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Approximately 151 million people visit emergency departments (EDs) each year. The most common complaint is abdominal pain, as shown in our cover story by Kimberly Sapre, DMSc, PA-C, CAQ-EM. Health care providers may apply cognitive heuristics, or gut instincts, to make treatment choices in the chaotic environment of the ED. However, Dr Sapre believes that “heavy reliance on cognitive heuristics may lead to unconscious or implicit biases when caring for patients.”
Findings from Dr Sapre’s restrospective review of medical records from 17,401 ED visits at a single institution showed that racial/ethnic minority patients and women often receive fewer pain medications compared with White men. Many researchers have tried to understand the undertreatment of pain in EDs. Because pain can’t be measured objectively, assessments must rely on a subjective numerical pain scale, or visual pain scale, which rates a patient’s pain on a scale of 0 to 10. Often, a patient’s perception of pain does not match the clinician’s assessment of the patient’s pain, leading to inadequate pain management in the ED, as found in previous clinical studies.
Clinicians have gone back and forth over the under- vs overtreatment of acute and chronic pain for decades. To help guide treatment decisions, the Centers for Disease Control and Prevention (CDC) recently released recommendations for prescribing opioid pain medication for acute, subacute, and chronic pain, which update the 2016 CDC Guideline for Prescribing Opioids for Chronic Pain that was released amid the opioid crisis, led in part by the overprescribing of oral opioids in EDs.
“Patients with pain should receive compassionate, safe, and effective pain care,” Christopher M. Jones, PharmD, DrPH, MPH, acting director of the CDC’s National Center for Injury Prevention and Control, said in a press release. “We want clinicians and patients to have the information they need to weigh the benefits of different approaches to pain care, with the goal of helping people reduce their pain and improve their quality of life.”
Being aware of our bias and the appropriate use/amount of opioids and nonopioid medications can help improve acute pain management for all.
Nikki Kean, Director The Clinical Adviso r
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Advanced age should not exclude surgical interventions that can improve function, improve quality of life, or provide curative intent. However, careful screening of candidates is necessary to produce the best outcomes.1 Approximately 50% of Americans will have a surgical procedure after the age of 65 years.1 Postoperatively, some functional decline will occur in 31% of patients2 and greater than 20% may not be able to live independently after hospital discharge.3 Approximately 50% of older adults experience a complication related to hospitalization.4
Management of elderly patients with cancer who require a surgical procedure is challenging, with a greater risk for complications and mortality related to an increased incidence of cardiovascular, pulmonary, and renal disease. A decrease in physiologic reserves, multiple chronic conditions, and functional impairments are all associated with an increased risk for adverse surgical complications in patients with cancer.1-5 For the management of solid tumors, surgical removal provides the best curative opportunity. The International Society of Geriatric Oncology recommends a Comprehensive Geriatric Assessment (CGA) be completed on all patients older than 65 years who require surgical procedures.6
Three-quarters of women with ovarian cancer have advanced-stage disease and require treatment
More than 20% of older adults will not live independently after surgery.
A decrease in physiologic reserves, chronic conditions, and functional impairments are associated with increased risk for poor surgical outcomes.
with extensive procedures, chemotherapy, and/or radiation. Almost half of patients with newly diagnosed ovarian cancer are 65 years or older.5 Older women derive the same cancer-related survival benefit from aggressive procedures for advanced-stage disease as younger women but have a higher risk for surgical morbidity and mortality.7 Older women are commonly excluded from clinical trials and are less likely to be offered surgical procedures for ovarian cancer, despite the evidence demonstrating feasibility in this age group. 8
The following 2 cases illustrate the importance of preoperative screening in women with ovarian cancer.
Case 1
GK is a 76-year-old woman who is scheduled for a cytoreductive procedure for advanced ovarian cancer. Her medical history includes hypertension (well controlled with an angiotensin receptor blocker), hypothyroidism (levothyroxine), and osteopenia (calcium 1200 mg/d and vitamin D). She lives with her partner of 50 years and enjoys salsa dancing weekly. She quit smoking 25 years ago. Review of her systems is negative except for an increased feeling of bloating and early satiety. Blood work and testing reveal an elevated creatinine level (1.3 mg/dL; normal range: 0.1-0.4 mg/dL), normal 12-lead electrocardiogram (ECG) with good R wave progression, and normal weight (body mass index [BMI] 24).
Case 2
MT is a 65-year-old woman who is scheduled for a cytoreductive procedure for advanced ovarian cancer. Her medical history includes diabetes (metformin discontinued, started insulin: recent hemoglobin A1c 9%), osteoarthritis, and poorly controlled hypertension. She walks her dog twice a day to the mailboxes in her community. Her daughter assists with independent activities of daily living. Review of systems is negative except for increased urination and bilateral knee pain. She has an elevated creatinine level (2.3 mg/dL), 12-lead ECG shows poor R wave progression possibly indicating left ventricular hypertrophy, and obese (BMI 35).
Risk stratification begins with a focused history and physical examination. Review of systems should explore potential cardiopulmonary prodromes such as dyspnea, palpitations, or near syncopal events accounting for the potential presentation in the older adult.9
Several associations have collaborated to develop a classification system for preoperative assessment in older patients. The American College of Surgeons (ACS), American Society of
Anesthesiologists (ASA), and American Geriatrics Society (AGS)10,11 formed the ACS Geriatric Surgical Verification Program (GSV).12 The pilot project included enhancements to the original ACS National Surgical Quality Improvement Program (NSQIP) to include geriatric risk factors.13
The GSV Standard 5.6 Geriatric Vulnerability Screens Preoperative Assessment includes components of the CGA,13,14 which in some cases is more predictive of morbidity than the ASA Physical Status Classification System.15,16 GSV Standard 5.7 and 5.8 provide examples of management of high-risk vulnerable older adults and recommend interprofessional collaborations in cases of elective risk procedures (anesthesia, cardiology, physical therapy, pharmacy, social work, nutrition, and nursing). The ASA, using data from the NSQIP, applied a mixed effects model to sort elective noncardiac operations into low, intermediate, and high-risk categories. Examples of these procedures and their cardiac risk odds ratios are displayed in Table 1 17
• High-risk surgical procedures (such as vascular and any open intraperitoneal or intrathoracic procedures)
• History of ischemic heart disease (myocardial infarction or positive exercise test, current complaint of chest pain considered to be secondary to myocardial ischemia, use of nitrates, or electrocardiogram with pathological Q waves not counting prior coronary revascularization procedure unless other criteria of ischemia are noted)
• History of congestive heart failure
• History of cerebrovascular disease
• Diabetes mellitus requiring treatment with insulin
• Preoperative serum creatinine >2.0 mg/dL
Rate
No risk factors: 0.4% (95% CI, 0.1-0.8)
1 risk factor: 1.0% (95% CI, 0.5-1.4)
2 risk factors: 2.4% (95% CI, 1.3-3.5)
3 or more risk factors: 5.4% (95% CI, 2.8-7.9)
Major adverse cardiac events (MACE) are a leading cause of mortality in noncardiac procedures.18 Patients older than 65 years of age account for nearly 73% of all cases of MACE in noncardiac procedures.19 Cardiac death is the first symptom in 50% of patients with heart disease.19,20 Multimorbidity is not sufficient to determine risk.21 The Revised Cardiac Risk Index (RCRI) uses 6 risk factors for prediction of cardiac risk for noncardiac procedures. It has also been used to stratify risk for noninvasive testing preoperatively (Table 2).22,23 The Geriatric-Sensitive Perioperative Cardiac Risk Index (GSCRI) contains 7 questions, including variables from the NSQIP geriatric subset, that when answered predicts the probability of perioperative myocardial infarction or cardiac arrest.24
Assessment of functional capacity should be used to guide risk assessment and aims to determine if the patient has the physiologic reserve capacity to undergo an operation without complication, which is most commonly estimated from the ability to perform activities of daily living expressed as metabolic equivalents (MET) of oxygen consumption. One MET (3.5 mL/kg/min) is equal to the resting oxygen consumption of a 40-year-old man weighing 70 kilograms.25 The Duke Activity Status Index (DASI) is a 12-item patient self-report questionnaire that measures functional capacity, aspects of quality of life, and estimates of peak oxygen uptake to assist in clinical decision-making.26 Over time, the DASI has been used to identify patients at increased risk for MACE during preoperative assessment with a point total of less than 34.27
ASA
GK, who salsa dances with her partner, has significant aerobic activity and her high functional capacity is indicated in a DASI score of 50.2. With a normal BMI, her procedure can proceed initially as a laparoscopic procedure. Normal renal function and well-controlled blood pressure also add to her risk stratification. Overall cardiac risk for GK is low and she can proceed with the operation (Table 3).
ASA, American Society of Anesthesiologists; BSO, bilateral salpingo-oophorectomy; DASI, Duke Activity Status Index; GSCRI, Geriatric-Sensitive Perioperative Cardiac Risk Index; RCRI, Revised Cardiac Risk Index; TAH-BSO, total abdominal hysterectomy and bilateral salpingo-oophorectomy
MT has limited functional capacity due to osteoarthritis in her knees as indicated by a DASI score of 18.45. Her BMI is elevated requiring an open surgical procedure. Open procedures increase the risk for hospital mortality associated with MACE.28 Evidence of her poorly controlled diabetes and blood pressure further add to her risk. Renal insufficiency is a risk variable that is consistent across instruments. Poor R-wave progression is another common clinical finding and may reflect left ventricular hypertrophy possibly related to
Review of systems should explore potential cardiopulmonary prodromes such as dyspnea, palpitations, or near syncopal events.
poorly controlled blood pressure or ventricular systolic or diastolic dysfunction, which can be elevated by a transthoracic echocardiogram.29
Considering the need for further cardiac evaluation, which may include nuclear testing with myocardial perfusion imaging, MT will require pharmacologic stress agents such as regadenoson or adenosine because of her inability to perform a stress test on a treadmill.30 With a history of obesity and other risk factors, MT is at high risk and may require a computed tomography (CT) coronary angiography or invasive coronary angiography with careful attention to her renal function.31 The Cardiac Comorbidity Risk Score (CCoR) tested in arthroplasty outperformed the RCRI.32
For the older adult requiring elective noncardiac surgery, a CGA along with careful assessment of function, type of surgery, and risk for major cardiovascular events aids in determination of risk stratification (Figure).6,33 The practical relevance of patient-reported outcome measures should have clinical and practical relevance.34 Identifying the limitations in functional
reserves in the older adult leads to improved decision-making related to cardiac risk and elective procedures. ■
Cassandra Vonnes, DNP, GNP-BC,APRN, is the geriatric oncology Nurses Improving Care for Healthsystem Elders (NICHE) coordinator at Moffitt Cancer Center in Tampa, Florida. Dr Vonnes has taught clinical and didactic courses at the University of South Florida College of Nursing. Under her leadership, Moffitt Cancer Center was the first hospital in Florida to be recognized as Committed to Care Excellence for the Older Adult. In 2022, the Gerontological Advanced Practice Nurses Association awarded her the Excellence in Leadership 2022 Award.
1. Kim S, Brooks AK, Groban L. Preoperative assessment of the older surgical patient: honing in on geriatric syndromes. Clin Interv Aging. 2015;10:13-27.
2. Rønning B, Wyller TB, Jordhøy MS, et al. Frailty indicators and functional status in older patients after colorectal cancer surgery. J Geriatr Oncol. 2014;5(1):26-32.
3. van Abbema D, van Vuuren A, van den Berkmortel F, et al. Functional status decline in older patients with breast and colorectal cancer after cancer treatment: a prospective cohort study. J Geriatr Oncol. 2017;8(3):176-184.
4. Gajdos C, Kile D, Hawn MT, Finlayson E, Henderson WG, Robinson TN. Advancing age and 30-day adverse outcomes after nonemergent general surgeries. J Am Geriatr Soc. 2013;61(9):1608-1614.
5. Tew WP. Ovarian cancer in the older woman. J Geriatr Oncol. 2016;7(5):354-361.
6. Wildiers H, Heeren P, Puts M, et al. International Society of Geriatric Oncology consensus on geriatric assessment in older patients with cancer. J Clin Oncol. 2014;32(24):2595-2603.
7. Langstraat C, Aletti GD, Cliby WA. Morbidity, mortality and overall survival in elderly women undergoing primary surgical debulking for ovarian cancer: a delicate balance requiring individualization. Gynecol Oncol. 2011;123(2):187-191.
8. Ferrero A, Fuso L, Tripodi E, et al. Ovarian cancer in elderly patients: patterns of care and treatment outcomes according to age and modified frailty index. Int J Gynecol Cancer. 2017;27(9):1863-1871.
9. Vonnes C, El-Rady R. When you hear hoof beats, look for the zebras: atypical presentation of illness in the older adult. J Nurse Pract. 2021;17(4):458-461.
ACC/AHA, American College of Cardiologists/American Heart Association; ASA, American Society of Anesthesiologists; DASI, Duke Activity Status Index; GSCRI, GeriatricSensitive Perioperative Cardiac Risk Index; MACE, major cardiovascular event; NSQIP, National Surgical Quality Improvement Program; RCRI, Revised Cardiac Risk Index
FIGURE . Noncardiac surgical risk determinants.
10. Chow WB, Rosenthal RA, Merkow RP, Ko CY, Esnaola NF. Optimal preoperative assessment of the geriatric surgical patient: a best practices guideline from the American College of Surgeons National Surgical Quality Improvement Program and the American Geriatrics Society. J Am Coll Surg. 2012;215(4):453-466.
Patients older than 65 years account for approximately 73% of all cases of major adverse cardiac events in noncardiac procedures.
11. Doyle JD, Hendrix JM, Garmon EH. American Society of Anesthesiologists Classification. StatPearls [Internet]. Updated December 4, 2022. Accessed December 14 2022. https://www.ncbi.nlm.nih.gov/books/NBK441940/
12. Hornor MA, Ma M, Zhou L, et al. Enhancing the American College of Surgeons NSQIP surgical risk calculator to predict geriatric outcomes. J Am Coll Surg. 2020;230(1):88-100e1.
13. Ma M, Zhang L, Rosenthal R, Finlayson E, Russell MM. The American College of Surgeons Geriatric Surgery Verification Program and the Practicing Colorectal Surgeon. Semin Colon Rectal Surg. 2020;31(4):100779.
14. Samuelsson KS, Egenvall M, Klarin I, Lökk J, Gunnarsson U. Preoperative geriatric assessment and follow-up of patients older than 75 years undergoing elective surgery for suspected colorectal cancer. J Geriatr Oncol. 2019;10(5):709-715.
15. Shahrokni A, Vishnevsky BM, Jang B, et al. Geriatric assessment, not ASA physical status, is associated with 6-month postoperative survival in patients with cancer aged ≥75 Years. J Natl Compr Canc Netw. 2019;17(6):687-694.
16. Hurwitz EE, Simon M, Vinta SR, et al. Adding examples to the ASA-Physical Status Classification improves correct assignment to patients. Anesthesiology 2017;126(4):614-622.
17. Liu JB, Liu Y, Cohen ME, Ko CY, Sweitzer BJ. Defining the intrinsic cardiac risks of operations to improve preoperative cardiac risk assessments. Anesthesiology. 2018;128(2):283-292.
18. Devereaux PJ, Sessler DI. Cardiac complications in patients undergoing major noncardiac surgery. New Eng J Med. 2015;373(23):2258-2269.
19. Banco D, Dodson JA, Berger JS, Smilowitz NR. Perioperative cardiovascular outcomes among older adults undergoing in-hospital noncardiac surgery. J Am Geriatr Soc. 2021;69(10):2821-2830.
20. Reinier K, Stecker EC, Uy-Evanado A, et al. Sudden cardiac death as first manifestation of heart disease in women. Circulation. 2020;141(7): 606-608.
21. Bilimoria KY, Liu Y, Paruch JL, et al. Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surg. 2013;217(5):833-842e3.
22. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100(10):1043-1049.
23. Devereaux PJ, Goldman L, Cook DJ, Gilbert K, Leslie K, Guyatt GH. Perioperative cardiac events in patients undergoing noncardiac surgery: a review of the magnitude of the problem, the pathophysiology of the events and methods to estimate and communicate risk. CMAJ. 2005;173(6):627-634.
24. Alrezk R, Jackson N, Rezk MA, et al. Derivation and validation of a Geriatric‐Sensitive Perioperative Cardiac Risk Index. J Am Heart Assoc. 2017;6(11):e006648.
25. Ainsworth BE, Haskell WL, Leon AS, et al. Compendium of physical activities: classification of energy costs of human physical activities. Med Sci Sports Exerc. 1993;25(1):71-80.
26. Hlatky MA, Boineau RE, Higginbotham MB, et al. A brief self-administered questionnaire to determine functional capacity (the Duke Activity Status Index). Am J Cardiol. 1989;64(10):651-654.
27. Wijeysundera DN, Beattie WS, Hillis GS, et al. Integration of the Duke Activity Status Index into preoperative risk evaluation: a multicentre prospective cohort study. Br J Anaesth. 2020;124(3):261-270.
28. Sanaiha Y, Juo YY, Aguayo E, et al. Incidence and trends of cardiac complications in major abdominal surgery. Surgery. 2018;164(3):539-545.
29. Schröder LC, Holkeri A, Eranti A, et al. Poor R-wave progression as a predictor of sudden cardiac death in the general population and subjects with coronary artery disease. Heart Rhythm. 2022;19(6):952-959.
30. Matta M, Harb SC, Cremer P, Hachamovitch R, Ayoub C. Stress testing and noninvasive coronary imaging: what’s the best test for my patient? Cleve Clin J Med. 2021;88(9):502-515.
31. Chang H-J, Lin FY, Gebow D, et al. Selective referral using CCTA versus direct referral for individuals referred to invasive coronary angiography for suspected CAD: a radonmized, controlled, open-label trial. JACC Cardiovas Imaging. 2019;12(7_Part_2):1303-1312.
32. Onishchenko D, Rubin DS, van Horne JR, Ward RP, Chattopadhyay I. Cardiac Comorbidity Risk Score: zero-burden machine learning to improve prediction of postoperative major adverse cardiac events in hip and knee arthroplasty. J Am Heart Assoc. 2022;11(15):e023745.
33. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130(24):2215-2245.
34. Pardo Y, Garin O, Oriol C, Zamora V, Ribera A, Ferrer M. Patient-centered care in coronary heart disease: what do you want to measure? A systematic review of reviews on patient-reported outcome measures. Qual Life Res. 2022 Nov 9.
A patient in their mid-40s with a history of HIV presents to the emergency department with a 3- to 4-week history of vomiting and testicle pain that is associated with alternating constipation and diarrhea. The testicular pain is on the right side and the patient reports swelling plus intermittent dysuria. Can you make the diagnosis? See the full case at: clinicaladvisor.com/case_january_february23
Approximately 151 million patients visited emergency departments (EDs) in 2019 and the most common complaint was abdominal pain, according to data from the National Hospital Ambulatory Medical Care Survey (NHAMCS).1 Even though acute pain is a common concern triggering ED visits, the undertreatment of pain remains an emergency medicine issue.2 In 2019, non-Hispanic Black people visited EDs at twice the rate of nonHispanic White people.1,2 However, research suggests that racial/ethnic minority patients and women often receive fewer pain medications than non-Hispanic White men.3-7
In the 1990s, increased efforts to treat pain as the fifth vital sign were intended to improve pain treatment.8 Although overuse of opioids precipitated an epidemic, racial/ethnic and sex treatment differences persisted.2-4 Unconscious biases of clinicians may attribute to these treatment differences.6-7,9-10
Emergency medicine clinicians may be susceptible to treatment biases because of their chaotic work environment with multiple interruptions. These clinicians treat patients unknown to them and must rely on previous experiences, evidencebased medicine, and instincts to make quick, justifiable medical decisions for patients possibly experiencing life-threatening conditions. Because of their need to make quick decisions, many clinicians rely heavily on cognitive heuristics to make treatment choices.7 Cognitive heuristics are
mental shortcuts that rely on intuitive thinking, known better as gut instinct. However, heavy reliance on cognitive heuristics may lead to unconscious or implicit biases when caring for patients.7 The purpose of the current study was to evaluate whether racial/ethnic minority patients and women received different acute pain treatments compared with non-Hispanic White men in an ED that serves a diverse population.
The retrospective chart review included data from adult patients (aged 18 years and older) treated at a large Level 1 trauma center in northernVirginia from January 1, 2018, to December 21, 2019. A total of 180,210 adult ED visits occurred during the study period, and 19,624 patients had a chief complaint of abdominal pain.
Exclusion criteria included critical patients categorized as Code STEMI (ST-elevated myocardial infarction),11 Code stroke,12 or trauma team activations. Patients were also excluded if they were pregnant, treated for chronic pain, or sought psychiatric care or inpatient detoxification treatment.
Before analysis, the data were stripped of patient identifiers and a unique code was assigned to each patient encounter. Patients were categorized by self-reported sex, race, and ethnicity. The sex category included female and male patients; no other genders met the study’s inclusion criteria.The races reported by patients included non-Hispanic/Latino White, non-Hispanic/Latino Black or African American, Hispanic/
Latino, Asian, Middle Eastern, American Indian or Alaskan Native, Pacific Islander or Native Hawaiian, more than 1 race, or other. For this analysis, race categories were combined to include non-Hispanic/Latino White, non-Hispanic/Latino Black,Asian, or other, which included all other racial categories.
Ethnicity was reported as Hispanic/Latino or non-Hispanic/ Latino and patients had the option to report Hispanic/Latino for both race and ethnicity. For the current study, racial and ethnic Hispanic/Latino groups were combined into 1 group of Hispanic/Latino ethnicity. Patients’ records that were missing data for sex, race, and ethnicity were excluded. Additional data collected from patients’ charts included age, patient acuity level, diagnosis, and disposition information.
The primary outcome measures were pain score and pain medication. Specifically, the patient’s pain was reported using the numerical pain scale (0-10). Based on the pain scale score, the pain was rated as mild (1-3), moderate (4-6), or severe (7-10). Patients’ records that were missing a pain score or those with a pain score of 0 were excluded from the analysis. Pain medication data included time of ED arrival to medication ordered by the clinician, type of medications given to patients, and length of stay (LOS) in the ED. The type of medication was divided into 2 categories: nonopioids and opioids. Nonopioids included acetaminophen, ibuprofen, naproxen, aspirin, and ketorolac. Opioids included tramadol, hydrocodone, oxycodone, morphine, hydromorphone, and fentanyl. The opioid category also included combined medications, such as hydrocodone-acetaminophen, oxycodone-acetaminophen, or acetaminophen-codeine.
Statistical analyses were conducted using SPSS Statistics version 27 (IBM Corp., Armonk, NY). A P <.05 was considered significant. Cross-tabulation tables were used to evaluate the relationship between abdominal pain diagnoses and other independent variables. An χ2 test was performed when applicable. A 1-way analysis of variance (ANOVA) was used to calculate differences in pain treatment among racial/ethnic groups. If homogeneity of variances was violated, a Welch ANOVA was performed. An independent samples t test was used to calculate differences in pain treatment between sexes. If homogeneity of variances was violated, the Welch t test was performed. A 2-way ANOVA was used to calculate treatment differences between combined sex and racial/ethnic groups.
A total of 19,624 ED visits with the chief complaint of abdominal pain and data from 17,401 ED visits were included in the current study after exclusion criteria. The patients ranged in age from 18 to 101 years. Hispanic/Latino patients had the youngest mean age of 39.84 years (95% CI, 39.45-40.24) and accounted for 41.5% of the 18 to 44 age group (Figure 1).
The remaining mean ages were 50.71 years (95% CI, 49.8051.63) for Asian patients, 49.85 years (95% CI, 49.36-50.33) for non-Hispanic/Latino White patients, 42.73 years (95% CI, 41.86-43.59) for other patients, and 42.71 years (95% CI, 42.05-43.37) for non-Hispanic/Latino Black patients. Women had a mean age of 44.31 years (95% CI, 43.95-44.65), which was younger than that for men (46.37 years; 95% CI, 45.93-46.80).
A majority of patients identified as non-Hispanic/Latino White, non-Hispanic/Latino Black, Hispanic/Latino, or Asian (Figure 2). A smaller number of patients identified as other (871/17401, 0.05%), Middle Eastern (365/17401, 2%), more than 1 race (186/17401, 1%), American Indian or Alaskan Native (29/17401, 0.002%), or Native Hawaiian or Pacific Islander (31/17401, 0.002%); these patients were grouped into the category labeled other (1482/17401, 8.5%). Most patients were female (10778/17401, 61.9%). Most women were Hispanic/Latino (3845/10778, 35.3%), and most men were non-Hispanic/Latino White (2547/6524, 39%).
The majority of patients were assigned an acuity level of 3; however, non-Hispanic/Latino White patients were given an acuity level of 2 at a higher rate than non-Hispanic/Latino Black, Hispanic/Latino, and other patients (Table 1, page 12). More than half of patients (11369/17401, 65.3%) reported severe pain on arrival at the ED. Patients’ acuity level by sex was also examined (Table 2, page 12). Patients with a pain rating of 10 received pain medications faster than patients with any other pain rating (Table 3, page 13).
Overall, 60% (10436/17401) of patients were treated with either a nonopioid medication (3700/17401, 21.3%)
or opioid medication (6965/17401, 38.7%), whereas 40% (6965/17401) of patients did not receive any pain medications. Non-Hispanic/Latino White patients received more opioid medications than racial/ethnic minorities (Table 4, page 13). The differences persisted when factoring in the pain rating. Non-Hispanic/Latino White patients with a severe pain rating were more likely to receive opioids than non-Hispanic/ Latino Black, Hispanic/Latino, and Asian patients with severe pain, (P =.03).
Some ethnic/racial minority patients waited longer for room assignments on arrival at the ED. Non-Hispanic/Latino White patients were assigned a room 8.5 minutes faster than Hispanic/Latino patients (95% CI, 6.16-10.83) and 3.83 minutes faster than Asian patients (95% CI, 0.37-7.30). No differences were found between non-Hispanic/Latino Black patients (2.46 minutes; 95% CI, 0.73-5.65) or other patients (3.42 minutes; 95% CI, 0.28-7.11).
Hispanic/Latino patients waited 7.53 (95% CI, 2.27-12.79) minutes longer than non-Hispanic/Latino White patients before receiving their first pain medication. No statistical differences in time to first pain medication were found between non-Hispanic/Latino White patients and non-Hispanic/ Latino Black patients (4.58 minutes; 95% CI, 2.74-11.89), Asian patients (6.40 minutes; 95% CI, 1.80-14.60), and other patients (0.19 minutes; 95% CI, 8.40-8.78).
Non-Hispanic/Latino White patients experienced a longer LOS than all racial/ethnic minority patients (Table 4). They remained in the ED 15.08 minutes longer than non-Hispanic/ Latino Black patients (95% CI, 4.23-25.89), 22.12 minutes longer than Hispanic/Latino patients (95% CI, 14.23-30.01),
AMA, against medical advice; LPTC, left prior to treatment complete
Data are reported as no. (%) of total in each column
a Data missing for 6 non-Hispanic/Latino White patients, 3 Hispanic/Latino patients, and 1 Asian patient
b Data missing for 5 non-Hispanic/Latino White patients, 2 Hispanic/Latino patients, and 2 Other patients
c Includes patients sent to the operating room, admitted for observation or for inpatient admission, and transferred to another facility
AMA, against medical advice; LPTC, left prior to treatment complete
Data are reported as number (%) of total in each column
a Data missing for 4 women and 6 men
b Data missing for 7 women and 2 men
c Includes patients sent to the operating room, admitted for observation or for inpatient admission, and transferred to another facility
a Significant difference between total non-Hispanic/Latino White and racial/ethnic minority patients (P <.05) b Significant difference between total Hispanic/Latino and non-Hispanic/Latino White (P <.05)
and 29.87 minutes longer than other patients (95% CI, 17.37-42.37). No significant difference was found in the LOS between non-Hispanic/Latino White patients (335.29 minutes; 95% CI, 331.15-339.43) and Asian patients (334.59 minutes; 95% CI, 326.47-342.70).
Women waited 9 minutes longer than men for their first dose of medication after arrival (95% CI, 5.71-12.31).Women were also less likely to receive an opioid medication. Fewer women (27.9%) than men (36.4%) were admitted to the hospital. A statistically significant interaction effect between sex and racial/ethnic group was found for the type of medication given, (P =.03). Both non-Hispanic/Latino White men and women were more likely to receive opioids than men or women from other racial/ethnic groups. No interaction effect was found for the time of first medication after arrival, number of medications given, or LOS (Table 4).
The most common diagnosis was nonspecific abdominal pain (6051/17401, 34.8%), which included far more visits than the second most common diagnosis of colitis (1201/17401, 6.9%) (Figure 3).The top 10 diagnoses accounted for 70% of the diagnoses (12181/17401) at discharge. Significantly more women were diagnosed with cholelithiasis, urinary tract infection, and cholecystitis, whereas significantly more men were diagnosed with kidney stones. A greater number of Hispanic/ Latino patients were diagnosed with cholelithiasis (305/613, 49.8%), urinary tract infection (243/559, 43.4%), cholecystitis (190/398, 47.7%), and ovarian cysts (166/475, 34.9%) than non-Hispanic/Latino White patients. A greater percentage of non-Hispanic/Latino White patients were diagnosed with bowel obstruction, colitis, and kidney stones.
The current retrospective chart review found a significant difference in pain management between non-Hispanic/Latino White patients and racial/ethnic minority patients and women.
Non-Hispanic/Latino White patients were more likely to receive opioids during their ED visit than non-Hispanic/ Latino Black, Hispanic/Latino, Asian, or other racial/ethnic groups. Furthermore, women waited longer for pain medications and received fewer opioid medications.These observed treatment differences support previous studies that indicated disparities in acute pain treatment for minority and female populations.2-6
When patients arrive at an ED, they receive a brief initial assessment by a nurse, who assigns an acuity level using the Emergency Severity Index (ESI) triage algorithm.13 Patients requiring direct lifesaving intervention are considered level 1.13 Level 1 is the most objective; the remaining 4 levels are assessed using objective and subjective patient evaluations that require experience, clinical gestalt, and vital signs review. Since the decision to categorize a patient as level 2 or 3 is subjective, assessment of these acuity levels may be biased.
In the current study, non-Hispanic/Latino White patients were assigned a higher acuity level than those in racial/ ethnic minority groups, which suggests that non-Hispanic/ Latino White patients presented with more urgent needs and required more resources. However, Zhang et al noted racial disparities in ESI assignment, where non-Hispanic/Latino White patients were assigned more urgent ESI levels than non-Hispanic/Latino Black and other minority patients.14
Unfortunately, because of bias in the subjective component
of the ESI, minority patients may receive lower acuity scores than their non-Hispanic/Latino White counterparts. For the same reason, a higher percentage of men than women in the current study were assigned a level 2 acuity score. As with racial/ethnic minority patients, gender bias may also influence the ESI score during triage. Study results also showed that racial/ethnic minority patients had a shorter LOS than nonHispanic/Latino White patients. One possible explanation for this result is that more non-Hispanic/Latino White patients were assigned higher acuity levels, which likely required more complex treatments and more resources that increased the LOS. Overall, the role of bias and its relation to quick, efficient care of racial/ethnic minority patients remains unclear.
Hispanic/Latino patients also waited longer for pain medications after arrival at the ED. A possible factor contributing to these longer wait times may be an existing language barrier. The population served by the hospital in northern Virginia in the current study is diverse and includes more than 728,000 immigrants.15 This foreign-born population accounts for 31% of the local population, which is higher than the state (13%) and US (14%) averages.15,16 Eight of 10 immigrants are from Asian or Latin American countries; the most common country of origin is El Salvador (12%).15 A large percentage of these immigrants are highly educated and speak English “very well.”15 However, 4 out of 10 immigrants speak English at lower levels.15 Of those in the Hispanic/Latino community, 53% are not fluent in English and require interpretation assistance when seeking care.17
Women of all racial/ethnic groups in the current study also waited longer than men to receive pain medications after arrival.These results support those of Chen et al,18 who found women waited longer than men to receive medication for acute abdominal pain in the ED.Treatment of abdominal pain in women is complex.Although clinicians perform pelvic examinations on women presenting with this complaint,19 abdominal and pelvic causes of pain must be considered as possible diagnoses. In general, pelvic examinations should not delay pain medications, but this delay for women may be caused by clinicians waiting for results of a pregnancy test. If the patient is pregnant, it changes the differential diagnosis and limits safe medication treatment options.
Women were less likely than men to receive opioid medications.The finding suggests that a woman’s pain is considered less severe than a man’s pain in the ED setting, resulting in more opiate use in men. Samulowitz et al20 reported that clinicians often undertreat women’s pain because these patients may not be taken seriously. Because of traditional gender norms for women, clinicians may consider their pain symptoms as complaining, malingering, emotional, hysterical, or psychogenic.20 In contrast, men are seen as stoic, pain tolerant, and less likely
to seek health care, which makes their pain complaints seem more severe to clinicians.20,21 Therefore, the undertreatment of acute pain in women may be related to gender biases. Similarly, unconscious biases of clinicians may also affect how racial/ ethnic minority patients are treated.
One limitation of the current study is related to the study design. It is a single-center retrospective chart review, so it limits generalizability. Furthermore, data extracted during a chart review is limited by the information originally recorded in the electronic medical record. Although the use of technology in health care makes it easier to aggregate large data sets of patient treatments, extracting that data to determine the full extent of the patient’s health care treatment can be tedious. Another limitation of the current study is that the race/ethnicity or gender of the clinician ordering the pain medication was not recorded. Research suggests that patients prefer being treated by clinicians who look like them, which creates a more trustworthy relationship between parties.22,23 However, additional research is needed to determine how race/ethnicity or gender of the clinician or nursing staff affects treatment. The current study is also limited regarding medication data since all medications given to the patient were not recorded. For several abdominal conditions, patients are typically given medications other than anti-inflammatory or opiate medications.24,25 For instance, the gastrointestinal cocktail (viscous lidocaine, aluminum hydroxide, and magnesium hydroxide) and intravenous famotidine are often given for gastritis. Dicyclomine, an antispasmodic, is usually provided for abdominal spasms.
In 2019, which racial/ethnic group had the highest rate of ED visits?
Patients with urinary tract infections are often given phenazopyridine for bladder spasms. Although these medications treat pain, they were not evaluated in the current study.
The current retrospective chart review evaluated whether racial/ethnic minority patients and women received different acute pain treatments from non-Hispanic/Latino White men in the ED. Results indicated that non-Hispanic/Latino White patients were more likely to receive opioids, and women waited longer for pain medications and received fewer opioid medications. Treatment of pain is complicated because no objective way to determine pain intensity is available. The clinician must rely on subjectivity and trust the patient’s perception of pain based on a basic rating system from 0 to 10 points.7 This lack of objectivity for determining pain intensity creates treatment biases such as less or delayed treatment for racial/ ethnic minority patients and women. ■
Kimberly Sapre, DMSc, PA-C, CAQ-EM, is a medical consultant for an insurtech company. She is a clinical instructor in Washington, DC, and practices emergency medicine in Falls Church, Virginia. She has 11 years of experience as a PA with previous experience in neurosurgery and interventional pain medicine.
1. Cairns C, Ashman JJ, Kang K. Emergency department visit rates by selected characteristics: United States, 2019. NCHS Data Brief. 2022;(434):1-8.
2. Shah AA, Zogg CK, Zafar SN, et al. Analgesic access for acute abdominal pain in the emergency department among racial/ethnic minority patients: a nationwide examination. Med Care. 2015;53(12):1000-1009.
3. Berger AJ, Wang Y, Rowe C, Chung B, Chang S, Haleblian G. Racial disparities in analgesic use amongst patients presenting to the emergency department for kidney stones in the United States. Am J Emerg Med. 2021;39:71-74.
4. Lee P, Le Saux M, Siegel R, et al. Racial and ethnic disparities in the management of acute pain in US emergency departments: meta-analysis and systematic review. Am J Emerg Med. 2019;37(9):1770-1777.
5. Pletcher MJ, Kertesz SG, Kohn MA, Gonzales R. Trends in opioid prescribing by race/ethnicity for patients seeking care in US emergency departments. JAMA. 2008;299(1):70-78.
6. Hall WJ, Chapman MV, Lee KM, et al. Implicit racial/ethnic bias among health care professionals and its influence on health care outcomes: a systematic review. Am J Public Health. 2015;105(12):e60-76.
7. Johnson TJ, Hickey RW, Switzer GE, et al. The impact of cognitive stressors in the emergency department on physician implicit racial bias. Acad Emerg Med. 2016;23(3):297-305.
8. Levy N, Sturgess J, Mills P. “Pain as the fifth vital sign” and dependence on the “numerical pain scale” is being abandoned in the US: why? Br J Anaesth. 2018;120(3):435-438.
9. FitzGerald C, Hurst S. Implicit bias in healthcare professionals: a systematic review. BMC Med Ethics. 2017;18(1):19.
10. Maina IW, Belton TD, Ginzberg S, Singh A, Johnson TJ. A decade of studying implicit racial/ethnic bias in healthcare providers using the implicit association test. Soc Sci Med. 2018;199:219-229.
11. Koh JQ, Tong DC, Sriamareswaran R, et al. In-hospital ‘CODE STEMI’ improves door-to-balloon time in patients undergoing primary percutaneous coronary intervention. Emerg Med Australas. 2018;30(2):222-227.
12. Seah HM, Burney M, Phan M, et al. CODE STROKE ALERT-concept and development of a novel open-source platform to streamline acute stroke management. Front Neurol. 2019;10:725.
13. Gilboy N, Tanabe P, Travers DA, Rosenau AM, Eitel DR. Emergency Severity Index, Version 4: Implementation Handbook. AHRQ Publication No. 05-0046-2. Agency for Healthcare Research and Quality. May 2005. https://www.sgnor.ch/ fileadmin/user_upload/Dokumente/Downloads/Esi_Handbook.pdf
14. Zhang X, Carabello M, Hill T, Bell SA, Stephenson R, Mahajan P.Trends of racial/ ethnic differences in emergency department care outcomes among adults in the United States from 2005 to 2016. Front Med (Lausanne). 2020;7:300.
15. A profile of our immigrant neighbors in northern Virginia.The Commonwealth Institute. Accessed September 9, 2022. https://thecommonwealthinstitute.org/ research/a-profile-of-our-immigrant-neighbors-in-northern-virginia/
16. U.S. Census Bureau QuickFacts: Fairfax County, Virginia. Accessed September 9, 2022. https://www.census.gov/quickfacts/fairfaxcountyvirginia
17. Goren L, Cassidy M. A closer look: the contributions of hispanic and latino immigrants to virginia’s economy. Accessed September 9, 2022. https:// thecommonwealthinstitute.org/research/a-closer-look-the-contributions-ofblack-immigrants-to-virginias-economy/
18. Chen EH, Shofer FS, Dean AJ, et al. Gender disparity in analgesic treatment of emergency department patients with acute abdominal pain. Acad Emerg Med. 2008;15(5):414-8.
19. Naamany E, Reis D, Zuker-Herman R, Drescher M, Glezerman M, Shiber S. Is there gender discrimination in acute renal colic pain management? A retrospective analysis in an emergency department setting. Pain Manag Nurs 2019;20(6):633-638.
20. Samulowitz A, Gremyr I, Eriksson E, Hensing G. “Brave men” and “emotional women”: a theory-guided literature review on gender bias in health care and gendered norms towards patients with chronic pain. Pain Res Manag. 2018;2018:6358624.
21. Hoffman KM, Trawalter S, Axt JR, Oliver MN. Racial bias in pain assessment and treatment recommendations, and false beliefs about biological differences between blacks and whites. Proc Natl Acad Sci U S A. 2016;113(16):4296-4301.
22. Shen MJ, Peterson EB, Costas-Muñiz R, et al. The effects of race and racial concordance on patient-physician communication: a systematic review of the literature. J Racial Ethn Health Disparities. 2018;5(1):117-140.
23. Ashton-James CE, Nicholas MK. Appearance of trustworthiness: an implicit source of bias in judgments of patients’ pain. Pain. 2016;157(8):1583-1585.
24. Macaluso CR, McNamara RM. Evaluation and management of acute abdominal pain in the emergency department. Int J Gen Med. 2012;5:789-797.
25. Natesan S, Lee J, Volkamer H, Thoureen T. Evidence-based medicine approach to abdominal pain. Emerg Med Clin North Am. 2016;34(2):165-190.
A 67-year-old man presents to the office for a yearly skin check. The patient has a history of basal cell carcinoma, which was treated with Mohs surgery 2 years ago without incident. Because of his history of skin cancer, the patient is careful to routinely perform a skin check. He recently noticed several hard scaly spots on his forehead and scalp that he would like evaluated. He had similar lesions in the past that were treated at his last visit with liquid nitrogen without an issue. On physical examination, the patient has several papules with an erythematous base and white gritty scale of varying thickness scattered on the scalp, forehead, nose, forearms, and dorsal hands.
A 72-year-old woman presents to the dermatology clinic for a routine annual skin check. The patient has a fair complection and history of sun exposure during her youth. She has a history of numerous nonmelanoma skin cancers and actinic keratoses that she has monitored over the years. On her current visit, she points to a lesion on her left shin that has been present for approximately 3 months and is growing. The patient notes that the lesion is tender and sometimes bleeds. She does not have any similar lesions elsewhere on her body. On physical examination, a 1.2- x 1.3-cm pink scaly plaque with focal areas of ulceration is noted on the left anterior lower leg.
Actinic keratosis (AK; also known as solar keratosis or senile keratosis) was first described by Duhreuilh in 1896 as keratosis senilis. The lesions were first called actinic keratoses by Pinkus in 1958 to emphasize their keratotic (thickened and scaly) aspects.1,2 These lesions are generally diagnosed in individuals 45 years and older and are more common in men and light-skinned individuals in geographical areas with increased sunlight exposure such as Australia.3,4
Actinic keratosis arises from keratinocyte proliferation at the dermoepidermal junction, disturbing regular epidermal differentiation and causing hyperkeratosis.5 This abnormal keratinocyte proliferation stems from DNA mutations as a result of exposure to UV light from sunlight and artificial sources such as tanning beds and psoralen and UV-A (PUVA) therapy.3,5 The most important cause of AK is exposure to UV-B radiation from sunlight.2
Actinic keratoses are considered premalignant by many researchers, while others have classified them as small, localized squamous cell carcinoma in situ.1,2,5 Mutations of TP53 are the most common mutation seen in AKs.2-4 Generally, once the lesion reaches the depth of the deep reticular dermis or if the atypical keratinocytes extend throughout the entire epidermis, the lesion is considered to have progressed to squamous cell carcinoma (SCC).5 Conversion rate of AKs to SCC is approximately 0.25% to 1% per year. The number of SCCs that develop from AKs is considered to be approximately 60%.5
Actinic keratoses present as scaly, rough, flesh-colored or erythematous papules and patches that may be tender, itchy, or asymptomatic.2,3,6 The lesions are divided into 3 grades depending on clinical presentation. Grade I lesions are thin and easier to feel than to see; grade II AKs are readily felt and seen; and grade III AKs are thick, hypertrophic, and hyperkeratotic.5 The texture of AKs is gritty and similar to sandpaper.2,3 Some lesions may contain pigment or telangiectasias.2,3 Their size can vary from millimeters to more than 2 centimeters and occur with the greatest frequency in sun-exposed areas including the upper extremities, upper back, neck, face, and areas of the scalp with thinning or absent hair.2-4,6 Lesions on the upper extremities often have greater thickness and more hyperkeratosis than those found on the head and neck.3
Histologic analysis of AKs reveals atypical keratinocytes, loss of polarity, nuclear pleomorphism, and increased mitotic
figures.2-4 Abnormal keratinocyte development can lead to alternating hyperkeratosis and parakeratosis in the stratum corneum.2,3 Keratinocytes in hair follicles and sweat glands will appear normal.3 The dermis may contain inflammatory infiltrates with plasma cells and lymphocytes as well as solar elastosis.2,3 Actinic keratoses are classified histologically as acantholytic, atrophic, bowenoid, hypertrophic, lichenoid, or proliferative. Some AKs may be confused as SCC, especially since there are no clear guidelines for differentiating between AKs and SCC.2,3 Invasive SCC will spread into the dermis, unlike AKs.4
Actinic keratoses are usually diagnosed clinically and can either spontaneously resolve, remain stable, or progress to SCC.2-4 Since it is impossible to predict which AKs may become malignant, they must be treated.3 Cryotherapy, topical fluorouracil cream, imiquimod cream, carbon dioxide lasers, chemical peels, dermabrasion, curettage and electrodessication, and photodynamic therapy are typically used for treatment of AKs.3,5
Treatment with liquid nitrogen had a 99% cure rate after 1 year in a study.5 Cryotherapy results vary with aggressiveness of application and the location and depth of the lesion. This therapy modality is most effective when treating single lesions.4-6 Side effects often include erythema and pain with possible scarring and depigmentation. Cryotherapy can be less effective in treating hyperkeratotic lesions.4,6
Topical fluorouracil treatment is most effective in treating multiple lesions located on the head and neck by triggering inflammatory processes within the lesions.3-5 The inflammatory process may cause ulceration and erosion.4 A study by Jansen et al compared the effectiveness of 5% topical fluorouracil cream with 5% imiquimod cream, methyl aminolevulinate photodynamic therapy (MAL-PDT), and 0.015% ingenol mebutate gel after 12 months.7 The differences in success rates between the 4 treatment options were significant, with fluorouracil cream having a 74.7% success rate and imiquimod, MAL-PDT, and ingenol mebutate showing 53.9%, 37.7%, and 28.9% success rates, respectively. The authors defined treatment success as a 75% or greater reduction in the number of AKs. The group randomized to receive fluorouracil treatment also reported higher rates of treatment satisfaction and in health-related
Actinic keratoses present as scaly, rough, flesh-colored or erythematous papules and patches that may be tender or itchy.
quality of life.7 Curettage and electrodessication are typically only used for hyperkeratotic AKs and can cause scarring.4,6
The patient in this case was diagnosed clinically with actinic keratoses and was treated with liquid nitrogen in clinic and was also given a prescription for topical fluorouracil for treatment of numerous AKs on his scalp.
The first description of squamous cell carcinoma in situ (SCCIS) was made by Bonney in 1914.8 The incidence of SCC is 356 per 100,000 White men in the US and 16 per 100,000 people in central Europe.9 Patients with a history of organ transplantation are up to 250 times more likely to develop SCC and their tumors are more likely to metastasize.9
Squamous cell carcinoma is most commonly found among older individuals in their mid-60s and is more common in White persons.10 Notable risk factors include high amounts of sun exposure, immunosuppression, and male gender (3:1 male to female ratio). Among people of color, including those of African, Asian, and Hispanic descent, cutaneous SCC is the most common skin cancer. Black patients with SCC have a higher mortality rate than non-Black patients because of delays in diagnosis and greater likelihood of occurrence of SCC in areas of prior trauma or scars, which also leads to a worse prognosis.10
Squamous cell carcinoma develops because of several different mutations in DNA. Mutations in tumor protein 53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), RAS, and NOTCH1 genes are commonly implicated in the development of SCC. Of these gene mutations, TP53 is the most common cause.Tumor protein 53 mutations often arise as a base mutation where cytosine is replaced with thymine at dipyrimidine sites, which allows SCC cells to evade apoptosis and continue to grow. Cyclin-dependent kinase inhibitor 2A mutations affect regulation of the cell cycle, while RAS gene mutations lead to changes in cell cycle transduction. These mutations are primarily caused by UV light damage.10,11
Histologic and physical characteristics of SCCs are important for management and prognosis. Squamous cell carcinoma has 2 well-differentiated histologic subtypes: keratoacanthoma and verrucous carcinoma. Keratoacanthomas appear crateriform
with a central keratin plug.9 Verrucous carcinomas are further differentiated into 2 subtypes: Buschke-Lowenstein, which are found in the genital and groin areas, and epithelioma cuniculatum, which are found on the bottom of the feet. Desmoplastic and adenosquamous histologic subtypes have a worse prognosis, with a higher risk for metastasis and recurrence after treatment.10,12-14
Other prognostic factors associated with a greater chance of metastasis and recurrence include a diameter of 2.0 cm or greater; a depth greater than 2 mm; perineural invasion of nerves greater than 0.1 mm; poorly differentiated tumors; previously treated or recurrent SCC; SCCs arising within chronic wounds or scars; and lesions arising in a patient with a suppressed immune system.10 Location of the SCC is another prognostic factor: SCCs on the lip and ear have the greatest risk of metastasizing than those in other locations.9,10
Diagnosis of SCC depends on clinical presentation and biopsy of the lesion. Lesions are most often found on the scalp, face, neck, dorsal hands, and forearms. They are erythematous to skin-colored papules or plaques and have varied degrees of scale. Lesions may have crust, erosions, or ulcerations. Some are cutaneous horns that contain actinic keratoses at the base that can progress to SCC. Keratoacantomas present as a rapidly enlarging papule with a central keratotic plug.15,16
keratoacanthoma and verrucous.
Dermoscopy is helpful in making a diagnosis.Vascular patterns that are present on dermoscopy are either small dotted vessels, glomerular vessels, or elongated vessels resembling hairpins. Erosions or ulcerations will appear as brown-red or black-colored surface blotches.10,15
Biopsy is needed to confirm the diagnosis of SCC.16 On biopsy, well-differentiated SCC will have atypical keratinocytes in the epidermis with disordered maturation as well as hyperkeratosis and parakeratosis. A downward proliferation of nests of keratinocytes extending into the dermis is also found. Nuclei of these keratinocytes will display varying degrees of pleomorphism and mitoses as well as prominent nucleoli. Degrees of cellular differentiation vary among tumors.15
Lesions that can mimic SCC include melanoma, where suspicious lesions should also be completely biopsied; actinic keratoses, which appear red, scaly, and inconsistent in texture compared with the surrounding skin; and basal cell carcinoma,
Two histologically differentiated subtypes of squamous cell carcinoma exist:
Dermatologic presentation
• Scaly, rough, flesh-colored or erythematous papules and patches
• May be tender, itchy, or asymptomatic
• Gritty texture similar to sandpaper
• May contain pigment or telangiectasias
• Can vary from 1 mm to >2 cm
• Ulcerated red plaque
• Central plug
Characteristic locations
• Head
• Neck
• Scalp
• Upper back
• Upper extremities
Potential risk factors
• UV and sunlight exposure
• Immunosuppression
• Lighter skin pigmentation
• Baldness
• Male gender
• Age greater than 70 years
Etiology
• DNA mutations (eg, in TP53) resulting from UV exposure
• Arise from keratinocyte proliferation at dermoepidermal junction
• Irregular epidermal differentiation and hyperkeratosis
Histology
• Acantholytic, atrophic, bowenoid, hypertrophic, lichenoid, or proliferative
• Atypical keratinocytes in basal epidermis or throughout entire epidermis in advanced lesions
• Lack polarity and nuclear pleomorphism
• Usually have increased mitotic figures
• Anaplastic and pleomorphic nuclei may be seen in stratum spinosum and stratum basale
• Alternating hyperkeratosis and parakeratosis in stratum corneum
• Dermis may contain inflammatory infiltrates with plasma cells/lymphocytes and solar elastosis
Diagnosis
Treatment
• Diagnosed clinically
• May be biopsied
• Carbon dioxide lasers
• Chemical peels
• Cryotherapy
• Curettage and electrodessication
• Dermabrasion
• Fluorouracil
• Imiquimod
• Photodynamic therapy
CDKN2A, cyclin-dependent kinase inhibitor 2A; TP53, tumor protein 53
• Forearms
• Hands
• Head
• Neck
• Scalp
• UV and sunlight exposure
• Immunosuppression
• Lighter skin pigmentation
• Baldness
• Male gender
• Age greater than 60 years
• UV exposure
• Mutations in TP53, CDKN2A, RAS, and NOTCH1
• Keratoacanthoma, verrucous carcinoma, desmoplastic, and adenosquamous
• Atypical keratinocytes in the epidermis with disordered maturation
• Hyperkeratosis and parakeratosis
• Downward proliferation of nests of keratinocytes extending into the dermis
• Atypical keratinocytes with pleomorphism, mitoses, and prominent nucleoli
• Clinical presentation
• Biopsy to confirm diagnosis
• Cryotherapy
• Electrodessication
• Fluorouracil
• Imiquimod
• Mohs surgery
• Radiotherapy
• Surgical excision
which is often described as a pearly telangiectatic papule, though biopsy is also needed to confirm this diagnosis.16
Treatment of SCC involves excision, surgery, cryotherapy, and biologic agents. Low-risk, nonmetastatic SCC requires excision with a margin of 4- to 6-mm. Electrodesiccation, cryotherapy, and radiotherapy can be used for some low-risk SCCs. However, treatment with radiotherapy has a higher recurrence rate and cannot be used in patients younger than 55 years of age.16 Some high-risk tumors or tumors in anatomic areas needing tissue conservation may be candidates for Mohs surgery.16 Off-label use of topical imiquimod and fluorouracil can be somewhat effective in treating SCC.16 Follow-up appointments should occur once every 6 months for the first year and then at least yearly to check for recurrence and development of new lesions.16
Patients with high-risk SCC may require additional workup and treatment. Those with palpable lymphadenopathy need an ultrasound-guided fine-needle aspiration or biopsy of the lymph nodes. Lesions that are high risk may also require adjuvant radiation or chemotherapy in some instances.12
Patients who are at increased risk for SCC can be treated prophylactically with oral retinoids or niacinamide. Other options include field therapy with topical chemotherapy agents or photodynamic therapy to target AKs or SCCIS that could progress to SCC.12
The patient in this case was diagnosed with SCC via biopsy and given the size and location of her lesion, was referred to Mohs surgery for treatment. ■
Briana Fernandez and Shangyi Fu are medical students at Baylor College of Medicine in Houston, Texas; Tara L. Braun, MD, is a dermatologist at Elite Dermatology in Houston,Texas.
1. Werner RN, Sammain A, Erdmann R, Hartmann V, Stockfleth E, Nast A. The natural history of actinic keratosis: a systematic review. Br J Dermatol. 2013;169(3):502-518.
2. Röwert-Huber J, Patel MJ, Forschner T, et al. Actinic keratosis is an early in situ squamous cell carcinoma: a proposal for reclassification [published correction appears in Br J Dermatol. 2007;157(2):431]. Br J Dermatol. 2007;156 Suppl 3:8-12.
3. Siegel JA, Korgavkar K, Weinstock MA. Current perspective on actinic keratosis: a review. Br J Dermatol. 2017;177(2):350-358.
4. Dodds A, Chia A, Shumack S. Actinic keratosis: rationale and management. Dermatol Ther (Heidelb). 2014;4(1):11-31.
5. Jeffes EW 3rd, Tang EH. Actinic keratosis. Current treatment options. Am J Clin Dermatol. 2000;1(3):167-179.
6. Ceilley RI, Jorizzo JL. Current issues in the management of actinic keratosis. J Am Acad Dermatol. 2013;68(1 Suppl 1):S28-S38.
7. Jansen MHE, Kessels JPHM, Nelemans PJ, et al. Randomized trial of four treatment approaches for actinic keratosis. N Engl J Med. 2019;380(10):935-946.
8. Bonney V. Uterus showing squamous cell carcinoma of the cervix and adeno-carcinoma of the body. Proc R Soc Med. 1914;7(Obstet Gynaecol Sect):227-228.
9. Brantsch KD, Meisner C, Schönfisch B, et al. Analysis of risk factors determining prognosis of cutaneous squamous-cell carcinoma: a prospective study. Lancet Oncol. 2008;9(8):713-720.
10. Que SKT, Zwald FO, Schmults CD. Cutaneous squamous cell carcinoma: Incidence, risk factors, diagnosis, and staging. J Am Acad Dermatol. 2018;78(2):237-247.
11. Xiang F, Lucas R, Hales S, Neale R. Incidence of nonmelanoma skin cancer in relation to ambient UV radiation in white populations, 1978-2012: empirical relationships. JAMA Dermatol. 2014;150(10):1063-1071.
12. Que SKT, Zwald FO, Schmults CD. Cutaneous squamous cell carcinoma: management of advanced and high-stage tumors. J Am Acad Dermatol. 2018;78(2):249-261.
13. South AP, Purdie KJ, Watt SA, et al. NOTCH1 mutations occur early during cutaneous squamous cell carcinogenesis. J Invest Dermatol. 2014;134(10):2630-2638.
14. Azorín D, López-Ríos F, Ballestín C, Barrientos N, Rodríguez-Peralto JL. Primary cutaneous adenosquamous carcinoma: a case report and review of the literature. J Cutan Pathol. 2001;28(10):542-545.
15. Soyer HP, Rigel DS, McMeinman E. Actinic keratosis, basal cell carcinoma, and squamous cell carcinoma. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier Limited; 2018:1872-1893.
16. Firnhaber JM. Basal cell and cutaneous squamous cell carcinomas: diagnosis and treatment. Am Fam Physician. 2020;102(6):339-346.
Acute decompensated heart failure is associated with new or worsening symptoms such as shortness of breath, orthopnea, and volume overload.
A56-year-old man with a history of hypertension and type 2 diabetes presents to the emergency department with a chief complaint of increased bilateral pedal edema and shortness of breath with dyspnea on exertion for 6 weeks. He admits he has not been on any outpatient medical management for the last 3 years because of a variety of social and financial barriers. He denies any fevers, chills, nausea, or vomiting. He has no chest pain, pressure, tightness, or palpitations. He denies a history of claudication or history of prior diagnosis of heart failure.
On physical examination, the patient’s temperature, respiratory rate, and oxygen saturation on room air are within normal limits. He is tachycardic with a heart rate of 130 beats per minute and hypertensive with a blood pressure of 158/102 mm Hg. He is alert, conversational, and cooperative but is ill-appearing and grossly volume overloaded. His breath sounds are diminished in his lung bases bilaterally. He has a regular rhythm with no murmurs, gallops, or rubs. His jugular veins are distended to the jawline. His abdomen is distended and nontender, and he has normoactive bowel sounds in all 4 quadrants. He has 3+ bilateral lower extremity edema with edema noted up to his abdomen. Chronic venous ulcers are noted on his lateral lower extremities bilaterally. Blistering wounds are noted on his right and left index fingers and left middle finger, which the patient notes were caused by touching
a hot pan at home. Cranial nerves II to XII are grossly intact and the patient demonstrates no gross focal deficits. The patient’s chemistry panel is within normal limits except for serum glucose, which is elevated to 165 mg/dL. The patient’s hemoglobin is decreased at 12.7 g/dL and the remainder of the complete blood cell count is within normal limits. Coagulation studies are also without abnormality. Point-of-care troponin level is negative at 0.03 ng/mL. Brain-type natriuretic peptide (BNP) is elevated to 221 pg/mL and hemoglobin A1c is 8.4%, confirming that the patient’s diabetes is uncontrolled over time. His D-dimer is elevated at 1.87 μg/mL, however, a chest computed tomography (CT) scan is negative for pulmonary embolism. Chest CT and chest radiography demonstrate moderate-sized bilateral pleural effusions. Electrocardiography reveals typical atrial flutter with rapid ventricular response and rates of approximately 130 to 140 beats per minute, but the patient denies any symptoms or personal history of atrial fibrillation or flutter.
Following emergency department workup, the patient is admitted to the cardiology service for acute decompensated heart failure (ADHF; NYHA class III stage C) and typical atrial flutter with rapid ventricular response.
The patient is begun on rapid diuresis protocol and potassium/magnesium replacement protocol. Endocrinology is consulted on day 1 of hospitalization and the patient is initiated on a diabetic diet, supplemental insulin lispro, and dapagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor. The patient’s medication management includes high-dose IV furosemide, guideline-directed medical therapy including an angiotensin II receptor blocker (ARB), β-blocker, and mineralocorticoid receptor antagonist (MRA). Hydralazine 10 mg is also added for management of hypertensive urgency. He is initiated on apixaban 5 mg twice a day for oral anticoagulation for atrial flutter. Wound care is initiated for management of the patient’s venous ulcers and finger blisters.
Transthoracic echocardiogram on day 2 demonstrates left ventricular ejection fraction (LVEF) 50% to 55%, low normal left ventricular systolic function (LVSF), decreased left ventricular stroke volume (LVSV), moderate concentric left ventricular hypertrophy, normal right ventricular systolic pressure (RVSP), no valvular disease, and normal right atrium and left atrium sizes. Cardiovascular magnetic resonance imaging (cMRI) on day 5 demonstrates LVEF 69%, no vasodilator stress-induced perfusion deficits or macroscopic scar or fibrosis, and biatrial enlargement with normal LVSF/ right ventricular systolic function, likely indicating a persistent atrial flutter over time.
Diuretics are stopped on day 6 because of acute kidney injury and contraction alkalosis secondary to brisk diuresis and large volume loss. The patient’s serum creatinine level increases to 1.26 mg/dL from 0.95 mg/dL on admission, and his arterial blood gas values are as follows: pH 7.52; carbon dioxide, 53.2 mm Hg; and bicarbonate, 43.5 mEq/L. Per endocrinology, linagliptin is added to the patient’s diabetes medication regimen on day 7 with subsequent improvements in blood glucose level found.
The patient undergoes successful cavotricuspid isthmus ablation as indicated for definitive treatment of typical atrial flutter on day 9 of hospitalization. A transesophageal echocardiogram is deemed not necessary by the electrophysiology team following their review of the patient’s CT angiogram and cMRI, which show no thrombus present in the left atrial appendage.
A postprocedure review of the patient’s telemetry record on day 10 confirms sustained normal sinus rhythm. The patient has lost greater than 40 liters of fluid and his weight has decreased by more than 90 pounds since admission. The patient is discharged on day 10 with a follow-up scheduled with electrophysiology and heart failure clinic for continued outpatient management.The patient’s discharge medications include apixaban, baby aspirin, furosemide as needed, metoprolol succinate, saxagliptin, and dapagliflozin.
Acute decompensated heart failure is characterized by new or worsening signs of heart failure such as shortness of breath, orthopnea, and volume overload that often lead to an emergency department visit and/or hospitalization for inpatient management.1-3 Major causes of ADHF include acute coronary syndrome, arrhythmias, myocarditis, acute valve syndromes, progressive valve disease, cardiomyopathic state, and poorly controlled hypertension.1 Acute decompensated heart failure affects a heterogenous patient population and is the most common discharge diagnosis among patients older than 65 years of age.4 Etiology and pathophysiologic mechanism of ADHF may be multifactorial in an individual patient, posing a challenge to long-term management and resulting in high postdischarge readmission rates.4,5
Inpatient management of ADHF should be tailored within the context of the individual patient’s presentation. General pillars of management include the following: volume management with diuresis, monitoring of electrolytes, renal function and hemodynamic status, vasodilator therapy, sodium and fluid restriction, venous thromboembolism prophylaxis, and
continuation or initiation of long-term therapy.6,7 Ejection fraction is an important consideration for determining the specific therapeutic management strategy.
New guidelines from the American College of Cardiology, American Heart Association, and the Heart Failure Society of America (2022 AHA/ACC/HFSA) for the management of heart failure with preserved ejection fraction (HFpEF) recommend the use of SGLT2 inhibitors, MRAs, ARBs, angiotensin receptor/neprilysin inhibitors (ARNi), as well as treatment of hypertension and atrial fibrillation, avoidance of the routine use of nitrates or phosphodiesterase-5 inhibitors, and management of comorbidities.7 First-line management of heart failure with reduced ejection fraction (HFrEF) follows guideline-directed medical therapy (GDMT) including an ARNi,ACEI, or ARB, 1 of 3 β-blockers (bisoprolol, carvedilol, or sustained-release metoprolol succinate), MRA, SGLT2 inhibitor, and diuretics as needed.7 Robust evidence supporting the use of SGLT2 inhibitors in patients with HFrEF recently led to the inclusion of this class in the GDMT per the updated American and European guidelines in 2021 and the 2022 AHA/ACC/ HFSA guidelines.7,8
Sodium-glucose cotransporter-2 inhibitors are an established class of medications commonly used in the management of
type 2 diabetes.The known mechanism of action of SGLT2 inhibitors for type 2 diabetes is the reduction of blood glucose via the promotion of urinary glucose excretion. These agents also have a protective effect on the risk for progression to diabetic kidney disease.9,10 The mechanism of action for heart failure is not currently known, but proposed mechanisms include the reduction of preload by promotion of osmotic diuresis and natriuresis, reduction of afterload by the promotion of vasodilation and improved endothelial function, improved cardiac efficiency via improved myocardial metabolism, and possible reduction of the risk for atrial arrhythmias.9,10
Several landmark trials established the evidence for inclusion of SGLT2 inhibitors in current GDMT for chronic HFrEF and recent approval for use in HFpEF (Table). The EMPEROR-Reduced trial demonstrated that among patients with symptomatic stable HFrEF (EF ≤40%), empagliflozin was superior to placebo in improving heart failure outcomes regardless of diabetes status.11,12 The DAPA-HF trial also demonstrated superior prevention of cardiovascular deaths and heart failure events among patients with HFrEF who received dapagliflozin versus placebo regardless of diabetes status.13 A meta-analysis of the EMPEROR-Reduced and
TABLE.
SGLT2 InhibitorChronic/Acute Heart FailureApproved Use
Empagliflozin Chronic: Beneficial –EMPEROR-Reduced trial –EMPEROR-Preserved trial
Acute: Beneficial –EMPULSE trial
Dapagliflozin Chronic: Beneficial –DAPA-HF trial
Acute: TBD; DICTATE-AHF trial currently in progress
Canagliflozin N/A
Ertugliflozin N/A
• Type 2 diabetes with or without CV disease
• HFrEF
• HFpEF
• Type 2 diabetes with or without CV disease or multiple CV risk factors
• HFrEF
• Chronic kidney disease at risk for progression
Type 2 diabetes with or without CV disease or diabetic nephropathy
Type 2 diabetes only
Diabetes Status
With type 2 diabetes or without11,12,15
With type 2 diabetes or without13
With type 2 diabetes only
With type 2 diabetes only
AHF, acute heart failure; CV, cardiovascular; DAPA-HF, Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure; DM, diabetes mellitus; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; TBD, to be determined
Diuretics are stopped on day 6 because of acute kidney injury and contraction alkalosis secondary to brisk diuresis and large volume loss.
DAPA-HF trials showed a 13% reduction in all-cause death, 14% reduction in death due to cardiovascular events, 31% reduction in first hospitalization for HF, and 38% reduction in adverse renal outcomes in patients on SGLT2 inhibitor management.14 The EMPEROR-Preserved trial demonstrated that among patients with symptomatic stable HFpEF (EF >40%), empagliflozin was superior to placebo in improving outcomes regardless of diabetes status or sex.15 A recent meta-analysis has further suggested that the use of SGLT2 inhibitors in patients with HFpEF may reduce the risk for hospitalization for heart failure and improve the severity of heart failure and quality of life.16
In cases of new-onset ADHF or cases of acute or chronic heart failure with variable outpatient management or compliance, patients may not be on an SGLT2 inhibitor prior to hospitalization. Relative uncertainty regarding safety, tolerability, and efficacy of inpatient initiation of SGLT2 inhibitors for patients with acute heart failure may lead hospital clinicians to defer this decision-making until outpatient follow-up.17
Findings from a recent systematic review and meta-analysis support the initiation of SGLT2 inhibitors for inpatients hospitalized with acute heart failure.18 Included in the metaanalysis were the EMPA-RESPONSE-AHF and EMPULSE trials, which found that empagliflozin was superior to placebo regardless of ejection fracture or diabetes status in patients with ADHF.19,20 Also included was the SOLOIST-WHF trial, which demonstrated that sotagliflozin was superior to placebo in patients with type 2 diabetes and worsening heart failure.21 The systematic review showed an overall 48% reduction in the odds of rehospitalization because of heart failure among those initiated on an SGLT2 inhibitor during an acute heart failure hospitalization or early postdischarge (within 3 days).14 Additional findings were improved patient-reported outcomes and no excess risk for acute kidney injury, hypotension, or hypoglycemia.18
Notable contraindications to the use of SGLT2 inhibitors include the following: type 1 diabetes, type 2 diabetes with prior or predisposition to diabetic ketoacidosis, volume depletion or symptomatic hypotension, estimated glomerular filtration rate less than 30 mL, frequent urinary tract infections or yeast infections, and risk factors for foot amputation.9,10
This case features a 56-year-old man admitted to the hospital for typical atrial flutter with rapid ventricular response and a new diagnosis of ADHF (HFpEF). His typical atrial flutter was surgically resolved with a successful cavotricuspid isthmus ablation, and he was medically managed with aggressive diuresis, resulting in a greater than 90-lb reduction in his weight during the course of the admission. Given that this patient’s ejection fraction was preserved, his discharge medications were focused on blood pressure management, rate and rhythm control, and management of comorbidities, rather than complete GDMT. He was discharged on an oral anticoagulant, β-blocker, diuretic to take as needed, dipeptidyl peptidase-4 inhibitor for diabetes, and SGLT2 inhibitor.
This patient was an appropriate candidate for initiation of an SGLT2 inhibitor because of his history of type 2 diabetes as well as acute hospitalization for heart failure. The patient should continue taking the SGLT2 inhibitor as part of his outpatient medication regimen not only for management of his diabetes but also for reduced risk for rehospitalization for heart failure and improved quality of life. ■
Ana-Maria Drobeniuc, MPA, PA-C, MPH, is a graduate of the Physician Assistant Program at Augusta University in Augusta, GA, and has accepted a position as a physician assistant at Piedmont Heart Institute in Atlanta, GA; E. Rachel Fink, MPA, PA-C, is a physician assistant at Augusta Urology Associates and an assistant professor in the Physician Assistant Program at Augusta University.
LESSONS LEARNED:
Lesson 1: SGLT2 inhibitors are a safe and effective secondary therapy for the treatment of acute heart failure in patients with and without type 2 diabetes and are guidelinerecommended agents.
Lesson 2: Failure to initiate SGLT2 inhibitors in patients with acute heart failure during or shortly following hospitalization or failure to continue an SGLT2 inhibitor initiated during an acute heart failure hospitalization may be a significant missed opportunity to prevent rehospitalization and improve patient quality of life.
recommend the addition of SGLT2 inhibitors.
References
1. Alla F, Zannad F, Filippatos G. Epidemiology of acute heart failure syndromes. Heart Fail Rev. 2007;12(2):91-95.
2. Joseph SM, Cedars AM, Ewald GA, Geltman EM, Mann DL. Acute decompensated heart failure: contemporary medical management. Tex Heart Inst J. 2009;36(6):510-520.
3. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J. 2005;26(4):384-416.
4. Metra M, Felker GM, Zaca V, et al. Acute heart failure: multiple clinical profiles and mechanisms require tailored therapy. Int J Cardiol. 2010;144(2):175-179.
5. De Luca L, Fonarow GC, Adams KF, Jr., et al. Acute heart failure syndromes: clinical scenarios and pathophysiologic targets for therapy. Heart Fail Rev. 2007;12(2):97-104.
6. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA 2010 comprehensive heart failure practice guideline. J Card Fail. 2010;16(6):e1-194.
7. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022;79(17):1757-1780.
8. Writing C, Maddox TM, Januzzi JL, Jr, et al. 2021 update to the 2017 ACC expert consensus decision pathway for optimization of heart failure treatment: answers to 10 pivotal issues about heart failure with reduced ejection fraction: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2021;77(6):772-810.
9. Tamargo J. Sodium-glucose cotransporter 2 inhibitors in heart failure: potential mechanisms of action, adverse effects and future developments. Eur Cardiol. 2019;14(1):23-32.
10. Tamargo J. Corrigendum to: Sodium-glucose cotransporter 2 inhibitors in heart failure: potential mechanisms of action, adverse effects and future developments. Eur Cardiol. 2019;14(3):201.
11. Anker SD, Butler J, Filippatos G, et al. Effect of empagliflozin on cardiovascular and renal outcomes in patients with heart failure by baseline diabetes status: results from the EMPEROR-reduced trial. Circulation 2021;143(4):337-349.
12. Packer M, Anker SD, Butler J, et al. Cardiovascular and renal outcomes with empagliflozin in heart failure. N Engl J Med. 2020;383(15):1413-1424.
13. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381(21):1995-2008.
14. Zannad F, Ferreira JP, Pocock SJ, et al. SGLT2 inhibitors in patients with heart failure with reduced ejection fraction: a meta-analysis of the EMPERORReduced and DAPA-HF trials. Lancet. 2020;396(10254):819-829.
15. Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.
16. Fukuta H, Hagiwara H, Kamiya T. Sodium-glucose cotransporter 2 inhibitors in heart failure with preserved ejection fraction: a meta-analysis of randomized controlled trials. Int J Cardiol Heart Vasc. 2022;42:101103.
17. Rao VN, Murray E, Butler J, et al. In-hospital initiation of sodium-glucose cotransporter-2 inhibitors for heart failure with reduced ejection fraction. J Am Coll Cardiol. 2021;78(20):2004-2012.
18. Salah HM, Al’Aref SJ, Khan MS, et al. Efficacy and safety of sodium-glucose cotransporter 2 inhibitors initiation in patients with acute heart failure, with and without type 2 diabetes: a systematic review and meta-analysis. Cardiovasc Diabetol. 2022;21(1):20.
19. Damman K, Beusekamp JC, Boorsma EM, et al. Randomized, double-blind, placebo-controlled, multicentre pilot study on the effects of empagliflozin on clinical outcomes in patients with acute decompensated heart failure (EMPARESPONSE-AHF). Eur J Heart Fail. 2020;22(4):713-722.
20. Voors AA, Angermann CE, Teerlink JR, et al. The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial. Nat Med. 2022;28(3):568-574.
21. Bhatt DL, Szarek M, Steg PG, et al. Sotagliflozin in patients with diabetes and recent worsening heart failure. N Engl J Med. 2021;384(2):117-128.
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Ms J was a 36-year-old nurse working in an after-hours medical clinic. She had worked at the clinic for approximately 18 months. When she was hired by the clinic, Ms J was asked to sign an employee confidentiality agreement that stated, “I will not intentionally share or release confidential information about the patient to anyone not directly involved in the patient’s care.” All employees of the clinic were required to review and sign the agreement each year. The policy went on to state that coworkers not directly involved in a patient’s care should not be told confidential information about the patient.
The clinic also had a wireless communication devices policy prohibiting the use of personal cell phones in patient treatment areas to take photographs. Other policies that Ms J was informed about and agreed to were a social media policy prohibiting employees from sharing information about patients on social media and a confidential matters policy, which provided that “reasons for admission and information about diagnosis and treatment are absolutely confidential and must be respected as such.”
A nurse questioned the diagnosis of a skin lesion and shared her concerns with colleagues. She was fired for privacy violations.
As part of her onboarding process, Ms J was also trained on how to report a concern regarding patient safety or care issues.
During one of Ms J’s night shifts, a patient presented at the clinic with a spot on the back of her thigh. The physician with whom Ms J was working believed it was a chemical burn. Ms J disagreed with this diagnosis and thought it was skin cancer and most likely melanoma, but the physician disagreed. Ms J believed the doctor had misdiagnosed the spot and she took a picture of it with her personal cell phone. After taking the photo, Ms J began showing it to her coworkers, asking what they thought.
She showed the picture to 9 coworkers, 8 of whom were not involved in the patient’s care. After showing the ninth person (a physician) the photo, the second physician re-diagnosed the lesion as melanoma, confirming Ms J’s suspicions.
Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.
Concerned nurse is fired over photo of skin lesion shared with colleagues.
When the patient learned that Ms J had been showing the photo to other workers at the clinic, she reported Ms J to the clinic’s management. Management suspended Ms J without pay while they investigated.When the investigation was concluded, Ms J was fired for violations of various clinic policies.
Ms J sought the counsel of an attorney and together they decided to file a lawsuit against the clinic.The lawsuit alleged that Ms J had been fired in retaliation for questioning the patient’s diagnosis, in violation of a state statute that prohibits employers from retaliating against employees who make reports regarding their reasons for “believing that the quality of care of a health care patient is in jeopardy.” Ms J alleged that her actions fell under the protection of the state statute and, thus, she was wrongfully terminated from her employment.
quite clear that showing the photo to 8 other people, none of whom was involved in the patient’s care, was not protected activity.
The court concluded that Ms J’s actions violated both the clinic’s policies and the statute requiring reports be made in such a way as to protect the confidentiality of the patient. Thus, the clinic was free to terminate her employment and the court deemed it nonretaliatory to do so.
Ms J, in trying to do something good for the patient, ended up doing something very bad for her career. It need not have been that way. Ms J could have protected both her career and the patient by reporting her concerns properly — according to the clinic’s clear policies.
This case had many concerning aspects such as the use of a cell phone in an examination room and whether or not the patient consented to the photograph in the first place (this wasn’t discussed by the court).The court seemed particularly concerned that Ms J had shown the photo to so many coworkers. Ms J noted she was only seeking information in an attempt to help the patient, but it was at the expense of the patient’s privacy and confidentiality.
The clinic made a motion to dismiss the case, which the trial court granted. Ms J appealed, and the case went to the Court of Appeals.
On appeal, the court looked at the state statute to determine whether Ms J had established a claim of retaliation against the clinic. To establish a claim for retaliatory firing, Ms J had to show that 1) she was engaging in protected activity, 2) the clinic knew about the protected activity, 3) the clinic took an adverse employment action against her because of it, and 4) a causal connection was established between the adverse employment action and the protected activity.
In this case, Ms J believed that taking the picture and showing it to her coworkers was protected because she was reporting a situation where a patient’s health or safety was in jeopardy. However, the court held that her actions were only partly protected and pointed out that her conduct didn’t just violate the clinic’s policies, but also violated the state statute requiring that all “protected” reports and investigations must maintain the confidentiality of patients.The statute also requires that a report be made to the health care facility itself, not to coworkers unrelated to the patient’s care, so that someone in an “administrative or supervisory capacity” can investigate.
The court acknowledged that Ms J’s showing the photograph to the other physician was protected as he was an individual in a “supervisory or administrative capacity,” however, the court was
Privacy is paramount these days. Treat your patient’s private information as if it were your own. To best protect your employment, know what your facility’s policies are and stick to them. ■
Medicine vs Food: the Patient Care Dilemma of ‘Financial Toxicity’
The plaintiff alleged that her actions fell under the protection against retaliation statute and was wrongfully terminated.Jody A. Charnow Clinicians are calling on colleagues to bring up the cost of care and its potential impact when discussing treatment options with patients. See the full case at: clinicaladvisor.com/ mypractice_january_february23
