diff --git "a/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_1_v1.json" "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_1_v1.json" new file mode 100644--- /dev/null +++ "b/data/data_annotator_data/new_v1/crowdsourcing_input_en_shard_1_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": "Death of Mrs Armstrong\nIn May 1919, Katharine Armstrong's health first began to weaken, with certain symptoms that the local physician, Dr Thomas Hincks, diagnosed as a case of brachial neuritis. From this she appeared to recover, and did not need to consult Dr Hincks for over a year. But in August 1920, Mrs Armstrong's health, both physical and mental, deteriorated again. Armstrong kept in close contact with Hincks, and showed great concern for his wife, consulting relatives and friends as well. Hincks found that Mrs Armstrong was showing signs of mental collapse and came to the conclusion that it was connected to her illness. At the end of August, Mrs Armstrong was admitted to Barnwood, a private mental asylum near Gloucester. On admission she had pyrexia, vomiting, heart murmurs, and albumen in the urine. There was also partial paralysis in the hands and feet and loss of muscle tone. Mrs Armstrong was also delusional.", + "doc_fkgl": 4.138157894736846, + "wiki_fkgl": 9.169247311827956, + "doc_tree_depth": 4.5, + "wiki_tree_depth": 6.555555555555555, + "fkgl_delta": -5.03108941709111 + }, + { + "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": "Pathophysiology\nThis condition is due to ischemia of the renal papillae, the portion of the kidney that collects urine from the nephron. The papillae are vulnerable to ischemia as they are supplied by small caliber arteries which are liable to obstruction. All of the underlying causes of papillary necrosis cause diminished flow through these arteries, either through direct mechanical obstruction (sickle cell), obstruction secondary to inflammation (vasculitides), or vasoconstriction (NSAIDs). Papillary necrosis is more likely to develop when multiple of these underlying factors are present. Ultimately, necrosis of the papillae results in sloughing into the lumen, causing hematuria. If the degree of necrosis is substantial post-renal failure may occur, though this is uncommon.", + "doc_fkgl": 15.20401179941003, + "wiki_fkgl": 14.20632743362832, + "doc_tree_depth": 4.888888888888889, + "wiki_tree_depth": 6.5, + "fkgl_delta": 0.9976843657817085 + }, + { + "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": "Primary (genetic) causes \nMutations in the following five genes account for greater than 80% of the genetic causes of congenital nephrotic syndrome:\n NPHS1 (Finnish Type): The gene NPHS1 encodes for the protein nephrin. This genetic variant is characterized by severe protein loss in the first several days to weeks of life. Fin-major and Fin-minor were the first two main genetic mutations identified in Finnish newborns, however, numerous mutations have now been identified in patients all over the world from various ethnic groups. NPHS1 mutations are the most common cause of primary congenital nephrotic syndrome, accounting for 40-80% of cases.\n NPHS2: This gene encodes for the protein podocin. Patients with this genetic mutation develop nephrotic syndrome in the first few weeks of infancy, but can also manifest symptoms later in life. Urinary protein loss is less severe when compared with the Finnish type. Both nephrin and podocin play important roles in the structure and function of the podocyte filtration slit diaphragm and disease involvement is typically limited to the kidneys\n WT1: The Wilms' tumor suppressor gene regulates the expression of many genes involved in kidney and urogenital development. Mutations lead to several types of developmental syndromes, including Denys-Drash syndrome, Frasier syndrome, WAGR syndrome (Wilms tumor, aniridia, genitourinary abnormalities, and intellectual disability), and isolated nephrotic syndrome in infants. Depending on the specific syndrome, patients are at risk for Wilms' and other tumors, genital abnormalities, and nephrotic syndrome.\n LAM\u03b22 (Pierson syndrome): This gene encodes for the protein laminin \u03b22, which helps attach podocytes to the glomerular basement membrane. Patients with Pierson syndrome have eye abnormalities, including nonreactive narrowing of the pupils (microcoria), and neurologic deficits.\n PLC\u03b51: Codes for the enzyme Phospholipase C\u03b51, which is expressed in podocytes.", + "doc_fkgl": 17.108284910965327, + "wiki_fkgl": 13.995492957746482, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 7.461538461538462, + "fkgl_delta": 3.1127919532188457 + }, + { + "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": "At the age of 16, Parlette began experiencing pain in the area of her right hip that forced her to drop out of cross country running. An MRI scan revealed a spot that was interpreted as a hemangioma. Six years later, after she developed a severe cough, further scans showed spots in her lungs. Half a year later, she developed a lump in her right breast, which was excised and biopsied, leading to the correct diagnosis of the cancer she had probably been carrying for at least seven years.", + "doc_fkgl": 3.5813553113553134, + "wiki_fkgl": 9.925702247191008, + "doc_tree_depth": 5.142857142857143, + "wiki_tree_depth": 8.75, + "fkgl_delta": -6.344346935835695 + }, + { + "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": "Phlegmasia cerulea dolens (PCD) (literally: 'painful blue inflammation'), not to be confused with preceding phlegmasia alba dolens, is an uncommon severe form of lower extremity deep venous thrombosis (DVT) that obstructs blood outflow from a vein. Upper extremity PCD is less common, occurring in under 10% of all cases. PCD results from extensive thrombotic occlusion (blockage by a thrombus) of extremity veins, most commonly an iliofemoral DVT, of the iliac vein and/or common femoral vein. It is a medical emergency requiring immediate evaluation and treatment.", + "doc_fkgl": 11.942105263157895, + "wiki_fkgl": 14.631617647058828, + "doc_tree_depth": 6.4, + "wiki_tree_depth": 7.5, + "fkgl_delta": -2.689512383900933 + }, + { + "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": "Postictal paresis (PP), although familiar to neurologists, has not been well-studied. One retrospective observational study evaluated 328 selected patients from ages 16 to 57 years who had prolonged video-electroencephalogram (EEG) monitoring for medically intractable epilepsy and focal seizure onset; those with nonepileptic seizures, status epilepticus, and Lennox-Gastaut syndrome were excluded. The following observations were made:\n PP occurred in 44 patients (13.4 percent)\n PP was always unilateral and always contralateral to the seizure focus\n The mean duration of PP was 174 seconds (range 11 seconds to 22 minutes)\nOf all seizures followed by PP, the following features were noted:\n Obvious ictal motor activity was seen in 78 percent (Todd's paresis is more common after any clonic seizure activity)\n Very slight ictal motor activity was seen in 10 percent\n No ictal motor activity was seen in nearly 10 percent\n The most common ictal lateralizing sign was unilateral clonic activity in 56 percent\n Ictal dystonic posturing occurred in 48 percent\n Ictal limb immobility occurred in 25 percent\nThe results of this study are valuable because few other data exist on the frequency, duration, and seizure characteristics associated with PP. However, the study is likely biased by the inclusion only of patients with medically intractable seizures who had undergone video-EEG monitoring, and the results may not extrapolate to a general epilepsy population.", + "doc_fkgl": 16.247417695473253, + "wiki_fkgl": 23.877302752293577, + "doc_tree_depth": 6.083333333333333, + "wiki_tree_depth": 8.8, + "fkgl_delta": -7.629885056820324 + }, + { + "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": "Medical importance\nEikenella corrodens is a commensal of the human mouth and upper respiratory tract. It is an unusual cause of infection and when it is cultured, it is most usually found mixed with other organisms. Infections most commonly occur in patients with cancers of the head and neck, but can occur in human bite infections, especially \"reverse bite\", \"fight bite\", or \"clenched fist injuries\". It can also cause infections in insulin-dependent diabetics and intravenous drug users who lick their needles (\"needle-licker's osteomyelitis\"). It is one of the HACEK group of infections which are a cause of culture-negative endocarditis. In general, the HACEK organisms are responsible for approximately 3% of all cases of infective endocarditis (IE). IE due to E. corrodens is usually a result of poor oral hygiene and or periodontal infection. Manipulation of the gingival or oral mucosa for dental procedures also can predispose patients to infection since E. corrodens is a constituent of the human oral flora. E. corrodens can coexists and is frequently detected with other pathogens including Staphylococcus and Streptococcus.", + "doc_fkgl": 4.63312375249501, + "wiki_fkgl": 12.393974025974025, + "doc_tree_depth": 5.277777777777778, + "wiki_tree_depth": 7.555555555555555, + "fkgl_delta": -7.760850273479015 + }, + { + "index": 2, + "label": "intermediate_health_literacy", + "original_doc": "A 22-year-old woman presented with a month of painful stomatitis that made eating and drinking difficult. The illness began with a fever and pimple-like lesions on the lips. She had been vaping regularly for about one year. Examination showed no skin lesions elsewhere. The lips had serosanguineous crusts and erosions at the labial commissures that tended to bleed. Intraorally, there were multiple irregular white ulcers with yellowish borders on several sites of the oral mucosa. Anti\u2013HSV-1 IgG was non-reactive. The diagnosis was oral erythema multiforme, likely related to vaping. Management included normal saline compresses to the lips, a dexamethasone mouth rinse mixed with hyaluronic acid, 2% miconazole cream applied to the lip corner, petroleum jelly for dry lips, and stopping vaping. Her oral condition improved within one week.", + "wiki_anchor": "Signs and symptoms\nIt presents itself in the mouth, most frequently as a thick, bilateral, symmetrical white plaques with a spongy, corrugated or velvety texture. Most usually, the lesions are on the buccal mucosa, but sometimes on the labial mucosa, alveolar ridge, floor of the mouth, ventral surface of the tongue or soft palate. The gingival margin and dorsum of the tongue are almost never affected. Less commonly, sites outside the mouth are affected, including the nasal, esophageal, laryngeal, anal and genital mucosae. It usually is present from birth, or develops during childhood. Rarely, the lesions may develop during adolescence. Apart from the appearance of the affected areas, there are usually no other signs or symptoms.", + "doc_fkgl": 10.328562500000004, + "wiki_fkgl": 11.421133004926109, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 6.142857142857143, + "fkgl_delta": -1.0925705049261047 + }, + { + "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": "In 1881 a Scottish professor of surgery, Kenneth MacLeod described lesions of dermal ulcer in Madras as \"serpiginous ulcer\". In 1896 J.H. Conyers and C.W. Daniels reported the same disease as \"lupoid form of the so-called groin ulceration\" in New Guinea. In 1897 similar symptom was described by J. Galloway as \"ulcerating granuloma of the pudendum\" from one infected person in London. This became a commonly used medical term. Even after twenty years the nature of the causative agent was elusive. In 1905 Charles Donovan prepared tissue smears from the ulcerative mouth of a ward boy in Madras hospital. Under the microscope he found intracellular bodies as the cause of the lesion. He described these bodies as like \"gagantic bacilli with rounded ends.\" Even though he regarded them as parasitic protozoans, the nature of these bodies was a matter of dispute. They were simply referred to as \"Donovan's bodies\". In 1910 R.M. Carter demonstrated a large number of the pathogens in large monocytes and he noted their resemblance to protozoans such as Crithidium and Herpetomonas. The description was similar to Donovan's bodies, hence, they were considered to be members of Sporozoa, and the scientific name Donovania granulomatis was introduced. In 1913 H.D. Arag\u00e3o and G. Vianna gave the binomial Calymmatobacterium granulomatis noting their similarities to bacteria from their (rather dubious) cell culture. The scientific name was ultimately changed to Klebsiella granulomatis based on the phylogenetic relationship with the genus Klebsiella.", + "doc_fkgl": 14.527236842105264, + "wiki_fkgl": 10.084166666666668, + "doc_tree_depth": 7.214285714285714, + "wiki_tree_depth": 6.5, + "fkgl_delta": 4.443070175438596 + }, + { + "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": "The history of tuberous sclerosis (TSC) research spans less than 200 years. TSC is a rare, multi-system genetic disease that can cause benign tumours to grow on the brain or other vital organs such as the kidneys, heart, eyes, lungs, and skin. A combination of symptoms may include seizures, developmental delay, behavioural problems and skin abnormalities, as well as lung and kidney disease. TSC is caused by mutations on either of two genes, TSC1 and TSC2, which encode for the proteins hamartin and tuberin respectively. These proteins act as tumour growth suppressors and regulate cell proliferation and differentiation. Originally regarded as a rare pathological curiosity, it is now an important focus of research into tumour formation and suppression.", + "doc_fkgl": 4.623939393939395, + "wiki_fkgl": 12.380000000000003, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 8.166666666666666, + "fkgl_delta": -7.756060606060608 + }, + { + "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": "Clinical services \nThe Fetal Treatment Center specializes in the diagnosis and treatment of fetal birth defects:\n Agenesis of the corpus callosum\n Amniotic band syndrome\n Bowel obstructions\n Congenital cystic adenomatoid malformation\n Congenital diaphragmatic hernia (CDH)\n Congenital heart disease\n Fetal anemia & thrombocytopenia\n Gastroschisis\n Inherited Genetic diseases treatable with Stem Cells\n Spina bifida (myelomeningocele)\n Omphalocele\n Pulmonary sequestration\n Sacrococcygeal teratoma\n Twin pregnancy complications\n Twin-to-twin transfusion syndrome (TTTS)\n TRAP sequence (acardiac twin)\n Unequal placenta sharing\n Urinary tract obstruction\n Ventriculomegaly", + "doc_fkgl": 11.214120481927715, + "wiki_fkgl": 42.451081081081085, + "doc_tree_depth": 5.4, + "wiki_tree_depth": 14.0, + "fkgl_delta": -31.23696059915337 + }, + { + "index": 3, + "label": "proficient_health_literacy", + "original_doc": "A 29-year-old gravida V para IV (3 spontaneous vaginal deliveries, prior cesarean for failed induction 4 years earlier) presented for ANC at 32 weeks by LNMP. Maternal labs: VDRL, HBsAg, and urinalysis negative; CBC within normal limits; blood group A Rh-positive. Obstetric ultrasound revealed normal fetal anatomy except the heart. Fetal echocardiography showed normal situs; atria of comparable size; normally positioned atrioventricular and semilunar valves with normal motion; ventricles comparable in size and contractility; left ventricle forming the apex; no ventricular septal defect. Two circumscribed, round, echogenic masses were noted on the left ventricular papillary muscles, measuring 18.2 \u00d7 8.3 mm and 13.5 \u00d7 8.3 mm. LVOT and RVOT anatomy and function were normal on 2D and color flow. Impression: cardiac rhabdomyoma. Given the association with tuberous sclerosis complex (TSC), detailed neurosonography and systemic evaluation were performed and were unremarkable. She continued routine ANC without complications to 39 weeks. At 39 weeks + 1 day, a cesarean section (repeat on request at term) delivered a 3200 g female, Apgar 10 and 10 at 1 and 5 minutes. Postoperative courses for mother and neonate were uneventful; discharge occurred on postoperative day 3. The neonate was evaluated on days 1, 7, and 30: physical examinations were normal; no seizure activity or new cutaneous lesions; mass dimensions were similar to the antenatal findings. At 7 months, development was age-appropriate; pediatric echocardiography showed well-circumscribed hyperechoic masses on both left ventricular papillary muscles measuring 21.8 \u00d7 9.2 mm and 14.7 \u00d7 8.5 mm, without left ventricular inflow obstruction. At 12 months, anthropometric and neurobehavioral development remained normal. Echocardiography again demonstrated well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and no left ventricular inflow obstruction. Up to one year of age, apart from the persistent intracardiac rhabdomyomas, the child met none of the clinical diagnostic criteria for TSC. Notably, while cardiac rhabdomyomas often regress spontaneously in infancy, these lesions were stable through 12 months.", + "wiki_anchor": "Diagnosis\n The classic triad of the vasa praevia is: membrane rupture, painless vaginal bleeding and fetal bradycardia or fetal death.\n Prior to the advent of ultrasound, this diagnosis was most often made after a stillbirth or neonatal death in which the mother had ruptured her membranes, had some bleeding, and delivered an exsanguinated baby. In these cases, examination of the placenta and membranes after delivery would show evidence of a velamentous cord insertion with rupture of the vessels. However, with almost universal use of ultrasound in the developed world, many cases are now detected during pregnancy, giving the opportunity to deliver the baby before this catastrophic rupture of the membranes occurs. Vasa previa is diagnosed with ultrasound when echolucent linear or tubular structures are found overlying the cervix or in close proximity to it. Transvaginal ultrasound is the preferred modality. Color, power and pulsed wave Doppler should be used to confirm that the structures are fetal vessels. The vessels will demonstrate a fetal arterial or venous waveform.\nAlkali denaturation test detects the presence of fetal hemoglobin in vaginal blood, as fetal hemoglobin is resistant to denaturation in presence of 1% NaOH. Tests such as the Ogita Test, Apt test or Londersloot test were previously used to attempt to detect fetal blood in the vaginal blood, to help make the diagnosis. These tests are no longer widely used in the US, but are sometimes used in other parts of the world.\n Also detection of fetal hemoglobin in vaginal bleeding is diagnostic.", + "doc_fkgl": 13.580182389937107, + "wiki_fkgl": 13.303, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.916666666666667, + "fkgl_delta": 0.2771823899371064 + }, + { + "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": "Three-fourths of abnormalities within a persistent thyroglossal duct involve the formation of a cyst. If a persistent thyroglossal duct becomes fluid filled it will form a thyroglossal duct cyst, which accounts for 70% of congenital neck masses and is the most likely diagnosis if the mass is along the midline of the neck. These cysts are often diagnosed in children under the age of ten and have no particular gender prevalence. The cysts are normally asymptomatic at this age and are noticed because of the swelling that will move if the patient swallows. Over 80% of these cysts are located at or below the hyoid bone.", + "doc_fkgl": 2.581463963963966, + "wiki_fkgl": 11.045924528301889, + "doc_tree_depth": 4.583333333333333, + "wiki_tree_depth": 6.6, + "fkgl_delta": -8.464460564337923 + }, + { + "index": 4, + "label": "intermediate_health_literacy", + "original_doc": "A 13-year-old boy with recurrent respiratory papillomatosis since age two presented with breathing difficulty, noisy breathing (stridor), and hoarseness. Airway evaluation showed multiple nodules narrowing the larynx and trachea. Chest CT revealed several pulmonary cysts. He underwent surgical removal of the papillomatosis lesions and a tracheostomy. He received a single 400 mg intravenous dose of bevacizumab and respiratory therapy. He recovered well, and there has been no recurrence on follow-up.", + "wiki_anchor": "Pulmonary pathology is the subspecialty of surgical pathology which deals with the diagnosis and characterization of neoplastic and non-neoplastic diseases of the lungs and thoracic pleura. Diagnostic specimens are often obtained via bronchoscopic transbronchial biopsy, CT-guided percutaneous biopsy, or video-assisted thoracic surgery (VATS). The diagnosis of inflammatory or fibrotic diseases of the lungs is considered by many pathologists to be particularly challenging.", + "doc_fkgl": 12.728571428571431, + "wiki_fkgl": 20.066774193548394, + "doc_tree_depth": 5.166666666666667, + "wiki_tree_depth": 8.0, + "fkgl_delta": -7.3382027649769626 + }, + { + "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": "NPC may present as a lump or a mass on both sides towards the back of the neck. These lumps usually are not tender or painful but appear as a result of the metastatic spread of the cancer to the lymph nodes, thus causing the lymph nodes to swell. Lymph nodes are defined as glands that function as part of the immune system and can be found throughout the body. Swelling of the lymph nodes in the neck is the initial presentation in many people, and the diagnosis of NPC is often made by lymph node biopsy. Signs of nasopharyngeal cancer may appear as headaches, a sore throat, and trouble hearing, breathing, or speaking. Additional symptoms of NPC include facial pain or numbness, blurred or double vision, trouble opening the mouth, or recurring ear infections. If the ear infection does not present with an upper respiratory tract infection, then an examination should be done on the nasopharynx. This is due to the fact that, in adults, ear infections are less common than in children. Signs and symptoms related to the primary tumor include trismus, pain, otitis media, nasal regurgitation due to paresis (loss of or impaired movement) of the soft palate, hearing loss and cranial nerve palsy (paralysis). Larger growths may produce nasal obstruction or bleeding and a \"nasal twang\". Metastatic spread may result in bone pain or organ dysfunction. Rarely, a paraneoplastic syndrome of osteoarthropathy (diseases of joints and bones) may occur with widespread disease.", + "doc_fkgl": 15.644583333333337, + "wiki_fkgl": 10.488739837398377, + "doc_tree_depth": 6.769230769230769, + "wiki_tree_depth": 6.666666666666667, + "fkgl_delta": 5.15584349593496 + }, + { + "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": "Early signs of disease in the chest include wheezing, cough, and feeling short of breath, which is often misdiagnosed as asthma. The pain that accompanies bone involvement may be attributed to \"growing pains\" in younger children. With bone involvement the first indication for disease may be a pathological fracture. Symptoms may not raise concern, or even be noted, until the disease process has advanced to a point where it causes restrictive compression of vital structures. Further, the occurrence of chylous effusions seems to be unrelated to the pathologic \"burden\" of the disease, the extent of involvement in any particular tissue or organ, or the age of the patient. This offers one explanation as to why, unfortunately, the appearance of chylous effusions in the chest or abdomen may be the first evidence of the disease.", + "doc_fkgl": 5.415573678290215, + "wiki_fkgl": 12.669253731343286, + "doc_tree_depth": 4.785714285714286, + "wiki_tree_depth": 7.833333333333333, + "fkgl_delta": -7.2536800530530705 + }, + { + "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": "Infection/Pneumocystis pneumonia (PCP), which is common in infants with hyper IgM syndrome, is a serious illness. PCP is one of the most frequent and severe opportunistic infections in people with weakened immune systems. Many CD40 Ligand Deficiency are first diagnosed after having PCP in their first year of life. The fungus is common and is present in over 70% of healthy people's lungs, however, Hyper IgM patients are not able to fight it off without the administration of Bactrim\n Hepatitis (Hepatitis C)\n Chronic diarrhea\n Hypothyroidism\n Neutropenia\n Arthritis\n Encephalopathy (degenerative)", + "doc_fkgl": 16.420789473684213, + "wiki_fkgl": 14.963904494382025, + "doc_tree_depth": 6.166666666666667, + "wiki_tree_depth": 8.75, + "fkgl_delta": 1.4568849793021883 + }, + { + "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": "Young acute lymphoblastic leukemia patients with methotrexate-induced leukoencephalopathy appear asymptomatic. However, toxic leukoencephalopathy induced by substance use or environmental toxins have had more damaging side effects. Heroin-induced leukoencephalopathy has had three stages described. The first stage features soft (pseudobulbar) speech, cerebellar ataxia, motor restlessness, and apathy/bradyphrenia. The intermediate stage includes pyramidal tract and pseudobulbar signs, spastic paresis, myoclonic jerks, and choreoathetoid movements. The final or terminal stage is characterized by stretching spasms, akinetic mutism, hypotonic paresis, central pyrexia, and death. Similarly, leukoencephalopathy induced by orally administered methotrexate for arthritis patients presents similar symptoms including ataxia, dysarthria, and seizures; however, long-term cognitive effects remain unknown. Symptoms of leukoencephalopathy caused by overdose of metronidazole medication include dysarthria, gait disturbance, weakness of extremities, and mental confusion. Despite the pharmacological agent or source of toxicity, some patients completely recover from toxic leukoencephalopathy.", + "doc_fkgl": 16.479367816091955, + "wiki_fkgl": 15.785652173913043, + "doc_tree_depth": 6.15, + "wiki_tree_depth": 6.333333333333333, + "fkgl_delta": 0.6937156421789119 + }, + { + "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": "This indicates that either:\n There is not enough specimen for the lab tests ordered to be performed.\n In the case of Vacutainers or other tubes with pre-added anticoagulant, the amount of blood invacuated into the tube at the time of phlebotomy was insufficient to attain the correct blood:anticoagulant ratio. This can cause false results in assays such as coagulation assays (causing falsely increased clotting times) or blood cell differentials (causing a false increase in poikilocytes, particularly burr cells.)", + "doc_fkgl": 4.512113821138211, + "wiki_fkgl": 15.426923076923078, + "doc_tree_depth": 4.444444444444445, + "wiki_tree_depth": 7.666666666666667, + "fkgl_delta": -10.914809255784867 + }, + { + "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": "When she was twenty years old, Marcel was diagnosed with endometriosis, and it was also discovered that she had a blood clotting disorder: \"I was bleeding for about four months then I passed out in the shower and had to be rushed to hospital for an emergency blood transfusion. The doctors told me I'd almost bled to death and further tests revealed I had a blood clotting problem, the female form of haemophilia.\" Six years later she suffered further problems when she developed the rare condition Beh\u00e7et's disease, an inflammatory disease in which the white blood cells attack healthy cells.", + "doc_fkgl": 11.051032608695653, + "wiki_fkgl": 15.110000000000003, + "doc_tree_depth": 5.0, + "wiki_tree_depth": 7.333333333333333, + "fkgl_delta": -4.05896739130435 + }, + { + "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": "Diagnosis\n The classic triad of the vasa praevia is: membrane rupture, painless vaginal bleeding and fetal bradycardia or fetal death.\n Prior to the advent of ultrasound, this diagnosis was most often made after a stillbirth or neonatal death in which the mother had ruptured her membranes, had some bleeding, and delivered an exsanguinated baby. In these cases, examination of the placenta and membranes after delivery would show evidence of a velamentous cord insertion with rupture of the vessels. However, with almost universal use of ultrasound in the developed world, many cases are now detected during pregnancy, giving the opportunity to deliver the baby before this catastrophic rupture of the membranes occurs. Vasa previa is diagnosed with ultrasound when echolucent linear or tubular structures are found overlying the cervix or in close proximity to it. Transvaginal ultrasound is the preferred modality. Color, power and pulsed wave Doppler should be used to confirm that the structures are fetal vessels. The vessels will demonstrate a fetal arterial or venous waveform.\nAlkali denaturation test detects the presence of fetal hemoglobin in vaginal blood, as fetal hemoglobin is resistant to denaturation in presence of 1% NaOH. Tests such as the Ogita Test, Apt test or Londersloot test were previously used to attempt to detect fetal blood in the vaginal blood, to help make the diagnosis. These tests are no longer widely used in the US, but are sometimes used in other parts of the world.\n Also detection of fetal hemoglobin in vaginal bleeding is diagnostic.", + "doc_fkgl": 11.779287370862324, + "wiki_fkgl": 13.303, + "doc_tree_depth": 6.208333333333333, + "wiki_tree_depth": 6.916666666666667, + "fkgl_delta": -1.5237126291376768 + }, + { + "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": "Plot \nDavid Coleman (Ben Gazzara) is a young doctor hired by a hospital's pathology department. The head of the department, Dr. Joseph Pearson (Fredric March), sees Coleman as a rival, and they fight over many medical issues. Coleman falls in love with Cathy Hunt (Ina Balin), a student nurse at the hospital, who develops a tumor in her knee. Pearson believes that the tumor is malignant and that the leg should be amputated, but Coleman disagrees. Coleman orders three blood tests on Mrs. Alexander (Phyllis Love), an expectant mother whose baby may have hemolytic disease, but Pearson believes that the tests are excessive and cancels the third test. Mrs. Alexander is married to a young intern at the hospital (Dick Clark), who, along with Coleman, tried to push for the third test. When the baby is born seriously ill, Dr. Charles Dornberger (Eddie Albert), Mrs. Alexander's OB/GYN, berates Pearson and conducts a blood transfusion to save the baby's life. Pearson's future at the hospital becomes uncertain, and he resigns. Coleman has changed his mind about Cathy's tumor and agrees with Pearson's decision, while Pearson says that Coleman reminds him of himself when he was young and urges him not to let hospital bureaucracy wear him down.", + "doc_fkgl": 3.26104347826087, + "wiki_fkgl": 9.26378640776699, + "doc_tree_depth": 4.0, + "wiki_tree_depth": 6.777777777777778, + "fkgl_delta": -6.00274292950612 + }, + { + "index": 7, + "label": "intermediate_health_literacy", + "original_doc": "A full\u2011term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non\u2011tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra\u2011operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.", + "wiki_anchor": "A testicular nubbin is the residual tissue of the human testis after a supposed perinatal vascular accident involving the testicular blood supply. The blood supply of the testis twists (called torsion) thereby cutting off the blood supply to the testis and results in testicular atrophy (shrinking). The nubbin is usually identified in childhood by the absence of a palpable testis in the scrotal sac. The tissue remnant usually includes fibrous tissue and signs of old infarction with hemosiderin deposition identified histologically. There is some disagreement as to whether these should be removed and whether there is a risk of future malignancy. They are typically removed surgically by pediatric urologists or pediatric general surgeons through either a scrotal or inguinal (or both) incision.", + "doc_fkgl": 11.784036259541985, + "wiki_fkgl": 13.908852459016394, + "doc_tree_depth": 5.375, + "wiki_tree_depth": 7.5, + "fkgl_delta": -2.1248161994744095 + }, + { + "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": "Male case\nIn 1994, a 28-year-old man was diagnosed with EIS after presenting to an orthopedic surgeon for correction of knock knees. He was fully masculinized. At 204\u00a0cm, he had tall stature. His epiphyses were unfused, and there was evidence of still-occurring slow linear growth (for comparison, his height at 16 years of age was 178\u00a0cm). He also had markedly delayed skeletal maturation (bone age 15 years), a severely undermineralized skeleton, evidence of increased bone resorption, and very early-onset osteoporosis. The genitalia, testes, and prostate of the patient were all normal and of normal size/volume. The sperm count of the patient was normal (25 million/mL; normal, >20 million/mL), but his sperm viability was low (18%; normal, >50%), indicating some degree of infertility. The patient also had early-onset temporal hair loss. He reported no history of gender dysphoria, considered himself to have strong heterosexual interests, and had normal sexual function, including morning erections and nocturnal emissions.", + "doc_fkgl": 15.11899521531101, + "wiki_fkgl": 12.257919320594478, + "doc_tree_depth": 6.5, + "wiki_tree_depth": 6.222222222222222, + "fkgl_delta": 2.8610758947165316 + }, + { + "index": 8, + "label": "low_health_literacy", + "original_doc": "A 4-year-old boy had blood in his pee and swelling for 5 days. He then had headaches, nausea, and vomiting. He came to the hospital with seizures and very high blood pressure. Blood tests showed a low level of a protein called C3 and signs of a recent strep infection. This meant his kidney filters were inflamed after strep. His brain was affected by the very high blood pressure. Doctors suspected a problem called PRES, which is brain swelling from high pressure. A brain MRI confirmed this. His immune system also attacked his red blood cells. This made his blood level drop very low, to 5 g/dL. He was treated with medicines to lower his blood pressure, steps to protect his brain, and steroid medicines. He left the hospital after 31 days. Six months later, he had no symptoms.", + "wiki_anchor": "Posterior reversible encephalopathy syndrome (PRES), also known as reversible posterior leukoencephalopathy syndrome (RPLS), is a rare condition in which parts of the brain are affected by swelling, usually as a result of an underlying cause. Someone with PRES may experience headaches, changes in vision, and seizures, with some developing other neurological symptoms such as confusion or weakness of one or more limbs. The name of the condition includes the word \"posterior\" because it predominantly though not exclusively affects the back of the brain (the parietal and occipital lobes). Common underlying causes are severely elevated blood pressure, kidney failure, severe infections, certain medications, some autoimmune diseases, and pre-eclampsia. The diagnosis is usually made by a brain scan (MRI) on which areas of swelling can be identified.", + "doc_fkgl": 4.794388489208632, + "wiki_fkgl": 16.532799999999998, + "doc_tree_depth": 4.923076923076923, + "wiki_tree_depth": 7.6, + "fkgl_delta": -11.738411510791366 + }, + { + "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": "Evidence of hypertensive damage\nIn the context of hypertension, features include:\n Heart\u00a0\u2014 evidence on electrocardiogram screening of the heart muscle thickening (but may also be seen on chest X-ray) suggesting left ventricular hypertrophy) or by echocardiography of less efficient function (left ventricular failure).\n Brain- hypertensive encephalopathy, hemorrhagic stroke, subarachnoid hemorrhage, confusion, loss of consciousness, eclampsia, seizures, or transient ischemic attack.\n Kidney\u00a0\u2014 leakage of protein into the urine (albuminuria or proteinuria), or reduced renal function, hypertensive nephropathy, acute renal failure, or glomerulonephritis.\n Eye\u00a0\u2014 evidence upon fundoscopic examination of hypertensive retinopathy, retinal hemorrhage, papilledema and blindness.\n Peripheral arteries\u00a0\u2014 peripheral vascular disease and chronic lower limb ischemia.", + "doc_fkgl": 14.753525835866263, + "wiki_fkgl": 18.731615384615385, + "doc_tree_depth": 6.333333333333333, + "wiki_tree_depth": 7.8, + "fkgl_delta": -3.9780895487491215 + }, + { + "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": "Pathophysiology\nTwo pathophysiologic mechanisms are thought to play a role in the development of gray baby syndrome after exposure to chloramphenicol. This condition is due to a lack of glucuronidation reactions occurring in the baby (phase II hepatic metabolism), thus leading to an accumulation of toxic chloramphenicol metabolites:\n Metabolism: The UDP-glucuronyl transferase enzyme system in infants, especially premature infants, is not fully developed and incapable of metabolizing the excessive drug load needed to excrete chloramphenicol.\n Elimination: Insufficient renal excretion of the unconjugated drug.\nInsufficient metabolism and excretion of chloramphenicol leads to increased blood concentrations of the drug, causing blockade of the electron transport of the liver, myocardium, and skeletal muscles. Since the electron transport is an essential part of cellular respiration, its blockade can result in cell damage. In addition, the presence of chloramphenicol weakens the binding of bilirubin and albumin, so increased levels of the drug can lead to high levels of free bilirubin in the blood, resulting in brain damage or kernicterus. If left untreated, possible bleeding, renal (kidney) and/or hepatic (liver) failure, anemia, infection, confusion, weakness, blurred vision, or eventually death are expected. Additionally, chloramphenicol is significantly insoluble due to an absence of acidic and basic groups in its molecular compound. As a result, larger amounts of the medication are required to achieve the desired therapeutic effect. High volumes of a medication that can cause various toxicities is another avenue how chloramphenicol can potentially lead to grey baby syndrome.", + "doc_fkgl": 14.958653673835126, + "wiki_fkgl": 17.496760330578514, + "doc_tree_depth": 5.866666666666666, + "wiki_tree_depth": 7.5, + "fkgl_delta": -2.5381066567433876 + }, + { + "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": "On 27 August 1903, one of his patients undergoing external urethrotomy under chloroform anaesthesia developed cardiac arrest, and he performed open chest cardiac massage. He also defined the \"Do not resuscitate\" code in cases involving serious heart disease and other diseases, where life expectancy is very short. He introduced novel vascular suture techniques, which he presented at the International Medical Congress in Moscow in August 1897 and at the annual Congress of the Soci\u00e9t\u00e9 de Chirurgie de Paris in July 1904, where he reported two cases of arterial tear during breast carcinoma resection and repair within the same session. He also reported the removal of a pen cover from the right main bronchus of a 7-year-old girl through a tracheotomy in 1903.", + "doc_fkgl": 6.522207792207791, + "wiki_fkgl": 16.90663934426229, + "doc_tree_depth": 5.571428571428571, + "wiki_tree_depth": 8.25, + "fkgl_delta": -10.384431552054501 + }, + { + "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": "An oxygenator is typically utilized by a perfusionist in cardiac surgery in conjunction with the heart-lung machine. However, oxygenators can also be utilized in extracorporeal membrane oxygenation in neonatal intensive care units by nurses.\nFor most cardiac operations such as coronary artery bypass grafting, the cardiopulmonary bypass is performed using a heart-lung machine (or cardiopulmonary bypass machine). The heart-lung machine serves to replace the work of the heart during the open bypass surgery. The machine replaces both the heart's pumping action and the lungs' gas exchange function. Since the heart is stopped during the operation, this permits the surgeon to operate on a bloodless, stationary heart.", + "doc_fkgl": 13.480000000000004, + "wiki_fkgl": 13.564150943396228, + "doc_tree_depth": 7.166666666666667, + "wiki_tree_depth": 6.0, + "fkgl_delta": -0.08415094339622442 + }, + { + "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": "Diagnosis\nIt can be diagnosed with a standard echocardiogram. An echocardiogram can also aid in classifying the type of defect. The diagnosis can also be made prior to birth via ultrasound. Patients will have a loss of appetite, appear tired and weak, and exhibit rapid breathing and a rapid heart rate. If the condition progresses, the infant may turn pale, feel cold in the lower half of the body, and have a weak pulse due to insufficient blood flow. The pattern of pulse abnormalities is dependent upon the classification; e.g., for type B interrupted aortic arch, the right brachial pulse will be palpable and the left brachial and femoral pulses will be impalpable due to closure of the ductus arteriosus. Rarely, an interrupted aortic arch can be associated with an intracranial aneurysm. Signs of ischemia due to interrupted aortic arch can be separated by the organ system involved:\n Liver injury: elevated serum glutamic oxaloacetic transaminase (SGOT) (also known as aspartate transaminase, AST) and lactic acid dehydrogenase (LDH)\n Kidney injury: elevated serum creatinine\n Intestinal injury: signs of necrotizing enterocolitis, such as bloody stools", + "doc_fkgl": 9.065632911392406, + "wiki_fkgl": 13.627435897435898, + "doc_tree_depth": 6.684210526315789, + "wiki_tree_depth": 6.222222222222222, + "fkgl_delta": -4.561802986043492 + }, + { + "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": "Endophthalmitis, or endophthalmia, is inflammation of the interior cavity of the eye, usually caused by an infection. It is a possible complication of all intraocular surgeries, particularly cataract surgery, and can result in loss of vision or loss of the eye itself. Infection can be caused by bacteria or fungi, and is classified as exogenous (infection introduced by direct inoculation as in surgery or penetrating trauma), or endogenous (organisms carried by blood vessels to the eye from another site of infection and is more common in people who have an immunocompromised state). Other non-infectious causes include toxins, allergic reactions, and retained intraocular foreign bodies. Intravitreal injections are a rare cause, with an incidence rate usually less than 0.05%.", + "doc_fkgl": 6.597509398496243, + "wiki_fkgl": 16.614, + "doc_tree_depth": 5.875, + "wiki_tree_depth": 7.0, + "fkgl_delta": -10.016490601503758 + }, + { + "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": "Signs and symptoms\nSome clinically observed signs and symptoms include:\n Orbital pain\n Eyes displaced posteriorly into sockets (enophthalmos)\n Limitation of eye movement (restrictive strabismus)\n Loss of sensation (hypoesthesia) along the trigeminal (V2) nerve distribution\n Seeing-double when looking up or down (vertical diplopia)\n Orbital and lid subcutaneous emphysema, especially when blowing the nose or sneezing\n Nausea and bradycardia due to oculocardiac reflex \n Inability to elevate eyeball, and move eyeball downward due to inferior rectus entrapment\n Bruising/ecchymosis \n Decreased movement of eyes\n Cranial nerve palsies (III, IV, VI)\n subconjunctival hemorrhage", + "doc_fkgl": 11.54186046511628, + "wiki_fkgl": 42.753793103448274, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 9.5, + "fkgl_delta": -31.211932638331994 + }, + { + "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": "Eye manifestations:\nBilateral ocular manifestations are usually pathognomonic of the disease. In the case of children who develop glaucoma, they may attend the consultation with signs and symptoms of buphthalmos, photosensitivity, tearing, corneal decompensation, which associated with poor vision, can be completed with a strabismus. In the case of the adult, there is a greater chance of not presenting symptoms, so an ophthalmological control may be required to detect the problem. Using a slit lamp, a posterior embryotoxon characterized by a prominent anteriorly displaced Schwalbe's ring near the temporal corneal limbus can be revealed. The unexpected finding of a posterior embryotoxon as a single whitish irregular arcuate ridge, on routine examination, is not necessarily a diagnosis of ARS, as this occurs in a percentage estimated in the literature from 8% to 15% of the normal population. In the case of gonioscopy, we can observe that the extension of the posterior embryotoxon can be greater and be present in the 360\u25cb, with a variable thickness of the annulus and unusually detached and hanging within the anterior chamber. Regarding the iris, we can observe peripheral extensions to Schwalbe's line, which can be thin or thick and extend over the trabecular meshwork, obscuring the scleral spur and even pulling the iris and producing corectopia in iris tissue that can range from atrophy mild stromal to the presence of uveal ectropion, pseudopolycoria or even absence of iris or pseudoacorea. These chamber sinus anomalies predispose half of the cases to open-angle glaucoma, which can manifest throughout life and therefore require regular ophthalmological check-ups. Other related anomalies are strabismus due to alteration in the insertions of the extraocular muscles or secondary to amblyopia, and with a predisposition to exotropia and retinal detachment.", + "doc_fkgl": 14.661870129870131, + "wiki_fkgl": 19.330606060606062, + "doc_tree_depth": 5.473684210526316, + "wiki_tree_depth": 9.222222222222221, + "fkgl_delta": -4.668735930735931 + }, + { + "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": "In the 1940s and 1950s, Canadian surgeon Wilfred Bigelow demonstrated in animal models that the length of time the brain could survive stopped blood circulation could be extended from 3 minutes to 10 minutes by cooling to 30\u00a0\u00b0C before circulation was stopped. He found that this time could be extended to 15 to 24 minutes at temperatures below 20\u00a0\u00b0C. He further found that at a temperature of 5\u00a0\u00b0C, groundhogs could endure two hours of stopped blood circulation without ill effects. This research was motivated by a desire to stop the heart from beating long enough to do surgery on the heart while it remained still. Since heart-lung machines, also known as cardiopulmonary bypass (CPB), had not been invented yet, stopping the heart meant stopping blood circulation to the whole body, including the brain.\n \nThe first heart surgery using hypothermia to provide a longer time that blood circulation through the whole body could be safely stopped was performed by F. John Lewis and Mansur Taufic at the University of Minnesota in 1952. In this procedure, the first successful open heart surgery, Lewis repaired an atrial septal defect in a 5-year-old girl during 5 minutes of total circulatory arrest at 28\u00a0\u00b0C. Many similar procedures were performed by Soviet heart surgeon, Eugene Meshalkin, in Novosibirsk during the 1960s. In these procedures, cooling was accomplished externally by applying cold water or melting ice to the surface of the body.", + "doc_fkgl": 6.542719298245618, + "wiki_fkgl": 12.788740585774061, + "doc_tree_depth": 4.823529411764706, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": -6.246021287528443 + }, + { + "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": "Although studies in the past have shown a benefit of the use of CPM in those individuals having undergone a TKA, recent research has shown that the benefits are questionable. When groups that only received standard mobilization therapies were compared to groups that received CPM treatment in addition to this same therapy, the results suggest that there is no significant increase in functional outcomes or length of hospital stay, or a decrease in adverse affects related to the surgery. These results weren\u2019t adequate for supporting the use of CPM over potentially more successful interventions, such as active exercise that is both high in intensity and velocity. Given the lack of support in current literature, the use of CPM over other treatment is not advised for most patients having undergone a TKA, nor is its use recommended as a standard procedure in clinical practice.", + "doc_fkgl": 12.910294117647059, + "wiki_fkgl": 18.321730769230772, + "doc_tree_depth": 6.444444444444445, + "wiki_tree_depth": 10.0, + "fkgl_delta": -5.411436651583713 + }, + { + "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": "Effects in congestive heart failure\nCongestive heart failure (CHF) is characterized by a reduction in ventricular performance and abnormalities in peripheral circulation and organs. A reduced release of endothelium derived relaxing factor (EDRF) causes a decrease in the stimulation of guanylate cyclase, and cyclic GMP (cGMP) levels fall in vascular smooth muscle. This impairs relaxation in the vasculature and is a part of the vicious cycle of CHF. Patients with CHF have a down-regulation of their \u03b2-1 adrenergic receptors which alters their ability to activate intracellular adenylate cyclase, which catalyzes cAMP formation. cAMP is the second messenger that controls the level of calcium available to allow the heart to contract. An IV administration of amrinone has been shown to increase cardiac output (CO) and stroke volume (SV), while concurrently reducing the filling pressure of the left ventricle and decreasing the resistance in the peripheral vasculature. This does not lead to an increase in heart rate or blood pressure. The improvement in performance of the ventricles is likely to result from a direct stimulation of the depressed myocardium as well as a decrease in peripheral vascular resistance.", + "doc_fkgl": 13.475840409207162, + "wiki_fkgl": 14.857069892473117, + "doc_tree_depth": 6.2631578947368425, + "wiki_tree_depth": 8.25, + "fkgl_delta": -1.3812294832659546 + }, + { + "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": "The larva, a caterpillar, is completely covered in long, hairlike setae arranged in spreading tufts. Most are white, but there are black tufts along the middle of the back, and four long black hair pencils, two near the front, and two near the back. There are black spots along the sides, and the head capsule is black. The hairs cause itchy rashes (contact dermatitis) in many people, particularly those prone to allergies, and may resemble exposure to urushiol. They are microscopically barbed and may rarely cause serious medical complications if they are transferred from the hands to the eyes, but in over 350 documented cases, most were asymptomatic within 24 hours, and none involved anaphylaxis.", + "doc_fkgl": 6.041, + "wiki_fkgl": 11.746956521739133, + "doc_tree_depth": 5.125, + "wiki_tree_depth": 6.4, + "fkgl_delta": -5.705956521739132 + }, + { + "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": "Diagnosis\nUrachal cysts are rare defects found mostly in young children and hence medical ultrasound of the abdomen, bladder and pelvis is the most used diagnostic tool combined with MRI scan and CT scan in older patients who can remain still during a scan.", + "doc_fkgl": 12.18240740740741, + "wiki_fkgl": 19.27, + "doc_tree_depth": 5.5, + "wiki_tree_depth": 11.0, + "fkgl_delta": -7.087592592592589 + }, + { + "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": "Signs and symptoms\n It is most commonly seen in females.\n It is reported among patients from lower socioeconomic groups.\n The nasal cavities become roomy and are filled with foul smelling crusts which are black or dark green and dry, making expiration painful and difficult.\n Microorganisms are known to multiply and produce a foul smell from the nose, though the patients may not be aware of this, because the nerve endings (responsible for the perception of smell) have become atrophied. This is called merciful anosmia.\n Patients usually complain of nasal obstruction despite the roomy nasal cavity, which can be caused either by the obstruction produced by the discharge in the nose, or as a result of sensory loss due to atrophy of nerves in the nose, so the patient is unaware of the air flow. In the case of the second cause, the sensation of obstruction is subjective.\n Bleeding from the nose, also called epistaxis, may occur when the dried discharge (crusts) are removed.\n Septal perforation and dermatitis of nasal vestibule can occur. The nose may show a saddle-nose deformity.\n Atrophic rhinitis is also associated with similar atrophic changes in the pharynx or larynx, producing symptoms pertaining to these structures. Hearing impairment can occur due to Eustachian tube blockage causing middle ear effusion.", + "doc_fkgl": 14.957394957983198, + "wiki_fkgl": 10.725471698113207, + "doc_tree_depth": 5.411764705882353, + "wiki_tree_depth": 6.75, + "fkgl_delta": 4.2319232598699905 + }, + { + "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": "Diagnosis\nIt can be diagnosed with a standard echocardiogram. An echocardiogram can also aid in classifying the type of defect. The diagnosis can also be made prior to birth via ultrasound. Patients will have a loss of appetite, appear tired and weak, and exhibit rapid breathing and a rapid heart rate. If the condition progresses, the infant may turn pale, feel cold in the lower half of the body, and have a weak pulse due to insufficient blood flow. The pattern of pulse abnormalities is dependent upon the classification; e.g., for type B interrupted aortic arch, the right brachial pulse will be palpable and the left brachial and femoral pulses will be impalpable due to closure of the ductus arteriosus. Rarely, an interrupted aortic arch can be associated with an intracranial aneurysm. Signs of ischemia due to interrupted aortic arch can be separated by the organ system involved:\n Liver injury: elevated serum glutamic oxaloacetic transaminase (SGOT) (also known as aspartate transaminase, AST) and lactic acid dehydrogenase (LDH)\n Kidney injury: elevated serum creatinine\n Intestinal injury: signs of necrotizing enterocolitis, such as bloody stools", + "doc_fkgl": 5.827348837209307, + "wiki_fkgl": 13.627435897435898, + "doc_tree_depth": 5.066666666666666, + "wiki_tree_depth": 6.222222222222222, + "fkgl_delta": -7.800087060226591 + }, + { + "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": "Takotsubo cardiomyopathy occurs worldwide. The condition is thought to be responsible for 2% of all acute coronary syndrome cases presenting to hospitals. Although TTS has generally been considered a self-limiting disease, spontaneously resolving over the course of days to weeks, contemporary observations show that \"a subset of TTS patients may present with symptoms arising from its complications, e.g. heart failure, pulmonary edema, stroke, cardiogenic shock, or cardiac arrest\". This does not imply that rates of shock/death of TTS are comparable to those of acute coronary syndrome (ACS), but that patients with acute complications may co-occur with TTS. These cases of shock and death have been associated with the occurrence of TTS secondary to an inciting physical stressor such as hemorrhage, brain injury sepsis, pulmonary embolism or severe COPD.", + "doc_fkgl": 14.593809523809526, + "wiki_fkgl": 14.486250000000002, + "doc_tree_depth": 5.888888888888889, + "wiki_tree_depth": 7.8, + "fkgl_delta": 0.10755952380952394 + }, + { + "index": 13, + "label": "proficient_health_literacy", + "original_doc": "A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nEmergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99\u2013100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.\n\nLaboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.\n\nComputed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700\u20131,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.\n\nImmunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.\n\nContext: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach\u2014urgent culprit-vessel PCI followed by immunosuppression and delayed CABG\u2014is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.", + "wiki_anchor": "Diagnosis\nIt can be diagnosed with a standard echocardiogram. An echocardiogram can also aid in classifying the type of defect. The diagnosis can also be made prior to birth via ultrasound. Patients will have a loss of appetite, appear tired and weak, and exhibit rapid breathing and a rapid heart rate. If the condition progresses, the infant may turn pale, feel cold in the lower half of the body, and have a weak pulse due to insufficient blood flow. The pattern of pulse abnormalities is dependent upon the classification; e.g., for type B interrupted aortic arch, the right brachial pulse will be palpable and the left brachial and femoral pulses will be impalpable due to closure of the ductus arteriosus. Rarely, an interrupted aortic arch can be associated with an intracranial aneurysm. Signs of ischemia due to interrupted aortic arch can be separated by the organ system involved:\n Liver injury: elevated serum glutamic oxaloacetic transaminase (SGOT) (also known as aspartate transaminase, AST) and lactic acid dehydrogenase (LDH)\n Kidney injury: elevated serum creatinine\n Intestinal injury: signs of necrotizing enterocolitis, such as bloody stools", + "doc_fkgl": 16.972754430379748, + "wiki_fkgl": 13.627435897435898, + "doc_tree_depth": 6.380952380952381, + "wiki_tree_depth": 6.222222222222222, + "fkgl_delta": 3.3453185329438497 + }, + { + "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": "While the definitive presentation of the disease is a patient having bowed lower limbs and sex reversal in 46,XY males, there are other clinical criteria that can be used, absent these characteristics, to make the diagnosis. Patients may present with shortened and angulated lower limbs, a vertically oriented and narrow pelvis, an enlarged head, an undersized jaw, cleft palate, flat nasal bridge, low set ears, club feet. On radiographs, underdeveloped shoulder blades, dislocated hips, hypoplastic vertebral pedicles in the thoracic region, 11 pairs of ribs instead of 12, or kyphosis of the cervical spine are useful diagnostic clues. Respiratory distress can be caused by an underdeveloped trachea which collapses on inhalation or by insufficient rib cage development.", + "doc_fkgl": 5.730088652482269, + "wiki_fkgl": 16.99698717948718, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 9.0, + "fkgl_delta": -11.266898527004912 + }, + { + "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": "Diagnosis\nIn patients who have dysphagia, testing may first be done to exclude an anatomical cause of dysphagia, such as distortion of the anatomy of the esophagus. This usually includes visualization of the esophagus with an endoscope, and can also include barium swallow X-rays of the esophagus. Endoscopy is typically normal in patients with nutcracker esophagus; however, abnormalities associated with gastroesophageal reflux disease, or GERD, which associates with nutcracker esophagus, may be seen. Barium swallow in nutcracker esophagus is also typically normal, but may provide a definitive diagnosis if contrast is given in tablet or granule form. Studies on endoscopic ultrasound show slight trends toward thickening of the muscularis propria of the esophagus in nutcracker esophagus, but this is not useful in making the diagnosis.", + "doc_fkgl": 11.984808362369339, + "wiki_fkgl": 17.5712, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 8.4, + "fkgl_delta": -5.586391637630662 + }, + { + "index": 14, + "label": "proficient_health_literacy", + "original_doc": "A 36-year-old female presented with dysphagia and longstanding cervical and upper thoracic pain; she also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit after barium ingestion showed a posterior and lateral right impression on the proximal esophagus extending 3.5 cm craniocaudally, with an estimated maximal esophageal stenosis of 60%. Cervical and thoracic CT revealed a congenital anomaly of the aortic arch: a right aortic arch with mirror-image branching. The arch originated from the aortic root, coursed above the right stem bronchus, and gave rise to the three supra-aortic trunks as follows: (1) left brachiocephalic artery (giving rise to the left common carotid artery and the left subclavian artery), (2) right common carotid artery, and (3) right subclavian artery. The aortic arch then passed posterior to the esophagus and exhibited a small anterior saccule measuring 1.3 cm, consistent with a Kommerell diverticulum. This configuration formed a vascular ring around the tracheo-esophageal pair, bounded posterolaterally on the right by the aortic arch, posterolaterally on the left by the Kommerell diverticulum, laterally on the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. Gastroscopy confirmed endoluminal impact of extrinsic compression. Given minimal clinical repercussions and absence of nutritional disorders, no surgical cure was performed. The evolution was favorable with patient-reported spontaneous amelioration of symptoms.\n\nContext: Right aortic arch with mirror-image branching is a rare anomaly of embryologic development. The vast majority of patients are asymptomatic unless mediastinal structures are compressed. Indications for surgery include major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm. There is no standardized treatment; management is individualized according to clinical presentation and anatomic configuration.", + "wiki_anchor": "Structure\nIn the developing heart, the truncus arteriosus and bulbus cordis are divided by the aortic septum. This makes its appearance in three portions.\n Two distal ridge-like thickenings project into the lumen of the tube; these increase in size, and ultimately meet and fuse to form a septum, which takes a spiral course toward the proximal end of the truncus arteriosus. It divides the distal part of the truncus into two vessels, the aorta and pulmonary artery, which lie side by side above, but near the heart the pulmonary artery is in front of the aorta.\n Four endocardial cushions appear in the proximal part of the truncus arteriosus in the region of the future semilunar valves; the manner in which these are related to the aortic septum is described below.\n Two endocardial thickenings\u2014anterior and posterior\u2014develop in the bulbus cordis and unite to form a short septum; this joins above with the aortic septum and below with the ventricular septum. The septum grows down into the ventricle as an oblique partition, which ultimately blends with the ventricular septum in such a way as to bring the bulbus cordis into communication with the pulmonary artery, and through the latter with the sixth pair of aortic arches; while the left ventricle is brought into continuity with the aorta, which communicates with the remaining aortic arches.", + "doc_fkgl": 16.455087719298245, + "wiki_fkgl": 16.711003861003864, + "doc_tree_depth": 7.0, + "wiki_tree_depth": 8.571428571428571, + "fkgl_delta": -0.2559161417056188 + }, + { + "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": "In 2014, a case of parasite-to-host cancer transmission occurred in a 41-year-old man in Colombia with a compromised immune system due to HIV. The man's tumor cells were shown to have originated from the dwarf tapeworm, Hymenolepis nana. In the 1990s, an undifferentiated pleomorphic sarcoma was transmitted from a 32-year-old patient to his 53-year-old surgeon when the surgeon injured his hand during an operation. Within five months, a tumor had developed on the hand of the surgeon and was subsequently excised. Histologic examinations of the tumor tissues from the patient and surgeon showed that both were morphologically identical. In 1986, a 19-year-old laboratory worker mistakenly punctured her hand with a needle previously used to extract human colonic cancer cells. No injection of the substance occurred, and the worker suffered a small puncture wound with bleeding. Within 19 days, she had developed a small cancerous nodule on her hand. The tumor was removed soon after, and has since shown no sign of reoccurrence.", + "doc_fkgl": 5.262667512690356, + "wiki_fkgl": 10.95098765432099, + "doc_tree_depth": 5.15, + "wiki_tree_depth": 6.111111111111111, + "fkgl_delta": -5.6883201416306335 + }, + { + "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": "In 1926, Lindau was the first to describe a coherent link between the retinal, cerebellar and visceral components of a disease he called \"angiomatosis of the central nervous system\". This disease is characterized by tumors of the retina and the brain, along with cysts of several visceral organs such as the kidneys, pancreas, and adrenal glands. Lindau's research soon attracted the attention of famed neurosurgeon Harvey Cushing, who named the disorder \"Lindau's disease\". By 1964 the medical community had become more aware of early 20th century research on retinal angiomata conducted by ophthalmologist Eugen von Hippel, and today the disease is named Von Hippel\u2013Lindau disease.", + "doc_fkgl": 13.893053097345135, + "wiki_fkgl": 15.213214285714287, + "doc_tree_depth": 6.666666666666667, + "wiki_tree_depth": 10.5, + "fkgl_delta": -1.320161188369152 + }, + { + "index": 15, + "label": "proficient_health_literacy", + "original_doc": "A 62-year-old Tunisian Arab postmenopausal woman with Von Hippel\u2013Lindau (VHL) disease (diagnosed 2021) had multisystem involvement. In 2021 she had a 6 cm left petrous bone endolymphatic sac tumor managed with radiotherapy; a 6 cm left pheochromocytoma treated with left adrenalectomy (pathology: pheochromocytoma); and a ruptured left renal mass treated with left nephrectomy (microscopy: multifocal clear-cell renal cell carcinoma, nuclear grade 2). In 2022 she underwent cephalic duodenopancreatectomy for a pancreatic mass; histology showed three serous cystadenomas and two well-differentiated neuroendocrine tumors. In January 2021, surveillance abdominal\u2013pelvic CT incidentally identified a 4 cm solid\u2013cystic left adnexal mass suspected to be malignant; this was confirmed on transvaginal ultrasound and pelvic MRI and classified O-RADS 5. Gynecologic exam was unremarkable. At laparotomy via a midline infraumbilical incision, a well-defined solid\u2013cystic mass was found in the left adnexa. There was no ascites, no peritoneal carcinomatosis, and the right adnexa appeared grossly normal without exocystic vegetations. Peritoneal cytology was obtained. Left adnexectomy was performed and the specimen sent for frozen section, which was inconclusive, raising the differential of a borderline tumor versus a VHL-associated tumor. Given her postmenopausal status, total hysterectomy with right adnexectomy was completed. Final histology demonstrated bilateral clear-cell papillary cystadenomas of the Fallopian tubes and broad ligament, measuring 0.5 cm on the right and 4 cm on the left. The tumors were composed of tightly packed papillae with fibrous cores lined by monolayered epithelium, consistent with VHL-associated mesosalpinx/broad ligament lesions. The postoperative course was uneventful; 1-month postoperative evaluation was normal. She has been followed every 4 months with normal pelvic ultrasound for 2 years, and was recently readmitted to neurosurgery for recurrence of a brain tumor.", + "wiki_anchor": "The most commonly used classification system for endometrial hyperplasia is the World Health Organization (WHO) system, which previously had four categories: simple hyperplasia without atypia, complex hyperplasia without atypia, simple atypical hyperplasia and complex atypical hyperplasia. In 2014, the WHO updated the classification system and removed the distinction between simple or complex hyperplasia, instead only on presence or absence of atypia. \n Endometrial hyperplasia (simple or complex) - Irregularity and cystic expansion of glands (simple) or crowding and budding of glands (complex) without worrisome changes in the appearance of individual gland cells. In one study, 1.6% of patients diagnosed with these abnormalities eventually developed endometrial cancer.\n Atypical endometrial hyperplasia (simple or complex) - Simple or complex architectural changes, with worrisome (atypical) changes in gland cells, including cell stratification, tufting, loss of nuclear polarity, enlarged nuclei, and an increase in mitotic activity. These changes are similar to those seen in true cancer cells, but atypical hyperplasia does not show invasion into the connective tissues, the defining characteristic of cancer. The previously mentioned study found that 22% of patients with atypical hyperplasia eventually developed cancer.", + "doc_fkgl": 15.117090909090908, + "wiki_fkgl": 18.75166666666667, + "doc_tree_depth": 6.071428571428571, + "wiki_tree_depth": 9.857142857142858, + "fkgl_delta": -3.6345757575757602 + }, + { + "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": "Paeniclostridium sordellii is a rare anaerobic, gram-positive, spore-forming rod with peritrichous flagella that is capable of causing pneumonia, endocarditis, arthritis, peritonitis, and myonecrosis. C. sordellii bacteremia and sepsis occur rarely. Most cases of sepsis from C. sordellii occur in patients with underlying conditions. Severe toxic shock syndrome among previously healthy persons has been described in a small number of C. sordellii cases, most often associated with gynecologic infections in women and infection of the umbilical stump in newborns. It has also been described in post-partum females, medically induced abortions, injection drug users and trauma cases. So far, all documented post-partum females who contracted C. sordellii septicaemia have died, and all but one woman who contracted the bacterium post-abortion have died .", + "doc_fkgl": 7.468333333333334, + "wiki_fkgl": 12.718333333333334, + "doc_tree_depth": 6.125, + "wiki_tree_depth": 7.833333333333333, + "fkgl_delta": -5.25 + }, + { + "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": "Angina animi, a subjective sense that one is dying, which may accompany cardiac ischemia or other conditions\n Abdominal angina, postprandial abdominal pain that occurs in individuals with insufficient blood flow to meet visceral demands\n Ludwig's angina, a serious, potentially life-threatening infection of the tissues of the floor of the mouth\n Prinzmetal's angina, a syndrome typically consisting of cardiac chest pain at rest that occurs in cycles\n Vincent's angina, an infection of the tonsils caused by spirochaeta and treponema\n Angina tonsillaris, an inflammation of the tonsils\n Angina bullosa haemorrhagica, blood blisters in the mucous membranes of the mouth\n Herpangina, pharyngeal blisters caused by Coxsackie A virus or Echovirus", + "doc_fkgl": 12.996079027355623, + "wiki_fkgl": 48.968037383177574, + "doc_tree_depth": 5.714285714285714, + "wiki_tree_depth": 29.0, + "fkgl_delta": -35.971958355821954 + }, + { + "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": "In the 1940s and 1950s, Canadian surgeon Wilfred Bigelow demonstrated in animal models that the length of time the brain could survive stopped blood circulation could be extended from 3 minutes to 10 minutes by cooling to 30\u00a0\u00b0C before circulation was stopped. He found that this time could be extended to 15 to 24 minutes at temperatures below 20\u00a0\u00b0C. He further found that at a temperature of 5\u00a0\u00b0C, groundhogs could endure two hours of stopped blood circulation without ill effects. This research was motivated by a desire to stop the heart from beating long enough to do surgery on the heart while it remained still. Since heart-lung machines, also known as cardiopulmonary bypass (CPB), had not been invented yet, stopping the heart meant stopping blood circulation to the whole body, including the brain.\n \nThe first heart surgery using hypothermia to provide a longer time that blood circulation through the whole body could be safely stopped was performed by F. John Lewis and Mansur Taufic at the University of Minnesota in 1952. In this procedure, the first successful open heart surgery, Lewis repaired an atrial septal defect in a 5-year-old girl during 5 minutes of total circulatory arrest at 28\u00a0\u00b0C. Many similar procedures were performed by Soviet heart surgeon, Eugene Meshalkin, in Novosibirsk during the 1960s. In these procedures, cooling was accomplished externally by applying cold water or melting ice to the surface of the body.", + "doc_fkgl": 12.497337640821737, + "wiki_fkgl": 12.788740585774061, + "doc_tree_depth": 5.96, + "wiki_tree_depth": 8.222222222222221, + "fkgl_delta": -0.2914029449523241 + }, + { + "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": "If cancer cells are found in the nodes it increases the risk of metastatic breast cancer. Another method of determining breast cancer spread is to perform an endoscopic axillary sentinel node biopsy. This involves injecting a dye into the breast lump and seeing which node it first spread to (the sentinel node). This node is then removed and examined. If there is no cancer present, it is assumed the cancer has not spread to the other lymph nodes. This procedure is often less invasive and less damaging than the axillary lymph node dissection. The estimated risk of lymphedema following sentinel lymph node procedure is less than 3%. The approximate risk of lymphedema following axillary lymph node dissection is 10-15% and this can slightly increase with the addition of radiotherapy and chemotherapy to as much as 20-25% depending on the extent of dissection, extent of radiotherapy fields, and history of chemotherapy.", + "doc_fkgl": 5.185050449959093, + "wiki_fkgl": 11.231833333333334, + "doc_tree_depth": 4.526315789473684, + "wiki_tree_depth": 6.75, + "fkgl_delta": -6.046782883374242 + }, + { + "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": "For lower down tumours in the middle and lower third of the rectum a new procedure has been developed known as Transanal-Total Mesorectal Excision (TaTME). Instead of the dissection via the abdomen TaTME combines an abdominal and transanal endoscopic approach (endoscopic instruments are inserted into the anus) allowing easier dissection of the most difficult part of the surgery deep down in the pelvis (particularly in male patients or patients with visceral obesity or a narrow pelvis). The perceived benefits of this technique may include ease of procedure due to better views, decreased operative time and reduced complications.", + "doc_fkgl": 16.9342905982906, + "wiki_fkgl": 18.187010309278353, + "doc_tree_depth": 5.8, + "wiki_tree_depth": 7.333333333333333, + "fkgl_delta": -1.2527197109877548 + }, + { + "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": "Scientific career\nAfter spending brief periods in England and France, he joined the Italian Cancer Institute in Milan as a volunteer. Veronesi challenged the dominant paradigm among surgeons that cancer could only be treated with aggressive surgery. He championed a paradigm shift in cancer care from \"maximum tolerated\" to \"minimum effective\" treatment. He was a pioneer of breast-conserving surgery in early breast cancer as an alternative to a radical mastectomy. He developed the technique of quadrantectomy, which limits surgical resection to the affected quarter of the breast. Between 1973 and 1980 he led the first prospective randomised trial of breast conserving surgery (the Milan I trial), which compared outcomes from radical mastectomy against quadrantectomy. The results, published in 1981, and confirmed in 2002 in a 20-year follow-up study, played a key role in establishing breast conserving surgery as standard of care for patients with early breast cancer, alongside results from trials of lumpectomy led by the US breast surgeon Bernard Fisher.\nVeronesi supported and promoted scientific research aimed at improving conservative surgical techniques, including sentinel lymph node biopsy, which resulted in axillary dissection in breast cancer with clinically negative lymph nodes no longer being performed. He also contributed to breast cancer prevention conducting studies on tamoxifen and retinoids and verifying their capabilities to prevent the formation of carcinoma. He was an activist in anti-tobacco campaigns. In 1994 he founded the European Institute of Oncology, which he directed until his death. He was appointed President of the Scientific Committee of the Italy-USA Foundation in 2010. In 2009, through his foundation (Fondazione Veronesi), he started the project \"Science for Peace\", in order to promote peaceful relations through scientific development.", + "doc_fkgl": 14.549020678891925, + "wiki_fkgl": 14.871624548736467, + "doc_tree_depth": 6.681818181818182, + "wiki_tree_depth": 8.0, + "fkgl_delta": -0.32260386984454215 + }, + { + "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": "Signs and symptoms\nDisproportionate short stature, deformity of the lower limbs, short fingers, and\nligamentous laxity give pseudoachondroplasia its distinctive features. The average height of adult males with the condition is around 120 centimeters (3\u00a0ft, 11 in), while adult females are typically around 116\u00a0cm (3\u00a0ft, 9in). Affected individuals are not noticeably short at birth. Patients with pseudoachondroplasia present with gait abnormalities, lower limb deformity, or a retarded growth rate that characteristically appear at age 2\u20133 years. Disproportionate short stature is characterized by shortening of proximal limb segments (humeri and femora) also called rhizomelic shortening. Other known clinical features include, genu valgum/varum, brachydactyly (short fingers), supple flexion deformity of the hips, knees, hyperlordosis of lumbar spine, rocker bottom feet and broadening of the metaphyseal ends of long bones especially around the wrists, knees and ankles. Patients with pseudoachondroplasia have normal intelligence and craniofacial features.", + "doc_fkgl": 5.560996503496504, + "wiki_fkgl": 14.851135029354207, + "doc_tree_depth": 4.916666666666667, + "wiki_tree_depth": 7.571428571428571, + "fkgl_delta": -9.290138525857703 + }, + { + "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": "Palindromic rheumatism is a syndrome presented with inflammatory para-arthritis (soft tissue rheumatism) and inflammatory arthritis both of which cause sudden inflammation in one or several joints or soft tissue around joints. The flares usually present with mono- or oligo-articular involvement, which have onset over hours and last a few hours to a few days, and then go away completely. However episodes of recurrence form a pattern, with symptom-free periods between attacks lasting for weeks to months. The most commonly involved joints were knees, metacarpophalangeals and proximal interphalangeal joints of the hands or feet. Constitutionally, there may or may not be a fever and swelling of the joints. The soft tissues are involved with swelling of the periarticular tissues, especially heel pads and finger pads. Nodules may be found in the subcutaneous tissues. The frequency of attacks may be variable over the course but there is no joint damage after attacks.", + "doc_fkgl": 9.454666666666668, + "wiki_fkgl": 11.703833333333336, + "doc_tree_depth": 5.454545454545454, + "wiki_tree_depth": 6.75, + "fkgl_delta": -2.2491666666666674 + }, + { + "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": "Diagnosis\nGamekeeper's thumb and skier's thumb are two similar conditions, both of which involve insufficiency of the ulnar collateral ligament (UCL) of the thumb. The chief difference between these two conditions is that skier's thumb is generally considered to be an acute condition acquired after a fall or similar abduction injury to the metacarpophalangeal (MCP) joint of the thumb, whereas gamekeeper's thumb typically refers to a chronic condition which has developed as a result of repeated episodes of lower-grade hyperabduction over a period of time. There are four types of Skier's thumb injury:\n Avulsion of distal UCL causing the pulling off of a bone chip off the proximal phalanx base.\n Partial-thickness tear of the UCL\n Full-thickness tear of the middle part of the UCL\n Full-thickness tear of the middle part of the UCL with the proximal fragment displaced superficial to the aponeurosis of adductor pollicis, thus preventing the healing of proximal and distal segments of UCL. This condition is called Stener lesion.", + "doc_fkgl": 11.863529411764706, + "wiki_fkgl": 16.93118518518519, + "doc_tree_depth": 5.75, + "wiki_tree_depth": 9.4, + "fkgl_delta": -5.0676557734204835 + }, + { + "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": "Death\nOn March 19, 2015, Colagrossi was on her way back to the station after filing a report on a house fire in Queens. As she sat in the news van, Colagrossi began feeling ill and her condition quickly worsened. The cameraman who accompanied her to the story got out of the van and flagged down an ambulance and she was transported to NewYork\u2013Presbyterian Hospital/Weill Cornell Medical Center, where it was discovered she had suffered a massive cerebral hemorrhage caused by a ruptured aneurysm. Colagrossi was immediately taken to the intensive care unit and placed on life support, but doctors were unable to save her, and she died the next day.", + "doc_fkgl": 4.0628178694158095, + "wiki_fkgl": 13.410878378378381, + "doc_tree_depth": 4.777777777777778, + "wiki_tree_depth": 7.25, + "fkgl_delta": -9.348060508962572 + }, + { + "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": "Angor animi (also referred to as angina animi, Gairdner's disease and also angina pectoris sine dolore), in medicine, is a symptom defined as a patient's perception that they are in fact dying. Most cases of angor animi are found in patients with acute coronary syndrome (cardiac-related chest pain) such as myocardial infarction. It is, however, occasionally found in patients with other conditions. Pheochromocytoma also can present with angor animi, accompanied by other symptoms that include; profuse sweating, palpitations and characteristically a pounding severe headache. Irukandji syndrome is also another reported cause.", + "doc_fkgl": 13.757534883720933, + "wiki_fkgl": 14.71898901098901, + "doc_tree_depth": 6.0, + "wiki_tree_depth": 6.2, + "fkgl_delta": -0.9614541272680768 + }, + { + "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": "Diagnosis\nIt can be diagnosed with a standard echocardiogram. An echocardiogram can also aid in classifying the type of defect. The diagnosis can also be made prior to birth via ultrasound. Patients will have a loss of appetite, appear tired and weak, and exhibit rapid breathing and a rapid heart rate. If the condition progresses, the infant may turn pale, feel cold in the lower half of the body, and have a weak pulse due to insufficient blood flow. The pattern of pulse abnormalities is dependent upon the classification; e.g., for type B interrupted aortic arch, the right brachial pulse will be palpable and the left brachial and femoral pulses will be impalpable due to closure of the ductus arteriosus. Rarely, an interrupted aortic arch can be associated with an intracranial aneurysm. Signs of ischemia due to interrupted aortic arch can be separated by the organ system involved:\n Liver injury: elevated serum glutamic oxaloacetic transaminase (SGOT) (also known as aspartate transaminase, AST) and lactic acid dehydrogenase (LDH)\n Kidney injury: elevated serum creatinine\n Intestinal injury: signs of necrotizing enterocolitis, such as bloody stools", + "doc_fkgl": 12.237704402515725, + "wiki_fkgl": 13.627435897435898, + "doc_tree_depth": 5.529411764705882, + "wiki_tree_depth": 6.222222222222222, + "fkgl_delta": -1.3897314949201736 + } +] \ No newline at end of file