Poster Day 2023: Abstracts: Clinical Vignettes

Shirley Gandhi, OMS - III, Pruthvi Patel, OMS-III    

Advancements in pharmaceutics have led to the development of medications that help clot blood during times of unwanted bleeding and degrade clots to prevent a hypercoagulable state. In addition to these classes of drugs, the human body has its own natural glycoproteins which serve to maintain hematological homeostasis. Protein S is a glycoprotein created by the body which aids in the prevention of a hypercoagulable state. Protein S deficient patients are placed on anticoagulant regimens as there is no definitive cure. Failure to bring balance to the hematological system in these patients will lead to complications such as widespread clot formation and pulmonary embolisms.  

Here we present a 74-year-old female who was admitted to the ICU after collapsing. She presented with respiratory failure, urinary tract infection (UTI), and pneumonia. Magnetic resonance imaging (MRI) scans depicted a thrombus in the distal right transverse sinus and sigmoid sinus. Her hematologic workup showed normal levels of homocysteine, fibrinogen, and protein C levels but protein S levels were reduced to 24%. This case displays the intricate presentation of a rare hematological disease as well as the importance of proactive screening and preventative medicine to be the forefront of healthcare in underserved areas.

Diamond McNeil, OMS-IV; Samantha Le, PharmD, OMS-IV; Mark Haygood, DO, MS, FAPA

The glomus tumor is a rare benign tumor commonly misdiagnosed as a neuroma by general practitioners and presents as a bluish-red temperature-sensitive tender nodule under the nail. It can be diagnosed on clinical exams and by imaging studies such as X-ray, MRIs, or ultrasonography and is treated with excision. A solitary lesion on the fingertip can easily be confused with a glomus tumor, myxoid cyst, and a neuroma. Our goal is to describe the characteristics of a glomus tumor and the methods that could be used to clinically differentiate it from other common tumors of the same region. The diagnosis can be confirmed using a biopsy with a histopathological analysis. A simple way to biopsy a lesion on the finger and excise the tumor is with a minimally invasive procedure using a punch biopsy followed by extensive electrocautery.

Paramjit Kaur, MD; Paarmit S. Chhabra, MD; Benjamin Easow, MD; Sindhu Yarrabelli, MD; and Syed Fatmi, MD.

Introduction:

Atherosclerotic cardiovascular disease remains a predominant cause of illness and death in the contemporary world, and its prevalence has shown a continuous increase ^[1]. The process of atherogenesis is well-documented, with a strong association with lipoprotein B-100, notably low-density lipoprotein cholesterol (LDL-C) ^[2]. Statins are employed to lower LDL levels. According to established literature, cholesterol is produced through a 30-step pathway originating from acetyl co-enzyme A ^[3]. The critical step controlling cholesterol biosynthesis is regulated by 3-hydroxy-3-methylglutaryl-CoA reductase. Statins were initially developed to inhibit HMG-CoA reductase to reduce LDL cholesterol levels, with the ultimate goal of enhancing survival and reducing the morbidity and mortality linked to atherosclerotic cardiovascular disease ^[4]. Statins rank as one of the most commonly recommended medications in the United States, particularly for managing hyperlipidemia and mitigating the risk of cardiovascular diseases in individuals with an increased likelihood of atherosclerotic cardiovascular disease (ASCVD). In 2019, a staggering 92 million individuals were prescribed statins, with Atorvastatin emerging as the most frequently prescribed statin within this category, closely followed by simvastatin ^[5].

We present a case of statin-induced autoimmune necrotizing myositis, wherein this patient developed necrotizing myositis within just three weeks of initiating statin therapy.

A 71-year-old female patient with a medical history of coronary artery disease (CAD), hypertension (HTN), and mixed hyperlipidemia presented to our medical facility, reporting chest pain. She underwent a left heart catheterization, revealing significant stenosis in the proximal right coronary artery (RCA), which was successfully treated with percutaneous transluminal coronary angioplasty (PTCA) and the placement of a drug-eluting stent. Additionally, during the procedure, she was found to have 50-70% ostial diagonal artery stenosis and opted for medical management. Her medication regimen included Aspirin 81 mg, Clopidogrel 75 mg, and a low dose of Atorvastatin 10 mg.

The patient had previously tried Atorvastatin in 2018 at a higher dose of 80 mg but experienced myalgia and discontinued it after three weeks. Therefore, this time, a lower dose of 10 mg was prescribed. After three weeks on this medication, she reported experiencing the same symptoms she had encountered a few years prior. She ceased taking the statin after this period. Initially, she developed generalized myalgia, which did not improve upon discontinuation but instead progressed. Consequently, she was referred to rheumatology for further evaluation to rule out other potential causes of myopathy. During the evaluation process, her condition deteriorated to the point where she became generally weak and reliant on a cane for mobility, ultimately losing the ability to walk. Initial creatine kinase (CK) levels were elevated at 7528 and increased to 9492 despite discontinuing Atorvastatin. Aldolase levels were measured at 90.7. A comprehensive workup for alternative causes of myositis was conducted, including tests for hepatitis B and C, gamma-glutamyl transferase (GGT), thyroid-stimulating hormone (TSH), and Myositis assessR Plus JO-1 antibody, all of which yielded unremarkable results. Additional assessments, such as Flexitest for Aldolase with repeat analysis, were performed. Mild elevations in transaminase levels were noted but remained relatively stable over time. Subsequently, an HMG-CoA reductase antibody (HMGCR Ab) test was conducted, revealing a high value of 314, typically associated with necrotizing myopathy induced by statins. This finding prompted a thigh muscle biopsy, which confirmed the diagnosis of necrotizing myopathy, specifically Type 2 muscle atrophy. The patient was advised to avoid statin medications and received aggressive physical therapy. CK levels have since shown a decreasing trend, with a recent level measuring 848. Thanks to aggressive physical therapy, she has progressed from using a cane to walking with the assistance of a walker, albeit at a gradual pace.

Statins represent the most commonly prescribed class of drugs for lowering lipid levels, providing substantial benefits in the prevention and management of vascular diseases ^[6]. Generally, statins are considered safe and well-tolerated; however, they can produce a range of side effects, spanning from myalgia to the severe condition of rhabdomyolysis. In rare instances, statins have been identified as a causative factor in the development of autoimmune necrotizing myositis. Although the exact pathophysiology of statin-induced myositis is not fully elucidated, current research suggests that individuals with an over-expression of HMG-CoA reductase may be more susceptible to the formation of autoimmune antibodies against this receptor ^[7].

 In our specific case, the patient had previously been prescribed statins a few years before her current presentation. When she experienced proximal muscle weakness, she discontinued the statin medication, resulting in the resolution of her muscle weakness. Subsequently, after encountering an atherosclerotic event and undergoing stent placement, an attempt was made to use a lower dose of atorvastatin. However, while on atorvastatin, she developed myalgias and muscle weakness, which progressed to a severe decline in her ability to walk, almost reaching a state of paralysis. Extensive diagnostic investigations were undertaken, encompassing muscle biopsy and autoimmune testing, revealing a positive result for HMG-CoA receptor antibodies. Notably, the patient's creatine phosphokinase (CPK) levels were initially elevated and continued to rise, even after discontinuing statins. The CPK levels reached their peak within three weeks but returned to a normal range over the course of three months.

From this case, we draw the conclusion that individuals with a history of statin intolerance should undergo a comprehensive evaluation for the presence of HMG-CoA reductase antibodies, rather than simply reducing the statin dose. If these antibodies are detected, it is advisable to avoid statin therapy in such patients. Furthermore, we recommend that if a patient currently taking statins develops proximal muscle weakness, prompt CPK assessment should be conducted, and statin use should be discontinued in the event of an elevated CPK level.

Immediate clinical assessment is imperative when a patient presents with complaints of proximal muscle weakness while undergoing statin therapy, and it is crucial to promptly measure their creatine phosphokinase (CPK) levels. Furthermore, we conclude that for patients who have previously experienced intolerance to statins, rather than attempting an alternative statin class or a reduced dosage, it is advisable to conduct an HMG-CoA antibody test before initiating statin therapy. This proactive approach is essential for averting potentially life-threatening complications.

Taylor F. Faust BS, MS, OMS-III, Jackson Carlyle BS, OMS-III, Grace Williams MD

Medical literature does not currently report a case of co-occurring congenital scoliosis, thumb aplasia, and radioulnar synostosis. This potential syndromic association deserves to be explored as it consists of a constellation of symptoms that are rather rare on their own in the general population. Furthermore, there is great overlap with other documented syndromes and associations that have potential cardiac, gastrointestinal, hematologic, and nephrological implications, thus contributing to increased morbidity and mortality if left undetected.

Daniel I. Mazzorana OMS-III, Kamil Arif MD, Junjian Huang MD

A 54-year-old female with a gastrostomy tube presents with persistent nausea, vomiting, and abdominal pain. On physical examination, the gastrostomy tube was completely advanced into the abdominal cavity with only the external retention ring and hub on the exterior. The first step in the workup was obtaining a scout radiograph. This imaging was appropriate to show the location of the gastrostomy catheter which was overlying the left upper quadrant. The distal tip was heading in the direction of the left lower quadrant. Proceeding forward, contrast was injected through the existing catheter which showed opacification of the jejunal bowel loops. Following this, a stiff Glidewire was advanced through the existing catheter all the way into the jejunum. Deflation of the balloon and removal of the catheter caused an almost instantaneous change in the course of the Glidewire. A sheath was then advanced over the wire which was now shown crossing the midline in the proper gastroduodenojejunal course. The final step was to advance a new 22 French MIC gastrostomy catheter over the Glidewire. The contrast was then injected to demonstrate proper opacification of the rugal folds and gastric fundus. The patient reported an immediate resolution of symptoms and was later discharged.

Benjamin M Easow, MD  Greeshma Thomas, MD  Tijin Mathew, MD Lydia George, MD

The mainstay treatment for symptomatic Wolff-Parkinson-White (WPW) syndrome is radiofrequency catheter ablation, which can be intricate, especially when dealing with right antero-septal and right anterolateral accessory pathways due to their close proximity to the normal cardiac conduction system.

We present a case involving a 33-year-old male who has a history of Wolff-Parkinson-White syndrome. He was admitted to the hospital due to recurrent chest pain and palpitations persisting for a duration of two weeks. The initial electrocardiogram (EKG) displayed a type B WPW pattern (as depicted in Figure A). All other diagnostic assessments, including troponin levels, yielded inconclusive results.

Subsequently, following an electrophysiology (EP) study, the patient underwent cardiac ablation with a focus on targeting the right anteroseptal and anterolateral accessory pathways. Nonetheless, achieving complete elimination of these pathways presented a challenge due to their proximity to the bundle of His.

Post-procedure, a recurrence of supraventricular tachycardia was observed, which was successfully terminated through the application of a vagal maneuver. Further assessment is planned, and there is consideration for potential repeat ablation.

Recurrent accessory pathway ablation remains a formidable task, even for experienced practitioners. Research highlights the rarity of right anteroseptal and anterolateral accessory pathways and their close proximity to the conduction system, raising the risk of complete AV block during ablation and the likelihood of reablation. Success and safety hinge on profound anatomical knowledge, thorough mapping (including pacing as needed), and stable catheter placement with precise energy delivery.

To summarize, even though the left accessory pathway exhibits a higher reablation rate compared to the right, the persisting risk of cardiac reablation associated with the right accessory pathway, due to its proximity to the conduction system, remains a concern.

This case features a 12-year-old male with a complex psychiatric history, focusing on an unexpected adverse reaction to Depakote, resulting in acute pancreatitis.

This case serves as a poignant reminder of the unanticipated medical perils posed by Depakote, particularly its capacity to trigger pancreatitis, especially in pediatric patients struggling with psychiatric comorbidities.

Sreenidhi Kosuri MD, Rabia Salman Mahfooz MD, Omer Farooq MD, William D. Hewitt MD

Introduction:

Omer Farooq MD, Sindhu Yarrabelli MD, Rabia Mahfooz MD, Sreenidhi Kosuri MD, Kristy Johnson-Pich DO

This case highlights the significance of considering enteropathogenic Escherichia coli (EPEC) as a potential cause of hemolytic uremic syndrome (HUS), especially when initial tests for Shiga toxin-producing E. coli (STEC) yield negative results. It emphasizes adopting a systematic and comprehensive diagnostic approach to identify rare pathogens.

Unaiza Batool OMS-III, Roy Schwartz M.D.

Gastrointestinal (GI) bleeding is a common diagnosis that results in a significant number of hospitalizations in the United States. 80% of GI bleeds are due to an upper source, defined as a bleed proximal to the ligament of Treitz. Peptic ulcer disease is the most common cause of upper GI bleeds, representing nearly 40% of all cases. However, the high incidence of peptic ulcer disease can skew clinical judgment when a patient presents with a less common source of an upper GI bleed, resulting in delays in diagnosis and treatment.

Here we present a 67-year-old female with a history of peptic ulcer disease and a recent non-diagnostic esophagogastroduodenoscopy (EGD) presenting with an acute GI bleed secondary to a hemorrhaging dieulafoy’s lesion (DL) in the proximal duodenum. DL is an abnormally dilated submucosal artery that protrudes through the mucosa into the GI lumen. DL is prone to trauma due to its location and can result in bleeds of varying severities. They are usually found in the proximal stomach but can occasionally occur in other places along the GI tract. Duodenal DL consist of only 15% of all occurrences and 3.5% of all GI bleeding. Significant hemodynamic instability in this case required exploratory laparotomy for definitive diagnosis and treatment. The atypical etiology of the bleed is a challenging diagnosis that was further hindered by clinical bias due to the patient’s prior history. In this case we discuss the patient’s initial presentation, the challenges surrounding diagnosis and treatment, and their recovery.

Tijin Mathew, MD, Bhoomi Shah, MD, Maheen Jawaid MD, Rabia Mahfooz, MD

Paarmit S. Chhabra, MD, Muhammad Qureshi, MD, Saikiran Mandyam, MD, Chang Hwan Park, MD, Mashal Awais, MD, Fnu Anshul, MD

Thiamine is an essential cofactor for 4 enzymes involved in the production of ATP and the synthesis of essential cellular molecules. The total body stores of thiamine are relatively small, and thiamine deficiency can develop in patients secondary to inadequate nutrition, alcohol use disorders, gastrointestinal disorders, and acute metabolic stress.[1] In adults, thiamine deficiency can present as encephalopathy, dry beriberi (peripheral neuropathy, muscle wasting, paralysis, and confusion), wet beriberi (cardiomegaly, edema, and high output cardiac failure due to dilated cardiomyopathy). The role of thiamine has gained prominence in critically ill patients.

A 46 year old female with a past medical history of congestive heart failure (CHF), chronic kidney disease (CKD), and hypertension (HTN) presented to the ED with complaints of severe respiratory distress. Patient was hypoxic and diaphoretic on initial presentation and became unresponsive with brief seizure like activity. Patient subsequently underwent cardiopulmonary resuscitation (CPR) and return of spontaneous circulation (ROSC) was achieved. Patient was unable to maintain her airway and therefore was intubated and admitted to the ICU. In the ED, patient’s ABG showed a pH of 7.1, PCO2 of 56.2, Bicarbonate of 21.2 Complete blood count showed a white blood count of 15.2 and was otherwise normal. Initial high sensitivity troponin were 117. Brain natriuretic peptide was elevated to a level of 2540. Rapid drug screen was positive for tetrahydrocannabinol and cocaine. Pneumonia panel was positive for Streptococcus agalactiae, Human rhino virus, and Haemophilus influenza. CT scan of the head showed age indeterminate lacunar infarcts in the bilateral basal ganglia. MRI showed no acute findings. During the earlier part of her hospital admission, patient was given a regimen of thiamine which included 500mg IV for two days and then 250mg IV for 3 days. This thiamine regimen showed no improvement in the patients clinical status. At this time, other causes of encephalopathy were suspected and other workup was completed including infectious causes. Patient had difficulty weaning off the ventilator and continuously required pressure support. Patient was scheduled for a tracheostomy and percutaneous endoscopic gastrostomy. A few days prior to the procedure, the patient presented with new onset nystagmus and Wernicke encephalopathy was again a differential. The patient was given another recommended regimen of thiamine at 500mg IV for two days and 250mg IV for three days. The patient subsequently improved clinically and was able to avoid a tracheostomy, percutaneous endoscopic gastrostomy, and an extended ICU admission. In a few days, the patient was transferred out of the ICU on to the medical floor and was discharged in stable condition back to her home.

Thiamine is a relatively safe and low cost medication, with cost being as low as 89 cents per 100mg.[2] Although there is no universally accepted dosage for thiamine infusion in critically ill patients, the generally acceptable dosage is 500mg per 100mL normal saline given by IV over a period of 30 minutes, for 2 to 3 days and 250mg IV or IM  for the next 3 to 5 days.[3] Due to the facts described above, we would like to recommend that patients with encephalopathy, whether the cause is known or not, should receive 500mg of thiamine for two days and then a continuous 250mg infusion until symptoms resolve or patient becomes clinically stable. Our patient made a significant improvement after the second round of thiamine infusion which further supports our recommendation. We also recommend that clinical trials be initiated comparing ICU outcomes in encephalopathic patients receiving a continuous infusion of thiamine versus patients who do not. 

In the ICU setting, critical illness and metabolic stress that the body endures requires an increased demand for thiamine. It is crucial to have a high degree of suspicion for thiamine deficiency and/or increased demand. In situations where critical illness is present, a thiamine replenishment protocol should be initiated. This protocol should include 500mg of thiamine infusion for two days and 250mg of thiamine infusion continuously until symptoms resolve or the patient becomes clinically stable.  

Devam Parghi, MD, Priyanka Patel, MD, Priya Pohani, OMS-II, Saikiran Mandyam, MD

A 34-year-old African American post-partum female who presented with right flank pain was found to have Inferior vena-cava (IVC), renal vein, and gonadal vein thrombosis with no known thrombophilia which was confirmed with computed tomography (CT) scan. The patient was initially treated with a heparin drip which was later switched to therapeutic enoxaparin. Patient had a hypercoagulable workup after completing anticoagulation which was unremarkable. We briefly review the epidemiology, presentation, imaging findings, diagnosis, evaluation, and treatment of post-partum thrombosis.

Courtnee Stagner CRNP, Will Baker OMS-III, Camila Vega OMS-III, Jillian Weiss OMS-III

Six patients admitted to an inpatient hospice unit without pre-existing DELC were observed during the same 1-month period. Regular comfort care was provided and development of DELC was documented as well as other common signs of imminent death.

• Case 1: 84 year old male with CAD and dementia.
• Case 2: 71 year old female with COPD and stage II lung cancer.
• Case 3: 67 year old female with history of CVA.
• Case 4: 69 year old female with CVA.
• Case 5: 68 year old female with breast cancer.
• Case 6: 63 year old male with stage IV lung cancer, COPD, and CAD.

This case report discusses a rare occurrence of Atypical Teratoid Rhabdoid Tumor (AT/RT) in the pituitary region of a 37-year-old female. AT/RTs are typically embryological tumors and are more common in children under 6 months old, with adult cases being extremely rare. There have been only 45 documented cases of pituitary AT/RTs.

A G1P0, 22-year-old female presented to the clinic at 19 weeks’ gestation with a referral from her OBGYN. She had recently been prescribed 20 mEq of potassium twice a day and over the counter 500 mg magnesium supplements twice a day because her recent lab work demonstrated low magnesium and potassium. She comments that prior to her pregnancy, she had noticed some lower levels in her electrolytes. However, she had not known about the severity of her values. Her vitals were BP: 99/69, Pulse: 96, and respiratory rate: 18. Her labs showed K: 2.7, Creatinine: 0.35, and Mg: 0.9.

Since electrolyte imbalances are considered a normal physiological change during pregnancy, pregnant patients with Gitelman could easily be overlooked, misdiagnosed, and inappropriately managed". There is currently little knowledge about the impact that Gitelman has on pregnancy. However, studies have shown higher rates or miscarriage, intrauterine growth restriction and morbidity".

Gitelman syndrome still requires long term research to determine the best treatment methods for its associated symptoms of CKD and arrhythmias. Furthermore, this case demonstrates the importance of continuously analyzing pregnant patient’s electrolytes.

Deep vein thrombosis is a significant medical emergency; findings indicative of DVT warrant  expeditious scrutiny and treatment.

Coronary Subclavian Steal Syndrome represents a fascinating yet intricate phenomenon within the realm of cardiovascular medicine, where blood flow within the coronary arteries deviates from its physiological pathways, causing potentially detrimental consequences, particularly in patients who underwent coronary artery bypass grafting using the left internal mammary artery. We recommend prompt identification of this condition by taking a detailed history and performing a thorough physical exam. Most patients will need a heart catheterization to confirm stenosis of the proximal subclavian artery along with patency of the left anterior descending artery. Management includes a subclavian artery stent with aggressive risk factor modifications including strict blood pressure control, reducing LDL cholesterol and increasing HDL cholesterol, and smoking cessation.