The patient is a 52-year-old man from Bangladesh.

The patient had exertional angina Canadian Cardiovascular Society III.

A stress myocardial scintigraphy was performed.

The stress myocardial scintigraphy revealed deep hypoperfusion in the antero-apical, septo-apical, and lateral walls.

The stress test showed electric positivity.

The resting left ventricle ejection fraction was 61%.

The patient's blood pressure was 127/85 mmHg.

The patient's oxygen saturation was normal.

The electrocardiogram showed a sinus rhythm.

The electrocardiogram showed no significant repolarization abnormalities.

A diagnostic coronary angiogram was performed.

Left injection revealed a stenosis on a third significant diagonal branch.

The LAD appeared to stop at its mid-segment without wrapping around the apex.

The LAD did not present a stump that could suggest a chronic occlusion.

The right coronary sinus injection revealed a dominant RCA free of stenosis.

A vessel opening into the ostium of the RCA was noted.

A non-selective injection into this artery identified an ostial-proximal stenosis.

Percutaneous coronary intervention of the third diagonal was performed.

The CT scan identified an artery whose course is compatible with a mid and distal LAD.

This artery connects in the right coronary ostium.

This artery joins the interventricular groove.

This artery wraps around the apex of the heart.

The guiding catheter was accessed through the right radial artery.

A workhorse wire was positioned in the right posterolateral artery.

A polymerjacket wire with a hydrophilic coating was used to navigate within the AAOCA.

A distal injection through a microcatheter revealed a severe stenosis in the mid LAD.

The distal lesion was treated with a drug-eluting stent 2.25 × 15 mm.

The mid lesion was treated with a drug-eluting balloon 2.0 × 15 mm.

The ostial-proximal segment was treated with a drug-eluting stent 2.5 × 15 mm.

The final angiographic result was satisfactory.

A contralateral injection confirmed the discontinuity of the AAOCA with the native LAD.

The post-procedural course was uneventful.

The patient was discharged the following day.

The patient is a 52-year-old from Bangladesh.

The patient has dual-origin LAD arising from both left and right sinus.

The patient presented with exertional angina.

The patient had documented myocardial ischaemia.

Computed tomography (CT) scan confirmed the anatomical course of the AAOCA.

Percutaneous coronary intervention was successfully performed.

Tailored techniques were used to treat significant atherosclerotic lesions.

The stress test showed electric positivity.

The patient's oxygen saturation was normal.

The electrocardiogram showed a sinus rhythm.

The post-procedural course was uneventful.

The patient was discharged the following day.


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 has chronic rheumatic heart disease.

She has severe mitral stenosis with pulmonary hypertension.

She had percutaneous balloon mitral valvotomy 6 weeks prior.

A left atrial thrombus was detected after the procedure.

She started warfarin 5 mg, po, daily for 4 weeks.

She escalated to warfarin 7.5 mg, po, daily.

She had a severe headache and repeated episodes of vomiting for 1 day.

She had fever, malaise, and generalized weakness for 1 week.

She had an accentuated P2 on cardiovascular examination.

She had a mid-diastolic and pan-systolic murmur at the mitral area.

Meningeal irritation signs were negative.

Diagnoses included chronic rheumatic heart disease.

Diagnoses included subarachnoid hemorrhage.

A lumbar puncture was deferred due to higher INR.

ECG showed ST depression and inverted T wave at V1-V3.

Trans-thoracic echocardiography revealed moderate mitral stenosis.

Trans-thoracic echocardiography revealed mild mitral regurgitation.

Trans-thoracic echocardiography revealed severe pulmonary hypertension.

She was started on Ceftriaxone 2 gm, IV, twice daily.

She was started on Vancomycin 1 gm, IV, twice daily.

She developed sudden onset, frequent tonic-clonic convulsive episodes.

Pupils were mid-sized but poorly reactive to light.

A non-contrast brain CT scan revealed left-sided acute subdural hematoma.

A non-contrast brain CT scan revealed ventricular bleeds.

She was diagnosed with status epilepticus secondary to intracranial hemorrhage.

She was initiated on diazepam, 10 mg IV.

She was initiated on Phenytoin 1 gm IV bolus.

Vitamin K, 10 mg IV once daily for 3 days, was given.

IV ceftriaxone and vancomycin were continued.

Mannitol (20%), 50 gm IV bolus, was given.

Valproic acid, 400 mg po 3 times daily, was added.

Repeat laboratory values showed WBC=34,000/µL.

Repeat laboratory values showed hemoglobin=9 gm/dl.

Repeat laboratory values showed platelets=550,000/µL.

Repeat coagulation profiles showed PT=49.8 sec.

Repeat coagulation profiles showed PTT=63.2 sec.

Repeat coagulation profiles showed INR=4.38.

She had paroxysms of increase in pulse rate.

She had paroxysms of increase in blood pressure.

She had paroxysms of increase in respiratory rate.

She had paroxysms of increase in temperature.

She was started on morphine 2 mg, IV, as required.

She was started on paracetamol 1 gm, po, as required.

She was started on propranolol, 40 mg po 3 times a day.

She was started on diazepam 5 mg, IV 3 times a day.

She was started on gabapentin 150–300 mg po 3 times a day.

Her GCS started to improve on the second week of ICU admission.

The frequency and severity of sympathetic storm declined.

IV antibiotics were discontinued after 2 weeks of therapy.

On the third week of admission, she developed asystole.

She has echo-proven chronic rheumatic heart disease.

She had percutaneous balloon mitral valvotomy 6 weeks previously.

Left atrial thrombus was detected after the procedure.

She presented with severe headache and repeated vomiting of 1 day duration.

She had frequent seizure attacks with subsequent loss of consciousness on the third day of admission.

CT-scan revealed acute subdural hematoma and ventricular bleeding.

Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made.

She was transferred to medical intensive care unit (ICU), intubated, and put on mechanical ventilator.

Anti-epileptic drugs, antibiotics, vitamin K, and fresh frozen plasma were given.

She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis, and decerebrate posturing after 7 days of neurological insult.

She had normal inter-ictal EEG tracing during cyclic autonomic surge.

PSH-AM score suggested 'probable' diagnosis of PSH.

Morphine, diazepam, propranolol, and gabapentin were given in combination to treat PSH.

Severity of autonomic storm started to improve on the second week of ICU admission.

On the third week of admission, her clinical condition deteriorated suddenly.

She developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR).

She has chronic rheumatic heart disease.

She started warfarin 5 mg, po, daily for 4 weeks.

She escalated to warfarin 7.5 mg, po, daily.

Meningeal irritation signs were negative.

Diagnoses included chronic rheumatic heart disease.

Diagnoses included subarachnoid hemorrhage.

A lumbar puncture was deferred due to higher INR.

She was started on Ceftriaxone 2 gm, IV, twice daily.

She was started on Vancomycin 1 gm, IV, twice daily.

Pupils were mid-sized but poorly reactive to light.

She was initiated on diazepam, 10 mg IV.

She was initiated on Phenytoin 1 gm IV bolus.

Vitamin K, 10 mg IV once daily for 3 days, was given.

IV ceftriaxone and vancomycin were continued.

Mannitol (20%), 50 gm IV bolus, was given.

Valproic acid, 400 mg po 3 times daily, was added.

Repeat laboratory values showed WBC=34,000/µL.

Repeat laboratory values showed hemoglobin=9 gm/dl.

Repeat laboratory values showed platelets=550,000/µL.

Repeat coagulation profiles showed PT=49.8 sec.

Repeat coagulation profiles showed PTT=63.2 sec.

Repeat coagulation profiles showed INR=4.38.

She had paroxysms of increase in pulse rate.

She had paroxysms of increase in blood pressure.

She had paroxysms of increase in respiratory rate.

She had paroxysms of increase in temperature.

She was started on morphine 2 mg, IV, as required.

She was started on paracetamol 1 gm, po, as required.

She was started on diazepam 5 mg, IV 3 times a day.

**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 was transferred to our hospital because of LV thrombus found on transthoracic echocardiogram.

Transthoracic echocardiogram showed global hypokinetic LV with an EF of 28%.

A pedunculated apical thrombus measuring 1.75 × 1.68 cm was found.

Coronary angiogram revealed no significant obstructive lesion.

He was discharged and took warfarin 3.75 mg/day for AF and LV thrombus.

He developed sudden onset of right-hand clumsiness and expressive aphasia after 1 month.

Right eye blurred vision and drooling from the right mouth angle were noted.

The prothrombin time and INR were in the supratherapeutic range (INR 7.64).

His symptoms totally recovered within 1 day.

Brain MRI showed multiple acute infarctions in the cortex of the bilateral frontal lobes, left parietal lobe, and bilateral central semiovale.

The infarctions highly suggested embolic stroke.

Transthoracic echocardiogram on the same day of stroke still revealed LV thrombus (1.27 × 0.90 cm).

Warfarin was discontinued due to acute infarction under high INR.

Edoxaban (60 mg/day) was started after INR decreased to less than 2.

Follow-up echocardiography showed resolution of LV thrombus after 23 days of edoxaban.

He did not have recurrent stroke in the following 6 months.

He presented with acute onset of right-hand clumsiness.

He had an international normalized ratio of 7.64.

He was previously treated with warfarin for the LV thrombus.

He was previously treated with warfarin for non-valvular AF.

Brain MRI showed multiple acute infarction in the cortex of the bilateral frontal lobes.

Brain MRI showed multiple acute infarction in the left parietal lobe.

Brain MRI showed multiple acute infarction in the bilateral central semiovale.

The repeated transthoracic echocardiogram still revealed LV thrombus.

The LV thrombus measured 1.27 × 0.90 cm.

The LV thrombus failed to respond to warfarin therapy.

Acute infarctions occurred under supratherapeutic range of INR.

Warfarin was switched to edoxaban after INR decreased to less than 2.

The thrombus disappeared after receiving edoxaban for 23 days.

No more recurrent stroke was noted for more than 6 months.


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 outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).

The patient was 174 cm tall and weighed 47 kg.

The patient had an American Society of Anesthesiologists physical classification of 3.

The patient was scheduled for elective left nephroureterectomy.

A left calyx tumor was incidentally discovered during a routine medical examination.

A biopsy performed 1 month ago during ureteroscopy suggested a urothelial carcinoma.

The patient had a past medical history of intraductal papillary mucinous neoplasm of the liver that was surgically removed 6 years ago.

Chest computed tomography (CT) revealed pulmonary thromboembolism in the left lower lobe.

A lower extremity ultrasonogram showed no evidence of deep vein thrombosis.

Arterial blood gas analysis and D-dimer were within the normal ranges.

The patient was instructed to fast for 8 hours before undergoing general anesthesia.

Premedication involved an intramuscular injection of glycopyrrolate (0.2 mg) and famotidine (20 mg).

Noninvasive monitoring devices were placed on the patient, including a blood pressure cuff, electrocardiogram, a pulse oximeter, a bispectral index signal device, and a quantitative monitor for neuromuscular blockade.

General anesthesia was induced using 80 mg propofol.

Rocuronium (30 mg) was used for neuromuscular blockade after confirming no response to stimuli.

Sevoflurane (1.7%) was used to maintain the appropriate anesthesia depth after intubation.

An arterial line was inserted into the right radial artery.

Right internal jugular vein central venous catheterization was planned.

Real-time ultrasound-guided catheterization was initially planned.

The hospital’s portable ultrasonography device was in use in other operating rooms.

A blind catheterization technique was used based on the patient’s anatomical structure without ultrasound guidance.

The patient was positioned in the Trendelenburg position with the head 15° below the horizontal plane and tilted 40° to the left.

The Bermuda triangle was clearly identified.

The carotid artery pulse was palpated at the superior angle of the triangle and followed to the center of the triangle.

A 10 ml syringe connected to a 23-gauge finder needle was inserted perpendicularly to the surface while aspirating.

The presence of dark venous blood was confirmed at a depth of 2.2 cm.

No pulsation was observed after separating the finder needle from the syringe.

An 18-gauge puncture needle connected to the syringe was inserted toward the nipple at a 75° angle from the skin while targeting the finder needle tip.

The aspiration of venous blood flow was confirmed.

A guidewire was inserted to a depth of 20 cm from the skin through the puncture needle without any resistance felt during the procedure.

The puncture needle was removed while leaving the guidewire in place.

The practitioner and colleagues attempted to investigate the anatomy of the puncture site by utilizing ultrasonography to detect the previously inserted guidewire.

The guidewire was found to be located in a vein as which we presumed the vessel based on its location that was lateral from the common carotid artery and collapsibility when pressure was applied using the probe.

A larger vessel presumed to be a vein was located superiorly and more laterally than the identified vessel.

Real-time ultrasound-guided guidewire insertion was performed at the same view in this vessel using another central venous catheter kit.

Both guidewires were left in place while the probe was tilted to visualize their paths.

It was confirmed that they were both descending toward the right brachiocephalic vein.

The first guidewire was removed, and manual compression using sterile gauze was applied for over 5 min.

No resistance was felt during the removal.

The second guidewire was used to complete the central venous catheterization.

Free regurgitation was observed at each port.

The central venous pressure measured using the central venous catheter was 15 mmHg.

The patient was transferred to the post-anesthesia care unit after extubation.

A simple anterior-to-posterior chest X-ray taken immediately after the surgery confirmed that the catheter tip was located near the right atrium, following the superior vena cava.

We reviewed the contrast-enhanced chest CT performed for preoperative evaluation and confirmed that the right internal jugular vein coursed laterally to the right common carotid artery on the axial view.

A large vessel was also observed behind the common carotid artery and internal jugular vein.

It was traced upward and downward, confirming that it enters into the transverse foramen at the level of the sixth cervical vertebra and drains into the right brachiocephalic vein.

The same findings were observed in the coronary view.

The radiologist indicated this vessel as the vertebral vein.

After considering the ultrasonographic findings and the radiologist’s official reading, we confirmed that the vein that we had initially punctured was indeed the right cervical vertebral vein.

On the third day after surgery, the central venous catheter was removed.

The patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms.

The patient was suspected to have a urothelial carcinoma.

The patient was scheduled for elective left nephroureterectomy.

During central venous catheterization, the anatomic landmark technique was used to target the internal jugular vein.

A guidewire was inadvertently inserted into the suspected vertebral vein.

The radiologist reviewed the preoperative enhanced computed tomography.

The radiologist confirmed that the initially punctured vessel was the vertebral vein.

The central venous catheter was removed on the third day after surgery.

The patient was 174 cm tall and weighed 47 kg.

The patient was scheduled for elective left nephroureterectomy.

A lower extremity ultrasonogram showed no evidence of deep vein thrombosis.

Arterial blood gas analysis and D-dimer were within the normal ranges.

General anesthesia was induced using 80 mg propofol.

An arterial line was inserted into the right radial artery.

Right internal jugular vein central venous catheterization was planned.

Real-time ultrasound-guided catheterization was initially planned.

The hospital’s portable ultrasonography device was in use in other operating rooms.

The Bermuda triangle was clearly identified.

The presence of dark venous blood was confirmed at a depth of 2.2 cm.

No pulsation was observed after separating the finder needle from the syringe.

The aspiration of venous blood flow was confirmed.

The puncture needle was removed while leaving the guidewire in place.

No resistance was felt during the removal.

The second guidewire was used to complete the central venous catheterization.

Free regurgitation was observed at each port.

The central venous pressure measured using the central venous catheter was 15 mmHg.

The patient was transferred to the post-anesthesia care unit after extubation.

The same findings were observed in the coronary view.

The radiologist indicated this vessel as the vertebral vein.

On the third day after surgery, the central venous catheter was removed.


The patient was a 10-year-old Kurdish boy.

The patient had fever associated with night sweats.

The patient had weight loss of 5kg/month.

The patient had purple purpuric spots over the skin.

The patient’s history dated back to 1 month before admission.

On examination, we observed tachycardia.

On examination, we observed multiple petechiae and ecchymoses all over the skin.

On examination, we observed dilated tortuous veins over the chest.

The respiratory rate was 23cycles/minute.

We found multiple small cervical lymphadenopathies.

We found mild splenomegaly 3cm below the left costal margin.

The liver was tender 7cm below the right costal margin.

The patient had gross abdominal distention.

The initial blood counts were hemoglobin 64g/L.

The initial blood counts were white blood cell count 34 × 109/L.

The initial blood counts were platelets 25 × 109/L.

The initial blood counts showed blasts 38%.

The blasts were homogeneous with a high nuclear to cytoplasmic ratio.

There was mediastinal widening visualized on a chest X-ray.

MRI showed lumbosacral vertebrae with diffuse infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae.

The MRI findings were suggestive of bony metastases predominantly osteolytic in nature.

Bone marrow aspiration showed no fragments.

Bone marrow aspiration showed few areas of necrosis.

The first immunophenotyping was not conclusive.

The second immunophenotyping was positive for CD3.

The second immunophenotyping was positive for terminal deoxynucleotidyl transferase.

The second immunophenotyping was negative for CD20.

The second immunophenotyping was negative for CD79a.

The second immunophenotyping was negative for CD10.

After admission, the patient’s condition deteriorated.

The patient developed frank superior vena cava syndrome.

The patient was treated with chemotherapy according to the ALL protocol.

Complete remission was achieved on day 28.

At the 24th week of chemotherapy, the patient’s condition relapsed on treatment.

The patient returned to the hospital with fever.

The patient returned to the hospital with chest infection.

The patient returned to the hospital with 60% blasts observed on peripheral blood film.

The complete blood count revealed severe pancytopenia.

The bone marrow biopsy showed hypercellular marrow.

The bone marrow biopsy showed extensive infiltration by mononuclear cells.

The bone marrow biopsy showed disappearance of necrosis.

Treatment was reinitiated according to the ALL protocol.

The patient developed uncontrolled septicemia.

The patient developed electrolyte imbalance.

The bone marrow aspiration at the time of diagnosis was diluted.

The slides showed artefact with a few necrotic cells.

The biopsy consisted of a fragment of trabecular bone.

The result of immunohistochemistry was not interpretable for the first specimen.

The result of immunohistochemistry for the second specimen was definitive as precursor T-cell ALL.

During admission, the patient received intravenous fluid 3000ml/m2/day.

During admission, the patient received allopurinol tablets 100mg/m2/dose.

During admission, the patient received antibiotics.

The patient developed progressive dyspnea.

The patient developed abdominal distention.

The patient was near to developing frank features of superior vena cava syndrome.

The patient developed bilateral lower-limb weakness.

The straight leg raising test was positive bilaterally.

MRI of the dorsolumbosacral spine showed diffuse focal infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae.

The MRI showed altered hypointense T1-weighted signal intensity.

The image was suggestive of bony metastasis that was predominantly osteolytic in nature.

Incidental hepatosplenomegaly was observed.

Incidental bilateral renal enlargement was observed.

There was no pressure on the spinal cord.

Dexamethasone intravenous infusion at 6mg/m2 was started.

Seven days after admission, induction therapy with vincristine 1.5mg/m2 intravenous bolus was started on days 7, 14, 21 and 28.

Dexamethasone 6mg/m2 was administered daily.

Daunorubicin 25mg/m2 was given on days 1 and 7.

Upon starting induction, the patient developed attacks of tonic-clonic contractions.

Computed tomography of the brain without contrast was negative.

Electrolyte measurements showed severe hypocalcemia.

Correction of hypocalcemia stabilized the convulsions.

On day 28, bone marrow aspiration indicated a few fragments.

On day 28, erythroid and myeloid series were present with all stages of maturation.

On day 28, the data indicated predominant neutrophils and histiocytes.

On day 28, the cellular elements could not confirm an excess of blast cells.

The bone marrow biopsy report showed 95% cellularity.

The bone marrow biopsy showed predominant early-stage granulocytes.

The bone marrow biopsy showed normal maturation stages of hematopoietic cells.

The blasts constituted about 2% of total marrow nucleated cells.

The myeloid to erythroid cell ratio was 8:1.

After a 4-week induction period, complete remission was observed.

Early consolidation chemotherapy was continued.

At the 24th week of treatment, the patient returned with fever.

At the 24th week of treatment, the patient returned with chest infection.

At the 24th week of treatment, the patient returned with neutropenia.

At the 24th week of treatment, the patient returned with thrombocytopenia.

We found the presence of a few blasts in the peripheral blood film.

The patient was not responding to supportive treatment that included antibiotics and antipyretics.

Follow-up analysis of bone marrow aspiration showed excessive bone marrow infiltration by mononuclear cells.

Follow-up analysis of bone marrow aspiration showed multiple inconspicuous nucleoli.

Both erythroid and megakaryocytic precursors were suppressed in bone marrow aspiration.

In the relapsed biopsy, no necrosis was observed.

On the reinduction therapy date, we followed a bone marrow relapsed protocol.

On the 14th day of treatment reinduction, the patient developed severe anemia.

On the 14th day of treatment reinduction, the patient developed thrombocytopenia.

On the 14th day of treatment reinduction, the patient developed neutropenia.

The patient developed grade IV mucositis.

The patient could not tolerate the complications.

The patient’s death was an inevitable outcome.

The overall survival period was 26 weeks after first diagnosis.

The patient is a 10-year-old Kurdish boy.

He had generalized bone pain and fever of 1 month's duration.

The fever was associated with easy fatigability.

The fever was associated with nose bleeding.

The fever was associated with breathlessness.

The fever was associated with severe weight loss.

On examination, tachycardia was observed.

On examination, low blood pressure was observed.

On examination, petechial hemorrhage was observed.

On examination, ecchymoses were observed.

On examination, tortuous dilated veins over the chest and upper part of abdomen were observed.

On examination, multiple small cervical lymph node enlargements were observed.

On examination, a mildly enlarged spleen was observed.

On examination, a palpable liver was observed.

On examination, gross abdominal distention was observed.

Blood analysis revealed elevated lactate dehydrogenase.

Blood analysis revealed elevated erythrocyte sedimentation rate.

Imaging results showed mediastinal widening on a planar chest X-ray.

Imaging results showed diffuse focal infiltration of the axial bone marrow on magnetic resonance imaging of the lumbosacral vertebrae.

Bone marrow aspiration and biopsy examination showed extensive bone marrow necrosis.

Immunophenotyping analysis of the bone marrow biopsy confirmed T-cell acute lymphoblastic leukemia.

Terminal deoxynucleotidyl transferase markers were positive.

The patient was a 10-year-old Kurdish boy.

The patient had fever associated with night sweats.

The patient had weight loss of 5kg/month.

The patient had purple purpuric spots over the skin.

The patient’s history dated back to 1 month before admission.

On examination, we observed tachycardia.

On examination, we observed dilated tortuous veins over the chest.

The respiratory rate was 23cycles/minute.

We found multiple small cervical lymphadenopathies.

We found mild splenomegaly 3cm below the left costal margin.

The liver was tender 7cm below the right costal margin.

The patient had gross abdominal distention.

The initial blood counts were hemoglobin 64g/L.

The initial blood counts were white blood cell count 34 × 109/L.

The initial blood counts were platelets 25 × 109/L.

The initial blood counts showed blasts 38%.

The blasts were homogeneous with a high nuclear to cytoplasmic ratio.

There was mediastinal widening visualized on a chest X-ray.

Bone marrow aspiration showed no fragments.

Bone marrow aspiration showed few areas of necrosis.

The first immunophenotyping was not conclusive.

The second immunophenotyping was positive for CD3.

The second immunophenotyping was negative for CD20.

The second immunophenotyping was negative for CD79a.

The second immunophenotyping was negative for CD10.

After admission, the patient’s condition deteriorated.

The patient developed frank superior vena cava syndrome.

The patient was treated with chemotherapy according to the ALL protocol.

Complete remission was achieved on day 28.

The patient returned to the hospital with fever.

The patient returned to the hospital with chest infection.

The complete blood count revealed severe pancytopenia.

The bone marrow biopsy showed hypercellular marrow.

The bone marrow biopsy showed disappearance of necrosis.

Treatment was reinitiated according to the ALL protocol.

The patient developed uncontrolled septicemia.

The patient developed electrolyte imbalance.

The bone marrow aspiration at the time of diagnosis was diluted.

The slides showed artefact with a few necrotic cells.

The biopsy consisted of a fragment of trabecular bone.

During admission, the patient received intravenous fluid 3000ml/m2/day.

During admission, the patient received allopurinol tablets 100mg/m2/dose.

During admission, the patient received antibiotics.

The patient developed progressive dyspnea.

The patient developed abdominal distention.

The patient developed bilateral lower-limb weakness.

The straight leg raising test was positive bilaterally.

The MRI showed altered hypointense T1-weighted signal intensity.

Incidental hepatosplenomegaly was observed.

Incidental bilateral renal enlargement was observed.

There was no pressure on the spinal cord.

Dexamethasone intravenous infusion at 6mg/m2 was started.

Dexamethasone 6mg/m2 was administered daily.

Daunorubicin 25mg/m2 was given on days 1 and 7.

Computed tomography of the brain without contrast was negative.

Electrolyte measurements showed severe hypocalcemia.

Correction of hypocalcemia stabilized the convulsions.

On day 28, bone marrow aspiration indicated a few fragments.

On day 28, the data indicated predominant neutrophils and histiocytes.

The bone marrow biopsy report showed 95% cellularity.

The bone marrow biopsy showed predominant early-stage granulocytes.

The blasts constituted about 2% of total marrow nucleated cells.

The myeloid to erythroid cell ratio was 8:1.

After a 4-week induction period, complete remission was observed.

Early consolidation chemotherapy was continued.

At the 24th week of treatment, the patient returned with fever.

At the 24th week of treatment, the patient returned with chest infection.

At the 24th week of treatment, the patient returned with neutropenia.

We found the presence of a few blasts in the peripheral blood film.

In the relapsed biopsy, no necrosis was observed.

The patient developed grade IV mucositis.

The patient could not tolerate the complications.

The patient’s death was an inevitable outcome.

The overall survival period was 26 weeks after first diagnosis.

The patient is a 10-year-old Kurdish boy.

He had generalized bone pain and fever of 1 month's duration.

The fever was associated with easy fatigability.

The fever was associated with nose bleeding.

The fever was associated with breathlessness.

The fever was associated with severe weight loss.

On examination, tachycardia was observed.

On examination, low blood pressure was observed.

On examination, petechial hemorrhage was observed.

On examination, ecchymoses were observed.

On examination, a mildly enlarged spleen was observed.

On examination, a palpable liver was observed.

On examination, gross abdominal distention was observed.

Blood analysis revealed elevated lactate dehydrogenase.

Blood analysis revealed elevated erythrocyte sedimentation rate.

Imaging results showed mediastinal widening on a planar chest X-ray.

Terminal deoxynucleotidyl transferase markers were positive.


A 56-year-old woman was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission.

The patient had nausea and vomiting in the morning.

The patient had no history of seizures or decreased consciousness.

The examination of neurological symptoms was completely normal.

The patient's blood pressure was 130/85 mmHg.

The patient had undergone tympano-mastoidectomy surgery and resection of the cholesteatoma 1 week earlier.

A canalwall down mastoidectomy was performed due to right ear cholesteatoma.

Microtrauma was inflicted in the dural plate during surgery.

No significant cerebrospinal fluid leak occurred during the procedure.

The Mount Fuji sign was found on the brain CT scan.

No evidence of brain abscess or intracranial hemorrhage was found.

The patient was immediately admitted to the intensive care unit.

Initial treatments such as CBR, 30-degree head elevation, anti-fever therapy, analgesics, oxygen therapy, and phenytoin were prescribed.

The patient did not undergo surgery due to a lack of neurological symptoms, decreased level of consciousness, or seizures.

The patient was maintained under regular and continuous monitoring of vital and neurological signs.

The patient’s headache had completely resolved the day after admission.

The patient was admitted to the ICU for 5 days.

The patient was monitored for the volume of pneumocephalus every day with a CT scan.

The patient's pneumocephalus was resolved completely at the end of 5 days.

The patient was transferred to the ward.

The patient was discharged after complete recovery.

The patient was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission.

The patient experienced nausea and vomiting in the morning.

Examination of neurological symptoms was completely normal.

The patient had undergone tympanomastoidectomy surgery and resection of the cholesteatoma 1 week previously.

Treatments such as CBR, 30-degree head elevation, anti-fever, analgesics, oxygen therapy, and phenytoin were prescribed.

At the end of 5 days, the patient's pneumocephalus was resolved completely.


The patient was a 22-year-old male soldier.

The patient received multifragmental combined with thoraco-abdominal injuries as a result of shelling from MLRS “Grad”.

The entrance wound was detected in the region of 5–7 ribs between the anterior and the posterior right axillary lines.

The patient received first medical aid immediately at the place of injury.

The time taken between injury and evacuation was less than 60 min.

The patient was transported to the Military Medical Hospital #66 at Pokrovsk.

The patient was diagnosed with a penetrating thoracic wound.

The blood loss was approximately 1500 ml.

Thoracentesis was performed to eliminate the right hemopneumothorax.

A hemorrhagic content was received at the laparocentesis.

Ruptures of the liver’s parenchyma were detected.

The entrance wound was detected only in the chest area.

The exit wound was not identified neither in chest, nor in abdomen wall.

A conclusion was made that damage of the liver was in result of “hydrodynamic shock”.

Suturing of liver ruptures was performed.

Excision of necrotic tissues was performed.

Suturing of gunshot wounds of limbs was performed.

In an early post-operative period, a hemorrhage and bile were detected on drainage.

Liver damage within the area of gallbladder fossa was detected.

A patch of omentum was used to fill the gap in injured S3–6 of liver.

The patient was transported to the Mechnikov Regional Clinical Hospital in Dnipro.

Antibacterial therapy was administrated.

The patient was transported to the ICU at the National Military Medical Clinical Center of Ukraine in Kyiv.

Drainage from the subhepatic area showed daily bile volume up to 300 ml.

Endoscopic papillosphincterotomy was performed.

Endoscopic retrograde cholecystopancreatography was performed.

Stenting of the common bile duct was performed.

A feeding tube was placed behind the Treitz ligament.

Implementation of endoscopic decompression of the bile duct had resulted in gradual reduction of bile volume.

The liver demonstrated zones with ischemic lesions.

A liver resection of the affected segment was planned.

Erosion of the right hepatic artery was detected.

Tissue softening and color changes of liver S5–6 parenchyma were detected.

Anatomic resection of the liver S5–6 was performed.

The patient was transferred to the surgery ward from ICU.

The patient was diagnosed with multiple fragmental injuries of soft tissues of the skull, chest, abdomen, as well as extremities.

The most serious soft tissue injury was detected at the right lower limb.

The patient was discharged from hospital in good condition on the 49th day after receiving injuries.

The patient was injured after the multiple launcher rocket system 'Grad' shelling.

The patient was diagnosed with hydrodynamic liver rupture.

Medical management with application of damage control (DC) tactic was used.

The patient underwent endoscopic papillosphincterotomy.

The patient underwent endoscopic retrograde cholecystopancreatography.

Stenting of the common bile duct was performed.

Applied treatment modalities were effective.

The patient was discharged on the 49th day after injury.

The patient was a 22-year-old male soldier.

The blood loss was approximately 1500 ml.

Ruptures of the liver’s parenchyma were detected.

Suturing of liver ruptures was performed.

Excision of necrotic tissues was performed.

Antibacterial therapy was administrated.

Endoscopic papillosphincterotomy was performed.

Stenting of the common bile duct was performed.

Erosion of the right hepatic artery was detected.


She had a painful lump in her left breast 3 months ago.

She had bloody discharge from the left nipple four years ago.

The patient decided not to follow-up despite recommendations for diagnostic procedure.

On physical examination, an erythematous tender mass with hard consistency was detected around the nipple.

Sonography showed a lobulated hypoechoic mass with microcystic areas measuring 20×17 mm at 3 o'clock beside the areola.

Mammography showed a hyperdense mass in the retroareolar site.

The patient was admitted and underwent surgery.

Intraoperative pathology consultation based on multiple frozen sections from the mass was performed.

A left modified radical mastectomy and lymph node dissection were done.

On serial sectioning, there were tan-brown firm masses with multiple cystic areas.

The surgical margins were free from tumoral cells.

Sections were taken and stained by hematoxylin and eosin.

Microscopically, neoplastic tissue composed of dilated ducts filled by papillary projections, cribriform and fused glands was seen.

The neoplastic tissue was lined by mild to moderate atypical cells with scattered mitoses.

There was no distinct myoepathelial layer.

The neoplastic tissue was mostly floating in mucinous lakes with invasion to surrounding stroma.

Foci of ductal carcinoma in situ including cribriform, papillary, and micropapillary patterns were present in about 30% of the tumor bulk.

All surgical margins were free of tumor.

An in situ component with papillary features was seen in the nipple.

Nearby skin-deep dermis was involved by tumor.

All 16 lymph nodes showed reactive changes.

Immunohistochemistry profile showed positive estrogen and progesterone receptors.

Immunohistochemistry profile showed negative for HER2.

The patient was discharged with regular follow-up.

The patient had a painful mass in her left breast.

Intraoperative pathology consult showed neoplastic tissue mostly floating in mucinous lakes.

Invasion to surrounding stroma was seen.

Immunohistochemistry profile showed positive estrogen receptors.

Immunohistochemistry profile showed positive progesterone receptors.


The patient was a 48-year-old caucasian male.

He had an extensive psychiatric history of depression.

He was admitted to the intensive care unit following intoxication of approximately 20 g venlafaxine, 450 mg zolpidem, and 250 mg propiomazine.

His past history included intensive care hospitalization due to two suicidal attempts through pharmacological intoxication.

His Glasgow Coma Scale (GCS) was 13 of 15.

His electrocardiography (ECG) was normal with a sinus rhythm of 57 beats per minute.

Laboratory findings were within normal range.

Admission occurred approximately 2 hours after intake of the pills.

Activated charcoal suspension was administered via a nasogastric tube upon arrival at the intensive care unit.

The patient was stable during the first 5 hours at the intensive care unit.

Seven hours post-intoxication, he experienced tonic–clonic seizures.

This was successfully treated with diazepam 10 mg intravenously.

He was intubated and sedated with propofol and remifentanil.

Vasopressor support with low-dose norepinephrine was initiated.

Nine hours after ingestion, his circulation began to slowly fail.

Increased doses of norepinephrine were required.

The patient developed metabolic acidosis with lactate elevation.

Fifteen hours after ingestion, the patient’s blood pressure fell rapidly despite high doses of norepinephrine.

Prompt echocardiography revealed prominent hypokinesia with akinesia from the mid-left ventricle to the apex, as in TTC.

The left ventricle ejection fraction (EF) was 20%.

The right ventricle was also affected with a tricuspid annular plane systolic excursion (TAPSE) measuring 10 mm.

Only a few micrograms of dobutamine were infused prior to cardiac arrest.

The patient suffered a cardiac arrest with an initial rhythm of asystole.

Advanced cardiac life support was initiated according to national guidelines.

The patient was given three doses of epinephrine 1 mg intravenously.

After 5 minutes without return of spontaneous circulation, the ECMO center at a tertiary hospital was contacted.

Fifteen minutes post cardiac arrest, the patient regained circulation temporarily for approximately 10 minutes.

The patient’s circulatory status and blood pressure were inadequate during these 10 minutes.

High-dose epinephrine infusion (1.0 µg/kg/minute) was initiated.

Manual CPR continued for another 30 minutes.

The patient was transported by helicopter to a tertiary hospital using mechanical CPR (AutoPulse Resuscitation System) and ongoing epinephrine infusion.

Transportation time was approximately 30 minutes.

One hour 15 minutes after the cardiac arrest, the patient was delivered to the tertiary hospital for ECMO initiation.

Upon arrival at the tertiary hospital, the patient had a sinus rhythm but very low cardiac output.

Blood pressure was 55/45 mmHg without cardiac arrest.

External compression was continued whilst ECMO system treatment was established.

Short pauses were taken during specifically vulnerable periods of the cannulation procedure.

Two hours after the cardiac arrest, the patient was on ECMO.

After ECMO initiation, treatment with sedation and circulatory drugs continued.

Continuous renal replacement therapy (CRRT) was initiated.

CRRT was initiated due to anuria and creatinine level of 265 µmol/L.

Sedation was reinitiated using midazolam and morphine instead of propofol and remifentanil.

The amount of epinephrine was significantly decreased during the initial hours of ECMO treatment.

Norepinephrine and milrinone were used instead.

Multiple plasma and red cell concentrate (RCC) transfusions were also required due to significant bleeding from the femoral artery catheter.

The patient was successfully weaned after 32 hours of ECMO.

Epinephrine infusion was terminated the same day.

Milrinone continued until the following day.

The patient was transported back to the primary hospital with decreasing doses of norepinephrine the day after ECMO termination.

Three days after the cardiac arrest, his cardiac function was echodynamically restored with an EF of above 55%.

Values of the cardiac biomarker NT-proBNP decreased from 8360 ng/L the day after the cardiac arrest to 1190 ng/L 36 days after the intoxication.

Two days after extubation, the patient gradually regained consciousness.

Thirty days after the intoxication, he had regained normal cardiac and cognitive function.

He left the hospital for further psychiatric treatment.

The patient’s renal function was fully restored with normal creatinine level (82 µmol/L) 7 weeks after the intoxication.

He was finally discharged in good health without his former prescribed psychiatric medications.

Two years later, his cardiac and renal function were normal.

His psychiatric medication was reinstated.

The serum venlafaxine concentration 24 hours after ingestion was 12.6 mg/L.

This laboratory result was not received until 1 week after ingestion.

The patient is a 48-year-old caucasian male.

The patient has an extensive psychiatric history.

The patient ingested a high dose of venlafaxine.

The serum venlafaxine concentration was 12.6 mg/L 24 hours after ingestion.

Seven hours post-ingestion, the patient experienced tonic-clonic seizures.

Eight hours post-ingestion, takotsubo cardiomyopathy was recognized.

The patient was resuscitated with prolonged cardiopulmonary resuscitation.

Ongoing automatic external compressions were used during helicopter transportation.

The patient was transported to a tertiary hospital for extracorporeal membrane oxygenation treatment.

The cardiopulmonary resuscitation duration was 2 hours.

The patient received 36 hours of extracorporeal membrane oxygenation.

The patient spent a total of 30 days in the intensive care unit.

The patient was a 48-year-old caucasian male.

He had an extensive psychiatric history of depression.

His Glasgow Coma Scale (GCS) was 13 of 15.

Laboratory findings were within normal range.

Admission occurred approximately 2 hours after intake of the pills.

Seven hours post-intoxication, he experienced tonic–clonic seizures.

This was successfully treated with diazepam 10 mg intravenously.

He was intubated and sedated with propofol and remifentanil.

Vasopressor support with low-dose norepinephrine was initiated.

Nine hours after ingestion, his circulation began to slowly fail.

Increased doses of norepinephrine were required.

The patient developed metabolic acidosis with lactate elevation.

The left ventricle ejection fraction (EF) was 20%.

The patient suffered a cardiac arrest with an initial rhythm of asystole.

The patient was given three doses of epinephrine 1 mg intravenously.

High-dose epinephrine infusion (1.0 µg/kg/minute) was initiated.

Manual CPR continued for another 30 minutes.

Transportation time was approximately 30 minutes.

Blood pressure was 55/45 mmHg without cardiac arrest.

Two hours after the cardiac arrest, the patient was on ECMO.

Continuous renal replacement therapy (CRRT) was initiated.

CRRT was initiated due to anuria and creatinine level of 265 µmol/L.

Norepinephrine and milrinone were used instead.

The patient was successfully weaned after 32 hours of ECMO.

Epinephrine infusion was terminated the same day.

Milrinone continued until the following day.

Two days after extubation, the patient gradually regained consciousness.

He left the hospital for further psychiatric treatment.

Two years later, his cardiac and renal function were normal.

His psychiatric medication was reinstated.

This laboratory result was not received until 1 week after ingestion.


The patient was a 46-year-old male with end-stage renal disease of unknown cause.

He had been on hemodialysis for 3 years.

He underwent cadaveric renal transplantation 15 months ago.

There was no other remarkable medical history except for 3 years of hypertension.

During harvesting of the donor’s kidneys, a branch of right renal artery to renal superior polar was inadvertently cut off.

The artery branch with a diameter 0.3 mm arose from the bifurcation of abdominal aorta and renal artery.

The severed renal artery branch was anastomosed in situ with 7–0 prolene during the repair of the kidney.

The cold ischemia time of the kidney was 5 min.

The warm ischemia time of the kidney was 6 h.

The right kidney of donor was transplanted in the right iliac fossa.

The donor renal artery with a Carrel patch of donor aorta was anastomosed end-to-side to the recipient right external iliac artery with 6–0 prolene.

The renal vein was anastomosed end-to-side to the recipient right external iliac vein with 5–0 prolene.

The graft ureter was anastomosed to the urinary bladder of the recipient with a double J stent.

Basiliximab was used as immunity induction on the day of surgery and the fourth day after transplantation.

His immunosuppression regimen consisted of tacrolimus, mycophenolate sodium, and prednisolone.

His immediate postoperative course was unremarkable.

His blood pressure was controlled to 140–156/90–105 mmHg with nicardipine, spironolactone, and furosemide.

The 24-h urine volume was between 1937 and 4100 ml.

His renal function significantly improved, reaching a creatinine of 151 μmol/L on 11st day posttransplantation.

From the 12nd day after transplantation, his blood pressure began to gradually increase to 170–174/103–109 mmHg.

There was no positive presentation on clinical examination and ultrasonography.

The level of creatinine and urine volume were also stable.

It was still difficult to control his blood pressure even though three antihypertensive medications were administered.

His blood pressure reached 190/120 mmHg on 20th day after transplantation.

There was a decrease in 24-h urine volume with 1620–1725 ml.

There was mild impairment of renal function with a creatinine of 194 μmol/L.

A bruit became audible over the site of the transplanted kidney.

Color Doppler ultrasonography indicated a decreased RI in intrarenal arteries.

Color Doppler ultrasonography indicated increased blood flow of the transplant renal artery.

The peak systolic velocity was 305 cm/s.

The velocity gradient between stenotic and prestenotic segment was more than 3:1.

A vascular complication of TRAS was suspected.

Diagnostic arteriography showed a 90% stenosis of transplant renal artery.

The TRAS occurred in the distal site of the anastomosis instead of the anastomosis.

We considered that the reconstructional renal artery branch stretched the trunk of renal artery, which resulted in the stenosis distal to the suture line.

Renal artery angioplasty was undertaken through a retrograde ipsilateral femoral artery approach.

Percutaneous transluminal stent implantation was performed.

A bare stent (6 × 14 mm, Express Vascular SD) had to be chosen to avoid affecting the flow of the artery branch.

After the bare stent was successfully deployed, a second angiographic evaluation verified the effectiveness of the intervention was obvious.

After the interventional treatment, the renal function and urine volume recovered.

His blood pressure was stably controlled to 121/80 mmHg with only two antihypertension medications (nifedipine and arotinolol).

He was discharged on 28 day after transplantation with a creatinine of 108 μmol/L.

The patient’s renal function remains stable at clinical follow-up of 15 months.

The patient has end-stage renal disease of unknown cause.

The patient received a cadaveric renal transplant one year ago.

Three antihypertensive medications were administrated.

His blood pressure increased to 190/120 mmHg 3 weeks posttransplantation.

The level of creatinine increased to 194 μmol/L.

Color Doppler ultrasonography indicated a decreased resistance index in intrarenal arteries.

A vascular complication of TRAS was suspected.

Percutaneous transluminal bare stent implantation treatment was successfully performed.

Satisfactory clinical efficacy with improvement in transplant renal function was achieved after the interventional treatment.

Satisfactory clinical efficacy with improvement in renovascular hypertension was achieved after the interventional treatment.

He had been on hemodialysis for 3 years.

He underwent cadaveric renal transplantation 15 months ago.

The cold ischemia time of the kidney was 5 min.

The warm ischemia time of the kidney was 6 h.

The right kidney of donor was transplanted in the right iliac fossa.

His immediate postoperative course was unremarkable.

The 24-h urine volume was between 1937 and 4100 ml.

The level of creatinine and urine volume were also stable.

His blood pressure reached 190/120 mmHg on 20th day after transplantation.

There was a decrease in 24-h urine volume with 1620–1725 ml.

A bruit became audible over the site of the transplanted kidney.

The peak systolic velocity was 305 cm/s.

A vascular complication of TRAS was suspected.

Diagnostic arteriography showed a 90% stenosis of transplant renal artery.

Percutaneous transluminal stent implantation was performed.


The carcinoembryonic antigen level was 5.6 ng/mL.

Chest computed tomography revealed a tumor with a maximum diameter of 13 mm in the left lower pulmonary lobe.

The tumor was suspected to be left lower lobe lung cancer (cT1bN0M0 stage1A2).

Three-dimensional CT was performed using the Fujifilm Synapse Vincent system.

A displaced B1 + 2 was running behind the main pulmonary artery.

An anomalous V1 + 2 joined the left inferior pulmonary vein.

Hyperlobulation between S1 + 2 and S3 with a completely fused interlobar fissure between S1 + 2 and S6 was observed.

The interlobar plane between S1 + 2 and S6 ran perpendicular to the cranio-caudal direction.

Bronchoscopy revealed that three bronchi branched from the left main bronchus.

VATS was planned for surgical diagnosis and treatment.

Non-anatomical wedge resection of the lesion was performed.

The patient was diagnosed with adenocarcinoma.

Left lower lobectomy and systematic nodal dissection were performed.

The major pitfalls were to avoid injuring the displaced B1 + 2 and to avoid cutting the anomalous V1 + 2.

The inferior pulmonary vein was identified on the posterior side of the hilum.

The anomalous V1 + 2 joined the inferior pulmonary vein.

The distal branch of A8 was identified using the interlobar fissure.

A6 and V1 + 2 ran near A6 and a branch of V1 + 2 ran between S1 + 2 and S6.

The branch of V1 + 2 was used as a landmark when dividing the fissure between S1 + 2 and the inferior lobe.

Forceps were passed from the anterior to posterior side between a branch of V1 + 2 and A6.

The largely fused fissure between S1 + 2 and the inferior lobe was divided using a stapler.

A6 and A9 + 10 were identified and divided.

The inferior bronchus branched from the left main bronchus at the level of the branches of B3 + B4 + 5 and the displaced B1 + 2.

The displaced B1 + 2 was located at a more proximal site than normal.

The station 11 lymph nodes were identified.

Forceps were passed from the anterior to posterior side along the station 11 lymph nodes.

The incomplete fissure between S5 and inferior lobe was divided using the stapler.

The inferior bronchus was divided, which completed the lobectomy ND2a-2 procedure.

The tumor was diagnosed as an invasive mucinous adenocarcinoma with a maximal diameter of 15 mm.

The pathological stage was p-T1aN0M0 stage I A1.

The patient was discharged from hospital 6 days after the surgery.

The patient had suspected lung cancer in the left lower lobe.

The patient was scheduled to undergo surgery.

Chest computed tomography revealed a displaced B1 + 2.

Chest computed tomography showed hyperlobulation between S1 + 2 and S3.

The interlobar fissure between S1 + 2 and S6 was completely fused.

Three-dimensional computed tomography revealed an anomalous V1 + 2 joining the left inferior pulmonary vein.

A branch of the V1 + 2 ran between S1 + 2 and S6.

The operation was a left lower lobectomy via video-assisted thoracic surgery.

The strategy included confirming the locations of B1 + 2 and B6 when dividing the fissure.

The patient was diagnosed with adenocarcinoma.

A6 and A9 + 10 were identified and divided.

The station 11 lymph nodes were identified.


She had recurrent upper abdominal fullness discomfort for almost 10 years.

She experienced exacerbation of intermittent nausea, vomiting with chyme (5 mL), heartburn, acid regurgitation, and eructation for 6 months.

No history of hypertension, diabetes mellitus, or coronary heart disease was noted.

A 5 × 4 cm mass with a hard texture and poor mobility was observed in the upper abdomen.

Routine blood and tumor marker test results were within normal range.

Abdomen CT showed a 32 mm × 22 mm soft tissue mass shadow with homogeneous density in the descending duodenum.

The mass was protruding into the duodenal lumen.

Thickening of the adjacent intestinal wall was noted.

Upper abdomen MRI revealed significant thickening of the wall of the duodenal bulb and descending duodenum.

The signals were slightly low in T1-weighted images.

The signals were slightly high in T2-weighted images.

Endoscopic ultrasonography showed a protrusion in the duodenal bulb of about 26 × 18 mm in size.

The protrusion had a clear boundary, smooth surface, and irregular shape.

The base of the protrusion was about 17 mm.

Neoplasm resection of the duodenum was performed.

A mass measuring about 25 × 30 × 10 mm was found in the descending duodenum.

The pathological result revealed multiple Brunner’s glands with tubes, fibers, and smooth muscle diffuse distribution.

No dysplasia was noted on the epithelium.

It was diagnosed as Brunner’s gland adenoma of the duodenum.

The patient was discharged from the hospital a week after recovery.

The patient had upper gastrointestinal obstruction for almost 10 years.

The patient was pathologically diagnosed with large Brunner's gland adenoma of the duodenum.

Postoperatively, no sign of recurrence has been noted until now.


Intuto is located 172 km from the city of Iquitos.

He has a history of untreated type 2 diabetes mellitus.

He presented to the emergency department of the Regional Hospital of Loreto.

The illness began with convulsions of 1 to 2 minutes.

The convulsions occurred 5 to 6 times a day.

Two days before admission, he had loss of consciousness.

Two days before admission, he had limited motor function.

He was transferred to the nearest health center.

At the health center, a thick and extended gout examination was performed.

Plasmodium vivax trophozoites were observed.

The doctor decided to refer him to a health center of greater complexity.

He went to the emergency department of the Regional Hospital of Loreto.

He received intravenous artesunate 14.4 mg at admission.

Intravenous artesunate was repeated at 12 and 24 h.

Each dose was diluted with 5% dextrose in a volume of 5 to 10 ml.

Each dose was administered as a 5 min bolus.

Artesunate was continued at 24 mg orally until day 5.

600 mg of clindamycin was infused over 20 to 30 min every 12 h for 5 days.

Clindamycin was diluted in 50 ml of 0.9% sodium chloride.

A packed red blood cell transfusion was performed.

A new thick blood examination was performed.

No parasite was observed in the thick blood examination.

The laboratory examinations showed depression of the three series of blood cells.

The peripheral sheet extension was typical granulocytes ++.

The peripheral sheet extension showed atypical lymphocytes +.

The erythrocyte series showed microcytosis.

The erythrocyte series showed anisocytosis.

The erythrocyte series showed basophilic punctate.

The abdominal ultrasound showed splenomegaly.

The abdominal ultrasound showed bilateral pleural effusion.

Cerebrospinal fluid analysis was performed.

The patient showed clinical improvement.

The patient had a neurological sequela of monoparesia of the motor nerves in the lower left.

The patient has cerebral malaria by Plasmodium vivax.

The patient starts with general discomfort and fever.

The patient presents convulsions more than twice a day.

The patient has motor functional limitation.

A thick drop shows Plasmodium vivax trophozoites.

A thick drop shows depression of the three blood series.

The patient is given treatment with artesunate and clindamycin for five days.

The patient receives a blood transfusion.

The patient continues with primaquine for seven days.

The patient has neurological sequelae in the left lower extremity.

Plasmodium vivax trophozoites were observed.

Each dose was administered as a 5 min bolus.

A new thick blood examination was performed.

The erythrocyte series showed microcytosis.

The erythrocyte series showed anisocytosis.

Cerebrospinal fluid analysis was performed.

The patient showed clinical improvement.


The patient was a 59-year-old morbidly obese, African-American female.

She had a history of Stage IIIc recurrent endometrial carcinosarcoma with para-aortic and pelvic lymph node involvement.

She had a 1-month history of numbness of the left vulva.

She had worsening left lower extremity pain/numbness.

The thoracic/lumbar MR revealed a 1.4 × 1.8 cm enhancing intradural extramedullary mass inferior to the conus at the L1 and L4-L5 levels.

There was abnormal enhancement of the left-sided intradural nerve roots.

There were bilateral, perihilar lung metastases.

The patient underwent a T12-L2 laminectomy for gross total resection of the L1 intradural/extramedullary mass.

The main aim of surgery was to provide neurological symptomatic relief.

Intraoperatively, diffuse carcinomatosis of the cauda equina was observed.

A large lesion was located anteroinferior to the conus.

The tumor appeared vascular and involved multiple, swollen, engorged nerve roots.

Dissection ceased once intraoperative electromyographic monitoring showed significant changes.

The permanent pathology showed a mesenchymal malignant Mullerian mixed tumor (carcinosarcoma) without an epithelial component.

The postoperative MR revealed residual intradural extramedullary tumor.

The pain and numbness improved in her left lower extremity.

She returned to the hospital 2 weeks later complaining of increased lower extremity symptoms.

She had the new onset of right-sided facial weakness, numbness, and blurry vision.

Imaging of the brain and spinal cord revealed leptomeningeal spread of her disease.

Imaging revealed multiple, new intracranial metastases.

Two months later, she succumbed to her metastatic disease.

The patient has a history of recurrent UCS.

The patient had new onset of left lower extremity pain.

The patient had episodic urinary incontinence.

MR revealed an enhancing intradural extramedullary mass posterior to the L1 vertebral body.

The patient underwent a focal decompressive laminectomy.

The patient improved neurologically postoperatively.

The patient succumbed to the leptomeningeal spread of her disease.

The patient died within 2 postoperative months.


The patient is a 69-year-old Tunisian female.

She has no family history of auto-immune disease.

She was explored 4 years prior to admission for transient arthralgias and arthritis.

She experienced photosensitivity, malar rash, and diffuse discoid lesions in her trunk and face.

She reported weight loss of approximately 3 kg in the last three months.

The physical examination showed synovitis of the wrists.

The autoimmune profile confirmed a strong positivity of Antinuclear antibodies (ANA) with titre 1:400.

The autoimmune profile showed anti-double-stranded DNA (anti-dsDNA) at 115 UI/ml.

The autoimmune profile showed normal serum complements.

The patient was non-reactive for anti-La antibodies.

The patient was non-reactive for anti-cardiolipin antibodies.

The patient was non-reactive for lupus anticoagulant.

The patient was non-reactive for anti-SM antibodies.

The patient was non-reactive for anti-RNP antibodies.

The patient was non-reactive for anti-SCL-70 antibodies.

The patient was non-reactive for anticentromere antibodies.

The patient was non-reactive for rheumatoid factor.

The patient was non-reactive for autoantibodies against citrullinated protein.

The presence of 6 of 11 American College of Rheumatology criteria allowed the diagnosis of SLE.

The patient was treated with Chloroquine (200 mg/day).

The patient showed improvement of her general state of health.

One year later, she developed liver dysfunction.

Antimitochondrial antibodies (AMA) were positive (1:164).

Antimitochondrial antibodies were positive with positive anti-E2 fraction.

Serologic markers for hepatitis B and hepatitis C viruses were negative.

Abdominal echo showed no fatty change of the liver.

Abdominal echo showed no abnormality of the bile ducts.

Microscopic examination reveals a focal florid duct lesion characterized by a portal lymphocytic infiltrate and epitheloid cells that are centred on interlobular ducts with evidence of destruction.

These lesions are associated with a lymphocytic cholangitis and a portal inflammation containing conspicuous plasma cells and numerous lymphocytes.

These findings led to a diagnosis of stage I PBC according to Scheuer’s classification.

Based on the hematology and liver-tissue results, she was diagnosed with asymptomatic PBC.

Treatment with ursodeoxycholic acid (600 mg daily) was started.

The transaminase levels normalized with one month.

The patient has not complained liver dysfunction.

She was followed up regularly with stable health.

The patient was diagnosed with SLE at 69 years.

The patient was admitted for further examination of liver dysfunction.

PBC was confirmed based on elevated serum levels of transaminase.

PBC was confirmed based on high levels of antimitochondrial antibodies.

PBC was confirmed following a liver biopsy.

The oral administration of ursodeoxycholic acid stabilized the liver dysfunction.

The patient is a 69-year-old Tunisian female.

She has no family history of auto-immune disease.

One year later, she developed liver dysfunction.

The patient has not complained liver dysfunction.

She was followed up regularly with stable health.


A previously healthy 64-year-old male was admitted to the hospital with headache, fever and later imbalance, blurred vision and general slowness.

Patient’s neurological examination revealed nuchal rigidity and general clumsiness.

Blood tests showed leukocytosis (11.90 × 109/l) and an increased C-reactive protein (47 mg/l).

A computer tomography (CT) scan of the brain showed normal results.

The cerebrospinal fluid (CSF) was clear but yellowish.

The CSF had a slightly elevated count of erythrocytes (10 × 106/l).

The CSF had high levels of leukocytes (940 × 106/l; 40% lymphocytes and 56% granulocytes).

The CSF had elevated protein levels (1,696 mg/l).

The CSF had hypoglycorrhachia (0.9 mmol/l).

Bacterial cultures and CSF staining remained negative.

The patient was treated with intravenous (IV) dexamethasone (10 mg four times a day).

The patient was treated with ceftriaxone (4 g daily).

The patient was treated with acyclovir (750 mg three times a day).

Four days after admission, when his C-reactive protein had decreased to 10 mg/l, viral meningitis was considered the most probable cause.

The treatment with ceftriaxone and dexamethasone was discontinued.

Nine days after admission, the patient’s general condition slowly deteriorated.

The patient became increasingly somnolent.

The patient was restarted on IV ceftriaxone (2 g daily, which was increased to 4 g daily one day later).

The patient was treated with doxycycline (100 mg twice a day) due to the suspicion of borreliosis.

Brain magnetic resonance imaging (MRI) was performed.

The MRI revealed signs compatible with ventriculitis in the right lateral ventricle and the third ventricle.

Eleven days after admission, the patient’s consciousness rapidly declined.

A new CT scan of the brain revealed hydrocephalus and a mild midline shift, attributed to the enlarged right lateral ventricle.

An emergency ventriculostomy was performed.

Cerebrospinal fluid obtained during the operation appeared clear but yellowish.

Later debris was observed in the CSF collector bag.

Due to the neurosurgeon’s suspicion of a poor clinical response to ceftriaxone, it was switched to IV cefotaxime (2 g three times a day).

The dosage of cefotaxime was increased to 2 g four times a day by an infection consultant two days later.

No signs of renal dysfunction were detected.

Serum creatinine levels remained within the normal range.

The patient’s condition rapidly improved after the ventriculostomy and antibiotic treatment.

On the 21st day after admission, the ventriculostomy was closed.

In the Gram staining of the CSF sample obtained from the ventriculostomy at the time of the operation, chains of gram-positive cocci were observed inside polymorphonuclear leukocytes.

The bacteria’s morphology resembled that of streptococci.

Bacterial cultures of both CSF and blood remained negative.

The sample, which displayed bacteria in the Gram staining, and another CSF sample taken one day later, were analyzed using in-house bacterial 16s ribosomal RNA gene amplification by polymerase chain reaction (PCR) with high sensitivity for both aerobic and anaerobic bacteria, followed by sequencing.

The analysis of both samples tested positive for S. intermedius.

No clinical signs of infective endocarditis were observed in further assessments.

The patient mentioned a history of chronic dental problems.

An orthopantomography revealed advanced periodontal destruction in several teeth.

Periapical abscesses were found in teeth 33 and 31.

Maxillary teeth 15 and 16 were urgently extracted.

Teeth 17, 23, 24, 31, 32, 33, and 43 were extracted.

During the latter operation, prophylactic metronidazole (500 mg three times a day) was initiated for three days.

The patient continued to improve and was discharged in good condition one month after admission, with only slight left-sided hemiparesis.

The patient was admitted to the hospital with a headache.

Neurological examination revealed nuchal rigidity.

Neurological examination revealed general clumsiness.

The patient was treated with dexamethasone.

The patient was treated with ceftriaxone.

The antibacterial treatment was discontinued.

Nine days after admission, the patient's condition deteriorated.

The antibacterial treatment was restarted.

In CSF Gram staining, chains of gram-positive cocci were observed.

A bacterial PCR detected Streptococcus intermedius.

An orthopantomography revealed periapical abscesses.

The teeth with periapical abscesses were subsequently operated on.

The patient was discharged in good condition after one month.

The cerebrospinal fluid (CSF) was clear but yellowish.

The CSF had elevated protein levels (1,696 mg/l).

The CSF had hypoglycorrhachia (0.9 mmol/l).

Bacterial cultures and CSF staining remained negative.

The patient was treated with ceftriaxone (4 g daily).

The patient became increasingly somnolent.

Brain magnetic resonance imaging (MRI) was performed.

An emergency ventriculostomy was performed.

Later debris was observed in the CSF collector bag.

No signs of renal dysfunction were detected.

Serum creatinine levels remained within the normal range.

The bacteria’s morphology resembled that of streptococci.

The patient mentioned a history of chronic dental problems.

Periapical abscesses were found in teeth 33 and 31.

Maxillary teeth 15 and 16 were urgently extracted.

Teeth 17, 23, 24, 31, 32, 33, and 43 were extracted.


The patient is a 43-year-old nonsmoking and nondrinking white male.

The patient had oral cancer on the left side of the tongue.

A biopsy sample taken from the tumor revealed G2 keratinizing squamous cell carcinoma.

A CT scan performed two months before the operation showed a primary tumor measuring 15 × 10 mm with peripheral contrast enhancement.

The CT scan showed two suspected, probably metastatic lymph nodes on the left side of the neck in groups III and IV, size 17 × 14 mm and 26 × 16 mm, respectively.

Distant metastases were ruled out on chest X-ray and abdominal ultrasound.

Anamnesis proved previous lower extremity deep vein thrombosis.

Doppler ultrasound ruled out active deep vein thrombosis.

The surgical procedure included excision of the left half of the tongue, the floor of the mouth, and the sidewall of the throat.

The surgical procedure included bilateral cervical lymph node dissection in groups I-V on the left side and I-III on the right side.

The second part of the operation involved reconstruction using an anterolateral thigh flap.

Reoperation was performed three days after surgery due to hemorrhage from the wound after lymphadenectomy.

The final histopathology report revealed G2 keratinizing squamous cell carcinoma, stage IVa (pT3 pN2b, AJCC 8th edition).

The histopathology report noted perineural invasion of small nerves.

The histopathology report noted an unfavorable pattern of invasion with small islands (the worst pattern of invasion, 4).

The histopathology report noted a closest margin below 1 mm.

The histopathology report noted five metastatic lymph nodes (of 49 lymph nodes dissected) without extracapsular extension at levels II, IV, V on the left side.

The novel prognostic histopathological grading system in oral squamous cell carcinoma based on tumor budding revealed G-2.

102 budding foci were detected per 10 high-power fields.

Two to four cell-sized nests or single-cell invasion was observed.

A multidisciplinary case conference qualified the patient for postoperative radiochemotherapy.

Five-point head, neck, and shoulder masks were employed for patient immobilization.

A CT scan (3 mm slice thickness) without intravenous contrast was performed in the planning radiotherapy process.

The dose prescription involved the bilateral lymph nodes I-V to a total dose of 50 Gy in 25 fractions.

The dose prescription involved the left side neck in groups II-V to a total dose of 60 Gy in 30 fractions.

The dose prescription involved the tumor bed with bilateral submandibular lymph nodes to a total dose of 66 Gy in 33 fractions.

In the first stage of treatment, three full arcs were used.

In the second stage, three arcs lateralized to the left side of the neck were used.

In the third stage, two frontal arcs were applied.

Radiotherapy was performed by linear accelerators (Clinac 23EX; Varian Medical Systems, Palo Alto, CA, USA) with an energy of 6 MV and maximal dose rate of 600 MU/min.

Two weeks after the beginning of radiotherapy, ultrasound of the neck was performed due to a suspected lump in group III on the right side.

The ultrasound revealed a 16 × 9 mm lymph node.

Fine-needle aspiration biopsy was performed, confirming metastasis of the squamous cell carcinoma.

The multidisciplinary case conference urged the application of a single-fraction stereotactic radiosurgery (SRS) boost of 18 Gy to the metastatic lymph node.

After 29 days of conventional treatment, a new 5-point mask, a new CT scan without contrast, and an MR scan with gadolinium intravenous contrast were performed in the planned stereotactic boost process.

A 3 mm margin was added to the GTVboost to create a PTVboost volume of 3.1 cm3.

A new treatment plan consisting of four arcs was prepared.

Four 6 MV FFF (flattening filter-free) photon beams with a maximal dose rate of 1400 MU/min were utilized.

The dose that fully covers target volume was selected as the prescribed isodose level.

The minimum dose in the target volume was 100% of the prescribed dose.

The angle range of arcs was adapted to the boost localization and was limited to the right and front sides of the patient.

The boost was delivered two days after the last fraction of conventional radiotherapy with the same linear accelerator.

During radiotherapy, oral mucositis and moist desquamation (grade 3, CTCAE v5.0) were observed in the irradiated area.

Oral mucositis and moist desquamation subsided within three months of follow up.

Staphylococcus aureus and Klebsiella oxytoca were identified from the throat culture in the sixth week of conventional treatment.

Antibiotic therapy consistent with the antibiogram (clindamycin, amoxicillin/clavulanate potassium) was used.

Blood tests showed grade 1 anemia after 24 fractions.

Blood tests showed grade 1 leukopenia after 33 fractions.

Blood tests normalized seven months after treatment.

CT scans and laryngological examinations did not prove locoregional recurrence three, ten, and thirteen months after the end of radiotherapy.

Chest X-ray and abdominal ultrasound did not detect any metastatic changes one year after treatment.

Xerostomia G2 was the only symptom of late toxicity fifteen months after radiotherapy.

At 17 months of follow-up, the patient reported coughing, suffocation, and bloody sputum.

A CT scan revealed infiltration (64 × 65 × 100 mm) in the 3rd segment of the right lung, encompassing the hilum and central part of the mediastinum.

Pathological examination after EUS-FNA proved squamous cell carcinoma with moderate PD-L1 membrane expression (< 50%).

Acknowledgment of the tumor in the chest as lung cancer or metastatic disease due to oral cancer was difficult.

The patient was qualified for palliative radiotherapy to a total dose of 30 Gy in 10 fractions (VMAT technique, single arc, gantry angle 30.0–210.0 deg) for the tumor in the chest.

Systemic treatment was contraindicated in terms of performance status—ECOG 2.

Three months later, multiple metastases in the mediastinum, right lung, spleen, and bones were detected by PET/CT.

The most painful osteolitic lesion in the left ischium and femoral head was irradiated in one fraction to 8 Gy.

Two-dimensional radiotherapy technique, two coaxial opposite beams from AP and PA directions were used.

During adjuvant radiotherapy, a metastatic cervical lymph node was diagnosed based on fine-needle aspiration biopsy.

A stereotactic radiosurgery boost of 1 × 18 Gy was performed two days after the last fraction of conventional radiotherapy.

The early and late tolerance of this treatment were positive.

During the 18-month follow-up, locoregional recurrence was not detected.

The patient died due to secondary malignancy.

The patient is a 43-year-old nonsmoking and nondrinking white male.

The patient had oral cancer on the left side of the tongue.

A biopsy sample taken from the tumor revealed G2 keratinizing squamous cell carcinoma.

Distant metastases were ruled out on chest X-ray and abdominal ultrasound.

Anamnesis proved previous lower extremity deep vein thrombosis.

Doppler ultrasound ruled out active deep vein thrombosis.

The second part of the operation involved reconstruction using an anterolateral thigh flap.

The histopathology report noted perineural invasion of small nerves.

The histopathology report noted a closest margin below 1 mm.

102 budding foci were detected per 10 high-power fields.

Two to four cell-sized nests or single-cell invasion was observed.

A multidisciplinary case conference qualified the patient for postoperative radiochemotherapy.

Five-point head, neck, and shoulder masks were employed for patient immobilization.

In the first stage of treatment, three full arcs were used.

In the second stage, three arcs lateralized to the left side of the neck were used.

In the third stage, two frontal arcs were applied.

The ultrasound revealed a 16 × 9 mm lymph node.

Fine-needle aspiration biopsy was performed, confirming metastasis of the squamous cell carcinoma.

A 3 mm margin was added to the GTVboost to create a PTVboost volume of 3.1 cm3.

A new treatment plan consisting of four arcs was prepared.

The dose that fully covers target volume was selected as the prescribed isodose level.

The minimum dose in the target volume was 100% of the prescribed dose.

Oral mucositis and moist desquamation subsided within three months of follow up.

Blood tests showed grade 1 anemia after 24 fractions.

Blood tests showed grade 1 leukopenia after 33 fractions.

Blood tests normalized seven months after treatment.

Chest X-ray and abdominal ultrasound did not detect any metastatic changes one year after treatment.

Xerostomia G2 was the only symptom of late toxicity fifteen months after radiotherapy.

At 17 months of follow-up, the patient reported coughing, suffocation, and bloody sputum.

Systemic treatment was contraindicated in terms of performance status—ECOG 2.