2018 FOEM Case Study Poster Competition Winners*Winning abstracts featured below Congratulations to the winners of FOEM’s 2018 Case Study Poster Competition! Thank you to all that participated.
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FOEM Case Study Poster Competition
Winning Abstracts
1st Place: Samantha Margaritas, DO from Midwestern University in Downers Grove, IL for her case Time for a Change of Pace.
Title: Time for a Change of Pace
Authors: Samantha Margaritis, DO, Rodney Fullmer, DO, Midwestern University, Downers Grove, IL; Swedish Covenant Hospital.
Introduction:
Hypertrophic cardiomyopathy (HCM) causes enlargement of the cardiac myocardium, mitral valve abnormalities, and obstruction of the outflow tract leading to lethal arrhythmias, often leading to sudden cardiac death. The gold standard of treatment for HCM is septal myotomy (SM) with mitral valve (MV) repair. Common complications of SM with MV repair include LBBB, aortic regurgitation and ventricular septal defect. Literature on MR rupture post SM is scant and with varying presenting symptoms. When patients with history of HCM present in unstable arrhythmia, MR rupture needs to be considered as a life threatening cause. This is a unique case as it is an uncommon complication of a disease requiring emergent intervention.
Case Description:
65 y/o M physician brought into the ED externally paced for third degree heart block. Initial history obtained through EMS as patient was A&Ox1-2. Pt was rounding when he had a syncopal episode at a nursing home. An AED noted v-fib and delivered a shock, CPR followed. EMS EKG strip showed a-flutter with variable conduction, v-tach and v-fib with a second shock delivered. Pt then had third degree heart block and was paced externally by EMS. While transferring the patient, transcutaneous pacemaker was dislodged and patient lost consciousness with a heart rate of 10. A transvenous pacemaker (TVP) was required for stabilization and placed emergently at bedside. Subsequent ECG showed LBBB. Troponin elevated to 0.09. After TVP placement, patient’s mental status improved and provided history that he had a SM for HCM and MR repair 2 months prior. Three days PTA, patient had a syncopal episode and was admitted to another hospital and diagnosed with MR rupture. Patient requested to be discharged home on Eliquis that morning with plan to return following day for MR repair. Also, the patient had occipital abrasion on exam and subsequent CT head showed traumatic SAH.
Discussion:
This case involved addressing a cascade of three life threatening conditions related to one initial event, with few similar case reports. Our patient presented with two rare complications of a routine treatment as one study found that 0.8% of patients who had SM with MV repair had subsequent MV rupture1. Another study demonstrated that only 43/482 patients had complete heart block requiring pacemaker after SM with MVR3. In ER setting, it is prudent to immediately place external pads and keep a broad differential of potential causes. Maintain a wide knowledge base and a high index of suspicion for MV rupture in patients with HCM presenting in labile arrhythmia. In our practice, it is imperative to maintain proficiency in infrequently performed procedures such as emergent TVP placement to prevent death. This also demonstrates importance of completing a primary and secondary survey of patients to evaluate the full extent of injuries. Had we focused solely on the cardiac problem presented, we would have missed the diagnosis of traumatic SAH. Recognize that patients with history of HCM are likely anticoagulated and have a low threshold to do head CT.
Resources
- Iacovoni A, Spirito P, Simon C, et al. A contemporary European experience with surgical septal myectomy in hypertrophic cardiomyopathy. European Heart Journal. 2012;33(16):2080-2087. doi:10.1093/eurheartj/ehs064.
- Kotkar KD, Said SM, Dearani JA, Schaff HV. Hypertrophic obstructive cardiomyopathy: the Mayo Clinic experience. Annals of Cardiothoracic Surgery. 2017;6(4):329-336. doi:10.21037/acs.2017.07.03.
- Rastegar H, Boll G, Rowin EJ, et al. Results of surgical septal myectomy for obstructive hypertrophic cardiomyopathy: the Tufts experience. Annals of Cardiothoracic Surgery. 2017;6(4):353-363. doi:10.21037/acs.2017.07.07.
2nd Place: Jacob Smith, DO from Doctor’s Hospital in Columbus, OH for his case May Thurner Syndrome: An Uncommon Cause of a Frequent Diagnosis.
Title
May Thurner Syndrome: An Uncommon Cause of a Frequent Diagnosis
Authors
Jacob Smith, DO, PGY 3, Emergency Medicine Resident, Doctors Hospital, Columbus, OH
Andrew Little, DO, Core Faculty, Doctors Hospital, Columbus, OH
Introduction
This case describes a young patient who presented to the ED with the complaint of leg pain and swelling after suffering a fall 2 weeks prior. She was found to have a large multi-vessel DVT in this leg. What is unique about this patient’s case is the cause of her DVT. Patient was found to have findings consistent with May-Thurner Syndrome, a nonthrombotic iliac vein lesion.
Case Description:
28-year-old Caucasian female with history of seizures and IVDA presented to the emergency department with left leg pain and swelling after a fall 2 weeks prior. She had increasing pain and swelling in her left leg and shortness of breath with productive sputum and subjective fevers. She also had generalized abdominal discomfort with nausea. She admitted to ongoing skin popping of heroin. She had no additional VTE risk factors.
Physical exam revealed a heart rate in the 100s and blood pressures in the mid to low 90s. She was noted to have diffuse left lower quadrant tenderness and a palpable cord in the left inguinal region. She also had 1+ pitting edema of the left lower extremity with intact pulses and sensation.
She underwent radiologic and laboratory testing revealing evidence of dehydration. Left lower extremity duplex revealed acute DVT’s in the left external iliac vein, common femoral, proximal femoral, and mid femoral vein. Patient additionally had a CT chest, abdomen, pelvis revealing extensive bilateral multifocal nodular consolidations and extensive thrombus within the left iliac vessels with extension of subocclusive thrombus into the IVC secondary to compression of the left common internal iliac vein via the right common internal iliac artery.
Patient was discussed with vascular surgery and admitted to stepdown. She underwent a pharmacomechanical thrombectomy, IVC filter placement and angioplasty of the left external iliac vein. Blood cultures also confirmed streptococcal viridans bacteremia. Unfortunately, patient signed out on POD #1 after completion thrombectomy, and her final outcome, although improved at disposition, is unknown.
Discussion
May-Thurner syndrome manifests as obstruction of the left common iliac vein due to the overlying right common iliac artery. This occurs due to either direct compression or intimal hypertrophy of the iliac vein due to pulsatile trauma. This occurs in 2% to 5% of patients with lower extremity venous disorders. Incidence of lower extremity DVT is higher on the left side than on the right and within these patients, 18-49% of these cases are due to May-Thurner syndrome. This predominantly occurs in women (8:1) of childbearing age with long periods of immobility or pregnancy.
Treatment options include endovascular thrombolysis followed by venous dilation and endovascular stent placement as well as even left common iliac vein bypass. Emergency providers should be aware of additional causes of VTE such as anatomic etiologies as May-Thurner’s as these are not amenable to traditional treatment therapies such as long-term anticoagulation. With increased pressures to decrease hospital admissions including patients with VTE, providers must take note to ensure that anticoagulation alone is the appropriate therapy for each case to prevent further clinical problems.
References
- Zhou, Q., Lee, B., Lee, R., & Stewart, M. (2015). An atypical cause of extensive left-lower-extremity DVT: May-Thurner syndrome. Radiology Case Reports,10(2), 1019. doi:10.2484/rcr.v10i2.1019
- Mousa, A. Y., & Aburahma, A. F. (2013). May–Thurner Syndrome: Update and Review. Annals of Vascular Surgery,27(7), 984-995. doi:10.1016/j.avsg.2013.05.001
- Durack, J. C., & Kohi, M. P. (2011). Venous Anatomy of the Abdomen and Pelvis. In Cardiovascular imaging(pp. 1005-1018). St. Louis, MO: Elsevier Saunders.
- Durack, J. C., & Kohi, M. P. (2011). Venous Anatomy of the Abdomen and Pelvis. In Cardiovascular imaging(pp. 1005-1018). St. Louis, MO: Elsevier Saunders.
- Demir, M. C., Kucur, D., Çakır, E., Aksu, N. M., Onur, M. R., Sabuncu, T., & Akkaş, M. (2016). May-Thurner syndrome: A curious syndrome in the ED. The American Journal of Emergency Medicine,34(9). doi:10.1016/j.ajem.2016.02.045
- Kaltenmeier, C. T., Erben, Y., Indes, J., Lee, A., Dardik, A., Sarac, T., & Chaar, C. I. (2017). Systematic review of May-Thurner syndrome with emphasis on gender differences. Journal of Vascular Surgery: Venous and Lymphatic Disorders. doi:10.1016/j.jvsv.2017.11.006
3rd Place: Kevin McLendon, DO from Merit Health Wesley in Hattiesburg, MS for his case Old Timer’s Toxin: Caramel Kalemia.
Case Report Abstract
Title: Old Timer’s Toxin: Caramel Kalemia
Authors: Kevin McLendon, D.O., Matthew Wiggins, M.D., Alex Gauthier, D.O., Deepu Thoppil, M.D., Jacob Fenster, D.O.
Introduction:
Hyperkalemia is a laboratory diagnosis with devastating consequences. In the Emergency Department we often focus on the initial stabilization of a patient found to have irregular potassium levels and may easily overlook the cause of the electrolyte imbalance. We focus on the EKG, calcium administration, and our immediate efforts to return potassium to a safe level. However, for our patients’ health it is imperative that we discover the cause of their ailments in efforts to best prevent them from recurring.
Potassium regulation is controlled by the kidneys and often clinically significant changes require more than a single source or influence. Impaired excretion, increased intake, and/or intracellular shifts are the root causes of hyperkalemia. The clinical manifestations are not an effect of the absolute elevation of potassium, but acuity of the elevation.
Without treatment hyperkalemia may lead to cardiac irritability with subsequent dysrhythmias and death.
Case description:
An 84-year-old Caucasian male presented to the emergency department with one day of nausea/vomiting and severe diffuse abdominal pain. He notes intermittent diarrhea over the last month that resolved one week prior and he was in usual health until his onset of abdominal pain and cramping. He reports his vomitus looked just like the tea he regularly drinks. He likens his pain to his previous peritonitis; however, it is much better than when he awoke and spontaneously resolves in the ED. He denies any associated symptoms of fever, chills, weakness, or body aches. He is compliant with medications and regularly follows with his nurse practitioner.
Discussion:
Review of diet discovered the patient eats approximately 10 pounds of Werther’s weekly, along with a daily 1-gallon intake of Chrystal Light Peach Iced Tea. It is estimated that the patient was consuming a daily additional 2.8g of Potassium from the Werther’s alone, plus a minimum 16 servings of potassium-based sweetener in his tea. During an office visit in December he was switched from Lasix to Spironolactone and had been encouraged to decrease his sugar intake. After which he incidentally switched to sugar-free Werther’s (1/800th the potassium content). His use of enalapril with spironolactone was stable as reported by his visit to his NP in mid-January. When he returned to Werther’s Originals he rapidly developed hyperkalemia within a week.
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