data/new_exp/few_shot_examples.json

{
    "intermediate_health_literacy": [
        {
            "doc_id": 9,
            "label": "intermediate_health_literacy",
            "gen_text": "A 69-year-old man with prior coronary bypass surgery presented with two months of severe shortness of breath with mild activity (NYHA class III). He was diagnosed with heart failure due to ischemia after failure of a saphenous vein graft to the right coronary artery. This was supported by an abnormal ECG, elevated NT-proBNP, and a coronary angiogram; echocardiography also showed reduced pumping function. The team reopened a chronic total occlusion in the native right coronary artery using a retrograde approach through septal channels (septal surfing). To enable that route, they first re-opened the totally occluded left coronary artery. After the procedure, his dyspnea improved before discharge, and at 6 months he had no recurrence of shortness of breath.",
            "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 \u00d7 15\u200amm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 \u00d7 15\u200amm balloon and stented with 2 overlapping drug-eluting stents (2.5 \u00d7 38\u200amm and 3.0 \u00d7 38\u200amm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
            "gs_summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
            "metadata": "Cardiology | Technical"
        },
        {
            "doc_id": 13,
            "label": "intermediate_health_literacy",
            "gen_text": "A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.\n\nUrgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.\n\nShe started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.",
            "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
            "gs_summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n",
            "metadata": "Cardiology | Technical"
        },
        {
            "doc_id": 19,
            "label": "intermediate_health_literacy",
            "gen_text": "A 23-year-old man came to the emergency department with a sudden severe headache, nausea, vomiting, and chest heaviness. His initial vital signs showed high blood pressure and a fast breathing rate. An emergency ECG showed a heart attack pattern (STEMI), so he was urgently sent for percutaneous coronary intervention; the angiogram revealed normal coronary arteries. Further evaluation with a brain CT identified a cisternal subarachnoid hemorrhage (bleeding around the brain). Despite coordinated care by multiple teams, his condition rapidly worsened, leading to cardiac arrest and death.",
            "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9\u00b0C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
            "gs_summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality.",
            "metadata": "Cardiology | Technical"
        },
        {
            "doc_id": 15,
            "label": "intermediate_health_literacy",
            "gen_text": "A 62-year-old white North African woman with Von Hippel\u2013Lindau (VHL) disease diagnosed in 2021 developed several VHL-related tumors: a left petrous bone tumor, a left pheochromocytoma, left renal cell carcinoma, a multicystic right kidney, and pancreatic masses. She was treated with radiotherapy to the petrous bone lesion, left adrenalectomy, left nephrectomy, and cephalic duodenopancreatectomy for the pancreatic tumors. During surveillance, ultrasound and MRI showed a solid\u2013cystic mass in the left adnexal (ovary/tube) region. Laparoscopy then identified cystic tumors in the mesosalpinx on both the right and left sides. She underwent hysterectomy with removal of both adnexa. Pathology confirmed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, a pattern consistent with VHL.",
            "fulltext": "A 62-year-old Tunisian Arab postmenopausal female diagnosed with Von Hippel\u2013Lindau disease in 2021 presented with various manifestations related to the disease. She had a history of multiple surgeries, primarily for renal, adrenal, and pancreatic tumors, with incidental findings of ovarian masses.\n\nThe patient was asymptomatic from a gynecological standpoint, but primarily complained of headaches before undergoing brain surgery. She had no significant family or psychosocial history.\n\nHer surgical history included\n2021: A non-operable tumor (6 cm) of the left petrous bone endolymphatic sac, managed with radiotherapy.\n\n2021: Left adrenalectomy for a 6 cm pheochromocytoma. Pathological examination revealed pheochromocytoma.\n\n2021: Left nephrectomy for a ruptured left renal tumor. Microscopy showed multifocal clear-cell renal carcinoma of nuclear grade 2.\n\n2022: Cephalic duodenopancreatectomy for a mass in the pancreas. Histological examination confirmed three serous cystadenomas and two well-differentiated neuroendocrine tumors.\n\nIn January 2021, during postoperative surveillance with an abdominal\u2013pelvic computed tomography (CT) scan, a 4 cm solid cystic left adnexal mass was incidentally discovered, which raised suspicion of malignancy. The mass was confirmed by transvaginal ultrasound and pelvic MRI, classified as Ovarian-Adnexal Reporting and Data System (O-RADS) 5 (high suspicion for malignancy).\n\nGynecological examination and surgical history\nPhysical examination: No abdominal\u2013pelvic mass detected.\n\nSpeculum examination: Healthy cervix observed.\n\nSurgical scars from previous left nephrectomy and cephalic duodenopancreatectomy were noted.\n\nA multidisciplinary staff meeting concluded that surgery was necessary. A laparotomy was performed via a midline incision below the umbilicus, revealing a well-defined solid cystic mass in the left adnexa. No ascites or signs of peritoneal carcinomatosis were present, and the right adnexa appeared normal, with no macroscopic signs of malignancy observed intraoperatively, including the absence of exocystic vegetations.\n\nCytology was performed along with left adnexectomy, and the specimen was sent for frozen section examination. The results were inconclusive, raising the possibility of borderline tumors or tumors specific to Von Hippel\u2013Lindau syndrome. Considering the patient\u2019s postmenopausal status, a right adnexectomy and total hysterectomy were performed.\n\nHistological examination later revealed bilateral clear-cell papillary cystadenomas of the Fallopian Tubes and broad ligament, characteristic of Von Hippel\u2013Lindau disease (0.5 cm on the right side and 4 cm on the left side).The tumors consisted of tightly packed papillae with fibrous cores, covered by monolayered epithelium.\n\nThe immediate postoperative period was uneventful, and at the 1-month follow-up, no abnormalities were detected. The patient has since been followed up with every 4 months with normal pelvic ultrasounds. During these 2 years of follow-up, no complications have arisen, but the patient was recently readmitted to the neurosurgery department for recurrence of a brain tumor.",
            "gs_summary": "A 62-year-old white North African woman diagnosed with Von Hippel-Lindau disease in 2021 presented with multiple manifestations, including a left petrous bone tumor, left pheochromocytoma, left renal cell carcinoma, multi-cystic right kidney, and pancreatic masses. She underwent various treatments, including radiotherapy, adrenalectomy, nephrectomy, and cephalic duodenopancreatectomy. Ultrasonographic and magnetic resonance imaging examinations revealed a solid cystic mass in the left adnexal region. Laparoscopy identified cystic tumors in the right and left mesosalpinx. Following a hysterectomy with bilateral adnexectomy, histological examination revealed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, consistent with Von Hippel-Lindau disease.",
            "metadata": "Gynecology | Technical"
        },
        {
            "doc_id": 0,
            "label": "intermediate_health_literacy",
            "gen_text": "A 20\u2011year\u2011old woman had a 12\u2011year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid\u2011sparing agent. A comprehensive thrombophilia work\u2011up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small\u2011bowel necrosis not compatible with survival. She died 48 hours later.",
            "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/\u00b5L. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
            "gs_summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours.",
            "metadata": "Nephrology | Technical"
        }
    ],
    "low_health_literacy": [
        {
            "doc_id": 11,
            "label": "low_health_literacy",
            "gen_text": "A 78-year-old man from the Amhara region of Ethiopia had a permanent heart pacemaker because of a complete heart block. He was scheduled for prostate surgery. Before surgery, the anesthesia and heart doctors advised switching his pacemaker to a steady, fixed beat to lower the chance of problems. He could not afford that change. He chose to go ahead with the operation. He signed consent for the plan. After surgery, he also gave permission to share his case. For anesthesia, he got a numbing injection in the lower back (a combined spinal\u2013epidural). The team used 2.5 ml of strong numbing medicine (0.5% bupivacaine) and a tiny dose of fentanyl (50 micrograms). Standard monitors were used, and his heart was watched closely. His vital signs stayed steady, with only small changes. His blood pressure stayed good with IV salt water. After surgery, he went to the recovery room. He got pain medicine after 4 hours and an extra dose through the epidural. Six hours after surgery, he moved to the ward in stable condition. The epidural pain control continued for 72 hours. He went home in stable condition about 88 hours after surgery.",
            "fulltext": "An elderly 78-year-old patient from the Amhara region of Ethiopia, who has had a permanent cardiac pacemaker for 7 years, was scheduled for retropubic prostatectomy due to benign prostatic hyperplasia (BPH). This condition developed following a previous transurethral resection of the prostate 3 months earlier. The patient in the preoperative anesthesia evaluation was fully evaluated, and all the routine investigations required for the proposed surgery, which were within normal limits, were investigated. The patient presented with a history of frequency, urgency, nocturia, and dribbling for the past 2 months. Additionally, the patient had been known to have hypertension for the past 16 years and was taking amlodipine 5 mg orally daily, enalapril 10 mg orally twice daily (BID), and atorvastatin 10 mg orally daily. He had also been known to have type II diabetes mellitus for the past 25 years and was on metformin 500 mg orally BID and neutral protamine Hagedorn (NPH) 20 IU and 10 IU. He was admitted to a hospital for further evaluation, and complete bundle branch block (BBB) was detected via electrocardiogram (ECG). In an electrophysiology study, the patient was diagnosed with left ventricular hypertrophy secondary to hypertensive heart disease, mild diastolic dysfunction, and an ejection fraction of 62%. Abdominal ultrasound revealed an enlarged prostate size of 82 ml; anterior\u2013posterior (AP) chest X-ray revealed a normal chest region with a left-side pacemaker in situ, and all the other blood parameters, including electrolytes and serum troponin levels, were within normal limits.\n\nA cardiologist was involved preoperatively as a multidisciplinary approach and risk determination tool for cardiac risk assessment. The patient had a frailty score of 5.5 with a poor functional cardiopulmonary reserve of metabolic equivalent (MET)\u2009=\u20093.4 and Revised Cardiac Risk Index (RCRI) class III, which accounts for 10.1% of major cardiac adverse events (myocardial infarction [MI], cardiac arrest, or death) within 30 days of the postoperative period, and intermediate risk on the basis of surgery type and patient risk factors. After preoperative evaluation and risk disclosure regarding the un-reprogrammed pacemaker and the associated complications during anesthesia and surgery, the patient was unable to afford the necessary health coverage for pacemaker reprogramming. This is because the cardiac surgery was performed in Addis Ababa, Ethiopia, which has a long waiting list with few cardiac surgeons for millions of people and is a considerable distance from the patient\u2019s home institution, and there is a period of monitoring after pacemaker reprogramming for considerable post-reprogramming complication. As a result, the patient chose to proceed with the surgery, accepting the potential risks and harm associated with the situation. Continuous cardiac monitoring during the intraoperative period is highly advocated. Despite these factors, the patient did not experience cardiorespiratory failure, and he was stable. The patient continued on medication until the day of surgery, which included amlodipine, enalapril, atorvastatin, and a morning lower dose of two-thirds of the NPH. He also took 5 mg of diazepam orally for anxiolytics at midnight before the day of surgery.\n\nOn the day of surgery, the patient\u2019s random blood sugar (RBS) was measured, and sliding scale glycemic control was implemented. Communication among the anesthetist, surgeon, and nurses was emphasized, ensuring that the cautery pad was placed away from the pacemaker, and that emergency drugs and a defibrillator were ready. The patient was premedicated with dexamethasone for nausea prophylaxis and paracetamol for pain relief as preemptive analgesia. American Society of Anesthesiology (ASA) standard monitoring was applied, and baseline parameters were recorded. Combined epidural\u2013spinal anesthesia was administered via 0.5% isobaric bupivacaine (12.5 mg) and 50 \u00b5g fentanyl at the L3\u2013L4 interspace. The block achieved anesthesia up to the umbilicus, and the sensory block was performed at T7. The surgery involved a midline incision below the umbilicus, with monopolar cautery used at low voltage (20 mA). Hemostasis was achieved through bipolar low-voltage cautery. Throughout the procedure, the patient\u2019s vital signs remained stable. The patient\u2019s vital signs did not change by more than 10% from the baseline vital signs. The intravenous fluid was resuscitated intraoperatively. During the postoperative period, the patient was transferred to the postanesthesia care unit (PACU) with vigilant monitoring, and 10 ml of 0.125% epidural top-up analgesia was given. Postop investigations were within normal limits. The patient was observed in the PACU for 12 hours and later transferred to the ward in stable condition with regular follow-up with the cardiology team. After 88th day of postsurgery the patient was discharged and advised to have regular checkups for pacemaker\u2019s in situ status.",
            "gs_summary": "A 78-year-old male from the Amhara region, Ethiopia, with a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy. Preoperative assessments by the anesthetist and cardiologist recommended reprogramming the pacemaker to asynchronous mode to reduce risks related to its dual-chamber, rate-modulated mode setting. However, the patient could not afford reprogramming and opted to proceed with the existing perioperative plan. Informed consent was obtained, and case report publication permission was obtained after operation. The patient received combined epidural-spinal anesthesia with 2.50 ml of 0.5% isobaric bupivacaine and 50 \u00b5g fentanyl at the L3-L4 interspace. Standard American Society of Anesthesiology monitoring was applied, with a focus on cardiac stability. The patient remained stable with minimal vital sign fluctuations and maintained adequate blood pressure using isotonic saline. Postoperatively, the patient was transferred to the postanesthesia care unit, receiving analgesia after 4 hours and an epidural top-up. After 6 hours, he was transferred to the ward in stable condition. Epidural analgesia was continued for 72 hours, and the patient was discharged on the 88th postoperative hour in stable condition.",
            "metadata": "Anesthesia | Technical"
        },
        {
            "doc_id": 14,
            "label": "low_health_literacy",
            "gen_text": "A 36-year-old woman had trouble swallowing. Tests found she was born with an unusual shape of the main body artery in her chest. The artery curves to the right in a mirror-image pattern. It wraps around a main branch of the airway. The side branches of the artery come off in the reverse order from normal. Most people with this have no symptoms. Problems happen only if the artery squeezes the space in the middle of the chest. This can press on the food pipe or the windpipe. Surgery may be needed if there is strong pressure on these tubes, a bulge or a tear in the chest artery, or a pouch on the artery bigger than 2 cm. There is no one-size-fits-all treatment. Care is tailored to the person\u2019s symptoms and body anatomy. This patient did not receive any treatment.",
            "fulltext": "A 36-year-old female patient complained of dysphagia with longstanding cervical and upper thoracic pain. She also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit was performed. It showed a posterior and lateral right impression of the proximal esophagus after ingestion of baryte, extending 3.5 cm cephalocaudal. A maximum esophageal stenosis of 60% was estimated. A cervical and thoracic CT scan revealed a congenital anomaly of the aortic arch: a mirror image of the right aortic arch. The aortic arch originates from the root of the aorta and runs above the right stem bronchus, giving rise to the three supra-aortic trunks as follows: the first is the left brachiocephalic artery (which gives rise to the left common carotid artery and the left subclavian artery); the second is the right common carotid artery; and the third is the right subclavian artery. The aortic arch then enters posteriorly to the esophagus and gives rise to a small anterior saccule of 1.3 cm, known as the Kommerell diverticulum. This configuration forms a ring around the tracheo-esophageal pair, whose edges are formed posterior-lateral to the right by the aortic arch, posterior-lateral to the left by the Kommerell diverticulum, lateral to the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. A gastroscopy confirmed the endoluminal impact of extrinsic compression. In view of minimal clinical repercussions and the absence of nutritional disorders, no surgical cure was ultimately performed. The evolution was favorable with, according to the patient, a spontaneous amelioration of symptoms.\n",
            "gs_summary": "We report the case of a 36-year-old female patient whose dysphagia presented a congenital anomaly of the thoracic aorta: the right aortic arch with mirror image. This is a rare anomaly of embryonic development where the aorta winds around the right stem bronchus and the supra-aortic trunks emerge from the crown in the reverse and opposite order to normal. The vast majority of patients are asymptomatic unless there is a compression of the mediastinal structures. Major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection or the presence of a Kommerell diverticulum of more than 2 cm may warrant surgical intervention. There is no standard treatment and it must be adapted to the clinical presentation and anatomical configuration of the patient. Our patient did not receive any treatment for her condition.\n",
            "metadata": "Cardiology | Technical"
        },
        {
            "doc_id": 0,
            "label": "low_health_literacy",
            "gen_text": "This is about a 20-year-old woman. She had a kidney problem since age eight that made protein leak into her urine. The problem first showed up when a big blood clot blocked veins in her brain, and a clot also went to her lungs. She took blood thinners and steroid pills. Later she took a medicine that calms the immune system to help her use fewer steroids. Tests showed no inherited blood-clotting problem. She had several flare-ups of the kidney problem. Steroid pills controlled them until 2017. After that she had no relapses. Her doctors stopped the blood thinner and the immune-calming medicine. One year later she had sudden, very bad belly pain all over. She threw up after eating. Both legs were swollen. Tests showed the kidney problem was back. A special X-ray picture (CT scan) showed a new clot in the main artery that feeds the small intestine. It was like a plug in a pipe that stops water. Blood could not reach the intestines. In surgery, most of her small intestine was dead. Taking out that much bowel would not allow life. She died 48 hours later.",
            "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/\u00b5L. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
            "gs_summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours.",
            "metadata": "Nephrology | Technical"
        },
        {
            "doc_id": 19,
            "label": "low_health_literacy",
            "gen_text": "A 23-year-old man came to the emergency room with a sudden, very bad headache. He also felt sick, threw up, and felt heavy pressure in his chest. His blood pressure was high and he was breathing fast. A quick heart test looked like a major heart attack. He was rushed for a procedure to check and open the heart arteries. The heart arteries looked normal. A head CT scan then showed bleeding in the space around his brain. A team of specialists cared for him, but he got worse quickly. He went into cardiac arrest and died.",
            "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9\u00b0C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
            "gs_summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality.",
            "metadata": "Neurology | Technical"
        },
        {
            "doc_id": 4,
            "label": "low_health_literacy",
            "gen_text": "This is about a 13-year-old boy. He has had small growths in his throat since he was two years old. The growths were in his voice box and windpipe. They narrowed his breathing tube, so he had trouble breathing. It was like trying to breathe through a pinched straw. A chest scan showed several small cysts in his lungs. Doctors removed the throat growths. They also placed a breathing tube through a small hole in his neck to help him breathe. He got one dose of a medicine called bevacizumab (400 mg) through a vein. He also had breathing therapy. He got better. The problem has not come back during follow-up.",
            "fulltext": "13-year-old boy from Cusco with a history of laryngeal papillomatosis since the age of two (at the age of three he required a tracheostomy) and a mother with a history of genital papilloma. The patient was admitted to the San Borja National Institute of Child Health in Lima, after a 16-day illness characterised by respiratory difficulties predominantly at night, inspiratory laryngeal stridor and moderate dysphonia; he previously received azithromycin and oxygen support, without improvement.\n\nThe physical examination revealed mild subcostal retraction, decreased vesicular murmurs in the left hemithorax and scanty wheezy breath sounds with predominance in the right hemithorax, which required oxygen support with a binasal cannula at 4 liters. The rest of the evaluation had no relevant findings. At the laboratory level, leukocytes were found at 8.03 \u00d7 103/u, platelets 209 \u00d7 103/u, hemoglobin 13.2 g/dL, C-reactive protein at 36.6 mg/L. As part of the imaging studies, a chest radiograph and a head and neck tomography were performed.\n\n48 hours after admission, she presented with increased stridor and respiratory difficulty, so admission to the emergency operating room for tracheostomy, microsurgery and excision of papillomatosis lesions was decided. An appendicular tumour of papillomatose appearance with ventricular bands in the epiglottis, glottic face, vocal cords, subglottis and trachea up to ring 5 was evident. The anatomopathological report reported coilocitic atypia due to HPV and mild focal dysplasia.\n\nIn the immediate postoperative period, he was transferred to the paediatric intensive care unit for respiratory monitoring, with weaning from oxygen at 48 hours. He received a single dose of bevacizumab 400 mg intravenous and subsequently improved clinically. The patient remained hospitalised for seven days, achieving clinical stability through normalisation of oxygen saturation levels and progressive weaning from oxygen, and was subsequently referred to the hospital in Bre\u00f1a to continue his management. Telemonitoring was carried out after eight months and the family indicated that there was no evidence of relapse or other intercurrences.\n",
            "gs_summary": "A 13-year-old boy with a history of laryngeal papillomatosis since the age of two years was presented. The patient presented respiratory distress and multiple stenosing nodules in the larynx and trachea, and several pulmonary cysts were visualized on a chest tomography. The patient underwent exeresis of the papillomatosis lesions and tracheostomy. He received a single dose of 400 mg bevacizumab intravenous and respiratory therapy with a favorable evolution, without recurrence in the follow-up.\n",
            "metadata": "Pediatrics | Technical"
        }
    ],
    "proficient_health_literacy": [
        {
            "doc_id": 16,
            "label": "proficient_health_literacy",
            "gen_text": "A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C\u2011peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow\u2011up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.\n\nEight days after a routine visit, he developed dyspnea and fever >38\u2103. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/\u03bcL, CRP 6.06 mg/dL, CK\u2011MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1\u2013V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non\u2011invasive positive pressure ventilation and nitrates.\n\nTransthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5\u00d76\u2011mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2\u00d75\u2011mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.\n\nRetrospective review revealed subtle abnormalities starting four months pre\u2011admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4\u2011kg weight loss. EGD and whole\u2011body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre\u2011admission visit (8 days prior), WBC was 9,300/\u03bcL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.\n\nEmpiric antibiotics were initiated with ampicillin\u2013sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase\u2011negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S \u22648 \u03bcg/mL; GM \u22641 \u03bcg/mL; CEZ \u22642 \u03bcg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III\u2013IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.\n\nAfter four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence\u2011free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.",
            "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38\u2103. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /\u03bcL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5\u00d76-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2\u00d75-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /\u03bcL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S \u22648 \u03bcg/mL; MIC to GM \u22641 \u03bcg/mL; MIC to cefazolin (CEZ) \u22642 \u03bcg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
            "gs_summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. ",
            "metadata": "Endocarditis | Technical"
        },
        {
            "doc_id": 0,
            "label": "proficient_health_literacy",
            "gen_text": "A 20\u2011year\u2011old woman had been followed since age eight for idiopathic nephrotic syndrome (NS) inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism, without sequelae and without personal or family thrombotic history. Kidney biopsy was deferred because there was no kidney failure, gross hematuria, hypertension, or extra\u2011renal signs suggestive of secondary NS at presentation. She was treated with an oral vitamin K antagonist and oral corticosteroids with good evolution. Subsequently, she had multiple steroid\u2011dependent relapses and was started on mycophenolate mofetil (MMF) as background therapy to spare corticosteroids and ensure normal growth. An exhaustive thrombophilia assessment was negative: homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden, JAK\u20112, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and anti\u2011\u03b22\u2011glycoprotein I antibodies were all normal. Anticoagulation was stopped after nine years. Several relapses occurred but were controlled with oral corticosteroids. NS remission was documented from 2017; MMF was gradually discontinued in 2019, and she remained asymptomatic without relapse.\n\nOne year later, she presented to the emergency department with acute intense diffuse abdominal pain without irradiation, associated with postprandial vomiting and bilateral lower\u2011limb edema for six hours. Examination showed intense epigastric tenderness with normal vital signs (BP 120/70 mm Hg, HR 83 bpm, SpO2 100% on room air) and no fever or neurological impairment. Urinalysis detected proteinuria. Hemogasanalysis showed metabolic acidosis with respiratory compensation. Labs revealed hypoalbuminemia, hypercholesterolemia, prothrombin time 90%, elevated D\u2011dimer, LDH, and creatine phosphokinase, with inflammatory markers (CRP 37 mg/L) and leukocytosis (26.4 \u00d7 10^3/\u00b5L); renal and liver function were normal. Urgent abdominal ultrasound showed a low\u2011to\u2011moderate intra\u2011abdominal effusion. Contrast\u2011enhanced CT demonstrated acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. She underwent emergency laparotomy: intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost the entire small bowel, rendering resection incompatible with life. She died 48 hours later.\n\nThis case illustrates catastrophic arterial thrombosis in the setting of NS despite a negative thrombophilia work\u2011up. NS is a hypercoagulable state with multifactorial mechanisms, including urinary loss of anticoagulant proteins (e.g., antithrombin III, protein S), increased fibrinogen, hemoconcentration, dyslipidemia, and systemic inflammation. While venous thromboembolism is more common in NS, superior mesenteric artery thrombosis is rare but often fatal, underscoring the need for high clinical suspicion and rapid imaging when severe acute abdominal pain occurs in patients with active or relapsing NS.",
            "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/\u00b5L. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
            "gs_summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours.",
            "metadata": "Nephrology | Technical"
        },
        {
            "doc_id": 19,
            "label": "proficient_health_literacy",
            "gen_text": "A 23-year-old male with a 23 pack-year smoking history, no alcohol use, and no illicit drug use presented with 2 hours of sudden severe frontal headache, nausea, vomiting, and chest heaviness. He was distressed but alert and oriented. Vitals: BP 178/103 mmHg, RR 26/min, T 38.9\u00b0C, HR 87/min, SpO2 94%. Exam: normal vesicular breath sounds; cardiovascular and abdominal exams inconclusive; neurological exam notable for neck stiffness, dilated but light-reactive pupils, normal plantar reflexes, and no focal deficits. ECG showed ST-segment elevation >2 mm in V2\u2013V5, consistent with STEMI; he received a 300 mg aspirin load and was urgently transferred for PCI. Troponin was elevated at 1.48 mg/dl (normal <0.16 mg/dl). Femoral-access coronary angiography demonstrated normal coronary arteries with TIMI 3 flow. Post-angiography ECG showed normal sinus rhythm with LVH; echocardiography revealed normal ventricular function without RWMA. Subsequent workup found lymphocytosis and mildly elevated CRP. Non-contrast CT brain demonstrated a cisternal subarachnoid haemorrhage with extension anterior to the right temporal lobe. Abdominal ultrasound was negative for polycystic kidney disease; cerebral CT angiography was planned to exclude aneurysm. Nimodipine 60 mg q4h was initiated with a BP target of 160/100 mmHg. On day 2, he acutely deteriorated with cardiac arrest; after CPR, GCS was 6, and he was intubated and mechanically ventilated in the ICU. Owing to instability, repeat CT brain and planned cerebral CTA were not performed. He received multidisciplinary ICU care with NG feeding, IV fluids, antibiotics, a proton pump inhibitor, and nimodipine. On day 8, he developed ventricular fibrillation and, despite CPR and more than five defibrillation attempts, could not be resuscitated and died.",
            "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9\u00b0C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
            "gs_summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality.",
            "metadata": "Neurology | Technical"
        },
        {
            "doc_id": 18,
            "label": "proficient_health_literacy",
            "gen_text": "A 65-year-old male presented with six months of swelling and boutonniere deformity of the right digit III following a motorcycle accident on January 1, 2023. He initially self-managed with analgesics and did not seek care. He reported inability to fully extend the right middle finger. Examination demonstrated edema and a boutonniere posture (PIP flexion, DIP hyperextension). Active PIP ROM was 45\u2013110 degrees, with passive PIP ROM within normal limits. Radiographs of the right hand (AP/lateral) revealed no osseous pathology, supporting a soft-tissue etiology consistent with a central slip injury. \n\nSurgical technique: Central slip defect reconstruction was performed using the partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. Under anesthesia and tourniquet control in the supine position, a midlateral incision was made on the ulnar aspect of the middle phalanx centered at the PIP joint with dorsal oblique extension, and a transverse incision was made over the MCP flexion crease proximal to the A1 pulley. The ulnar digital neurovascular bundle was identified and protected. Full-thickness dorsal flaps were elevated to expose the central slip and extensor mechanism to the PIPJ. Scar and pseudotendinous tissue were excised. The central slip was not amenable to primary repair; therefore, the ulnar slip of the FDS was selected for reconstruction. The ulnar neurovascular bundle was mobilized to visualize the periosteal insertion of the A3 pulley. The extensor tendon was mobilized and tenolyzed; the dorsal PIP capsule was incised with removal of interposed tissue. The A3 pulley periosteal insertion and the volar capsule of the PIP joint were incised longitudinally. A 2\u20130 non-absorbable monofilament suture was placed around the ulnar FDS slip at the PIP level. Through the proximal incision, the flexor sheath and A1 pulley were incised longitudinally to expose the FDS; the ulnar slip was isolated and transected, preserving the radial slip. The previously placed 2\u20130 suture facilitated delivery of the distally based ulnar FDS slip distally. A 2.8\u2011mm dorsal-to-volar bone tunnel was drilled at the base of the middle phalanx; an elevator protected the FDP, volar plate, and volar structures. With the PIP reduced in full extension, the FDS slip was passed through the tunnel and routed through the intact proximal segment of the central slip/extensor tendon. A tendon weaver completed a Pulvertaft weave under appropriate tension with the PIP in full extension and reduction, secured with 3\u20130 non-absorbable suture. The capsule and central slip reconstruction margins were approximated; adhesions were released and lateral bands mobilized. Tenodesis effect, posture, stability, and motion were assessed. Wounds were irrigated, the tourniquet deflated, hemostasis obtained, and capillary refill confirmed. Skin was closed with horizontal mattress sutures. A sterile dressing and a well-padded PIP extension splint were applied to allow early DIP and MCP motion.\n\nPostoperative course: First wound check at postoperative day 4; the patient received meloxicam 7.5 mg PO BID and doxycycline 100 mg PO BID for 3 days. A second wound visit occurred 3 days later. At 2 weeks, the back slab and external sutures were removed, and active and passive PIP ROM exercises were initiated. By 3 weeks, the wound had healed and PIP ROM was 0\u201390 degrees. At 1 month, PIP ROM improved to 0\u2013100 degrees, with continued functional gains. After 7 weeks of rehabilitation, he returned to work with PIP ROM 0\u2013110 degrees. Overall function improved substantially, with the DASH score decreasing from 50 to 4.2.\n\nInterpretation: Clinical and radiographic findings were concordant with a chronic central slip injury producing boutonniere deformity (PIP flexion, DIP hyperextension due to dorsal apparatus disruption and volar migration of lateral bands). Reconstruction using an ulnar FDS slip via bone tunnel and Pulvertaft weave restored PIP extension and yielded progressive ROM gains and marked functional recovery.",
            "fulltext": "A 65-year-old male presented with swelling and boutonniere deformity on the right middle finger for six months after a motorcycle accident on January 1st, 2023. Initially, he managed the injury with painkillers and did not seek medical attention. After six months of persistent symptoms, including an inability to fully extend the finger and noticeable edema, he sought treatment.\n\nClinical findings\nThe inspection of the right hand showed the presence of deformity with edema. The active range of motion (ROM) was impaired in PIP joint in digiti III of the right hand. The active ROM of PIP joint digiti III of the right hand 45\u2013110 degrees. The passive ROM of PIP joint digiti III of the right hand within normal.\n\nDiagnostic assessment\nWe performed X-ray of the right hand AP/Lateral which showed there are no abnormality in the bone and we diagnosed the deformity from soft tissue which is central slip injury.\n\nSurgical technique\nA central slip defect reconstruction utilizing partial ulnar side of flexor digitorum superficial tendon was performed. Under anesthesia, the patient was positioned supine with a tourniquet applied to the upper arm. A midlateral incision was made on the ulnar aspect of the right middle phalanx, centered at the PIP joint. The incision extended dorsally in an oblique manner. A transverse incision was made over the MCP joint flexion crease, just proximal to the A1 pulley. The procedure involves identifying and protecting the ulnar digital neurovascular bundle, exposing the central slip and extensor tendon to the PIPJ, full-thickness dorsal flaps are elevated. Scar tissue and pseudotendinous tissue is identified and excised. The central slip cannot be repaired primarily, so the ulnar slip of the FDS tendon is used for reconstruction. The ulnar neurovascular bundle is mobilized to visualize the periosteal insertion of the A3 pulley.\n\nThe extensor tendon is mobilized and tenolyzed, followed by incision of the dorsal capsule of the PIP joint and removal of interposed tissue. The A3 pulley's periosteal insertion is incised longitudinally, and the PIP joint's volar capsule is incised longitudinally. The ulnar slip of the FDS tendon is identified and a 2\u20130 non-absorbable, monofilament suture is placed around it. A transverse incision is made at the MCP joint flexion crease, proximal to the A1 pulley revealing the flexor tendon sheath. The tendon sheath and A1 pulley are incised longitudinally. The FDS tendon is identified. The ulnar slip of the FDS tendon is isolated and transected to release the ulnar slip, avoiding entrapment or catching of the radial slip. The 2\u20130 suture that was placed around the ulnar slip at the level of the PIP joint is used to release distally based FDS tendon slip and deliver the ulnar slip of the FDS tendon distally.\n\nA 2.8-mm drill is used to create a vertically oriented bone tunnel dorsal to volar. An elevator is placed between the flexor digitorum profundus tendon, volar plate, and volar aspect of the base of the middle phalanx protecting the volar anatomic structures. The FDS tendon slip passes through the tunnel while maintaining the PIP joint in extension and reduced position. The FDS tendon slip passed through the intact proximal section of the central slip and extensor tendon. A tendon weaver completes a Pulvertaft weave, confirming the appropriate tension with the PIPJ in the reduced, full extension position. A 3\u20130 non-absorbable suture secures the pulvertaft weave. The margins of the capsule and central slip reconstruction are approximated across the PIP joint, and adhesions are released and the lateral bands mobilized.\n\nThe overall posture, stability, and motion with tenodesis assessed. All the incisions are copiously irrigated. The tourniquet is deflated and hemostasis is obtained. Capillary refill of all fingers is assessed. The skin is closed using horizontal mattress stiches. A sterile dressing is applied with an appropriately padded PIP joint extension splint to allow for early DIP joint and MCP joint motion.\n\nFollow-up and outcomes\nFirst follow-up was done 4 days after for wound treatment. The patient was given oral meloxicam 7,5 mg twice a day and doxycycline 100 mg twice a day for 3 days. The second follow-up was done 3 days after for wound treatment. After 2 weeks, we remove the back slab, remove the external suture and begin the active and passive ROM exercise. After 3 weeks, the wound was healed, and we found the ROM of PIP joint 0 to 90 degrees. And after a month, the patient came with improved ROM of PIP joint 0 to 100 degrees, and improved functional outcome. After 7 weeks of physical rehabilitation, patients already back to work with improve ROM of PIP joint 0 to 110 degrees. The function of the patient's right hand is evaluated with DASH score, which improves significantly from 50 to 4.2.",
            "gs_summary": "A 65-year-old male patient presented with swelling and boutonniere deformity on the digiti III of the right hand. The patient had previously fallen from a motorcycle, and the patient's right middle finger got was by a motorcycle six months ago. After the incident, the patient's right middle finger cannot be fully extended. The patient's right hand showed edema with flexion of the interphalangeal (PIP) joint and hyperextension of the distal interphalangeal (DIP) joint. The Range of Motion (ROM) of the PIP joint right middle finger was 45-110 degrees. The X-ray of the right hand AP/oblique showed no bone involvement in the deformity. The patient underwent central slip defect reconstruction utilizing the partial ulnar side of the flexor digitorum superficial tendon. A PIP joint extension splint was applied for 2 weeks. Active and passive exercise of the ROM of the PIP joint began after 2 weeks of PIP extension joint splinting. The patient's ROM of the PIP joint (0-90 degrees) significantly improved 1 month after surgery. The patient's ROM of the PIP joint returned to normal after 2 months after surgery. The function of the patient's right hand is evaluated with the DASH score, which improves significantly from 50 to 4.2.",
            "metadata": "Orthopedic Surgery | Technical"
        },
        {
            "doc_id": 13,
            "label": "proficient_health_literacy",
            "gen_text": "A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nEmergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99\u2013100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.\n\nLaboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.\n\nComputed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700\u20131,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.\n\nImmunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.\n\nContext: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach\u2014urgent culprit-vessel PCI followed by immunosuppression and delayed CABG\u2014is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.",
            "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
            "gs_summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n",
            "metadata": "Topic: Cardiology | Complexity: Technical"
        }
    ]
}