. Iron deficiency results in increased pediatric and maternal mortality; decreased work production; delayed childhood development; and with mild to moderate defi-ciency, an increased risk for developing infec-tious diseases. There are estimates that 4% of U. S. women between the ages of 20 and 49 years have iron deficiency anemia with the higher rates in Mexican-American women (Killip, Bennett, & Chambers, 2007). African-American women, adolescents, and women of low socioeconomic status are at increased risk for iron and folic acid deficiencies (Laubach & Bendell, 2008). The incidence of anemia increases with age with 10% seen in the 65 years and older age group (Schrier, 2010). This increase is associated with a significant increase in morbidity and mortality, impaired cognition, decrease in exercise toler-ance, and decrease in quality of life measures. 2. Th alassemia a. D efinition and overview: Thalassemia syn-dromes are a group of inherited autosomal-recessive anemias classified by defects in the synthesis of one or more of the hemoglobin globin chain subunits. These defects can occur either in the α or β globin chains of hemoglobin. The combined imbalances of globin and inad-equate hemoglobin production result in a variety of clinical manifestations. The former causes hypochromia and microcytosis; the latter leads to ineffective erythropoiesis. Both types cause hemolysis (Giardina & Forget, 2008). The diag-nosis of thalassemia is made by a hemoglobin electrophoresis test (T able 43-3). i. α-Thalassemia trait: loss of one α gene, not anemic but mean cell volume may be low. Table 43-3 Thalassemia Percent of Abnormal Hgb and Degrees of Anemia Hgb A Hgb A2 Hgb F Comments Normal 97-99% 1-3% <1% β-Thalassemia (minor) 80-95% 4-8% 1-5% MCV 55-75 f L, Hematocrit (Hct) 28-40%, peripheral smear mildly abnormal, heterozygous trait β-Thalassemia (intermediate) 0-30% 0-10% 6-100% Moderate anemia β-Thalassemia (major) 0% 4-10% 90-96% Homozygous trait, marked microcytosis with severe anemia α-Thalassemia trait Normal Normal Normal Heterozygous trait, 2/4 genes normal, MCV 60-70 f L, Hct 28-40%, diagnosis of exclusion Reproduced from Collins-Bride, G., & Saxe, J. (Eds. ). (1998). Nurse practitioner/physician collaborative practice: Clinical guidelines for ambulatory care. San Francisco, CA: UCSF Nursing Press. Used with permission from the UCSF Nursing Press. 403 Introduction and general background
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sideroblasts in the bone marrow accompanied by moderate to severe microcytic anemia. The classification of sideroblastic anemias is distin-guished between diseases of the heme synthesis pathway and those diseases of mitochondrial DNA or those with defects in the nuclear DNA. There are two primary X-linked inherited forms that are recognized early in life. Acquired types are caused by exposures from toxins or drugs (alcohol, lead, or zinc). Once the offend-ing toxin is removed, recovery occurs within 1-2 weeks (Gehrs & Friedberg, 2002). Others are associated with ringed sideroblasts, the myelodysplastic syndrome of refractory anemia. b. P revalence and incidence: The incidence of sideroblastic anemia is low. Acquired types are more prevalent than hereditary types. Many individuals are stable for years but in a subset of patients who belong to the myelodysplastic syndrome category, 5% go on to develop leukemia. Acquired sideroblastic anemias are not fully established because of the multiple triggers and clinical presentations (Schwartz, 2007). B. Normocytic anemias 1. D efinition and overview: The MCV is within normal limits but hemoglobin and hematocrit are decreased mildly to moderately. Individuals are generally asymptomatic. Nearly all anemias are normocytic in their initial stages (Brill & Baumgardner, 2000). 2. A nemia of chronic disease and anemia of chronic inflammation (ACD). a. D efinitions and overview: This is an anemia of underproduction of RBCs often associated with chronic inflammatory disease. A decreased life span of the RBC and inhibition of hematopoi-esis, deregulation of iron absorption and trans-port, and decreased erythropoietin production defines this anemia (Gardner & Benz, 2008). Hepcidin, an iron regulatory peptide produced by the liver, is thought to be the central regula-tor in iron metabolism and is controlled by the erythropoietic activity in the bone (Kemna, 2008). ACD is usually seen as normocytic, nor-mochromic, or mildly microcytic with a low reticulocyte count. Iron stores may be normal or increased. The most common causes are usually multifactorial. i. C hronic systemic diseases, such as diabetes, congestive heart failure, and chronic obstructive pulmonary disease ii. C hronic inflammation, such as rheumatoid arthritis and inflammatory bowel disease iii. N eoplasmiv. C hronic liver and kidney disease v. C hronic infection, such as HIV/AIDS vi. E ndocrine deficiencies, such as hypo-thyroidism, diabetes, adrenal or pituitary insufficiencies, and hypogonadism vii. U ncompensated blood loss viii. H ypersplenism b. P revalence and incidence: This is the second most common form of anemia worldwide, second to iron deficiency. In a review of hospi-talized patients, estimated prevalence is 20-40% for ACD (T efferi, 2007). 3. H emolytic anemia a. D efinition and overview: Hemolytic anemia is a normocytic, normochromic anemia where there is a premature destruction of RBCs for which the bone marrow cannot compensate. This occurs when RBC survival is less than normal (120  days) or when the bone marrow is impaired (Linker, 2007). This can be seen congenitally with recognition early in life as in sickle cell disease or later in life when exposed to a stressor, such as G6PD (glucose-6-phosphate dehydrogenase) deficiency. The acquired type usually occurs in adulthood, in those persons older than 40 years of age and in those with mechanical hemolysis, paroxysmal nocturnal hemolysis, or warm and cold reactive antibodies. b. P revalence and incidence: Hemolytic anemia represents 5% of all anemias (Schick, 2010). Autoimmune hemolytic anemia occurs in 10% of systemic lupus erythematosus, most occurring in women older than 65 years of age (Schwartz, 2007). The underlying disorder and etiology of hemolysis dictates survival. C. Macrocytic anemias Macrocytosis can be seen without megaloblastic changes in liver disease, hypothyroidism, aplastic anemia, autoimmune hemolytic anemia, and some forms of myelodysplasia. Megaloblastic anemias are a group of diverse anemias that share the failure in the synthesis and assembly of DNA resulting in ineffective erythropoiesis. Findings of MCV greater than 100 suggest megaloblastic anemia, but with MCV greater than 110 it is much more likely to be present. The most common causes of megaloblastosis are vitamin B 12 and folate deficiencies. Deficiencies of one of these vitamins can cause malabsorption of the other vitamin. Megaloblastic disease, especially when combined with microcytic anemia, can be present as normocytic. 1. V itamin B12 deficiency a. D efinitions and overview: Vitamin B12 (cobalamin) deficiency is a problem of either inadequate intake over several years or of inadequate absorption. 404 CHAPTER 43 | Anemia
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iv. M edications interfering with absorption, such as methotrexate, phenytoin, acyclovir, oral contraceptives, colchicine, and trim-ethoprim. v. I ncreased demand in pregnancy and lacta-tion; hyperemesis gravidarum; and intrinsic hematologic disease, such as malignancy infiltration in the bone marrow. b. P revalence and incidence: The United States Food and Drug Administration mandated that folic acid be added to enriched grain products in 1998, which resulted in a significant decrease in folate deficiency. In temperate zones, folate deficiency is most common in alcoholics. T ropical sprue, which is endemic near the equator, results in malabsorption of this critical vitamin. II. Database (may include but is not limited to) A. Subjective: microcytic 1. I ron deficiency anemia, thalassemia, and sideroblastic anemia a. P ast health history i. M edical illnesses: recurrent iron deficiency anemia, anorexia, gastrointestinal or geni-tourinary malignancy, celiac disease, atro-phic gastritis, Helicobacter pylori, helminthic infections, and chronic inflammatory conditions ii. S urgical history: partial or total gastroenter-ostomy, gastric resection, or splenectomy iii. Obs tetric and gynecological history: heavy menses, multiparty, recent pregnancy, and parturition iv. M edication history: nonsteroidal anti-inflammatory drugs, steroids, chemo-therapy, iron or multivitamins, salicylates, antacids that block iron absorption, and health food products v. E xposure history: toxic exposures, such as lead poisoning (exposure to lead-based paint, lead-contaminated dust, and lead-contaminated residential soil) and potent marrow toxic agents b. F amily history i. A nemia ii. C hronic inflammatory diseases iii. M alignancy iv. L ead poisoning Lifelong subclinical vitamin B12 deficiency, 50% with normal vitamin B12 levels, when challenged with abnormal absorption or altered metabolism can tip individuals into symptomatic deficiency (Langan & Zawistoski, 2011). Low levels of vitamin B 12 elevate homocysteine, which is asso-ciated with cardiovascular disease (CVD); how-ever, replacement with vitamin B12 does not change CVD risk (Elmadfa & Singer, 2009; Langan & Zawistiski, 2011). Consider screening high-risk individuals for megaloblastic anemia. Common causes are:i. P ernicious anemia associated with autoim-mune disorders, atrophic gastritis. ii. G astrectomy, bariatric surgery, and intesti-nal surgeries. iii. S mall-bowel disorders, such as inflamma-tory bowel disease, bacterial overgrowth, tapeworms, enteritis, sprue, and celiac disease all affecting the terminal ileum. iv. L ong-term vegan diets without dairy products or eggs. v. M edications inhibiting absorption, such as metformin, proton pump inhibitors, and histamine 2 blockers. vi. F ood: cobalamin malabsorption syndrome when nutritional intake is adequate and there is no evidence of other causes of malabsorption or pernicious anemia. b. P revalence and incidence: Determining the frequency of vitamin B12 deficiency anemia is difficult because the etiologies are diverse. It is estimated that vitamin B 12 deficiency occurs in 5. 3% of those older than 60 years. In the elderly, rates increase from 5 to 20%. Those 31-51 years old have 3. 5% incidence and have a subclinical presentation (Centers for Disease Control and Prevention [CDC], 2009). Although usually seen in adults older than 40 of Scandinavian or Northern European ancestry, it can also be seen in any population. Nutritional deficiency is seen worldwide; however, in affluent countries, inad-equate absorption is most common. 2. F olic acid deficiency a. D efinitions and overview: Folic acid is present in most fruits and vegetables. A typical diet of 50 mg/d should be adequate. Folic acid stores of 5-20 mg last about 4 months. Common causes of folic acid deficiency include:i. I nadequate diet of fruits and vegetables. ii. I nflammatory bowel disease, such as sprue. iii. C ultural or ethnic cooking destroying folate, as in prolonged stewing. 405 Database
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c. P ersonal and social history i. Die t inadequate in iron, dairy, or animal products ii. H eavy alcohol use iii. I ntravenous drug use and sharing needles iv. T ravel to sub-Sahara Africa exposing the person to Schistosoma, such as Trichuris infections, and malarial zones v. R egular blood donations 2. Th alassemia a. P ast health history i. M edical illnesses: chronic microcytic ane-mia and iron overload. ii. S urgical history: splenectomy or hemato-poietic stem cell transplant. iii. Obs tetric history: pregnancy or stillborn fetus caused by hydrops fetalis. iv. M edication history: chelation therapy and RBC transfusions. b. F amily history i. Th alassemia and hemoglobinopathies ii. E thnicity: Mediterranean, Southeast Asian, Chinese, and African-American descent 3. S ideroblastic anemia a. P ast health history i. M edical illness: copper deficiency, vita-min B6 deficiency, and myelodysplastic syndrome ii. M edication history: excessive use of zinc supplements, antibiotics, copper chelat-ing agents, antituberculosis agents, and chemotherapy iii. E xposure history: lead poisoning and pro-longed exposure to cold b. F amily history i. S ideroblastic anemia ii. M itochondrial disease c. P ersonal and social history i. C hronic excessive alcohol intake ii. C oin ingestion 4. R eview of systems for microcytic anemias a. C onstitutional: degree of symptoms depends on the degree and rate of anemia development. Marked fatigue and decreased exercise tolerance may be the earliest symptoms along with weak-ness, postural faintness, headache, and weight loss. Pica, especially eating ice, is common. b. S kin and nails: pallor; bruising; koilonychia (spoon nails); and brittle nails. c. Ea rs, nose, and throat: bleeding, fissures at corners of mouth, and painful mouth. d. N eck: swollen neck glands. e. P ulmonary: cough, shortness of breath, and hemoptysis. f. C ardiac: chest pain, palpitations, and tachycardia g. A bdomen: tenderness, masses, changes in bowel habits, bleeding hemorrhoids, hematemesis, melena or bright red blood per rectum, disten-tion, and difficulty swallowing. h. Ge nitourinary: bloody urine i. G ynecological: heavy and or irregular menses, pregnancy, and multiple pregnancies j. S keletal: bone tenderness B. Subjective: normocytic anemias 1. A nemia of chronic disease a. P ast health history i. M edical illness: anemia; chronic diseases, such as renal disease; inflammatory bowel disease; autoimmune disorders; malignan-cies; sickle cell disease; and liver disease ii. S urgical history: cholecystectomy, prosthetic cardiac valves, and stem cell transplant iii. M edication history: penicillin, quinine, and quinidine iv. E xposure history: parvovirus B19 b. F amily history i. G6PD deficiency ii. S ickle cell disease iii. H ereditary anemia disorders iv. Aut oimmune disorders v. R enal or liver disease c. P ersonal and social history i. Die t including fava beans 2. H emolytic anemia a. P ast medical history i. M edical illnesses: previous hemolysis, chronic hemolytic anemia, systemic lupus erythema-tosus, rheumatoid arthritis, chronic lympho-cytic leukemia, non-Hodgkin's lymphoma, various carcinomas, idiopathic thrombocyto-penic purpura and thrombotic thrombocyto-penic purpura, G6PD deficiency, malaria, and cold agglutinin disease ii. S urgical: prosthetic heart valves, patches, and vascular grafts iii. M edications: antimalarials, sulfonamides, nitrofurantoin, sulfonylureas, quinine, quin-idine, interferon, phenacetin, high-dose penicillin, and blood transfusions iv. E xposures: infectious agents, such as para-sites; viruses, such as Epstein-Barr or cyto-megalovirus; measles; syphilis; enteric bacteria; spider bites and snake venom; copper; and organic compounds406 CHAPTER 43 | Anemia
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i. M edical history: vitamin B12 deficiency, chronic hemolytic anemia, sprue, atrophic gastritis, small bowel disease, psoriasis, epilepsy, and chronic hemodialysis ii. Obs tetric and gynecological history: pregnancy iii. M edications: methotrexate, pentamidine, trimethoprim, cancer chemotherapy, tri-ampterene, phenytoin, primadone, pheno-barbital, cholestyramine, and sulfasalazine b. F amily history i. H ereditary disorders ii. Glut en sensitivities c. P ersonal and social history i. A lcohol abuse ii. N arcotic addiction iii. I nadequate diet 3. R eview of systems: macrocytic or megaloblastic anemia, vitamin B12 or folic acid deficiency. a. C onstitutional: fatigue, decreased exercise toler-ance, weakness, and weight loss b. S kin: yellow skin, pallor, vitiligo, and rashes. c. M outh: cheilosis, stomatitis, sore smooth tongue, and atrophic glossitis d. N eck: sense of fullness in the thyroid region e. P ulmonary: shortness of breath f. C ardiac: tachycardia, chest pain, palpitations. g. A bdominal: diarrhea, pain, anorexia, nausea, constipation, bowel incontinence, and sense of fullness h. B ladder: incontinence i. N eurologic: paresthesias, balance problems, and difficulty walking j. E xtremities: edema k. N europsychiatric: depression, irritability, dementia, and insomnia D. Physical examination 1. E valuate weight and height. 2. C omplete vital signs: postural blood pressure and pulse, respiratory rate, and temperature. 3. Se e T able 43-4 for physical examination findings seen in anemia. III. Assessment A. Determine the diagnosis After the health history and physical examination. Guide the workup based on the clues found. Review previous complete blood cell count (CBC) to evaluate what might be the individual's trend of blood counts. b. F amily history i. G6PD deficiency ii. Aut oimmune hemolytic anemia iii. R ed cell membrane disorders c. P ersonal and social history i. A ggressive exercise causing microvascular trauma 3. R eview of symptoms for normocytic anemia and anemia of chronic disease and hemolysis a. C onstitutional: fatigue, weakness, postural faint-ness, poor exercise tolerance, and abrupt or gradual onset. b. S kin: rash, yellowing color, bruising, petechiae, pale skin, and nails c. N eck: swollen lymph nodes. d. P ulmonary: shortness of breath e. C ardiac: palpitations, tachycardia, and chest pain f. A bdominal: right upper quadrant pain, abdom-inal fullness, and decreased appetite g. E xtremities: leg ulcers and edema h. J oints: swollen painful joints i. B ladder: dark or bloody urine C. Subjective: macrocytic and megaloblastic 1. V itamin B12 deficiency a. P ast health history i. M edical history: autoimmune thyroid dis-ease, type I diabetes mellitus, Addison's disease, idiopathic hypoparathyroidism, autoimmune hemolytic diseases, tropical sprue, atrophic gastritis, regional enteritis, or gastric cancer ii. S urgical: gastrectomy, bariatric surgery, or intestinal surgery iii. M edications: metformin, thyroid replace-ment, colchicine, cholestyramine, hista-mine 2 blockers, proton pump inhibitors, and azidothymidine iv. E xposures: intestinal tape worm infesta-tion and repeated and prolonged (> 6 hr) nitrous oxide inhalation especially in the elderly (Longo, 2009) b. F amily history i. P ernicious anemia ii. Aut oimmune disorders, such as diabetes mellitus type 1 and thyroid disorders, vitiligo, hypoparathyroidism, and Addison's disease. c. P ersonal and social history i. V egan diet, high folate intake ii. A lcohol use 2. F olate deficiency a. P ast health history407 Assessment
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B. Differentiate the anemia and assess the severity of the disease. 1. M icrocytic anemias a. I ron deficiency anemia i. C BC: white cell and platelet abnormalities give clues about bone marrow malfunction, such as myelodysplastic or myeloprolifera-tive disorder. ii. A ssess anemia based on the MCV (T able 43-1). iii. Or der iron studies: ferritin, iron, total iron binding capacity, and reticulocyte count with a peripheral blood smear (T able 43-5). iv. D etermine the type of microcytic anemia. If iron deficiency, order stool guaiac and urinalysis to rule out blood loss from the gastrointestinal and genitourinary tracts, respectively. It is critical not to miss an occult gastrointestinal lesion, frequently a malignancy. Refer patients older than age 50, or younger than age 50 with a positive family history of colon cancer, to gastroenterology for endoscopy and colonoscopy. Y oung patients with iron deficiency anemia, weight loss, and persis-tent abdominal discomfort should also be referred to gastroenterology. Table 43-4 Physical Examination Findings Seen with Anemia Location Finding Implication Skin and nails Pallor Decreased number of red blood cells Petechiae Thrombocytopenia, leukemia, disseminated intravascular coagulation Telangiectasia and spider angiomas Liver disease Jaundice, icterus Hemolytic and megaloblastic anemia, liver disease Decreased elasticity of skin, brittle nails Long-standing anemia Koilonychia (spoon nails) Hair loss Long-standing anemia, especially iron deficiency Rash Systemic lupus erythematosis Neck Thyromegaly or masses Endocrinopathies Mucous membranes Pallor, cheilosis, and stomatitis Leukemia, pernicious anemia, or severe iron deficiency Smooth red tongue and atrophic glossitis Vitamin B 12 deficiency Lymph nodes Lymphadenopathy Leukemia, lymphoma, HIV Heart Tachycardia, loud murmurs, decreased PMI, congestive heart failure, functional murmurs, hypertension Severe anemia, pregnancy, renal disease Pulmonary Tachypnea Severe anemia Abdomen Splenomegaly, hepatomegaly, or hepatic tenderness Leukemia, lymphoma, hemolytic anemia, liver disease, autoimmune disease Central nervous system Decreased vibratory and position sense/ataxia, and decreased vibration of 256-degree tuning fork Pernicious anemia Lead poisoning causing ringed sideroblasts Skeletal Bone tenderness, swollen joints Hematologic disease, rheumatoid arthritis, autoimmune disorders Rectal Guiaic-positive stool, or bright red blood per rectum Gastrointestinal bleeding Extremities Edema Heart failure, renal failure, cirrhosis, hepatitis Leg ulcers Chronic hemolytic anemia, iron deficiency408 CHAPTER 43 | Anemia
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Milder forms of thalassemia need to be dis-tinguished from iron deficiency and more severe forms need to be distinguished from other hemoglobinopathies. ii. Th alassemias are congenital. Compare cur-rent CBC to previous CBCs. Microcytosis is usually significant, whereas the RBC count is normal or elevated. iii. I f no diagnosis, order hemoglobin A2, globin chain synthesis ratio, and hemo-globin electrophoresis including Hgb H (T able 43-3). iv. I f a pregnant woman is thought to be a carrier, the father of the baby should be tested. A CBC and hemoglobin electro-phoresis should be done. v. P regnant women and young menstruating women who are asymptomatic and otherwise healthy likely have iron deficien-cy anemia caused by menses or increased iron demands from a growing fetus in the context of inadequate dietary iron intake (ACOG, 2008). vi. A the rapeutic trial of iron reevaluating the results can be helpful because only an iron-deficient state will (see the treat-ment section) will improve with iron supplementation. b. Th alassemia anemia i. I f iron studies are normal and abnormal peripheral smear is reported, consider thal-assemia based on the individual's history. Table 43-5 Red Blood Cell Morphology Description of Red Blood Cell Associated with Disease Anisocytosis Excessive number of red blood cells of various sizes Larger size = vitamin B12 or folate deficiency, drug effect Smaller size = iron deficiency Hypochromia (decreased hemoglobin content in the red blood cell)Central pallor Iron deficiency Macro-ovalocytes Oval red blood cell Vitamin B12 or folate deficiency, liver disease, myelodysplastic syndrome Polychromasis Wright's stain: large grayish blue with pink Reticulocytes Increased levels in a peripheral smear are a result from a variety of anemias or from damage to the bone marrow Poiklocytosis Abnormal red blood cell shapes, such as:(the following is not inclusive list) Acanthocytes (spur cells) Severe liver disease Echinocytes (burr cells) Uremia, red blood cell volume loss Schistocytes (schizocytes) Microangiopathic or macroangiopathic hemolytic anemia Spherocytes Autoimmune hemolytic anemia, G6PD deficiency, hereditary spherocytosis T arget cells Thalassemia, liver disease, hemoglobin C, sickle cell disease T eardrop cells Myelofibrosis, infiltrative processes of marrow Rouleaux formation Paraproteinemia, such as multiple myeloma Red blood cell inclusions (the following is not inclusive list) Basophilic stippling Lead poisoning, thalassemia, myelofibrosis Pappenheimer (iron) bodies Sideroblastic anemia, lead poisoning Parasites Malaria, babesiosis Hypersegmentation Neutrophil nuclei with more than seven lobes Vitamin B12 or folate deficiency, drug effects409 Assessment
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c. S ideroblastic anemia i. R eview the CBC and iron studies; iron overload is suggestive of congenital or acquired clonal sideroblastic anemia. ii. A bone marrow biopsy with appropriate staining ultimately is the gold standard for this diagnosis. d. L ead poisoning i. R eview the CBC and iron studies. ii. C onsider getting a zinc protoporhyrin or free erythrocyte protoporphyrin (an elevated level suggests lead poisoning or iron deficiency anemia) as either test can be used as an indication of lead exposure over the past 3 months. iii. Obt ain a serum lead level. 2. N ormocytic anemia a. A nemia of chronic disease. This is a diagnosis of exclusion when CBC and iron stores are normal. Identify potential causes of this anemia. i. C onsider ordering an erythrocyte sedi-mentation rate and a C-reactive protein to look for chronic inflammatory states, both elevated in infection and inflammation. ii. R ule out liver disease with liver func-tions tests, thyroid disease with a thyroid-stimulating hormone level and thyroid function tests, and renal disease with a serum creatinine and urinalysis. b. H emolytic anemia i. W ith a careful health and medication history and physical examination, look at the normocytic anemia MCV for reticulocytosis. ii. Or der an indirect bilirubin and lactate dehy-drogenase blood test. iii. C onsider ordering a direct antiglobin test or Coombs to confirm immune-mediated hemolysis. Order a G6PD blood test 1-2 months after acute hemolysis. iv. C onsider ordering a cold agglutinin titer. 3. M acrocytic and megaloblastic anemias a. V itamin B12 deficiency i. C BC with elevated MCV and a peripheral smear with macro-ovalocytes and hyper-segmented polymorphonuclear cells are seen with vitamin B 12 and folate deficiency. ii. Or der a vitamin B12 and a folate level to differentiate the common causes of mega-loblastic anemia. Consider screening high-risk individuals especially those with health conditions resulting in a high cell turnover as after a prolonged or critical illness and normal MCV (Bryan, 2010; Langan & Zawistoski, 2011). iii. C onsider serum methylmalonic level, which has increased sensitivity and speci-ficity for confirming vitamin B12 deficiency. Additional serologic testing for gastrin and intrinsic factor (IF) are used to diagnose pernicious anemia (Oberly & Yang, 2013). iv. L ow cobalamin distinguishes vitamin B12 from myelodysplastic syndrome. b. F olate deficiency: with normal vitamin B12 level, low serum folate level, normal methylma-lonic level, and elevated homocysteine, folate deficiency is the probable diagnosis. IV. Goals of clinical management A. Choose a cost-effective approach for diagnosing anemia. B. Choose a treatment plan that normalizes serum RBC level and minimizes the risk of anemia relapse (Table 43-6 ). C. Select an approach that maximizes the patient's short-and long-term adherence to treatment. V. Plan A. Microcytic anemias 1. I ron deficiency anemia a. E ncourage intake of iron-rich foods: lean red meat, poultry, egg yolks, beans, dried fruit, dark leafy greens, broccoli, asparagus, or infusion of dried nettle. b. R eview foods that interfere with iron absorp-tion: coffee, tea, soda, dairy, and antacids. c. F errous sulfate therapy, 325 mg (65 mg elemental iron) daily to twice daily, depending on severity of anemia treatment. In pregnancy, this should be given in addition to prenatal vitamins (CDC, 1998; Graves & Barger, 2001). A 4-week trial of iron supplementation for mild anemia before a definitive diagnosis of iron deficiency anemia with iron studies is an acceptable initial inter-vention. If the follow-up complete blood count (CBC) is normal, it is reasonable to assume the anemia was caused by a deficiency in iron. Plan to give iron 1-2 months for anemia correction then an additional 4-5 months to replenish iron stores (ferritin level to 50 mcg/m L). 410 CHAPTER 43 | Anemia
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f. I f iron is poorly tolerated because of side effects, consider switching to ferrous fumarate, 325 mg, or ferrous gluconate, 325 mg. g. Ke ep iron tablets out of reach of children, because they can be fatal if ingested in quantities of only 10-20 pills. d. Di scuss ways to increase iron intake and absorption: take with juice with vitamin C and in-between meals. e. R eview side effects of supplementation: consti-pation, nausea, bloating, almost dark, charcoal-colored stool, and abdominal cramps. Table 43-6 Laboratory T ests with Normal Values *Note each lab has their own result standards. Test n ormal Comment Complete blood count Hgb Hct Hemoglobin:F: 12-15. 5 g/d LM: 13. 6-17. 5 g/d LHematocrit:F: 35-49%M: 39-49Physiologic variation because of age, smoking, and altitude. Hemogloblin reflects amount of oxygen carrying protein. Hematocrit measures percentage of Hgb in blood Red blood cell indices Red blood count F: 3. 5-5. 2 10 × 6th/mc L M: 4. 3-6 10 × 6th/mc LElevated in dehydration, lung disease, smoking, polycythemia vera Mean cell volume 80-100 f L Reflects size of red cell Mean cell hemoglobin concentration31-36 g/d L Increased with spherocytosis, hemolysis; decreased in other anemias Mean cell Hgb 26-34 pg Is calculation of average amount of Hgb in RBC Red cell distribution width 11. 5-14. 5% Is calculation of variation of red blood cell size; decreased in iron deficiency White blood cell count 4. 5-11 10 × 3rd/mc L Platelets 15,000-450,000 μL Reticulocyte count 33-137 10 × 3rd/mc L > 400 reflects RBC loss or destruction< 200 reflects low production, macrocytosis, ACD, or myelodysplastic disease Expect increase of two to three times in 10 days after anemia starts if normal erythropoietin and bone marrow Iron supply studies 50-175 mcg/d L Serum iron, total iron binding capacity250-460 mcg/d L Is decreased in iron deficiency anemia % transferring saturation 25-50% low in iron deficiency < 16% Ferritin M: 10-300 μg/m L F: 10-200 μg/m LMost useful in separating iron deficiency from ACD, thalassemia; lowest levels correlate with depleted bone marrow Haptoglobin 4-316 High levels helpful in ruling out significant intravascular hemolysis Folate 165-760 ng/m L Vitamin B 12140-820 pg/m L Data from Gomella, L., & Haist, S. (2007). The famous scut monkey handbook: Clinician's pocket reference (11th ed. ). New York, NY Mc Graw-Hill; Nicoll, D., Mc Phee, S., Pignone, M., & Lu, C. (2007). Pocket guide to diagnostic tests (5th ed. ). New York, NY. Mc Graw-Hill Medical. 411 Plan
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h. I f the patient has mild anemia, consider inter-mittent dosing (120 mg elemental iron one to two times weekly). i. C onsider informing the patient of the availability in health food stores of Floridex Liquid Iron Supplement. Floridex has very little elemental iron and thus is better tolerated. However, it may not be as effective in treating anemia. j. Ele mental iron interferes with zinc absorption, so consider zinc supplementation (25 mg, which is the amount found in prenatal vitamins) is recommended in pregnant patients (Graves & Barger, 2001). k. R epeat CBC and reticulocyte count in 2-4  weeks after initiation of treatment. An increased reticulocyte count confirms that the patient is taking iron supplementation. l. A lthough medication nonadherence is the most common cause of response failure, having the incorrect diagnosis has to be considered. m. P lan for patient follow-up with laboratory values at 1, 2, 4, and 6 months to ensure full recovery. n. I n pregnancy, obtain medical consultation if severe anemia (Hgb is less than 9 g/d L) despite initiation of therapy or if anemia is chronic. 2. Th alassemia a. I ndividuals with mild disease should be identi-fied to prevent repeated unnecessary diagnostic anemia evaluations and to prevent patients from taking iron unnecessarily. b. F or those with hemoglobin H disease, 1 mg of folate daily should be prescribed. c. I ndividuals who have severe anemia and need to be treated with red cell transfusions and chelation therapy should be referred to a hematologist. d. P regnant women who are found to be carriers and whose partner is also a carrier of either a thalassemia or sickle cell trait should have genetic counseling because of the risk of fetal hemoglobinopathy. Women who either have a thalassemia or sickle cell disease may have profound anemia with considerable neonatal morbidity and therefore should be cared for by a specialist in obstetrics and hematology (ACOG, 2008). 3. S ideroblastic anemia a. I f medically stable, no treatment is needed. Patients often do not respond to erythropoietin therapy. b. O ccasionally, these patients need RBC transfu-sions. A hematologist should be managing their anemia. 4. L ead poisoning a. F urther investigate the patient's possible lead exposures: exposure to lead-based paint, lead-contaminated dust, lead-contaminated residen-tial soil (U. S. Environmental Protection Agency, 2010). b. R efer patient to the public health department to help with investigation of lead exposure. c. C onsult with a hematologist to evaluate for a plan of treatment (e. g., need for therapeutic administration of a chelating agent). B. Normocytic anemias 1. A nemia of chronic disease a. T reat underlying conditions. b. I n most cases, correction of anemia is not indi-cated. However, erythropoietin can be effective for those individuals with renal failure, cancer, and inflammatory disorders. 2. H emolytic anemias a. T reat illness and discontinue drugs that may have triggered this anemia. b. P rednisone is the standard initial treatment in autoimmune hemolytic anemia. Symptomatic individuals should receive transfusions. In those who fail remission or cannot sustain remission, a splenectomy is recommended. Immunosuppressive agents are used in those persons who fail to respond with splenectomy. c. I nstruct patients to take 1 mg of folate daily. In those individuals with G6PD deficiency, avoid giving oxidant medications (e. g., sulfamethoxa-zole). In those susceptible to hemolysis, avoid giving medications known to trigger hemolytic anemia. d. H ematology evaluation and management are indicated. e. F or pregnant patients with sickle cell trait, the father of the baby should be tested (CBC and Hgb electrophoresis). If the father is found to be a sickle cell trait carrier, refer to genetics for counseling regarding the risk of sickle cell disease in the neonate. Urine culture and sensi-tivity screening every trimester should be done, because pregnant women who are a carrier for sickle cell trait have an increased risk of urinary tract infection (Pastore, Savitz, & Thorp, 1999). f. F or pregnant patient with a child with sickle disease, refer to genetics for counseling. C. Macrocytic and megaloblastic anemias 1. V itamin B12 deficiency anemia a. Admini ster cobalamin, 1,000 mg, parenter-ally daily for 1 week, then weekly for 1 month, 412 CHAPTER 43 | Anemia
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and other links for additional information for patients. B. The National Institutes of Health has a collection of patient information sites that discuss anemia with handouts under links on dietary supplementation: www. nhi. gov. Re Fe Ren Ce S American College of Obstetricians and Gynecologists. (2008). ACOG practice bulletin No. 95: Anemia in pregnancy. Obstetrics & Gynecology, 112(1), 201-207. Beutler, E., & Waalen, J. (2006). The definition of anemia: What is the lower limit of normal of the blood hemoglobin concentration? Blood, 107(5), 1747-1750. Brabin, B. J., Hakimi, M., & Pelletier, D. (2001). An analysis of anemia and pregnancy-related maternal mortality. Journal of Nutrition, 131, 604S. Brill, J., & Baumgardner, D. (2000). Normocytic anemia. American Family Physician, 62(10), 2255. Bryan, R. (2010). Are we missing vitamin B12 deficiency in the primary care setting? Journal of Nurse Practitioners, 6(7), 519-523. Centers for Disease Control and Prevention. (2009). Vitamin B 12 deficiency. National Center on Birth Defects and Developmental Disabilities Centers for Disease Control and Prevention. (1998). Recommendations to prevent and control iron deficiency in the United States. Morbidity and Mortality Weekly Report, 47, 1-29. Collins-Bride, G., & Saxe, J. (Eds. ). (1998). Nurse practitioner/physician collaborative practice: Clinical guidelines for ambulatory care. San Francisco, CA: UCSF Nursing Press. Elmadfa, I., & Singer, I. (2009). Vitamin B12 and homocysteine status among vegetarians: A global perspective. American Journal of Clinical Nutrition, 89(5), 1693S-1698S. Gardner, L., & Benz, Jr., E. (2008). Anemia of chronic disease. In R.  Hoffman, H. Heslop, B. Furie, E. Benz, Jr., P. Mc Glave, L.   Silberstein,  & et al. (Eds. ), Hematology: Basic principles and practice (5th ed., pp. 469-474). Philadelphia, PA: Elsevier Churchill Livingstone. Gehrs, B., & Friedberg, R. (2002). Autoimmune hemolytic anemia. American Journal of Hematology, 69(4), 258-271. Giardina, P., & Forget, B. (2008). Thalassemia syndromes. In R. Hoffman, H. Heslop, B. Furie, E. Benz, Jr., P. Mc Glave, L. Silberstein, & et al. (Eds. ), Hematology: Basic principles and practice (5th ed., pp. 535-563). Philadelphia, PA: Elsevier Churchill Livingstone. Gomella, L., & Haist, S. (2007). The famous scut monkey handbook: Clinician's pocket reference (11th ed. ). New Y ork: Mc Graw-Hill. Graves, B. W., & Barger, M. K. (2001). A “conservative” approach to iron supplementation during pregnancy. Journal of Midwifery & Women's Health, 46(3), 159-160. Hoffman, R., Benz, E. J., Shatti, S. S., Mc Glave, P., Silberstein, L. E., & Shattil, S. J. (Eds. ). (2008). Hematology: Basic principles and practice (5th ed. ). Philadelphia, PA: Elsevier Churchill Livingstone. Kemna, E. H. (2008). Hepcidin: From discovery to differential diagnosis. Haematologia, 9(3), 90-97. Killip, S., Bennett, J., & Chambers, M. (2007). Iron deficiency anemia. American Family Physician, 75(5), 671-678. Langan, R., & Zawistoski, K. (2011). Update of vitamin B12 deficiency. American Family Physician, 83(12), 1425-1430. then monthly lifelong. In severe anemia, serum potassium and hematocrit may drop with initial treatment with cobalamin. b. Or al cobalamin, 1,000-2,000 mcg daily, can be substituted with equal effect as parental admin-istration (Vidal-Alaball, Butler, Cannings-John, & Goringe, 2009). Follow-up serum vitamin B 12 levels need to be monitored to ensure there is adequate absorption. Lifelong compliance is critical, especially for the elderly who are more prone to have atrophic gastritis. T reat subclinical deficiency with 500 mcg to 1g dose, just enough to correct the deficiency. c. I t is important to appropriately investigate macrocytosis. All patients with suspected myelo-dysplastic disease need a hematologic evaluation. d. Thos e individuals who do not respond to vita-min B12 treatment, who are medically unstable, or whose vitamin B12 and folic acid levels are normal should be referred to a hematologist. 2. F olate deficiency anemia a. A void treating patients with potential cobalamin deficiency with folate alone unless vitamin B12 deficiency anemia has been ruled out and treated because this may lead to progressively severe neuropsychiatric disease caused by untreated vitamin B 12 deficiency. b. Admini ster folate, 1 mg daily. In 1 week, the patient should begin to have a sense of improve-ment with increase in reticulocytes. CBC corrects in 2 months, and then the patient may be tapered to folate, 0. 5 mg/d long term. D. Client education 1. P rovide verbal and written information regarding a. The d isease process, including signs and symp-toms and underlying etiologies. b. Di agnostic tests that include a discussion about preparation, actual procedures, and follow-up care. c. M anagement plan: rationale, action, use, side effects, and cost of therapeutic interventions, and the need for adhering to the long-term treat-ment plans. VI. Self-management r esources and tools A. The American Society of Hematology's website is www. bloodthevitalconnection. org. This website provides both an overview of anemia 413 References
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Laubach, J., & Bendell, J. (2008). Hematologic changes of pregnancy. In R. Hoffman, H. Heslop, B. Furie, E. Benz, Jr., P. Mc Glave, L.   Silberstein, & et al. Hematology: Basic principles and practice (5th ed., pp. 2385-2396). Philadelphia, PA: Elsevier Churchill Livingstone. Linker, C. (2007). Blood. In S. Mc Phee & M. Papadakis (Eds. ), Current medical diagnosis & treatment (pp. 493-507). New Y ork, NY: Mc Graw-Hill. Longo, D. (2009). Examination of blood smears and bone marrow and red blood cell disorders. In A. Fauci, E. Braunwald, D. Kasper, S. Hauser, D. Longo, J. Jameson, et al. (Eds. ), Harrison's manual of medicine (17th ed., pp. 321-328). New Y ork, NY: Mc Graw-Hill. Makipour, S., Kanapuru, B., & Ershler, W. B. (2008). Unexplained anemia in the elderly. Seminars in Hematology, 45(4), 250-254. Nicoll, D., Mc Phee, S., Pignone, M., & Lu, C. (2007). Pocket guide to diagnostic tests (5th ed. ). New Y ork: Mc Graw-Hill Medical. Oberly, M. J., & Yang, D. T. (2013). Laboratory testing for cobalamin deficiency in megaloblastic anemia. American Journal of Hematology, 88, 522. Pastore, L. M., Savitz, D. A., & Thorp, J. M., Jr. (1999). Predictors of urinary tract infection at the first prenatal visit. Epidemiology, 10, 282. Schick, P. (2010). Hemolytic anemia, Version 2010. Retrieved from http://emedicine. medscape. com/article/201066-overview. Schrier, S. (2010). T o be old is to be inflamed? Blood, 115(18), 3651-3652. Schwartz, R. (2007). Autoimmune and intravascular hemolytic anemias. In L. Goldman, D. Ausiello, W. Arend, J. Armitage, D. Clemmons, J.  Drazen, et al. (Eds. ), Goldman Cecil medicine: Expert consult (23rd ed., pp. 1194-1202). Philadelphia, PA: W. B. Saunders. Sifakis, S., & Pharmakides, G. (2000). Anemia in pregnancy. Annals of the New York Academy of Sciences, 900, 125. T efferi, A. (2007). Nonhemolytic normochromic, normocytic anemias. In L. Goldman, D. Ausiello, W. Arend, J. Armitage, D. Clemmons, J.  Drazen, et al. (Eds. ), Goldman Cecil medicine: Expert consult (23rd ed., pp. 1228-1230). Philadelphia, PA: W. B. Saunders. Umbreit, J. (2005). Iron deficiency: A concise review. American Journal of Hematology, 78, 225-231. U. S. Environmental Protection Agency. (2010, May 19). Lead in paint, dust and soil. Retrieved from www. epa. gov/lead/. Vidal-Alaball, J., Butler, C., Cannings-John, R., & Goringe, A. (2009). Oral vitamin B 12 versus intramuscular vitamin B12 for vitamin B12 deficiency (review). The Cochrane Collaboration. Retrieved from www. thecochranelibrary. com. Yaish, H. (2013). Pediatric thalassemia. Medscape reference: Drugs, diseases & procedures. Retrieved from http://emedicine. medscape. com/article /958850-overview. 414 CHAPTER 43 | Anemia
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(and the only one available in the United States). Whether or not generic warfarin is dispensed, it is often referred to by both clinicians and patients by its trade name Coumadin ®. The term “blood thinner” is a useful though misleading way to describe the action of warfarin to patients. In reality it does not make blood more watery. The action of a VKA is to inter-fere with hepatic synthesis of vitamin K dependent proteins. The net effect is to slow down or delay fibrin clot formation in the systemic circulation. In this way, the ability to easily make harmful thrombi is limited. In most cases, this effect translates to roughly 10-15 seconds delay in clot formation. A. Monitoring warfarin therapy The prothrombin time (PT) measures the speed of clot formation but the reagents used to perform the test vary in their sensitivities among manufacturers. The INR is a ratio that corrects for this variation and therefore its inter-pretation is consistent among laboratories and institu-tions (Nicoll, Mc Phee, Pignone, & Lu, 2007). The INR is intended to be used only for warfarin monitoring. Unlike the PT, it is not a measure of liver function. Individuals not on a VKA usually have a baseline INR value between 0. 8 and 1. 2; under the influence of a VKA, the PT and the INR both rise indicating delay in the onset of clot formation, and the blood is described as being “thinner” than it was at baseline. B. Target population Indications associated with increased clot risk are shown in T able 44-1, along with the recommended target INR for that indication; the target INR may be amended to suit the health and safety profile of the individual. For instance, consider the rare patient who develops a clot despite being at their therapeutic target of 2. 0-3. 0. In such a case the therapeutic target may be raised to 3. 0-3. 5. A polar opposite example is the patient whose bleeding risk is very high because of high fall risk. In this situation, the INR tar-get may be lowered to as little as 1. 5-2. 0. Older patients also deserve special consideration. Common barriers to an older patient taking warfarin safely include cognitive I. Intr oduction and general background Authors' note: Since the previous publication of this chapter in 2011, treatment options for oral anticoagulation have been broadened by the introduction and the increasingly widespread use of the target-specific oral anticoagulants (TSOACs); these have been approved by the Food and Drug Administration (FDA) for most but not all indications. The new agents have both advantages and disadvantages over warfarin; as clinical experience and research accumulates with the new agents, recommendations for their use will undoubt-edly be further refined. Because warfarin continues to be the most widely used and best understood oral anticoagulant, this chapter continues to focus on its use but also includes basic information about the TSOACs. Updated expert clinical practice guidelines are expected to be published by the American College of Chest Physicians (ACCP) within the near future. The 9th (2012) edition of these guidelines was consulted for the preparation of this chapter. Long-term oral anticoagulation (OAC) with warfarin (Coumadin ®) is indicated for numerous conditions (T able 44-1). Used for primary and secondary prevention of thromboembolism (TE), OAC requires careful and meticu-lous management by the clinician to achieve effective and safe outcomes. Although the best practice model for anticoagula-tion management is a dedicated anticoagulation service, the primary clinician often oversees warfarin therapy. Warfarin management can be complex because the drug possesses what one anticoagulation expert (Ansell, 2009) describes as a “high risk/benefit profile. ” Warfarin has a narrow therapeutic index and thus requires careful follow-up at regular intervals because what may be a therapeutic dose at one time may be subthera-peutic or supratherapeutic at other times. The discussion that follows is intended to increase clinician comfort with managing warfarin for the patient on OAC. Warfarin belongs to the class of OAC called vitamin K antagonists (VKA) and of these, it is the most commonly used Fran Dreier and Linda Ray Ant Ico Agu LAt I on t he RA py ( o RAL )© Eliks/Shutterstock; © donatas1205/Shutterstock 415 44Chapt Er
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C. Associated risk of vitamin K antagonists (VKAs) The potential for bleeding is the primary side effect of OAC with warfarin. As reported by the Centers for Medicare and Medicaid Services (2009), those at increased risk of bleeding are patients with the following: INR greater than 4. 0, labile INR pattern, history of gastrointestinal bleeding, existing cerebrovascular disease, serious heart disease, anemia, malignancy, trauma, renal insufficiency, concomitant drugs, advanced age, and prior stroke. It is axiomatic that the higher the INR, the greater the risk for bleeding complications. However, it is important to point out that an elevated INR is a measure of risk of harmful bleeding, which is not the same as having harmful bleeding. D. Treatment duration The ACCP guidelines include recommendations for treat-ment duration. Patients who are at high risk of TE need lifelong OAC (T able 44-1). Short-term therapy, which usually lasts 3 months, is appropriate for indications where clot risk is transitory or triggered by a provoking event, such as the case of a single-event deep venous thrombosis after hip replacement. E. Variables that affect response to warfarin 1. Die t The most frequent cause for a change in INR in a patient who has been otherwise stable is a change in oral vitamin K intake or absorption. For impairment, increased fall risk, visual or hearing impair-ment, or dependency on others for warfarin administra-tion (Evans-Molina, Henault, Regan, & Hylek, 2003). In patients diagnosed with atrial fibrillation (AF), war-farin is highly effective in preventing complications of TE, particularly stroke, in patients of any age (Wolf, Abbott, & Kannel, 1991). The CHADS 2 score (T able 44-2A) is a widely used scheme for evaluating stroke risk in patients with lone or nonvalvular AF (Gage et al., 2001). Patients with a score of greater than or equal to 1 are likely to benefit from warfarin, unless risk for bleeding outweighs the potential for clotting. Patients with AF and a score of 0 have traditionally been treated with aspirin (Fang et al., 2008). The CHA2DS 2-VASc score (T able 44-2B) is a more recently developed risk scheme that has been adopted by the American Heart Association and some other groups. This scheme includes additional risks factors: age 65-74, female gender, and vascular disease. Age 75 years and older gains extra weight, with 2 points. The result is to further subdivide the low-risk group of patients with AF so that anticoagulation is recommended for a greater proportion of the group. However, as pointed out by Fang in 2015, to date it has not been shown that treating these additional AF patients results in improved stroke outcome without unjustified increase in bleeding. The clinician should keep in mind that an individual's risk of complications of thrombosis versus bleeding risk may change over time and, as such, the assessment of need for OAC treatment should be reexamined from time to time. Table 44-1 Indications with Therapeutic International Normalized Ratio (INR) Range of 2-3 Indications with Therapeutic INR Range of 2-3 Duration of OAC Treatment of deep vein thrombosis/pulmonary embolism (DVT/PE), collectively known as venous thromboembolism (VTE) Provoked by transient risk factor Unprovoked Recurrent3 months Reevaluate at 3 months Long term Stroke/TIA/systemic arterial embolism, secondary prevention Long term Prevention of systemic embolism (acute coronary syndrome, atrial fibrillation, valvular heart disease, severe left ventricular dysfunction [ejection fraction < 30%], postsurgical VTE prophylaxis)Varies with indication Pulmonary hypertension Long term Mechanical prosthetic valves in the aortic position* Long term Indications with Therapeutic INR Range of 2. 5-3. 5 Duration of OAC Recurrent thromboembolism while on therapeutic warfarin Long term Mechanical prosthetic valves in the mitral position or ball and cage valves in any position Long-term * Goal INR 2. 5-3. 5 if patients have additional risk factors (e. g., AF) Data from Guyatt, G., Akl, E., Crowther, M., Gutterman, D., & Schünemann, H. J. (2012). Executive summary: Antithrombotic therapy and prevention of thrombosis (9th ed. ). Chest, 141(2, Suppl. ), 7S-47S. 416 CHAPTER 44 | Anticoagulation Therapy (Oral)
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example, warfarin effect is enhanced in the presence of decreased appetite or acute diarrhea. For optimal stability, patients should be encouraged to maintain a consistent amount of vitamin K in their diet from week to week. Vitamin K is a nutrient that is present in varying quantities in most foods, and deficiency is rare for the individual who is not starving. The daily value (DV) recommended by the U. S. Department of Agriculture (2001) is 120 mcg for men and 90 mcg for women. Certain foods are very rich in vitamin K, and far exceed the DV in a single serving. The foods highest in vitamin K are the dark green leafy vegetables, such as kale and spinach. Several other vegetables are moderately high in vitamin K. A patient's vitamin K intake should be assessed at every visit, and patients should be reminded periodically that it is their responsibility to maintain consistent vitamin  K intake. Some common vitamin K-rich foods are listed in T able 44-3. A comprehensive list can be found at: U. S. Department of Agriculture, Agricultural Research Service, Nutrient Data Laboratory. (2015). USDA National Nutrient Database for Standard Reference, Release 28. Retrieved from www. ars. usda . gov/nea/bhnrc/ndl. Supplements, both tablet and liquid forms, and multivitamins may contain significant amounts of Table 44-2 b CHADS2-VASc Score for Assessment of Stroke Risk in Patients with Atrial Fibrillation Congestive Heart Failure* 1 pt Hypertension 1 pt Age ≥ 75 years 2 pt Diabetes 1 pt Stroke (previous TIA or CVA) 2 pts Vascular Disease (myocardial infarct, aortic plaque, peripheral artery disease)1 pt Age 65-74 years 1 pt Sc Sex category (i. e., female sex) 1 pt *Ejection fraction < 25% or have had a heart failure exacerbation in the last 90 days Risk of events per year without OAC: 0 points = 0. 0 low risk 1 point = 1. 3% moderate risk2 points = 2. 2% high risk3 points = 3. 2% high risk4 points = 4. 0% high risk5 points = 6. 7% high risk6 points = 9. 8% high risk7 points = 9. 6% high risk8 points = 6. 7% high risk9 points = 15. 2% high risk Data from Odum, L., Cochran, K., Aistrope, D., & Snella, K. (2012). The CHADS 2 vs the New CHA2DS2-VASc scoring systems for guiding antithrombotic treatment of patients with atrial fibrillation: review of the literature and recommendations for use. Pharmacotherapy, 32(3), 285-296. Table 44-2 a CHADS2 Score for Assessment of Stroke Risk in Patients with Atrial Fibrillation Congestive Heart Failure* 1 pt Hypertension 1 pt Age ≥ 75 years 1 pt Diabetes 1 pt Stroke (previous transient ischemic attack [TIA] or cerebrovascular accident [CVA])2 pts *Ejection fraction < 25% or have had a heart failure exacerbation in the last 90 days Risk of events per year without OAC: 0 points = 1. 9% 1 point = 2. 8%2 points = 4%3 points = 5. 9%4 points = 8. 5%5 points = 12. 5%6 points = 18. 2% Data from Gage, B. F., Waterman, A. D., Shannon, W., Boechler, M., Rich, M. W., & Radford, M. J. (2001). Validation of clinical classification schemes for predicting stroke: Results from the National Registry of Atrial Fibrillation. JAMA, 285, 2864-2870. Table 44-3 Foods Rich in Vitamin K Beet greens* Kale* Broccoli Lentils Brussels sprouts Lettuce† Cabbage Mustard greens* Cauliflower Seaweed (nori) Chard* Soybean oil‡ Collard greens* Spinach* Garbanzo beans Turnip greens* * Extremely high in vitamin K. † Except iceberg. ‡ In large quantities. Data from U. S. Department of Agriculture, Agricultural Research Service. National Nutrient Database for Standard Reference, Release 27. 417 Introduction and general background
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vitamin K; clinicians should ask about supplement use at each visit. A change in multivitamin brand or in frequency of use can significantly affect the INR. 2. A lcohol intake Alcohol can affect the INR unpredictably. Paradoxically, chronic alcohol use tends to lower the INR, whereas acute binge drinking tends to increase the INR. Light to moderate drinking (i. e., up to two servings of alcohol [12 oz of wine, 24 oz of beer, 2 oz of hard liquor] at one time) may be less problematic. Alcohol also increases the likelihood of injury if ingested in excess, may cause bleeding by irritating the upper gastrointestinal tract, and may impair platelet function. Abstention from alcohol does simplify warfarin management (Wittkowsky, 2009b). 3. C omorbidities An acute illness or a worsening of a chronic illness may affect warfarin stability. Changes in liver, cardiac, or thyroid function are likely to alter usual dose require-ments. In general, severe illness tends to increase one's sensitivity to warfarin and necessitates dose reduction to achieve target INR. For reasons not fully understood, fever itself may independently cause an increased response to warfarin (Self, 2000). 4. I nteractions a. Dr ug interactions and other medications Many drug interactions with warfarin have been documented. For most agents, there is significant individual variability among patients as to timing and extent of the interaction. Drug interactions may vary both among individuals and within a drug class itself (see T able 44-4 for a partial list of interactions). It is important that the clinician very clearly educate patients to report any acute illness, new medicines, or change in medicines. It is critical that clinicians maintain meticulous communication to ensure that all members of the healthcare team are aware of new drugs that have been prescribed. If a new medication is recommended for which there is no reasonable alternative and if it is likely to interact, the clini-cian may choose to preemptively alter warfarin dose or increase the frequency of INR checks. This is often done in consultation with an anti-coagulation specialist. A comprehensive list of interactions can be found in the article by Holbrook and colleagues (2005). Fortunately, first-generation penicillins do not interact with warfarin. Pain medications represent a special category of consideration because the need for acute or chronic analgesia arises so frequently in the primary care setting. Nonsteroidal anti-inflammatory drugs (NSAIDs), both nonselec-tive and selective (cyclooxygenase-2 inhibitors), should be avoided in patients taking warfarin because they increase the risk of gastrointesti-nal bleeding (Battistella, Mamdani, Juurlink, Rabeneck, & Laupacis, 2005; Cheetham, Levy, Niu, & Bixler, 2009). If a patient must take an NSAID, it is best to take the shortest acting agent, at the smallest dose, for the briefest time. If a patient must be on chronic NSAID therapy, the clinician should consider monitoring stool with fecal occult blood testing (FOBT) Although adding a drug from the class of proton pump inhibitors theoretically confers some protection to the upper gastrointestinal tract, this does not protect the lower gastrointestinal tract. The safest alternative for a patient requiring short-term pain relief is acetaminophen. Although it does not relieve inflammation, when the dosage does not exceed 2 g/day, there is very small likelihood that an interaction will occur. However, the INR may increase with the use Table 44-4 W arfarin-Drug Interactions Increase in I n R Decr ease in I n R Alcohol Alcohol Amiodarone* Antiretrovirals (some)† Antiretrovirals (some)†Carbamazepine Azoles‡*Phenobarbital* Cimetidine* Rifampin/rifabutin* Erythromycin* Vitamin K (phytonadione)* Fibrates* Fluoroquinolones (some)*Phenytoin Statins Prednisone*Allopurinol Tramadol This is not a comprehensive list. INR should be monitored after initiating or modifying any drug therapy. * Significant interaction. † The reader is advised to go to literature for specifics of individual drugs of this class. ‡ Azoles include antifungals, metronidazole, and sulfamethoxazole, a component of Bactrim®/Septra®. Modified from UCSF Medical Center. (Updated February 2009). Comprehensive Hemostasis and Antithrombotic Service (CHAS). 418 CHAPTER 44 | Anticoagulation Therapy (Oral)
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a. B ased on the 7-day week, tell me what dose you take on what days. b. D o you recall having missed any doses recently, particularly in the last 7 days? Additional areas to cover at each visit are shown in T able 44-6. 3. P ast guidelines indicated that the stable patient with therapeutic INR readings should undergo follow-up testing every 4 weeks (Ansell, 2009), although there is evidence suggesting that the stable patient without significant comorbidities might be followed less frequently (Witt et al., 2009). ACCP guidelines (2012) suggest (grade 2B) that for stable patients, follow-up may safely be extended up to 12-week intervals. T esting every 1 to 2 weeks is recommended if the INR is not within therapeutic range or if warfarin dose is changed. In certain situations, such as a very high (supratherapeutic) INR, it may be advisable to retest in 1 or 2 days. G. Managing variations in INR 1. One of the ch allenges of managing OAC is deciding how to respond to INR variations. Small INR variations occur from visit to visit for even the more stable patient, and not all INR variations require new dose adjustment. The trend of a patient's INR readings is more important than any single INR. Abrupt change in dosing should be avoided, because it is responsible for some of the difficulty that can occur in attempting to maintain INRs within target range. 2. W hen presented with an INR that is out of target range, the clinician should look for variables that of 4 g/day (Carrier, Grégoire, & Wells, 2009). T ramadol may increase the INR; narcotics do not by themselves alter the INR or platelet func-tion. However in the setting of acute pain, oral intake including vitamin K is likely to decrease and result in a rise in INR. b. I nteractions and supplements It has been estimated that 50% of patients are taking some form of nutritional supplement and that up to 60% do not report use of alter-native therapies to their healthcare providers (Wittkowsky, 2009a). Although there are rela-tively few case reports of supplement-warfarin interactions to date and these are poorly docu-mented, potential interactions do exist, either by diminishing platelet activity or by directly affecting the INR (T able 44-5). The clinician is advised to check Web-based information systems for further information regarding these products (www. naturaldatabase. com) F. Issues of dosing and follow-up in OAC 1. O AC is best managed using a systematic approach of patient assessment, addressing dose adjustment, and scheduling the next follow-up interval. The use of a flow sheet or electronic record is strongly advised to help the clinician interpret the visit data in the context of overall INR trends and usual dose patterns (Garcia et al., 2008). 2. A t each visit the clinician should assess the patient's overall health status. The clinician should confirm actual dosing at each visit with direct and specific questions: Table 44-5 W arfarin and Commonly Used Dietary Supplements/Herbal Medicines herbs and Dietary Supplements Impact or e ffect American ginseng May either potentiate warfarin or inhibit warfarin effect Chinese herbs and medicines Impact determined by active ingredients Coenzyme Q-10 Mixed reports on its effects; avoid or monitor closely for 3 months at time of supplement initiation Echinacea No case reports of interaction with warfarin Fish oil and omega-3 fatty acids Antiplatelet activity; may increase bleeding risk Garlic Antiplatelet activity when taken in large quantities Ginkgo biloba Antiplatelet activity; may increase bleeding risk (hemorrhagic stroke case reports) Glucosamine May increase INR (based on a few isolated case reports) Multivitamins containing vitamin K Inhibits warfarin; choose product with ≤ 30 mcg vitamin K Data from Dennehy, C. (2010, April 9-11). An evidence based look at popular dietary supplements. Presented at Clinical Pharmacotherapy 2010, University of California, Davis. 419 Introduction and general background
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affect warfarin stability, determine if these variables are transient or continuing, and review or reinforce topics in patient education that may explain the variation in the INR reading. If a subtherapeutic or supratherapeutic value can be explained by a transient change in a variable, the provider should adjust the dose for 1 or 2 days and then resume the prior dose, usually with follow-up in 1 or 2 weeks. 3. V ariables affecting warfarin stability (Carrier et al., 2009) include the following a. C hanges in other medications, including addi-tions or deletions of routine, over-the-counter, and herbal medications and dose changes of current medications b. I ntercurrent illness, especially febrile or diarrheal illness c. Die tary habits (wide swings in amount of intake or type of foods) d. A lcohol intake e. T ravel, which can alter lifestyle habits and dosing schedules f. I ssues of patient adherence 4. A p atient's response to chronic warfarin treatment may vary over time, and occasionally a previously stable patient requires a new weekly warfarin dose in the absence of any clear influencing variables. 5. The de gree of response to an INR out of range should also be based on the patient's risk category. For example, a single low value is more concerning for patients with a mechanical mitral valve than it is for  one with lone AF. A supratherapeutic value is more concerning when there is a high risk for falls or a past history of gastrointestinal bleeding. Patients at higher risk for complications require closer follow-up than patients at lower risk. 6. A lthough computer-based programs and warfarin dos-ing tables are available to aid clinicians in predicting maintenance dose (e. g., www. warfarindosing. org) these are not likely to take the place of a clinician's familiarity with a patient's case history. Some guide-lines for dose adjustments include the following: a. C hange the total weekly dose by approximately 10-15%, depending on the magnitude of the INR variation and the stability and risk profile of the patient. b. U se a single-strength tablet to propose a weekly dose schedule (e. g., two and three tablets alternating) or fractions (e. g., dose reduction from one tablet daily to half a tablet Monday, Wednesday, and Friday, and one tablet the other 4 days). Although dosing with one tablet strength is easier for some patients to manage than using tablets of different strengths, using a combination of 1-and 5-mg tablets offers good dosing flexibility for most patients. c. Befor e changing to a new dose, evaluate the patient's risk for confusion, dose error, practicality and cost of dose adjustment, and patient prefer-ence (Wong, Wilson, & Wittkowsky, 1999). 7. P atients with persistently unstable INRs may benefit from switching to brand Coumadin® or dispensing a generic from the same manufacturer each time (Wittkowsky, 2009b). 8. S ubtherapeutic INRs If an INR is below goal, inquire about recent change in vitamin K intake, along with the possibility of missed doses or an error in dosing. See T able 44-7 for addi-tional guidelines for evaluating a subtherapeutic INR. 9. S upratherapeutic INRs If an INR is above goal, inquire whether the patient has increased bruising or frank bleeding. An INR greater than 4 carries an increased risk of serious bleeding (Beyth, 2005). Inquire about intercurrent illness, acute dose error, recent addition of antibi-otics, or reduction in dietary vitamin K intake or in total dietary intake (T able 44-8). See T able 44-9 for specific guidelines for managing supratherapeutic INRs. Table 44-6 W arfarin Management: Questions to Ask at Follow-up Visits Current dose and tablet strength? Any changes in health status?Any unusual bruising or bleeding?Any change in diet?Any new medicines or supplements?Any change in medicines or supplements?Any falls?Any questions? Table 44-7 Evaluation of Subtherapeutic INR Dose error? (particularly missed dose)Increase in vitamin K intake? New medication or supplement? Change in medication or supplement?Improvement in heart or liver function?Change in usual manufacturer of tablet?420 CHAPTER 44 | Anticoagulation Therapy (Oral)
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B. To promote adherence and minimize error, warfarin dosing should be tailored to the individual patient. Some patients achieve their best INR control with one single-strength daily dose, although those less susceptible to confusion or error can manage a variable dose. Equal daily dosing causes less confusion and is associated with lower rates of dose error. However, using the same dose every day may require the patient to have tablets in more than one strength or to split tablets. Although warfarin comes in multiple strengths, many patients need a dose that falls somewhere in between these strengths. In many cases it is not possible to achieve a target INR with 7 days of equal dosing. C. The fundamentals of safe warfarin therapy should be reinforced frequently: 1. C larify warfarin tablet strength and dosing schedule at each visit. It should be clear to the patient whether the dosing instructions are given in terms of milligrams or tablets. It is most precise to talk with patients about their weekly dosing schedule in terms of specific milligrams per day rather than number of tablets per day. However, many patients know their warfarin only by its color and prefer instructions given in tablets per day. It is critical to patient safety that the patient, caregiver, and clinician have a clear mutual understanding of what dose is being recommended. II. patient education and safety A. Patient education is the cornerstone of safe and effective warfarin management. This requires that the patient have a basic understanding of the purpose and mechanism of anticoagulation. At the beginning of treatment it should be made clear to patients that although warfarin does slow clotting, it does not initiate bleeding. Warfarin comes in nine strengths; each strength is uniquely color coded, although shape and manufacturer do vary. The coding of color to strength helps to prevent dosing errors and to discover them quickly when they occur. Table 44-8 Possible Causes of Supratherapeutic INR Dose error Diet change Change in medicine or supplement Acute illness Decrease in liver function Decrease in cardiac function Change in usual manufacturer of tablet Laboratory error Table 44-9 Recommendations for the Management of Excessive Oral Anticoagulation or Bleeding INR supratherapeutic, but < 5 with no significant bleeding Lower or omit dose, monitor more frequently, resume at lower dose when INR is therapeutic. If only minimally elevated or associated with a transient variable, dose adjustment may not be necessary. INR > 5 but < 9, no significant bleeding Omit the next one or two doses, monitor more frequently, resume therapy at adjusted dose when INR is therapeutic. Alternatively, omit dose and give 1-2. 5 mg vitamin K orally, particularly for those at increased risk of bleeding. If more rapid reversal is required because the patient needs urgent surgery, give vitamin K ≥ 5 mg orally, expecting INR reduction within 24 hours. If INR remains high, give additional vitamin K of 1-2 mg. INR > 9, no significant bleeding Hold warfarin therapy and give a higher dose of vitamin K (2. 5-5 mg) orally, expecting INR to reduce significantly within 24-48 hours. Monitor the INR more frequently, give additional vitamin K if needed, and resume therapy at an adjusted dose when the INR is in therapeutic range. INR therapeutic or elevated with serious or life-threatening bleeding Hold warfarin therapy and give vitamin K by slow intravenous infusion along with fresh frozen plasma, prothrombin complex concentrate, or recombinant factor VIIa. For life-threatening bleeding, recombinant factor VIIa is supplemented with vitamin K, 10 mg by slow infusion, repeated as necessary. Data from Guyatt, G., Aki, E., Crowther, M., Gutterman, D., Schünemann, H. (2012). Executive Summary: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest, 141(Suppl. 2), 7S-47S. 421 Patient education and safety
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2. R einforce dietary guidelines and the need to report any significant changes. 3. R eport any signs of possible warfarin complications, which include unusual bruising, epistaxis, bleeding gums, hematuria, hematochezia, or melena. 4. R eport if any medicines or supplements have been started, changed, or discontinued. Avoid aspirin, NSAIDs, and all nonprescription medications unless approved by the clinician. 5. R eport any acute illness, especially vomiting or diarrhea, or significant change in health status. 6. A void activities that increase risk of injury, particularly contact sports. 7. C all the clinic or go to an acute care setting in case of a fall or serious injury, particularly head trauma. Because the most devastating potential complication of warfarin therapy is intracranial bleeding, even minor head trauma should prompt a call to the clinic or an urgent care visit. D. Special considerations 1. M ultiple providers: it is best to identify a single provider for warfarin management and prescription refills. This simple strategy can help to avoid potentially serious errors in dosing. 2. W omen and gynecological issues: women who are of childbearing age must be informed about the teratogenic risks of warfarin. They should be advised to use contraception at all times and to tell their clinician about future plans to become pregnant. They should also be counseled that warfarin may increase menstrual flow and/or duration. Because warfarin can unmask an existing gynecological issue in a woman of any age, patients should report unusual, heavy, or intermenstrual bleeding. 3. C ombined warfarin and antiplatelet therapy (often referred to as “dual” or “triple” therapy): some patients, such as those with coronary artery disease, may be prescribed warfarin as well as one or two antiplatelet agents (i. e., aspirin and clopidogrel [Plavix ®]). Because the bleeding risk has been shown to be significantly higher in these patients, the need for antiplatelet therapy should be carefully evaluated (Douketis et al., 2008). If the patient does require dual or triple therapy, one option is to lower the INR target within the limits of safety given the patient's indication for warfarin: For example, for a patient with AF and coronary artery disease (CAD) who is on an antiplatelet agent, the usual goal of 2-3 might be lowered to 2-2. 5 (Rossini et al., 2008). 4. P lanned interruptions of OAC: the relative risk of bleeding during a procedure versus developing a thrombus off anticoagulation determines whether and when an individual may need to interrupt warfarin. In a case of low risk for thrombosis, the dose  may be safely stopped 5 days before the procedure and resumed when the clinician performing the procedure deems it safe, usually the day of or day after the procedure. More complicated situations require  a decision tree as to whether to bridge the patient with low-molecular-weight heparin (LMWH) or lengthen the time off warfarin. A minority of patients considered high risk may require hospitalization for heparinization preceding and following their procedure. The CHADS 2 score can help with risk stratification for patients with AF who need to interrupt OAC treatment. A patient with a CHADS 2 score of 5-6 is considered to be high risk for TE when OAC is suspended (T able 44-10). Consensus regarding bridging for warfarin interruptions has been favoring not to bridge the AF patient except in certain high-risk situations. In a recent well-designed large study, not bridging was found to be noninferior to bridging and, as expected, bleeding risk was lowered (Douketis et al., 2015). 5. Or al procedures: some oral procedures can be safely performed at an INR of 2. The decision to alter warfarin dosing is based on how much bleeding the procedure may induce. See T able 44-11 for guidelines for oral procedures. 6. T ravel: Diets often change significantly when patients travel. Counsel patients to maintain their intake of vitamin K-rich food at its usual level and to maintain the usual 24-hour dosing interval across changing time zones. Table 44-10 Risk of Thromboembolism for Patients with AF Interrupting W arfarin Low risk CHADS2 score of 0-2 No history of CVA or TIA Moderate risk CHADS2 score of 3 or 4 High risk CHADS2 score of 5-6 Recent (i. e., within 3 months) stroke or TIA Rheumatic valvular heart disease Data from Douketis, J. D., Spyropoulos, A. C., Spencer, F. A., Mayr, M., Jaffer, A. K., Eckman, M. H., et al. (2012). Perioperative management of antithrombotic therapy: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest, 141(Suppl. 2), e326S-e350S. doi:10. 1378/chest. 11-2298. 422 CHAPTER 44 | Anticoagulation Therapy (Oral)
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Table 44-11 Guidelines for the Management of Anticoagulation During Oral Surgery Patients who require interventional or surgical procedures while they are taking anticoagulants can pose a therapeutic dilemma for clinicians. The need for alteration of anticoagulant therapy in patients undergoing general dentistry, periodontal, and oral surgical procedures is dependent on several factors including the intensity of anticoagulation, the type of procedure, and the likelihood of thrombosis versus bleeding. Because of the risk for thromboembolism, patients undergoing invasive procedures who require interruption of their anticoagulant therapy should have it interrupted for the shortest possible time period. The trend to lower intensity of anticoagulation allows many procedures to be performed without interruption of therapy while maintaining the INR at approximately 2. 0. All patients undergoing any procedure associated with a risk for bleeding should have the INR evaluated within 24 hours before the procedure. If interruption of therapy is necessary, it must be individualized. When therapy is interrupted, it should usually be resumed the evening of the procedure if hemostasis has been achieved. Low-Risk or Routine Procedures can usually be performed with an INR of 2-3 and include a. Routine hygiene and light scaling. b. Routine restorative procedures including fillings performed under local infiltrative anesthesia. c. Simple, single extractions. Multiple and surgical extractions may require modification of anticoagulant therapy. d. Sockets should be sutured and packed with a local hemostatic agent, such as Gelfoam or Surgicel®. Moderate-Risk Procedures can be performed with an INR of approximately 1. 5. a. Procedures requiring mandibular blocks to accomplish adequate local anesthesia. b. Deep scaling. c. Multiple extractions or other extensive periodontal surgery. d. Sockets should be sutured and packed with a local hemostatic agent, such as Gelfoam or Surgicel®. High-Risk Procedures should be performed only when the INR is normalized. Periprocedural heparinization in the hospital setting may be necessary for some patients, for example those with mechanical heart valves who are at a high risk of both bleeding and development of thrombosis. a. Multiple extractions or extraction of impacted teeth. b. Major reconstructive procedures. General Guidelines a. Aspirin and other nonsteroidal anti-inflammatory drugs should not routinely be used in most patients for postoperative analgesia because of their antiplatelet ef fect. An exception is once-daily aspirin, 81-325 mg, when prescribed for patients with a cardiovascular or cerebrovascular indication. This therapy should not be interrupted at any time and should be continued before and after the dental procedure. In addition, therapy with clopidogrel (Plavix ®) should not be interrupted when it is used in patients with drug-eluting stents. b. A thorough medication history should be obtained before the planned procedure. Keep in mind that herbal medications may also influence hemostasis. c. Prophylactic antibiotics are required for patients at risk of bacterial endocarditis. See the American Heart Association guidelines for recommendations. d. Patients should be instructed to avoid chewing hard foods, to avoid hot liquids, and to perform vigorous mouth washing for 24-48 hours after procedures. They should use external ice packs and biting pressure on gauze pads to control localized bleeding. e. T ranexamic acid mouthwashes have been suggested as an intervention to minimize bleeding after oral surgical procedures. In a well-designed 2003 study, a 5% solution of tranexamic acid used immediately after surgery and four times a day for 2 days was as effective as a 5-day course to reduce bleeding (Carter & Goss, 2003). f. Patients undergoing major procedures who have had anticoagulant therapy interrupted should be scheduled for a follow-up anticoagulation clinic appointment within 7-14 days. Patients who have required bridging with low-molecular-weight heparin need earlier follow-up. References Carter, G., & Goss, A. (2003). Tranexamic acid mouthwash: A prospective randomized study of a 2-day regimen vs. 5-day regimen to prevent post-operative bleeding in anticoagulated patients requiring dental extractions. International Journal of Oral and Maxillofacial Surgery, 32, 504-507. Carter, G., Goss, A., Lloyd, J., & Tocchetti, R. (2003). Tranexamic acid mouthwash versus autologous fibrin glue in patients taking warfarin undergoing dental extractions: A randomized prospective clinical study. Journal of Oral and Maxillofacial Surgery, 61, 1432-1435. (continues)423 Patient education and safety
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Table 44-11 Guidelines for the Management of Anticoagulation During Oral Surgery Dalen, J. E., & Hirsh, J. (Eds. ). (2008). Eighth ACCP Consensus Conference on Antithrombotic Therapy. Chest, 133, 67S-887S. Douketis, J. D. (2003). Perioperative anticoagulation management in patients who are receiving oral anticoagulant therapy: A practical guide for clinicians. Thrombosis Research, 108, 3-13. Douketis, J. D., Berger, P. B., Dunn, A. S., Jaffer, A. K., Spyropoulos, A. C., Becker, R. C., et al. (2008). The perioperative management of antithrombotic therapy: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest Supplement, 133(6, Suppl. ), 299S-339S. Dunn, A. S., & Turpie, A. G. G. (2003). Perioperative management of patients receiving oral anticoagulants. Archives of Internal Medicine, 163, 901-908. Ferrieri, G. B., Castiglioni, S., Carmagnola, D., Cargnel, M., Strohmenger, L., & Abati, S. (2007). Oral surgery in patients on anticoagulant treatment without therapy interruption. Journal of Oral and Maxillofacial Surgery, 65, 1149-1154. Nishimura, R. A., Carabello, B. A., Faxon, D. P., Freed, M. D., Lytle, B. W., O'Gara, P. T., et al. (2008). ACC/AHA 2008 guideline update on valvular heart disease: Focused update on infective endocarditis. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation, 118, 887-896. Wilson, W., Taubert, K. A., Gewitz, M., Lockhart, P. B., Baddour, L. M., Levison, M., et al. (2007). Prevention of endocarditis. Guidelines from the American Heart Association. Circulation, 116, 1736-1754. Addendum: preparation of 5% tranexamic acid mouthwash Tranexamic acid is freely soluble in water. A 500-mg tablet of tranexamic acid can be crushed and dispersed in 10 m L of water immediately before administration. Alternatively, a liquid can be prepared by mixing crushed tablets with water and then filtering out the insoluble excipients to give a clear solution. A maximum expiry date of 5 days is suggested for this preparation, which has not been formally tested. Adapted from Kayser, S. R., Kearns, G., & Smith, R. (2009). The Anticoagulation Clinic, Division of Oral Surgery, University of California San Francisco. III. tar get-specific anticoagulants No text discussing OAC would be complete without some focus on the recently introduced target-specific oral anti-coagulants (TSOACs), also called novel oral anticoagu-lants (NOACs) and direct oral anticoagulants (DOACs). There are currently two groups of TSOACs approved for use in the United States: direct thrombin inhibitors, dabi-gatran (Pradaxa ®) and factor Xa inhibitors [rivaroxaban (Xarelto®), apixaban (Eliquis®), and edoxaban (Savaysa®)] Both these groups act further down the clotting cascade than warfarin and thus have more predictable pharma-codynamics. Although the prothrombin time (PT) and partial thromboplastin time (PTT) are prolonged with all the TSOACs, this occurs in an unpredictable manner, and so these measures are not useful or reliable for drug activity monitoring. A. Advantages of the TSOACs: 1. F ixed oral dosing 2. R apid onset of action 3. F ew drug-drug interactions. However, patients do need to be screened for these since there are drugs that do interact. See the individual prescribing information (see Hellwig and Gulseth, 2013). 4. N ot affected by diet(Continued) 7. Di scontinuing warfarin: if a patient is at high risk of falls or of dose error (as may occur in dementia), or if the patient is unable or unwilling to adhere to monitoring schedules, the clinician should reevaluate if the risk of bleeding outweighs the possible benefits of treatment. Chronic warfarin treatment should prompt periodic review of the risk/benefit ratio for each individual patient. 8. S elf-testing: patients on lifelong anticoagulation sometimes ask about the possibility of self-testing at home with their own point-of-care-testing (POCT) device. This is a viable option for some, and many insurance companies now reimburse for the use of the machine and the testing supplies. Because POCT is not reliable for every patient, it is wise to run at least two simultaneous venipunctures to evaluate for concordance. Some patients show a persistent discordance and, in that case, are not candidates for self-testing. POCT/venipuncture discordance can also be a problem when the clinician is relying on home health POCT reports to evaluate warfarin levels. 9. S pecialty referral: patients at higher risk for bleeding (e. g., INR goal of >/= 3. 0) or thrombosis (an example of the latter is a patient who has had an arterial clot) may do best with services offering specialty management, such as a hematology or dedicated anticoagulation clinic. References (Continued)424 CHAPTER 44 | Anticoagulation Therapy (Oral)
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5. S evere hepatic dysfunction or any hepatic disease-associated coagulopathy 6. P regnant or breastfeeding women (insufficient data) 7. P rosthetic heart valve or severe valvular disease 8. M edication interactions (for instance, chronic use of an azole) 9. N o prescription insurance or unable to afford the copay 10. P ediatric patients (not FDA approved for pediatric use) F. Baseline studies recommended for good candidates for TSOAC use: 1. C omplete blood count with differential 2. L iver function tests (aspartate aminotransferase, alanine aminotransferase, total bilirubin) 3. R enal function studies (serum creatinine and creatinine clearance) 4. C oagulation studies (PT, PTT) G. Counseling patients about TSOACs When discussing and initiating a TSOAC, it is important to remind patients of the need for strict adherence to their dos-ing schedule. Although warfarin is fairly forgiving of minor dosing errors, this is not the case with the TSOACs. As is the case with warfarin, patients taking TSOACs should carry with them something that identifies them as taking an anticoagulant. There are a few medications that need to be avoided with TSOACS, and the patient should be given a list of these: (a) P-glycoprotein inhibitors/inducers: vera-pamil, amiodarone, dronedarone, macrolide antibiotics; and (b) CYP3A4 inhibitors/inducers: rifampin, phenytoin, carbamazepine, phenobarbital, St. John's wort, antifungals (econazole, ketoconazole), protease inhibitors. If a long-term interacting medication is needed, the TSOAC would be contraindicated because currently there is no way to dose adjust for interactions. As is the case with warfarin, patients on TSOACs should avoid NSAIDs and should not take aspirin (ASA) unless specifically recommended (ASA is often indicated for cardiac protection in CAD). Any surgery needs to be carefully planned, taking TSOAC use into account. We recommend consulting with an anticoagulation specialist when preparing these patients for treatment interruption. In conclusion, the TSOACs are probably as effective as warfarin for many indications and may result in fewer serious bleeds. However the decision whether to use a TSOAC must take into account in each case the individual patient risk-benefit profile. 5. N o need for routine coagulation monitoring (This can also be seen as a disadvantage, because there is no validated lab assay for measuring drug effect in patients on active medication. ) B. Disadvantages of TSOACs are: 1. Ad herence must be strict due to the short half-lives of these agents 2. A nticoagulant effect cannot be immediately reversed (The development of reversal agents is an area of continuing research. ) 3. M ore difficult to determine whether there is residual anticoagulant effect 4. M ore costly than warfarin, not always covered by insurance C. Indications and dosing T able 44-12 compares indications and dosing of the TSOACs currently approved for use in the United States. It should be noted that these agents are currently contraindicated for patients with prosthetic valves or significant valvular heart disease. Research to date shows noninferiority of the TSOACs to warfarin for approved indications. Bleeding rates are similar, but the TSOACs seem to confer a consistently lower risk for intracranial hemorrhage. The direct thrombin inhibitor dabigatran confers a higher risk of gastrointestinal bleeding compared to warfarin. Again, a major disadvantage to all the TSOACs is the lack of a reversal agent or antidote, although reversal agents are currently in trials. If a patient has been doing well on warfarin (i. e., has stable therapeutic INRs), it is not recommended that therapy be changed. As always, decisions regarding OAC should be individualized. D. Appropriate candidates for TSOAC: 1. H istory of medication adherence 2. H istory of unstable INRs unrelated to adherence problems 3. Di fficulty or hardship with INR monitoring E. Do not meet the following exclusions: 1. H istory of medication nonadherence2. H istory of underlying bleeding disorder or increased risk for bleeding 3. C reatinine clearance < 15 m L/min. Modified doses have not been well studied to date 4. L ow body weight (Use in patients with low body weight has not been well studied. )425 Target-specific anticoagulants
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Table 44-12 Indications and Dosing of TSOACs Approved for Use in the United States Dabigatran ( pradaxa®) Dosing Indication Renal Function ( c r c l m L/min) Recommended Dose Atrial fibrillation > 30 150 mg po twice daily 15-30 75 mg po twice daily Cr Cl < 15 or dialysis Avoid use Treatment of DVT/PE Cr Cl > 30 150 mg po twice daily after 5-10 days of parenteral therapy Cr Cl < 30 or on dialysis Avoid Rivaroxaban (Xarelto®) Dosing Indication Renal Function ( c r c l m L/min) Recommended Dose Atrial fibrillation (stroke prevention)> 50 20 mg po daily with evening meal 15-50 15 mg po once daily with evening meal < 15 Avoid use Treatment of DVT/PE ≥ 30 15 mg twice daily with food for 21 days, then 20 mg once daily with food < 30 Avoid use Knee replacement ≥ 30 10 mg once daily for 12-14 days < 30 Avoid use Hip replacement ≥ 30 10 mg once daily for 35 days < 30 Avoid use Apixaban ( e liquis®) Dosing Indication Recommended Dose Dose Adjustments Atrial fibrillation (stroke prevention)5 mg twice daily 2. 5 mg twice daily if any 2 of the following: Age ≥ 80 years Body weight ≤ 60 kg Serum creatinine ≥ 1. 5 mg/d L Treatment DVT/PE 10 mg twice daily x 7 d Followed by 5 mg twice daily After 6 months 2. 5 mg twice daily Prophylaxis after total knee arthroplasty/total hip arthroplasty (TKA/THA)2. 5 mg twice daily TKA 12 days, THA 35 days e doxaban (Savaysa) Dosing Indication Renal Function ( c r c l m L/min) Recommended Dose Atrial fibrillation (stroke prevention)> 50 ≤ 95 Do not use if > 9560 mg po once daily < 50 > 15 30 mg po once daily Treatment DVT/PE > 50 60 mg po once daily following 5-10 days parenteral anticoagulation 15-50 or body weight ≤ 60 kg 30 mg po once daily Used with permission from Dr. Steve Kayser, anticoagulation pharmacist, University of California, San Francisco. 426 CHAPTER 44 | Anticoagulation Therapy (Oral)
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Re Fe Rence S Ansell, J. E. (2009). The value of an anticoagulation management service. In J. Ansell, L. Oertel, & A. Wittkowsky (Eds. ), Managing oral anticoagula-tion therapy (3rd ed., pp. 1-8). St. Louis, MO: Wolters Kluwer Health. Battistella, M., Mamdani, M. M., Juurlink, D. N., Rabeneck, L., & Laupacis, A. (2005). Risk of upper gastrointestinal hemorrhage in warfarin users treated with nonselective NSAIDs or COX-2 inhibitors. Archives of Internal Medicine, 165, 189-192. Beyth, R. (2005). Assessing risk factors for bleeding. In J. Ansell, L. Oertel,  & A. Wittkowsky (Eds. ), Managing oral anticoagulation therapy (2nd ed., pp. 1-6). St. Louis, MO: Wolters Kluwer Health. Carrier, M., Grégoire, L. G., & Wells, P. S. (2009). Factors that influence warfarin effect. In J. Ansell, L. Oertel, & A. Wittowsky (Eds. ), Managing oral anticoagulation therapy (3rd ed., pp. 183-191). St. Louis, MO: Wolters Kluwer Health. Centers for Medicare and Medicaid Services. (2009). 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Retrieved from www. medscape. com/viewarticle/410539. U. S. Department of Agriculture, Agricultural Research Service, Nutrient Data Laboratory. (2015). USDA National Nutrient Database for Standard Reference, Release 28. Retrieved from www. ars. usda. gov/nea /bhnrc/ndl. Witt, D. M., Delate, T., Clark, N. P., Martell, C., T ran, T., & Crowther, M. A. ; Warfarin Associated Research Projects and other En Deavors (WARPED) Consortium. (2009). Outcome and predictors of very stable INR control during chronic anticoagulation therapy. Blood, 114, 952-956. Wittkowsky, A. K. (2009a). Initiation and maintenance dosing of warfarin and monitoring the INR. In J. Ansell, L. Oertel, & A. Wittkowsky (Eds. ), Managing oral anticoagulation therapy (3rd ed., pp. 173-182). St. Louis, MO: Wolters Kluwer Health. Wittkowsky, A. K. (2009b). Pharmacology of warfarin and related antico-agulants. In J. Ansell, L. Oertel, & A. Wittkowsky (Eds. ), Managing oral anticoagulation therapy (3rd ed., pp. 149-160). St. Louis, MO: Wolters Kluwer Health. Wolf, P. A., Abbott, R. D., & Kannel, W. B. (1991). Atrial fibrillation as an independent risk factor for stroke: The Framingham Study. Stroke, 22, 983-988. Wong, W., Wilson, N. J., & Wittkowsky, A. K. (1999). Influence of warfarin regimen type on clinical and monitoring outcomes in stable patients on an anticoagulation management service. Pharmacotherapy, 19, 1385-1391. 427 References
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previously known, especially for persons who are homeless or of low socioeconomic status who may be chronically exposed to violence and other forms of trauma (Bobo, Warner, & Warner, 2007; Meredith et al., 2009). Diagnosis of anxiety disorders in the primary care setting is often influenced by a number of factors. Many patients pres-ent with somatic complaints or problems with sleep. Some patients use substances to self-medicate symptoms. Substance use, although a separate problem, is often a symptom of an underlying disorder. It is imperative that providers adequately assess for such disorders. Cultural factors may also confound the diagnosis of anxiety disorders (Brenes et al., 2008). Each culture or demographic group has a set of norms for addressing mental health disorders, which may be influenced by stigma. Cultural identity involves not only ethnicity, acculturation and biculturalism, and language but also age, gender, socioeco-nomic status, sexual orientation, religious and spiritual beliefs, disabilities, political orientation, and health literacy, among other factors (APA, 2000). Anxiety disorders across a spectrum of intensity and clinical relevance may present at any time during the course of a primary care visit. It is normal for patients to feel nervous on first meeting with a stranger, including a new primary care provider. This must not be overinterpreted as a sign of a significant or enduring psychiatric condition for which treat-ment is indicated. Visiting an unfamiliar treatment center may cause a patient to present as anxious or distressed. Actual or perceived sociocultural differences between the provider and the patient may contribute to a greater chance of initial anxiety. T raditional office settings can be noisy, congested, and stressful environments, often requiring the patient to wait well beyond their appointment time. A sincere apology for causing a patient any inconvenience often goes far to help their situ-ational anxiety subside. Providers must evaluate anxiety symptoms for the pres-ence of an anxiety disorder. A provider should be aware of his or her personal biases, prejudices, or lack of knowledge pertaining to particular personal issues or cultural stan-dards of a given patient. Privacy must be ensured, and the I. Intr oduction and general background Anxiety disorders are commonly encountered, although often not adequately addressed, in the primary care setting. It is estimated that 8% of patients presenting for primary care services have a form of anxiety disorder, and the presence of such disorders may increase the disability of existing chronic medical conditions (Kroenke, Spitzer, Williams, Monahan, & Lowe, 2007). Despite increased awareness of the prevalence of these disorders, less than 40% of patients with anxiety are diagnosed and treated in the primary care setting (Kroenke et al., 2007). Although some providers hold the sentiment that treatment of mental health disorders in the primary care setting is too time consuming, lack of treatment prevents one from being able to adequately address physical health issues. In a study conducted by Weisberg, Beard, Moitra, Dyck, and Keller (2014), 51% of patients with anxiety disorders received pharmacotherapy from a primary care provider. Anxiety disorders can be adequately treated in primary care (Bandelow et al., 2012). Anxiety disorders contribute to functional impairments, disability, decreased health outcomes, comorbidity, and high use of health services. Given the impact of these disorders and the emerging trend toward the provision of integrated services, primary care providers should be equipped to properly screen and treat patients presenting with anxiety symptoms. The etiology of anxiety disorders involves environmental, biochemical, psychosocial, and genetic factors. Many types of anxiety disorders exist; however, this guideline focuses on the identification and treatment of the most common anxi-ety disorders: generalized anxiety disorder, social anxiety disorder, and panic disorder as well as posttraumatic stress disorder (PTSD) (American Psychiatric Association [APA], 2013). The most commonly found anxiety disorder is gener-alized anxiety, followed by panic disorder and social phobia (Kroenke et al., 2007). With improved screening by primary care providers, PTSD may be found to have higher rates than Esker-D Ligon Anx IEty© Eliks/Shutterstock; © donatas1205/Shutterstock 428 45Chapt Er
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l. P recipitating stressors, events, and losses (includ-ing community violence and vicarious trauma) m. S ubstance use: changes in types, frequency, and quantity of alcohol or drugs, including street drugs or prescribed medications n. P ast health history: history of other mental health disorders and medical illnesses causing or exacerbating signs and symptoms of anxiety (e. g., hyperthyroidism, attention deficit hyper-activity disorder [ADHD], major depression, bipolar disorder, and schizophrenia) B. Objective 1. A ppearance and kinetic behavior: restlessness, wringing hands, biting nails, shaking legs or feet, rocking, sitting unusually still, appearing tense, and altered grooming and hygiene. 2. M ental status examination which includes: appearance, mood, affect, speech, thought content, thought process, memory and concentration, and assessment of insight and judgment. 3. E vidence-based screening tools: it is advisable that primary care practice settings adopt a screening tool for early identification of comorbid anxiety disorders: a. The Ge neralized Anxiety Disorder 7-item (GAD-7) scale (see Figure 45-1) is a useful anxi-ety screening tool (Spitzer, Kroenke, Williams, & Lowe, 2006). The tool should be used to screen for the emergence of anxiety disorder symptoms. Screening should be repeated periodically to objectively measure changes after behavioral or psychotherapeutic intervention. b. DR EAMS mnemonic is a useful interview tool to screen for PTSD (Lange et al., 2000). i. D etachment (alexithymia) or feeling emotionally numb ii. R eexperiencing the event via nightmares, flashbacks iii. E vent with emotional effects, such as distress, feeling unsafe, fear iv. A voidance of reminder places, activities, or people v. M onth duration of symptoms or longer vi. Sy mpathetic hyperactivity (e. g., tachycardia, tachypnea, and insomnia) 4. Di agnostic studies: include laboratory testing for thyroid disorders, hormonal imbalances, substance intoxication or occult use, electrolyte imbalances, vitamin B 12 deficiency, hypo-or hyperglycemia. 5. C ollateral data: include information from members of a multidisciplinary treatment team when possible. With the permission of the patient, a brief discussion provider must assume a nonjudgmental tone about anything that the patient may be encouraged to reveal. Even when the provider inquires in a warm, nonjudgmental manner, some topics are inherently difficult for patients to discuss. They may feel embarrassed and guarded, and the interviewer may need to phrase questions in different ways and repeatedly. Throughout any clinical encounter the provider needs to be alert for signs of increased agitation, such as increasing rest-lessness or pacing, clenched fists, verbal threats or pressured or loud speech. When one detects such agitation, it is advis-able to refrain from further discussion of distressing topics that are not germane to the patient's current presentation (Lange, Lange, & Cabaltica, 2000). II. Database (may include but is not limited to) A. Subjective 1. S ymptomatology and relevant supporting data Patients may present with a variety of complaints related to anxiety disorders. Providers should inquire about the duration of symptoms, effect of symptoms on patient's functioning, and relationships between symptoms and contributory factors. Providers should assess for the following:a. F eelings of nervousness, anxiety, panic, excessive worry, or feeling generally stressed and overwhelmed b. N egative thoughts, ruminative or obsessive thinking; unrelenting pessimism, feelings of foreboding, and excessive guilt c. Adr energic effects: irregular heartbeat, tachy-cardia, and palpitations; shortness of breath, diaphoresis, lightheadedness, paresthesias, and tremor d. S leep disturbances including insomnia, hyper-somnia, nightmares, and restless sleep e. M arked avoidance of specific situations and social withdrawal f. R estlessness, irritability, agitation, and excessive anger g. A ppetite disturbance h. Di fficulty with memory or concentration i. P ersistent sense of fear, foreboding, apprehen-sion, and hypervigilance j. S uicidality: ideation, thoughts of being better off dead or that life is not worth living, and planned or attempted suicidal acts k. S omatic complaints: headaches, gastrointestinal complaints, back and neck pain, chest pain, and excessive concern with physical health429 Database
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Figure 45-1 Generalized Anxiety Disorder 7-Item (GAD-7) Scale Reproduced from Pfizer. (n. d. ). GAD-7. Retrieved from www. phqscreeners. com. Developed by Drs. Robert L. Spitzer, Janet B. W. Williams, Kurt Kroenke, and colleagues, with an educational grant from Pfizer Inc. No permission required to reproduce, translate, display, or distribute. Scoring and interpretation table modified from www . lifesolutionsforyou. com. GAD-7 Over the last 2 we eks, how often have you been bothered by the following problem s? (Use “” to indica te your answer)Not at all Several days More than half the days Nearly every day 1. Feeling nervous, anxious or on edge 0 1 2 3 2. Not be ing ab le to stop or control worrying 0 1 2 3 3. Worrying too much about differen t things 0 1 2 3 4. Trouble relaxing 0 1 2 3 5. Being so restless that it is hard to sit still 0 1 2 3 6. Becoming easily a nnoyed or irritable 0 1 2 3 7. Feeling af raid as if something aw ful 0 1 2 3 might happen Total Score __ __ =____ + ____ + ____ Scoring and Inte rpretation: GAD-2 Scor e Provisio nal Diag nosis 0-2 No ne 3-6 Probable anxiety di sorder *GAD-2 is the fi rst 2 questions of the GAD-7GAD-7 Scor e Provisio nal Diag nosis 0-7 None 8+ Pr obable anxiety di sorder430 CHAPTER 45 | Anxiety
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with family members or friends may yield corrobo-rating or missing information about manifestations of the patient's anxiety or provide perspective on the cause, duration, intensity, and possible remedies of the patient's condition. Collateral contacts may also yield helpful information regarding suicidal state-ments, failure to eat or function normally, or use of substances. III. Assessment A. Determining a diagnosis Refer to the diagnostic criteria and/or decision trees for anxiety in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, published by the American Psychiatric Association (2013), or the DSM-5 Handbook of Differential Diagnosis (First, 2013). The DSM-5 classi-fication and the specific diagnostic criteria are meant to serve as guidelines to be informed by clinical judgment in the categorization of the patient's conditions and are not meant to be applied in a rote fashion. The following are summarized criteria for anxiety and trauma and stressor-related disorders common to primary care settings. In gen-eral, symptoms should not be attributable to the effects of a substance or another medical or psychiatric condition. 1. P anic attack: a feature of many anxiety disorders characterized by the following: a. P alpitations or rapid heart rate b. Sw eating c. T rembling or shaking d. S hortness of breath e. F eeling of choking f. C hest pain, pressure, or discomfort g. N ausea or stomach upset h. Di zziness or lightheadedness i. F eelings of unreality or self-detachment j. F ear of dying k. N umbness or tingling of extremities l. C hills or hot flushes 2. P anic disorder: recurrent unexpected panic attacks and at least one of the attacks has been followed by at least a month of one of the following symptoms: persistent worry about having another attack, worry about the consequences of the attack, or significant change in behavior related to attacks. 3. Ge neralized anxiety disorder: excessive anxiety and worry about a variety of situations. Patients report difficulty controlling the anxiety, and it interferes with their ability to function. Anxiety is associated with at least three of six symptoms as noted previously. 4. S ocial anxiety disorder: fear of being embarrassed or humiliated in social or performance situations when exposed to unfamiliar people or possible scrutiny by others. Exposure to feared situation provokes anxiety, and in some cases a panic attack. In most cases, the patient recognizes fear is excessive or unreasonable. The feared situation is avoided or experienced with intense anxiety; avoidance may interfere with normal functioning or cause marked distress. 5. A goraphobia a. F ear about being in situations that would be difficult to escape or in which help would not be available if a panic attack was experienced b. S ignificant avoidance of such situations, enduring situations in distress, or requiring a companion to function 6. P TSD a. C ondition may be acute (lasting > 1 month but < 3 months) or chronic (lasting > 3 months). b. P erson has been exposed to an event in which they witnessed or experienced something that threatened life, serious injury, or damage to per-sonal integrity; their response included intense fear, helplessness, or horror and lasts for longer than 1 month. The traumatic event is reexperi-enced in one of four ways:i. I ntrusive distressing recollections of the event. ii. Di stressing dreams or nightmares of the event. iii. H aving a sense of reliving the event, including flashbacks and hallucinations. iv. I ntense psychologic or physiologic response to triggers and cues reminiscent of the event c. P ersistent avoidance of stimuli associated with the trauma including avoidance of triggers associated with trauma, inability to remember important details of trauma, anhedonia, isola-tion, restricted emotions, and sense of shortened lifespan. d. I ncreased state of arousal evidenced by sleep disturbance, irritability, poor concentration, hypervigilance, or becoming easily startled. B. Functional assessment and severity of illness 1. C onsider the patient's current clinical status, psychosocial factors affecting the clinical situation, the patient's highest level of past functioning, and the patient's quality of life. 2. A f unctional assessment may be useful for assessing strengths and disease severity and should focus on the patient's ability to perform essential activities of daily living. Information gathered may also facilitate the monitoring of treatment by assessing important beneficial and adverse effects of treatment. 431 Assessment
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IV. Plan Anxiety disorders are a common and often disabling mental disorder. T reatment is indicated when symptoms of the disorder interfere with functioning or cause significant distress. Effective treatment for anxiety disorders should lead not only to reduction in frequency and intensity of symp-toms but should optimally yield full remission of symptoms and return to a premorbid level of functioning. A range of evidence-based psychosocial and pharmacologic interven-tions exist for treatment of anxiety disorders and should be instituted for all patients requiring treatment. The treatment plan is ideally collaboration between the patient, the provider, and other members of the treatment team. It should include a combination of biologic and socio-cultural interventions to create an integrated treatment plan. Optimally, interventions should encourage recovery from illness through community integration and empower patients to make choices that improve their quality of life. Considerations that guide the choice of an initial treatment modality include patient preference, the risks and benefits of treatment, past treatment history, presence of co-occurring conditions, cost, and treatment availability. A. Medication selection When making the decision to use pharmacologic treat-ments, providers must consider a patient's ability to remain compliant with treatment. Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reup-take inhibitors (SNRIs) are regarded as first-line agents for treatment of anxiety disorders. Before selecting a specific medication one must balance the risks associated with the medication against the benefits of treatment and con-sider the following: potential side effects, potential drug interactions or contraindications, pharmacologic prop-erties, co-occurring medical and psychiatric conditions, and the strength of the evidence for the particular medi-cation in treatment of anxiety disorders. With regard to co-occurring psychiatric conditions, it is imperative that the potential for bipolar disorder be assessed. T reatment with certain agents can precipitate mania. Please refer to the chapter on depression for a list of medications commonly used to treat anxiety and depres-sion. The use of benzodiazepines is often a controver-sial issue. Additionally, the treatment of PTSD is often complex and may require a specialty referral. Benzodiazepines are appropriate as monotherapy only in the absence of a co-occurring mood disorder and may be preferred (as monotherapy or in combination with antidepressants) for patients with very distressing or impairing symptoms in whom rapid symptom con-trol is critical. The benefit of rapid response must be bal-anced against the potential for depressive and sedative side effects and physiologic dependence that may lead to difficulty discontinuing the medication. Addition of ben-zodiazepines to an SSRI or SNRI is a common augmen-tation strategy to target residual symptoms. They are also commonly used to treat severe presentations initially with another agent, followed by a gradual taper of the benzodi-azepine. When the goal is to prevent panic attacks rather than reduction of symptoms after an attack has occurred, a regular dosing schedule rather than an “as needed” sched-ule is preferred. In such instances, agents with a longer half-life, such as clonazepam, may provide better coverage than short half-life agents, such as lorazepam. PTSD may manifest with a variety of physical and psychiatric symptoms, which must be addressed to successfully treat this disorder. T reatment often requires a multidisciplinary approach, including polypharmacy in some cases (Bobo et al., 2007). Severe cases should be referred to a psychiatric or mental health clinician. Refer to T able 45-1 for possible pharmacotherapeutic options to treat PTSD. B. Medication management 1. E ducate patients about the likely course of treatment associated with a particular medication. Pharmacotherapy should generally be continued for 1 year or more after acute response to promote further symptom reduction and decrease risk of recurrence. 2. P atients with anxiety disorders can be sensitive to medication side effects; thus, low starting doses of medications are recommended with a gradual increase to a full therapeutic dose over several days and as tolerated by the patient. Underdosing of antidepressants is common in treatment of anxiety disorders and is a frequent source of partial response or nonresponse. 3. M edication monitoring involves assessment of the change in symptoms, such as frequency and intensity of panic attacks, level of anticipatory anxiety, degree of agoraphobic avoidance, quality of sleep, persistence of somatic symptoms, and severity of interference and distress related to anxiety disorders. a. P atients typically require monitoring every 1-2 weeks when first starting a new medication, then every 2-4 weeks until the dose is stabilized. b. L ess frequent monitoring is required after stabilization and reduction of symptoms. 4. Di scontinuation of medication should be performed in a gradual and collaborative manner. This allows for continual assessment of the effects of the taper, the patient's response to any changes that emerge, and, if required, treatment may be reinitiated at a previously effective dose. However, medications can be discontinued much more quickly in urgent conditions, such as pregnancy. Before advising a 432 CHAPTER 45 | Anxiety
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Table 45-1 Pharmacotherapeutic Options for T reating PTSD Medication Starting Dose (mg) Effective Dose (mg) Maximum Dose/Day First line Fluoxetine (Prozac®) 20 mg/day 20-40 mg/day 200 mg/day Paroxetine (Paxil®) 20 mg/day 20-50 mg/day 50 mg/day Sertraline (Zoloft®) 50 mg/day 50-200 mg/day 80 mg/day Citalopram (Celexa®) 20 mg/day 20-40 mg/day 60 mg/day Escitalopram (Lexapro®) 10 mg/day 10-20 mg/day 20 mg/day Fluvoxamine (Luvox®) 50 mg/day 50-300 mg/day 300 mg/day Non-SSRI antidepressants Venlafaxine, Venlafaxine ER (Effexor®)37. 5-75 mg BID 75-225 mg Most people use venlafaxine ERVaries from 225-375 mg/day depending on the targeted condition and the medication preparation Mirtazapine (Remeron®) 15 mg q. h. s. 15-45 mg q. h. s. 45 mg/day Trazodone (Desyrel®) 25-50 mg q. h. s. 25-150 mg q. h. s. 200 mg/day Amitriptyline (Elavil®, Amitid®, Amitril®)—TCA25-100 mg q. h. s. 50-150 mg/day 300 mg/day Doxepin (Adapin®, Sinequen®)—TCA 25 mg q. h. s. 150-300 mg q. h. s. 300 mg/day Imipramine (Tofranil®, Presamine®, Janimine®)—TCA*off-label use25 mg q. h. s. 150-300 mg q. h. s. 300 mg/day Nortriptyline (Pamelor®, Aventyl®)—TCA*off-label use25 mg q. h. s. 50-150 mg q. h. s. 150 mg/day Augmenting agents Antiadrenergic agents Prazosin 1 mg BID 5-20 mg/day 40 mg/day Clonidine 0. 1 mg BID 0. 2-1. 2 mg/day 2. 4 mg/day Guanfacine 1 mg q. h. s. 1-2 mg/day 3 mg/day Propranolol (Inderal ®) 20-40 mg BID 160-480 mg/day 640 mg/day Mood stabilizers/anticonvulsants *Should refer to a psychiatric specialist if required for treatment Lamotrigine (Lamictal®) 25-50 mg/day 50-250 mg BID 500 mg/day Gabapentin (Neurontin®) 300 mg q. h. s. 300-600 mg TID 3,600 mg/day Atypical antipsychotics *Should refer to a psychiatric specialist if required for treatment Risperidone (Risperdal®) 1 mg/day 1-3 mg BID 6 mg/day Olanzapine (Zyprexa®) 25-5 mg/day 5-20 mg/day 20 mg/day Quetiapine (Seroquel®) 25 mg/day 150-750 mg/day divided BID-TID800 mg/day Miscellaneous agents Zolpidem (Ambien®) 5 mg q. h. s. 5-10 mg q. h. s. 10 mg/day Zaleplon (Sonata®) 5 mg q. h. s. 5-10 mg q. h. s. 20 mg/day Diphenhydramine (Benadryl®) 25 mg q. h. s. 25-50 mg q. h. s. 50 mg/day Buspirone (Bu Spar) 7. 5 mg BID 30 mg/day 60 mg/day *Hydroxyzine is an additional antihistamine medication that is useful for the treatment of anxiety at doses of 10-100 mg daily, in split doses. Modified from Bobo, W., Warner, C., & Warner, C. (2007). The management of post traumatic stress disorder (PTSD) in the primary care setting. Southern Medical Journal, 100(8), 797-801. 433 Plan
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regimens have been proven helpful at addressing anxiety in some cases (van der Watt, Laugharne, & Janca, 2008). D. Referral to specialty care As a primary care provider, it is important to have the ability to differentiate cases that can be managed in one's own setting from more severe cases that require consultation or referral to dedicated psychiatric care. If  response to an adequate trial of a first-line treatment (e. g., CBT, SSRI, or serotonin-norepinephrine reuptake inhibitor) is unsatisfactory, it is appropriate for the provider and the patient to consider a change to another treatment. Decisions about whether and how to make changes depends on the level of response or lack thereof to the initial treatment, the feasibility of other treatment options, and the severity of remaining symptoms and impairment. After first-and second-line treatments and augmentation strategies have been exhausted, either because of lack of efficacy or patient intolerance, pro-viders are encouraged to consult with experienced colleagues or refer the patient to dedicated psychiatric services. V. Special populations A. Dually diagnosed patients There is a high prevalence of self-medication with alcohol and other substances by persons with anxiety disorders (Arch, Craske, Stein, Sherbourne, & Roy-Byrne, 2006). It is often advantageous for patients to receive inte-grated treatment of both conditions (Mueser, Noordsy, Drake, & Fox, 2003). Patients often decrease their use of substances once the underlying anxiety is effectively addressed (Denning & Little, 2000). Providers should exercise caution when prescribing medications because of potential interactions with substances of abuse. Extreme caution should be used when using benzodiazepines to treat patients using alcohol or opiates. Patients should be educated about the additive effects of the previously mentioned substances. B. Pregnant women For women with anxiety disorders who are pregnant, nursing, or planning to become pregnant, psychosocial interventions should be implemented. Pharmacotherapy may be indicated but requires discussion of the poten-tial benefits and risks with the patient and, her obstetri-cian. Such discussions should also consider the potential risks to the patient and the child of untreated psychiatric illness, including anxiety disorders and any co-occurring psychiatric conditions. taper of effective pharmacotherapy, one should consider the patient's history of previous mood or anxiety disorder episodes, the duration of symptom remission, the presence of current or impending psychosocial stressors in the patient's life, and the extent to which the patient is motivated to discontinue the medication. This discussion should also include the possible outcomes of taper, including discontinuation symptoms and recurrence of panic symptoms. C. Psychosocial interventions Psychosocial treatment is recommended for pregnant women and other patients who prefer nonpharmacologic treatment and can invest the time and effort required to attend weekly sessions. Psychosocial treatments for anxiety disorders should be conducted by professionals with an appropriate level of training and experience in the relevant approach. 1. C ognitive-behavioral therapy (CBT): CBT is a time-limited treatment, generally 10-15 weekly sessions, that yields durable effects. It can be successfully administered individually or in a group format. CBT and other psychosocial treatments are not readily available in some geographic areas. Self-directed forms of CBT may be useful for patients who do not have ready access to a trained CBT therapist. CBT for anxiety disorders generally includes psychoeducation, self-monitoring, countering anxious beliefs, exposure to fear cues, modification of anxiety-maintaining behaviors, and relapse prevention. 2. C ombined treatment should be considered for patients who have failed to respond to monotherapy, and may also be used under certain clinical circum-stances (e. g., using pharmacotherapy for temporary control of severe symptoms that are impeding the patient's ability to engage in psychosocial treatment). Such treatment may also enhance long-term out-comes by reducing the likelihood of relapse when pharmacologic treatment is stopped. 3. Othe r group therapies: patient support groups are not recommended as monotherapy, although they may be useful adjuncts to other effective treatments for some patients. 4. C ouples or family therapy may be helpful in addressing co-occurring relationship dysfunction. When initiating treatments for anxiety disorders, educate significant others about the nature of the disorder, enlisting their assistance to improve treatment adherence. 5. C omplementary and alternative medicine methods, such as tai chi and meditation, and regular exercise 434 CHAPTER 45 | Anxiety
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REf EREnc ES American Psychiatric Association. (2013). Diagnostic and statistical manual of mental health disorders (5th ed. ). Washington, DC: Author. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental health disorders (4th ed. ), text revision. Washington, DC: Author. Arch, J., Craske, M., Stein, M., Sherbourne, C., & Roy-Byrne, P. (2006). Correlates of alcohol use among anxious and depressed primary care patients. General Hospital Psychiatry, 28, 37-42. Bandelow, B., Sher, L., Bunevicius, R., Hollander, E., Kasper, S., Zohar, J., et al. (2012). Guidelines for the pharmacological treatment of anxiety disorders, obsessive-compulsive disorder, and posttraumatic stress disorder in primary care. International Journal of Psychiatry in Clinical Practice, 16(2), 77-84. Bobo, W., Warner, C., & Warner, C. (2007). The management of post traumatic stress disorder (PTSD) in the primary care setting. Southern Medical Journal, 100(8), 797-801. Bourne, E. (2005). The anxiety and phobia workbook (4th ed. ). Oakland, CA: New Harbinger. Brenes, G., Knudson, M., Mc Call, W., Williamson, J., Miller, M., & Stanley, M. (2008). Age and racial differences in the presentation and treatment of generalized anxiety disorder in primary care. Journal of Anxiety Disorders, 22, 1128-1136. Denning, P., & Little, J. (2000). Practicing harm reduction psychotherapy: An alternative approach to addictions. New Y ork, NY: Guilford. First, M. (2013). DSM-5 handbook of differential diagnosis. Arlington, VA: APA. Kroenke, K., Spitzer, R., Williams, J., Monahan, P., & Lowe, B. (2007). Anxiety disorders in primary care: Prevalence, impairment, comorbidity, and detection. Annals of Internal Medicine, 146(5), 317-325. Lange, J., Lange, C., & Cabaltica, R. (2000). Primary care treatment of post-traumatic stress disorder. American Family Physician, 62(5), 1035-1040, 1046. Meredith, L., Eisenman, D., Green, B., Basurto-Davila, R., Cassells, A., & T obin, J. (2009). System factors affect the recognition and management of posttraumatic stress disorder by primary care clinicians. Medical Care, 47(6), 686-694. Mueser, T., Noordsy, D., Drake, R., & Fox, L. (2003). Integrated treatment for dual disorders: A guide to effective practice. New Y ork, NY: Guilford. Spitzer, R. L., Kroenke, K., Williams, J. B. W., & Lowe, B. (2006). A brief measure for assessing generalized anxiety disorder: The GAD-7. Archives of Internal Medicine, 166, 1092-1097. van der Watt, G., Laugharne, J., & Janca, A. (2008). Complementary and alternative medicine in the treatment of anxiety and depression. Current Opinion in Psychiatry, 21(1), 37-42. Weisberg, R. B., Beard, C., Moitra, E., Dyck, I., & Keller, M. B. (2014). Adequacy of treatment received by primary care patients with anxiety disorders. Depression and Anxiety, 31(5), 443-450. C. Older adults There are important safety considerations for SSRIs, tricyclic antidepressants, and benzodiazepines, which include increased risk of falls and osteoporotic fractures in patients age 50 and older. Caution and careful moni-toring are indicated when prescribing medications to elderly patients, because they may produce sedation, fatigue, ataxia, slurred speech, memory impairment, and weakness. Check the American Geriatrics Society Beers Criteria Medication List at www. dcri. org for potentially harmful medications in the elderly. D. Children and adolescents Children and adolescents may present with different symptoms than adults. Please refer to the DSM-5 for further information. There is also a higher risk of suicidality as a potential adverse effect of SSRIs and other antidepressants in this population. Psychotherapy is the first-line treatment for children and adolescents with anxiety disorders. VI. Self-management r esources and tools A. Patient and client educational handouts and resources 1. E ducational handouts for patients and families can be found at www. nimh. nih. gov. Many handouts are available in multiple languages and are updated periodically. 2. The Anxiety and Phobia Workbook (Bourne, 2005). 3. N ational Alliance for the Mentally Ill (NAMI), www . nami. org 4. N ational Center for PTSD website (www. ptsd. va . gov/) has factsheets and resources for patients and providers. 5. A nxiety Disorders Association of America website (www. adaa. org) has resources for patients and providers. 435 References
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civilizations, where exposure to infections is limited resulting in persistence of Th2 dominance in genetically susceptible children (Brooks, Pearce, & Douwes, 2013; Busse & Lemanske, 2001). B. Prevalence Asthma affects 25 million people in the United States (Centers for Disease Control and Prevention, 2011) and more than 300 million worldwide (World Health Organization, 2007). Early in life the prevalence of asthma is higher in boys, but at puberty the gender ratio shifts toward girls and asthma is seen predominantly in women after puberty. Asthma exacerbations are responsible for more than $37 billion in direct costs annually in the United States (Kamble & Bharmal, 2009). Severe asthma affects approxi-mately 10% of the population with asthma and accounts for 50% of asthma-related health costs (Sullivan et al., 2007). C. Factors that precipitate or aggravate asthma 1. A llergens: Exposure to aerosolized allergens (aero-allergens) for people who are sensitized to them is an important precipitant of asthma. Outdoor allergens are primarily pollens from trees and plants that occur in seasonal waves. Patients with these sensitivities have more frequent exacerbations during the time of heavy pollination if they are sensitized. Even more important are the perennial indoor allergens (molds, house dust mites, cockroaches, and animal dander) because of the length of time people stay indoors. 2. I rritants: The most important airway irritant exposure is environmental tobacco smoke. Other irritants include bleach, sprays like perfume, strong odors (paint fumes, cooking gas, and wood smoke) and air pollution, with increased exposure in closed, poorly ventilated areas. 3. M edication and drugs: Some medications are known to trigger airway constriction through neural or metabolic pathways. These include β-blockers, aspirin, and nonsteroidal anti-inflammatory drugs. I. Intr oduction and general background Asthma is an inflammatory disease of the airways character-ized by airflow obstruction that is reversible (at least partially) either spontaneously or with treatment. Airway inflammation and bronchospasm cause recurring symptoms of wheezing, coughing, breathlessness, and the sensation of chest tight-ness that occurs particularly at night or early morning. The obstruction to airflow in the airways is the result of mucosal inflammation caused by inflammatory cell infiltration with neutrophils, eosinophils, and lymphocytes, in addition to mast cell activation and epithelial cell injury. Airway inflam-mation contributes to hyperresponsiveness of the airway and airway narrowing caused by bronchoconstriction of airway smooth muscle. In some patients, persistent changes in airway structure occur, resulting in airway remodeling and airflow limitation that are not fully reversible. A. Pathogenesis The etiology of asthma is unknown but the strongest predictor for developing asthma is atopy, the genetic predisposition for development of an immunoglobulin (Ig) E-mediated response to common aeroallergens. Viral respiratory infections may also contribute and are the most important cause of asthma exacerbations. There is considerable variability in the pattern of airway inflamma-tion indicating phenotypic differences of expression that may influence response to treatment. Onset of asthma for most people begins early in life with recurrent wheezing, atopic disease, and a history of parental asthma. Understanding of the pathogenesis of asthma is evolv-ing as genetic and phenotypic variations are identified. Research has focused on an imbalance of Th1 and Th2 cytokines in allergic diseases including asthma that result in either overexpression of Th2 or underexpression of Th1 cells. Th2 cells mediate inflammation, whereas Th1 cells respond to infection. The “hygiene hypothesis” illus-trates how this imbalance may occur, as in westernized Susan L. Janson ASthm A I n Ado L e S cent S A nd Adu Lt S© Eliks/Shutterstock; © donatas1205/Shutterstock 436 46Chapt Er
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x. M edications (e. g., aspirin, other nonsteroidal anti-inflammatory drugs, β-blockers) xi. F ood, food additives, and preservatives (e. g., sulfites) xii. C hanges in weather and exposure to cold air xiii. E ndocrine factors (e. g., menses, pregnancy, and thyroid disease) xiv. C omorbid conditions (e. g., sinusitis, allergic rhinitis, GERD, and allergic responses to specific foods or alcohol) 2. P ast health history a. A ge of onset of disease b. H istory of emergency department visits, hospi-talizations, need for intubation, and mechanical ventilation c. N eed for systemic or oral corticosteroids and frequency of use d. H istory of exacerbations i. P rodromal signs and symptoms ii. R apidity of onset and duration and frequency iii. S everity (need for urgent care, hospitaliza-tion, or intensive care unit care) iv. I mpact (number of days missed from work or school, limitation of activities, nocturnal awakening, and economic impact) 3. F amily history: Allergies, atopy, or asthma 4. O ccupational and environmental history: Work-related exposures, such as vapors, gas, dusts, fumes, isocyanates, or cedar 5. P ersonal and social history: T obacco smoking and secondhand tobacco exposure 6. R eview of systems a. C onstitutional signs and symptoms: fatigue caused by sleep disruption. b. Ea r, nose, and throat: congestion, sneezing, runny nose, sinus headache, and postnasal drip. c. R espiratory: recurrent wheezing, cough, breath-lessness, chest tightness, and increased mucus production. d. C ardiac: palpitations during times of severe breathlessness. e. G astrointestinal: heartburn or dyspepsia. f. P sychiatric: anxiety or depression. B. Objective 1. P hysical findings a. Ge neral appearance: anxious, labored breathing, hyperexpansion of the chest (especially in chil-dren), use of accessory muscles, hunched shoul-ders, and deformed chest b. Ea r, nose, and throat: pale and boggy nasal mucosa, thin and watery nasal secretions, red 4. Othe r factors that can worsen asthma: Sulfites found in beer, wine, and food; strong emotions; cold air; weather changes; exercise; and viral infections are common triggers for asthma symptoms. 5. C omorbid conditions that exacerbate asthma: Among the chronic conditions that make asthma harder to control are gastroesophageal reflux disease (GERD), rhinitis and sinusitis, obesity, and chronic stress and depression. Evidence is stronger for the first two, but efforts should be made to treat and control all of these conditions when present. II. d atabase (may include but is not limited to) A. Subjective 1. S ymptom description: The most common signs and symptoms of asthma are intermittent dyspnea, cough, and wheezing. These symptoms occur together creating a well-recognized syndrome. a. P resenting symptoms: recurrent wheezing, shortness of breath, chest tightness, cough that is worse at night, and sputum production b. P attern of symptoms i. P erennial, seasonal, or both ii. C ontinual, episodic, or both iii. On set, duration, and frequency (number of days or nights per week or month) iv. Diur nal variations, especially nocturnal and on awakening in early morning c. P recipitating or aggravating factors i. V iral respiratory infections ii. E nvironmental allergens, indoor (e. g., mold, house dust mite, cockroach, and animal dander or secretions) and outdoor (e. g., pollen) iii. H ome characteristics (age, location, heating and cooling system, wood-burning stove, humidifier, carpeting over concrete, molds or mildew, floor coverings, and stuffed or upholstered furniture) iv. S moking (patient or others in home or work) v. E xercise vi. O ccupational chemicals or allergens vii. E nvironmental change (relocation or remodeling) viii. I rritants (secondhand tobacco smoke, strong odors, air pollutants, dusts, particu-lates, vapors, gases, and aerosols) ix. E motions (e. g., fear, anger, frustration, hard crying or laughing) or stress437 Database
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visits or hospitalizations in the last year, intubation or intensive care unit admission for asthma in the last 5 years, patient report of feeling in danger from asthma, depression, and certain demographic charac-teristics (female, nonwhite, not using corticosteroid medication, and current smoking). 2. C lassify asthma control (T able 46-2): Asthma can be classified as well controlled, not well controlled, or very poorly controlled. Asthma control is classified when the patient is currently on a controller medication, considering domains of impairment and risk. Control is the degree to which the symptoms, impairments, and risk are minimized and the goals of therapy are met. Control is assessed by symptoms, night-time awakenings, need for a short-acting β-agonist for relief of symptoms, ability to engage in usual activities and the frequency of exacerbations requiring treatment with oral corticosteroids. Several standardized questionnaires have been developed for the assessment of asthma control as reported by patients. 3. A ssess responsiveness to therapy: Responsiveness is the ease with which asthma control is achieved by therapy. C. Significance and motivation Assess the significance of asthma to the patient and family, including how much asthma interferes with quality of life, work, and play. Determine willingness and ability to follow the treatment plan and properly inhale medications. IV. Goals of clinical management to control asthma A. Reduce impairment 1. P revent chronic symptoms and night-time awakenings 2. R equire only infrequent use of short-acting β-agonist (infrequent use is ≤ 2 d/wk) for quick relief of symptoms 3. M aintain normal (or near normal) lung function 4. M aintain normal activity levels: exercise and attendance at work and school B. Reduce risk 1. P revent recurrent exacerbations and minimize need for urgent care 2. P revent progressive loss of lung function; for youth, prevent reduced lung growth 3. P rovide optimal pharmacotherapy with minimal or no adverse effectsor streaked posterior pharynx, and thrush (associated with inhaled corticosteroid use [ICS]) c. L ungs: diffuse or scattered expiratory wheezes, prolonged expiration, wheezing with forced exha-lation, and decrease in air entry and movement d. C ardiac: tachycardia (if hypoxic or if recently used beta-agonists) e. S kin: atopic dermatitis or eczema; pallor or cyanosis (if hypoxic) 2. S upporting data from relevant diagnostic tests, such as bronchoprovocation and especially spirometry. III. Assessment A. Differential diagnosis 1. A sthma 2. C hronic obstructive pulmonary disease (COPD) (e. g., emphysema and/or chronic bronchitis) 3. U pper airway disease: allergic rhinitis and sinusitis 4. V ocal cord dysfunction 5. Obs tructions of large airways (foreign body, tumor, and lymph nodes) 6. Obs tructions of small airways (cystic fibrosis, bronchiolitis, and bronchopulmonary dysplasia) 7. R ecurrent cough secondary to medications 8. A spiration 9. C ongestive heart failure B. Asthma severity, control, and response to treatment 1. C lassify asthma severity (T able 46-1) as intermittent, mild persistent, moderate persistent, or severe persistent. Severity of asthma is the intrinsic intensity of the disease and is most easily determined when the patient is not on long-term treatment. Severity is measured in two domains: impairment and risk. Impairment is assessed by history of symptoms, nocturnal awakenings, short-acting beta 2-agonists use for relief of symptoms, activity limitation and by spirometry to assess airway caliber. It is impor-tant to assess the quantity and quality of sleep, limits to desired activity, and need for medication to gain a full picture of impairment. If these components are missed in history-taking asthma severity may be misclassified. Risk is assessed by the likelihood of frequent exacerbations, also assessed by history and by forced expiratory volume in 1 second (FEV 1). Predictors of asthma exacerbation include severe air-flow obstruction, two or more emergency department 438 CHAPTER 46 | Asthma in Adolescents and Adults
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and physical examination are not reliable ways to exclude other causes of respiratory impairment. The key measures are FEV 1, forced vital capacity (FVC), and FEV1/FVC ratio. For those who cannot sustain expiration for the length of time necessary to measure FVC, FEV in 6 seconds is used as a substitute for FVC. Significant reversibility is demonstrated by an V. Plan A. Diagnostic tests 1. P ulmonary function testing (spirometry) (Figure 46-1): Spirometry, which measures airflow obstruction, is needed to diagnose asthma because medical history Table 46-1 Classifying Asthma Severity and Initiating T reatment in Adolescents ≥ 12 Years of Age and Adults components of Severity  c lassifying of Asthma Severity Intermittent Persistent m ild m oderate Severe Impairment Normal FEV1/FVC: 8-19 yr 85% 20-39 yr 80% 40-59 yr 75% 60-80 yr 70%      Symptoms ≤ 2 d/wk ≥ 2 d/wk but not daily Daily Throughout the day Nighttime awakenings≤ 2 times per month3-4 times per month> 1 per week but not nightly Often 7 times per week Short-acting β 2-agonist use for symptom control (not prevention of EIB)≤ 2 d/wk > 2 d/wk but not daily, and not more than one time on any day Daily Several times per day Interference with normal activity None Minor limitation Some limitation Extremely limited Lung function Normal FEV 1 between exacerbations FEV 1 > 80% predicted FEV 1/FVC normal FEV1 > 80% predicted FEV 1/FVC normal FEV1 > 60% but < 80% predicted FEV 1/FVC reduced 5%FEV1 < 60% predicted FEV 1/FVC reduced > 5% Risk Exacerbations requiring oral systemic corticosteroids  0-1/yr (see note) ≥ 2/yr (see note) ← Consider severity and interval since last exacerbation. Frequency and severity may fluctuate over time for patients in any severity category. Relative annual risk of exacerbation may be related to FEV 1. Recommended step for initiating treatment    Step 1  Step 2 Step 3  Step 4 or 5 and consider short course of oral systemic corticosteroids In 2-6 weeks, evaluate level of asthma control that is achieved and adjust therapy accordingly. Abbreviations: EIB, exercise-induced bronchospasm; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity. ICU, intensive care unit. The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs. Level of severity is determined by assessment of both impairment and risk. Assess impairment domain by patient's and caregiver's recall of previous 2-4 weeks and spirometry. Assign severity to the most severe category in which any feature occurs. At present, there are inadequate data to correlate frequencies of exacerbations with different levels of asthma severity. In general, more frequent and intense exacerbations (e. g., requiring urgent, unscheduled care, hospitalization, or ICU admission) indicate greater underlying disease severity. For treatment purposes, patients who had ≥ 2 exacerbations requiring oral systemic corticosteroids in the past year may be considered the same as patients who have persistent asthma, even in the absence of impairment levels consistent with persistent asthma. Reproduced from National Heart, Lung and Blood Institute, National Asthma Education and Prevention Program, & National Institutes of Health. (2007). Expert panel report 3: Guidelines for the diagnosis and management of asthma (Publication No. 08-5846). Bethesda, MD: Author. 439 Plan
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Table 46-2 Assessing Asthma Control and Adjusting Therapy in Adolescents ≥ 12 Y ears of Age and Adults    c lassifying of Asthma c ontrol Well c ontrolled n ot Well c ontrolled Very Poorly c ontrolled Impairment     Symptoms ≤ 2 d/wk > 2 d/wk Throughout the day Nighttime awakenings ≤ 2 times per month 1-3 times per week ≥ 4 times per week Interference with normal activity None Some limitation Extremely limited Short-acting β 2-agonist use for symptom control (not prevention of EIB)≤ 2 d/wk > 2 d/wk Several times per day FEV 1 or peak flow > 80% predicted/ personal best60-80% predicted/personal best< 60% predicted/personal best Validated questionnaire ATAQACQACT0≤ 0. 75*≥ 201-2≥ 1. 516-193-4N/A≤ 15 Risk  Exacerbations requiring oral systemic corticosteroids 0-1/yr ≥ 2/yr (see note) Consider severity and interval since last exacerbation Progressive loss of lung function Evaluation requires long-term follow-up care Treatment-related adverse effects:Medication side effects can vary in intensity from none to very troublesome and worrisome. The level of intensity does not correlate to specific levels of control but should be considered in the overall assessment of risk. Recommended action for treatment Maintain current step. Regular follow-ups every 1-6 months to maintain control. Consider step down if well controlled for at least 3 months. Step up 1 step and Reevaluate in 2-6 weeks. For side effects, consider alternative treatment options. Consider short course of oral systemic corticosteroids. Step up 1-2 steps, and Reevaluate in 2 weeks. For side effects, consider alternative treatment options. Abbreviations: EIB, exercise-induced bronchospasm; ICU, intensive care unit. *ACQ values of 0. 76-1. 4 are indeterminate regarding well-controlled asthma. The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs. The level of control is based on the most severe impairment or risk category. Assess impairment domain by patient's recall of previous 2-4 weeks and by spirometry or peak flow measures. Symptom assessment for longer periods should reflect a global assessment, such as inquiring whether the patient's asthma is better or worse since the last visit. At present, there are inadequate data to correspond frequencies of exacerbations with different levels of asthma control. In general, more frequent and intense exacerbations (e. g., requiring urgent unscheduled care, hospitalization, or ICU admission) indicate poorer disease control. For treatment purposes, patients who had ≥ 2 exacerbations requiring oral systemic corticosteroids in the past year may be considered the same as patients who have not-well-controlled asthma, even in the absence of impairment levels consistent with not-well-controlled asthma. Validated questionnaires for the impairment domain (the questionnaires do not assess lung function or the risk domain). ATAQ = Asthma Therapy Assessment Questionnaire © (see sample in “Component 1: Measures of Asthma Assessment and Monitoring”). ACQ = Asthma Control Questionnaire© (user package may be obtained at www. qoltech. co. uk or juniper@qoltech. co. uk). ACT = Asthma Control Test TM (see sample in “Component 1: Measure of Asthma Assessment and Monitoring”). Minimal important difference: 1. 0 for the ATAQ; 0. 5 for the ACQ; not determined for the ACT. Before step up in therapy:Review adherence to medication, inhaler technique, environmental control, and comorbid conditions. If an alternative treatment option was used in a step, discontinue and use preferred treatment for that step. Reproduced from National Heart, Lung and Blood Institute, National Asthma Education and Prevention Program, & National Institutes of Health. (2007). Expert panel report 3: Guidelines for the diagnosis and management of asthma (Publication No. 08-5846). Bethesda, MD: Author. 440 CHAPTER 46 | Asthma in Adolescents and Adults
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B. Management 1. M edications: A stepwise approach to pharmacologic therapy is recommended (T able 46-3) a. Quick relief “rescue” medications are short-acting β2-agonists. These include albuterol-HFA and levalbuterol-HFA, which are prescribed for any severity of asthma. Patients should be instructed to inhale two puffs every 4-6 hours as needed for symptoms of asthma. They also may be used 20-30 minutes before exercise to prevent exercise-induced bronchospasm. b. L ong-acting “controller” medications i. IC S are the most effective to reduce airway inflammation and control persistent asthma. (See T able 46-4 showing the estimated comparative daily doses for inhaled corticosteroids. ) For patients who have had well-controlled asthma for at least 3  months, it is essential to step down therapy to identify the minimum medica-tion necessary to maintain control. ii. L ong-acting β2-agonists (LABA) added if asthma is not controlled with ICS alone. Do not use LABA as monotherapy. Consider discontinuing LABA when control is achieved. iii. C onsider combined ICS and LABA in one inhaler if asthma is not controlled by ICS alone. iv. W hen initiating therapy monitor at 2-to 4-week intervals to ensure that asthma control is achieved. v. C onsider adding a leukotriene receptor antagonist (e. g., montelukast [sold as Singulair®] if allergies are a strong compo-nent of the asthma. c. A nti-Ig E therapy: Omalizumab (Xolair®) i. C onsider for adolescents older than 12  years and adults with severe uncon-trolled asthma, skin or in vitro test positive to perennial allergens, and elevated Ig E. Omalizumab is given subcutaneously under direct observation. ii. Be ale rt to the possibility of anaphylaxis which has been reported to occur up to 24 hours after giving this medication. 2. E nvironmental control a. R educe exposure to allergens to which the patient is sensitized and exposed (dust mites, animal dander, mold, cockroach, and pollens). increase in FEV 1 or FVC of 200 m L and greater than or equal to 12% change from baseline after inhaling two puffs of albuterol at 90  mcg/puff (Pellegrino et al., 2005). Some patients with the symptoms of asthma do not demonstrate reversibility until they have a 2-week trial of oral corticosteroids. 2. C hest radiograph to exclude other causes of airway obstruction 3. A llergy testing by skin tests or in vitro tests 4. E xhaled nitrous oxide testing to detect inflammation 5. Add itional pulmonary function tests that are not routinely necessary but can be useful when considering alternative diagnoses: a. Flo w-volume loops to assess the presence of inspiratory airflow obstruction b. B ronchoprovocation challenge testing with metha-choline or cold air may be helpful when asthma is  suspected but spirometry is normal or near normal. c. Di ffusing capacity to assess for emphysema d. T otal lung volumes to assess for restrictive venti-latory defects. 8 6420Flow L-s-1-2-4-6-8 024 Volume LInspiration Expiration 6 Figure 46-1 Flow-V olume Loop Generated by Spirometry Reproduced from Pellegrino, R., Viegi, G., Brusasco, V., Crapo, R. O., Burgos, F., Casaburi, R., et al. (2005). Interpretive strategies for lung function tests. European Respiratory Journal, 26, 948-968. Reprinted with permission from the European Respiratory Society. 441 Plan
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Table 46-3 Stepwise Approach for Managing Asthma in Adolescents ≥ 12 Y ears of Age and Adults Key: Alphabetical order is used when more than one treatment option is listed within either preferred or alternative therapy. EIB, exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, long-acting inhaled beta2-agonist, LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting beta2-agonist. Notes: The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs. If alternative treatment is used and response is inadequate, discontinue it and use the preferred treatment before stepping up. Zileuton is a less desirable alternative due to limited studies as adjunctive therapy and the need to monitor liver function. Theophylline requires monitoring of serum concentration levels. In step 6, before oral corticosteroids are introduced, a trial of high-dose ICS + LABA + either LTRA, theophylline, or zileuton may be considered, although this approach has not been studied in clinical trials. Step 1, 2, and 3 preferred therapies are based on Evidence A; step 3 alternative therapy is based on Evidence A for LTRA, Evidence B for theophylline, and Evidence D for zileuton. Step 4 preferred therapy is based on Evidence B, and alternative therapy is based on Evidence B for LTRA and theophylline and Evidence D zileuton. Step 5 preferred therapy is based on Evidence B. Step 6 preferred therapy is based on Expert Panel Report 3 (EPR3; National Heart, Blood, and Lung Institute, 2007) and Evidence B for omalizumab. Immunotherapy for steps 2-4 is based on Evidence B for house dust mites, animal dander, and pollens; evidence is weak or lacking for molds and cockroaches. Evidence is strongest for immunotherapy with single allergens. The role of allergy in asthma is greater in children than in adults. Clinicians who administer immunotherapy or omalizumab should be prepared and equipped to identify and treat anaphylaxis that may occur. Reproduced from National Heart, Lung and Blood Institute, National Asthma Education and Prevention Program, & National Institutes of Health. (2007). Expert panel report 3: Guidelines for the diagnosis and management of asthma (Publication No. 07-4051). Bethesda, MD: Author. Persistent Asthma: Daily Medication Consult with asthma specialist if step 4 care or higher is required. Consider consultation at step 3. Intermitt ent Asthma Preferred: SABA PRNPreferred: Low-dose ICS Alternative: Cromolyn,LTRA,Nedocromil, or Theophylline Preferred: Low-dose ICS+ LABA ORMedium-dose ICS Alternative: Low-dose ICS+ either LTRA,Theophylline,or Zileuton Preferred: Medium-dose ICS+LABA Alternative: Medium-dose ICS+either LTRA,Theophylline,or Zileuton Preferred: High-dose ICS +LABA AND Consider Omalizumab forpatients whohave allergies Preferred: High-dose ICS+LABA+oral corticosteroid ANDConsider Omalizumab forpatients whohave allergies Step up if needed (/f_irst, check adherence, environmental control, and comorbid conditions) Each step: Patient education, environmental control, and management of comorbidities. Steps 2-4: Consider subcutaneous allergen immunotherapy for patients who hav e allergic asthma (see notes). Quick-relief medication for all patients SABA as needed for symptoms. Intensity of treatment depends on se verity of symptoms: up to 3 treatments at 20-minute intervals as needed. Short course of oral syste mic cort icostero ids may be needed. Use of SABA >2 days a week for symptom relief (not pr evention of EIB) generally indicates inadequate control and the need to step up treatment. Step down if possibl e (and asthma is well controlled at least 3 months)Assess control Step 1Step 2Step 3Step 4Step 5Step 6 442 CHAPTER 46 | Asthma in Adolescents and Adults
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Table 46-4 Estimated Comparative Daily Doses: Ages 12 Y ears and Older medication daily dose Low m edium h igh Beclomethasone MDI 80 to 240 micrograms more than 240 to 480 microgramsmore than 480 micrograms 40 micrograms per puff 1 to 3 puffs twice a day 4 to 6 puffs twice a day   80 micrograms per puff 1 puff a. m., 2 puffs p. m. 2 to 3 puffs twice a day 4 or more puffs twice a day Budesonide DPI 180 to 540 microgramsmore than 540 to 1,080 microgramsmore than 1,080 micrograms 90 micrograms per inhalation1 to 3 inhalations twice a day    180 micrograms per inhalation1 inhalation a. m., 2 inhalations p. m. 2 to 3 inhalations twice a day4 or more inhalations twice a day Budesonide Nebules not applicable not applicable not applicable 0. 25 mg not applicable not applicable not applicable 0. 5 mg not applicable not applicable not applicable 1. 0 mg not applicable not applicable not applicable Ciclesonide MDI 160 to 320 microgramsmore than 320 to 640 microgramsmore than 640 micrograms 80 micrograms per puff 1 to 2 puffs twice a day 3 to 4 puffs twice a day   160 micrograms per puff   2 puffs twice a day 3 or more puffs twice a day Flunisolide MDI 320 micrograms more than 320 to 640 microgramsmore than 640 micrograms 80 micrograms per puff 2 puffs twice a day 3 to 4 puffs twice a day 5 puffs or more twice a day Fluticasone MDI 88 to 264 micrograms more than 264 to 440 microgramsmore than 440 micrograms 44 micrograms per puff 1 to 3 puffs twice a day     110 micrograms per puff   2 puffs twice a day 3 puffs twice a day 220 micrograms per puff   1 puff twice a day 2 or more puffs twice a day Fluticasone DPI 100 to 300 microgramsmore than 300 to 500 microgramsmore than 500 micrograms 50 micrograms per inhalation1 to 3 inhalations twice a day    100 micrograms per inhalation  2 inhalations twice a day 3 or more inhalations twice a day 250 micrograms per inhalation  1 inhalations twice a day 2 or more inhalations twice a day Mometasone DPI 110 to 220 micrograms more than 220 to 440 microgramsmore than 440 micrograms 110 micrograms per inhalation1 to 2 inhalations p. m. 3 to 4 inhalations p. m. or 2 inhalations twice a day3 or more inhalations twice a day 220 micrograms per inhalation1 inhalation p. m. 1 inhalation twice a day or 2 inhalations p. m. 3 or more inhalations divided in two doses Reproduced from National Heart, Lung, and Blood Institute, & National Institutes of Health. (2012). Asthma care quick reference: Diagnosing and managing asthma. Retrieved from http://www. nhlbi. nih. gov/health-pro/guidelines/current/asthma-guidelines/quick-reference-html#estimated-comparative-daily-doses. 443 Plan
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b. Effe ctive allergen avoidance requires a multi-faceted, comprehensive approach (e. g., carpets harbor dust mites so remove or vacuum often; use allergen-proof mattress and pillow covers to protect against dust mites; wash all bed linens in hot water at least every 2 weeks; eliminate any cockroach infestation and do not leave food or garbage out or exposed; remove mold and mildew; and repair leaks). c. A void exposure to environmental tobacco smoke and other respiratory irritants (wood smoke, perfume, strong odors and fumes, bleach, and cleaning products). d. A void exertion outside when air pollution levels are high. e. A void use of nonselective β-blockers. f. A void sulfite-containing food and foods to which the patient is sensitive. 3. T reat and control comorbid diseases that aggravate asthma a. A llergic rhinitis or sinusitis (consider leukotriene receptor antagonist, antihistamine, nasal cortico-steroid spray, and nasal saline washes). b. GER D: consider use of a proton pump inhibitor; elevate head of bed at night; no food at bedtime; and decrease use of alcohol and caffeine. See chapter on GERD for further suggestions. c. Othe r conditions that make asthma harder to control include obesity, depression, family barriers to self-management, and vocal cord dysfunction. 4. C onsider specialty consultation for uncontrolled asthma that has not responded to maximal therapy, when allergy immunotherapy or omalizumab is being considered, or when exacerbations require hospitalizations. 5. F ollow-up should be at frequent intervals until control is achieved and then at 3-to 6-month intervals to maintain control. More frequent follow-up is determined by individual characteristics, past history, and psychosocial factors that increase risk. C. Patient education and training in self-management of asthma 1. El icit the patient's concerns and questions regarding asthma. Box 46-1 Instructions for u sing a m etered-d ose Inhaler With or Without a Spacer 1. T o begin, shake the inhaler five or six times. 2. Remove the mouthpiece cover. If using a spacer, place the spacer over the mouthpiece at the end of the inhaler. 3a. Use of a metered-dose inhaler without a spacer: Put your lips and teeth over the inhaler mouth-piece and breathe in slowly. As you do so, squeeze the top of the canister once. Keep inhaling even after you finish the squeeze. Continue inhaling slowly and deeply. 3b. Use of the metered-dose inhaler with a spacer: Put your lips and teeth over the mouthpiece. Squeeze the top of the canister once and then breathe in slowly. Keep inhaling even after you finish the squeeze. Continue inhaling slowly and deeply. 4. After inhaling, remove the inhaler or spacer from your mouth and hold your breath for up to 10 seconds. 5. Rinse your mouth after using the inhaler. If you need another dose of medication, repeat the previous steps. Box 46-2 P atient Instructions for u sing a d ry Powder d isk Inhaler 1. Hold the disk level in one hand. With the other hand, put your thumb in the appropriate notch and push it away from you as far as it goes. The mouthpiece will appear and snap into place. 2. Keep the disk horizontal. Again with your thumb, slide the lever away from you until it clicks. The disk is now ready to deliver medication. Breathe out all the way away from the mouthpiece prior to inhalation from the dry powder inhaler. 3. Put your lips around the mouthpiece. Breathe in quickly and deeply through your mouth—not your nose. 4. After inhaling, remove the disk from your mouth and hold your breath for up to 10 seconds. 5. T o close the disk, put your thumb in the notch and slide it back toward you as far as it goes. The disk will click shut, and the lever will automatically return to its original position. The disk is now ready for your next dose. 6. Rinse your mouth after using the inhaler. Ask your pharmacist for a demonstration when you pick up the medication from the pharmacy. 444 CHAPTER 46 | Asthma in Adolescents and Adults
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2. D escribe airway inflammation and bronchospasm. 3. T each the patient how to recognize and avoid individual triggers: explain the cumulative effect of precipitating factors. 4. I nstruct the patient not to smoke and to avoid secondhand smoke. 5. R eview all of the patient's medications, including the purpose, actions, dosage, side effects, and interactions. Explain how each medication works to relieve, control, or prevent asthma signs and symptoms. Box 46-3 Instructions for u sing a d ry Powder tube Inhaler Flexhaler® 1. T o begin, hold the inhaler in the upright position and twist the cover off and set it down. 2. Next, load the dose of medication. T wist the base grip to the right as far as it will go. Twist it back to the left. You will hear a click, which means it is ready to go. 3. Y ou do not need to shake the inhaler. Breathe out all the away from the mouthpiece prior to inhalation from the dry powder inhaler. 4. Bring the inhaler to your lips in a horizontal posi-tion. Put your lips over the tube and take a fast and powerful deep breath. Continue inhaling quickly and deeply. 5. Hold your breath for up to 10 seconds. 6. If you need another dose of medication, repeat the previous steps. The tube inhaler is designed to deliver one dose at a time. 7. Do not blow into your inhaler after loading a dose because the medication will become saturated with condensation and dif ficult to dispense. 8. When you are finished, place the cover back on the inhaler and twist shut. Keep your inhaler dry and store it at room temperature. 9. Rinse your mouth after using the inhaler. Asthmanex Twisthaler® 1. T o begin, hold the inhaler in the upright position and grip the white cap. 2. T urn the cap counter-clockwise while keeping the inhaler in an upright position, then lift off the cap. As the cap is lifted off, the dose counter counts down. 3. Breathe out all the way away from the inhaler. 4. Bring the inhaler to your lips in a horizontal posi-tion. Put your lips over the mouthpiece and take a fast and powerful deep breath. Continue inhaling quickly and deeply. Do not cover the ventilation hole while inhaling. 5. Remove the inhaler from your mouth and hold your breath for about 10 seconds. 6. Wipe the mouthpiece dry and put the cap back on, Turn the cap in a clockwise direction as you gently press down. You will hear a click to let you know the cap is fully closed. 7. Rinse your mouth after using the inhaler. Box 46-4 P atient e ducation Supplement: Peak e xpiratory Flow Rate m onitoring What is a peak expiratory flow rate? Peak expiratory flow rate is a measurement of the highest speed at which you can blow out air when you exhale as hard and as fast as you can. This measure-ment tells us how much impediment, or obstruction, there is in your airways. Flow rates decrease when asthma obstructs, or narrows, your airways. Flow rates are normal when there is no, or minimal obstruction of your airways. What are the steps to measuring a peak expiratory flow rate? 1. Place the indicator at the base of the numbered scale. 2. Stand up or sit up straight with head erect. 3. T ake a deep breath. 4. Place the meter in your mouth and close your lips around the mouthpiece. 5. Blow out as hard and as fast as possible. 6. W rite down the achieved measurement. This is where the indicator stops. 7. Repeat this process two more times. 8. Record the highest of the three measurements. When and how often should you measur e and record peak flow rates? You and your provider will plan this during your visits. Modified from National Heart, Lung, and Blood Institute, National Asthma Education and Prevention Program. (1997). Expert panel report 2: Guidelines for the diagnosis and management of asthma (NIH Publication No. 97-4051). Bethesda, MD: Author. 445 Plan
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patient should call his or her provider, increase or add medications, or go to the emergency department (Figure 46-2). 9. E ncourage adequate hydration, proper nutrition, and adequate rest. 10. E ncourage the patient to keep regular appointments for follow-up and evaluation, even if the symptoms of asthma are not present. Step 1, 2, and 3 preferred therapies are based on Evidence A; step 3 alternative therapy is based on Evidence A for LTRA, Evidence B for theophylline, and Evidence D for zileuton. Step 4 preferred therapy is based on Evidence B, and alternative therapy is based on Evidence B for LTRA and theophylline and Evidence D zileuton. Step 5 preferred therapy is based on Evidence B. Step 6 preferred therapy is based on EPR 2 (National Heart, Blood, and Lung Institute, 1997) and Evidence B for omalizumab. Immunotherapy for steps 2-4 is based on Evidence B for house dust mites, animal danders, and pollens; evidence is weak or lacking for molds and cock-roaches. Evidence is strongest for immunotherapy with single allergens. The role of allergy in asthma is greater in children than in adults. Clinicians who administer immunotherapy or omalizumab should be prepared and equipped to identify and treat anaphylaxis that may occur. Source: National Heart, Lung, and Blood Institute. (2007). Expert panel report3: Guidelines for the diagnosis and management of asthma (NIH Publication No. 07-4051). Bethesda, MD: Author. D. Asthma education resources 1. A merican Academy of Allergy, Asthma, and Immunology: www. aaaai. org 2. A merican Lung Association: www. lung. org 3. A ssociation of Asthma Educators: www . asthmaeducators. org 4. N ational Heart, Lung, and Blood Institute Information Center: www. nhlbi. nih. gov 5. U. S. Environmental Protection Agency: www. airnow . gov VI. Futur e update topics in asthma A. The National Heart, Lung, and Blood Advisory Council Asthma Expert Working Group 1. The N ational Heart, Lung, and Blood (NHLB) Advisory Council Asthma Expert Working Group recently released an assessment of potential areas for 6. D emonstrate the proper use of the metered-dose inhaler or dry powder inhaler and also spacer device for metered-dose, inhaler containing corticosteroid medication (Boxes 46-1 through 46-3). Have the patient demonstrate proper use periodically or at each follow-up visit. 7. F or patients who meet the criteria for moderate-persistent or severe-persistent asthma, demonstrate the use and rationale of peak flow meters (for use at home or in the office) before the initiation of therapy. See the Patient Education Supplement: Peak Expiratory Flow Rate Monitoring (Box 46-4). Recommend daily morning measurements on awakening before inhaling medications. T each the patient how to measure and interpret the peak flow rate readings (Box 46-5). Provide written guidelines for what the patient should do when the readings fall below a specified level. 8. H ave a written action plan directing the patient what to do during an exacerbation. Include when the Box 46-5 Instructions for u sing a Peak Flow  m eter The peak flow meter helps you to monitor your asthma by measuring the maximum airflow you can blow out of your lungs. Ask your clinician about where to set the color-coded indicators. They can help determine the status of your airflow. 1. T o begin, hold the meter by the handgrip. Slide the measurement arrow to the bottom of the scale, next to the mouthpiece. (One device requires you to shake the arrow to the bottom of the device). 2. Raise the meter horizontally, inhale deeply from room air, then place your mouth over the mouth-piece and blow forcefully. Make sure your lips act as a seal over the mouthpiece so that no air escapes. Make sure your tongue is not in the mouthpiece. 3. The measurement arrow will slide up the scale. The number that it stops on is your peak flow reading. 4. Repeat the test two more times. Each time, remem-ber to slide the measurement arrow back to its start position near the mouthpiece. Remember the high-est reading of your three blows. 5. Record the highest reading, with the date and time. Y our clinician will help determine a personal-ized scale to use with your meter, dependent on your age, height, and gender. 446 CHAPTER 46 | Asthma in Adolescents and Adults
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Asthma Action Plan PROVIDERINSTRUCTIONS Atinitialpresentation,determinethelevelofasthmaseverity Level of severity is determined by both impairment and risk and is assigned to the most severe category in which any feature occurs. Stepwiseapproachformanagingasthma: Therapy is increased (stepped up) if necessary and decreased (stepped down) when possible as determined by the level of asthma severity or asthma control. Atsubsequentvisits,assesscontroltoadjusttherapy Level of control is determined by both impairment and risk and is assigned to the most severe category in which any feature occurs. Address adherence to medication, inhaler technique,and environmental control measures. Sample patient self-assessment tools for asthma control can be found at http://www. asthmacontrol. com/index. html http://www. asthmacontrolcheck. com FORMOREINFORMATION: Toaccess the August 2007 full version of the NHLBI Guidelines for the Diagnosis and Treatment of Asthma (EPR-3) or the October 2007 Summary Report, visit http://www. nhlbi. nih. gov/guidelines/asthma/index. htm. Asthma severity and asthma control include the domainsof current impairment and future risk. Impairment: frequency and intensity of symptoms and functional limitations the patient is currently experiencing or has recently experienced. Risk: the likelihood of either asthma exacerbations, progressive decline in lung function (or, for children, reduced lung growth), or risk of adverse effects from medication. HOWTOUSETHEASTHMAACTIONPLAN: Topcopy(forpatient): Enter specific medication information and review the instructions with the patient and/or family. Educate patient and/or family about factors that make asthma worse and the remediation steps on the back of this form. Completeandsignthebottomoftheform andgivethiscopyoftheformtothepatient. Middlecopy(forschool,childcare,work,etc): Educate the parent/guardian on the need for their signature on the back of the form in order to authorize student self-carry and self-administration of asthma medications at school and also to authorize sharing student health information with school staff. Providethiscopyoftheformtothe school/childcarecenter/work/caretakeror otherinvolvedthirdparty. (Thiscopymay alsobefaxedtotheschool,etc. ) Bottomcopy(forchart): Filethiscopyinthepatient'smedicalchart. 2008, Public Health Institute (RAMP)ASTHMAMANAGEMENTRECOMMENDATIONS: — Ensure that patient/family receive education about asthma and how to use spacers and other medication delivery devices. — Assess asthma control at every visit by self-administered standardized test or verbal history. — Perform spirometry at baseline and at least every 1 to 2 years for patients >5 years of age. — Update or review the Asthma Action Plan every 6 to 12 months. — Perform skin or blood allergy tests for all patients with persistent asthma. — Encourage patient/family to continue follow-up with their clinician every 1 to 6 months even if asthma is well controlled. — Refer patient to a specialist if: there are difficulties achieving or maintaining control OR step 4 care or higher is required (step 3 care or higher for children 0-4 years of age) OR immunotherapy or omalizumab is considered OR additional testing is indicated OR if the patient required 2 bursts of oral systemic corticosteroids in the past year or a hospitalization. ENGLISH Figure 46-2 Asthma Action Plan447 Future update topics in asthma
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potential update in the Guidelines of the Diagnosis and Management of Asthma (NHLB Advisory Council Asthma Expert Working Group, 2015). These five topics have the highest priority for new systematic literature review and potential update of the guidelines in the future: a. R ole of adjustable medication dosing in recur-rent wheezing and asthma b. R ole of long-acting antimuscarinic agents (LAMAs) in asthma management as add-on to inhaled corticosteroids c. R ole of bronchial thermoplasty in adult severe asthma d. R ole of fractional exhaled nitric oxide (Fe NO) in diagnosis, medication selection, and monitoring treatment response in asthma e. R ole of remediation of indoor allergens (house dust mites/pets) in asthma management Re Fe Rence S Brooks, C., Pearce, N., & Douwes, J. (2013). The hygiene hypothesis in allergy and asthma: An update. Current Opinion Allergy Clinical Immunology, 13(1), 70-77. Busse, W. W., & Lemanske, R. F., Jr. (2001). Asthma. New England Journal of Medicine, 344(5), 350-362. Centers for Disease Control and Prevention. (2011). Asthma in the U. S. Vital Signs. Retrieved from www. cdc. gov/Vital Signs/Asthma/index. html. Kamble, S., &. Bharmal, M. (2009). Incremental direct expenditure of treating asthma in the United States. Journal of Asthma, 46(1), 73-80. National Heart, Lung, and Blood Advisory Council Asthma Expert Working Group. (2015). Needs assessment for potential update of the Expert Panel Report-3 (2007): Guidelines for the diagnosis and management of asthma. Retrieved from www. nhlbi. nih. gov/sites/www. nhlbi. nih. gov/files /Asthma-Needs-Assessment-Report. pdf. National Heart, Lung, and Blood Institute. (2012). Estimated comparative daily doses: Inhaled corticosteroids for long-term asthma control. In Asthma care quick reference: Diagnosing and managing asthma guidelines from the National Asthma Education and Prevention Program: Expert Panel Report 3. Retrieved from www. nhlbi. nih. gov/health-pro/guidelines/current/asthma-guidelines /quick-reference-html#estimated-comparative-daily-doses. National Heart, Lung, and Blood Institute. (1997). Expert panel report 2: Guidelines for the diagnosis and management of asthma (Publication No. 97-4051). Bethesda, MD: Author. National Heart, Blood, and Lung Institute. (2007). Expert panel report 3: Guidelines for the diagnosis and management of asthma (Publication No. 07-4051). Bethesda, MD: Author. Pellegrino, R., Viegi, G., Brusasco, V., Crapo, R. O., Burgos, F., Casaburi, R., et al. (2005). Interpretative strategies for lung function tests. European Respiratory Journal, 26, 948-968. Sullivan, S. D., Rasouliyan, L., Russo, P. A., Kamath, T., Chipps, B. E., & TENOR Study Group (2007). Extent, patterns, and burden of uncontrolled disease in severe or difficult-to-treat asthma. Allergy, 62, 126-133. World Health Organization. (2007). Global surveillance, prevention and control of chronic respiratory diseases: A comprehensive approach. Retrieved from www. who. int/gard/publications/GARD%20Book%202007. pdf. Key: Alphabetical order is used when more than one treatment option is listed within either preferred or alternative therapy. EIB, exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, long-acting inhaled beta 2-agonist, LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting beta2-agonist. Notes: The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs. If alternative treatment is used and response is inadequate, discontinue it and use the preferred treatment before stepping up. Zileuton is a less desirable alternative due to limited studies as adjunctive therapy and the need to monitor liver function. Theophylline requires monitoring of serum concentration levels. In step 6, before oral corticosteroids are introduced, a trial of high-dose ICS + LABA + either LTRA, theophylline, or zileuton may be considered, although this approach has not been studied in clinical trials. Reproduced from National Heart, Lung and Blood Institute, National Asthma Education and Prevention Program, & National Institutes of Health. (2007). Expert panel report 3: Guidelines for the diagnosis and management of asthma (NIH Publication No. 08-5846). Bethesda, MD: Author. Figure 46-2 Asthma Action Plan (Continued)448 CHAPTER 46 | Asthma in Adolescents and Adults
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over a period of years. As BPH progresses, the affected individual may or may not develop lower urinary tract symptoms (LUTS), which may include urinary frequency, hesitancy, urgency, nocturia, decreased force of stream, intermittent stream, incomplete bladder emptying, and incontinence or dribbling. Prostatic enlargement may cause obstruction of the bladder outlet and compression of the urethra. If this occurs, compromised urinary flow and deterio-ration of the upper urinary tract and renal failure can result (Emberton et al., 2008). Does BPH increase the risk for development of prostatic carcinoma? Most current clinical research suggests that although BPH may not result in pros-tatic carcinoma, pathologic changes that are asso-ciated with BPH may be associated with prostatic carcinoma (Bushman, 2009). An extensive study by Negri et al. (2005) concluded that the development of BPH seemed to be increased in those with a family history of bladder cancer but not with those having a family history of prostatic carcinoma. Some studies have indicated an association between chronic inflammation and both BPH and prostatic carcinoma (Abdel-Meguid, Mosli, & Al-Maghrabi, 2009) and have found that prostatic cancer develops in 83% of prostate glands where BPH is also found (Bostwick et al., 1992). A study conducted by Hammarsten and Högstedt (2002) suggests that fast-growing BPH is a factor that increases the risk of developing clinical prostate cancer. The authors note that these findings support the hypothesis of an association between the development of BPH and clinical prostate cancer. The association between BPH and prostate cancer is complicated and controversial. T o date, no clear-cut answers exist as to the actual association and risk. 2. P revalence and incidence BPH is very common, beginning around age 45 with development of accompanying symptoms by the age of 65 in whites and 60 in blacks (Longo et al., 2014). I. Intr oduction and general background The prostate is a muscular gland roughly triangular in shape and located in the lower abdomen between a man's bladder and rectum. According to some anatomic descriptions it has a median lobe and two lateral lobes and physically surrounds the neck of the bladder and the urethra (Venes, 2013). Other sources, such as the classification system of Lowsley, attribute five lobes to the prostate: (1) anterior, (2) posterior, (3) media, (4) right lateral, and (5) left lateral (T anagho & Lue, 2013). Partly muscular and partly glandular, the prostate has ducts opening into the prostatic portion of the urethra. Normally the prostate is roughly 2 × 4 × 3 cm and weighs approximately 20  g; it is enclosed in a fibrous capsule containing smooth muscle fibers in its inner layer. Muscle fibers also separate the glandular tissue and encircle the urethra. The gland secretes a thin, opalescent, slightly alkaline fluid that forms part of the seminal fluid (Venes, 2013). The gland is responsible for secreting liquid that then mixes with additional fluids secreted by the seminal vesicles and with the sperm produced by the testicles. A. Benign prostatic hyperplasia 1. D efinition and overview Benign prostatic hyperplasia (BPH) is generally considered to be a progressive disease and is consid-ered to be the most common benign tumor in men (Meng, Walsh, & Chi, 2014). The etiology of BPH is not known, but it is believed to be multifactorial with testicular androgens being the most probable controlling factor for the prostatic enlargement (Barry, 2009; Meng et al., 2014). Hyperplasia of the prostate occurs in a nodular pattern, increasing the cell numbers and occurring in varying amounts in the stroma or epithelium and glandular tissue of the prostate (Barry, 2009; Meng et al., 2014). The hyperplasia begins in the area around the urethra and gradually increases in nodules Jean N. Taylor-Woodbury Be NIg N Pros Ta TI c Hy P er P las I a© Eliks/Shutterstock; © donatas1205/Shutterstock 449 47Chapt Er
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viii. T rauma history: brain trauma including infarct or hemorrhagic stroke; trauma to bladder, urethra, or penis ix. E xposure history: any prior chemical or radioactive exposures to the lower genito-urinary tract or perineal area. x. M edication history: medications and sup-plements that may affect urinary flow or retention (e. g., antihistamine and deconges-tant use). Note any history of use of medi-cations or supplements for treatment of existing or prior genitourinary disorders or disease or prostatic disease. xi. A hi story of eye disease or cataracts should also be evaluated. Boehringer Ingelheim and the Food and Drug Administration noti-fied healthcare professionals of revisions to the precautions and adverse reactions sections of the prescribing information for tamsulosin (Flomax®), indicated for the treatment of the signs and symptoms of BPH. A surgical condition termed “intraoperative floppy iris syndrome” (IFIS) has been observed during phacoemulsification cataract surgery in some patients treated with α 1 blockers including Flomax®. Most of these reports were in patients taking the α 1 blocker when IFIS occurred, but in some cases the α1 blocker had been stopped before surgery. It is recommended that male patients being considered for cataract surgery, as part of their medical history, be specifically questioned to ascertain whether they have taken Flomax® or other α 1 blockers. If so, the patient's ophthalmologist should be prepared for possible modifications to their surgical technique that may be warranted should IFIS be observed during the procedure (U. S. Food and Drug Administration, 2005). c. F amily history i. P rostatic disease, particularly in first-degree relatives, includes age of onset of disease ii. D iabetes iii. N eurologic disorders iv. C ancer d. O ccupational and environmental history i. W ork-related exposures, such as chemical or radiation exposures ii. D egree of access to appropriate facilities for voiding e. P ersonal and social history i. R ecreational drug use, including metham-phetamines, and tobacco ii. Die tary intake and caffeine It  affects up to 80% of men 80 years or older (Barnard  & Aronson, 2009). Not all men, however, who have histologic BPH are symptomatic with lower urinary tract symptoms (LUTS). Twenty-five percent of men age 55 and 50% age 75 report signs and symptoms (Meng et al., 2014). Up to 80% of men 80 years of age and older report being affected by BPH (Barnard & Aronson, 2009). It is difficult to predict who will develop BPH because the risk factors are poorly understood, although some studies have indicated racial differences and some have indicated a genetic link. Age is considered a correlate to likelihood of BPH and its progression. For those who progress early, findings have suggested that approximately half of all men younger than age 60 who require surgical inter-vention for BPH may have an inherited form of BPH that is an autosomal-dominant trait. According to Meng, Walsh, and Chi (2014), the first-degree male relatives of those with the heritable form of BPH have a fourfold increased relative risk of developing BPH. More recent studies have also indicated that diabetes and obesity increase the risk of BPH and BPH symptom progression, whereas exercise and moderate alcohol consumption seem to decrease the risk of BPH and BPH progression (Parsons, 2007; Platz et al., 1998; Sea, Poon, & Mc Vary, 2009). II. Database (may include but is not limited to) A. Subjective 1. BPH a. C urrent symptoms and severity: The American Urological Association (Mc Vary et al., 2010) offers effective tools for screening symptoms and severity (Appendices 47-1 and 47-2). b. P ast health history i. M edical illnesses: any prostatic disease, renal disease, renal infection, or renal cal-culi; and any bladder disease, dysfunction, or recurrent infections. ii. S exual history to include practices and any history of infection. iii. H istory of diabetes mellitus and obesity. iv. H istory of physical trauma to the bladder or the urethra. v. H istory of neurologic disease or injury. vi. A ny history of cancer. vii. S urgical history: bladder surgery, urethral surgery, or penile surgery. 450 CHAPTER 47 | Benign Prostatic Hyperplasia
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4. Othe r conditions that may explain the patient's presentation a. Di abetes mellitus b. U rethral stricture c. B ladder neck contracture d. B ladder stone e. N eurogenic bladder B. Assess the severity of the disease 1. The A merican Urological Association's Symptom Index for Benign Prostatic Hyperplasia and the Disease Specific Quality of Life Question (Appendices 47-1 and 47-2) are helpful tools for assessing the severity of the condition. C. Assess the significance of the problem to the patient and significant others IV. g oals of clinical management A. Choose a cost-effective approach for screening or diagnosing BPH B. Select a treatment plan that returns the client to a symptom-free state in a safe and effective manner C. Select an approach that maximizes client adherence V. Plan A. Screening 1. The re are no screening tests for BPH. Examination is usually done in response to complaints of symptoms, although prostatic hyperplasia may be detected during a routine digital rectal examination. B. Diagnostic tests (see Box 47-1 for a description of relevant diagnostic studies and Figure 47-1 for the suggested approach for BPH diagnosis and treatment) C. Management (includes treatment, consultation, referral, and follow-up care) 1. I f symptoms are mild (American Urological Association Symptom Scale of less than or equal to 7 or no bothersome symptoms), then watchful waiting is indicated. 2. I f symptoms are moderate to severe, then discuss treatment options with the patient. f. R eview of systems i. A bdomen: suprapubic pain (suggestive of acute urinary retention) and flank pain. ii. Ge nitourinary: urethral discharge; dysuria; irritative symptoms (urgency, frequency, or nocturia); or obstructive symptoms (hesi-tancy, decreased or intermittent stream flow, sensation of incomplete void, and dribbling incontinence). iii. N eurologic: focal neurologic findings sug-gestive of neurologic etiology of the pre-senting urinary symptoms, such as lower extremity weakness or radiculopathic or neu-ropathic symptoms (e. g., saddle anesthesia). B. Objective 1. P hysical examination findings a. A n abdominal examination may demonstrate a palpable, distended bladder, which may be asymptomatic if LUTS are otherwise mild or absent. b. A bsence of costovertebral angle pain c. A bsence of urethral discharge or other genital findings suggestive of infection or sexually trans-mitted infection as a source of the LUTS d. A d igital rectal examination should be done and may reveal an enlarged prostate, which may be focal or diffuse. However, the size of the prostate correlates poorly with either the symptoms or the signs of BPH. e. A foc used neurologic examination should be accomplished to rule out a neurogenic bladder. 2. S upporting data from relevant diagnostic tests a. U rinalysis by either dipstick or microscopic examination to evaluate for hematuria or urinary tract infection. b. M easurement of the serum prostate-specific antigen (PSA) should be considered for those patients with at least a 10-year life expectancy and for whom the knowledge of prostate cancer would change symptom or disease management and for those whose PSA level might change the management of their LUTS (Mc Vary et al., 2010). III. a ssessment A. Determine the diagnosis 1. BPH 2. P rostatitis 3. P rostatic neoplasms (benign or malignant)451 Plan
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guideline for the management of BPH [Mc Vary, et al., 2010], there is insufficient evidence to support the use of either phenoxybenzamine or prazosin for the treatment of LUTS with BPH) c. A lfuzosin, 10 mg orally daily d. D oxazosin, 1-8 mg orally daily e. T amsulosin, 0. 4 or 0. 8 mg orally daily f. T erazosin, 1-10 mg orally daily g. S ilodosin, 8 mg orally daily h. I n using α-blockers, a gradual upward titration is recommended to minimize the risk of ortho-static hypotension that may occur with the use of this class of medications i. 5α-Reductase inhibitors (used for individuals with prostates > 40 m L by ultrasonographic examination) (Meng et al., 2014)i. Dut asteride, 0. 5 mg orally daily ii. F inasteride, 5 mg orally daily iii. C ombination therapy: α-blocker and 5α-reductase inhibitor j. Die tary supplements i. B ased on expert panel recommendations, and noted in the American Urological Association guideline for the management of benign prostatic hyperplasia (Mc Vary et al., 2010), phytotherapeutics and other dietary supplements—e. g., saw palmetto (Serenoa repens), African prune tree (Pygeum africanum), and rye pollen (Secale cereale)—are not currently recommended for the treatment of LUTS with BPH (Barry et al., 2011; Dedhia & Mc Vary, 2008; Dreikorn, 2002). k. I f the patient desires invasive therapy, refer to the urology service. i. The spe cialist may consider additional optional diagnostic tests, such as pressure flow, urethrocystoscopy, or prostate ultrasound. ii. M inimally invasive surgical options include transurethral laser-induced prostatec-tomy, transurethral needle ablation of the prostate, transurethral electrovaporization of the prostate, and hyperthermia. iii. C onventional surgical therapy includes transurethral resection of the prostate, transurethral incision of the prostate, and open simple prostatectomy. 4. Adv erse effects of treatment Regardless of treatment approach, patient education around both desired and the potential for undesired or adverse effects of the treatment should be thor-ough. The adverse effects depend on the treatment 3. I f patient chooses noninvasive therapy, may choose watchful waiting or the following medical therapy. a. P henoxybenzamine, 5-10 mg orally twice daily b. P razosin, 1-5 mg orally twice daily (according to the current American Urological Association Box 47-1 Description of r elevant Diagnostic s tudies Common prostate studies may include, but are not limited to the following: 1. Urinalysis (may be done by dipstick testing or microanalysis). According to the American Urological Association, routinely measuring the serum creatinine levels in the initial assessment of men with lower urinary tract symptoms is not indi-cated (Mc Vary et al., revised 2010). 2. The U. S. Preventive Services T ask Force (USPSTF) recommends against routine prostate cancer and prostate-specific antigen screening, citing that risk of harm outweighs the benefits of screening. However, the American Urological Association continues to recommend digital rectal exam and PSA screening in asymptomatic males aged 40  years and older with a life expectancy of more than 10 years. Other agencies, such as the American Cancer Society and the American College of Preventive Medicine recommend education-based informed decision making regarding the risks and benefits of screening men 50 years or older (USPSTF, 2012). 3. Urine cytology may be considered if there is a predominance of irritative (versus obstructive) symptoms and if the patient has a history of smoking or other significant risk factors for bladder carcinoma. 4. Optional tests for men with moderate to severe urinary symptoms include test of postvoid residual and urinary flow. If there is significant postvoid residual volume, transabdominal kidney ultrasound or intravenous urography by radiograph may be helpful in evaluating for hydronephrosis (American College of Radiology, 1995, revised 2014). Data from American College of Radiology. (1995, last reviewed 2014). ACR appropriateness criteria®: Lower urinary tract symptoms: Suspicion of benign prostatic hyperplasia. Retrieved from https://acsearch. acr. org/docs/69368/Narrative/. ; Mc Vary, K. T., Roehrborn, C. G., Avins, A. L., Barry, M. J., Bruskewitz, R., Donnell, R. F., et al. (2010). Management of benign prostatic hyperplasia (BPH) (rev. ed. ). Baltimore, MD: American Urological Association Education and Research, Inc. 452 CHAPTER 47 | Benign Prostatic Hyperplasia
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Figure 47-1 Benign Prostatic Hyperplasia (BPH) Diagnosis and T reatment Reproduced from Mc Vary, K. T., Roehrborn, C. G., Avins, A. L., Barry, M. J., Bruskewitz, R. C., Donnell, R. F., et al. (2010). American Urological Association: Management of benign prostatic hyperplasia (BPH) (rev. ed. ). Baltimore, MD: American Urological Association Education and Research, Inc. AUA/IPSS Symptom Index Assessment of Patient Bother Mild Symptoms (AUA/IPSS ≤ 7) or No Bothersome Symptoms Moderate/Severe Symptoms (AUA/IPSS ≥ 8) Discussion of Treatment Options Patient Chooses Noninvasive Therapy Patient Chooses Invasive Therapy Surgery Watchful Waiting *In patients with clinically significant prostatic bleeding, a course of a 5 alpha-reductase inhibitor may be used. If bleeding persists, tissue ablative surgery is indicated. †Patients with at least a 10-year life expectancy for whom knowledge of the presence of prostate cancer would change management or patients for whom the PSA measurement may change the management of voiding symptoms. ‡After exhausting other therapeutic options as discussed in detail in the text. §Some diagnostic tests are used in predicting response to therapy. Pressure-flow studies are most useful in men prior to surgery. AUA, American Urological Association; DRE, digital rectal exam; IPSS, International Prostate Symptom Score; PE, physical exam; PSA, prostate-specific antigen; PVR, postvoid residual urine; UTI, urinary tract infection. Medical Therapy Minimally Invasive Therapies Surgery Presence of Refractory Retention or Any of the following clearly related to BPH Persistent Gross Hematuria ‡ Bladder Stones‡ Recurrent UTIs‡ Renal Insufficiency History DRE & Focused PE Urinalysis* PSA in Select Patients †Initial Evaluation Optional Diagnostic Tests Uroflow PVR Optional Diagnostic Tests § Pressure Flow Urethrocystoscopy Prostate Ultrasound453 Plan
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course and may range from no adverse effects to either asymptomatic or symptomatic hypotension with the use of α-blockers to more severe side effects with surgical intervention. For example, beyond the risk of immediate surgical complications, transure-thral resection of the prostate has the potential to result in retrograde ejaculation, erectile dysfunction, urinary incontinence, inability to void, and infection (Du Beau, 2009). D. Client education 1. A ssist the patient and significant others in expressing and coping with concerns and feelings related to the respective prostate disease process and disease management. 2. P rovide oral and, preferably, written information regarding: a. The d isease process, including signs and symp-toms and underlying etiologies. b. Di agnostic tests, including a discussion about preparation, cost, the actual procedures, and aftercare. c. M anagement (rationale, action, use, side effects, and cost of therapeutic interventions; and the need for adhering to long-term treatment plans). VI. s elf-management resources and tools A. Patient and client education brochures or frequently asked question documents: 1. The N ational Institutes of Health's website (www. nlm. nih. gov/medlineplus/prostatediseases . html) has patient and client education brochures and frequently asked question documents in English and Spanish. The documents include visual resources and include a link to a number of other resources, including to the American Urological Association Foundation Urology Care Foundation website (www. urologyhealth. org). 2. The M erck Medicus Resource Library (Merck Sharp & Dohme Corp., now called univadis, 2001-2014) provides a range of patient information and patient teaching resources for BPH, which include a high-quality interactive 3-D human atlas. For more information go to www. merckmedicus. com/. 3. J ohns Hopkins Medical School offers a Health Alerts electronic subscription service for BPH, which provides regular updates on BPH and treatments. refere Nces Abdel-Meguid, T., Mosli, H., & Al-Maghrabi, J. (2009). Prostate inflam-mation. Association with benign prostatic hyperplasia and prostate cancer. Saudi Medical Journal, 30(12), 1563-1567. American College of Radiology. (1995, last reviewed 2014). ACR appro-priateness criteria®: Lower urinary tract symptoms: Suspicion of BPH. Retrieved from https://acsearch. acr. org/docs/69368/Narrative/. Barnard, R. J., & Aronson, W. J. (2009). Benign prostatic hyperplasia: Does lifestyle play a role? Physician and Sportsmedicine, 37(4), 141-146. Barry, M. J. (2009). Approach to benign prostatic hyperplasia. In A. H. Goroll & A. G. Mulley, Primary care medicine: Office evaluation and management of the adult patient (6th ed. ) (pp. 974-979). Philadelphia: Wolters Kluwer/Lippincott, Williams & Wilkins. Barry, M. J., Meleth, S., Lee, J. Y., Kreder, K. J., Avins, A. L., Nickel, J. C., et al. (2011). Effect of increasing doses of saw palmetto on lower urinary tract symptoms: A randomized trial. JAMA, 306(12), 1344-1351. doi:10. 1001/jama. 2011. 1364 Retrieved from www. ncbi. nlm. nih. gov /pmc/articles/PMC3326341/. Bostwick, D., Cooner, W., Denis, L., Jones, G. W., Scardino, P. T., & Murphy, G. P. (1992). The association of benign prostatic hyperplasia and cancer of the prostate. Cancer, 70(Suppl. 1), 291-301. Bushman, W. (2009). Etiology, epidemiology, and natural history of benign prostatic hyperplasia. Urologic Clinics of North America, 36(4), 403-415. Dedhia, R. C., & Mc Vary, K. T. (2008). Phytotherapy for lower urinary tract symptoms secondary to benign prostatic hyperplasia. Journal of Urology, 179(6), 2119-2125. Dreikorn, K. (2002). The role of phytotherapy in treating lower urinary tract symptoms and benign prostatic hyperplasia. World Journal of Urology, 19(6), 426-435. Du Beau, C. E. (2009). Chapter 50. Benign prostate disorders. In J. B. Halter, J. G. Ouslander, M. E. Tinetti, S. Studenski, K. P. High, & S. Asthana (Eds. ), Hazzard's geriatric medicine and gerontology (6th ed. ). New Y ork: Mc Graw-Hill. Retrieved from http://accessmedicine. mhmedical. com /book. aspx?book ID=371. Emberton, M., Cornel, E. B., Bassi, P. F., Fourcade, R. O., Gómez, J. M., & Castro, R. (2008). Benign prostatic hyperplasia as a progressive disease: A guide to the risk factors and options for medical management. International Journal of Clinical Practice, 62(7), 1076-1086. Hammarsten, J., & Högstedt, B. (2002). Calculated fast-growing benign prostatic hyperplasia—a risk factor for developing clinical prostate cancer. Scandinavian Journal of Urology and Nephrology, 36(5), 330-338. Longo, D. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Jameson, J., & Loscalzo, J. (2014). Urinary tract obstruction. In D. L. Longo, A.   S.   Fauci, D. L. Kasper, S. L. Hauser, J. Jameson, & J. Loscalzo (Eds. ), Harrison's Manual of Medicine (18th ed. ). New Y ork: Mc Graw-Hill. Retrieved from http://accessmedicine. mhmedical. com/book . aspx?book ID=1140. Mc Vary, K. T., Roehrborn, C. G., Avins, A. L., Barry, M. J., Bruskewitz, R. C., Donnell, R. F., et al. (2010). Management of benign prostatic hyperplasia (BPH) (rev. ed. ). Baltimore, MD: American Urological Association Education and Research, Inc. Retrieved from https://www. auanet. org /education/guidelines/benign-prostatic-hyperplasia. cfm. Meng, M. V., Walsh, T. J., & Chi, T. D. (2014). Urologic disorders. In M. A. Papadakis, S. J. Mc Phee, & M. W. Rabow (Eds. ), Current medical diagnosis & treatment 2015. Retrieved from http://accessmedicine. mhmedical. com/book. aspx?book ID=1019. 454 CHAPTER 47 | Benign Prostatic Hyperplasia
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T anagho's general urology (18th ed. ). New Y ork: Mc Graw-Hill. Retrieved from http://accessmedicine. mhmedical. com/book. aspx?book ID=508. U. S. Food and Drug Administration. (2005). T amsulosin: Safety warning /recommendation statement. Retrieved from www. fda. gov/Safety /Med Watch/Safety Information/Safety Alertsfor Human Medical Products /ucm151211. htm. U. S. Preventive Services T ask Force. (2012). Final recommendation statement: Prostate cancer: Screening, May 2012. Retrieved from http://www . uspreventiveservicestaskforce. org/Page/Document/Recommendation Statement Final/prostate-cancer-screening#recommendations-of-others. Venes, D. (Ed. ). (2013). T aber's cyclopedic medical dictionary (22nd ed. ). Philadelphia, PA: F. A. Davis Company. Negri, E., Pelucchi, C., T alamini, R., Montella, M., Gallus, S., Bosetti, C., et al. (2005). Family history of cancer and the risk of prostate cancer and benign prostatic hyperplasia. International Journal of Cancer, 114(4), 648-652. Parsons, J. (2007). Modifiable risk factors for benign prostatic hyperplasia and lower urinary tract symptoms: New approaches to old problems. Journal of Urology, 178, 395-401. Platz, E., Kawachi, I., Rimm, E., Colditz, G., Stampfer, M., Willett, W., et al. (1998). Physical activity and benign prostatic hyperplasia. Archives of Internal Medicine, 158(21), 2349-2356. Sea, J., Poon, K., & Mc Vary, K. (2009). Review of exercise and the risk of benign prostatic hyperplasia. Physician and Sportsmedicine, 37(4), 75-83. T anagho, E. A., & Lue, T. F. (2013). Chapter 1. Anatomy of the genitourinary tract. In J. W. Mc Aninch & T. F. Lue (Eds. ), Smith and 455 References
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a PPe NDIx 47-1: T H e a mer I ca N Urolog I cal a ssoc I a TI o N ( a Ua ) s ym PTom I ND ex for Be NI g N Pros Ta TI c Hy P er P las I a (BPH) a ND TH e D I sease s P ec I f I c Q Ual IT y of l I fe Q U es TI o N Patient Name: Date of birth: Date completed Not at alll ess than 1 in 5 Timesl ess than Half the Timea bout Half the Timem ore than Half the Timea lmost a lwaysyour s core 1. Over the past month, how often have you had a sensation of not emptying your bladder completely after you finished urinating?0 1 2 3 4 5 2. Over the past month, how often have you had to urinate again less than 2 hours after you finished urinating?0 1 2 3 4 5 3. Over the past month, how often have you stopped and started again several times when you urinated?0 1 2 3 4 5 4. Over the past month, how often have you found it dif ficult to postpone urination?0 1 2 3 4 5 5. Over the past month, how often have you had a weak urinary stream?0 1 2 3 4 5 6. Over the past month, how often have you had to push or strain to begin urination?0 1 2 3 4 5 None 1 Time 2 Times 3 Times 4 Times 5 or Mor e 7. Over the past month, how many times did you most typically get up to urinate from the time you went to bed at night until the time you got up in the morning?0 1 2 3 4 5+ T otal Symptom Score Score: 1-7: Mild 8-19: Moderate 20-35: Severe The possible total runs from 0 to 35 points with higher scores indicating more severe symptoms. Scores less than seven are considered mild and generally do not warrant treatment. The International Prostate Symptom Score uses the same seven questions as the AUA Symptom Index (presented here) with the addition of the following Disease Specific Quality of Life Question (bother score) scored on a scale from 0 to 6 points (delighted to terrible): “If you were to spend the rest of your life with your urinary condition just the way it is now, how would you feel about that?” Reproduced from Mc Vary, K. T., Roehrborn, C. G., Avins, A. L., Barry, M. J., Bruskewitz, R. C., Donnell, R. F., et al. (2010). Management of benign prostatic hyperplasia (BPH) (rev. ed. ). Baltimore, MD: American Urological Association Education and Research, Inc. 456 CHAPTER 47 | Benign Prostatic Hyperplasia
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a PPe NDIx 47-2: Be NI g N Pros Ta TI c Hy P er P las I a (BPH) Im Pa c T I ND ex (“Bo TH er” s core) Patient Name: DOB: ID: Date of assessment Initial Assessment q Monitor during: Therapy q after: Therapy/surgery q BPH Impact Index 1. Over the past month how much physical discomfort did any urinary problems cause you?None q Only a little q Some q A lot q 2. Over the past month, how much did you worry about your health because of any urinary problems?None q Only a little q Some q A lot q 3. Overall, how bothersome has any trouble with urination been during the past month?Not at all bothersome q Bothers me some q Bothers me a little q Bothers me a lot q 4. Over the past month, how much of the time has any urinary problem kept you from doing the kind of things you would usually do?None of the time q Most of the time q A little of the time q All of the time q Some of the time q T otal Score: (Scoring based on 0-4 point scale) Reproduced from Mc Vary, K. T., Roehrborn, C. G., Avins, A. L., Barr, M. J., Bruskewitz, R. C., Donnell, R. F., et al. (2010). Management of benign prostatic hyperplasia (BPH) (rev. ed. ). American Urological Association Education and Research, Inc. 457 Appendix
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ensure that all of a person's health needs are met (Hewitt et al., 2005). The American Society for Clinical Oncology (ASCO) further defined high-quality cancer survivorship care by recommending that providers address psychoso-cial effects of cancer diagnosis, provide health education, promote a healthy lifestyle including diet and exercise guidance, provide resources for financial hardships, and empower cancer survivors to be their own healthcare advocate (Mc Cabe et al., 2013). Oncology providers have historically been responsible for coordinating cancer survivorship care. The projected increase in the number of survivors requiring follow-up care will place a serious burden on oncology providers. There is evidence to suggest that the increased time pres-sure on healthcare providers and the shrinking oncology workforce will make it difficult for practicing oncologists to adequately manage this increasing number of cancer survivors and meet the goal of delivering high-quality cancer survivorship care. These pressures in combination with increased access to care through the Affordable Care Act will compound the burden of oncology providers (Chandak et al., 2014; Edwards et al., 2014). This growing burden signals the need for a multidisciplinary approach that includes primary care providers is warranted to ensure continuity and complete cancer survivorship care. Many models of care for survivorship have been iden-tified including shared care nurse-led, primary care, and oncology provider led (Hewitt, Bamundo, Day, & Harvey, 2007; Keesing, Mc Namara, & Rosenwax, 2014; Rowland, Hewitt, & Ganz, 2006). There is no consensus across insti-tutions on the optimal model of healthcare delivery to cancer survivors at this time, but because of the growing demands on oncology specialists, it is evident that primary care providers will be key members of the cancer survivors, care team. Figure 48-1 shows the Cancer Care T rajectory taken from the IOM report From Cancer Patient to Cancer Survivor: Lost in Transition (Hewitt et al., 2005). I. Intr oduction and background A. Definition and overview There are an estimated 14. 5 million cancer survivors cur-rently living in the United States, and that number is expected to increase by 31% to approximately 19 million by 2024 (American Cancer Society [ACS], 2014). This represents an increase of more than 4 million cancer survi-vors over 10 years (De Santis et al., 2014). The concept of “cancer survivorship” is relatively young, dating back to a 1985 New England Journal of Medicine arti-cle by Fitzhugh Mullan, a physician and cancer survivor, in which he wrote, “The challenge in overcoming cancer is not only to find therapies that will prevent or arrest the disease quickly, but also to map the middle ground of survivor-ship and minimize its medical and social hazards” (Mullan, 1985, p. 273). In 1986 the National Coalition for Cancer Survivorship (NCCS) formalized the first definition of the term and laid the foundation for the current definition developed by the National Cancer Institute (NCI). The definition states that the term survivor applies to “an indi-vidual from the time of diagnosis, through the balance of his or her life. Family members, friends, and caregivers are also impacted by the survivorship experience and are there-fore included in this definition” (Hewitt, Greenfield, & Stoval, 2006, p. 29). In 2006, the seminal report from the Institute of Medicine (IOM) titled From Cancer Patient to Cancer Survivor: Lost in Transition (Hewitt et al., 2005) highlighted the importance of cancer survivorship and the multifaceted aspects of caring for those affected by cancer. The IOM report outlined essential components of survivorship care including (1) prevention and detection of new and recurrent cancers; (2) surveillance for cancer spread, recurrence, or second cancers; (3) intervention for consequences of cancer and its treatment; and (4) coordi-nation between specialists and primary care providers to Tara D. Lacey and Sheila N. Lindsay Ca NCer Surv Ivor Sh Ip IN a D u LT p r I mary Care© Eliks/Shutterstock; © donatas1205/Shutterstock 458 48Chapt Er
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A. Subjective 1. C ancer history: specific site and type, stage at diagnosis, and histology; age at diagnosis 2. C ancer treatment history: a. C hemotherapy: therapeutic agents used includ-ing dose, date initiated and completed b. R adiotherapy: region treated, radiation dose, date initiated and completed c. S urgery: Surgical procedure, date of surgical pro-cedure, pathology, and surgical complications d. H ereditary risk and genetic testing: Assess if genetic counseling was completed including results. Follow screening guidelines for moderate-to high-risk cancer survivors (Wood et al., 2012). e. C omplications from treatment course: hospi-talizations, toxicities during treatment, ongoing toxicity at completion of treatment, and func-tional and performance status 3. M edications: current medications for ongoing cancer therapy, current medications for cancer treatment sequelae, complementary and alternative medicine practices. 4. P ast medical history: Comorbid conditions both pre and post cancer diagnosis, gynecologic and obstetric history including menstrual history, contraception, B. Epidemiology In 2014, the Surveillance, Epidemiology, and End Results (SEER) database showed that 46% of survi-vors were 70 years or older. Only 5% of survivors were under the age of 40. The three most common cancers in males were prostate (43%), colorectal (9%), and melanoma (8%). In women, the three most com-mon cancers were breast (41%), uterine corpus (8%), and colorectal (8%). Survival rates and survivor ages vary between cancer types. In all cancer sites, the rela-tive 5-year cancer survival rate is estimated at 66% (De Santis et al., 2014; Howlader et al., 2014). The largest group of survivors, about 36%, are less than 5 years from diagnosis, 10% are 15 to 20 years from diagnosis, and only 5% are more than 30-year cancer survivors (De Santis et al., 2014). The number of can-cer survivors who are living 5 or more years beyond their diagnosis is projected to increase by 37%, reach-ing nearly 12 million over the next decade (de Moor et al., 2013). II. Database The clinical assessment of the cancer patients in the survivor-ship phase of care should include the following:Figure 48-1 Cancer Care T rajectory Reproduced from Institute of Medicine and National Research Council of the National Academies. From Cancer Patient to Cancer Survivor: Lost in Transition. M. Hewitt, S. Greenfield, and E. Stovall (Eds. ). Washington, DC: The National Academies Press. Cancer-Free Survival Treatment with Intent to Cure Managed Chronic or Intermittent Disease Recurrence/ Second Cancer Diagnosis and Staging Palliative Treatment Death Treatment Failure Survivorship Care Late effects management andsurveillance for recurrence andsecond cancers459 Database
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k. H ematologic and lymphatic: bleeding, easy bruising, and recurrent or chronic infections, lymphedema. l. M usculoskeletal: chronic pain, height changes, joint swelling, and joint stiffness, decreased range of motion, new lumps or bumps. m. N eurologic: peripheral neuropathy, neuropathic pain, hearing loss, decreased cognitive function, mental acuity, and headaches. n. P sychiatric/psychosocial: depression, posttrau-matic stress disorder, and cancer related changes in health, relationships, and finance, fear of recur-rence or new cancers. B. Objective 1. P hysical examination A problem-focused physical exam should occur at regular intervals. T able 48-1 shows the late effects of both radiotherapy and chemotherapy on organ systems including spe-cific chemotherapy drugs as a reference for physical exam findings. 2. Di agnostics a. Di agnostic testing should be based on the fol-lowing: Review of systems and physical exam findings, surveillance tests based on specific cancer history and hereditary risk factors, and standard of care cancer screening and prevention (Smith et al., 2014). b. I mmunizations: influenza vaccine (only inactive or recombinant) for all cancer survivors, pneu-mococcal vaccine, T dap, human papillomavirus in survivors aged 26 or younger. Zoster vaccine (a live attenuated vaccine) in survivors aged 60 or older without active or ongoing immuno-deficiency, no history of cellular immunodefi-ciency or hematopoietic stem cell transplant, or who have not received chemotherapy or radiotherapy in the past 3 months (National Comprehensive Cancer Network [NCCN], 2014). III. a ssessment The NCI guidelines and NCCN clinical practice guidelines in oncology for survivorship recommend that a provider see an adult cancer survivor at regular intervals. These intervals are driven by individual cancer history and follow-up recom-mendations (NCCN, 2014). At each visit, the differential diagnosis is based on the survivor's symptoms. The guide-lines recommend addressing the following subjects at regular sexually transmitted diseases, gravida/para, hormone replacement use, and fertility. 5. F amily history: cancer history in family. Obtain a three-generation pedigree for hereditary cancer risk (Rowland et al., 2006). 6. P ersonal and social history: past and current alcohol intake and tobacco use, obesity history, exercise or activity level pre and post treatment, sexual history including fertility preservation, desire to have children, current sexual practices, relationship and living situation, and ethnicity 7. O ccupational history: environmental exposures and cancer-related employment changes 8. R eview of systems: A complete review of systems should be assessed at regular intervals. These intervals are individualized depending on the diagnosis. Generally it is recommended that a complete review of systems be assessed at least once a year for all cancer survivors. a. C onstitutional: weight gain or loss, fatigue, fevers, sweats, pain, changes or limitations in exercise ability b. S kin and integument: treatment-related skin changes from radiotherapy, surgery, or chemo-therapy; skin changes including fibrosis, telangi-ectasia, or thinning of skin; hair loss. c. H ead, eyes, ear, nose, throat, and mouth: vision or hearing changes, dental problems, jaw pain or nonhealing sores, and xerostomia. d. P ulmonary: cough, hemoptysis, shortness of breath or dyspnea on exertion e. C ardiovascular: signs or symptoms of congestive heart failure, palpitations, coronary ischemia, pleural or pericardial chest pain, claudication or vascular ischemic symptoms, Reynaud's phe-nomenon, hypertension. f. B reast: new lumps or bumps, nipple or skin changes, nipple discharge. g. G astrointestinal: diarrhea, constipation, nausea, emesis, abdominal pain, ostomy site problems, hepatitis, and cirrhosis. h. Ge nitourinary: incontinence, dysuria, hema-turia, urinary frequency or hesitancy, erectile dysfunction. i. G ynecologic: premature menopause, vasomotor symptoms. j. E ndocrine, reproductive, and sexual func-tioning: symptoms of hypothyroidism, meta-bolic syndrome, vaginal dryness, dyspareunia, decreased libido, body image issues, decreased sexual functioning, and vasomotor changes. 460 CHAPTER 48 | Cancer Survivorship in Adult Primary Care
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Table 48-1 Late Ef fects for Cancer Treatment o rgan/System Late e ffects of r adiotherapy Late e ffects of Chemotherapy Some of the Drugs r esponsible Cardiovascular Pericardial effusion, pericarditis, coronary artery disease Cardiomyopathy, congestive heart failure, hypertension Anthracyclines (doxorubicin, daunorubicin, epirubicin, mitoxantrone), cyclophosphamide, monoclonal antibodies (trastuzumab & pertuzumab) Central Nervous System Cognitive deficits, structural changes, hemorrhage, increased risk of stroke, hearing loss, psychiatric and psychosocial distress Cognitive deficits, seizure, hemiplegia, hearing loss, psychiatric and psychosocial distress Methotrexate Cisplatin Gastrointestinal Malabsorption, stricture, liver abnormalities Abnormal liver function tests, hepatic fibrosis/failure, cirrhosis Methotrexate, carmustine (BCNU ®) Genitourinary Bladder fibrosis, contractures Bladder fibrosis, hemorrhagic cystitis, urination dysfunction and malignancy Cyclophosphamide, ifosfamide Hematology/Lymph Cytopenias, myelodysplasia Myelodysplastic syndrome, acute myeloid leukemia Alkylating agents, platinum agents (cisplatin, carboplatin, & oxaliplatin) Musculoskeletal/Soft Tissue Fibrosis, atrophy, osteonecrosis, secondary malignancies, cosmetic changes, lymphedema Avascular necrosis, osteoporosis, pain Steroids, methotrexate, aromatase inhibitors (letrozole, anastrozole, exemestane) Ophthalmologic Cataracts, retinopathy, double vision Cataracts Steroids, tamoxifen, busulfan Oral Health Poor enamel and root formation, xerostomia Xerostomia, increased incidence of caries All chemotherapies Peripheral Nervous System Peripheral neuropathy Peripheral neuropathy, hearing loss Cisplatin, taxanes (paclitaxel, docetaxel, & albumin bound paclitaxel), vinca alkaloids (vincristine, vinorelbine), proteasome inhibitors (thalidomide) Pulmonary Pulmonary fibrosis, decreased lung volumes Pulmonary fibrosis, interstitial pneumonitis Bleomycin, BCNU, methotrexate, anthracyclines (doxorubicin, daunorubicin, epirubicin, mitoxantrone), MTOR/PI3K inhibitors (temsirolimus & everolimus) Renal Decreased creatinine clearance, hypertension Decreased creatinine clearance, increased serum creatinine Methotrexate, nitrosoureas, ifosfamides, Platinum agents (cisplatin, carboplatin, & oxaliplatin) Reproductive Men: risk of sterility, Leydig cell dysfunction Women: ovarian failure, premature menopause Men: sterility, deficient or insufficient testosterone Women: sterility, premature menopause Alkylating agents (cyclophosphamide and ifosfamide), procarbazine, antiestrogen therapies (tamoxifen, anastrozole, letrozole, and exemestane), platinum agents Endocrine Hypothyroidism, nodules, growth hormone deficiencies, pituitary deficiencies    Data from Ganz, P. A. (2001). Late effects of cancer and its treatment. Seminars in Oncology Nursing, 17(4), 241-248. doi: http://dx. doi . org/10. 1053/sonu. 2001. 27914; Oeffinger, K. C., Hudson, M. M., & Landier, W. (2009). Survivorship: Childhood cancer survivors. Primary Care, 36(4), 743-780. doi: 10. 1016/j. pop. 2009. 07. 007. 461 Assessment
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Iv. Goals of clinical management The 2005 IOM report created the foundation of survivor-ship care and its essential components (Hewitt et al., 2005). These principles of cancer survivorship care have been used intervals to see if there are contributing and/or reversible factors affecting health, current disease status, performance status, medications, comorbid conditions, and cancer his-tory (NCCN, 2014). Figure 48-2 is the NCCN survivorship baseline assessment guideline (NCCN, 2014). SURVIVORSHIP BASELINE ASSESSMENT (Patient version) Survivorship Concerns Survivorship Care Survey Anxiety and Depression 1. Do you often feel nervous or do you worry? Yes/No 2. Do you often feel sad or depressed? Yes/No 3. Have you lost interest in things you used to enjoy? Yes/No Cognitive Function 4. Do you have difficulties with multitasking or attention? Yes/No 5. Do you have difficulties with remembering things? Yes/No6. Does your thinking seem slow? Yes/No Fatigue 7. Do you feel persistent fatigue despite a good night's sleep? Yes/No8. Does fatigue interfere with your usual activities? Yes/No9. How would you rate your fatigue on a scale of 0 (none) to 10 (extreme) over the past month? 0-10 Pain 10. Are you having any pain? Yes/No11. How would you rate your pain on a scale of 0 (none) to 10 (extreme) over the past month? 0-10 Sexual Function 12. Are you dissatisfied with your sexual function? Yes/No13. Do you have any concerns regarding sexual function or sexual activity? Yes/No Sleep Disorder 14. Are you having problems falling asleep or staying asleep? Yes/No15. Are you experiencing excessive sleepiness (ie, sleepiness or falling asleep in inappropriate situations or sleeping more during a 24-hour period than in the past)?Yes/No Physical Activity16. Are you exercising or doing some physical activity for less than 150 minutes a week? Yes/No 17. Do you have any limitations to participating in the physical activities that you enjoy? Yes/No Immunizations and Infections18. Have you received your flu vaccine this year? Yes/No19. Have you received any vaccinations recently? Yes/No Please answer the following questions regarding possible symptoms that you may have experienced over the past 4 weeks: Note: All recommendations are category 2A unless otherwise indicated. Clinical Trials: NCCN believes that the best management of any cancer patient is in a clinical trial. Participation in clinical trials is especially encouraged. Figure 48-2 NCCN Survivorship Baseline Assessment Guideline Reproduced from National Comprehensive Cancer Network. (2014). NCCN clinical practice guidelines in oncology™: Survivorship (v. 2. 2014). Retrieved from www. nccn. org/professionals/physician_gls/f_guidelines . asp#survivorship. 462 CHAPTER 48 | Cancer Survivorship in Adult Primary Care
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as the backbone for subsequent discussions and represent the overarching goals of management of the cancer survivor: (1) prevention and detection of new cancers and recurrent cancer, (2) surveillance for cancer spread and secondary cancers, (3) intervention for the consequences of cancer and its treatment, and(4) coordination between specialists and pri-mary care providers to ensure health needs are met. Many factors including lifestyle, environment, hereditary risks and the late effects of cancer treatment contribute to the development of secondary malignancies or disease recurrence in cancer survivors (Wood et al., 2012). It is important to iden-tify those at higher risk and employ lifestyle interventions that mitigate risks including counseling on smoking cessation and alcohol usage, increasing physical activity, improving nutrition, and limiting sun exposure (NCCN, 2014). The timing and patterns of local regional recurrence and metastatic disease are disease-site specific, and surveillance must be highly individualized. The NCCN has created disease specific guidelines that can help the primary care provider navigate the care of the cancer survivor (Morgan & Denlinger, 2014). In addition, interventions to prevent new cancers including standard age-appropriate cancer screening should be considered (Smith et al., 2014). Cancer is more than just a disease of the body. The conse-quences of cancer and the downstream effects of a cancer diagnosis and its often multimodal treatments affect each individual patient and family differently. Cancer can leave its mark on all aspects of patients' lives including their physical condition, psychosocial and financial well-being, employment status, and interpersonal relationships. The late effects of treat-ment can be long lived and contribute to chronic physical and psychosocial changes such as fatigue, pain, anxiety, depression, and fear of recurrence. Regular assessments of these areas are essential and profoundly affect the quality of life of the can-cer survivor. Cancer survivorship requires a multidisciplinary team of specialists who along with the primary care provider can help navigate the transition from patient to survivor. A physical exam should be completed at every visit, and sites of previous cancers should be assessed (Wood et al., 2012). In addition, appropriate screening guidelines should be imple-mented at each visit. ASCO and the American College of Surgeons Commission on Cancer Program Standard for 2012 recommend treatment summaries and survivorship care plans for all cancer survivors to enhance both communication between the oncology team and the primary care provider and patient-provider communi-cation (Mc Cabe et al., 2013). The survivorship care plan should consist of two components: the treatment summary and follow-up plan. T ogether, these two components help to facilitate con-tinuity of care and promote high-quality survivorship care. The treatment summary should include the malignant diagnosis, stage at diagnosis (including histology), specific treatment modalities, ongoing toxicities of all treatments, and genetic or hereditary risk factors. The specific treatment modalities include surgical procedures, individually listed chemotherapy names and end date of chemotherapy, and radiotherapy treatment including anatomic location, dura-tion, total dose, and end date (Mayer et al., 2014). The follow-up plan should include oncology team mem-bers' names and contact information, ongoing need for adju-vant therapy with planned duration, schedule for follow-up visits, recommended surveillance tests for recurrence, cancer screening for new cancers, and other periodic testing needed as applicable. The patient should be given a list of symptoms concerning recurrence and a list of clinically significant late or long-term effects of treatment. The plan should end with a general statement educating the patient about healthy life-style including diet and exercise plans and a list of resources to address ongoing psychosocial, financial, employment, or par-enting issues (Mayer et al., 2014). Figure 48-3 is the ASCO survivorship care plan template. v. p lan A. Diagnostic tests Diagnostic testing is based on the specific cancer history, symptoms at presentation, and subjective and objective findings. These diagnostic tests can include laboratory tests including tumor markers and/or imaging studies, which may include CT scan, bone scan, or PET scan. The NCCN and ASCO guidelines outline specific follow-up recom-mendations based on cancer diagnosis, stage at presenta-tion, and risk. These guidelines are widely available and useful to all providers managing cancer survivors (ASCO, n. d. ; NCCN, 2014). Included in these guidelines are recom-mendations for ongoing cancer screening and preventative imaging studies for cancer survivors, including screening tests for breast, prostate, cervical, colorectal, and lung cancer (Smith et al., 2014). B. Patient education It is important for survivors to be reminded that recovery takes time. They need to understand that their journey is not completed at the end of acute treatment but contin-ues throughout their lives. Cancer survivors should be provided information about their individual care plan, symptoms to watch for, and lifestyle modifications that can aid in managing long-term effects and reduce risks for a second malignancy. 1. L ifestyle interventions Cancer survivors often request information and advice from providers about what they can do to improve their quality of life following cancer treat-ment and increase survival. Healthcare providers have a significant opportunity to counsel cancer survivors 463 Plan
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ASCO Treatment Summary and Survivor ship Care Plan General Information Patien t Name: Patient DOB: Patien t pho ne: Email: Healthcare Providers (Inc luding Names, Institution) Prima ry Care Pr ovider : Surgeon: Radiation Onco logist: Medical Onco logist: Other Providers: Diagnosis Treatment Summary Cancer Type/Locat ion/Histolog y Subtyp e: Diagnosi s Date (year): Stage: I II III Not applicable Treatment Surgery Yes No Surgery Date(s) (year): Surgical procedure/location/findings: Radiation Yes No Body area treated: End Date (year): Systemic Therapy (chemotherapy, hormonal therapy, other) Yes No Names of Agents Used End Dates (year) Persistent symptoms or side effects at completi on of treatm ent: No Yes (enter type(s)) : Familial Cancer Risk Assessment Genetic/he reditary risk factor(s) or predisposing cond itions: Genetic couns eling: Yes No Genetic testing results: Need for on going (adjuva nt) treatment for cancer Yes No Additional trea tment na me Planned durati on Possible Side effects Schedule of clinical visits Coordinating Pr ovider When/H ow often Figure 48-3 ASCO Survivorship Care Plan T emplate Reproduced from American Society of Clinical Oncology. (2016). ASCO Cancer Treatment and Survivorship Care Plans. Retrieved from www. cancer. net. 464 CHAPTER 48 | Cancer Survivorship in Adult Primary Care
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ASCO Survivorship Care Plan Updated based on consensus conference held on 9. 27. 13 and the ASCO Survivorship Co mmittee Cancer surveillance or other recommended related tests Coordinating Pr ovider What /When/How Often Please continue to see your primary care provider for all general health care recommended for a (man) (woman) your age, including cancer screening tests. Any symptoms should be brough t to the attentio n of your provider: 1. Anything that represents a brand new symptom; 2. Anything that represents a persistent symptom; 3. Anything you are worried about that might be related to the cancer coming back. Possible late-and long-ter m effects that someone wi th this type of ca ncer and treatm ent may experien ce: Cancer su rvivors may experience issu es wi th the areas listed below. If you have any concerns in these or othe r areas, please speak with your doctors or nur ses to find out how you can get help with them. Emot ional and me ntal health Fatigue Weight changes Stopping smoking Physical Functi oning Insurance School/Work Financial advice or assistance Memory or concentration loss Parenting Fertility Sexual functi oning Other A number of lifestyle/ behaviors can affect your on going health, including the risk for the cancer coming back or developing anot her cancer. Discuss thes e recommenda tions with your doctor or nurse: Tobacco use/ces sation Diet Alcohol use Sun screen use Weight management (l oss/gain) Physical activity Resour ces you may be interested in : Other comments : Prepared by: Delivered on: This Survivorship Ca re Plan is a cancer treatment summary and follow-up plan is provided to you to keep wi th your healthcare records and to share with your pr imary ca re provider. This summar y is a brief record of major aspects of yo ur cancer trea tment. You can share your copy with any of your doctors or nurses. However, this is not a detail ed or comp rehensive record of your care. Figure 48-3 ASCO Survivorship Care Plan T emplate (Continued) Reproduced from American Society of Clinical Oncology. (2016). ASCO Cancer Treatment and Survivorship Care Plans. Retrieved from www. cancer. net. 465 Plan
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on lifestyle modifications that may decrease their risk of recurrence, manage cancer treatment effects, and improve overall quality of life. The lifestyle modifica-tions that have shown to make the greatest benefit are increased physical activity, weight management, and nutrition (Pekmezi & Demark-Wahnefried, 2011). a. The c urrent physical activity recommendations from both ACS and NCCN are that cancer sur-vivors engage in regular physical exercise with the goal of 150 minutes of moderate to vigorous aerobic exercise per week. In addition, they rec-ommend 2 days a week of resistance or strength training and that exercise programs are tailored to individual needs (NCCN, 2014; Rock et al., 2012). b. N utrition and dietary choices have also been shown to play a role in cancer recurrence risk, improved quality of life after cancer treatment, and overall survival (Pekmezi & Demark-Wahnefried, 2011). Though more data are needed to further investigate the role nutrition and weight management play in cancer survi-vorship, current recommendations follow those of the general population. It is recommended that cancer survivors maintain a healthy weight with body mass index < 25 and consume a plant-based diet high in vegetables, fruits, and whole grains (Kushi et al., 2012; Rock et al., 2012). Many studies have attempted to include supple-ments from isolated nutrients as chemopreven-tion from cancer or recurrence. Unfortunately, to date, there are no trials that have confirmed addi-tional supplementation to be beneficial in cancer prevention. Some of these trials have revealed high-dose isolated nutrients can actually be det-rimental. Evidence for supplementation in can-cer is not supported, with best advice currently being portion-controlled consumption of whole foods to obtain nutrients (Kushi et al., 2012). The recommendations for alcohol consump-tion are no different from the general population guidelines. C. Consultations and Referrals The care of the adult cancer survivor is complex. Each sur-vivor has his or her own specific cancer story and follow-up recommendations. It is imperative to consult the oncology team with any questions or concerns regarding surveil-lance and possible recurrence. The open line of communi-cation will ensure high-quality care. In addition, the mental, psychosocial, and financial health of the cancer survivor should not be overlooked. Referrals to psycho-oncology, psychology, psychiatry, and social work should be used to address those needs. v I. Self-management r esources Cancer survivors are a unique population. They have medical needs that reach beyond physical well-being, and navigating those needs can be challenging. The survivorship care plan is an individualized road map for providers to help facilitate and direct follow-up care. It is also a tool for cancer survivors and families to help them understand their individualized history and risks, and it empowers them to be active members in their follow-up care. As the cancer survivor population increases it will be essential that both oncology and primary care providers work together as the cancer survivorship care team to ensure continued, coordinated, and high-quality care for this unique population. A. Educational resources www. cancer. org/treatment/survivorshipduringandafter treatment/indexwww. canceradvocacy. orghttp://cancercontrol. cancer. gov/ocs/index. htmlhttp://journeyforward. orgwww. cancer. net/survivorshipwww. cdc. gov/cancer/survivorshipwww. livestrong. org/we-can-help/healthy-living-after -treatment/www. mskcc. org/cancer-care/integrative-medicine/about -herbs-botanicals-other-products B. Community support groups 1. A CS provides a resource link where survivors can look up local support groups based on location: www. cancer. org/treatment/supportprogramsservices /app/resource-search. 2. C ancer Care is a national organization that provides free, professional support services and information to help survivors manage the emotional, practical, and financial challenges of cancer. They provide online, telephone, and face-to-face support groups: www. cancercare. org/support_groups. refere NCe S American Cancer Society. (2014). Cancer facts & figures 2014. Atlanta: American Cancer Society. American Society of Clinical Oncology. (n. d. ). Practice guidelines. Retrieved from www. instituteforquality. org/practice-guidelines. Chandak, A. N., Loberiza, F. R., Deras, M., Armitage, J. O., Vose, J. M., & Stimpson, J. P. (2014). Estimating the state-level supply of cancer care providers: Preparing to meet workforce needs in the wake of healthcare reform. Journal of Oncology Practice. [Epub 2014, Nov. 12] doi: 10. 1200 /JOP. 2014. 001565. de Moor, J. S., Mariotto, A. B,, Parry, C., Alfano, C. M., Padgett, L., Kent, E. E., et al. (2013). Cancer survivors in the United States: Prevalence 466 CHAPTER 48 | Cancer Survivorship in Adult Primary Care
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across the survivorship trajectory and implications for care. Cancer Epidemiology, Biomarkers and Pprevention, 22(4), 561-570. doi: 10. 1158/1055-9965. EPI-12-1356. [Epub 2013 Mar 27]. De Santis, C. E., Lin, C. C., Mariotto, A. B., Siegel, R. L., Stein, K. D., Kramer, J. L., et al. (2014). Cancer treatment and survivorship statistics, 2014. CA: A Cancer Journal for Clinicians, 64(4), 252-271. doi: 10. 3322 /caac. 21235 Edwards, B. K., Noone, A. M., Mariotto, A. B., Simard, E. P., Boscoe, F. P., Henley, S. J., et al. (2014). Annual report to the nation on the status of cancer, 1975-2010, featuring prevalence of comorbidity and impact on survival among persons with lung, colorectal, breast, or prostate cancer. Cancer, 120(9), 1290-1314. doi: 10. 1002/cncr. 28509 Ganz, P. A. (2001). Late effects of cancer and its treatment. Seminars in Oncology Nursing, 17(4), 241-248. doi: http://dx. doi. org/10. 1053 /sonu. 2001. 27914 Ganz, P. A. (2006). Monitoring the physical health of cancer survivors: A survivorship-focused medical history. Journal of Clinical Oncology, 24(32), 5105-5111. doi: 10. 1200/jco. 2006. 06. 0541 Hewitt, M., Greenfield, S., & Stoval, E. (2005). From cancer patient to can-cer survivor—Lost in transition. Washington, DC: National Academies Press. Hewitt, M. E., Bamundo, A., Day, R., & Harvey, C. (2007). Perspectives on post-treatment cancer care: Qualitative research with survivors, nurses, and physicians. Journal of Clinical Oncology, 25(16), 2270-2273. doi: 10. 1200/jco. 2006. 10. 0826 Howlader, N., Noone, A. M., Krapcho, M., Garshell, J., Miller, D., Altekruse, S. F., et al. (Eds. ). (2014). SEER cancer statistics review 1975-2011. Bethesda, MD: National Cancer Institute. Retrieved from http://seer. cancer. gov/archive/csr/1975_2011/. Keesing, S., Mc Namara, B., & Rosenwax, L. (2014). Cancer survivors' experiences of using survivorship care plans: A systematic review of qual-itative studies. Journal of Cancer Survivorship, 9(2), 1-9. doi: 10. 1007 /s11764-014-0407-x Kushi, L. H., Doyle, C., Mc Cullough, M., Rock, C. L., Demark-Wahnefried, W., Bandera, E. V., et al. (2012). American Cancer Society guidelines on nutrition and physical activity for cancer prevention: Reducing the risk of cancer with healthy food choices and physical activity. CA: A Cancer Journal for Clinicians, 62(1), 30-67. doi: 10. 3322/caac. 20140 Mayer, D. K., Nekhlyudov, L., Snyder, C. F., Merrill, J. K., Wollins, D. S., & Shulman, L. N. (2014). American Society of Clinical Oncology clinical expert statement on cancer survivorship care planning. Journal of Oncology Practice, 10(6), 345-351. doi: 10. 1200/jop . 2014. 001321 Mc Cabe, M. S., Bhatia, S., Oeffinger, K. C., Reaman, G. H., Tyne, C., Wollins, D. S., et al. (2013). American Society of Clinical Oncology statement: Achieving high-quality cancer survivorship care. Journal of Clinical Oncology, 31(5), 631-640. doi: 10. 1200/jco. 2012. 46. 6854 Morgan, M. A., & Denlinger, C. S. (2014). Survivorship: T ools for transi-tioning patients with cancer. Journal of the National Comprehensive Cancer Network, 12(12), 1681-1687. Mullan, F. (1985). Seasons of survival-Reflections of a physician with can-cer. New England Journal of Medicine, 313(4), 270-273. doi: 10. 1056 /nejm198507253130421 National Comprehensive Cancer Network. (2014). NCCN clinical prac-tice guidelines in oncology: Survivorship (v. 2. 2014). Retrieved from www. nccn. org/professionals/physician_gls/f_guidelines. asp# survivorship. Oeffinger, K. C., Hudson, M. M., & Landier, W. (2009). Survivorship: Childhood cancer survivors. Primary Care, 36(4), 743-780. doi: 10. 1016/j. pop. 2009. 07. 007 Pekmezi, D. W., & Demark-Wahnefried, W. (2011). Updated evidence in support of diet and exercise interventions in cancer survivors. Acta Oncologica, 50(2), 167-178. doi: 10. 3109/0284186X. 2010. 529822. [Epub 2010 Nov 24. ] Rock, C. L., Doyle, C., Demark-Wahnefried, W., Meyerhardt, J., Courneya, K. S., Schwartz, A. L., et al. (2012). Nutrition and physical activity guidelines for cancer survivors. CA: A Cancer Journal for Clinicians, 62(4), 243-274. doi: 10. 3322/caac. 21142 Rowland, J. H., Hewitt, M., & Ganz, P. A. (2006). Cancer survivorship: A new challenge in delivering quality cancer care. Journal of Clinical Oncology, 24(32), 5101-5104. doi: 10. 1200/jco. 2006. 09. 2700 Smith, R. A., Manassaram-Baptiste, D., Brooks, D., Cokkinides, V., Doroshenk, M., Saslow, D., et al. (2014). Cancer screening in the United States, 2014: A review of current American Cancer Society guide-lines and current issues in cancer screening. CA: A Cancer Journal for Clinicians, 64(1), 31-51. doi: 10. 3322/caac. 21212 Wood, M. E., Vogel, V., Ng, A., Foxhall, L., Goodwin, P., & T ravis, L. B. (2012). Second malignant neoplasms: Assessment and strategies for risk reduction. Journal of Clinical Oncology, 30(30), 3734-3745. doi: 10. 1200/jco. 2012. 41. 8681467 References
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causes. Exposure to fumes from cooking and burning of biomass is recognized as a significant risk in devel-oping countries. Occupational exposures can also cause COPD (GOLD, 2014). Examples include but are not limited to silica, coal dust, cotton dust, grain dust, toxic chemicals, secondhand smoke, biomass smoke, diesel exhaust, welding flames, and wood fin-ishing fumes (Balmes & Speizer, 2015). Several comorbidities are associated with COPD: cardiovascular disease, osteoporosis, metabolic syn-drome, diabetes mellitus, bronchiectasis, lung cancer, anxiety, and depression (GOLD, 2014). Additionally, COPD is recognized as a systemic disease evidenced by nutritional depletion and skeletal muscle dysfunc-tion (Decramer, De Benedetto, Del Ponte, & Marinari, 2005; Maltais et al., 2014). An asthma-COPD overlap syndrome (ACOS) has also been described (Global Initiative for Asthma [GINA], 2014). 2. P revalence and incidence According to U. S. National Center for Health Statistics data collected between 2007 and 2012, 14. 7% of adults aged 40-79 reported some degree of lung obstruction (including COPD and asthma), with adults aged 60-79 having a higher prevalence (17%) compared to younger adults aged 40-59 (13. 6%) (Tilert, Paulose-Ram, & Brody, 2015). Currently, COPD is the third leading cause of death in the United States (Centers for Disease Control and Prevention [CDC], 2015a). According to the CDC (2015a), COPD deaths among men have declined: 57. 0 per 100,000 in 1999 falling to 47. 6 per 100,000 in 2010 There has not been a similar decline in death rates in women (35. 3 per 100,000 in 1999 and 36. 4 per 100,000 in 2010) (CDC, 2015a). U. S. state-level data reported in 2012 revealed that people living in the Ohio and Mississippi River valleys had the highest incidence of COPD (CDC, 2012). I. Intr oduction and general background Chronic obstructive pulmonary disease (COPD) is an umbrel-la name for two major pulmonary obstructive disorders: chronic bronchitis and emphysema. Although each disorder has its own distinctive pathophysiology, many COPD patients have a combination of chronic bronchitis and emphysema. A. COPD 1. D efinition and overview COPD is defined as “a common preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles and gases. Exacerbations and comorbidities contribute to the overall severity in individual patients” (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2015, p. 2). The main pathophysiologic problem in COPD is expiratory airflow limitation. In the case of chronic bronchitis, loss of structural integrity and bron-chospasm in the larger airways, plus excess mucous production, are the cause of expiratory airflow limita-tion. The classic definition of chronic bronchitis is a productive cough for 3 months for 2 successive years (American Thoracic Society, 1962). In emphysema, smaller, more distal airways and alveoli are damaged, resulting in loss of structural integrity plus destruction of the alveolar-capillary membrane. The small airway changes result in early collapse during expiration, caus-ing airflow limitation. Additionally, the loss of surface area at the alveoli-capillary level impairs gas exchange. Smoking is recognized to be the most common cause of COPD. Environmental toxin exposures, including outdoor and indoor air pollution, are also known Lynda A. Mackin Chron IC obstru Ct Ive Pu LM on A ry D I se A se© Eliks/Shutterstock; © donatas1205/Shutterstock 468 49Chapt Er
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iii. R espiratory: chronic cough (with or without sputum production; may be inter-mittent); chronic sputum production; and progressive, persistent dyspnea (worsens with activity or on exertion), wheezing, hemoptysis iv. C ardiac: chest pain, fluid retention and peripheral edema, and dysrhythmias v. G astrointestinal: heartburn, reflux, cough with meals B. Objective The GOLD Guidelines (GOLD, 2014) recommend that assessment focus on an objective determination of disease severity and impact on functional and personal activities and determine risk of future events such as hospitaliza-tions, exacerbations, and death. 1. P hysical examination findings (T able 49-1). 2. S pirometry: Spirometry is an important tool in classifying the severity of chronic airflow limitation and is particularly useful as a confirmatory test. Key spirometric values are the forced vital capacity (FVC) and the forced expiratory volume in 1 second (FEV 1), percentage predicted and is performed before and after inhaled bronchodilator administration. A postbronchodilator FEV 1/FVC ratio of less than 0. 7 confirms airflow limitation. Classification of airflow limitation severity is further defined by FEV 1 value. See T able 49-2 (GOLD, 2014) for GOLD classification of severity of airflow obstruction in COPD. 3. C ombined assessment of COPD: The GOLD Guidelines recommend the combination of spirometric data, objective symptom measurement, and frequency of exacerbation be considered together to determine risk. Based on these data, II. Database A. Subjective 1. C OPD COPD is symptomatically characterized by chronic, progressive cough, dyspnea, and sputum production that can vary from day to day (GOLD, 2014). The clinician should elicit information about these key symptoms, as well as query progression of symptoms over time. The comprehensive history should also include the following:a. P ast health history i. M edical illnesses: asthma, allergies, nasal polyps, sinusitis, gastroesophageal reflux disease, childhood respiratory infections, adult respiratory illnesses, hospitalizations and other respiratory diseases. Elicit if there has been any pattern to symptom develop-ment over time. ii. S urgical history: chest or lung iii. E xposure history: environmental tobacco smoke exposure, occupational dusts and fume exposures toxins; indoor and out-door air pollution, cooking fumes, and biomass fuel combustion fumes (GOLD, 2014) iv. M edication history: medications taken to relieve symptoms currently and in the past (oral or inhaled bronchodilators and oral or inhaled steroids) b. F amily history: obstructive pulmonary disease (COPD, asthma, bronchiectasis) c. O ccupational and environmental history i. W ork-related exposures: toxins and fumes ii. E xposure to home cooking or biomass fuel fumes d. P ersonal and social history i. H istory of or current smoking; impact of symptoms on physical function and occu-pational activities. ii. Die t: caloric intake iii. E xercise capacity iv. S ocial support resources. e. R eview of systems i. C onstitutional signs and symptoms: fatigue, activity intolerance, weight change, and fevers; impact of symptoms on activities of daily living and occupational and recre-ational pursuits ii. Ea r, nose, and throat: allergic rhinitis, sinus symptoms, and postnasal drip Table 49-1 Classic Physical Examination Findings in Chronic Bronchitis and Emphysema Chronic bronchitis e mphysema Overweight Thin Cyanotic but breathing comfortably at rest Not cyanotic, breathing looks comfortable Noisy breath sounds, rhonchi, wheezing Quiet, distant breath sounds Peripheral edema No peripheral edema Note: Most chronic obstructive pulmonary disease patients have clinical characteristics of both chronic bronchitis and emphysema to varying degrees. 469 Database
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patients are grouped into one of four groups (A, B, C, D) with groups C and D being at the highest risk. Either the modified British Medical Research Council Questionnaire for Assessing the Severity of Breathlessness (m MRC) (Bestall et al., 1999) or the COPD Assessment T est (CAT) ( Jones et al., 2009) can be used to assess symptoms. See T able 49-3 for the m MRC Scale. The CAT can be accessed at http://www. catestonline. org/. Exacerbation fre-quency, and specifically if hospitalized, is considered. See T able 49-4 for the combined assessment of risk matrix. Table 49-2 Classification of Severity of Airflow Limitation in COPD (Based on Postbronchodilator FEV 1) In patients with F ev1/Fv C < 0. 70: GOLD 1: Mild FEV1 ≥ 80% predicted GOLD 2: Moderate 50% ≤ FEV1 < 80% predicted GOLD 3: Severe 30% ≤ FEV1 < 50% predicted GOLD 4: Very Severe FEV1 < 3 0% predicted 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. Table 49-3 Modified Medical Research Council Questionnaire (m MRC) for Assessing the Severity of Breathlessness Please check the box that applies to you (one box only) m MRC Grade 0. I get breathless only with strenuous exercise. ☐ m MRC Grade 1. I get short of breath when hurrying on the level or walking up a slight hill. ☐ m MRC Grade 2. I walk slower than people of the same age on the level because of breathlessness, or I have to stop for breath when walking on my own pace on the level. ☐ m MRC Grade 3. I stop for breath after walking about 100 meters or after a few minutes on the level. ☐ m MRC Grade 4. I am too breathless to leave the house or I am breathless when dressing or undressing. ☐ Reproduced from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2015). Pocket guide to COPD diagnosis, management, and pre-vention. Available from http://www. goldcopd. org/. Used with permission. Table 49-4 Combined Assessment of COPD 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. When assessing risk, choose the highest riskBDDPSEJOHUP(0-%HSBEFPSFYBDFSCBUJPOIJTUPS Z 0OFPSNPSFIPTQJUBMJ[BUJPOTGPS$01%FYBDFSCBUJPOTTIPVMECFDPOTJEFSFEIJHISJTL Patient Characteristic Spirometric Classification Exacerbations per year CAT m MRC ALow Risk Less Symptoms GOLD 1-2 ≤ 1< 10 0-1 BLow Risk More Symptoms GOLD 1-2 ≤ 1≥ 10 ≥ 2 CHigh Risk Less Symptoms GOLD 3-4 ≥ 2< 10 0-1 DHigh Risk More Symptoms GOLD 3-4 ≥ 2≥ 10 ≥ 2(C) (D) (A) (B) Risk (Exacrbation History)Risk (Gold Classification of Airflow Limitation ) Symptoms Breathlessness CAT < 10 CAT ≥ 10 m MRC 0-1 m MRC ≥ 2   ≥2 or ≥1 leading to hospitaladmission 1 (not leading to hospitaladmission) 0470 CHAPTER 49 | Chronic Obstructive Pulmonary Disease
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4. C hest radiograph: Does not confirm diagnosis of COPD but may demonstrate hyperinflation and flattened diaphragms and may reveal other conditions. In the absence of obstruction on pulmonary function tests, chest CT scan can provide evidence of nonobstructive emphysema. 5. C heck complete blood count (may see polycythemia in chronic hypoxemia) and complete metabolic panel. When vitamin D25 hydroxy serum levels are low, patients may be more likely to have respiratory symptoms. Hyperthyroid symptoms can sometimes mimic COPD. 6. P ulse oximetry: Saturation is reduced in cases of hypoxemia. Six-minute walk is used to evaluate oxygen need with exercise. Nocturnal oximetry can be ordered through a durable medical equipment (DME) company to evaluate oxygen need with sleep. 7. C onsider arterial blood gases: reflects hypoxemia and possible hypercapnia. 8. C onsider α1-antitrypsin deficiency screen (in cases of younger onset of symptoms and more extensive disease). 9. Add itional pulmonary function testing (lung volumes, diffusing capacity) and exercise testing may be useful in further differentiating diagnosis. Emphysema is often associated with air trapping (increased TLC and RV) and decreased diffusing capacity. 10. T o assess systemic effect of disease, composite assess-ments such as the BODE Index (Celli et al., 2004) may be useful: the BODE Index is a multidimen-sional mortality prediction that incorporates body mass index, severity of airflow obstruction, dyspnea, and exercise capacity as measured by 6-minute walk performance. III. Goals of clinical management of stable C o PD (GOLD, 2014) A. Reduce symptoms B. Improve activity tolerance Management of stable COPD focuses on improving activity tolerance and overall health status in addition to reducing symptoms. This goal is achieved through use of pharmacologic and nonpharmacologic therapeutics. C. Reduce risk Management of stable COPD also focuses on reducing future risk of the disease. The focus is on strategies to prevent disease progression, prevent and treat exacerbations, and reduce overall mortality. As with symptom reduction, both pharmacologic and nonpharmacologic therapeutics are used. Iv. Plan (components of COPD management) A. Pharmacologic therapy 1. P harmacologic therapeutics include short-acting (SA) and long-acting (LA) beta2-agonist or anticholinergic bronchodilators, oral and/or inhaled corticosteroids, phosphodiesterase-4 (PDE-4) inhibitor (for preven-tion of exacerbation), and in highly selected cases, theophylline or carbocysteine (GOLD, 2014). When clinically indicated, supplemental oxygen should also be used; oxygen flow rate can be determined though an oxygen prescription test with exercise (arranged through a pulmonary function laboratory) and at night (arranged through a DME company). 2. The G OLD Patient Group Classification provides a basis for initial pharmacologic therapy in stable COPD. See T able 49-5 for an overview of recommended pharmacologic therapy by COPD patient group. See T able 49-6 for formulations and typical doses of COPD medications 3. Ge neral pharmacotherapy recommendations for stable COPD per the GOLD Guidelines (GOLD, 2014) are as follows: a. B ronchodilators: Long-acting bronchodilators are preferred, but short-acting bronchodilators may be helpful if symptoms are not sufficiently relieved with long-acting bronchodilators alone. Inhaled bronchodilators are preferred over oral bronchodilators. Theophylline is not recom-mended unless other agents are not available or unaffordable. b. C orticosteroids: A trial of oral corticosteroid to determine steroid responsiveness is not recom-mended. Long-term treatment with oral or inhaled corticosteroids alone is not recommended. It is not recommended to use inhaled corticosteroids at doses outside typical dose range. c. PDE-4 inhibitor: May reduce the frequency of exacerbation in patients with chronic bronchitis, severe or very severe airflow limitation (category 3 or 4), or frequent exacerbations not controlled by a long-acting bronchodilator. B. Nonpharmacologic therapy 1. M anagement of stable COPD should incorporate regular exercise, including participation in a formal pulmonary rehabilitation program if available and qualified. C. Risk reduction strategies 1. S moking cessation or prevention 2. El iminate or reduce occupational exposures and indoor and outdoor pollution. 471 Plan
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