Case Report or Series Posters

Introduction/Background:

Kounis Syndrome is a hypersensitivity-mediated acute coronary syndrome (ACS) classified into three types: Type I (coronary vasospasm), Type II (plaque rupture with thrombosis), and Type III (stent thrombosis). Type III is the rarest and presents significant challenges in percutaneous coronary intervention (PCI). We report a case of recurrent in-stent thrombosis following PCI, suspected to be due to Type III Kounis Syndrome.

Description:

A 67-year-old female with type 2 diabetes and hyperlipidemia presented with substernal chest pressure radiating to the left shoulder. Symptoms worsened with exertion but were not associated with dyspnea or indigestion. Electrocardiogram (EKG) showed an inferior ST-elevation myocardial infarction (STEMI), with troponin elevated to 1.7K. Emergent coronary angiography demonstrated a 99% stenosis in the mid-right coronary artery stenosis with acute occlusion, treated with a drug-eluting stent. Shortly after PCI, she developed recurrent chest pain, and repeat angiography revealed in-stent thrombosis requiring an additional stent and eptifibatide infusion. Post-procedure transthoracic echocardiogram showed an ejection fraction of 59% with basal inferoseptal and inferior wall hypokinesis. She later developed hypotension, dizziness, and a hemoglobin drop from 13.6 to 7.7 g/dL. CT imaging revealed a retroperitoneal hematoma. Given her history of contrast allergy and recurrent thrombosis, Type III Kounis Syndrome was suspected. She was stabilized on dual antiplatelet therapy with aspirin and prasugrel and managed conservatively, with plans for staged PCI of the left anterior descending artery.

Discussion:

Type III Kounis Syndrome occurs when allergic reactions induce coronary stent thrombosis through mast cell degranulation, leading to platelet activation and thrombus formation. This patient’s contrast allergy suggests a possible allergic trigger, highlighting the need for heightened clinical suspicion in post-PCI patients with recurrent thrombosis. Management involves addressing allergic mechanisms with corticosteroids and antihistamines alongside standard ACS therapy. This case emphasizes the need to recognize allergic reactions as potential contributors to adverse cardiac events, particularly in patients with known hypersensitivities.

Introduction/Background:

A fully vaccinated 16-year-old female from Mexico with PMH of sinusitis requiring surgery, presented with a three-month history of chronic pharyngitis despite multiple courses of antibiotics, difficulty swallowing, voice changes, fevers, chills, and a 30-pound weight loss. ROS revealed acute-onset worsening throat pain, right-sided headache, ear pain, cough, and biliteral lacrimation. On exam, she was non-toxic, visibly uncomfortable. She had a severely muffled voice, lacrimation, bilateral tonsillar hypertrophy, pseudomembranes on right tonsil/pharynx, and difficulty swallowing thick secretions. Her neck was supple with normal ROM and no tenderness. She saturated well on room air but was tachycardic, had mild hepatosplenomegaly, and mild non-pitting edema of bilateral lower extremities.

Description:

Serum studies revealed pancytopenia, lymphopenia, elevated inflammatory markers, elevated EBV IgG, and significant depletion of T and B cells. She tested negative for HIV twice. Throat biopsy cultures were positive for resistant pseudomonas and yeast, negative for diphtheria. CT and MRI identified significant retropharyngeal edema, tonsillitis, supraglottitis, thickening of the epiglottis creating a critical airway, diffuse pansinusitis, and gallstones. Bone marrow and tonsil biopsy flow cytometry were negative. Her symptoms never resolved despite multiple rounds of antibiotics while inpatient. Given the cytopenias and chronicity and progression of symptoms, there was high suspicion for underlying immunodeficiency. Immunology testing revealed a diagnosis of autosomal recessive hereditary major histocompatibility complex class I deficiency, also known as Bare Leukocyte Syndrome (BLS) Type I. This is an extremely rare subtype of severe combined immunodeficiency syndrome (SCID), with only 30 cases reported in medical literature. It can sometimes be treated with a stem cell transplant. Three days before this patient’s scheduled transplant she suffered an episode of massive hematemesis, and despite several attempts to secure her airway, she went into cardiac arrest and expired.

Discussion:

BLS typically presents in the first year of life with recurrent infections and often results in death before puberty, like other congenital immunodeficiencies. Rarely, patients with a heterotypic phenotype can present later in life, as in this case. Therefore, when presenting symptoms are chronic or resistant to treatment, suspicion should remain high for immunodeficiencies regardless of age.

Introduction/Background:

Rotational Vertebral Artery Syndrome, or Bow Hunter’s Syndrome, is characterized by vertebral artery occlusion or stenosis due to compression from cervical vertebrae or bony abnormalities, leading to ischemia with head movement. Its prevalence is not well documented, but it is most common in the fifth to seventh decades of life, more common in men, and the left vertebral artery is more often affected. The gold standard of diagnosis is cerebral angiogram.

Description:

A 9-year-old male with a recent diagnosis of abdominal migraines with aura presented with acute right-sided numbness, weakness, and unsteady gait. There was no recent illness or trauma. The patient had three recent ED visits for headache, blurry vision, dizziness, and right-sided facial and upper extremity numbness, typically resolving within 15 minutes. Workups, including MRI/MRV/MRA, only revealed a Chiari I malformation. However, this episode had been ongoing for several hours. In the ED, vitals were normal. Mental status was appropriate, and strength was normal. However, he had mild pronator drift of the right arm and leg, dysmetria on the right finger-to-nose test, right facial droop, and intermittent unsteadiness, prompting a stroke code. MRI showed a nonhemorrhagic left thalamic infarct. MRA head and neck were unremarkable. Basic labs, cardiac, and coagulation tests were normal. Hematology and neurology teams were consulted, and daily aspirin was started. On day three of admission, he had a new right leg weakness that lasted 10 minutes. Given the brief intermittent nature of his symptoms, it raised concern for TIAs. A cerebral angiogram was obtained and showed an irregularity in the distal V2/proximal V3 of the left vertebral artery, with focal stenosis exacerbated by head movement, confirming Bow Hunter’s Syndrome.

Discussion:

Both migraines and strokes can present suddenly. In patients with a history of migraines, any sudden, intense symptoms should raise concern for serious underlying conditions. Symptoms of stroke exacerbated by head movement can be a significant clue for Bow Hunter’s Syndrome. In this case, the family recalled an episode when the patient developed symptoms while looking down and kicking a ball, prompting consideration of head/neck positioning as a trigger. Clinicians should maintain a high index of suspicion for structural or vascular abnormalities in cases with recurrent or progressive features.

Introduction/Background:

Immune checkpoint inhibitors (ICI) are being incorporated in treatment of various malignancies, activating T-cell responses against tumor cells, but occasionally triggering immune related adverse events (irAEs) by inadvertently attacking healthy tissue. Endocrinopathies due to ICI occur in 10% of patients, frequently manifesting as hypophysitis or thyroid dysfunction. ICI-induced diabetes is much rarer, with a 0.45% prevalence, as noted in a cohort study of 14,328 patients between 2010-2022 (1). Early detection is difficult due to nonspecific symptoms. This report details a case of ICI-induced diabetes and diabetic ketoacidosis (DKA) caused by ipilimumab and nivolumab therapy.

Description:

A 48-year-old female with metastatic ovarian clear cell carcinoma, receiving ipilimumab and nivolumab treatment for the past three months, presented with nausea, vomiting, anorexia, and polydipsia for a week. She had prior ICI-induced hypophysitis, requiring prolonged steroids. On admission she was alert and oriented, but lethargic. Vitals were notable for tachycardia and hypertension. Labs confirmed DKA with hyperglycemia of 492 (70-99 mg/dL), metabolic acidosis with pH 7.22 (7.35-7.45 units), bicarb 13 (21-32 mmol/L), anion gap 26 (7-19 mmol/L), and ketosis with beta-hydroxybutyrate >8 (0.0-0.3 mmol/L). C-peptide was 0.1 (0.8-3.9 ng/mL), indicating lack of insulin production. She received fluids, electrolyte repletion, and insulin drip before transitioning to basal-bolus insulin for ICI-induced diabetes. Post discharge, she is now followed by endocrinology and uses a continuous glucose monitor to guide insulin requirements. Her immunotherapy is temporarily held and may be discontinued given multiple irAEs.

Discussion:

This case highlights the insidious nature of ICI-induced diabetes. Unlike other irAEs treated with a steroid course, endocrine toxicities can require lifelong hormone replacement. It is important clinicians recognize these irreversible effects and counsel patients accordingly. Endocrinopathies typically emerge 14.5 weeks after ICI initiation but can occur within a week or years later. Cohort studies have shown that the incidence of ICI-induced diabetes is 124.8 per 100,000 person-years, a 7-fold increase compared to type I diabetes in ICI-naïve patients (1). Combination ICI therapy and preexisting type 2 diabetes further heighten the risk, making frequent screening and early endocrinology evaluation essential to prevent life-threatening presentations such as DKA.

Introduction/Background:

Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN) is a rare hematologic malignancy that can present with or without involvement of bone marrow, skin, peripheral blood, and central nervous system. Pediatric BPDCN is less aggressive with more favorable outcomes than the more common adult BPDCN.

Description:

Our case is a 14-year-old otherwise healthy female who presented with prolonged right calf discoloration and swelling. While otherwise asymptomatic, walking and hot showers exacerbated the swelling and discoloration. Fevers, night sweats, weight loss, and bone pain were denied. The calf lesion measured a 5 x 3 cm area of presumed ecchymosis that was non-fluctuant, non-indurated, and nontender. The initial laboratory workup was unremarkable. A punch skin biopsy performed at an outside hospital was read as lymphoblastic lymphoma. On initial visit at Advocate Children’s Hospital-Oak Lawn she was noted to have a dry, non-pruritic, hyperpigmented nodular plaque measuring 13 x 12 cm. Smaller hyperpigmented lesions were present on the legs, arms, right buttock as well as a 2 x 3 cm nodular lesion on the left cheek. Repeat biopsy with flow cytometry and cytogenetics confirmed the diagnosis of BPDCN. There was no evidence of leukemic involvement. Chemotherapy utilizing the high-risk ALL protocol AALL1732 was initiated with resolution of cutaneous lesions within a month. A repeat biopsy done six months later showed no evidence of disease.

Discussion:

Pediatric BPDCN is uncommon with fewer than 100 cases reported. Clinical presentation can range from a single nodule to widespread cutaneous manifestations followed by rapid leukemic dissemination. In a case series, 73% of patients only had nodular lesions, 12% had bruise-like patches, and 14% had mixed lesions. Current treatment regimens are not standardized. Best outcomes are reported with high-risk ALL chemotherapy regimens. The role of biologic agents and stem cell transplants (SCT) are undetermined. Tagraxofusp is a biologic agent that targets CD123, a marker that is commonly overexpressed in BPDCN. Tagraxofusp has been shown in clinical trials to induce a 72% remission rate in adult patients. Additionally, both autologous and allogenic SCTs have been used successfully but are reserved for cases of second complete remission or when initial treatment does not result in rapid complete remission. Additional studies are required to further define optimal treatment in pediatric patients.

Introduction/Background:

Cutaneous sequelae of COVID-19 infections and vaccinations are increasingly recognized, with pustular dermatoses emerging as rare manifestations that can mimic generalized pustular psoriasis (GPP) or acute generalized exanthematous pustulosis (AGEP). This report details a case of pustular dermatosis following COVID-19 infection in a 24-year-old male.

Description:

The patient was presented with a three-day history of a painful pustular rash on his face, chest, and back developing 35 days post-COVID infection. No improvement with doxycycline for presumed folliculitis. He had a recent 16-day hospitalization for several multi-systemic post-COVID complications including encephalomyelitis, optic disc edema, and SIADH, which resolved with IVIG, pulsed methylprednisolone, and acetazolamide. Examination revealed multiple tender pustules with erythematous backgrounds, but no mucosal involvement. Laboratory findings were notable for leukocytosis with neutrophilic predominance. Dermatology and infectious disease guided further evaluation. Broad-spectrum antimicrobials, including IV vancomycin, fluconazole, and acyclovir, were initiated. Acetazolamide was discontinued. A punch biopsy spongiosis and ballooning degeneration of keratinocytes with superficial and deep perivascular and periadnexal dense neutrophilic infiltrate, focal sebaceus necrosis. No evidence of viral cytopathic change was seen. HSV and ZVZ PCR and IHC were negative. All other infectious workup was negative, including orthopoxvirus, EBV, CMV, and monkeypox virus. Given the absence of eosinophils in histology, AGEP was deemed unlikely. He was diagnosed with post-infectious COVID-19 pustular eruption. Clinical resolution occurred with symptomatic treatment, and acetazolamide was later reintroduced without recurrence.

Discussion:

This case underscores the diagnostic complexity of pustular eruptions post-COVID-19. Dermatologists should integrate clinical, histopathologic, and multidisciplinary perspectives when evaluating pustular dermatoses, ensuring exclusion of life-threatening infections while considering post-viral inflammatory dysregulation as a potential etiology.

Introduction/Background:

Thrombotic microangiopathy (TMA) is a syndrome causing thrombocytopenia and microangiopathic hemolytic anemia. It can be induced by drugs, pathogens, or the immune system. Drug-induced TMA is most often caused by chemotherapy agents, while cocaine-induced TMA is rare. A case of a patient with TMA, acute renal failure, thrombocytopenia, and MAHA after crack cocaine use is presented.

Description:

A 50-year-old male with COPD, hypertension, and crack cocaine use was initially hospitalized at an outside hospital for bloody diarrhea, shortness of breath, hematuria, fever, and chills after smoking crack cocaine. Initially treated for COPD exacerbation with antibiotics and steroids, he developed acute urinary retention, worsening creatinine (2.23 to 11.93 mg/dL), and metabolic acidosis requiring bicarbonate infusion. His hemoglobin dropped from 10.3 to 7.0 g/dL, and platelets from 123 to 10 K/mcL. Transferred to our hospital for suspected thrombotic microangiopathy (TMA) and plasmapheresis, he presented with elevated creatinine (12.80 mg/dL), severe anemia, low C3, schistocytes, and normal ADAMTS13. Testing for autoimmune and infectious causes was negative. Hemodialysis and plasmapheresis sessions were initiated. After treatment, kidney function gradually improved, and weekly eculizumab infusions were done. Nephrology and hematology advised continued hemodialysis and eculizumab with outpatient follow-up.

Discussion:

TMA is caused by various factors, including drug-induced, complement-mediated, hemolytic uremic syndrome (HUS), and thrombotic thrombocytopenic purpura (TTP). Our patient's TMA was likely due to crack cocaine use given the symptom onset after consumption, presence of schistocytes, low C3 levels, and normal ADAMTS13. Cocaine-induced TMA can result from activating the complement cascade, vasoconstriction, vascular damage, and platelet activation. Reports show cocaine depletes platelets by triggering the alternative complement pathway, leading to low C3 and normal C4, mirroring our patient’s findings. Cocaine-induced vasoconstriction impairs renal blood flow, leading to acute tubular necrosis and renal failure. Although renal biopsy could confirm TMA, it is unnecessary for diagnosis and contraindicated in acute kidney injury (AKI). In TMA cases, obtaining a thorough medical history, including drug use, is essential. Treating drug-induced TMA involves stopping the offending agent and providing supportive care. When TTP or TMA is suspected, initiating anti-complement therapy like eculizumab is prudent.

Introduction/Background:

Iatrogenic esophageal perforation (IEP) is a rare but serious complication that may occur during transesophageal echocardiography (TEE). The high mortality of this condition implores rapid identification for urgent antibiotic administration and potential surgical repair.

Description:

A 66-year-old female with gastric arteriovenous malformations and paroxysmal atrial fibrillation with recent left atrial appendage (LAA) closure presented with submandibular pain, swelling, and acute onset dysphagia. IEP was suspected as TEE had been performed within the preceding 24 hours for routine assessment of the LAA closure device. CT neck and esophagram were obtained exhibiting submandibular edema and gas locules without contrast extravasation concerning for Ludwig angina (diffuse cellulitis of bilateral submandibular, sublingual, and submental spaces) rather than perforation. Broad spectrum IV antibiotics were administered, and the patient underwent emergent incision and drainage. The patient was discharged without complication on oral amoxicillin-clavulanate and doxycycline.

Discussion:

TEE course was unremarkable with only minimal blood-tinged secretions observed post-procedure and the patient was discharged following a 2-hour observation and an unimpeded swallow challenge. The new onset of profound dysphagia, oral bleeding, increased volume of blood-tinged secretions, and pain prompted workup. CT neck without frank perforation and esophagram without contrast extravasation ruled out acute traumatic injury. As a result, an alternative diagnosis was considered, such as an infectious process. The patient was diagnosed with Ludwig angina in context of symptoms and additional imaging findings and was subsequently treated with empiric antibiotics and surgical intervention. Formulating a broad multisystem differential remains crucial to the expedient recognition of less common but highly morbid conditions. Developing and maintaining a broad knowledge base across multiple systems and critical pathologies remains essential for all clinicians to combat diagnostic bias and promote appropriate intervention. Pathologies may have a diverse range of symptoms and even mimic the characteristic presentation of unrelated disease mechanisms. Although critical to identify, the relative infrequency of IEP substantiates alternative diagnoses, such as infection of the oral cavity, e.g. Ludwig angina. This patient was successfully treated before incurring further sequelae and has recovered.

Introduction/Background:

Illness anxiety disorder is a mental health condition that often leads to frequent emergency room (ED) visits due to excessive worry about health and impulsive behaviors surrounding medical evaluation. This case report follows a 59-year-old male patient with illness anxiety disorder who was seen by a primary care physician (PCP) on a weekly basis over three years. Prior to these weekly visits, the patient had an average of 12 ED visits per month, often related to health anxieties. Over the course of the three-year period, alongside psychiatry support for medication management, cognitive behavioral therapy, and access to a 24-hour triage line, this resulted in a dramatic reduction of his ED visits to an average of 4 ED visits per month.

Description: Current literature highlights that individuals with illness anxiety disorder often experience heightened health-related anxiety and compulsive behaviors surrounding medical evaluation, which contributes to frequent ED visits. While there are limited published studies on illness anxiety alone, a greater depth of literature surrounding health anxiety supports comprehensive management, including regular medical follow-up, psychiatric care, and psychotherapy. This approach can significantly reduce unnecessary ED utilization in these populations. The role of the PCP remains the cornerstone of the management of illness anxiety disorder; however, this case uniquely demonstrates the efficacy of more frequent PCP follow-up and the significance of rapport building as well as providing continuity of care, reassurance, and addressing both physical and mental health concerns in an integrated manner.

Discussion:

The clinical importance of this case lies in the potential to not only reduce healthcare costs but also improve patient outcomes by offering a comprehensive, accessible care model. Future directions may include research into optimizing PCP involvement in patients with illness anxiety disorder and health anxiety, particularly exploring the long-term effects of weekly follow-up visits on both mental and physical health outcomes as well as evaluating the sustainability of reduced ED visits. The key takeaway from this case is the potential of frequent PCP follow-up and the power of the therapeutic relationship to substantially decrease unnecessary ED visits in patients with illness anxiety disorder and health anxiety. This approach promotes patient empowerment and reduces unnecessary healthcare utilization.

Introduction/Background:

Acute onset focal neurological change of the lower extremity is a medical emergency with a broad differential including stroke, transverse myelitis, acute inflammatory demyelinating polyneuropathy, acute flaccid paralysis, spinal tumor, epidural abscess, and tick paralysis. In this case series, we describe two pediatric cases of spinal cord ischemia (SCI) of which there are limited reports in the literature.

Description:

Case 1: An 11-year-old female with a history of autism spectrum disorder presented with acute onset ataxia, lower extremity weakness, loss of lower extremity deep tendon reflexes and urinary incontinence. She had a viral illness the week prior and a suspected allergic reaction the day prior. Initial work up for stroke, including magnetic resonance imaging (MRI) of the brain and spinal cord and lumbar puncture were negative. 96 hours later, with no clinical improvement, subsequent MRI with diffusion weighted sequence (DWI) revealed a stroke of the spinal artery territory from C3/C4 to T3/T4, along with a tear in the posterior annulus fibrosis of the C6-C7 disc. This was suggestive of fibrocartilaginous embolism (FCE). Case 2: A 13-year-old healthy male presented with acute onset right lower extremity weakness, numbness, and inability to urinate. The day prior, he felt a few minutes of right foot numbness while gardening. On exam, he had complete paralysis and hyperreflexia of his right lower extremity, numbness in both legs, and a loss of sharp/ cold sensation and areflexia in the left lower extremity. Initial MRI was normal; subsequent MRI with DWI identified an acute infarction in the spinal cord from C6-T4 and a small central disc protrusion with an annular fissure at C6-C7.

Discussion:

SCI occurs due to disrupted blood supply to the spinal cord, due to generalized hypotension, vascular injury/compression, thrombosis, or embolization to the spinal arteries. In both cases, the likely etiology for these patients’ SCI was an FCE. The first case had no known inciting event, but the second case was likely precipitated by increased intradiscal pressure associated with gardening maneuvers. As it is not always evident on typical MRI spine sequences, a high index of suspicion is needed to ensure DWI sequencing is obtained. Once diagnosed, treatment is supportive, focusing on intensive rehabilitation. Valsalva maneuvers should be avoided in the first 48 hours to limit extension of the stroke. The degree of recovery is variable.

Introduction/Background:

Extravascular implantable cardioverter defibrillator (EV-ICD) implantation is contraindicated in patients who have had a prior sternotomy. We describe the surgical implantation of an EV-ICD lead in a patient with Ebstein’s anomaly during repeat tricuspid valve (TV) surgery and clinical sustained ventricular tachycardia (VT).

Description:

A 49-year-old man with a history of Ebstein’s anomaly and TV repair without mobilization of posterior and septal leaflets presented with heart failure symptoms. He was in atrial flutter (AFL) with uncontrolled ventricular rates. Echocardiography showed Ebstein’s anomaly with torrential TV regurgitation. TV surgery was planned, but sustained VT occurred while awaiting the operation. Electrophysiology and cardiothoracic surgery teams jointly planned the treatment of AFL and VT. The electrophysiologist performed a preoperative AFL cavotricuspid isthmus ablation. Then an intraoperative right atrial maze procedure, redo TV replacement due to inadequate leaflets from prior repair, plication of the atrialized right ventricle, and left internal mammary artery to left anterior descending coronary artery grafting were completed. To avoid placing a lead across the new TV, an EV-ICD lead was sutured to the anterior surface of the right ventricle. Lead testing showed excellent sensing with an R wave of 4.0 mV and no P wave oversensing. Postoperative heart block was treated with a permanent pacemaker with atrial and coronary sinus branch leads to avoid crossing the TV and desynchronizing the left ventricle.

Discussion:

This is the first case in the United States of a surgically placed EV-ICD lead in a patient with a prior sternotomy. It highlights the importance of collaboration between electrophysiology and cardiothoracic surgery in the innovative treatment of complex arrhythmias in patients with congenital heart disease.

Introduction/Background:

Botulism is caused by botulinum neurotoxin (BONT), produced by the anaerobe Clostridium botulinum which causes descending paralysis due to irreversible blockade of pre-synaptic acetylcholine release. Forms include foodborne, infant, wound and iatrogenic. Foodborne botulism is uncommon in the United States and due to improper food preservation, resulting in bacterial contamination, growth and toxin production. Treatment is with botulinum antitoxin (BAT) which binds unbound toxin.

Description:

62-year-old F presented to the Emergency Department (EDP) with GI and neurological complaints 16h after ingesting broccoli cheddar soup (single-serving plastic package, commercially prepared). No PMH or medications. Alert, fully oriented, normal strength. BP 225/106. Sinus tachycarida 120 bpm. Otherwise normal exam. EDP +3h: Neurologist described “heaviness around her eyes and generalized fatigue.” Full visual fields, reactive pupils, conjugated gaze, but significant ophthalmoplegia. Face symmetric, decreased smiling. Dysarthric and dysphonic speech was difficult to understand. Strength decreased: arms 4+/5 and legs 1+/5. Reflexes decreased by 1+. EDP +4h: Transferred to ICU. Desaturation, severe hypercapnia and respiratory acidosis prompted tracheal intubation and mechanical ventilation. The differential diagnosis included Guillan-Barré Syndrome and variants such as Miller Fisher Syndrome, stroke and myasthenia gravis. Myelitis and tick-borne disease seemed improbable. Evaluation included CT head and neck, CBC, chemistries, MRI x2, CT head, EEG and lumbar puncture—all (-) as were cultures, meningitis panel, GM1, GD1b and GC1b antibodies. EDP+5d: Patient paralyzed. History from husband emphasized baseline high-energy state. He mentioned “eyelid heaviness” and diplopia, indicating descending paralysis and the possibility of botulism. CDC and WI Department of Health Services were consulted. Plasma and stool sampling were approved for testing and heptavalent BAT was released by the CDC and infused. EDP +10d: PCR for BONT type A (+). Subsequently, BoNT type A was confirmed by mouse bioassay. EDP +122d: Awake, moving digits, mechanically ventilated in long-term acute care hospital.

Discussion:

Our patient with food-borne botulism presented atypically: Urban, industrialized, sealed plastic container, spoiled taste inconsistent with contamination by C. botulinum as the toxin has no odor or taste. Botulism should be considered early in the differential of descending paralysis and prompt consultation with DPS to request BAT. Only BAT-eligible patients undergo botulism testing.

Introduction/Background:

Spontaneous coronary artery dissection (SCAD) is a rare, non-atherosclerotic cause of acute coronary syndrome, primarily affecting young women, often associated with pregnancy and hormonal changes, including in vitro fertilization (IVF). Pregnancy-associated SCAD (P-SCAD) presents diagnostic and management challenges due to physiological cardiovascular adaptations. This case highlights a recurrent SCAD event occurring both antenatally and postpartum, leading to ST-elevation myocardial infarction (STEMI).

Description:

A 38-year-old woman at 34 weeks of gestation via IVF presented with substernal chest pain. Initial ECG was unremarkable, but troponins rose from 191 to 5500. A repeat ECG showed T-wave abnormalities. Given hemodynamic stability, conservative management was initiated. She later developed non-sustained ventricular tachycardia, prompting coronary angiography, which revealed a Type II SCAD in the mid-left anterior descending (LAD) artery with 50% stenosis and TIMI III flow. She was treated with aspirin, labetalol, and nifedipine.

Hours later, she developed hypertensive emergency and pre-eclampsia symptoms with recurrent chest pain. A nitroglycerin infusion was initiated, later switched to labetalol. An urgent cesarean section was performed, after which her chest pain resolved without coronary intervention. She was discharged in stable condition.

In the postpartum period, she re-presented with chest pain and dyspnea. ECG showed an inferior STEMI. Coronary angiography revealed a long Type II SCAD in the right posterior descending artery with TIMI II flow, while the previous LAD SCAD had resolved. Due to inconclusive intravascular ultrasound, she was managed conservatively with an intra-aortic balloon pump, which was removed the following day.

Discussion:

SCAD should be recognized as a potential cause of acute coronary syndrome during pregnancy and postpartum. This case highlights the risk of recurrence in the postpartum period, emphasizing the need for close monitoring. Conservative management remains the first-line approach in stable cases, but individual considerations must guide treatment. Future research should focus on optimizing risk stratification and management strategies for P-SCAD to improve maternal cardiovascular outcomes.

Introduction/Background:

Historically, using beta blockers in patients with active cocaine use was considered taboo due to concerns about unopposed alpha stimulation, which can present life-threatening complications. While emerging studies suggest beta blockers' safety in cocaine users, this risk remains significant. Beta blockers are effective in managing hypertension and tachycardia from cocaine use but can worsen the clinical course in some patients.

Description:

A 42-year-old male presented to the Emergency Department with severe left shoulder pain radiating down the arm after a night of heavy alcohol use. His blood pressure was 175/119, and his heart rate was 114. He was moved quickly from triage due to his discomfort and agitation. He received 20 mg IV Labetalol before a CT scan. Subsequently, he became tachycardic, hypoxic, and his blood pressure increased. The patient was started on supplemental O2 and admitted for further management. A urine drug screen revealed cocaine use, which he either did not disclose or was unaware of. His initial complaint of left arm pain was found to be a chronic issue. A chest X-ray and CT scan suggested pulmonary edema. Labetalol was discontinued, and clonidine was started to manage both hypertension and post-cocaine anxiety. He was also restarted on his prior medications, amlodipine and lisinopril-hydrochlorothiazide, and given Ativan for additional anxiolytic benefits. By the next morning, heart rate normalized, and he was weaned off supplemental oxygen. With his blood pressure under control, he was discharged home with close follow-up with his primary care physician.

Discussion:

This case illustrates that while the interaction between cocaine and beta blockers may be rare, it is far from theoretical. Cocaine use is unfortunately common, with resultant nonischemic cardiomyopathy (NICM), hypertensive emergencies, and frequently presenting tachycardia. High clinical suspicion and risk stratification should be exercised before using beta blockers to prevent unintended negative outcomes.

Introduction/Background:

Transcatheter aortic valve replacement (TAVR) has revolutionized the treatment of severe aortic stenosis, especially in high-risk patients. Despite its minimally invasive nature, TAVR carries risks, including conduction abnormalities, vascular injury, and coronary obstruction. Left main (LM) coronary artery dissection is a rare but life-threatening complication. This case highlights a delayed LM dissection post-TAVR, requiring emergent coronary artery bypass grafting (CABG) and venoarterial extracorporeal membrane oxygenation (VA-ECMO).

Description:

A 79-year-old female with hypertension, hyperlipidemia, antiphospholipid syndrome on warfarin, and bilateral carotid artery stenosis underwent TAVR for symptomatic aortic stenosis. Preprocedural catheterization showed non-obstructive coronary disease. The procedure was complicated by transient complete heart block, requiring transvenous pacing. Postoperatively, she had a peri-arrest event with hypotension and bradycardia, responding to atropine and pressors. Electrocardiogram (ECG) revealed a new left bundle branch block and first-degree AV block, prompting implantation of a Micra pacemaker. Four days post-TAVR, she developed acute chest pain, dyspnea, and troponin >16K ng/L. Echocardiography showed ejection fraction (EF) 20% with regional wall motion abnormalities. Angiography revealed LM dissection extending from the aorta. Percutaneous intervention was unsuccessful due to hemodynamic instability, necessitating emergency CABG. Intraoperatively, she developed cardiogenic shock with EF 5%, requiring VA-ECMO. She was transferred to the ICU with an open chest on VA-ECMO and vasopressors. Over two days, she stabilized, allowing ECMO weaning and decannulation. Postoperative complications included cardiogenic shock, acute kidney injury requiring dialysis, and severe malnutrition. Despite challenges, she engaged in rehabilitation and was transferred to a long-term acute care facility.

Discussion:

Coronary dissection post-TAVR is rare and usually occurs intraoperatively. Delayed presentation, as seen here, is uncommon and complicates diagnosis. Potential mechanisms include guidewire or catheter trauma and altered coronary flow dynamics. Prompt recognition of ischemic symptoms and emergent intervention are critical. This case underscores the importance of vigilance, timely imaging, and a multidisciplinary approach to improving outcomes despite severe complications.

Introduction/Background:

The most common etiologies of intracardiac masses include myxoma, fibroelastoma, sarcoma, endocarditis, and metastatic tumors. Cardiac masses of testicular origin are rare. These are commonly found due to respiratory distress, cerebrovascular event, or severe anemia. Given the dynamic nature of these masses, our case supports the need for repeat cardiac imaging to prevent embolization.

Description:

A 37-year-old male with a noncontributory history presented with shortness of breath and right leg pain. He was diagnosed with intracardiac mass in the setting of suspected testicular cancer. A grade 4/6 systolic murmur at the left upper sternal border was appreciated. Imaging showed a right testicular mass, retroperitoneal lymphadenopathy, DVT, PE, and a right ventricular (RV) filling defect. Cardiac MRI displayed a 6.5 cm mass in the right ventricle causing outflow tract obstruction. A lymph node biopsy showed embryonal carcinoma, likely testicular in origin. His shortness of breath was attributed to PE and obstructive RV mass. He was anticoagulated and started on chemotherapy. Surgical intervention was deferred due to the likelihood that the RV mass would respond to chemotherapy. Two weeks later, he returned with worsening right leg pain after apixaban was held for 48 hours for chemotherapy port placement. Repeat imaging showed increasing mobile RV mass prolapsing through the pulmonic valve and advancing DVT. Percutaneous removal of the thrombus using expression thrombectomy catheter was considered. However, since the mass was directly below the tricuspid valve, he underwent surgical open approach embolectomy through the right atrium. Pathology showed atypical endothelial cells which stained positive for cytokeratin, a diagnostic marker for embryonal carcinoma metastases.

Discussion:

In young, healthy individuals, the presence of a RV mass and VTE should raise concern for malignancy. Holding anticoagulation may increase the risk of thromboembolism and should be limited. Clinicians must consider whether to pursue chemotherapy, percutaneous intervention, or surgical intervention accounting for risk factors, comorbidities, and decompensation. Increased mobility, location, and size of the mass may necessitate an expedited surgical approach over less invasive options. Close follow-up with repeat ECHO or cardiac MRI may improve outcomes by monitoring mobility to help prevent embolization. Future studies to determine the appropriate interval for imaging of intracardiac masses are needed.

Introduction/Background:

Lithium has long been used for treatment of bipolar disorder. However, its long-term use has been associated with renal toxicity. Most well documented is arginine vasopressin resistance, which often is self-limiting. While most patients on lithium do not have chronic kidney disease (CKD), studies demonstrate a positive association between lithium use and CKD. Unfortunately, the risk of developing CKD remains increased even once patients discontinue lithium use. Renal damage typically can be observed histologically, requiring renal biopsy. However, radiographic findings may also be present, and an astute clinician may consider less-invasive imaging instead. This case highlights the diagnostic utility of ultrasound in suspected lithium-induced nephrotoxicity.

Description:

A 68-year-old male with bipolar disorder on lithium and ziprasidone and hypertension on lisinopril and amlodipine presented for annual follow-up. He was taking 600 mg lithium nightly for over 10 years and was tolerating his medications well. Baseline creatinine for the prior 2 years was in the 1.2 to 1.4 range. His creatinine worsened to 1.50, and a referral to nephrology was placed, who saw him 2 months later. Urinalysis was unrevealing and the patient denied any symptoms nor significant renal history. Given lithium use, bilateral renal ultrasound was obtained, demonstrating innumerable echogenic foci with small cysts bilaterally. These findings suggested lithium-induced renal injury, and the nephrologist attributed his CKD to longstanding hypertension and lithium use. Lithium was not discontinued, with management focused on blood pressure control instead. Follow-up ultrasound 6 months later demonstrated persistence of multifocal cysts and echogenic foci, with a plan to discuss lithium alternatives with psychiatry should CKD worsen.

Discussion:

This case demonstrates the use of renal ultrasound in patients suspected to have CKD from long-term lithium use. While lithium therapy was not discontinued for this patient, future therapeutic decisions may be guided by a known diagnosis of lithium-induced nephrotoxicity. In patients with this diagnosis, ultrasound often demonstrates numerous uniform microcysts with punctate echogenic foci. These findings may also be observed on abdominal CT or with T2-weighted MRI. As such, in patients on long-term lithium therapy with new or worsened CKD, a renal ultrasound may aid in the diagnosis of lithium-induced nephrotoxicity.

Introduction/Background:

Acute cholangitis is a serious infection of the biliary tree with dire implications if not recognized early including up to 50% mortality. The classic triad of fever, right upper quadrant (RUQ) pain, and jaundice developed by Jean-Martin Charcot is often relied on to identify these patients. Acute cholangitis, however, can be missed or misdiagnosed when relying solely on these criteria. Our case series demonstrates a heterogeneous sample of patients who did not fulfill the classic criteria for acute cholangitis but indeed had cholangitis. Our aim is to emphasize the atypical nature of some cases to consider expanding or reforming Charcot’s Triad.

Description:

We reviewed the cases of 5 (3 F and 2 M) patients with a mean age of 51.2 years who were diagnosed with acute cholangitis but did not fulfill the classical triad of fever, jaundice, and RUQ pain. Patient 1: 70-year-old female who presented with fever but no RUQ pain or jaundice. Occult infection was suspected. ERCP showed a retained stone and pus in the proximal bile duct and was managed by sphincterotomy, stone removal, and intravenous (IV) antibiotics. Patient 2: 56-year-old male who presented with RUQ pain without fever or jaundice. ERCP showed common bile duct (CBD) stone with upstream purulent material. He was managed with IV antibiotics, sphincterotomy, stone extraction, stent placement, and cholecystectomy. Patient 3: 31-year-old female who presented with RUQ pain without fever or jaundice. ERCP showed pus flowing from the ampulla and numerous stones in the CBD. She was managed by IV antibiotics as well as sphincterotomy, stone extraction, and stent placement. Patient 4: 66-year-old male who presented with fever and jaundice but denied RUQ pain. ERCP showed bulging ampulla and pus flowing right after cannulation. Multiple stones and sludge were seen in the CBD. He was managed with IV antibiotics, sphincterotomy, stone extraction, and stent placement. Patient 5: 33-year-old female patient who presented with RUQ pain but no fever or jaundice. ERCP showed numerous stones and pus in the CBD with a dilated biliary system. She was managed with IV antibiotics, sphincterotomy, stone extraction, and stent placement.

Discussion:

Patients with acute cholangitis can present with a variety of symptoms that do not consistently fulfill Charcot’s triad. Care should be taken to apply these criteria as appropriate but to also consider expanding the classic definition of cholangitis.

Introduction/Background:

Neonatal hemoptysis is a rare but life-threatening presentation requiring rapid intervention.

Description:

We report the case of a 36-week infant born via repeat C-section who developed severe respiratory distress and massive pulmonary hemorrhage within hours of birth. Initial stabilization included high-flow nasal cannula (HFNC) and continuous positive airway pressure (CPAP), but progressive hemoptysis and hemodynamic instability necessitated endotracheal intubation and aggressive resuscitation. Despite interventions with epinephrine, tranexamic acid (TXA), and surfactant, the infant exhibited persistent hemorrhage and worsening metabolic acidosis (lactate 31.9), prompting venoarterial extracorporeal membrane oxygenation (VA-ECMO) initiation. In the pediatric cardiac intensive care unit (PCICU), the patient demonstrated cardiovascular dysfunction (EF 25%, moderate patent ductus arteriosus [PDA]), coagulopathy, and persistent bleeding, requiring Factor VII, TXA, and cryoprecipitate. The hemorrhage resolved by Day 3, allowing for ECMO decannulation by Day 7. Subsequent evaluation, including bronchoscopy, CTA chest, and cardiac catheterization, failed to identify a definitive source of bleeding. However, mild pulmonary hypertension and a small PDA were noted. The infant was successfully extubated and weaned off anticoagulation and inotropic support. By discharge on Day 34, the patient was stable on enalapril and furosemide with follow-up arranged for pulmonary hypertension and NICU teams.

Discussion:

This case highlights the complexities of neonatal pulmonary hemorrhage, coagulopathy, and cardiopulmonary instability, underscoring the importance of multidisciplinary management and ECMO support in refractory cases.

Introduction/Background:

Since 2019 the volume of Transcatheter Aortic Valve Replacements (TAVR) performed annually has surpassed Surgical Aortic Valve Replacements because of its favorable outcomes and reduction in median length of hospital stay. Potential complications such as high-grade AV block, tamponade, and hemorrhage can occur with TAVR. Non-occlusive mesenteric ischemia (NOMI) is a rare complication of TAVR but carries a high mortality. Our report presents a case of NOMI resulting in extensive bowel necrosis and patient mortality.

Description:

Patient is a 79-year-old female with history of abdominal aortic aneurysm status post Endovascular Aneurysm Repair (EVAR), and stable thoracic aortic aneurysm being evaluated for recurrent heart failure exacerbations and progressive dyspnea. Transthoracic echocardiogram (TTE) demonstrated low-flow low-gradient severe aortic stenosis with ejection fraction (EF) of 45%. A SAPIEN Ultra Resilia 26 mm valve was successfully implanted, and temporary pacemaker was placed due to transient AV block. TTE post-procedure revealed improved EF of 65%. Twenty-four hours later the patient developed profuse diarrhea and severe left sided abdominal pain. Labs at that time demonstrated leukocytosis with neutrophilic predominance and lactic acidosis. CT abdomen showed extensive mesenteric and gastric pneumatosis. Emergent laparotomy was performed which revealed necrosis from the gastroesophageal junction to the distal small bowel. Given the extent of necrosis and poor prognosis, the decision was made to proceed with palliative treatment.

Discussion:

Our patient had known non-obstructive stenosis of the eliac arteries with high grade stenosis of the Superior and Inferior Mesenteric arteries. Rapid pacing during TAVR deployment likely led to subsequent mesenteric ischemia. Therefore, special attention must be paid to patients with history of endovascular interventions such as EVAR or thoracic endovascular aortic repair, particularly in regard to the pre-procedural assessment of the mesenteric vasculature. Imaging modalities such as mesenteric CTA or MRA could allow for further risk stratification and prevention of NOMI. Additionally, post-procedural monitoring of lactic acid trends and interval abdominal examinations may afford earlier detection and subsequent intervention. Further investigation is necessary to identify effective pre-procedural risk stratification methods as well as post-procedural assessments and interventions.

Introduction/Background:

Tumor lysis syndrome (TLS) is a feared complication of anticancer therapy that results from massive tumor cell death and release of tumor cell contents into the circulation. It is commonly seen in hematologic malignancies such as acute leukemias and clinically aggressive lymphomas and rarely occurs in solid tumors. TLS can rapidly lead to permanent kidney damage and death even with appropriate, aggressive treatment.

Description:

A 67-year-old male began neoadjuvant treatment with cisplatin, gemcitabine, and nivolumab for stage IIIA squamous cell carcinoma of the lung. On day four, he presented to the emergency room for confusion and anuria and was found to be in acute renal failure with potassium 6.8 mmol/L, blood urea nitrogen 106 mg/dL, creatinine 6.67 mg/dL (baseline 0.7-1.0 mg/dL), calcium 8.2 mg/dL, phosphorus 11.9 mg/dL, uric acid 14.1 mg/dL, and LDH 351 U/L (normal range 86-234 U/L). He was treated with rasburicase, IV fluids, and urgent hemodialysis with improvement in his electrolyte disturbances, but unfortunately his kidney function did not recover, and he subsequently required three times weekly hemodialysis.

Discussion:

Tumor lysis syndrome is rare in lung cancers, and even more so in non-small cell lung cancer (NSCLC). There are currently 12 reported cases of TLS in NSCLC indexed in PubMed, 11 of which occurred in the setting of metastatic disease. Our case appears to be the first report of TLS in non-metastatic squamous cell carcinoma of the lung following initiation of systemic therapy. Known risk factors for TLS in solid tumors include bulky disease, rapidly growing tumors, and high sensitivity to anticancer therapy. Combination cytotoxic chemotherapy is the most commonly implicated trigger in TLS; the relative risk of TLS following immunotherapy is unknown. Currently, routine prophylaxis with urate-lowering medication is not recommended for most solid tumors including NSCLC. Understanding risk factors for solid tumor TLS is key for prevention and early intervention in order to minimize its frequently devastating outcomes.

Introduction/Background:

Bioprosthetic mitral valve stenosis is a condition in which the mitral valve prosthesis becomes narrowed and difficult to open for both passive filling and active filling. This case is unique as there are very few articles published of fulminant bioprosthetic mitral valve failure only 2 years after implantation.

Description:

This is a case discussing a 67-year-old male with a past medical history of severe stenosis of a bioprosthetic 29mm Magna Ease mitral valve who presented with acute decompensated heart failure and found to have a completely degenerated bioprosthetic mitral valve two years after placement. After medical management, he was taken for surgical mitral valve replacement. This case report aims to discuss the mechanism, etiology, incidence, and prevalence of rapidly degenerated bioprosthetic mitral valves.

Discussion:

Modes of bioprosthetic valve degeneration include structural dysfunction (affecting the leaflets) or nonstructural (affecting the area around the leaflet but sparing the leaflets). Additional causes include thrombus and endocarditis. This patient was experiencing both etiologies with symptoms, with decreased leaflet mobility and pannus formation around the leaflets. Etiologies that may have led to rapid structural and non-structural bioprosthetic valve dysfunction in our patient include: uncontrolled hypertension, chronic kidney disease, diabetes mellitus, chronic smoking, excessive alcohol intake, atrial fibrillation, and increased mechanical wear and tear such as dilation of the left atrium and left ventricle. Other causes include hyperparathyroidism, end stage renal disease, and patient-prosthesis mismatch as our patient required an increased 31 mm replacement valve. Bioprosthetic heart valves do not have an ability for self-repair as native valves do and the lack of chordae tendinae attachments to the underside of the mitral valve can place greater stress on the bioprosthetic mitral valve, all leading to a higher grade of wear and tear over time.

Introduction/Background:

Patients with cardioembolic strokes suffer greater debility than those with ischemic strokes from other etiologies. Thrombi formed from the left atrial appendage or left ventricle (LV), from a vegetation, or an intracardiac tumor can potentiate the stroke. This case documents the successful diagnosis and conservative management of a left atrial mass in the setting of an ischemic stroke.

Description:

A 73-year-old male with a history of presumed cocaine-induced cardiomyopathy with reduced ejection fraction, chronic lymphocytic leukemia, and chronic hepatitis C was admitted to the intensive care unit with altered mentation requiring emergent intubation. Magnetic resonance imaging of the brain revealed multiple subacute bilateral infarcts suggestive of cardioembolic etiology. A contrast-enhanced transthoracic echocardiogram (TTE) demonstrated a dilated, hypertrabeculated LV with a moderately reduced LV ejection fraction of 32% with a LV apical thrombi and a 25x20 mm left atrial mass attached to the interatrial septum that was suspicious for atrial thrombus versus myxoma. Subsequent transesophageal echocardiography confirmed a large, pedunculated mass attached to the superior aspect of the interatrial septum. Anticoagulation was initiated and continued throughout an extended hospitalization. The patient was lost to follow-up before obtaining additional cardiac testing.

Discussion:

The patient’s clinical status and pre-existing comorbidities made the usual surgical management of the left atrial mass risk prohibitive. A series of three subsequent echocardiograms showed gradual and complete resolution of the left atrial mass after heparin was started, suggesting its etiology as thrombus. This case represents the successful diagnosis and conservative management of a left atrial mass in the setting of an ischemic stroke. Further studies are needed to determine whether conservative management with anticoagulation alone is safe and effective for undifferentiated atrial masses.

Introduction/Background:

Cardiogenic shock due to right ventricular (RV) dysfunction poses significant risks, with few treatment options when fluid optimization and inotropes fail. The Impella right-sided heart pump (Impella RP) offers rapid hemodynamic restoration, which is crucial for patients in cardiogenic shock.

Description:

A 68-year-old female presented with syncope, hypotension, and cardiac arrest. Coronary angiography revealed a small right coronary with an ostial occlusion, too small for intervention. She remained unstable despite fluids and inotropes. After cardiac arrest, echocardiography demonstrated RV dilation and hypokinesis with preserved apical function which suggested acute RV dysfunction. Right heart catheterization demonstrated a severely reduced cardiac index of 0.9 L/min/m2 and pulmonary artery pulsatility index of 0.7, which led to the timely consideration of mechanical support. Due to single ventricle shock, the heart team felt she was an ideal candidate for Impella RP. An Impella RP was placed, resulting in immediate hemodynamic improvement. Support was able to be weaned and successfully removed without major complications. RV function normalized on echocardiogram prior to discharge.

Discussion:

Treating isolated RV shock is complex. Abnormal RV strain with preserved apical function suggested RV reserve. Impella RP is a promising percutaneous therapy offering early RV unloading, potentially hastening recovery from RV shock, particularly when reperfusion is not feasible.

Introduction/Background:

Uncommon in developed countries, Shigella infection can present with mild symptoms such as abdominal pain and loose stools, to severe manifestations such as hemolytic uremic syndrome and septicemia. Gastrointestinal complications can include colitis and toxic megacolon. While rarely leading to surgical complications, there are reports of acute appendicitis in children with shigellosis severe enough to lead to perforation and peritonitis. These cases have primarily been historical and seen in developing countries. We present the case of a recent immigrant who was admitted for bloody diarrhea and abdominal pain found to have shigellosis and subsequent acute appendicitis.

Description:

A 7-year-old under-immunized female who recently immigrated to the United States from Venezuela presented with two days of abdominal pain and bloody diarrhea. Initial workup included an ultrasound which was equivocal for appendicitis. A subsequent CT scan showed findings consistent with colitis and an appendix at the upper limit of normal measuring 7mm with thickened hyper-enhancing mucosa consistent with early appendicitis. A gastrointestinal pathogen panel was sent and resulted positive for Shigella species, for which treatment was initiated. Serial abdominal exams and repeat imaging remained highly concerning for acute appendicitis. She underwent laparoscopic appendectomy with pathology reporting neutrophilic inflammation compatible with acute appendicitis. She recovered well from both shigellosis colitis and associated acute appendicitis.

Discussion:

This case is a stark example of the importance of keeping a broad differential in mind throughout caring for a patient as the clinical course progresses. While Occam’s Razor poses that most symptoms can be attributed to a single cause, it is imperative to remain open-minded and avoid anchoring to a single diagnosis. While there are reported cases of shigellosis with concomitant appendicitis, most cases are historical and in developing countries. This case highlights the importance of assessing for risk factors such as recent immigration when addressing a chief complaint and initiating a diagnostic workup. Although the development of appendicitis secondary to shigellosis is rare, it is essential for providers to be acutely aware of the ongoing risk of surgical complications that may be encountered given the significant morbidity and mortality associated with delayed diagnosis, including intestinal perforation and peritonitis.

Introduction/Background:

Hypertriglyceridemia is the third most common cause of acute pancreatitis after alcohol use and gallstones. While plasmapheresis and insulin are key treatments for hypertriglyceridemia-induced pancreatitis, logistical factors must be considered when selecting a regimen.

Description:

A 38-year-old male with no significant medical history presented with one day of severe abdominal pain. He had consumed a large amount of fatty foods at a party the night before. He was diagnosed with acute necrotizing hypertriglyceridemia-induced pancreatitis. Due to delays in initiating plasmapheresis, concerns over equipment availability, and cost barriers for this unemployed patient, plasmapheresis was not pursued. Instead, he was started on an insulin drip, D5 infusion, normal saline, and pain management. The patient had an elevated blood glucose level and hemoglobin A1c of 8.7. Gastroenterology and endocrinology were consulted, and he was started on daily insulin glargine, lispro, fenofibrate, and pantoprazole for duodenitis. His IV fluids were transitioned to a D5 normal saline infusion. Due to recurrent nausea and vomiting, he was placed NPO, a nasogastric tube was inserted, and meropenem was initiated on day 3 for fevers and leukocytosis. However, infected necrosis was ruled out via CT, and meropenem was discontinued on day 6 as his white blood cell count improved. His diet was slowly advanced. By day 7, his triglyceride levels had decreased to an acceptable level, and the insulin drip was stopped. D5 normal saline was transitioned to lactated ringers. By day 9, the nasogastric feeds and IV fluids were discontinued. On day 10, he was discharged home with insulin, fenofibrate, and atorvastatin.

Discussion:

This case highlights the complexity of managing hypertriglyceridemia-induced pancreatitis in critically ill patients and underscores the importance of early diagnosis and intervention. Given the potential for severe complications, logistical factors such as time, cost, and equipment availability should be considered early in treatment planning.

Introduction/Background:

This case highlights an exceedingly rare presentation of malignant atrial sarcoma with metastases to the brain and potentially bone. There are almost no documented similar case presentations given the rarity of atrial sarcomas to metastasize. When they do metastasize, the lungs and liver are the most common sites, rather than the brain or humerus. Of note, it is far more common for metastatic tumors to spread to the heart rather than be of cardiac origin.

Description:

A 51-year-old female with PMH of atrial sarcoma status post resection and chemotherapy (doxorubicin) and past neurocysticercosis presented from an outside hospital for a right-sided cerebellar brain mass. Her sarcoma was originally diagnosed after presenting 1 month prior for chest pain and dyspnea. An atrial intimal sarcoma was diagnosed and resected with pacemaker implantation for postoperative complete heart block. The patient was discharged on rivaroxaban for heparin-induced thrombocytopenia (HIT) during that admission. On admission, she reported worsening headaches, nausea, vomiting, and left sided blurry vision. CT head revealed a 4 cm right cerebellar mass with vasogenic edema and mass effect flattening the left ventricle. She was started on levetiracetam and dexamethasone. Neurosurgery performed surgical resection via a right suboccipital craniotomy, and biopsy confirmed metastatic intimal sarcoma. She was discharged with oncology follow-up. Subsequently, outpatient imaging identified a heterogeneously enhancing mass from the distal humerus to the antecubital fossa, with differential diagnoses including soft tissue sarcoma and angiomatoid fibrous histiocytoma. Metastasis is under investigation.

Discussion:

Atrial sarcomas are exceedingly rare. Primary cardiac sarcomas make up ~20% of all primary cardiac tumors. This case is unique due to the rarity of the atrial sarcoma as its own entity, but even more so with metastases to the brain and humerus. These tumors typically spread to the liver, lungs, and adrenal glands. This case provides bolstering data on atrial sarcomas’ preference for metastasis. These tumors are highly aggressive and may recur. This case demonstrates that atrial sarcomas cannot be ruled out based solely on location of the metastases. Overall, close monitoring is recommended in these patients including 3–6-month CT chest, abdomen, pelvis, MRI, and echocardiography, and for at least 5 years if the sarcoma has been resected, since recurrence is highest during this time.

Introduction/Background:

This case study details chiropractic treatment resulting in long-term improvement for pubic symphysis dysfunction in a female patient.

Description:

A 35-year-old female with pelvic girdle and low back pain, worsened by running and driving, and a history of unresolved post-partum pubis symphysis dysfunction of 10-year duration, diagnosed by a gynecologist as Lightning Crotch, was referred for chiropractic evaluation. Initial examination revealed right-sided pain provoked when performing Yeomans, Kemp’s, and Nachla’s and a positive sacral apex test. Palpatory findings were point tenderness of the right gluteus medius, right piriformis, and right hamstring. Chiropractic treatment including pin and stretch of the hypertonic muscles, side posture manipulation, and supine lumbar long-axis distraction to address lumbar, sacral, and pelvic somatic dysfunction along with a home exercise program was initiated. Pubic symphysis dysfunction and low back pain were resolved after 9 visits and patient was discharged following 12 visits, having adhered consistently to the care plan.

Discussion:

Unintended relief of chronic pubis symphysis dysfunction and correlating pain via chiropractic management of low back pain, which continued to be resolved at 7-month follow-up, noted in this case warrants further exploration in patient populations with this condition.

Introduction/Background:

An 18-month-old male presented to clinic with limp for 1 week. Patient was recovering from a cold with resolved rhinorrhea and was treated with NSAIDs every 6 hours with minimal improvement in ambulation. In the clinic, the patient was very irritable with limited use of left leg. Mother denied any recent falls/trauma, fevers, joint swelling, rashes, changes in behavior, cough, congestion. Reported Father was at home sick with diagnosed strep throat. Due to non-improving symptoms, the patient was transferred to ED for further workup and admitted to the floor in stable condition.

Description:

Initial exam in the ED: Afebrile with stable vitals. No swelling, erythema, or warmth noted on b/l hip, knee, and ankle joints. No tenderness to palpation over hip, femur, knee, leg or ankle. Pain with passive range of motion (PROM) of left hip and knee. No pain with PROM of ankles. Sporadically moved left lower extremity. 5/5 strength. 2+ dorsalis pedis pulse. Throughout exam the patient was grimacing in pain. On ambulation, patient favored the right leg and upon bearing weight with left leg, patient immediately buckled. No neurological symptoms or signs. Initial XR imaging was all negative, but after persistence of fevers, an MRI was obtained. Final diagnosis was osteomyelitis with intraosseous abscess of the distal left femur. Upon discovery of osteomyelitis on MRI, blood cultures x2 were taken and patient was started on Cefazolin 50mg/kg IV q8h and transitioned to Cephalexin 50 mg/kg/dose PO TID for 6 weeks on discharge. Orthopedic surgery performed irrigation and excisional debridement of osteomyelitis, left distal femur. Bone biopsy sent out for culture. Safe ambulation and mobility education left leg strengthening and gentle knee PROM. No physical activity restrictions. Patient was safe for discharge home from a mobility standpoint, no assisted device or further physical therapy needed.

Discussion:

Differentiating septic arthritis from transient synovitis in children with an irritable hip is crucial but challenging due to overlapping symptoms. The Kocher criteria, though commonly used, have shown limited reliability for the knee. Persistent symptoms despite NSAID therapy, normal imaging, and elevated inflammatory markers (ESR, CRP) should raise suspicion for a more serious condition like septic arthritis or osteomyelitis.

Introduction/Background:

While the exact mechanism of fistula formation in cases of gastroduodenal fistulas (GDFs) is unclear, we present a case in which the primary suspect for GDF formation is fistulation originating from a previous gastric antral ulcer, compounded by persistent NSAID usage. This case also underscores the possibility of concomitant gastric ulcers along the GDF tract in individuals continuing NSAID therapy.

Description:

A 74-year-old male with a history of joint pain and non-steroidal anti-inflammatory (NSAID) use presented for weight loss. On physical examination, he appeared well without distress, abdominal pain, or discomfort. Laboratory findings showed a hemoglobin (Hb) level of 10.7 g/dL and mean corpuscular volume (MCV) of 86.0 fL. Esophagogastroduodenoscopy (EGD) revealed a 12mm Forrest III ulcer in the antrum. Biopsies revealed mild chronic gastritis, without evidence of H. pylori infection. The patient was told to stop NSAIDs and was prescribed twice daily PPI. An EGD three months later displayed a 3mm remnant ulcer with granulation tissue and patchy erythema in the antrum, indicative of mucosal healing. A year later, the patient presented with dizziness. He had been using supratherapeutic doses of NSAIDs for several months for knee pain. He denied nausea, vomiting, or abdominal pain, but reported melena. Laboratory findings showed a Hb of 4.3 g/dL and MCV of 76.0 fL. On examination, he appeared well without acute distress or abdominal pain. Repeat Hb following transfusion of three units of packed red blood cells was 8.3 g/dL. Repeat EGD identified a GDF at the previous ulcer site in the antrum. Additionally, a 3cm Forrest IIa ulcer was observed along the luminal wall of the fistula. Hemostasis was successfully achieved using epinephrine injection and bipolar electrocautery. Biopsies showed benign gastric mucosa without H. pylori infection. The patient experienced no post-procedural complications or recurrence of gastrointestinal hemorrhage. He was discharged with strict instructions to stop NSAIDs and was given twice daily PPI therapy.

Discussion:

While the exact mechanism of fistula formation in cases of GDFs is unclear, we present a case in which the primary suspect for GDF formation is fistulation originating from a previous gastric antral ulcer, compounded by persistent NSAID usage. This case also underscores the possibility of concomitant gastric ulcers along the GDF tract in individuals continuing NSAID therapy.

Introduction/Background:

Semi-acute progressive lower extremity musculoskeletal pain has a broad differential diagnosis including infections (e.g., osteomyelitis), MSK (e.g., slipped capital femoral epiphysis [SCFE]), and oncological (e.g., leukemia and bone tumors) etiologies. In the setting of subtle neurological findings, it is important to consider spinal lesions such as a primary tumor, congenital anomaly, or infection.

Description:

A 6-year-old male with a history of chronic lower leg complaints presented with one month of right proximal tibia pain and a new limp. His pain increased during the day and often woke him from sleep. He also reported decreased activity, anorexia, weight loss and intermittent night sweats. The pain was treated with acetaminophen and ibuprofen with minimal relief. He noted upper respiratory symptoms and fever with pain onset, but none at admission. He had no joint swelling or history of trauma, and the review of systems was otherwise negative. Initially he was felt to be experiencing growing pains, however given the progression of pain and systemic symptoms, he was admitted to the hospital for further work up. On exam, patient was non-toxic appearing. His right lower extremity had pain to palpation over the proximal outer tibia, without erythema, swelling, or limitations in range of motion. He had pain to palpation over his lower lumbosacral spine and paraspinal musculature with radiation to the right tibial region. Neurological exam revealed a right sided limp with ambulation, 4/5 strength in right lower extremity, normal reflexes and no focal deficits. Labs including inflammatory markers, creatinine kinase, and tumor lysis markers were unremarkable. X-rays of hip, femur and tibia revealed a slight displacement of the right femoral head that was clinically insignificant. He underwent an MRI spine that demonstrated an extramedullary intradural lesion at the L4 level.

Discussion:

The patient’s MRI finding was consistent with an epidermoid inclusion cyst, likely a rare sequela of a lumbar puncture he had received at 4 weeks of age during a septic workup. Epidermoid cysts can result from iatrogenic implantation of ectodermal tissue during procedures like lumbar punctures. These cysts can present later in life with neurological deficits, including pain, motor weakness, or sphincter dysfunction. This case underscores the importance of avoiding diagnostic anchoring bias, as maintaining a “working differential” can be crucial to uncovering rare conditions and allow for timely imaging and appropriate therapies.

Introduction/Background:

Venous thromboembolism (VTE) is a common phenomenon in sedentary individuals with risk factors including malignancy and trauma and includes both deep venous thrombosis (DVT) and pulmonary embolism (PE). There are individuals with notable unprovoked DVTs that may embolize to the lungs, causing a PE. When there are indications of hypotension, right ventricular strain, and/or troponinemia, these are indications of a massive pulmonary embolism. Approximately 25 to 50% of thromboembolisms are unprovoked, prompting further evaluation for hypercoagulable states or malignancy. According to the American Society of Hematology (ASH), VTE may recur after 2 years in 10% of patients who were treated with anticoagulation, and up to 30% by 10 years. This case is unique in the fact that this patient had a fatal PE secondary to stopping her rivaroxaban for only 5 weeks.

Description:

We present a case of a 69-year-old female with a medical history of heart failure with preserved ejection fraction (HFpEF), pulmonary hypertension, history of DVT and PE who was unable to afford her anticoagulation, CAD, CKD, HTN, and COPD found to have lower extremity DVT which was complicated by massive pulmonary embolization and pulseless electrical activity (PEA) cardiac arrest secondary to DVT embolization to lungs while ambulating (with return of spontaneous circulation achieved). Intravascular ultrasound (IVUS) was performed, demonstrating group I and II pulmonary HTN and right segmental PE; the patient was started on a heparin drip and epoprostenol. Catheter directed thrombolysis was unable to be performed due to significant pulmonary hypertension and increased risk of bleeding, requiring transfer to higher level of care at a pulmonary hypertension center. The hospital course at an outside facility was complicated by renal failure requiring continuous renal replacement therapy, intubation, and atrial fibrillation. The patient then further decompensated and expired.

Discussion:

This case stresses the need for early treatment for pulmonary hypertension and policy changes to help improve the cost of anticoagulation and the complications that may arise from discontinuing life-saving medications based on affordability. According to The American Journal of Managed Care, it was found that 14 to 17.8% of patients with atrial fibrillation were not able to receive any oral anticoagulation after an initial rejection for apixaban. If approved, delays may take up to 2 months before approval. Other common barriers include formulary restrictions including quantity limitations, insurance limitations, high copayments, and racial disparities. This highlights the need for better access to the care needed.

Introduction/Background:

According to Molina and Faulk's journal article, "Lower Extremity Amputation," approximately 150,000 individuals in the United States undergo lower extremity amputations each year. Limikatso et al. found in "The Prevalence and Risk Factors for Phantom Limb Pain in People with Amputations: A Systematic Review and Meta-Analysis," that 64% of these individuals experience phantom limb pain (PLP). This persistent and often debilitating condition can significantly impact an amputee's quality of life. This case study describes the therapeutic benefit experienced by a patient with PLP while being treated for low back pain with radicular symptoms into the residual limb.

Description:

A 66-year-old male with history of left-sided below-the-knee amputation presented for care of chronic low back pain and radicular symptoms to the left residual limb. He also noted left-sided PLP that began two days after amputation, which was five years prior to the initial visit. Aggravating factors included standing, walking, and sleeping. Alleviating factors included pain medications. The patient reported worsening PLP in relation to the severity of low back and left radicular pain. Lumbar long-axis distraction and soft-tissue therapy were initiated to address the LBP and radicular symptoms. He self-reported two weeks of complete symptomatic relief from PLP at visit 5. A flare up of LBP and PLP was reported at visit 6. However, he chose to discontinue care citing insurance limitations. At discharge from care, scores on the Numeric Pain Rating Scale improved from 8/10 to 4/10 and the DoD/VA Pain Supplemental Questions score improved from 32/40 to 18/40.

Discussion:

This case illustrates an unexpected improvement in phantom limb pain coinciding with chiropractic treatment for low back pain and radicular symptoms. The favorable response warrants further investigation into the effects of lumbar spine long-axis distraction and soft-tissue therapy on phantom limb pain.

Introduction/Background:

Blue rubber bleb nevus syndrome (BRBNS) is a rare congenital disorder caused by a mutation in the TEK gene, which disrupts normal cellular communication and leads to the development of abnormal blood vessels. The TEK gene expresses a TIE2 tyrosine kinase receptor predominantly present in the vascular endothelium. The TIE2 pathway, activated by angiopoietin 1 and 2, is responsible for angiogenesis and endothelial maintenance. Clinically, patients exhibit distinctive dome-shaped, blister-like lesions known as blebs, characterized by a rubbery texture and blue or purple appearance, that can develop throughout the body.

Description:

85-year-old caucasian female with a past medical history of atrial fibrillation on xarelto, heart failure with preserved ejection fraction (HFpEF), CAD, COPD on home oxygen, CKD3a, and HTN presented with dark stools, abdominal pain, and weakness. CT abdomen and pelvis with contrast showed extravasation in the small bowel, a push enteroscopy revealed several esophageal venous blebs, and capsule endoscopy showed active bleeding in the small bowel. Her hospital course was further complicated by a DVT in the right lower extremity and several pulmonary emboli. Patient was treated with amicar and octreotide. She ultimately required 19 units of packed red blood cells. Double balloon enteroscopy was significant for several nonbleeding venous blebs in the jejunum. Full dose lovenox was resumed to treat her pulmonary embolism and she was bridged to eliquis before discharge.

Discussion:

BRBNS is an exceedingly rare disease with only a few hundred case reports published since 1860. There appears to be an autosomal dominant inheritance pattern linked to chromosome 9, but most cases are sporadic. Symptoms typically present at birth or in early childhood but can present at any time. The classic blue blebs can form in any solid organs, the central nervous system, and anywhere along the GI tract. Systemic therapies such as sirolimus, corticosteroids, IVIG, INF-a, and vincristine have been utilized with reported success as well. However, dosing and duration of treatment have not been extensively studied. Supportive care with iron supplementation is commonplace for these patients. Given our patient's age and comorbidities, she decided to pursue supportive care. Younger, healthier patients would benefit from pharmacotherapy trials with the drugs mentioned above in order to potentially reduce the long-term complications of hospitalizations, blood transfusions, and to avoid bowel resections.