diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_19_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_19_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_19_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": "Side effects\n Tumor lysis syndrome (TLS). Clofarabine quickly kills leukaemia cells in the blood. The body may react to this. Signs include hyperkalemia, hyperuricemia, and hyperphosphatemia. TLS is very serious and can lead to death if it is not treated right away.\n Systemic inflammatory response syndrome (SIRS): symptoms include fast breathing, fast heartbeat, low blood pressure, and fluid in the lungs. \nBone marrow problems (suppression). Clofarabine can stop the bone marrow from making enough red blood cells, white blood cells, and platelets. Serious side effects that can happen because of bone marrow suppression include severe infection (sepsis), bleeding, and anemia.\nEffects on pregnancy and breastfeeding. Girls and women should not become pregnant or breastfeed during treatment which may harm the baby.\nDehydration and low blood pressure. Clofarabine can cause vomiting and diarrhea which may lead to low body fluid (dehydration). Signs and symptoms of dehydration include dizziness, lightheadedness, fainting spells, or decreased urination.\nOther side effects. The most common side effects are stomach problems (including vomiting, diarrhea, and nausea), and effects on blood cells (including low red blood cells count, low white blood cell count, low platelet count, fever, and infection). Clofarabine can also cause tachycardia and can affect the liver and kidneys.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 8.772477542741235, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 4.764705882352941, + "fkgl_delta": -4.634319648004389 + }, + { + "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": "Because of its similarities to deep vein thrombosis (DVT), May-Thurner's syndrome is rarely diagnosed amongst the general population. In this condition, the right iliac artery sequesters and compresses the left common iliac vein against the lumbar section of the spine, resulting in swelling of the legs and ankles, pain, tingling, and/or numbness in the legs and feet. The pain is often presented as dull, and may progress up and down the leg depending on the patient. Lower extremities may feel warm to the touch, and swelling may maintain or dissipate throughout the day.", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 12.636639784946237, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 8.0, + "fkgl_delta": 2.5673720144637926 + }, + { + "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": "Causes\nA number of conditions may cause the appearance of livedo reticularis:\nCutis marmorata telangiectatica congenita, a rare congenital condition\nSneddon syndrome \u2013 association of livedoid vasculitis and systemic vascular disorders, such as strokes, due to underlying genetic cause\nIdiopathic livedo reticularis \u2013 the most common form of livedo reticularis, completely benign condition of unknown cause affecting mostly young women during the winter: It is a lacy purple appearance of skin in extremities due to sluggish venous blood flow. It may be mild, but ulceration may occur later in the summer.\nSecondary livedo reticularis:\nVasculitis autoimmune conditions:\nLivedoid vasculitis \u2013 with painful ulceration occurring in the lower legs\nPolyarteritis nodosa\nSystemic lupus erythematosus\nDermatomyositis\nRheumatoid arthritis\nLymphoma\nPancreatitis\nChronic pancreatitis\nTuberculosis\nDrug-related:\nAdderall (side effect) \nAmantadine (side effect)\nBromocriptine (side effect)\nBeta interferon treatment, e.g. in multiple sclerosis\nLivedo reticularis associated with rasagiline\nMethylphenidate and dextroamphetamine-induced peripheral vasculopathy\nGefitinib\nObstruction of capillaries:\nCryoglobulinaemia \u2013 proteins in the blood that clump together in cold conditions\nAntiphospholipid syndrome due to small blood clots\nHypercalcaemia (raised blood calcium levels which may be deposited in the capillaries)\nHaematological disorders of polycythaemia rubra vera or thrombocytosis (excessive red cells or platelets)\nInfections (infective endocarditis, syphilis, tuberculosis, Lyme disease)\nAssociated with acute kidney injury due to cholesterol emboli status after cardiac catheterization\nArteriosclerosis (cholesterol emboli) and homocystinuria (due to Chromosome 21 autosomal recessive Cystathionine beta synthase deficiency)\nIntra-arterial injection (especially in drug addicts)\nEhlers-Danlos syndrome \u2013 connective tissue disorder, often with many secondary conditions, may be present in all types\nPheochromocytoma\nLivedoid vasculopathy and its association with factor V Leiden mutation\nFILS syndrome (polymerase \u03b51 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature)\nPrimary hyperoxaluria, oxalosis (oxalate vasculopathy)\nCytomegalovirus infection (very rare clinical form, presenting with persistent fever and livedo reticularis on the extremities and cutaneous necrotizing vasculitis of the toes)\nGeneralized livedo reticularis induced by silicone implants for soft tissue augmentation\nAs a rare skin finding in children with Down syndrome\nIdiopathic livedo reticularis with polyclonal IgM hypergammopathy\nCO2 angiography (rare, reported case)\nA less common skin lesion of Churg\u2013Strauss syndrome\nErythema nodosum-like cutaneous lesions of sarcoidosis showing livedoid changes in a patient with sarcoidosis and Sj\u00f6gren's syndrome\nLivedo vasculopathy associated with IgM antiphosphatidylserine-prothrombin complex antibody\nLivedo vasculopathy associated with plasminogen activator inhibitor-1 promoter homozygosity and prothrombin G20210A heterozygosity\nAs a first sign of metastatic breast carcinoma (very rare)\nLivedo reticularis associated with renal cell carcinoma (rare)\nBuerger's disease (as an initial symptom)\nAs a rare manifestation of Graves hyperthyroidism\nAssociated with pernicious anaemia\nMoyamoya disease (a rare, chronic cerebrovascular occlusive disease of unknown cause, characterized by progressive stenosis of the arteries of the circle of Willis leading to an abnormal capillary network and resultant ischemic strokes or cerebral hemorrhages)\nAssociated with the use of a midline catheter . ( atheroempolic renal DX )due to angioplasty \nFamilial primary cryofibrinogenemia.", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 47.07600000000001, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 10.545454545454545, + "fkgl_delta": -29.96771508903468 + }, + { + "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": "Illness and death\nShe experienced the first symptoms of her illness shortly after her father's death and her involvement in the family business. In 1996, she suffered aphonia. The next year, her hands began to fall asleep, and one year later, she began to lisp. She was diagnosed in the Houston Methodist Hospital with amyotrophic lateral sclerosis (ALS), a specific disease that causes the death of neurons which control voluntary muscles.", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 10.61137323943662, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 6.0, + "fkgl_delta": -7.030017928081307 + }, + { + "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": "Causes\nthe causes for this condition are the following:\n Obstruction by deep vein thrombosis or tumors (most commonly renal cell carcinoma)\n Compression through external pressure by neighbouring structures or tumors, either by significantly compressing the vein or by promoting thrombosis by causing turbulence by disturbing the blood flow. This is quite common during the third trimester of pregnancy when the uterus compresses the vein in the right side position.\n Iatrogenic causes may be suspected in patients with a medical history of liver transplantion, vascular catheters, dialysis and other invasive procedures in the vicinity\n Budd-Chiari syndrome", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 19.117894736842107, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 9.666666666666666, + "fkgl_delta": -7.175789473684212 + }, + { + "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": "Frontal lobe\nLateral frontobasal (orbitiofrontal): This artery branches out anteriorly, superiorly and laterally to vascularize the inferior frontal gyrus. It \"competes\" in size with the frontal polar branch of the anterior cerebral artery\nPrefrontal arteries: These arteries fan out over the insula and exit to the cortex via the medial surface of the frontal operculum. The arteries fan superiorly over the pars triangularis and vascularize the inferior and middle frontal gyrus. Near the superior frontal gyrus these arteries anastomose with branches from the pericallosal artery of the anterior cerebral artery.\nPre-Rolandic artery (precentral): The artery extends out on the medial surface of the operculum and supplies the posterior parts of the middle and inferior frontal gyri as well as the lower parts of the pre-central gyrus. This artery branches once or twice and is relatively invariant across anatomies. \nRolandic arteries (central): The artery extends out and exits from the central portion of the operculum then passes inside the central sulcus. This artery bifurcates in 72% of individuals and irrigates the posterior pre-central gyrus and the inferior portion of the post-central gyrus.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 16.1166229281768, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 6.625, + "fkgl_delta": 0.13079476729645378 + }, + { + "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": "Aphthous stomatitis (canker sores) is the recurrent appearance of mouth ulcers in otherwise healthy individuals. The cause is not completely understood, but it is thought that the condition represents a T cell mediated immune response which is triggered by a variety of factors. The individual ulcers (aphthae) recur periodically and heal completely, although in the more severe forms, new ulcers may appear in other parts of the mouth before the old ones have finished healing. Aphthous stomatitis is one of the most common diseases of the oral mucosa, and is thought to affect about 20% of the general population to some degree. The symptoms range from a minor nuisance to being disabling in their impact on eating, swallowing, and talking, and the severe forms can cause people to lose weight. There is no cure for aphthous stomatitis, and therapies are aimed at alleviating the pain, reducing the inflammation and promoting healing of the ulcers, but there is little evidence of efficacy for any treatment that has been used.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 15.277619047619051, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 8.5, + "fkgl_delta": -10.644495295124042 + }, + { + "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": "The oral mucosa is the mucous membrane lining the inside of the mouth. It comprises stratified squamous epithelium, termed \"oral epithelium\", and an underlying connective tissue termed lamina propria. The oral cavity has sometimes been described as a mirror that reflects the health of the individual. Changes indicative of disease are seen as alterations in the oral mucosa lining the mouth, which can reveal systemic conditions, such as diabetes or vitamin deficiency, or the local effects of chronic tobacco or alcohol use.\nThe oral mucosa tends to heal faster and with less scar formation compared to the skin. The underlying mechanism remains unknown, but research suggests that extracellular vesicles might be involved.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 13.498928571428575, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 8.0, + "fkgl_delta": -3.170366071428571 + }, + { + "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": "Angular cheilitis is a fairly non specific term which describes the presence of an inflammatory lesion in a particular anatomic site (i.e. the corner of the mouth). As there are different possible causes and contributing factors from one person to the next, the appearance of the lesion is somewhat variable. The lesions are more commonly symmetrically present on both sides of the mouth, but sometimes only one side may be affected. In some cases, the lesion may be confined to the mucosa of the lips, and in other cases the lesion may extend past the vermilion border (the edge where the lining on the lips becomes the skin on the face) onto the facial skin. Initially, the corners of the mouth develop a gray-white thickening and adjacent erythema (redness). Later, the usual appearance is a roughly triangular area of erythema, edema (swelling) and breakdown of skin at either corner of the mouth. The mucosa of the lip may become fissured (cracked), crusted, ulcerated or atrophied. There is not usually any bleeding. Where the skin is involved, there may be radiating rhagades (linear fissures) from the corner of the mouth. Infrequently, the dermatitis (which may resemble eczema) can extend from the corner of the mouth to the skin of the cheek or chin. If Staphylococcus aureus is involved, the lesion may show golden yellow crusts. In chronic angular cheilitis, there may be suppuration (pus formation), exfoliation (scaling) and formation of granulation tissue.", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 11.225062240663902, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": 3.3021746014413615 + }, + { + "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": "Neonatal form \nThe neonatal form is the least common clinical presentation of this disorder and is almost invariably fatal in rapid fashion regardless of intervention. Symptomatic onset has been documented just hours after birth to within 4 days of life. Affected newborns typically experience respiratory failure, low blood sugar, seizures, liver enlargement, liver failure, and heart enlargement with abnormal heart rhythms leading to cardiac arrest. In most cases, elements of abnormal brain and kidney development are apparent, sometimes even at prenatal ultrasound. Infants with the lethal neonatal form usually live no longer than a few months. Neuronal migration defects have also been documented, to which the CNS pathology of the disorder is often attributed.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 14.902456140350878, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 7.166666666666667, + "fkgl_delta": -10.278516746411483 + }, + { + "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": "Presentation\nSymptoms vary, but usually result in dysmorphisms in the skull, nervous system problems, and developmental delay. Dysmorphisms in the heart, kidneys, and musculoskeletal system may also occur. An infant with complete trisomy 9 surviving 20 days after birth showed clinical features including a small face, wide fontanelle, prominent occiput, micrognathia, low set ears, upslanting palpebral fissures, high-arched palate, short sternum, overlapping fingers, limited hip abduction, rocker bottom feet, heart murmurs and a webbed neck.", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 15.71466666666667, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 8.0, + "fkgl_delta": -4.500546184738955 + }, + { + "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": "Presentation\nSymptoms of ML I are either present at birth or develop within the first year of life. In many infants with ML I, excessive swelling throughout the body is noted at birth. These infants are often born with coarse facial features, such as a flat nasal bridge, puffy eyelids, enlargement of the gums, and excessive tongue size (macroglossia). Many infants with ML I are also born with skeletal malformations such as hip dislocation. Infants often develop sudden involuntary muscle contractions (called myoclonus) and have red spots in their eyes (cherry red spots). They are often unable to coordinate voluntary movement (called ataxia). Tremors, impaired vision, and seizures also occur in children with ML I. Tests reveal abnormal enlargement of the liver (hepatomegaly) and spleen (splenomegaly) and extreme abdominal swelling. Infants with ML I generally lack muscle tone (hypotonia) and have mental retardation that is either initially or progressively severe. Many patients suffer from failure to thrive and from recurrent respiratory infections. Most infants with ML I die before the age of one year.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 10.517021943573667, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.8, + "fkgl_delta": 3.0631604463634403 + }, + { + "index": 4, + "label": "low_health_literacy", + "original_doc": "This is about a 13-year-old boy. He has had small growths in his throat since he was two years old. The growths were in his voice box and windpipe. They narrowed his breathing tube, so he had trouble breathing. It was like trying to breathe through a pinched straw. A chest scan showed several small cysts in his lungs. Doctors removed the throat growths. They also placed a breathing tube through a small hole in his neck to help him breathe. He got one dose of a medicine called bevacizumab (400 mg) through a vein. He also had breathing therapy. He got better. The problem has not come back during follow-up.", + "wiki_anchor": "Signs and symptoms \nA common symptom of laryngeal papillomatosis is a change in voice quality. More specifically, hoarseness is observed. As a consequence of the narrowing of the laryngeal or tracheal parts of the airway, shortness of breath, chronic cough and stridor (i.e. noisy breathing which can sound like a whistle or a snore), can be present. As the disease progresses, occurrence of secondary symptoms such as dysphagia, pneumonia, acute respiratory distress syndrome, failure to thrive, and recurrent upper respiratory infections can be diagnosed. The risk of laryngeal papillomatosis spreading to the lungs is higher in the juvenile-onset than the adult-onset. In children, symptoms are usually more severe and often mistaken for manifestations of other diseases such as asthma, croup or bronchitis. Therefore, diagnosis is usually delayed.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 12.342982283464568, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 7.857142857142857, + "fkgl_delta": -9.761518319500603 + }, + { + "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": "In general, physicians are unsure why only certain people who have been exposed to the HPV types implicated in the disease develop laryngeal papillomatosis. In the case of the juvenile form of the disease, the likelihood of a child born of an infected mother developing laryngeal papillomatosis is low (between 1 in 231 to 1 in 400), even if the mother's infection is active. Risk factors for a higher likelihood of transmission at childbirth include the first birth, vaginal birth, and teenaged mother.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 15.245783132530125, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 8.666666666666666, + "fkgl_delta": -2.5172117039586936 + }, + { + "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": "Complications \nMajor complications of CAP include:\n Sepsis - A life-threatening reaction to infection. A common cause of sepsis is bacterial pneumonia, frequently the result of infection with streptococcus pneumoniae. Patients with sepsis require intensive care with blood pressure monitoring and support against hypotension. Sepsis can cause liver, kidney and heart damage.\n Respiratory failure - CAP patients often have dyspnea, which may require support. Non-invasive machines (such as bilevel positive airway pressure), a tracheal tube or a ventilator may be used.\n Pleural effusion and empyema - Microorganisms from the lung may trigger fluid collection in the pleural cavity, or empyema. Pleural fluid, if present, should be collected with a needle and examined. Depending on the results, complete drainage of the fluid with a chest tube may be necessary to prevent proliferation of the infection. Antibiotics, which do not penetrate the pleural cavity well, are less effective.\n Abscess - A pocket of fluid and bacteria may appear on X-ray as a cavity in the lung. Abscesses, typical of aspiration pneumonia, usually contain a mixture of anaerobic bacteria. Although antibiotics can usually cure abscesses, sometimes they require drainage by a surgeon or radiologist.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 13.019032258064517, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 5.3076923076923075, + "fkgl_delta": 2.6255510752688203 + }, + { + "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": "According to the US CDC definition, one has AIDS if he/she is infected with HIV and present with one of the following:\n A CD4+ T-cell count below 200 cells/\u03bcl (or a CD4+ T-cell percentage of total lymphocytes of less than 14%)\nOR\n he/she has one of the following defining illnesses:\n Candidiasis of bronchi, trachea, or lungs\n Candidiasis esophageal\n Cervical cancer (invasive)\n Coccidioidomycosis, disseminated or extrapulmonary\n Cryptococcosis, extrapulmonary\n Cryptosporidiosis, chronic intestinal for longer than 1 month\n Cytomegalovirus disease (other than liver, spleen or lymph nodes)\n Encephalopathy (HIV-related)\n Herpes simplex: chronic (for more than 1 month); or bronchitis, pneumonitis, or esophagitis\n Histoplasmosis, disseminated or extrapulmonary\n Isosporiasis, chronic intestinal (for more than 1 month)\n Kaposi's sarcoma\n Lymphoma Burkitt's, immunoblastic or primary brain\n Mycobacterium avium complex\n Mycobacterium, other species, disseminated or extrapulmonary\n Pneumocystis carinii pneumonia\n Pneumonia (recurrent)\n Progressive multifocal leukoencephalopathy\n Salmonella sepsis (recurrent)\n Toxoplasmosis of the brain\n Tuberculosis\n Wasting syndrome due to HIV", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 67.70389261744967, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 10.0, + "fkgl_delta": -62.28831893915945 + }, + { + "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": "Causes\nSpecific instances of fungal infections that can manifest with pulmonary involvement include:\n Coccidioidomycosis, which begins with an often self-limited respiratory infection (also called \"Valley fever\" or \"San Joaquin fever\")\n Pneumocystis pneumonia, which typically occurs in immunocompromised people, especially AIDS\n Sporotrichosis \u2014 primarily a skin disease, but can involve the lungs as well\n Cryptococcus species can sometimes invade the lungs\n Aspergillosis, resulting in invasive pulmonary aspergillosis\n rarely, candidiasis has pulmonary manifestations in immunocompromised patients.\n Histoplasmosis or Spelunker's lung", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 25.47694805194806, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": -9.056158578263847 + }, + { + "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": "Children/adolescents \n IgA nephropathy (Note: Contrast time of onset with Post-streptococcal Glomerulonephritis) - Most commonly diagnosed in children who recently had an upper respiratory tract infection (URI). Symptoms typically present within 1\u20132 days of a non-specific URI with severe flank/abdominal pain, gross hematuria (characterized by dark brown or red colored urine), and edema of the hands, feet, and/or face.\n Post-streptococcal glomerulonephritis (PSGN) - Similar to IgA nephropathy, post-streptococcal glomerulonephritis (PSGN) most often occurs in children who have recently had an upper respiratory infection (URI). In contrast with IgA nephropathy, however, PSGN typically presents 2\u20133 weeks after recovering from an URI that was caused specifically by a Streptococcus bacteria. The symptoms at onset are very similar to IgA nephropathy and include abdominal pain, hematuria, edema, and oliguria.\n Henoch\u2013Sch\u00f6nlein purpura (HSP) - Often considered a systemic form of IgA nephropathy, Henoch\u2013Sch\u00f6nlein purpura (HSP) is a systemic small-vessel vasculitis that is characterized by deposition of IgA antibody immune complexes in different key areas throughout the body. Most often, the condition presents in children with palpable purpura, abdominal pain, and arthritis. When the kidneys are affected, the IgA immune complexes deposit in the glomerulus very similarly to IgA nephropathy and will present in a similar way.\n Hemolytic uremic syndrome - Most cases occur immediately following infectious diarrhea caused by a specific type of E. coli (O157:H7). The bacteria produces a toxin that causes widespread inflammation and numerous blood clots in small blood vessels (thrombotic microangiopathy). When the inflammation reaches the kidney, or the by-products of systemic inflammation build up in the kidney, the patient will begin showing signs of nephritic syndrome or potentially acute kidney failure (elevated creatinine, BUN, etc.).", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 17.008587722240865, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 7.909090909090909, + "fkgl_delta": -0.52921990614891 + }, + { + "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": "Occasionally, a person with a LGIB will not present with any signs of internal bleeding, especially if there is a chronic bleed with ongoing low levels of blood loss. In these cases, a diagnostic assessment or pre-assessment should watch for other signs and symptoms that the patient may present with. These include, but are not limited to, hypotension, tachycardia, angina, syncope, weakness, confusion, stroke, myocardial infarction/heart attack, and shock.", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 13.73072463768116, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 9.0, + "fkgl_delta": -9.218610816542949 + }, + { + "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": "Pathophysiology\nAPC (with protein S as a cofactor) degrades Factor Va and Factor VIIIa. APC resistance is the inability of protein C to cleave Factor Va and/or Factor VIIIa, which allows for longer duration of thrombin generation and may lead to a hypercoagulable state. This may be hereditary or acquired. The best known and most common hereditary form is Factor V Leiden, which is responsible for more than 95% of cases. Other genetic causes include Factor V Cambridge (VThr306) and the factor V HR2 haplotype (A4070G mutation). Acquired forms of APC resistance occur in the presence of elevated Factor VIII concentrations. Antiphospholipid antibodies, pregnancy, and certain forms of estrogen therapy, such as ethinylestradiol-containing birth control pills, have been found to produce acquired APC resistance.", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 13.966958525345628, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 6.714285714285714, + "fkgl_delta": -2.915925916649975 + }, + { + "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": "A \"hypertensive emergency\" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure, an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 16.232121212121214, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": -4.45283384125889 + }, + { + "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": "Scrotoplasty, also known as oscheoplasty, is a type of surgery to create or repair the scrotum. The history of male genital plastic surgery is rooted in many cultures and dates back to ancient times. However, scientific research for male genital plastic surgery such as scrotoplasty began to develop in the early 1900s. The development of testicular implants began in 1940 made from materials outside of what is used today. Today, testicular implants are created from saline or gel filled silicone rubber. There are a variety of reasons why scrotoplasty is done. Some transgender men and intersex or non-binary people who were assigned female at birth may choose to have this surgery to create a scrotum, as part of their transition. Other reasons for this procedure include addressing issues with the scrotum due to birth defects, aging, or medical conditions such as infection. For newborn males with penoscrotal defects such as webbed penis, a condition in which the penile shaft is attached to the scrotum, scrotoplasty can be performed to restore normal appearance and function. For older male adults, the scrotum may extend with age. Scrotoplasty or scrotal lift can be performed to remove the loose, excess skin. Scrotoplasty can also be performed for males who undergo infection, necrosis, traumatic injury of the scrotum.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 11.497758215962442, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": -8.236714737701572 + }, + { + "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": "Symptoms and signs\nSymptoms and signs in the newborn can be sepsis, abdominal mass, and respiratory distress. Other abdominopelvic or perineal congenital anomalies frequently prompt radiographic evaluation in the newborn, resulting in a diagnosis of coincident vaginal atresia. Symptoms for vaginal atresia include cyclical abdominal pain, the inability to start having menstrual cycles, a small pouch or dimple where a vaginal opening should be, and pelvic mass when the upper vagina becomes filled with menstrual blood. Signs and symptoms of vaginal atresia or vaginal agenesis can often go unnoticed in females until they reach the age of menstruation. Women may also experience some form of abdominal pain or cramping.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 15.321174311926608, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 7.4, + "fkgl_delta": -3.5371380523846234 + }, + { + "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": "The use of ultrasound has become the standard of care when preparing a patient for paracentesis. Confirmation of an ascitic effusion reduces the risks associated with a dry or blind tap of the abdomen. Anatomic landmarks, such as the midline linea alba approach, were traditionally used as reference points for needle insertion. Phased array or curvilinear ultrasound transducers are typically used in the hospital and outpatient setting to identify ascites in the abdominal cavity. Fluid within the abdominal cavity appears hypoechoic or anechoic (black) on ultrasound. Morison's pouch (hepatorenal recess) is a common starting location in concordance with ultrasound FAST (focused assessment with sonography for trauma) exam. Fluid collection can occur in a number of different locations and may be difficult to find, especially if the patient only exhibits a small volume of ascites. Measurement of the amount of fluid within the abdominal cavity is not necessary or very successful. Identification of sufficient fluid within the abdominal cavity for fluid analysis or to achieve a therapeutic benefit is all that is required to proceed to paracentesis. Ultrasound guidance of the paracentesis can also be used as an additional safety measure to ensure the needle stays within the ascitic fluid and avoidance of important vessels within the abdominal cavity.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 14.930653846153849, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 7.0, + "fkgl_delta": 0.18834136915716115 + }, + { + "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": "Brain herniation frequently presents with abnormal posturing, a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the medulla oblongata. Severe headaches and seizures as a result of increased intracranial pressure are not uncommon. Cardiovascular and pulmonary symptoms may also be present as the brain loses function, but might also be associated with bleeding. These symptoms are known as Cushing's Triad: hypertension (with widening pulse pressure), irregular respirations (commonly Cheyne-Stokes), bradycardia and in severe cases cardiac arrest.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 13.191097992916177, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.0, + "fkgl_delta": -8.396709503707545 + }, + { + "index": 8, + "label": "intermediate_health_literacy", + "original_doc": "A 4-year-old boy presented after 5 days of visible blood in the urine and leg swelling, plus new headaches, nausea, and vomiting. He developed seizures with a hypertensive emergency. Labs showed low complement C3 and a high anti-streptolysin O (ASO) titer, consistent with acute post-streptococcal glomerulonephritis. He developed encephalopathy, and MRI confirmed posterior reversible encephalopathy syndrome (PRES) secondary to the hypertensive crisis. He also developed autoimmune hemolytic anemia, with hemoglobin falling to 5 g/dL. Treatment included antihypertensive therapy, neuroprotective measures, and corticosteroids. He was discharged after 31 days and remained asymptomatic at 6-month follow-up.", + "wiki_anchor": "Although the pathogenesis is uncertain, it is probable that the symptoms are a consequence of hemorrhagic pulmonary edema, as the hematocrit is lower than normal blood (usually 15-20% less) and the concentration of small proteins is higher than in plasma. It is postulated that the infant suffers from asphyxia with resultant heart attack; this increases pulmonary microvascular pressure, resulting in pulmonary edema. Contributing factors include factors that favor increased filtration of fluid from pulmonary capillaries (e.g., low concentration of plasma proteins, high alveolar surface tension, lung damage, hypervolemia).", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 16.724090909090908, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 9.0, + "fkgl_delta": -1.9705650732246447 + }, + { + "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": "Side effects\n Tumor lysis syndrome (TLS). Clofarabine quickly kills leukaemia cells in the blood. The body may react to this. Signs include hyperkalemia, hyperuricemia, and hyperphosphatemia. TLS is very serious and can lead to death if it is not treated right away.\n Systemic inflammatory response syndrome (SIRS): symptoms include fast breathing, fast heartbeat, low blood pressure, and fluid in the lungs. \nBone marrow problems (suppression). Clofarabine can stop the bone marrow from making enough red blood cells, white blood cells, and platelets. Serious side effects that can happen because of bone marrow suppression include severe infection (sepsis), bleeding, and anemia.\nEffects on pregnancy and breastfeeding. Girls and women should not become pregnant or breastfeed during treatment which may harm the baby.\nDehydration and low blood pressure. Clofarabine can cause vomiting and diarrhea which may lead to low body fluid (dehydration). Signs and symptoms of dehydration include dizziness, lightheadedness, fainting spells, or decreased urination.\nOther side effects. The most common side effects are stomach problems (including vomiting, diarrhea, and nausea), and effects on blood cells (including low red blood cells count, low white blood cell count, low platelet count, fever, and infection). Clofarabine can also cause tachycardia and can affect the liver and kidneys.", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 8.772477542741235, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 4.764705882352941, + "fkgl_delta": 6.186176131093891 + }, + { + "index": 9, + "label": "low_health_literacy", + "original_doc": "This 69-year-old man had heart bypass surgery in the past. For 2 months, he got very short of breath with light activity. Tests\u2014a heart tracing, a blood test, and an X-ray movie with dye of the heart arteries\u2014showed heart failure from poor blood flow after a bypass vein to the right heart artery failed. Doctors first opened a totally blocked artery on the left side of his heart. Then they used tiny natural detours between heart arteries to reach the right heart artery from the far end and open it. His breathing was better when he left the hospital. Six months later, his shortness of breath had not come back.", + "wiki_anchor": "Pathophysiology\nWhen pulmonic stenosis (PS) is present, resistance to blood flow causes right ventricular hypertrophy. If right ventricular failure develops, right atrial pressure will increase, and this may result in a persistent opening of the foramen ovale, shunting of unoxygenated blood from the right atrium into the left atrium, and systemic cyanosis. If pulmonary stenosis is severe, congestive heart failure occurs, and systemic venous engorgement will be noted. An associated defect such as a patent ductus arteriosus partially compensates for the obstruction by shunting blood from the left ventricle to the aorta then back to the pulmonary artery (as a result of the higher pressure in the left ventricle) and back into the lungs.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 16.744298245614036, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 6.75, + "fkgl_delta": -10.222090453406246 + }, + { + "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": "Indications\nThe following situations may benefit from this device.\n Cardiogenic shock when used alone as treatment for myocardial infarction. 9\u201322% survive the first year.\n Reversible intracardial mechanical defects complicating infarction, i.e. acute mitral regurgitation and septal perforation.\n Unstable angina pectoris benefits from counterpulsation.\n Post cardiothoracic surgery\u2014most common and useful is counterpulsation in weaning patients from cardiopulmonary bypass after continued perioperative injury to myocardial tissue.\n Preoperative use is suggested for high-risk patients such as those with unstable angina with stenosis greater than 70% of main coronary artery, in ventricular dysfunction with an ejection fraction less than 35%.\n Percutaneous coronary angioplasty\n In high risk coronary artery bypass graft surgery where cardiopulmonary bypass time was shortened, as well as during intubation period and hospital stay.\n Thrombolytic therapy of acute myocardial infarction.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 16.597312500000005, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 5.444444444444445, + "fkgl_delta": -3.1173125000000006 + }, + { + "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": "A much smaller incision (made through the rib cage as opposed to cutting the sternum and opening the rib cage) than with traditional bypass surgery.\n Less pain for the patient and quicker recovery time. Particularly in high risk patients, morbidity and mortality decreases in comparison to conventional surgery. A study from FuWai Hospital in Beijing reports on 104 patients with multivessel coronary artery disease who were compared with the same sized group of patients undergoing off pump surgery using propensity score matching. The patients treated with the hybrid approach had a significantly lower ICU stay and intubation time and experienced less complications in terms of bleeding and transfusions needs. At a median follow up of 18 months, patients undergoing the hybrid procedure also had a significantly higher freedom from major adverse cardiac or cerebrovascular events (99% vs. 90.4%; p = 0.03). HCR is also associated with a significant decrease in the need for blood transfusion and a significant reduction in the duration of intubation.\n Less risk of complications, infections etc. and also decreases the necessity for two separate cardiac procedures (bypass and stenting). However, it requires the implementation of suitable X-ray equipment in the OR, i.e. a hybrid operating room. Helpful in this regard is the regular use of completion angiography. In a study designed and published by the Vanderbilt Heart and Vascular Institute, routine intraoperative completion angiography performed in a fully functional hybrid operation room detected important defects in 97 of 796 (12% of the grafts) venous coronary artery bypass grafts in 366 adult patients (14% of the patients) with complex coronary artery disease. Their findings in completion angiography at the end of the operation included suboptimal anastomoses, poor lie of the venous bypass graft, and bypasses to not diseased vessels. The angiography findings led to a change in the management, including minor adjustments of the graft, traditional surgical revision or percutaneous coronary interventions, resulting in optimal bypass outcomes.\n In the study from FuWai, the hybrid procedure was also less costly than an exclusively percutaneous strategy.", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 14.524187675070028, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 7.928571428571429, + "fkgl_delta": -5.458554763677622 + }, + { + "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": "In the third decade of the condition, individuals develop further visual problems including retinitis pigmentosa, and bilateral cataracts. Affected individuals experience the restriction of visual fields, night blindness, and eventually severe or complete blindness.\nIndividuals with this syndrome exhibit many physical deformities including skeletal, epidermal, and subcutaneous abnormalities. The skeletal problems are characterized by scoliosis and muscle weakness indicative of the kyphoscoliotic type which follow muscle wasting and peripheral neuritis (nerve inflammation). Osteoporosis is also observed in many cases. Skin and subcutaneous atrophy is common as well as skin ulcerations due to inability of the skin to heal. One of the final manifestations of disease is baldness. There is no evidence that the progression of Flynn\u2013Aird syndrome shortens the patient's life-span, but the terrible conditions certainly increase morbidity.", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 16.278125, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 6.625, + "fkgl_delta": -9.680615601503757 + }, + { + "index": 10, + "label": "intermediate_health_literacy", + "original_doc": "A 51-year-old man presented with 3 days of sudden, painful vision loss in the left eye. Visual acuity was 20/20 in the right eye and hand motion in the left eye. Left fundus findings included optic nerve head swelling, choroidal bulging, multiple areas of subretinal fluid, and RPE corrugations. Orbital/brain MRI with gadolinium showed a retrobulbar nodular mass enhancing at the junction of the optic nerve and sclera. Oncology and rheumatology evaluations were unremarkable. The clinical diagnosis was nodular posterior scleritis, and oral prednisolone was started.", + "wiki_anchor": "Optic nerve sheath meningiomas (ONSM) are rare benign tumors of the optic nerve. 60\u201370% of cases occur in middle age females, and is more common in older adults (mean age 44.7 years). It is also seen in children, but this is rare. The tumors grow from cells that surround the optic nerve, and as the tumor grows, it compresses the optic nerve. This causes loss of vision in the affected eye. Rarely, it may affect both eyes at the same time.", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 5.554012345679016, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 4.833333333333333, + "fkgl_delta": 5.987848119437263 + }, + { + "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": "Signs and symptoms\n Hypermetropia: Without the focusing power of the lens, the eye becomes very farsighted. \n Loss of accommodation: Since the lens and its zonules are responsible for adjusting the focus of vision to different lengths, patients with aphakia will have a total loss of accommodation.\n Defective vision: High degree hypermetropia and total loss of accommodation cause defective vision for both distance and near.\n Cyanopsia: Absence of lens cause cyanopsia or blue vision. Some individuals have said that they perceive ultraviolet light, invisible to those with a lens, as whitish blue or whitish-violet.\n Erythropsia: Sometimes, objects appear reddish.\n Deep anterior chamber: Since the lens is absent, anterior chamber will be deep.\n Iridodonesis: Iridodonesis is the vibration or agitated motion of the iris with eye movement.\n Purkinje test shows only two images; the reflection from anterior and posterior corneal surfaces. \n Iridectomy mark may be seen in surgical aphakia.\n Astigmatism: With-the-rule astigmatism due to corneal wound healing may occur in surgical aphakia, mainly after intracapsular cataract extraction or extracapsular cataract extraction.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 12.395901022054868, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 5.75, + "fkgl_delta": 2.2659691078152626 + }, + { + "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": "Local anesthetic nerve block\nLocal anesthetic nerve block (local anesthetic regional nerve blockade, or often simply nerve block) is a short-term nerve block involving the injection of local anesthetic as close to the nerve as possible for pain relief. The local anesthetic bathes the nerve and numbs the area of the body that is supplied by that nerve. The goal of the nerve block is to prevent pain by blocking the transmission of pain signals from the affected area. Local anesthetic is often combined with other drugs to potentiate or prolong the analgesia produced by the nerve block. These adjuvants may include epinephrine (or more specific alpha-adrenergic agonists), corticosteroids, opioids, or ketamine. These blocks can be either single treatments, multiple injections over a period of time, or continuous infusions. A continuous peripheral nerve block can be introduced into a limb undergoing surgery\u00a0\u2013 for example, a femoral nerve block to prevent pain in knee replacement.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 13.678311688311691, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 7.142857142857143, + "fkgl_delta": -7.135592390066073 + }, + { + "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": "Local anesthetic nerve block\nLocal anesthetic nerve block (local anesthetic regional nerve blockade, or often simply nerve block) is a short-term nerve block involving the injection of local anesthetic as close to the nerve as possible for pain relief. The local anesthetic bathes the nerve and numbs the area of the body that is supplied by that nerve. The goal of the nerve block is to prevent pain by blocking the transmission of pain signals from the affected area. Local anesthetic is often combined with other drugs to potentiate or prolong the analgesia produced by the nerve block. These adjuvants may include epinephrine (or more specific alpha-adrenergic agonists), corticosteroids, opioids, or ketamine. These blocks can be either single treatments, multiple injections over a period of time, or continuous infusions. A continuous peripheral nerve block can be introduced into a limb undergoing surgery\u00a0\u2013 for example, a femoral nerve block to prevent pain in knee replacement.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 13.678311688311691, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 7.142857142857143, + "fkgl_delta": -0.7680175706646324 + }, + { + "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 much smaller incision (made through the rib cage as opposed to cutting the sternum and opening the rib cage) than with traditional bypass surgery.\n Less pain for the patient and quicker recovery time. Particularly in high risk patients, morbidity and mortality decreases in comparison to conventional surgery. A study from FuWai Hospital in Beijing reports on 104 patients with multivessel coronary artery disease who were compared with the same sized group of patients undergoing off pump surgery using propensity score matching. The patients treated with the hybrid approach had a significantly lower ICU stay and intubation time and experienced less complications in terms of bleeding and transfusions needs. At a median follow up of 18 months, patients undergoing the hybrid procedure also had a significantly higher freedom from major adverse cardiac or cerebrovascular events (99% vs. 90.4%; p = 0.03). HCR is also associated with a significant decrease in the need for blood transfusion and a significant reduction in the duration of intubation.\n Less risk of complications, infections etc. and also decreases the necessity for two separate cardiac procedures (bypass and stenting). However, it requires the implementation of suitable X-ray equipment in the OR, i.e. a hybrid operating room. Helpful in this regard is the regular use of completion angiography. In a study designed and published by the Vanderbilt Heart and Vascular Institute, routine intraoperative completion angiography performed in a fully functional hybrid operation room detected important defects in 97 of 796 (12% of the grafts) venous coronary artery bypass grafts in 366 adult patients (14% of the patients) with complex coronary artery disease. Their findings in completion angiography at the end of the operation included suboptimal anastomoses, poor lie of the venous bypass graft, and bypasses to not diseased vessels. The angiography findings led to a change in the management, including minor adjustments of the graft, traditional surgical revision or percutaneous coronary interventions, resulting in optimal bypass outcomes.\n In the study from FuWai, the hybrid procedure was also less costly than an exclusively percutaneous strategy.", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 14.524187675070028, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 7.928571428571429, + "fkgl_delta": -1.0483472658628656 + }, + { + "index": 12, + "label": "low_health_literacy", + "original_doc": "A 52-year-old woman had burning when she peed and had to pee very often for a long time. She tried many treatments for bladder infections, but the problem did not go away. Regular scans and lab tests looked normal. A camera test that looked inside her bladder showed the lining was red and irritated, with tiny bits floating in the urine. Later, the lab saw a live larva (a baby insect) in her urine under the microscope. That finding explained her symptoms. She was told to keep very clean. She was also told to drink plenty of water every day.", + "wiki_anchor": "Clinical features\nPatients with urinary tract infections caused by S. saprophyticus usually present with symptomatic cystitis. Symptoms include a burning sensation when passing urine, the urge to urinate more often than usual, a 'dripping effect' after urination, weak bladder, a bloated feeling with sharp razor pains in the lower abdomen around the bladder and ovary areas, and razor-like pains during sexual intercourse. Flank pain may occur due to infection of the upper urinary tract, such as pyelonephritis. Signs and symptoms of renal involvement are also often registered.", + "doc_fkgl": 6.041, + "wiki_fkgl": 12.897149425287356, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 9.25, + "fkgl_delta": -6.856149425287356 + }, + { + "index": 12, + "label": "intermediate_health_literacy", + "original_doc": "A 52-year-old woman had ongoing dysuria and urinary frequency despite multiple treatments for presumed infections. Cystoscopy showed bladder redness and debris, while imaging and routine lab tests were unremarkable. Eventually, a live larva was identified in the urine, confirming the cause of her symptoms. Management focused on better personal hygiene and increased fluid intake.", + "wiki_anchor": "Hemorrhagic cystitis or haemorrhagic cystitis is an inflammation of the bladder defined by lower urinary tract symptoms that include dysuria, hematuria, and hemorrhage. The disease can occur as a complication of cyclophosphamide, ifosfamide and radiation therapy. In addition to hemorrhagic cystitis, temporary hematuria can also be seen in bladder infection or in children as a result of viral infection.", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 15.480000000000004, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 8.333333333333334, + "fkgl_delta": -3.2975925925925935 + }, + { + "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": "Symptoms\nC. cayetanensis causes gastroenteritis, with the extent of the illness varying based on age, condition of the host, and size of the infectious dose. Symptoms include \"watery diarrhea, loss of appetite, weight loss, abdominal bloating and cramping, increased flatulence, nausea, fatigue, and low-grade fever\", though this can be augmented in more severe cases by vomiting, substantial weight loss, excessive diarrhea, and muscle aches. Typically, patients with a persistent watery diarrhea lasting over several days may be suspected of harboring the disease, especially if they have traveled to a region where the protozoan is endemic. The incubation period in the host is typically around a week, and illness can last six weeks before self-limiting. Unless treated, illness may relapse. The more severe forms of the disease can occur in immunocompromised patients, such as those with AIDS.\nHuman cyclosporiasis is clinically similar to cryptosporidiosis, isosporiasis, giardiasis and microsporidiosis because of the similar clinical features. Flu like syndrome with myalgias and arthralgias may precede the onset of diarrhea. Fever is low grade and is unusual. There is presence of moderate to severe dehydration, compensatory tachycardia, systolic blood pressure (SBP<90 mmHg) and decreased skin turgor may occur. But mild infection produces few or no clinical symptoms. The immune system may determine the appearance of symptoms; that is, from symptomatic to asymptomatic stage depends on resistivity of the immune system.", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 13.475353982300884, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.416666666666667, + "fkgl_delta": 1.4820409756823132 + }, + { + "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": "Cardiac examination of individuals with variant angina is usually normal in the absence of current symptoms. Two-thirds of these individuals do have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of their symptoms. Persons who have atherosclerosis-based occlusion that is \u226570% in a single coronary artery or that involves multiple coronary arteries are predisposed to develop a variant angina form that has a poorer prognosis than most other forms of this disorder. In these individuals but also in a small percentage of individuals without appreciable atherosclerosis of their coronary arteries, attacks of coronary artery spasm can have far more serious presentations such as fainting, shock, and cardiac arrest. Typically, these presentations reflect the development of a heart attack and/or a potentially lethal heart arrhythmia; they require immediate medical intervention as well as consideration for the presence of, and specific treatment regimens for, their disorder.", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 20.404516129032263, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 8.6, + "fkgl_delta": -14.577167291822956 + }, + { + "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": "Variant angina, also known as Prinzmetal angina, vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina (cardiac chest pain). Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 18.194662162162164, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 11.5, + "fkgl_delta": -3.600852638352638 + }, + { + "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": "A \"hypertensive emergency\" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure, an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 16.232121212121214, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": 0.7406332182585338 + }, + { + "index": 14, + "label": "low_health_literacy", + "original_doc": "A 36-year-old woman had trouble swallowing. Tests found she was born with an unusual shape of the main body artery in her chest. The artery curves to the right in a mirror-image pattern. It wraps around a main branch of the airway. The side branches of the artery come off in the reverse order from normal. Most people with this have no symptoms. Problems happen only if the artery squeezes the space in the middle of the chest. This can press on the food pipe or the windpipe. Surgery may be needed if there is strong pressure on these tubes, a bulge or a tear in the chest artery, or a pouch on the artery bigger than 2 cm. There is no one-size-fits-all treatment. Care is tailored to the person\u2019s symptoms and body anatomy. This patient did not receive any treatment.", + "wiki_anchor": "The aortic arch has three main branches on its superior aspect. The first, and largest, branch of the arch of the aorta is the brachiocephalic trunk, which is to the right and slightly anterior to the other two branches and originates behind the manubrium of the sternum. Next, the left common carotid artery originates from the aortic arch to the left of the brachiocephalic trunk, then ascends along the left side of the trachea and through the superior mediastinum. Finally, the left subclavian artery comes off of the aortic arch to the left of the left common carotid artery and ascends, with the left common carotid, through the superior mediastinum and along the left side of the trachea. An anatomical variation is that the left vertebral artery can arise from the aortic arch instead of the left subclavian artery.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 14.777179856115108, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 7.6, + "fkgl_delta": -9.047091203632839 + }, + { + "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": "The aortic arch has three main branches on its superior aspect. The first, and largest, branch of the arch of the aorta is the brachiocephalic trunk, which is to the right and slightly anterior to the other two branches and originates behind the manubrium of the sternum. Next, the left common carotid artery originates from the aortic arch to the left of the brachiocephalic trunk, then ascends along the left side of the trachea and through the superior mediastinum. Finally, the left subclavian artery comes off of the aortic arch to the left of the left common carotid artery and ascends, with the left common carotid, through the superior mediastinum and along the left side of the trachea. An anatomical variation is that the left vertebral artery can arise from the aortic arch instead of the left subclavian artery.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 14.777179856115108, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 7.6, + "fkgl_delta": -2.792371493745769 + }, + { + "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": "Arches 1 and 2\nThe first and second arches disappear early. A remnant of the 1st arch forms part of the maxillary artery, a branch of the external carotid artery. The ventral end of the second develops into the ascending pharyngeal artery, and its dorsal end gives origin to the stapedial artery, a vessel which typically atrophies in humans but persists in some mammals. The stapedial artery passes through the ring of the stapes and divides into supraorbital, infraorbital, and mandibula branches which follow the three divisions of the trigeminal nerve. A remnant of the second arch also forms the hyoid artery. The infraorbital and mandibular branches arise from a common stem, the terminal part of which anastomoses with the external carotid artery. On the obliteration of the stapedial artery, this anastomosis enlarges and forms the internal maxillary artery; branches formerly of the stapedial artery are subsequently considered branches of the internal maxillary artery. The common stem of the infraorbital and mandibular branches passes between the two roots of the auriculotemporal nerve and becomes the middle meningeal artery; the original supraorbital branch of the stapedial is represented by the orbital twigs of the middle meningeal.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 14.611634615384613, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 7.125, + "fkgl_delta": 1.8434531039136317 + }, + { + "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": "Merkel-cell carcinoma (MCC) usually presents as a firm nodule (up to 2\u00a0cm diameter) or mass (>2\u00a0cm diameter). These flesh-colored, red, or blue tumors typically vary in size from 0.5\u00a0cm (less than one-quarter of an inch) to more than 5\u00a0cm (2 inches) in diameter and may enlarge rapidly. Tumors can present as painless, tender or itchy, and other MCC manifestations as papules or plaques have also been reported. Although MCC may arise almost anywhere on the body, it is most commonly found in sun-exposed areas such as the head, neck or extremities. Five key attributes of MCC were summarized in 2008 in the acronym AEIOU (Asymptomatic/lack of tenderness, Expanding rapidly, Immune suppression, Older than 50 years, and Ultraviolet-exposed site on a person with fair skin). Ninety percent of MCC's have three or more of those features.\nMCC is sometimes mistaken for other histological types of cancer, including basal cell carcinoma, squamous cell carcinoma, malignant melanoma, lymphoma, and small cell carcinoma, or as a benign cyst. Merkel-cell carcinomas have been described in children, however pediatric cases are very rare.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 12.593664825046044, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 7.25, + "fkgl_delta": -7.330997312355688 + }, + { + "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\nThis mass can be detected and removed before transformation and metastasis. The tumor is often detected by imaging such as ultrasound. The location and size of the tumor may cause pressure and pain to the patient. But often the tumor goes undetected. After detection, the mass is tested using an invasive fine-needle aspiration biopsy.\nH\u00fcrthle cell adenoma is the benign analogue of H\u00fcrthle cell carcinoma. This adenoma is extremely rare; when it occurs, it usually occurs in women. Often the adenoma is harmless but is removed after detection because its future course cannot be trusted.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 10.354583333333334, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 4.625, + "fkgl_delta": 3.5384697640118006 + }, + { + "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": "Diagnosis\nH\u00fcrthle cell adenomas are most likely diagnosed much more frequently than H\u00fcrthle cell carcinomas. The female to male ratio for Hurthle cell adenomas is 8:1, while the ratio is 2:1 for the malignant version. H\u00fcrthle cell cancer tends to occur in older patients. The median age at diagnosis for H\u00fcrthle cell carcinomas is approximately 61 years old. Typically a painless thyroid mass is found in patients with this type of cancer. As expected, patients with carcinoma usually present larger tumors than patients with adenoma. Rarely, the cancer can spread to the lymph nodes. On few occasions, patients with H\u00fcrthle cell carcinoma have distant metastases in the lungs or surrounding bones. H\u00fcrthle cell neoplasms are somewhat difficult to differentiate between being benign or malignant. Since the size and growth pattern of the tumor cannot be used to determine malignancy, although larger tumors have higher incidence of malignancy, H\u00fcrthle cell adenomas and carcinomas have to be separated by the presence, in the case of carcinomas, or absence, in the case of adenomas, of both capsular invasion and vascular invasion. Tumors displaying only capsular invasion tend to behave less aggressively than those with vascular invasion. H\u00fcrthle cell carcinomas are characterized as either minimally invasive or widely invasive tumors. While the minimally invasive or encapsulated carcinoma is fully surrounded by a fibrous capsule, the widely invasive carcinoma shows extensive area of both capsular and vascular invasion with the leftover capsule typically difficult to identify. Classification is important since widely invasive tumors can have outcomes with a 55% mortality rate.", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 13.620334821428575, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 6.428571428571429, + "fkgl_delta": 1.4967560876623338 + }, + { + "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": "Staphylococcus epidermidis is a Gram-positive bacterium, and one of over 40 species belonging to the genus Staphylococcus. It is part of the normal human microbiota, typically the skin microbiota, and less commonly the mucosal microbiota and also found in marine sponges. It is a facultative anaerobic bacteria. Although S. epidermidis is not usually pathogenic, patients with compromised immune systems are at risk of developing infection. These infections are generally hospital-acquired. S. epidermidis is a particular concern for people with catheters or other surgical implants because it is known to form biofilms that grow on these devices. Being part of the normal skin microbiota, S. epidermidis is a frequent contaminant of specimens sent to the diagnostic laboratory.", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 13.359827586206897, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 6.285714285714286, + "fkgl_delta": -5.891494252873564 + }, + { + "index": 16, + "label": "intermediate_health_literacy", + "original_doc": "A 59-year-old man with long-standing type 1 diabetes presented with acute heart failure. An echocardiogram showed large vegetations on the mitral and aortic valves. Blood cultures were positive for Staphylococcus warneri, a coagulase\u2011negative staphylococcus commonly found on the skin. He was diagnosed with native valve endocarditis. After medical stabilization, he ultimately underwent replacement of both the mitral and aortic valves. In retrospect, mild laboratory abnormalities and several months of weight loss beginning about four months earlier were likely early signs of endocarditis. He had no history of immunosuppressive therapy and no implanted medical devices.", + "wiki_anchor": "Underlying structural valve disease is usually present in patients before developing subacute endocarditis, and is less likely to lead to septic emboli than is acute endocarditis, but subacute endocarditis has a relatively slow process of infection and, if left untreated, can worsen for up to one year before it is fatal. In cases of subacute bacterial endocarditis, the causative organism (streptococcus viridans) needs a previous heart valve disease to colonize. On the other hand, in cases of acute bacterial endocarditis, the organism can colonize on the healthy heart valve, causing the disease.", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 18.815652173913048, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": -5.819573146557424 + }, + { + "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": "A \"hypertensive emergency\" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure, an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 16.232121212121214, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": -3.7347835712994772 + }, + { + "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": "A hepatectomy is considered a major surgical procedure performed under general anesthesia. Access is accomplished by laparotomy, historically by a bilateral subcostal (\"chevron\") incision, possibly with midline extension (Calne or \"Mercedes-Benz\" incision). Nowadays a broadly used approach for open liver resections is the J incision, consisting in a right subcostal incision with midline extension. The anterior approach, one of the most innovative, is made simpler by the liver hanging maneuver.\nIn most recent years the minimal invasive approach, consisting in laparoscopic and then robotic surgery, has become increasingly common in liver resective surgery.\nHepatectomies may be anatomic, i.e. the lines of resection match the limits of one or more functional segments of the liver as defined by the Couinaud classification (cf. liver#Functional anatomy); or they may be non-anatomic, irregular or \"wedge\" hepatectomies. Anatomic resections are generally preferred because of the smaller risk of bleeding and biliary fistula; however, non-anatomic resections can be performed safely as well in selected cases.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 14.825786163522015, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 7.0, + "fkgl_delta": -9.640735713562922 + }, + { + "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": "Process\nThis test is usually done in a doctor's office. The patient is required to remove their underwear, and must either lie on their side on top of an examining table, with their knees bent up towards the chest, or bend forward over the table. The anoscope is 3 to 4\u00a0inches long and the width of an average-to-large bowel movement. The doctor will coat the anoscope with a lubricant and then gently push it into the anus and rectum. The doctor may ask the patient to \"bear down\" or push as if they were going to have a bowel movement, and then relax. This helps the doctor insert the anoscope more easily and identify any bulges along the lining of the rectum.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 9.289552845528458, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": 7.64473775276214 + }, + { + "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": "Recovery and function\nThe surgery itself along with recovery time depends on the patient. Robotic surgery can take approximately 6\u201312 hours. A patient's time in the hospital can take 7\u201310 days if no complications present themselves. Depending on the type of surgery the abdominal incision for this surgery may be up to eight inches in length and is typically closed with staples on the outside and several layers of dissolvable stitches on the inside. After surgery, patients will have three drainage tubes place while tissues heal: one through the newly created stoma, one through another temporary opening in the abdominal wall into the pouch, and an SP tube (to drain non-specific post-surgical abdominal fluid). In the hospital, the SP tube and external staples will be removed, after several days. The remaining two tubes will each be connected to collection bags worn on each leg and the patient is usually sent home like this. After sufficient healing, and another doctor's visit, the tube will be removed from the stoma. The patient will now begin to catheterize the pouch every two hours. Since one other tube will still be in place, patients can still sleep through the night, since a larger collection bag is attached to that tube at night time. After approximately one month, patients will return to the hospital for a special x-ray. Dye will be instilled into the pouch to verify that there is no leakage of urine. If there is no leakage, this last tube will be removed. Emptying time now may be increased to 3 hours, however, now the patient will need to wake up during the night (every 3 hours) to empty the pouch. Over time, emptying time can possibly be increased up to 4\u20136 hours. Although to decrease the potential for infections and deterioration of the pouch it is best to continue to cath every 3\u20134 hours. The pouch will continue to expand and will reach its final size at approximately six months. The pouch will then hold up to 1,200 cubic centimeters (cc). Depending on your doctor's orders, each day, the pouch may need to be irrigated with 60 cc of sterile water in an effort to remove membrane mucus, salts, and bacteria. It can take 6\u201312 months for your body to adjust to the Indiana pouch.", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 10.056045691906004, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 5.6, + "fkgl_delta": 4.492974986985921 + }, + { + "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": "Symptoms\nAffected individuals experience pain and swelling in the middle part of the foot and usually limp as a result. Patients who walk with a limp tend to walk with increased weight on the lateral side of the foot. Also, there can be tenderness over the navicular. Patients often complain of pain over the apex.\nAn X-ray of both feet is used to diagnose disease. The affected foot tends to have a sclerotic and flattened navicular bone. Symptoms may last for a few weeks or may continue to be present for up to 2 years. An indication of the symptoms residing is the resolution of the acute inflammation and obvious healing of the foot. This means that the affected bone and the Tarsal Navicular begin to regain their normal size, density and structure.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 8.53874686716792, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 6.555555555555555, + "fkgl_delta": -2.977750363671415 + }, + { + "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": "Signs and symptoms\nPain and soft-tissue swelling are present at the distal-third radial fracture site and at the wrist joint. This injury is confirmed on radiographic evaluation. Forearm trauma may be associated with compartment syndrome. Anterior interosseous nerve (AIN) palsy may also be present, but it is easily missed because there is no sensory component to this finding. A purely motor nerve, the AIN is a division of the median nerve. Injury to the AIN can cause paralysis of the flexor pollicis longus and flexor digitorum profundus muscles to the index finger, resulting in loss of the pinch mechanism between the thumb and index finger. Galeazzi fractures are sometimes associated with wrist drop due to injury to radial nerve, extensor tendons or muscles.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 11.505133565621371, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 6.571428571428571, + "fkgl_delta": -2.050466898954703 + }, + { + "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": "Rheumatism, excluding the back (725\u2013729)\n Polymyalgia rheumatica\n Peripheral enthesopathies and allied syndromes\n Adhesive capsulitis, shoulder\n Rotator cuff syndrome, NOS (Not Otherwise Specified)\n Bicipital tenosynovitis\n Enthesopathy of elbow region\n Medial epicondylitis\n Lateral epicondylitis\n Olecranon bursitis\n Enthesopathy of wrist and carpus\n Enthesopathy of hip region\n Enthesopathy of knee\n Pes anserinus tendinitis\n Tendinitis, patellar\n Prepatellar bursitis\n Metatarsalgia, NOS (Not Otherwise Specified) \n Tendinitis, achilles\n Tendinitis, tibialis\n Calcaneal spur\n Other disorders of synovium, tendon and bursa\n Synovitis and tenosynovitis\n Synovitis/tenosynovitis, unspec.\n Trigger finger, acquired\n de Quervain's disease\n Tenosynovitis, hand/wrist\n Tenosynovitis, foot/ankle\n Bunion\n Ganglion and cyst of synovium, tendon, and bursa\n Ganglion, tendon sheath\n Ganglion, unspec.\n Rupture of tendon, nontraumatic\n Rupture, biceps tendon\n Rupture, achilles tendon\n Other disorders of synovium, tendon, and bursa\n Plica syndrome\n Abscess, bursa\n Disorders of muscle, ligament, and fascia\n Infective myositis\n Muscular calcification and ossification\n Muscular wasting, atrophy\n Other specific muscle disorders\n Laxity of ligament\n Hypermobility syndrome\n Dupuytren's contracture\n Other fibromatoses\n Plantar fasciitis\n Other disorders of muscle, ligament, and fascia\n Diastasis recti\n Muscle spasm\n Necrotizing fasciitis\n Muscle weakness\n Rhabdomyolysis\n Iliotibial band syndrome\n Other disorders of soft tissues\n Rheumatism unspecified and fibrositis\n Myalgia and myositis, Fibromyositis\n Neuralgia neuritis and radiculitis unspecified\n Panniculitis unspecified\n Fasciitis unspecified\n Pain in limb\n Foreign body in soft tissue\n Nontraumatic compartment syndrome", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 37.71330049261084, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 13.666666666666666, + "fkgl_delta": -25.849771080846136 + }, + { + "index": 19, + "label": "low_health_literacy", + "original_doc": "A 23-year-old man came to the emergency room with a sudden, very bad headache. He also felt sick, threw up, and felt heavy pressure in his chest. His blood pressure was high and he was breathing fast. A quick heart test looked like a major heart attack. He was rushed for a procedure to check and open the heart arteries. The heart arteries looked normal. A head CT scan then showed bleeding in the space around his brain. A team of specialists cared for him, but he got worse quickly. He went into cardiac arrest and died.", + "wiki_anchor": "In November 1981, Antognoni fractured his skull in two places and went into a coma for two days following an accidental collision with Genoa's goalkeeper Silvano Martina, which saw the latter's knee come into heavy contact with Antognoni's head; according to FIFA.com, the playmaker went into cardiac arrest for 30 seconds, which led Genoa's captain, Claudio Onofri, to exclaim \"he\u2019s dead, he\u2019s dead!\" However, Genoa's team doctor \u2013 Pierluigi Gatto \u2013 was able to act quickly and revive Antognoni's pulse by untwisting his tongue and giving him CPR through chest compressions and mouth-to-mouth resuscitation.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 16.122173913043483, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 11.5, + "fkgl_delta": -12.059356043627673 + }, + { + "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": "Intraparenchymal hemorrhage accounts for approximately 8-13% of all strokes and results from a wide spectrum of disorders. It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 16.34121621621622, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.0, + "fkgl_delta": -2.5836813324952885 + }, + { + "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": "A \"hypertensive emergency\" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure, an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 16.232121212121214, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": -3.9944168096054895 + } +] \ No newline at end of file