A 5-year-old girl initially presented to our department due to worsening pain in the left proximal thigh.

Osteosarcoma was suspected radiographically.

Open biopsy revealed a high-grade conventional osteosarcoma.

The tumor was initially staged as IIB (T2b N0 M0).

Neoadjuvant chemotherapy was commenced in accordance with the NECO-95J protocol.

After three cycles of neoadjuvant chemotherapy, the pain was alleviated.

The extra-osseous mass was dramatically reduced.

The tumor had already invaded the epiphyseal plate and epiphysis of the left distal femur at initial presentation.

Osteo-articular resection was thought necessary so as to obtain a negative surgical margin.

At 6 years and 2 months old, distal femoral resection and temporary spacer insertion was performed.

Both medial and lateral meniscuses were preserved.

The spacer was hand-made, using an intramedullary nail of 7 mm in diameter and molded polymethylmethacrylate (PMMA).

Because there were no commercially available molds fitting the distal femur of such a young child, we made the spacer by hand, imitating the original distal femur of the patient that had been just removed.

After surgery, the left leg was externally fixed in a cast for 4 weeks.

Partial weight bearing on the affected leg, supported by a hinged knee brace, was thereafter commenced.

The spacer was dislocated at 7 months post-operatively.

The spacer dislocation prevented the patient from bearing weight.

Bone atrophy in the left leg was observed.

At 7 years and 8 months old, secondary surgery was performed with the aim of enabling weight bearing on the affected leg.

A custom-made ceramic spacer (Kyocera Corp., Japan) with a smooth straight stem of 8 mm in diameter had been ordered 3 months prior to the surgery.

Intra-operatively, after the removal of the initial spacer, a 1-cm length of the distal edge of the residual femur was removed.

The periosteum and reactive membrane around the molded PMMA was preserved.

The junction between the residual femur and the ceramic spacer was fixed with PMMA.

The junction was covered with the preserved periosteum and membrane.

After surgery, the left leg was placed in a cast for 4 weeks.

The patient re-started partial weight bearing using a hinged knee brace as with the first spacer.

The bone atrophy in the left leg was gradually resolved.

At 18 months after the second surgery, the cortexes of the femur and tibia had thickened sufficiently for expandable mega-prosthesis.

Loosening of the stem and varus deformity was observed.

A third surgical intervention was, therefore, planned.

At 9 years and 7 months old, the second spacer was removed, and the knee joint was reconstructed using a custom-made growing femoral prosthesis (Stryker Corp., Germany) with a curved porous stem of 8.5 mm in diameter fixed to the residual femur with two screws.

Intra-operatively, the PMMA around the junction was already loosened, and the stem was easily removed.

The residual femur was carefully reamed, and the stem was inserted.

Cancellous bone chips from the proximal tibial epiphysis were grafted around the bone-prosthesis junction and then wrapped with the preserved periosteum and pseudo-periosteum membrane.

The proximal surface of the tibia was also replaced, but the growth plate was preserved.

Immediately after surgery, range of motion (ROM) exercise was started.

Six weeks after surgery, partial weight bearing was permitted.

Ten months after the third surgery, the patient was able to walk unsupported.

A radiograph showed further thickening of the cortex of the residual femur.

At 10 years and 7 months old, the growing femoral prosthesis was extended by 1.1 cm.

At the latest follow-up, at 11 years and 1 month old, the patient was 143 cm in height with a limb length discrepancy (LLD) of 5 cm.

The patient was able to walk unsupported using a 2.5 cm shoe lift.

The Musculoskeletal Tumor Society (MSTS) score was 24 out of 30 points.

The muscle strength of quadriceps recovered to manual muscle test (MMT) level 3.

Active straight leg raising became possible without extension lag.

The patient was receiving a second extension of growing femoral prosthesis.

The patient is a 5-year-old girl with high-grade conventional osteosarcoma in the left distal femur.

The patient underwent three cycles of neoadjuvant chemotherapy.

Limb-salvage surgery was planned because femoral rotationplasty had been refused.

At 6 years and 2 months old, distal femoral resection and temporary spacer insertion using a 7-mm-diameter intramedullary nail and molded polymethylmethacrylate was performed.

At 7 years and 8 months old, secondary surgery was performed because the first spacer had been dislocated and the residual femur became atrophic.

The distal end of the residual femur was removed by 1 cm.

The periosteum and induced membrane around polymethylmethacrylate was preserved.

A custom-made ceramic spacer with a smooth straight 8-mm-diameter stem was utilized.

The bone-spacer junction was fixed with polymethylmethacrylate.

The bone-spacer junction was covered with the preserved periosteum and induced membrane.

After surgery, the bone atrophy improved.

At 9 years and 7 months old, the second spacer was removed because it had loosened.

The knee joint was reconstructed using a custom-made growing femoral prosthesis with a curved porous 8.5-mm-diameter stem.

Cancellous bone tips from the proximal tibia were grafted around the bone-prosthesis junction underneath the induced membrane.

At 10 years and 5 months old, the patient was able to walk unsupported.

A radiograph showed further thickening of the cortex of the residual femur without any stress shielding.

The patient had 5 cm of limb length discrepancy.

The patient and her mother were satisfied with the function.

Repeated limb length extensions are planned.

Osteosarcoma was suspected radiographically.

Open biopsy revealed a high-grade conventional osteosarcoma.

The tumor was initially staged as IIB (T2b N0 M0).

After three cycles of neoadjuvant chemotherapy, the pain was alleviated.

The extra-osseous mass was dramatically reduced.

Both medial and lateral meniscuses were preserved.

After surgery, the left leg was externally fixed in a cast for 4 weeks.

The spacer was dislocated at 7 months post-operatively.

The spacer dislocation prevented the patient from bearing weight.

Bone atrophy in the left leg was observed.

The periosteum and reactive membrane around the molded PMMA was preserved.

The junction was covered with the preserved periosteum and membrane.

After surgery, the left leg was placed in a cast for 4 weeks.

The bone atrophy in the left leg was gradually resolved.

Loosening of the stem and varus deformity was observed.

A third surgical intervention was, therefore, planned.

The residual femur was carefully reamed, and the stem was inserted.

Immediately after surgery, range of motion (ROM) exercise was started.

Six weeks after surgery, partial weight bearing was permitted.

Ten months after the third surgery, the patient was able to walk unsupported.

A radiograph showed further thickening of the cortex of the residual femur.

The patient was able to walk unsupported using a 2.5 cm shoe lift.

The Musculoskeletal Tumor Society (MSTS) score was 24 out of 30 points.

Active straight leg raising became possible without extension lag.

The patient was receiving a second extension of growing femoral prosthesis.

The patient underwent three cycles of neoadjuvant chemotherapy.

The distal end of the residual femur was removed by 1 cm.

The bone-spacer junction was fixed with polymethylmethacrylate.

After surgery, the bone atrophy improved.

At 10 years and 5 months old, the patient was able to walk unsupported.

The patient had 5 cm of limb length discrepancy.

The patient and her mother were satisfied with the function.

Repeated limb length extensions are planned.


Your body needs to keep your blood clean and your organs working well. If your kidneys aren’t doing their job, it’s like having a leaky faucet — waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.

Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.

The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.

She was seen in the emergency department with three days of severe abdominal pain.

Her medical history included menometrorrhagia due to uterine fibroids.

She had a previous endometrial ablation in 2015.

She used a contraceptive vaginal ring for three months prior to presentation.

She used Provera for 2 days prior to presentation for persistent vaginal bleeding.

Physical examination revealed a temperature of 39.2°C.

Physical examination revealed a pulse of 132 beats/min.

Physical exam showed tenderness throughout the lower abdomen with voluntary guarding.

Laboratory data revealed a white blood cell count of 12,000/µL.

Laboratory data revealed a hemoglobin of 7.8 gm/dL.

Laboratory data revealed a hematocrit of 25.7%.

Laboratory data revealed a sodium of 127 mmol/L.

Laboratory data revealed a chloride of 96 mmol/L.

Initial CT scan showed uterine masses consistent with known fibroids.

Initial CT scan showed minimal pelvic fluid.

She was admitted to the medical service for sepsis.

Gynecology was consulted for presumed pelvic inflammatory disease.

She was started on empiric antibiotics for PID: ceftriaxone IV 1 g every 24 hours, azithromycin IV 500 mg every 24 hours, and metronidazole IV 500 mg every 8 hours.

Blood, urine, and stool cultures were sent upon admission.

Her white blood cell count rose to 20,000/µL.

A repeat CT scan on hospital day four showed interval development of ascites.

She was taken for a diagnostic laparoscopy.

Diagnostic laparoscopy revealed a dense fibrinous exudate and significant ascites in all four quadrants of the abdomen.

Multiple peritoneal biopsies were taken.

Peritoneal fluid was sent for gram stain, cultures, and cytology.

Postoperatively, carcinoembryonic antigen (CEA) and CA-125 levels were obtained.

CA-125 was mildly elevated at 56.8 U/mL.

Her white blood cell count fluctuated between 15,000 and 25,000/µL.

Peritoneal fluid gram stain did not reveal any bacteria.

Cytology revealed rare mesothelial cells and abundant neutrophils.

Cytology did not reveal malignant cells.

Final pathology report stated the presence of benign fibromembranous tissue with severe acute inflammation and extensive necrosis.

The final pathology report was consistent with 'severe necrotizing acute peritonitis.'

Group A Strep (GAS) peritonitis was suspected.

Recommendations were made to continue ceftriaxone at 1 g IV every 24 hours in addition to one dose of clindamycin 600 mg IV.

Azithromycin was added to ceftriaxone three days later (IV 500 mg every 24 hours).

A streptolysin O antibody (ASO) titer was sent.

The ASO titer argued against GAS peritonitis.

Azithromycin was transitioned to oral 500 mg daily.

She continued to have persistent abdominal pain and anorexia.

A repeat CT scan obtained nine days after surgery showed peritoneal enhancement and several fluid collections.

A diagnostic paracentesis was performed.

Peritoneal fluid was sent to an outside institution for 16S ribosome analysis.

Her abdominal pain and leukocytosis slowly improved.

She continued to have severe anorexia and food aversion.

On hospital day 23, she was discharged home on oral azithromycin.

16S ribosome testing revealed Mycoplasma hominis RNA within the peritoneal fluid.

Her outpatient antibiotic was changed to oral doxycycline 100 mg twice daily for three months.

She was closely followed as an outpatient.

She gradually demonstrated clinical improvement.

She remains well ten months after hospitalization.

She had intraperitoneal fluid of unknown etiology.

She was initially managed nonoperatively.

She was empirically treated with broad spectrum antibiotics.

Blood and urine cultures were unrevealing.

Diagnostic laparoscopy revealed a dense fibrinous exudate covering the entire peritoneal cavity.

Peritoneal fluid and biopsies were sent for cytology and culture.

The peritoneal fluid was sent for 16 s ribosomal analysis.

She had a previous endometrial ablation in 2015.

Physical examination revealed a temperature of 39.2°C.

Physical examination revealed a pulse of 132 beats/min.

Laboratory data revealed a hemoglobin of 7.8 gm/dL.

Laboratory data revealed a hematocrit of 25.7%.

Laboratory data revealed a sodium of 127 mmol/L.

Laboratory data revealed a chloride of 96 mmol/L.

Initial CT scan showed minimal pelvic fluid.

She was admitted to the medical service for sepsis.

Her white blood cell count rose to 20,000/µL.

She was taken for a diagnostic laparoscopy.

Multiple peritoneal biopsies were taken.

CA-125 was mildly elevated at 56.8 U/mL.

Cytology did not reveal malignant cells.

Group A Strep (GAS) peritonitis was suspected.

A streptolysin O antibody (ASO) titer was sent.

The ASO titer argued against GAS peritonitis.

Azithromycin was transitioned to oral 500 mg daily.

A diagnostic paracentesis was performed.

Her abdominal pain and leukocytosis slowly improved.

She was closely followed as an outpatient.

She gradually demonstrated clinical improvement.

She remains well ten months after hospitalization.

**System Role:**

You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.

**User Prompt:**

Please process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.
### Instructions for Each Level:

1. Level: Low Health Literacy (High Readability)

Target: Individuals needing the simplest terms for immediate action.

Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").

Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.

Strategy: High paraphrasing using analogies. One idea per sentence.

Faithfulness: Must align perfectly with the Gold Summary.

2. Level: Intermediate Health Literacy (Medium Readability)

Target: The general public (news-reading level).

Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.

Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.

Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.

Faithfulness: Maintains the main narrative of the Gold Summary.

3. Level: Proficient Health Literacy (Low Readability)

Target: Researchers, clinicians, or highly informed patients.

Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.

Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.

Strategy: Minimal paraphrasing. Retain all original technical terminology.

Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.

I will provide the following information:

- Input Language: <<<SOURCE_LANGUAGE>>>
- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>
- Source Text (detailed content): <<<FULL_TEXT>>>

**Output Format (JSON only):**
    {
    "low_health_literacy": "...",
    "intermediate_health_literacy": "...",
    "proficient_health_literacy": "..."
    }


He presented with sudden onset pain in his left hip and shoulder.

The pain followed an episode of slip and fall at home 2 days ago.

He had been taking treatment for hypertension for the past 15 years.

Clinical examination revealed extensive bruising over the chest, left arm, forearm, and the medial aspect of the entire left thigh.

Movements of the involved hip and shoulder joints were extremely painful and restricted.

There was no distal neurovascular deficit in any of the involved limbs.

Laboratory investigations revealed anemia (Hb 8.5 g/dl).

Coagulation profile was within normal limits.

The fracture of the left inter-trochanteric femur was confirmed.

An associated fracture of the left proximal humerus was confirmed.

X-rays did not reveal any bony injury to the chest/thigh and forearm.

The patient received intravenous fluids (normal saline).

Serum creatinine decreased to 0.68 mg/dl.

Creatinine phosphokinase (CPK) was 865 U/L.

The patient underwent closed reduction and internal fixation with the proximal femoral nail for the inter-trochanteric femur fracture.

The proximal humerus fracture was managed non-operatively.

The patient was discharged after 7 days of hospitalization.

At 3 months follow-up, he was able to walk with the help of crutches.

There was still residual pain and stiffness in his left shoulder.

The patient was a 77-year-old hypertensive male.

He presented to the emergency following an episode of slip and fall at home.

Radiological evaluation revealed fractures of the left inter-trochanteric femur and left proximal humerus.

Laboratory investigations showed grossly deranged renal parameters.

Serum creatinine phosphokinase levels were more than 5 times the baseline.

A diagnosis of acute kidney injury secondary to traumatic rhabdomyolysis was made.

Medical management included adequate intravenous fluid administration.

Medical management included strict input-output monitoring.

The patient underwent closed reduction and internal fixation of the inter-trochanteric femur fracture with a proximal femoral nail.

The fracture of the proximal humerus was managed non-operatively with sling immobilization.

The patient refused to give consent for a second surgery.


The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.

The patient was a 52-year-old White man.

The patient presented with intermittent constipation.

The patient had a history of a decrease in lymphocyte count two months prior.

Initial computed tomography scans revealed stage T4 prostatic adenocarcinoma.

The tumor had invasion into adjacent structures.

The tumor had metastasis to regional lymph nodes (stage N1).

The tumor had metastases to the liver, bone, and a distant lymph node (stage M1).

A retroperitoneal lymph node was biopsied to confirm histology.

The patient's prostate-specific antigen (PSA) level was 1291ng/mL.

The patient started the antiandrogen bicalutamide (oral) shortly after confirmed diagnosis.

A gonadotrophin-releasing hormone agonist, leuprorelin (depot injection), was subsequently initiated.

The patient received treatment until PSA values began to rise ≈15 weeks later.

Docetaxel (intravenous infusion; 4 cycles) plus prednisone (oral; continuous dosing) was administered as standard of care.

Prednisone was continued for 1 week after the end of docetaxel treatment for symptom control.

The patient discontinued docetaxel/prednisone due to radiographic disease progression and PSA progression.

The patient immediately started on abiraterone as an androgen receptor targeting therapy.

The patient received palliative radiation of the right femur and acetabula around the time abiraterone was initiated.

After discontinuing abiraterone, the patient was enrolled in the TRITON2 study.

Local genomic testing of an archival tissue biopsy (retroperitoneal lymph node metastasis, 90% tumor purity) was obtained at initial diagnosis.

Local testing utilized the Oncomine™ Comprehensive Assay v3.

The local test indicated the presence of a BRCA1 T1399I (allelic fraction [AF], 19%) mutation.

A deleterious or probably damaging ATM G1663C mutation was also detected.

A damaging TP53 P191del mutation was also detected.

An oncogenic, activating BRAF K601E mutation was also detected.

TRITON2 patients provided plasma samples for central genomic analysis prior to starting rucaparib.

The patient’s pre-rucaparib plasma sample was analyzed using the FoundationOne Liquid CDx assay.

The FoundationOne Liquid CDx assay detected the same alterations as the Oncomine analysis of the archival tissue biopsy.

The FoundationOne Liquid CDx assay also revealed the presence of a BRCA2 homozygous loss (whole gene, 26 of 26 exons).

The patient started at the recommended dose of rucaparib, 600 mg twice daily.

The dose was reduced to 500 mg twice daily due to nausea/fatigue.

The patient ultimately received rucaparib for 32 weeks.

At enrollment into TRITON2, the patient had >21 bone-associated lesions.

Treatment with rucaparib resulted in a confirmed partial response per modified Response Evaluation Criteria In Solid Tumors, version 1.1.

The partial response was ongoing as of the last radiographic assessment before subsequent anti-cancer therapy.

There was no confirmed progression in bone.

The patient had a confirmed PSA response (maximum decrease, 95%).

The PSA response lasted 28 weeks from the first dose of rucaparib.

The patient discontinued rucaparib treatment due to clinical disease progression after 32 weeks on study.

The patient received carboplatin and cabazitaxel for 2 cycles.

Subsequent scans indicated progressive disease in nontarget liver lesions two months later.

The patient discontinued carboplatin/cabazitaxel.

The patient did not receive any further anticancer therapies.

The patient died ≈23 months after initial diagnosis due to progression of his disease.

The patient had BRCA-mutated metastatic castration-resistant prostate cancer.

The patient had a response to the PARP inhibitor rucaparib.

The patient remained on rucaparib for 32 weeks.

The duration of treatment with rucaparib was >2 times longer than the duration of each of his prior therapies.

The patient's prior therapies included bicalutamide, docetaxel, and abiraterone.

The patient enrolled in TRITON2 based on results of local genomic testing of an archival biopsy.

Local genomic testing indicated the presence of a BRCA1 T1399I mutation.

The allelic fraction of the BRCA1 T1399I mutation was 19%.

Local testing also identified an ATM G1663C mutation.

Local testing also identified a TP53 P191del mutation.

Local testing also identified a BRAF K601E mutation.

Analysis of a plasma sample obtained before starting rucaparib detected the same alterations as those in the archival biopsy.

Analysis of the plasma sample also revealed the presence of a BRCA2 homozygous loss.

The BRCA2 homozygous loss involved the whole gene, 26 of 26 exons.

The plasma sample analysis also revealed several other alterations of unknown functional impact.

We hypothesize the response of the patient's tumor to rucaparib was likely driven by DNA damage repair deficiency.

The DNA damage repair deficiency was caused by homozygous loss of all BRCA2 exons.

The patient discontinued rucaparib due to clinical disease progression.

Following discontinuation from rucaparib, the patient received carboplatin and cabazitaxel.

The patient received carboplatin and cabazitaxel for ≈3 weeks.

The patient died due to progression of his disease.

The patient was a 52-year-old White man.

The patient presented with intermittent constipation.

The patient had a history of a decrease in lymphocyte count two months prior.

Initial computed tomography scans revealed stage T4 prostatic adenocarcinoma.

The tumor had invasion into adjacent structures.

The tumor had metastasis to regional lymph nodes (stage N1).

A retroperitoneal lymph node was biopsied to confirm histology.

The patient's prostate-specific antigen (PSA) level was 1291ng/mL.

Local testing utilized the Oncomine™ Comprehensive Assay v3.

A deleterious or probably damaging ATM G1663C mutation was also detected.

A damaging TP53 P191del mutation was also detected.

An oncogenic, activating BRAF K601E mutation was also detected.

The patient started at the recommended dose of rucaparib, 600 mg twice daily.

The dose was reduced to 500 mg twice daily due to nausea/fatigue.

The patient ultimately received rucaparib for 32 weeks.

At enrollment into TRITON2, the patient had >21 bone-associated lesions.

There was no confirmed progression in bone.

The patient had a confirmed PSA response (maximum decrease, 95%).

The PSA response lasted 28 weeks from the first dose of rucaparib.

The patient received carboplatin and cabazitaxel for 2 cycles.

The patient discontinued carboplatin/cabazitaxel.

The patient did not receive any further anticancer therapies.

The patient had BRCA-mutated metastatic castration-resistant prostate cancer.

The patient had a response to the PARP inhibitor rucaparib.

The patient remained on rucaparib for 32 weeks.

Local genomic testing indicated the presence of a BRCA1 T1399I mutation.

The allelic fraction of the BRCA1 T1399I mutation was 19%.

Local testing also identified an ATM G1663C mutation.

Local testing also identified a TP53 P191del mutation.

Local testing also identified a BRAF K601E mutation.

The BRCA2 homozygous loss involved the whole gene, 26 of 26 exons.

The patient discontinued rucaparib due to clinical disease progression.

The patient received carboplatin and cabazitaxel for ≈3 weeks.

The patient died due to progression of his disease.


The patient is a 44-year-old black African man of Burkinabè origin.

He has been taking 5 mg of folic acid daily.

He has no notion of tuberculosis infection.

He was admitted to the rheumatology department for chronic inflammatory lower back pain.

He had inflammatory left knee pain that had been going on for about seven months.

On physical examination, clinical anaemia was observed that was not decompensated.

A soft, purulent swelling of 4x5 cm was observed in the sterno-clavicular joint.

The knee puncture revealed a purulent, fluid liquid.

The respiratory tract examination showed a condensation syndrome in the left pulmonary field.

A purulent pleural effusion on the right was observed.

A right inguinal lymphadenopathy with pus was observed.

A biological inflammatory syndrome was observed.

The microcytic hypochromic anaemia was 8.1 g/dl.

The C reactive protein (CRP) was 98 mg/l.

The intradermal reaction (IDR) to the tuberculin was positive at 18 mm.

The cytobacteriological examination did not find any germ.

The GeneXpert MTB/RIF test did not find any germ.

The search for acid-fast bacilli (AFB) in the pus from the different sites did not find any germ.

The thoracic computed tomography showed a right sterno-clavicular arthrosis with anterior muscular and mediastinal extension.

The thoracic computed tomography showed a pyothorax.

The thoracic computed tomography showed a right lung abscess.

The thoracic computed tomography showed a L3-L4 spondylodiscitis with calcifying abscesses of the psoas and paravertebral muscles.

The standard radiography of the left knee showed signs in favour of arthritis.

The diagnosis of tuberculosis with multifocal, pleuropulmonary and lymph node involvement was retained.

The patient was put on rifampicin 600 mg daily.

The patient was put on isoniazid 300 mg daily.

The patient was put on pyrazinamide 2000 mg daily.

The patient was put on ethambutol 1600 mg daily for two months.

The same doses of rifampicin and isoniazid were continued for 10 months.

The patient received thoracic drainage of the pyothorax in the operating theatre.

The patient received a joint lavage of the left knee.

The patient received a drainage of the cold abscess in the sterno-clavicular joint.

Local care with antiseptic was applied to the fistula of the inguinal lymphadenopathy.

Local care with antiseptic was applied to the cold abscess until complete healing.

Folic acid treatment was continued in the context of sickle cell anaemia.

The immediate evolution was marked by a clinical and biological improvement.

The evolution at three months was characterised by an improvement of the psoitis.

The evolution at three months was characterised by an improvement of the lower back pain.

The weight gain estimated at 3 months was 5%.

The patient is a 44-year-old African black patient of Burkinabe origin.

The patient had chronic inflammatory low back pain.

The patient had inflammatory right knee pain.

The symptomatology had been developing for seven months.

The symptomatology was in a febrile context.

The patient had a general deterioration in health.

The examination showed oligoarthritis of the right sternoclavicular joint.

The examination showed oligoarthritis of the left knee.

The examination showed a pulmonary condensation syndrome.

The examination showed pleural effusion.

The examination showed a cold abscess at the level of the right sternoclavicular joint.

The examination showed a fistulous and purulent right inguinal lymphadenopathy.

The biology showed an inflammatory syndrome.

The GeneXpert test was positive in the sputum.

The GeneXpert test showed no resistance to rifampicin.

The intradermal reaction to the tuberculin was positive.

The thoracic tomodensitometry showed a right sternoclavicular osteoarthritis.

The thoracic tomodensitometry showed a spondylodiscitis of the L3-L4 spine.

The standard radiography of the left knee objectified signs in favour of arthritis.

The diagnosis of tuberculosis with multifocal, pleuropulmonary and ganglionar bone involvement was retained.

He has been taking 5 mg of folic acid daily.

He has no notion of tuberculosis infection.

The knee puncture revealed a purulent, fluid liquid.

A purulent pleural effusion on the right was observed.

A right inguinal lymphadenopathy with pus was observed.

A biological inflammatory syndrome was observed.

The microcytic hypochromic anaemia was 8.1 g/dl.

The C reactive protein (CRP) was 98 mg/l.

The GeneXpert MTB/RIF test did not find any germ.

The thoracic computed tomography showed a pyothorax.

The patient was put on rifampicin 600 mg daily.

The patient was put on isoniazid 300 mg daily.

The patient was put on pyrazinamide 2000 mg daily.

The patient received a joint lavage of the left knee.

The weight gain estimated at 3 months was 5%.

The patient had chronic inflammatory low back pain.

The patient had inflammatory right knee pain.

The symptomatology had been developing for seven months.

The symptomatology was in a febrile context.

The patient had a general deterioration in health.

The examination showed oligoarthritis of the left knee.

The examination showed a pulmonary condensation syndrome.

The examination showed pleural effusion.

The biology showed an inflammatory syndrome.

The GeneXpert test was positive in the sputum.

The GeneXpert test showed no resistance to rifampicin.

The intradermal reaction to the tuberculin was positive.


The infant was born at 27 weeks and four days.

The infant's birth weight was 1135 grams.

The pregnancy was a dichorionic diamniotic twin pregnancy.

The mother experienced premature membrane rupture in the 27th week of pregnancy.

The mother experienced contractions in the 27th week of pregnancy.

The mother experienced bleeding in the 27th week of pregnancy.

The mother was treated with antenatal steroids.

Cesarean delivery was planned due to an arrested birth.

The neonate required intubation one minute after birth.

The intubation was due to respiratory failure.

The neonate was transferred to the newborn intensive care unit.

A diagnosis of respiratory distress syndrome was made.

Treatment with endotracheal poractant alfa 200 mg/kg was initiated.

Treatment with parenteral ampicillin-gentamicin was initiated.

Treatment with caffeine citrate was initiated.

Ventilation settings were arranged to assist control and volume guaranteed mode.

The maximum inspiring pressure was 20 cm/H²O.

The cranial ultrasound showed no abnormalities.

On hospital day 3, the neonate was extubated to nasal intermittent positive pressure ventilation.

On hospital day 3, the neonate required reintubation for recurrent respiratory failure.

Antibiotics were escalated to vancomycin-meropenem due to clinical deterioration.

On hospital day 5, the baby had worsening acute hypoxic respiratory failure.

A chest x-ray revealed mediastinal pneumothorax.

A follow-up x-ray one hour later showed accelerated pneumothorax on the left side.

A follow-up x-ray one hour later showed mediastinal shift to the right.

A thorax tube was placed through the left 5th intercostal space.

Repeat x-rays showed an expanded lung on the left side.

Repeat x-rays showed air bronchograms on the right.

Ten hours later, the neonate had persistent acidosis.

Ten hours later, the neonate had persistent hypoxia.

An x-ray ten hours later displayed a repeat pneumothorax on the left side.

The thorax tube was set to continuous suction.

The thorax tube resulted in a reduction of pneumothorax on subsequent imaging.

An echocardiogram revealed a 3 mm patent ductus arteriosus.

The patent ductus arteriosus had mostly left to right two-way shunts.

The echocardiogram showed pulmonary hypertension.

The oxygen saturation levels were approximately 80%.

The arm-leg saturation differences were higher than 15 mm Hg.

These findings were suspicious for persistent fetal circulation.

Pediatric cardiology advised against the closure of PDA.

A new chest x-ray showed a collapsed left lung.

A second chest tube was placed in the left hemithorax.

A decision was made to perform a surgical intervention.

A left posterolateral thoracotomy was performed.

A 1 cm perforated area between the left bronchus and carina was found.

The perforated area was repaired by using a pleural patch.

Suturing with 6.0 prolene was performed.

There was no visible bleeding or air leak at the end of the procedure.

The anesthesiologist applied high-pressure air via the endotracheal tube.

The thoracotomy incision was closed by layers.

A post-procedure chest x-ray showed an expanded left lung.

Three days later, the neonate experienced another episode of hypoxia.

The hypoxia was found to be secondary to a repeat left-sided pneumothorax.

A second thoracotomy was performed using the same technique as the prior surgery.

An air leak emanated from the same area.

The perforated area was repaired using a pleural patch.

The left 5th intercostal muscle long peduncle was used.

Fibrin glue and spongestan were used as anchorage on top of the patch.

No leak was found with the use of maximal airway pressure.

A PDA ligation operation was performed simultaneously during the procedure.

There was no air leakage in the repeat x-ray.

Both the first and second thorax tubes were removed on postoperative days 0 and 5, respectively.

There were no signs of air buildup or pneumothorax on the following days.

On the 161st day of admission, the patient was discharged home.

The patient was discharged with a home-type ventilator.

The patient was discharged with 30% oxygen support.

The patient developed pneumomediastinum.

The pneumothorax persisted despite placement of a thorax tube.

A thoracotomy was performed to detect and treat the bronchial rupture.

The infant was born at 27 weeks and four days.

The infant's birth weight was 1135 grams.

The pregnancy was a dichorionic diamniotic twin pregnancy.

The mother was treated with antenatal steroids.

Cesarean delivery was planned due to an arrested birth.

The neonate required intubation one minute after birth.

The intubation was due to respiratory failure.

A diagnosis of respiratory distress syndrome was made.

Treatment with caffeine citrate was initiated.

The maximum inspiring pressure was 20 cm/H²O.

The cranial ultrasound showed no abnormalities.

A chest x-ray revealed mediastinal pneumothorax.

Repeat x-rays showed an expanded lung on the left side.

Repeat x-rays showed air bronchograms on the right.

Ten hours later, the neonate had persistent acidosis.

Ten hours later, the neonate had persistent hypoxia.

The thorax tube was set to continuous suction.

The echocardiogram showed pulmonary hypertension.

The oxygen saturation levels were approximately 80%.

Pediatric cardiology advised against the closure of PDA.

A new chest x-ray showed a collapsed left lung.

A second chest tube was placed in the left hemithorax.

A decision was made to perform a surgical intervention.

A left posterolateral thoracotomy was performed.

The perforated area was repaired by using a pleural patch.

Suturing with 6.0 prolene was performed.

The thoracotomy incision was closed by layers.

A post-procedure chest x-ray showed an expanded left lung.

An air leak emanated from the same area.

The perforated area was repaired using a pleural patch.

The left 5th intercostal muscle long peduncle was used.

No leak was found with the use of maximal airway pressure.

There was no air leakage in the repeat x-ray.

The patient was discharged with a home-type ventilator.

The patient was discharged with 30% oxygen support.


He presented with a complaint of recurrent pain and swelling on his right cheek of three-month duration.

He visited a general practitioner each time.

The condition was resolved with analgesic and antibiotics.

He attended the Oral Surgery Clinic for consultation.

The patient is a fit and healthy young man.

He had undergone bimaxillary orthognathic surgery one and a half years earlier.

The surgical team informed him that there was a dislodged orthodontic appliance in his right cheek that must have occurred during the operation.

The molar tube from the right maxillary second molar was found missing the next day after the surgery.

Its presence was confirmed high up in the right maxillary-zygomatic buttress area shown in the postoperative X-ray image taken the next day.

A series of further postoperative radiographs confirmed its location, lying outside the right maxillary antrum.

No attempt was made to remove the appliance due to the pronounced postoperative facial oedema.

The absence of signs and symptoms during further follow-up sessions confirmed the decision to leave it in-situ.

On examination, there was no extraoral swelling noted.

There was a sinus with slight pus discharge on the upper right buccal sulcus region adjacent to the upper right first premolar.

Tenderness was elicited upon palpation on the upper right vestibular region.

A periapical view was taken with gutta-percha inserted into the sinus for foreign body localization.

The radiograph revealed the gutta-percha pointed towards the site of titanium plate and screws used for rigid fixation.

A cone beam CT was performed to provide a 3D detailed location of the appliance.

The presence of the molar orthodontic tube foreign body reaction was suspected as the most probable cause of the recurrent right cheek pain and swelling.

Exploration of the site was performed through the sulcular incision under general anesthesia.

The dislodged molar tube was identified lying on the zygomatic bone just beneath the raised flap.

It was removed by dividing some surrounding fibrous tissue strands.

One titanium straight bone plate with four screws used for fixing the previous Le Fort I osteotomy site was inspected.

A decision was made to remove them based on the fact that they are present in an infected area.

The Le Fort I osteotomy site showed good healing with new bone formation.

The orthognathic surgical team who attended him previously was informed of his progress.

A 25-year-old gentleman presented with recurrent upper right vestibular abscess three months following a bimaxillary orthognathic surgery.

A bonded molar orthodontic tube had dislodged into the wound during the operation.

The clinical presentation initially mimics an odontogenic infection.

Our investigations revealed that the abscess originated from the dislodged appliance.

The molar tube and neighbouring rigid fixation plates and screws were removed.

The patient recovered well following the procedure.


A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction.

The right radial access was chosen for the performance of percutaneous coronary intervention.

After the introduction of 6 F sheath, there was difficulty in the advancement of 0.035 J wire.

The 0.035 J wire was exchanged with a Terumo hydrophilic wire (0.035 × 180).

The Terumo hydrophilic wire was advanced easily to the aortic root.

Coronary angiography revealed tortuous coronary arteries without significant lesions.

Radial arteriography before sheath removal revealed perforation.

Protamine sulfate (1 mg per 100 USP units of heparin) was administered intravenously.

APTT was monitored 15 min after the protamine dose.

Prolonged balloon inflation 2.5/3.0 was performed.

A 7-F-long vascular sheath was inserted to internally tamponade the vessel.

The patient was sent to the coronary care unit for monitoring of the forearm hematoma and the distal pulses.

Over the next 3 days, serial radial angiographies were done.

Serial radial angiographies revealed the persistence of the perforation.

After 4 days, angiography revealed multiple thrombi.

Thrombus aspiration was done using Pronto V4 extraction catheter.

The implantation of a covered stent was performed.

The stent was dislodged, mostly secondary to under expansion.

The perforation was sealed spontaneously.

There were no signs of intra-arterial thrombi.

The 0.035 J wire was exchanged with a Terumo hydrophilic wire.

After the procedure and before sheath removal, radial arteriography was done.

Radial arteriography revealed perforation.

Prolonged balloon inflation was attempted.

Prolonged balloon inflation failed to seal the perforation.

The patient was sent to the coronary care unit for monitoring.

On the fourth day, angiography revealed multiple thrombi.

Thrombus aspiration was followed by the deployment of a covered stent.

The dislodged stent was successfully snared.

The perforation was sealed spontaneously.

The perforation was sealed spontaneously.

There were no signs of intra-arterial thrombi.

Radial arteriography revealed perforation.

Prolonged balloon inflation was attempted.

The dislodged stent was successfully snared.

The perforation was sealed spontaneously.

There were no signs of intra-arterial thrombi.


A 16-year-old Ukrainian boy was admitted to the Department of Children’s Infectious Diseases in Warsaw, Poland.

The boy had jaundice lasting for four days.

The boy had lived in Poland for 1.5 years.

The boy was working (training) in the profession of a hairdresser.

The boy had a tattoo made at home by his mother’s partner six months earlier.

The boy had a finger cut by hairdressing scissors six weeks before the admission.

The patient confirmed that he had two secured heterosexual encounters during the last six months.

In Ukraine, he had been vaccinated against tuberculosis, diphtheria, tetanus, pertussis, poliomyelitis, measles, mumps, and rubella.

He has not been vaccinated against hepatitis B.

He had never had blood transfusion nor surgery.

He was once hospitalized due to acute gastroenteritis in Ukraine.

The physical examination revealed jaundice.

The physical examination revealed hepatomegaly (2 cm below the rib arch).

The physical examination revealed a tattoo on the right forearm.

Laboratory tests showed a significantly elevated level of aminotransferases.

Alanine aminotransferase (ALT) was 2439 IU/L.

Aspartate aminotransferase (AST) was 1418 IU/L.

Serological testing was positive for HBsAg.

Serological testing was positive for anti-Hbc IgM antibodies.

Serological testing was negative for hepatitis A and hepatitis C viruses.

During observation, hepatic parameters were firstly elevated.

After 14 days, hepatic parameters improved.

The patient was discharged home with the recommendation to appear for follow-up examinations after six months.

The patient did not appear for the visit.

After 15 months, he wrote a message on Facebook to his practitioner asking if he had to report on a follow-up.

A visit in the clinic was arranged for him.

Testing towards the hepatitis B antigen was negative.

The extended interview revealed a urinary tract infection a year before.

The extended interview revealed unprotected sexual encounters of both homo and heterosexual relations.

During physical examination, a small ulcer around his anus was found.

Additional tests for HIV, syphilis, gonorrhoea, and chlamydia trachomatis were ordered.

All tests were negative except for syphilis.

Due to risky sexual behaviour, the patient was offered pre-exposure prophylaxis.

The patient applied for further treatment of syphilis to the Clinic of Dermatology and Venereology in Warsaw.

The patient is a 16-year-old Ukrainian boy.

The patient had not been previously vaccinated against hepatitis B.

Possible sources of infection included a tattoo made at home.

Possible sources of infection included a finger cut made with hairdresser scissors during work.

Possible sources of infection included unprotected sexual encounters.

The clinical course of the disease was typical with jaundice.

The clinical course of the disease was typical with elevated aminotransferases levels.

During the follow-up visit 16 months after the onset of the disease, chronic hepatitis B was excluded.

Additional tests for sexually transmitted diseases were ordered.

The extended interview revealed that the patient had several unprotected bisexual encounters.

The patient's unprotected bisexual encounters may have indicated a potential source of infections including the hepatitis B virus.

The boy had jaundice lasting for four days.

The boy had lived in Poland for 1.5 years.

The physical examination revealed jaundice.

Serological testing was positive for HBsAg.

After 14 days, hepatic parameters improved.

The patient did not appear for the visit.

A visit in the clinic was arranged for him.


The patient had 5 months of intermittent cervicalgia.

The patient had several weeks of a progressive right hemiparesis, up to hemiplegia (0/5).

The patient had brisk upper and lower extremity reflexes.

The patient had bilateral Hoffmann’s and Babinski signs.

The patient had left hemisensory dysesthesias.

The cervical spinal MRI revealed an intramedullary expansive lesion (10 mm×15 mm) at C1–C2.

The lesion at C1–C2 markedly enhanced with gadolinium.

The CT scan revealed a large mass (about 85 mm in size) involving the upper polar region and the middle third of the right kidney.

The mass extended to the ipsilateral psoas muscle.

A CT-guided fine-needle ago-biopsy established the diagnosis of an RCC.

The C1–C2 lesion was most likely an RCC metastasis.

Intraoperative neurophysiological monitoring was used.

The lesion was macroscopically fully resected.

Postoperatively, the patient had a slight motor improvement.

The histological examination revealed large cells with marked anaplasia.

Immunostaining was negative for cytokeratin.

Immunostaining was positive for intermediate vimentin filaments.

The histological and immunostaining studies confirmed the diagnosis of an RCC.

The 1-week postoperative cervical spine MRI showed postoperative changes.

The 1-week postoperative MRI showed full lesion excision.

The patient was discharged to a neuromotor rehabilitation center.

The patient underwent chemotherapy and radiotherapy for RCC.

Fourteen months later, the patient died due to metastatic RCC.

The patient had intermittent cervicalgia of 5 months duration.

The patient had progressive severe right hemiparesis for a few weeks.

The MRI revealed an intramedullary expansive lesion at the C1-C2 level.

The lesion readily enhanced with contrast.

The CT scan documented an 85 mm mass involving the right kidney.

The mass extended to the ipsilateral adrenal gland.

The mass posteriorly infiltrated the ipsilateral psoas muscle.

The CT-guided fine-needle biopsy confirmed the diagnosis of an RCC.

The patient underwent total surgical removal of the C1-C2 intramedullary mass.

After surgery, the patient exhibited a slight motor improvement.

The right hemiparesis was 2/5 after surgery.

The cause of death was global RCC tumor progression.


The patient has non-ischemic dilated cardiomyopathy.

The patient had an implantable cardioverter defibrillator implanted.

The patient was in New York Heart Association (NYHA) IV class.

The patient had left bundle branch block (LBBB; QRS duration of 145 ms).

The patient was referred for CRT-D upgrade.

The patient was awaiting cardiac transplantation.

The patient was receiving optimal medical therapy.

The patient was receiving loop-diuretic.

The patient was receiving angiotensin-converting enzyme (ACE) inhibitor.

The patient was receiving K-sparing agent.

Standard clinical imaging protocol revealed a dilated left ventricle.

The end-systolic volume (ESV) was 380 ml.

The ejection fraction (EF) was 4.8% as measured by the modified Simpson’s method.

Severe functional mitral regurgitation (FMR) was assessed by qualitative estimation with two-dimensional color flow Doppler approach.

The FMR showed a very large central jet.

The FMR jet reached the posterior wall of the left atrium.

The patient underwent the implant of a CRT-D device.

A quadripolar left ventricular (LV) lead was placed in the posterolateral branch of the coronary sinus.

The right ventricle (RV)-to-LV electrical delay was recorded at each of the four LV rings.

The A1 unipolar vector was chosen for LV pacing.

The greatest electrical delay was 80 ms.

At 13-day post-implant follow-up, the patient showed worsening heart failure (HF) symptoms.

Only A2 unipolar LV vector configuration was suitable for simultaneous biventricular activation.

The interventricular (VV) interval was 0 ms.

Echo-PIV was used during the acute study with contrast agent bubbles.

Echo-PIV evaluated the orientation and relative magnitude of blood-induced intraventricular forces.

Without pacing stimulation (CRT OFF), the intraventricular flow was dominated by rotation.

The intraventricular forces were predominantly transverse.

A first setting option (CRT ON, VV delay 0 ms) changed the orientation of intraventricular forces.

Increasing the delay (CRT ON, VV delay − 30 ms) improved the alignment.

Sequential biventricular activation with delay − 50 ms provided the best alignment.

No reduction of FMR by three-dimensional FVCD was observed.

The data acquisition time for each three-dimensional color Doppler data set was approximately 5 seconds.

The analysis of average regurgitation volume took less than 3 minutes.

Automated anatomy detection of the LV endocardial border, mitral annulus (MA), LV outflow (LVOT), and placement of three-dimensional hemispheric flow sampling planes in the MA and LVOT was performed.

The software of three-dimensional FVCD computed the flow volumes as the area under the curve of both the MA and LVOT flow in three cardiac cycles.

FMR volume was calculated by subtracting LVOT stroke volume from MA stroke volume.

At 6-month follow-up, the patient showed an improvement of NYHA class to III.

Persistent improvement of diastolic function was obtained.

A significant reduction of FMR (mean value regurgitant volume, 42.2 ml) was estimated.

The intraventricular forces estimated by echo-PIV were still partially dominated by the longitudinal path of pressure gradient.

The patient showed worsening heart failure symptoms a few days after an implant.

The two technologies are used in combination during acute echocardiographic optimization of left pacing vector.

The effect of the device’s optimization is assessed at 6-month follow-up.

The patient was referred for CRT-D upgrade.

The patient was awaiting cardiac transplantation.

The patient was receiving optimal medical therapy.

The patient was receiving loop-diuretic.

The patient was receiving K-sparing agent.

The end-systolic volume (ESV) was 380 ml.

The FMR showed a very large central jet.

The patient underwent the implant of a CRT-D device.

The A1 unipolar vector was chosen for LV pacing.

The greatest electrical delay was 80 ms.

The interventricular (VV) interval was 0 ms.


A 68-year-old man was admitted to our hospital with dyspnea and general fatigue in July 2018.

He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy.

The patient had a history of severe coronary heart disease.

The patient had chronic kidney disease (CKD Stage II-III).

During his last hospitalization in 2017, coronary angiography showed severe triple vessel coronary artery disease.

Holter revealed paroxysmal ventricular tachycardia and frequent ventricular premature beats.

He received implantable cardioverter defibrillator (ICD) treatment.

Aspirin, atorvastatin, furosemide, spironolactone, perindopril, and metoprolol were taken regularly at home.

On the current admission, his blood pressure was 135/82 mmHg.

On the current admission, his heart rate was 75 beats/min.

A S3 and systolic murmur were identified.

Inspiratory moist rales were found in the bilateral lung fields.

Slight edema of both lower limbs was noted.

Estimated glomerular filtration rate was 38 ml/min/1.73 m2.

Electrocardiogram revealed a sinus rhythm with a heart rate of 75 beats per minute.

Chest X-ray showed left small pleural effusion.

Echocardiography demonstrated severe left ventricular enlargement.

Left ventricular ejection fraction was 28%.

The patient was diagnosed with acute decompensated heart failure caused by volume overload.

Intravenous loop diuretics and nesiritide were administered.

The patient was insensitive to intravenous diuretics.

The patient's clinical symptoms did not improve significantly.

Diuretic resistance could be considered.

Low-dose TLV (7.5 mg qd) was performed on day 3.

The administration of TLV dramatically relieved dyspnea.

The administration of TLV increased urinary output.

After 3 days of TLV treatment, the patient became delirious.

We suspected a high sensitivity to the side effect of TLV.

Gastric tube was inserted orally to increase the intake of fresh water.

Serum sodium was restored to normal (135 mmol/L) on day 10.

Estimated glomerular filtration rate was 62 ml/min/1.73 m2.

The patient remained insensitive to intravenous diuretics.

We tried again to use a lower dose of TLV (3.75 mg qd).

We confirmed that hypernatremia was caused by TLV.

After the suspension of TLV, his serum sodium decreased to 138 mmol/L.

We had to give the patient a larger dose of intravenous loop diuresis.

The patient was discharged on the 21st day after admission.

After hospital discharge, the patient eventually died of cardiac arrest due to critically ill heart failure.

A 68-year-old man was admitted to our hospital with dyspea and general fatigue.

After the 3-day treatment using TLV, he became delirious and his limbs shook uncontrollably.

High serum sodium 173 mmol/L was noted compared to the results of the first examination (137 mmol/L).

After intensive rescue, serum sodium was restored to normal (135 mol/L).

When the patient refused continuous renal replacement therapy (CRRT), we tried again to use a lower dose of TLV to improve diuretic resistance.

Two days later, serum sodium rose again (162 mol/L).

During the course of therapy, we did not strictly require the patient to control the fluid intake.

No other medication could cause elevation of serum sodium.

Stop the use of TLV and encourage the patient to drink plenty of water.

His serum sodium decreased gradually and his psychiatric symptom recovered.

During this period, overall condition of the patient was stable.

After being discharged from the hospital, the patient eventually died of cardiac arrest due to critically ill heart failure.

The patient had chronic kidney disease (CKD Stage II-III).

On the current admission, his heart rate was 75 beats/min.

A S3 and systolic murmur were identified.

Slight edema of both lower limbs was noted.

Chest X-ray showed left small pleural effusion.

Left ventricular ejection fraction was 28%.

The patient was insensitive to intravenous diuretics.

Diuretic resistance could be considered.

Low-dose TLV (7.5 mg qd) was performed on day 3.

The administration of TLV dramatically relieved dyspnea.

The administration of TLV increased urinary output.

We suspected a high sensitivity to the side effect of TLV.

The patient remained insensitive to intravenous diuretics.

We tried again to use a lower dose of TLV (3.75 mg qd).

We confirmed that hypernatremia was caused by TLV.


An 84-year-old white male presented with a pale, ulcerated lesion (1.3 cm in diameter) on the middle of his lower lip.

There was no associated lymphadenopathy.

Histopathological and immunoistochemical features revealed a Merkel cell carcinoma.

The patient was scheduled for a wider excision in the following 2 months.

The patient returned with a protruding white lesion of 1.1 cm in diameter.

A wider excision, with an 8 mm margin, was performed.

Histopathology confirmed the nature of MCC.

The second excision was within healthy margins.

Two months later, the patient was referred to the Department of Plastic Surgery.

The patient had a protruding ulcerated lesion, 3 cm in diameter, on his lower lip.

Multiple palpable lymph nodes in the submandibular and cervical area were present.

The patient had been diagnosed with chronic lymphocytic leukemia 8 years earlier.

The patient did not receive any treatment for CLL.

A CT scan showed a soft tissue lobular mass, 3 cm in diameter, on the lower lip.

The mass had a possible extension to the mandible.

A W-excision (4 × 3.5 × 1 cm) of the lip lesion was performed.

An open biopsy of one submandibular lymph node was performed.

Histopathology confirmed recurrence of MCC.

An undifferentiated small cell carcinoma with hyaluronated stroma was identified.

The cells arranged in nodules or rosettes.

The cells had dense nuclear chromatin, with mitoses and nuclear debris.

Immunoistochemical procedures showed Neuron Specific Enolase (NSE) positivity.

Antibodies for Epithelial Membrane Antigen (EMA) and Chromogranin were negative.

The submandibular lymph node was positive for malignancy.

The lymph node was associated with the CLL (non Hodgkin's, B cell small lymphocytic lymphoma).

There was no evidence of metastatic infiltration by MCC.

This was confirmed immunoistochemically with the positive expression of CD5 and CD20 antibody.

The expression of CD10 antibody and NSE was negative.

Due to the age of the patient, chemotherapy was not considered.

A month later, a new CT scan depicted a soft tissue mass consistent with recurrence of MCC.

Multiple enlarged superficial and deep cervical lymph nodes were present.

Fine needle aspiration of the submandibular swelling was performed.

The patient underwent one month of neck radiotherapy with Cobalt 60.

A total dose of 4600cGy in 23 days was administered.

A further boost of 600cGy in 2 days on the left submandibular area was administered.

The treatment was successfully completed with full remission of the cervical lymphadenopathy.

Two months following the radiotherapy, a new CT scan showed reduction and obscurrence of the pre-existing mass on the left mandibular area.

There is no evidence of progression or further recurrence of MCC 9 months post-radiotherapy.

The patient had an aggressively recurrent form of MCC on the lower lip.

The patient had an 8-year history of untreated CLL.

During the recurrences of MCC, coexisting regional lymphadenopathy posed a problem in the differential diagnosis.

Histopathology and immunoistochemistry showed submandibular lymphadenopathy coexisting with the second recurrence of MCC.

The submandibular lymphadenopathy was due to B-cell small lymphocytic lymphoma.

The subsequent recurrence of the skin tumor involved the superficial and deep cervical lymph nodes.

Surgical excision followed by involved field radiation therapy has been proven effective for both malignancies.

There was no associated lymphadenopathy.

A wider excision, with an 8 mm margin, was performed.

Histopathology confirmed the nature of MCC.

The second excision was within healthy margins.

The patient did not receive any treatment for CLL.

The mass had a possible extension to the mandible.

Histopathology confirmed recurrence of MCC.

The cells arranged in nodules or rosettes.

The expression of CD10 antibody and NSE was negative.

A total dose of 4600cGy in 23 days was administered.


The patient has a diagnosis of long-standing arterial hypertension of difficult control.

The patient has severe heart failure with a left ventricular ejection fraction of 30%.

The patient is receiving pharmacological treatment with carvedilol, ivabradine, and losartan.

The patient has a history of stage IIIB chronic renal failure without dialysis therapy.

A year before the current admission, he consulted for urinary symptoms.

The urinary symptoms rapidly evolved to systemic compromise with fever, diaphoresis, low back pain, hypotension, dyspnea, and increased acute phase reactants.

He required hospitalization in the intensive care unit for multidisciplinary treatment.

The diagnosis was sepsis of urinary origin.

Alterations in calcium behavior were detected.

The alterations in calcium behavior were associated to the underlying renal disease.

The alterations in calcium behavior were associated to a severe hyperparathyroidism secondary to a functional adenoma in the lower left parathyroid.

The functional adenoma in the lower left parathyroid was treated with surgery.

Surgery achieved control of symptoms and levels of calcium and phosphorus.

Chest x-ray showed 2 lesions of tumor aspect with internal lytic areas in the fourth right and eighth left costal arches.

The first lesion measured 25 × 21 mm with involvement of fourth right costal arch.

The second lesion measured 77 × 54 mm in eighth left costal arch showing growth toward the left pleural cavity.

Both lesions were suggestive of a tumor of chondral origin, enchondroma.

It was not possible to rule out malignancy with the images.

He was admitted in our institution for excisional biopsy.

The physical examination revealed a thin patient with chronic disease.

The physical examination revealed a deformity in the neck with anterior flexion pronounced by severe dorsal kyphoscoliosis.

The physical examination revealed secondary asymmetry of the right ribcage, which was retracted with decreased intercostal spaces.

He referred increased dyspnea with the activities of daily life, with NYHA functional class III.

Breathing frequency was 16 breaths per minute.

The heart was tachycardic and rhythmic with no murmurs or gallop.

Breath sounds were decreased at both lung bases.

No identifiable lesions in the chest wall other than deformity by kyphoscoliosis were found.

Blood work was unremarkable, except for mild anemia of normal volumes.

Spirometry showed a moderate restrictive ventilatory pattern.

There were no significant post-bronchodilator changes.

Diffusing capacity of carbon monoxide was in normal limits (DLCO: 109%).

Thoracic computed tomography (CT) scan showed a heterogeneous rounded lytic lesion with sclerotic edges and growth toward the pulmonary cavity.

The lesion was of expansive type, causing displacement of pulmonary parenchyma.

The lesion measured approximately 77 × 54 mm and depended on the eighth left costal arch.

It was very difficult to determine if the lung was surrounding the lesion or if the mass was infiltrating the parenchyma.

In the fourth right costal arch, an image of similar characteristics, but smaller in size, was found, measuring 25 × 21 mm.

A severe dorsal kyphoscoliosis was identified.

The decision was made to perform a surgical resection of the mass with the possibility of having to do a lobectomy.

The patient was hospitalized in the intensive care unit for pre-surgical conditioning.

A left ventricular ejection fraction of 30% was evidenced.

A cycle of intravenous levosimendan was initiated.

He underwent resection of the left costal mass by thoracoscopy.

During the surgical procedure, only 1 hard lesion was found that involved the eighth rib and soft tissues of the seventh to ninth left ribs.

The lesion did not infiltrate into the lung tissue or pleural cavity.

Only partial resection of these 3 ribs was necessary.

In the immediate postsurgical period, the patient presented a difficult evolution.

The patient had hemodynamic instability.

The patient required vasoactive support with norepinephrine.

The patient had prolonged mechanical ventilation.

The patient needed a tracheostomy to assist a long-standing recovery process.

Subsequently, it was possible to remove the vasoactive drugs.

The invasive ventilatory support was removed.

The patient had complete physical and respiratory rehabilitation.

The patient had a history of multiple diseases.

Two tumor-like lesions with internal lytic areas were detected.

One lesion was located in the fourth right costal arch.

One lesion was located in the eighth left costal arc.

The diagnosis was sepsis of urinary origin.

Alterations in calcium behavior were detected.

It was not possible to rule out malignancy with the images.

He was admitted in our institution for excisional biopsy.

Breathing frequency was 16 breaths per minute.

The heart was tachycardic and rhythmic with no murmurs or gallop.

Breath sounds were decreased at both lung bases.

Spirometry showed a moderate restrictive ventilatory pattern.

There were no significant post-bronchodilator changes.

A severe dorsal kyphoscoliosis was identified.

A left ventricular ejection fraction of 30% was evidenced.

A cycle of intravenous levosimendan was initiated.

He underwent resection of the left costal mass by thoracoscopy.

The lesion did not infiltrate into the lung tissue or pleural cavity.

Only partial resection of these 3 ribs was necessary.

The patient had hemodynamic instability.

The patient required vasoactive support with norepinephrine.

The patient had prolonged mechanical ventilation.

Subsequently, it was possible to remove the vasoactive drugs.

The invasive ventilatory support was removed.

The patient had complete physical and respiratory rehabilitation.


The patient is a 56-year-old Caucasian male.

He has a past medical history of hypertension.

He has a past medical history of acute coronary syndrome.

He has a past medical history of atrial fibrillation.

He presented to the emergency department with acute epigastric pain.

His complaints had started 2 weeks earlier.

The pain had worsened 1 day prior to ED presentation.

Physical examination showed a sweating man.

Physical examination showed an obese man.

His oxygen saturation was 95% on room air.

His respiratory rate was 13 breaths/min.

The international normalised ratio (INR) was 2.4.

Abdominal ultrasound showed an inhomogeneous aspect of the spleen.

Contrast-enhanced computed tomography (CT) imaging of the abdomen revealed splenic haemorrhage.

Contrast-enhanced CT imaging showed subcapsular hematoma.

An acute operation was deemed unnecessary.

Oral anticoagulation was reversed with 10 mg vitamin K.

The patient was admitted to the hospital for observation.

The patient was discharged in good condition after 3 days.

The patient was on oral anticoagulation.

The patient presented to the emergency department with epigastric pain.

The patient had left upper quadrant tenderness.

Contrast-enhanced CT imaging revealed a large subcapsular haematoma of the spleen.

Oral anticoagulation was antagonised with vitamin K.

The patient was discharged in good condition after 3 days of clinical observation.


The patient was a 78-year-old Greek male.

The patient was classified as an ASA physical status grade III.

The patient had osteoarthritis of the left hip.

The patient was scheduled for an elective total hip replacement.

The patient had type II diabetes managed by oral metformin.

The patient had a normal pre-operative echocardiography with an ejection fraction of 60%.

The patient had no history of pulmonary disease.

The patient had a total knee replacement in the past without complications.

The patient's preoperative laboratory examination was within normal parameters.

The patient was hemodynamically stable with blood pressure 137/67 mmHg, heart rate 77 bpm, and SpO2 99%.

The anesthesia plan included combined lumbar epidural and spinal anesthesia.

Standard monitoring including ECG, SpO2, and non-invasive blood pressure was commenced in the OR.

An oxygen mask administering 6 lt/min was used throughout the procedure.

The neuraxial spinal technique was performed by a second-year anesthesia trainee.

The spinal block was performed at the L4-L5 intervertebral space using a midline approach.

Local anesthesia with 5 ml of 2% lidocaine was used.

An 18-Gauge Tuohy needle was used with a syringe filled with 8 ml of air.

The epidural space was located after a single redirection of the needle.

A needle-through-needle approach was used to locate the subarachnoid space.

Cerebrospinal fluid flowed freely through the spinal needle.

A mixture of 1.9 ml of ropivacaine 0.75% and 0.2 ml of fentanyl was introduced into the subarachnoid space.

The epidural catheter was placed in the epidural space.

The spinal block was confirmed using the temperature differentiation method.

An arterial catheter was inserted in the radial artery.

The patient was placed on the right lateral side with the left hip facing upwards.

The patient received no intravenous anesthetic or analgesic medication.

Approximately 2 hours after the spinal block, the patient's blood pressure dropped from 163/84 mmHg to 82/45 mmHg.

The patient's heart rate decreased to 45 bpm.

Sinus bradycardia was apparent on the ECG.

The anesthesiologist administered 5 mg of ephedrine and 1 mg of phenylephrine.

O2 administration was increased to 15 lt/min.

Intravenous fluid administration was increased.

There was no improvement in the patient's hemodynamic state.

The patient's blood pressure dropped further to 55/35 mmHg.

1 mg of adrenaline was given intravenously.

This produced an immediate rise in blood pressure to 183/88 mmHg.

Small 0.05 mg/ml boluses of nitroglycerin were administered.

The patient's mental status returned to normal.

A point of care echocardiogram demonstrated no new cardiac abnormalities.

A CTPA was performed and was negative for pulmonary embolism.

A chest and abdomen CT demonstrated air in the subcutaneous tissue, intermuscular space, spinal canal, and mediastinum.

The patient was discharged home on the fifteenth postoperative day.

A combined lumbar epidural and spinal anesthesia was performed using the loss of resistance to air technique.

The patient was a 78-year-old Greek (Caucasian) male.

The patient was undergoing a total hip replacement.

The patient was hemodynamically stable throughout the operation.

Two hours following epidural analgesia, the patient manifested a sudden drop in blood pressure and heart rate.

The patient's drop in blood pressure and heart rate required the administration of adrenaline.

A Computed Tomography scan demonstrated pneumomediastinum.

A Computed Tomography scan demonstrated pneumorrachis.

A Computed Tomography scan demonstrated paravertebral soft tissue emphysema.

We believe that injected air from the epidural space and surrounding tissues slowly moved towards the mediastinum.

We believe that the movement of air stimulated the para-aortic ganglia.

We believe that the stimulation caused parasympathetic stimulation.

We believe that the parasympathetic stimulation caused hypotension and bradycardia.

The patient was a 78-year-old Greek male.

The patient had osteoarthritis of the left hip.

The patient had type II diabetes managed by oral metformin.

The patient had no history of pulmonary disease.

Local anesthesia with 5 ml of 2% lidocaine was used.

The epidural catheter was placed in the epidural space.

An arterial catheter was inserted in the radial artery.

The patient's heart rate decreased to 45 bpm.

Sinus bradycardia was apparent on the ECG.

O2 administration was increased to 15 lt/min.

Intravenous fluid administration was increased.

The patient's blood pressure dropped further to 55/35 mmHg.

1 mg of adrenaline was given intravenously.

Small 0.05 mg/ml boluses of nitroglycerin were administered.

The patient's mental status returned to normal.


The patient was diagnosed with acquired aplastic anemia in December 2019.

Cytogenetic studies showed 46XX karyotype.

Paroxysmal nocturnal hemoglobinuria clone was absent.

Clinical exome did not show any genetic mutation for inherited bone marrow failure syndrome.

The patient had no matched sibling or matched unrelated donor.

She received a haploidentical stem cell transplant in July 2020.

The conditioning regimen included Rabbit ATG from Day-9 to Day-7.

Fludarabine was given at 40 mg/m2 for 4 days (Day-6 to Day-3).

Cyclophosphamide was given at 14.5 mg/kg for 2 days (Day-6 and Day-5).

A single fraction TBI (400 cGy) was given on Day-1.

On the day of transplantation, she received a peripheral blood stem cell graft from the father.

The graft contained 10 million CD34+ cells/kg.

The graft contained 2.41 × 108 CD3+ T cells/kg.

Post-transplant Cyclophosphamide (50 mg/kg) was given on Day+3 and Day+4.

Ciclosporin and Mycophenolate mofetil were started on Day+5 as GvHD prophylaxis.

On Day+9, she developed high-grade fever with the onset of engraftment.

A diagnosis of Candida tropicalis-driven macrophage activation syndrome was established on Day+13.

She was treated with caspofungin and posaconazole.

She received intravenous immunoglobulin (1 g/kg for 5 days).

She received intravenous Methylprednisolone (2 mg/kg).

One dose of intravenous Alemtuzumab (0.1 mg/kg) was administered.

The patient developed hypertension from Day+13.

On Day+14, she had loose motions with abdominal pain.

An ultrasound scan was suggestive of pan-colitis.

Oral Budesonide was started for possible gut GvHD.

The patient had neutrophil engraftment on Day+16.

TA-TMA was suspected based on anemia, thrombocytopenia, hypertension, gastrointestinal bleeding, decreased serum albumin, and raised lactate dehydrogenase.

Blood smear showed 1 fragmented RBC per high power field on Day+20.

Urine protein:creatinine ratio was 0.47 on Day+20.

Soluble C5b-9 assay is not available nationally.

The diagnosis of TA-TMA was confirmed based on the Overall-TMA criteria.

There was no evidence of pathogenic variation in TMA-associated genes on clinical exome.

Eculizumab was considered but not used due to cost.

Narsoplimab was accessed through an expanded access program.

Narsoplimab was commenced at a dose of 4 mg/kg twice a week on Day+30.

Severe colitis with inflammatory thickening measuring 5.5 mm extending up to the caecum and base of the appendix was seen on ultrasound.

She was started on a TNF-α inhibitor (Etanercept).

She developed pneumatosis coli after two doses of Etanercept.

She continued to have significant intestinal bleeding.

Narsoplimab was increased to thrice a week on Day+45.

Her lactate dehydrogenase improved dramatically after starting Narsoplimab.

Her hypertension improved and antihypertensive requirement was reduced to a single medication from Day+59.

Intestinal bleeding reduced from Day+50 and completely stopped on Day+82.

Inj Methylprednisolone was tapered and stopped on Day+92.

There were no schistocytes in the peripheral blood smear after Day+70.

The patient received the last packed cell transfusion on Day+70.

The patient received the last platelet transfusion on Day+77.

Narsoplimab was reduced to twice a week on Day+109.

Narsoplimab was reduced to once a week on Day+133.

The patient had CMV reactivation on Day+59 with CMV copy numbers of 16,500/ml.

She had a herpes zoster skin infection on Day+111.

The patient developed liver GvHD from Day+217.

She had severe reticulocytopenia secondary to parvovirus infection on Day+246.

Parvovirus infection was managed with immunoglobulin infusion.

She developed a second episode of TA-TMA.

The second episode was manifested by circulating schistocytes, anemia, thrombocytopenia, low albumin, and an increase in lactate dehydrogenase and creatinine.

Urine protein:creatinine ratio increased to 0.89.

Narsoplimab was given twice a week for 3 weeks.

Narsoplimab was escalated to thrice a week from Day+274.

Narsoplimab was tapered to twice weekly from Day+290.

Liver GvHD resolved with steroids and Ruxolitinib.

The patient had no features of TA-TMA on the last follow-up of Day+650.

The six-year-old girl underwent a human leucocyte antigen (HLA) haploidentical hematopoietic stem cell transplant using post-transplant Cyclophosphamide for severe aplastic anemia.

In the second week of the transplant, the patient developed macrophage activation syndrome.

The diagnosis of hepatosplenic candidiasis was made based on USG abdomen and blood fungal PCR.

Candida-triggered macrophage activation syndrome responded to antifungals, steroids, intravenous immunoglobulin, and alemtuzumab.

The patient developed hypertension in the 2nd week.

The patient had high lactate dehydrogenase (1010 U/L), schistocytes (5 per hpf), low haptoglobin (< 5 mg/dl), thrombocytopenia, and anemia in the 3rd week.

The patient was treated with 10 days of defibrotide without response.

The course was further complicated by the involvement of the gastrointestinal tract and kidneys.

Narsoplimab was started in the 5th week of the transplant.

A fall in lactate dehydrogenase was observed after starting Narsoplimab.

The resolution of gastrointestinal symptoms, proteinuria, and recovery of cytopenia followed starting Narsoplimab.

The second episode of TA-TMA occurred with parvoviraemia.

The second episode of TA-TMA was successfully treated with Narsoplimab.

Cytogenetic studies showed 46XX karyotype.

Paroxysmal nocturnal hemoglobinuria clone was absent.

The patient had no matched sibling or matched unrelated donor.

Fludarabine was given at 40 mg/m2 for 4 days (Day-6 to Day-3).

A single fraction TBI (400 cGy) was given on Day-1.

The graft contained 10 million CD34+ cells/kg.

The graft contained 2.41 × 108 CD3+ T cells/kg.

She was treated with caspofungin and posaconazole.

She received intravenous immunoglobulin (1 g/kg for 5 days).

She received intravenous Methylprednisolone (2 mg/kg).

The patient developed hypertension from Day+13.

On Day+14, she had loose motions with abdominal pain.

An ultrasound scan was suggestive of pan-colitis.

Oral Budesonide was started for possible gut GvHD.

The patient had neutrophil engraftment on Day+16.

Urine protein:creatinine ratio was 0.47 on Day+20.

Soluble C5b-9 assay is not available nationally.

Eculizumab was considered but not used due to cost.

Narsoplimab was accessed through an expanded access program.

She was started on a TNF-α inhibitor (Etanercept).

She developed pneumatosis coli after two doses of Etanercept.

She continued to have significant intestinal bleeding.

Narsoplimab was increased to thrice a week on Day+45.

Inj Methylprednisolone was tapered and stopped on Day+92.

The patient received the last platelet transfusion on Day+77.

Narsoplimab was reduced to twice a week on Day+109.

Narsoplimab was reduced to once a week on Day+133.

She had a herpes zoster skin infection on Day+111.

The patient developed liver GvHD from Day+217.

Parvovirus infection was managed with immunoglobulin infusion.

She developed a second episode of TA-TMA.

Urine protein:creatinine ratio increased to 0.89.

Narsoplimab was given twice a week for 3 weeks.

Narsoplimab was escalated to thrice a week from Day+274.

Narsoplimab was tapered to twice weekly from Day+290.

Liver GvHD resolved with steroids and Ruxolitinib.


A 6-year-old girl presented to the pediatric emergency department with the chief complaints of vomiting blood and blood in stool.

Her mother reported that she noticed the blood in her daughter’s stool three days ago.

The baby was delivered at 34 weeks gestation with cesarean section.

The baby had intrauterine growth restriction (IUGR).

The baby was hospitalized in a neonatal intensive care unit for 1 month.

The baby was treated with laser photocoagulation due to the vision loss in the left eye.

The cranial magnetic resonance imaging (MRI) was performed at the age of 6 months.

The cranial MRI revealed diffuse symmetric calcifications.

The cranial MRI showed changes suggesting hemorrhage.

The cranial MRI showed dilated lateral ventricles.

The cranial MRI showed septated cystic lesions in the area extending from the roof of the third ventricle to the lateral ventricle.

The cranial MRI showed hemorrhage in the globe in the left orbit.

The patient was diagnosed with Coats plus syndrome.

The patient’s weight and height were below the 3rd percentile.

The patient’s mid-upper arm circumference was <115 mm.

The patient’s peak heart rate was 120/min.

The patient’s blood pressure was 70/40 mmHg.

Leukocoria and glaucoma were detected in the left eye.

The patient’s muscle strength in bilateral lower and upper extremities was 3/5.

The percussion over Traube’s space produced dull sounds during the abdominal examination.

The patient’s hemoglobin (Hb) was 6.5 gr/dL.

The patient’s thrombocyte count was 292000/mm3.

The patient’s white blood cell (WBC) count was 2010/mm3.

The patient’s international normalized ratio (INR) was 1.3.

The patient’s alanine aminotransferase (ALT) was 113 U/L.

The patient’s aspartate aminotransferase (AST) was 115 U/L.

The patient’s gamma-glutamyl transferase (GGT) was 245 U/L.

The metabolic studies did not show any abnormalities.

The levels of viral markers, alpha 1 antitrypsin, alpha fetoprotein, ceruloplasmin, autoantibody, and tissue transglutaminase were normal.

Abdominal ultrasonography showed linear echogenicity and heterogeneity in the liver.

Abdominal doppler ultrasonography suggested portal hypertension.

Upper and lower gastrointestinal endoscopy revealed folded vascular appearance reminiscent of esophageal varices.

Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the pyloric antrum, duodenum, and colon.

A liver biopsy revealed portal fibrosis.

The patient was initially received nothing-by-mouth diet.

The patient was given intravenous (IV) proton pump inhibitors.

The severe gastrointestinal bleeding of the patient was later stopped after receiving IV octreotide and erythrocyte transfusion.

The patient was treated with propranolol, ursodeoxycholic acid, and anticonvulsant.

The patient was followed in the pediatric gastroenterology, neurology, and eye clinics.

The patient continued to have intermittent gastrointestinal system bleeding.

The patient was admitted to the emergency department and hospitalized multiple times.

The patient was treated with tranexamic acid when she had mild bleeding.

The patient received IV octreotide when the bleeding was severe.

The patient was admitted to the intensive care unit due to multi-organ failure secondary to severe gastrointestinal system bleeding.

An emergency endoscopy could not be performed.

The patient received IV octreotide and erythrocyte transfusion again.

The patient’s condition did not improve.

The patient presented with vomiting blood.

The patient presented with blood in stool.

Upper and lower gastrointestinal endoscopy revealed esophageal varices.

Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the pyloric antrum.

Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the duodenum.

Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the colon.

The patient received intravenous octreotide.

The bleeding was stopped after receiving intravenous octreotide.

The patient was followed in the pediatric gastroenterology clinic.

The patient was followed in the pediatric neurology clinic.

The patient was followed in the pediatric ophthalmology clinic.

The patient was hospitalized and admitted to the intensive care unit.

The patient eventually died due to severe gastrointestinal system bleeding.

The baby had intrauterine growth restriction (IUGR).

The cranial MRI revealed diffuse symmetric calcifications.

The cranial MRI showed changes suggesting hemorrhage.

The cranial MRI showed dilated lateral ventricles.

The patient was diagnosed with Coats plus syndrome.

The patient’s mid-upper arm circumference was <115 mm.

The patient’s peak heart rate was 120/min.

The patient’s blood pressure was 70/40 mmHg.

Leukocoria and glaucoma were detected in the left eye.

The patient’s hemoglobin (Hb) was 6.5 gr/dL.

The patient’s thrombocyte count was 292000/mm3.

The patient’s white blood cell (WBC) count was 2010/mm3.

The patient’s international normalized ratio (INR) was 1.3.

The patient’s alanine aminotransferase (ALT) was 113 U/L.

The patient’s aspartate aminotransferase (AST) was 115 U/L.

The patient’s gamma-glutamyl transferase (GGT) was 245 U/L.

The metabolic studies did not show any abnormalities.

A liver biopsy revealed portal fibrosis.

The patient was initially received nothing-by-mouth diet.

An emergency endoscopy could not be performed.

The patient’s condition did not improve.


A 9 days-old male neonate weighing 3.60 kg was referred to the National Cardiac Center Harapan Kita Hospital.

The neonate was ventilated because of severe metabolic and respiratory acidosis.

The neonate had circulatory dynamics instability.

The neonate had a history of respiratory distress.

The neonate was born at 40 weeks of gestation by normal labour.

The neonate's oxygen saturation at birth was 90%.

On the 6th day postpartum, the neonate presented with feeding difficulty.

On the 6th day postpartum, the neonate had severe cyanosis.

On the 6th day postpartum, the neonate had congestive heart failure.

The neonate was ventilated at the emergency room with oxygen saturation 82%.

The neonate was transferred to the center for possible surgical repair.

The neonate's oxygen saturation was 75%.

Differential oxygen saturation was noted between the upper and lower limbs.

No apparent cardiac murmur was detected.

The chest X-ray showed mild cardiomegaly.

The chest X-ray showed congestion of the lungs.

The electrocardiogram showed normal rhythm.

The electrocardiogram showed right axis deviation.

The electrocardiogram showed mild right ventricular hypertrophy.

The neonate was admitted to the pediatric cardiac intensive care unit.

The neonate's oxygen saturation was between 40% and 70%.

Two-dimensional echocardiography revealed an interrupted aortic arch type A.

Two-dimensional echocardiography revealed an aortopulmonary window type II.

Two-dimensional echocardiography revealed a restricted patent ductus arteriosus.

Two-dimensional echocardiography revealed pulmonary hypertension.

Two-dimensional echocardiography did not reveal a ventricular septal defect.

The baby had disseminated intravascular coagulation.

The baby had several epileptic episodes.

Brain sonography showed no intracranial bleeding.

Operation was deferred because of the risk of infection.

Operation was deferred because of sepsis.

Operation was deferred because of the good general condition.

Operation was performed on the 20th day of life.

A one-stage surgical correction was performed through a median sternotomy.

The surgery was performed under profound hypothermia (26 °C).

Before the administration of heparin, the entire ascending aorta and the arch vessels were mobilized.

Before the administration of heparin, the pulmonary trunk and both branch were mobilized.

The external anatomy confirmed an interrupted aortic arch type A.

The external anatomy confirmed a large aortopulmonary window type II.

The right pulmonary artery was recognized to originate from the posterolateral part of the ascending aorta.

The right pulmonary artery was recognized to have connection with the common pulmonary artery.

The ascending aorta gave three branches including the brachiocephalic artery.

The ascending aorta gave three branches including the left common carotid artery.

The ascending aorta gave three branches including the left subclavian artery.

There was no evidence of descending aorta.

The proximal part of the patent ductus arteriosus arose from the pulmonary artery trunk.

The distal part of the patent ductus arteriosus became the descending aorta.

The left pulmonary artery arose from the pulmonary artery trunk.

Cardiopulmonary bypass was established by right hemicerebral perfusion.

Cardiopulmonary bypass was established by bicaval drainage.

Right hemicerebral perfusion was obtained via an expanded 4-0 mm polytetrafluoroethylene graft.

The graft was sewn to the right brachiocephalic artery.

The aortic arch vessels were clamped at the origin of the brachiocephalic artery.

The aortic arch vessels were clamped at the origin of the left common carotid artery.

The aortic arch vessels were clamped at the origin of the left subclavian artery.

Snaring of both pulmonary arteries precluded overflooding the lungs.

Ductal tissue was ligated near its pulmonary origin.

Ductal tissue was resected until normal aortic tissue appeared.

The ascending aorta was longitudinally incised.

An extended end-to-side anastomosis of the descending aorta to the distal ascending aorta was performed.

The anastomosis was performed with a continuous 7-0 polypropylene suture.

After removal of the aortic cross-clamp, full flow bypass was resumed.

The anastomosis was checked for bleeding.

The anastomosis was checked for undue tension.

The aortic cross-clamp was reapplied proximal to the aortic cannula.

The aortopulmonary window repair was started.

The ascending aorta was transversely incised distal to the aortopulmonary window.

The aortopulmonary window was confirmed to be very large, 10 mm diameter.

The right pulmonary artery originated from the ascending aorta.

The left pulmonary artery arose from the pulmonary artery trunk in the normal fashion.

The coronary arteries were normally positioned.

The aortic cross clamp was removed and reapplied for right hemicerebral perfusion again.

A 4-0 Gore-tex patch was used to close the aortopulmonary window.

A 4-0 Gore-tex patch was used to separate the right pulmonary artery from the aortic origin.

After rewarming, cardiopulmonary bypass was easily weaned.

Peritoneal dialysis was performed post operatively for 3 days.

Peritoneal dialysis was switched with lasix intermittently.

The postoperative recovery was uneventful.

The neonate was extubated on the 7th day post operatively.

No clinical signs of neurologic disturbances were observed.

Cardiopulmonary function was satisfactory.

Early postoperative echocardiography demonstrated an excellent early surgical result.

Early postoperative echocardiography showed a minimal pressure gradient of 12 mmHg across the aortic reconstruction.

Early postoperative echocardiography showed good left ventricular function.

Early postoperative echocardiography showed no residual aortopulmonary window.

In 2021, the patient was a 9 year old child.

The patient had entered elementary school in grade 2.

There were no abnormalities of the heart and lungs according to the patient's mother.

The cerebral palsy sequela was being treated by a pediatric neurologist.

A 9 days-old male neonate weighing 3.85 kg was referred to our center.

The neonate was ventilated with a history of respiratory distress and severe infection since birth.

A 2D echo showed an IAA type A associated with a huge APW type II and restrictive PDA.

The baby experienced several epileptic episodes during the following days.

Surgery was performed on the 20th day of life in 2011.

A successful one-stage repair of the anomalies was performed.

The repair included cutting of the PDA that arose from the PA trunk and distally became the descending aorta.

An extended end-to-end anastomosis was used to conduct ascending aortic blood flow into the descending aorta.

A 4-0 Gore-Tex baffle was used to close the APW and separate the RPA from the aortic origin.

The result was good, as the child recently grew up as a cheerful 9 year old.

The child is growing actively and has entered elementary school in grade 2.

The neonate had circulatory dynamics instability.

The neonate had a history of respiratory distress.

The neonate was born at 40 weeks of gestation by normal labour.

The neonate's oxygen saturation at birth was 90%.

On the 6th day postpartum, the neonate presented with feeding difficulty.

On the 6th day postpartum, the neonate had severe cyanosis.

On the 6th day postpartum, the neonate had congestive heart failure.

The neonate was transferred to the center for possible surgical repair.

The neonate's oxygen saturation was 75%.

Differential oxygen saturation was noted between the upper and lower limbs.

No apparent cardiac murmur was detected.

The chest X-ray showed mild cardiomegaly.

The chest X-ray showed congestion of the lungs.

The electrocardiogram showed normal rhythm.

The electrocardiogram showed right axis deviation.

The electrocardiogram showed mild right ventricular hypertrophy.

The neonate was admitted to the pediatric cardiac intensive care unit.

The neonate's oxygen saturation was between 40% and 70%.

Two-dimensional echocardiography revealed an aortopulmonary window type II.

Two-dimensional echocardiography revealed pulmonary hypertension.

The baby had disseminated intravascular coagulation.

The baby had several epileptic episodes.

Brain sonography showed no intracranial bleeding.

Operation was deferred because of the risk of infection.

Operation was deferred because of sepsis.

Operation was deferred because of the good general condition.

Operation was performed on the 20th day of life.

A one-stage surgical correction was performed through a median sternotomy.

The surgery was performed under profound hypothermia (26 °C).

The external anatomy confirmed an interrupted aortic arch type A.

The external anatomy confirmed a large aortopulmonary window type II.

There was no evidence of descending aorta.

The left pulmonary artery arose from the pulmonary artery trunk.

Cardiopulmonary bypass was established by right hemicerebral perfusion.

Cardiopulmonary bypass was established by bicaval drainage.

The graft was sewn to the right brachiocephalic artery.

Snaring of both pulmonary arteries precluded overflooding the lungs.

Ductal tissue was ligated near its pulmonary origin.

Ductal tissue was resected until normal aortic tissue appeared.

The ascending aorta was longitudinally incised.

The anastomosis was performed with a continuous 7-0 polypropylene suture.

After removal of the aortic cross-clamp, full flow bypass was resumed.

The anastomosis was checked for bleeding.

The anastomosis was checked for undue tension.

The aortic cross-clamp was reapplied proximal to the aortic cannula.

The aortopulmonary window repair was started.

The aortopulmonary window was confirmed to be very large, 10 mm diameter.

The right pulmonary artery originated from the ascending aorta.

The coronary arteries were normally positioned.

A 4-0 Gore-tex patch was used to close the aortopulmonary window.

After rewarming, cardiopulmonary bypass was easily weaned.

Peritoneal dialysis was performed post operatively for 3 days.

Peritoneal dialysis was switched with lasix intermittently.

The postoperative recovery was uneventful.

The neonate was extubated on the 7th day post operatively.

No clinical signs of neurologic disturbances were observed.

Cardiopulmonary function was satisfactory.

Early postoperative echocardiography showed good left ventricular function.

In 2021, the patient was a 9 year old child.

The patient had entered elementary school in grade 2.

The cerebral palsy sequela was being treated by a pediatric neurologist.