diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_17_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_17_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_17_v1.json" @@ -0,0 +1,662 @@ +[ + { + "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": "Signs and symptoms\nThe presence of antiphospholipid antibodies (aPL) in the absence of blood clots or pregnancy-related complications does not indicate APS (see below for the diagnosis of APS).\nAntiphospholipid syndrome can cause arterial or venous blood clots, in any organ system, or pregnancy-related complications. In APS patients, the most common venous event is deep vein thrombosis of the lower extremities, and the most common arterial event is stroke. In pregnant women affected by APS, there is an increased risk of recurrent miscarriage, intrauterine growth restriction, and preterm birth. A frequent cause of such complications is placental infarctions.\nIn some cases, APS seems to be the leading cause of intellectual and/or developmental disabilities in the newborn, due to an aPL-induced inhibition of trophoblast differentiation. The antiphospholipid syndrome is responsible for most of the miscarriages in later trimesters seen in concomitant systemic lupus erythematosus and pregnancy.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 14.623743842364533, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 7.0, + "fkgl_delta": -10.485585947627687 + }, + { + "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": "PE usually results from a blood clot in the leg that travels to the lung. The risk of blood clots is increased by advanced age, cancer, prolonged bed rest and immobilization, smoking, stroke, long-haul travel over 4 hours, certain genetic conditions, estrogen-based medication, pregnancy, obesity, trauma or bone fracture, and after some types of surgery. A small proportion of cases are due to the embolization of air, fat, or amniotic fluid. Diagnosis is based on signs and symptoms in combination with test results. If the risk is low, a blood test known as a D-dimer may rule out the condition. Otherwise, a CT pulmonary angiography, lung ventilation/perfusion scan, or ultrasound of the legs may confirm the diagnosis. Together, deep vein thrombosis and PE are known as venous thromboembolism (VTE).", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 11.17233665559247, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 7.285714285714286, + "fkgl_delta": 4.031675143817559 + }, + { + "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": "The cause of multiple myeloma is unknown. Risk factors include obesity, radiation exposure, family history, age and certain chemicals. There is an increased risk of multiple myeloma in certain occupations. This is due to the occupational exposure to aromatic hydrocarbon solvents having a role in causation of multiple myeloma. Multiple myeloma may develop from monoclonal gammopathy of undetermined significance (MGUS) that progresses to smoldering myeloma. The abnormal plasma cells produce abnormal antibodies, which can cause kidney problems and overly thick blood. The plasma cells can also form a mass in the bone marrow or soft tissue. When one tumor is present, it is called a plasmacytoma; more than one is called multiple myeloma. Multiple myeloma is diagnosed based on blood or urine tests finding abnormal antibody proteins - (often using electrophoretic techniques revealing the presence of a monoclonal spike in the results - termed an m-spike), bone marrow biopsy finding cancerous plasma cells, and medical imaging finding bone lesions. Another common finding is high blood calcium levels.", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 12.585606060606064, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.8, + "fkgl_delta": 4.522678850359263 + }, + { + "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": "The symptoms observed in patients included respiratory distress, panic attacks, seizures, severe muscle spasms (one woman was described as having her feet touching the back of her head), nausea, vomiting, diarrhea, hallucinations (often accompanied by disturbing laughter), muscle weakness, amnesia, coma, severe headaches, numbness, pain (initially in the eyes and mucous membranes), chills, high blood pressure, and nosebleeds. Doctors attending the patients could not identify a specific cause but diagnosed the cases as the result of \"an intoxication of unknown aetiology\".", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 22.930925925925923, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 9.0, + "fkgl_delta": -19.34957061457061 + }, + { + "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": "Venous thrombosis is blockage of a vein caused by a thrombus (blood clot). A common form of venous thrombosis is deep vein thrombosis (DVT), when a blood clot forms in the deep veins. If a thrombus breaks off (embolizes) and flows to the lungs to lodge there, it becomes a pulmonary embolism (PE), a blood clot in the lungs. The conditions of DVT only, DVT with PE, and PE only, are all captured by the term venous thromboembolism (VTE).", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 8.094778481012657, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 6.5, + "fkgl_delta": 3.847326782145238 + }, + { + "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": "The affected infant tends to be short, with a disproportionately large head. The fetal head of infants born with iniencephaly are hyperextended while the foramen magnum is enlarged and opens through the widened pedicles. The defective neural arches directly into the upper cervical reach of the spinal canal, causing the formation of a common cavity between most of the spinal cord and the brain. The skin of the anterior chest is connected directly to the face, bypassing the formation of a neck, while the scalp is directly connected to the skin of the back. Because of this, those born with this anomaly either have a highly shortened neck or no neck at all. This causes extreme retroflexion, or backward bending, of the head in a \"star-gazing\" fashion. The spine is severely distorted as well along with significant shortening due to marked lordosis. The vertebrae, especially cervical, are fused together in abnormal shapes and their numbers are reduced. The spinal cord is almost always defective while the ventricular system is often dilated and the cortex is thinned. Sometimes, in the case of iniencephaly apertus, an encephalocele (sac-like protrusions of the brain through an opening in the cranium) forms.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 11.02091878172589, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 6.8, + "fkgl_delta": 5.226498913747363 + }, + { + "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\nFifth disease starts with a low-grade fever, headache, rash, and cold-like symptoms, such as a runny or stuffy nose. These symptoms pass, then a few days later, the rash appears. The bright red rash most commonly appears in the face, particularly the cheeks. This is a defining symptom of the infection in children (hence the name \"slapped cheek disease\"). Occasionally, the rash will extend over the bridge of the nose or around the mouth. In addition to red cheeks, children often develop a red, lacy rash on the rest of the body, with the upper arms, torso, and legs being the most common locations. The rash typically lasts a few days and may itch; some cases have been known to last for several weeks. Patients are usually no longer infectious once the rash has appeared.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 7.9824275362318815, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 5.75, + "fkgl_delta": -3.3493037837368718 + }, + { + "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": "Most people with hand, foot, and mouth disease get better on their own in 7 to 10 days. Most cases require no specific treatment. No antiviral medication or vaccine is available, but development efforts are underway. For fever and for painful mouth sores, over-the-counter pain medications such as ibuprofen may be used, though aspirin should be avoided in children. The illness is usually not serious. Occasionally, intravenous fluids are given to children who are dehydrated. Very rarely, viral meningitis or encephalitis may complicate the disease. Because HFMD is normally mild, some jurisdictions allow children to continue to go to child care and schools as long as they have no fever or uncontrolled drooling with mouth sores, and as long as they feel well enough to participate in classroom activities.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 11.005726744186049, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 4.75, + "fkgl_delta": -0.677164244186045 + }, + { + "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": "Bulimia typically involves rapid and out-of-control eating, which may stop when the person is interrupted by another person or the stomach hurts from over-extension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day and may directly cause:\n Chronic gastric reflux after eating, secondary to vomiting\n Dehydration and hypokalemia due to renal potassium loss in the presence of alkalosis and frequent vomiting\n Electrolyte imbalance can lead to abnormal heart rhythms, cardiac arrest, and even death\n Esophagitis, or inflammation of the esophagus\n Mallory-Weiss tears\n Boerhaave syndrome, a rupture in the esophageal wall due to vomiting\n Oral trauma, in which repetitive insertion of fingers or other objects causes lacerations to the lining of the mouth or throat\n Russell's sign: calluses on knuckles and back of hands due to repeated trauma from incisors\n Perimolysis, or severe dental erosion of tooth enamel\n Swollen salivary glands (for example, in the neck, under the jawline)\n Gastroparesis, or delayed gastric emptying\n Constipation or diarrhea\n Tachycardia or palpitations\n Hypotension\n Peptic ulcers\n Infertility\n Constant weight fluctuations are common\n Elevated blood sugar, cholesterol, and amylase levels may occur\n Hypoglycemia may occur after vomiting", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 45.888999999999996, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 15.5, + "fkgl_delta": -31.361763157894732 + }, + { + "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": "In 2017, a girl born of consanguineous Iranian parents was described in medical literature. Aside from the characteristic findings of the condition, she was found to have intrauterine growth restriction, severe respiratory distress, transient hypothyroidism (which resolved by age 1 year old), and small ventricular septal defect. Dysmorphic findings included small nipples, frontal bossing, smooth philtrum, hypertelorism, unilateral low-set ear, and high-arched palate. She developed low extremity lymphedema in infancy, and had mild developmental delays which were thought to have been caused by the surgeries and prolonged NICU stay she had to go through.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 14.66436170212766, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 8.5, + "fkgl_delta": -10.040422308188266 + }, + { + "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": "In 2017, a girl born of consanguineous Iranian parents was described in medical literature. Aside from the characteristic findings of the condition, she was found to have intrauterine growth restriction, severe respiratory distress, transient hypothyroidism (which resolved by age 1 year old), and small ventricular septal defect. Dysmorphic findings included small nipples, frontal bossing, smooth philtrum, hypertelorism, unilateral low-set ear, and high-arched palate. She developed low extremity lymphedema in infancy, and had mild developmental delays which were thought to have been caused by the surgeries and prolonged NICU stay she had to go through.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 14.66436170212766, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 8.5, + "fkgl_delta": -3.4502412201999455 + }, + { + "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": "Cesarean Scar Disorder \nAlthough studies are increasing, an international debate can be about their relevance. If 60 to 70% of women after cesarean section actually get a niche, maybe it's not that relevant because not all these people have symptoms. Therefore in 2023, a paper discussed the cesarean scar disorder. \u00a0This is a combination of having a niche on ultrasound with a minimum amount of symptoms that the woman has. Apart from having a niche and symptoms, it's also important to exclude other causes of the \u00a0symptoms other than the niche. The Cesarean Scar Disorder paper defined primary and secondary symptoms. \u00a0The primary symptoms are those that are directly caused because of the defect in the wall of \u00a0the uterus. \u00a0These are postmentrual spotting, pain during menstrual bleeding, technical difficulty inserting the catheter during embryo transfer and secondary unexplained infertility combined with intrauterine fluid (fluid inside of the uterine cavity after the ovulation). Secondary symptoms are symptoms that are caused usually because of the primary symptoms. \u00a0These are dyspareunia (pain during sex), abnormal vaginal discharge, chronic pelvic pain, avoiding sexual intercourse, door associated with abnormal blood loss, secondary unexplained infertility or secondary infertility despite Assisted Reproductive Treatment (for example IVF), a negative self-image or discomfort during participation in leisure activities. Because there are other reasons that women can have these symptoms, these other causes should \u00a0be excluded. Things are, for example, cervical dysplasia, vaginal/uterine infection, uterine pathology like polyps and fibroids, etc. \u00a0When woman has a niche, symptoms started \u00a0after the cesarean section and there is not other good explanation for the symptoms, she has a cesarean scar disorder. Having a cesarean scar disorder does not mean it needs treatment, but it might be an important diagnosis.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 14.85378048780488, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.866666666666666, + "fkgl_delta": -1.2735980978677723 + }, + { + "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": "Causes \nThere are a variety of causes of NPPE, which can theoretically result from any upper airway obstruction. In adults, the most frequent cause is laryngospasm (involuntary contraction of the vocal cords) after extubation, making up approximately 50% of all adults cases of NPPE. The incidence of NPPE as a result of postextubation laryngospasm has been estimated to be between 0.1-3.0%. In the pediatric setting, the reported most common causes of NPPE are both infectious in nature: croup and epiglottitis. Other reported causes include endotracheal tube obstruction (e.g., from patient biting down on tube), tumors/masses compressing the upper airway, choking on foreign objects, strangulation. Interestingly, the use of sugammadex to reverse neuromuscular blockade (the mechanism of paralysis during surgery) has also been associated with increased incidence of NPPE", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 14.035178571428574, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 6.5, + "fkgl_delta": -11.453714607464608 + }, + { + "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": "A primary spontaneous pneumothorax is one that occurs without an apparent cause and in the absence of significant lung disease. A secondary spontaneous pneumothorax occurs in the presence of existing lung disease. Smoking increases the risk of primary spontaneous pneumothorax, while the main underlying causes for secondary pneumothorax are COPD, asthma, and tuberculosis. A traumatic pneumothorax can develop from physical trauma to the chest (including a blast injury) or from a complication of a healthcare intervention.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 15.730526315789472, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 7.0, + "fkgl_delta": -3.001954887218041 + }, + { + "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": "The second case was her younger, 4-year-old toddler brother. He was born weighing 3042 grams, and was noted to have cyanosis at birth, which was an indicator for a possible heart anomaly. He learned how to control his head at 3 months of age and learned how to walk when he was 20 months old, at the age of 2 he was found to have a speech delay and could only say a handful of words. Physical examination done on him in July 1984 showed a height of 72.7\u00a0cm, a weight of 7.7\u00a0km, and a head circumference of 44.5\u00a0cm. He had the same skin tone, hair color, and facial characteristics as his proband sister. A systolic ejection murmur (grade 4/6) could be heard at his second left intercostal face, this same murmur was later discovered to be caused by pulmonary valve stenosis. Like his sister, he also had whorls and loops in his fingerprints (4 and 6, respectively), and he had routine laboratory tests and a karyotype which turned back normal. Physical examination done in him again in May 1987 showed a height of 94.3\u00a0cm, a weight of 45.2\u00a0kg, and a head circumference of 49.7\u00a0cm. His bone age was appropriate for his age.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 6.657990430622011, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 7.777777777777778, + "fkgl_delta": 8.986592902711326 + }, + { + "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, + "fkgl_delta": -4.294281394173556 + }, + { + "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": "Acute bronchitis, also known as a chest cold, is short-term bronchitis \u2013 inflammation of the bronchi (large and medium-sized airways) of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterward with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 7.319683544303796, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": 9.101105929380417 + }, + { + "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": "Amaral AF, Strachan DP, Burney PG, Jarvis DL (2017). \"Female smokers are at greater risk of airflow obstruction than male smokers: UK Biobank\". American Journal of Respiratory and Critical Care Medicine. 195: 1226-1235.\n Amaral AFS, Newson RB, Abramson MJ, Anto JM, Bono R, Corsico AG, de Marco R, Demoly P, Forsberg B, Gislason T, Heinrich J, Huerta I, Janson C, Jogi R, Kim JL, Maldonado J, Martinez-Moratalla Rovira J, Neukirch C, Nowak D, Pin I, Probst-Hensch N, Raherison-Semjen C, Svanes C, Urrutia Landa I, van Ree R, Versteeg SA, Weyler J, Zock JP, Burney PGJ, Jarvis DL (2015). \"Changes in IgE sensitization and total IgE levels over 20 years of follow-up\". Journal of Allergy and Clinical Immunology. 137: 1788-1795.e9.\n Canova C, Heinrich J, Maria Anto J, Leynaert B, Smith M, Kuenzli N, Zock J-P, Janson C, Cerveri I, de Marco R, Toren K, Gislason T, Nowak D, Pin I, Wjst M, Manfreda J, Svanes C, Crane J, Abramson M, Burr M, Burney P, Jarvis D (2013). \"The influence of sensitisation to pollens and moulds on seasonal variations in asthma attacks\" European Respiratory Journal. 42: 935-945.\n Ghosh RE, Cullinan P, Fishwick D, Hoyle J, Warburton CJ, Strachan DP, Butland BK, Jarvis D (2013). \"Asthma and occupation in the 1958 birth cohort\" Thorax. 68: 365-371.\n Ramasamy A, Curjuric I, Coin LJ, Kumar A, McArdle WL, Imboden M, Leynaert B, Kogevinas M, Schmid-Grendelmeier P, Pekkanen J, Wjst M, Bircher AJ, Sovio U, Rochat T, Hartikainen A-L, Balding DJ, Jarvelin M-R, Probst-Hensch N, Strachan DP, Jarvis DL (2011). \"A genome-wide meta-analysis of genetic variants associated with allergic rhinitis and grass sensitization and their interaction with birth order\". Journal of Allergy and Clinical Immunology. 128: 996-1005.", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 12.744626334519577, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 8.875, + "fkgl_delta": 3.734741481572378 + }, + { + "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": "Symptoms of factor V Leiden include:\n Having a first DVT or PE before 50 years of age.\n Having recurring DVT or PE.\n Having venous thrombosis in unusual sites in the body such as the brain or the liver.\n Having a DVT or PE during or right after pregnancy.\n Having a history of unexplained pregnancy loss in the second or third trimester.\n Having a DVT or PE and a strong family history of venous thromboembolism.", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 7.557837837837841, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 5.666666666666667, + "fkgl_delta": -3.04572401669963 + }, + { + "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": "One common early indicator of haemophilia is prolonged bleeding from venepuncture or heelpricks. These signs often prompt blood tests that confirm the presence of haemophilia. In individuals, especially those with moderate or mild haemophilia, any form of trauma can trigger the first significant bleed. Haemophilia substantially elevates the risk of protracted bleeding from ordinary injuries, and in severe cases, bleeding can occur spontaneously without an apparent cause. Bleeding episodes can manifest anywhere in the body. Superficial bleeding resulting from abrasions or shallow lacerations may persist, with scabs easily breaking due to the deficiency of fibrin, potentially leading to re-bleeding. While superficial bleeding poses challenges, more critical sites of bleeding include:\n Joints\n Muscles\n Digestive tract\n Brain", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 13.083229813664598, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 6.0, + "fkgl_delta": -2.032197204968945 + }, + { + "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": "Cesarean Scar Disorder \nAlthough studies are increasing, an international debate can be about their relevance. If 60 to 70% of women after cesarean section actually get a niche, maybe it's not that relevant because not all these people have symptoms. Therefore in 2023, a paper discussed the cesarean scar disorder. \u00a0This is a combination of having a niche on ultrasound with a minimum amount of symptoms that the woman has. Apart from having a niche and symptoms, it's also important to exclude other causes of the \u00a0symptoms other than the niche. The Cesarean Scar Disorder paper defined primary and secondary symptoms. \u00a0The primary symptoms are those that are directly caused because of the defect in the wall of \u00a0the uterus. \u00a0These are postmentrual spotting, pain during menstrual bleeding, technical difficulty inserting the catheter during embryo transfer and secondary unexplained infertility combined with intrauterine fluid (fluid inside of the uterine cavity after the ovulation). Secondary symptoms are symptoms that are caused usually because of the primary symptoms. \u00a0These are dyspareunia (pain during sex), abnormal vaginal discharge, chronic pelvic pain, avoiding sexual intercourse, door associated with abnormal blood loss, secondary unexplained infertility or secondary infertility despite Assisted Reproductive Treatment (for example IVF), a negative self-image or discomfort during participation in leisure activities. Because there are other reasons that women can have these symptoms, these other causes should \u00a0be excluded. Things are, for example, cervical dysplasia, vaginal/uterine infection, uterine pathology like polyps and fibroids, etc. \u00a0When woman has a niche, symptoms started \u00a0after the cesarean section and there is not other good explanation for the symptoms, she has a cesarean scar disorder. Having a cesarean scar disorder does not mean it needs treatment, but it might be an important diagnosis.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 14.85378048780488, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 6.866666666666666, + "fkgl_delta": -3.0744931169425556 + }, + { + "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": "Signs and symptoms\nTesticular torsion usually presents with severe testicular pain or pain in the groin and lower abdomen. Pain generally begins suddenly and typically involves only one side. There is often associated nausea and vomiting. The testicle may lie higher in the scrotum due to twisting and subsequent shortening of the spermatic cord or may be positioned in a horizontal orientation. Mild warmth and redness of the overlying area may be present. Elevation of the testicle may worsen the pain. Urinary symptoms, such as pain or increased frequency of urination are also typically absent. Symptom onset often follows physical activity or trauma to the testes or scrotum. Children with testicular torsion may awaken with testicular or abdominal pain in the middle of the night or in the morning. There may be a history of previous, similar episodes of scrotal pain due to prior transient testicular torsion with spontaneous resolution.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 12.208000000000006, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 6.1, + "fkgl_delta": -8.946956521739136 + }, + { + "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": "Signs and symptoms\nTesticular torsion usually presents with severe testicular pain or pain in the groin and lower abdomen. Pain generally begins suddenly and typically involves only one side. There is often associated nausea and vomiting. The testicle may lie higher in the scrotum due to twisting and subsequent shortening of the spermatic cord or may be positioned in a horizontal orientation. Mild warmth and redness of the overlying area may be present. Elevation of the testicle may worsen the pain. Urinary symptoms, such as pain or increased frequency of urination are also typically absent. Symptom onset often follows physical activity or trauma to the testes or scrotum. Children with testicular torsion may awaken with testicular or abdominal pain in the middle of the night or in the morning. There may be a history of previous, similar episodes of scrotal pain due to prior transient testicular torsion with spontaneous resolution.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 12.208000000000006, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 6.1, + "fkgl_delta": -0.42396374045802077 + }, + { + "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": "Thorax\nThe scutum is black with inconspicuous, very minute, brownish pubescence on mesonotum. There is an oblique, oval spot on presutural callus. An elongated spot is on the mesopleurae along the mesopleural suture. Below it is an oval oblique yellowish spot along the posterior end of the sterno-pleural suture. The scutellum is reddish brown, towards the sides it is yellowish brown with the extreme base and lateral angles black and the posterior margin narrowly brown. The thorax sides have oblong longitudinal yellow spot on posterior anepisternum directed downward, and another smaller, oblong yellow spot directed sideways below it just above the coxa of midlegs. A wide, curved light yellow mark is below scutellum. Each side of mesonotum is reddish brown, from above seen as an outwardly arched stripe, beginning a little in front of the scutellar ridge and extending to the transverse suture. Along the middle of mesonotum, in front, are two parallel, narrow, yellowish pollinose stripes, not quite reaching the anterior border, but each one terminating in a transverse, yellowish pollinose spot on the transverse suture, behind which the stripes are faintly visible. The black ground color is concealed by the pollen of those stripes. The sternum is very thinly whitish pollinose. Note: small spots behind the ocelli may seem like two yellow spots on base of thorax, depending on angle of head.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 10.654285714285717, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 6.833333333333333, + "fkgl_delta": 4.464709501025293 + }, + { + "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": "This initial stage of sepsis is followed by suppression of the immune system. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion. There may also be symptoms related to a specific infection, such as a cough with pneumonia, or painful urination with a kidney infection. The very young, old, and people with a weakened immune system may have no symptoms of a specific infection, and the body temperature may be low or normal instead of having a fever. Severe sepsis causes poor organ function or blood flow. The presence of low blood pressure, high blood lactate, or low urine output may suggest poor blood flow. Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 9.691904761904762, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.0, + "fkgl_delta": -4.89751627269613 + }, + { + "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": "Symptoms \nAcute necrotizing encephalopathy typically appears in infancy or early childhood, although some people do not develop the condition until adolescence or adulthood. People with this condition usually show typical symptoms of an infection, such as fever, cough, congestion, vomiting, and diarrhea, for a few days. Following these flu-like symptoms, affected individuals develop neurological problems, such as seizures, hallucinations, difficulty coordinating movements (ataxia), or abnormal muscle tone. Eventually, most affected individuals go into a coma, which usually lasts for a number of weeks. The condition is described as \"acute\" because the episodes of illness are time-limited.", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 17.21883333333334, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 7.0, + "fkgl_delta": -2.4653074974670766 + }, + { + "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": "Thioridazine prolongs the QTc interval in a dose-dependent manner. It produces significantly less extrapyramidal side effects than most first-generation antipsychotics, likely due to its potent anticholinergic effect. Its use, along with the use of other typical antipsychotics, has been associated with degenerative retinopathies (specifically retinitis pigmentosa). It has a higher propensity for causing anticholinergic side effects coupled with a lower propensity for causing extrapyramidal side effects and sedation than chlorpromazine, but also has a higher incidence of hypotension and cardiotoxicity. It is also known to possess a relatively high liability for causing orthostatic hypotension compared to other antipsychotics. Similarly to other first-generation antipsychotics it has a relatively high liability for causing prolactin elevation. It is moderate risk for causing weight gain. As with all antipsychotics thioridazine has been linked to cases of tardive dyskinesia (an often permanent neurological disorder characterised by slow, repetitive, purposeless and involuntary movements, most often of the facial muscles, that is usually brought on by years of continued treatment with antipsychotics, especially the first-generation (or typical) antipsychotics such as thioridazine) and neuroleptic malignant syndrome (a potentially fatal complication of antipsychotic treatment). Blood dyscrasias such as agranulocytosis, leukopenia and neutropenia are possible with thioridazine treatment. Thioridazine is also associated with abnormal retinal pigmentation after many years of use.\nThioridazine has been correlated to rare instances of clinically apparent acute cholestatic liver injury.", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 17.24593939393939, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 7.7272727272727275, + "fkgl_delta": -2.287285720104265 + }, + { + "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": "Aortic stenosis (AS or AoS) is the narrowing of the exit of the left ventricle of the heart (where the aorta begins), such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occur due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without narrowing is known as aortic sclerosis.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 8.92799180327869, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 5.625, + "fkgl_delta": -2.4057840110708995 + }, + { + "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": "Cardiopulmonary bypass is commonly used in operations involving the heart. The technique allows the surgical team to oxygenate and circulate the patient's blood, thus allowing the surgeon to operate on the heart. In many operations, such as coronary artery bypass grafting (CABG), the heart is arrested (i.e., stopped) because of the difficulty of operating on the beating heart. Operations requiring the opening of the chambers of the heart, for example, mitral valve repair or replacement, requires the use of CPB to avoid engulfing air systemically and to provide a bloodless field to increase visibility for the surgeon. The machine pumps the blood and, using an oxygenator, allows red blood cells to pick up oxygen, as well as allowing carbon dioxide levels to decrease. This mimics the function of the heart and the lungs, respectively.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 12.48168443496802, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 7.5, + "fkgl_delta": 0.9983155650319837 + }, + { + "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": "In common usage, in clinical practice including angiology and vascular surgery, the femoral artery includes the common femoral artery, and the superficial femoral artery however, the Terminologia Anatomica (TA) only lists the femoral artery. (The TA is the international standard for human anatomical terminology developed by the Federative International Programme on Anatomical Terminology).\nThe common femoral artery (CFA) is located between the inferior margin of the inguinal ligament, and the branching point of the deep femoral artery. Its first three or four centimetres are enclosed, with the femoral vein, in the femoral sheath. In 65% of people, the common femoral artery lies anterior to the femoral vein in the upper thigh. The CFA is, after the popliteal artery, the most common peripheral site of general dilatation or aneurysmal formation, at a frequency of 1/10 of the aorta. Highly calcific arterial stenosis in the CFA is very difficult to treat by endovascular intervention. Stent positioning in CFA may be limited by compressive or torsional forces, leading to stent fracture and/or restenosis. On the other hand, lithoplasty balloon angioplasty may represent a safe tool to treat CFA stenosis.\nThe superficial femoral artery is a designation for the segment between the branching point of the deep femoral artery and the adductor hiatus, passing through the subsartorial canal. However, this term is not listed in Terminologia Anatomica, and usage of the term superficial femoral is discouraged by many physicians because it leads to confusion among general medical practitioners, at least for the femoral vein that courses next to the femoral artery. In particular, the adjacent femoral vein is clinically a deep vein, where deep vein thrombosis indicates anticoagulant or thrombolytic therapy, but the adjective \"superficial\" leads many physicians to falsely believe it is a superficial vein, which has resulted in patients with femoral thrombosis being denied proper treatment. Therefore, the segment is alternatively termed the subsartorial artery. The segment enters the adductor hiatus and becomes the popliteal artery which goes through the popliteal fossa.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 16.451948051948055, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 7.0, + "fkgl_delta": -7.386315140555649 + }, + { + "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": "Diseases associated with myelitis\nConditions associated with myelitis include:\n Acute disseminated encephalomyelitis: autoimmune demyelination of the brain causing severe neurological signs and symptoms\n Multiple sclerosis: demyelination of the brain and spinal cord\n Neuromyelitis optica or Devic's disease: immune attack on optic nerve and spinal cord\n Sj\u00f6gren's syndrome: destruction of the exocrine system of the body\n Systemic lupus erythematosus: a systemic autoimmune disease featuring a wide variety of neurological signs and symptoms\n Sarcoidosis: chronic inflammatory cells form as nodules in multiple organs\n Atopy: an immune disorder of children manifesting as eczema or other allergic conditions. It can include atopic myelitis, which causes weakness.\n Immune-mediated myelopathies, heterogeneous group of inflammatory spinal cord disorders including autoimmune disorders with known antibodies", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 24.93452991452992, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 7.666666666666667, + "fkgl_delta": -18.33702051603368 + }, + { + "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": "History \nThe first case of orbital compartment syndrome causing monocular blindness was published in 1950 due to a complication of a zygomatic fracture repair. In 1953 the first surgical orbital decompression was performed. Two incisions below and above the external canthus were made and surgical drains were put in place. In 1990 the first lateral canthotomy procedure as presently performed was completed. In 1994 lateral canthotomy was first published in a review of procedures that emergency physicians can perform. Today a canthotomy is almost always performed with cantholysis of the inferior canthal tendon as this provides the best decompression of intraocular pressure.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 13.020392156862744, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.166666666666667, + "fkgl_delta": -1.4785316917464648 + }, + { + "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": "First stage: This is the initial phase of the condition, and it takes place from birth to the age of 14 years old; it is characterized by the appearance of a large, perforated chorioretinal atrophic lesion at the central part of the macula which contains the vascular arch, alongside extra-macular white deposits and localized areas of hyperpigmentation in the retinal pigment epithelium. The heads of the optic nerve start taking a vertical ovaloid shape during this stage.\nSecond stage: This stage of the condition takes place from the age of 15 to 45 years old. In this phase of the condition, the previously mentioned macular perforation starts growing outside its original starting point, beyond the vascular arch, with relatively new spots of atrophy in the nasal retina starting to join into one, making one white, chorioretinal atrophic lesion as a result. Patients also start reporting visual hallucinations of flashing lights (photopsias) during this stage. Myopia, which is previously absent in affected patients, starts becoming apparent during one's 20th years of life.\nThird stage: This is the final stage, and it takes place at the age of 46 years old and later. In this stage, the previously mentioned atrophic lesions of the macula and the nasal retina expand and grow towards the optic disc, which consequently results in a narrow bridge of intact retina that passes through the optic disc in a vertical manner. During this stage, patients are more likely to report having difficulties seeing in low-light conditions.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 14.712311827956992, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 8.666666666666666, + "fkgl_delta": -0.0504416980868605 + }, + { + "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": "Diagnosis is based on symptoms, physical findings, and echocardiography. Blood tests, and a chest x-ray may be useful to determine the underlying cause. Treatment depends on severity and case. For people with chronic, stable, mild heart failure, treatment usually consists of lifestyle changes, such as not smoking, physical exercise, and dietary changes, as well as medications. In heart failure due to left ventricular dysfunction, angiotensin-converting-enzyme inhibitors, angiotensin receptor blockers, or angiotensin receptor-neprilysin inhibitors, along with beta blockers, mineralocorticoid receptor antagonists and SGLT2 inhibitors are recommended. Diuretics may also be prescribed to prevent fluid retention and the resulting shortness of breath. Depending on the case, an implanted device such as a pacemaker or implantable cardiac defibrillator may sometimes be recommended. In some moderate or more severe cases, cardiac resynchronization therapy (CRT) or cardiac contractility modulation may be beneficial. In severe disease that persists despite all other measures, a cardiac assist device ventricular assist device, or, occasionally, heart transplantation may be recommended.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 15.975833333333334, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": -9.433114035087716 + }, + { + "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": "Career\nHe has served in various medical organizations such as a Locum Medical Officer at Paragon Hospital (Bukoto Branch) (2009), a Medical officer at AAR Health Services Uganda (2010\u20132012), had an 8 weeks emergency medicine stint at Villa Somalia Medical Facility at Presidential Palace in Somalia, was Head of Department of Anaesthesia at CoRSU Rehabilitation Hospital (January 2012 \u2013 December 2012). He eventually started lecturing at the Department of Anesthesia and Critical Care at Makerere University, School of Medicine, College of Health Sciences in 2012 where he took up the Emergency Medicine Curriculum and oversaw the accreditation process to final registration by the National Council for Higher Education, that culminated in first MMED-EM class intake in the academic year 2018\u20132019 of Makerere University's From 2018\u2013 2021, he served as the Course Director for the new MMED Emergency Medicine program of the Department of Anesthesia. In 2018 he was promoted to senior lecturer and in May 2021 he was appointed the first substantive Chair of the Department of Anesthesia.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 28.87209580838324, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 8.75, + "fkgl_delta": -15.96180169073618 + }, + { + "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 Vaseghi M, Gima J, Kanaan C, Ajijola OA, Marmureanu A, Mahajan A, Shivkumar K. Cardiac sympathetic denervation in patients with refractory ventricular arrhythmias or electrical storm: intermediate and long-term follow-up. Heart Rhythm. 2014 Mar;11(3):360-6. doi: 10.1016/j.hrthm.2013.11.028. Epub 2013 Nov 28. PMID 24291775; PMCID: PMC4253031.\n Marelli D, Laks H, Patel B, Kermani R, Marmureanu A, Patel J, Kobashigawa J; University of California at Los Angeles Heart Transplant Group. Heart transplantation in patients with diabetes mellitus in the current era. J Heart Lung Transplant. 2003 Oct;22(10):1091-7. doi: 10.1016/s1053-2498(02)01219-6. PMID 14550818.\n Wieder JA, Laks H, Freitas D, Marmureanu A, Belldegrun A. Renal cell carcinoma with tumor thrombus extension into the proximal pulmonary artery. J Urol. 2003 Jun;169(6):2296-7. doi: 10.1097/01.ju.0000065432.22782.0d. PMID 12771776.\n Crisera CA, Connelly PR, Marmureanu AR, Li M, Rose MI, Longaker MT, Gittes GK. TTF-1 and HNF-3beta in the developing tracheoesophageal fistula: further evidence for the respiratory origin of the distal esophagus'. J Pediatr Surg. 1999 Sep;34(9):1322-6. doi: 10.1016/s0022-3468(99)90003-9. PMID 10507421.\n Crisera CA, Connelly PR, Marmureanu AR, Colen KL, Rose MI, Li M, Longaker MT, Gittes GK. Esophageal atresia with tracheoesophageal fistula: suggested mechanism in faulty organogenesis. J Pediatr Surg. 1999 Jan;34(1):204-8. doi: 10.1016/s0022-3468(99)90258-0. PMID 10022173.", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 10.637632653061228, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 4.6521739130434785, + "fkgl_delta": 2.838207756145934 + }, + { + "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": "Symptoms and signs\nThe symptoms of urethritis can include pain or a burning sensation upon urination (dysuria), a white/cloudy discharge and a feeling that one needs to pass urine frequently. For men, the signs and symptoms are discharge from the penis, burning or pain when urinating, itching, irritation, or tenderness. In women, the signs and symptoms are discharge from vagina, burning or pain when urinating, anal or oral infections, abdominal pain, or abnormal vaginal bleeding, which may be an indication that the infection has progressed to Pelvic Inflammatory Disease.", + "doc_fkgl": 6.041, + "wiki_fkgl": 16.26539325842697, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 7.0, + "fkgl_delta": -10.224393258426968 + }, + { + "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": "Content\n1,188 images include those of pathological specimens, photographs at endoscopy of the bladder and diagrams that explain urological diagnostic procedures. It contains a collection of X-rays including a comparison of spread to bone from prostate cancer and Paget's disease. 70 images relate to lesions of the penis and scrotum. These include priapism, spermatocele, and hydrocele.", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 11.995000000000001, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 8.25, + "fkgl_delta": 0.18740740740740947 + }, + { + "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": "Human infection \nIn June 2022, a neurosurgeon in an Australian hospital found a roundworm in a woman's brain while investigating her mysterious symptoms. The woman initially reported diarrhea and abdominal pain, along with night sweats and dry cough, and was originally diagnosed with a rare lung infection. Though her symptoms improved with treatment, she subsequently returned with symptoms of fever and cough, resulting in an additional diagnosis of a blood disorder. Worsening symptoms of forgetfulness and depression resulted in a MRI that revealed a brain lesion. The biopsy resulted in the discovery and extraction of the live worm. This was the first known instance of such an occurrence, as this type of worm had never been identified as a human parasite before. The woman, who lived near carpet python habitat and foraged for native vegetation to cook, was believed to have been exposed by consuming the roundworm\u2019s eggs. These eggs, which were commonly shed in snake droppings due to the snakes' diet of infected animals, likely contaminated the grass eaten by small mammals. Doctors theorize that the various symptoms experienced by the patient resulted from the migration of the parasitic eggs and larva from the bowel, through various other organs, before arriving in the brain.", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 13.612357723577237, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.444444444444445, + "fkgl_delta": 1.345037234405961 + }, + { + "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": "Coronary artery disease is caused when coronary arteries of the heart accumulate atheromatous plaques, causing stenosis (narrowing) in one or more arteries and risking myocardial infarction, the interruption of blood supply to the heart. CAD can occur in any of the major vessels of coronary circulation: the left main stem, left ascending artery, circumflex artery, and right coronary artery, and branches thereof. CAD symptoms vary from none, to chest pain only when exercising (stable angina), to chest pain even at rest (unstable angina). It can even manifest as a myocardial infarction; if blood flow to the heart is not restored within a few hours, whether spontaneously or by medical intervention, the blood-deprived part of the heart becomes necrotic (dies) and is scarred. It may lead to other complications such as arrhythmias, rupture of the papillary muscles of the heart, or sudden death.", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 16.426845070422534, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 8.2, + "fkgl_delta": -10.599496233213227 + }, + { + "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": "Coronary artery disease is caused when coronary arteries of the heart accumulate atheromatous plaques, causing stenosis (narrowing) in one or more arteries and risking myocardial infarction, the interruption of blood supply to the heart. CAD can occur in any of the major vessels of coronary circulation: the left main stem, left ascending artery, circumflex artery, and right coronary artery, and branches thereof. CAD symptoms vary from none, to chest pain only when exercising (stable angina), to chest pain even at rest (unstable angina). It can even manifest as a myocardial infarction; if blood flow to the heart is not restored within a few hours, whether spontaneously or by medical intervention, the blood-deprived part of the heart becomes necrotic (dies) and is scarred. It may lead to other complications such as arrhythmias, rupture of the papillary muscles of the heart, or sudden death.", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 16.426845070422534, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 8.2, + "fkgl_delta": -1.833035546613008 + }, + { + "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": "Diagnosis is based on symptoms, physical findings, and echocardiography. Blood tests, and a chest x-ray may be useful to determine the underlying cause. Treatment depends on severity and case. For people with chronic, stable, mild heart failure, treatment usually consists of lifestyle changes, such as not smoking, physical exercise, and dietary changes, as well as medications. In heart failure due to left ventricular dysfunction, angiotensin-converting-enzyme inhibitors, angiotensin receptor blockers, or angiotensin receptor-neprilysin inhibitors, along with beta blockers, mineralocorticoid receptor antagonists and SGLT2 inhibitors are recommended. Diuretics may also be prescribed to prevent fluid retention and the resulting shortness of breath. Depending on the case, an implanted device such as a pacemaker or implantable cardiac defibrillator may sometimes be recommended. In some moderate or more severe cases, cardiac resynchronization therapy (CRT) or cardiac contractility modulation may be beneficial. In severe disease that persists despite all other measures, a cardiac assist device ventricular assist device, or, occasionally, heart transplantation may be recommended.", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 15.975833333333334, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": 0.996921097046414 + }, + { + "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": "The low oxygen level leads to physiologic constriction of the pulmonary arteries to correct ventilation-perfusion mismatching, which puts excessive strain on the right side of the heart. When this leads to right sided heart failure, it is known as cor pulmonale. Symptoms of this disorder occur because the heart has difficulty pumping blood from the body through the lungs. Fluid may, therefore, accumulate in the skin of the legs in the form of edema (swelling), and in the abdominal cavity in the form of ascites; decreased exercise tolerance and exertional chest pain may occur. On physical examination, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to blood leaking through the tricuspid valve, hepatomegaly (an enlarged liver), ascites and leg edema. Cor pulmonale occurs in about a third of all people with OHS.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 13.261643356643358, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.833333333333334, + "fkgl_delta": -7.531554704161088 + }, + { + "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": "Aortic stenosis (AS or AoS) is the narrowing of the exit of the left ventricle of the heart (where the aorta begins), such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occur due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without narrowing is known as aortic sclerosis.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 8.92799180327869, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 5.625, + "fkgl_delta": 3.056816559090649 + }, + { + "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": "Thorax\nThe scutum is black with inconspicuous, very minute, brownish pubescence on mesonotum. There is an oblique, oval spot on presutural callus. An elongated spot is on the mesopleurae along the mesopleural suture. Below it is an oval oblique yellowish spot along the posterior end of the sterno-pleural suture. The scutellum is reddish brown, towards the sides it is yellowish brown with the extreme base and lateral angles black and the posterior margin narrowly brown. The thorax sides have oblong longitudinal yellow spot on posterior anepisternum directed downward, and another smaller, oblong yellow spot directed sideways below it just above the coxa of midlegs. A wide, curved light yellow mark is below scutellum. Each side of mesonotum is reddish brown, from above seen as an outwardly arched stripe, beginning a little in front of the scutellar ridge and extending to the transverse suture. Along the middle of mesonotum, in front, are two parallel, narrow, yellowish pollinose stripes, not quite reaching the anterior border, but each one terminating in a transverse, yellowish pollinose spot on the transverse suture, behind which the stripes are faintly visible. The black ground color is concealed by the pollen of those stripes. The sternum is very thinly whitish pollinose. Note: small spots behind the ocelli may seem like two yellow spots on base of thorax, depending on angle of head.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 10.654285714285717, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 6.833333333333333, + "fkgl_delta": 5.800802005012528 + }, + { + "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": "The second case was her younger, 4-year-old toddler brother. He was born weighing 3042 grams, and was noted to have cyanosis at birth, which was an indicator for a possible heart anomaly. He learned how to control his head at 3 months of age and learned how to walk when he was 20 months old, at the age of 2 he was found to have a speech delay and could only say a handful of words. Physical examination done on him in July 1984 showed a height of 72.7\u00a0cm, a weight of 7.7\u00a0km, and a head circumference of 44.5\u00a0cm. He had the same skin tone, hair color, and facial characteristics as his proband sister. A systolic ejection murmur (grade 4/6) could be heard at his second left intercostal face, this same murmur was later discovered to be caused by pulmonary valve stenosis. Like his sister, he also had whorls and loops in his fingerprints (4 and 6, respectively), and he had routine laboratory tests and a karyotype which turned back normal. Physical examination done in him again in May 1987 showed a height of 94.3\u00a0cm, a weight of 45.2\u00a0kg, and a head circumference of 49.7\u00a0cm. His bone age was appropriate for his age.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 6.657990430622011, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 7.777777777777778, + "fkgl_delta": -1.3953229179316544 + }, + { + "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": "Pheochromocytoma is a rare tumor of the adrenal medulla composed of chromaffin cells, also known as pheochromocytes. When a tumor composed of the same cells as a pheochromocytoma develops outside the adrenal gland, it is referred to as a paraganglioma. These neuroendocrine tumors typically release massive amounts of catecholamines, metanephrines, or methoxytyramine, which result in the most common symptoms, including hypertension (high blood pressure), tachycardia (fast heart rate), and diaphoresis (sweating). Rarely, some tumors (especially paragangliomas) may secrete little to no catecholamines, making diagnosis difficult. While tumors of the head and neck are parasympathetic, their sympathetic counterparts are predominantly located in the abdomen and pelvis, particularly concentrated at the organ of Zuckerkandl.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 15.376357142857142, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.8, + "fkgl_delta": -1.483304045512007 + }, + { + "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": "The microscopic histopathology of PACB tumors prepared with hematoxylin and eosin staining shows that >90% of the tumors consist of apocrine gland-like tissue. The lesions must also show that tumor cells have broken through their ducts of origin to invade adjacent tissue in at least one area. Most of the tumor cells (termed type A cells) typically appear somewhat more irregular than normal apocrine gland cells. They have abundant eosinophilic (i.e. pink due to the uptake of the eosin dye) cytoplasm which contain numerous granules and large mitochondria. Their nuclei are large, variably sized and shaped, have multiple nucleoli (which are eosinophilic and may be distinctively large in size), and are surrounded by highly visible nuclear membranes. The cells are arranged into solid sheets, nests, papillae, and/or cords (see Figs. 1 and 2). The tumor cells' cytoplasmic granules test positive when treated with the PAS diastase stain. Binucleated cells, i.e. cells with two nuclei, are common. Less commonly, type B apocrine cells are present; these cells have a more foamy and vacuolated cytoplasm (i.e. containing multiple vacuoles) than type A cells and often resemble foamy histiocytes or sebaceous gland cells. The tumor cells have low to moderate rates of proliferation based on their Ki-67 protein levels. PACB tissues may have localized areas that contain mucin-like secretions within their luminal ducts, localized areas of necrosis (i.e. foci containing dead or dying cells), and/or microcalcifications spotted throughout the apocrine tissue. The stroma (i.e. connective tissue between the sheets, nests, papilla and cords of cells) typically contains non-malignant, infiltrating lymphocytes (see Fig. 3). In an examination of 41 PABC tumors, 33 (80.5%) had <50% of their stroma tissues infiltrated with these cells while 8 (19.5%) had \u226550% of their stroma tissues infiltrated with them. Tumors with \u226550% of their stroma infiltrated with lymphocytes tended to have carcinoma cells that had high rates of proliferation. Metastatic and recurrent PACB tumors have a histopathology similar to their original primary tumors.", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 9.708561872909701, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 6.8125, + "fkgl_delta": 5.408529036181207 + }, + { + "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": "Most cases are caused by a viral infection. Strep throat, a bacterial infection, is the cause in about 25% of children and 10% of adults. Uncommon causes include other bacteria such as gonococcus, fungi, irritants such as smoke, allergies, and gastroesophageal reflux disease. Specific testing is not recommended in people who have clear symptoms of a viral infection, such as a cold. Otherwise, a rapid antigen detection test or throat swab is recommended. PCR testing has become common as it is as good as taking a throat swab but gives a faster result. Other conditions that can produce similar symptoms include epiglottitis, thyroiditis, retropharyngeal abscess, and occasionally heart disease.", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 10.72689384010485, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 6.857142857142857, + "fkgl_delta": -3.2585605067715164 + }, + { + "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": "Typically, the infection enters the body through a break in the skin such as a cut or burn. Risk factors include poor immune function such as from diabetes or cancer, obesity, alcoholism, intravenous drug use, and peripheral artery disease. It does not typically spread between people. The disease is classified into four types, depending on the infecting organism. Between 55 and 80% of cases involve more than one type of bacteria. Methicillin-resistant Staphylococcus aureus (MRSA) is involved in up to a third of cases. Medical imaging is often helpful to confirm the diagnosis.", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 10.653794162826422, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 5.714285714285714, + "fkgl_delta": 2.3422848645292014 + }, + { + "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": "The third and final case was the youngest brother of the three, a 2-year old infant boy. He weighed 2962 grams at birth and he was found to have heart murmur when he was 3 months old. Physical examination done on him in May 1986 showed a height of 63\u00a0cm, a weight of 5.3\u00a0kg, and a head circumference of 41.5\u00a0cm. His skin color, hair color and facial features were the same as his siblings'. His heart murmur was found to be a grade 3/6 systolic murmur that could be heard in his lower left sternal border, after cardiac echography and other tests, the murmur was ruled out to be benign and harmless. He was noted to have ankyloglossia and hypospadias. He was also found to have whorls and loops in his fingerprints just like his siblings (5 and 5, respectively). A karyotype done on him gave back normal results. Physical examination done on him a year later in May 1987 showed a height of 73.9\u00a0cm, a weight of 8.8\u00a0kg, and a head circumference of 47.4\u00a0cm. He could control his head at the age of 6 months but even at the age of 18 months he was found to have a walking delay and a speech delay. Routine laboratory tests and bone age examination turned back normal.", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 6.221312741312744, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 7.0, + "fkgl_delta": 6.276024899508993 + }, + { + "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": "Purpose \nGenerally, an antrectomy is performed to treat bleeding and blockage of the stomach. This could be caused by a variety of gastric disorders, including: \n Peptic ulcer disease (PUD): The disease is characterized by ulcers developed either by impaired mucus protection or an excess of gastric acid production. Antrectomy could either lead to the reduction of gastric acid levels or the removal of the peptic ulcer altogether. Antrectomy is rarely warranted in this case since PUD rarely recurs and is usually manageable via medications.\n Zollinger\u2013Ellison syndrome: The condition features excessive gastric acid production. Antrectomy removes gastrin-producing G-cells in the stomach antrum, in turn reducing gastric acid levels.\n Gastric cancer: Antrectomy could remove gastric tumors developing in the antrum.\n Gastric antral vascular ectasia syndrome (GAVE): The disease is characterized by excessive bleeding in the stomach. By removing the bleeding site and reconnecting the upper stomach with the intestines, antrectomy controls chronic bleeding and ensures gastric continuity.\n Gastric outlet obstruction (GOO): It is a condition where the passage between the stomach and the duodenum is blocked. Removal of the blocked stomach parts by antrectomy could ensure continuity of the gastrointestinal system.\n Penetrative wounds in the duodenum, stomach, or pancreas: The removal of devitalized tissue by antrectomy could prevent continuous bleeding and inflammation from wound infection.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 13.990715962441314, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 7.083333333333333, + "fkgl_delta": -8.805665512482221 + }, + { + "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, + "fkgl_delta": -9.514541177410344 + }, + { + "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": "In general terms, the procedure for an open appendectomy is:\n Antibiotics are given immediately if signs of actual sepsis are seen (in appendicitis, sepsis and bacteremia usually only occurs at some point after rupture, once peritonitis has begun), or if there is reasonable suspicion that the appendix has ruptured (e.g., on imaging) or if the onset of peritonitis - which will lead to full sepsis if not quickly treated- is suspected; otherwise, a single dose of prophylactic intravenous antibiotics is given immediately before surgery.\n General anaesthesia is induced, with endotracheal intubation and full muscle relaxation, and the patient is positioned supine.\n The abdomen is prepared and draped and is examined under anesthesia.\n If a mass is present, the incision is made over the mass. Otherwise, the incision is made over McBurney's point (one-third of the way from the anterior superior iliac spine to the umbilicus), which represents the most common position of the base of the appendix.\n The various layers of the abdominal wall are opened. In order to preserve the integrity of abdominal wall, the external oblique aponeurosis is split along the line of its fibers, as is the internal oblique muscle. As the two run at right angles to each other, this reduces the risk of later incisional hernia.\n On entering the peritoneum, the appendix is identified, mobilized, and then ligated and divided at its base.\n Some surgeons choose to bury the stump of the appendix by inverting it so it points into the caecum.\n Each layer of the abdominal wall is then closed in turn.\n The skin may be closed with staples or stitches.\n The wound is dressed.\n The patient is brought to the recovery room.", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 11.842316546762593, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 5.928571428571429, + "fkgl_delta": 2.7067041321293317 + }, + { + "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": "Clinical significance\nThe radius and scaphoid articulate deep to the snuffbox to form the basis of the wrist joint. In the event of a fall onto an outstretched hand (FOOSH), this is the area through which the brunt of the force will focus. This results in these two bones being the most often fractured of the wrist. In a case where there is localized tenderness within the snuffbox, knowledge of wrist anatomy leads to the speedy conclusion that the fracture is likely to be of the scaphoid. This is understandable as the scaphoid is a small, oddly shaped bone whose purpose is to facilitate mobility rather than confer stability to the wrist joint . In the event of inordinate application of force over the wrist, this small scaphoid is likely to be the weak link . Scaphoid fracture is one of the most frequent causes of medico-legal issues.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 9.920998043052837, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 7.857142857142857, + "fkgl_delta": -4.3600015395563325 + }, + { + "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": "The mainstay of treatment for infectious tenosynovitis includes symptom relief, antibiotic therapy, and surgery. Early recognition of the disease with early initiation of antibiotics are important for better range of movement of the affected finger. Minimally invasive procedures into the flexor tendon sheath such as catheter irrigation give better outcomes (74% chance of good outcome) when compared to open surgery (26% chance of good outcome). However, wound irrigation with antibiotics has no clear benefits. Most infectious tenosynovitis cases should be managed with tendon sheath irrigation and drainage, with or without debridement of surrounding necrotic tissue, along with treatment with broad-spectrum antibiotics. In severe cases, amputation may even be necessary to prevent the further spread of infection. Following surgical intervention, antibiotic therapy is continued and adjusted based on the results of the fluid culture.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 15.242556390977445, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 6.714285714285714, + "fkgl_delta": -5.7878897243107765 + }, + { + "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": "The olecranon is a large, thick, curved eminence, situated at the upper and back part of the ulna. It is bent forward at the summit so as to present a prominent lip which is received into the olecranon fossa of the humerus in extension of the forearm. Its base is contracted where it joins the body and the narrowest part of the upper end of the ulna. Its posterior surface, directed backward, is triangular, smooth, subcutaneous, and covered by a bursa. Its superior surface is of quadrilateral form, marked behind by a rough impression for the insertion of the triceps brachii; and in front, near the margin, by a slight transverse groove for the attachment of part of the posterior ligament of the elbow joint. Its anterior surface is smooth, concave, and forms the upper part of the semilunar notch. Its borders present continuations of the groove on the margin of the superior surface; they serve for the attachment of ligaments: the back part of the ulnar collateral ligament medially, and the posterior ligament laterally. From the medial border a part of the flexor carpi ulnaris arises; while to the lateral border the anconeus is attached.", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 12.98948979591837, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 8.125, + "fkgl_delta": -1.1259603841536645 + }, + { + "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": "In 2003, Loughren was approached by detectives who suspected Cullen of poisoning hospital patients. The patient who triggered law enforcement interest was Florian Gall. As a patient at Somerset Medical, Gall had been improving, then he suddenly died of a massive heart attack. An autopsy showed that he had been administered digoxin. It was not on his prescription list. In small doses, digoxin can improve heart function, but the amount Gall had received was lethal. After consulting with her 11-year-old daughter, Loughren agreed to assist law enforcement.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 8.110016420361248, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.857142857142857, + "fkgl_delta": -4.0471985509454385 + }, + { + "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": "\"Health Minister Naba Das was admitted to Apollo with gunshot wounds to the left chest. A team of doctors led by Dr Debashish Nayak immediately attended to and operated on him. During the operation, it was found that a single bullet had entered and exited the body, injuring the heart and left lung and causing massive internal bleeding and injury. The injuries were repaired, and steps were taken to improve the pumping of the heart. He was given urgent ICU care. But despite best efforts, he could not be revived and succumbed to his injuries,\" the statement read.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 8.961632653061226, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.0, + "fkgl_delta": 4.795902230659706 + }, + { + "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": "Signs and symptoms\nFindings are due to brain stem and lower cranial nerve dysfunction. Onset of symptoms are less likely to be present during adulthood in most patients. Younger children generally have a substantially different presentation of clinical symptoms from older children. Younger children are more likely to have a more rapid neurological degeneration with profound brain stem dysfunction over several days.\n Neurogenic dysphagia: Difficulty swallowing. Seen by poor feeding in patient.\n Cyanosis: Bluish discoloration of skin while feeding.\n Weak crying\n Facial weakness\n Aspiration\n Headaches aggravated by Valsalva maneuvers, such as yawning, laughing, crying, coughing, sneezing or straining, bending over, or getting up suddenly\n Tinnitus (ringing in the ears)\n Lhermitte's sign (electrical sensation that runs down the back and into the limbs)\n Vertigo (dizziness)\n Nausea\n Schmahmann syndrome\n Nystagmus (irregular eye movements; typically, so-called \"downbeat nystagmus\")\n Facial pain\n Muscle weakness\n Impaired gag reflex\n Dysphagia (difficulty swallowing)\n Restless leg syndrome\n Sleep apnea\n Sleep disorders\n Impaired coordination\n Severe cases may develop all the symptoms and signs of a bulbar palsy\n Paralysis due to pressure at the cervico-medullary junction may progress in a so-called \"clockwise\" fashion, affecting the right arm, then the right leg, then the left leg, and finally the left arm; or the opposite way around.\n Papilledema on fundoscopic exam due to Increased intracranial pressure\n Pupillary dilation\n Dysautonomia: tachycardia (rapid heart), syncope (fainting), polydipsia (extreme thirst), chronic fatigue\n Apnea: Sudden pause of breathing, usually during sleep.\n Opisthotonos: Spasm of the head which causes head to arch backwards. More common in infants than adults.\n Stridor", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 15.071529581529585, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.538461538461538, + "fkgl_delta": -2.8338251790138607 + } +] \ No newline at end of file