Volume 69Number 3

March 2016

THE JOURNAL OF THE SOUTH DAKOTA STATE MEDICAL ASSOCIATION

Volume 69 lNumber 3March 2016

The Journal of the South Dakota State Medical Association

ContentsPresident’s Comments99 Back to Basics – Tim M. Ridgway, MD, FACP

Editorial101 When to Order – Keith Hansen, MD

The Journal103 Preconception Counseling – Kailey Witt, MD; Mark K. Huntington, MD, PhD

109 Diagnostic Yield of Brain Imaging in persons with Parkinson’s – Brian Westerhuis, MSIV; Bassel Salem, MD; Eugenio Matos, MD; Paul A. Thompson, PhD; Joanne Landis, RN; Jerome W. Freeman, MD

113 Treatment of Skin Abscesses: A Review of Wound Packing and Post-Procedural Antibiotics – Mark List, MD; Donella Headlee, MD; Katherine Kondratuk, MS I

Primers in Medicine121 Polymyalgia Rheumatica and Giana Cell Arteritis: A Review Article

– Ukamaka Nwadibia, MD; Eric Larson, MD, FACP; Joseph Fanciullo, MD, FACP

124 Clostridium difficile Associated Diarrhea – Noah Wiedel, MD, MS; Jorge Gilbert, MD; Brett Baloun, MD; Chelsea Nelson, CNP

Pharmacology Focus128 Emerging Evidence of Corticosteroids in Community-Acquired Pneumonia

– Claire Larson; Tadd Hellwig, PharmD, BCPS

Special Features130 Extenuating Circumstances: The Calling – Jacquelyn Gunnarson

132 Board News – Margaret B. Hansen, PA-C, MPAS

134 Quality Focus: National Colorectal Cancer Initiative – Stephan D. Schroeder, MD

137 Patient Education: When to Get Help for a Headache – Richard P. Holm, MD

Member News139 For Your Benefit: Get Involved in the SDSMA

Save the Date: SDSMA 2016 Annual Leadership Conference is June 3

140 The Issue Is…Bipartisan Bill Would Expand Telemedicine

Legal Brief Highlight: Restrictive Covenants

141 Avoid Meaningful Use Penalties

2016 SDSMA Annual Conference Sponsorship and Advertising Opportunities

For the Record142 CME Events

Advertisers In This Issue143 Physician Directory

144 Classified Ads

Office of PublicationPO Box 74062600 W. 49th Street, Suite 200Sioux Falls, SD 57117-7406605.336.1965Fax 605.274.3274www.sdsma.org

EditorKeith Hansen, MD

SDSMA PresidentTim M. Ridgway, MD

Chief Executive OfficerBarbara A. Smith

SDSMA Vice PresidentMark East, MS

Staff Editor Elizabeth Reiss, MS–ereiss@sdsma.org, 605.336.1965

Advertising RepresentativeElizabeth Reiss, MS–ereiss@sdsma.org, 605.336.1965

South Dakota Medicine(ISSN 0038-3317)Published 12 times per year with one special issue in the spring by the South Dakota State Medical Association.

Subscription price: $50 per year domestic$65 per year foreign, $8.95 for single copy

Periodicals postage paid at Sioux Falls,South Dakota and additional mailing offices.

Postmaster: Send address changes toSouth Dakota Medicine PO Box 7406 Sioux Falls, SD 57117-7406

SDSMA Home Page: www.sdsma.org

AMA Home Page: www.ama-assn.org

Printer:The Ovid Bell Press, Inc.P.O. Box 370Fulton, Missouri 65251-0370

Cover photo by Tony Gorder

99March 2016

President’s Comments

Back to Basics By Tim M . R i d gwa y, MD , FACP

SDSMA P r e s i d e n t

Being a physician in 2016 is not for the faint of heart. Thepractice of medicine has become extraordinarily complicated. Health care reform, navigating the electronic

medical record, dealing with increasing regulation, and complicated coding with ICD-10 are just a few of the challengeswe have. These and other issues physicians face tend to takeaway from their personal fulfillment. How many of us enteredmedical school with the goal of practicing medicine in the present environment? Everywhere we turn, we are hearing about theincreasing numbers of our profession suffering from burnout.Richard Gunderman, in an excellent editorial, suggests the solution does not lie in incentivizing physicians with money orrestructuring systems to minimize stress on physicians, but ratherfinding earnest professional fulfillment.1 He references the workof noted psychologist Frederick Herzberg, who argued there is little gain in trying to reduce our “dissatisfiers,” such as reducingall the regulations, increasing compensation, etc. In essence,reducing one’s dissatisfaction does little to improve one’s sense offulfillment or quality of work. Gunderman goes on to say oneneeds to focus less on reducing stress and more on promotingwhat is best in us: compassion, courage, and wisdom.

The medical literature in recent years has placed increasedattention to the basic skills of the physician. How many timeshave we all heard “Listen to your patients. They will tell youwhat is wrong?” In JAMA Internal Medicine, a recent series ofmonthly articles emphasizing the “teachable moment” can befound. One such submission described a middle-aged womanwho presented to the emergency room with severe ankle pain,malaise, and a rash.2 Extensive lab tests, imaging, and whole-body scintigraphy were all normal. She was prescribed pain medications and antidepressants. After more than $40,000 wasspent on the medical work-up, a further dietary history wasobtained and a diagnosis was then made of scurvy–a diagnosiswhich could have been made with a good history, physical examination, and a serum vitamin C level. With increasingtechnological advancement, clinicians have become more andmore reliant on laboratory tests, imaging, and other high-techmodalities. Yet, data suggests this increased reliance on imagingis not associated with better outcomes, but certainly increasedcosts. The value of the history and physical examination is gaining increasing attention in the present cost containmentand outcomes based environment. The social history, somethingwe many times overlook, also has been shown to be increasinglyimportant (a discussion of the social determinants of health is

beyond the scope of this editorial).3

So what, you may ask, does this have to do with professional fulfillment? A few years ago, a middle aged woman was referredto me because of a concern she had a gastrointestinal cancer. Shehad been losing weight, had no appetite, and had abnormalabdominal imaging. The findings on imaging proved to be a normal variant, and she had an appropriate investigation prior toseeing me. I sat down and spoke with the patient and her daugh-ter, and asked if there had been any substantial changes in herlife, perhaps anything occurring socially which could be affectingher. There were no answers. Approximately two hours later, Ireceived a call from the patient’s daughter, explaining that onthe drive home her mother tearfully opened up about the yearsof abuse she had been suffering at the hands of her husband. Thedaughter profusely thanked me for being the vehicle to allow hermother to open up, and explained how she was going to work ongetting appropriate help for her mother. That day was very ful-filling for me, and reminded me of why I enjoy the practice ofmedicine. I did not make any “unusual” diagnosis, and did notperform some state of the art, technically challenging procedure.I simply would like to think I made a positive difference in thisperson’s life. My point is this: We often can get caught up in theday to day grind – see patients, order tests, make referrals, make diagnoses, and move on. We can complain bitterly about all theregulations and impersonal nature of medicine. Some of this isbeyond our control. But in the end, we still have the skill andacumen to make a difference in people’s lives. To me, that is fulfillment! Let’s all devote ourselves to a reemphasis on theimportance of taking a good history, doing a focused but complete physical examination, and above all demonstrate kindness. “Let us not forget these fundamental resources of ourprofession – the power of our hands, our voices, and our rationalthought – for these are free but priceless, so if value is the ratio ofcost to worth, theirs is infinite.”4 Let us refocus our work withthis principle in mind, and perhaps we can achieve more fulfillment is this wonderful profession in which we work.

REFERENCES1. Gunderman, R. The root of Physician Burnout. The Atlantic. Aug, 2012.2. Ziki M et al. The value of the history and physical examination – sailing through

with modern tools. JAMA Intern Med. 2015;175(12):1901-2.3. Srivastava R. Complicated lives – taking the social history. N Engl J Med.

2011;365(7):587-9.4. Humikowski C. For what it’s worth. 2015;313(8):799-800.

“Each morning we are born again. What we do today is what matters most – Buddha

101March 2016

In this month’s issue of South Dakota Medicine, we havea number of very interesting manuscripts. Dr. Freemanet al. discuss the utility of performing imaging in

patients with a diagnosis of a chronic neurological disease– Parkinson’s. They found that the frequency of discovering clinically significant information with imagingin Parkinson’s disease was low and that it remains a clinical diagnosis. In their series, the authors did note ahigh incidence of vascular disease, in fact one patient hadan acute stroke. It is important to remember that the history and physical examination remain the cornerstoneof diagnosis, and that laboratory tests simply assist thephysician and are not meant to stand on their own. In thismanuscript these patients had CNS imaging after a thorough neurological evaluation by a trained neurologistwho diagnosed them with Parkinson’s disease. This articleelegantly raises the question of when to perform a diagnostictest in a patient with clinical evidence of a chronic, progressive disease. This article also highlights the importance of the clinician being familiar with and interpreting the literature about the validity of a new test.

1

Also in this issue, Huntington et al. discuss the importanceof preconception counseling of the woman who is plan-ning to become pregnant. This is a unique opportunity toevaluate the patient’s past medical and surgical history,substance use/abuse, medication use and family history. Inthis manuscript, the authors outline a thoughtful approachto these patients and the importance of a thorough medical evaluation to reduce the risk for the mother andinfant. Preconception counseling also allows one theopportunity to review the family history for potentialinherited illnesses as well as offer carrier screening for highrisk genetic illnesses. The American College ofObstetricians and Gynecologists (ACOG) have notedthat screening to determine carrier status for cystic fibrosis should be offered to all non-hispanic white individuals who are attempting pregnancy, since 2001.

Recently this recommendation has been upgraded toinclude screening for all couples who are attempting pregnancy, but especially in those of non-hispanic ancestory. ACOG and the American College of MedicalGenetics suggest screening for other diseases based onancestory/ethnicity.

2,3

This issue also includes a manuscript on the managementof skin abscesses by List et al. and two Primers in Medicinereview articles on polymyalgia and Clostridium difficile.These are three interesting articles with up-to-date recommendations. We also have a wonderful ExtenuatingCircumstances piece on Fr. Ed Anderson and his journeyfrom anesthesiology to the priesthood. I hope you enjoythis thought-provoking issue of South Dakota Medicine.

Editorial

When to Order? B y K e i t h Han s e n , MD

Ed i t o r, S o u t h D a k o t a M e d i c i n e

REFERENCES1. Jaeschke R, Guyatt G, Sackett DL, for evidence-based medicine working group.

Users’ guide to the medical literature: III. How to use an article about a diagnostictest. A. Are the results of the study valid? JAMA. 1994:271;389-91.

2. American College of Obstetricians and Gynecologists Committee on Genetics.ACOG Committee Opinion No. 486: Update on carrier screening for cystic fibrosis.Obstet Gynecol. 2011 Apr;117(4):1028-31.

3. Grody WW, Cutting GR, Klinger KW, Richards CS, Watson MS, Desnick RJ,Subcommittee on Cystic Fibrosis Screening, Accreditation of Genetic ServicesCommittee, ACMG. American College of Medical Genetics. Laboratory standardsand guidelines for population-based cystic fibrosis carrier screening. Genet Med.2001 Mar-Apr;3(2):149-54.

IntroductionPreconception counseling (PCC) is a time whereproviders identify and modify risk factors of reproductiveage women to improve health and birth outcomes. Thegoal is to ensure that women are as healthy as possibleprior to conception. During this time, providers shouldaddress social, behavioral, environmental, and medicalrisks to a woman’s health and pregnancy outcome andmake recommendations to reduce these risks.1-3

Preconception intervention is more important than pre-natal intervention; important fetal development happensprior the woman’s first prenatal visit.2 Maternal risk factorsare associated with preterm birth, spontaneous abortion,stillbirth, fetal death, sudden infant death syndrome, lowbirthweight, fetal growth restriction, fetal alcohol disor-ders, and neural tube defects.4

The American College of Obstetricians and Gynecologists,American Academy of Pediatrics, American College ofNurse Midwives, and March of Dimes all promote PCC asa way to enhance maternal and infant outcomes. In 2006,the Centers for Disease Control and Prevention (CDC)released 10 recommendations to improve preconceptionhealth and health care for women in the U.S. One ofthese recommendations was to provide risk assessmentand educational and health promotion counseling during

primary care visits for all women of reproductive age,regardless of desire to become pregnant.1 This is importantas nearly 50 percent of pregnancies in the U.S. are unintended.5

Studies have shown that only approximately one-third ofwomen receive PCC. The lowest levels of receiving PCCwere in women whose pregnancy was unintended, thosewho had no health insurance prior to pregnancy, wereunmarried, ages less than 20 years, and those who had lessthan 12 years of education. PCC is particularly importantin primary care as a study found that women with highertrust in their providers are more likely to discuss healthconcerns in relation to their reproductive health. Anotherstudy found that primary care physicians and obstetrician/gynecologists were preferred sources of PCC.1

Preconception Care PromotionDuring a visit for health maintenance exam is always agood time to discuss preconception health but otheropportunities exist as well. Such visits might include avisit for premarital exam and testing, contraception counseling, after a negative pregnancy test, and evaluation for sexually transmitted diseases or vaginalinfection. Other ways to aid in preconception care includepreconception care checklists, patient brochures andhandouts, and waiting room posters.6

103March 2016

Journal

Preconception Counseling By Ka i l e y Wi t t , MD ; and Ma rk K . Hun t i n g t on , MD , PhD

AbstractPreconception counseling is a way to discuss optimizing reproductive age women’s health and chronic medicalissues to facilitate the healthiest pregnancy possible. Preconception counseling is an important piece of care forreproductive aged women especially as nearly 50 percent of pregnancies in the U.S. are unplanned and important fetal development has already taken place prior to the initial obstetrics visit. Many opportunities aremissed to provide this counseling; only approximately one-third of women receive it. Visits to primary care arethe ideal time for this to occur. In this paper, topics to discuss will be presented along with some guides to optimizing chronic medical problems to improve pregnancy outcomes.

Components of Preconception CareReproductive Life PlanThe risk of infertility, fetal aneuploidy, miscarriage, gestational diabetes, preeclampsia, and still birth allincrease as maternal age increases. These risks should bediscussed with women as they contemplate having children or delaying childbirth until later for career purposes. If thinking about delaying childbirth the risk-benefits should be discussed including the increasedrisks associated with increased maternal age.Contraception should be discussed if they are not intending to have children immediately.7,8 Preconceptionhealth and women’s health can be improved by reducingunintended pregnancy and reducing risky behaviors.2

Medical HistoryA thorough review of a woman’s medical history, familyhistory and medications should be performed, along withreview of chronic diseases to make sure they are optimallycontrolled with nonteratogenic medications prior to conception.2

Pregestational diabetes increases riskof miscarriage, congenital fetal anomalies, and perinatal death (Table1). Glucose is teratogenic at high lev-els. Glycemic control in the firsttrimester is essential as this is whenorganogenesis takes place. Ideally,hemoglobin A1c levels prior to conception should approach levels inpatients without diabetes (less than7). Hyperglycemia and hypoglycemiaawareness are decreased in pregnancy.There are increased rates of diabeticketoacidosis and progression of diabetic retinopathy and nephropathy.8

Chronic hypertension in pregnancy isassociated with higher rates of complications (Table 1). The risk ofsuperimposed preeclampsia is 25 per-cent in all women with hypertension.It is important to have good controlof blood pressure with nonteratogenicmedications. Treating mild hyperten-sion has not shown improvements in perinatal outcomes but treatingsevere hypertension (systolic greaterthan or equal to 180 mm Hg or

diastolic greater than or equal to 110 mm Hg) improvespregnancy outcomes.8,9

Thyroid disease also increases complications (Table 1). Inthe first trimester, hypothyroidism is associated with cognitive impairment in children. When treated adequately before pregnancy and those treated early inpregnancy have no increased risk of complications. Goalthyroid stimulating hormone levels vary with trimester:0.1 to 2.5 mU/L in first trimester, 0.2 to 3.0 mU/L in second trimester, and 0.3 to 3.0 mU/L in the finaltrimester. Hypothyroidism affects 2.5 percent of womenof reproductive age. Euthyroidism should be achievedprior to pregnancy. However, only women with risk factorsand symptoms of thyroid disease should be screened.8

Seizure disorders are the most common neurologic diseasein pregnant women. During pregnancy, about one-third ofwomen with a seizure disorder will experience more frequent seizures. Both the disease itself and the medications to treat them can affect the pregnancy

104

Journal

Information from references 2, 8, and 10.

Medical Problem Risks Interventions Diabetes Miscarriage, congenital fetal

anomalies, perinatal death. Optimize A1c prior to conception.

Hypertension Preterm birth, placental abruption, intrauterine growth restriction, preeclampsia, fetal death.

Good control with nonteratogenic medications Avoid ACE inhibitors, ARBs and atenolol.

Hypothyroidism Preterm birth, low birth weight, placental abruption, fetal death.

Medication dosages usually increases by 4-6 weeks of gestation.

Hyperthyroidism Significant maternal and neonatal morbidity.

Propylthiouracil preferred in first trimester while methimazole is preferred in second and third trimesters.

Seizure Disorder Miscarriage, low birth weight, developmental disabilities, microcephaly, hemorrhagic disease, and congenital anomalies.

Monotherapy at the lowest dose possible should be used when able. Supplement with 4mg folic acid daily.

Overweight Diabetes, gestational diabetes, and hypertension.

Achieve healthy weight prior to conception, limit weight gain during pregnancy.

Underweight Preterm birth, low birth weight, and gastroschisis.

Obtain ideal weight prior to pregnancy.

Psychiatric Illness Maternal suffering can lead to poor compliance with prenatal care, poor nutrition, substance abuse, or disturbed relationship between mother and infant.

Women on medication with no or mild symptoms can be considered for a taper and discontinuation. Discontinuation of medication not advised for women with severe recurrent depressive disorders, psychosis, bipolar illness, psychiatric comorbidity requiring medication, or history of suicidal ideation.

Table 1. Chronic Medical Conditions, Risks, and Preconception Interventions

105March 2016

Journal

adversely. Seizure disorders are associated with a numberof risks (Table 1). Congenital anomalies are more common with seizure disorders whether or not the mother is taking medications. With this being said it isvery important to try and control the disorder with theleast teratogenic medications possible.8

Some authorities recommend screening for depression,anxiety, domestic violence, and major psychosocial stressors. The risks of anxiety and depression should bediscussed as well as counseling on treatment options during pregnancy (Table 1).2,14

Family HistoryA woman’s family history should be reviewed to screen forhistory of congenital anomalies or genetic disorders inboth the mother and the father’s families. Consider referral to genetic counseling when risk factors are present.2 Some heritable conditions have strong association with the individual’s ethnic background, andcarrier screening may be offered (Table 2).

MedicationsCurrent medication use should be reviewed prior to pregnancy. This should include all medications includingany over the counter medications, supplements, or vitamins the woman may be taking. Discontinuing unnecessary medications or finding safe alternatives isimportant to accomplish prior to conception.2,8

Nutrition and Weight Women should be counseled on proper diet includingfoods to avoid while pregnant. Folic acid supplementation(400 to 800 mcg daily) and intake of folate fortified foodscan reduce risk of neural tube defects. The neural tubecloses between 18 and 26 days after conception so supplementation should be started prior to attemptingconception.

A healthy prepregnancy weight (ideal BMI is 19.8 to26.0) through exercise and nutrition should be encouraged. Overweight or obese women are at increasedrisk of diabetes, gestational diabetes, and hypertension.These can be associated with macrosomia, shoulder dystocia, operative delivery, congenital anomalies,intrauterine growth restriction, spontaneous abortion,stillbirth, preeclampsia, and eclampsia. Interventionsshould be taken to help women get to a normal weightprior to pregnancy. A review found that out of five commercial diets, Weight Watchers was least costly, andwomen maintained a 3.2 percent weight loss after twoyears.

On the other hand, low prepregnancy weight is associatedwith preterm birth, low birth weight, and a higher rate ofgastroschisis. It is also associated with nutrient deficiencies,osteoporosis, amenorrhea, infertility, and maternalarrhythmias.8,10

Substance AbuseWomen should be screened for alcohol, tobacco, anddrug use. Abstinence from alcohol and illicit drugsshould be encouraged. A safe level of alcohol intakehas not been established. In a national survey in theU.S., 87 percent of women who drank alcohol beforepregnancy abstained during pregnancy, 6.6 percentreduced their alcohol intake, and about 6.4 percentreported no reduction. Preconception counseling hasbeen shown to lead to an increased rate of cessation ofdrinking prior to pregnancy.1 Fetal alcohol spectrumdisorders can manifest with different severities. Noexact dose-response relationship has been establishedbetween the amount of consumption and the severityof the complications to the infant.11

Smoking cessation should be achieved prior to conception. Smoking and secondhand smoke exposureincreases the risk of infertility, placental abruption,preterm premature rupture of membranes, and placentaprevia.12

Infections and ImmunizationInclusion of screening for periodontal, urogenital, and sexually transmitted infections as indicated and updatingimmunizations is beneficial, as is counseling about prevention of TORCH [toxoplasmosis, other (syphilis,varicella-zoster, parvovirus B19), rubella, cytomegalovirus,herpes ] infections.

Infectious diseases that should be screened for include

Ethnic Background Disease Screening Non-hispanic white Cystic fibrosis Eastern European (Ashkinazi) Jewish Tay-Sachs disese

Canavan disease Familial dysautonomia Cystic fibrosis Mucolipidosis IV* Niemann-Pick disease type A* Fanconi anemia group C* Bloom syndrome* Gaucher disease*

*offered based on individual family history African, Mediterranean, Southeast Asian Thalassemias

Sickle cell disease

Table 2. Carrier Screening Tests and Populations

106

chlamydia, gonorrhea, herpes simplex virus, syphilis, HIV,and tuberculosis according to standard guidelines. Ifchlamydia or gonorrhea is treated during pregnancy, fol-low up testing for resolution needs to be performed.

Immunizations that should be performed include hepatitisB, rubella, varicella, tetanus, diphtheria, pertussis, humanpapillomavirus, and influenza vaccines as needed. Some ofthese vaccines should be administered during pregnancyand others should be given at least three months prior toconception.8,13 A summary of immunization practices inpregnancy is shown in Table 3.

Environmental ExposuresIdentification of potentially toxic exposures by discussingthe woman’s work, hobbies, home environment, and petscan help identify potential toxic exposures including mercury, lead, pesticides, and endocrine disrupting chemicals. If the woman has cats inher life, she needs to be educated onavoiding cleaning up the kitty litteras this poses a risk of toxoplasmosis.2,15

Physical ExamThe physical examination shouldfocus on assessment of periodontal,thyroid, heart, lungs, abdominal, andpelvic exams. The physical exam canhelp detect conditions that can affectmaternal health and pregnancy outcomes, as noted in the sectionsabove.2

Special Populations in South Dakota:RefugeesRefugee women may experience barriers to accessing health care,including preconception care.Research has shown that foreign-bornwomen have better birth outcomesthan U.S.-born women. On the otherhand, refugee women have worsebirth outcomes than U.S.-bornwomen. Refugee women have oftenexperienced stressful conditions intheir home country and spent time inrefugee camps. They face many barri-ers including social, language, andcultural barriers that may affect theirpreconception health. They havelower overall health if they did not

have access to health care in their home country.Immigrants from certain areas of the world are more at riskof tuberculosis (see Box) and hepatitis B infections.16,17

Preconception counseling can be integrated into refugeeentrance examinations as this may be one of the onlyhealth care visits these women have before conception.Routine infectious disease screening and updating immu-nizations should be done at this time as well.Preconception counseling should then contain the samecomponents as with non-refugee patients. In addition,preconception care messages can be provided at non-health care settings such as at English classes.

ConclusionsPreconception counseling can help ensure that women areas healthy as possible prior to conception. This can helpreduce maternal and fetal complications. Providers should

Vaccine BEFORE pregnancy DURING pregnancy AFTER pregnancy Type

Hepatitis A Yes, if indicated Yes, if indicated Yes, if indicated Inactivated

Hepatitis B Yes, if indicated Yes, if indicated Yes, if indicated Inactivated

Human Papillomavirus

(HPV)

Yes, if indicated,

through 26 years of

age

No, under study

Yes, if indicated,

through 26 years of

age

Inactivated

Influenza IIV Yes Yes Yes Inactivated

Influenza LAIV

Yes, if less than 50

years of age and

healthy; avoid

conception for 4

weeks

No

Yes, if less than 50

years of age and

healthy; avoid

conception for 4

weeks

Live

MMR

Yes, if indicated,

avoid conception for

4 weeks

No

Yes, if indicated,

give immediately

postpartum if

susceptible to

rubella

Live

Meningococcal:

• polysaccharide

• conjugate

If indicated If indicated If indicated

Inactivated

Inactivated

Pneumococcal

Polysaccharide If indicated If indicated If indicated Inactivated

Tdap Yes, if indicated

Yes, vaccinate

during each

pregnancy ideally

between 27 and 36

weeks of gestation

Yes, immediately

postpartum, if not

received previously

Toxoid/

inactivated

Tetanus/Diphtheria Td Yes, if indicated Yes, if indicated,

Tdap preferred Yes, if indicated Toxoid

Varicella

Yes, if indicated,

avoid conception for

4 weeks

No

Yes, if indicated,

give immediately

postpartum if

susceptible

Live

Adapted from Centers for Disease Control and Prevention, http://www.cdc.gov/vaccines/pubs/downloads/f_preg_chart.pdf.

Table 3. Vaccine use in pregnancy

Journal

107March 2016

Journal

Box. Tuberculosis in Pregnancy

Active tuberculosis in pregnant and postpartum women from high-burden countries is found in greater than 60 cases per 100,000per year and in less than 20 cases per 100,000 in low-burden countries. Latent tuberculosis in the U.S. is 4.2 percent and is up to 10times higher in foreign-born Americans. Tuberculosis increases mortality during pregnancy and postpartum period. There is increasedrisk of complications and miscarriages in pregnant women with pulmonary or extrapulmonary tuberculosis. Tuberculosis symptomscan be masked by pregnancy. CDC recommends screening for high risk populations, employing the tuberculin skin test (the bloodtest has not been validated in pregnancy).

Treatment for active tuberculosis during pregnancy is very similar to treatment when not pregnant. INH, rifampin (RIF), and ethambutol (EMB) are all FDA category C. Pregnant women on INH should take pyridoxine to prevent peripheral neuropathy. Someexperts recommend vitamin K for infants born to mothers taking RIF due to potential association with hemorrhagic disease of newborns.

Treating latent tuberculosis in pregnancy is controversial. CDC recommends delaying treatment of latent tuberculosis until two tothree months postpartum unless there has been recent contact with known tuberculosis. WHO does not comment on whether latenttuberculosis should be treated during pregnancy. Women with latent tuberculosis have a 10 percent lifetime risk of reactivation.

In a small study in South Africa, vertical transmission occurred at a rate of 16 percent. Infant mortality varies greatly between studies. Studies are also inconsistent on adverse effects to the infant. There was no difference in outcomes between infants born tomothers treated for tuberculosis during pregnancy and those without tuberculosis in the U.S. Infants born to Indian mothers with pulmonary or extrapulmonary tuberculosis other than lymphadenitis had increased risk of fetal distress, low birth weight, prematurity, and infant mortality.

Reference from 17.

address past medical history, work to optimize chronicmedical problems, review medications, discuss nutrition,update immunizations and screen for infectious diseases.As half of pregnancies are unintended, it is important toincorporate preconception counseling into visits for otherreasons for reproductive age women.

It is especially valuable to integrate preconception

counseling into refugee physicals as this is often the onlyencounter with health care these women may have priorto conception. It is important to screen for tuberculosisand complete treatment prior to conception if possible, asthere is controversy over treatment of latent tuberculosisduring pregnancy. There is also risk of complications tothe infant and risk of vertical transmission if the motherhas tuberculosis.

REFERENCES1. Willams L, Zapata L, D’Angelo D, et al. Associations between preconception

counseling and maternal behaviors before and during pregnancy. Maternal ChildHealth Journal. 2012;16:1854-61.

2. Sackey J. The preconception office visit. Uptodate. 2014. 3. Ruhl C, Moran B. The clinical content of preconception care: preconception care

for special populations. American Journal of Obstetrics & Gynecology. 2008Dec;199(6 Suppl 2):S384-8.

4. Robbins C, Zapata L, Farr S, et al. Core state preconception health indicators-pregnancy risk assessment monitoring system and behavioral risk factor surveillance system, 2009. MMWR. 2014;63(3):1-62.

5. Finer LB, Zolna MR. Unintended pregnancy in the United States: incidence anddisparities, 2006. Contraception. 2011;84(5):478-85.

6. Mazza D, Chapman A, Michie S. Barriers to the implementation of preconceptioncare guidelines as perceived by general practitioners: a qualitative study. BMCHealth Serv Res. 2013;12:36.

7. Leuzzi RA, Scoles KS. Preconception counseling for the primary care physician.Med Clin North Am. 1996;80(2):337-74.

8. Farahi N, Zolotor A. Recommendations for preconception counseling and care.American Family Physician. 2013:88(8):499-506.

9. Dunlop AL, Jack BW, et al. The clinical content of preconception care: womenwith chronic medical conditions. American Journal of Obstetrics and Gynecology.2008;199(6 Suppl 2): S310-27.

10. American College of Obstetricians and Gynecologists. Good health before preg-nancy: preconception care. Retrieved from www.acog.org/-/media/For-Patients.

11. Chang, G. Alcohol intake and pregnancy. Uptodate. May 2014. 12. Rodriguez-Thompson, D. Cigarette smoking and pregnancy. Uptodate. February

2015. 13. Barss, V. Immunizations during pregnancy. Uptodate. April 2015. 14. Yonker KA, Wisner KL, et al. The management of depression during pregnancy: a

report from the American Psychiatric Association and the American College ofObstetricians and Gynecologists. General Hospital Psychiatry. 2009;31(5):403-13.

15. McDiarmid MA, Gardiner PM, Jack BW. The clinical content of preconceptioncare: environmental exposures. American Journal of Obstetrics and Gynecology.2008;199(6 Suppl 2):S357-61.

16. U.S. Department of Health and Human Services. Centers for Disease Control andPrevention. Preconception clinical care for women special populations. Retrievedfrom www.cdc.gov/preconception/documents/Clinical-Content_WomensSpecialPopFactsheet9.pdf.

17. Gupta, Amita, Mathad, Jyoti. Tuberculosis in pregnant and postpartum women:epidemiology, management, and research gaps. Clinical Infectious Disease. 2012Dec;55(11):1532-49.

18. Whitworth M, Dowswell T. Routine pre-pregnancy health promotion for improvingpregnancy outcomes. Cochrane Database of Systematic Reviews.2009;(4):CD007536.

About the Authors:Kailey Witt, MD, Sioux Falls Family Medicine Residency Program.Mark K. Huntington, MD, PhD, Sioux Falls Family Medicine Residency Program; Department of Family Medicine, University of South Dakota Sanford School of Medicine.

108

109March 2016

Journal

IntroductionBrain imaging is frequently performed in patients withdegenerative neurologic conditions. Scant data exists as tothe yield of brain imaging in patients with features suggesting Parkinson’s disease. In 2013, several of theauthors of this manuscript published a case report of a 48-year-old woman who presented with typicalParkinson’s symptoms and findings. She proved to have alarge, left hemisphere meningioma and when this was surgically resected, her symptoms entirely abated.1 Thisdramatic case has prompted us to systematically look atthe diagnostic value of brain imaging in persons withParkinson’s features.

The diagnosis of Parkinson’s disease is a clinical one.There are no definitive, confirmatory tests. Often thediagnosis is only established, with certainty, based on apatient’s response to medication over time. In the initialstages, the clinician may not be certain whether a patientwill prove to have drug-responsive Parkinson’s disease or acondition less responsive to therapy (so-called“Parkinsonism”). For instance, people with some featuressuggestive of Parkinson’s will ultimately be judged to havesome variant of multiple system atrophy. Some patientswith multiple system atrophy who have the so-called “striatonigral degeneration” may exhibit prominentParkinson’s features.2 Patients with this latter conditiongenerally do not respond dramatically to drug therapy.

Given the lack of diagnostic certainty with Parkinson’sand the fact that persons with Parkinson’s have a lifelongand progressive disease, many clinicians opt to do earlybrain imaging. Magnetic resonance imaging (MRI) orcomputerized axial tomography (CAT) can be used butMRI offers much more diagnostic information. When ourliterature review did not reveal definitive data on the yieldof brain imaging in Parkinson’s, we decided to do a retrospective analysis looking at the results of brain imaging in persons who had Parkinson’s features (i.e.,Parkinson’s disease or some form of Parkinsonism such as

multiple system atrophy). We postulated that brain imaging would often be abnormal, and would have a reasonable yield in terms of demonstrating various findings that might require treatment.

MethodsFor the purposes of this study, all patients seen by an eight-member neurology group within a two-year period (Jan. 12, 2012 through Feb. 12, 2014) were included. Eachpatient was identified by a neurologist as havingParkinson’s features such as tremor, rigidity or gait impair-ment. Some of these patients were seen as initial consultsand others had been followed by a neurologist in the groupover a number of years. A piloted data collection form wasmodified for this study. Each of the authors (excluding thebiostatistician) participated in chart review and data collection. Care was taken to ensure the accuracy of datacompilation. The chart review identified 179 patients whofit the inclusion criteria. Of this number, 135 had brainimaging and 44 did not. Of those who had brain imaging,110 had an MRI and 25 had a CAT scan. Patients wereexcluded from this retrospective study if the records of aninitial evaluation or brain imaging results at another facility were no longer available. Imaging performed within a year prior to the initial diagnosis of Parkinson’sfeatures was included in the study. As this analysis focusedon brain imaging around the time of diagnosis, long termfollow-up was not undertaken. Appropriate institutionalreview board (IRB) approval for this chart review studywas obtained (Sanford 03-13-026).

ResultsThe mean age of our patients at the time of brain imagingwas 69 years. Notably, 99 (63.7 percent) patients hadMRIs that suggested small vessel ischemic disease and 80(47.4 percent) showed diffuse atrophy. While five (8.9percent) showed evidence of a previous stroke, threepatients demonstrated small areas of acute ischemia in themonths leading up to their initial neurologic evaluationfor Parkinson’s. Another patient, suspected of having

Diagnostic Yield of Brain Imaging in Persons with Parkinson’s By B r i a n We s t e r h u i s , MD ; B a s s e l S a l em , MD ; E u g en i o Ma t o s , MD ;

P a u l A . Thomp s on , P hD ; J o a nn e L and i s , RN ; a n d J e r ome W. F r e eman , MD

Parkinson’s, had a contemporaneous MRI that revealed asmall acute ischemic focus in the left cerebellar hemisphere, in addition to diffuse small vessel ischemicchanges and evidence of remote lacunar infarcts. Nopatient, other than our sentinel patient with meningioma,demonstrated a new tumor. The MRI of one patient witha known acoustic neuroma documented the lesion to beunchanged. Our finding of a single new brain tumor in thestudy group is comparable to a previously reported seriesthat found an incidence of tumor in patients withParkinson’s features of 0.3 percent.3

While many of our patients’ scans thus showed abnormal-ities, these findings rarely resulted in altered treatment. Inthree patients, antiplatelet therapy was started or adjustedbased on imaging findings. The brain imaging in onepatient led to subsequent magnetic resonance angiography(MRA) of the neck and brain vasculature and one patientreceived carotid stenting based on further investigation.Certainly, the majority of patients with abnormal imaginghad evidence for small vessel ischemia or brain atrophy,both of which are fairly common, age-related changes.

ConclusionThe results of this study do not provide definitive evidence for the utility of brain imaging in persons presenting with Parkinson’s symptoms and features.Indeed, one could argue that based on the relativelybenign findings of brain imaging in this series, a cliniciancould opt for empiric treatment or observation, ratherthan proceeding to brain imaging. However, we urge caution in foregoing routine brain imaging for persons presenting with Parkinson’s symptoms. In our series, thereis a high incidence of vascular disease. The 8.9 percentincidence of prior stroke and 63.7 percent patients withsmall vessel ischemia are notable findings. As described,one patient who was imaged to evaluate his Parkinson’ssymptoms also proved to have a small acute stroke.Certainly, the MRI is much more sensitive than the CATscan at revealing both acute ischemia and the extent ofsmall vessel ischemic change. Vigorous secondary prevention measures for stroke seem warranted in allpatients whose brain imaging reveals ischemic changes.Limited literature exists supporting the benefit of treatingasymptomatic MRI or CAT ischemic findings. The argument has been advanced that silent lacunar infarctsand chronic small vessel ischemic disease frequently coexist and have been associated with an increased risk ofstroke and cognitive decline.4 In our cohort of patients,

the degree to which follow-up of vascular risk factors wasaccomplished was not assessed. Also, a matched controlgroup to compare MRI findings with our Parkinsonpatients was not incorporated into this study.

When considering the appropriateness of early brainimaging in Parkinson’s, the clinician must ponder theimplications of a slowly progressive neurologic condition.If brain imaging is not performed initially, the clinicaldesire for such testing (not to mention patient and familypressures) may inevitably increase as a patient continuesto demonstrate progression of symptoms. In a disease likeParkinson’s, in which there is no definitive way for diagnostic verification, due diligence may warrant earlybrain imaging to exclude significant structural andischemic abnormalities. And arguably, the incidence ofcerebral vascular disease in our series, coupled with theknown utility of vigorous secondary stroke preventionmeasures, provides impetus for MRI imaging in personswith Parkinson’s symptoms.

Journal

110

REFERENCES

About the Authors:Brian Westerhuis, MD, Department of Surgery, University of Michigan. Bassel Salem, MD, Department of Neurosciences, University of South Dakota SanfordSchool of Medicine; Sanford Clinic Neurology, Sioux Falls.Eugenio Matos, MD, Department of Neurosciences, University of South Dakota SanfordSchool of Medicine; Sanford Clinic Neurology, Sioux Falls.Paul A. Thompson, PhD, Sanford Health, Sioux Falls. Joanne Landis, RN, Sanford Clinic Neurology, Sioux Falls. Jerome W. Freeman, MD, Department of Neurosciences, University of South DakotaSanford School of Medicine; Sanford Clinic Neurology, Sioux Falls.

1 Freeman J, Westerhuis B, Asfora W, Free T, Salem B. Meningioma mimickingParkinson’s disease: a case report and analysis. South Dakota Medicine.2013;66(4):101-3.

2 Fanciulli A, Wenning, GK. Multiple system atrophy. New England Journal ofMedicine. 2015;372(3):249-63.

3 Kraus JK, Paduch T, Mundinger F, Seeger W. Parkinsonism and rest tremor sec-ondary to supratentorial tumors sparing the basal ganglia. Acta Neurchir (Wien).1995;133 (1-2):22-9.

4 Norrving, B. Lucunar infarcts: no black holes in the brain are benign. PracticalNeurology. 2008;8:222-8.

112

113March 2016

Journal

Introduction

A skin abscess is a localized collection of pus that generallydevelops in response to infection or to the presence ofother foreign materials under the skin. Abscesses are acommon source of significant pain and morbidity forpatients encountered by physicians and advance practiceprofessionals (APPs) across the nation. The increase in

incidence of skin and soft tissue infections, includingabscesses, has been well-documented. In 1993, 1.2 millioncases were diagnosed in the U.S., a number that increasedto 3.4 million in 2005.1 This rise in cases of skin and softtissue infections has also overlapped the emergence ofcommunity-acquired methicillin-resistant Staphylococcusaureus (CA-MRSA). Several studies over the past decade

Treatment of Skin Abscesses: A Review of WoundPacking and Post-Procedural Antibiotics By Ma r k L i s t , MD ; Don e l l a H e a d l e e , MD ; a n d

K a t h e r i n e Kond r a t u k , MS I

AbstractObjective: Skin abscesses can be a significant source of morbidity and are frequently encountered by physiciansacross the country. Incision and drainage (I&D) remains the standard of care; however, significant variabilityexists in the treatment of abscesses after I&D. Some recent evidence has suggested that routinely performedtreatment modalities may not be beneficial. We examine the available evidence investigating if I&D alone issufficient as the sole management for the treatment of uncomplicated abscesses, specifically focusing on woundpacking and post-procedural antibiotics.

Methods: We reviewed available literature for any published observational or randomized control trials on thetreatment of abscesses via packing and antibiotics. Only recent manuscripts published in the English language and in the past 10 years (2004 through 2014) were included due to the emergence of methicillin-resistant Staphylococcus aureus (MRSA) as one of the leading causative organism of soft tissue infections in thepast decade.

Results: Three randomized control trials (RCT) and one observational study investigated wound packing versusno packing following I&D. None of the studies demonstrated a difference in treatment failure rates, recurrencerates, or need for secondary interventions in non-packed wounds; however, packing groups had more pain. Sixstudies investigated the post-procedural use of antibiotics. The RCTs failed to show decreases in treatment failure rates with antibiotics, but two studies demonstrated a short-term decrease in new lesion formation. Theobservational studies demonstrated mixed results regarding rates of treatment cure with appropriate antibioticselection, specifically in patients with positive wound cultures for MRSA.

Discussion: Regardless of supplemental post-procedural treatment, all studies demonstrate high rates of clinicalcure following I&D. While the number of studies is small, there is data to support the elimination of abscesspacking and routine avoidance of antibiotics post-I&D in an immunocompetent patient; however, antibioticsshould be considered in the presence of high risk features. Due to limited studies and conflicting data, we areunable to make a recommendation in support or opposition of adjunctive post-procedural packing and antibiotics in an immunocompromised patient.

have shown that the most common etiologic agent ofthese infections is now CA-MRSA.2-4

While their incidence has increased in recent years,abscesses are not a new phenomenon, and the primarymeans to achieve clinical cure remains surgical incisionand drainage (I&D). For centuries, physicians have passedalong the Latin phrase ubi pus, ibi evacua translated as“where pus, there evacuate.”5 Even so, practice patternsfor I&D technique are not standardized, and significantvariability exists in the type of incision, use of irrigation,decision to pack the wound, concomitant antibiotic use,anesthetic and pain control, and obtaining wound cultures.6-8 For decades, supplemental post-I&D interven-tions were utilized and taught, often despite limited evidence supporting their use. In this review, we focus onthe available medical literature regarding the use ofwound packing following the procedure and evaluate theneed for antibiotics following I&D. The collection andassessment of pertinent, recent studies will allow physicians and APPs to choose post-procedural care wisely, not only providing the best possible rates of clinical cure, but also decreasing any unnecessary concomitant antibiotic exposure or unnecessary discomfort from packing. Additionally, we hope to assistmedical educators in providing evidence-based medicinefor clinical instruction on this topic. When applicable, wepresent the level of evidence using the Strength ofRecommendation Taxonomy System (Figure 1).9

MethodsLiterature SearchOur search strategy, selection of publications, and thereporting of results for the review were conducted inaccordance with the most recent Preferred ReportingItems for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Randomized control trials andobservational studies on the management of skin abscesseswere acquired through PubMed, MEDLINE and CINAHL

through EBSCOhost. We limited results to the Englishlanguage. All articles were published in a 10-year timeframe from Jan. 1, 2004 through Sept. 25, 2014, ensuringthey were applicable for modern medical practice in theMRSA-era. All publications with medical subject headings (MeSH) and keywords in title, abstract, and full-body text containing “abscess AND packing” and “abscessAND antibiotics AND skin” were investigated. Resultswere then narrowed by author defined inclusion andexclusion guidelines designed for relevance for this systematic review.

Selection and Quality Assessment of ArticlesAll identified papers were critically appraised by theauthors. The inclusion criteria were as follows: studieswith full text available and having practical application tothe management of skin abscesses regarding either packing and/or antibiotic use following I&D. Exclusion

Journal

114

Figure 1. Strength of Recommendation Taxonomy (SORT)

Figure 2. Flow Sheet Representing Database Literature Search and Selection for Articles Regarding Wound Packing

Following Skin Abscess Incision and Drainage

Figure 3. Flow Sheet Representing Database Literature Search and Selection for Articles Regarding Antibiotic

Administration Following Skin Abscess Incision and Drainage.

115March 2016

Journal

criteria were all studies prior to 2004 to eliminate anyresults not applicable to modern MRSA-era, studies comparing I&D techniques other than standard linearincisions, single case reports, and those specificallyfocused on abscess management in non-cutaneous abscesses or in perianal abscesses. Figures 2 and 3 illustratethe search process and selection of articles.

ResultsThree randomized control trials (RCT) and one observational study were selected based on predeterminedselection criteria regarding the use of wound packing following abscess incision and drainage. In 2009,O’Malley et al. produced an emergency department basedRCT reporting results from 48 adults randomized toreceive one-quarter inch non-iodophor-impregnatedgauze packing. Follow ups were scheduled in the ED at 48hours and a phone call between 11 and 14 days. Resultsshowed no difference in treatment failure or need for secondary inventions, but the non-packed group had statistically significant reductions in pain scores andrequired less narcotic medications to control post-procedural pain.3 Another randomized control trialinvolved 57 pediatric patients and similarly showed nostatistically significant differences in need for repeat interventions [5/22 non-packing group (NPG) vs. 3/27packing group (PG)] and had similar low rates of treatment failure and satisfaction scores at one month (96percent NPG vs. 93 percent PG).10 The most recent RCTwas done on 85 pediatric patients, showing no differencesin rates of abscess recurrence (1/42 NPG vs. 1/43 PG).4

The lone non-randomized trial investigated pediatricpatients who had packing placed at the time of the I&D.Researchers then chose to post-operatively remove thepacking from 16 pediatric patients and compared them to19 historical matched controls who had packing left inplace. The group who was packed were more likely torequire post-operative IV pain control (6/19 PG vs. 0/16NPG), hospitalization (11/19 PG vs. 0/16 NPG), followup visits (7/19 PG vs. 0/16 NPG); however, there was noincrease in treatment failure or abscess recurrence (0/19PG vs. 1/16 NPG, p= 0.15).11

The results for antibiotic use following abscess drainageare less uniform in their outcomes. One RCT of 166patients randomized to QID cephalexin vs. placebo founda 90.5 percent cure rate observed in the placebo arm and84.1 percent cure rate in the antibiotic arm (p=0.25).12 Intwo RCT comparing two tablets of Bactrim BID to an

identical regimen of placebo, Schmitz et al. found no statistically significant difference in failure rates betweenthe groups (15/88 treatment vs. 27/102 placebo, absoluterisk reduction (ARR) 9 percent, p= 0.12), as did Duong etal. (failure rate 3/73 treatment vs. 4/76 placebo, ARR 1.2percent). Both of these studies, however, showed anincrease in short-term recurrence or formation of newlesions (10 day: 26.4 percent placebo vs. 12.9 percenttreatment; one month: 28 percent placebo vs. 9 percenttreatment; p=0.02).13-14

In observational trials, one small study of 68 pediatricpatients with MRSA abscesses showed no difference inrates of treatment failure in patients who were appropri-ately treated vs. those given ineffective antibiotics (0/26susceptible antibiotics vs. 4/37 resistant antibiotics; ARR11 percent, p= 0.1).15 Again, a similar result was found ina larger (n=408) observational study in adults (failure rate2/166 susceptible antibiotics vs. 1/242 resistant antibiotics;P=.74).16 However, one retrospective cohort study showedthat treatment of abscess specifically from MRSA withappropriate antibiotics did lead to a statistically significantdecrease in failure rates (16/312 susceptible antibiotics vs.29/219 resistant antibiotics; ARR 8 percent, p= 0.001).17

DiscussionWound PackingWe summarize our clinical recommendations in Figure 4.The treatment of skin abscesses with incision anddrainage alone has a high rate of clinical cure (SORT =A).3,4,10-17 The packing of wounds following incision anddrainage of cutaneous abscesses has historically been amainstay in medical treatment, with its origins datingback to ancient Mesopotamia when oil soaked linens wereused to pack recently drained abscesses. 18 More than 3,000

SORT: KEY RECOMMENDATIONS FOR EVIDENCEPRACTICE RATING

• Incision and drainage alone is often sufficient for the treatment of uncomplicated skin abscesses in Aan immunocompetent patient.

•Wound packing following incision and drainage is Bnot necessary and is usually painful.

•Antibiotics following incision and drainage are Boften not necessary for clinical cure.

•Antibiotics following incision and drainage may Bdecrease recurrence rates of abscesses.

•When antibiotics are prescribed following incision and drainage, medications with MRSA coverage Cshould be selected.

Figure 4. SORT Recommendations

116

Journal

years later, we describe several recent studies which consistently demonstrate that wound packing does notproduce superior outcomes compared to wounds notpacked after I&D. Wound packing following incision anddrainage of abscesses is not necessary and is usuallypainful. (SORT = B).3,4,10-11

Outcomes were not improved by packing, and patientsexperienced more pain than non-packing. However, thestudies are quite small with the largest study containingonly 85 patients. In addition, although the data, whilelimited, is supportive of avoiding packing following incision and drainage, it is difficult to make firm conclusionsfor standardized treatment of skin abscesses for all patientsbased on four studies, only one of which is in adults. Otherstudies have been done also showing no benefit to woundpacking, but these were excluded due to their focus onperianal abscesses and their limited relevance to treatment of other generalized, uncomplicated skinabscesses.19,20 The studies reviewed are by no means uniform in methodology. There was no standard of followup, no uniform exclusion of patient populations, andantibiotics use was not standardized, as one study usedantibiotics randomly based on physician decision at a rateof 43 percent. Additionally, O’Malley et al. limited theirinvestigation to abscesses less than 5 cm in diameter,while the other two made no exclusions based on size: 18percent of all cases in Kessler et al. had abscesses greaterthan 5 cm and Leinwald et al. had very large abscess, withthe mean abscess diameters of 5.7 cm in the packing groupand 4.6 cm in the non-packing group. The non-random-ized trial is less comparable to the others as both controland treatment groups were packed after I&D, but investigators post-operatively removed the packing in thecontrol group. This study resulted in much higher rates ofhospitalization compared to the other studies (of whichone study excluded hospitalized patients), but still showedlow rates of recurrence and need for secondary interventionsafter initial I&D. Although there is great diversity in thesefour studies, the vast differences in the study populationsand methods may make the case for non-packing evenstronger, as they all showed a very high cure rate with lowrates of recurrence and low numbers of secondary interventions needed on follow up. All studies reviewedlist immunocompromised status as an exclusion criterion.To our knowledge, there has been no study investigatingthe use of packing in treatment of abscesses in animmunocompromised patient.

We feel that a recommendation of opposition to packing

is appropriate due to the lack of benefits (no change incure rates, no change in need for secondary interventions)and significant increase in pain caused by wound packing.Additionally, wound packing is still a frequent practice,highlighted in one 2013 study demonstrating a 75 percentpacking rate among surveyed emergency departmentphysicians, residents, and APPs.21 Clearly, large scale studies are needed, but the uniformity of results despitethe diversity of patient characteristics, size of abscess, and need for hospitalization due to severity supports that packing abscesses following incision and drainage is likely unnecessary in an immunocompetent patient.Unfortunately, given the dearth of information availableon packing use in the immunocompromised patient, thereis insufficient evidence to make a recommendation supporting or opposing the use of packing in the immuno-compromised.

Antibiotic TreatmentAntibiotic use after incision and drainage is a controversialtopic, with no clear consensus on whether or not their useimproves outcomes. Yet, they are commonly and routinelyprescribed in clinical practice.6,21,22 We describe two RCTsin which antibiotic administration, specifically 320 mg to1600 mg trimethoprim-sulfamethoxazole twice daily, following I&D demonstrated no statistically significantimprovement over placebo, but may reduce abscess recurrence (SORT = B).13,14 At the time of writing thisreview, a much larger clinical trial (n=1247) investigatingthe treatment of abscesses with placebo or high dosetrimethoprim-sulfamethoxazole remains unpublished, butit has publically released its preliminary data, documentingtreatment failure in 123/630 (19 percent) patients withantibiotics vs. 163/617 (26 percent) patients with placebo.23

Another recent, large clinical trial regarding Clindamycinvs. trimethoprim-sulfamethoxazole did not address theissue of antibiotics versus placebo, but showed a high curerate in both treatment groups and stated, “although incision and drainage alone may be sufficient for treatmentin many cases, there are likely to be subgroups in whichantibiotic therapy is needed. Outcomes in antibiotic-treated patients with abscesses in our relatively low riskpopulation could reflect either similar true efficacies orthe adequacy of incision and drainage alone.”24

For immunocompetent patients with mild, uncomplicatedinfections; there is not enough evidence to support theroutine use of antibiotics following I&D (SORT = B).12-17,25

However, with the number of abscesses treated each yearin the U.S., the absolute risk reductions shown in these

117March 2016

Journal

studies leads to a reduction of treatment failures leading tosecondary interventions that number in the hundreds ofthousands. This does not even include the statistically significant decrease in recurrence rates, which lead toadditional interventions.

Recent guidelines recommend that purulent abscesses beempirically treated with antibiotics when infections aredeemed moderate to severe, recommended stronglyalthough based on “evidence from opinions of respectedauthorities, based on clinical experience, descriptive studies,or reports of expert committees.” These guidelines definemoderate infections as patients with systemic signs ofinfection and define severe infections as those who havefailed incision and drainage plus oral antibiotics or thosewith systemic signs of infection or immunocompromisedpatients.25 In our review, several studies include immuno-compromised patients (diabetics, HIV/AIDs, etc.); however, the results are mixed. Rajendran et al. andPaydar et al. both included immunocompromised patientsand found no benefit to post-procedural antibiotics. Ruheet al. did demonstrate an ineffective antibiotic regimen tobe an independent risk factor for treatment failure in apopulation that included immunocompromised patients;but in sub-group analysis, immunocompromised status wasnot found to be statistically significant between clinical

cure and failure groups. While these studies seem to suggest that immunocompromised status is not a risk factor in treatment failure, we find insufficient evidence tomake a recommendation supporting or opposing the use of post-procedural antibiotics in immunocompromisedpatients.

Another possibility to guide treatment would be to onlytreat high risk cases that were likely to cause treatmentfailure and lead to complications like hospitalization or asecondary intervention. Lee et al. describe a study involving children, in which abscesses larger than 5 cmwere associated with treatment failure; however, a separate study of adults found that size of abscess greaterthan 5 cm or area of cellulitis greater than 5 cm was notassociated with treatment failure. The presence of MRSA,in that study, was associated with an increased risk fortreatment failure.15,26 When antibiotics are chosen, due tothe rise of CA-MRSA as the leading bacterial cause ofabscesses, an antibiotic with MRSA coverage should bechosen as first line therapy (SORT=C).

2-4 The decisionwhen to obtain culture is also somewhat controversial, but newer guidelines suggest obtaining culture for susceptibilities only when choosing to initiate antibiotictherapy following I&D.25

REFERENCES1. Pallin D, Egan J, Pelletier A, et al. Increased US emergency department visits for

skin and soft tissue infections, and changes in antibiotic choices, during the emergence of community associated methicillin-resistant Staphylococcus aureus.Ann Emerg Med. 2008;51:291-8.

2. Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med.2006;355:666-74.

3. O'Malley GF, Dominici P, Giraldo P,et al. Routine packing of simple cutaneousabscesses is painful and probably unnecessary. Acad Emerg Med. 2009May;16(5):470-3.

4. Leinwand M, Downing M, Slater D, et al. Incision and drainage of subcutaneousabscesses without the use of packing. J Pediatr Surg. 2013 Sep;48(9):1962-5.

5. The Necessary Peroxide of Hydrogen. The American Medical Journal. Vol 19.1891 pg 226.

6. Schmitz G, Goodwin T, Singer A, et al. The treatment of cutaneous abscesses:comparison of emergency medicine providers' practice patterns. West J EmergMed. 2013 Feb;14(1):23-8.

7. May L, Harter K, Yadav K, , et al. Practice patterns and management strategies forpurulent skin and soft-tissue infections in an urban academic ED. Am J EmergMed. 2012 Feb;30(2):302-10.

8. LoVecchio F, Perera N, Casanova L, et al.Board-certified emergency physicians'treatment of skin and soft tissue infections in the community-acquired methicillin-resistant Staphylococcus aureus era. Am J Emerg Med. 2009 Jan;27(1):68-70.

9. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy(SORT): a patient-centered approach to grading evidence in the medical literature.Am Fam Physician. 2004;69(3):548-56.

10. Kessler DO, Krantz A, Mojica M. Randomized trial comparing wound packing to nowound packing following incision and drainage of superficial skin abscesses inthe pediatric emergency department. Pediatr Emerg Care. 2012 Jun;28(6):514-7.

11. Koehler MB and Nakayama DK. Treatment of cutaneous abscesses without postoperative dressing changes. AORN J. 2009 Oct;90(4):569-74.

12. Rajendran PM, Young D, Maurer T, et al. Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in apopulation at risk for community-acquired methicillin-resistant Staphylococcusaureus infection. Antimicrob Agents Chemother. 2007 Nov;51(11):4044-8.

13. Schmitz GR, Bruner D, Pitotti R, et al. Randomized controlled trial of trimethoprimsulfamethoxazole for uncomplicated skin abscesses in patients atrisk for community-associated methicillin-resistant Staphylococcus aureus infection. Ann Emerg Med. 2010 Sep;56(3):283-7.

14. Duong M, Markwell S, Peter J, et al. Randomized, controlled trial of antibiotics inthe management of community-acquired skin abscesses in the pediatric patient.Ann Emerg Med. 2010 May;55(5):401-7.

15. Lee MC, Rios AM, Aten MF, et al. Management and outcome of children with skinand soft tissue abscesses caused by community-acquired methicillin-resistantStaphylococcus aureus. Pediatr Infect Dis J. 2004;23:123-7.

16. Paydar KZ, Hansen SL, Charlebois ED, et al. Inappropriate antibiotic use in soft tissue infections. Arch Surg. 2006; 141:850-4. Discussion 855-6.

17. Ruhe JJ, Smith N, Bradsher RW, et al. Community-onset methicillin-resistantStaphylococcus aureus skin and soft-tissue infections: impact of antimicrobialtherapy on outcome. Clin Infect Dis. 2007;44:777-84.

About the Authors:Mark List, MD, Avera McGreevy Clinic, Sioux Falls, South Dakota; Clinical Assisant Professor, University of South Dakota Sanford School of Medicine.Donella Headlee, MD, Center for Family Medicine, Sioux Falls Family Medicine Residency.Katherine Kondratuk, MS I, University of South Dakota Sanford School of Medicine.

Please note: Due to limited space, we are unable to list all references. You may contact South Dakota Medicine at 605.336.1965 for a complete listing.

118

119March 2016

120

IntroductionPolymyalgia rheumatic (PMR) is almost exclusively a disease of adults over the age of 50 with a peak incidencebetween the ages of 70 to 80.3 Geographically, it is mostcommon in Scandinavian countries and in people ofNorthern European descent.5 In the U.S., it is most common in the upper Midwest where a significant portionof the population is of Scandinavian descent.5 It is morecommon in women than in men and is rare in black,Asian and Latino populations.5,7

PMR is an inflammatory rheumatic condition character-ized clinically by aching and morning stiffness in theshoulders, hip girdle and neck.9 Most commonly PMRoccurs in isolation, but it may be seen in 40 to 50 percentof patients with giant cell arteritis (GCA).5 In addition,approximately 10 to 20 percent of patients who initiallypresent with features of PMR later go on to developGCA.6 The strong clinical association together with datafrom pathophysiologic studies suggest that GCA and PMR

are closely related diseases; however, the exact mechanismof these two conditions remains unknown.5 Despite thesimilarities, PMR and GCA have distinct symptoms withsignificantly different corticosteroid requirements andprognosis.7

GCA is also referred to as temporal arteritis or cranialarteritis and is an inflammation of medium and large sizedarteries.8 It is a systemic disease that can involve arteriesin multiple locations including the aorta and its mainbranches but more characteristically involves one or morebranches of the common carotid arteries, particularly thetemporal artery.5

The annual incidence rate of GCA in individuals greaterthan 50 years ranges from 6.9 to 32.8 per 100,000 population. Familial aggregation has been reported as ithas an association with HLA-DR4.5 In addition, geneticlinkage studies have demonstrated an association of GCAwith alleles at the HLA-DRB1 locus, particularly HLA-DRB1-04 variant.5

121March 2016

Primers in Medicine

Polymyalgia Rheumatica and Giant Cell Arteritis: A Review Article By Ukamak a Nwad i b i a , MD ; E r i c L a r s o n , MD , FACP ; a n d

J o s e ph F a n c i u l l o , MD , FACP

AbstractPolymyalgia rheumatic (PMR) and giant cell arteritis (GCA) are two rheumatological conditions with significant overlap that typically affect the older white population.1 PMR is the most common inflammatoryrheumatic disease of the elderly and shares many pathogenetic and epidemiological features with GCA.2

Diagnosis is made primarily on clinical grounds with supporting laboratory evidence.1,3 Typical symptoms ofPMR are bilateral aching of the shoulders and pelvic girdle associated with stiffness.4 PMR is associated withGCA and is considered to be on a disease continuum.5 Approximately half of patients diagnosed with GCAhave already been or will be diagnosed with PMR.6

GCA is the most common vasculitis in adults and affects medium and large arteries and can result in blindnessif untreated.3 Clinically it may present either gradually or abruptly.2 The most common presentation is headachewith an aching pain classically localizing to the temporal region of moderate intensity which responds poorly toanalgesics.5 Patients may also experience jaw or tongue claudication with weakening or pain in the muscles ofmastication that is relieved by rest.7 The temporal artery may exhibit palpable beading, diminished pulses, bruitsand tenderness.8

122

Primers in Medicine

Pathogenesis The etiology of PMR and GCA is not clearly defined.5

Both genetic and environmental factors appear to play arole.5 Both conditions are associated with specific allelesof HLA-DR4.9 There has been demonstration of sequencepolymorphism inside the hyper variable region of theHLA DRB1 gene that maps to the antigen binding cleft ofHLA DR molecules suggesting an important role for antigenselection and presentation.10 Patients with GCA and PMRshare this sequence polymorphism which is not found inpatients with rheumatoid arthritis.10

Histopathologically, GCA is a pan arteritis with inflammatory mononuclear cell infiltrate in the vesselwall with frequent giant cell formationand proliferation ofthe intima and fragmentation of the internal elastic lamina.5 The pathogenesis of GCA is thought to start inthe adventitia where CD 4+ T cells are triggered, settingoff macrophage differentiation.5 The T cells that areenrolled to vasculitic lesions in patients with GCA produce predominantly IL-2 and IFN-gamma, and the latter has been suggested to be involved in the progressionto overt arteritis.5 Seasonal variations suggest a role ofinfectious agents such as viruses and mycoplasma as possible triggers, although specific causative agents andpathological mechanisms have not been identified.11

Signs and SymptomsPolymyalgia RheumaticaPMR primarily affects the muscles and joints of the neckand hip girdles with prominent bilateral pain and morningstiffness.7 The shoulders are affected in about 70 to 95 percent of cases.1 Proximal myalgia and arthralgia typicallydevelop over weeks to months, worsening at night andwith movement.12 Up to 50 percent of patients with PMRdisplay distal, transient, asymmetrical or symmetricalarthritis primarily in the knee or wrist.7 Tenosynovitissuch as carpal tunnel syndrome is common.7 Pitting edemacan affect the wrists, hands, ankles and feet and occasion-ally is the presenting finding.7 Systemic symptoms such aslow grade fever, fatigue, malaise and weight loss occur in30 to 50 percent of patients.7

GCAPatients with GCA usually have constitutional featuresincluding fever and fatigue.8 Cranial vessel involvementmay precipitate jaw claudication, scalp tenderness andtemporal or occipital headache.5 Inflammation of theophthalmic artery may cause ischemia of the optic nerveresulting in visual loss.8 Involvement of the subclavian

vessels may result in upper extremity limb claudication orsubclavian steal syndrome.7 Aortic involvement occurs in15 percent of cases and presents with decreased or absentperipheral pulses, discrepancies of blood pressure betweenboth arms and arterial bruit.14 Aortic valve regurgitationmay occur with GCA involvement of the proximalascending aorta.8

Evaluation

Patient evaluation starts with a detailed history and physical examination with suggestive clinical history andfindings.7 Also, laboratory testing includes C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)which are classically elevated in both conditions.9

Complete blood count to evaluate for anemia and thrombocytos is seen in some cases, liver function testsand creatinine phosphokinase may also be abnormal.7

Other laboratory studies to assist in differentiating PMRand GCA from other conditions include thyroid studies, complete metabolic panel, rheumatoid factor measurement,cyclic citrullinated peptide (CCP) antibody, urinalysis aswell as protein electrophoresis.7 For suspected GCA, temporal artery biopsy is indicated, though not requiredprior to starting steroid therapy to avoid serious complications of untreated disease especially blindness.5

Biopsy could be done up to five days, maybe even later following commencement of therapy without a significanteffect on the histopathology. Since involvement of thevessel may be segmental, accuracy is increased by obtaining a biopsy segment of 3 to 5 cm together with serial sectioning of biopsy specimens.5 If disease suspicionremains strong after a negative biopsy, a biopsy of the contralateral temporal artery could be considered, therebyincreasing diagnostic sensitivity by 9 to 12 percent.15

In the circumstance of a negative temporal artery biopsyand a high clinical suspicion for GCA involving the aorta,diagnosis may be aided by CT angiography.13 Other imaging modalities including MRI and ultrasound of thetemporal artery may also show lesions of GCA but are notgenerally clinically useful.13 PET scans have also been suggested to have a role in the diagnosis of large vessel vasculitis but data is limited.13

Differential Diagnosis Due to the sometimes nonspecific features of both PMRand GCA, it is necessary for the clinician to consideralternative diagnosis. Various vasculitides and connectivetissue diseases share common features with GCA andPMR. Paraneoplastic conditions, occult malignancy and

123March 2016

Primers in Medicine

hypothyroidism may present similarly as can drug inducedmyopathy.5

TreatmentTreatment of both GCA and PMR is with glucocorticoidsbut at significantly different doses.5 Most treatment recommendations and guidelines are based on clinicalexperience rather than results of randomized clinical trials.6 PMR is treated with lower doses of prednisone 10to 20 mg daily and then gradually tapered over one to twoyears.8 GCA requires higher doses of prednisone, typically40 to 60 mg daily for approximately one month, followedby a gradual taper to lower doses depending on patients’response for a total of about two years of therapy.5 It is recommended to start therapy immediately if GCA is suspected to avoid visual loss.5 ESR and CRP serve as useful indicators of inflammatory disease activity in monitoring and tapering steroid therapy.7 Aspirin, 325 mgdaily, has been found to reduce the occurrence of cranialischemic complications in GCA and should be given inaddition to glucocorticoids in patients with no contraindi-cations.5 The use of weekly methotrexate is controversialas a steroid sparing agent but is used occasionally in clinical practice.16 In such situations, patients should beadvised of the limitations of available data regarding theefficacy of potentially glucocorticoid-sparing therapies.Bisphosphonates should be used to maintain bone mineral density and decrease vertebral fractures inpatients on long-term glucocorticoid therapy.16 Durationof glucocorticoid treatment varies from one to two yearsbut could be continued or restarted if the patient is stillsymptomatic or having flares.16 It is recommended to consider Pneumocystis jiroveci pneumonia prophylaxis inpatients receiving up to 20 mg or more of prednisonedaily.6

ConclusionGCA and PMR are two rheumatologic conditions withsignificant overlapping findings and pathophysiology.Clear differentiation between them is required for appropriate management. PMR is characterized by bilateral shoulder and pelvic girdle pain and respondsbriskly to low dose steroid therapy. GCA is a vision threatening vasculitis that requires prompt initiation ofhigh dose prednisone with early temporal artery biopsy toconfirm diagnosis. Both disorders are characterized byhigh ESR and CRP, which however, may not be presentearly in the course of disease. Prognosis is good withprompt diagnosis and treatment.

REFERENCES1. Salvarani C, Cantini FL, Hunder GG. Polymyalgia rheumatic and giant-cell arteritis.

N Eng J Med. 2002;347(4):261-712. Butler N, Mundy J, Shah P. Aortic complications of Giant cell arteritis: a diagnostic

and management dilemma. J Card Surg. 2010;25(5):572-81.3. Salvarani C, Macchioni P, Zizi F, et al. Epidemiologic and immunogenetic aspects

of polymyalgia rheumatic and giant cell arteritis in Northern Italy. Arthritis Rhuem.1991;34(3):351-6.

4. Brooks RC,Mc Gee SR. Diagnostic dilemma in PMR and GCA. N Eng J Med.2002;347:261.

5. Borchers AT, Gershwin M.E. Giant cell arteritis: a review of classification, patho-physiology, geoepidemiology and treatment. Autoimmune Rev. 2012;6-7:544-54.

6. Weyand CM, et al. Clinical practice: giant cell arteritis and polymyalgia rheumati-ca. N Eng J Med. 2014;371:50-7.

7. Caylor T Perkins Allen. Recognition and management of Polymyalgia rheumaticaand giant cell arteritis. Am Fam Physician. 2013;88:676-84.

8. Waldman C, et al. Giant cell arteritis. Med Clin N Am. 2013;(97):329-359. Salvarani C, Cantini F, Hunder G. Polymyalgia rheumatic and giant cell arteritis.

Lancet 2008;372:234.10. Weyand CM, Hunder N, Hicok et al. HLA-DRB1 alleles in PMR, GCA and RA.

Arthritic Rheum. 1994;37:514.11. Elling P, Olsson AT, Elling H. Synchronous variations of the incidence of temporal

arteritis and Polymyalgia rheumatica in different regions of Denmark; associationwith epidemics of mycoplasma pneumonia infection. J Rheumatol.1996;23(1):112-9

12. Chuang TY, et al. Polymyalgia rheumatic: a 10 year epidemiologic and clinic study.Ann Intern Med. 1982;97(5):672-80

13. Levine SM, Hellman DB. Giant cell arteritis. Curr Opin Rheumatol. 2002Jan;14(1):3-10

14. Butler N, Mundy J, Shah P. Aortic complications of GCA, a diagnostic and management dilemma. J Card Surg. 2010;25(5):572-81.

15. Breuer GS, Nesher G, Nesher R. Rate of discordant findings in bilateral temporalartery biopsy to diagnose giant cell arteritis. J Rheumatol. 2009;36(4):794-6.

16. Mackie SL, Pease CT. Diagnosis and management of giant cell arteritis andpolymyalgia rheumatic: challenges, controversies and practical tips. PostgradMed J. 2013;89:284-92.

About the Authors:Ukamaka Nwadibia, MD, Internal Medicine Resident, PGY2, University of South DakotaSanford School of Medicine.Eric A. Larson, MD, FACP, Academic Associate Professor of Medicine, University ofSouth Dakota Sanford School of Medicine. Joseph Fanciullo, MD, FACP, Academic Associate Professor of Medicine and ProgramDirector, Internal Medicine, University of South Dakota Sanford School of Medicine.

124

BackgroundClostridium difficile associated diarrhea (CDAD) is diarrheasecondary to Clostridium difficile infection, usually in thesetting of disturbed gut microbiota. Clostridium difficile is agram positive anaerobic bacillus which has the ability toform spores, and is spread via fecal-oral transmission.CDAD is becoming more prevalent, with a two- to four-fold increase in the past 20 years. Clostridium difficileinfection is the most common cause of hospital acquiredinfection in parts of the U.S., exceeding hospital acquiredMRSA,1 causing the Centers for Disease Control andPrevention (CDC) to deem this an immediate publichealth threat that requires urgent and aggressive action.

The reason for the increase in CDAD is multifactorial,with contributions from poor antibiotic stewardship, virulent strains (NAP1/B1/027), sub-optimal preventionstrategies (i.e., isolation practices for patients withCDAD), and increasing long-term facility residencewhere residents are more frequently colonized withClostridium difficile. It is important to note that while 5 to15 percent of the general adult population are carriers,2

non-toxigenic strains typically do not cause diarrhea andcarriers are often asymptomatic. Of hospitalized or nursinghome residing adults, 10 to 43 percent are carriers of C.difficile.3 Treatment is usually not recommended for

asymptomatic carriers.

Nationwide, there are greater than 300,000 new casesyearly,4 and in South Dakota, 1,032 cases were reported to the South Dakota Department of Health in 2015 – 312of which were in hospitalized patients.5 It is important tonote that this disease is not mandatorily reported and thusthe prevalence is underestimated. More than $1 billion isspent treating this disease annually in the U.S. This disease is most frequently associated with antibiotic use.Other predisposing factors include inflammatory boweldisease, use of proton pump inhibitors, cirrhosis, and theperipartum state. Forty percent of CDAD is acquired in anon-hospital setting, and in one study, 22 percent of community acquired CDAD occurred in patients withoutpreceding exposure to antibiotics.6

Pathogenesis

CDAD often occurs when healthy colonic flora is disruptedby antibiotics, most frequently clindamycin, fluoro-quinolones, and cephalosporins.7 After these broad-spectrum antibiotics kill the normal gut flora, susceptiblepatients are then exposed to and colonized withClostridium difficile. As C. difficile multiplies, toxin A andB act synergistically to glucosylate Rho GTPase, interferingwith signal transduction which leads to cytoskeleton

Clostridium difficile Associated DiarrheaBy No ah Wi e d e l , MD , MS ; J o r g e G i l b e r t , MD ; B r e t t B a l o un , MD ; a n d

Ch e l s e a Ne l s o n , CNP

AbstractClostridium difficile associated diarrhea (CDAD) is increasingly important in primary care, and associated withhigh cost, significant morbidity and mortality. As the preferred treatment for different groups of patients variesconsiderably, it is important to stratify CDAD patients into mild versus severe and uncomplicated versus complicated. While treatment with either metronidazole or oral vancomycin cures a majority of patients, anddespite improvement in early diagnosis and therapy, recurrence continues to be a significant problem. In appropriately selected patients, fecal bacteriotherapy has emerged as an effective treatment for the patient withmultiple recurrences. Addressing CDAD should include antibiotic stewardship, improved hygiene, prompt diagnosis, appropriate treatment, and infection precautions in hospitals and skilled nursing facilities.

Primers in Medicine

125March 2016

Primers in Medicine

dysfunction, resulting in enterotoxicity and cytotoxicity.8

Evidence of dysfunction of cytoskeleton and cell-celladhesion may be seen on microscopy of cultured fibroblasts, which upon exposure to toxin B, becomerounded and undergo apoptosis. The hypervirulentClostridium difficile strain NAP1/BI/027 produces higherquantities of toxins A and B. This strain likely has othermechanisms promoting virulence, including fluoroquinoloneresistance, increased sporulation and adherence.9

Another potential contributing mechanism is an alteredimmune response to infection with inadequate productionof IgG antibodies against toxin A. Whereas a healthyimmune system may keep Clostridium difficile activity to alevel where the carrier is asymptomatic, low levels of IgGantibody against toxin A are associated with developmentof diarrhea10 and recurrence of CDAD.11

Clinical PresentationClostridium difficile infection exists with remarkable variability. Those infected may indeed be asymptomatic orpersistent carriers, or CDAD may progress to painful fulminant colitis that mimics an acute abdomen. ClinicalCDAD most frequently presents with watery diarrheaafter antibiotic use. In this mild presentation, patients typically note frequent watery or bloody stools, abdominalpain and cramping, nausea, vomiting and fever.12 Markersof severe CDAD include leukocytosis (WBC greater than15,000 cells/uL), acute kidney injury (50 percent rise ofcreatinine over baseline), lactic acidosis, or shock presentation. CDAD may be complicated by hypotension,ileus, toxic megacolon, or colectomy from lack of responseto therapy or colonic perforation. An occasionally over-looked scenario is that of a post-operative patient who hasileus, and in whom a septic picture without diarrheaemerges. As the presenting picture varies widely, and asprevalence is increasing, a high index of suspicion is warranted.

DiagnosisCDAD is best diagnosed with PCR testing for toxin B,performed on liquid feces. Sensitivity and specificity ofPCR is greater than 90 percent, and results from PCR canbe available in one hour. If the patient is unable to have abowel movement but CDAD is suspected, rectal swabsmay be used to obtain a test sample. Other methods oftesting include enzyme immunoassay (EIA) for toxins Aand B, EIA for C. difficile glutamate dehydrogenase, cytotoxicity assay and anaerobe culture, or an algorithmcombining EIA with PCR.

While a majority of CDAD is diagnosed with stool testing,lower endoscopy (colonoscopy or sigmoidoscopy) is occasionally performed in carefully selected patients withnegative stool testing but high clinical suspicion. Findingsare variable, and include non-specific colitis-type changesto classic pseudomembrane formation with yellow-whiteplaques (giving the name pseudomembranous colitis,pathognomonic for CDAD, which correlates with severity). However, lower endoscopy should be minimizedgiven the potential risk of perforation.

TreatmentTreatment of mild CDAD on its first occurrence is withmetronidazole 500 mg three times daily for 10 to 14 days.If possible, precipitating systemic antibiotics should be discontinued. Initial treatment of CDAD cures 80 to 90percent of patients. While a majority of CDAD patientsare cured, recurrence continues to be a significant clinicalproblem, and roughly 10 to 20 percent of patients willhave a first recurrence. Per Infectious Disease Society ofAmerica guidelines, CDAD on its first recurrence shouldbe treated with a repeat 14-day course of oral metronidazole versus oral vancomycin 125 mg orally fourtimes per day.13 Severe CDAD is treated with vancomycinorally 125 mg QID for 10 to 14 days, and complicatedCDAD is treated with vancomycin 500 mg QID PO andmetronidazole 500 to 750 mg IV Q8h. Vancomycin enemasmay be employed for patients with ileus. Early surgicalconsultation is recommended in complicated CDAD, particularly in the ICU. A study of ICU patients with fulminant CDAD revealed that colectomy in selectedpatients reduced mortality (34 percent of patients whoreceived a colectomy died, versus 58 percent who did not).14

Recurrence, as mentioned previously, is a significant issueresulting in re-hospitalization and health care expenditure.

Mild CDAD Metronidazole 500mg PO TID for 10 to 14 days.

Severe Vancomycin PO 125mg QID 10 to 14 days.CDAD

Severe, Higher dose vancomycin, IV metronidazole.complicated Ileus may need vancomycin enema. EarlyCDAD surgery consult.

First Recurrence Metronidazole vs. Vancomycin

Second Recurrence Prolonged vancomycin course or pulsed vancomycin, or fidaxomicin.

Third Recurrence Controversial, consider FMT.

Table 2.

Table 1.

Fidaxomicin (Dificid), a macrolide antibiotic, is anotheroption for patients with recurrent CDAD. When compared to vancomycin, fidaxomicin achieved similarcure rates, but with fewer recurrences.15 Dosing of fidaxomicin is 200 mg orally BID for 10 days.

Unfortunately standard antibiotic treatment of subsequentrelapses is less efficacious, with cure rates of approximately50 percent. A second relapse may be treated with vancomycin with prolonged tapering or pulse dose of vancomycin. Tapering involves gradually smaller doses oforal vancomycin, often over the course of 21 days. Pulseddoses (125 to 500 mg) of oral vancomycin are given onceevery three days for 27 days. Variations or combinations ofthese regimens are often utilized. The use of probiotics(Saccharomyces boulardii or Lactobacillus plantarum) is controversial, with insufficient evidence to recommendtheir use.16

It is important to rehydrate patients who have a fluiddeficit, ideally by oral rehydration. IV fluid repletion maybe warranted if adequate rehydration is not achieved bysimple oral rehydration. It is important that anti-motilityagents such as loperamide not be used, as this class of drugsmay worsen CDAD.

Treatment for a third recurrence should include consider-ation of fecal microbiota transplant (FMT) with the aimof restoring balanced microbiota. FMT has been practicedin the veterinary world for over 300 years in the treatmentof ruminant disease and equine digestive disease. In theearly 17th century, Hieronymus Fabricius noted thattransplanting cud from a healthy cow into particular ailingcows cured them of their digestive illnesses.16 In subsequentveterinary literature, this is termed “transfaunation.”Human FMT was described in medical literature as earlyas 1958.17 Under 2013 American College ofGastroenterology CDAD guidelines,15 FMT should beconsidered after three recurrences. One study used rRNA

sequencing to investigate fecal microbiota in patients withrecurrent CDAD, and found a paucity of normal microbiota such as of Bacteroidetes and Firmicutes species,often replaced with atypical Streptococcal, Clostridium andLactobacillus species.18 FMT was successful at restoring normal flora, more closely representing the healthy donor.

Multiple trials with FMT have proven highly successful inpreventing further recurrence of CDAD, with an approximately 90 percent cure rate. FMT involves instilling fecal material from a healthy donor into apatient with recurrent CDAD. Meta-analysis of 27 studieswith a total of 317 pooled participants showed a cure rateof 92 percent.19 van Nood et al.20 published a three-armrandomized trial studying FMT for recurrent CDAD. Armone received vancomycin followed by bowel lavage andFMT via nasoduodenal tube, arm two received a standardoral vancomycin course, and arm three received an oralvancomycin course with bowel lavage. Of the 16 patientsreceiving FMT, 13 were cured with one infusion, and 15after two (94 percent cure). Four of the 13 (31 percentcure) in the arm two vancomycin group had resolution oftheir recurrent CDAD, and three of 13 in arm three werecured.

During FMT, fecal material is delivered to the colon withcolonoscopy or enema, or alternatively to the small bowelusing naso-enteric tube. While the ideal route of FMT iscurrently not firmly established, trials are ongoing toanswer this question.21 Transplant of purified feces is typically (although not always) from related donors.Donor stool is homogenized in a blender with 350 mL ofsterile saline. It is then filtered twice using saline-moistened gauze in a funnel and collected in syringes forinjection into endoscopes used during FMT. In trials, bothmethods of delivery have achieved cure rate of approximately 90 percent.22, 23 The FDA considers FMT anexperimental therapy, and administration is typically inthe setting of a clinical trial, or with informed consent.

FMT is being performed locally in South Dakota.24

Patients are usually enrolled after three recurrences ofCDAD, and donors are recruited from relatives or spouses.Potential donors are screened for potentially transmissiblediseases (see table) and feces are emulsified prior to transplant. Donor feces is prepared and a liquid suspensionis transplanted using colonoscopy. FMT performed at theauthors’ facility, taking place over one year and involving36 patients has achieved greater than 90 percent success,defined as resolution of diarrhea without recurrence.

126

Primers in Medicine

Donor Serology Donor Stool Tests

• HIV• HTLV I/II• RPR• HAV IgM• HBsAg• HBsAb, • HCV Ab

• Bacterial culture• Ova & Parasite• Giardia Ag• Cryptosporidium Ag• Microsporidia smear• AFS for Cyclospora• AFS for Isospora• C. diff toxin B (PCR)

Table 3.

127March 2016

Primers in Medicine

PreventionPrevention is mainly aimed at: 1) antibiotic stewardship;and 2) containing infectious spores in hospitals. The CDCrecommended prevention strategies include contact precautions, isolation, and optimized testing (PCR asabove). Patients who are diagnosed with CDAD should beisolated with their own bathroom or commode. Closingtoilet seat lids prior to flushing is recommended. Staffshould be instructed to wear gown and gloves, and washtheir hands with soap and water prior to leaving the roomof a CDAD patient, as well as universal glove use on unitswith high CDI rates. Environmental cleaning of CDADpatient rooms needs to involve agents containing bleach.25

ConclusionCDAD is increasingly important in primary care as well asspecialized medical care as a result of increasing prevalenceand resulting health care expenditure, as well as significantmorbidity and mortality. Steps in counteracting the current swell in cases include antibiotic stewardship,improved hygiene, prompt diagnosis, appropriate treatment,

and infection precautions in hospitals and skilled nursingfacilities. It is important to stratify patients into mild versus severe and uncomplicated versus complicated, as treatment for the different groups varies considerably.Despite improvement in early diagnosis and therapy,recurrence continues to be a significant problem. Inappropriately selected patients, fecal bacteriotherapy hasemerged as an effective alternative for patient with multiple recurrences.

REFERENCES1. Miller B, et al. Comparison of the burdens of hospital-onset, healthcare facility-

associated Clostridium difficile infection and of healthcare-associated infectiondue to methicillin-resistant Staphylococcus aureus in community hospitals.Infection Control and Hospital Epidemiology. 2011 Apr;32(4):387-90.

2. Ozaki, et al. Clostridium difficile colonization in healthy adults: transient colonization and correlation with enterococcal colonization. J Med Microbiol.2004 Feb;53(Pt 2):167-72.

3. Gursoy S et al, Clostridium difficile infection frequency in patients with nosocomialinfections or using antibiotics. Hepatogastroenterology. 2007 Sep;54(78):1720-4.

4. Bassetti M, Villa G, Pecori D, Arzese A, Wilcox M. epidemiology, diagnosis andtreatment of Clostridium difficile infection. Expert Rev Anti Infect Ther.2012;10(12):1405-23.

5. South Dakota Health and Disease Summary – December 2015. South DakotaDepartment of Health. Retrieved fromhttp://doh.sd.gov/documents/statistics/ID/Dec2015.pdf.

6. Khanna S, et al. The epidemiology of community-acquired Clostridium difficile infection: a population-based study. The American Journal of Gastroenterology.2012;107:89.

7. Gerding, et al. Clindamycin, Cephalosporins, Fluoroquinolones, and Clostridium difficile–associated diarrhea: this is an antimicrobial resistance problem. ClinicalInfectious Diseases. 2004;38(5):646-8.

8. Lyras D, et al. Nature. 2009;458:1176..9. O’Connor J, et al. Clostridium difficile infection caused by the epidemic

BI/NAP1/027 strain. Gastroenterology. 2009;136(6):1913-24.10. Kyne, L, et al. Asymptomatic carriage of Clostridium difficile and serum levels of

IgG antibody against toxin A. NEJM. 2000;342(6):390.11. Kyne, L. Association between antibody response to toxin A and protection against

recurrent Clostridium difficile diarrhea. The Lancet. 2001;357(9251):189.12. Wanahita A, et al. Conditions associated with leukocytosis in a tertiary care

hospital, with particular attention to the role of infection caused by clostridium difficile. Clin Infect Dis. 2002;34(12):1585.

13. Cohen S, et al. Clinical practice guidelines for Clostridium difficile infection inadults: 2010 update. Infection Control and Hospital Epidemiology. 2010;31(5).

14. Lamontagne F, et al. Impact of emergency colectomy on survival of patients withfulminant Clostridium difficile colitis during an epidemic caused by a hypervirulentstrain. Ann Surg. Feb 2007;245(2): 267-72.

15. Louie T, et al. Fidaxomicin versus vancomycin for Clostridium difficile infection. N Engl J Med. 2011;364:422-31.

16. Surawicz C, et al. Guidelines for diagnosis, treatment, and prevention ofClostridium difficile infections. Am J Gastroenterol. 2013;108:478-98.

17. Borody, T et al, Bacteriotherapy using fecal flora. Journal of ClinicalGastroenterology. 2004;38(6):475.

18. Khoruts A, et al. Changes in the composition of the human fecal microbiome afterbacteriotherapy for recurrent CDAD. J Clin Gastroenterol. 2010;44:354-60.

19. Gough, et al. Systematic review of intestinal microbiota transplantation (fecal bacteriotherapy) for recurrent Clostridium difficile infection. Clinical InfectiousDiseases. 2011;53:994-1002.

20. van Nood, et al. Duodenal infusion of donor feces for recurrent Clostridium difficile. NEJM. 2013;368(5):407-15.

21. Kao D, et al. FMT delivered by capsule versus colonoscopy for recurrent C. diff. Retrieved from https://clinicaltrials.gov.

22. Khanna S, Pardi D. Clostridium difficile infection: management strategies for a difficult disease Therapeutic Advances in Gastroenterology. 2014;7(2):72-86

23 Youngster et al. Fecal microbiota transplant for relapsing Clostridium difficile infection using a frozen inoculum from unrelated donors: a randomized, open-label,controlled pilot study. Clinical Infectious Diseases. 2014;58(11):1515-22

24 Wiedel N, Nelson C, Baloun B, Gilbert J. Recurrent Clostridium difficile infection:fecal microbiota transplant Sanford Medical Center poster presentation at GI symposium 4/2014.

25 Update on IDSA practice guidelines symposium: C difficile. 8/2007 abstract#1165.

About the Authors:Noah Wiedel, MD, MS, PGY-2, Internal Medicine Resident, University of South Dakota Sanford School of Medicine. Jorge Gilbert, MD, Gastroenterologist, Sanford Medical Center, Sioux Falls, South Dakota.Brett Baloun, MD, Gastroenterologist, Sanford Medical Center, Sioux Falls, South Dakota. Chelsea Nelson, CNP, Gastroenterology, Sanford Medical Center, Sioux Falls, South Dakota.

128

Community-acquired pneumonia (CAP) alongwith other lower respiratory infections have a significant impact on morbidity and health-care

costs.1 Hospitalizations secondary to CAP are commonand may lead to acute respiratory distress syndrome(ARDS), sepsis, or death.

CAP results from an inability of the immune system toclear bacterial pathogens in the lower respiratory tract.Inflammatory cytokine responses help clear bacteria butthey may also exacerbate pulmonary dysfunction byimpairing alveolar gas exchange possibly leading to sepsisor end organ damage.2-3 Use of systemic corticosteroids inpatients with CAP may help reduce inflammatory processes in the lungs.

The use of adjunctive corticosteroids in patients withCAP has been studied for decades with results demonstrating inconsistent decreases in ARDS, sepsis andmortality. Previous systematic reviews have been unableto demonstrate conclusive benefits of corticosteroids inCAP and current practice guidelines do not recommendcorticosteroids for CAP.4-7 However, two recent trials anda meta-analysis have once again brought attention to thepotential benefits of corticosteroids in patients withCAP.2,3,8

A systematic review and meta-analysis, recently publishedin the Annals of Internal Medicine evaluated the use of corticosteroids in patients hospitalized with CAP.3 Thismeta-analysis included studies that randomly assignedCAP patients to receive either corticosteroids or placebo.Eligible studies also had to report at least one of the following outcomes: need for mechanical ventilation,development of ARDS, need for ICU admission, time toclinical stability, duration of hospitalization or all-causemortality. This analysis evaluated potential adverse effectsassociated with corticosteroid use such as hyperglycemiarequiring treatment, rehospitalization, gastrointestinal(GI) hemorrhage and severe neuropsychiatric symptoms.

A total of 13 randomized controlled trials, involving 2005patients, were included in the analysis. The addition oftwo recently released trials in Lancet and JAMA wereincluded in this analysis, therefore, making it differentthan previous meta-analysis on this topic.2,8 Studies thatwere limited to patients with chronic obstructive pulmonary disease, ventilator-associated pneumonia, aspiration pneumonia, or Pneumocystis jirovecii pneumoniawere excluded from the analysis. Most of the studies wereconducted in Europe and excluded patients at high risk foradverse effects from corticosteroids such as GI hemorrhagewithin three months, immunosuppression, and pregnantwomen. Most patients were male in their early 60s. Thestudies used a variety of corticosteroid agents with theduration of treatment ranging from 1 dose to 10 days.

The use of corticosteroids in CAP was found to decreasethe need for mechanical ventilation and the rate ofARDS. The relative reduction in the need for mechanicalventilation was found to be larger in patients with lesssevere pneumonia than those with severe pneumonia.Corticosteroids were also found to significantly decreasetime to clinical stability and duration of hospitalization.Time to clinical stability was defined as having all vitalsigns within normal range and not requiring supplementaloxygen. As far as duration of hospitalization, in all studies,patients were discharged at the discretion of the admittingphysician. Detailed results are included in Table 1.

There were no differences noted between corticosteroidgroups and control groups in the rate of ICU admission orall-cause mortality. However, a mortality benefit wasdemonstrated in patients that met the criteria for severepneumonia (RR 0.39 [CI, 0.20 to 0.77]), but not in thosewith less severe pneumonia (RR 1.00 [CI, 0.79 to 1.26]).Definitions of severe pneumonia are provided in Table 2.

No effect was found on the risk of GI hemorrhage, neuropsychiatric complications, or rehospitalizations withcorticosteroid therapy. However, most studies excluded

Emerging Evidence of Corticosteroids in Community-Acquired Pneumonia By C l a i r e L a r s o n ; a n d Ta d d He l lw i g , P h a rmD , BCPS

Pharmacology Focus

129March 2016

Pharmacology Focus

patients at high risk for these adverse effects. There was asignificantly higher risk of hyperglycemia requiring treatment in those patients who were treated with corticosteroids compared to those who were not.

The use of corticosteroids was found to significantlydecrease the need for mechanical ventilation, rate ofARDS, time to clinical stability, duration of hospitalization,and mortality in severe CAP compared to no corticos-teroid therapy. There are still questions, however, aboutthe optimal corticosteroid, dose of corticosteroid, andduration of therapy in CAP. These results cannot beapplied to those patients excluded from the trials, including patients who are immunosuppressed, pregnant,at risk for neuropsychiatric events, or have had a recentGI hemorrhage.

An ongoing phase 3 randomized trial, with an estimatedenrollment of 1,450 patients, will further clarify the rolethat corticosteroids may play in patients with severe CAP(ClinicalTrials.gov: NCT01283009). This trial will alsohelp define which corticosteroid to use, what dose to use,and the optimal duration of treatment.

In conclusion, a recent meta-analysis that included tworecently released trials has demonstrated beneficial effectsof corticosteroids in patients with CAP highlighted by asignificant decrease in mortality in patients with severeCAP.

REFERENCES

About the Authors:Claire Larson, PharmD Candidate, South Dakota State University. Tadd Hellwig, PharmD, BCPS, Associate Professor, Department of Pharmacy Practice,College of Pharmacy, South Dakota State University; Clinical Pharmacist, SanfordMedical Center.

Please note: Due to limited space, we are unable to list all references. You may contact South Dakota Medicine at 605.336.1965 for a complete listing.

1. Thomas CP, Ryan M, Chapman JD, et al. Incidence and cost of pneumonia inMedicare beneficiaries. Chest. 2012;142:973-81.

2. Blum CA, Nigro N, Briel M, et al. Adjunct prednisone therapy for patients withcommunity-acquired pneumonia: a multicenter, double-blind, randomized, placebo-controlled trial. Lancet. 2015;385:1511-18.

3. Siemieniuk RAC, Meade MO, Alonso-Coello P, et al. Corticosteroid therapy forpatients hospitalized with community-acquired pneumonia. Ann Intern Med.2015;163:519-28.

4. Nie W, Zhang Y, Cheng J, Xiu Q. Corticosteroids in the treatment of community-acquired pneumonia in adults: a meta-analysis. PLoS One 7(10):e47926.Doi:10.1371/journal.pone.0047926.

5. Chen Y, Li K, Pu H, et al. Corticosteroids for pneumonia. Cocchrane Database Syst Rev. 2011:CD007720. Doi.10.1002/14651858.CD007720.pub2.

6. Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, et al. Infectious DiseasesSociety of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007;44 Suppl 2:S27-72.

7. Woodhead M, Blasi F, Ewig S, et al. Joint Taskforce on the European RespiratorySociety and European Society for Clinical Microbiology and Infectious Diseases.Guidelines for the management of adults lower respiratory tract infections- fullversion. Clin Microbiol Infect. 2011;17 Suppl 6:E1-59.

8. Torres A, Sibila O, Ferrer M, et al. Effect of corticosteroids on treatment failureamong hospitalized patients with severe community-acquired pneumonia and highinflammatory response: a randomized clinical trial. JAMA. 2015;313:677-86.

Table 1. Outcomes of corticosteroids in patients with CAP3

Outcome # of Studies Event Rates, n/N (%) Level of (# of Patients) Corticosteroids Control RR (CI) Certainty

Mechanical Ventilation (%) 5 (1060) 17/550 (3.1) 29/510 (5.7) 0.45 (0.26 to 0.79) Moderate

ICU Admission (%) 3 (950) 25/476 (5.3) 36/474 (7.6) 0.69 (0.46 to 1.03) Moderate

ARDS (%) 4 (945) 2/473 (0.4) 14/472 (3.0) 0.24 (0.10 to 0.50) Moderate

Time to Clinical Stability (days) 5 (1180) 3.5 d 4.7 d -1.22 (-2.08 to -0.35) High

Duration of Hospitalization (days) 3 (1288) 7.9 d 9.1 d -1 (-1.79 to -0.21) High

All-cause Mortality (%) 12 (1974) 52/977 (5.3) 79/997 (7.9) 0.67 (0.45 to 1.01) Moderate

Hyperglycemia Requiring6 (1534) 88/640 (13.8) 50/640 (7.7) 1.49 (1.01 to 2.19) HighTreatment (%)

Table 2. Definition of Severe Pneumonia6,9-13

Pneumonia Severity Index: score of IV or V

CURB-65 score: 2 or greater

2007 IDSA/ATS guidelines: 1 major or 3 minor criteria

British Thoracic Society: score of 3 or greater

ATS 2001 rule: 1 major or 2 minor criteria

ATS 1993: 1 criteria

IDSA: Infectious Diseases Society of America

ATS: American Thoracic Society

130

Special Features

E x t e n u a t i n g C i r c u m s t a n c e s

The Calling By J a c q u e l y n Gunn a r s o n

Question: Where was your home of origin and what wasinvolved in your early years to prepare for your futurecareer path?

Answer: I was born in Philadelphia in 1943, four monthsafter my father, a Naval aviator and test pilot, was killedin a plane crash while on active duty. I had an older brother, and we were raised by a courageous and devoutmother. I graduated from Notre Dame with a B.A. in liberal studies in 1965 and B.S. in mechanical engineeringin 1966.

Q: You mentioned your “call” to medicine. When didthat occur?

A:While still at Notre Dame, I felt I was being called toserve other people through the practice of medicine, so Ientered Georgetown University School of Medicine in1966 and received my MD from Georgetown in 1970.

Q: Did knowing of your father’s service in the Navyhave any influence on your life?

A:While attending Georgetown, I joined a Navy programfor medical students, and after graduating I did a rotatinginternship at Great Lakes Naval Regional Medical Centerin Chicago. Then for three years I did an anesthesiologyresidency at the National Naval Medical Center,Bethesda, Maryland, completing that in 1974. For thenext few years I returned to Great Lakes as the assistantchief of the anesthesiology department. I had 11 years inthe Navy, including two years of inactive service whileattending medical school.

Q: How did you end up in Sioux Falls?

A: In late 1977, I received a phone call from Dr. BobWillix, who invited me to join Sioux Valley Hospitalbecause they were getting ready to start an open heart surgery program. In February 1978, I joined with Dr. EdDaw, an anesthesiologist at Sioux Valley.

Q: In what ways did your responsibilities as an anesthesiologist increase at Sioux Valley Hospital?

A: In March 1978, I administered anesthesia for the firstopen heart surgery in Sioux Falls. In February 1981, Dr.Richard Belatti and I formed Anesthesia Physicians Ltd.,the anesthesiology group at what was then Sioux ValleyHospital. That group continues to this day. Although initially part of the surgery department, anesthesiologybecame a separate department in 1985. I served as medicaldirector of anesthesiology at Sioux Valley from 1985through 2000.

Q: Was there any event in your life which impacted youimmensely?

A: In 2000, after 28 years of marriage, my wife and I weredivorced. That impacted me immensely. After receivingmy annulment and looking back at this experience, Ibelieve that this event, in part, began to lead me to eventually consider my “call” to the priesthood and wouldallow this, and other experiences, to be used for the benefits of others. My former wife and I remain goodfriends to this day.

Q: Because of your willingness to be vulnerable in sharing that part of your life, how did your calling to the priesthood all come together?

“I was called to the practice of medicine to serve others...and I was called toserve others in a different way once I retired from my medical practice,”explained Fr. Ed Anderson when interviewed about his journey in life. Hisstory serves as an example of a lifetime dedicated to healing, both physicallyand spiritually.

Ed Anderson, MD,Anesthesiologist

Fr. Ed Anderson,Catholic Priest

131March 2016

A: In August 2004, I became a seminarian for theCatholic Diocese of Eastern South Dakota, and at age 61,entered Blessed John XXIII National Seminary in Weston,Massachusetts.

That is a seminary for the formation of priests who hadprevious careers. After having surgery for cancer of thebladder and prostate in Boston on May 1, 2008, I wasordained as a priest on May 30, 2008, in Sioux Falls.

Q: In what areas have you served after becoming a priest?

A: I spent two years as an associate pastor at SaintLambert Catholic Church in Sioux Falls. Since 2010, Ihave been the Catholic chaplain at Avera Prince Of Peaceand the Dougherty Hospice House. In addition, sinceJune 2014, I have been the Catholic chaplain at the Royal C. Johnson Veteran’s Hospital. Furthermore, forthe past four years I have been president of the Sioux FallsMinisterial Association. I am also the Bishop’s representativefor medical ethics.

Q: Having spent nearly four decades of service in SouthDakota, how would you summarize the areas of your lifein which you’ve been called?

A: Physicians have a calling of the heart and I’ve alwaysthought there was a certain spirituality in practicing medicine because God is involved in the healing. My callto the priesthood was a continuation of spirituality in theprofession of medicine. It was also one from the heart,almost a longing for God, who seemed to be telling me toserve others’ spiritual health, not just their emotional andphysical health. I believe that my experiences both in thepractice of medicine and in life have helped me become abetter and more understanding priest to those I serve.Understanding where they are emotionally and physicallyalso helps me to understand where those I serve are spiritually.

A final question is addressed for the reader to answer.Would you be willing to respond to a second “calling”when you retire from serving in your profession?

About the Author:Jacquelyn Gunnarson, Sioux Falls; BS, Nursing; SoDak Medical Auxiliary News Editor,1978-1991, South Dakota State Medical Association Alliance President, 1988-1989,Married 54 years to the late Richard Gunnarson, MD, Otolaryngologist.

Special Features

132

sdbmoe.gov

Board News is a monthly feature sponsored by the South Dakota Board of Medical and Osteopathic Examiners. For more information, contact the Board at SDBMOE@state.sd.us or write to SDBMOE, 101 N. Main Avenue, Suite 301, Sioux Falls, SD 57104.

133March 2016

REFERENCES1. http://nccrt.org/tools/80-percent-by-2018.

134

Q u a l i t y F o c u s :

National Colorectal Cancer Initiative B y S t e ph an D . S c h r o e d e r, MD , Med i c a l D i r e c t o r,

S o u t h D a k o t a F o und a t i o n f o r Med i c a l C a r e

“80% by 2018” is a National ColorectalCancer Roundtable initiative in whichorganizations are committing to eliminating colorectal cancer as amajor public health problem and areworking toward the shared goal ofreaching 80 percent of adults aged 50and older screened for colorectal cancer by 2018. The National ColorectalCancer Roundtable, an organization co-founded by the American Cancer Society andthe Centers for Disease Control and Prevention, is usingthis March, National Colorectal Cancer AwarenessMonth, to rally organizations behind this shared goal.

Thanks in part to the work of many of these leaders, colorectal cancer mortality rates have dropped by over 30percent in the U.S. and over 37 percent in South Dakotaamong adults 50 and older in the last 15 years, with a substantial fraction of these declines due to screening.This evolving public health success story is good news;however, colorectal cancer remains the second-leadingcause of cancer death in the U.S and in South Dakotawhen men and women are combined. To reach the 80 percent goal in South Dakota, we must reach the thousands of South Dakotans between the ages of 50 and75 who are not being regularly screened.

The principal challenge to reaching the 80 percent goal isthat those who are still unscreened will be the most difficult to reach. This calls for a robust, coordinated effortto extensively reduce colorectal cancer as a major publichealth problem, to make sure that all South Dakotans arebenefitting equally from life-saving technology and to sustain the progress we make. The map on the followingpage illustrates where we have the most work to do.

Achieving the 80 percent by 2018 is an ambitious goal,but leaders have led us to this moment. Utilizing an ambitious strategic plan that focuses on moving

consumers to action, promoting practiceimprovement and systems change, andbringing down policy barriers anddefining accountability, we can assureour continued successes. Over 500organizations – including medical professional societies, academic centers,survivor groups, government agencies,cancer coalitions, cancer centers, payers

and many others – have signed a pledge tomake this goal a priority.1

As a primary care physician, here are five things that youcan do to be a part of 80 percent by 2018:

1. Understand the power of the physician recommendation.

2. Measure the colorectal cancer screening rate in your practice; it may not be as high as you think.

3. Use evidence-based practice changes to systematize screening in your office. More screening doesn’t have to mean more work for you.

4. Understand the screening options for colorectal cancer. Educate your patients and staff on the various, often less expensive, testing options.

5. Make sure that patients and staff understand that most insurance companies are required to cover colorectal cancer screening.

For more information, please contact Great Plains QIN/South Dakota Foundation for Medical Care at 605.336.3505or email me at stephan.schroeder@area-a.hcqis.org.

Adapted from NCCRT’s new 80% by 2018 blog at http://nccrt.org/welcome-2016-nccrt-new-blog/.

Special Features

135March 2016

“Quality Focus “ is a monthly feature sponsored by SDFMC, South Dakota’s Quality Improvement Organization. For more information about the SDFMC, visit their website at www.sdfmc.org.

Special Features

This material was prepared by the Great Plains Quality Innovation Network, the Medicare Quality Improvement Organization for Kansas, Nebraska, North Dakota and South Dakota, under contract with the Centersfor Medicare & Medicaid Services (CMS), an agency of the U.S. Department of Health and Human Services. The contents presented do not necessarily reflect CMS policy. 11SOW-GPQIN-SD-SIP1-124/0216

?If not, contact us to reach over 2,000 physicians!

CONTACT:Elizabeth Reiss,

South Dakota MedicinePO Box 7406,

2600 W. 49th Street, Suite 200Sioux Falls, SD 57117-7406

605.336.1965E-mail: ereiss@sdsma.org

Is

In Your Advertising Budget?

136

There are some 200 different kinds ofheadaches, and about 90 percentare of the non-dangerous type.

We're not talking about how miserably orpainful headaches can be, just that most are not dangerous. This is about how torecognize when a headache might be dangerous, and when to come in and seethe doctor or care provider.

I was an intern working in a big city hospital emergency room one late after-noon autumn day in Georgia, when a tall40-something-year-old guy lumbered intomy tiny exam room with the worstheadache he'd ever had. He was a hikerwho spent a lot of time out in the woodswith his dog, but who was so miserable hewanted nothing to do with hiking this day.

He was running a 102 degree fever and he hurt everywhereI touched, especially when I bent his head forward. He hada light pink rash especially on the palms and he reportedplenty of exposure to ticks lately. To make a long storyshort, the tests take a week to come back, but we treatedhim for Rocky Mountain spotted fever and later provedthat was the case.

What clues are there to know when to do more than justcover up a headache with pain medicines?

In general people are safe if the headache is associated witha viral syndrome; is something similar to headaches in thepast and has been defined already as migraine, tension, orneck arthritis headache; is occurring in a person otherwisehealthy; or is accompanied by no other significant newphysical or neurological symptom.

On the other hand, people are not so safe if the headacheis completely different than any previous headache; is theworst headache ever; strikes suddenly like a thunderclap; isassociated with a significant fever, generalized illness, stiffneck, or weight loss; comes with new one-sided face, arm,leg weakness, or vision change; or is a new progressivelyworsening headache that is happening in someone over 40years of age.

Of course, these are just guidelines. If you have any question, seek professional help.

My woods walker had an unusual and severe headachewith a generalized illness, and if not treated early, mighthave resulted in his death. As an intern, I was glad I hadbeen listening during the lecture on the causes ofheadaches.

P a t i e n t E d u c a t i o n :

When to Get Help for a HeadacheBy R i c h a r d P. Ho lm , MD

Dr. Rick Holm wrote this Prairie Doc Perspective for “On Call, “ a weekly program where medical professionals discuss health concerns for the general public.“On Call “ is produced by the Healing Words Foundation in association with the South Dakota State University Journalism Department. “On Call “ airs Thursdays on

South Dakota Public Broadcasting-Television at 7 p.m. Central, 6 p.m. Mountain. Visit us at OnCallTelevision.com.

The Patient Education Page is a monthly feature sponsored by the Healing Words Foundation. For more information, visit www.prairiedoc.com.

137March 2016

Special Features

138

THE JOURNAL OF THE SOUTH DAKOTA STATE MEDICAL ASSOCIATION

Date:

Name:

Company:

Address:

City, State, Zip:

Phone: Fax:

E-mail:

Mailing Address For Publication (if different from above):

Name:

Company:

Address:

City, State, Zip:

Subscription Begin Date:

Prices: Single Issue: $8.95 Tax Exempt ID#:Annual Subscription Fee: $50.00 (U.S.)

$65.00 (Foreign)Subscription Agency Fee: $40.00 (U.S.)

$50.00 (Foreign)

Please return order form and payment to: South Dakota MedicinePO Box 7406Sioux Falls, SD 57117-7406Fax: 605.274.3274 Email: ereiss@sdsma.org

Please direct any questions to: Elizabeth ReissStaff Editor, South Dakota MedicinePhone: 605.336.1965 Fax: 605.274.3274Email: ereiss@sdsma.org

FOR OFFICE USE ONLY

Received By: Date:

Amount Paid: Date Paid:

SUBSCRIPTION ORDER FORM – 2016

BENEFITMember News

Visit www.sdsma.org for the latest news and information.

139March 2016

For Your Benefit:

“For Your Benefit “ is the SDSMA’s monthly update on programs and services available to physicians

through their affiliation with the SDSMA.

Thank you for your membership in the SouthDakota State Medical Association. As a member, you have several direct opportunitiesto become more involved in the importantwork of the SDSMA:

• Doctor of the Day – serve as the physicianfor the South Dakota State Legislature forone day during session;

• Physician lobbyist – serve as a volunteerlobbyist during the legislative session;

• SDSMA PAC – help friends of medicinebecome elected officials and lawmakers;

• SDSMA committees and task forces – servethe organization and yourself;

• SDSMA appointments to state boards, committees and commissions – the SDSMAis asked to nominate and recommend physicians to fill positions to numerousvacancies every year;

• Membership sections for medical students,residents, young physicians, and seniorphysicians – needs vary at different pointsthroughout a physician’s career, and weneed leaders at each stage; and

• Districts and specialty societies – for localinvolvement.

If you’d like to get involved, give us a call at605.336.1965 or visit www.sdsma.org formore information.

Get Involved in the SDSMA

Registration Now Open For the 2016SDSMA Annual Leadership Conference Save the Date! The 2016 SDSMA Annual Leadership Conference – with a new schedule and new events – heads back to the Hilton Garden Inn, Downtown Sioux Falls on Friday, June 3.

WHAT: 2016 SDSMA Annual Leadership Conference

WHEN: Friday, June 3

WHERE: Hilton Garden Inn, Downtown Sioux Falls

With presentations, discussions, networking opportunities and social events, theAnnual Leadership Conference is a great time to share ideas and learn from fellowmembers.

Check out the new schedule and new events! Do you have an issue you’d like tobring to the SDSMA’s attention? Schedule a time to address the Council by contacting the SDSMA office at 605.336.1965 or visit www.sdsma.org. Visitwww.sdsma.org for more information and registration.

The Annual Leadership Conference is a benefit of your membership. For the latestdetails about exciting events taking place during the 2016 SDSMA AnnualLeadership Conference, visit www.sdsma.org.

New Schedule & Events! Register at sdsma.org 8:30 a.m. Membership Meeting with presentations from AMA President

Dr. Steven Stack and SSOM Dean Dr. Mary Nettleman

9:30 a.m. Medical Marijuana Panel Discussion

11 a.m. Open Forum

12 p.m. SDSMA PAC Lunch on Human Trafficking

1:30 p.m. Council Meeting

6 p.m. Membership Mixer

7 p.m. Awards Banquet & Scholarship Recognition

Source: SDSMA staff

ISSUEThe Issue Is...

The Creating Opportunities Now for Necessary and Effective CareTechnologies (CONNECT) for Health Act recently introduced inCongress would expand the use of telemedicine to achieve qualitycare for patients.

The bill reflects that the appropriate use of telemedicine can greatly improve access to quality care while maintaining patientsafety. According to an independent study by Avalere Health, thebill could save $1.8 billion over 10 years.

“This legislation has the potential to remove barriers to new healthcare delivery models that promote coordinated and patient-centered care. Importantly, the bill aims to maintain high standardswhether a patient is seeing a physician in an office or via telemedicine,” said American Medical Association PresidentSteven J. Stack, MD. “Telemedicine can strengthen the patient-physician relationship and improve access for patients with chronic conditions and limited access to quality care.”Source: AMA staff

“The Issue Is” is the SDSMA’s monthly update on key policy issues of importance to physicians.

Bipartisan Bill Would Expand Telemedicine

140

Member News

?If not, contact us to reach over 2,000 physicians!

CONTACT:Elizabeth Reiss, South Dakota Medicine

PO Box 7406, 2600 W. 49th Street, Suite 200Sioux Falls, SD 57117-7406

605.336.1965E-mail: ereiss@sdsma.org

Is

In Your Advertising Budget?

Legal Brief Highlight: Restrictive CovenantsSouth Dakota law generally restricts geographic and length of timeprovisions in employment agreements that prohibit former employees from competing with a former employer. Restrictivecovenants are unethical if they are excessive in geographic scopeor duration, or if they fail to make reasonable accommodation ofpatients’ choice of a physician.

The SDSMA has adopted the position of the AMA Council onEthical and Judicial Affairs that restrictive covenants restrict competition, disrupt continuity of care, and potentially deprive thepublic of medical services, and because of those reasons, the

SDSMA believes restrictive covenants should be discouraged inphysician employment agreements.

For more information, download the SDSMA legal brief RestrictiveCovenants at www.sdsma.org. Through the SDSMA Center forPhysician Resources, the SDSMA has developed more than 40legal briefs that are available to members. In addition, the Centerdevelops and delivers and programs for members in the area ofpractice management, leadership and health and wellness.Source: SDSMA staff

141March 2016

Member News

Physicians have until March 15 to apply for a hardship exemptionfrom the electronic health record (EHR) meaningful use financialpenalties for the 2015 program year. Those who don’t apply couldface up to a 3 percent cut in their Medicare payments in 2017 sincethe meaningful use program operates on a two-year look-back period. The good news is that exemptions will be granted broadlythis year.

The Centers for Medicare & Medicaid Services (CMS) has statedthat it will broadly grant hardship exemptions as a result of thedelayed publication of the Stage 2 meaningful use modificationsrule, which left physicians with insufficient time to report under themodified program requirements issued in late 2015.

This inclusive approach to hardship exemptions is a result of thePatient Access and Medicare Protection Act, passed just beforeCongress adjourned for the holidays, which directed CMS to makeAMA-supported changes to the previously limited exemptionprocess.

All physicians are encouraged to apply for the exemption. Evenphysicians who believe they met the requirements of the meaningful use program in 2015 can apply. Submitting an application for a hardship exemption will not prevent those whoqualify from receiving an incentive payment.

Applications must be submitted before 12 a.m. ET March 15. To getstarted, download an application from www.cms.gov. TheAmerican Medical Association website at www.ama-assn.org provides step-by-step instructions to help simplify the submissionprocess. New this year, individuals can apply on behalf of a groupof physicians.

While CMS has given a deadline for applications, it has not yet indicated when physicians will receive confirmation of theirexemption status.Source: AMA

Avoid Meaningful Use Penalties

The SDSMA Annual Conference is a perfect opportunity for organizations of all sizes to advertise their products and services tocurrent and potential customers. The 2016 Annual Conference willbe held on Friday, June 3, 2016 at the Hilton Garden Inn inDowntown Sioux Falls. As a sponsor or advertiser, you will havethe opportunity to market your technologies, services, pharmaceu-ticals and other products. This is a valuable opportunity to reachkey health care leaders from across South Dakota.

Diamond sponsors have the opportunity to attend the MembershipMixer and Awards Banquet on Friday evening to visit with

physician members. Sponsorship and advertising options are available in many varieties to meet the needs of all organizations.

Check out the all NEW sponsorship and advertising opportunities for 2016 at sdsma.org. The sponsor and advertiserregistration form along with a description of each sponsorship category and advertising option is available there. Complete theregistration form and reach South Dakota physicians. Those withquestions may contact Laura Olson at 605.336.1965 orlolson@sdsma.org.

2016 SDSMA Annual Conference Sponsorship and Advertising Opportunities

Don’t forget to send in your favorite scenic photo forSouth Dakota Medicine front cover consideration.

Send photos to ereiss@sdsma.org.

142

Continuing Medical Education events which are being held throughout the United States (Category 1 CME credit available as listed)

CME EventsMarch 2016 March 2016 March 2016March 9DermatopathologyConference/Pathology Grand Rounds AMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 9Internal Medicine Grand RoundsAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 16Internal Medicine Grand RoundsAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 16Surgery Grand Rounds: Striving forUtopia – The Uphill Battle for BetterSurgical EducationAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 16VA Tumor ConferenceAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 17Pediatric Grand RoundsAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 23Internal Medicine Grand RoundsAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 24Pediatric Grand RoundsAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 30Internal Medicine Grand RoundsAMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

March 31Pediatric Grand Rounds AMA PRA Category 1 Credit(s)™ availableRegister online: usdssom.learningexpressce.com

DO YOU HAVE A CME EVENT COMING UP? WOULD YOU LIKE TO HAVE IT LISTED HERE?Contact: Elizabeth Reiss, South Dakota Medicine,

2600 W. 49th Street, Suite 200, Sioux Falls, SD 57105 Phone: 605.336.1965Fax: 605.274.3274

Email: ereiss@sdsma.org

Don’t forget to send in your favorite scenic photo for

South Dakota Medicine front cover consideration.

Send photos to ereiss@sdsma.org.

CME Events

143March 2016

Physician Directory

PATHOLOGY

144

Classified Ads

?If not, contact us to reach over 2,000 physicians!

CONTACT:Elizabeth Reiss,

South Dakota MedicinePO Box 7406,

2600 W. 49th Street, Suite 200Sioux Falls, SD 57117-7406

605.336.1965E-mail: ereiss@sdsma.org

Is

In Your Advertising Budget?

SD State Penitentiary, Sioux Falls, SD

Family Medicine or Internal Medicine PHYSICIAN,PHYSICIANS ASSISTANT (PA), CERTIFIED NURSEPRACTITIONER (CNP)

Work in SDSP Health Services

Clinics seeing adult male inmate patients for generalphysical exams and care for chronic medical problemsEither contract or state employee options available.

• Large nursing staffs in both clinics.

• Criminal background check and drug screening required.

• Full or Part-time provider positions available

Contact: Kayla Tinker, DirectorSouth Dakota Department of Health/Correctional Health600 East Capitol, Pierre, SD 57501Phone: (605)773-2707E-Mail: Kayla.Tinker@state.sd.us

An Equal Opportunity Employer