diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_18_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_18_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_18_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 of hemolytic disease of the newborn include a positive direct Coombs test (also called direct agglutination test), elevated cord bilirubin levels, and hemolytic anemia. It is possible for a newborn with this disease to have neutropenia and neonatal alloimmune thrombocytopenia as well. Hemolysis leads to elevated bilirubin levels. After delivery, bilirubin is no longer cleared (via the placenta) from the neonate's blood and the symptoms of jaundice (yellowish skin and yellow discoloration of the whites of the eyes, or icterus) increase within 24 hours after birth. Like other forms of severe neonatal jaundice, there is the possibility of the neonate developing acute or chronic kernicterus, however the risk of kernicterus in HDN is higher because of the rapid and massive destruction of blood cells. Isoimmunization is a risk factor for neurotoxicity and lowers the level at which kernicterus can occur. Untreated profound anemia can cause high-output heart failure, with pallor, enlarged liver and/or spleen, generalized swelling, and respiratory distress.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 14.785535714285718, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 6.285714285714286, + "fkgl_delta": -10.647377819548872 + }, + { + "index": 0, + "label": "intermediate_health_literacy", + "original_doc": "A 20\u2011year\u2011old woman had a 12\u2011year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid\u2011sparing agent. A comprehensive thrombophilia work\u2011up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small\u2011bowel necrosis not compatible with survival. She died 48 hours later.", + "wiki_anchor": "Signs and symptoms\nMost people will present as nephrotic syndrome, with the triad of albuminuria, edema and low serum albumin (with or without kidney failure). High blood pressure and high cholesterol are often also present. Others may not have symptoms and may be picked up on screening, with urinalysis finding high amounts of protein loss in the urine. A definitive diagnosis of membranous nephropathy requires a kidney biopsy, though given the very high specificity of anti-PLA2R antibody positivity this can sometimes be avoided in patients with nephrotic syndrome and preserved kidney function", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 14.414782608695656, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 7.0, + "fkgl_delta": 0.7892291907143729 + }, + { + "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 nephrotic syndrome is characterised by the finding of edema in a person with increased protein in the urine and decreased protein in the blood, with increased fat in the blood. Inflammation that affects the cells surrounding the glomerulus, podocytes, increases the permeability to proteins, resulting in an increase in excreted proteins. When the amount of proteins excreted in the urine exceeds the liver's ability to compensate, fewer proteins are detected in the blood \u2013 in particular albumin, which makes up the majority of circulating proteins. With decreased proteins in the blood, there is a decrease in the oncotic pressure of the blood. This results in edema, as the oncotic pressure in tissue remains the same. Although decreased intravascular oncotic (i.e. osmotic) pressure partially explains the patient's edema, more recent studies have shown that extensive sodium retention in the distal nephron (collecting duct) is the predominant cause of water retention and edema in the nephrotic syndrome. This is worsened by the secretion of the hormone aldosterone by the adrenal gland, which is secreted in response to the decrease in circulating blood and causes sodium and water retention. Hyperlipidemia is thought to be a result of the increased activity of the liver.", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 13.431666666666668, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.5, + "fkgl_delta": 3.676618244298659 + }, + { + "index": 1, + "label": "low_health_literacy", + "original_doc": "She is 34 years old and pregnant. She had a seizure and trouble speaking clearly. She was sent right away for a head MRI scan. The scan showed a pattern doctors call the \u201cMedusa head.\u201d This means the veins in her brain are arranged in an unusual way that she was born with. There is a small blood clot at the outer part of this vein pattern. The blood is also moving slowly closer to the main vein.", + "wiki_anchor": "Caput medusae is the appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen. The name caput medusae (Latin for \"head of Medusa\") originates from the apparent similarity to Medusa's head, which had venomous snakes in place of hair. It is also a sign of portal hypertension. It is caused by dilation of the paraumbilical veins, which carry oxygenated blood from mother to fetus in utero and normally close within one week of birth, becoming re-canalised due to portal hypertension caused by liver failure.", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 13.645217391304353, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 9.0, + "fkgl_delta": -10.06386207994904 + }, + { + "index": 1, + "label": "intermediate_health_literacy", + "original_doc": "A 34-year-old woman who is 8 weeks pregnant had a first-time generalized seizure with temporary slurred speech. Because she is pregnant and this was her first seizure, doctors obtained an urgent brain MRI. The MRI showed the classic \u201cMedusa head\u201d sign, which indicates a developmental venous anomaly (DVA)\u2014a vein pattern you are born with. Imaging also suggested a partial clot along the peripheral portion of the draining system and slower blood flow closer to the main draining vein. These findings support the diagnosis: a developmental venous anomaly with peripheral partial thrombosis and proximal slow flow.", + "wiki_anchor": "In up to 30% there is a coincidence of CCM with a venous angioma, also known as a developmental venous anomaly. These lesions appear either as enhancing linear blood vessels or caput medusae, a radial orientation of small vessels that resemble the hair of Medusa from Greek mythology. These lesions are thought to represent developmental anomalies of normal venous drainage. These lesions should not be removed, as venous infarcts have been reported. When found in association with a CCM that needs resection, great care should be taken not to disrupt the angioma.", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 11.722956521739132, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 7.2, + "fkgl_delta": 0.2191487414187634 + }, + { + "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": "Case #2: A 56-year-old man, KS, was admitted to the hospital with signs of a putaminal hemorrhage, including dense paralysis on the left side of his body and face, difficulty swallowing, and visual field defects on his left side. On the fifth day of hospitalization, he was alert and cooperative with no disorientation, delusion, or emotional lability. He then became euphoric and outspoken, speaking in puns and witticisms with an exaggerated smile. The content of his conversations, however, was not bizarre or random. He would work in puns and jokes while speaking his concerns about his other physical symptoms from the stroke in a coherent manner. Sometimes he would not crack a smile at something he said to make others around him laugh hysterically, while other times he could not appreciate others' jokes. During this time, KS also developed hypersexuality, using erotic words and inappropriate behavior toward the female hospital staff. Before his stroke, KS's family reported he did make jokes on occasion, but never in this bizarre manner, and never behaved impolitely to women. MRI tests showed bleeding at the right putamen, extending into the posterior and lateral portions of the right thalamus and defects in the thalamus and right basal ganglion. Another test showed deficits in recent memory, orientation, abstract thinking, drawing, and verbal fluency.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 13.42783870967742, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 7.3, + "fkgl_delta": 2.8195789857958324 + }, + { + "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": "The oral cavity is part of the gastrointestinal system and as such the presence of alterations in this district can be the first sign of both systemic and gastrointestinal diseases. By far the most common oral conditions are plaque-induced diseases (e.g., gingivitis, periodontitis, dental caries). Oral symptoms can be similar to lesions occurring elsewhere in the digestive tract, with a pattern of swelling, inflammation, ulcers, and fissures. If these signs are present, then patients are more likely to also have anal and esophageal lesions and experience other extra-intestinal disease manifestations. Some diseases which involve other parts of the GI tract can manifest in the mouth, alone or in combination, including:\n Gastroesophageal reflux disease can cause acid erosion of the teeth and halitosis.\n Gardner's syndrome can be associated with failure of tooth eruption, supernumerary teeth, and dentigerous cysts.\n Peutz\u2013Jeghers syndrome can cause dark spots on the oral mucosa or on the lips or the skin around the mouth.\n Several GI diseases, especially those associated with malabsorption, can cause recurrent mouth ulcers, atrophic glossitis, and angular cheilitis (e.g., Crohn's disease is sometimes termed orofacial granulomatosis when it involves the mouth alone).\n Sideropenic dysphagia can cause glossitis, angular cheilitis.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 12.430519480519482, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 7.222222222222222, + "fkgl_delta": -7.797395728024473 + }, + { + "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": "Causes\nThe white appearance is created by hyperkeratosis (overproduction of keratin) and epithelial hyperplasia. The causative agent implicated is Epstein-Barr virus, the same virus that causes infectious mononucleosis (glandular fever). After the primary EBV infection has been overcome, the virus will persist for the rest of the host's life and \"hides\" from the immune system by latent infection of B lymphocytes. The virus also causes lytic infection in the oropharynx, but is kept in check by a normal, functioning immune system. Uncontrolled lytic infection is manifested as oral hairy leukoplakia in immunocompromised hosts. OHL usually arises where the immunocompromise is secondary to HIV/AIDS. Rarely are other causes of immunocompromise associated with OHL, but it has been reported in people who have received transplants and are taking immunosuppressive medication. OHL may also accompany chronic graft versus host disease. Even more rare are reports of OHL in persons with competent immune systems.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 13.251333333333335, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 6.444444444444445, + "fkgl_delta": -2.922770833333331 + }, + { + "index": 2, + "label": "proficient_health_literacy", + "original_doc": "A 22-year-old woman presented to Oral Medicine with a 1-month history of painful oral ulcers causing difficulty eating and drinking. The episode began with fever followed by pimple-like lesions on the lips. She had used pod-type vapes for approximately one year, often trying different e-liquid flavors; she had never smoked conventional cigarettes. She reported no medication exposure prior to onset (no antibiotics, analgesics, anticonvulsants, NSAIDs, or antifungals), no drug or food allergies, and unhealthy eating habits. Extraorally, there were no lesions elsewhere on the body. The lips exhibited serosanguineous crusts with an erosive area at the right labial commissure that tended to bleed. Intraoral examination showed multiple painful white ulcers with yellowish edges, irregular and variable in size, on the labial and buccal mucosa, lateral and ventral tongue, and floor of mouth. Anti-HSV-1 IgG was non-reactive. Based on isolated oral mucosal involvement, absence of cutaneous lesions, and negative HSV serology, a diagnosis of vaping-related oral erythema multiforme, minor type, was established. Management comprised 0.9% NaCl\u2013moistened gauze compresses to the lips three times daily; a dexamethasone mouthrinse (1 mg in 10 mL hyaluronic acid) three times daily with a 30-minute post-rinse fasting period; 2% miconazole cream applied to the wound at the right labial commissure twice daily; and vaseline album (petrolatum) for dry lips. Adjunctive advice included brushing teeth and tongue twice daily (after breakfast and before bed), cessation of vaping, and avoidance of foods containing monosodium glutamate. At 1-week follow-up, the oral condition had improved. Ethical considerations: written informed consent was obtained; the case conformed to the Helsinki Declaration and had institutional approval. Context: Erythema multiforme is a mucocutaneous hypersensitivity reaction classically triggered by infections (e.g., HSV) or drugs; in this case, vaping exposure and frequent e-liquid flavor changes were considered plausible triggers in the absence of medication exposure and with non-reactive anti-HSV-1 serology.", + "wiki_anchor": "Signs and symptoms\n Clinical symptoms of the disease:\n Seborrhoeic areas\n This is defined as areas where excess oil and sebum is released.\n Overall greasy or scaly skin either in the central chest and back or in the folds of the skin.\n Fragile or poorly formed fingernails\n Nail disease leading to V-shaped nicks at the edge of the nail.\n Rash that covers many areas of the body\n The rash is often associated with a strong unpleasant odor\n The rash can be aggravated by heat, humidity, and exposure to sunlight.\n Mucosal manifestation\n White cobblestone pattern of small papules\n Overgrowth of gums\n Usually affects the mouth, esophagus, rectum, vulva, vagina\n Oral symptoms\u00a0 can be diagnosed by a routine dental examination\n Other symptoms and their overall prevalence in the affected population:\n In 80 to 90% of patients\n Acrokeratosis verruciformis\n Acrokeratosis is characterized by several small wart-like and flat-topped bumps that line the skin on typically the hand and feet.\n Hypermelanotic macule\n Patches on the skin that contain excess pigment, they often appear as dark patches in the skin.\n Pruritus\n Itching\n Subungual hyperkeratotic fragments\n Thickened skin that is often discolored, under nails, on either hands or feet.\n Palmar pits\n Usually red in color, they are pits or depressions in the palms or soles of the hands and feet.\n In 30 to 79% of patients\n Abnormal hair morphology\n Acne conglobata\n Typically described as cystic acne", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 14.583988355167396, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 7.0, + "fkgl_delta": -0.056751513062131664 + }, + { + "index": 3, + "label": "low_health_literacy", + "original_doc": "At 32 weeks of pregnancy, a routine scan found one small lump inside the baby\u2019s heart. It caused no symptoms. This was the only problem seen. Doctors watched it with clinic visits until 39 weeks plus 1 day. Then the baby was delivered by C-section (a surgery to deliver the baby). After birth, the child had checkups on day 1, day 7, day 30, month 7, and month 12. At each visit, the child\u2019s growth and behavior were healthy for age. The heart lump stayed the same size; it did not grow or shrink. By 1 year old, there were no signs of a related condition called tuberous sclerosis complex.", + "wiki_anchor": "It is much more common to find metastasis from an alternate site than a primary heart tumor. However, primary cardiac tumors do occur. One of these is the cardiac rhabdomyoma. Approximately 80-90% of these tumors are found in patients with tuberous sclerosis, a genetic condition causing multiple tumors, with most found prior to the age of one. Although these tumors are most commonly treated with resection, symptomatic tumors in fetuses have been shown to decrease in size after maternal sicrolimus administration. If clinically silent, they can be watched with routine imaging as the tumor will likely spontaneously regress.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 11.490204081632655, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 5.833333333333333, + "fkgl_delta": -6.86626468769326 + }, + { + "index": 3, + "label": "intermediate_health_literacy", + "original_doc": "This case describes an isolated, asymptomatic fetal cardiac rhabdomyoma first detected at 32 weeks\u2019 gestation. The pregnancy was monitored as an outpatient until 39 weeks plus one day, when delivery occurred by cesarean section. Postnatal follow-up at day 1, day 7, day 30, 7 months, and 12 months showed normal growth and neurodevelopment. The intracardiac mass remained stable in size across all visits. Up to one year of age, the child did not meet any clinical diagnostic criteria for tuberous sclerosis complex (TSC).", + "wiki_anchor": "It is much more common to find metastasis from an alternate site than a primary heart tumor. However, primary cardiac tumors do occur. One of these is the cardiac rhabdomyoma. Approximately 80-90% of these tumors are found in patients with tuberous sclerosis, a genetic condition causing multiple tumors, with most found prior to the age of one. Although these tumors are most commonly treated with resection, symptomatic tumors in fetuses have been shown to decrease in size after maternal sicrolimus administration. If clinically silent, they can be watched with routine imaging as the tumor will likely spontaneously regress.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 11.490204081632655, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 5.833333333333333, + "fkgl_delta": -0.2760835997049398 + }, + { + "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": "There are three types of aortic coarctations:\n Preductal coarctation: The narrowing is proximal to the ductus arteriosus. Blood flow to the aorta that is distal to the narrowing is dependent on the ductus arteriosus; therefore severe coarctation can be life-threatening. Preductal coarctation results when an intracardiac anomaly during fetal life decreases blood flow through the left side of the heart, leading to hypoplastic development of the aorta. This is the type seen in approximately 5% of infants with Turner syndrome.\n Ductal coarctation: The narrowing occurs at the insertion of the ductus arteriosus. This kind usually appears when the ductus arteriosus closes.\n Postductal coarctation: The narrowing is distal to the insertion of the ductus arteriosus. Even with an open ductus arteriosus, blood flow to the lower body can be impaired. This type is most common in adults. It is associated with notching of the ribs (because of collateral circulation), hypertension in the upper extremities, and weak pulses in the lower extremities. Postductal coarctation is most likely the result of the extension of a muscular artery (ductus arteriosus) into an elastic artery (aorta) during fetal life, where the contraction and fibrosis of the ductus arteriosus upon birth subsequently narrows the aortic lumen.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 13.507909090909092, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 7.2727272727272725, + "fkgl_delta": 0.07227329902801571 + }, + { + "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": "Bronchiolitis typically presents in children under two years old and is characterized by a constellation of respiratory symptoms that consists of fever, rhinorrhea, cough, wheeze, tachypnea and increased work of breathing such as nasal flaring or grunting that develops over one to three days. Crackles or wheeze are typical findings on listening to the chest with a stethoscope. The child may also experience apnea, or brief pauses in breathing. After the acute illness, it is common for the airways to remain sensitive for several weeks, leading to recurrent cough and wheeze.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 12.992390109890113, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 10.75, + "fkgl_delta": -10.410926145926148 + }, + { + "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": "Lung destruction in LAM is a consequence of diffuse infiltration by neoplastic smooth muscle-like cells that invade all lung structures including the lymphatics, airway walls, blood vessels and interstitial spaces. The consequences of vessel and airway obstruction include chylous fluid accumulations, hemoptysis, airflow obstruction and pneumothorax. The typical disease course displays progressive dyspnea on exertion, spaced by recurrent pneumothoraces and in some patients, chylous pleural effusions or ascites.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 16.850000000000005, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 8.333333333333334, + "fkgl_delta": -4.121428571428574 + }, + { + "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": "Signs and symptoms\nSigns and symptoms of familial dysautonomia usually commence during infancy and worsen with age, and may include gastrointestinal dysmotility (including erratic gastric emptying, gastroesophageal reflux, abnormal esophageal peristalsis, oropharyngeal incoordination), dysphagia (as poor suckling in infancy) and frequent choking/gagging, recurrent vomiting, poor weight gain/growth, delayed development (especially walking) and puberty (especially in girls), recurrent aspiration pneumonia (due to inhalation of food or vomitus) with possible secondary chronic lung disease, absence of overflow tears during crying, corneal ulcers, red skin blotches and excessive sweating (often during eating or excitement), breath-holding spells, slurred speech/nasal voice, tongue ulcers (from accidental self-injuries), hyporeflexia (variable absence of deep tendon reflexes), hypotonia, enuresis, arrhythmias, hypertension (including episodic hypertension in response to emotional stress or visceral pain), hypotension (including orthostatic hypertension with compensatory tachycardia (invariably present)), impaired (but not absent) temperature and pain perception (leading to frequent accidental injury), impaired proprioception, a smooth glossy tongue, scoliosis (with possibly secondary restrictive lung disease), abnormal gait, short stature, chronic renal failure (common), visual impairment, variable cognitive ability, characteristic facial features that develop with time, impaired vibration perception, lack of fungiform papilla of the tongue, and impaired taste perception (especially for sweetness).\n Autonomic crises - In children with FD, recurrent episodes of vomiting may occur. Such episodes may be triggered by physical (e.g. infection) or emotional stress, may occur every 15\u201320 minutes for over 24 hours, and may be accompanied by significant hypertension, drenching sweat, breathing issues, fever, tachycardia, aspiration pneumonia, skin blotches, drooling, and negative personality change.\n Pain insensitivity - Insensitivity or indifference to painful stimuli may lead to frequent/progressive self-mutilation, burns, and ulcers. There may be self-mutilation of the tongue (especially in toddlers during teething), lips, and cheeks, or loss of teeth. Compulsive oral biting may result in ulcers, or tumour-like masses (Riga-Fede disease).", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 26.22582972582973, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 8.0, + "fkgl_delta": -10.581246392496393 + }, + { + "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": "The anti\u2013glomerular basement membrane (GBM) antibodies primarily attack the kidneys and lungs, although, generalized symptoms like malaise, weight loss, fatigue, fever, and chills are also common, as are joint aches and pains. 60 to 80% of those with the condition experience both lung and kidney involvement; 20-40% have kidney involvement alone, and less than 10% have lung involvement alone. Kidney symptoms usually include blood in the urine, protein in the urine, unexplained swelling of limbs or face, high amounts of urea in the blood, and high blood pressure. Lung symptoms usually antedate kidney symptoms and usually include: coughing up blood, chest pain (in less than 50% of cases overall), cough, and shortness of breath. Some other signs and symptoms that could be used to identify Goodpasture syndrome during a physical exam include an increased respiratory rate, cyanosis, crackles, hepatosplenomegaly, and hypertension.", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 14.907290780141846, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 8.8, + "fkgl_delta": -9.49171710185163 + }, + { + "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": "A patient presenting one of the above conditions but with laboratory evidence against HIV infection is not normally considered to have AIDS, but an AIDS diagnosis may be given if the patient has had Pneumocystis jirovecii pneumonia, and has not:\n undergone high-dose corticoid therapy or other immunosuppressive/cytotoxic therapy in the three months before the onset of the indicator disease\n been diagnosed with Hodgkin's disease, non-Hodgkin's lymphoma, lymphocytic leukemia, multiple myeloma, or any cancer of lymphoreticular or histiocytic tissue, or angioimmunoblastic lymphoadenopathy\n or been diagnosed with a genetic immunodeficiency syndrome atypical of HIV infection, such as one involving hypogammaglobulinemia.", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 47.43408163265306, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 17.0, + "fkgl_delta": -31.01329215896885 + }, + { + "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": "Signs and symptoms\nSigns and symptoms of familial dysautonomia usually commence during infancy and worsen with age, and may include gastrointestinal dysmotility (including erratic gastric emptying, gastroesophageal reflux, abnormal esophageal peristalsis, oropharyngeal incoordination), dysphagia (as poor suckling in infancy) and frequent choking/gagging, recurrent vomiting, poor weight gain/growth, delayed development (especially walking) and puberty (especially in girls), recurrent aspiration pneumonia (due to inhalation of food or vomitus) with possible secondary chronic lung disease, absence of overflow tears during crying, corneal ulcers, red skin blotches and excessive sweating (often during eating or excitement), breath-holding spells, slurred speech/nasal voice, tongue ulcers (from accidental self-injuries), hyporeflexia (variable absence of deep tendon reflexes), hypotonia, enuresis, arrhythmias, hypertension (including episodic hypertension in response to emotional stress or visceral pain), hypotension (including orthostatic hypertension with compensatory tachycardia (invariably present)), impaired (but not absent) temperature and pain perception (leading to frequent accidental injury), impaired proprioception, a smooth glossy tongue, scoliosis (with possibly secondary restrictive lung disease), abnormal gait, short stature, chronic renal failure (common), visual impairment, variable cognitive ability, characteristic facial features that develop with time, impaired vibration perception, lack of fungiform papilla of the tongue, and impaired taste perception (especially for sweetness).\n Autonomic crises - In children with FD, recurrent episodes of vomiting may occur. Such episodes may be triggered by physical (e.g. infection) or emotional stress, may occur every 15\u201320 minutes for over 24 hours, and may be accompanied by significant hypertension, drenching sweat, breathing issues, fever, tachycardia, aspiration pneumonia, skin blotches, drooling, and negative personality change.\n Pain insensitivity - Insensitivity or indifference to painful stimuli may lead to frequent/progressive self-mutilation, burns, and ulcers. There may be self-mutilation of the tongue (especially in toddlers during teething), lips, and cheeks, or loss of teeth. Compulsive oral biting may result in ulcers, or tumour-like masses (Riga-Fede disease).", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 26.22582972582973, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 8.0, + "fkgl_delta": -9.746461909737775 + }, + { + "index": 6, + "label": "low_health_literacy", + "original_doc": "A 34-year-old woman had new lower back pain. She saw blood in her urine. She also had a big bruise under the skin on her right buttock. She had never had bleeding problems before. Because these bleeding signs were serious, she was sent to the emergency room. Doctors did blood-clotting tests. One test mixed her blood with normal blood to see how it clotted. Another test looked for a blocker against a clotting protein called factor eight. These tests confirmed the diagnosis.", + "wiki_anchor": "A person with this disease may also complain of malaise, fatigue, and general weakness (with or without accompanying blood loss). Acquired thrombocytopenia may be associated with the use of certain drugs. Inspection typically reveals evidence of bleeding (petechiae or ecchymoses), along with slow, continuous bleeding from any injuries or wounds. Adults may have large, blood-filled bullae in the mouth. If the person's platelet count is between 30,000 and 50,000/\u03bcL, bruising with minor trauma may be expected; if it is between 15,000 and 30,000/\u03bcL, spontaneous bruising will be seen (mostly on the arms and legs).", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 11.324978723404257, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 6.6, + "fkgl_delta": -6.812864902266046 + }, + { + "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": "Diagnosis\nThe diagnosis of haemophilia C (factor XI deficiency) is centered on prolonged activated partial thromboplastin time (aPTT). One will find that the factor XI has decreased in the individual's body. In terms of differential diagnosis, one must consider: haemophilia A, haemophilia B, lupus anticoagulant and heparin contamination. The prolongation of the activated partial thromboplastin time should completely correct with a 1:1 mixing study with normal plasma if haemophilia C is present; in contrast, if a lupus anticoagulant is present as the cause of a prolonged aPTT, the aPTT will not correct with a 1:1 mixing study.", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 15.3994587628866, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 6.75, + "fkgl_delta": -4.348426154190946 + }, + { + "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": "Early symptoms include anemia, jaundice, splenomegaly, and fatigue. Acute cases can threaten to cause hypoxia secondary to anemia and acute kernicterus through high blood levels of bilirubin, particularly in newborns. Most cases can be detected soon after birth. Testing for HS is available for the children of affected adults. Occasionally, the disease will go unnoticed until the child is about 4 or 5 years of age. A person may also be a carrier of the disease and show no signs or symptoms of the disease. Late complications may result in the development of pigmented gallstones, which is secondary to the detritus of the broken-down blood cells (unconjugated or indirect bilirubin) accumulating within the gallbladder. Also, patients who are heterozygous for a hemochromatosis gene may exhibit iron overload, despite the hemochromatosis genes being recessive. In chronic patients, an infection or other illness can cause an increase in the destruction of red blood cells, resulting in the appearance of acute symptoms, a hemolytic crisis. On a blood smear, Howell-Jolly bodies may be seen within red blood cells. Primary treatment for patients with symptomatic HS has been total splenectomy, which eliminates the hemolytic process, allowing normal hemoglobin, reticulocyte and bilirubin levels. The resultant asplenic patient is susceptible to encapsulated bacterial infection, and prevented with vaccination. If other symptoms, such as abdominal pain persist, the removal of the gallbladder may be warranted for symptomatic cholelithiasis.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 13.152121212121212, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 6.461538461538462, + "fkgl_delta": -1.3728338412588883 + }, + { + "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": "Pregnancy\nDrexler kept her pregnancy secret from the baby's father, her parents and friends. At tall, and about , she apparently showed no signs of her pregnancy. On June 6, 1997, Drexler gave birth in a bathroom stall at her senior prom, twenty minutes after complaining of stomach cramps in the car she had arrived in. She retrieved the baby from the toilet bowl, placed it in a plastic bag, and deposited it in a trash can. It is thought that she severed the umbilical cord on the serrated edge of a sanitary napkin dispenser and suffocated the child. According to the prosecutor, a friend asked if she was all right, and she replied \"I'll be done pretty soon. Go tell the boys we'll be right out.\" She then returned to the dance floor, ate a salad, and danced with her boyfriend. When Drexler and her friends were asked by teachers about the blood in the bathroom, she replied that she was having a heavy menstrual period. The baby was discovered in a trash bin by a janitor, after a school nurse cleaned the bloody bathroom stall, emptied the trash can, and became suspicious of the weight of the trash bag.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 8.73, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 6.5, + "fkgl_delta": -5.4689565217391305 + }, + { + "index": 7, + "label": "intermediate_health_literacy", + "original_doc": "A full\u2011term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non\u2011tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra\u2011operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.", + "wiki_anchor": "A hydrocele testis feels like a small fluid-filled balloon inside the scrotum. It is smooth, and is mainly in front of the testis. Hydrocele testes vary greatly in size and are typically painless and harmless. However, as the fluid continues to accumulate and the scrotum further enlarges, more discomfort can be expected. Large hydroceles will cause discomfort because of their size. Sometimes pain can be in both testicles as pressure from the enlarged area puts pressure against the unaffected area which can cause discomfort to the normal testicle. It has also been found to decrease a man's sex drive and makes him less active for fear of enlarging the mass. As the fluid of a hydrocele testis is transparent, light shone through the hydrocelic region will be visible from the other side. This phenomenon is called transillumination.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 9.295571776155722, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 6.0, + "fkgl_delta": 2.488464483386263 + }, + { + "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": "Complications\nAmong the complications of hydrocele are:\n Rupture usually occurs as a result of trauma but may be spontaneous. On rare occasions cure results after the fluid has been absorbed.\n Transformation into a haematocele occurs if there is spontaneous bleeding into the sac or as a result of trauma. Acute haemorrhage into the tunica vaginalis sometimes results from testicular trauma and it may be difficult without exploration to decide whether the testis has been ruptured. If the haematocele is not drained, a clotted haematocele usually results.\n The sac may calcify. Clotted hydrocele may result from a slow spontaneous ooze of blood into the tunica vaginalis. It is usually painless and by the time the patient seeks help, it may be difficult to be sure that the swelling is not due to a testicular tumour. Indeed, a tumour may present as a haematocele.\n Occasionally, severe infection can be introduced by aspiration. Simple aspiration, however, often may be used as a temporary measure in those cases where surgery is contraindicated or must be postponed.\n Postherniorrhaphy hydrocele is a relatively rare complication of inguinal hernia repair. It is possibly due to interruption to the lymphatics draining the scrotal contents.\n Infection which may lead to pyocele.\n Atrophy of testis in long standing cases.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 10.846870813397132, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 5.666666666666667, + "fkgl_delta": 4.272124401913878 + }, + { + "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": "Signs and symptoms\nThe symptoms of the disease include a high fever with frontal headaches, chills, severe muscle pain, vomiting, and other gastrointestinal symptoms. Bleeding problems may occur 3\u20134 days after initial symptom onset. Patients may experience abnormally low blood pressure, and low platelet, red blood cell, and white blood cell count. After 1\u20132 weeks of symptoms, some patients recover without complication. However, the illness is biphasic for a subset of patients (10-20%) who experience a second wave of symptoms at the beginning of the third week. These symptoms include fever and signs of neurological manifestations, such as severe headache, mental disturbances, tremors, and vision deficits. The convalescent period is typically very long, lasting several months. Muscle aches and weakness also occur during this period, and the patient is unable to engage in physical activities.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 11.881620370370374, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.25, + "fkgl_delta": -7.087231881161742 + }, + { + "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": "Hemolytic\u2013uremic syndrome (HUS) is a group of blood disorders characterized by low red blood cells, acute kidney failure, and low platelets. Initial symptoms typically include bloody diarrhea, fever, vomiting, and weakness. Kidney problems and low platelets then occur as the diarrhea progresses. Children are more commonly affected, but most children recover without permanent damage to their health, although some children may have serious and sometimes life-threatening complications. Adults, especially the elderly, may present a more complicated presentation. Complications may include neurological problems and heart failure.", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 12.702058823529416, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 5.666666666666667, + "fkgl_delta": 2.051467012336847 + }, + { + "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": "Symptoms\nPhysical dependence can manifest itself in the appearance of both physical and psychological symptoms which are caused by physiological adaptions in the central nervous system and the brain due to chronic exposure to a substance. Symptoms which may be experienced during withdrawal or reduction in dosage include increased heart rate and/or blood pressure, sweating, and tremors. More serious withdrawal symptoms such as confusion, seizures, and visual hallucinations indicate a serious emergency and the need for immediate medical care. Sedative hypnotic drugs such as alcohol, benzodiazepines, and barbiturates are the only commonly available substances that can be fatal in withdrawal due to their propensity to induce withdrawal convulsions. Abrupt withdrawal from other drugs, such as opioids can cause an extremely painful withdrawal that is very rarely fatal in patients of general good health and with medical treatment, but is more often fatal in patients with weakened cardiovascular systems; toxicity is generally caused by the often-extreme increases in heart rate and blood pressure (which can be treated with clonidine), or due to arrhythmia due to electrolyte imbalance caused by the inability to eat, and constant diarrhea and vomiting (which can be treated with loperamide and ondansetron respectively) associated with acute opioid withdrawal, especially in longer-acting substances where the diarrhea and emesis can continue unabated for weeks, although life-threatening complications are extremely rare, and nearly non-existent with proper medical management.", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 24.758912280701754, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 9.6, + "fkgl_delta": -9.800258606866628 + }, + { + "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": "Cardiogenic\n Congestive heart failure which is due to the heart's inability to pump the blood out of the pulmonary circulation at a sufficient rate resulting in elevation in pulmonary wedge pressure and edema \u2013 this usually is due to left ventricular failure, but may also be from arrhythmias, or fluid overload, (e.g. from kidney failure or intravenous therapy).\n Hypertensive crisis can cause pulmonary edema as the elevation in blood pressure and increased afterload on the left ventricle hinders forward flow in blood vessels and causes the elevation in wedge pressure and subsequent pulmonary edema.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 18.70430107526882, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 12.0, + "fkgl_delta": -12.182093283061029 + }, + { + "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": "Coronary catheterization is one of the several cardiology diagnostic tests and procedures. Specifically, through the injection of a liquid radiocontrast agent and illumination with X-rays,\n angiocardiography allows the recognition of occlusion, stenosis, restenosis, thrombosis or aneurysmal enlargement of the coronary artery lumens; heart chamber size; heart muscle contraction performance; and some aspects of heart valve function. Important internal heart and lung blood pressures, not measurable from outside the body, can be accurately measured during the test. The relevant problems that the test deals with most commonly occur as a result of advanced atherosclerosis \u2013 atheroma activity within the wall of the coronary arteries. Less frequently, valvular, heart muscle, or arrhythmia issues are the primary focus of the test.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 16.631726495726493, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 6.8, + "fkgl_delta": -3.151726495726489 + }, + { + "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": "There are three types of aortic coarctations:\n Preductal coarctation: The narrowing is proximal to the ductus arteriosus. Blood flow to the aorta that is distal to the narrowing is dependent on the ductus arteriosus; therefore severe coarctation can be life-threatening. Preductal coarctation results when an intracardiac anomaly during fetal life decreases blood flow through the left side of the heart, leading to hypoplastic development of the aorta. This is the type seen in approximately 5% of infants with Turner syndrome.\n Ductal coarctation: The narrowing occurs at the insertion of the ductus arteriosus. This kind usually appears when the ductus arteriosus closes.\n Postductal coarctation: The narrowing is distal to the insertion of the ductus arteriosus. Even with an open ductus arteriosus, blood flow to the lower body can be impaired. This type is most common in adults. It is associated with notching of the ribs (because of collateral circulation), hypertension in the upper extremities, and weak pulses in the lower extremities. Postductal coarctation is most likely the result of the extension of a muscular artery (ductus arteriosus) into an elastic artery (aorta) during fetal life, where the contraction and fibrosis of the ductus arteriosus upon birth subsequently narrows the aortic lumen.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 13.507909090909092, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 7.2727272727272725, + "fkgl_delta": -4.442276179516686 + }, + { + "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": "Many people with Stickler syndrome are very nearsighted (described as having high myopia) because of the shape of the eye. People with eye involvement are prone to increased pressure within the eye (ocular hypertension) which could lead to glaucoma and tearing or detachment of the light-sensitive retina of the eye (retinal detachment). Cataract may also present as an ocular complication associated with Stickler's Syndrome. The jelly-like substance within the eye (the vitreous humour) has a distinctive appearance in the types of Stickler syndrome associated with the COL2A1 and COL11A1 genes. As a result, regular appointments to a specialist ophthalmologist are advised. The type of Stickler syndrome associated with the COL11A2 gene does not affect the eye.", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 13.108620689655172, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 9.0, + "fkgl_delta": -6.5111112911589295 + }, + { + "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": "The second most common initial manifestation of the disease is inflammation of the optic nerve and/or optic chiasm (optic neuritis, ON). ON may lead to varying degrees of visual impairment with decreased visual acuity, although visual field defects, or loss of color vision, may occur in isolation or prior to formal loss of visual acuity. Compared to idiopathic ON and ON due to multiple sclerosis (MS), ON due to NMOSD more often results in severe visual loss at onset, with bilateral involvement, and permanent visual deficits.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 17.680697674418607, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 7.333333333333333, + "fkgl_delta": -6.138837209302327 + }, + { + "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": "It is commonly associated with diabetes. Chronic or uncontrolled diabetes type 2 can affect peripheral blood vessels including those of the retina which may leak fluid, blood and occasionally fats into the retina causing it to swell.\nAge-related macular degeneration may cause macular edema. As individuals age there may be a natural deterioration in the macula which can lead to the depositing of drusen under the retina sometimes with the formation of abnormal blood vessels.\nReplacement of the lens as treatment for cataract can cause pseudophakic macular edema. (\u2018pseudophakia\u2019 means \u2018replacement lens\u2019) also known as Irvine-Gass syndrome The surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. Less common today with modern lens replacement techniques. \nChronic uveitis and intermediate uveitis can be a cause. \nBlockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina. The blockage may be caused, among other things, by atherosclerosis, high blood pressure and glaucoma.\nA number of drugs can cause changes in the retina that can lead to macular edema. The effect of each drug is variable and some drugs have a lesser role in causation. The principal medication known to affect the retina are:- latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others.\nA few congenital diseases are known to be associated with macular edema for example retinitis pigmentosa and retinoschisis.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 12.634700460829496, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 6.714285714285714, + "fkgl_delta": 2.027169669040635 + }, + { + "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": "On 16 August 1898, Bier performed the first operation under spinal anesthesia at the Royal Surgical Hospital of the University of Kiel. The patient was scheduled to undergo segmental resection of his left ankle, which was severely infected with tuberculosis, but he dreaded the prospect of general anesthesia because he had suffered severe adverse side effects during multiple previous operations. Therefore, Bier suggested \"cocainization\" of the spinal cord as an alternative to general anesthesia. Bier injected 15\u00a0mg of cocaine intrathecally, which was sufficient to allow him to perform the operation. The subject was fully conscious during the operation, but felt no pain. Two hours after the operation, the subject complained of nausea, vomiting, severe headache, and pain in his back and ankle. The vomiting, back and leg pain improved by the following day, but the headache was still present. Bier performed spinal anesthetics on five more subjects for lower extremity surgery, using a similar technique and achieving similar results.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 13.745000000000001, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 6.625, + "fkgl_delta": -7.202280701754383 + }, + { + "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": "Epidural anaesthesia causes a loss of sensation, including pain, by blocking the transmission of signals through nerve fibres in or near the spinal cord. For this reason, epidurals are commonly used for pain control during childbirth and surgery. The technique is considered safe and effective for providing pain relief during childbirth and surgery, and is considered more effective and safer than giving pain medication by mouth or through an intravenous line. An epidural injection may also be used to administer steroids for the treatment of inflammatory conditions of the spinal cord. It is not recommended for people with severe bleeding disorders, low platelets, or infections near the intended injection site. Severe complications from epidural administration are rare, but can include problems resulting from improper administration, as well as side effects of the medicines administered. The most common complications of epidural injections include bleeding problems, headaches, and inadequate pain control. Epidural analgesia during childbirth may also impact the mother's ability to move during labor. Very large doses of anesthetics or analgesics may result in respiratory depression.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 14.379619047619048, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 7.111111111111111, + "fkgl_delta": -1.4693249299719895 + }, + { + "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": "A supraventricular tachycardia with a ventricular heart rate of 150 beats per minute is suggestive (though not necessarily diagnostic) of atrial flutter. Administration of adenosine in the vein (intravenously) can help medical personnel differentiate between atrial flutter and other forms of supraventricular tachycardia. Immediate treatment of atrial flutter centers on slowing the heart rate with medications such as beta blockers (e.g., metoprolol) or calcium channel blockers (e.g., diltiazem) if the affected person is not having chest pain, has not lost consciousness, and if their blood pressure is normal (known as stable atrial flutter). If the affected person is having chest pain, has lost consciousness, or has low blood pressure (unstable atrial flutter), then an urgent electrical shock to the heart to restore a normal heart rhythm is necessary. Long-term use of blood thinners (e.g., warfarin or apixaban) is an important component of treatment to reduce the risk of blood clot formation in the heart and resultant strokes. Medications used to restore a normal heart rhythm (antiarrhythmics) such as ibutilide effectively control atrial flutter about 80% of the time when they are started but atrial flutter recurs at a high rate (70\u201390% of the time) despite continued use. Atrial flutter can be treated more definitively with a technique known as catheter ablation. This involves the insertion of a catheter through a vein in the groin which is followed up to the heart and is used to identify and interrupt the electrical circuit causing the atrial flutter (by creating a small burn and scar).", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 13.24533910533911, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 8.625, + "fkgl_delta": 0.2305013038680528 + }, + { + "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": "Urinary tract\nOne of the most common causes of dysuria is urinary tract infection. Urinary tract infections are more common in females than in males due to anatomical differences between them. Females have a comparatively shorter and straight urethra, whereas males have a longer and curved urethra. In females, bacteria can reach the bladder more easily, as they have less distance to travel. Most urinary tract infections are uncomplicated.\n Chlamydia\n Cystitis\n Hemorrhagic cystitis\n Kidney stones\n Malignancy, i.e., bladder cancer, prostatic cancer, or urethral cancer\n Prostatic enlargement, i.e., benign prostatic hyperplasia (male), prostatic cancer\n Prostatitis (male)\n Pyelonephritis\n Sexually transmitted disease\n Trichomoniasis\n Urethral stricture\n Urethritis\n Urinary schistosomiasis\n Urinary tract infection (UTI) caused by bacterial infection", + "doc_fkgl": 6.041, + "wiki_fkgl": 14.771847345132745, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 6.5, + "fkgl_delta": -8.730847345132744 + }, + { + "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": "Signs and symptoms\nThe symptoms of a cystocele may include:\n a vaginal bulge\n the feeling that something is falling out of the vagina\n the sensation of pelvic heaviness or fullness\n difficulty starting a urine stream\n a feeling of incomplete urination\n frequent or urgent urination\n fecal incontinence\n frequent urinary tract infections\n back and pelvic pain\n fatigue\n painful sexual intercourse\n bleeding", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 29.220000000000002, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 14.0, + "fkgl_delta": -17.037592592592592 + }, + { + "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": "Ureaplasma spp. as human pathogens \nBoth Ureaplasma urealyticum and Ureaplasma parvum have been identified as important human pathogens, causing infection in the urogenital tract and, rarely, at distal sites. Their role in neonatal disease and adverse pregnancy outcomes has been well established, and semantic classifications are changing to reflect the nature of the detrimental outcomes these infections are associated with. In the 2010s, Mycoplasma genitalium has been re-classified as an STI, and it is likely that with more research, Ureaplasma spp. will follow this trend. Similar to other pathogens such as Chlamydia trachomatis, infection with Ureaplasma spp. is associated with adverse fertility outcomes in both men and women. Both cause non-gonococcal urethritis. Ureaplasma spp. were implicated in conditions such as prostatitis and chronic pelvic pain syndrome as early as the 1980s. Research in women has lagged several decades behind, but it is now becoming more clear how Ureaplasma spp. contribute to etiologies such as interstitial cystitis/painful bladder syndrome. Ureaplasma spp. are associated with alterations in host environment that increase susceptibility to other infections such as bacterial vaginosis and vaginal candidiasis. Ureaplasma spp. can cause reactive arthritis as well as directly infect the synovium. Some case studies have suggested a causative role in complex regional pain syndrome/reflex sympathetic dystrophy syndrome.", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 13.26373205741627, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.083333333333333, + "fkgl_delta": 1.6936629005669275 + }, + { + "index": 13, + "label": "low_health_literacy", + "original_doc": "A 36-year-old woman had a long-term bowel disease (ulcerative colitis). She came in with chest pain that kept getting worse. She also had shortness of breath, sweating, and felt sick to her stomach. For months she had felt very tired and had night sweats. Her heart test (EKG) showed signs of a heart attack in the lower part of the heart. Doctors did a dye X-ray to look at the heart arteries. It showed bad blockages in two heart pipes. They opened the most blocked pipe right away with a balloon and a tiny mesh tube (stent). While looking, the team worried the main body artery (aorta) was swollen. Blood tests showed mild inflammation. A special CT scan showed the aorta wall looked thick and scarred, with tight narrow spots in several arteries. This pointed to a rare illness that causes swollen big arteries, called Takayasu arteritis. She started strong anti-inflammatory and immune medicines (prednisone and methotrexate). Later she had heart bypass surgery to improve blood flow. She did well after treatment.", + "wiki_anchor": "Of note is the function of renal artery stenosis in the causation of high blood pressure: Normally perfused kidneys produce a proportionate amount of a substance called renin. Stenosis of the renal arteries causes hypoperfusion (decreased blood flow) of the juxtaglomerular apparatus, resulting in exaggerated secretion of renin, and high blood levels of aldosterone, eventually leading to water and salt retention and high blood pressure. The neurological symptoms of the disease vary depending on the degree; the nature of the blood vessel obstruction; and can range from lightheadedness to seizures (in severe cases). One rare, important feature of the Takayasu's arteritis is ocular involvement in form of visual field defects, vision loss, or retinal hemorrhage. Some individuals with Takayasu's arteritis may present with only late vascular changes, without a preceding systemic illness. In the late stage, weakness of the arterial walls may give rise to localized aneurysms. As with all aneurysms, the possibility of rupture and vascular bleeding is existent and requires monitoring. In view of the chronic process and good collateral development, Raynaud's phenomenon or digital gangrene are very rare in Takayasu arteritis. A rare complication of this condition are coronary artery aneurysms.", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 14.470274914089348, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 7.111111111111111, + "fkgl_delta": -8.642926076880041 + }, + { + "index": 13, + "label": "intermediate_health_literacy", + "original_doc": "A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.\n\nUrgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.\n\nShe started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.", + "wiki_anchor": "Those with the disease often notice symptoms between 15 and 30 years of age. In the Western world, atherosclerosis is a more frequent cause of obstruction of the aortic arch vessels than Takayasu's arteritis. Takayasu's arteritis is similar to other forms of vasculitis, including giant cell arteritis which typically affects older individuals. Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery, Takayasu's arteritis can present as pulseless upper extremities (arms, hands, and wrists with weak or absent pulses on the physical examination) which may be why it is also commonly referred to as the \"pulseless disease.\" Involvement of renal arteries may lead to a presentation of renovascular hypertension.", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 15.397495934959352, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 8.4, + "fkgl_delta": -0.8036864111498261 + }, + { + "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": "abrupt cessation of physical exertion (resulting in heart output in excess of current muscular need for blood flow)\n abdominal cutaneous nerve entrapment syndrome (ACNES), usually in patients who have had abdominal surgery \n alcohol flush reaction\n antiestrogens such as tamoxifen\n atropine poisoning\n body contact with warm or hot water (hot tub, bath, shower)\n butorphanol reaction with some narcotic analgesics (since butorphanol is also an antagonist)\n caffeine consumption\n carbon monoxide poisoning\n carcinoid tumor\n chronic obstructive pulmonary disease (COPD), especially emphysema (also known as \"pink puffer\")\n cluster headache attack or headache\n compression of the nerve by the sixth thoracic vertebrae\n coughing, particularly severe coughing fits\n Cushing's syndrome\n dehydration\n dysautonomia\n emotions: anger, embarrassment (for this reason it is also called erythema pudoris, from the Latinized Greek word for \"redness\" and the Latin \"of embarrassment\")\n fever\n fibromyalgia\n histamines\n homocystinuria (flushing across the cheeks)\n Horner's syndrome\n hot flush\n hyperglycaemia\n hyperstimulation of the parasympathetic nervous system, especially the vagus nerve\n hyperthyroidism\n inflammation (for example, caused by allergic reaction or infection)\n iron poisoning\n Jarisch-Herxheimer reaction (caused by antibiotics)\n keratosis pilaris rubra faceii\n Kratom\n mastocytosis\n medullary thyroid cancer\n mixing an antibiotic with alcohol\n neuroendocrine tumors\n niacin (vitamin B3)\n pheochromocytoma \n polycythemia vera\n powerful vasodilators, such as dihydropyridine calcium channel blockers\n severe pain\n sexual arousal, especially orgasm (see following section)\n sexual intercourse (see below)\n sneezing (red nose)\n some recreational drugs, such as alcohol, heroin, cocaine and amphetamines\n spicy foods\n sunburn (erythema)\n tachycardia\n vinpocetine", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 99.86327586206897, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 16.0, + "fkgl_delta": -82.89052143168922 + }, + { + "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": "In nearly all cases one or more chest tubes are placed. These tubes are used to drain air and fluid until the patient heals enough to take them out (usually a few days). Complications such as pneumothorax, tension pneumothorax, or subcutaneous emphysema can occur if these chest tubes become clogged. Furthermore, complications such as pleural effusion or hemothorax can occur if the chest tubes fail to drain the fluid around the lung in the pleural space after a thoracotomy. Clinicians should be on the look out for chest tube clogging as these tubes have a tendency to become occluded with fibrinous material or clot in the post operative period, and when this happens, complications ensue.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 12.260000000000002, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.2, + "fkgl_delta": -6.529911347517732 + }, + { + "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": "Characteristic features are edema (swelling due to excess fluid) of the face and arms and development of swollen collateral veins on the front of the chest wall. Shortness of breath and coughing are quite common symptoms; difficulty swallowing is reported in 11% of cases, headache in 6% and stridor (a high-pitched wheeze) in 4%. The symptoms are rarely life-threatening, though edema of the epiglottis can make breathing difficult, edema of the brain can cause reduced alertness, and in less than 5% of cases of SVCO, severe neurological symptoms or airway compromise are reported. Resolution of superior vena cava syndrome is directly related to the treatment of the underlying compression.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 15.389793577981653, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 8.5, + "fkgl_delta": -3.4049852156123137 + }, + { + "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": "Gastrointestinal tract diverticula \nEsophageal diverticula may occur in one of three areas of the esophagus:\nPharyngeal (Zenker's) diverticula usually occur in the elderly, through Killian's triangle above the cricopharyngeal muscle.\nMidesophageal diverticula\nEpiphrenic diverticula are due to dysfunction of the lower esophageal sphincter, as in achalasia.\nA duodenal diverticulum can be found incidentally in 23% of normal people undergoing imaging. It can be either congenital or acquired, but the acquired form is more common and is due to the weakness of the duodenal wall, which causes protrusions. It is usually found at the second or third part of duodenum, around the ampulla of Vater. Food debris may enter the diverticular outpouchings, causing inflammation or diverticulitis. On CT or MRI imaging, it appears as a sac-like outpouching. If the diverticulum is filled with contrast agents, the wall would be thin and may contain air, fluid, contrast material, or food debris. If the food debris is broken down by bacteria, the outpouching may show \"faeces sign\". Inflammation of the duodenal wall shows thickening of the wall. Rarely, on barium studies in congenital duodenal diverticula, the contrast material fills up the true lumen, causing \"windsock\" deformity.\nA jejunal diverticulum is a congenital lesion and may be a source of bacterial overgrowth. It may also perforate or result in abscesses.\nA Killian-Jamieson diverticulum is very similar to a pharyngeal esophageal diverticulum, differing in the fact that the pouching is below the cricopharyngeal muscle.\nColonic diverticula, although found incidentally during colonoscopy, may become infected (see diverticulitis) and can perforate, requiring surgery.\nGastric diverticula are very infrequent.\nMeckel's diverticulum, a persistent portion of the omphalomesenteric duct, is present in 2% of the population, making it the most common congenital gastrointestinal malformation.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 14.25841073271414, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 5.823529411764706, + "fkgl_delta": 2.196676986584105 + }, + { + "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": "Birt\u2013Hogg\u2013Dub\u00e9 syndrome affects the skin and increases the risk of tumors in the kidneys and lungs. The condition is characterized by multiple noncancerous, dome-shaped tumors of the hair follicles (fibrofolliculomas), particularly on the face, neck, and more rarely, the upper chest. The fibrofolliculomas are generally described as having an opaque white color or a yellowish tone and have a waxy, smooth texture. The tumors are always found on and around the nose and on and behind the outer ear. Typically, they first appear in a person's 20s or 30s, and are found in more than 80% of people with the syndrome above the age of 40. The tumors become larger and more numerous over time. Tumors differ between individuals; they may appear merged in plaques, look similar to a comedo with a plug of keratin, or include epidermoid cysts. A large number of tumors on the face can be associated with hyperseborrhea (abnormally elevated sebum production). The presence of fibrofolliculomas on a person's face can cause significant psychological distress.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 11.632741617357002, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 7.0, + "fkgl_delta": -6.370074104666646 + }, + { + "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": "Diagnosis is typically delayed 5 to 6 years. The condition is often misdiagnosed as asthma or chronic obstructive pulmonary disease. The first pneumothorax, or lung collapse, precedes the diagnosis of LAM in 82% of patients. The consensus clinical definition of LAM includes multiple symptoms:\n Fatigue\n Cough\n Coughing up blood (rarely massive)\n Chest pain\n Chylous complications arising from lymphatic obstruction, including\n Chylothorax\n Chylous ascites\n Chylopericardium\n Chyloptysis\n Chyluria\n Chyle in vaginal discharge\n Chyle in stool\n Angiomyolipomas (fatty kidney tumors) are present in about 30% of patients with sporadic LAM and up to 90% of patients with TSC-LAM. Angiomyolipomas can sometimes spontaneously bleed, causing pain or low blood pressure.\n Cystic lymphangiomas or lymph nodes with hypodense centers, which mimic necrotizing lymphomas, ovarian or renal cancers, or other malignancies can occur in the retroperitoneum, pelvis or mediastinum.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 15.324172932330828, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": -1.4311198349856937 + }, + { + "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": "Granulosa cell tumour. This tumour produces granulosa cells, which normally are found in the ovary. It is malignant in 20% of women diagnosed with it. It tends to present in women in the 50-55yo age group with post menopausal vaginal bleeding. Uncommonly, a similar but possibly distinct tumour, juvenile granulosa cell tumour, presents in pre-pubertal girls with precocious puberty. In both groups, the vaginal bleeding is due to oestrogen secreted by the tumour. In older women, treatment is total abdominal hysterectomy and removal of both ovaries. In young girls, fertility sparing treatment is the mainstay for non-metastatic disease.\n Sertoli cell tumour. This tumour produces Sertoli cells, which normally are found in the testicle. This tumour occurs in both men and women.\nThecoma. This tumour produces theca of follicle, a tissue normally found in the ovarian follicle. The tumour is almost exclusively benign and unilateral. It typically secretes estrogen, and as a result women with this tumour often present with postmenopausal bleeding.\nLeydig cell tumour. This tumour produces Leydig cells, which normally are found in the testicle and tend to secrete androgens.\nSertoli\u2013Leydig cell tumour. This tumour produces both Sertoli and Leydig cells. Although both cell types normally occur in the testicle, this tumour can occur in the ovary.\nGynandroblastoma. A very rare tumour producing both ovarian (granulosa and/or theca) and testicular (Sertoli and/or Leydig) cells or tissues. Typically it consists of adult-type granulosa cells and Sertoli cells, but it has been reported with juvenile-type granulosa cells. It has been reported to occur in the ovary usually, rarely in the testis. Due to its rarity, the malignant potential of this tumour is unclear; there is one case report of late metastasis.\nSex cord tumour with annular tubules, abbreviated SCTAT. These are rare tumours that may be sporadic or associated with Peutz\u2013Jeghers syndrome.", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 10.157427242524918, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 4.962962962962963, + "fkgl_delta": 4.959663666565991 + }, + { + "index": 16, + "label": "low_health_literacy", + "original_doc": "A 59-year-old man with type 1 diabetes came to the hospital with heart failure. A heart ultrasound showed big clumps of germs stuck to two heart valves, the mitral and the aortic valves. His blood test grew a germ called Staphylococcus warneri. This is a kind of staph that usually lives on the skin and is normally harmless. Doctors found he had an infection on his own heart valves (native valve endocarditis). He later had surgery to replace both the mitral and the aortic valves. Looking back, small lab changes and weight loss that began about four months earlier may have been early warning signs. He had not been on immune-weakening medicines and did not have any implanted medical devices.", + "wiki_anchor": "Rheumatic fever (RF) is an inflammatory disease that can involve the heart, joints, skin, and brain. The disease typically develops two to four weeks after a streptococcal throat infection. Signs and symptoms include fever, multiple painful joints, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of the cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks but can sometimes occur after one. The damaged valves may result in heart failure, atrial fibrillation and infection of the valves.", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 11.152113402061858, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 6.833333333333333, + "fkgl_delta": -3.683780068728524 + }, + { + "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": "Presentation\nAll of these organisms are part of the normal oropharyngeal flora, which grow slowly (up to 14 days), prefer a carbon dioxide\u2013enriched atmosphere, and share an enhanced capacity to produce endocardial infections, especially in young children. Collectively, they account for 5\u201310% of cases of infective endocarditis involving native valves and are the most common Gram-negative cause of endocarditis among people who do not use drugs intravenously. They have been a frequent cause of culture-negative endocarditis. Culture-negative refers to an inability to produce a colony on regular agar plates because these bacteria are fastidious (require a specific nutrient).", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 16.60173469387755, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 7.75, + "fkgl_delta": -3.605655666521926 + }, + { + "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": "New South Wales \n Armidale Regional Hospital - Armidale - University of New South Wales Faculty of Medicine\n Batemans Bay Hospital, Batemans Bay - Australian National University Medical School\n Bega District Hospital, Bega - Australian National University Medical School\n Bega Valley Private Hospital, Bega - Australian National University Medical School\n Sapphire Coast Medical Practice at Bega and Tathra - Australian National University Medical School\n Blacktown Hospital, Blacktown - University of Sydney & Western Sydney University\n Camden and Campbelltown Hospitals (Campbelltown, Camden, Sydney) - Western Sydney University\n Cessnock District Hospital - Cessnock - University of New South Wales Faculty of Medicine\n Dubbo Base Hospital and Orange Base Hospital, Dubbo - Sydney Medical School\n Glen Innes District Hospital - Glen Innes- University of New South Wales Faculty of Medicine\n Gloucester Soldiers' Memorial Hospital- Gloucester - University of New South Wales Faculty of Medicine\n Gosford Hospital, Gosford - University of Newcastle, University of New England\n Goulburn Base Hospital, Goulburn - Australian National University Medical School\n Katungal Aboriginal Medical Service - Australian National University Medical School\n Kenmore Hospital, Goulburn - Australian National University Medical School\n St John of God Hospital, Goulburn - Australian National University Medical School\n Chisholm Ross Centre, Goulburn - Australian National University Medical School\n Gunnedah District Hospital - Gunnedah - University of New South Wales Faculty of Medicine\n Hornsby Ku-ring-gai Hospital, Hornsby - University of Sydney\n Inverell District Hospital- Inverell - University of New South Wales Faculty of Medicine\n Nepean Hospital, Kingswood(suburb of Sydney) - Sydney Medical School\n Liverpool Hospital, Liverpool - University of New South Wales & Western Sydney University\n Maitland Hospital- Maitland - University of New South Wales Faculty of Medicine\n Sapphire Clinic, Merimbula\n Moree District Hospital - Moree - University of New South Wales Faculty of Medicine\n Moruya Hospital, Moruya\n Muswellbrook District Hospital- Muswellbrook - University of New South Wales Faculty of Medicine\n Nelson Bay and District Polyclinic - Nelson Bay - University of New South Wales Faculty of Medicine\n Newcastle Mater Misericordiae Hospital - Newcastle - University of New South Wales Faculty of Medicine\n John Hunter Hospital - Newcastle - University of New South Wales Faculty of Medicine\n Orange Health Service, Orange - University of Sydney\n Pambula Hospital, Pambula\n Scott Memorial Hospital - Scone - University of New South Wales Faculty of Medicine\n Shoalhaven District Memorial Hospital, Nowra - University of Wollongong and University of New South Wales\n Singleton District Hospital - Singleton - University of New South Wales Faculty of Medicine\n Macquarie University Hospital, Sydney - Macquarie University Australian School of Advanced Medicine\n Prince of Wales Hospital (Sydney) - University of New South Wales\n Royal Prince Alfred Hospital, Sydney - Sydney Medical School \n Westmead Hospital, Sydney - Sydney Medical School\n Royal Alexandra Hospital for Children, Sydney - Sydney Medical School\n Concord Repatriation General Hospital, Sydney - Sydney Medical School\n Royal North Shore Hospital, Sydney - Sydney Medical School\n Royal Hospital for Women, Sydney - University of Sydney, University of New South Wales\n Royal Prince Alfred Hospital, Sydney - University of Sydney\n St George Hospital (Sydney) - University of New South Wales\n St Vincent's Hospital, Sydney - University of New South Wales\n Sydney Adventist Hospital, Sydney - Sydney Medical School\n Sydney Children's Hospital, Sydney - University of New South Wales\n Sydney Dental Hospital, Sydney - University of Sydney\n Manning Base Hospital - Taree - University of New South Wales Faculty of Medicine\n Tamworth Base Hospital - Tamworth - University of New South Wales Faculty of Medicine\n Prince Albert Memorial Hospital - Tenterfield - University of New South Wales Faculty of Medicine\n Wollongong Hospital, Wollongong - University of Wollongong", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 215.7971482889734, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 14.6, + "fkgl_delta": -203.29981064815166 + }, + { + "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": "Flexible sigmoidoscopy \nFlexible sigmoidoscopy enables the physician to look at the inside of the large intestine from the rectum to the left side of the colon, called the sigmoid. Physicians may use the procedure to find the cause of diarrhea, abdominal pain, or constipation. They also use it to look for benign and malignant polyps, as well as early signs of cancer in the descending colon and rectum. With flexible sigmoidoscopy, the physician can see intestinal bleeding, inflammation, abnormal growths, and ulcers in the descending colon and rectum. Flexible sigmoidoscopy is not sufficient to detect polyps or cancer in the ascending or transverse colon (two-thirds of the colon). However, although in absolute terms only a relatively small section of the large intestine can be examined using sigmoidoscopy, the sites which can be observed represent areas which are most frequently affected by diseases such as colorectal cancer, for example the rectum.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 14.770666666666667, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 8.0, + "fkgl_delta": -9.585616216707574 + }, + { + "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": "Diseases of the large intestine which may require surgical removal include Crohn's disease, ulcerative colitis, familial adenomatous polyposis, and total colonic Hirschsprung's disease. An ileostomy may also be necessary in the treatment of colorectal cancer or ovarian cancer. One example is a situation where the cancer tumor is causing a blockage (obstruction). In such a case the ileostomy may be temporary, as the common surgical procedure for colorectal cancer is to reconnect the remaining sections of colon or rectum following removal of the tumor provided that enough of the rectum remains intact to preserve internal/external anal sphincter function.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 16.60173469387755, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 7.0, + "fkgl_delta": 0.3325559044130486 + }, + { + "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": "Medical procedures\n Amniotomy \u2013 An incision created to accelerate labor.\n Androtomy \u2013 Dissection of the human body .\n Bilateral cingulotomy \u2013 Psychosurgery, treatment for depression and addiction .\n Bronchotomy \u2013 A procedure that ensures there is an open airway between a patients lung/s and the outside world.\n Clitoridotomy \u2013 Plastic surgery of the clitorial hood.\n Coeliotomy \u2013 A large incision through the abdominal wall to gain access into the abdominal cavity\n Colpotomy \u2013 Extraction of fluid from the pouch of Douglas (a rectouterine pouch[1] posterior to the vagina) through a needle\n Cordotomy \u2013 Procedure that disables selected pain-conducting tracts in the spinal cord, in order to achieve loss of pain and temperature perception\n Craniotomy \u2013 A bone flap is temporarily removed from the skull to access the brain\n Cricothyrotomy \u2013 An incision made through the skin and cricothyroid membrane to establish a patent airway during certain life-threatening situations\n Escharotomy \u2013 Procedure used to treat full-thickness (third-degree) circumferential burns\n Episiotomy \u2013 Surgical incision of the perineum and the posterior vaginal wall\n Fasciotomy \u2013 Surgical procedure where the fascia is cut to relieve tension or pressure commonly to treat the resulting loss of circulation to an area of tissue or muscle\n Heller myotomy \u2013 Muscles of the cardia (lower oesophageal sphincter or LOS) are cut, allowing food and liquids to pass to the stomach\n Hymenotomy \u2013 Surgical removal or opening of the hymen\n Hysterotomy \u2013 Incision in the uterus, and is performed during a Caesarean section\n Laminotomy \u2013 The partial removal (or by making a larger opening) of the lamina.\n Laparotomy \u2013 Large incision through the abdominal wall to gain access into the abdominal cavity\n Lithotomy position \u2013 Medical term referring to a common position for surgical procedures and medical examinations involving the pelvis and lower abdomen\n Lobotomy \u2013 Cutting or scraping away most of the connections to and from the prefrontal cortex, the anterior part of the frontal lobes of the brain.\n Meatotomy \u2013 Form of penile modification in which the underside of the glans is split\n Myotomy \u2013 Procedure in which muscle is cut\n Osteotomy \u2013 A bone is cut to shorten or lengthen it or to change its alignment\n Phlebotomy \u2013 An incision in a vein with a needle\n Pulpotomy \u2013 Removal of a portion of the pulp, including the diseased aspect\n Radial keratotomy \u2013 a refractive surgical procedure to correct myopia\n Sphincterotomy \u2013 Treating mucosal fissures from the anal canal/sphincter\n Thoracotomy \u2013 Incision into the pleural space of the chest\n Thyrotomy \u2013 Incision of the larynx through the thyroid cartilage\n Tracheotomy \u2013 An incision on the anterior aspect of the neck and opening a direct airway through an incision in the trachea (windpipe)\n Trans-orbital lobotomy \u2013 Cutting or scraping away most of the connections to and from the prefrontal cortex, the anterior part of the frontal lobes of the brain", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 27.959769362186794, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 9.333333333333334, + "fkgl_delta": -13.41074868329487 + }, + { + "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": "A sprain is a soft tissue injury of the ligaments within a joint, often caused by a sudden movement abruptly forcing the joint to exceed its functional range of motion. Ligaments are tough, inelastic fibers made of collagen that connect two or more bones to form a joint and are important for joint stability and proprioception, which is the body's sense of limb position and movement. Sprains may be mild (first degree), moderate (second degree), or severe (third degree), with the latter two classes involving some degree of tearing of the ligament. Sprains can occur at any joint but most commonly occur in the ankle, knee, or wrist. An equivalent injury to a muscle or tendon is known as a strain.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 12.084363636363637, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 8.6, + "fkgl_delta": -6.523367132867133 + }, + { + "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": "Treatment of sclerodactyly is by physical therapy, phototherapy, surgery, topical corticosteroids or vitamin D analogues, and systemic immunosuppressive drugs when the condition is part of systemic scleroderma. Localized treatment won't halt systemic disease, but can restore function and cosmetic aspects of the affected digits. The mild to moderate proximal interphalangeal (PIP) joint flexion and extension contractures and stiff distal interphalangeal (DIP) joints in slight flexion often seen in sclerodactyly can be addressed somewhat with physical therapy. In a few cases when immune involvement isn't apparent (in these cases environmental causes are suspected), the condition may gradually clear up by itself If the trigger is avoided. In other cases, early treatment while the disease is in the inflammatory stage is much more likely to be successful than on established lesions.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 16.791379844961245, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 7.6, + "fkgl_delta": -7.336713178294577 + }, + { + "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 following situations may result in wrist drop:\n Stab wounds to the chest at or below the clavicle\u2013The radial nerve is the terminal branch of the posterior cord of the brachial plexus. A stab wound may damage the posterior cord and result in neurological deficits, including an inability to abduct the shoulder beyond the first 15 degrees, an inability to extend the forearm, reduced ability to supinate the hand, reduced ability to abduct the thumb and sensory loss to the posterior surface of the arm and hand.\n Broken humerus\u2013The radial nerve can be damaged if the humerus (the bone of the arm) is broken because it runs through the radial groove on the lateral border of this bone along with the deep brachial artery.\n Lead poisoning\u2013Wrist drop is associated with lead poisoning due to the effect of lead on the radial nerve.\n Persistent injury\u2013Persistent injury to the nerve is a common cause through either repetitive motion or by applying pressure externally along the route of the radial nerve as in the prolonged use of crutches, extended leaning on the elbows, or regular upper body rope suspension. The colloquial terms for radial nerve palsy are derived from this cause. \n Correcting dislocated shoulders\u2013Radial nerve palsy can result from the now discredited practice of correcting a dislocated shoulder by putting a foot in the person's armpit and pulling on the arm in attempts to slide the humerus back into the glenoid cavity of the scapula.\n Neuropathy in the hands and/or arms in patients with rheumatoid arthritis may in rare cases cause wrist drop. \"When a joint swells, it can pinch the nerves of sensation that pass next to it. If the swelling irritates the nerve, either because of the inflammation or simply because of pressure, the nerve can send sensations of pain, numbness, and/or tingling to the brain. This is called nerve entrapment. Nerve entrapment most frequently occurs at the wrist (carpal tunnel syndrome) and elbow (ulnar nerve entrapment). A rare form of nerve disease in patients with rheumatoid arthritis that causes numbness and/or tingling is neuropathy. Neuropathy is nerve damage that in people with rheumatoid arthritis can result from inflammation of blood vessels (vasculitis).\"", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 13.954506708760857, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 8.0, + "fkgl_delta": -2.090977296996151 + }, + { + "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": "Levy died of a heart attack on 29 April 2005 during a robbery attempt in Mexico City, Distrito Federal, Mexico. The heart attack was attributed to the stress she experienced after an assailant approached her car on a city street and tried to steal her watch. The death shook the Mexican entertainment world. It was one of the highest-profile deaths in Mexico\u2019s wave of common crime since TV comedian Francisco \u201cPaco\u201d Stanley was gunned down in 1999. \u201cHer heart apparently could not take the shock,\u201d Mexican journalist Lolita Ayala said.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 10.834444444444443, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 6.4, + "fkgl_delta": -6.771626575028634 + }, + { + "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": "Causes include falls, vehicle collisions and violence. Brain trauma occurs as a consequence of a sudden acceleration or deceleration within the cranium or by a complex combination of both movement and sudden impact. In addition to the damage caused at the moment of injury, a variety of events following the injury may result in further injury. These processes may include alterations in cerebral blood flow and pressure within the skull. Some of the imaging techniques used for diagnosis of moderate to severe TBI include computed tomography (CT) and magnetic resonance imaging (MRIs).", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 13.646869565217393, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 8.4, + "fkgl_delta": 0.11066531850353911 + }, + { + "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\nPulmonary infection\n Produces a virulent form of pneumonia (progressive)\n Night sweats, fever, cough, chest pain\n Pulmonary nocardiosis is subacute in onset and refractory to treatment with standard antibiotics\n Symptoms are more severe in immunocompromised individuals\n Radiologic studies show multiple pulmonary infiltrates, with a tendency to central necrosis\nNeurological infection\n Headache, lethargy, confusion, seizures, sudden onset of neurological deficit\n CT scan shows cerebral abscess\n Nocardial meningitis is difficult to diagnose\nCardiac conditions\n Nocardia has been highly linked to endocarditis as a main manifestation\n In recorded cases, it has caused damage to heart valves whether natural or prosthetic\nLymphocutaneous disease\n Nocardial cellulitis is akin to erysipelas but is less acute\n Nodular lymphangeitis mimics sporotrichosis with multiple nodules alongside a lymphatic pathway\n Chronic subcutaneous infection is a rare complication and osteitis may ensue\n May be misidentified and treated as a staph infection, specifically superficial skin infections\n Cultures must incubate more than 48 hours to guarantee an accurate test\nOcular disease\n Very rarely, nocardiae cause keratitis\n Generally there is a history of ocular trauma\nDisseminated nocardiosis\n Dissemination occurs through the spreading enzymes possessed by the bacteria\n Disseminated infection can occur in very immunocompromised patients\n It generally involves both lungs and brain\n Fever, moderate or very high can be seen\n Multiple cavitating pulmonary infiltrates develop\n Cerebral abscesses arise later\n Cutaneous lesions are very rarely seen\n If untreated, the prognosis is poor for this form of disease", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 100.42982905982906, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 14.0, + "fkgl_delta": -88.19212465731334 + } +] \ No newline at end of file