A hypertensive, diabetic, 67-year-old man was admitted to an outside hospital for the treatment of inferior wall myocardial infarction. Angiography, in the same hospital, demonstrated 80% stenosis of calcified proximal RCA, total occlusion in distal RCA (Fig. , 30% stenosis in left main coronary artery, and 50% in mid left anterior descending artery (LAD) with a small non-dominant left circumflex artery. At that time, DES implantation in RCA was attempted. The RCA was crossed with a BMW wire and predilated with 1.5 × 10 mm and later with 2 × 10 mm balloons at 16 atm for 20 s. But it was not successful as no balloon could be negotiated beyond the lesion in proximal RCA after successful wire crossing. Thereafter, patient was referred to our hospital for further management.
After analyzing his CAG records, due to significant calcification in proximal RCA, rotablation was performed with a 1.25-mm burr at 165,000 rpm. Then, distal lesion was stented with 2.5 × 20 mm PROMUS Element (Boston Scientific, Marlborough, MA), and everolimus-eluting stent (EES) and proximal lesion were stented with 2.75 × 20 mm PROMUS Element stent (Fig. . This procedure was successful with thrombolysis in myocardial infarction (TIMI) III flow, and there was no visible dissection or residual lesion. Further follow-up up to 2 months was unremarkable.
After 2 months, the patient complained of chest pain and was admitted with non-ST-elevation myocardial infarction and moderate left ventricular dysfunction. A repeat angiogram showed giant RCA aneurysms besides restenosis, along with progression of left main disease. Two aneurysms were detected: one in proximal RCA (15 × 25 mm) and other in acute marginal artery (10 × 30 mm) (Fig. . Taking into account the patient’s condition and the size of the aneurysms, off-pump coronary artery bypass surgery (CABG) was planned (Fig. . Left internal mammary artery (LIMA) graft to LAD and saphenous vein graft (SVG) to posterior descending artery (PDA) were carried out. RCA ligation was carried out at the ostio-proximal end and the distal end to seal off the blood flow to the aneurysms.
The patient’s condition was stable at the end of the operation. Post CABG, patient was discharged on dual antiplatelet therapy and statin. At further follow-up, patient was doing well and asymptomatic.


A 48-year-old female patient presented with abnormal behavior and urinary incontinence for 1 month. The patient was on oral telmisartan 20 mg once daily for hypertension. Magnetic resonance imaging scan of the brain revealed a large lobulated bilateral falcine homogenous contrast-enhancing mass lesion measuring 6.5 cm × 6.0 cm × 6.5 cm [Figure and ], with mass effect on adjacent structures and displacement of the bilateral anterior cerebral artery. Rest of the preoperative investigations was unremarkable. The bifrontal craniotomy was carried out under general anesthesia with invasive blood pressure and central venous pressure monitoring. During tumor resection, the patient had continuous bleeding, with fluctuating hemodynamic despite using oxidized cellulose polymer. Intravascular volume was maintained with crystalloid, colloid, and packed red cells transfusion. After 3 h of surgery and following loss of almost 2 L of blood, we decided to quit. However, it appeared difficult to achieve hemostasis. The bleeding continued from the tumor bed despite repeated attempts in spite using available hemostats during surgery to control it. There prevailed a situation of uncertainty. Based on our previous experience, it was decided to administer tranexamic acid at a dose of 10 mg/kg.[] Within 10 min of administration of tranexamic acid, there was a significant decrease in the bleeding from the tumor bed and in the next 20 min, we noted satisfactory hemostasis. This also coincided with the improvement in the hemodynamic profile of the patient and reduction of fluid to the maintenance dose. Postoperatively, the patient was shifted for elective ventilatory support and gradual reversal of neuromuscular blockade. The postoperative noncontrast computed tomography scan showed no major collections of blood in the operated field []. Subsequently, the patient was weaned off the ventilatory support and was discharged on the 10th postoperative day. Histopathological examination is suggestive of Grade 1 transitional meningioma.


A 30-year-old female patient presented with a 8 months history of a swelling located in the midline of the hard palate (). The swelling was persistent and firm with no increase in the size over a period of 3 months. There was no history of trauma, bleeding, or discomfort from the lesion. Family history and review of systems were non-contributory.
On examination, no changes were seen extra-orally. Head and neck examination demonstrated no palpable cervical or submandibular lymph nodes. Intra-orally, a well-defined solitary nodular swelling of size 1 cm × 1 cm was present in the region of the mid-palatine raphe. The overlying mucosa was slightly erythematous at the periphery. On palpation, the swelling was nontender, firm and attached to the underlying mucosa. The surface of the swelling was smooth and was neither compressible nor reducible ().
Based on the above clinical findings, a provisional diagnosis of a benign mesenchymal non-odontogenic tumor was considered. A fine needle aspiration cytology revealed hemorrhage with few squamous cells suggesting no evidence of inflammation or malignancy. A maxillary occlusal radiograph and digital volumetric tomography did not reveal any significant finding in relation to maxillary anterior teeth.
The differential diagnosis considered was benign soft tissue tumors like fibroma, neural tumors such as neurofibroma and traumatic neuroma. A benign minor salivary gland tumor such as a pleomorphic adenoma was considered on account of its site, their slow growths, and absence of neural symptoms. The possibility of oral focal mucinosis though rare was also included.
An excisional biopsy was performed under general anesthesia, and it was subsequently followed by a histopathological examination to conclude the provisional diagnosis. The histopathological examination revealed a highly cellular well-circumscribed encapsulated spindle cell tumor, which is separated from the overlying surface epithelium by fibrous stroma (). Sheets of spindle cells with vesicular nuclei, intermingled with ovoid cells are arranged in the form of fascicles (). At the periphery of the lesion, peripheral nerve bundles are seen. These features are suggestive of cellular schwannoma. Immunohistochemical evaluation revealed intense nuclear staining for S-100. More than 50% of cells were positive and confirmed the diagnosis (). The patient was followed up after 10 days with satisfactory healing and no fresh complaints.


A woman aged 66 years presented with decreased right visual acuity over several months. On admission, her visual acuity was 0.04 on the right and 0.1 on the left. Right abducens palsy was noted. Conventional MRI and MR angiography (MRA) revealed a giant right ICA aneurysm (diameter 30 mm) and a left ICA aneurysm (5 mm) [Figure -]. T1-weighted MRI (T1WI) showed a mixed iso–low-intensity area in the lumen of the right giant ICA aneurysm, although a flow artifact originating from the aneurysm was present []. T2-weighted MRI (T2WI) revealed an iso–high-intensity area at the center of the aneurysm [].
In ASL-MRI with PLDs of 1.5 and 2.5 seconds, although the left aneurysm was not demonstrated, the right ICA aneurysm was depicted as a hyperintense signal area in nearly the same configuration [Figure and ]. This area was large enough to extend to the axial level of the basal ganglia [Figure and ], while the aneurysm was not seen at this level in conventional MRI []. Hyperintensity circles were also noted in a concentric arrangement central to the right aneurysm [Figure and ]. Although there was no laterality in the bilateral middle cerebral artery (MCA) territories on MRA [], ASL-MRI with PLD 1.5 seconds demonstrated decreased signals in the right hemisphere, especially the right MCA territory []. ASL-MRI with PLD 2.5 seconds showed improvement in this decreased area, although a slight right laterality was still present [].
Carotid angiography (CAG) at 1.5 and 2.5 seconds after contrast medium injection into the right and left ICA, respectively, clearly demonstrated the nonthrombosed giant aneurysm at the cavernous portion of the right ICA [] and the aneurysm at the cavernous portion of the left ICA [], respectively. At 4.5 seconds PLD, the contrast in the right ICA aneurysm was still stagnant [, right], while the contrast in the left aneurysm had completely disappeared [, right]. In the left CAG at 1.5 seconds, the trunks of the left MCA and ACA were well opacified, and their peripheries had started to be visualized [, left]. In contrast, in the right CAG at 1.5 seconds, the trunks of the right MCA and ACA were barely visualized due to stagnation of the contrast in the giant aneurysm [, left]. At 2.5 seconds, the trunks and peripheries of the right MCA and ACA were opacified [, middle] but not fully visualized compared with the left [, middle].
The balloon Matas and Allcock test revealed robust collateral flows through the anterior communicating artery (ACoA) and the right posterior communicating artery (PCoA), respectively. During 20 minutes of balloon test occlusion (BTO), her neurological findings and somatosensory evoked potentials (SEPs) following left median nerve stimulation did not show any decline. For the treatment of the “symptomatic” giant right IC aneurysm, proximal ligation of the right cervical ICA was indicated. The patient underwent right superficial temporal artery (STA)-MCA bypass just before the proximal ICA ligation on the same day with monitoring of SEPs and transcranial motor evoked potentials.
During postoperative (PO) 2 months, conventional MRI revealed a gradual signal change of the right aneurysm, although the aneurysm's size had not changed. T1WI depicted the aneurysm as homogenous and iso–low-intensity at PO 1 day [], iso-intensity surrounded by hyperintensity at PO 2 weeks [], and having an onion skin appearance with flow void signs at PO 2 months []. In T2WI, the aneurysm was depicted as mixed iso–low-intensity with a low-intensity peripheral rim at PO 1 day [], mixed iso–hyperintensity at PO 2 weeks [], and having an onion skin appearance with flow void signs at PO 2 months []. MRA did not demonstrate the aneurysm at PO 1 day [], but the reappearance of the aneurysm was noted at PO 2 weeks [] and 2 months []. The STA-MCA bypass was patent at PO 1 day [] and 2 weeks [], but there was no visualization of the bypass at PO 2 months [].
Perioperative ASL-MRI with a PLD of 1.5 seconds demonstrated a gradual decrease in the size of the aneurysm. At PO 1 day, the size of the ASL hyperintense signal area had markedly decreased in size compared with that shown by preoperative ASL-MRI, and the hyperintense signal area was not demonstrated at the level of the basal ganglia []. Furthermore, no concentric artifact was noted. ASL-MRI at PO 2 weeks [] and 2 months [] showed further size decreases of the aneurysm. At PO 1 day, ASL signals increased throughout both hemispheres compared with preoperative ASL-MRI []. The decreased ASL signals on the right hemisphere were mostly improved, although there was still a slight laterality. At PO 2 weeks and 2 months, the increased ASL signals in both hemispheres showed gradual improvement, although the right side still showed slightly decreased ASL signals compared with the left side [Figure and ].
DSA was performed at PO 5 days. Right common CAG (CCAG) demonstrated complete patency of the bypass, and part of the right MCA territory was visualized through this bypass at 2.5 and 3.5 seconds (equivalent to 1.5 and 2.5 seconds in CAG, respectively) []. Through cross flow via the ACoA, left CAG revealed that the trunk of the right MCA was faintly visualized at 1.5 seconds, and the periphery of the right MCA was visualized at 2.5 seconds []. DSA did not show opacity of the aneurysm in the right ICA.
At PO 1 year, the patient had completely recovered from her right visual disturbance and abducens palsy and underwent coil embolization of the left ICA aneurysm. At that time, right CCAG failed to reveal the patency of the bypass []. Left CAG confirmed successful embolization of the left ICA aneurysm []. At 1.5 seconds, the trunk of the right MCA was visualized through cross flow via the Acom, but it was not fully visualized compared with the left side. The aneurysm of the right ICA was not opacified. At 2.5 seconds, left CAG [] and left VAG [] revealed visualization of the right MCA periphery, but right laterality was still present.
At PO 2 years, conventional MRI and MRA demonstrated a marked size decrease of the right ICA aneurysm. The aneurysm was detected as a small hyperintensity surrounded by a low-intensity region in T1WI [] and a small low-intensity area surrounded by a hyperintensity in T2WI []. MRA depicted the aneurysm as a small spot without any communication with the artery []. There was no visualization of the STA-MCA bypass.
ASL-MRI with dual PLDs demonstrated the aneurysm as a tiny spot of low-intensity signal at PLD 1.5 seconds [] and an iso-intense signal area at 2.5 seconds []. The intensity and configuration of the spot were not identical between PLDs of 1.5 and 2.5 seconds. To compare with pre- and perioperative ASL-MRI findings, the intensity and size of the ASL signal was markedly decreased. Furthermore, preoperative decreased signals in the right hemisphere, especially in the right MCA territory, were markedly improved at PLD 1.5 seconds []. Although there was a slight signal decrease in the right hemisphere, this laterality was somewhat improved at PLD 2.5 seconds [].


A 70-year-old man visited Samsung Medical Center complaining of chest wall pain. Chest computed tomography (CT) revealed a 9.6-cm-sized cystic lesion in the anterior and left upper mediastinum with direct extension to the mediastinal fat and the left upper lobe of the lung. Multiple enlarged lymph nodes were found in the mediastinum. The patient underwent endobronchial ultrasound (EBUS)–transbronchial needle aspiration (TBNA) of the subaortic lymph node. FNA slides revealed some epithelial clusters in bloody background (). Three-dimensional (3D) clusters consisted of variably sized cells with moderate to high nuclear atypia. Their nuclei had irregular contours, margination, a coarse chromatin pattern, and single or two prominent nucleoli. Cytoplasmic borders were indistinct, and the amount of cytoplasm was variable (). Some of the tumor cells contained intracytoplasmic vacuoles (, arrow). Core needle biopsy (CNB) was conducted a day after the EBUS-TBNA. The tumor was diagnosed as thymic adenocarcinoma with enteric differentiation (). The histologic characteristics were well correlated with the features identified in cytologic specimens: a tubulo-glandular pattern with nuclear atypia and occasional intracytoplasmic mucin.


A 50-year-old man visited the hospital for an evaluation of his weight loss (8 kg during the past two months). Chest CT revealed an 8.1-cm-sized, heterogeneously enhancing mass in the anterior mediastinum with sternum destruction. Multiple small nodules in the lung parenchyma and necrotic lymphadenopathy in the right supraclavicular area were also identified. FNA of the right supraclavicular lymph node revealed a large amount of three-dimensional epithelial cell clusters in a background of blood and inflammatory cells (, ). The cells at the edge of the clusters were stratified. Small to large clusters consisted of columnar cells with abundant eosinophilic cytoplasm and occasional intracytoplasmic vacuoles (). The elongated nuclei of the columnar cells had irregular membranes with margination, coarse to vesicular chromatin, and prominent nucleoli. CNB for the mediastinal mass was subsequently performed. A tubular growth pattern, pseudostratified nuclei with atypia, and a few instances of intracytoplasmic mucin were also found in the CNB specimen (). Considering the cytology and histology of the tumor, enteric type adenocarcinoma was an appropriate diagnosis.
After 6 months of prolonged chemotherapeutic treatment, pericardial effusion from the patient was obtained by aspiration. Liquid-based cytology showed crowded epithelial cells with nuclear overlapping (). Pleomorphic nuclei, vesicular chromatin, and single or two prominent nucleoli were also shown ().


A 62-year-old man presented to the hospital with chest discomfort. Chest CT showed an infiltrative anterior mediastinal mass, measuring 3.2 cm in size, along with massive pericardial effusion. The possibility of lymphoma or thymic malignancy was suggested considering the patient’s clinical and radiologic features. FNA of the anterior mediastinum was conducted. In the aspirated specimen, a few cells could be identified with extensive mucinous material in the background (). Tumor cells were round and small to medium in size. A relatively fine chromatin pattern and indistinct nucleoli favored benign cells; however, slight nuclear margination, irregular arrangement, and cellular overlapping suggested malignancy (). The patient underwent surgical excision. According to the cytologic and histologic features of the specimen, a diagnosis of enteric type mucinous adenocarcinoma was made (). One major histologic characteristic of the surgical specimen was floating tumor clusters in the extracellular mucin that were cribriform, tubular, or single cell types.


The patient had provided written informed consent for publication of this case study.
A 63-year-old woman was admitted for evaluating gastric submucosal lesion incidentally detected during a health check-up. Upon endoscopic examination, a single smooth surfaced polypoid lesion sized 1 cm was identified. Under the clinical impression of submucosal benign mesenchymal tumor, ESD was performed. Normal saline and indigo carmine dye mixed with hyaluronic acid was injected into the submucosal layer to lift up the lesion and distinguish the muscle layer from the submucosal layer. The endoscopist did not detect any visible mucosal changes before injecting the solution (). However, the release of air bubbles from the lesion was clearly observed during the submucosal dissection (). Microscopic examination of the submucosal tumor was consistent with inflammatory fibroid polyp. The lamina propria contained numerous unlined empty spaces without inflammatory reaction, measuring 40–600 μm in diameter and extending to the submucosa and submucosal tumor (, ). Neither specific cytological abnormalities nor architectural destruction was found in the mucosa. Helicobacter pylori was not identified. The lesion showed negative immunohistochemical staining results for D2-40, CD31, CD34, vimentin, and S100 protein. Therefore, lymphangiomatous lesion and lipomatous metaplasia were ruled out (). These histologic findings were similar, if not identical, to those of gastrointestinal pseudolipomatosis reported previously [,]. Based on histological and immunohistochemical findings, a final diagnosis of gastric pseudolipomatosis was made.


A 24-year-old female was admitted to the emergency room (ER) with sudden onset of abdominal pain, nausea and vomiting after eating a heavy meal 6 hours previously. Patient reported eating an excessive amount of grapes and pomegranates hours prior. Her pain was sharp, severe, and worst in the epigastrium.
Physical examination revealed a thin, uncomfortable-appearing young woman. Patient exhibited abdominal swelling, rigidity, and diffuse tenderness with peritonitis on palpation. All other examination findings were non-contributory. When the patient presented to the ER, vital signs were as follows: blood pressure (BP) 125/80 mmHg, pulse 75 beats/minute, respiratory rate 16 breaths/minute, and a body temperature of 36.5°C. Amount of urine from urinary catheter placed in bladder was approximately zero. Nasogastric tube inserted into the stomach was not effective because it was full of undigested stomach contents. Chemistries and hemogram were normal. Abdominal computed tomography (CT) showed a grossly distended stomach occupying the entire abdominal cavity.
Coronal image of abdominal CT scan revealed distended stomach containing air and radiodense material, later determined to be grapes and pomegranates (). Sagittal image of abdominal CT showed that stomach over-distended with food content led to displacement of intra-abdominal structures ().
During systemic examination, patient was checked for cyanotic condition and no pulse could be detected in either of lower extremities. Moreover, pulse rose to tachycardic rate of 125-135 beats/minute, respiratory rate was 30-35 breaths/minute and BP was 70/45 mmHg 2 hours after first checked. The patient was intensively resuscitated preoperatively with crystalloid intravenous (IV) fluids and plasma expander. Shock occurred and patient’s breathing worsened (oxygen saturation of 65% on air). An emergency operation was performed.
The patient underwent laparotomy (epigastric midline incision) that revealed massively distended stomach with perforation of gastric antrum. Stomach was filled with nearly 5 liters of partially and minimally digested food, including whole grapes and pomegranate matter. Following adequate decompression, stomach was moved from wound site, remaining contents were emptied, and perforation was closed (). No discrete bezoar or mechanical gastric outlet obstruction was identified.


The patient was a 74-year-old woman, para 2, gravida 2. She consulted with a doctor at another hospital with the complaint of abdominal distension and constipation. A firm irregular mass larger than 10 cm was found in the intra-pelvis by ultrasound sonography, after which she was admitted to our hospital.
Computerized tomography (CT) and magnetic resonance imaging revealed a pelvic mass of over 10 cm and containing solid parts, leading to our suspicion of a malignant tumor. Small hemorrhagic ascites were also discovered. Moreover, the tumor was found to be adhering to the bilateral fallopian tubes, small intestine, and broad ligament of the uterus. The size and irregularity of the tumor made it unclear whether it also involved the bilateral ovaries CT found neither distant metastasis nor enlarged lymphadenopathy. In a blood examination, the CA125 value, a tumor marker of ovarian cancer, was elevated to 409 U/mL.
The patient underwent an operation as the primary treatment. The operative findings included normal uterus and bilateral ovaries. The tumor seemed to have developed from the broad ligament of the uterus (). The tumor was diagnosed as a differentiated malignant Brenner tumor or large cell NEC by intraoperative pathological diagnosis. Therefore, we performed a total abdominal hysterectomies with bilateral salpingo-oophorectomy, subtotal omentectomy, and extensive pelvic and para-aortic lymphadenectomies, in accordance with the standard procedure for ovarian cancer. The histological findings included various sizes of cells with high N/C ratios, which were forming sheets (). In addition, chromogranin A, neural cell adhesion molecule (NCAM), and synaptophysin were all positive in immunohistochemical staining (). We finally reached a diagnosis of NEC arising from the broad ligament of the uterus (pT3cN1M0). And in this present case, there are no evidence of neither serous carcinomas nor mesothelial carcinomas, which are thought to be common peritoneal cancer, by histologic or immunophenotypic examination.
Postoperatively, we strongly recommended that our patient begin adjuvant chemotherapy. She sought out a second opinion, then consistently refused any kind of additional treatment. Fortunately, she has been alive without recurrence.


A previously healthy, 61-year-old right-handed woman without history of epilepsy was transferred to our hospital for further evaluation and treatment of hypokalemia, hypercalcemia, confusion, and a brief seizure. Initial magnetic resonance imaging (MRI) revealed a 3.5 × 3.3 × 2.8 cm right frontotemporal meningioma with an accompanying midline shift of 3 mm (Fig. ).
Upon arrival, her neurological exam was notable for confusion and otherwise was nonfocal. Two clinical seizures with semiology of lip smacking, left head and eye deviation, and altered awareness were also observed. Both seizures ceased following intravenous lorazepam 2 mg without any improvement in mental status. Electroencephalography (EEG) revealed two right temporoparietal seizures with frequent T8/P4 sharp waves. She was treated with intravenous fosphenytoin 15 mg/kg. Continuous video-EEG monitoring showed nonconvulsive SE (NCSE). The patient was intubated and admitted to the neuro-intensive care unit. Stepwise treatment with propofol, midazolam, and ketamine was started, with burst suppression achieved in less than 24 h. Her antiepileptic drug (AED) management consisted of levetiracetam, lacosamide, and phenobarbital. Unfortunately NCSE recurred each time with weaning of general anesthesia. Three days after admission, she underwent resection of the right frontotemporal mass which was consistent with a WHO grade I meningioma (Fig. ). During her hospital stay, she was also treated for hyperparathyroidism secondary to a parathyroid adenoma that was treated medically and then surgically. Postoperatively, she remained seizure free, but her mental status did not improve. Intermittent EEGs showed diffuse slowing with focal right hemispheric arrhythmic delta slowing and continued right T8/P4 sharp waves. She was discharged to a long-term care facility in a minimally responsive state with tracheostomy and percutaneous endoscopic gastrostomy. Her mental status improved after discharge, but she had persistent generalized weakness due to critical illness myopathy from her prolonged intensive care unit stay. At 2-month follow-up, she had normal memory, attention, and language functions.
Two weeks later, she presented with confusion and left face twitching. EEG showed continuous right hemispheric spike and wave activity consistent with focal NCSE. Her preadmission AEDs were continued with the addition of valproic acid without subsequent improvement. EEG burst suppression was achieved with propofol, ketamine, midazolam, and pentobarbital. Brain MRI showed right superior temporal encephalomalacia and gliosis (Fig. ). NCSE emerged each time anesthetic medication was lowered despite four antiepileptic medications. Due to her previous SRSE with prolonged recovery phase and current poor prognosis, the family agreed for recurrent surgical treatment. She underwent tailored right temporal lobectomy 8 days after admission with removal of the superior, middle, and inferior temporal gyri (6 cm from the tip). Hippocampectomy was guided by intraoperative electrocorticography with resultant cessation of epileptiform activity along the margin of the resections (Fig. ). Postoperative EEG continued to show frequent right posterior temporal periodic epileptiform discharges for another 15 days without clinical improvement. Topiramate was added to her AED regimen, and propofol and midazolam was again titrated to EEG burst suppression for 2 days. As general anesthesia was weaned, the EEG slowly improved to diffuse theta and delta range slowing. Surgical pathology showed nonspecific leptomeningeal necrotizing inflammation in medium-sized arteries, focal cortical neuronal loss, and gliosis. The patient received high-dose fosphenytoin steroids for 5 days for possible autoimmune encephalitis. Tests for autoimmune markers and paraneoplastic antibodies as well as imaging studies for neoplasia in any other part of the body were negative except for a nonspecific elevated antinuclear antibody. She was transferred to a long-term care facility on topiramate 400 mg/day, valproic acid 3,000 mg/day, phenobarbital 300 mg/day, lacosamide 400 mg/day, and levetiracetam 5,000 mg/day.
At 9-month follow-up, neuropsychological testing could not be performed due to somnolence and lack of cooperation. Over 3 years the patient gradually improved her interaction and alertness, with concomitant decrease in her AEDs. As her cognitive status improved, a clinical picture of sensory aphasia was revealed. This manifested as relatively fluent and articulate speech with notable paraphasic errors, verbal perseveration, word salad, and alexia. Neuropsychological testing 34 months postoperatively could not be completed due to her dense sensory aphasia. The Mississippi Aphasia Screening Test showed an improving Wernicke-type aphasia that was evolving into a transcortical sensory aphasia profile with relatively fluent and articulate speech, paraphasic errors, poor comprehension, inconsistent response to questions and command following, restricted repetition of single words only, agraphia, and inability to read complex sentences.


A 30-year-old male patient presented to us with gradual diminution of vision in both eyes for 1 year. There was no history of night blindness and no history of niacin intake in the past. Family history was not significant. Best-corrected visual acuity was 20/30; N6 in both eyes. Anterior segment was normal with clear lens. There was no evidence of inflammation in the anterior chamber. Vitreous was clear. In both eyes, discs were healthy, retinal vessel caliber was normal, and pars plana was clear. Both eyes had cystoid macular edema at the posterior pole []. Multicolor imaging showed a greenish hue with central orange reflectance suggestive of gross cystoid macular edema []. Both short wave autofluorescence and near infra-red autofluorescence (NIR-AF) showed central multispot hyperautofluorescence and an area of hyperautofluorescence involving the posterior pole and extending up to the arcades []. NIR-AF showed an additional area of hyperautofluorescence, nasal to the disc in both eyes []. Spectral domain optical coherence tomography showed cystoid spaces involving all the retinal layers in both eyes []. Fluorescein angiography (FA) showed faint petaloid leakage at the fovea in both eyes []. The patient refused electrophysiological tests. Based on history, clinical examination and imaging findings a diagnosis of DCMD was made.


A 65-year-old male, a known case of old healed multifocal choroiditis and peripheral vasculitis in both eyes, presented to the uvea clinic for routine follow-up examination. His best-corrected visual acuity was 20/20 in both eyes. Anterior segment was quiet in both eyes. Dilated fundus examination showed patches of healed multifocal choroiditis in both eyes and sclerosed vessels in the left eye periphery. A bright red elevated nodular lesion protruding above the retinal surface was noted along the inferotemporal arcade. Fundus FA was done which showed a feeding artery filling up the entire lesion and a draining vein in the early phase of the angiogram with an interesting meteor-like leak emanating from the lesion and rising toward the superior retina in the late frames of the angiogram [Figs. and ]. Peripheral retina showed collaterals with areas of capillary nonperfusion (CNP) anterior to it. No CNP areas were identified close to the lesion. Optical coherence tomogram (OCT) using the RTVue-100 was done through the macula and the lesion. A shallow pocket of subretinal fluid was noted at the macula. OCT scan through the pathology showed the lesion to be elevated from the retinal surface and protruding toward the vitreous cavity [Fig. and ]. The clinical and retinal imaging findings were suggestive of an active VPT secondary to uveitis. Laser photocoagulation was done around the VPT. OCT imaging was repeated after 3 months []. Subretinal fluid at the macula has resolved. Our photo highlights this unusual FA finding in a patient with VPT secondary to multifocal choroiditis and vasculitis and pictorially, we call it the “retinal meteor.”


A 50-year-old male presented with a hyperkeratotic nodule 6 mm in diameter with a brown surface on the extensor surface of his left lower leg (Fig. ). The lesion had developed over the course of a few years without any tendency to heal. He had been suffering from asteatotic dermatitis on his four extremities, and admitted that he had scratched his lower legs frequently before the tumor developed. He was treated for hyperlipidemia and hyperglycemia, in addition to control of abdominal obesity. The laboratory examinations from half a year before demonstrated serum total cholesterol levels ranging from 344 to 479 mg/dL (reference interval: 125–220 mg/dL) with a low-density lipoprotein cholesterol level between 236 and 311 mg/dL (reference interval: 70–140 mg/dL), a triglyceride level of 1,650 mg/dL at the maximum (reference interval: 45–150 mg/dL), and hemoglobin A1c ranging from 6.1 to 8.7% (reference interval: 4.3–5.8%).
A skin biopsy performed on the tumor showed acanthosis and basal hypermelanosis of the epidermis. The poorly demarcated tumor mass was located in the dermis, separated by a clear zone from the epidermis, extending into the deep reticular area (Fig. ). The tumor was composed of an admixture of fibroblast-like spindle cells, rounded histiocytes, and capillaries. Spindle cells were arranged irregularly in the collagen strands. There were neither atypical cells nor bizarre cells in the lesion. Within the center of the lesion there were abundant cleft spaces compatible with cholesterol clefts (Fig. ), surrounded by foam cells and giant cells. Immunohistochemistry of the tumor revealed CD68-positive cells as well as numerous factor XIIIa-positive cells, in contrast to a negativity for CD34. Based on these findings, we diagnosed this lesion as cholesterotic fibrous histiocytoma.
Later, we performed total excision of this tumor, and the patient has remained free from recurrence for more than 5 years.


A 65-year-old man visited our hospital because of his gradually worsening back pain for 2 months. He was administered Nonsteroidal Antiinflammatory Drugs (NSAIDs) and paracetamol for pain relief, but these did not relieve the pain. He denied any persistent fevers, night sweats, chills, and respiratory symptoms. His past medical history and review of systems were unremarkable. A physical examination showed that the patient had a clear consciousness, upper thoracic (over the T4 and T6 vertebrae) percussion pain of the spine, myodynamia was V, and reflexes were all normal. The cervical and lumbosacral spine was clinically normal. Laboratory tests showed a white blood cell (WBC) count of 7.1 × 109/L and the percentage of neutrophilic granulocytes was 83.2%, the C-reactive protein (CRP) level was 63.0 mg/L, and a T-spot was negative. A bone marrow biopsy was normal.
An X-ray of the thoracic spine showed slight compression of the body of T6 (). Ultrasonic examination of the pelvis and abdomen was normal. A computed tomography (CT) scan showed lytic lesions of the right side of the T4, T5, and T6 vertebral bodies (). Magnetic resonance imaging (MRI) displayed abnormal marrow signals in T4, T5, and T6 vertebral bodies (low signal on T1, high signal on T2 and short time inversion recovery), with some compressed fracture of the T5 body and the lesions partly extended into the right pedicle (). Which is mimicking malignancy, such as haematological malignancy and metastatic bone cancer. The spinal cord was normal. There was no intra-spinal or extra-osseous component. A Positron Emission Computed Tomography (PET-CT) scan demonstrated increased uptake in T4, T5, and T6 vertebrae on late films. A CT-guided transpedicular biopsy of T6 showed a lesion (). A histopathological examination showed granulomatous inflammation with necrosis, which was highly suggestive of tuberculosis. Therefore, the patient was administered isoniazid, rifampicin, pyrazinamide, and ethambutol for 2 weeks. The CRP level was 5.6 mg/L. Thoracic spinal surgery using the anterior approach was performed (). An intraoperative frozen section examination showed thoracic histoplasmosis infection (). Routine postoperative pathology, and specific mycological stains, such as Giemsa, PAS, and periodic acid-silver methenamine, also confirmed thoracic histoplasmosis infection (). The patient’s back pain was relieved. He was treated with itraconazole for 12 months. At a 26-month follow-up, the lesions had not progressed. The patient was pain-free and asymptomatic, and was able to return to his active lifestyle.


A 72 year old man was admitted to our department with a nine month history of gradually enlarging mass in the volar aspect of the hypothenar area of his left hand. The patient reported that the size of the mass had been increasing during the past 3 months. As far as the rest medical record is concerned he was under medication for diabetes mellitus type 2 with metformin and he had undergone an operation for colorectal malignancy 6 years before presentation. He had no previous hand injury. The patient experienced persistent pain and altered sensation on the ulnar side of the hand, accompanied with progressively diminishing grip strength. Physical examination revealed a small, mobile, and painless palpable mass in the hypothenar area. The skin overlying the mass was normal. The range of motion of the finger joints was not restricted and there was no vascular impairment.
Laboratory exams were within normal limits and radiographs of the hand demonstrated no osseous involvement or radio-opaque lesion. Ultrasound (U/S) examination revealed a solid, hypoechoic and homogeneous tumor with capsule in the ulnovolar aspect of the left hand (). Magnetic Resonance Imaging (MRI) indicated a multi-lobulated mass, located in the volar aspect of the fourth web space of the hand, not infiltrating adjacent structures or having bony involvement and bone edema (). No biopsy was performed preoperatively, since all radiological studies suggested a benign tumor.
The patient was operated under axillary nerve block. Using a Brunner incision volarly the skin and the palmar fascia were divided carefully. The neurovascular bundles were identified and protected. The mass was removed en block with clear margins. The gross specimen consisted of a lobulated, well-circumscribed, gelatinous mass ().
The histopathology of the specimen revealed () uniform, cytologically bland spindle-shaped cells with eosinophilic cytoplasm separated by abundant extracellular myxoid stroma containing very sparse capillary – sized blood vessels.
After the last follow up, 12 months following the excision, the ring and the little finger of the patient had normal sensation and range of motion (). No signs of tumor recurrence were noticed during follow up.


In March 2015, a 17-year-old man was referred to our hospital by infectious disease specialists for the evaluation of fever for over 20 days. He was treated for viral infection at first by infectious disease specialists. Then antibiotic therapy was conducted due to painful oral and skin lesions on scrotum. Patient suffered from bilateral vision loss and photophobia initiated 3 days before admission to hospital. His body temperature was 38.8 °C, systolic/diastolic blood pressure was 115/70 mmHg and heart rate was 96 bpm when physically examined.
The heart sounds were normal without any murmurs and the lung fields were clear to auscultation. The electrocardiogram showed normal sinus rhythm. The chest X ray was normal. We noted an inflammatory syndrome in the laboratory results (white blood cell count: 113,000 mm3, neutrophil: 60%, C-reactive protein: 62 mg/l, erythrocyte sedimentation rate: 71 mm/hour). Therefore, antibiotics were started due to endocarditis. Blood cultures and serology tests for fever, Legionella, Bartonella, Tropheryma whipplei, Chlamydia, Mycoplasma, and Brucella were negative. The transthoracic echocardiography (TTE) showed a left ventricle ejection fraction of about 65% and a mobile mass seen in RV apex which was hyperechoic and well circumscribed ().
A thoracic multi detector computed tomography (MDCT) confirmed the diagnosis of bilateral segmental pulmonary thromboembolism (PTE) and infarction. A transesophageal echocardiogram (TEE) did not show the nature of RV mass. Three differential diagnosis were introduced for RV mass including fever including infection, malignancy and clot. Thus, cardiac magnetic resonance imaging (MRI) was performed and showed that the nature of mass was clot in RV trabeculae ().
Oral ulcers had a nonspecific pathology with a variable infiltrate of lymphocytes, macrophages, and neutrophils at the base of the ulcer that showed autoimmune disorder in histopathologic examination. We started treatment with anticoagulant since the patient was at risk of PTE and RV clot caused by leukocytoclastic and lymphocytic vasculitis which may also be seen in severe inflammation. The thrombophilia study did not show any abnormalities, and antinuclear antibody, anti-DNA antibody, anti-extractable nuclear antigen (anti-ENA) antibody, and anti-neutrophil cytoplasmic antibody tests and tumor markers were all negative. We noted a positive HLA-B51 and HLA-B5 serologic typing. Taking these findings together, the patient was diagnosed with BD.
Corticosteroid (methylprednisolone 1 g per day for 3 days and followed by oral prednisone 1 mg/kg) with cyclophosphamide (1 gram monthly) treatment was started. In addition, warfarin was administered to maintain the international normalized ratio (INR) at 2.5 or above. Two months later, the RV clot had disappeared on TTE.


A 60-year-old post-menopausal female presented to her primary care provider for intractable nausea, diarrhea, vomiting, and unintentional weight loss of 25lb over 2 months. She had a history of poorly controlled type II diabetes mellitus with peripheral neuropathy, and previous cholecystectomy. The patient was adopted, and thus her family history was unknown. Her physical exam was unremarkable. Her primary care provider referred her to a gastroenterologist for an endoscopy due to her clinical picture and a screening mammogram due to never having received one before.
Screening mammography performed six weeks after her initial encounter showed an oval mass in the upper outer quadrant and focal asymmetry with architectural disturbances in the anterior third of the left breast. Subsequent diagnostic mammography was concerning for breast cancer and biopsies of the mass and suspicious lymph nodes were performed. Her pathology demonstrated the lesion to be grade 2 ER positive (90%), PR positive (2%), HER2/neu positive invasive ductal adenocarcinoma with a Ki67 of 20% (). Due to the size of the oval mass and the presence of cancerous cells on lymph node biopsy, her initial stage was T2N1 stage II triple positive adenocarcinoma of the left breast.
A week later, an abdominal ultrasound demonstrated a dilated common bile duct of 14mm without obvious stones. Further work-up included an MRI of her abdomen, which demonstrated liver enlargement and a 3.5cm mass in the uncinate process of her pancreas, and diffuse thickening of the stomach wall (). The MRI also demonstrated enhancing vertebral lesions concerning for metastatic disease. Esophagogastroduodenoscopy was performed, visualizing the lesion in the stomach wall (). To determine if the gastrointestinal lesions represented another primary cancer, biopsies of the lesions in the stomach and pancreas were taken. The lesion biopsies were demonstrated to be metastatic breast adenocarcinoma due to immunohistochemical staining positive for estrogen receptors, E-cadherin, and GATA3 ().
The patient was ultimately diagnosed as having stage IV triple positive invasive ductal adenocarcinoma of the breast. Once the diagnosis was confirmed, systemic therapy was initiated with docetaxel, pertuzumab, and trastuzumab.


This case report was confirmed by the patient and the patient signed the informed consent form, A 16-year-old female visited our clinic complaining about progressive neck pain and left arm abduction weakness (grade III) over the past 2 years. She was examined by plain X-ray, three-dimensional (3D)-computed tomography, magnetic resonance imaging, and vertebral artery angiogram. The analyses indicated a calcified extradural mass with a size of about 3 cm×2.4 cm, ill-defined, compressing the cord in the C3–4 portion, and extending into the neural foramen with eroded vertebral body. A vertebral angiography showed a left side hypoplastic vertebral artery ().
There was no evidence of family history and long bone deformities revealing the multiple hereditary exostosis.
The tumor was successfully excised using a modified combined anterior oblique and posterior approach. In this approach, the extraforaminal portion of the tumor was first removed through the anterior oblique approach. For this, the patient’s body including the neck was tilted to the right side for a proper surgical view to avoid vertebral artery injury using an intraoperative doppler. In the second part, the intracanal portion of the tumor was removed via a posterior approach with C3/C4 laminoplasty under intraoperative neuro-monitoring (). The tumor showed a dark-red colored leather-like consistency with some calcification.
A histopathologic study of the resected material showed a cartilaginous cap and an underlying bone with enchondral ossification. The cartilaginous cap demonstrated chondrocytes without cytologic atypia comparable with osteochondroma ().
Postoperative, the symptoms of the female were improved. Clinical and radiological assessments were performed in the 5 years after the operation. Clinically, she was symptom-free and there was neither a spinal instability nor kyphosis or tumor recurrence in the imaging studies ().


A 64-year-old male, current smoker (20 cigarettes daily) and drinker (20 g alcohol daily), presented with pain in the lower right limb that had begun several months previous. Initially, the pain was attributed to lumbar degenerative pathology in the fourth and fifth lumbar vertebrae. A multidetector computed tomography (MDCT) scan of thorax-abdomen-pelvis with intravenous and oral contrast showed a large, solid, contrast-enhanced mass affecting psoas, iliac and gluteus minor muscles with iliac bone infiltration. This great lytic lesion affected the iliac paddle wall, thinning the acetabular roof. Pelvic magnetic resonance imaging (MRI) study confirmed the destructive, heterogeneous and highly vascularized tumor (Figure and B), resembling an osteochondroma.
Histologically, a solid neoformation formed by cells of epithelioid habit that showed large eosinophilous cytoplasm compartments and irregular, vesiculous nuclei with patent nucleolus and frequent figures of mitosis was observed, accompanied by a rich vascular network adjacent to a soft tissue. Tumor cells were strongly positive for cytokeratin AE1/AE3, cytokeratin 8 and hepatocytes. Cytokeratin 20, 7, 19 and EMA were completely negative. This was conclusive for HCC. A second biopsy performed later over the same site, just if a mistake had been made in the processing or identification of tissue, showed the presence of a proliferation, composed of cells that mimic hepatocytes, with marked incipient anisopleomorphism, extended in sheets and infiltrating different soft tissues. Immunohistochemical staining was performed, showing hepatocyte, cytokeratin AE 1 and AE 3 positivity; the rest of the requested immunohistochemical tests (alpha-fetoprotein (AFP), prostate antigen) were negative again. Therefore, metastasis from a well-differentiated HCC (Figure ) was confirmed.
Tests of peripheral blood showed AFP level of 3.4 ng/mL (upper normal value 8 ng/mL), aspartate aminotransferase (AST) of 133 U/L, alanine aminotransferase (ALT) of 35 U/L, alkaline phosphatase (ALP) of 161 U/L, gamma-glutamyl transpeptidase (GGT) of 95 U/L and bilirubin of 1 mg/dL. Liver stiffness measurement value was 12.5 kPa, suggestive of significant fibrosis. Upper endoscopy revealed no signs of portal hypertension. Hepatitis B and C chronic infection were excluded.
Multiphasic hepatic TCMD depicted a 24-mm, ill-defined area that enhanced in the arterial phase, with washout in delayed phases, in segment IV that was associated with vascular invasion of the left portal vein and with left lobe hypertrophy in a polylobed liver (Figure -F). This imaging impressed the finding of tumor injury meeting non-invasive diagnosis criteria for HCC. Taking into account the symptoms, defined as ECOG PS 2[], and the results of biopsies and radiological staging, BCLC-C hepatocellular carcinoma was diagnosed.
Treatment with analgesics plus external palliative radiotherapy in the pelvic area was initiated. Once the patient’s pain and discomfort were alleviated, sorafenib was started at October 11, 2014. Clinical evolution was good, with progressive recovery of general status to ECOG PS 0 together with radiological regression of intra- and extra-hepatic disease. The bone metastases at initial scan (July 21, 2014) measured 47 mm × 132 mm × 181 mm, and measurement of the same lesion at the last study (September 15, 2016) showed it to be 40 mm × 80 mm × 80 mm.
The patient has been taking sorafenib up to the writing of this report, with minor adverse events at full dose. He has been able to stop morphine-derived and non-steroidal anti-inflammatory drugs. Due to excellent tolerance to sorafenib, in case of radiological progression, the patient will be assessed to switch to regorafenib.


This is a 66-year-old male, former drinker of 80 g alcohol daily, with chronic hepatitis C virus infection, secondary iron overload, porphyria cutanea tarda, arterial hypertension and obesity. He frequented Traumatology and Emergency Departments due to left inguinal mechanical pain that distally radiated through the left leg since August of 2011. He presented with spontaneous fracture of the left hip (October 16, 2012) that needed a total hip prosthesis placement (October 22, 2012). Examination of the surgical specimen determined a bone metastasis of undifferentiated carcinoma.
A thorax-abdomen-pelvis MDCT was performed to find the primary tumor. An ill-defined hypodense nodule of less than 1 cm in the right hepatic lobe that cannot be assessed due to its size was seen, together with a small peripancreatic adenopathy and a left femoral neck fracture that did not present sclerotic borders, and represented the location where a hypodense lytic lesion was observed (Figure ). A multiphasic liver TCMD informed of normal liver size and morphology.
Upper endoscopy revealed erosive gastritis without esophageal varices. Laboratory values were AFP of 4.2 ng/mL, AST of 227 U/L, ALT of 181 U/L, ALP of 311 U/L, GGT of 629 U/L and bilirubin of 1 mg/dL. A dynamic hepatic MRI was performed and showed multiple small focal lesions, tenuously hypointense in T1 and hyperintense in T2, with intense contrast uptake in the arterial phase and washout in the portal phase in the larger ones (Figure -D). An ultrasonographic-guided biopsy-trucut with an 18-gauge needle was taken over one of the larger liver lesions, and demonstrated a well-differentiated hepatocellular carcinoma, thus identifying the primary focus.
The patient was finally diagnosed with advanced ECOG PS 0 BCLC-C HCC and sorafenib was started on December 18, 2012. Due to radiological progression, he was assessed for second-line clinical trials (February, 2014) but ultimately died due to tumor progression on January 20, 2015.


This is a 74-year-old diabetic man, who is a current drinker (40 g alcohol daily) and occasional smoker. In January 2014, he complained of pain in the upper hemiabdomen and pain in the lumbosacral region which radiated to the lateral face of the right thigh. He also presented functional impotence of the right lower limb and dysesthesia. No anorexia, asthenia nor weight lose were present. He was ECOG PS 2.
Blood count, biochemistry, including liver function tests and AFP, were mostly within the normal range (AFP of 4.2 ng/mL, AST of 128 U/L, ALT of 93 U/L, ALP of 192 U/L, GGT of 459 U/L and bilirubin of 1 mg/dL). Abdominal ultrasound detected a 15-mm hypoecogenic liver focal lesion in the left lobe. The study was completed with a multiphasic abdomen-pelvis MDCT with the finding of a 40 mm × 39 mm focal liver lesion in the right lobe that could correspond with metastases (Figure -C). A pathological fracture with significant stenosis of the central spinal channel provoking compromise of neurological structures was detected in the body of the fourth lumbar vertebrae. Lumbar MRI confirmed this lesion and another very similar one in the second lumbar vertebrae (Figure and E).
The Neurosurgery Team performed a cementation of the fourth lumbar vertebra after an intraoperative biopsy at 14-AUG-2014. The pathological description was compatible with a metastatic focus of HCC, with the following immunophenotypic profile: Cytokeratin AE1/AE3, cytokeratin 8, CD138 and TTF1 positivity, but hepatocyte, cytokeratin 7, CDX, synaptophysin, S100, P40 and P53 negativity (Figure ). This patient also presented with several very painful lesions in the dorsal spine.
The patient was administered intrathecal perfusion of fentanyl, intravenous zoledronic bolus and external radiotherapy (total dose of 20 Gy) to ameliorate symptoms. In spite of all efforts, his quality of life was poor and he worsened very fast. He was so fragile that he was not a candidate for sorafenib drug therapy and home-based palliative care provided support during the last 5 mo of his life. He finally deceased on October 26, 2015.


A 25-year-old male presented with bowel incontinence and difficulty in micturition for 4 days. He also had a history of low back pain for 4 years with radiation to the left leg till toes. For past 15 days, he complained of the right leg pain along with numbness. On neurological examination, his power of both extremities, proximal, and distal was found to be 5/5 on Medical Research Council scale. The deep tendon reflexes on the affected side were reported to be normal. However, they were found to be brisk on the left side. His straight-leg raise test was found to be 30° on the right side. He had absent anal reflex and decreased perianal sensation, typical of saddle anesthesia.
The patient had an arachnoid cyst reported at the level of conus medullaris on a magnetic resonance imaging (MRI) 4 years ago when he had lower back pain with leg radiation. His pain settled with medications and the patient was symptom-free since then. A repeat MRI of Dorsolumbar Spine was done, which showed an increase in the size of the cyst. He underwent laminectomy for excision of an arachnoid cyst, at the level of L1 and L2.
MRI images obtained through lumbosacral spine were acquired both with and without intravenous contrast. The conus medullaris had asymmetry at the level of L1/L2, and filum terminale was deviated anteriorly and superiorly with arching of the nerves. There was an increase in angulation compared to the previous scan, as the size had increased [Figure –].
He underwent an L2–L3 laminectomy and after dural opening had near total excision of the arachnoid cyst under microscope. At surgery, the cyst appeared to be filled with clear fluid, delineated on outer and inner aspect by a delicate transparent membrane [Figure and ]. On microscopic examination, a cystic lesion of delicate fibrovascular tissue lined by cuboidal to low columnar meningothelial lining was found [].
The patient's pain settled, and he regained sphincter control immediately after surgery. However, slight numbness persisted in the right leg. He was discharged after 3 days, and a follow-up MRI scan showed resolution of cyst with decompressed conus.


An 85-year-old woman was diagnosed with a left asymptomatic PCOM aneurysm during a prophylactic brain evaluation by magnetic resonance imaging (MRI) 2 years ago. She had a medical history of hypertension and mild emphysema. Angiography revealed a 12-mm diameter aneurysm originated from the PCOM []. Because of her age, follow-up was recommended to her. The aneurysm, however, enlarged to be 30 mm in diameter in the subsequent 2 years and compressed the brainstem and thalamus with the contained thrombotic material []. Clinical deficits progressed to right hemiparesis and left oculomotor nerve palsy, approximately 5 months before admission. Moreover, deterioration of the level of consciousness occurred 1 month before admission. She was referred to our institution for surgical treatment of the aneurysm when the lesion reached 35 mm in diameter as seen on MRI [].
On admission, she had an impaired level of consciousness (Glasgow coma scale [GCS] E4V2M5 = 11), left total oculomotor nerve palsy, and right hemiparesis (3/5 manual muscle testing [MMT]). Oral intake was not possible and she was completely bedridden (score of 5 on the modified rankin scale [mRS]). Three-dimensional computed tomography (3D-CT) angiography revealed that the giant aneurysm originated from the PCOM, almost obscuring this structure; it had blebs and was directed ventrally and superiorly [].
A left frontotemporal craniotomy was created. The Sylvian fissure was opened wide. Sylvian veins were dissected from the temporal lobe, and the temporal tip was retracted posteriorly. The aneurysm was approached and its origin only from the PCOM was confirmed. The oculomotor nerve was severely displaced medially. The midbrain was also severely compressed. Vasa vasorum were not present on the aneurysmal surface, and there were no perforating arteries originating from the aneurysmal wall. The origin of the PCOM was detected by retraction of the anterior part of temporal lobe, facilitating placement of the proximal clip. The aneurysm was located medially to the tent and the distal part of the PCOM (dPCOM) running behind the tent was not initially observed because it was severely compressed inferiorly by the aneurysm. After placement of the proximal clip at the origin of the PCOM, the tent was cut and the dPCOM from the aneurysm could be seen behind the tent. The other trapping clip was placed just distal to the aneurysm on the PCOM. The aneurysmal dome was opened and thrombectomy was performed []. The thrombus was relatively soft and easy to remove completely. The anterior choroidal artery could be dissected away from the aneurysmal wall. The aneurysmal wall was incompletely resected because of severe adhesion to the brainstem. During surgery, sensory- and motor-evoked potentials were stable. Postoperative CT confirmed brainstem decompression without ischemic lesions [Figure and ].
The patient had an uneventful postoperative course. Complete aneurysm exclusion was confirmed on 3D-CT angiography 2 weeks after operation. The patient's neurological condition improved, with consciousness recovering to GCS 15 and right hemiparesis decreasing to 4/5 MMT. She could walk and eat with assistance 1 month after operation. The preoperative complete oculomotor nerve palsy improved partially. The Glasgow outcome scale was 3 and mRS improved from 5 to 4 at discharge 1 month after operation.


A 74-year-old man was scheduled for cardiac operation because of severe mitral regurgitation and coronary stenosis. During preoperative screening, all initial preoperative routine test results were normal, except for the presence of the non-specific cold antibodies confirmed by the saline method. The direct antiglobulin test was negative for anti-immunoglobulin G, but we did not perform further testing of anti-C3. These findings had not been assessed until the preoperative evaluation by anaesthesiologists. On the basis of these indications, we postponed the operation and performed further tests, which resulted in the detection of cold agglutinins by the haemagglutination assay. The titre of the cold agglutinin was 1:512 at 4°C, and the thermal amplitude, defined as the highest temperature at which haemagglutination occurs, was 32°C. The patient had no history of anaemia, prior blood transfusion or any disease other than prostate cancer, for which he had undergone operation without complications.
Haematologists diagnosed him as having idiopathic cold agglutinin disease because of a lack of prior infection or haematological malignancy. There is no consensus on the clinical significance of the cold antibody titre and thermal amplitude that warrant appropriate precautions. However, he had no clinical symptoms, and his agglutinin titre was not extremely high compared with those of previously reported cases; there was no indication for preoperative plasmapheresis or the administration of immunoglobulin, corticosteroids and alkylating agents and rituximab therapy. However, thermal amplitude, which is more important than the titre in predicting the likelihood of complications, was 32°C; therefore, management using hypothermic cardiopulmonary bypass (CPB) with cold cardioplegia would have caused the temperatures of his core, peripheral and coronary arteries to reach unsafe levels.
Therefore, we performed normothermic cardiac operation with warm cardioplegia. We usually use a single infusion of cold blood cardioplegia in an antegrade and retrograde delivery system every 30 min, which was modified from the one-dose method.
To avoid inadequate protection of the heart due to warm conditions and excessive cardiac activity and oxygen consumption, we added a continuous retrograde hyperkalaemic infusion to the intermittent antegrade infusion of cardioplegia. The patient was protected from exposure to hypothermia using warming blankets and a fluid warming system.
Retrograde cardioplegia (36°C) was performed continuously, except when antegrade cardioplegia was administered. We used blood cardioplegia made of the patient’s blood and potassium chloride (KCl, 8–20 mEq/L). We maintained cardiac arrest during almost the entire CPB period while keeping the patient’s temperature >35°C.
The patient had uneventful intraoperative and postoperative courses, with no clinically significant haemagglutination or haemolysis.
Written informed consent was obtained from the patient for publication of this case report.


At 7 wk of gestation, a 34-year-old Japanese woman, gravida 0, para 0, was referred to our emergency department from a reproductive clinic for abdominal pain that had lasted for 12 h and was accompanied by vomiting and hematochezia. Nausea had appeared 4 d prior and was treated as hyperemesis gravidarum. The patient had a history of infertility related to endometriosis, and pregnancy was achieved after her first IVF procedure with frozen-thawed embryo transfer. As part of that procedure, oral conjugated equine estrogen (3.75 mg/d) was administered for hormone replacement for 49 d; the patient also received intramuscular injections of progesterone (50 mg/4 d) and a vaginal progesterone suppository (800 mg/d). She was a nonsmoker and had no prior history suggestive of thrombosis. She had no family history of coagulopathies or thromboembolic events. The patient underwent a laparoscopic ovarian cystectomy for endometriosis 4 years prior to her presentation at our hospital. Her body mass index was 24 kg/m2.
Upon arrival, the patient exhibited the following vital signs: A temperature of 36.8 °C, a heart rate of 119 beats/min, a blood pressure of 89/76 mmHg, a respiratory rate of 28/min, and oxygen saturation of 97% in room air. A physical examination showed tenderness without guarding, rigidity or rebound tenderness throughout the entire abdomen, and a hematologic examination revealed leukocytosis with a left shift (white blood cell count, 21000/μL; segmented neutrophils, 94.9%). The platelet count was 142000/μL. The patient had a C-reactive protein level of 5.13 mg/dL, aspartate aminotransferase level of 23 U/L (normal, 13-30 U/L), alanine aminotransferase level of 29 U/L (normal, 7-23 U/L), serum creatinine level of 0.58 mg/dL, and blood urea nitrogen level of 14.3 mg/dL. Her D-dimer level was elevated (46.8 μg/mL; normal, < 1.0 μg/mL), the prothrombin time was 13.4 s (normal, 10.2-13.6 s), and the activated partial thromboplastin time was 24.1 s (normal, 23.0-36.0 s). The findings of a hypercoagulability workup, including results for protein S, protein C, and antithrombin, were within normal limits. Anticardiolipin antibodies, antiphospholipid antibodies, and lupus anticoagulant were not detected. She refused screens of the FV Leiden mutation and FII G20210A mutations, which are not found in Japanese people. JAK2 V617F mutation was also not screened because hemoglobin and platelets were in the normal range.
Obstetric ultrasound indicated that the embryo had a normal appearance compatible with its gestational age. Computed tomography (CT) scanning demonstrated thrombosis in the superior mesenteric vein (SMV) extending into the portal vein (Figure ). A moderate amount of ascites was observed, and the affected small bowel had an edematous and thickened wall with decreased enhancement, which suggested bowel ischemia.
Emergency surgical exploration was performed; this exploration found hemorrhagic fluid and a gangrenous portion of the small intestine extending from 80 cm distal to the ligament of Treitz to 160 cm proximal to the ileocecal valve (Figure ). After the surgical removal of SMV thrombi (Figure ), the necrotic portion of the small bowel, which was approximately 170 cm in length, was resected, and end-to-end anastomosis was performed. Following surgery, the patient was transferred to the intensive care unit, and anticoagulation therapy with unfractionated heparin was started immediately. We confirmed cardiac activity in the embryo by ultrasonography.
The subsequent postoperative course was not favorable. CT scanning on postoperative day 4 demonstrated re-occlusion of the SMV and portal vein and no improvement in small bowel congestion. Thrombolysis therapy via a catheter placed in the superior mesenteric artery (SMA) was performed by continuously administering unfractionated heparin with urokinase via the SMA at a dose of 240000 units/d for 5 d. In addition to thrombolysis therapy, we discussed artificial abortion with the patient; after obtaining consent, we performed this procedure due to the early pregnancy stage and the recurrence of thrombosis despite heparin administration. Following the artificial abortion, the patient’s condition improved, and she was discharged on postoperative day 18 with bridging to warfarin from unfractionated heparin.
Four months later, the patient continued to receive anticoagulation therapy uneventfully, and a follow-up CT scan revealed complete recanalization of the portal vein, and the SMV was completely occluded from the distal to the first jejunal branches (Figure ). The first jejunal vein was expanding and functioning as a collateral pathway. The follow-up laboratory data were as follows: Platelet count, 260000/μL; aspartate aminotransferase level, 19 U/L (normal, 13-30 U/L); alanine aminotransferase level, 17 U/L (normal, 7-23 U/L); serum creatinine level, 0.54 mg/dL; blood urea nitrogen level, 11.1 mg/dL; D-dimer level, 0.5 μg/mL (normal, < 1.0 μg/mL); prothrombin time on warfarin, 19.3 s (normal, 10.2-13.6 s); and activated partial thromboplastin time, 31.5 s (normal, 23.0-36.0 s). She had normal liver function, no symptoms of portal hypertension, and had no ascites. We plan to continue anticoagulation therapy for one year.


The patient was an 87-year-old male, nonsmoker, with a known history of pulmonary tuberculosis 14 years previously and complete recovery from prostate cancer 10 years earlier, who was also diagnosed with type 2 diabetes mellitus, hypertension, and hypothyroidism. Previous diagnosis of pulmonary tuberculosis was confirmed based on a positive culture for Mycobacterium tuberculosis. He was treated with a standard four-drug therapy for drug-susceptible tuberculosis. However, a negative sputum culture for M. tuberculosis was not confirmed during the 6-month treatment, owing to improvement of his respiratory symptoms. After recovery, the patient was subsequently rehospitalized for treatment of prostate cancer. Although the patient lived in South Korea, which has a high prevalence of tuberculosis, he did not report of any memorable exposure to patients with active tuberculosis.
He was regularly taking the following medications: metformin and saxagliptin for diabetes, levothyroxine sodium hydrate for hypothyroidism, and ramipril for hypertension.
The patient presented to our hospital with a week-long history of intermittent fever and general weakness. On admission, he had a cough, poor oral intake, and experienced dyspnea after walking for a few minutes on level ground. General physical examination revealed bilateral crackles and rales on both lung fields. There was no evidence of cardiac murmur, lymphadenopathy, hepatosplenomegaly, or skin lesion. No Osler nodes, Janeway lesions or splinter hemorrhages were observed.
In the initial laboratory results, the patient's complete blood counts were as follows: hemoglobin 9.9 g/dL (normal limits 12∼16 g/dL), white blood cell (WBC) count 9500 /μL (normal limits 4,500∼11,000 /μL), and platelet count 376,000 /μL (normal limits 150,000∼400,000 /μL). WBC differential count with neutrophilia was 7837 /μL (82.5%, normal limits 45%∼75%). Erythrocyte sedimentation rate (ESR) of 57 mm/hr (normal limits 0∼20 mm/hr) and C-reactive protein (CRP) of 57.4 mg/L (normal limits 0∼5 mg/L) were mildly elevated; procalcitonin was 0.14 ng/mL (normal limits 0∼ 0.05 ng/mL). A chest radiograph and computed tomography (CT) scan showed multifocal patchy consolidations with nodular lesions of variable sizes and irregular margins combined with right pleural effusion, but there was no hilar or mediastinal lymphadenopathy (Fig. A and B).
Early differential diagnosis of fever and lung nodules included tuberculosis, pulmonary septic emboli, fungal infection, vasculitis, and malignancy. Transthoracic echocardiography demonstrated no evidence of infective endocarditis. Analysis of pleural effusion showed a WBC count of 340 /mm3 with 94% lymphocytes, 4% neutrophils, and 2% monocytes, protein of 1.9 g/dL, lactate dehydrogenase (LDH) of 231 U/L, and pH of 8.0. Polymerase chain reaction for M. tuberculosis and cytology for malignancy were all negative. Fiber optic bronchoscopy with bronchoalveolar lavage (BAL) was inconclusive. All blood culture using the BacT/ALERT 3D Microbial Detection System (bioMérieux, Inc., Durham, NC) and sputum cultures using Vancomycin-Bacitracin-Clindamycin agar, MacConkey agar, and blood agar plates were negative for bacterial or fungal growth. Respiratory specimens, including BAL fluid, taken for acid fast bacillus (AFB) staining on more than three occasions were negative. A viral work-up for hepatitis B surface antigen (HBsAg), antihepatitis C antibody (anti-HCV) and human immunodeficiency virus (HIV), respectively; an autoimmune disease work-up for antinuclear antibodies (ANA) and a fungal work-up for Aspergillus antigen were also negative.
Under the clinical diagnosis of bacterial pneumonia, cefepime (2 g, twice daily) and intravenous teicoplanin (400 mg, once daily) were administered as empirical antibiotic therapy. However, after 2 weeks of antimicrobial treatment, follow-up chest radiograph and chest CT scans showed numerous aggravated nodular densities with cavities (Fig. C and D), and his Eastern Cooperative Oncology Group (ECOG) scale of performance status deteriorated from grade II to grade IV. Thus, amphotericin B deoxycholate was prescribed concurrently based on a suspicion for fungal pneumonia.
Percutaneous core needle biopsy (PCNB) of the left lung was performed to differentiate between the suspected diagnoses of fungal pneumonia and malignancy. However, histological examination revealed only nonspecific findings of interstitial chronic inflammation with fibrosis and focal necrosis. After maintaining the combination antimicrobial therapy for 28 days, multifocal patchy consolidations with nodular lesions on chest CT scan showed no further improvement. Accordingly, open lung biopsy using video-assisted thoracic surgery (VATS) was conducted for wedge resection of the right lung (middle and lower lobes). The histopathology showed grade III lymphomatoid granulomatosis, composed of polymorphous infiltrate with large atypical and small lymphoid cells showing angiocentricity with fibroblastic stroma (Fig. ).
The large atypical cells and small lymphocytes were positive for CD20 and CD3, respectively. The atypical lymphoid cells were positive for Epstein-Barr virus-encoded small RNA (EBER) with > 50/high-power field (hpf). Grocott–Gomori's methenamine silver (GMS) and periodic acid–Schiff (PAS) stains revealed no fungal organisms. The AFB stain was negative and there was no granulomatous lesion consistent with mycobacterial infection on our biopsy specimen.
On the 30th day of hospitalization, a therapeutic plan for PLG was carefully established with intensive CHOP and rituximab; however, the initiation of chemotherapy was delayed because of general weakness of the patient. Subsequently, M. tuberculosis complex, which is susceptible to all antituberculous drugs, was identified on the 36th day of hospitalization from the culture of sputum samples collected at admission. Therefore, anticancer treatment was deferred until after antituberculous treatment. After 34 days of antituberculosis medication, the patient showed a consciousness deterioration and became completely disabled. The patient's subsequent death was attributed to have resulted because of the disease progression of PLG.


A 62-year-old man initially presented to his primary care physician with a 3-month history of bilateral nasal airway obstruction (left greater than right), intermittent facial pressure, rhinorrhea, and postnasal drip. The patient was subsequently treated with multiple courses of antibiotics and topical and systemic steroids as well as saline solution irrigations, with only temporary relief. The patient was then referred to the rhinology service in January 2007 for further management of presumed chronic rhinosinusitis. Although the patient continued to have persistent sinonasal symptoms, he did not have any headache, facial pain, epistaxis, numbness, visual changes, or anosmia. However, his occupational history was significant for long-standing exposure to fumes, chemicals, resins, dusts, and solvents as a professional painter. He also had a 45 pack-year history of smoking and admitted to drinking 4–5 highballs daily for the past 40 years.
On nasal endoscopy, the patient was found to have a large polypoid mass that occluded the entire left nasal cavity from the roof to the floor of the nasal vestibule. On the right, an inferior septal spur was seen, along with polypoid changes of the mucosa of the lateral nasal wall. Polyps were seen in the middle meatus but were not as extensive as the contralateral side. A biopsy of the left nasal mass was performed in the clinic, which showed hyperplastic surface epithelium associated with acute and chronic inflammation and reactive atypia. There was no evidence of malignancy on histopathologic examination. A sinus computed tomography also was obtained, which showed partial opacification of the ethmoid sinuses bilaterally, complete opacification of the left maxillary sinus, and mucosal thickening of the right maxillary and bilateral sphenoid sinuses. The Lund-McKay score was 11 of 24 ().
In February 2007, the patient was taken to the operating room for bilateral endoscopic sinus surgery. Specifically, maxillary antrostomies and total sphenoethmoidectomies were performed bilaterally, including complete resection of the left sinonasal lesion. During surgery, polypoid tissue was not only seen filling the nasal vestibule on the left but also extending into the anterior and posterior ethmoid cavities as well as the sphenoethmoidal recess. The left maxillary sinus was also filled with polyps and mucopurulent material, all of which were removed with curved instrumentation. No polypoid tissue was seen in the left sphenoid sinus, and no discrete attachment site was appreciated at the time of surgery. In addition, no frontal sinusotomy was performed because the frontal recess and sinus were clear of any polypoid inflammation both on nasal endoscopy and imaging. Interestingly, on the right side, the patient was also found to have copious polyps within the maxillary sinus as well as the anterior and posterior ethmoid cavities. However, the polyps did not fill the nasal vestibule and were not as extensive as the contralateral side. Specimens from both sinonasal cavities were then sent to pathology.
Histopathologic analysis of the tissue from the right sinonasal cavity showed findings consistent with benign inflammatory polyps. However, the specimen from the left side demonstrated two concurrent processes, inverted schneiderian papilloma with a focus of malignant transformation into SNUC (
A–D). The focus of undifferentiated carcinoma was found deep in the stroma of the IP, with the contour of the IP preserved. The focus also showed a syncytial-type grown pattern, with a high nuclear-to-cytoplasmic ratio. The cells were dark blue in appearance, with round-to-oval nuclei that contained vesicular nuclear chromatin and small nucleoli. Mitoses were markedly increased within the focus of SNUC. There was no squamous or glandular differentiation. Immunohistochemistry was performed. The neoplastic cells showed a strong pancytokeratin reaction and a positive result for cluster of differentiation 56 but negative results for S100 protein, Human Melanoma Black 45, chromogranin, synaptophysin, tumor protein 63, cytokeratin 5/6, CD45RB, desmin, and smooth muscle actin consistent with SNUC. HPV testing results were negative.
The patient was then seen by a head and neck oncologist, and his case was presented to a multidisciplinary tumor board. Concurrent chemoradiation therapy was recommended. A postoperative positron emission tomography (PET) and computed tomography (CT) was performed before radiation and chemotherapy, which showed no evidence of distant metastasis. The patient was then treated with 70.29 Gy of radiation with concurrent cisplatin therapy. Combined treatment began on April 2, 2007, and concluded May 16, 2007. Cisplatin was administered over 1 hour once a week for 7 weeks throughout the treatment. Radiation treatment was completed over the same length of time 5 days each week for a total of 33 treatments. The patient did not require a break-in treatment at any time. He then underwent adjuvant chemotherapy after this initial treatment with four courses of cisplatin, docetaxel, and 5-fluorouracil, which concluded in September 2007. The patient was subsequently followed up by his rhinologist and his head and neck surgeon with serial nasal endoscopy examinations and imaging. Specifically, posttreatment magnetic resonance images were obtained in October 2007, April 2008, December 2008, April 2009, and June 2010, with no evidence of recurrent disease (). Postoperative PET/CT was also obtained in June 2008 and April 2009, without evidence of local or distant disease. There has been no evidence of recurrent disease after 9 years of follow-up on imaging or examination.


A 69-year-old male presented with a 3-month history of weight loss, watery non-bloody diarrhoea, low energy, and pain in the left hip radiating to the leg. His history consisted of stroke with no residual deficit 6 years ago and non-deforming rheumatoid arthritis. He was on aspirin and sulfasalazine. He was a smoker of 20 pack-years having stopped 7 years ago. He consumed alcohol socially.
Systemic examination was normal. He had recently been diagnosed with CD and commenced a GFD. MRI followed by a PET scan showed a mass at the fourth lumbar vertebra with no disease elsewhere, and the subsequent biopsy revealed a diagnosis of T-cell lymphoma with anaplastic large cell morphology, CD30 positive and ALK-1 negative. The patient was treated with CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) × 8 cycles and radiotherapy 40 Gy/20 fractions. A follow-up PET scan 6 months after completion of therapy suggested a residual soft tissue mass in the left posterior element of L4 with minimal FDG accumulation (residual disease). However, a repeat L4 biopsy showed therapy-related changes only, with no evidence of lymphoma. The patient was admitted again 24 months later with diarrhoea and 2-stone weight loss. He looked cachectic with generalised oedema, but on examination, there was no lymphadenopathy or organomegaly. His laboratory work-up revealed a normocytic anaemia, hypoalbuminaemia with normal anti-transglutaminase antibody titre (Table ). Given significant risk of enteropathy-associated T-cell lymphoma (EATL), investigations to exclude this diagnosis were performed. Scans including whole-body CT and PET showed no evidence of recurrence of his anaplastic large cell lymphoma, but an MRI of the small bowel showed mildly thickened loops of the jejunum in the central abdomen and right flank without dilatation. Oesophagogastroduodenoscopy revealed severely active CD (Fig. ), and colonoscopy was macroscopically normal with normal colonic and terminal ileal biopsies. Biopsy results from the second part of the duodenum showed total villus atrophy with intraepithelial lymphocytes that were within normal limits. Subsequent immunostaining confirmed a normal number of aberrant intraepithelial T lymphocytes (IELs) (Fig. ). A diagnosis of RCDII was made, and the patient was treated with total parenteral nutrition, blood products (red cell concentrate, platelet, fibrinogen, albumin), parenteral steroids followed by “naked” unencapsulated budesonide. He was later treated with oral cladribine, a synthetic purine nucleoside homologue with cytotoxic activity, but was not considered a candidate for autologous stem cell transplant given his age and poor performance status. He did not respond to cladribine, and developed a catastrophic upper gastrointestinal bleed 4 weeks after admission which could not be controlled endoscopically. A mesenteric angiogram with embolisation of jejunal branches was performed, and haemostasis was achieved (Fig. ). Unfortunately, he went on to develop severe systemic sepsis with multiple organ dysfunction after the procedure. Given the poor prognosis, treatment was not escalated, and he died 3 days later. A limited post-mortem examination (requested by next of kin) showed axillary lymph node T-cell lymphoma likely related to the CD.


A 79-year-old woman with chronic lymphocytic leukemia was referred by her oncologist for a skin check. The patient noted changes in the appearance and texture of her nails within 6 months of starting systemic treatment for chronic lymphocytic leukemia with ibrutinib at an oral daily dose of 420 mg. She was not receiving any other chronic lymphocytic leukemia-directed therapy.
Cutaneous skin examination was significant for changes of her toenails (Figs. , , ) and fingernails, which appeared fragile and brittle; biotin 2.5 mg daily was prescribed. In addition, she had ecchymoses on her arms and legs. Ten actinic keratosis were discovered and treated with cryotherapy. No cutaneous malignancies were diagnosed.
At follow-up evaluation 3 months after starting biotin, her toenails were less brittle. New ecchymoses on her extremities continued to develop.


A 53-year-old man with chronic lymphocytic leukemia was referred by his oncologist for a skin check. The patient noted that the appearance of his nails had changed within 4 months of starting systemic treatment for chronic lymphocytic leukemia with ibrutinib at an oral daily dose of 420 mg. ABT199 (Venetoclax), a Bcl-2 inhibitor, had been added 3 months after the initiation of ibrutinib. He was not receiving any other chronic lymphocytic leukemia-directed therapy.
Cutaneous skin examination was significant for changes to the nails on his thumb (Fig. ), finger (Figs. and ) and toe (Fig. ); they appeared fragile and brittle. Biotin 2.5 mg daily was prescribed. In addition, desquamative dermatitis with red-brown macules and petechiae was present on the tip of the left great toe (Fig. ). No cutaneous malignancies were observed.


A 44-year-old female was hypertensive treated with ramipril 5 mg twice daily. She had a family history of kidney disease and a medical history of IgA nephropathy (Berger's disease). Then, she had become uremic, requiring chronic hemodialysis due to renal failure following Berger's disease for 8 years. Furthermore, an arteriovenous fistula (FAV) was created in the left forearm. Following hemodialysis training, the patient performed hemodialysis three times a week at home.
She had been hospitalized at the Nephrology Department 1 year previously because of bilateral pleural effusion and fever during hemodialysis.
Then, she was admitted to our hospital to evaluate if she was eligible for a kidney transplant. At the admission, the patient was asymptomatic. There was a mild leg swelling. On clinical examination, she was apyretic with a pulse rate of 96/min, blood pressure of 150/100 mmHg, and arterial saturation of 96%. On cardiac examination, we found normal first heart sound, fixed splitting of the second heart sound, hardening P2, and pansystolic murmur four of six in left parasternal line of intercostal space II–III. On lung auscultation, vesicular breath sound was heard over the most of the lung surface. Laboratory tests showed serum creatinine 9.91 mg/dl, serum urea 191 mg/dl, serum potassium 5.6 mmol/l, serum phosphorus 5.9 mg/dl, and Hb 9.5 g/dl.
Her electrocardiogram showed sinus rhythm of 90 bpm. Transthoracic echocardiography (TTE) showed enlargement of the right ventricle (right ventricular basal diameter of 51 mm) [] and truncus of pulmonary artery (diameter of 36 mm), a markedly dilated CS: 25 mm × 21 mm (normal value: <15 mm) [Figure and ], mildly enlarged left atrium (42 mm parasternal long axis), normal size left ventricle (42 mm), and mild ejection fraction reduction (50%) along with altered diastolic pattern (Grade 1 diastolic dysfunction). There were also moderate mitral regurgitation and evidence of right ventricular volume overload with right ventricular-right atrial gradient of 43 mmHg [], tricuspid regurgitation of 3.4 m/s with estimate pulmonary artery systolic pressure of 65 mmHg. There was also a mild pericardial effusion.
We also proceeded with a transesophageal echocardiographic (TEE) study which demonstrated a septal defect of the sinus venous type, ranging 18–20 mm [Figure and ], with normal return of the pulmonary veins. The resulting left-to-right shunt is hemodynamically significant with Qp/Qs: 2.2 (systemic blood flow of 7.6 l/min and pulmonary blood flow of 17.4 l/min due to the association of ASD and FAV).
Dilatation of the CS raised suspicion of PLSVC. A saline contrast echocardiography to confirm the presence of PLSVC was not performed because of FAV on the left forearm. Therefore, computed tomography (CT) angiography was performed, and it showed the PLSVC draining into the right atrium through a dilated CS [Figure and ].
Right heart catheterization (RHC) was performed to better estimate the magnitude of the shunt (pulmonary to systemic flow ratio, Qp: Qs) and measurement of the pulmonary artery pressure. The results of the RHC revealed a mean pulmonary arterial pressure of 21 mmHg, a pulmonary artery wedge pressure of 13 mmHg, and a pulmonary vascular resistance of 2.6 Wood units. Therefore, the RHC ruled out the diagnosis of precapillary pulmonary hypertension. There was only a right ventricular volume overload because of the ASD hemodynamically significant and high flow fistula. During RHC, oxygen saturations of single blood specimens were measured from the PLSVC, right atrium, and pulmonary artery. The oxygen saturations in PLSVC were 99% because of the FAV on the left forearm; in the right atrium, mid-high was higher than normal value, ranging from 98% to 95%, because of the shunt determined by the ASD. At the right atrium low, near tricuspid valve, there was an oxygen saturation of 80% for the reason why it received deoxygenated blood from the body through the inferior vena cava (O2: 56%).
Now, the patient is waiting for the elective surgery for ASD closure.


A 78-year-old male patient was admitted to hospital due to onset of shortness of breath on exertion over the past month. Patient was diabetic and suffered from chronic obstructive pulmonary disease but had no other cardiovascular risk factors. He has never experienced angina symptoms even though approximately 2 months before admission had experienced some abdominal pain with vomit and fever that lasted for <48 h. At admission, he was tachycardic with an otherwise unremarkable clinical examination. Electrocardiogram showed sinus tachycardia with q wave and ST segment elevation on the lateral leads. Cardiac troponin was mildly elevated but stable during three consecutive measurements over 24 h, and the brain natriuretic peptide was elevated. Transthoracic echocardiogram, due to a very poor acoustic window, was deemed almost inconclusive. Parasternal long axis view and very poor apical views did not show evidence of global systolic dysfunction, significant valve disease, or pericardial effusion. Contrast echocardiography might have provided crucial additional information improving diagnostic accuracy, but at the time, it was not being routinely performed. Therefore, to better characterize cardiac function, a cardiac magnetic resonance (CMR) was arranged.
CMR scan showed a giant pseudoaneurysm [] of the lateral wall [, arrows] with laminar thrombus [, arrowheads] and bilateral pleural effusion [, curved arrows]. Pseudoaneurysm with a “guitar-like” appearance [, panel A] was expanding in systole [, panel B] and restricting in diastole [, panel C] causing an ejection fraction of nearly 10% despite normal contractility and viability [, panel D] of all other segments. Pseudoaneurysm wall showed no late gadolinium enhancement [, panel D] since myocardium was absent and only pericardium was impeding the heart from a lethal rupture.
Urgent coronary angiogram was performed showing proximal left circumflex occlusion with diffuse atherosclerosis but no significant lesions on the other coronary vessels. Cardiac surgery consult was deemed necessary to decide following management. An urgent cardiac surgery was performed that confirmed CMR findings. A big pseudoaneurysm with some thrombotic deposition was observed and was excluded with a Dacron patch. Coronary artery bypass graft was not performed.


A 38-year-old male patient reported to the department of periodontics with chief complaint of bleeding gums and also with the history of seizures for 3 years and on medication for the same. He first noticed that his gums had become thick and swollen before 1½ years which gradually started to bleed while brushing for 6–8 months. Medical history revealed that the patient was a known case of APLA syndrome and had a history of cerebrovascular thrombosis before 3 years and had undergone a burr hole craniotomy for the same to relieve the decompression. The patient also gave history of generalized tonic–clonic seizures since then and was on medication, i.e., phenytoin sodium for the same. The patient was on oral anticoagulants (warfarin sodium 5 mg 1-0-0, i.e. sofarin tablet and anticonvulsants tablet eptoin 100® 1-0-2).
On intraoral examination, there was presence of moderate amount of local factors, generalized bleeding on probing (Muhlemann and Son bleeding index score was 4), and suppuration was present. The gingiva revealed generalized puffy and erythematous enlargement []. Generalized pockets were present with Grade I mobility (tooth #11–18, 24, 35, 37, and 38), Grade II mobility (tooth #28, 31, 32, 41, and 42), and Grade II furcation involvement (tooth #27). Routine blood examination revealed that there was slight increase in total white blood cell count of 11,300 cells/mcL and a slight raise in the international normalized ratio values of 2.03. Full-mouth radiographs revealed generalized bone loss whereas panoramic X-ray revealed vertical bone loss in relation to 13–21, 26, and 32–42 []. Many teeth had a questionable prognosis because of the simultaneous occurrence of gingival enlargement and chronic periodontitis. Clinically, inflammatory gingival enlargement, drug-induced enlargement, conditioned gingival enlargement, and gingival enlargement associated with systemic diseases were considered in the differential diagnosis. Based on the clinical findings and medical history, it was diagnosed as phenytoin-induced gingival enlargement combined with inflammatory enlargement. The patient's neurologist was consulted, and medication could not be deferred or changed.
Considering compromised medical condition, conventional flap therapy was avoided because of the risk of hemorrhagic episodes. Hence, a conservative treatment (scaling and root planing with maintenance and regular follow-up) under antibiotic coverage was planned for this patient after taking opinion from neurologist and consent from patient's caretaker. The periodontal treatment included several scaling sessions and gingival debridement, accompanied by ample washings with oxygenated water and 3% chloramine solution. Systemic antibiotic therapy included administration of amoxicillin 500 mg and metronidazole 400 mg three times a day, for 7 days. Antiseptic mouthwash 0.2% chlorhexidine mouthrinse was prescribed twice daily for 3 weeks. As a result of the antibiotics and periodontal therapy, satisfactory results were seen at the follow-up visit, with the presence of pockets and gingival enlargement in some areas []. Oral hygiene practice was stressed to the patient during regular follow-up visit with the continuation of the drugs for the main disease.


JP is currently a 58 year old man with multifocal urothelial tumors of the urinary bladder despite two courses of intravesical mitomycin C and one six week course of BCG.
The patient appears well but has a significant past medical history consisting of diabetes mellitus, coronary artery disease, mild congestive heart failure, chronic renal disease, and peripheral neuropathy. He stopped cigarette smoking at age 35 after 15 years of smoking 1.5 packs/day. He has had a coronary artery stent placed.
The patient has a BMI of 38 kg/m2. He weighs 106 kg and is 168 cm in height. He is thus markedly overweight with a large abdominal girth. His recent creatinine is 2.13, BUN 38. This has been stable for 3 years.
He presented with gross hematuria in 8/15. Imaging disclosed left hydronephrosis with a filling defect in the left renal pelvis. Ureteroscopy and biopsy revealed a low grade urothelial tumor in the renal pelvis. In April 2016 he underwent a robotic assisted left nephroureterectomy. The pathology indicated high grade pT3 urothelial cancer in the renal pelvis with small HG Ta and CIS in the ureter. There was Ta tumor at the distal margin. Adjuvant chemotherapy was discussed but was not given because of his renal failure. Subsequent serial imaging has been negative for any metastasis.
Beginning in July 2016 he has developed multifocal low or high grade Ta urothelial cancer of the bladder. After the resection of over 10 HG Ta tumors in 7/16 he received intravesical mitomycin for six weeks. In 11/16 he had a TUR BT of multiple tumors from one to 5 cm, LG Ta. Although BCG is not likely to be effective for LG Ta he was given intravesical BCG for six weeks. The next TUR BT was 3/17 and once again there was mutifocal HG Ta tumors. This was followed with weekly mitomycin again.
The most recent TUR BT was in 7/17 and the pathology was LG Ta. The largest tumor was at the 1 o’clock position just inside the bladder neck and required a bugby electrode with the 70 degree lens to visualize and remove, as it was not visible with the 12 or 30 degree lens. His most recent cystoscopy was 10/17 and not surprisingly he has developed multiple small and large tumors which all appear Ta.
The patient’s quality of life has not changed as a result of the multiple resections. He has not had gross hematuria since the left nephrectomy. He has not developed an invasive tumor of the bladder.
Alternative considerations for therapy are welcome such as a PDL inhibitor or other experimental treatment.
Photos will be of the tumor and the use of the blue bugby electrode for the tumor at the 1 pm location at the bladder neck.


A 32-year-old man presented with complaints of metamorphopsia in his right eye (RE) for 1-month duration. There was no prior history of intraocular inflammation, surgery, or trauma. His best-corrected visual acuity (BCVA) was 20/25 in the RE and 20/20 in left eye (LE). Anterior segment examination of both the eyes was unremarkable. Fundus examination of the RE showed an ERM involving the supertemporal arcade with inner retinal folds radiating toward the fovea [] and the presence of multiple peripheral bulb-like dilatations of vessels in the temporal periphery []. Ultra-wide-field (UWF) fluorescein angiography (Optos Inc.,) demonstrated typical light bulb-like dilatations of telangiectatic vessels characteristic of Coats’ disease along with interspersed capillary nonperfusion (CNP) areas []. Spectral domain optical coherence tomography (SD-OCT, Carl Zeiss Inc.,) confirmed the presence of ERM, an intact ellipsoid zone, and inner retinal folds in the area nasal to fovea []. The LE fundus was normal. A diagnosis of adult-onset Coat's disease with ERM was made.
After obtaining informed consent, the supertemporal lesion along with the CNP areas as depicted on the UWF autofluorescence (UWFA) was subjected to laser ablation (532 nm green laser). No surgical intervention was recommended as the patient was comfortable with his visual status and a regular follow-up was advised. At 8 weeks’ follow-up, the patient reported worsening of metamorphopsia and diminution of vision in his RE. BCVA RE was 20/40. SD-OCT showed worsening changes in the inner retina as well as external limiting membrane []. After informed consent, the patient underwent 25-gauge PPV, posterior vitreous detachment induction, ERM and internal limiting membrane peeling, fluid-air exchange, and endolaser augmentation of supertemporal Coats’ lesion. The patient was advised standard postoperative regimen with topical steroids and cycloplegic drops.
At 4 weeks’ follow-up, the patient reported the improvement in metamorphopsia and BCVA in the RE improved to 20/30. Dilated fundus examination showed normal appearing macula []. Laser photocoagulation scars were seen in the temporal periphery on UWFA []. SD-OCT revealed macula devoid of ERM along with flattened foveal contour []. At 6 months, the patient had no complaints of metamorphopsia and BCVA (RE) improved to 20/25.