United States

This is a case of a patient who underwent an elective laparoscopic cholecystectomy after previously presenting with acute cholecystitis. His operation was complicated by a high common hepatic duct (CHD) injury requiring complex surgical repair. This case highlights the importance of early recognition of this type of injury and the utility of a Kasai portoenterostomy as an operative repair in high CHD injuries in the absence of a viable extrahepatic duct viable for repair.

AMA Research Challenge 2025 

Surgical Management of a Complex High Hepatic Duct Injury: A Case Report

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Diaphragmatic hernias result from a defect in the diaphragm that allows abdominal contents to herniate into the thoracic cavity. The most common cause is acute trauma, particularly blunt force trauma, more than penetrating trauma. Congenital causes are the second most common cause. Such as Bochdalek and Morgagni hernias. There are other types and the most uncommon is a spontaneous diaphragmatic hernias (SDH). This paper presents a novel case of SDH, leading to gastric fundus protrusion and incarceration, resulting in abscess formation. The patient’s medical history did not suggest trauma or congenital anomalies, making this case an acquired SDH, with fewer than 40 documented occurrences. Diagnosis is often delayed due to the overlap of symptoms with other conditions, and SDH frequently presents with nonspecific gastrointestinal or respiratory symptoms. Imaging, particularly CT, is crucial for diagnosis. The patient underwent successful repair using a transabdominal robotic approach with the Da Vinci Xi system, marking the first documented case of SDH repaired exclusively with robotic techniques. This case highlights the importance of considering SDH in patients with unexplained thoracoabdominal pain, particularly in the absence of trauma, and demonstrates the efficacy of robotic surgery in minimizing complications and reducing morbidity in such cases.

Trans-abdominal Approach in a Spontaneous Diaphragmatic Hernia: A Case Report

Introduction
Intracholecystic papillary neoplasm (ICPN) is a rare, visibly distinct lesion arising
from the gallbladder lining and projecting into its lumen. It is often discovered
incidentally when asymptomatic but may sometimes cause symptoms such as pain,
jaundice, weight loss, or ascites. ICPN is very rarely reported in Nepal, highlighting
the need for careful evaluation and management.
Presentation of case
We report a 63-year-old man diagnosed incidentally with ICPN during routine
evaluation. The patient had no symptoms such as abdominal pain. He underwent
laparoscopic cholecystectomy and recovered well without complications.
Discussion
ICPN is a preinvasive gallbladder tumor that can show different histologic patterns,
typically appearing as papillary or polypoid growths. Imaging like ultrasound and CT
can suggest ICPN, but a definitive diagnosis requires surgical removal and
microscopic confirmation. Intraoperative frozen section assessment of tumor invasion
and margins is helpful for surgical decision-making, as demonstrated in this case.
Early diagnosis and surgery generally result in better outcomes than those seen in
invasive gallbladder cancer.
Conclusion
Because ICPN is rare and often presents subtly, a thorough clinical workup with
appropriate imaging is essential. Early surgical intervention supported by
intraoperative pathology evaluation can improve prognosis and patient outcomes.

An incidental finding of Intracholecystic Papillary Neoplasm- A rare case report

Background: 
Extramedullary plasmacytoma (EMP) is a rare form of plasma cell neoplasm characterized by monoclonal plasma cell infiltration without systemic evidence of multiple myeloma. It represents 1.6-4% of all plasma cell tumors. The most common sites of involvement are the upper respiratory and gastrointestinal tracts, while anterior chest wall involvement is rare and can mimic other common thoracic malignancies. Here, we report a case of a 50-year-old man presenting with a large anterior chest wall mass diagnosed as extramedullary soft tissue plasmacytoma occurring years after blunt thoracic trauma. Plasmacytoma should be considered in the differential diagnosis of anterior chest wall masses, especially when associated with a history of trauma and presence of invasive features on imaging. A combination of clinical presentation, imaging, and biopsy is critical for diagnosing atypical soft tissue neoplasms.
Case Presentation: 
A 50-year-old man presented with a progressively enlarging anterior chest wall mass, initially noticed 5–6 years after blunt thoracic trauma. The mass remained stable for years but rapidly increased in size over six months, causing dyspnea, dysphagia, and odynophagia. Physical examination revealed an 18 cm, firm, non-mobile mass with superficial venous prominence. The initial differentials included thymoma, teratoma, thyroid neoplasm, and lymphoma. However, the history of trauma, chronic presentation, recent progression, and normal tumor markers raised suspicion for a soft tissue or bony lesion. Contrast-enhanced CT showed a lobulated, calcified mass in the superoanterior mediastinum with scattered enhancement, sternal erosion, invasion of the first rib, anterior chest wall extension, and tracheal compression. Laboratory workup revealed hemoglobin 11.6 g/dL, calcium 9 mg/dL, creatinine 0.8 mg/dL, and normal TSH, LDH, β-hCG, and AFP levels, but urine electrophoresis demonstrated an M spike with significantly elevated free kappa light chains (1956.2 mg/L). Histopathology showed diffuse sheets of plasma cells with eosinophilic cytoplasm and eccentric nuclei. Immunohistochemistry was positive for CD138, MUM1, CD56, and kappa light chain, consistent with a diagnosis of kappa-restricted extramedullary plasmacytoma.
Discussion: 
This case demonstrates a rare post-traumatic extramedullary plasmacytoma with extensive local invasion, highlighting the need to consider plasma cell neoplasms in the differentials of anterior mediastinal masses. In this case, scar tissue from prior injury may have created a permissive microenvironment, allowing delayed plasma cell proliferation. Imaging revealed aggressive features suggestive of soft tissue plasmacytoma, and biopsy confirmed the presence of plasma cells. While radiotherapy is the primary treatment modality, chemotherapy may also be used in combination based on the tumor characteristics.


Post-Traumatic Extramedullary Plasmacytoma Presenting as an Anterior Chest Wall Mass

Abstract Title : 
An Uncommon Case of BRAF V600E–Mutated Colorectal Adenocarcinoma in an African American Patient: Case Report and Therapeutic Implications 
Background:
BRAF V600E mutations occur in 8% to 15% of colorectal cancers (CRC) and are linked to aggressive tumors, poor prognosis, and chemotherapy resistance. These mutations occur less frequently in African American patients (1.8% to 6.4%). Early molecular profiling is essential to guide personalized treatment. Case Presentation A 77-year-old African American man with hypertension and type 2 diabetes presented with fatigue and iron deficiency anemia. Colonoscopy identified a transverse colon mass; biopsy confirmed invasive adenocarcinoma. Molecular testing revealed a BRAF V600E mutation with loss of MLH1 and PMS2. The patient underwent right hemicolectomy, which showed a 5.0 × 3.5 × 1.2 cm high-grade tumor invading through the muscularis propria into the subserosal fat (pT3) with lymphovascular invasion. Five of 15 lymph nodes were positive (pN2a), and a contrast-enhanced computed tomography (CT) scan showed no distant metastasis consistent with stage IIIC (T3N2aM0). He completed 12 cycles of FOLFOX (oxaliplatin, leucovorin, and 5-fluorouracil) per National Comprehensive Cancer Network (NCCN) guidelines with mild peripheral neuropathy. Carcinoembryonic antigen (CEA) is being monitored. A post-treatment CT is pending to assess distant metastasis and treatment response. 
Discussion:
BRAF V600E mutation causes aggressive tumor behavior, rapid progression, and resistance to treatment. In metastatic colorectal cancer (CRC), BRAF inhibitor monotherapy is ineffective due to epidermal growth factor receptor (EGFR)–mediated resistance. Combination therapies targeting BRAF and EGFR, such as encorafenib plus cetuximab, have shown improved outcomes. Our patient completed 12 cycles of FOLFOX, the standard first-line chemotherapy for stage IIIC CRC without distant metastasis. Post-treatment imaging will guide next steps; if metastases are found, targeted therapy with BRAF and EGFR inhibitors will be considered. The phase III BEACON trial demonstrated median survival of 9 months and response rates up to 26% with encorafenib plus cetuximab, with or without the MEK (mitogen-activated protein kinase kinase) inhibitor binimetinib. MEK inhibitors increased response rates from 10% with doublet therapy to 21% with triplet therapy. The BREAKWATER trial showed first-line encorafenib, cetuximab, and chemotherapy improved response to 60.9% versus 40.0% with chemotherapy alone, with durable disease control in 69% and no added toxicity. Early genomic testing enables timely, personalized therapy. Though BRAF mutations are less frequent in African American patients, comprehensive molecular profiling is essential to detect early mutations and guide appropriate treatment. Addressing disparities in testing and access remains key to improving outcomes in this aggressive CRC subtype.

An Uncommon Case of BRAF V600E–Mutated Colorectal Adenocarcinoma in an African American Patient: Case Report and Therapeutic Implications

Authors: 
Muneeba Ali, MD, Lubaba Mukhtar, MD, Warda Naqvi, MD, Muhammad Ayub, MD. 

Background:
Today, we present the case of Mollaret’s meningitis in a 49-year-old male who was acutely distressed with a severe headache and associated back pain upon presentation to the emergency department. Remarkably, he experienced a complete resolution of symptoms within 24 hours of admission. This case provides an opportunity to highlight the clinical behavior of this rare condition, the critical role of detailed history-taking , the importance of maintaining a high index of suspicion in patients with a history of viral meningitis, and the eventual bold decision to discontinue all intravenous management in a patient exhibiting signs of meningitis, provided the symptomatology is consistent with a diagnosis of Mollaret’s meningitis.

Case Presentation:
A 49-year-old male with a past medical history of viral meningitis presented to the emergency department (ED) with the chief complaint of a gradually worsening headache, associated with lower back pain. A lumbar puncture was performed, revealing cerebrospinal fluid with 180/μL red blood cells, 228/μL white blood cells, a glucose level of 37 mg/dL, and a protein level of 152 mg/dL. His symptoms surprisingly resolved completely within 24 hours. HSV-2 was detectable on CSF DNA PCR, and his clinical course was highly consistent with Mollaret’s meningitis. All intravenous therapy was discontinued, and the patient was discharged home on oral valacyclovir 1 g every 8 hours to complete a 10-day course.

Discussion:
Mollarets Syndrome or benign recurrent aseptic meningitis collectively refers to two distinct medical conditions which are Mollaret’s meningitis and Mollaret's lymphocytic meningitis. Mollaret’s meningitis is characterized by recurrent episodes, which typically goes away within a week or so, whereas Mollaret's lymphocytic meningitis is a recurrent chronic inflammation of the meninges.

Symptoms of moderate syndrome typically include meningeal signs, as well as various neurological symptoms including confusion, altered consciousness, seizures, paresthesia and cranial nerve palsies. However, these symptoms vary between episodes and may not always be present. The most implicated causative organisms are varicella-zoster virus (VZV) and herpes simplex virus (HSV). Autoimmunity and genetic factors also play a role in pathogenesis.

The diagnosis of Mollaret’s syndrome often proves to be a challenge, as there are no specific diagnostic tests available for this rare neurological disorder. CSF analysis is usually a critical lab test to diagnose the syndrome and usually shows elevated levels of lymphocytes and protein in the CSF. Viral testing can identify the underlying causative agent.

Treatment of Mollaret’s syndrome usually includes managing the acute episode and preventing further attacks. The literature regarding the use of antiviral therapy in an acute episode or as longer term prophylaxis is currently mixed.

The Back Burn: A Case Report of Mollaret’s Meningitis in a Young Male.

Background: Intracranial hypertension (IH) is a rare but serious complication of growth hormone (GH) therapy. Incidence is roughly 13 per 100,000 cases. Risk factors for GH-induced IH include obesity, chronic renal failure, and Turner Syndrome. Blindness and intractable headache are primary concerns. GH therapy discontinuation is commonly sufficient for resolution of IH, but some patients require additional therapies. Most cases resolve within 12 months of GH discontinuation with favorable outcomes. We describe an unusual case of a very prolonged course of IH after GH therapy.

Case Presentation: A 19-year-old non-obese female developed persistent intracranial hypertension at age eleven within two months of starting GH therapy (0.264 mg/kg/week) for GH deficiency. Initially, she presented with new-onset headaches, pulsatile tinnitus, visual obscurations, and bilateral grade 1 papilledema. Lumbar puncture (LP) revealed an opening pressure of 44 cm H2O, and neuroimaging revealed a congenital hypoplastic transverse sinus. Despite promptly discontinuing GH therapy, symptoms remained persistent eight years later (opening pressure: 29 cm H2O; elevated OCT RNFL measurements: OD 120 um, OS 121 um). Her course was resistant to multiple standard diuretics (acetazolamide, topiramate, furosemide) and she was treated with repeated LPs for symptom relief. Her headache phenotype evolved into chronic migraine (16 days/month, MIDAS=69, severe) with medication overuse headache.

Discussion: Through our literature review of 169 reported cases, we found that symptom onset of GH-induced IH was typically within three months. Growth hormone discontinuation alone was often sufficient for symptom resolution, but up to 43% of patients underwent additional treatments– most commonly with acetazolamide, but interventions also included serial LPs, and, rarely, ventriculoperitoneal shunts. The prognosis is favorable. In those with detailed data, an estimated 95% reported resolution by 6 months and 98% by 12 months. Two cases reported complete resolution at 2 years after discontinuation. At 8 years, our patient’s duration is unusually prolonged. Although CSF pressures have improved over time, this is the longest persistence of GH-induced IH to the best of our knowledge. IH is an uncommon event during GH treatment, but our patient's course demonstrates the potential for long-lasting and debilitating adverse effects. Routine ophthalmological monitoring and a high index of suspicion is essential for early recognition, enabling timely interventions to prevent vision loss and headache disability.

Eight-Year Persistence of Growth Hormone-Induced Chronic Migraine and Intracranial Hypertension

Abstract Title
A Clot Conundrum: Reassessing Interstitial Lung Disease as Pulmonary
Embolisms with Aubagio Use
Background
Interstitial lung disease and pulmonary embolism are rare side effects reported post
teriflunomide use. Based on a trial evaluating the potential long-term effects of teriflunomide, reports of such adverse reactions have emerged from the TOWER extension study1 as well as several case studies2,3,4 . There are case reports of suspected pneumonia with a CT angiogram performed upon lack of clinical improvement, with pulmonary embolisms found there after. Here we report a case of suspected interstitial lung disease in the setting of teriflunomide use and upon further investigation, multiple pulmonary embolisms were discovered.
Case Presentation
A 46 year old female with a past medical history of multiple sclerosis, who was started on Teriflunomide four years prior, presented with progressive dyspnea, with persistent deoxygenation for one year based on an Apple watch monitoring device. The patient had several CT chest without contrast studies that were suggestive of interstitial lung pneumonitis prompting discontinuation of Teriflunomide and initiation of steroids. When the patient had no clinical improvement, a CT Angiogram with contrast later revealed extensive pulmonary artery emboli at multiple levels. Transthoracic echocardiogram revealed significant right heart strain. She was then started on a heparin drip and underwent a bilateral pulmonary endarterectomy.
Following this, the patient was started on oral anticoagulation and was continued on steroids.
Discussion
There have been a few reported cases of either interstitial lung disease and pulmonary embolism linked to Aubagio use in multiple sclerosis patients. In our case, a patient presumed to have interstitial lung disease was later diagnosed with multiple pulmonary embolisms. A more comprehensive evaluation of potential side effects could have resulted in earlier, more effective treatment. Thus, we caution against solely attributing symptoms to one side effect and recommend early consideration of multifactorial and broader adverse effects of Aubagio.

A Clot Conundrum: Reassessing Interstitial Lung Disease as Pulmonary Embolism with Teriflunomide Use

Background
Gradenigo syndrome is an uncommon complication of otitis media, first described by Giuseppe Gradenigo in 1904. The infection spreads from the middle ear to the petrous apex of the temporal bone, irritating cranial nerves V and VI. It classically presents with a triad: otorrhea, abducens palsy, and facial pain in the V1/V2 distribution. Although less common today due to antibiotics, diagnosis and management remain challenging, particularly when caused by atypical etiologies such as neoplasms.
We present a rare case of Gradenigo syndrome secondary to a meningioma in a 78-year-old female, emphasizing the importance of considering neoplastic causes and utilizing neuroimaging in patients with progressive cranial neuropathies and a history of brain tumors.
Case Presentation
A 78-year-old female with a history of four meningiomas and immune thrombocytopenic purpura (ITP) presented with generalized weakness, 3-4 months of painless diplopia, and significant unintentional weight loss.
Neurologic exam revealed bilateral lateral gaze palsies, left proptosis, suspected CN III/IV/VI palsies on the left, right CN VI palsy, and mild left facial droop. She also had left-sided hemiplegia from a prior stroke. Rinne test was positive on the right, negative on the left; Weber test was normal.
Labs showed hemoglobin of 9.4, platelets 51,000 (rising to 78,000), and ESR of 120 mm/hr.
Head CT showed no acute findings. MRI revealed a 3.7 cm enhancing lesion at the left cavernous sinus involving the dura, prepontine cistern, and sella, consistent with a meningioma compressing the pons. Another lesion at the petrous temporal bone was compressing cranial nerves.
Neurosurgery was consulted, and outpatient follow-up was advised.

Discussion 
This case illustrates a rare instance of Gradenigo syndrome mimicking infectious petrositis but caused by a skull base meningioma. Persistence of symptoms despite antibiotics and absence of infection signs pointed to a structural lesion.
Although the full triad was not present, many cases are incomplete. Accurate diagnosis requires maintaining a broad differential and early neuroimaging. Without it, tumors may be mistaken for infection, delaying care.
Other mimics include skull base infections, thrombosis, coagulopathies, Lemierre’s syndrome, and neoplasms. While antibiotics are standard for infectious cases, mass lesions often require surgery, thus, early recognition of atypical causes is critical to prevent lasting deficits. Even benign meningiomas can present deceptively at the skull base, warranting timely imaging.


A Rare Presentation of Gradenigo Syndrome Secondary to Skull Base Meningiomas: A Case Report

Background:
Ulnar neuropathy is the second most common upper extremity entrapment neuropathy, typically occurring at the cubital tunnel or Guyon’s canal. Simultaneous compression at both sites, referred to as “double crush syndrome” is not common; examples of double entrapment involving compression and cubital tunnel entrapment unrelated to trauma are rare. Reports of dual-site entrapment in otherwise healthy athletes, particularly from overuse, are exceedingly uncommon. We present a novel case of unilateral, double-site ulnar neuropathy in a hypermobile gymnast following repetitive handstands; an activity not previously associated with this condition.
Case Presentation:
A 30-year-old left-handed professional gymnast presented with acute paresthesia, weakness, and pain in the fourth and fifth digits of her left hand following a performance involving prolonged handstands. She repeated the routine the next night, after which symptoms intensified. Neurological examination showed decreased grip strength, weakness in finger abduction, and reduced sensation in the ulnar distribution. Tinel’s sign was positive at both the cubital tunnel and Guyon’s canal. Froment’s sign and the elbow flexion test were also positive. The patient reported frequent long-duration handstands several times per week and demonstrated hypermobility at the wrists and elbows. Radiographs were unremarkable; electromyography and nerve conduction studies was deferred due to improvement. At one-month follow-up, after pausing performances but continuing to coach, her symptoms largely resolved, consistent with overuse-related ulnar neuropathy exacerbated by joint laxity and load-bearing mechanics.
Discussion:
Hypermobility increases joint laxity and amplifies tensile and compressive forces on the ulnar nerve. Anatomical variations may further predispose to entrapment; close to 60% of patients had anatomical changes in the cubital tunnel that caused the ulnar nerve neuropathy, of which nearly 20% of patients had a subluxation of the ulnar nerve.
Hypermobile athletes may have unrecognized variants that tolerate extreme ranges but place neural structures at risk. During handstands, prolonged elbow extension and wrist hyperextension stress the ulnar nerve at multiple points. At the elbow, compression may occur at the retrocondylar groove, beneath Osborne’s ligament, between the flexor carpi unaris heads, or due to variants like the Arcade of Struthers or anconeus epitrochlearis. At the wrist, Guyon’s canal and pisohamate arch can entrap the motor branch, while trauma to the nearby ulnar artery may produce secondary compression (Hypothenar Hammer Syndrome). Unilateral symptoms may reflect dominance or asymmetric loading. Recognizing handstands as a potential biomechanical risk factor may guide early intervention and inform preventive strategies in similar athletic populations.

A Balancing Act: Dual Ulnar Nerve Entrapment In AHypermobile Handstand Performer

Background: Chimeric Antigen Receptor T-cell (CAR-T) therapy has transformed treatment for hematologic malignancies but is associated with immune effector cell-associated neurotoxicity syndrome (ICANS), a complication typically marked by cortical dysfunction such as encephalopathy, aphasia, and seizures. Current ICANS grading criteria uses the Immune Effector Cell-Associated Encephalopathy (ICE) score and relevant neurologic findings, with motor deficits falling under grade 4. However, spinal cord–predominant presentations are rare and not well represented in existing grading criteria.

Case Presentation: A 30-year-old female with refractory B-cell acute lymphoblastic leukemia and KMT2A rearrangement underwent CAR-T therapy with brexucabtagene autoleucel. After developing cytokine release syndrome (CRS), she experienced a progressive decline in mental status consistent with grade 2 ICANS. Despite aggressive immunosuppression with corticosteroids, tocilizumab, and anakinra, she developed sudden paraplegia and bowel/bladder dysfunction by day 8 post-infusion. MRI revealed diffuse T2 hyperintensities and cord expansion throughout the cervical and thoracic spinal cord, consistent with inflammatory myelitis. Intrathecal cytarabine and hydrocortisone were administered, followed by intravenous immunoglobulin (IVIG). While her cognitive status fully recovered, motor deficits persisted and only some sensory function recovered. At one-year follow-up, she remained paraplegic with persistent spinal cord atrophy and T2 intensities demonstrated on MRI.

Discussion: Spinal cord-predominant ICANS is a distinct clinical presentation that challenges current pathophysiologic models centered on cortical dysfunction. The decoupling of cognitive recovery from persistent motor deficits suggests a localized spinal cord injury, likely mediated by cytokine-induced blood–spinal cord barrier disruption. Spinal MRI was key to diagnosis, and earlier imaging may have facilitated more targeted intervention. Current ICANS grading systems, which rely heavily on ICE scores and encephalopathy, may overlook spinal presentations, delaying diagnosis and treatment. Revised grading criteria that account for spinal cord involvement, as well as research into optimal management strategies, are warranted to better identify and treat this rare but serious form of neurotoxicity.

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