A 51-year-old woman presented to our hospital with vomiting, delirium for 12 h, weakness in all four limbs, abnormal behavior, and aconuresis. For approximately 1 month, she had experienced xerostomia, and she had been febrile, especially in the afternoon. The patient had no history of risk factors for venous thrombosis (e.g., long-term usage of oral contraceptives, recurrent miscarriages, and diet) and no family history of thrombotic disease. On examination, the patient was unconscious, and her blood pressure was 133/88 mmHg. Myodynamia of all four limbs was diminished, and electropositive cone bundle pathology and neck stiffness were present. Cranial nerve examination was unremarkable, and Kernig's sign was negative. Laboratory investigations showed anti-SS-related antigen A (anti-Ro/SSA) antibodies (+++), anti-SS antigen B (anti-SSB) antibodies (+++), beta 2 glycoprotein antibody (−), antiphospholipid antibody (−), and anti-nuclear ribonucleoprotein/Sm antibodies (+) and an increased immunoglobulin G level (23.2 g/L). The function of blood coagulation including detection of thrombin time, prothrombin time, activated partial prothrombin time, international normalized ratio, prothrombin time activity percentage, and fibrinogen is normal. The activity of Protein C, Protein S, and antithrombin is normal. The level of homocysteine is normal. Lumbar puncture revealed an elevated intracranial pressure (240 mmH2O), but cerebrospinal fluid cell count and protein levels were normal. Antinuclear antibodies, immunoglobulin G4, rheumatoid factor, and C-reactive protein levels were also normal. Neurological imaging aided diagnosis. Brain computed tomography demonstrated a bilateral low-density shadow on the thalamus [], and brain magnetic resonance imaging suggested deep vein thrombosis associated with brain edema [Figure -]. Magnetic resonance venography images showed that the straight sinus, vein of Galen, left middle cerebral vein, and inferior sagittal sinus were not visible [Figure and ]. Color Doppler ultrasonography of the lymph nodes in the salivary glands and their drainage area implied that the outline of the bilateral parotid gland and submandibular gland were unclear, with a coarse heterogeneous echo pattern in the parenchyma. Blood flow parameters were increased, and the surrounding soft tissue was thickened and hyperechoic. Schirmer's I test: 1 mm in 5 min for both eyes. Schirmer's II test: 4 mm in 5 min for both eyes. Labial salivary gland biopsy confirmed a diagnosis of SS []. After diagnosis, a rheumatologist prescribed oral hydroxychloroquine sulfate and total glucosides of peony. In addition, the patient was treated with anticoagulants, diuretics, and antibiotics. Subsequently, the patient's symptoms improved.


A 44-year-old female patient living in Purano-baneshwor, Kathmandu, Nepal was referred from the National Center for Rheumatic disease (NCRD) for laboratory investigation in the Modern Diagnostic Laboratory and Research Center on 24 July 2019, presenting with hyperpigmented erythematous rash all over her body along with V-shaped rashes on the neckline since 2 months. Initial symptoms as mentioned by the patient included itchy rashes and photosensitivity. She had no history of headache, fever, and weight loss with a normal vital test. In addition, she had no surgical as well as medical history of chronic disease. She had progressed symptoms like muscle pain (especially in the left arm and thigh), unable to walk upstairs, inability to stretch hands, unable to turn neck, and difficulty in swallowing food.
Physical examination showed signs of inflammation supported by laboratory findings, i.e. erythrocyte sedimentation rate (ESR) done by Wintrobe’s method found to be 30 mm/1st hour (normal 0–20 mm/1st hour), leukocytosis (14,920 cells/µL) with neutrophilia 13,080 cells/µL (normal range 2500–8000 cells/µL), and carbohydrate reactive protein (CRP) done by nephelometry found to be 25.3 mg/L (normal <3 mg/L). Hematological parameters were measured using Sysmex XN-350 and are presented in . Biochemical parameters () were measured by a fully automated Dimension RxL Max integrated chemistry analyzer that revealed an elevated level of serum creatinine kinase 17,160 IU/L (normal 26–192 IU/L), and normal plasma glucose level and renal function test. Her liver enzymes revealed an elevated level of alanine aminotransferase (ALT), i.e. 370 IU/L (normal 5–45 IU/L), and aspartate aminotransferase (AST) 616 IU/L (normal 5–45 IU/L). Nailfold capillaroscopy of 8 fingers findings showed variant and simple Raynaud's. Urine analysis, chest X-ray, and thyroid function test were normal. Serum lactate dehydrogenase (LDH) 1657 IU/L (reference 25–250 IU/L), Jo-1 antibodies, and dsDNA antibodies were negative while anti-Mi-2 antibody was positive. Raynaud’s phenomenon and anti-Mi-2 antibody are highly specific to dermatomyositis. Based on the above findings, a diagnosis of dermatomyositis was made.
She was administered with 50 mg prednisolone with a significant improvement of muscular activities within a month; with a modest fall in serum creatinine kinase level as shown in and 25 mg azathioprine once a day as immunosuppressive drugs. At present, she is orally administered 50 mg prednisolone therapy for maintenance therapy and still being followed up.


A 35-year-old male was admitted to our cardiology unit with a 15-day history of unremitting fever, chest and abdominal pain, and palpitation. Although the patient's vitals were stable, general conditions appeared critical. Unspecific ECG abnormalities were present at entry. Signs of endocarditis were disclosed at transthoracic echocardiography to involve both the aortic and mitral valve leaflets [].
Optimal medical therapy was initiated in the cardiac care unit, with challenging clinical efficacy. He was established to be at a high risk for cardiac surgery due to multiorgan (pulmonic, kidney, and metabolic) failure from a septic condition. A daily echocardiographic examination was then scheduled.
However, on the 5th day, his clinical course complicated with CA. High-quality chest compressions and advanced cardiac life support procedures warranted a ROSC in 16 min. This allowed the rescuer performing further echocardiographic check for cardiac function. Unexpectedly, a large TF was seen in the right atrium [, movie]. The decision was made to administer rapid endovenous heparin (5000 + 5000 IU) and continued chest compressions until the thrombus disappeared [Figure and ]. The patient was then moved to the intensive care department, but his prognosis remained poor.


A 67-year-old man with past medical history of coronary artery disease (CAD) status post coronary artery bypass graft (CABG), history of alcoholism, and history of chronic kidney disease stage 3 presented with chest pain for 1 week. Chest pain was intermittent, left sided, 8/10 in severity, non-radiating, dull in nature, exacerbated by exertion and mildly relieved by rest. Remaining review of system was negative. He stopped taking all his cardiac medications for 1 year. Vitals were as follows: blood pressure 130/76 mm Hg, pulse 142/beat per minute respiratory rate 18/min. Pulse oximetry was 97% on 2 L nasal cannula. Cardiac examination was significant for tachycardia with irregularly irregular pulse but no murmur, rub or gallops. Lungs were clear to auscultation. Other system examinations were unremarkable. Laboratory data showed sodium 137 (136 - 145 mmol/dL), potassium 5.1 (3.5 - 5.2 mmol/dL), chloride 105 (96 - 110 mmol/dL), bicarbonate 22 (24 - 31 mmol/dL), blood urea nitrogen (BUN) 37 (5 - 25 mg/dL), creatinine 1.85 (0.44 - 1.0 mg/dL), glucose 130 (70 - 99 mg/dL), aspartate transaminase (AST) 176 (10 - 42 IU/L), alanine transaminase (ALT) 208 (10 - 60 IU/L), international normalized ratio (INR) 1.39, and thyroid stimulating hormone (TSH) 6.87 (0.3 - 4.5 IU/mL). Serum troponin was 0.01 (reference value < 0.04 ng/mL). Electrocardiogram (EKG) showed 2:1 atrial flutter. Initially patient was given cardizem and β-blocker boluses but heart rate did not improve. He was loaded with amiodarone 150 mg intravenous push (IVP) over 10 min and continued on amiodarone drip 1 mg/min over 6 h. Heparin drip was started for anticoagulation. On the following day morning labs showed significantly elevated liver enzymes and worsening renal function from his base line on the day of admission. AST was 4,250 (10 - 42 IU/L), ALT 2,422 (10 - 60 IU/L), and INR 2.28. Creatinine was 3.2 mg/dL (0.44 - 1.0 mg/dL), and BUN 44 mg/d reference value (5 - 25 mg/dL). At that moment patient was hemodynamically stable with blood pressure (BP) of 105/55 mm Hg, HR 70 beats per min and pulse ox of 95% on room air. Six hours later, patient became confused and unable to protect his airways. A rapid response was called, and the patient was intubated for airway protection and transferred to intensive care unit (ICU). Amiodarone was immediately stopped. Right upper quadrant ultrasound, a computed tomography (CT) of the chest, abdomen and pelvis without contrast were normal. Blood cultures, toxicology screen including acetaminophen level, hepatitis panel, antinuclear antibodies (ANAs), anti-smooth muscle antibody (ASMA), antimitochondrial antibody (AMA) were all negative. Alpha-1 antitrypsine (A1AT) was 126 (90 - 200 mg/dL), and ceruloplasmin 18 (17 - 54 mg/dL). Hereditary hemochromatosis mutation with C282Y heterozygote and H63D was negative. Patient was immediately started on N-acetylcysteine drip for 72 h. Patient’s liver enzymes continued to rise and peaked at 21,000 (10 - 42 IU/L) for AST and 9,020 (10 - 60 IU/L) for ALT (, ). Total bilirubin increased to 3.9 (, ). INR was 3.8 (day 3 of admission) (). Patient was deemed not a candidate for liver transplant due to history of alcoholism and acute-on-chronic kidney injury. As patient’s kidney function continued to worsen, he was started on hemodialysis (on the fifth day). His platelets count began to drop on day 3. Heparin-induced thrombocytopenia was suspected and heparin was stopped. Heparin-induced platelet antibodies with reflex to serotonin were positive. Patient was started on argatroban but serotonin release assay came back negative. Patient was successfully extubated to nasal cannula on day 8. LFTs improved and came down AST 79, ALT 192, and albumin of 2.5. INR was falsely high when patient was receiving argatroban () but improved after argatroban was stopped. Kidney function eventually improved, and he did not need more hemodialysis.


A 13-year-old girl reported to the department of pedodontics and preventive dentistry with the chief complaint of pain and food accumulation in the right posterior mandibular region for the past 4 days. Dental history revealed root canal treatment in that region three years ago and upon clinical examination, a stainless-steel crown was cemented onto tooth #46. Intraoral periapical radiograph confirmed the root canal treatment and the presence of an angular bone defect with respect to the mesial root of 46 with a probing pocket depth of 8 mm.
The patient was provided with oral hygiene instructions, brushing demonstration prior to intervention. Corresponding inferior alveolar nerve was anaesthetised using 2% lignocaine (2% lignocaine in 1:200,000 dilution adrenaline, Neon Laboratories Ltd. Mumbai, India), following which full-mouth supra and subgingival scaling were performed using ultrasonic scalers (Cavitron™ Bobcat™ Pro Ultrasonic scaler, Dentsply USA). The stainless-steel crown was removed using crown remover and root planing was performed using hand instruments (Gracey curettes, Hu-Friedy USA) until the removal of necrotic cementum.


A 46-year-old female patient with medical history of bipolar disorder presented to an outside hospital after she was found in an obtunded state by her family on the morning of presentation.
Per family, the patient developed a sudden severe headache during her father’s funeral. She was given ibuprofen, which initially helped with her headache. She described this as the worst headache of her life. Her son later gave her 1–2 tablets of naproxen which did not seem to help. She then vomited and subsequently went to bed. She had no prior history of headaches or migraines.
One day later, the patient woke up and was able to walk a few steps, but became obtunded and unresponsive shortly thereafter. Emergency medical services (EMS) were called, and she was transferred to an outside hospital. On arrival, the patient’s vital signs were blood pressure (BP): 103/84, heart rate (HR): 66 and temperature: 36.4. She was intubated for airway protection given her decreased level of consciousness.
Head CT revealed a left basal ganglia/fronto-parietal haematoma measuring 33 mL in volume with mild subarachnoid haemorrhage near the vertex (). She was transferred to MedStar Georgetown University Hospital for neurosurgical evaluation. A CT angiogram of the head and neck performed on arrival showed no vascular abnormalities. The patient underwent emergent craniotomy, haematoma evacuation and external ventricular drain placement after transfer from the outside hospital. There was no history of hypertension (HTN), bleeding disorders, tobacco use or substance abuse. The patient’s only home medication was lithium, and she had been on a stable dose for several years. Family history was significant for father with Lewy body dementia.


A 13-year-old girl presented to the emergency room with generalized, acute abdominal pain (worst in the hypogastric region) with fever 38.9°, anorexia and vomiting started 2 days prior to presentation.
The parents mentioned that they brought her 5 months ago with mild pain and abdominal mass; an ultrasonography showed no splenic tissue in upper left quadrant, which suggested a wandering spleen and a CT scan was ordered, but the parents ignored. She did not have history of trauma or any remarkable past medical history.
On examination, the abdomen was rigid with generalized tenderness and rebound tenderness. There was an evident mass bulging under the umbilicus. Heart rate was 123 bpm with otherwise normal cardiorespiratory function.
On admission, her hemoglobin was 11.3 g/dL, white cell count 19.6 × 109/L, granulocytes 78.1% and CRP 21.6 mg/L. Her renal, liver function, amylase and lactate were within normal limits.
A Doppler ultrasonography showed that the spleen was in the hypogastric region with a diameter of 14 cm and a very low perfusion. The abdominal radiograph and the chest radiograph were normal.
She was prepared for an emergency laparotomy; the spleen was infarcted without any ligamentous attachments. The hilar vessels of the spleen were within a long mesentery. The splenic vessels were twisted three rounds around themselves. The other organs in the abdomen were normal (). A splenectomy was performed and the splenic vessels were ligated and then cut.
Her recovery was uneventful, and she took vaccines dedicated for splenectomy patients.


A 52-year-old male presented to the Outpatients’ Hand Clinic with a history of significant pain, skin changes and itchiness in the right little finger for 15 years. He was referred from the dermatology clinic for a skin biopsy, suspecting either dermatitis, Lichen Simplex or viral warts. Over the past 15 years, the patient was seen by numerous specialists as of failure in proper diagnosis.
At the clinic, the patient was examined thoroughly. He was suffering from a constant deep throbbing pain (9/10 numeric pain scale) throughout the day and night. He required non-steroidal anti inflammatory drugs (NSAIDs) and opiates regularly to alleviate the pain. Yet, the itching of the ulnar aspect of the hand and little finger was not relieved with medication. The patient described paroxysmal pain on dishwashing, especially with cold water. Clinical examination showed exquisite pressure tenderness over the tip of the right little finger with positive Love’s pin test and Hildreth’s test. The signs, symptoms and clinical tests supposed the condition to be a GT. X-rays, ultrasound scan and contrast-enhanced MRI confirmed the lesion of 16 × 8 × 7mm to be a GT ( and ).
A large, bone-boring GT was found to penetrate through distal phalanx, reaching the volar aspect of the pulp. Surgical excision of the tumor was performed under local anesthesia using a hockey-stick incision.
Complete pain relief was noted immediately after the surgery. Follow-up after 1 year did not reveal any evidence of recurrence.


We report the case of a 69-year-old transgender woman. The patient underwent genital reconstruction surgery at the age of 25, by combined penile and scrotal skin inversion, and has been on hormone therapy ever since.
Our patient was found having a left renal mass at the age of 65; therefore, she underwent left radical nephrectomy and retroperitoneal lymph node dissection. The pathology showed a left kidney renal cell carcinoma of clear cell type, grade 4. It invaded into the perinephric fat, and grossly extended into the renal vein. 0/4 lymph nodes were involved. The resection margins were negative for tumor. She developed an osseous metastasis in her left posterior rib 1 year after nephrectomy (at the age of 66), and received local radiation for the bone metastasis, as well as systemic targeted therapy by tyrosine kinase inhibitors.
In the fourth year after nephrectomy (at the age of 68), CT scans showed a new 1.5 × 1.5 cm nodule in the left lower lung of the patient. This lesion was presumed to be a new metastatic renal cell carcinoma. However, the nodule slowly grew to 3.3 cm in size during the next 12 months despite the systemic therapy for renal cell carcinoma.
A transbronchial biopsy of the left lower lung lesion was performed, which showed a basaloid poorly differentiated carcinoma (Fig. ). Immunohistochemical stains showed that the tumor cells were diffusely positive for CK5/6 (Fig. ) and p40 (Fig. ), and negative for TTF1, PAX8, synaptophysin, and chromogranin. Ki67 stained approximately 80% of the tumor cell nuclei (Fig. ). These results supported a diagnosis of poorly differentiated SCC rather than a metastatic renal cell carcinoma or small cell carcinoma.
Since the CT scan did not demonstrate abnormalities other than the lung lesion and the bone metastases, a PET-CT was performed. Consistent with the previous CT scan, PET-CT showed an FDG-avid density within the left lower lung (Fig. ), with multiple additional nodular densities within both lungs. Additionally, an irregular region of marked increasing FDG activity that measures approximately 6 cm in the craniocaudal dimension was present within the pelvis with multiple moderate- to high-grade FDG-avid lymph nodes present within the left external iliac region and left inguinal region (Fig. ). Due to marked reduced sensitivity on the associated non-contrast CT component of the PET-CT, the female transgender anatomy within the pelvis was not clearly identified. The case was reviewed at the multidisciplinary tumor board rounds. On discussion, the transgender status of the patient was noted, and the FDG avidity within the pelvis was localized to the neovagina. Retrospective review of the CT imaging identified subtle changes within the soft tissues of the neovagina region over time (Fig. ). An MRI was also performed in the interim and identified a tumor within the neovagina (Fig. ).
Given the above information, additional immunohistochemical stains were performed and showed that the tumor cells were strongly positive for p16 (Fig. ), suggesting a HPV-related SCC. In situ hybridization study further confirmed that the tumor cells are strongly positive for high-risk HPV RNA (Fig. ). The above study results were highly suggestive of a metastatic HPV-related SCC from the mucosa/skin of the oral cavity or anogenital region. A transvaginal biopsy was attempted but was not successful due to heavy bleeding. Nonetheless, a diagnosis of metastatic HPV-related SCC of the neovagina is established.
Due to the terminal stage of the disease, the patient was provided palliative radiotherapy and unfortunately passed away 4 months after the diagnosis.


The patient was a 26-year-old woman who presented to the emergency department with palpitations and breathlessness for 3–4 weeks and worsening for 8 h. She had a history of VSD repair which was performed 14 years earlier after she was diagnosed with CCTGA. Seven years after the operation one healthy child was born after uneventful pregnancy. She also reported a ‘syncopal event’ 10 years after VSD repair although no further detail regarding the event could be elucidated. Holter’s study at that time only demonstrated no significant tachy- or bradyarrhythmias. Her transoesophageal atrial and ventricular pacing study demonstrated normal sinus node function and AV conduction without inducible ventricular tachycardia (VT). Multiple follow-up electrocardiograms (ECGs) 11 and 13 years after open-heart surgery only showed mild first-degree AV block and intraventricular conduction delay, with one ECG illustrated in . On this admission, her ECG showed high degree AV block () with a ventricular rate of 44 b.p.m. A fusion beat be could be seen (the 3rd QRS). Her blood pressure was 102/57 mmHg. Respiratory rate was 25/min and oxygen saturation was 98% on room air. The remainder of the examination was unremarkable. Her B-type natriuretic peptide was mildly elevated at 1623 pg/mL (normal 0–450 pg/mL). Other relevant biochemical and haematologic parameters were within normal limits. Her weakness and shortness of breath further worsened shortly after admission and she ‘passed out’ twice, both required electric defibrillation. Her ECG rhythm strip at one such event was shown in . After a bedside Echo study confirming CCTGA [right ventricle (RV) is the systolic ventricle] and preserved right ventricular systolic function [ejection fraction (EF) 55–60%] the patient was taken to the EP lab with implantation of a temporary pacemaker. She was ventricularly paced at 90 b.p.m. and remained completely haemodynamically stable overnight. She received a dual-chamber pacemaker (XL DR 5826, St. Jude Medical, USA), the next day after a thorough discussion with patient and her family members regarding various treatment options including single-chamber, dual-chamber, and resynchronization pacemaker or defibrillator. The atrial and ventricular leads were fixed in the right atrium and high interventricular septum, respectively. Her paced ECG was shown in , with QRS morphology being consistent with high septal pacing. The Echo study with four-chamber views, the chest X-rays before and after pacemaker implantation were shown in , respectively. The ventricular lead was intentionally implanted in the mid- to high septum so that the paced QRS duration was similar to the native QRS prior to pacemaker implantation. This was achieved with careful mapping. The high resolution computed tomography (CT) reconstruct of three-dimensional imaging for the patient’s CCTGA anatomy after pacemaker implantation was shown in . The CT study also confirmed the high septal ventricular lead location. Patient was discharged home in clinically stable condition. She has been physically active at 3, 6, and 9-month follow-ups. Repeat Echo study at a 6-month follow-up showed systolic ventricular function at 57%. Her pacemaker interrogation demonstrated atrial sensing and ventricular pacing rhythm without ventricular tachyarrhythmia. Atrial sensing was 4.4 mV, threshold was 0.5 V at 0.5 ms, and impedance was 538 ohms. Ventricular sensing was 6.8 mV, threshold was 0.5 V at 0.5 ms, and impedance was 326 ohms. Atrial pacing was 19% and ventricular pacing was >99% being in complete AV block. Those parameters were essentially unchanged from previous interrogation at hospital discharge.


A 52-year-old Aboriginal female with longstanding HIV-1 infection presented in November 2015 with a 4-month history of choreiform movements. She required increased assistance in activities of daily living and demonstrated dysarthria, confusion and poor oral intake. There were no fevers, focal infective symptoms or loss of weight. Infection with HIV-1 had been diagnosed in August 2003, but adherence to treatment had been erratic until a CD4 T cell count nadir of 96 × 106/L (12%) was reached in 2012 (). At this time, genotyping had shown an M184V nucleoside reverse transcriptase inhibitor (NRTI) resistance mutation. There were no major resistance mutations to protease inhibitors or non-nucleoside reverse transcriptase inhibitors. The patient underwent subsequent directly-observed therapy with good adherence (, ) but still maintained ongoing low-level viremia (87–347 HIV-1 copies/mL).
Medical history included rheumatic fever at age 14 years with no witnessed chorea, ischaemic heart disease, dyslipidaemia and depression. Interestingly, she had been diagnosed with meningoencephalitis secondary to parainfluenza virus in 2012 when she presented with confusion and coryzal symptoms. Cerebrospinal fluid (CSF) biochemistry was consistent with viral meningitis, but the sample was inadequate to perform parainfluenza and HIV1 PCR testing. The diagnosis of parainfluenza meningoencephalitis was made as concurrent serum parainfluenza titre was significantly elevated at titre >320 (<80). Other medications included aspirin, atenolol, mirtazapine, rosuvastatin and thiamine. She was a smoker of 10 cigarettes/day and, despite a history of alcohol excess, no longer used alcohol.
At presentation, she appeared disorientated and had choreiform movements involving her head, tongue and upper limbs with unsteady gait, left-sided dysdiadochokinesis and past pointing. Reflexes and power were normal. Cardiorespiratory examination was unremarkable.


A 27-year-old male professional rugby player was admitted to his local district general hospital with a 2-day history of chest tightness and breathlessness. He had no other significant past medical history and was not taking any regular medications. He admitted to regularly taking cocaine and performance-enhancing steroids. He was haemodynamically stable with normal saturation. The main findings on physical examination were an irregularly irregular pulse and bibasal crackles. His admission electrocardiogram (ECG) showed AF and his chest X-ray findings were in keeping with pulmonary oedema. Initial bloods tests were within normal range. Transthoracic echocardiogram (TTE) revealed bi-atrial dilatation and a moderately dilated left ventricle (left ventricular end diastolic diameter 7 cm) with mild concentric left ventricular (LV) hypertrophy with an ejection fraction (EF) 35–40%.
He was acutely managed with intravenous diuretics and initiated on evidence-based heart failure medications including beta-blockers and angiotensin-converting enzyme inhibitors. In view of his drug history, a working diagnosis of drug-induced dilated cardiomyopathy (DCM) was made. Once stabilized, he was discharged on bisoprolol 2.5 mg and ramipril 2.5 mg. In anticipation of a direct current cardioversion (DCCV), he was started on rivaroxaban 20 mg. He was counselled not to participate in any competitive sports.
To further investigate his cardiomyopathy, he underwent an outpatient coronary angiogram which revealed unobstructed coronary arteries. In addition, a cardiac magnetic resonance (CMR) confirmed a dilated left ventricle with globally impaired systolic function and a calculated EF of 37%. There was no evidence of scarring or fibrosis on delayed enhancement images. He was unable to maintain sinus rhythm following DCCV and relapsed back into persistent AF. His CHA2DS2-VASc score was 1 (LV dysfunction) which does not strictly mandate anticoagulation; however, he made an informed decision to continue rivaroxaban.
On a follow-up TTE performed 3 months later, LV systolic function remained unchanged. His ramipril was increased and he was initiated on eplerenone. Left ventricular function gradually improved on optimal medical therapy and, at 8 months of follow-up, had returned to near-normal (EF 50–55%). He remained in AF and experienced a brief episode of left arm weakness and paraesthesia suggestive of a transient ischaemic attack (TIA) despite being compliant with anticoagulation. As his CHA2DS2-VASc score increased to 3 (TIA, LV dysfunction) he now had a clear indication for anticoagulation. Connective tissue disorders, syphilis, and Fabry disease screening were negative.
At 1-year follow-up, he was asymptomatic (New York Heart Association 1) but remained in AF and continued to participate in competitive rugby, whilst on oral anticoagulation despite counselling regarding the high bleeding risk. He was reluctant to terminate his professional rugby career prematurely and sought alternative stroke prevention strategies that obviated the need for continuous anticoagulation. He was referred to a Tertiary Cardiology Centre for further management of his AF and consideration of a left atrial appendage occlusion (LAAO) device. A 27 mm Watchman Flx (Boston Scientific, MA, USA) device was successfully deployed under general anaesthetic in the left atrial appendage with a good seal and no leaks (, ). He was discharged home on a 6-week course of aspirin and clopidogrel therapy with a follow-up transoesophageal echocardiogram to assess LAAO device position and guide cessation of antiplatelet strategy.


An 11-year-old male patient presented to a healthcare facility with fever and cough for 2 days and had been referred to our hospital for a preliminary diagnosis of complicated pneumonia. On physical examination, he weighed 30 kg, body temperature was 39°C, maximum heart rate was 125 bpm, respiratory rate was 30 breaths per minute, and a blood pressure reading of 115/77 mm Hg was noted. On auscultation, he had diminished breath sounds over the right hemithorax. There were palpable submandibular lymph nodes of 1.5 cm × 0.5 cm on both sides and palpable right axillary lymph node of 1 cm × 0.5 cm in size. Other physical examination findings were normal. Complete blood count results were as follows: leukocyte count, 8290/mm3; hemoglobin, 9.8 g/dL; and platelet count, 545000/mm3. The sedimentation rate was 38 mm/hour. A thoracic ultrasonography revealed septated pleural fluid with a dense content, which reached a depth of up to 30 mm. A thoracic catheter was placed, and intrapleural tissue plasminogen activator was administered three times. Intravenous ceftriaxone and clindamycin were administered. A thoracic computed tomography was taken, showing multiple lymph nodes having a conglomerated appearance, the largest of which measured 18 mm × 13 mm, in the mediastinal pretracheal, subcarinal, and right hilar regions. There existed a dense pleural effusion with a depth of up to 35 mm in the basal part of the right hemithorax. We also observed intensive pleural fluid in the right hemithorax from apex to the basale in coronal and sagittal images ( and ). As the pleural biopsy material was necrotic and mycobacteria polymerase chain reaction was positive, pathological examination could not be done. An echocardiogram revealed normal findings. As the patient's fever and respiratory difficulty persisted and his radiological signs did not improve, his antibiotic therapy was switched to piperacillin plus teicoplanin. Pleural fluid and blood cultures were negative. Serological tests for human immunodeficiency virus, Epstein–Barr virus, cytomegalovirus, hepatitis B and C, chlamydia, and mycoplasma were all negative. His clinical symptom did not improve with nonspecific therapy, and he was started on pyrazinamide, isoniazid, rifampicin, and ethambutol as antituberculosis treatment empirically. He could not use antituberculous therapy for the first week due to vomiting.
Purified protein derivative measured 10 mm; acid-resistant bacilli were negative in the sputum and fasting gastric juice. He had QuantiFERON positive. His family screen for tuberculosis turned negative. He was noted to have bicytopenia in full blood count on the 35th day of follow-up, and a bone marrow aspiration was performed, which revealed signs of dysplasia in normoblasts and two hemophagocytosis. His laboratory results were as follows: ferritin: 11.735 ng/mL (N: 5.6–216), fibrinogen: 159 mg/dL (N: 200–400), alanine aminotransferase (ALT): 154 U/L (N: 0–55), aspartate aminotransferase (AST): 1,196 U/L (N: 5–34), gamma-glutamyl transferase: 464 U/L (38–54), cholesterol: 102 mg/dL, triglyceride: 164 mg/dL, lactic acid dehydrogenase (LDH): 2936 U/L (N: 110–295), albumin: 2.4 g/dL (3.5–5), direct bilirubin (D.Bil): 1.78 mg/dL, c-reactive protein (CRP): 6.6 mg/dL (N: 0–0.5), procalcitonin: 16.4 ng/mL (N: <0.05), sodium: 132 mEq/L (N: 138–145), and international normalized ratio (INR): 1.62. A hemophagocytic syndrome secondary to tuberculosis infection was primarily considered. As his fever did not subside and his tachypnea persisted, he was transferred to the pediatric intensive care unit. There he was started on intravenous immunoglobulin (IVIG) 400 mg/kg/day for 5 days. An 11.5 Fr hemodialysis catheter was placed, and 10 sessions of TPE with adjunctive fresh frozen plasma were performed. A cervical lymph node biopsy was taken, which was consistent with tuberculosis infection. As his clinical condition did not improve, dexamethasone 10 mg/m2 was commenced. Subsequently, during follow-up, his fever subsided, rash, tachypnea eliminated, and appetite returned to normal. Subsequent laboratory values were as follows: ferritin: 297 ng/mL, fibrinogen: 356 mg/dL, ALT: 26 U/L, AST: 22 U/L, triglyceride: 164 mg/dL, LDH: 295 U/L, albumin: 23.8 g/dL, D.Bil: 0.3 mg/dL, CRP: 0.2 mg/dL, procalcitonin: 0.14 ng/mL, sodium: 138 mEq/L, and INR: 0.99. The patient was transferred to the Department of Pediatrics. Sequencing of PRF1 from peripheral blood mononuclear cells showed heterozygous mutation (Exon 2, codon 91 GCG/GTG, and Ala/Val).


A 53-year-old man, with dyslipidaemia and an alcohol consumption of 100 g per day, presented a progressive unspecific malaise which culminated in a witnessed loss of consciousness after 6 hours of physical work at a temperature of 33ºC. He was locally assisted by an emergency response team and was found comatose and hypotensive. He was intubated, fluid challenge was initiated and he was admitted half an hour later to the emergency room. He remained hypotensive (mean arterial pressure <65 mmHg), tachycardic (sinus rhythm) and was sweaty with a tympanic temperature of 39.9ºC. Fluid challenge was maintained and therapeutic cooling with intravenous cold saline and through gastric tube infusion was immediately undertaken.
Initial workup revealed: metabolic acidosis with hyperlactacidaemia (lactate 5.9 mmol/l, normal (N) <2), acute kidney injury (creatinine 6.8 mg/dl, N 0.7–1.2), rhabdomyolysis (myoglobin 3,670 ng/ml, N <116), mild elevated total bilirubin (1.7 mg/dl, N <1.0) and mild elevated alanine aminotransferase (ALT 177 U/l, N <78). The complete blood count, coagulation, glucose, troponin, remaining liver panel, drug testing and alcohol dosage were normal. An electrocardiogram, echocardiogram and brain and chest-abdomen-pelvis computed tomography with angiography showed no alterations.
After 1 hour of cooling, the patient’s tympanic temperature was 37.9ºC. He was further monitored and supported in the Intensive Care Unit (ICU), with cold saline infusion and application of ice packs maintained. The maximal core temperature in the following 12 hours was 38.2ºC. Despite the improvement in cardiocirculatory, renal and neurological dysfunction allowing early extubation on the next day, there was worsening of the liver injury (), without signs of encephalopathy, and evolution to disseminated intravascular coagulation (DIC) (). Early referral and transfer to a Liver Transplant Unit was made at day 3 due to the possible progression to acute liver failure (ALF). In addition, other causes of liver disease were excluded: abdominal ultrasound with Doppler imaging, virus screening and general and hepatic-specific autoimmune, immunological and metabolic studies were normal. From the 5th day on, there was a progressive improvement of the liver panel and coagulation without specific treatment. The patient remained without encephalopathy and evolved without the need for hepatic clearance techniques or liver transplantation (LT).


In June 2018, a 73-year-old Caucasian male was diagnosed with stage 4 colorectal adenocarcinoma with hepatic metastasis. From his past medical history, he had essential hypertension and diabetes mellitus type II. He was an ex-smoker. In July 2018, he started treatment with a combination therapy of panitumumab and folinic acid, fluorouracil and oxaliplatin (FOLFOX) every 2 weeks. After the eighth cycle of panitumumab and FOLFOX chemotherapy, the patient suddenly developed multiple, eruptive, large, sharply defined, light-brown plaques with a velvety to finely verrucous surface, mainly on the face (), scalp () and upper trunk (), clinically in keeping with eruptive seborrhoeic keratosis.
A dermatology referral was made and the diagnosis of eruptive seborrhoeic keratosis was clinically confirmed. Upon dermatology review, the patient was advised to topically apply betamethasone 0.05% and gentamicin ointment once daily for 7 days. Panitumumab was discontinued for the ninth cycle, and 7 days later, almost all the previous new seborrhoeic keratosis resolved spontaneously. The close temporal association between panitumumab treatment and the sudden onset of multiple seborrhoeic keratoses, together with the complete recovery after 7 days of discontinuation of panitumumab treatment, pointed to a drug-related adverse event. The patient continued treatment with FOLFOX for the ninth cycle and then completed 2 more cycles of combination therapy of panitumumab and FOLFOX. The patient thereafter remained on maintenance treatment with panitumumab every 2 weeks. The patient remains to the present time under medical oncology follow-up, with no recurrence of the seborrhoeic keratosis.


A 37-year-old male presented with dysesthesia of 4 months' duration involving his both upper limbs. On enquiring further, it was revealed that his symptoms started all on a sudden before 4 months and has been gradually increasing ever since. There was no history of neck pain. There was no history of trauma to the neck. On examination, general examination was unremarkable. There were no cranial nerve palsies. Motor system examination revealed that he had Grade 5 power in both upper and lower limbs and deep tendon reflexes were normal. There was sensory loss involving upper limbs from the nape of the neck downward. Local skull and spine examination were normal.
He underwent a magnetic resonance imaging (MRI) of the brain along with cervical spine which showed an intra-axial tumor with a cystic component in the medullary region extending below to the second cervical vertebra [Figure and ]. The tumor was mildly hyperintense on T1-weighted image and hyperintense on T2-weighted image. There was minimal contrast enhancement of the cystic wall of the tumor. There was fluid level in the cavity which was hypointense on both T1 and T2 weighted images suggestive of previous hemorrhage [Figure -]. Our preoperative differential diagnosis included pilocytic astrocytoma, hemangioblastoma, and ependymoma.
He was taken up for surgery under neuromonitoring. He underwent a posterior fossa midline craniotomy along with a laminectomy of the first cervical vertebra in the prone position. The tumor was exposed in the midline. The cystic part of the tumor was let out which contained xanthochromic fluid, suggestive of previous bleeding. The tumor was soft and moderately vascular which had a well-demarcated margin with that of the normal cervical cord in the superficial part []. However, as the dissection progressed to the deeper parts, this demarcation was less well defined. The tumor was removed in piecemeal and intraoperative frozen section was done which was suggestive of high-grade glioma. The debulking of the tumor was performed during which profuse bleeding from the base was observed. A sudden drop in the transcranial motor evoked potentials as well as in blood pressure occurred associated with occurrence of arrhythmias after which the decision to proceed further was abandoned. Postoperatively, he was examined clinically and there were no new focal neurological deficits.
The histopathology of the tumor showed round cell tumor with rosette formation []. There was no evidence of calcification, necrosis, or neovascular proliferation. The MIB index was 3.7%. There was no mitosis. The tumor cells were positive for GFAP and EMA and negative for P53, synaptophysin, and NSE, suggestive of Grade 2 ependymoma.
A repeat MRI with contrast was taken [] which showed residual tumor involving the base of the excision cavity. The option of a repeat surgery or wait and watch with serial imaging was discussed with the patient. After discussions with the family, the patient decided against surgery and is now on follow-up.


A 65-year-old male patient was referred to our hospital with urinary retention. The patient suffered from an intellectual disability and mental retardation.
The CT scan of the abdomen disclosed a complete scrotal shift of both small intestine and sigmoid colon and a bilateral Grade II hydronephrosis (). The patient was then referred to our surgical department for the operative hernia repair.
Clinically, the hernia reached to a level just above the knees (Akpo Classification 3b) [] ().
We applied a novel therapeutic concept based on the combination of three separate components, an intra-abdominal catheter [PleurX™ Catheter, Care Fusion, IL, USA] was laparoscopically placed into the abdominal cavity in order to create a PPP. At the same time, an intramuscular injection of 100 IU of botulinum toxin of five doses of 20 IU each was given on each side of the anterolateral abdominal wall. The application was sonographically guided in the space between the abdominal external and internal oblique muscle ().
Following laparoscopy, a PPP was created with insufflation of room air through the abdominal catheter (1500 ml of room air/day in the first 5 days up to 2000 ml/day for the next 10 days).
We performed a Stoppa procedure as following: median laparotomy with progressive reduction of the viscera without opening the sac. The space behind the rectus muscle, from the internal part of the pubic symphysis and the Cooper ligament to the umbilicus, was prepared. The Retzius space, the iliac vein and artery in the Bogros space, the obturator region and the psoas region were dissected on both sides. One ~20 × 30 cm PVDF Mesh [DynaMesh®-CICAT-Aachen, Germany] was placed into a preperitoneal position according to the standard Stoppa procedure []. The scrotum and testicles were intraoperatively examined by our urologists. No orchiectomy was necessary and scrotal skin was left intact ().
The patient’s postoperative course was uneventful. After a short recovery on the ICU, he was readmitted to the normal surgical ward on the second postoperative day. The patient was released at a stable condition on the 10th postoperative day. Fifteen months after surgery, the patient is doing well.


An 11-year-old female patient reported to the department of pediatric dentistry with the chief complaint of pain and swelling over the lower right back tooth region for 3 months. The patient had taken medication for the same, but there was no cure. History revealed that the patient was apparently normal 3 months back; slowly the patient started experiencing pain which was intermittent in nature and dull aching type and pain was aggravating on touching the affected side and relieved on taking analgesics. Following this, the patient developed swelling in the right lower one-third of the face 2 months back. The patient had visited a primary health center, where medications were given, and the patient was referred to our department for further investigation and treatment. On extraoral examination, swelling was noted on the right lower one-third of the face extending anteroposteriorly from the angle of the mouth to the angle of the mandible and from ala-tragus line to the lower border of the mandible. No abnormalities were seen on the skin and mucous membrane. On palpation, the swelling was hard in consistency and was tender on palpation. The right submandibular lymph nodes were palpable, mobile and nontender.
Intraoral examination showed a small (1 cm × 1.5 cm size), single, bony hard, nontender swelling in the mandibular right primary second molar region with obliteration of the buccal vestibule []. The teeth in the affected region were noncarious. The involved tooth was vital and nontender on percussion. There was no associated tooth mobility and any purulent discharge, and the patient's oral hygiene was good. The orthopantomogram [] examination revealed an approximately 1–1.5 cm radiopaque mass attached to the distal root of the primary right mandibular second molar, and it was well demarcated by a radiolucent halo. The observed clinical and radiographic findings led us to the provisional diagnosis of benign cementoblastoma. The clinical differential diagnosis included juvenile ossifying fibroma, osteoma, osteoblastoma, odontoma, periapical cemental dysplasia, condensing osteitis and hypercementosis.
The surgical excision of the tumor along with the extraction of the associated primary molar under general anesthesia was planned. Pediatrician's opinion was taken regarding the general health and fitness of the patient. The surgical excision was carried out by an oral and maxillofacial surgeon with the help of an anesthesiologist. At the time of surgery, the lesion could be easily differentiated from the normal bone [] and was removed along with the involved tooth. The surgical wound was closed by suturing. The excised tissue was irregularly shaped, white-colored structure with rough surface, hard in consistency and 1.6 cm × 0.8 cm × 0.5 cm in size []. The specimen was sent to histopathological examination.
The microscopic examination of H and E-stained (×10) section showed trabeculae of cementum-like calcified material lined by cementoblasts in the background of loose vascular connective tissue []. The center of the lesion showed trabeculae exhibiting reversal lines and numerous lacunar spaces filled with cementocytes. At the periphery of the lesion, radiating columns of unmineralized matrix oriented perpendicular to the connective tissue capsule were seen; in few areas, multinucleated cementoclast-like giant cells were also seen.
Thus, the final diagnosis of benign cementoblastoma was confirmed. The patient was recalled for regular clinical and radiographic follow-up. On 6-month follow-up, clinical and orthopantomogram [] evaluation showed satisfactory healing without any signs of recurrence. The eruption path of the underlying second premolar was normal.


A 29-year-old male patient reported to the department of conservative dentistry and endodontics with a chief complaint of sensitivity in the lower front teeth for 8 months. Here, the severity of sensitivity increased on occluding teeth. Few months later, he noticed swelling in the lower front jaw, which had slight tenderness on touch, not associated with fever or any discharge.
Extraoral examination revealed no gross asymmetry, discharge or sinus tract. On palpation of the lower chin, no tenderness was present.
Intraoral examination [] revealed tenderness on percussion with respect to tooth nos. 32, 31 and 41. A solitary diffuse swelling was observed with respect to the lower anterior region, with vestibular obliteration extending mediolaterally from 33 to 42 regions. The overlying mucosa was inflamed as compared to the surrounding mucosa with no sinus tract observed. The mouth opening was approximately 35 mm. To palpate, the swelling was soft in consistency and compressible due to labial cortical perforation. Cold test and electric pulp test were performed. Negative response was obtained on testing with respect to 31, 32, 33 and 41. Radiovisiograph revealed a well-corticated, multiple coalescent radiolucency with respect to the apical regions of 33, 32, 31, 41 and 42 []. A provisional diagnosis of radicular cyst associated with 33, 32, 31 and 41 was made. Treatment protocol planned was endodontic treatment followed by surgery.
Access opening was done for 33, 32, 31 and 41. On negotiating two canals, one buccal and one lingual canals were located for all teeth.
Working length was established, and cleaning and shaping was done up to ISO 30/0.02 size.
For disinfection, calcium hydroxide medicament was placed for 4 weeks []. As there were no signs of healing of the periapical lesion noticed, periapical surgery was planned after obturation of 33, 32, 31 and 41 [].
Enucleation of cyst with respect to 33, 32, 31 and 41 was done under local anesthesia. A full-thickness mucoperiosteal flap was elevated from the regions of 34–43 []. Cystic lining was separated from the bone and dissected from the underlying mucosa and removed in toto [Figure and ]. Apicectomy and retrograde filling was done with glass ionomer cement with respect to 33, 32, 31 and 41. Sharp bony margins were reduced, and the socket was debrided with betadine and saline solution. 4-0 vicryl sutures were placed to close the surgical site. Pressure pack and postoperative instructions were given. The patient was recalled after 1 day for follow-up and after 7 days for suture removal.
The cyst enucleated in toto was sent to the department of oral pathology for histological examination []. The histopathological report revealed that the section showed lining of corrugated parakeratinized stratified squamous epithelium with basal cell layer, showing typical tombstone appearance. The cystic lumen showed keratin flakes. The epithelium was lifted away from the underlying connective tissue capsule at few areas. The connective tissue showed dense inflammatory infiltrate with areas of vascularity.
An impression of OKC was made by the histopathological report [].
Considering the aggressive nature and high chance of recurrence of OKC, a decision to revisit the surgical site was taken. Vestibular incision was given from the distal aspect of 33 to the distal aspect of 42 region after administration of local anesthesia. A full-thickness mucoperiosteal flap was elevated. Curettage of granulation tissue was done within the cystic cavity followed by peripheral ostectomy and Carnoy's solution application. Socket toileting was done with betadine-saline solution. 3-0 interrupted silk sutures were used to close the surgical site. Pressure pack and postoperative instructions were given. The patient was recalled after 1 day for follow-up and after 7 days for suture removal.
Suture removal was done after 7 days.
The patient was recalled after 1 month, 3 months, 6 months and 1 year for follow-up. The radiographs revealed complete resolution of the periapical lesion, with the teeth being asymptomatic [].


A 57-year-old man presented to the outpatient clinic with a complaint of thin stools since three months; he reported anal bleeding, outlet dysfunction constipation with incomplete emptying, and lower pelvic heaviness 1 week before his visit. The patient had undergone hemorrhoidectomy 8 years ago, and had no underlying diseases such as hypertension and diabetes. He had never undergone a colonoscopy before. Four centimeters proximal to the anal verge, at the 6 o’clock position, a smooth, round huge palpable mass estimated to be more than 5 cm in diameter could be felt outside the rectum, accompanied by a small amount of bleeding on digital rectal exam. There was no visible tumor in the rectal mucosa, but mucosal modification was seen due to external compression at the same location on colonoscopy. Pelvic computed tomography (CT) revealed a 7.8 × 6.3 × 7.2-cm cystic lesion with thin, enhancing wall lining in the right retrorectal space. The tumor was located just below the level of the right seminal vesicle, superiorly abutting onto the right posterolateral wall of the rectum, pushing the rectum to the left (). On colonoscopy, there were no tumors in the mucosa, but external compression was noted, arising from the retrorectal space.
Preoperative bowel preparation was not done, and prophylactic intravenous 2nd generation cephalosporin was administered just before the operation. The patient was placed in the lithotomy position after induction of general anesthesia, to enable digital rectal exam during surgery. A 12-mm trocar was inserted into the umbilicus for the camera, and four 5-mm trocars were inserted into the right and left upper and lower quadrants, respectively. The small intestine was shifted upward with the Trendelenburg position with a slight tilt to the left side. Dissection was conducted to separate the left side of the tumor and the rectum (), and the anterior peritoneum was fixed to the abdominal skin using 2-0 Prolene with linear needles following dissection of the peritoneal reflection (). The separated rectum was tied with a nylon tape and controlled with a needle holder by an assistant (). The cystic lesion was seen after additional rectal mobilization (), and meticulous dissection was carried out around the cyst (). The tumor was resected without damage, and no remnant sac was observed (). There was little bleeding during the operation, which was completed after insertion of a drainage catheter in the pelvic cavity. The time from skin incision to closure of the trocar sites was around 120 minutes.
The tumor was an 8 × 5 × 5-cm-sized round cyst () that had a 3-mm-thick shell filled with nonodorous, mud-like material (). The patient started oral feeding on the day after surgery and was discharged without complications on the fifth day. The pathologic report confirmed a tailgut cyst, or retrorectal cystic hamartoma without evidence of malignancy, 7.5 cm × 5.0 cm × 2.0 cm in size. The patient had no abdominal or anal symptoms at the 1-month outpatient follow-up visit.
The study was approved by the Institutional Review Board of Chonnam National University Hospital (CNUH-EXP-2018-088); even though the patient’s informed consent was exempted, the risk to the patient was extremely low.


The patient was a 48-year-old woman who worked as a healthcare professional with a medical history notable for four renal transplantations for idiopathic renal failure beginning at age eight. She was on chronic immunosuppression with tacrolimus and mycophenolic acid. She presented initially with cutaneous SCC two years previously with a nodule of the dorsal right hand involving the 3rd and 4th webspace. Biopsy confirmed squamous cell carcinoma and she underwent Mohs resection of the mass with subsequent reconstruction with chest wall flap. Resection included at least partial excision of the ring finger radial digital nerve due to perineural invasion. A year later, she noted a recurrent mass of the same webspace and underwent re-resection with negative margins. Over the next several months, the mass slowly re-grew in the same webspace, prompting a biopsy with pathology consistent with recurrent SCC. Magnetic resonance imaging (MRI) at that time showed a dorsal mass to the interspace between the heads of the third and fourth metacarpals measuring approximately 7 mm transverse × 5 mm volar-dorsal × 16 mm proximal-distal. The tumor significantly involved the webspace with some penetration of the lesion into the volar neurovascular bundle. Clinically, there was suspicion of dorsal, dermal invasion; however, MRI did not show bone invasion. She was seen in consultation at an outside institution where single (4th digit) to double ray resection (3rd and 4th digits) was recommended.
The patient presented to our institution for a second opinion. The recommendation of upfront surgical management was reinforced. As the patient refused ray amputation due to functional loss and cosmetic deformity, the option of initial external beam radiation therapy followed by surgical tumor debulking was discussed. The potential serious complications of surgery and radiation therapy were discussed in detail []. Due to the increased risk of wound healing complications, significant impairment of lymphatic drainage, fibrosis, swelling, and continued pain which could have limited the function of her hand, she declined this option as well. The option of EBRT alone using electrons was proposed. An initial plan using electrons was generated but the dose inhomogeneity was deemed unacceptable given the complexity of the target. Subsequently, she was referred to the brachytherapy group for consideration of interstitial brachytherapy (). After much discussion, a plan of surface and interstitial HDR brachytherapy was generated with the goal of balancing tumor control with preserving organ function.


The patient was a 67-year-old woman with severe kidney disease (3 rejected renal transplants), severe peripheral vascular disease (Fig. A), hypertension and suffered a recent ischaemic stroke during AF. She was hospitalized with a non-ST elevation myocardial infarction and known with paroxysmal AF for 9 months (CHA2DS2-VASc = 6).


Our patient was a 70-year-old man with severe dysphagia as a result of accidental ingestion of sulfuric acid while intoxicated when he was roughly 30 years old. He was initially treated by subtotal esophagectomy with gastric tube–cervical esophageal anastomosis. Severe dysphagia continued afterwards, and in 2005 (at the age of 58 years) he visited the Department of Surgery of Nakagami Hospital. Despite undergoing endoscopic esophageal dilatation several times every year, his symptoms did not improve, and he underwent contracture release and PMMC flap transfer in 2009 (at the age of 62 years). He also underwent periodic endoscopic esophageal dilatation thereafter (up to five times per year). He was referred from the department of surgery to the department of plastic surgery in May 2016. On examination, there was a surgical scar on his neck, and a scar where the right PMMC flap had been harvested. There was also a scar in the center of his abdomen from the first operation, as shown in . He complained of extreme difficulty in swallowing, leading him to squeeze his neck manually to pass food. Endoscopic examination by an otolaryngologist showed no major problems in his larynx, and it was considered that the food that he consumed entered the gastric tube via the PMMC flap from the right piriform sinus. It was impossible to advance the endoscope forward due to the severe stenosis. Three-dimensional multi-detector CT (MDCT) and VE were performed. MDCT was performed using a 64-slice CT apparatus (Aquilion 64; Toshiba Medical Systems Corp., Otawara, Japan). The technical parameters were 120 kVp, 150 mA, collimation of 64×0.5, a rotation time of 0.5, a slice thickness of 1 mm, and an increment of 1 mm. On VE, the stenosis was about 2–3 cm in length. A contrast swallowing examination also showed a similar result, as shown in . Based on the VE findings, we decided to utilize a patch graft, for which we expected that the luminal mucosa could be used to some extent. Thus, surgery was planned to release the stenosis and replace it with a FJPG.
In August 2016, a joint operation took place. A U-shaped skin incision was made in the neck. The transplanted right PMMC flap was dissected. Using a nerve-stimulating device, peeling of the flap and esophageal stricture was performed. Ultimately, the PMMC flap was excised, and the leftover epithelium remained in the lumen. As shown in the preoperative VE image of the right piriform sinus, pinhole-like stenosis was observed.
The stenosis was incised and expanded sufficiently with fingers on both the cephalad and caudal sides. The right piriform sinus remained only on the left wall (inner wall), and it was decided to reconstruct the three sides of the front, the rear, and the outer walls with a FJPG. The defect length was about 5 cm, in a spindle shape. The harvested jejunum was split in the longitudinal direction, and was divided into a patch graft and a monitoring segment. The FJPG was transferred in a 90°-transposed fashion. The third jejunal artery and the right transverse cervical artery were end-to-end anastomosed with 9-0 nylon sutures. The third jejunal vein and the right internal jugular vein were end-to-side anastomosed with 9-0 nylon sutures.
The flap survived completely. Videofluorography was performed at 3 months postoperatively, and good passage was confirmed, as well as at 2 years postoperatively. There were no complications, such as an abdominal wall hernia. The patient was able to enjoy meals and his body weight increased by 10 kg. Upper gastrointestinal endoscopy was performed at 2 years and 3 months after surgery. Superficial gastritis was found in only a part of the gastric tube, and no evidence of stricture or cancer was seen, as shown in .


A 44-year-old Taiwanese male, an office worker, represented to us with a 2-year history of a productive cough.
He had experienced 3 episodes of pneumonia in the previous 2 years. After empiric treatment with antibiotics including levofloxacin 750 mg PO for 1 wk in the past 3 episodes, the symptoms subsided. At the time of presentation, the patient seemed uncomfortable and feverish.
He had been healthy before the cough developed.
He was a non-smoker and no specific family history.
Physical examination showed decreased breathing in the right lower lung field.
Serum laboratory data, including tumor markers such as carcinoembryonic antigen (1.91 ng/mL) and anti-squamous cell carcinoma antigen antibody (0.60 ng/mL), were within normal limit.
A plain chest radiograph demonstrated focal atelectasis of the right lower lobe of the lung. Contrast-enhanced thoracic computed tomography was also performed, and revealed bronchiectasis, right lower lobe, and a nodule with a lower density material over the right hilar region (Figure ). The differential diagnosis included hematoma or mucoid impaction soft-tissue lesions (Figure ).
Bronchoscopy revealed an endobronchial lobulated protruded mass in front of bronchi 9 and 10 (Figure ). An endobronchial biopsy was performed with forceps. The pathological report revealed atypical cell nests with hyperchromatic nuclei. But it did not lead to a diagnosis. Therefore, he underwent surgical intervention. The final pathological report revealed glandular papilloma of lung.


A 65-year-old Caucasian female presented to the emergency department with a 3-day history of haematuria, exertional dyspnoea, abdominal pain, myalgia and profound fatigue. She reported profuse non-bloody diarrhoea the day before onset of symptoms, having eaten at a seafood restaurant. Her past medical and drug history are shown in . Upon clinical examination, she had marked conjunctival pallor, scleral icterus and marked tachypnoea with a respiratory rate of 24 breaths per minute and oxygen saturation of 95% on room air. Left iliac fossa tenderness and voluntary guarding were noted on abdominal palpation and rectal examination was unremarkable.
Initial blood tests () revealed a normocytic anaemia, raised reticulocyte counts and hyperbilirubinaemia, raising the possibility of a haemolytic process. Urinalysis demonstrated 3+ of both protein and blood, with microscopy () demonstrating renal tubular cells and red cell casts. At presentation, she had an acute kidney injury (AKI) which subsequently worsened throughout the admission. ECG was normal and her chest x-ray showed small bilateral pleural effusions.
The differential diagnoses considered at this stage were gastrointestinal blood loss, haemolytic anaemia secondary to sepsis, haemolytic uraemic syndrome (HUS), infective endocarditis and malignancy. Initial management included IV fluids and fluid balance monitoring in the context of the AKI.
Subsequent blood tests were noted to haemolyse and her haemoglobin rapidly fell to 6 g/dl. No clotting samples could be processed. The peripheral blood smear revealed a few spherocytes, mild polychromasia, no fragments and toxic looking neutrophils (). The lack of red cell fragments and normal platelet count made HUS an unlikely differential. Transthoracic ECHO revealed a functioning porcine aortic valve without evidence of infective endocarditis and renal ultrasound showed normal kidneys.
A haemolysis screen noted a raised LDH, undetectable haptoglobin levels and a positive direct antiglobulin test (DAT) (3+ IgG), suggesting an autoimmune haemolytic anaemia (AIHA) (). Cold agglutinins and a viral screen were negative. A paroxysmal nocturnal haemoglobinuria (PNH) screen was requested given the possibility of haemoglobinuria (urinalysis positive for blood but absence of red cells on microscopy) and an intravascular source of the haemolysis. This identified marked clonal expansion of GPI-anchor deficient blood cells by flow cytometry, with 17% red cell clone and 78% monocyte and granulocyte clones. A bone marrow aspiration and trephine (BMAT) showed no evidence of an underlying myelodysplastic syndrome or aplastic anaemia.
A diagnosis of concurrent AIHA and PNH, precipitated by a presumed acute gastrointestinal infection was formulated. The patient received packed red cell transfusions and was commenced on oral prednisolone (at a dose of 1 mg/kg) for AIHA. The patient was transferred to PNH National Service centre and subsequently commenced on eculizumab. She was also treated with thromboembolic prophylaxis (following resolution of the AKI) and was vaccinated against meningitis, due to increased risk conferred with eculizumab treatment.
She made a good recovery with eculizumab therapy and was under surveillance. At 3 years following her initial presentation, the PNH clone had persisted. Despite her good recovery and haematological stability, our patient died unexpectedly at 3 years following complications of her underlying (bio-prosthetic) valvular heart disease.


A 60-year-old Chinese male visiting from Australia presented to our hospital with syncope. He had been having cough, fever, myalgia, and malaise for the past 4–5 days. Past medical history included atrial fibrillation (AF) and hypertension. Drug history includes aspirin, perindopril, and atenolol. No history of illicit drug use. He reported contact with water from his outdoor inflatable pool 2 weeks ago in Australia.
Patient was hypotensive on arrival at the emergency department and required fluid resuscitation with improvement in blood pressure. He had Type 1 respiratory failure requiring non-rebreathable mask. Pulse was irregularly irregular, heart rate was 100 b .p.m. There were no audible murmurs. Coarse crepitations were heard in the left lung.
Laboratory investigations on admission were notable for elevated transaminases and elevated troponin T levels. Serum troponin T was 1041 ng/L. Serum alanine transaminase was 181 U/L while aspartate transaminase was 137 U/L. Chest radiograph showed cardiomegaly with bilateral infiltrates and a right pleural effusion. Ultrasound-guided pleural aspiration revealed haemorrhagic contents. Electrocardiogram showed AF with a right bundle branch block pattern (Figure ).
Transthoracic echocardiogram (TTE) on admission showed moderately depressed left ventricular ejection fraction (LVEF) of 42%.
Patient was initially treated as for respiratory tract infection and possible Type 2 myocardial infarction with intravenous (IV) ceftriaxone and doxycycline.
On Day 2 of admission, the patient’s rhythm was noted to be in alternating right and left bundle branch block (Figure ). He then developed a transient episode of pulseless electrical activity. There was return of spontaneous circulation within seconds after resuscitation with a bolus dose of IV adrenaline 1 mg and cardiopulmonary resuscitation. Monomorphic ventricular tachycardia (VT) followed. This was terminated within a minute with a bolus dose of IV amiodarone 150 mg. He subsequently developed recurrent runs of non-sustained VT (NSVT) and was given 100 mg of IV lignocaine.
Dual inotropes were required to maintain blood pressure. Patient was in bradycardia with ventricular escape rhythm and had recurrent runs of NSVT. Temporary pacing wire was inserted. Coronary angiogram showed minor coronary artery disease. Veno-arterial extracorporeal membrane oxygenator was implanted for refractory cardiogenic shock. A centrifugal ECMO pump system was used with cannulation of the right femoral artery and left femoral vein. A distal perfusion cannula was inserted at the right proximal superficial femoral artery to reduce risk of right lower limb ischaemia. Extracorporeal membrane oxygenation flow was maintained between 3 to 4 L per minute.
Urgent endomyocardial biopsy was performed to confirm the clinical diagnosis of fulminant myocarditis and to determine the underlying aetiology. Endomyocardial histology demonstrated features consistent with myocarditis with predominantly lymphocytic infiltrates.
After ECMO implantation, patient continued to have runs of monomorphic VT of varying morphologies. The recurrent runs of VT were not amenable to chemical and electrical cardioversion or overdrive pacing. Ablation was not considered in view of varying morphologies of VT and underlying aetiology was deemed secondary to myocardial inflammation.
Repeat TTE showed severely depressed LVEF of <10%. There was subsequently no pulse pressure or cardiac rhythm while patient was on VA-ECMO support. Continuous renal replacement therapy was commenced for acute kidney injury. Decision was made to empirically pulse high -dose IV methylprednisolone as endomyocardial histology confirmed acute myocarditis without obvious pathogens or viral cytopathic features present. One gram of IV methylprednisolone was given, then 500 mg per day over the next 2 days, followed by tapering doses of prednisolone, 30 mg b.i.d. for 2 days, 25 mg b.i.d. for 2 days, 20 mg b.i.d. for 2 days, and then 15 mg b.i.d. for 2 days. Haemodynamic status improved over the following week. Inotropes were weaned off by Day 6 of admission. Veno-arterial extracorporeal membrane oxygenator was successfully explanted after ten days of support. A total of 14 days of IV ceftriaxone and oral doxycycline was given.
He was extensively evaluated for an underlying infective aetiology. Multiple blood cultures were negative. Respiratory virus polymerase chain reaction test was negative. A search for evidence of parvovirus, Epstein–Barr virus, cytomegalovirus, herpes simplex virus, dengue virus, Zika virus, chikungunya virus, human immunodeficiency virus, hepatitis B/C virus, toxoplasma, rickettsia from blood, serum, and urine did not yield any positive results except for a paired convalescent leptospira enzyme-linked immunosorbent assay (ELISA). The initial leptospira IgM at admission was negative, but a convalescent repeat 2 weeks later returned positive, supporting the diagnosis of acute leptospirosis.
After recovery of haemodynamics, patient was started on heart failure treatment, including bisoprolol and hydralazine, isosorbide dinitrate combination. Angiotensin-converting enzyme inhibitors were not started, while renal function was recovering.
There were no further episodes of malignant arrhythmia. Transthoracic echocardiogram done before discharge showed normal LV cavity size and LVEF of 65%. He was discharged stable 3 weeks after admission.


A 37-year-old Chinese man was admitted to the Xuanwu Hospital Capital Medical University (Beijing, China) with the major complaints of coughing and mild fever for 2 weeks, with daily expectoration of yellow or white sputum. The patient was a non-smoker and also denied use of alcohol or any illicit drugs. The patient also presented with a medical history of recurrent pneumonia during childhood. During chest auscultation, a few moist rales were audible from basilar areas of the right back. Chest X-ray analysis showed a large opaque area in the lower right lobe, with a slightly blurred edge. Chest radiography was not improved after intravenous administration of 2.0 g cefminox twice daily for 7 days. Tests of liver and renal function, blood cell counts, and coagulation tests were normal. Both sputum culture and acid-fast staining were negative. Galactomannan and β-D-glucan detection, latex agglutination, and a T-SPOT test for tuberculosis were also negative. Remarkably, laboratory analysis of tumor markers in the patient’s serum showed a significant increase in CA125 levels ().
After admission, a chest computed tomography (CT) examination was performed. The CT scan showed a heterogeneous mass in the right S10 region that was scattered in the low attenuation area. A single systemic artery provided vascular supply from the descending aorta (, arrow), while venous drainage was via the pulmonary venous system. The patient was diagnosed with right intralobar pulmonary sequestration and eventually underwent thoracotomy to remove the right sequestrated lung (measured size of the mass = 12 × 6×3 cm3). Epithelioid cells, lymphocytes, and polynuclear giant cells were visualized in the mucus-containing dilated bronchi by standard microscopy (). Immunohistochemical staining of the sequestrated lung showed positive staining for CA125 in some area of bronchial epithelial cells and epithelioid cells ().
After surgery, the patient was discharged according to standard procedures. No further treatments were administered after discharge. Six months after surgery, the patient was clinically re-assessed and no post-surgical complaints were noted. A set of exams to evaluate whole blood cell counts, liver and kidney function, coagulation function, and other indicators were also performed. All test results were within the normal range. Additionally, CA125 levels were within the normal range (14.08 U/mL).
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. Ethics approval was not applicable because there was no special treatment for the patient.


Proband (, IV1) is a male child aged 8 years, the oldest of two siblings from non-consanguineous parents. Clinical history included uneventful perinatal development, although he was born by caesarean delivery, weighing 3055 g and with a head circumference of 49 cm at birth, with no reported complications before or after birth. The mother (, III2) presents tiredness, headaches and muscle weakness and had three pregnancies with one previous miscarriage (at the sixth week). Brother and father were reported to be healthy. Several members of the family report muscle weakness, neurological problems and lactic acidosis.
The proband presented at 2 years with vomiting, fever and diarrhoea accompanied by progressive developmental delay, irritability, fatigue, hypotonia, weight loss, gastrointestinal and body temperature dysautonomia, repetitive infections, cognitive impairment and autistic behaviour. The first suspected diagnosis was autism spectrum disorder due to speech regression, hand stereotypies and flapping, with worsening of these symptoms during infections. Blood tests such as lactate and pyruvate were consistently elevated; venous blood examination showed severe metabolic acidosis and altered carnitine profile (increased C4, C5, C5:1, C5-OH), suggesting the possibility of a mitochondrial disease.
Brain MRI showed hyperintense signals in T2/FLAIR sequences in the white matter of the peritrigonal region, possibly corresponding to gliosis (). The mother also presented hyperintense signals in T2/FLAIR in the white matter of the subcortical parietal frontal lobe ().
Treatment was started with L-carnitine, biotin and CoQ10, and was associated with normalisation of MRI, weight gain, decreased fatigue, irritability and autistic behaviour. The mother was also treated with good response to L-carnitine and CoQ10. The patient is currently undergoing reposition of immunoglobulins with decreasing of repetitive infections and consequently improving general clinical presentation.


A 62-year-old female with a medical history of diffuse large B-cell lymphoma, nongerminal cell type was diagnosed in 2004. The patient received 2 salvage therapy lines. She was given 6 cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, hydrochloride, vincristine sulfate, prednisone) in March 2004 with remission. She experienced a recurrence in February of 2017 and was given 4 unsuccessful cycles of R-GCD (rituxan, gemzar, cisplatin, dexamethasone). As a second-line therapy, she received an ABMT, which was not T-cell depleted. The patient’s stem cell collection was performed in July 2017, 5 months after receiving her second round of high-dose chemotherapy with R-GCD. The patient did not receive any other unusual chemotherapy regimens, nor any investigational drugs prior to her graft. Prior to her transplant, the patient received BEAM conditioning [carmustine (bis-chloroethylnitrosourea, BCNU), Etoposide, Ara-C, and Melphalan]. The patient was placed in remission after receiving ABMT July 2017. The patient was not on any immunosuppressive therapy following ABMT. She has not experienced recurrence since receiving her ABMT.
During the first year after her ABMT, the patient experienced recurrent sinusitis and was treated with antibiotic therapy approximately once every 2 to 3 months, with temporary resolution of symptoms between recurrences. During the second year after her ABMT, she developed pneumonia twice, the second of which required hospitalization for sepsis secondary to Streptococcus pneumonae. Prior to receiving her ABMT, the patient was not subject to recurrent infections.
Serum immunoglobulins (Igs), Ig subclasses, antibody responses, lymphocyte subsets, complete blood cell count, and immunofixation were performed 2 years posttransplant. and demonstrate the results of the patient’s initial testing. As described in , the Ig levels demonstrated an elevated total IgG with IgG1, IgG2, and IgG4 subclass deficiencies. IgG3 was found to be significantly elevated >220 g/dL. The immunofixation demonstrated a monoclonal IgG without light chain detected at 0.4 g/dL (). Antipneumococcal titers were unresponsive to both Pneumovax and Prevnar vaccinations. Lymphocyte subsets were within normal limits.
The patient received intravenous immunoglobulin (IVIG) diagnosis of hyper-IgG3 gammopathy with total IgG deficiency and IgG1, IgG2, and IgG4 subclass deficiencies. This therapy successfully decreased the frequency and quantity of recurrent infections.


A 20-year-old male patient was referred to our hospital with a small black-colored polyp on the upper lip. On clinical examination, a small polyp measuring 10 × 8 mm in size at the right side of the upper lip mucosa with a brown–black patch expanding from gingivolabial sulcus to the attached gum of incisor tooth was observed (). He was clinically diagnosed with a mucosal malignant melanoma with a metastatic right submaxillary lymph node (). The brown–black patch was melanoma in situ. The polyp was found to be a malignant melanoma following a biopsy. Tumor resection with radical neck dissection was performed 5 days after the biopsy. The tumor excision site was planned, involving some orbicularis oris muscle, including oral mucosa, gingiva and alveolar bone extending from the right canine tooth to the left central incisor tooth (). The defect in the red lip was reconstructed using a musculomucosal flap from the lower lip; simultaneously, the perioral defect was reconstructed using a tongue flap. Initially, the intraoral defect was filled using a tongue flap to the greatest extent possible (). A 10-mm width musculomucosal flap including the right inferior labial artery, in which blood flow had been detected using Doppler ultrasound after right side neck dissection, was designed at the lip mucosa, reaching the left side beyond the center of the lip (). Both the right vermillion border and the shortage of intraoral reconstruction by the tongue flap were repaired using a lip musculomucosal flap (). Both flaps healed well without any congestion or necrosis. They were separated at 2 weeks after primary surgery under deep sedation. The patient could eat and speak without trouble. Nevertheless, cupid’s bow was conspicuous for the gap and the postoperative scar contracted after 3 months. Therefore, correction of the cupid’s bow using Z-plasty of the white lip and reduction of the tongue flap was performed. The secondary operation to correct the misalignment of cupid’s bow and to remove the contraction was successful ().


The patient is a 28-year-old female with history of drug abuse previously on suboxone 5 months prior and migraine headaches who overdosed on intravenous recreational drugs. She has a family history of bipolar disorder in a paternal aunt but had no psychiatric disorders herself.
While out of state, the patient was initially found unconscious for an unknown duration in the field by EMS with agonal breathing and acute hypoxic respiratory failure to an unknown degree requiring a nonrebreather mask. She had some positive response to naloxone via intranasal and intravenous administration with the patient less obtunded. Upon arrival at the Emergency Department, she became more alert but was confused and combative. Initial noncontrast head Computed Tomography (CT) was unremarkable for acute changes, as well as repeat imaging 24 hours later. Initial urine toxicology screening was positive for benzodiazepines but negative for opiates. Serum alcohol level was negative. A boyfriend reported intravenous heroin use immediately prior to this presentation, and the patient was noted to have track marks on her right upper extremity. The patient also used benzodiazepine immediately prior to the inciting event for anxiety, although no prescriptions were in the state's reporting system for controlled substances. On the second day of her hospitalization, the patient required elective intubation due to status epilepticus from suspected benzodiazepine withdrawal. She was uneventfully extubated the following day. She was alert and oriented ×3 with no focal neurologic deficits and left against medical advice on day 3 of the hospitalization.
Five days following the initial hospitalization in the same state as the initial inciting event, the patient was noted by her family to have retrograde amnesia and an inability to care for herself due to confusion. Upon admission to a different hospital, the patient was noted to be only oriented to self and unable to provide history regarding her recent hospitalization. Urine drug screen was negative. Liver enzymes were elevated on admission (ALT 384 μ/L, AST 227 μ/L) due to Hepatitis C. She had an electroencephalogram (EEG) which showed frequent epileptiform activity in the occipital region without electrographic seizures. The patient was started on topiramate 50 mg BID and levetiracetam 500 mg BID for seizure prophylaxis. Imaging with head CT without contrast showed low attenuation of the caudate heads and lentiform nucleus, suggestive of hypoxic injury with clinical encephalopathy (Figure ). MRI of the brain was unremarkable during this admission (Figure ). Due to labile emotions, she was started on 0.25mg q8h lorazepam as needed. After 2 days of hospitalization, the patient was discharged, as she was alert and oriented ×3 without confusion and with a nonfocal neurologic examination.
Four weeks after the initial event, the patient presented to our hospital due to acute psychosis of 2 days' duration, including confusion, agitation, lack of sleep, flat affect, and hallucinations. Family reported that she was doing well at home following discharge from the second hospitalization, except for short-term memory loss. Upon admission, the patient was alert and oriented to self only with a nonfocal neurologic examination. Montreal Cognitive Assessment (MOCA) administered on admission showed significant cognitive impairment with a score of 16/30. Urine drug screen during this hospitalization was negative. Liver enzymes were mildly elevated. Head CT without contrast revealed bilateral symmetric areas of abnormal low attenuation in the basal ganglia involving the caudate heads and anterior aspect of the putamen due to anoxic brain injury (Figure ). Brain MRI with contrast demonstrated a hyperintense T2 signal in the basal ganglia with mild white matter changes in bilateral frontal paraventricular areas (Figure ). Infectious Disease was consulted, and the workup was negative, including HIV, CMV, HSV, Lyme disease, syphilis, and acute EBV. No cerebral spinal fluid analysis was done due to patient's clinical condition and parent's wishes to monitor clinically with low to no index of suspicion for infectious etiology, as no fevers, leukocytosis, or meningeal signs were present. Arylsulfatase A level in leukocytes was within normal limits. The patient had multiple EEG's which failed to show any significant seizure activity, including during the patient's delusional episodes.
Psychiatry was consulted, who declared there was no underlying primary psychiatric condition. Her home topiramate 50 mg BID and levetiracetam 500 mg BID were discontinued due to concern of worsening her clinical features. She was started on olanzapine 5 mg q6h, trazodone 100 mg nightly, and scheduled lorazepam 2 mg q6h. However, she had minimal response to this regimen with frequent agitation and delusional outbreaks. She was transitioned to quetiapine (50 mg, 50 mg, and 100 mg) TID with 50 mg PRN and lorazepam 2 mg q6h PRN with good response, which were continued as outpatient. Carbamazepine 200 mg BID was started during the admission for seizures and continued at discharge. Propranolol 10 mg TID was initiated and continued upon discharge for tachycardia due to agitation. The patient was alert and oriented to person, place, and time without hallucinations or paranoia upon discharge home. She was calm, relaxed and more interactive. She had improved sleep, with seven hours per night.


A 48-year-old female patient presented with a several-year history of a slowly increasing asymptomatic mass in the lateral surface of the left auricle, near the concha. The patient could not recall any history of trauma at the site of swelling. The lesion appeared as a solitary 0.8 cm skin-colored, dome-shaped nodule with irregular borders. In detail, the round mass had central small pitted umbilication and a tuft of fine hair protruding out of it (). In palpation, it was smooth, rubbery to firm in consistency, and fixed to the the intertragal notch of the left auricle without cartilage component. The remainder of the physical examination was unremarkable. There were no local lymphadenopathy and any other masses in the body in physical examination. Clinical diagnosis of accessory tragus, hair follicle nevus, other adnexal tumor, and basal cell carcinoma were also made due to irregular surface.
Because the patient wanted to remove the mass, wide local excision was planned. The mass was removed completely. Intraoperatively, it was adherent to the auricular epidermis so that it was inevitable to expose the auricular perichondrium. After removal of the mass, the exposed wound and perichondrium was covered with split-thickness skin graft. The biopsied tissue was single, firm, globular grey white and measured 0.6×0.5×0.5 cm in size.
Histopathological examination showed a dilated central cystic follicle that communicated with the overlying skin surface. The dilated follicular opening showed keratin debris and hair. The follicle was lined with squamous epithelium and surrounded by numerous smaller secondary follicles, many of which contained fragments of hair shafts along with many variables sized hair follicles exhibiting varying degree of maturation (). Epidermis and dermis unremarkably showed strands of stratified squamous epithelium. Many fibroblasts was observed at the the stroma. The histopathological analysis was consistent with TF. There was no recurrence after a follow up of 1 year.


A 25-year-old male patient was referred to the Department of Prosthodontics and Crown and Bridge, MCODS, Manipal, Manipal Academy of Higher Education, for the replacement of maxillary front teeth. A history of uneventful extraction of proclined maxillary central incisors and right lateral incisor occurred 2 months back was reported. On examination, the patient had a right unilateral cleft lip without involvement of alveolus and secondary palate []. There was no contributory family and medical history. Intraoral examination revealed healthy and sound remaining maxillary tooth structure []. The patient's concern for missing anterior teeth was considered and an interim partial denture was delivered. The patient was also explained about various rehabilitative procedures for congenital lip defect. On positive reinforcement, the patient recognized the importance of a comprehensive prosthesis and consented for the same. To improve the cosmetic appearance, a magnet-retained silicone lip prosthesis with cast partial denture was designed.
A preliminary impression of the maxillary and mandibular arch was made in irreversible hydrocolloid (Alginate, DPI, New Delhi, India), and facial impression of the lower third of the face that involved the upper lip defect was made with polysulfide impression material (Reprosil, Dentsply India Pvt. Ltd.). The preliminary and lower facial impression cast was poured with type III dental stone (Goldstone, Asian Chemicals, Rajkot, India) [].
Intraoral maxillary cast was surveyed, and cast partial denture with the retentive elements was designed to achieve more stable and retentive silicone prosthesis. The entire framework was casted using cobalt–chromium alloy (Remanium®, DENTAURUM GmbH and Co. KG, Ispringen, Deutschland) and try-in was performed. Teeth arrangement was done, and the cast partial denture was processed with heat-cured acrylic resin (Trevalon, Dentsply India Pvt. Ltd. Gurgaon) [].
Extraoral master cast obtained was sculpted with wax pattern anatomically []. Marginal fit of the contoured wax pattern was then evaluated on the patient's face. The wax trial prosthesis along with the master cast was flasked. The biomedical-grade silicone (SILASTIC MDX4-4210, Dow Corning India Pvt. Ltd.) was shade matched with intrinsic colorants to the adjacent skin []. The colored silicone was packed in the dewaxed mold and processed based on the manufacturer's instructions. After the prosthesis was retrieved, extrinsic coloration was coated to merge it esthetically with the patient's skin color.
The tissue surface of the silicone prosthesis was affixed with (1.5 mm width) an autopolymerizing clear acrylic resin substructure (Rapid Repair Powder, Dentsply India Pvt. Ltd.). This substructure served as a base to house the retentive magnets (cobalt–samarium, Ambica Co., New Delhi, India). Perforations measuring approximately 2 mm were created on the substructure to serve the purpose of retaining overlaying silicone material []. The counterpart magnet was guided and centered on the cast partial denture labially and bonded with autopolymerizing acrylic resin (Rapid Repair Powder, Dentsply India Pvt. Ltd.) []. The whole assembly of extraoral and intraoral prosthesis was then positioned at the cleft lip defect []. By means of retentive magnet, lip prosthesis supported by the cast partial denture was delivered to the patient []. A skin biomedical-grade adhesive (MG 7-1010, Dow Corning®, India Pvt. Ltd.) was applied to form a better seal of the thin margin of the silicone with the adjacent skin.
At the delivery appointment, postoperative instructions with the removal and wear of the prosthesis were explained. The prosthesis marginal fit was enhanced after application of silicone skin adhesive. The patient experienced better magnetic retention, but reduced smile as the maxillary lip defect was small; hence, the prosthesis coverage provided limited movements on the skin. The patient was made well aware of the initial discomfort and maintenance and hence recalled for routine follow-up at 1 week, 1 month, and 6 months.


A 45-year-old man who complained of a 1-week history of swelling, erythema, and pain around his left upper eyelid (Fig. ) was referred to our hospital. The patient had Graves' disease but had discontinued anti-thyroid medications for 1 year. Cellulitis had already been diagnosed and treated with meropenem 0.5 g/day for 3 days at the local hospital. However, the patient's condition failed to improve.
The patient was already subjected to orbital MRI at the local hospital, which showed left upper palpebral cellulitis, sinusitis in the left frontal and ethmoid sinuses, and no intracranial complications (Fig. ). The best-corrected visual acuity was 1.2, and the intraocular pressure was 25 mm Hg in the left eye. Slit-lamp and fundus examinations of the left eye were normal. On blood tests, CRP was slightly high at 1.36 mg/dL, and the white blood cell count and procalcitonin were within normal limits, HbA1c was 6.5%, and thyroid hormone was elevated. The patient's temperature was 37.6°C. The patient was initially given cefazolin 1 g/day for 3 days but showed no improvement on MRI. Therefore, the skin of the left upper eyelid was successfully incised under local anesthesia, and a large amount of pus and blood was excreted (Fig. ). Postoperatively, there was significant improvement in the left upper eyelid (Fig. ). CT examination on the operation day showed left frontal sinus osteomyelitis and osteolysis of the inferior wall of the left frontal sinus connected to the left upper eyelid (Fig. ). Ceftriaxone 4 g/day, clindamycin 1.2 g/day, and fosfomycin 4 g/day were administered postoperatively. As for sinusitis, endoscopic sinusitis surgery (frontal sinus single sinus surgery [Draf III] and Kilian surgery) was performed. There was no recurrent palpebral cellulitis or sinusitis postoperatively. Bacterial cultures from the cellulitis and sinusitis were negative.


A 49-year-old man with chronic thromboembolic pulmonary hypertension (CTEPH)
(pre-procedural mean pulmonary artery pressure: 36 mmHg) underwent balloon pulmonary
angioplasty (BPA). Chronic total occlusion (CTO) of the left inferior pulmonary
artery trunk was observed (). To evaluate the collateral vessels of the CTO, time-resolved 4D CT
angiography (4D-CTA) was performed. The examination was performed using a 256-row
detector CT system (Revolution CT; GE Healthcare, Milwaukee, WI, USA) using the test
bolus tracking method. First, the test bolus was injected for 2 s, followed by a 0.9% saline
solution for another 4 s. Then, after waiting for 20 s, the main bolus injection for
18 s was automatically started, followed by the injection of a saline solution for
4 s. The CT operator then manually pressed the acquisition trigger button at the
beginning of the enhancement of the right ventricle in the test bolus (the trigger
point), visually assessing the monitor images along with the enhancement curve
measured in the region of interest (ROI) placed on the right ventricle. After the
subsequent scan delay of 23 s from the trigger point, an intermittent image
acquisition was automatically started. This image acquisition consisted of an
initial 24 intermittent volume scans with a rotation time of 0.28 s and a scan
interval of 0.6 s (scan duration: 20.52 s), followed by a secondary 13 intermittent
volume scans with a rotation time of 0.28 s and a scan interval of 1.47 s (scan
duration: 21.28 s). The CT operator manually stopped the image acquisition when the
contrast medium had sufficiently reached the systemic collaterals and the distal
pulmonary arteries of the targeted CTO. In this patient, the acquisition was
performed until the 31st scan. A 0.9% saline solution and an iodine contrast medium
with an iodine concentration of 370 mg/mL were delivered via a 20-gauge catheter
inserted into the right antecubital vein with an injection flow rate of 5 mL/s. The
acquisition was performed under automatic exposure control (tube current modulation)
with a noise index of 30 (for a slice thickness of 5 mm), and the tube current
ranged from 10 mA to 200 mA. Other scanning parameters were as follows: peak tube
voltage, 100 kVp; rotation speed, 0.28 s; scan coverage, 160 mm; a matrix size of
512 × 512 pixels; and reconstruction section thickness and section interval,
0.625 mm. The CT dose index volume for this examination was 28.84 mGy, and the
dose-length product was 461.46 mGy*cm. Consequently, the effective dose estimate was
6.46 mSv, which was determined by the dose-length product measurements and
appropriate normalized coefficients for chest CT (0.014 mSv/(mGy*cm)). 4D-CTA showed the bronchial artery-to-left inferior pulmonary artery
collateral supply, which was confirmed by a selective bronchial artery angiography
(; Video 1
in supplementary material). The patient’s symptoms improved with BPA of the other
stenotic lesions.