A 63-year-old Asian male with hypertension was admitted due to recent attacks of transient right upper extremity weakness and numbness, lasting 3 to 5 min. On admission, his blood pressure was high at 170/90 mmHg and heart rate was 80 beats/min. Neurologic examination was normal. Doppler ultrasound examination showed normal right internal carotid artery velocities (0.92 m/s of peak systolic velocity) and elevated velocities in the left internal carotid artery (2.79 m/s of peak systolic velocity) suggesting critical stenosis. Six months before this admission, he had undergone arch aortography at an outside institution using a femoral artery approach, which confirmed critical stenosis in the proximal right internal carotid artery (ICA), variant origin of the left CCA from the proximal brachiocephalic trunk, and also critical stenosis in the proximal left ICA (). After selective cannulation of right CCA, successful carotid stent placement had been performed with distal protection at the bifurcation level (). Left carotid stenosis had not been stented at that time. Because of the right sided transient ischemic attack episodes on admission to our institution, we decided to perform stenting to the stenosis in left ICA. Firstly, femoral approach was tried. However, selective engagement to the left CCA could not be possible in this way using standard catheters and Simmons catheter; therefore, right brachial approach was considered.
After pretreatment with aspirin (325 mg daily) and clopidogrel (75 mg daily) for five days, a 7 Fr sheath was inserted in the right brachial artery. A 5 Fr hydrophilic coated vertebral catheter (Merit Medical Systems, Inc., Utah, USA) was then advanced into the brachiocephalic trunk to engage selectively the left CCA (). 0.035′′ flexible guidewire (Merit Medical Systems, USA) was positioned at the left external carotid artery using this vertebral catheter and exchanged with a 0.035′′ Amplatz extra-support guidewire. After that, a 7 Fr Asahi Zenyteex guiding catheter (Asahi-Intecc, USA) was positioned at the left common carotid artery and extra-support guidewire was removed. Selective left carotid angiography confirmed critical stenosis at the bifurcation level of ICA (). Distal embolic protection system (Emboshield, Abbot, IL, USA) was deployed in the distal ICA under fluoroscopic guidance. A 6 × 9 × 40 mm Sinus Carotid (Optimed, Ettlingen, Germany) self-expandable stent was successfully deployed in the left common and internal carotid artery, and postdilation was performed using a 5 × 20 mm Pyxis-c balloon (Stron Medical, Winsen, Germany) with the inflation at 10 atm for 10 sec (). After postdilation, the follow-up angiogram showed complete coverage of the lesion without residual stenosis or dissection (). The embolic protection system was removed and moderate debris was identified. The brachial artery sheath was removed and excellent hemostasis was achieved. The patient tolerated the procedure well and did not suffer any complications. He was discharged within 24 hours without any neurologic deficit and is now followed up at the outpatient clinic in a stable condition.


A 71-year-old man was admitted to our outpatient clinic, with nausea, epigastric pain, and weight loss that had lasted for seven months. Laboratory findings showed anaemia. The patient underwent an endoscopic evaluation, which revealed a huge ulcerative and infiltrative mass in the upper and middle third of the stomach and the biopsy specimen taken showed a moderated tubular adenocarcinoma. Contrast-enhanced computerised tomography (CT) scan revealed a thick engrossment of the two upper thirds of the stomach with enlarged perigastric lymph nodes and not liver, nor peritoneal metastases findings were shown. The patient underwent a D2 total gastrectomy with distal pancreatectomy and splenectomy. At surgery, the tumour was located in the upper two-thirds of the posterior wall of the stomach with enlarged lymph nodes at the lesser curvature and celiac trunk. There was serosal invasion and fixation to the anterior surface of the pancreas body. No liver or peritoneal metastases were found.
On gross examination of the specimen, we identified two attached ulcerative tumours located on the posterior wall of the stomach (). The proximal one close to the cardial region measured 6.5 × 5.5 cm, with a whitish grey coloration and with an elastic consistency; and closely attached, a fungating ulcerative reddish lesion (Borrmann type III) measured 8.5 × 8.0 cm and occupied the posterior surface of the middle third of the stomach. The latter fixedly attached to the anterior surface of the body of the pancreas. The spleen did not show alterations. In addition to the gastric specimen, 41 resected regional lymph nodes were submitted and studied. Microscopically, two separated gastric lesions were identified with different patterns in morphology and the distance in between was of 1 mm (). The proximal lesion corresponds to a large-cell neuroendocrine carcinoma composed of atypical cells with faint cytoplasmic features and prominent hyperchromatic nuclei (occasionally pleomorphic). The cells are distributed in an organoid architecture with solid nests and broad trabeculae solid pattern without glandular formation (). The distal tumour corresponds to a moderated tubular adenocarcinoma, composed mainly of tubules infiltrating the gastric wall with serosal exposure. The cells contain variable amounts of eosinophilic cytoplasm with scattered mucin material ().
The neuroendocrine phenotype of the large-cell neuroendocrine carcinoma was immunohistochemically confirmed with synaptophysin, which stain all (). Additionally, it showed focal expression for keratin (AE1/AE3) (). Other markers, such us CD45, CD3, CD20, CD30, and S100, were negative.
The tumour cells invaded veins as well as lymphatic nodes. Regional lymph node metastasis was detected in 17 out of 41 lymph nodes. Sections showed adenocarcinoma in all lymph nodes retrieved, but only one lymph node showed metastasis from the neuroendocrine carcinoma.


A 79-year-old male, with terminal lung cancer at the right upper lobe, had been in another hospital and intubated for 3 weeks since an accidental airway obstruction. His doctor performed the tracheostomy in a surgical manner at the bedside. During the procedure, continuous arterial bleeding at the surgical site occurred. The doctor could not detect the bleeding artery clearly, but direct manual compression with an index finger at the surgical site provided temporary hemostasis. On arrival at our emergency department, he was intubated and in severe hemorrhagic shock despite having received transfusion of six units of packed red blood cells concentration (PRBC) and six units of fresh frozen plasma (FFP).
Arterial blood gas assessment revealed metabolic and respiratory acidosis and anemia [pH 7.09, pCO2 71 mmHg, pO2 193 mmHg, HCO3− 21.0 mmol/L, base excess (BE) −8.3 mmol/L, lactate (Lac) 5.5 mmol/L, hemoglobin (Hb) 7.9 g/dL, hematocrit (Ht) 22 %, FiO2 1.0], and blood tests showed coagulopathy [PT 35.3 %, PT-INR 1.68, activated partial thromboplastin time (APTT) 56.2 s, fibrinogen (Fib) 84 mg/dL]. These data showed that his condition was in severe hemorrhagic shock and coagulopathy.
The patient was taken up for emergency surgery in view of the serious nature of the injury.
During surgery, because of the clinical impression of an injury to the distal IA or proximal common carotid artery, a right supraclavicular incision was made, followed by dissection of the platysma, division of the right sternocleidomastoid muscle, and resection of the right clavicular head. The exposure revealed that both innominate and right common carotid arteries were injured (Fig. ). After innominate, the right subclavian and right common arteries were isolated and primary repair and graft interposition of the arteries was attempted, but proved too difficult because of atherosclerosis. After an hour into the surgery, the patient showed worsening hypothermia (34 °C), metabolic acidosis, and clinical evidence of coagulopathy; therefore, we decided a damage control strategy. Despite clamping of the IA for about 10 min in attempting primary repair, the regional oxygen saturation (rSO2) of the forehead, measured by near-infrared spectroscopy (NIRS; INVOS 5100C Cerebral/Somatic Oximetry Monitors™; Covidien, USA), was approximately 60 % without laterality. It seemed that adequate blood circulation to the brain was maintained through the collateral flow; therefore, we decided to ligate the innominate, right carotid, and subclavian arteries. The wound was packed with gauze for temporary wound closure. Overall, the operation lasted for 1 h and 25 min, with a recorded blood loss of 1190 g and transfusion of 16 units PRBCs and 10 units of FFP.
Postoperative contrast-enhanced computed tomography revealed no apparent acute cerebral ischemia and extravasation, and the distal right common carotid and right subclavian arteries were enhanced through the circle of Willis (Fig. ). A right tracheal shift due to adhesions caused by lung cancer was also revealed, indicating a course of the IA anterior to the third tracheal ring.
After admission to the intensive care unit, coagulopathy and hypothermia were corrected with massive transfusion (overall transfusions: PRBCs 24 units and FFP 26 units).
No symptoms of hypo-perfusion of the right upper limbs and brain were observed; therefore, an extra-anatomical bypass was deemed unnecessary. On postoperative day 1, we closed the wound definitively. On postoperative day 7, the patient was transferred to a sub-acute, community hospital.


A 76-year-old man came to the Department of Oral and Maxillofacial Surgery, University of Tsukuba Hospital, with a three-month history of swelling of the left mandible. He had been diagnosed with stage IV prostatic carcinoma and multiple distant metastases and had been treated with zoledronic acid 4 mg for 22 times and denosumab 120 mg for 4 times. His face was symmetrical, with a fistula and pus discharge on the skin of the left mandible. The regional lymph nodes were normal, and there was no trismus. Examination of the oral cavity showed gingival swelling, redness, pus discharge, and loosening of teeth 35 and 36. Tooth 17 was lost naturally 2 months after the first visit, which revealed a sequestrum in the mouth; the sequestrum expanded over the next 8 months (). A panoramic radiograph revealed separated sequestra of the right maxilla and the left mandible (). Computed tomography (CT) revealed maxillary osteitis and sinusitis (). An abscess had formed in the right maxillary sinus, and the patient complained of mild ophthalmalgia. Therefore, we performed a sequestrectomy of the right maxilla and drained the maxillary sinus under local anesthesia. The postsurgical course on day 0 was uneventful, and the patient was discharged from the hospital; however, he was found unconscious in his house on the day after surgery and was brought by ambulance to the emergency room (ER) at our hospital. The patient's consciousness level was 13 in the Glasgow Coma Scale (eye opening 4, verbal response 4, motor response 5), and he had left conjugate deviation and left hemiparesis. General convulsions occurred continuous to the left upper and lower limb convulsions. The convulsions were resolved by administering diazepam (5 mg) twice and fosphenytoin (900 mg) once. Laboratory results showed elevated WBC (10,300/μL) and CRP (2.08 mg/dL). A brain CT revealed a hypodense lesion in the right frontal lobe (). A T2-weighted MRI revealed a right frontal-lobe abscess and ethmoid sinusitis. The maxillary sinus was connected to the oral cavity, and the abscess in the maxillary sinus had disappeared (). Diffusion-weighted imaging (DWI) MR imaging showed a low apparent diffusion coefficient (ADC) (). A fall in the ADC in the fluid-filled lesion was highly suggestive of abscess.
The infection was suspected to have originated from the maxillary sequestrum and spread through the maxillary sinus, ethmoid sinus, and frontal sinus, and, by contiguity, to the frontal lobe. Although a bacterial culture of the maxillary sinus revealed only gram-positive and gram-negative bacilli and gram-positive cocci, these species were not found.
The patient was treated with ceftriaxone 2 g q12h and metronidazole 500 mg q8h for 50 days, with valproate Na 800 mg for convulsions. The enhanced area of brain infection disappeared in follow-up MR images (). This case was treated conservatively, without surgery, because the patient had terminal-stage cancer. The patient was discharged from the hospital after 2 months, without any left-limb paralysis.


A 60-year-old woman presented with a three-year history of intermittent postprandial
epigastric pain, and weight loss of 6 kg. The abdominal pain was relieved with fasting.
She denied nausea, vomiting and diarrhea. Physical examination was normal. Several
exams, including abdominal ultrasonography, upper gastrointestinal endoscopy,
colonoscopy, small bowel radiographic study, tomography failed to reveal any
abnormality. Finally, an angiotomography showed high-grade stenosis of the anterior wall
of the proximal celiac axis caused by extrinsic compression of the median arcuate
ligament (A).
The patient underwent laparoscopic section of the ligament and celiac ganglionectomy.
The patient was placed in reverse Trendelenburg position with the legs abducted and
supported on cushioned spreader bars. The operation was performed through five trocars
inserted in the upper abdomen, similar to that of Nissen-Rosetti procedure. A right
subcostal retractor was used to retract the left lobe of the liver laterally and the
stomach was retracted to the patient's left side with a Babcock clamp. After dividing
the gastrohepatic omentum and identifying the right crus of the diaphragm inferiorly to
the cardia, the junction of both crus was carefully separated to expose the anterior
surface of the aorta and identify the median arcuate ligament and celiac plexus. The
median arcuate ligament that was compressing the proximal celiac axis was sectioned and
all neural tissue overlying the celiac axis was resected. The operation was uneventful
and lasted 70 min.
The patient was discharged from the hospital 12 h after the operation completion and had
an uneventful recovery. At two-month follow-up, she referred only two episodes of mild
abdominal pain and gained 3 kg. An angiotomography obtained at that time showed no
celiac axis stenosis (B).


A 44-year-old woman with unremarkable medical history was admitted to our clinic for recurrent attacks of pressing headache, with abrupt onset and brief duration, accompanied by nausea, transient hearing loss and tinnitus. These symptoms were relieved by supine position. The clinical picture progressively worsened, with episodes of vomiting during headache. Neurological examination was negative. A magnetic resonance imaging (MRI) scan showed a spherical mass lesion with lipid signal at the intraventricular foramina of Monro causing compression of the third ventricle and expansion of the ventricular system, suggestive of hydrocephalus.
After neurosurgical evaluation the patient underwent an endoscopic removal of the lesion. Histological findings were compatible with colloid cyst of the third ventricle. After surgical treatment the patient recovered completely from symptoms and the follow-up MRI demonstrated the complete excision of the lesion.


A 50-year-old male patient was taken to catheterization laboratory at the third hour of his pain with the diagnosis of acute posterolateral myocardial infarction (MI). The patient was pretreated with acetylsalicylic acid 300 mg, prasugrel 60 mg, and unfractionated heparin 100 mg/kg. Infarct related artery was first obtuse marginalis (OM) (). Total occlusion was crossed with a 0.014 inch floppy wire and the lesion was predilated with a 2.5/20 mm monorail balloon at 12 atm pressure. Control angiography revealed a thrombus shift to circumflex artery (Cx) which ceased the distal flow (). The occlusion was crossed with a second 0.014-inch floppy wire and the occlusion site was dilated with a 1.5/20 mm monorail balloon at 16 atm pressure (). After balloon angioplasty no-reflow developed. Intracoronary adenosine (250 mcg) was administered, but distal flow could not be restored (). Therefore we decided to give adenosine at the distal part of Cx and the previously used 1.5/20 mm monorail balloon was retrieved and perforated with a needle at four different sites. The perforated balloon was flushed from the hub with adenosine solution (1 cc/100 mcg) and bubbles were removed (Figures and ). Then it was inserted to the distal part of the Cx and 250 mcg adenosine was injected via the balloon. Control angiography revealed TIMI 3 flow (). First OM was stented with a 3.5/12 mm bare metal stent and the procedure was terminated without any other complication.


An 87-year-old female patient admitted with acute inferior MI and complete AV block at the thirteenth hour of her symptoms. The patient was taken to catheterization laboratory for primary PCI. She was pretreated with acetylsalicylic acid 300 mg, ticagrelor 180 mg, and 85 mg/kg unfractionated heparin. Right coronary artery (RCA) was totally occluded at the midportion. A 0.014-inch floppy wire was inserted to the distal part of the RCA. The lesion was predilated with 1.20/12 mm and 3.0/15 mm monorail balloons, respectively, and a 3.0/18 mm drug eluting stent was implanted at 16 atm (). No-reflow developed after stent deployment. We administered 250 mcg adenosine via the guiding catheter but could not achieve any distal flow (). Afterwards, previously used 1.20/12 mm monorail balloon was perforated and flushed with adenosine solution (1 cc/100 mcg) and bubbles were removed. Then it was inserted to the distal part of the RCA and 250 mcg adenosine was injected via the balloon (). TIMI 3 flow was restored ().


A 35-year-old woman was referred to our clinic with a diagnosis of ITP resistant to medical treatment in whom a splenectomy was indicated. For 7 years, she had been treated regularly with 1 mg/kg/day methylprednisolone and episodic intravenous immunoglobulin (IVIG) in the hematology clinic and had persistent thrombocytopenia of 3,000–60,000/mm3, ongoing menorrhagia, and ecchymosis. The patient had two healthy births after IVIG treatment. Preoperatively, dextrocardia was detected on an electrocardiogram and thoracoabdominal computed tomography (CT) showed situs inversus totalis. In addition to mirror imaging of the normal anatomic locations of all organs, the spleen measured 13 × 6 cm and there was a 1.5 cm accessory spleen in the right upper quadrant (). Although no abnormalities were seen in the head and body of the pancreas, no pancreatic tail was seen. In other words, the pancreas had not crossed over to the right side of the superior mesenteric vascular axis and there was no pancreatic tissue near the splenic hilum (). The patient underwent a laparoscopic splenectomy () with no complications or adverse events following surgery. She was discharged on the third postoperative day with thrombocyte count of 155,000/mm3.


A 33-year-old woman with a history of intermittent jaundice was referred to our radiology department. She had complained of recurrent abdominal pain for 5 years. At the age of 30 years she had been diagnosed of cholelitiasis by an ultrasound performed in another centre. Her liver function tests were abnormal with slight elevation of bilirubin.
First an abdominal ultrasound was realized. It showed an intussusception involving the duodenum and proximal jejunum. An anechoic cystic lesion was observed inside the lesion (). Besides, the biliary tree was dilated.
The study was continued with computed tomography with contrast and obtainment in portal phase, and after a complementary magnetic resonance (MR) with axial and coronal T2 weighted single-shot turbo spin echo, MR Cholangiopancreatography and contrast enhancement sequences were performed. Gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid was used for the dynamic study. We realized vascular acquisitions and a delayed hepatobiliary phase. The axial CT images and T2 weighted sequences confirmed that the distal duodenum with surrounding fat, vessels, and the pancreatic head were invaginated into the proximal jejunum. Inside the intussusception a cystic lesion was also visualized. The stomach was not distended (Figures and ). The MR Cholangiopancreatography depicted that the extrahepatic bile duct was slightly dilated and pulled leftward towards the cyst mass. The contrast enhancement sequences corroborated the simple cystic nature of the cause of intussusception (). In the hepatocytic acquisition phase the contrast filled the biliary tree and the bowel lumen, but not inside the cyst lumen (). An open surgery was the treatment elected. A laparotomy was realized and a cystic lesion measuring 4 × 4 × 3 cm was removed. At histopathologic analysis the cyst presented definitive criteria of duplication cyst (). The postoperative period was uneventful and ten days later the patient was discharged.


A 47-year-old male was treated with a salvage vertical partial hemilaryngectomy after failed radiation for an early stage (cT1a) squamous cell carcinoma of the glottis. The recurrent tumor was initially staged as rT1a with normal vocal cord mobility (). Although surgical margins were free of disease, the lesion was found to invade the thyroid cartilage on final pathology, prompting it to be restaged as rT4a (). The patient subsequently rapidly developed extensive disease involving the subglottis with extension into the overlying strap muscles and underwent a salvage total laryngectomy. The patient was free from disease 24 months after laryngectomy.


An 81-year-old woman whose platelet count was 184,000/μL 3 months before admission was referred to our hospital because of thrombocytopenia. Her platelet count reduction was found unexpectedly during a medical examination; she had no symptoms caused by thrombocytopenia. She had received an influenza vaccination 4 weeks before developing thrombocytopenia. Her laboratory data at the time of thrombocytopenia diagnosis were as follows: platelet count, 39,000/μL; white blood cell count, 4,900/μL without atypical cells; hemoglobin concentration, 14.1 g/dL; and platelet-associated IgG (PAIgG), 97 ng/107 cells. Bone marrow was normocellular; the megakaryocyte count was 56/μL. A urea breath test for HP was positive. The patient was diagnosed with ITP. HP was eradicated with 400 mg of clarithromycin, 1,500 mg of amoxicillin hydrate, and 20 mg of rabeprazole per day for 7 days. The patient's platelet count gradually increased and within 5 months had normalized. The patient's platelet count has remained within the reference range for over 2 years.


A 75-year-old woman received an influenza vaccination; her platelet count measured the same day was 251,000/μL. Five weeks after the vaccination, she was referred to our hospital because of thrombocytopenia with purpura combined with gingival and nasal hemorrhaging. Her laboratory data at admission were as follows: platelet count, 5,000/μL; white blood cell count, 10,600/μL without atypical cells; hemoglobin concentration, 15.9 g/dL; and PAIgG, 3780 ng/107 cells. Bone marrow was normocellular. A urea breath test for HP was positive and a diagnosis of ITP was established. She experienced massive bleeding because of marked thrombocytopenia; hence, we started HP eradication as well as steroid treatment (1 mg/kg of prednisolone per day). Four weeks after the initiation of treatment, her platelet count had increased to within the normal range, so the steroid treatment was gradually tapered off over 2 months. No evidence of relapsed thrombocytopenia has been seen for over 15 months.


An 87-year-old woman who showed no signs of platelet reduction such as purpura received an influenza vaccination. Two weeks after the vaccination, she was referred to us because of genital bleeding and purpura. Her laboratory data on admission were as follows: platelet count, 2,000/μL; white blood cell count, 9,200/μL without atypical cells; hemoglobin concentration, 9.3 g/dL; and PAIgG, 950 ng/107 cells. The bone marrow megakaryocyte count was 111/μL. We diagnosed the patient with ITP and began treatment with 1 mg/kg of prednisolone per day. The steroid treatment resulted in a rapid increase in the patient's platelet count, so it was tapered off over several months. The patient exhibited no evidence of relapsed thrombocytopenia after treatment.


A 12-year-old boy presented with progressive exertional dyspnea NYHA class III of 7 months duration. Blood pressure was 100/76 mm Hg in right arm in supine position. Pulse rate was 70/min, regular, low volume, with no special character with all peripheral pulses palpable. Jugular venous pulse pressure was elevated 6 cm above sternal angle with prominent a wave and v-y descent. Apex beat was located in right fifth intercostals space, tapping in character. There was grade II right parasternal heave. P2 was palpable. S1 was loud. S2 was loud; loud P2 component with narrow split. Opening snap (OS) was present with narrow A2-OS gap. There was long grade IV mid diastolic rumbling murmur with presystolic accentuation. Pansystolic murmur grade III/VI of tricuspid regurgitation was present in left parasternal area. The electrocardiograph (ECG) showed inverted P wave in all leads except aVR and V1, upright R wave in aVR, reduction in the R wave voltage across the chest leads with evidence of right ventricular hypertrophy (). Chest X-ray PA view showed dextrocardia (). Subcotal window showed aorta on the right and inferior vena cava on the left side, i.e. situs inversus (). Transthoracic echocardiography showed critical mitral stenosis with mitral valve area (MVA) of 0.6 cm2 by pressure half time () and planimetry () and mild mitral regurgitation. His Wilkin’s score was 8/16 (C2, T2, M2, S2). Mean gradient across mitral valve was 36 mm Hg. Transesophageal echo ruled out any LA or LAA clot. Dextrocardia, atrio-ventricular (AV) and ventriculo-arterial (VA) concordance were present. Left femoral artery and venous access was obtained with a 5F arterial and 8F venous sheaths, respectively after proper consent. A 5F pigtail catheter was passed retrograde into the aorta and parked in the non-coronary sinus of the aortic root. A 0.035" J-tip guide wire was then passed up the femoral vein into the inferior vena cava (IVC) and up into the left-sided superior vena cava (SVC) via the left-sided “right atrium” (). An 8F Mullins sheath was passed up on the guide wire, into the left SVC (). A curved Brockenbrough septal puncture needle was introduced into the sheath stopping just short of the tip and was oriented to 9 o’clock position in the SVC. Septal descent was done by withdrawing the needle and the sheath in tandem into the heart with the needle pointer in 9 o’clock position. Septal puncture was done in right anterior oblique (RAO) 40° and also confirmed in left lateral projection which was contrary to our conventional view, i.e., left anterior oblique (LAO) 40° projection (). LA was entered and pressure was recorded. The septum was dilated and heparin 100 IU/kg IV was given. A “loopy” LA wire was then passed through the sheath into LA and the latter was withdrawn leaving the LA wire inside (). The 14F dilator was then used to dilate the septum (). Subsequently, the accura balloon (Vascular Concepts, Essex, UK) was introduced over the LA wire to enter the LA (). The LA wire was withdrawn and the balloon was flushed and simultaneous LA/LV pressures were recorded. Now, director was used to guide the balloon () towards mitral valve by slight counter clock rotation till flip at the balloon tip was noted (). Director was pulled and balloon was pushed in a symphony to facilitate its entry into the LV (). Mitral valve was negotiated and dilation was performed successfully in LAO 40° projection which was contrary to our conventional view, i.e., RAO 40° projection (). Post-procedural MVA was 2.0 cm2 and MR still remained mild (). Patient was discharged in stable condition on third day.


A 48-year-old male was brought to the emergency department in cardiac arrest after collapsing at a grocery store. Bystanders called emergency medical services (EMS). The patient was found to have pulseless electrical activity (PEA), and EMS initiated cardiopulmonary resuscitation. During the resuscitation, the patient was bag-ventilated and intubated. Following administration of three doses of intravenous epinephrine (1 mg in 10 mL), the cardiac rhythm converted to ventricular tachycardia, and, after two shocks of 360 J, the patient reverted to sinus rhythm with good cardiac output. The total duration of cardiopulmonary resuscitation was 15 minutes.
The patient's past medical history was significant only for controlled hypertension. There was no history of smoking, illegal drug use, or other behaviors that might increase his risk of cardiac disorders. He had no family history of sudden cardiac arrest and no reported allergies. His medications included daily losartan (100 mg) and hydrochlorothiazide (25 mg).
Physical exam on arrival to the emergency department revealed a middle-aged, intubated patient with a temperature of 98.6 F, pulse rate of 98 beats per minute, respiratory rate of 18 breaths per minute, and blood pressure of 98/65 mm Hg. His oxygen saturation was 100% while on a ventilator receiving 40% FiO2. He had no conjunctival pallor. Auscultation of the lungs demonstrated bilateral air entry with no adventitious sounds. Precordial exam revealed normal heart sounds with no murmur, rub, or gallop. Abdominal exam revealed no hepatosplenomegaly. Glasgow Coma Scale (GCS) score was three on initial assessment. Electrocardiogram showed normal sinus rhythm with T wave inversions in I, AVL, and V3–V6. Portable chest radiograph revealed an appropriately placed endotracheal tube (ETT) (). Computed Tomography (CT) of the brain did not reveal any significant pathology. No arrhythmias were identified during cardiac monitoring. Cardiac enzymes and an initial echocardiogram did not show any ischemia.
The patient was deemed a candidate for postresuscitation hypothermia and was managed according to the current hypothermia guidelines. Cardiac catheterization was performed and demonstrated patent coronary vessels. Further history was then provided by family members, who reported that the patient was choking on food prior to his collapse. In the absence of another clear etiology for cardiac arrest and with no significant arrhythmias or ischemia identified, foreign body aspiration was considered as the most plausible explanation for the patient's arrest. The patient underwent bronchoscopy, revealing a piece of meat and bone lodged in the left main stem bronchus (Figures and ). During the retrieval process, pieces of foreign body were dislodged in the right mainstem (). Biopsy forceps were used to remove the foreign body (). Follow-up flexible bronchoscopy performed 48 hours later revealed complete removal of the foreign body and diffuse tracheobronchial mucosal edema. The patient went on to have an excellent clinical recovery and was discharged after 15 days in the hospital, with no cardiac, respiratory, or neurological sequelae.


A 48-year-old man was admitted to our hospital because of fever, dyspnea, and chest pain. The patient had a history of hepatitis C virus infection, opioid-use disorder treated with buprenorphine, chronic venous insufficiency, and severe chronic respiratory failure due to chronic obstructive pulmonary disease treated with long-term oxygen therapy and non invasive ventilation at home. He was not admitted to the hospital and did not use any healthcare facilities in the last 12 month period. He reported recent use of cotton balls soaked in buprenorphine for injection in his venous ulcers.
On examination, the patient was noted to be short of breath with a respiratory rate of 24/min, and an oxygen saturation of 70 % on room air. The temperature was 39 °C, and the blood pressure 90/50 mmHg. There were scattered focal crackles in the right lung. The heart sounds were normal. Skin examination found chronic venous ulcers on both legs, no marks consistent with intravenous injection, no abscesses. Oral and dental health examination was normal. The remainder of the examination was normal. Arterial blood gas analysis revealed a PaO2 of 154 mmHg, a PaCO2 of 90 mmHg, a pH of 7.18 on 12 L/min of oxygen. The patient was admitted to the intensive care unit and placed under non-invasive ventilation. Blood cultures were taken before intravenous cefotaxime and gentamicine were started. Laboratory results disclosed the following: hemoglobin, 12.0 g/dL; white blood cells, 5710/mm3; platelets, 94,000/mm3; creatinine, 13 mg/L; blood urea nitrogen, 0.49 g/L; C-reactive protein, 89 mg/L; aspartate aminotransferase, 37 units/L; alanine aminotransferase, 16 units/L; total bilirubin, 5 mg/L. HIV serologic test and hepatitis C virus RNA quantitative PCR were negative. Chest X-ray showed distension with no infiltrate. Computed tomography of the chest revealed consolidation of the left upper lobe. The patient’s condition improved rapidly allowing his transfer to the department of infectious diseases. Two sets of blood cultures taken at admission grew yeasts on hospital day 2. Caspofungin 70 mg once a day was started. Identification to the species level was performed by Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF mass spectrometry) (Vitek MS, BioMerieux®, Marcy l’Etoile, France). A portion of one colony isolated from a Sabouraud agar plate (BioMérieux®, Marcy l’Etoile, France) was applied directly onto the Vitek MS disposable target (single deposit) and was lysed with 0.5 μl of 25 % formic acid. After drying completely at room temperature (1–2 min), 1 μL of ready-to-use α-cyano-4-hydroxycinnamic acid (CHCA) matrix (BioMérieux®, Marcy l’Etoile, France) was applied to the spot, which was allowed to dry completely again (1 min). Final identification result led to the diagnosis of C. pulcherrima blood-stream infection. Antifungal drug susceptibility testing was performed by E-test (BioMérieux®, Marcy l’Etoile, France). In vitro minimal inhibitory concentrations for fluconazole, voriconazole, caspofungin, and amphotericin B were: 0.25, 0.004, 0.25, and 0.047 mg/L respectively. Culturing of the patient’s injection drug apparatus could not be obtained.
Trans-oesophageal echocardiogram revealed no valvular abnormalities or vegetations. Optic fundus examination was normal. Abdominal computed tomography revealed no deep abcess. Yeasts were eradicated at the 2nd day of the antifungal therapy. Treatment was modified for fluconazole 400 mg once a day, according to the pathogen’s susceptibility pattern. The patient completed 2 weeks of antifungal therapy and recovered without complications.


In September 2010, an 81-year-old male with hemafecia visited a public hospital in Beijing of China, and the progressive symptoms of fever, couch, and pulmonary infection were observed after hospitalization. The patient had the underlying diseases hypertension, diabetes, multiple cerebral infarction, and chronic renal insufficiency. The patient received long-term hospital care under the hospital and was bed-ridden with indwelling catheter. His symptoms of hemafecia were generally well controlled during hospitalization, but he started to suffer from the recurrent urinary tract infections since August 2013. About 2 weeks later, bacterial colonies were observed after cultivation of the urine specimens on the Mueller-Hinton agar, and the bacterial isolate designated 10265 was identified as P. aeruginosa. Based on the antimicrobial susceptibility test results, the patient received the intravenous administration with amikacin, and his symptoms associated with urinary tract infections progressively disappeared.


A 15 year old Caucasian girl of Dutch ancestry was admitted to the pediatric critical care unit for the management of her first episode of status epilepticus. She was the first child of non-consanguineous parents (). Pregnancy and delivery were uneventful and early development was reportedly normal.
Despite control of seizure activity, during the recovery phase, the patient continued to need ventilation support, and after extubation, remained confused with inconsistent responses, fluctuating awareness and an encephalopathic state. Investigative work up for infectious causes was normal and a urine toxicology screen was found to be negative at admission. Further, on reviewing the history, long standing symptoms of easy fatigability, generalized weakness were noted. Her weight was 35.7 kg (< 3rd centile) and height was 173 cm (75th centile). Neurological examination during recovery disclosed additional clinical findings that included; bilateral ptosis, significant limitation of extra ocular movements (external ophthalmoplegia) (this had been previously missed) (), eyelid myoclonia and distal polymyoclonus in the hands. During the recovery phase and subsequent follow up over the course of a year, recurrent stroke -like episodes, signs of gastroparesis, poor gut motility manifesting with constipation became evident.
The proposita's mother was 36 years old at diagnosis and has suffered from migraine headaches. There was also a history of migraine headaches in the maternal grandmother and a maternal great aunt. The proposita's siblings, an 18 year old brother has recently developed some fatigue and a 16 year old sister has presented with headaches but overall the siblings are relatively asymptomatic. The lactate levels are normal for all the three maternal relatives. The EKG and cardiac evaluation is normal in the mother. The mother is also on the mitochondrial cocktail including riboflavin 400 mg once a day, Carnitor 330 mg 1 tablet 3 times a day, alpha-lipoic acid 100 mg 3 capsules twice daily, CoQ 100 mg 2 capsules 3 times daily, l-arginine 100 mg/mL 60 mL 3 times a day.
Laboratory tests demonstrated a persistent elevation in blood lactate levels 4–7 (normal 0.5–2.2 mmol/L) in the proposita. EEG (Electroencephalogram) confirmed the presence of diffusely slow background rhythms with no epileptiform activity consistent with a moderately severe encephalopathy. Brain magnetic resonance imaging (MRI) showed multifocal ill-defined hyperintense lesions in the grey and white matter of the temporal lobes and orbito-frontal regions (). There was an inverted lactate peak on brain magnetic resonance spectroscopy (MRS) (). A muscle biopsy was performed in the proposita on the left thigh. Histopathology of the stained muscle biopsy of the left thigh showed numerous scattered ragged red fibers which were highlighted by the modified Gomori trichome stain. There were numerous ragged blue fibers positive for succinate dehydrogenase reaction. Many fibers were devoid of cytochrome c oxidase (COX). Electron microscopy revealed increased subsarcolemmal accumulation of mitochondria. These mitochondria showed marked variation in size and shape with abnormal cristae architecture. The results of respiratory chain enzyme assays on muscle homogenate were within reference ranges but demonstrated a relatively reduced activity of complex I + III (ratio to citrate synthase 0.041 (0.033–0.110)) in comparison with other complexes. A diagnosis of a mitochondrial cytopathy, likely MELAS was made.
DNA samples were prepared from the muscle biopsy and blood and urine specimens from the proposita. Sanger sequencing after PCR amplification of tRNAleu (UUR) demonstrated a heteroplasmic m.3291T > C mutation in the proposita. The percent heteroplasmy was calculated using densitometry software (GelDoc-Bio-Rad Image analyzer) after polyacrylamide gel electrophoresis of restriction enzyme (TSP509I New England Biolabs, Whitby, Ontario, Canada) fragments after PCR amplification. The level of heteroplasmy varied with tissue sampled: muscle biopsy contained 75% mutated mtDNA, urine 35%, blood 30%, and cultured primary skin fibroblasts 25%. Negative results were obtained with targeted mtDNA analysis for m.3243A > G, m.3260A > G, m.3303C > T, m.8344A > G, m.8993T > G/C and deletions.
The m.3291T > C mutation was also demonstrated in the blood of proposita's mother, brother and sister with 11%, 14% and 5% lymphocyte mutant mtDNA respectively. Urine DNA and other tissues were not tested for the proposita's mother, brother and sister.
The patient is currently in a stable clinical condition and is maintained on a mitochondrial cocktail and anticonvulsants including; Coenzyme Q 120 mg TID, vitamin C 500 mg BID, Thiamin 100 mg OD, Vitamin E 400 IU BID, Creatine 2.5 g BID, lamotrigine 175 mg BID, topiramate 25 mg AM and 50 mg HS and oral L-Arginine (0.15 g/kg) TID.
The patient is presently 22 years old and continues to demonstrate ptosis, external ophthalmoplegia, easy fatigability and occasional headaches. Further she has also been diagnosed with Wolff-Parkinson-White syndrome (WPW) on the basis of EKG findings, but remains asymptomatic from a cardiac point of view. She has not had any further hospitalizations since the introduction of arginine to her mitochondrial cocktail. Prior to this she was having at least 2–3 hospitalizations per year.
Initial neuropsychological assessment (15 years of age) was limited due to fatigue, poor attention, distractibility, poor comprehension of task demands, and significant anxiety. She demonstrated weak comprehension of vocabulary (7th percentile) and impaired comprehension of spoken instructions (< 1st percentile) and expressive language (1st–3rd percentiles). Verbal immediate and working memory, and estimates of verbal intellectual and performance (non-verbal) reasoning skills were within the extremely low range (≤ 1st percentile). Performance on a test of verbal learning was average (25th percentile). Although reported to have an academic average over 75% in Grade 9, tests of academic achievement were well below age expectations (< 1st–3rd percentiles). Subsequent assessments carried out at 16 and 17 years of age document improvements in her verbal intellectual skills (10th percentile), understanding of language (13th–30th percentiles), and verbal memory (25th–84th percentile). Impairments in perceptual reasoning (1st percentile), working memory (1st percentile), visual memory (5th–16th percentile), and processing speed (1st percentile) persist with significant difficulty noted in aspects of executive functioning such as cognitive flexibility in day-to-day activities and concept formation (9th percentile). Performance on tests of academic achievement improved but continued to range from just below average to low (3rd–13th percentiles). Currently, she requires guidance and supervision to complete activities of daily living. Due to ongoing fatigue, she completed high school at the pace of one or two subjects at home or in school. She has received counseling in her community for anxiety and helping her cope with the many medical issues and social implications of her diagnosis.


A 36-year-old female patient presented to dermatology clinic with a complaint of rash along the anterior parts of both lower legs for 2 weeks. An incisional skin biopsy was performed due to presence of widespread nonblanchable maculopapular eruptions on the anterior parts of tibias at the physical examination of the patient. Skin biopsy revealed leukocytoclastic vasculitis. The walls of the small blood vessels are infiltrated by mixed inflammatory cells (Figures and ). Treatment of vasculitis was started for the patient diagnosed with leukocytoclastic vasculitis. An increase was observed in the lesions of the patient during follow-up. It was learned that similar lesions were observed on the anterior parts of tibias previously for 2 times and she was diagnosed with vasculitis after biopsy performed. It was stated that the reason of vasculitis developing in the patient was determined to be brucellosis in both of attacks and cure was achieved after treatment for brucellosis. In her personal history, patient had complaints of muscle and joint paints, malaise, chill, shivering, and rash lasting about 2 months. When the risk factors for Brucella were examined, it was learned that the patient consumes fresh cheese.
In laboratory, the following were determined: white cell count: 8400/μL, erythrocyte sedimentation rate: 50 mm/h (0–15), C Reactive Protein: 26,3 mg/L (<5), RF: 14 IU/mL (<14). The Rose Bengal test was positive. Standard tube agglutination (STA) test for Brucella was positive at titers of 1/320 and Coombs anti-Brucella test was positive at titers of 1/640. Also ELISA test for Brucella was positive for IgM and IgG antibodies. The patient was given a combination therapy of rifampicin (1 × 600 mg/day, po) and doxycycline (2 × 100 mg/day, po). It was determined that lesions were regressed at first week visit during follow-up. Rifampicin discontinued due to rifampicin-induced hepatotoxicity and ciprofloxacin therapy was added. A complete cure was achieved in the clinic of the patients at the end of 6-week treatment.


A 58-year-old female was referred to our hospital from a local hospital. She had complaints of abdominal pain, jaundice for the last two months, and weight loss. On clinical examination, she had slight icteric sclera and tenderness in the right upper quadrant on palpation. Laboratory studies showed markedly elevated hepatic enzymes. Aspartate transaminase, alanine transaminase, and gamma-glutamyl transferase levels were 259, 412, and 1289 IU/L, respectively. Bilirubin levels were slightly elevated with a direct bilirubin level of 1.2 mg/dL and total bilirubin level of 2.61 mg/dL. Other blood tests were unremarkable. On subsequent ultrasound examination, cystic and choledochal ducts were dilated. There was a polypoid mass at the junction of cystic and choledochal duct. The patient underwent magnetic resonance cholangiopancreatography (MRCP) for better delineation of the ultrasonography findings. On MRCP, cystic duct was fusiformly dilated having a wide opening to the common bile duct which was also fusiformly dilated. There was a hypointense, heterogeneous mass filling the distal parts of both ducts. Intrahepatic bile ducts were minimally dilated in the central part but were in normal caliber in the remainder (). An endoscopic retrograde cholangiopancreatography (ERCP) procedure was performed for mass sampling. ERCP confirmed the findings of MRCP. After the procedure, the patient complained of severe abdominal pain and underwent computed tomography (CT) which showed free intra-abdominal air and periduodenal contrast leakage () consistent with perforation along with the other findings (). There was no sign of lymphadenopathy or distant metastasis on CT. The patient urgently underwent Whipple procedure. It was not until then that all the findings of fusiform dilatation of the cystic and choledochal ducts were interpreted as a cystic duct cyst which was proposed as a type VI biliary cyst. On histopathological examination, there was a polypoid mass which was characterized by atypical epithelial cells lining a fibrovascular core extending from the cyst wall that was lined by columnar epithelium (). The histopathological diagnosis of the polypoid mass was consistent with cholangiocarcinoma. To our knowledge, this is the second case of cholangiocarcinoma arising from a type VI biliary cyst.


A 21-year-old female, who has underwent renal transplantation 1 week ago, was referred to the department of nuclear medicine for renal transplant scintigraphy. She had end stage renal disease as a consequence of nephritic syndrome for the past 4 years, and was maintained on regular hemodialysis. Both her previous right and left brachial-cephalic arterio-venous fistulas had become dysfunctional, and she had been on a renal transplant waiting list since then. A catheter had been implanted in her right internal jugular vein (IJV), and she underwent hemodialysis via this route for 10 months. The catheter has been removed a few days after transplantation. Dynamic renal scintigraphy was obtained in an anterior view after bolus injection of 7 mCi 99mTechnetium-diethylenetriaminepentaacetic acid (99mTc-DTPA) through an 18-gauge venous cannula in the right antecubital vein intravenously. The images were obtained with a single-head gamma camera (Siemens ecam) fitted with a low energy high-resolution collimator. In the angiographic phase, sequential 1-second images revealed an unusual vascular filling pattern along with patent iliac arteries and transplanted kidney (). In order to gather further information on the abnormal finding, an additional angioscintigraphy of the chest in the anterior view was performed following bolus injection of 5 mCi 99mTc-DTPA through the same venous cannula 4 hours later (). Sequential 1-second images demonstrated rapid filling of the right basilic and cephalic veins followed by the axillary and subclavian veins (). Unexpectedly, two parallel channels appeared and the right heart, left heart and aorta became visible in turn. Regurgitation into the lateral thoracic and IJVs was also noted (). All findings were suggestive of SVC obstruction, which was attributed to the prolonged IJV catheterization, accompanied by blood flow through the azygos system (). The patient did not have any symptoms or signs, except some dilated collateral veins over the chest and abdominal wall that were retrospectively detected on physical examination. Due to the risk of contrast nephropathy and the patient’s being asymptomatic, the referring physician did not agree to perform computed tomography (CT) angiography to obtain detailed anatomical information.


A 36 year old previously healthy man with no family history of sudden cardiac death or LQTS suffered a witnessed cardiac arrest while exercising. At the time of his arrest his medications included amitriptyline, pseudoephedrine, and famotidine. His initial rhythm was ventricular fibrillation from which he was successfully resuscitated with an external countershock. Coronary angiography showed no evidence of coronary artery disease. Cardiac MRI showed an EF of 65% with no evidence of right ventricular dysplasia. ECGs in the post-arrest period were notable for prolonged QT intervals (repeated QTc measurements > 480 ms; the longest was 597 ms) (). ECGs obtained in the month after the arrest and in all follow up visits showed normal QT intervals (all QTc measurements <440 ms) after discontinuation of amitriptyline, pseudoephedrine, and famotidine ().
The patient was prescribed β-blocker therapy and underwent implantable cardioverter-defibrillator (ICD) implantation. He received one ICD shock for polymorphic ventricular tachycardia after re-initiation of vigorous exercise while he was only intermittently compliant with β-blocker therapy.


The patient was a 52-year-old female that presented with progressive cough and dyspnea for 8 weeks. Her medical history was unremarkable; she did not suffer from chronic disease. She had never smoked and had no known allergies or exposure to toxics. She had no family history suggestive of telomere syndromes or lung disease and she had two healthy daughters. She was admitted to a general hospital, where she was diagnosed with IPF based on high-resolution computed tomography scan and open lung biopsy findings. Simultaneously, laboratory analysis revealed that she had severe panhypogammaglobulinemia (IgM 0.32 g/L; IgA < 0.1 g/L; and IgG 2.2 g/L), and she was given the diagnosis common variable immunodeficiency (CVID). There were no clinical features suggestive of telomere disease or autoimmune disease. The patient had no history of recurrent infections. Bronchoalveolar lavage fluid showed no lymphocytosis or other abnormalities, and antinuclear antibody and anti-neutrophil cytoplasmic antibody tests were negative. She was started on oral corticosteroid treatment for her pulmonary fibrosis (as was common practice at the time) and gammaglobulin replacement therapy, both of which she would receive during her entire course of disease.
Her situation was relatively stable for 48 months, and she showed no signs of infections. When she became progressively dyspnoic, she was screened for lung transplantation. Because there were no contraindications for lung transplantation, she was placed on the waiting list 65 months after diagnosis. Unfortunately, a donor was not available in time and she passed away 71 months after diagnosis at the age of 58. As this all occurred a decade ago, we have retrospectively reviewed the case based on current guidelines [] in our multidisciplinary interstitial lung diseases team. Based on pathological and radiological findings, and in the absence of features suggestive of other diagnoses, our patient can be classified as a case of possible IPF (). There was multidisciplinary consensus on the clinical diagnosis of IPF, additionally supported by the progressive nature of the fibrosis in this patient and the failed response to corticosteroid treatment. We retrospectively measured the T/S ratio in DNA extracted from peripheral blood monocytes obtained 65 months after diagnosis and found a T/S ratio of 1.03, indicating normal telomere length in this cell compartment.


A seventy-seven-year-old female with history of hypertension, gastroesophageal reflux, hypercholesterolemia, and an episode of pericarditis at the age of thirty-five was admitted to the hospital in February 2014 for significant dyspnea, lower extremity edema, and a painful tongue lesion.
The patient described gradual deterioration of her general health over months: generalized fatigue, inability to perform daily activities, lower extremity edema, and transient red bullae on the lips that subsided on their own.
Her primary care physician referred her to a rheumatologist where she was diagnosed with nonspecific arthritis. Electromyogram revealed bilateral carpal tunnel syndrome and right sided injury to the ulnar nerve. Laboratory evaluation was significant for positive antinuclear antibodies (ANA) and anti-double stranded DNA antibodies (anti-ds-DNA). Based on a tentative diagnosis of systemic lupus erythematosus, the patient started hydroxychloroquine and prednisolone. During the monthly follow-up visit, the patient had anemia, and she was referred to a hematologist. At the same time, she became increasingly unable to eat because of a lesion on the left side of her tongue.
She was thus brought to the emergency room and the tongue lesion was evaluated by an otolaryngologist, who found her to be debilitated and in distress. The patient was admitted to the hospital by the medical oncology team since the tongue lesion was thought to be cancerous. On admission, the patient was an obese, ill-looking woman with shortness of breath on minimal exertion. Lung auscultation revealed bilateral wet rhonchi and she was tachycardic with bilateral pitting edema on lower extremities. Her tongue appeared beefy red. There was no cervical lymphadenopathy.
The patient was treated initially with oxygen, diuretics, inhalers, and a blood transfusion. Her general condition remained poor and unstable, with increasing need for respiratory support. The next morning she deteriorated to the point where she suffered a cardiac arrest while being transferred to the ENT suite for a tongue biopsy.
After resuscitation, she was transferred to the intensive care unit. Computed tomography of the chest and abdomen showed bilateral, well-defined, dense pulmonary infiltrates and diffuse opacification of the abdominal subcutaneous fat (). Echocardiogram showed global hypokinesis, most prominent in the anterior wall; B-type natriuretic peptide (BNP) was elevated while creatinine kinase MB (CKMB) and troponin enzymes were borderline. Coronary catheterization was negative for myocardial ischemia or coronary stenosis. Her disease course was complicated by takotsubo cardiomyopathy with a pathognomonic echocardiogram of hypokinetic left ventricle wall except for the base. The patient underwent biopsy of the tongue lesion while being intubated in the unit.
In the ICU, she required high doses of vasopressors and antiarrhythmic agents but soon developed adult respiratory distress syndrome (ARDS) and renal dysfunction. She eventually succumbed in the ICU from multiorgan system failure.
The biopsy of the tongue yielded amyloidosis (). In particular, the lesion exhibited homogenous eosinophilic amyloid-like material. Special staining with Congo red showed amyloid material as peach-red color under light microscopy with apple-green birefringence under polarized light.


This 56-year-old lady underwent augmentation mammaplasty in September 2013 with 285 cc moderate profile, round cohesive polyurethane coated silicone implants placed in the subglandular region via the inframammary approach. Intraoperative breast sizers were used during surgery.
In February 2014, she noted a progressive distortion of her left breast which was painful on palpation (). We assigned a Baker IV capsular contracture.
The left breast implant was removed and capsulectomy was carried out with reinsertion of 285 cc polyurethane coated implants in the subglandular pocket in August 2014. Note that residual distortion is still evident postoperatively ().


This 35-year-old patient underwent augmentation mammaplasty in March 2013 with 275 cc high profile, anatomic cohesive polyurethane coated silicone implants inserted in the subglandular plane via a periareolar approach with use of intraoperative breast sizers.
She returned on post-op day 20 with fullness and mild serous discharge at the suture line of the periareolar regions bilaterally. Ultrasonographic assisted drainage was carried out for seroma collection. There were no systemic or local signs of infection but drained material was sent for culture and sensitivity. No implicating organisms or bacteria were isolated on cultures. Patient was started on Ciprofloxacin 500 mg twice a day and Augmentin 875 mg twice a day for 14 days.
However, the patient continued to present with recurring seroma of minimal volume (about 3 to 5 ccs on each occasion) over the next 3 months. Although we recommended removal on basis of subclinical infection, patient strongly opposed the removal. In the 3rd month, a trial of Diprospan (Betamethasone 7 mg per ampoule) was injected intramuscularly once a week for 2 weeks in an attempt to resolve inflammation. As the clinical picture improved with no more seroma, the breast implants were not removed as per request of patient. Again no particular organism was isolated on repeated culture including Mycobacterium.
Patient is still on 6-month follow-up and recent ultrasound scan is normal.


This 23-year-old woman underwent primary breast augmentation in December 2013 (). She had 280 cc high profile anatomic, cohesive polyurethane coated silicone implants inserted via the inframammary approach with intraoperative use of implant sizers. Implants were placed in the subglandular plane ().
She returned in February 2014 (post-op day 52) complaining of redness and clear discharge from her right breast. On examination, she was hemodynamically stable and afebrile. A small fistula measuring 0.5 × 0.6 cm was noted medially with a 1 cm wound dehiscence at the lateral suture line. Antibiotic therapy with Ciprofloxacin 500 mg twice a day was initiated.
A swab was taken and 8 cc of seroma was drained via aseptic technique. The culture results returned a diagnosis of M. abscessus.
When reexamined at the clinic on post-op day 57, it was noted that more seroma had developed and the decision was made to remove the implants surgically with debridement and commence antibiotic therapy with Clarithromycin 500 mg twice a day for 4 months ().
Culture results obtained during implant removal and debridement reconfirmed the Mycobacterium infection. Patient subsequently had reinsertion of implant after concluding the 4 months of antibiotic therapy with satisfactory results ().


A 29-year-old healthy man presented to the emergency room with progressive history of urinary frequency, urgency, weak stream, and sense of incomplete emptying over the previous year. His postvoid residual was 300 mL. Urine analysis showed > 3 RBC/Hpf, which prompted a computed tomography (CT) with and without contrast and it showed a cystic lesion around the bulbar urethra (). Cystoscopy and retrograde urethrography showed a cyst and filling defect, respectively, bulging into the bulbar urethra without communication into the urethra (). A urethral catheter was placed for a few days, and he underwent percutaneous cyst aspiration by interventional radiology through the perineum. He experienced a temporary improvement but had worsening obstructive symptoms over the ensuing 8 months. Ultrasound and cystoscopy confirmed the recurrence of the imperforate Cowper's syringocele. Subsequently a transurethral unroofing of the syringocele using loop cautery was performed, creating a wide communication between the urethra and the syringocele (). A urethral catheter was maintained for 1 week and the patient completed a 7-day course of ciprofloxacin. He was asymptomatic at 1-year follow-up. There was no retrograde ejaculation, and his erectile dysfunction rates were unaffected. Repeat urethroscopy demonstrated persistence of the communication between the urethra and syringocele.


A 24-year-old male patient was admitted to our hospital due to a mass lesion with regular contours located in costodiaphragmatic sinus in the right inferior zone which was detected in posteroanterior chest X-ray during his routine control (). The patient had no complaints. Computed tomography of thorax revealed a mass lesion measuring 6 × 10 × 3 cm, neighboring to chest wall and diaphragm in inferior lobe of the right lung, consistent with hydatid cyst (). Laboratory data were normal. Right lateral thoracotomy was performed. On exploration, a firm, extraparenchymal cystic lesion measuring 10 × 6 cm, beginning from the inferior of the 6th rib, adhered to pleura was totally resected. The cyst had no association with parenchyma (Figures and ). The patient was discharged on postoperative day 7. Pathology result was reported as hydatid cyst. 15–20 mg/kg daily albendazole was administered to him for 2 postoperative months. No postoperative complications or recurrence occurred in the patient who is on postoperative month 18.


The 32-year-old male patient had received medical therapy due to hepatic hydatid cyst 2 years ago. The patient who had chest pain 2 years after the first diagnosis was detected to have a cystic lesion measuring 6 × 6 × 10 cm in apex of the right hemithorax and 4 × 4 × 10 cm in intercostal space basal on his control chest X-ray and computed tomography of thorax (Figures , , and ). The extraparenchymal firm cystic lesions were totally resected with right thoracotomy (). The patient was discharged on postoperative day 7. Pathology result was reported as hydatid cyst. 15–20 mg/kg daily albendazole was administered to the patient for 2 months postoperatively. He is on 3rd postoperative year and he did not develop any problems or recurrence.


A 56-year-old Caucasian male presented with a sensation of swelling in the throat, hoarseness, difficulty swallowing, and slight soreness in the right side of the throat. The symptoms were present when the patient awoke in the morning and progressed in a few hours, which caused him to seek medical assistance. At the local emergency department, a swollen tongue was found and the on-call otorhinolaryngologist was contacted. The patient had no known food allergies and no previous history of angioedema or urticarial eruptions. The patient did not present any signs of anaphylaxis (e.g., urticarial eruption, pruritus, hypotension, bronchospasm, or vomiting). It was unravelled that the patient 5 years ago was taking an ACE-inhibitor as an antihypertensive drug on a daily basis and thus bradykinin mediated angioedema was suspected. The patient was immediately transferred to the department of otorhinolaryngology. On admission, the symptoms were unchanged and the vital signs were normal. Lung and heart auscultation were normal. The clinical otorhinolaryngological assessment showed a moderate angioedema of the right side of the base of the tongue, the uvula, and the right palate-pharyngeal arch. Fibre-optic assessment of the pharynx showed a moderate swelling of the right side of the lingual tonsil and a severe mucosal swelling of the right side of the hypopharynx, the piriform sinus, the right aryepiglottic fold, and the right ventricular fold. The vocal folds were unaffected. Articulation was slightly impaired by the swelling. The voice was hoarse, but the respiration was unaffected. Besides a single small and sore lymph node on the right side of the neck, there were no palpable cervical lymph nodes. A bedside sonography of the neck revealed an inconspicuous lymph node with normal hilar flow in level Ib/II equivalent to the palpable lymph node. Blood samples (electrolytes, red and white blood cell count, and C-reactive protein) were normal except for a subnormal level of P-potassium 3.0 mmol/L (3.5–4.5 mmol/L). Since there were no signs of an anaphylactic reaction, tryptase was not measured. The patient did not present with symptoms and clinical findings compatible to upper airway infection (no fever, odynophagia, mucosal hyperaemia, or lymphadenitis). The patient had earlier suffered from a single deep vein thrombosis and was known to have type 2 diabetes, hypertension, hypercholesterolemia, and secondary polycythaemia due to smoking. He had no positive family history for angioedema and no prior swelling episodes. The medical history did not reveal any signs of allergic disease or malignancy. Complement analysis was not performed in the acute phase, as the biochemical analysis requires several days.
On admission, 40 milligrams of corticosteroid (Solu-Medrol®) had initially been administered intravenously. However, as the history revealed, ACEi-AE was suspected and an effect of corticosteroid could not be expected and was not awaited. Treatment with antihistamine was expected to be ineffective; thus, an antihistamine was not administrated. On suspicion of ACEi-AE, 2000 units of (18 units/kg) plasma-derived C1-inhibitor concentrate (Berinert) was administered intravenously over a course of 10 minutes. The patient rapidly reported to have decreased symptoms, but a fibre-optic reassessment was not performed until 5 hours after the infusion. A significant decrease in severity of the angioedema was observed. The patient was observed in the in-patient department for 24 hours and at discharge the angioedema had completely resolved, which was confirmed by fibre-optic reassessment. At the time of admission, the patient received an ACE-inhibitor, a calcium-antagonist, acetylsalicylic acid, a statin, and a non-beta-cell stimulating antidiabetic drug (Metformin®). The patient was thoroughly instructed never to take ACE-inhibitor again. The patient was enrolled in a large international multicenter DNA sequencing study (Prediction-ADR) in which further evaluation, including DNA testing for genetic mutations in the bradykinin pathway, is currently performed.


A 67-year-old man presented with low back pain, sciatica, and weakness of the lower limbs for 2 years. His back and leg pain exacerbated after standing or walking and relieved by lying supine with the knees and hips flexed. Overall, his pain was tolerable. He can walk well, though he felt his legs were weaker than usual. He sought treatment at a local hospital, and magnetic resonance (MR) imaging revealed a herniation disc at L3/4 level. Two months ago, however, his back pain worsened considerably and he started to have intermittent claudication. His symptoms failed to respond to conservative treatments, and his walking distance decreased to approximately 100 m. He was referred to us for further treatment. His bowel and bladder functions were normal since he was sick.
On physical examination, there was mild tenderness on L3-5 spinous processes. While straight leg raising test was negative, femoral stretch test was positive at both sides. Neurological examinations revealed decreased muscle power for the right quadriceps femoris and left tibialis anterior (Manual Muscle Test grade IV). His knee and ankle reflexes at the right leg disappeared, and sensation at the medial side of his left calf diminished. Pathological reflexes were negative at both legs. Lumbar spine MR imaging revealed an intradural lesion (14 × 8 mm2) at the left side of the dural sac and a herniated disc of moderate size at the right lateral recess of the L3/4 spinal canal (Figs. and ).
The patient underwent laminectomy and intrathecal tumor resection. Intraoperatively, the lesion was found to be encapsulated and stuck to a nerve root. After tumor removal, discectomy and posterior lumbar intervertebral fusion were performed. Histological studies revealed a herniated disc and a schwannoma. At the 6-month postoperative follow-up, the patient did not have back and leg pain. Neurological deficits at the extremities fully recovered, and he returned to normal life.
The current case highlights a rare situation that symptomatic disc herniation and spinal tumor present simultaneously in a spinal segment. To our knowledge, there are only four similar cases of lumbar disc herniation coexisting with intradural tumor reported in English literatures [–]. Albert et al. reported a case of L4/5 disc herniation presented together with a neurinoma at the L5 nerve root in a 52-year-old man []. The clinical manifestations revealed typical signs of L5 root compression from the herniated disc, and the tumor was an accidental finding on myelography. Liu et al. reported a 51-year-old man with L2/3 disc herniation coexisting with a schwannoma causing cauda equina syndrome []. The patient had suffered from low back pain for 3 years and was diagnosed with L2/3 lumbar disc herniation. To begin with, his back pain was relieved by conservative treatment but deteriorated progressively till cauda equina syndrome occurred. Bhatia et al. reported a paraganglioma coexisting with L5/S1 disc herniation in a 33-year-old man []. The clinical presentation was left sciatica associated with paresthesia in the left S1 dermatome. In 2014, Baek et al. described another case of intradural schwannoma coexisting with lumbar disc herniation at L4/5 disc level in a 71-year-old woman who suffered from lower back pain and L5 radiculopathy []. Intrathecal tumor resection and discectomy were performed using a posterior approach in these cases. In our case, right leg radiculopathy resulted from L4 nerve root compression due to L3/4 disc herniation. Some other symptoms, such as claudication and leg weakness, may be the results of both pathologies. We used a single operation to address both conditions, as did others [–].
Spinal schwannoma is a benign nerve sheath tumor, which comprises approximately 15 % of all spinal tumors []. The vast majority of schwannomas was located at the intradural space and occasionally presented as extradural or a dumbbell-shaped lesion []. Intradural schwannoma may produce symptoms similar to those of disc herniation, such as back pain and neurological deficits []. On MR images, schwannoma typically presents as an isolated and encapsulated mass, as hypointense or isointense on T1W images and hyperintense on T2W images []. Contrast MR imaging may reveal a well-delineated enhanced mass and, thus, is useful for differential schwannoma from disc degeneration []. In the present case, gadolinium contrast MR images revealed two heterogeneous signal masses at the same level, with one at the right extradural space and another at the left intradural space. As a result, the establishment of diagnosis was relatively easy.
In general, posterior epidural migration of a herniated lumbar disc fragment, a rare situation of disc herniation, should also be included in the differential diagnosis for extradural and intradural tumors [–]. Extradural disc fragment presents signals similar to those of a disc on both T1-weighted and T2-weighted MR sagittal images []. Moreover, disc fragment may demonstrate peripheral enhancement on contrast MR images [, ]. Even rarer, calcified disc sequestration may mimic an intradural spinal tumor and had MR findings similar to that of schwannoma []. Occasionally, a histological study is the only way to verify the diagnosis.
When clinical symptoms cannot be fully explained by an identified pathology, the coexistence of another spinal pathology should be considered. It is easy to establish the diagnoses when a spinal tumor and a herniated disc present in the same spinal region, as both pathologies are displayed on a MR study. It is noteworthy, however, that spinal tumor and lumbar disc herniation may present at different spinal regions and a single MR study may not be able to reveal both. Knafa reported a patient who presented rapidly progressive spinal cord compression following discectomy []. Her symptoms temporally restored but soon developed progressing paralysis in her right leg. Retrospective MR revealed an extramedullary tumor at T1/2 level. Another scholar reported a similar case of misdiagnosed thoracic tumor with neurological deficits deteriorated after decompression surgery for lumbar spinal stenosis []. Symptoms of upper neuron compression in patients who suffer from lumbar degenerative disorders, therefore, should be carefully examined to exclude possible concomitant pathology in the thoracic or cervical regions.


A Caucasian male infant was born to a 33 year old G7P5SA2 mother and her non-consanguineous partner at 37 weeks gestation. The pregnancy was complicated by morning sickness treated with Diclectin® (doxylamine succinate/pyridoxine hydrochloride). There were no other exposures to known teratogens. Intrauterine growth restriction was noted on ultrasound at 20 weeks gestation (head circumference, weight, femur length all < 5%ile). Oligohydramnios was noted at 34 weeks gestation, and the mother was placed on bed rest.
Labour was induced at 37 weeks gestation for asymmetric growth restriction. The infant was delivered by caesarean section for failure to progress. Birth weight was 1580 grams (<3rd %ile), length was 40 centimeters (<3rd %ile) and head circumference was 31 centimeters (3rd-10th %ile). Apgar scores were 9 and 9 at 1 and 5 minutes. Newborn examination revealed a small, non-dysmorphic baby with minimal body fat, a heart murmur and a right sided inguinal hernia.
Hyperglycemia was noted at 12 hours of age and an insulin infusion was started. An echocardiogram identified truncus arteriosus type III, hypoplastic pulmonary arteries, a ventricular septal defect and atrial septal defect (VSD and ASD respectively). He underwent cardiac repair on day 7 of life. Surgical repair involved the construction of a right ventricular – pulmonary artery conduit, patch closure of the VSD and suture closure of the ASD.
The pancreas was not identified on ultrasound. Abdominal magnetic resonance imaging (MRI) demonstrated minimal ectopic pancreatic tissue, absent gall bladder, liver steatosis and normal kidneys and spleen. Cerebral MRI was normal. C-peptide levels were undetectable, amylase and lipase were low and fecal fat was elevated suggesting pancreatic endocrine and exocrine deficiencies. Pancreatic exocrine replacement therapy was started week 3 of life (Creon® pancrelipase delayed release capsules 2500 u lipase/kg/d).
Family history revealed no history of cardiac or other congenital abnormalities. The mother is known to be a carrier of a balanced Robertsonian translocation (45, XX der(13;14)(q11;q10). She had had two early miscarriages, thought to be related to an unbalanced translocation. The maternal aunt and grandfather have type 2 diabetes.
Our patient was found to carry the same balanced Robertsonian translocation as his mother. Microarray testing was normal. Based on the combination of a congenital heart defect and pancreatic agenesis, GATA6 gene mutation testing was performed. A frameshift deletion in exon 2 (c744del) was found predicting a premature stop codon. Neither parent carries this mutation.
At four months of age the infant was transitioned from a continuous insulin infusion to subcutaneous injections. His course has been complicated by congenital hip dysplasia, developmental delay, and recurrent episodes of bronchiolitis. At 22 months of age, the child presented with facial edema, abdominal distension and poor feeding. Serum albumin was 20 g/L (normal range 35-47 g/L ). Subsequent investigations revealed a normal urinalysis and normal urine albumin. Testing for celiac disease was negative. Upper endoscopy with video capsule placement demonstrated diffuse erythema and superficial ulceration of the stomach and edema throughout the small bowel. Small bowel lymphangiectasia was also noted. Sigmoidoscopy to 20 cm did not demonstrate any abnormalities of the colon. These findings lead to the diagnosis of protein losing enteropathy. Treatment with enoxaparin and oral budesonide was initiated with good clinical response.
At 30 months of age he weighs 11.59 kilograms (15th %ile) and he has a height of 80 centimeters (<3rd %ile). His diabetes is managed on a basal-bolus regime with insulin glargine and lispro (diluted) for carbohydrate intake and correction. HbA1c is 7.4 % (normal 4-6 %). Average total daily dose is 0.15 - 0.2 units/kg/day. His low insulin requirements are thought to be due to endogenous production of insulin by ectopic pancreatic tissue identified on MRI. Fortunately, the child has not experienced any episodes of severe hypoglycemia.


A 71-year-old man with a history of chronic hepatitis C virus infection, DM, hypertension and benign prostate hypertrophy presented with a tender mass in the right subcostal area in June 2015. Results of needle biopsy were diagnostic of metastatic HCC. Laparoscopic right hepatectomy was performed in August, 2015 and histopathologic examination of resected specimens revealed HCC. Positron emission tomography–computed tomography (PET-CT) scan showed multiple bone metastases. A total radiation dose of 45 Gy was delivered in 15 fractions to the mass located near lumbar spine (L spine) 4 to 5 and a total dose of 39 Gy was delivered in 13 fractions to the right 7th rib. The radiation course began on September 9 and was completed on October 16, 2015. Sorafenib (200 mg) 400 mg twice daily was prescribed beginning on September 7, 2015. Approximately 1 week after beginning sorafenib, the patient began to complain of hiccups, epigastric distress, anorexia, heart burn, and fatigue. Empiric antiemetic agents, antacids, and pain killers were prescribed but the symptoms persisted. Panendoscopy revealed diffuse white lesions in the esophagus (Figure ). A diagnosis of candida esophagitis, grade IV, was made according to Kodsi classification. Periodic acid-Schiff (PAS) staining was indicative of candidiasis involving the squamous epithelium of the esophageal mucosa (Figure ). Fluconazole (150 mg) 300 mg per os (p.o.) quaque die (qd) in 1 week was prescribed. At 2-week follow-up, panendoscopy demonstrated regression of candida esophagitis (Figure ). Physical examination at the same follow-up visit revealed complete resolution of hiccups and epigastric distress as well as significant weight gain.


An 80-year-old man with goiter and benign prostatic hyperplasia underwent laparoscopic segmentectomy for segment 5 of liver in October 2014 and cholecystectomy on November 11, 2014. Alpha-fetoprotein (AFP) level decreased from 265.2 ng/ml before surgery to 3.52 ng/ml after surgery; however, at follow-up in April 2015 the AFP level was 1260 ng/ml. PET-CT scan in May 2015 revealed multiple bone metastases, including metastasis to the right scapula, the left 7th rib, the 10th thoracic (T) spine, and the 1st lumbar (L) spine but no local recurrence. Sorafenib (200 mg) 400 mg twice a day was prescribed in addition to local radiation therapy comprising a total dose of 30 Gy in 10 fractions delivered to T12 to L2 in May 2015. Grade II hand-foot syndrome was noted during the course of sorafenib and RT. In August 2015, the patient presented with persistent bone pain and an AFP level of 31,526 ng/ml. A total dose of 30 Gy in 10 fractions was delivered to T10-L1 and a total dose of 39 Gy in 13 fractions was delivered to lesions in the right scapula and left 7th rib concurrent with sorafenib (200 mg) 400 mg per day beginning in September 2015. Epigastric pain, hiccups, anorexia, and tarry stool were noted during the periods of treatment. Empiric agents were administered but the patient still complained of retrosternal pain on swallowing and persistent hiccups. Panendoscopy revealed plaques in the upper and mid esophagus indicative of candida esophagitis as well as esophageal and gastric ulcers. An 1-week regimen of fluconazole (150 mg) 300 mg p.o. qd for candidiasis and Takepron, 30 mg p.o. qd for the esophageal and gastric ulcers was administered. Physical examination at 2-week follow-up revealed complete resolution of hiccups and epigastric distress as well as significant weight gain.
The need for informed consent was waived by the Institutional Review Board of the Far Eastern Memorial Hospital (FEMH-IRB-104172-C) and retrospective data were collected after receiving approval from the Institutional Review Board of the Far Eastern Memorial Hospital (FEMH-IRB-104172-C).


A 27-year-old female patient with good general health presented to endodontic department of Dental School, Shahid Sadooghi University of Medical Sciences, Yazd, Iran, with a chief complaint of pus discharge from buccal mucosa adjacent to maxillary left lateral incisor for the past 6 months (). The periodontal pocket was traced with #35 a gutta-percha point and revealed the extension of lesion to the apical third of the root ().
The patient did not mention any previous trauma to the maxillary anterior region and had no history of pain in the area. Tooth #10 had an intact crown without caries or fracture. The response to refrigerant spray and Electric pulp tester (Analytic Technology, Redmond, WA, USA) was negative while adjacent and opposite teeth responded normally. The mobility of the tooth and its response to percussion and palpation tests were within the normal limits. Periodontal examination revealed a 12-mm pocket in mid palatal region (). Purulent exudate was excreted from palatal sulcus which was associated with a palatal groove on cingulum of the tooth, extending to gingival sulcus. Probing depth of the buccal gingival sulcus was within normal limits. Maxillary right lateral incisor was also examined for similar condition, a shallow groove was evident but probing depth of buccal and lingual sulcus was within normal limits. Radiography showed a periradicular radiolucency involving the apical one-third of the root and a para pulpal radiolucent line that is a typical radiographic representation of the palatal groove ().
Based on history, clinical and radiographic examination, the lesion was provisionally diagnosed as primary periodontal lesion with secondary endodontic involvement according to Simon’s classification [] in a maxillary lateral incisor because of a radicular groove. The patient was informed about the questionable long-term prognosis of the tooth #10 related to the length and depth of the radicular groove. Treatment options were offered to the patient including collaborative management using a combination of endodontic therapy, sealing the groove and periodontal regenerative procedure. Patient opted for this procedure and informed consent was gained.
Endodontic treatment was started under rubber dam isolation. Cleaning and shaping of the canal was carried out using the crown-down technique up to #40 master apical ﬁle using hand K-files (Mani, Tochigi, Japan). Root canal was irrigated with 1% sodium hypochlorite. The tooth was obturated with gutta-percha (Gapadent Co Ltd, Tianjin, China) and AH-26 sealer (Dentsply, De Trey, Konstanz, Germany) using lateral condensation technique (). One week later the crown was restored permanently with composite resin (Z250, 3M ESPE, St Paul, MN, USA).
At one-week endodontic follow-up evaluation, the buccal sinus tract and pus drainage from palatal sulcus was eliminated and the sulcus adjacent to the palatal groove could be still probed with gutta-percha cone to a depth of 12 mm. Three-month recall showed no abnormal symptoms while palatal probing depth did not change.
Upon further consultation with the periodontist, an exploratory surgery was planned. After flap reflection, a narrow palatal bony defect was noted along the root adjacent to radicular groove. Transillumination revealed no apparent cracks or fractures. The diseased granulation tissue filling the bony defect was curetted to leave the soft tissue more conducive to regeneration and the root surfaces exposed to the defect were planned with an ultrasonic scaler (Odontoson, Odonto-Wave, Fort Collins, CO, USA) and hand curettes. Also 3 mm of the root apex was resected in order to eliminate probable extra radicular microbial biofilm. Odontoplasty was performed on the lingual aspect of the root, but the groove was too deep to be totally eliminated. Chemical conditioning of the groove was performed by 10% poly acrylic acid and glass ionomer cement (Fuji I, GC Corporation, Tokyo, Japan) was applied into the groove (). The area was kept isolated of blood and tissue ﬂuids during the setting of glass ionomer. Then, GTR was carried out by means of 0.5 mL of decalcified freeze dried bone (DFDB) allograft with particle size of 1000×75 µm (Cenobone, Tissue Regeneration Corporation, Kish Island, Iran) and a 10×10 mm thin bioabsorbable collagenous membrane (CenoDerm, Tissue Regeneration Corporation, Kish Island, Iran) (). The ﬂap was approximated and continuous sling suturing was done.
with nonresorbable 3-0 silk suture material (). Patient was instructed on post-surgery precautions and maintenance protocol which included rinsing with 0.12% solution of chlorhexidine twice a day.
The healing of the periodontium was uneventful. Sutures were removed 14 days after the surgery. No attempt for probing or deep scaling was made before the 6-months follow-up. A radiography taken 6 months after the surgery revealed partial disappearance of the radiolucency around the lateral incisor due to bone grafting and simultaneous bone regeneration (). Also palatal probing depth did not exceed 3 mm (). Thus a 9-mm gain of clinical attachment was achieved in an area where the original pocket depth had been 12 mm.
Follow up after 2 years showed normal periodontal and endodontic condition. Palatal probing depth was 3 mm and periapical radiographies showed bone regeneration and healing of periapical bone defect (). Permission was gained from the patient.


A 48-year-old man suffered from ADO without prior family history of the disease and complained of deficiencies in speaking, swallowing, and mastication due to acquired maxillary and mandibular bone defects. He had been first diagnosed with a right femoral fracture in the 2000s. The patient had purulent drainage in the maxilla in 2003 and he informed no treatment performed in this clinical condition. He underwent surgical procedures, including the extraction of the left maxillary central and lateral incisor and right mandibular second molar tooth under local anesthesia in 2011 (Figures and ) and the sequestrectomy of right mandible under general anesthesia in 2013 (). The patient was referred to the Department of Prosthodontics, Faculty of Dentistry, Istanbul University, for dental rehabilitation in 2014 ().
At radiographic and oral examination, an unerupted third maxillary molar tooth and extensive bone defects in both jaws without any sign of sequestrum were diagnosed. Extraction of the right maxillary first molar, mandibular central incisors, and right mandibular lateral incisor was planned due to severe periodontal disease. Several treatment options were considered and the patient did not agree to any surgical treatment, so the decision was made to replace missing teeth and separation of nasal cavity from oral cavity with removable dentures in maxillary and mandibular jaw (Figures and ).
Antibiotics were provided for prophylaxis to prevent the infection of the bone due to extraction of the teeth. Tooth extractions and preparations were performed under local anesthesia, and the irreversible hydrocolloid impression material was used for making the preliminary impression and fabricating acrylic tray. Adhesive was applied to the tray and condensation silicone (Zetaplus System; Zhermack SpA, Badia Polesine, Italy) was loaded into the tray for master impression. Master casts were fabricated and maxillary master cast was mounted to the semiadjustable articulator (Artex CT; Amann Girrbach AG, Koblach, Austria) to locate the condylar (hinge) axis and mandibular master cast was than mounted to the articulator in centric relation. A maxillary obturator and a mandibular resection prosthesis with a fully balanced occlusion were fabricated. A permanent resilient liner was used to increase the comfort of the affected soft and hard tissues in the maxilla (). Determination of the occlusal plane and occlusal adjustment was important for obtaining aesthetic and comfortable results.
The patient was satisfied with the aesthetic results and function. The patient has been followed up for 1 year and an oral hygiene program on a 1-month recall schedule was applied (). At 1-year follow-up visit, the patient has reported better masticatory and speech efficiency, and also self-esteem improvement and family interaction.


A 70-year-old mentally challenged man was admitted to our hospital because of bradycardia and an altered state of consciousness. On the day of hospitalization, he suddenly suffered from disturbance consciousness after breakfast, and his heart rate was 40 beats/min. Electrocardiogram indicated sinus arrest and a junctional escape rhythm; hence, a pacemaker was implanted. There was no congenital heart disease on transthoracic echocardiogram on admission so we had not observed duplication of the LIV before the procedure. Left subclavian venography showed two vessels that were connected to the superior vena cava: a narrow, normally positioned LIV and a tortuous vein (Fig. ). The tortuous vein turned inferiorly and ran a course similar to that of the PLSVC. Before reaching the LA, the tortuous vein turned rightward and coursed horizontally into the SVC. There was only a short distance from where the RAIV entered the SVC. The normally positioned LIV was too narrow to pass through with a guide wire. Therefore, we chose the tortuous vein for pacemaker implantation. However, the procedure was difficult because of the vein’s tortuosity. Finally, leads at the right atrium and ventricle were successfully implanted using a steerable stylet (Locator™, St. Jude Medical, Inc., St. Paul, MN, USA). After the procedure, computed tomography showed two innominate veins: a RAIV and a narrow LIV that was a duplication of the LIV (Fig. ).


This 45-year-old female patient was hospitalized for a sizeable tumor of the right buttock (Fig. ) that impaired daily life and social activities. A diagnosis of neurofibroma was established by incisional biopsy.
Contrast-enhanced computed tomography (CT) revealed an enormous dumbbell-shaped mass (68.3 cm superoinferiorly), occupying the mid-abdomen, pelvic cavity, and buttock. The rectum, uterus, and urinary bladder were compressed and shifted to the left (Fig. ). On CT angiography, the tumor was supplied in part by the right internal iliac artery and by the right femoral and left internal iliac arteries.
The patient was placed in lithotomy position for the two-part tumor resection. First, a 20-cm midline incision was made from the umbilicus to pubic region, exposing a bulky encapsulated tumor of the abdomen and pelvis. The mass displayed solid and cystic areas, reaching a diameter of 30 cm. It was soft to the touch and grossly intact, completely displacing the peritoneal and pelvic contents. The bowel, uterus, and bladder were compressed and shifted laterally. The ureters and bladder were secured while freeing the encapsulated edge of the mass and severing its pelvic floor attachment, thus enabling en bloc abdominopelvic tumor removal. The protuberant skin-covered gluteal component, still communicating with the pelvic tumor, was incised along its base to maximize excision and skin procurement.
Having no clear boundary, the narrowest segment of the dumbbell-shaped mass also involved the vagina and anus, creating compressive displacement (to the left) and preventing complete excision without mutilation. The remainder of this segment was isolated along its border and removed. Ultimately, the excised mass measured 50 cm across and weighed ~25 kg (Fig. ). Postoperative pathology studies confirmed a diagnosis of neurofibroma (positive: vimentin, CD34; negative: S-100, smooth muscle actin [SMA], desmin, CD117, cytokeratin [CK], epithelial membrane antigen [EMA]) (Fig. ).
Postoperatively, the patient became febrile. B-scan ultrasonography indicated a seroperitoneum of moderate degree that was evacuated on postoperative day 6 via B-scan ultrasound-guided paracentesis. The fever thereafter abated. Three months postoperatively, a residual perianal tumor was presumptively identified in follow-up CT images. The gluteal and perineal regions were otherwise satisfactory, and the patient’s quality of life had measurably improved (Fig. ).
Infiltrative neurofibromas (with ill-defined borders) cannot be treated radically []. The neurofibromas can reoccur after surgical intervention []. However, surgical intervention is the most effective means for improving quality of life []. A giant tumor of this nature, involving the peritoneal and pelvic cavities, retroperitoneal space, and buttock, is truly a surgical challenge. Although resection is the accepted practice, a number of surgeons find this controversial and prefer clinical observation []. As a less aggressive measure, the gluteal mass alone could have been targeted, but our multidisciplinary team felt that near-total resection was needed to relieve abdominal organ compression. Because radical resection was prohibitive, our objective was visceral and genitoanal functional preservation. The resultant gluteal and perineal defects were too extensive for reparative local flaps; therefore, skin resected with the tumor was reserved for reconstruction purposes.


A 49-year-old male patient presented with pruritus, abdominal discomfort, jaundice,
choluria, hypocholic stools, and weight loss (of 13 kg in five months). Physical
examination revealed jaundice and no fever, as well as a soft abdomen that was
painful on palpation of the right side. The patient had a history of smoking and
alcoholism. Laboratory tests showed elevated liver enzymes and bilirubin levels
(with an obstructive pattern), serum amylase and lipase levels being within the
normal range.
After an ultrasound showing bile duct dilatation, an endoscopic retrograde
cholangiopancreatography revealed common bile duct stenosis. An endoscopic
papillotomy was performed, and a biliary stent was placed. Brush biopsy of the bile
duct was negative for neoplasia.
Abdominal CT and MRI scans showed diffuse pancreatic enlargement with loss of the
normal pancreatic lobulation and roughness, a hypoenhancing peripancreatic halo in
the tail of the pancreas, and hypoenhancing renal nodules with partially ill-defined
borders ( and ). Magnetic resonance cholangiography showed bile duct
dilatation ().
Given the suspicion of IgG4-related disease, renal and pancreatic biopsies were
performed. Examination of the biopsy samples showed dense, mixed lymphoplasmacytic
inflammatory infiltrate with no evidence of epithelial neoplasia, most of the plasma
cells in the infiltrate being IgG4-positive. Taken together, the imaging and
histopathological findings confirmed the diagnosis of IgG4-related disease; the
patient was started on corticosteroid therapy, which resulted in significant
clinical and radiological improvement after approximately 16 weeks (). At this writing, the patient is
receiving outpatient follow-up care and responding well to treatment.


An 8-year old male child presented after 10 days of sustaining electric burn over left forearm, chest, and abdominal wall. He sustained electrical burn accidently after touching electrical cable which was described as low voltage current. After sustaining electric burn, patient was brought to the private hospital. They managed patient with dressing and medications. There were no abdominal complaints at that time so he was discharged. After a week he developed abdominal pain with distension. On examination, there was necrosis of skin with eschar on the left lower abdomen with entry wound on left forearm and exit wound over left lower abdomen. He was dehydrated with pulse 100/mint. It was 2nd degree burn. Abdomen was distended and tender. On investigation hemoglobin was 11.7 gm%, TLC- 17000/mm3, serum electrolytes, liver function test, serum amylase and lipase were in normal limits. In urine analysis albumin was present. ECG was normal. Ultrasound abdomen showed thick inter-loop collection, dilatation of small bowel loops, and collapsed colon. X-ray abdomen revealed free gas under both domes of diaphragm. He was diagnosed as having bowel perforation leading to peritonitis. Immediate exploratory laparotomy was performed. There was around 50 cc of bilious fluid in peritoneal cavity with plenty of flakes over intestine. On further exploration, a perforation (0.5x0.5cm) found in the proximal ileum. Refreshing of the margins of perforation was done and primary closure performed (Fig. 1). Patient recovered uneventfully and was discharged on 7th postoperative day. Electric burn healed at the time of discharge. At follow up patient remained healthy.