A 74-year-old man presented with obstructive jaundice and appetite loss. Computed tomography showed unresectable pancreatic head cancer. Duodenoscopy revealed that the duodenum was obstructed by tumor from just anal side of the papilla to the third portion about 2 cm, so both biliary and duodenal stents were necessary for symptom palliation (). The endoscope (GIF-2T240; Olympus, Tokyo, Japan) was advanced into the duodenum and duodenography showed severe stenosis in the horizontal portion of the duodenum. A 0.035-inch guidewire (Revowave; Piolax Medical Devices, Kanagawa, Japan) was passed through the stenosis under endoscopic and fluoroscopic guidance. An uncovered expandable metal stent (WallFlex Duodenal; Boston Scientific, Natick, MA, USA) was advanced over the guidewire through the endoscopic channel and released under endoscopic and fluoroscopic guidance (). Immediately after stent placement, duodenography showed contrast fluid passing through the stent smoothly. However we could not identify the orifice of the papilla through the endoscope and perform transpapillary stenting. Then the endoscope was withdrawn and a curvilinear array echoendoscope (GF-UCT240; Olympus, Tokyo, Japan) was advanced into the duodenum. The dilated extrahepatic bile-duct was punctured at the bulb of the duodenum with a 19-gauge needle (Echotip Ultra; Cook Medical, Winston-Salem, NC, USA) and contrast was instilled through the needle under fluoroscopic guidance to confirm successful biliary access. A 0.035-inch guidewire (Revowave; Piolax Medical Devices) was introduced through the needle and advanced into the intrahepatic duct. After removing the needle, the puncture channel was expanded with 7 Fr biliary dilator catheters and a 4-mm balloon catheter. Then, a 7 Fr straight plastic stent (Flexima; Boston Scientific) was placed over the guidewire (). The patient could tolerate a regular solid diet after the procedure and 7 Fr plastic stent was electively replaced with 8.5 Fr plastic stent (Flexima; Boston Scientific) using Soehendra stent retriever without complications 32 days after EUS-CDS. After the replacement, stent occlusion did not occur.


A 63-year-old man underwent covered SEMS placement for malignant biliary obstruction due to pancreatic head cancer on December 2008. He had been suffering from recurrent cholangitis without stent occlusion and SEMS was replaced with two plastic stents on January 2009. He presented with appetite loss and vomiting on March 2009. Duodenography revealed severe duodenal stenosis from the oral side of the papilla to the third portion due to tumor invasion about 2 cm (). Furthermore, the papilla was involved with tumor, so the duodenal metal stent placement would blocked the papilla. Therefore, we needed to perform EUS-CDS instead of transpapillary stenting. After removal of biliary plastic stents with snare, a curvilinear array echoendoscope (GF-UCT240; Olympus) was advanced to the duodenal bulb. From the bulb of the duodenum, we punctured the bile duct with 19-gauge needle, which was not dilated due to previous biliary stent. A 0.035-inch guidewire (Jagwire; Boston Scientific) was advanced into the intrahepatic duct through the needle. After removing the needle, the puncture channel was expanded with 7 Fr biliary dilator catheters and a 4-mm balloon catheter. Then, a 7 Fr straight plastic stent (Flexima) was inserted over the guidewire (). Then, a covered expandable metal stent (ComVi; Taewoong Medical, Seoul, Korea) was placed through the endoscopic channel across the duodenal stenosis (). The patient could eat a solid diet and the stent remained patent within 111 days until the patient died.


A 1-year-old male child presented with a discharging sinus over the right hemiscrotum since the age of 3 months []. The child had a history of scrotal abscess, which got burst spontaneously, followed by intermittent episodes of pus discharge. The right spermatic cord was thickened and tender. An impulse on cry was present suggestive of inguinal hernia. The sinus could not be cannulated. The ultrasound of the right inguinoscrotal area revealed bowel herniation. A diagnosis of inguinal hernia with some bizarre congenital fistula was made. On inguinal exploration, there was a sliding hernia with cecum and appendix herniating into the sac. Grossly the appendix appeared to be edematous. It was densely adherent to the scarred sinus in the upper scrotum []. The right testis was slightly bulky and spermatic cord was thickened. The appendix adherent to the scrotal sinus was dissected. Appendicectomy followed by herniotomy was done. The postoperative period was uneventful and the child is asymptomatic at 1-year followup. Histopathology of the appendix revealed acute inflammation.


A 2-year-old boy presented with recurrent episodes of abdominal pain with distension, bilious vomiting and fever for 3 weeks. He weighed 8 kg and had a history of failure to thrive since early infancy. He was a known case of ventricular septal defect (VSD) and was on digoxin. He was dehydrated and lethargic with a pansystolic cardiac murmur. The abdomen was mildly distended with a nontender hepatomegaly. The chest radiograph was normal. The abdominal radiograph showed a prominent gas shadow in the upper half of the abdomen that was initially mistaken for a dilated colonic shadow by the treating physician. []. An ultrasonography suggested dilated large bowel loops that were peristalsing and moderate free fluid. He had a hemoglobin of 14.1 gm% and total leucocyte count of 9800/mm3 with blood urea 89 mg/dL and serum creatinine of 1.3 mg/dL. The 2D-echo revealed situs solitus with levocardia and a small 3 mm peri membranous VSD. The child was kept nil per oral and the fluid and electrolyte imbalance corrected. Due to persistent bilious aspirates, an upper gastrointestinal (GI) contrast study was performed that suggested malrotation with volvulus and situs inversus []. The abdomen was explored through an upper abdominal transverse incision. The stomach and duodenum were in mirror image position with gross distension up to the third part of the duodenum. There was a single 360° counterclockwise torsion at the base of the mesentery. The entire small bowel was healthy but enclosed in a thin transparent sac containing jelly-like material in the left half of the abdomen []. The ascending and transverse colon were posterior to the duodenum. The liver was slightly medially positioned. Multiple splenunculi (five in number) of variable sizes, were seen in the right upper quadrant related to the greater curvature of the stomach []. The bowel was derotated after excising thick Ladd's bands, sac excised and inversion appendectomy performed. The superior mesenteric vessels were seen to lie more toward the posterior aspect of the mesentery after the procedure. The child recovered uneventfully and was discharged on sixth postoperative day. At 2 years follow up, he is asymptomatic and thriving well.


The patient was a 27 year old female who was married for 5 years. She was a case of secondary infertility with previous one spontaneous abortion at 8 weeks. It was a natural conception. The patient had undergone intrauterine insemination (IUI) seven times previously.
The patient was investigated for secondary infertility. Husband's semen analysis revealed severe oligospermia. She was advised IVF/ICSI in view of male factor and previous failed IUI attempts. The patient underwent a gonadotropin with antagonist protocol. Recombinant Follicle Stimulating Hormone was given (total units 1275 IU). Fixed antagonist protocol starting from fifth day of stimulation was given. Trigger was given with recombinant human chorionic gonadotropin (HCG) 250 mcg on Day 9. Oocyte retrieval was done under general anesthesia on Day 11 of cycle. Five oocytes were retrieved.
Out of the five oocytes, three fertilized. Day 3 embryo transfer (ET) was done (Day 14 of cycle). One embryo was 6 cellar Grade 1, second one was 4 cellar Grade 1, and third one was 6 cellar Grade 2. Embryos were placed 1.1 cm away from fundus under ultrasound guidance with K-soft 1000(Cook) (William A. Cook Australia Pty. Ltd, Brisbane, Australia) embryo transfer catheter.
Urine pregnancy test on Day 19 after ET showed a positive result. Serum beta HCG on Day 24 after ET was 1270.93 mIU/mL. So, transvaginal sonography (TVS) was advised, which did not reveal any intrauterine or extra uterine gestational sac (GS).
Repeat serum beta HCG after 48 h (Day 26 after ET) was raised to 3495.99 mIU/mL. TVS revealed an empty uterus with endometrial thickness of 11.5 mm. A well-defined GS was seen in right ovary with good decidual reaction and a yolk sac. The GS size was 7.1 mm × 6.2 mm × 6.8 mm. There was no free fluid in the pelvis. The patient was diagnosed as a case of unruptured ovarian pregnancy [Figures and ].
Thorough counseling of the couple regarding different treatment options was done. The couple opted for conservative medical management. She weighed 57 kg and was hemodynamically stable. The pulse was 82/min and blood pressure was 110/70 mmHg. The patient was given inj. methotrexate 50 mg, i.e., 50 mg/m2, under supervision. Pulse and blood pressure was monitored. There were no signs of methotrexate toxicity.
Repeat serum beta HCG on Day 3 after methotrexate (Day 1 being the day of methotrexate administration) was found to be raised to 5147.97 mIU/mL.
Repeat TVS revealed intact GS with fetal pole and good cardiac activity. There was minimal free fluid in the pelvis. The couple was counseled and the decision for laparoscopic surgery was taken.
There was collection of blood, approximately 200 mL, in the peritoneal cavity. Left ovary and left fallopian tube were normal. Right ovarian fossa was filled with blood clots. Right ovary was stuck to the right ovarian fossa. Clots were separated and ovary was separated from the ovarian fossa. Right ovary revealed an intact ectopic pregnancy, which started bleeding after separation from ovarian fossa. The ovary was held with grasping forceps and a wedge resection of right ovary along with the ectopic pregnancy was done using harmonic current. Remaining ovarian tissue was observed for hemostasis. GS with part of ovary (specimen) was sent for histopathological examination [].
Postoperatively, the patient was stable. She was discharged on Day 2 of surgery.
Histopathology revealed ectopic products of conception. Ovarian tissue was seen with the products of conception. Rest of ovarian tissue showed luteal changes.


A 50 year old male presented with abnormal movements in the form of jerky movements of all four limbs associated with tongue bite and urinary incontinence. These abnormal movements were episodic and each episode lasted for 3-4 minutes and was followed by clouding of consciousness for few minutes. The patient started to experience these seizure episodes when he was 25 years of age, the frequency of seizures was initially one to two episodes in 5-6 months. But since last one month the frequency had markedly increased and patient was having convulsions on almost daily basis. Patient was prescribed phenytoin tablets by local practitioner in dose of 300 mg/day but the seizures were not controlled. Patient also developed tremors of both the hands since last 2 months, tremors were more in the left hand as compared to right and they were more prominent at rest.
On examination there was painful spasm of hand on inflating sphygmomanometer cuff above systolic blood pressure (i.e. Trousseau's sign was positive), he was fully conscious well oriented, appearance and behavior were normal, there were no hallucination and delusions and his memory and speech were normal, all the cranial nerves were intact, coarse pill rolling type of tremors were present at rest in both the hands but more in left hand as compared to right hand. Cog wheel rigidity was present in both the upper limbs, power was normal in all four limbs and sensations were intact.
No scar on the neck to suggest any previous neck surgery was seen, there was no candidiasis or vitiligo neither there was any hearing loss. However cataracts were present in both the eyes.
On investigation his haemoglobin was 13.2 gm/dl, total leucocyte count 9400/μL, differential leucocyte count showed 76% neutrophils and 24% lymphocytes. Blood sugar 90 mg%, blood urea 27 mg% and serum creatinine 0.8 mg%. Alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase and serum bilirubin were all with in normal range. His serum albumin was 4.0 gm/dl. Serum electrolytes were sodium 136 meq/L, potassium 4.2 meq/L, calcium 6.11 mg/dl (normal range 8.0-10.4 mg/dl), ionized calcium 3.0 mg/dl (normal range 4.6-5.4 mg/dl), serum phosphate 5.7 mg/dl (normal range 2.5-4.5 mg/ dl) and serum magnesium was 2.12 mg/dl (normal range 1.3-2.5 mg/dl). His parathormone level was 3.6 pg/ml (normal range 15-68 pg/ml). CT scan of the brain revealed bilaterally symmetrical hyperdense lesions with CT value of calcification in basal ganglia, thalami, white matter of cerebellar hemispheres and subcortical white matter of bilateral frontal and parietal lobes [Figures and ].
On the basis of seizures, extrapyramidal features, bilateral cataracts, positive Trousseau's sign, hypocalcemia, high phosphate levels and low PTH levels our patient was diagnosed as a case of hypoparathyroidism with extrapyramidal features and seizures due to hypocalcemia.
Calcitriol 0.5 μg/day and calcium 1 gm/day was started. Patient's calcium levels returned to normal range with this treatment. Although antiepileptic drugs were not indicated in this patient but we put him on sodium valproate 500 mg twice daily with the aim to withdraw the drug slowly, this was done as the patient was taking phenytoin tablets for a very long duration. With the normalization of serum calcium patient became seizure free and the parkinsonian features (tremors and cog wheel rigidity) also improved remarkably, patient was not prescribed any anti-parkinsonian drug for control of extrapyramidal features. Patient is in follow up for the last four months and did not have even a single seizure episode.


A 42-year-old man with no past significant medical illness presented with headache. CT scan done showed subarachnoid hemorrhage (SAH) predominantly in the perimesencephalic cisterns []. Magnetic resonance imaging T1 gradient sequence also showed the hypointense signal suggestive of blood products in the perimesencephalic cisterns []. Fetal posterior cerebral arteries are seen on both the sides arising from the internal carotid artery [Figures and ]. DSA (digital subtraction angiogram) done subsequently revealed fusiform bulbous dilation involving both the cisternal and cortical segments of the left SCA []. Endovascular treatment in the form of parent artery occlusion was done under general anesthesia, with complete exclusion of the aneurysm from the circulation as seen on post-coiling angiogram []. Standard heparin protocol was followed and activated clotting time greater than 250 s was maintained during the procedure. Six-French (6F) Envoy (cordis) guiding catheter was placed in the distal vertebral artery. A combination of echelon-10 microcatheter (ev3) and transcend 0.014 microwire (Stryker) were used to access the aneurysms. Multiple Axium (ev3) coils were used to occlude the aneurysm. There were no intra- and periprocedural complications and patient was discharged on the 5th day after operation. The post-operative course was uneventful. The patient's neurological examination after 1 month was completely normal. Control angiogram done after 1 year showed stable occlusion of the aneurysm with endovascular coil in place [].


A 50-year-old lady, who had a history of hypertension, presented with severe headache and ataxia. CT scan done at admission showed acute right cerebellar hematoma []. DSA done subsequently revealed fusiform aneurysm of the cisternal segment of the SCA []. Endovascular treatment was done under general anesthesia with inside out coiling of the aneurysm with platinum coils []. Standard heparin protocol was followed and an activated clotting time greater than 250 s was maintained during the procedure. 5F Envoy (cordis) guiding catheter was placed in the distal vertebral artery. A combination of echelon-10 micro-catheter (ev3) and transcend 0.014 micro-wire (Stryker) were used to access the aneurysms and multiple axiom (ev3) coils were used to occlude the aneurysm. Post-coiling angiogram showed complete exclusion of the aneurysm from the circulation. The post-operative period was uneventful. The patient's neurological examination done after 1 month was completely normal. Control angiogram done at the end of 1 year showed stable occlusion with no re-canalization of the aneurysm [].


A 64-year-old man, who had a history of hypertension, presented with headache and vomiting. CT scan showed SAH in the superior cerebellar cisterns []. DSA done revealed a fusiform aneurysm of the distal SCA, predominantly involving the branch of the cortical segment [Figures and ]. Standard heparin protocol was followed and an activated clotting time greater than 250 s was maintained during the procedure. 5F Envoy (cordis) guiding catheter was inserted in the distal vertebral artery. The aneurysm was accessed with a combination of micro-catheter (echelon-10) and micro-wire (traxcess12). Meticulous pre-shaping of the micro-catheter according to the shape of the target aneurysm aided in proper positioning of the micro-catheter in the aneurysm which was subsequently packed densely with the platinum micro-coils. Post-procedure angiogram showed complete exclusion of the aneurysm along with the branch of the cortical segment and preservation of the flow in the superior cerebellar artery (SCA) []. There were no untoward events in the post-procedure hospital stay and patient was discharged after 1 week. No neurological deficit was seen during the clinical follow-up after 1 month. Control angiogram carried out after 1 year showed stable occlusion of the aneurysm with preservation of the ante-grade flow in the SCA [].


A 64-year-old African American female was referred to our center with a complaint of new bilateral palpable breast masses and a reported history of diffuse increasing bilateral breast densities on the mammogram taken at another center. She denied skin changes, nipple discharge, or other breast problems. The patient denied family history of breast or ovarian cancer and had no history of trauma to her breasts. Her past medical history included hypothyroidism and hypertension. Physical exam was remarkable for multiple palpable masses throughout both breasts with no overlying skin or nipple changes. No axillary, supraclavicular, or cervical lymphadenopathy was noted bilaterally.
The patient presented to our Breast Imaging Department with printed copies of her digital bilateral mammogram images which were taken at an outside facility on 11/11/2011. Bilateral mediolateral oblique (MLO) and craniocaudal (CC) views were reviewed and demonstrated multiple new irregular spiculated masses within all quadrants of both breasts most prominent in the right upper outer quadrant and the left lower inner quadrant []. There were triangle skin markers denoting the areas of palpable abnormality in the patient and these corresponded to the areas of greatest increase in density. These mammograms were compared to her prior images which were dated 06/01/2010, also from an outside facility []. Additional compression views of the irregular masses in the right lower outer quadrant and the left lower central breast demonstrated that the irregular masses persisted. Further evaluation with bilateral breast ultrasound was recommended to evaluate the new masses.
Ultrasound examination of both breasts was performed utilizing a 12 MHz transducer (Toshiba Alplio MX, Japan). Ultrasound of the bilateral breasts demonstrated multiple hypoechoic, taller than wide irregular masses with angular margins throughout both breasts at nearly every clock position []. These masses correlated with the mammographic findings. Normal axillary lymph nodes were present bilaterally.
The mammographic and ultrasound findings were suggestive of malignancy, and the patient subsequently underwent bilateral ultrasound guided core biopsy using a 14 gauge Achieve biopsy device (Cardinal Health, McGraw Park, IL) of the most suspicious appearing masses bilaterally at 6:00 and 11:00 o’clock position in the left breast and at 6:00 and 12:00 o’clock positions in the right breast. Pathology results of the left breast lesion at the 6:00 o’clock position showed invasive lobular carcinoma Nottingham combined histologic Grade II/III moderately differentiated []. Estrogen and progesterone receptors were positive, and HER2 was unamplified. There was an additional finding of granulomatous inflammation consistent with sarcoid. Pathology results of the left breast at the 11:00 o’clock and right breast at 6:00 and 12:00 o’clock positions all showed granulomatous inflammation consistent with sarcoid. Auramine rhodamine and Grocott's methenamine silver stains were negative for acid-fast bacteria and fungus at all four biopsy sites.
Breast MRI (Magnetom Verio 3T, In vivo Breast Coil, Siemens, Germany) was performed with intravenous contrast to evaluate the extent of disease. The MRI demonstrated patchy areas of non-mass enhancement throughout all quadrants of both breasts []. The patient's known invasive lobular carcinoma in the left breast at the 6:00 o’clock position was indistinguishable from the known sarcoid lesions []. No abnormal lymph nodes were identified by MRI.
The patient underwent CT (Lightspeed, GE Healthcare, UK) of the chest to evaluate for sequela of sarcoid which revealed upper lobe predominant perihilar ground glass opacities with mild bronchiectasis consistent with sarcoidosis. On CT of the abdomen and pelvis, multiple soft tissue nodules of the omentum, left flank, and gluteal regions were noted which were all subsequently biopsy-proven to be granulomas consistent with sarcoid.
The patient initially desired breast conserving therapy and was treated with left partial mastectomy and sentinel lymph node biopsy. Surgical pathology revealed the presence of a 4.5 cm invasive lobular carcinoma of the left breast with ductal carcinoma in situ nuclear Grade II/III (intermediate) and lobular carcinoma in situ. The margins were involved by invasive lobular carcinoma. The sentinel lymph node biopsy revealed metastatic carcinoma. There was also extensive involvement of the breast tissue by sarcoid granulomas.
Given the margin positivity, extent of the cancer, the complexity of the mammographic, sonographic, and MRI imaging, and the need for treatment with steroids as well as adjuvant chemotherapy, the patient ultimately underwent a completion mastectomy with complete axillary lymph node dissection on the left side. The patient also underwent a right prophylactic mastectomy. Final staging was T2 N2 (5/13 lymph nodes positive). The patient's treatment plan for adjuvant therapy included cytotoxic chemotherapy, post mastectomy radiation, and endocrine therapy.


A 70-year-old man with history of calcified, rheumatic aortic stenosis who underwent aortic valve replacement 16 years ago (31-mm St. Jude Medical bi-leaflet mechanical valve prosthesis) developed severe shortness of breath in the last weeks. Additionally, he reported gastroenteritis few weeks ago. Clinical examination on admission showed orthopnoea, tachypnoea, tachycardia, and hypotension. Cardiac auscultation revealed systolic murmur and absence of the metallic click sound. The chest X-ray demonstrated enlargement of the heart [], and the echocardiography revealed dilation of the left ventricle and reduced contractility with an ejection fraction of 15%. Flow velocity over the prosthetic valve was 4 m/s in combination with severe regurgitation into the left ventricle. The International Normalized Ratio (INR) at admission was 2.3.
The patient underwent emergency reoperation immediately. The mechanical aortic prosthesis showed complete immobilization of both leaflets due to thrombotic material located in both sides of the leaflets pivots [Figures and ]. The mechanical valve was removed and a bio-prosthesis was implanted. Postoperative recovery was uneventful. Thrombotic material was sent for microbiological examination and there were no bacteria.


A 22-year-old primigravida weighing 46 kg, known case of Eisenmenger's syndrome at 37 weeks of gestation, was scheduled for an elective caesarean section. At the age of 15 years, a cardiac catheterization was performed, which revealed a large mid-muscular VSD with severe pulmonary arterial hypertension (120/50 mmHg). She was explained about the existing cardiac condition and advised to avoid strenuous work.
Pre-operatively, apart from exertional dyspnoea (grade II), she was asymptomatic. Physical examination revealed grade II clubbing, pulse rate of 92/min, blood pressure of 130/90 mmHg and room air oxygen saturation (SpO2) of 90–92% with no rise in jugular venous pressure (JVP). No peripheral oedema or cyanosis was observed. Her lungs were clear to auscultate and cardiac examination showed regular rate and rhythm with loud P2 and pansystolic murmur over the lower left sternal border. Electrocardiography showed right axis deviation with right ventricular hypertrophy. Two-dimensional echocardiography (2D Echo) with colour Doppler revealed a large muscular VSD (19 mm × 20 mm) with a bidirectional shunt and a good left ventricular function with ejection fraction of 58% with severe pulmonary hypertension. Her haemoglobin was 12.6 g%, with a haematocrit of 40% and platelet count of 1,50,000/mm3. Arterial blood gas (ABG) on room air was pH-7.32, PaCO2-35 mmHg, PaO2-59 mmHg, and SaO2-91%. Cardiologist opinion was taken and she was advised to undergo elective caesarean section.
She was pre-medicated with Ranitidine 150 mg orally the night before surgery. Infective endocarditis prophylaxis was given. In the operation theatre, standard monitors, an arterial line and a central venous catheter were placed. Prophylactic dopamine infusion 10 μg/kg/min was started to maintain the systemic vascular resistance (SVR). After 3 min of pre-oxygenation, SpO2 increased to 100%. The pre-induction blood pressure (BP) and central venous pressure (CVP) were 130/90 mmHg and 10 mmHg, respectively. Intravenous induction was carried out with a low dose of thiopentone sodium 150 mg and fentanyl 50 μg titrated to anaesthetic and haemodynamic effects. The patient was intubated endotracheally with suxamethonium 50 mg. Anaesthesia was maintained with 50% oxygen and 0.5% halothane in air and neuromuscular blockade was achieved with vecuronium 5 mg. The end tidal carbon dioxide (EtCO2) was maintained between 32 and 35 mmHg.
A live female baby with Apgar score of 5 at 1 min and 8 at 5 min, weighing 1.9 kg, was extracted. Intravenous infusion of oxytocin 15 units was administered slowly over 30 min. Intraoperative analgesia was obtained with morphine 6 mg i.v. Blood loss was estimated to be about 500 mL. The patient remained haemodynamically stable throughout the procedure, which lasted for 45 min. Low-molecular weight heparin (LMWH) 5000 IU was given subcutaneously towards the end of the surgery. Neuromuscular blockade was reversed with neostigmine 2.5 mg and glycopyrrolate 0.5 mg and the patient was extubated and shifted to the post-operative ward with oxygen by mask for observation. Post-operatively, the patient was haemodynamically stable and dopamine was tapered off. Anticoagulation with heparin and analgesia with morphine 4 mg i.v. 8th hourly were continued for the next 1 week. Perioperatively, CVP was used as a guide to administer i.v. fluids and was maintained around 10 cm of H2O. Volume overload was avoided as it could easily precipitate right ventricular failure in these cases.[]
On the third post-operative day, she was found to have cyanosis with tachycardia, tachypnoea and hypotension (90/60 mmHg) with SpO2 of 75% despite supplemental oxygen. Her ABG revealed pH-7.42, PaCO2-32 mmHg, PaO2-45 mmHg and SaO2-72%. Dopamine was restarted at 10 μg/kg/min to maintain the systolic BP above 100 mmHg. SpO2 remained between 75% and 80% despite oxygen therapy. She improved gradually over a period of 3 days and dopamine was tapered off. She was discharged on the 15th post-operative day.


A 14-yr-old girl complained of nasal blockage accompanied by yellowish mucopurulent rhinorrhea. No history of asthma, other allergic diseases, or medical or surgical treatment was identified. No potential risk factors such as diabetes mellitus, immunodeficiency, or previous facial trauma were found. Laboratory investigations revealed a white blood cell count of 15,600/mm3 with 3.7% eosinophils and a high level of serum IgE, 149 IU/mL (0-100 IU/mL). The results of the multiple antigen simultaneous test (MAST) for specific serum IgE antibodies against Aspergillus, Penicillium, Cladosporium, and Alternaria were negative. The results of the Uni-CAP system (Pharmacia, Sweden) for specific serum IgE antibodies against Aspergillus fumigatus, Cladosporium herbarum, and Alternaria tenuis were in the normal range. A non-enhanced computed tomography (CT) scan of the ostiomeatal unit revealed soft-tissue opacification in the right frontal, ethmoid, and maxillary sinuses (). Bony remodeling and destruction was found in the right lamina papyracea. Endonasal endoscopic surgery was undertaken. Mucosal swelling and polyposis were found in the right middle meatus, maxillary sinus, ethmoid sinus, and frontal sinus, which encroached on the right lamina papyracea. The frontal recess was filled with mucoid secretions, which were collected for histological and microbiological investigations. Histological examination of the material obtained from the frontal recess showed allergic mucin, characterizing Charcot-Leyden crystals, numerous eosinophils, and a few septate fungal hyphae ().
The material was plated onto PDA plates and incubated at room temperature, 30℃, and 37℃. Growth of a white, densely woolly mold with a yellow-to-brown reverse was observed after 3 days at all temperatures (). The fungus was sensitive to cycloheximide (400 µg/mL) and produced a tart and disagreeable smell, particularly at 37℃. Microscopic examination of the mycelia showed no conidia or sporangiospores, but revealed both narrow and wide hyphal filaments, which were hyaline, septate, branched hyphae without clamp connections and spicules (). Macroscopic examination did not reveal structures such as fruiting bodies even after 2 months of culture.
The ITS and D1/D2 regions of the 26S ribosomal DNA was sequenced. The ITS region (including the 5.8S rRNA gene) and the 26S rRNA gene D1/D2 domains were amplified with the following primer pairs: pITS-F (5'-GTCGTAACAAGGTTAACCTGCGG-3') and pITS-R (5'-TCCTCCGCTTATTGATATGC-3'), and NL1 (5'-GCATATCAATAAGCGGAGGAAAAG-3') and NL4 (5'-GGTCCGTGTTTCAAGACGG-3') []. The fungus was identified (Basic Local Alignment Search Tool, ) as S. commune (accession number HM595605.1) with 100% homology. The patient was given oral corticosteroids and antibiotics for 1 week after surgery. Topical nasal steroids were administered to suppress the immune response and minimize recurrence. The patient has been followed up for 3 months and shows no signs of recurrence, except mild mucosal swelling.


A 42 year old male patient with a complaint of intermittent abdominal pain lasting for 5-7 days presented to the Internal Medicine Outpatient Clinic of Ankara Education and Research Hospital in August 2010. He did not have any other complaint or history of any disease. He was not smoking. On physical examination, he was alert and oriented with a temperature of 36.8°C, a pulse of 82 bpm and a blood pressure of 120/60 mmHg. Cardiac exam was normal with regular heart rate and rhythm, normal heart sounds and no murmurs. Physical examination was unremarkable other than mild generalized tenderness. Laboratory data included a hemoglobin of 13.3 g/dl (normal range: 11.7-15.5), white blood count of 10,500 cells/mm3 (normal range: 4.5-11) and platelets of 131,000 cells/mm3 (normal range: 150-450). Biochemical tests were all within normal limits except a slight elevation in aminotransferases (aspartate aminotransferase: 54 U/L (normal range: 0-35), alanine aminotransferase: 57 U/L (normal range: 0-35)). Chest X ray film did not show any acute process and electrocardiogram showed normal sinus rhythm and no ST and T wave changes. Abdominal ultrasonography (USG) revealed portal vein thrombosis. In order to ascertain the hematological status of the patient, a blood sample was withdrawn to determine thrombophilic parameters.
After the patient was accepted in our clinic, treatment was commenced with low molecular weight heparin (enoxaparin, 0.4 cc, once a day). On the eighth day of his admission, abdominal pain worsened and abdominal defence was detected. A new USG was done and all branches of the portal vein, inferior mesenteric vein and proximal part of splenic vein were found to be thrombotic. Moreover, necrosis was seen in some parts the small bowel. The patient was transferred to the surgery department for an emergent operation. During the operation, small bowel resection, 250 cm from the ligament of Treitz, was performed. Cholecystectomy was also conducted as gallbladder was distended and necrosed. After the operation, the patient did not experience short bowel syndrome, his status stayed stable and his abdominal pain subsided.
There was no abnormality in the plasma sent to the laboratory before the operation. The thrombophilic parameters on admission are presented in . Extensive laboratory workup for thrombophilia including measurements of factor V Leiden, factor VR2, prothrombin G20210A and lupus anticoagulants showed no abnormality. However, the patient was found to be heterozygous for the MTFHR gene both in C677T and A1298C alleles.
In order to exclude any malignancy or IBD, colonoscopy was performed and caecum was reached. In the regions of rectum, rectosigmoid junction, descending colon, splenic flexure, and approximately through the middle of transverse colon, hyperemic fragile, oedematous mucosa and decreased vascular pattern were observed. There were several pseudopolyps, especially in descending colon section. The mucosa after the middle of transverse colon was normal. These findings revealed UC. While the patient had chronic portal vein thrombosis and had been operated because of acute splenic and mesenteric venous thrombosis, subcutaneous enoxaparin (0.6 cc, twice a day) and oral warfarin treatment (2.5 mg, once a day) were started. After three days, according to suitable international normalized ratio (INR) levels, enoxaparin was stopped and warfarin dose was adjusted to 5 mg. Meselamine (500 mg, three times a day) was also prescribed. He was discharged home in a stable condition on meselamine and warfarin.


A 56-year-old Malay man with chronic hepatitis B, not on regular follow-up, who first presented to a private medical center with abdominal distension in July 2010, was diagnosed with hepatocellular carcinoma and referred to our institute for further management.
At our institute, a dynamic CT scan of the liver revealed five hypervascular lesions at segments IVa, VII and VIII in the background of cirrhosis. The largest lesion at segment IVa, measured 4.3 × 3.5 cm and associated splenomegaly and esophageal varices but no ascites was observed ().
Local treatment of the multicentric HCC using RFA was planned in agreement with the patient. During the pre-procedural assessment, the patient was incidentally found to have a small ventricular septal defect with left to right shunting. However, the chamber sizes and left ventricular ejection fraction were normal.
At the time of treatment, he had Child Class A compensated liver disease with the following laboratory test results: serum albumin, 32 g/L; serum bilirubin, 21 µmol/L; alanine aminotransferase (ALT), 45 IU/L; aspartate aminotransferase (AST), 54 IU/L; platelet count, 61 × 109/L; International Normalised Ratio, 1.2; and alpha fetoprotein (AFP), 23.8 ng/mL.
The procedure was performed under general anesthesia and fluoroscopic CT guidance (Somatom Definition AS, Siemens Medical Solutions, Erlangen, Germany) using a 10 cm long expandable 15 G StarBurst XL radiofrequency (RF) needle (RITA Medical System, Mountain View, CA, USA) with an array diameter of 5 cm. The RF current generator used was the 1500X RF generator system (RITA Medical System, Mountain View, CA, USA). Four grounding pads were placed on the patient's thighs. The patient's pulse-oximetry, arterial blood pressure, and cardiac activity were monitored during the entire procedure. Under CT fluoroscopic guidance, the largest tumour in segment IVa was identified. The needle tip was placed such that the thines at 2 cm deployment covered the outer margins of the tumour. Deployment was monitored under CT fluoroscopic guidance. This lesion was ablated to 5 cm after which the needle was repositioned twice to ablate the medial and lateral margins to provide a 5 mm margin around the tumour. The entire process was constantly monitored using CT fluoroscopy. The area of coagulation necrosis was seen within the tumour () with no evidence of any pericardial fluid. During the attempt to remove the RF needle from segment IVa, the thines would not retract. Significant force was finally used to retract the thines.
The operator then decided to ablate the lesion in segment VI. During placement of the needle, it was noted that there was an expanding pericardial effusion (). The procedure was aborted to facilitate the management of the cardiac tamponade. Immediate pericardiocentesis performed by a cardiologist, was noted to be haemorrhagic. Approximately 300 mL of blood was aspirated but the patient was persistently hypotensive and an emergency sternostomy was performed. Intra-operatively, two litres of blood was evacuated from the pericardium. A puncture wound was noted at the anterior cardiac vein (right marginal vein) (), which could have led to the haemorrhagic cardiac tamponade. In addition, inflammatory changes are also seen in the adjacent diaphragm but no evidence of any ablation change was seen in the pericardium. The anterior cardiac vein (right marginal vein) was repaired and haemostasis was secured.
The patient was stable post-surgery. While in the intensive care unit, his condition gradually deteriorated with the development of liver failure, upper gastrointestinal bleeding, pneumonia, and sepsis. The patient expired 19 days after the primary event.


A 72 year-old man developed right side weakness after a left ACA infarction and was transferred to the department of rehabilitation medicine 7 weeks after the attack. He had no remarkable medical history but was diagnosed with diabetes at our hospital. He had a family history of ischemic stroke (affecting his younger brother). On transfer to our department, he was alert but had cognitive impairment with a K-MMSE (Korean version of the Mini-Mental Status Examination) score of 13. Manual muscle test (MMT) grades of his right upper extremity-were all 3/5, lower extremity test grades were 2/5 except for ankle plantar flexor grades of 1/5, and dorsiflexor grades were 0/5. He had no spasticity in his elbow and knee joints, and had a modified Ashworth scale (MAS) score of zero. His sensory function was intact and deep tendon reflex was normoactive. He complained that his hand moved abnormally against his will. He could grasp and release with his bare hands on the doctor's order, but when grasping some objects with his palm, he was unable to release them. Brain magnetic resonance imaging (MRI) revealed acute cerebral infarction at the left ACA region (). For TMS, we used a Magstim 200 monopulse® (Magstim co., Whiteland, UK) connected to a figure-eight coil (7 cm outer diameter for each loop) with a maximum magnetic strength of 2.0 tesla. The coil was initially centered on the vertex, perpendicular to the scalp, with the handle pointing posteriorly at a 45 degree angle from the median sagittal line and then moved in 1 cm steps in anterior-posterior and medial-lateral directions. Motor evoked potentials (MEP) were recorded from the first dorsal interosseous (FDI) muscle with a surface gel electrode. The active electrode was placed over the muscle belly and the reference electrode over the distal interphalangeal joint of the index finger. The signals were displayed by Keypoint® EMG (Dantec, Skovlunde, Denmark) and stored in a laboratory computer. Using a paired pulse magnetic stimulation technique, we studied intracortical inhibition (ICI) and intracortical facilitation (ICF). In this case, when we stimulated the left motor cortex area, the resting motor threshold (rMT) was 54% of the maximum magnetic strength and the MEP amplitude was 287 µV. At the right motor cortex area, the rMT was 57% and the MEP amplitude was 579 µV. In the ICF study, when we stimulated the left motor cortex area, the MEP amplitude was increased to 1,697 µV. In the ICI study, the amplitude was not suppressed, but rather increased to 1,170 µV (). The SEP studiesusing median nerve stimulation showed normal values with no statistically significant difference between sides ().


A 47 year-old woman developed left side weakness after a right ACA infarction and was transferred to the department of rehabilitation medicine 3 weeks post onset. She had no remarkable medical history but was diagnosed with diabetes at our hospital. She had no family history of stroke. On transfer to our department, her mental status was alert but she had mild attention deficit. Her speech was normal and a K-MMSE score was 25. MMT grades of her left upper and lower extremities were all 3/5, except the wrist flexor and wrist extensor scores were both 2/5. She could perform fine motor activity with her left hand. She had no spasticity in her elbow and knee joints, with a MAS score of zero. Her deep tendon reflex was normoactive. Her superficial sensory responses were intact, but proprioception was impaired. She complained that her left hand was out of her control; her left hand "took away" objects out of her right hand. Her hands appeared to be directed at opposing purposes, showing 'intermanual conflict'. A brain MRI revealed acute cerebral infarction at the right ACA region, mainly at the right frontal lobe and corpus callosum (). In this case, when we stimulated the right motor cortex area, the rMT was 44% and the MEP amplitude was 314 µV. At the left motor cortex area, the rMT was 44% and the MEP amplitude was 456 µV. In the ICF study, when we stimulated the right motor cortex area, the MEP amplitude was increased to 876 µV. In the ICI study, theamplitude was not suppressed, but rather increased to 867 µV (). The SEP studies using median
nerve stimulation were normal with no significant differences between sides ().


A healthy 18-year-old female patient reported to our dental clinic with a complaint of pain and swelling in her upper left lateral incisor []. Patient history indicated repeated palatal swelling and pain in the same tooth for the past 2 years. On clinical examination, the upper left lateral incisor was found discoloured with folding of the tooth crown palatally. The tooth did not respond to electric pulp vitality test using an Analytic Pulp Tester (Analytic Technology Corp., Richmond, VA, USA.), although all the adjacent teeth responded within normal limits. Radiographic examination revealed the presence of an invagination along the entire length of the root [].
Based on the clinical and radiographic finding, presence of Type III dens in dente was confirmed and a definite treatment plan was formulated. The treatment planned included non-surgical endodontic therapy, crown lengthening, raising a palatal flap to seal the groove, reinforcement of crown, permanent restoration, and surgical apical curettage, if necessary.
Treatment started with conventional endodontic procedure. Without local anesthesia, rubber dam (Hygenic dental dam, Coltene whaldent Switzerland) was applied on the tooth, and endodontic access was performed with a tapered safe-ended endoacess diamond point (Maillefer-Dentisply, Baillagues, Switzerland). Using a DG16 endodontic explorer (Hu-Friedy, Germany) and a size 15 K file (Mani Inc, Tochigi, Japan) two orifices were identified. The two canals were negotiated, and working length was established using radiography []. The two canals were prepared to working length by step back technique to a size 55 K file (Master apical file, Mani Inc, Tochigi, Japan) and to a size 80 K file (Final file, Mani Inc, Tochigi, Japan); the canal was then flared by using Gates Glidden drills sizes 1-4 (Maillefer-Dentisply, Baillagues, Switzerland). During the instrumentation, the canals were irrigated with 5.25% sodium hypochlorite (KMC Pharmacy, Manipal, India). Following the final irrigation with 15% ethylenediaminetetraacetic acid (Sigma Aldrich, Germany) and then 5.25% sodium hypochlorite (KMC Pharmacy, manipal, India), the canals were dressed with calcium hydroxide paste (UltraCalâ, Ultradent) and the access was sealed with temporary filling material (Caviton; GC Corporation). After 3 weeks, obturation was done using cold lateral condensation of Gutta-percha cones (Maillefer-Dentisply, Baillagues, Switzerland)) using zinc oxide eugenols cement (Kalzinal, Dentsply UK) as sealer.
Post-obturation radiograph showed a dentine bridge along the entire length of the root canal []. Post endodontic rehabilitation was started with crown lengthening, which was done using electrocautery []. Crown lengthening revealed the presence of invagination as a developmental groove on the labial aspect [].
The palatal flap was raised to expose the root surface. Palatal surface of the root also had similar type of invagination. Infolding of the tooth crown was evident from the palatal aspect. Palatal and labial grooves were sealed with Light cure glass ionomer cement (GC Corporation, Tokyo, Japan) and sutures (5-0 TevedkR) were placed []. A provisional crown was placed in order to maintain the gingival contour.
CBCT (KODAK 900 cone beam CT digital X-ray) scan of the maxilla was taken and a three dimensional reconstruction of the involved tooth was done []. The 3D reconstruction showed the developmental groove along the entire length of the root, both labially and palatally [].
The CBCT showed a bony lesion, with eroded palatal and labial cortical plates []. In the next appointment, the temporary restoration was placed inside the access cavity and some amount of obturation material was removed. The tooth was reinforced by allowing composite (3M Espee) to flow into the access cavity. A provisional crown was fabricated and placed over the tooth. In the following appointment, a permanent porcelain fused metal crown was cemented []. The patient returned six months later and was found to be asymptomatic. Clinical examination was unremarkable; there was a reduction in the size of the periradicular radiolucency.


A 63-year-old male presented to the eye emergency on 30 July 2011 with a 10-day history of bilateral (B/L) redness and photophobia. He had no history of ophthalmic ailments before this. Eight weeks prior to presentation he had been diagnosed with superficial transitional cell bladder carcinoma for which transurethral resection of bladder tumor (TURBT) was done, followed by intravesical BCG therapy (one instillation per week). Following the fourth dose of intravesical BCG vaccination, he developed fever, hematuria, and swelling over the parotid and neck glands for which anti-tubercular drugs consisting of rifampicin 450 mg, pyrazinamide 1500 mg, ethambutol 800 mg, isoniazide 300 mg (AKT4), broad spectrum antibiotic, and oral prednisolone (60 mg daily) were started by the treating urologist. Two days after the BCG injection, he developed B/L redness of eyes for which he was treated by a local ophthalmologist with topical antibiotic and lubricant gel, without any improvement.
His best-corrected visual acuity (BCVA) at presentation was 20/80 and 20/200 in the right eye (RE) and left eye (LE), respectively. Eyelashes were matted with thick mucopurulent discharge. After cleaning the eyes with normal saline, slit lamp (S/L) examination was done which showed subconjunctival hemorrhage, conjunctival and ciliary congestion, and corneal ulceration. In both the eyes, the ulcer was in the inferior part of the cornea extending to the limbus with surrounding infiltration [Figures and ]. Limbal ischemia adjacent to the ulcer was noted. Multiple Descemet's folds were found radiating towards the central cornea from the ulcer margin (BE). The ulcer bases were clear, devoid of any suppuration. Both cornea and conjunctiva appeared dry and lusterless. Anterior chamber (A/C) was deep and quiet and pupils were regular and reacting to light in BE. Direct and indirect ophthalmoscopy revealed normal fundus in RE, but the LE fundus could not be properly visualized due to corneal haze and mild cataractous change. Conjunctival swab from eyelids, fornices, and scraping from ulcer margin were sent for Gram and acid fast bacilli (AFB) stain and culture, which were bacteriologically negative. Corneal scraping was not done from ulcer base to avoid perforation. Schirmer's test detected severe dry eye (<2 mm BE). Laboratory studies showed an erythrocyte sedimentation rate of 56 mm in 1st hour with the rest of hematological studies normal. Biochemistry showed raised serum sodium, urea, and creatinine. Tests for antinuclear antibodies and rheumatoid factor were negative. We diagnosed the case as B/L sterile corneal ulcer with mucopurulent conjunctivitis and dry eyes following intravesical BCG instillation. He was treated with moxifloxacin o.5% eye drops eight times daily, timolol eye drops (0.5%) twice daily, cyclosporine eye drops (0.05%) four times daily, atropine sulfate eye drops (1%) thrice daily, and lubricant gel six hourly. AKT4 and oral prednisolone were continued as before.
Follow-up (F/U) on day 1: BCVA was reduced to 20/200 (RE) and finger counting at 2 feet (LE). Conjunctival congestion and discharge decreased but descemetocele developed in both eyes [Figures and ]. Bandage contact lenses (BCL) were inserted in BE and medications were continued as before. He was advised for admission and pulse steroid therapy but he refused.
F/U on day 2: A/C was shallow, pupils irregular, and iris prolapsed through the perforated ulcer bilaterally. The perforation measured 2 mm × 1 mm RE and 3 mm × 2 mm LE. The patient refused to get admitted and received two doses of pulse steroid therapy (intravenous methylprednisolone) as day care basis. Intravenous antibiotic was not given as he was already getting broad spectrum oral antibiotics (Tab cefixime 200 mg bd). Paramedian tarsorraphy was done (BE). The ulcers showed signs of regression but the patient was subsequently lost to follow-up, prior to completion of pulse steroid therapy.


A 30-year-old man presented to our outpatient department with sudden loss of visibility in his left visual field for one week. There was a history of headache and low-grade fever for five weeks. He had no other neurological or systemic signs and symptoms. On ocular examination Snellen visual acuity was 20/20 in both eyes, ocular adnexa and motility were also normal in both eyes. The pupils of both eyes were equal, round, regular. Direct and consensual light reflexes were symmetrical and normal in both eyes. Ocular media were clear and fundus examination did not show any abnormalities of the optic nerve head or the retina in both eyes. On confrontation visual field testing left-sided field defect was noted in both eyes. Color vision and contrast sensitivity were normal in both eyes.
Automatic static threshold perimetry (Humphrey Field Analyser) [] showed left-sided incongruous homonymous hemianopsia denser above the horizontal meridian. Brain computed tomography (CT) scan showed a hypodense lesion in the right parieto-temporal lobe []. Magnetic resonance imaging (MRI) revealed irregular well-marginated lobulated lesions with mild perifocal edema of altered signal intensity showing irregular contrast enhancement in the right temporo-occipital (39×34×24 mm3) and left high fronto- parietal region (26×22×17 mm3) []. Ultrasonography of the abdomen and chest X- ray were normal. There was no evidence of retroperitoneal and mediastinal lymph node enlargement. A repeat systemic and neurologic examination was unremarkable. Serological tests for HIV were reactive. Other investigations showed a CD4 (cluster differentiation 4) count of 396 cells/μl, an erythrocyte sedimentation rate (ESR) of 60 mm/1sth, negative sputum for acid fast bacillus (AFB) {Ziehl-Nielsen staining} and negative toxoplasma IgG (Immunoglobulin G) titers.
The patient was started only on anti-tubercular drugs with the presumptive diagnosis of primary cerebral tubercular abscess. The regime consisted of an intensive phase of two months with Isoniazid (300 mg/day), Rifampicin (600 mg/ day), Pyrazinamide (1500 mg/day), Ethambutol (800 mg/day) followed by a continuation phase of 10 months with Isoniazid (300 mg/day), Rifampicin (600mg/day) and pyridoxine (20 mg/day). After four weeks of the intensive phase of anti-tubercular therapy (ATT), the patient's initial constitutional symptoms improved. MRI after two-month intensive phase followed by 10-month continuation phase of ATT showed significant decrease in the size of the lesions which measured 21× 17 mm for the right and 11× 9 mm for the left with minimal edema. In addition the central cores of the lesions were now hypointense on T2-weighted (T2W) images []. But repeat perimetry after one year did not reveal any significant improvement in visual fields.


A 39-year-old female presented with non-union of the left humerus fracture following trauma. The surgeon found the cystic lesion intraoperatively. Curettage with evacuation of the cyst was done and the fracture was fixed with dynamic compression plate. Analysis of resected specimen reconfirmed the diagnosis and the patient was referred for chemical therapy. After 2 years, the patient was re-admitted with the diagnosis of non-union humeral fracture. In physical examinations, motion of fractured site decreased and pain was eminent, but neuromuscular examination was normal. The laboratory findings were not specific and the routine serological tests were normal. Before operation, radiological plans including X-ray [], CT scan [], and MRI [] showed a cystic lesion in the proximal part of the left humerus in the presence of non-union.
We administered albendazole (10 mg/kg/day) and praziquantel (40 mg/kg/day) for 2 weeks before surgery. During surgery, we found a highly viscous, yellowish liquid which was aspirated. After curettage, we cleaned the wound with a solution of H2O2 and hypertonic saline solution to prevent recurrence of cysts. Because of massive resection, we used autographs from fibula and iliac bones, and the fracture was fixed with LCP [].
The histopathologic tests revealed the characteristic trilamellar hydatid cyst wall and scolices of E. granulosus scattered amidst fragments of bone and marrow. An ultrasound and CT scans of the brain, breast, and abdomen were performed later, which revealed no cysts in these organs. After the operation, we performed serological investigations which showed negative results for complement fixation test (CFT) and latex agglutination test (LAT). The patient was discharged on albendazole (10 mg/kg/day) and praziquantel (40 mg/kg/day) to prevent recurrence of cysts. At the last follow-up (9 months), the patient was doing well. She was pain-free and completely asymptomatic. X-ray did not show any local recurrences.


Forty-year-old man, no co-morbidities, RTA as motor-bike driver with left dorso-lateral tibial head impression facture, left middle foot fracture and closed, displaced comminuted
fracture of the distal lower right leg with C3-fracture of the tibial pilon and luxation fracture of the ankle including a fracture of the distal fibula. Initial treatment involved applying external fixation and plate osteosynthesis of the fibula fracture. Within 12 hours, the patient developed compartment syndrome. After decompression of the compartments of the lower leg and temporary wound coverage with artificial skin coverage, the tibia was
reconstructed using small fragment screws and secondary wound closure. At 61 months FU mobilisation in the right ankle joint was actively possible with a range of pain-free movement of 10 – 0 – 30 degrees (left 20 – 0 – 35 degrees). AOFAS score: 82 points (Fig. ).


20.06.2005: 49-year-old man, lorry driver, BMI 37.8, CVI II degree with atrophy of the skin and brown skin pigmentation, smoker with 25 pack years, arterial hypertension. Closed, isolated C3-tibial pilon fracture on right. Continued driving his lorry for about 5 hours after sustaining the injury, on admission already presenting with compartment syndrome of the lower leg. Primary treatment included compartment decompression and stabilisation using external fixation followed by osteosynthesis with nine small fragment screws after 7 days and secondary wound closure. FU 09/2011 with active movement of 5 –0 – 25 degrees in the ankle joint (left 15 – 0 – 30). AOFAS score: 76 points. Patient has been able to continue working as a lorry driver (Fig. ).


21.08.2007: 55-year-old woman, no co-morbidities. RTA, collision in a car. Closed pilon tibial fracture, B-3 with high left fibula fracture without syndesmotic injury, additional left ulna shaft fracture. Primary treatment using external fixation, secondary osteosynthesis 8 days after initial surgery with five small-fragment interfragmentary screws. FU 06/2011 with active movement of the left ankle joint of 15 – 0 – 45 degrees (right 15 – 0 – 45 degrees). AOFAS score: 100 points (Fig. ).


06.10.2007: 19-year-old man, no co-morbidities, sustaining a fall from 8 m height through a roof. Closed right tibial pilon fracture type B-3, accompanying fracture of 2 (Fig. ).


27.02.2008: 66-year-old male, no co-morbidities, fall from 4 m height from scaffolding onto concrete ground, sustaining a closed pilon tibial C3-fracture including right proximal fibula fracture without syndesmotic injury and Grade II soft tissue contusion with early tension blistering of the overlying skin. Accompanying central mid-face fracture. Primary treatment using external fixation followed by treatment of the mid-face fracture 14 days after initial surgery. Osteosynthesis of distal tibia with screws and removal of external fixation on April 30th 2008 followed by mobilisation with partial weight-bearing walking aid. FU 02/2011 with active movement of the ankle joint of 0 – 0 – 10 degrees (left 10 – 0 – 20). AOFAS score: 62 points (Fig. ).


A 65-year-old male reported to the clinic with a complaint of enlarged gums in relation to the right side upper and lower jaw for the past 2 years. His past medical history revealed that he was hypertensive and was taking Tab. nifedipine 30 mg BID for the past 3 years, as prescribed by his physician. History of the presenting illness revealed that the patient noticed the swelling which started before 2 years and progressed to the present stage. On intraoral examination, there was bulbous enlargement of the gingival mucosa in relation to 13, 14, 44, and 45; surface was lobulated and reddish pink in color []. On palpation, it was nontender and firm in consistency. Assessment of plaque accumulation was done using Silness and Loe plaque index (1964) which gave in a score of 3 (marking abundance of soft matter within the gingival pocket and/or on the tooth and gingival margin). Assessment of gingival inflammation was made using gingival index of Silness and Loe (1963), which gave a score of 1 (which includes mild inflammation, slight change in color, slight edema, and no bleeding on palpation). The gingival hyperplasia was graded by using Angelopoulos and Goaz (1972) criteria, which was graded as grade I (which presents with hyperplastic gingiva extending to the cervical third or less of the anatomic crown).


A 12-year-old male epileptic child with phenobarbital-induced SJS of one-week duration was referred to the Department of Paediatric Dentistry for the management of severe toothache since two days and non-healing ulcerations in the buccal mucosa. Medical history revealed that SJS developed following a change in medication for epilepsy from phenytoin to phenobarbital (60 mg/day) by a local physician. Within 7 days of intake of the medication, the patient developed blisters preceded by high grade fever and headache. They ruptured to form painful erosions in eyes and oral cavity. Subsequently he reported to the hospital where the offending drug was withdrawn immediately. The laboratory investigations [], history and causality assessment score of 7 (Naranjo's criteria) were indicative of probable phenobarbital-induced SJS.[]
Systemic corticosteroid (injection dexamethasone, 1 mg once daily intravenously for ten days) along with tablet clobazam (a benzodiazepine derivative) 5 mg twice daily was administered. Topical mupirocin cream was prescribed for the skin lesions, tobramycin cream and artificial tear drops for the eye lesions.
Examination in the Department of Paediatric Dentistry revealed erosive ulcerations in the oral cavity. The lips were encrusted []. There was abundant plaque accumulation with inflamed and bleeding gingiva. The mucosal ulcerations were aggravated by sharp cusps of grossly decayed painful teeth.
At first dental visit, his oral hygiene was improved with supragingival cleaning. Coronoplasty of the sharp cusps was done to prevent further irritation to the ulcerated buccal mucosa. The patient was advised to use an ultrasoft toothbrush and alcohol-free chlorhexidine digluconate mouthrinse (0.2%) as an antiplaque agent. Lidocaine hydrochloride gel (2% W/W) was prescribed to reduce the pain associated with the lesions.
At the next visit after 2 days, there was improvement in his oral condition. Extraction of the offending tooth was performed under local anesthesia.
His overall condition improved over a period of 2 weeks following the admission and change of medication. He was discharged with instructions to continue tablet clobazam (5 mg twice daily) as an antiepileptic agent, artificial tear drops, topical antibacterial and steroid creams (fluticasone) for skin lesions.
At subsequent follow-up examination, no adverse sequelae were reported by him.


During routine upper limb dissection for first year medical students, the BP of 43-year-old female cadaver showed the complete absence of MCN and variant branches of MN in the arm of both the upper limbs.
In the right axilla, the lateral cord of BP had three branches i.e. lateral pectoral nerve, nerve to CB and lateral root of MN. The lateral pectoral nerve pierced the clavipectoral fascia and supplied the pectoralis major as usual but during its course it communicated with the medial pectoral nerve (MPN) of medial cord of BP (). The MCN was completely absent. The nerve to the CB was a small motor twig arising directly from the lateral cord which innervated the CB muscle. The lateral and medial root of MN formed the MN proper and descended between the biceps brachii and brachialis muscle. It then crossed the brachial artery from lateral to medial and finally entered the cubital fossa. In the arm, deep in the biceps brachii, the MN gave two branches: a direct branch to the biceps brachii and another long branch which, after supplying the brachialis muscle, continued as the LCNF and supplied the lateral side of the skin of forearm. The medial cord also varied in the origin of medial cutaneous nerve of arm and forearm arising from a single common trunk, which became separated in the middle of the arm ().
The lateral cord of BP in the left axilla branched four times: the lateral pectoral nerve; nerve to CB and lateral root of MN and an additional lateral root of MN. The MCN was absent and the nerve to CB was a small twig which supplied and terminated in the muscle itself (). No communication between lateral and MPNs was found.
The MN was formed by two lateral roots from the lateral cord and one from medial root from the medial cord. After the formation, the left MN had the same course as the right side. During its course between the biceps brachii and brachialis, the MN split off a single long branch from which branches to the biceps brachii and brachialis were derived. After supplying these two muscles it continued as LCNF, which supplied the lateral side of the skin of forearm. The medial cutaneous nerve of arm and forearm arose from a common trunk, and separated in the middle of the arm, similarly to the right side ().


A 36-year-old man was hospitalized due to abdominal discomfort with fatigue. His family history states that his mother died of liver cirrhosis associated with the hepatitis B virus (HBV). Physical examination indicated no abnormal findings. All laboratory findings were normal, but serum hepatitis B surface antigen, hepatitis B e antigen, and HBV DNA were positive. The human immunodeficiency virus (HIV) antibody tests were all negative. The abdominal computed tomography did not show any abnormality in the liver, but a 2.4 cm sized enhancing renal mass in the left upper pole was incidentally found. An enlarged lymph node was seen in the left paraaortic area (). A whole body isotope scan to assess for metastasis did not show any abnormal uptake.
The renal mass and the enlarged lymph node were excised by robotic-assisted laparoscopic partial nephrectomy based on the preoperative impression of renal cell carcinoma, renal oncocytoma, or adenoma. Microscopic pathologic examination was performed intraoperatively, and lymphoproliferative lesion with negative margins was demonstrated by a frozen section.
The wedge resected specimen was 5×3×2.5 cm in size and 20 g in weight. The cut surface showed a well demarcated, white tan and solid mass measuring 2.2×1.8 cm in the renal parenchyma (). The paraaortic lymph node was 1 cm in its greatest dimension. The histopathological examination revealed the features of the HVCD. There were many lymphoid follicles with hyalinized germinal centers and broad mantle zones. Blood vessels were prominent in the germinal centers and the interfollicular areas. These findings were seen in the renal cortex, medulla, and the paraaortic lymph node ().
Both renal tissue and lymph node tested negative for human herpsevirus 8 (HHV-8) and Epstein-Barr virus infection. The levels of interleukin 6 (IL-6) and erythrocyte sedimentation rate (ESR) were not assessed.


A 75-year-old man was admitted to Inha University Hospital with a three-month history of language deterioration. He was also presenting gait disturbance and urinary and fecal incontinence. He had an eight-year history of hypertension and had undergone stent insertion for myocardial infarction five years previously. In computed tomography (CT) and magnetic resonance imaging, a 6.5 cm-sized heterogeneous enhancing mass with central necrosis was seen in both the frontal lobes and the anterior genu of the corpus callosum. Radiologically, the mass was suspected to be lymphoma or glioblastoma multiforme, and a stereotactic biopsy was therefore performed. A piece of the biopsy sample was sent for frozen section evaluation. The cytologic crush material was composed mainly of large single cells with indistinct cytoplasmic borders in a granular background. The tumor cells had abundant eosinophilic granular cytoplasm and round oval nuclei with prominent nucleoli. Some tumor cells with mild nuclear atypia were also discerned (). No endothelial proliferation or mitosis was identified.
The biopsy samples for permanent section consisted of three pieces of brain tissue. They showed cellular lesions predominantly composed of infiltrates of large round cells without endothelial proliferation. Reticulin deposition was seen only in the endothelial cells. The tumor cells had abundant intracytoplasmic eosinophilic granules, either dispersed uniformly or confined to the cell periphery (targetoid appearance) (). The granules were positive for periodic acid-Schiff (PAS) and resistant to diastase digestion. The nuclei were bland, round to oval, varied in size and often eccentrically located. Occasionally, mild atypical nuclei and small nucleoli were observed. In the entire field, no mitosis or necrosis was identified.
The granular cells were diffusely and strongly immunoreactive with GFAP showing cytoplasmic staining and targetoid appearance. The S-100 protein showed diffuse strong cytoplasmic immunoreactvity (). The tumor cells overexpressed the p53 protein and showed positive immunoreactivity for CD68 (KP), but were negative for CD68 (PGM). Epithelial membrane antigen (EMA), lysozyme, CD43, and albumin were not expressed. The Ki-67 labeling index was 5%. The patient was discharged without additional management.


A 54-year-old male admitted to the ER complaining of headache
from 13 days ago. It did not occur when lying down but became intensely squeezing around the occipital area within 10 seconds after being seated or standing. Symptoms were accompanied by nausea and vomiting. Visual analog score (VAS) was 8 at standing. Past medical history was insignificant other than undergoing L4-5 laminectomy and discectomy at a local hospital 15 days ago. Physical examination did not display any neurologic findings such as neck stiffness and laboratory results as well as brain MRI findings were not remarkable. Under the strong impression of intracranial hypotension, he admitted to neurology department and underwent conservative therapy including absolute bed rest (ABR) and hydration. A MR myelogram was performed, showing a pseudomeningocele accompanied by large CSF leakage in the lumbosacral area ().
Because resolution of symptoms was unsatisfactory, an epidural blood patch was placed on the sixth admission day. After placing the patient in a prone position, a 22 gage touhy needle was inserted through the L5-S1 epidural space through a paraspinal method. After confirming the epidural space by the loss-of-resistance technique, a dye was injected to confirm the epidural space with the C-Arm. Then the epidural patch was placed with 12ml of autologous blood.
VAS one day after intervention was reduced from 6 to 2. After three days of ABR following the procedure, the patient practiced changing positions by sitting. Symptoms were not aggravated when standing up. Five days after the procedure, the patient did not complain of any symptoms (VAS 0). Follow up MR myelogram showed decreased pseydomeningocele size caused by CSF leakage ().
We decided to perform one more procedure of epidural patch placement because of the residual CSF leakage 6 days after the first intervention. A total of 10 mL autologous blood was injected, and the patient was discharged the next day. Follow up for six months confirmed no recurrence of symptoms ().


A 48-year-old man underwent RF ablation due to AF. Since then, the patient complained of intermittent hemoptysis and dyspnea upon exertion. However, symptoms were transient and improved after conservative treatment. The patient was re-admitted 6 months after the procedure because of an 1-month history of right chest pain.
The chest posteroanterior view at admission showed right pleural effusion and patchy consolidations in the right lower lung field. Smooth reticular opacities overlapped and the volume of the right lung was smaller than that of the left side. Comparison with a prior chest radiography taken before RF ablation revealed that the lesions were newly developed.
Chest CT showed ill-defined soft tissue infiltrations in the right mediastinum, which encased the bronchovascular bundle. The right superior PV was faintly opacified and disconnected. The right inferior PV was not opacified and its entry to the left atrium was obliterated by the soft tissue infiltrations. Small collateral vessels were noted around the soft tissue infiltrations (). Pulmonary vein stenosis after catheter ablation was diagnosed. In the lung setting, parenchymal pulmonary venous infarction was also noted. A lung perfusion scan revealed the absence of right lung perfusion (). For the evaluation of pulmonary vein flow, pulmonary TR-MRA (TR = 2.7 ms, TE = 1.0 ms, flip angle = 19°, a sample interval = 1 sec) was performed using a 3 Tesla system (Magnetom VERIO, Siemens Healthcare, Erlangen, Germany). On pulmonary TR-MRA, the right pulmonary artery was shown to be opacified later than the left pulmonary artery. Prominent systemic arteries were also noted in the right thorax that connected with the right pulmonary artery, suggesting pulmonary to systemic collaterals. Systemic venous collaterals were opacified instead of filling the pulmonary vein (). On a velocity-encoded cine (VEC) image (TR = 38.2 ms, TE = 2.3 ms, signal average 1, matrix size = 256 × 256, FOV = 320 × 320 mm, slice thickness = 6 mm, flip angle = 20°, velocity encoding range -100 to 100 cm/sec), the flow direction of the right pulmonary artery was reversed in the diastolic phase and displayed a continuous diastolic forward flow in the left pulmonary artery (), which was similar to that of congenital PV atresia.
An attempt to insert a stent into the pulmonary vein was unsuccessful. However, symptoms and abnormalities on chest PA improved after heparin anticoagulation therapy. The patient was discharged and followed-up at an outpatient clinic.


A 68-year-old woman with a previous history of paraplegia after traumatic spinal epidural hemorrhage from a ruptured L3 arteriovenous fistula (AVF) was admitted to our institute with high fever above 38℃ and severe back pain. About 10 days earlier, she suffered a superficial burn to her back and was admitted into the local hospital because of acute renal failure due to rhabdomyolysis. On neurologic examination, the patient was alert but mildly disoriented. Examination of the motor system revealed intact muscle strength in the upper extremity and flaccid paraplegia with areflexia. An examination of the sensory system revealed that all sensory modalities had decreased below the T10 dermatome level. An abdominal computed tomography scan demonstrated a suspicious pyogenic spondylitis of multiple lumbar spines with multiple perivertebral abscess formation and fluid collections around the pyriform muscles and parasacral area. A drainage catheter was inserted by a radiologist and the patient was admitted into the infectious diseases ward for antibiotic therapy. Empirical antibiotic therapy with ampicillin and sulbactam was started. On culture of aspirated fluid, methicillin-sensitive Staphylococcus aureus was identified. Thus, the antibiotic was changed to nafcillin. Drug fever developed after nafcillin was given, so the antibiotic was changed to cefazolin. This antibiotic was maintained until the culture of the draining catheter was identified. On culture of the draining catheter, methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa were identified. Therefore, the antibiotic was changed to a combined vancomycin and ciprofloxacin regimen. After 14 days on that regimen, the antibiotic was changed to teicoplanin because the patient developed a skin rash. Despite conservative therapy using the appropriate antibiotics for 3 months and surgical drainage being performed twice, the spondylitis of her lumbar spine was not controlled. We thought that the fluid collection in the dead space between the intra-/inter-muscular area and the scar of the previously embolized AVF was the main source of infection recurrence (). We believed that by filling the dead space, we would be able to control the spondylitis. Therefore, we designed a staged operation.
First, we performed multiple posterior screw fixations from L1 to the sacrum with wide debridement of infected soft tissue and obliteration of dead space using RLDMF (). Second, we performed anterior column reconstruction with an expandable mesh cage via an anterolateral reptroperitoneal approach to correct deformity and bone fusion. After the staged operation and antibiotic therapy, the multiple infectious spondylitis completely resolved without recurrence () and there were no signs of spinal instability or pseudoarthrosis ().


SA, a 27 years old morbidly obese male with weight above 180 Kg had been showing at our clinic with recurrent lymphangitis since 1997. In 2000, during an attack of cellulitis of the leg, he developed a large gangrenous patch on the posterior and dependent side of the right calf. Following debridement, he persisted with a nonhealing ulcer which reached a size of 13 × 9 cms []. He later developed two secondary ulcers, one near the ankle which was 4 × 3 cm and one anteriorly which was 6 × 4 cm. These ulcers did not heal with antibiotics and various other forms of ancillary therapy. He did purchase a compression pump in 2001 which helped the associated oedema but the ulcer kept waxing and waning and never completely disappeared. Skin grafting was tried four times. []. In between he required three visits to the ICU for septicemia, with adult respiratory distress syndrome (ARDS). He was put on a Bi PAP machine following the first attack. Surgery for morbid obesity was not an option as the risks were stated to be too high. The presence of the ulcers was declared to be adding to the risk.
In early 2010, he was started on multilayer lymphoedema bandaging (MLLB) [] – this was done a few times at the clinic where the process was taught so that after learning and purchasing a set of bandages and related consumables he could continue the same at home. Benzathine penicillin injections (Pencom 12®) were continued every 3 weeks as before. When he came back to us around 3 months later, all the ulcers had miraculously healed []. During his last follow-up a year later, he was still ulcer free and continued using a compression pump as well as penicillin. Thus, in summary, MLLB resulted in healing of more than one large recalcitrant ulcer (s) in a morbidly obese individual.


MJ, a 45-year-old male, a resident of Lucknow had suffered fractures of the right leg 12 years back following a road traffic accident. He had been given a plaster cast initially along with external fixators. After the cast was removed, he was found to have multiple ulcers in the leg. Since then, the ulcers have persisted with occasional attacks of cellulitis. Various treatment methods including four surgeries (split skin grafting) did not result in long-lasting wound closure.He was referred to our clinic and seen first time on 17th May 2012. After cleaning the leg, and a single shot of benzathine penicillin, he was given compression therapy using a multichambered pump. This was followed by multilayer bandaging after local application of commercially available micronized Silver in the form of cream as well as dressing. Foam packing ensured uniformity of the pressure across the pressure points like the malleoli. The bandaging process is shown in .
The dressing was opened every 3 -4 days and then reapplied after washing and following the same protocol as above. After the fourth session, he wanted to go back with a promise of applying the bandage and dressing himself and regular follow-up. When he came back on 7th of June 2012, all the original ulcers had healed completely. However, there was a small fresh superficial ulcer higher up at the shin, which he attributed to a small injury caused by a local graze. It was also noticed that his self application had the problem of using knots to tie the bandages which caused pressure points. We suspect an imperfect self-bandaging technique to be the possible cause for the abrasion in the shin.
A final course of pumping, followed by bandaging was done []. Only a very light dressing was required. His leg circumference measured at various points showed that the concomitant oedema also improved alongside []. A repeat follow-up visit after another month showed continued healing with only a mild scar breakdown at one place [Figures and ]. In summary, his ulcers healed completely in less than 3 weeks with the use of compression therapy and multilayer bandaging. shows the leg date wise at various stages of healing. shows how healing was parallel to decrease in limb oedema


A 41-year-old woman presented at our hospital complaining of chest discomfort and pain. She had been healthy with no significant preceding symptoms, allergic history or past medical history.
The initial examination showed the following findings; body temperature 37.8℃, blood pressure 94/60 mmHg, heart rate 100 beats/min and a cardiac gallop rhythm.
Laboratory data on admission revealed decrease in the total white blood cell count (1040/mm3), elevated enzymes (creatinine phosphokinase 236 IU/L, aspartate aminotransferase 112 IU/L, alanine aminotransferase 87 IU/L, lactic dehydrogenase 588 IU/L, Troponin-I 4.070 ng/mL, CK-MB 12.32 ng/mL and proBNP 8760 pg/mL). Electrocardiogram (ECG) showed a regular sinus rhythm with low voltage in all limb and precordial leads (). Transthoracic echocardiogram (TTE) showed marked edematous left ventricular (LV) myocardium and global hypokinesis (), resulted in mild left ventricular systolic dysfunction (LV ejection fraction = 48%) (). There was no significant valvular dysfunction and small pericardial effusion without tamponade physiology was noted. We diagnosed that she had acute myocarditis of unknown etiology. Empirical treatment such as intravenous antibiotics injection, bed rest, pain control and close vital sign monitoring were performed. On the tenth day of admission, total white blood cell count (17160/mm3) and eosinophil count (8430/mm3) markedly increased (49% of her total white blood cell count). We started oral administration of prednisolone 1 mg/kg for 3 days and performed ventricular endomyocardial biopsy. Histopathologic findings revealed myocyte necrosis and degeneration (). The antibody test against parasitic infection demonstrated that toxocara immunoglobulin G (IgG) was positive. Taken together, we diagnosed that she had myocarditis caused by T. canis VLM. We started oral administration of albendazol 400 mg twice a day for two weeks after oral prednisolone 1 mg/kg administration for 3 days. Three days after starting steroid therapy, eosinophil count decreased promptly (130/mm3). One week after steroid therapy, TTE was followed up. TTE finding showed that echogenicity of LV myocardium was markedly decreased and wall thickness was normalized (). M mode evaluation of LV showed completely recovered myocardial contractility (). After the completion of the treatment, physical examination, laboratory tests, ECG and echocardiogram showed no abnormal findings and she was able to return to work.


The patient was 26-year-old man who was diagnosed as ulcerative colitis (UC) at other hospital 6 years ago. Since then, he had been taking medication irregularly by himself. One month ago, he received surgical treatment for anal fistula and started to take mesalazine-containing regimen (Asacol 2.4 g per day) regularly. He did not feel uncomfortable while taking medication for about 1 month. At 3 days before admission, he intermittently felt febrile sensation and anterior chest discomfort on resting. The chest discomfort was aggravated by positional change and deep breathing but relieved by stable supine position. He was admitted to our hospital via emergency room to evaluate his symptoms.
At the time of admission, body temperature was 38.3℃, systolic/diastolic blood pressure was 100/60 mmHg, heart rate was 124 beats/min and respiratory rate was 20 times/min. Laboratory tests including serum liver enzymes, serum blood urea nitrogen/creatinine levels, serum cardiac enzyme levels were within normal range, however, the N-terminal pro-brain natriuretic peptide (NT-proBNP) level was increased to 1877 pg/mL (reference value: 0-349 pg/mL). White blood cell count was 10900/mm3 (reference value: 4100-10200/mm3), neutrophil count was 9232/mm3 (84.7%, reference value: 38.3-69.3%) and eosinophil count was 32/mm3 (0.3%, reference value: 0.7-8.1%). Hemoglobin level was slightly low (10.4 g/dL). The erythrocyte sedimentation rate (ESR) (reference value: 2-30 mm/hr) and C-reactive protein (CRP) (reference value: ≤ 0.59 mg/dL) were elevated up to 93 mm/hr and 15 mg/dL, respectively. The electrocardiogram (ECG) revealed distinct ST segment elevations in leads I, II, aVL, and V2-6 (). Echocardiogram showed mild pericardial effusion (about 0.2 cm) in the posterior space and slightly increased pericardial thickness, and global hypokinesis of the left ventricle (). Left ventricular ejection fraction was 60.3% and left ventricular internal dimension at diastole was 4.73 cm.
He was diagnosed as acute myopericarditis. After taking oral aspirin of 2 g per day and prednisolone of 40 mg per day with cessation of mesalazine medication, he felt no more chest pain and fever was disappeared at 3 days after medical treatment. The abnormal ECG findings were gradually normalized within 7 days. On echocardiogram at 11 days after treatment, pericardial effusion, increased pericardial thickness, and wall motion abnormality were completely improved. Finally, he was discharged with aspirin 2 g per day and prednisolone 20 mg per day. Unfortunately, the mesalazine (3 g per day) was re-administered at 6 days after discharge by his gastroenterologist. At 3 days after mesalazine re-medication, he felt chest pain and febrile sensation again, although he had been taking aspirin (2 g per day) and prednisolone (20 mg per day) at that time. He was readmitted to our hospital, and the echocardiographic findings showed minimal pericardial effusion and mild global hypokinesia of the left ventricle again, although the findings were milder than those at the time of first admission. Acute phase reactants were also elevated without leukocytosis nor eosinophilia (ESR 88 mm/hr, CRP 18.30 mg/dL, white blood cell count 6590/mm3 and eosinophil fraction 8%). Mesalazine was immediately stopped with maintaining other medications including aspirin and prednisolone. After then, he showed dramatic improvement of chest pain and fever within 3 days after cessation of mesalazine. There was no abnormal arrhythmic rhythm change in ECG monitor except intermittent ventricular premature beats during admission. When discharge, we recommended not to prescribe mesalazine for him ever again to his doctor. However, we have no more information on the patient because he did not return for any treatment ever since.


Ms. S, a 35-year-old, married lady presented with a one-year history of marked social withdrawal, muttering to herself, and suspiciousness. On clarification with her husband regarding her ‘suspiciousness’ it was found that she kept enquiring from him whether their acquaintances had visited her or not, subsequently she would report about her belief that she felt her acquaintances were not visiting her often, and hence, they could possibly be cheating her, but would not elaborate further. She firmly held on to these beliefs in spite of her husband telling her otherwise. For the last two weeks there had been a worsening of illness, characterized by crying spells, along with two suicidal attempts of high intentionality and lethality. After hospitalization, she was found to be tearful and withdrawn, reported of being fearful and expressed death wishes. An initial impression of psychosis, with a phenomenological inference of delusion of persecution, was made as per the longitudinal course of the illness from the available information, and she was started on tablet risperidone 2 mg. She continued to express fearfulness and did not show much improvement with risperidone. During the course of hospitalization, she was noticed to be repeatedly asking others to forgive her for ‘a mistake’ she had committed. On further clarification, she elaborated that she had been getting repeated thoughts that she had done something wrong, which could be the reason for her feeling that her acquaintances were not visiting her often. This had been interpreted to be ‘suspicious behavior’. She would get these repetitive, anxiety provoking thoughts so often that she started wondering whether she had actually done something wrong. The level of conviction regarding this thought was quite high and she did not feel that this thought was in anyway irrational. Hence, she had started feeling ‘suspicious’ about the reason for others not visiting her. To decrease her anxiety, she would constantly ask reassurance from others, would check with her husband as to why a particular acquaintance had not visited her, and would keep repeatedly muttering to herself about this issue. The thoughts were very repetitive, stereotyped, and distressing, while they remained uncontrollable. As the frequency of these thoughts increased, she started feeling sad throughout the day, along with ideas of hopelessness, guilt, and suicidal ideas. Subsequently, her diagnosis was revised to obsessive compulsive disorder (OCD), with obsessions of intrusive thoughts / images and compulsion of reassurance seeking as denoted in the Yale Brown Obsessive Compulsive Scale (YBOCS) symptom checklist. The YBOCS obsession score was 16 and compulsion score was 10 (YBOCS total score of 26). She was started on fluoxetine 20 mg / day, which was increased to 40 mg per day in a week. The depressive symptoms began to improve initially. The frequency of thoughts began to gradually decrease later. After two months follow-up, she had significant improvement in her symptoms with the YBOCS total score decreasing to 10.


A 37-year-old man, diagnosed with CD in 1999, presented with diarrhea and a perianal fistula. He had been treated with mesalazine, 3 g/day, but had not undergone a colonoscopy since the diagnosis because of a high-grade stricture in the anorectum. In 2002, he was referred to our gastrointestinal department for a second opinion on his CD. Diarrhea and intermittent abdominal pain developed three months before admission. An abdominal computed tomography (CT) scan demonstrated diffuse bowel-wall thickening and enhancement throughout the ileum and colon with multifocal strictures (). Laboratory data were unremarkable. After informed consent had been obtained, a colonoscopy was performed to assess disease activity and as surveillance for cancer. At three centimeters from the anal verge, however, passage of both a standard colonoscope and gastroscope (GIF-P230, 8.5 mm Ø; Olympus Co.) was blocked due to severe anal stricture (). We, therefore, performed a colonoscopy with an ultra-slim upper endoscope (GIF-XP260N, Olympus Co.), which passed through the rectal stricture without any resistance (). Although other focal strictures were found in his transverse () and sigmoid () colon, we succeeded in reaching the cecum () in 3 minutes, but we failed to reach the terminal ileum due to a narrowed ileocecal valve (). Careful examination of the colon revealed a huge ulcer in the transverse colon. Biopsies were taken from the mucosa of the anal stricture to rule out colon cancer. These biopsies showed no evidence of malignancy.


The patient, a 25-year-old Japanese woman, the second child of non-consanguineous healthy parents, was born after 39 weeks of gestation with no prenatal or perinatal problems. Her early developmental milestones were normal, except for two episodes of febrile seizures at 1 year of age, which never recurred. From the age of three, her food intake was relatively small, and malnutrition delayed her physical growth, but her mental development was normal. From the age of nine, she suffered from episodic vomiting after eating, which caused anorexia. At the age of 11, she was referred to our hospital for further investigation of progressive weight loss (−1.4 kg/year). Her height was 123 cm (−3.0 SD) and she weighed 18.6 kg (−2.5 SD). She had normal intelligence and no neurological deficits, except for episodic postprandial vomiting. Detailed physical investigations showed no significant abnormalities, except for scoliosis. Gastrointestinal, metabolic, endocrinological and psychological disorders were ruled out. No neurophysiological examinations were performed, although, brain MRI revealed a 7-mm-sized lesion in the posterior dorsal portion of the cervicomedullary junction, which was enhanced with Gd-DTPA (Fig. A). Signal changes were also detected bilaterally in the dentate nuclei without enhancement. No other signal abnormalities were noted. During follow-up on MRIs, taken twice a year, the enhancement of the lesion disappeared after 2 years, although the plaque remained. Her episodic vomiting also vanished almost simultaneously. Her growth stopped at the age of 17. At age 25, she is frail 140 cm/33.4 kg with scoliosis. She has normal intelligence and is asymptomatic. A tiny plaque without enhancement, the same size as before, is still visible in the dorsal part of medulla oblongata (Fig. C), although cervicomedullary atrophy without a signal change has advanced (Fig. B).
Sequencing of the GFAP gene with informed consent revealed a heterozygous missense mutation in exon 5 (c.827G>T), causing a change of arginine to leucine at amino acid position 276 (p.R276L). The mutation was not found in her mother. The father, who died in traffic accident in his forties, could not be investigated. This mutation has already been described as responsible for pathologically proven hereditary [] and sporadic [] cases of adult-onset AxD. According to an interview, there was no relationship between the present patient and the families previously reported, although they originated from the same region of Japan.


A 30-year-old male patient presented to our clinic with a history of tender swelling on the dorsum of middle phalanx of left index finger. The patient noted the mass since 12 months, which gradually became larger. The mass was 13 mm in diameter [], with mild tenderness and firm in palpation, slightly mobile and, without marked movement on interphalyngeal motion, and no obvious adhesion to adjacent skin. The sensation of the finger was normal. Flexor and extensor tendons were intact; however, finger motion was slightly limited.
There was no history of major trauma, sharp injury, infection, or constitutional symptoms such as malaise, fever, or weight loss. Laboratory tests (CBC diff, ESR, CRP, Ca, P, Alk-P) were within normal limit. Tests for tuberculosis, brucella and syphilis were negative. Chest roentgenogram was normal.
Other imaging investigations included simple x-ray and CT-scan of the index finger. Conventional posteroanterior and lateral radiography revealed a paraosteal sclerotic lesion just abutting middle phalanx with bone density similar to adjacent bone and slight periosteal reaction [], and further evaluation with CT-scan noted that the lesion has a patchy irregular border without cortical destruction or sauccerization and there is no typical zonal pattern in the lesion [].
An excisional biopsy with dorsolateral incision was performed. The lesion was 1 × 1 × 1.5 cm in size, white-grayish in color, with hard consistency, and no adhesion to adjacent tendons or soft tissues. Histopathologic examination revealed proliferation of fibroblasts that are loosely arranged, a prominent myxoid matrix, and deposits of osteoid rimmed by uniform osteoblasts. Multinucleated giant cells were also existed [].


A 36-year-old Asian male presented with seven years of intermittent melena and maroon-stools, requiring at least five hospitalizations and multiple blood transfusions at outside institutions. Previous examination at other hospitals including endoscopy, colonoscopy, Meckel's scan and VCE had shown only gastric angioectasia as a possible bleeding source. Active bleeding secondary to the gastric angioectasia was never observed. Nevertheless, these lesions were treated with argon plasma coagulation (APC) as recently as two days prior to admission to our institution.
He presented to our institution with melena and maroon colored stools. He was not on aspirin or any NSAID. We performed upper endoscopy, colonoscopy which surveyed approximately 80 cm of the ileum, technetium-99m-tagged red blood cell scan and VCE. VCE showed non-bleeding gastric angiodysplasia which were again ablated with APC. The patient's rectal bleeding subsided and hemoglobin remained stable after four units of packed red blood cell (RBC) transfusion. Two months later, his rectal bleeding recurred required a four unit RBC transfusion. Patient was on Ranitidine one hundred and fifty milligrams orally; daily prior to the admission. Repeat examinations were performed, which revealed a normal Meckel's scan and a tagged RBC scan showing active bleeding in the right lower quadrant of the abdomen. VCE was again performed which showed blood in the terminal ileum. A total of at least of four upper endoscopies, five colonoscopies, three VCE's, two tagged-RBC scans, and two Meckel's scans were performed at multiple institutions. Based on the VCE findings, the source of bleeding was localized to the terminal ileum.


A 47-year-old man had basal cell carcinoma 1.5 cm in diameter of the left nasolabial fold, which was resected with a free margin of 0.5 cm. The circular skin defect of approximately 2.5 cm in diameter was reconstructed using a unilateral V-Y advancement flap. In particular, the lower limb of the V flap was consistent with the relaxed skin tension line (RSTL). This procedure did not cause any undue deformity of the adjacent tissue, and good cosmetic results were obtained ().


A-30-year-old male with alleged history of consumption of ALP tablets came to the emergency department, with pungent odour vomiting and pain abdomen. On presentation, patient was drowsy, pulse and blood pressure was un-recordable. Abdominal examination and CVS examination were within normal limits. Baseline investigations were as under: Hemoglobin: 16 gm/dl, total leukocyte count: 11,000/cumm, differential leukocyte counts: normal (77-20-1-2), serum sodium: 137 mEq/L, serum potassium: 3.8 mEq/L, blood urea: 27 mg/dl, and serum creatinine: 1.3 mg/dl. Resuscitation was started with intravenous fluids, inotropes like dopamine and noradrenaline, hydrocortisone, pantoprazole, sodium bicarbonate, calcium gluconate, magnesium sulphate, and prophylactic antibiotics.
Patient remained hypotensive and finally inotropic support was withdrawn after 1 week. Patient developed respiratory distress after few days and was shifted to the ICU. His chest X-ray was suggestive of right pleural effusion []. Serial pleural aspirations from right pleural cavity were done initially in emergency, subsequently in ICU, and then in the ward. Diagnostic thoracentesis revealed an exudative fluid with 80 percent lymphocytes. Gram stain and AFB stain were negative with no growth after 48 hours of culture for pyogenic organisms. In the ICU, the patient was initially on oxygen support and non invasive ventilation. Subsequently he was on ventimask with reservoir bag. Then the patient was shifted to the pulmonary medicine ward while on oxygen supplementation by ventimask. There was no history of fever during the stay in the hospital. He was discharged after about a week of stay in the ward. During follow-up he was healthy with a normal chest X-ray [] and investigations were normal.