Dyspnea following high-altitude hike

CONTENTS

J U LY / A U G U S T 2 0 2 2

6 Dyspnea following high-altitude hike.

23 Unknown rash in sexually active adult.

25 Hyperpigmented scaly patch.

30 Beware of what you post on social media.

FEATURES

6 A Case of Dyspnea and Cough in Young Man

After Climb in Colorado

The patient develops cough and dyspnea while climbing

Pike’s Peak in Colorado.

12 Anxiety and Depression Mushroomed in US at Start of Pandemic

Anxiety disorders are the most common mental illness in the

US and affect 40 million adults every year. 19 Adults Without Diabetes Benefit From

GLP-1 Agonists for Obesity

Review of the pathophysiology of obesity and the mechanism of action, efficacy, and safety of GLP-1 receptor agonists.

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Rising Temperatures Can Be Deadly

4 Web Roundup

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25 Dermatologic Look-Alikes

Lower Leg Ulcers

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A Case of Dyspnea and Cough in Young Man After Climb in Colorado

The patient develops cough and dyspnea while climbing Pike’s Peak in Colorado, climbing 4000 feet to the elevation of 12,400 ft.

© GALEN ROWELL / GETTY IMAGES

Case involves a 27-year-old hiker from Georgia.

A27-year-old man presents to the emergency department with symptoms of dyspnea and cough for the past 3 days. Four days earlier, the patient (Mr M) and a friend arrived at Woodland Park, Colorado (elevation: 8400 ft) from their hometown of Atlanta, Georgia (elevation: 1050 ft). The patient states that their goal was to hike a 21-mile trail to the top of Pike’s Peak (elevation: 14,100 ft) in 2 days.

On the second day of their arrival at Woodland Park, they embarked on their hike covering 10 miles, climbing 4000 ft (elevation: 12,400 ft), before setting up camp for the night. During the rst evening, Mr M reported the onset of a nonproductive cough, mild headache, and shortness of breath when lying down to sleep. The following day, Mr M’s cough worsened and was associated with dyspnea during the ascent. He states that he had to take multiple breaks to catch his breath. Based on these symptoms, his friend decided to discontinue the hike and begin their descent. During the descent, Mr M began coughing up pink, frothy sputum and experienced dyspnea during rest. A park ranger was noti ed and Mr M was taken to the nearest hospital.

Upon arrival at the emergency department, Mr M reports chest tightness, drowsiness, and headache. He denies nausea, vomiting, abdominal pain, chest pain, edema, hemoptysis, or medical history of asthma. No signi cant family history of cardiac or respiratory conditions is noted. Mr M

Continues on page 8

TABLE 1. Vital Signs

Height, in

Weight, lb

BMI 70

175

25.1

Blood pressure, mm Hg 132/85

Heart rate, bpm 115

Respiratory rate, per min 23

Temperature 98.7 °F/37 °C

Pulse oximetry, % 81

BMI, body mass index; bpm, beats per minute

lives a healthy lifestyle, is an avid hiker in the Appalachian Mountains of Georgia, is physically fit, and does not have a history of smoking cigarettes or use of any street drugs.

Physical Examination

Upon physical examination, the patient is alert and oriented to person, place, time, and situation. He appears to be in mild respiratory distress with signs of dyspnea while sitting with his arms leaning on his legs to assist in breathing. The patient also has a productive-sounding cough. Cyanosis is present around his lips and throughout his oral mucosa. The patient is tachypneic and tachycardic and has decreased oxygen saturation (Table 1). Upon auscultation of the posterior lung fields, inspiratory crackles and bronchial breath sounds are heard bilaterally. No other abnormalities are noted on his physical examination.

Diagnostic Workup/Diagnosis

Based on the patient’s history and presentation, the emergency department physician suspects high-altitude pulmonary edema (HAPE) and wants to confirm the diagnosis by ruling out other possible differentials through laboratory tests and imaging studies. Given the patient’s condition, he is quickly started on high-flow supplemental oxygen therapy via facemask. Complete blood cell count and metabolic panel findings indicate a mild elevation of white blood cells (11,000/µL). A respiratory pathogen panel was negative for common viral and bacterial causes such as pneumonia, influenza, and SARSCoV-2. Electrocardiography findings are normal, ruling out any associated cardiac complications. Bedside ultrasonography of the lung parenchyma reveals comet tail artifact, also known as lung rockets. This type of artifact is the ultrasonography equivalent of Kerley B lines indicating interstitial edema (Figure). Chest radiography reveals patchy opacities and alveolar infiltrates bilaterally.

High-Altitude Pulmonary Edema

High-altitude pulmonary edema is defined as noncardiogenic pulmonary edema caused by exaggerated hypoxic pulmonary vasoconstriction, high pulmonary artery pressure, and increased capillary pressure in individuals exposed to altitudes above 8200 ft.1 Environmental conditions at elevations above 8200 ft include lower oxygen concentrations, lower barometric air pressure, and lower temperatures. Hypobaric hypoxia causes the body to go through maladaptive responses, which can result in impairment of gas exchange from abnormal accumulation of plasma and reticulocytes in alveoli because of breakdown of pulmonary blood-gas barriers.2 Impairment of gas exchange can be fatal if no interventions are performed during initial symptom onset.

High-altitude pulmonary edema can occur in 2 distinct forms. The first form occurs in people who live at low altitudes and ascend rapidly to altitudes greater than 8200 ft. The second form, also known as re-entry HAPE, occurs in people who live at high altitudes and return home after a period of being at a lower altitude.3 The onset of HAPE usually presents within 2 to 4 days of ascent at an elevation above 8200 ft and rarely occurs after more than 4 to 5 days at the same altitude because of remodeling and adaptation.4

Major risk factors for HAPE include higher or greater changes in altitude, rapid ascent rate, and individual susceptibility;

FIGURE. Ultrasonography of comet tail artifact.

the effects of these risk factors are cumulative (Table 2).2 Furthermore, individuals with cardiopulmonary circulation abnormalities that may lead to pulmonary hypertension, such as mitral stenosis, primary pulmonary hypertension, unilateral absence of pulmonary artery, and patent foramen ovale, may be at an increased risk for HAPE at moderate and even low altitudes.5

Genetics can also play a role in susceptibility to developing HAPE. The genes associated with the occurrence of HAPE include polymorphisms in renin-angiotensin-aldosterone system (RAAS) pathway genes, more specifically with the angiotensin conversion enzyme (ACE), nitric oxide (NO) pathway genes (ie, NOS3), endothelin-1, and pulmonary surfactant proteins A1 and A2.6 Hypoxia-inducible factors (HIF), also known as the master regulators of oxygen homeostasis, are key transcription factors consisting of 1α (or 2α) and 1β subunits that form active transcriptional complexes under hypoxic conditions to stimulate expression of target genes.7 Hypoxia-inducible factors are involved in the release of vascular endothelial growth factor (VEGF) in the brain, erythropoiesis, and other pulmonary and cardiac functions at high altitudes.7 EPAS1 is a gene that codes for transcriptional regulator HIF-2α and is involved in decreasing inflammatory and vasoconstrictive responses to hypoxia, which allowed for the adaptation of people from Tibet and the Andes to live at high altitudes.5,7 Genetic predisposition determines how different groups of individuals will be affected and be able to adapt to high-altitude stress by a mechanism of minute ventilation.8

The incidence of HAPE among individuals at 14,763 ft is 0.6% to 6% and at 18,044 ft is 2% to 15%, with a faster ascent resulting in a higher incidence.8 In addition, those with a prior history of HAPE have a recurrence rate as high as 60% and should be managed accordingly.8

Signs and Symptoms

High-altitude pulmonary edema presents within 2 to 4 days of ascent to a high altitude and it is rarely observed at altitudes below 8200 ft or after 1 week of acclimatization to the exposed altitude.3 High-altitude pulmonary edema symptoms have an insidious onset and include nonproductive cough, decreased exercise tolerance, chest pain, and exertional dyspnea.8 As HAPE progresses, the cough and dyspnea worsen and orthopnea develops.2 In advanced HAPE progression, individuals can experience dyspnea at rest, severe exertional dyspnea, and the cough may become productive of bloodtinged, frothy sputum.8

Physical examination reveals tachycardia, tachypnea, cyanosis, and elevated body temperature that generally does not exceed 38.5 °C.4 Auscultation of the lung fields reveals discrete initial rales located over the middle lung fields.3 Furthermore, crackles may be unilateral or bilateral, but initially are auscultated in the right middle lobe and are heard first in the right axilla.9 Oxygen saturation is often 10% less than expected for altitude and the patient will often appear better than expected given their level of hypoxemia and oxygen saturation value.8

Treatment

Depending on the resources that are available at a medical facility, nonpharmacologic or pharmacologic interventions may be used. In the nonpharmacologic approach, immediate improvement of oxygenation either by supplemental oxygen, hyperbaric treatment, or rapid descent is the treatment of choice.3 Further studies have found that descent is the mainstay of treatment and individuals should try to passively descend at least 3280 ft or until symptom resolution.8 It is vital to minimize exertion on descent because exertion may increase hypoxemia from metabolic demands that can further increase pulmonary artery pressure and exacerbate edema formation.10

A suitable alternative to descent is supplemental oxygen delivery by nasal cannula or face mask at flow rates sufficient enough to achieve an oxygen saturation greater than 90%.10 Additionally, patients who have access to oxygen, whether in a hospital or high-altitude medical clinic, can be treated with oxygen at the current elevation without needing to descend to a lower elevation.10 When descent and supplemental oxygen administration are not feasible, simulated descent with the use of a portable hyperbaric chamber should be used at 2 to 4 pounds per square inch for several hours as a temporary measure until real descent can be achieved.4

Pharmacotherapy should not be regarded as a substitute for descent or supplemental oxygen and should only be used when the nonpharmacologic approaches are not feasible or available.11 Staying at the same altitude, receiving supplemental

TABLE 2. Risk Factors for HAPE

Cold temperatures Pre-existing respiratory infection

Heavy exertion Prior history of HAPE

Higher altitudes achieved Rapid ascent rates

Male sex

HAPE, high-altitude pulmonary edema

PULMONOLOGY HEALTH: HAPE HAPE presents within 2 to 4 days of ascent at an elevation above 8200 ft and rarely occurs after more than 4 to 5 days at the same altitude.

low flow oxygen for 24 to 48 hours to maintain an arterial saturation above 90%, and bed rest can lead to relief of symptoms within hours and complete clinical recovery within several days.4

Pharmacotherapy focuses on reduction of pulmonary artery pressure through the use of vasodilators, such as the calcium channel blocker nifedipine, which can reduce systolic pulmonary artery pressure by 50%.11 In hikers who develop HAPE at 14,957 ft elevation, taking extended-release nifedipine 20 mg every 6 hours leads to “a persistent relief of symptoms, improvement of gas exchange, and radiographic clearance of pulmonary edema over an observational period of 34 hours.”3 If nifedipine is unavailable, phosphodiesterase inhibitors such as tadalafil or sildenafil may help decrease pulmonary artery and capillary pressure.8 In one study, tadalafil was found to be effective in reducing the incidence of HAPE in susceptible adults, those with a previous history of HAPE, and those exposed to hypoxic high-altitude environments.12

Prognosis

High-altitude pulmonary edema is the more severe end of the high-altitude illness spectrum and it is the leading cause of death from altitude illness.13 If HAPE is left untreated, it can progress to dyspnea at rest and cyanosis. In a report by Jensen et al, the mortality rate from untreated HAPE is as high as 50%; when treated, the mortality rate is up to 11%.8 However, HAPE is completely and easily reversible if recognized early and treated properly.3 Individuals treated for HAPE may consider resuming ascent at an appropriate rate once they are asymptomatic, no longer require oxygen or vasodilator therapy, and have an increased exercise tolerance compared with symptom onset.8,9

Conclusion

The diagnosis of HAPE is based on results of a thorough history and physical examination.14 This case demonstrates the importance of recognizing the initial signs and symptoms of HAPE. If symptoms are recognized early, HAPE is an easily and completely reversible condition. Not only is it imperative for providers to accurately identify early signs of HAPE, but also it is important to educate patients traveling to high-altitude environments about the effects of hypoxic conditions. Simple interventions, such as having information readily available at trailheads warning of the condition and how to avoid it with acclimatization techniques, could better inform the public and decrease the incidence of HAPE. It is vital for hikers to recognize initial symptoms of HAPE so they can pursue treatment without developing long-term consequences. ■

Danila Teptsov, PA-S, is currently a PA student at Augusta University in Georgia. E. Rachel Fink, MPA, PA-C, is an assistant professor at the Augusta University Physician Assistant Program.

References

1. Bärtsch P, Swenson ER. Acute high-altitude illnesses. N Engl J Med. 2013 13;368(24):2294-302. 2. Luks AM, Swenson ER, Bärtsch P. Acute high-altitude sickness. Eur Respir Rev. 2017;26(143):160096. 3. Paralikar SJ. High altitude pulmonary edema—clinical features, patho physiology, prevention and treatment. Indian J Occup Environ Med. 2012;16(2): 59-62. 4. Korzeniewski K, Nitsch-Osuch A, Guzek A, Juszczak, D. High altitude pulmonary edema in mountain climbers. Respir Physiol Neurobiol. 2015;209: 33-38. 5. Basnyat B, Tabin G. Altitude illness. In: Loscalzo J, Fauci As, Kasper DL, Hauser SL, Longo DL, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21st ed. McGraw Hill; 2022;462. 6. Luo Y, Zou Y, Gao Y. Gene polymorphisms and high-altitude pulmonary edema susceptibility: a 2011 update. Respiration. 2012;84(2):155-162. 7. Woods P, Alcock J. High-altitude pulmonary edema. Evol Med Public Health. 2021;9(1):118-119. 8. Jacob D, Jensen JD, Vincent AL. High altitude pulmonary edema. In: StatPearls [Internet]. StatPearls Publishing; May 1, 2022. 9. Zafren K, Thurman RJ, Jones ID. High-altitude pulmonary edema. In: Koop KJ, Stack LB, Storrow AB, Thurman J. The Atlas of Emergency Medicine, 5th ed. McCraw Hill; 2021;16-01:548. 10. Luks AM, Auerbach PS, Freer L, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness: 2014 update. Wilderness Environ Med. 2019;30(4S):S3-S18. 11. Pennardt A. High-altitude pulmonary edema: diagnosis, prevention, and treatment. Curr Sports Med Rep. 2013;12(2):115-119. 12. Leshem E, Caine Y, Rosenberg E, Maaravi Y, Hermesh H, Schwartz E. Tadalafil and acetazolamide versus acetazolamide for the prevention of severe high-altitude illness. J Travel Med. 2012;19(5):308-310. 13. Bliss A, Mahajan S, Boehm K M. Systematic review of the effects of phosphodiesterase-5 inhibitors and dexamethasone on high altitude pulmonary edema (HAPE). Spartan Med Res J. 2019;3(3):7111. 14. Wimalasena Y, Windsor J, Edsell M. Using ultrasound lung comets in the diagnosis of high altitude pulmonary edema: fact or fiction? Wilderness Environ Med. 2013;24(2):159-164.

Anxiety and Depression Mushroomed in US at Start of Pandemic

Rates of anxiety and depression among US adults were 4 times higher between April 2020 and August 2021 compared with rates in 2019.

Anxiety disorders affect 40 million adults in the US.

The COVID-19 pandemic brought to light the growing mental health crisis in America, which has a ected patients of all ages. Before 2020, mental health disorders were among the leading causes of the global health-related burden, with depressive and anxiety disorders the most disabling.1 The ongoing pandemic has exacerbated many determinants of poor mental health. As a result, rates of anxiety and depression among US adults were 4 times higher between April 2020 and August 2021 compared with rates in 2019 (Figure).2,3 Men, Asian Americans, young adults, and parents with children in the home had the greatest increases in rates of anxiety and depression, according to the Centers for Disease Control and Prevention.3

The COVID pandemic further highlighted the need to monitor children’s mental health as well. The 2020 National Survey of Children’s Health (NSCH) examined 5-year trends in children’s well-being, including potential e ects of the COVID-19 pandemic. Between 2016 and 2020, signi cant increases in the rates of children diagnosed with anxiety (from 7.1% to 9.2%) and depression (3.1% to 4.0%) were found along with decreases in daily physical activity (24.2% to 19.8%) and in caregiver mental health (69.8% to 66.3%; trend P < .001 for all comparisons).4

Primary care settings often serve as the only point of contact for individuals experiencing mental health problems. Primary care providers play a crucial role in the management of these patients.

The Truth About Anxiety

Anxiety disorders are the most common mental illness in the US and affect 40 million adults (or 19.1% of the population) every year.5 Anxiety disorders are highly treatable, yet only 36.9% of those diagnosed with these disorders receive treatment.5 Lack of access to mental health providers and limited insurance coverage prevent patients from obtaining proper treatment.1,2,5 People with anxiety disorders are 3 to 5 times more likely to go to the doctor and 6 times more likely to be hospitalized for psychiatric disorders than those without anxiety disorders.5 Anxiety develops from a complex set of risk factors, including genetics, brain chemistry, personality, and life events.5 Depression is a common comorbidity in patients with anxiety with approximately 50% of those diagnosed with depression also diagnosed with an anxiety disorder.5

Anxiety disorders affect 31.9% of children between the ages of 13 and 18 years.4 Children with untreated anxiety are at higher risk of performing poorly in school, missing important social experiences, and engaging in substance abuse (often as self-medication).4,5 Anxiety disorders in children and adolescents often co-occur with other disorders such as depression, eating disorders, and attention-deficit/hyperactivity disorder (ADHD).4,5 Identifying anxiety disorders at an early age may be important because childhood onset of some psychiatric disorders has been linked to a worse prognosis compared with adult onset.6

In older adults, generalized anxiety disorder (GAD) is the most commonly diagnosed anxiety disorder.5,7 Anxiety disorders in this older population are frequently associated with traumatic events such as a fall (or fear of a fall), safety, or onset of illness. When symptoms of anxiety become pervasive, are consistent with the Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria, and affect the patient’s ability to function, the presumed diagnosis is an anxiety disorder (Table 1).5,7,8

Diagnosing Anxiety in Adults

Anxiety disorders can negatively impact a patient’s quality of life and disrupt important activities of daily living. Screening questions to ask in primary care include the following8: • Over the past 2 weeks, how often have you been bothered by either feeling nervous, anxious, or on edge? • Have you been unable to stop or control your worrying? • Please tell me a bit more about the difficulties your anxiety is causing for you in terms of how you are functioning in your daily life at work and at home

The Generalized Anxiety Disorder 7-item Scale (GAD-7) is a free self-administered questionnaire that can be used to support diagnosis and as a severity measure for GAD. The tool can be introduced to patients by saying “Please complete this form so I can get a bit more information on the nature of your worries. It won’t take very long, there are only 7 questions, and it will help

Rates of Anxiety, %

40 35 30 25 20

15 10

5

Jan 2019-Dec 2019 April 2020-August 2021

FIGURE. Percentage of US adults reporting symptoms of anxiety, January to December 2019 (monthly average) and April 2020 to August 2021 (submonthly average)2,3

TABLE 1. Common Types of Anxiety Disorders Treated in Primary Care5,7,8

Generalized anxiety disorder • The most common anxiety disorder • Chronic disorder involving excessive, long-lasting anxiety and worries about nonspecific life events, objects, and situations that occur more days than not for at least 6 months, about several different events/activities • People with this disorder are not always able to identify the cause of their anxiety and find it difficult to control their worry • Women are twice as likely as men to be affected • Often occurs with MDD • Physical symptoms include restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance • Hallmark signs: excessive, persistent, out-of-control worry about various domains

Panic disorder • Includes recurrent or unexpected brief and sudden attacks of intense terror and apprehension • ≥1 attack has been followed by ≥1 month of persistent concern about additional attacks or their consequences and/or a significant maladaptive change in behavior related to attacks • Attacks may be expected (response to a typically feared object) or unexpected (occurs for no apparent reason) • Panic attacks tend to occur and escalate rapidly, peaking after 10 minutes (however, a panic attack may last for hours) • Hallmark signs: shaking, sweating, palpitations, fear of dying, confusion, dizziness, nausea, and breathing difficulties

Social anxiety disorder • The fear of negative judgment from others in ≥1 social situations or of public embarrassment • Includes a range of feelings such as stage fright, fear of intimacy, and anxiety around humiliation and rejection • Can cause people to avoid public situations and human contact to the point that everyday living is rendered extremely difficult • Fear, anxiety, or avoidance is persistent and lasts for ≥6 months • Equally common among men and women • Onset is typically around age 13 years • Many of these patients will wait 10 years or more before seeking help • Hallmark sign: fear of being scrutinized

MDD, major depressive disorder

me to work out how best to help you.” In addition to assessing a person’s symptoms and associated functional impairment, consider how the following factors may affect the development, course, and severity of the person’s presenting problem7,8: • History of any mental health problem • History of a chronic physical problem • Any past use of, and response to, treatments • Quality of interpersonal relationships • Living conditions and social isolation • Family history of mental illness • History of domestic violence or sexual abuse

The rates of underdiagnosis and misdiagnosis of GAD and panic disorder in primary care are high, with symptoms often ascribed to physical causes.8,9 Careful evaluation of an anxious patient will help to determine if the cause of the anxiety is organic or psychological (Table 2).9-11

Clinical guidelines for pharmacologic treatment of anxiety in adults recommend a selective serotonin reuptake inhibitor (SSRI), such as paroxetine and escitalopram, as first-line treatment (Table 3).12 Current treatment guidelines discourage the use of benzodiazepines (except as a short-term measure during crises) and antipsychotics for the treatment of anxiety disorders in primary care.12

Anxiety Disorders in Children and Adolescents

The median age of onset of anxiety disorders in children is approximately 11 years and onset typically occurs during a specific developmental phase such as specific phobias in the school-age years; social anxiety in the early adolescent years; and GAD, panic, and agoraphobia in the later adolescent/ young adult years.13 While no universal recommendation for screening for anxiety disorders in children and adolescents exists, free screening tools such as the GAD-7 and the Screen

TABLE 2. Disease States Associated With Anxiety9

Cardiac arrhythmia Neoplasms

Chronic obstructive pulmonary disease Pheochromocytoma

Congestive heart failure Pneumonia

Encephalitis Porphyria

Hyperadrenalism Pulmonary embolism

Hyper- or hypothyroidism Vestibular dysfunction

Hyperventilation Vitamin B12 deficiency

Continues on page 16

TABLE 3. Medications Used to Treat Anxiety Disorders Among Adults in Primary Care10-12

Antidepressants • Antidepressants are typically first-line treatment for anxiety, particularly SSRIs • SSRIs take 6-8 weeks to be fully effective • SSRIs are not addictive • Examples include paroxetine, sertraline, fluoxetine, and escitalopram • Some serotonin and norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine and duloxetine, are indicated for anxiety

Benzodiazepines • Have largely replaced barbiturates in the treatment of anxiety as they are safer and more effective • Work quickly, often within 1 hour • Typically prescribed for no more than 1 month when used for GAD, panic disorder, and social anxiety disorder • Addiction/abuse is possible and withdrawal symptoms may occur if stopped suddenly; important to taper off when discontinuing use • Safe for short-term use with antidepressants • Examples include alprazolam, clonazepam, lorazepam (preferred in the elderly), and diazepam

Azapirones • Weak dopamine D2 receptor blocking action • Does not produce antipsychotic or extrapyramidal side effects • Often prescribed with an antidepressant • Have little potential for producing tolerance or physical dependence; no abuse liability • Slow onset of action; not suitable for an acute episode of anxiety • Buspirone is commonly used to treat GAD; this agent does not produce significant sedation or cognitive impairment • Avoid use in patients with renal or hepatic impairment

Sedative antihistamine • Hydroxyzine is used for short-term treatment of anxiety and tension symptoms as well as to treat allergic reactions • Acts quickly by rapidly absorbing into the stomach; begins working as soon as 15-30 minutes after administration • Most common side effect is sleepiness; this agent is also commonly used to treat insomnia

β-blockers • Many symptoms of anxiety (heart palpitations, increase in blood pressure, shaking, tremors) are caused by sympathetic overactivity • Propranolol and other nonselective beta-blockers can help with these symptoms • Do not affect psychological symptoms such as worry, tension, and fear but are valuable in acutely stressful situations (examinations, public speaking)

GAD, generalized anxiety disorder; SSRIs, selective serotonin reuptake inhibitors

for Child Anxiety Related Disorders are readily available. Treatment guidelines for children are similar to those for adults. The American Academy of Child and Adolescent Psychiatry (AACAP) recommends that SSRIs be o ered to patients 6 to 18 years old with social anxiety, GAD, separation anxiety, or panic disorder.13 All SSRIs have a boxed warning for suicidal thinking and behavior through age 24 years with the rate for suicidal ideation across all antidepressant classes reported to be 1% compared with 0.2% for placebo.13 The US Food and Drug Administration recommends close monitoring of children for suicidality, especially during the rst months of treatment.11,12

Nonpharmacologic Recommendations

Low-intensity psychological interventions for anxiety disorders include psychoeducation groups and individual guided self-help with written or electronic materials of appropriate reading age.12 High-intensity treatment recommendations include 12 to 15 weekly sessions of cognitive behavioral therapy (CBT) delivered by trained and competent practitioners.12 Adult CBT usually combines several di erent interventions such as psychoeducation, worry exposure, applied relaxation, problem-solving, cognitive restructuring, and interpersonal psychotherapy.12 The AACAP recommends that CBT be o ered to patients 6 to 18 years old with social anxiety, GAD, separation anxiety, speci c phobia, or panic disorder.13 Cognitive behavioral therapy in children is aimed at both the child and parents with a focus on learning positive self-talk, coping skills training, and thought challenging.13

Conclusion

Given the marked increase in anxiety rates among both adults and children during the COVID-19 pandemic, primary care clinicians should ask patients about anxiety symptoms and use simple screening tools such as the GAD-7 at regular visits. ■

POLL POSITION

What percentage of children between the ages of 13 and 18 years have anxiety disorders?

■ 25.1%

■ 31.9%

■ 39.2%

■ 42.6% 21.15% 19.23%

23.08% 36.54%

For more polls, visit ClinicalAdvisor.com/Polls. Jennifer Allain, DNP, MSN, APRN, FNP-C, is the NP program coordinator and master teacher of mental health psychiatric nursing at The LHC Group, Myers School of Nursing of the University of Louisiana at Lafayette College of Nursing and Health Sciences. Shirley Gri ey, DNP, PMHNP, is a psychiatric nurse practitioner at Baton Rouge General Medical Center and an instructor at Southeastern Louisiana University School of Nursing. Christy Cook-Perry, DNP, PMHNP, ANP, is assistant professor at Southeastern Louisiana University College of Nursing and Health Sciences.

References

1. COVID-19 Mental Disorders Collaborators. Global prevalence and burden of depressive and anxiety disorders in 204 countries and territories in 2020 due to the COVID-19 pandemic. Lancet. 2021;398(10312):1700-1712. 2. Terlizzi EP, Schiller, JS. Estimates of mental health symptomatology, by month of interview: United States, 2019. National Center for Health Statistics. March 2021. Accessed June 18, 2022. www.cdc.gov/nchs/data/nhis/mental-health-monthly-508.pdf 3. National Center for Health Statistics. Household pulse survey — anxiety and depression. Centers for Disease Control and Prevention. Accessed June 21, 2022. www.cdc.gov/nchs/covid19/pulse/mental-health.htm 4. Lebrun-Harris LA, Ghandour RM, Kogan MD, Warren MD. Five-year trends in US children’s health and well-being, 2016-2020. JAMA Pediatr. 2022 Mar 14:e220056. 5. Facts and statistics. Anxiety and Depression Association of America. June 18, 2022. Accessed June 21, 2022. https://adaa.org/understanding-anxiety/facts-statistics 6. Scheeringa MS, Burns LC. Generalized anxiety disorder in very young children: rst case reports on stability and developmental considerations. Case Rep Psychiatry. 2018;2018:7093178. 7. National Institute for Health and Clinical Excellence. Common mental health problems. Clinical case scenarios for primary care. May 2012. Accessed May 27, 2022. https://www.nice.org.uk/guidance/cg123/resources/ clinical-case-scenarios-pdf-version-pdf-181726381 8. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. American Psychiatric Association; 2013. 9. Chen JP, Reich L, Chung H. Anxiety disorders. West J Med. 2002;176(4):249-253. 10. Stahl MS. Stahl’s Essential Psychopharmacology. 4th ed. Cambridge University Press; 2011. 11. Stahl MS. Stahl’s Essential Psychopharmacology: Prescriber’s Guide. 6th ed. Cambridge University Press; 2017. 12. National Institute for Health and Care Excellence. Generalized anxiety disorder and panic disorder in adults: management. Updated June 2020. Accessed June 27, 2022. https://www.nice.org.uk/guidance/cg113 13. Walter HJ, Bukstein OG, Abright AR, et al. Clinical practice guideline for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2020;59(10):1107-1124.

Conference Roundup

2022 AANP National Conference

American Association of Nurse Practitioners June 21 to 26, 2022, Orlando, Florida

WORKFLOW PROTOCOL IMPROVES UTI CARE IN OLDER ADULTS

The implementation of a standardized workflow for the diagnosis and management of urinary tract infections (UTIs) in patients using home health care did not increase emergency department visits or hospitalization rates, according to the results of a pilot study.

“Antimicrobial use for suspected UTI among older adults is very common and often inappropriate,” said the study authors. Homebound older adults are at higher risk for infection and UTI diagnosis can be challenging. “This often results in high antibiotic use, which can lead to multidrug-resistant infections, drug interactions, and medication-related adverse effects,” noted the authors. Delay in administering empiric antibiotics raises the risk for sepsis in older patients.

The lack of a clinical standard for diagnosis and management of UTIs in homebound older adults led the team to embark on a quality improvement project. This included the development of a standardized workflow protocol for the initial diagnosis and management of urinary symptoms.

Half of all patients enrolled in the Senior Services Homebound Program received the intervention. Calls from patients and caregivers were managed by a nurse care coordinator who triaged symptom-based calls. The nurse would then report findings to a nurse practitioner or PA. The researchers compared infection rates among 15 enrolled patients with those among nonenrolled homebound patients. Among the patients enrolled in the protocol, 73% were women, 53% lived in assisted living facilities, and 53% were between 80 to 90 years of age.

The total number of UTIs in the protocol group was 23 compared with 20 in the control group; the number of UTI-related hospitalizations was lower in the protocol group than in the control group (2 vs 6).

“This clinically significant project offers a standardized method for addressing this condition in an evidence-based paradigm. A workflow protocol for urine testing for these patients resulted in appropriate treatment based on laboratory results rather than just taking an often inappropriate educated guess. Hospitalization in this population results in another myriad of problems and this easy to implement framework decreases the chance that hospitalization will be the treatment outcome,” Dr Koslap-Petraco said.

The workflow protocol was easy for nurses to implement, according to the authors. Patients who were triaged for urinary testing were more likely to receive testing following implementation of the protocol; those with symptoms not appropriate for empiric treatment were provided with supportive care instructions and revisited 2 days later, the authors concluded.

CAGE-AID HELPS IDENTIFY PATIENTS WITH SUD FOR RECOVERY

The use of the CAGE-AID screening tool in an emergency department (ED) was linked to increased referral to an addiction recovery coach for treatment of alcohol and drug use disorders, the authors of a poster reported.

Approximately 1 in 4 ED patients screen positive for risky alcohol and/or drug use. However, previous attempts to integrate screening for alcohol and drug use into ED nurses’ workflow have had mixed results.

The researchers studied the benefits of administration of CAGE-AID and SBIRT (screening, brief intervention, and referral to treatment) over a 10-week

TOP, BOTTOM IMAGES: © GETTY IMAGES Antibiotic use for suspected UTIs is common and often inappropriate in older adults.

Conference Roundup

period compared with standard of care during the preceding 10 weeks.

All patients who presented to Jefferson Health older than 18 years and did not qualify for emergency or mental health services were assessed for social history by a licensed provider (physician, nurse practitioner, or PA). All patients who answered yes to either question about history of alcohol or drug use were administered CAGE-AID by the ED physician. Those who answered yes to 1 or more of the CAGE-AID questions were encouraged by the provider to accept a referral to an addiction recovery coach.

Over the 10-week control period, 15.7% of 209 patients were referred to an addiction recovery coach. According to lead author Julie M. Daly, DNP, MSN, APN, “recovery coaches serve as personal guides and mentors to people seeking or already in long-term recovery.” They connect patients to resources, develop wellness plans, monitor progress with recovery, and provide encouragement. They complement counseling, 12-step recovery programs, and other recovery support systems.

During the intervention period, the percentage of patients referred to an addiction recovery coach rose to 33% and included 77 patients. “It was noted that 59% of patients with a documented positive CAGE-AID screening were also documented as having agreed to and received a referral to ARC,” noted Dr Daly.

MINDFULNESS IMPROVES MOOD AND BEHAVIOR IN UNDERSERVED STUDENTS

A nurse practitioner (NP)-led, mindfulness- based intervention for underserved elementary students led to improvements in emotional regulation and behavior, explained Cara C. Young, PhD, RN, FNP-C, FAANP, FAAN.

The study was designed to investigate the effects of the standardized mindfulness-based intervention A Still Quiet Place when used in at-risk, predominantly Hispanic (75%) elementary school students in fourth and fifth grades (N=16) before they transitioned from elementary to middle school.

The mindfulness sessions were conducted after school hours. The A Still Quiet Place program is an 8-week mindfulness-based stress reduction program designed for therapists, teachers, and other professionals to use with children and adolescents. A majority of the students (88%) completed the intervention. Outcomes were based on parent reports.

A majority of parents reported improvement in their child’s mood, attitude, and behavior (ie, sibling and family interactions) at home. Parents said they appreciated the movement and stillness practices, take-home materials, and after-school timing. Parents also suggested the need for improved feedback loops, additional parent-involved group sessions, and the ability to track mindfulness homework. School staff reported “excitement of the children in their participation” in the mindfulness training and noted logistical challenges with implementation, Dr Young said.

The benefits of an NP-school partnership during mindfulness training in this population include the potential for increased identification of at-risk students in need of health care services and for the NP to act as an advocate and liaison to ensure that additional services are provided to students in need, Dr Young said.

LIFESTYLE MODIFICATIONS ALLEVIATE VESTIBULAR MIGRAINE SYMPTOMS

Vestibular migraine is a common cause of vertigo and can significantly impact quality of life. Interventions to treat vestibular migraine include lifestyle modifications as well as prophylactic and rescue medications. While lifestyle modifications can improve symptoms of other forms of migraine, these strategies have yet to be studied in vestibular migraine.

The current study was comprised of 28 patients with vestibular migraine as defined by ICHD-3 criteria. All participants agreed to be treated without pharmacological intervention. Participant were asked to adhere to the following lifestyle modifications for 60 days: • Restful sleep • Mealtime regularity • Exercise • Elimination of dietary triggers

Dizziness Handicap Inventory (DHI) and Headache Disability Inventory (HDI) were used to calculate results.

Dizziness scores improved by a mean of 14 points overall and 39.2% of patients experienced an 18-point or greater decrease in DHI score postintervention. Headache scores also decreased by a mean of 14 points with 17.9% of the group experiencing a 29-point or greater decrease in HDI score.

The sleep intervention appeared to be linked to the greatest improvement in symptoms, according to the researchers. ■

A majority of parents reported improvement in their child’s mood, attitude, and behavior.

Adults Without Diabetes Benefit From GLP-1 Agonists for Obesity

Obesity is associated with an increased risk of developing diabetes, heart disease, stroke, and some types of cancer and reduced quality of life.

New treatments reduce appetite and food intake and increase satiety.

Obesity was first recognized by the American Medical Association as a chronic disease requiring medical interventions in 2013.1 Although medications promoting weight loss have been available since the 1930s, few remain on the market because of side effects, including cardiotoxicity, psychiatric disturbances, and dependency.2,3 The US Food and Drug Administration (FDA) has approved 6 agents for the long-term management of obesity: liraglutide, lorcaserin, naltrexone/bupropion, orlistat, phentermine/topiramate, and semaglutide.2

This review will focus on the 2 most recently approved antiobesity medications — liraglutide and semaglutide. These agents are glucagonlike peptide-1 (GLP-1) receptor agonists, which were first approved for the treatment of type 2 diabetes. The new indications include weight loss in adults with obesity (body mass index [BMI] ≥30) without diabetes and adults with a BMI of 27 or greater and 1 weight-related comorbidity (hypertension, type 2 diabetes, or dyslipidemia).2 The agents were approved based on clinical studies supporting the use of these GLP-1 agonists as targeted antiobesity therapies.2,3

Prevalence of Obesity

The prevalence of obesity among adults in the US has been increasing and has reached 41.9%, with the highest rates found among non-Hispanic Black adults (49.9%) followed by Hispanic adults (45.6%), according to data from the 2017-2020

WEIGHT MANAGEMENT: GLP-1 RECEPTOR AGONISTS The incretin effect is a 2- to 3-fold increase in insulin stimulation after oral glucose consumption, which leads to GIP and GLP-1 secretion.

National Health and Nutrition Examination Survey.4,5 Obesity is associated with an increased risk of developing diabetes, heart disease, stroke, and some types of cancer.4 Obesity is also associated with poorer mental health outcomes and reduced quality of life.6

Pathophysiology of Obesity

While weight gain is commonly thought to be caused by an imbalance of calorie intake to calorie expenditure, the risk of developing obesity also is associated with environmental and genetic factors.2 Data from the genome project have identified more than 140 genetic chromosomal regions related to obesity.7 Weight gain also is related to use of certain medications such as antidepressants and corticosteroids as well as certain illnesses, including Cushing disease and hypothyroidism.6 Research into the role of the gastrointestinal (GI) system has found that an altered microbiome also appears to play a role in the development of obesity.2

Role of Incretin Hormones in Metabolism

The latest antiobesity agents target GLP-1 receptors, which are concentrated within the pancreas, GI system, central nervous system, heart, lungs, kidneys, blood vessels, and peripheral nervous system.1 Incretin hormones are GI peptides secreted following food intake and an elevation of blood glucose level.1 The focus on incretin hormones as an obesity treatment evolved after observing the incretin effect.1 This effect describes the 2- to 3-fold increased insulin stimulation from the pancreas following oral glucose consumption as compared with intravenous infusion.1 Ingestion of oral glucose leads to the secretion of glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 from specialized cells in the gut.1 K-cells produce GIP in the duodenum and upper jejunum, and L-cells produce GLP-1 in the lower GI system.1 The combined effect of GIP and GLP-1 secretion in healthy adults results in increased insulin secretion and delayed gastric emptying.1 In people with type 2 diabetes, however, this incretin effect is decreased or nonexistent.1

Incretin Effects on Organs Glucagon-like peptide-1 uptake in the hypothalamus reduces appetite and food intake and increases satiety.7-10 Alpha cells of the pancreas produce glucagon and beta cells of the pancreas secrete insulin.8 Both cell types have GIP and GLP-1 receptors on their membranes.1 The presence of GLP-1 delays gastric emptying and acid secretion while slowing transit through the gut.8 Uptake of GLP-1 in the liver decreases gluconeogenesis, increases glycogen storage, and decreases lipogenesis.8-10

Mechanism of Action of GLP-1 Receptor Agonists

Glucagon-like peptide-1 receptor agonists improve glycemic control by enhancing insulin secretion from the beta-pancreatic cells and inhibiting glucagon release from the alpha-pancreatic cells.9,10 Additionally, the agonists slow gastric emptying, increase satiety, and reduce appetite, resulting in weight reduction.9,10 Endogenous GLP-1 has a half-life of less than 2 minutes because it is rapidly degraded by dipeptidyl peptidase IV (DPP4).9 Glucagon-like peptide-1 receptor agonists are identified as short- or long-acting agents.10 Short-acting receptor agonists circulate for a few hours, followed by periods of GLP-1 inactivity.10 Long-acting receptor agonists produce a long-lasting drug concentration with little fluctuation in drug levels.10 Short-acting GLP-1 receptor agonists lower glucose levels by slowing gastric emptying, while long-acting GLP-1 receptor agonists lower glucose levels by slowing gastric emptying, increasing insulin production, and inhibiting glucagon.10 Both liraglutide and semaglutide are long-acting agents; no short-acting agents are currently approved for weight loss.10-12

GLP-1 Receptor Agonists Approved for Obesity

Liraglutide (Victoza) and semaglutide (Ozempic) are longacting GLP-1 receptor agonists made by the same manufacturer (Novo Nordisk) and currently approved for the treatment of type 2 diabetes.3 Both medications also are approved as adjuncts to a reduced-calorie diet and increased exercise for chronic weight management at different doses than those used for diabetes treatment and under the brand names Saxenda and Wegovy, respectively.3,11,12

Lack of Insurance Coverage for Antiobesity Medications

Many health insurance companies do not cover the cost of GLP-1 receptor agonists when used for weight loss or other antiobesity medications. Patients may be counseled that coupons and patient assistance programs may assist in getting access to these GLP-1 receptor agonists in the near future. Semaglutide manufacturing problems have also limited the supply of this agent; this issue is expected to be resolved later this year. (Kolata G. The doctor prescribed an obesity drug. Her insurer called it ‘vanity.’ New York Times. May 31, 2022).

Few patients stopped GLP-1 receptor agonists because of drug-related adverse events, and those that did cited GI-related events.

Liraglutide In 2015, the FDA approved liraglutide (3 mg) as the first GLP-1 receptor agonist for chronic weight management in adults with obesity and overweight.11 In December 2020, the FDA approved an updated label for use of liraglutide in the treatment of obesity in adolescents (12-17 years).13 The initial dose is 0.6 mg once daily for 1 week to be increased weekly to a target dose of 3 mg once daily.11 Liraglutide is long-acting and administered by daily subcutaneous injections and has a half-life of 12.6 to 14.3 hours.3

Semaglutide In June 2021, the FDA approved semaglutide for chronic weight management in adults with obesity and overweight.12 With a starting dose of 0.25 mg, the once-weekly subcutaneous injection should be increased in 4-week intervals to 2.4 mg.12 Semaglutide has an extended half-life of approximately 1 week, making it suitable for once-weekly administration.9,12,14

Safety Profiles and Side/Adverse Effects

The most common side effects of GLP-1 agonists reported in clinical trials for weight management were nausea, diarrhea, vomiting, constipation, abdominal pain, headache, fatigue, dyspepsia, dizziness, abdominal distension/pain, injection site reactions (liraglutide), increased lipase (liraglutide), pyrexia (liraglutide), eructation (semaglutide), flatulence (semaglutide), hypoglycemia in patients with type 2 diabetes, gastroenteritis, and gastroesophageal reflux disease (semaglutide).11,12

Most adverse events reported were mild (69%) and severe adverse events were rare.3 Few patients stopped the medications because of drug-related adverse events, and those that did cited GI-related events.3,11,12 The discontinuations occurred during escalating doses of semaglutide rather than after reaching the final dose.3 Both acute pancreatitis and acute gallbladder disease have been observed in patients treated with GLP-1 receptor agonists, including semaglutide and liraglutide.3,11,12 Reports of cholelithiasis and cholecystitis increased across the semaglutide dosing range (2%-7%).3 An increased risk of developing upper respiratory infections has been reported with the use of GLP-1 receptor agonists.14 The increased risk is listed as an adverse reaction in some package inserts of this class but is not a contraindication to use and is not listed as a warning or precaution.14

Efficacy of Liraglutide and Semaglutide

O’Neil and colleagues compared liraglutide with semaglutide in adults without diabetes and with a BMI of 30 or greater (mean BMI, 39.3). The authors, who disclosed that the study was funded by the drug’s manufacturer, reported that liraglutide 3.0 daily was associated with an estimated mean weight loss of 7.8% at week 52, while semaglutide 0.2 mg, 0.3 mg, and 0.4 mg resulted in an 11.6%, 11.2%, and 13.8% weight reduction. Estimated mean weight loss was 2.3% for the placebo group.3

The weight loss observed with semaglutide is greater than that reported for other approved antiobesity drugs: orlistat (6%), lorcaserin (6%), phentermine-topiramate (8%-10%), and naltrexone-bupropion (5%).3 Most established guidelines define meaningful weight loss as 5% to 10% of initial weight at which point an improvement in cardiovascular risk factors is observed.2

Once-weekly administration may improve patient compliance and quality of life over once-daily dosing as has been demonstrated in the management of type 2 diabetes with GLP-1 receptor agonists as well as administration of medications for other chronic diseases.15,16

Conclusion

Glucagon-like peptide-1 receptor agonists access specific brain areas important for appetite regulation, resulting in weight loss.17 These mechanisms may help explain how treatment with GLP-1 agonists leads to reduced appetite and food cravings and better control of eating.3,17 Evidence supports both GLP-1 agonists liraglutide and semaglutide as effective agents for weight loss in patients with obesity without diabetes, with semaglutide data providing a more significant weight loss in clinical trials. Although GLP-1 agonists have side effects, the weight loss benefits may outway their risks. ■

Darlene M. Sanders, DMSc, MPAS, PA-C, is a family practice PA in rural Montana.

Disclosure: Dr Sanders has no relevant financial disclosures.

References

1. Pollack A. AMA recognizes obesity as a disease. New York Times June 18, 2013. Accessed June 1, 2022. https://www.nytimes.com/2013/06/19/business/ ama-recognizes-obesity-as-a-disease.html 2. Bays HB, Fitch A, Christensen S, Burridge K, Tondt J. Antiobesity medications and investigational agents: an Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022. Obesity Pillars. 2022. Published online April 15, 2022. 3. O’Neil PM, Birkenfeld AL, McGowan B, et al. Efficacy and safety of semaglutide compared with liraglutide and placebo for weight loss in patients with

obesity: a randomised, double-blind, placebo and active controlled, doseranging, phase 2 trial. Lancet. 2018;392(10148):637-649. 4. Adult obesity facts. Centers for Disease Control and Prevention. Updated May 17, 2022. Accessed May 31, 2022. https://www.cdc.gov/obesity/data/adult.html 5. Stierman B, MPH, Afful J, et al. National Health and Nutrition Examination Survey 2017-march 2020 pre-pandemic data files-development of files and prevalence estimates for selected health outcomes. National Health Statistics Reports Number. 2021;158. 6. Obesity basics. Centers for Disease Control and Prevention. Updated April 7, 2022. Accessed May 31, 2022. https://www.cdc.gov/obesity/basics/ index.html 7. Fall T, Mendelson M, Speliotes EK. Recent advances in human genetics and epigenetics of adiposity: pathway to precision medicine? Gastroenterology. 2017;152(7):1695-1706. 8. Nauck MA, Meier JJ. Incretin hormones: Their role in health and disease. Diabetes Obes Metab. 2018;20 Suppl 1:5-21. 9. Tilinca M, Tiuca R, Burlacu A, Varga A. A 2021 update on the use of liraglutide in the modern treatment of ‘Diabesity’: A narrative review. Medicina (Kaunas). 2021;57(7):669. 10. Brown E, Cuthbertson DJ, Wilding JP. Newer GLP-1 receptor agonists and obesity-diabetes. Peptides. 2018;100:61-67. 11. Saxenda® (liraglutide). Prescribing information. Novo Nordisk; 2021. Accessed June 2, 2022. https://www.novo-pi.com/saxenda.pdf 12. Wegovy™ (semaglutide). Prescribing information. Novo Nordisk; 2021. Accessed June 2, 2022. https://www.novo-pi.com/wegovy.pdf 13. Novo/Nordisk. FDA approves Saxenda® for the treatment of obesity in adolescents aged 12-17. Press release. December 2, 2020. https://www.novonordiskus.com/content/nncorp/us/en_us/media/news-archive/news-details.html?id=39225 14. Wilding JPH, Batterham RL, Calanna S, et al; STEP 1 Study Group. Onceweekly semaglutide in adults with overweight or obesity. N Engl J Med. 2021;384(11):989-1002. 15. Polonsky WH, Arora R, Faurby M, Fernandes J, Liebl A. Higher rates of persistence and adherence in patients with type 2 diabetes initiating once-weekly vs daily injectable glucagon-like peptide-1 receptor agonists in US clinical practice (STAY Study). Diabetes Ther. 2022;13(1):175-187. 16. Iglay K, Cao X, Mavros P, Joshi K, Yu S, Tunceli K. Systematic literature review and meta-analysis of medication adherence with once-weekly versus oncedaily therapy. Clin Ther. 2015;37(8):1813-21.e1. 17. Blundell J, Finlayson G, Axelsen M, Flint A, Gibbons C, Kvist T, Hjerpsted JB. Effects of once-weekly semaglutide on appetite, energy intake, control of eating, food preference and body weight in subjects with obesity. Diabetes Obes Metab. 2017;19(9):1242-1251.

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