Bilateral Extremity Research Articles

Can Talaromyces marneffei Infection Cause Acute Liver Failure? A Case Report

Introduction: Talaromyces marneffei is a pathogen that causes talaromycosis, a systemic fungal infection. Cases in which hepatic failure is the primary clinical presentation are exceedingly rare. Case Presentation: This report details the case of a 49-year-old male with no prior liver disease, presenting to the hospital with persistent symptoms, including a fever lasting over ten days, abdominal distension for five days, and jaundice for three days. The patient’s history included immune thrombocytopenia and prolonged glucocorticoid therapy. Physical examination revealed yellowing of the skin and sclera, abdominal distension, firmness of the abdominal wall, absence of abdominal tenderness, positive shifting dullness, and pitting edema in the lumbosacral region and bilateral lower extremities. An HIV antibody test was negative. The patient developed hepatic failure and received artificial liver support along with routine therapy. Despite these interventions, the patient was automatically discharged without improvement and subsequently passed away. Post-discharge, cultures from pleural and abdominal effusions identified Talaromyces marneffei. Conclusions: Talaromyces marneffei infection should be considered in the differential diagnosis of immunocompromised patients, particularly those with no history of liver disease but with long-term glucocorticoid or immunosuppressant use who present with acute liver failure. Early and aggressive investigation for the causative pathogen is essential to minimize diagnostic and treatment delays. Given the prolonged incubation period of Talaromyces marneffei, metagenomic next-generation sequencing may offer a more rapid approach for etiological diagnosis.

Abstract 4118070: High Output Heart Failure After Leadless Pacemaker Placement In a Heart Transplant Recipient

Introduction: The advent of leadless pacemaker (LP) technology has revolutionized cardiac rhythm management by minimizing risks associated with traditional transvenous pacemakers. LP use is expected to increase as dual-chamber LP systems emerge into clinical practice. The LP requires a large-bore venous sheath (27-Fr) through a femoral vein. One risk of large bore femoral cannulation is creation of an occult arteriovenous fistula (AVF), which can cause high output heart failure (HOHF) over time. In the LEADLESS II trial, the event rate for AVF was 0.2%. HOHF as a complication of LP implant has not been previously reported. We describe the first case of HOHF in a heart transplant (HT) recipient after LP. Case Presentation: An 82-year-old male with a history of HT 26 years earlier underwent leadless pacemaker for recurrent syncope, deemed associated with conduction system disease. He had no history of cardiac allograft rejection, angiographic coronary allograft vasculopathy or left ventricular dysfunction. Six months post-implant he presented with shortness of breath and bilateral lower extremity edema. Management: Evaluation included: 1) Chest X-ray which was suggestive of pulmonary edema 2) natriuretic peptide level of 5,500 pg/ml (6-fold increase from 6 months prior) 3) echocardiogram showing EF of 69%, and 4) bilateral lower extremity Doppler ultrasound where he was found to have a large AVF between the right superficial femoral artery and superficial femoral vein. Subsequent right heart catheterization was notable for a PCWP of 18 mmHg and a cardiac output/index of 11 L/min and 5.8 L/min/m2 respectively, hence confirming HOHF. Treatment with intravenous diuretic was initiated and percutaneous stent placement to correct the AVF was performed with symptomatic relief. Conclusion: This case highlights the rare but serious complication of unrecognized AVF following leadless pacemaker implant. Given that this event occurred in a HT recipient, a more exhaustive work-up was required to rule-out expected causes of congestion. To our knowledge there is only one other case report describing AVF post-LP implant for which no intervention was performed due to absence of symptoms at 6-month follow up and HOHF was not reported. Our case emphasizes that the differential diagnosis of new onset of signs and symptoms of heart failure that develop post LP implant in general and in HT recipients specifically, should include HOHF related to an unrecognized procedural AVF.

Abstract 4129839: Successful Left Atrial Appendage Occlusion (LAAO) with WATCHMAN FLX via Transhepatic Approach

Left atrial appendage occlusion (LAAO) with the WATCHMAN FLX (Boston Scientific) has been proven to reduce stroke risk in patients with paroxysmal atrial fibrillation (PAF). Certain circumstances may preclude LAAO1. In this case, transhepatic vein access was used to successfully deploy a WATCHMAN FLX in a 72 year old male with PAF not on anticoagulation due to recent subdural hemorrhage and recurrent bilateral lower extremity deep venous thrombosis (DVT) post IVC filter placement. Recent attempt at LAAO was unsuccessful due to total occlusion of bilateral femoral veins (Figure 1 A-B) and inability to cross the IVC. Access to the inferior branch of the right hepatic vein was achieved by micropuncture technique at the right mid-axillary line at the level of the 12th rib, which was confirmed by venogram (Figure 2A). The 4F microsheath was upsized to 16F. Intraoperative TEE was used for device sizing and delivery (Figure 3A). The transseptal sheath and dilator were positioned in the right atrium at the level of the fossa ovalis (Figure 3B) before successfully crossing into the left atrium (Figure 2B). After confirming placement (Figure 3C), a pigtail catheter was positioned within the LAA (Figure 3D) and an angiogram was performed (Figure 2C). A 24 mm WATCHMAN FLX was partially unsheathed and positioned (Figure 3E). Repeat LAA angiogram was performed through the WATCHMAN delivery sheath (Figure 2D). A Tug test was performed. The device was released (Figure 3F). Repeat venogram was performed to confirm location (Figure 2E) of the access site, and coil embolization closure of the venotomy access site was performed (Figure 2F). The patient was discharged the following day on dual antiplatelet (aspirin, clopidogrel) without complication. Venous access via right hepatic vein is a viable option for LAAO using the WATCHMAN FLX device.

Abstract 4121816: Viral Venture: A Case of Myocarditis and IgA Vasculitis from Adenovirus Infection

Case Description: A 19-year-old man presented to the emergency department for 3 days of shortness of breath, progressive bilateral lower extremity rash, generalized fatigue, and diffuse joint following an earlier visit to urgent care for pharyngitis symptoms. Physical exam was notable for tachycardia, pain with active wrist and ankle range of motion, pharyngeal erythema, cervical adenopathy, and confluent erythematous palpable purpura and petechiae noted on bilateral lower extremities with scattered lesions on his thighs, arms, and back. Laboratory workup notable for markedly elevated high-sensitivity troponin to 3398 ng/L, and elevated CRP. Further workup was notable for normal urinalysis, negative streptococcus antigen, negative ANCA antibodies, ANA, Hepatitis B and C, and cryoglobulins. Imaging and cardiac workup were notable for normal left ventricular function and cardiac MRI notable for late gadolinium enhancement in the anteroapical mid-myocardial region suggestive of myocarditis. Skin biopsy ultimately revealed immunodeposition of IgA on superficial capillaries compatible with a diagnosis of IgA vasculitis. The patient was started on steroids for IgA vasculitis with rapid improvement in his symptoms and he was discharged home in good condition. Discussion: Recognizing the severe complications of viral infection can lead to prompt treatment and prevention of progression to severe end organ damage. Our case highlights rarely reported cardiac involvement of IgA vasculitis secondary to adenovirus infection based on laboratory and imaging diagnosis with cardiac MRI. To date, only 16 cases of cardiac involvement in IgA vasculitis have been reported. This case adds to the limited body of published cases describing this presentation of IgA vasculitis and is also consistent with the results of prior cases suggesting that an immunosuppressive regimen including glucocorticoids may help to prevent disease progression and induce remission in cases with cardiac involvement without the need for endomyocardial biopsy.

Abstract 4136539: Management of Malignant SVC Syndrome and Acute SVC Thrombosis with Complex Endovascular Intervention

Superior vena cava (SVC) syndrome occurs when there is SVC occlusion or obstruction. SVC obstruction can cause an increase in venous return pressure up to 40 mm Hg, producing edema of the face, neck and chest wall. Blood flow can be diverted to the right atrium through collateral venous networks in cases of gradual SVC compression. The most common cause of SVC syndrome is malignancy, as seen in 70% of cases. Traditionally, treatment is with radiation therapy but advances have now allowed for an endovascular approach. We present a case of malignant SVC syndrome with a complex percutaneous treatment approach that provided palliation with near immediate symptom improvement. A 64 year-old-female with history of cerebrovascular accident on Eliquis, right upper lobe squamous cell carcinoma of the lung in remission, and a mediastinal nodule under surveillance presented with facial and bilateral upper extremity edema. CT revealed bilateral pulmonary embolism and a large SVC thrombus causing impaired venous return. Invasive angiogram confirmed a 95% thrombotic tubular stenosis for which she underwent aspiration thrombectomy with alpha VAC F-18, then angioplasty with an Armada (Abbott) 10 x 40 mm compliant balloon and stenting with the Express (Boston Scientific) 10 x 37 mm stent. There was 0% residual stenosis and immediate clinical improvement. Oncological workup confirmed the right mediastinal mass to be a recurrence of squamous cell carcinoma. SVC syndrome occurred due to mediastinal mass compression and a near occlusive SVC thrombus. Aspiration thrombectomy was effective in treating the SVC thrombosis and was performed alongside pulmonary embolism thrombectomy. The Armada balloon is intended for lesion dilation in the peripheral arteries, but was safely used here for venous dilation. The Express stent is intended for palliation of malignant biliary neoplasms but has versatility and was utilized here for malignant neoplasm surrounding the SVC. Peripheral endovascular stenting is an advantageous treatment option for malignant SVC syndrome given the challenges due to recurrence from mass effect. This provides additional support to maintain vessel patency and is a safe palliation option for improvement in quality of life.

Abstract 4124430: Calcinosis Cutis and Heart Failure---A Rare Manifestation Which Should Never Be Ignored!

Introduction: Heart failure can be a manifestation of underlying immune mediated myopathies like dermatomyositis/polymyositis which can present in broad range of clinical manifestations and sometimes dermatologic lesions can be the only manifestation of these underlying pathologies without typically involving the muscle weakness. Calcinosis cutis is the deposition of calcium salts in the skin and subcutaneous tissue. There are five subtypes of calcinosis cutis, dystrophic, metastatic, idiopathic, iatrogenic and calciphylaxis. Case summary: 70-year-old female was evaluated for bilateral lower extremity swelling. Past medical history was significant for Graves’ disease, atrial fibrillation, mechanical aortic valve on warfarin, hypertension, hyperlipidemia, ascending aortic aneurysm. Work up showed BNP of 4700 pg/ml with normal cardiac enzymes. Transthoracic echocardiogram revealed newly reduced ejection fraction of 25—30% with severely dilated left ventricle. Patient refused cardiac catheterization. Nuclear stress test showed no evidence of ischemia. Patient was started on guideline directed medical therapy and biventricular Implantable cardioverter defibrillator device was placed as per cardiology recommendation. Six months later patient developed multiple calcinosis cutis lesions on abdominal wall requiring surgical excisions. Endocrine work up including PTH, serum Ca level was normal, however creatin kinase level was high normal (150 U/L). Serum aldolase was ordered which was found to be elevated(25U/L). Muscle biopsy was performed as per recommendations of rheumatology which was diagnostic of dermatomyositis. Patient was started on high dose steroids and methotrexate and eventually IV immunoglobulins as per rheumatology recommendation. Follow up echocardiogram revealed improved ejection fraction to 40--45% with resolution of any further lesion of calcinosis cutis afterwards. Conclusion: Cardiac involvement such as congestive heart failure can be a part of presentation of underlying untreated myopathies. Calcinosis cutis can be the only clinical manifestation of dermatomyositis affecting heart. Etiology of calcinosis cutis in patients with heart failure should be worked up properly. Dystrophic calcinosis cutis is the subtype associated with underlying autoimmune connective tissue diseases.

Abstract 4112944: A diagnostic challenge overcome with persistent clinical suspicion in a case of cardiac AL amyloidosis

Case: A 62-year old male with a history of chronic kidney disease and paroxysmal atrial fibrillation presented with several months of fatigue, a progressive decline in functional status (NYHA IIIb-IV), weight loss, and intermittent lower extremity swelling. Blood pressure was 92/72 mmHg on presentation, and heart rate was 90 bpm. Physical examination revealed a jugular venous pressure of 12-14 cm H2O and 2+ bilateral lower extremity edema with mild wheezing. Methods/workup: Laboratories are shown in Table 1 and were notable for a serum free light chain ratio of 0.14. Transthoracic echocardiogram (figure 1) revealed a left ventricular (LV) ejection fraction of 33% with increased LV wall thickness and severe bi-atrial enlargement. Bone marrow biopsy revealed 2% lambda restricted plasma cells without evidence of amyloid deposits; metastatic bone survey was negative. A fat pad biopsy and endomyocardial biopsy stained negative for amyloid with Congo red. Cardiac MRI showed diffuse, circumferential subendocardial late gadolinium enhancement, most compatible with cardiac amyloidosis (figure 2). The patient also had a chest CT scan that demonstrated a few patchy nodular pulmonary infiltrates. Given his extensive negative workup, he was referred to pulmonary and endobronchial biopsy was positive for amyloid on Congo red staining (figure 3). Biopsy tissue typing revealed Lambda subtype AL amyloidosis. Management: The patient was started on Daratumumab, Cyclophosphamide, Bortezomib, and Dexamethasone by Hematology. Unfortunately, about a month after his diagnosis, he developed worsening heart failure despite treatment. He was admitted to an outside hospital with refractory cardiogenic shock and passed away during that admission. Discussion: The diagnosis of AL amyloidosis requires a high index of suspicion for prompt diagnosis and treatment. We present a case in which cardiac amyloidosis was suspected based on the patient’s clinical picture and cardiac imaging; however, multiple initial biopsies were negative. An expedited, multimodal and interdisciplinary diagnostic assessment is imperative as prognosis with chemotherapy is highly dependent on extent of AL disease, patient functional status, and presence of cardiac compromise. Elevated natriuretic peptides, troponins, autonomic dysfunction, and hypotension are negative prognostic features.

NCMP-28. CASE REPORT: REFRACTORY MYASTHENIA GRAVIS FLARE INDUCED BY IMMUNE CHECK POINT INHIBITOR

Abstract Immune checkpoint inhibitors (ICIs) are used for treating many types of cancers. Neurological adverse effects are uncommon (incidence of 7.2%), however these effects can have life-threatening outcomes when they occur. We present a case of a 78-year-old male with an existing diagnosis of Myasthenia Gravis (MG) with metastatic Basal Cell Carcinoma (BCC). He was diagnosed in 2015 with ocular myasthenia gravis that was acetylcholine receptor antibody positive. He developed an exacerbation with double vision, fatigue, and upper extremity weakness that resolved with intravenous immunoglobulin (IVIG). During this year, he also had a thymectomy and he was controlled on Mestinon. Five months after his MG diagnosis, he was diagnosed with BCC and was given Vismodegib, however he had metastasis to the spine and lymph nodes. Unfortunately, he had no other treatment options besides immunotherapy, thus Cemiplimab was given in 2023. Ten days after receiving his 2nd dose, he developed left eye ptosis, neck weakness, shortness of breath, dysphagia, bilateral lower extremity weakness, and urinary retention. Workup additionally revealed concern for myocarditis and myositis. He received IVIG and intravenous methylprednisolone initially, and then had maintenance IVIG 1g/kg every 2 weeks with a prednisone taper. Due to ongoing symptoms, he got Rituximab which improved most of the symptoms except for dysphagia. He then received Efgartigimod alfa-fcab (Vyvgart) but had no improvement in dysphagia. Later, plasmapheresis (PLEX) was trialed but there was a partial response. Unfortunately, he obtained a PEG tube for dysphagia and declined significantly due to disease progression and multiple medical comorbidities. Myasthenia Gravis crisis from ICI therapy is a rare but serious treatment complication. In addition to the challenging nature of treating this condition, our case highlights the importance of a comprehensive work up to include consideration of overlap syndromes, such as myocarditis and myositis as identified in this case.

Isolated peripheral neuroleukemiosis mimicking Guillain‐Barré syndrome in an adolescent with relapsed B‐lymphoblastic leukemia

AbstractBackgroundNeuroleukemiosis, leukemic infiltration of the peripheral nervous system (PNS), is rare. Very few cases of isolated neuroleukemiosis, PNS leukemic infiltration without leukemia blasts in the blood or bone marrow, have been reported in pediatrics. Most cases have occurred in adults with acute myelogenous leukemia (AML) in remission who presented with peripheral neuropathy. We describe a pediatric patient presenting with isolated neuroleukemiosis mimicking Guillain‐Barré syndrome.Patient descriptionA 15‐year‐old boy presented 1 month after IVIG treatment for Guillain‐Barre syndrome with worsening ataxia and weakness. He had a past medical history of B‐cell acute lymphoblastic leukemia (B‐ALL) in remission for 8 years. Examination revealed distal greater than proximal weakness of the bilateral lower extremities, areflexia at the Achilles tendon, and 1+ patellar and upper extremity reflexes. Initial magnetic resonance imaging (MRI) of the brain and spine were normal, and lumbar puncture revealed increased protein with uninterpretable white count due to excessive red blood cells. Repeat MRI brain and spinal cord showed extensive enlargement of all nerve roots and enhancement of the cauda equina and portions of cranial nerve VII bilaterally. Repeat lumbar puncture with cytology revealed leukemic blast cells. Blasts were not detected in peripheral blood smear or by flow cytometry. Bone marrow biopsy was also free of blast cells, confirming the diagnosis of relapsed B‐ALL restricted to the nervous system.ConclusionsNeuroleukemiosis is a rare entity with typical clinical features of mono‐ or polyneuropathy. It most often occurs in adults in remission from AML. However, neuroleukemiosis should also be on the differential for pediatric patients in remission from ALL presenting with neuropathy.

The occurrence of remitting seronegative symmetrical synovitis with pitting edema (RS3PE) after arthroplasty mimicking a periprosthetic joint infection: A case report and literature review.

As the elderly population grows, the number of joint arthroplasty surgeries is also increasing. Periprosthetic joint infection (PJI) is a postoperative complication that occurs in 1%-2% of the arthroplasties. Once it occurs, PJI is refractory to treatment. Similar symptoms of PJI, including joint synovitis and elevated body temperature, sometimes arise because of crystal arthritis, rheumatoid arthritis, or other inflammatory diseases. Precise diagnosis is essential for determining the optimal treatment strategy. An 81-year-old female patient with a history of bilateral knee arthroplasty presented with a high fever of 38 °C and was unable to walk due to swelling and pain in the bilateral lower extremities. Infectious conditions, such as cellulitis or PJI, were suspected. Imaging findings revealed bilateral knee joint synovitis with pitting edema around the lower extremities, and cultures of bilateral joint fluids were negative. No crystals were observed in the joint fluid. Laboratory data revealed highly elevated levels of inflammatory marker; however, antinuclear antibodies, including rheumatoid factor and cyclic citrullinated peptide, were not detected. Based on bilateral synovitis with pitting edema in the lower extremities, in addition to negative culture findings and normal antinuclear antibodies, the diagnosis of remitting seronegative symmetrical synovitis with pitting edema (RS3PE) was made. Steroid therapy was performed. The dose was gradually reduced, with the improvement of the symptoms. The inflammatory reaction promptly decreased and then normalized. With improved inflammation, the symptoms of pitting edema, pain in the bilateral lower extremities, and fluid effusion of the knee joints were reduced. She was able to walk without a cane, and her activities of daily living fully recovered. High fever and synovitis after joint arthroplasty do not necessarily indicate an infectious condition. Clinicians should be familiar with the occurrence of RS3PE, regardless of whether arthroplasty is performed.

Unilateral Biportal Endoscopic Decompression for Thoracic Spinal Stenosis Secondary to Ossification of the Ligamentum Flavum

Ossification of the ligamentum flavum (OLF) in the thoracic spine is a cause of thoracic myelopathy that is more commonly found in East Asian populations (Koreans, Japanese, Chinese) than in others. Early diagnosis and sufficient surgical decompression can improve the functional prognosis for thoracic OLF. Surgical decompression is necessary and should be done as soon as the symptoms develop. There is a wide range of possible treatments, from standard open laminectomy to endoscopic decompression surgery. This video demonstrates the least invasive technique of decompressive laminectomy with bilateral decompression and removal of thoracic OLF through unilateral biportal endoscopic spinal surgery. The authors present the case of an 81-year-old male patient who presented with bilateral lower extremity weakness, numbness, pain, and ataxia. Magnetic resonance imaging and computed tomography scans of the whole spine showed the presence of OLF with severe spinal canal stenosis and a cord signal change at the T9–10 level. He underwent biportal endoscopic decompression and removal of thoracic OLF at T9–10. On the discharge day (postoperative day 7), motor power and pain had significantly improved. He could stand and independently ambulate with a walker.

Atypical Milroy's disease with predominant unilateral involvement: a case report

Milroy's disease (MD), known as hereditary lymphedema type I, is a rare autosomal dominant primary lymphedema. It accounts for about twenty percent of all primary lymphedema. MD typically presents clinically with bilateral lower extremity lymphedema. Our case report describes a rare case of MD presenting with unilateral upper and lower extremity lymphedema in a patient admitted to our clinic. A 24-year-old woman who had been followed for lymphedema since the age of 8 was diagnosed with MD at our hospital by physical examination, venous Doppler ultrasound, whole-body lymphoscintigraphy, and molecular genetic testing. Partial improvement was observed with complete decongestive therapy, considered the gold standard treatment for lymphedema. Genetic counseling may be beneficial for the patient and family. Although MD is uncommon in the literature, many more studies are needed to identify carrier variants in the community.

Cervical Myeloradiculopathy With Bilateral Foraminal Stenosis Treated by Unilateral Biportal Endoscopic Decompression with Alternating Hemilaminectomy and Bilateral foraminotomy: A Case Report and Technical Note

Cervical myeloradiculopathy is a debilitating condition characterized by progressive spinal cord dysfunction commonly caused by degenerative changes in the cervical spine. It typically exhibits an insidious onset and progressive functional decline, along with multiple exiting nerve root entrapments bilaterally in some patients. Traditional surgical interventions, such as discectomy and fusion, are associated with some complications and limitations. Unilateral biportal endoscopic (UBE) decompression can have significant advantages over traditional techniques when cervical central and bilateral foraminal decompression is required. In this case report and technical note, we describe our experience with this novel surgical technique for the treatment of cervical myelopathy. A 67-year-old patient presented with progressive neck pain; bilateral upper extremity radiculopathy; loss of power and sensation in the C5, C6, and C7 nerve root distribution; gait imbalance, and spasticity. Magnetic resonance imaging revealed multilevel cervical spondylosis with central canal and bilateral foraminal stenosis. The patient underwent UBE central and bilateral foraminal decompression. At a 9-month follow-up visit, he was able to walk unassisted, his reflexes had returned to normal, no spasticity was observed, and he had good grip strength in both hands. This is a novel technique of UBE decompression with bilateral foraminotomy at the C4–5, C5–6, and C6–7 levels and laminectomy named “the floating tip technique.” The procedure involved bilateral 3-level lamino-foraminotomy and hemilaminotomy on both C5 and C6. A hemilamina was removed on the opposite sides, and flavectomy was performed. Postoperative computed tomography findings showed an intact, complete muscular mass with an intact central spinous process. Therefore, this method was labelled the “floating tip technique.”

Thoracic aortic coarctation with asbestos-induced pleural fibrosis presenting as lower limb claudication

Asbestos exposure is a well-documented cause of pulmonary diseases. However, its systemic effects, particularly on the cardiovascular system, are less understood. We expose a case that highlights an unusual cardiovascular manifestation in a patient with a history of pleural asbestosis compressing the aorta and clinically manifested as lower limb claudication. A 65-year-old individual presented with bilateral short-distance lower extremity claudication. The patient’s clinical presentation prompted advanced imaging studies, including CT angiography, to assess the extent of vascular involvement. The imaging confirmed the presence of substantial calcification and narrowing of the thoracic aorta. The patient had a documented history of pleural asbestosis. This case underscores the potential for asbestos-related diseases to extend beyond pulmonary manifestations, affecting cardiovascular health. The observed aortic calcification and coarctation represent an atypical progression of asbestosis related pathology.

Development of the scoliosis research society spinal deformity surgery safety checklist.

Spine deformity surgery is a complex multi-step procedure that has a relatively high complication rate. The use of surgical safety checklists has been shown to reduce perioperative adverse events, but existing lists are varied and non-specific for spinal deformity surgery. Thus, the purpose of this study was to develop a comprehensive surgical checklist for complex spinal corrective surgery. An electronic survey consisting of 187 surgical checklist items that had been developed and used by a group of SRS members over a 5-year period was distributed to the Scoliosis Research Society Safety and Value Committee membership. The survey sections included: (1) pre-operative area, (2) initial operating room visit, (3) before turning, (4) positioning, (5) prepare and drape, (6) pre-incision timeout, (7) intraoperative, (8) finishing implant placement and confirming imaging, (9) final rods and locking, (10) prior to closure, (11) closure, (12) turn to supine, and (13) checkout/debriefing. Respondents graded each item on a five-point Likert scale based on their perceived importance and feasibility for inclusion in the checklist. Features graded as "moderately important" or "very important" to include by at least 70% of respondents were considered to meet the cutoff for inclusion-based standard Delphi practices. Study data were collated using REDCap. A total of 25 surgeons completed the survey in its entirety. The overall checklist "package" was shortened to 9 individual checklist modules, with 2 to 16 items per checklist. In terms of individual checklist items, 40% of items (74 of 187) met the cutoff for inclusion; 17 of these items were graded as "very important," which included verifying the presence of implantable devices, reviewing the surgical plan and positioning with the surgical staff, securing the endotracheal tube, bite block confirmation, prone and lateral positioning, neuromonitoring baseline readings, double-checking that the implant screw caps were locked prior to closure, and confirming that the patient was moving bilateral lower extremities before leaving the operating room when possible. This study has led to the development of a specific spinal deformity surgical checklist of 74 (many specific to spine surgery) items that were considered important for inclusion; 17 were considered "very important".

Effects Of Bilateral Upper Extremity Exercises Training On Trunk Performance, Posture And Gait In Patients With Subacute Stroke-A Quasi Experimental Study

Background and objective: Stroke is one of the neurological disorders which is caused by disturbance in blood supply to the brain resulting in weakness in contralateral limbs and axial musculature. Stroke is the leading cause of physical impairment where the most prominent motor deficit is paresis of one side of body, which is contralateral to the event. This study was conducted with an aim to assess the effectiveness of bilateral upper extremity training on trunk performance, posture and gait in patients with subacute stroke. Method: 30 subjects with subacute stroke were selected for the study. Subjects were treated for 3 days/week for 12 sessions with 45 minutes of task oriented, strengthening training and PNF technique for bilateral upper extremity along with conventional training. The rehabilitation protocol consists of bilateral functional exercises, activity of daily living goal, exercises in multiple movement games, strengthening exercises for lower limb, controlled sitting training, sit to stand training, weight bearing and balance training Conclusion: Significant improvement in all items of TIS, PASS and DGI were observed after intervention (P< 0.001). The study concluded that bilateral upper extremity training is more effective in improving trunk control, posture and gait in subacute stroke patients.

Establishing an upper extremity transplantation program: lessons learnt over 12 years.

As one of the early hand transplant programs in the world, we are often asked to educate other programs on the lessons we have learned and on how to set up a successful hand transplantation program. Two decades of global experience with vascularized composite allotransplantation (VCA) of the upper limb have demonstrated improved functional outcomes and quality of life for carefully screened patients. Despite initial reticence about VCA, over 30 patients in the USA have benefited from hand transplantation, with around 80% long-term successes. We have experience with four bilateral upper extremity patients who have undergone bilateral upper extremity allotransplants. This review article highlights our personal experience and lessons with respect to VCA team assembly, logistics, patient selection, perioperative planning, the operative procedure, and postoperative management. Continual learning and critical evaluation are crucial to maintaining a successful upper extremity VCA program. This will ensure that patients who stand to benefit most from this life-enhancing procedure are identified and are others optimized to achieve the best possible outcomes.

8269 Euglycemic Diabetic Ketoacidosis Secondary to Rapid Weight Loss in a Patient on Dapagliflozin

Abstract Disclosure: A. Sridhar: None. A. Iqbal: None. A. Prabha Kumar: None. F. Haider: None. M. Babic: None. Background: Euglycemic DKA (eDKA) is a potentially life-threatening complication in patients taking SGLT 2 inhibitors (SGLT2i). Common precipitating factors include strenuous exercise, carbohydrate restriction, starvation, and alcohol use. Clinical case: The patient is a 71-year-old female with past medical history of Type 2 diabetes mellitus (DM), gastro-esophageal reflux disease, hypertension, hyperlipidemia, coronary artery disease and chronic pain syndrome. She presented with complaints of nausea, vomiting, reduced appetite and generalized weakness for the past 4 days. She also reported an intentional weight loss of 35 pounds in the last 6 weeks achieved with daily exercise and a carbohydrate restricted diet. She had been taking Dapagliflozin-Metformin 5-1000 mg twice daily and pioglitazone 30 mg once daily for 2 years and Ozempic subcutaneous injection 1 mg weekly for 6 months. Physical examination in the ED showed normal vital signs, dry mucous membranes, and trace bilateral lower extremity edema. Blood work was significant for venous blood gas pH 7.24, bicarbonate 9 mmol/L, anion gap 30 mmol/L, blood glucose 94 mg/dL, HbA1c 5.8 % and WBC 13.2 K/uL. Urinalysis was positive for glucose and ketones. The patient was admitted for management of eDKA and was started on intravenous 10% dextrose infusion and insulin infusion. Endocrinology was consulted and they recommended following DKA protocol and stopping Dapagliflozin at discharge. She was maintained on insulin infusion for 48 hours after which her anion gap normalized, and she was transitioned to subcutaneous insulin with Lantus 8 units and sliding scale insulin. During this time the patient’s symptoms resolved, and she was able to tolerate oral diet. She eventually resumed her home medications with oral Metformin 1000 mg twice daily and pioglitazone 30 mg once daily. Dapagliflozin and Ozempic were discontinued at discharge. Strenuous exercise and carbohydrate restriction which caused rapid weight loss, were likely the triggers for eDKA in our patient. A diabetes educator was involved at discharge and the patient was counseled to avoid possible triggers and identify warning signs and symptoms in the future. The patient was discharged with a follow up appointment with her Endocrinologist. Conclusion: High index of clinical suspicion is important to promptly diagnose eDKA in patients taking SGLT2i. Patient education on avoiding precipitating factors and early recognition of signs and symptoms is necessary to reduce mortality. Presentation: 6/3/2024

7148 Fake Fingerstick: Artifactual Hypoglycemia in a Hospitalized patient with Systemic Sclerosis

Abstract Disclosure: S. Shteyman: None. F. Mirza: None. Introduction: Artifactual hypoglycemia is a problem in hospitalized patients. It often leads to unnecessary use of resources and creates anxiety for the patient and medical team. We describe a case of a 60-year-old female with history of systemic sclerosis (Raynaud, telangiectasias, esophageal dysmotility, interstitial lung disease, pulmonary hypertension), rheumatoid arthritis, autoimmune hepatitis and hypothyroidism who initially presented to the hospital emergency department with bilateral lower extremity radiculopathy, and new onset urine incontinence. She underwent spine surgery initially, followed by emergent left upper extremity thrombectomy two days later. Postoperatively, she was noted to have fingerstick glucose of 34 mg/dL. Dextrose and juice were given, and endocrinology service was consulted. The patient was monitored with 2 hourly fingerstick glucose and was noted to have frequent hypoglycemia on fingerstick monitoring. Serum glucose in AM labs was consistently within normal limits. Patient denied both adrenergic and neuroglycopenic symptoms during periods of “hypoglycemia”. She was asked to fast till fingerstick glucose was noted to be at 43 mg/dl, when blood was drawn for serum glucose, insulin, proinsulin, C-peptide, B-hydroxybutyric acid, IGF-2, insulin AB, and sulfonylurea panel, prior to giving her any dextrose. She was asymptomatic at the time. All labs were within normal limits, with serum glucose at 119 mg/dL. At that point, artifactual hypoglycemia was suspected. Serum glucose was checked twice again when fingerstick glucose was noted to be <45mg/dL, and corresponding serum glucose was noted to be normal at both times (>100 mg/dL). Decision of artifactual hypoglycemia was made and fingerstick glucose monitoring was discontinued in this non-diabetic patient, with recommendation to check serum glucose only if symptoms of hypoglycemia occur, as fingerstick glucose values were not reliable. Fasting serum glucose continued to be normal for the remainder of the hospitalization. Discussion: There have been a handful cases of artifactual hypoglycemia reported in patients with CREST, systemic sclerosis, and Raynaud’s disease. It is thought to be due to abnormal small vasculature causing delayed transit of blood through capillaries, and increased uptake of glucose into the interstitial tissue. Some recommend using earlobe sticks as a replacement for fingerstick glucose monitoring in these patients. Future research can explore if continuous glucose monitoring can be used reliably in these patients. Presentation: 6/1/2024

7743 A Case Study of Ectopic Adrenocorticotropic Hormone Secretion from Pancreatic Neuroendocrine Tumor

Abstract Disclosure: K.S. Wei: None. J. Huang: None. Introduction: Pancreatic neuroendocrine tumors (PanNETs) are uncommon cancers that account for less than 2% of pancreatic malignancies. Even rarer are ACTH-producing NETs which may only become symptomatic until after metastasis. This case study examines the distinct presentation and diagnostic complexities associated with ectopic adrenocorticotropic hormone (ACTH) secretion from a PanNET. Clinical Case:A 42 year-old male with hypertension and type 2 diabetes initially presented to the hospital with increased abdominal girth for one month, bilateral lower extremity edema for two weeks, and generalized abdominal pain. He had unremarkable surgical, family, and social histories. Patient was afebrile, normotensive, saturating well on room air, with exam notable for a distended abdomen and 2+ bilateral pitting edema. Admission labs were notable for potassium of 2.4 (ref: 3.5-5.1 mmol/L). MRI abdomen showed hepatomegaly with numerous heterogeneously enhancing masses and an ill-defined pancreatic tail mass with involvement of the spleen. Liver biopsy showed well-differentiated neuroendocrine tumor, grade 2. He was started on octreotide 20mg q4weeks and capecitabine/temozolomide q4weeks. Two months later, the patient was readmitted after presenting with back pain for two days, found to have acute compression fractures of T9-L1 without spinal PET activity. At follow-up visit with endocrinology, he endorsed easy bruising and muscle weakness and had hypertension (161/96 mmHg) with hypokalemia. Random cortisol was 43.7 (ref: 2.5-11.9 mcg/dL). ACTH was 124 (ref: 6-50 pg/mL) despite receiving chemotherapy. 24-hour urine cortisol was 3,049 (ref: 4-50 mcg/24 hrs). He was diagnosed with ectopic Cushing’s disease from ACTH-producing PanNET leading to osteoporosis and fracture of the vertebral bodies. For the ectopic Cushing’s disease, he was started on ketoconazole 200mg BID with plan to start osilodrostat once approved. For the fracture, he is scheduled for Zometa infusion and IR kyphoplasty. Conclusion: This case offers several important clinical insights. In patients with PanNET with Cushingoid exam findings, ACTH-producing PanNET should be high on the differential. Most ACTH NETs are aggressive often with liver metastases, whereby metastatic disease will have already occurred by the time the Cushingoid features develop. The initial severe hypokalemia and hypertension should have prompted investigation for mineralocorticoid excess from hypercortisolism, which may have led to an earlier diagnosis of ectopic ACTH Cushing’s disease, thereby decreasing the possibility of developing vertebral fractures, uncontrolled diabetes and hypertension. Ketoconazole or osilodrostat may be used to treat Cushing’s disease from ACTH NETs. Presentation: 6/1/2024