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As the global population becomes older, physicians are increasingly navigating the complexities of geriatric medicine. Older adults often have multiple chronic conditions that require ongoing treatment, which frequently results in the practice of polypharmacy — typically defined as the concurrent use of 5 or more medications.1

Although polypharmacy begins as a well-intentioned effort to manage cooccurring conditions, the interaction of these different medications can become a health hazard instead of an optimal solution. Given the increased risks for adverse drug interactions, medication errors, and cognitive impairment, addressing polypharmacy and developing a nuanced approach to geriatric care is crucial to safeguarding the health of older adults.

Increasing Prevalence of Polypharmacy in Older Adults

In a chapter on polypharmacy published in Geriatric Rehabilitation, co-authors Parulekar and Rogers noted that while only 13% of the United States population was aged 65 years and older, this age group accounted for 33% of total prescription medications.2 More than 50% of older adults with multimorbid conditions receive 5 or more medications, with the rate varying between 10% and 55% globally.3 Furthermore, a study of survey data from the Centers for Disease Control and Prevention (CDC) found that the majority of older adults in the US had major polypharmacy and nonsteroidal anti-inflammatory drugs (NSAIDs) were the most common medication type.4

The prevalence of polypharmacy is even higher among women. Research suggests that women are more likely than men to require more than 1 or more specialized medications,1 and older women have higher rates of multimorbidity relative to men — with a consequently higher prevalence of polypharmacy.5

"
Managing polypharmacy requires careful monitoring and coordination by health care providers to deprescribe, optimize medication regimens, and minimize risks for patients.

Erika Ramsdale, MD, an associate professor at the Department of Medicine, Hematology/Oncology at the University of Rochester Medicine, has studied the effects of polypharmacy on older adults initiating cancer treatment6 and spoke about this issue. “Polypharmacy and potentially inappropriate medications are very, very common in older adults, and especially within certain populations, such as older adults with cancer. [However], there is not an easy way to estimate the burden of medication-related adverse effects on patients and the health care system as a whole,” she remarked.

Risk factors for polypharmacy include both patient-level factors (eg, increased age, difficulty self-managing medications, multimorbidity, disabilities) as well as health care system-level components, such as poor continuity of care, prescribing cascades, the use of multiple pharmacies, and inadequately updated medical records.7,8

While polypharmacy is often deemed necessary to treat multimorbidity, the concurrent use of medications has been shown to cause harm in and of itself. In a retrospective cohort study published in 2023, older adults who received multiple medications experienced significantly higher rates of severe comorbidity relative to those who did not experience polypharmacy. Patients with polypharmacy also had a greater rate of all-cause hospitalizations and emergency department (ED) visits.9

Polypharmacy also carries specific neurologic and psychiatric risks. Older adults with polypharmacy and multimorbidity demonstrate greater levels of cognitive impairment, relative to their peers with fewer comorbidities and medications,10 and has been associated with worse self-reported health and depression in older adults.11

Given the risks associated with multiple medications in older adults, many experts have called into question the “appropriate” vs “inappropriate” use of polypharmacy.2 To this aim, Mohamed and colleagues conducted a study to examine the associations between polypharmacy, potentially inappropriate medications, and adverse treatment outcomes in a large national cohort of older adults with advanced cancer. They found that 67% of patients received 1 or more inappropriate medications, and the use of inappropriate medications increased the odds of unplanned treatment-related hospitalization. Additionally, polypharmacy overall was associated with increased risk for postoperative complications, hospitalizations, and mortality risk.8

Dr Ramsdale emphasized the importance of not just the number of medications prescribed to a patient, but also their appropriateness. “Some patients have polypharmacy by number, but all their medications are needed and appropriate.”

Further complicating this medication management issue, Dr Ramsdale addressed the challenge of differentiating between patients who develop symptoms from polypharmacy vs a root cause issue, such as comorbidities/disease. “Often, there is not one ‘root cause’ for a symptom or adverse effect in older adults. There are generally multiple contributing factors and you have to look at all of them and also how the factors interact with each other. One thing you can say is that medications are very often contributing and need to be considered each time something happens.”

Concerns & Barriers in the Management of Polypharmacy in Clinical Practice

Although a wealth of evidence has demonstrated the adverse health risks associated with polypharmacy, the question remains as to how health care systems should best manage this issue. Researchers conducted a study across 14 countries, including the US and UK, to identify the barriers associated with addressing polypharmacy in primary care. They found the most common barriers were a lack of evidence-based guidance, a lack of communication and decision-making systems, and gaps in support.12

From a clinician’s perspective, Dr Ramsdale stated,

Older adults tend to have many doctors who are all prescribing [medications], sometimes in different health systems, leading to fragmentation of care. Providers also may not want to alter [a medication] that another provider has prescribed.

In-depth review of medications takes a lot of time and thought, as each patient’s situation is unique and everyone has different goals and preferences. In addition, clinicians often do not have the time or resources to accomplish this for all patients because of the way our health care system is set up and [the type] of care it prioritizes.

Because one of the major concerns regarding polypharmacy is the increased risk for drug-to-drug interactions that are associated with adverse events and even death,13 there is a critical need to support physicians in these complicated — but increasingly common — cases of medication management.

How Can Providers Manage Polypharmacy in Older Adults?

Researchers have agreed that screening and interventional tools to optimize medication usage for improved outcomes may be beneficial.9 However, the frequency of prescribing multiple medications needs to be evaluated to reduce adverse events and medication burden in this patient population.4 Clinical studies have shown that one of the ways of reducing exposure to polypharmacy is through the practice of “deprescribing” medications.12

Deprescribing medications involves the identification of inappropriate or unnecessary medications to ultimately taper or discontinue their use. In 2019, the American Academy of Family Physicians (AAFP) developed recommendations for clinicians to help in deprescribing medications and reducing the risks for polypharmacy.7 Some of the key guidelines include the identification and prioritization of medications to discontinue, conducting informed decision-making with the patient, ensuring routine follow-up visits, and considering the risks vs benefits when refilling medications.

“Patients and their caregivers can be excellent advocates. All older adults should be [encouraged to] ask questions about the [safety] of their medications. The US Deprescribing Research Network and the Canadian Medication Appropriateness and Deprescribing Network have excellent patient resources available,” Dr Ramsdale recommended.

One of the key aspects in reducing polypharmacy is medication reconciliation, which can be more effectively achieved by improving the communication between provider and patient and the process of discharge from hospitalization. With the increased use of artificial intelligence and clinical decision support systems, the risks for polypharmacy may be minimized.14

Given that many older patients experience some degree of polypharmacy, pharmacists, specialist nurses, and physician assistants play a vital role in medication management, quality prescribing practices, and safety monitoring.4 Managing polypharmacy requires careful monitoring and coordination by health care providers to deprescribe, optimize medication regimens, and minimize risks for patients. Overall, polypharmacy in older adults is directly related to health care service outcomes,9 which warrants the need for a multidisciplinary, holistic approach to address and evaluate its use among patients.

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A 26-year-old Black man is referred for evaluation of a skin condition affecting his underarms and groin that has waxed and waned in intensity over the past 5 years. A female cousin is similarly affected. He has had several sites treated surgically and one boil recently drained. He complains of pain and malodor. Current medications are doxycycline and mirtazapine. Examination of the affected areas reveal scattered abscesses, sinus tracks, and hypertrophic scars.

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Idiopathic pulmonary fibrosis (IPF), a type of interstitial lung disease and the most common type of idiopathic interstitial pneumonia, is characterized by chronic fibrosis and progressive scarring of the lung tissues.1 The disease is of clinical significance because of its misdiagnosis and high mortality rate.1 The cause of IPF remains unknown; however, alveolar epithelial injury and abnormal injury repair are thought to be the main causative agents.2 Its estimated prevalence in the US ranges from 10 to 60 cases per 100,000 people.1 As IPF progresses, patients experience increasing episodes of dyspnea, eventually leading to respiratory failure.3 The average survival rate after diagnosis is 3 to 5 years; the probability of surviving 5 years after diagnosis is estimated to be 20% to 40%.2   

Differential Diagnosis 

A workup to diagnose IPF includes laboratory blood test, chest radiographs, high resolution computed tomography (HRCT), and lung biopsy.1 The first step in diagnosing IPF is ruling out other known causes of interstitial lung disease (ILD), with the most common being chronic hypersensitivity pneumonitis, sarcoidosis, connective tissue disease–related ILD, drug-induced ILD, and pneumoconiosis (Table 1).1 They share similar clinical and radiologic findings of the usual interstitial pneumonia (UIP) pattern.4 

Making an accurate diagnosis of IPF is critical because treatments vary amongst the different types of ILD. The incorrect treatment regimen may lead to a degradation in the patient’s quality of life and shorten their lifespan.4 

Another potential differential diagnosis is COVID-19 pneumonia. Findings of COVID-19 pneumonia can present in a similar way to idiopathic interstitial pneumonias on HRCT.5 An acute exacerbation of IPF will show ground-glass opacities on HRCT, comparable with findings of COVID-19 pneumonia.5 However, if the patient is presenting with the common symptoms of COVID-19 and had a known exposure to the virus, this can aid in ruling out IPF as a differential diagnosis. Radiologists play a vital role in discerning between COVID-19 pneumonia, idiopathic interstitial pneumonias, and chronic fibrosing lung diseases.5 

History and Physical Exam Findings 

A detailed patient history is necessary to rule out other causes of ILD. A history of co-morbidities, environmental exposures, medication use, family history, connective tissue disorders, high-risk occupations (such as those in dusty environments, including farming, hairdressing, and metal work) and history of tobacco smoking should be inquired about.6 There are more than 380 medications that are known to cause lung disease, some of the medications that are noted to cause ILD are Amiodarone, Macrobid, chemotherapy, Methotrexate, Amphotericin B, sulfonamides, biological agents, anti-inflammatories. 7 There are many environmental and occupational exposure risk factors of ILD, including, but not limited to, asbestos, silica, coal, organic and metal dusts, chemicals, mold, farm animals, and birds. 8  A history of smoking tobacco is associated with a 2-fold increase in developing IPF.8 The disease is more prevalent in people older than 50 years and in men.3 In a study by Luppi et al, an estimated 60% of patients with IPF had up to 3 of the following comorbidities: pulmonary hypertension, emphysema, obstructive sleep apnea, lung cancer, venous thromboembolism, chronic obstructive pulmonary disease, coronary artery disease, anxiety, depression, sarcopenia, osteoporosis, diabetes mellitus, hypothyroidism, and gastroesophageal reflux disease.9 

Patients with IPF most commonly present with complaints of progressive dyspnea, at rest or with exertion, and a nonproductive cough.1 Positive physical examination findings for IPF include inspiratory fine crackles and clubbing.3 Crackles may be present in all lung fields, correlating with fibrotic areas.10 Cyanosis, fatigue, right-sided heart failure, and respiratory failure are associated with more advanced disease.10 Patients may also report experiencing episodes of a sudden onset of respiratory failure with new abnormalities on HRCT unexplained by other causes.1 

Workup in Primary Care Setting  

The primary care provider can initiate the workup for IPF with laboratory testing, chest radiographs, and HRCT until the patient is referred to a pulmonologist. If the patient’s symptoms, history, and physical examination are suggestive of ILD, the clinician may proceed with obtaining laboratory testing to further rule out diagnoses closely associated with the symptoms of IPF. An extensive laboratory panel to include in the workup for IPF is indicated in Table 2.11 

Genetic testing should be included in the workup of IPF in all patients who have interstitial lung disease or those with a positive family history of interstitial lung disease.11 There are sporadic and familial forms of IPF and it is estimated that 33% of these forms can be diagnosed through genetic testing for certain genetic variants.12 A list of gene mutations is included in Table 3.12 Telomere length should also be tested when evaluating for sporadic and familial forms of IPF, as one third of patients with IPF will have short telomeres.12  

A complete workup of IPF includes spirometry, serologic testing, imaging, and lung biopsy.1 Pulmonary function tests including forced vital capacity (FVC), total lung capacity and diffusion capacity of the lungs for carbon monoxide (DLCO); 6-minute walk distance should also be assessed.1 A positive finding is a reduction in FVC, total lung capacity, DLCO, and 6-minute walk distance; however, these tests are imprecise in that the results may be normal in early disease or positive in the presence of other restrictive lung diseases.1 Serologic tests commonly included in the workup of IPF aid in exclusion, rather than being specific for IPF.1 However, serum lactate dehydrogenase, though non-specific, can be used as a biomarker for the severity of acute exacerbations and activity of the disease.10 

Chest radiographs are used for evaluating disease location, changes in volume loss, and the presence of pulmonary hypertension.10 The typical findings on chest radiograph are bilateral reticulonodular opacities, more commonly in the lower lobes.6 The disease presents with a UIP pattern on HRCT, consisting of heterogeneous paraseptal fibrosis.1 Peripheral, subpleural, and lower lobar reticulation, honeycombing, and single-layered clusters of cystic airspaces suggest the presence of IPF in the absence of other causes.1,10 Another feature of lung fibrosis is the presence of traction bronchiectasis and bronchiolectasis seen on HRCT.13 Findings on HRCT can be classified as typical, probable, indeterminate, or non-IPF based on the criteria shown in Table 4.10 If the pattern seen on HRCT is atypical or unclear, surgical lung biopsy or bronchoscopic lung cryobiopsy can be performed to provide a more definitive diagnosis.10 However, lung biopsies are restricted to certain patients because of potential complications.1 A patient presenting with a clinical history highly suggestive of IPF, a history of tobacco use and older than 60 years of age, with a probable UIP pattern on HRCT, does not need a lung biopsy.4 

Treatment 

The American Thoracic Society, European, Respiratory Society, Japanese Respiratory Society, and Asociación Latinoamericana de Tórax updated the IPF guidelines on diagnosis and treatment of IPF in 2022.14 The guidelines state that the treatments of IPF should include nonpharmacological and pharmacological, as discussed below.14 It is mentioned that patients’ comorbidities, most notable being pulmonary hypertension, gastroesophageal reflux, obstructive sleep apnea, and lung cancer, should be diagnosed and treated.14 However, in the treatment of gastroesophageal reflux, the updated guidelines recommend not treat patients with IPF with antacid medications or anti reflux surgery to improve respiratory outcomes.14 

Shared decision making between the patients, family members and provider can be utilized to also offer palliative care to patients.14 The guidelines state that providers should monitor patients’ disease progression, utilizing pulmonary function tests and the six-minute walk test, every four to six months.14 HRCT scans can also be used to monitor progression, presence of lung cancer or acute exacerbations.14 Acute exacerbations should be treated with corticosteroids, and it is recommended to avoid mechanical ventilation for most patients with respiratory failure.14 

"
Making an accurate diagnosis of IPF is critical because treatments vary amongst the different types of interstitial lung disease. The incorrect treatment regimen may lead to a degradation in the patient’s quality of life and shorten their lifespan.

Nonpharmacologic and pharmacologic treatments are implemented to slow the progression of IPF, enhance quality of life, and improve symptoms and survival.1 Nonpharmacologic treatment includes supplemental oxygen, pulmonary rehabilitation, and lung transplantation.1 Supplemental oxygen therapy should be started when oxygen saturation declines to 88% or less at rest or during activity.1 Pulmonary rehabilitation enhances physical exertion capacity, thus minimizing dyspnea during activity.1 

Undergoing lung transplantation can increase survival and improve quality of life; however, transplants are limited to select candidates.1 Clinicians should educate the patient about a lung transplant if they experience a sudden reduction in pulmonary function, decline in oxygen saturation, pulmonary hypertension, or need treatment in the emergency department for an acute exacerbation, respiratory deterioration, or pneumothorax.2 

Pirfenidone and nintedanib are the 2 antifibrotic medications approved for the treatment of IPF.2,6 Pirfenidone, a modified pyridine, slows the rate of fibrosis by reducing the production of collagen and suppressing transforming growth factor-β (TGFβ).2 Nintedanib, a tyrosine kinase inhibitor, reduces fibroblast activity by suppressing signaling pathways of vascular endothelial, fibroblast and platelet-derived growth factor receptors.2 Both medications slow FVC decline by 50% per year and are used to prevent acute exacerbations.10 

Pirfenidone and nintedanib have similar efficacy and tolerability; therefore, selecting between the 2 should be individualized to patient preference, comorbidities, and current medications.15 Side effects of pirfenidone include skin rash, weight loss, nausea, fatigue, and increased liver enzymes.2 Side effects of nintedanib include diarrhea, nausea, and hepatotoxicity; patients taking either antifibrotic therapy require liver-function monitoring.2 There are no definitive guidelines in predicting disease progression; it is recommended to initiate antifibrotic therapy early in the disease despite the patient’s baseline impairments.15   

Cost-Effectiveness of Antifibrotic Therapy 

The economic burden to the patient must be considered when treating patients with IPF. In the US, the annual cost of pirfenidone averages $113,193, and $112,357 for nintedanib.16 These prices were estimated from a database including patients who have commercial private insurance and those with Medicare Advantage.16 The lifetime analysis of cost and benefits demonstrates that symptom management treatment costs $79,815 with 3.78 quality-adjusted life years (QALYs), nintedanib costs $675,544 with 4.15 QALYs, and pirfenidone costs $688,778 with 4.10 QALYs.16 Though antifibrotics are clinically efficacious, there is a lower-than-expected number of patients with IPF receiving antifibrotics, possibly because of  their high price.16 A potential solution to the high cost of antifibrotic therapy is assistance programs through the drug’s manufactuer; however, these programs are highly individualized and not all patients will meet inclusion criteria.16 

Conclusion 

The complexity of IPF makes the diagnosis challenging. More research is still needed to accurately understand the disease pathophysiology and treatment. Prevention and early detection of IPF are necessary in developing a management plan for patients since a diagnosis carries a poor prognostic outcome. A multidisciplinary approach that includes primary care providers, pulmonologists, radiologists, and pathologists is essential to accurately make the diagnosis of IPF.10  

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A 56-year-old man presents with a right middle finger injury that occurred 1 month earlier and has progressively become more deformed. The patient notes that his finger hit the sharp edge of a fan and he sustained a laceration to the dorsum of the proximal interphalangeal (PIP) joint. He originally went to a local urgent care for sutures and wound management but over the past few weeks, the finger has become deformed (Figures 1 and 2). On physical examination, the patient has a healing laceration to the dorsum of the PIP joint. The PIP joint is hyperflexed and the distal interphalangeal (DIP) joint is in hyperextension consistent with a boutonniere deformity.

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