A 38-year-old woman had a weak heart since she was 17, after a bad cold that might have hurt her heart muscle. Her heart couldn’t pump blood well, so she was in the hospital for 10 months. She was very sick and close to dying, but her heart started to get better. Doctors treated her heart failure, kept her heart from beating too fast or too slow, and stopped blood clots. After 4 years, her heart function improved and stayed strong — that’s rare, only 1 in 6 people get this. Then it got worse again for 2 years, but she stayed stable. She had a baby, and after the second pregnancy, her heart got weaker again, especially after giving birth — this is common in women with heart problems. Now, in 2017, she’s stable. She takes medicine every day — for her heart, to control fluid, and to slow her heartbeat. She can do normal daily activities, has two children, and doesn’t work. Her heart is still weak, but it’s working better than before. She checks her heart regularly and watches her weight and fluid intake. No need for a special heart device right now.


A 27-year-old man broke his right thigh bone after a small fall, where the bone twisted and bent. He had a bone condition called fibrous dysplasia in his thigh since childhood, and 20 years ago, doctors removed part of the bone, added bone graft, and fixed it with a metal device. They later took out the metal device one year later. This time, because the break was serious and in a weak area, they removed a large part of the broken bone and replaced it with a hip implant. They also took a small tissue sample, which confirmed it was the same bone problem from when he was a child. Now, he can walk and do daily things, though he still has some pain when walking long distances. He’s happy with how well it’s working and can now walk and do light activities like walking without much trouble.


A 27-year-old man came to the emergency department with a fracture in the upper part of his right thigh bone (femur), specifically at the base of the neck. The break happened after a minor fall that involved pressure and twisting of the hip. This type of fracture is classified as Garden II, Pauwells III, AO 31B2.3r, and is considered serious due to the way it occurred and the patient’s medical history. He had been treated 20 years ago for fibrous dysplasia — a condition where abnormal bone tissue grows in the bone — with a procedure that included removing part of the bone (curettage), adding bone graft, and using a device (osteosynthesis material) to stabilize the area. That device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia (DF). Because of the fracture’s location and the patient’s history, doctors decided on a wide removal of the upper femur and a total hip replacement using a modular prosthesis, along with placing a cerclage wire to help stabilize the bone. A biopsy after surgery confirmed it was the same fibrous dysplasia seen in childhood. The patient recovered well, with no major complications. He was able to walk with support and gradually returned to daily activities. He still has some walking difficulty due to a scar in the gluteal muscle, but he is now able to do 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) and then a cord blood transplant (allogeneic CBT). After the transplant, he developed worsening breathing problems on day 194. His older brother had a cold, and a test showed he had a respiratory syncytial virus (RSV) infection about a month before. He also had symptoms like coughing and shortness of breath. A lung biopsy showed signs of lung damage, including inflammation from the virus and changes consistent with pulmonary vascular dysplasia (PVOD). The doctors believe the RSV infection may have triggered or contributed to the development of PVOD. The lung injury was seen in the cells of the lungs, especially in the air sacs and blood vessels, and the findings suggest that the virus played a key role in starting the condition.


A 65-year-old man started feeling a persistent cough, shortness of breath, and lost 10 pounds in just 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked under a microscope — it showed strange cells that grew in sheets, surrounded by many immune cells. These cells were found to be from a rare cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). The cancer cells had signs of a virus called Epstein-Barr, and they were also positive for a protein called PD-L1, which means the cancer can hide from the body’s immune system. He got chemotherapy with drugs like gemcitabine and cisplatin, and later switched to carboplatin because of side effects. He also took durvalumab to help fight the cancer. After 6 rounds of treatment, the cancer got worse and he died 9 months after first being diagnosed, due to breathing problems.


A 13-year-old boy had a lump in his groin that could be felt and moved. He didn’t have fever, pain, or other symptoms. The doctors took out the lump to make sure it wasn’t something serious like cancer. After checking the tissue under a microscope, they found a rare condition called Castleman’s disease, specifically the plasma cell type, which is very rare in kids. This case is the first time this kind of disease has been found in the groin area. For 12 months after the surgery, the boy had no new lumps or symptoms, and all tests showed everything was normal. He’s doing fine and doesn’t need more treatment.


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 comprised a clinical diagnosis of myotonia, presence of the warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as molecular confirmation via mutation analysis in the CLCN1 gene. Data collected included demographic variables (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical evolution), family history, and response to therapeutic interventions. Five patients with a clinical diagnosis of congenital myotonia were identified: three with Becker congenital myotonia and two with Thomsen congenital myotonia. The estimated incidence was 1:15,000 live births for the Becker phenotype and 1:21,000 live births for the Thomsen phenotype.

The cohort was predominantly female, with the sole male patient presenting before the age of 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 for one patient whose family declined testing. All patients exhibited worsening of myotonia with cold exposure; the warm-up phenomenon, a hallmark of the Becker phenotype, was observed only in patients with the Becker genotype.

Patients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, both clinically affected, with no clinical signs in their parents. The mother of patient 1 exhibited mild, cold-exacerbated myotonic symptoms, suggesting a possible carrier state. The patient who declined genetic evaluation had a positive family history of myotonia in the maternal lineage.

Serum creatine kinase levels were not elevated in any of the patients, indicating that 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 (out of 12 years of follow-up); subsequent EMG testing was not repeated due to clinical stability and institutional protocol. The primary pharmacological intervention was oxcarbazepine, particularly in patients with the recessive form, with generally favorable response. However, patient 2 experienced loss of efficacy over time and was subsequently treated with mexiletine. Patient 4 attempted multiple medications without sustained benefit due to either therapeutic failure or adverse effects. Patient 5 declined treatment due to a mild clinical presentation.

Patient 1 was found to carry a previously unreported, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from the mother. Cases 1 to 3 exhibited the Becker phenotype and presented with composite heterozygosity—i.e., a combination of two different pathogenic variants in the CLCN1 gene—consistent with autosomal recessive inheritance. Cases 4 and 5 presented with the Thomsen phenotype, which is associated with a single pathogenic variant and typically manifests with more severe myotonia and earlier onset. Patient 5 declined genetic testing, limiting the ability to confirm the specific mutation in that individual.

The pathophysiological mechanism underlying congenital myotonia involves dysfunction of the voltage-gated chloride channel encoded by CLCN1, which leads to impaired repolarization of skeletal muscle fibers during depolarization. This results in prolonged muscle membrane depolarization, causing delayed relaxation and the clinical manifestation of myotonia. The specific mutation c.824T>C (p.Leu275Pro) is predicted to disrupt the channel's pore-forming domain, reducing chloride conductance and contributing to the observed myotonic phenotype. This mutation has not been previously described in the literature and may represent a novel pathogenic variant in the CLCN1 gene spectrum associated with congenital myotonia.


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 an AVM, which didn’t get better even after treatment. Recently, she started feeling tired and short of breath, which means her heart was struggling. Her doctor found her heart was enlarged and not working well, and her blood markers showed high pressure on the heart. She was diagnosed with a serious, long-time leg blood vessel problem and heart failure. The doctors tried to fix it by placing a stent in her leg to block the bad blood flow, which helped her heart feel better. After the surgery, her leg swelling went down and her heart started working better. A second step was done to stop the blood flow from the AVMs in the leg. After one year, her leg swelling was much less, and her heart was stronger. This shows the treatment worked.


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 didn’t stop the swelling. Over time, she developed symptoms of heart failure, including fatigue and shortness of breath, which led her to seek care at a specialized hospital. Tests showed her heart was enlarged and had weakened function, with high levels of a heart failure marker (BNP), and her leg blood flow was very high—3400 ml/min—due to the AVM.

The doctors decided to treat the AVM using a combination of procedures. First, they placed a covered stent in her femoral artery to block the abnormal blood flow from the AVM. This helped reduce the blood flow to the leg from 3400 ml/min to 1600 ml/min, and her heart failure symptoms improved. The stent was placed in the area where the AVM was most active, and follow-up imaging showed much less blood flow and better leg circulation.

A second procedure followed, where they used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow and helped seal off the malformation. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels dropped significantly. Her left ventricular ejection fraction improved from 60% to 71%, showing better heart pumping ability. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs in the lower limb and improving heart failure in patients with such conditions.


{
  "proficient_health_literacy": "A 67-year-old female presented with a six-year history of progressive left lower limb edema, initially diagnosed with a lower limb arteriovenous malformation (AVM) one year prior. Two months before admission, she underwent embolization using two coils (20 mm × 40 cm, BSX, USA) in the superficial femoral artery (SFA), yet no clinical improvement in swelling was observed. Over the preceding month, she developed progressive fatigue and dyspnea, indicative of acute decompensated heart failure, leading to transfer to Chengdu University of Traditional Chinese Medicine Hospital. She had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported seven years of oral estrogen therapy for menopausal symptoms.\n\nPhysical examination revealed marked edema and skin sclerosis in the left lower limb, 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 elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary abnormalities. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, significant dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex congenital AVMs involving the SFA and profunda femoris artery. Arterial phase imaging showed marked enlargement of both femoral and superficial veins. The popliteal and anterior tibial arteries were nonvisualized, supporting diagnosis of complex congenital lower limb AVMs with associated venous congestion.\n\nThe patient was classified as New York Heart Association (NYHA) Class IV due to severe symptoms of acute heart failure. Preoperative CFA flow volume was 3400 ml/min. Given the persistence of high flow through the AVMs despite coil embolization, and the lack of effective flow reduction with conventional embolization, a covered stent graft was selected as a therapeutic strategy to occlude the high-flow AVM nidus and reduce venous congestion, thereby alleviating cardiac preload and improving hemodynamics. CTA measurements indicated maximum vessel diameters of 32 mm (iliac artery), 27 mm (CFA), and 22 mm (SFA), with the SFA mid-segment measuring 19 mm, leading to selection of a 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China).\n\nUnder general anesthesia, antegrade access was achieved via the common femoral artery using a 14 F (Cook Medical, USA) catheter sheath. A 0.035 guidewire was initially used, subsequently replaced with a 0.035 super-hard guidewire for enhanced stability during stent deployment. The stent was implanted at the distal SFA, the region of highest AVM burden. Completion angiography demonstrated significant reduction in venous opacification around the stent and clear visualization of the popliteal artery, confirming successful stent placement and hemodynamic stabilization. Postoperatively, the left femoral artery was sutured using a 6-0 vascular risk suture.\n\nThe surgical procedure was performed with minimal duration to avoid exacerbation of heart failure, consistent with the patient’s unstable cardiac status. A staged embolization was planned for the second phase to target the AVM nidus and draining venous pathways. One week post-intervention, CFA flow reduced to 1600 ml/min, and BNP levels decreased to 1198 ng/L, indicating early clinical improvement. Right CFA access was used to perform angiographic guidance, with puncture of the AVM drainage vein and introduction of a 5 F vascular sheath. 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) to achieve occlusion of the nidus and draining veins.\n\nCompletion angiography showed near-complete disappearance of AVM and draining vein visualization. At one-year follow-up, the CFA flow volume decreased to 780 ml/min, echocardiography revealed mild atrial enlargement,


A 28-year-old man got two red, bump-like spots on his right arm and forearm that had small blisters and sores in the middle. They were sore and itched, but he didn’t feel sick inside. He was vacationing in a coastal area of Ecuador when this happened. The doctor took a small skin sample and saw signs that matched a skin problem from bugs in that area. The doctor called it Paederus dermatitis. He treated it with anti-itch medicine, cream to calm the skin, and cold compresses. After 8 days, the bumps went away, but the skin stayed a little darker in those spots.


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, located 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, without systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key epidemiological context. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending into the superficial, middle, and deep dermis. These findings are characteristic of a delayed-type hypersensitivity reaction to Paederus beetle-derived cuticular proteins, specifically the Paederus toxin (Paederus toxin, a member of the cysteine-rich protein family), which induces a type IV hypersensitivity response mediated by CD4+ T cells and subsequent release of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13. The clinical presentation, geographic exposure, and histopathological profile collectively support the diagnosis of Paederus dermatitis. Management consisted of antihistamines to mitigate pruritus, topical corticosteroids to suppress local inflammation, and cold compresses to reduce vascular permeability and symptom severity. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a result of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering environmental exposures in tropical regions, particularly in endemic areas where Paederus beetles (family Paederidae) are prevalent, as a potential etiology of acute, non-infectious, pruritic dermatoses with a distinct histopathological signature.


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. Instead, they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through a vein, and the doctors used a scope to look inside his bile duct. They placed a small light tube into the duct and shone light on the blocked area to help open it. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, they checked the duct again to make sure everything was okay. The treatment worked for three months, but the blockage came back. He had other treatments, but eventually died from lung cancer that spread from the tumor, 15 months after the light treatment. The most important thing is that the light treatment helped him feel better for a while, even though it didn’t cure the disease.


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 confirmed choledocholithiasis, and endoscopic retrograde cholangiopancreatography (ERCP) revealed inability to remove stones due to disproportionate ductal dilation, necessitating placement of a plastic biliary stent. Clinical improvement was transient, with cholestasis returning 45 days post-ERCP. Subsequent ERCP attempts failed to clear the stones. On repeat EUS, a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm was identified in the dilated common hepatic duct, compressing the duct lumen, and extending into 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 therapy. Multidisciplinary consensus supported adjunctive photodynamic therapy (PDT) to manage the obstructive lesion. The PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) administered 24 hours prior to the session. The photosensitizer has a peak light absorption at 630 nm, enabling targeted activation within biliary tissue. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla and achieve retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct for direct visualization, allowing precise identification of the neoplastic stenosis. Under real-time cholangioscopic guidance, an illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. The 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 stabilization; the third port serves as the injection site for the photosensitizer. The illumination was delivered 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 stenotic segment. Post-procedure, the bile duct was re-evaluated via cholangioscopy to assess immediate outcomes and detect any adverse events. The patient was maintained on a fasted state for 24 hours post-procedure, with oral diet initiated if no adverse events were observed. Discharge was accompanied by strict photoprotection protocols, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT. The procedure lasted 150 minutes and concluded with placement of a 10 Fr plastic biliary stent for drainage, as a self-expanding metal stent was unavailable at the time. The patient remained asymptomatic for three months, the longest period since disease onset. However, early recurrence of cholestasis with cholangitis occurred, which was attributed to stent obstruction by tumor debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by re-drainage resolved the acute episode. Subsequently, a self-expanding metal stent was placed to maintain patency. The patient continued on systemic oncologic therapy and eventually required a duodenal stent for palliation of dysphagia. 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 immediate adverse events, and the PDT provided symptomatic relief and disease stabilization for an extended period, although the underlying malignancy progressed to metastatic disease.


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), accompanied by anaemia (haemoglobin: 9.6 g/dL), consistent with upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steep flexure of the third part of the duodenum on the right side of the aorta, with a caudal course that did not cross 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 suggestive of 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, where forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—specifically, its steep rightward flexure 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 seven days later showed spontaneous resolution of this rightward deviation, with the jejunum returning to a central or left-sided position. This transient, self-resolving malposition is inconsistent with true malrotation, which typically presents as a congenital anomaly with persistent anatomical abnormality and risk of volvulus. The patient was discharged after stabilization.

Two months later, she presented with a recurrent episode of haematemesis. Dynamic CT performed prior to endoscopy revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was found 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 laceration at the gastric cardia, reinforcing the diagnosis of Mallory-Weiss syndrome. Subsequent non-contrast CT, performed two months after the second haematemesis, showed no persistent duodenal deviation, but revealed oedematous wall thickening in the second part of the duodenum. Without prior imaging, this might have been interpreted as duodenitis; however, the history of repeated, spontaneous rightward deviations of the small intestine provided a critical clue to an underlying anatomical variant.

Given the pattern of transient, reversible right-sided displacement of the duodenum and jejunum—without evidence of malrotation or volvulus—dysplasia of the ligament of Treitz was diagnosed. The ligament of Treitz, which normally anchors the duodenum to the jejunum in the retroperitoneum, is typically formed and fixed during embryogenesis. In this case, CT imaging and surgical exploration revealed a formed ligament of Treitz, but with incomplete fixation to the upper jejunum—specifically, it was attached only to the duodenum and not securely anchored to the retroperitoneum. The duodenal-jejunal junction was not fixed to the retroperitoneal space, resulting in mechanical instability and allowing the jejunum to fold freely around the ligament as a fulcrum, thereby producing transient rightward displacement during gastrointestinal motility or increased intraluminal pressure.

Laparotomy 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 incomplete fixation of the ligament of Treitz was the primary pathophysiological mechanism underlying the recurrent, spontaneous rightward deviations observed on imaging. Surgical correction involved fixation of the upper jejunum with four sutures to the retroperitoneum on the left side, which stabilized the anatomical configuration. The postoperative course was uncomplicated, and the patient has remained asymptomatic since. This case illustrates that transient, reversible small intestinal deviations in the absence of malrotation may represent a functional variant due to dysplasia of the ligament of Treitz, with implications for both imaging interpretation and surgical management in patients with recurrent upper gastrointestinal bleeding.


A 28-year-old man from Morocco had pain in his belly, especially on the right side, for about a month. He also had fever, chills, sweating, loss of appetite, and lost 6 pounds. His doctor found a swollen liver with small spots on it that looked strange. These spots were not cancer or infection from other causes. Tests showed signs of a slow, hidden infection — like tuberculosis — in the liver. A small surgery was done to take a piece of the liver tissue, and the lab confirmed it was tuberculosis. After starting medicine to fight the tuberculosis, his symptoms got better fast. The pain went away, the fever stopped, and the spots on his liver got smaller over time. This treatment works well for this kind of liver problem.


A 28-year-old Moroccan man with no smoking or drinking habits presented with a month-long history of abdominal pain, especially in the upper right part of his belly, along with fever, chills, night sweats, loss of appetite, and a 6-kilogram weight loss. He had no known family history of illness and was vaccinated for tuberculosis (BCG). Initially, his symptoms were mild, but they worsened over time, leading to significant weight loss of 12 kilograms over three months. Tests showed signs of infection, including high white blood cells and inflammation markers, but no evidence of common infections like hepatitis or bacterial infections. Imaging scans revealed multiple nodules in his liver that were not clearly explained. These nodules appeared on both ultrasound and MRI, and they were not enhancing after contrast was given. Liver function tests were normal, and blood tests for viruses and tuberculosis (using GeneXpert and quantiferon) were negative at first. A liver biopsy during laparoscopy showed characteristic tissue changes — epithelioid and giant cells with caseous necrosis — which are typical of tuberculosis. This confirmed a diagnosis of focal liver tuberculosis. The patient was started on standard anti-tuberculosis medication: a four-drug combination for the first two months, followed by a two-drug regimen for four months. Within days of starting treatment, his symptoms improved significantly. By the third month, follow-up scans showed that the liver nodules had shrunk in number and size, and his overall condition had stabilized.


A 28-year-old male military personnel presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peaking at 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss over one month. He had no history of alcohol use, smoking, or significant comorbidities; he was BCG-vaccinated and had no familial or personal history of infectious or hepatic disease. Physical examination revealed an asthenic appearance, tachycardia (124 beats/min), tachypnea (22 breaths/min), and moderate right upper quadrant tenderness with hepatomegaly (liver size 17 cm). No pulmonary or lymphadenopathic findings were detected on physical exam.

The clinical picture evolved from an initial presentation of diffuse abdominal pain with alternating diarrhea and constipation, persisting over several weeks, initially with only low-grade nocturnal fever and preserved general condition. This was followed by progressive deterioration, including a 12 kg weight loss over three months, prompting emergency admission for further evaluation.

Laboratory findings demonstrated a neutrophilic leukocytosis (17,800 cells/mm³), elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), consistent with a systemic inflammatory response syndrome. Initial biomarkers of liver injury were within normal limits: ALT (22 IU/L), AST (17 IU/L), GGT (42 IU/L), ALP (115 IU/L), bilirubin, prothrombin time (78%), and albumin (39 g/L). Renal function and electrolyte balance were normal. 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. Blood cultures and urine cytobacteriological analysis during febrile peaks were negative. GeneXpert assay for Mycobacterium tuberculosis in respiratory specimens and in liver biopsy material was negative; quantiferon tuberculin test was negative, indicating no evidence of latent or active TB in the immunological screening.

Imaging studies revealed multiple, well-defined, rounded hypodense lesions in the liver on thoraco-abdomino-pelvic CT, with no enhancement after contrast administration. The largest lesions were located in segment I (21 × 16 mm) and segment V (36 × 27 mm). Abdominal ultrasound showed no focal abnormalities. Liver MRI demonstrated dysmorphic liver architecture with heterogeneous T2 signal intensity, with peripheral hyperintense walls surrounding the lesions, showing peripheral contrast enhancement. The largest lesions were in segment I (20 × 22 mm) and segment V (33 × 31 mm), consistent with a pattern suggestive of granulomatous inflammation. No deep lymphadenopathy was observed in thoracic or pelvic regions.

Echographic-guided liver biopsies initially revealed subacute, fibro-inflammatory changes without evidence of malignancy or specific infectious etiology. Diagnostic laparoscopy was performed to obtain histological specimens from hepatic nodules. Histopathological examination revealed epithelioid and gigantocellular granulomas with central caseous necrosis, a classic histological hallmark of tuberculosis, supporting a diagnosis of focal hepatic tuberculosis.

The patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy—isoniazid, rifampicin, pyrazinamide, and ethambutol—administered as single oral doses in the morning on an empty stomach. Phase 2 (4 months) involved continuation with bitherapy (isoniazid and rifampicin) under the same dosing regimen. Clinical and biological monitoring demonstrated a rapid and favorable response to treatment, with resolution of systemic inflammatory markers and improvement in symptoms within days. After three months of therapy, follow-up imaging showed a significant reduction in the number and volume of hepatic lesions, indicating therapeutic efficacy. The clinical course reflects a rare presentation of extrapulmonary tuberculosis involving the liver, with a delayed recognition due to non-specific symptoms and negative initial microbiological screening, ultimately confirmed by histopathological analysis of hepatic nodules.


A 12-year-old boy with Down Syndrome and trouble moving his hands and feet had a sore spot on his tongue that looked serious, like a cancer, but it was actually just a long-lasting wound from sharp teeth. His lips were dry and cracked. Because he wore a collar, doctors couldn’t check his neck lymph nodes. The wound was 1 cm wide, had a hard edge, and was white-yellow, which made it look scary. The sharp tooth on the side of his mouth was hurting his tongue and was causing the soreness. Doctors said the problem was caused by the sharp tooth and dry lips, not cancer. He was given salt water, iodine mouthwash, and lip cream to clean and heal the sore spot. His mom was told to use salt water to clean his mouth, apply iodine three times a day to the sore spot, and use lip cream to keep his lips soft. The sharp teeth were planned to be removed, and the space where they went will be fixed with a special device. After a few days, the sore spot got better. But later, he had surgery on his neck because of spine problems. After surgery, he had breathing trouble and passed away two weeks later.


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 progressive lower extremity and upper limb weakness, initially presenting with a fall approximately one year prior, leading to hospitalization. The patient's mother reported chronic difficulties in performing routine oral hygiene due to motoric impairments, contributing to poor oral care and increased risk of mucosal injury. The patient was diagnosed with Down Syndrome and myeloradiculopathy, a condition characterized by degeneration of spinal nerve roots, resulting in motor dysfunction and sensory deficits.

Extraorally, the patient exhibited a dysmorphic facial appearance, consistent with the phenotypic features of 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 reduced lip mobility, impaired salivary flow, and inadequate moisturization. Lymph node examination was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.

Intraorally, 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 malignancy of the epithelial lining of the oral cavity, due to its indurated border and surface appearance. However, the diagnosis of a chronic traumatic ulcer was established based on clinical correlation, patient history, and exclusion of neoplastic pathology. The traumatic origin was attributed to the sharp occlusal surface of the maxillary right central incisor (tooth 55), which caused persistent mechanical irritation against the tongue's lateral border, leading to tissue breakdown and ulceration. Additionally, the patient had dentinal caries involving tooth 63, and radicular gangrene (radix gangrene) affecting teeth 55, 62, 74, and 85, indicating advanced pulp necrosis and periapical tissue destruction. These tooth remnants were recommended for extraction by a pediatric dentist, with a space maintainer to be placed to preserve dental arch integrity and prevent malocclusion.

Laboratory findings revealed hyponatremia (serum sodium 130 mEq/L), which may reflect impaired renal sodium reabsorption or osmotic imbalances associated with chronic neurological dysfunction or medication effects. Lymphocytosis (lymphocyte count 46%) was noted, potentially indicating a chronic inflammatory state or immune dysregulation, which may be exacerbated by recurrent mucosal trauma and poor oral hygiene. An MRI of the cervical spine confirmed cervical spine dislocation, consistent with the pathophysiology of myeloradiculopathy, which directly contributes to the patient's motor deficits and may have secondary effects on orofacial control and posture.

The differential diagnosis included exfoliative cheilitis, reversible pulpitis of tooth 63, and radix gangrene of multiple teeth. The chronic traumatic ulcer was confirmed through clinical evaluation, with no evidence of dysplasia, cellular atypia, or invasive growth on biopsy. The patient received a multimodal treatment regimen: paracetamol 120 mg/5 mL and amoxicillin 125 mg/5 mL for symptomatic management and possible bacterial infection; sodium chloride 0.9% solution for oral rinsing to maintain osmotic balance; povidone-iodine 1% mouthwash applied three times daily as an antiseptic and anti-inflammatory agent to reduce bacterial load and modulate local inflammation; and petroleum jelly applied to the lips to address desiccation and promote epithelial integrity.

The patient's oral lesions showed progressive improvement over time: at the 3-day follow-up, there was initial healing of the oral ulcer; at the 1-week follow-up, the ulcer size decreased and lip lesions improved; by the 10-day follow-up, significant healing of the tongue ulcer was observed. However, despite clinical improvement, the patient underwent neurosurgery for correction of cervical spine dislocation two days after the 10-day visit. Postoperatively, the patient was admitted to the Pediatric Intensive Care Unit (PICU) due to respiratory compromise. After two weeks of PICU observation, the patient developed acute respiratory failure and was declared deceased. The clinical course underscores the complex interplay between genetic syndrome, neurologic pathology, oral trauma, and systemic complications in pediatric patients with Down Syndrome and motoric disorders. The case highlights the importance of multidisciplinary management, including oral medicine, neurology, and pediatrics, in addressing both local and systemic manifestations of these conditions.


A 59-year-old woman had blurry vision in both eyes for a few weeks. She has multiple sclerosis and was taking medicine for seizures, including levetiracetam. Right after starting levetiracetam, her vision got worse, and her corneas (the clear front part of the eye) became swollen. Doctors found this swelling with a special eye test. When they slowly reduced the levetiracetam dose and stopped it, her vision got better and the swollen corneas went away. Now, her vision is clear and her eyes look normal. This suggests the medicine caused the swelling.


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 a special eye test called corneal topography.

Her vision and corneal swelling improved when her levetiracetam dose was reduced and eventually stopped altogether. After six months without the medication, her vision returned to normal and the corneal swelling went away. Follow-up exams showed no further changes in her eyes or vision over the next year. Doctors believe the blurriness was caused by the levetiracetam, not her multiple sclerosis or other eye conditions.


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 disease, and previous ocular examinations had not identified signs of Fuchs' endothelial corneal dystrophy. Her medication regimen included amantadine 100 mg twice daily for seven years, administered for symptomatic management of multiple sclerosis-related motor and cognitive symptoms, and levetiracetam 250 mg twice daily, initiated as an adjunctive antiepileptic agent in response to new seizure activity.

Visual acuity was measured at 0.5 logMAR in both eyes, indicating moderate visual impairment. Slit-lamp examination revealed bilateral corneal edema without evidence of uveitis or anterior segment inflammation. Intraocular pressures were within normal limits at 16 mmHg (right) and 18 mmHg (left). Corneal topography demonstrated significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with substantial epithelial and stromal hydration.

Amantadine is well-documented to induce corneal edema via its known effect on corneal endothelial cell function, particularly through inhibition of Na+/K+ ATPase activity and disruption of ion homeostasis in the corneal endothelium, leading to impaired fluid transport and accumulation of aqueous humor within the stroma. Given this pharmacological mechanism, the treatment team decided to discontinue amantadine and substitute it with lamotrigine, a second-line anticonvulsant with no known association with corneal toxicity. Levetiracetam was continued during this transition, but no improvement in visual acuity was observed over a two-month period.

The patient reported a direct temporal correlation between the initiation of levetiracetam and the onset of visual symptoms, prompting a trial of levetiracetam dose reduction. Following a partial taper, visual symptoms began to resolve within days, and complete cessation of levetiracetam resulted in full normalization of vision. Repeat corneal topography six months post-discontinuation demonstrated regression of corneal thickening to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR bilaterally. Slit-lamp examination confirmed resolution of corneal edema and absence of corneal guttata, a histological feature of endothelial dysfunction.

At a follow-up visit thirteen months after initial presentation, the patient remained stable on amantadine and lamotrigine, with no further changes in medication. Visual acuity remained at 0.2 logMAR in both eyes, and repeat corneal topography showed no progressive thickening, indicating sustained resolution of the endothelial dysfunction. This case supports the hypothesis that levetiracetam may induce corneal edema through mechanisms involving direct or indirect effects on corneal endothelial cell function, potentially via disruption of ion transport, altered membrane permeability, or secondary metabolic stress. While not a well-documented adverse effect in the literature, this case provides clinical evidence for a previously underrecognized side effect of levetiracetam in patients with underlying neurodegenerative conditions, particularly those with compromised ocular homeostasis. The temporal association, reversal upon discontinuation, and normalization of corneal parameters following cessation strongly support a causal relationship between levetiracetam use and the observed corneal pathology.


A 77-year-old man had a seizure at home and fell, breaking both hip bones and pushing them out of place. He was in the hospital for several days, checked with X-rays and scans, and found to have serious hip fractures on both sides. The doctors fixed the hips in two steps, seven days apart, to make sure the bones healed well. In each surgery, they used a special ring to hold the hip socket in place and a special hip replacement with a stem that fits into the thigh bone. The ring was placed in the pelvis and held with screws to keep it strong. The man did not have any problems after surgery. At one year, he could walk fully with a walking stick, had a good hip score (77 on the right, 79 on the left), and only had a little pain or limp. He hasn’t had any serious issues since and is doing well.


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 polytrauma code was activated due to hemodynamic instability, not 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 evaluate for intra-abdominal pathology, and 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, 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 fibrotic consolidation at the fracture sites and to minimize intraoperative bleeding. Surgery 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 thromboprophylaxis. The left hemipelvis was operated first due to greater pelvic protrusion, which increased the risk of soft tissue hematoma formation during femoral head extraction, potentially leading to vascular injury or excessive bleeding. The procedure employed a posterior lateral approach with Moore's autograft placement to reconstruct the acetabular fracture bed. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Prior to ring placement, dissection of the gluteal musculature (gluteus minimus and medius) was required to accurately reposition the femoral head. The ring was verified under direct visualization. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsule and pelvic musculature were closed using transosseous trochanteric suture points. The right hemipelvis was operated seven days later. For the longitudinal iliac wing fracture, a six-hole anatomical plate was used via an ilio-inguinal approach. The same surgical sequence—anti-protrusion ring with double-mobility cemented acetabular ring and non-cemented femoral stem—was repeated. Anti-protrusion rings are indicated in acetabular fractures involving the acetabular background (e.g., Type IV AAOS classification), where pelvic disjunction is possible, and require anchorage in both ischium and ilium to provide structural support. They are not indicated for isolated anterior or posterior wall fractures without acetabular bed involvement. The patient remained bedridden during admission and was mobilized to prevent pressure ulcers. After the second surgery, clinical tolerance permitted initiation of wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with full weight-bearing delayed until six weeks due to the need for initial graft consolidation in the acetabular background to ensure stable ring support, and due to bilateral hip pathology, which precluded safe partial loading with one hip serving as a functional support. The patient began full load with a walking stick at six weeks. At 12-month follow-up, the patient achieved full weight-bearing with a Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12, indicating minimal pain and functional limitation. No postoperative complications have been reported to date. The patient reports occasional discomfort and a mild right-sided limp, but maintains full range of motion and no episodes of hip instability. The surgical approach successfully addressed bilateral acetabular fractures with associated femoral head protrusion, utilizing staged reconstruction with biomechanically stable fixation to restore joint integrity and function in a high-risk, cognitively impaired elderly population.


A 19-month-old boy fell from a highchair and hit his head. He was fine at first, but then started vomiting and became very irritable. He was breathing fast and not getting enough oxygen. His chest looked like it was pulling in, and one side of his lung wasn’t working well. Doctors gave him a breathing tube to help him breathe, but his oxygen levels kept dropping. A scan showed the left lung was completely collapsed, and the main airway to that lung was blocked. The doctors thought a small almond, about 2 cm, had gotten stuck there. The boy had never eaten almonds before and probably swallowed it by accident. After the almond was removed, his breathing got better and he was able to breathe on his own again. He stayed in the hospital for a few days and is now doing well.


A 19-month-old male was admitted to the Emergency Department following a fall from a baby feeding highchair. The fall occurred while the child was in apparent well-being, with no prior signs or symptoms of distress. The mechanism of injury involved initial gluteal contact followed by a direct impact to the occiput (back of the head). The child presented with three episodes of vomiting and was markedly irritable. 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 diminished breath sounds localized to the left basal lung region. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to supplemental oxygen and continuous pulse oximetry. However, despite this intervention, oxygen saturation progressively declined below 70%, and ventilation-induced worsening of hypoxemia was observed, suggesting impaired gas exchange. Lung ultrasound revealed the absence of normal A lines and evidence of pulmonary consolidation, interpreted as solid parenchymal opacification consistent with alveolar collapse or obstruction. Given the severity of respiratory compromise, orotracheal intubation with a cuffed endotracheal tube was performed to secure airway patency and ensure adequate oxygenation. Following stabilization, a chest computed tomography (CT) scan was obtained, which demonstrated complete atelectasis of the left lung and a discrete interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation (i.e., the point where the left and right main bronchi divide). This radiographic finding, combined with the clinical history of a recent, self-limiting cough episode in the days prior, raised a strong suspicion of foreign body aspiration (FBA). The mother reported that the infant had experienced a severe cough attack that resolved spontaneously within 24 hours without medical intervention. Rigid bronchoscopy was subsequently performed, during which a 2 cm diameter almond was identified within the proximal left main bronchus and was successfully removed. Notably, the child had no prior exposure to nuts or any known history of food ingestion, and the almond was ingested incidentally during routine feeding. Post-intervention, the patient exhibited a progressive clinical recovery, with oxygenation improving steadily. At 24 hours post-intubation, the patient was extubated and transferred to the general pediatrics ward for continued observation. Over the following days, full respiratory function was restored, and the child was discharged without further complications. The case highlights the potential for asymptomatic or transient respiratory symptoms to precede significant airway obstruction, and underscores the importance of high index of suspicion for foreign body aspiration in pediatric patients presenting with acute respiratory distress following minor trauma, particularly when associated with a history of cough or atelectasis on imaging.


{
  "proficient_health_literacy": "A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axilla, prompting medical evaluation. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who received pharmacological intervention. The infant was born with normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother was incarcerated in a prison cell with the infant and two other individuals, living in a crowded environment. At 4 months of age, the infant was admitted to a pediatric hospital following a chest X-ray that demonstrated suggestive radiographic findings of rib fractures, leading to suspicion of child abuse. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized pain, redness, and warmth 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 revealed a left axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological analysis of the axillary abscess demonstrated suppurative panniculitis and myositis. 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. \n\nAt 8 months of age, the infant was readmitted with fever, irritability, and extension of the suppurative process to the left scapula. Repeat laboratory values 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 associated with the scapular abscess. The infant was initially treated with piperacillin-tazobactam, which was subsequently replaced with voriconazole after *Aspergillus fumigatus* was isolated from the abscess secretion. Given the recurrent and progressive nature of the infection, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) fluorescence assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and immunofluorescence 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, specifically c.80_83del/Y (p.Val27Glyfs*33), which results in a frameshift mutation and premature termination of the gp91phox protein. The mother was identified as a carrier of the same variant (c.80_83del/WT), consistent with X-linked recessive inheritance. The two older male siblings, who were clinically asymptomatic, 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 for bacterial infection


{
  "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 and lip lesions. The lesions initially appeared as canker sores in the oral cavity four days prior to presentation, subsequently extending to the upper and lower labial mucosa two days later. The patient reported exacerbation of symptoms during eating and speech. Initial self-management with petroleum jelly failed to provide relief; he then used triamcinolone acetonide 0.1% in orabase ointment, applied once daily, which resulted in partial symptomatic improvement but no complete resolution of the lesions.\n\nThe patient reported a preceding febrile illness lasting approximately one week prior to lesion onset, with no cutaneous or systemic manifestations elsewhere. He described a history of chronic poor nutritional intake over the past one and a half months, associated with high work-related stress. There was no known medical history, food allergies, medication use, alcohol consumption, or tobacco use. However, he had a documented history of chickenpox in childhood. He maintained a habit of frequent lip-licking and lip-peeling, which was identified as a potential contributing behavioral factor.\n\nGeneral examination revealed normal vital signs and no lymphadenopathy. Extra-oral examination demonstrated serosanguineous crusts on the lips, which were tender and prone to bleeding. Intra-oral examination revealed diffusely erythematous, irregularly bordered, painful lesions on the upper and lower labial mucosa. Additional findings included hyperkeratotic, non-scrapable white plaques with diffuse borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques covering one-third of the posterior dorsal tongue with associated dental impression indentations (non-painful), and a painless, 2×1×0.5 cm hard nodule in the midline of the hard palate. Dental evaluation identified carious lesions, root caries, and edentulism in multiple teeth (teeth 28, 36, 37, and 46), with diagnoses of reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis due to root caries (tooth 15), and associated periodontal disease. Oral hygiene was assessed as suboptimal.\n\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6). Based on clinical presentation and history, the working diagnosis was suspected to be Herpes Simplex Virus-1-associated Erythema Multiforme (HAEM), with concomitant findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, and multiple dental pathologies. Differential diagnosis considered exfoliative cheilitis, which was excluded due to the absence of herpesvirus involvement. Serological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (positive when ratio > 1.1), confirming active HSV-1 seropositivity and supporting the diagnosis of HAEM.\n\nOral health-related quality of life (OHRQoL) was assessed using the OHIP-14, with an initial score of 35, indicating moderate impairment. The treatment plan included both pharmacological and non-pharmacological interventions. Non-pharmacological measures comprised instruction in daily oral hygiene (soft-bristled toothbrush, twice daily; non-detergent toothpaste), increased daily water intake (≥2 liters), balanced nutrition, avoidance of acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods, and cessation of lip-licking and lip-peeling behaviors. Pharmacological therapy included topical application of triamcinolone acetonide 0.1% in orabase (three times daily), gauze compression with 0.9% NaCl solution (three times daily), and systemic administration of multivitamins (once daily). Following one week of treatment, acyclovir 200 mg tablets were initiated orally, administered five times daily for one week to target viral replication.\n\nClinical improvement was observed at the first follow-up (two days post-initial visit), with significant reduction in lip pain, though the canker sores remained incomplete. At the second follow-up (five days later), complete healing of all oral lesions was achieved. The final OHIP-14 score improved to 4, indicating excellent OHRQoL. The patient’s physical, psychological, and social functioning returned to baseline within seven days of treatment. The patient was referred for continued management in periodontics,


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 was discontinued for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological decline (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly documented. Physical examination revealed a large cervical mass measuring 8 × 8 cm extending into the parametrium and bilateral pelvic side walls, 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 biopsy of the cervix confirmed an extra-nodal Burkitt lymphoma (BL), with immunohistochemical staining positive for CD20, CD75a, CD10, PAX5, and BCL6; CD44 and c-Myc were also positive, with focal EBER in situ hybridization (ISH) positivity. The Ki67 proliferation index was nearly 100%, indicating extremely high cellular proliferation, and PAX5 and BCL6 showed moderate expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), serum creatinine of 187 mmol/L (indicating significant renal impairment), urea 11.1 mmol/L, albumin 21 g/L, aspartate transaminase 41 U/L, and alkaline phosphatase 100 U/L. The patient was recommenced on ART, transitioning from a TLD (Tenofovir-Lamivudine-Dolutegravir) regimen to a renal-sparing Lamivudine-Abacavir-Dolutegravir combination to mitigate further nephrotoxicity. Following histological confirmation and multidisciplinary oncology review, a treatment plan of chemoradiation was recommended. However, due to a prolonged waiting list at the referral oncology unit, the patient waited 43 days before receiving any treatment—exceeding the recommended 48-hour window for initiating therapy in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was performed due to technical limitations in the available equipment. The patient received supportive care including blood transfusions and analgesia. She died in the gynecological ward on day 43, with the interval between diagnosis of BL and death remaining 43 days. A postmortem histopathological examination was not conducted, as both the Burkitt lymphoma and HIV infection were already established and well-documented. The primary cause of death remains difficult to assign due to the coexistence of multiple severe comorbidities; however, given the aggressive nature of BL in the context of advanced HIV infection with high viral load and profound immunosuppression, the attending physician concluded that BL was the most likely primary cause. The secondary cause of death was multiple organ failure, encompassing both renal and hematological dysfunction, reflecting the systemic impact of the disease and the underlying immunodeficiency. This case underscores the critical importance of timely diagnosis and initiation of oncological intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of high-risk lymphoma subtypes such as extra-nodal BL.


{
  "proficient_health_literacy": "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 findings on chest X-ray consistent with 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. Computed tomography of the chest (CNYCT) showed an enlarged pulmonary trunk, right atrium, and right ventricle, supporting the diagnosis of pulmonary hypertension. Objective signs of Sjögren’s syndrome included dry mouth, dry eyes, cracked tongue mucosa (Schirmer’s test <5 mm), positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and a positive anti-Ro antibody test. The patient was initiated on sildenafil (Revatio) 20 mg three times daily (TID) for PAH management, with addition of bosentan (Tracleer) in 2016 due to disease progression. Right heart catheterization (RHC) in 2017 confirmed pre-capillary, group I PAH with a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, consistent with chronic pulmonary hypertension and right heart strain. Based on these findings, the patient was eligible for opsumit (macitentan) 10 mg once daily (QD), which replaced bosentan in 2017. From 2017 to 2020, she required repeated hospitalizations for corticosteroid therapy to manage active Sjögren’s syndrome. Prior to 2017, her PAH was classified as low to intermediate risk and managed with dual therapy (sildenafil and macitentan), with stable disease progression. However, in October 2020, she presented with worsening dyspnea, cough, and white sputum, suggestive of respiratory infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and SpO2 of 70%, requiring 100% oxygen via face tent. 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 pulmonary vasodilator agents. Her condition stabilized, with successful weaning from vasopressors on November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support tapered to nasal cannula at 2 L/min. Follow-up RHC continued to demonstrate elevated pulmonary artery pressure, reflecting persistent right heart strain and likely progression toward right heart failure. The patient was subsequently referred to National Taiwan University Hospital for evaluation for heart-lung transplantation. Over time, her 6-minute walk distance progressively declined, and her pulmonary artery pressure trajectory showed a steady upward trend, leading to current classification as high-risk. Despite stabilization, dyspnea remains her primary clinical complaint. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur indicative of severe valvular heart disease. In 2020, ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023 using PURE HYDROGEN capsules manufactured by 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. Adjuvant administration of hydrogen therapy was associated with significant immunomodulatory effects: flow cytometry and serological analyses revealed an increase in CD127+ regulatory T cells (Tregs), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These changes were assessed via standardized fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA) using immun


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 had strange eye movements, muscle jerks on one side of his face and chest, and then a full seizure. After that, he had weakness on his left side. Tests showed the virus was in his brain fluid, which means it may have spread to his brain. But over time, his symptoms got better, and he fully recovered. He was able to go home after 31 days with no need for medicine to stop seizures and will see his doctor for follow-up.


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. After 16 days in the hospital, he suddenly developed a change in consciousness, with his eyes turning toward the right and strange, brief jerking movements on his left side (face and chest). This was followed by a full seizure, and he ended up with weakness on his left side that didn’t go away. Tests showed the virus was present in his cerebrospinal fluid, which is the fluid around the brain and spinal cord. This finding suggested the virus had affected his brain, possibly causing encephalitis. However, there was no sign of bacterial infection or other common causes of seizures. The patient’s condition gradually improved, and by day 31, he was able to leave the hospital without needing anti-seizure medication. His recovery was considered favorable, and follow-up care was arranged.


{
  "proficient_health_literacy": "A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted with a history of grade 3 obesity and no other significant comorbidities or pharmacological therapy. He presented to emergency care with a four-day course of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. On initial neurological examination, no abnormalities were noted. Respiratory evaluation revealed tachypnea and bilateral rough vesicular murmurs on auscultation, consistent with diffuse pulmonary involvement. Laboratory findings showed mild elevation in inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal opacities on chest radiography. A positive reverse-transcription real-time polymerase chain reaction (RT-PCR) for SARS-CoV-2 was obtained from nasal and oropharyngeal exudates, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a diagnosis of SARS-CoV-2-associated pneumonia.\n\nOver the first 48 hours, progressive deterioration in fatigue, dyspnea, and respiratory function necessitated escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow oxygen via nasal cannula was then implemented without clinical benefit. The patient was subsequently transferred to a level III intensive care unit (ICU), where sedoanalgesia was administered and orotracheal intubation with invasive mechanical ventilation was performed.\n\nOn day 11 of hospitalization, the patient received remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) on suspicion of secondary bacterial superinfection. Despite persistent fever refractory to antipyretics, inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious etiologies, intravenous lines were replaced, and blood cultures, catheter tip cultures, bronchial secretions, urinalysis, urine culture, and transthoracic echocardiography were performed. Only one positive blood culture was obtained: Klebsiella pneumoniae, which is susceptible to amoxicillin/clavulanic acid—antibiotic 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) along with 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 ruled out.\n\nInotropic support with dobutamine was required during ventilatory weaning and post-extubation phases. On day 16 of hospitalization (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, conjugate gaze deviation to the right, left-sided myoclonus involving the face and thoracic region, followed by a generalized tonic-clonic seizure, which was terminated with midazolam. Hypoxic-ischemic etiology was excluded due to sustained normotension, absence of peri-event hypoxemia or hypoxia, normal serum lactate levels, and preserved diuresis. Electrolyte and glucose levels were within normal limits, ruling out metabolic or ionic triggers for the seizure.\n\nPost-ictal assessment revealed a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, no localizing to pain), with persistent left hemiparesis of grade 3/5. Due to airway compromise, the patient remained intubated and received anticonvulsant therapy. Lumbar puncture was performed, yielding turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF was tested for neurotropic viruses, venereal disease research laboratory (VDRL) activity, acid-alcohol resistant bacteria, and SARS-CoV-2 via RT-PCR; the latter was positive, confirming the presence of SARS-CoV-2 RNA in CSF without pleocytosis. This finding excluded bacterial meningitis and supported a diagnosis of SARS-CoV-2 encephalitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity. MRI performed on day 17 revealed multiple artifacts attributable to patient movement, necessitating repeat imaging.\n\nFollowing discontinuation of sedoanalgesia, the patient exhibited a gradual improvement in mental status with a GCS of 14, persistent left hemiparesis (muscle strength grade


The person had a long-lasting cough, ear pain, and a foul-smelling pus coming out of their right 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, and no bacteria were found in the ear or stomach. They also started taking HIV medicine again and got better overall. Now they are fully healed and healthy.


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 the fluid from the stomach and in the pus from the ear, which pointed to tuberculosis. The patient also had HIV, which weakened his immune system, making him more susceptible to tuberculosis. He was treated with a 6-month course of anti-tuberculosis medication, including four drugs in the first two months, followed by two drugs for the next four months. He also received treatment for HIV again, and was given antibiotics to prevent complications. After treatment, his symptoms fully improved, the bacteria tests became negative, and his overall health returned to normal. His HIV virus levels dropped significantly, showing the treatment was effective.


{
  "proficient_health_literacy": "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 included artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media, which failed to resolve the symptoms. The patient is HIV-1 infected, with a diagnosis established 7 months prior, and has been on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir; however, adherence to this regimen has been poor due to denial of his HIV status.\n\nPhysical examination revealed a fever of 38.2 °C, altered general condition, right-sided otalgia, purulent foul-smelling otorrhea, and a right basal pulmonary condensation consistent with bronchovascular hyperactivity. Neurological examination was normal, with no cranial nerve involvement, particularly the facial (VII) and cochleovestibular (VIII) nerves. Otoscopic evaluation of the right ear demonstrated inflammatory changes in the external auditory canal with purulent exudate and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was intact. Rinne and Weber tests confirmed a right conductive hearing loss.\n\nImmunological and virological assessments showed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL at the time of HIV diagnosis. Following 6 months of ART, the CD4 count increased to 193 cells/μL and the viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (7 months post-HIV diagnosis), the CD4 count declined to 89 cells/μL and the viral load was 10,230 copies/mL, reflecting immunosuppression conducive to opportunistic infections.\n\nMicrobiological testing via Ziehl-Neelsen bacilloscopy was positive for acid-fast bacilli in gastric washings upon admission and again 19 days later in a right ear swab due to persistent otorrhea. The Xpert-MTB/GeneXpert assay, which detects *Mycobacterium tuberculosis* and rifampicin resistance, was negative for rifampicin resistance, indicating susceptibility to first-line anti-tuberculosis agents.\n\nChest radiography revealed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. The clinical and radiological findings, combined with the positive acid-fast bacilli in both gastric fluid and ear pus, support a diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-induced immunosuppression.\n\nThe patient was initiated on a 6-month standard first-line anti-tuberculosis regimen: an intensive phase of quadruple therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months (2RHZE), followed by a maintenance phase of dual therapy (isoniazid and rifampicin) for 4 months (4RH) at a dose of 3 tablets/day 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) to improve HIV suppression. ART was restarted on 4 May 2023 with patient consent, using tenofovir/lamivudine/dolutegravir (1 tablet/day) plus an additional dolutegravir 50 mg tablet (1 tablet/day) in accordance with current HIV management guidelines. Chemoprophylaxis with cotrimoxazole (960 mg once daily) was administered, and the external auditory canal was cleaned via aspiration, with ciprofloxacin ear drops (2 drops, three times daily) administered for 14 days to manage ear infection.\n\nClinical improvement was observed within 14 days of treatment, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy became negative in both the gastric washings and the right ear pus swab. At the end of the 6-month anti-tuberculosis treatment, complete clinical healing was achieved, with normalization of ENT and neurological examinations. Follow-up bacilloscopy and Xpert-MTB/GeneXpert testing were negative at the end of the intensive phase (month 2), at month 5, and at the end of the maintenance phase (month 6). Post-treatment


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 special tube to clear the blocked blood vessel and fixed it successfully. The boy was small for his age but 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 and preserved brain motor potential, exhibiting normal psychomotor development, was diagnosed with restrictive cardiomyopathy and enrolled in a cardiac transplant programme at 16 months of age. He received external biventricular support via an implantable Berlin Heart device to bridge to transplantation. To mitigate the risk of embolic complications, he was maintained on 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, he presented with acute disconnection and right hemiparesis, consistent with a left middle cerebral artery (MCA) occlusion. Non-contrast computed tomography (CT) revealed a hyperdense left MCA, indicative of thrombus, and a chronic right parietotemporal infarct, suggesting prior ischemic injury. Laboratory parameters showed red blood cell count of 4.16 × 10⁶ µ/L and hemoglobin of 11.4 g/dL, within normal limits. Intravenous thrombolytic therapy was contraindicated due to active anticoagulation. Consequently, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and placement 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. Recanalisation 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 within 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 system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. During the procedural control run, an iatrogenic dissection of the left internal carotid artery was identified, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately supplied via the anterior communicating artery. Post-procedure, the patient underwent successful cardiac transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with residual corticospinal tract dysfunction following the stroke. The case demonstrates the feasibility and clinical efficacy of intra-arterial mechanical thrombectomy in a young pediatric patient with complex comorbidities, including congenital cardiomyopathy and anticoagulated state, and highlights the importance of meticulous vascular mapping and perfusion monitoring during such interventions.


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 before. When doctors checked him, they found a broken shoulder on his left side too — a problem that wasn’t seen at the first hospital. The injury got worse in the left shoulder because he was held down and moved too much during his stay. Doctors used X-rays and CT scans to see the damage. They fixed both shoulders at the same time with metal plates and strong stitches. The right shoulder healed well, but the left one needed two more surgeries — one to fix the broken piece and another to open up the joint. Two years later, he can move his shoulders a lot better, with a score of 5% on a pain scale and 72 and 76 on a mobility scale for left and right shoulders, which means he’s doing better than most people in similar cases.


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. When first evaluated, he had visible bruising on both shoulders and limited ability to move his arms, especially rotating them outward. He was physically restrained due to agitation.

Initial X-rays showed a dislocation in his right shoulder and a simple posterior dislocation in his left shoulder — a problem that had not been seen at the previous hospital. A follow-up CT scan revealed that the left shoulder injury had worsened since admission, likely because of the physical restraint. Both shoulders were surgically treated at the same time with a procedure called open reduction and internal fixation using locked plates to realign and stabilize the bones.

The right shoulder had a fracture that was partially fixed with a screw and strong sutures. The left shoulder had a smaller bone defect, which was filled using a piece of the shoulder bone itself (a technique similar to McLaughlin’s method). However, the left shoulder needed two additional surgeries: one to fix the broken bone properly and another to release the stiff joint.

After two years, the patient is doing well. He scores 5% on the Quick DASH scale (which measures 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. He was able to return to work five months after the injury and is now progressing toward full recovery, though his left shoulder still has limited range of motion, especially in external rotation.


A 52-year-old male with no prior 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. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. Radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had been missed at the referring facility and was only identified after a 48-hour delay.

Computed tomography (CT) of both shoulders demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission to a full LFGHP within 48 hours, likely attributable to mechanical stress from prolonged physical restraint. This intrahospital aggravation underscores the role of external forces in the destabilization of glenohumeral joint integrity, particularly in the setting of altered neuromuscular control.

Preoperative imaging of the right shoulder revealed glenoid bone integrity with 40% articular surface involvement of the humeral head, including a large fragment that was amenable to osteosynthesis in continuity with the lesser tuberosity. A 4.0 mm spongy screw with high-strength sutures was planned for fixation to preserve humeral head stability. In contrast, the left shoulder demonstrated intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed via repositioning and fixation of the lesser tuberosity fragment during osteosynthesis, mimicking the surgical technique described by McLaughlin.

Surgical intervention consisted of open reduction and internal fixation (ORIF) using bilateral locked plates. The patient was positioned in a beach chair position, and both shoulders were approached via classic deltopectoral incisions. 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 fixation with a 4.0 mm spongy screw and high-strength sutures. Definitive stabilization was accomplished with a Philos (Depuy Synthes®) locked plate, with additional fixation of the rotator cuff tendons to the plate to enhance biomechanical stability. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.

The left shoulder was operated on immediately after, using the same deltopectoral approach with an accessory posterior portal for digital reduction. Fixation was performed similarly, except that the anterior humeral fragment was stabilized exclusively with high-strength sutures due to insufficient anatomical support for a spongy screw. Postoperative management included bilateral shoulder immobilization for four weeks, followed by a progressive rehabilitation protocol beginning at the second postoperative week. Exercises included pendular flexion-extension of the elbow and fist mobilization, administered as tolerated based on pain levels.

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 achieve adequate fixation using high-strength sutures. The patient continued with immobilization for an additional four weeks on the left side. Bilateral self-administered 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 rehabilitation, the patient returned to work five months following the initial trauma.

One-year follow-up demonstrated full recovery of strength and range of motion in the right shoulder. The left shoulder, however, retained significant limitations, particularly in external rotation. At this point, arthroscopic joint release was performed with removal of the osteosynthesis hardware to address chronic joint contractures and mechanical impingement. Two years post-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 sustained improvement in pain, function, and daily activity capacity. These results reflect both the efficacy of early surgical intervention and the importance of staged rehabilitation in managing complex glenohumeral injuries, especially in the context of secondary trauma from restraint and delayed diagnosis.


A 70-year-old man had a weak heart that was leaking badly, so doctors put in a new valve (TAVI) through his chest to fix it. After that, his heart started failing again, so they added a machine (LVAD) to help his heart pump. One year later, the machine was giving warning signs, and scans showed the old valve was still leaking badly. The doctors decided to fix the old valve from the inside with another new valve (valve-in-valve). They slowed down the machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, the man is doing great — no more leaks, better heart strength, and can walk much farther without trouble.


A 70-year-old man with severe heart valve problems was treated first with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a condition called aortic regurgitation, where blood leaks backward through the aortic valve, caused by past heart infection. Because his heart function was very weak and he had other serious health issues, surgery was too risky, so TAVI was chosen. The procedure used a new valve (JenaValve) and worked well initially, with only a small amount of leakage. However, four weeks later, his heart failed again due to poor pumping ability, so he received a left ventricular assist device (LVAD) to help his heart pump blood. After one year, the LVAD showed signs of high flow and echocardiograms showed worsening leakage through the aortic valve, even though the original valve itself looked normal. The medical team decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve (CoreValve Evolut R) was placed inside the existing one. During this procedure, the LVAD flow was reduced to the lowest level and the heart was paced at 140 beats per minute to help the new valve settle properly. The placement was carefully guided using imaging. The procedure was successful, and at 12 months, the patient had no significant leakage, improved heart function (LVEF increased to 33%), and could walk much farther without symptoms. He is now doing well and living a normal daily life.