A 52-year-old man presented with gradually increasing pain in his neck and left upper arm over a 3 month period. When he had visited our hospital, he could not move his neck as a result of the pain. The plain radiographs demonstrated a collapsed vertebral body at C-6 (). The CT scan findings of the lung revealed a solitary round tumor with an irregular margin in the left upper lobe. The size was 2 cm in diameter. Technetium-99 bone scintigraphy demonstrated multiple spinal bone metastases, which were diagnosed as a stage IV (T1N0M1).
The patient underwent posterior decompression and spinal fusion as palliative surgery. The visual analog scale (VAS) improved to 2 cm from 10 cm. The pathological diagnosis was adenocarcinoma. Although platinum-based chemotherapy was administered, the tumor marker and size did not improve. The patient rejected additional therapy. Four months after the first operation, the C3-6 vertebral body collapsed and he could sit up (). Therefore, the patient underwent C2-7 anterior body fusion as palliative surgery again. After surgery, the neck pain was reduced, and the VAS was improved to 4 cm from 10 cm. However, two months after the second operation, he presented with intolerable neck pain. The performance status deteriorated to 3. Since the radiograph showed the progress of osteolysis () and the primary focus progressed, the oral administration of gefitinib 250 mg/day was started as a second-line chemotherapy with informed consent. After administration for one month, the pain was reduced to allow walking. The performance status improved to. The VAS improved to 4 cm from 10 cm. At three months after administration, the cervical metastatic lesions showed remarkable increasing bone formation (). The CT scan findings of the cervical vertebrae confirmed osteosclerosis matched with the metastatic bone tumor lesion (). The patient survived for a further two years after having a recognized bone metastasis. The activity of daily living (ADL) continued during the term of gefitinib administration.


A 78-year-old woman presented with cough and weight loss over a 3 month period. The plain radiographs and CT scan findings revealed a tumor in the left upper lobe of the lung. A pathological diagnosis by sputum suggested an adenocarcinoma. In addition, to the brain metastases, there were multiple bone metastases of the pelvis, spine and femur. She was diagnosed with stage IV (T4N3M1) lung cancer. The oral administration of gefitinib 250 mg/day was commenced with informed consent. One week later, she suffered from the pathological fracture of the femur, and underwent internal fixation. Three months after surgery, remarkable bone formation and union was observed in the plain radiograph (). She was able to walk without pain. The cervical metastatic lesions revealed remarkable bone formation in the plain radiographs and CT scan findings (). She was still alive one year after the recognized bone metastasis with an improvement in the pain and ADL after gefitinib administration.


A twenty year old male patient visited our outpatient clinic complaining of low back pain. He was a new recruit in the army, and the acute back pain had occurred approximately one month earlier after entering an army training camp for recruits. He had previously experienced back pain after hard work or hard exercise for several years. The findings of a physical examination were unremarkable, except for mild tenderness at the left lumbar paravertebral area. No pathological reflexes were noted. The straight leg raising test was negative.
The plain radiograph showed an absence of the left inferior articular process at the fourth lumbar vertebra. A hypoplastic defect of the left lamina was also noted ().
A CT scan confirmed the absence of the unilateral lumbar apophyseal joint due to an inferior articular process defect and a hypoplastic defect of the unilateral lamina (). However, the contralateral apophyseal joint was normal and did not show any pathological changes, such as arthrosis or hypertrophy. There was no evidence of disc herniation.
The patient was managed conservatively and a role change to the administrative department in the army was recommended. He returned to activity as an administrative office soldier and the severe low back pain has not returned for 2 years.


The patient was a 64-year-old male diagnosed with acinar-type prostate adenocarcinoma with a Gleason score of 6 (3+3) by prostate biopsy. His prostate volume was 25 g, and his prostate-specific antigen (PSA) was 2.34 ng/ml. The patient had undergone a three-piece IPP (AMS-700CX, American Medical Systems, USA) implantation 15 years previously because of diabetic erectile dysfunction. The 60 ml reservoir was placed in the left retropubic space through an external inguinal ring from a penoscrotal vertical incision. All devices worked well. Because we perform magnetic resonance imaging in all prostate cancer patients preoperatively (), the surgeon who performed this case was fully aware of the anatomical structure of the patient before surgery. The patient was informed in advance of the risks of malfunction, infection, and the possibility of IPP removal.
The RARP was done in the usual manner []. Initially, all six ports were placed after the pneumoperitoneum was established with a Veress needle. A 12 mm Visiport was placed at the umbilicus for the camera. The 8 mm ports for the robotic arms were placed laterally below the level of the umbilicus. In addition, a 12 mm assistant port was inserted between the camera port and the outer robot port and the suction cannula was put through a 5 mm port between the camera and robotic port ipsilateral to the assistant's side. In this case, the inflated reservoir was easily found in the lateral pelvic wall. We carefully dissected the encapsulated reservoir by electrocautery (monopolar curved scissor) so as not to injure it. After separating the reservoir capsule, deflation was performed on the pelvic wall to empty the reservoir, creating more prevesical space. There were no adhesions in the pelvic cavities (). Then, RARP was successfully performed []. After finishing the urethrovesical anastomosis with an 18Fr silicone Foley catheter and placing a drain, we inflated the reservoir ().
The operating time was 120 min, and the estimated blood loss during the surgery was 320 ml. There was no damage to the adjacent organs. The encapsulated reservoir was well inflated and was easily separated from the surrounding tissues. Reservoir change was not suspected. Pathologic examination revealed acinar type adenocarcinoma and the Gleason score was 6 (3+3). The tumor volume was 1.50 cc, and the surgical margin was negative. The length of hospital stay was 9 days. The drain was removed on day 4, and the urethral catheter was removed on day 9. The preserved IPP continued to function properly in 1 month. No other complications were reported. The 6-month follow-up PSA level was <0.01 ng/ml and the patient achieved pad-free status.


The patient was a 2 month-old girl with cyanosis, irritability, respiratory difficulty, poor oral intake and seizure-like movements, and had cardiopulmonary resuscitation on arrival. Her body weight was 5.6 kg (5 percentile). She was born at 38 weeks of gestational age with a birth-weight of 2.8 kg. She had been exclusively breast-fed. There were no medical or familial histories except an admission at an age of 10 days for hypocalcemic tetany. She was treated with calcium replacement therapy for a week. There were moist rales on both middle lung fields and chest wall retraction without cardiac murmurs or hepatomegaly. The patient had frequent episodes of muscular tetany. A chest X-ray showed an apparent cardiomegaly and pulmonary congestion (). An echocardiogram revealed a markedly enlarged left ventricular cavity and a hypokinetic ventricular wall motion. Left ventricular end diastolic diameter (LVDd) was 38 mm, left ventricular end systolic diameter (LVDs) was 35 mm, ejection fraction (EF) was 17%, and fractional shortening (FS) was 8%, without any structural abnormalities (). Electrocardiography showed sinus tachycardia (heart rate 191 beat/min), and normal QTc (0.415 seconds) (). Initial portable electroencephalography (EEG) showed a multiple, epileptic form discharge. Arterial blood gas analysis were pH 6.988, pO2 325.9 mmHg, pCO2 31.0 mmHg, and HCO3 7.3 mmol/L under a 40% O2 mask. Hypocalcemia as total serum calcium was 5.8 mg/dL, hyperphosphatemia as inorganic phosphorus was 10.9 mg/dL, and alkaline phosphatase was elevated (643 IU/L). Creatine kinase was 544 IU/L and creatine kinase-muscle and bone was 33.3 ug/L. Other chemistries and electrolytes studied were in the normal range. Hormone levels that were changed included elevated parathyroid hormone (155 pg/mL; normal 12-72 pg/mL), decreased 25-hydroxy vitamin D (2.6 ng/mL; normal 9.1-37.6 ng/mL) and decreased 1α,25(OH)2 vitamin D (9.2 pg/mL; normal 20.1-46.2 pg/mL). There were no metabolic disorders by amino acid and organic acid tests. Tests for viral infection were not performed. A fluorescence in situ hybridization study for chromosome 22q11 deletion was negative. A left wrist X-ray revealed mild fraying signs. After calcium and vitamin D replacement, the patient showed rapid reductions in hypocalcemic tetany, and a rapid recovery of cardiac function and cardiomegaly on chest X-ray ( and ). Follow-up EEG revealed improvements as there was no evidence of epileptiform discharges. The patient was discharged on the 15th hospital day and followed up by the outpatient department with calcium gluconate and calcitriol replacement.
The mother had a vitamin D deficiency as indicated by a decreased level of 25-hydroxy vitamin D (4.3 ng/mL). Her bone densitometry study revealed osteomalacia.


A 52-year old woman with Marfan syndrome was admitted to the emergency department complaining of acute resting chest pain for one hour. Three years prior she had undergone a total aortic arch replacement due to aortic arch dissection with descending thoracic aortic aneurysm. The patient also had a Cabrol-type Bentall operation in another hospital using a St. Jude's mechanical aortic valve for progressive severe aortic regurgitation 12 days previously. Her electrocardiogram on arrival showed ST-elevation in the inferior leads and ST-depression in the I, aVL, V3-6. She was diagnosed with acute inferior ST-elevation myocardial infarction. Initial cardiac biomarkers showed a slightly elevated troponin T of 0.15 ng/mL but were otherwise unremarkable. Though she took warfarin, the prothrombin time expressed as a normalized international ratio was 1.6 on admission. Because her initial blood pressure was too low to measure, she was started on hydration with normal saline, inotropic support and transferred immediately to the catheter laboratory for primary PCI.
During coronary angiography, a 6 Fr EBU guiding catheter (Medtronic, Minneapolis, MN, USA) was easily inserted into the left Cabrol composite graft ostium. The left limb of the graft was found to be fully patent with normal flow {Thrombolysis in Myocardial Infarction (TIMI) grade 3} down to the left coronary artery. However, the right limb of the Cabrol composite graft ostium was not found initially. Aortic root angiography did not show the right limb of the Cabrol graft ostium. With eager, we could insert a 7 Fr multipurpose guiding catheter (Cordis, Johnson and Johnson, Cordis, Miami Lakes, FL, USA) into the right limb of the Cabrol composite graft ostium. The right limb of the graft was totally obstructed (TIMI grade 0) by heavy thrombi at the Cabrol graft to the right coronary artery (RCA) anastomosis site (). Initially, we tried to aspirate with an intracoronary suction catheter using an Export aspiration catheter (Medtronic, Minneapolis, MN, USA), but it was not passed due to tortuosity. After ballooning of the anastomosis site, the whole right coronary arterial system was visible angiographically. The anastomosis site between the Cabrol graft and the RCA was significantly narrowed, angulated and twisted (). An intravascular ultrasound (IVUS) study revealed a kinked and narrowed anastomotic site (). Pre-dilatation was performed using a 4.0×20 mm Sprinter™ semi-compliant balloon (Medtronic, Minneapolis, MN, USA) and then a 5.0×20 mm Liberte™ (Boston Scientific, Natick, MA, USA) bare metal stent was deployed at the Cabrol graft to the RCA anastomosis site. The entire lesion including the anastomosis site was postdilated using a 5.0×8 mm Quantum™ non-compliant balloon (Boston Scientific, Natick, MA, USA). An optimal angiographic result was obtained with TIMI grade 3 flow distally (). After post-dilation, the IVUS study revealed optimal stent deployment and lesion coverage (). The patient was stabilized in the intensive care unit. The coronary CT angiography showed severe angulation and tortuosity between the RCA and the right limb of the Cabrol graft (). She was discharged five days after the primary PCI without complications.


A female patient aged seventy-five years was admitted to the emergency room with abdominal pain ten days after an angioplasty plus coronary stent implantation, which had been performed through the femoral artery. Three days after the angioplasty; i.e., one week prior to presentation to the emergency room, an inguinal hematoma developed as complication of the femoral arteriography had to be drained. Thereafter, the patient suffered from constipation and had difficulties with evacuation. On the day the woman presented to the emergency room, she felt a sudden and dull abdominal discomfort during evacuation and noticed a loop of bowel protruding from her vagina. There was no history of abdominal or vaginal trauma.
Thirty years prior to the present admission, the woman had undergone a total abdominal hysterectomy for a benign pathology. The operation had no complications, and the patient’s recovery was uneventful. After the hysterectomy and ten and twelve years prior to the present admission, the woman had undergone two perinea surgeries for a prolapsed bladder. Apart from these three surgeries, the she had no past medical or gynecological history worthy of note.
Upon admission to the emergency room, the patient’s blood pressure was 110 × 70 mmHg, her heart rate was 88 bpm, and an abdominal examination indicated significant pain. The pelvic examination revealed 40 cm of small bowel prolapsing through her vagina (). After resuscitation of the patient, she received intravenous broad-spectrum antibiotics (1 g of Ceftriaxon and 500 mg of Metronidazole), and her bowel was wrapped with warm, sterile, and saline-soaked gauze for transfer to the operating room. There, under rachianesthesia, the woman was placed in lithotomy position, so that the viability of her small bowel could be assessed. The examination revealed that the bowel was edematous and thick-walled, but still viable. There was no evidence of necrosis. The inguinal hematoma, which looked infected, was drained (). The patient was then placed in the Trendelenburg position. Because the vault defect was located high in the vagina, all attempts to transvaginally reduce the small bowel into the peritoneal cavity were unsuccessful. Consequently, a midline subumbilical incision was made, and the prolapsed bowel was reduced into the abdomen and inspected for damage throughout its length. Thereafter, the vaginal vault defect was closed with absorbable sutures (Polygleprone 2.0) by a vaginal route (), and a 30-cm segment of bowel was excised. Although the bowel was viable, we decided to carry out this procedure because there was an expansible hematoma in the mesum. Broad-spectrum antibiotics were postoperatively given for six days. The patient had no postoperative complications and was discharged from the hospital after six days. In a follow-up examination three months later, the woman exhibited no evidence of recurrence, and the vaginal vault had healed satisfactorily.


A healthy 69-year-old man initially noticed slower reactions while playing tennis and during the next year developed a more complex clinical picture. During the course of each day, his gait became slower and unstable. Furthermore, he noticed short memory disturbances, occasional dysphasia, the daily need for an afternoon nap, frequent headaches, nausea and blurred vision by the end of the day, as well as frequent miction overnight. Finally, he suffered three episodes of ophistotonus after a long, strenuous walk. Because the clinical presentation to some extent resembled the normal pressure hydrocephalus triad, the neurologist presented the patient for evacuating lumbar punctures. Interestingly, we diagnosed a BPC (Fig. ) indicating an obstructive hydrocephalus and therefore contraindicating evacuating lumbar punctures. Instead, we recently performed an ETV and we are now closely following the patient.


A healthy 51-year-old man presented to the emergency department with ataxia after a bicycle fall. Surprisingly, his CT scan did not reveal any posttraumatic hemorrhage but a moderate tetraventricular hydrocephalus. Two months thereafter, he still complained of minimal concentration difficulties; however, his neuropsychological examination was within normal range. MR imaging was consistent with BPC (Fig. ) and an apparently arrested (compensated) hydrocephalus. Therefore, no therapy was instituted, and he is doing fine with a follow-up of nearly 2 years.


A 49-year-old, 72 kg man with voice color change was diagnosed with laryngeal and vocal cord polyp. He had no history of other medication, surgery or significant illness. Microlaryngeal polypectomy was scheduled. Preoperative investigations were unremarkable. Monitoring methods included electrocardiography, noninvasive blood pressure monitoring, pulse oximetry, and capnography. The electrocardiograph showed a normal sinus rhythm of 85 beats per minute, and the patient's blood pressure (BP) was 129/82 mmHg before anesthesia induction in the operating room. Glycopyrrolate, 0.2 mg, was given intravenously for premedication just before anesthesia induction. Anesthesia was induced with propofol, 140 mg, and followed by remifentanil, 210 µg; the patient's lungs were ventilated with 100% oxygen. Propofol was mixed with 1% lidocaine 35 mg for reducing injection pain and the remifentanil was diluted to 10 ml with normal saline and injected slowly during a 90-second period.
One minute after administration of remifentanil, BP and heart rate (HR) were 89/60 mmHg and 57 beats per minute, respectively. The trachea was intubated with an endotracheal tube (ID 6.5 mm) using a curved-blade direct laryngoscope. Immediately after intubation, BP was 100/60 mmHg, HR was 64 beats per minute, and the oxygen saturation was 100%. There were no significant adverse events during intubation. We confirmed proper position of the endotracheal tube and adequate ventilation with stethoscope. Sevoflurane (1.0-2.5 vol%) was used to maintain anesthesia without a neuromuscular blocking agent. The BP and HR just before surgery began were 112/70 mmHg and 75 beats per minute, respectively.
However, when the surgeon placed a suspension laryngoscope (Laryngoscope 8590C, Karl-Storz, Tuttlingen, Germany) to secure a view of the vocal cords, HR progressively decreased to <30 beats per minute. Atropine, 0.5 mg, was given intravenously but was ineffective. The lowest heart rate was 18 beats per minute. At our request, the surgeon withdrew the suspension laryngoscope promptly, and then HR progressively increased to 70 beats per minute of itself; BP was 115/70 mmHg. On a second attempt of suspension laryngoscopy, HR decreased to <30 beats per minute, just as it did during the first attempt, so the surgeon again withdrew the suspension laryngoscope. The HR recovered to 68 beats per minute, and the BP was 120/79 mmHg. Five minutes later, we administered 0.5 mg of atropine intravenously again; then suspension laryngoscopy was performed without any problem. Surgery proceeded without further complications. The patient was discharged from ambulatory surgery 3 hours later without any problem.


An 18-year-old male presented with a complaint of chest discomfort, exertional dyspnea, and an intractable dry cough. Chest radiography revealed a mass like lesion in left upper mediastinum and trachea deviated to the right-side. Multi detector computed tomography (MDCT) revealed a 12 × 9 × 15 cm sized heterogenously enhancing mass in anterior mediastinum extending ventrally into the left pectoralis major muscle, and dorsally into the aortic arch, pulmonary artery trunk, and descending aorta, and encroaching the left lung field ( and ). However, the diameters of involved vessels were preserved (not shown), and the trachea and both main bronchi were patent ( and ). Transthoracic echocardiography demonstrated minimal pericardial effusion with moderate mitral regurgitation and a left ventricular ejection fraction of 52%. Pulmonary function test (PFT) findings were within normal limits, and including a peak expiratory flow rate (PEFR) of 50% the predicted value.
Although the patient underwent a fluoroscopy-guided percutaneous needle lung biopsy twice, the type of tumor was not confirmed, and thus, a thoracotomic incisional biopsy was decided upon under general anesthesia. After intravenously injecting 1% propofol and succinylcholine in the supine position, a Univent tube was successfully intubated by direct laryngoscopy. Anesthetic maintenance was then carried out by the target-controlled infusion of propofol and remifentanil with O2, air, and intermittent intravenous rocuronium. During the first 45 minutes after induction in the supine position, end-tidal carbon dioxide partial pressure (PetCO2), heart rate (HR) and systolic/diastolic blood pressures were 37-39 mmHg, 109-120 bpm, and 121-181/85-103 mmHg, respectively. Even after closing the left main bronchus using a bronchial blocker, pulse oximetry O2 saturation (SpO2) was maintained at 97-99%, and central venous pressure (CVP) was maintained at 14-15 mmHg under controlled positive pressure ventilation. He was then placed in the right lateral decubitus for the left thoracotomy approach, and for the first 30 minutes after this positional change, his vital signs remained unchanged. However, SpO2 then began to decline, and fiberoptic bronchoscopy demonstrated the left main bronchus was almost totally obstructed, and that the ballooned bronchial blocker had been dislodged into the carina. Accordingly, we immediately turned patient supine to relieve the mass effect on the main bronchi. However, hypoxemia was further aggravated up to 65% even after two lung ventilation and increasing the inspiratory oxygen fraction (FiO2) to 1.0. The sitting position also failed to improve oxygenation. Furthermore, CVP increased gradually from 17 to 65 mmHg after the SpO2 decreased. Nevertheless, blood pressure (112-123/72-77 mmHg) and PetCO2 (32-36 mmHg) remained in their normal ranges.
Eventually, the patient was placed in the left lateral decubitus position to detach the mass from the site of obstruction by gravity, and thereafter, SpO2 improved from 79% to 93 and then to 97-99%, and CVP simultaneously decreased from 65 to 18-20 mmHg. Surgery was then undertaken under a partial (femoro-femoral) cardiopulmonary bypass (CPB) in the right lateral decubitus position. The total bypass time was 150 minutes, and blood pressures and heart rates perioperatively were 89-120/44-50 mmHg and 95-115 bpm, respectively. During bypass, core temperature was maintained at normothermia (36℃) and PetCO2 was 36-43 mmHg. A frozen biopsy later confirmed Hodgkin's lymphoma. After weaning the patient off CPB, his SpO2 was 100%, PetCO2 42-46 mmHg, and CVP 12-16 mmHg under controlled positive pressure ventilation supplying FiO2 1.0. Muscle relaxation was reversed using glycopyrrolate and pyridostigmine. After observing full recovery of spontaneous respiration and of extremity muscle power, we extubated the Univent tube and transferred the patient to an intensive care unit (ICU) with O2 5 L/min administered through a venturi mask. In the ICU, no signs of hypoxemia were evident (SpO2 98%), and no cardiorespiratory or neurologic abnormalities were found. On postoperative day 2 , the patient was moved to a general hospital ward.


A 22-year-old Korean male visited our clinic in 2009 due to the onset of a major depressive episode. The presenting symptoms were depressed mood, avolition, idea of reference, insomnia, guilty feeling, and suicidal ideation. The last symptom resulted in him being admitted to a closed psychiatric ward.
The patient had no medical history and no history of substance abuse; his laboratory tests were also normal. He was diagnosed with MDD. He was initially treated with mirtazapine at 15 mg, which was subsequently escalated to 45 mg. However, the patient had only a partial response to this drug. As a result, an initial dose of 30 mg duloxetine was added to mirtazapine, and subsequently escalated to 60 mg. The patient's symptomatology largely remitted after this combination treatment, and so he was discharged to day-clinic treatment. Just prior to his discharge, laboratory tests were repeated, and all of them (including the liver function test) produced normal results; his total bilirubin was 1.0 mg/dL and alkaline phosphatase (ALP) was 88 U/L.
After discharge, the patient maintained the mirtazapine (45 mg) and duloxetine (60 mg) combination therapy for 3 months. During this time he developed jaundice in his eyes. Liver function tests were repeated again, and although he did not complain of any symptoms, his total bilirubin level had increased to 3.3 mg/dL, while other test results were within normal limits (e.g., ALP 111 U/L). Duloxetine was discontinued immediately. At 1 month after discontinuation of duloxetine, the patient's total bilirubin had decreased to 1.8 mg/dL, ALP remained normal at 109 U/L, and the jaundice had disappeared.


A 27 year-old female who had a two-year history of non-insulin dependent diabetes mellitus (NIDDM) underwent an abdominal ultrasonography for unrelated causes. Multiple hepatic nodules and liver enlargement were observed (). The patient reported the use of oral contraceptives for the last 5 years and had a positive family history for diabetes mellitus. An abdominal CT-scan was performed and multiple hypervascularized hepatic nodules were observed, consistent with the diagnosis of LA. The largest nodule (18 cm) was resected and histological analysis revealed a liver adenoma.


A 43-year-old woman had undergone surgery for a myoid hamartoma in the lower outer quadrant of the patient's left breast. Twelve months later, she presented with a palpable lump under the surgical scar. A clinical breast examination revealed a 3.0-cm sized firm mass with slight mobility under the scar. A mammography showed two oval isodense masses with a partially obscured margin in the left subareolar area (). Ultrasound images showed a 2.3-cm sized irregular isoechoic mass with a microlobulated margin situated in the surgical bed (). Another 2.0-cm sized, oval hypoechoic mass with a circumscribed margin was found in the lower outer quadrant of the patient's left breast (). US examination results indicated that the mass in the surgical bed was considered to be suspicious. To further evaluate the suspicious mass, MRI was performed on a 1.5 Tesla system (General Electric Medical Systems, Milwaukee, WI) with a specially developed double breast coil. The MR revealed two, circumscribed, oval-shaped masses which appeared to be of isosignal intensity relative to skeletal muscle on the T1-weighted images (WI) and with high-signal intensity on the T2-WI. On contrast enhanced T1-WI and subtracted images, the masses showed strong enhancement. On dynamic MRI, the mass situated in the surgical bed showed early intense enhancement and progressive signal loss over time (). This finding was considered to be suspicious for malignancy. The lesion found in the lower outer quadrant of the left breast showed progressive enhancement () and thought to be benign.
A 14-gauge core needle biopsy was performed on the mass under the scar using ultrasound guidance. A microscopic evaluation revealed that the lobules and ducts of the mammary gland and stroma had no malignant component and reported to be a fibroadenoma. The patient requested and then underwent a surgical excision in order to obtain a definitive diagnosis. The gross pathology evaluation of the specimen revealed a 2.5×1.8×2.0-cm-long rubbery, white, solid mass situated in the surgical bed and a 2.3×1.4×2.4-cm-long rubbery, white, solid mass in the lower outer quadrant of the left breast; both masses were round and had smooth margins. The microscopic evaluation of the mass situated in the surgical bed revealed lobules and ducts of the mammary gland, stroma with a high collagen concentration, and many bundles of smooth muscle fiber without atypia (). An immunohistochemical investigation was positive for vimentin, smooth muscle actin, CD34 in the smooth muscle cells, but negative for S100 protein. The final pathology diagnosis was myoid hamartoma, whereas the other mass was a fibroadenoma.


A 64-year-old man was hospitalized due to frequent chest pain, despite oral medication. He had a longstanding history of hypertension. An electrocardiogram (EKG) on admission showed atrial fibrillation and Q waves in leads II, III, aVF, and V2-4. On chest X-ray, there were findings suggestive of cardiomegaly. An echocardiography revealed a severe degree of inferior and posterior wall hypokinesis, left and right ventricular dilatation, and a decreased left ventricular ejection fraction of 30%. Coronary angiography performed via the right femoral artery showed 97% stenosis and calcifications from the proximal to mid-right coronary artery (RCA), 99% stenosis and calcifications in the proximal left circumflex (LCX) artery, and complete obstruction of the left anterior descending (LAD) artery (). Percutaneous coronary artery intervention was performed. For the RCA lesion, a 6-Fr Judkins right type 4 (Medtronic, Danvers, MA, USA) guide catheter was used to advance the guide wire into the lesion, a 2.0/15 mm Ryujin™ balloon (Terumo Corporation, Fujinomiya, Japan) was expanded up to a pressure of 6 atm, and because of a residual stenosis of 80-90%, a 2.5/15 mm Ikazuchi™ balloon (Kaneka Corporation, Kanagawa, Japan) was expanded up to a pressure of 6 atm and a Taxus™ (Boston Scientific, Galway, Ireland) 3.5/32 mm stent was implanted, leaving a residual stenosis of 10%. For the LCX lesion, a 6-Fr Judkins left type 4 guide catheter was used, a 2.0/15 mm Ryujin™ balloon was expanded to a pressure of 6 atm, leaving a residual stenosis of 70%; an attempt was made to pass a Taxus™ 3.0/20 mm stent was rendered unsuccessful because of severe calcifications. The guide catheter was replaced with a 6-Fr Extra Back-Up (EBU) 3.5 (Medtronic), but passage could not be performed. Resistance was perceived for the additional expansion during stent removal and it was observed that the stent was left at the lesion site (). Residual stent removal was then unsuccessfully attempted with a small balloon. The guide catheter was replaced with an 8-Fr EBU 3.5 and unsuccessful attempts were made to remove the residual stent with the use of a Snare (Multi-snare Micro Set; Produkte fur die Medizin AG, Germany). Finally, the lost stent was compressed with a Xience V™ (Abbott Vascular, Santa Clara, CA, USA). A 3.0/28 mm stent was transferred to the left main branch and removed using a Snare (). Following the procedure, although the patient had persistent mild chest pain, no complications were apparent due to stent loss and the patient was discharged on medical treatment.


A 57-year-old woman with a 5-year history of hypertension and diabetes under treatment presented to the emergency care center with a 3-day history of respiratory difficulty. An admission EKG showed a sinus rhythm and ST-segment depression in leads V4-6. On chest X-ray, there were findings suggestive of pulmonary edema and cardiac enlargement. Echo-cardiography revealed overall decreased left ventricular mobility and the left ventricular ejection fraction which was decreased to 25%. Percutaneous coronary angiography performed via the right femoral artery revealed 99% stenosis and calcifications in the proximal LAD, a normal LCX (), and 50% stenosis in the mid-RCA. For the LAD lesion, a 6-Fr EBU 3.5 guide catheter was used to advance a guide wire and a 2.0/15 mm Ikazuchi™ balloon was dilated to a pressure of 8 atm after coronary artery dissection developed with acute obstructive findings. Passage of a Xience V™ 3.0/15 mm stent to the lesion was unsuccessfully attempted. A 2.5/15 mm Kaneka RX balloon™ (Kaneka Corporation) was then dilated to 12 atm and a subsequent attempt at stent passage resulted in leaving the stent in the proximal LAD lesion (). To remove the lost stent, a guide wire was passed into the lost stent and removal was attempted without success with a small balloon. To fix the lost stent to the original site, a 2.0/15 mm Ikazuchi™ balloon was placed into the stent and dilatation was performed to 14 atm (). With progression of coronary artery detachment up to the mid-LAD portion, however, a thrombolysis in myocardial infarction (TIMI) flow grade 1 persisted. Again, using Xience V™ 2.5/18 mm and Xience V™ 2.5/23 mm stents, the stent was placed in the mid-portion lesions and dilatation was performed with a residual stenosis of approximately 30%. The rate of blood flow was improved to TIMI 3, which finalized the procedure (). The patient was discharged and then followed in an outpatient setting.


A 79-year-old man with no history of hypertension, diabetes, smoking, or alcohol consumption was hospitalized because of a >1-month history of exertional chest pain. Sixteen years ago the patient had undergone thrombolytic therapy for an anterior and inferior wall myocardial infarction. Admission EKG showed sinus rhythm and Q waves in leads II, III, and aVF, while echocardiography revealed no abnormal findings in the left ventricular ejection fraction or cardiac wall movement. Percutaneous coronary artery intervention was performed via the right femoral artery. Coronary angiography revealed a complete mid-LAD obstruction, 70% stenosis in the proximal LCX, 90% stenosis in the distal LCX (), 40% stenosis in the proximal RCA, and 90% stenosis in the mid-RCA. A 6-Fr EBU guide catheter (Cordis Britetip, Miami, FL, USA) was used to advance the guide wire into the lesion, a 2.5/20 mm Ryujin™ balloon was dilated, and passage of a Pico™ stent (Amg Vacular, Bucharest, Romania) was attempted unsuccessfully. Again, a successful re-attempt was made with an Endeavor™ 3.0/24 mm stent (Medtronic Ireland, Galway, Ireland). For the LAD artery, a 6-Fr Judkins left type 4 guide catheter was passed, a 2.5/20 mm Ryujin™ balloon was dilated, and unsuccessful attempts were made with an Endeavor stent. After replacement with a 6-Fr EBU guide catheter, re-attempts at passage into the middle portion lesion resulted in stent retention because of severe resistance in the lesion (). Because the lesion was already a complete obstruction, lack of stent removal was not deemed problematic and we proceeded with intervention of the proximal and distal LCX lesions, with insertion of a Pico™ 3.0/24 mm stent and an Endeavor™ 2.75/18 mm stent, respectively (). The patient completed the procedure in stable condition and was discharged.
One month later, the patient presented to the emergency care center with severe chest pain. The creatine kinase-MB fraction level was 149 ng/mL and the troponin T level was 2.4 ng/mL. An EKG showed new Q waves in leads V1-5 and echocardiography revealed a severe decrease in left ventricular anterior wall mobility. Percutaneous coronary artery intervention was performed emergently. There wa°). A 6-Fr guide catheter was used to pass a guide wire into the lesion and stent (), a 3.0/15 mm Kaneka RX™ balloon was dilated to 6 atm, and using an Endeavor™ 3.5/15 mm stent, the lost stent was compressed and inserted (). Coronary angiography showed recovery of the hemodynamic profile (). The patient was discharged in stable condition and followed in an outpatient setting.


A 24-year-old male was admitted to our hospital with a 1 week history of progressive headache and fever. His previous medical history was clear. On the neurologic examination, his mental status was normal without focal neurological deficits. The laboratory examination revealed nonspecific findings. HIV antibodies were negative. Lumbar cerebrospinal fluid (CSF) analysis showed pleocytosis, increased total protein level (167 mg/dL) and decreased glucose (32 mg/dL). Tubercle bacillus was detected in the CSF and the adenosine deaminase (ADA) level was elevated (12 IU/L). Brain MRI revealed small, multiple high signal intensity lesions on the diffusion weighted image. His chest X-ray showed diffuse ill-defined patches and nodules with increased density in both apical lungs. Tuberculosis meningitis and pulmonary tuberculosis were suspected and antituberculous treatment with rifampicin, isoniazid, ethambutol and pyrazinamide was started. Nine days after the antituberculous treatment, his general condition and headache had improved significantly. However, four weeks after antituberculous treatment, he developed acute sensory disturbance below T10 dermatome as well as urination disturbances. A neurological examination revealed grade 3/3 paraparesis and hyporeflexia. Spinal MRI showed a long segmentally located soft tissue mass mimicking a meningioma in the intradural, extramedullary space of the posterior spinal canal from T2 to T6 with severe cord compression and displacement (). Surgical decompression and a biopsy were performed. During the operation, a T3, T4, T5 and T6 laminectomy was performed. The dura was thickened and the cord was infiltrated with an adhesive mass. The dura was opened and closed in the normal manner after removing the mass under microscope guidance. Grossly, the mass was very soft with a dark green color. Optical microscopy of the mass revealed chronic granulomatous inflammation with neutrophil infiltration (). The cultures were negative for Mycobacterium tuberculosis, and the stains for fungi and acid-fast micro organisms were negative. Twelve weeks after surgery, the patients reported low back discomfort. MRI of the thoracic and lumbar areas showed lumbosacral tuberculosis spondylitis with multiple abscesses (). Anti-tuberculous medication was continued for 18 months. At the one year follow-up, the patient could walk without assistance and urinate normally.


A 30-year-old female patient presented to the emergency department with dyspnea on exertion and severe left anterior chest pain that had begun about 30 minutes prior to arrival, and which increased in intensity over time. She reported a history of exertional chest pain that had begun 10 days prior to her presentation. Previous studies, including electrocardiography (ECG), cardiac biomarkers, echocardiography, and an exercise treadmill test had shown no abnormalities. Her chest pain had been slightly alleviated by sublingual nitroglycerine. The patient had no smoking history and had no cardiovascular risk factors such as hypertension, dyslipidemia, or diabetes mellitus. The patient had been diagnosed with ET 6 months previously at a workplace health screening, and was being treated with 100 mg aspirin, 500 mg hydroxyurea twice a day, and 1 mg anagrelide three times daily. Her ET was relatively well controlled without any other complications, and her platelet counts had been within the normal range. Initial vital signs were stable, with a blood pressure of 110/80 mmHg, a heart rate of 78 beats/min, and a respiratory rate of 18 breaths/min. S1 and S2 were normal and S4 was faintly audible at the apex. An ECG showed T-wave inversions in leads I, aVL, and in V2 through V5, which were consistent with myocardial ischemia (). Neither cardiomegaly nor pulmonary congestion was noted on a chest X-ray. The MB fraction of creatinine phosphokinase (CK-MB) was 8.5 ng/mL and cardiac troponin I was 3.08 ng/mL (upper normal limit, 0.07 ng/mL). B-type natriuretic peptide (100 pg/mL) was also slightly elevated. A complete blood count showed the following: a leukocyte count of 3.70×103/µL, hemoglobin of 10.5 g/dL, and a platelet count of 388×103/µL. Low density lipoprotein (LDL) cholesterol level was 54 mg/dL. An echocardiograph revealed hypokinesis in the anteroseptal wall and a left ventricular ejection fraction of 55%. These results were compatible with an acute, non-ST-elevation MI. Immediately, the patient was treated with anti-platelet therapy (300 mg aspirin and 600 mg clopidogrel). In addition, according to the early invasive strategy, coronary angiography was performed, which revealed significant segmental stenosis (90%) of the mid left anterior descending artery (LAD) (). The segmental lesion in the mid LAD did not respond to intracoronary nitroglycerin injection, which excluded coronary spasms as the causative factor (). An intravascular ultrasound (IVUS) scan showed a focal soft plaque with a ruptured cap and thrombus formation (). Percutaneous coronary angioplasty and stenting (Promus, 3.5×18 mm) were performed successfully. After coronary angioplasty, the chest pain and T-wave inversions on ECG disappeared. Anagrelide was discontinued, anti-platelet and anti-anginal agents were added to the treatment, and the patient was discharged without further cardiac symptoms.


A 65-year-old female, suffering from an OSCC of the right anterior floor of the mouth (pT1N2bM0), was treated in November 2002 with a wide excision in combination with a lateral neck dissection at the right side. To achieve radical removal, the lower teeth had to be extracted, and the alveolar process was reduced in height. Subsequently, two endosseous implants (TiUnite Mark III RP, Nobel Biocare®, Gothenburg, Sweden) were placed into the symphyseal region of the mandible to facilitate early prosthetic rehabilitation [, ].
Postoperatively, the patient was subjected to a fractionated radiotherapy schedule up to a cumulative dose of 64 Gy (32 times, receiving 2 Gy at each session) because of a spidery growth pattern and two ipsilateral positive lymph nodes of level Ib. After a healing period of 3 months postradiation, the patient desired prosthetic rehabilitation. Consecutively, healing abutments were placed (June 2002), and a bar-retained overdenture was fabricated. Since then, this construction functioned satisfactorily for about 4 years without further complications.
Unfortunately, in October 2006, 4 years postradiation, a recurrent OSCC (cT2N0M0) developed. Between the two implants, an exophytic tumor was observed in the floor of the mouth extending to the attached keratinized peri-implant mucosa of both implants (Fig. ). Radiographically (OPG and CT scan), no osteolytic lesions around the dental implants, indicative for bone invasion, could be observed [].
To achieve radical removal, first, a tumor-free mucosal margin of 1 cm was outlined. Subsequently, the mandibular bone surface was exposed by careful elevation of the mucoperiosteum in caudal direction, thereby preserving the attachment of the soft tissue to the aimed cranial bone segment (Fig. ). Then, the marginal mandibulectomy was performed, utilizing a standard drill unit (Elan-EC, Aesculap®, Tuttlingen, Germany) connected to a saw using a standard saw blade (Braun-Aesculap® sterile blades, Ref GC615R; Tuttlingen, Germany). During the osteotomy, consecutively, the implants were also cut into two parts (Fig. ).
Postoperatively, the lower denture was not worn for 6 months. The mucosal defect was closed primarily. In addition, the patient was warned of the risk of fracture and instructed about oral hygiene and soft diet. The soft tissues healed well (Fig. ).
Histology showed a radically removed tumor with an 8-mm free mucosal margin. The tumor had an infiltrative spidery-type growth pattern in the lamina propria. Fortunately, no bone, perineural, or intravascular invasion was observed.
Two years postoperatively (November 2008), it was decided to insert dental implants again. After exposing the mucoperiostal flap, the apical parts of the cut implants could be easily identified (Fig. ). Three years after resection of the recurrent tumor and 1 year after reimplantation, the patient is disease free and has a good oral function.


A 63-year-old woman from Campinas, SP, Brazil was admitted to the ICU on August 21, 2009 (Day 1) because of respiratory failure. She had a five-day history of dry cough, myalgia, wheezing, and fever (38°C) and had been using clarithromycin for three days. Her past medical history was significant for hypertension, type 2 diabetes mellitus, obesity (body mass index of 30.1 kg/m2), and total hip replacement 10 months before admission complicated by deep-vein thrombosis (DVT) and pulmonary embolism, both of which were successfully treated. Upon admission, she was placed in respiratory isolation with negative pressure, and nasopharyngeal washings were collected for detection of influenza A (H1N1) by reverse-transcriptase polymerase chain reaction (RT-PCR). The blood and tracheal aspirate cultures were negative, as was the urinary assessment for Pneumococcus and Legionella. Arterial blood gas analysis confirmed severe hypoxemia, and an X-ray computed tomography (CT) scan () of the thorax showed bilateral pulmonary infiltrates.
Orotracheal intubation was performed after a failed attempt at noninvasive ventilation. Oseltamivir (150 mg b.i.d.) administered through the enteral route and intravenous ceftriaxone (1 g IV b.i.d.), levofloxacin (500 mg IV q.d.), vancomycin (1 g IV b.i.d.) and methylprednisolone (2 mg/kg/day) were started. A Doppler ultrasound of the lower limbs was negative for DVT, and an echocardiogram showed a systolic pulmonary artery pressure of 26 mm Hg with no signs of right ventricular dysfunction and a left ventricular ejection fraction of 66%.
Severe hypoxemia (PaO2 55 mm Hg) was present despite ventilation with a positive end-expiratory pressure (PEEP) of 16 cm H2O and pure oxygen, so a recruitment maneuver was performed for two minutes using a PEEP of 35 cm H2O and a plateau pressure of 50 cm H2O. After the recruitment, the PEEP was titrated at 18 cm H2O according to the best dynamic compliance, but there was no significant improvement in the PaO2/FiO2 ratio (). A decision was then made to repeat the recruitment maneuver with the patient in the prone position, which resulted in significant improvement in gas exchange (). Mechanical ventilation in the prone position for an average of 12 hours/day and one daily recruitment maneuver were continued for three consecutive days, with progressive improvement in the gas exchange (). At all times, we maintained a protective ventilatory strategy with low tidal volumes (6 mL/kg of ideal body weight) and a plateau pressure of <30 cm H2O.
On the 12th day of her ICU stay, amantadine was added to the treatment regimen, and importation of intravenous zanamivir (not approved in Brazil) was requested because the RT-PCR for influenza A (H1N1) remained positive. On the 19th day of her stay in the ICU, intravenous zanamivir was started, and the RT-PCR for influenza A (H1N1) became negative two days later. Because the patient still had diffuse, patchy ground-glass opacities on chest CT and had signs of incipient interstitial fibrosis, pulse therapy with methylprednisolone (1 g/day) for three consecutive days was given. The patient showed progressive radiological and gas exchange improvement and was released from mechanical ventilation 26 days after intubation. She was discharged from the ICU 30 days after admission and discharged home 3 weeks later.


A 24-year-old man had a palpable tough mass on his left chest wall accompanied by mild pain and no redness of the skin. The lump developed in 2014 and had continued to grow slowly during the 5 years of follow-up with no medical intervention. The patient had no previous medical history. Physical examination found a hard, regularly shaped, mobile mass of approximately 1 cm in diameter which was palpable under the left areola. Lymph nodes of axilla were not palpable.
A March 2017 breast ultrasound revealed a 0.8 × 0.5 cm hypoechoic mass on the retroareolar region of the left breast () (The earliest ultrasound results in 2014 were unavailable). In May 2019, the mass had grown to 1.3 × 0.7 cm in size and was hypoechoic with a clear margin and uneven internal echo (). Therefore, the patient underwent lumpectomy in May 2019. According to the pathological examination results, the mass was described as a biphasic tumor composed of glandular epithelial cells and myoepithelial cells arranged in a tubular, cribriform, solid structure, which supports the diagnosis of breast ACC (). Immunohistochemical staining showed that the tumor cells were negative for ER, PR and HER-2 and positive for E-cadherin, P120-catenin, P63, CK5/6, and CD117. Approximately 20% of the cells expressed Ki67. Then the patient immediately returned to the Department of Breast and Thyroid Surgery for further treatment and received a breast ultrasound and 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET-CT). The breast ultrasound revealed a 1.8 × 0.9 cm hypoechoic area under the areola of the left breast (possible postoperative change) (). Lymph nodes were visible in the bilateral axilla and left clavicle, and an enlarged lymph node approximately 2.3 × 0.6 cm in size was observed in the left axilla (). The 18F-FDG PET-CT revealed a disordered subcutaneous structure in the left breast region accompanied by increased metabolism, indicating postoperative changes. Small lymph nodes with low metabolism were found in the bilateral neck and axilla. No significant metabolic abnormalities were observed anywhere else in the patient ().
Based on the breast ultrasound, 18F-FDG PET-CT, pathological examination and the preference of the patient, we performed modified radical mastectomy and left axillary lymph node dissection in June 2019. After the surgery, the patient did not receive subsequent radiotherapy, chemotherapy or endocrine therapy.
Mastectomy histopathological examination showed no residual carcinoma tissue around the primary tumor bed in the left breast. No vascular tumor embolus was evident by pathological analysis. No nerve invasion was detected, and the surgical margin was negative. None of the 22 ipsilateral axillary lymph nodes resected showed metastatic carcinoma. The patient recovered well and was discharged 1 week later. The patient remained healthy over 28 months of regular follow-up, with no signs of local relapse or distant metastases (, ).


A 46-year-old female patient with no past medical history presented to the emergency department (ED) with worsening dizziness and weakness resulting in a presyncope. The episode was witnessed by her family members who reported that she reached down to tie her shoelaces and upon rising endorsed dizziness, isolated paresthesias in the right hand, and dysarthria for approximately 15 min. Upon presentation to the ED, her symptoms had largely resolved. The patient was awake, alert, and oriented to person, place, and time. Physical examination revealed minor numbness in the thumb of the right hand. Otherwise, cranial nerves II-XII were grossly intact. There were no signs of pronator drift and the patient had intact muscle strength with flexion and extension of the upper and lower extremities. Cardiovascular examination was significant for a loud P2 with tumor plop at the cardiac apex as can be appreciated in (). Vital signs on admission were as follows: heart rate of 103 beats per minute, blood pressure of 173/105 mm Hg, temperature of 36.7 °C, respiratory rate of 16 breaths per minute, and pulse oximetry of 94% on room air.
Laboratory data, as summarized in , including complete blood count, complete metabolic panel, and troponin were significant only for borderline elevation of troponin level of 0.04 ng/mL (reference < 0.04 ng/mL). EKG was significant for sinus tachycardia, left axis deviation with no signs of fascicular block, incomplete right bundle branch block with T-wave inversions in the inferior leads, and a classic “S1-T3-Q3”' pattern (). In the setting of mildly elevated troponins and characteristic EKG pattern, there was concern for PE. A reflex chest computed tomography angiogram (CTA) was negative for PE; however, it did reveal a 1.6 × 3.6 cm filling defect in the left atrium (). We continued to trend the troponin and it had peaked to 0.16 ng/mL approximately 4 h later. Transthoracic echocardiogram (TTE) results revealed a 1.6 × 3.4 cm mass fixed to the mitral leaflet (). M-mode confirmed the localization of the mass to the mitral valve (). Definity scan confirmed the mass but did not reveal any further masses within the left ventricle (). The extent of outflow tract obstruction is demonstrated by ).
Given the presenting symptoms and laboratory data, there was concern for a transient ischemic attack with underlying non-ST elevation myocardial infarction, thus the patient was administered 324 mg of aspirin and high intensity atorvastatin. Maintenance intravenous fluids were ordered to promote volume expansion of the heart in the setting of a mobile mass and prevent left ventricular outflow tract obstruction. Systemic anticoagulation was initially deferred due to concern for thromboembolic masses to the brain. Although the initial CT scan of the head was negative, magnetic resonance imaging (MRI) of the brain revealed findings consistent with multiple bilateral microinfarcts in a vascular distribution. After further consultation with neurology and cardiothoracic surgery, it was deemed that the benefits of initiating anticoagulation with a heparin drip outweighed the risks of intracranial hemorrhaging given the small size of the infarcts. The patient underwent further evaluation including a left heart catheterization to rule out coronary artery disease in addition to cardiothoracic surgery evaluation for mass removal. Cardiac catheterization was negative for significant obstructive coronary artery disease.
The patient ultimately underwent mass removal by cardiothoracic surgery and had an uncomplicated hospital course. The mass was sent for histopathological evaluation. Tissue evaluation was significant for a myxoid neoplasm that was composed of spindle shaped cells and capillaries on a myxoid stroma consistent with an atrial myxoma. The neurological symptoms had resolved, and the patient was discharged safely to home.


A 10-year-old female child reported to the Department of Pedodontics and Preventive Dentistry with a chief complaint of pain on the upper front tooth for 4 days. In a clinical examination, it showed yellowish discoloration of the 11, 22, and missing 21, with protrusive maxillary anterior segment (A). The parent recalled a history of trauma to the anterior maxillary region 5 years back. Based on the history and clinical examination, we made a provisional diagnosis of turner's hypoplasia on 11, and 22. IOPA radiograph and panoramic radiograph revealed that 21 is within the alveolar bone and was associated with a radiopaque mass (B). To confirm the position and structural relationship with adjacent structures, cone-beam computed tomography (CBCT) was advised and was suggestive of 21 with dilacerated root and single supernumerary tooth positioned palatally between 11 and 21 (C). After the consultation with an orthodontist, it was inferred that the forced eruption of 21 seemed practically impossible or technically difficult due to the position and morphology of the tooth. So, we planned the surgical extraction of the 21 along with the supernumerary tooth under local anesthesia. A full-thickness mucoperiosteal flap was raised, selective and circumferential removal of bone was done to expose the tooth till above the CEJ of 21 and the crown showed hypoplastic enamel (D). Following which odontectomy was done to section out the crown portion. The supernumerary tooth which was found fused with the root of 21 was surgically removed (E) and sutures were placed (F) and the patient was prescribed antibiotics and analgesics.


A 9-year-old female patient reported to the Department of Pedodontics, Govt Dental College and Hospital Shimla, Himachal Pradesh with a chief complaint of missing anterior front teeth. There was no history of trauma. On clinical examination, there was a missing maxillary right central incisor. A supernumerary tooth was present palatally with respect to 11 (A). An eruption bulge was palpable on the labial gingiva of the 21 region. Occlusal and panoramic radiographs of 21 revealed that a tooth-like structure was placed superior to the horizontally impacted 21 (B). A CBCT was advised to know the exact position and morphology of the tooth-like structure and also the impacted 21. CBCT images disclosed an impacted supernumerary tooth within the alveolar bone palatal to 11 and 21 having a complete crown and single root. It was positioned vertically, with crown tipped toward the occlusal plane. The crown of the supernumerary tooth is in close proximity to the CEJ of 11 and 21; positioned palatally with a little displacement of 11 and 21. Labially, the crown of supernumerary teeth was positioned superior to the crown of 21 (C). Our treatment plan was an extraction of supernumerary tooth associated with 11 and surgical extraction of 21 (since 21 cannot be extruded by orthodontic traction), under local anesthesia ( and ). Following which extraoral endodontic treatment was done on 21 and replanted into its anatomic position (F). Sutures were placed, antibiotics and analgesics were prescribed.


An 8-year-old male patient reported to the Department of Pedodontics, Govt Dental College and Hospital Shimla, Himachal Pradesh with a chief complaint of an irregularly placed upper front tooth. The parent of the patient noticed this irregularity for 1 year. Clinical examination revealed that an extra tooth was present in between 11 and 21 suggestive of a mesiodens (A). IOPA radiograph showed a tooth-like structure was found impacted in relation to the apical third of 11 which is in an inverted direction (crown toward the apex) suggestive of mesiodens (B). To determine the position of mesiodens, occlusal radiograph was advised and was located palatally (C). Surgical extraction of the mesiodens was planned under local anesthesia. Mesiodens which was visible on the oral cavity was extracted first. The palatal flap was elevated, and selective removal of the palatal bone by using bur, the supernumerary tooth was exposed and was extracted ( and ). The flaps were sutured and a periodontal pack was placed (F).


A 6-year-old girl presented to our clinic with a 2-year history of hair loss. Prior to therapy, the patient had seen three to four dermatologists but lost the records. Along with extensive hair loss on the scalp, eyelashes, and eyebrows, the patient was hyperactive and short []. She had dystrophic fingernails toenails with erythematous areas (striated lunulae), pitting, and nail fragility []. No other systemic abnormalities were found. Alopecia universalis with nail degeneration was diagnosed clinically. Minoxidil 2% solution was initially used with bimatoprost. After the second appointment, tofacitinib 2.5 mg daily single oral dose was administered due to lack of improvement. All examinations, including complete blood count, serum creatinine, liver function test, lipid profile, HBsAg, HCV, HIV 1 and 2, Mantoux test, tuberculosis interferon gold, and thyroid functions, were all normal prior to starting tofacitinib. Patient was also referred to a geneticist to rule out Down's syndrome. Three months into treatment, 50% of the scalp's hair grew [], and the nails improved []. All other medications were discontinued after 3 months, except for tofacitinib. Near-complete hair growth on the scalp, eyebrows, and eyelashes was seen after 6 months of treatment []. After 6 months of tofacitinib treatment, nail irregularities [] and pain were gone. Subsequent investigations were normal. No side effects were seen due to the medication.


A 49-year-old Caucasian female with hypertrophic cardiomyopathy underwent orthotopic heart transplantation (OHTx) complicated by primary graft dysfunction. Veno-arterial extracorporeal membrane oxygenation was instituted intraoperatively due to failure to wean from cardiopulmonary bypass. She remained stable in the intensive care unit requiring a median dose of 4 µg/min epinephrine and 2 µg/min norepinephrine over the next 10 days. At that time, she was able to be weaned from ECMO and decannulated. However, over the next 12 h, she developed worsening right ventricular dysfunction necessitating the insertion of a temporary right ventricular assist device (Jostra-Rotaflow). She remained stable over the next 5 days and her sedation was weaned. At this time, it was noted that she had flaccid paralysis and areflexia of her lower limbs. Upper limb function was preserved. After a further 5 days, the patient was uneventfully weaned from mechanical support. Magnetic resonance imaging (MRI) revealed extensive central spinal cord oedema from T1-2 level to the conus suggestive of infarction ( and ). Over the next 6 weeks, the patient developed multi-organ failure and sepsis and treatment was withdrawn.


A 72-year-old Caucasian male underwent coronary artery bypass grafting, aortic valve replacement, and Maze procedure. He required an intra-aortic balloon pump (IABP) to be weaned off cardiopulmonary bypass. Over the next few hours, he had persistently low cardiac output (on 4 µg/min of epinephrine and 14 µg/min of norepinephrine), acidosis (pH 7.2), and rising lactate (8 mmol/L) was placed on peripheral VA ECMO and the IABP was removed. Due to ongoing severe left ventricular dysfunction (requiring up to 4 µg/min of epinephrine and 24 µg/min of norepinephrine) and an inability to wean off ECMO, 6 days after the index operation, a repeat coronary angiogram was performed. This demonstrated patent grafts to the circumflex and first diagonal territories. However, an ostial left main stenosis, which had not been previously demonstrated, was noted. He underwent repeat surgery the following day with a bypass graft to the left anterior descending artery. He was subsequently weaned from VA ECMO and decannulated uneventfully 72 h later (a total of 10 days on VA ECMO). At this time, he was noticed to have bilateral lower limb paralysis. Spinal MRI revealed extensive central thoracic cord T2-weighted signal hyperintensity, swelling and diffusion restriction from T6 down to the conus, consistent with spinal cord infarction ( and ). Over the next 3 days, he developed biliary sepsis with rising lactate, rising vasopressor requirements, and renal failure requiring haemofiltration. Treatment was withdrawn in view of these complications.


A 38-year-old Caucasian female with post-partum cardiomyopathy, supported for 7 months on continuous flow left ventricular assist device (HeartWare, Medtronic, MA, USA), underwent OHTx. She developed primary graft failure within 12 h requiring the institution of peripheral VA ECMO. She was successfully weaned and decannulated after 13 days on VA ECMO. Sedation was subsequently weaned over the next week, but she was noticed to have paralysis of bilateral lower limbs. Spinal MRI demonstrated hyperintense T1-weighted non-enhancing lesions predominantly affecting the central cord grey matter from T9 to T12, suggestive of cord infarction ( and ). Her intensive care unit stay was protracted, and she eventually succumbed to sepsis and multi-organ failure 3 months after her initial heart transplantation.
All three patients were on mechanical ventilation when VA ECMO was instituted and remained sedated and on mechanical ventilation for the duration of the VA ECMO run. They had all had a normal neurological status prior to their operation, having presented from home for surgery. Veno-arterial extracorporeal membrane oxygenation was instituted within 12 h of surgery for all three patients. None of the patients required left ventricular venting. All patients received a downflow cannula into the superficial femoral artery and none were complicated by lower limb ischaemia. All patients had pulmonary artery catheters placed as part of their surgery, although these are generally removed after 7 days to reduce infection risk. Veno-arterial extracorporeal membrane oxygenation was instituted using HLS Bioline coated cannulae (Getinge AB, Gothenburg, Sweden), a Bio-Medicus Pump driver and head (550 Bio-Console, Medtronic Inc., Dublin, Ireland), and Quadrox D oxygenator (Getinge AB, Gothenburg, Sweden). Parameters were adjusted to achieve adequate end-organ perfusion maintaining mean blood pressure above 65 mmHg, mixed venous oxygen saturation above 70% and aiming for a cardiac index above 2.2 L/min/body surface area (m2), as per our hospital protocol. This generally requires flows of 3.5–5 L/min to achieve these parameters and the flow is controlled by manually adjusting the revolutions per minute on the centrifugal pump console, and modified by utilising vasodilator infusions to reduce afterload as required. When possible we aim to maintain some pulsatility and utilise intravenous inotropic infusions to achieve this, as well as regular echocardiography to identify (and maintain) aortic valve opening. Heparin was commenced at 12 h post-institution of VA ECMO if there was no surgical bleeding, aiming for an activated partial thromboplastin time of 60–80 s. None of the patients had any other embolic phenomena to suggest that the spinal cord injury was the result of an embolic shower, although this cannot be excluded.
There was no suspicion of spinal cord injury in any of the three patients until they were weaned from sedation. This occurred at about 15 days post-operatively in the two female heart transplant patients and at 10 days in the male post-cardiotomy patient. The actual timing of the spinal cord injury is unknown. In identifying that the patients had profound lower limb weakness, the following differential diagnoses were considered: intensive care myopathy, critical illness polyneuropathy, ischaemic stroke, and disc herniation. However, the clinical features were highly suspicious of a spinal cord pathology and so spinal cord MRI was performed confirming the diagnosis in each patient.


A 48-year-old African American woman was referred to our institution for further evaluation and management of recently diagnosed IgA nephropathy. Her baseline serum creatinine was 1.2 mg/dL (ref: 0.5–1.1). She was initially evaluated at an outside facility three months prior to presentation, when the serum creatinine was 1.4 mg/dL with a urine protein–creatinine ratio of 1.7 g/g (ref: less than 150 mg/g) and 60/hpf red blood cells (ref: 0–5) in the urine. She did not have gross haematuria. A month later, her serum creatinine increased to 1.7 mg/dL, which prompted a renal biopsy. Unfortunately, the sample was inadequate, but it was suggestive of crescentic IgA nephropathy. Serologic tests for antinuclear antibodies, antineutrophil cytoplasmic antibodies, HIV and viral hepatitis were negative, and serum complements were within normal limits. In our clinic, the patient’s blood pressure was 110/78 mmHg while taking amlodipine 10 mg and losartan 25 mg/day. Serum creatinine was 1.4 mg/dL and urine protein–creatinine ratio was approximately 1.2 g/g. We elected to rebiopsy her to confirm the diagnosis of crescentic IgA nephropathy in a non-HIV-positive female African American patient, and the possibility of treatment with an alkylating agent. This time, an adequate sample was obtained and, interestingly, it was consistent with IgA nephropathy (). As there were fibrocellular crescents in only 2 of the 11 glomeruli and the renal function remained stable, there was no indication for therapy with an alkylating agent. However, because of proteinuria exceeding 1 g/g despite being on an angiotensin receptor blocker, we treated her with a tapering course of prednisone. Six months later, her urine protein–creatinine ratio reduced to 437 mg/g and serum creatinine remained relatively stable at 1.6 mg/dL.


The patient was a 31-year-old woman who was admitted at 27 weeks of gestation for abnormal fetal development identified on a routine prenatal checkup. Ultrasonography revealed anencephaly with a biparietal diameter of 5.4 cm and femur length of 2.8 cm. The fetal position was right sacrum anterior. The placenta was mostly located on the anterior uterine wall and completely covered the cervical os. Placenta accreta was ruled out on both ultrasonography and magnetic resonance imaging (). At admission, her temperature was 37.1℃, and laboratory tests revealed a white blood cell (WBC) count of 13.0 × 109 cells/L with 81.4% neutrophils and a C-reactive protein (CRP) level of 1.8 mg/L. Her coagulation profile and liver and renal function tests results were normal.
On the second day following admission, 100 mg of ethacridine lactate was injected into the amniotic cavity to induce labor. Two hours later, UAE was performed by the Seldinger technique (). Four hours following UAE, the patient was found to have a temperature of 41.1℃. Laboratory tests revealed a WBC count of 3.9 × 109 cells/L with 69.2% neutrophils and a CRP level of 28.2 mg/L. She was administered intravenous moxifloxacin at 0.4 g once daily. Her inflammatory marker levels were higher when tested 10 hours following UAE (WBC count, 21.5 × 109 cells/L with 98.1% neutrophils; CRP, 30.8 mg/L; procalcitonin, 48.34 ng/mL; activated partial thromboplastin time, 67.2 s; prothrombin time, 19.8 s; alanine transaminase, 142 U/L; and aspartate transaminase, 251 U/L). Her blood pressure decreased to 75/40 mmHg. She exhibited no evidence of uterine contraction or cervix dilatation. Septic shock was suspected, and an emergency cesarean section was performed to remove the infected tissues. The weight of the fetus was 400 g. Intravenous moxifloxacin (0.4 g once daily) and vancomycin (0.5 g twice daily) were administered for 1 week postoperatively. Both uterine cavity culture and blood cultures revealed Serratia marcescens sensitive to moxifloxacin. The patient was discharged on postoperative day 9, after her temperature and inflammatory markers had normalized.
The present study was approved by the ethics committee of Zhejiang University, and the termination of the pregnancy because of anencephaly was performed according to the Chinese law. The patient provided written informed consent for publication of her information and images.


A 60-year-old male presented with gradually enlarging asymptomatic mass in his right buccal mucosa from the past 3 months []. The asymptomatic lesion was initially peanut-sized which gradually enlarged to the present size of 4 cm × 3.5 cm [], which was well-circumscribed and pedunculated on a broad-based stalk. The overlying mucosa presented with dilated vascular channels. The mass was rubbery in consistency. No lymphadenopathy. The examination of other subsites of oral cavity was normal.
An attempted incomplete surgical excision was done at a dental clinic which aggravated the lesion. He has no compounding medical history or any recent history of trauma to the offending site.
After a through surgical workup and a written consent from the patient for both surgical procedure and for use of the photographs for scientific publication, the lesion was excised with wide surgical margins under local anesthesia under proper aseptic conditions [Figures and ].
Excisional biopsy of the lesion was performed, and the tissue sent for histopathological examination.
Histopathology report revealed the presence of highly cellular connective tissues and numerous dilated, large, and small endothelial lined capillaries. Some blood vessels exhibited characteristic “staghorn pattern” of branching. These vessels were lined by thin endothelial lining and surrounded by cellular areas composed of cells with moderate cytoplasm, round nuclei, and inconspicuous nucleoli. At places, these cellular areas were separated by fibrous septa. The tumor was labeled as benign HPC because of its lack of cellular atypia, absence of mitotic activity, and absence of hemorrhage and necrosis [].


An asymptomatic 20-year-old female visited our institute for treatment of her malaligned teeth []. Her orthopantomogram revealed a unilocular, well-defined radiolucency extending from the right mandibular second molar to condylar and coronoid process involving the entire ramus. Root resorption of mandibular right second molar was present. The lesion had mandibular right third molar located inferiorly toward the lower border of the mandible []. Calcifications were not evident in the radiograph. There was no limitation in temporomandibular joint movements or sensory disturbances in lower lip. The oral examination was also within normal limits []. Mandibular right second molar was nonvital. A differential diagnosis of cystic ameloblastoma, dentigerous cyst, and odontogenic keratocyst was made. The lesion was enucleated with removal of second and third molars through intraoral approach followed by chemical cauterization using carnoy's solution []. The excised lesion [] was sent to Department of Oral Pathology in the same institute for histopathological examination. Closure was performed using silk sutures []. Histopathological report revealed thin odontogenic epithelial lining in some region and luminal proliferation in some region. Tall columnar ameloblast like basal cells were present with hyperchromatic nuclei. Above the basal layer, cells were loosely arranged resembling stellate reticulum. The presence of ghost cell in the cystic lining was noted. Underlying connective tissue showed dentinoid-like material with mature collagen fiber bundles. Ameloblastic follicles and odontogenic islands were present in some regions along with presence of nonkeratinized stratified squamous epithelium [Figure and ]. These features were confirmatory for ameloblastomatous COC. The bone healing is satisfactory [] and there has been no recurrence of the lesion since the past 6 years. Written consent and approval for publication were obtained from the patient.


A 26-year-old female was referred from an outside hospital to our hospital in view of persistent chest pain and abdominal pain for 3 days. The patient was a known for SCD, not on regular medication, last Hydroxyurea was taken a year ago, and last blood transfusion was also done a few years back. The patient was referred in view of hypotension and worsening clinical condition. On examination in the emergency department, she was conscious, afebrile, tachycardic, and hypotensive. Fluid resuscitation was started, appropriate cultures were sent, and broad-spectrum antibiotics started. On arrival to Medical Intensive Care Unit (ICU), she was hemodynamically unstable; bilateral crepitations were present on auscultation. She was started on vasopressors in view of persistent hypotension and connected to noninvasive ventilation (NIV) for respiratory support. Arterial blood gas analysis showed severe metabolic acidosis and laboratory parameters showed grossly deranged renal function test and liver function test (LFT), a likely diagnosis of sickle cell crisis was made.
The patient had persistent anuria and severe metabolic acidosis; hence, the patient was planned for sustained low-efficiency dialysis (SLED). Peripheral smear showed sickle cells, spherocytes, and plenty of nucleated RBCs, which was suggestive of sickle cell crisis and the sickling test was also positive [Figures and ]. Packed RBC (PRBC) transfusion was done to maintain Hb level >10 g%, and Hb electrophoresis was also sent. Liver viral markers, dengue, malaria, leptospira, and scrub typhus tests were negative. The patient had persistent severe chest pain suggestive of acute chest syndrome in spite of PRBC transfusion; hence, she was planned for red cell exchange transfusion during SLED.
During the exchange transfusion, whole blood was removed, which was replaced by PRBC and fresh frozen plasma (FFP) in equal proportion, at the same time of SLED. The patient tolerated the exchange transfusion without any complications and showed good clinical improvement after exchange transfusion. Two more cycles of exchange transfusion were done along with SLED and patient clinical condition further improved. The patient was off vasopressors, off NIV, chest pain had reduced, and LFT and LDH levels started improving. The patient gradually started producing urine and was shifted with to the ward in stable condition with dialysis catheter in situ. In the ward, her renal function improved further and she was discharged home with oral medications.


A 56-year-old woman presented with a several-month history of left upper quadrant discomfort and a poor appetite. Her medical history included laparoscopic cholecystectomy due to chronic cholecystitis performed 3 years previously. Physical examination revealed moderate tenderness in the upper quadrant. Gastroscopy revealed a metal clip in the duodenum (). The clip was about to drop from the duodenum; therefore, we did not remove the clip surgically or gastroscopically. Two months later, gastroscopy revealed that the metal clip had dropped.


A 59-year-old woman who had undergone laparoscopic cholecystectomy 1 year previously was admitted for investigation of a 1-week history of middle upper quadrant pain. Laparoscopic findings revealed an acutely inflamed, thick-walled gallbladder with surrounding pus. The patient’s postoperative course was uneventful. Gastroscopy revealed two metal clips in the duodenum (). The patient went to another institution to undergo duodenotomy. After the operation, she became asymptomatic. Unfortunately, the patient died of depression-induced suicide 3 months after the operation.
This study was approved by the ethics committee of the People’s Hospital of Zhuji. Both patients provided written informed consent.


J.S. (a 54-year-old man) underwent a routine dental extraction in which a 30-gauge needle was used to perform a local injection. This needle broke off at the hub and was lost in the right gingival buccal sulcus. The dentist was unable to remove it and referred J.S. to an oral surgeon at St. Joseph’s Health Care (London, Ontario). A radiopaque foreign body was seen in the right masticator space and ITF on CT. An attempt at removal of the foreign body in the operating room was unsuccessful. A postoperative CT showed the object pushed deeper into the infraorbital fissure (). The patient was subsequently seen by a specialist in the otolaryngology service and described trismus, pain with mastication, intermittent right otalgia, and right cheek numbness. The patient had no visual changes. On examination, the patient had masseter swelling and trismus (2 cm). Results of an examination of the cranial nerve indicated that the nerve was intact except decreased sensation in the V2 distribution.
After careful consideration, the patient and surgeon decided to attempt endoscopic (nasal) extraction by using image guidance assistance. The patient first underwent a right middle turbinate resection, complete ethmoid dissection, and right sphenoidotomy. By using image guidance, the right inferomedial orbital wall was drilled and the periorbita was incised. The infraorbital fat was searched, but the needle was not visible. After this, a right medial maxillectomy was performed. The sphenopalatine artery was ligated. The posterior maxillary wall was then removed and the internal maxillary artery was ligated, after which the fat could be diligently searched. The needle was eventually located in the ITF fat (in the infraorbital fissure) at the junction of the fissure and previously opened orbital wall, and, now that it was found, it was removed intact (). The defect was reconstructed by using Gelfoam (Ethicon, Sommerville NJ, USA) and Tisseel (Baxter, Mississauga, Canada), and was covered with mucosa. After extraction, his symptoms resolved, and recovery was complete.


A 77-year-old woman with no declining of activities of daily living (ADL) was brought to the emergency department by ambulance after being found with severe disturbance of consciousness and fecal incontinence while taking a bedrock bath for around 2 hours. On physical examination, she was in a deep coma with a Glasgow Coma Scale of 3, blood pressure of 93/67 mm Hg, heart rate of 175 beats per minute, regular respiratory rate of 24 breaths per minute, and a tympanic temperature of 40.1°. She had a history of untreated hypertension. A laboratory test revealed increased serum creatinine and creatine kinase at 1.38 mg/dL and 1545 IU/L, respectively. A head CT and MRI scan showed no significant lesion. All other examinations including abdominal ultrasonography, transthoracic echocardiography, lumbar puncture, and EEG disclosed no specific abnormalities. The possibility of epilepsy or encephalitis was negligible.
After detailed examination, we initiated immediate cooling and intensive care including a blood transfusion and mechanical ventilation in the intensive care unit for the treatment of severe heatstroke. Tracheal intubation was performed and a sedative and analgesic were also administered. Despite intensive medical care, her clinical course was severe as shown in Figure A. Her initial SOFA score at hospitalization was 8 and reached a peak of 16 on hospital day 4.
On hospital day 4, severely fluctuating blood pressure was found without certain causes. Her vital signs showed hypertensive crisis without counter-regulation of heart rate, followed by the consecutive circulatory collapse every 2 hours, shown in Figure B. It was similar to “autonomic storm” found in amyotrophic lateral sclerosis, suggesting that limbic system may have been involved. The fluctuating blood pressure probably due to central sympathetic hyperactivity quitted on hospital day 5 without life-threatening events.
On hospital day 5, sedation using midazolam was discontinued. Despite the discontinuation, she remained unconscious for the following 2 days, and her EEG on the day 6 showed very low amplitude (<10 μV, Figure ), suggesting an unfavorable prognosis. (Over 98% of the patients with this type of EEG died.) As per her family’s wishes, treatment was withheld and further attempts at resuscitation were discontinued.
However, contrary to our expectations, the patient responded to intensive supportive care. She gradually recovered consciousness on hospital day 8 and was extubated on hospital day 11 with a Glasgow Coma Scale of 15. Her EEG eventually normalized, and she was discharged. She had no significant neurological sequelae. Mini–Mental State Examination score was 29 at 2 years after discharge.


A 39-year-old woman with disseminated tuberculosis and bilateral solitary choroidal tubercles [Fig. and ] was subjected to multimodal imaging including enhanced depth imaging spectral-domain optical coherence tomography (EDI-OCT), near-infrared reflectance (NIR), and fundus autofluorescence (FAF) imaging. FAF imaging revealed hyperautofluorescent lesion with central hypoautofluorescence [Fig. and ]. NIR imaging revealed hyperreflective lesion with a hyporeflective halo [Fig. and ]. EDI-OCT [Fig. and ] showed lobulated hypo/isoreflective choroidal lesion with loss of vascular pattern and dome-shaped elevation of the overlying retina. Characteristic “increased transmission effect” was seen beneath the lesion. A small cap of subretinal fluid at the apex of lesion was noted in the right eye. Antituberculous therapy resulted in systemic improvement and regression of choroidal tubercles [Figs. and -].


This is a case of a 52-year-old female, with a recent history of panic attack and depression, according to DSM-IV-TR criteria, triggered by a recent retirement. Laboratory and clinical evaluations during the last years had never revealed any pathological findings. At her referral to our department (community mental health service), the patient was suffering from depressed mood most of the day, fatigue, diminished ability to think or concentrate, insomnia, feelings of worthlessness and periods of sweating, chest pain, dizziness and fear of losing control. ESC was administered with an initial dose of 10 mg once a day for a week, and thereafter to 20 mg per day. Three weeks later the patient’s depressive symptoms improved significantly; however she complained about a swelling in both of her feet and she could hardly wear her shoes. The clinical examination revealed a bilateral ankle edema.
Clinical and laboratory evaluations (electrocardiogram, ultrasonography, blood tests, albumins, renal and thyroid function tests, serum electrolytes) did not reveal any pathological findings. There was also no history of arterial hypertension, and after repeated measurements her arterial pressure was within normal range. The patient’s edema resolved completely within ten days after escitalopram discontinuation with no reappearing.


A 4-year-old boy with unremarkable past health presented to a regional hospital with dehydration and tachycardia with history of recent increased fluid intake. Patient was cachexic with multiple café-au-lait spots. Neurological examination was unremarkable. On admission he had high blood pressure. Initial blood test results were nonspecific apart from some electrolyte disturbances. Chest radiograph showed increased cardiothoracic ratio (0.57) with clear lungs. Echocardiogram showed left ventricular hypertrophy with small left ventricular volume, but normal left ventricular systolic function. Pericardial effusion was detected. Bedside ultrasound examination showed absent right kidney. A computed tomography (CT) of brain performed for workup of diabetes insipidus showed brainstem swelling with obstructive hydrocephalus. He was then transferred to the pediatric intensive care unit of our institution, a tertiary referral center.
Urgent magnetic resonance imaging (MRI) of brain and spine [] showed abnormal T1-weighted (T1W) hypointense and T2W hyperintense signal with swelling in medulla oblongata, anterior pons, and bilateral medial cerebellar hemispheres. Neither abnormal contrast enhancement nor restricted diffusion was noted. Swelling in brainstem caused obstructive hydrocephalus. No abnormal signal was seen in bilateral cerebrum. In the spine, there was diffuse swelling of whole spinal cord, most severe in cervical cord. Whole-cord generalized swelling with increase in T2W signal was noted. No abnormally enhancing focal lesion was evident. No evidence of leptomeningeal lesion was seen along the whole thecal sac.
Initial differential diagnoses included inflammatory causes as in longitudinally extensive myelitis such as neuromyelitis optica (NMO) associated with systemic lupus erythematosus (SLE) (presence of pericardial effusion); neoplastic causes including lymphoma or diffusely infiltrative ependymoma. Subsequent laboratory studies revealed negative immune markers, except elevated erythrocyte sedimentation rate, rendering systemic inflammatory conditions, including SLE and NMO unlikely. Cerebrospinal fluid (CSF) analysis also revealed no evidence of infection or oligoconal band. Neoplastic causes were not supported by serum tumor markers, as well as CT scan and metaiodobenzylguanidine scan, in particular for pheochromocytoma.
On CT scan, right renal agenesis was confirmed. Compensatory hypertrophy of left kidney was noted with poor enhancement. The patient had two left renal arteries in which the superior one showed focal narrowing in its proximal segment (0.3 cm in length) sparing ostium. Wedge-shaped renal parenchymal nonenhancement suggestive of infarcts was also noted. Ultrasonography Doppler of renal artery confirmed the diagnosis of renal artery stenosis []. Renal scintiscan study also showed slow uptake and retention of tracer in left kidney, compatible with renal artery stenosis. Focal lack of uptake confirming renal infarct was also evident.
Renal artery stenosis was identified as cause of persistent hypertension. To exclude underlying vasculitis causing renal artery stenosis, positive emission tomography–computed tomography was done, which was negative.
Considering the renal artery stenosis and multiple café-au-lait spots, NF 1 was suspected. Slit-lamp examination showed Lisch nodules in bilateral retina. Diagnosis of NF 1 was established by criteria by National Institutes of Health.[] Radiograph of lower limbs of patient showed anterior bowing of left tibia with cortical thickening, suspected to be NF 1 associated bone lesion []. The patient had no first-degree relative suffering from NF 1.
Patient's hypertension was difficult to control. It required titration of multiple antihypertensive medications. Initially, the patient was dependent on intravenous infusion of labetalol, infusion phentolamine, amlodipine, captopril, hydralazine, frusemide, minoxidil, and aldactone. Blood pressure slowly came down and he was able to take off phentolamine and changed to oral labetalol. Blood pressure was controlled on high side: systolic blood pressure of 140–180 mmHg and diastolic blood pressure 60–80 mmHg. Renal artery angioplasty was considered but not done in the acute setting due to high risk associated with small caliber artery and single kidney status. The plan was to delay the procedure to when the patient is older and bigger, giving a lower risk and higher rate of success in renal angioplasty.
After blood pressure was gradually controlled, serial CT brain scans showed gradual resolution of swelling in brainstem and cerebellum. Obstructive hydrocephalus also resolved. Follow-up MRI [] was performed 6 weeks after the presentation. Abnormal spinal cord swelling and signal changes were resolved. Changes in brainstem and bilateral cerebellar hemispheres also resolved. Only minimal residual swelling of medulla was evident, with no abnormal signal. Hydrocephalus also resolved. The diagnosis of PRES precipitated by hypertensive crisis from NF 1-related renal artery stenosis was postulated. Patient remained clinically stable and was discharged.


A 33-year-old man presented to the emergency department of our regional hospital with left upper quadrant pain after dinner, accompanied by distension and nausea. Computed tomography (CT) revealed a mass near the body of the stomach, which was first considered to be a gastrointestinal stromal tumor (GIST). The patient underwent further evaluation at our hospital 1 week later. The patient did not smoke or drink alcohol. Following admission, his vital signs were stable, and physical examination revealed no organomegaly or palpable lump. His abdominal pain had improved, and no tenderness or rebound phenomenon was present. The results of routine blood and liver function tests were normal, and negative results were obtained for alpha-fetoprotein, carcinoembryonic antigen, and carbohydrate antigen 19-9. The patient had no history of trauma, but he had undergone ocular surgery 9 years previously at a hospital in Shanghai; however, the results of histopathological examination conducted at that time were lost. Re-examination of the abdomen using CT showed a lesion occupying the greater curvature of the stomach; thus, GIST and gastric schwannoma were considered (Fig. ). Endoscopic ultrasonography (EUS) showed a hypoechoic exogenous mass, 4 cm in diameter, which was in contact with the greater curvature of the stomach. No protrusive lesion was found on the gastric wall (Fig. ). The imaging findings strongly suggested a GIST.
Subsequently, robot-assisted laparoscopic abdominal mass resection was performed; we found a 3 × 4-cm cystic mass between the posterior gastric wall and the pancreas, and removed it by radical excision (Fig. ). Melanin pigmentation was observed in the neoplastic cells (Fig. A), and immunohistochemistry revealed that the tumor cells were positive for HMB-45 (Fig. B), S-100 protein (Fig. C), and the melanocyte/melanoma tumor antigen melan A (Fig. D), which supported the diagnosis of malignant melanoma. However, solitary primary abdominal melanoma is a rare entity, and no such case has been reported in the literature. Bearing in mind the histopathological results and the complexity of the clinical case, we carefully reviewed the patient's medical history again. As the patient had undergone ocular surgery 9 years previously, we urged his family to consult the pathological results from this surgery, which revealed primary choroidal melanoma. A definitive diagnosis of solitary abdominal metastatic melanoma from uveal melanoma (UM) was finally made. To exclude the possibility of other metastasis, the patient underwent thorough postoperative dermatologic and ophthalmologic examinations, including ophthalmoscopy and positron emission tomography/CT of the whole body; no suspicious lesion was found at any other site. The postoperative period was uneventful and the patient was discharged 6 days later. The patient was followed-up for nearly 3 years, and appeared to be in good condition. The study was approved by the Ethical Committee of the First Affiliated Hospital, College of Medicine, Zhejiang University and written informed consent was obtained from the patient prior to the publication of the present study.


An 8-year-old male child who was operated for meningomyelocele presented to our department on June 6, 2017. The child had a history of urinary incontinence for the last 2 years and severe constipation since the time of surgery. Clinical examination of the child revealed a severe symptomatic anemia, multiple scars in lumbosacral area, insensate urethra, and a loaded rectum. The child had a weight of 19 kg, height of 147 cm, and blood pressure of 100/50 mm/hg. Baseline laboratory investigations revealed hemoglobin of 6.6 g/dl; serum urea of 140 mg/dl; serum creatinine of 3.74 mg/dl; 24-h urinary protein of 0.1 g/l; and normal serum calcium, magnesium, electrolytes, and arterial blood gas analysis. Ultrasound abdomen revealed bilateral Grade III hydroureteronephrosis with thick-walled trabeculated bladder. Micturating cystourethrography showed small capacity trabeculated bladder, oblong in shape with no reflux. A urodynamics and uroflowmetry were done. The child was diagnosed as a case of neurogenic bladder with chronic kidney disease (CKD).
The child was catheterized. Nephrology consultation was sought, and the advice was followed. The child was planned for augmentation cystoplasty and Mitrofanoff procedure using appendix. After proper optimization, an augmentation colocystoplasty with a bladder drainage procedure was done on June 11, 2017. The child behaved well till 12th postoperative day while still being in the hospital he started having rapid onset of symptoms such as headache, seizures, altered consciousness, and visual disturbances. Pediatric medicine consultation was sought suspecting metabolic derangement which usually follows a colocystoplasty. The child's metabolic profile was normal which ruled out a metabolic cause. A cerebrospinal fluid examination was done to rule out an infective cause. The child was not on any specific drugs responsible for the above clinical picture. The child was diagnosed as having hypertensive encephalopathy with seizures. Magnetic resonance imaging (MRI) brain was done which showed features of PRES []. The child was managed as PRES with labetalol infusion, intravenous phenytoin, and mannitol on pediatric medicine side for 7 days. The child was shifted back to pediatric surgery on June 30, 2017, on oral antihypertensives with a controlled blood pressure. The child was discharged on July 1, 2017, on oral antihypertensives, and a clean intermittent self-catheterization program was started. Nephrology follow-up was advised. Strict monitoring of blood pressure was advised on discharge.