An 82-year-old male patient with a history of type 2 diabetes mellitus, hypertension, chronic obstructive lung disease, coronary artery disease, coronary artery bypass grafting in 2005, and ischaemic dilated cardiomyopathy with reduced systolic function presented with a picture of congestive heart failure. He had frequent admissions to different hospitals with similar picture and discharges after adjustment of his heart failure medications. The patient had no history of recent coronary events. His mobility had limited him to his home. After starting intravenous diuretics, he improved clinically. A routine transthoracic echocardiography showed dilated left ventricle with global hypokinesia, reduced systolic function of the left ventricle and an estimated ejection fraction of 30%. There was also a dilated left atrium and evidence of moderately severe mitral regurgitation. These parameters were similar to previous echocardiographic findings four months prior. Surprisingly a small endocardial defect in the inferolateral wall (posterior wall) of the left ventricle was observed, followed by a large oval anechoic area measuring 7.5 × 6.0 cm () containing a thrombotic mass surrounding its thin wall (). This picture was suggestive of a large left ventricle pseudoaneurysm with a narrow neck of 5 mm. A colour-flow Doppler on the neck of the left ventricle pseudoaneurysm showed turbulence flow (). The patient underwent a cardiac computed tomography and a computed tomography coronary angiography, which revealed an outpouching sac measuring 7.6 × 5.9 cm with a narrow neck and thrombotic mass adjacent to the wall of the sac and was strongly suggestive of a pseudoaneurysm ( and ). Patent grafts with severe native coronary artery disease were obtained on computed tomography coronary angiography. A surgical approach was considered the most effective way to avoid the dramatic scenario of the progression to spontaneous rupture; however, patient’s age and comorbidity limited the surgical option, and a conservative approach was taken.


An obese 21-year-old male with no other past medical history presented to the emergency
department (ED) with 3 days of cough, fevers, shortness of breath, pleuritic chest pain, and
1 day of light-headedness with near syncope as well as acutely worsened dyspnoea. He denied
contact with sick persons, exertional chest pain, weight loss, night sweats, abdominal pain,
changes in bladder or bowel habits, and recent travel, surgery, or prolonged immobilization.
Upon arrival, he was febrile (38.9°C), tachycardic (121 beats per minute), normotensive
(104/66 mmHg), and hypoxic saturating 82% on room air, however, improved to 100% with
non-rebreather mask at 15 L/min.
Obesity: body mass index (BMI) 37.
This patient’s presentation with chest pain, dyspnoea, and near syncope preceded by cough
and fever in the midst of a global pandemic raised concerns for COVID-19 and
community-acquired pneumonia as well as pneumothorax and pulmonary embolism.
Severe Acute Respiratory Syndrome Coronavirus 2 nasopharyngeal qualitative polymerase chain
reaction (PCR) was positive. electrocardiogram (ECG) demonstrated evidence of right heart
strain as well as S wave in lead I, Q wave and inverted T wave in lead III (S1Q3T3), a
pattern associated with acute PE (). Point of care ultrasound demonstrated right ventricular free wall
hypokinesis with preserved apical contractility (McConnel’s sign), also consistent with PE.
Initial D-Dimer was elevated at 3.71 mcg/mL (Ref. range ≤0.49), troponin-T was elevated at
0.04 ng/mL (Ref. range ≤0.00), and pro-BNP NT was elevated at 4573 pg/mL (Ref. range ≤125).
A computed tomography pulmonary angiogram (CTPA) demonstrated pulmonary emboli involving the
bilateral pulmonary arteries, including the central, segmental, and subsegmental branches.
There was also enlargement of the pulmonary trunk and flattening of the interventricular
septum, with right ventricle to left ventricle ratio of 1.4 to 1 ().
The patient was admitted to the intensive care unit (ICU) on high-flow nasal cannula and
intravenous (IV) unfractionated heparin (UFH) infusion (goal PTT 60–80 s) with stable vital
signs. Twelve hours after initial presentation, the patient became increasingly hypoxic and
persistently hypotensive with systolic blood pressure <90 mmHg. At this point, he was
presumptively diagnosed with massive PE, and urgently underwent CDT of the bilateral
pulmonary arteries utilizing the EKOS™ Endowave Infusion Catheter System (1 mg/h tissue
plasminogen activator (tPA) per side over 6 h). Intravenous heparin infusion was continued
(goal PTT 40–60 s during tPA infusion, 60–80 s post-tPA infusion). Following CDT, the
patient improved clinically and was transferred to the general medicine floor on hospital
Day 3 with minimal supplemental oxygen and plan to discharge with oral anticoagulation.
On hospital Day 4, the patient was initially normotensive with blood pressure 114/64 mmHg
and saturating 99% on 2 L/min of oxygen via nasal cannular when he developed acute
respiratory failure with oxygen saturation of 65% requiring non-re-breather mask and
hypotension with blood pressure 70/30 mmHg. The patient was subsequently intubated and
developed cardiac arrest regaining spontaneous circulation after two rounds of
cardiopulmonary resuscitation and one electrical shock. Vasopressor support was initiated
with norepinephrine, epinephrine, vasopressin, and phenylephrine. Due to persistent
haemodynamic instability, veno-arterial extracorporeal membrane oxygenation was initiated at
bedside. Recurrence of massive PE was suspected, but a repeat CTPA could not be obtained due
to clinical instability. Instead, the patient was taken to the catheterization laboratory
where a pulmonary angiogram demonstrated bilateral pulmonary emboli with interval worsening
of clot burden compared to index CTPA (). Repeat CDT of the bilateral pulmonary arteries was performed (2 mg/h
tPA per side over 6 h) with continuous systemic IV UFH infusion (goal PTT 50–60 s during tPA
infusion, 60–80 s post-tPA infusion).
Over the next 48 h, ventilation parameters improved, and vasopressors were discontinued.
Repeat pulmonary angiography demonstrated significant improvement in the right central
pulmonary embolism, with residual obstruction of the left central pulmonary artery
(). Venous duplex
ultrasound was then performed demonstrating non-occlusive thrombus of the right femoral vein
and right popliteal vein. An inferior vena cava filter was placed, and the patient’s
anticoagulation regimen was transitioned from UFH to low-molecular-weight heparin (LMWH)
(Enoxaparin, 1 mg/kg every 12 h) due to concern for failure of anticoagulation.
Hypercoagulable workup consisting of Beta-2 Glycoprotein, Cardiolipin, and Phospholipid
Antibodies as well as Prothrombin A and Factor V Leiden gene mutations was unremarkable. The
patient was successfully weaned from ECMO on hospital Day 10 and extubated on hospital Day
31.
The remainder of the hospital course was notable for septic shock treated with broad
spectrum antibiotics and development of a right thigh haematoma and compartment syndrome
requiring surgical debridement on hospital Day 40. Postoperatively, the patient was
transitioned to rivaroxaban 15 mg twice daily for 21 days and 20 mg once daily thereafter.
On hospital Day 52, the patient was discharged to an acute rehabilitation facility.
The patient returned home 67 days after admission and was able to perform activities of
daily living independently. The patient remained anticoagulated on rivaroxaban 20 mg daily
and had no major adverse events 4 months following discharge.


A 69-year-old man presented to the emergency department with a 1-week history of worsening generalised abdominal pain, abdominal distension and loss of appetite. His clinical examination indicated the presence of ascites associated with generalised mild abdominal tenderness. He was haemodynamically stable with no evidence of systemic infection. There were no features suggestive of peritonism.
This presentation occurred 5 months following a laparoscopic left radical nephrectomy for an 80 mm contrast-enhancing, Bosniak IV left lower pole cystic renal mass. The procedure was performed via a transperitoneal approach, with care taken to avoid spillage by first aspirating the cystic content, which was sent for cytological analysis. Gauze was then used over the ruptured portion of the cyst to further minimise spillage during dissection until the specimen was bagged and delivered through a separate left abdominal incision. The renal bed was then irrigated with distilled water. The patient had an uneventful recovery and was discharged the following day.
Histopathology of the specimen showed a pT2 Nx type 1 pRCC, nuclear grade 2, with the greatest tumour dimension of 80 mm (). Necrotic features were evident. Negative surgical margin was achieved, and all tumours were shown to be confined within the renal capsule without lymphovascular invasion. There was no evidence of rhabdoid or sarcomatoid differentiation. The cytology from the aspirated cystic content showed no evidence of malignancy.
He had no other surgical or malignancy history. His other comorbidities included hypertension, gastro-oesophageal reflux disease, scoliosis and previous occupational asbestos exposure. He was a non-smoker and non-alcohol drinker.


A 51-year-old man presented to our Emergency Department with chest tightness that had been ongoing for 5 hours. The patient had a well-controlled history of hypertension for longer than 1 year by taking amlodipine and metoprolol. His vital signs on admission were a blood pressure of 132/93 mmHg, heart rate of 97 beats/minute, and respiratory rate of 18 breaths/minute. ECG showed 1- to 2-mm upsloping ST-segment depression in the precordial leads, with tall and positive symmetric T waves, loss of precordial R wave progression, and a small ST-segment elevation (0.5 mm) in lead aVR (). However, the troponin I level at presentation was negative. Bedside transthoracic ultrasound showed mild tricuspid and mitral valve regurgitation with an overall left ventricular ejection fraction (LVEF) of 60%. In the next 30 minutes, ongoing ECG monitoring showed a similar static pattern, without evolving to precordial ST-segment elevation. These ECG changes suggested de Winter syndrome, which is a condition associated with acute occlusion of the LAD coronary artery and no ST-segment elevation. Dual antiplatelet therapy with aspirin and a direct-acting P2Y12 receptor inhibitor (clopidogrel) was provided in the Emergency Department. Urgent coronary angiography showed nearly complete occlusion of the proximal LAD coronary artery (), which was then successfully treated with angioplasty and two drug-eluting stents (). After angiography, the cardiac troponin I level rose to a peak of 0.76 ng/mL. One month later, outpatient ECG showed sinus rhythm with mild T wave changes in the anterior wall (). Repeated transthoracic cardiac ultrasound showed that the overall LVEF was improved to 72.3%.


A 4-year-old girl was admitted to the pediatric intensive care unit (PICU) of Peking University First Hospital as an emergency (day 1) with intermittent fever, convulsions, and abnormal mental behavior over 15 d of evolution.
Fever (In China, fever is diagnosed when a body temperature is ≥ 37.3 °C) occurred 15 d ago with the highest body temperature of 37.5 °C and without obvious inducement. The symptoms were accompanied by headache. The girl developed convulsions 10 d after the initial symptom onset, lasting a few seconds to 3 min with spontaneous remission occurring 2-3 times a day. Her parents sent her to a local hospital for treatment first. Routine blood tests were normal, and the serum immunoglobulin M antibodies against coxsackie virus and adenovirus were positive. Electroencephalogram (EEG) indicated a small number of low-medium amplitude spikes in the left parietal and central regions and midline during the sleep period. Brain magnetic resonance imaging (MRI) was performed without obvious pathological findings. The patient was diagnosed with viral encephalitis and treated with antiviral drugs at the local hospital. During admission, the condition of the patient worsened on day 13 of symptom onset with intermittent psychiatric symptoms and behavioral changes, including agitation, pressured speech, and dyskinesias of the arms and legs. Thereafter, her parents took her to the outpatient department of pediatrics at our hospital, and she was admitted to the PICU as an emergency.
The patient had a free previous medical history.
There was no special personal or family history.
After admission, physical and neurological examinations were unremarkable except for a slightly higher temperature at 37.5 °C.
Routine laboratory tests were unremarkable. Tumor markers and autoimmune profiles were within normal limits. Blood and urine cultures revealed no findings of bacteria or other microorganisms. The detection of thyroid function was also normal.
Brain MRI was performed without obvious pathological findings. Brain MRI was re-examined on day 9 and demonstrated small flaps of T2 fluid-attenuated inversion recovery hyperintensity in the right frontal lobe. On day 12, abdominal-pelvic ultrasound revealed a 3.4 cm × 3.1 cm × 2.8 cm cystic tumor in the left adnexal region, suggesting ovarian teratoma.


A 33-year-old Chinese female patient (G1P1) was admitted to our hospital for abdominal discomfort, pelvic pain, and palpable abdominal masses in January 2018.
The patient felt intermittent abdominal discomfort 8 mo ago. At that time, there were no other discomforts including abdominal pain or bloating, so she did not pay much attention. However, in the past 4 mo, she felt pelvic pain and touched a lower abdominal mass. The size of the mass slowly increased, and the symptoms of abdominal discomfort and pelvic pain became more and more serious.
The past medical history was notable for four surgeries because of UL without morcellation from 2007 to 2015. The details are summarized in Table .
The patient denied any family history of UL or LPD and previous oral contraceptive (OC) use.
On abdominal examination, an 8 cm × 8 cm fist-sized palpable right lower-quadrant near midline anterior abdomen mass was observed. There was no tenderness or rebound tenderness.
Laboratory testing including tumor markers, sex hormones, and other tests yielded normal results. The pathology of the core-needle biopsy showed a spindle-shaped smooth-muscle cell tumor with features of leiomyoma without necrosis and atypia. Immunohistochemistry staining was positive for Caldesmon, smooth-muscle actin (SMA), Desmin, estrogen receptors (ERs), and progesterone receptors (PRs) but negative for SOX-10, and CD117 (Figure ), and the Ki-67 index was 5%.
Whole exon sequencing of 120 cancer-related genes by next-generation sequencing for determining the possibility of malignant transformation was also performed. However, no germline variants were found.
Computed tomography confirmed multiple nodules involving the abdominal wall and pelvic cavity ranging from 3-7 cm in diameter, in which the largest nodule was approximately 78 mm × 66 mm × 40 mm. No distant metastasis or intravenous proliferation was found (Figures , and ).
Caldesmon, SMA, and Desmin are three markers characteristically found in smooth muscle cells, which can distinguish UL or leiomyosarcoma. SOX-10 expression can be found in myoepithelial neoplasms. CD117 is typically positive in gastrointestinal stromal tumors (GIST). These markers helped eliminate potential differential diagnoses and determine the diagnosis of leiomyomatosis. No distant metastasis or intravenous proliferation excluded the diagnosis of BML and IVL.


A 30-year-old primigravida who was a diagnosed case of severe aortic stenosis presented at term for lower segment cesarean section (LSCS). Invasive monitoring (invasive blood pressure, central venous pressure) was planned for the patient anticipating heart failure intraoperatively or postoperatively. Induction was done with injection etomidate and fentanyl, and trachea was intubated in a single attempt with rocuronium. She was extubated in a deep plane and shifted to ICU for monitoring.


A 35-year-old primigravida at 35 weeks gestation COVID-19 positive presented to our tertiary care health center for safe confinement. She was a known case of sickle cell disease who presented in vaso-occlusive crisis for the last 10 days, with overlapping features of COVID-19 infection. She was planned for emergency LSCS under regional anesthesia. Combined spinal epidural anesthesia with epidural catheter in situ (Epidural Anesthesia Set, imported by B. Braun Medical [India] Pvt. Ltd, Spinocan, imported by B. Braun Medical [India] Pvt. Ltd.) was the technique of choice in view of normal arterial blood gas analysis, but deranged liver function tests (serum bilirubin - 7.2), and increased D-dimer (4.63) []. Intraoperatively, Grade-2 placenta previa was managed conservatively with blood transfusion and drugs. The patient was shifted to postoperative ICU for further management. Postoperative pain was managed with local anesthetics and opioids through epidural catheter. All further management was continued with antibiotics, antivirals, anticoagulants, and steroids as per the COVID-19 protocol and was then discharged uneventfully after 10 days of surgery.


A 39-year-old female presented to the hospital with preterm contractions at 32 weeks. She had a previous history of LSCS and was a diagnosed case of gestational hypertension, controlled on oral antihypertensives. As blood pressure was 180/110 mm of Hg, she was started on loading dose of magnesium sulfate which had to be stopped due to oliguria. Her investigations revealed severe preeclampsia in hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome. Cardiotocography showed fetal distress, so the decision to terminate the pregnancy through LSCS was taken. As her platelet count was 30,000, 4 units of random donor plasma was transfused and 2 units of fresh whole blood was cross-matched for surgery. On examination, she had tachycardia (heart rate - 138/min), and her blood pressure was 180/110 mm of Hg which was controlled with 1 mg metoprolol intravenous. SpO2 on room air showed 89% which improved to 100% with 8 l/minute of oxygen with face mask. She complained of orthopnea and had productive cough. She also had anasarca with facial puffiness and bilateral petechial hemorrhages on the shin. Airway examination revealed anticipated difficult airway as she was morbidly obese and had a short neck, with Modified Mallampatti Grade-IV, large breasts. Hence, a plan of endotracheal intubation using videolaryngoscope and controlled ventilation was done. Ramp position had to be made to facilitate intubation and ventilation. The baby after delivery had poor APGAR but responded well to resuscitation. There was an episode of postpartum hemorrhage which was managed by uterine massage. The patient was shifted to ICU for elective ventilation and was extubated the next day after adequate surgical hemostasis.


A 29-year-old morbidly obese hypothyroid, primigravida at 36 weeks of gestation was tested COVID positive and was admitted to hospital for safe confinement. She had twin pregnancy after in vitro fertilization conception presented with breech and was planned for elective surgery under regional anesthesia (subarachnoid block). All her investigations were under normal reference values except deranged liver function tests, D-dimer, and C-reactive protein (CRP) levels (D-dimer - 6.2, CRP - 6.18). Difficulty in regional anesthesia was encountered due to reduced interspinous spaces, but preoperative ultrasonogram assessment was done to locate space, and paramedian approach was used to advocate the block. Intraoperatively, the case was uneventful except for atonic hemorrhage which was managed conservatively. The patient remained positive for the infection for a total duration of 35 days which had a bad perinatal outcome and one loss of the neonate occurred.


A 30-year-old female at gestation age of 37 weeks, being COVID positive, was admitted to ICU with a history of fever, respiratory illness, and ground-glass infiltrates on chest X-ray, with altered liver enzymes, deranged renal function tests, raised D-dimer levels, and altered mental sensorium, was on ventilator support and invasive monitoring, and was posted for emergency LSCS to save the baby. The baby survived but mother succumbed on the 2nd postoperative day [].


A 26-year-old, G4P2L1A1 female presented at 24 weeks' gestation with a positive indirect antiglobulin test reported from an outside laboratory. The patient's transfusion history revealed a red blood cell transfusion during her first pregnancy. The husband's and first child's blood group was B Positive. Patient's blood group showed an ABO discrepancy. Forward group was B Negative while reverse group showed unexpected reaction with reagent pooled B cells and pooled O cells. The antibody screen showed a positive reaction with Cell 1 (R1R1) and Cell 2 (R2R2) and a negative reaction with Cell 3 (rr) of antibody screening panel (Surgiscreen, Ortho Clinical Diagnostics, Raritan, NJ, USA). Antibody identification panel (Resolve Panel A, Ortho Clinical Diagnostics, Raritan, NJ, USA) gave a pattern which aroused high suspicion for multiple alloantibodies.
For ruling out/ruling in antibodies, select cells from a second panel (Resolve Panel B, Ortho Clinical Diagnostics, Raritan, NJ, USA) were identified. Three alloantibodies, namely anti-D, anti-C, and Anti-E were suspected. While the patient tested negative for all three antigens, father and first child tested positive for only two; D and C, questioning the source of immunization of E antigen. Anti-E could have been formed after the transfusion episode during her first pregnancy but this could not be established as extended phenotype of the transfused unit was not available at the time of work-up. Since the presence of anti-E in the patient's plasma was not supported by the father's or child's phenotype and the possibility of anti-G could not be excluded, differential adsorption was planned.
The department was conducting a study to gain knowledge about the prevalence of 18 clinically significant blood groups antigens. Coincidently, at the time this patient presented, the department had recently been visited by a very rare donor with D - - phenotype. With the help of the pilot samples, sequential adsorption and elution studies were proposed []. shows sequential adsorption and elution studies to check for the presence of anti-G along with other Rh alloantibodies. An alternative approach to identify specificities of these antibodies without use of D - - red cells is suggested in . The presence of anti-G was ruled out and presence of anti-D, anti-C, and anti-E were confirmed. Serial doubling dilution titration by conventional tube technique was performed with r'r (dCce) adsorbed patient plasma and R1R1 red cells for anti-D, R2R2 (DcE) adsorbed plasma and R1R1 (DCe) red cells for anti-C and R1R1 adsorbed plasma from and R2R2 red cells for anti-E. Titration revealed anti-D titer to be 1024, anti-C to be 4, and anti-E to be 32. In view of multiple antibodies, Doppler ultrasound was done which revealed middle cerebral artery peak systolic velocity >41.9 cm/s, i.e., >1.5 standard deviation above the normal mean for gestation suggesting fetal anemia. A request for 30 ml red cells was received. Group “O” RhD negative, fresh red cells (within 5 days of collection), negative for C, E, and K antigens, hematocrit 75%–85%, leukoreduced, crossmatch compatible with maternal plasma, sickle negative, and irradiated were transfused.
A total of eight intrauterine transfusions were performed till induction of labor. Each time a request was received, antibody screening and antibody titration were performed and an aliquot of patient's plasma was preserved. No RhD prophylaxis was given to the mother. The neonate developed pathological jaundice after birth which required phototherapy mainly and exchange transfusion once. The unit prepared for exchange transfusion involved reconstituting red cells without additive solution and fresh frozen plasma to a hematocrit of 45%–55%. The red cell unit selected was group “O” RhD negative, fresh, negative for C, E, and K antigens, anti-human globulin phase crossmatch compatible with both the neonate and the patient, sickle negative, leukoreduced, and irradiated. The neonate was able to recover from hyperbilirubinemia and was discharged from the hospital at day 42 of birth. The infant continues to do well.


A 39-year-old female kidney transplant recipient was admitted to our hospital in September 2018 (Fig. ) due to general malaise, weight loss, fevers up to 38.5°C, diarrhea, and moderate anemia in follow-up laboratory tests. Her primary renal disease was lupus nephritis with kidney involvement resulting in end-stage renal disease. For this reason, she was on hemodialysis for 3 years while being prepared for the transplantation. The patient received a renal graft from a deceased donor in March 2016. A kidney biopsy was performed in August 2018, and its histopathological examination showed no signs of either transplant rejection or drug toxicity. High antinuclear antibody count (including elevated anti-double-stranded DNA antibody count) and low C3 and C4 complement components suggested SLE as the cause of the graft failure, despite an ongoing triple immunosuppressive treatment. Aside from that, patient's medical history included the very intensive courses of immunosuppresion including cyclophosphamide, mycophenolate mofetil, cyclosporine A and pulses of intravenous steroids. The patient also suffered from cytomegalovirus (CMV) early after transplantation and a recurrent CMV infection in August 2018.
On the admission, the immunosuppressive regimen consisted of mycophenolate sodium, tacrolimus, and prednisone. The patient was also receiving valganciclovir due to the recent CMV infection. The physical examination showed the signs of dehydration and an enlarged single left submandibular node. The routine laboratory tests revealed the signs of pancytopenia (hemoglobin 9.5 g/dL; leukocyte count 1.91 × 103/µL; and platelet count 117 × 103/µL) and renal failure with metabolic acidosis (serum creatinine 462.5 μmol/L; urea 31.9 mmol/L and pH 7.153; and sHCO3− 11.8 mEq/L). Serum C-reactive protein level was within normal range. The abdominal ultrasound was significant only for gallbladder polyps and revealed a single cyst in the upper pole of the transplanted kidney and an accessory spleen. No enlargement of internal organs was seen. The intravenous fluid therapy was promptly started, resulting in a partial improvement of graft function. Since we considered valganciclovir as a potential cause of pancytopenia, CMV-DNA laboratory test was carried out and upon receiving a negative result the drug was discontinued. One unit of leukoreduced and irradiated blood was transfused, and the patient received a single dose of an erythropoiesis-stimulating agent and 2 doses of granulocyte colony-stimulating factor (G-CSF). Despite all this, no significant improvement of blood count was observed (Fig. ). Among numerous other laboratory tests performed 3 were especially worthy of attention, that is, increased activity of lactate dehydrogenase (LDH) (341 U/L), elevated triglycerides (2.35 mmol/L), and highly increased serum ferritin (>2,000 ng/mL). The patient was then transferred to the Hematology Clinic, where she had a bone marrow aspiration performed. The histopathological examination of the bone marrow specimen revealed an intensive hemophagocytosis which alongside the aforementioned laboratory and clinical findings raised a suspicion of sHLH.
After the patient returned to our nephrology ward in October 2018, the possible treatment plans were discussed. Etoposide therapy was considered inordinately toxic given the presence of graft failure and hypoalbuminemia (25 g/L). The immunosuppressive regimen was modified, and tacrolimus was converted to everolimus and oral prednisone to an intravenous dexamethasone. Based on the available literature, plasma exchange (PE) therapy was initiated. In total, 4 PEs were performed, resulting in a remarkable improvement of blood count parameters (Fig. ) and the patient's general condition.
In search for a potential cause of sHLH CMV-DNA and Epstein Barr Virus DNA (EBV-DNA), tests were performed. The results of both tests were positive with 1.25 × 103 copies/mL EBV-DNA and CMV-DNA detectable levels but too low to estimate the viral load. Hence, intravenous ganciclovir was started. The patient was referred to a rheumatologist who suggested a possible SLE exacerbation based on newly presented oral ulcers, right wrist pain, bilateral Reynaud's phenomenon, and previously described signs of renal failure present in laboratory tests. Gastrointestinal malignancies were ruled out after negative results of colonoscopy and gastroscopy. Lastly, a chest radiograph was taken, revealing a single cavitary lesion in the right lung which was not present in the previous radiograph (Fig. ). Following that, a computed tomography was performed and precise measurements were taken (Fig. ). According to the radiologist, the observed lesion presented no active inflammation and it was most likely post-inflammatory, although it could also be caused by tuberculosis. At the moment sustained therapy with reduced doses of immunosuppressants and follow-up of the lesion progression was deemed the reasonable approach. The patient was discharged from the hospital with frequent follow-up visits at our outpatient clinic.
In January 2019, a significant enlargement of the lung lesion was noticed in a chest radiograph (Fig. ). At this point, a preemptive therapy for the mycobacterium tuberculosis would be useful for the diagnosis; however, it was not administered. Instead, the patient was referred to a pulmonologist, who raised a suspicion of the fungal pulmonary infection. A bronchofiberoscopy was performed, which did not reveal any macroscopic changes. The samples for bacterial and fungal cultures, BK-virus test, Mycobacterium tuberculosis culture, and PCR-DNA were taken. At the same time, blood galactomannan level was also assessed. All these test results came negative. The patient was also referred to a thoracic surgeon who advised an active monitoring of the lesion with no immediate indication for its surgical removal. In the following months, chest radiographs and CT scans showed a slow increase of the size of the cavitary lesion with the thickening of its wall (Fig. ).
At the same time, the patient suffered from a prolonged course of sHLH. High levels of ferritin, that is, 2,761 ng/mL in January 2019; 1,149 ng/mL in June 2019; and 1,946 ng/mL in August 2019, and cytopenia affecting from 1 to 3 cell lines were observed during subsequent hospitalizations. The patient had additional courses of PE performed from November 2018 to June 2019–17 in total. Moreover, 2 courses of intravenous immunoglobulin (IVIG) therapy were necessary to maintain disease control. Due to high serum creatinine and urea levels in follow-up laboratory tests, the patient had a second graft biopsy performed in August 2019. The histopathological examination revealed the signs of tubulointerstitial graft rejection and coexisting thrombotic microangiopathy.
In September 2019, a further progression and consolidation in lung CT within the cavity wall was observed; therefore, the patient was referred to a pulmonary disease center. There, a second bronchofiberoscopy was performed which included bronchoalveolar lavage and carinal forceps biopsy. Since changes of the lesion observed in CT were highly suspicious for pulmonary fungal infection, the patient was started on voriconazole. Another set of samples for bacterial, fungal, and Mycobacterium tuberculosis cultures was taken. Cytological examination of the lavage fluid revealed increased amount of neutrophils (11.3% of all counted leukocytes, with normal range <3%); distribution of the other leukocyte populations, including macrophages, was normal; however, the histopathologist observed signs of activation and phagocytosis in some of the macrophages; additionally, numerous erythrocytes, sparse bacteria, and sparse fungi hyphae were described in the sample. Examination of the specimen from the carinal biopsy showed active inflammation within the mucosa with no fungi hyphae. Bacterial cultures were positive for Escherichia coli and Streptococcus mitis, cultures for Mycobacterium tuberculosis and fungi were once again negative. Antibiotic therapy was administered according to the antibiotic susceptibility testing results.
She was initially qualified to thoracic surgery, but due to severe flu, zoster, and graft failure, the procedure has been postponed. As the graft function gradually worsened, the patient returned to hemodialysis in April 2020.


An 11-year-old boy was seen as an emergency in our clinic, complaining of severe photophobia and right eye pain. He reported having been spat at in his right eye by a beetle when he was holding it between his fingers and trying to place it inside an anthill. He had been seen previously on the same day at the casualty department of the local hospital, where he was diagnosed with corneal erosion and burn affecting the upper and lower eyelids of the right eye and treated with topical antibiotics and steroids.
The patient was healthy, with no allergies and taking no medication. He was treated for purulent conjunctivitis when aged 6 months. Ocular examination was very difficult as he was severely photophobic and in significant pain. His unaided visual acuity was 0.1 in the right eye and 1 in the left eye. Slit-lamp examination of the right eye revealed swollen upper and lower eyelids with localized skin erythema (Fig. ), marked mixed conjunctival hyperemia, and an erosion affecting the lower half of the cornea (Fig. ). There was no activity in the anterior chamber. Steroids were stopped and tobramycin ointment 0.3% (Tobrex Ointment®; Novartis Pharmaceutical) maintained (3 times a day to the conjunctival sac and to the eyelids).
When seen 3 days later, his unaided visual acuity in the right eye was 0.8. The corneal epithelium was closed, leaving only mild pooling of fluorescein and a scab in the area of the eyelid burn. Twice daily fluorometholone 0.1 (FML®; Allergan Ltd.) eyedrops were added to the treatment.
After 7 days of treatment, his condition had completely resolved. The corneal epithelium was intact, and there was no pooling of fluorescein. Both the upper and the lower eyelids affected by the burning were slightly pigmented (Fig. ). The patient was discharged with the recommendation to taper the treatment.


A 42-year-old obese woman presented to her optometrist after she noticed “after images” following bright light exposure in her left eye (OS). She also noticed transient blurred vision with position changes but denied any regular headaches or pulsatile tinnitus. She denied ever having a severe onset headache. She was referred to neuro-ophthalmology and was found to have a visual acuity of 20/20 in both eyes. Humphrey 24-2 SITA-Fast visual fields showed nonspecific depressed points right eye (OD; MD −6.18 dB) and showed an enlarged blind spot OS (MD −4.84 dB). Dilated fundus examination showed moderate optic disc edema in both eyes with preretinal, intraretinal, and subretinal hemorrhages around the left optic disc (shown in Fig. ). Her blood pressure measured 140/100 and her hemoglobin was normal. Magnetic resonance imaging/magnetic resonance venography was performed and showed signs of raised ICP without a secondary cause. Lumbar puncture showed an opening pressure of 32 cm of water and normal cerebrospinal fluid (CSF) contents. She was started on acetazolamide 500 mg twice-daily (BID) and telmisartan 40 mg daily and the optic disc edema improved and resolved after 4 months with significant weight loss. She maintained normal visual function and the ODH resolved at 3 months. The final Humphrey mean deviation was −3.42 dB OD and −2.98 dB OS.


A 44-year-old obese woman with a medical history of iron-deficiency anemia (pretreatment hemoglobin of 8.8 g/dL) presented with blurred vision in her right eye and new headaches over 1 month. She described the headaches as holocephalic, rated them 4–5 out of 10 (where 1 is minimal intensity and 10 is maximal intensity) without any diurnal or positional variation. She had associated intermittent nausea, but no vomiting. She denied any characteristics consistent with a thunderclap headache. She initially saw her optometrist and was referred to neuro-ophthalmology for bilateral optic disc edema. Examination revealed a visual acuity of 20/30 OD and 20/20 OS, and Humphrey visual field testing showed an enlarged blind spot OD (MD −4.60 dB) and was normal OS (MD −2.10 dB). Slit-lamp examination revealed a posterior subcapsular cataract in the OD and dilated fundus examination showed moderate optic disc edema in both eyes with hemorrhages in all 3 retinal layers in the OD (shown in Fig. ). Her blood pressure was 128/78, and her hemoglobin was found to be 9.0 g/dL with mean corpuscular volume of 70.4 fL. Magnetic resonance imaging/magnetic resonance venography of the head was normal apart from signs of raised ICP, and lumbar puncture showed an opening pressure of 34 cm of water with normal CSF contents. She was started on acetazolamide 500 mg BID and continued her recent supplementation with ferrous fumarate. With significant weight loss, her optic disc edema resolved after 4 months, and she continued to maintain normal visual function. The final Humphrey mean deviation was −2.80 dB OD and −0.72 dB OS.


It is a case of a 66-year-old Palestinian male patient, a heavy smoker with multiple comorbidities including hypertension, Type 2 diabetes mellitus, and renal impairment. He was presented with a 2 months history of progressively increasing neck swelling and left ear pain associated with hearing loss and difficulty speaking that worsened the last 3 days before admission. The patient has a previous history of stroke with sequelae of left-sided weakness.
The patient appeared pale with ecchymosis patches over both arms. Clinical examination was significant for multiple enlarged submental, submandibular, periauricular lymph nodes (LNs) described as fixed, firm, and not tender with no overlying skin redness. No hepatosplenomegaly appreciated. No focal neurological deficit apart from sensorineural hearing loss. Complete blood count revealed marked leukocytosis with white blood cell count (WBC) 66 × 103/μL (4–10), moderate macrocytic anemia with hemoglobin 9.0 g/dL (13–17), and mild thrombocytopenia with platelets 138 × 103/μL (150–400).
Peripheral blood (PB) smear showed moderate macrocytic anemia with some NRBCs. There was marked leukocytosis with (24%) blasts. Some were medium to large with abundant cytoplasm, irregular/convoluted nuclear borders, fine chromatin, prominent one or more nucleoli, and a few with cytoplasmic granules. Others appeared smaller with a very high N/C ratio and inconspicuous nucleoli. There was a marked shift to the left, different stages of maturation seen with basophilia. Monocytic cells were markedly increased and including some immature forms (promonocytes). Platelets were mildly reduced in number (Fig. ). The differential count segmented neutrophils (15%), lymphocytes (7%), eosinophils (1%), basophils (2%), promyelocytes (2%), myelocytes (7%), metamyelocytes (3%), monocytes and promonocytes (39%), and blasts (24%).
Bone marrow (BM) examination was done. The aspirate was infiltrated with 22% blasts with preserved trilineage hematopoietic cells. The blasts have the same morphology as that of the PB with pseudopods, fine azurophilic granules, and or vacuoles. The monocytic component was significantly increased (26%). Granulopoiesis was hyperplastic, left-shifted, in different maturational stages with an increased M/E ratio (7.3), and relatively reduced erythropoiesis (Fig. ). No significant dysplasia was noted. The trephine BM biopsy was mildly hypercellular for age (60–70%) and showed infiltration with many primitive cells with active granulopoiesis, increased eosinophils, markedly increased monocytic cells, decreased erythropoiesis, and preserved megakaryocytes (Fig. ).
Immunohistochemical stains showed increased positivity for CD34, CD1a, TdT, and CD10. There was diffuse strong positivity for CD99 and lysozyme. CD163 and CD68 highlighted increased monocytic cells (Fig. ).
Flowcytometry analysis performed on BM aspirate showed an abnormal population of blasts expressing cytoplasmic CD3 (20%) and including 2 subpopulations: one population with dim CD45 (9%) and expressing CD34, CD7, CD5, CD33, and CD11b with aberrant partial cCD79 and negative for CD1a and another population with moderate CD45 (11%) and expressing cytoplasmic CD3, CD7, CD5, aberrant partial CD11b, and partial CD1a. These cells were negative for CD34, CD33, and cCD79a.
Both populations were negative for cMPO, CD117, CD13, CD15, CD64, CD14, HLADR, CD11c, CD36, GP, CD41, CD61, sCD3, CD2, CD4, CD8, TCR alpha/beta, TCR gamma/delta, CD19, CD20, CD10, CD56, and TdT. There was increase in the monocytic cells (28%) expressing (CD64 and CD14) (Fig. ).
The fluorescence in situ hybridization (FISH) analysis was performed on interphase nuclei obtained from a BM sample. The analysis revealed dual fusion hybridization signal pattern for BCR and ABL1 probes on chromosomes 9 and 22, indicated t(9:22) in 92%, which resulted in Ph+. Further, the iFISH analysis was performed using BCR/ABL1 dual fusion extra signal probe to discriminate between major and minor breakpoints (m-bcr). The analysis revealed a m-bcr associated with the p190 transcript (Fig. ).
Cytogenetic analysis revealed abnormal complex Karyotype: 46, XY, t(9;22) (q34;q11.2) [29]/46, idem, add (10) (q24) [11]/46, idem, der(7) t(7;10) (q32;q22) [3]/46, and idem, add (16) (q?22) [2]. The G-banding chromosome analysis of 45 metaphase cells from the BM sample revealed an abnormal karyotype with 4 subclones. The main clone was with a reciprocal translocation between chromosome 9 at band q34 and chromosome 22 at band q11.2, which result was Ph+. Each of the subclones had additional nonrecurrent structural abnormalities involving chromosomes 7, 10, and 16.
PB and BM findings were consistent with T-ALL/LBL with t(9;22); BCR-ABL1 (Ph+) However, the possibility of T-cell LBL/lymphoma blast phase of CML could not be ruled out as was suggested from morphology. The patient's neurological complaints raised suspicion for CNS involvement, but lumbar puncture was not feasible with such a poor patient's performance. CT Head showed no recent infarction or hemorrhage. MRI head and posterior fossa without contrast did not reveal any obvious sizable brain lesion or cerebellopontine angle mass.
Positron emission tomography showed mild-to-moderate fluorodeoxyglucose avid uptake present in multiple bilateral para jugular, jugulodigastric, posterior triangular, submental, and bilateral axillary LNs. Bilateral pleural fluid was noted. An irregular ground-glass opacity in the right upper lobe and in the apical segment of the lung with minimal uptake that might represent lung involvement. The liver and spleen were unremarkable with no obvious adenopathy in the abdomen or pelvis. The initial plan of the leukemia MDT meeting was to start the patient on GMALL chemotherapy protocol (adopted from German Multicenter Study Group for Adult ALL).
The patient was started on tumor lysis measures, imatinib, and steroids. He could not tolerate the chemotherapy (one dose of idarubicin, vincristine, and cyclophosphamide), therefore, given the patient's age, comorbidities, and overall poor prognosis of Ph+ T-ALL, he was considered not fit for aggressive chemotherapy and the best available treatment option for him would be TKIs, steroids +/− vincristine, along with antimicrobial prophylaxis.
He was started on Imatinib 600 mg daily but could not tolerate that dose due to fluid retention. Imatinib dose was reduced several times according to tolerance, which barely controlled his disease for few months.
Four months later, he attained complete hematological remission (CHR) but not molecular remission. BCR-ABL1 e1a2 rearrangement resulting in a p190 protein, the fusion transcript type commonly associated with de novo ALL, was detected in the blood (Fig. ).
Two months later, he presented with high WBCs 36 × 103/μL. Flowcytometry analysis performed on the PB showed 32% blasts expressing cytoplasmic CD3 and including two subpopulations: one subpopulation with dim CD45 (9%) expressing CD34, cytoplasmic CD3, CD7, CD33, partial dim CD5, with aberrant cCD79a and negative for CD1a and another subpopulation with slightly brighter CD45 (23%) expressing cytoplasmic CD3, CD7, partial dim CD5, with partial aberrant cCD79a and partial CD1a and negative for CD34 and CD33. There were increased monocytic cells (20%) expressing (CD64 and CD14) which proved relapse by morphology and flow cytometry.
The case was discussed in the hematology department. The agreement was to shift to dasatinib along with steroids, with close follow-up. He was started on dasatinib 50 mg daily then increased to 100 and 140 mg daily once tolerated.
The patient was kept on dasatinib and again attained CHR. Unfortunately, he could not tolerate that TKI as well when developed a refractory cough and bilateral chest crepitations upon auscultation. ECHO showed pulmonary hypertension; RVSP of 44 mm Hg and high-resolution. CT chest showed bilateral subpleural ground-glass attenuation areas associated with interstitial thickening and reticular infiltration. Dasatinib was then changed to nilotinib 300 mg BID which was well tolerated for 2 months. The patient was kept in CHR. The patient developed QT prolongation so nilotinib was held for 2 weeks.
After another 5 months, the patient presented to the emergency with a history of sudden painless left monocular visual loss, associated with a fluctuation of the level of consciousness and irritability. MRI head displayed a subtle enhancing area in the pons associated with areas of meningeal thickening and enhancement, raising the possibility of leukemic involvement. MRI whole spine with contrast revealed subtle areas of meningeal thickening and enhancement in the cervical, dorsal, and lumbar regions raising the suspicion of meningeal leukemic deposits.
The patient had clinical and radiological CNS leukemic involvement despite maintained CHR. He was not fit for any kind of aggressive treatment, a family meeting was held, and agreed to keep the patient on best supportive care. He was shifted under palliative team and rendered Do Not Resuscitate (DNAR code), shortly after expired.


A 27 year old previously healthy male was referred to a hospital with a two-week history of vomiting, high-grade fever, and abdominal pain, which was diagnosed as appendicitis. On admission to the referral facility, he was diagnosed with a new presentation of type 1 diabetes mellitus. Postappendectomy, he was referred to our facility for further management. On arrival, he was semi-conscious, barely responsive to pain, and had labored breathing. He also had electrolyte imbalance with severe hypokalemia of 1.6 mmol/L and an elevated random blood glucose level.
Physical examination revealed a well-nourished albeit severely dehydrated male weighing about 53kg. He was febrile and had Kussmaul breathing. His vitals were as follows: BP = 151/69 mm Hg, HR = 132 beats per minute, RR = 32 breaths per minute, SPO2 = 96% on room air, temperature =38.9℃, and random blood glucose =16.6 mmol/L. A bedside ultrasound revealed a collapsed inferior vena cava (IVC). His initial point-of-care venous blood gas showed metabolic acidosis (pH =7.20, PCO2 = 21.5 mmHg, HCO3 = 10.1 mmol/L) with severe hypokalemia of 2.2 mmol/L (3.5–5.0 mmol/L), hypernatremia of 167 mmol/L (135–145 mmol/L), and hyperchloremia of 125 mmol/L (98–109 mmol/L). Serial venous blood gases and electrolytes were performed every 3 to 6 hours (Table ). Urine analysis was unremarkable including the absence of urinary ketones.
Central venous access was obtained in the right subclavian vein, and a 4-L bolus of Ringers lactate was administered followed by a free water deficit maintenance using 5% dextrose water admixed with potassium chloride (KCl) 40 – 80 mmol which ran at 125 ml/h (KCl rate of 10 – 20 mmol/h). Simultaneously, a fast-acting insulin infusion at 0.05 U/kg/h (2.5 U/h) was also administered. Post-operative broad-spectrum parenteral antibiotics were initiated, and the patient was admitted to the ICU.
After 24 hours of admission, we noted the patient had a urinary output of 9 L of dilute urine with a negative fluid balance of 3 L. His serum potassium was persistently low despite receiving a continuous KCl infusion for over 24 hours. At this point, his serum potassium level was 1.94 mmol/L. Serum magnesium levels were ordered to rule out probable cause of refractory hypokalemia, which revealed hypomagnesemia of 0.50 mmol/L (0.66 −1.25 mmol/L). All other blood investigations including brain and abdominal CT scan were unremarkable except for the ECG which showed diffuse U-wave morphology (Figure ) correlating with hypokalemia and/or hypomagnesemia. Urinary specific gravity was found to be low with a value of 1.005. Plasma levels of antidiuretic hormone (ADH) and urine osmolality were not available at our center.
Based on these findings, a diagnosis of nephrogenic diabetes insipidus (NDI) was made secondary to hypomagnesemia induced severe hypokalemia. The treatment was modified by the addition of 4g of magnesium sulfate along with 40 mmol of KCl in 5% dextrose water (500 ml bottle) which ran at a rate of 125 ml/h, along with the same insulin rate of 0.05 U/kg/h (2.5 U/h). This treatment plan continued for 48 hours until his electrolytes normalized. In addition, oral bendroflumethiazide 5 mg twice a day, indomethacin 50 mg thrice a day, eplerenone 25 mg twice a day, and magnesium trisilicate 250 mg thrice a day were added to his treatment.
Improvement in potassium and magnesium levels were seen on the 3rd day postadmission with significant ECG improvement with the disappearance of U waves (Figure ). A decrease in the exaggerated amount of urine output was also observed with an improvement in the patient's hydration status. On the 8th day in the ICU, the patient had significant clinical improvement with normal serum electrolytes and an adequate positive fluid balance (input of 3.5 L and output of 2.9 L in 24 h). Thereafter, he was transferred from the ICU to the general ward to continue with the management and follow-up. Further follow-up as an outpatient postdischarge has yielded normal electrolyte results.


A 52-year-old male had no obvious inducement of epigastric pain for >3 months presenting persistent stabbing pain, accompanied by back pressure, fatigue, loss of appetite and hiccup. He went to a local hospital for treatment because of aggravated abdominal pain. Gastroscopy showed: (i) gastric polyps and (ii) chronic atrophic gastritis. The symptoms were not relieved after oral medication. Two weeks later he had jaundice with clay-like stool, so he went to the local hospital and underwent a color Doppler ultrasound examination. The results showed that: (i) visceral inversion; (ii) solid space-occupying at the head of the pancreas; (iii) dilated inner diameter of the intrahepatic and extrahepatic bile ducts and main pancreatic duct; (iv) fatty liver and (v) enlarged gallbladder volume and wall rough. The patient was admitted to our hospital complaining of ‘epigastric pain >3 months ago, jaundice with clay-like stool for 1 week’. The patient had no significant medical, surgical or drug history. Physical examinations were unremarkable except for a weight loss of ~20 kg since the onset of the disease. Blood and laboratory tests were carried out, and they showed elevated values of liver enzymes, with a clear elevation in the values of Enzyme gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP), as well as tumor markers CA19-9, CEA and CA72-4, which are indicative of the presence of an obstructive lesion (). After preoperative examinations, he was diagnosed with pancreatic cancer. His CT scan () showed: (i) mirror dextrocardia; total visceral inversion; (ii) pancreatic space-occupying lesions; (iii) intrahepatic and extrahepatic bile duct dilation; (iv) intrahepatic calcification and (v) multiple small cysts in the left kidney, and the MRI scan has confirmed the previous results (). A perioperative plan has been made for a LPD. The patient was put under general anesthesia in a supine split–leg position. The laparoscopic instruments were connected (). Diagnostic laparoscopy confirmed a mirror transportation of organs hence confirming SIT, considering the preoperative assessments and intraoperative exploration, a LPD, and intestinal adhesiolysis was performed. Major vessels along with thoracic and abdominal organs were transposed as mirror images of the normal anatomy, a 17-cm paramedian incision in the upper left abdomen was made to accomplish the resection of the organs which includes the distal stomach—the duodenum, the upper segment of the jejunum, the common bile duct and the gallbladder. According to conventional loop reconstruction, the reconstruction of the alimentary tract was performed. Three drainage tubes were placed at the sites of the anastomoses. Although there were anatomical variations, the operation went smoothly. The blood pressure of the patient was stable and the anesthesia effect was satisfactory within 150-ml intraoperative blood loss. The postoperative specimens were sent to the pathological lab. Postoperative fluoroscopy was normal (). The patient had a total hospital stay of 26 days; 15 days postoperative hospital stay, and was discharged without any complications.
Postoperative pathological report () indicated the following:
Tumor site: pancreatic-head.
Pathological stage: T3N0M0.
Tumor size: 7.3 × 6.8 × 3 cm.
Histological type: ductal adenocarcinoma.
Histological grade: grade IIA.
Surgical margin invasion: there is a cancer involvement found into the duodenal wall, no cancer involvement found in the gastric cutting edge, common bile duct stump.
Lymph node involvement: no lymph node involvement.
Nerve invasion is present. However, no vascular invasion was seen.


A 9-year-old female in mixed dentition was reported with a chief complaint of missing upper front tooth. The patient had a convex profile and asymmetric smile. Intraorally, the patient had a class 1 molar relationship bilaterally with crowding in maxillary and mandibular arch (). Three supernumerary teeth between upper right central incisor and upper left lateral incisor teeth had been diagnosed radiographically and surgically removed 5 months earlier. The maxillary left central incisor was impacted and the adjacent teeth had drifted into the unoccupied space. The impacted tooth was tipped mesially with the crown height at the middle third of the adjacent incisor (). The cause of impaction was established as an obstruction to the path of eruption due to supernumerary teeth.
The follow-up radiograph taken 5 months after extraction of supernumerary tooth showed no improvement of the vertical position of the affected incisors, so it was decided to proceed with active orthodontic eruption. A Nance holding appliance and lower lingual arch were placed to maintain space in the arches. The maxillary first premolars and deciduous canines were extracted to relieve crowding and facilitate canine eruption in the maxillary arch. The permanent teeth were bonded in the maxillary arch after the eruption of the canines to align the teeth. An open coil spring was placed post alignment to create space for the impacted incisor. A closed eruption technique was planned as the tooth was apical to the mucogingival junction. Orthodontic vertical traction was applied 1-week post-surgery using an e-chain tied to a modified 0.018 SS wire containing a helix. Over the next 6 months, the progress of incisor eruption was evaluated monthly. Once sufficiently erupted, the crown was bonded with an incisor bracket to align the maxillary arch (). A lower right central incisor was extracted to relieve the crowding in the lower arch. The active treatment took 18 months. At the end of treatment, the upper and lower arches were aligned, there was a class 2 molar relation and class 1 canine relation ().


An 11-year-old male in permanent dentition was reported with a chief complaint of missing upper front teeth. The patient had a convex profile and competent lips. On intraoral examination, the patient had a class 1 molar relationship bilaterally with missing maxillary right central and lateral incisors, retained deciduous canine, mandibular arch crowding, and retroclined maxillary left central and lateral incisors (). Routine panoramic radiograph revealed impacted incisors, unerupted canine, and a supernumerary tooth as well. Cone-beam computed tomography scan done to evaluate the shape and exact position of the supernumerary tooth revealed that it was lying between right central and lateral incisors. Cone-beam computed tomography scan also revealed the presence of dilaceration of impacted central incisor root which was curved distobuccally near the apical third (). The cause of impaction was established as an obstruction to the path of eruption due to supernumerary teeth.
The treatment plan was the removal of deciduous canine, supernumerary tooth, and surgical exposure of impacted incisors and unerupted canine followed by evaluation at a later date for all first premolar extraction depending on the soft tissue profile.
An open coil spring was placed post alignment to create space for the impacted incisor on an 018 round SS wire. An open eruption technique was planned as the tooth was below the mucogingival junction near the alveolar crest along with the extraction of deciduous canine and supernumerary teeth. The impacted incisor and unerupted canine were bonded at the same time as the exposure. Spontaneous eruption of the teeth occurred while space was maintained with an open coil NiTi spring. Over the next 3 months, the progress of incisor eruption was evaluated monthly. Once sufficiently erupted, the crown was bonded with an incisor bracket to align the maxillary arch (). Proximal stripping was done to relieve the crowding in the lower arch. The active treatment took 18 months. At the end of treatment, the upper and lower arches were aligned, there was a class 1 molar and class 1 canine relation ().


A 7-year-old male in mixed dentition was reported with a chief complaint of missing upper front tooth. On intraoral examination, the patient had a class 1 molar relationship with a missing maxillary left central incisor. A bulge could be felt in the palate in the anterior region (). A routine panoramic radiograph revealed an impacted incisor. The lateral cephalogram revealed a dilaceration in the incisor with the crown displaced palatally. The CBCT showed a palatally impacted dilacerated central incisor with root placed labially (). As the patient was in mixed dentition, a 2 × 4 appliance was planned. There was adequate space for the incisor therefore initial alignment followed by surgical exposure was planned. For the surgical protocol, an open surgical procedure was selected because the crown was covered only with palatal mucosa. A vertical loop was fabricated that was pushed back and ligated to the button to aid in the eruption of the tooth (). Once the crown was brought into the oral cavity with traction, a piggyback 0.012 NiTi wire on an 0.018 SS wire was placed. After the alignment of the tooth in the arch, root torque was given in a 17 × 25 TMA wire to bring the root in the proper position. The active treatment took 18 months. At the end of treatment, the upper incisor was well aligned ().


On May 4, 2021, a 9-year-old boy confirmed with COVID-19 was referred to our hospital. . shows the timeline before hospitalization to our hospital. Because his uncle, whom he had contact with at a family reunion, was confirmed with asymptomatic COVID-19, he had been in self-quarantine since 10 days earlier. He had a cough on the seventh day of self-quarantine (nine days after the last exposure) and developed a fever of ≥ 38°C the next evening. He was eventually confirmed with COVID-19 12 days after the last exposure and was hospitalized in a designated hospital. Upon admission to the outside hospital, the initial chest X-ray showed diffuse pneumonic consolidations in both lung fields and chest computer tomography was performed on the same day (). He had a fever of up to 40.5°C, cough, and sputum, but no dyspnea, and his saturation of percutaneous oxygen (SpO2) was maintained at ≥ 95% on room air. However, the next day, his fever and cough became worse, and he complained of respiratory difficulty.
The patient was previously healthy and had no specific medical history other than obesity (body mass index, 27.6, 99.8th percentile; body weight, 62 kg, 99.8th percentile; height, 150 cm, 97.3rd percentile). The initial vital signs at our hospital showed a blood pressure of 124/106 mmHg, pulse rate of 133 beats per minute, respiratory rate of 29 breaths per minute, a body temperature of 38.6°C, and an SpO2 of 95–98% on room air. The initial laboratory results were as follows: white blood cell count 6,760/μL (13.9% lymphocytes), hemoglobin 11.7 g/dL, platelet count 238,000/μL, C-reactive protein 8.29 mg/dL (range, 0–0.5), procalcitonin 0.86 ng/mL (range, 0-0.05), and D-dimer 0.7 μg/mL (range, 0-0.5). The cardiac biomarkers were normal. The results of arterial blood gas analysis were pH 7.48, pCO2 31 mmHg, pO2 103 mmHg, and O2 saturation 98%. However, he gradually complained of respiratory difficulty starting on the night of hospitalization day and had oxygen desaturation. Oxygen supplementation was needed to maintain an SpO2 of ≥ 95%. He received supplemental oxygen via nasal prongs initially. The clinical course and selected relevant laboratory parameters are shown in .
On hospital day 2, he developed markedly increased tachypnea (respiratory rate up to 48 breaths per minute) and decreasing SpO2, thus requiring oxygen enrichment (up to 5 L flow of 100% oxygen). The chest X-ray showed the progression of pneumonia (). We assessed the patient's COVID-19 severity based on clinical criteria, which was regarded as severe. Remdesivir is suggested for children with severe COVID-19, so remdesivir administration was initiated (body weight ≥ 40 kg: 200 mg loading dose on the first day, followed by 100 mg every 24 hours intravenously). Although hypotension was not noted, other vital signs remained unstable. He had sustained and recurrent fever with poor response to antipyretics, tachycardia, tachypnea, and repeated need for increase in oxygen. He complained of severe general aches, and the C-reactive protein level was high. We decided to administer corticosteroids. He received dexamethasone at 6 mg (0.15 mg/kg, maximum dose 6 mg) once daily for 10 days.
The patient showed defervescence by hospital day 4. However, he complained of severe cough and had frequent desaturation of SpO2. In the episodes of deterioration, his oxygen requirement increased up to 10 L/min and slowly recovered. There were no significant findings in testing for additional bacterial and viral respiratory pathogens. The echocardiography results were unremarkable. The five days of remdesivir therapy were finished on hospital day 6. Hepatic and renal function tests were monitored daily during remdesivir therapy, and there were no adverse events. Although there was no significant improvement in the chest X-ray on hospital day 6, his oxygen requirements were gradually weaning. On hospital day 8, the chest X-ray showed a marked improvement in pneumonic consolidations in both lung fields (), and the C-reactive protein level was normal. Supplemental oxygen was stopped on hospital day 9.
The follow-up polymerase chain reaction (PCR) test for SARS-CoV-2 on hospital day 18 was equivocal (negative for E gene; positive for ORF 1ab; cycle threshold value, 35.11). However, no pneumonic consolidations were noted on the follow-up chest X-ray, and his symptoms had nearly resolved. The patient was discharged from the hospital on day 21.
This study was approved by the Institutional Review Board (IRB) of Pusan National University Hospital and the requirement for informed consent was waived (IRB No. 2105-024-103).


We report the case of an 83-year-old female who presented to the emergency department for lower abdominal pain. The pain started 1 month prior to the presentation and progressively got worse. A computed tomography (CT) scan of the abdomen and pelvis showed significant left-sided hydronephrosis, hydroureter, mass in left side of the base of the bladder (), and 4.6 × 4.7 cm mass medial to the left common femoral artery (). The patient underwent transurethral resection of the bladder tumor, which showed large necrotic mass involving left posterior bladder/trigone and left side of bladder wall (likely cause of left-sided hydronephrosis, hydroureter), and pathology was consistent with high-grade urothelial carcinoma with invasion of muscularis propria. The patient was diagnosed with metastatic bladder cancer. The patient was not a chemotherapy candidate based on the age and performance status and immunotherapy was started with pembrolizumab. The patient got 7 cycles of pembrolizumab (every 3 weeks) and then presented to hospital for breathing difficulty and CT scan of the chest showed pneumonitis. The patient was initiated on steroids, pembrolizumab permanently stopped, and eventually discharged home. The patient continued to follow-up as outpatient off therapy and repeat CT chest, abdomen, and pelvis 6 month post last treatment showed no evidence of metastatic disease in chest, abdomen, and pelvis–complete response ().


A 61-year-old male presented with rectal bleeding for 3–4 months. Rectal digital examination and proctoscopy revealed a mass in the anorectal region, and in view of suspicion of malignancy, the patient was referred for whole-body FDG PET/CT scan. The staging of PET/CT scan [Figure –] showed an intensely FDG-avid intraluminal mass in the anorectum with FDG-avid regional lymph nodes. Subsequently, surgery was planned, and APR with colostomy was performed, and histopathology report [] confirmed rectal melanoma. Postsurgery, the patient received concurrent chemotherapy and radiotherapy. Follow-up PET/CT scan after 6 months [Figure –] revealed the absence of FDG-avid visible mitotic disease. PET/CT scan [Figure –] done 10 months after staging was suggestive of recurrence with FDG-avid metastatic lesions in the liver, abdominal deposits, and FDG-avid skeletal lesion.


A 68-year-old female presented with symptoms of intestinal obstruction. Post evaluation, anterior resection and diversion colostomy surgery were performed, and the resected specimen was sent for histopathological examination. On histopathology [], it was reported as rectal malignant melanoma. Subsequently, the patient was sent for PET/CT scan to rule out distant disease. Initial scan [Figure –] showed postoperative changes in the pelvis and postcolostomy status. Follow-up scan after three cycles of chemotherapy and after 3 months of initial scan showed postoperative changes and no evidence of any FDG-avid visible disease. However, PET/CT scan performed 24 months after the initial scan showed multiple FDG-avid lesions involving the liver suggestive of recurrence.


A 41-year-old male presented with rectal bleeding for 4–5 months. A rectal mass was palpated on examination. The patient was sent for FDG PET/CT scan for initial evaluation. The whole-body FDG PET/CT scan [Figure –] showed a FDG-avid polypoidal intraluminal mass involving the anorectal region with FDG-avid regional lymph nodes. APR was performed, and histopathology report [] was suggestive of rectal melanoma. Postsurgery and radiotherapy, follow-up PET/CT scan [Figure –] done after 9 months of the initial scan was suggestive of an absence of FDG-avid visible disease.


A 71-year-old male presented with a 3-month history of word-finding difficulties, confusion, and left leg weakness. CT head demonstrated several ill-defined hypodense areas within the right parietal and occipital subcortical white matter. MRI of the brain demonstrated a contrast-enhancing 3.2 cm lesion in the right occipital lobe, a 1.8 cm enhancing lesion in the right precentral gyrus, and multiple smaller enhancing lesions in the right periventricular region with associated vasogenic edema but no mass effect []. PET/CT showed no evidence of systemic malignancy but visualized right posterior temporal, occipital and parietal lobe lesions [ and ]. Susceptibility-weighted angiography (SWAN) imaging demonstrated a hemorrhagic component of the right occipital lobe lesion [].
A needle core biopsy was obtained of the right occipital lesion, and intraoperative frozen pathology was thought to be consistent with a lymphoma. Formal pathology, however, only showed an intense inflammatory process [ and ] comprised foamy macrophages and T-cells with scattered small B-cells. These cells were CD3 [], CD163, Iba1, and CD68 positive. B cell immunohistochemistry was scantly positive []. The T-cell population was found to be composed of more CD4+ than CD8+ cells.
Postoperatively, he was started on high-dose dexamethasone. However, this was discontinued once the formal pathology was available. A follow-up brain MRI after 1 month demonstrated a decrease in the size of all enhancing lesions. MRI of the total spine was without evidence of disease. Dexamethasone was subsequently tapered off given initial concern for sentinel lymphomatous lesions.
CSF studies, ordered 2 months after the patient’s biopsy, were unremarkable for autoimmune, bacterial, viral, fungal, parasitic, or inflammatory etiologies. CSF flow cytometry was limited by the low cellularity of the specimen but revealed a predominance of CD5+ T cells. Repeat MRI brain off of corticosteroids demonstrated an interval increase in size and conspicuity of all previously observed enhancing lesions, and the decision was made to perform an excisional biopsy of the right occipital lesion.
The patient was brought to the operating room for excisional biopsy of the right occipital lesion. He was positioned supine with his head placed in the Mayfield head holder. The field was prepped and draped, and an incision was made down to the bone. A burr hole was made, and a craniotomy was turned over the lesion as confirmed with image-guidance. There was a pale tan pink discoloration of the brain. Several biopsies were obtained, and then the lesion was resected under the microscope and sent for pathology.
Further histological analysis demonstrated areas of macrophages/lymphocytes with markedly reactive astrocytes that showed quick transition to reactive less inflamed cortex. The lymphocytic population appeared small, but polymorphous, containing scattered plasma cells. There was marked perivascular inflammation but no fibrinoid necrosis. Flow cytometric and immunohistochemical workup failed to demonstrate a definitely clonal lymphocyte population. There was no evidence of demarcated myelin loss or a vasculitic process.
Two weeks postoperatively, he had worsening behavioral outbursts, frequent mood fluctuations, poor comprehension, and worsening balance. Given the clinical deterioration, he was restarted on high-dose dexamethasone. The following MRI demonstrated post-surgical changes with significant decrease in the size of the right occipital lesion []. His steroids were changed to a Prednisone taper starting at 60 mg that was tapered to 20 mg over the course of 6 weeks. Upon follow-up, he was noted to have improved cognitive processing and improved left-sided weakness. Given the clinical and radiographic responsiveness to steroids in the absence of infectious, inflammatory, or neoplastic etiologies, the diagnosis of SLIPPERS was made.


A 48-year-old male patient was diagnosed with stage II HIV infection 11 years back after presenting with cutaneous fungal infections. He was treated with topical antifungals, and started on ART (AZT-3TC-EFV) and cotrimoxazole preventive therapy (CPT) with a baseline CD4+ count 175 cells/mm3. The patient achieved an undetected viral load after 6 months of ART initiation. The ART regimen was shifted to TDF-3TC-DTG after 10 years as recommended by the National Comprehensive HIV Care Guideline. His fasting blood sugar (FBS) level was 101 mg/dl at time of the DTG-based ART initiation. He was told to have hypertension on medical follow up and was prescribed amlodipine, 10 mg po daily, and advised on lifestyle modification. He was diagnosed to have diabetic ketoacidosis (DKA) with clinical evidence of polyuria, polydipsia and fatigue, severe hyperglycemia (RBS=320–466 mg/dl, HbA1c=9.3%), and ketonuria (3+)), which occurred after 7 months of DTG-based ART regimen (). No documented preceding infections. No personal or family history of diabetes mellitus or dyslipidemia. Serum C-peptide level, anti-insulin antibody or anti-glutamic acid decarboxylase (GAD) antibody were not determined due to limited clinical setup. He was treated with intravenous fluids, regular insulin and IV KCl, and recovered from DKA after 4 days of admission. NPH insulin 20/10 IU s/c daily was started, which later changed to metformin 850 mg/day. Good glycemic control (FBS=101–130 mg/dl, HbA1c=7.1%) was obtained with metformin, while the DTG-based ART regimen was continued.


A 49-year-old female patient was diagnosed with stage III HIV infection 11 years back after presenting with smear negative pulmonary tuberculosis and oropharyngeal candidiasis with a baseline CD4+ count 74 cells/mm3. She was covered with fluconazole as antifungal therapy. She was treated with anti-tuberculosis treatment (ATT) for 6 months and declared treatment completed. ART (AZT-3TC-NVP) and CPT were started two weeks after ATT initiation. She had records of undetected viral load after 2 years of ART initiation. The ART regimen was shifted to TDF-3TC-DTG after 10 years as recommended by the National Comprehensive HIV Care Guideline. She was diagnosed with hypertension and dyslipidemia on follow-ups, and advised on lifestyle modification. She was diagnosed with type 2 diabetes after presenting with polyuria, polydipsia, fatigue and blurred vision, and hyperglycemia (RBS=313 g/dl) which occurred after 1 year of the DTG-based ART regimen (). No documented preceding infections. No personal or family history of diabetes mellitus. Serum C-peptide level, anti-insulin antibody or anti-GAD antibody were not determined due to limited clinical setup. No documented plasma glucose level prior to changing ART regimen. She was started on NPH insulin 24 IU s/c daily, which later changed to metformin 1 gm po daily. Good glycemic control (FBS=109–135 mg/dl) was achieved with metformin, while the DTG-based ART regimen was continued.


A 46-year-old female patient was diagnosed with stage I HIV infection after voluntary counseling and testing (VCT) for HIV 13 years back. She was initiated on ART (AZT-3TC-NVP) and CPT 2 years later with a CD4+ count 119 cells/mm3. The ART regimen was shifted to TDF-3TC-DTG after 11 years as recommended by the National Comprehensive HIV Care Guideline. She was diagnosed to have DKA with clinical evidence of polyuria, polydipsia and fatigue, severe hyperglycemia (RBS=350–450 mg/dl, HbA1c=11.4%) and ketonuria (3+), which occurred after 1 month of the DTG-based ART regimen (). No documented preceding infections. No personal or family history of diabetes mellitus or dyslipidemia. Serum C-peptide level, anti-insulin antibody or anti-GAD antibody were not determined due to limited clinical setup. No documented plasma glucose level prior to changing ART regimen. She was treated with intravenous fluids, regular insulin and IV KCl, and recovered from diabetic ketoacidosis after 3 days of admission. NPH insulin 10/8 IU s/c daily was initiated, which later changed to metformin 750 mg po daily. Good glycemic control (FBS=106–140 mg/day, HbA1c=5.6%) was obtained with metformin, while the DTG-based ART regimen was continued.


During a routine follow-up for gallbladder adenomyomatosis, a 65-year-old woman underwent an abdominal ultrasound which revealed a hypoechogenic lesion in the pancreatic head, measuring 2.2 × 1.7 cm. An abdominal MRI confirmed a solid hypovascularized mass in the uncinated pancreatic process, without lymphadenopathies or vascular involvement. CA19-9 was normal (12 UI/mL). In January 2018, she underwent a duodenopancreatectomy with lymphadenectomy. Pathology confirmed a pT3 pN1 (5/17 positive lymph nodes) ductal adenocarcinoma of the pancreas. Nine days after being discharged, the patient developed fever with rigors, followed by explosive diarrhea. She was admitted and tested positive for C. difficile, which was treated with orally administered metronidazole for 14 days with complete resolution of the infection.
From March to August 2018, she received adjuvant gemcitabine and capecitabine without any adverse events. Subsequently, she was asymptomatic and on routine follow-up. However, in December 2019, she started complaining of abdominal pain, especially in the left upper quadrant, associated with intermittent diarrhea and abdominal cramps. At that time, CT scans showed only discrete fat densification at the root of the mesenterium, which was stable according to the CT scans from 6 months before, and CA19-9 was normal. The abdominal pain and diarrhea aggravated and new CT scans were ordered in May 2020, revealing the emergence of diffuse intestinal pneumatosis along the colic frame as well as multiple small gaseous foci of pneumoperitoneum in the pericolic fat, as shown in Figures , , . In addition, the tissue located circumferentially to the emergence of the superior mesenteric artery became better defined, extending along its proximal segment, and at the level of the bifurcation of the celiac trunk, measuring up to 2.6 cm. Given the suspicion of severe bowel infection, the patient was admitted and several tests were ordered, which confirmed CDI. Oral vancomycin was started with resolution of the diarrhea. Seven days later, there was almost complete resolution of the intestinal pneumatosis. In order to rule out locoregional recurrence, an echoendoscopy was requested, which unfortunately revealed ductal adenocarcinoma.


An eight-year-old girl was referred to our outpatient clinic with complaints of neck asymmetry, restricted cervical movements, and pain on the right side of her neck. Her parents noticed an asymmetry on her neck at three years of age. She had no history of head and neck trauma. She had no history of upper cervical or head infection, or otolaryngologic procedure, either. She had painful torticollis which was misdiagnosed during multiple visits to the pediatric, neurosurgical, and orthopedic departments. Initially, it was thought that this condition was a muscular torticollis and stretching and strengthening exercises were recommended by previous physicians from different specialties. On her physical examination, the throat was normal. She had no fever. Her head was in the cock-robin position (Figure 1); i.e., tilted toward the affected side and flexed anteriorly, and the chin was turned to the opposite side.[] Torticollis and shortness of the right sternocleidomastoid muscle (SCM) were observed on inspection. Cervical lateral flexion and cervical rotation to the left and cervical extension were restricted by approximately 20°. Her neurological examination findings were normal. The results of all biochemical blood tests were within normal ranges. The cock-robin position was visualized on the anteroposterior cervical plain graph (Figure 2). The three-dimensional (3D) computed tomography (CT) revealed atlantoaxial rotatory subluxation at an angle of 10° on the transverse plane (Figure 3). Additionally, cervical magnetic resonance imaging (MRI) confirmed the atlantoaxial rotatory subluxation without any soft tissue pathology. Based on these clinical and radiological findings, the diagnosis of GS was made. The patient was consulted to neurosurgery department and resection myotomy on the right SCM was decided. Atlantoaxial joint surgery was not considered due to the fixed rotatory subluxation persisting without any neurological complication. A written informed consent was obtained from each parent. A resection myotomy was successfully performed and the patient was discharged with a cervical orthosis on the fifth day of the surgery.


A 34-year-old Asian male with hyperechoic masses in the RV found incidentally on the transthoracic echocardiogram during a routine physical examination was admitted to our cardiology department. There was no past medical history of coronary artery disease, cardiomyopathy, heart failure, dysrhythmia, sudden death, or autoimmune disease. On admission, the physical examination, vital signs, and laboratory profile were normal, and the patient had a normal sinus rhythm.
The repeated transthoracic echocardiogram showed three solitary and well-demarcated masses in the RV (Supplementary material online, TableS1, Video 1). The size of these three lumps of poplar homogeneous isoechoic shadows were about 23 mm × 17mm, 12 mm × 33mm, and 21 mm × 25mm, respectively. The boundaries were clear and their internal echo was similar to that of point-like particles. The residual cardiac structure (including pericardial thickness), intracardiac flow, and left ventricular function (ejection fraction 65%) were unremarkable. The preliminary diagnosis was multiple solitary and well-demarcated masses in the pericardium (considering the possibility of lipoma or fibrinous cystadenoma).
The computed tomography also demonstrated multiple circular low-density shadows near the interventricular septum in the RV with a mean value of −56 HU (). The preliminary consideration was lipomas. It was not possible to identify the degree of subvalvular apparatus involvement.
Given these findings, CMR was performed for better tissue characterization. CMR demonstrated four irregular but well-circumscribed masses (the largest size being 20.5 mm × 13.6m × 15.7 mm). Two bases were attached to the interventricular septum and arranged up and down, the other two were attached to the lower wall of the RV (). The CMR diagnosis was intracardiac partially occluding the right ventricular outflow tract (RVOT) (, Video 2), and similar findings were found on the echocardiography (). The T1-weighted image revealed a hyperintense signal and was uniformly suppressed in the fat-suppression mode, but an unusual malignant tumour with high-fat content could not be excluded (, Video 3).
Considering the age of the patient and the concrete possibility of the future development of significant RVOT obstruction, the surgical treatment was recommended. Surgical excision was performed to avoid potentially fatal embolism and obtain a definitive diagnosis, excluding the small possibility of malignancy. Thus, an operation involving tricuspid valve repair and resection of the tumour was electively planned.
Once the patient was intubated, a transoesophageal echocardiography was performed (Supplementary material online, VideoS1). The operation was carried out through a median sternotomy with standard hypothermic cardiopulmonary bypass. After opening the pericardium, the masses were seen. Through the right atrium incision, the tricuspid valve and papillary muscle were covered by four adipose masses in the RV that arose from the interventricular septum and the tricuspid chordae tendineae, which partially occluding the RVOT (, white asterisks). These multiple yellowish masses partly merged with each other, integrated with packs of chordae and papillary muscle of the tricuspid septal leaflet, as well as the right interventricular septum. While trying to maintain the integrity of papillary muscles and tricuspid valve chords, a part of the chordae tendineae was severed and four masses were fully exfoliated (). After that, saline was injected into the RV and severe tricuspid valve insufficiency was found. The severed chordae tendineae were sutured to the papillary muscle using a prolene 4–0 suture for two stitches. Again, it was found that the tricuspid closure improved and only with a small amount of reflux. After an aortic cross-clamp time of 3 h, the patient was weaned from cardiopulmonary bypass. A transthoracic echocardiogram was performed 1 day after surgery (Supplementary material online, TableS1). The S′, peak systolic tissue velocity at the tricuspid annulus was 8.6 cm/s, and there was no sign of tricuspid regurgitation or RVOT obstruction, which indicated that the patient had an uneventful in-hospital recovery without any signs of right-sided cardiac failure. The macroscopic appearance of the four ovoid fat masses was histopathologically confirmed as lipomas, characterized by the mature adipocytes with entrapped myocardial cells. No atypical features or malignancy were identified ().
The patient had no complaints and his echocardiogram was unremarkable in the scheduled 1-month follow-up after the surgery.


A 9-year-old male patient with severe intellectual impairment and limited mobility was referred to local cardiology services with a soft ejection systolic murmur. The electrocardiogram showed an incomplete right bundle branch block with QRS duration of 95 ms and right axis deviation. Chest X-ray results showed mild cardiomegaly. The patient was diagnosed with a large secASD with evidence of right ventricular volume overload based on a focused TTE. Foetal alcohol syndrome was determined as the most likely overriding aetiology for his cardiac abnormality and co-morbidities. The patient resided in the South Pacific islands and was referred to the regional overseas paediatric cardiac centre for transcatheter secASD closure.
A full cardiac anatomy scan was completed using TTE at the cardiac centre. A diagnosis of secASD suitable for transcatheter device closure was confirmed. The patient had normal left ventricular dimensions and ejection fraction with no evidence of regional wall motion abnormalities. The right ventricle was severely dilated and had normal systolic function. Trivial mitral regurgitation was present. The patient had a severely dilated RCA origin from the right aortic sinus that measured 4.6 mm with a Boston Z-score of +4.65 ( and Video 1). There was no evidence of a left main coronary artery (LMCA) originating from the left aortic sinus ( and Video 2). On further interrogation using colour Doppler, only retrograde flow was noted in the region of the proximal LAD ( and Video 3). The LCX was not observed.
The coronary artery origins were further assessed using transoesophageal echocardiography (TOE) due to suspicion of a coronary artery abnormality. This was undertaken as part of the secASD imaging pre-intervention. An aortic angiogram was chosen as the next step if a coronary artery anomaly could not be ruled out. The TOE was unable to identify an LMCA and demonstrated abnormal coronary artery colour Doppler signal near the left atrial appendage ( and ).
An aortic root angiogram showed a single dilated RCA originating from the right aortic sinus, supplying the inferoseptal and inferior myocardium and retrogradely filling the LCX back to the expected position of the LMCA. There was no LMCA originating from the aorta ( and ).
A selective RCA angiogram was subsequently performed to further define coronary supply and confirmed the above findings ( and ). There was adequate retrograde filling of the LCX as far as the LAD and LCX bifurcation. No LMCA was evident. The LAD was antegradely filled from the LCX and retrogradely by a large collateral artery from an RCA ventricular branch that extended to the cardiac apex. The middle third of the LAD was diffusely hypoplastic.
A dobutamine stress echocardiogram (DSE) was immediately performed to determine the potential need for surgical coronary artery intervention. DSE analysis confirmed good left ventricular function with no evidence of regional wall motion abnormalities.
The transcatheter secASD closure was deferred pending cardio-surgical evaluation of the coronary artery findings. The overall appearance was judged to be a congenital coronary artery anomaly, but the diffusely hypoplastic LAD raised the question of an inflammatory, and thus acquired aetiology.
It was decided that the risks of surgical coronary artery intervention to bypass graft or re-anastomose the left coronary arteries to the aortic root outweighed the benefits. Contributing factors to this decision included no inducible ischaemia or wall motion abnormalities, adequate collateral and retrograde supply, distance from the aortic root to the reconstitution of the LAD and LCX, and the small calibre of both the LAD and obtuse marginal branch. An interval transcatheter secASD closure was successfully performed using a 24-mm Figulla Flex II ASD occluder (Occlutech GmbH, Jena, Germany), and the patient then returned to his country of origin. A follow-up stress echocardiogram will be performed in adolescence.


The case concerns a 62-year-old male, active cigarette smoker with hypertension, hyperlipidemia, chronic mild anemia, chronic kidney disease on hemodialysis, with lower extremity peripheral artery disease (PAD) after surgical revascularization (left femoral → popliteal artery bypass), with active ulcer of the left foot, history of myocardial infarction without ST-segment elevation (NSTEMI) treated percutaneously with a bare metal stent (BMS) to the right coronary artery (RCA), and in subsequent scheduled BMS implantation to the left anterior descending artery (LAD) and the circumflex (Cx), 11 years prior to the current hospitalization. He had a history of NSTEMI 1 year previously treated with implantation of drug eluting stents (DES) to the proximal part of the RCA and an unsuccessful attempt of crossing a lesion in the distal part of the RCA (due to heavily calcification in the body of the lesion the patient was qualified for optimal medical therapy of CAD).
He was admitted to hospital with chest pain (class IV in the CCS scale) ongoing for 2 h. An electrocardiogram showed sinus rhythm 80/min conducted with the right bundle branch block (RBBB) and the serum high-sensitivity troponin-I was positive. Coronary angiogram revealed: chronic total occlusion of the LAD with two coexisting culprit lesions in the RCA (proximal in-stent restenosis and distal highly calcified subtotal lesion) (). Accumulated Syntax Score was 39.5 points. Due to advanced atherosclerosis, comorbidities and ongoing ischemic symptoms a rescue PCI was performed by the right femoral approach using the AL 1.0 Guide-Catheter (7F) (Medtronic Ireland, Galway, Ireland). We managed to cross the distal lesion with a Choice ES guidewire (Boston Scientific, Marlborough, United States). Despite use of the 7F guiding extension TrapLiner (Teleflex Incorporated, Wayne, United States) all attempts to cross the lesion with the FineCross microcatheter (Terumo Corporation, Tokyo, Japan) and a low-profile balloon Ryurei 1.0 × 10 mm (Terumo) failed. The successful crossing was achieved using an additional support by TrapLiner (Teleflex) and Turnpike Gold 135 (Vascular Solutions LLC, Minneapolis, United States) () – a microcatheter with a threaded tip, providing rotational advancement when rotated clockwise. In the next step we performed ineffective predilation with Ryurei (Terumo) 1.5 × 20 mm. Significant underexpansion of the balloon catheter at 18 atm was observed (). Therefore, we exchanged the guidewire on the Rotawire-Extra-Support (Boston Scientific) and performed successful rotational atherectomy (RA) with the ROTAPRO Rotational Atherectomy System (Boston Scientific) using a Rotablator burr size of 1.75 mm (). Despite lesion preparation with the RA, we still observed a significant “dogbone effect” on the non-compliant (NC) Emerge (Boston Scientific) balloon 3.0 × 15 mm (22 atm) (). Hence, we performed the S-IVL using a 3.5 × 12 mm catheter. Delivery of the device was facilitated by use of a guiding extension. After application of 40 ultrasonic pulses, full expansion was obtained (). Implantation of three overlapping drug eluting stents – Resolute ONYX (Medtronic) 3.5 × 38 mm, 4.0 × 38 mm and 4.0 × 34 mm (16 atm) – was followed by a 4.0 × 20 mm (22 atm) NC Emerge (Boston Scientific) postdilation. Finally, we obtained a satisfactory angiographic result (). On the 7th day after the procedure, the patient was discharged. Follow-up transthoracic echocardiography showed an enlarged hypokinetic left ventricle with coexisting thinning and lack of vitality related to the anterior wall, interventricular septum and apex (LVEDd/LVESd = 64 mm/50 mm) with reduced ejection fraction (EF~30%) and coexisting moderate functional mitral regurgitation, without other mechanical complications. Due to the previously observed analogical impairment of myocardial contractility, ICD implantation was scheduled.


A 72-year-old male came with a complaint of rapidly increasing swelling in the right upper gingival region for 3 months []. Along with this, he also had right cervical lymph node enlargement. On examination, he had massive splenomegaly. Incisional biopsy performed from the gingival mass showed a tumor composed of monomorphic proliferation of large plasmacytoid and immunoblastic cells showing vesicular nuclei, moderate cytoplasm, and 1–3 prominent nucleoli. Frequent mitosis and apoptosis were noted []. The tumor cells were positive for LCA and CD138 and focally positive for EMA; and negative for CK, p63, CD20, CD79a, CD3, ALK-1, CD56, and lambda restricted. Ki67 index was 95%. EBER ISH (EBV encoded RNA in situ hybridization) for EBV infection was positive []. Based on these findings, he was diagnosed with PBL.
Simultaneously, routine hemogram revealed anemia, leukocytosis, and thrombocytopenia. WBC count was 86.8 × 109/L with absolute lymphocytosis showing 90% mature lymphocytes suggesting a possibility of CLL. Bone marrow examination showed 78% atypical lymphoid cells on the aspirate with diffuse pattern of infiltration on the biopsy []. The lymphoid cells were positive for CD20, CD5, CD23, and negative for CD 138. Plasma cell percentage on bone marrow was within normal limits. HIV viral serology was negative. There was no monoclonal spike in the serum or urine electrophoresis and no lytic lesion on the skeletal survey. As he was in the high-risk category of CLL according to modified Rai staging, he was started on bendamustine and rituximab therapy and his counts came back to normal within 2 months of treatment. Interestingly, the gingival tumor regressed in size after the biopsy and within 1 month had disappeared completely.


The patient, female, 24 years old, self-reported that she had repeated vomiting without obvious inducement 5 d ago.
The vomit was food, occasionally bloodshot, accompanied by abdominal pain, and alleviated after eating, no acid reflux, no belching. Gastroscopy in the outside hospital indicated that the Gastric occupying lesions. Laboratory examination: Blood and biochemical test index are close to normal, Tumor indicators and coagulation function are negative; Helicobacter pylori staining was positive.
During the course of the disease, there was no fever, no chills, no diarrhea, no hematemesis, no cough or sputum and good spirits, good diet and sleep, normal stools, and no significant weight loss.
No history of cancer in individuals and families.
The skin and sclera were not yellowish, the liver and spleen were not touched under the ribs, the abdomen was soft, no tenderness, no rebound pain, and mobile dullness was negative.
The blood analysis revealed that the average hemoglobin was a mild decreased, the test result was 26.7 pg (normal range 27-34 pg), and the reticulocytes were slightly decreased, the test result was 0.023 × 1012/L (normal range 0.024 × 1012/L-0.084 × 1012/L) Prothrombin and partial thromboplastin times were normal. The blood biochemistries, as well as urine analysis were normal. Electrocardiogram, chest X-ray and arterial blood gas were also normal.
Plain computed tomography(CT) scan and contrast enhancement CT scan examination showed that the gastric body, stomach fundus, and gastric antrum were diffusely and uniformly thickened, showing gyrus-like changes, focusing on the greater curvature side. After enhancement, it was significantly enhanced. The plain scan, arterial phase and venous phase CT values were about 50 HU, 129 HU, and 113 HU, respectively. The serosal surface of the gastric wall showed smoothness and the density of perigastric fat was clear (Figure ). Magnetic resonance imaging (MRI) showed that the gastric body, fundus and gastric antrum were diffusely and uniformly thickened, showing slightly longer T1 and T2 signal shadows. DWI showed high signal. The measured ADC value ranged from 1.387 × 10-3 mm2/s-1.467 × 10-3 mm2/s. The mucosa showed smoothness (Figure ).
Gastroscopy and pathological: The cardia extends to the stomach, fundus and antrum, with irregular mucosal bulges, medium texture, poor peristalsis, and narrow gastric cavity. The pylorus is round and can be opened and closed (Figure ). The diagnosis suggests that the Gastric occupying lesions, possibly gastric cancer. The pathological results showed: Chronic inflammation of the gastric mucosa, hyperplasia and lengthening of the gastric pits, and a small number of glands with mild atypical hyperplasia (Figure ).
Gastric lymphoma: It is a tumor originating from the lamina propria and submucosal lymphoid tissues of the gastric mucosa. This case is characterized by a small number of CD45-positive lymphocytes scattered among the hyperplastic glands (Figure ), while the lymphoma is characterized by uniform round tumor cells diffusely distributed under the pathological microscope, so this case does not match.
Gastric cancer: It is a malignant tumor that originates from the gastric mucosa, the structural and cellular atypia of the glands are very obvious, accompanied by obvious invasive growth, so this case does not meet. Figure is an immunohistochemical picture of CK, showing that the hyperplastic glands are arranged regularly.
Gastric polyp: It is a benign tumor derived from gastric epithelium or gastric interstitium. The characteristics of lesion distribution and enhancement characteristics are not consistent with this disease.
Stomach stromal tumor: In gastric stromal tumors, proliferating spindle cells can be seen arranged in bundles and weaves. In this case, only a few proliferating spindle cells are seen between the hyperplastic glands, which is not consistent with this case. The immunohistochemical marker DOG1 was negative (Figure ), which ruled out the possibility of gastric stromal tumor.
Gastric mucosal prolapse: It refers to the abnormally loose gastric mucosa passing through the pylorus or cardia, protruding into the duodenal ampulla or protruding into the esophagus, which can be distinguished by observation of different positions of upper gastrointestinal angiography.