A 40-year-old man with HIV who had been consistently taking his medication came in with recurring fevers over two years. These fevers didn’t follow a regular pattern and were only temporarily relieved with anti-inflammatory drugs. In the past two months, he developed widespread abdominal pain, especially on the right side, along with swelling in his liver and spleen. He also had enlarged lymph nodes throughout his body. Lab tests showed low blood cell counts, blood clotting problems, low protein levels, and signs of inflammation. Imaging scans showed enlarged liver and spleen and widespread lymph node swelling. Tests for bacteria like Mycobacterium were mostly negative, except for a detection of HHV-8 in a lab test. A biopsy of a lymph node in his pelvis found signs of Castleman’s disease. Even after restarting his HIV treatment, his symptoms got worse. He was started on corticosteroids and ganciclovir, but after one week, he developed severe organ failure and swelling (anasarca), which made the treatment unsafe. A new chest scan showed tree-like patterns in the upper right lung and fluid around both lungs, and his liver and spleen continued to grow larger with more abdominal fluid. He was admitted to the intensive care unit 48 hours later and died shortly after from sudden liver failure. After death, tests on a sample from his airway found Mycobacterium tuberculosis, and a liver biopsy showed small, non-destructive granulomas.


A 4-month-old baby from a rural village in Panama, far from any hospital, was sick with diarrhea and could not keep fluids down. She was very weak, had no weight, and was dehydrated — her body was dry and she couldn’t cry properly. She didn’t get breast milk and was fed powdered milk, which wasn’t enough. Her family had no electricity, no clean water, and lived in a simple house with a thatched roof. She didn’t get vaccines or any medical care for the first four months of life. When she came to a health center, she had diarrhea for four days, no fever, no cough, but she was vomiting. Doctors gave her a medicine called Enterogermina to help her gut. Because she kept getting worse, she was taken to a bigger hospital and then to a major hospital in Panama City. There, she had trouble breathing, her skin was cold and pale, her heart was racing, and her blood pressure was very low. Tests showed she had a dangerous bacteria in her blood called MRSA and also had a gut infection from Clostridiodes difficile. A good bacteria called Bacillus clausii was found in her blood over several days. Even with strong antibiotics, she kept getting sicker. She developed heart problems, her kidneys stopped working, and her body failed in many ways. After 12 days, she died. No autopsy was done because the mother didn’t want to.


A 4-month-old indigenous infant from a rural area in Panama, living 3 hours by canoe from the nearest health center, arrived at a hospital with severe diarrhea and dehydration. She had not been breastfed and was given powdered milk instead, which may have contributed to her poor health. Her family lived in a basic home without electricity or running water, relying on a well and a river for waste disposal. She did not receive any vaccines or prenatal care during her early life.

She first visited a local health center with 4 days of diarrhea, vomiting, and no fever or breathing problems. Doctors gave her oral fluids and a medication called Enterogermina (which contains B. clausii bacteria) to help her gut recover. Because she was severely dehydrated, she was transferred to a larger hospital and then to a major hospital in Panama City.

When she arrived at the hospital, she was very weak, with dry mouth, no tears, and signs of shock — including cold hands and feet, a fast heartbeat, and low blood pressure. She had swelling in her hands, feet, face, and belly. Tests showed she had a serious infection, including methicillin-resistant Staphylococcus aureus (MRSA) in her blood, and later, Clostridiodes difficile (a harmful gut bacteria) was found. B. clausii, a beneficial bacteria, was also found in her blood over several days.

She received multiple antibiotics, but the infection kept getting worse. Her body began to fail in many systems — her heart, kidneys, and organs stopped working properly. She developed acute heart inflammation (myocarditis) and kidney failure. Despite treatment, including IV antibiotics, fluids, and medications to support her organs, she died 12 days after being admitted to the hospital. No autopsy was done because the mother refused, due to cultural reasons.


A 2-year-old girl was brought in with a 1-year history of painless swelling in her left eye, where the eye had slowly moved forward and was pointing inward and upward. Her vision was very limited, with only light sensation in the left eye. Examining her eye, doctors found that the eye was stuck in position and couldn’t move properly. A soft, well-defined lump was felt in the lower part of her left eye socket, and her lower eyelid was turned outward. The pupil was large and didn’t react to light. MRI scans showed a clear mass inside the eye socket that appeared dark on T1-weighted images and bright on T2-weighted images. The mass did not take up contrast, which helped rule out some other conditions. The diagnosis of orbital teratoma — a type of tumor containing different tissues like skin, cartilage, and brain tissue — was confirmed through tissue testing and lab analysis. The doctors removed the tumor using a small incision inside the lower eyelid, along with cutting the lower eyelid and outer corner of the eye to give better access. During surgery, they found a grayish-white cystic mass with a clear border, and it was tightly attached to the optic nerve. Because the tumor was large and the space was limited, they removed most of the fluid and completely excised the mass. One month after surgery, the child developed a sunken eye (enophthalmos), redness of the eyelid (conjunctival hyperemia), and inflammation of the cornea (keratitis). This happened because the tumor had previously stretched the eye socket, and after removal, the space collapsed. To fix this, a second surgery was done, where a donated sclera (the white part of the eye) was implanted into the socket to restore volume and help the eye sit properly again. After one year of follow-up, no tumor came back, and there were no other serious complications. The child’s vision stayed the same, though she still has a slight sunken eye and a small issue with the outer corner of her eye.


This study follows a 9-year-old girl who has both high intellectual abilities and dyslexia, a learning disorder that makes reading and writing difficult. The goal was to see how her reading, writing, and phonological skills improved after targeted therapy. Before the intervention, she was reading at an early stage (alphabetic level), writing in a transitional phase between syllabic and alphabetic systems, and had weak phonological processing skills. After six months of weekly therapy focused on phonological skills—like recognizing sounds, blending sounds, and improving memory—the child showed clear progress. Her phonological processing improved, her writing became more consistent and reached the alphabetic level, and her reading speed increased significantly—from about 20 to 94 words per minute. She also showed better ability to access words quickly in her mind. However, some writing problems remained, such as mixing up similar letters and making small spelling errors. The therapy helped her catch up in key areas, especially in reading and sound processing, even though she still faces some challenges typical of dyslexia. This case shows that with focused support, children with high abilities and dyslexia can make meaningful progress in learning to read and write.


We report the first case of heatstroke occurring at the same time as a severe SARS-CoV-2 infection in a 52-year-old man. He first tested positive for the virus after having a cold, then returned to work without fever. But while working outdoors in very hot weather (35°C) for five hours, he lost consciousness. When brought to the hospital, his body temperature was extremely high at 40°C, and he was in a coma. Doctors diagnosed him with heatstroke and a serious COVID-19 infection, which caused multiple organ damage. He received treatment including intravenous antibiotics, fluids, blood pressure support, mechanical ventilation, and care for his blood clotting problems. Despite initial improvement, he later developed shortness of breath and a brain bleed. He also had a multi-pathogen lung infection and a severe blood clotting disorder that led to failure of several organs (MODS), which ultimately caused his death. This case shows that heatstroke can happen alongside severe COVID-19, and it can lead to serious complications even in people with no known health problems.


A 19-year-old woman was admitted to the hospital with severe headaches, nausea, vomiting, fever, and very high blood pressure. She had a large adrenal mass found on imaging, and initial tests suggested possible infection or heart inflammation. Her blood pressure was extremely high (189/120 mmHg), and her heart rate was fast, leading to concerns about heart damage. She had a history of similar symptoms a year earlier, when she was diagnosed with myocarditis and hypertension, but she did not follow up on her blood pressure treatment. Her father had a history of sudden death, which raised concerns about a genetic condition.

Tests showed very high levels of certain hormones, including catecholamines, which are produced by the adrenal glands. These findings pointed to a condition called pheochromocytoma — a tumor of the adrenal gland that can cause high blood pressure and other symptoms. Genetic testing revealed a mutation in the RET gene, linked to a condition called MEN2A, which can cause tumors in multiple endocrine glands.

Further testing found a small thyroid nodule with slightly elevated calcitonin levels, but normal parathyroid hormone and calcium levels. After surgery to remove the adrenal tumor, the patient remained stable. Over the next 15 months, her thyroid nodule stayed the same size, and her calcitonin levels remained mildly high. However, her parathyroid hormone and blood calcium levels slowly increased. A scan for parathyroid tumors came back negative, meaning no parathyroid tumor was found.

The patient is now doing well after surgery and is being followed up regularly without any signs of recurrence.


A 13-year-old boy came to the emergency department with sudden chest pain on the sides of his chest, which worsened when he coughed. The pain was not severe, and he didn’t have shortness of breath, fever, or other symptoms like joint pain or fatigue. He had a mild cold and a single fever spike, but otherwise felt fine. He was active, doing canoeing twice a week, and had no known exposure to infections or environmental irritants. His past chest X-ray, taken four years earlier during a cold, showed a similar lung pattern that was treated with azithromycin and has not returned since.

At the hospital, his breathing was normal, oxygen levels were good, and his physical exam showed reduced breath sounds in the lower part of his lungs. A new chest X-ray showed a similar lung pattern as before. A detailed lung scan (CT) found widespread, cloudy areas in both lungs, covering more than 65% of the lung tissue, which is typical of a condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including COVID-19, came back negative. A lung fluid sample (bronchoalveolar lavage) showed a milky appearance and tested positive for a specific stain (periodic acid-Schiff), which supports the diagnosis of PAP. Lung function tests showed a mild restriction in how much air he could breathe out (FVC at 77%) and a moderate drop in lung capacity to transfer oxygen (DLCO at 48.6%).

Genetic testing ruled out known causes of PAP related to surfactant problems. Testing for antibodies against a protein called GM-CSF was strongly positive, which suggests the body is attacking its own lung cells — pointing to an autoimmune form of PAP. At 20 months of follow-up, the boy is still symptom-free, breathing normally, and continues to exercise regularly. His lung function has improved slightly and remains stable. Since he has no symptoms and is doing well, treatment has been delayed, and he is being monitored regularly at the clinic.


A 17-year-old boy was found to have a small metal object in his nose during a routine dental exam. He had no symptoms like nosebleeds, congestion, or discomfort. His parents remembered when he was seven that he had inserted a small object into his nose, but at that time, no imaging was done and the issue was never followed up. Over the years, they thought the object had fallen out on its own. Later, imaging showed a shiny, metallic snap button stuck in the floor of his right nasal cavity, likely there for over 10 years. The object was covered in mucus and crust, showing signs of long-term exposure. It was safely removed under local anesthesia with a simple procedure that caused little bleeding. After removal, the nose healed well, and the patient is doing fine now. He’s being given nasal rinses to keep the area clean and is doing well at his follow-up visit.


A 17-year-old male with no significant past medical or family history was referred to the clinic from the dental department following an incidental discovery of a nasal foreign body (NFB) during preoperative orthodontic planning, which included routine dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. Parental recall indicated that at age seven, the patient had inserted a small object into his nose; at that time, no imaging was performed, and an anterior rhinoscopy was attempted due to non-cooperative behavior, leading the physician to recommend removal under sedation. However, the family did not pursue follow-up, and given the absence of symptoms, they assumed the foreign body had spontaneously expelled. Endoscopic evaluation of the right nasal cavity revealed a deviated nasal septum with inferior turbinate hypertrophy, erythematous and mildly edematous mucosa, and a foreign body lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate. The object was partially obscured by mucus and crusted material, exhibiting a shiny surface consistent with metallic composition. Radiographic assessment using lateral and frontal x-rays demonstrated a circular, radiopaque lesion located in the floor of the right nasal cavity, morphologically consistent with a metallic snap button. No abnormalities in adjacent bony structures were observed. CBCT further confirmed the presence of the foreign body and revealed mild inflammatory changes within the nasal mucosa, with no evidence of significant bony erosion, sinus involvement, or spread to adjacent anatomic spaces. With informed parental consent, the foreign body was removed under local anesthesia in a semi-sitting position to minimize the risk of dislodgment into the airway. Prior to retrieval, the nasal cavity was decongested with Xylometazoline 0.1%, and Lidocaine spray (10 mg/spray) was administered to the right nostril. A hook was used to disengage the object, which was then extracted using bayonet forceps. The procedure was uncomplicated, with minimal bleeding effectively controlled by saline irrigation. Post-removal examination showed no significant mucosal injury or tissue necrosis. The retrieved object, identified as a metallic snap button measuring 1 cm in diameter, demonstrated extensive corrosion and accumulation of biological material, consistent with prolonged retention over a period exceeding ten years. The patient was discharged in stable condition and prescribed daily nasal rinses with 0.9% sodium chloride irrigation solution. At a two-week follow-up, the patient was clinically stable with no signs of recurrence, inflammation, or obstruction, and endoscopic examination remained unremarkable. This case underscores the potential for long-term retention of small metallic foreign bodies in the nasal cavity, particularly in children, with delayed presentation due to asymptomatic course, highlighting the importance of thorough imaging evaluation and timely intervention when such objects are incidentally detected, even in the absence of clinical symptoms. The presence of corrosion and biofilm formation suggests prolonged exposure, which may contribute to chronic local inflammation and tissue remodeling, although no structural damage was observed in this case.


A 18-year-old boy came to the emergency room with sudden chest pain, fever, and trouble breathing, especially when lying down. He had no history of heart problems, but his family had a heart condition in the past. Tests showed his heart was enlarged, his heart muscles were thick, and there was fluid around the heart. Doctors thought it was a virus called Coxsackie, which can cause heart and chest lining inflammation. He got medicine for that, but his breathing got worse and his blood pressure dropped. The fluid around the heart grew so big it was pressing on his heart, causing a life-threatening situation. They drained the fluid, but during that, he had a sudden stop in his heart rhythm and needed a machine to keep his heart and lungs working. Tests on his heart tissue showed no virus or inflammation, but a small lump on his arm was found to have a rare cancer called Epstein-Barr virus (EBV) positive natural killer/T-cell lymphoma. This cancer was likely causing the heart and heart lining problems. After starting cancer treatment, his heart function improved — the thick heart muscles got thinner, the fluid went away, and his breathing got better. He’s now on heart failure medicine and is doing well, with plans to finish chemotherapy and possibly get radiation or a stem cell transplant in the future.


An 18-year-old male came to the emergency department with new chest pain, fever, and shortness of breath, especially when lying down. He had a dry cough and felt unwell for 3 to 4 days. His family history included a grandfather with heart disease, but he had no known heart problems himself. He worked at a car parts shop and planned to go to college.

Initial tests showed high levels of a heart damage marker (troponin), widespread changes on his ECG, and an enlarged heart on X-ray. An echo test (TTE) revealed thickened heart muscle (severe biventricular concentric hypertrophy) and a small amount of fluid around the heart (pericardial effusion). Viral tests found high levels of Coxsackie virus A and B, which can cause viral pericarditis. His symptoms improved slightly with medications like ibuprofen and colchicine, and a heart catheterization showed no blocked arteries.

However, by the fourth day, his condition worsened. He became very weak, had very low blood pressure, and developed a large pericardial effusion that was threatening to stop his heart (cardiac tamponade). A needle was inserted to remove the fluid (pericardiocentesis), but during the procedure, he went into cardiac arrest with no pulse. He needed emergency life support with a machine that takes over heart and lung functions (VA ECMO), and received blood transfusions due to bleeding.

A biopsy of his heart tissue showed no signs of inflammation or infection, which made the initial diagnosis of viral pericarditis less likely. A skin biopsy from a small, painless lump on his right arm revealed a rare type of cancer called Epstein-Barr virus (EBV)-positive natural killer/T-cell lymphoma. This finding changed the diagnosis — the heart and pericardium were likely affected by this cancer, not just a virus.

He started chemotherapy for the lymphoma, and within days, his heart function began to improve. His heart pump strength (ejection fraction) increased from 10%–15% to 55%, the fluid around the heart went away, and the thickened heart muscle started to normalize. He is now on heart failure treatment and cardiac rehab.

He has completed five out of six chemotherapy sessions and is expected to finish the full course. He may now receive radiation therapy or a stem cell transplant. His care involves both cardiology and oncology teams, and he is doing much better overall.


A woman had a weak heart after giving birth and got a new heart transplant. After the transplant, her kidneys were working fine at first. But later, her kidneys started to fail because of a virus called BK virus. The doctors found the virus in her blood and saw damage in her kidney tissue. They cut back on the medicines that weaken the immune system, which helped. After two years, her kidneys stayed stable, with a kidney function level that is still okay, even though her kidney numbers are low.


A 39-year-old woman had a heart transplant due to peripartum cardiomyopathy. After the transplant, her kidneys initially worked well, with normal kidney function and no signs of kidney disease. However, in 2016, her kidney function started to decline, and by 2017, her creatinine had risen to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2. She was hospitalized, and tests showed no signs of infection or other common causes of kidney problems. A kidney biopsy was done and found to have active chronic tubulointerstitial nephritis linked to late-stage BK virus infection. The blood test showed a high BK virus load (log 4.5). Her immunosuppressive medications, especially tacrolimus, were reduced. After two years of follow-up, her kidney function stabilized at a serum creatinine of 2.5 mg/dL and a GFR of 23.4 mL/min/1.73m2. The virus load gradually decreased to undetectable levels, and she has had no further kidney issues or heart rejection episodes.


A 56-year-old Italian woman with a serious blood disorder called β-thalassemia major had a magnetic resonance imaging (MRI) scan to check how much iron was building up in her heart, liver, and pancreas. She has been needing regular blood transfusions since she was 7 years old and had previously had her spleen and gallbladder removed. At the time of the scan, she had no major problems with her heart, liver, or hormones, and was taking medications including deferasirox to remove iron, vitamin D, and luspatercept to help reduce her need for transfusions.

The MRI found a mass in the mediastinum (the area in the chest between the lungs), which had been seen before in a 2020 scan but had slightly grown. This mass showed only mild activity on a PET scan, which made doctors think it might be a type of thymoma — a tumor that develops in the thymus gland. However, a chest CT scan revealed multiple thin-walled cysts in both lungs, which are a sign of a condition called lymphangioleiomyomatosis (LAM), a rare lung disease often linked to certain conditions like thalassemia.

The patient had no symptoms like coughing or shortness of breath and was not a smoker. After a team of specialists reviewed her case, she had surgery to remove the thymoma mass and a small piece of lung tissue affected by LAM. The surgery results showed a type B2 thymoma with some cells at the edge of the removed tissue, meaning it wasn’t completely removed. The lung tissue showed signs of LAM, with cysts lined by specific cells and mild inflammation.

Following surgery, she was recommended to receive adjuvant radiation therapy for the thymoma and to take sirolimus, a medication that helps control LAM, especially in people with thalassemia. This treatment plan is designed to manage both conditions and reduce the risk of future complications.


A 49-year-old woman with long-term lupus (SLE) developed both kidney and heart failure over many years. She had lupus since childhood and was treated with several medications, including steroids and immunosuppressants, but stopped in 2002 due to hepatitis C. Over time, her kidneys failed, requiring dialysis, and her heart suffered damage, including heart attacks and weakened heart muscle. By 2007, her kidney function had worsened enough to need a biopsy, which showed active kidney disease. Despite treatments, her heart continued to fail, leading to serious heart problems like valve damage and a need for surgery in 2014. After surgery, her heart function remained poor, and she needed dialysis for 4 years before being ready for a kidney transplant.

Before the transplant, her heart was very weak—only 26% of its normal pumping ability—and she had high levels of a heart stress marker (BNP). Because of this, doctors added a heart-protective drug called Levosimendan to help her heart during surgery. The transplant was done with careful planning to protect her kidneys and heart, avoiding harmful medications and using fluid therapy to keep her stable. During recovery, her heart function slowly improved: by one month after surgery, her heart was pumping better (EF improved to 30%) and her exercise ability increased from very limited to normal. By five months, her heart function was much better, her BNP dropped to normal levels, and her kidneys were working properly again. The transplant was successful, and she is now recovering well.


A 42-year-old woman with a chronic headache condition could not use certain medications because of side effects. When her headaches were very severe — scoring 9 out of 10 — she came to the pain clinic. Doctors took her to a local operating room and performed a nerve block using ultrasound guidance. This procedure targeted the greater occipital nerve in the neck and used a local anesthetic called bupivacaine. Right after the block, her headache pain dropped from 9/10 to just 2/10. The block was repeated once a week for a month. By the end of two months, her headaches had greatly improved: the number of attacks dropped from daily to just two per month, and the pain intensity decreased to 4/10. She had no side effects from the treatment and hasn’t had any attacks by the sixth month.


A baby was born early by C-section because the baby was not getting enough oxygen. The baby had a weak heart from birth and had serious problems with the heart valves, making it hard for blood to flow properly. The baby’s hands and feet were long and bent, the fingers couldn’t straighten, and the joints at elbows and knees were stuck. The face looked old, the eyes were deep-set and slanted, the ears were small and soft, and the mouth hung down. The baby also had a flat foot and a swollen belly. Tests showed the heart was too big, the blood pressure in the lungs was too high, and the lens in the eyes had moved out of place. A genetic test found a new change in a gene that causes a rare condition called neonatal MFS, which affects the body’s connective tissue. Doctors tried medicines to help the heart pump better, used sedation, and gave diuretics to reduce swelling, but the heart problems got worse. The baby’s breathing and heart function kept getting worse, and the body started to shut down. Even with treatment, the baby could not survive. The family chose to focus on comfort instead of surgery, and the baby passed away 32 days after birth.


A newborn boy was born early via emergency cesarean section because of fetal distress. He had several serious physical problems from birth, including long, thin fingers and toes (arachnodactyly), fingers that could not fully straighten (camptodactyly), stiff elbows and knees, a wrinkled, aged-looking face, flat feet, and a deep, downward-slanting eye opening. His ears were small and soft, and his mouth sagged. He also had a short head shape (brachycephaly) and a lens that was out of place in his eyes (ectopia lentis), which is a sign of a genetic condition called Marfan syndrome.

Genetic testing found a new mutation in a gene called fibrillin-1, specifically in a section known as the neonatal region (exons 24 to 32). This mutation is linked to a severe form of Marfan syndrome that affects the heart and blood vessels.

At birth, the baby had a weak heart, severe heart valve problems (especially mitral and aortic regurgitation), and high blood pressure in the lungs (pulmonary hypertension). These issues led to low blood pressure, poor breathing, and heart failure. Doctors tried medications to help, including drugs to reduce the heart’s workload, sedation, and diuretics to manage fluid buildup. However, the heart problems continued to get worse.

Because the disease was progressing too quickly and surgery was not expected to help, the family chose to focus on palliative care — care aimed at making the child comfortable rather than trying to cure the condition. Over the next few months, the baby developed severe lung and liver problems, including bleeding in the lungs, and eventually died at 32 days old.


A 20-year-old woman had a long history of nephrotic syndrome (NS) that started when she was 8 years old. Her condition was first noticed after she developed a blood clot in her brain veins and a large blood clot in her lungs. She didn’t have any lasting effects from this. Tests showed no family history of blood clots, and no other signs pointed to a secondary cause of her NS. She was treated with blood-thinning medication (anticoagulation) and steroid pills, which worked well. Over time, she had several relapses of her disease, each controlled with high-dose steroids. To reduce the need for steroids and support her growth, she started taking mycophenolate mofetil (MMF). Thrombophilia tests — which check for blood clotting disorders — came back normal. After nine years, her blood thinners were stopped. From 2017 onward, she stayed in remission and didn’t have any relapses. Her MMF was stopped in 2019, and she remained healthy without symptoms. One year later, she suddenly developed severe abdominal pain, vomiting after eating, and swelling in both legs. Lab tests confirmed a relapse of her nephrotic syndrome. An abdominal CT scan showed a blood clot in the superior mesenteric artery, causing acute mesenteric ischemia (lack of blood flow to the intestines). During surgery, doctors found widespread tissue death in her small intestine, and the damage was so severe that removing the affected parts was not possible. The patient died four days later.


A 20-year-old girl had a kidney disease called nephrotic syndrome since she was 8 years old. It started with blood clots in her brain and lungs, but she got better. She was treated with medicine to stop clots and steroids to calm her kidneys. Over time, she had several flare-ups that were controlled with steroids, but after 2017, her kidneys stayed healthy and no more flares happened. So, her doctors stopped the clot medicine and the kidney medicine (MMF). One year later, she got sudden, severe stomach pain, threw up after eating, and her legs swelled. Tests showed her kidney disease came back. A scan found a blood clot in a major blood vessel in her abdomen, cutting off blood to part of her intestines. When doctors opened her belly, they saw that most of her small intestine was dead and could not be saved. She died two days later.


A 20-year-old female with a 12-year history of idiopathic nephrotic syndrome (NS) presented with a clinical course initiated at age eight, marked by cerebral venous thrombosis extending to the right jugular vein and a massive pulmonary embolism, which resolved without sequelae. No history of medical comorbidities, surgical interventions, or family history of thrombotic events was reported. Initial evaluation excluded secondary causes of nephrotic syndrome, as she lacked gross hematuria, hypertension, or renal biopsy findings, and no extra-renal manifestations were present. Consequently, she was initiated on anticoagulation therapy with oral vitamin K antagonist and oral corticosteroids, which resulted in stable disease control. Subsequent relapses of NS were managed with high-dose corticosteroid pulses, leading to long-term maintenance therapy with mycophenolate mofetil (MMF) to reduce corticosteroid dependence and support normal growth and development. A comprehensive thrombophilia workup—including homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and beta-1-glycoprotein antibodies—was performed and all results were within normal limits, ruling out inherited or acquired thrombophilic predispositions. Anticoagulant therapy was discontinued after nine years of use. The patient experienced multiple relapses of NS, all of which were controlled with oral corticosteroids, achieving sustained remission by 2017. MMF was gradually tapered and discontinued in 2019, with no further relapses or clinical symptoms observed thereafter.

One year after the last remission, the patient presented to the emergency department with severe, diffuse acute abdominal pain, non-radiating, associated with postprandial vomiting and bilateral lower limb edema lasting six hours. Physical examination revealed intense epigastric tenderness, with normal vital signs (blood pressure 120/70 mm Hg, heart rate 83 bpm, oxygen saturation 100% on room air), afebrile status, and intact consciousness. No other systemic abnormalities were identified. Urinalysis using labstix demonstrated proteinuria. Arterial blood gas analysis revealed metabolic acidosis with respiratory compensation. Laboratory findings included hypoalbuminemia, hypercholesterolemia, a prolonged prothrombin time (90%), markedly elevated D-dimer, lactate dehydrogenase, and creatine phosphokinase, and a systemic inflammatory response characterized by a C-reactive protein (CRP) level of 37 mg/L and leukocytosis (26.4 × 10³/µL). Renal and hepatic function tests remained within normal ranges.

The patient was admitted to the intensive care unit for close hemodynamic and metabolic monitoring. An urgent abdominal ultrasound revealed a low-to-moderate volume intra-abdominal effusion. Abdominal computed tomography (CT) demonstrated acute thrombosis of the superior mesenteric artery with concomitant acute mesenteric ischemia. Immediate surgical intervention was performed. Intraoperative exploration confirmed extensive mesenteric ischemia with nearly complete necrosis of the small intestine, rendering resection of the bowel segments non-viable and incompatible with survival. The patient succumbed to multi-organ failure within 48 hours of presentation. This case highlights the potential for severe, life-threatening complications in patients with long-standing idiopathic nephrotic syndrome, particularly in the context of underlying hypercoagulable states or unrecognized vascular vulnerability, even in the absence of thrombophilia. The pathophysiological link between chronic immune dysregulation in NS and a pro-thrombotic milieu—potentially mediated by persistent inflammation, endothelial dysfunction, and increased expression of tissue factor—may contribute to the development of acute arterial thrombosis in critical vascular territories such as the superior mesenteric artery, leading to ischemic bowel necrosis and death.


A 34-year-old pregnant woman had seizures and trouble speaking, which went away in less than two hours. She had no other health problems. Doctors did an MRI of her brain and saw a special pattern called the 'Medusa head' sign. This means there’s a problem with how veins develop in the brain, with some blood clots at the edges and slow blood flow near the center. The brain tissue around the veins is swollen, which causes the symptoms. She started taking medicine to prevent more seizures and clots, and her symptoms got better in a week.


A 22-year-old woman visited the Oral Medicine Department with painful mouth sores that had been bothering her for one month. The sores started with a fever and appeared as small, pimple-like bumps on her lips. She had been using pod-type vapes for about a year, mostly during free time or with friends, and had recently switched to a new e-liquid flavor without telling anyone. She had never smoked cigarettes before and had no history of taking medications or having allergies. She also didn’t eat healthy foods regularly, often skipping vegetables and fruits.

On examination, her lips had crusts that looked like a mix of blood and fluid, and the corner of her mouth was sore and easily bled. Inside her mouth, she had white ulcers with yellow edges, of different sizes, on the lips, tongue, and floor of her mouth. There were no signs of illness on her body outside the mouth. Lab tests showed no evidence of a common virus (HSV-1) linked to these sores, which helped doctors rule out other causes.

The diagnosis was oral erythema multiforme, a condition that can be triggered by vaping, and it was classified as mild. Treatment included applying a saltwater solution (0.9% NaCl) to her lips three times a day, using a mouthwash with dexamethasone and hyaluronic acid three times a day (after waiting 30 minutes before eating or drinking), applying a 2% miconazole cream to the sore corner of her mouth twice daily, and using vaseline album cream for dry lips. She was also advised to stop vaping and avoid foods with MSG.

After one week of treatment, her mouth sores improved significantly. The case was reviewed with her consent, and it followed ethical medical guidelines.


A baby was born at 39 weeks and had a small, harmless lump inside the heart that was found during pregnancy. The lump didn’t grow or shrink, and the baby didn’t have any seizures or skin spots. The doctor checked the baby right after birth, at 1 month, 7 months, and 1 year, and everything was normal. The baby grew well, stayed healthy, and developed like other babies her age. The heart lump was only in the heart and didn’t cause any problems. No other signs of a rare condition called tuberous sclerosis were found, so the baby doesn’t have that condition.


A 29-year-old gravida V par IV woman, with a history of three spontaneous vaginal deliveries and one previous cesarean section for failed induction of labor (four years prior), presented for antenatal care follow-up at 32 weeks' gestation based on her last normal menstrual period (LNMP). Comprehensive medical history revealed that all four of her children are healthy, thriving in school, and have no known genetic or seizure-related disorders. Laboratory investigations including Venereal Disease Research Laboratory (VDRL) testing, Hepatitis B surface antigen (HBsAg), and urine analysis were negative. Complete Blood Count (CBC) showed normal cellular parameters; blood group was A, Rh-positive. Obstetric ultrasound demonstrated a normal fetal anatomy except for the cardiac structure. Detailed fetal echocardiography revealed normal atrial size and situs, with appropriately positioned and functioning atrioventricular and semilunar valves. Both ventricles exhibited comparable size and contractile function, with normal left ventricular apex formation and no ventricular septal defect. However, two circumscribed, round, echogenic masses were identified on the left ventricular papillary muscles, measuring 18.2 mm × 8.3 mm and 13.5 mm × 8.3 mm, respectively. The left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT) demonstrated normal anatomy and hemodynamics on two-dimensional (2D) and color flow (CF) ultrasound assessment. Based on these findings, a diagnosis of isolated fetal cardiac rhabdomyoma was established. Given the strong association between cardiac rhabdomyoma and tuberous sclerosis complex (TSC), a comprehensive evaluation for TSC was performed, including neurosonography and systemic screening for cutaneous, renal, and neurological manifestations. No additional features consistent with TSC were identified beyond the cardiac mass. The patient maintained regular antenatal care from 32 weeks through 39 weeks plus 1 day, with no complications. At 39 weeks plus 1 day, a cesarean section was performed for full-term delivery and patient request for repeat cesarean delivery, resulting in the birth of a 3200-gram female infant with an APGAR score of 10 at both 1 and 5 minutes. Both maternal and neonatal postoperative courses were uncomplicated, and both were discharged on postoperative day three. Postnatal evaluations were conducted on days 1, 7, and 30, with no evidence of tumor regression, growth, or emergence of skin lesions or seizures. Physical examination findings remained normal, and the cardiac mass size was stable compared to the prenatal assessment. At 7 months of age, developmental history and neurodevelopmental screening were performed, revealing age-appropriate developmental progress. Anthropometric measurements confirmed normal growth. A pediatric echocardiogram revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, measuring 21.8 mm × 9.2 mm and 14.7 mm × 8.5 mm, respectively, with no evidence of left ventricular inflow obstruction or functional compromise. At 12 months of age, comprehensive evaluation including physical examination, anthropometric assessment, and neurobehavioral testing was completed. The child demonstrated healthy growth parameters and normal neurobehavioral development, consistent with age-matched peers. The cardiac rhabdomyoma remained stable in size and did not exhibit any growth or regression. No clinical criteria for tuberous sclerosis complex were met, including absence of cutaneous hamartomas, subependymal nodules, renal angiomyolipomas, or other systemic manifestations. This case represents an isolated, asymptomatic cardiac rhabdomyoma without evidence of tuberous sclerosis complex, with stable tumor morphology and normal developmental and physiological outcomes through one year of age.


A 13-year-old boy had a problem in his throat since he was 2 years old, with small growths called papillomas that blocked his airway. By age 3, he needed a tube (tracheostomy) to breathe. His mom also had a similar skin growth. The boy had trouble breathing, especially at night, with a loud breathing sound and hoarseness. He got medicine and oxygen but it didn’t help. Tests showed growths in his voice box and windpipe, and small lung pockets. After surgery, the doctor removed the growths and put in a breathing tube. He got one shot of a medicine called bevacizumab to help stop the growths. He started breathing better and didn’t need oxygen after a few days. He stayed in the hospital for 7 days and then went to another hospital. After 8 months, the family said the problem didn’t come back. He is doing well and no signs of return.


A 13-year-old male from Cusco with a longstanding history of laryngeal papillomatosis since age two, who required tracheostomy at age three, was admitted to the San Borja National Institute of Child Health in Lima following a 16-day course of progressive respiratory distress, primarily nocturnal, characterized by inspiratory laryngeal stridor and moderate dysphonia. Prior treatment with azithromycin and supplemental oxygen failed to improve symptoms. Physical examination revealed mild subcostal retraction, diminished vesicular breath sounds in the left hemithorax, and scattered wheezing predominantly in the right hemithorax, necessitating oxygen via binasal cannula at 4 liters per minute. Laboratory findings included leukocyte count of 8.03 × 10³/μL, platelets at 209 × 10³/μL, hemoglobin 13.2 g/dL, and C-reactive protein of 36.6 mg/L, indicating a moderate inflammatory response without evidence of sepsis. Imaging studies consisted of chest radiography and head and neck tomography, which revealed multiple stenosing nodules involving the larynx and trachea, as well as several pulmonary cysts consistent with chronic airway obstruction and alveolar damage. At 48 hours post-admission, the patient experienced worsening stridor and respiratory compromise, prompting urgent intervention in the emergency operating room. The procedure included tracheostomy, microsurgical excision of papillomatosis lesions, and removal of a large appendicular tumor with papillomatous morphology and ventricular banding structures involving the epiglottis, glottic region, vocal cords, subglottis, and trachea extending to tracheal ring 5. Histopathological analysis confirmed coilocytic atypia and mild focal dysplasia, consistent with human papillomavirus (HPV)-induced epithelial dysregulation, most likely HPV-16 or HPV-18 based on typical patterns of HPV-associated laryngeal papillomatosis. Postoperatively, the patient was transferred to the pediatric intensive care unit (PICU) for close respiratory monitoring and initiated weaning from oxygen, which was successfully achieved by 48 hours post-surgery. He received a single intravenous dose of 400 mg bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), administered to inhibit angiogenesis and reduce tumor neovascularization in recurrent or persistent papillomatosis. Clinically, the patient showed significant improvement within 72 hours, with normalization of oxygen saturation and progressive reduction in respiratory support. He remained hospitalized for seven days before being transferred to the Hospital in Breña for continued outpatient management. Eight-month follow-up via telemonitoring demonstrated no evidence of disease recurrence, no new lesions, and no additional respiratory complications, supporting the durability of the intervention. The clinical course underscores the role of HPV-driven epithelial proliferation in laryngeal and tracheal stenosis, the efficacy of combined surgical excision and anti-angiogenic therapy, and the importance of long-term surveillance in patients with familial or recurrent papillomatosis, particularly in those with a maternal history of genital human papillomavirus infection.


A 54-year-old man with a long history of kidney problems and medicines that weaken his immune system got sick with fever, cough, and trouble breathing. He had been smoking for a long time and was on strong medicines for his kidneys. Before he got sick, his chest X-ray was normal. When he got sick, he had a high fever, shortness of breath, and his body wasn’t getting enough oxygen. His lungs made crackling sounds, and scans showed cloudy spots in both lungs. Tests showed signs of infection — bacteria, virus, or fungus — and he had antibodies for RSV, a common virus. Because his immune system was weak from long-term medicine use, he couldn’t fight off the infection well. Doctors gave him antibiotics, antifungal medicine, and steroids to calm his body’s reaction. Even with all this care, his condition got worse fast. He needed a breathing machine, but still didn’t improve. Two days later, he passed away from not being able to breathe.


A 34-year-old woman had lower back pain and blood in her urine. She also had a big bruise on her right buttock and no history of bleeding before. The bleeding started after she had a C-section during pregnancy two months ago. Doctors found that her body couldn't stop bleeding properly because of a problem with a blood protein called factor VIII. This problem was made worse after giving birth. Tests showed she had a high level of an antibody that attacks this protein. This confirmed she had acquired haemophilia, which happened after childbirth. She got treatment with medicines to stop the bleeding and help her blood work, and her symptoms got better over time. She is now doing well and can go home.


A two-day-old baby was admitted to Children’s Hospital with a swelling on the right side of the scrotum that had been present since birth. The baby was born at full term by cesarean section at a private hospital and stayed in the nursery for one day before being referred for surgery. When they arrived at the hospital, the baby was healthy, well-hydrated, pink, and had good circulation. On exam, the right testis was enlarged, firm, not painful, and had a red color with skin damage. The testis did not allow light to pass through (negative trans-illumination), while the left one did (positive). Both testicles had normal openings, with no signs of hernia. An ultrasound showed the right testis was enlarged (15.6 mm x 9.4 mm), had an uneven texture, and showed a thickened network of tissue (rete testis) with no blood flow, which is a sign of poor circulation. The left testis was normal in size and shape, with only a small amount of fluid around it. Surgery was urgently performed. During the operation, the right testis was found to be completely dead (necrotic) and twisted inside the scrotum (intravaginal torsion), with only a small amount of fluid. The doctors removed the damaged right testis (right orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to prevent future issues.


A two-day-old baby was born by C-section and had a swelling on the right side of his scrotum from the start. When they checked him, he was healthy, warm, and breathing well. The swollen testicle was big, stiff, red, and had small skin scratches. A light test showed the right side didn’t let light through (which means it’s not normal), but the left side did. The baby’s groin openings were fine. A scan showed the right testicle was enlarged and had a bad, patchy look with no blood flow — this means it was dying. The left testicle was normal but had a little fluid. Doctors had to do an emergency surgery. Inside, they found the right testicle was dead and twisted, with only a small amount of fluid. They removed the dead testicle (right orchidectomy) and fixed the left testicle (contralateral orchidopexy) to keep it in place.


We present a case of a two-day-old male neonate presenting with an inborn right scrotal swelling admitted to the pediatric emergency department of Children’s Hospital. The infant was born at term via cesarean section at a private facility and remained in the nursery for one day prior to referral for urgent surgical evaluation. Transfer to our institution was delayed by a full day, during which time the clinical condition was stable. On arrival, the neonate was well-hydrated, had normal room temperature skin color, and exhibited adequate peripheral perfusion, indicating no signs of systemic compromise. Physical examination revealed a markedly enlarged, tense, non-tender right testis with visible erythema and overlying skin excoriation, suggestive of localized ischemia or inflammatory processes. Trans-illumination testing was negative in the right testis (indicating a non-reflective, solid tissue mass), while it was positive in the left contralateral testis, consistent with a normal, fluid-containing structure. Both inguinal hernial orifices were anatomically intact, ruling out inguinal hernia as a primary etiology. An urgent Doppler ultrasound of the inguinoscrotal region was performed, revealing the right testis to be enlarged (dimensions: 15.6 × 9.4 mm) with a heterogeneous hypoechoic echotexture, characterized by prominent rete testis architecture and absence of detectable arterial or venous flow on color Doppler imaging—findings consistent with ischemic compromise and loss of vascular perfusion. The left testis was normal in size, shape, and echotexture, with a minimal hydrocele present, indicating preserved vascular integrity and normal testicular development. Intraoperative findings confirmed a frank necrotic right testis with intravaginal torsion (i.e., twisting of the testicular parenchyma around its vascular pedicle), leading to complete arterial occlusion and irreversible tissue damage. Minimal hydrocele was also noted in the right scrotum. The surgical intervention consisted of a right orchidectomy (removal of the necrotic testis) and contralateral orchidopexy (surgical fixation of the normally developing left testis to the scrotal wall) to prevent future complications such as testicular descent failure or torsion. The absence of flow on Doppler imaging is a critical indicator of testicular ischemia, and the presence of necrosis and intravaginal torsion confirms a diagnosis of testicular torsion with secondary ischemic necrosis, likely occurring in the perinatal period due to delayed presentation and inadequate perfusion. This case underscores the importance of prompt evaluation and intervention in neonates with scrotal swelling, as delayed diagnosis significantly increases the risk of irreversible testicular loss.


A 4-year-old boy had a skin infection (impetigo) two weeks before his illness. For 5 days, he had blood in his urine and swelling in his legs. Then he started having headaches, nausea, vomiting, and suddenly had a seizure. His blood pressure became very high, causing a dangerous situation. Tests showed his body was missing some important proteins (C3) and had high levels of a strep infection marker (ASO), which pointed to a condition called GNAPE. Because of the high blood pressure, his brain started to swell (PRES), which can cause brain damage. He also developed a type of anemia where his red blood cells were being destroyed, and his hemoglobin dropped to 5 g/dL. He needed medicine to lower his blood pressure, protect his brain, and stop the body from attacking his red blood cells (steroids). He stayed in the hospital for 31 days, and after that, he was back to normal. Six months later, he had no symptoms and was doing well with medicine to keep his blood pressure and kidneys healthy.


{
  "proficient_health_literacy": "A 4-year-old male presented with a 5-day history of macroscopic glomerular hematuria and lower extremity edema, which progressed over the preceding 12 hours to include headaches, nausea, vomiting, and a generalised tonic-clonic seizure. On emergency department admission, the patient was afebrile, with non-evaluable blood pressure, and exhibited quantitative consciousness impairment, generalized hypertonia, and bilateral pretibial edema. Endotracheal intubation was performed, and phenobarbital (10 mg/kg) was administered to control seizure activity.\n\nPhysical examination in the intensive care unit (ICU) revealed a blood pressure of 134/94 mmHg (BP 110 mmHg), with a p95 of 108/66 mmHg and p95+12 of 120/78 mmHg. Initial laboratory findings included hematuria (>100 erythrocytes per field), proteinuria 3+, leucocyturia (10–25 per field), creatinine 0.3 mg/dL, hemoglobin 7 g/dL, hematocrit 21%, normal mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC), leukocytosis (23,900/mm³), thrombocytosis (756,000/mm³), absence of acute-phase reactants, hypocomplementemia (C3 25 mg/dL; normal range 80–150 mg/dL), and normal C4. A rapid antigen test for Streptococcus pyogenes (group A beta-hemolytic streptococcus) was positive, and Anti-Streptolysin O (ASO) titers were elevated, consistent with recent streptococcal infection. Non-contrast brain CT showed no acute abnormalities. Renal ultrasound revealed bilateral nephromegaly with increased cortical echogenicity and reduced corticomedullary differentiation.\n\nThe patient was diagnosed with nephritic syndrome secondary to group A streptococcal infection (GNAPE) complicated by hypertensive emergency and convulsive status. Within 24 hours of ICU admission, mechanical ventilation and continued phenobarbital therapy were required. Electroencephalography (EEG) and cerebrospinal fluid analysis were normal on day one. Empirical antibiotic therapy with cefotaxime was initiated for eradication of Streptococcus pyogenes, and furosemide was administered for diuresis.\n\nOn post-admission day two, the patient developed acute kidney injury with creatinine rising to 0.99 mg/dL, persistent hypertension, and 24-hour proteinuria of 36.6 mg/m²/h, without oliguria. Antihypertensive therapy was initiated with amlodipine and intravenous labetalol, achieving initial control. At 48 hours, extubation was performed, which was well tolerated. However, within 24 hours of extubation, the patient's mental status deteriorated to Glasgow Coma Scale (GCS) 8 (ocular opening and limb withdrawal only to painful stimuli), with poor verbal response, and blood pressure remained above p95+12 despite continuous infusion of labetalol (up to 3 mg/kg/h), amlodipine (10 mg/day), and furosemide. This necessitated reintroduction of mechanical ventilation and administration of sodium nitroprusside (up to 3 mcg/kg/min) to achieve a gradual reduction of blood pressure by 25% per day to prevent secondary neurological injury. Given the presence of acute neurological symptoms in the context of severe hypertension in a patient with glomerulonephritis, posterior reversible encephalopathy syndrome (PRES) was suspected and confirmed by magnetic resonance imaging (MRI) on day 5. MRI demonstrated bilateral, symmetric subcortical hyperintensities in the occipital regions, without diffusion restriction, consistent with vasogenic edema. Ophthalmological examination was normal, and subsequent EEG showed occasional episodes of generalized voltage depression.\n\nHemoglobin declined to 5 g/dL during ICU stay, with normal MCV and MCHC, and no plateletopenia, prompting suspicion of autoimmune hemolytic anemia. A positive direct Coombs test and hemoglobinuria supported this diagnosis. Two red blood cell transfusions were required. Corticosteroid therapy with methylprednisolone (1 mg/kg/day) was initiated for 72 hours. Serological testing for Epstein-Barr virus, parvovirus B19, extractable nuclear antigens (ENA), anti-neutrophil cytoplasmic antibodies (AN


A 69-year-old man with a history of heart surgery (coronary artery bypass grafting) came in with severe shortness of breath even during light activity, which had been going on for two months. He was diagnosed with heart failure caused by reduced blood flow to part of his heart, specifically due to a blockage in the right coronary artery (RCA) that had previously failed to work properly. This diagnosis was made based on his heart test results, blood markers, and a detailed heart imaging study (coronary angiogram).

To fix the blocked artery, doctors used a technique called 'retrograde recanalization' — meaning they started from the opposite side of the heart, using natural blood channels (collaterals) from the left side to reach the blocked RCA. They first cleared a major blockage in the left coronary artery, then used a method called 'septal surfing' to travel through the septal branches and reach the blocked RCA. Once there, they opened the blockage with a balloon and placed two drug-coated stents to keep the artery open.

After the procedure, his shortness of breath improved and went away by the time he was discharged. At a 6-month check-up, he had no return of symptoms and was doing much better.


A 69-year-old man had trouble breathing even when doing small things like walking, for two months. He had had heart surgery before (CABG) and now his heart isn’t pumping well, which caused this breathing problem. Doctors found that a part of his heart’s blood supply (the right coronary artery) was completely blocked, and that damage from a heart attack years ago made the heart weaker. They fixed the blocked blood vessel by going backward through a small channel in the heart muscle, using a special method called 'septal surfing.' After fixing it, his breathing got better right away. Six months later, he still doesn’t have any breathing problems.


A 69-year-old male with a prior history of coronary artery bypass grafting (CABG) presented with severe dyspnea at mild exertion, classified as New York Heart Association (NYHA) class III, lasting for two months. The patient had a documented history of inferior ST-segment-elevation myocardial infarction (STEMI) in 2009 at age 59, with coronary angiography at that time revealing severe three-vessel disease, including a complete occlusion (CTO) in the proximal left anterior descending artery (LAD), 90% stenosis in the mid and distal left circumflex artery, and 95% stenosis in the mid-right coronary artery (RCA). In 2009, he underwent CABG utilizing the left internal mammary artery (LIMA) to the LAD, followed by sequential saphenous vein graft (SVG) to the first obtuse marginal branch (OM1), second obtuse marginal branch (OM2), and posterolateral artery (PL). At presentation, coronary angiography via 6 French left radial artery access demonstrated patency of the LIMA-to-LAD and SVG-to-OM1, OM2 conduits, but a complete occlusion of the SVG-to-PL graft. Native left main coronary artery was occluded at its ostium, and the native RCA was occluded in the mid-portion with bridging collaterals. Given the functional significance of the occluded native RCA, a targeted intervention was initiated to recanalize the native right coronary artery CTO. Dual arterial access was established using a second 6 Fr sheath in the right femoral artery. Left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach via the left radial artery was attempted; however, neither the Fielder XTR wire (Asahi Intec) nor the Gaia 3 wire (Asahi Intec) with Finecross microcatheter (Terumo) successfully navigated to the true lumen of the distal RCA. A parallel wire technique using Crusade microcatheter (Kaneka) and two Gaia 3 wires was attempted but failed to achieve coronary artery crossing. Consequently, a retrograde approach via the septal collaterals originating from the left anterior descending artery (LAD) through the occluded left main coronary artery was employed. The Gaia 3 wire crossed the occluded left main (LM) and LAD and reached the true lumen of the distal LAD. The Sion wire was then exchanged for a Finecross microcatheter (Terumo) and advanced into the distal LAD. The left main and proximal LAD were predilated with a 2.0 × 15 mm balloon. Subsequently, the septal surfing technique (SST) was applied to facilitate retrograde crossing of the CTO. Multiple septal channels were evaluated from proximal to distal LAD, and the Sion wire was retrogradely delivered through a distal septal branch into the distal RCA, supported by a 150-cm Finecross microcatheter. The Gaia 3 wire successfully traversed the CTO lesion retrogradely into the true lumen of the proximal RCA and was advanced into the Guidezilla guide extension catheter (Boston Scientific) positioned within the antegrade guiding catheter. The Finecross microcatheter was then delivered to the antegrade catheter, and an RG3 wire (Asahi Intec) was externalized. The CTO was predilated with a 2.0 × 15 mm balloon and treated with two overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm), resulting in excellent angiographic restoration with TIMI 3 flow in all distal coronary branches. Post-procedure, the patient’s dyspnea improved significantly and was fully resolved at discharge. At 6-month follow-up, there was no recurrence of dyspnea. The diagnosis of heart failure due to ischemic etiology was established based on electrocardiographic findings of ST depression in leads II, III, aVF, and V4–V6, elevated plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (2640 pg/mL), and echocardiographic evidence of left ventricular systolic dysfunction with a left ventricular ejection fraction of 30%, consistent with ischemic cardiomyopathy secondary to prior SVG failure in the right coronary artery.


A 51-year-old man came in with sudden, painful vision loss in his left eye three days earlier. His right eye had normal vision, but his left eye could only see hand movements. Examining the back of his left eye showed swelling around the optic nerve, bulging of the choroid, fluid buildup under the retina, and wrinkling of the retinal pigment epithelium. Imaging tests, including MRI of the orbit and brain, showed a nodular mass at the junction of the optic nerve and sclera. Tests for cancer and autoimmune diseases were normal. Based on these findings, the doctor diagnosed nodular posterior scleritis, a type of eye inflammation. The patient was started on oral prednisolone at 50 mg per kilogram of body weight. After surgery to remove a small nodule, the fluid in the eye improved, and vision stabilized. The treatment was gradually reduced over three months. All tests and follow-up showed no signs of serious disease.


A 51-year-old man woke up 3 days ago with a sudden, painful blurry vision in his left eye. His right eye was fine. He could see clearly with his best eye, but the left eye only showed hand motion. When doctors looked inside his left eye, they saw swelling around the back of the eye, bulging tissue, fluid buildup, and wrinkled layers of the eye’s lining. A scan of his eye and brain showed a small lump near where the optic nerve meets the eye socket. Tests for cancer and other diseases came back normal. The doctor diagnosed it as a type of eye inflammation called nodular posterior scleritis. He started taking a strong steroid pill (prednisolone) at a high dose to reduce the swelling and pain. The lump went down, the fluid cleared, and his vision improved. After a week, he had surgery to remove a small part of the eye socket tissue, and the steroid was injected. He didn’t go to the hospital for IV medicine, but still got better with the pills. After three months, the medicine was slowly stopped. His vision stayed good.


A 51-year-old male presented with acute, painful visual loss of the left eye (LE) onset three days prior. Best-corrected distance visual acuity (BCDVA) was 20/20 in the right eye (RE) and hand motion (HM) in the LE. Ocular motility was intact bilaterally. Anterior segment examination was normal. Fundus examination of the LE revealed optic disc (ONH) swelling, choroidal bulging, multiple subretinal fluid accumulations, and retinal pigment epithelial (RPE) corrugations. The RE fundus was unremarkable. Multimodal imaging was performed: Optical coherence tomography (OCT; OptoVue, Inc., 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. Fundus blue-autofluorescence (BAF) showed a geographic area of speckled autofluorescence at the macula, consistent with RPE disruption. Indocyanin green angiography (ICGA) revealed a geographic hypofluorescent area with speckled hyperfluorescent margins measuring three disc diameters (DD), suggesting focal vascular leakage and RPE dysfunction. Fluorescein angiography (FA; Heidelberg Eye Explorer v1.9.13.0, Spectralis Viewing Module 6.5.2.0) demonstrated vascular leakage at the optic disc (hot spot), supporting active inflammation. B-scan ultrasonography confirmed optic nerve enlargement, consistent with retrobulbar infiltration. Orbital and brain MRI with gadolinium enhancement identified a retrobulbar nodular mass at the optic nerve-sclera junction, showing intense enhancement, raising concern for both inflammatory and neoplastic etiologies. Oncology evaluation was negative for malignancy. Rheumatology work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable. Given the clinical suspicion of nodular posterior scleritis, the patient underwent transconjunctival lateral orbitotomy one week after presentation, revealing a pink, localized scleral nodule with edematous tenon. Sub-tenon triamcinolone acetonide was administered as a local anti-inflammatory intervention. The patient declined admission and intravenous corticosteroid therapy. Oral prednisolone was initiated at a dose of 50 mg/kg/day, targeting immunomodulation and suppression of inflammatory cascades within the ocular and orbital tissues. At follow-up one week post-intervention, BCDVA remained 20/20, with counting fingers at 2 meters in both eyes. Subretinal fluid (SRF) was completely absorbed, and the macular region exhibited atrophy, indicating resolution of active fluid accumulation and chronic RPE damage. Oral prednisolone was tapered over a three-month period to minimize long-term corticosteroid effects. The clinical course supports a diagnosis of nodular posterior scleritis, with imaging findings consistent with inflammatory-mediated RPE and choroidal disruption, optic nerve edema, and focal vascular leakage, all without evidence of systemic autoimmune or infectious pathology or malignancy. The pathophysiological mechanism likely involves chronic inflammation at the posterior sclera-optic nerve interface, leading to RPE dysfunction, fluid accumulation, and structural changes in the retinal layers, with potential activation of local cytokine networks (e.g., IL-1, IL-6, TNF-α) contributing to tissue swelling and vascular permeability.


A 78-year-old man from the Amhara region of Ethiopia had a permanent pacemaker because he had complete heart block. He needed surgery for an enlarged prostate (benign prostatic hyperplasia), which had developed after a previous prostate procedure. Before surgery, doctors checked his heart and overall health and found that his heart function was stable, though he had high blood pressure and type 2 diabetes. His pacemaker was set to a mode that could be risky during surgery, so doctors recommended changing it to a safer setting. However, the patient could not afford the cost of reprogramming the device due to limited access to cardiac care in Ethiopia and the long wait times for specialists. After discussing the risks, he chose to proceed with the surgery using his current pacemaker setup. Informed consent was given, and the surgery went ahead. He received combined epidural-spinal anesthesia (a mix of bupivacaine and fentanyl) at the L3-L4 level, which provided good pain relief. His vital signs stayed stable during surgery and recovery, with no major heart or breathing issues. After the operation, he was monitored in the recovery room for 12 hours, then moved to the ward. He got pain relief after 4 hours and had a small dose of epidural medicine to keep pain under control. He stayed in the hospital for about 24 hours and was discharged after 88 hours of recovery, in stable condition. He continues to take his medications and is advised to have regular check-ups to ensure his pacemaker is working properly.


A 78-year-old man from Ethiopia had a pacemaker in his heart because his heart wasn’t beating properly. He needed surgery to fix a swollen prostate, and the doctors said his pacemaker was set in a way that could be risky during surgery. They suggested changing the pacemaker setting to make it safer, but he couldn’t afford the cost and chose to go ahead with the old setting. He gave permission to have the surgery and to share his story later. Before surgery, he was checked well and had normal blood tests. He was given pain medicine through a tube in his back (epidural) and a small shot of pain medicine (fentanyl) to help him stay comfortable. The doctors watched his heart and blood pressure closely and found nothing wrong. During the surgery, the team kept his heart safe by staying away from the pacemaker and having emergency tools ready. His body stayed steady the whole time. After surgery, he stayed in a recovery room for 12 hours, got more pain medicine, and was moved to a regular room. He stayed in the hospital for about 2 days and got pain relief for 3 days. He was finally sent home after 88 hours, and the doctors said he’s doing well and should keep checking his pacemaker regularly.


A 52-year-old woman had trouble urinating for years, going to the bathroom often and feeling pain when she did. She saw red and black thread-like stuff in her urine, and sometimes had headaches, fever, and chills. She tried many treatments for infections, but nothing helped. No bugs or travel was linked to her symptoms. She had surgery before, but that didn’t fix it. Tests showed no infections or blockages. A bladder check showed redness and dirt in the bladder. Doctors thought it might be a worm, so they gave medicine, but symptoms stayed. Later, a tiny worm was found in her urine under a microscope. It was a type of fly larva. The doctor told her to clean herself better and drink at least 3 liters of water every day. That helped her feel better.


A 36-year-old woman with ulcerative colitis had been doing well on medication but started experiencing worsening chest pain, shortness of breath, and symptoms like fatigue and night sweats. Her electrocardiogram showed abnormal changes in the lower part of her heart, and tests revealed signs of inflammation and heart damage. An emergency heart scan found severe blockages in two major coronary arteries, with the worst blockage in the right coronary artery. She had successful treatment with a stent placed in that artery. During the procedure, doctors noticed signs that might point to a condition called aortitis, which can cause inflammation in the aorta and its branches. Further testing, including blood work and a detailed imaging scan (CTA), showed thickening of the aortic walls and narrowing in several arteries, strongly suggesting Takayasu arteritis — a rare inflammatory disease that affects large arteries. She was started on prednisone and methotrexate to reduce inflammation. After three weeks, she had surgery to improve blood flow to her heart using a blood vessel from her chest. The surgery was successful, and she is now recovering well at home with regular follow-up.


A 36-year-old woman had a long-time stomach problem called ulcerative colitis, which she was managing with medicine. She started feeling chest pain that got worse over a week, along with shortness of breath and feeling tired and sweating at night. Tests showed her heart had damage, especially in the lower part, and two major blood vessels feeding the heart were badly blocked. Doctors fixed one of the blocked vessels with a stent and did a surgery later to fix the other. They also found signs of a rare inflammation in her blood vessels, especially around the aorta, which pointed to a condition called Takayasu arteritis. She was given steroids and a medicine to calm her immune system. After a few weeks, she had heart surgery that worked well, and she’s now doing fine at home.


A 36-year-old female with a history of ulcerative colitis, well-controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares, was admitted to the emergency department with a one-week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms, including fatigue and night sweats. She reported a six-month history of generalized malaise, with prior episodes of effort-related precordial pain that had progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.

Electrocardiography demonstrated sinus rhythm with supradesnivel (supra- or superior) ST-segment elevation in the inferior wall, indicating acute ischemia or infarction. Emergency coronary angiography revealed severe two-vessel coronary artery disease: a 90% ostial lesion in the left coronary trunk and a 99–100% subocclusive lesion at the ostial level of the right coronary artery (culprit vessel). Primary percutaneous coronary intervention (PCI) was performed with successful deployment of a drug-eluting stent in the right coronary artery. The hemodynamic team observed vascular friability during balloon advancement in the aortic arch, raising suspicion for aortic inflammation, prompting a targeted evaluation for systemic inflammatory or autoimmune etiology prior to surgical revascularization of the left coronary trunk.

Laboratory findings included mild anemia (hemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm³), elevated erythrocyte sedimentation rate (ESR: 42 mm/h), elevated C-reactive protein (CRP: 4.9 mg/L; normal <1 mg/L), and elevated ultra-sensitive troponin, consistent with myocardial injury. Autoimmune workup showed normal complement levels (C3 and C4), negative anti-nuclear antibodies (ANA), anti-double-stranded DNA, negative extracellular nuclear antigen (ENA) profile, and non-reactive VDRL, excluding systemic lupus erythematosus and syphilis.

Cardiac magnetic resonance (CMR) with contrast revealed acute non-transmural infarction of the inferior wall of the left ventricle and subendocardial ischemia in the anteroseptoapical region at rest. Mild aortic and mitral regurgitation were noted, with preserved biventricular systolic function.

Computed tomography angiography (CTA) of the chest, abdomen, and pelvis demonstrated periaortic fibrotic wall thickening involving the aortic root, aortic arch, and abdominal aorta, with severe stenosis of the left coronary trunk and mild stenosis of the left subclavian and left vertebral arteries. Severe stenosis of the lower mesenteric artery was also identified. These findings are consistent with Takayasu arteritis, a rare large-vessel vasculitis primarily affecting young women. Immunological evaluation revealed IgG level of 1,600 mg/dL (within reference range of 700–1,600 mg/dL), with elevated IgG1 (1024 mg/dL), and normal IgG2 (456 mg/dL), IgG3 (98.8 mg/dL), and IgG4 (13.6 mg/dL)—a pattern suggestive of IgG4-related disease, although the clinical diagnosis of Takayasu arteritis was established primarily through imaging and clinical context.

The patient was diagnosed with Takayasu arteritis based on clinical presentation, inflammatory markers, and imaging findings. Treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by intramuscular injection, and folic acid 1 mg daily to mitigate methotrexate-induced toxicity. After three weeks of immunosuppressive therapy, the patient underwent delayed myocardial revascularization surgery using the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta were found to be structurally intact, without evidence of significant inflammatory or fibrotic involvement. Postoperative recovery was uneventful, and the patient is currently stable at home under ambulatory follow-up with ongoing monitoring for disease activity and cardiovascular complications. The case illustrates the importance of considering large-vessel vasculitides in young patients with unexplained cardiovascular symptoms, particularly in the context of chronic inflammatory conditions such as inflammatory bowel disease.


A 36-year-old woman had trouble swallowing (dysphagia) and long-standing pain in her neck and upper chest. She also had a multinodular goiter, but no other major health issues. Imaging tests showed a rare birth defect called a mirror image right aortic arch. In this condition, the aorta (the main blood vessel from the heart) forms around the right bronchus and the arteries that supply the neck and arms develop in the opposite order to normal. This creates a ring around the esophagus and trachea, which can press on them and cause symptoms. In her case, the aortic arch and a small pouch called a Kommerell diverticulum (1.3 cm) were pressing on the esophagus, causing a narrowing of 60%. However, she had no serious complications like breathing problems, aneurysms, or aortic dissection, and her symptoms improved on their own over time. Because her condition was not causing major harm and she was doing well, no surgery was done. This rare condition usually doesn’t cause problems unless there is significant pressure on the airway or esophagus, or if there are other serious complications. Treatment is not standard and depends on the individual case.


A 36-year-old woman had trouble swallowing and pain in her neck and upper chest. She didn’t have other health problems. Doctors found a rare birth difference in her chest where the main blood vessel (aorta) loops around the right side of her airway and windpipe. This causes a small pouch (called Kommerell diverticulum) that presses on her esophagus. Most people with this don’t have symptoms, but if the pressure is strong or the blood vessel weakens or bursts, surgery might be needed. In this case, her symptoms were mild and didn’t affect her eating or health, so no surgery was done. Her symptoms got better on their own over time.


A 62-year-old woman of North African descent, diagnosed with Von Hippel-Lindau disease in 2021, had several tumors involving her kidneys, adrenal glands, pancreas, and ovaries. She had a left bone tumor, a pheochromocytoma in her adrenal gland, a kidney cancer on the left side, a multi-cystic right kidney, and masses in her pancreas. She also had ovarian cysts that were found during imaging and surgery.

She underwent several surgeries: radiotherapy for a bone tumor, removal of her left adrenal gland and left kidney, and a major surgery to remove part of her pancreas. A tumor in her left ovary was found during a scan and later confirmed with imaging, raising concerns for cancer. Laparoscopic surgery revealed cystic tumors in both fallopian tubes and the area around the uterus. After a hysterectomy with removal of both ovaries, tissue tests showed clear-cell papillary cystadenomas in both tubes and the broad ligament — a known sign of Von Hippel-Lindau disease.

She recovered well after surgery and has been followed every four months with normal ultrasounds. However, she recently returned to the hospital for a new brain tumor, which is a known possible complication of this condition.


A 62-year-old woman from Tunisia had a rare disease called Von Hippel-Lindau. In 2021, she was found to have tumors in several parts of her body, including her brain, kidneys, adrenal glands, pancreas, and ovaries. She had surgeries to remove tumors from her left kidney, left adrenal gland, and part of her pancreas. A tumor in her left ear bone was treated with radiation. An ovarian tumor was found during a scan and later confirmed as a cystic mass. Surgery showed tumors in her fallopian tubes and pelvic area, which are normal for this disease. After removing her uterus and both ovaries, the doctors found the tumors were clear-cell papillary cystadenomas, which match the disease. She has been doing well since, with no new problems, but recently came back because a brain tumor came back.


A 59-year-old man with type 1 diabetes developed heart failure and was found to have infections on his heart valves. Tests showed large growths (vegetations) on both the mitral and aortic valves, which are signs of native valve endocarditis (NVE) — an infection of the heart valves caused by bacteria. The bacteria identified was Staphylococcus warneri, a type of common skin bacteria that can cause serious infections in people with weakened hearts or poor blood sugar control. He had no history of medical devices or immune problems, and the infection likely started from bacteria that had been living in his body for years. Before getting sick, he had mild signs like slight lab abnormalities, weight loss, and low blood counts, which may have been early warning signs of the infection. He was treated with antibiotics first, and after four weeks, he had surgery where both his mitral and aortic valves were replaced with mechanical valves. His heart function improved, and he has not had any problems since, over two years later. His poor diabetes control and high blood sugar likely made the surgery risky, so it was delayed until his health stabilized.


A man in his 50s with type 1 diabetes had heart problems that got worse. He started feeling short of breath and had a fever, but didn’t notice any other symptoms before. Doctors found big, sticky spots on his heart valves — these are signs of an infection called endocarditis. The infection was caused by a type of bacteria that lived in his body all along, not from a cut or injury. Before this, he had been losing weight slowly and had small signs like a slightly high white blood cell count and low blood proteins, which might have been early warning signs. He didn’t have any devices or medicines that weaken his immune system. Doctors treated him with antibiotics first, which helped his heart stop failing. After his heart stabilized, they did surgery to replace both his aortic and mitral heart valves because the infections were too serious. He recovered well and hasn’t had any problems since, two years later.


{
  "proficient_health_literacy": "A 59-year-old Japanese man with a 28-year history of type 1 diabetes presented with acute heart failure and was diagnosed with native valve endocarditis (NVE) caused by Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS). The patient had long-standing, poorly controlled diabetes, evidenced by severely depleted insulin secretion (serum C-peptide undetectable), persistent hyperglycemia (HbA1c ≈ 9.0%), and marked glycemic variability despite intensive multiple-dose insulin therapy. His body mass index was 18.4 kg/m² (height 168 cm, weight 52 kg), indicating underweight status, which may have contributed to impaired immune surveillance and increased susceptibility to infection. He had a pre-existing diagnosis of asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years prior, which he had actively declined to monitor, leading to progressive valvular deterioration. No prosthetic devices or immunosuppressive therapies were implanted, and no prior history of medical device use or immunocompromise was reported.\n\nEight days prior to presentation, the patient presented to an emergency clinic with acute dyspnea and fever (>38°C), with no prior history of fever, chills, weakness, or systemic symptoms. On admission, vital signs included hypertension (192/82 mmHg) and tachycardia (118 bpm), orthopnea, and hypoxemia (SpO₂ 80%). Physical examination revealed a Levine 3/6 systolic murmur, a finding not previously documented during routine follow-up. No classic signs of infective endocarditis (IE) such as Osler nodes, Janeway lesions, or conjunctival petechiae were observed. Laboratory findings showed marked leukocytosis (WBC 20,800 /μL), elevated C-reactive protein (CRP 6.06 mg/dL), normal serum creatine phosphokinase MB (6.0 IU/L), and negative troponin T, suggesting myocardial injury was not present. Chest X-ray demonstrated pulmonary congestion and cardiac enlargement (cardiothoracic ratio 55%). Electrocardiography showed ST elevation in leads V1–V4, consistent with acute strain or ischemia, but emergency transthoracic echocardiography revealed preserved left ventricular contractility, indicating that the hemodynamic compromise was primarily due to valvular dysfunction.\n\nTransthoracic echocardiography revealed severe aortic and mitral regurgitation, with a mobile vegetation detected on the mitral valve. Transesophageal echocardiography confirmed a 16.5×6-mm mobile vegetation on the anterior mitral valve leaflet and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings met the clinical criteria for native valve endocarditis, particularly given the size and mobility of the vegetations. Imaging with head CT and MRI showed no evidence of cerebral infarction or hemorrhage, though the presence of a mobile vegetation was confirmed, raising concern for embolic risk. Retrospective review of pre-admission laboratory data revealed subtle abnormalities: four months prior to admission, a slight elevation in WBC was noted; subsequently, serum albumin declined to 3.0 g/dL, hemoglobin showed a gradual decline over two months, and the patient experienced a 4-kg weight loss. These findings, though non-specific, may represent early signs of systemic infection or malignancy. Esophagogastroduodenoscopy and whole-body CT were unremarkable. One month later, the patient regained weight and laboratory values nearly normalized (except for mild CRP elevation at 0.54 mg/dL). However, at the visit eight days before admission, WBC rose to 9,300 /μL, Hb and albumin dropped again to 13.1 g/dL and 3.0 g/dL, and CRP increased to 4.18 mg/dL, with a concomitant drop in diastolic blood pressure, suggesting a recurrent inflammatory or infectious process.\n\nEmpirical intravenous antibiotic therapy was initiated with 12 g/day ampicillin sulbactam (ABPC/S) and 120 mg/day gentamicin (GM). Three blood culture sets obtained upon admission were positive for S. warneri, with minimal inhibitory concentrations (MICs) of ≤8 μg/mL for ABPC/S, ≤1 μg/mL for GM, and ≤2 μg/mL for cefazolin (CEZ), confirming susceptibility to these agents. The organism was identified as a member of the CoNS family, known for its


A 27-year-old woman with a family history of colorectal cancer (familial adenomatous polyposis) had multiple cancers in her colon and rectum. To treat this, she underwent a complex robotic surgery called robot-assisted total proctocolectomy (TPC), which included removing lymph nodes from the entire colorectal area using the Hugo RAS system. The surgery was done in three main steps: first, the ascending colon was removed along with its surrounding tissue (complete mesocolic excision) while the patient was in a Trendelenburg position; second, the descending colon was removed, and the rectum was fully excised with detailed lymph node removal (D3 dissection); and third, the superior mesenteric artery was ligated to stop blood flow to the colon. After the surgery, the tumor sample was removed through the anus, and a new pouch made from part of the small intestine was created and connected to the anus (ileal pouch-anal anastomosis). The entire procedure took 632 minutes and involved only minimal blood loss. The patient recovered smoothly, started eating liquids on day 1, and returned to a regular diet by day 3. Pathology showed two sigmoid colon cancers and one rectal cancer, with 18 of 89 lymph nodes found to be positive, indicating the cancer had spread to nearby lymph nodes. The cancer stage was classified as pT1bN2b.


A 65-year-old man had a motorcycle accident six months ago, which injured his right middle finger. After the fall, he couldn't fully extend his finger and noticed swelling. Over time, the finger developed a deformity called boutonniere deformity, where the middle joint bends and the tip of the finger extends too far. An X-ray showed no bone damage, so the problem was caused by soft tissue injury — specifically, a tear in the central slip of the finger's extensor tendon.

The doctor repaired the injury by using a part of the ulnar side of the flexor tendon (FDS) to replace the damaged central slip. The surgery was done under anesthesia, with the finger carefully opened and the damaged tissue removed. The new tendon was passed through a small tunnel in the bone and secured with sutures to restore normal movement.

After surgery, the patient wore a splint for two weeks to keep the finger extended. Once the wound healed, he started gentle exercises to improve finger movement. After one month, his middle finger could move from 0 to 100 degrees, and after two months, movement returned to normal (0 to 110 degrees). His hand function improved dramatically, as shown by the DASH score, which went from 50 (indicating poor function) to 4.2 (indicating nearly normal function). He was able to return to work and daily activities with much better finger control.


A 65-year-old male patient presented with a six-month history of swelling and boutonniere deformity involving the right middle finger (digiti III) following a motorcycle accident on January 1, 2023. The initial injury resulted in traumatic disruption of the central slip of the flexor digitorum superficialis (FDS) tendon, leading to impaired extension of the proximal interphalangeal (PIP) joint. The patient initially managed symptoms with analgesics without seeking medical evaluation. Clinical examination revealed persistent edema, active range of motion (ROM) of the PIP joint limited to 45–110 degrees, and passive ROM within normal limits, indicating a soft tissue pathology rather than bony involvement. Radiographic assessment via anteroposterior (AP) and lateral views of the right hand demonstrated no osseous abnormalities, confirming the deformity as originating from a central slip defect.

Surgical intervention was performed via a midlateral incision on the ulnar aspect of the right middle phalanx, centered at the PIP joint, extending dorsally in an oblique fashion. A transverse incision was made proximal to the A1 pulley at the metacarpophalangeal (MCP) joint flexion crease. The ulnar neurovascular bundle was identified and preserved throughout the procedure. The central slip was exposed, and interposed scar tissue and pseudotendinous tissue were excised. Due to the inability to repair the central slip primarily, reconstruction was achieved using the ulnar slip of the FDS tendon.

The extensor tendon was mobilized and tenolyzed, and the dorsal capsule of the PIP joint was incised and debrided. The A3 pulley's periosteal insertion was longitudinally incised, and the volar capsule of the PIP joint was similarly opened. The ulnar slip of the FDS tendon was isolated and transected to release it from its proximal attachment, avoiding entrapment of the radial slip. A 2–0 non-absorbable monofilament suture was placed around the ulnar slip at the PIP joint level and used to release the distal portion of the FDS tendon slip, enabling distal transposition of the ulnar slip. A 2.8-mm drill was used to create a vertically oriented dorsal bone tunnel, positioned posterior to the volar plate. An elevator was placed between the flexor digitorum profundus (FDP) tendon, the volar plate, and the volar base of the middle phalanx to protect adjacent anatomic structures. The FDS tendon slip was passed through the tunnel while maintaining the PIP joint in full extension and reduced position, traversing the intact proximal segment of the central slip and extensor tendon. A pulvertaft weave was completed using a tendon weaver to ensure proper tension and biomechanical stability, with a 3–0 non-absorbable suture securing the weave. The margins of the joint capsule and central slip reconstruction were approximated, and adhesions were released with mobilization of the lateral bands.

Postoperative care included a 4-day follow-up for wound management, with administration of oral meloxicam 7.5 mg twice daily and doxycycline 100 mg twice daily for three days. A second follow-up was conducted three days later. At two weeks postoperatively, the posterior splint was removed, external sutures were discontinued, and both active and passive range of motion exercises were initiated. At three weeks, wound healing was confirmed, and the PIP joint ROM improved to 0–90 degrees. One month postoperatively, ROM reached 0–100 degrees, with significant functional improvement. By seven weeks, the patient achieved full active ROM of 0–110 degrees and returned to work. Functional outcome was assessed using the DASH (Disability of Arm, Shoulder, and Hand) score, which decreased from 50 (indicating moderate disability) to 4.2 (indicating minimal disability), reflecting a substantial restoration of hand function. The surgical reconstruction successfully restored biomechanical alignment, joint stability, and functional capacity of the PIP joint through precise tendon transfer and pulvertaft tenodesis, with no evidence of bony pathology on imaging.


A 23-year-old man came to the emergency room with a sudden, very severe headache that lasted for two hours, along with nausea, vomiting, and a feeling of chest heaviness. He had high blood pressure and a fast breathing rate. An emergency heart test (ECG) showed signs of a heart attack (STEMI), so he was quickly taken to a specialized center for treatment. During the procedure, his coronary arteries were found to be normal, meaning there was no blockage. However, a brain scan (CT) later revealed a cisternal subarachnoid hemorrhage (SAH), which is bleeding in the space around the brain. This condition was likely the cause of his symptoms. Despite being treated with medications, monitored closely, and given supportive care, his condition worsened rapidly. He suffered a cardiac arrest and could not be revived. He died after seven days in the intensive care unit.


A 23-year-old man came to the hospital with a sudden, very bad headache that lasted two hours. He also had nausea, vomiting, and felt like his chest was heavy. His blood pressure was very high, and he was breathing fast. An emergency heart test showed a sign of a heart attack, so they rushed him to get treated. But when they looked at his heart tubes, they found no blockage — the heart was fine. Instead, a brain scan showed bleeding around the brain, which can be deadly. Even with doctors working together to help, his condition got worse quickly. He had a heart stoppage and couldn't be saved. He passed away.