United States

Abstract Title
How Did It Get There? A Case of Thoracic discitis and paraspinal abscesses caused by a vaginal flora in a 73-year-old man.

Background
Gardnerella vaginalis (G. vaginalis) is a small, gram-variable rod typically part of the vaginal flora. The overgrowth of G. vaginalis is a well-known cause of bacterial vaginosis. Only a few cases document infection with G. vaginalis in men, the most common source being genitourinary. We present a case of a 73-year-old man with altered mental status and sepsis who was found to have multilevel thoracic discitis/osteomyelitis with paraspinal and mediastinal abscesses secondary to G. vaginalis.

Case Presentation
A 73-year-old man presented to Loyola University Medical Center (LUMC) as a transfer for escalated care for septic shock. He initially presented to an outside hospital after being found down for two days. He had altered mental status, chest discomfort, shortness of breath, and an inability to move his bilateral lower extremities (LE). He was afebrile, hypotensive, tachycardic, and tachypneic with cold LE bilaterally. Computed tomography of chest, abdomen and pelvis revealed T7-T10 discitis/osteomyelitis, a complex fluid collection along the left posterior mediastinum, and emphysematous cystitis. Magnetic resonance imaging of the thoracic spine confirmed the presence of discitis/osteomyelitis, mediastinal and paraspinal abscesses and revealed an epidural abscess (T1-T7-8) and canal stenosis (T9-10). He was empirically treated with vancomycin and piperacillin-tazobactam. He rapidly decompensated requiring intubation and was therefore transferred to LUMC.

At LUMC, neurosurgery was consulted for concerns of acute cord compression. He underwent T7-T10 laminectomy, T8-9 transpedicular decompression and T5-11 fusion for spinal infection with unstable T8 spine fracture. Frank purulence was noted upon fascial opening. Intraoperative cultures of thoracic epidural fluid, epidural swab and deep fascia wound cultures grew few colonies of G. vaginalis. Blood cultures were negative. After treatment of emphysematous cystitis, he was transitioned to ampicillin-sulbactam for 6 weeks. He remained afebrile with improved leukocytosis and negative blood cultures but was still unable to move his bilateral LE upon discharge (hospital day 27). Later, he was unfortunately readmitted to an outside hospital for unknown reasons and was lost to follow up. 

Discussion
This case demonstrates the pathogenic ability of G. vaginalis to cause extensive spinal abscesses and osteomyelitis. Although G. vaginalis can cause bacterial vaginosis and treatment for this is well-established, the management of this case is much more complex. This patient’s diagnosis is uncommon, so being aware of the pathogenicity of G. vaginalis to cause substantial infection and analyzing treatment outcomes for these cases is important for management of future cases. 


AMA Research Challenge 2024 

How Did It Get There? A Case of Thoracic Discitis and Paraspinal Abscesses Caused by a Vaginal Flora in a 73-year-old Man

Welcome to the largest national, multi-specialty research event **featuring research from 750 medical students, residents and fellows, and international medical graduates.**


#### Event Details
The 2022 American Medical Association Research Challenge includes a poster symposium hall and a semifinals hall with the top scored research. Log in at any time throughout the event to:
* **View posters and presentations** on a variety of topics and specialties
* **Score posters in the semifinals** to help decide the top five finalists (AMA member exclusive opportunity)
* **Connect with participants** and provide feedback to help advance their research

At the conclusion of this event, the AMA will announce the top five finalists who will advance to the AMA Research Challenge finals, present their research to an elite panel of judges and compete to win a $10,000 grand prize sponsored by Laurel Road.
 

#### Attend Live Forums
**Oct. 20, 6 — 7 p.m. Central**
 **How to plan a career in academic medicine** 
 Learn how to plan a career in academic medicine and get your questions answered. [Access Here](https://underline.io/events/363/lounge)
 
 **Speakers**
![](https://assets.underline.io/uploads/markdown_image/1/image/d5adb133dfc58eb0a6d469e9cedcd5d4.jpg)
Ricardo Correa, MD, EdD
![](https://assets.underline.io/uploads/markdown_image/1/image/5f9437ab87861538bf02b9ca7c0d926e.jpg)
Stuart M. Greenstein, MD
![](https://assets.underline.io/uploads/markdown_image/1/image/05b1b637c99286d558c371f8e8b185ce.jpg)
Stephanie Strohbeen, MD
 
 **Oct. 22, 11 a.m. — Noon Central**
 **How to get published**
 Learn tips to get your research published and get your questions answered. [Access Here](https://underline.io/events/363/lounge)
 
 **Speakers**
![](https://assets.underline.io/uploads/markdown_image/1/image/8ce6235e957d31cb5e6f9097cc6f6972.jpg)
Jessica Li, MD/PhD Candidate
![](https://assets.underline.io/uploads/markdown_image/1/image/9950ef2e0237f54cb3d8280334d42491.jpg)
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.

![](https://assets.underline.io/uploads/markdown_image/1/image/611e331d4a0eba0920f240cfc04b4d77.png)

**There is no registration fee for this event! **

Register to explore research in a variety of topics. AMA members get exclusive access to score posters in the semifinals.

**Please use the link below to register for free if you have not already done so:**

https://www.ama-assn.org/about/events/ama-research-challenge

Registration Is Required

AMA Research Challenge 2022

Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


poster

Welcome to the **largest national, multi-specialty research** event featuring research from more than 750 medical students, residents, fellows, and international medical graduates.

Use the buttons below or navigation menu to access the event.
 

[![](https://assets.underline.io/markdown_image/1/image/20e1e77aa954efeac7a15d84c85eb383.jpg)](https://underline.io/events/468/sessions?searchGroup=all)
 
[![](https://assets.underline.io/markdown_image/1/image/068522d81aca0b68a369787c7dfccd1b.jpg)](https://underline.io/events/468/posters?searchGroup=all)
 
[![](https://assets.underline.io/markdown_image/1/image/d3971ece79d5e5575b178bdc2c8bbfae.jpg)](https://underline.io/events/468/help-desk)
 

#### Event Details

The 2024 American Medical Association Research Challenge includes a poster symposium hall and a semifinals hall with the top scored research. **Log in at any time throughout the event to:**

* **View posters and presentations** on a variety of topics and specialties
* **Score posters in the semifinals** to help decide the top five finalists (AMA member exclusive opportunity)
* **Connect with participants** and provide feedback to help advance their research

At the conclusion of this event, the AMA will announce the top five finalists who will advance to the AMA Research Challenge finals, present their research to an elite panel of judges, and compete to win a $10,000 grand prize presented by Laurel Road. 

### Grand Prize 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 winner selection process. The winner will be announced on February 20, 2025 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.

[![](https://assets.underline.io/uploads/markdown_image/1/image/611e331d4a0eba0920f240cfc04b4d77.png)](https://www.laurelroad.com/)

You need to log in with the email address you registered with. Access credentials have been sent to your email. 

Please be sure to check your spam and other email folders if you do not see an email confirmation right away.

Please log in to explore this event.

**There is no registration fee for this event! **

If you have used the AMA Research Challenge platform previously, please click the ‘Log-in’ button below. If you do not remember your password, please click “forgot password” and follow prompts to reset your password. After resetting your password, please refresh your webpage to access the platform.

Register to explore research in a variety of topics. AMA members get exclusive access to score posters in the semifinals. 

**Please use this link [here](https://www.ama-assn.org/member-benefits/events/ama-research-challenge) to register for free.**

Join the AMA Research Challenge poster symposium and semifinals to explore top research posters and score posters in the semifinals (an AMA member exclusive opportunity).

Hydralazine-Associated Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Lupus with Crescentic Pauci-Immune Rapidly Progressive Glomerulonephritis - A Case Report
Cynthia Andrade, Adam Ostrovsky, Nairuti Sanghavi, Eunae Ko, Vandana Bandari, Sangeetha Satyan

Introduction
Hydralazine, a commonly prescribed medication for hypertension and heart failure, has been linked with anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis and lupus. We present a unique case of hydralazine associated ANCA vasculitis and lupus with crescentic pauci-immune type rapidly progressive glomerulonephritis (RPGN) requiring renal replacement therapy treated with immunosuppression and Avacopan.

Case Presentation
A 58-year-old male with hypertension treated with hydralazine 100 mg three times a day for about three years presented to the hospital with fatigue, poor appetite, twenty-pound weight loss, exertional dyspnea, intermittent fevers, and erythematous rash for about three months.
Serum creatinine was elevated at 2.4 mg/dL on admission with a previous baseline of 1.0 mg/dL four months prior to hospitalization. Urinalysis showed proteinuria and microscopic hematuria. Hemoglobin was 11.8 g/dL. Urine protein/creatinine ratio was 0.6 g/g. Renal ultrasound revealed normal sized echogenic kidneys. Further evaluation revealed elevated inflammatory markers, high anti-nuclear antibody (ANA) in a homogeneous pattern (titer of 1:1280), normal anti-ds DNA, hypocomplementemia with low C3 and lower limits of normal C4, positive anti-histone antibody at 3.1 U, and anti-cardiolipin IgM antibodies at 30.8 MPL-U/mL. Kidney biopsy revealed focal segmental necrotizing and crescentic pauci-immune type glomerulonephritis (GN) with mild tubular atrophy and interstitial fibrosis and severe acute tubular injury. Immunofluorescence revealed low level immune complex deposition; electron microscopy revealed global small electron dense deposits in mesangial areas and rare endothelial tubulo-reticular inclusions. ANCA screen was positive for p-ANCA (titer of > 1: 640) with high anti-MPO and anti-PR3 antibodies at 652.7 and 5.5 AI, respectively.
Hydralazine was discontinued. He was treated with high dose methylprednisolone along with rituximab for induction therapy followed by prednisone taper. Renal function progressively worsened requiring initiation of renal replacement therapy. He was also treated with Avacopan. Hemodialysis was discontinued after about four months due to renal recovery but with residual stage four chronic kidney disease. ANA and ANCA titers decreased with treatment and anti-MPO and anti-PR3 antibodies were 3.5 and 0.3 Units respectively at four months. 

Discussion 
Hydralazine induced Lupus and ANCA vasculitis with pauci-immune type RPGN is rare. Certain serologic markers and pathologic features are suggestive of drug associated ANCA-GN rather than primary ANCA-GN as demonstrated in our case. ANCA-GN including that complicated by hydralazine has high morbidity and mortality. Vigilance, prompt diagnosis, discontinuation of the offending medication, and immunosuppressive treatment for severe disease are necessary. Clinicians must be cognizant of this potentially life-threatening condition associated with hydralazine and consider alternative available treatments for hypertension and heart failure when feasible.


Hydralazine-Associated Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Lupus with Crescentic Pauci-Immune Rapidly Progressive Glomerulonephritis - A Case Report

Abstract Title
Atrial Fibrillation Presenting as Renal Infarction
Background
Renal infarction is caused by occlusion of renal artery or its branches, due to emboli from cardiac sources or in situ thrombosis. It presents as sudden flank or abdominal pain, with labs showing elevated LDH, hematuria, proteinuria. Prompt diagnosis is crucial to initiate timely revascularization therapies.

Case Presentation
A 78-year-old male with past medical history of hypertension, diabetes mellitus, hyperlipidemia, COPD, meningioma presented to the emergency department with complaints of pain in the left flank and umbilical region which started gradually over the past few days and was described as dull and non-radiating. Physical evaluation revealed stable vital signs with hypertension, chronic normocytic anemia, irregularly irregular pulse, Left costovertebral angle (CVA) tenderness, bilateral chronic hand tremors. No focal neurological deficits. Denies fever, nausea, vomiting, diarrhea, constipation, anorexia, alcohol use, changes with meal, similar pain, incontinence, dysuria, hematuria, changes with urine output, urinary frequency, chest pains, palpitations, syncope, orthopnea, PND, edema. Initial Diagnostic workup included negative troponin, COVID-19/flu/RSV tests, and a chest X-ray showing mediastinal widening. Further investigations with a CT angiography chest ruled out aortic aneurysm or dissection but noted a region of low density in the left kidney parenchyma suggestive of multiple cortical infarcts. Urinalysis was positive for microscopic blood and 1 RBC. An EKG demonstrated new-onset atrial fibrillation (Afib). Cardiology consulted recommended to start anticoagulation therapy for atrial fibrillation and electrophysiology with no immediate plan for cardioversion. Later, CTAP with and without contrast show findings consistent with multiple acute renal infarcts (ARI) in the left kidney. Urology was consulted and determined no surgical intervention was indicated, recommending anticoagulation to prevent further complications from kidney infarcts. The patient was educated about his condition and discharged with appropriate outpatient follow-up.

Discussion
ARI is potentially serious medical condition but its clinical presentation of is often
nonspecific, leading to delays in diagnosis and treatment. Autopsy studies suggest the incidence of renal infarction is 14 per 1000, or 1.4%. Other retrospective studies of ER admissions found an incidence of 0.004% to 0.007%. In our case, the patient's abdominal pain with no previous history of arrhythmias prompted further evaluation, revealing new-onset AFib on EKG and subsequent diagnosis of renal infarction on imaging. Afib can cause thrombotic complication to any body part, most commonly being ischemic stroke. Clinicians should suspect other systemic embolization phenomena in patients with Afib.


Internal Medicine Resident PGY-3

We report a case of Lemierre Syndrome caused by Arcanobacterium haemolyticum bacteremia in a previously healthy immunocompetent 29-year-old male. Two blood cultures revealed the exclusive presence of A. haemolyticum. 

A 29-year-old male with no past medical history presented with a 5-day history of fever, chills, and severe odynophagia. Physical exam revealed asymmetrical tonsillar swelling and a CT Neck with contrast showed an infectious process surrounding the left palatine tonsil and inflammatory phlegmonous changes and gas abutting the left carotid sheath. Given this, patient was to be transferred to a tertiary care center for further evaluation by ENT. 
His symptoms continued to worsen, and he presented to the tertiary care center the following day. Initially, the patient was afebrile with a leukocytosis 13.5. A CT neck showed an infectious abscess around the left parapharyngeal and left carotid spaces with thrombophlebitis of the left internal jugular vein with complete thrombosis suggestive of Lemierre’s syndrome. Septic emboli were also noted in the upper lungs. Antibiotics were broadened to linezolid and piperacillin-tazobactam. The patient was taken to the OR for left neck exploration, left peritonsillar abscess drainage, and excision of the left jugular vein. During the procedure, it was noted that the thrombosed internal jugular vein had purulent material expressed. 
Two blood cultures were positive exclusively for Arcanobacterium haemolyticum at 3.6 days and the BCID panel was negative for all targets including Streptococcus. Intra-operative cultures had no growth. His leukocytosis gradually returned to normal range, and he remained afebrile. Patient was discharged with plan for 2 weeks of IV ampicillin-sulbactam and 4 additional weeks of PO amoxicillin/clavulanate. 

In 1936, Andre Lemierre described a series of cases of septicemia caused by Fusobacterium necrophorum and complicated with internal jugular vein thrombophlebitis and septic emboli to distant organs. F. necrophorum is the most common causative agent of Lemierre’s syndrome, followed by Fusobacterium nucleatum. Lemierre's syndrome is a rare condition, estimated to affect approximately one in a million individuals annually. Typically, affected individuals are young, previously healthy adults, with a male-to-female ratio of 2:1. 
To date, only 6 cases of Lemierre’s syndrome caused exclusively by A. haemolyticum have been reported in the medical literature and no cases have been reported from the United States. We present the first case of Lemierre's disease stemming from infection solely involving A. haemolyticum.

Lemierre Syndrome caused by Arcanobacterium haemolyticum: First reported case in the United States

Abstract Title
Losing Fat or Muscle? A Case of Rhabdomyolysis Following Initiation of Semaglutide (Wegovy)
Background
GLP-1 receptor agonist semaglutide has gained popularity due to its glycemic control, positive cardiovascular effects, and role in weight management. Common side effects include fatigue, headache, injection site reactions, and gastrointestinal symptoms, like abdominal pain, nausea, and gastroparesis.
Case Presentation
A 56-year-old female with past medical history of systemic lupus erythematosus (SLE) on hydroxychloroquine (HCQ) for 30 years, gastroesophageal reflux disease, autoimmune hepatitis on budesonide, asthma, and fibromyalgia presented to the emergency department (ED) with five days of worsening fatigue, bilateral lower extremity weakness, and pain. One week prior, she experienced nausea, heartburn, and pruritus of the breast, back, and buttocks. Primary care visit labs revealed a creatine kinase (CK) above 27,000 u/L (n=30-184 u/L) prompting ED evaluation. On admission, she endorsed worsening pain, weakness, and decreased appetite. She denied new excessive exertion, foods or supplements, trauma, or statin use but did disclose starting semaglutide (Wegovy) 0.25 mg injections two weeks prior for weight loss. Family history includes polymyositis in her father. Admission vital signs were notable for pulse 113 beats per minute, blood pressure 137/99 mmHg, and BMI 36.85 kg/m2. Physical exam demonstrated bilateral calf tenderness, positive Homan’s sign, hip flexor weakness, normal range of motion, and no joint tenderness. Serum studies demonstrated CK above 34,000 u/L, aspartate aminotransferase (AST) 1018 u/L, alanine aminotransferase (ALT) 297 u/L, creatinine 0.60 mg/dL, estimated glomerular filtration rate (eGFR) >90 mL/min/1.73m2, and no leukocytosis. Rheumatological studies including C3/C4, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), urine protein-creatinine ratio, and double-stranded DNA (dsDNA) were within normal limits. Aldolase was elevated to 176.5 u/L (normal <7.7 u/L). Duplex doppler ultrasonography showed no venous thromboembolism bilaterally. She was diagnosed with rhabdomyolysis and admitted for three days during which her HCQ was held, and she received aggressive IV fluids. CK levels dropped nearly 10,000 u/L daily. At discharge, CK was below 6,000 u/L with no renal injury and improved liver enzymes; she reported near resolution of symptoms. Repeat CK four days post-discharge was 192 u/L.
Discussion
Limited information exists on the association between semaglutide and rhabdomyolysis; one case report details a similar presentation, both in timing and symptomology. This patient had significantly elevated CK levels and liver enzymes. Despite stable autoimmune conditions on long-term treatment, laboratory results suggest her rhabdomyolysis is attributable to recent semaglutide initiation instead of another etiology.

Losing Fat or Muscle? A Case of Rhabdomyolysis Following Initiation of Semaglutide (Wegovy)

Title: Lurasidone (LATUDA)-Induced Pancreatitis: A Case Report

Background: Lurasidone (LATUDA) is a second-generation antipsychotic used in the management of schizophrenia and bipolar disorder. There have been reports of drug-induced pancreatitis (DIP) associated with antipsychotics such as haloperidol, olanzapine and clozapine. However, there is limited documented literature on the association between Lurasidone and pancreatitis. Although rare, DIP is a severe adverse effect of various medications. Here, we present a compelling case of
Lurasidone-induced pancreatitis that sets itself apart from other cases of DIP.

Methods: A 60-year-old African-American woman with a past medical history of Type-1 bipolar disorder presented to the ER with complaints of nausea, multiple episodes of vomiting, and constant, sharp abdominal pain that radiates to her back. These symptoms began approximately a month after she started taking Lurasidone. A thorough examination revealed tenderness to palpation in the umbilical and lower abdominal area without rebound tenderness or guarding. Laboratory tests
showed significantly elevated serum Lipase (997 U/L) and serum Amylase (533 U/L), consistent with the diagnosis of acute pancreatitis. We considered a diagnosis of Lurasidone-induced pancreatitis due to the correlation between the initiation of Lurasidone therapy and the manifestation of her symptoms. Subsequently, we discontinued the patient's Lurasidone therapy and initiated supportive management, including bowel rest, intravenous fluids, and pain control. Her symptoms improved progressively and successive laboratory assessments revealed downward
trending pancreatic enzyme concentrations (serum Lipase of 25 U/L after a week).

Results: Despite the absence of documented literature linking Lurasidone specifically to pancreatitis, patient presentation and laboratory findings confirmed drug-induced pancreatitis. Much like the other antipsychotics implicated in drug-induced pancreatitis (DIP), the mechanism of this reaction, although unclear, is believed to stem from either direct toxicity on pancreatic cells, immune-mediated mechanisms, or hypertriglyceridemia.

Conclusion: Since there are no documented cases of Lurasidone-induced pancreatitis, this case report necessitates healthcare providers to maintain a high index of suspicion for DIP in patients presenting with acute abdominal pain when they are on Lurasidone therapy. The patient's clinical presentation, laboratory findings, and the temporal relationship between the start of Lurasidone
treatment and the onset of symptoms, combined with the lack of any other identifiable causes for pancreatitis, established the diagnosis of Lurasidone-induced pancreatitis. Further studies are warranted to elucidate the underlying pathophysiological mechanisms and guide appropriate clinical practice for prompt patient management.

Lurasidone (LATUDA)- Induced Pancreatitis: A case Report

In-stent thrombosis (ISR) is one of the dreaded complications of percutaneous coronary angioplasty. Despite marked reductions in ISR since the transition from bare metal stents to drug-eluting stents, ISR still occurs at a rate of 1%-2% per year. 

We present the case of a 64-year-old Caucasian male who was admitted for staged angioplasty after a left heart catheterization had shown significant stenosis to the LAD and mid ramus intermedius. He had DES placed to the mid-LAD and mid-ramus intermedius. Despite being placed on dual antiplatelet therapy after the stent placement, six hours later, he complained of chest pain and EKG showed new ST elevations in leads I, aVL, and V2-V6. Repeat LHC showed thrombosis to recently placed LAD and mid ramus-intermedius stents, so a new set of stents was placed, and the patient was loaded with eptifibatide and then restarted on dual antiplatelet therapy after the procedure.

However, only 48 hours later, the patient started complaining of chest pain again. EKG showed new ischemic changes and a high sensitivity troponin of 5000. He was taken to the catheterization lab, and LHC once again revealed late stenosis of the previously stented LAD and mid-ramus intermedius. He underwent percutaneous coronary angioplasty to these stents. Post-LHC, he was started on prasugrel and aspirin instead of the 2 other times when he was on clopidogrel and aspirin, then ticagrelor and aspirin.

In addition to the dual antiplatelet therapy, he was also started on a Factor X inhibitor, rivaroxaban. Our hypercoagulability investigations did not yield any positive results; however, we found out the patient was on testosterone replacement.

This case is very unique in that we had early re-stenosis of a drug-eluting stent, and it did not only occur once, it occurred twice. One of the questions raised in this unique case is: when you have patients who have early restenosis of their stents, what is the preferred antiplatelet agent, and is a Factor Xa inhibitor indicated in this scenario? In the case of our patient, we went for prasugrel + aspirin + rivaroxaban, and we did not have any re-stenosis.


Managing Recurrent Acute In-Stent Thrombosis: Insights from a Single Case Study


Background
Vasculitides encompass a diverse group of rare inflammatory disorders that affect blood vessels, each presenting with distinct clinical and pathological characteristics. Over 30 types of vasculitides have been identified, differentiated by their patterns of vessel involvement, serological markers, and histopathological features. Accurate diagnosis is crucial for determining long-term survival and appropriate therapy, necessitating a thorough evaluation to classify the specific type of vasculitis and exclude other conditions that mimic it.
Case Presentation
We present a 59-year-old female who presented with oral mucositis, purpuric skin lesions, and bilateral cyanosis of the toes. Upon presentation, necrosis of the toes was identified, and the patient underwent ten-toe amputation. Despite the resolution of mucositis and purpuric lesions, she now presents with acute skin changes to her left index finger concerning for additional necrosis. An angiogram revealed arteriographic evidence of vasculitis in small tributaries, displaying a beaded appearance along the plantar surface of the foot. Histological examination was nonspecific, showing necrosis with inflammatory cell infiltration. A comprehensive rheumatologic workup was negative for antiphospholipid antibodies, ANCA, anti-DNA, ANA, CCP, MPO, RF, and Proteinase 3. The patient was started on steroids, which halted the progression of necrosis in her index finger. Despite an extensive serological and histopathological workup, no clear predisposing cause or diagnosis was established. The working diagnosis remained thromboangiitis obliterans, attributed to a remote history of smoking. Through her stay and discharge, the treatment team conducted patient-centered rounds by engaging in open dialogue with the patient and involving her physician acquaintances.
Discussion
With an elusive diagnosis, the type of vasculitis afflicting our patient remained unidentified. Her constellation of findings does not align with any known form of vasculitis, and the work-up provides no evidence to corroborate a specific pathology. Despite a leading diagnosis of thromboangiitis obliterans, empiric steroid therapy provided clinical benefit, which is not typical for the condition. Furthermore, the lack of a definitive diagnosis complicates prognostic assessments and the selection of concurrent immunosuppressive treatments. While our patient was equally frustrated at the lack of definitive answers regarding a diagnosis, the team's open communication fostered a relationship of trust, resulting in the patient's cooperation, thus enabling the team to stabilize our patient's symptoms in the setting of diagnostic uncertainty. Frequent updates and patient-centered rounds increased transparency about the goals of the patient and medical team. Our case demonstrates the importance of a systematic, evidence- based approach to vasculitis workup and establishing a therapeutic alliance with our patients.

Navigating Diagnostic Uncertainty in a Case of Atypical Vasculitis

Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiographic diagnosis that can be visualized as symmetric posterior white matter vasogenic edema in the occipital and parietal lobes that arises as a consequence of endothelial damage in vulnerable vasculature. PRES can present clinically as visual changes, headaches, seizures, and altered mental status. Although most cases of PRES have been described in the setting of hypertension, a rare subset has developed in the setting of blood transfusion in chronic anemia.

Here, we present the first case of an adult male who developed PRES following a blood transfusion. The patient is a 69-year-old caucasian male who had an acute exacerbation of chronic anemia and went on to develop PRES following the transfusion of three units of packed red blood cells. 

21 total cases of PRES following a blood-transfusion have been documented. 20 of these cases are reported in females and 1 in an adolescent male. In the setting of chronic anemia correction in patients with identifiable risk factors (i.e., hypoalbuminemia or metabolic acidosis), care should be taken to transfuse blood products over long periods of time with close monitoring of hemoglobin levels to mitigate the risk of developing PRES. In patients with PRES, early identification and discontinuation of inciting factors are critical to a favorable prognosis.

Posterior Reversible Encephalopathy Syndrome Related to Blood Transfusion in a Male Chronic Anemic: A Case Report

Introduction:
Primary rib neoplasms are uncommon, making up only 5-10% of all bony tumors and 5% of thoracic neoplasms. Primary rib neoplasms are also not typically considered in the list of common differential diagnoses for thoracic musculoskeletal pain alongside conditions such as costochondritis. Additionally, primary rib neoplasms can present similar to other conditions, such as Tietze Syndrome. Because of the prevalence of primary rib neoplasms as well as its wide range of presenting symptoms, the time to diagnosis is typically prolonged. Primary rib neoplasms are typically treated surgically. We discuss a patient presenting with a 5-year history of intermittent left chest pain who was found to have a chondroid lesion of the left rib after years of extensive cardiac and radiologic workup. This case highlights the importance for physicians to consider primary rib neoplasms in the differential for patients with musculoskeletal chest pain.

Clinical Vignette Summary:
A 39 y/o F with a PMH of bilateral avascular necrosis of the hips presents with a 5-year history of intermittent left chest pain. Patient reports that the pain began after shutting the hatchback of a car in 2018. She notes that the pain is exacerbated by movement of her left arm and shoulder and occurs roughly once a week. Patient was initially given a diagnosis of costochondritis in 2018. However, in 2021, an EKG and Echo were ordered due to patient report of chest tightness; both tests returned within normal limits. In November 2022, extensive imaging was conducted due to persistence of pain. CT Chest w/o contrast revealed a 10 x 5 mm lesion in the left third costal cartilage with appearance of a benign chondroid lesion, corresponding with a T2 hyperintense focus on MRI of the Left Upper Extremity. Patient was sent to Cardiothoracic Surgery for evaluation and ultimately opted for conservative management with acupuncture and topical diclofenac and lidocaine due to stability of symptoms. 

Conclusions/Clinical Relevance:
This case highlights the importance of broadening one’s differential when it comes to the workup of musculoskeletal pain. While diagnoses such as costochondritis are common causes of musculoskeletal pain, quickness to diagnose patients with this condition may lead clinicians to miss other potentially more serious causes of musculoskeletal pain.

Primary Rib Neoplasms: Considerations For Providers in the Workup of Musculoskeletal Pain – A Clinical Vignette

Background

Statins, widely prescribed for cardiovascular disease, effectively reduce cardiovascular risk in primary and secondary prevention. However, muscle pain is a common side effect, affecting 2% to 11% of users. It is crucial to differentiate between benign muscle pain and serious myopathies, as severe myopathy (characterized by a creatine kinase (CK) level greater than 10 times the reference value) occurs in approximately 0.5% of patients. Immune-mediated necrotizing myopathy (IMNM), associated with anti-HMGCR antibodies, anti-SRP auto-antibodies, HIV, hepatitis C virus (HCV), connective tissue disorders, paraneoplastic disease, or idiopathic causes, is one such severe condition. IMNM presents with acute or subacute mild to moderate symmetrical muscle weakness, and discontinuing statins does not halt muscle weakness and elevated CK levels in HMGCR antibody-associated IMNM.

Case Presentation

A 67-year-old female presented with muscle weakness and elevated creatine phosphokinase (CPK) levels. Initially active, she began experiencing muscle weakness, particularly with overhead movements, in October 2023. She consulted her primary care doctor and was referred to a rheumatologist, who discontinued her statin medication in March 2024. Her symptoms temporarily improved but then worsened, with leg weakness and difficulty swallowing. By April 2024, her CPK level rose to 4806. 

Laboratory findings revealed anemia of inflammatory condition, elevated AST (175 U/L) and ALT (195 U/L) levels, a low A/G ratio, and low serum potassium. CT scans of the chest, abdomen, and pelvis with contrast did not indicate malignancy. Immunological testing revealed an elevated HMGCR Antibody IgG at 95 and SSA-52 (RO52) at 43. A muscle biopsy indicated skeletal muscle necrosis and regeneration. 

The patient received 1 gram of Solu-Medrol (Methylprednisolone sodium succinate), significantly improving her muscle strength and mobility, with CPK levels decreasing to 2779 and then to 855. The treatment plan included IV Solu-Medrol for three days, followed by oral Prednisone, Vitamin D, a proton pump inhibitor (PPI), and scheduled IVIG therapy for 2 days. Follow-up showed symptom relief and normalization of CPK levels.

Discussion

This case underscores the importance of recognizing statin-induced myopathy, particularly HMGCR antibody-mediated IMNM. Before diagnosing statin-induced myopathy, various differential diagnoses, including dermatomyositis, myopathy/myositis with significant CK elevation, polymyalgia rheumatica, and HMGCR antibody-mediated IMNM, must be considered. Understanding its natural course, particularly in cases of HMGCR antibody-mediated IMNM, is essential for informed patient consent and effective management. This case highlights the need for thorough differential diagnosis and appropriate treatment to ensure optimal patient outcomes.

Premium content

Next from AMA Research Challenge 2024

Hydralazine-Associated Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Lupus with Crescentic Pauci-Immune Rapidly Progressive Glomerulonephritis - A Case Report

Similar lecture

Spine strangler: A case of spinal epidural lipomatosis in a young male