A 38-year-old woman had a weak heart since she was 17, after a bad throat infection that might have hurt her heart muscle. Her heart couldn’t pump blood well, and she was in serious danger. She stayed in the hospital for 10 months and got treatment to help her heart work better, including medicines to stop her heart from beating too fast and to reduce fluid buildup. After a while, her heart started to get stronger and stayed that way for 4 years. Then it got worse again for 2 years, but later she got stable again. She had a baby the first time, and her heart stayed strong. During her second pregnancy, in the second trimester, her heart weakened again and stayed weak for a few months. But now, in May 2017, she is doing fine. She takes medicines every day — for her heart, to control fluid, and to keep her heart steady. She can do normal daily activities, has two children, and doesn’t work. Her doctor says her heart is stable and she doesn’t need a special heart device. She just needs to keep taking her medicines, watch her fluid intake, stay healthy, and go to check-ups regularly.


A 27-year-old man broke his right thigh bone after a small fall, where his hip twisted. He had a bone problem called fibrous dysplasia in his thigh years ago, which was fixed with surgery and bone graft 20 years ago. The old surgery part was removed a year later. This time, because the bone broke again, doctors took out a big piece of the upper thigh bone and replaced it with a hip implant. They also took a small tissue sample to make sure it was the same bone problem from when he was a child. Now, he can walk and do light activities, though he still has some pain when walking long distances. He’s doing well and feels happy with how his hip is working.


A 27-year-old man came to the emergency department with a broken right femur, specifically at the base of the neck, after a fall that involved pressure and twisting of the hip. The fracture was classified as a serious type (Garden II, Pauwells III, AO 31B2.3r) and occurred despite a low-energy injury. He had a history of fibrous dysplasia — a bone condition — in his right hip area, which was treated 20 years ago with surgery to remove abnormal bone (curettage), bone grafting, and the use of a metal fixation device. This device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia. Because of the nature of the fracture and the underlying disease, doctors decided on a wide removal of the upper part of the femur and a total hip replacement using a modular prosthesis, along with a biopsy to confirm it was the same fibrous dysplasia from his childhood. The surgery was successful, and the patient is now stable, walking with support and able to do daily activities. He still has some walking limitations due to a scar in the gluteal muscle, but he enjoys low-impact activities like walking and is very satisfied with his recovery.


A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT), then a transplant from a donor using cord blood (allogeneic CBT). After the transplant, he developed symptoms of a respiratory infection about a month before, including upper respiratory issues, and tested positive for RSV (a common virus that causes colds in children). On day 194, he started having severe breathing difficulties and was admitted to the hospital. Tests showed signs of lung damage, including inflammation and scarring in the small blood vessels of the lungs, which led to a diagnosis of PVOD (a condition where the lungs become stiff and hard to breathe). Pathology from a lung biopsy showed both signs of past viral infection and the lung injury linked to PVOD. The doctors believe that the RSV infection may have triggered or worsened the development of PVOD in this child.


A 65-year-old man started feeling a bad cough, short of breath even doing small things, and lost 10 kilograms in 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked at under a microscope. The cells were large and spread out, with lots of immune cells around them. This type of cancer is rare and not like regular lung cancer. The cancer cells had markers that match a specific kind of cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). It had a very high level of a protein called PD-L1 and was found to have Epstein-Barr virus. He got 6 rounds of chemo using platinum and durvalumab, but the cancer grew worse. He had side effects like hearing loss and kidney problems, so the chemo was changed. After 9 months, he died from not being able to breathe.


A 13-year-old boy found a lump in his groin that could be moved, but wasn't painful or red. No other symptoms were present. Doctors removed the lump to make sure it wasn't cancer or a serious disease. The test results showed the lump was made of special cells called plasma cells, which is a rare kind of disease in kids. This is the first time such a case has been found in the groin area. After 1 year of checking, no new lumps or symptoms came back. The boy is doing fine and has no other problems.


The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria included a clinical diagnosis of myotonia accompanied by a warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as a molecular diagnosis involving mutations in the CLCN1 gene. Demographic data (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical progression), family history, and response to therapeutic interventions were systematically extracted from the electronic medical records. All patients underwent comprehensive clinical evaluation, including laboratory testing and EMG assessment.

Five patients with a clinical diagnosis of congenital myotonia were identified: three with Becker disease and two with Thomsen disease. The estimated incidence per 10,000 live births was 1:15,000 for the Becker phenotype and 1:21,000 for the Thomsen phenotype. The majority of patients were female; the only male patient presented with onset prior to age six. Initial clinical manifestations included lower-limb myotonia in four patients and upper-limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except in one case where the family declined testing. All patients exhibited worsening of myotonia with exposure to cold, with the warm-up phenomenon—defined as improvement of muscle tone following prolonged rest—observed exclusively in those with the Becker phenotype.

Patients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, with no clinical manifestations in their parents, suggesting an autosomal recessive inheritance pattern. The mother of patient 1 exhibited mild, cold-exacerbated myotonia, raising the possibility of subclinical carrier status. The patient who declined genetic testing had a reported history of myotonia in the maternal lineage, consistent with an inherited predisposition.

Serum creatine kinase levels were not elevated in any of the patients, indicating that skeletal muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (at 2.8/12 years of age); subsequent EMG studies were not repeated due to clinical stability and the established diagnostic certainty. The absence of significant muscle enzyme elevation supports the notion that the pathophysiology is primarily due to impaired chloride channel function rather than active muscle degeneration.

Initial pharmacological management primarily involved oxcarbazepine, particularly in patients with the recessive form (Becker disease), with generally favorable responses. However, in patient 2, oxcarbazepine lost efficacy over time, prompting the initiation of mexiletine. Patient 4 required multiple medications, all of which failed due to either therapeutic resistance or adverse effects. Patient 5, who had a mild clinical presentation, declined treatment. Patient 1 was found to carry a previously undescribed, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from his mother. Cases 1 to 3 exhibited the Becker phenotype and displayed composite heterozygosity, involving two distinct CLCN1 mutations. Cases 4 and 5 presented with the Thomsen phenotype, characterized by a more severe, early-onset form of myotonia. Patient 5 declined genetic testing, limiting the ability to confirm the specific inheritance pattern in this individual. The CLCN1 gene encodes the chloride channel subunit responsible for regulating membrane potential in skeletal muscle fibers; mutations in this gene lead to reduced chloride conductance, resulting in prolonged depolarization of the sarcolemma and subsequent muscle hyperexcitability, which manifests clinically as myotonia. This mechanism underlies the pathophysiology of both Becker and Thomsen congenital myotonias, with differences in severity and age of onset likely attributable to the nature and combination of mutations, including the novel c.824T>C variant identified in this cohort.


A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called AVMs, which didn’t go away even after treatment. Recently, she started feeling very tired and short of breath, which means her heart was struggling. Doctors found her heart was enlarged and not working well, and her leg swelling was getting worse. The problem was caused by a rare birth defect in her leg’s blood vessels that was sending too much blood to her heart. To fix it, doctors first placed a special stent in her leg to block the bad blood flow. This helped her heart feel better. After that, they did a second treatment to stop the blood from flowing into the wrong veins. After the treatments, her leg swelling went down and her heart started working better. She’s now much stronger and her symptoms are much better.


A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils did not stop the swelling. Over the past month, she developed symptoms of heart failure, including fatigue and shortness of breath, and was taken to a hospital for further care. Tests showed her heart was enlarged and her heart function had worsened, with high levels of a heart failure marker (BNP). She also had poor blood flow in her leg arteries and no pulses in her lower leg. Imaging revealed a large AVM in the femoral and superficial femoral arteries, along with a swollen femoral artery and vein, which was likely causing the heart to work harder.

Because the AVM was too complex to be fully treated with coils alone, doctors used a covered stent placed in the femoral artery to block part of the abnormal blood flow. This helped reduce the amount of blood flowing into the leg, which in turn improved her heart failure symptoms. The surgery was done under general anesthesia using a catheter inserted through the leg, and the stent was placed exactly where the AVM was most active. After the procedure, her leg swelling and heart function improved significantly. One week later, blood flow in the leg dropped from 3400 ml/min to 1600 ml/min, and her BNP levels dropped, showing better heart health.

In a follow-up treatment, doctors used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels were much lower. The patient is now doing better, with improved daily function and reduced symptoms of heart failure. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs that cause heart failure.


{
  "proficient_health_literacy": "A 67-year-old female patient with a six-year history of progressive left lower limb edema was diagnosed with complex congenital arteriovenous malformations (AVMs) in the lower extremity, following a prior embolization intervention involving two coils (20 mm × 40 cm, BSX, USA) one year prior. Despite this, her lower limb swelling remained unresponsive, and she developed symptomatic acute heart failure characterized by progressive fatigue, dyspnea, and cardiac dysfunction. She was referred to Chengdu University of Traditional Chinese Medicine Hospital for comprehensive evaluation. The patient had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported lifelong oral estrogen use for menopausal symptoms. Physical examination revealed severe edema, skin sclerosis, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and markedly elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) and left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary pathology. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, marked dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex AVMs involving both the SFA and profunda femoris artery. The femoral and superficial veins were significantly dilated during arterial phase imaging, with non-visualization of the popliteal and anterior tibial arteries. The patient was diagnosed with complex congenital lower limb AVMs, acute decompensated chronic heart failure, and classified as New York Heart Association (NYHA) Class IV. Preoperative CFA flow volume was measured at 3400 ml/min. Given the persistence of high shunt flow and inadequate response to coil embolization, a covered stent graft was deemed necessary to reduce venous shunting and alleviate hemodynamic burden on the heart. Access was achieved via antegrade surgical puncture of the right CFA using a 14 F (Cook Medical, USA) catheter sheath under general anesthesia. A 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China) was selected based on preoperative CTA measurements showing a middle SFA diameter of 19 mm. A 0.035 guidewire and single-curve catheter were used to navigate to the popliteal artery, followed by transition to a 0.035 super-hard guidewire for stable catheterization during stent deployment. The stent was placed at the distal SFA, where AVM burden was highest. Completion angiography demonstrated marked reduction in venous opacification and restoration of arterial visualization, including the popliteal artery. Postoperatively, the left femoral artery was closed with a 6–0 vascular risk suture. The procedure was performed with minimal duration to avoid exacerbating cardiac stress in the setting of acute heart failure. One week postoperatively, CFA flow decreased to 1600 ml/min, and BNP levels dropped to 1198 ng/L, indicating early improvement in cardiac function. A second-stage embolization was planned to target the nidus of the AVM. Under ultrasound guidance, the draining venous system was punctured via the right CFA, with a 5 F vascular sheath introduced. Contrast injection confirmed the presence of the AVM nidus and its draining veins. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL). Completion angiography showed near-complete obliteration of the AVM nidus and draining venous pathways. At one-year follow-up, the CFA flow reduced to 780 ml/min, echocardiography revealed mild atrial enlargement, minor mitral and tricuspid regurgitation, and an improved left ventricular ejection fraction (LVEF) of 71%, with BNP levels significantly reduced. This case illustrates the clinical utility of staged intervention—initial covered stent graft placement to reduce shunt volume and stabilize hemodynamics, followed by targeted embolization to achieve complete nidus occlusion in complex congenital lower


A 28-year-old man developed two red bumps on his right arm and forearm, with small blisters and sores in the middle, after being on vacation in coastal Ecuador. The area felt hot and itched a lot, but he didn’t have fever or other symptoms. Doctors took a small skin sample and saw signs of irritation and inflammation. Because of the location and his trip to a tropical area, they figured out it was caused by a bug called Paederus. He was treated with anti-itch medicine, creams to calm the skin, and cold compresses. After 8 days, the sores went away, but the skin stayed a bit darker in those areas.


A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration situated on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, with no systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key environmental exposure factor. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, along with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending through the superficial, middle, and deep dermis. These findings reflect a type IV hypersensitivity reaction mediated by T-helper 1 (Th1) cells, driven by exposure to Paederus beetles (Paederus fuscipes or Paederus spp.), whose defensive secretions contain cytotoxic compounds such as pederin and other sesquiterpene lactones that induce direct epidermal damage and immune activation. The diagnosis was confirmed based on the clinical presentation, geographic exposure context, and histopathological correlation. Management consisted of antihistamines to mitigate pruritus and histamine-mediated inflammation, topical corticosteroids to suppress dermal immune cell activity and reduce epidermal hyperplasia, and cold compresses to alleviate vascular congestion and symptomatic discomfort. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a consequence of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering endemic arthropod exposures in tropical regions when evaluating acute, localized, non-infectious dermatoses with a characteristic vesiculobullous and ulcerative pattern in flexural skin folds.


A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed, so they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through his vein 24 hours earlier. During the procedure, a doctor used a tube to look inside the bile duct and guided a light tool through it to shine on the blocked area. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, the doctor checked the bile duct again to make sure everything was okay. The treatment worked well at first — he didn’t feel sick for three months. But later, the blockage came back, and he had infections and other problems. He died 15 months after the treatment because of cancer spreading to his lungs.


The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with choledocholithiasis, confirmed by endoscopic retrograde cholangiopancreatography (ERCP), which failed to extract stones due to disproportionate ductal dilation. A plastic biliary stent was placed initially, resulting in transient improvement, but cholestasis recurred at 45 days, with two subsequent ERCP attempts also failing. During the third ERCP, a long, irregular stenosis of the common hepatic duct was identified, and EUS revealed a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm compressing the common hepatic duct, with evidence of involvement of the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative photodynamic therapy (PDT).

The PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) 24 hours prior to intervention. Photogen® is a porphyrin derivative with peak light absorption at 630 nm, enabling selective activation within tumor tissue upon illumination. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla, followed by retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct to directly visualize the stenotic segment. Neoplastic stenosis was identified via cholangioscopic examination. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. This catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter guidance; the third port serves as an injection port for photosensitizer delivery. The illumination was administered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the obstructed area. The procedure lasted 150 minutes and concluded with a final cholangioscopic evaluation to assess immediate outcomes and detect adverse events. A 10 Fr plastic biliary stent was placed at the end of the session due to unavailability of a self-expanding metal stent.

Post-procedure, the patient was maintained on a fasted state for 24 hours, with oral diet initiated if no adverse events were observed. Strict photoprotection measures were enforced, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT, to mitigate photosensitivity risk. The patient exhibited no signs of photosensitivity within the first week. However, early recurrence of cholestasis occurred, complicated by cholangitis. ERCP revealed stent obstruction due to biliary sludge and tumor necrotic debris. A biliary scan followed by re-drainage resolved the acute episode. The patient remained asymptomatic for three months, the longest period since disease onset. Subsequent recurrence was managed with a self-expanding metal stent, and systemic oncologic therapy was continued. Eventually, the patient developed dysphagia, requiring placement of a duodenal stent for palliative relief. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no intra-procedural complications, and the clinical benefit was sustained for a significant duration despite the underlying malignancy progression.


A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), along with anaemia (haemoglobin: 9.6 g/dL), suggesting upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steeply flexed third part of the duodenum on the right side of the aorta, running caudally without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents consistent with a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, wherein forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—particularly its steep rightward flexion and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.

Initial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT performed seven days later showed spontaneous resolution of this rightward deviation, indicating a non-malrotational etiology. The patient was discharged after this transient finding. Subsequently, two months later, she presented with a recurrent episode of haematemesis. Dynamic CT revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent gastric cardial laceration, consistent with Mallory-Weiss syndrome.

A follow-up non-contrast CT two months after the second haematemesis revealed no persistent duodenal deviation, but demonstrated oedematous wall thickening in the second part of the duodenum. Without prior imaging, this would have been interpreted as duodenitis; however, the clinical context of repeated, spontaneous right-sided deviations of the duodenal-jejunal junction and jejunum—despite their eventual resolution—led to the diagnosis of dysplasia of the ligament of Treitz. This condition is characterized by an abnormal, redundant, or poorly anchored ligament of Treitz, which normally anchors the duodenojejunal junction to the retroperitoneum and stabilizes the small intestine. In this case, the ligament of Treitz was anatomically formed but exhibited incomplete fixation to the upper jejunum, with attachment limited to the duodenum and absence of retroperitoneal anchoring. This results in a fulcrum-like mechanism allowing the jejunum to fold or deviate freely, particularly during increased intra-abdominal pressure (e.g., from vomiting), thereby reproducing transient right-sided displacement of the duodenum and jejunum.

Laparotomy was performed, which confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The ligament of Treitz was present and formed, but its fixation to the upper jejunum was incomplete, with only partial attachment to the duodenum and no secure retroperitoneal anchoring. The duodenal-jejunal junction was not fixed to the retroperitoneum, allowing for dynamic mobility. Surgically, the upper jejunum was secured with four sutures to the retroperitoneum on the left side to stabilize the anatomical relationship. The postoperative course was uncomplicated, and the patient has remained asymptomatic with no further episodes of haematemesis. The transient, spontaneous rightward deviations observed on CT imaging are attributable to the mechanical instability of the ligament of Treitz, rather than true malrotation, supporting the diagnosis of dysplasia of the ligament of Treitz as the underlying pathophysiological mechanism.


A 28-year-old man from Morocco had pain in his belly, especially on the right side, and had a fever, chills, and lost weight over a month. He didn’t drink or smoke, and had been vaccinated for tuberculosis. His doctor found a swollen liver with small spots on it that looked like signs of infection. Tests showed these spots were likely caused by tuberculosis, not cancer or another disease. A small surgery was done to take a piece of the liver for testing, and the result confirmed it was tuberculosis. He started taking medicine to fight the tuberculosis, and within days, his fever and pain went away. After three months, the spots on his liver got smaller and fewer. He’s getting better.


A 28-year-old Moroccan man with no smoking or drinking habits was admitted to the hospital after experiencing abdominal pain for about a month, along with fever, chills, sweating, loss of appetite, and a 6-kilogram weight loss. The pain was mainly in the upper right part of his abdomen, and he had been experiencing digestive issues like alternating diarrhea and constipation. Initially, his symptoms were mild, but they worsened over time, leading to a significant weight loss of 12 kilograms over three months.

Physical exams showed signs of inflammation, including a high fever and fast heart rate. Blood tests revealed elevated white blood cells and inflammation markers, but no evidence of liver damage or viral hepatitis was found. Imaging scans showed multiple small nodules in the liver that were not enhancing after contrast was given. These nodules were most noticeable in two areas of the liver.

Although initial tests for tuberculosis (TB) and other infections were negative, the liver biopsies taken during a laparoscopic procedure showed characteristic signs of tuberculosis, including granulomas with caseous necrosis — a hallmark of TB infection. This confirmed a diagnosis of focal liver tuberculosis.

The patient was started on standard anti-tuberculosis medication, which includes four drugs for the first two months, followed by two drugs for the next four months. After starting treatment, his symptoms improved quickly. His fever and inflammation went away, and follow-up scans after three months showed that the liver nodules had shrunk in number and size. The overall clinical and lab results improved significantly, indicating a good response to treatment.


A 28-year-old male, single, without children, active military personnel, presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peak 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss. No history of alcohol use, tobacco consumption, or significant comorbidities was reported; he had received BCG vaccination and no positive family or personal history of infectious or hepatic disease. Physical examination revealed an asthenic patient with hepatomegaly and moderate right hypochondrial tenderness, consistent with a systemic inflammatory response syndrome (SIRS): tachycardia (124 bpm), tachypnea (22 breaths/min), and elevated body temperature. Laboratory findings included neutrophilic leukocytosis (17,800 cells/mm³), markedly elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), suggesting a bacterial or infectious etiology. Hepatic function tests were within normal limits: ALT 22 IU/L (normal <40 IU/L), AST 17 IU/L (<35 IU/L), GGT 42 IU/L (<50 IU/L), alkaline phosphatase 115 IU/L (normal 40–150 IU/L), bilirubin normal, prothrombin time 78%, and albumin 39 g/L. Renal function and electrolyte balance were unremarkable. Imaging studies, including chest radiography and abdominal ultrasound, were non-contributory. Blood and urine cultures, performed during febrile peaks, were negative. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. GeneXpert testing for Mycobacterium tuberculosis in respiratory specimens and biopsy samples was negative; quantiferon tuberculin test was also negative, excluding latent tuberculosis infection. A thoraco-abdomino-pelvic CT scan revealed an enlarged liver (17 cm), with multiple well-defined, rounded hypodense lesions, non-enhancing after contrast administration, primarily in segments I (21×16 mm) and V (36×27 mm). Echo-guided liver biopsy demonstrated subacute fibro-inflammatory changes with no evidence of malignancy or viral hepatitis. Hepatic MRI further characterized the lesions as dysmorphic, with heterogeneous T2 signal intensity, hyperintense perilesional rims on T2, peripheral enhancement post-contrast, and largest lesions in segments I (20×22 mm) and V (33×31 mm). No deep lymphadenopathy was observed. Diagnostic laparoscopy was performed to obtain biopsy specimens from hepatic nodules, which showed histologically confirmed epithelioid and gigantocellular granulomas with caseous necrosis—pathological findings consistent with focal hepatic tuberculosis. The patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy (isoniazid, rifampicin, pyrazinamide, ethambutol) administered orally in the morning on an empty stomach, followed by Phase 2 (4 months) of bithiapine (isoniazid and rifampicin) with identical dosing regimen. Clinical and biological response was observed within days of therapy initiation, with resolution of fever, chills, and systemic inflammatory markers. At three months post-treatment, follow-up imaging demonstrated a significant reduction in both the number and volume of hepatic lesions, supporting a favorable clinical course. This case represents a rare presentation of focal hepatic tuberculosis in a young, previously healthy individual, with non-specific initial symptoms and imaging findings, underscoring the importance of considering tuberculous hepatopathy in patients with chronic abdominal pain, unexplained weight loss, and persistent low-grade fever despite negative standard infectious workups.


A 12-year-old boy with Down Syndrome and trouble moving his arms and legs had a sore spot on the inside of his tongue. The sore spot was about 1 cm wide, hard around the edge, and had a white-yellow color. His lips were dry and cracked. He had sharp teeth, especially one tooth on the side of his tongue, which kept rubbing against it and caused the soreness. This soreness looked like a serious mouth cancer, but doctors said it was just from long-term rubbing, not cancer. The doctors treated it with salt water, iodine rinse, and lip cream to heal and protect the area. His mom was told to clean his mouth with salt water, use iodine three times a day on the sore spot, and apply lip cream to keep his lips soft. Some of his teeth were broken or gone, so they were taken out and a device was put in to keep space. The boy got better over time, but later had surgery on his neck due to spine problems. After that, he had breathing trouble and passed away.


{
  "proficient_health_literacy": "A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes bilateral lower extremity and upper limb weakness, with a prior fall approximately one year prior, leading to hospital admission. His mother reported inconsistent oral hygiene practices, contributing to chronic oral mucosal exposure to trauma and infection. The patient was diagnosed with Down Syndrome, a genetic disorder caused by trisomy 21, and myeloradiculopathy, a neurological condition involving degeneration of spinal nerve roots, likely due to congenital or progressive cervical spinal cord compression.\n\nExtraorally, the patient exhibited dysmorphic facial features consistent with Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to impaired lip lubrication, reduced mucosal integrity, and altered keratinization. Lymph node assessment was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\n\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignant neoplasm of the oral epithelium, due to its well-defined, chronic, non-healing appearance. However, histopathological confirmation was not performed, and the diagnosis of chronic traumatic ulcer was established based on clinical correlation with the patient's occlusal trauma and history of dental malocclusion. The 55 tooth, which was sharp and malpositioned, was identified as the primary source of occlusal trauma, leading to direct mechanical injury to the tongue's lateral border. Additionally, the patient had dentinal caries on tooth 63, reversible pulpitis in 63, and radix gangrene (necrotic root apex) in teeth 55, 62, 74, and 85, indicating advanced dental pathology and potential bacterial invasion.\n\nRadiographic and imaging evaluation revealed cervical spine dislocation, confirmed by MRI, which is a known complication in patients with Down Syndrome and myeloradiculopathy, often resulting from developmental anomalies of the cervical vertebrae and ligamentous laxity. This structural abnormality may contribute to neurogenic weakness and impaired motor function. Laboratory findings included hyponatremia (sodium level: 130 mEq/L), likely secondary to impaired renal sodium reabsorption or SIADH (syndrome of inappropriate antidiuretic hormone secretion), and lymphocytosis (lymphocyte percentage: 46%), which may reflect a chronic inflammatory or immune-mediated state.\n\nThe patient was managed with a multimodal approach: systemic therapy including paracetamol 120 mg/5 mL oral suspension for pain control and amoxicillin 125 mg/5 mL oral suspension for potential bacterial superinfection; local therapy with 0.9% sodium chloride solution for oral rinsing, 1% povidone-iodine mouthwash applied three times daily for antiseptic and anti-inflammatory effects, and petroleum jelly applied to the lips to address desiccation and promote mucosal hydration. The patient's mother was instructed to perform daily oral care using gauze saturated with 0.9% NaCl, apply povidone-iodine to the ulcer site three times daily, and use petroleum jelly for lip protection.\n\nDental management included extraction of teeth 55, 62, 74, and 85 due to extensive root necrosis and irreversible pulpitis, with a space maintainer recommended to preserve arch alignment and prevent malocclusion progression. The diagnosis of the oral lesion was confirmed as a chronic traumatic ulcer, not malignancy, based on clinical features, absence of malignant histopathology, and temporal correlation with occlusal trauma.\n\nClinical follow-up showed progressive improvement: at the second visit (3 days post-intervention), the oral lesion showed early signs of healing; at the third visit (1 week), the ulcer size decreased and lip lesions improved; at the fourth visit (10 days), significant ulcer healing was observed. Two days after the fourth visit, the patient underwent neurosurgical intervention to correct the cervical spine dislocation. Postoperative care was provided in the Pediatric Intensive Care Unit (PICU), where the patient developed respiratory failure due to postoperative complications, including possible aspiration, airway compromise, or neurogenic pulmonary edema, and was declared dead two weeks after surgery. This outcome underscores the high morbidity associated with cervical spine instability in pediatric patients with Down Syndrome and associated neurological impair


A 59-year-old woman had blurry vision in both eyes for a few weeks. She had multiple sclerosis and was taking medicine for seizures, including levetiracetam. Soon after starting levetiracetam, her vision got worse. Doctors found her corneas were swollen, which can happen when eyes get too full of fluid. When they slowly cut back on levetiracetam, her vision started to get better. After stopping the medicine completely, her vision returned to normal and her corneas stopped being swollen. Six months later, the swelling was gone and her eyes looked healthy again. After 13 months, her vision stayed the same and no changes were seen.


A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with corneal topography. This swelling was linked to the start of levetiracetam use. After reducing the dose of levetiracetam, her vision began to improve and eventually returned to normal. When the medication was stopped completely, the corneal swelling went away and her vision stabilized. Follow-up tests six months later showed no signs of swelling or vision problems. The doctors made a provisional diagnosis of levetiracetam-induced corneal edema. Her vision has remained stable since then, with no further changes after 13 months.


A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal dystrophies, and previous ocular examinations had been unremarkable for signs of Fuchs' endothelial corneal dystrophy. Her medication history included long-term amantadine therapy (100 mg twice daily for 7 years), which is a known cause of corneal edema due to its effect on corneal endothelial cell function, particularly through inhibition of Na⁺/K⁺-ATPase and disruption of ion homeostasis in the endothelium. She was initiated on levetiracetam (250 mg twice daily) as an adjunctive antiepileptic agent for breakthrough seizure activity. Within weeks of starting levetiracetam, she developed progressive bilateral visual deterioration.

Ophthalmic examination revealed best-corrected visual acuity of 0.5 logMAR in both eyes. Slit-lamp biomicroscopy demonstrated bilateral corneal edema with normal anterior chamber and absence of uveitis. Intraocular pressures were 16 mmHg (right) and 18 mmHg (left), within normal limits. Corneal topography confirmed significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with epithelial and stromal fluid accumulation due to impaired corneal endothelial pump function.

Given the established association between amantadine and corneal edema, the patient and her neurologist agreed to discontinue amantadine and switch to lamotrigine, with levetiracetam continued at the same dose. No improvement in visual acuity was observed after two months, suggesting that the corneal edema was not solely attributable to amantadine withdrawal. The patient then requested a trial discontinuation of levetiracetam due to the temporal correlation between the initiation of levetiracetam and the onset of visual symptoms.

Levetiracetam was tapered over several days, and within a few days of dose reduction, visual symptoms began to improve. Upon complete cessation of levetiracetam, vision stabilized and corneal edema resolved. Follow-up corneal topography six months later demonstrated normalization of central corneal thickness to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR in both eyes. Slit-lamp examination confirmed a clear cornea without corneal guttata, indicating resolution of endothelial dysfunction and fluid accumulation.

At a 13-month follow-up, the patient remained stable on amantadine and lamotrigine, with no further changes in medication or ocular findings. Visual acuity remained at 0.2 logMAR bilaterally, and repeat corneal topography showed no progression of corneal thickening. This case supports the hypothesis that levetiracetam may induce corneal edema via endothelial dysfunction, possibly through interference with endothelial cell metabolism, membrane integrity, or ion transport mechanisms, particularly in the context of preexisting neurodegenerative disease and altered neurovascular coupling. While no direct evidence of levetiracetam’s mechanism in corneal endothelium is established, the temporal association, clinical course, and resolution upon discontinuation strongly suggest a causal relationship. This represents a rare but clinically significant adverse effect of levetiracetam, particularly in patients with underlying neurological conditions involving chronic neuroinflammation or altered cellular homeostasis.


A 77-year-old man had a seizure at home and fell, causing both hips to pop out of place. He was rushed to the hospital, where doctors found broken bones in his pelvis and both femur heads sticking out. His legs were shorter and twisted, and he couldn’t move them well. He was given fluids and blood to stabilize, and a special brace was used to keep the bones in place. After a few days, doctors did surgery in two steps: first on the left hip, then the right hip, seven days apart. In both surgeries, they fixed the broken hip socket with a ring that holds it in place and replaced the ball of the hip with a new joint that lets it move freely. The new parts were not glued in, so they needed time to settle. The patient had no problems after surgery and was able to walk with a walking stick after six weeks. At one year, he could do all normal activities, had no pain or falls, and his hips were working well. He still has a slight limp on the right side, but everything else is fine.


{
  "proficient_health_literacy": "A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The activation of a polytrauma protocol was driven by hemodynamic instability, not by the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to assess for intra-abdominal pathology, and a 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally to maintain reduction, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow for fibrovascular consolidation at the fracture sites and to minimize intraoperative bleeding. The procedure was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for anticoagulation. The left hemipelvis was operated on first due to greater pelvic protrusion and higher risk of soft tissue hematoma formation during femoral head extraction, which could lead to vascular injury or excessive bleeding. The patient was placed in lateral decubitus position and underwent a posterior-lateral approach with Moore's autograft placement at the acetabular fracture focus. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Gluteal musculature (gluteus minimus and medius) was dissected to facilitate accurate femoral head positioning. The ring was verified under endoscopic control. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsular and pelvic musculature closure was achieved using transosseous trochanteric fixation points. The right hemipelvis was operated on seven days later. A first window of the ilio-inguinal approach was utilized to address the longitudinal iliac wing fracture, which was stabilized with a six-hole anatomical plate. The same surgical protocol was repeated: anti-protrusion ring implantation, double-mobility cemented acetabular ring, and non-cemented femoral stem placement. Anti-protrusion rings are indicated in acetabular fractures classified as type IV by the American Academy of Orthopaedic Surgeons (AAOS), where there is disruption of the acetabular background and risk of pelvic disjunction, requiring bony anchorage at the ischium and ilium. They are contraindicated in isolated anterior or posterior wall fractures without acetabular body involvement. The patient remained in bed during admission and was mobilized to prevent pressure ulcer formation. After tolerating the second surgery, he began wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with loading initiated only at six weeks using a walking stick. Delayed loading was implemented due to the need for initial graft consolidation in the acetabular background to provide biomechanical support for the anti-protrusion ring, and due to bilateral involvement, which precluded safe partial loading without a stable, healthy hip to serve as a functional baseline. At 12-month follow-up, the patient achieved full weight-bearing with a walking stick, with Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12. No postoperative complications have been reported. Clinically, the patient is satisfied, reporting occasional discomfort and a mild right-sided limp. Full range of motion is preserved, and no episodes of hip instability have occurred since surgery. The surgical strategy reflects a biomechanically sound approach to managing


A 19-month-old boy fell from a highchair and hit his head. He was acting irritable, vomiting, and had trouble breathing. His breathing was fast and his oxygen levels were very low. When doctors checked him, they saw he was struggling to breathe on his left side. They gave him a tube to help him breathe, but his oxygen kept dropping. Tests showed his left lung was completely collapsed, and there was a blockage in the main airway. A scan found a small piece of almond stuck in the airway, about 2 cm big. The boy had never eaten almonds before and probably swallowed it by accident. After the piece was removed, his breathing got better, and he was able to breathe on his own within 24 hours. He was then taken out of the hospital and sent to a regular pediatric ward to recover.


A 19-month-old male was admitted to the Emergency Department following a fall from a highchair, during which he initially landed on his gluteal region and subsequently experienced a blunt head impact to the occiput. The child presented without prior warning signs or symptoms, and upon arrival, exhibited three episodes of vomiting and marked irritability. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and decreased breath sounds localized to the left basal lung zone. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to oxygen, but despite this intervention, oxygen saturation progressively declined below 70%, indicating worsening hypoxemia. The clinical course suggested a severe impairment in gas exchange, prompting the decision for orotracheal intubation with a cuffed endotracheal tube to secure the airway. Post-intubation, the patient's respiratory status stabilized. Chest computed tomography (CT) revealed complete atelectasis of the left lung, with a discrete abrupt interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation, consistent with a foreign body obstruction. The clinical presentation, including the acute onset of severe respiratory distress following a minor trauma, and the history of a prior, self-limiting cough episode in the days preceding the event, led to a high clinical suspicion of foreign body aspiration (FBA). Rigid bronchoscopy was performed, which identified a 2 cm diameter almond lodged in the proximal left main bronchus. The foreign body was successfully removed. Notably, the patient had no prior exposure to nuts or almonds, and the ingestion was accidental. Post-removal, the child demonstrated a progressive clinical recovery, with oxygenation improving steadily. After 24 hours of intensive care, the patient was extubated and transferred to the general pediatrics ward, where he achieved full respiratory function recovery over several days. The radiological and bronchoscopic findings, combined with the clinical trajectory, support the diagnosis of acute left main bronchial obstruction due to accidental almond aspiration, with the respiratory failure secondary to impaired ventilation and alveolar collapse, likely exacerbated by the altered state of consciousness induced by head trauma. The mechanism of respiratory compromise involved obstructive atelectasis, leading to reduced lung compliance and ventilation-perfusion mismatch, which were confirmed by lung ultrasound showing absent A lines and solid, consolidated parenchymal patterns. This case underscores the importance of considering foreign body aspiration in pediatric patients presenting with acute respiratory distress, particularly when there is a history of sudden-onset cough or no prior risk factors, even in the absence of overt aspiration signs.


{
  "proficient_health_literacy": "A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axillary region. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who was receiving pharmacological therapy. The infant had normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother resided in a prison cell with the infant and two other individuals, in a crowded environment. At 4 months of age, the infant was evaluated for the axillary mass; a chest X-ray revealed suggestive rib fractures, leading to suspicion of child abuse and hospitalization. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized swelling, erythema, warmth, and pain in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography demonstrated an axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological examination of the axillary abscess revealed myositis and suppurative panniculitis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for Mycobacterium tuberculosis complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. Two months later, at 8 months of age, the infant was readmitted with fever, irritability, and progression of the suppurative process to the left scapula. Repeat laboratory evaluation showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula connecting the scapular abscess to the underlying tissue. The infant was initially treated with piperacillin-tazobactam, which was later replaced with voriconazole after isolation of Aspergillus fumigatus from secretion culture. Given the recurrent, severe, and progressive nature of the infections, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and flow cytometric analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the CYBB gene, c.80_83del/Y (p.Val27Glyfs*33), resulting in a frameshift mutation and premature termination of the gp91phox protein. The mother was found to be a heterozygous carrier (c.80_83del/WT) of this variant, consistent with X-linked recessive inheritance. The two older male siblings, who appeared clinically healthy, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis and weekly fluconazole for antifungal proph


{
  "proficient_health_literacy": "A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral ulcers affecting the upper and lower labial mucosa, exacerbated by eating and speech. The lesions initially appeared as canker sores four days prior to presentation, with subsequent extension to the lips two days later. The patient initially attempted self-treatment with petroleum jelly, which provided no symptomatic relief. He subsequently applied triamcinolone acetonide 0.1% in orabase ointment once daily, which resulted in partial improvement but incomplete healing of the lesions.\n\nThe patient reported a preceding one-week history of fever, with no cutaneous or systemic lesions elsewhere. He described a prolonged period of suboptimal nutritional intake—approximately one and a half months—due to high work-related stress. There was no history of medical comorbidities, food allergies, medication use, alcohol consumption, or tobacco use. However, a chronic habit of lip-licking was noted. The patient had a documented history of varicella (chickenpox) in childhood, which is clinically relevant given the role of herpes simplex virus type 1 (HSV-1) in mucocutaneous infections.\n\nOn general examination, vital signs were within normal limits, with no lymphadenopathy. Extra-oral examination revealed serosanguineous crusts on the lips that were tender and prone to bleeding. Intra-oral examination demonstrated diffuse, irregular erythematous lesions with well-defined borders on both upper and lower labial mucosa, consistent with mucosal inflammation. Additional findings included hyperkeratotic white plaques with non-scrapable consistency and irregular borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques on one-third of the posterior dorsal tongue, and shallow dental impression indentations on the lateral tongue surfaces without pain. A painless, firm nodule measuring 2×1×0.5 cm was identified in the midline of the hard palate. Dental assessment revealed carious lesions, root caries, and edentulous status in teeth 28, 36, 37, and 46, with evidence of reversible pulpitis in tooth 18 and irreversible pulpitis in tooth 47, as well as chronic apical periodontitis due to root caries in tooth 15. Oral hygiene was suboptimal.\n\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6), suggesting no significant psychiatric comorbidity. Based on clinical presentation and history, the working diagnosis was suspected to be Herpetic Angina of the Mucosa (HAEM), a condition characterized by recurrent or persistent mucocutaneous ulceration associated with HSV-1 infection. Differential diagnosis considered exfoliative cheilitis, which lacks viral etiology and is typically linked to irritant exposure or chemical dermatitis; however, the presence of HSV-1 seropositivity ruled this out.\n\nSerological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (ratio >1.1), confirming prior exposure and active viral involvement. This result, in conjunction with the clinical picture, established a definitive diagnosis of HAEM. The patient’s oral health-related quality of life (OHRQoL) was assessed using the OHIP-14 instrument, with an initial score of 35 (indicating moderate impairment), which improved to 4 (indicating excellent OHRQoL) at the final follow-up.\n\nTherapeutic management included both pharmacological and non-pharmacological interventions. Non-pharmacological measures involved patient education on maintaining rigorous oral hygiene—specifically, brushing teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste—increasing daily water intake to at least two liters, adopting a balanced nutritional diet, and avoiding acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods. The patient was specifically instructed to discontinue lip-licking and lip-peeling behaviors, which are known to exacerbate mucosal trauma and promote viral replication.\n\nPharmacological therapy consisted of topical and systemic agents. Topically, the patient was instructed to apply a thin layer of triamcinolone acetonide 0.1% in orabase three times daily and to compress the lips with gauze soaked in 0.9% NaCl solution at least three times daily to reduce inflammation and promote epithelial healing. Systemically, the patient was prescribed multivitamin supplementation once daily to address potential micronutrient deficiencies, which may contribute to


A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis, but she defaulted treatment for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological deterioration (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly established. Physical examination revealed a large cervical mass measuring 8 × 8 cm, extending into the parametrium and bilateral pelvic sidewalls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch cervical biopsy was performed, and histopathological examination confirmed an extra-nodal Burkitt lymphoma (BL). Immunohistochemical staining was positive for CD20, CD75a, CD10, PAX5, and BCL6, with additional positivity for CD44 and c-Myc. In situ hybridization for Epstein-Barr virus (EBER-ISH) showed focal positivity, consistent with EBV-associated BL. The Ki67 proliferation index was nearly 100%, indicating aggressive tumor cell proliferation, with moderate PAX5 and BCL6 expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), elevated serum creatinine (187 mmol/L), urea (11.1 mmol/L), and reduced albumin (21 g/L), reflecting significant renal and systemic compromise. Aspartate transaminase (41 U/L) and alkaline phosphatase (100 U/L) were within mild upper limits, suggesting minimal hepatic dysfunction. Following histological confirmation, the patient was reviewed at an oncology multidisciplinary team (MDT) meeting, where chemo-radiation therapy was recommended as the standard of care for stage 3B extra-nodal BL. However, due to a prolonged waiting list at the referral oncology unit, treatment initiation was delayed by 43 days—exceeding the recommended 48-hour window for initiating oncological intervention in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was conducted due to technical limitations in available equipment. The patient received supportive care, including blood transfusions and analgesia, but ultimately died in the gynecological ward on day 43 while awaiting treatment. Postmortem histopathology was not performed, as both the BL diagnosis and HIV infection were already established. The primary cause of death remains difficult to attribute definitively due to the presence of multiple comorbidities; however, the attending physician concluded that Burkitt lymphoma was the most likely primary cause, given its rapid progression and high mortality in HIV-positive individuals with high viral loads. The secondary cause of death was multiple organ failure, encompassing both renal and hematological failure, which likely resulted from the combined effects of aggressive lymphoma biology, immunosuppression, and progressive organ dysfunction. This case underscores the critical importance of timely diagnosis and intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of EBV-associated extra-nodal BL, where delays in treatment significantly impact survival outcomes.


A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and signs of pulmonary vascular congestion on chest X-ray, including interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation, consistent with right heart strain. Cardiac catheterization (RHC) in 2017 confirmed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, classifying the condition as pre-capillary, group I, CTD-related PAH. These findings supported insurance approval for Opsumit (macitentan) 10 mg once daily, which replaced Tracleer (bosentan) in 2017. Treatment with sildenafil (Revatio) 20 mg three times daily and macitentan was initiated and maintained until 2020, during which the patient remained stable with low-to-intermediate risk classification. However, in October 2020, she presented with worsening dyspnea, productive cough with white sputum, and signs of systemic infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and hypoxemia (SpO2 = 70%), requiring 100% oxygen via face tent. Arterial blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pharmacological agents for PAH management. Her condition stabilized, with successful weaning from vasopressors by November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support reduced to nasal cannula at 2 L/min. Follow-up RHC continued to show elevated pulmonary artery pressures, reflecting progressive right ventricular dysfunction due to chronic pulmonary hypertension. Despite stabilization, her 6-minute walk distance progressively declined, and she was reclassified as high-risk. She continues to require frequent hospitalizations for disease control. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur suggestive of severe valvular heart disease. In 2020, Ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment, consisting of daily administration of 1 capsule of PURE HYDROGEN (HoHo Biotech Co., Ltd., Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7 × 10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 mL of water. Whole-blood flow cytometry and serological analyses were performed pre- and post-treatment using standard fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA), following established immunophenotypic gating protocols. Results demonstrated a significant increase in CD127+ regulatory T cells (Treg), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These immunological changes correlated with clinical stabilization, including improvement in dyspnea and respiratory function, without any reported adverse events. The study adheres to the CARE (Consolidated Standards of Reporting Trials) 2013 reporting guidelines.


A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and his eyes turned to the right. His face and chest twitched on one side, then he had a full seizure. After that, he had weakness on his left side. Doctors found the SARS-CoV-2 virus in his brain fluid, which means the virus got into his brain. But he slowly got better over time and is now doing well. He doesn’t need medicine for seizures anymore and is back in a regular room. No serious brain damage was found.


A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. For the first few days, he had symptoms like fever, dry cough, shortness of breath, and chest pain. Tests confirmed the pneumonia was due to SARS-CoV-2, and he needed increasing oxygen support as his condition worsened. He was placed in the intensive care unit and given medications including remdesivir, dexamethasone, and antibiotics, which helped reduce inflammation and fight infection.

On the 16th day of hospitalization, he suddenly had a change in consciousness, with his eyes turning to the right and involuntary jerking movements on his left side (face and chest). This was followed by a full seizure. After treatment with midazolam, the seizure stopped. Tests showed no signs of low oxygen, low blood sugar, or other common causes of seizures. A key finding was that the virus SARS-CoV-2 was detected in his cerebrospinal fluid (the fluid around the brain and spinal cord), which suggests the virus may have affected his brain.

After this event, he remained in a coma-like state for a short time, with no ability to respond to pain or speak, and had weakness on his left side. He was eventually able to wake up and regain some function. His brain scans showed no major damage, and after a few weeks, he was discharged with no need for anti-seizure medication. His overall recovery was favorable, and he continued to improve over time.


{
  "proficient_health_literacy": "A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted to the intensive care unit (ICU) with a diagnosis of SARS-CoV-2-associated pneumonia. He had a history of grade 3 obesity and no significant comorbidities or prior pharmacological therapy. The initial presentation included fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia, evolving over four days. On admission, neurological examination was unremarkable, with tachypnea and bilateral rough vesicular breath sounds on pulmonary auscultation, consistent with diffuse pulmonary involvement. Laboratory findings revealed elevated inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal pulmonary opacities on chest radiography. Reverse-transcription real-time polymerase chain reaction (RT-PCR) testing of nasal and oropharyngeal exudates confirmed active SARS-CoV-2 infection, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a primary viral etiology of pneumonia.\n\nOver the first 48 hours, progressive clinical deterioration was observed, including worsening fatigue, dyspnea, and respiratory failure, necessitating escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow nasal cannula oxygen was then applied without clinical benefit. The patient was subsequently transferred to a level III ICU, where he received sedoanalgesia and orotracheal intubation with invasive mechanical ventilation.\n\nOn day 11 of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) was continued, administered on suspicion of secondary bacterial superinfection. Persistent fever with suboptimal response to antipyretics was noted, though inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious sources, intravenous lines were changed, and blood cultures, catheter tip cultures, bronchoalveolar lavage, urinalysis, urine culture, and transthoracic echocardiography were performed. Blood culture yielded Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid—therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) and ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were excluded.\n\nDuring the weaning phase, the patient required inotropic support with dobutamine and continued to need noninvasive ventilation post-extubation, which occurred on day 15. On day 16 (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, accompanied by conjugate gaze deviation to the right, left-sided myoclonus of the face and thoracic region, and a generalized tonic-clonic seizure, which resolved with midazolam administration. Hypoxic-ischemic encephalopathy was ruled out due to sustained normotension, absence of peri-event hypoxemia or hypoxemia, normal serum lactate, and preserved diuresis. Electrolyte, glucose, and metabolic imbalances were also excluded as etiologies for the seizure.\n\nPost-ictal status included a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, failure to localize to pain), persistent left hemiparesis (grade 3/5), and requirement for airway protection. The patient remained sedated and underwent repeated orotracheal intubation and initiation of anticonvulsant therapy. Cranial computed tomography (CT) showed no acute structural abnormalities. Lumbar puncture revealed turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF analysis included testing for neurotropic viruses, venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria, and RT-PCR for SARS-CoV-2; the latter was positive, confirming the presence of SARS-CoV-2 RNA in the CSF without evidence of bacterial or viral pleocytosis. This finding supported the diagnosis of SARS-CoV-2 encephalitis rather than bacterial meningitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity.\n\nMagnetic resonance imaging (MRI) performed on


The person had a long-lasting cough, ear pain, and a foul-smelling yellow discharge from one ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, the bacteria test turned negative, and they felt better. They also started taking HIV medicine again and now have a much lower virus level in their body. The treatment worked and they are fully recovered.


The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in both the liquid from the stomach and a swab from the ear pus, which pointed to tuberculosis. The patient also had HIV, which weakened their immune system, making them more susceptible to tuberculosis. Despite initial treatment for malaria and ear infection, the symptoms did not improve. Imaging and exams confirmed tuberculosis in both the ear and the lungs. The patient was treated with a 6-month course of anti-tuberculosis medication, including isoniazid, rifampicin, pyrazinamide, and ethambutol in the first two months, followed by isoniazid and rifampicin for the next four months. They also received treatment for HIV, restarted after adjusting their medication, and were given preventive antibiotics and ear cleaning. After 14 days, their symptoms improved, and the bacteria tests became negative. By the end of treatment, the patient was fully recovered with no signs of infection, and their HIV viral load dropped to a very low level.


A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases Department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center with artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media was ineffective. The patient is HIV-1 positive, diagnosed seven months prior, and was previously on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir, which was discontinued due to patient non-adherence. Immunological evaluation at diagnosis revealed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL; after six months of ART, the CD4 count increased to 193 cells/μL and viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (at seven months post-HIV diagnosis), CD4 count was 89 cells/μL and viral load was 10,230 copies/mL, indicating ongoing immunosuppression. Otoscopic examination of the right ear demonstrated inflammation of the external auditory canal with purulent discharge and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was normal. Rinne and Weber tests confirmed a right conductive hearing loss. Radiographic findings on frontal chest X-ray showed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. Ziehl-Neelsen bacilloscopy was positive in both gastric washings (on admission and at 19 days later) and in the right ear swab due to persistent purulent otorrhea, supporting the presence of acid-fast bacilli. The Xpert-MTB/GeneXpert assay was negative for rifampicin resistance, confirming drug-susceptible Mycobacterium tuberculosis. The diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-associated immunosuppression was established. The patient was initiated on a standard first-line anti-tuberculosis regimen: a 2-month intensive phase of quadritherapy comprising isoniazid, rifampicin, pyrazinamide, and ethambutol (2RHZE), followed by a 4-month continuation phase of isoniazid and rifampicin (4RH) at a dose of three tablets daily in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART), with ART restarted on 4 May 2023 following good tolerance of anti-tuberculosis drugs. The ART regimen was re-established with tenofovir/lamivudine/dolutegravir (1 tablet/day) and an additional dolutegravir 50 mg (1 tablet/day) as per standard HIV management protocols. Chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) was initiated, and the external auditory canal was cleared via aspiration, followed by instillation of ciprofloxacin ear drops (2 drops, three times daily) for 14 days. Clinical improvement was observed within 14 days of therapy, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy results became negative in both gastric washings and the right ear pus swab during treatment. At the end of the 6-month anti-tuberculosis regimen, complete clinical healing was achieved, with normal ENT and neurological examinations. Sputum and ear swab bacilloscopy, as well as Xpert-MTB/GeneXpert testing, remained negative at the end of the intensive phase (month 2), at month 5, and at the completion of the maintenance phase (month 6). Post-treatment HIV viral load, assessed three months after ART restart, was 329 copies/mL, indicating effective suppression of viral replication. This case demonstrates the clinical and pathological interplay between HIV-induced immunosuppression, pulmonary and otological tuberculosis, and the successful management through integrated anti-tuberculosis and antiretroviral therapy, with sustained virological and microbiological responses.


A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a small tube to clear the blocked blood vessel and fixed it successfully. The boy was only 10 kg at 23 months, which is small for his age, but he stayed healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm.


A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth, exhibiting preserved brain motor potential and normal psychomotor development, was managed for restrictive cardiomyopathy. He was enrolled in a cardiac transplant programme at 16 months of age and subsequently required implantation of an external biventricular support device (Berlin Heart) to maintain circulatory function. To mitigate the risk of embolic complications associated with chronic cardiac dysfunction and mechanical support, he received dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months of age, he presented with acute neurological deterioration manifesting as disconnection syndrome and right hemiparesis. A non-contrast computed tomography (CT) scan revealed a hyperdense left middle cerebral artery (MCA), consistent with acute thrombosis, and a chronic right parietotemporal infarction, indicating prior ischemic damage. Given the concomitant anticoagulation, intravenous thrombolytic therapy was contraindicated due to hemorrhagic risk. Therefore, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and insertion of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalization was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned in the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire catheter system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. A control run during the procedure identified an iatrogenic dissection of the left internal carotid artery, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately irrigated via the anterior communicant artery. Post-procedure, the patient underwent a successful heart transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with the initial stroke lesion. The case highlights the feasibility and efficacy of intra-arterial mechanical thrombectomy in a pediatric population with complex comorbidities, including congenital cardiomyopathy and chronic anticoagulation, and underscores the importance of pre-procedural vascular mapping and intra-procedural monitoring in pediatric neurointerventional practice.


A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught at the first hospital. When checked, his right shoulder had a dislocation and his left shoulder had a simple dislocation that wasn't seen before. The doctors found that the left shoulder injury got worse during his stay, probably because he was held down too tightly. They did surgery on both shoulders at once to fix the bones. The right shoulder was fixed with screws and strong stitches. The left shoulder needed two extra surgeries — one to fix the broken piece and another to open the joint. Two years later, he can move his shoulders a little, with scores showing he's doing better than most. He can now work again and is moving toward full recovery.


A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. At first, X-rays showed a right shoulder dislocation and a simple posterior dislocation of his left shoulder — a problem that had not been seen at the previous hospital and took about 48 hours to diagnose. A CT scan later showed that the left shoulder injury had worsened during his hospital stay, likely because of physical restraint. Both shoulders were surgically repaired in one operation using plates and screws to realign and stabilize the bones. The right shoulder had a fragment of bone that was fixed with a screw and strong sutures, while the left shoulder used strong sutures to hold the bone pieces together, since a screw wasn’t needed. After surgery, the patient wore a shoulder immobilizer for four weeks. By the second week, he began gentle exercises to improve movement, but at one month, the left shoulder’s bone alignment started to loosen, so he had a second surgery to fix it with stronger sutures. He then wore the immobilizer for another four weeks and resumed exercises. After 30 sessions of physical therapy, he returned to work five months later. One year after the injury, his right shoulder was doing well, but his left shoulder still had limited motion, especially in rotating outward. A final surgery was done to release the joint and remove the earlier screws in the left shoulder. Two years later, the patient was doing well — he scored 5% on the Quick DASH scale (a measure of shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. This shows he is making steady progress in recovery.


A 52-year-old male with no significant medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation on both shoulders. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. The initial radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had not been identified at the referring facility and was only diagnosed approximately 48 hours after admission.

A computed tomography (CT) scan of both shoulders was performed to assess the extent and evolution of the injuries. The CT demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission radiographs to a full posterior glenohumeral fracture (LFGHP) by the 48-hour mark, likely secondary to the mechanical stress imposed by physical restraint during immobilization. This progression highlights the role of external forces in exacerbating glenohumeral instability in the setting of acute trauma.

Preoperative imaging of the right shoulder revealed glenoid bone integrity with 40% involvement of the humeral articular surface, including a large fragment that was anatomically positioned to maintain continuity with the lesser tuberosity. This fragment was planned to be stabilized using a 4.0 mm spongy screw with partial threading and high-strength sutures. In contrast, the left shoulder showed intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed by repositioning and osteosynthesizing the lesser tuberosity fragment—mirroring the surgical technique described in McLaughlin’s protocol for humeral head fracture repair.

The surgical approach involved open reduction and internal fixation (ORIF) with bilateral locked-plate fixation using a Philos (Depuy Synthes®) plate. The patient was positioned in a beach chair position, and both shoulders were accessed via a classic deltopectoral approach. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by definitive fixation with a 4.0 mm spongy screw and high-strength sutures. The final reduction and stability were achieved with the Philos plate, supplemented by fixation of the rotator cuff tendons to the plate using high-strength sutures. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.

The left shoulder was operated on immediately after the right. A second deltopectoral approach was performed with an accessory posterior portal for digital reduction of the humeral head. Fixation was accomplished similarly to the right shoulder, except that the spongy screw was not used due to the anterior fragment's inability to achieve adequate stability without high-strength suture fixation alone.

Postoperative management included bilateral shoulder immobilization for four weeks. Passive and active pendular flexion-extension exercises of the elbow and finger flexion were initiated from the second postoperative week, progressing according to pain tolerance. At the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to re-stabilize the fragment with high-strength sutures. The patient was then placed in additional immobilization for four weeks on the left shoulder. Bilateral rehabilitation exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured kinesiological rehabilitation, the patient returned to work five months after the initial injury.

One-year follow-up revealed full recovery of strength and range of motion in the right shoulder, while the left shoulder continued to exhibit significant limitations, particularly in external rotation. At this stage, arthroscopic joint release surgery was performed, with removal of the osteosynthesis hardware in the left shoulder to address chronic joint stiffness and functional impairment. Two years after the initial trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating substantial recovery and satisfactory functional performance despite persistent limitations in the left shoulder. The case underscores the importance of timely diagnosis, accurate imaging interpretation, and surgical intervention in managing complex glenohumeral fractures, particularly in the context of acute trauma and physical restraint-related injury progression.


A 70-year-old man had a serious heart problem where blood was leaking backward through the aortic valve. Doctors fixed it with a tiny valve placed inside his heart using a catheter (not open surgery) from the top of his heart. After that, his heart started to fail again, so they added a machine to help his heart pump blood. One year later, the machine showed the valve wasn’t working well, and the leak got worse. The doctors decided to fix the old valve by placing a new one inside it, like putting a new door in an old one. They slowed down the heart machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, there was no more leak, his heart was strong, and he could walk much farther without trouble. He’s doing great now.


A 70-year-old man with severe heart valve problems was treated with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a history of heart infection that had healed, and his heart was very weak, with only 20% of its normal pumping ability. Because of his poor heart function and other health issues, surgery was too risky, so TAVI was chosen instead. After the first procedure, his heart improved, but he had a relapse of symptoms four weeks later due to continued weakness. As a result, he received a left ventricular assist device (LVAD), which helps the heart pump blood. He stayed symptom-free for a year, but the LVAD started giving warning signs of high flow, and tests showed worsening leakage through the aortic valve, even though the original valve appeared structurally normal. After careful discussion with his medical team, they decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve was placed inside the existing one. This was done while reducing the LVAD flow to the lowest level and using a pacemaker to keep his heart beating at 140 beats per minute during the procedure. The new valve was placed carefully using imaging guidance to avoid damaging the original valve. The procedure was successful, and at 12 months follow-up, the patient had no significant leakage from the aortic valve, his heart function improved to 33%, and he could walk much farther without shortness of breath. He is now doing well and living a normal life.