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AISC Team B1 5

3957451-1

noncomm/PMC003xxxxxx/PMC3957451.xml

Percutaneous device closure of persistent ductus venosus presenting with hemoptysis

An eight-year-old boy, presented with a history of hemoptysis (50 ml per episode, thrice) for one week. The X-ray of the chest was unremarkable and the screening echocardiography was normal. Pulse oximetry and blood gas showed oxygen saturation of 80%, when the patient was comfortable at rest. Contrast echo with agitated saline done to rule right to left shunt, showed delayed appearance of bubbles in the left atrium after four cycles, suggestive of pulmonary arteriovenous fistula (PAVF). Contrast-enhanced computed tomography (CECT) revealed two small (2 mm) aortopulmonary collaterals at T6 - T7, one on each side, no major PAVF, features of aspiration in the right upper lobe, and an incidentally detected persistent ductus venosus (PDV) []. The ultrasonogram and echocardiography confirmed a PDV of 6.5 mm diameter, opening into the inferior vena cava (IVC) [ and ] and no evidence of liver disease or portal hypertension. The diagnosis of congenital portosystemic shunt due to PDV, causing PAVF was made. The aortopulmonary collateral arteries (APCA) were considered to be secondary to systemic hypoxemia. However, the cause of hemoptysis was not clear (aortopulmonary collateral or PAVF). The patient was taken up for percutaneous intervention of PDV and aortopulmonary collateral. A pulmonary angiogram showed diffuse bilateral multiple small PAVFs []. The PDV was entered from the internal jugular vein access. Test balloon occlusion showed adequate hepatic portal circulation and no increase in portal pressure from the basal 10 mmHg [ and ]. Through a 7F Mullin sheath, a 12 mm Amplatzer vascular plug II (St. Jude Medical, St. Paul, Minnesota) was deployed [ and ]. The APCAs on both sides were selectively cannulated []. The right APCA was cannulated with a 4F right coronary artery (RCA) catheter and coiled with two 035 inch 2 mm – 30 mm platinum fiber coils (COOK MEDICAL INC. Bloomington). The left APCA could not be coiled. There was no recurrence of hemoptysis in the next 48 hours and the patient was discharged. The follow-up plan was to monitor the oxygen saturation for regression of PAVF and an ultrasonogram to rule out portal hypertension.

[[8.0, 'year']]

M

{'18161055': 1, '21976894': 1, '14694396': 1, '25684892': 2, '30644348': 1, '24688239': 2}

{'4322406-1': 1}

3957453-1

noncomm/PMC003xxxxxx/PMC3957453.xml

Surgical removal of a left ventricular myxoma in an infant

A five-month-old male infant presented with incidental detection of a murmur during an evaluation for upper respiratory tract infection. The child was otherwise symptom-free, with normal growth and development. The examination revealed normal pulse volume and blood pressure. There was no tachypnea. Auscultation of the heart revealed an ejection systolic murmur in the left third intercostal space, radiating to the right second intercostal space. The chest roentgenogram was normal. The child was in sinus rhythm with no echocardiographic (EKG) evidence of LV hypertrophy.\nTransthoracic echocardiography revealed a single tumor mass, with varying echo density, which was 20 mm in its largest dimension, protruding in and out of the left ventricular outflow tract causing significant outflow tract obstruction []. The tumor was arising from the anterior, lateral, and superior aspect involving the lateral papillary muscles. Three-dimensional echocardiography demonstrated an irregular surface []. The Doppler revealed a peak gradient of 88 mmHg across the left ventricular outflow tract. There was no mitral stenosis, mitral regurgitation or aortic regurgitation. The left ventricular function was normal.\nThrough a midline sternotomy and under cardiopulmonary bypass, the aorta was clamped and the left atrium was opened in the Sondergaards plane.[] A vent was introduced and a mitral valve retracted. The tumor was not visualized well from the left atrium. An aortotomy revealed that the tumor was found fully occluding the left ventricular outflow, extending to just below the aortic valve. It was not possible to define the tumor margins and tissue planes completely from the aortotomy.\nA decision was then made to access the LV via the conal septum. The right ventricle (RV) outflow was opened and the conal septum was incised (like in a modified Konno operation) and retracted.[] The tumor was visualized and removed from the superior, lateral, and anterior wall of the LV. Some tumor was left alone in the region of the lateral papillary muscle, as removing it would have damaged the papillary muscle.\nThe tumor on gross appearance was a grayish white tissue with a thin capsule, measuring about 20 × 15 × 8 mm. The histological sections showed a neoplasm with spindle cells having round-to-elongated nuclei, with a vesicular chromatin, and oval-to-elongated spidery cytoplasmic processes, set in a myxoid stroma, along with large areas of hemorrhage, suggestive of a myxoma [].\nThe child was noted to have a complete heart block in the immediate postoperative period that reverted to sinus rhythm spontaneously after – eight days. A pre-discharge echo showed normal ventricular function and a small residual tumor mass in the vicinity of the papillary muscle. At the three-month follow-up there was no increase in the size of the residual tumor. At the six-month follow-up, the child was noted to have a prolonged PR interval, wide QRS interval, and an intermittent Wenckebach phenomenon, on a 24 hour Holter recording. In view of the rhythm abnormality and associated history of the previous transient postoperative complete heart block a permanent pacemaker was inserted into an abdominal pocket. An epicardial lead was used. There was no tumor recurrence at the nine-month follow-up visit.

[[5.0, 'month']]

M

{'12537208': 1, '9424072': 1, '19329501': 1, '24987268': 2, '22108931': 1, '8651800': 1, '8219827': 1, '21095370': 1, '8215825': 1, '7477198': 1, '1873035': 1, '24688241': 2}

{'4070211-1': 1}

3957454-1

noncomm/PMC003xxxxxx/PMC3957454.xml

Remission of congenital complete heart block without anti-Ro/La antibodies: A case report

A single-term, appropriate-for-date, girl baby, with birth weight 2478 g, born out of a non-consanguineous marriage to a 24-year-old primigravida mother, presented at birth with a heart rate of 45/minute. The baby was born by normal vaginal delivery and had APGAR scores of 7 and 8 at one and five minutes. The obstetric history revealed documented fetal bradycardia during labor, but normal heart rate on the ultrasound scans at 18 and 35 weeks of gestation. The mother had no history of gestational diabetes, hypertension, hypothyroidism, any fever with rash, or drug intake during pregnancy, nor did she have any symptoms suggestive of connective tissue disease. There was no history of cardiac disease in the family.\nAt birth, the baby was otherwise healthy with a heart rate of 45/minute, without any symptoms of congestive cardiac failure. Serum electrolytes were normal and echocardiography revealed no structural heart disease. The baby was put on continuous electrocardiographic monitoring. The electrocardiogram (EKG) on day one revealed complete AV dissociation with an atrial rate of 115/minute, ventricular rate of 45/minute, QRS duration of 0.08 seconds (occasionally > 0.08 seconds), corrected QT interval (QTc) of 0.48 seconds, and an left bundle branch block (LBBB) pattern []. EKG on day three revealed no AV dissociation with both atrial and ventricular rates of 93/minute and QRS duration of 0.08 seconds []. Although the EKG reverted to sinus rhythm, the PR interval (0.18 seconds) was prolonged, the QRS duration was at the upper limit of normal, and the EKG showed a right bundle branch block (RBBB) pattern. There was marked ST depression in V1 and marked right axis deviation, indicating normal right ventricle (RV) dominance in the newborn period. The EKG on day four showed a similar picture as on day three with a rate of 107/minute. On day six, however, the bradycardia again worsened. This time the ventricular rate varied between 45 and 60/minute, atrial rate was 150/minute, and QRS duration was 0.08-0.1 seconds. This pattern prevailed over the next seven days. From day 13 onward, there was spontaneous improvement, with disappearance of AV dissociation and atrial–ventricular rates improving to 100/minute. The baby remained asymptomatic during the hospital stay. Cardiac function was regularly monitored using functional echocardiography, and the fractional shortening (FS%) was found to range between 32 and 38% during this period, which was normal for term neonates. Hence, cardiac pacing was withheld. The baby was discharged on day 29 of life. During this period, the heart rate varied between 85 and 120/minute, but no further episodes of AV dissociation were noted. The mother was tested for serum anti-nuclear antibody using the indirect immunofluorescence technique. Subsequently the mother's serum was subjected to antigen-specific enzyme immunoassay, using microtiter plates coated with a combination of antigens SSA/Ro, SSB/La, Sm, U1-RNP, Jo-1, and Scl70. The test results were negative.\nThe baby was followed up weekly for two months, then every fortnight for the next 14 months []. The baby did not develop any such episodes further. Serial echocardiography during this one-year follow-up revealed no evidence of any cardiac dysfunction. EKGs were done in both the parents and were found to be normal.

[[24.0, 'year']]

F

{'16219517': 1, '4273004': 1, '15937979': 1, '14999207': 1, '14987746': 1, '28251027': 2, '14705240': 1, '15692198': 1, '19567621': 1, '9626848': 1, '16020601': 1, '8116991': 1, '21920962': 1, '24688242': 2}

{'5322508-1': 1}

3957455-1

noncomm/PMC003xxxxxx/PMC3957455.xml

Transjugular closure of a two-hole atrial septal defect in a child with iliac vein thrombosis

A 4-year-old girl, who weighted 13 kg, presented to our department for a scheduled follow-up for the transcatheter closure of a multiple secundum ASD. She also had a history of a transcatheter closure of a large patent ductus arteriosus at the age of 10 months, because of congestive heart failure. A transthoracic echocardiographic examination revealed two atrial septal defects measuring 12 and 4 mm, respectively, thatwere 5 mm apart. The total septum was 32 mm in length and had adequate surrounding rims []. In addition, a dilated right ventricle and tricuspid valve regurgitation were present, and no remarkable findings were observed in the other investigations.\nCardiac catheterization was performed under general anesthesia using transesophageal echocardiography control. We originally intended to place a 5-French (Fr) sheath in the right femoral vein and the right femoral artery for hemodynamic measurements and monitoring. However, we could not pass the guidewire into the inferior vena cava. Manual contrast injection was performed in the femoral vein, and an obstruction in the inferior vena cava was observed and identified as a thrombus. Catheterization was continued by using the right internal jugular venous access with a 5 Fr sheath. Heparin 100 units per kilogram of body weight was administered, and a 5 Fr Judkins right catheter with a hydrophilic guidewire was introduced, under transesophageal echocardiographic control through the larger defect into the left atrium and the left lower pulmonary vein instead of the left upper pulmonary vein. A manually curved, stiff exchange guidewire then replaced the catheter in that position, over which a 7F long sheath and a 16 mm Amplatzer septal occluder (St. Jude Medical, Inc.; Plymouth, MN, USA) device were glided into the left atrium. The left and right device discs were opened sequentially under fluoroscopic and transesophageal echocardiographic guidance, and a successful deployment of the device was accomplished after several and repeated trials, aiming for an ideal device orientation []. Transesophageal echocardiography revealed no residual shunts, normal atrioventricular valve function, and normal superior and inferior vena cava blood flow. The next day, a transthoracic echocardiographic examination was normal. Aspirin therapy was started with a six-month course, and a follow-up was planned for the patient. The coagulation profile tests were normal, and the patient was discharged the next day.

[[4.0, 'year']]

F

{'22719163': 1, '16998405': 1, '34760057': 2, '16598389': 1, '16951839': 1, '15170723': 1, '34521236': 2, '15320573': 1, '14624437': 1, '24688243': 2}

{'8574097-1': 1, '8574097-2': 1, '8574097-3': 1, '8574097-4': 1, '8447089-1': 1}

3957457-1

noncomm/PMC003xxxxxx/PMC3957457.xml

Unusual systemic venous Collateral channels to left atrium causing desaturation after Fontan operation closed percutaneously

A 7-year-old girl child, had tetralogy of Fallot with hypoplastic right ventricle and adequate branch pulmonary arteries (tricuspid valve measured 8.5 mm, “Z” score -4.2 at the time of Fontan completion). She had undergone modified right Blalock–Taussig (BT) shunt in infancy followed by bidirectional Glenn shunt and ligation of pulmonary artery and takedown of BT shunt at 16 months of age. She was regularly followed up and underwent extracardiac Fontan at the age of 5½ years.\nPre-Fontan cardiac catheterization had revealed normal left ventricular (LV) filling pressure, mean pulmonary artery pressure, and pulmonary vascular resistance index.\nShe had a smooth postoperative course and was discharged after 9 days of surgery. Her oxygen saturation at the time of discharge was 95% in room air. A gradual return of cyanosis, exertional dyspnea, and easy fatigability was noted by the parents for the past 6 months. Her saturation was 85% at rest and 78% after (10 min) walking.\nCross-sectional echocardiography revealed normally functioning Fontan circuit. The ventricular function was normal, and there was no atrio-ventricular valve incompetence and no pericardial or pleural effusions. One small venous channel was seen arising from the brachiocephalic vein.\nPatient underwent cardiac catheterization; intracardiac pressures and Fontan pressures were normal. There was no fenestration. Innominate vein angiogram revealed a small venous channel descending on the left side. On selective injection, the venous channel was found to be communicating with the left atrium (LA). This channel was occluded using 0.038-inch, 5 mm × 5 cm Cook coil.\nInferior vena cava (IVC) angiogram revealed a large tortuous venous channel arising at T8-T9 level and draining into the LA [Figure and ]. Selective venous channel injection was also done which showed maximum diameter of venous channel 12 mm and the opening into LA measured 9.5 mm. An additional small vein was seen connecting the larger venous channel to the LA separately.\nLarger venous channel was test occluded using a 15 mm × 4 mm Tyshak balloon []. During occlusion, no hemodynamic instability was noted. There was no significant rise in systemic venous/Fontan pressure. The Fontan pressures before and after balloon occlusion were 12 mmHg and 13 mmHg, respectively. Systemic arterial saturation improved to 94% on balloon occlusion.\nThe smaller venous channel was first occluded using a 0.35-inch 5 mm × 5 cm Cook coil, whereas an 18-mm Amplatzer vascular plug was deployed in the larger channel []. Post-deployment IVC angiogram revealed complete occlusion of both the venous channels. Patient was discharged after 48 h of observation and has remained well at 6 months follow-up without any evidence of desaturation.

[[7.0, 'year']]

F

{'11388633': 1, '16541221': 1, '11458423': 1, '14694936': 1, '18407962': 1, '18412082': 1, '24688245': 2}

{}

3957458-1

noncomm/PMC003xxxxxx/PMC3957458.xml

Hemitruncus with ventricular septal defect in a 6-year-old child

A 6-year-old girl had presented with history of recurrent episodes of lower respiratory tract infection since 3 months of age and easy fatigability of 4 years duration. The frequency of chest infections had decreased during the last 2 years. There was no history of cyanosis. On examination the child was fairly built and nourished. Her pulse rate was 102/min, and blood pressure was 110/64 mm Hg. The apex beat was in the 6th intercostal space lateral to mid clavicular line. On auscultation thesecond heart sound was loud and single. A soft systolic murmur of grade 2/6 was heard in left 2nd/3rd intercostal space.\nChest roentgenogram [] showed cardiomegaly with a cardiothoracic ratio of 0.70 and left ventricular type of apex with dilatation of pulmonary trunk and proximal pulmonary arteries. Transthoracic echocardiography showed an enlarged left ventricle, a large malaligned sub aortic ventricular septal defect (VSD) with bidirectional shunt. There was evidence of severe pulmonary arterial hypertension. The pulmonary artery confluence was not clear. Cardiac catheterization revealed a systemic saturation of 93% and systemic pulmonary artery pressures. The left pulmonary artery (LPA) pressure and saturation was 106/46 and 83% respectively. The aortic pressures and saturation was 120/69 and 93% respectively. The superior vena cava saturation was 65%. Calculation of flows and resistances in this situation using Fick's principle has many fallacies. The relative contribution of the right lung in real oxygenation is likely to be small as the saturation at entry is 93%. The whole right sided cardiac output, in the absence of significant right-to-left shunt traverses the left lung. Based on these assumptions, the calculated PVRI for left lung was 8.9 Wood Units. Calculation of right sided PVRI may be impossible with conventional principles. The angiogram showed a large sub aortic VSD with aortic override of < 50%, and the RPA arising anomalously from the ascending aorta. The LPA was seen to be a continuation of the main pulmonary artery that was arising normally from the right ventricle. In this case, aortic saturation of 93%, wide pulse pressure and low left lung PVRI supported the clinical assessment of operability. CT angiogram [] showed the RPA (1.08 × 1 cm) was arising from aorta approximately 2 cm from aortic valve leaflet without ostial narrowing, and main pulmonary artery (1.6 × 1.5 cm) was continuous with the left pulmonary artery (1.1 × 1 cm). An echocardiogram was repeated that showed continuous flow signals into the RPA without ostial narrowing. There was no pulmonary regurgitation.\nSingle stage repair was planned. Through a standard median sternotomy approach, aorta, LPA, and RPA were dissected and mobilized. On cardiopulmonary bypass (CPB), the RPA was divided from the ascending aorta and its aortic end was sutured primarily. An arteriotomy was made in the MPA at the lateral aspect just opposite to MPA-LPA junction and RPA was anastomosed to MPA with a continuous 6-0 prolypropylene suture. The VSD was then closed through the right atrium using a patch; the surgically created 4mm atrial septal defect was left open. The saturation at the time of weaning from CPB was 88% on FiO2 of 100%. The measured pulmonary artery pressure was equal to the systemic arterial pressure. Transesophageal echocardiography revealed right-to-left shunting through the atrial septal defect. In the intensive care unit, elective nitric oxide was started in the usual doses in view of severe pulmonary arterial hypertension. Over the next 5 days the systemic oxygen saturations improved, the catecholamine support and nitric oxide were gradually withdrawn and she was removed from mechanical ventilator support on the 5th post-operative day. Oral medications consisted of a diuretics and sildenafil 10 mg thrice a day and she was discharged on day 9. Post operative chest X-ray [] showed normal lung vascularity on both the sides and a lung perfusion scan [] three weeks following surgery showed normal perfusion of both the lungs. At follow-up transthoracic echocardiogram, the estimated right ventricular systolic pressure was 60 mm Hg.

[[6.0, 'year']]

F

{'6834873': 1, '22467006': 1, '3354450': 1, '21395684': 1, '17467452': 1, '2979975': 1, '15016045': 1, '24688246': 2}

{}

3957459-1

noncomm/PMC003xxxxxx/PMC3957459.xml

Coronary artery thrombus resulting in sudden cardiac death in an infant with Kawasaki disease and giant coronary artery aneurysms

A six-month-old Hispanic male presented to the ER with seven-day history of fever, cough and congestion and he was treated with antibiotics for possible pneumonia. Two days later due to persistent fevers, irritability and gastrointestinal symptoms, he was admitted for septic work up. He was continued on antibiotics for possible urinary tract infection and aseptic meningitis (had elevated white cell counts in the urine and CSF). He continued to have recurrent fevers, and seventeen days into the illness he was noted to have increasing white cell count (29.5 K mm3), high platelet count (1061 K mm3), elevated CRP (138 mg/L), high ESR (>100 mm/hr) with mild peeling of his fingertips which prompted an echocardiogram. He had a transient conjunctivitis, dry lips and skin rash early in the course of his illness by history but had a normal exam at presentation. Echocardiogram showed extensive, multiple, giant CAA of the right coronary artery (RCA), fusiform shape, the largest measuring 19 m × 20 mm [], the proximal left anterior descending artery (LAD) measuring 22 mm × 24 mm [, [Videos and ].\nHe had a large pericardial effusion, which was drained. He was treated with IVIG and Abciximab. Due to risk of coronary artery thrombus and for myocardial protection, he was treated with enoxaparin, Clopidogrel, Aspirin, Captopril, and Propranolol, which were continued at the time of discharge. He was closely followed up as outpatient with serial echocardiograms. At his last follow up four months later, he was doing well, with stable giant CAA with no thrombus and normal biventricular function by echocardiography. A cardiac catheterization was planned in next 1-2 months.\nA month later he presented to the ER with nonspecific gastrointestinal symptoms and irritability, he was presumed to have a viral illness, and was discharged. The next day he died suddenly at home. Autopsy showed giant fusiform CAA of the RCA measuring 20 mm in diameter and 65 mm in length with occluding thrombus []. The giant LAD aneurysm was oval and measured 20 mm in diameter and 40 mm in length with occluding thrombus []. The myocardium showed multifocal grayish scar formation particularly of the inter-ventricular septum suggestive of infarction. Microscopic cross section showed a completely occluding mural thrombus in RCA aneurysm with intimal wall thickening.

[[6.0, 'month']]

M

{'18025079': 1, '17576863': 1, '12911476': 1, '15505111': 1, '16511387': 1, '22454602': 1, '16511388': 1, '20300241': 1, '15805345': 1, '8822996': 1, '24688247': 2}

{}

3957460-1

noncomm/PMC003xxxxxx/PMC3957460.xml

VACTERL association with double-chambered left ventricle: A rare occurrence

A 2-year-old male asymptomatic child came for echocardiogram referred from an orthopedic center. His past history was significant for various limb and urachal anomalies of VACTERL association including bilateral radial aplasia, club hand, absent thumbs, sacral agenesis, and urachal sinus. At 9 months of age, he was diagnosed to have apical muscular ventricular septal defects and secundum atrial septal defect by echocardiography done elsewhere. On examination, he had normal development and normal intelligence for his age. There were dysmorphic facial features with bilateral radial club hand, absent thumbs, and short upper and lower limbs []. Chest examination was normal with cardiac auscultation revealing regular heart sounds with no murmur. His ECG and Chest X-ray were unremarkable. Sacral X-ray showed partial sacral agenesis [].\nTransthoracic echocardiography demonstrated situs solitus with normal atrioventricular and ventriculoarterial concordance. There were no ventricular septal defects. The left ventricle (LV) was abnormally configured with a muscle band extending from the interventricular septum toward the apex dividing the LV into two separate contracting LV chambers. A typical “figure-of-eight” appearance was seen in the parasternal short-axis view in diastole indicating double-chambered left ventricle (DCLV) [ arrowheads, ]. During systole, the LV was seen leading to aorta []. There was laminar flow inside the LV with no intraventricular gradient. Rest of the cardiac examination was normal with good biventricular function.

[[2.0, 'year']]

M

{'9215761': 1, '11343333': 1, '6824545': 1, '18490276': 1, '30571578': 1, '15262602': 1, '19543847': 1, '21340234': 2, '21846383': 1, '19520641': 1, '24688248': 2}

{'3020356-1': 1}

3957461-1

noncomm/PMC003xxxxxx/PMC3957461.xml

A rare pediatric cardiac anomaly: Quadricuspid aortic valve with aortic regurgitation

A 9-year-old male was referred to the cardiology clinic for evaluation of an asymptomatic diastolic heart murmur. On physical examination, a 2/4 early, medium-frequency, diastolic murmur was audible at the right mid-sternal border. The remainder of his physical examination was unremarkable and an electrocardiogram was normal. Transthoracic echocardiography showed a type B quadricuspid aortic valve (QAV) (three cusps of equal size and one smaller cusp) associated with mild aortic regurgitation by color Doppler imaging, likely from a coaptation defect [ and ].[] The left ventricular end-diastolic dimension measured by M-mode was normal (4.58 cm, z-score + 0.3) with a shortening fraction of 31%. The remainder of the cardiac anatomy was normal, including the origins of the coronary arteries.\nTwo years later, the patient remained asymptomatic and the echocardiography showed stable, mild aortic regurgitation [], now associated with mild left ventricular dilation []. By M-mode the left ventricular end-diastolic dimension measured 5.82 cm (z-score + 2.8), the end-systolic dimension was 3.7 cm (z-score + 1.9), and the shortening fraction was 35%.

[[9.0, 'year']]

M

{'4698133': 1, '2181849': 1, '12492123': 1, '15311857': 1, '25926908': 1, '24688249': 2}

{}

3958499-1

noncomm/PMC003xxxxxx/PMC3958499.xml

Axial length estimation error caused by hidden double-peak on partial coherence interferometry in an eye with epiretinal membrane: a case report

A 52-year-old female presented with ERM in her left eye (). Her visual acuity at the first visit was 20/25, with mild cataract on slit-lamp examination. The spherical equivalent was −1.5 D. ERM was identified on fundus examination and spectral domain optical coherence tomography (Spectralis®; Heidelberg Engineering, Dossenheim, Germany); this clearly showed a strained line with high intensity above the retina corresponding to the ERM. After 6 months, her retinal thickening became severe due to proliferating ERM, and her visual acuity dropped to 20/100 (). Combined cataract surgery with pars plana vitrectomy was planned.\nOn preoperative examination, the IOLMaster® (version 5.4; Carl Zeiss AG, Oberkochen, Germany) was used for measurement of axial length by PCI. The measurement was repeated 20 times, and a signal curve synthesized from individual curves using an algorithm built into the IOLMaster was displayed as a summary.\nThe highest peak in the summary display was used for measurement of axial length because the signal curve appeared to be, at a glance, a single peak (). Keratometry readings were obtained by the automated keratometer incorporated in the IOLMaster. The SRK/T formula was used for intraocular lens power calculation.\nAfter giving informed consent, the patient underwent combined cataract surgery with pars plana vitrectomy. Phacoemulsification was performed with a 2.2 mm superior self-sealing clear corneal incision, and a foldable acrylic intraocular lens (AcrySof® IQ Model SN60WF; Alcon, Fort Worth, TX, USA) was injected in the capsular bag with full covered continuous curvilinear capsulorhexis. Transconjunctival pars plana vitrectomy was performed using the Alcon 25 gauge vitrectomy system (Alcon). The internal limiting membrane was peeled using indocyanine green staining after removing the ERM.\nOne month postoperatively, her best-corrected visual acuity was improved to 20/20 (). The spherical equivalent was −2.62 D despite aiming for −1.04 D, ie, the postoperative refractive error was −1.58 D.\nRetrospectively viewing all the individual signal curves in the IOLMaster, eight of 20 curves showed more than two peaks. When the amplitude of the second highest peak was higher than 30% of the highest peak and the amplitude of the third highest peak was lower than 50% of the second highest peak, the curve was defined as a double peak, and when the third highest peak was higher than 50% of the second highest peak, the curve was defined as a multi-peak. According to this rule, six eyes showed a double peak and two eyes showed a multi-peak. In cases with a double peak, five curves had a higher anterior peak, whereas one curve had a higher posterior peak. The distance from the anterior peak to the posterior peak of these curves was approximately 0.6 mm. If the posterior peak of the double peak is applied to obtain the axial measurement, the postoperative refractive error is reduced to −0.37 D.\nThe other 14 curves showing single peaks might correspond to the retinal surface because the distance was almost equal to that of the anterior peak of the double peak ().

[[52.0, 'year']]

F

{'22998208': 1, '9780097': 1, '17331581': 1, '11738911': 1, '18851731': 1, '20471687': 1, '12457677': 1, '12614744': 1, '2355321': 1, '11045345': 1, '24648720': 2}

{}

3958542-1

noncomm/PMC003xxxxxx/PMC3958542.xml

Cutaneous factitia in elderly patients: alarm signal for psychiatric disorders

A 77-year-old woman was hospitalized in a dermatology department for atrophic skin lesions, with discrete erythema at the edges on the preauricular area and hyperpigmented macules on the frontal and malar area (). She described the lesions as being present for several months, accompanied by slight pruritus on the face and scalp. The patient was diagnosed 10 years before with arterial hypertension well controlled by indapamide; a cardiological examination revealed no anomaly or no neurological symptoms. Dermatological examination failed to unfold other skin lesions, except the one on the face strictly related to the patient’s age.\nShe was referred to the hospital under suspicion of discoid lupus; a punch biopsy was taken from the preauricular area. The histopathological report excluded lupus and concluded orthokeratosis, spongiosis, and sparse lymphocytic perivascular infiltrate in the dermis ().\nAll the routine lab tests were within normal range. Based on clinical grounds, histological report, and lab investigations, the suspicion of discoid lupus was excluded. A psychiatric consult was demanded, and a transfer to the psychiatric department was accepted. New dermatological advice was asked for 1 month later, the patient being in very good condition, with no new lesions and minor hyperpigmentation on the face. The patient admitted the self-mutilation by causing the skin lesions herself, but without being able to explain the automutilation, most of the time being unaware of doing it; furthermore, she did not claim any delusions of parasitosis. She was transferred to the psychiatric unit and not followed up in the dermatology unit.

[[77.0, 'year']]

F

{'24091067': 1, '20864649': 1, '34463642': 1, '23326202': 1, '24053087': 1, '21482231': 1, '21437061': 1, '1552059': 1, '21548659': 1, '23927062': 1, '10972090': 1, '24648724': 2}

{'3958542-2': 2}

3958542-2

noncomm/PMC003xxxxxx/PMC3958542.xml

Cutaneous factitia in elderly patients: alarm signal for psychiatric disorders

A 61-year-old woman was hospitalized in a dermatology department for evaluation of atrophic scars disseminated on the face, trunk, and upper limbs (). She could not recall when she had first noticed the lesions, but her medical documents were filled with hospitalizations, investigations, and therapies for the last 2 years, varying from chronic eczema, anetoderma, morphea, prurigo, discoid lupus erythematosus, mycosis fungoides, and others not remembered by the patient. The patient was in good medical condition, with no comorbidities, treatments, or complaints. Clinical examination did not reveal anything worthy.\nA complete battery of blood tests was performed, but did not reveal the cause of the disorder. On the fifth day of hospitalization, during the night, she attempted suicide by taking an aspirin overdose. She was transferred to a psychiatric hospital, where she was diagnosed with severe depressive syndrome. Thereafter, she underwent stabilization and treatment, with no information on the therapeutic plan being available. The patient finally admitted the self-mutilation that had been going on for years.\nBased on the elusive history of the lesions, chronic evolution, and weird cutaneous impairments displayed upon attainable areas of the body, which did not mirror any of the known dermatoses, and associated to inconclusive biopsy (), with remission after specific psychiatric therapy, we finally reached a diagnosis of factitial dermatitis.

[[61.0, 'year']]

F

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{'3958542-1': 2}

3958572-1

noncomm/PMC003xxxxxx/PMC3958572.xml

Supratentorial Intraparenchymal Haemorrhages during Spine Surgery

A 28-year-old woman presented with an acute onset of bilateral lower weakness. She had a history of Ewing's sarcoma involving the thoracic spine with metastases to the right lung, right kidney and brain (). Palliative systemic chemotherapy, radiotherapy to the right thorax, and whole brain irradiation were given seven months prior. She had no bleeding diathesis. On examination, she did not have any sign of raised intracranial pressure (ICP). Her lower limb motor power was grade 1/5 bilaterally. The sensory level was at T10 dermatome. There was acute urinary retention but intact anal tone. Computerized tomography (CT) of the brain showed multiple cerebral and cerebellar metastases with perifocal oedema (). There was no hydrocephalus. Magnetic resonance studies showed an intradural extramedullary lesion at T4/5 that was causing significant cord compression ().\nBecause of previous radiotherapy, surgery was the only treatment option for her. Laminectomy for tumour excision was therefore performed. Intra-operatively, spinal CSF was drained under normal pressure. Her haemodynamics were stable during surgery. The spinal cord was well decompressed after tumour removal. The procedure lasted three hours and 15 minutes. Immediately after surgery, the patient was found to have dilated and non-reactive pupils. CT brain scan showed significant brain swelling and multiple ICHs (). Her family declined further surgery in view of the poor prognosis. She died two days later despite medical therapy. Histological examination of the spinal lesion showed metastatic Ewing's sarcoma. No autopsy was performed.

[[28.0, 'year']]

F

{'16741465': 1, '15987597': 1, '20461178': 1, '12015857': 1, '21294099': 1, '17355028': 1, '12634578': 1, '16007466': 1, '20829719': 1, '26692705': 2, '24653806': 2}

{'4660504-1': 1}

3958573-1

noncomm/PMC003xxxxxx/PMC3958573.xml

Spinal Arteriovenous Fistula with Progressive Paraplegia after Spinal Anaesthesia

A 20-year-old female was referred to our hospital, with a history of progressive sensory-motor paraplegia and a spinal magnetic resonance imaging (MRI) demonstrating conus medullaris edema as well as dilated vessels on the cord surface. Her history began two years prior to her admission to our hospital, while she was admitted to another hospital with acute abdomen and the suspicion of a ruptured ectopic pregnancy. For some reason, most likely related to the fact that she had eaten shortly before her admission, spinal anaesthesia was decided instead of general anesthesia. Several unsuccessful attempts for access were made. She described that during those attempts she felt a sharp electric current-like sensation in both the lower extremities followed by pins and needles-like sensation. She complained intensely and further attempts were aborted. Thereafter and during her hospitalisation she was complaining of disturbing sensory symptoms involving her legs. Over the following weeks, she started to have a progressive 'numbness' of her lower limbs followed by slowly progressive spastic paraplegia over the next twenty months. During that period and especially soon after her discharge, she visited her family doctor and described her problem, which was not properly evaluated and further investigation was not followed. She was getting worse in spite of physiotherapy, which was suggested. During the last six months she developed clear spasticity and paraparesis and was investigated by MRI, which revealed conus medullaris edema and dilated vessels on the surface of the spinal cord. A vascular lesion was suspected and the patient was referred to us for further investigation and treatment. On admission the general physical and systemic examination was unremarkable except for the neurological findings. No family history or sign of any genetic disease related to a central nervous system vascular lesion was discovered. Her neurological findings included severe spastic paraplegia-she came on a wheelchair-with hypoesthesia below the twelfth thoracic (T12) dermatome. Tone was markedly increased, and knee reflexes were exaggerated. Both the plantar reflexes were elicited with an up-going great toe and both her legs were affected by some atrophic changes. Bladder and intestinal sphincter function were preserved.\nAfter her admission she underwent a spinal angiogram that revealed a single, direct, moderate flow, single-hole type AVF at the left first lumbar (L1) level supplied by the anterior spinal artery (ASA), which presented a small dilatation just at the shunt site (). The draining vein and the superficial venous network were dilated with slow flow indicating venous congestion (). In the same session and under general anaesthesia we approached the lesion endovascularly using a Magic 1.2 Fr microcatheter (Balt, Montmorency, France) which was advanced over a Mirage 0.008-inch guidewire (ev3, Irvine, CA, USA). A single drop of N-butyl cyanoacrylate glue 50% was delivered just at the shunt site, which resulted to a complete occlusion of the fistula ().\nAfter awakening, she reported some immediate sensory improvement. Six months after the operation she was able to walk again with assistance. No complete motor recovery was achieved after one year despite of intensive rehabilitation.

[[20.0, 'year']]

F

{'10419371': 1, '15321178': 1, '15321239': 1, '16284566': 1, '8678281': 1, '17624210': 1, '16534285': 1, '12182775': 1, '12973972': 1, '16798451': 1, '17097107': 1, '18774513': 1, '15376294': 1, '17253336': 1, '9316950': 1, '9855649': 1, '18020083': 1, '20678351': 1, '8134010': 1, '12823872': 1, '11368250': 1, '24653807': 2}

{}

3958574-1

noncomm/PMC003xxxxxx/PMC3958574.xml

Microsurgical Excision of Symptomatic Sacral Perineurial Cyst with Sacral Recapping Laminectomy : A Case Report in Technical Aspects

This 61-year-old man presented with 2-year history of increasing lumbosacral pain and hypesthesia. On neurologic exam, he showed right L5 and S1 radiculopathy. His symptoms were aggravated by standing, walking, climbing, coughing and lifting, and relieved by sitting. The patient rated his pain 7 of 10 on the visual analogue score (VAS). He had bladder dysfunction and abnormal sensation for urination, and reported insertion of a Foley catheter 2 months ago. Preoperative MR imaging demonstrated 30×17×11 mm sized sacral cyst with another small cyst from L5 to S2 level (). Myelogram and CT showed the contrast-filled bridge between the thecal sac and the cystic mass and sacral cyst causing compression of adjacent nerve roots (). An L5 laminectomy and S1-3 en bloc laminectomy were performed. After careful dissection of the cyst wall, we observed the superior surface of the cyst compressing S1 nerve root ventromedially and S2 nerve root dorsally (). It was connected with a small cyst that was adhesive to right S2 and S3 nerve roots. The main cyst originated from inferomedial side of right L5 nerve root. The cyst was opened and its content appeared the same as the CSF content. We ligated the neck of the cyst and its wall was cut down away from the adjoining root sleeve. The sacral lamina was recapped at the back again with using heavy silk sutures (). His lumbosacral pain and radiculopathy improved progressively after surgery. Postoperative two weeks, he removed the Foley catheter. Follow up MR imaging after 6 months demonstrated complete resolution of the cyst (). At one year follow up, he had mild back pain (2 of 10 on the VAS).

[[61.0, 'year']]

M

{'10917349': 1, '12648906': 1, '16508691': 1, '11518008': 1, '2274142': 1, '3576493': 1, '26131126': 1, '14025208': 1, '32043000': 1, '33879717': 2, '602855': 1, '9016209': 1, '16322904': 1, '3975809': 1, '11453427': 1, '27554352': 1, '9092864': 1, '8192075': 1, '31270612': 1, '3343608': 1, '24653808': 2}

{'3958574-2': 2, '3958574-3': 2, '8078352-1': 1}

3958574-2

noncomm/PMC003xxxxxx/PMC3958574.xml

Microsurgical Excision of Symptomatic Sacral Perineurial Cyst with Sacral Recapping Laminectomy : A Case Report in Technical Aspects

This 21-year-old man complained of worsening radiating pain and hypesthesia on left leg for 1 year. His motor weakness was grade 4 on left leg, especially when extending the left ankle. Because of worsening symptoms he eventually visited our department. He had mild claudication, positive on left straight leg raising test at 45 degree. We confirmed a mild left S1 radiculopathy on electromyography. He had no neurologic deficit associated with cauda equina syndrome. Preoperative MR imaging showed a 20×13×14 mm sized sacral cyst (). We performed myelogram and CT and found the contrast-filled stalk between the thecal sac and the cyst. The cyst compressed a contiguous structure including nerve roots ().\nWe performed surgery the same as patient 1 () and symptoms disappeared after one week. Follow up MR imaging after 2 months demonstrated complete resolution of the lesion. We checked with MR imaging after 1 year and ascertained that there was no further cystic formation and complication ().

[[21.0, 'year']]

M

{'10917349': 1, '12648906': 1, '16508691': 1, '11518008': 1, '2274142': 1, '3576493': 1, '26131126': 1, '14025208': 1, '32043000': 1, '33879717': 2, '602855': 1, '9016209': 1, '16322904': 1, '3975809': 1, '11453427': 1, '27554352': 1, '9092864': 1, '8192075': 1, '31270612': 1, '3343608': 1, '24653808': 2}

{'3958574-1': 2, '3958574-3': 2, '8078352-1': 1}

3958574-3

noncomm/PMC003xxxxxx/PMC3958574.xml

Microsurgical Excision of Symptomatic Sacral Perineurial Cyst with Sacral Recapping Laminectomy : A Case Report in Technical Aspects

This 60-year-old female patient visited our department with 6-year history of increasing lumbosacral pain and right leg radiculopathy. On neurologic examination, she complained right L5 and S1 radiculopathy. The patient rated her pain 9 of 10 on the VAS. She did not have bladder dysfunction. Preoperative MR imaging demonstrated 15×17×22 mm sized sacral cyst with S1 nerve root (). Myelogram and CT showed the contrast-filled bridge between the thecal sac and the cystic mass, and sacral cyst causing compression of adjacent nerve roots (). After careful dissection of the cyst wall, we observed the superior surface of the cyst. The main cyst originated from inferomedial side of right L5 nerve root. We performed surgery the same way but we used miniplate instead of silk for recapping (). The symptoms improved progressively after surgery. MR imaging 4 months later demonstrated complete resolution of the cyst (). At one year follow up, she had only mild back pain (3 of 10 on the VAS).

[[60.0, 'year']]

F

{'10917349': 1, '12648906': 1, '16508691': 1, '11518008': 1, '2274142': 1, '3576493': 1, '26131126': 1, '14025208': 1, '32043000': 1, '33879717': 2, '602855': 1, '9016209': 1, '16322904': 1, '3975809': 1, '11453427': 1, '27554352': 1, '9092864': 1, '8192075': 1, '31270612': 1, '3343608': 1, '24653808': 2}

{'3958574-1': 2, '3958574-2': 2, '8078352-1': 1}

3958578-1

noncomm/PMC003xxxxxx/PMC3958578.xml

Demographic and Clinical Characteristics of Patients with Restless Legs Syndrome in Spine Clinic

A 68-year-old woman was presented with severe paresthesia in the left leg and tingling sensation in the right lower leg (Type E). She had no underlying disease. Spine MRI shows left L4-5 foraminal LDH with Grade 3 foraminal stenosis (). She was treated with a L5 transforaminal epidural steroid injection and was followed up. She felt much improvement on left L5 paresthesia, but still had unpleasant sensation on both lower legs with aggravation during night time. We diagnosed as mixed conditions; left L4-5 LDH and RLS. She took additional pramipexole and then paresthesia of the lower legs disappeared.

[[68.0, 'year']]

F

{'3206054': 1, '18274269': 1, '14725821': 1, '11509198': 1, '23121149': 1, '7565839': 1, '21795081': 1, '22772928': 1, '20671589': 1, '20308517': 1, '22704403': 1, '11160969': 1, '22834914': 1, '23211049': 1, '8723377': 1, '21412893': 1, '10566915': 1, '15016424': 1, '2312537': 1, '11435804': 1, '20191944': 1, '16874755': 1, '15223000': 1, '10751293': 1, '15222997': 1, '23179641': 1, '14592343': 1, '14592341': 1, '11053528': 1, '11152983': 1, '11391765': 1, '34768519': 1, '8990055': 1, '22505854': 1, '11909990': 1, '11346069': 1, '10752578': 1, '23183234': 1, '22435397': 1, '11295915': 1, '20466589': 1, '15364685': 1, '20531433': 1, '17566123': 1, '11244268': 1, '10904456': 1, '12473756': 1, '22406784': 1, '17131226': 1, '23345489': 1, '21370262': 1, '24653801': 2}

{}

3958579-1

noncomm/PMC003xxxxxx/PMC3958579.xml

Chronic Encapsulated Intracerebral Hematoma Associated with Cavernous Malformation

A 12-year-old female was admitted to our hospital because of a one-week history of progressive headache and nausea. She had no prior history of radiation therapy or surgery. She had a past history of a simple febrile seizure at 21 months of age, and a brain magnetic resonance imaging (MRI) study was performed on a 1.5 tesla device and was judged normal (). On admission, neurological examination showed no abnormality. A brain computed tomography (CT) scan and MRI on a 3 tesla device showed an intracerebral hematoma surrounded by edema in the right frontal lobe (). One week later, her headache and nausea worsened, and a brain CT scan revealed the enlargement of hematoma (). A right frontal craniotomy was performed. The capsule was opened at a depth of 1 cm from the cortex. The cavity was filled with brownish fluid hematoma similar to chronic subdural hematoma. A lobulated mass was also found on the capsule. The capsule, mass, and hematoma were totally removed (). Histological examination confirmed the diagnosis of CM, and also revealed that the capsule consisted of an outer collagenous layer and an inner granulated layer with deposits of hemosiderin, which was compatible with CEIH (). Immunohistochemical analysis revealed increased expression of vascular endothelial growth factor (VEGF) and the VEGF receptor (VEGFR)-1 in the endothelium and fibroblasts in the capsule (). Postoperative cerebral angiography showed no abnormality. The postoperative course was uneventful and the patient was discharged without neurological deficit.

[[12.0, 'year']]

F

{'12639533': 1, '21891948': 1, '1919693': 1, '19597762': 1, '20809765': 1, '29662588': 1, '15661718': 1, '26855712': 1, '18812682': 1, '21430981': 1, '10874148': 1, '20931239': 1, '7472549': 1, '2330096': 1, '8468616': 1, '22234209': 1, '19479188': 1, '22396841': 2, '32698881': 1, '3993333': 1, '21273746': 1, '14623736': 1, '21052741': 1, '24653802': 2}

{'3291704-1': 1}

3958580-1

noncomm/PMC003xxxxxx/PMC3958580.xml

Spontaneous Carotid-Cavernous Fistula in the Type IV Ehlers-Danlos Syndrome

A 46-year-old female presented with diplopia and conjunctival ecchymosis for 5 days. She had suffered from headache and pulsatile tinnitus on the right side for 2 months. She had repeated medical histories of easy bruisability, rupture of the tendon and ligament as well as the subluxation of multiple joints. She had a thin, translucent, and fragile skin with prominent veins, especially on the hands. Ophthalmologic evaluation showed chemosis with mild exophthalmia and lateral gaze limitation on the right side, without any problem of visual acuity or field. She had a senile-looking face, hair loss, metacarpophalangeal joint dislocation, radial head dislocation at extension on the right side, distal radioulnar joint instability, fourth brachymetatarsia, and Lisfranc (tarsometatarsal) joint dissociations bilaterally (). Two daughters of 22 and 17 years old showed similar appearances (). Brain magnetic resonance (MR) angiography demonstrated the CCF on the right side associated with the right superior ophthalmic vein (SOV) dilatation. Thoracoabdominal computed tomographic angiography demonstrated multifocal splenic artery aneurysms. On genetic investigation, her COL3A1 gene mutation was identified by polymerase chain reaction assays. A splice site mutation in intron 23 of one allele of the COL3A1 gene [c. 1662+1 (intervening sequence 24) G→A] was found to be the causative mutation. Her daughters had the same genotype. Because of the high risk of vascular damage from conventional angiography and intervention, further investigation and treatment was deferred.\nTwo months later, she was readmitted due to the generalized tonic-clonic seizure. Brain MR imaging revealed venous infarction at the right anterior insular cortex and right frontal lobe with micro-bleeds on gradient-echo images (). As we considered these features as ominous signs of impending intracranial hemorrhage and poor prognosis, the decision was made to precede embolization of CCF. Under the ultrasonographic guidance, her femoral artery was carefully punctured and 4 Fr sheath was introduced. Then, cerebral angiography was carefully performed with a 4 Fr angiocatheter. On angiography, direct CCF accompanied multiple venous drainage into the right SOV, right inferior petrosal sinus (IPS), and right cavernous sinus (CS) with reflux to the superficial middle cerebral vein and medullary veins (). Notably, the right IPS was stenosed. On right common carotid artery angiography with the left neck compression, fistular point was identified at the medial compartment of CS.\nAfter the angiographic evaluation, a 5 Fr guiding catheter was positioned at the right internal jugular vein via femoral vein. A microcatheter was placed at the right CS near the proximal portion of right SOV via the right IPS. The CS near the fistular point was completely embolized with fibered coils. There were no fistulous flow and venous reflux, and normal antegrade flow through the right internal carotid artery (ICA) was restored with subtle venous hyperemia on the perisylvian area (). The clinical course was uneventful after the embolization. Bruit disappeared and right eye movement improved at discharge. Chemosis, proptosis and limitation of the ocular motion were completely resolved on 6-month follow-up after the transvenous embolization.

[[46.0, 'year']]

F

{'3287925': 1, '27511817': 1, '30147886': 2, '8456380': 1, '10815681': 1, '5556792': 1, '1055406': 1, '8781594': 1, '11014550': 1, '3819843': 1, '10233664': 1, '6664673': 1, '2033461': 1, '8880727': 1, '3076851': 1, '8160237': 1, '8526472': 1, '29201856': 2, '27796449': 1, '2362658': 1, '10706896': 1, '20670529': 1, '2676388': 1, '6018786': 1, '3968564': 1, '9399899': 1, '5147941': 1, '9557891': 1, '29940997': 1, '24653803': 2}

{'6099022-1': 1, '5702757-1': 1}

3958581-1

noncomm/PMC003xxxxxx/PMC3958581.xml

Renal Subcapsular Hematoma after Percutaneous Transfemoral Angiography

A 54-year-old female was admitted to our hospital for the evaluation of unruptured cerebral aneurysm. She had a 5-year history of diabetes mellitus and hypertension. Eighteen months earlier, she had chest pain and underwent transfemoral cardiac angiogram at a different institute. Since then, she had been taking aspirin 100 mg under the diagnosis of angina. Percutaneous cerebral angiogram was performed through the right femoral artery. She was diagnosed as having multiple aneurysms in both the anterior communicating artery and in the paraclinoid portion of the internal carotid artery. The whole procedure of percutaneous cerebral angiogram was uneventful. However, about 3 hours later, she complained of left flank pain. Her blood pressure was 90/60 mm Hg and the body temperature was 36.4℃. On physical examination, the abdomen was soft but tender on the left upper quadrant. There was no evidence of puncture site bleeding or petechiae. Laboratory findings were white blood cell 6100/mm3, Hb 10.8 g/dL, platelets 174000/mm3. We performed abdominal computed tomography (CT). Abdominal CT showed a left renal subcapsular hematoma in the lower pole portion (). She was consulted by Urology Department and was advised to undergo supportive treatment. She had a followed-up abdominal CT seven days later. The follow-up abdominal CT showed a slight regression of the hematoma. She was discharged with improved conditions after 14 days of hospital stay. Six months later, her 64-cut multislice CT scan showed complete regression of the subcapsular hematoma (). Interestingly, in her three-dimensional angiogram, small accessory renal arteries supplying the lower pole of the kidney were found at both sides (). She has remained symptom free since then.

[[54.0, 'year']]

F

{'8025931': 1, '9157852': 1, '20639669': 1, '2952137': 1, '8179080': 1, '33887860': 1, '27867458': 2, '11259702': 1, '15026593': 1, '27621950': 2, '17349702': 1, '3518559': 1, '2720767': 1, '30445948': 2, '24653804': 2}

{'5018549-1': 1, '5105220-1': 1, '6240213-1': 1, '6240213-2': 1}

3958582-1

noncomm/PMC003xxxxxx/PMC3958582.xml

Sphenoid Ridge Meningioma Presenting as Acute Cerebral Infarction

A 52-year-old man with no significant prior medical history was brought to our emergency room with drowsy mental status that lasted ten hours after the onset of left hemiparesis and dysarthria. The patient's left extremities were weak, and muscle power was of grade 4 in upper and lower limbs. Brain computed tomography (CT) and magnetic resonance examinations revealed acute cerebral infarction in the right MCA territory and an extra-axial mass with homogenous enhancement in the medial portion of the right sphenoid ridge (). Magnetic resonance angiogram showed complete occlusion of the right ICA terminus (). The infarction included the right uncus, insula, medial occipitotemporal gyrus, basal ganglia, corona radiate, and precentral gyrus (). The tumor, which was consistent with a sphenoid ridge meningioma, encased and compressed the right ICA terminus. Cerebral angiography demonstrated complete occlusion of the right proximal M1 portion with slightly limited collateral circulation to the right MCA territory and a radiographic blush from the surrounding meningioma (). Flow in the right MCA had been partially reconstituted by supply from the ipsilateral anterior cerebral artery and the posterior cerebral artery, but was much reduced. A CT perfusion study obtained shortly after arrival showed dramatic prolongation of time to peak and mean transit time of the right MCA territory, indicating obviously decreased regional cerebral blood flow in the involved territory ().\nThe patient was admitted and started on dual antiplatelet therapy, induced hypertension, and volume expansion. However, over the ensuing 48 hours, the left hemiparesis deteriorated steadily to muscle power grade 2 in upper and lower limbs, and follow-up magnetic resonance imaging demonstrated enlargement of the area of the diffusion weighted abnormality (). Emergency extracranial-intracranial (EC-IC) bypass was performed uneventfully. We have adopted a "double-barrel" technique whereby both branches of the superficial temporal artery are joined with MCA recipients to augment flow to the whole territory of the MCA, while leaving the tumor as is (). The patient awoke in the recovery room with exhibited a dramatic improvement of his preoperative weakness over the next 48 hours. He was maintained on oral aspirin at 100 mg/day and clopidogrel at 75 mg/day. CT perfusion scans obtained on the 14th postoperative day revealed improved cerebral blood flow in the involved territory (). At the time of writing the plan was to follow the tumor. We are considering a gamma knife radiosurgery for meningioma, if needed.

[[52.0, 'year']]

M

{'9574636': 1, '23266265': 1, '23821132': 1, '12486289': 1, '11386821': 1, '22068990': 1, '19499983': 1, '26846762': 1, '2796031': 1, '8045068': 1, '16908574': 1, '3366148': 1, '8178634': 1, '11386838': 1, '29901637': 1, '2512784': 1, '20671387': 1, '22295325': 1, '2865674': 1, '24653805': 2}

{}

3958605-1

noncomm/PMC003xxxxxx/PMC3958605.xml

Unprotected Left Main Percutaneous Coronary Intervention in a 108-Year-Old Patient

A 108-year-old man was referred with ongoing chest pain on minimal or no exertion (Canadian Cardiovascular Society class III-IV) despite optimum medical therapy. He was an ex-smoker, hypertensive, but non-diabetic, and had chronic kidney disease, Parkinsonism and below-knee amputation of the left leg due to a previous road-traffic accident. His pulse was 80/min, blood pressure 140/90 mm Hg, and the lung bases were clear. His resting electrocardiogram (ECG) showed sinus rhythm, ST depression and T inversion in leads V 5, V 6, I and aVL, and ST elevation in aVR (); echocardiography revealed distal septal and basal inferior left ventricular wall hypokinesia with a left ventricular ejection fraction of 45-50%. Blood counts and biochemistry including the sugar and lipid profile were normal. Serum creatinine was 1.6 mg/dL, and the glomerular filtration rate was 40.8 mL/min. CAG was done because of ongoing chest pain; there was triple vessel disease with involvement of the left main coronary artery (LMCA); there was 75% stenosis in the distal LMCA, 95% stenosis in the proximal segment and 75% stenosis in the mid segments of the left anterior descending (LAD) artery, 75% osteo-proximal and 90% distal stenosis in the left circumflex (LCX) artery, and total occlusion of the right coronary artery from the origin (). The calculated Euroscore was 20, and the SYNTAX score 37. Coronary artery bypass graft (CABG) surgery was advised, but the surgeons declined to perform it. So, percutaneous transluminal coronary angioplasty and stenting were done for the LMCA and LAD lesions; LMCA was hooked by a JL 3.5, 7 Fr guide catheter, and the LAD lesion was navigated with a hydrophilic guidewire (BMW guidewire, Abbott Vascular, Santa Clara, CA, USA), while another hydrophilic guidewire (Runthrough™ NS Coronary Guidewire, Terumo Medical Corporation, Tokyo, Japan) was kept in the distal LCX. Predilatation was done with a 2.5×12 mm noncompliant balloon (NC Sprinter RX Noncompliant Balloon Dilatation Catheter, Medtronic Vascular, Minneapolis, MN, USA) at 12-14 atm. A 2.75×36 mm biodegradable polymer drug-eluting stent (DES) (BioMatrix Flex, Biosensors International, Bulach, Switzerland) was deployed over the proximal to mid LAD lesion at 14 atm for 20 seconds. Another 3.5×33 mm BioMatrix Flex stent (Biosensors International) was deployed over the left main to proximal LAD lesion at 14 atm for 20 seconds, and overlapped with the previous stent. Post-dilatation was done with a 3.5×12 mm Quantum balloon (Quantum™ Maverick® Balloon Catheters, Boston Scientific Corp.) that was deployed at up to 22 atm. The LCX wire was re-crossed, and the ostial lesion was dilated with a 2.5×12 mm noncompliant balloon (NC Sprinter RX Noncompliant Balloon Dilatation Catheter, Medtronic Vascular) at 12 atm. Finally, kissing balloon dilatation was done with LAD (3.5×12 mm Quantum) and LCX (2.5×12 mm Sprinter) balloons at 18 and 12 atm respectively. Thrombolysis in Myocardial Infarction III flow was established (). A temporary pacemaker and intra-aortic balloon pump, and provisions for an emergency CABG were kept ready. The immediate post-procedural period was uneventful. The patient was free of chest pain; ECG changes became normal (), echocardiography revealed improvement in regional left ventricular wall motion, with an ejection fraction of 58%, and the troponin I was negative (0.118 ng/mL). However, on the first post-procedural day, the patient developed an acute confusional state and abdominal distension. A CT scan of the brain and an ultrasonogram of the abdomen revealed no significant abnormalities. Blood biochemistry including the serum creatinine was normal. On day 2, the confusional state and abdominal distension improved with conservative measures, and on the third post-procedure day, the patient was oriented and able to converse well. He was discharged with aspirin 75 mg and clopidogrel 75 mg daily. During the subsequent 3 months' follow-up, the patient remained free of symptoms.

[[108.0, 'year']]

M

{'22009446': 1, '16844881': 1, '18825133': 1, '23726179': 1, '20605241': 1, '21939824': 1, '22210689': 1, '27326065': 1, '20031689': 1, '19406337': 1, '23439102': 1, '19824825': 1, '19303634': 1, '21139558': 1, '20494044': 1, '18498954': 1, '24653741': 2}

{}

3958606-1

noncomm/PMC003xxxxxx/PMC3958606.xml

Transvenous Pacemaker Lead Removal in Pacemaker Lead Endocarditis with Large Vegetations: A Report of Two Cases

A 63-year-old male was admitted for fever and confusion of three days. He had undergone pacemaker (VDD type) implantation for symptomatic sick sinus syndrome three months prior.\nUpon admission, the patient was febrile with a temperature of 38.3℃, confused and had dysarthric speech. Physical examination was remarkable for warmth, erythema, and tenderness of the skin overlying the pacemaker pocket, which was exposed. His white blood cell (WBC) count was 18.40×103/µL, and C-reactive protein (CRP) concentration was 148.27 mg/L. Transthoracic echocardiogram (TTE) revealed vegetations attached to the tricuspid valve (2.4×1.1 cm) (, arrow), right atrium (0.8×0.8 cm) (, broken arrow), and mitral valve (0.7×0.5 cm) (, arrow). Brain magnetic resonance imaging results were consistent with multiple acute embolic infarcts (). Computed tomography scan of the chest and abdomen showed multiple cavitary nodules in both lungs () and small, low-attenuated lesions in segment 6 of the liver (), suggesting septic embolism.\nOn the same day, the patient underwent transvenous removal of the pacemaker lead (). Pocket site swab cultures and three separate sets of blood cultures were collected and later revealed methicillin-resistant, Staphylococcus aureus. The patient was treated with vancomycin 1000 mg every 12 hours. On the tenth day, blood cultures were negative for the first time. The patient's fever relapsed at day 14 and three of three blood cultures grew Candida tropicalis (C. tropicalis). Repeated blood cultures were positive for C. tropicalis until day 18. Antifungal treatment was started intravenously and continued for a total of six weeks, including four weeks with liposomal amphotericin B 350 mg/day (5 mg/kg) and two weeks with fluconazole 400 mg/day. After 22 days, vegetations of tricuspid valve and right atrium were no longer visible on TTE (). The patient was discharged after eight weeks of admission and no relapse was documented at the six months clinical visit.

[[63.0, 'year']]

M

{'12891205': 1, '21707667': 1, '17724263': 1, '17481444': 1, '11033588': 1, '9133520': 1, '33435384': 2, '16606389': 1, '8353245': 1, '24653742': 2}

{'3958606-2': 2, '7827933-1': 1}

3958606-2

noncomm/PMC003xxxxxx/PMC3958606.xml

Transvenous Pacemaker Lead Removal in Pacemaker Lead Endocarditis with Large Vegetations: A Report of Two Cases

A 19-year-old woman was admitted for chills of three days. She had a history of pacemaker (VDD type) implantation five years prior for high-degree atrioventricular block with recurrent syncope.\nUpon admission she was afebrile and did not reveal pacemaker skin redness or tenderness. Her WBC count was 12.75×103/µL and CRP concentration was 26.4 mg/L. TTE revealed a large vegetation (2.5×1.7 cm) attached to the tricuspid valve (). We began treatment with intravenous vancomycin 1000 mg every 12 hours.\nOn the third day, three different sets of blood cultures grew Staphylococcus epidermidis and blood cultures were positive until day 12. At day 15, the size of the largest vegetation increased to 3.2×0.8 cm. We then completely removed the previous pacemaker and leads () transvenously with a temporary pacemaker. Blood cultures were negative for the first time at day 17, but TTE revealed no interval change in vegetation size until day 32. Despite the lack of interval vegetation size change, a new pacemaker (VDD type) was implanted at day 32 (). After successful re-implantation, treatment with intravenous vancomycin was continued for a total of six weeks and TTE showed complete resolution of the vegetation. At the five-year follow-up, the TTE showed no relapse ().

[[19.0, 'year']]

F

{'12891205': 1, '21707667': 1, '17724263': 1, '17481444': 1, '11033588': 1, '9133520': 1, '33435384': 2, '16606389': 1, '8353245': 1, '24653742': 2}

{'3958606-1': 2, '7827933-1': 1}

3958607-1

noncomm/PMC003xxxxxx/PMC3958607.xml

A Case of Sudden Cardiac Death due to Pilsicainide-Induced Torsades de Pointes

An 84-year-old male visited our hospital due to palpitations and shortness of breath that began two days previously. He underwent physical examination, 12-lead ECG, chest X-ray, and blood tests. The patient's heart rate was 150 beats/min, and his blood pressure was 126/76 mm Hg. Chest X-ray revealed no cardiomegaly (cardiothoracic index=46%) and no congestion. An ECG examination showed atrial fibrillation, which was considered to be of recent onset (within 48 hours). Although ECG showed a tendency for poor progression of R in V 1-3, the patient had no chest pain and no history of coronary artery disease. In addition, an echocardiography, which was performed in a private clinic two months before the patient visited our hospital, showed normal left ventricular wall motion; during the past two months, there were no significant differences of ST-T changes in ECG. Routine laboratory tests revealed serum sodium of 142 mEq/L, potassium of 4.8 mEq/L (no hypokalemia and hyperkalemia) and creatinine of 1.0 mg/dL, which were indicative of mild renal dysfunction. Thus, oral low-dose pilsicainide at 50 mg twice daily was prescribed to convert atrial fibrillation to a sinus rhythm, and a Holter ECG was ordered in the outpatient clinic. In addition, he started anticoagulant treatment with warfarin but did not receive any other drugs, including any other antiarrhythmic drugs.\nOne day after receiving an oral administration of pilsicainide, he visited our hospital again, and a Holter monitor was fitted to evaluate the efficacy of pilsicainide and initiated at 13:30 in the afternoon. At this time, he felt no palpitations and showed a sinus rhythm with normal QT and QTc intervals (320 msec and 400 msec, respectively) in the CM5 lead of the Holter ECG (). However, the patient died during his sleep 18 hours after the Holter ECG was started. He reported no discomfort during the day or before his sudden death.\nThe analysis of the Holter ECG recording revealed that the cause of sudden death was an episode of TdP (). The Holter ECG showed that the patient developed atrial fibrillation followed by repetitive non-sustained and sustained TdP ( and ). As shown in , the QTc interval in the Holter ECG showed gradual elongation from 13:30 at the start until 6:00 the next day. At 7:00 the next day, TdP was observed, and it continued for approximately one hour; at 8:00, cardiac arrest was detected in the Holter ECG. The electrophysiological parameters, QRS complexes, RR, and QTc interval were measured. The segments with excessive noise, ectopic activity and atrial fibrillation were excluded from the analysis. illustrates the trend of the electrophysiological parameters. The QTc interval was clearly prolonged compared with that of initial Holter ECG. At the same time, the width of the QRS complexes was slightly prolonged compared with that of the initial Holter ECG.

[[84.0, 'year']]

M

{'22333385': 1, '30210355': 1, '32461529': 1, '15575054': 1, '8831412': 1, '2473403': 1, '27878411': 1, '24653743': 2}

{}

3958608-1

noncomm/PMC003xxxxxx/PMC3958608.xml

An Unusual Pattern of All Three Coronary Arteries Originating from a Single Coronary Artery Arising from the Right Sinus of Valsalva

A 48-year-old woman presented with exertional angina and palpitations for a long time. She a had medical history of hypertension and dyslipidemia, and a family history of coronary artery disease. Her father had a heart attack at an early age. The electrocardiogram showed normal sinus rhythm and nonspecific ST-T wave changes. Labaratory examinations were unremarkable. The exercise electrocardiogram showed dynamic changes with ST-segment depression in the V 1-4 leads. Echocardiography revealed preserved left ventricle systolic function and concentric left ventricle hypertrophy. The coronary angiography procedure was started with a LCA cannulation attempt, but left anterior descending coronary artery and Cx imaging was unsuccessful even though contrast was injected into the left coronary sinus. The right coronary artery was cannulated and visualized with a right Judkins catheter. At this time, we noticed the left coronary arteries arising from the right sinus of Valsalva. The right Judkins catheter was gently pull back and the left coronary arteries were clearly visualized ( and ). There was no significant stenosis of any of the three coronary trees. Coronary CT angiography confirmed that the left coronary arteries arose from the right sinus of Valsalva and that all three coronary arteries originated from the single sinus (). The patient was managed with conservative treatment and has had no symptoms on clinical follow-up.

[[48.0, 'year']]

F

{'15640543': 1, '11262367': 1, '758666': 1, '25953581': 1, '2208265': 1, '23508331': 2, '2918156': 1, '30524556': 1, '24653744': 2}

{'3596660-1': 1}

3958635-1

noncomm/PMC003xxxxxx/PMC3958635.xml

Ranibizumab Injection for Corneal Neovascularization Refractory to Bevacizumab Treatment

A 32-year-old female with known corneal opacity and decreased visual acuity of the right eye, which was noticed three weeks prior to visit, was referred to our clinic. Previously, in 2008, she visited an ophthalmologist due to decreased visual acuity measuring 20 / 50, and a pannus-like elevated nodular opacity was found at the right superotemporal cornea (). Following suspicion of herpetic keratoconjunctivitis, she received two subcon-junctival and intrastromal bevacizumab (Avastin; Genentech Inc., South San Francisco, CA, USA) injections with a one month interval. Within one month after the last injection, the diameter of abnormal new vessels decreased to some degree, but the extent of corneal NV and opacity remained stationary (). Further bevacizumab treatment was abandoned because the lesion showed no improvement during the next six months and no other treatment was given to the patient for the next four years.\nAt her first visit to our clinic, the patient's best-corrected visual acuity (BCVA) measured 20 / 250 in the right eye and a central corneal opacity was observed along with new, abnormal vessels growing in from the superotemporal side (), suggestive of herpetic keratoconjunctivitis. After administration of Virgan (0.15% ganciclovir; Samil, Seoul, Korea) ointment and Gatiflo (0.3% gatifloxacin; Handok, Seoul, Korea) eye drops for six months, the patient underwent two subconjunctival and intrastromal ranibizumab (Lucentis, Genentech Inc.) injections in the right eye, with a one month interval. At two months postoperatively, there was significant decline in both the neovascular area (by 8.02%) and vessel caliber compared to the initial lesion (). Anterior segment photograph taken by a built-in camera on a surgical microscope (Leica F40; Microsystems, Wetzlar, Germany) at three months after the initial injection also revealed reduction of the lesion extent (). The BCVA was improved to 20 / 160 on her last visit at six months postoperatively and neither adverse reactions nor recurrence was apparent. Alteration in the corneal neovascular area was determined by sequential standardized digital slit-lamp pictures, which were analyzed morphometrically using image analysis software (Image J 1.40 g; Wayne Rasband at the Research Services Branch, National Institutes of Health, Bethesda, MD, USA). The procedure was approved by institutional review board of the Catholic University of Korea and the patient was provided with thorough explanation and filled out an informed consent form.

[[32.0, 'year']]

F

{'6205680': 1, '31713747': 1, '19324856': 1, '20100589': 1, '18329626': 1, '22482468': 1, '15136787': 1, '11507336': 1, '21212709': 1, '2446823': 1, '6794043': 1, '15106938': 1, '21593862': 1, '22003112': 1, '8756718': 1, '27610242': 1, '23407316': 1, '29908870': 1, '21712359': 1, '17471348': 1, '12045060': 1, '21245949': 1, '19413229': 1, '24688262': 2}

{}

3958637-1

noncomm/PMC003xxxxxx/PMC3958637.xml

Bilateral Acute Anterior Uveitis and Optic Disc Edema Following a Snake Bite

A 35-year-old male farmer was brought to the emergency department after being bitten by a viper on the dorsum of the right foot. He had received first aid following the bite in the form of local wound incision and application of tourniquet. The patient was stable and vitals were normal. There were no signs of internal or external bleeding. Examination revealed a wound on the dorsum of the right foot with cellulitis of the lower limb. The patient was started on anti-snake venom (ASV) injection 70 mL stat, followed by 30 ml every six hours for two days. On the second day the patient complained of sudden onset pain and blurring of vision in both eyes (OU) which gradually worsened over the next four days. He was referred to the eye department on sixth day following the bite. On examination, the best-corrected visual acuity (BCVA) in OU was 20/200. Extraocular movements were full and free in all directions of gaze. Anterior segment examination of OU revealed fresh keratic precipitates with grade 3 anterior chamber (AC) cells and flare with posterior synechiae (). Pupils showed a sluggish and ill-sustained reaction to bright light. Fundus examination through hazy media revealed disc hyperemia with blurred margins and disc edema (). The rest of the fundus was within normal limits. On color vision testing by pseudoisochromatic plates of Ishihara, the patient responses from the second plate to the ninth plate were incorrect, and he was not able to identify the number in tenth to thirteenth plates in OU, which indicated total red green deficiency. Visual fields could not be tested, as the patient was irritable and uncooperative. Visual evoked potential testing showed prolonged latency and decreased amplitude. Optical coherence tomography (OCT) revealed a retinal nerve fiber layer (RNFL) thickness of 247 microns in the right eye (OD) and 245 microns in the left eye (OS) superiorly, 117 microns (OD) and 113 microns (OS) nasally, 260 microns (OD) and 258 microns (OS) inferiorly, and 169 microns (OD) and 162 microns (OS) temporally, suggesting an increase in RNFL thickness. Neuroimaging of the brain was normal. Magnetic resonance imaging of the orbit showed abnormal signal intensity from the optic nerve of OU. A diagnosis of acute anterior uveitis and optic disc edema OU following snake bite was established and the patient was started on topical steroid drops six times a day and homatropine drops two times a day, and was given intravenous methylprednisolone 250 mg daily in normal saline over one hour for 3 days. On the fourth day, the visual acuity in OU improved to 20/80. Examination showed a decrease in the AC cells, flare and disc edema. OCT revealed that the disc edema had resolved. The patient was continued on topical steroids and cycloplegics, and was started on oral prednisolone in doses tapered over three weeks. At the end of three weeks, visual acuity improved to 20/30 with AC exhibiting no cells or flare, and disc edema resolved completely.

[[35.0, 'year']]

M

{'7346436': 1, '9567021': 1, '13032366': 1, '4775470': 1, '7169408': 1, '13618532': 1, '24688264': 2}

{}

3958638-1

noncomm/PMC003xxxxxx/PMC3958638.xml

Acetazolamide for Cystoid Macular Oedema in Bietti Crystalline Retinal Dystrophy

A 32-year-old male of Maltese heritage who was known to have electroretinogram-confirmed Bietti crystalline retinal dystrophy presented with acute bilateral central visual impairment. Upon examination, best-corrected visual acuity (BCVA) was 6 / 60 in the right eye and 6 / 45 in the left eye. At an examination one year previously, BCVA had been 6 / 7.5 in the right eye and 6 / 18 in the left.\nDilated retinal examination revealed the presence of peripheral corneal and retina crystalline changes characteristic of Bietti dystrophy (). Flourescein angiography showed patchy hypof luorescence indicative of chorioretinal atrophy. No evidence of late leakage was observed, excluding the diagnosis of choroidal neovascularisation (). Time-domain (TD)-OCT was performed and demonstrated bilateral cystic macular lesions () with a central foveal thickness (CFT) of 242 µm in the right eye and 253 µm in the left.\nOn the basis of the OCT findings, the patient was diagnosed with cystoid macular oedema. Acetazolamide therapy at a dose of 500 mg daily was initiated, and one month later, visual acuity improved to 6 / 18 bilaterally and CFT reduced to 221 µm in the right eye and 225 µm in the left eye. Following one year of acetazolamide therapy, BCVA was 6 / 15 in the right eye and 6 / 24 in the left eye, and CFT had stabilised at 221 µm in the right eye and 219 µm in the left eye ().

[[32.0, 'year']]

M

{'2783846': 1, '15042513': 1, '17420384': 1, '22205354': 1, '25738160': 1, '23221965': 1, '10664057': 1, '18835469': 1, '34049507': 1, '28698241': 1, '2803090': 1, '31544053': 1, '17173010': 1, '24949209': 1, '25505979': 1, '28791069': 2, '24688265': 2}

{'5525505-1': 1}

3958639-1

noncomm/PMC003xxxxxx/PMC3958639.xml

Reversal of Early Central Retinal Vein Occlusion by Alleviating Optic Nerve Edema with an Intravitreal Dexamethasone Implant

A 44-year-old female without any previous medical history visited our clinic because of the sudden onset of intermittent blurred vision in her left eye. Her best-corrected visual acuity (BCVA) was 20 / 22 and fundus examination revealed multiple retinal, preretinal, and subretinal hemorrhages throughout the retina with tortuous retinal veins in her left eye (). The right eye showed a completely normal fundus. Fluorescein angiography revealed delayed retinal venous filling. Arteriovenous transit time was slightly prolonged to 19 seconds and there was faint leakage in the late phase, but no signs of any vascular non-perfusion (). Cardiologic and neurologic work-up and laboratory tests (homocysteine, protein C and S, fibrinogen, anticardiolipin antibodies, and lupus anticoagulants) were normal except for weakly positive anticardiolipin IgM and mild iron deficiency anemia. The patient denied any valsalva episodes. We decided to observe the patient for the following two weeks without making a diagnosis. Two weeks later, her BCVA was slightly decreased to 20 / 25, and an increased number of retinal hemorrhages with severe disc swelling were noted (), but there was still no sign of ME (). At this time, the patient preferred to undergo medical intervention to improve her subjective symptom. We discussed with her that the drainage site of the retinal vein is located in the lamina cribrosa within the optic nerve and an intravitreal dexamethasone implant may help alleviate the progression of the vein occlusion by reducing optic nerve edema. The patient agreed to the treatment and an intravitreal dexamethasone implant 0.7 mg was injected.\nFive days later, her BCVA was 20 / 22 and there were improvements in disc swelling and retinal hemorrhage (). One month later, her BCVA improved to 20 / 20 and her subjective visual symptom was completely improved. Fundus examination revealed marked improvement of retinal hemorrhages and vascular tortuosity along with almost complete resolution of disc swelling ().

[[44.0, 'year']]

F

{'30999889': 1, '20417567': 1, '20381871': 1, '19752419': 1, '24688266': 2}

{}

3958640-1

noncomm/PMC003xxxxxx/PMC3958640.xml

A Case of Ocular Myasthenia Gravis Presenting as Double Depressor Palsy

A 65-year-old man who had been experiencing diplopia in front and down gaze for 15 days visited our hospital. His medical history revealed no contributing factors such as diabetes mellitus, hypertension, and cerebral ischemic attack. Ophthalmic examinations revealed normal vision in both eyes and no abnormal pupillary reflex. Fourteen prism diopter hypertropia was noted in the patient's left eye and limitation of depression was found in the adduction, primary gaze, and abduction (). Forced duction test revealed no restriction. Brain magnetic resonance imaging showed no remarkable findings. Two weeks after the first visit, the patient complained of ptosis in the left eye. An ice test was performed and the ptosis was resolved after the test (). Then, anti-acetylcholine receptor binding antibody levels were checked and found to be slightly elevated (0.416 nmol/L). We prescribed methylprednisolone per os 24 mg for 2 weeks, and his symptoms improved after 2 weeks. Three weeks after medication, the patient showed an ortho result in the alternate prism cover test, normal ocular movements, and complete resolution of diplopia ().

[[65.0, 'year']]

M

{'10406606': 1, '4696014': 1, '6662574': 1, '23047171': 1, '24688267': 2}

{}

3958977-1

noncomm/PMC003xxxxxx/PMC3958977.xml

Vanishing Bile Duct Syndrome in a Hodgkin's Lymphoma Patient with Fatal Outcome Despite Lymphoma Remission

A previously healthy 33-year-old Saudi man was admitted with a progressive left-sided neck swelling for 1 year. He developed yellowish discoloration of the skin and sclera, pale stools, and dark urine associated with abdominal distension 1 week prior to admission. He also complained of unexplained weight loss of 8 kg, low-grade fever, and fatigability. There was no history of liver disease or use of any herbs or other medication. Physical examination revealed pallor, jaundice, and a nontender, firm lymph node in the neck measuring 5 × 5 cm with unremarkable examination of other systems.\nComplete blood count showed mild leukopenia with a total WBC count of 3.1 × 109/L (normal 4-11), neutrophils 2 × 109/L, lymphocytes 0.7 × 109/L, mild normocytic normochromic anemia (Hb 12.6 g/dL), and a normal platelet count. Liver function tests (LFT) revealed a predominant cholestatic pattern with a total bilirubin (TBil) of 88 μmol/L (normal up to 18 μmol/L), direct bilirubin 74 umol/L, alkaline phosphatase 524 U/L, gamma-glutamyl transferase (GGT) 518 U/L, alanine aminotransferase 194 U/L, aspartate aminotransferase 106 U/L, and serum albumin 42 g/L. His renal function tests were normal and autoimmune work up was negative. Virology screening revealed negative results for hepatitis A, B, C, HIV, Epstein-Barr virus (EBV), and cytomegalovirus (CMV).\nAbdominal ultrasound showed a normal-sized liver (13 cm) with multiple hyper-echoic lesions seen in both lobes; the largest one in the left lobe (3.8 × 2.7 cm), and mild splenomegaly (14.9 cm). Common bile duct (CBD), portal vein, and hepatic veins were normal. Baseline computed tomography (CT) scan of the neck, chest, abdomen, and pelvis revealed multiple lymph nodes in the left side of the neck (largest 4.8 × 4.1 cm), left supraclavicular, mediastinal, both hilar areas, and intra-abdominal regions, suggestive of lymphoma. In addition, at least three hypodense focal hepatic lesions were present (largest 4 × 3.6 cm) with features suggestive of hemangiomas. Other findings were noncontributory.\nThe patient underwent left cervical lymph node excisional biopsy, which showed classical HL of nodular sclerosis type [] with a positive immunohistochemical staining for CD 30 and CD 15 but negative for CD 45 and CD 20. Bone marrow biopsy showed no evidence of lymphoma infiltration, so he was staged as III-B.\nThe patient received first cycle of chemotherapy, ABVD regimen (doxorubicin, bleomycin, vinblastine, and dacarbazine) with 30% dose reduction due to liver dysfunction. His jaundice improved initially but after 1 week he presented again with generalized weakness, anorexia, nausea, and worsening of jaundice. Repeat liver function tests revealed deterioration with elevated bilirubin (159 μmol/L) and liver enzymes consistent with a cholestatic pattern. There was no evidence of intrahepatic biliary dilatation on ultrasound. He underwent endoscopic retrograde cholangiopancreatography (ERCP), which showed normal CBD and a sphincterotomy and insertion of a biliary stent were performed. No improvements in liver function were noted so an ultrasound-guided liver biopsy was performed, which revealed cholestasis and nonspecific portal inflammation with no evidence of lymphoma. CK7 staining showed significantly reduced number of bile ducts consistent with a diagnosis of VDBS [].\nIn view of the persistent liver dysfunction, the patient received a modified ESHAP chemotherapy regimen (methylprednisolone 250 mg IV daily for 4 days, cisplatin 25 mg/m2 IV continuous infusion for 4 days and cytarabine 2 g/m2 IV on day 5 but without etoposide) because of the liver friendly nature of this regimen to prevent any further liver damage. The patient remained jaundiced with TBil fluctuating between 400 and 600 μmol/L, although a drop in TBil was noted (232 μmol/L) for a brief period. A repeat CT scan performed after the second chemotherapy cycle revealed significant regression of the lymph nodes in the neck, supraclavicular, mediastinal and retroperitoneal areas.\nAt this stage he received the second cycle of modified ESHAP chemotherapy (3rd cycle in total) but with a higher dose of methylprednisolone (500 mg daily for 4 days). After 2 weeks, he developed febrile neutropenia with positive blood cultures for Klebsiella species. He was treated with broad spectrum antibiotics. He also sustained drug-induced acute kidney injury, which improved initially but serum creatinine remained elevated, which hindered administration of further chemotherapy. His liver function showed no improvement. A positron emission tomography-CT of the whole body did not show significant fluorodeoxyglucose activity suggesting remission of HL. He was referred for a liver transplant but his condition rapidly deteriorated. He developed severe coagulopathy and hepatic encephalopathy, and died 4 months after the initial diagnosis of HL.

[[33.0, 'year']]

M

{'16879775': 1, '28127210': 2, '3317863': 1, '19406729': 1, '34182468': 1, '17906981': 1, '11521175': 1, '7678577': 1, '14959910': 1, '25125318': 2, '18188038': 1, '30061135': 1, '19131796': 1, '24195983': 2}

{'4143581-1': 1, '5236516-1': 1}

3958989-1

noncomm/PMC003xxxxxx/PMC3958989.xml

Non-zoonotic Pasteurella multocida Infection as a Cause of Septic Shock in a Patient with Liver Cirrhosis: A Case Report and Review of the Literature

A 52-year-old African American female was brought to the emergency department for generalized abdominal discomfort, altered mental status, diarrhea, fevers and chills for 4-5 days. Her past medical history was significant for alcohol abuse and alcohol-related liver cirrhosis. In the emergency department, vital signs were as follows: Blood pressure of 74/42 mmHg, heart rate of 112 beats/min, respiratory rate of 20 breaths/min and temperature of 98.6 F. Remarkable findings on physical examination included jaundice as well as abdominal distention and tenderness to palpation, especially in the right upper quadrant. There was no rash or ulcers. As per family, she did not have recent travels or exposure to sick people. They denied having domestic animals at home or any contact to the patient with pets. She was placed on mechanical ventilation and admitted to the medical intensive care unit. Admission diagnosis was systemic inflammatory response syndrome with sepsis and septic shock with multi-organic dysfunction syndrome, presumptively secondary to community-acquired pneumonia, possible biliary tract infection (ascending cholangitis), probable spontaneous bacterial peritonitis (SBP) and alcoholic hepatitis. Aggressive intravenous fluids resuscitation with crystalloids along with vasopressors was initiated. Blood, urine, respiratory cultures and Legionella urine antigen were obtained. Empiric intravenous antimicrobial therapy, composed by piperacillin/tazobactam (2.25 g every 8 h) and azithromycin (500 mg every 24 h), was initiated.\nLaboratory results on admission were: A complete blood cell count of 21,000/mm3(90% neutrophils), a platelet count of 51,000/mm3, a sodium level of 127 mEq/L, a potassium level of 5.3 mEq/L, a bicarbonate level of 15 mEq/L and a creatinine level of 6.3 mg/dl. Aspartate aminotransferase and alanine aminotransferase levels were 121 and 65 IU/L, respectively. Alkaline phosphatase level was 290 IU/L, gamma-glutamyl transpeptidase level was 290 U/L and lactate dehydrogenase level was 482 U/L. Total bilirubin level was 14.5 mg/dl, with a direct bilirubin level of 10.1 mg/dl. Lactic acid level was 6.4 mg/dl. Prothrombine time was 25.2 s, with an INR of 2.29. Serum alcohol level was within the normal limits. Arterial blood gases showed a pH of 7.15, a pCO2 of 23, and a pO2 of 132 while the patient was receiving mechanical ventilation with FIO2 of 60%. Chest X-ray showed left lung infiltrate with pleural effusion.\nAfter 24 h of admission, patient remained in critical condition and requiring maximum doses of vasopressors, despite of what it seems to be the appropriate empiric antimicrobial therapy. Blood cultures drawn of admission grew P. multocida. Blood culture system Bact-Alert 3D® was used for the recovery of the organism. No polymerase chain reaction analysis was performed. Isolate was tested sensitive to piperacillin/tazobactam and azithromycin. No minimal inhibitory concentrations for these antimicrobials were reported. In spite of all medical efforts, general medical condition deteriorated and patient expired on day 3 of admission.

[[52.0, 'year']]

F

{'3313679': 1, '6371440': 1, '8678013': 1, '26942025': 2, '19452350': 1, '479068': 1, '7421926': 1, '27840749': 2, '6999394': 1, '15586605': 1, '9097378': 1, '34707957': 2, '14108437': 1, '1452670': 1, '8011850': 1, '11347675': 1, '30559948': 2, '33129238': 1, '24672181': 2}

{'5093256-1': 1, '8532189-1': 1, '4752973-1': 1, '6292365-1': 1}

3958990-1

noncomm/PMC003xxxxxx/PMC3958990.xml

Spontaneous Pneumorrhachis and Transverse Myelitis Complicating Purulent Meningitis

The patient is a 21-year-old male without significant medical history. He was admitted in the emergency department for cephalalgia, fever, and frequent easy vomiting lasting 1 week duration. Symptoms were associated to a puffiness of the face and dyspnea of level I according to Sadoul classification.\nAt admission, the patient was conscious with a fever of 39°C. The blood pressure was 120/70 mmHg with a heart rate of 80 beats/min and a respiratory frequency of 24 cycles/min. The neurological examination objectified signs of meningeal irritation without any motor and sensory deficit. The pleuropulmonary examination found subcutaneous emphysema in the top part of the thorax and upper limbs extending to the cervical region and the face. Associated air effusion syndrome was not evidenced.\nThe initial cerebral computed tomography (CT) scan was normal. Afterward, a lumbar puncture was performed and revealed a blurred liquid with predominant polynuclear neutrophils (80%). The glycorrhachia was 0.40 g/l (with concomitant glycemia of 1.20 g/l); total albumin level was 0.98 g/l, and the classical cerebrospinal fluid (CSF) gram’s stain and culture was negative. The immunochemistry study of lumbar puncture was in favor of meningitis diagnosis, which oriented to start the antibiotherapy. The routine biological and hematological studies included blood cells count and blood culture, ionogram, and sedimentation rate were found to be normal. The hepatic assessment was also without abnormalities. The diagnosis of bacterial meningitis was retained. The patient was treated using adequate antibiotherapy consisting of 2.0 g of ceftriaxone every 12 h. Ceftriaxone dose was maintained at the meningitis rate of 100 mg/kg/day.\nThe thorax X-ray showed a pneumomediastinum in the left paratracheal border along the left edge of the heart; the image also showed subcutaneous emphysema without associated pneumothorax []. Evermore, thorax CT scan confirmed all abnormalities described in the thorax X-ray and revealed the presence of air collection in the spinal canal between C7 and D6 levels []. The laryngoscopy, bronchoscopy, and digestive opacification did not show any abnormality in the respiratory-digestive tracts. These invasive gestures were achieved under general anesthesia without remarkable event.\nThe clinical evolution within 48 h was marked by the occurrence of apyrexia, coupled with disappearance of the subcutaneous emphysema and the meningeal steepness. However, the neurological status of the patient worsened gradually; a paraparesis occurred and was followed by a tetraparesis. The patient started with presenting neurovegetative disorders with hemodynamic instability which was in favor of central affection. The sepsis was discarded since the patient was afebrile. The patient experienced acute respiratory syndrome that required artificial ventilation. Afterward, a spinal magnetic resonance imaging (MRI) was performed and showed a cervical medullary edema extending from C2 to C6 without any sign of spinal cord compression. This result was consistent with a general clinical profile of acute transverse myelitis []. The hemodynamic support consisted initially of administrating vasoactive Drugs and dopamine then adrenaline since nor adrenaline was not available. The patient died within 15 days with a profile of vasoparalysis resistant to vasoactive drugs.

[[21.0, 'year']]

M

{'34955642': 2, '15136999': 1, '20837275': 1, '10025027': 1, '16920430': 1, '9757286': 1, '15826793': 1, '10592919': 1, '18375187': 1, '12006470': 1, '20010389': 1, '9051898': 1, '10195480': 1, '16950703': 1, '865671': 1, '16835735': 1, '24672182': 2}

{'8694274-1': 1}

3958991-1

noncomm/PMC003xxxxxx/PMC3958991.xml

Atypical Dengue Meningitis in Makkah, Saudi Arabia with Slow Resolving, Prominent Migraine like Headache, Phobia, and Arrhythmia

A 27-year-old Saudi female, living in Makkah, was referred from ophthalmology clinic, with severe retro-orbital headache and neck pain started 3 days before admission. There was no myalgia, arthralgia, bleeding manifestation, cutaneous rash, or any similar or significant past medical history. On examination, she was in pain, febrile with a temperature of 38.3°C, respiratory rate of 20/min, heart rate of 112/min, and blood pressure 116/63 mmHg. Her chest, cardiovascular, abdomen, and neurological examinations including fundus were unremarkable, except of mild neck rigidity. She was admitted with professional diagnosis of acute meningitis and started on intravenous dexamethasone, vancomycin, ceftriaxone, and acyclovir with good hydration. Brain CT scan was normal. CSF was normal except of pleocytosis (85% lymphocytes). The complete blood count was as follows: WBC 4.5 cell/mm3, 60% lymphocytic, Hb 12.1 gm/dL, platelets count 135/mm3. The blood tests for malaria, brucella, cytomegalovirus (CMV), Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), and swine flu virus (H1N1) in the blood were negative. Dengue serology sent to Makkah central laboratory due to relative low platelets and low grade fever. Upon these result dexamethasone, vancomycin, and ceftriaxone were stopped on the next day and the patient was kept on intravenous acyclovir only. Throughout the 7 days admission period, the patient was almost afebrile but showed bizarre headache appearing as persistent diffuse headache with attacks of severe retro-orbital pain, eye tearing, and blurring vision mainly on left eye that respond only to pethidine intravenous injection in spite of trial of multi analgesic and neuropathic medication including amitriptyline, topiramate, pregabaline, and tramadol. The headache attacks predominantly appeared between 3 and 11 pm, associated with anxiety and fear of death in addition to episodes of arrhythmia range between bradycardia down to 45/min and supraventicular tachycardia up to 180/min, that required many cardiology and psychiatry on call review. On 4th day of admission, serum dengue IgM reported to be positive. To further strengthen the diagnosis, we repeated the CSF test for dengue IgM. On the 7th day, the patient was so much upset and asked discharge against medical advice to seek abroad management. 20 days later, the patient was seen in neurology out-patient clinic complaining of persistence migraine like headache and the CSF test for dengue IgM was found to be positive. Over several months later, the patient was on amitriptyline and tramadol on need. Then gradually and slowly, headache attacks diminished in frequency and severity, resolving almost completely 4 months after onset.

[[27.0, 'year']]

F

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{'3958991-2': 2, '7354550-1': 1, '7354550-2': 1, '7354550-3': 1}

3958991-2

noncomm/PMC003xxxxxx/PMC3958991.xml

Atypical Dengue Meningitis in Makkah, Saudi Arabia with Slow Resolving, Prominent Migraine like Headache, Phobia, and Arrhythmia

A 48-year-old Egyptian obese woman, not known to have any medical illness before, was referred by ENT specialist as possible central dizziness with history of severe dizziness, nausea, and vomiting associated with blurring of vision and headache 1 day before. On examination, she was looking ill, with a temperature of 38.4°C, respiratory rate of 21/min, heart rate of 124/min, and blood pressure of 167/93 mmHg. Her chest, cardiovascular, abdomen, and neurological examination were unremarkable, except of mild early bilateral papilledema, neck rigidity, and ataxic gait. A CT scan of brain done with/without contrast in emergency department showed possible left sigmoid sinus partial occlusion. She was admitted and started on heparin infusion and ceftriaxone with good hydration plus amitriptyline, betahistine, cinnarizine, and heparin 5000 IU 6 hourly sc injections. Next day, MRI/MRV of brain was done and reported to be normal, but the platelet count dropped to 109/mm3, and GPT raised to 87 compared to normal result on baseline admission result; this supports stopping heparin therapy. On the third day afternoon, she was suffering from severe diffuse burning quality headache mainly on right tempro-occipital with severe central scalp scratching and pressing like pain last several hours and aborted only on pethidine intravenous injection. On the 4th day, lumbar puncture was done and the CSF was normal. The blood tests for CV, EBV, HIV, and H1N1 were also negative but serum dengue IgM was positive. A CSF sample for dengue IgM sent to private lab reported as positive. Throughout the 23 days admission period, the patient was almost afebrile but showed significant fatigue with bizarre headache appearing as persistent diffuse pressure like headache with attacks of severe bilateral temproparietal burning and central scratching pain associated with nausea, vomiting, dizziness, phonophobia, photophobia, anxiety, and near death phobia and bradycardia (4060) that required many cardiology and psychiatry on call review. On the 22nd day, the patient was discharged after showing reduction of headache attacks severity and frequency with normal blood count and liver enzymes. Then patient was on weekly out-patient neurology clinic follow up for several months using amitriptyline, respridone, and tramadol on need. Then gradually and slowly, headache attacks diminished in frequency and severity, resolving completely about 3 months after onset.

[[48.0, 'year']]

F

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{'3958991-1': 2, '7354550-1': 1, '7354550-2': 1, '7354550-3': 1}

3959025-1

noncomm/PMC003xxxxxx/PMC3959025.xml

Depression is More Than Just Sadness: A Case of Excessive Anger and Its Management in Depression

Mr. A, a 27-year-old single Hindu male, educated up to intermediate, with no significant past history of any psychiatric or medical illness, presented with chief complaints of depressed mood, initial and terminal insomnia and diminished appetite, excessive easy fatigability, anhedonia, excessive irritability, frequent anger outbursts, physical and verbal abuse, acts of deliberate self-harm for a duration of 3-4 months with progressive increase in intensity of symptoms over the time. His pre-morbid history revealed impulsive traits, frequent irritability and outbursts of anger, inability to handle criticism and difficulty in maintaining friends and relationships. However, there was no history of physical violence or conflict with others. However, currently, there was a significant increase in intensity and frequency of anger outbursts and irritability along with the depressive symptoms. Birth and developmental history was unremarkable.\nDepressive episode of moderate intensity was diagnosed and rating on beck depression inventory (BDI) and Hamilton Depression Rating Scale (HDRS) were 11 and 18 respectively. Escitalopram was started, which was gradually increased from 5 to 20 mg/day. Though his depressive symptoms showed response to medications, there was no improvement in anger and irritability.\nNon-pharmacological treatment based on cognitive-behavioral approach was started mainly to deal with his anger-related problem. The total therapy lasted over 4 weeks, which included a total of 11 sessions of 45-90 min/session. The objective of the therapy was to decrease impulsivity, arousal and expression of anger, increase his capacity to tolerate anger, channel his energy in prosocial ways and exert a better control over tension and anxiety even in tense situations. Psychoeducation, activity scheduling, self-monitoring of anger and associated physical cues and negative thoughts, relaxation and distraction techniques and cognitive restructuring were used to attain the above objectives.\nFirst, patient was psychoeducated about depression and nature and importance of anger. Second, he was asked to maintain a diary of his anger outbursts, which included recording the antecedents, behaviors and consequences of his anger. In addition, patient was also instructed to rate and record the intensity of anger on a scale of 0 to 10. An activity schedule was prepared in collaboration with the patient and he was advised to follow it regularly in a proper way. Themes that emerged out of the assessment was that trivial events like things not done as per subject's wish and cues like heartbeat, hot flushes and irregular breathing increased his anger. This often led to impulsive acts like self-harm or violent behavior, which later led to the deep sense of guilt and disturbed his inter-personal relationship(s). To control the autonomic cues, Jacobson's progressive muscular relaxation training and deep breathing was taught. Distraction technique was suggested in the form of moving away from the arousing situation, keep calm and at the same time imagine pleasurable image or fantasy and feel good about it. Cognitive restructuring helped in replacing anger-provoking thoughts with more rational ones. Patient was instructed to practice repeatedly.\nFollowing 11 sessions of CBT, there was a significant improvement in his anger and impulsivity. He reported that whenever he got angry, he was able to identify the feeling that caused anger (e.g., fear, hurt, disappointment). Further, he could contain his anger, used positive thoughts and expressed it in a respectful way. Overall, there was about 70% improvement in his perceived ability to control his anger. A decrease in BDI and HDRS scores from moderate to mild severity was also noticed during this time, which finally resolved over time. Before termination of sessions, importance of practicing the techniques even after resolution of depressive symptoms was emphasized to manage his anger outbursts.

[[27.0, 'year']]

M

{'2809577': 1, '11140922': 1, '17763117': 1, '9133758': 1, '26009674': 1, '12457634': 1, '34840989': 1, '24701016': 2}

{}

3959026-1

noncomm/PMC003xxxxxx/PMC3959026.xml

A Case Report on Myxedema Madness: Curable Psychosis

Mrs. X, a 30-year-old female without a known significant past medical history was brought with a 1½ year continuous disturbance in the form of having suspiciousness, fearfulness and quarrel with neighbors with gradual and progressive work impairment.\nShe, on provocation, anxiously reported that “someone has done black magic on her. She along with her children would be harmed and daughters sold off in flesh trade by the neighbors.”\nFor self-defense, she used to sleep with a knife under her pillow.\nAt home, mostly she was noted to be withdrawn and fearful. Whenever husband went out to work then she’d run to her sister's house and had to be fetched back home for which she was reluctant always in coming.\nOn active enquiry; she reported a voice commanding her to run away from the house if she wished to be safe, also of having other auditory hallucinations of people (neighbors) talking amongst themselves about ways of harming her and her family.\nPatient was admitted to our psychiatry ward for evaluation and work-up.\nAfter admission Mrs. X's vitals were normal. Facial puffiness was observed in physical examination. Her neurological examination was normal. On mental status examination, she was conscious and oriented to time, place and person with poor eye contact, low tone rough voice with a paucity of speech, psychomotor activity was decreased and affect was apathetic. She was guarded about her hallucinations but came out easily with her delusions with a BPRS score of 41. Depressive features or death wish were not reported.\nGeneral blood profile was normal with a normal chest X-ray and electrocardiography. Thyroid profile was altered with thyroid stimulating hormone - 63.71 mIU/L, Free tri iodo thyronine (FT3) - 2.1 pg/ml, Free tetra iodo thyronine(FT4) - 0.6 ng/ml and normal ulltrasound-thyroid. Patient was started on thyroxin 100 μg after consultation from the endocrine department of our hospital and a low dose risperidone 2 mg, which was then withdrawn over a week with the recovery of her behavioral abnormalities and then she was continued with thyroxin alone. She was discharged after about 2 weeks of hospitalization with the absence of any hallucinations and delusions with a BPRS score of 8. After 1 month, on second follow-up, relatives reported a 90% overall improvement and absence of delusions and hallucination. Brief Psychiatric Rating Scale score was three.

[[30.0, 'year']]

F

{'34447249': 1, '9365336': 1, '18148089': 1, '6381038': 1, '7234630': 1, '5568196': 1, '33321556': 1, '5936575': 1, '24701017': 2}

{}

3959027-1

noncomm/PMC003xxxxxx/PMC3959027.xml

The Denial of Death: A Three-decade Long Case of Absent Grief

Mrs. SM, an 80-year-old woman admitted to the surgical unit for a gluteal abscess, was referred for psychiatric evaluation. The referring physician said that the patient believed that her deceased son was still alive. She had two sons and a daughter, who provided the psychiatric history. The deceased son was her favorite, but her relationship with other family members was depleted. When he was in his twenties, he was accused of fraud at his workplace, following which he developed depressive symptoms. At 10 days later he committed suicide by consuming poison, leaving separate notes for his mother and sister. When taken to the morgue, the patient claimed that he was not dead. The suicide note was not shown to her.\nOver the next few months, the patient displayed behaviors indicating that she believed her son was alive. She maintained his room and belongings exactly as before. She often rushed up to the terrace at the sound of airplanes and would say that her son was returning home. The above behaviors persisted for the next 35 years. Her self-care, sleep and appetite were unchanged. Her daughter reported that during the current admission the patient had been looking for her son among the medical interns.\nPatient was an emotionally restrained person who was not demonstrative about her affection for her children. There was a family history of suicide in her paternal uncle, sister and her son as described above and depression in her grandson.\nOn mental status examination, her higher mental functions were intact. When asked about her son she said she could not talk about him, but requested us to arrange for his return.\nBased on the history and examination, we considered differential diagnoses of delusional disorder and atypical bereavement. The family refused any psychiatric intervention for her. She passed away 2 months later. Her daughter subsequently presented to us with depression.

[[80.0, 'year']]

F

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{}

3959028-1

noncomm/PMC003xxxxxx/PMC3959028.xml

Restless Legs Syndrome in Opioid Dependent Patients

A 25-year-old male patient presented with a past history of opioid-dextropropoxyphene (DPP) intoxication seizure with no family history of either seizure or any substance abuse, after remaining abstinent for ~1.5 years restarted DPP, which was followed by another episode of generalized seizure. However, he continued DPP in dependent pattern for last 4 months.

[[25.0, 'year']]

M

{'28017182': 1, '15907642': 1, '30071007': 1, '26874840': 1, '25883472': 1, '12734764': 1, '17235431': 1, '20005913': 1, '14592341': 1, '26045290': 1, '24701019': 2}

{'3959028-2': 2, '3959028-3': 2}

3959028-2

noncomm/PMC003xxxxxx/PMC3959028.xml

Restless Legs Syndrome in Opioid Dependent Patients

A 26-year-old male patient with no significant past and family history was dependent to opioid (DPP) for last 4 years. He had four episodes of generalized seizure once in withdrawal and others during intoxication. In addition, he started abusing steroid (dexamethasone) for last 6 months and developed exogenous Cushing's disease, which was followed by acute Addison's disease due to abrupt stoppage of steroid. For which steroid supplementation was given.

[[26.0, 'year']]

M

{'28017182': 1, '15907642': 1, '30071007': 1, '26874840': 1, '25883472': 1, '12734764': 1, '17235431': 1, '20005913': 1, '14592341': 1, '26045290': 1, '24701019': 2}

{'3959028-1': 2, '3959028-3': 2}

3959028-3

noncomm/PMC003xxxxxx/PMC3959028.xml

Restless Legs Syndrome in Opioid Dependent Patients

A 32-year-old male with no significant family history and past history of trichotillomania was dependent to opioid (DPP and codeine containing cough syrup) for last 12 years. He tried to quit multiple times, also underwent rapid detoxification under anesthesia a year back, but relapsed eventually.\nAll these three patients were brought to Drug Deaddiction and Treatment Center, Postgraduate Institute of Medical Education and Research, Chandigarh. They had received clonidine (0.6-0.3 mg/day), non-steroidal anti-inflammatory drugs (ibuprofen/ketorolac) and benzodiazepine (BZD) (clonazepam/nitrazepam) as standard detoxification regime to relieve the withdrawal symptoms. With these medications rhinorrhea, lacrimation, loose motion, bodyache, anxiety had been resolved, but sleep problem persisted in the form of sleep induction and maintenance problem The dose of BZD was increased in each case (nitrazepam up to 30 mg and clonazepam up to 4 mg), but sleep disturbances continued even after 2 weeks.\nOn further enquiry, they complained creeping/crawling/burning sensation in both the lower limbs especially at night when they lie down, relieved partially by stamping feet on the bed or by walking around. Clinically, this was fulfilling the criteria for RLS. So a neurology consultation was taken to substantiate the diagnosis. Serum urea, creatinine, ferritin, thyroid function test were conducted along with electroencephalogram. All these investigations came out to be normal.\nThe patients were started on ropinirole 0.75 mg/day. Two of them improved with in next 2 days and the third patient required dose escalation to 1.5 mg/day to have clinical improvement. BZDs were tapered off successfully, but ropinirole was continued for next 1 month then was tapered of over 2 weeks uneventfully.

[[32.0, 'year']]

M

{'28017182': 1, '15907642': 1, '30071007': 1, '26874840': 1, '25883472': 1, '12734764': 1, '17235431': 1, '20005913': 1, '14592341': 1, '26045290': 1, '24701019': 2}

{'3959028-1': 2, '3959028-2': 2}

3959029-1

noncomm/PMC003xxxxxx/PMC3959029.xml

Typical Neuroleptic Malignant Syndrome Presented in Patient on Maintenance Quetiapine

A 46-year-old male patient was brought to Emergency Department of Tertiary Care Centre at Bhavnagar, with, generalized stiffness, fever, generalized tremulousness mutism, perspiration, inability to swallow, intermittent tongue protrusion, sialorrhea, restlessness and insomnia for the last 3 days. Patient was seen by emergency team and was hospitalized in critical care unit. He was diagnosed with schizoaffective disorder of 11 year duration. He was under regular treatment of quetiapine 200 mg/day, divalproex sodium 500 mg/day and lorazepam 4 mg in two divided doses/day since 2006, confirmed by relatives and clinical case records. There was no past history suggestive of similar symptoms, medical disorder or substance use. The paternal uncle was having symptoms of self-talking, abusive, poor self-hygiene, roaming on roads who died at the age of 50 years.\nOn examination, patient was confused, not oriented to time and place. His temperature was 102°F, blood pressure 150/90 mm of Hg, heart rate 104/min, respiratory rate 20/min. He had generalized tremors, cog wheel rigidity in all extremities and orofacial dystonias. The pupils were normal size and reactive to light. Planters were flexor both sides. He was agitated and was pulling intravenous (IV) lines.\nClinically, NMS was suspected. Other differential diagnoses such us meningitis, encephalitis, substance/overdose or withdrawal, metabolic disturbances, seizure, heat stroke were ruled out. Serotonin syndrome was ruled out because of presence of severe rigidity, absence of hyperreflexia, clonus, diarrhea, in coordination and no use of serotonergic reuptake inhibitors. Lethal catatonia was ruled out because patient did not have initial psychotic symptoms. Blood and urine and cerebrospinal fluid (CSF) samples were sent for examination and culture. A head computed tomography scan, chest X-ray and urine analysis and CSF analysis were unremarkable. The physical and laboratory parameters are shown in .\nPatient was admitted in intensive care unit and nasogastric tube and urine catheter was inserted. Quetiapine and divalproex were discontinued. Patient was given 6000 ml/day including dextrose and saline for hydration. Cold water sponging was done regularly to control hyperthermia. Bromocriptine 10 mg in four divided doses through nasogastric tube and intramuscular lorazepam 8 mg/day in two divided doses was started. There was hypernatremia (151 mEq/L) on day 1, which was corrected with successful fluid resuscitation. Vitals, electrocardiogram and urine output were monitored daily. As shown in clinical condition improved on day 3 and patient was able to take oral fluids. The patient was clinically stable and was ambulatory on day 5. There was reemergence of psychotic symptoms such as delusion of jealousy, auditory hallucinations, increased talkativeness and psychomotor activity on the 10th day. Clozapine 25 mg in divided was started with divalproex 500 mg/day. Dose was increased and patient was discharged on the 22nd day with 150 mg/day of clozapine and divalproex 1000 mg/day. Patient significantly improved on discharge and was advised for regular follow-up. Patient well- maintained with the same treatment on follow-up.

[[46.0, 'year']]

M

{'2873715': 1, '19299325': 1, '9699705': 1, '7249508': 1, '13815606': 1, '24701020': 2}

{}

3959031-1

noncomm/PMC003xxxxxx/PMC3959031.xml

Teratogenicity with Olanzapine

Ms. A, a 25-year-old married lady presented in the hospital's Walk-in clinic with the symptoms of suspiciousness and hearing voices. The symptoms had been present for about 5 years. She was very irritable and was unable to sleep. She also suffered few episodes suggestive of dissociative spells in which she would call herself “Goddess Kali.” There was also occasional history of disinhibition in the form of taking of her clothes in front of her family members.\nDetailed evaluation revealed delusions of persecution and second person auditory hallucination. There were no features suggestive of a mood disturbance or organicity. She was diagnosed as having unspecified non-organic psychosis on International Classification of Diseases, tenth edition.[] Olanzapine was started and gradually increased to 15 mg/day. The psychotic symptoms were controlled over a period of 2 months with olanzapine. After 1 month of treatment with olanzapine, the patient became pregnant (this was her first pregnancy) and sought consultation for safety of medications during the 2nd month of gestation. Considering the severity of the symptoms in the past and duration of illness, on mutual discussions, it was decided to continue olanzapine. She was referred to the obstetrics service of the hospital to keep a close watch for any untoward event. She followed-up there regularly as advised by the obstetrician. A discussion with the consulting obstetrician and review of records revealed no major untoward event during pregnancy. Careful history revealed absence of fever, rashes or other skin lesions. Antibody titers for herpes simplex, varicella, cytomegalovirus, toxoplasma and rubella were conducted and found to be normal. Fasting and postprandial blood glucose levels performed at the time of first consultation and repeated in the 2nd and 3rd trimesters were found to be in the normal range. On follow-up, the fetus was detected to have microcephaly on ultrasonography. No other major anomalies were detectable.\nMs. A delivered a female baby weighing 3.4 kg with microcephaly and congenital anopthalmos (bilateral) at full term. The head circumference was 30.5 cm at birth, which falls below the third percentile.[] The baby was seen at department of pediatrics, genetics and ophthalmology. B scan ultrasound revealed absence of ocular tissue. No additional causative factors could be elicited despite the above mentioned specialist referrals. However, detailed imaging and genetic investigations could not be done due to cost limitations. She was not on any other medication known to cause teratogenicity during the period. There was no history of any substance use or family history of congenital anomalies. Patient had adequate nutrition and rest during her pregnancy. There was no history of trauma or exposure to radiation either. The history was corroborated by the patient's mother as well as husband Although this adverse event scored only three on the the Naranjo et al. adverse drug reaction probability scale,[] the lower scores were due to non-applicability of some questions to this situation. For instance, the issue of improvement on discontinuation of drug or administration of antagonist obviously does not apply to this case. Similarly, re-administration and replication of the adverse effect also cannot be done in this case for ethical reasons.

[[25.0, 'year']]

F

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{'4211849-1': 1}

3959032-1

noncomm/PMC003xxxxxx/PMC3959032.xml

Organic Depression and Terson's Syndrome in Adult Polycystic Kidney Disease: Case Report and Review of Literature

A 50-year-old lady, receiving treatment for hypertension for the past 8 years, was diagnosed as having comorbid organic depression as per ICD-10 diagnostic criteria,[] and was symptomatic for the past 4 months. She was managed with escitalopram (10 mg/day) and mirtazapine (15 mg/day), but was in partial remission. She presented to the psychiatry out-patient services with exacerbation of symptoms of pervasive depression, apathy, insomnia, anorexia, fatigue, reduced social interactions, and frontal headache for the past 4 months, with diminished vision and vomiting for the past 1 week. Episodic frontal headache was followed by unresponsiveness and sudden fall without tonic — clonic limb movements or injuries, lasting for about 10 min with amnesia for the event. She had no history of head trauma, epilepsy, substance (alcohol, nicotine, or drug) abuse, or psychosocial stressors. She had second-degree consanguineous marriage. Family history of late-onset kidney diseases and hypertension was noted in both her parents and ADPKD was diagnosed in both her sons.\nOn admission, the Glasgow Coma Scale[] score was E4V5M6 and Hunt — Hess scale[] was grade-1, with blood pressure of 190/110 mm Hg. Neuromuscular and cardiovascular examination was normal. Mental status examination revealed depressed mood, apathy, negative cognitions, impaired judgment with preserved attention, orientation, memory, and intelligence, with grade-4 insight. Hamilton depression rating[] (HAMD-17 item) score was 16 and the score on the mini-mental status examination[] was 28/30. Ophthalmological evaluation revealed reduced visual acuity in the right eye (1/60) and normal left eye (6/6), bilaterally normal anterior segments, normal pupils (bilaterally 3 mm, round, regular, and reacting to both direct and consensual light reflexes), and normal intraocular pressures. Fundoscopy showed boat-shaped subhyaloid hemorrhage involving the posterior pole extending below the inferior arcade, with multiple hemorrhages seen around the normal optic disc in the right eye [] and normal left fundus [], with evidence of bilateral grade-1 hypertensive retinopathy []. Hematological and biochemical investigations revealed moderate normocytic and normochromic anemia (hemoglobin 8.7 g/dL), mild leukocytosis (12,240/mm3), raised serum creatinine (2.5 mg/dL) with normal blood urea (42 mg/dL), serum electrolytes, blood glucose, lipid, liver, and thyroid profiles. Ultrasonography (USG) of abdomen showed bilateral renal ill-defined multiple (>6) cysts and calculi []. Echocardiography revealed mitral valve prolapse along with trivial mitral and aortic regurgitation. Electrocardiograph and carotid Doppler studies were normal. Electroencephalography showed right frontal polyspikes and sharp waves with preserved alpha background activity suggestive of epileptogenic foci. Cranial magnetic resonance imaging (MRI) revealed minimal SAH in the anterior inter-hemispheric fissure and adjacent cortical sulci with edema in adjacent frontal lobes, and hyper-acute SDH in bilateral fronto-temporo-parietal regions along the cerebral convexities (5 mm), with no mass effect or midline shift [], confirming the diagnosis of TS. Cerebral angiography showed small bi-lobed aneurysm (6 × 6 × 4 mm) arising from the ACoA with the neck of aneurysm measuring 1.5 mm in medio-lateral direction [].\nManagement included anti-hypertensives, antiepileptics, zolpidem, and hematonics. Antidepressants were withheld for the risk of re-bleed. Neodymium: YAG (Nd: YAG) laser posterior hyaloidotomy was performed by transcorneal route using frequency doubled Nd: YAG laser 532 nm (Zeiss-Visulas YAG laser 532 nm; laser setting: 9 spots, 100 msec duration, 50 μm spot size for penetration burn, 130 mW power) delivered via a slit lamp using Goldmann lens.[] The aiming beam was focused on the sloping edge of the most dependent portion of posterior hyaloid membrane at the inferior edge of subhyaloid hemorrhage to facilitate gravity-induced drainage. Blood flowed from hyaloidotomy opening and dispersed into inferior vitreous. Patient was advised for head-end elevation, and later discharged with anti-hypertensives, antiepileptics, and zolpidem. A week later, near-complete resolution of subhyaloid hemorrhage [] and ICH, with mild ventriculomegaly [] was noted. A month later, aneurysm clipping was successfully done by the neurosurgeon in liaison with a nephrologist. A month later, patient was asymptomatic with HAMD-17[] score of 3, and was regularly followed up for a year following neurosurgical intervention. She remained euthymic without any active psychiatric interventions and was managed with antihypertensives and antiepileptics alone. This sequential presentation with full remission of symptoms following neurosurgical interventions led to the diagnosis of “possible” organic depression due to intracranial ACoA aneurysm as per ICD-10 diagnostic criteria.[]

[[50.0, 'year']]

F

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{}

3959040-1

noncomm/PMC003xxxxxx/PMC3959040.xml

Pigmented Hypopyon in Association with Listeria Monocytogenes Endopthalmitis: An Interesting Case Report Following Refractive Surgery Procedure with Literature Review

A 28-year-old male presented to the emergency room (ER) with pain and redness in the right eye over the last 5 days. He was otherwise healthy and gave a past history of appendicectomy. His ocular history revealed laser refractive surgery procedure in both eyes 6 months prior to his presentation in another institution in Jordan. His history also revealed prior recent admission to a local hospital where he was found to have a high intraocular pressure of 50 mmHg which was managed by antiglaucoma medications: Latanoprost (Xalatan by Allergan) drops. He also received fortified antibiotics and topical steroids. No exact details of his treatment were available at the time of his presentation to our ER facility. He presented with vision of hand motion in the affected eye and intraocular pressure of 18 mmHg. His slit lamp examination of the right eye revealed severe conjunctival congestion with ciliary injection, opaque hazy cornea, and deep anterior chamber (AC) with 3 mm of dark pigmented hypopyon. There was no localized corneal infiltrate, but ring deep corneal dense haze was noticed possibly representing the edges of a previous laser-assisted in situ keratomileusis (LASIK) flap [ and ]. There was no further view of the posterior cavity. The left eye examination was within normal limits.\nThe patient was admitted as a case of uveitis. His initial B-scan showed very mild vitreous opacity and no RC layer thickening, therefore was not considered to be typical of endophthalmitis []. However, he was continued on fortified antibiotic drops (vancomycin 25 mg/ml and ceftazidime 50 mg/ml every 3 h around the clock, OD) and topical steroids: Prednisolone (Predforte by Allergan) drops four times/day, OD.\nHis differential diagnosis included post-refractive herpetic keratouveitis and masquerade syndrome. He was started on valtrex 500 mg twice daily, orally, in addition to the moxifloxacin 400 mg orally once daily. He was also kept on antiglaucoma medication: Combination of dorzolamide and timolol (Xolomol by Jamjoom Pharma) drops twice daily, OD.\nHis repeated B scans over 4 days following admission revealed increasingly dense organized vitreous opacities and significant retina and choroid (RC) layer thickening suggestive of early endophthalmitis [] for which AC washout, vitreous tap and intravitreal antibiotics were given in the form of vancomycin 1 mg/0.1 ml, ceftazidime 2.25 mg/0.1 ml, and cefuroxime 1 mg/0.1 ml. Meanwhile his systemic investigations were within normal limits. His human immunodeficiency virus (HIV) testing, urine, and blood cultures were negative. His chest X-ray was clear.\nThe smears prepared from his AC washout showed necrotic debris insterspersed with both extra- and intracellular melanin granules. Moderate number of polymorphonuclear leukocytes were also present []. The Grocott's methenamine silver (GMS), gram, and acid-fast stains were all negative. No malignant cells were seen to suggest a masquerade syndrome. The AC aqueous was sent for polymerase chain reaction (PCR) to rule out infectious etiology including herpetic infection, cytomegalovirus, varicella zoster, tuberculosis, and Chlamydia which were all negative. The aqueous fluid culture proved bacterial growth identified as Listeria monocytogenes in the blood agar plate [] and brain heart infusion (BHI) broth. The organism was sensitive to gentamicin and penicillin G. The culture of the vitreous fluid showed few gram positive bacilli which were not further identified. Valtrex and moxifloxacin were stopped and the patient was given intravenous penicillin G 15 million units every 6 h (following a negative skin test) for 2 weeks and then shifted to oral augmentin 1 g twice daily for another 2 weeks.\nThe patient subsequently developed cataract for which he underwent phacoemulsification with posterior chamber intraocular lens (PC-IOL) implantation 4 weeks after his admission []. Another AC fluid was sent for culture at the time of his cataract procedure which was negative. His last examination 1 month following surgery showed vision of 2/200 in the right eye which improves with pinhole to 20/160 and intraocular pressure (IOP) 12 mmHg controlled on a single antiglaucoma medication (Xolamol drops). The slit lamp examination showed corneal + 2 edema and haze, total peripheral anterior synechia with shallow AC, stable IOL, and hazy fundus view [].

[[28.0, 'year']]

M

{'2309867': 1, '15090435': 1, '19840735': 1, '3608514': 1, '27424034': 2, '26552393': 1, '26437938': 2, '15013893': 1, '1455294': 1, '29086326': 1, '1078953': 1, '21103198': 1, '4964814': 1, '10606462': 1, '11738433': 1, '2297040': 1, '11427612': 1, '3134816': 1, '21475652': 2, '1486086': 1, '19648890': 1, '10230593': 1, '24669144': 2}

{'4947317-1': 1, '3062758-1': 1, '4593987-1': 1}

3959048-1

noncomm/PMC003xxxxxx/PMC3959048.xml

Severe Bilateral Paralimbal Sterile Infiltrates after Photorefractive Keratectomy

A 47-year-old male patient underwent bilateral PRK for myopic astigmatism. The patient was in good health, did not take any systemic medications and the ocular history was unremarkable. The pre-operative manifest refractions were −1.25 −1.00 × 110 right eye and −1.75 −0.50 × 70 left eye.\nBilateral PRK was performed on the same day. Two drops of topical anesthetic were instilled in the eye undergoing surgery. The eyes were draped with a plastic sheet. A lid speculum was inserted for maximum globe exposure. The corneal epithelium was removed by mechanical debridgement using a sponge soaked in topical oxybuprocaine hydrochloride 0.4% (benoxinate) and a surgical blade. The surgical procedure was uneventful and a bandage contact lens was placed at the end of surgery. The patient was discharged with instructions to instill topical ofloxacin 4 times a day and diclofenac sodium (Voltaren; Novartis AG, Basel, Switzerland) 6 times a day for pain. No topical steroids were prescribed.\nOne day post-operatively, the visual acuity was 20/25. Slit lamp examination revealed bilateral corneal infiltrates outside the treatment zone with intact epithelium and clean central epithelial defects and quiet anterior chambers [].\nThe contact lenses were removed and corneal scrapings were sent for microbial studies. The patient was placed on topical steroid 4 times a day and topical ofloxacin hourly and the voltaren was stopped.\nMicrobiology studies were negative for any microorganisms. Two days post-operatively, the corneal infiltrates were less prominent than at original presentation. By the sixth post-operative day, the epithelium had completely healed bilaterally. The patient improved on topical steroid and antibiotics within 2 weeks. The central corneas remained clear throughout follow-up. Steroids were tapered over a month and the infiltrates resolved with faint peripheral corneal scarring and final CDVA of 20/25 [].

[[47.0, 'year']]

M

{'3085488': 1, '8117641': 1, '16105612': 1, '7473111': 1, '14640433': 1, '27689081': 1, '33229677': 1, '33292492': 2, '19251159': 1, '24669152': 2}

{'7661148-1': 1}

3959049-1

noncomm/PMC003xxxxxx/PMC3959049.xml

Intraoperative Fracture of Phacoemulsification Tip

Phacoemulsification with intraocular lens (IOL) implantation in the left eye was performed in a 61-year-old female. Preoperatively, the best-corrected visual acuity (BCVA) was 20/200. The patient had grade II nuclear sclerosis with grade II cortical cataract in the left eye. Intraocular pressure (IOP) was 14 mmHg, and no other significant ocular abnormality was noted.\nSurgery was performed under topical anesthesia with 2% Xylocaine gel. A 2.75 mm temporal clear corneal incision was made with a keratome. Continuous curvilinear capsulorrhexis, hydrodissection and hydrodelineation were performed without complications. Phacoemulsification was then performed using a standard 20-gauge ABS (Aspiration Bypass System) phaco tip (Infiniti, Alcon laboratories, Inc., Fort Worth, TX, USA). As soon as the phaco tip was inserted into the nucleus, the surgeon realized there was no vacuum build up and carefully evaluated the problem. The phaco parameters were verified to be appropriate. The same steps were repeated, however it was noted that a segment of the titanium tip was broken. The broken fragment remained inside the silicone sleeve []. The phaco probe was carefully taken out ensuring the removal of the phaco needle with the broken end in toto. The anterior chamber (AC) was reformed with viscoelastic and a thorough search for any potential fragments under the operating microscope did not reveal any residual material. The surgery was completed uneventfully with a new titanium tip. Thereafter, we meticulously examined the broken tip under the operating microscope [-]. The broken ends matched perfectly with no missing fragments, thus confirming no retained foreign body within the AC. It was noted that the tip had broken in the area where the ABS microhole was present (i.e., 3 mm from the distal open end). Electron microscopy (EM) of the broken ends revealed a smooth break near the microhole of the ABS tip [-]. The postoperative course was uneventful, and the patient achieved BCVA of 20/25 with normal IOP and a quiet AC at 3 months postoperatively.

[[61.0, 'year']]

F

{'17222793': 1, '31856507': 1, '16863978': 1, '10511940': 1, '9373491': 1, '33880008': 1, '12660486': 1, '19020637': 1, '16473241': 1, '8972380': 1, '33732949': 1, '9640206': 1, '9642593': 1, '24669153': 2}

{}

3959050-1

noncomm/PMC003xxxxxx/PMC3959050.xml

Repositioning of Pedicle Conjunctival Flap Performed for Refractory Corneal Ulcer

A 50-year-old male had complaints of pain, redness, watering, and diminution of vision in the right eye for 4 weeks. The patient had a previous history of a 5.0 × 4.5 mm corneal ulcer and marked corneal thinning in the right eye. He did not show any improvement after 2 weeks of topical and systemic antifungal treatment. The referring ophthalmologist performed a CF in the right eye. After 2 weeks, patient did not show any improvement in symptoms and was referred to us for further treatment.\nOn examination, the patient's visual acuity was count fingers in the right eye and 20/20 in the left eye. Slit-lamp biomicroscopy revealed a thick CF including Tenon's capsule, extending 6.5 mm on the right cornea. The limbal conjunctiva had been removed from 6:30 to 9:30 clock h []. The projecting 10-0 nylon sutures were removed. Left eye on examination was normal. We elected to reposit the CF with the method described below.\nA low-dose peribulbar anesthesia (5 mL) was delivered containing 2.5 mL each, of xylocaine (2%) and bupivacaine (1%). The eye was prepared in a sterile fashion and draped. A Barraquer wire eyelid speculum was inserted for adequate globe exposure. First, the wound was evaluated. The peritomy area was deepithelialized. The CF was disengaged, fibrous tissue was excised and the CF was resutured to the original position with interrupted 8-0 vicryl sutures. The excision of the CF left behind a corneal epithelial defect, corneal opacity, and corneal thinning. A bandage contact lens (BCL) was applied. The patient was placed on moxifloxacin 0.3%, natamycin suspension 5%, and cyclopentolate hydrochloride 1% three times daily. The epithelial defect healed within a week and the BCL was removed. The corneal ulcer healed resulting in avascular corneal opacity [].\nAt 3 months follow-up, corneal opacity persisted and best corrected visual acuity was 20/200. The patient underwent an uneventful PKP. Over 4 years of follow-up, the patient achieved a best corrected visual acuity of 20/40 and the graft remained clear.

[[50.0, 'year']]

M

{'9097795': 1, '9436878': 1, '12912699': 1, '26976834': 1, '12578769': 1, '31334396': 1, '22553762': 1, '19464670': 1, '34179583': 1, '17198015': 1, '29245335': 1, '29456673': 1, '32905115': 1, '17251805': 1, '20818073': 1, '15803178': 1, '24669154': 2}

{}

3959051-1

noncomm/PMC003xxxxxx/PMC3959051.xml

Alternaria Keratitis after Deep Anterior Lamellar Keratoplasty

A 30-year-old male patient presented with the complaints of decreased vision in both eyes for 25 years. His best corrected visual acuity (BCVA) was 20/60, N6 and 20/80, N10 in the right and left eyes respectively. On examination, he had bilateral central, leucomatous, vascularized corneal opacity, which was larger in the left eye [] as compared with the right eye. The rest of the ocular and systemic examination was normal. Patient was not a diabetic or hypertensive.\nPatient underwent deep anterior lamellar keratoplasty (DALK) in the left eye. Post-operatively, patient was prescribed topical 0.5% moxifloxacin, 0.3% tobramycin, 0.1% dexamethasone and 2% hydroxypropyl methyl-cellulose 6 times/day and 1% atropine once at night. Patient developed a recurrent epithelial defect over the next 3 months with a BCVA of 20/60. The defect was treated with a bandage contact lens (BCL). At the 3 month follow-up visit, patient presented with reduced vision in the left eye (BCVA 20/200) along with redness and pain. Patient was a driver by occupation and resumed his work 2 days prior when he had an episode of dust particles entering into the left eye. On examination, dust particles were present along with an epithelial defect in the graft. Patient was started on topical 0.3% fluconazole, 0.5% moxifloxacin 0.3% tobramycin along with 2% hydroxypropyl methyl-cellulose eye ointment 6 times/day and 1% carboxymethyl-cellulose hourly.\nOne week later, a large brown pigmented dry lesion was present on the graft []. With a working diagnosis of keratitis, corneal scrapping was performed, which showed segmented filamentous fungi on 10% potassium hydroxide mount [] as well as on lactophenol blue stain [].\nCulture on sabouraud dextrose agar at 30°C yielded colonies of Alternaria species within 7 days of incubation []. Oral fluconazole (150 mg) twice daily were started in addition to the topical medications. Patient did not respond to medical therapy and had to undergo a repeat DALK. After removal of the old graft button, four drops of amphotericin B (5 μ/0.1 ml) were place on Descemet's membrane. Patient was prescribed oral fluconazole 150 mg twice daily, ofloxacin 200 mg twice daily and acetazolamide 250 mg twice daily along with topical 5% natamycin, 0.5% moxifloxacin, 0.3% tobramycin, 0.1% dexamethasone, in addition to 2% hydroxypropyl methyl-cellulose 6 times/day and 1% carboxymethyl-cellulose CMC 8 times/day. A BCL was placed for the epithelial defect. Patient improved with complete epithelial healing in 2 weeks and topical 5% natamycin was changed to 1% voriconazole. At 1 month follow-up, the left eye BCVA was 20/60 that remained stable at 11 months follow-up []. The graft remained clear with no signs of recurrence of fungal infection.

[[30.0, 'year']]

M

{'16371794': 1, '32476722': 1, '31517855': 2, '20215384': 1, '7927819': 1, '15126145': 1, '20335812': 1, '27716123': 1, '18661446': 1, '2055034': 1, '1081406': 1, '34307431': 1, '12472731': 1, '24669155': 2}

{'6750735-1': 1}

3959052-1

noncomm/PMC003xxxxxx/PMC3959052.xml

Alopecia Following Oral Acyclovir for the Treatment of Herpes Simplex Keratitis

A 32-years-old female presented with complaints of redness, watering, photophobia, and diminution of vision in the left eye with duration of two weeks. She disclosed a history of a similar attack in the left eye one year previously. She had a visual acuity of 20/20 in the right eye and count fingers close to face in the left eye. Examination of the right eye did not reveal any abnormality. There was mild conjunctival congestion in the left eye. Slit lamp biomicroscopy showed corneal edema, medium-sized keratic precipitates, cells (++) and flare (++). Fluorescein staining of the cornea did not reveal any epithelial defect. There was a marked decrease of corneal sensation in the left eye. A diagnosis of keratouveitis due to recurrent herpes simplex virus infection in the left eye was considered. She was placed on prednisolone acetate (1%) suspension four times daily, atropine sulfate (1%) thrice a day, and oral acyclovir 400 mg twice-daily. At one week follow-up, there was decrease in her symptoms. The visual acuity in the left eye improved to counting fingers at three meters. Slit lamp biomicroscopy revealed mild corneal edema, decrease keratic precipitates, cells (+) and flare(+). She was advised to continue the same treatment. At three weeks, she felt symptomatically better, but complained of diffuse loss of hair from scalp. There was no history of drug eruptions. Her visual acuity in the left eye was 20/200. Slit lamp biomicroscopy revealed residual corneal opacity and few old keratic precipitates in the left eye. Examination of the scalp revealed a diffuse hair loss and no drug eruptions []. The color and the texture of the hair were normal.\nOral acyclovir was discontinued, and topical prednisolone was reduced to thrice a day for two weeks and then twice a day for two weeks. A follow up after three months of discontinuation of oral acyclovir revealed hair re-growth in the affected area on her scalp []. Examination of the left eye revealed a corneal opacity, and she was advised to undergo penetrating keratoplasty for the left eye. The patient was not on any other oral, topical or over-the-counter medication. In addition, she did not receive any holistic, natural or home remedies during this period. Patient was moderately-built and did not suffer from any nutritional deficiency. She had not been pregnant recently. In addition, she did not have any other systemic problem that may lead to hormonal imbalance. She did not suffer from lupus erythematosus, hypothyroidism, hyperthyroidism, syphilis, sarcoidosis, HIV infection or any systemic malignancy.

[[32.0, 'year']]

F

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{'3099514-1': 1}

3959059-1

noncomm/PMC003xxxxxx/PMC3959059.xml

Transcatheter therapy for Lutembacher's syndrome: The road less travelled

An 18-year-old male, presented with history of dyspnea on exertion New York Heart Association (NYHA) class II. Physical examination revealed loud first heart sound, wide and fixed split second heart sound, mid diastolic murmur at the apex, and lower left sternal border with grade 4/6 ejection systolic murmur in the left second parasternal region. Electrocardiogram (ECG) showed incomplete right bundle branch block with right atrial enlargement. Chest X-ray findings were increased pulmonary vascular markings with prominent right pulmonary artery. Transthoracic echocardiography (TTE) showed a 27 mm ostium secundum ASD with severe rheumatic MS []. The mitral valve area (MVA) was 0.67 cm2 by planimetry. Color flow mapping revealed a left-to-right shunt across the ASD. As both the ASD and MS appeared suitable for percutaneous treatment, concurrent transcatheter therapy was planned.\nPatient received 300 mg of clopidogrel and 325 mg of aspirin 1 day prior to procedure. After antibiotic prophylaxis, right femoral arterial and venous access was obtained, and 5,000 units of heparin administered. Right and left heart catheterization with oximetry run confirmed a left to right shunt with step up at the atrial level with Qp/Qs of 5.37 as measured by Fick's principle. The mean left atrial pressure and transmitral gradients were relatively low, in spite of significant MS.\nBalloon mitral valvotomy (BMV) was first undertaken. Multiple attempts with standard Inoue technique proved futile with repeated jumping of Inoue balloon back into the right atrium (RA) and right ventricle (RV). Hence, an over -the -wire (OTW) technique was adopted with the available hardware on shelf. The mitral valve (MV) was crossed using a balloon floatation catheter (Swan Ganz) and an Inoue wire was placed directly into the LV. However, an attempt to introduce the Inoue balloon over the Inoue wire failed because of poor support. Modifying OTW technique, we recrossed the MV with a balloon floatation catheter, parking an Inoue wire directly into the left ventricle (LV). With the Inoue wire in situ, the Swan Ganz catheter was removed and a Mullins sheath was introduced into the LV. With adequate support provided by Mullins sheath, the Inoue wire was exchanged for a J tip Amplatz extra stiff wire (ESW). After removing the Mullins sheath, an Inoue balloon was successfully introduced into the LV over the ESW. With Inoue balloon stabilized in the LV cavity, the ESW was changed to Inoue wire for better conformation to the LV anatomy and provide safe support to Inoue balloon during mitral valvotomy []. The MV was successfully dilated using a 26 mm Inoue balloon with abolition of the transmitral gradient and a MVA of 1.8 cm2.\nAfter successful BMV, ASD device closure was undertaken. Based on our experience of device closure of ASDs without balloon sizing under trans-thoracic (TTE) guidance in young patients, we decided to deploy a 30 mm Amplatzer (AGA Medical, Golden Valley, MN) ASD device under TTE guidance. Postprocedure TTE showed a well-deployed device across the ASD. Twelve hours postprocedure TTE showed a malpositioned device, which was confirmed later on transesophageal echocardiography (TEE) []. After arranging for full surgical backup, percutaneous retrieval of malpositioned ASD device was undertaken under cinefluroscopic and TEE guidance. Intentional bevel was created at the end of a 12 French Amplatzer sheath and a 1-cm Amplatz GooseNeck snare (Amplatz, ev3 Inc., Phymouth, MN, USA) was chosen with intention to grasp the microscrew of the right atrial disk of the ASD device. Using alternate orthogonal views to align the snare in the plane of the ASD device, the device was successfully pulled from the RA into the inferior vena cava below the kidneys and retrieved through the femoral sheath [Figure –]. Careful reassessment of ASD diameter under TEE guidance showed a procedural diameter of 30 mm and total interatrial septal length of 52 mm. Final ASD device closure [] was done with a 36 mm Heartr™ atrial septal occluder device (Lifetech Scientific Inc., Shenzhen, China). There were no further postprocedural complications and patient has done excellently with no clinical sequelae at 16 months follow-up.

[[18.0, 'year']]

M

{'10506780': 1, '16082575': 1, '17985381': 1, '21205423': 1, '15065154': 1, '15224314': 1, '1394421': 1, '18706243': 1, '28228300': 1, '22388316': 1, '9600517': 1, '15550747': 1, '3687695': 1, '10348582': 1, '25984452': 1, '1858633': 1, '30627291': 2, '24701084': 2}

{'6306122-1': 1}

3959060-1

noncomm/PMC003xxxxxx/PMC3959060.xml

Transcatheter device closure of a traumatic ventricular septal defect

A previously well 7-year-old boy was hit and run over by a truck. He presented to the local emergency department with evidence of head, chest, and abdominal injury. Clinical examination also revealed a harsh pansystolic murmur at the left sternal border. Echocardiography showed an 8-mm muscular VSD near the apex, which was initially thought to be a congenital defect []. The patient was hemodynamically stable and did not require inotropic support. Electrocardiogram showed normal sinus rhythm. Cardiac enzymes were not assayed on presentation.\nCT of head showed base of skull fracture. The CT chest and abdomen showed lung contusions at both bases and liver laceration []. Over the course of the next 24 hours, he developed progressive tachycardia, hypotension with hepatomegaly and elevated central venous pressure. He had also developed a right-sided pleural effusion. He underwent emergency laparotomy to exclude persistent hemorrhage from the liver laceration. A moderate volume of old blood was found and this was not able to explain the degree of hypotension. Repeat echocardiography documented ragged walls around the muscular VSD near the apex and significant left heart dilatation and right ventricular strain.\nThe patient was clinically in severe heart failure, which was very difficult to manage medically. In the context of multiple organ injuries, coagulopathy, hemodynamic instability, and technical difficulty in closing the VSD surgically, a decision was taken to close the defect percutaneously. In order to achieve the maximal coverage of the lacerated ventricular septum and in the context of his relatively small weight (23 kg), a 25-mm cribriform Amplatzer PFO device (St Jude Medical, Plymouth, MN USA) was selected. This was placed after forming an arterio-venous guidewire loop through a 7-Fr delivery system [Figures and ]. There were no complications. Post-procedure echocardiogram showed the presence of only a small residual VSD, which was anticipated due to the unusual morphology and ragged edges of the traumatic VSD [Figures and ].\nDespite apparent successful device placement, the patient required high-dose infusion of adrenaline to maintain adequate blood pressure. He also developed acute renal dysfunction and required continuous veno-venous hemofiltration. He had bilateral chest drains inserted for pleural effusions. His hypotension progressively worsened over the next 2 days. In spite of the multiple inotropes, the heart function was moderately reduced. He was already being treated with broad-spectrum antibiotics, adrenaline, vasopressin, and corticosteroids for inotrope-resistant shock. At this juncture, extracorporeal membrane oxygenation (ECMO) was considered as an alternative means of supporting the patient, despite the increased risk involved in view of liver laceration and lung contusion. The role of ECMO support provision in the post-trauma patient was discussed with international centers and it was decided that ECMO would be provided if further deterioration occurred, despite the risk of hemorrhage with systemic anticoagulation.\nHis clinical condition improved progressively with the inotropes stopped at day 5. His recovery over the next 2 weeks was complicated by episodes of pulmonary hemorrhage, bronchial occlusion with casts in left main bronchus, and critical illness myopathy. He was discharged from our intensive care unit after 20 days. At discharge, his heart function had returned to normal. The occluder device was in a good position. There remained a small residual VSD of 5 mm size, with a highly restrictive left-to-right shunt. There were no obvious signs of neurological damage except for the evidence of resolving myopathy.\nAfter 6 months of his first device closure, he underwent elective closure of his residual VSD with a duct occluder device (Amplatzer ADOII 6 mm, St Judes Medical, Plymouth, MN, USA) for persistent mild left ventricular dilatation. Following the second procedure, he had no residual shunt with complete resolution of left ventricular dilatation (Figures and ).

[[7.0, 'year']]

M

{'12173854': 1, '20661334': 1, '32547656': 1, '19642200': 1, '32467927': 1, '22787351': 2, '11410583': 1, '3396173': 1, '22272462': 1, '12796201': 1, '24701085': 2}

{'3391845-1': 1}

3959062-1

noncomm/PMC003xxxxxx/PMC3959062.xml

Prenatal diagnosis of isolated interrupted inferior vena cava with azygos continuation to superior vena cava

A 38-year-old second gravida was referred to us for fetal echocardiography at 25 weeks in view dilated superior vena cava (SVC) and suspicion of interrupted IVC with persistent right umbilical vein. Biometry was consistent with fetal age. No other abnormalities were detected within the heart or other organs. Fetal karyotype was normal. Fetal echocardiography showed the presence of a vessel posterior to the descending aorta in the four-chamber view (“Double vessel sign,” ). The next clue came from the three-vessel view, which showed a dilated, prominent SVC []. In the bi-caval view, the intra-hepatic portion of the inferior vena cava was found to be interrupted []. Rostral to this point, a thinner vessel with venous flow was detected as a continuation of the infra-hepatic portion of the IVC. On tracing this vessel cranially, its connection with the superior vena cava was documented []. The hepatic veins and ductus venosus reached the right atrium normally. No other anomalies of the heart were detected.\nA female baby weighing 2.8 Kg was delivered by elective caesarian section at 38 weeks. Clinical evaluation of the cardio-vascular system was unremarkable. A detailed cardiac evaluation was performed at 6 weeks post-natal age. ECG was unremarkable and showed sinus rhythm with normal atrio-ventricular conduction. Echocardiography confirmed the prenatal diagnosis of isolated inferior vena cava with azygos continuation to superior vena cava []. No other cardiac/extracardiac abnormalities were detected. The patient was advised follow-up and periodic monitoring for the development of any rhythm anomalies in future.

[[38.0, 'year']]

F

{'10835118': 1, '13683264': 1, '19829946': 2, '8644662': 1, '21183652': 1, '19304670': 1, '15772175': 1, '34760057': 2, '7614500': 1, '262529': 1, '22726404': 1, '20060092': 1, '31741603': 2, '7609017': 1, '10773801': 1, '24701087': 2}

{'6857260-1': 1, '8574097-1': 1, '8574097-2': 1, '8574097-3': 1, '8574097-4': 1, '2740028-1': 1}

3959065-1

noncomm/PMC003xxxxxx/PMC3959065.xml

Percutaneous closure of patent ductus arteriosus in interrupted inferior caval vein through femoral vein approach

A 12-year-old girl who presented with dyspnea on moderate exertion and palpitation since three years was admitted for percutaneous closure of a patent arterial duct. Her infancy and childhood period were unremarkable and without cardiac symptoms. Her weight was 39 kg and height was 149 cm. Her blood pressure was 120/60 mmHg. Peripheral pulses were bounding. Precordial examination revealed active precordium with the point of maximum intensity shifted downward and laterally. There was thrill and continuous murmur over the left second intercostal space. Chest X-ray showed marked cardiomegaly. Electrocardiogram (ECG) showed sinus rhythm with a rate of 80 bpm and left ventricular hypertrophy. Echo showed dilated left atrium, left ventricle, and pulmonary artery, and a patent ductus arteriosus (PDA) of about 6 mm with a continuous left-to-right shunt.\nUnder general anesthesia, arterial access was established through the right femoral artery with a 4F introducer and aortic pressure was measured (86/53 mmHg, mean: 69 mmHg). Then, aortic angiogram was done []. A duct measuring 5 mm was seen. On right heart catheterization, it was found that the inferior caval vein was interrupted and that there was azygos continuation. A Terumo catheter was advanced and snared in the descending aorta. An AGA exchange wire (.035" × 260 cm) was advanced through the catheter and snared in the descending aorta. While snaring the wire, an Amplatzer TorqVue 2 delivery sheath 6F, 60 cm long (AGA Medical Corporation, Golden Valley, MN) was advanced over the wire from the venous side and again snared in the descending aorta [Figures and ]. An Amplatzer duct occluder (ADO) size 8/6 was advanced through the sheath while still holding the sheath with a snare [Figure –]. The device was opened, again with the sheath still snared. The sheath was then unsnared once the aortic disc was completely out. The sheath and the device were pulled back into the duct and the device was successfully implanted []. The device was then released and it attained a stable position []. An aortic angiogram was done after the device was released, showing complete occlusion. The patient remained stable and there was no hemodynamic instability anytime during the procedure. She was extubated immediately.

[[12.0, 'year']]

F

{'20607224': 1, '20808632': 2, '16933065': 1, '20808631': 2, '17674085': 1, '32642857': 2, '20060092': 1, '26995443': 1, '34276894': 2, '24701089': 2}

{'2922666-1': 1, '2922667-1': 1, '7343687-1': 1, '8254156-1': 1, '8254156-2': 1, '8254156-3': 1, '8254156-4': 1}

3959066-1

noncomm/PMC003xxxxxx/PMC3959066.xml

Dysphagia Lusoria with atrial septal defect: Simultaneous repair through midline

A four-year-old female child presented to us with complaints of dysphagia and regurgitation of solid food. A contrast-enhanced CT scan (CECT) of the chest done elsewhere revealed an aberrant right subclavian artery []. A 256 slice CECT scan was ordered in our hospital for the exact anatomical characterization of the aberrant vessel. The scan showed an aberrant origin of the right subclavian artery from the medial wall of the descending thoracic aorta, just distal to the origin of the left subclavian artery [Figures and ]. The artery crossed to the right side at the level of the fourth thoracic vertebra, causing posterior compression of the esophagus. An additional finding that was noted was the common origin of the right and left common carotid arteries. The arch was left-sided, with a left descending thoracic aorta. An echocardiogram done showed a large ostium secundum atrial septal defect (ASD) of 20 mm, with a dilated right atrium and right ventricle.\nUnder general anesthesia a median sternotomy was performed. The arch was followed down from the top and the aberrant right subclavian artery was identified just distal to the origin of the left subclavian artery on the medial wall of the descending thoracic aorta. Loss of the right radial artery trace on clamping the aberrant vessel confirmed that the vessel was indeed the right subclavian artery. The artery was carefully divided at its site of origin and the aortic end oversewn with two layers of continuous polypropylene sutures. The artery was next brought to the right side from behind the esophagus and the anastomosed end side to the right common carotid artery, after confirming that there was no torsion of the mobilized vessel []. Pericardial patch closure of the ostium secundum ASD was performed in a routine manner, under cardiopulmonary bypass, under mild hypothermia using the standard cannulation techniques. The patient had an uneventful postoperative course and was discharged on day six from the hospital. The patient had no complaints of dysphagia or regurgitation of food on discharge.

[[4.0, 'year']]

F

{'8362621': 1, '5829979': 1, '15216311': 1, '32004900': 1, '17858859': 1, '17958718': 1, '8415218': 1, '26904341': 1, '21519490': 2, '5947142': 1, '3509606': 1, '5057835': 1, '22084776': 1, '7224699': 1, '5549289': 1, '24701090': 2}

{'3079082-1': 1}

3959067-1

noncomm/PMC003xxxxxx/PMC3959067.xml

Redux valvular surgery with coronary artery bypass graft in familial hypercholesterolemia

We report the case of a 12-year-old girl; she had a medical history of FH like her brother with tendon xanthomas of the upper and lower extremities []. She was operated two years previously for aortic stenosis associated with mitral valve regurgitation grade 3 without coronary artery disease []. She had a Ross intervention with mitral annuloplasty with positive results. Currently, she was admitted in emergency for acute coronary syndrome with negative ST and positive troponin I with initially stable hemodynamic constants. A transthoracic echocardiography was done which showed a dilated left ventricle with an ejection fraction of 61%, mitral regurgitation grade 2, absence of aortic insufficiency, and a good functioning of a Contegra tube in pulmonary position. The patient was directly sent to the catheterization laboratory where angiography showed stenosis of the distal left main trunk, subocclusive stenosis of the proximal circumflex coronary, a stenosis of the second and distal parts of the interventricular coronary, and proximal subocclusive stenosis of the right coronary artery []; it also showed stenosis of both left and right subclavian arteries []. She was hospitalized in the surgical intensive care unit and antianginal treatment was initiated. Her hospital course was complicated by the deterioration of hemodynamic status with several outbreaks of left heart failure related to mitral regurgitation grade 3-4 with a low ejection fraction of 35%, requiring the introduction of vasoactive drugs in gradually high doses.\nThe patient was operated and three aortocoronary grafts using the two saphenous veins taken at the thigh because of the presence of stenosis of subclavian arteries, in addition to the replacement of the mitral valve by a mechanical prosthesis. The postoperative course and medium-term follow-up were excellent with improved hemodynamic status and the disappearance of angina and dyspnea.

[[12.0, 'year']]

F

{'19843551': 1, '19214450': 1, '19301565': 1, '7089781': 1, '19341213': 1, '9564940': 1, '16368327': 1, '16261269': 1, '10925239': 1, '24701091': 2}

{}

3959068-1

noncomm/PMC003xxxxxx/PMC3959068.xml

Pseudo interruption of the inferior vena cava complicating the device closure of patent ductus arteriosus: Case report and short review of venous system embryology

A nineteen-months-old girl presented with recurrent respiratory infection and patent ductus arteriosus (PDA). There was no other significant past medical or surgical history. An echocardiogram showed a 3.4 mm PDA with adequate ampulla and mild hyperkinetic pulmonary arterial hypertension. The patient was taken up for percutaneous device closure of the PDA. A diagnostic catheter (5 F Goodale Goodale-Lubin) from the right femoral venous access entered the right atrium through azygos vein into superior vena cava (SVC). A diagnosis of IVC interruption with azygos continuity was made. The PDA was crossed from venous end. The catheter course was via the right femoral vein, azygos vein, SVC, right atrium (RA), right ventricle, pulmonary artery, PDA to the descending aorta []. In view of the tortuous course, difficulty in tracking the delivery sheath was anticipated. Interventional options available in such a situation are: (a) Arterial side snaring of the distal end of the wire (for support), and tracking the femoral venous sheath, (b) Jugular venous approach, and (c) Trans arterial Amplatzer duct occluder II (ADO II). An ADO II device of appropriate size was not available then in the catheterization laboratory. Arterial side snaring was not attempted, anticipating cardiac stretch-related bradycardia. Therefore, the right internal jugular vein (IJV) access was used for PDA closure. An aortogram from the femoral arterial access showed 4.7 mm PDA. Through an 8F Mullin sheath, in the right internal jugular vein access, a 10 × 12 mm Heartr™ duct occluder device (Lifetech Scientific Inc., Shenzhen, China) was deployed. The post procedure angiogram and echo showed stable device position, with no residual flow. On the following day, a repeat echocardiogram revealed patent IVC connection into the right atrium. The patient was taken up for a venogram to rule out interrupted IVC. A right femoral venous angiogram showed filling of the iliac veins and azygos system, in addition to normal drainage into the IVC [Figures and , ]. Similarly, the left femoral venous angiogram showed filling of both the IVC and the hemi azygos system [, ]. Hence, the misdiagnosis of IVC interruption was revealed. The catheter has had tracked through the congenital communication between the iliac veins and the azygos system, bypassing the IVC. Had it been recognized earlier, internal jugular vein (IJV) access could have been avoided.

[[19.0, 'month']]

F

{'10835118': 1, '29707375': 1, '34760057': 2, '12136323': 1, '26995443': 1, '34276894': 2, '24701092': 2}

{'8254156-1': 1, '8254156-2': 1, '8254156-3': 1, '8254156-4': 1, '8574097-1': 1, '8574097-2': 1, '8574097-3': 1, '8574097-4': 1}

3959069-1

noncomm/PMC003xxxxxx/PMC3959069.xml

Ebstein anomaly and Trisomy 21: A rare association

A male infant was born to a 23-year-old woman with intermittent prenatal care, at 35 weeks and 2 days gestation. The prenatal ultrasound revealed a 10-fold risk of Trisomy 21 based on nuchal translucency; however, additional workup, including a fetal echocardiogram, was not performed. On the day of birth, an obstetric ultrasound revealed oligohydramnios and intrauterine growth restriction with the fetus at less than the first percentile, therefore, induction of labor ensued and the baby was born via uncomplicated vaginal delivery.\nAfter birth, continuous positive airway pressure at 5 mmHg and supplemental oxygen at 50% was instituted due to clinical cyanosis and poor respiratory effort, with a resulting oxygen saturation of 70%. The Apgar scores were 7 and 9. On physical examination there was typical facies associated with Trisomy 21 and a 2-3/6 holosystolic murmur was auscultated at the left lower sternal border. Genetic testing confirmed karyotype 47, XY + 21. A chest X-ray revealed significant cardiomegaly and increased pulmonary vascularity []. An electrocardiogram (EKG) demonstrated sinus rhythm, right atrial enlargement, intraventricular conduction delay, with an extreme rightward axis, and no pre-excitation.\nTransthoracic echocardiography performed on the first day of life [Figure –] revealed (S,D,S) normal segmental anatomy with atrioventricular and ventriculoarterial concordance. An apically displaced and tethered tricuspid septal leaflet, with a deficient posterior leaflet, resulted in mild-to-moderate tricuspid regurgitation. The right atrium (atrialized ventricle) was dilated with a right-to-left flow across a stretched patent foramen ovale. There was a moderate perimembranous ventricular septal defect (VSD) with muscular extension and mostly left-to-right flow, at a low velocity, which predicted a peak gradient of 14 mmHg. The pulmonary valve was normal without stenosis or regurgitation. A large ductus arteriosus shunted left-right on the initial echocardiogram. The left ventricular morphology was normal.\nThe patient was monitored in the Neonatal Intensive Care Unit (NICU). Once ductal closure had been confirmed on day of life #6 and as oxygen saturations remained above 90%, ensuring adequate pulmonary blood flow, the patient was discharged home on day of life #25, with close follow up and consideration of surgical intervention once symptomatic.\nFollowing initial discharge, the patient was readmitted multiple times to the hospital for failure to thrive despite maximal caloric intake. Therefore, the patient underwent tricuspid valvuloplasty and VSD closure, with maintenance of an atrial level communication on day of life #108. A postoperative echocardiogram revealed moderate-to-severe tricuspid regurgitation, estimating a gradient of 39 mmHg from right ventricle to right atrium and right-to-left shunting across the atrial communication. Initially, weight gain was steady and oxygen saturations remained above 80%; however, over several months the patient again failed to gain weight despite adequate caloric intake. An echocardiogram 6.5 months postoperatively [Figure –] demonstrated severe tricuspid regurgitation, right-to-left shunting across the atrial communication, and new mild left upper pulmonary vein stenosis, with a mean gradient of 3-4 mmHg. Cardiac catheterization revealed diffuse pulmonary vein hypoplasia and left-sided pulmonary vein stenosis, with mean gradients of 4-11 mmHg. Repeat surgical intervention of the tricuspid valve was considered, however, given the low likelihood of improvement on account of pulmonary vascular disease and high-expected morbidity, surgery was not recommended.

[[23.0, 'year']]

M

{'15865831': 1, '14694960': 1, '1462038': 1, '34849279': 1, '14494652': 1, '4267846': 1, '138359': 1, '10364665': 1, '17098303': 1, '7801301': 1, '11675224': 1, '15320560': 1, '2527505': 1, '24701093': 2}

{}

3959086-1

noncomm/PMC003xxxxxx/PMC3959086.xml

The central retinal artery occlusion in the right eye followed by a branch retinal artery occlusion in the left eye four days later

A 65-year-old woman was admitted to our clinic with complaints of sudden, painless, decrease in vision, and sectoral visual field defect in the left eye for the past 3 days. On examination, the corrected visual acuity by the Snellen chart was 20/40 OS and 20/20 OD. Intra-ocular pressures were 13 mm Hg bilaterally. A relative afferent pupillary defect was observed in the left eye. External and slit lamp examinations were unremarkable in both eyes. Fundus examination of the left eye showed a patchy area of partially faded retinal whitening in the inferotemporal quadrant of the macula, just encroaching into the fovea. There was an emboli at the disc margin within the inferotemporal artery []. Fluorescein angiogram of the left eye showed a delay in arterial filling in the affected vessels [] and late leakage from the embolus site [Fig. and ]. Confrontation visual field revealed a loss of superior visual field in the left eye. She had a history of uncontrolled hyper-tension and hypercholesterolemia. She had no history of amaurosis fugax, diabetes mellitus, coronary artery disease, or stroke. A fundus examination of the right eye showed an emboli and segmentation in the inferotemporal artery. Due to these findings, cardiology consultation, carotid Doppler ultrasound, echocardiography and blood tests were requested from the patient. Four days after the initial examination, she was presented to our clinic again with a history of sudden loss of vision in her right eye for the last 4 h. Visual acuity in the right eye was reduced to perception of light only. The right eye fundus examination demonstrated a diffuse disc pallor, severe attenuation of retinal arteries, retinal edema, and a “cherry-red spot” appearance on the macula []. The red-free photograph greatly accentuates the retinal whitening surrounding the macula and with segmentation of blood columns in inferotemporal retinal artery because of the multiple emboli plaques []. She was immediately given a vigorous digital ocular massage, breathing carbogen (95% oxygen, 5% carbon dioxide), started on intra-venous mannitol and systemic carbonic anhydrase inhibitor. Unfortunately, visual acuity in the right eye was not changed after the treatment. In the cardiovascular evaluation, there was a fibro-fatty plaque in the right internal carotid artery at carotid Doppler ultrasonography. There were also calcified mitral and aortic valves in the echocardiography. Serum cholesterol level was 231 mg/dL and serum low-density lipoprotein level was 166 mg/dL. Prothrombin time and partial thromboplastin time were in the normal range. An urgent erythrocyte sedimentation rate, C-reactive protein, and complete blood count were normal. The patient's blood pressure was measured at 170/100 mm Hg. One month after the admission, visual acuity did not change in either eye. There was no iris neovascularization in both the eyes. However, there was a neovascularization of optic disc in the right eye. Optical coherence tomography (OCT) revealed diffuse thickening of the inner retinal layers. Increased reflectivity was noted in the inner retinal layers from the surface of the retina to the photoreceptor layers. Colored fundus photographs and OCT images in the 1st month are shown in .

[[65.0, 'year']]

F

{'21757667': 1, '20609991': 1, '17895823': 1, '18441166': 1, '758898': 1, '3808517': 1, '8533103': 1, '26958113': 1, '23070637': 1, '24145559': 2}

{}

3959087-1

noncomm/PMC003xxxxxx/PMC3959087.xml

Successful treatment of Fusarium keratitis after photo refractive keratectomy

A 39-year-old woman presented to our hospital with a history of photorefractive keratectomy (PRK), performed two weeks prior. She complained severe visual loss, photophobia, redness and pain in right eye.\nThe patient was receiving therapy with topical steroids and antibiotic eye drops. The best corrected visual acuity (BCVA) of the affected eye was limited to hand motion. Slit lamp examinations revealed diffuse conjunctival congestion and a corneal ulcer with stromal infiltration [].\nThe ulcer bed and edges were scraped and were sent for bacteriological and mycological examination analysis.\nTreatment with corticosteroid eye drops was suspended and the patient was started on the following drugs: Topical fortified 5% vancomicin, tobramicin 0.3%, moxifloxacin 0.5%, amphotericin B 0.15% at 4 h intervals; systemic antifungal and antibacteric drugs consisted of oral itraconazole at a dose of 200 mg daily with oral ciprofloxacin 1g daily, and intramuscolar ceftriaxone 1 g daily respectively.\nAfter two days the cornea revealed a full thickness infiltrate with 1 mm hypopyon []. The infiltrate and the hypopyon progressively increased in size. After 5 days, the patient underwent a therapeutic penetrating keratoplasty with an 8-mm graft on a 7.75-mm bed using Barron Corneal Trephine. The explanted cornea was sent to the microbiology laboratory for further testing.\nPost-surgery treatment consisted in topical norfloxacin 0.3% (6 times per day) and amphotericin B (4 times per day); systemic ciprofloxacin 1 g daily, ceftriaxone 1 g daily, itraconazole 200 mg daily and intramuscolar metilprednisolone 20 mg daily [].\nAfter 8 days, the culture of corneal scraping revealed the presence of fungal filaments. We decided in agreement with the infectious disease specialist, to add therapy with oral voriconazole, (800 mg per day on the first day, followed by 400 mg per day on successive days) and topical amphothericin B eye drops 6 times per day. The donor cornea and anterior chamber remained free from infiltrates until day 12, after keratoplasty, when the patient showed eye redness, pain, 1/50 of visual acuity, endothelial dusting and aqueous flare and cells [Figs. and ]. Oral voriconazole was changed to intravenous formulation, 8 mg/Kg twice per day.\nTwenty days after surgery the patient had recurrent fungal infiltrate in the donor cornea with wound dehiscence []. We decided to perform a second penetrating keratoplasty.

[[39.0, 'year']]

F

{'14748803': 1, '33412407': 1, '27380973': 1, '16488012': 1, '4537911': 1, '27990375': 1, '11425685': 1, '24881619': 1, '17667615': 1, '20079930': 1, '21797693': 1, '34163127': 1, '34829196': 1, '12777034': 1, '15909252': 1, '22623874': 2, '33916767': 1, '24178402': 2}

{'3353683-1': 1}

3959088-1

noncomm/PMC003xxxxxx/PMC3959088.xml

Ophthalmomyiasis externa by Musca domestica in a case of orbital metastasis

A 70-year-old male presented with a foul smelling and discharging ulcer around the right eye of seven days duration. He complained of a crawling sensation over the area for the past two days.\nA diabetic, he was diagnosed with follicular carcinoma thyroid one year ago. He refused therapy, but came back after four months of alternative medicine treatment. In view of widespread metastasis then, he underwent chemotherapy. During the chemo, he developed painful swelling of the right eye with loss of vision and was subsequently lost to follow-up. He remained largely symptom free till the present complaints.\nOn examination of the right eye [], lids were thickened and inflammed; medial and lateral orbital walls showed deep ulcer cavities teeming with maggots; eye was proptosed down and out; exposure keratitis was present. He had no perception of light and the corneal haze precluded any fundus view.\nLeft eye anterior segment and fundus were within normal limits with a Best Corrected Visual Acuity (BCVA) of 20/20.\nHe was started on intravenous antibiotics and insulin doses adjusted to control his high glycaemic values. Under sedation, turpentine oil was instilled into the ulcer cavities and the maggots were manually picked out. The ulcers extended into the lids and inferomedially into the nose. Few maggots were caught wriggling out of the nostrils. Over 200 maggots ranging from three to ten mm size were retrieved in multiple sittings over the next three days. Sterile dressings were given. The fellow eye was thoroughly irrigated and antibiotic-steroid drops were applied following each maggot retrieving session.\nThe maggots were identified by the entomologist as those of the common housefly, Musca domestica. The patient was a coastal area inhabitant and he acknowledged that his neighbourhood with its fish markets were notorious for housefly infestation. ENT consultation showed extensive crusting of the nasal cavity, but no evidence of maggots. CT scanning [], showed a moderately enhancing soft tissue density encasing the recti and orbital apex structures, with widespread bony destruction extending to the infratemporal fossa, maxillary sinus, nasal cavity and through the lamina papyracea to the ethmoidal sinus, suggesting the possibility of metastasis from follicular carcinoma thyroid. Over the course of one week, the patient's general condition improved and the ulcer cavities filled up with healthy granulation tissue []. He was referred for palliative care.

[[70.0, 'year']]

M

{'20644320': 1, '711280': 1, '6026599': 1, '2086474': 1, '31977893': 2, '15688059': 1, '2086473': 1, '30930673': 1, '15453857': 1, '24145557': 2}

{'7004749-1': 1}

3959089-1

noncomm/PMC003xxxxxx/PMC3959089.xml

Cataract surgery in juvenile xanthogranuloma: Case report and a brief review of literature

A 2-month-old girl was brought to us with haziness of both eyes for the past 20 days. She was a full-term baby delivered by cesarean section with a birth weight of 2.75 kg. Her antenatal period was uneventful. The parents denied any history of trauma and the child was otherwise healthy. On examination (under general anesthesia), she was noted to have conjunctival hyperemia, increased corneal diameter (13.5 mm OD, 11 mm OS), corneal haze with small blood clots in the anterior chamber of both eyes. No iris nodules were evident []. Intraocular pressure (IOP) was noted to be 20 mm Hg OD and 8 mm Hg OS by Perkin's tonometer. A B-scan ultrasound of the posterior segment was normal OU. A few yellowish-orange skin nodules were noted on the forehead and neck [], that progressively increased on follow-up. Remainder of her systemic and neurological examination was normal. Her hemogram and coagulation profile were within the normal limits. Excision biopsy of a forehead skin lesion was performed under general anesthesia and histopathological examination of the specimen showed non-langerhans histiocytic proliferation []. Immunohistochemistry was negative for CD1a and cytokeratin; positive for CD68. With the above clinical picture and laboratory finding, a diagnosis of JXG was made.\nShe was started on a topical antibiotic steroid combination, cycloplegic and dorzalamide OU. On her review visits, she developed posterior synechiae and a few iris nodules in the left eye, which resolved with intensive topical steroids. Her IOP and fundus examination were within the normal limits. The steroids were tapered off after 2 months. She maintained a steady central fixation throughout her treatment and was also on regular review with a pediatrician. Four months after her first presentation, she developed bilateral anterior subcapsular cataract, which gradually progressed. She underwent cataract surgery in the left eye under general anesthesia. Topical prednisolone acetate 4 times a day was added to topical antibiotics a day before surgery. A superior bridle suture was placed. After peritomy, the bleeders were cauterized and a limbal groove made with a blade breaker. The anterior chamber was entered by deepening the groove and trypan blue was injected under an air bubble. Intracameral adrenaline was used to achieve pupillary dilatation and reduce intraoperative bleeding. Subsequently, 2% hydroxypropyl methylcellulose was injected into the anterior chamber. Iridocapsular adhesions were gently lysed by sweeping a cyclodialysis spatula under the iris. The anterior capsule was punctured by a bent 26 G needle and capsulorhexis done with a Utrata forceps. The lens matter was aspirated by a Simcoe cannula. The bottle height was raised to increase pressure in the anterior chamber and tamponade any bleeding. Subsequently, the posterior capsule was punctured by a bent 26 G needle in a sideways fashion and capsulorhexis completed by an Utrata forceps. Sufficient anterior vitrectomy and a peripheral iridotomy were done by an automated vitrector. An intraocular lens (IOL) was not implanted given the age of the patient (<1 year). Tight wound closure with 10-0 monofilament nylon suture was ensured. After surgery, she was started on topical steroid antibiotic combination and cycloplegics, which were tapered over 6 weeks. The right eye cataract surgery was done 6 weeks after the left eye surgery and a similar procedure was followed. Her perioperative period was uneventful. On her last follow-up, 1 year after surgery, the child was comfortable with aphakic correction and the visual axis was clear. The IOP was monitored with Pulsair tonometer. The IOP was noted to be normal on all occasions and no antiglaucoma medications were needed. The skin lesions appeared to be regressing.

[[2.0, 'month']]

F

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{}

3959090-1

noncomm/PMC003xxxxxx/PMC3959090.xml

Delayed diagnosis of ocular syphilis that manifested as retinal vasculitis and acute posterior multifocal placoid epitheliopathy

A 55-year-old female patient hospitalized with a history of bilateral progressive visual loss for 4 months. Initial work-up done elsewhere revealed all tests including rapid plasma reagin (RPR) were negative. She then, had been treated with the high dose systemic steroids followed by bilateral intravitreal triamcinolone injection, but her eyes continued to deteriorate.\nBest corrected visual acuity (VA) was light perception in both eyes. Biomicrocopy revealed a few inflammatory cells and fundoscopy showed disc edema, multiple yellow placoid lesions and vasculitis in both eyes [Fig. and ]. Fluorescein angiography demonstrated early hypofluorescence and late leakage from the placoid lesions [Fig. and, ]. Indocyanine green angiography was not performed. Optical coherence tomography revealed severe macular intraretina edema in both [Fig. and ] eyes as well as a serous retinal detachment in the right eye [].\nWe repeated serologic tests including viral polymerase chain reaction, toxoplasma antibody, rheumatoid factor, antinuclear antibody, human leukocyte antigen B27, human immunodeficiency virus (HIV) antigen/antibody and fluorescent treponemal antibody-absorption (FTA-ABS). Whereas all other tests were negative, FTA-ABS test was positive. Subsequent tests for cerebrospinal fluid also revealed positivity in FTA-ABS and Venereal Disease Research Laboratory (VDRL). The titer of VDRL was 1:8. While she denied any history of previous systemic diseases, systemic evaluation revealed recent skin rashes on her palms and soles, which appeared to be characteristic signs of secondary syphilis [Fig. and ].\nTaken all together, she was diagnosed as secondary syphilis. After 2 weeks of intravenous penicillin G treatment (4 million units of aqueous penicillin G, 6 times a day), her vision slightly improved to hand motion in the right eye and finger count 30 cm in the left eye. Ocular examination showed a resolution of vasculitis and macular edema in her both eyes.\nDue to the delayed diagnosis, despite the massive intravenous antibiotic treatment, visual recovery was poor. On the last follow-up of 4 months following treatment, her VA was hand motion in the right eye and 0.03 in the left eye. There was no sign of active inflammation, but visual recovery was poor due to optic atrophy [Fig. and ] and macular ischemic thinning [Fig. and ]. While the central retinal thickness was significantly decreased, the subfoveal choroidal thickness seemed to be unaffected when examined with an enhanced depth imaging optical coherence tomography (Spectralis HRA-OCT; Heidelberg Engineering, Heidelberg, Germany) [Fig. and ]. Scotopic electroretinogram showed extinguished wave in both eyes.[]

[[55.0, 'year']]

F

{'27461014': 1, '32163642': 1, '18574118': 1, '16935333': 1, '32676271': 2, '22863970': 1, '16282150': 1, '30923777': 1, '11734683': 1, '21059839': 1, '20606871': 2, '18751717': 1, '24145569': 2}

{'7332998-1': 1, '2886223-1': 1}

3959091-1

noncomm/PMC003xxxxxx/PMC3959091.xml

Dislocation of polyfocal full-optics accommodative intraocular lens after neodymium-doped yttrium aluminum garnet capsulotomy in vitrectomized eye

A 55-year-old male patient visited our clinic for the chief complaint of sudden-onset vision decrease after Nd: YAG capsulotomy in a local clinic. At the time of admission, the uncorrected visual acuity was 20/1000 and the intraocular pressure was 15 mm Hg.\nAt 22 months before the dislocation of the IOL, the patient underwent uneventful phacoemulsification with WIOL-CF® IOL implantation in the local clinic and 10 months after the cataract surgery, the patient was transferred to our clinic for the treatment of rhegmatogenous retinal detachment (RRD) with 3 disc diameter-sized horseshoe tear located at 12 o’clock. Patient underwent pars plana vitrectomy, endolaser photocoagulation and 14% C3F8 gas tamponade and recovered the vision up to 20/20 of the best corrected visual acuity (BCVA) with well-attached retina, 3 months after the RRD surgery.\nAt 9 months after RRD surgery, the BCVA decreased to 20/25 and in the slit lamp examination, the inferonasal continuous curvilinear capsulorhexis (CCC) margin was dragged superotemporally and anterior capsule was folded. However, the IOL was not subluxated and definite signs of damaged posterior capsule or zonules were not identified []. At 2 days later, the patient visited our clinic after Nd: YAG posterior capsulotomy in the local clinic and in fundus examination, the dislocated IOL was identified []. Slit lamp examination revealed the ovoid Nd: YAG capsulotomy site and the larger linear break, which is the suspected route of the IOL dislocation, in the posterior capsule [].

[[55.0, 'year']]

M

{'19365027': 1, '27921205': 1, '34040808': 1, '15599585': 1, '7837077': 1, '9051519': 1, '32511121': 1, '8603875': 1, '9818350': 1, '31238464': 2, '24145560': 2}

{'6611258-1': 1}

3959092-1

noncomm/PMC003xxxxxx/PMC3959092.xml

IIH with normal CSF pressures?

A 52-year-old woman presented with blurred vision and headache. She said her headache started abruptly a week previously and that this co-occurred with impaired color perception and blurred vision. When she visited our office, she still complained of blurred vision, especially in her left eye, but her vision was 20/20 and color vision was normal in both eyes. Both of her optic discs were swollen and Goldmann perimetry showed enlarged blind spots bilaterally [Figs. and ]. Lumbar puncture was performed and the opening pressure was checked at 130 mm H2O; the CSF composition was normal. Brain magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) neuroimaging results were also normal; and no empty sella, globe flattening, or venous narrowing was detected by brain imaging. She was on no medication regimen, and had no other significant past medical history. We recommended another lumbar puncture, but she refused; and thus, because of the definite bilateral disc swelling and headache, which are typical features of IIH, we prescribed acetazolamide 500 mg twice daily. A week later, she told us that her headache and blurred vision had subsided, and thus, we gradually tapered the dosage during follow-up. At last visit, 4 months after the onset of her symptoms, both optic discs were normal without any swelling or temporal pallor and she no longer complained of a headache or visual symptoms. The sizes of enlarged blind spots were prominently reduced on follow-up Goldmann perimetry [].

[[52.0, 'year']]

F

{'12649214': 1, '33715026': 1, '21696699': 1, '12455560': 1, '30692759': 1, '31875114': 1, '8956158': 1, '1859302': 1, '30820297': 2, '31875113': 1, '30488256': 1, '24145570': 2}

{'3959092-2': 2, '6388523-1': 1}

3959092-2

noncomm/PMC003xxxxxx/PMC3959092.xml

IIH with normal CSF pressures?

A 15-year-old girl presented with a headache, pulsatile tinnitus, and transient visual obscuration of 2 months duration. She had bilateral disc swelling with a blurred disc margin and Goldmann perimetry showed enlarged blind spots in both eyes [Figs. and ]. The lumbar CSF opening pressure was 200 mm H2O and CSF composition was normal. Brain MRI/MRV was also normal with no empty sella, globe flattening, or venous narrowing. A few days after the initial lumbar puncture, the puncture was repeated, and the rechecked CSF opening pressure was 205 mm H2O. Even though her ICP was still within the normal range, IIH was strongly suspected since she had several typical symptoms, and she told us her headache improved after the lumbar punctures. We prescribed acetazolamide 250 mg twice daily and made frequent follow-ups. Her symptoms improved after taking acetazolamide and Goldmann perimetry returned to normal []. Three months after her first visit, she had minimal swelling of both optic discs, but did not have headache or tinnitus. Currently (at 7 months after her initial visit), she is on acetazolamide 250 mg twice daily. We intend tapering the drug dosage when the disc swelling and symptoms resolve.

[[15.0, 'year']]

F

{'12649214': 1, '33715026': 1, '21696699': 1, '12455560': 1, '30692759': 1, '31875114': 1, '8956158': 1, '1859302': 1, '30820297': 2, '31875113': 1, '30488256': 1, '24145570': 2}

{'3959092-1': 2, '6388523-1': 1}

3959176-1

noncomm/PMC003xxxxxx/PMC3959176.xml

A Schizophrenia-Like Psychotic Disorder Secondary to an Arachnoid Cyst\nRemitted with Neurosurgical Treatment of the Cyst

The patient was a 37-year-old Caucasian man who was the second of three siblings. He was married, the father of two sons, and worked in his family's business. He came, as an outpatient, to our department because he was suffering psychopathological symptoms of psychotic characteristics.\nThe patient's family members reported that two months before the first consultation he started coming out with strange ideas: he thought that people he passed in the street somehow knew him and were following him in order to harm him or his family. He also expressed unusual beliefs, such as, that his digital television tuner stopped working in his presence and that radio commentaries of court cases were really subliminal messages directed at him. In association with these perceptions, he suffered an anxiety crisis with a sense of his imminent death and somatic symptoms (trembling, palpitations and feelings of suffocation); he was treated with Alprazolam 1.5mg/day. His state of mind worsened, and in the three weeks prior to the first consultation he suffered apathy, anhedonia and desperation. Two weeks before the first consultation, his family doctor prescribed him Alprazolam 0.5 mg/day, Alprazolam retard 1 mg/day, and Escitalopram 15 mg/day, but no improvement was reported.\nAlthough the above symptoms clearly began two months before the first consultation, the patient's wife reported that for the previous year the patient had been especially worried about some judicial proceedings in which he was implicated.\nWith regard to personal antecedents, the patient was diagnosed with serious depression with intention to self-harm when 14 years old. This depression remitted without medication within six months. Coinciding with the depression, there was an episode of involuntary movements of the left arm. The patient did not report any addictions or substance abuse. The patient had no history of head trauma or other medical or metabolic conditions.\nIn the first consultation, the patient was partially disoriented in time but oriented in space and person. He was confused, of labile attention, and with slowed speech. He gave answers unrelated to questions, was slow to answer even simple questions and suffered blocking in his thinking. He presented delusional interpretations and intuitions and a delusional paranoid reference of events to himself. He showed sadness, emotional lability, apathy, anhedonia, but did not express thoughts of death or self-harm. He reported anxiety and had somatic manifestations of this (paraesthesias, palpitations, trembling in the hands, and diaphoresis) and a sense of restlessness. We did not detect any alterations in sensory perception or in the experience of self-identity. The patient reported fragmented sleep with nightmares. His appetite was normal.\nWeight: 70 kg. Height: 180cm. Blood pressure: 100/60mmHg. Body mass index: 21.6kg/m2. Pulse rate: 70 bpm. Temperature: 36.7°C. Arterial oxygen saturation: 98%.\nLungs were well ventilated without noise. Heart beat was rhythmical, without murmur. Adbomen was soft and depressible, the lower part being slightly painful to palpation. There were no masses, enlarged organs, or evidence of peritoneal irritation. There was no costovertebral angle tenderness.\nThere was no motor or sensory deficit. There was no signs of a neurological focus. Osteotendinous reflexes were normal. Gait was normal.\nAfter psychiatric evaluation the patient was hospitalized. Brain Magnetic Resonance Imaging was undertaken and revealed a large arachnoid cyst in the right hemisphere (Fig. ). Study of the parietal calvarial region and brain stem showed relative thinning adjacent to the cyst, a finding suggestive of a congenital anomaly (Fig. ).\nOur neurosurgery department proposed surgical treatment of the cyst.\nSurgical fenestration (the making of small perforations) of the cyst was done by minimally invasive endoscopic surgery through right temporal trephine. This fenestration created a communication between the arachnoid cyst and cisterns located in the base of the skull allowing a wide circulation of cerebrospinal fluid. The tissular observation through intra-operative imaging confirmed the presence of normal arachnoid tissue and ruled out features of malignancy. There were no complications during surgery. To reduce possible cerebral edema after surgery, dexamethasone 4mg/day was prescribed for a week. Phenytoin 300mg/day was prescribed as a prophylactic against convulsive crises for a week also. The patient complained of headache during the first week after the surgery, which was controlled with a standard analgesic protocol (paracetamol and metamizole). One week after the surgery a brain computed axial tomography revealed a small left subdural hematoma without mass effect (Fig. ). The surgical wound healed without complications. Six months later another brain computed axial tomography showed no signs of the mentioned hematome. A magnetic resonance imaging 10 mounths after surgery ruled out recurrence of the cyst. There was a transitory worsening of the affective symptoms during the first week after surgery.\nFor four weeks prior to surgery the patient had received psychopharmacological treatment (escitalopram at a dose of up to 20mg/day, quetiapine at a dose of up to 300mg/day, clonazepam at a dose of up to 3mg/day, mirtazapine 15mg/day and lormetazepam 2mg/day). Despite this treatment, psychopathological symptoms (confusion, paranoid reference of events to self, delusional intepretations and fears that others intended harm, rumination on negative thoughts, sadness, emotional lability, apathy, anhedonia and social withdrawal) persisted. Improvement in this respect only occurred after surgery, when there was a 64% reduction in the Hamilton Anxiety Rating Scale Score [], a 60% reduction in the Hamilton Depression Rating Scale Score [] and a 55% reduction in PANSS General Psychopathology Scale Score [] (Fig. ).\nThe duration of hospitalization was six weeks.\nIn follow-up consultations, the patient showed global improvement with complete remission of delusional symptoms. He resumed his professional life and returned to normality in his family and social roles. Family members confirmed the improvement.\nThe provisional diagnosis was: Psychotic disorder with delusions due to known physiological condition (in this case, an arachnoid cyst) (ICD-10: F06.2 / DSM-IV:293.2). The diagnosis was confirmed by the patient's progression.

[[37.0, 'year']]

M

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{'1933420-1': 1, '5703589-1': 1, '5385751-1': 1, '8685962-1': 1, '8685962-2': 1}

3959291-1

noncomm/PMC003xxxxxx/PMC3959291.xml

Idiopathic cystic artery aneurysm complicated with hemobilia

A 35-year-old male patient presented with severe hematemesis and upper right quadrant abdominal pain. He had a history of recurrent vague abdominal pain and melena for the last 3 months and was treated symptomatically at a local hospital. He did not undergo any surgeries or diagnostic\nprocedures. He had a known history of hypertension, a family history of hypertension, and was under amlodipine. He had no history of smoking, alcohol consumption, or drug abuse. On admission, the patient was afebrile and non-icteric. His blood pressure was 110/60 mmHg, respiratory rate was 20/min, and pulse rate was 100 bpm. Physical examination revealed a well-nourished and oriented young man. The upper right quadrant appeared full and tender to palpation but without rebound tenderness. Rectal examination showed fresh blood. The remainder of the physical examination was normal. Laboratory investigation revealed an elevated white blood cell count of 20×103/μL, hemoglobin of 8.5 g/dL and platelet count of 22 7×103/μL. Blood chemistry showed SGOT:149 U/L (0-37), SGPT:203U/L (0-40), Bilirubin total/conjugated:1.27/0.52 (units?), GGT:872 U/L, total protein/albumin:5.70/3.10 g/dL. Upper GI endoscopy revealed blood was likely to be coming out from pylorus. CT scan revealed markedly distended gallbladder lumen filled with high Hounsfield Unit (H.U.) (60-70) content suggestive of blood along with a 20 mm x 16 mm in size, well-defined, intensely enhanced lesion arising from the wall of the body of the gallbladder and very likely representing vascular pathology []. MR angiography revealed a 21×17 mm sized aneurysm arising from the terminal end of the cystic artery with a secondary bleeding within gallbladder lumen [,].\nThe patient was referred for surgery due to radiological findings of associated cholecystitis. He underwent open cholecystectomy and aneurysm repair. Intraoperatively the gallbladder was hugely distended and there was dense adhesion surrounding the gallbladder and the Callot’s triangle anatomy was distorted. Gallbladder was opened on fundus and blood clots were drained []. There was active spurt from the body of the gallbladder following removal of clot-like material which was controlled using 4’0 synthetic, monofilament, nonabsorbable polypropylene suture. Cholecystectomy was then performed following dissection of Callot’s triangle and individually ligating the cystic artery and duct. The condition of the patient remained clinically stable and subsequent follow-up showed normal hemoglobin levels. Histopathological examination revealed chronic cholecystitits. The patient was discharged after 7 days with a plan for outpatient follow-up.

[[35.0, 'year']]

M

{'1898577': 1, '10520869': 1, '11412246': 1, '31489197': 2, '32027010': 2, '28660824': 1, '28641193': 1, '29459583': 1, '15041503': 1, '15236123': 1, '9732939': 1, '12658412': 1, '9464443': 1, '3823426': 1, '34869829': 2, '8887048': 1, '32874789': 2, '24714720': 2}

{'6710687-1': 1, '6966396-1': 1, '7455374-1': 1, '8635945-1': 1}

3959296-1

noncomm/PMC003xxxxxx/PMC3959296.xml

Development of non-Hodgkin’s lymphoma in a patient with primary biliary cirrhosis: A case report and review of the literature

A 75-year-old woman, was admitted with a 4-week-duration abdominal pain reflecting to the lumbar area bilaterally. She also mentioned malaise and loss of 5 Kg of weight. She had a past medical history of PBC diagnosed ten years previously, positive for antimitochondrial antibodies, histologically stage 3 at diagnosis. Portal hypertension (gastro-esophageal varices) was identified 2 years before current admission. She has been on ursodeoxycholic acid (VDCA) since PBC diagnosis. Pulmonary fibrosis was also documented 1 year previously. Physical examination on admission revealed hepatosplenomegaly and generalized lymphadenopathy (submandibular, right axillary and left inguinal-femoral nodes). Laboratory tests showed: hemoglobin 9.9 g/dL; white blood cells, 4,000 per mm3 (neutrophils 67%, lymphocytes 21%, monocytes 12%); platelets 200,000 per mm3 erythrocyte sedimentation rate 52mm/h; negative direct antiglobulin test; IgG, 1730g/dL (700-1600); IgM and IgA within normal limits; polyclonal gammopathy and ^-microglobulin 8.18mg/L. Antibodies for hepatitis virus B and C were negative. A lymph node biopsy revealed infiltration by large lymphocytes. Immunochemistry results were positive for CD45, CD20, PAX-5, CD79a and negative for Bcl2, Bcl6, MUM1, CD138, CD30, CD15, CD3, CD4, CD8 and ALK1. Bone marrow aspiration and biopsy showed infiltration by the same B cell population. Interestingly, the number of cell proliferation, Ki-67+, was increased to 60%. Imaging studies demonstrated enlarged mediastinal and, paraortic lymph nodes inducing ureter obstruction bilaterally, enlarged hilar nodes without focal lesions of the liver, left iliac and inguinal nodes. There was no evidence of ascitic fluid. A diagnosis of DLBCL, stage IV, was established and International Prognostic Index score (IPI) was calculated to 4 points. The patient received treatment with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Clinical, laboratory and imaging improvement was ensued. The patient died from pneumonia five months after the diagnosis of lymphoma, following five cycles of chemotherapy.

[[75.0, 'year']]

F

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{'2722057-1': 1}

3959297-1

noncomm/PMC003xxxxxx/PMC3959297.xml

Caroli’s disease: Description of a case with a benign clinical course

A 12-year-old boy was admitted to the Pediatrics Department of our Hospital, because of high fever (40.5°C) with shivers and moderate pain in the right upper quadrant of the abdomen, for the previous two days. The pain increased during the rise in fever. Before his admission a course of antibiotics (amoxicilline-clavulanic acid) had preceded without any response. On physical examination the liver and spleen were just palpable, liver (+1 cm) and spleen (+1cm) under costal margins. Interestingly a slight tenderness in the right hypochondrium was found only as the fever rose. No jaundice, ascites, splenomegaly or venous dilatation of abdominal wall were observed. The physical examination of the other systems was normal. Blood pressure was repeatedly between 100-110 / 60-70 mmHg.\nA month before this episode, he had been hospitalized again because of an episode with similar clinical picture (fever for 8 days: 38-40.5°C, with shivers, muscle aches and diffuse abdominal pain) and he was treated for suspected bacteremia for 10 days. The laboratory findings on these two admissions appear on and it is noteworthy that during the second admission the laboratory findings of bacterial infection were more obvious (although with negative cultures) in addition to a slight elevation of transaminases. His medical history was extremely interesting in that he had had two consecutive hospitalizations at the age of 2.5 years, because of suspected bacteremia. At that time he presented again with elevated WBC, CRP, ESR, negative cultures, normal immune profile and normal liver function tests, so an ultrasound (U/S) of the abdomen was not considered necessary. In the intermediate period (the last 10 years) he was asymptomatic with normal growth (weight and height: between 50th to 75th percentile, according to our national charts) and without any other chronic illness.\nDuring the last hospitalization (4th episode), because of the localization of moderate pain in the right upper quadrant of abdomen during the rise in fever, an U/S of the abdomen was performed and revealed two small cystic formations in the superior part of right upper lobe of the liver.\nAccording to the clinical picture and to the above U/S findings, more extensive radiological investigation was performed. CT scan of abdomen revealed several small cystic formations in the VII segment of the liver. MRI of the liver showed several well-defined round lesions (maximum diameter 2 cm), hyperintense on T2 and hypointense on T1 -weighted images. There was no contrast enhancement after intravenous contrast (Gadolinium DTPA) injection, therefore these findings were thought to be cysts [, ].\nIn addition, there were no specific findings from other organs (kidneys, pancreas, spleen etc) or signs of portal hypertention.\nA subsequent MRCP revealed communication of the cystic formations with the biliary tree [], compatible with Caroli’s disease.\nThe child was treated for cholangitis. He was afeverish on the 4th day of treatment. The abdominal pain subsided later (on 9th day).\nHe was discharged in generally good condition with the advice of frequent follow-up studies, including liver function tests (AST, ALT, γGT, CEA, CA19-9, aFP etc.) and U/S of the liver.\nSince, he has been followed-up systematically for ten years and remains asymptomatic, with normal blood pressure, normal growth, normal laboratory findings and unchanged imaging (U/S and MRI) parameters, in follow-up studies.

[[12.0, 'year']]

M

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{'7021243-1': 1}

3959301-1

noncomm/PMC003xxxxxx/PMC3959301.xml

A ruptured infected mesenteric cyst diagnosed on laparoscopy for suspected appendicitis

A 25-year-old woman presented to the acute surgical team with a 24-hour history of sudden onset generalized abdominal pain, worsening in severity. She had an associated fever, malaise and anorexia. She did not complain of any urinary symptoms, dyspareunia or vaginal discharge. At the time of presentation, she was approximately midway through a regular menstrual cycle. She was otherwise fit and well with no previous medical history and on no regular medications. She did admit to a diarrheal illness one month previously during which an out-patient stool culture had grown Campylobacter jejuni.\nOn examination, she was noted to be tachycardic with a heart rate of 110 beats per minute and fever at 38.0°C. She was tender throughout the lower abdomen, mostly in the suprapubic area with guarding. Urinalysis was negative for blood, nitrites and leukocytes and a urinary pregnancy test was negative. Her blood investigations revealed a raised white cell count of 19.1 (normal range 4 – 11 109/L) and a C-reactive protein of 3 (normal range 0 – 10 mg/L). An ultrasound examination was not performed. She was discussed with the gynecology team who agreed with our management plan to perform a diagnostic laparoscopy and was available to attend theater if required.\nDiagnostic laparoscopy was performed via a 10 mm infraumbilical camera port and a 5 mm left iliac fossa instrument port. A small collection of pus was noted in the pelvis although the uterus, ovaries and appendix were macroscopically normal. The pus subsequently showed pus cells on microscopy but no organisms were cultured. On inspection of the small bowel, primarily in search of a Meckel’s diverticulum, a 160 mm length of cystic and nodular change involving the mid-ileum and neighboring mesentery was found. The rest of the small bowel was normal. One cystic lesion on the posterior aspect of the mesentery had ruptured with evidence of surrounding induration []. The left iliac fossa stab incision was lengthened to 40mm, creating a mini-laparotomy incision to enable resection of the effected length of small bowel and a hand-sewn end-to-end bowel anastomosis was performed. The resected bowel was opened along its antimesenteric border and cystic disease affecting both the mesentery and bowel wall was confirmed []. Her post-operative course was uneventful and she was discharged home 5 days after surgery.\nHistology identified these changes as localized intestinal and mesenteric lymphatic cyst disease. Dilated lymphatic channels were noted to extend throughout the full thickness of bowel wall and into the mesentery [].

[[25.0, 'year']]

F

{'11319324': 1, '15334326': 1, '11053936': 1, '19609826': 1, '9314483': 1, '16033626': 1, '14976800': 1, '26064760': 2, '15278036': 1, '15168049': 1, '18604575': 1, '24713757': 2}

{'4438157-1': 1, '4438157-2': 1}

3959323-1

noncomm/PMC003xxxxxx/PMC3959323.xml

Chronic abdominal pain secondary to mesh erosion into cecum following incisional hernia repair: a case report and literature review

The patient is a 56-year-old female with a past medical history of hypertension, morbid obesity, and uterine fibroids. She had a history of abdominal surgery with two cesarean sections, total abdominal hysterectomy, and bilateral salpingooophorectomy. Five months after her last surgery in 1996, the patient was re-admitted with a large incisional hernia. She had open hernia repair with inlay polypropylene mesh under general anesthesia. Her post-operative course was uncomplicated. In general, polypropylene is cheap, available readily and is usually first choice for most hernias. It causes intense scarring, which is what is desired for repair of hernias.\nApproximately 14 years (June 2010) after hernia repair, the patient presented to the Emergency Department complaining of intermittent abdominal pain rated 6/10 starting at right lower quadrant and migrating upwards and diffusely over the entire abdomen, associated with 2-3 episodes of nausea/ week. She had felt this pain on and off for the past 2 years but came to the Emergency Department because she felt it was worsening. She denied any other complaints. She was passing gas and having bowel movements. All lab work was normal. Computed tomography (CT) scan of abdomen and pelvis was unremarkable. Physical exam showed moderate tenderness at right lower quadrant but was otherwise benign. Prior screening colonoscopy showed diverticulosis but was otherwise unremarkable. Repeat colonoscopy was performed on this admission which showed mesh in the cecum. In light of the patient’s past history of incisional hernia repair with polypropylene mesh, this finding was consistent with partial migration of the previous surgical mesh into the cecum and mesh was intact. The mesh appeared to have eroded into the lumen, but there was no enterocutaneous fistula or any other enteric fistula. This would have been evident by clinical exam and CT scan. The patient had no external leakage of stool or gas to suggest an enterocutaneous fistula, and she did not have peritoneal signs to suggest an enteric leak into the abdomen ().\nMesh migration often results in significant bleeding or a fistula and requires operation. However, based on the patient’s minimal symptoms, morbid obesity, and probability of significant surgical morbidity (postoperative wound infection, recurrent hernia, fistula, etc.), we elected to observe. The patient was discharged with instructions to return in case of significant bleeding or increased, disabling pain. Surgery would be a better choice but the operation would be complicated; she was morbidly obese and had had multiple hernia repairs in the past. Her mesh migration was in the right lower quadrant, a difficult area to repair hernias because mesh fixation around the iliac bone is difficult. After initial presentation, she was advised to be followed up as she was minimally symptomatic from it and had no bleeding. The operation would have involved removing the mesh, removing the cecum, re-anastamosing the bowel and then repairing the hernia with a biologic mesh, so that the mesh would not get infected. A two-stage operation might have to be done since bowel resection would have contaminated the field.

[[56.0, 'year']]

F

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{'6214886-1': 1, '6637341-1': 1, '7602325-1': 1, '6545489-1': 1, '6545489-2': 1, '8449232-1': 1}

3959327-1

noncomm/PMC003xxxxxx/PMC3959327.xml

Complicated hepatic hydatid cyst with simultaneous biliary tree and intraperitoneal rupture: can we treat it in a minimally invasive way?

An 87-year-old woman, with senile dementia, diabetes mellitus, hypertensive diastolic heart failure and chronic renal disease presented at the Accident and Emergency Department with jaundice (total bilirubin 15.8 mg/dL, direct 12.4 mg/dL), significant bile duct dilatation at ECHO examination and obstructing cholangitis. Since 1987, when she has had an open cholecystectomy for symptomatic cholecystolithiasis, she was known to have three calcified asymptomatic hydatid cysts. One cyst was located at the spleen and another at the left liver lobe, both heavily calcified. The third one, that was barely calcified radiologically, was at the periphery of the right liver lobe, about 45-50mm in diameter. An ERCP performed the next day visualized at least five round bile duct contents (), which proved to be, after sphincterotomy and debriment of the bile duct, hydatid cyst remnants. A 10F plastic stent was inserted and broad spectrum antibiotics were initiated. Bilirubin level dropped to a total of 5.31 mg/dL (direct 4.95 mg/dL) on day 3 of admission.\nOn the third day of hospitalization, the patient developed dyspnea, tachypnea and clinical signs of right pleural effusion and ascitic fluid. An emergency CT scan of the thorax and abdomen was performed that revealed a large right pleural effusion with atelectasis (which proved to be reactive after laboratory analysis), a small left effusion and a large diffuse peritoneal effusion around the liver and down to the pelvis. Air was present inside the right hepatic lobe hydatid cyst, consistent with a biliary tree communication and the antecedent sphincterotomy (). The CT scan suggested a simultaneous free intraperitoneal cyst rupture. Due to the concomitant biliary tree communication, not only hydatid cysts and remnants, but also bile leak, was probably the cause of patient’s large effusions.\nAfter thorough discussion with the patient’s family and considering her poor general status and possible technical difficulties, a minimal invasive approach was selected. After a second ERCP that removed the plastic stent and another debridement that confirmed an efficient sphincterotomy and a clear duct, a subdiaphragmatic drainage was placed radiologically. Albendazole at a dose of 15 mg/kg/day was initiated.\nPeritoneal fluid drainage gradually fell from 300 cc to about 50 cc/day over a two-week period. X-ray chest film showed a complete resolution of the pleural effusions () and CT scan revealed the absence of ascites (). After 3 months of albendazole, the drainage tube was extracted and patient remained both clinically and radiologically improved at the first monthly scheduled follow-up.

[[87.0, 'year']]

F

{'12122725': 1, '11577320': 1, '16878513': 1, '11213153': 1, '19350321': 1, '24714038': 1, '24713778': 2}

{}

3959328-1

noncomm/PMC003xxxxxx/PMC3959328.xml

An unusual infection on an unusual gastroenteritis

A 35-year-old lady was admitted due to fever (39°C), abdominal pain, diarrhea and a non-productive cough for 3 days. She reported a history of asthma, atopic dermatitis, nephrolithiasis and smoking (30 pack/year). Her abdominal problems started 1 year ago when she underwent multiple urgent or semi-elective operations: appendectomy with subsequent gallbladder removal, followed by diagnostic laparotomy (6 months ago) with biopsies from a thickened jejunum to identify evidence of eosinophilic enteritis (muscular and serosal layers). She received treatment with steroids that was discontinued 2 months prior to admission.\nOn admission she presented with tachypnea, tachycardia, fever, and fine crackles in the right upper pulmonary field. Abdominal examination identified diffuse rebound tenderness and ascites. Chest-radiograph showed a consolidation in the right upper pulmonary field (), air blood gases (ABGs) revealed hypocapnea, and blood tests showed leukocytosis (without eosinophilia), high CRP and D-dimers, low albumin and marginally low sodium (). She received oxygen (28%), i.v. clarithromycin and cefuroxime, fluids, ranitidine, analgesics, and low-molecular-weight heparin subcutaneously.\nBecause of the severe clinical picture, impaired ABGs and the lung infiltrate, she underwent a ventilation/perfusion scan indicating a low probability for PE. On day 2 she had an unenhanced (due to strong history of allergy and no time for desensitization) spiral abdominal CT (), which showed a large amount of free fluid collection and thickening of several small bowel loops, without evidence of perforation. She did not consent to abdominal paracentesis. Viral and microbiology serological tests, as well as blood, urine and stool cultures were screened. Sputum induction gave suboptimal material for cultures.\nThe patient gradually improved. An upper GI endoscopy was unremarkable and biopsies showed mild gastritis. As diarrhea gradually improved and ceased, and given that the patient had twice had a lower GI endoscopy over the previous months, with unremarkable findings, a third colonoscopy was postponed. PPD was negative. She underwent a spiral chest-CT negative for PE, while the lung lesion resolved. Her immunological tests showed very high IgE, with IgA, IgM, IgG, RF, ANA, ANCA within normal values. Hepatotropic viruses, adenovirus, CMV, HIV, EBV, Coxiella burnetii, Yersinia enterocolitica, and Entamoeba histolytica were negative. Stool for parasites and stool-urine-blood cultures were also negative. On admission the patient had a titer for Legionella sp. IgG 1/64 in serum which, when repeated at week 4 from the onset of illness, diagnostically rose to titer 1/128. Urinary test for Legionella was not performed and PCR for Legionella was unavailable from our lab at that time. The final diagnosis for this patient was Legionella pneumophila pneumonia – eosinophilic gastroenteritis.\nAbbreviations: CT, computed tomography; CMV, cytomegalovirus; HIV, Human Immunodeficiency Virus; EBV, Epstein Barr Virus\nShe completed 14 days of antibiotic treatment and had for her EG prednisolone 40 mg slowly tapered, ranitidine 300 mg, ketotifen, and calcium and vitamin-D supplementation. The patient had a straightforward recovery, and she subsequently underwent an MRI-enteroclysis to further study the affected small bowel (). Three years after the episode she remains asymptomatic without relapses.

[[35.0, 'year']]

F

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{}

3959345-1

noncomm/PMC003xxxxxx/PMC3959345.xml

Antibody-mediated rejection after adult living-donor liver transplantation triggered by positive lymphocyte cross-match combination

A 46-year-old female was admitted suffering from well-developed liver cirrhosis. Hepatitis C virus infection was diagnosed at 39 years of age and she had been treated at another hospital for the last seven years. Although the number of different medications used to treat the condition (furosemide, spironolactone, ursodeoxycholic acid, lactulose, and branched-chain amino acids) and their dosages had slowly increased over the last year, her condition was not well-controlled. She had frequent episodes of esophageal variceal rupture over the last year and had suffered from intractable ascites and a right pleural effusion. Because of her deteriorating condition, she was referred to our division for LDLT. On admission, she had a low-grade fever and cell counts in the ascites and pleural effusion were 2270 /mm3 and 2580 /mm3, respectively. We diagnosed spontaneous bacterial peritonitis and pleuritis which were managed pre-operatively by drainage, hydration and cefotaxime i.v. The low-grade fever disappeared after treatment. Her status according to the United Network for Organ Sharing was IIB. Her scores for Child-Pugh and the model for end-stage liver disease were 14 and 25, respectively.\nPre-transplant lymphocyte cross-match tests were performed using direct complement-dependent cytotoxicity (CDC) and anti-human globulin assays (anti-human immunoglobulin lymphocytotoxicity test, AHG-LCT) [,]. The results of these tests were positive. Moreover, the patient showed strong reactions against donor HLA Class I antigens (). Also, flow cytometry (FCM) showed that the lymphocytes of the recipient were reactive against HLA Class I antigens (). The HLA typing of both the recipient and the donor is shown (). We also performed additional tests to assess the patient’s immunoreactivity to specific HLA Class I antigens. The lymphocytes of the recipient showed strong immunoreactivity against HLA Class I loci including HLA B 55. Tests showed that the donor had this HLA B locus (), which meant that the patient could potentially mount a donor-specific anti-HLA antibody response after transplantation.\nAlthough the results of the cross-matching tests were positive for this particular donor and recipient, the ABO blood group was compatible and the patient had no history of receiving blood transfusions from the donor. As we were unable to find a more suitable donor, the ethics committee of our institution granted approval for the procedure and written informed consent was obtained from both the recipient and the donor. During surgery we found that the patient had splenomegaly and developed collateral vessels (umbilical vein and coronary vein) and so we performed a splenectomy and ligation of collateral vessels to obtain improved intra-operative control of portal venous pressure. We reported that portal venous pressure <15 mmHg is a key for successful LDLT [,], and the final pressure was 13 mmHg in this case. The surgery lasted 822 minutes and intra-operative blood loss was 7700 mL. The graft was a left-lobe graft and the graft weight was 450 g. The graft:recipient weight ratio was 0.91. The patient received 24 units of red cells, 16 units of plasma and 30 units of platelets during the procedure. We used tacrolimus, methylprednisolone and mycophenolate mofetil as immunosuppressants and the trough level of tacrolimus was kept at 8–10 ng/mL during the early post-operative period. Methylprednisolone was given intravenously (1 mg/kg) once daily from post-operative Day (POD) 1 to POD 3 followed by 0.5 mg/kg once daily for the next 3 days. The dosage of mycophenolate mofetil was 10 mg/kg/d from POD 1.\nPost-operative splanchnic in-flow and out-flow were excellent as assessed by Doppler ultrasound studies. The post-operative course was uneventful until POD 3 when the patient experienced a sudden elevation of serum lactate dehydrogenase (LDH) levels, a decrease in the platelet count and severe fragmentation of red blood cells. Serum total bilirubin (T-Bil) levels were increased after POD 3 leading to a prolonged case of jaundice. On POD 4 a chest X-ray was taken and showed an acute respiratory distress syndrome-like condition. Blood gas analysis revealed significant respiratory insufficiency. The patient’s respiratory function worsened to a point where she required mechanical ventilation. Plasma exchange (PE) (80 mL/kg/d) was performed daily after POD 4 () and she received steroid pulse therapy (methylprednisolone at 10 mg/kg, i.v.) from POD 5. The gated area represented immunoreactivity against Class I antigens, and the percentages were calculated as the counts in the gated area/the whole counts. The percentages at pre-LDLT, PODs 2, 5, 6, 8 and 9 were 71.7, 1.7, 1.9, 11.2, 7.3 and 25.8 %, respectively. Although immunoreactivity against HLA Class I antigen was down-regulated during the early period after LDLT it increased again from POD 6. Note that this immunoreactivity was down-regulated on POD 5 even though graft dysfunction began on POD 3 and that this immunoreactivity remained from POD 6 even after repeated PE. On POD 8, peripheral blood examination showed evidence of hemolysis and that haptoglobin levels had fallen (<5.0 mg/dL). Percutaneous microecchymosis was noted and coagulation profiles were consistent with disseminated intravascular coagulation (DIC). The patient’s condition worsened and she did not respond to further treatment, including daily PE. On POD 9 we performed a liver needle biopsy under US guidance. Histopathological examination clearly showed severe graft damage (). We diagnosed HR mediated by an antigen-specific immune response to the donor tissue based on the clinical, immunological and histopathological findings. The patient experienced multi-organ failure accompanied by DIC and died at POD 9 despite intensive treatment.

[[46.0, 'year']]

F

{'15084176': 1, '16741901': 1, '11374419': 1, '12614293': 1, '16146554': 1, '17220802': 1, '21336085': 1, '12962837': 1, '10083233': 1, '19191764': 1, '19077886': 1, '9233701': 1, '3047927': 1, '8475557': 1, '8438192': 1, '11699030': 1, '17431411': 1, '7940711': 1, '19708453': 1, '12200775': 1, '14526401': 1, '17496547': 1, '15787786': 1, '18945283': 1, '14752842': 1, '16313323': 1, '18581485': 1, '4174539': 1, '4162350': 1, '18162984': 1, '21185796': 1, '19005402': 1, '9724473': 1, '17929298': 1, '20517905': 1, '17318084': 1, '8514248': 1, '24714061': 2}

{}

3959351-1

noncomm/PMC003xxxxxx/PMC3959351.xml

A giant type IVA choledochal cyst

A 25-year-old female was referred to our GI Surgery Unit for unexplained fever, jaundice, and right upper quadrant abdominal pain for the last 10 days. There was a past history of similar episodes over the last year. At presentation, she had jaundice, fever and large soft cystic swelling occupying the entire upper abdomen. Laboratory investigations revealed total bilirubin 8 mg/dL, alkaline phosphatase 1230 U/L, ALT 200 U/L and AST 93 U/L. The ultrasonographic examination demonstrated a huge thick walled cystic lesion with internal echogenic particles and septations that extended from the subhepatic area to the left hypochondrium, separate from liver. There were cystic dilatations of intrahepatic ducts. An MRCP examination disclosed a huge cystic dilatation of the common bile duct measuring 12 cm in diameter (). Another separate, large-septated cystic lesion with homogenous fluid signal intensity, measuring 12 cm×10 cm×9 cm (), was seen at porta hepatis contiguous with an extrahepatic segment of left hepatic duct extending to the left hypochondrium. With these findings, the provisional diagnosis of a huge type, IVA choledochal cyst with enormous tortuous dilatation of the extrahepatic segment of the left hepatic duct was considered.\nPercutaneous transhepatic biliary drainage was done as the patient went into toxic cholangitis and she was not fit for endoscopic retrograde cholangiopancreaticography (ERCP). Subsequently, cholangitis subsided and she was taken up for the surgery after optimization of the coagulation and nutritional status. Intraoperative findings were a large thick walled folded cyst measuring approximately 15 cm arising from the extrahepatic segment of left hepatic duct in continuation with a huge dilatation of CBD confirming the finding of MRCP.\nThe extrahepatic component of the cyst was excised and biliary-enteric flow was re-established through a wide mucosa to mucosa Roux-en-Y hepaticojejunostomy at the level of the hilum. At 10 months of follow up, the patient was doing well.

[[25.0, 'year']]

F

{'5401505': 1, '341380': 1, '889044': 1, '31632886': 2, '6776832': 1, '7979612': 1, '15549778': 1, '12611583': 1, '13625059': 1, '9358787': 1, '7899614': 1, '10436795': 1, '18332966': 1, '27011558': 1, '19196083': 1, '24714178': 2}

{'6797019-1': 1}

3959352-1

noncomm/PMC003xxxxxx/PMC3959352.xml

Acute gastrointestinal bleeding from a submucosal gastric mass

A 44-year-old male with a history of hypertension, chronic kidney disease and reflux disease, presented with upper gastrointestinal bleeding and hemodynamic instability. A month prior to admission he underwent GDS and colonoscopy because of melena. No bleeding source was found, but GDS did reveal a submucosal mass in the lesser curvature of the stomach with central erosion suggestive for ectopic pancreas therefore no biopsies or endoscopic ultrasound (EUS) were performed. shows the submucosal mass in the lesser curvature of the stomach with central erosion (black arrow).\nAt the time of admission the patient complained about melena and syncope. Physical examination revealed hypotension and tachycardia, but was otherwise unremarkable. Laboratory tests revealed low hemoglobin 5.1 mg/dL. Subsequent GDS revealed a submucosal protruding mass in the lesser curvature of the stomach with an eroded surface and bleeding stigmata, which is shown in (black arrow). This was treated with epinephrine injection and hemoclips. Computed tomography (CT) showed a mass in the stomach with a diameter of 3 × 7 cm without lymphadenopathy or signs of distant metastases. The patient was admitted to the ICU and continuous intravenous proton pump inhibitor was started. However, fluid resuscitation and blood transfusion remained necessary. Therefore, two days after admission, the patient underwent a partial gastrectomy. shows the wedge resection of the gastric mass with central hemorrhage (black arrow).\nThe submucosal mass with central erosion seen with endoscopy and CT scan was characteristic for a GIST. Histopathologic examination confirmed the diagnosis, describing an epithelioid type GIST with focal necrosis and hemorrhage with clear resection margins. Immunohistochemical examination demonstrated partial positive CD117 and CD34. shows the brown coloration of the CD117 positive tumor cells. Twelve days after admission the patient was discharged. GDS, two months after partial gastrectomy, showed no signs of recurrent disease. Seven months later the patient remains recurrence free.

[[44.0, 'year']]

M

{'15648083': 1, '16136600': 1, '18023108': 1, '20661913': 1, '19454466': 1, '24714393': 1, '16550259': 1, '10202065': 1, '8571202': 1, '24713788': 2}

{}

3959364-1

noncomm/PMC003xxxxxx/PMC3959364.xml

Obscure gastrointestinal bleeding persisting for a decade: a rare manifestation of a common disease

A 60-year-old lady was referred to us for melena of 12 years duration. She had earlier undergone repeat evaluations at multiple private hospitals. She was initially diagnosed with duodenal ulcer and underwent exploratory laparotomy with pyloroplasty and truncal vagotomy. However, she rebled and thereafter underwent antrectomy with retrocolic gastrojejunostomy. She also received proton pump inhibitors, and eradication therapy for Helicobacter pylori. Despite the aggressive treatment, the patient continued to have melena episodes and required multiple blood transfusions (~170 transfusions over a decade). Her esophagogastroduodenoscopy, colonoscopy and barium meal follow through did not reveal any abnormality. Contrast enhanced computed tomography (CECT) of abdomen and the technetium-99m red blood cell scan were also non-contributory. A capsule endoscopy was performed by placing capsule in efferent limb under endoscopic guidance (). It revealed multiple ulcers of varying sizes throughout the small bowel (). As there was no history of non steroidal anti inflammatory drugs (NSAID) ingestion, a possibility of chronic non-specific small bowel ulcers was kept. Antinuclear antibodies and anti-neutrophil cytoplasmic antibodies were negative. However, IgA anti-tissue transglutaminase and anti-gliadin antibodies were positive. Antegrade double balloon enteroscopy was performed and biopsies were obtained from ulcer edge as well as mucosal folds. Histological examination of the biopsies from the ulcer edge revealed chronic inflammation and from the mucosal folds revealed increased intraepithelial lymphocytes. She was started on prednisolone 40 mg daily along with gluten-free diet. The melena subsided and thereafter steroids were tapered off. She remains well after one-year follow up, there has been no recurrence of bleeding and her hemoglobin has risen to 13.4 mg/dL.

[[60.0, 'year']]

F

{'8602182': 1, '11079196': 1, '7409396': 1, '17960014': 1, '18596537': 1, '14695710': 1, '20682594': 1, '20066591': 1, '15990820': 1, '16616349': 1, '24874805': 1, '12692066': 1, '9412920': 1, '16733138': 1, '1083465': 1, '24714068': 2}

{}

3959365-1

noncomm/PMC003xxxxxx/PMC3959365.xml

Intramural hematoma of the ascending colon leading to intraperitoneal hemorrhage: a possible post-polypectomy complication

A 61-year-old male was admitted to our hospital due to lymphadenopathy of unknown origin. He was an obese, ex-smoker, receiving acenocoumarol due to aortic valve replacement and coronary artery bypass graft surgery. A colonoscopy with ileal intubation was conducted as part of a thorough work-up. Acenocoumarol was discontinued 5 days before the endoscopic procedure and was substituted by low molecular weight heparin (LMWH). Last LMWH injection was administered the day before endoscopy and was reinstituted the day after []. His laboratory tests on the day of colonoscopy were: hemoglobin 9.48 g/dL (11-14), platelet count 150 K/μL (150-400) and INR 1.3 (0.9-1.2). Three polyps (d=0.4-0.8 cm) were detected and removed: a sessile in the proximal ascending colon using hot snare and two in the sigmoid (a sessile and a pedunculated) using cold snare technique. The diathermy used for hot snare polypectomy (ERBE ICC 200, Tübingen, Germany) was set in endo-cut mode at 120 Watt. The patient was discharged 2 days later without any signs of short-term complications, with instructions for continuing LMWH injections. Two days later he presented with rectal bleeding. A new colonoscopy revealed a red clot on every polypectomy site with oozing bleeding at the ascending colon. Adrenaline solution was injected initially, then clots were removed with a snare and metallic clips (Resolution Clip, Boston Scientific Corporation, Natick, MA) were placed in all three polypectomy sites with resolution of hemorrhage. The patient was discharged 2 days later with instructions for initiating LMWH injections the day after. Ten days later, he presented with lower abdominal pain, three vomiting episodes and gas and stool retention over the last 24 h. Physical examination revealed an acutely ill, afebrile patient with a palpable mass on his right lower abdominal quadrant and a suggestion of ileus in the plain radiograph. A nasogastric tube was placed and intravenous antibiotic therapy (cefoxitin, metronidazole) and decongestive enemas were introduced. On the following day, his condition deteriorated with an exacerbation of the abdominal pain and a sharp decrease in hemoglobin (11.3 to 9.1 g/dL). He underwent an abdominal CT scan, which provided a suspicion for intussusception of the cecum into the ascending colon () and a new colonoscopy was conducted. Clips remained intact but in the ascending colon a protruding violet-reddish mass with edematous rims was seen next to the polypectomy site (). The patient was urgently operated, where extensive intra-abdominal hemorrhage was the initial finding. The bleeding source was a wide rupture of both the serosal and muscular layers of the proximal ascending colon. A right hemicolectomy was performed. The patient died, while in the Intensive Care Unit, 4 days later due to recurrent cardiac arrest episodes. Pathology report confirmed the existence of an intramural hematoma in the proximal ascending colon with hemorrhagic infiltration of all layers and no signs of intussusception, vasculitis or other noteworthy coexistent lesions ().

[[61.0, 'year']]

M

{'19177292': 1, '20889070': 1, '31620527': 2, '31181384': 1, '22079510': 1, '29118689': 2, '12024126': 1, '21126738': 1, '16246699': 1, '12556798': 1, '24714100': 2}

{'6722354-1': 1, '5662997-1': 1}

3959372-1

noncomm/PMC003xxxxxx/PMC3959372.xml

Jodhpur disease revisited: a rare cause of severe protein energy malnutrition

A 3.5-year-old unimmunized developmentally normal female child presented with vomiting for 6 months, intermittent fever for 5 months, abdominal distention for 4 months and painful abdomen for 1 month. Vomiting was non bilious, non projectile, 4-5 episodes/day, occurring 1-2 h after meal and contained food particles. Fever was on and off, low-grade, not associated with chills and rigor. Pain was localized to upper abdomen, non colicky, aggravated by food intake, relieved by vomiting or medications. The child had significant weight loss (>5 kg) during the past 4 months and had received one unit packed red cell transfusion at some other center. There was no history of loose stools at any point of time, constipation, jaundice, bleeding from any site or contact with a tuberculosis patient. On examination, she was malnourished with her weight only 6.5 kg and height 84 cm, both below the 3rd percentile of WHO standards. She was pale and dehydrated, with sparse and lusterless hair. Abdomen was soft and distended, with tympanic note on percussion, normal bowel sounds and without organomegaly. The rest of the systemic examination did not show any abnormality.\nOn investigation, her hemogram and chest X-ray were normal, but serum electrolytes were abnormal (hyponatremia with hypokalemia). HIV serology, PPD test and gastric aspirates (n=3) for tuberculosis were negative. Stool examination was negative for ova, cysts or opportunistic pathogens. X-ray abdomen showed no air-fluid level but only gaseous distention of stomach and intestine. Ultrasound of abdomen showed distended stomach with normal pyloric canal. Barium meal showed grossly distended stomach with slow passage of barium from the antero-pyloric region distally (). Suspecting gastric outlet obstruction, exploratory laparotomy was done that revealed hugely distended stomach with normal smooth muscle thickness but no intra-luminal valve, ring or diaphragm or extra-luminal compression was seen (). Heineke-Mikulicz pyloroplasty was done. Pyloric biopsy showed sub-mucosal edema and mild congestion and no inflammatory cells were seen. The diagnosis of primary acquired gastric outlet obstruction during infancy and childhood (Jodhpur disease) with severe malnutrition was made. The child recovered well postoperatively, became asymptomatic gradually and gained 2.5 kg in one month post surgery.

[[3.5, 'year']]

F

{'9200104': 1, '15991158': 1, '18926227': 1, '14760495': 1, '17187970': 1, '17270531': 1, '24714224': 2}

{}

3959373-1

noncomm/PMC003xxxxxx/PMC3959373.xml

Possible Strongyloides stercoralis infection diagnosed by videocapsule endoscopy in an immunocompetent patient with devastating diarrhea

A 70-year-old, housewife, living in a small village, presented with a six-month history of more than 10 watery diarrheas per day and loss of 18 kilos of body weight. Laboratory data were normal, including hemoglobin, white cell count and differential, CRP, serum albumin and immunoglobulin, iron, feritin, vitamin B12, and folate. Chest x-ray was normal. ESR was 40 mm/h. Stool examination for hemoglobin, leukocytes, parasites and cultures for pathogens was negative (twice). Colonoscopy with biopsies was normal. Duodenal biopsies showed mild, non-diagnostic changes of mucosa villi. Antibodies to tissue transglutaminase, endomysial antibodies and serum chromogranin-A were negative, including HIV infection. A small bowel videocapsule endoscopy (SBVCE) study showed mucosal areas of denuded villi and prominent small bowel submucosal vessels in the jejunum, multiple linear whitish lesions surrounded by reddish mucosa (), and parasites within the ileal fluid, entering the ileal mucosa (). These SBVCE findings favored the diagnosis of Strongyloides stercoralis infection. Review of previous histology of small bowel and colon, two more stool examinations for parasites and serum IgG antibodies against Strongyloides stercoralis (ELISA) were negative. She also tested negative for the HTLV-1 co-infection. The patient was treated with two cycles of albendazole 400 mg/d for 7 days. At 6-month follow up, she had no diarrhea and gained 4 kg of body weight.

[[70.0, 'year']]

F

{'20540646': 1, '12578162': 1, '19899045': 1, '21173914': 1, '32503315': 2, '19530103': 1, '30157619': 2, '18321548': 1, '19807271': 1, '21175501': 1, '20518090': 1, '21198912': 1, '19788836': 1, '21070870': 1, '20733481': 1, '3783811': 1, '19624080': 1, '20541203': 1, '11528578': 1, '33928798': 1, '24713813': 2}

{'6370920-1': 1, '7350350-1': 1}

3959384-1

noncomm/PMC003xxxxxx/PMC3959384.xml

Hypercalcemic crisis due to adult T cell leukemia: a rare cause of paralytic ileus

A 54-year-old diabetic male presented with diffuse abdominal pain, distension and obstipation for 3 days following an alcoholic binge. The patient had severe anorexia and nausea. The patient had become irritable with incomprehensible speech and abnormal behavior over the last two days and his relatives reported an 8 kg decrease in his body weight over the past 2 months. Six years ago he had undergone patellectomy and was transfused with 6 units of whole blood. There was no family history of malignancy. On examination he was dehydrated, tachypneic and cyanosed with a heart rate of 116 bpm and a blood pressure of 200/110 mmHg. His face and trunk were erythematous. He had generalized lymphadenopathy. Abdominal examination revealed hepatosplenomegaly, generalized tympanitic resonance and absent bowel sounds. Auscultation of the chest revealed diffuse crepitations. Neurological examination showed no signs of meningeal irritation. Cardiac examination was unremarkable. The clinical findings were suggestive of paralytic ileus and the differential diagnosis considered included acute pancreatitis, diabetic ketoacidosis (DKA), porphyria and hypercalcemia.\nHis hemogram was as follows: hemoglobin, 13.8 g/dL; leukocyte count, 174 × 109 /L with 70% lymphocytes; platelet count, 156 × 109 /L; and ESR, 63 mm. His urea was 112 mg/dL and creatinine level 3.9 mg/dL. He also had hyperkalemia (6.0 mg/dL), hyperuricemia (10.6 g/dL) and LDH levels >5 times the upper limit of normal (ULN) suggesting the possibility of increased cell turn over. His pancreatic enzymes were normal, urine ketones and porphyrinogen negative, thereby ruling out pancreatitis, DKA and porphyria. He had high calcium (15.8 mg/dL), high phosphate (5.8 mg/dL), normal magnesium and low parathormone levels of 8.8 pg/mL (normal 13-55 pg/mL). His alkaline phosphatase was >3 times the ULN. The results were suggestive of a malignancy-associated hypercalcemia. His duodenal aspirate and biopsy were negative for strongyloides larvae. There was evidence of reticulonodular opacities in both lung fields. ABG analysis showed acute lung injury (PaO2/ FiO2 = 252). Sputum cytology showed malignant cells and was negative on silver stain. ECG showed a corrected QT interval of 0.36 sec. Spinal fluid study was normal and was negative for Cryptococcus on Indian ink staining. Dilated bowel loops were seen in the abdominal X-ray. Ultrasound of the abdomen revealed hepatosplenomegaly and intra-abdominal lymphadenopathy. His peripheral smear showed marked leukocytosis, predominantly atypical mononuclear cells with high nucleo-cytoplasmic ratio. Few lymphocytes had convoluted nuclei suggestive of flower cells (), characteristic of ATLL. Bone marrow was studded with abnormal cells () and immunophenotyping showed CD3+, CD4+, CD7−, CD8−, CD25+ lymphocytes. His HTLV-1 serology was positive.\nThe patient was diagnosed with paralytic ileus secondary to hypercalcemic crisis due to adult T cell leukemia caused by HTLV-1. The patient was treated with aggressive hydration, corticosteroids, furosemide, hemodialysis and chemotherapy was initiated. His calcium levels reduced to 12 g/dL and his bowel sounds reappeared. However his leukocyte count increased to 345 × 109 /L. The patient developed anuria with progressive worsening of renal function (creatinine of 6.4 g/ dL) and succumbed one week after admission.

[[54.0, 'year']]

M

{'6272125': 1, '11781248': 1, '17183844': 1, '16106073': 1, '15353320': 1, '23198151': 1, '29384906': 2, '1468864': 1, '25657421': 2, '11042682': 1, '16155612': 1, '12481881': 1, '12612113': 1, '24714244': 2}

{'4318027-1': 1, '4318027-2': 1, '4318027-3': 1, '4318027-4': 1, '4318027-5': 1, '6393021-1': 1}

3959392-1

noncomm/PMC003xxxxxx/PMC3959392.xml

Mediastinal lymphadenopathy in ampullary adenocarcinoma: not always metastatic

A 65-year-old female presented to our clinic with a two-month history of painless progressive jaundice with pruritus and clay colored stools, anorexia and weight loss. On examination she had icterus and a palpable gallbladder which was cystic in consistency. She had normal hematological parameters. Serum bilirubin was 16.9 mg/dL (0.2-1.1 mg/dL) with a conjugated fraction of 13.3 mg/dL, serum alkaline phosphatase was 678 IU/mL (<128 IU/mL), serum aspartate aminotransferase (AST) was 76 IU/mL (<35 IU/mL) and serum alanine aminotransferase (ALT) was 57 IU/mL (<40 IU/mL). She had normal coagulation parameters. Transabdominal ultrasound showed hugely distended gallbladder, dilated common bile duct up to its lower end along with dilated intrahepatic biliary radicles (IHBR). CECT of the abdomen showed dilated pancreatic duct and biliary system. However, a definite cause of the distal obstruction could not be identified. Side viewing endoscopy showed a bulky ulcerated papilla. Biopsies from the papilla showed adenocarcinoma of the ampulla. PET-CT scan was done to look for metastatic disease before surgery. It showed increased [18F]-Fluoro-Deoxy-Glucose (FDG) tracer uptake in the periampullary region (SUV max 4.1) () as well as in the enlarged subcarinal nodes (SUV max 14.7) (). There were no positive loco-regional lymph nodes on PET-CT scan. Endoscopic ultrasound (EUS) showed a small hypoechoic lesion in the ampullary region with dilated common bile duct and IHBR (). Also large hypoechoic subcarinal nodes with echogenic foci were noted (, ) and fine needle aspiration of the node was done using a 22 Gauge needle (EchoTip, Wilson−Cook, Winston−Salem, North Carolina, USA) was performed (). Cytological examination of the aspirate showed granulomatous inflammation consistent with tuberculosis. Stain for AFB was negative but PCR (polymerase chain reaction) was positive for Mycobacterium tuberculosis. She underwent pancreatioco-duodenectomy and achieved complete resection. Following six months of tuberculosis treatment she improved and is asymptomatic after 1 year of follow up.

[[65.0, 'year']]

F

{'20504861': 1, '21264165': 1, '18274842': 1, '8635381': 1, '15138336': 1, '14654474': 1, '21830397': 1, '16720142': 1, '17941009': 1, '19352560': 1, '18656049': 1, '15967899': 1, '16928527': 1, '17629078': 1, '24714280': 2}

{}

3959401-1

noncomm/PMC003xxxxxx/PMC3959401.xml

Secondary rectal linitis plastica as first manifestation of urinary bladder carcinoma

A 68-year-old man presented to the Department of Endoscopy with a six-month history of anal outlet obstruction, constipation and tenesmus. The patient had no relevant past medical history. Digital examination revealed a circumferential rectal narrowing with a firm, mass-like area, palpable all around the rectal wall and extending to a few centimeters of the anal margin. Laboratory tests, including urinalysis, were unremarkable. Subsequent endoscopy demonstrated a narrow distal rectum, with the overlying mucosa being indurated, non-ulcerated, with a cobblestone appearance (). Several biopsies and fine-needle aspiration were taken, but none was conclusive for diagnosis. T2-weighted MRI showed a double-layered thickening of the rectal wall with an inner iso-intense circumferential thickening of the submucosa and outer hypo-intense circumferential thickening of the muscular rectal wall, as well as a thickened bladder wall. Transrectal ultrasonography showed circumferential infiltration of the submucosa, whereas the other layers were normal (); an image compatible with “linitis plastica”. The patient underwent rectal extirpation and total cystectomy with lymph node dissection. Macroscopic examination of a sagittal section of resected rectum demonstrated an expanded submucosal layer due to infiltration with cancer cells, with intact mucosa and muscular layer (). Histological examination of the resected bladder showed a grade III papillary transitional cell carcinoma. In the rectum clusters of tumor cells of a poorly differentiated adenocarcinoma were observed. Immunostaining was positive for both CK7 and CK20; PSA was negative. Combining the cytokeratine profile histology and transrectal ultrasonography findings, the diagnosis of a primary urinary bladder tumor with hematogenous spread to rectal submucosal layer was established.\nThe patient received postoperative radiation followed by gemcitabine (100 g/m2 on days 1, 8, 15) and cisplatin (70 mg/ m2 on day 2) for a 28-day cycle for six months, but he died eight months later due to disseminated peritoneal carcinomatosis.

[[68.0, 'year']]

M

{'18635171': 1, '10385739': 1, '10658725': 1, '16417562': 1, '12518144': 1, '1568609': 1, '9434221': 1, '1397867': 1, '17565636': 1, '34759661': 2, '6653567': 1, '13769272': 1, '30949339': 2, '26322720': 1, '1642587': 1, '15729254': 1, '30980194': 1, '18796553': 1, '24714188': 2}

{'8525488-1': 1, '6439517-1': 1}

3959411-1

noncomm/PMC003xxxxxx/PMC3959411.xml

Klippel-Trénaunay syndrome, pregnancy and the liver: an unusual interplay

In January 2008, a 29-year-old woman was referred from the Obstetrics Unit because of fever and the development of ascites, 3 days after a Caesarian section (gravida 3) performed because of vaginal-cervical varices. She had had no previous spontaneous vaginal deliveries and bilateral stripping of varicose veins. She was a non-smoker and she abstained from alcohol.\nAt referral, she was normotensive without encephalopathy. Pyrexia (38.8oC), mild tachycardia and moderately distended and tender abdomen were present. There were no cutaneous markers of chronic liver disease and no cardiac, respiratory or neurological abnormalities. However, she had limb asymmetry with the right side (length 95 cm, circumference 35 cm), larger than the left (length 93 cm, circumference 29 cm) (), together with right sided enlargement of the face compared to the left. She had capillary (port-wine) hemangiomas in the right cervical area and right upper limb (). She was diagnosed with the KTS.\nHemoglobin was 8.9 g/dL, white cell count 16500 K/ μL and platelet count 173000 K/μL. The liver and renal function tests were normal apart from an albumin of 2.5 mg/dL. The INR was 1.4. Viral and autoimmune markers were negative. A computed tomography (CT) scan showed hepatomegaly with arteriovenous anastomoses within the liver parenchyma, splenoportal hilar varices, splenomegaly (length 15.5 cm), a moderate amount of ascites and phlebolithiasis in intra-abdominal varicose dilated veins. Smallesophageal varices were seen endoscopically. A brain magnetic resonance imaging (MRI) and echocardiography were unremarkable.\nShe was treated empirically with piperacillin/tazobactam and metronidazole. Subsequently bacterial cultures from the lochia isolated Escherichia coli and Enterococcus faecalis. Piperacillin/tazobactam was continued and linezolid was added according to sensitivities. She responded to these antibiotics. The ascites responded to diuretics. Prophylactic low molecular weight heparin was started and continued for 6 weeks because of persistent tachycardia and raised D-dimers.\nAfter 3 months a percutaneous liver biopsy was performed which showed non-specific features. The ascites had resolved completely and blood biochemistry was normal. A thrombophilia screening was weakly positive for lupus anticoagulant and hyperhomocysteinemia (28.4 μmol/L, normal range 3.7-11). A chest CT was normal whilst CT of skull–cervical region showed muscle enlargement and projection of the right pharyngeal wall.\nReferral for further evaluation was made at 8 months after initial presentation. A transjugular liver biopsy and hepatic venous pressure measurements were performed. Liver histology and hepatic venous pressures were essentially normal. An MRI scan revealed portal vein (PV) thrombosis with cavernoma. There was no evidence of PV aplasia. She was commenced on warfarin for PV thrombosis on a procoagulant background and she has been well for four years since the initial diagnosis.

[[29.0, 'year']]

F

{'16911369': 1, '7698593': 1, '9468262': 1, '18274338': 1, '16284144': 1, '12037456': 1, '12452471': 1, '29225678': 1, '9820414': 1, '16490119': 1, '10428616': 1, '24714267': 2}

{}

3959419-1

noncomm/PMC003xxxxxx/PMC3959419.xml

Endoscopic submucosal dissection for the diagnosis and treatment of a gastric submucosal tumor: initial experience in Greece

A 78-year-old woman with a history of right heart failure on anticoagulant therapy was referred to our department due to persistent dyspeptic symptoms. Upper gastrointestinal (GI) endoscopy revealed a submucosal lesion, ulcerated on top, measuring approximately 35 mm × 10 mm, on the anterior-inferior wall of the antrum (). Boring biopsies were obtained. Endoscopic ultrasonography revealed a well-circumscribed homogenous, hypoechoic mass 35 mm × 12 mm in size originating from the second gastric wall layer – muscularis mucosa (). Pathologic examination proved insufficient to provide a definitive diagnosis, setting the differential diagnosis among PDGFRA(+) GIST, leiomyoma and leiomyosarcoma. Immunohistochemistry revealed SMA(+), suggestive of a leiomyoma/leiomyosarcoma although desmin(-) and CD34(+), suggestive of GI stromal tumor although CD117(c-kit) (-). Moreover S-100 was negative, excluding tumors of neural origin and Schwannoma. Since the patient was not an eligible surgical candidate due to comorbidities and advanced age, she was referred for ESD after obtaining informed consent.\nMidazolam plus propofol were used for sedation under anesthesiological supervision. A triangle-tip electrocautery knife (TT-Knife, KD-640L; Olympus Optical) was used through a standard-size video endoscope (GIF-1T140; Olympus Optical). A soft transparent straight-type cap device (MH595; Olympus Optical) was attached to the tip of the endoscope to obtain proper direct views of the submucosal layer.\nResection of the submucosal lesion was performed according to the previously published experience [,]. Initially, the demarcation of the marginal dissection line was performed, approximately 5 mm distant from the tumor margin, by applying argon plasma coagulation (35W, 0.8 L/min) using a 2.3 mm diameter probe (APC-Sonde 2200 A; ERBE Elektromedizin GmbH). Complete lift of the lesion was achieved by submucosal injection of a solution of 0.5 mL of epinephrine 0.1% added in 100 mL Glycerol with 1 mL indigo carmine dye. Additional submucosal injections of epinephrine solution were applied to maintain the lift effect, when needed. Exposed blood vessels of the ulcer bed were thoroughly coagulated either with the bottom of the triangular plate or using hemostatic forceps (Coagrasper, Olympus Optical), to prevent bleeding. Finally, the resection site was carefully observed to evaluate the presence of any residual tumor and sucralfate was sprayed onto the ulcer (). The duration of the procedure was 55 min, consistent with the published data, while no immediate complications, such as perforation or postoperative bleeding, occurred.\nAfter complete en bloc resection, tissue specimen was fixed along its edges using thin needles, inserted onto a wooden plate and fixed in formalin solution. Histopathology examination confirmed complete resection and set the diagnosis of leiomyoma.\nUpper GI endoscopy was carried out six days after the procedure in order to evaluate the ulcer bed and to initiate per os anticoagulation therapy (). Follow-up upper GI endoscopy 3 months later did not reveal any signs of recurrence.

[[78.0, 'year']]

F

{'14997145': 1, '20171632': 1, '20354939': 1, '22032850': 1, '20457867': 1, '16762644': 1, '1871670': 1, '11293753': 1, '29725533': 1, '15326574': 1, '24714393': 1, '10502173': 1, '17058168': 1, '19032991': 1, '19961528': 1, '20623442': 1, '24714207': 2}

{}

3959423-1

noncomm/PMC003xxxxxx/PMC3959423.xml

Lymphocytic esophagitis mimicking eosinophilic esophagitis

A 74-year-old male with a history of 3 years duration of dysphagia presented with acute food impaction. The patient had a history of lymphoma and esophagitis with stricture without the symptoms of gastro-esophageal reflux disease (GERD). Following endoscopic removal of the impacted meat he had severe chest pain with evidence of perforation of the esophagus with pneumomediastinum on chest CT scan which resolved uneventfully. A later endoscopy showed a tight distal stricture and course rings at the middle third of the esophagus (). A mucosal split occurred during endoscopy (, black arrow). Biopsies taken from the middle third of the esophagus showed marked infiltration of exclusive intraepithelial lymphocytes in a peripapillary distribution (). There was no eosinophilic component, thus ruling out eosinophilic esophagitis.\nThe immunostains showed presence of CD3 and CD5 lymphocytes (T cell markers) in the epithelium (). The specimen was negative for CD 20 lymphocytes (B cell marker). The esophageal manometry showed diffuse esophageal spasm with partial relaxation of the lower esophageal sphincter. The patient had prior chemotherapy for non-Hodgkin lymphoma present in his nostril and leg. The lymphoma was monoclonal B-cell CD20 positive. Thus, the lymphocytes (CD3 and CD5) present in the esophageal epithelium are distinct from the lymphoma (CD20). Four year follow up with 5 endoscopies shows persistence of the endoscopic and biopsy findings. The patient was dilated each time and received botox twice.

[[74.0, 'year']]

M

{'26866393': 1, '18794041': 1, '22157333': 1, '28573181': 1, '28246468': 1, '27231454': 1, '34099042': 2, '27231461': 1, '28035315': 2, '28429201': 1, '30370453': 1, '16613348': 1, '24714246': 2}

{'5156879-1': 1, '5156879-2': 1, '5156879-3': 1, '8186211-1': 1}

3959436-1

noncomm/PMC003xxxxxx/PMC3959436.xml

Combined use of band ligation and detachable snares (endoloop) in a patient with blue rubber bleb nevus syndrome

A 20-year-old woman was admitted with iron deficiency anemia and history of melena. Upper endoscopy demonstrated normal esophagus, stomach and proximal duodenum. At colonoscopy, two bluish pedunculated angiectatic polypoid lesions (1 to 2 cm in diameter) were noted due to BRBNS (). The small intestine was screened for further lesions with the use of capsule endoscopy. The capsule identified four more lesions at the proximal jejunum. The small bowel lesions were smaller (0.5 to 1 cm in diameter at their bases). She had a similar venous malformation at the gingival area which was embolized. CT scan of abdomen, chest and brain did not reveal any other lesion.\nWe performed enteroscopy to approach the jejunal lesions (). All lesions were ligated in one session using the band ligation technique with a multi-band ligator device (Fig. , ). In order to avoid entrapment of all intestinal layers, high suction pressure was not used. In addition, two trigger cords, tied together, were used in order to match the length of the colonoscope's channel. A colonoscopy was performed and detachable snares - endoloops were inserted at the colonic lesions (Fig. , ).\nA tissue specimen was obtained using the snare after endoloop insertion from one of the lesions. No bleeding occurred during the procedure. Histopathological examination revealed submucosal large blood-filled spaces lined by a single layer of endothelial cells with presence of some thrombi in the cavernous spaces ().\nThe patient made an uneventful recovery and was discharged 3 days later without any abdominal pain or signs of bleeding. Three weeks following the interventions further endoscopic evaluations were performed; these revealed scars at all sites treated with either technique. No bleeding or new venous malformations were observed ().

[[20.0, 'year']]

F

{'15729077': 1, '26908380': 2, '1603744': 1, '12024162': 1, '17137850': 1, '7783168': 1, '19691801': 1, '22392180': 1, '34781211': 1, '18974470': 1, '29851802': 1, '7748841': 1, '24714239': 2}

{'4763553-1': 1}

3959438-1

noncomm/PMC003xxxxxx/PMC3959438.xml

Pancreatic mass as an initial presentation of severe Wegener's granulomatosis

A 62-year-old woman was admitted to the hospital with ten-day history of acute epigastric pain, radiating to the back and associated with nausea, persistent fever up to 38°C and headache. She had a history of cough and sinusitis a month ago, complicated with otitis media, with insignificant improvement on antibiotic treatment and antitussive drugs. The patient had no other significant past and family history except laparoscopic cholecystectomy for lithiasis 15 years ago. She denied alcohol use, herbal or over-the-counter medications and allergies.\nExamination revealed epigastric tenderness without rebound and no palpable organomegaly, peristalsis was normal. There was purulent discharge from the left ear, pain in maxillary sinus and left mastoid. No other pathological findings were present.\nThe initial laboratory tests showed slight leukocytosis, trombocytosis, normal ESR, CRP 15.8 mg/dL (normal range <0.6 mg/dL), elevated fibrinogen, ALT and GGT were up to 2xURL (upper reference level) and 3xURL respectively. Serology for HBV and HCV infection was negative. Serum amylase and lipase, cholesterol and triglycerides were within normal range. Albumin was 2.95 g/dL; blood glucose was 148 mg/dL. Serum iron (8.4 μg/dL) and TIBC (38 μmol/L) were low. Hemoglobin was normal at admission to hospital but dropped to 8.8 g/dL within a week without signs of bleeding and prothrombin time also decreased to 53%. Urinalysis showed increased numbers of leukocytes and erythrocytes with proteinuria 0.276 g/L/24h. Blood cultures and urine cultures were sterile. Coombs and Schirmer tests were negative. Serum IgG, IgA, IgM and serum tumor markers (CA 19-9, CEA) were within normal range. RF (rheumatoid factor), ANA (anti-nuclear antibodies) and anti-MPO (anti-myeloperoxidase) were tested negative, while anti-Pr3 (anti-proteinase 3, c-ANCA) were 15xURL (89.63 U/mL; negative <6 U/mL).\nInitial abdominal ultrasound (US) revealed slightly enlarged and hypoechoic pancreatic body and tail with blurry margins, as in acute pancreatitis. Computed tomography of the abdomen also confirmed edema of the pancreatic tail without fluid collections or other abnormal findings. Control US in several days showed blight echoes scattered among the enlarged pancreas, compression of the splenic vein and spleenomegaly. Further magnetic resonance was performed and revealed a 3 cm soft-tissue formation in the pancreas tail without pancreatic duct abnormalities, which compressed the splenic vein, without infiltration or enlarged regional lymph nodes. Imaging studies of the kidneys showed no alterations and chest X-ray was normal.\nThe initial diagnosis was acute pancreatitis but normal levels of serum amylase and lipase in the course of the disease, normal billiary tree imaging and lack of pancreatic disease history or alcohol consumption did not support this diagnosis. Normal immunoglobulin levels and absence of pancreatic duct abnormalities ruled out autoimmune pancreatitis, but positive c-ANCA suggested the possibility of other autoimmune diseases. However, pancreatic neoplasm was also suspected because of the presence of pancreatic tail mass. US-guided fine needle aspiration was performed twice but only detritus without atypical cells was established. However malignancy could not be entirely ruled out.\nDespite treatment with antibiotics, IV fluids, proton pump inhibitors and analgesia for a week, fever and severe abdominal pain still persisted. On the fifth day of hospitalization the patient suffered phlebothrombosis of left lower leg and low-molecular-weight heparin was added to therapy. Immunosuppressive treatment was discussed as an option, but the severe intractable abdominal pain and lack of cytological confirmation along with the possibility of pancreatic carcinoma indicated surgery. A solid tumor-like formation in the pancreatic body and tail with well-defined margins was resected and pancreato-jejunoanastomosis a modo Roux and splenectomy were performed ().\nThe histology from the surgical specimens confirmed WG of the pancreas and spleen – typical vasculitis with fibrinoid necrosis, granulomas and giant cells ().\nThe patient was further treated with steroids and azathioprine and a clinical remission followed. She was doing well at 6 months of follow up.

[[62.0, 'year']]

F

{'2071011': 1, '26900301': 1, '31434674': 1, '17602941': 1, '27876769': 1, '31832480': 1, '31289155': 1, '21386646': 1, '2202308': 1, '6336643': 1, '24714250': 2}

{}

3959450-1

noncomm/PMC003xxxxxx/PMC3959450.xml

Achalasia cardia associated with esophageal varices: a therapeutic dilemma

A 63-year-old male, chronic alcohol consumer, presented with progressively increasing dysphagia of 6 months duration. There was history of loss of weight. He was a known diabetic with blood sugar well controlled with oral drugs. However, after onset of dysphagia, his blood sugar control was erratic and had frequent episodes of hypoglycemia. Clinical examination revealed hepatomegaly. Laboratory examination revealed hypoalbuminemia with mildly elevated liver enzymes. Upper gastrointestinal endoscopy revealed dilated esophagus with residue. Esophageal varices were also noted but there was no history of gastrointestinal bleed (). Esophageal manometry revealed high resting lower esophageal sphincter (LES) pressure with non transmitted low amplitude contractions in esophageal body () suggesting classic achalasia cardia. A contrast-enhanced computed tomography of chest and abdomen revealed dilated esophagus enlarged liver with irregular outline and intra-abdominal collaterals. Endoscopic ultrasound (EUS) examination revealed peri-esophageal collaterals as well as prominent perforators at lower end of esophagus (). Patient was started on calcium channel blockers with no relief of symptoms. The co-existence of varices with achalasia is very rare and this case poses a difficult therapeutic dilemma as risk of bleeding from the varices limit the treatment options available. What to do next?\nBecause of risk of bleeding from varices following balloon dilatation, the patient underwent EUS-guided botulinum toxin injection. Using a linear echoendoscope with color Doppler, carefully avoiding varices and perforators, 80 units of botulinum toxin was injected into LES in four quadrants (20 units in each quadrant) (). Following this, the patient had marked improvement in his symptoms and was completely free of dysphagia 7 days later and also blood sugar was controlled with oral drugs. He is asymptomatic till the last follow up 3 months after injection. As the patient has chronic liver disease along with portal hypertension, he has been referred for work up for liver transplantation.

[[63.0, 'year']]

M

{'22217358': 1, '16948803': 1, '9041010': 1, '10223381': 1, '9013174': 1, '22180005': 1, '19106675': 1, '31065374': 1, '15075653': 1, '16416206': 1, '24714325': 2}

{}

3959462-1

noncomm/PMC003xxxxxx/PMC3959462.xml

Wilke’s syndrome. A rare cause of duodenal obstruction

A 15-year-old female patient was urgently admitted with symptoms of dehydration, loss of appetite and persistent vomiting for 10 weeks. For four months she was vomiting two to three times weekly and this increased to three to four times daily during the last week before admission. The vomitus consisted of undigested meals eaten recently without any blood. During the last four months the patient reported a significant weight loss (21 kg). Her past medical history was free. On admission the patient was very thin and extremely weak with signs of severe dehydration. A nasophagogastric tube was inserted and the fluid and electrolyte balance was corrected by parenteric infusion of crystalloid fluids with electrolytes. Two days later the patient was subjected to gastroscopy which showed mild inflammation of the lower esophageal mucosa and gastritis. The instrument could not pass further than the third part of the duodenum, due to extraluminal pressure on the duodenal wall. Barium meal follow through confirmed the extrinsic obstruction of the third part of the duodenum and proximal dilation of the stomach and duodenum [] with normal motility of the upper GI tract. CT scan of the upper and lower abdomen excluded the possibility of a tumor or an annular pancreas being the cause of the compression of the duodenum. Thus based on the history, the clinical and imaging findings of the patient, the diagnosis of Wilke’s syndrome was concluded.\nThe patient denied the initially suggested conservative treatment and therefore she was subjected to laparotomy. The first and second parts of the duodenum were dilated and hypertrophied. The dilated duodenum was abrupted at the point where the superior mesenteric artery crossed the third part of the duodenum []. These findings confirmed the diagnosis and a site to site duodenojejunostomy in two layers was performed []. The postoperative course was uneventful and barium meal a month postoperatively showed unobstructed passage of the contents from the duodenum to the jejunum. One year later the patient gained the lost weight and remained asymptomatic.

[[15.0, 'year']]

F

{'19547692': 2, '19357930': 1, '1571759': 1, '15957095': 1, '20349665': 1, '10086410': 1, '17476104': 1, '19525600': 1, '9798861': 1, '19342937': 1, '17198067': 1, '18646483': 1, '1265660': 1, '29479421': 2, '24714262': 2}

{'2699079-1': 1, '5814821-1': 1}

3959485-1

noncomm/PMC003xxxxxx/PMC3959485.xml

Synchronous gastric gastrointestinal stromal tumor (GIST) and other primary neoplasms of gastrointestinal tract: report of two cases

A 50-year-old male presented with history of two episodes of melena and drop in hemoglobin for 3 months. Barium meal study showed an eccentric rounded impression in the gastric fundus. Additionally there was an eccentric impression on the superior wall of the duodenal bulb. Upper GI endoscopy revealed a nodular lesion in the gastric fundus with a central ulcer. Another sessile polyp of about 1 cm size was seen in the first part of duodenum (Fig. , ). Both were thought to be leiomyomas endoscopically. Contrast-enhanced computed tomography (CT) of upper abdomen showed a large nodular lesion in the fundus of stomach and another small lesion in first part of duodenum.

[[50.0, 'year']]

M

{'28951716': 1, '20707247': 1, '17193825': 1, '21360271': 1, '21744758': 1, '29992077': 2, '24995213': 1, '1694655': 1, '31086397': 1, '17701127': 1, '20380900': 1, '32180871': 1, '31435178': 1, '22340419': 1, '22457867': 1, '18932294': 1, '25197591': 2, '24714328': 2}

{'3959485-2': 2, '4150523-1': 1, '6016216-1': 1}

3959485-2

noncomm/PMC003xxxxxx/PMC3959485.xml

Synchronous gastric gastrointestinal stromal tumor (GIST) and other primary neoplasms of gastrointestinal tract: report of two cases

A 62-year-old male was admitted with chief complaints of decrease in appetite and painful abdomen for two months. Colonoscopy revealed a large constricting mass in the rectosigmoid colon. CT of the abdomen showed thickening of sigmoid colon and ileum with multiple mesenteric lymph nodes and heterogeneous nodular opacities in pelvis. The patient was taken up for surgery of advanced adenocarcinoma of colon. A nodule was found perioperatively in fundus of stomach which was thought to be metastatic in nature. In view of extensive spread with adhesions of small intestine, sigmoidectomy, right hemicolectomy along with wedge resection of stomach was done.

[[62.0, 'year']]

M

{'28951716': 1, '20707247': 1, '17193825': 1, '21360271': 1, '21744758': 1, '29992077': 2, '24995213': 1, '1694655': 1, '31086397': 1, '17701127': 1, '20380900': 1, '32180871': 1, '31435178': 1, '22340419': 1, '22457867': 1, '18932294': 1, '25197591': 2, '24714328': 2}

{'3959485-1': 2, '4150523-1': 1, '6016216-1': 1}

3959491-1

noncomm/PMC003xxxxxx/PMC3959491.xml

Spontaneous bacterial peritonitis in extrahepatic portal venous obstruction

A 48-year-old male presented with melena of 2 days duration. He was diagnosed to have idiopathic EHPVO at the age of 14 years and had undergone multiple endotherapies and later splenectomy at the age of 15 years. At admission the vitals were stable and physical examination was normal except for pallor and the presence of abdominal scar. On the fourth day of admission the patient developed fever with abdominal pain and mild abdominal distension due to ascites. Hemogram revealed; hemoglobin 6.1 g/dL, total leukocyte count 6500 cells/mm3, platelet count 3.56 lakhs/mm3, mean corpuscular volume 65.2 fL and International Normalized Ratio (INR) 1.04. Doppler ultrasound abdomen revealed normal liver, multiple tortuous collaterals replacing portal vein and moderate ascites. Upper gastrointestinal endoscopy revealed mucosal tags in the esophagus (post endotherapy), single column of grade 1 esophageal varix and severe portal hypertensive gastropathy. Ascitic fluid analysis revealed a total leukocyte count of 2400 cells/mm3, polymorphonuclear cell count of 1680 cells/mm3, with ascitic fluid protein 1.9 g/dL, albumin 0.8 g/dL and serum ascites albumin gradient (SAAG) 2.3. Culture of ascitic fluid yielded heavy growth of Escherichia coli (E. coli) species.

[[48.0, 'year']]

M

{'20667529': 1, '17090853': 1, '7264497': 1, '17335715': 1, '9928769': 1, '9693222': 1, '10673079': 1, '10052502': 1, '7095741': 1, '15723320': 1, '24714664': 2}

{'3959491-2': 2}

3959491-2

noncomm/PMC003xxxxxx/PMC3959491.xml

Spontaneous bacterial peritonitis in extrahepatic portal venous obstruction

A 58-year-old male presented with melena, abdominal pain and fever. He was diagnosed to have EHPVO and had undergone splenectomy at the age of 19 years when he presented with massive variceal bleeding in 1973. Physical examination revealed pallor and moderate ascites. Laboratory investigations were as follows; hemoglobin 9.1 gm/dL, total leukocyte count 11700 cells/mm3, platelet count 4.04 lakhs/mm3 and INR of 1.1. Ascitic fluid analysis showed a total leukocyte count of 1600 cells/mm3, polymorphonuclear cell count of 1472 cells/mm3, total protein 2.5 g/dL, albumin 1.4 g/dL and SAAG 1.9. Ascitic fluid culture yielded growth of E. coli. Ultrasound abdomen with Doppler study showed normal liver, cavernous transformation of the portal vein and moderate ascites. Upper gastrointestinal endoscopy revealed severe portal hypertensive gastropathy and gastric fundal varix. Computerized tomography of the abdomen was consistent with the diagnosis of EHPVO; there was no evidence of cirrhosis of the liver or any features of perforation or inflammation of other organs.\nThe liver and renal function tests, serum amylase and lipase levels, serum electrolytes and blood glucose levels were normal in both patients. Ascitic fluid glucose, lactate dehy-drogenase, triglycerides and adenosine deaminase were also within normal limits. Both patients did not show any features of perforation or obstruction on plain x-ray of the abdomen.\nBoth patients were managed with infusion of octreotide, proton pump inhibitors, transfusions, hematinics and beta blockers. SBP was treated with Cefotaxime 2 g IV t.i.d. Both patients had relief of fever, abdominal pain and abdominal distension. Repeat ascitic fluid analysis after 48 h of antibiotic therapy showed a decrease in polymorphonuclear cell count to 68 cells/mm3 and 165 cells/mm3 in the first and second case respectively. Antibiotics were continued for 5 days and both patients were discharged in a stable state.

[[58.0, 'year']]

M

{'20667529': 1, '17090853': 1, '7264497': 1, '17335715': 1, '9928769': 1, '9693222': 1, '10673079': 1, '10052502': 1, '7095741': 1, '15723320': 1, '24714664': 2}

{'3959491-1': 2}

3959507-1

noncomm/PMC003xxxxxx/PMC3959507.xml

Inflammatory pseudotumor of liver secondary to migrated fishbone - a rare cause with an unusual presentation

A 35-year-old woman presented to the surgical gastroenterology outpatient department with a short history of vague epigastric pain for one day only. She had no other gastrointestinal symptoms like vomiting or anorexia or weight loss. She had no history of fever or jaundice and no history of similar episodes before, with a normal physical examination. She was referred to us with an ultrasound abdominal scan done in another public hospital, showing a 3×3.5 cm mass in the left lobe of liver. A contrast-enhanced CT scan in our hospital showed an abnormal hypodense lesion with mild enhancement in the arterial phase and with a central calcification (). Complete blood count, liver function test and alpha-fetoprotein were within normal limits.\nA diagnostic laparoscopy was done as a routine protocol in our unit, followed by an exploratory laparotomy, since a definitive diagnosis could not be established. Intraoperatively, a dense fibrotic lesion was felt in the region of liver segments II and III. No peri-hepatic adhesions were seen. Right lobe was normal. A left lateral segmentectomy was done. Dissection of the specimen revealed a 3 cm long fish bone within the fibrotic mass (). There was no purulent material in the lesion. A thorough search for evidence of healed perforation in stomach, duodenum and colon was made and none was found. She had an uneventful post-operative period. The histopathological examination revealed chronic non-specific inflammation with fibrosis consistent with an inflammatory pseudotumor.

[[35.0, 'year']]

F

{'2155699': 1, '5457244': 1, '6622330': 1, '4019845': 1, '34509175': 2, '15188521': 1, '18516543': 1, '7283022': 1, '9606806': 1, '18286779': 1, '27900327': 2, '30882633': 1, '11490814': 1, '8382011': 1, '8884330': 1, '3335676': 1, '9333363': 1, '24714409': 2}

{'8435090-1': 1, '5112358-1': 1, '5112358-2': 1, '5112358-3': 1}

3959509-1

noncomm/PMC003xxxxxx/PMC3959509.xml

Deveopment of hepatocellular carcinoma in a non-cirrhotic, long-term responder to antiviral therapy, chronic hepatitis C patient: what kind of surveillance?

A Caucasian 61-year-old man was referred to our Hospital in 1993 due to elevated aspartate aminotransferase (AST) (eight times the upper limit of normal) with a slight increase in the gamma-glutamyl transferase (GGT) and was diagnosed as having CHC. He had no history of alcohol abuse, intravenous drug use, blood transfusions and drug intake. The patient’s medical history was notable for lung silicosis and hypertension without any secondary complication. His body mass index (BMI) was 25.51 kg/m2. He tested positive for HCV antibodies and negative for other causes of liver disease (other viral infections, hepatic autoimmunity, medications, hyperferritinemia, metabolic diseases). In 1993 the assessment of HCV-RNA and genotype by serum polymerase chain reaction (PCR) were not available, so no relative data at the time of the diagnosis exist. Other laboratory findings included a preserved liver function and a normal platelet count (). Abdominal examination and ultrasonography excluded hepatosplenomegaly and hepatic nodules. The liver biopsy, performed in 1994, showed stage 2 fibrosis with a moderate necro-inflammatory activity (A2 grade) according to the Desmet’s classification [], and a mild microvescicolar hepatic steatosis.\nOne year later, in January 1994, he was treated with 3MU of interferon-alpha 2a (Roferon) three times a week for 48 weeks, achieving a biochemical and SVR.\nFrom 1996 to 2009 HCV-RNA was undetectable with normal AST/ALT.\nIn August 2009 the patient was referred to our emergency room for the onset of severe abdominal pain. On abdominal examination, there was distention, rebound and guarding with moderate ascites. The remaining physical examination and vital signs were normal. Laboratory findings showed mild anemia with normal platelet count and a preserved liver function. HCV RNA was undetectable and alpha-fetoprotein was elevated ().\nContrast-enhanced computed tomography (CT) found a large (8.6 cm) hepatic mass in segment IV, with a vascular pattern typical of HCC, ascites and no evidence of portal vein thrombosis. The subsequent diagnostic paracentesis confirmed the presence of hemoperitoneum.\nDuring his hospital stay, there was a spontaneous stabilization of hemoglobin levels and a progressive pain relief. The gastroscopy was negative for esophageal and gastric varices. Therefore, on 4th November 2009 he underwent a left hepatectomy extending to the fifth hepatic segment. Intraoperatively a plurinodular mass of 7 cm in diameter was found, well demarcated from the remaining liver parenchyma. Histological evaluation revealed a moderately-differentiated HCC (grade G2 according to Edmondson and Steiner) [], in the absence of vascular invasion; the number of mitosis was less than 1 per 10 high power fields. His liver fibrosis on the resected specimen remained at stage 2.\nHe was discharged at home on hospital day 24 and has returned to full activity. Three months after surgery the level of alpha-fetoprotein decreased from 49.6 ng/mL pre-resection to 2.4 ng/mL. At the last visit in June 2011 he was well and CT-scan showed no evidence of recurrent tumor.

[[61.0, 'year']]

M

{'17311612': 1, '30705715': 1, '27049708': 2, '30341715': 1, '15770398': 1, '21374666': 1, '21435968': 1, '21129375': 1, '17876888': 1, '13160935': 1, '10428733': 1, '15853990': 1, '8188183': 1, '24714548': 2}

{'4727140-1': 1}

3959514-1

noncomm/PMC003xxxxxx/PMC3959514.xml

Splenic abscess due to chronic melioidosis in a patient previously misdiagnosed as tuberculosis

A 47-year-old Indian male, presented with high-grade fever and left-sided pleuritic chest pain of 3-week duration. He complained of anorexia and significant weight loss of 6 kg in the last 1 month. There were no other respiratory symptoms, jaundice or bowel symptoms. The patient was diagnosed with diabetes and was on insulin therapy for the past 5 years. Two years ago, the patient was evaluated for hemoptysis, diagnosed as sputum-negative pulmonary TB on the basis of X-ray finding suggestive of right upper lobe fibrosis. He was treated with Isoniazid (H), Rifampicin (R), and Pyrazinamide (Z) for 2 months and with H, R and Z for 4 months. He was treated for small joint arthritis for 3 months prior to presentation. There was no history of recent exposure to pulmonary TB. There was no history of malignancies in the family. He is a reformed smoker and a chronic alcoholic. No history of recent travel to North Australia or Southeast Asia. There is no history of exposure to soil. There was no history of sexual promiscuity.\nOn examination his vitals were stable and he had a body mass index of 17.8 kg/m2. Abdominal examination revealed tenderness in the left hypochondrium and moderate hepatosplenomegaly. Per rectal examination did not reveal bleeding or deposits. On chest examination, there were fine crepitations and diminished air entry in the right upper chest. Examination of other systems was within normal limits.\nHis hemogram showed polymorphonuclear leukocytosis and an erythrocyte sedimentation rate of 70 mm/h. He had a fasting blood sugar value of 236 mg/dL and a postprandial value of 300 mg/dL with a urine sugar of 2%. His renal function and electrolytes were normal. His liver function tests and prothrombin time were within normal limits (WNL). His amylase and lipase levels were WNL. His chest X-ray showed right upper zone fibrosis. His upper and lower gastrointestinal endoscopies were normal. Ultrasonography of the abdomen showed a collection of heterogeneous echogenicity near the inferior pole of spleen suggestive of a perisplenic abscess. Contrast-enhanced CT scan of the abdomen revealed a splenic abscess with a breech in the capsule and extension of abscess into the perisplenic area (). His viral serology was negative for hepatitis B, C and human immunodeficiency virus.\nThe possibilities considered in this middle-aged gentleman presenting with fever, weight loss and arthritis with evidence of right upper lobe fibrosis, hepatosplenomegaly and perisplenic abscess were TB, brucellosis, melioidosis, lymphoma, salmonellosis and connective tissue disorders. His sputum was negative for acid-fast bacillus. Infectious screen was negative for enteric fever, malaria and brucella serology. He had positive rheumatoid factor and anti-cyclic citrullinated protein was negative. Anti-nuclear antibodies were absent and tumor markers were WNL. Trephine biopsy of the bone marrow was normal. The aspirate from the abscess revealed catalase- and oxidase-positive, gram-negative bacillus with bipolar staining and violet colonies with central umbonation in Ashdown’s selective agar (), diagnostic of Burkholderia pseudomallei. Polymerase chain reaction for TB was negative in the aspirate. Blood, sputum and urine cultures were sterile.\nThe patient was diagnosed as melioidosis and treated with 2 weeks of parenteral ceftazidime (2 g t.i.d.) followed by oral co-trimoxazole (160/800 mg t.i.d.) for 12 weeks upon which he became symptom-free. His fever and arthritis subsided and follow-up ultrasound showed resolution of abscess. Chest X-ray showed improvement in the right upper lobe lesion. The response to the therapy confirmed our diagnosis of melioidosis.

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