diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_fully_merged_v2.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_fully_merged_v2.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_fully_merged_v2.json" @@ -0,0 +1,602 @@ +[ + { + "index": 0, + "label": "low_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Donald J Sherrard, Gavril Hercz, York Pei, Norma A Maloney, Celia Greenwood, Arif Manuel, Carl Saiphoo, Stanley S Fenton, Gino V Segre. The spectrum of bone disease in end-stage renal failure\u2014an evolving disorder. Kidney International. 1993.\n Julian Paul Midgley, Andrew Glenday Matthew, Celia Margaret T Greenwood, Alexander Gordon Logan. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA. 1996.\n Brent W Zanke, Celia MT Greenwood, Jagadish Rangrej, Rafal Kustra, Albert Tenesa, Susan M Farrington, James Prendergast, Sylviane Olschwang, Theodore Chiang, Edgar Crowdy, Vincent Ferretti, Philippe Laflamme, Saravanan Sundararajan, St\u00e9phanie Roumy, Jean-Fran\u00e7ois Olivier, Fr\u00e9d\u00e9rick Robidoux, Robert Sladek, Alexandre Montpetit, Peter Campbell, Stephane Bezieau, Anne Marie O'Shea, George Zogopoulos, Michelle Cotterchio, Polly Newcomb, John McLaughlin, Ban Younghusband, Roger Green, Jane Green, Mary EM Porteous, Harry Campbell, Helene Blanche, Mourad Sahbatou, Emmanuel Tubacher, Catherine Bonaiti-Pelli\u00e9, Bruno Buecher, Elio Riboli, Sebastien Kury, Stephen J Chanock, John Potter, Gilles Thomas, Steven Gallinger, Thomas J Hudson, Malcolm G Dunlop. Genome-wide association scan identifies a colorectal cancer susceptibility locus on chromosome 8q24. Nature Genetics. 2007.\n Jean-Philippe Fortin, Aur\u00e9lie Labbe, Mathieu Lemire, Brent W Zanke, Thomas J Hudson, Elana J Fertig, Celia MT Greenwood, Kasper D Hansen. Functional normalization of 450k methylation array data improves replication in large cancer studies. Genome Biology. 2014.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 18.072553317535547, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 6.5625 + }, + { + "index": 0, + "label": "intermediate_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Signs and symptoms\nThe symptoms experienced in cholesterol embolism depend largely on the organ involved. Non-specific symptoms often described are fever, muscle ache and weight loss. Embolism to the legs causes a mottled appearance and purple discoloration of the toes, small infarcts and areas of gangrene due to tissue death that usually appear black, and areas of the skin that assume a marbled pattern known as livedo reticularis. The pain is usually severe and requires opiates. If the ulcerated plaque is below the renal arteries the manifestations appear in both lower extremities. Very rarely the ulcerated plaque is below the aortic bifurcation and those cases the changes occur only in one lower extremity.", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 13.475353982300884, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 6.0 + }, + { + "index": 0, + "label": "proficient_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Signs and symptoms\nAside from the occasional flank or lower back pain caused by a sudden clot in the major veins to the kidneys, RVT produces few symptoms. Some patients may not display any symptoms while other patients may experience bloody urine, decrease in urine output, edema and worsening proteinuria. Usually the diagnoses of RVT is first made when a nephrotic syndrome patient experiences a pulmonary embolism or a sudden decrease in kidney function or kidney failure. These symptoms may vary in duration since a blood clot can resolve itself, but precautions should be taken to prevent the migration of the clot to other parts of the body. The most severe complication of RVT is a pulmonary embolism, caused by a clot, also called a thrombus, that originates from the renal vein or any other vein in the body and migrates to the pulmonary artery. A pulmonary embolism is a serious condition because; it can damage the lungs due to pulmonary hypertension and cause low blood oxygen, damaging other organs in the body. This condition can cause death if left untreated; about 30% percent of patients who have a pulmonary embolism will die, usually within one hour.", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 15.511602610587385, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.428571428571429 + }, + { + "index": 1, + "label": "low_health_literacy", + "original_doc": "She is 34 years old and pregnant. She had a seizure and trouble speaking clearly. She was sent right away for a head MRI scan. The scan showed a pattern doctors call the \u201cMedusa head.\u201d This means the veins in her brain are arranged in an unusual way that she was born with. There is a small blood clot at the outer part of this vein pattern. The blood is also moving slowly closer to the main vein.", + "wiki_anchor": "Caput medusae is the appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen. The name caput medusae (Latin for \"head of Medusa\") originates from the apparent similarity to Medusa's head, which had venomous snakes in place of hair. It is also a sign of portal hypertension. It is caused by dilation of the paraumbilical veins, which carry oxygenated blood from mother to fetus in utero and normally close within one week of birth, becoming re-canalised due to portal hypertension caused by liver failure.", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 13.645217391304353, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 9.0 + }, + { + "index": 1, + "label": "intermediate_health_literacy", + "original_doc": "A 34-year-old woman who is 8 weeks pregnant had a first-time generalized seizure with temporary slurred speech. Because she is pregnant and this was her first seizure, doctors obtained an urgent brain MRI. The MRI showed the classic \u201cMedusa head\u201d sign, which indicates a developmental venous anomaly (DVA)\u2014a vein pattern you are born with. Imaging also suggested a partial clot along the peripheral portion of the draining system and slower blood flow closer to the main draining vein. These findings support the diagnosis: a developmental venous anomaly with peripheral partial thrombosis and proximal slow flow.", + "wiki_anchor": "In up to 30% there is a coincidence of CCM with a venous angioma, also known as a developmental venous anomaly. These lesions appear either as enhancing linear blood vessels or caput medusae, a radial orientation of small vessels that resemble the hair of Medusa from Greek mythology. These lesions are thought to represent developmental anomalies of normal venous drainage. These lesions should not be removed, as venous infarcts have been reported. When found in association with a CCM that needs resection, great care should be taken not to disrupt the angioma.", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 11.722956521739132, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 7.2 + }, + { + "index": 1, + "label": "proficient_health_literacy", + "original_doc": "A 34-year-old woman, 8 weeks pregnant and without other relevant history, presented with generalized convulsions and postictal dysarthria that resolved within two hours. On examination she was alert, oriented, and without focal language, motor, or sensory deficits; a right lateral tongue bite was noted. Laboratory tests and ECG were unremarkable. Given a first epileptic seizure in pregnancy, an urgent cranial MRI was performed. The protocol included 3D T1 pre- and post-contrast (axial, coronal, sagittal), axial FLAIR, axial T2, VEN BOLD and magnetic susceptibility sequences, as well as axial diffusion and ADC mapping. MRI demonstrated multiple venous cortico-medullary vascular structures converging centripetally to a large central draining vein that emptied via the inferior anastomotic vein into the left transverse sinus, forming the classic \u201cMedusa head\u201d sign. On T1 post-contrast, the drainage vein showed increased signal with central hyphocaptation, suggesting partial thrombosis versus slow flow. On T2 and FLAIR, the parenchyma surrounding the drainage vein was hyperintense, without diffusion restriction, compatible with edema. Overall, the findings are diagnostic of a developmental venous anomaly with signs of partial peripheral thrombosis and more proximal slow flow, causing perilesional edema. Management was initiated with clexane 60 mg every 12 hours and levetiracetam 500 mg every 12 hours, with symptomatic improvement and stability after one week. Contextually, DVAs are typically benign venous variants; however, pregnancy-associated hypercoagulability may predispose to thrombosis. Partial thrombosis and impaired outflow in a DVA can lead to venous congestion and edema, manifesting clinically with seizures.", + "wiki_anchor": "Perinatal stroke is a disease where an infant has a stroke between the 140th day of the gestation period and the 28th postpartum day, affecting up to 1 in 2300 live births. This disease is further divided into three subgroups, namely neonatal arterial ischemic stroke, neonatal cerebral sinovenous ischemic stroke, and presumed perinatal stroke. Several risk factors contribute to perinatal stroke including birth trauma, placental abruption, infections, and the mother's health. Detection and diagnosis of perinatal stroke are often delayed due to prenatal onset or inadequacy of neonatal signs and symptoms. A child may be asymptomatic in the early stages of life and may develop common signs of perinatal stroke such as seizures, poor coordination, and speech delays as they get older. Diagnostic tests such as magnetic resonance imaging, electroencephalogram, and blood tests are conducted when doctors suspect the patients have developed signs of a perinatal stroke. The prognosis of this disease is associated with the severity and the development of the symptoms. This disease can be treated by anticoagulant and anticonvulsant drugs, surgical procedures, and therapeutic hypothermia, depending on the condition of the patient.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 14.923885135135137, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 8.0 + }, + { + "index": 2, + "label": "low_health_literacy", + "original_doc": "A 22-year-old woman had painful mouth sores. The sores made eating and drinking hard. The problem started after a fever. Small pimples showed up on her lips. She had been vaping for about one year. The checkup found no spots on the rest of her body. Her lips had crusts with a little blood. The corners of her mouth were raw and bled easily. Inside her mouth there were white sores with yellow edges. The sores were different shapes and sizes and were in several places. A test for the cold-sore virus was negative. The doctor said this was a mouth reaction called oral erythema multiforme. She was treated with salt-water compresses on the lips. She used a mouth rinse with an anti-swelling medicine (dexamethasone) mixed with a coating gel (hyaluronic acid). She put 2% miconazole cream on the sores at the mouth corners. She used petroleum jelly on her dry lips. She was told to stop vaping. Her mouth got better after one week of treatment.", + "wiki_anchor": "Signs and symptoms\nRarely is any soreness associated with the condition. Apart from the appearance of the lesion, there are usually no other signs or symptoms. The typical appearance of the lesion is an oval or rhomboid shaped area located in the midline of the dorsal surface of the tongue, just anterior (in front) of the sulcus terminalis. The lesion is usually symmetric, well demarcated, erythematous and depapillated, which has a smooth, shiny surface. Less typically, the lesion may be hyperplastic or lobulated and exophytic. There may be candidal lesions at other sites in the mouth, which may lead to a diagnosis of chronic multifocal oral candidiasis. Sometimes an approximating erythematous lesion is present on the palate as the tongue touches the palate frequently. The lesion is typically 2\u20133\u00a0cm in its longest dimension.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 11.90070895522388, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 6.625 + }, + { + "index": 2, + "label": "intermediate_health_literacy", + "original_doc": "A 22-year-old woman presented with a month of painful stomatitis that made eating and drinking difficult. The illness began with a fever and pimple-like lesions on the lips. She had been vaping regularly for about one year. Examination showed no skin lesions elsewhere. The lips had serosanguineous crusts and erosions at the labial commissures that tended to bleed. Intraorally, there were multiple irregular white ulcers with yellowish borders on several sites of the oral mucosa. Anti\u2013HSV-1 IgG was non-reactive. The diagnosis was oral erythema multiforme, likely related to vaping. Management included normal saline compresses to the lips, a dexamethasone mouth rinse mixed with hyaluronic acid, 2% miconazole cream applied to the lip corner, petroleum jelly for dry lips, and stopping vaping. Her oral condition improved within one week.", + "wiki_anchor": "Signs and symptoms\nThe lesions are located on the mucosa, usually bilaterally in the central part of the anterior buccal mucosa and along the level of the occlusal plane (the level at which the upper and lower teeth meet). Sometimes the tongue or the labial mucosa (the inside lining of the lips) is affected by a similarly produced lesion, termed morsicatio linguarum and morsicatio labiorum respectively. There may be a coexistent linea alba, which corresponds to the occlusal plane, or crenated tongue. The lesions are white with thickening and shredding of mucosa commonly combined with intervening zones of erythema (redness) or ulceration. The surface is irregular, and people may occasionally have loose sections of mucosa that comes away.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 14.514000000000003, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 7.4 + }, + { + "index": 2, + "label": "proficient_health_literacy", + "original_doc": "A 22-year-old woman presented to Oral Medicine with a 1-month history of painful oral ulcers causing difficulty eating and drinking. The episode began with fever followed by pimple-like lesions on the lips. She had used pod-type vapes for approximately one year, often trying different e-liquid flavors; she had never smoked conventional cigarettes. She reported no medication exposure prior to onset (no antibiotics, analgesics, anticonvulsants, NSAIDs, or antifungals), no drug or food allergies, and unhealthy eating habits. Extraorally, there were no lesions elsewhere on the body. The lips exhibited serosanguineous crusts with an erosive area at the right labial commissure that tended to bleed. Intraoral examination showed multiple painful white ulcers with yellowish edges, irregular and variable in size, on the labial and buccal mucosa, lateral and ventral tongue, and floor of mouth. Anti-HSV-1 IgG was non-reactive. Based on isolated oral mucosal involvement, absence of cutaneous lesions, and negative HSV serology, a diagnosis of vaping-related oral erythema multiforme, minor type, was established. Management comprised 0.9% NaCl\u2013moistened gauze compresses to the lips three times daily; a dexamethasone mouthrinse (1 mg in 10 mL hyaluronic acid) three times daily with a 30-minute post-rinse fasting period; 2% miconazole cream applied to the wound at the right labial commissure twice daily; and vaseline album (petrolatum) for dry lips. Adjunctive advice included brushing teeth and tongue twice daily (after breakfast and before bed), cessation of vaping, and avoidance of foods containing monosodium glutamate. At 1-week follow-up, the oral condition had improved. Ethical considerations: written informed consent was obtained; the case conformed to the Helsinki Declaration and had institutional approval. Context: Erythema multiforme is a mucocutaneous hypersensitivity reaction classically triggered by infections (e.g., HSV) or drugs; in this case, vaping exposure and frequent e-liquid flavor changes were considered plausible triggers in the absence of medication exposure and with non-reactive anti-HSV-1 serology.", + "wiki_anchor": "Signs and symptoms\nWhile the presence of lesions is the denominator among patients with PNP, the characteristics of the lesions differ. The five clinical presentations of lesions associated with PNP include:\n \"Pemphigus-like\": Flaccid blister (discrete), crusts over the raw exuding skin lesions\n \"Pemphigoid-like\": Tense blister(s) on brick red erythema\n \"Erythema multiforme-like\": Severe polymorphic skin and/or mucous membrane lesions\n \"Graft-vs.-host disease-like\": Widespread lichenoid eruption with severe mucous membrane involvement\n \"Lichen planus-like\": Small red flat-topped scaly papules\nIt is most common that mucous membrane lesions of the oral cavity are presented first. They can involve the oropharynx, nasopharynx, tongue, and vermilion (red portion) of the lips. They are also known to develop in the conjunctiva of the eye, anogenital (perineum) region, and esophagus. Cutaneous lesions tend to follow the onset of mucosal lesions. The blisters often erupt in waves, usually affecting the upper trunk, head, neck, and proximal extremities. Pemphigoid-like lesions are seen more often on the extremities. Lichenoid lesions are more common among children, presenting on the trunk and limbs, ranging from small red scaly papules to extensive violet to brown papules extending to the face and neck. Within the spectrum of lichenoid presentations are wounds that have features of erythema multiforme and graft-vs.-host disease. Scaly lesions on the palms of the hand and soles of the feet have been noted to coincide with the lichenoid lesions. Lesions of varying morphology may present simultaneously and transform from one type to another as the disease progresses.", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 12.506393442622954, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 7.454545454545454 + }, + { + "index": 3, + "label": "low_health_literacy", + "original_doc": "At 32 weeks of pregnancy, a routine scan found one small lump inside the baby\u2019s heart. It caused no symptoms. This was the only problem seen. Doctors watched it with clinic visits until 39 weeks plus 1 day. Then the baby was delivered by C-section (a surgery to deliver the baby). After birth, the child had checkups on day 1, day 7, day 30, month 7, and month 12. At each visit, the child\u2019s growth and behavior were healthy for age. The heart lump stayed the same size; it did not grow or shrink. By 1 year old, there were no signs of a related condition called tuberous sclerosis complex.", + "wiki_anchor": "It is much more common to find metastasis from an alternate site than a primary heart tumor. However, primary cardiac tumors do occur. One of these is the cardiac rhabdomyoma. Approximately 80-90% of these tumors are found in patients with tuberous sclerosis, a genetic condition causing multiple tumors, with most found prior to the age of one. Although these tumors are most commonly treated with resection, symptomatic tumors in fetuses have been shown to decrease in size after maternal sicrolimus administration. If clinically silent, they can be watched with routine imaging as the tumor will likely spontaneously regress.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 11.490204081632655, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.833333333333333 + }, + { + "index": 3, + "label": "intermediate_health_literacy", + "original_doc": "This case describes an isolated, asymptomatic fetal cardiac rhabdomyoma first detected at 32 weeks\u2019 gestation. The pregnancy was monitored as an outpatient until 39 weeks plus one day, when delivery occurred by cesarean section. Postnatal follow-up at day 1, day 7, day 30, 7 months, and 12 months showed normal growth and neurodevelopment. The intracardiac mass remained stable in size across all visits. Up to one year of age, the child did not meet any clinical diagnostic criteria for tuberous sclerosis complex (TSC).", + "wiki_anchor": "It is much more common to find metastasis from an alternate site than a primary heart tumor. However, primary cardiac tumors do occur. One of these is the cardiac rhabdomyoma. Approximately 80-90% of these tumors are found in patients with tuberous sclerosis, a genetic condition causing multiple tumors, with most found prior to the age of one. Although these tumors are most commonly treated with resection, symptomatic tumors in fetuses have been shown to decrease in size after maternal sicrolimus administration. If clinically silent, they can be watched with routine imaging as the tumor will likely spontaneously regress.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 11.490204081632655, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 5.833333333333333 + }, + { + "index": 3, + "label": "proficient_health_literacy", + "original_doc": "A 29-year-old gravida V para IV (3 spontaneous vaginal deliveries, prior cesarean for failed induction 4 years earlier) presented for ANC at 32 weeks by LNMP. Maternal labs: VDRL, HBsAg, and urinalysis negative; CBC within normal limits; blood group A Rh-positive. Obstetric ultrasound revealed normal fetal anatomy except the heart. Fetal echocardiography showed normal situs; atria of comparable size; normally positioned atrioventricular and semilunar valves with normal motion; ventricles comparable in size and contractility; left ventricle forming the apex; no ventricular septal defect. Two circumscribed, round, echogenic masses were noted on the left ventricular papillary muscles, measuring 18.2 \u00d7 8.3 mm and 13.5 \u00d7 8.3 mm. LVOT and RVOT anatomy and function were normal on 2D and color flow. Impression: cardiac rhabdomyoma. Given the association with tuberous sclerosis complex (TSC), detailed neurosonography and systemic evaluation were performed and were unremarkable. She continued routine ANC without complications to 39 weeks. At 39 weeks + 1 day, a cesarean section (repeat on request at term) delivered a 3200 g female, Apgar 10 and 10 at 1 and 5 minutes. Postoperative courses for mother and neonate were uneventful; discharge occurred on postoperative day 3. The neonate was evaluated on days 1, 7, and 30: physical examinations were normal; no seizure activity or new cutaneous lesions; mass dimensions were similar to the antenatal findings. At 7 months, development was age-appropriate; pediatric echocardiography showed well-circumscribed hyperechoic masses on both left ventricular papillary muscles measuring 21.8 \u00d7 9.2 mm and 14.7 \u00d7 8.5 mm, without left ventricular inflow obstruction. At 12 months, anthropometric and neurobehavioral development remained normal. Echocardiography again demonstrated well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and no left ventricular inflow obstruction. Up to one year of age, apart from the persistent intracardiac rhabdomyomas, the child met none of the clinical diagnostic criteria for TSC. Notably, while cardiac rhabdomyomas often regress spontaneously in infancy, these lesions were stable through 12 months.", + "wiki_anchor": "Diagnosis\n The classic triad of the vasa praevia is: membrane rupture, painless vaginal bleeding and fetal bradycardia or fetal death.\n Prior to the advent of ultrasound, this diagnosis was most often made after a stillbirth or neonatal death in which the mother had ruptured her membranes, had some bleeding, and delivered an exsanguinated baby. In these cases, examination of the placenta and membranes after delivery would show evidence of a velamentous cord insertion with rupture of the vessels. However, with almost universal use of ultrasound in the developed world, many cases are now detected during pregnancy, giving the opportunity to deliver the baby before this catastrophic rupture of the membranes occurs. Vasa previa is diagnosed with ultrasound when echolucent linear or tubular structures are found overlying the cervix or in close proximity to it. Transvaginal ultrasound is the preferred modality. Color, power and pulsed wave Doppler should be used to confirm that the structures are fetal vessels. The vessels will demonstrate a fetal arterial or venous waveform.\nAlkali denaturation test detects the presence of fetal hemoglobin in vaginal blood, as fetal hemoglobin is resistant to denaturation in presence of 1% NaOH. Tests such as the Ogita Test, Apt test or Londersloot test were previously used to attempt to detect fetal blood in the vaginal blood, to help make the diagnosis. These tests are no longer widely used in the US, but are sometimes used in other parts of the world.\n Also detection of fetal hemoglobin in vaginal bleeding is diagnostic.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 13.303, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.916666666666667 + }, + { + "index": 4, + "label": "low_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Signs and symptoms \nA common symptom of laryngeal papillomatosis is a change in voice quality. More specifically, hoarseness is observed. As a consequence of the narrowing of the laryngeal or tracheal parts of the airway, shortness of breath, chronic cough and stridor (i.e. noisy breathing which can sound like a whistle or a snore), can be present. As the disease progresses, occurrence of secondary symptoms such as dysphagia, pneumonia, acute respiratory distress syndrome, failure to thrive, and recurrent upper respiratory infections can be diagnosed. The risk of laryngeal papillomatosis spreading to the lungs is higher in the juvenile-onset than the adult-onset. In children, symptoms are usually more severe and often mistaken for manifestations of other diseases such as asthma, croup or bronchitis. Therefore, diagnosis is usually delayed.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 12.342982283464568, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 7.857142857142857 + }, + { + "index": 4, + "label": "intermediate_health_literacy", + "original_doc": "A 13-year-old boy with recurrent respiratory papillomatosis since age two presented with breathing difficulty, noisy breathing (stridor), and hoarseness. Airway evaluation showed multiple nodules narrowing the larynx and trachea. Chest CT revealed several pulmonary cysts. He underwent surgical removal of the papillomatosis lesions and a tracheostomy. He received a single 400 mg intravenous dose of bevacizumab and respiratory therapy. He recovered well, and there has been no recurrence on follow-up.", + "wiki_anchor": "Pulmonary pathology is the subspecialty of surgical pathology which deals with the diagnosis and characterization of neoplastic and non-neoplastic diseases of the lungs and thoracic pleura. Diagnostic specimens are often obtained via bronchoscopic transbronchial biopsy, CT-guided percutaneous biopsy, or video-assisted thoracic surgery (VATS). The diagnosis of inflammatory or fibrotic diseases of the lungs is considered by many pathologists to be particularly challenging.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 20.066774193548394, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 8.0 + }, + { + "index": 4, + "label": "proficient_health_literacy", + "original_doc": "A 13-year-old male from Cusco with recurrent respiratory papillomatosis (RRP) since age two (tracheostomy at age three) and a maternal history of genital papilloma presented after 16 days of predominantly nocturnal respiratory difficulty, inspiratory laryngeal stridor, and moderate dysphonia. He had previously received azithromycin and supplemental oxygen without improvement. On exam, there was mild subcostal retraction, decreased vesicular breath sounds over the left hemithorax, and scant wheezes predominating on the right; he required 4 L/min oxygen via binasal cannula. Laboratory studies showed WBC 8.03 \u00d7 10^3/\u03bcL, platelets 209 \u00d7 10^3/\u03bcL, hemoglobin 13.2 g/dL, and CRP 36.6 mg/L. Imaging included a chest study and head and neck tomography; chest tomography visualized several pulmonary cysts. Forty-eight hours after admission, he developed worsening stridor and respiratory distress, prompting emergent OR transfer for tracheostomy, microlaryngoscopy, and excision of papillomatous lesions. Intraoperative findings demonstrated extensive papillomatous disease with appendicular tumor-like lesions and ventricular bands involving the epiglottis, glottic surface, vocal cords, subglottis, and trachea to ring 5. Histopathology showed koilocytotic atypia consistent with HPV and mild focal dysplasia. Postoperatively, he was managed in the PICU with respiratory monitoring and was weaned off oxygen within 48 hours. He received a single intravenous dose of bevacizumab 400 mg and showed prompt clinical improvement. He completed a seven-day hospitalization with normalization of oxygen saturation and progressive oxygen weaning, then was transferred for ongoing care. He also received respiratory therapy. On telemonitoring at eight months, there was no evidence of recurrence or intercurrent events. Clinical context: RRP is typically HPV-related (often low-risk types) and can cause multifocal papillomas leading to airway stenosis; anti-VEGF therapy such as bevacizumab is used off-label to reduce angiogenesis and disease recurrence, and in this case was associated with a favorable short- to mid-term outcome.", + "wiki_anchor": "Procedure\nDuring a total laryngectomy, the entire voicebox (larynx) is removed, which leads to a permanent disconnection of the upper and lower airways and a permanent tracheostoma (a breathing hole in the neck). Prior to the operation, breathing primarily occurs through the nasal airways. In the upper airways, the inhaled air is warmed up or cooled down, to prepare the optimal temperature before the air reaches the lungs. After a total laryngectomy, the upper airways are bypassed and breathing in and out occurs through the tracheostoma in the neck which means that the inhaled air flows directly into the lungs. These anatomical changes lead, among others, to changes in voice production, breathing, and olfaction. The nasal functions of regulating the temperature, humidifying, and filtering of the inhaled air are lost. The lack of these functions impairs the lower airways and the activity of the cilia, which leads to pulmonary problems such as tracheobronchial mucus, excessive sputum production, crusting, which can also cause fatigue and shortness of breath. To at least partially reduce these restrictions and compensate the nasal functions, an HME cassette can be attached over the tracheostoma to provide a means for conditioning, humidifying and to a certain extent filtering the inhaled air.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 14.195196078431373, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 8.875 + }, + { + "index": 5, + "label": "low_health_literacy", + "original_doc": "This 54-year-old man had long-term kidney disease. He took steroids and other medicines that weaken the body\u2019s defenses for a long time. He came to the lung department with fever, cough with mucus, and trouble breathing. A scan showed many cloudy spots in both lungs, like frosted glass. Blood tests showed a lot of inflammation. This suggested an infection from germs such as bacteria, a virus, or a fungus. A blood test was positive for RSV antibodies. Tests for other germs were not positive. His immune system was weak. His antibody level (IgG) was low. His infection-fighting T cells (CD4 and CD8) were also low. Doctors gave strong medicines for infection and support to help his breathing. His illness got worse quickly. He died from breathing failure.", + "wiki_anchor": "In more than 90% of cases, the cause is a viral infection. These viruses may be spread through the air when people cough or by direct contact. Risk factors include exposure to tobacco smoke, dust, and other air pollution. A small number of cases are due to high levels of air pollution or bacteria such as Mycoplasma pneumoniae or Bordetella pertussis. Diagnosis is typically based on a person's signs and symptom. The color of the sputum does not indicate if the infection is viral or bacterial. Determining the underlying organism is typically not needed. Other causes of similar symptoms include asthma, pneumonia, bronchiolitis, bronchiectasis, and COPD. A chest X-ray may be useful to detect pneumonia.", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 9.709855072463771, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 5.444444444444445 + }, + { + "index": 5, + "label": "intermediate_health_literacy", + "original_doc": "A 54-year-old man with chronic kidney disease on long-term corticosteroids and immunosuppressants was admitted to respiratory medicine with fever, cough with sputum, and shortness of breath. Chest CT showed multiple bilateral ground-glass opacities. Laboratory studies showed elevated inflammatory markers, indicating possible bacterial, viral, or fungal infection. RSV antibodies were positive, while tests for other pathogens were negative. He was immunocompromised from prolonged corticosteroid and immunosuppressant use, with low total IgG and reduced CD4 and CD8 T-lymphocyte counts. Despite intensive anti-infective therapy and escalating respiratory support, his condition deteriorated rapidly, and he died from respiratory failure.", + "wiki_anchor": "Coccidioidomycosis is amazingly diverse in terms of its scope of clinical presentation, as well as clinical severity. About 60% of Coccidioides infections as determined by serologic conversion are asymptomatic. The most common clinical syndrome in the other 40% of infected patients is an acute respiratory illness characterized by fever, cough, and pleuritic pain. Skin manifestations, such as erythema nodosum, are also common with Coccidioides infection. Coccidioides infection can cause a severe and difficult-to-treat meningitis in AIDS and other immunocompromised patients, and occasionally in immunocompetent hosts. Infection can sometimes cause acute respiratory distress syndrome and fatal multilobar pneumonia. The risk of symptomatic infection increases with age.", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 14.871428571428577, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 6.0 + }, + { + "index": 5, + "label": "proficient_health_literacy", + "original_doc": "A 54-year-old male with membranous nephropathy II and nephrotic syndrome on long-term oral glucocorticoids and immunosuppressants (immunocompromised) presented to the Department of Respiratory Medicine with 5 days of fever, cough, expectoration, and progressive dyspnea. He had a 20 pack-year smoking history and no family history of hereditary disease. A chest x-ray one month prior was normal. On admission (August 8, 2016): BMI 24.5 kg/m2, T 39.0\u00b0C, tachypnea 35 breaths/min, severe hypoxemia (SaO2 86%). Auscultation revealed good bilateral air entry with scattered diffuse crackles and rhonchi. Chest CT demonstrated multiple bilateral ground-glass opacities. Initial labs showed a normal WBC count with elevated neutrophils and increased inflammatory markers (CRP, ESR) and elevated (1\u21923)-\u03b2-D-glucan. Serology was positive for RSV antibodies on hospital day 4; other pathogen testing was negative. He had laboratory evidence of immunosuppression with decreased total IgG and reduced CD4 and CD8 T-lymphocyte counts, consistent with chronic exposure to corticosteroids and immunosuppressants.\n\nManagement: Immediate respiratory monitoring and supplemental oxygen were initiated. Empiric anti-infective therapy included antibiotics (moxifloxacin for 4 days, then cefminoxine for 8 days) and antifungal therapy (voriconazole for 10 days). The glucocorticoid and immunosuppressant doses were largely unchanged. After 10 days, clinical status and oxygenation worsened with radiographic progression. He was transferred to the Emergency ICU for noninvasive mechanical ventilation, broad-spectrum antibiotics (i.v. meropenem, oral moxifloxacin, cotrimoxazole), antifungal therapy (micafungin), systemic corticosteroids (methylprednisolone 40 mg bid i.v.), and supportive care. Ganciclovir was added for possible viral coinfection (e.g., CMV). Five days later, chest x-ray showed further aggravation. Despite escalation to invasive ventilator-assisted ventilation, higher-dose methylprednisolone (80 mg bid), additional antibacterials (cefoperazone-sulbactam, tigecycline, cotrimoxazole), and continued micafungin, he developed rapid progression culminating in respiratory failure and death two days later.\n\nInterpretation: The presentation is consistent with severe viral pneumonia due to RSV in an immunocompromised host, with imaging showing multifocal ground-glass opacities and laboratory evidence of systemic inflammation. Elevated (1\u21923)-\u03b2-D-glucan prompted antifungal coverage, while broad-spectrum antibacterial and antiviral regimens addressed possible coinfections. Profound immunosuppression (low IgG, reduced CD4/CD8 T cells) likely contributed to rapid deterioration and refractory hypoxemic respiratory failure despite intensive anti-infective therapy and advanced respiratory support.", + "wiki_anchor": "In 1847 Bennett described Geotrichum candidum causing a superinfection in the tuberculous cavity. Bennett was able to differentiate infection by Geotrichum candidum from candidiasis, and diagnose the first case of geotrichosis. Other early medical case reports in 1916 and 1928 also described lung infections. Most cases affect the bronchopulmonary tree, although other sites can be involved, such as oral mucosa and vagina. Skin and gut infections are also known. Reported cases of geotrichosis have been characterized with symptoms of chronic or acute bronchitis. Exogenous geotrichosis may arise from contact with contaminated soil, fruits or dairy products.\n Pulmonary geotrichosis is the most frequent form of geotrichosis. The symptoms appear to be secondary symptoms of tuberculosis. This includes symptoms such as light, thick, grey sputum, which in some cases may be blood-tinged. Patients often have a cough that produces clear or yellow sputum. Another symptom of pulmonary geotrichosis includes fine to medium rales. Patients may develop fever, rapid pulse and leukocytosis. The condition appears chronic with the presence of a little debilitation and fever. There is no chest pain and occasional wheezing can occur.\n Bronchial geotrichosis does not involve the lung instead the disease persists within the bronchial. Geotrichum candidum grows in the lumen of the bronchi. The disease is characterized as an endobronchial infection. Bronchial geotrichosis is similar to the allergic reaction of aspergillosis. Symptoms include prominent chronic cough, gelatinous sputum, lack of fever and medium to coarse rales. Patients with the bronchial condition their pulse and respiration are rarely elevated. Fine mottling may be present in the middle or basilar pulmonary region. Colonization of the bronchi can be associated with Candida albicans and usually occur with patients with chronic obstructive lung disease.\n Oral and vaginal geotrichosis is similar to thrush in its appearances and was often confused with this infection. The difference between oral and vaginal geotrichosis can be determined using microscope analysis. The infected area forms a white plaque and patients usually report burning sensation in the affected areas. The vaginal geotrichosis is more common in pregnant women and is often associated with vaginitis.\n Gastrointestinal geotrichosis is enterocolitis associated with glutamic therapy. The symptoms usually stop once the glutamic therapy is discontinued. Establishment of the etiology of the fungi is difficult since G. candidum is found within the gut normal flora. The difference between normal gut flora form and the disease causing form is the production of toxins.\n Cutaneous geotrichosis has two different types of variants which include superficial and deep infection. The superficial form the infection occurs on skin folds including submammary, inguinal, perianal and interdigital folds. The deep form develops nodules, tumours and ulcers on legs, face and hands. Geotrichosis can cause a cystic lesion appears as soft tissue on the skin.", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 10.812573260073261, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 5.942857142857143 + }, + { + "index": 6, + "label": "low_health_literacy", + "original_doc": "A 34-year-old woman had new lower back pain. She saw blood in her urine. She also had a big bruise under the skin on her right buttock. She had never had bleeding problems before. Because these bleeding signs were serious, she was sent to the emergency room. Doctors did blood-clotting tests. One test mixed her blood with normal blood to see how it clotted. Another test looked for a blocker against a clotting protein called factor eight. These tests confirmed the diagnosis.", + "wiki_anchor": "A person with this disease may also complain of malaise, fatigue, and general weakness (with or without accompanying blood loss). Acquired thrombocytopenia may be associated with the use of certain drugs. Inspection typically reveals evidence of bleeding (petechiae or ecchymoses), along with slow, continuous bleeding from any injuries or wounds. Adults may have large, blood-filled bullae in the mouth. If the person's platelet count is between 30,000 and 50,000/\u03bcL, bruising with minor trauma may be expected; if it is between 15,000 and 30,000/\u03bcL, spontaneous bruising will be seen (mostly on the arms and legs).", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 11.324978723404257, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 6.6 + }, + { + "index": 6, + "label": "intermediate_health_literacy", + "original_doc": "A 34-year-old woman with no prior bleeding history developed lower back pain, passed a kidney stone, and then had three days of haematuria. She later developed painful thigh and right gluteal bruising after an intramuscular injection. Because the bleeding was extensive, she was transferred to the emergency department. Her coagulation work-up showed a markedly prolonged aPTT. A mixing study only partially corrected the aPTT, and factor VIII activity was very low with a measurable factor VIII inhibitor (8.64 BU/mL), confirming acquired haemophilia A, likely postpartum. She was treated with prednisone and cyclophosphamide, and received bypassing therapy (initially FEIBA, then switched to recombinant factor VIIa due to side effects). Her bleeding improved and she was discharged.", + "wiki_anchor": "Alfredo Pavlovsky (24 November 1907 \u2013 26 April 1984) was an Argentinian physician who discovered that haemophilia has two types (A and B). Pavlovsky graduated with his medical degree in 1931, then worked as Bernardo Houssay's assistant professor in physiology. In 1947 he reported in Buenos Aires that \"occasionally (in vitro) the blood of some of the haemophilic patients with a greatly prolonged clotting time ... when added to other haemophilic blood possessed a coagulant action nearly as effective as normal blood\". This was later shown to be due to the blood of people with haemophilia B providing the clotting factor factor VIII to correct the defect in those with the more common haemophilia A.", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 12.124884955752215, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 8.5 + }, + { + "index": 6, + "label": "proficient_health_literacy", + "original_doc": "A 34-year-old female, 2 months post\u2013cesarean section (37 weeks) with persistent postoperative wound bleeding and no childhood/adolescent bleeding history, presented with a 4-week illness. The clinical course began with lower back pain attributed to bilateral renal lithiasis; after spontaneous passage of a stone she had 3 days of haematuria and was given tranexamic acid q12h. Three weeks later she developed progressive pain and induration of the left distal thigh. Following intramuscular diclofenac for persistent pain, she developed ecchymosis and ongoing bleeding in the gluteal area despite compression. An outside \u201cparticular Doppler ultrasound\u201d reportedly showed deep venous thrombosis (left lower limb), and she was started on enoxaparin 30 mg SC q24h plus morphine and hospitalized. The next day she developed epigastralgia, blurred vision, HR 117 bpm, BP 113/85 mmHg, and SpO2 93%; enoxaparin was discontinued. Hemoglobin fell from 10.4 g/dL (day prior to admission) to 6.4 g/dL, prompting 2 units of packed red cells. With a working diagnosis of vasculitis, methylprednisolone was started and she was referred for further evaluation.\n\nOn admission she had severe pallor, extensive ecchymosis of the left thigh and lateral knee, and a right thigh haematoma. Hemogram: Hb 9.8 g/dL, normocytic, normochromic. Chemistry notable for glucose 160 mg/dL; AST 52 U/L, ALT 86 U/L. Coagulation profile showed isolated prolongation of the activated partial thromboplastin time (aPTT) to 91.2 s; the remainder of hemogram, biochemistry, electrolytes, liver profile, and coagulation parameters were within reference limits. Soft-tissue ultrasound of the right gluteal region revealed a subcutaneous collection (TCSC) with oedema extending to the upper third of the thigh. Repeat Doppler ultrasound of the left lower limb showed normal flow without thrombosis in the common femoral, superficial, or deep venous systems. Blood and urine cultures were negative. ANA, C3, C4, and ferritin were within reference ranges.\n\nGiven suspected acquired haemophilia, a mixing test demonstrated partial correction of the aPTT. Factor VIII activity was <1.0 U/dL, and a factor VIII inhibitor was detected at 8.64 Bethesda units/mL, confirming acquired haemophilia A, likely postpartum in onset. Therapy included prednisone 50 mg PO at breakfast plus 10 mg at lunch, cyclophosphamide 50 mg (2 tablets) PO q24h, and FEIBA for haemostasis. After 5 days, FEIBA was discontinued due to chest tightness, dyspnoea, and nausea (suspected adverse drug reaction) and replaced with activated recombinant factor VII (rFVIIa; NovoSeven). Clinical evolution was favourable, with decreasing ecchymoses and no new symptoms, and she was discharged.\n\nContext: Postpartum acquired haemophilia A is mediated by autoantibodies to factor VIII and typically presents with isolated aPTT prolongation, low FVIII activity, and an inhibitor measured in Bethesda units. Partial correction on mixing supports an inhibitor pattern. First-line immunosuppression (e.g., prednisone with or without cyclophosphamide) and bypassing agents (FEIBA or rFVIIa) are standard to control bleeding while eradicating the inhibitor.", + "wiki_anchor": "Prevention\nOnly qualified, chemotherapy-certified nurses who have been trained in venipuncture and administration of medications with vesicant and irritant potential should be allowed to administer vesicants.\nChoose a large, intact vein with good blood flow for the venipuncture and placement of the cannula. Do not choose inadvertently \"dislodgeable\" veins (e.g. dorsum of hand or vicinity of joints) if an alternative vein is available.\nThe digits, hands, and wrists should be avoided as intravenous sites for vesicant administration because of the close network of tendons and nerves that would be destroyed if an extravasation occurred.\nPlace the smallest gauge and shortest length catheter to accommodate the infusion.\nMonitor the venipuncture site closely for evidence of infiltration and instructing patients to report any pain, discomfort, or tightness at the site.\nThe IV infusion should be freely flowing. The arm with the infusion should not begin to swell (oedema), \"get red\" (erythema), \"get hot\" (local temperature increase), and the patient should not notice any irritation or pain on the arm. If this occurs, extravasation management should be initiated.\nThe infusion should consist of a suitable carrier solution with an appropriately diluted medicinal/chemotherapy drug inside.\nAfter the IV infusion has finished, flush the cannula with the appropriate fluid.\nFinally, depending on clinical circumstances, central line access may be most appropriate for patients who require repeated administrations of vesicants and irritants.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 12.440442477876108, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 6.75 + }, + { + "index": 7, + "label": "low_health_literacy", + "original_doc": "This is about a 2-day-old newborn boy. He was born at full term by C-section at a private hospital. He came to the children\u2019s hospital because the right side of his scrotum (the sack that holds the testicles) was swollen since birth. In the emergency room, he looked well. His skin was pink and warm. His blood flow looked good. On exam, the right testicle was big and tight. It was not sore when touched. The skin was red and looked rubbed. A light test did not shine through the right side. The light did shine through the left side. There were no signs of a hernia. An urgent ultrasound scan was done. The scan showed the right testicle was larger and looked uneven inside. No blood was flowing to it. The doctors took him quickly to surgery to look inside the scrotum. In surgery, the right testicle was dead because it had twisted, like a kinked hose that stops flow. There was a small amount of fluid. They removed the right testicle. They fixed the left testicle in place to help prevent twisting.", + "wiki_anchor": "Assessing biology\nAfter anesthesia and scrubbing the scrotum with soap and water, the vas deferens is exposed through a small, 1\u20132\u00a0cm incision in the upper scrotum on each side. The vas deferens is cut sharply in half, both above and below the vasectomy site. A special bipolar microcautery is used to judiciously control any bleeding. One end of the vas deferens, termed the abdominal end, is inspected and flushed with salt solution to ensure that it is not blocked as it courses from the scrotum to the prostate (a \u201csaline vasogram\u201d). In order to assess for the presence of possible obstruction above the vasectomy site the testicular end of the vas deferens can be compressed and inspected for fluid. This fluid is examined with a microscope for color, consistency and for sperm. This information is used by some surgeons to decide whether or not a secondary epididymal obstruction is present (see Table below).", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 12.375714285714285, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 7.571428571428571 + }, + { + "index": 7, + "label": "intermediate_health_literacy", + "original_doc": "A full\u2011term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non\u2011tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra\u2011operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.", + "wiki_anchor": "A hydrocele testis feels like a small fluid-filled balloon inside the scrotum. It is smooth, and is mainly in front of the testis. Hydrocele testes vary greatly in size and are typically painless and harmless. However, as the fluid continues to accumulate and the scrotum further enlarges, more discomfort can be expected. Large hydroceles will cause discomfort because of their size. Sometimes pain can be in both testicles as pressure from the enlarged area puts pressure against the unaffected area which can cause discomfort to the normal testicle. It has also been found to decrease a man's sex drive and makes him less active for fear of enlarging the mass. As the fluid of a hydrocele testis is transparent, light shone through the hydrocelic region will be visible from the other side. This phenomenon is called transillumination.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 9.295571776155722, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 6.0 + }, + { + "index": 7, + "label": "proficient_health_literacy", + "original_doc": "A 2\u2011day\u2011old term male neonate, delivered by cesarean section at a private hospital, was referred for a congenital right scrotal swelling and presented to our children\u2019s hospital one day later. On ED arrival he was well hydrated, pink on room air with good perfusion. Physical exam: right hemiscrotum with an enlarged, tense, non\u2011tender, visibly reddish testis and overlying skin excoriation; transillumination negative on the right and positive contralaterally; both hernial orifices normal. Laboratory studies were obtained, and urgent inguinoscrotal Doppler ultrasonography demonstrated an enlarged right testis measuring 15.6 \u00d7 9.4 mm with heterogeneous hypoechoic echotexture, prominent rete testis, and absent intratesticular color Doppler flow. The left testis was normal in size, shape, and echotexture; there was minimal hydrocele. The patient underwent urgent scrotal exploration. Intra\u2011operatively there was frank necrosis of the right testis secondary to intravaginal testicular torsion, with minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed. Contextually, perinatal testicular torsion often presents at or shortly after birth and Doppler evidence of absent flow with heterogeneous hypoechoic parenchyma correlates with nonviability; salvage rates are low when presentation is delayed. Contralateral orchidopexy is commonly performed to mitigate future torsion risk.", + "wiki_anchor": "Imaging technique\nFor any scrotal examination, thorough palpation of the scrotal contents and history taking\nshould precede the sonographic examination. Patients are usually examined in the supine\nposition with a towel draped over their thighs to support the scrotum. Warm gel should\nalways be used because cold gel can elicit a cremasteric response resulting in thickening of\nthe scrotal wall; hence a thorough examination is difficult to be performed. A high\nresolution, near-focused, linear array transducer with a frequency of 7.5\u00a0MHz or greater is\noften used because it provides increased resolutions of the scrotal contents. Images of both\nscrotum and bilateral inguinal regions are obtained in both transverse and longitudinal\nplanes. Color Doppler and pulsed Doppler examination are subsequently performed,\noptimized to display low-flow velocities, to demonstrate blood flow in the testes and\nsurrounding scrotal structures. In evaluation of acute scrotum, the asymptomatic side\nshould be scanned first to ensure that the flow parameters are set appropriately. A\ntransverse image including all or a portion of both testicles in the field of view is obtained to\nallow side-to-side comparison of their sizes, echogenicity, and vascularity. Additional views\nmay also be obtained with the patient performing Valsalva maneuver.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 13.944121212121214, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 7.555555555555555 + }, + { + "index": 8, + "label": "low_health_literacy", + "original_doc": "A 4-year-old boy had blood in his pee and swelling for 5 days. He then had headaches, nausea, and vomiting. He came to the hospital with seizures and very high blood pressure. Blood tests showed a low level of a protein called C3 and signs of a recent strep infection. This meant his kidney filters were inflamed after strep. His brain was affected by the very high blood pressure. Doctors suspected a problem called PRES, which is brain swelling from high pressure. A brain MRI confirmed this. His immune system also attacked his red blood cells. This made his blood level drop very low, to 5 g/dL. He was treated with medicines to lower his blood pressure, steps to protect his brain, and steroid medicines. He left the hospital after 31 days. Six months later, he had no symptoms.", + "wiki_anchor": "Posterior reversible encephalopathy syndrome (PRES), also known as reversible posterior leukoencephalopathy syndrome (RPLS), is a rare condition in which parts of the brain are affected by swelling, usually as a result of an underlying cause. Someone with PRES may experience headaches, changes in vision, and seizures, with some developing other neurological symptoms such as confusion or weakness of one or more limbs. The name of the condition includes the word \"posterior\" because it predominantly though not exclusively affects the back of the brain (the parietal and occipital lobes). Common underlying causes are severely elevated blood pressure, kidney failure, severe infections, certain medications, some autoimmune diseases, and pre-eclampsia. The diagnosis is usually made by a brain scan (MRI) on which areas of swelling can be identified.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 16.532799999999998, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.6 + }, + { + "index": 8, + "label": "intermediate_health_literacy", + "original_doc": "A 4-year-old boy presented after 5 days of visible blood in the urine and leg swelling, plus new headaches, nausea, and vomiting. He developed seizures with a hypertensive emergency. Labs showed low complement C3 and a high anti-streptolysin O (ASO) titer, consistent with acute post-streptococcal glomerulonephritis. He developed encephalopathy, and MRI confirmed posterior reversible encephalopathy syndrome (PRES) secondary to the hypertensive crisis. He also developed autoimmune hemolytic anemia, with hemoglobin falling to 5 g/dL. Treatment included antihypertensive therapy, neuroprotective measures, and corticosteroids. He was discharged after 31 days and remained asymptomatic at 6-month follow-up.", + "wiki_anchor": "Although the pathogenesis is uncertain, it is probable that the symptoms are a consequence of hemorrhagic pulmonary edema, as the hematocrit is lower than normal blood (usually 15-20% less) and the concentration of small proteins is higher than in plasma. It is postulated that the infant suffers from asphyxia with resultant heart attack; this increases pulmonary microvascular pressure, resulting in pulmonary edema. Contributing factors include factors that favor increased filtration of fluid from pulmonary capillaries (e.g., low concentration of plasma proteins, high alveolar surface tension, lung damage, hypervolemia).", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 16.724090909090908, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 9.0 + }, + { + "index": 8, + "label": "proficient_health_literacy", + "original_doc": "A 4-year-old male, two weeks post nasal impetigo treated with topical mupirocin and oral cefadroxil (dose/duration/adherence unknown), presented with 5 days of macroscopic glomerular haematuria and lower-extremity oedema, followed by 12 hours of headache, nausea, and vomiting, and arrived to the ED in convulsive status after 20 minutes of generalized tonic\u2013clonic seizures. On ED arrival he was afebrile, with non-evaluable BP, depressed consciousness, generalized hypertonia, and bilateral pretibial oedema. He was intubated and loaded with phenobarbital 10 mg/kg. In the ICU, BP was 134/94 mmHg (p95 for age 108/66; p95+12 120/78), consistent with hypertensive emergency. Initial labs: urinalysis with haematuria (>100 RBC/hpf), proteinuria 3+, leucocyturia 10\u201325/hpf; creatinine 0.3 mg/dL; anaemia Hct 21%, Hb 7 g/dL with normocytic, normochromic indices; leukocytosis 23,900/mm3; thrombocytosis 756,000/mm3; no elevation of acute-phase reactants; hypocomplementemia with C3 25 mg/dL (VN 80\u2013150) and normal C4. Throat rapid antigen for group A Streptococcus was positive and ASO positive. Non-contrast head CT was unremarkable. Renal ultrasound showed bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullary differentiation. The working diagnosis was nephritic syndrome due to complicated GNAPE with hypertensive emergency and status epilepticus. He required mechanical ventilation and phenobarbital; EEG the next day was normal; CSF was normal. Cefotaxime was started for Streptococcus pyogenes eradication and furosemide for diuresis. By day 2 he developed AKI (creatinine 0.99 mg/dL), hypertension, and 24-hour proteinuria 36.6 mg/m2/h without oliguria. Antihypertensive therapy included amlodipine and IV labetalol with initial control. After extubation at 48 hours, he deteriorated neurologically within 24 hours (GCS 8) with BP > p95+12 despite labetalol infusion up to 3 mg/kg/h, amlodipine 10 mg/day, and furosemide, necessitating reintubation and sodium nitroprusside infusion up to 3 mcg/kg/min with a planned gradual BP reduction of 25% per day to mitigate secondary neurologic injury. Given acute neurologic deficits with severe HTN in GN, PRES was suspected and confirmed by brain MRI on day 5 showing increased subcortical T2/FLAIR signal in bilateral symmetric occipital regions without diffusion restriction, consistent with vasogenic edema. Ophthalmologic exam was normal; repeat EEG showed occasional generalized voltage depression. Enalapril was added. Over 10 days, BP normalized with slow pharmacologic weaning; follow-up MRI on day 12 showed radiologic regression, and he was successfully extubated after 5 days. During the ICU course, Hb fell to 5 g/dL with normocytic, normochromic indices and no thrombocytopenia; hemolytic anemia was diagnosed given a positive direct Coombs test and hemoglobinuria. He required two packed RBC transfusions. Methylprednisolone 1 mg/kg/day was given for 72 hours. Stool culture and urinary antigen for Streptococcus pneumoniae were negative. Serologies for EBV and Parvovirus B19, ENA profile, ANCA, anti-dsDNA, anti-\u03b22 glycoprotein I, anticardiolipin, and lupus anticoagulant were all negative; all cultures (blood, urine, endotracheal aspirate, pharyngeal) were negative. ANA was positive at 1:160. Clinical status improved with BP control, rising complement levels, and resolution of proteinuria and haematuria; the direct Coombs remained positive on hospital day 9. He was discharged on day 31 normotensive, non-anaemic, with preserved renal function, no proteinuria or haematuria, normalized C3, and asymptomatic neurologically. Discharge medications: prednisone, amlodipine, enalapril, and folic acid. He remained asymptomatic with no recurrence at 6 months. Overall, the case represents GNAPE with hypocomplementemia (low C3) and elevated ASO complicated by hypertensive emergency causing encephalopathy and secondary PRES, plus autoimmune hemolytic anemia with Hb nadir 5 g/dL, successfully managed with antihypertensives, neuroprotective measures, and corticosteroids, with full clinical and radiologic recovery.", + "wiki_anchor": "Agranulocytosis, a potentially fatal drop in white blood cell count, basically an exaggerated form of leukopaenia.\n Thrombocytopaenia. A drop in blood platelet counts which are involved in blood clotting. \n Thromboembolism (blood clots; including pulmonary embolism and deep vein thrombosis)\n Rhabdomyolysis (breakdown of muscle tissue leading to the release of myoglobin into the bloodstream which in turn damages the kidneys)\n Alkaline phosphatase increased (an abnormal laboratory parameter)\n Priapism (a painful and enduring erection)\n Urinary hesitation\n Pancreatitis, swelling of the pancreas which supplies the body with insulin. \n Neuroleptic malignant syndrome a potentially fatal complication of antipsychotic drug treatment. Presents with hyperthermia, tremor, tachycardia (high heart rate), mental status change (e.g. confusion), etc.\n Jaundice, which is basically when the body's ability to clear a by product (called bilirubin) of the breakdown of an essential component of the blood called haem, is impaired leading to yellow discolouration of the skin, eyes and mucous membranes. \n Diabetic coma\n Diabetic ketoacidosis. Type II diabetes mellitus is basically where the body cannot effectively utilise sugars to produce energy due to the fact that its cells have become unresponsive to the hormone, insulin, which allows cells to utilise sugars for energy. This in turn forces the body to burn fats for energy and fats require conversion to ketone bodies in order to be utilised by the cells of the body as an energy source. The ketone bodies are acidic hence when the body is entirely reliant on these ketone bodies for energy the levels in the blood reaches a point where it overwhelms the body's natural mechanisms to keep blood pH (a measure of acidity) within a safe range, leading to the blood becoming acidic which is potentially damaging to the tissues of the body due to the ability of acidic environments to denature the proteins of the body. \n Anaphylactic reaction a potentially life-threatening allergic reaction\n Sudden cardiac death", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 16.983489736070386, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 8.5 + }, + { + "index": 9, + "label": "low_health_literacy", + "original_doc": "This 69-year-old man had heart bypass surgery in the past. For 2 months, he got very short of breath with light activity. Tests\u2014a heart tracing, a blood test, and an X-ray movie with dye of the heart arteries\u2014showed heart failure from poor blood flow after a bypass vein to the right heart artery failed. Doctors first opened a totally blocked artery on the left side of his heart. Then they used tiny natural detours between heart arteries to reach the right heart artery from the far end and open it. His breathing was better when he left the hospital. Six months later, his shortness of breath had not come back.", + "wiki_anchor": "Pathophysiology\nWhen pulmonic stenosis (PS) is present, resistance to blood flow causes right ventricular hypertrophy. If right ventricular failure develops, right atrial pressure will increase, and this may result in a persistent opening of the foramen ovale, shunting of unoxygenated blood from the right atrium into the left atrium, and systemic cyanosis. If pulmonary stenosis is severe, congestive heart failure occurs, and systemic venous engorgement will be noted. An associated defect such as a patent ductus arteriosus partially compensates for the obstruction by shunting blood from the left ventricle to the aorta then back to the pulmonary artery (as a result of the higher pressure in the left ventricle) and back into the lungs.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 16.744298245614036, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 6.75 + }, + { + "index": 9, + "label": "intermediate_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Off-pump coronary artery bypass or \"beating heart\" surgery is a form of coronary artery bypass graft (CABG) surgery performed without cardiopulmonary bypass (heart-lung machine) as a treatment for coronary heart disease. It was primarily developed in the early 1990s by Dr. Amano Atsushi. Historically, during bypass surgeries, the heart is stopped and a heart-lung machine takes over the work of the heart and lungs. When a cardiac surgeon chooses to perform the CABG procedure off-pump, also known as OPCAB (Off-pump Coronary Artery Bypass), the heart is still beating while the graft attachments are made to bypass a blockage.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 14.79561224489796, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 7.5 + }, + { + "index": 9, + "label": "proficient_health_literacy", + "original_doc": "A 69-year-old male with prior CABG presented with 2 months of severe dyspnea on mild exertion (NYHA III). ECG showed ST depression in II, III, aVF, and V4\u20136; NT-proBNP was 2640 pg/mL. Echocardiography demonstrated LV systolic dysfunction with LVEF 30%. His history included an inferior STEMI in 2009 with severe 3-vessel disease (proximal LAD CTO, 90% mid/distal LCx stenoses, 95% mid RCA stenosis) treated with CABG (LIMA\u2013LAD; sequential SVG to OM1, OM2, and PL). Current angiography via 6 Fr left radial access showed patent LIMA\u2013LAD and SVG\u2013OM1/OM2, but complete occlusion of the sequential SVG to PL. The native LM was occluded at the ostium and the native RCA was occluded in the mid segment with bridging collaterals. The strategy was to treat the native RCA CTO. Dual arterial access was obtained with an additional 6 Fr right femoral sheath. The right and left coronaries were engaged with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach from the left radial artery failed: neither a Fielder XTR nor a Gaia 3 with a Finecross microcatheter could enter the distal true lumen. A parallel wire technique with a Crusade microcatheter and two Gaia 3 wires also failed. The team then switched to a retrograde approach via septal channels from the LAD through the occluded left coronary system. A Gaia 3 crossed the occluded LM and LAD to reach the distal LAD true lumen. A Sion wire was exchanged via a Finecross into the distal LAD, followed by dilation of the LM and proximal LAD with a 2.0 \u00d7 15 mm balloon. Septal surfing technique (SST) was then used to identify a viable septal channel. A Sion wire, supported by a 150-cm Finecross, was advanced retrogradely through a distal septal branch into the distal RCA. A Gaia 3 traversed the RCA CTO retrogradely into the proximal RCA true lumen and was advanced into a Guidezilla guide extension catheter positioned in the antegrade guide. The Finecross was delivered to the antegrade guide and an RG3 wire was externalized. The CTO segment was predilated with a 2.0 \u00d7 15 mm balloon and stented with two overlapping DES (2.5 \u00d7 38 mm and 3.0 \u00d7 38 mm), achieving an excellent angiographic result with TIMI 3 flow in all distal branches. Dyspnea was relieved at discharge, and at 6-month follow-up there was no recurrence of dyspnea.", + "wiki_anchor": "Assessment of coronary stenoses\nCoronary artery blockages or stenoses that limit blood flow to the heart muscle can cause angina and can be treated by stenting or bypass surgery. Relief of a stenosis by stenting aims to restore vessel patency with improvement in blood flow leading to a reduction in angina symptoms. However, if stenoses are not flow limiting, then they can be safely left alone without stenting or surgery and this help reduce patient's exposure to unnecessary procedures and potential complications. Identifying stenoses that cause flow limitation, or ischaemia, can be done in a variety of ways. Non-invasive tests can include stress testing such as exercise electrocardiograms, stress echocardiography, or perfusion imaging tests such as scintigraphy or SPECT. Alternatively, invasive tests can be performed at the time of angiography, and these include those that measure coronary flow velocity in the vessel, CFR or index flow against pressure gradients such as hyperaemic or basal stenosis resistance (HSR or BSR). More commonly coronary pressure measurements are used as a surrogate for flow measurement and techniques include iFR and fractional flow reserve (FFR). Cardiologists use a combination of these investigations together with the patient's history, symptoms and clinical risk factors to decide if a stenosis requires further treatment. An example of use in clinical practice is seen here.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 15.020925925925926, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 8.666666666666666 + }, + { + "index": 10, + "label": "low_health_literacy", + "original_doc": "A 51-year-old man came to us with sudden, painful vision loss in his left eye for three days. His right eye could see clearly (20/20). His left eye could only see hand movements. The back of his left eye showed swelling of the seeing nerve, a bulge in the layer under the retina, several patches of fluid under the retina, and wrinkles in the thin lining there. An MRI scan with contrast dye of the eyes and brain showed a small lump behind the eye where the eye nerve meets the white part of the eye. Tests for cancer and immune diseases were normal. The doctors diagnosed inflammation in the back part of the eye\u2019s white coat that forms a small lump (nodular posterior scleritis). They started high-dose steroid pills by mouth (prednisolone).", + "wiki_anchor": "Signs and symptoms \nThe onset of ocular symptoms are usually preceded by episode of viral or flu-like symptoms such as fever, cough or sore throat (however this is not always the case). Patients can typically present erythema nodosum, livido reticularus, bilateral uveitis, and sudden onset of marked visual loss associated with the appearance of multiple lesions in the retina. These lesions may be colored from grey-white to cream-shaded yellow.\nOther symptoms include scotomata and photopsia. In weeks to a month times the lesions begin to clear and disappear (with prednisone) leaving behind areas of retinal pigment epithelial atrophy and diffuse fine pigmentation (scarring). Rarely choroidal neovascularization occur as a late onset complication.", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 13.182857142857145, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 7.5 + }, + { + "index": 10, + "label": "intermediate_health_literacy", + "original_doc": "A 51-year-old man presented with 3 days of sudden, painful vision loss in the left eye. Visual acuity was 20/20 in the right eye and hand motion in the left eye. Left fundus findings included optic nerve head swelling, choroidal bulging, multiple areas of subretinal fluid, and RPE corrugations. Orbital/brain MRI with gadolinium showed a retrobulbar nodular mass enhancing at the junction of the optic nerve and sclera. Oncology and rheumatology evaluations were unremarkable. The clinical diagnosis was nodular posterior scleritis, and oral prednisolone was started.", + "wiki_anchor": "Optic papillitis is a specific type of optic neuritis. Inflammation of the optic nerve head is called \"papillitis\" or \"intraocular optic neuritis\"; inflammation of the orbital portion of the nerve is called \"retrobulbar optic neuritis\" or \"orbital optic neuritis\". It is often associated with substantial losses in visual fields, pain on moving the globe, and sensitivity to light pressure on the globe. It is often an early sign of multiple sclerosis.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 13.270528169014085, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.25 + }, + { + "index": 10, + "label": "proficient_health_literacy", + "original_doc": "A 51-year-old male presented with acute, painful visual loss of the left eye (LE) for 3 days. Best-corrected distance visual acuity (BCDVA) was 20/20 OD and hand motion (HM) OS. Ocular motility and anterior segment were unremarkable OU. Fundus OS showed optic nerve head (ONH) swelling, choroidal bulging, multiple patches of subretinal fluid (SRF), and retinal pigment epithelial (RPE) corrugations; OD fundus was unremarkable.\n\nMultimodal imaging was obtained: OCT (OptoVue, Inc., Fremont, CA, USA; software version 2018.0.0.18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Indocyanine green angiography (ICGA) showed a geographic macular hypocyanescent area OS. Blue-autofluorescence (BAF) revealed a geographic macular area with speckled autofluorescence. B-scan ultrasonography showed optic nerve enlargement. Fluorescein angiography (FA) demonstrated vascular leakage at the ONH (hot disc) and a geographic patchy hypofluorescent area with speckled hyperfluorescent margins measuring approximately three disc diameters. Orbital and brain MRI with gadolinium revealed a retrobulbar nodular enhancing mass at the optic nerve\u2013sclera junction. Oncology consultation was unremarkable.\n\nGiven concern for malignancy and the enhancing orbital nodule, the patient underwent transconjunctival lateral orbitotomy one week after presentation. Intraoperatively, a pink localized scleral nodule with edematous Tenon was identified. With a clinical diagnosis of nodular posterior scleritis, sub-Tenon triamcinolone acetonide was administered. The patient declined admission and intravenous corticosteroids; oral prednisolone 50 mg/Kg was initiated. Rheumatologic and infectious work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable.\n\nAt the one-week postoperative follow-up, BCDVA was 20/20 OD and counting fingers at 2 meters OS. SRF had resolved, and the macula was atrophic. Oral prednisolone was tapered over three months.", + "wiki_anchor": "Indications\nIndications for indocyanine green angiography include:\n Choroidal neovascularisation (CNV): Indocyanine green angiography is widely used to study choroidal neovascularization in patients with exudative age-related macular degeneration. In ICGA, CNV is seen as hyperflourescent spot or plaque. It is also useful in diagnosing and classifying CNV associated to serous pigment epithelial detachments in Nonexudative macular degeneration.\n Idiopathic polypoidal choroidal vasculopathy (IPCV)\n Pigmented choroidal melanomas\n Choroidal haemangioma: ICGA can be used to differentiate choroidal haemangioma from other intraocular tumors.\n Choroiditis: In multifocal choroiditis, lesions are visualized as hypoflourescent spots.\n Chorioretinopathy: In Central serous chorioretinopathy, using ICGA multifocal areas of choroidal hyperpermiability can be visualized. In birdshoot chorioretinopathy, lesions appear as symmetrical round or oval hypoflourescent spots. ICGA allows better visualization of lesions in serpiginous chorioretinopathy, punctate inner chorioretinopathy, acute zonal occult outer retinopathy etc. In multiple evanescent white dot syndrome, numerous hypoflourescent spots can be visualized using ICGA.\n Pigmented epithelial detachment\n Retinal angiomatous proliferation (RAP)\n Chorioretinal atrophy: ICGA help evaluating different stages of chorioretinal atrophy.\n Anterior uveitis: ICGA is rarely indicated in anterior uveitis, but it might be used to find out associated choroidal pathology.\n Stargardt disease: Numerous hypoflourescent spots are seen in ICGA.\n Angioid streaks: ICGA can be used for diagnosing angioid streaks and their associated ocular pathologies.\n Vogt\u2013Koyanagi\u2013Harada disease (VKH): ICGA is useful in diagnosing VKH. In VKH, delay in filling of the choriocapillaris along with larger choroidal vessel perfusion and multiple hypofluorescent spots are visible with ICGA.\n Sympathetic ophthalmia: Sympathetic ophthalmia is a bilateral, granulomatous form of uveitis. In sympathetic ophthalmia, numerous dark spots may be visible during the intermediate phase of ICGA.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 16.04865704772475, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 6.0 + }, + { + "index": 11, + "label": "low_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Methods\nProtocols vary depending on local standard procedures and the extremity being operated on. A vast majority of practitioners begin by exsanguinating the limb as Bier did with an elastic bandage (Esmarch bandage), squeezing blood proximally toward the heart, then pneumatic tourniquets are applied to the limb and inflated 30mmHg above arterial pressure to occlude all blood vessels and then the elastic bandage is removed. A high dose of local anesthetic, typically lidocaine or prilocaine without adrenaline, is slowly injected as distally as possible into the exsanguinated limb. The veins are filled with the anesthetic, with the anesthetic setting into local tissue after approximately 6\u20138 minutes, after which the surgery, reduction, or manipulation of the region may begin. It is important that the region is isolated from active blood flow at this time. Analgesic effect typically remains for up to two hours depending on the dosage and type of anesthetic agent being used. The wait time and isolation of blood flow from the region is important for avoiding an overdose of the anesthetic agent in the blood which can lead to hypotension, convulsions, arrhythmia and death. Cardiotoxic local anesthetic agents like bupivacaine and etidocaine are strictly contraindicated.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 15.577201776649748, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 7.625 + }, + { + "index": 11, + "label": "intermediate_health_literacy", + "original_doc": "A 78-year-old man from the Amhara region, Ethiopia, with a permanent pacemaker placed for complete heart block was scheduled for retropubic prostatectomy. The anesthesia and cardiology teams recommended switching his dual-chamber, rate\u2011modulated pacemaker to an asynchronous mode perioperatively to reduce the risk of electromagnetic interference during surgery. He could not afford reprogramming and chose to proceed with the existing plan after informed consent; permission to publish the case was obtained after the operation. He received combined spinal\u2013epidural anesthesia at L3\u2013L4 using 0.5% isobaric bupivacaine 2.5 ml (12.5 mg) plus fentanyl 50 \u00b5g. Standard ASA monitoring was applied with special attention to cardiac stability. Intraoperatively, he remained stable with minimal changes in vital signs; blood pressure was supported with isotonic saline as needed. Postoperatively, he was monitored in the PACU, received analgesia at 4 hours with an epidural top\u2011up, and was transferred to the ward about 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in good condition.", + "wiki_anchor": "Methods\nProtocols vary depending on local standard procedures and the extremity being operated on. A vast majority of practitioners begin by exsanguinating the limb as Bier did with an elastic bandage (Esmarch bandage), squeezing blood proximally toward the heart, then pneumatic tourniquets are applied to the limb and inflated 30mmHg above arterial pressure to occlude all blood vessels and then the elastic bandage is removed. A high dose of local anesthetic, typically lidocaine or prilocaine without adrenaline, is slowly injected as distally as possible into the exsanguinated limb. The veins are filled with the anesthetic, with the anesthetic setting into local tissue after approximately 6\u20138 minutes, after which the surgery, reduction, or manipulation of the region may begin. It is important that the region is isolated from active blood flow at this time. Analgesic effect typically remains for up to two hours depending on the dosage and type of anesthetic agent being used. The wait time and isolation of blood flow from the region is important for avoiding an overdose of the anesthetic agent in the blood which can lead to hypotension, convulsions, arrhythmia and death. Cardiotoxic local anesthetic agents like bupivacaine and etidocaine are strictly contraindicated.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 15.577201776649748, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 7.625 + }, + { + "index": 11, + "label": "proficient_health_literacy", + "original_doc": "A 78-year-old male from the Amhara region of Ethiopia with a 7-year history of a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy for BPH after prior TURP 3 months earlier. Comorbidities included long-standing hypertension (amlodipine 5 mg daily, enalapril 10 mg BID, atorvastatin 10 mg daily) and type 2 diabetes mellitus (metformin 500 mg BID; NPH insulin 20 IU AM/10 IU PM). Preoperative evaluation showed complete bundle branch block on ECG; electrophysiology assessment demonstrated LVH due to hypertensive heart disease with mild diastolic dysfunction and an EF of 62%. Abdominal ultrasound showed an 82-ml prostate; AP chest X-ray was normal with a left-sided pacemaker in situ; electrolytes and troponin were normal. He had a frailty score of 5.5, METs 3.4, and an RCRI class III, indicating an estimated 10.1% risk of major adverse cardiac events within 30 days and intermediate surgical risk. Multidisciplinary planning recommended reprogramming the dual-chamber, rate\u2011modulated pacemaker to an asynchronous mode to mitigate intraoperative electromagnetic interference risk. Due to financial and logistical constraints, reprogramming was not performed; risks were disclosed, and he consented to proceed. Preoperatively, usual medications were continued (with a lower morning NPH dose at two\u2011thirds); diazepam 5 mg PO was given at midnight for anxiolysis. On the day of surgery, random blood glucose was checked and managed with a sliding scale. Team communication emphasized CIED precautions (electrosurgery pad positioned away from the device; emergency drugs and defibrillator immediately available). Dexamethasone was given for PONV prophylaxis and paracetamol for preemptive analgesia. ASA standard monitoring was applied and baselines recorded. An L3\u2013L4 combined epidural\u2013spinal anesthetic was performed using 0.5% isobaric bupivacaine 12.5 mg (2.5 ml) plus fentanyl 50 \u00b5g, achieving a sensory level to T7. The procedure used a midline infraumbilical incision; monopolar cautery at low voltage (20 mA) with bipolar low\u2011voltage cautery for hemostasis. Intraoperative hemodynamics remained within 10% of baseline without cardiorespiratory events; blood pressure was maintained with isotonic saline. Postoperatively, he was transferred to PACU with vigilant monitoring; analgesia was administered at 4 hours with an epidural top\u2011up, and he was transferred to the ward approximately 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in stable condition, with cardiology follow\u2011up advised. Informed consent was obtained, and permission for case report publication was granted after the operation.", + "wiki_anchor": "Selected publications\n Diastolic properties predict short-term postoperative risk and duration of pleural effusions after the fontan operation. Garofalo CA, Cabreriza SE, Quinn TA, Weinberg AD, Quaegebeur JM, Spotnitz HM, Mosca RS. Circulation. 114(1 Suppl):I56-61. 4 July 2006.\n Left ventricular pacing site-timing optimization during biventricular pacing using a multielectrode patch. Berberian G, Cabreriza SE, Quinn TA, Garofalo CA, Spotnitz HM. Ann. Th. Surg. 82(6):2292-4. Dec 2006.\n Surgical Considerations of Pacemakers and Automatic Defibrillators, in Cohn L, Cardiac Surgery in the Adult. Spotnitz HM. 2nd Ed., McGraw-Hill, 2003.\n Booth JH, Quinn TA, Richmond ME, Cabreriza SE, Weinberg AD, Johnston T, Spotnitz HM. Cardiac output measurement by arterial pressure waveform analysis during optimization of biventricular pacing after cardiac surgery. ASAIO J 2009 Nov-Dec;55(6):587-91.\nQuinn TA, Cabreriza SE, Richmond ME, Weinberg AD, Holmes JW, Spotnitz HM. Simultaneous variation of ventricular pacing site and timing with biventricular pacing in acute ventricular failure improves function by interventricular assist. Am J Physiol Heart Circ Physiol 2009 Dec; 297(6): H2220-6. \nSpotnitz HM. Ventricular function in surgery for congenital Heart Disease. World J of Surg [Epub ahead of print 2009 Nov 17].\nRusanov A, Spotnitz HM. 15-year experience with permanent pacemaker and defibrillator lead and patch extractions. Ann Thorac Surg 2010;89:44-50.\nBonney WJ, Spotnitz HM, Liberman L, Silver ES, Ceresnak SR, Hordof AJ, Pass RH. Survival of transvenous ICD leads in young patients. Pacing Clin Electrophysiol 2010;33:186-91.\nGeorge E, Cabreriza SE, Quinn TA, Rusanov A, Gerrah R, Broyles JM, Weinberg AD, Spotnitz HM. Validation of automated monitoring of cardiac output for biventricular pacing optimization. ASAIO J. Abstract. 2010; 56:265\u2013269.\nGray RG, Cabreriza SE, Quinn TA, Weinberg AD, Spotnitz HM. Feasibility of in vivo pressure measurement using a pressure-tip catheter via transventricular puncture. 2010; 56:194\u2013199.\nSpotnitz ME, Richmond ME, Quinn TA, Cabreriza SE, Wang DY, Albright CM, Weinberg AD, Dizon JM, Spotnitz HM. Relation of cardiac output to QRS duration during temporary resynchronization therapy after cardiac surgery. ASAIO J. 2010; Epub ahead of print", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 11.051111111111112, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 4.972222222222222 + }, + { + "index": 12, + "label": "low_health_literacy", + "original_doc": "A 52-year-old woman had burning when she peed and had to pee very often for a long time. She tried many treatments for bladder infections, but the problem did not go away. Regular scans and lab tests looked normal. A camera test that looked inside her bladder showed the lining was red and irritated, with tiny bits floating in the urine. Later, the lab saw a live larva (a baby insect) in her urine under the microscope. That finding explained her symptoms. She was told to keep very clean. She was also told to drink plenty of water every day.", + "wiki_anchor": "Clinical features\nPatients with urinary tract infections caused by S. saprophyticus usually present with symptomatic cystitis. Symptoms include a burning sensation when passing urine, the urge to urinate more often than usual, a 'dripping effect' after urination, weak bladder, a bloated feeling with sharp razor pains in the lower abdomen around the bladder and ovary areas, and razor-like pains during sexual intercourse. Flank pain may occur due to infection of the upper urinary tract, such as pyelonephritis. Signs and symptoms of renal involvement are also often registered.", + "doc_fkgl": 6.041, + "wiki_fkgl": 12.897149425287356, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 9.25 + }, + { + "index": 12, + "label": "intermediate_health_literacy", + "original_doc": "A 52-year-old woman had ongoing dysuria and urinary frequency despite multiple treatments for presumed infections. Cystoscopy showed bladder redness and debris, while imaging and routine lab tests were unremarkable. Eventually, a live larva was identified in the urine, confirming the cause of her symptoms. Management focused on better personal hygiene and increased fluid intake.", + "wiki_anchor": "Hemorrhagic cystitis or haemorrhagic cystitis is an inflammation of the bladder defined by lower urinary tract symptoms that include dysuria, hematuria, and hemorrhage. The disease can occur as a complication of cyclophosphamide, ifosfamide and radiation therapy. In addition to hemorrhagic cystitis, temporary hematuria can also be seen in bladder infection or in children as a result of viral infection.", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 15.480000000000004, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 8.333333333333334 + }, + { + "index": 12, + "label": "proficient_health_literacy", + "original_doc": "A 52-year-old woman presented with a three-year history of urinary frequency, dysuria, and dribbling, along with intermittent passage of red and black thread-like material in the urine. Episodes with these discharges were associated with headache, fever, and chills, and she reported intermittent periurethral and genital pruritus. She had been repeatedly treated for recurrent urinary tract infections without clinical improvement. She denied recent travel, camping, hiking, farming, swimming, or insect bites. Past surgical history included pilonidal sinus surgery (8 years prior) and hysterectomy (7 years prior). Two years before the current visit, she was hospitalized for evaluation. Examination revealed a well-appearing patient with normal vital signs. Laboratory testing, including complete blood count, urinalysis, and serum chemistries, was within normal limits. Abdominopelvic CT was unremarkable. Cystoscopy demonstrated erythema and hyperemia of the bladder mucosa, suspended intravesical debris, and dilatation of the left ureteral orifice. Schistosomiasis was suspected and she received praziquantel at appropriate dose and duration, without improvement. A second infectious diseases consultation raised suspicion for urinary myiasis, and ivermectin was prescribed, again without benefit. She underwent bladder irrigation with polyethylene glycol; no visible larvae were recovered from the washings, and she experienced self-limited hematuria for two days post-procedure. A subsequent random urinalysis was normal. However, a 24-hour urine collection demonstrated a live larva on light microscopy. The specimen was isolated and identified morphologically by an entomologist as Sarcophaga spp. Final management emphasized personal hygiene measures and liberal oral hydration.", + "wiki_anchor": "Diagnosis \nDue to the atypical presentation and rarity of the infection, it takes a physician longer to diagnose than more common types of bladder infections. Diagnosis requires a personalized investigation with consideration to risk factors and symptoms. Radiology of the abdominal or pubic region has proven to be an important tool in reaching a definitive diagnosis of conditions causing gas in the urinary tract. Computer tomography, or CT scans, are of most help due to their high sensitivity in detecting gas and air bubbles. However, radiology is normally not the first tool used to diagnose. Most diagnoses are made by chance after imaging examination. Sometimes, even when patients don't show symptoms, their Emphysematous cystitis infection level can be very advanced already. Gas in the bladder wall will often have the appearance of cobblestone or a \u201cbeaded necklace\u201d with the use of conventional radiography. Delayed diagnosis can lead to a severe infection, extension of the uterus, rupturing of the bladder, and death. Emphysematous cystitis has an overall mortality rate of 7%. However, surgery is only considered in severe cases where the disease progresses involving the ureters, kidneys, or adrenal glands. When required, surgery may be extensive.", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 13.258269230769233, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.416666666666667 + }, + { + "index": 13, + "label": "low_health_literacy", + "original_doc": "A 36-year-old woman had a long-term bowel disease (ulcerative colitis). She came in with chest pain that kept getting worse. She also had shortness of breath, sweating, and felt sick to her stomach. For months she had felt very tired and had night sweats. Her heart test (EKG) showed signs of a heart attack in the lower part of the heart. Doctors did a dye X-ray to look at the heart arteries. It showed bad blockages in two heart pipes. They opened the most blocked pipe right away with a balloon and a tiny mesh tube (stent). While looking, the team worried the main body artery (aorta) was swollen. Blood tests showed mild inflammation. A special CT scan showed the aorta wall looked thick and scarred, with tight narrow spots in several arteries. This pointed to a rare illness that causes swollen big arteries, called Takayasu arteritis. She started strong anti-inflammatory and immune medicines (prednisone and methotrexate). Later she had heart bypass surgery to improve blood flow. She did well after treatment.", + "wiki_anchor": "Of note is the function of renal artery stenosis in the causation of high blood pressure: Normally perfused kidneys produce a proportionate amount of a substance called renin. Stenosis of the renal arteries causes hypoperfusion (decreased blood flow) of the juxtaglomerular apparatus, resulting in exaggerated secretion of renin, and high blood levels of aldosterone, eventually leading to water and salt retention and high blood pressure. The neurological symptoms of the disease vary depending on the degree; the nature of the blood vessel obstruction; and can range from lightheadedness to seizures (in severe cases). One rare, important feature of the Takayasu's arteritis is ocular involvement in form of visual field defects, vision loss, or retinal hemorrhage. Some individuals with Takayasu's arteritis may present with only late vascular changes, without a preceding systemic illness. In the late stage, weakness of the arterial walls may give rise to localized aneurysms. As with all aneurysms, the possibility of rupture and vascular bleeding is existent and requires monitoring. In view of the chronic process and good collateral development, Raynaud's phenomenon or digital gangrene are very rare in Takayasu arteritis. A rare complication of this condition are coronary artery aneurysms.", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 14.470274914089348, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 7.111111111111111 + }, + { + "index": 13, + "label": "intermediate_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Those with the disease often notice symptoms between 15 and 30 years of age. In the Western world, atherosclerosis is a more frequent cause of obstruction of the aortic arch vessels than Takayasu's arteritis. Takayasu's arteritis is similar to other forms of vasculitis, including giant cell arteritis which typically affects older individuals. Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery, Takayasu's arteritis can present as pulseless upper extremities (arms, hands, and wrists with weak or absent pulses on the physical examination) which may be why it is also commonly referred to as the \"pulseless disease.\" Involvement of renal arteries may lead to a presentation of renovascular hypertension.", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 15.397495934959352, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 8.4 + }, + { + "index": 13, + "label": "proficient_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Assessment of coronary stenoses\nCoronary artery blockages or stenoses that limit blood flow to the heart muscle can cause angina and can be treated by stenting or bypass surgery. Relief of a stenosis by stenting aims to restore vessel patency with improvement in blood flow leading to a reduction in angina symptoms. However, if stenoses are not flow limiting, then they can be safely left alone without stenting or surgery and this help reduce patient's exposure to unnecessary procedures and potential complications. Identifying stenoses that cause flow limitation, or ischaemia, can be done in a variety of ways. Non-invasive tests can include stress testing such as exercise electrocardiograms, stress echocardiography, or perfusion imaging tests such as scintigraphy or SPECT. Alternatively, invasive tests can be performed at the time of angiography, and these include those that measure coronary flow velocity in the vessel, CFR or index flow against pressure gradients such as hyperaemic or basal stenosis resistance (HSR or BSR). More commonly coronary pressure measurements are used as a surrogate for flow measurement and techniques include iFR and fractional flow reserve (FFR). Cardiologists use a combination of these investigations together with the patient's history, symptoms and clinical risk factors to decide if a stenosis requires further treatment. An example of use in clinical practice is seen here.", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 15.020925925925926, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 8.666666666666666 + }, + { + "index": 14, + "label": "low_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Complications\nComplications are not common but include infection, lung abscess, and bronchopleural fistula (a fistula between the pleural space and the bronchial tree). A bronchopleural fistula results when there is a communication between the laceration, a bronchiole, and the pleura; it can cause air to leak into the pleural space despite the placement of a chest tube. The laceration can also enlarge, as may occur when the injury creates a valve that allows air to enter the laceration, progressively expanding it. One complication, air embolism, in which air enters the bloodstream, is potentially fatal, especially when it occurs on the left side of the heart. Air can enter the circulatory system through a damaged vein in the injured chest and can travel to any organ; it is especially deadly in the heart or brain. Positive pressure ventilation can cause pulmonary embolism by forcing air out of injured lungs and into blood vessels.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 14.241315789473685, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 7.833333333333333 + }, + { + "index": 14, + "label": "intermediate_health_literacy", + "original_doc": "A 36-year-old woman had dysphagia due to a congenital right aortic arch with mirror-image branching.\nIn this rare pattern, the aorta runs to the right, wraps around the right main bronchus, and the head-and-arm arteries branch in the reverse order of normal.\nMost people have no symptoms unless the aorta or an associated bulge compresses the esophagus or trachea.\nSurgery is considered for major airway or esophageal compression, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm.\nThere is no standard operation; treatment is tailored to the person\u2019s anatomy and symptoms.\nIn this case, imaging showed external compression of the upper esophagus with a small Kommerell diverticulum (about 1.3 cm), so no intervention was performed and her symptoms improved.", + "wiki_anchor": "Presentation\nThis condition is usually asymptomatic. The aberrant artery usually arises just distal to the left subclavian artery and crosses in the posterior part of the mediastinum on its way to the right upper extremity. In 80% of individuals it crosses behind the esophagus. Such course of this aberrant vessel may cause a vascular ring around the trachea and esophagus.\nDysphagia due to an aberrant right subclavian artery is termed dysphagia lusoria, although this is a rare complication. In addition to dysphagia, aberrant right subclavian artery may cause stridor, dyspnoea, chest pain, or fever. An aberrant right subclavian artery may compress the recurrent laryngeal nerve causing a palsy of that nerve, which is termed Ortner's syndrome.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 13.150443349753697, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.428571428571429 + }, + { + "index": 14, + "label": "proficient_health_literacy", + "original_doc": "A 36-year-old female presented with dysphagia and longstanding cervical and upper thoracic pain; she also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit after barium ingestion showed a posterior and lateral right impression on the proximal esophagus extending 3.5 cm craniocaudally, with an estimated maximal esophageal stenosis of 60%. Cervical and thoracic CT revealed a congenital anomaly of the aortic arch: a right aortic arch with mirror-image branching. The arch originated from the aortic root, coursed above the right stem bronchus, and gave rise to the three supra-aortic trunks as follows: (1) left brachiocephalic artery (giving rise to the left common carotid artery and the left subclavian artery), (2) right common carotid artery, and (3) right subclavian artery. The aortic arch then passed posterior to the esophagus and exhibited a small anterior saccule measuring 1.3 cm, consistent with a Kommerell diverticulum. This configuration formed a vascular ring around the tracheo-esophageal pair, bounded posterolaterally on the right by the aortic arch, posterolaterally on the left by the Kommerell diverticulum, laterally on the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. Gastroscopy confirmed endoluminal impact of extrinsic compression. Given minimal clinical repercussions and absence of nutritional disorders, no surgical cure was performed. The evolution was favorable with patient-reported spontaneous amelioration of symptoms.\n\nContext: Right aortic arch with mirror-image branching is a rare anomaly of embryologic development. The vast majority of patients are asymptomatic unless mediastinal structures are compressed. Indications for surgery include major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm. There is no standardized treatment; management is individualized according to clinical presentation and anatomic configuration.", + "wiki_anchor": "Structure\nThe aorta begins at the level of the upper border of the second/third sternocostal articulation of the right side, behind the ventricular outflow tract and pulmonary trunk. The right atrial appendage overlaps it. The first few centimeters of the ascending aorta and pulmonary trunk lies in the same pericardial sheath. and runs at first upward, arches over the pulmonary trunk, right pulmonary artery, and right main bronchus to lie behind the right second coastal cartilage. The right lung and sternum lies anterior to the aorta at this point. The aorta then passes posteriorly and to the left, anterior to the trachea, and arches over left main bronchus and left pulmonary artery, and reaches to the left side of the T4 vertebral body. Apart from T4 vertebral body, other structures such as trachea, oesophagus, and thoracic duct (from front to back) also lies to the left of the aorta. Inferiorly, the arch of aorta is connected to ligamentum arteriosum while superiorly, it gives rise to three main branches. Arch of aorta continues as the descending aorta after T4 vertebral body.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 12.532222222222224, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 5.8 + }, + { + "index": 15, + "label": "low_health_literacy", + "original_doc": "This story is about a 62-year-old white North African woman. She was diagnosed in 2021 with a rare condition called Von Hippel\u2013Lindau disease. This condition caused growths in several parts of her body. She had a tumor in a bone near her left ear. She had a tumor in the left adrenal gland, which sits above the kidney. She had cancer in her left kidney. Her right kidney had many cysts. She also had growths in her pancreas. She received several treatments. She had radiation treatment. She had surgery to remove the left adrenal gland. She had surgery to remove the left kidney. She had major surgery on the pancreas and nearby small intestine. Later, ultrasound and MRI scans showed a lump with both fluid and solid parts near the left ovary and tube. Keyhole surgery looked inside the pelvis. It found cyst-type tumors in the thin support tissue next to both fallopian tubes. Doctors then removed the uterus and both ovaries and tubes. The lab checked the tissue. It showed tumors of the same type on both sides in the thin support tissue around the tubes and the uterus. These findings fit with Von Hippel\u2013Lindau disease.", + "wiki_anchor": "Presentation\nLPF presents as an ill-defined, slow growing tumor mass located in or below the subcutaneous tissue (area of the skin below the dermis) of an extremity or, less commonly, the thigh, trunk, or head areas. Rare single cases of these tumors have been reported in occur in the heart and eye socket. These tumors are often painless but in some cases become painful when manipulated during examination. LPF tumors occur almost exclusively in children at birth (~18% of cases) up to age 8 years with most cases presenting before age 2 years; they are extremely rare in adults. The disorder has a 2:1 male predominance. LPD tumors are usually 5\u00a0cm. or smaller and obvious on physical examination. Uncommonly, LPF tumors present after they have invaded adjacent underlying structures such as blood vessels, nerves, and muscles although significant functional impairment of the invaded tissues is uncommon. Individuals have also presented with recurrences of these tumors at the site of surgery in up to 1/3 of all surgically treated cases.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 12.322549019607845, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 6.333333333333333 + }, + { + "index": 15, + "label": "intermediate_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Pathogenesis \nThe von Hippel\u2013Lindau tumor suppressor gene generally has a germline mutation. This suppressor gene is also called elongin binding protein and G7 protein. The VHL protein is involved in up-regulation of hypoxic response via the [[hypoxia inducible factor [HIF]-1 alpha]]. Mutations generally prevent the production of any functional VHL protein or result in a change of structure of VHL protein. This genetic disorder shows an autosomal dominant inheritance pattern, with about 20% of patients possessing a new mutation. There are usually several other tumors which are part of the syndrome, including tumors of the central nervous system, kidneys, pancreas, adrenal glands, epididymis, broad ligament, along with the endolymphatic sac. The vast majority of patients with an endolymphatic sac tumor have von Hippel-Lindau syndrome.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 13.015345622119813, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.857142857142857 + }, + { + "index": 15, + "label": "proficient_health_literacy", + "original_doc": "A 62-year-old Tunisian Arab postmenopausal woman with Von Hippel\u2013Lindau (VHL) disease (diagnosed 2021) had multisystem involvement. In 2021 she had a 6 cm left petrous bone endolymphatic sac tumor managed with radiotherapy; a 6 cm left pheochromocytoma treated with left adrenalectomy (pathology: pheochromocytoma); and a ruptured left renal mass treated with left nephrectomy (microscopy: multifocal clear-cell renal cell carcinoma, nuclear grade 2). In 2022 she underwent cephalic duodenopancreatectomy for a pancreatic mass; histology showed three serous cystadenomas and two well-differentiated neuroendocrine tumors. In January 2021, surveillance abdominal\u2013pelvic CT incidentally identified a 4 cm solid\u2013cystic left adnexal mass suspected to be malignant; this was confirmed on transvaginal ultrasound and pelvic MRI and classified O-RADS 5. Gynecologic exam was unremarkable. At laparotomy via a midline infraumbilical incision, a well-defined solid\u2013cystic mass was found in the left adnexa. There was no ascites, no peritoneal carcinomatosis, and the right adnexa appeared grossly normal without exocystic vegetations. Peritoneal cytology was obtained. Left adnexectomy was performed and the specimen sent for frozen section, which was inconclusive, raising the differential of a borderline tumor versus a VHL-associated tumor. Given her postmenopausal status, total hysterectomy with right adnexectomy was completed. Final histology demonstrated bilateral clear-cell papillary cystadenomas of the Fallopian tubes and broad ligament, measuring 0.5 cm on the right and 4 cm on the left. The tumors were composed of tightly packed papillae with fibrous cores lined by monolayered epithelium, consistent with VHL-associated mesosalpinx/broad ligament lesions. The postoperative course was uneventful; 1-month postoperative evaluation was normal. She has been followed every 4 months with normal pelvic ultrasound for 2 years, and was recently readmitted to neurosurgery for recurrence of a brain tumor.", + "wiki_anchor": "Presentation\nIndividuals presenting with SEF tumors are 3 to 87 years old (median age 44.6 years) with most individuals aged 30-60\u202fyears. These tumors involve the lower limb and shoulder areas (28.3% of cases), trunk (18.7%), head and neck areas (11.7%), lung and its pleura (10.0%), bone (including the spinal vertebrae) (10.0%), soft tissues (9.1%), upper limb and shoulder areas (7.5%), kidney (3.9%), pancreas (0.9%), liver (0.4%), and brain (0.4%). Rare cases of SEF tumors have developed in the ovary and lower gastrointestinal tract. In two separate studies, 17% and 27% of patients presented with metastases at the time of the initial diagnosis of their disease. While most individuals present with a painless mass, about 33% report having a painful and enlarging mass. The tumor may have been noticed and even painful for a few months to years. Tumors developing in the head, abdominal cavity, or other space-constrained sites often present with symptoms and signs related to their tumors' mass effects. For example, 5 of 5 patients diagnosed with SEF tumors in the spinal vertebrae presented with pain that they had experienced for 3 to 6 months and 2 of 2 patients with a SEF located in the buttock presented with highly painful sciatica. SEF tumors have varied in size from 1 to 25 cm in diameter (average diameter, 8.3 cm). In one small study, all individuals treated with surgical resection of their tumors, re-presented with recurrences of their tumors at the sites of their surgical removal and 91% re-presented with metastases (67% to the lung, 50% to bone, and 1 case each to the liver, brain and abdomen).", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 8.355900159320235, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 8.4 + }, + { + "index": 16, + "label": "low_health_literacy", + "original_doc": "A 59-year-old man with type 1 diabetes came to the hospital with heart failure. A heart ultrasound showed big clumps of germs stuck to two heart valves, the mitral and the aortic valves. His blood test grew a germ called Staphylococcus warneri. This is a kind of staph that usually lives on the skin and is normally harmless. Doctors found he had an infection on his own heart valves (native valve endocarditis). He later had surgery to replace both the mitral and the aortic valves. Looking back, small lab changes and weight loss that began about four months earlier may have been early warning signs. He had not been on immune-weakening medicines and did not have any implanted medical devices.", + "wiki_anchor": "Rheumatic fever (RF) is an inflammatory disease that can involve the heart, joints, skin, and brain. The disease typically develops two to four weeks after a streptococcal throat infection. Signs and symptoms include fever, multiple painful joints, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of the cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks but can sometimes occur after one. The damaged valves may result in heart failure, atrial fibrillation and infection of the valves.", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 11.152113402061858, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 6.833333333333333 + }, + { + "index": 16, + "label": "intermediate_health_literacy", + "original_doc": "A 59-year-old man with long-standing type 1 diabetes presented with acute heart failure. An echocardiogram showed large vegetations on the mitral and aortic valves. Blood cultures were positive for Staphylococcus warneri, a coagulase\u2011negative staphylococcus commonly found on the skin. He was diagnosed with native valve endocarditis. After medical stabilization, he ultimately underwent replacement of both the mitral and aortic valves. In retrospect, mild laboratory abnormalities and several months of weight loss beginning about four months earlier were likely early signs of endocarditis. He had no history of immunosuppressive therapy and no implanted medical devices.", + "wiki_anchor": "Underlying structural valve disease is usually present in patients before developing subacute endocarditis, and is less likely to lead to septic emboli than is acute endocarditis, but subacute endocarditis has a relatively slow process of infection and, if left untreated, can worsen for up to one year before it is fatal. In cases of subacute bacterial endocarditis, the causative organism (streptococcus viridans) needs a previous heart valve disease to colonize. On the other hand, in cases of acute bacterial endocarditis, the organism can colonize on the healthy heart valve, causing the disease.", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 18.815652173913048, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 6.333333333333333 + }, + { + "index": 16, + "label": "proficient_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Some examples of reported cardiovascular causes include:\n Congenital abnormalities:\nAtrial septal defect\nAortopulmonary window\nEbstein's Anomaly\nPatent Ductus Arteriosus (PDA)\nSurgical intervention:\nTranscatheter closure of a PDA \nIncidence: due to the close proximity of the LRLN to the aortic arch, transient paralysis can occur in 10% of cases while permanent effects can occur in 1% of cases. This can further be attributed to using metal clips (used to control bleeding) during the surgical procedure and is more common in premature infants.\n Cardiac disease:\nLeft atrial enlargement due to valvular heart disease\nNotable case: A middle-aged male had ongoing cough, hoarseness of voice, and shortness of breath for two years without a history of smoking was found to have mitral valve stenosis due to calcification. This led to left atrial enlargement, elevated pulmonary artery pressure, pulmonary artery hypertension, and right ventricular enlargement. This cardiomegaly, or enlargement of the heart, led to compression of the LRLN.\nAtrial Myxoma\nAorta:\nTraumatic injury\nIncidence: Although injury to the thoracic aorta is often fatal, in 10% of cases that take longer to present, hoarseness may be the first symptom.\nAortic dissection\nMore commonly affects the right recurrent laryngeal nerve as the most common type of aortic dissection is type A (Figure 2).\nPseudoaneurysm\nNotable case: A male with long-standing uncontrolled hypertension and hoarseness of voice attributed to life-long smoking was found to have a pseudoaneurysm of the aortic arch which was compressing the LRLN.\nPulmonary disease:\nPathophysiology: Due to vascular congestion in the lung, the pulmonary artery (Figure 3) becomes dilated and can compress the aorta and the LRLN.\nPrimary pulmonary hypertension\n Pulmonary emboli\nMalignancy (pulmonary, mediastinal)\n Autoimmune:\nMixed connective tissue disease\nNotable case: A young female with a history of mixed connective tissue disease presented with hoarseness of voice and was found to have secondary pulmonary artery hypertension. This was causing right heart enlargement and therefore compression of the LRLN.\nIdiopathic", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 17.909027817608266, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 7.071428571428571 + }, + { + "index": 17, + "label": "low_health_literacy", + "original_doc": "A 27-year-old woman had many cancers in her large intestine and rectum. She also had an inherited condition that causes many polyps.\n\nShe had robot-assisted surgery to remove the entire colon and rectum. The team also removed lymph nodes from the whole area. They used a surgical robot called Hugo RAS.\n\nThe robot work had three steps.\n\nStep 1: Her head was tilted down. The team removed the right side of the colon with its nearby tissue, up to the bend near the liver.\n\nStep 2: They removed the left side of the colon with its nearby tissue. They also removed the rectum with the tissue around it. They took deeper lymph nodes.\n\nStep 3: Her body was kept flat. The team tied off the main blood vessels along the main artery that feeds the intestines.\n\nAfter the robot part was finished, they took the removed bowel out through the anus. Through a small cut at the belly button, they made a pouch from the small intestine. They connected this pouch to the anus.\n\nThe surgery took about 10 and a half hours. Blood loss was very small. Recovery after surgery went smoothly.", + "wiki_anchor": "Small bowel resection \nOnce the abdomen is accessed, the surgeon \"runs\" the small bowel, viewing the entire small bowel from the ligament of treitz to the ileocecal valve. This allows for total evaluate of the small bowel to identify any and all pathologic sections. Once the area of concern is located, two small holes are created in the mesentery on either end of the segment. These holes are used to place a surgical stapler across the bowel and separate the segment of injured bowel from the healthy bowel on each end. Then bowel is then dissected away from the mesentery. Following this the remaining bowel is observed to verify continued blood flow. After resection the surgeon will create an anastomosis between the two ends of the bowel. Following this the hole in the mesentery created by removing the section of bowel is closed with sutures to prevent internal herniation. The resected section of bowel will then be removed from the abdomen and the abdomen closed. This concludes the procedure.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 10.202183431952665, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 5.454545454545454 + }, + { + "index": 17, + "label": "intermediate_health_literacy", + "original_doc": "A 27-year-old woman with familial adenomatous polyposis and multiple colorectal cancers underwent robot-assisted total proctocolectomy with complete lymph node dissection using the Hugo RAS system. The robotic work was organized into three steps: 1) in Trendelenburg position, ascending colon complete mesocolic excision up to the hepatic flexure; 2) descending colon complete mesocolic excision and total mesorectal excision with D3 lymph node dissection; and 3) in a flat position, central vessel ligation along the superior mesenteric artery. After undocking, the specimen was removed transanally. An ileal pouch was created through a small umbilical incision and then connected to the anus (ileal pouch\u2013anal anastomosis). The operation lasted 632 minutes with minimal blood loss, and the postoperative course was uneventful.", + "wiki_anchor": "R. John Nicholls is best known for his work in the development of ileal pouch surgery. With the advancement of ileal-anal pouch surgery, selected patients with ulcerative colitis and familial adenomatous polyposis were successfully relieved of the disease through removing the colon and rectum, but in contrast to the conventional operation of a total proctocolectomy used at the time, ileal pouch-anal anastomosis surgery also called reconstructive procotocolectomy added the optional choice for the person to avoid the need for a stoma and external appliance bag by internally holding stool in a pouch made from ileum (small bowel) that connects to the anus and restores traditional anal evacuation.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 26.448831775700942, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 10.5 + }, + { + "index": 17, + "label": "proficient_health_literacy", + "original_doc": "A 27-year-old woman with multiple colorectal cancers on a background of familial adenomatous polyposis (FAP) underwent robot-assisted total proctocolectomy (TPC) with lymph node dissection of the entire colorectal region using the Hugo RAS system. Preoperative CT showed multiple nodal swellings along the inferior mesenteric artery (IMA) and middle colic artery without distant metastases. After multidisciplinary review, robot-assisted TPC was performed under approvals from the Evaluating Committee for Highly Difficult New Medical Technologies (H-0051) and the Kyoto University IRB.\n\nUnder general anesthesia in lithotomy with arms tucked, a 5-cm vertical umbilical incision was made and a wound protector placed. After pneumoperitoneum, 4 robotic and 2 assistant trocars were inserted. Instruments included a camera, monopolar curved shears (right hand), bipolar fenestrated forceps (left hand), and Cadiere/double-fenestrated forceps (reserve arm). Two table positions (Trendelenburg and flat) were used with specific docking tilts; arm cart angles were unchanged. The robotic procedure comprised three steps, followed by transanal specimen extraction, ileal pouch construction via a small umbilical laparotomy, and ileal pouch\u2013anal anastomosis (IPAA).\n\nStep 1: Ascending colon complete mesocolic excision (CME) from a caudal approach, completed through hepatic flexure mobilization.\n\nStep 2: Central vessel ligation (CVL) of the IMA, descending colon CME to completion of splenic flexure mobilization, and total mesorectal excision (TME) to full exposure of the intersphincteric space. This corresponds to a D3 lymph node dissection of the left colon/rectum.\n\nStep 3: After undocking and repositioning the patient flat, CVL along the superior mesenteric artery (SMA) was performed, ligating the ileocolic, right colic, and middle colic vessels; the inferior mesenteric vein (IMV) was ligated at its root (exposed in Step 2).\n\nTransanal and small laparotomy procedures: After transection of the terminal ileum, a transanal specimen extraction was performed with complete rectal mucosectomy from just below the dentate line due to multiple adenomas in the anal canal. An ileal pouch was constructed via the small umbilical incision, its reach to the anal canal confirmed, and a transanal hand-sewn IPAA was completed. No diverting ileostomy was created.\n\nAll three steps were completed without conversion. Following undocking after Step 3, laparoscopy confirmed hemostasis, specimen extraction, and anastomotic integrity. Total operative time was 632 minutes (Step 1: 36 min; Step 2: 160 min; Step 3: 188 min; positioning/docking/specimen extraction/anastomosis: 248 min). Estimated blood loss was 20 mL. Postoperatively, the course was uneventful: flatus and initiation of liquids on POD 1, advancement to a solid diet on POD 3, with a functional ileal pouch and satisfactory anal function.\n\nFinal pathology identified two sigmoid cancers (S1: Type 0-Ip, 55 \u00d7 50 mm, tub1, T1b, ly0, v0; S2: Type 0-Isp, 55 \u00d7 50 mm, tub1, Tis, ly0, v0) and one rectal cancer (R1: Type 0-Ip, 40 \u00d7 35 mm, tub1, Tis, ly0, v0). Lymph node status: 18/89 positive, all in sigmoid/rectosigmoid stations (#241, #242, #251), yielding UICC pT1bN2b stage.", + "wiki_anchor": "Laboratories \n Intravascular therapeutic Microbot Lab - Microrobot moving controlled through blood vessel for drug delivery and treatment of coronary artery disease such as CTO(chronic total occlusion) and thrombus. The lab achieved the world's first microrobot navigation through artery in a live pig.\n Bacteria-based Biomedical Microbot Lab - Development of the fundamental technology for intelligent theragnostic bacteria-based microrobot.(Using bacteria with the abilities such as active movement, fluorescence expression, recombination and replication)\n Telesurgical robot for brain surgery Lab - Development of an Articulated multi-DOF Manipulator for Minimal Invasive Surgery.(Master and Slave System with force reflection control & image guided surgical robot system)\n Robotic Couch for Heavy Ion Therapy Lab - Development of a Novel Robotic Couch System to adjust Patient's position to treat using Heavy Ion Therapy. (An articulated robotic arm to carry a human & respiration synchronization method)\n Surgeon-Robot Interaction for Bone-Fracture Reposition Robot Lab - Robotic Assistant Robot for Bone-Fracture Reposition Surgery, which replaces assistant surgeons who align the broken bone to reduce their exposure to X-ray and labor-intensive work. Surgeon-robot interaction method including an interactive mode and a remote mode will be developed and integrated into the robotic system.\n Cable Robotics Lab - The establishment of Fraunhofer-IPA, one of the Europe's largest robotics institutes, is expected to facilitate the technical improvement through the collaboration in intelligent robotics. The research topic is \u201cdevelopment of core and application technologies on high dynamic parallel cable robotics.\u201d", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 20.04846607669617, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 10.714285714285714 + }, + { + "index": 18, + "label": "low_health_literacy", + "original_doc": "A 65-year-old man had a swollen right middle finger after a motorcycle crash 6 months earlier. The middle joint stayed bent, and the fingertip bent backward. He could not fully straighten the finger. An X-ray showed no broken bones. The problem was in the soft tissues and tendon on top of the finger. Before surgery, the middle joint could bend from 45 to 110 degrees but could not straighten. The doctors repaired the top tendon using a small strip from another tendon in the same finger. They put the middle joint in a straight splint for 2 weeks. After 2 weeks, he started gentle bending and straightening exercises for that joint. One month after surgery, the middle joint moved from 0 to 90 degrees. Two months after surgery, movement went back to normal. His hand function score (DASH) improved from 50 to 4.2.", + "wiki_anchor": "In cubital tunnel syndrome (a proximal impingement), sensory and motor symptoms tend to occur in a certain sequence. Initially, there may be numbness of the small and ulnar fourth finger which may be transient. If the impingement is not corrected, the numbness may become constant and progress to hand weakness. A characteristic resting hand position of \"ulnar claw,\" where the small and ring fingers curl up, occurs late in the disease and is a sign of severe neuropathy.\nBy contrast, in Guyon's canal syndrome (distal impingement) motor symptoms and claw hand may be more pronounced, a phenomenon known as the ulnar paradox. Also, the back of the hand will have normal sensation.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 10.338214285714287, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 5.666666666666667 + }, + { + "index": 18, + "label": "intermediate_health_literacy", + "original_doc": "A 65-year-old man developed persistent swelling and a boutonniere deformity of the right middle finger after a motorcycle fall six months earlier. He could not fully extend the finger. On exam, the finger showed edema with flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Active PIP range of motion (ROM) was 45\u2013110 degrees. X\u2011rays of the right hand (AP/oblique) showed no bone injury, indicating a soft-tissue problem consistent with a central slip injury. The patient underwent reconstruction of the central slip using a partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. A PIP extension splint was used for 2 weeks. Active and passive PIP ROM exercises began after 2 weeks. One month after surgery, PIP ROM improved to 0\u201390 degrees, and by 2 months it returned to normal. Hand function, measured by the DASH score, improved markedly from 50 to 4.2.", + "wiki_anchor": "At the level of the PIP joint the extensor mechanism splits into three bands. The central slip attaches to the dorsal tubercle of the middle phalanx near the PIP joint. The pair of lateral bands, to which contribute the extensor tendons, continue past the PIP joint dorsally to the joint axis. These three bands are united by a transverse retinacular ligament, which runs from the palmar border of the lateral band to the flexor sheath at the level of the joint and which prevents dorsal displacement of that lateral band. On the palmar side of the joint axis of motion, lies the oblique retinacular ligament [of Landsmeer] which stretches from the flexor sheath over the proximal phalanx to the terminal extensor tendon. In extension, the oblique ligament prevents passive DIP flexion and PIP hyperextension as it tightens and pulls the terminal extensor tendon proximally.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 12.781111111111112, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 6.833333333333333 + }, + { + "index": 18, + "label": "proficient_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Treatment\nManagement of pulley injuries of the fingers is to follow the RICE method. Other treatment suggestions are listed below:\n The patient is to immediately cease climbing and any other activity that puts stress on the injured finger, and consult a doctor if there is noticeable \"bowstringing\" on the flexor tendon or if unsure about the nature of the injury.\n There are different theories out there for the preferred line of approach. Some argue for the use of NSAIDs and ice for visible swelling only.\n Light massage can be used to increase blood flow to the injured area, aiding recovery. Massage tools such as acupressure rings can be beneficial in the same way.\n Protein supplements may help the tendons recover faster by providing much needed building block nutrients.\n When the pain and swelling is gone (depending on the grade of the injury, 1\u20134 weeks), the patient can begin with an active healing process \u2013 containing squeezing putty clay or a stress ball. This can be combined with mild exercise, such as finger flexions, to ensure the finger will heal properly and better prepared for future stress. The use of heating pads and cold water baths are also mentioned in several sources in order to increase blood flow. \n The patient can gradually return to climbing while using prophylactic taping when climbing. There is some research supporting the use of taping, especially concerning bowstringing, but more research is needed. It is advised to spend the first weeks climbing relatively easy routes with big holds, good footholds and keeping sessions short. Stay away from overhangs and campus areas/boards.\n The patient can return to full-force climbing if easy climbing yields no pain. Continue taping (it will also serve as a mental note of the previous injury) and avoid tweaky crimps and pockets for several months, since complete tendon healing can take 100 days or more.", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 10.351411290322584, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 6.5 + }, + { + "index": 19, + "label": "low_health_literacy", + "original_doc": "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.", + "wiki_anchor": "Five days later, her fianc\u00e9, a young Navajo man, was en route to her funeral in Gallup when he suddenly became severely short of breath. By the time paramedics brought him to the Indian Medical Center emergency room, he had stopped breathing and the paramedics were performing cardiopulmonary resuscitation. The young man could not be revived by doctors and died. The physicians, recalling the similar symptoms and death of the young woman, reported his death to the New Mexico Department of Health.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 12.119634146341465, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.5 + }, + { + "index": 19, + "label": "intermediate_health_literacy", + "original_doc": "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.", + "wiki_anchor": "In a true subarachnoid hemorrhage, there is higher attenuation on CT scans of the basal cisterns, and blood that has leaked from a vessel or formed a hematoma is more highly attenuated due to the absorption of plasma. Pseudosubarachnoid hemorrhages have been observed in as much as 20% of patients resuscitated from non-traumatic cardiopulmonary arrest. Patients with pseudosubarachnoid hemorrhages may have worse prognoses than those with true subarachnoid hemorrhages because of underlying disease processes and decreased cerebral perfusion with elevated intracranial pressure. The identification of a pseudosubarachnoid hemorrhage as opposed to a true subarachnoid hemorrhage may therefore change a patient's treatment plan.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 17.029509803921574, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 7.25 + }, + { + "index": 19, + "label": "proficient_health_literacy", + "original_doc": "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.", + "wiki_anchor": "ST elevation MI\nThe 2018 European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Health Federation Universal Definition of Myocardial Infarction for the ECG diagnosis of the ST segment elevation type of acute myocardial infarction require new ST elevation at J point of at least 1mm (0.1 mV) in two contiguous leads with the cut-points: \u22651 mm in all leads other than leads V2-V3. For leads V2-V3: \u22652 mm in men \u226540 years, \u22652.5 mm in men <40 years, or \u22651.5 mm in women regardless of age. This assumes usual calibration of 1mV/10mm. These elevations must be present in anatomically contiguous leads. (I, aVL, V5, V6 correspond to the lateral wall; V3-V4 correspond to the anterior wall ; V1-V2 correspond to the septal wall; II, III, aVF correspond to the inferior wall.) This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. Over 90% of healthy men have at least 1\u00a0mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 12.617924528301888, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 7.25 + } +] \ No newline at end of file