United States

Introduction
Early administration of intramuscular epinephrine can be life-saving in the acute management of anaphylaxis. Rarely, intracranial hemorrhage (ICH) can occur after epinephrine use due to rapid elevations in blood pressure. We report a rare case of a man who developed ICH following epinephrine injection for acute anaphylaxis.
Case Description
A 70-year-old man with end-stage renal disease on dialysis, hypertension, and diabetes presented to the emergency department with a 1-month history of left ear pain. He had no prior history of anaphylaxis, intracranial hemorrhage, stroke, or allergies. Initial vital signs showed blood pressure of 203/87 mmHg. Physical exam revealed left edematous ear canal and mastoid tenderness, with no focal neurologic deficits. Suspected mastoid infection prompted a CT temporal bone scan with contrast, which was consistent with otomastoiditis and showed no evidence of intracranial hemorrhage or other intracranial pathology. Empiric antibiotic treatment was given with cefepime and vancomycin. Within 10 minutes of initiating vancomycin infusion, he developed shortness of breath and tongue/facial swelling, with blood pressure 152/116 mmHg. The patient then rapidly decompensated, developing altered mental status, bradycardia (30 bpm), hypoxia (40% O2 on pulse oximetry), and minimally palpable pulse. Anaphylaxis was suspected, and 0.3 mg intramuscular epinephrine, diphenhydramine, and dexamethasone were given. A repeat BP 5 minutes later showed hypertension up to 261/102 mmHg. Due to altered mental status and for airway protection, an emergent surgical airway was established with subsequent blood pressure 114/108 mmHg twenty minutes after sedation and ventilation with tracheostomy tube. Patient was subsequently admitted to the intensive care unit. Four days later, MRI brain with/without contrast for evaluation of osteomyelitis showed incidental bilateral intraventricular hemorrhage and acute pontine hemorrhages, confirmed stable by subsequent CT six hours later. Patient had no neurologic deficits and was discharged to a rehabilitation facility 35 days later with a tracheostomy collar.
Discussion
First-line treatment of anaphylactic shock is administration of epinephrine; however, adverse events can occur. Epinephrine can cause short term elevations in systolic blood pressure. Factors that can cause precipitation of intracranial hemorrhage include platelet dysfunction in the setting of chronic kidney disease with dialysis and hypertensive urgency. Physicians should be aware of ICH as a rare cerebrovascular complication of epinephrine injection in the setting of anaphylaxis, particularly in elderly patients with hypertension and high bleeding risk.

AMA Research Challenge 2024 

Intracranial Hemorrhage Following Epinephrine Injection for Anaphylactic Shock: A Rare Complication 


Congratulations to all the researchers who have qualified for the AMA Research Challenge virtual poster symposium and semifinals!

Welcome to the **largest national, multi-specialty research event** featuring research from nearly 1,000 medical students, residents, fellows, and international medical graduates across six topic areas - basic science, clinical and translational research, clinical vignettes, health systems science, medical education, and public health and health policy.

#### Access the Event
Use the buttons below or navigation menu to access the event. 

[![](https://assets.underline.io/markdown_image/1/image/d4076f2146939317a29eb9f69c53ad41.png)](https://underline.io/events/506/sessions?searchGroup=all)
[![](https://assets.underline.io/markdown_image/1/image/6bcee0b523a4874c4292ca0415d88dde.png)](https://underline.io/events/506/posters?searchGroup=all)

#### Event Details
The 2025 AMA Research Challenge includes the following symposium halls:
* **Semifinals hall:** Features research from 54 medical students, residents and international medical graduates that received top scores during first round scoring. 
* **Poster symposium hall:** Features research from nearly 1,000 medical students, residents and international medical graduates categorized by topics and subtopics.

**Here’s how to participate:**
* **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 presenters** and provide feedback to help advance their research
* **New this year: Watch live poster presentations** by topic area and engage directly with researchers

At the conclusion of this event, the AMA announced the top five finalists who advanced to the AMA Research Challenge final round, presented their research to an elite panel of judges, and competed to win a $10,000 grand prize presented by Laurel Road.

**Addison Shenk, a fourth-year medical student from Edward Via Virginia College of Osteopathic Medicine, was the winner of the 2025 AMA Research Challenge and was awarded the grand prize of $10,000, presented by Laurel Road.**

#### A message from Dr. Bobby Mukkamala, AMA President
<div style="position: relative; width: 100%; padding-bottom: 56.25%; height: 0; overflow: hidden;">
  <iframe 
    src="https://underline.io/embed/136894-ama-video?t=0"
    title="AMA Welcome Video"
    allowfullscreen
    style="position: absolute; top: 0; left: 0; width: 100%; height: 100%; border: 0;">
  </iframe>
</div>


#### Recognized Institutions
In 2025, 1,400 abstracts were submitted across six topic areas representing 174 medical schools and more than 150 residency and health care institutions. [See if your institution is represented this year!](https://drive.google.com/file/d/1eFrTqCmCeobx9pr5drJK2hllvsIpFNOY/view?usp=drive_link)

#### Grand Prize Sponsor
AMA would like to thank Laurel Road, a brand of KeyBank, for sponsoring a $10,000 grand prize for the winner of the AMA Research Challenge. Laurel Road and KeyBank are not involved in winner selection process. The winner will be announced during the AMA Research Challenge final round. Payment of the grand prize will be directly from Laurel Road/KeyBank. See the [AMA Research Challenge Official Rules for terms and conditions](https://www.ama-assn.org/system/files/research-challenge-official-rules.pdf).

[![](https://assets.underline.io/uploads/markdown_image/1/image/611e331d4a0eba0920f240cfc04b4d77.png)](https://www.laurelroad.com/)

#### Code of Conduct
<html>
AMA has a code of conduct for its meetings – we ask all attendees to adhere to this code to participate in this year’s meeting. Please read and <a href="https://www.ama-assn.org/about/code-conduct" target="_blank">learn more here</a> about your conduct requirements.
<br><br>
	</html>
	

#### Semifinals Judges

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.

Need help? Contact us at <support@underline.io>.

Please log in to explore 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. **

Registration Is Required

AMA Research Challenge 2025 

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).

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.
<br><br><br>

[![](https://assets.underline.io/markdown_image/1/image/20e1e77aa954efeac7a15d84c85eb383.jpg)](https://underline.io/events/468/sessions?searchGroup=all)
<br>
[![](https://assets.underline.io/markdown_image/1/image/068522d81aca0b68a369787c7dfccd1b.jpg)](https://underline.io/events/468/posters?searchGroup=all)
<br>
[![](https://assets.underline.io/markdown_image/1/image/d3971ece79d5e5575b178bdc2c8bbfae.jpg)](https://underline.io/events/468/help-desk)
<br><br>

#### 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.<br><br>

### 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/)

<br><br>

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.

**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.**


Abstract Title:
Navigating Anaplasmosis: A Case Report Highlighting Diagnosis and Treatment
Background:
Human Granulocytic Anaplasmosis caused by Anaplasma phagocytophilum is an emerging concern in the United States, spread by Ixodes scapularis and Ixodes pacificus in the Northeastern and Midwestern regions and in the Western regions, respectively. Tick-borne infections are increasingly reported during the summer months, especially in Pennsylvania. Lyme disease remains the most reported tick-borne illness in the state. Anaplasmosis presents unique challenges due to its nonspecific clinical manifestations and potential to mimic other tick-borne diseases. Preventing tick bites prevents the spread of infections.
Case Presentation:
The case of a 68-year-old male patient highlights the critical importance of recognizing and diagnosing anaplasmosis promptly. He presented to the ED with sudden onset high-grade fevers at 103°F, chills, abdominal pain with nausea and vomiting, and generalized weakness. His heart rate was 105/min and BP was 146/87 mm Hg. Fever panel was negative. With alarming findings such as profound thrombocytopenia (platelets decreasing from 102 K/mcL to 56 K/mcL within a day), transaminitis, and elevated CRP levels at 322.1 mg/dL, admission for suspected sepsis of unclear origin was necessitated. Empirical treatment with IV Doxycycline, Atovaquone, and Azithromycin was initiated to cover potential tick-borne infections. Radiological investigations, including CT scans and echocardiography, were unremarkable, further complicating the diagnostic process. The patient's history of living in wooded areas, owning dogs, and previous deer rearing raised suspicion for a tick-borne illness, despite no recollection of a recent tick bite. Definitive diagnosis was achieved through a tick-borne PCR panel, which confirmed Anaplasma phagocytophilum infection. This gram-negative intracellular bacterium selectively infects neutrophils, leading to the characteristic intracytoplasmic inclusions known as morulae, observed on peripheral blood smear. Given the patient's old age, he was at increased risk for severe complications such as systemic inflammatory response syndrome and multiorgan failure. Following a five-day course of IV Doxycycline, the patient's clinical status improved with resolution of fever and thrombocytopenia. He was discharged on oral Doxycycline and Atovaquone, emphasizing the importance of timely intervention and appropriate antimicrobial therapy in managing anaplasmosis.
Discussion:
This case underscores the challenges in diagnosing tick-borne illnesses, particularly in non-endemic regions with limited awareness. Heightened clinical suspicion due to drastic thrombocytopenia, prompt empirical treatment, and utilization of specific diagnostic tools such as NAAT/Tick-borne PCR panels are crucial in achieving favorable patient outcomes. Early recognition of clinically compatible symptoms associated with thrombocytopenia remains paramount in combating the rising incidence of tick-borne infections across the United States.



Navigating Anaplasmosis: A Case Report Highlighting Diagnosis and Treatment

Background 

Patients with Limb Girdle Muscular Dystrophy (LGMD) and other RYR1 variants present unique challenges to the anesthesiologist because of muscle weakness and potential for malignant hyperthermia (MH). We describe the anesthetic management of a patient with LGMD and a potentially difficult airway. 

Case Presentation 

A 55-year-old male with LGMD and no prior exposure to anesthesia presented for resection of colon cancer. The patient’s LGMD predominantly affected his shoulders. Pre-anesthesia examination and routine blood tests were within normal limits. While LGMD is not associated with difficult airways, there was concern for one because of the patient’s small mouth opening and beak-shaped mouth and jaw. Thus, an awake-fiberoptic intubation was performed and the airway was secured with a 7.0 mm endotracheal tube. The anesthesia team took precautions for MH and used a new anesthesia machine to avoid triggers. In the operating room, the patient was positioned at 45 degrees and semi-reclined. Maintenance of anesthesia was achieved with total intravenous anesthesia (TIVA) with propofol, dexmedetomidine, fentanyl, and paralysis with rocuronium. The patient was managed conservatively in the postoperative period and extubated without incident the following day. 

Discussion 

Literature on safe anesthetic management of LGMD is limited. In this case report, we highlight the successful use of TIVA in avoiding MH triggers, and the use of awake-fiberoptic intubation as an effective technique for securing a difficult airway in a patient with LGMD. 
Inhaled anesthetics and succinylcholine are contraindicated in LGMD patients because of an increased risk of developing MH, rhabdomyolysis, and hyperkalemia [1]. Using TIVA avoids the triggers of MH while maintaining appropriate anesthetic depth. Interval measurement of lactate and CK are also important in monitoring for development of MH. Dantrolene should be readily available for suspected MH. 
LGMD increases the risk of respiratory compromise under anesthesia, particularly since muscle relaxants can further exacerbate existing respiratory weakness. Awake-fiberoptic intubation requires thorough pre-anesthesia airway assessment and planning, preserves spontaneous ventilation, and mitigates the risk of respiratory decompensation associated with muscle relaxation, allowing for a controlled and gradual approach to securing the airway. In this case, a thorough airway assessment revealed potential challenges (limited mouth opening, and beak-shaped mouth and jaw) that could have complicated conventional intubation. Anticipation of potential airway challenges and advanced planning for an awake-fiberoptic intubation ensured a safe intubation and successful anesthetic for this patient.

Anesthetic Challenges of a Patient with Limb Girdle Muscular Dystrophy

Although uncommon, the loss of artificial valve components during surgery has been documented in the literature. If a valve fracture occurs intraoperatively, parts of the valve can either remain within the heart cavities or migrate distally into the thoracoabdominal aorta or aortic bifurcation. When the disc fragments, it may be found in the iliac, femoral, or even popliteal arteries. Historically, computed tomography (CT) scans have proven more effective in locating these fragments compared to plain radiography, angiography, and ultrasound.

Missing Aortic Valve Leaflet in Double Valve Replacement Surgery

Background
Pacemaker implantation is routine in modern day medicine, with nearly one million performed annually worldwide, and 200,000 in the United States alone. Despite being so commonplace, cardiac device implant can be associated with serious complications which require awareness for prevention and appropriate treatment. We present an unusual case of pneumomediastinum, pneumopericardium and contralateral pneumothorax following pacemaker implantation.

Case Presentation
A 71-year-old male with a history of coronary artery disease requiring multiple stents, ischemic cardiomyopathy causing heart failure with mildly reduced ejection fraction (40-45%), abdominal aortic aneurysm requiring endovascular aorta repair, hypertension, type II diabetes, and atrial fibrillation presented to the hospital after a significant conversion pause was noted by event monitoring. He subsequently underwent dual chamber pacemaker placement via the left subclavian vein with creation of a left chest wall pocket; insertion of the ventricular lead in the left bundle branch area was noted to be challenging requiring multiple attempts. However, the dual chamber pacemaker implantation was otherwise routine without immediate complications. Proper lead position was confirmed via fluoroscopy.

The patient was admitted overnight for observation. The following morning, routine chest x-ray discovered a right apical pneumothorax and pneumomediastinum. Subsequent CT chest revealed moderate-volume right pneumothorax and pneumopericardium, with the atrial lead extending into the right pleural space. The right atrial lead tip bored through the atrium into the lungs, creating a channel leading to communication between lung parenchyma, pleural space and the pericardium. The surgery service subsequently placed a right-sided chest tube. Imaging the next day demonstrated resolution of pneumothorax and pneumopericardium. The chest tube was removed the following morning, with the patient remaining asymptomatic throughout his post-procedural recovery. Due to concern for potential dislodgement or further extension of the right atrial lead into the right pleural space, it was successfully extracted prior to discharge. 

Discussion
This case represents an unusual mechanism of pneumothorax after pacemaker implant, which typically occurs due to inadvertent lung puncture ipsilateral with vascular access. Patients with pneumothorax and pneumopericardium may initially present asymptomatically, then later develop symptoms days later including pleuritic chest pain and shortness of breath. Findings may not be readily apparent on chest x-ray depending on burden of air and may require lead removal or repositioning. Clinicians must maintain a high index of suspicion when thoroughly analyzing post-procedural images.

A Lighthearted Case: Pneumopericardium and Contralateral Pneumothorax following Pacemaker Implantation

Background:
Lyme disease is the most common tick-borne illness in the United States, with a prevalence of approximately 500,000 cases annually. Myocarditis is a rare Lyme complications recent data demonstrated prevalence of Lyme myocarditis to be 1% and usually appears 1-2 months after initial infection. We hereby present a rare case of early-onset Lyme Myocarditis.

Case Presentation: 
A 35-year-old male with no significant past medical history presented to the hospital with four days of fever, myalgia, and headache. The day prior to admission, he found a tick at his home and developed a circular rash. He denies chest pain, SOB, palpitations, dizziness. He had no prior medical or family history of cardiac disease and denied tobacco, alcohol, and illicit drug use. He lives with his wife and owns a dog. On physical examination, T 102.6F, HR 103, BP 109/68, RR 19, SpO2 96% on room air. A target lesion was noted on his right thigh; rest of the physical examination was benign. His labs revealed positive serology for B. Burgdorferi IgM antibody, positive western blot, high sensitivity troponin 240; EKG was normal sinus rhythm with no ST or T wave changes. The patient was diagnosed with early localized Lyme disease and discharged home on doxycycline; the troponin elevation was attributed to the fever. He returned to the hospital the next day with chest pain and palpitations; exam was normal, high sensitivity troponin was 267 and ECG was unchanged. Echocardiogram demonstrated EF of 60% without any valvular abnormalities or effusions. He declined cardiac catheterization; a pharmacological nuclear stress test did not show perfusion defects. He was diagnosed with Lyme myocarditis and treated with two-weeks course of ceftriaxone with clinical improvement. 

Discussion: 
Myocardial involvement in Lyme disease results from spirochete colonization in cardiac tissue and subsequent exaggerated immune response, most commonly leading to myocarditis and subsequent heart block; which occurs 1-2 months after Borrelia infection. Typical clinical manifestations of Lyme myocarditis include palpitations, chest pain, conduction abnormalities, pericarditis and heart failure. The diagnosis is clinical and made by, positive Lyme serology accompanied by EKG changes and symptoms. other tests that can point to cardiac involvement include troponins, positive echocardiogram, and negative CAD testing. Treatment depends on clinical status; asymptomatic patients with 1° AV block can be treated with oral antibiotics, whereas symptomatic patients will require IV antibiotics, and patients with 3° heart block may require temporary pacemakers. 


A rare-case of early stage lyme myocarditis

Background: The incidence of gastro-intestinal stromal tumors is 1-2% of all gastrointestinal malignancies [1]. These rarely metastasize to the heart [2], causing atrial fibrillation. The drug of choice is imatinib. This is known to have GI side effects, and infrequently, direct cardiac toxicity. Here, we present a case of atrial fibrillation in a patient with GIST on imatinib therapy, and outline the workup of this rare presentation. 
Case: 84 year old male with spindle cell GIST (4.9 X 3.5 cm) in the gastric fundus, on imatinib 400mg OD for 3 weeks was hospitalized for new onset atrial fibrillation (Figure 1), fever and lymphadenopathy. No history of shortness of breath, chest pain, headaches or palpitations. There is history of severe diarrhea, vomiting and weakness in the last week.  On examination, vitals were normal. Bloodwork showed an eosinophil manual count of 73% (normal: <7%) and atypical lymphocytosis. Workup for the cause of atrial fibrillation (echo, cardiac CT, chest X ray, electrolytes) was done and was normal. Patient was started on eliquis 2.5 mg BD and rate control for atrial fibrillation. Patient developed AKI and transaminitis during the course of hospitalization. Imatinib was held, and patient was started on steroids. On steroids, his eosinophil count normalized, rhythm returned to sinus, renal and liver function dropped back to baseline. The patient was referred to oncology to switch to a different tyrosine kinase inhibitor. Steroids were tapered and discontinued. Patient was asked to review in cardiology clinic for follow – up of atrial fibrillation. 
Discussion: Four potential causes of AF were considered in this patient: cardiac metastasis from the GIST, direct drug toxicity, dehydration induced, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome due to imatinib [3,4]. Imaging revealed no evidence of cardiac metastasis. Electrolytes were normal, ruling out dehydration as a cause. AF is an uncommon side effect of imatinib (0.55% of patients) [5]. In this case, temporal correlation suggested a possible association. However, the markedly elevated eosinophil count raised suspicion for DRESS [6]. Scoring according to RegiSCAR system suggested probable DRESS. The patient markedly improved on steroids, further confirming our theory. Several studies have reported cases of imatinib-induced DRESS syndrome, and atrial fibrillation in DRESS (7.1%) [3] supporting our clinical findings.  In conclusion, this case is a good example of the importance of considering multiple etiologies for AF in cancer patients undergoing targeted therapy. Clinicians should remain vigilant, follow a comprehensive diagnostic approach and promptly intervene to mitigate adverse events. 

Atrial Fibrillation in a Patient with GIST on Imatinib – What are the causes?

Background: 
Pulmonary embolism (PE) is a life-threatening condition characterized by the blockage of a pulmonary artery or one of its branches. The intricate relationship between substance abuse and thromboembolic events has emerged as a significant concern in clinical medicine. Cocaine, a potent vasoconstrictor, has been associated with both arterial and venous thrombotic events due to its prothrombotic effects on the coagulation cascade and its impact on the vascular endothelium. We present a case of a 42-year-old male with a history of cocaine abuse who presented with a life-threatening PE. 
Case Presentation: 
A 42-year-old male with a past medical history of cocaine abuse presented after a syncopal episode. He described the episode as passing out from a standing position and regaining consciousness quickly on the ground. He endorsed a 3 day history of worsening dyspnea and lightheadedness. On examination, the patient was experiencing mild respiratory distress and was found to be tachycardic. ECG revealed sinus tachycardia with evidence concerning for right heart strain. Laboratory findings were significant for elevated troponin and pro-BNP. 
A ventilation/perfusion lung scan was ordered which showed a high probability of PE. A subsequent CT angiography of the chest was performed which confirmed acute bilateral pulmonary emboli with moderate-large clot burden and evidence of right heart strain with a right ventricle to left ventricle size ratio of 1.35. Lower extremity doppler ultrasound was positive for deep vein thrombosis in the right popliteal vein. 
The patient was evaluated by the interventional cardiology team and was taken for mechanical thrombectomy of the pulmonary emboli. Pre-intervention right heart catheterization was significant for a mean pulmonary artery pressure of 47 mmHg and a pulmonary capillary wedge pressure of 23 mmHg. The clot burden was reduced by greater than 90% and excellent filling with a good venous phase of all pulmonary arteries was noted. The patient improved symptomatically after the procedure. 
Discussion: 
Cocaine's prothrombotic properties are multifaceted, involving the activation of the coagulation process and the secretion of von Willebrand factor (VWF), among other factors, which collectively contribute to thrombus formation. The presence of adulterants in cocaine, such as levamisole, further complicates its pathophysiological impact, potentially exacerbating pulmonary damage and fibrosis, thus predisposing individuals to thromboembolic events. The reported case emphasizes the need for a high index of suspicion for cocaine-induced PE in patients with a history of substance abuse presenting with symptoms suggestive of thromboembolic events.

BEYOND TRADITIONAL RISK FACTORS: COCAINE ABUSE AND PULMONARY
EMBOLISM

Background:
Complete heart block (CHB) is a potentially life-threatening conduction disorder characterized by the complete absence of electrical impulse transmission from the atria to the ventricles. While commonly associated with advanced age and structural heart disease, CHB can also present atypically, particularly in elderly patients. Potential consequences of delayed diagnosis of CHB can consist of syncope, heart failure and even cardiac arrest. This case report describes a 79-year-old male with a history of hypertension and tobacco abuse who presented with atypical symptoms of CHB.
Case Presentation:
A 79-year-old male with a past medical history of hypertension and tobacco abuse presented with shortness of breath of several days duration. He noted body aches, upper respiratory symptoms, and malaise during the week prior. In the past month, he reports having intermittent episodes of lightheadedness. He was previously hospitalized a few months before for similar episodes of lightheadedness, but refused workup. At home in the morning before admission, a low oxygen saturation and heart rate were noted.
On examination the patient was alert, oriented, and answering questions appropriately. He was breathing comfortably on supplemental oxygen via nasal cannula. An ECG was then performed and the patient was found to have a complete heart block with a rate in the 30s. On continuous monitoring, his heart rate continued to drop into the 20s without worsening symptoms. He was then moved to the ICU for placement of transvenous pacemaker.
The patient was not taking any pharmacological agents that could have caused his condition. A transthoracic echocardiogram showed a preserved ejection fraction. Left heart catheterization revealed non-occlusive disease. He was taken for permanent pacemaker placement which led to resolution of all symptoms.
Discussion:
This case highlights the often atypical presentation of CHB in elderly patients. While the classic presentation involves syncope or near-syncope due to bradycardia, this patient primarily reported shortness of breath and malaise. Additionally, despite experiencing prior episodes suggestive of CHB, he initially declined a workup. This stresses the need for thorough clinical evaluation in elderly patients, even when symptoms appear mild or unrelated to cardiac dysfunction. The absence of structural heart disease on echocardiogram and non-occlusive coronary arteries on angiography suggest an idiopathic or functional etiology for the CHB in this case. The prompt diagnosis and placement of a permanent pacemaker resulted in complete symptom resolution. This emphasizes the critical role of early intervention in managing CHB and preventing potential complications such as heart failure or syncope-related injuries.

Complete Heart Block in an Elderly Male with Atypical Presentation


Abstract Title
Myocarditis post-COVID-19 Vaccination

Background: 
Reports to the Vaccine Adverse Event Reporting System (VAERS) have highlighted a possible association between mRNA COVID-19 vaccines and myocarditis, particularly in males between 12 and 39.1 This case report investigates a rare instance of myocarditis in an adult male following mRNA vaccination, emphasizing the need for heightened clinical awareness.

Case Presentation :
A 38-year-old male with no prior medical history presented with acute chest pain and shortness of breath one day after receiving his second Moderna COVID-19 vaccine dose. An EKG showed nonspecific ST elevations and elevated troponin levels, peaking at 16 ng/mL. Coronary angiography ruled out coronary artery disease, and cardiac MRI indicated myocarditis, characterized by delayed intramural enhancement.

Discussion :
This case exemplifies myocarditis as a potential adverse effect post-COVID-19 vaccination, a phenomenon that demands attention due to its potentially severe implications. Immunological reactions like those elicited by viral infections may play a role, potentially involving an exaggerated inflammatory response to the vaccine's spike protein, leading to myocardial injury.1 The rapid symptom onset post-vaccine and elevated cardiac biomarkers strongly suggest a causal relationship.
While vaccine-associated myocarditis generally follows a benign course, severe outcomes like arrhythmias and heart failure require vigilant monitoring and management. Treatment focuses on anti-inflammatory medications and, if necessary, immunosuppressive therapy, especially when cardiac function is compromised.1
Despite the low incidence of myocarditis relative to the millions of vaccine doses administered, these cases highlight the need for ongoing surveillance and research to refine our understanding and management strategies. Improved knowledge of vaccine-related myocarditis is essential for developing educational programs for healthcare providers and informing the public to ensure early detection and treatment.


Covid-19 Vaccine Induced Myocarditis

BACKGROUND
Immuno-oncology (IO) therapy is often associated with immune-related adverse effects (irAEs) varying in severity and involving different organs. There are many common irAEs; however, the rare irAEs include myocarditis, pericarditis, colitis, pneumonitis, dermatitis, and hepatotoxicity, which are associated with higher rates of morbidity and mortality. Approximately 0.06%–2.4% of SCLC patients develop IO-related myocarditis.
CASE PRESENTATION
A 74-year-old female with a past medical history of hypertension, O2-dependent COPD, pAF, SCLC, and a 40-pack-year history of tobacco abuse presented to the hospital with chest and back pain. Her pain radiated towards the epigastric region, and she was also experiencing nausea. She received two cycles of carboplatin/etoposide followed by two cycles of chemoradiation, during which substantial tolerance issues were noted, even with dose reductions and treatment delays due to AF, respiratory failure, and influenza. After deferring therapy, her condition relapsed within several months, and she was started on Nivolumab monotherapy four weeks prior to her admission.
Upon presentation, it was noted that the patient’s troponin T was elevated (177 ng/L). She also had an abnormal NT-proBNP (10,279 pg/ml), and the ECG suggested NSTEMI changes. The CT thoracic spine reports indicated a T9 compression fracture, which correlated with the site of back pain. For the concurrent chest pain, a TTE was performed, showing depressed RV systolic function, grade I diastolic dysfunction, and LVEF of 45-49% (previous LVEFs of 50–54%). Since multiple abnormalities were noted on TTE and ESR, CRP were elevated, and a cardiac MRI was performed. Due to a drop in EF, a diagnosis of immune-mediated myocarditis due to Nivolumab was suspected. The patient was started on Solumedrol-1 mg/kg, resulting in clinical improvement. A cardiac MRI was performed four days after initiation of treatment, demonstrating wall motion abnormalities in the mid/distal septal wall with patchy segments of non-CAD LGE in the mid-distal septum and apical septal wall. Findings were consistent with IO-associated myocarditis.
DISCUSSION
PD-1 inhibitors, such as Nivolumab, represent an effective treatment option for SCLC that induces irAEs. Myocarditis associated with ICIs necessitates immediate and continuous monitoring after starting immunotherapy. This case seeks to raise awareness for early detection and intervention, which are essential in managing ICI-induced myocarditis. Elevated cTnI levels and ECG changes are key biomarkers. Frequent ECG changes include T waves, ST segment abnormalities, and arrhythmias. As seen in this case, high doses of glucocorticoids are effective in alleviating symptoms, especially in cases of severe myocarditis.

Premium content

Downloads

Next from AMA Research Challenge 2024

Navigating Anaplasmosis: A Case Report Highlighting Diagnosis and Treatment

Similar lecture

Neuraxial Anesthesia for Cesarean Delivery in a Patient with Intracranial Hemorrhage and Chronic Anticoagulation