The first patient, a 53 years old man, was diagnosed of high risk microgranular variant APL, presenting gingivorrhagia and fever. Anemia (Hb: 7.8 g/dL), more than 10×109/L leucocytes (11.8×109/L), and thrombocythopenia (platelets: 2.75×109/L) were present as well as coagulopathy (prothrombine time: 54%; fibrinogen: 114 mg/dL). The bone marrow aspirate showed infiltration by 93% of promyelocytes, and 80% of them were hypogranular. The diagnosis was confirmed by conventional cytogenetic, FISH and molecular studies, identifying the t(15,17) and PML/RAR (bcr3) isoform.
The patient was included in the LPA 2005 PETHEMA protocol and received idarrubicin, 12 mg/m2 on days 2, 4, 6 and 8 and ATRA, 45 mg/m2 since day 1. According to the protocol, the patient received dexamethasone at dose of 5 mg/12 hours during 15 days as DS prophylaxis because of leucocytes count at diagnosis was >5×109/L.
Twenty-four hours after stopping dexamethasone, when he had just recovered from neutropenia (neutrophils: 1.2×109/L), the patient developed fever without any clinical focus or microbiological documentation. Although wide spectrum antibiotics (piperazilin-tazobactam and teicoplanin) were administered, febrile syndrome was maintained. Six days later, on day 22, with neutrophil counts of 2.8×109/L, the patient developed hemodynamic instability with maintained hypotension, tachycardia, tachypnea and oliguria with fluid retention, respiratory insufficiency and evidence of hepatic failure. The chest radiography showed bilateral alveolar infiltrates and venocapillary hypertension signs. The patient was admitted to the Intensive Care Unit (ICU), requiring invasive mechanical ventilation and vasoactive drugs. At that moment, in absence of any microbiological documentation, late DS was suspected and ATRA was discontinued. Dexamethasone was administered and significant clinical and radiological improvement was observed 4 days after initiation. After complete recovery, ATRA was reintroduced without further complications. Eight months after achieving molecular complete remission (CR), the patient relapsed with central nervous system involvement, and promyelocytic infiltration was detected in the cerebrospinal fluid analysis. Rescue therapy, that included arsenic trioxide (ATO) plus intrathecal liposomal cytarabine, leaded to achievement of molecular remission and the patient received allogeneic stem cell transplantation. At the present time, he remains and disease free, 20 months after transplantation. The second patient was a 56 years old lady, diagnosed of low risk APL based on laboratory investigation due to hemorrhagic diathesis and fever. At diagnosis she presented anemia (Hb: 7.8 g/dL), leucopenia (0.4×109/L) and thrombocytopenia (platelets: 46×109/L). The bone marrow aspirate showed 38% of blasts, all of them abnormal promyelocytes, and the diagnosis was confirmed by cytogenetic and molecular analysis, detecting t(15,17) and PML/RAR (bcr1) isoform, respectively.
She was also included in the LPA 2005 PETHEMA protocol and received idarrubicin 12 mg/m2 days 2, 4, 6 and 8 and ATRA 45 mg/m2 since day 1. Since it was classified as of low risk, no DS prophylaxis was required.
Seventeen days after treatment initiation, the patient developed fever with no clinical focus and no microbiologic documentation. Wide spectrum antibiotics (piperacilin/tazobactam, teicoplanin and amikacin) were administered without improvement. At day +22, when granulocyte count started to recover (0.350×109/L), the patient evidenced crepitants on right pulmonary base, without dyspnoea or cough. Bilateral pulmonary infiltrates were observed in thorax X-ray and the computerized tomography reported the presence of bilateral pulmonary opacities, with areas of unpolished glass. This was radiologically suggestive of fungal infection and empiric treatment with B-amphotericin, cotrimoxazol and oseltamivir was given together with enlarged spectrum antibiotics.
Seven days later, on day +28, the patient developed respiratory failure with dyspnea, requiring large debit oxigenotherapy. Intensive care unit admission was required, requiring non-invasive mechanical ventilation. At that time, DS was suspected and ATRA was discontinued starting treatment with dexamethasone at dose of 10 mg twice per day. Forty-eight hours later, significant improvement was observed, with disappearance of fever and respiratory symptoms. ATRA was reintroduced during the consolidation without any further complications.


A 35-year-old Caucasian male diagnosed with FMF in childhood was admitted to the hospital in 2010 with widespread cutaneous eruptions on the lower limbs, which gradually intensified within the 5 days prior to the admission. The patient also had swelling and pain over his right wrist and left knee. He was on regular colchicine treatment with 1.5 mg/day for the last 17 years. No recent exposure to other drugs was recorded. There were no symptoms of infectious diseases such as fever, abdominal pain, and diarrhea prior to the cutaneous disease. The main complaints for the past 10 years were low back pain and morning stiffness.
On physical examination there were macular, brown cutaneous eruptions with confluence on both legs. In addition to right wrist and left knee arthritis, the patient had restricted painful spinal movements in all directions, suggestive of AS with modified Schober test of 3 cm.[] The rest of the physical examination was unremarkable.
On laboratory examination, level of hemoglobin was 9.3 g/dL (normal (N) −12-14 g/dL), consistent with anemia of chronic disease. Erythrocyte sedimentation rate (ESR) and C- reactive protein (CRP) were 59 mm/h (N −0-20 mm/h) and 7.27 mg/dL (N −0-0.8 mg/dL), respectively. Sacroiliac joints radiography was compatible with bilateral grade IV sacroiliitis []. A skin biopsy from the frontal aspect of tibia showed fibrin deposits, nuclear debris, endothelial swelling and neutrophils infiltrating capillary wall, suggestive of small-vessel vasculitis []. Immune fluorescence staining did not detect immune deposits. Serum IgA level was elevated at 617 mg/dL (N −82-453 mg/dL). HLA-B27 antigen was positive. Antinuclear antibodies (ANA), antineutrophil cytoplasmic antibody (ANCA), and cryoglobulins were undetectable. Levels of complement fractions and urine examination were within normal limits. Biochemical profile, hepatitis B and C serology, chest X-ray, and abdominal ultrasonography were also unremarkable. Mutational genetic analysis of the MEFV gene was consistent with compound heterozygote state (R202Q/R726A).
Treatment with oral prednizolone (15 mg/day), sulfasalazine (2 g/day), acemetacin (120 mg/day), and colchicine (1.5 mg/day) was commenced. After 10 days of the treatment the skin eruptions completely disappeared, arthritis and low back pain substantially subsided.
Subsequently, dose of prednizolone was tapered and then stopped. Other drugs were continued at lower doses.


A 45-year-old man presented to the clinic with a year's history of a painless growth on the right side of the palate. The lesion was initially the size of a peanut and had gradually enlarged to attain the present size of 3 cm. Patient had noticed ulceration over the surface of the growth 15 days prior to seeking our opinion. Personal history showed that he had been a smoker for 25 years and smoked 5–10 cigars/day. The medical, dental, and family histories were non-contributory to the complaint.
Extra-oral examination showed bilateral palpable submandibular lymph nodes. The lymph nodes were single, tender, firm in consistency, and mobile. The other facial structures appeared normal. Intra-oral examination revealed a well-defined ovoid ulcero-proliferative growth approximately 3.5 × 2.5 cm in size. Anteroposteriorly, the growth extended from the posterior-most rugae to the junction of hard and soft palate. Mediolaterally, it extended from the midline of the palate toward the palatal gingiva. Mucosa over the growth showed focal areas of ulceration, and the base of the ulcer contained yellowish white slough. Surrounding mucosa appeared normal and no secondary changes were seen. On palpation, the growth was non-tender, firm in consistency, and fixed to the underlying bone [].
Maxillary cross-sectional occlusal radiograph showed a faint radiolucency on the right half of the hard palate suggestive of bony erosion. Panoramic radiograph showed a well-defined radiolucent shadow exactly over the right maxillary sinus [].
Thin spiral CT sections of the neck were studied before and after intravenous IV contrast administration. All the images were studied for soft tissue, bone, as well as air window settings. The findings showed a faintly enhancing lesion, 26 × 11 mm in size, in the soft tissue of the hard palate to the right of the midline, associated with slight thinning of the underlying hard palate and a few small calcific densities within the mass [].
With the patient fasting for 6 h, 10 mci of (18) F-fluorodeoxyglucose (FDG) was injected intravenously and three-dimensional positron emission tomography (3D PET) scan was performed. Physiological concentration was observed in the heart, gut, brain, kidneys, and bladder. Increased concentration of FDG was seen in the following regions [standardized uptake values (SUV) as per body weight]: focal lesion on the right hard palate- SUV maximum (max) 16.5, right level II lymph node- SUVmax 4.8, and left posterior cervical lymph node- SUVmax 4.4. The PET impression was that of a focal erosion of the hard palate, associated with 1.9 × 1.2 × 1.6 cm nodular enhancing soft tissue, possibly of neoplastic etiology, and few mildly prominent right upper jugular and left posterior cervical lymph nodes raising suspicion of metastatic or reactive nature of the lesion [].
Considering the history, clinical and imaging findings, incisional biopsy of the lesion and fine needle aspiration cytology of the lymph nodes were performed []. Histopathology of the specimen showed presence of stratified squamous parakeratinized epithelium. The underlying connective tissue showed sheets of proliferating mucus cells and epidermoid cells, with areas of cystic degeneration. Intermediate cells were also seen occasionally. Concentric lamellated calcifications were evident suggestive of mucoepidermoid carcinoma (MEC) – intermediate grade []. Cytology of the aspirate collected from the lymph nodes showed hyperplastic follicles with round to plump chronic inflammatory cells. The findings were suggestive of reactive lymphadenopathy.
Based on PET/CT and histological analysis, a combination therapy of surgical excision, radiotherapy, and chemotherapy regimen, followed by prosthetic rehabilitation of the tumor site was planned. Partial maxillectomy (right side) was performed to excise the tumor mass along with a margin of 1 cm normal tissue around it. Later the surgical defect was rehabilitated with a palatal obturator. Two weeks post surgery, the patient was treated with 4 weeks of chemotherapy with cisplatin followed by 6600 cGy of radiation therapy for 6 weeks using image-guided radiotherapy (IGRT). The patient tolerated the treatment protocol well and showed good signs of healing. The patient reported for the first 6-month follow-up and was found to be tumor free [].


A 55-year-old male had difficulty in passing urine and was sexually impotent. On examination, there was absence of ankle reflexes and hypoaesthesia in the L5, S1 dermatomes on the left side and neurogenic claudication. He had retention of urine with a distended bladder. Lumbar MRI revealed a prolapsed disc herniation at the level L5-S1 []. An urgent, hemipartial laminectomy of left side L5 was performed and a massive disc prolapse, compressing the CE, was removed. The bladder control returned by the eight week after operation and although he was able to pass urine on his own, it took 4 months to recover normal bladder function. His sensation was gradually improved. However, sexual function and tendon reflexes had not returned to normal even 2 years after the operation.


A 54-year-old male was admitted for acute retention of urine. He had no history of backache. Two days before his admission, he had developed left-sided sciatica, followed by urinary retention and impotence. Clinical examination revealed saddle anesthesia, a distended bladder, and loss of anal tone. The straight legraising test was normal on both sides, there was no motor weakness inthe lower limbs and the Achilles reflexes were absent on the right side. Lumbar MRI revealed a L5-S1 disc herniation []. A right side hemipartial laminectomy of L5 was performed immediately and a large disc prolapse at the L5-S1 level was removed. On the two months after surgery, he was able to pass urine but it took six months for him to recover normal bladder function. One year after operation he was able to have a sustained erection.


A 29-year-old woman admitted with transient difficulty in passing urine, sexual dysfunction, and perianal hypoaesthesia. Clinically, both the Achilles reflexes were absent and there was perianal hypoaesthesia but no motor weakness. A lumbar MRI revealed a prolapse at the level of the left side L5-S1 disc space, and at operation, disc prolapse was removed []. The perianal hypoaesthesia diminished and bladder control was returned to normal after three months of operation. However, there was no recovery of her sexual dysfunction.


A 31-year old woman, she has had left side L5-S1 disc herniation; however, it was not prolapsed, only bulging was noted on the lumbar MRI []. Urinary retention and sexual dysfunction were main problems. After initial evaluation, emergent, standard left L5-S1 partial hemilaminotomy and microdiscectomy performed. The post-operative period of patient was uneventful. They discharged on the fourth post-operative day. At 6-month follow-up, although bladder was nearly normal, the reduced sensation in the sacral area, and her sexual dysfuntion were continuing.


An 81-year-old woman presented to the preoperative assessment clinic (PAC) prior to an elective robotic total hysterectomy for biopsy-proven adenocarcinoma of the endometrium, FIGO grade 2. She had a medical history of rheumatic heart disease, with a previous mitral valve replacement with a tissue valve, atrial fibrillation with chronic anticoagulation and pacemaker placement, and coronary artery disease. She denied any cardiac symptoms except for mild shortness of breath on exertion. The patient was taking metoprolol, valsartan, aspirin, simvastatin, and warfarin. Her blood pressure was 150/81 mmHg, heart rate was 78 beats/min, and oxygen saturation was 98% on room air. Her heart beat was irregularly irregular without murmurs. Her lung sounds were clear. There was no pitting edema. Per the Revised Cardiac Risk Index (RCRI) for preoperative risk, the patient had one risk factor (coronary artery disease) with an expected risk of having a major postsurgical adverse cardiac event of 0.9%–1.1%. Per the American College of Cardiology/American Heart Association (ACC/AHA) guidelines on perioperative cardiac evaluation, she underwent robotic total laparoscopic hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymph node dissection, with continuation of metoprolol for heart rate control. Perioperatively, she was also bridged with low molecular weight heparin and unfractionated heparin. Her postoperative course was uneventful, and she was discharged on postoperative day (POD) 1 to home with home health services. She returned to the gynecology clinic 1 month later for surgical follow-up and was found to be doing well without any overt complications.


A 72-year-old woman presented to the PAC prior to her scheduled robotic total hysterectomy for complex atypical hyperplasia of the endometrium. Her medical history included benign essential hypertension, schizophrenia, gastroesophageal reflux disease, and irritable bowel syndrome. She was taking hydrochlorothiazide, labetalol, olanzapine, lovastatin, trazodone, lansoprazole, amlodipine, potassium chloride, and vitamin E. She denied any cardiovascular (CV) symptoms. Her schizophrenia was well controlled on antipsychotic medications and, although she has received assistance from a social worker, she was independent on all her activities and instrumental activities of daily living (ADLs and IADLs). In the PAC, her blood pressure was 136/64 mmHg, heart rate was 74 beats/min, and oxygen saturation was 98% on room air. Her heart beat was regular without murmurs. Her lung sounds were clear. There was no pitting edema. Per the RCRI, the patient had no major CV risk factors and the expected risk of having a major adverse postoperative cardiac event was 0.4%–0.5%. Per the ACC/AHA guidelines on perioperative cardiac evaluation, it was advised that she proceed with the surgery without further work-up. She underwent a robotic total hysterectomy, bilateral salpingo–oophorectomy, ureteral stent placement, and pelvic washing. The pathology later was reported as stage I adenocarcinoma grade 2. Her immediate postoperative course was uncomplicated, and she was discharged, accompanied by her son, to her home on POD 2, without home health services. Unfortunately, on POD 32, she was admitted to the hospital after sustaining a fall in her apartment and was found to have an open tarsometatarsal fracture dislocation of her left foot. She underwent a closed reduction and debridement, and was discharged to a skilled nursing facility.


A 49-year-old and otherwise healthy man underwent a traffic accident and was transferred to emergency room in an unconscious state. Brain computed tomography (CT) revealed traumatic subdural and epidural hemorrhage at the bilateral frontal lobes and right temporal lobe. No abnormality in the extrapyramidal motor system including the basal ganglia was present (). The initial Glasgow Coma Scale (GCS) score was 5 (eye opening response [E]=1, verbal response [V]=0, motor response [M]=4). After receiving burr-hole trephination and hematoma drainage, the patient was reevaluated to have a GCS score of 11 (E1, V5, M5). Although verbal and motor responses improved after surgery, he was unable to open his eyes even with a strong painful stimulus. In spite of gradual recovery of mental status and motor function, voluntary eye opening was still not observed. After being transferred to the rehabilitation unit, the patient was examined for the neurological function with mental status being alert and the Mini-Mental State Examination score at 7. He exhibited left side weakness that was graded fair to good in a manual muscle test. The pupils were 3 mm in diameter, symmetrical, and equally reactive with extraocular movements fully intact. With the patient unable to open his eyes on command, an examiner elevated the patient's eyelid and found no abnormality in the ocular motor function. No evidence of other apraxia, such as buccofacial and limb apraxia, was present. He received comprehensive rehabilitation treatment, but AEO did not improve. We planned on treating the patient with levodopa/benserazide 200/50 mg twice a day with the informed consent of the patient. On the fifth day of the treatment, he started to open his eyes on command intermittently (). We confirmed no visual loss since he was able to recognize color and count fingers during spontaneous eye opening. With continued treatment, the interval between command and eye opening gradually shortened while the duration of spontaneous eye opening increased. This result was even more apparent when eating and undergoing physical training. We presumed that the dopaminergic treatment had a beneficial effect on AEO and tried to increase dose frequency from twice to three times daily to investigate a dose-dependent response. However, in the third day of the dosage modulation, aggressive behaviors emerged, and the treatment was withheld for three days. Even though the aggressiveness subsided shortly thereafter, the patient again exhibited difficulty in voluntary eye opening. After the resolution of the behavioral problem, the treatment was resumed twice a day. With AEO ameliorated, as evident in spontaneous eye opening during eating and physical training, the patient was discharged and has been closely followed up on an outpatient basis with the treatment of levodopa/benserazide 200/50 mg twice a day. He is currently capable of voluntary eye opening that is sustained much longer than before being discharged.


A 71-year-old male presented with aphasia and muscle weakness of the left side of his body. He was suspected of having a central nervous system disorder and underwent head brain CT that showed a 50 × 50 mm mass lesion in the right frontal lobe (fig. ). His chest X-ray showed a mass shadow with a cavity in the right-middle lung field (fig. ). The chest CT also showed a 70 × 68 mm mass with a cavity in the right lower lobe (fig. ). The level of tumor markers like carcinoembryonic antigen, cytokeratin 19 fragments and pro-gastrin-releasing peptide were not elevated. Based on these clinical findings, the patient was diagnosed with lung cancer with a single brain metastasis.
Craniotomy was performed because the patient's central nervous system's symptoms were severe and his Eastern Cooperative Oncology Group performance status was zero. The brain tumor in the right frontal lobe was completely removed, and the pathological diagnosis was confirmed as sarcomatoid pattern carcinoma. A CT-guided percutaneous lung biopsy proved that the pathological diagnosis of the right lung mass was spindle cell carcinoma. The patient was therefore diagnosed as having pleomorphic carcinoma of the lung with a single brain metastasis (clinical T3N0M1b stage IV).
After craniotomy, the patient underwent 6 courses of chemotherapy (carboplatin AUC 4 on day 1 and gemcitabine 800 mg/m2 on days 1 and 8, repeated every 3 weeks). After chemotherapy, the chest CT showed a reduced nodular shadow (62 × 50 mm) (fig. ), while 18F-fluorodeoxyglucose positron emission tomography showed no uptake in the lymph nodes (data not shown). The patient achieved a partial response by preoperative chemotherapy and underwent a right-lower lobectomy, partial resection of a right S2 segment, parietal pleurectomy, and mediastinal lymph node dissection through a posterolateral thoracotomy. This surgery was required because of the possibility of invasion into the right upper lobe and the parietal pleura.
Macroscopically, the tumor was 64 × 48 mm in size (fig. ). Microscopically large, spindle-shaped atypical cells had sarcomatously proliferated into most of the tumor portions (fig. ). The tumor had invaded the parietal pleura but not the S2 segment. There was no lymph node metastasis. The final diagnosis was pathological T3N0M1b PC of the lung stage IV. Immunohistochemically, the MIB-1 index of the specimen obtained by CT-guided percutaneous lung biopsy before preoperative chemotherapy was high at 60% (fig. ), whereas that of the resected tumor was low at 10% (fig. ).
The patient is alive after 7 years, with no signs of tumor recurrence.


A 19-year-old Caucasian female from Brazil was admitted with focal neurological deficit 3 days after symptom onset. The patient had been diagnosed in another center with anxiety. She presented asymmetry of brachial and radial pulses, aphasia, dysarthria and right hemiplegia. A CT scan showed extensive ischemia in the left cerebral hemisphere (fig. ). Cerebral angiography displayed occlusion of the right subclavian and left common carotid arteries, stenosis of the brachiocephalic trunk and flow inversion of the right vertebral artery and left posterior communicating artery, irrigating the territory of the left common carotid artery (fig. ). Abdominal ultrasonography showed celiac trunk stenosis (fig. ). Stroke was investigated extensively in this young patient. Only nonspecific inflammatory markers such as velocity of hemosedimentation and C-reactive protein were elevated. During hospitalization, clinical treatment was performed using pulse therapy with methylprednisolone 1 g/day for 3 days as well as methotrexate 15 mg/day, acetylsalicylic acid 200 mg/day and simvastatin 20 mg/day. After pulse therapy, prednisone 60 mg/day was initiated, showing progressive neurological recuperation on the subsequent days. After 4 months, the patient was submitted to medicated angioplasty of the brachiocephalic trunk with paclitaxel, with significant improvement of the stenosis. At the 6-month follow-up, the neurological exam presented mild dysarthria, faciobrachial predominant disproportionate hemiparesis, an NIHSS score of 4 and a modified Rankin Scale score of 3 (moderate incapacity).


A 68-year-old female presented to the general surgery outpatient clinic with a day history of right lower quadrant abdominal pain. Otherwise, the patient was well. The patient had undergone no surgical procedure in the past with no bowel habit change or gastrointestinal bleeding. Physical examination revealed tenderness of right lower quadrant abdomen with no palpable mass. Initial laboratory data showed slightly increased white blood cell count (10,300/mm3). Other laboratory data including C-reactive protein were within normal range. Plain radiography of the abdomen showed no remarkable finding. Abdominal US using an ultrasound unit (LOGIQ E9; GE Healthcare, Berlin, Germany) was performed to rule out the possibility of appendicitis; and it showed wall thickening of terminal ileum with diffusely increased echogenicity of surrounding fat suggesting inflammation. US also revealed several small hypoechoic projections with hyperechoic center, connected to the thickened terminal ileum, indicating inflamed diverticula (). Wall layering of thickened terminal ileum was relatively well preserved. Color Doppler image showed increased vascularity around small diverticula (). The entire appendix was well delineated to the tip with normal diameter (). Subsequent contrast-enhanced abdominal CT with a dual-energy unit (Discovery CT750 HD; GE Healthcare) showed several diverticula of the terminal ileum. The terminal ileum showed diffuse mural thickening and prominent contrast enhancement with preservation of the layering pattern and soft tissue stranding in the surrounding fat suggesting inflammation (, ). Intraperitoneal free air was not depicted. The entire appendix was well delineated without mural thickening or periappendiceal fat stranding. The patient received conservative treatment with antibiotics and was discharged after symptom relief during four hospital days.


A 38-year-old pregnant Hispanic woman, gravida 4, para 4, with a gestational age of 22 weeks was referred to a tertiary center with complaints of intermittent abdominal pain for the past 3 months, and worsening symptoms over the past 3 to 4 weeks. The nonradiating pain originated in the epigastric region, was of moderate to severe intensity, and worsened upon food ingestion, with no obvious relieving factor. The patient also had nausea with a few intermittent episodes of bilious vomiting; however, she denied any hematemesis, melena, or hematochezia. During routine prenatal care at another hospital, her symptoms were attributed to the underlying pregnancy. She was prescribed ranitidine, which failed to alleviate her symptoms. She denied any past medical problems and was not taking any medications prior to her pregnancy. Her prior pregnancies were full term, normal vaginal deliveries and were uneventful. She denied the use of alcohol, smoking, or illicit drugs.
On examination she was afebrile, with a heart rate of 87 bpm, blood pressure of 123/87 mmHg, and was saturating well on room air. The physical exam was remarkable, indicating a gravid uterus at around 28 weeks' of gestation. She had mild epigastric tenderness and was found to have a tender mass from midline to the left flank. The patient had no pedal edema, and (I think the physical exam should be in a separate sentence from the labs.) laboratory findings revealed normal electrolytes and creatinine; hemoglobin was 11.5 g/dl, and platelets were 277 K/µl. While carcinoembryonic antigen (CEA) and cancer antigen 19-9 (CA 19-9) levels were normal, the cancer antigen 125 (CA 125) was found to be elevated to 846 U/ml. An ultrasound revealed a normal intrauterine pregnancy (), and a left adnexal mass of heterogeneous echodensity of ~13.4 cm in the diameter at its largest side, which was distinct from the uterine mass, displaying characteristics of an ovarian neoplasm (). Magnetic resonance imaging (MRI) was recommended for further evaluation, and confirmed a large pelvic mass arising from the left adnexa, with ascites and demonstrated edema of the mesentery and omentum ().
Physicians from the Maternal Fetal Medicine (high-risk obstetrics) and gynecology oncology departments discussed the findings with the patient and decided to continue the pregnancy while proceeding with surgical staging. However, a few days after admission and prior to the scheduled date for surgery, she had worsening abdominal pain and was found to be in active labor. The patient subsequently delivered a viable infant via vaginal delivery. Gestational age at birth was 23 weeks, with the female infant weighing 510 g and having Apgar scores of 2, 6, 7. There were no fetal anomalies and the infant was admitted to the neonatal intensive care unit for further care. Postpartum, the patient underwent an exploratory laparotomy, which revealed straw colored ascites upon entry and a large mass originating from the left ovary. The neoplasm had ruptured intraoperatively, and only the solid tumor was visible. The left ovary was processed for frozen section investigation, which revealed the presence of a Krukenberg tumor (). Subsequently, an abdominal examination noted that the omentum harbored marked reactive tissue, which indicated metastases, and a tumor was palpated along the lesser curvature of the stomach, which suggested a primary gastric cancer. Palliative gastrectomy was not performed.
Based on the intraoperative exams, an esophagogastroduodenoscopy was performed, which revealed patchy areas of erythema on the non-peristaltic stomach wall, with superficial ulceration along the lesser curvature (). Multiple biopsies were obtained that showed the presence of a poorly differentiated adenocarcinoma. The patient was diagnosed as having stage IV gastric cancer and was scheduled for palliative chemotherapy. She underwent multiple hospital admissions after the advanced-cancer diagnosis for reasons including development of submassive pulmonary embolism, seizures secondary to acute ischemic stroke, and hospital-associated pneumonia. She received 2 cycles of FOLFOX before succumbing to cancer.


A 60-year-old male nondiabetic, nonsmoker, hypertensive, obese, presented with intermittent right-sided, severe, sharp, and lancinating facial pain for the past 4 years, with an identifiable trigger area located at upper right canine teeth. The patient had difficulties for chewing, eating, drinking, shaving, washing his face, altering his daily activities. The pain used to come in sudden bursts lasting 1-5 min and recurs more than 15 times a day. On physical examination, arterial hypertension and obesity were found. Neurologic examination showed facial trigger points in the right maxillary region and nasogenian fold without other neurological findings. Patient had longstanding pain resistant to medical management with agents such as carbamazepine (1200 mg/day), alone or in combination with gabapentin or pregabaline. The patient underwent multiple punctures and local infiltration with alcohol and steroids without improvement. He did not have previous surgical procedures. No sensory loss over a particular nerve division was reported by the patient at any time. Facial sensory exam with pin or light touch was normal before the radiosurgical procedure. Corneal blink reflex was normal.


A 20-year-old female presented with sudden onset of severe headache associated with nausea followed by disturbance of consciousness, and was admitted to another hospital. The diagnosis of cerebellar and subarachnoid hemorrhage from AVM supplied by the posterior inferior cerebellar artery (PICA) was based on the findings of computed tomography (CT) [] and cerebral angiography. Emergency evacuation of the hematoma was performed via a midline suboccipital approach. Four months after surgery, vertebral angiography demonstrated left cerebellar hemispheric AVM supplied by the PICA []. Fourteen months after the initial hemorrhage, gamma knife radiosurgery was performed to treat the AVM nidus with a volume of 0.487 cm3 at another institution using a Leksell Gamma Knife model B unit (Elekta AB). The procedure was planned using GammaPlan software based on stereotactic digital subtraction angiography and magnetic resonance (MR) imaging. A prescribed dose of 20 Gy was delivered to the lesion margin at the 50% isodose line. Three years after the first radiosurgery, vertebral angiography showed a small residual nidus in the left cerebellar hemisphere []. The patient underwent repeat radiosurgery at the previous institution using a Leksell Gamma Knife model C unit (Elekta AB) 4 years after initial radiosurgery. The target volume of the nidus was 1.5 cm3, a larger volume than that at the initial radiosurgery, and was intended to improve the treatment efficacy. The procedure was planned using GammaPlan software and a prescribed dose of 24 Gy was delivered to the lesion margin at the 60% isodose line. Vertebral angiography obtained at 5 years after the second radiosurgery revealed complete disappearance of the AVM []. However, T2-weighted MR imaging and postcontrast T1-weighted MR imaging obtained at 7 years after the second radiosurgery revealed an enhanced lesion adjacent to the cyst formation in the left cerebellar hemisphere [Figure , ]. The patient was lost to follow up during the 18 months after the last examination. The patient subsequently presented with headache and nausea, which had persisted over 3 weeks, at age 34 years in the 32nd week of pregnancy, and was referred to our institution 9 years after the second radiosurgery.
The patient had headache and nausea, but no other neurological deficits were identified except for House–Brackmann grade 3 facial palsy persisting since her childhood. Other medical history was unremarkable. On admission, CT demonstrated an irregularly shaped, heterogeneous high density hematoma with perifocal edema in the vermis extending to the left cerebellar hemisphere []. Her infant was delivered by cesarean section immediately after admission and osmotic therapy was started. Despite conservative management, disturbance of consciousness developed and deteriorated due to the extensive perifocal edema and hydrocephalus. Three-dimensional CT angiography revealed no vascular abnormality around the lesion.
Midline suboccipital craniotomy was performed and cerebrospinal fluid was released from the ventricular drainage. A very firm, reddish angiomatous nodular granuloma with adjacent cyst was visualized in the cerebellar hemisphere. Indocyanine green videoangiography confirmed the absence of abnormal vasculature around the lesion. The lesion contained angiomatous capsule and firm organized hematoma. Gross total resection was achieved without injury to the surrounding structures. No AVM nidus was observed during surgery. Her symptom was completely resolved immediately after surgery and the postoperative course was uneventful. Postoperative MR imaging revealed total resection of the hematoma with the adjacent cyst []. Postoperative angiography confirmed disappearance of the AVM. Her baby's growth and development was also normal.
Histological examination of the lesion obtained during surgery demonstrated encapsulated hematoma consisting of a dense collagenous outer layer and a granulated, newly vascularized, angiomatous inner layer with extensive multinodular hemorrhage at various stages of organization []. Hemosiderin deposits and coagulation necrosis were also observed []. The microvasculature in the inner layer demonstrated inflammatory infiltration in the vascular walls and thickening of the vessel walls with hyaline degeneration, which are characteristic findings of vasculitis []. Immunohistochemical examination demonstrated strong staining for CD34 in the microvasculature [].


A 5-year-old female child presented with two months history of tense fluid filled lesions. Two weeks prior to appearance of these lesions, she had dark coloured, scaly, itchy skin lesions over her trunk and extremities. Fluid filled lesions appeared on normal skin as well as over the pre-existing scaly lesions. She recently had an episode of chickenpox one month prior to the scaly skin lesions. Physical examination revealed multiple erythematous-to-violaceous papules and plaques varying in size from 0.3 mm to 5 cm distributed over the trunk and the extremities [Figures and ]. Multiple tense bullae are distributed predominantly over the upper and lower extremities, a few of them hemorrhagic. Hyperkeratotic plaques with fissures were present over the central aspects of both the palms and soles in addition to a few deep-seated vesicular lesions []. There was no oral involvement.
Skin biopsies were taken from two sites: one from an intact bulla and the second from an erythematous papule. Histopathology of the bullous lesion revealed orthokeratosis, hypergranulosis, acanthosis, and subepidermal bulla with no acantholytic cells []. Adjacent basal cells showed liquefactive degeneration with scattered mixed inflammatory infiltrate of lymphocytes and occasional plasma cells in the upper dermis []. Apoptotic keratinocytes or civatte bodies were scattered in the epidermis []. Biopsy from the papule revealed hyperkeratosis, hypergranulosis, acanthosis with pointed rete ridges, focal basal cell degeneration, melanin incontinence, perivascular and periappendageal inflammatory infiltrate of eosinophils, neutrophils and mononuclear cells. Direct immunoflourescence of biopsy drawn from peribullous skin revealed immunoglobulin G (IgG) and C3c deposition at BMZ and C3c deposition at appendages and vessel walls consistent with the diagnosis of LPP. Routine hemogram, urinalysis and chest X-ray are within normal limits.
The patient was treated with oral prednisolone 20 mg daily and showed significant clinical improvement within a span of 10 days. She is currently on maintenance dose of prednisolone and follow up.


In October 2010, a 16-year-old girl was referred to our maxillofacial radiology clinic for radiographic examination for orthodontic treatment. Accidentally, in the panoramic radiograph, a unilocular mixed lesion was detected in the left mandibular angle.
The posterior borders of the lesion were poorly-defined; whereas, the anterior borders were ill-defined. In the panoramic view, intra-lesion calcifications were evident (). In the panoramic radiography and lateral cephalography, a mild expansion was observed in the posterior and inferior borders of the mandibular angle (). The mandibular cortical borders appeared completely intact. Root resorption was not present on any of the teeth adjacent to the lesion. The approximate dimensions of the lesion were 3 × 5 cm. The patient had no noteworthy medical history.
She did not experience pain in the region, and the lesion was non-tender on palpation. On clinical examination, a slight swelling was observed in the left mandibular angle. No enlarged lymph nodes were detected on palpation.
On intra-oral examination, the overlying mucosa of the region was smooth and of normal color.
To localize the intraosseous lesion and perform further investigations on the effects of the lesion on the surrounding structures, we performed cone beam computed tomography.
On CBCT examination, a multilocular lesion with coarse septa, without sclerotic borders was observed.
The cortical borders of the mandible and follicular space of the unerupted left third molar were normal. No displacement and root resorption was found on the teeth adjacent to the lesion ().
Moreover, no displacement in the inferior alveolar nerve canal position was noted, but the cortical borders of the canal were thinned ().
Based on age, clinical behavior, and radiographic findings, the differential diagnoses of fibrous dysplasia and desmoplastic ameloblastoma were made. Incisional biopsy of the lesion was performed.
Histologic examination of the lesion revealed sheets and islands of large eosinophilic cells with abundant granular cytoplasm with small islands of odontogenic epithelium (). Foci of dystrophic and cementum-like calcifications were detectable in the lesion (). The fibrous stroma contained fibroblasts, and in the decalcified sections, bone trabecules were evident (). Histologic examination confirmed the diagnosis of central granular cell odontogenic tumor (CGCOT). Resection of the lesion was carried out to treat the patient. For mandibular reconstruction, allogen graft from the fibula was applied (). Histopathological examination of the excised specimen confirmed the diagnosis of CGCOT.
The patient is on follow-up periodic check and there has not been any radiographic evidence of recurrence on the follow-up radiograph after 2 years of operation ().


A 13-year-old, unmarried, female patient presented with complaints of oligomenorrhoea, masculinizing features of enlarged clitoris, facial hair, deep voice and rapidly growing abdominal lump in left side since one month. Magnetic resonance imaging revealed normal right ovary and a 10-cm neoplastic isointense to hypointense capsulated mass in the left ovary. Uterus and cervix were unremarkable. Hormonal study showed CA 125-37.5 IU/mL, AFP 8.6 ng/mL, HCG-4 IU/L and testosterone 1196 ng/mL. Unilateral salpingooophorectomy was done and specimen was sent for histological examination. Histologically, these cases usually show predominant luteinized/steroid cells with less than 5% area of sertoliform cells
Received ovarian mass measuring 10 cm in diameter with attached tube. Outer surface was nodular. Cut surface was solid with focal cystic and hemorrhagic areas ().
Sections examined from ovary showed a well-encapsulated mass with proliferation of plumped, ovoid to spindle cells arranged in bundles and fascicles forming nodules, with mild degree of anisonucleosis and hyperchromasia and infrequent mitosis and lacking nuclear grooving. A few interspersed large, polygonal cells with pale cytoplasm (luteinized/steroid cells), lacking reinke’s crystalloids were also seen. Tiny foci of cuboidal cells (less than 5%) arranged in cords, micro and macrotubules (sertoliform cells of intermediate differentiation) were seen at the periphery (). Reticulin fibers showed pericellular pattern in spindle cell area with grouping around sertoliform cells. Spindle cells were positive for vimentin, weakly for inhibin, but negative for calretenin, CD34 and cytokeratin. Strong positivity for calretenin was seen in sertoliform cells and in pale, luteinized, steroid cells. However, these sertoliform cells were inhibin, cytokeratin, vimentin and S-100 negative, though steroid cells were strongly inhibin positive (). On the basis of histology and immunohistochemistry, final diagnosis of ovarian fibrothecoma with minor sex cord stromal elements was made.
All masculinizing features were significantly reduced in post operative follow-up of four months. Ostradiol was 100.96 pg/mL and testosterone dropped to 5 ng/dL. She hasn’t reported back to our center again.


A 40-year-old woman was referred to the Department of Oral and Maxillofacial Surgery with the complaint of a painless swelling in the left cheek region with duration of 8 months [ and ]. The patient revealed that she had got her left upper molars extracted 2 months prior to her presentation to us. The swelling was initially small and had gradually increased to the present size. No neurological deficit was evident on subjective and objective examination. On extraoral examination, an ill-defined diffuse swelling of 6 × 5 cm size over the left cheek region was seen extending superiorly to the infraorbital region, and inferiorly 1 cm lateral to the angle of the mouth. The swelling extended medially till the ala of the nose and laterally to the preauricular region. It was firm to palpation and was not fixed to the underlying structures. There was no associated lymph node enlargement.
On intraoral examination, a diffuse swelling of 6 × 5 cm in size was noted on the left buccal mucosa, which extended superiorly until the maxillary tuberosity with obliteration of the buccal sulcus in relation to left maxillary molars. The lesion was firm in consistency with a smooth surface, and the overlying mucosa was normal. The lesion was evaluated with a panoramic radiograph and subsequently with a computed tomography (CT) scan. The panoramic radiograph showed destruction of the alveolar bone corresponding to the extracted molar region. The CT scan showed a hypodense lesion involving the infratemporal fossa [–]. It was interpreted as a benign mesenchymal tumor.
An incisional biopsy was performed and submitted for histopathological evaluation. The report revealed interlacing fascicles of spindle cells with dark staining wavy nuclei with less prominent amorphous eosinophilic zones representing verocay bodies and perivascular hyalinization. The cellular proliferations were intermixed with large foamy histiocytes along with areas of hemorrhage and cystic degeneration [–]. Although in certain fields there were nuclear hyperchromatism and mitosis, the overall histo-architecture was consistent with a diagnosis of ancient schwannoma.
In keeping the indolent nature and imaging findings, surgical excision of the lesion was planned through a transantral approach to the infratemporal fossa. A Weber-Fergusson incision was made, and the maxillary bone over the lesion was exposed till the pterygoid plates. The lesion was dissected from the buccal mucosa and traced to infratemporal fossa through transantral approach and was excised in toto. The immediate postoperative period was uneventful. The surgical specimen was submitted for histopathological evaluation, which confirmed the diagnosis of ancient schwannoma [–]. The patient is periodically monitored and is disease free at the last follow-up (2 years after surgery) [ and ].


The patient was a 48-year-old Chinese woman with a history of thalassemia minor but otherwise well. She first presented to the hospital for a routine health screening at which she had complained of a persistent cough for a few months and reported a reduction in exercise tolerance during this period. On the physical examination, she was found to have a pansystolic murmur radiating to the axilla. An electrocardiogram (ECG) revealed left ventricular hypertrophy with atrial enlargement. Chest x-ray confirmed an increased cardiothoracic ratio, left atrial enlargement, and blunting of the left costophrenic angle. In view of findings suggestive of heart failure, the patient was referred to a cardiologist for further management.
On further questioning, the patient reported that she had experienced a loss of appetite and loss of weight over the preceding 2 months and was having occasional left-sided abdominal discomfort. In addition to the systolic murmur, the cardiologist found an abdominal mass measuring 10 cm in the left hypochondrium, which he could not get above cranially and which descended with respiration. With an initial working diagnosis of possible infective endocarditis with splenomegaly, a transthoracic echocardiogram and an ultrasound of the abdomen were obtained.
The transthoracic echocardiogram showed a lef t ventricular ejection fraction (LVEF) of 34%. There was moderate global left ventricular hyperkinesia, mild concentric left ventricular hypertrophy, and a severely dilated left atrium (). No valvular vegetations were seen. The results of an ECG and measurement of cardiac enzyme markers were also unremarkable. A computed tomography (CT) coronary angiogram was ordered for further evaluation, revealing normal coronary arteries and an Agatston calcium score of 0.
The abdominal ultrasound done after the echocardiogram revealed a large left kidney measuring 14 cm with a large heterogeneous solid mass-like component predominantly in the mid and upper pole with adjacent increased vascularity, suspicious for a renal malignancy. The patient was referred to our urology department for further management. We performed a CT intravenous pyelogram (, ), which clearly illustrated a large left renal mass measuring 14 cm×13 cm×11 cm and arising from the mid/lower pole with involvement of the renal pelvis, ureter, and left adrenal gland. The staging scans showed no evidence of metastasis. The patient was offered an open left radical nephrectomy.
Intraoperatively, a locally advanced left renal tumor was noted, with involvement of the mesentery of the descending colon. A decision was made to perform en bloc left hemi colectomy along with radical nephrectomy.
Postoperatively, the patient recovered well without any complications. On postoperative day 8, we repeated a transthoracic echocardiogram. Heart function had dramatically improved, with an increased LVEF of 45% to 50%, whereas the global left hyperkinesia was noted to have resolved. The patient was eventually discharged on postoperative day 8.
Final histology revealed a clear cell RCC with predominant sarcomatoid features, involving at least 90% of the lesion. The tumor measured 14 cm and was noted to have invaded into the perinephric tissues, beyond Gerota's fascia, and into the adrenal gland. The tumor was of Fuhrman's nuclear grade 4 and vascular invasion was seen but the resection margins were free of tumor. A regional lymph node was negative for metastasis, whereas 1 of 3 nodules invading into the descending colon was positive for disease.


Our case was a 20-year-old man who had a gunshot trauma to the abdomen, which had exited from his back. The patient was admitted and underwent laparotomy three times. There was a debrided ulcer on his back with leakage of CSF. One week after his discharge, the patient became febrile (T ≥ 39°C) and was admitted to our unit with a diagnosis of meningitis and treated with meropenem, vancomycin and amikacine. Cerebrospinal fluid analysis was as follows: total cell count = 230, total white blood cells (WBC) = 200, polymorph nuclear (PMN) = 70%, lymphocytes (LYM) = 30%, glucose 39 mg/dl and protein 40 mg/dL. The radiological study revealed hydrocephalus, therefore extra ventricular drainage (EVD) was implanted. After four days, samples from the ulcer, urine and CSF yielded A. baumannii. Finally the patient was referred to our center (Golestan Hospital, Ahvaz, southwest of Iran). At this center, EVD was revised twice and the patient received antibiotic therapy with ampicillin/sulbactam, piperacillin/tazobactam, rifampin and ciprofloxacin in different combinations.
On the day of the admission a CSF sample was taken and cultured. After growth, colistin sensitive A. baumannii (isolate number 1) was recovered. After four days, colistin (intravenous and intrathecal) was initiated. Five days after administration of colistin, another CSF sample was taken and cultured again, and colistin resistant A. baumannii (isolate number 2) was recovered. The patient was still ill and did not improve. On the thirteenth day of treatment with colistin, a CSF sample was taken again, analyzed and cultured. However, the culture was negative for A. baumannii but CSF analysis showed meningitis pattern that was as follows: total cell count = 11600, total white blood cells (WBC) = 1600, polymorph nuclear (PMN) = 85%, Lymphocytes (LYM) = 15%, glucose 25 mg/dL and protein 65 mg/dL. Colistin treatment was continued until the last day of his life. The patients expired after 26 days of hospitalization. According to the importance of diagnosis and treatment of A. baumannii meningitis, and since this case of meningitis was particular and rare, we decided to do some additional experiments on two isolates of the A. baumannii.
Conventional microbiology tests were performed for initial identification of A. baumannii (). DNA was extracted by sodium dodecyl sulfate (SDS) and the proteinase K method () and, blaOXA-51-like gene and partial sequencing of rpoB gene were performed by specific primers (, ). A. baumannii NCTC 12156 (ATCC 19606) was used as the positive control (). Antimicrobial susceptibility testing of the two isolates to the following antibiotics was evaluated by the disk diffusion method (). The tested antibiotics were as follow: imipenem 10 µg, meropenem 10 µg, ceftazidime 30 µg, cefepime 30 µg, ceftriaxone 30 µg, colistin 10 µg, piperacillin 100 µg, piperacillin-tazobactam 100/10 µg, polymyxin B 300 unit, gentamicin 10 µg, tobramycin 10 µg, amikacin 30 µg, tetracycline 30 µg, ciprofloxacin 5 µg, trimethoprim-sulfamethoxazole 1.25/23.75 µg, rifampin 5 µg, aztreonam 30 µg and ampicillin-sulbactam (10/10 µg) (MAST, Group Ltd, Merseyside, UK). Minimum inhibitory concentration (MIC) of colistin, imipenem, meropenem and tigecycline were determined by the E-test (Liofilchem, Italy). The results of disk diffusion and E-test were interpreted according to CLSI guidelines. The United States Food and Drug Administration-approved criteria for Enterobacteriaceae was used for the tigecycline breakpoint ().
Multiplex PCR for detection of oxacillinase genes such as: blaOXA23-like, blaOXA-24-like and blaOXA-58-like were performed as previously described (). Metallo ß-lactamase production and encoding genes such as: blaIMP, blaVIM, blaSPM and blaNDM were investigated by PCR (, ). Both isolates were examined by REP-PCR with primers according to the Bou et al. protocol with some modifications (). According to the PCR results, both isolates were blaOXA-51-like positive and according to sequences of rpoB gene alignment, both isolates were confirmed as A. baumannii. Isolate 1 was resistant to all of tested antimicrobial disks except polymyxin B, colistin and ampicillin-sulbactam. Results of E-test showed that isolate 1 was resistant to imipenem and meropenem with MIC > 32 µg/mL and 12 µg/mL, respectively, yet was sensitive to colistin with MIC 0.25 µg/mL. Although disk diffusion results showed that isolate 1 was resistant to tigecycline yet the E-test result revealed tigecycline MIC 1.5 µg/mL, and isolate 1 was categorized as sensitive to tigecycline according to the E-test result. However isolate 1 was sensitive to colistin, but within the colistin zone of inhibition, eight colonies grew, which are indicated in .
Antibiogram results of the second isolate that was recovered after colistin therapy was similar to the first isolate but some changes had occurred. The second isolate was completely resistant to colistin with MIC 256 µg/mL (). By disk diffusion, isolate 2 was resistant to both of polymyxin B and colistin but remained sensitive to ampicillin-sulbactam. The MIC results for imipenem, meropenem and tigecycline were unchanged for the second isolate. Multiplex PCR revealed that two isolates had the blaOXA23-like gene (). Other investigated genes were negative for both isolates. By phenotypic tests, metallo-ß-lactamase production was negative for the two isolates. Results of REP-PCR revealed that the two isolates were derived from a single strain and were same ().


A healthy 69-year-old woman was referred to the Osaka University Hospital with a diagnosis of a macular tumor. She complained of distorted vision in her left eye. Her medical and family history was unremarkable. Before referral, there were no systemic workups for tuberculosis, sarcoidosis and toxoplasmosis. We excluded other diseases such as choroidal melanoma, pigmented choroidal metastasis and retinal pigment epithelial tumors by N-isopropyl-p-[123I]-iodoamphetamine single photon emission CT, and her general condition was good.
At our initial examination, her best-corrected visual acuity was 20/20 in both eyes, and the intraocular pressure was 18 mm Hg in both eyes. A slit-lamp examination showed no abnormalities in the anterior segment of either eye. An ophthalmoscopy of the left eye revealed a slightly elevated juxtafoveal chorioretinal lesion and polyp-like reddish-orange lesions (fig. ). There was also a PED around the lesion. In the macular area, there were no exudative changes such as hard exudates and macula edema.
Fluorescein angiography (TRC-50LX; Topcon, Tokyo, Japan) showed juxtafoveal hyperfluorescence due to the underlying CNV (fig. ). Indocyanine green angiography (Heidelberg Retinal Angiograph 2, Heidelberg, Germany) showed branching choroidal vascular networks (fig. ), and magnified images showed that the lesions resembled those from eyes with PCV (fig. ). The FAF images had a darker hypoautofluorescence than the surrounding areas and slight hyperautofluorescence suggesting an exudation from the CNV within the nevus (fig. ).
We also performed OCT examinations with 3 OCT instruments: a Heidelberg Spectralis (Cirrus HD-OCT; Carl Zeiss Meditec, Inc., Dublin, Calif., USA), a Heidelberg Spectralis HRA + OCT (Heidelberg Engineering), and a prototype high-penetration OCT Topcon). The OCT examinations confirmed the CNV with an overlying PED, and the PED maintained (fig. ). Because of the PED, aflibercept was injected intravitreally which improved the PED (fig. ). Her VA remained stable for the 12-month follow-up period.
The patient provided her written informed consent for the treatment. The study adhered to the tenets of the Declaration of Helsinki.


A 45-year-old woman presented with a 20-year history of a lump in the mid-third of the left clavicle, which had recently increased in size to 10 cm in diameter. Plain X-ray, computed tomography (CT) chest and clavicle, and bone scans were used to image the lesion (Figs –). Radiology reported the lesion as a parosteal osteosarcoma, based on the CT appearance of tumour growing into the medulla of the mid-third of the clavicle; not usually a feature of an osteochondroma or an osteoma. Biopsies showed dense sclerotic bone, with no obvious malignant features. To confirm diagnosis complete excision of the tumour was needed, with a partial excision and scraping the lump off the surface deemed unsafe. The patient was informed that, following a total claviculectomy, a 30% functional loss (29.5% []) in her left shoulder power would be expected. Her active lifestyle meant this result was unacceptable, so she opted instead for excision of the tumour plus the adjacent clavicle, irradiation and reimplantation of the bone with internal fixation, despite this being relatively experimental. If successful, she would have virtually normal function. Although possible risks included infection or development of non-union, which would require further surgery or possible complete claviculectomy, it was deemed oncologically safe with a low risk of complications.
The surgery was carried out through an incision over the clavicle and the tumour was carefully dissected leaving a layer of normal tissue over the mass. The clavicle was then removed by resection through the sterno-clavicular and acromio-clavicular joints and careful division of the subclavius muscle, preserving the underlying neurovascular structures. The main mass of the tumour was then stripped from the clavicle, leaving the residual bone and the attached ligaments. The bone was then soaked in a solution of vancomycin 1 g dissolved in 200 ml of saline, wrapped in swabs and then two sterile bowel bags. Irradiation of the bone with 90 Gy was then carried out at the local radiotherapy unit. After 1.5 hours, the bone was removed from the sterile bowel bags and reimplanted. The conoid and trapezoid ligaments were repaired as were the ligaments and capsule at either end of the bone, with a plate applied to the bone to strengthen it. The wound was closed and the patient advised to use a sling for 6 weeks. Post-op histology confirmed that the lump was a benign giant osteoma.
The patient had 3 monthly follow-up and at 2 years, there was no evidence of local recurrence or complications. She had a full and pain-free range of motion of the shoulder and was completely asymptomatic (Fig. ).
Four years following the procedure, after discomfort in her shoulder, X-rays revealed that the plate had broken and there was a fracture of the clavicle. This plate was subsequently removed and an underlying non-union was found, but no evidence of recurrence of the tumour. She has been managed symptomatically since and has a full range of shoulder movements but some discomfort when doing heavy lifting, which she therefore avoids (Figs and ).


A 49-year old male presented with history of pedal edema and breathlessness of 2 months duration. There was history of facial flushing, but no history of wheezing, diarrhea or abnormal blood pressure changes. There was no weight loss or abdominal symptoms. He did not have significant comorbid illnesses except for a long-standing right testicular swelling of 10 years duration. On examination, he had an early ejection systolic murmur in the pulmonary area and diastolic murmur in the tricuspid area. He had hepatomegaly secondary to the severe right heart failure. He had an enlarged, firm and nontender right testis while the left testis was normal. Lymph nodes including the supraclavicular lymph nodes were not palpable. His chest X-ray showed cardiomegaly [] with clear lung fields. Electrocardiogram showed right bundle branch block. Echocardiography revealed the presence of severe right heart disease in the form of dilated right heart chambers, dysplastic tricuspid, and pulmonary valves, with stenosis and regurgitation in both valves. Hence, we evaluated him for carcinoid syndrome. His 24-h urine 5-hydroxy indoleacetic acid (5-HIAA) was elevated, whereas other serum markers for testicular tumors were normal []. Computed tomography of the abdomen showed hepatomegaly and infrarenal para-aortic lymphadenopathy, but there were no intestinal tumors. The right testis was enlarged (4.8 × 5.0 × 7.6 cm), vascular, showing heterogeneous density, necrosis, and calcifications [] along with minimal hydrocele. Combined together, these findings favored the diagnosis of a testicular carcinoid tumor. Under local cord block, sedationand continuous cardiac monitoring, he underwent right radical high inguinal orchidectomy []. The right testis measured 3 × 4.5 × 8 cms, with the cut section showing a well-circumscribed tumor with pale white to pale yellow surface and with areas of hemorrhage and necrosis. Histological analysis showed a well-circumscribed encapsulated tumor composed of cells arranged in an acini, insular, and trabecular pattern []. The cells were round to oval with round nuclei, granular chromatin, and eosinophilic granular cytoplasm with collagenous stroma. Immunohistochemistry staining for synaptophysin expression was positive. All these features confirmed a carcinoid tumor. We made a diagnosis of a primary testicular carcinoid with carcinoid heart syndrome. He was advised repeat biochemical evaluation during follow-up visits, but he lost to follow up.


The present case report is about a 30-year-old female patient who was referred to the hospital due to right knee pain, which had started since she was 4 months of age. There was nothing of significance in her past or family history. Her pain was not relieved by aspirin and not aggravated during the night. Physical examination showed nothing of significance.
Radiography study: On anteroposterior (AP) [], lateral [] and axial [] views of right knee, there is a large bony excrescence originating from tibial tubercle and is extended toward the knee joint between the tibia, femur and patella. The lesion appears to be mostly hyperdense, containing hypodense lacunae with a sharp border. It seems to be intra-articular. The fat lines are normal. No signs of fracture or dislocation can be seen.
The differential diagnoses at this point include synovial chondromatosis, osteochondroma, large osteophyte and pigmented villonodular synovitis.
Computed tomography (CT) scanning study: On axial spiral CT scanning of the right knee joint [Figure –] without contrast with 3-mm slices (kV = 100, mA = 100), the cortex and the medulla of tibia appears to be in continuation the lesion. The soft-tissues are normal. Therefore, the diagnosis of osteochondroma is more probable.
During surgery, a lobulated, pink and firm bony mass lesion was seen to have extended from the tibial tubercle toward the knee joint but surprisingly not into the actual joint space. On AP and lateral views of right knee after surgery [], the tumor is completely resected and the joint space is intact.
Pathology study: Microscopic examination [Figure and ] reveals proliferation in the osteoid and chondroid tissues. Lamellar and mature trabeculae of the bone are located in the center and are separated by fibro-fatty tissue and capillary vessels. These bony trabeculae are covered by a thick layer of hyaline cartilage. There is no evidence of malignancy and the features are those of benign osteochondroma.


A 53-year-old woman presented with sudden stuporous mentality. Brain CT scan showed a hemorrhage in the left basal ganglia, which was extended into the lateral ventricle. She was diagnosed with MMD 2 years ago on MRI performed for evaluation of chronic headache. Based on her past history and CT findings, diagnostic angiography was performed to detect any bleeders, and revealed a ruptured aneurysm in the left medial LSA, supplying the frontal cortex via medullary vessels (). The aneurysm was located in a branch of this LSA, which was another medullary vessel connected with the insular branch of the M2 segment ().
Because the patient was uncooperative, the procedure was performed under general anesthesia. Echelon-14 microcatheter (EV3, Irvine, CA, USA) was positioned directly at the target branch with the aneurysm using Synchro-14 wire (Stryker, Fremont, CA, USA) in order to save medullary vessels from this LSA. Selective angiogram showed that delayed filling defect in the M2 branch, which was connected with the LSA. This finding confirmed another collaterals to this lesion (). The target branch was perfectly wedged by the microcatheter. To prevent a retrograde filling of the aneurysm from the M2 branch, the target branch of the LSA was embolized with a 33% NBCA mixture with lipiodol up to the point connecting with the insular branch of the M2 (). Postembolization angiogram showed no aneurysmal filling. Patent distal vessels of the LSA and M2 branches were also confirmed ().
Follow-up CT scan showed the aneurysm and target branch filled with NBCA (). No infarction in the adjacent structure and cortex area was detected on diffusion weighted imaging (DWI). The patient fully recovered and no rebleeding occurred for 1 year after embolization. Aneurysm recurrence was not detected on 1-year follow-up angiography.


A 44-year-old woman presented with stuporous mental status. Brain CT scan revealed intraventricular hemorrhage extended from a focal hemorrhage in the left caudate nucleus. The patient had a history of intracerebral hemorrhage in the right temporal lobe 8 years ago and had been diagnosed with MMD. Diagnostic angiography showed a ruptured aneurysm on medullary vessel from the LSA connected with cortical branches supplying frontal area. Additional aneurysmal dilatation was noted in these cortical branches, but its location was not in the hemorrhage site ().
Under general anesthesia, Echelon-14 microcatheter was navigated into the target LSA using Synchro-14 wire. To avoid a reflux of NBCA into M1 and another vessels, the microcatheter was inserted up to proximal segment of the target LSA over its origin. Selective angiogram showed the aneurysm and cortical branches via medullary vessels (). These cortical branches were found to disappear after brief opacification on selective angiogram, suggesting collateral vessels from other LSA. Occlusion of the target LSA with wedging microcatheter into the LSA induce no perfusion defect and branch loss on repeated angiograms. A 25% NBCA mixture with lipiodol was slowly injected via the microcatheter up to the aneurysm (). Postembolization angiogram revealed complete obliteration of the aneurysm and patent cortical braches (). No retrograde filling of the aneurysm was noted on venous phase of angiogram.
CT scan taken 3 days after embolization showed the aneurysm and LSA filled with NBCA (). No infarction was detected on DWI. The patient also fully recovered without neurologic deficit. One-year follow-up angiography did not reveal the aneurysmal recurrence. No rebleeding developed during 2 years after embolization.


A 20-year-old unmarried girl attended the outpatient clinic of KangNam Sacred heart Hospital because of gradually expanding and painless tumor of the vulva. She noticed a small mass on left labium majus five years ago that had been increasing in size over the past year. She had attained menarche at 14 years with regular cycles and was not sexually active. She had no unremarkable medical and surgical history. Physical examination revealed soft, pedunculated skin-covered mass, about 10 cm in diameter, arising from the left labium majus (). Transrectal and transabdominal ultrasonography revealed no abnormal findings of the uterus, bilateral ovaries or other pelvic organ. The result of blood test were within normal limit and the rest of gynecologic and general examinations were normal. Under general anesthesia, a circular incision was made around the base of the stalk and vulva mass was resected. In pathologic findings, macroscopically the mass was relatively well demarcated with covering skin, measuring 10×9×3 cm. On section, the cut surface showed small cystic spaces containing clear fluid. Microscopically, dilated lymphatic vessels, often cystic and ectatic, were lined by flattened endothelial cells with the paucicellular fibrous background in the mid and the deep dermis (). The lymphatic endothelial cells were positive in D2-40 immunohistochemical stain and positive nuclear staining for estrogen and progesterone receptor (PR) was noted in the stromal fibroblasts. After one year the patient is in good condition without evidence of recurrence.


A 76-year-old female had experienced unstable gait for 3 months. Because her disability was gradually progressing, she consulted a local hospital. When she came to our hospital for further examination 1 week later, she could not move without a wheel chair. Neurological examination revealed cerebellar truncal ataxia without Romberg's sign. Magnetic resonance imaging (MRI) of the head showed a cystic lesion in the foramen of Magendie, which was compressing the inferior part of the vermis and the medial part of the cerebellar hemisphere without causing hydrocephalus [].
She had previously consulted her local hospital with a complaint of headache 3 years ago. MRI performed at that time revealed the same cystic lesion to be present. The intensity of the cyst was similar to that of the cerebrospinal fluid (CSF), and the cyst was divided into two portions, suggesting the presence of a multilobular cyst. Because the patient's symptoms were believed to attribute to the presence of this cystic lesion, surgical decompression was planned.
Median suboccipital craniectomy was performed such that after the dural incision, the cyst was exposed. The retromedullary cistern was open, but the cyst had not shrunk, and the cyst was found not to communicate with the surrounding cistern []. Most of the cyst wall was successfully removed. A small part of the cyst that was still attached to the choroid plexus at the foramen of the Magendie was allowed to remain [], and the fourth ventricle was not opened via the obex.
Pathohistological examination demonstrated that the cyst wall was composed of a collagenous membrane lined by multiple layers of arachnoid cells []. Chronic inflammation and hemosiderin pigmentation were absent on the wall. This result confirmed the diagnosis of the cyst as an AC.
The patient's postoperative clinical course was excellent and her neurological recovery was remarkable. She regained her mobility and could walk without a cane. MRI performed 2 weeks after the operation revealed that the cyst had diminished and clearly demonstrated a flow artifact entering into the foramen of Magendie []. Recurrence of the cyst has not been detected on follow-up MRI for 4 years.


A 62-year-old man, who had undergone cardiac transplantation for advanced heart failure, was referred to our catheterization laboratory for a regular surveillance coronary angiogram and concomitant intravascular ultrasound (IVUS) imaging. After identifying a normal right coronary angiogram (), the clinician attempted to insert a 0.014-inch BMW (Abbott Vascular, Melno Park, CA, USA) wire for IVUS evaluation. However, resistance was quickly met, and the wire failed to pass through the proximal portion of the right coronary artery (RCA). A subsequent angiogram revealed a spiral luminal filling defect from the proximal to the distal RCA indicating coronary dissection and Thrombolysis in Myocardial Infarction (TIMI) 2 flow (). The ST segment elevation appeared in lead II and III on electrocardiography (ECG) monitoring, while hemodynamic parameters were stable. Urgent bailout stenting was performed: the RCA was engaged with 8 Fr guiding catheter (JR 4.0, Cordis, Bridgewater, NJ, USA); a BMW wire was inserted using a 1.8 Fr Finecross (Terumo Medical, Tokyo, Japan) micro-guiding catheter; the true lumen was confirmed by IVUS-virtual histology; and three ZES stents (Resolute Integrity 2.75×30 mm, 3.0×38 mm, 3.5×30 mm, Medtronic, Santa Rosa, CA, USA) were deployed in order from distal to proximal at 12, 16, and 16 atm, respectively, with overlap between adjacent stents. Although the right ventricular branches were compromised, final RCA angiography showed optimal angiographic results with TIMI 3 flow; ECG abnormalities eventually returned to baseline.
During close clinical observation, a follow-up ECG, performed six hours after the procedure, showed new ST segment elevation of 2 mm in leads V 1-2, and a blood test revealed elevated levels of troponin I (29.834 ng/mL, normal level <1.5 ng/mL). The patient was hemodynamically stable and did not complain of chest pain, likely due to anatomical denervation of the allograft during transplantation. Considering the occurrence of the previous adverse event, a follow-up coronary angiography was performed and showed a complete linear transverse fracture of the previously inserted stent (). The fracture site was close to the stent overlap, at the distal edge of the first proximal stent; hinge motion was noted during the cardiac cycle. Although there was evidence of some misalignment observed, the two fractured segments still maintained contact without definite displacement. Since there was no evidence of obstruction at that time and TIMI 3 flow was observed, the procedure was terminated after ascertaining the left coronary artery was normal. Echocardiography showed new right ventricular dysfunction, but the patient remained hemodynamically stable without any discomfort.
The patient was discharged from the hospital three days later with standard dual antiplatelet drugs and immunosuppressive agents (tacrolimus, prednisone and mycophenolate mofetil). After 12- months of clinical follow-up without further issues, routine surveillance coronary angiography was performed. Previous stents were deemed stable without restenosis at the original site of stent fracture.


A 75-year-old man was admitted with a history of effort-related chest pain persisting for two years. Prior to being admitted, his chest pain increased in intensity and frequency despite taking appropriate medications. The patient had a 10-year documented history of hypertension and was an ex-smoker. An ECG showed a left ventricular hypertrophy pattern without ST segment change. A Thallium-201 myocardial perfusion scan showed severe reduction of tracer uptake in the septum and anterior walls. Coronary angiography revealed diffuse eccentric stenosis in the left anterior descending artery (LAD) (). A minimally invasive direct bypass surgery was planned because the lesion was long, originated from the ostium of the LAD, and was accompanied by very heavy calcification: this indicated that the patient was not suitable for coronary intervention. However, the patient also had comorbid psychological issues including anxiety disorder and claustrophobia, which were not ameliorated by professional psychotherapy; the patient strongly refused surgery. Considering the patient's extant physical and psychological issues, coronary intervention was a suboptimal option for him.
The LAD was engaged with a 7 Fr guiding catheter (JL 4.0, Cordis, Bridgewater, NJ, USA), predilatation was performed with a TREK 2.5×20 mm balloon (Abbott Vascular, Santa Clara, CA, USA), and two ZES stents (Resolute Integrity 2.5×30 mm, 3.0×34 mm, Medtronic, Santa Rosa, CA, USA) were deployed at 9 atm in an overlapping manner. Additional high-pressure postdilation with a Nimbus Salvo non-compliant balloon (3.0×17mm, Clearstream Tech, Wexford, Ireland) at 16 atm and Empira non-compliant balloon (4.0×10 mm, Cordis) at 24 atm was performed.
During the final angiography, a gap was found in the proximal portion of the second distally implanted stent, which was indicative of a fracture; rotational fluoroscopic images showed consistent findings (). Similar to the first reported case, the fracture site was close to the overlap at the distal edge of the first proximal stent, and hinge motion was also noted during the cardiac cycle. IVUS with an automated pullback speed of 0.5 mm/s revealed partial absence of the stent struts corresponding to the area of the stent fracture (). Except for the stent fracture, IVUS showed good results with complete stent apposition and sufficient expansion. We opted not to perform any further interventions, and the patient was discharged with antianginal medications including triple antiplatelet agents with the regimen of aspirin, clopidogrel and cilostazol. At the 6-month clinical follow-up point, the patient was asymptomatic for chest pain or dyspnea and exercise stress tests were negative.


The first case is a 20-year-old African-American female with NS and systemic manifestations of short stature (58 inches), webbed neck and prior surgery for atrial septal defect (ASD) presented with cloudy vision in the right eye that had acutely worsened over 1 month. She also had complained of intense eye rubbing as an associated symptom. The patient was prescribed glasses at 4 years of age by an optometrist with whom she followed-up annually. Her best corrected visual acuity was hand motions in the right eye and 20/50 in the left eye. The intraocular pressures were 10 and 12 in the right and left eye respectively. Her extra ocular motility was full in all fields of gaze. Upper eyelid examination revealed mild bilateral ptosis []. There was a positive Munson's sign in the right eye. Slit lamp exam of the right eye showed central corneal edema and a very prominent cone. Slit lamp exam in the left eye showed early keratoconus. Dilated fundus exam on follow-up visit showed a cup-to-disk ratio of 0.6 in both eyes.
To address her acute corneal hydrops in the right eye, the patient was immediately started on the topical hypertonic agent Muro 128 5% ophthalmic solution 4 times a day in the right eye. At the 3-month follow-up visit, the acute corneal hydrops had largely resolved with paracentral scarring, prominent cone and stromal thinning []. Further improvement was seen at the 7-month follow-up with limited regain of visual acuity of 20/100. The patient had very high myopia with a refraction of − 18.75D sphere − 2.00D cylinder × 15 in the right eye and − 13.50D sphere − 7.00D cylinder × 165 in the left eye. Topography with Pentacam in both eyes showed high keratometric readings with thin paracentral pachymetry, consistent with keratoconus [].


A 60-year-old male retired soldier presented with a 4-month history of recurrent low-grade fever, cough, abdominal distention and remarkable weight loss. He was chronically ill looking, wasted, moderately pale, splenomegaly of 16 cm, and hepatomegaly of 6 cm. Haematological investigation showed packed cell volume (PCV) of 21.7% (37.0-53.0%), total white blood cell (WBC) count of 30.5 × 109/L (3.0-13.2 × 109/L) with differentials of granulocyte of 36.3%, lymphocyte 53.6%, medium sized (MID) 10.1%. Platelet count was 324 × 109/L. Other investigations revealed erythrocyte sedimentation rate (ESR) ˃80 mm in the first hour. Chest radiograph (hilar opacities), mantoux test (negative) and sputum acid bacilli (negative). The patient was then classified as smear-negative tuberculosis. He was then placed on empirical anti tuberculosis therapy according to the Nigerian national guideline for tuberculosis therapy. However, there was no clinical response after 4 weeks.
On haematological review he was found to be emaciated, mildly pale, mildly dehydrated without significant peripheral lymphadenopathy. The chest was clinically clear, and the cardio-vascular system was stable. He has an enlarged spleen measuring 24 cm below the left coastal margin. Repeat haematological investigations revealed a PCV of 20.8%, WBC count of 48.8 × 109/L differentials were neutrophils 70%, lymphocyte 8%, monocyte 4%, band forms 2%, metamyelocyte 10% and myelocyte 6%. The platelet count was 769 × 109/L. The peripheral blood film showed 416 nucleated red blood cells (NRBC) per 100 WBC, macrothrombocyte, leuco-erythroblastosis, tear drop poikilocytes, target cells, fragment cells and hypogranular granulocyte with bizarre segmentation. Bone marrow aspiration (BMA) revealed myeloid:Erythroid reversal and increased megakaryocytopoiesis. Biopsy findings were consistent with increase dysplastic megakaryocyte and moderate fibrosis.
These laboratory and clinical findings led to a diagnosis of CML (accelerated phase) to rule out cellular phase of myelofibrosis (MF); thus, cytoreductive therapy was started with hydroxyurea (HU) for 3 months while awaiting results of molecular biologic test. The test turned out positive for BCR-ABL1 (e14a2/e13a2) 61.6%. The patient was then commenced on Imatinib at 400 mg once daily. However, response to Imatinib was sub-optimal; thus, JAK2 analysis was requested on the same sample, and it turned out to be positive for the JAK2 mutation (exon14V617F). He was then maintained on Imatinib, blood transfusion support, erythropoietin and regular follow-up, but the patient died in a peripheral hospital about 10 months after diagnosis.


A 50-year-old male was admitted with sudden onset of markedly painful erythematous nodules on bilateral lower limbs since 3 days. There was a history of generalized weakness and malaise but no complaints of fever, loose stools, joint pains, or sore throat. On the second day of admission, an erythematous plaque was observed over the dorsal aspect of the right hand and radial aspect of the index finger. These lesions gradually progressed, and similar plaques subsequently developed over the index finger of the left hand. He was on telmisartan and metformin for hypertension and diabetes mellitus, respectively, since five years. Examination revealed multiple tender, erythematous nodules over the anterior aspect of both lower legs and knees []. There was a large, erythematous, boggy, tender plaque on the dorsum of the right hand extending over to the dorsum of right index finger []. There were large bullous and pustular lesions on an erythematous base over the radial aspect of right index finger []. General physical and systemic examination was normal.
Investigations revealed a total leukocyte count of 12.4 × 109/L with 61% neutrophils, 30% lymphocytes. His erythrocyte sedimentation rate was 65 mm in first hour, and C-reactive protein was 104 mg/L (0–6 mg/L). Creatine kinase, rheumatoid factor, and antinuclear antibody were negative. His urine analysis, serum electrolytes, liver and renal function tests, and thyroid profile were normal. Serology for HIV, HBs Ag, and hepatitis C virus (HCV) was nonreactive. No abnormality was detected on chest X-ray and electrocardiogram. Blood cultures and pus culture from the finger lesion showed no growth. A skin biopsy taken from the hand lesion revealed a dense infiltrate of mature neutrophils in the papillary dermis associated with leukocytoclastic debris. Within this area, vessel wall dilatation and fibrinoid necrosis were also seen. Few inflammatory cells were seen infiltrating the vessel wall; however, there was no extravasation of erythrocytes [Figures and ]. No organisms were identified on hemotoxylin and eosin stain. Microbiologic cultures were negative. Based on the clinicopathologic features, diagnosis of neutrophilic dermatoses of dorsal hands was made. The patient did not consent for the skin biopsy from the leg lesions; these were presumptively diagnosed as erythema nodosum. During his hospital course, papulopustular lesions were seen to develop at sites of venepunture which were interpreted clinically as positive pathergy phenomena. Treatment with prednisolone 1 mg/kg/day was initiated, and remarkable improvement was observed over the next few days. The leg lesions were observed to become ecchymotic and then yellowish before fading. Corticosteroids were gradually tapered and dapsone 100 mg/day was initiated. Complete resolution of all lesions was observed over the next four weeks. Dapsone was safely continued, with no recurrence over a follow-up of 10 months.


A 62-year-old man presented to the emergency department with 3 weeks of intermittent right upper quadrant pain. CT of the abdomen demonstrated acute cholecystitis complicated by a contained perforation of the gallbladder at the hepatic aspect. A Type 3 laparoscopic subtotal cholecystectomy was performed the day after his admission due to an inability to safely dissect inflammatory adhesions, which held the duodenum in close proximity to the structures of Calot's triangle. The remaining gallbladder tissue was diathermied and a drain was placed in the gallbladder fossa.
This patient remained in hospital for 1 month with postoperative complications. Ongoing leakage of bile prompted insertion of a percutaneous drain and endoscopic retrograde cholangiopancreatography with stent insertion. Ultrasound of the abdomen performed on Day 14 postoperatively demonstrated a collection with lobulated margins (Fig. ). Concurrent hepatobiliary iminodiacetic acid scan confirmed that this represented an ongoing bile leak contained within the gallbladder fossa.
Further ultrasound studies on Days 21 and 31 demonstrated an ongoing organizing collection (Fig. ). He was discharged with the percutaneous drain in place, which was removed on Day 37 when drainage eventually ceased.
The patient presented to the hospital 4 months after the initial operation with right upper quadrant pain. CT abdomen established the appearance of a normal gallbladder despite his history of subtotal cholecystectomy (Fig. ). He underwent an elective laparoscopic cholecystectomy 1 month later, which revealed an apparently complete gallbladder that was extensively walled off by omentum. An intraoperative image is shown in Fig. .
The postoperative recovery was uneventful and the patient remained pain and gallbladder free. Acute on chronic cholecystitis and contiguous gallbladder mucosa were demonstrated by histopathological analysis.


The patient was a 52-year-old woman with no history of systemic disease or parafunctional occlusion. The patient presented to our facility with a main request to replace her missing maxillary left second premolar and first molar with implants. An orthopantomogram was taken (), and after clinical and radiographic examination, a taper implant with a 4.0 mm width and a 10 mm length was selected for replacement of both teeth. Using local anesthesia, a crestal incision was performed without vertical extension. The bone was then exposed and prepared according to the manufacturer’s recommendations. During preparation of the first molar socket, the resistance to drilling decreased, indicating sinus floor penetration. Because the bone density was poor, the final drill was inserted halfway, and two implants with a diameter of 4.0 mm and length of 10 mm were placed, replacing the first molar and second premolar. The implant design was a tapered, modified surface (sand-blasted, large grit, acid-etched [SLA]) that was threaded to the top (Superline™, Dentium, Cypress, CA, USA) to achieve better implant stability and increase the implant surface area in contact with the surrounding bone. Implants were placed approximately 1 mm subcrestally, and resonance frequency analysis (RFA) measurements were taken for both implants (). The reading for the second premolar implant was 73 ISQ (implant stability quotient) in all four directions, and for the first molar implant, the reading was 69 ISQ in all directions except for the buccolingual direction, which was 64 ISQ. A cover screw was placed on the second premolar implant and covered with gingival tissue to obtain primary closure and allow healing using the submerged technique. The first molar implant was immediately loaded with a temporary plastic abutment, and a crown was fabricated from a light-cured composite resin material (). At this stage, the crown was out of occlusion, with a narrow occlusal table and no interproximal contact ( and ). The tissue flap was adapted to the temporary crown, and the gingiva was sutured around it (). A periapical radiograph was taken postoperatively for both implants and was considered a basic radiograph (). The radiograph shows the implant in the molar area penetrating the maxillary sinus approximately 2–3 mm.
Postoperative instructions were given, and after 10 days the patient returned for suture removal and follow-up. Both implant sites healed uneventfully, and the sutures were removed. No signs or symptoms of maxillary sinus infection or inflammation were reported by the patient. One month after implant placement, the temporary abutment and crown were removed. The RFA measurements taken at that time were 73 ISQ in the mesiodistal and distomesial directions and 70 ISQ in the buccolingual and lingobuccal directions. The crown was modified () by increasing the width of the occlusal table and obtaining distal contact with the adjacent tooth (upper right second molar). At this stage, the crown remained out of occlusion (no increase in crown height). The crown was polished and again screwed into the fixture. Again, the patient was examined for any signs or symptoms of maxillary sinus infection, and none were found.
Two months after implant placement, the patient returned for the third stage of crown modification. The temporary abutment and crown were removed, and the RFA measurements taken at this time were 75 ISQ in the mesiodistal and distomesial directions and 70 ISQ in the buccolingual and lingobuccal directions. The crown was modified by increasing the vertical height and obtaining occlusal contact with the opposing tooth in the axial direction only (). Occlusal contacts during excursive movements were removed, and only central contact remained. During the same appointment, the second premolar implant was uncovered, and the RFA measurements taken were 76 ISQ in the mesiodistal and distomesial directions and 66 ISQ in the buccolingual and lingobuccal directions. A healing abutment was placed and left for 1 month to allow healing of the soft tissue ().
Three months after implant placement (), the RFA measurement for the first molar was 75 ISQ in the mesiodistal, lingobuccal, and distomesial directions and 71 ISQ in the buccolingual direction. For the second premolar, the RFA values were 75 ISQ in the mesiodistal direction, 79 ISQ in the distomesial direction, and 70 ISQ in the buccolingual and lingobuccal directions. Impressions were taken at this appointment using a closed-tray technique and hex coping. Jaw relationships and bite registration were obtained using a wax bite rim and O-bite. Titanium hex abutments were placed using 30 Ncm of force for both implants, and provisional crowns were cemented with temporary cement (). Occlusion was checked and adjusted, leaving only centric occlusal contacts and removing all contacts found during excursive movements (). A periapical radiograph after abutment installation was taken (). Final crowns will be placed 6 months after cementation of provisional crowns.


A 22-year-old female patient visited the outpatient department with a complaint of pain in the left jaw joint region since 1½ months. On eliciting the history, patient had pain on mastication and difficulty in opening the mouth due to which she was on the soft diet. Medical history revealed that she was diagnosed with RA 6 months back. The patient took homeopathy medicines for 1 month. But presently was not on any medication. On clinical examination of TMJ, the following signs and symptoms were assessed: Left side TMJ was associated with pain, TMJ range of motion was limited, associated with pain while maximum unassisted mouth opening (18 mm) and while lateral excursion [], deviation of mandible toward left side while opening mouth was noticed. No clicking sounds on opening, closing and lateral movements. Muscles of mastication were tender on palpation. Intra orally, no teeth were carious, no occlusal prematurity was noticed. On radiological examination, panoramic radiograph depicted irregular erosions in the left condyle and decreased joint space both on right and left side. The findings were of degenerative joint disease but nonspecific due to the overlapping of structures []. TMJ tomography both open and closed mouth revealed slight erosion in the anterior surface of the left condyle but was not clearly appreciated []. Further evaluation was carried out by CBCT.
Cone beam computed tomography images revealed sclerosis of the outer surface of the condylar head, narrowing of the articular space bilaterally (more on the left). Coronal left closed mouth view revealed loss of joint space, loss of cortical bone on the superior surface and condylar head erosions compared to right side, which shows normal joint space and condylar structure [Figure and ]. Coronal left open mouth view revealed narrowing of the articular space and erosions on superior head of condyle and right side depicting no changes in the joint space [Figure and ]. Sagittal view open and closed mouth revealed decrease in joint space with erosions of the superior surface of the condyle on the left side [Figures and , and ]. Hand wrist radiograph revealed the joint space narrowing of the distal phalange of the right thumb, narrowing of 3rd and 4th proximal phalanges and erosion of the middle phalange seen of index finger []. Knee and shoulder joint radiographs revealed no changes. Serum investigations were advised and it revealed rheumatoid factor (RF)-340 IU/ml (normally <40 IU/mL), C-reactive protein (CRP)-368 mg/dl (normally <0.8 mg/dL), erythrocyte sedimentation rate (ESR)-40 mm/h (normally <20 mm/h in females). All serum markers for RA were elevated. Final diagnosis of RA affecting TMJ was arrived at.
Patient was referred to rheumatologist for the further treatment, and she was prescribed Tab Methotrexate 75 mg once a week for 2 months and anti-inflammatory drug twice a day for 15 days and patient responded well to the treatment. Liver function test was also monitored with periodic follow-up. After 2 months of the follow-up, patient reported relief of pain and improvement in mouth opening.


A 31 year old, 50 kg American Society of Anaesthesiologists (ASA) physical status-I female patient was posted for open myomectomy. In the operating room standard monitoring with 5-lead electrocardiogram, pulse oximetry, non-invasive blood pressure (NIBP) were attached. After securing intravenous access with 18G cannula, 250 ml of crystalloid was administered. The patient was placed in right lateral position, and subarachnoid block with 26G Quincke® needle was performed at L4-L5 interspace and 2.5 ml 0.5% heavy bupivacaine with 25 μg fentanyl (0.5 ml) was given. NIBP was measured every 3 min and no significant haemodynamic changes were noted following subarachnoid block. Peak cephalad level of sensory blockade (loss of temperature sensation with a alcohol swab) was T6 dermatome at 30 min. Thirty minutes following skin incision, 30 ml normal saline (NS) containing 4 units of vasopressin (20 units vasopressin diluted in 150 ml NS, 0.133 units/ml) was injected intramyometrially after negative aspiration of blood. Two minutes after vasopressin injection patient developed severe conjunctival pallor, hypotension (NIBP - 70/30 mmHg) and complete heart block (heart rate [HR] <40/min) with absent peripheral pulses. Three doses of injection atropine 0.6 mg (30 s between doses) administered intravenously and oxygen 6 L/min was supplemented through face mask.[] HR and blood pressure were restored with palpable peripheral pulses. The total duration of the event was <2 min and throughout this period the patient remained conscious with palpable central pulses, normal respiration and oxygen saturation. Sensory blockade at this point remained at T6 level. Arterial blood gas analysis performed 15 min later showed no significant abnormality.
Since the patient remained haemodynamically stable, surgery was resumed and completed with no further complications. Post-operatively electrocardiography, cardiac enzymes, echocardiogram, and renal function tests were done and found to be normal. After an uneventful post-operative stay of 5 days, the patient was discharged.