United States

2022 AMA Research Challenge

A rare case of anti-tubercular drug induced cardiomyopathy

Truth and Responsibility
“Truth and Responsibility” is a call to reimagine anthropology to meet the demands of the present moment. The imperative to bear witness, take action, and be held accountable to the truths we write and circulate invites us to reflect on our responsibility in reckoning with disciplinary histories, harms, and possibilities. To whom are we giving evidence and toward what ends? For whom are we writing? To whom are we accountable, and in what ways? We are thrilled to announce the theme of the 2021 AAA Annual Meeting to be held in Baltimore, MD: Truth and Responsibility.

Many consider anthropology to be a holistic social science dedicated to cross-cultural understanding as a way to reduce bigotry and more fully comprehend “what it means to be human.” Others push against this readily circulated origin story, arguing that “human” remains a highly contested, political category—evident as the presumed set of rights and protections associated with the “human” continue to be stripped away violently in the communities in which some of us live and work. Which violent histories and epistemologies must anthropologists take responsibility for in telling truth(s) about the discipline’s development? How do the dual histories of settler colonialism and slavery continue to influence anthropological thought and practices? In these political times, how can anthropologists throughout the globe work to secure a capacious, progressive vision of the human? How might movements for anti-racism, decoloniality, queer liberation, and healing such as #BlackLivesMatter, #ProtectMaunaKea, and #MeToo push a future anthropology out of the ashes of the anthropological past? Finally, what are the limits and possibilities of the anthropological imagination?

Across subfields, we find truths in patterns of human behavior, language, evolution, and cultural worlds. Industry-positioned anthropologists do this by extending the boundaries of the discipline not as an administrative solution to job shortages but as a source of intervention and knowledge production. Increasingly, anthropologists who make use of the scientific method question how status and identity help to decide which facts come to represent truth. How might quantitative researchers use our methods to identify patterned truths, and what responsibility do we hold in challenging conventional wisdom about these patterns? What responsibility do we have to both our colleagues and larger publics, to push toward increased transparency and ethical grounding in our data collection, analysis, and presentation?

Pedagogy is a key medium for the communication of anthropological truths. Which (and whose) truths are foregrounded in our curricula? What are the possibilities for a liberatory pedagogy in a precarious, “post-truth” era? Conferences, museums, organizing spaces, and classrooms are sites where pedagogy and various forms of communication can help us interrogate the performativity of truth. How might anthropologists conceive of truth performances? Might visual, aural, and choreographic performances during AAA sessions offer anthropologists alternative genres for truth-telling and truth-making that provoke discussions about responsibility?

In accordance with the urgency of the year’s theme, the questions posed in this call for papers do not have easy answers. The hope is that those who submit proposals will take up these questions and engage in collective thinking and imagining about the truths we hold, the truths we challenge, and the responsibilities we bear in co-creating a free and more equitable world. All panel proposals should have a statement about how the panel has incorporated the goals of equity, diversity, and inclusion, and/or analysis of power.

Executive Session proposals have already been selected and speak directly to the theme “Truth and Responsibility.” To practice the critical reflexivity this call for papers invites, we asked that Executive Session submissions explicitly address the diversity of session participants, such as organizational/institutional affiliation, career stage, race, ethnicity, disability, sexuality, class, religion, national identity, and gender. Proposals for Executive Sessions that demonstrated a commitment to equity and inclusion and/or a clear analysis of power (i.e. anti-imperialist, anti-white supremacist, decolonial, anti-ableist, feminist, anti-transphobic, anti-xenophobic, etc) were given priority. We are excited to be in conversation with residents of the Baltimore region and look forward to the discussions, performances, and actions generated by the dynamic group of anthropologists attending the 2021 AAA Annual Meeting.

AAA Annual Meeting 2021

“Truth and Responsibility” is a call to reimagine anthropology to meet the demands of the present moment. The imperative to bear witness, take action, and be held accountable to the truths we write and circulate invites us to reflect on our responsibility in reckoning with disciplinary histories, harms, and possibilities. To whom are we giving evidence and toward what ends? For whom are we writing? To whom are we accountable, and in what ways? We are thrilled to announce the theme of the 2021 AAA Annual Meeting to be held in Baltimore, MD: Truth and Responsibility.

poster

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#### Event Details
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Ricardo Correa, MD, EdD
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Stephanie Strohbeen, MD
 
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Jessica Li, MD/PhD Candidate
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Charles Lopresto, DO

### Sponsor
AMA would like to thank Laurel Road for sponsoring a $10,000 grand prize for the winner of the AMA Research Challenge. Laurel Road is not involved in the judging or scoring process to select the winner. The winner will be announced on Dec. 7 during the AMA Research Challenge finals. Payment of the grand prize will be directly from Laurel Road. See the AMA Research Challenge Official Rules for terms and conditions.

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Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


Abstract Title: 
A Rare Case of Infective Endocarditis caused by Serratia marcescens

Background: 
Serratia marcescens is a gram-negative bacillus that usually causes respiratory and CNS infections but it rarely can cause infective endocarditis.

Case Presentation: 
A 62-year-old male with PMH of intravenous drug use and Hepatitis C presented to the ED with palpitations and back pain for three weeks with no reported fevers. In the ED, his vitals were: temperature 103.9° F, BP 105/72, HR 125, RR 20 and O2 saturation 100% on room air. The remainder of his examination revealed bilateral subconjunctival hemorrhages and multiple track marks; there were no neurological deficits, petechiae, or murmurs. Laboratory studies revealed WBC 12.82, bandemia of 13%, and lactic acid 4.1. An MRI brain revealed scattered acute infarcts; subsequent spinal MRIs were negative for abscesses. He was admitted for sepsis possibly secondary to endocarditis and started on broad spectrum antibiotics; an initial TTE was negative for vegetations, and blood cultures later grew S. marcescens. The patient subsequently developed an intermittent AV block. Repeat TTE revealed a linear echo-density on the aortic leaflets; TEE showed a 2cm vegetation on the aortic valve with perforation. He was transferred to a tertiary center for further care; he underwent aortic valve replacement, which was complicated by aortic root rupture. He also developed sick sinus syndrome and required a pacemaker. The remainder of his hospitalization was unremarkable and he was discharged on a prolonged antibiotic course.

Discussion: 
Infective endocarditis with S. marcescens is rare; some studies report only 0.14% of IE cases are caused by Serratia. Although IV drug users typically have higher rates of right-sided valvular endocarditis, S. marcescens tends to involve left-sided valves. S. marcescans is rapidly progressive. Typical symptoms include fever, myalgias, or dyspnea. Exam findings can include cardiac murmurs, splinter hemorrhages, Janeway lesions, Osler nodes, and Roth spots. IE diagnosis is made via positive blood cultures and vegetations on echocardiography. Surgical intervention is recommended within 7-10 days; mortality is as high as 85% in patients with Serratia who only received medical therapy. After prompt surgical intervention, antimicrobial treatment includes combination therapy of B-lactam and an aminoglycoside or fluroquinolone for at least six weeks. 


A Rare Case of Infective Endocarditis by Serratia Marcescens

Drug-Induced Interstitial Lung Disease (DILD) describes an inflammatory response to various drugs that can result in fibrosis of the lung. It can present with dose-dependent toxicity or as an immune-mediated response, with respiratory illness ranging from benign infiltrates to debilitating respiratory fibrosis. This report describes a patient with a history of chronic, recurrent pneumonia suspected to be gabapentin-induced pneumonitis and severe gastroesophageal reflux disease (GERD). Respiratory symptoms initially improved after abstinence from gabapentin but then recurred postoperatively, after a GERD-related hiatal hernia repair. Diagnosis of DILD remains difficult and a diagnosis of exclusion, and our case may provide evidence for a relationship between gabapentin, GERD, and DILD: chronic aspiration combined with depressed cough reflexes characteristic of drugs like gabapentin may contribute to lung injury. Future research may provide a better understanding of how GERD may act to exacerbate DILD and give insight into a mechanism of similar adverse drug interactions.

A Rare Presentation of Suspected Gabapentin-Induced Idiopathic Pneumonitis

Background: Multiple studies have shown that a majority of community-acquired pneumonia (CAP) associated mortalities are due to cardiovascular disorders. Up to 30 % of patients with CAP are at risk of cardiovascular complications during the first thirty days of hospital admission, especially older than 65 years or with underlying cardiac conditions. However, mechanisms involved in this pathogenesis are not fully understood in younger healthy patients. We are presenting a case of acute onset of systolic heart failure in the setting of community-acquired pneumonia.

Case Presentation: A 45-old male patient presented to the emergency department with a complaint of upper respiratory tract infection symptoms of 4 days duration. He received oseltamivir but worsening of symptoms, including nausea and vomiting, were noted. Vital signs were normal except for tachycardia, and the physical exam was non-focal. FLU A and B and COVID-19 testing were negative. Chest x-ray (CXR) revealed right lower lobe infiltrates. The patient was started on Levofloxacin for CAP coverage. The patient was stable, but on day three, oxygen desaturation (85%) with tachycardia and dyspnea were found. Physical examination revealed bilateral coarse crackles, especially lower lobes. CT angiography Chest ruled out pulmonary embolism but revealed diffuse bilateral alveolar and interstitial infiltrates suspicious for vascular congestion with superimposed pneumonia. Echocardiography revealed dilated cardiomyopathy, systolic heart failure (HF) with reduced left ventricular ejection fraction to 15%, and mild to moderate mitral regurgitation. Guideline-directed medical therapy for HF was initiated. Left heart catheterization excluded significant coronary artery disease.

Discussion: We present a case of acute onset of systolic heart failure in a young immunocompetent male patient who presented with CAP. The workup for CAP includes sputum cultures, blood cultures, methicillin-resistant staphylococcus aureus PCR, legionella antigen testing, cytomegalovirus, Epstein-Barr virus IgM, herpes simplex virus type I and II, and human immunodeficiency virus were negative.


Acute Onset of Systolic Heart Failure in The Setting of Community-Acquired Pneumonia in an Immunocompetent Patient

Background
Atypical hemolytic uremic syndrome (aHUS) is a rare condition characterized by hemolytic anemia, thrombocytopenia and acute renal failure. The mechanism of aHUS consists of a genetic mutation in complement regulation incited by a strong trigger leading to uninhibited activation of the complement system. Trigger events include infection, medications, malignancy or a systemic illness that initiates inflammatory reaction like pancreatitis. We present a case of a patient that presented in an extreme hyperglycemic state with acute pancreatitis and was subsequently diagnosed with aHUS. 
Case Presentation
38-year-old obese Hispanic male with no past medical history who presented to the emergency department with altered mental status. On physical exam, he was lethargic and hemodynamically unstable. Initial labs showed metabolic acidosis with anion gap, acute kidney injury, glucose of 1500, moderate serum acetone and a hemoglobin A1C of 11.9. Lipase was 1766 (upper limit of normal 60) and computed tomography of the abdomen without contrast revealed multiple loculated fluid collections around the pancreas. His renal function progressively worsened, requiring hemodialysis. On hospital day 2, his platelet count decreased to 20 and peripheral blood smear revealed schistocytes. Heparin-induced thrombocytopenia, disseminated intravascular coagulation and viral infections from Hepatitis B, C and human immunodeficiency virus were all ruled out. Also, shiga-like toxin antigen and stool culture were negative. Given the fevers, renal failure, hemolytic anemia, thrombocytopenia and altered mental status; thrombotic thrombocytopenia purpura (TTP) was suspected and immediate plasmapheresis was initiated. He completed 11 sessions of plasmapheresis in conjunction with 11 days of methylprednisolone 40 mg every 8 hours. ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) level resulted at 43%, making aHUS more likely. The patient was then started on eculizumab with improvement in his mental status and renal function. 
Discussion
Although rare, patients can develop both TTP and aHUS, with hemolytic anemia, thrombocytopenia and acute renal dysfunction following pancreatitis. Due to the high mortality of TTP, patients should be promptly treated with plasmapheresis while awaiting results of ADAMTS13 levels. If ADAMTS13 is normal, the physician should consider aHUS as a possible diagnosis and start eculizumab as soon as possible to salvage renal function.

Acute pancreatitis causing aHUS in a patient with new-onset diabetes mellitus

Association between statin use and Morbidity-Mortality outcome in stroke patient with LDL <70 mg/dl: A retrospective study from a stroke registry

Background 
Encountering direct complications of absorbable antibiotic carriers is rare. When treating prosthetic joint infections, absorbable antibiotic calcium-sulfate beads have a superior elution profile to other traditional antibiotic loaded beads which eventually require removal. In a case of persistent polymicrobial post-operative infection, an unexpected turn of events manifested with heightened serum calcium after carrier insertion.

Case Presentation 
A 74-year-old woman with advanced osteoarthritis of the hip presented with progressive right hip pain. Right total hip arthroplasty (THA) was successfully performed; however, she developed a hip abscess, fever, and chills shortly after staple removal. Abscess cultures resulted positive for methicillin-resistant Staphylococcus aureus and Finegoldia magna. Rifampin and vancomycin were initiated, and she underwent arthroplasty revision. Despite implant exchange, continued polymicrobial infection necessitated a second revision.
A second THA revision was performed with the insertion of Stimulan calcium-sulfate antibiotic carriers to optimize control of the persisting polymicrobial infection. Rifampin therapy was continued, and daptomycin substituted vancomycin due to acute kidney injury. Post-operative day five, she was found to be hypercalcemic with corrected serum calcium peaking at 12.6 mg/dL; prior labs confirmed serum levels within normal limits. Only notable symptoms were nausea and features of delirium. A broad differential was explored for this acute abnormality. Suppressed parathyroid hormone (PTH) and vitamin D metabolites favored a PTH-independent process. Granulomatous disease was suspected as a bone biopsy showed non-caseating granuloma. Hypercalcemia of malignancy was considered, with raised suspicion for multiple myeloma as elevated monoclonal protein were found. 
Serum calcium levels and delirium improved with fluids and bisphosphonate therapy. We suspected calcium-sulfate antibiotic bead spacers as the most likely calcium source after immunofixation showed no overt evidence of monoclonal proteins, diagnostics of granulomatous disease origins remained negative, and repeat PTH, vitamin D metabolites, and PTHrP remained inconsistent with primary parathyroid or paraneoplastic-mediated processes. She was discharged with downtrending inflammatory markers and normal calcium levels.

Discussion 
Calcium-sulfate antibiotic beads are effective for managing surgical site and prosthetic joint infections; however, the risk of transient hypercalcemia remains. Further studies are necessary to determine if there is a threshold amount of calcium-sulfate antibiotic beads which correlates with higher risk of developing hypercalcemia. 


Beads of Calcium, the Culprit of Confusion

Background
Syncope is the result of cerebral hypoperfusion with underlying etiologies classified as neurally mediated, cardiac, or orthostatic hypotension. Risk stratification based on etiology of syncope is crucial since cardiac syncope is associated with increased morbidity and mortality and may have specific treatment options, whereas neurally mediated syncope and orthostatic hypotension are often benign and are treated with supportive care. It is estimated that 5-21% of syncope is of cardiac etiology. Signs and symptoms, listed with the associated positive likelihood ratio (+LR) that predict increased risk of cardiac syncope include age >35 at initial episode of syncope (3.3), history of existing heart disease (2.7-7.3), exertional syncope (1.4-15), syncope while supine (1.1-4.9), prodromal chest pain, dyspnea, or palpitations (1.9-3.8), cyanotic during episode (6.2), and abnormal ECG (2.3).

Case Presentation
A 50-year-old woman presented with syncope while walking up a flight of stairs. Syncope was preceded by palpitations, dizziness, and dyspnea. ECG demonstrated sinus rhythm, 1st degree AV block, RBBB, and LAFB without ischemic changes. CT Coronary revealed multiple perilymphatic pulmonary nodules with hilar lymphadenopathy concerning for sarcoidosis. Transthoracic echocardiogram showed normal LVEF of 66% and proximal septal wall thickening. On hospital day 2, the patient experienced syncope while supine with bradycardia to the 20s and hypotension to 70s/40s. Repeat ECG and showed complete heart block. The patient received emergent transvenous pacing along with IV dopamine and norepinephrine infusions. On hospital day 3, she received a permanent dual chamber pacemaker-defibrillator. She underwent fluorodeoxyglucose positron emission tomography (FDG-PET) and biopsy confirming the diagnosis of cardiac sarcoidosis.

Discussion
This case demonstrates the importance of recognizing signs and symptoms associated with high-risk cardiac syncope, which should prompt hospital admission and further diagnostic evaluation. After identifying cardiac syncope, it is important to determine the underlying cause which can be due to arrythmias or structural heart disease. This patient’s arrhythmogenic cardiac syncope was due to cardiac sarcoidosis, an infiltrative granulomatous disease that impacts multiple organs. Clinical manifestations of cardiac sarcoidosis occur in only 5% of patients and typically presents as conduction abnormalities, ventricular arrythmias, and heart failure. Diagnosing cardiac sarcoidosis is crucial to identify patients that will benefit from appropriate treatment.


Cardiac Sarcoidosis Presenting as Syncope due to Complete Heart Block

Background
In patients with cavitary lesions it is important to consider Aspergillosis in the differentials. In the past it was more associated in immunosuppressed patients with malignancies and HIV. However, recent studies suggest risk factors such as chronic obstructive pulmonary disease (COPD), steroid use, viral infections, and occupational risk factors should also increase the suspicion.

Case Presentation
Patient is a 56 year old male with past medical history of CAD s/p PCI, COVID-19 infection 2 months ago, and COPD who presented to the hospital due to persistent cough and fevers. His occupation involved repairing air conditioners. CT chest showed RUL cavitary lesion with thickened wall. AFB cultures were negative times three. Serum studies were negative for Cryptococcus and Blastomycosis. ANCA titers were also negative. 1,3-Beta-D-glucan assay was negative.
Bronchoscopy was performed with bronchoalveolar washings (BAL), bronchial brushings and
transbronchial biopsies; culture of washings showed growth of normal respiratory flora, acid fast smear negative. Pathology examination of transbronchial biopsies showed inflammation but no malignant cells noted. Positive Aspergillus galactomannan antigen was found in BAL, and Aspergillus growth in the pulmonary cavitary lesion was confirmed. Patient was started on Voriconazole.

Discussion
In patients presenting with upper respiratory symptoms and cavitary lesion on imaging it is important to consider fungal infections like Aspergillosis, especially in patients who were treated for COVID-19 infection. Our patient also had underlying emphysematous bullous changes due to long term tobacco use, and bullae are known as a potential risk factor for this fungal infection. His occupation working to repair air conditioners could have also put him at risk for Aspergillosis. 


Cavitary Lesion in an Immunocompetent Patient with Recent COVID-19 infection


As clopidogrel demonstrates both long-term and short-term situational benefits for morbidity and mortality, it has become one most prescribed medications in the medical field. The mechanism of clopidogrel hepatotoxicity is not known, is difficult to reproduce, and may be due to the complex hepatic metabolism of the clopidogrel molecule. Immunologic features are usually not prominent, but hypersensitivity reactions to clopidogrel have been described. We describe the case of a patient who experienced clopidogrel-induced liver injury. The patient was an elderly woman who presented to the emergency department with nausea and generalized weakness. She had 1 prehospital episode of nonbilious, non-bloody vomiting, along with hyperchromic urine and constipation for 3 days pre-hospitalization. 13 days prior to this admission she was hospitalized for a transient ischemic attack (TIA) and discharged with clopidogrel and aspirin for 21 days. She had an uncomplicated posthospital course until the onset of these new symptoms. On admission, patients showed a new-onset dramatic elevation in liver markers. Abdominal MRI revealed moderate edema along the portal triad and a HIDA scan came back normal. Acetaminophen level and hepatitis screen were noncontributory. Her liver enzymes steadily elevated to the several thousands without reasonable explanation until Clopidogrel was isolated as the cause of the patient’s liver injury, and was discontinued with success. Her liver enzymes steadily down trended with discontinuation of clopidogrel and she improved dramatically. As more tests came back inconclusive for the underlying etiology of this patient’s liver injury, and her clinical condition remained undefined. A reasonable explanation for this patient’s condition was a diagnostic challenge. This was until her relatively recent initiation of Clopidogrel was considered. Clopidogrel was the only new medication this patient began taking between her two hospitalizations, and its discontinuation was followed by dramatic success. As these medications have become a mainstay of primary care in medicine, Clopidogrel side effects are critical for providers to be aware of and to understand thoroughly as they prescribe this incredibly beneficial class of medications.



Clopidogrel: A Case Report of Suspected Drug Induced Liver Injury

Background:
A rare consequence of DRESS syndrome is eosinophilic myocarditis. Our case discusses this condition in conjunction with utilization of the lifesaving modality Extra-Corporeal Membrane Oxygenation, and treatment options.

Case Presentation:
A 30-year-old female patient with a PMHx of DM1, adrenal insufficiency, vitiligo and seizure disorder, which all developed following DRESS syndrome from lamotrigine exposure presented for chest pain. She had no prior cardiac history. EKG showed low voltage QRS. Echocardiogram revealed a small pericardial effusion, pericardial thickening, EF of 55 to 60%, and no tamponade physiology. Labs showed: BNP 4194, CRP 1.48, ESR 7, and a troponin peak of 3121. The patient was treated for acute pericarditis with colchicine and prednisone with resolution of her symptoms.
Sixteen days later, she presented back with recurrent chest pain and hypotension. Labs showed: BNP 14,981 CRP 2.94, troponin peak of 24,097. TTE showed EF 30-35%. EKG showed new RBBB and inferior q waves. Repeat TTE showed EF 10-15%. Left heart catherization revealed normal coronary arteries. Following LHC, multiple episodes of ventricular tachycardia were noted, requiring defibrillated and intubation. Following intubation, she became pulseless requiring CPR and placed on VA ECMO. The patient remained on ECMO support and was started on immunosuppressive modalities following endocardial biopsy confirming eosinophilic myocarditis. Four days after discontinuing ECMO, TTE showed EF 45% with normal RSVP.

Discussion:
DRESS is a rare and potentially life-threatening condition caused by delayed hypersensitivity reaction. Although many cardiac imaging tests assist in the diagnosis, the most definitive remains endomyocardial biopsy. This case report is unique in that there is no other case report that emphasizes the importance of early ECMO support and an anti-IL- 5 antibody in the treatment of eosinophilic myocarditis. In this case, the role of ECMO was significant in the bridge to recovery.
Typical, long-term treatments of eosinophilic myocarditis include steroids in adjunct with immunosuppressive strategies. Our patient’s regimen included prednisone daily, mycophenolate twice a day, and mepolizumab injections monthly. Eosinophils acquire IL-5 receptor on their surface during the early stages of differentiation, and maturation. Mepolizumab, is an anti-IL-5 recombinant humanized monoclonal antibody, which stops the interaction between IL-5 and its receptor on eosinophils.

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A Rare Case of Infective Endocarditis by Serratia Marcescens

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