Let Your Poster Speak for Itself Best Practices in Academic Poster Creation

1. Let Your Poster Speak for ItselfBest Practices in Academic Poster Creation Justin Roesch, MD, FACP Assistant Professor, Hospital Medicine

2. Objectives • Review essential elements of scientific and vignette posters • Discuss best practices of poster creation • Review posters and discuss: • Strengths and Potential Problems

3. What attributes make a visually appealing?

4. SWOT: Harnessing Resident Feedback to Drive Institutional Change University of New Mexico Implementing a SWOT analysis Background Results • The ACGME graduation survey is a valuable tool that is intended to improve the quality of the education provided to residents • However, the data only highlights broad areas requiring improvement rather than providing specific details • Program Evaluation Committees are often seeking new methods for identifying actionable results from the survey which they can address.   • Four sessions have been performed: 2 sessions were performed with Internal Medicine, 1 with Pediatrics and 1 with OB/GYN • Thematic strengths included identification of attending physicians that were education-focused or delivered high quality feedback. • Weaknesses included perceived reduction in education due to resident scheduling, need/want for additional board review sessions, and lack of feedback. • Specific actions residents suggested were the creation of a system to prevent scheduling difficulties, restructuring rounds to avoid duty hour issues, developing service agreements to standardize care, developing board-focused interactive sessions, and additional teaching on administration of feedback. What is a SWOT? • A business tool that gives a comprehensive look at a project using the following acronym • Strengths – Things you are currently doing well (i.e. teaching time, resident autonomy?) • Weaknesses – Areas that can be improved (i.e. lack of feedback, insufficient procedure numbers) • Opportunities – Ideas for future development (i.e. new rotations, faculty involvement) • Threats – Things out of your control which could cause problems (i.e duty hours, funding) Sample Data Conclusions • Using a resident-focused SWOT analysis to address areas of concern from the ACGME survey results is a valuable way to glean useful and actionable feedback. • SWOT analyses also provided granular detail of not only which areas are important to residents, but also generated interventions for the areas of concern and allowed for resident buy-in for these interventions. • This is a simple, easy to use method to focus feedback that can easily be performed by a new Chief Resident who may be unfamiliar or uncomfortable with running these sessions. Keys to a Successful SWOT • Residents need to feel like they can speak openly and honestly. Utilizing external facilitators may encourage unbiased discussion. • Focus each analysis on a specific issue, such as a single rotation or an educational conference. • Constructive feedback is key. Encourage them the use what they identified in the SWOT analysis to come up with ways the program can improve. • Most importantly, this is a tool to gather information. The ultimate success of this activity depends on using the issues identified in this analysis to improve your program.

5. General Rules • Prior to creating your poster you should: • Consider conference theme and review the conference website for Judging Criteria • Review the Rules/Logistic Requirements • Size of poster • How it will be displayed? • Who needs to be involved? Authors or acknowledgements? • What is the BOTTOM LINE point I am trying to convey?

6. Two Types of Posters Research/Innovation Poster Clinical Vignette Title Introduction History of Present Illness Hospital Course Family History Social History Pertinent Exam Findings Labs, Images, Studies Discussion Conclusion References Acknowledgements • Title • Introduction • Materials and Methods • Results • Discussion • Conclusion • References • Acknowledgements

7. Selecting a Clinical Vignette • Why is the case interesting? • Diagnostically Challenging • Novel Treatment • Novel Application of Ethics Principles • How will this help others? • What are the specific teaching points?

8. Vignette Abstract

9. Vignette Abstract • Case Description: • Use chronological order • Pertinent Hx/PE/Lab • Add normal values for uncommon lab: “free triiodothyronine 235 ng/dL (normal 55-172 ng/dL)” • Discussion: • What is the importance of your case? • How does it compare to previously reported cases? • What is the applicability to practice?

10. Best Practices: Visual Aesthetics • Visual Aesthetics • Legible Font and Size (85-72 point [title], 20-24 point [text]) • Tasteful Color Scheme • Use dark letters on white background • Not crowded with text • Rule: Should be able to read poster in < 8 minutes • Not too much “white” space

11. Best Practices: Organization • Organization • Clearly Labeled Sub-titles • Logical Flow = Left Right and Top to Bottom • Optimize Use of Figures • Figures graphically represent data = less time spent reading • Visually attractive and ‘draw-in’ audience attention • Use Arrows to Direct the Reader

12. CAN’T SEE, CAN’T PEE, CAN’T STAND LIKE ME University of New Mexico School of Medicine Autoimmune AUTONOMIC GANGLIONOPATHY (AAG) AUTONOMIC NERVOUS SYSTEM Case Presentation A 47-year-old Taiwanese male without significant past medical history presented with complaints of dizziness, decreased urination and diarrhea. On exam he was noted to be markedly orthostatic. The abdomen was slightly distended. After voiding, foley catheterization returned approximately one liter of residual urine. Laboratory evaluation was remarkable for hyponatremia. The patient was admitted for intravenous hydration with a presumptive diagnosis of dehydration secondary to gastroenteritis. Despite aggressive fluid resuscitation his orthostasis did not resolve. He could not tolerate sitting up for more than a few minutes as his systolic blood pressure would acutely drop to 50-60mm Hg. He also exhibited dry skin, dry mouth, dry eyes, blurry vision and poor heart rate variability. An extensive evaluation for causes of autonomic insufficiency did not reveal adrenal insufficiency, paraneoplastic syndrome, myasthenia gravis, Parkinson’s or cancer. A ganglionic acetylcholine receptor antibody test for autoimmune autonomic ganglionopathy was negative. Given the patient’s extensive negative evaluation and his constellation of symptoms consistent with autonomic failure, a diagnosis of autoimmune autonomic ganglionopathy was made. No benefit was noted after treatment with fludrocortisone and midodrine hydrochloride. Plasmapheresis and intravenous immunoglobin (IVIG) was initiated and the patient had significant symptomatic improvement. Discussion Autoimmune autonomic ganglionopathy (AAG) is a type of autonomic insufficiency that includes both parasympathetic and sympathetic dysfunction and is thought to have an immunologic basis. It may occur after a viral illness or with cancer, most commonly non-small cell lung cancer. AAG usually develops subacutely over days to weeks. Characteristic clinical features include gastrointestinal dysmotility and an abnormal pupillary response to light and accommodation. Serologic testing may be positive for an autonomic ganglionic acetylcholine receptor antibody, but a negative result does not exclude the diagnosis. Treatment is supportive and fludrocortisone and midodrine hydrochloride help with orthostatic hypotension. There is no definitive course-modifying treatment. Recovery after plasma exchange and IVIG therapy has been reported. Spontaneous recovery may also occur. Conclusions Review of this case may help practitioners recognize this rare form of autonomic insufficiency. • Background • AAG first described by Young et al. in 1969 • Auto-antibodies to the ganglionic AChR identified 10 years ago • AAG is a distinct disorder but may share many clinical features with other • types of autoimmune disorders that affect the ANS (paraneoplastic, acute • inflammatory demyelinating polyradiculopathy (Guillain-Barre), diabetic • autonomic neuropathy) • AAG is an acquired neurological disorder characterized by diffuse autonomic • failure • Sympathetic (orthostatic hypotension, anhidrosis) • Parasympathetic (dry eyes and mouth, fixed pupils, bladder and • sexual dysfunction) • Enteric (ileus, colic, diarrhea, and constipation) • Key distinction: AAG spares somatic nerve function • Pathophysiology • Alpha-3 subunit of the AChR is the target in AAG • AAG is an antibody mediated disorder caused by reversible disruption of fast • synaptic transmission in autonomic ganglia • Clinical Presentation • Mean age 52 years (22-82) with slight female predominance (60-65%) • Acute and subacute AAG can affect children, although they are uniformly • seronegative for ganglionic AChR antibodies) • Typically presents in previously healthy individual • May follow viral prodrome (upper respiratory or gastroenteritis) = 60% cases • No specific association, but Epstein-Barr virus most commonly reported • Constellation of tonic pupils with gastrointestinal dysmotility (70%) in the • setting of severe orthostatic hypotension(70%) is suggestive of AAG • Most common presentation is severe and subacute (66% cases) • 25% patients report neuropathic symptoms (tingling distal extremities) but • sensory and nerve conduction studies are normal • Diagnosis • AAG diagnosed on clinical grounds after excluding other etiologies • Up to 50% of patients with acute or subacute AAG have high antibody levels • High antibody levels correlate with severe phenotype and rapid onset • High antibody levels are specific for AAG and not found in other neurological • disorders • Sensitivity of the antibody is only around 50% • Patients may be seronegative • Autoimmune mechanism still postulated due to clinical similarity to • seropositive AAG • Some seronegative patients respond to immunomodulatory treatments • Cerebrospinal fluid analysis may show modest elevation in protein • Treatment • Decrease in antibody levels is associated with improvement • Typically not diagnosed for many months after patient presents • AAG is rare • Similarity with other forms of autonomic failure • Lack of routine diagnostic tools • Initial treatment is largely symptomatic (volume expansion, fludrocortisone, • erythropoietin, midodrine, lower extremity support hose, bowel and bladder • management, supplemental moisture agents for dry eyes and mouth, • pyridostigmine or other cholinesterase inhibitors) • In severe cases immunomodulatory treatment (corticosteroids, plasma • exchange, intravenous immunoglobulin as well immunosuppression with • azathioprine, mycophenolate mofetil or rituximab) • Long-term management needs to be tailored to the individual patient. Figure 1 - Anatomy of the Autonomic Nervous System • AUTONOMIC NERVOUS SYSTEM (ANS) • Controls involuntary or “autonomic” functions of the body • Typically divided into three components • Sympathetic (Craniosacral) • Parasympathetic (Thoracolumbar) • Enteric • Signals from spinal autonomic neurons synapse with ganglionic neurons • Ganglionic neurons send axons to innervate target organs (Figure 1) • Nicotinic acetylcholine receptors (AChR) are the same in sympathetic and parasympathetic ganglia (Figure 2) • Pentameric transmembrane complex (2 alpha ,3 beta subunits) • Ligand-gated ion channel • Fast synaptic transmission • Immunologically distinct from AChR at the neuromuscular junction • Summary Points • AAG is a severe, potentially treatable, form of antibody-mediated autonomic failure. • 2) AAG manifests as gastrointestinal dysmotility, abnormal pupillary light • response, bladder dysfunction, sicca complex, anhidrosis and orthostatic • hypotension. • 3) Ganglionic AChR antibodies are very specific for AAG and levels correlate with • disease severity. • 4)There are no proven therapies, but immunomodulatory treatments (plasma • exchange, intravenous immunoglobulin and immunosupressants) can be • considered for severe cases. • REFERENCES: • Vernino, S, et al. Autonomic ganglia, acetylcholine receptor antibodies, and autoimmune gangliopathy. Autonomic Neuroscience: Basic and Clinical. • 146 (2009) 3-7. • 2) Vernino, S, Winston, N. Autoimmune autonomic ganglionopathy. Front Neurol Neurosci. (26) 85-93, 2009. • 3) Iodice, V, et al. Immunotherapy for autoimmune autonomic ganglionopathy. Autonomic Neuroscience:Basic and Clinical. (146) 22-25, 2009. • 4) Vernino, S. Antibody testing as a diagnostic tool in autonomic disorders. Clin Auton Res. (19) 13-19, 2009. • 5) Vernino, S, et al. Autonomic ganglia: Target and novel therapeutic tool. Neurology. 70(20) 1926-1932, 2008. • 6) Schroeder, C, et al. Plasma exchange for primary autoimmune autonomic failure. New England Journal of Medicine. 353:1585-1590, 2005. • 7) Harrison's Principles of Internal Medicine, 17th edition. Fauci, A, et al. McGraw-Hill Companies, Inc. 2008. • 8) Adams and Victor’s Neurology, 9th edition. Samuels, M.A. McGraw-Hill Companies, Inc. 2009. Figure 2 – Nicotinic AChR a)Muscle AChR b) Ganglionic AChR c) Transmembrane AChR receptor, antibodies recognize extracellular alpha subunits (Reproduced from Vernino, S., Winston, N. Autoimmune autonomic ganglionopathy. Front Neurol Neurosci. (26) 85-93, 2009.)

13. Best Practices: What to Avoid • Catchy (but vague) Titles • Photos/figures that don’t add to understanding • Small Figures with legends written in size 8 font • Missing Conclusions • Conclusions are vital, but should be succinct

15. The University of New Mexico School of Medicine Feedback Initiative University of New Mexico Hospital What do participants say? Background & History Feedback Concept Based on insights from the Accreditation Council for Graduate Medicat Education (ACGME )survey, the Feedback Initiative was created in 2010 with the goal of improving both the quality and quantity of feedback given and received across the UNM School of Medicine. The Feedback Initiative (FI) is based on the Harvard model termed ‘Debriefing With Good Judgment.’ FI is under the guidance of the Office for Medical Educator Development (OMED). “I would like to make feedback part of our culture” “Interactions and role play really helped me learn the concepts in this workshop. Allowing extra time for discussion was extremely helpful!” “I am going to incorporate Feedback With Good Judgment more into my practice” “I am going to keep a list of feedback items on my patient list (love this!)” Feedback With Good Judgment Observation Advocacy FEEDBACK GIVER Inquiry Feedback Initiative Goals What We’ve Accomplished To educate all faculty, trainees and students in order to improve the amount and frequency of feedback given across the institution 2) To educate all faculty, trainees and students in order to improve the quality of feedback given across the institution 3) Create a culture of feedback, which fosters collaboration and professional development to improve the care of our patients. FEEDBACK RECEIVER • Residents As Educators Conference since 2010 • Harvard Training for >20 faculty members in 2013 • Residency Program SWOT analyses: Pediatrics, ObGyn, Internal Medicine • GME Housestaff orientation since June 2014 • Publication AAIM Insight September 2014 • OMED Workshops since July 2015 • Regional presentation at the Society for General Internal Medicine Conference October 2015 • At least 4 yearly “On demand” presentations Best Practices of Feedback • *Does NOT use • ‘sandwich’ method What can we do for you? • OMED Workshop 3 times per year • Department visitations to conduct 1, • 2, or 3 hour workshops • SWOT (Strengths, Weaknesses, • Opportunities, Threats) analyses • Feedback consultations to any • department/residency/other program Involved Faculty & Staff Leadership Patrick Rendon, MD Justin Roesch, MD David Stromberg, MD Faculty Lanier Lopez, MD Darra Kingsley, MD Ann Morrison, MD Steve McLaughlin, MD John Rask, MD Pamela Arenella, MD Craig Timm, MD Gary Smith, PhD Edward Auyang, MD Key Staff Elizabeth Sanchez Jamie Tenorio Contact Information HSC-Feedback@salud.unm.edu

16. Poster Pearls • “10x10 Rule” • Avoid Migraine-Inducing Auras in your color scheme selection • Use Professional Templates • Poster can be printed on canvas so it can be packed

17. The University of New Mexico School of Medicine Feedback Initiative University of New Mexico Hospital What do participants say? Background & History Feedback Concept Based on insights from the Accreditation Council for Graduate Medicat Education (ACGME )survey, the Feedback Initiative was created in 2010 with the goal of improving both the quality and quantity of feedback given and received across the UNM School of Medicine. The Feedback Initiative (FI) is based on the Harvard model termed ‘Debriefing With Good Judgment.’ FI is under the guidance of the Office for Medical Educator Development (OMED). “I would like to make feedback part of our culture” “Interactions and role play really helped me learn the concepts in this workshop. Allowing extra time for discussion was extremely helpful!” “I am going to incorporate Feedback With Good Judgment more into my practice” “I am going to keep a list of feedback items on my patient list (love this!)” Feedback With Good Judgment Observation Advocacy FEEDBACK GIVER Inquiry Feedback Initiative Goals What We’ve Accomplished • To educate all faculty, trainees and students in order to improve the amount and frequency of feedback given across the institution • 2) To educate all faculty, trainees and students in • order to improve the quality of feedback given • across the institution • 3) Create a culture of feedback, which fosters • collaboration and professional development to • improve the care of our patients. FEEDBACK RECEIVER • Residents As Educators Conference since 2010 • Harvard Training for >20 faculty members in 2013 • Residency Program SWOT analyses: Pediatrics, ObGyn, Internal Medicine • GME Housestaff orientation since June 2014 • Publication AAIM Insight September 2014 • OMED Workshops since July 2015 • Regional presentation at the Society for General Internal Medicine Conference October 2015 • At least 4 yearly “On demand” presentations Best Practices of Feedback • *Does NOT use • ‘sandwich’ method What can we do for you? • OMED Workshop 3 times per year • Department visitations to conduct 1, • 2, or 3 hour workshops • SWOT (Strengths, Weaknesses, • Opportunities, Threats) analyses • Feedback consultations to any • department/residency/other program Involved Faculty & Staff Leadership Patrick Rendon, MD Justin Roesch, MD David Stromberg, MD Faculty Lanier Lopez, MD Darra Kingsley, MD Ann Morrison, MD Steve McLaughlin, MD John Rask, MD Pamela Arenella, MD Craig Timm, MD Gary Smith, PhD Edward Auyang, MD Key Staff Elizabeth Sanchez Jamie Tenorio Contact Information HSC-Feedback@salud.unm.edu

18. The Presentation: Preparation • Know the Judging Criteria for Presentation • Usually 4 minutes of oral presentation, 6 minutes of questions • Prepare 2 minute a synopsis of the poster • Anticipate Questions You May Face • If you can’t answer= “That’s a great question, and may be a great future direction of research…” • Practice with colleagues • “What could I improve?” • “What didn’t make sense?”

19. The Presentation: Delivery • Know Your Poster • Familiar with content, ‘geography’, and references • Prepare answers for tough/controversial questions or inconsistencies • Engage Your Judges • “May I tell you a bit more about my vignette/research/QI project…” • Maintain Eye Contact • Thank the Judge

20. Examples Take 2 minutes to individually review each poster Annotate comments Bring it back to the large group

21. A RARE CAUSE OF RECTAL PAIN University of New Mexico School of Medicine Extrapulmonary Tuberculosis Anorectal Tuberculosis Case Presentation A 64 year-old Hispanic male without a significant past medical history presented with a complaint of “rectal pain.” The pain was worse with bowel movements and as a result the patient reported a fear of eating. The patient denied any associated nausea, vomiting, fevers, chills, melena or bright red blood per rectum. He did report a two week history of a dry nonproductive cough. Additionally he had a 50 pack-year smoking history and multiple sexual partners without consistent use of protection. On examination the patient was hypotensive with a blood pressure of 80/60 mmHg, tachycardic and had a decrease in weight from 60kg to 45kg in less than 6 months. Breath sounds were clear bilaterally and rectal examination revealed a 4 cm by 4 cm rectal ulceration. Stool exam was brown and guiac positive. Laboratory examination revealed a mild leukocytosis with normal differential and chest radiology showed diffuse patchy opacifications. Given the patient’s social history, weight loss and chest radiology findings there was concern for human immunodeficiency virus (HIV) infection and Pneumocystis jiroveci pneumonia. He was started on trimethoprim-sulfamethoxazole and admitted for further evaluation. The patient’s hypotension responded to fluids. He was evaluated by gastroenterology and infectious disease services. HIV testing was negative. A new working diagnosis of rectal malignancy with lymphangitic spread to the lungs was made. The patient underwent colonoscopy with biopsies. Sigmoid ulcerations were also noted. Rectal biopsies revealed caseating granulomas and 2+ acid fast bacilli (AFB). Induced sputum later showed 4+ AFB. The patient was placed in isolation and started on a four drug regimen for treatment of miliary tuberculosis (TB).  Discussion National TB surveillance data reveals that almost one-fifth of TB cases in the United States are extrapulmonary. Gastrointestinal TB is a diagnostic challenge in the absence of a pulmonary infection. Only 2% of gastrointestinal TB cases present after 60 years of age. Most commonly the intestinal lesions are ulcerative. Symptoms include abdominal pain, diarrhea, weight loss, fever, melena and rectal bleeding. Rectal lesions usually present as anal fissures, fistulas or perirectal abscesses. It is essential to distinguish TB enteritis from inflammatory bowel disease such as Crohn’s disease as the initiation of immunosuppressive therapy in a patient with tuberculosis can lead to dissemination. Our patient presented with rectal involvement and likely had disseminated TB. Classic miliary TB is defined as millet like seeding of TB bacilli in the lung and is seen in 1-3% of all TB cases. It can mimic many diseases and in some cases up to 50% are diagnosed ante mortem. A high index of clinical suspicion is important as early diagnosis and treatment correlate with improved outcomes. Conclusions Rectal tuberculosis is rare. A case of undiagnosed rectal TB presenting as an acute perianal abscess is reported. Lack of suspicion for rectal TB in such a case can lead to delays in diagnosis and significant risks of exposure to healthcare personnel. • Incidence: • One-third world population is infected with TB • Extrapulmonary forms of TB are present in 10-15% of all cases of TB, but can be • found in 40 to 60% of patients with concomitant HIV infection • Gastrointestinal (GI) tract is the 6th most frequent site of extrapulmonary TB • (From most to least common: lymphatic, genitourinary, bone/joint, miliary, • meningeal, gastrointestinal) • Anorectal TB compromises less than 2% of cases of abdominal TB • Only 3 cases of anorectal TB reported in the last 22 years in the United Kingdom • Presentation: • Fourth decade of life with a 4:1 male predominance • Symptoms: weight loss (40-90%), abdominal pain (80-95%), fever (40-70%), • change in bowel habits (50%), anorexia and malaise • Hematochezia (due to mucosal trauma by stool) is common (88%) • Massive hemorrhage is rare due to obliterative endarteritis caused by TB • Pathogenesis: • TB bacilli can reach the GI tract by four different mechanisms: 1) hematogenous spread, 2) ingestion of bacilli from sputum or unpasteurized milk from infected bovine, 3) direct spread from adjacent organs and 4) lymphatic spread from infected lymph nodes • Pathology: • GI TB can involve any part of the GI tract from mouth to anus • Most common site of GI involvement is the ileocecal region due to abundance of • lymphoid tissue (M cells and Peyer’s patches) • Ulcers are superficial and do not penetrate the muscularis • They tend to be transversely oriented versus the longitudinal and serpiginous • appearance of Crohn’s ulcers • There are 4 morphological types of anorectal TB lesions: ulcerative (most common), • verrucous, lupoid and miliary • The ulcerative form typically presents as a superficial ulceration with a hemorrhagic • necrotic base that is covered with thick purulent secretions of mucous • Diagnosis: • Chest radiology shows pulmonary lesions <25% of cases • Colonoscopy requires multiple biopsies from the ulcer edge • Cultures are positive in 40% of biopsies • Acid-fast bacilli (AFB) staining is variable and polymerase chain reaction (PCR) • testing for TB DNA is helpful in difficult to diagnose cases • Treatment: • Conventional anti-TB therapy for 6 months (99% cure rate) although some expand • to 12-18 months (94% cure rate) • Surgery is indicated only if there is a complication. Most commonly it is intestinal • obstruction (15-60%), fistula (25%), perforation (15%) and rarely hemorrhage Prevalence • Globally prevalence of tuberculosis (TB) infection is estimated at 32% • The percentage of US cases that occur among foreign-born persons is • increasing (53% in 2003) • Extrapulmonary TB seen in over 50% of patients with concurrent AIDS • Risk of extrapulmonary TB increases with immunosuppression Figure 1 – Prevalence of all forms of tuberculosis per 100,000 inhabitants, 2005 (Source: World Health Organization) Clinical Clues Suggesting Extrapulmonary TB • Ascites with lymphocyte predominance and negative bacterial cultures • Chronic lymphadenopathy (especially cervical) • Cerebral spinal fluid lymphocytic pleocytosis with elevated protein and • low glucose • Exudative pleural effusion with lymphocyte predominance, negative • bacterial cultures, and pleural thickening • Joint inflammation (monoarticular) with negative bacterial cultures • Persistent sterile pyuria • TB-endemic country of origin • Unexplained pericardial effusion, constrictive pericarditis or pericardial • calcification • Vertebral osteomyelitis involving the thoracic spine SUMMARY POINTS Gastrointestinal tuberculosis is a diagnostic challenge in the absence of pulmonary infection. It can involve any part of the alimentary tract from the mouth to anus. Include evaluation for anorectal tuberculosis in the management of recurrent anorectal fistulas, ulcers and abscesses. Histological demonstration of chronic granulomatous inflammation with caseation is pathognomonic of tuberculosis. In most instances superficial biopsies may not reveal the bacilli and only 36% of cultures yield a positive result. Consider PCR testing. Anorectal tuberculosis usually responds well to anti-tubercular drugs and these patients seldom require any further surgical intervention. A high suspicion leads to prompt diagnosis and treatment and avoids unnecessary exposure to health care staff. Figure 3 - Chest CT scan later in the admission Figure 2 - Chest X-ray on initial presentation Extrapulmonary Manifestations Tuberculous Lymphadenitis Pleural Tuberculosis Skeletal Tuberculosis Central Nervous System TB Abdominal Tuberculosis Genitourinary Tuberculosis Gastrointestinal Tuberculosis Milliary Tuberculosis Tuberculous Peritonitis TuberculousPericarditis References: 1) Samarasekera, DN, Nnayakkara, PR. Rectal tuberculosis: a rare cause of recurrent rectal suppuration. Colorectal Disease. 2008: 846-848. 2) Kamani L, et al. Rectal tuberculosis: the great mimic. Endoscopy 2007: E277-E228. 3) Golden, MP, Vikram, HR. Extrapulmonary tuberculosis: an overview. American Family Physician 2005: 1761-1768. 4) Sharma, MP, Bhatia, V. Abdominal tuberculosis. Indian Journal of Medical Research 2004: 305-315. 5) Saenz, EV, et al. Colonic tuberculosis. Digestive Diseases and Sciences. 2002: 2045–2048. 6) Subnis, BM, et al. Primary tuberculosis of rectum mimicking malignancy: a case report. Bombay Hospital Journal. 2008: 283-285. Acknowledgements Michael Gilles, MD – Department of Gastroenterology, University of New Mexico Mark Hubbell, MD – Department of Pathology, University of New Mexico Figure 4 – Colon, sigmoid ulcer Figure 5 – Sigmoid ulcer biopsy, submucosal caseating granuloma

22. Pyogenic liver abscess vs. Hepatocellular carcinoma, the challenge of diagnosis without a biopsy. University of New Mexico Health Sciences Center, Albuquerque, NM, USA BACKGROUND CASE DESCRIPTION According to current guidelines, a mass found incidentally or on screening in the setting of a patient with known hepatitis B or cirrhosis of other etiology is likely to be HCC [4]. Whenever a liver lesion of more than 1 cm is present in the right clinical setting, this should be either evaluated by MRI or CT with contrast and if the appearance is typical of HCC, then no further investigations are required [4]. Unfortunately in our case the initial CT was concerning but still equivocal for HCC, in such cases the next approach can be either pursuing another imaging modality or trying to biopsy the lesion. But after consultation with interventional radiology it was deemed that the risk of the percutaneous biopsy might be too elevated since the patient had an elevated INR and thrombocytopenic , therefore the second imaging modality was chosen. Another widely used tool is the serum marker AFP, it is a glycoprotein that is normally produced during gestation by the fetal liver and yolk sac, the serum concentration of which is often elevated in patients with HCC. However the serum levels do not correlate well with other clinical features of HCC, such as size, stage, or prognosis. It could be elevated in other conditions such as pregnancy, gonadal origin neoplasms and other GI malignancies. It is accepted that a level ˃500mcg/L in a high risk patient is diagnostic of HCC [5]. However over 40% of cases have normal levels [6]. Also a variant of HCC called fibrolamellar carcinoma have normal serum levels generally. Still its use can be practical since its Sensitivity 41-65 %, specificity 80-94 % positive likelihood ratio 3.1 - 6.8 and negativelikelihood ratio 0.4 - 0.6 with a cutoff of >20 mcg/L [7]. Applying this information into our case the level of AFP was measured on admission but was reported as normal, therefore still HCC could not be ruled out since the sensitivity of the test is not high. CONCLUSION A liver mass in a cirrhotic liver should always raise the concern for hepatocellular carcinoma (HCC), and expert guidelines state that diagnosis can be made with imaging alone in some settings. The causes of focal liver lesions are diverse, and may range from benign lesions with an indolent clinical course to aggressive malignant tumors. They are common findings as a result of the increasing use of cross-sectional imaging techniques in patients with nonspecific abdominal complaints. Clinical evaluation and noninvasive radiologic imaging are critical for decision making in the management of most patients with liver lesions [1]. Our case illustrates that care must be taken to consider other etiologies before making that diagnosis. A 57 year old man with alcoholic liver cirrhosis came to the ED complaining of 1 month of severe, intermittent abdominal pain with associated subjective fever and chills. A CT abdomen on admission reported 2 ill-defined hypodense liver lesions concerning for HCC (left image). In the setting of liver cirrhosis and a hepatic mass, work up for HCC was initiated, including an AFP which was later found to be normal. IR was consulted for possible biopsy, however because the patient had an elevated INR and thrombocytopenia it was deferred and a triple phase MRI was instead recommended to further evaluation. Infection was initially lower on the differential due to lack of fever and normal WBC. On hospital day 2 one of the BCXs from admission revealed Streptococcus viridians (later updated to Strep milleri). On hospital day 3, fevers, tachycardia and leukocytosis developed. An abscess was now more likely. The patient was initially monitored without antibiotics, but after the positive culture and the episode of fever, he was started on ceftriaxone and a second set of BCX were drawn which later revealed the same organism. The MRI showed two rim enhancing lesions in the right hepatic lobe which in the setting of infectious symptoms, were favored to represent abscesses (right image). ID was consulted and recommended 6 weeks of IV ceftriaxone. A TEE showed no evidence of endocarditis. A repeat CT showed the masses to be decreased in size and the patient was discharged with Clindamycin 300mg TID for an additional month. His last CT continued to show evidence of improvement and he was clinically improved as well, so clindamycin was discontinued and he was discharged from the Infectious Disease clinic. By following these recommendations, our patient who had the common risk factors and worrisome radiological findings of HCC was spared from an invasive procedure and negative impact in his quality of life by being diagnosed with cancer. Other factors that contributed to pursue another diagnosis was obtaining blood cultures on admission, which is important to consider in the setting of a possible septic picture. All these was achieved with out obtaining a biopsy or culture from the mass, which even in the setting of an abscess would be important to consider. However the therapy was deemed appropriate since subsequent CT scans showed regression of the abscess. DISCUSSION A mass lesion seen in a patient with hepatitis B or C infection, particularly when associated with features of chronic liver disease, should raise the threshold for suspicion of a malignancy, such as hepatocellular carcinoma (HCC) [1]. Our patient came to the ED complaining of vague symptoms of abdominal pain and had concerning risk factors that makes a malignancy higher in the differential diagnosis. The initial signs and symptoms are typically indolent and advance lesions may have mild to moderate upper abdominal pain, weight loss, early satiety, or a palpable mass in the upper abdomen [2]. Theoretically the anatomopathological assessment is the gold standard for the diagnosis of any liver mass, however given the invasiveness and procedural risks of the intervention is not the initial tool for the diagnosis, specially with accessible imaging modalities such as CT and MRI or tumor markers such as Alpha-Fetoprotein (AFP). In a setting such as our patient, a contrast CT scan of the liver and/or magnetic resonance imaging (MRI) study is often the initial diagnostic test. In patients with cirrhosis, any dominant solid nodule that is not clearly a hemangioma should be considered a HCC unless proven otherwise  [3]. WHY THIS CASE MATTERS? Reminds the clinician which risk factors are concerning for a liver malignancy such as HCC but still having in mind that other differential diagnosis exist. Provides the primary care provider in the outpatient setting the guidelines to work up a liver mass found incidentally on abdominal imaging such as ultrasound, CT or MRI. Demonstrates that HCC can be diagnosed without the need of pathological confirmation, since most of the patients have certain degree of coagulopathy that can put them at periprocedural risk of bleeding among others. REFERENCES: 1. Alan Bonder, NezamAfdhal, Evaluation of Liver Lesions, Clinics in Liver Disease, Volume 16, Issue 2, May 2012, Pages 271-283, ISSN 1089-3261 2. Kew MC, Dos Santos HA, Sherlock S. Diagnosis of primary cancer of the liver. Br Med J 1971; 4:408. 3. Gogel BM, Goldstein RM, Kuhn JA, et al. Diagnostic evaluation of hepatocellular carcinoma in a cirrhotic liver. Oncology (Williston Park) 2000; 14:15. 4. Bruix J, Sherman M, American Association for the Study of Liver Diseases. Management of hepatocellular carcinoma: an update.Hepatology 2011; 53:1020. 5. Wu JT. Serum alpha-fetoprotein and its lectin reactivity in liver diseases: a review. Ann Clin Lab Sci 1990; 20:98. 6. Chen DS, Sung JL, Sheu JC, et al. Serumalpha-fetoprotein in theearlystage of human hepatocellular carcinoma.Gastroenterology 1984; 86:1404. 7. Gupta S, Bent S, Kohlwes J. Test characteristics of alpha-fetoprotein for detecting hepatocellular carcinoma in patients with hepatitis C. A systematic review and critical analysis. Ann Intern Med 2003; 139:46.

23. Post-operative pain management in an elderly, opioid-tolerant patient undergoing initiation of hemodialysis. Division of Hospital Medicine, University of New Mexico, Albuquerque, New Mexico Opioids for ESRD Comparison World Health Organization (WHO) Analgesic Ladder • Hydromorphone: Preferred short acting, hepatic metabolism, dialysis removes 40-55%. • Methadone: Preferred long acting (when clinician experienced in prescribing). Hepatic metabolism, dialysis removes 15%. Monitor for QT prolongation. • Fentanyl: Preferred for chronic pain, avoid if opioid naïve. Deliver transdermal for chronic use or IV for acute pain. Hepatic metabolism into inactive products. Low dialysis clearance. • Oxycodone: Primarily hepatic metabolism but up to 19% of parent drug excreted in urine. Accumulates if dosed regularly. Use with caution. Dialysis removes 32-52%. • Tramadol : Hepatic metabolism into active metabolites (95% renally excreted), minimally cleared by dialysis. • Buprenorphine: Strong and potentially useful but minimal studies. • AVOID codeine, hydrocodone, meperidine, morphine and tapentadol. Discussion References • Over 58% of CKD patients are affected by pain with approximately 49% in the moderate to severe range. Higher rates of depression, insomnia, and irritability are common. Those with poor pain control are more likely to consider stopping dialysis. The WHO analgesic ladder can guide pain management, with some adjustments for ESRD: • Chronic pain complicates acute pain • Dose adjustments are often needed • Peripheral nerve block if possible • Acetaminophen for mild pain • Add opioids for moderate/severe pain • Consider non-opioid adjunctive drugs • Avoid NSAIDs Conclusions • Treat chronic pain in dialysis patients to prevent misdiagnosis, avoidable pain, and complications. • Fentanyl and hydromorphone are the safest opioids for the renally impaired. Use oxycodone with caution. • Do a thorough medication reconciliation. • Utilize your state’s PMP. CASE PRESENTATION References Davison, S., (2007). The prevalence and management of chronic pain in end-stage renal disease. Journal of Palliative Medicine, 10(6), 1277-1287. Koncicki, H., Brennan, F., Vinen, K., & Davison, S. (2015). An approach to pain management in end stage renal disease: Considerations for general management and intradialytic symptoms. Seminars in Dialysis, April 2015, 1-8. Qutaiba, T., & Bellingham, G. (2015, Jan-Mar). Postoperative pain management in patients with chronic kidney disease. J AnaesthesiolClinPharmacol, 31(1): 6-13. • Chronic pain is common in end stage renal disease (ESRD) and requires careful management prior to and at the time of hemodialysis initiation, particularly when the patient is undergoing a simultaneous surgical intervention. • A 69-year-old diabetic male with chronic kidney disease (CKD) stage V was admitted for volume overload, initiation of hemodialysis, and previously scheduled amputation of a gangrenous toe. • Next day he developed severe delirium with agitation. • Delirium was attributed to hydromorphone intoxication • Intravenous medications were discontinued • Was started on scheduled oxycodone every 6 hours • Delirium and agitation waxed and waned over the next several days, delaying and at times precluding medical therapy: medication refusals, shorter dialysis sessions, and delayed consent for recommended below the knee amputation (BKA). • Exam was notable for hyperactive delirium as well as a poorly healing surgical wound of left foot • Chemistries, complete blood count, thyroid function tests, serum ammonia, blood cultures, chest radiograph, computed tomography of the head, and lumbar puncture were all nondiagnostic • The New Mexico Prescription Monitoring Program (PMP) report for controlled substances was reviewed, and a prescription for acetaminophen-oxycodone 325-10 milligrams (120 tabs monthly) was discovered. Monthly refills suggested chronic opiate use with delirium due to uncontrolled pain after oxycodone was dialyzed off. • Was started on a fentanyl patch for chronic pain • IV hydromorphone was restarted for breakthrough pain • His orientation and agitation rapidly improved • He regained decisional capacity and consented to surgery • Eight days after his BKA, he continued to be oriented and participating fully in his medical decisions. Pain management consisted of a fentanyl patch 75 micrograms per hour with risperidone and trazodone at bedtime for sun-downing behaviors.

25. Questions?

26. Presumed vs Confirmed Full Code University of New Mexico School of Medicine, Albuquerque A PATIENT’S STORY - DOES THIS SOUND FAMILIAR? Mr. Adams is a 70 yo man admitted to the hospital for altered mental status at 2AM. He has never been a patient at this hospital, cannot provide his story, and there are no family members with him. On the admission orders the patient is listed as FULL CODE. The patient is passed off to a daytime team. Over the course of he next 3 days, the family arrives and is bedside, and work up and therapies continue with some improvement in his mental status. On Day 3 the patient experiences a PEA arrest and the team begins resuscitation efforts. The family intervenes and shows paperwork that has been present for the last day at bedside stating the patient is DNR. The code is halted after significant distress to family. On review of the records, a code status note was not written and no information about code status was mentioned in the H&P. The covering team and nurses on the floor state that they assumed that the patient was full code, and that a discussion took place, due to the order placed stating “FULL CODE”. Description Purpose • Actions undertaken by the Task Force over a 2 year period included the following quality improvement measures: • Revision of the hospital Code Status Policy: • “All adult admissions will have a code status discussion, identification of a surrogate decision maker, and a code status note written. Code status orders are written for all adult inpatients and include the options of Presumed Full Code (for patients with whom a discussion cannot take place on admission), Confirmed Full Code (after discussion takes place with patient or surrogate), or DNR (eliminating “partial code” status orders)”. • 2. Process Improvements included: • a. Modification of existing orders and order sets in EMR • b. Development of standardized templates for code status discussion and surrogate decision maker identification notes (see below) • c. Revision of patient handouts about Advance Directives in literacy appropriate language • d. Education for physicians about “how to have a code status discussion” • e. Hospital-wide education to all staff about these changes At the University of New Mexico (UNM), an academic safety net hospital, a multidisciplinary Advance Directives Task Force formed to improve patient care at end of life. An initial survey found that <2% of inpatients had Advanced Directives (ADs). The goals of the task force were: a. To improve access to and completion of ADs, and b. Clarify patients’ wishes regarding CPR Background • Problems with Advance Directives (ADs) • ADs are rarely completed in outpatient and inpatient settings • Patients’ preferences regarding code status are often not elicited, or delayed to when a patient cannot participate or there is a crisis • Physicians do not provide adequate information to allow patients to make informed decisions about code status • Providers inappropriately extrapolate DNR orders to limit other treatments (such as artificial nutrition, ICU admission, etc.)  • Most hospitals default to “Full Code” as the status for patients admitted, particularly in patients with whom a code status discussion cannot or has not taken place. In many cases, confirmation of “Full Code” does not occur later when these discussions become possible. • These problems can result in patients receiving care they • would not wish or choose. Conclusions • Hospital Medicine needs to take a more proactive role in ensuring that patients make informed decisions and receive all and only the care they desire.  • 2. We submit these standards we hope to be adopted by other institutions including: • a. the use of ‘presumed’ and ‘confirmed’ code statuses • b. the expectation to have code status discussions on all admissions • c. identification of surrogate decision maker • d. increased education to hospitalists on code status discussions

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