A 26-year-old male, manual laborer presented with pain and swelling over left elbow following a fall on an outstretched hand while driving a two-wheeler. There were diffuse swelling and tenderness over lateral elbow joint line. Forearm rotation was associated with pain. Elbow was held in 30° flexion with painful restriction of further flexion. There was no distal neurovascular deficit.
An intra-articular displaced capitellum fracture was diagnosed on plain radiographs of the elbow (, ). Computed tomography (CT) images revealed a three-part capitellum fracture pattern with a Y-shaped split of distal humerus, a sheared anterior crescent-shaped fragment, and a single, large posterolateral fragment including the lateral epicondyle. The anterior crescent-shaped capitellum fragment extending up to the lateral part of trochlea was displaced proximally and laterally. The posterior arm of the Y-shaped fracture line exited the posterolateral cortex of distal humerus (, , ).
Open reduction and internal fixation (ORIF) was done through an anterolateral Kocher’s interval. Posterior soft-tissue sleeve was left undisturbed. Anatomical articular reduction was temporarily held with two 1.0 mm Kirschner wires (). Headless cannulated screws were not available at this trauma center which is a low-resource health-care setup. Instead, two divergent, countersunk, solid 3.5 mm cortical screws were used to stabilize the articular fragment. Both screws were applied obliquely from anterior-distal to posterior-proximal to ensure adequate far cortex purchase above the unstable posterolateral fragment and to prevent posterior column comminution (). An additional oblique, extra-articular screw was used to fix the posterolateral fragment. Primary LCL repair was done and additional absorbable sutures used to tag the LCL to the intact posterolateral soft-tissue sleeve. Elbow was taken through a full range of movement and valgus and rotational stability was assessed, wound was irrigated and closed over suction drain. Active-assisted elbow range of movement exercises initiated from the 7th post-operative day.
At 3 months follow-up, fracture united and the patient regained active elbow flexion from 5° to 130°. He complained of minor pain at terminal elbow extension. Persistent restriction of 5° terminal elbow extension was attributed to suspected impingement of olecranon tip against screw tip. Implant was not removed as the patient has good elbow function and was able to return to work 3 months after surgery.
At 1 year and 2 years’ follow-up, elbow range of 5–130° was recorded and Mayo elbow performance score was 95. There was no valgus or posterolateral rotational instability. The patient reported no pain, full elbow flexion, minimal restriction of elbow movement at terminal extension, and no elbow instability. Minimal asymptomatic anterior heterotopic ossification (HO) was noted but it did affect elbow function (, ).


A 23-year-old Korean female presented to our surgical department with epigastric pain of two-months’ duration. Her past surgical history included laparoscopic ovarian cyst excision 8 months previously. No history of prior abdominal trauma was noted. There was no family history to suggest a genetic hereditary disease. Clinical examination was normal. The liver function test was normal except elevated serum amylase 250 U/L (reference range: 28 to 100 U/L) and lipase level 708 U/L (reference range: l3 to 60 U/L). The levels of serum tumor markers were within normal limits: carcinoembryonic antigen, 0.6 ng/ml (reference range: 0 to 5 ng/ml); carbohydrate antigen 19 to 9, 6.27 IU/ml (reference range: 0 to 37 IU/ml) (). An abdominal computed tomogram (CT) demonstrated a 10-cm solid mass in the distal pancreas, with signs of splenic artery and vein occlusion, gastric and transverse colon invasion (). The pancreatic mass was ill-delineated with no evidence of metastasis. On MRI scan, a huge lobulated contour mass was found in the body and tail of the pancreas, showing low signal intensity on T1- and slightly high T2-weighted images with diffusion restriction and delayed enhancement pattern (). On EUS a showed an huge soft tissue mass with no cystic portion but multiple echogenic foci located in the distal pancreas (). PET CT showed heterogeneous hypermetabolic lesion in left quadrant abdomen (). Operative findings showed a mass involving distal pancreas, invasive to the posterior wall of the antrum of the stomach and transverse colon and 4th portion of the duodenum without lymph node involvement. The surgery consisted of a distal pancreatectomy, splenectomy and combined partial resection of the stomach, transverse colon and 4th portion of the duodenum. On gross pathology the tumor appeared as a grayish, white, dense and firm mass, without necrosis or hemorrhage (). On pathologic microscopic examination, the surgical margins were negative for a tumor. Histological sections showed a large number of spindle-shaped cells, with a regular nuclear pattern within a background of massive collagen fibers. No marked cell death but mitosis 8/50 HPF was observed (). Immunohistochemical analysis revealed that the tumor cells were diffuse immune-positive for vimentin and β-catenin (), but immune-negative for smooth muscle actin, S-100, and CD34. The immunohistochemistry and histopathological features were consistent with a confirmed diagnosis of intra-abdominal DTF. The patient received no adjuvant therapy after surgery. She exhibited good health and complained of no discomfort. No local recurrence or distant metastasis in CT was found during a 3 year follow-up.


We present the case of a 63-year-old female, with a past medical history of hypertension, diabetes, diverticulitis, and chronic low back pain. She did not have any significant cardiac history. She has had a hysterectomy, and multiple orthopaedic surgeries in the past. She takes lisinopril, trazodone, amlodipine, metformin, sertraline, cyclobenzaprine, and morphine at home. She is an active half a pack a day cigarette smoker, but no alcohol or illicit drug use.
She was found unresponsive at home and did not have a pulse and cardiopulmonary resuscitation was started. Emergency medical services arrived at the scene and she was found to have ventricular fibrillation (VF) on the monitor. She was defibrillated three times and received multiple rounds of epinephrine and sodium bicarbonate. Her total time from cardiopulmonary arrest (CPA) to return of spontaneous circulation (ROSC) was 37 min. After ROSC was achieved, electrocardiogram (ECG) showed non-specific ST-segment changes and T-wave inversions and soon progressed into high grade and third-degree AV block ( and ). Initial troponin I was negative. A bedside echocardiogram was performed by a cardiologist, showing an ejection fraction of 25% with akinesis of the apex and anteroseptum.
On presentation, the patient had a troponin I level of <0.015 ng/mL, lactic acidaemia of 10 mmol/L, potassium of 2.5 mmol/L, elevated creatinine of 1.4 mg/dL. Computed tomography angiogram of the chest was done to rule out pulmonary embolism or aortic dissection as the cause of the CPA, which was negative for any acute process; however, it did show calcification of left anterior descending and left circumflex arteries. She was taken for a right and left heart catheterization the same day which did not show any significant coronary occlusion (, Videos 1 and 2). Left ventriculogram showed ballooning of the left ventricle ().
A formal transthoracic echocardiogram performed hours after presentation showed an ejection fraction of 15–20% and severe hypokinesis of anterior, apical, anteroseptal, and lateral wall of the heart, resembling TCM (). An echocardiogram repeated 4 days after the cardiopulmonary arrests showed an ejection fraction of 60–65% with hypokinesis of mid anterior and antero-apical hypokinesis and absence of any other wall motion abnormalities compared to the previous echocardiogram.
The patient had a pulmonary artery catheter and transvenous pacemaker placed for closer monitoring of cardiac haemodynamic state and to pace her heart, respectively. The pulmonary artery catheterization revealed right atrial pressure of 11 mmHg, right ventricular systolic pressure of 39 mmHg, pulmonary artery pressure of 46/22 with a mean of 31 mmHg, pulmonary capillary wedge mean pressure of 20 mmHg, cardiac output of 5.27 L/min, and cardiac index of 2.9 L/min/m2. The patient was pacemaker dependent during her hospitalization, despite of improvement in her TCM per repeat echocardiogram. Hence, she eventually received a dual-chamber pacemaker/implantable cardioverter-defibrillator for her AV block and as primary prevention for her ventricular arrhythmia. The patient was intubated during CPA. She had a thorough neurological examination off sedation, and she was following commands and moving all extremities. She was eventually extubated and had a good neurological recovery. Subsequently, she was discharged home without any significant neurological deficits. In addition to her previous home medications, she was started on carvedilol, aspirin, and atorvastatin upon discharge. The patient followed up in an outpatient setting and continued to have a stable ejection fraction of 60–65%; in addition, she was pacemaker dependent without any ventricular arrhythmia events.


A 33-year-old lady with a background of essential hypertension was admitted with New York Heart Association Class (NYHA) IV breathlessness attributed to de novo acute HF and severe LVSD. In the preceding 5 years, extensive investigations by nephrology and endocrinology specialists had excluded secondary causes including phaeochromocytoma, renovascular, and renal parenchymal disease. Body mass index was 33 kg/m2 but the STOP-Bang screen for obstructive sleep apnoea proved negative.
Echocardiogram revealed a mildly dilated LV with mild posterior LVH (septum 1.1 cm, posterior wall 1.5 cm, indexed LV mass 129 g/m2), LVEF 18% and indexed SV (SVi) 11mLs/m2. Using single-beat analysis for non-invasive estimations of Ea and Ees, net arterial load was found to be significantly raised (Ea 7.0 mmHg/mL; normal range 2.2 ± 0.8 mmHg/mL) in excess of a normal index of contractility (Ees 2.7 mmHg/mL; normal range 2.3 ± 1.0 mmHg/mL) giving a VAC of 2.6. This indicated considerable inefficiency of the ventricle working against an opposing afterload. Cardiac MRI confirmed HHD with LVEF 14% after excluding infarction, infiltration, myocarditis and coarctation of aorta. Coronary angiography demonstrated normal coronary arteries.
Before the diagnosis of HFrEF, she was already on spironolactone, maximum doses of bisoprolol and ramipril for the preceding 2 years. Despite this, she had grade 3 hypertension, confirmed on 24-h ambulatory monitor (). With no evidence of interval injury, the HF team suspected a case of end-stage HHD prompting an urgent referral for cardiac transplant assessment. Hydralazine was concurrently added to optimize BP.
At the transplant clinic, BP improved to 126/76 and echocardiogram revealed normalization of LV systolic function associated with better exercise tolerance. She was therefore discharged from the transplant service. As presented in the timeline, subsequent BP escalations were associated with profound deteriorations in clinical and LV systolic function. When she became more compliant with the evening hydralazine doses, a reasonable BP 133/86 was achieved and echocardiogram showed a mildly impaired LV systolic function, LVEF 48%. Calculated Ea was 2.9 mmHg/mL, Ees 3.0 mmHg/mL with VAC ratio 0.97 indicating a closely matched elastance for greater ventricular efficiency.
Unfortunately, on recent follow-ups, she reported NYHA III breathlessness and was found again to have uncontrolled hypertension with severe LVSD. Despite 6 months of Sacubitril/Valsartan 97/103 mg BD, LV remained poor in the face of uncontrolled hypertension.


An 86-year-old gentleman was referred to the HF clinic with NYHA III breathlessness. He was known to have AS on a background of hypertension, diabetes, and coronary artery bypass grafting in 1998. Prior to referral, he was established on maximal doses of bisoprolol and losartan, and furosemide. N-terminal prohormone of brain natriuretic peptide was 1719 pmol/L. Compared with his baseline echocardiogram, repeat scan revealed new severe LVSD, LVEF 29%, SVi 23 mL/m2 with mild concentric LVH and low-flow low-gradient severe AS (mean gradient 25 mmHg, peak gradient 41 mmHg, aortic valve area 0.7 dimensionless valve index 0.2).(). There was no evidence of aortic coarctation. On review, BP was 156/111 and heart rate 86 b.p.m. To optimize BP control, hydralazine 25 mg twice daily was initiated.
Coronary angiography showed patent grafts without de novo lesions and no signs of tachyarrhythmia were found on Holter monitoring, excluding a second-hit injury. Dobutamine stress echocardiography (DSE) was arranged to assess for contractile reserve before potential transcatheter aortic valve implantation (TAVI). He returned a BP diary over 3 months, which showed significantly better control and reported improved exercise tolerance.
On the day of DSE, BP was 106/68. Resting echocardiogram (before dobutamine infusion) showed resolution of LVSD with an LVEF 60% and SVi 52.9mLs/m2. Dobutamine stress echocardiography excluded regional wall motion abnormalities on peak stress and recovery, and reaffirmed severe AS (mean gradient 68 mmHg, peak 104 mmHg, aortic valve area 0.7 cm2) (). Using steady data from echocardiography, VAC normalized to 0.99 (Ea 1.28 mmHg/mL over Ees 1.29 mmHg/mL) from an initial inefficient VAC 1.62 (Ea 3.42 mmHg/mL over Ees 2.11 mmHg/mL). Global haemodynamic load, characterized by ZVa, was calculated by dividing the estimated LV systolic pressure (systolic arterial pressure + mean transvalvular pressure) by SVi. At the time of severe LVSD, ZVa was significantly raised at 6.18 mmHg/mL/m2 indicating a high global impedance opposing ventricular ejection, absorbing most of the mechanical energy developed by the LV. On BP control, this improved to 3.3 mmHg/mL/m2. Accordingly, as symptoms and LV function improved, AVR was not required until 18 months later when he developed exertional breathlessness. Blood pressure remained well-controlled and echocardiogram showed LVEF 60%. He finally underwent a successful TAVI.


A 61-year-old woman presented to the emergency department with new-onset angina pectoris. She had a history of heterozygous familial hypercholesterolaemia, carotid artery stenosis, and CABG 3 years before the current episode (LIMA to left anterior descending artery (LAD), and sequential right internal mammary artery (RIMA) from LIMA to a ramus intermedius branch and left marginal artery). Medications before admission were losartan, amlodipine, bisoprolol, acetyl salicylic acid (ASA), ticagrelor, omeprazole, and atorvastatin. She was admitted to our hospital with unstable angina (recurrent episodes of angina on minimal effort or at rest). Blood pressure was 102/45 mmHg and heart rate was 66 beats per minute. Electrocardiographic extensive ST-segment depression was clearly documented (), but there were no segmental wall motion abnormalities on echocardiography and troponin values were 0.04 ng/mL (reference values ≤ 0.05 ng/mL). Renal function was normal (creatinine level 1.05 mg/dL; reference values 0.7–1.3 mg/dL). Physical examination showed weak pulses in the left arm and a left supraclavicular bruit. Gated myocardial perfusion scintigraphy with 99mTc-methoxyisobutylisonitrile (99mTc-MIBI gated-SPECT) was performed to demonstrate the presence and extension of myocardial ischaemia. During vasodilator stress, the patient had chest pain without ST-T changes. Gated-SPECT (non-corrected) images revealed a reversible hypoperfusion in LAD territory and several high-risk functional markers as biventricular dilation and left ventricular systolic dysfunction observed after pharmacological stress (). Invasive coronary angiography showed no changes in native coronary arteries. A retrograde blood flow was observed within both internal mammary artery grafts (; Video 1), and contrast injection into left SA confirmed a proximal severe stenosis (, Video 2). To better assess the ascending aorta and aortic arch branches, a chest computed tomography (CT) angiogram was performed. An extensively calcified ascending aorta, significant stenosis in both common carotid arteries as well as severe left SA stenosis was documented (). In a multidisciplinary heart team meeting, we decided to perform an endovascular SA repair. From right femoral and left axillary approach, a retrograde injection into the SA confirmed the stenosis severity (). Pre dilatation (Mustang balloons, 5 and 6 mm) was associated with electrocardiographic ST-segment elevation. Then, a balloon-expandable endoprosthesis (Gore Viabahn VBX, 8 × 29 mm) was deployed along the stenotic lesion. Post-procedural angiography () and chest CT angiogram () demonstrated the optimal SA dilatation with patency of LIMA and vertebral artery. There were no periprocedural complications. The patient was discharged 48 h after the procedure. The antithrombotic regimen chosen was dual antiplatelet therapy with ASA and ticagrelor for a duration of 1 year and single antiplatelet treatment with ASA afterwards. In the last medical follow-up, 5 months after hospital discharge, the patient is asymptomatic and physical examination showed symmetrical pulses in both arms and the supraclavicular bruit was not detected.


A 72-year-old man was admitted to the emergency department with a non-ST-elevation myocardial infarction (NSTEMI). He had a history of type 2 diabetes, chronic kidney disease, stent implantation in the left iliac artery 7 years previously, and chronic coronary artery disease treated with drug-eluting stents in the left circumflex artery 14 years ago, and in the right coronary artery 4 years ago. Five months before the current episode, the patient underwent CABG (LIMA to the LAD and a saphenous vein graft from LIMA to the left marginal artery). He was treated with ASA, ticagrelor, omeprazole, atorvastatin, valsartan, bisoprolol, and insulin before the current admission. He presented to the emergency department with prolonged chest pain. Physical examination was normal, and serial electrocardiograms did not show T wave or ST changes. Serum high-sensitivity troponin T level of 3270 ng/L (reference values ≤ 14 ng/L) confirmed the diagnosis of NSTEMI. Creatinine level was 1.9 mg/dL. An invasive coronary angiogram was performed and retrograde flow in both grafts was documented (, Video 3, ). A 50-mmHg pressure gradient was found across the proximal segment of the left SA. Left SA contrast injection confirmed the stenosis severity (, ). An endovascular treatment was decided in a multidisciplinary heart team. In this case, a left brachial artery approach was chosen. A Gore Viabahn VBX balloon-expandable endoprosthesis (8 × 29 mm) was implanted in the stenotic lesion () and post-dilatation was performed with a Mustang balloon (7 mm). The success of the procedure was angiographically confirmed (). There were no periprocedural complications and the patient was discharged 8 days after admission taking dual antiplatelet therapy with the intention of withdrawing clopidogrel after 12 months. Six months later, the patient is asymptomatic.


A 76-year-old man was seen in a follow-up visit. He had a history of arterial hypertension, left internal carotid artery stenosis treated with endarterectomy 3 years ago, and CABG 1 year prior to the current consultation (LIMA to the LAD and RIMA to a marginal artery). The patient was asymptomatic. He was taking ASA, atorvastatin, omeprazole, and bisoprolol. Physical examination during follow-up medical consultation revealed the absence of pulses in the left arm and normal pulses in the other limbs. A systolic blood pressure difference was found in the upper extremities (right arm: 170 mmHg, left arm: 132 mmHg; index: 0.78). A Doppler ultrasound was performed to assess the aortic arch branches detecting a retrograde flow in the left vertebral artery. Chest CT angiogram documented an 80% left SA stenosis (). Renal function was normal (creatinine level was 0.78 mg/dL). Electrocardiogram showed sinus rhythm without signs of acute ischaemia. Considering the high probability of developing future symptomatic myocardial ischaemia, we decided to perform an endovascular treatment. In this patient, a left brachial and right femoral artery approach was chosen. Retrograde subclavian injection confirmed a severe left SA stenosis (). Pre dilatation with a Mustang balloon (6 × 40 mm) was performed, and a balloon-expandable stent (Visipro 8 × 37 mm) was implanted in the SA at the site of the stenosis. Post-procedure angiographic result was optimal () with no complications The blood pressure index between the upper limbs after the procedure was 0.98. The patient was discharged 24 h after the procedure on treatment with ASA and clopidogrel. Clopidogrel was withdrawn 6 weeks later. A new chest CT angiogram performed 2 months after hospital discharge showed absence of stenosis in the left SA (). The last follow-up visit at the outpatient clinics was 10 months after discharge, the patient was asymptomatic and left arm pulses were present and symmetrical.


An 81-year-old man, former smoker, was admitted to our cardiology department for congestive heart failure with the complaint of recent onset of dyspnoea. He had a history of ischaemic heart disease with stenting of the mid-left anterior descending artery. Two months before his admission, the patient received an implantable cardioverter-defibrillator (ICD) for sustained ventricular tachycardia.
Upon arrival, blood pressure was 130/70 mmHg, heart rate 72 b.p.m., and oxygen saturation 95% with 3 L/min of oxygen. Physical examination demonstrated signs of decompensated heart failure with no evidence of any heart murmur.
The initial electrocardiogram (ECG) (Figure ) showed a sinus rhythm with abnormal R-wave progression and ST-segment elevation in leads V2–V5 and II, III, aVF, suggesting a late presentation of an acute myocardial infarction. The previous ECG, performed 2 months before, showed only negative T-waves in V2–V3 with normal R-wave progression (Figure ).
Blood tests demonstrated mild elevation of cardiac enzymes with ultrasensitive troponin I at 83 ng/L (normal <26 ng/L) and brain natriuretic peptide at 1400 pg/L (normal <100 pg/L). A moderate systemic inflammatory response syndrome was noted with an elevated C-reactive protein at 93 mg/L (normal <4 mg/L) and white blood cell counts at 14 G/L (normal <10 G/L).
As coronary angiography 2 months before, prior to his ICD implantation, had shown no new significant stenosis, it has been decided not to perform an emergency coronary angiography.
Transthoracic echocardiography (TTE) was performed and showed a known impaired left ventricular ejection fraction of 40% due to inferior and posterior wall akinesia. Transthoracic echocardiography also demonstrated a thickening or a mass of the apical and median portion of the interventricular septum (IVS) (Video 1, Figure ) measured 5 cm × 3 cm, associated with moderate pericardial effusion. Contrast-enhanced TTE using low mechanical index (MI) imaging settings (MI at 0.23) revealed a myocardial mass involving the apex of both left and right ventricles (Video 2, Figure ). Mechanical index was then decreased to 0.07 with an intermittent flash of a high mechanical index to assess the vascularization of the tumour (Video 3), demonstrating a peripheral contrast enhancement suggestive of a necrotic centre with peripheral hypervascularization, consistent with a myocardial malignant tumour (Figure ).
To better characterize the cardiac mass, cardiac CT was preferred as a second line exam to CMR, considering the recent ICD implantation. An ECG-gated cardiothoracic contrast-enhanced CT-scanner was performed (Figure ) demonstrating an important thickening of the apical part of the IVS at the arterial phase (Figure ) and moderate pericardial effusion. Delayed acquisition at 2 min confirmed an intra-septal apical mass of 6 cm × 4 cm × 8 cm with a hypodense centre and peripheral enhancement consistent with the diagnosis of a malignant tumour with a necrotic central area (Figure ).
Interestingly, cardiac-CT also revealed a voluminous mass of the lung’s left lower lobe (LLL) measured at 9 cm × 6 cm with multiple mediastinal lymph nodes and a possible left adrenal gland involvement. Computed tomography-guided percutaneous biopsy of the LLL mass demonstrated a squamous cell lung cancer (Figure ).
The final diagnosis was a Stage IVB (according to the Union for International Cancer Control) large squamous cell lung cancer possibly spreading to the heart and the left adrenal gland.
The signs of decompensated heart failure resolved after low-dose intravenous furosemide therapy and the patient was discharged home before chemotherapy with Carboplatin and Paclitaxel. He unfortunately died 2 days later at home from an unknown cause. We could not perform autopsy nor device interrogation because of the family’s opposition to further investigate the cause of death.


Our index case was a 52-year-old gentleman who presented with the complaints of gross, intermittent, and painless hematuria for 3 months. Digital rectal examination revealed a grade 1 enlarged benign prostate. On ultrasonography (USG), a cystic structure abutting the urinary bladder was seen, and right kidney was not visualized. Urine culture was sterile. Urine cytology was negative for malignant cells.
A computed tomography (CT) scan [Figure and ] revealed right renal agenesis and a tubular elongated structure extending from the right renal fossa to the pelvis 21 cm long and 6 cm wide closely abutting the urinary bladder. The distal end of the lesion was opening into the right SV. Hyperdense calcified structures were seen in the distal portion of the lesion. A cystopanendoscopy was done as a part of work up for hematuria []. Urethra and verumontanum were normal. No abnormal opening or utricle was appreciated on the verumontanum. There was a Grade II enlargement of the prostate and a high bladder neck. Prostatic urethra was deviated to the left. Right ureteric orifice was not visualized, and an indentation was noted on the right lateral wall. Bladder mucosa was healthy. A magnetic resonance (MR) urography [Figure and ] was also performed to better characterize the lesion before taking up the patient for invasive surgery. It revealed the findings of a large cyst with blood content within and an absent right kidney. The lesion was seen communicating distally with one of the cysts of the right SV. Right ejaculatory duct was prominent with its distal end in close proximity with urethra. With a diagnosis of Zinner syndrome in mind, the patient was planned for the excision of the large cyst in view of persisting hematuria. The patient underwent a prior cystopanendoscopy and bladder neck incision in view of high bladder neck. The cyst was removed with a robot-assisted laparoscopic approach. The console time was 110 min with minimal blood loss. Cutting the cyst open revealed hemorrhagic fluid and the diagnosis of stones within the cyst was confirmed. There were multiple stones with spiky configuration []. Histopathology of the cyst wall revealed chronic inflammation. The postoperative course was uneventful, and the patient was discharged on the second day. On 6 months follow-up, patients doing well.


A 7-year-old girl (15 kg), known case of AAS (FDG1 mutation as per documents) presented in emergency with traumatic corneal perforation and subsequently was posted for corneal repair surgery []. On examination, she had short stature (100 cm), clinodactyly, hypertelorism, high arched palate, macroglossia, irregular dentition, receding mandible, mild mental retardation and a 7 mm atrial septal defect (2D echo) []. There were no other fresh complaints and present biochemical investigations were with in normal limit. She had taken her last meal 3 hours back, so we waited for the next 5 hours for her fasting status to complete. In past history, she had episodes of repeated pneumonias in her early childhood with repair of right-sided diaphragmatic eventration at 2 years of age. At present, she had no complaint of respiratory tract infections or signs of respiratory compromise and had good functional capacity as per parents (METS >4).
Surgery was planned under general anaesthesia with controlled ventilation after completing an adequate NPO status (8 hours) and keeping in mind the coexisting conditions of child. We had kept a difficult intubation cart ready. Induction of anaesthesia was done with inj. Fentanyl 30 mcg and inj. Propofol 30-40 mg intravenously. After ensuring an adequate bag and mask ventilation inj. vecuronium 1.5 mg was administered. We secured the airway with PLMA# 2 (second generation supraglottic device) and ensured an optimal ventilation. However, soon after securing airway food particles were encountered in orogastric tube inserted via gastric drain tube of PLMA. An immediate head low was done and a continuous suction was attached to orogastric tube to decompress gastric contents. Under continuous suction and direct vision using a videolaryngoscope PLMA was removed and trachea was secured with cuffed ETT #5. Patient's vital remained stable and surgery was proceeded with following which child was extubated successfully. Intraoperative and postoperative period was also uneventful. On regular follow up in our hospital, child was later found to have a hiatus hernia.


A 19-year-old pregnant female at approximately 17 weeks gestation presented to the emergency department with headache, nausea, and emesis while at school. Initial neurosurgical evaluation in the ED demonstrated an awake and drowsy patient with Glasgow Coma Scale of 12 with a breakdown of E2 M6 V4 and plegia of her left upper and lower extremities. Initial computed tomography (CT) scan [] demonstrated a right-sided frontal-parietal intra-cerebral hemorrhage (ICH) measuring 5.5 cm × 7.7 cm with intraventricular extension and 8 mm of leftward midline shift. There was also a 2.5 cm × 3.5 cm partially calcified high attenuation lesion concerning for a varix or aneurysm. CT angiogram [] demonstrated a right fronto-parietal PAVF with dilated venous angioma and superficial cortical drainage in the parafalcine area with no discrete nidus. In the right temporal lobe, there was a suspected PAVF along the right M3 division of the middle cerebral artery (MCA) with a large venous varix with both superficial and deep drainage into the basal veins of Rosenthal and right sphenoparietal sinus and right transverse sinus.
The patient developed persistent vomiting and was intubated for airway protection prior to being brought to the endovascular suite for diagnostic digital subtraction angiogram (DSA). DSA confirmed the CTA findings and showed that the right fronto-parietal PAVF feeding vessels were from the left pericallosal artery and draining into the superior sagittal sinus along with a steal phenomenon with retrograde flow through the right anterior cerebral artery [Figure and ]. The right temporal lesion showed early venous filling of the large varix with no discernible feeding vessel aneurysm [Figure and ]. Vertebrobasilar injection demonstrated additional recruitment through a right posterior cerebral artery P3 segment supplying the right temporal PAVF [].
The patient did not require ventriculostomy and continued to follow commands throughout hospitalization and self-extubated without complication 7 days after presentation. On postbleed day 14, she was taken back to the neuroangiography suite for Onyx embolization of the right fronto-parietal feeding vessels followed by craniotomy for resection of this lesion and hematoma evacuation [Figure , and ]. During resection, an arterialized vein of Trolard was encountered and this turned blue in color after ligation of the PAVF. She tolerated the procedures well and was extubated on postoperative day one. Postoperative magnetic resonance imaging showed good evacuation of hematoma with reduced mass effect and midline shift []. She and her fetus continued to be stable and she was discharged to the physical medicine and rehabilitation service on postoperative day five.
During initial DSA as well as treatment angiogram, a lead apron shield was used over the patient's abdomen to reduce the radiation exposure to her fetus. The patient received a total dose of 784.3 mGy (milli-gray) during the DSA and 11 days later 1991.0 mGy during the embolization procedure.
The obstetrics team was involved at the time of admission and followed along with weekly Doppler tones and providing medication recommendations during the initial admission. During outpatient follow-up, we recommended consideration of urgent C-section due to hypervolemia gravidarum and increased headaches after a clinic visit at 33 weeks gestation to prevent rupture of the second PAVF. The patient went on to deliver via low transverse cesarean section at 35 weeks and 3 days gestation to a healthy girl with Apgar scores of 6 and 8 at birth.
Five months after delivery of her baby, the patient returned for elective staged embolization of the right temporal PAVF Figure -]. The procedure required a combination of Onyx embolization of PCA feeding vessel and coil embolization of venous varix from the right MCA branches. No complications occurred and the patient returned the following day for the second stage embolization of the MCA feeding vessels with Onyx. There were no complications after the procedure and she was discharged home after monitoring for 48 h. At 6 months postembolization, an angiogram was performed which showed complete obliteration of the giant right temporal PAVF and the right frontoparietal PAVF []. She recovered to a modified Rankin score of two and was ambulatory with a left ankle-foot orthosis with a left foot drop as only significant residual motor deficit.


A healthy, active woman in her 70s with a remote history of provoked pulmonary embolism presented to her primary care physician (PCP) with 2–3 months of dyspnoea on exertion during the COVID-19 pandemic. The patient is an active open-water swimmer and initially noticed reduction in exercise tolerance, both in the water and when walking up inclines, which she attributed to deconditioning. She also endorsed palpitations and occasional dizziness, but denied chest pain, cough, fevers, syncope and dyspnoea at rest. She had no recent surgery, periods of reduced mobility or known history of malignancy. However, she had a history of provoked pulmonary embolism in the setting of air travel 3 years prior, for which she had completed 3 months of dabigatran. The initial evaluation for this current episode was conducted through secure video visit as in-person visits were limited during the early COVID-19 pandemic. Through video, the PCP noted no acute distress and no laboured breathing.


A 67-year-old Caucasian male with a history of non-insulin-dependent diabetes mellitus and ocular rosacea presented with complaints of chronic facial edema and erythema. The facial edema had begun 4 years previously. The Patient denied a history of acne vulgaris. Physical examination revealed periorbital and maxillary facial edema with associated erythema extending over the malar region (). A 4-mm punch biopsy showed mild spongiosis with peri-adnexal mixed infiltrate and dermal edema (). The dermis showed perivascular and perifollicular lymphoplasmacytic inflammation, solar elastosis, and superficial dermal telangiectasia. No granulomata were observed. Colloidal iron and periodic acid–Schiff (PAS) stains were negative. The patient was initially treated with a regimen of 2.5% hydrocortisone cream, brimonidine 0.33% topical gel, and metronidazole gel. His treatment regimen was later expanded to include 100 mg doxycycline twice daily. This treatment regimen resulted in documented improvement at 3 months following doxycycline initiation with disease resolution at one-year follow-up.


A 50-year-old Caucasian male with a past medical history significant for latent autoimmune insulin-dependent diabetes mellitus, rosacea, and acne vulgaris presented with chronic periorbital edema (). He previously endorsed the presentation of reddish papules in conjunction with swelling that had resolved with oral antibiotic treatment. Physical examination revealed facial edema localized to the right periorbital region and several flesh-colored nodules along the right mandible. A 3-mm punch biopsy showed dermis with perivascular and perifollicular lymphoplasmacytic inflammation, solar elastosis, and superficial dermal telangiectasias (). No granulomata were observed. Colloidal iron and PAS stains were negative. The patient was started on doxycycline 100 mg twice daily and once-weekly topical permethrin with partial improvement at 3 months. At this time, permethrin was discontinued and brimonidine 0.33% topical gel and 2.5% hydrocortisone cream were added. Following three additional months, the patient noticed a majority clearance and resolution of edema and erythema. At 1-year follow-up, there was complete resolution of disease with no documented recurrence.


A 43-year-old woman presented at a local hospital with the chief complaint of fatigue for a month. Routine peripheral blood examination showed white blood cell count (WBC) 2.61*10^9/L, red blood cell count (RBC) 2.36*10^12/L, hemoglobin level (Hb) 83 g/L, and blood platelet count (PLT) 147*10^9/L. But no diagnosis and treatment were made. The fatigue increased progressively for half year. Then the patient took a visit to the hospital and was recommended to the department of hematology. Physical examination results were unremarkable, with no hepatosplenomegaly or lymphadenopathy. Peripheral blood was WBC 11.86*10^9/L, Hb 58g/L, RBC 1.37*10^12/L and PLT 58*10^9/L. Peripheral smear showed 11% blasts. Bone marrow aspirate smears were hypercellular with 54% lymphoid blasts. The blasts exhibited round-like shape in medium sizes, with less cytoplasm and granules in the cytoplasm. Burr like or pseudopod like protrusions and tailing could be seen in most of the cytoplasm. Scattered plasma plasmids, round like nucleus and coarse granules of chromatin could be seen, and 1 to 2 clear nucleoli could be seen in some of the cytoplasm. Auer rods could not be seen in the blasts. Cytochemistry revealed these blasts were negative for POX (peroxidase) staining (). In flow cytometry (FCM), the results were obtained by a FACSCanto II dual laser six color flow cytometer (Becton Dickinson, CA, USA) in a panel with 32 markers. The immunophenotypes of lymphoid blasts were displayed as CD7, CD117, CD34, CD33, CD38, CD3(dim), cytoplasmic CD3, and negative for TDT, CD123, CD36, HLA-DR, CD64, CD11b, CD13, CD16, CD14, CD15, CD64, CD11c, CD4, CD5, CD8, CD10, CD19, lambda, kappa, CD20, CD22, MPO, CD1a, CD99, CD2 (). The FCM findings fulfilled ETP-ALL criteria. 4/10 of metaphase chromosomes had an abnormal karyotype with a +4; 6/10 of chromosome karyotypes were 46 XX; Breakpoint cluster/Abelson tyrosine kinase (BCR/ABL) fusion was not detected by Fluorescence in situ hybridization (FISH). The next generation sequencing (NGS) was based on Illumina nextseq high-throughput sequencing platform. A Ph-like gene panel was used for NGS (). The NGS demonstrated mutations in FLT3-ITD, PAX5, IL7R, SH2B3, and other genes were negative (). The patient received hyper-CVAD (six doses of intravenous (IV) 300 mg/m2 cyclophosphamide over 3 hours every 12 hours on days 1 through 3, 2 mg of IV vincristine on days 4 and 11, 50 mg/m2 IV doxorubicin on day 4, and 40 mg of dexamethasone daily on days 1 through 4 and 11 through 14) chemotherapy but the treatment course was complicated by neutropenic fever. The chemotherapy failed. The peripheral blood and bone marrow aspirate smears did not indicate complete remission. Bone marrow assessment at day +14 showed 25% blasts. Then, the patient was given the second cycle of chemotherapy with FLAG-IDA regimen (25 mg/m2 IV fludarabine x 4 doses daily, 2 g/m2 IV cytarabine [Ara-C] on day 1, 10 mg/m2 IV idarubicin x 3 doses, 5–10 μg/kg granulocyte-colony stimulating factor [G-CSF] daily on days 0 through 5]) was given, combined with FLT3 inhibitor sorafenib (400 mg po bid) from day +8. The patient showed complete response (CR) and minimal residual disease (MRD)-negative. Then the patient received prophylactic intrathecal methotrexate (MTX) and Ara-C. After 2 courses of FLAG-IDA, the MRD maintained negative and FLT3-ITD mutation became negative. Subsequently, sorafenib was continued until a myeloablative (human leukocyte antigen) HLA-matched sibling donor allo-HSCT was performed. The bone marrow still remained CR, MRD-negative, and FLT3-ITD negative at current 12 months after transplantation.


A previously healthy 39-year-old Hispanic male presented with flu-like symptoms, including headache, fatigue, and myalgia for 8 days. He had no significant prior past medical history, never smoker, and took no medications. Progressive flu-like symptoms and new development of cough and chills prompted the patient to present to the hospital in late April 2020. He denied dyspnea on exertion, nausea, vomiting, diarrhea, or exposure to sick contacts. He lived at home with his girlfriend, who had no symptoms. He denied any alcohol, tobacco, or illicit drug use.
The patient presented to a level III trauma center. On presentation, physical examination was notable for a fever of 102.6°F, heart rate 133 beats/min, blood pressure 118/76 mmHg, respiratory rate 20 breaths/min and oxygen saturation 94% on room air. The patient was not in distress, but was warm to touch. Diminished vesicular breath sounds were present in all lung fields. Approximately 3 hours later, oxygen saturation decreased to 89% on room air, requiring oxygen supplementation via nasal cannula. Initial laboratory findings showed white blood cell count 7.8 K/uL, venous blood gas pH 7.37 and PaCO2 44 mmHg, ferritin 635 ng/ml, lactate dehydrogenase (LDH) 395 U/L. Chest x-ray showed multifocal infiltrates and the patient tested positive for SARS-CoV-2 RNA by real-time polymerase chain reaction testing. Blood and sputum cultures were negative. Echocardiogram revealed a left ventricular ejection fraction of 65%. The patient was admitted for acute hypoxic respiratory failure and sepsis secondary to COVID-19 pneumonia and was started on intravenous fluids, azithromycin and ceftriaxone.
Two days later, the patient developed respiratory distress, initially requiring high flow nasal cannula oxygen and subsequently intubation due to increased work of breathing. He was placed on lung protective ventilation, for which he received neuromuscular blockade and sedation. The patient was diagnosed with severe ARDS and was ventilated in the proned position on two separate occasions with progressive worsening PaO2/FiO2 ratios (initially 131 and finally 83). In addition to convalescent plasma, the patient received 40 mg methylprednisolone IV twice daily and 40 mg subcutaneous enoxaparin twice daily.
On hospital day 6, the patient developed worsening ARDS, remaining hypoxic despite 100% FiO2. Laboratory results showed increased inflammatory markers, including interleukin-6 (IL-6) 10 pg/ml, ferritin 1432 ng/ml, d-dimer 3670 ng/ml, LDH 1100 units/L, C-reactive protein (CRP) 35.1 mg/dl. Due to refractory hypoxia despite maximal therapy, the patient was transferred to a quaternary care referral center and was started on VV-ECMO on hospital day 7. Chest x-ray showed persistent bilateral multifocal infiltrates and chest computerized tomography (CT) scan showed diffuse lung opacities ( and ). His hospital course was complicated by delirium, Enterococcus faecalis bacteremia, and a non-occlusive deep vein thrombosis in the inferior vena cava (IVC) thrombus near the previous VV-ECMO site. He underwent a tracheostomy on hospital day 36. The patient slowly improved and was decannulated on hospital day 42, after 35 days on VV-ECMO. The following day, the patient was placed on mechanical ventilation via pressure support ventilation 8/8 cm H2O and tolerated tracheostomy collar the next day.
The patient tested negative for SARS-CoV2 on hospital days 30, 39 and 58. His overall clinical presentation significantly improved; he passed a speech-language assessment and was able to tolerate oral diet without signs of aspiration. CT chest on hospital day 58 showed significant improvement of the bilateral opacities compared to hospital day 25 (). The patient received aggressive daily rehabilitation treatment with physical therapy (PT) and occupational therapy (OT). By the time of discharge, PT and OT deemed that he was able to ambulate independently and perform all activities of daily living (ADLs) independently. Tracheostomy was decannulated on hospital day 62. The patient was discharged home without oxygen supplementation on hospital day 63 ().
Follow-up CT chest imaging showed complete resolution of the bilateral multifocal opacities 20 days after discharge (). Additionally, the patient’s SARS-CoV-2 test remained negative 17 days and 43 days post-discharge. The patient continues to do well and has returned to his baseline with respect to the activities of daily living as of 4 months post-discharge free of respiratory symptoms or complications.


An 81-year-old male with a past medical history of hypertension, diabetes mellitus type 2, coronary artery disease, atrial fibrillation, and myasthenia gravis presented to the hospital with complaints of left-sided abdominal pain for few hours. He denied any trauma or fall. The abdominal pain had an intensity of 6 out of 10 on the pain scale, with no aggravating or relieving factors. It was associated with dry cough without any fever. He underwent left main coronary artery stenting 60 days prior to the presentation and was taking apixaban, clopidogrel, and aspirin for the management of the atrial fibrillation and coronary artery disease. He had minimal left upper quadrant tenderness on palpation without any guarding or rigidity. A CT of the abdomen () revealed splenic laceration, hemoperitoneum, and grade 2 perisplenic hematoma according to the American Association for the Surgery of Trauma splenic injury scale. Serum hemoglobin ranged from 8.1 to 9.3 g/dL throughout the hospital stay. He was monitored in the critical care unit for hemodynamic instability and surgical intervention was deferred due to stable hematoma. The patient’s apixaban, aspirin, and clopidogrel were held during the hospital stay. Repeat CT of the abdomen showed interval resolution of the perisplenic hematoma. At discharge, only clopidogrel was resumed.


A 55-year-old woman was admitted to our hospital with a history of recurrent upper abdominal pain for 1 year. The patient had no symptoms of fever, nausea, vomiting, or weight loss.
The patient’s symptoms started 1 year ago, with recurrent episodes of upper abdominal pain that were relieved spontaneously.
The patient had no previous medical history.
The personal and family history was unremarkable.
The patient’s physical examination was unremarkable.
The laboratory findings, including liver function tests and tumor markers (carcinoembryonic antigen, alpha fetoprotein, and carbohydrate antigen 19-9), were all within normal limits.
On computed tomography (CT) (Figure ) and magnetic resonance imaging (Figure ), a large mass with contrast enhancement was observed in the descending part of the duodenum. On magnetic resonance cholangiography (Figure ), no cut-off sign or stricture was found on either the bile duct or pancreatic duct except for a mild dilation of the common bile duct.
EGD revealed a 3.5-cm-sized villous growth over the major duodenal papilla (Figure ). Pathology of the endoscopic biopsy indicated a villous adenoma with low-grade dysplasia.


A 75-years-old man presented to the emergency room of our hospital with a 4-day history of fever and dyspnea. His medical history was unremarkable. On admission (day 1), he had a temperature of 38°C, normal blood pressure (130/80 mmHg), and heart rate (80 bpm in SR). His physical examination was unremarkable, with normal breath sounds at lung bases. Continuous positive airway pressure (CPAP) was started (days 1, 2, and 3) as he was hypoxic with SpO2 of 88% in ambient air. In consideration of the local coronavirus epidemic outbreak, nasopharyngeal and oropharyngeal swabs were immediately obtained, confirming SARS CoV-2 positivity. The patient underwent orotracheal intubation plus invasive mechanical ventilation (day 4) because of worsening respiratory status. Chest high-resolution computed tomography (HRCT) [, Panel A] documented bilateral ground-glass opacities (GGOs) suggesting interstitial inflammatory lung disease. ECG (, Panel B) showed sinus rhythm with heart rate of 102 bpm, a new onset left bundle branch block with QRS duration of 128 ms and QTc of 414 ms. The high-sensitivity troponin T curve was 14-27–15 pg/mL (normal value <14), N-terminal pro-BNP (NT-proBNP) was 450 pg/mL (normal value <153), and C-reactive protein was 33 mg/L (normal value <6). Markers of coagulation showed a prothrombotic status confirmed by a high D-dimer (peak of 16.6 mcg/mL-normal value range: 0–5), high fibrinogen level (peak of 791 mg/dL; normal value range: 200–400), platelet count of 269 × 109 U/L, and an aPTT of 35.3 s (normal range: 30–40 s).
The initial ventilation parameters were volume ventilation with tidal volume 6–8 ml/kg, according to acute respiratory distress syndrome guidelines, positive end-respiratory pressure (PEEP) 14 cmH2O, FiO2 55%, and driving pressure <15 cmH2O.
Invasive hemodynamic monitoring indicated worsening cardiac status with a reduced cardiac output index of 2.9 L/min/m2, extravascular lung water index of 7 mL/kg, and a global end-diastolic volume index of 713 mL/m2. Dobutamine support was added to therapy to maintain the cardiac index above 3 L/min/m2.
Transthoracic echocardiogram (TTE) showed a mild left ventricular systolic dysfunction (left ventricular ejection fraction [LVEF] 45%), normal right ventricular function without chamber dilation, and normal valves. There was a small pericardial effusion (max 10 mm in diastole) anteriorly with an elongated (0.5 × 2 cm) and mobile clot [, Panel C, D]. There was near-complete resolution of the clot after therapy with 10 days of enoxaparin (1 mg/kg BID) along with lopinavir/ritonavir (400 mg BID), hydroxychloroquine, and metilprednisolone 1 mg/kg OD. The patient was extubated on the 17th day after intubation. He was on noninvasive ventilation and high-flow nasal cannula (HFNC) for 15 days and the final outcome was favorable.
At 6-month follow-up, the patient was in good conditions; HRCT demonstrated a complete resolution of lung lesions and the pericardial clot was significantly reduced in size on TTE, but it was still present.


A 68-year-old man presented to the the emergency system with severe dyspnea and hypoxia (SpO2: 87% in ambient air). His past medical history was significant for hypertension, obesity, diabetes, and chronic renal failure. On admission (day 1), he had a temperature of 39°C, high blood pressure (170/100 mmHg), and heart rate (110 bpm in sinus rhythm (SR)). Diffuse breath sounds (rales) were found on both lung fields and the chest HRCT [, Panel E] revealed bilateral GGOs consistent with interstitial inflammatory lung disease. Nasopharyngeal and oropharyngeal swabs were immediately obtained, confirming SARS-CoV-2 positivity. After a CPAP attempt (days 1 and 2), the patient was intubated (day 3) with ventilatory support parameters demonstrating a high (PEEP of 15 cm H2O), FiO2 80%, and driving pressure <15 cmH2O. Serum creatinine increased to 2.3 mg/dL (glomerular filtration rate of 31 mL/min), leukocytes were 8.3 × 109 U/L, lymphocytes were 0.9 × 109 U/L, and hemoglobin was 9.3 g/dL. The high-sensitivity troponin T curve was 59-43–35 ng/L (normal value <14), NT-proBNP reached to 10.650 pg/mL (normal value <153) and C-reactive protein peak was 29 mg/L (normal value <6) with procalcitonin peak of 6.3 ng/mL (normal value range: 0–0.15). Interleuchin-6 values were 91.83 pg/mL and 37.63 pg/mL and he was treated with intravenous tocilizumab. Coagulation markers demonstrated a pro-thrombotic status with a platelet count of 160 × 109 U/L, D-dimer of 17 mcg/mL, fibrinogen of 656 mg/dL, and an aPTT of 33.8 s. ECG [, Panel F] showed atrial fibrillation with high heart rate (111 bpm), mild ST depression, inverted T waves in V4–V6, and a QTc of 437 ms. TTE revealed a moderate left ventricular systolic dysfunction (LVEF 40%) with a mildly dilated left ventricle (end-diastolic diameter of 61 mm), normal right ventricle in size and function, and normal cardiac valves. There was a moderate pericardial effusion, anterior to the right ventricle (maximum 15 mm in diastole). A mobile and elongated (0.3 × 4 cm) clot was noted within the effusion (Panel G). The patient was treated with lopinavir/ritonavir (400 mg BID), hydroxychloroquine (200 mg BID), and enoxaparin (1 mg/kg BID). Metilprednisolone (1 mg/kg OD) was added (day 6) together with beta-blockers, diuretics, and nitrates. Due to persistent atrial fibrillation, enoxaparin was switched to edoxaban (30 mg OD) on day 9. To date (day 15), the clot continues to decrease as seen on the chest HRCT (Panel H).
The prone position was used for the first four nights in the ICU. He was extubated the 15th day after intubation; noninvasive ventilation and HFNC were used the following days to optimize oxygenation.
At 6-month follow-up, the patient was in good conditions, lung lesions appeared reduced on chest HRCT, but at TTE pericardial clot appeared unchanged [].


A 45-year-old male patient presented to us who required extraction of tooth #8 due to symptoms of gingival inflammation, oral fistula with exudate underpressure, pain, and discomfort for weeks before. On clinical examination, there were swelling, redness, and deep probing of 10 mm in the vestibular zone with purulent liquid originating from the crevicular sulcus; a scar area was observed along the attached gum, which is the product of a previous surgery. Periapical X-ray showed an enlargement of the periodontal ligament in the apex. Apical filling with an alloy metal was observed without relief of symptoms. Imageology examination was complemented with cone-beam computed tomography of the zone, showing a huge zone of bone loss in three-dimensional (3D) aspects of tooth #8. In addition, severe bone loss was observed. Tooth #8 was diagnosed as a chronic periodontal abscess,[] with a bad prognosis []. After the patient signed the informed consent, the surgical intervention was carried out. A Newman flap was designed for the extraction of # 8, the area was detoxified with tetracycline after tooth extraction and irrigated with saline solution to eliminate remaining infected tissue. Once it was confirmed that the buccal wall presented a perforation accompanied by bone loss, the area was filled with particulate xenograft of with particulate xenograft (LuminaBone by Criteria Inc) and a platelet-rich fibrin membrane was placed. A suture with nylon 6-0 was allowed to close the socket, and a hemostatic was used, followed by a aesthetic temporary restoration []. The extracted tooth showed signs of apical corrosion due to retrograde filling and multiple lines of fracture at the root. Finally, the patient was prescribed oral capsules of amoxicillin 500 mg and nimesulide tablets 100 mg. Control at 8 days and 6 weeks showed good stability of the tissues around the graft and good functional and esthetic condition of the temporary bridge []. The cone-beam tomography showed a bone neoformation at 4 months, with an increase in vestibular bone volume even with the immature bone. The clinical findings accompanied the results in the tomography []. After 8 months of follow-up, there is no relapse of abscess or inflammation in the surgical zone. The gingival tissue showed good healing and the regenerated bone volume was confirmed with CBT.


In October 2016, a 47-year-old man presenting with stroke syndrome was diagnosed with right frontoparietal infarct and multi-territory foci on magnetic resonance imaging-brain. Past medical history was notable for mitral valve (MV) repair in 2009 and current medications included Clopidogrel 75 mg and Omeprazole 20 mg once daily. There was no history of constitutional symptoms, and screening investigations for a central embolic source were normal. Outpatient transoesophageal echocardiography (TOE) was therefore planned.
TOE in December 2016 showed a strand-like structure (<10 mm) associated with a competent MV repair (, Video 1); he was admitted to differentiate IE from thrombus. He was afebrile with no significant findings on examination and normal inflammatory markers [white cell count (WCC) 7.3 ×109 g/L and high sensitivity C-reactive protein (CRP) <5 mg/L]. Four sets of peripheral blood cultures were sterile. Serology for Coxiella, Bartonella, Brucella, Syphilis, and an autoimmune screen was negative; whole blood polymerase chain reaction (PCR) is not performed in our Trust due to low sensitivity. 18F-fluorodeoxyglucose positron emission tomography–computed tomography (CT-PET) showed focal posterior mitral annular uptake, typical for IE (). IE was possible by mDC [one major plus two minor; possible vegetation on TOE (major), MV repair as a predisposing risk factor (minor) and multi-territory stroke as embolic phenomena (minor)] and so the Endocarditis Team recommended repeat TOE in 2 weeks, anticoagulation and Flucloxacillin, Benzylpenicillin, and Gentamicin for culture negative prosthetic valve IE (PVE). After 2 weeks however, the clinical team noted the negative blood cultures, persistently normal inflammatory markers and apyrexia; antibiotics were stopped and the patient anticoagulated with Apixaban 5 mg twice daily for valve thrombus.
Four days later, he re-presented with self-resolving objective facial and limb weakness. He remained apyrexial with normal inflammatory markers (WCC 7.7 ×109 g/L and CRP <5 mg/L). His mDC score was unchanged, but given recurrent embolic phenomena, inspection of the MV repair and resection of the underlying cause was mandated.
Intraoperative findings were of an irregular mass attached to the posterior mitral annuloplasty ring. There was regional dehiscence with areas of necrotic tissue suggestive of PVE. A 29 mm Carbomedics valve was implanted. Direct valve culture grew fully sensitive Streptococcus sanguinis on enrichment and was considered significant. Cutibacterium acnes ribosomal DNA (rDNA) was identified on 16S molecular testing and deemed a contaminant. Given the intraoperative findings, the previous antibiotics were recommenced for 2 weeks followed by 4 weeks of intravenous outpatient Ceftriaxone monotherapy.
In August 2018, 18 months later, he presented to his local hospital complaining of post-syncopal right frontal headache, diplopia, and transient left arm paraesthesia; stroke was confirmed on CT-Head. Since discharge, he had been diagnosed with presyncope secondary to 2:1 and 3:1 atrioventricular block and had been listed for pacemaker implantation.
He was apyrexial, had no significant findings on examination and near normal inflammatory markers (WCC 6.9 ×109 g/L and CRP 7 mg/L), and a normal electrocardiogram. His medications included: Warfarin [target INR (international normalized ratio) 2.5–3.5], Omeprazole 40 mg, Candesartan 4 mg, Atorvastatin 40 mg once daily. Given his previous history, he was transferred for urgent imaging at Barts Heart Centre. TOE was concerning for a small indeterminate lesion (10 mm) associated with the posterior MV replacement (MVR), with normal valve function (, Video 2). IE was initially possible by mDC [one major plus two minor; possible vegetation on TOE (major), MVR and previous PVE as predisposing risk factors (minor) and multi-territory stroke as embolic phenomena (minor)], but prolonged incubation of the blood cultures grew fully sensitive C. acnes (2/6 bottles), and was considered significant given the previously disregarded 16S findings. Focal avidity of the posterior MVR was demonstrated on repeat PET-CT (). Interval TOE at 1 week showed progression of the suspicious lesion to an 11 × 6 mm mobile vegetation attached to the posterior annulus, with good excursion of the disc and only trivial paravalvular regurgitation (, Video 3). The Endocarditis Team opted to manage the case medically with a 6-week course of Benzylpenicillin and Rifampicin. Fortnightly TOE was planned to monitor progress of the vegetation, given absence of elevated biomarkers. There were no surgical indications, and redo surgery was deemed high-risk given two previous sternotomies.
Sequential TOE showed progressive reduction and ultimately resolution of the vegetation. Throughout his 8-week admission, he remained well, with WCC 4.1–7.3 ×109 g/L and CRP <5 mg/L. Following 6 weeks of intravenous antibiotics, he was discharged on a 6-month course of oral Amoxicillin 3 g daily to complete treatment. Cardiac monitoring showed only Mobitz Type I heart block. Given the concurrent IE, pacemaker implant was deferred and an implantable loop recorder inserted. Endocarditis Clinic follow-up has been per protocol at 1, 3, 6, and 12 months, with TOE given the previously absent inflammatory response. This has been unremarkable for recurrent infection and embolic phenomena as of April 2021.


A 50-year-old male, smoker and hyperlipidemic was hospitalized with anterior STEMI in a second level center. Emergency coronary angiography revealed subocclusion of the proximal left anterior descending coronary artery and subcritical disease of the mid and distal segments of the vessel. Primary PCI was performed with implantation of a metallic zotarolimus-eluting stent (ZES) (Resolute Onyx 2.75 × 18 mm, Medtronic, Santa Rosa, CA) (Figure ). Ten days later, the mid and distal diseased segments of the LAD were treated with elective implantation of two everolimus-eluting BVS (Absorb 2.5 × 28 mm + 2.5 × 12 mm, Abbott Vascular, Santa Clara, CA), while a metallic everolimus-eluting stent (EES) (Sinergy 2.75 × 28 mm, Boston Scientific, San Josè, CA) (Figure ) was deployed proximally to the BVS. Intravascular imaging was not performed at that time.
At 4-month follow-up, the patient was referred to our center because of chest pain at rest. Coronary computed tomography angiography (CCTA) showed patency and correct apposition of both metallic drug-eluting stents and BVS with normal lumen appearance (Figure ).
After 9 months, he was admitted to our emergency department because of recurrent chest pain. A rise of high-sensitivity troponin prompted urgent coronary angiography that showed multiple saccular CAA involving the mid and distal segments of the LAD previously treated with the BVS (Figure ). Intracoronary imaging with OCT (OPTIS Integrated System and DragonFly Imaging Catheter, Abbot Vascular, Santa Clara, CA) confirmed the presence of multiple aneurysmal dilations surrounding the central portion of the BVS and showed unopposed and floating polymeric struts (Figure ). A small aneurysm was also visible at the level of the metallic EES. We decided for a conservative approach and indefinite dual antiplatelet therapy (DAPT) was prescribed to prevent thrombus formation.
Although the patient had no symptoms, a follow-up coronary angiography was performed 27 months after the index PCI. The exam showed that the CAA had significantly increased in diameter and longitudinal extension (Figure ). In view of the progressive growth and the perceived risk of thrombosis, we decided to proceed with a percutaneous treatment.
Via a radial access, a 6 F large lumen guide catheter was positioned in the left main coronary artery and a guide extension (GuideLiner, Vascular Solutions, Sycamore, MN) was advanced to the mid LAD in order to achieve good back-up support and to provide adequate blood exclusion required for OCT imaging. The OCT scan showed that BVS geometry was preserved at the distal edge with complete endothelialization, while further CAA enlargement was visible in most of the BVS-treated segment. In this segment, partial strut degradation interspaced with residual struts embedded in the arterial wall was also observed. Restenosis at the overlap between the BVS and the EES was also visible (Figure ). Furthermore, focal vessel ectasia persisted around the EES, while the ZES was completely opposed to the coronary artery wall. Considering that no major side branches took off from the coronary segment with multiple CAA, we decided to treat the patient with polyurethane membrane covered stent implantation (PK Papyrus, Biotronik, Bulach, Switzerland). The length of the aneurysmatic vessel segment was assessed with OCT automatic longitudinal reconstruction and measured 42.6 mm, which is longer than the maximal length of the available Papyrus covered stent (26 mm), thus requiring implantation of two devices. Our concern was the risk of articulation and dislodgement of the overlapping Papyrus covered stents due to the lack of apposition and anchoring inside the large aneurysmal segment., Therefore, we first deployed a long metallic EES (2.5 × 48-mm, Xience Xpedition; Abbot Vascular, Santa Clara, CA) across the CCA that was anchored to the proximal and distal ends of the aneurysmatic segment. We then implanted two Papyrus covered stents inside the metallic EES (2.5 × 20-mm + 3.0 × 26-mm) with approximately 3-mm overlapping. Finally, postdilation with 2.5 × 15-mm and 3.0 × 15-mm NC balloons at 20 atm was performed. Complete CAA exclusion without leaks was confirmed with angiography (Figure ), while OCT showed complete covered stent expansion with a minimal stent area of 5.48 mm2 and a minimal lumen diameter of 2.64 mm (Figure ).
The patient was discharged the following day with life-long DAPT. At 10-month follow-up after covered stent implantation, he was asymptomatic and CCTA showed vessel patency, no dislodgment of covered stents, and persistence of CAA exclusion (Figure ).


A 14-year-old boy was presented in outpatient department with severe kyphotic deformity of the thoracic spine and complete loss of power of both lower limbs. The patient had a history of a progressively increasing kyphotic deformity since the age of 4 years, almost 4–5 months back, he started developing weakness of both legs.
On physical examination, bossing of the thoracic cage was observed with short abdomen and both iliac crest almost touching the ribs []. There was a prominent kyphotic hump at the thoracic level, the lower extremities had 0/5 power bilaterally along with spasticity. Reflexes of knees and ankles were exaggerated and Babinski sign was positive. Flexion contracture of 40° was observed in both knees.
Radiographic picture of spine showed severe kyphosis of 141° from T1 to T10 thoracic vertebrae on lateral view with diffuse paraspinal calcifications, most likely representing a granulomatous lesion [Figure1b]. MRI revealed acute angle kyphotic deformity appreciated at the upper-mid dorsal spine due to multiple deshaped dorsal vertebrae (starting from T1 down till T10), resulting in significant canal narrowing posteriorly with cord compression and compressive myelopathic changes. Abnormal marrow signals were appreciated in vertebrae with pathological reduction in their heights, with indistinct/eroded adjacent end plates and involved intervening discs, suggesting squeal of chronic disco vertebral osteomyelitis (caries spine).
Pathological necrotic tissue was also appreciated in pre- and paravertebral spaces at the affected levels. Similarly, variable sized paraspinal collections were identified with areas of low-intensity signals/signal void suggested chronic calcified component []. Blood work-up was within normal limits.
Distraction using a modified halo-pelvic distraction assembly was planned to stretch out the soft tissues aiming to decrease the severity of the deformity and compression on the spinal cord and to improve the neurology.
An assembly was prepared with the following modifications:
Pelvic ring was substituted with two lateral arches which allowed the patient to lie supine in bed. Supra-acetabular region was chosen for half pin placement which provided a sturdy anchorage and gave a strong construct. Muscles were not pierced for the placement of wires or pins that minimized the risk of infection and pain. The assembly construct had four rods, two of them were placed anterolateral and the other two were posterolateral. The aim was to provide balanced distraction forces so that the sagittal or coronal balance should not be affected.
A halo ring according to the head size was chosen and connected to the head with 06 threaded pins.
A total of four Ilizarov half pins were used in the pelvic assembly. Two Ilizarov half pins of 6 mm each were passed in the supra acetabular area one on both sides. Anterior inferior iliac spine was approached through blunt dissection after giving a 2 cm incision, almost 2 cm below and medial to the anterior superior iliac spine (ASIS) on both sides. The outer cortex at anterior inferior iliac spine was drilled with a 4 mm drill bit and a 6 mm half pin was passed using a T handle.
The 2nd site for half pin placement was about 10 cm posterior to the ASIS. After making a small incision, the outer cortex was drilled and a 6 mm half pin was passed in between the inner and outer tables of the iliac bone on both sides using a T handle. Both half pins on either side were connected to an Ilizarov arch using male posts and rancho cubes. Both arches were connected with each other through two threaded rods to strengthen the construct [].
Distraction device consisted of four threaded rods, two anterolateral and two posterolateral connecting pelvic assembly to the halo assembly.
Distraction was started on the 1st postoperative day at the rate of 3 mm per day divided in three intervals of 1 mm each. On the 5th postoperative day, the patient started to move his right foot and started to feel touch sensations in his right leg. Distraction was continued at this constant pace of 3 mm per day for 35 days. The patient was closely monitored for his progress by getting weekly X-rays of the spine and measuring the trunk height and kyphotic angle.
After 35 days of distraction, rib hump and thoracic knuckle markedly improved and Cobb angle reduced from 141° to 56° [] and the patient height increased up to 8 cm. Power of the legs improved to 2/5 bilaterally.
At this time, resection of vertebral bodies, thorough debridement and stabilization using a vertebral standalone cage through anterior approach, was planned and surgery was performed by the senior author (AA). A cage was placed from T1 to T10 vertebral body after debridement []. After the definitive surgery, kyphotic angle was reduced to 46°.
GeneXpert analysis of the tissue revealed multidrug-resistant tuberculosis. Postoperatively, the patient is doing well and put on 2nd line antituberculous therapy.


A 54-year-old woman was admitted to our hospital in a comatose state. Radiological examinations revealed a subarachnoid hemorrhage from a ruptured aneurysm of the anterior communicating artery. She underwent urgent external ventricular drainage positioning followed by cerebral angiography, resulting in a successful occlusion of the aneurysm with endovascular coiling. After the procedure, she developed a status epilepticus, which was efficaciously treated. A cerebral angiography showed a moderate distal vasospasm and an MRI demonstrated an ischemic area in the left precentral frontal lobe with no clinical correlation. She was discharged and transferred to a rehabilitation hospital.
Seven months later, a follow-up cerebral angiography showed a recanalization of the aneurysm, which required retreatment. At that point, she had also developed severe hypertension and was able to suspend antiepileptic treatment. During retreatment, intravenous nimodipine was administered because of ongoing vasospasm throughout the procedure. Endovascular treatment was prolonged due to a complex vascular anatomy: after unsuccessfully attempting to perform a stent-assisted coiling procedure, a coiling-only procedure was carried out, thus resulting in a much larger volume of contrast medium administration. Final sequences documented no vessel occlusion or emboli. The patient emerged from general anesthesia with severe right hemiparesis and complete aphasia. A postoperative CT scan showed an edematous area in the left cerebral hemisphere, an abnormal subarachnoid contrast enhancement zone (probably secondary to contrast extravasation) and a focal left parasagittal frontal hyperdense area []. A new CT scan performed at about 20 h after a neurological deflection showed a new left parasagittal frontal hypodense area at the vertex and in the left precentral gyrus (territory of the middle cerebral artery). It also showed a resorption of the subarachnoid hyperdensity, supporting the hypothesis of contrast medium extravasation due to disruption of the blood–brain barrier (BBB) []. An EEG showed a significant epileptic activity, whereupon the patient was administered antiepileptic drugs.
During the following days, her speech and right hemiparesis gradually improved, although she could only compose short sentences and was still not able to walk autonomously. An MRI performed at 6 days revealed a hyperintense signal on FLAIR sequences in the left cortical precentral gyrus (as in case of vasogenic edema), corresponding to a hyperintense signal on DWI sequences with no alteration of the ADC maps, thus excluding any signs of new ischemia []. An MRI performed 6 months later showed the same radiological alterations [].
After 6 months of rehabilitation, the patient improved clinically, being left with a mild dysarthria and a mild right monoparesis, but having regained the capacity to walk and live autonomously.
The patient’s clinical course and radiological findings suggested a possible permanent neurotoxic effect of contrast medium during coil embolization.


An 11-year-old child, Asian male, brought to the ETU of our institution when he suddenly collapsed at home. At the time of presentation, he was in asystolic cardiac arrest. Following a prolonged uninterrupted resuscitation, signs of cardiocerebral revascularization were evident with spontaneous breathing and sinus rhythm in ECG. The patient was intubated and transferred to the ICU for post-resuscitation care. Corroborative history taken from the grandmother later revealed a similar past incidence of short-lived syncopal attack with spontaneous recovery about a year ago which was not investigated. She denied any recent history of trauma to head, past events of persistent headaches, seizures, visual symptoms, or behavioral changes. Except for the presumed syncopal event, neither the medical history nor the family history was significant.
On D1 of ICU care NCCT brain revealed diffuse, superficial subarachnoid hemorrhage (modified Fisher scale Grade 3) [] with evidence of cerebral edema, persistently low GCS (4/15) and WFNS grading of 5 (GCS <7 with deficits). According to the neurosurgical opinion, the patient was not amenable for any neurosurgical intervention at that time hence opted for conservative management with neuroprotective measures. ECG showed bradycardia with prolonged QT (QTc = 0.53 s). Correctable causes of prolong QT interval were excluded, and it was later attributed to subarachnoid hemorrhage (SAH). Elevated intracerebral pressure (ICP) was confirmed by increased optic nerve sheath diameter in ultrasonography since the fundoscopy was normal. (ICP manometry was not available at our institution).
Electroencephalogram performed on D3 suggested severely reduced cerebral activity. Neuroprotective management was continued with neuroprotective ventilation, maintaining a normocapnia (PaCO2 30–35 mmHg) and normoxia. All the metabolic parameters including serum glucose, electrolytes, lactate, and liver and renal function tests were stable at that moment.
On D7 patient was found to have deteriorating lung functions, setting hypoxia, tachycardia, and elevated temperature with lung signs. Presumptive diagnosis of sepsis with ventilator associated pneumonia was made and after taking appropriate cultures, intravenous antibiotics were escalated. Cerebral diabetes insipidus was diagnosed based on elevated serum Na+ (158–162 mmol/l), polyuria, and suggestive urinary and serum osmolalities (260 mOsmol/kg and 320 mOsmol/kg, respectively).
Despite every effort, the patient gradually deteriorated with acute renal failure with metabolic acidosis, persistent hypotension which warranted the use of multiple inotropes, deranged clotting profile with liver failure, and ultimately multiorgan dysfunction. A cluster type respiratory pattern was noticed on capnography []. On day 10 of ICU stay, brain stem reflexes were absent on two different occasions, bilateral pupils were found to be round, dilated, and nonreactive to light. Apneic test was negative. Ultimately, the patient succumbed to death by cardiac arrest while on ventilator on day 12.
Pathological postmortem revealed extensive SAH with diffused multiple tufts of irregular, dilated vessels in the occipital region of the basilar and interpeduncular cistern area of the cerebrum. Adjacent to the blood clots evidence of pressure effect causing sulci and gyri obliteration with extensive cerebral edema was found []. Liquefaction of brain parenchyma was noted in several foci []. Histopathological specimens revealed closely packed large cavernous vascular spaces, marginated by thin fibrous tissue with the absence of intervening glial tissue which is compatible with a CCM [ and ].


A 67-year-old man was transferred from another medical facility for worsening shortness of breath, fever, and chills that started approximately 6 h after administration of his second dose of the Moderna COVID-19 vaccine. He also had nausea, orthopnea, and increasing fatigue that developed 12 h following vaccine administration. He denied chest pain, palpitations, and syncope. His medical history was significant for hypertension, type 2 diabetes mellitus, hyperlipidemia, coronary artery disease with history of multiple stent placements and coronary artery bypass grafting surgery, congestive heart failure (CHF) with preserved ejection fraction, chronic obstructive pulmonary disease without any home oxygen requirement, hypothyroidism, and gastro-esophageal reflux disease. For these ailments, he was taking low-dose aspirin (81 mg daily), atorvastatin (80 mg daily), clopidogrel (75 mg daily), furosemide (80 mg twice daily), isosorbide mononitrate (120 mg daily), levothyroxine (25 mcg daily), lisinopril (40 mg daily), metformin (500 mg twice daily), metoprolol tartrate (50 mg twice daily), potassium chloride (10 mEq daily) along with albuterol and tiotropium inhalers. He had been compliant to all his medications. He had no similar symptoms after the first dose of vaccine. He denied history of previous COVID infection or contact with a patient with known COVID-19 infection.
At his presentation to the emergency room, he had oxygen saturations down to 86% on 6 L/min of oxygen via nasal canula. He was also hypertensive (169/96 mmHg), tachycardic (141 beats/min), tachypneic (40 breaths/min), and febrile (101.2°F) and was speaking in short sentences due to dyspnea (). He had coarse crackles in both lung bases, elevated jugular venous pressure, and 1+ pitting edema in his lower extremities. Initial labs were significant for leukocytosis (WBC count of 17.86 × 103/μL), an elevated ESR of 41 mm/h, an elevated proBNP of 43134 pg/mL, and an elevated high sensitivity troponin of 180.8 ng/L. His blood gases showed a pH of 7.294, HCO3 of 21 mmole/L, and PaCO2 of 39.9 mmHg. His serum lactate level (5.7 mmol/L) and total bilirubin (1.9 mg/100 mL) were elevated. His Hb was 18 g/dL at presentation. A chest x-ray showed cardiomegaly and pulmonary edema without any focal consolidation (). An ECG revealed sinus tachycardia with non-specific ST/T wave changes. A transthoracic echocardiogram showed a mildly dilated left atrium, a left ventricle ejection fraction of 50%-54%, mild hypokinesia in the mid-septal and mid-anterior walls, and grade 2 diastolic dysfunction. He tested negative for COVID-19 and influenza by PCR. His urinalysis was normal, and sputum and blood cultures were negative; however, his CRP level was elevated (15.5 mg/dL).
The patient was treated for his acute exacerbation of CHF with diuretics and supplemental oxygen therapy. His hypoxia and dyspnea significantly improved after placing him on BiPAP (12/8 cm H2O setting). His tachycardia and tachypnea improved with intravenous furosemide and bronchodilators, and his hypertension improved with hydralazine. summarizes his vitals and some inflammatory markers during the course of his hospital stay which showed gradual improvement. He was also empirically treated for sepsis with ceftriaxone and azithromycin to cover for community-acquired pneumonia as a possible source of infection. Despite antibiotic treatment, he continued to have heart failure symptoms and the pro-BNP remained elevated, suggesting an alternative etiology for his CHF exacerbation. Elevated troponin levels and mild hypokinesia of the ventricular wall in 2 regions on TTE with an acute presentation, including fever, led to the clinical diagnosis of myocarditis rather than type 2 non-ST elevation myocardial infarction associated with heart failure. The temporal association of his symptoms with COVID-19 vaccination and the absence of preceding symptoms of viral infection suggested that the acute myocardial injury was associated with his vaccination.
His subsequent clinical course showed remarkable improvement with resolution of symptoms over the next 2 days. His oxygen requirement decreased to 2 L/min of oxygen by nasal cannula. At a 2-month follow-up, he was at his baseline with normalization of troponin and inflammatory markers.


The patient is a 70-year-old man with a medical history of hypertension, gout, and rectal cancer with liver metastases who presented with 4 days of nausea, vomiting, and gait instability. On physical examination, he was found to have right ptosis, left arm tremor, and right arm dysmetria. CT head showed cerebellar infarction with surrounding cerebral edema in the territory of the right posterior inferior cerebellar artery (PICA). CT angiography of the head and neck showed right vertebral thrombus with distal reconstitution from retrograde flow along with moderate-to-severe stenosis in his bilateral posterior cerebral arteries. He was not a candidate for thrombolysis with tissue plasminogen activator or endovascular intervention being outside of the thrombectomy treatment window.
Stroke workup was completed, with a normal transthoracic echocardiogram, elevated hemoglobin A1c, and elevated LDL. He received an aspirin 325 mg load and then was started on aspirin 81 mg and a statin for secondary stroke prophylaxis. His blood pressure was slowly decreased from permissive hypertension with his home antihypertensives. MRI brain confirmed a subacute stroke of the right PICA territory with secondary right tonsillar herniation and no hemorrhagic transformation (Fig. ). Mass effect was also seen with compression of the fourth ventricle without hydrocephalus. He further underwent MR angiography of his head and neck, which was significant for occlusion of his right vertebral artery from V1 to the distal V2 segment, with distal reconstitution. That is, trickle flow at the V3 segment level and normal caliber at V4 reflecting clot burden and likely retrograde flow from the basilar artery.
Intravenous heparin infusion without bolus was started for the right vertebral thrombus with therapeutic partial thromboplastin time reached on the second day of admission. The patient began complaining of abdominal pain on the third day, with recurrence of nausea and vomiting. He became hypotensive and had tachycardia. Hemoglobin dropped from 9.4 to 5.9 mmol/L. Abdominal X-ray showed possible ileus, with bowel diameter >10 cm. CT abdomen showed left retroperitoneal hematoma from a ruptured 1.2 cm renal angiomyolipoma (mildly complex and posterior). Aspirin and heparin were stopped. He was given 3 units of packed red blood cells (PRBCs) and emergently taken for mesenteric/visceral angiography with embolization by interventional radiology (IR) (Fig. ).
Post-procedurally, he was initially hemodynamically stable but had new-onset atrial fibrillation with rapid ventricular response to the 160s on telemetry and his systolic blood pressure dropped to 70 mm Hg. Repeat angiography of the embolized site was reviewed with IR. There was no active extravasation. He was given 1 L of fluids, 2 units of PRBCs along with amiodarone bolus and then started on an amiodarone infusion which was stopped the next day. Repeat electrocardiograms showed sinus rhythms. His hemoglobin was repeated every 8–12 h, then daily. Due to a high CHADSVASC score of 5, it was felt strongly that he needed to be on antithrombotic therapy. Repeat CT abdomens showed a stable hematoma; thus, he was restarted on aspirin 81 mg, 4 days after his embolization.
The case was further discussed with IR, oncology, hematology, surgery, gastrointestinal, and urology. The decision was that the benefits of anticoagulation outweighed the risks of rebleeding after embolization. His hemoglobin remained stable. On day 7 after embolization, he was started on an aspirin to warfarin bridge. Device implantation or atrial ablation for atrial fibrillation management was not selected due to patient preference. At this point, he was discharged from the hospital with home health and close multispecialty follow-up. At 6 months follow-up, he was on anticoagulation and functioning close to his baseline at home.


A 70-year-old man who complained of nausea, vomiting, and weight loss was referred to our hospital for examination and treatment. He had a history of hyperthyroidism, diabetes, hypertension, osteoporosis, infectious uveitis, and retinal detachment. Computed tomography revealed thickening of the gastric wall from the gastric body to the prepyloric region, as well as retention of food residues (Fig. ). Esophagogastroduodenoscopy revealed friable and irregular mucosa, and a depressed lesion extending from the gastric antrum to the lower body (Fig. ). An esophagogastroduodenoscopy biopsy revealed poorly differentiated adenocarcinoma (por) (Fig. ). Surgery was performed for preoperative diagnosis of undifferentiated advanced gastric cancer. Total gastrectomy was initially planned but then was abandoned during the operation in favor of gastrojejunostomy because of a strong adhesion to the head of the pancreas. Systemic chemotherapy with the SOX regimen (S-1, 120 mg/day on days 1–14; oxaliplatin, 170 mg on day 1) was initiated as treatment because the patient tested HER2-negative in immunohistochemical staining.
After cycle 1 of oxaliplatin infusion, the patient realized that his right eye had visual field impairment, which he described as darkening of the right half of his visual field and loss of vision lasting about 1 min and occurring about 7 times a day. The daily frequency of this occurrence gradually decreased, and his visual field impairment improved in 1 week. No visual field impairment occurred in the left eye. Since the same symptoms recurred from the second to the fifth cycle of treatment, we consulted with an ophthalmologist. An ophthalmologic examination revealed no obvious damage to the retinal and optic nerves. The patient showed no abnormal findings in the brain or around the orbit on magnetic resonance imaging (MRI) (Fig. , b), no stenosis or aneurysm in the internal carotid artery or ophthalmic artery on 3D-MRI (Fig. ), and no plaque or stenotic lesion in the bilateral carotid arteries on carotid artery ultrasound. Thus, the ophthalmologist arrived at the diagnosis of amaurosis fugax, but without mentioning its cause or recommending any specific treatment. His clinical course led us to suspect oxaliplatin-associated amaurosis fugax and to discontinue oxaliplatin and switch to S-1 monotherapy from cycle 6. Subsequently, the patient's amaurosis fugax improved.
After an improvement shown after cycle 6 in gastric wall thickening on computed tomography, total gastrectomy was performed with D2 lymph node dissection. The gastric lesion in the patient was diagnosed as tubular adenocarcinoma, well-differentiated type (tub1 > tub2), 45 × 13 mm, ypT3 (SS), ly0, v1, N0, M0, grade 1b, stage IIA. The patient underwent adjuvant chemotherapy with S-1 and has shown no recurrence for 6 months. In addition, no visual field impairment occurred since.


A 54-year-old female presented with right upper quadrant pain for 2 months. It was dull aching, intermittent, non-radiating, and aggravated by meals. She had intermittent episodes of passage of black tarry stools associated with easy fatigability. Bilateral lower limb swelling with abdominal distension was noted for 1 month. She had anorexia and loss of weight. On examination, she had pallor, tachycardia, pedal edema, raised jugular venous pressure, and mild tender hepatomegaly. Investigations revealed microcytic hypochromic anemia, thrombocytopenia, and positive occult blood in the stool. Except for the reversal of albumin/globulin ratio, rest of the liver function tests were normal. Ultrasound abdomen showed hepatomegaly (16.5 cm) with mild ascites. Portal vein and spleen were normal. Ascitic fluid had high protein and high serum ascites albumin gradient (SAAG >1.1) with 300 white cells predominantly lymphocytes. Upper GI endoscopy showed multiple linear ulcers without active bleeding in the gastric body and fundus with thickened gastric folds; the rapid urease test was negative []. Esophageal and duodenal mucosa was normal. There was dense neutrophilic inflammation suggestive of acute gastritis on histology with no evidence of malignancy. Computed tomography of the abdomen revealed mild irregular wall thickening in fundus and body. The right and left atrial enlargement with diastolic dysfunction was noted on the 2D-echocardiogram. The patient was started on diuretics and pantoprazole. She improved and was discharged with a diagnosis of congestive cardiac failure secondary to anemia due to peptic ulcer bleed. She was readmitted after 2 months with a history of generalized weakness and easy fatiguability with melena for 8 days. On admission, hemoglobin was 4.5 g/dl, total leukocyte count and platelets were normal. The patient was transfused two units of blood. Repeat upper GI endoscopy showed partially healed gastric ulcers [] and multiple polypoidal lesions in the duodenum with intermittent ooze []. Bleeding was controlled with hemospray and injection adrenaline (1:10,000). After stabilization, biopsies were taken 3 days later from duodenal polypoidal lesions and the gastric ulcers. Histology revealed moderate chronic lymphoplasmacytic infiltrate with lamina propria showing glassy pink material separating glands suggestive of amyloidosis []. Rectal fat pad biopsy and gastric mucosal biopsy showed amyloid deposits with apple-green birefringence on polarized microscopy []. Serum electrophoresis showed increased IgG lambda light chains – 452 mg/L (N-0.57–2.63 mg/dl). Twenty-four hours urinary protein was normal. Bone marrow aspiration shows monoclonal population of plasma cells with positive amyloid staining with congo red stain. Based on gastrointestinal amyloid deposits with positive congo red staining, presence of IgG lambda-type M protein in serum and clonal plasma cells in bone marrow a diagnosis of primary systemic AL amyloidosis was made. Serum β2 microglobulin levels were 3400 mcg/ml (N-0–3 mcg/ml). Chemotherapy with Bortezomib and low-dose dexamethasone (M-Dex) was started by the hematologist. Follow-up endoscopy at 2 months showed a reduction in the size of the polypoidal lesions. The patient was asymptomatic at 6 months and then lost to follow-up. This was an unusual presentation of systemic amyloidosis in an elderly patient with melena, thickened gastric folds, and duodenal polypoidal lesions.


In October 2009, a 63-year-old man was diagnosed with refractory anemia of myelodysplastic syndrome (MDS) related to trisomy 8. One and a half years post-diagnosis, oral administration of low-dose prednisolone (PSL) and methenolone was initiated because he became transfusion-dependent. Four months later, he was hospitalized because of high fever. On hospitalization day (HD) 1, he had pancytopenia (white blood cell count, 500/μL [blasts, 8%]; hemoglobin level, 7.3 g/dL; platelet count, 12.3 × 104/μL), splenomegaly, and hyperferritinemia (serum ferritin level, 39,900 [normal, 21.8–274.7] ng/mL). Biochemistry examinations revealed an aspartate aminotransferase (AST) level of 51 (normal, 13–30) IU/L, alanine aminotransferase (ALT) level of 184 (normal, 6–27) IU/L, lactate dehydrogenase level of 363 (normal, 124–222) IU/L, and plasma fibrinogen level of 757 (normal, 200–400) mg/dL. Bone marrow aspiration yielded a hypocellular smear with 22.4% blasts and 5.2% hemophagocytes, suggesting the progression to acute myeloblastic leukemia with suspected HPS. Chromosome analysis revealed a complex karyotype, including 5q deletion and trisomy 8. Although we were unable to assess the triglyceride level, soluble interleukin-2 receptor (sIL-2R) level, and natural killer (NK) activity, we diagnosed him with definitive HPS because he met five of the eight factors comprising the hemophagocytic lymphohistiocytosis (HLH) 2004 criteria. In addition, chest X-ray and computed tomography (CT) demonstrated infiltration in the right middle lobe and multiple micronodules in both lungs (). Although serum galactomannan and β-D-glucan were negative, fungal pneumonia was suspected based on the imaging findings. He was intravenously treated using micafungin and tazobactam/piperacillin before treatment for MDS with HPS. These were subsequently switched to liposomal amphotericin B (LAMB) and meropenem due to refractoriness of the disease. However, his symptoms did not improve. We performed transbronchial lung biopsy of the right-sided infiltrative lesion and the diagnosis of AFOP was made on HD9 (). Although we performed culture of bacteria, fungi, and tuberculosis, in addition to Grocott-Gomori staining, we found no evidence of infection. Moreover, there was no histopathological evidence of other malignancies. We administered methylprednisolone (mPSL) pulse therapy (1 g/body) for 3 days, followed by PSL maintenance therapy. Although the infiltrative shadow disappeared immediately, the micronodules increased in size. These lesions were diagnosed as probable invasive aspergillosis based on the high serum galactomannan levels (1.8 [normal, 0.5] cut-off index) on HD23. After LAMB was switched to voriconazole, the lesions gradually became smaller and disappeared. Although the signs and symptoms of HPS also improved, pancytopenia and hyperferritinemia persisted. Thereafter, he underwent chemotherapy followed by cord blood transplantation for refractory acute myeloid leukemia 7 months after discharge. One month later, he died of primary disease in July 2012, without AFOP relapse.


In June 2011, a 38-year-old woman was diagnosed with primary mediastinal B-cell lymphoma (PMBCL). She achieved a partial response (PR) after receiving eight courses of rituximab, cyclophosphamide, doxorubicin, vincristine, and PSL regimen. She received 50-Gy radiation to the mediastinum and consequently achieved a first complete response at 1 year post-diagnosis. One month later, she was diagnosed with relapsed PMBCL because of the enlargement of mediastinal lymph nodes. Although we administered rituximab, etoposide, mPSL, high-dose cytarabine, and cisplatin, the treatment was not effective. We administered rituximab plus ranimustine, etoposide, cytarabine, and melphalan as the second salvage chemotherapy, and she achieved PR after receiving one course. On day (D) 7 of the second course, she exhibited pancytopenia (white blood cell count, 600/μL; hemoglobin level, 10.0 g/dL; platelet count, 7.0 × 104/μL) and mildly high transaminase levels (AST and ALT levels of 34 and 76 IU/L, respectively). On D18, she developed febrile neutropenia. She was initially treated using intravenous cefepime, which was subsequently changed to imipenem/cilastatin, teicoplanin, and caspofungin. However, the symptoms did not improve. Chest CT revealed an infiltration shadow with ground-glass opacity (GGO) in the left side of the lungs on D34. Imipenem/cilastatin and caspofungin were changed to tazobactam/piperacillin and LAMB. As severe pancytopenia with fever remained, we performed bone marrow aspiration on D40. Bone marrow aspiration yielded a markedly hypocellular smear with 2.0% hemophagocytes and no lymphoma invasion. The chromosome karyotype was normal. Biochemistry testing demonstrated a serum ferritin level of 1916 ng/mL, serum sIL-2R level of 2580 (normal, 124–466) IU/L, serum triglyceride level of 89 (normal, 50–150) mg/dL, and plasma fibrinogen level of 639 mg/dL. Although we were unable to evaluate NK activity and confirm splenomegaly, we diagnosed her with HPS because she met five of the eight HLH 2004 criteria. Thereafter, the infiltrative shadow with GGO gradually enlarged and a new GGO developed in the left side of the lungs (). We therefore performed transbronchial biopsy and diagnosed AFOP on D45 (). Although we performed culture of bacteria, fungi, and tuberculosis, in addition to Grocott-Gomori staining, we found no evidence of infection. Moreover, there was no histopathological evidence of other malignancies. After the initiation of PSL at 30 mg/day intravenously, the infiltration shadow gradually disappeared and finally became a scar shadow. Although the signs and symptoms of HPS also improved, pancytopenia and hyperferritinemia persisted. Thereafter, she underwent allogeneic peripheral blood stem cell transplantation from a haploidentical sibling for PMBCL in PR because of poor autologous stem cell mobilization. At 1 year and 11 months post-diagnosis, she obtained complete response of the primary disease without AFOP relapse.