Poster Day 2025: Abstracts: Clinical Vignettes

Case Presentation:

A 60-year-old female with history of prior cerebrovascular accident with post-stroke seizure disorder on levetiracetam, chronic kidney disease, diabetes, COPD, and recurrent urinary tract infections presented after a mechanical fall resulting in a displaced intertrochanteric femur fracture. Her course was complicated by urinary retention and sepsis secondary to Escherichia coli UTI. She underwent left hip cephalomedullary nail fixation and was initially treated with meropenem and vancomycin. Due to CT findings concerning for pneumonia, antibiotics were de-escalated to cefepime and metronidazole.

After completing seven days of cefepime, the patient developed acute encephalopathy with increasing lethargy. Laboratory evaluation was unrevealing for metabolic or infectious etiologies, and ammonia was normal. Despite being on maintenance levetiracetam, she experienced breakthrough seizures, and EEG demonstrated abundant triphasic discharges within the ictal–interictal continuum, consistent with nonconvulsive status epilepticus. Cefepime was immediately discontinued, and she was treated with high-dose levetiracetam and lacosamide. She required intubation and ICU transfer for airway protection and continuous EEG monitoring, which confirmed ongoing generalized status epilepticus. CSF analysis revealed elevated protein without pleocytosis or infectious organisms, and neuroimaging was unremarkable.

Cefepime, a fourth-generation cephalosporin, is a widely used broad-spectrum antibiotic, but neurotoxicity remains an underrecognized complication, particularly in patients with renal impairment. Manifestations range from confusion and myoclonus to nonconvulsive status epilepticus, often occurring within several days of therapy initiation. The mechanism involves inhibition of γ-aminobutyric acid (GABA) receptors, leading to neuronal hyperexcitability and a lowered seizure threshold. In this case, despite appropriate dosing and ongoing antiepileptic therapy, the patient’s underlying CKD and prolonged exposure likely predisposed her to cefepime accumulation and breakthrough seizures. Prompt recognition and discontinuation of cefepime, along with escalation of antiepileptic therapy, led to gradual improvement in mental status and cessation of electrographic seizures.

Milan Regmi, MD; Siddharth Sharma, MD; Abinaya Sivakumar, MD; Gaurab K C, MD; Mina M Saba, MD; Srushti Ghetiya, MD; Kevin Meek, DO, Yoseph Herpo, MD; Ananya Prakash, MD; Sagar Madan, MD; Sudha Bhattarai, BAMS; Walter Johnson, BS;

Abstract:

Clostridium subterminale is a gram-positive, spore-forming bacterium belonging to the Clostridiaceae family, which rarely grows in blood culture, with common colonization in the gastrointestinal tract and genitourinary tract. Clostridium subterminale, like Clostridium perfringens bacteremia, has been linked with potential occult gastrointestinal malignancy, including esophageal and colon cancer. We are presenting a unique case of Clostridium bacteremia, which prompted further workup to look for occult gastrointestinal malignancy. Our patient was a 78-year-old female with a history of autoimmune hepatitis and stroke who presented to the hospital with complaints of dark-colored stool. A CT scan of the abdomen was suggestive of possible colitis, and a blood culture was obtained, which was positive for Clostridium subterminale. The infectious disease team suggested an extensive workup to rule out occult gastrointestinal malignancy. On colonoscopy, we found localized edematous and ulcerated mucosa in the distal transverse colon and splenic flexure, 75 cm from the anal verge, suggestive of possible ischemic colitis, which was later confirmed by biopsy. Our case report highlights the importance of extensive workup in cases of atypical blood culture with Clostridium subterminale, but even with a breach in the colonic mucosa, it is possible to have Clostridium subterminale. Even with mucosal injury, Clostridium subterminale bacteremia may develop without a concurrent malignancy, emphasizing the need for careful clinical correlation.

Milan Regmi, MD, Mina M. Saba, MD; Paarmit Chhabra, MD; Roger Lin, MD, Namitha Thotli, MD

Authors:

Yoseph Herpo, MD; Gourab K.C., MD; Mina Saba, MD; Sagar Madan, MD; Siddhartha Sharma, MD; Milian Regmi, MD; Srushti Ghetiya, MD; Abinaya Sivakumar, MD; Mahmoud Ahmad, MD; Bahaa Batayneh, MD

The concurrent presentation of new-onset chest pain and Atrial Fibrillation with Rapid Ventricular Response (AFib with RVR) poses a significant diagnostic challenge. The rapid ventricular rate can independently cause supply-demand mismatch (Type 2 Myocardial Infarction) or, more critically, mask life-threatening conditions such as Acute Aortic Syndrome (AAS), leading to delayed diagnosis.

We present the case of a 79-year-old female with hypertension who initially presented with AFib with RVR (HR 190s). Her vague initial symptoms, including chest pounding, fatigue, and mild chest discomfort, resolved after successful pharmacological rate control. However, during subsequent workup with TTE, she rapidly decompensated with new-onset chest pain, dizziness, and hypotension. A stat CT Angiography (CTA) immediately revealed an ascending aortic rupture with active extravasation, extensive hemorrhage, and signs of tamponade physiology. The patient underwent emergent surgical repair via deep hypothermic circulatory arrest, Aortic repair, and graft placement.

This clinical vignette illustrates the complex relationship between AFib and AAS. Chronic hypertension provided the underlying substrate (shared risk factor), and the acute hemodynamic stress from the AFib with RVR likely acted as the immediate trigger for the aortic rupture due to sudden, excessive wall shear stress. Crucially, the non-specific AFib symptoms initially masked the catastrophic underlying pathology. This case emphasizes the imperative to maintain a high index of suspicion and broaden the differential diagnosis for patients presenting with new-onset AFib, particularly when acute decompensation occurs

Authors:

Milan Regmi, MD;  Roger Lin, MD;Abdelrahman Shehata, MD; Motunrayo Adeleye, MD; Kevin Meek, DO; Parmit Chhabra, MD; Darius Aliabadi, MD; Mina Saba, MD, Sudharani Kinthada, MD,  Ahsan Masod, MD; Gaurab K C, MD

Hypertrophic cardiomyopathy is a genetic disease defined objectively with a 2D echocardiogram with maximal end-diastolic myocardial wall thickness >= 15 mm in any part of the left ventricle associated with dynamic left ventricular obstruction that can cause mitral regurgitation and potentially pulmonary edema. We are presenting a case in which a patient with previously mild mitral valve regurgitation presented with acute severe flash pulmonary edema during elective cardiac catheterization not totally explained with HOCM physiology.  The patient was a 77-year-old female with a history of hypertrophic cardiomyopathy, non-sustained VT, VVIR ICD implant, and paroxysmal atrial fibrillation on Eliquis. During a right and left cardiac catheterization , the patient developed acute/flash pulmonary edema associated with acute worsening of MR, presumably related to hypertrophic physiology and the development of systolic anterior motion (SAM) of the mitral valve but not totally explained with HOCM physiology, leading to severe torrential MR resulting in flash pulmonary edema requiring aborting the elective cardiac catheterization.  Elective cardiac catheterization in HOCM patients with mild MR can potentially lead to torrential MR and acute flash pulmonary edema, leading to sudden deterioration of the patient in the cath lab. Continuous clinical monitoring and rapid management of underlying conditions are crucial. Further studies to better understand the pathophysiology of this specific and peculiar phenomenon is required

Milan Regmi, MD; Shekhar Bhatta, MD; Bibek Man Shrestha, MD

Two young males aged 25 presented with metastatic nonseminomatous germ cell tumors (NSGCT) exhibiting extremely high beta-hCG levels in the millions, primarily associated with extensive choriocarcinoma elements. The first case involved a 25-year-old male with major depressive disorder who presented with abdominal pain and weight loss; imaging revealed widespread metastases to the liver, lungs, and lymph nodes. His initial beta-hCG was >1.3 million. He received multiple cycles of EP and BEP chemotherapy, with complications including choriocarcinoma syndrome, pneumonia, gastrointestinal hemorrhage, prolonged intubation, and eventual tracheostomy. Despite intensive therapy and surgical intervention (orchiectomy, hepatic metatectomy, RPLND), beta-hCG levels declined from millions to undetectable, though residual disease persisted radiographically after completion of four cycles of BEP and surgery. The second patient, also a 25-year-old male, was diagnosed after presenting with hemoptysis and constitutional symptoms. Orchiectomy confirmed a mixed germ cell tumor (40% teratoma, 5% seminoma, 55% choriocarcinoma); baseline beta-hCG was 2,038,000. He completed four cycles of the VIP regimen complicated by significant cytopenias, infection, hemolytic anemia, and neurotoxicity. Beta-hCG declined rapidly to <200 by cycle four, but residual tumor masses persisted on imaging. Both cases demonstrated initially aggressive disease, life-threatening complications from tumor burden and therapy, and a notable decline in tumor marker levels with intensive, multidisciplinary management. Persistently elevated or detectable beta-hCG after therapy prompted surgical consolidation, highlighting the role of multimodality therapy in poor-risk metastatic NSGCT with massive beta-hCG elevation

Hira Javaid MD, Mahnoor Farooq Raja MBBS, Mishal Basit MBBS, Asma Mahmood MD, Syeda Hooria Imtiaz MD, Osama Kunwer Naveed MD

Case Presentation:

A 73-year-old woman with stage IV poorly differentiated lung adenocarcinoma (PD-L1 90%) was treated with atezolizumab, alongside radiation to the right lung and stereotactic body radiation to a hepatic metastasis, achieving partial response. Therapy was discontinued due to radiographic disease progression. Subsequent imaging revealed hypermetabolic lesions in the right adrenal gland and left kidney. Histopathology of the renal mass demonstrated poorly differentiated non-small-cell carcinoma with sarcomatoid features, positive only for pankeratin (AE1/AE3). A scalp lesion developed subsequently, biopsy revealing a low-grade sarcoma.

Discussion:

Atezolizumab, as part of immune checkpoint inhibitor (ICI) therapy, blocks PD-L1 and restores T-cell–mediated antitumor immunity. However, selective immune pressure may eliminate immunogenic epithelial clones, facilitating expansion of resistant subclones with mesenchymal and immune-evasive phenotypes. Sarcomatoid transformation represents epithelial-to-mesenchymal transition (EMT), characterized by loss of epithelial markers (E-cadherin), gain of mesenchymal markers (vimentin, N-cadherin), and enhanced migratory and invasive potential. EMT is driven by TGF-β signaling, Wnt/β-catenin activation, and transcription factors such as ZEB1, Snail, and Twist, which also suppress antigen presentation and reduce tumor-infiltrating lymphocyte activity. This case highlights a rare presentation of atezolizumab-associated histologic transformation manifesting as extra-thoracic sarcomatoid lesions that can mimic metastatic sarcoma. The immunophenotype, pankeratin positive but negative for lineage-defining markers, supports dedifferentiation rather than a de novo secondary malignancy.

Conclusion:

Hira Javaid MD, Mishal Basit MBBS, Asma Mahmood MD, Mahnoor Farooq Raja MD, Syeda Hooria Imtiaz MD, Hajelkhidir Bala MD, Osama Kunwer Naveed MD

Case Presentation:

A 64-year-old male with mixed small cell and non–small cell lung cancer (pT1N0) and a history of chronic obstructive pulmonary disease (COPD) underwent surgical resection with mediastinal lymph node dissection, followed by adjuvant cisplatin/etoposide and prophylactic cranial irradiation. Upon recurrence, he received thoracic radiation with concurrent chemotherapy and was started on durvalumab. After two cycles, he presented with rapidly worsening dyspnea and diffuse bilateral infiltrates on imaging. Infectious workup was unrevealing, and findings were consistent with grade 4 checkpoint inhibitor pneumonitis (CIP). Pulse-dose corticosteroids were administered with gradual improvement, followed by a slow taper.

Discussion:

Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of advanced lung cancer by substantially improving survival. However, CIP is a potentially life-threatening complication that demands prompt recognition. Diagnosis is challenging because clinical presentation and imaging findings are often nonspecific, overlapping with infectious pneumonia, lymphangitic carcinomatosis, tumor progression, or diffuse alveolar hemorrhage. Risk is compounded by pre-existing COPD, male sex, prior thoracic radiation, chemotherapy exposure, mixed histology tumors, and patient-specific genetic factors (e.g., PD-L1 expression, HLA haplotypes). The pathogenesis involves dysregulated T-cell activation, alveolar epithelial injury, and proinflammatory cytokine release (e.g., IFN-γ, TNF-α, IL-6). Management typically requires high-dose corticosteroids and immunosuppression, although recurrence upon ICI rechallenge is frequent, often necessitating permanent discontinuation and compromising long-term antitumor therapy.

Conclusion:

Prompt identification of high-risk patients, early immunosuppression, and coordinated multidisciplinary care are critical to reduce morbidity and optimize outcomes in CIP.

Hira Javaid MD, Mishal Basit MBBS, Asma Mahmood MD, Mahnoor Farooq Raja MD, Syeda Hooria Imtiaz MD, Hajelkhidir Bala MD, Osama Kunwer Naveed MD

Case Presentation:

A 56-year-old man presented with several days of melena and progressive fatigue. Laboratory evaluation revealed severe normocytic anemia (hemoglobin 5.6 g/dL) and hypercalcemia (10.2 mg/dL). He was stabilized with red blood cell transfusions. Upper endoscopy demonstrated diffuse gastritis without an adequate source for his profound anemia. The patient reported chronic low back pain self-managed with over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs). Persistent anemia, hypercalcemia, and bone pain raised suspicion for a plasma cell dyscrasia. Serum protein electrophoresis identified a monoclonal IgG kappa spike, urine protein electrophoresis demonstrated monoclonal light chain excretion, and bone marrow biopsy confirmed >10% clonal plasma cells. A skeletal survey revealed multiple lytic lesions.

Discussion:

Gastrointestinal bleeding in hematologic malignancies occurs in 10–30% of patients and is typically multifactorial, involving mucosal compromise, marrow suppression, infections, or direct neoplastic infiltration. Multiple myeloma, a malignant plasma cell disorder, predisposes to bleeding, paraprotein-mediated platelet dysfunction, thrombocytopenia from marrow replacement, and acquired coagulopathies. In this patient, NSAID-induced gastric mucosal injury acted synergistically with these hematologic derangements to precipitate overt hemorrhage. This case highlights the importance of considering systemic disorders when gastrointestinal bleeding persists despite local therapy, as unrecognized coagulopathy and marrow dysfunction may obscure the underlying etiology.

Conclusion:

In elderly patients with gastrointestinal bleeding of unclear etiology, especially when anemia persists despite endoscopic therapy, clinicians should evaluate for plasma cell dyscrasias such as multiple myeloma. Early identification allows for timely disease-directed therapy, reduces the risk of recurrent hemorrhage, and addresses systemic complications arising from marrow infiltration and coagulopathy.

Sonia Portillo, MD, MPH, Krishnamohan Basarakodu, MD, Bridget Herschap, MD

Background:

Colorectal cancer is the third most common cancer worldwide. The most common patient presentations include rectal bleeding, occult blood in the stool, and changes in bowel habits. Metastasis commonly occurs in the liver and lungs, and rarely with isolated metastasis to the bone marrow. This is an exceptional finding, with only a handful of cases reported in the literature. 

Case Summary:

An 82-year-old Caucasian male with past medical history of asthma, BPH, radiculopathy of lumbosacral region, and GERD was admitted to the hospital for gross hematuria. He underwent cystoscopy and scheduled to undergo a TURP procedure, however due to worsening thrombocytopenia Oncology was consulted. The patient endorsed a 10-12 pound weight loss the past few months, but denied hematochezia/melena, or changes in bowel habits. The physical exam was unremarkable, except for diluted blood in the foley catheter. Baseline platelet count was within normal range four months prior to hospitalization. The standard workup for new onset thrombocytopenia was initiated. Platelet transfusions were administered in hopes of resolution, however his counts continued to fall. After initial work up was negative, differentials of ITP and bone marrow pathology were considered. The patient underwent a bone marrow biopsy. While awaiting results, he completed a trial of pulse dexamethasone for possible ITP, of which he failed. The pathology report revealed metastatic carcinoma most compatible with colorectal primary.  

Discussion:

In this unique case, bone marrow infiltration represented the initial and sole site of metastatic spread, without evidence of hepatic, pulmonary, or peritoneal lesions. The tumor cells were negative for prostate markers, bladder markers, neuroendocrine markers, lung and hematopoietic markers. The cells stained strongly for CK20, SATB2 and CDX2. Positive CK20 markers, especially when paired with CK7 negativity, is typical for colorectal primary. In addition, the combination of CDX2 and SATB2 yields a >95% sensitivity and specificity for metastatic colorectal carcinoma. This atypical presentation highlights the diagnostic value of bone marrow biopsy in evaluating unexplained cytopenias, even in the absence of overt systemic symptoms or imaging.  

Conclusion:

Clinicians should maintain a high index of suspicion for occult solid malignancy when evaluating unexplained cytopenias. Immunohistochemical staining was crucial in determining the colorectal origin.

Gaurab K C, MD, Milan Regmi, MD, Abinaya Sivakumar, Siddhartha Sharma, MD;  Kevin Meek, DO; Mina Saba, MD;Yoseph Herpo, MD; Srushti Ghetiya, MD ; Sagar Madan, MD, Syeda Hooria Imtiaz, MD, Hannah Choi, MD ; Subhan ATA, MD

Background:

Neuromyelitis optica spectrum disorder (NMOSD) is a rare, relapsing autoimmune disorder characterized by attacks of optic neuritis and transverse myelitis, often affecting three or more vertebral segments and sometimes extending into the brainstem, resulting in life-threatening respiratory compromise. High cervical cord involvement is a recognized cause of neurogenic respiratory failure in NMOSD, particularly in untreated patients.

Discussion:

Acute neurological hypercapnic respiratory failure is a rare but life-threatening complication of NMOSD, usually due to high cervical cord or brainstem involvement. Acute management includes high-dose intravenous corticosteroids and plasma exchange, with adjunctive IVIG in refractory cases. Long-term relapse prevention now includes FDA-approved agents such as eculizumab, inebilizumab, and satralizumab, which target complement, B cells, and IL-6 pathways, respectively.

Conclusion:

This case underscores the importance of considering NMOSD in patients with unexplained acute respiratory failure and multifocal CNS lesions, especially in populations at higher risk for severe disease and delayed diagnosis. Early recognition and initiation of immunosuppressive therapy are critical to improving prognosis and reducing relapse-related disability.

Gaurab K C, MD; Kevin Meek, DO; Milan Regmi, MD; Yoseph Herpo,MD; Abinaya Sivakumar, MD; Siddhartha Sharma, MD; Srusti Ghetiya, MD; Sagar Madan, MD; Mina Saba, MD

Background:

Pulmonary embolism (PE) and deep vein thrombosis (DVT) represent a spectrum of venous thromboembolism (VTE). While DVT commonly precedes PE, simultaneous presentation can be clinically silent and potentially life-threatening. Early diagnosis and prompt management are critical to prevent hemodynamic compromise and mortality. 

Case Summary:

A 64-year-old male with a history of type 2 diabetes mellitus, hypertension, coronary artery disease status post triple-vessel CABG (2009), and recent left VATS with epicardial lead placement presented with one day of right lower extremity pain, swelling, and toe discoloration. He had no family history of coagulopathy but reported recent long-distance air travel. Venous Doppler ultrasound revealed diffuse occlusive thrombosis of the right lower extremity involving the common femoral, superficial femoral, popliteal, peroneal, and posterior tibial veins. CTA chest demonstrated multifocal pulmonary emboli throughout bilateral pulmonary arteries, including a saddle embolus, without initial right heart strain. Intravenous heparin was initiated, and vascular surgery and cardiology were consulted. Due to impending phlegmasia cerulea dolens, the patient underwent thrombectomy of the right lower extremity veins. Post-procedure, he developed hypoxemia and hypotension requiring ICU transfer, vasopressors, and supplemental oxygen. The following day, he underwent Penumbra-assisted pulmonary thrombectomy for massive PE. Repeat CTA showed marked improvement in clot burden and perfusion. Echocardiography revealed moderately reduced LV function (LVEF 37%) and RV dilation. Cardiology recommended lifelong anticoagulation with rivaroxaban due to provoked DVT with high recurrence risk.

Discussion:

This case highlights the diagnostic challenge of PE presenting as isolated DVT. Recognition of this overlap is vital, as both entities share pathophysiology and treatment. Early imaging and anticoagulation are essential to prevent progression and recurrence. 

Conclusion:

This case underscores the importance of integrated diagnostic strategies and prompt initiation of anticoagulation in patients with DVT, given the frequent coexistence of silent PE and the shared management approach for VTE.

Sagar Madan, MD; Kevin Meek, DO; Milan Regmi, MD; Abinaya Sivakumar, MD; Siddharth Sharma, MD; Mina Saba, MD; Gaurab K.C., MD; Ananya Prakash, MD; Srushti Ghetiya, MD; Yoseph Herbo, MD; Hira Javaid, MD; Syeda Imtiaz, MD; Walter Johnson, BS

This is a case report of Adult Onset Myasthenia Gravis, specifically presenting as a myasthenic crisis. A 70-year-old male with a past medical history of asthma who was brought to the ED with complaints of dysphagia, dysarthria, choking spells, blurred vision, generalized weakness, and drooping of his head for the past couple months. IV neostigmine was administered in the ED, after which he was admitted. IVIG and Mestinon were started; CT was negative for a thymoma. He continued to have progressively worsening respiratory function, thus the patient was electively intubated. Negative inspiratory force (NIF) is a key bedside measurement for assessing respiratory muscle strength and guiding management decisions, especially in the context of rapid symptom progression. NIF quantifies the maximal pressure a patient can generate during inspiration against a closed airway, reflecting diaphragmatic and accessory muscle strength. An NIF less negative than -20 cm H2O (i.e. closer to zero) is considered a threshold indicating significant respiratory muscle weakness and a high risk for respiratory failure, often prompting consideration for elective intubation and mechanical ventilation in myasthenic crisis as was done in this case.  Management in this scenario includes prompt airway protection, discontinuation of cholinesterase inhibitors after intubation, and initiation of fast-acting immunomodulatory therapies such as plasma exchange or intravenous immunoglobulin, as recommended by the literature (New England Journal of Medicine). Long-term immunosuppression is also necessary to prevent recurrence. Regular monitoring of NIF and other respiratory parameters is essential for guiding extubation readiness and ongoing care.

Sagar Madan, MD; Kevin Meek, DO; Mina Saba, MD; Gaurab K.C., MD; Milan Regmi, MD; Abinaya Sivakumar, MD; Siddharth Sharma, MD; Ananya Prakash, MD; Hira Javaid, MD; Syeda Hooria Imtiaz, MD; Osama Naveed, MD; Srushti Ghetiya, MD; Yoseph Herpo, MD; Walter Johnson, BS

This is a case report of Central Diabetes Insipidus development following a pituitary tumor resection. 26 y/o female with a h/o asthma who was admitted with c/o nausea, vomiting, headaches, loss of appetite, visual disturbances and unintentional weight loss. She underwent a CT scan of the head that showed evidence of a sellar mass with some associated edema. MRI revealed evidence of a large sellar and suprasellar mass with edema, measuring 1.8 x 2.3 x 2.8 cm. She was taken to the OR for resection of said suprasellar mass. Pathology showed a ruptured acute/chronically inflamed epidermoid cyst with adjacent pituitary gland. Consequently the patient developed post-operative DI with hypernatremia, and was placed on hydrocortisone. Central diabetes insipidus (CDI) is a well-recognized complication of pituitary tumor resection, resulting from disruption of vasopressin synthesis or release due to surgical manipulation of the neurohypophysis or pituitary stalk. The incidence of postoperative CDI varies by tumor type and surgical approach, with transient CDI occurring in approximately 5–25% and permanent CDI in 1–8% of cases. Risk factors include larger tumor size, craniopharyngioma pathology, intraoperative cerebrospinal fluid leak, and greater pituitary stalk traction. CDI typically presents within the first 24–48 hours postoperatively as hypotonic polyuria and polydipsia, and is diagnosed by high urine output, low urine osmolality, and hypernatremia in the absence of other causes. Most cases are transient, resolving within days to weeks, but a minority persist and require long-term desmopressin. The Endocrine Society recommends initial management with short-acting subcutaneous aqueous vasopressin, reserving scheduled desmopressin for persistent cases, and advises against routine fixed dosing in the first postoperative week to avoid hyponatremia. Periodic attempts to withdraw desmopressin are suggested to assess for recovery of endogenous vasopressin secretion.

Sudharani Kinthada MD, Kolli.H M.D

Case Presentation:

We describe a 35-year-old woman transferred from an outside ER for evaluation of a suspected spontaneous CSF leak. She reported a two-week history of unilateral clear nasal discharge that began abruptly following a forceful sneeze, accompanied by a dull, hollow headache, bilateral tinnitus, and transient visual obscurations. There were no focal neurological deficits, nausea, vomiting, or photophobia. Interestingly, the patient noted a marked reduction in headache severity—exceeding 50%—after the onset of rhinorrhea. Computed tomography (CT) of the head and maxillofacial region revealed no hemorrhage, mass effect, hydrocephalus, or skull base fracture. The cribriform plate appeared intact, with only mild bilateral maxillary sinus mucosal thickening. Biochemical testing of nasal fluid was positive for glucose, consistent with CSF leakage.

On admission, vital signs showed hypertension (170/103 mmHg) with normal respiratory and oxygen parameters. Physical examination confirmed continuous clear nasal drainage, particularly when leaning forward. Magnetic resonance imaging (MRI) of the brain demonstrated mild paranasal sinus inflammation and thickening of the left nasal turbinate, consistent with rhinitis. Lumbar puncture revealed an elevated opening pressure of 25 cm H₂O with normal CSF composition. Neurosurgical consultation supported the diagnosis of IIH with spontaneous CSF rhinorrhea. A lumbar drain was placed, producing 300 mL output on day one and 200 mL on day two. Empirical ceftriaxone therapy was initiated to prevent secondary infection; CSF cultures remained sterile throughout hospitalization. The patient’s symptoms improved progressively, and no recurrence of rhinorrhea was observed.

Discussion:

Conclusion:

Dr Kolli, Himabindu MD

Case Presentation:

A 46-year-old man (BMI 36.6 kg/m²) with T2DM on tirzepatide for four months, gastroesophageal refl ux disease, obstructive sleep apnea, depression, and anxiety presented with three days of progressive, sharp epigastric pain radiating to the back and right fl ank. The pain was constant, rated 10/10, and unrelieved by rest or medication. He denied nausea, vomiting, alcohol use, and had no history of pancreatitis or hypertriglyceridemia. On examination, he was alert but in mild distress. Abdominal exam revealed right upper quadrant tenderness without guarding; bowel sounds were normal. Cardiopulmonary fi ndings were unremarkable. Laboratory tests showed normal renal and hepatic function, mild leukocytosis, triglycerides of 181 mg/dL, and lipase of 32 U/L. Computed tomography of the abdomen and pelvis demonstrated mild peripancreatic fat stranding near the pancreatic head, consistent with acute uncomplicated pancreatitis. No necrosis, ductal dilation, or obstruction was identifi ed. The patient was managed conservatively with intravenous fl uids, analgesia, and gradual diet advancement. Symptoms improved, and he was discharged in stable condition. Tirzepatide was discontinued on discharge.

Discussion:

Conclusion:

Anastasiia Merkulova, MD, Juliana Stoilova, MD

 A 68-year-old male with chronic anemia presented to the emergency department (ED) with a 5-day history of band-like headache, somnolence, weakness, dizziness, and a prodrome of sore throat and ear pain. Initial evaluation a few days prior showed negative head CT; cefdinir was prescribed. Symptoms progressed to include gait instability requiring wheelchair assistance. He denied tick bites, fever, rash, or prior stroke, despite recent travel to Niagara Falls.

He returned to the ED with acute left facial palsy. Exam revealed peripheral left facial palsy, slurred speech, blurry vision, gait instability, and fatigue; vital signs, repeat head CT, and CT perfusion were unremarkable. While awaiting for MRI brain and lumbar puncture results, patient was started empirically on Doxycyline 100mg and Prednisone 60mg. A day later, patient developed Bell’s palsy-like right-sided weakness. Brain MRI without contrast showed focal enhancement of the left geniculate ganglion. LP results: protein 175 mg/dL, WBC 171/µL, RBC 0/µL. Meningitis panel positive for varicella-zoster virus (VZV). Acyclovir 10 mg/kg IV was added. Patient demonstrated marked improvement in left facial droop and clear speech upon hospital discharge.

This case represents the diagnostic challenge and neurological versatility of varicella-zoster virus. It serves as a critical reminder that VZV reactivation can present as zoster sine herpete, a rashless syndrome capable of mimicking strokes, idiopathic Bell's palsy, and autoimmune disorders like Guillain-Barré Syndrome.

Introduction:

The dangers of seizures as an adverse effect of antibiotic therapy is a serious, neurological complication in clinical practice. While antibiotics are essential for combating bacterial infections, beta-lactams (penicillins, cephalosporins, and carbapenems) and fluoroquinolones have been consistently linked to neurotoxicity, including a lowered seizure threshold.

Antibiotic-induced seizures represent a serious, and uncommon neurological complication, particularly with agents like beta-lactams (e.g., cephalosporins, carbapenems) and fluoroquinolones. These drugs lower the seizure threshold, primarily through antagonism of GABA-A receptors. The risk is significantly increased by factors like CNS pathology, renal/hepatic impairment, and advanced age.

Case Presentation:

After an extensive workup ruled out other etiologies, the seizure was attributed to the use of beta-lactam, cefepime, which was immediately discontinued. The patient showed a dramatic clinical response the next day, leading to successful extubation without further complications.

Conclusion:

Introduction:

Systemic sclerosis (scleroderma) is a chronic autoimmune disease characterized by progressive fibrosis and vascular dysfunction. Gastrointestinal involvement is common, with esophageal dysmotility being the most frequent manifestation. Impaired motility predisposes patients to reflux and aspiration, potentially leading to recurrent pneumonia or interstitial lung disease.

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Background:

Case Presentation:

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Conclusion:

Timely recognition and correction of hypophosphatemia can halt rhabdomyolysis and prevent systemic complications, prolonged ICU stays, and further metabolic deterioration.

Background:

Case Presentation:

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Conclusion:

This case underscores the importance of considering DIP in patients with new medications and unexplained pancreatitis. Prompt recognition and withdrawal of the offending agent are key to favorable outcomes.

Background:

Case Summary:

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Conclusion:

Prompt diagnosis, pathogen-specific antibiotics, and timely surgical intervention are essential to optimize outcomes and reduce morbidity in elderly patients with Enterococcus faecalis prosthetic joint infections.

Introduction:

Case Presentation:

Discussion:

Pulmonary mucormycosis is often diagnosed late due to non-specific symptoms and slow fungal culture, delaying treatment and surgery. While amphotericin B remains the mainstay therapy, timely molecular diagnostics and early infectious disease and thoracic surgery involvement may improve outcomes. Routine imaging to screen for vascular invasion can prevent catastrophic embolic events. Multidisciplinary care and vigilance are essential for timely intervention and improved survival in these cases.

Introduction:

Case Presentation:

Discussion:

Hypophosphatemia affects over 70% of DKA cases but rarely causes clinically significant encephalopathy. Profound depletion impairs ATP-dependent neuronal function and can mimic cerebral edema or hypoxic injury. While current guidelines do not recommend routine phosphate supplementation, severe hypophosphatemia with neurological symptoms warrants targeted repletion. EEG may help confirm toxic-metabolic encephalopathy. Vigilant phosphate monitoring and timely repletion are crucial for unremitting encephalopathy in DKA.

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Case Summary:

Discussion:

Conclusion:

This case highlights the diagnostic utility of careful clinical examination.Recognition of one-and-a-half syndrome and its variants is critical for accurate neuroanatomic localization and guiding further diagnostic evaluation and management.

Siddharth Sharma, MD; Abinaya Sivakumar, MD; Mina Saba, MD; Milan Regmi, MD; Gaurab K.C., MD; Srushti Ghetiya, MD; Kevin Meek, DO; Sagar Madan, MD; Yoseph Herpo, MD; Osama Naveed, MD, Syeda Hooria Imtiaz, MD; Walter Johnson, BS

Wernicke encephalopathy is an acute neurological emergency caused by thiamine deficiency. It typically presents as an incomplete triad of altered mental status, oculomotor abnormalities, and ataxia. WE can also arise from malnutrition, polysubstance use, and critical illness. A 40-year-old female with bipolar disorder and polysubstance use disorder presented with four days of altered mental status. She was drowsy, lethargic, and able to answer very few questions. Physical exam revealed nystagmus. Labs were significant for mild hyponatremia and a positive THC urine screen. Stroke imaging including CTA head were largely unremarkable. Neurology was consulted with consideration of toxic-metabolic encephalopathy, stroke, postictal state, and CNS infection as differentials. Lumbar puncture ruled out infection with a mildly elevated protein, few WBCs and negative cultures. EEG showed profound slowing without epileptiform activity. MRI brain revealed T2/FLAIR hyperintensities with restricted diffusion in bilateral medial thalami and periaqueductal gray matter consistent with WE. The patient was started on high-dose IV thiamine 500 mg bid x 7 days, followed by 250 mg bid x7 days. Her clinical course was complicated by respiratory distress requiring ICU transfer, intubation and mechanical ventilation.She showed significant clinical improvement with thiamine therapy.This case illustrates WE in a non-alcoholic patient with polysubstance use and nutritional deficiency. Awareness of WE beyond alcoholism can reduce permanent neurological damage and mortality. Maintaining a high index of suspicion for at-risk patients presenting with altered mental status ensures timely empiric thiamine therapy, optimizing patient outcomes.

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Conclusion:

Itraconazole-induced pseudohyperaldosteronism is an uncommon but clinically important adverse effect. Clinicians should maintain vigilance in patients on prolonged itraconazole therapy. Prompt recognition and withdrawal of the offending agent leads to full recovery and prevent potentially life-threatening metabolic derangements.

Siddharth Sharma, MD; Abinaya Sivakumar, MD; Mina Saba, MD; Milan Regmi, MD; Gaurab K.C., MD; Srushti Ghetiya, MD; Kevin Meek, DO; Sagar Madan, MD; Yoseph Herpo, MD; Osama Naveed, MD, Syeda Hooria Imtiaz, MD; Walter Johnson, BS

 A 34-year-old male with a history of osteogenesis imperfecta, chronic constipation, recurrent fecal impactions, and chronic anemia presented to the emergency department with worsening abdominal distension and decreased urine output. On examination, he was noted to have a small body habitus (height 114.3 cm, weight 31.8 kg). Laboratory evaluation revealed hypokalemia (serum potassium 3.1 mEq/L). CT imaging demonstrated severe constipation with extensive fecal impaction and marked colonic distention (up to 13 cm), as well as a distended urinary bladder with bilateral hydronephrosis and hydroureter, suggestive of urinary retention secondary to bowel obstruction. A Foley catheter was placed, resulting in good urine output. Gastroenterology was consulted and recommended GoLYTELY, enemas, and manual disimpaction. During his hospital course, the patient received an adult maintenance dose of oral potassium chloride, rather than a pediatric dose appropriate for his size. On transfer from the emergency department to the medical floor, he developed acute respiratory distress, became unresponsive, and was found pulseless. Cardiopulmonary resuscitation was initiated. ECG showed ST elevations progressing to ventricular tachycardia, ventricular fibrillation, and ultimately asystole with pulseless wide complex tachycardia. This case illustrates the critical importance of weight-based potassium dosing in patients with small body habitus, particularly those with underlying conditions such as osteogenesis imperfecta, to avoid potentially fatal outcomes.

Background:

Case Presentation:

Discussion:

Conclusion:

This case highlights the severe cardiopulmonary and systemic consequences of uncorrected large ASDs in adults and emphasizes the importance of early diagnosis and timely repair to prevent irreversible complications.

Siddharth Sharma, MD; Abinaya Sivakumar, MD; Mina Saba, MD; Milan Regmi, MD; Gaurab K.C., MD; Srushti Ghetiya, MD; Kevin Meek, DO; Sagar Madan, MD; Yoseph Herpo, MD; Osama Naveed, MD, Syeda Hooria Imtiaz, MD; Walter Johnson, BS

 A 76-year-old female with a history of untreated hypothyroidism presented with progressive confusion, hypothermia (32.5°C), bradycardia (HR 44 bpm), hypotension (BP 82/48 mmHg), and generalized edema. Initial laboratory evaluation revealed severe hyponatremia (Na 122 mmol/L), elevated TSH (68 mIU/L), and low free T4 (0.2 ng/dL), consistent with myxedema coma. Workup excluded infection, adrenal insufficiency, and other metabolic derangements.

Management was initiated in the intensive care unit with empiric intravenous hydrocortisone (100 mg every 8 hours), followed by intravenous levothyroxine (200 μg loading dose, then 75 μg daily), and low-dose intravenous liothyronine (5 μg loading, then 2.5 μg every 8 hours), in accordance with current guidelines.[1][3] Supportive measures included passive rewarming, ventilatory support, and correction of electrolyte imbalances. The patient demonstrated marked clinical and biochemical improvement within five days, with normalization of mental status and vital signs. She was transitioned to oral levothyroxine and discharged to rehabilitation on day 12.

Myxedema coma is a rare, life-threatening endocrine emergency, most often triggered by infection, cold exposure, or medication nonadherence in patients with longstanding hypothyroidism.[2][4-5] Prompt diagnosis and aggressive management with intravenous thyroid hormone and empiric glucocorticoids are essential to reduce mortality, which remains high despite advances in care.[1][3] This case highlights the importance of early recognition and adherence to evidence-based protocols in optimizing outcomes for elderly patients with decompensated hypothyroidism.

Introduction:

Case Presentation:

Conclusion:

This case underscores the need for multidisciplinary vigilance when managing complex infections with high-risk antimicrobials. Early identification of DEP requires considering it in any patient developing new pulmonary infiltrates while on daptomycin. Monitoring eosinophil counts and pulmonary symptoms, prompt discontinuation of daptomycin, consideration of corticosteroids, and communication among infectious disease, pulmonary, and critical care teams are essential to improving outcomes.

Introduction:

This case illustrates the potentially catastrophic embolic complications of a non-aneurysmal AMT, manifesting as acute bilateral limb ischemia. Given the multiple thrombotic events and the absence of clear predisposing factors besides the recent resolved sepsis, a hypercoagulable state, likely paraneoplastic, was strongly suspected. Initial management focused on acute limb salvage with thrombectomy and prevention of further embolization with therapeutic anticoagulation. However, the definitive long-term management requires the identification and treatment of the underlying cause, underscoring the necessity of the recommended outpatient malignancy workup. Timely diagnosis and aggressive antithrombotic therapy are paramount in managing this high-risk condition.

Introduction:

Case Presentation:

Discussion:

Conclusion:

Milan Regmi, MD; Motunrayo Adeleye, MD; Ahmed Al Sharie, MD;  Siddharth Sharma, MD; Abinaya Sivakumar, MD; Roger Lin, MD;  Sudharani Kinthada, MD; Abdelrahman Shehata, MD;  Mina Saba, MD; Kevin Meek, DO;  Humza Syed, MD; Paarmit Chhabra, MD;  Samid Bhatti, MD; Farhan Hashimi, MD; Mohamad Khedari, MD; Ahsan Masood, MD; Osama Naveed, MD; Syeda Hooria Imtiaz, MD; Saawan Patel, MD; Luis Ruiz Marrero, MD; Ananya Prakash, MD; Srushti Ghetiya, MD; Gaurab K C, MD; Jewell George, MD; Sagar Madan, MD; Yoseph Herpo, MD; Haider Malik, MD-; Franchesca Ramirez, MD; Hajelkhidir Bala, MD, Walter Jhonson, BS

Introduction:

Immune checkpoint inhibitors (ICIs), such as pembrolizumab, have become standard treatment for advanced non-small cell lung cancer (NSCLC). However, they can induce immune-related adverse events (irAEs), with colitis being a significant complication. Early recognition and aggressive management of ICI-colitis are critical. We are presenting a case of severe immune checkpoint inhibitor-related immune colitis. 

Case Presentation:

A 67-year-old male with stage IV non-small cell lung cancer (adenocarcinoma) and metastases to the brain and bone, receiving maintenance pembrolizumab for 21 cycles, presented with two weeks of intermittent midline abdominal pain, nausea, vomiting, constipation, and rectal bleeding. Symptoms began 1.5 weeks after his most recent radiotherapy. Initial evaluation showed tachycardia, hypertension, and abdominal tenderness. Labs were notable for a mildly elevated lipase (331 U/L), leukopenia (2.18), and thrombocytopenia (109 ). CT abdomen and pelvis suggested acute, inflammatory colitis with focal mural thickening and enhancement in the rectum. A colonoscopy revealed severe pancolonic edematous, erythematous, friable, hemorrhagic, and ulcerated mucosa, with biopsies confirming active colitis consistent with checkpoint inhibitor colitis.

Discussion:

The patient's clinical presentation, endoscopic findings, and history of recent ICI therapy established a diagnosis of severe checkpoint inhibitor colitis. The patient was initially treated with high-dose intravenous Solu-Medrol (1 mg/kg b.i.d., then 1000 mg daily) but had persistent, frequent bloody diarrhea (up to 10-12 bowel movements per hour). Due to the lack of response to high-dose steroids alone, he was escalated to infliximab (IFX), a TNF-alpha inhibitor, and subsequently transitioned to oral prednisone with a taper plan. His symptoms gradually improved after IFX initiation, with a decrease in bowel movements and resolution of bleeding. He was discharged on prednisone and scheduled for outpatient IFX continuation. Resuming pembrolizumab was deemed not feasible due to the severity of the colitis.

Conclusion:

This case illustrates a severe, refractory case of pembrolizumab-induced pancolitis that necessitated the addition of a biologic agent, infliximab, after failing high-dose corticosteroid therapy. Patients who develop Grade 3/4 ICI-colitis often require multidisciplinary management and may be ineligible for further ICI treatment

Jewell George, MD, Hajelkhidir Bala

Introduction:

The dangers of Euglycemic diabetic ketoacidosis (EDKA) is an uncommon diabetic complication associated with several risk factors that include fasting, surgery, pregnancy, and the use of sodium-glucose cotransporter 2 (SGLT2) inhibitors. The imbalance between insulin and counter-regulatory hormones with an elevated ratio of glucagon to insulin is the primary driving force of EDKA.

Case presentation:

A 63 year old male with multiple comorbidities including a history of hypertension, stage 3 chronic kidney disease, T2DM, asthma, spinal stenosis, seizures who presented with complaints of recurrent falls and presyncope. The patient takes glipizide, Farxiga, and Lantus at home, and eats only one meal. He was found to have recurrent hypoglycemia due to EDKA with low pH, elevated beta hydroxybutyrate and open anion gap. The patient was transferred to the ICU for close monitoring and was started on 0.054 unit/kg/hour insulin drip.

Management and Outcome:

After an extensive workup ruled out other etiologies, EDKA was managed with insulin drip with D10-0.9% saline infusion with hourly glucose checks and BMP. ABG and beta hydroxybutyrate were also checked every 4 hours and the patient's anion gap closed the following morning with transition to long-acting insulin and diabetic diet, prompting transfer out of the intensive care unit. Remainder of hospitalization, anion gap remained closed with well-controlled sugars without any insulin requirements 24 hours prior to discharge. 

Conclusion:

This case shows the risk of EKDA and importance of discontinuing anti-diabetic medications if needed in a timely manner which allows adequate compliance by the patient.

Milan Regmi, MD;  Siddharth Sharma, MD; Abinaya Sivakumar, MD; Abdelrahman Shehata, MD; Gaurab K C, MD;  Mina Saba, MD; Kevin Meek, DO;  Ahmed Al Sharie, MD; Sudharani Kinthada, MD; Saawan Patel, MD; Roger Lin, MD; Sagar Madan, MD; Yoseph Herpo, MD; Srushti Ghetiya, MD; Walter Johnson, BS

Introduction:

Cardiac tamponade is a life-threatening condition requiring immediate diagnosis and intervention, typically stemming from impaired diastolic ventricular filling due to causes like PCI, malignancies, or inflammation. We present a rare case of cardiac tamponade in a patient on apixaban that resolved following chest compression during cardiopulmonary resuscitation (CPR).

Case Presentation:

A 67-year-old female with hypertension and atrial fibrillation (on apixaban) presented with bradycardia and a large pericardial effusion suggesting impending cardiac tamponade. Shortly after arrival, the patient developed cardiac arrest, and CPR was initiated. Initial transthoracic echocardiogram (TTE) confirmed tamponade. As the patient was on apixaban, hemorrhagic effusion was suspected, and andexanet alfa was started. Before emergent pericardiocentesis could be performed, the patient lost pulse, and CPR resumed. Upon achieving ROSC, a repeat TTE showed no pericardial effusion, though left and right ventricular contractility remained limited. It was presumed that pericardial rupture occurred during CPR, leading to the loss of contained blood into the mediastinum. The initial X-ray showed an enlarged cardiac silhouette, while a repeat X-ray showed a decreased cardiac silhouette with a right-sided opacity, likely blood.

Discussion:

Apixaban, a Factor Xa inhibitor, is associated with bleeding risk. Hemorrhagic pericardial effusion causing tamponade is life-threatening, and its association with apixaban is rarely documented. Tamponade physiology limits diastolic filling. Crucially, CPR-related trauma can cause pericardial rupture, which has been previously reported in only two cases to lead to the resolution of pericardial tamponade.

Conclusion:

This case highlights apixaban-related hemorrhagic pericardial tamponade that unexpectedly resolved after chest compressions during CPR, likely due to pericardial rupture. This demonstrates CPR's potential to alter management. Clinicians must remain aware of bleeding risks with DOACs and the need for rapid diagnosis and emergent intervention. Further studies on CPR-related injuries are recommended.

Khedari, Mohamad. MD Sawaan, Patel. MD Jewell, George. MD

Resistant hypertension is a complex clinical condition typically managed with combination pharmacotherapy. However, treatment becomes exceptionally challenging when standard antihypertensives are poorly tolerated. We report a unique case of a 79-year-old female with longstanding, poorly controlled hypertension who was intolerant to over 60 medications, including nearly every class of antihypertensives. The patient presented with flash pulmonary edema and hypertensive emergency, requiring ICU admission. Her blood pressure on arrival exceeded 250 mmHg systolic. She had a 20-year history of uncontrolled hypertension and was labeled allergic to 61 medications. Only clonidine and propranolol were tolerated, offering limited control. Past imaging revealed 60% right renal artery stenosis. Despite her previous refusal of procedural interventions and multiple discharges against medical advice, she consented to care following this life-threatening episode.

Khedari, Mohamad. MD. Herpo, Yousef. MD Jewell, George. MD Patel, Saawan. MD

Neurocysticercosis, caused by Taenia solium infection, is the most common parasitic infection of the central nervous system. Although parenchymal involvement is typical, intraventricular lesions are rare and can present with nonspecific symptoms related to cerebrospinal fluid obstruction or raised intracranial pressure.

Khedari, Mohamad. MD. Jewell, George. MD Patel, Sawan.MD Syed, Humza. MD

Fabry disease is a rare X-linked lysosomal storage disorder resulting from a deficiency of α-galactosidase A, leading to systemic accumulation of glycosphingolipids. Its variable and often subtle presentation makes early diagnosis challenging.

Jewell George, MD, Hajelkhidir Bala, MD, Mohamad Khedari, MD

Introduction:

The dangers of Internationalized normalized ratio (INR) levels exceeding 5 and increasing bleeding risk for patients on chronic warfarin therapy following procedures that require prolonged chronic warfarin therapy like mechanical mitral valve replacement. It is important to have a good dietary plan to avoid leafy green vegetables, like kale, spinach, green tea, grapefruit, cranberry juice.

Case presentation:

A 57-year-old female with multiple comorbidities, including mitral valve replacement in 2021, end-stage renal disease on hemodialysis Monday, Wednesday, Friday, presented with left axillary swelling and tenderness and was found to have supratherapeutic INR in addition to influenza. The patient reported having lower abdominal pain exacerbated by worsening cough for several days prior and a tender left axillary swelling.

Management and outcome:

Patient underwent daily monitoring of INR along with abdominal binder in addition to Tessalon perles to help control cough and renally dosed oseltamivir following a positive influenza A viral panel. Following close monitoring of the INR, she was found to be subtherapeutic with levels as low as 1.2 during which the patient’s home warfarin was resumed. The patient also had a low hemoglobin of less than seven for which she received a unit of blood.

Conclusion:

This case shows the likelihood of developing hematomas and deviations in INR that can go unnoticed when periodic monitoring is not performed. The patient's INR was found to be 8.2 and she received vitamin K injection which helped adjust her warfarin administration in a timely manner.

Srushti Ghetiya, MD ; Siddhartha Sharma, MD; Gaurab K.C., MD; Milan Regmi, MD; Abinaya Sivakumar, MD; Mina Saba, MD; ; Kevin Meek, DO; Sagar Madan, MD; Yoseph Herpo, MD; Walter Johnson, DO

Introduction:

Massive pulmonary embolism (PE) complicated by obstructive shock and right ventricular (RV) failure is associated with high mortality and demands rapid hemodynamic stabilization. Mechanical circulatory support (MCS) devices, such as the Impella RP, have emerged as potential adjuncts to conventional therapies, aiming to restore RV output and tissue perfusion while definitive management of the embolic obstruction is pursued.

Case presentation:

A 46-year-old man with no prior medical history presented with a one-week history of progressive dyspnea, fatigue, and weakness. Initial imaging at an outside facility revealed bilateral pulmonary emboli with a saddle embolus, left lower lobe infarction, and right heart strain. He was started on intravenous heparin and transferred for advanced cardiac care.  Thrombolytic therapy with tenecteplase was administered for massive pulmonary embolism with right ventricular failure. Overnight, he developed hypotension, diaphoresis and desaturated to 88% spo2 requiring rapid response intervention; subsequently, he sustained a cardiac arrest with return of spontaneous circulation after four cycles of CPR. He was initiated on vasopressor support and mechanical ventilation. Bedside echocardiography confirmed severe right ventricular systolic dysfunction and acute cor pulmonale. Rescue mechanical thrombectomy with right ventricular Impella support was performed on same day. During this time he developed transient acute kidney injury, ischemic hepatitis in setting of cardiac arrest. Levophed requirement was decreased and oxygenation improved on day two. On day two, RV Impella was removed and patient was off pressors by day three.  He was successfully weaned off mechanical ventilation by end of one week, with resolution of a transient posterior pericardial effusion.Therapeutic anticoagulation was transitioned from heparin to apixaban, then rivaroxaban for long-term management. Coreg was initiated for sinus tachycardia. The patient was discharged hemodynamically stable with recommendations for close outpatient follow-up with primary care and cardiology. This case highlights the importance of rapid recognition and aggressive management with RV Impella for massive pulmonary embolism complicated by obstructive shock with right heart failure.

Discussion:

The Impella RP is a percutaneous, microaxial RV assist device capable of delivering up to 4 L/min of flow, approved for acute RV failure refractory to medical therapy. In the context of massive PE, the device can partially decompress the RV and augment cardiac output, potentially reversing shock and facilitating recovery.Case reports and small series have demonstrated successful hemodynamic stabilization and RV recovery in patients with massive PE and profound shock, with rapid reduction in vasopressor requirements and improvement in RV function following Impella RP implantation. However, the literature notes several limitations: downstream pulmonary artery obstruction may restrict device efficacy, and nonpulsatile RVADs may increase RV afterload, potentially impeding optimal RV recovery.Complications such as bleeding and hemolysis are not uncommon, and outcomes outside of controlled study protocols may be less favorable. Compared to venoarterial extracorporeal membrane oxygenation (VA-ECMO), which unloads both RV preload and afterload and improves oxygenation, Impella RP offers selective RV support but may be less effective in cases of severe pulmonary vascular obstruction.

Conclusion:

In patients with massive PE and refractory RV failure, Impella RP may provide rapid hemodynamic stabilization and bridge to definitive therapy, but its use should be individualized, considering anatomical and physiological constraints. While promising, further prospective studies are needed to clarify its safety, efficacy, and optimal role relative to other MCS modalities in this high-risk population.