President's Perspective

As President of IAPA, I would like to extend a formal invite to join us at our 2017 Fall CME event, being held September 15^th and 16^th at the Big Ten Conference Center in Rosemont. Our CME committee has put together a dynamic agenda which provides topics of interest for all PAs. Network with fellow PAs and interact with your IAPA Board while you earn CME! Attendance at the CME event helps IAPA raise the funds necessary to advocate on your behalf at the Capitol. 

Our PA Practice Act is awaiting signature from Governor Rauner.  Our deadline is approaching quickly and we will see movement by the end of August. Highlights of the major changes include moving all language from “supervision” to “collaboration.” As a result of the update, PAs will see easier Medicaid billing and reimbursement. Although ratio language will be somewhat improved, IAPA vows to continue to push for further changes which will allow PAs to remain competitive in the Illinois market. 

Membership numbers are improving for our organization, but not yet at goal. Please encourage your fellow PAs to join. IAPA has been reaching out to PAs across the state by holding presentations to explain our legislative agenda. I would love to continue meeting members! Please contact me to arrange a presentation in your area! 

Heat Illness 

by Jana K. Stedman, MS, PA-C

Heat waves are the deadliest weather-related exposure in the United States, with more deaths than tornadoes, floods, earthquakes, and hurricanes combined¹. Heat stroke in particular is a leading cause of preventable death in sports². Heat illness exists on a continuum where the hypothalamic “thermostat” is unable to balance heat gain and heat loss. Persons who are not acclimated to high temperature and humidity, and those unable to behaviorally respond to overheating are at an increased risk.

On a biochemical level, excessive heat results in protein denaturation and destabilization of lipid molecules and cell membranes. When the body’s cooling mechanisms fail, cardiovascular collapse and a cascade of multi-organ failure result from these high-temperature changes. 

The skin is the body’s major “radiator” to dissipate heat, largely through sweating. Heavy clothing and high humidity reduce heat transfer from skin back to the environment.  Persons who are not used to hot or humid environments sweat later, less profusely, and with less sodium resorption than those who are acclimated, and are at greater risk of heat injury and electrolyte disturbance. Anhidrosis is a late and inconsistent indicator of the severity of heat injury², so a high index of suspicion must be maintained even if a person is sweating. 

Early symptoms of heat injury include muscle cramping, dizziness, and weakness. As core temperature rises, tachycardia, hypotension, electrolyte disturbances, and syncope may result. “Heat stroke” occurs at body temperatures typically reaching 103-106F (39.5-41.1C) or higher with associated neurologic dysfunction^1,2. Heat stroke may be exertional (EHS) or nonexertional (NEHS), resulting simply from exposure.

Who is at risk for heat stroke? Perhaps more people than you think. Any condition that impairs sweating, reduces cardiovascular reserve, or prevents behavioral modification predisposes a person to severe heat illness.

• Persons exercising on a hot and humid day, especially when deconditioned or highly competitive
• Alcohol consumption, or use of cocaine, amphetamines, or MDMA in hot environments
• Infants, the bed-bound, or cognitively impaired persons unable to take measures to cool themselves
• Persons taking diuretics, anticholinergics, or neuroleptics 
• Classically, geriatric, low-income and homebound persons on multiple medications with poor access to cool environments who do not self-hydrate

Heat stroke is a medical emergency. Morbidity and mortality are directly related to the duration of temperature elevation. When heat loss fails and no intervention is taken, basal metabolism alone can raise the body temperature by 1.1∞C/hr simply at rest. Immediate cooling at the scene is necessary to minimize the time of heat exposure. Removal of restrictive clothing, spraying the person with cool water, and application of ice packs to the axillae and groin can be performed at the scene. Submersion in an ice water bath is a somewhat contested yet common method of cooling². Upon the arrival of medical personnel, hemodynamic stabilization and cooling the body to a goal temperature of 39∞C are priorities. Providers should look for evidence of organ complications due to poor perfusion, apoptosis, direct heat injury to proteins, and cell membrane breakdown. These commonly include rhabdomyolysis, compartment syndrome, AKI, pulmonary edema, and transamnitis³.

Heat injury is preventable with straightforward means, and “common sense” precautions should be reinforced despite their simplicity. People who are traveling to hot and humid locations and those beginning or intensifying exercise will need 7-10 days for their body’s heat response to acclimate². Educate patients taking related medications about side effects that can worsen in hot weather. Finally, caregivers and residents in poorly cooled homes should be informed of local “cooling centers,” or may call 3-1-1 for locations in Chicago, or to request a well-being check by local officials⁴.

References 

1. Centers for Disease Control and Prevention. Warning Signs and Symptoms of Heat-Related Illness. Natural Disasters and Severe Weather. https://www.cdc.gov/disasters/extremeheat/warning.html. Published 2017. Accessed August 4, 2017.

2. Helman RS. Heat Stroke. Medscape. http://emedicine.medscape.com/article/166320-clinical#b1. Published 2017. Accessed August 4, 2017.

3. Lumlertgul D, Chuaychoo B, Thitiarchakul S, Srimahachota S, Sangchun K, Keoplung M. Heat stroke-induced multiple organ failure. Ren Fail. 1992;14(1):77-80. http://www.ncbi.nlm.nih.gov/pubmed/1561392. Accessed August 4, 2017.

4. City Cooling Centers. City of Chicago. https://www.cityofchicago.org/city/en/depts/fss/provdrs/emerg/svcs/city_cooling_centers.html. Published 2017. Accessed August 4, 2017.

Sunburn

by Jana K. Stedman, MS, PA-C

Sunburn is the most common type of radiation burn. The cost of treating sunburn in 2013 reached $11.2 million in emergency departments alone¹. While sunburns are known to be an important risk factor for cutaneous melanoma, basal and squamous cell carcinomas, they can also result in acute complications requiring medical intervention. Severe sunburn may result in second-degree burns, dehydration, or secondary infection².

Unfortunately for those looking for a “healthy glow,” all tanning is skin damage, and tanning and burning are mechanistically interrelated through ultraviolet radiation (UVR)³. Ultraviolet radiation can be understood as a combination of UVA and UVB rays, with UVB rays being the primary cause of sunburn. UVA rays lead to skin damage such as wrinkling and hyperpigmentation, and can pass through window glass.

Immediate skin pigment darkening can occur during UVR exposure due to oxidation and redistribution of existing melanin, and initial erythema from sunburn may not appear until 3-4 hours of exposure. The acute cutaneous inflammation following exposure to UVR causes vasodilation and cellular apoptosis, along with the release of a host of pro-inflammatory compounds tipped off by direct damage to DNA². Sunburn erythema peaks around 24 hours, when delayed tanning begins to become visible. Repeated UVR exposure leads to thickening of the stratum corneum, and suppression of cutaneous cell-mediated immunity, an important mechanism in the development of neoplasms².

There is widespread belief that sunburns in childhood are more contributory to the development of cutaneous melanoma than those sustained in adulthood, which may lead adults to underestimate their risk with the mindset that “the damage is done.” However, the incidence of melanoma actually rises in a dose-response fashion, with increased risk correlated with an increasing number of sunburns across a lifetime⁴. 

Advising a person to “wear sunscreen” is easy enough, but what does that mean when faced with a store display of dozens of products to choose from? Many people aren’t sure what “SPF” means in practical terms, nor do they use the product they purchase appropriately. SPF, or Sun Protection Factor, is the ratio of UVR needed to produce erythema on protected versus unprotected skin. “Broad-spectrum” sunscreens protect against both UVA and UVB rays³.  A sunscreen with an SPF of 30 blocks 97% of UVB radiation, with diminishing returns with higher SPFs³. Inconveniently, a higher SPF does not give a product any longer protection time in the sun, and will have to be reapplied every 2-3 hours just like a product with a lower SPF. Higher-SPF sunscreens may give a false sense of security, leading people to apply less product, stay out longer in the sun, or reapply less often. This is risky because most people only apply one-fifth of the sunscreen they need in the first place, far below the ballpark goal of 30mL for an adult, and therefore only get a fraction of the protection on the package^3,5. 

Environmental conditions that affect UVR exposure can lead to surprising burns when they are least expected: 80-94% of radiation is reflected by snow, in contrast to 5-8% by ocean surfaces⁶. Light clouds attenuate only about 10% of UVR, and can be deceiving to those outdoors². Sun protection is a year-round priority.

There are some special considerations regarding sun exposure, particularly the risk of phototoxic or photoallergic reactions in persons taking a wide variety of medications or using topical therapies, sunscreens themselves included. While each reaction is the result of chemical photoactivation in the skin, the mechanisms differ. Phototoxicity is more common and occurs when light-activated compounds damage cell membranes, resembles an exaggerated sunburn, and appears quickly following sun exposure. Photoallergy is the result of cell-mediated responses to the light-activated compound, appears to be an allergic contact dermatitis distributed over sun-exposed skin, and tends to appear greater than 24 hours post exposure⁷. Common medications that may lead to these responses include antibiotics, diuretics, statins, sulfonylureas, and retinoids. Ironically, the increasingly rare chemical sunscreen PABA (para-aminobenzoic acid) can induce a photoallergic response, which should be suspected in those who develop an atopic rash following sun exposure despite proper sunscreen use⁸.

Other medical conditions that have dermatological manifestations following sun exposure should be kept in mind. Infants who sunburn easily, developing blistering skin even under phototherapy for hyperbilirubinemia, may be showing signs of an underlying disease such as porphyria⁹ or xeroderma pigmentosum¹⁰ and should be referred to dermatology for evaluation.

Sun exposure can trigger or worsen herpes simplex, the malar rash of systemic lupus erythematosus, and eczema¹¹.

If a sunny outdoor nap or ski trip leaves you burned, or you simply toweled off all your sunscreen, most burns can be treated symptomatically with cool water soaks, NSAIDs, and avoiding further sun exposure. Numbing topicals such as benzocaine should be avoided, as they can worsen dermatitis and cause further skin sensitization. Blistering skin is a sign of partial-thickness, or second-degree burns¹².

Patients with partial-thickness burns presenting with signs of dehydration may require intravenous fluid resuscitation if sufficient fluid has moved from the vasculature into vesicles and bullae. Those who have partial-thickness burns covering >10% of their body surface area may be referred to a burn center for further management. Consider admission to a burn unit if partial-thickness burns cover greater than 20% of BSA in patients under 10 or over 50 years of age, or over 25% of BSA in others¹³.

Lastly, a new consideration in the age of social media. Rising public interest in do-it-yourself projects, “natural” and organic products, and avoidance of “chemical” exposure has created new space for homemade sunscreens. Plant-derived oils, zinc oxide powder, and other ingredients are readily available for the home personal-care mixologist. Although well-intended, the true SPF, stability, and expiration of these compounds are unknown. Those wishing to avoid use of laboratory-tested sunscreens may be better encouraged to avoid the sun through protective clothing and shading.  

References 

1. Kennedy M. ED Visits for Severe Sunburn Rack Up Millions in Costs. Medscape. http://www.medscape.com/viewarticle/873015. Published 2016. Accessed August 3, 2017.

2. McStay C. Sunburn: Background, Pathophysiology, Epidemiology. Medscape. http://emedicine.medscape.com/article/773203-overview. Published 2017. Accessed August 3, 2017.

3. American Academy of Dermatology. Sunscreen FAQs. https://www.aad.org/media/stats/prevention-and-care/sunscreen-faqs. Accessed August 3, 2017.

4. Dennis LK, Vanbeek MJ, Beane Freeman LE, Smith BJ, Dawson D V, Coughlin JA. Sunburns and risk of cutaneous melanoma: does age matter? A comprehensive meta-analysis. Ann Epidemiol. 2008;18(8):614-627. doi:10.1016/j.annepidem.2008.04.006.

5. Wang SQ. ASK THE EXPERT: Does a higher-SPF (sun protection factor) sunscreen always protect your skin better? Skin Cancer Foundation. http://www.skincancer.org/skin-cancer-information/ask-the-experts/does-a-higher-spf-sunscreen-always-protect-your-skin-better. Published 2010. Accessed August 4, 2017.

6. Allen J. Ultraviolet Radiation: How It Affects Life on Earth : Feature Articles. September 2001. https://earthobservatory.nasa.gov/Features/UVB/uvb_radiation3.php. Accessed August 3, 2017.

7. Zhang A. Drug-Induced Photosensitivity: Background, Pathophysiology, Epidemiology. Medscape. http://emedicine.medscape.com/article/1049648-overview. Published 2017. Accessed August 3, 2017.

8. Scheuer E, Warshaw E. Sunscreen Allergy: Epidemiology, Characteristics, & Allergens. Dermatitis. 2006;17(1):3-11. http://www.medscape.com/viewarticle/528577_7. Accessed August 4, 2017.

9. Bonkovsky H, Rudnick SR. Overview of Cutaneous Porphyrias. Merck Manual Professional Version. http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/porphyrias/overview-of-cutaneous-porphyrias. Published 2017. Accessed August 4, 2017.

10. NIH. Xeroderma Pigmentosum. National Institutes of Health - Genetics Home Reference. http://ghr.nlm.nih.gov/gene/NF2. Published 2007. Accessed April 8, 2017.

11. Ichihashi M, Nagai H, Matsunaga K. Sunlight is an important causative factor of recurrent herpes simplex. Cutis. 2004;74(5 Suppl):14-18. http://www.ncbi.nlm.nih.gov/pubmed/15603217. Accessed August 4, 2017.

12. Berry J, Mancini M. Classification of Burns. University of Rochester Medical Center. https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=90&ContentID=P09575. Published 2017. Accessed August 4, 2017.

13. Lloyd ECO, Rodgers BC, Michener M, Williams MS. Outpatient Burns: Prevention and Care. Am Fam Physician. 2012;85(1):25-32. http://www.aafp.org/afp/2012/0101/p25.html. Accessed August 3, 2017.
 

IAPA News and Updates

by Kristin Mahr, MS, PA-C

In response to the increasing number of accredited Physician Assistant programs and limited availability of clinical rotation sites, AAPA and PAEA collaborated to allow PA programs to provide Category 1 CME to physician assistant clinical preceptors.  PA preceptors may claim a maximum of 10 Category 1 CME credits per calendar year, and 20 in a two-year certification maintenance cycle.  In order for PA programs to receive eligibility to provide Category 1 CME for PA clinical preceptors, programs must submit an annual CME application through AAPA. Similar to other Category 1 CME activities, participants receiving CME are required to complete the CME activity evaluation.  This evaluation process provides a valuable opportunity to receive feedback about the program, including aspects they find most and least beneficial to further their own professional development.  At the end of the clinical year, programs approved to provide CME must submit follow-up reconciliation including an evaluation summary and credits awarded to PA preceptors.  

Comments received through CME activity feedback include:

• “Being a preceptor provides me the opportunity to give back and train future generations of physician assistants.”
• “Although the time commitment of clinical precepting can interfere with efficiency, the act of clinical precepting is wholly valuable for continued development as a PA.” 

Physician Assistant clinical preceptors are an essential part of the education team. Providing Category 1 CME is a way to support the physician assistant profession and recognize the partnership between PA programs and PA clinical preceptors.  It is also a way to recognize their participation and contributions to the education of our students.  

For the second consecutive year, the Physician Assistant Program at Rosalind Franklin University of Medicine and Science has awarded Category 1 CME to our physician assistant clinical preceptors.  For the 2016- 2017 academic year we were able to provide a total of 261.50 Category 1 CME hours to our PA clinical preceptors.
 

The Student Section

PA Students in Corrections Medicine:
at the Intersection of Health & Justice

by  Vic Speedwell PA-S3

In the fall of 2015, Dr. David Ansell (author of County: Life, Death and Politics at Chicago’s Public Hospital and The Death Gap: How Inequality Killsl) hosted Rush University students in his home for a ‘Medicine in Action’ themed dinner and discussion. The guest speaker that evening was Dr. Jack Raba—former chief resident at Cook County Hospital and medical director of Chicago’s Cook County Jail—a lifelong social justice advocate with decades of experience putting medicine into action. His soft-spoken yet indignant stories of the conditions and health care challenges at both the hospital and jail so resonated with the students that within a few months of the event a new program was developed—the Incarceration Medicine Initiative (IMI).

This fledgling project, organized by a PA student, two medical students and PA Faculty Advisor Jessica Vlaming, PA-C, met with jail medical staff, toured the jail dormitories and healthcare facilities, recruited and trained an inter-professional team of student volunteers representing three of Rush University’s four colleges, produced and presented a series of health lessons to women detainees over ten weeks, and joined the family of student-run volunteer projects managed by Sharon Gates, Director of Community Engagement for Rush University Medical Center. This year the program won a grant from Rush Medical Center Women’s Board to further the continued growth and reach of the IMI.

The current coordinating team, (now comprised of another PA student and two nursing students) is forging connections with organizations working to win the release of men and women who are jailed prior to conviction and cannot afford the bond that would allow them to be with their families while awaiting trial.  Additionally, other organizations are working to reduce the number of people who are imprisoned by promoting diversion and restorative justice opportunities as alternatives to time behind bars. Outside of the walls, several volunteers have committed to understanding the health implications for residents who live in the same neighborhood as the jail and plan to support existing groups in Little Village and South Lawndale neighborhoods.

The work of teaching health topics behind bars will continue. The Incarceration Medicine Initiative has ambitious goals for the education sessions. Recently a new PA student at Rush was instrumental in getting a men’s program up and running at the jail. Future work includes translating the handouts and lessons into Spanish, offering a similar program to immigration detainees, and creating a youth-appropriate program for residents at the juvenile detention facility. In addition to the IMI serving as a model of inter-professional team building, the project may soon become inter-institutional. The group was approached by the representatives of the Radical Public Health Club at University of Illinois-Chicago and the Northwestern University PA program to discuss the potential for collaboration. Additional collaboration may be sparked by academic posters about the Incarceration Medicine Initiative presented at the Social Medicine Consortium in April of this year, and another for the PAEA 2017 Education Forum taking place in October.

Click here to view the Incarceration Medicine Initiative health education booklet distributed to detainees at Cook County Jail in Chicago.

Events

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