A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. At presentation, she was hemodynamically stable, without respiratory distress or requirement for supplemental oxygen. Physical examination revealed a painful, homolateral cervical adenopathy and significant trismus. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with all other parameters within normal limits. Imaging studies included a head and neck CT, which revealed a large thrombus in both the internal and external carotid arteries, consistent with a thrombotic event secondary to severe local inflammation or endothelial activation. Arterial Doppler ultrasound of the neck vessels showed no significant stenosis or flow abnormalities, but the presence of carotid thrombus suggests a systemic inflammatory response. A chest CT scan demonstrated bilateral pulmonary septic emboli, indicating dissemination of infected material via venous thrombus from the head and neck region to the pulmonary circulation. Initial empiric intravenous therapy was initiated with ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover potential Gram-positive and anaerobic pathogens, including those associated with odontogenic infections. Concomitant anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to prevent extension of the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging. Echocardiography excluded cardiac vegetations, ruling out endocarditis as a source of emboli. A repeat chest CT confirmed bilateral pulmonary septic emboli. Hemocultures obtained at admission were negative, leading to the decision to perform culture of pharyngeal exudate and initiate a broader-spectrum antibiotic regimen with piperacillin-tazobactam 4.5 g every 6 hours intravenously, replacing ceftriaxone. No pathogen was isolated from cultures, suggesting a possible non-bacterial or polymicrobial infection with limited cultivability. The patient responded favorably to treatment, with resolution of fever and clinical signs of infection. After 14 days of optimized therapy, follow-up chest CT showed absence of pulmonary lesions, and the patient was transitioned to oral clindamycin 300 mg every 6 hours for continued coverage of anaerobic organisms. Anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels, with the patient achieving stable coagulation parameters and being discharged. The clinical course reflects a rare but severe complication of odontogenic infection—systemic thrombosis and septic embolization—likely driven by intense local inflammation, endothelial injury, and hypercoagulability, with potential contributions from underlying comorbidities such as asthma and prior viral infection, which may predispose to dysregulated immune and coagulation responses.


A 5-year-old child swallowed a dangerous poison called chlorpyrifos and also breathed in a mixture of charcoal and palm oil. This caused serious problems: breathing stopped, the child went into a deep sleep, had no movement in the arms and legs, and was very weak. The child was rushed to the hospital where they gave breathing support, gave medicine to stop the poison, and used blood changes to help the body. The child started to get better within hours, didn’t have a later serious problem (called intermediate syndrome), and was home after 10 days. The doctors kept the child safe and helped them recover step by step.


A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after accidentally ingesting it. Shortly after, the child also aspirated (inhaled) a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, difficulty breathing, excessive sweating, vomiting, and eventually coma. At the time of arrival at the emergency department, the child had very low consciousness (Glasgow Coma Score of 3), pinpoint pupils, and signs of shock and respiratory failure.

The child was treated with non-invasive ventilation to help with breathing, intravenous atropine to counteract the poisoning, and medications to support blood pressure and reduce inflammation. Because the family could not afford intensive care, the treatment was kept manageable. The child also received exchange transfusions (a blood exchange to remove toxic substances) and antibiotics for lung infection. Hypoglycemia (low blood sugar) was treated with dextrose, and heart issues were managed with fluids and a dopamine infusion.

Over the next few days, the child’s condition improved steadily. Consciousness returned, breathing became easier, and lung symptoms improved. By day 10, the child was stable enough to be discharged home. The child did not develop a known complication called intermediate syndrome and recovered well from the poisoning. However, after discharge, the child was not followed up by healthcare providers.


{
  "proficient_health_literacy": "A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingesting chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The initial clinical presentation included generalized abnormal jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), severe dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient had lapsed into coma prior to arrival, with a presenting temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation included a heart rate of 180 beats per minute, blood pressure of 120/80 mmHg, and a random blood glucose of 14 mg/dL. Physical examination revealed widespread crackles on auscultation, indicating pulmonary edema or aspiration-related pulmonary injury. Serum cholinesterase activity and lactate levels were not measured due to institutional limitations.\n\nThe diagnosis was established as severe organophosphate poisoning (OPP) with concomitant aspiration pneumonitis. Given the severity of respiratory failure and the unavailability of intensive care resources, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which improved oxygen saturation to 99–100%. Hypoglycemia was managed with a dextrose bolus, and tachycardia was treated with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered for suspected aspiration-related pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose, with the first dose leading to a significant tachycardia, prompting discontinuation due to hemodynamic instability. Pralidoxime, a reactivating agent for organophosphate-inhibited acetylcholinesterase, was not administered due to unavailability.\n\nWithin 3 hours of presentation, the patient underwent a fresh-whole-blood exchange blood transfusion (FWB-EBT) of 500 mL to rapidly reduce circulating organophosphate metabolites and mitigate cholinergic toxicity. The GCS improved to 9/15 following this intervention. Over the subsequent 15 hours, blood glucose fluctuated between 41 and 259 mg/dL, eventually stabilizing with continued management. On day 2 of admission, the patient developed thready pulses and hypotension, prompting a second bolus of normal saline. Dopamine infusion was initiated at 5 mcg/kg/min via peripheral venous access, and intravenous mannitol was discontinued. A second FWB-EBT of 500 mL was performed.\n\nOver the first 30 hours, there was a progressive improvement in consciousness and resolution of respiratory distress. However, rhonchi were noted, managed with nebulized salbutamol and budesonide, and the patient was transitioned to nasal prong oxygen therapy, maintaining stable oxygen saturation at 97%. A chest radiograph on day 2 revealed bilateral pulmonary infiltrates consistent with aspiration pneumonia. Full recovery of consciousness was achieved by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B, and oral vitamin E and zinc to mitigate oxidative stress associated with acute organophosphate toxicity. A graded reintroduction of oral diet was implemented over the following 48 hours.\n\nThe patient’s clinical course remained stable, and he was discharged home after 10 days of hospitalization. However, follow-up care was not maintained, resulting in loss to follow-up. The patient did not develop the intermediate syndrome, a known risk in organophosphate poisoning characterized by delayed neuromuscular weakness typically occurring 24–96 hours post-exposure, which may have been attributed to the rapid clinical response, early intervention, and absence of prolonged cholinesterase inhibition.\n\nThis case underscores the pathophysiological mechanisms of organophosphate toxicity, including acetylcholinesterase inhibition leading to excessive acetylcholine accumulation at neuromuscular junctions and in the central nervous system, resulting in muscarinic and nicotinic cholinergic overstimulation. The clinical manifestations include bronchospasm, respiratory failure, hypotension, seizures, and coma. Aspiration of lipid-rich substances like palm oil may exacerbate pulmonary injury through direct chemical irritation and mechanical obstruction, contributing to secondary pneumonia. The use of exchange transfusion in this setting is a rare but effective strategy to rapidly remove toxic metabolites and restore physiological balance in severe OPP, particularly in resource-limited settings where advanced supportive care is not available. The absence of pralidoxime administration highlights a critical gap in access to antidotal therapy in


A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working hard, and there was no sign of a heart attack or heart muscle damage. After checking her heart with different scans, doctors found a birth defect: the main blood vessel going to her right heart was missing at the start. This missing part caused her heart to beat wrong and made her feel sick. Doctors found the problem spot on a small muscle in her heart, fixed it with a special treatment, and now she feels fine and has not had any problems since.


A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed high levels of markers for heart stress. A 12-lead ECG ruled out a heart attack, and a cardiac MRI did not show signs of heart muscle disease. Because of this, a cardiac CT scan (CCTA) was done to look for a congenital heart problem. The scan found that the opening of the right coronary artery was completely missing, and the rest of the artery was supplied by a collateral branch from another artery. This is a rare congenital anomaly. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was starting in the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has been symptom-free and is doing well with regular follow-up.


{
  "proficient_health_literacy": "A 19-year-old female presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicative of myocardial injury and cardiac stress, respectively. These findings prompted admission to the coronary care unit with a clinical suspicion of cardiogenic shock due to underlying structural or electrical cardiac pathology.\n\nFive years prior, she had experienced cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation with cardiac magnetic resonance (CMR) and transesophageal electrophysiological study (TEES) yielded inconclusive results, leading to a diagnosis of tachycardiomiopathy. She was initiated on standard medical therapy including angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with regular follow-up scheduled. Clinically, no further events were reported during this interval.\n\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive, reinforcing the need for further anatomical evaluation. Given the clinical history of recurrent arrhythmias and cardiogenic shock in the absence of obstructive coronary disease, cardiac computed tomography angiography (CCTA) was performed to assess for undiagnosed congenital coronary anomalies.\n\nCCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness. Intravenous contrast was administered at 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy). The imaging demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery featuring a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No evidence of significant stenosis or obstructive coronary artery disease was identified. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch arising from the distal LAD, which courses along the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a small branch originating from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to arrhythmogenic substrate.\n\nThe differential diagnosis of cardiogenic shock in a young, otherwise healthy adult must consider both acquired and congenital etiologies. While myocardial infarction is a common cause, it was ruled out by the absence of typical ST-segment changes on ECG and normal coronary anatomy in the absence of obstructive lesions. Similarly, conventional cardiomyopathies were excluded by CMR, which showed no evidence of diffuse myocardial fibrosis or structural remodeling. In such cases, undiagnosed congenital coronary anomalies, particularly ostial atresia of a major coronary artery, represent a critical but often overlooked cause of sustained ventricular arrhythmias and cardiogenic shock.\n\nFollowing CCTA, an echo-stress test was performed, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical origin of the arrhythmic focus. The patient was referred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the posteromedial papillary muscle, the identified site of sustained ventricular tachycardia. The procedure successfully eliminated the arrhythmic substrate. Post-procedural follow-up at 6 months demonstrated sustained clinical stability, with complete absence of symptoms and no recurrence of arrhythmias. She is currently managed with acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing congenital coronary anomalies in young patients with recurrent arrhythmias and cardiogenic shock, particularly when conventional tests fail to identify underlying pathology.\n\nScientific context: Ostial atresia of the right coronary artery is a rare congenital anomaly in which the origin of the RCA is completely obstructed or absent, leading to


A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was stuck under the floor of his nose, covered with mucus and crust, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. After getting permission from his parents, the button was gently removed with a small tool while he was sitting up. The nose healed well, and after the removal, he was given a salt water rinse to keep it clean. At his follow-up two weeks later, everything looked normal and he was doing fine.


{
  "proficient_health_literacy": "An 18-year-old Hispanic male with no significant medical history presents to the emergency department (ED) with substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history includes paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. Patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. Occupationally, he works at an auto parts shop and plans to begin college. Initial workup reveals elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiogram (TTE) demonstrates left ventricular ejection fraction (LVEF) of 40%, severe left ventricular concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres are elevated, consistent with viral myopericarditis. Symptoms initially improve with ibuprofen and colchicine. Cardiac catheterization shows no coronary artery disease. Repeat TTE reveals LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, elevated left ventricular end-diastolic pressure, and diastolic dysfunction. Chest CT angiogram demonstrates pneumonitis and pericardial effusion. Clinical picture is initially attributed to Coxsackie virus-induced myopericarditis, with continued medical management.\n\nOn day 4 of admission, the patient develops diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE shows large pericardial effusion with signs of impending cardiac tamponade. Pericardiocentesis is performed, during which the patient experiences pulseless electrical activity (PEA) cardiac arrest requiring 30 minutes of advanced cardiovascular support. He is intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated on vasopressor therapy (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannula necessitates multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). Transferred to a tertiary center, endomyocardial biopsy (EMB) is performed due to concern for fulminant myocarditis or infiltrative cardiomyopathy. Histopathology shows no evidence of inflammatory or infiltrative processes. Repeat Coxsackie serology confirms positivity for Coxsackie A9, B2, and B6. Epstein-Barr virus (EBV) DNA quantitative PCR is elevated at 133,000 IU/mL. Subsequent TTE reveals severely reduced LVEF (10%–15%) with persistent severe concentric left ventricular hypertrophy.\n\nThe patient is initiated on intravenous immunoglobulin (IVIG) for suspected Coxsackie myocarditis and broad-spectrum antibiotics due to worsening leucocytosis without identifiable infectious focus. Colchicine is discontinued due to concern for rhabdomyolysis, evidenced by serum creatine kinase of 2874 U/L. Vasopressors are withdrawn, and the patient is extubated. He subsequently develops flushing, fever, dyspnoea, and hypoxaemia, with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decline, cardiac function improves on repeat TTE with LVEF of 25%–30%, prompting consideration of ECMO removal—however, this is unsuccessful. The patient remains on ECMO and is evaluated for left ventricular assist device (LVAD) placement, which is deemed contraindicated due to global concentric hypertrophy. Multidisciplinary team consensus supports emergency listing for heart transplantation, with potential transition to intra-aortic balloon pump (IABP) and inotrope support.\n\nDuring evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity is performed. Pathology reveals aggressive EBV-positive natural killer/T-cell lymphoma (NK/TCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1), and diffuse co-expression of Epstein-Barr virus-encoded small RNAs (EBER) by in


A 50-year-old man who smoked a lot and had bad fats in his blood for years got a rare eye problem where one eye (right) swelled up fast and couldn’t move properly. This caused constant double vision that made daily life hard. His thyroid was normal, but his body made a little bit more of a certain immune protein. Steroid shots helped a little, but didn’t fix the double vision or the eye movement. Doctors had to do surgery on both sides of the eye socket to give room for the eye to move better. A tissue sample from the eye muscle showed it was full of scar tissue and fat. This scar tissue is what made the eye move so poorly.


A 50-year-old man with a history of smoking and high cholesterol developed a rare condition called euthyroid single muscular Graves' ophthalmopathy. He had no family history of thyroid problems, but he did have a family history of heart disease and diabetes. Over several years, he noticed swelling in the right eye, pain when moving his eyes, redness, and constant double vision (diplopia) that made daily life difficult. His eyesight was normal, but he could not move his right eye properly, especially upward, which worsened his double vision. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Imaging showed that only the right inferior rectus muscle was enlarged and damaged, while the rest of the eye muscles were normal. A biopsy confirmed massive scar tissue (fibrosis) in that muscle. The patient tried steroid treatment, which helped reduce inflammation but did not fix the double vision or muscle damage. He then had surgery to relieve pressure in the eye socket, and this helped slightly. However, the main problem — the scarred muscle — remained. This case highlights a rare form of eye swelling where only one muscle is affected, and it can cause serious vision problems even when the thyroid is healthy.


We report a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early, massive mono-muscular fibrosis in the right inferior rectus muscle of a 50-year-old male patient. The patient had a significant family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He was a daily smoker (20 cigarettes/day) since age 30 and had long-standing dyslipidemia, with laboratory values showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, accompanied by moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed a severe reduction in elevation and persistent depression of the right globe in primary position, as assessed by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and eyelid aperture was 14 mm (right) versus 10 mm (left), with Hertel measurements of 24 mm (right) and 18 mm (left), confirming significant orbital expansion. The muscle orbit area ratio in the right orbit was 0.25 (in-house Autocad method; normal threshold vn ≤ 0.20 ± 0.03), indicating pathological enlargement of the inferior rectus muscle. High-resolution CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked enlargement of the lower rectus body extending to the insertion tendon, while all other extraocular muscles in both orbits showed normal morphology. Thyroid function tests were euthyroid, with only a mild elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), suggesting a low-grade autoimmune component without overt thyroid dysfunction. Electrophysiological evaluation revealed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction possibly secondary to inflammatory or fibrotic muscle changes. Thyroid ultrasound demonstrated a thyroiditis-like pattern, consistent with chronic inflammation, but no evidence of nodules or thyroid autoimmunity was found. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment consisted of intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks), which effectively resolved inflammatory signs and symptoms such as swelling and pain. However, functional outcomes—including Gorman score, Hertel measurements, and diplopia—remained unchanged, and electrophysiological parameters and visual acuity deteriorated, suggesting irreversible or progressive neuro-ocular compromise. Due to the persistent symptoms and lack of response to medical therapy, the patient underwent two-wall orbital surgical decompression in conjunction with continued parenteral glucocorticoid therapy. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early and severe fibrotic transformation of the extraocular muscle, likely driven by chronic inflammation and/or metabolic stress. This case highlights the potential for rapid progression of mono-muscular fibrosis in euthyroid GO, even in the absence of overt thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with severe ocular motility dysfunction and persistent fibrotic changes, particularly in those with comorbidities such as smoking and dyslipidemia.


A 15-year-old boy had belly pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His stomach was swollen, and tests showed his small intestine was blocked. A scan found a piece of intestine stuck in a small opening in the belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of the belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had gotten trapped. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at a pediatric surgery clinic, doing well and able to eat again.


A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t improve. He was admitted for further testing.

His abdomen was distended and had signs of intestinal blockage, which was confirmed by an abdominal X-ray. A CT scan showed a small intestine loop trapped at the Winslow hiatus — a key opening in the abdomen — causing an intestinal obstruction. This condition is called an internal hernia.

The surgery began with laparoscopy, a minimally invasive procedure, but the view was poor due to the distended intestines and the position of the liver. Because of this, the surgery was changed to an open approach — a larger incision in the middle of the abdomen — to better see and fix the problem.

During the surgery, the doctors found a five-centimeter section of the ileum (a part of the small intestine) that had herniated through the Winslow hiatus. The loop was successfully reduced, and no part of the intestine needed to be removed. No preventive steps were taken to reduce the risk of it coming back.

After surgery, the boy had a temporary slowdown in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in the pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. He is doing well and has normal bowel function.


We present a clinical case of a 15-year-old male with no significant medical history or prior surgical interventions who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including ongoing epigastric pain and biliary vomiting, prompting admission for further investigation.

Physical examination revealed acceptable general condition, afebrile status, and mild signs of dehydration. Abdominal distension was noted, with absent peritoneal signs and diminished bowel sounds. Laboratory studies were unremarkable. Abdominal radiography demonstrated findings consistent with small bowel obstruction.

Urgent computed tomography (CT) imaging revealed ascites and marked dilation of small intestinal loops, indicating interposition of a small bowel segment at the proximal transition zone of the epiploic fat, specifically at the level of the Winslow hiatus. The CT showed a distinct change in caliber of the small intestine at this anatomical landmark, suggesting intraperitoneal herniation of a segment of ileum through the Winslow hiatus.

Surgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium, with the cecum exhibiting high mobility and no adhesions to the right parietocolic space. Proximal to the terminal ileum, multiple small bowel loops were identified in the depth of the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to interference from the lower edge of the liver and the distended bowel loops. A percutaneous puncture of a dilated loop was attempted to decompress gas and improve visualization, but this did not resolve the obstruction.

Given the poor visualization and inability to accurately localize the site of caliber change, a conversion to a supraumbilical midline laparotomy was performed. In the opened abdominal cavity, the site of caliber change in the ileum was identified at approximately 40 centimetres from the ileocecal valve, confirming a herniation of a 5-centimetre segment of ileum through the Winslow hiatus. The herniated loop demonstrated characteristic congestive imprints at both ends, consistent with mechanical compression and ischemic changes due to entrapment. The normal caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (such as hernia repair or mesh placement) was applied to reduce the risk of recurrence.

Postoperatively, the patient developed a transient paralytic ileus, which resolved over five days, allowing nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection developed, which was managed conservatively with broad-spectrum antibiotics and drainage via percutaneous catheterization, resulting in favorable clinical course. The patient was discharged ten days after surgery with preserved gastrointestinal transit, absence of fever, and stable general condition.

The patient is currently under outpatient follow-up in the paediatric surgery clinic. This case highlights the diagnostic challenge of internal hernias, particularly in adolescents, where clinical presentation may mimic common gastrointestinal disorders, and imaging findings can be subtle. The Winslow hiatus, a potential site for intraperitoneal herniation due to its anatomical variability and the presence of epiploic foramen, remains a critical anatomical consideration in the evaluation of small bowel obstruction. Internal hernias are often asymptomatic until obstruction occurs, and their diagnosis relies on high-resolution imaging and surgical exploration. The absence of preventive measures in this case underscores the need for further study into risk factors and long-term outcomes in pediatric populations, particularly given the potential for recurrence in cases involving small bowel entrapment through the Winslow hiatus.


A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or had any gynecological visits. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help with the pain and infection. She went home after being watched for 4 hours and her pain went away.