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We present the case of a 65-year-old Caucasian man without previous psychiatric history that presented to our outpatient clinic due to elevated mood, reduced need of sleep, pressured speech, thoughts race, elevated energy, and disinhibition with a month of evolution. The worsening of the symptoms led his niece and brother-in-law to make an appointment in our outpatient psychiatry services. According to his family, the patient also started money overspending and abuse of alcoholic drinks and had frequent conflicts with the rest of the family, especially with his son with whom he had an emotional break-up just after the beginning of the symptoms. There was no previous history of manic or depressive symptoms.\nThe patient is the older of two sons, in a family of middle socioeconomic status. He had a eutocic birth and had normal psychomotor development with no relevant health problems. At 6 years of age he was enrolled in primary school. He was a sociable child and his adolescence had no relevant issues. At 18 years he went to college and took a degree in economics. During that time he met his future wife with whom he would marry after he began working as an economist in a private company at the age of 24, and they had one son. His marriage lasted until 13 years ago when he got divorced and started living alone and after 3 years he also retired from his work.\nSix months before the beginning of symptoms the patient had a stroke and was admitted at the neurology inpatient service. Computed tomography (CT) scan and brain magnetic resonance imaging (MRI) revealed generalized cerebral atrophy with multiple subcortical biparietal lacunar infarctions (), a lacunar infarction in left putamen () and an ischemic lesion at the cerebral trunk evolving the right median portion ().\nAt the neurology inpatient service, he started taking acetylsalicylic acid 100 mg/day and irbesartan/hydrochlorothiazide 150/12.5 mg/day for a diagnosed hypertension. He was already taking simvastatin 20 mg/day for dyslipidaemia. His medical history also revealed that he had been smoking about 30 cigarettes per day for the last years but no illicit drugs consumption.\nThe patient was resistant to receiving treatment in our inpatient facilities so he was admitted to our day hospital for psychopathological compensation. On the mental examination at admission he presented with good appearance, was alert, cooperative, oriented in time and space, attention procurable but difficult to maintain, and easily irritable, and had elevated mood. He was unable to stay sited and gesticulated more than usual when talking, according to his niece.\nThe patient had pressure of speech and thoughts race with megalomaniac ideas of grandiosity. There was no hallucinatory activity and patient had no insight or critical appraisal for his clinical situation. Neurological examination revealed a stooped, stiff posture with the head and neck bent forward, dysarthric speech, and discrete hemiparesis in the right hemibody.\nWe ran a brief test battery to exclude other organic causes, including blood chemistry, thyroid function, folic acid, vitamin B12, C-reactive protein, summary analysis of urine type II, coagulation studies, illicit drugs on urine and alcohol in blood, EEG, chest radiography, HIV, HCV, and HBV viral markers, and syphilis serology, which revealed no significant alterations. He also had a brief screening neuropsychological assessment, scoring 29 points in the Saint Louis University mental status examination (SLUMS), demonstrating apparently normal cognitive functioning (normal score range for high school education patient between 27 and 30) [, ].\nThe patient started pharmacological therapy with diazepam 10 mg/day, olanzapine 10 mg/day, and sodium valproate 1000 mg/day. After a month of inpatient he was asymptomatic, with therapeutic plasmatic levels of sodium valproate (70 mg/L), was discharged, and maintained regular observations in our outpatient clinic.\nAfter 4 months he presented with hypomanic symptoms, so we made adjustments in pharmacotherapy to olanzapine 15 mg/day and diazepam 15 mg/day, maintaining sodium valproate 1000 mg/day that resulted in remission of the symptoms after one week. He remained euthymic in the next 6 months of follow-up till he progressively presented with psychomotor inhibition, terminal insomnia, anhedonia, depressed mood, despair, asthenia, and death thoughts as “a relief from this situation.” We proceeded to another pharmacotherapy adjustment adding bupropion 150 mg once a day and olanzapine and diazepam were slowly reduced each to 5 mg/day. After one month with this therapy he maintained depressive mood; however, the rest of the clinical picture improved and two months later he was asymptomatic.
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A 15-year-old female with a past medical history of obesity presented to the emergency department with a marked 90-degree flexion at the thoracolumbar region. She was able to walk only by using a walker in an unusual manner; she placed her axillae on the hand grips. The patient described constant back pain almost daily for which she took ibuprofen with moderate relief. These symptoms began three years ago following a sexual assault and have progressed significantly. As per the patient's mother, the only time the patient's spine straightened out was during deep sleep. She had no neurologic complaints, specifically denying any sensory or motor deficits, fatigue, ptosis, or any complaints consistent with any form of endocrinopathy. Her family history included siblings with epilepsy, ADHD, and mood disorders.\nThe patient denied any substance abuse, including use of alcohol or cigarettes, as well as being sexually active. She reported no history of mood or psychotic symptoms and no suicide attempts.\nDespite the pain, however, the patient was not concerned with her condition. The patient herself was not interested in physical therapy or additional diagnostic testing or counseling despite her mother's encouragement. She refused a gynecological examination due to anxiety following having been a victim of sexual assault; it was unclear the extent of counseling, if any, she received following the assault.\nThe patient was a seventh grader at a local school where she participated in extracurricular activities. She reported being well accepted by her peers. She stated having a good social support network including friends and family. Her parents were separated and she lived with her mother and brother.\nPhysical exam revealed an obese (BMI 39.2) Caucasian female, leaning forward with the spine nearly ninety degrees at the waist. Extremities showed normal strength, sensation, and range of motion. The patient was unwilling to attempt spinal extension. Tenderness to palpation of the paraspinal muscles was present. The rest of the physical examination was unremarkable.\nUpon Pediatric Neurology consultation, no evidence of neuromuscular disease was found. Plain radiography of the cervical, thoracic, and lumbar spine was limited due to her deformity, but no abnormalities were noted. Magnetic resonance imaging of the same was unrevealing. Psychiatric consultation was obtained; they concluded that the patient's symptoms were likely manifestations of Conversion Disorder, following exclusion of organic causes.\nWhile she is currently receiving social services support and physical therapy; she declines psychiatric outpatient care at this time.
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A 67-year-old male with past medical history of diabetes mellitus, opioid dependence, and prostate cancer fell down an embankment while attempting to urinate off the side of a road suffering a twisting injury to his left lower extremity. He was seen at an outside emergency department and found to have a closed, comminuted, oblique fracture of left distal tibia-fibula (see Figures and ). The patient was immobilized in a long-leg plaster splint and subsequently transferred to our hospital for definitive care. His left leg was swollen on presentation and tender to palpation over the distal aspect of the leg and globally around the knee. He had weakness of ankle and great toe dorsiflexion on presentation that was baseline from a previous spinal injury. He also had numbness over the left foot, which was present prior to the injury. Distal pulses were found to be intact. A mild to moderate effusion was present in the knee and the patient was unable to complete a straight leg raise, which was felt to be secondary to pain from the tibial fracture and a possible ligamentous knee injury. Initial radiographs revealed an oblique distal tibia and fibula fracture with concern for extension into the tibial plafond. A computed tomography scan was obtained which demonstrated a nondisplaced avulsion of the Chaput's tubercle and a nondisplaced fracture of the posterior malleolus. Due to the substantial comminution of the fracture as well as ipsilateral fibula shaft fracture, operative intervention was recommended.\nDuring the surgical procedure, the nondisplaced posterior malleolus fracture was stabilized initially with a percutaneous screw directed anteromedial to posterolateral. The knee was then examined which revealed a substantial gap in the suprapatellar region suggestive of a quadriceps tendon rupture. A midline incision was then made 6 centimeters proximal to the superior pole of the patella to the tibial tubercle. A complete rupture of the quadriceps tendon was found on exploration. The tibia fracture was then stabilized with an intramedullary rod inserted after splitting the patellar tendon in standard fashion (see Figures and ). Following completion of proximal and distal locking ankle external rotation stress test was performed to evaluate for syndesmotic widening. As there was no syndesmotic widening, the fibula fracture was left to heal without fixation. Repair of the quadriceps tendon followed. Krackow stitches were placed in the quadriceps tendon with No-2 Fiberwire® (Arthrex Inc, Naples, Florida) and were passed through 3 drill holes from the superior to inferior pole of the patella. The sutures were then tied with the knee in extension. Postoperatively he was placed in a knee immobilizer and a posterior splint and later transitioned to and ankle equalizer boot and kept nonweight bearing for 6 weeks. He was transitioned to a range-of-motion (ROM) brace allowing knee movement to 90-degree flexion at 4 weeks (see Figures and ). At 8 weeks full movement and partial weight bearing were allowed and the knee brace was discarded (see Figures –). At 3 months, he had regained 0 to 120 degrees of ROM and the fracture had healed completely, and at 6 months following surgery, he had discontinued ambulatory aids and had a lower extremity functional score of 84 points.
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A 56-year-old female patient was transferred to our department of critical care medicine, Huashan hospital in Shanghai in June 2016 after she received treatment in a local hospital for productive cough, tachypnea and respiratory distress. She complained of recurrent fever and asymmetric edema of the lower extremities for over 1 month, as well as painful swelling both in the thyroid and labium majus for 2 weeks. In the previous hospital, due to the finding of multiple bilateral cysts which were palpable nodules in her thyroid gland by ultrasound examination, a left lobe thyroid puncture and drainage had been conducted and an aspergillus fumigatus infection was detected. She had a history of systemic lupus erythematosus (SLE) and lupus nephritis for 8 years, and received prednisone treatment for these diseases. But from November 2015, prednisone was switched to methylprednisolone, and hydroxychloroquine has been added because of lupus nephritis aggravation, and tacrolimus has also been added to the medications in the following month. She was also diagnosed with renal hypertension and diabetes induced by steroids, and received antihypertension and antihyperglycemic therapy. She had no history of pulmonary diseases such as chronic obstructive pulmonary disease (COPD), asthma, or any repeated infections, and had no addiction to drugs, smoking or alcoholism. Previous examinations showed no evidence of neutropenia. The ratio of CD4/CD8 was 0.33. Only one aspergillus test was positive in repeated sputum cultures. The galactomannan aspergillus antigen and culture tests in BALF were negative, so were blood and urine cultures including fungi. Our chest computed tomography (CT) imaging revealed bilateral patchy lung opacities in the middle and lower lobes, along with multiple shadows of fibrotic streaks, high-density nodules and mediastinal calcification of lymph nodes (Fig. ). The diagnosis of pulmonary infection was established, and pathogen was highly suspected of aspergillus according to the previous finding of thyroid puncture and drainage. An ultrasound examination showed thrombosis in the bilateral femoral veins and popliteal veins. In addition, a 51 × 16 mm hypoechoic lesion was detected in the left subcutaneous perineal region. We continued voriconazole therapy in a standard treatment dose (200 mg twice a day), but her body temperature was still up to 37.6 °C intermittently. Her white blood cells were 15.61 × 109/L (neutrophils 90.8% and lymphocytes 5.4%), hemoglobin was 93 g/L, and platelets were 295 × 109/L. Except hyperglycemia, proteinuria, and hypoproteinemia, other routine laboratory tests were unremarkable, which including thyroid hormone levels. A neck CT showed findings consistent with a fluid collection in the right thyroid lobe (Fig. ). Cultures of aspirated purulent fluid showed aspergillus fumigatus growth, which was obtained from fine needle aspirations in both thyroid and perineum. Five days after being transferred to our hospital, the patient’s thyroid drainage tube was removed because no further fluid was drained out. We continued the voriconazole dose 400 mg per day as anti-aspergillosis therapy with 16 mg methylprednisolone and 400 mg hydroxychloroquine per day as immunosuppressive therapy, along with a therapeutic 4100 iu q 12 h dose of nadroparin calcium. The patient’s fever was relatively controlled and white blood cells decreased to 10.74 × 109/L (neutrophils 91.7%, and lymphocytes 4.7%). Lesions in the thyroid and subcutaneous labium majus became significantly smaller, and the pain was greatly relieved. On the eighth day of hospitalization, the symptoms had improved and the patient was discharged from our hospital. She continuously took voriconazole orally (400 mg per day) for 6 months, combined with caspofungin for the initial 2 weeks (first day 70 mg, then 50 mg per day). After 1 month of antifungal treatment, she was afebrile and all the clinical symptoms were relieved. The patient is on a follow-up for 1 year and has been free of aspergillosis for 6 months. Hydroxychloroquine treatment ceased in April 2017, and methylprednisolone dose was reduced in a tapered manner.
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A 12.5-year-old girl with a history of neurofibromatosis type 1 presented in January 2015 with a right inguinal tumor mass causing pain and impairment of movement of the right leg. Magnetic resonance imaging showed a heterogeneous solid-cystic tumor mass with focal necrosis, measuring 9.6 cm in the greatest dimension. Tumor biopsy was performed. Histologically, the material comprised focally necrotic tumor fragments, composed of atypical spindle to polygonal cells showing high mitotic activity, forming fascicles with focal palisading (). Immunohistochemically, tumor cells were positive for S-100 and negative for desmin. Considering the aforementioned, the case was signed out as malignant peripheral nerve sheath tumor. The girl was treated with two cycles of chemotherapy according to the CWS protocol and one cycle of vinblastine. The control imaging scans showed an evident progression of the tumor, which was then surgically excised in June 2015. The resected tumor was histologically completely necrotic; thus the previous pathohistological diagnosis could not be confirmed.\nOne year later, in June 2016, after falling down the stairs, a painful lesion of the right parietal region was found. Ultrasound and CT scans showed a soft tissue tumor measuring 3 cm in the greatest diameter, which was penetrating through the skull into epidural space. In July 2016 the tumor was surgically resected (Figures and ). Histologically, this tumor was composed of aberrant vascular, focally anastomosing spaces covered with atypical endothelial cells showing prominent nucleoli and high mitotic activity (Figures and ). Tumor infiltrated through the bone (). Immunohistochemically, the tumor cells were diffusely positive for CD31 (), CD34, and Factor VIII. The pathohistological findings were consistent with the diagnosis of angiosarcoma. This lesion of the scalp did not contain any spindle cell areas which could correspond to MPNST nor did it show connection to any peripheral nerve; therefore it was considered a de novo lesion, unrelated to previously diagnosed and treated MPNST of the right inguinal region.\nIn September 2016 the patient presented with recurrent MPNST of the right inguinum, measuring 2,5 cm, which led to the reintroduction of chemotherapy according to CWS protocol. After the third cycle of chemotherapy, in December 2016, a MR scan was performed, showing no evidence of previously described tumor mass.\nIn March 2017, 26 months after the initial diagnosis of MPNST of the inguinum and 9 months after the diagnosis of angiosarcoma of the scalp, the patient had no evidence of tumor masses. She is under the regular follow-up care.
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A 20-year-old male presented with painless right fronto-temporal forehead mass that was rapidly enlarging over a 4-week period. One month prior to presentation, our patient experienced intermittent headaches localized to the right fronto-temporal area unrelieved with analgesics. Our patient also noticed a rapid mass growth in the fronto-temporal area which upon was observed to be 5 cm × 5 cm, non-tender, and soft. Physical, neurological and laboratory assessments were all within normal limits.\nA computed tomography (CT) scan of the head 1-month after initial presentation revealed an aggressively appearing 5 cm × 5 cm soft tissue mass that was lytic and expansile involving the right frontal bone (Fig. ). The lesion also involved the occipital bone with extension into the central skull base, nasal cavity and right nasal bone. Given the evidence of bone expansion and ground-glass appearance involving the calvarium, diagnosis was determined to be FD. Two weeks later, MRI studies revealed an aggressively enhancing 11 cm × 8 cm soft tissue mass with loculated fluid levels in the right frontal bone (Fig. ). Extensive destruction of the outer table of the skull was noted with severe thinning of the skull inner table. Findings were thought to be consistent with ABC formation. Extensive bony involvement was noted primarily in the anterior and central skull base, but also in the occipital calvarium. Extension to the right zygoma and orbital walls with narrowing of the bony orbit was also visualized.\nFour days later, the patient was admitted to the hospital for immediate drainage of the enlarging cystic mass on the right forehead and considered for either biopsy or excision of the skull lesion the following day. Cytology following cystic drainage revealed signs of acute inflammation without malignant cells. Upon admission, a CT maxillofacial scan with contrast revealed multiple areas of ground-glass appearance with extension of the skull base and decreased right optic canal.\nChest x-ray revealed a destructive lesion in the posterolateral right fourth rib with associated soft tissue component consistent with FD. A CT of the chest revealed cortical thickening and ground-glass appearance of the right fourth rib (Fig. ). A lytic lesion was noticed in the posterolateral fourth rib with a soft tissue component and cortical thinning adjacent to the area of FD appeared consistent with ABC. MRI of the chest revealed a 7 cm × 3 cm complicated cystic lesion within the right fourth rib with fluid levels consistent with ABC (Fig. ). The skull lesion represented the most accessible site for biopsy and possible excision. For completeness, a bone scan was performed to evaluate other areas of involvement and remarkably the scan revealed increased uptake in the right frontal region, right fourth rib and in the right upper extremity. X-rays of the right upper extremity revealed non-expansile ground-glass process within the humerus and proximal one-third of the radius consistent with a history of FD with ABC formation (Fig. ). The patient denied right extremity pain and was not tender to palpation along upper extremity.\nThe patient underwent a right frontal craniotomy for resection of dysplastic bone, removal of cyst and soft tissue tumor, and epidural decompression as a part of a joint effort between neurosurgery and plastic surgery. After peeling away the scalp, a large cystic component was visualized and removed within the lytic portion of the right frontal bone. Soft tissue components involved with the capsular mass were resected including areas of pericranium and temporalis muscle. A soft tissue component was also visualized to be lining the dysplastic lytic portion of the right frontal bone and was resected. The lytic bone along with soft tissue components lining the dura were then resected resulting in the final appearance of bare dura. Pathology of the right frontal capsular mass, pericranium, temporalis muscle and lytic bone were consistent for FD with secondary ABC. At the three-week follow up in clinic, the patient was well and had a noticeable head deformity. At the six-month follow-up, the patient demonstrated clear indications of proper recovery with plans for cranioplasty of the right frontal region.
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A 75-year old Caucasian lady presented with acute onset of painless visual loss in her left eye, which she noted on waking up that morning. She denied any associated headaches, jaw claudication or any clinical symptoms suggestive of temporal arteritis. Past ophthalmic history was not significant apart from one episode of transient visual loss in the left eye of about 5 minutes duration with zigzag lines three months earlier. This was accompanied by spontaneously resolving short-duration headache. The general practitioner diagnosed an episode of migraine with no further investigations or recurrence. She had treated essential hypertension and suffered especially in cold weather with Raynaud's phenomenon for 20 years; this had worsened in severity in the last few months.\nOn examination visual acuity of 20/20 in the right and CF (counting fingers at 0.5 m) was noted in the left eye with a left relative afferent pupillary defect. Anterior segment examination was unremarkable with normal intraocular pressures. Dilated fundal examination showed a cherry-red spot in the left foveal area. No visible arteriolar embolus was noted (Fig ). Apart from presence of two cotton wool spots in the right eye the fundal examination was unremarkable (Fig ). Superficial temporal arteries were palpable, non-tender and not thickened or nodular with good flow. Cardiac examination & carotid artery auscultation was unremarkable. A clinical diagnosis of left acute central retinal artery occlusion with cotton wool spots in the right eye led to a suspected diagnosis of temporal arteritis. Urgent blood investigations were requested but the ESR, CRP, platelets counts and liver function tests were within normal limits. Fundus fluorescein angiography was carried out on the third day showing no evidence of choroidal ischaemia (Fig and ). She was initially started on 80 mg of oral prednisolone daily but with availability of all the blood tests, the angiogram features and lack of any clinical symptoms, the steroids were stopped after 3 days as temporal arteritis was deemed unlikely. She was commenced on 150 mg of aspirin. A closer examination of her hands showed tethered skin with spindly fingers. She was duly referred for a rheumatology opinion to rule out any vasculitic aetiology linking her hands, Raynaud's & ophthalmological features.\nFurther investigations revealed a positive ANA's at 8.1 U (0–1.0 reference range) with a positive anti-centromere antibody and a negative anti-Scl-70 and anti-ds DNA antibody. X-rays of the hands did not reveal any significant calcinosis or erosions. Barium swallow was unremarkable but echocardiography showed mild concentric hypertrophy of ventricular walls consistent with long-standing systemic hypertension.\nMild non-flow limiting plaque was also detected on coronary angiography. Her pulmonary hypertension was attributed to her cardiac status with atrial fibrillation and systemic hypertension rather than connective tissue disorder related. Carotid duplex scans revealed minor calcific plaques with no significant stenosis in either carotid arterial system. She remains under joint rheumatology and ophthalmology review on immunosuppression with methotrexate 10 mg per week, prednisolone 7.5 mg daily and anti-platelet therapy with no further visual symptoms after 12 months of follow up.
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A 60-year-old man visited the emergency room with projectile vomiting that had persisted for five days. There was a palpable mass located in the epigastric area. Seven months earlier, the patient presented with hematuria and was diagnosed with bladder cancer (). No definite abnormality in the stomach was seen on an initial image (). A pathological examination obtained from the initial diagnosis reported a poorly differentiated infiltrating urothelial carcinoma as a clear cell variant. Subsequently, the patient had undergone systemic chemotherapy and locoregional radiation therapy for bladder cancer. Due to the new symptoms, an abdominal computed tomography scan was performed with the use of a 64-channel multidetector CT (LightSpeed VCT; GE Healthcare, Waukesha, WI) scanner for the precontrast phase and portal phase after the administration of an intravenous iodinated contrast agent (Ultravist; Bayer Schering Pharma, Berlin, Germany). Axial and coronal reformatted images were obtained with a 5 mm thickness. The primary bladder tumor mass had markedly regressed in extent and size with residual tumor infiltration to the right pelvic side wall. The stomach showed diffuse and marked gastric wall thickening from the gastric cardia to the antrum (). Subsequently, gastroduodenoscopy was performed and there was an approximate 8 cm segmental infiltrative submucosal lesion resulting from luminal narrowing from the lower body to the pyloric ring. There was no ulcerative lesion in the involved mucosa. An endoscopic biopsy was performed, but only inflammatory neutrophils were seen. An upper gastrointestinal (GI) series was performed that revealed marked mucosal thickening from the gastric lower body to the pyloric antrum. There was abrupt narrowing in the gastric antrum with rigidity and loss of peristalsis, producing a linitis plastica appearance (). To relieve symptoms and to provide pathological confirmation, a feeding jejunostomy with a loop ileostomy and multiple biopsies were performed. On the operative field, multiple nodular lesions were seen in the stomach with direct invasion to the transverse colon. In addition, multiple seeding masses were seen in the ileum, greater omentum and mesentery. Multiple biopsies were performed for the stomach, transverse colon and multiple seeding masses located in the ileum, greater omentum and mesentery. The biopsy specimens of the stomach and the seeding masses were infiltrated by numerous poorly differentiated malignant cells with eccentric nuclei and moderate to abundant cytoplasm (seen at a magnification of ×200) (). Immunohistochemical analysis showed positive staining for cytokeratin (CK) 7, CK20, high-molecular-weight cytokeratin (CK34BE12) and p63 () and negative staining for CK20. The stomach tissue was pathologically confirmed as being poorly differentiated, with the presence of an infiltrating metastatic urothelial carcinoma confirmed by the use of special stains and immunohistochemical studies.
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We present a 43-year-old man with a past medical history only significant for a prior splenectomy who was admitted to the hospital due to right upper quadrant pain for two days. This was described as a dull “liver pain” in the right upper quadrant area. On physical exam, there was evidence of a midline scar, the abdomen was soft with mild tenderness to palpation of the right upper quadrant and the liver span was approximately 10 cm in the mid-clavicular line by percussion. A complete blood count and a basic metabolic panel were normal; however, alanine transaminase (ALT) and aspartate transaminase (AST) showed a mild elevation of 66 U/L and 51 U/L, respectively. Serum bilirubin levels and alkaline phosphatase levels were within normal limits. Due to the reported complaint of right upper quadrant pain and the associated abnormal liver function tests, an abdominal ultrasound (US) was ordered. This showed fatty liver disease and a left liver lobe isoechoic liver mass. A computed tomography (CT) triple phase abdomen scan was done demonstrating a 2.5 cm exophytic mass in the liver in segment 2 (Figure ). The next day of admission, the patient’s pain improved with analgesia. As no clear diagnosis was made, he was later discharged with an intention to perform an elective abdominal magnetic resonance imaging (MRI). This MRI revealed a single mass in segment 2 of the liver, with features of a hepatic adenoma (Figure ). The surgical team was consulted and evaluated the patient and an elective percutaneous liver biopsy was performed. Examination of hematoxylin and eosin (H&E) stained sections revealed histological evidence of splenic tissue with distinct red and white pulp areas, with evidence of passive congestion (Figure ). The red pulp included thin-walled venous sinusoids that were congested with red blood cells that were positive for CD8 stains (Figure ), with surrounding macrophages and few lymphocytes. The white pulp included thickened meshwork of cords showing arterioles sheathed by predominantly small T lymphocytes (CD3+) and scattered B-cell aggregates (CD20+), consistent with splenic Malpighian corpuscles (Figure ). On further questioning, the patient reported he had an exploratory laparotomy with subsequent emergent splenectomy at the age of 16 years due to a motor vehicle accident which caused a splenic rupture. As the patient was diagnosed with hepatic splenosis and was at this point asymptomatic, his benign diagnosis was explained, and no further workup was needed.
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The patient is a 50-year-old female who had a 4-year history of left lumbar radiculopathy which was precipitated from a lifting injury that did not resolve following L4-5 microdiscectomy. She had previously been unsuccessfully managed with epidural steroid injections and multimodal analgesics. A nerve conduction study was unremarkable for any pathology. She was diagnosed with failed back surgery syndrome and counseled regarding her treatment options, including spinal cord stimulation. She elected to pursue spinal cord stimulation with the Nevro Senza HF10 system. As part of her evaluation for SCS placement, the patient was seen at the behavioral medicine clinic and underwent presurgical psychological testing and evaluation by a board-certified psychologist. Her psychological assessment profile suggested a high likelihood of a good postoperative outcome. She had a history of depression and anxiety, both of which were stable and under medical management. The patient underwent an uneventful SCS trial with near 100% relief of her back and leg pain and wished to proceed with permanent implant. Her permanent placement procedure was uneventful with leads placed at the same levels as her trial leads (.) with the tip of the right lead at the top of the T8 vertebral body and left lead tip at the mid T9 vertebral body. The device was activated in the post-anesthesia care unit with bipole setting on electrodes 10 and 11.\nThe first day following her procedure, the patient noted a buzzing or a chirping sound predominately in her left ear as well as vertigo, intermittent involuntary left facial twitches, and perioral numbness, all of which were new to her. She also reported nausea, vomiting, and diarrhea, which she has attributed to anxiety in the past. She was subsequently evaluated by ENT around 4 weeks postoperatively and underwent an audiological evaluation with no abnormal findings. There was concern that the tinnitus could be related to her stimulator. She also later complained of implanted pulse generator (IPG) site pain and stinging sensations. Attempts at reprograming her SCS system with a bipole settings on leads 4 and 5 failed to resolve her ongoing neurologic symptoms. The patient was subsequently advised to deactivate her system to see if her symptoms would improve. Two days after deactivation of her system, the patient reported complete resolution of her symptoms. She was again evaluated and spine radiographs were performed which demonstrated unchanged position of her SCS leads. She was not interested in reactivating her system to assess for return of symptoms. The SCS system was subsequently explanted. At the time of explant, there were no visible defects in the SCS system.
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A 60-year old female underwent a phase III Oxford UKA [Biomet UK Ltd, Bridgend, United Kingdom] in 2006 for antero-medial osteoarthritis. A minimally invasive medial para-patellar approach was used and medium sized femur, 44 X 28mm tibia and 3mm meniscal bearing insert were implanted. She had an uneventful post-operative recovery. She was completely asymptomatic and was discharged from the follow-up at two years following the surgery with no symptoms and a range of motion of 0 to 130 degrees.\nShe presented to the Accident and Emergency (A&E) department in April, 2013 with history of a sudden onset of pain and swelling in the same knee. She heard a ‘pop’ in the knee while standing and did not report any obvious injury to the knee. On clinical examination, she was haemodynamically stable and afebrile and there was moderate effusion in the knee. The range of motion was from 30 to 60 degrees and she was unable to weight bear through the knee due to pain. The radiographs of her knee in the A&E department raised a suspicion of posterior dislocation of the polyethylene insert (). There was no evidence of loosening of femoral or tibial components.\nThe white cell count and CRP were normal, excluding an acute infection. She was admitted to the ward and surgical exploration was planned for the following day, with the view of changing the polyethylene insert or to revise the components if they were loose or damaged. The knee was opened through the previous scar of medial para-patellar approach. Intraoperatively, both the femoral and the tibial components were found to be well fixed with no scratches and rest of the knee did not show any evidence of osteoarthritis. The polyethylene insert was found to be fractured through the middle (). The anterior half was sitting on the tibial component and the posterior half was dislodged into the posterior compartment of the knee, stuck to the posterior capsule. It was not possible to retrieve that fragment from the front.\nThe operating surgeon had two options; either to remove both the components and then retrieve the fragment from the front or to retrieve it through a posterior incision. Eventually, rather than making a separate skin incision, the previous skin incision was extended and medial skin flap was raised to expose the postero-medial aspect of the knee. Deep fascia was incised to expose the pes anserinus. An interval was created between the pes anserinus and the medial collateral ligament anteriorly and medial head of Gastronemius posterioly (). Capsulotomy was performed through this\ninterval and the dislodged part of the polyethylene insert was retrieved through the opening. The polyethylene insert showed some pitting and whitening and it seemed to have fractured cleanly through the thinnest part (). A new polyethylene of the same size insert was implanted. The patient made uneventful recovery following the surgery. At two year follow-up she was completely asymptomatic with the range of knee movement from 0 to 125 degrees.
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A 40-year-old woman was referred to our Urology Department with a diagnosis of urinary sepsis and bilateral hydronephrosis; radical hysterectomy, bilateral salpingectomy with ovarian preservation as well as pelvic and para-aortic lymphadenectomy for squamous cell carcinoma of the cervix had been performed 8 years earlier. The patient received adjuvant concurrent cisplatin-based chemo radiotherapy up to a total dose of 50.4 Gy; next she underwent periodical surveillance examinations which resulted negative for long term. Twenty months earlier a CT scan revealed a right-sided pelvic recurrence involving the right ureter with concurrent hydronephrosis; treatment of the recurrence required 3 further cycles of Cisplatin, Paclitaxel and Bevacizumab, obtaining a partial response at 18F-FDG PET/CT, followed by additional cycles of Bevacizumab every 3 weeks as maintenance treatment. A right ureteral stent was placed with the retrograde cystoscopic approach at the time of recurrence diagnosis to treat the associated hydronephrosis and had already been substituted twice using the same approach without problems employing hydrophilic long-permanence stents.\nAt time of the admission, a urinary tract infection sustained by Enterococcus was under treatment with Linezolid; abdominal sonography revealed bilateral hydronephrosis, with the presence of the curled upper extremity of the stent inside the right kidney collecting system, but the lower extremity was not detected in the bladder. Substitution of the right ureteral stent was planned to treat the sepsis.\nAt cystoscopy the distal end of the stent was not visible inside the bladder, while a fistula orifice covered with fibrin was evident on the right side of the bladder trigone, so the planned procedure was suspended.\nA 64-detector row multiphase CT examination of the abdomen and pelvis was performed, showing a cross-over course of the ureteral stent from the right side to the left at the level of the sacrum, which was more evident with 3D rendering (Fig. ), presence of gas inside the right pyelocalyceal system, along the side of the upper coil of the stent (Fig. ) with displacement of the distal third of the stent and its lower loop inside the rectum, and right-sided pelvic tumor recurrence (Fig. ). A delayed scan revealed the presence of iodinated contrast material inside the rectal lumen, consistent with urinary fistulization. Subsequent treatment consisted in bilateral percutaneous nephrostomy in the prone position to relieve hydronephrosis and digital extraction of the stent from the rectal ampulla; an indwelling bladder catheter was placed. Two days later a left excluding colostomy was performed.
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One patient, the 57-year-old lady with schizoaffective disorder (see under results Case 1) experienced prolonged paralysis of her muscles during anesthesia due to abnormal CHE function. This was the most remarkable but rarely occurring finding among all ECT patients reported here. Butyrylcholinesterase, also called CHE, is an enzyme synthesized in the liver, which metabolizes neuromuscular blocking agents that are used in anesthesia, such as succinylcholine (). The latter or other muscle relaxants are essential during ECT to avoid unwanted muscle cramps induced by the seizure. Just one arm is kept without relaxation by a pneumatic cuff to visualize the ECT effect by an increase in muscle tone. The action of succinylcholine is short in onset and is used during a rapid induction of anesthesia, which at a dose of 1 mg/kg body weight is about 45 s, with 10–15 min duration (). This has to be seen in the light that wide variations in succinylcholine efficacy during ECT anesthesia may require a dose adjustment of 2 SDs either above or below the mean standard dose of around 1 mg/kg body weight ().\nNeuromuscular blockade can be affected by mutations in the CHE gene, where succinylcholine neuromuscular blockade is prolonged (5–10 min) by heterozygosity, while homozygosity may prolong blockade for several hours (). This butyrylcholinesterase deficiency may go undiagnosed for decades until succinylcholine is used. Studies in Europe estimate a 4% prevalence of congenital serum CHE deficiency in the population (). The neuromuscular blockade results in extended muscle relaxation and thereby impairs respiratory function after anesthesia as used for ECT (). The pathological dibucaine inhibition test in the patient reported here suggested that the adverse drug effect had a pharmacogenetic basis (). The value of inhibition, as well as moderate prolongation of muscle relaxation, suggests heterozygosity being present in the given patient. As a result, the rapid action of an anesthetist to prolong sedation and start manual respiration was required to prevent physical harm to the patient.\nIn summary, this event of prolonged neuromuscular blockade was not related to ECT per se but was life-threatening by affecting breathing functioning. This required proper management by an experienced anesthetist. The event may stimulate the discussion about optimizing adjunctive medication regimes in ECT anesthesia, where no consensus exists regarding the optimal anesthetic and muscle relaxing drugs ().
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A 7-year-old Hispanic female with an uneventful birth history presented to our referral institution for workup and management of balance and gait disturbance and an inability to walk that was first noted at 3 ½ years of age. She was noted to have increasing “clumsiness” in the months leading to her inability to walk. She was also noted to have chronic renal disease and liver disease with hepatomegaly and enlarged kidneys in the first 4 years of life. Her inability to walk was previously attributed to severe pain throughout her body.\nAt 6 years of age, she developed bilateral lower extremity fractures and an upper extremity fracture while attempting to stand. She was noted to have bowing of her lower extremities and elevated alkaline phosphatase and was subsequently diagnosed with rickets that was believed to be the result of chronic kidney disease. Shortly thereafter, she was referred to a local medical center where she underwent liver biopsy, kidney biopsy, and muscle biopsy. Her liver biopsy revealed cirrhosis with minimal chronic inflammation and her kidney biopsy revealed nonspecific glomerular and tubular changes with some parenchymal fibrosis. Her muscle biopsies revealed severe myopathic changes with myofiber atrophy. She was noted to have mitochondrial DNA quantification on her muscle biopsy which was reduced and less than 29% of controls. She was subsequently diagnosed with mitochondrial depletion syndrome.\nWhen her weakness and strength worsened further, she was referred to our institution’s mitochondrial clinic where she underwent additional workup. Extensive metabolic evaluation revealed an elevated succinylacetone which led to a diagnosis of HT-1. Analysis of the FAH gene revealed a homozygous splice mutation known to be associated with HT-1. She ultimately underwent treatment with dietary modification and 2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione (NTBC), but she was immediately referred for cadaveric liver transplantation after further workup revealed imaging findings consistent with hepatocellular carcinoma. Following this initial pre-transplant treatment, her condition improved substantially with significant improvement in her amino acid profile, improvement in her mental status, and reduction in her alpha-fetoprotein from 2320 ng/mL to 1585 ng/mL. Despite this metabolic improvement, she required liver transplantation as a result of her hepatocellular carcinoma. Since this lesion was felt to be adjacent to major blood vessels and liver transplantation was not ideal without improved nutrition and rehabilitation, she underwent transarterial chemoembolization for a 1.5 cm × 1.6 cm lesion in her liver (Figure ) after which time she had further reduction in her alpha-fetoprotein to 511 ng/mL. After continued improvement in nutrition and physical conditioning, she ultimately underwent liver transplantation 4 mo after her diagnosis was made. Explant of her liver revealed a yellow-orange and nodular liver, and histology revealed cirrhosis and multinodular well-differentiated hepatocellular carcinoma with bile duct proliferation felt to be consistent with tyrosinemia (Figure ).\nHer immediate postoperative course was unremarkable and, following transplant, she had further improvements in her cognitive function, nutrition, and physical conditioning. Within 6 mo, she was ambulating without assistance and attending regular school without difficulty. Her rickets had also improved and resolved with her bone mineral density Z-score in her hip improving from -4.1 prior to transplant to -1.1 fifteen months following transplant. Her renal function improved with her estimated GFR before and 6 mo after transplant noted to be 75 and 121 mL/min per 1.73 m2 respectively. She had no recurrence of tumor on follow-up imaging obtained 2 years following her transplantation, and her alpha-fetoprotein was normal during this time.
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A 6-day-old term male infant was brought to the emergency department by his parents for evaluation of irritability on passive movement of the right hip.\nThe infant was born via spontaneous vaginal delivery to a 28-year-old gravida 2 para 1 mother at 38 weeks. Pregnancy was complicated by group B Streptococcus colonization which was not known during the delivery so no antenatal prophylaxis was performed. He was 2800 g at birth, and received routine care in the delivery room. Metabolic screening tests and bilirubin controls were performed as routine by heel samples and were normal. Physical examination revealed an instability of the left hip, and he was discharged from the hospital after 72 hours with the indication to anticipate the ultrasound of the hips within the second month of life.\nOn the day of presentation, his parents noted a reduction of the movements of the lower right limb, so they referred him to the emergency department. Physical examination at the time of presentation revealed an afebrile infant, with vital parameters in the rule except for the absence of active movement and irritability to passive mobilization of the lower right limb. The baby was holding the right leg flexed with slight abduction and external rotation. The right hip was also noted to be slightly swollen without skin hyperemia or heat to the touch.\nThe complete blood count was unremarkable, hematocrit 44%, platelets 273,000/L, and white blood cell count 13180/L, C-reactive protein was 13.3 mg/L (normal values <10 mg/L). The presence of fractures was excluded by radiography of the pelvis and the right femur. Ultrasound documented an intra-articular circumferential effusion, with echogenic content, in the right coxo-femoral area, with a maximum thickness of 3.4 mm ().\nThe baby was admitted to the general pediatrics service for additional evaluation and management. After blood and urine cultures were obtained, antibiotic therapy was started with endovenous amikacin and ceftazidime. A magnetic resonance was performed confirming the presence of endoarticular effusion in the right coxo-femoral area with articular capsule relaxation and signal characteristics compatible with the presence of corpusculous component. No sign of adjacent bone or soft tissue infection was present. These findings were suggestive for arthritis, so, during the second day of hospitalization, ecoguided drainage of intrarticular fluid was performed with the suction of 1 mL of serous fluid.\nThe culture of the articular fluid was positive for Staphylococcus epidermidis 500 UFC/mL, while the urine culture was positive for group B Streptococcus 500 UFC and the blood culture was negative. From the third day of hospitalization, there was a clear improvement in the right hip objectivity, with complete normalization of mobility and disappearance of joint effusion at the ultrasound repeated after 7 days of antibiotic therapy. The C-reactive protein was negative at the 6th day of hospitalization. Antibiotic therapy with endovenous amikacin and ceftazidime was stopped after 14 days and the infant was resigned with orthopedic follow-up. At 1 week, 1 month, 3 and 6 months follow-up visit after discharge his conditions were good with normal right hip objectivity without pain or irritability to active or passive mobilization of the lower right limb.
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We report here the case of a 83-year-old white man with a two months history of a painful lesion in the gingiva followed by hematoma in the right then left palatine tonsil with spontaneous bleeding (). He complains of progressive odynophagia, dyspnea and weight loss. He has no antecedent beyond a benign prostatic hyperplasia. Complete blood cell count showed 12.3 g/dL hemoglobin and 400/mm lymphocytes. The coagulation factors are normal. A cervico-thoraco-abdominal computed tomography scan brings out tumoral syndrome in the two palatine tonsils with central necrosis (). Furthermore two necrotic lymph nodes in right level Ib and right level IIa and one non-necrotic lymph node in left level IIa were present ( and ). The patient underwent bilateral tonsillectomy and nodal puncture in right level IIa. Histological diagnosis has been made according to the 2002 World Health Organization classification and a pathological expert second opinion has been asked in another reference center. The final pathological findings conclude angiosarcoma in the gingiva, both palatine tonsils and IIa right lymph node. Microscopic examination reveals the presence of a tonsil whose epithelial structures of the surface coating, as that of the crypts, are colonized by many polymorphic leukocytes, predominantly lymphocytes but also include some unaltered neutrophils. At the lymphoid apparatus exist prominent germinal center follicles. Sampling also includes at its periphery small lobules of seromucous glands and striated muscle bundles. Are also observed neoplastic structures that include vascular cavities bordered by a more or less dense and thick collagenous fibrosis, with a coating of atypical nuclei cells or tumor foci with rounded or globular cells whose cytoplasm is eosinophilic and whose nuclei contains clear chromatin with a prominent central nucleolus, often atypical (). In some places the two (cavity and compact) aspects are in continuity. There are morphologically abnormal mitosis. There are six mitoses per ten fields at a magnification of 400. The tumor necrotic foci are rare. Immunohistochemical techniques were performed showing the following marks: marking of tumor cells for the CD31 antigen (clone JC/70A, Dako, 1/50) and CD34 (Clone QBEND, Cell Marque, 1/50). Marking of a part of the lesion for Actin (clone 1A4, Dako, 1/300) but not for BNH9 (clone Bnh9, Dako, 1/20). No marking for HHV8 (clone 13B10, Ventana, Prediluted). Furthermore the identification of KL1 (clone KL1, Immunotech, 1/200), epithelial membrane antigen (EMA) (clone E29, Dako, 1/200), CK5/6 (clone D5 16/B4, Dako, 1/50) pancytokeratin and P63 (clone 4A4, BIOSB, 1/100) shows no argument for carcinoma. Markings for the CD45 (clone 2B11 +PD7/26, Dako, 1/100), CD3 (polyclonal, DBS, 1/25) and CD20 (clone L26, THERMO SCIENTIFIC, 1/250) antigens do not argue for lymphoma. It is a grade two angiosarcoma (score 5 including 3 for differentiation, 1 for mitosis, 1 for necrosis). In the meantime the patient presents recurrent macroscopic hematuria, which require hemostatic surgery and several hospitalizations for transfusion. A month after the diagnosis a progression of the gingival tumor with bone involvement and a right tonsillar relapse were noted. Chemotherapy with paclitaxel 90 mg/m every week is initiated as first-line treatment. After five injections, deterioration of the general condition prevents further treatment. The patient underwent three sessions of hemostatic radiotherapy for oral bleeding, and likewise extreme exhaustion prevents further treatment. He died, seven months after the first symptoms and four months after the diagnosis of angiosarcoma, of gastrointestinal bleeding and mediastinal compression.
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A 15-year-old boy had complained of motility limitation in the right eye since a young age. His visual acuity was 20/20 in each eye, although an ocular motility examination revealed markedly limited abduction and mildly limited adduction in his right eye (). On attempted adduction of the right eye, globe retraction () with narrowing of the palpebral fissure was observed, and there mild upshoot and downshoot were also observed (). The palpebral fissure of the right eye was slightly widened on attempted abduction. An alternate prism cover test revealed a 16 prism diopters (PD) right esotropia (ET) in the primary position, 25 PD ET in right gaze, 10 PD ET in left gaze at distance fixation, and 4 PD ET at near fixation. He assumed a compensatory face turn to the right and did not complain of diplopia. No living member on either the paternal or maternal side had a squint. Duane's retraction syndrome was inferred as the diagnosis until we noted that the patient's right eye had slight enophthalmos. Hertel's exophthalmometry revealed a 1.5 mm difference between both eyes and the margin reflex distance 1 was 0.5 mm in the right eye. Computed tomography of the orbits was performed and demonstrated an old medial orbital wall fracture with entrapment of the medial rectus muscle and surrounding tissues (). However, there was no history of trauma or forceps delivery according to the patient or his parents. A forced duction test under topical anesthesia was definitely positive in the right eye. The patient's ocular motor impairment was concluded to have arose from a long-term medial orbital wall fracture and was diagnosed as 'pseudo-Duane's retraction syndrome'. Because open reduction surgery for an old orbital wall fracture would be very difficult, and fruitless for this patient, we decided only to perform surgery on the eye muscle. The 5 mm recession of the right medial rectus muscle was successfully performed in order to correct the patient's head turn and esotropia. Neither structural anomalies nor fibrosis of the medial rectus muscle was observed during surgery. Postoperatively, the patient had orthotropia in the primary position, and the anomalous head posture disappeared, though there were still some limitations in both abduction and adduction in the right eye one year after the surgery.
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An 18-year-old woman, 2-0-1-1, had experienced irregular vaginal bleeding over the course of 6 months and was admitted to the hospital with confusion for 4 hours. After admission, the patient continued to be confused and experienced frequent vomiting. Her pupils were round and of equal size, with sensitivity to light. She complained of a stabbing pain in the neck, and the muscle strength of the extremities was grade V. Head computed tomography (CT) showed multiple hemorrhages in the right temporal-parietal lobe and occipital lobe, right temporal-parietal hematomas, ventricle compression, and midline shift (Fig. ). As the patient was young and the bleeding site was atypical, cerebrovascular malformation could not be excluded. After preoperative examination, evacuation of the hematoma in the temporal-parietal lobe and decompressive craniotomy was performed under general anesthesia. During the surgery, the intracranial hematoma was removed. We did not observe vascular malformation. Because intraoperative intracranial pressure was high, we removed the patient's skull. No special treatment was provided as the volume of the posterior occipital hematoma was small. Postoperatively, the patient had a clear mind and was able to speak fluently. The extremities were normal, and she could eat and communicate normally. Irregular vaginal bleeding was still seen, and no abnormality was found by gynecologic ultrasound. One week after the surgery, the patient experienced frequent vomiting and severe headache. CT showed an increased right occipital hematoma, right hemisphere swelling, and high pressure at the decompression window. Based on the patient's symptoms and CT examination, dehydration and conventional therapy were performed. Follow-up CT examinations showed that the occipital hematoma was in the absorption period, and her symptoms improved. To determine the cause of bleeding, we performed digital subtraction angiography that indicated abnormal vessels in the right occipital lobe, which later proved to be the blood vessel of the tumor, and an anterior cerebral artery aneurysm (Fig. ). Pulmonary CT showed an occupying lesion in the chest without a clear nature. Abdomen CT, pelvic ultrasound examination, including uterus, uterine appendages, vagina showed no occupying lesion, Twenty-five days after the surgery, recurrence of the intracranial hypertension was seen. Head CT showed bleeding in the right occipital lobe, with a hematoma over 30 mL. Conventional medication was unable to relieve the symptoms of intracranial hypertension. Hence, we performed craniotomy to remove the hematoma. During the surgery, a purple and red goiter with rich blood transport was resected for pathological examination. Based on the previous medical history, we considered it a choriocarcinoma. Postoperative head CT showed a fresh hematoma in the right frontal lobe. Based on the hematoma volume, we performed conventional therapy. The pathological report suggested brain and lung metastases of choriocarcinoma with total human chorionic gonadotropin (THCG) > 1000 mIU/mL. Histological examination of the hematoma was compatible with a diagnosis of choriocarcinoma. The specimens showed several atypical pleomorphic trophoblastic cells on a necrotic background and some scattered trophoblasts in the hematoma and invading the vessel wall. Immunohistochemistry revealed positive staining for human chorionic gonadotrophin (HCG) the tumor cells, as well as neoplastic cells with a Ki-67 labeling index of 90%, positive immunoreactivity for placental alkaline phosphatase, cytokeratin, and inhibin, and negative immunoreactivity for glial fibrillary acidic protein (GFAP) (Fig. ). However, the endometrial biopsy specimen showed no evidence of chorionic villi, trophoblasts, or decidual reaction. Twelve days after pathological diagnosis, the intracranial hypertension symptoms recurred, accompanied by decline in vision (only light sensation). Head CT showed a fresh hematoma in the left occipital lobe, with a small hematoma volume. We chose conventional therapy, and head CT after 3 days indicated an enlarged hematoma. The patient had a clear mind, and conventional therapy was administered. Head magnetic resonance imaging (MRI) was then performed because we believed that the multiple bleeding sites were caused by brain metastasis of choriocarcinoma and no metastases were seen in other organs (Fig. ). Five days later, the patient asked to terminate the treatment and was discharged. One month later, the patient died of upper gastrointestinal bleeding. The patient and patient's family consented to publication of the case.
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A 56-year-old female smoker had a history of a pleomorphic adenoma in the left parotid gland treated with a superficial parotidectomy at the age of 18. Nineteen years following that surgery, the patient presented with multifocal recurrence. Surgical exploration was undertaken and the tumor was found inseparable from the facial nerve. At that time, the resection was abandoned and the facial nerve was not sacrificed and gross disease was left in the parotid bed. The patient underwent external beam radiation therapy and the size of the tumor remained stable for 10 years on serial computed tomography (CT) and magnetic resonance imaging (MRI) monitoring. The patient had been clinically asymptomatic until she started developing intermittent ipsilateral hemifacial spasms occurring spontaneously and involving all portions of the left facial musculature, which prompted her to return for evaluation.\nRepeat CT scan showed enlargement of avidly and uniformly enhancing solid tumor without areas of necrosis or extracapsular extension with extension into the left stylomastoid foramen, along with suspicious changes in enlarged (15 mm) left level IV lymph node (Figure ). Fine-needle aspiration biopsy of the tumor was suspicious for carcinoma ex pleomorphic adenoma. After a negative systemic metastatic work-up, the patient was brought to the operating room for a radical parotidectomy with facial nerve sacrifice, ipsilateral selective neck dissection (levels I-IV), and a de-epithelialized anterolateral thigh free flap for volume restoration and to enhance wound healing. The vertical segment of the facial nerve in the mastoid was exposed. Primary facial nerve repair was performed using sural nerve grafting from the main trunk to the temporal branch of the facial nerve, nerve to masseter grafting to the dominant midfacial branches of the facial nerve, together with construction of an oral commissure suspension with a fascia lata sling.\nFinal surgical pathology confirmed a 5.2 cm pleomorphic adenoma with a multinodular growth pattern. Well-circumscribed neoplastic nodules of variable sizes were embedded in densely fibrotic connective tissue (Figure ). Nerve bundles were also entrapped in the scar tissue in-between the nodules, but no true perineural invasion was detected. Within the nodules, two foci of early non-invasive carcinoma were noted. Within one nodule a 4 mm focus of malignant cells surrounded by benign epithelial elements was identified. In a separate nodule, an intraductal malignant neoplastic proliferation with an intact benign myoepithelial cell rim was also noted. None of the malignant neoplastic foci showed invasion into adjacent fibroadipose tissue and nerves. Thirteen level II-V lymph nodes were negative for tumor involvement. The primary tumor was staged as rT4N0M0.\nThe hemifacial spasms subsided after surgery, and the patient remains disease free at 6 mo of follow-up. The patient has recovered facial tone but has yet to develop dynamic muscular activity.
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The patient was a 73-year-old Chinese woman with osteoarthritis in both knees. In the recent half year, she had been suffering from intractable right knee pain with failed conservative treatment and prepared for right side TKA. She had a 27-year history of hypertension and her blood pressure was controlled well by medication. She had no other medical history, including smoking history. Her BMI was 24. The physical examination showed a limited range of motion (ROM) of 0°–120° without varus or valgus deformity. Preoperative X-ray showed narrow medial knee joint space and osteophyte formation without vascular calcification (Fig. ). The peripheral pulses and capillary refill were normal, although the preoperative Doppler ultrasound showed arteriosclerosis with plaque formation in the arteries in both legs.\nThe right side TKA with a posterior stabilized design (LPS, NexGen, Zimmer, Warsaw, USA) was performed under general anesthesia. A tourniquet was applied for 70 min at a pressure of 250 mmHg. The whole surgery was completed without any complications and there was normal intraoperative bleeding at the surgical site. The postoperative X-ray showed successful implantation for the right knee (Fig. ).\nHowever, immediately after the surgery, routine peripheral pulse check in the operating room found absent dorsalis pedis artery pulse in the right foot. The patient was closely monitored in the recovery room. After approximately 2 h, there was no improvement in peripheral pulses, capillary refill, and oxygen saturation. In consideration of the high possibility of arterial occlusion, the vascular consultant recommended using 1000 U heparin for anticoagulation and immediate evaluation by arteriography for diagnosis. An emergency arteriography under local anesthesia showed that there was a short segmental occlusion of the popliteal artery (Fig. ). Then the angioplasty was performed with a balloon with a diameter of 5 mm for 3 min. Follow-up imaging showed excellent blood flow although vascular stenosis was still observed in popliteal artery (Fig. ). There was a return of palpable pulses and a normal capillary refill and oxygen saturation.\nAfter the patient returned to the ward, 12 500 U heparin in 50 mL saline was pumped 1 mL/h and activated partial thromboplastin time (APTT) was controlled around 40 s. The peripheral pulses were closely monitored. On postoperative day 2, the patient was allowed to walk with aids. On postoperative day 6, the anticoagulation plan was changed to rivaroxaban 10 mg two times a day and aspirin 100 mg one time a day for 3 weeks orally. The patient was discharged home 2 weeks after surgery without any complaints.\nAt the most recent follow-up in the orthopaedic clinic (3 months after surgery), there were no orthopaedic or vascular complaints. The patient had an ROM of 0° to 125° with excellent muscle strength and could walk without aids for 1 km.
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A 2-year old girl was referred to the Jos University Teaching Hospital in north central Nigeria, with complains of progressive cough and difficulty in breathing in the preceding six months. She was treated at several health facilities for pneumonia and asthma without resolution of symptoms. Patient had no fever or features suggestive of tuberculosis. Pregnancy, delivery, neonatal and infant periods were uneventful and patient had received all immunization appropriate for her age. Examination at presentation showed a child in severe respiratory difficulty necessitating oxygen administration, with Spo2 89–90% at room air and 96% on oxygen by nasal prongs. There was bulging of the right side of her anterior chest wall and markedly reduced breath sounds on the right hemithorax. No features suggestive of congenital heart disease. Chest X-ray showed homogenous opacity continuous with the cardiac silhouette, involving almost the entire right thoracic cavity with a shift of the mediastinum to the left (Fig. ). Echocardiography confirmed a very large well defined mediastinal cyst compressing the right atrium, left atrium and right ventricle (Fig. ). Contrast-enhanced computed tomography scan of the chest showed a well defined large cyst of the anterior mediastinum compressing the right main bronchus (Fig. ). Blood investigations were all normal. A diagnosis of anterior mediastinal cyst was made and the patient had right posterolateral thoracotomy through the fifth intercostals space. Intraoperatively a large tense cyst measuring 20 × 16 × 3.5 cm was noted adjacent to the pericardium and attached loosely to the thymus compressing but not attached to the bronchus. The cyst was unilocular with a thick wall and contained serous fluid (Figs. & ); the cyst was excised en bloc. There was moderate pericardial fluid which was drained by a pericardiostomy. Histopathological sections showed ectopic pancreatic tissues in the wall of the cyst (Figs. , and ). The post operative course was uneventful; the patient has been asymptomatic after a followed-up period of twenty four months.
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A 70 year old man from Greece having Hellenic Nationality, came to the emergency department of our hospital with abdominal pain, anorexia and jaundice. The duration of symptoms prior to presentation was four weeks. Physical examination revealed moderate tenderness on palpation of the hypogastrium. His past medical history included essential hypertension and hyperlipidemia. There was no family history of gastrointestinal diseases. Laboratory studies showed elevated bilirubin and alkaline phosphatase levels and moderately elevated serum carbohydrate antigen 19-9 (Ca 19-9) of 380 U/ml (reference value ≤ 70 Uml). Abdominal ultrasound and computerized tomography scan showed a mass in the head of the pancreas measuring 4.5 cm in size and curative pancreaticoduodenectomy was performed. Histological evaluation of the pancreatic tumor showed an adenosquamous carcinoma which was extensively infiltrative with perineural invasion, involvement of peripancreatic lymph nodes and all the thickness of the duodenum wall. The tumor elicited an intense desmoplastic stromal reaction and areas of necrosis (Figure ). Focal areas of high grade pancreatic intraepithelial neoplasia were seen. The tumor exhibited a biphasic malignant growth identified as well to moderate differentiated adenocarcinoma and well to poorly differentiated squamous cell carcinoma (Figure ). The adenocarcinoma component contained ductal or glandular structures with focal intracellular or extracellular mucin (Figure ). Squamous differentiation was characterized by irregular and infiltrative nests or sheets of polygonal cells with distinct cellular borders, intercellular bridges, eosinophilic cytoplasm and varying degrees of keratinization (Figure ). These two different patterns could be seen separated topographically within the substance of the tumor or intimately admixed. Six of the 15 resected lymph nodes were positive for metastatic tumor which was composed of squamous carcinoma only (Figure ). The immunochistochemical study showed that the tumor cells were positive for cytokeratin AE1 and AE2. Cam 5.2 and Ker 7 were reactive predominantly in the adenocarcinoma component and in few squamous cells (Figure ). Immunoreactivity for CK 5/6 was restricted to the squamous component, while the glandular component was negative (Figure ). A few number of tumor cells were immunoreactive with CEA and Ca 19-9. All tumor cells were negative for Ker 20, chromogranin and synaptophysin. The patient received postoperative adjuvant chemotherapy and he is alive 6 months after surgery.
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A 70-year-old female without significant past medical history presented to the clinic after the results of a routine mammogram revealed the continued presence of a small mass in her right breast. A mammogram dated 3 years prior detected this mass and reported it as small and benign, located inferior to an implant of her right breast. The more recent mammogram findings reported no change in size. The patient was asymptomatic and denied previous history of cancer and no family history of breast cancer, or other malignancies. She denied weight loss, fever, night sweats, or change in appetite. However, she did report mild discomfort with self-palpation to her lower right breast. Her breast implants were placed 28 years ago in Argentina for cosmetic reasons and have not since been revised. Additionally, she reported a long history of smoking tobacco daily.\nTo rule out malignancy, an ultrasound was performed and confirmed the presence of an elongated nodular density benign in appearance. The mass had multiple areas of hyperechoic densities within it and was located at the 8 o'clock position 10 cm from the right nipple. The size was measured to be 3.4 × 1.3 × 3.2 cm, with no evidence of shadowing or implant rupture reported (). The impression of the ultrasound was the presence of a hamartoma, a benign lesion of the breast that corresponded with previous mammogram results. Despite recommendations for a follow-up mammogram at a later date, the patient was referred by her primary care provider for fine-needle biopsy and samples were sent for evaluation.\nBiopsy samples were sent to pathology for analysis using histology, immunohistochemistry, and FISH studies. Histologic sections of the core biopsy fragments showed malignant lymphoma of diffuse pattern. The tumor cells were large in size with anaplastic and focally spindled morphology. Additionally, there were increased mitotic figures and cellular apoptosis. Immunohistochemistry revealed lymphoma cells positive for CD20, PAX5, BCL2, BCL6, and vimentin and negative for CD3, CD5, CD10, cyclin D1, smooth muscle myosin, S100, CD31, CD20, E-cadherin, and keratin. It was determined that the neoplasm had a nongerminal center phenotype with a proliferative index of 80-90%. FISH studies were completed to determine the presence of MYC, BCL2, or BCL6 gene rearrangements. All were negative; however, an abnormal signal pattern suggestive of gains of BCL2 was detected. Overall, testing of the fine-needle biopsy confirmed DLBCL.\nThe patient underwent surgery for lumpectomy of the right breast, as well as bilateral breast implant removal. During the operation, the presence of a calcified capsule surrounding each nontextured implant was noted. Found within the capsules was silicone. It was unclear if the nontextured implants had ruptured prior to surgery or if there was a rupture during the procedure. Both capsules were removed, and silicone was irrigated and aspirated from the sites. The tumor was found to be in direct contact with the calcified capsule but without evidence of capsule invasion into the tumor. The tumor was also widely excised with ample samples sent to pathology for further testing. The patient was given a one-time dose of cefazolin 1 gm IV and hydrocodone for pain management. She was discharged 2 days later with a complaint of moderate breast pain that was being managed well with hydrocodone.\nIntraoperative tissue samples were sent to pathology. The breast lesion was noted to be well circumscribed and consisted of monomorphous cells with large lymphocytic features. No evidence of invasion from the calcified capsule was found. The cells had pleomorphic ovoid to round nuclei with occasional atypical mitotic figures. Atypical cells, as well as foamy macrophages, were present in the touch prep. Atypical lymphoid cells with anaplastic nuclear features were noted to infiltrate into collagenized-sclerotic stroma and at times adjacent fatty lobules. Immunohistochemistry was positive for CD45, BCL2, BCL6, CD43, CD79A, MUM1, and PAX5. Flow cytometry results, in addition to the histologic and immunohistochemistry staining, confirmed the diagnosis of DLBCL. The tumor was ultimately measured as 2.3 × 1.3 cm in maximal dimension, and the benign sclerotic capsule tissue provided evidence of the chronic rupture of implants.\nThe patient returned to the clinic 2 weeks after surgery and had well-healing scars without signs of infection. She returned again 6 months later and reported no pain at the surgical sites. Physical exam did not find any lymphadenopathy or mass with palpation. She continues to remain in good health.
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A 69-yr-old female presented with a 5-yr history of neck swelling caused by thyroid enlargement that had rapidly increased in size over the previous several months. She complained of orthopnea and dyspnea on exertion and was admitted for recent exacerbation of respiratory distress. The patient was a known case of hyperthyroidism on suppression therapy. No risk factor or suspicious history for amyloidosis was detected.\nOn physical examination, the patient had bilateral nodular enlargement of the thyroid gland. No lymphadenopathy was detected. Ultrasonography revealed that the thyroid was diffusely enlarged with a heterogeneous echotexture. Multiple echogenic lesions were found throughout the right lobe with the largest lesion measuring 1.8 × 1 cm. Thyroid scan revealed asymmetrical enlargement of the thyroid gland with a prominent cold nodule located in the lower portion of the right thyroid lobe. No retrosternal extension of the thyroid was found. Fine-needle aspiration of the right lobe showed normal follicular cells and colloid. Based on the clinical and imaging findings, a diagnosis of multinodular goiter with obstructive symptoms was made. The patient underwent a total thyroidectomy and the specimen was submitted for histopathological study.\nThe thyroid specimen measured 11 × 10 × 9 cm and weighed 290 gr. Cut sections showed multiple variable-sized nodules with areas of hemorrhage and cystic changes. One nodule was yellow and rubbery with a smooth regular outline measuring 2 cm at the greatest diameter in the right lower pole of thyroid (). Microscopic examination of the latter nodule revealed colloid-filled thyroid follicles lined by cuboidal cells with minimal variation in size in the presence of intermixed mature adipose tissue in the interfollicular stroma ().\nThe surrounding thyroid tissue showed multinodular goiter. No vascular or capsular invasion was identified. No lymphocytic infiltration, follicular destruction, or amyloid deposition was noted. No focus of papillary carcinoma was detected. A diagnosis of adenolipoma of the thyroid gland (thyrolipoma or thyroid hamartoma) in association with multinodular goiter was rendered.
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A 35-year-old male referred to the hospital with abdominal pain and intermittent food intolerance, concomitant with 6 kg of weight loss since 3 months earlier. No prior history of GI disease, drug use, abdominal pain and similar problems in his family were observed. In the abdominal examination, the abdomen appeared to be normal and no distension or organomegaly was observed. Also, no tenderness, rebound tenderness and guarding were noted. Prior to referral to the surgery clinic, the patient had undergone endoscopy and computed tomography (CT) scan, and the reports are as follows.\nStomach: normal fundus, normal body and a large submucosal mass lesion with partial obstruction of the gastric outlet.\nDuodenum: Bulbar deformity, normal D2.\nIncreased gastric wall thickness was observed with emphasis on antropyloric region and the lesser curvature with maximum thickness of 21 mm accompanied by fat stranding around the same areas. Evidence of partial stenosis with mild dilatation of stomach was seen. Contrast agent has penetrated through the distal region and no leak of contrast agent is observed. Liver, spleen and the pancreas looked normal. No apparent paraaortic lymphadenopathy was observed. No free fluid was observed in the abdomen and the pelvic cavity ( and ).\nConsidering the aforementioned reports, EUS was requested, and the report was as follows: two large sub epithelial lesions were seen in the antral territory that caused partial obstruction of gastric passage.\nUpper GI: There was large mixed echo mass 3244 mm in size with marked border with three cystic lesions in it and another one, a 26 × 22 mm SEL, both of which originated from forth layer of the gastric wall. The lesion is located between the left liver lobe and the outlet of the stomach. One lymph node was seen around the lesions.\nHepatobiliary: At visible range, there was no intrahepatic ducts dilation, with no intrahepatic masses or lesions.\nFinal diagnosis: GIST with worrisome signs is a highly probable diagnosis.
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A 76-year-old woman with medical history of cervical lymphoma presented to our hospital with diplopia and ptosis on the right caused by right oculomotor nerve palsy. Head T2-weighted magnetic resonance (MR) imaging disclosed a large intracavernous ICA aneurysm, and cerebral digital subtraction angiography revealed a large aneurysm at the ICA-PTA bifurcation with a maximum diameter of 18 mm [Figure –]. PTA originated at cavernous portion of ICA and terminated at basilar artery, below the level of the superior cerebral artery and above the union. Because she refused to undergo an operation, follow-up examination was continued.\nThree years later, she complained of a headache in addition to the right oculomotor nerve palsy. Head diffusion-weighted and T2-weighted MR imaging disclosed scattered cerebral infarctions in the right hemisphere and enlargement of the aneurysm to the maximum diameter of 22 mm with intra-aneurysmal thrombosis [Figure and ]. Computed tomography (CT) also disclosed partial thrombosis in the aneurysm sac []. We considered the cause of the infarction to be embolism from the aneurysm, and treatment with aspirin was started. She also refused to have a surgical procedure at this time.\nOne week later, her headache and diplopia worsened, and she was admitted to our hospital. Right abducens nerve palsy was detected as well as preexisting oculomotor nerve palsy. Head diffusion-weighted MR imaging revealed recurrence of embolic infarction [], and oral administration of cilostazol was added. Echocardiography and electrocardiography monitoring showed no apparent abnormalities indicating the presence of cardiac embolic sources. Cervical MR angiography did not show any carotid or vertebral artery stenosis that would cause stroke. In spite of the dual antiplatelet therapy, she developed left hemiparesis 6 days later, and diffusion-weighted MR imaging disclosed recurrence of cerebral infarction [], so intravenous heparin was added. The surgery was planned to prevent further cerebral infarction and aneurysm rupture under the agreement of the patient, first coil embolization of the PTA, then high-flow bypass from the cervical external carotid artery (ECA) to the middle cerebral artery (MCA) using RAG followed by ligation of the cervical portion of the ICA on the next day.\nUnder local anesthesia, systemic heparinization was initiated, and a 6 Fr Envoy XB catheter (Johnson and Johnson, Miami, FL) was placed in the right vertebral artery. An Excelsior SL-10 preshaped 45° catheter (Stryker, Kalamazoo, MI) was navigated into the PTA, and the PTA was occluded using a PRESIDIO Spherical 10 CERECYTE 4 mm × 11.5 cm coil, and two ULTIPAQ Helical 10 CERECYTE 2 mm × 8 cm coils (Johnson and Johnson). Throughout the procedure, care was taken to prevent coil protrusion into the aneurysm, ICA, and basilar artery. After tight packing of the PTA was obtained, the procedure was ended.\nOn the next day, high-flow bypass was conducted as described previously.[] Neuroanesthesia was induced under the monitoring of somatosensory evoked potentials (SSEPs) of the left extremities. The right cervical carotid bifurcation was exposed, a curvilinear frontotemporal skin incision was made, and the superficial temporal artery (STA) was meticulously prepared under the operating microscope. The RAG was harvested concurrently by another neurosurgeon. Frontotemporal craniotomy was performed, and a subzygomatic tunnel was formed for the RAG. The Sylvian fissure was split under the operating microscope, and the M2 and M3 portions of the MCA were exposed. First, an “insurance” STA-M3 bypass was made distal to the M2 portion for RAG anastomosis. Then, the harvested RAG was gently pulled through the subzygomatic tunnel, that is, between the lateral pterygoid muscle and the temporal muscle from the cranium to the neck through the lateral corridor of the stylohyoid muscle and the posterior belly of the digastric muscle toward the ECA.[] The distal end of the RAG was anastomosed to the M2 of the MCA, and the proximal end was anastomosed to the ECA. Microvascular Doppler flowmetry confirmed the patency of the anastomosis. The cervical ICA was permanently ligated after confirming no change in the SSEPs 5 min after temporary ligation. Microvascular Doppler flowmetry confirmed anterograde bypass flow from the STA and RAG. No significant SSEP changes were observed throughout the operation.\nCT obtained the day after the operation disclosed thrombosis of the entire aneurysm sac and cerebral angiography performed at 5 days after the operation demonstrated good patency of the bypasses and disappearance of anterograde flow to the aneurysm [Figure –]. Diffusion-weighted MR imaging revealed no new infarction. She gradually recovered with rehabilitation without new cerebral infarction over 8 months and was transferred to another hospital with modified Rankin scale 4.
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A 39-year-old woman (gravida 6, para 3-0-3-3) underwent a standard protocol of artificial cycle FET and had been transferred two in vitro fertilization-derived embryos at a fertility clinic. Detailed information about the transferred embryos was not available for this case. The patient had episodes of spontaneous and artificial abortions and a salpingectomy for an ectopic pregnancy, but had no history of a cesarean section. She became pregnant by FET and was treated with progesterone agents, an estrogen patch, and aspirin.\nAt 5-2/7 weeks of gestation, she presented to our hospital with hemorrhagic shock due to persistent genital bleeding. A transvaginal ultrasonography detected an intrauterine gestational sac of age-appropriate size and a squashed cystic lesion in the cervix. A blood examination indicated a hemoglobin level of 4.8 g/dL. Blood coagulum from the genitalia contained decidual tissues. Her genital bleeding was successfully controlled by manual compression of the external cervical os and the blood pressure and heart rate were stabilized after transfusing four units of red cell concentrates. She was diagnosed with a cervical heterotopic pregnancy. All the medications that had been prescribed at the fertility clinic were withdrawn, with the intention to terminate the pregnancy. However, despite the discontinuation of progesterone supplementation, the gestational sacs in the cervix and uterus continued to develop and formed yolk sacs (Figs a and b).\nAt 8 weeks of gestation, the patient expressed her desire to maintain the intrauterine pregnancy, despite being fully informed of the risk of hemorrhage and other complications. As there was growth discordancy in the two pregnancies and the fetal heartbeat was not observed in the gestational sac in the cervical canal, the gestational sac was manually removed with forceps under ultrasound guidance, instead of local potassium chloride injection. The cervical bleeding was controlled by astriction. Histological analyses of the removed specimen confirmed the presence of fetal tissues.\nThe subsequent course of the pregnancy was uneventful until delivery, except for a vasa previa that was detected at 28 weeks of gestation (Figs c and d). In order to avoid the rupture of the vasa previa, a cesarean section was performed at 36 weeks of gestation, which resulted in the birth of a healthy female infant. However, at the delivery, massive bleeding occurred from the region around the internal cervical os. A total hysterectomy was performed because the placenta was not able to be manually separated from the uterus. A histological examination of the uterus indicated a total placenta accreta; placental villi had invaded the myometrium (Figs a and b). There was no histological abnormality in the cervix or in the region around the internal os.
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A 34-year-old woman had come to our hospital with 45 days amenorrhea and 3 days of vaginal bleeding. She had a history of cesarean section 5 years ago. The transvaginal sonography revealed empty uterine cavity and empty cervical canal with a gestational sac in the anterior myometrium of lower uterine segment (). Anterior myometrium anterior to the gestational sac was thinned out. The laboratory test result for β-hCG revealed a level of 11,399 mIU/mL.\nAfter discussion about the possible benefits and risks of each of the treatments, she opted for the treatment of UAE and suction evacuation of the pregnancy under ultrasound guidance. So the next day, the patient’s uterine artery was selectively catheterized using a Rosch hepatic catheter and was embolized using gel foam sponge particles (900–1,200 μm, ). After that, dilation and curettage were performed guided by transabdominal ultrasound. However, during the process of anesthesia, the patient presented sudden cardiac arrest. Upon rapid resuscitation (external chest compression for 8–10 seconds), she recovered immediately. After return to the ward after dilation and curettage, she presented sudden cardiac arrest once again. Rapid resuscitation (external chest compression for 8 seconds and persistent mask oxygen-inspiration was performed) was carried out one more time. The subsequent urgent bedside electrocardiography (ECG) showed abnormal Q wave in III and aVF, and the computed tomography pulmonary angiogram scan showed extensive filling defects in the pulmonary trunk artery, the left and right trunk of pulmonary arteries, upper and lower arteries of the left pulmonary lobe, and lower artery of the right pulmonary lobe (). The next echocardiography revealed possibility of left pulmonary artery embolization, right atrium and ventricle enlargement, as well as moderate tricuspid regurgitation and mild pulmonary valve insufficiency. The patient was sent to the intensive care unit immediately, where she started to receive subcutaneous enoxaparin 100 IU/kg twice daily. A retrievable inferior vena cava filter was inserted, and the patient was kept under observation in the intensive care unit for 4 days until her condition was stabilized. After that, she was transferred to respiratory ward and remained there for 10 days. The enoxaparin was suspended, and she continued to take rivaroxaban for 2 weeks after discharge. During the next 4 months following-up, she recovered well without any complications.
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A 49-year-old Jamaican female with insignificant past medical history presented to the Emergency Department of an urban hospital with a chief complaint of progressively worsening shortness of breath of approximately 4 weeks evolution. Physical exam was remarkable for marked jugular venous distension, bilateral basal wet crackles, a distended and globally tender abdomen with positive fluid shift and positive hepatojugular reflex, as well as bilateral +2 lower leg edema. The patient's labs are shown in and were remarkable for anemia, elevated troponin, markedly elevated pro-BNP, transaminases, mildly elevated TSH, and CRP. ECG tracing showed atrial flutter with a ventricular rate of 126 bpm (). Chest X-ray showed a markedly enlarged cardiac silhouette with a water-bottle appearance suspicious for pericardial effusion (), for which an echocardiogram was done on hospital day 1, and confirmed the presence of a significantly dilated right ventricle, severe tricuspid, and moderate mitral regurgitation with no valvular structural abnormalities described. In addition, a moderately compromised left ventricular ejection fraction (LVEF) (30–40%) and a large pericardial effusion () were shown. CT of the chest with pulmonary artery protocol was not supportive of pulmonary embolism as the underlying etiology. While the syndromic diagnosis of dilated cardiomyopathy with right sided heart failure was made, the etiology remained unknown.\nThe patient was started on beta-blocker and diuretic therapy, and with close monitoring began to improve from her heart failure. While aggressive medical management continued, an etiologic search for the underlying pathology began. Toxicology and infectious disease markers were negative. A viral panel was sent out, and later returned as unremarkable. A search for underlying malignancy also was negative. Left heart catheterization showed normal coronaries but was remarkable for severe mitral and tricuspid regurgitation. Right heart catheterization was performed due to the patient's persistently labile hemodynamics intermittently requiring pressor support suggestive of cardiogenic shock due to right heart failure and to establish an initial baseline of pulmonary artery pressure in newly diagnosed heart failure without clear etiology. This revealed severe mitral and tricuspid regurgitation with moderate pulmonary regurgitation and only mildly increased pulmonary artery pressure, thereby supporting the mechanism of decompensated heart failure as secondary to dilated cardiomyopathy.\nIt was only when ANA titers came back strongly positive with low C3 and C4 complement levels that the etiology was suspected to be most likely autoimmune. The patient was immediately started on prednisone (40 mg daily), and further workup showed elevated levels of both anti-double-stranded DNA and anti-Smith antibodies along with decreased levels of C3 and C4, confirming a diagnosis of SLE and lupus myopericarditis. On further examination of the patient, no other clinical findings of Lupus could be identified besides microcytic-hypochromic anemia.\nOn subsequent follow-up, the patient showed continuous improvement with steroid therapy and was ultimately scheduled for valve replacement surgery. As heart function monitoring and prednisone therapy continued, surgical intervention was ultimately averted. The patient progressed with complete functional recovery. A year later, EKG showed a normal sinus rhythm; ECHO analysis showed a LVEF of 55%; and the patient remained clinically stable on maintenance hydroxychloroquine and prednisone therapy, avoiding surgical intervention.
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The patient was born prematurely (34 weeks and 1 day of gestation) at an outside hospital to a 29-year-old woman by elective cesarean section. The pregnancy had been complicated by preterm premature rupture of the membranes at 28 weeks and 2 days of gestation as well as prenatal diagnoses of cystic hygroma, pericardial and pleural effusions, left renal artery duplication, and bilateral ventricular hypertrophy with worsening myocardial function. This conglomeration of symptoms was later confirmed to result from Noonan syndrome. Specifically, this patient was found to have a PTPN11 gene mutation (c.923A>C; p.N308T).\nAt 12 hours of life, the patient became hypotensive and did not respond well to fluid resuscitation. Given the constellation of complications, the decision was made to transfer her to the tertiary care children's hospital for genetic assessment and cardiologic consultation. Upon arrival, the patient remained in respiratory distress and was hemodynamically unstable, and the placement of an umbilical catheter was attempted. A portable chest radiograph demonstrated a caudal loop of the catheter prior to ascending to the superior abdomen, so the catheter was assumed to be within an umbilical artery. However, the tip of the line was ultimately located to the right of the vertebral column (). Given this unusual position of the catheter, a cross-table lateral radiograph was performed. This demonstrated the tip of the umbilical line projecting over the expected location of the right atrium, at the level of the lower thoracic spine, and anteriorly and to the right of the expected position of the aorta (). A subsequent portable radiograph was obtained the following morning, redemonstrating the atypical position.\nAn ultrasound with Doppler assessment was performed to accurately determine the positioning of the line. The aorta was found to be unremarkable and without an intraluminal catheter. Instead, the catheter was identified within the inferior vena cava, with the tip positioned at the lower cavoatrial junction (). Confirming previous radiographs, the course of the catheter involved a caudal loop inferiorly and to the left, before coursing superiorly and to the right.\nFurther Doppler ultrasound imaging demonstrated an umbilical vein, which coursed inferiorly into the left iliac vein (). Sonographic imaging was unable to identify the ductus venosus. The development of the portal system, however, was not assessed in this patient. The patient's obstetrical records were obtained from the outside healthcare system, and these indicated a suspicion of atypical umbilical venous anatomy seen during prenatal ultrasound (). The umbilical catheter had no complications, and the remainder of the patient's hospital course was unremarkable. The patient is now one year old.
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The patient was a 29-year-old male who was electrocuted by 30,000 V of electricity while working. He was found in a coma, and woke up after 7 min. He was then sent to a local hospital immediately after the injury and transferred to our department for further treatment 6 h afterwards. The patient was very agitated when he entered our department. He had a hoarse voice and no nausea or vomiting. Wounds were located mainly on the left head, neck, back, and left upper limb. The skin surface of the wound was removed, and the basement was pale and could not be touched. There was also evident swelling of the head and neck. The wounds on the neck and back are shown in Fig. a. The wound was debrided 4 days after the injury, we observed deep electrical burns on the neck and back, reaching the deep fascia. After we removed the degenerated and necrotic upper trapezius, levator scapulae, and occipital muscles, the size of the skin and soft tissue defect was 28 cm × 10 cm, as shown in Fig. b. We designed the right trapezius myocutaneous flap to be about 30 cm × 12 cm in size, as shown in Fig. c. We cut the deep fascia deeply from the outside and separated it inwards under the trapezius muscle. Then, we raised the myocutaneous flap from deep inside the lower part and separated it along the nourishing blood vessels. The upper part of the myocutaneous flap was formed from a part of the rhomboid muscle sleeve, and the flap was rotated to the left to cover the wound. The donor site was repaired by medium-thickness skin grafting (Fig. d). After the operation, the tissue flap completely covered the wound surface and the electrical burn wound on the neck and back was effectively repaired, as shown in Fig. e. The donor site and the flap healed well without any major events. Good cosmetic appearance and function were achieved on the 7th day postoperatively. Half a year after the flap repair, neck and back functions returned to normal and the shape was satisfactory, as shown in Fig. f.
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A 37-year-old Iranian balochi male was shot with a firearm in the upper part of his right pelvis. He underwent primary closure on the same day and a suprapubic cystostomy was placed which was removed 3 weeks later. Ten months later, he developed urinary retention. He underwent retrograde urethrography and antegrade cystography, which showed a stricture measuring 5 cm in length. There was also a history of progressive pain in his right hip joint accompanied by low grade fever which started 2 months after the initial injury. A hip X-ray showed evidence of complicated septic arthritis (Figure ). There was also accumulation of contrast around the right femoral head and the presence of a fistulous tract between the posterior urethra and his right hip (Figure ). An axial computed tomography (CT) scan of his pelvis following retrograde urethrography confirmed a fistulous tract with destruction of the acetabular cavity and femoral head (Figure ). Laboratory tests showed active urinary sediment and positive synovial fluid culture (Table ). For this, he underwent delayed reconstructive surgery for the urethral stricture using a bladder epithelial graft and urethral fistula via a transperineal approach. The patient was placed in an exaggerated lithotomy position. An inverted Y incision was made in the bulbospongiosus muscle and the muscle displaced laterally. The urethra was released and the edges of the fistula were freshened by passing a curette, followed by a gracilis muscle flap which was placed between the urethra and fistulous tract. The stricture was located by placing a Van Buren sound and semicircular sound in the anterior and posterior urethra via the cystotomy tract, respectively. The stricture length was approximately 5 cm. Stricturectomy was performed and the edges were sutured to a graft from a bladder mucosa. An intraluminal catheter was placed to serve as a stent and a suprapubic cystotomy was done to divert the urine.\nThe intraluminal catheter was removed 3 weeks after surgery while the suprapubic cystostomy was clamped and the patient was instructed to void. An antegrade urethrography was performed which showed a widely patent urethra with no evidence of contrast extravasation (Figure ). After 1 week of normal voiding, the suprapubic catheter was removed. At the same time, the patient was under treatment with antibiotics for his septic arthritis. Four months later (14 months after the initial injury), he underwent non-cemented total hip arthroplasty. The patient was discharged on an antibiotic regimen and followed with post void imaging for 18 months. He was instructed to return for follow-up if he developed difficulty voiding or any reduction in urinary caliber. The patient was not symptomatic during routine follow-up. To our best knowledge, this kind of fistula following a gunshot injury has not been reported previously.
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A male famer aged 68 years old was admitted to our institute for a tumor in his lower lip. This patient has a history of smoking (30 pack-year) and consuming alcohol for more than 30 years (approximately 200 ml per day). He was diagnosed as systemic lupus erythematosus (SLE) 20 years ago and had been treated with methylprednisolone for 17 years. For the last three years, his SLE status has been stable and thus, he discontinued the SLE treatment.\nThe patient reported that the tumor in the middle of his lower lip had appeared for a year and gradually increased in size without any pain or bleeding. He did not receive any treatment because of his financial issue. For the last few months, the tumor had rapidly grown, bled and become painful, so that he could not eat or clean his teeth.\nOn examination, there was a 3 x 4 cm, raised, ulcerous, and bleeding tumor, developing in the lower lip and expanding to 1/3 external upper lip (). The submental lymph node was around 2 cm in diameter, firm, and hardly moveable. Ultrasound revealed a suspected metastatic submental lymph node with absent echogenic hilum. MRI Scan demonstrated a lesion in lower lip with size of 13 x 31 mm, which increased in T1W signal and T2W signal, strongly enhanced after contrast and did not invade surrounding tissue. A 2 cm and round lymph node was also identified (). The fine needle aspiration (FNA) result of the lymph node presented a metastatic squamous cell carcinoma and the biopsy result of the tumor confirmed squamous cell carcinoma (SCC). No abnormality was detected by a metastatic work-up. Therefore, the clinical staging of this patient was cT2N1M0. In addition, other para-clinical tests including full blood count, biochemistry profile, ds-DNA, ANA were normal, which indicated a stable status of SLE.\nThe patient underwent surgery including a complete removal of the lower lip and 1/3 external of upper lip, and dissection of the bilateral cervical lymph nodes. The lower lip was reconstructed with V-Y advancement flap (). This operation, performed by a team of head and neck surgeons, was proceeded within 4 h. Patient was discharged after 14 days without any complications. Final pathology presented SCC ().
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A 75-year-old female was initially admitted to the ICU after planned esophagogastrectomy for esophageal cancer with laparoscopic mobilization of stomach and duodenum by a left posterior lateral thoracotomy and subsequent gastric pull up and reconstruction. Patients esophageal cancer was a partially obstructing and circumferential T4N1 (stage IIIA) moderately differentiated adenocarcinoma at the gastroesophageal junction. Intraoperatively, the patient’s visceral pleura was violated necessitating the placement of two 24 Fr chest tubes. Upon subsequent chest X-ray (CXR) imaging 5 days after removal of the initial chest tubes it was noted that there was recurrence of a small apical pneumothorax and a percutaneous chest tube was subsequently placed. Post procedure imaging revealed the percutaneous tube was placed directly into the parenchyma of the right lung creating a large air leak. Subsequently an open chest tube was placed at bedside and 40 ml of blood was evacuated. Shortly after the passage of the new chest tube and the patient developed increasing ventilator requirements the patient began developing clinical signs of SE. Physical exam revealed widespread upper trunk tissue distention and crepitance to palpation. Within hours widespread tissue distention spread cephalad to involve the upper chest, neck and face. The patient progressively developed massive SE and increasing peak pressures (Fig. ). The following day the patient developed complete inability to open her eyes and her peak airway pressures became elevated to 70 cm H2O. The patient had a massive and persistent air leak and negative pressure was increased in the chest tube drainage system to −40 mmHg without any improvement in respiratory dynamics. In an effort to rapidly decompress the rapidly evolving SE we decide to place three 14 g 2 inch I.V. catheters (Acuvance® Plus Safety I.V. Catheter—Smiths Medical ASD, Inc. Southington, CT) into the tissue. The first needle was placed at the area of the greatest air accumulation in the right upper lateral chest wall (Fig. ). The trajectory of the needle was into the deep plane of the chest wall. Upon successful placement of the needle there was audible release of air immediately decompressed. Subcutaneous air subsequently continued to decompress and was noted to be in synchrony with the respiratory cycle. Lateral to the initial needle another 14 g angiocatheter was placed in an oblique and transverse direction in an effort to provide a drainage site to a more superficial tissue plane (Fig. ). Lastly a third 14 g needle was placed on the contralateral left upper lateral chest wall directed in a deep oblique direction (Fig. ). During the placement of all three needles there was an audible rush of air that was evacuated and continued to decompress once in final position. After successful placement, the inner needle was removed and the overlying plastic angiocatheter was left in place. Within the first three hours there was a noticeable change in both a decrease in the tissue distention and improvement in respiratory dynamics. The patient continued to progressively improve over the initial 24 h with near complete resolution of SE and normalization of ventilator dynamics, most notably in normalization of peak airway pressures indication alleviation of airway compression. The angiocatheters were subsequently left in place for 24 h and removed without difficulty. Measuring from the level of the skin to the proximal hub of the catheter proved to be a simple means to quantify the degree of decompression and in this patient, we were able to achieve 3 cm of circumferential decompression (Fig. ). At 24 h, there was nearly complete resolution of SE (Fig. ).
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A 28-year-old Caucasian man living in London presented at a walk-in GP clinic reporting four episodes of hematospermia over 10 days. In the first three episodes, the patient reported the semen being brown in color. On the fourth episode, there were distinct streaks of red blood within the semen.\nThe man was heterosexual, and this was his first and only sexual partner. His partner had no history of sexually transmitted infections (STI). The couple was sexually active and using barrier method contraception for family planning reasons.\nThe patient was otherwise fit and well with no past medical history apart from mild childhood asthma. He had no headaches or changes in vision. He had no cardiac or respiratory symptoms. There was no history of recent trauma. There were no changes in urinary or bowel habits. He had no pain, fever, sweats, weight loss, or fatigue. He had not travelled abroad recently. The patient had never smoked or taken illicit substances. His diet was reasonably healthy, and he walked approximately 5 km a day. He consumed approximately 32 units of alcohol per week and recognized that this as in excess of medical guidelines. There was no family history of inheritable diseases.\nOn examination, he was comfortable at rest and clinically euvolemic. His abdomen was soft and nontender. His kidneys were not palpable. There were no renal bruits. There was no enlargement or masses in the scrotum. A digital rectal examination was normal with no enlargement or nodularity of the prostate. Respiratory examination revealed normal breath sounds. Examination of the central and peripheral nervous system was entirely normal.\nOn cardiovascular examination, heart sounds were normal. There was no peripheral edema, and the jugular venous pressure was not raised. There was no radio-femoral delay, and fundoscopy was normal. His blood pressure was note to be 228/135 mmHg, and his heart rate was 90 beats per minute and regular. Pulse volume and character were normal. His oxygen saturations were 98% on room air. There were no signs of acromegaly or Cushing's syndrome.\nUrinalysis was completely negative. His electrocardiogram (ECG) showed normal sinus rhythm. There was no left ventricular hypertrophy, axis deviation, or strain pattern.\nHis full blood count was as follows: hemoglobin 174 g/L, platelets 234 × 109/L, white blood count 5.9 × 109/L, and mean corpuscular volume was 85 fl. His CRP was <1 mg/L. His urea and electrolytes were sodium 142 mmol/L, potassium 4.3 mmol/L, urea 4.7 mmol/L, and creatinine 96 mmol/L. His estimated glomerular filtration rate was slightly reduced at 84 mL/min. His chest radiograph was normal. Ultrasound and computerized tomography of the urinary tract were normal.\nTwenty four-hour urinary metanephrines and a serum renin–aldosterone level were with normal range, ruling out pheochromocytoma and hyperaldosteronism as causes of hypertension, respectively. An echocardiogram was entirely normal. More specifically, there was no left ventricular hypertension nor diastolic dysfunction, which would be the expected findings in a case of chronic hypertensive heart disease.\nA diagnosis of hematospermia secondary to severe essential hypertension was made. There were no clinical signs of malignant hypertension. The absence of other urological symptoms made inflammation or infection of the urinary tract unlikely, and the lack of proteinuria or left ventricular hypertrophy on ECG implied that the hypertension was of recent rather than chronic onset.\nThe patient was treated with an angiotensin-converting enzyme inhibitor (ACE-i), per National Institute for Health and Care Excellence guidelines. A dosage of 2.5 mg of ramipril daily was sufficient to control his blood pressure.\nThe patient purchased a home blood pressure machine and monitors his blood pressure daily. His systolic pressure lowered steadily to an average of 165 mmHg. Normotension led to complete resolution of the hematospermia.
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Patient 2 was a 74-year-old man suffering from heart failure, chronic atrial fibrillation, severe venous insufficiency, leg ulcers, type 2 diabetes, chronic obstructive lung disease, and severe obesity (160 kg, BMI 49). At hospital admission the patient was confused with delayed response time. Furthermore he presented with atrial fibrillation (140 beats/minute), hyperthermia (39.0°C), and elevated blood levels of creatinine. He was tachypnoeic with low oxygen saturation (91%). A urine test strip showed presence of blood, protein, and ketone bodies. Initial treatment included fluid therapy and antibiotics on the suspicion of sepsis. The patient was transferred to telemetry in the cardiology department where treatment with digoxin was initiated.\nDuring the following days urine output increased, but his level of consciousness decreased and he developed myoclonia. Due to accumulation of carbon dioxide he was transferred to the ICU, where intubation and mechanical ventilation were initiated. At admission GCS score was 3, pupil reactions were sluggish, and muscle spasms in the upper body were observed. Blood tests were normal except an increasing INR.\nDuring the first days in the ICU the patient improved with decreasing demand of oxygen and cardiac inotropes. Analysis of the cerebrospinal fluid and a head CT were both normal. Microbiological tests showed no sign of infection. Despite fanning and cold fluids the patient still had an elevated temperature and cooling was intensified using a thermoregulatory device with cooling pads. On day 5 the patient's temperature normalized and he gained consciousness. On day 7 the diagnosis of HS syndrome was suspected. The patient stabilized and was extubated, but he still received intermittent cooling. The patient developed hypercapnia and was reintubated and later a tracheostomy was performed. Due to anuria dialysis was performed until he regained his kidney function on day 23. The patient was again stabile and interacting with family and staff. Unfortunately the patient was infected with pneumonia. His overall condition thereafter gradually declines and he died 55 days after admission.
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A previously healthy 10-year-old female presented to our hospital with a 2-month history of intermittent abdominal pain. An abdominal computed tomography (CT) scan done to rule out appendicitis revealed a 4 × 3 cm cystic lesion in the region of pancreatic head, and whether the lesion involved the pancreas at its head or not was unknown based on the images (). The differential diagnoses included a choledochal cyst, a retroperitoneal lymphangioma, and a pancreatic cystic lesion. The patient therefore underwent an exploratory laparotomy to obtain a histologic diagnosis. The intraoperative frozen section diagnosis of the cyst wall biopsy was a true pancreatic cyst without malignancy. The cystic lesion was drained and unroofed. Cystic fluid analysis showed an amylase of 60 U/L. The patient's symptoms subsequently resolved after the procedure, and she was placed under close ultrasound surveillance. The surveillance interval period was 3 months for the first follow-up, 5 months for the second follow-up, 8 months for the third follow-up, and then extended to a year.\nFor the next fifteen years, the patient was asymptomatic without any complications and had a successful uncomplicated pregnancy. The abdominal ultrasound surveillance showed the tumor grew in size from 4.2 cm to 6.2 cm in diameter for 15 years. In the latest five months, the patient had noted occasional right mid abdominal pain and discomfort. A pylorus-preserving pancreaticoduodenectomy was then performed due to her recurrent pain and enlargement of the lesion.\nOn gross examination, a multilocular cystic lesion was identified in the head of the pancreas with cysts ranging from 0.5 to 3 cm in size (). The cysts were filled with clear fluid, and the cystic wall was smooth without any solid or papillary areas. Microscopically, the lesion consisted of multiple variable-sized cysts separated by fibrous stroma and residual islands of unremarkable pancreatic tissue (). The cysts contained eosinophilic secretions and were lined by a single layer of bland epithelium ranging from nondescript flat/cuboidal epithelium to apparent acinar cells (). Cytologic atypia and mitotic figures were absent. Occasional calcifications with fibrosis, histiocytes, and cholesterol clefts were noted. The immunohistochemical analysis was performed and demonstrated that the cyst lining cells were positive for trypsin (), CK7 (), and CK19 but negative for synaptophysin and chromogranin. Proliferative index marker (Ki-67) is less than 1%. Based on these histomorphological and immunohistochemical findings, the final diagnosis was confirmed to be ACT. The prior intraoperative biopsy was retrospectively reviewed to reveal similar epithelial lining to that seen in the resection specimen (Figures and ). One and a half years have passed after surgical resection and no recurrences of the lesion and symptoms were documented.
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A 60-year-old man was referred to our surgical colleagues for rectal bleeding in November 2006. He had a colonoscopy which showed a tumour few centimetres proximal to the anal verge, and the biopsy confirmed a moderately differentiated adenocarcinoma. A computed tomography (CT) scan of thorax, abdomen and pelvis showed the presence of multiple liver metastases which were confined to its right lobe. A magnetic resonance imaging (MRI) scan of his pelvis showed a 7-cm nodular tumour which circumferentially surrounded the rectum, and the local invasion of this tumour was also noted. The whole-body positron emission tomography–CT (PET–CT) scan confirmed the same and showed no evidence of tumour dissemination to any other sites (apart from local invasion and to the right lobe of the liver). He had a successful course of palliative radiotherapy for his rectal bleeding and was started on chemotherapy with 5-fluorouracil and leucovorin on a weekly schedule for 6 weeks with a 2-week break. However, the repeat CT scans in April 2007 showed no response to this treatment. His chemotherapy was then changed to a combination of oral capecitabine plus intravenous infusions of oxaliplatin in May 2007; however, he developed significant myelosuppression and hepatotoxicity, and was taken off this regimen. In September 2007, he had a synchronous resection of his liver metastases and the resection of primary rectal tumour with colostomy. Subsequently, his chemotherapy was changed to irinotecan. Unfortunately, in January 2008, his PET scan showed an uptake at the primary tumour site and also in the right lobe of liver; this was also accompanied by the episodes of rectal bleeding. In June 2008, he had resection of local recurrence, along with local radiotherapy to his primary site. His K-ras mutation status was of wild-type, and it was decided to commence him on monoclonal form of chemotherapy.\nHe had the first session of a combined therapy with cetuximab and 5-fluorouracil (5-FU) in March 2009; however, soon afterwards, he developed a gradually worsening nausea, feeling unwell, and lethargy. He did not seek medical attention for these complaints. He was reviewed in the outpatient clinic 10 days post-chemotherapy, and was noted to be very unwell and dehydrated; his blood tests on that day are shown in . He was urgently treated for his hyperkalaemia and was transferred to our nephrology services. The history of recent chemotherapy prompted us to request further blood biochemistry, and he was subsequently diagnosed with the tumour lysis syndrome on the basis of hyperphosphataemia (serum phosphate 3.54 with a normal range of 0.8–1.5 mmol/l), hypocalcaemia (calcium 1.83 with a normal range of 2.1–2.62 mmol/l), hyperuricaemia (uric acid 2589 with normal range of 212–482 µmol/l) and hyperkalaemia (serum potassium level of 6.2 with a normal range of 3.5–5.0 mmol/l), along with acute renal failure (creatinine 1424 with a normal range of 50–130 µmol/l). Clinically, he was dehydrated and was commenced on intravenous fluids. His arterial blood gases showed metabolic acidosis (pH 7.20, bicarbonate of 10). To our surprise, even within 2 h of commencing fluids, he had massive diuresis. He had a urine output of about 7 l in the first 12 h; his intake and output were balanced with isotonic saline and bicarbonate infusion. This caused a dramatic improvement of his renal profile and uric acid levels (). The patient subjectively felt much improved and was discharged home after 48 h of his admission with normal renal profile and baseline physical status. Repeat imaging to look for any interval change of his tumour burden since the infusion of cetuximab was not done; as after about a month, our patient developed a fatal massive intracerebral haemorrhage—the cause of which remains speculative.
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A 59-year-old man felt sudden headache and dizziness twice in a year. He visited a neighborhood clinic and a right VAFA (10 × 6 mm) was detected. Conservative therapy was selected. However, a third attack occurred with dysarthria and gait disturbance and he visited the emergency department of our hospital near his workplace. He had a medical history of hypertension and hyperlipidemia, and a heavy smoking history (30 cigarettes per day for 30 years).\nMRI after admission revealed expansion of the right VAFA (19 × 16 mm) that compressed the lower pons from the anterior side, while the intraluminal thrombus was increased compared with preadmission MRI (). Preoperative DSA showed that the dilated segment of the right VA started 12-mm proximal, and ended just proximal, to the VA union. The right side had a common trunk of the AICA-PICA, while the PICA was absent. However, there was a relatively thick branch (0.8 mm in diameter) feeding the lower vermis, lower pons, and medulla oblongata that arose from the V4 segment just distal to the penetrating part of the posterior dura (, blue arrowhead). In addition, no angiographically identifiable branch was found. The contralateral VA was well-developed.\nNo other cause was found to explain his symptoms. Thus, brainstem compression caused by expansion of the thrombotic part of the aneurysm was considered the main cause. For treatment, the distal end of the aneurysm was positioned high and contralaterally displaced, making it difficult to perform reconstructive clipping as for case 1 or VA reconstruction as for case 2. Thus, we selected proximal ligation. The strategy was to reduce blood flow into the dilated segment of the aneurysm while maintaining the VA perforators by allowing the retrograde blood flow via the VA union to pass through the aneurysm and outflow to the VA perforator (). In this situation, we had no choice but to make the distal segment of the ligation clip the so-called “perforator end,” which is hemodynamically prone to obstruction. Nevertheless, the potential for perforator obstruction was considered to be relatively low compared with aneurysmal trapping.\nIntraoperatively, a perforator arose from the V4 segment just proximal to the aneurysm and there was no distance for clip application between the proximal neck to this perforator (, , black arrowhead). Thus, the proximal portion of this perforator was ligated while ensuring visually that there was no other conspicuous VA perforator. The anterograde blood flow of the VA was allowed to flow out to the aforementioned relatively thick branch from the V4 (, , blue arrowhead). Additionally, a flow-augmentation to the right PICA through the V3-RAG-PICA bypass secured the perfusion of the right AICA-PICA region to reduce the hemodynamic load on the contralateral VA. This was expected to be a detour to substitute for the VA trunk (, blue arrow) in case the contralateral VA become occluded in the future. The actual surgical procedures of case 3 is shown in .
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A 52-year-old farmer was referred to us 7 hours after he had met with a high-velocity road traffic accident. He was resuscitated as per the ATLS protocol at the hospital where he was initially treated and when he arrived at the casualty department of our hospital, he was conscious and all his vital parameters were within normal limits. He also gave the history that he was under treatment for segmental myoclonus which was characterised by semirhythmic involuntary muscle contractions.\nHis radiographs showed a left-sided posterior acetabular wall fracture (AO type 6 2 A1). He also had an ipsilateral femoral neck fracture with the femoral head displaced anteriorly (Figures and ) and also an associated middle-third fracture of the shaft of the femur (). He also had an extra-articular distal femur fracture on the opposite side (AO type 3 3 A1). On arrival, his serum lactate level was 1.9 mmol/l indicating that he had been adequately resuscitated.\nHe was taken for definitive surgery 9 hours after arrival. The patient was positioned in the lateral position and a posterolateral approach was planned to address the acetabular and femoral head fractures. Upon dissection, the femoral head () was found to have buttonholed and displaced anteriorly through the capsule which was found to be torn. The posterior wall of the acetabulum was addressed using two contoured reconstruction plates (). Using the trochanteric flip osteotomy, better access to the femoral neck was achieved and the femoral head was reduced anatomically and secured with K-wires. Then the femoral shaft fracture was reduced by opening the fracture site and held with a clamp. The femoral head fracture and the shaft fracture were fixed with an antegrade femoral nail with two screws securing the femoral head (Figures and ). The flip osteotomy was fixed using a tension band wire and the joint was reduced. The torn capsule was sutured. Closure was done in layers. The operating time was 4 hours and the intraoperative blood loss was 600 ml. Three days following this surgery, the contralateral distal femur fracture was addressed using a titanium locking plate. The postoperative period was uneventful.\nThree weeks after the initial surgeries, the patient experienced an episode of rhythmic contractions of the lower limbs at his home. He presented to us with an anterior dislocation of the left hip joint (Figures and ). An open surgery was done to reduce the left hip joint (). Considering the displacement of the femoral head at the time of initial presentation, the chances of avascular necrosis of the femoral head was explained to the patient. The patient was also on follow-up treatment with a neurologist to manage the myoclonus problem.\nFour weeks after the surgery to relocate the femoral head, non-weight-bearing mobilization was initiated. As expected, avascular necrosis of the femoral head occurred () and we waited for union of the femoral shaft to occur as any procedure to address the femoral head would require removal of the intramedullary nail.\nEight months after the initial surgery and after union of the femoral shaft fracture, the patient was planned for total hip replacement surgery. Through a posterior approach, the antegrade femoral nail was removed. The acetabulum was reconstructed using a cage, and an uncemented hydroxyapatite-coated stem was used for the femur (). A ceramic on a polybearing surface was used. Postoperatively, there was no shortening of the limb. Immediate full weight-bearing mobilization was started using walker support. One year following the hip replacement surgery and 22 months following the initial trauma, the patient was ambulatory without any support and able to do all activities with an LEFS (lower extremity functional score) of 72. The radiographs showed complete union of all the fractures and there was no loosening of the femoral prosthesis.
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A 34-year-old, married, previously healthy man presented to our hospital outpatient department on December 7, 2017, with pain, tenderness, and swelling in his left leg for one week. The pain was sudden in onset and sharp, movement made the pain worse, and rest relieved it. The pain was localized to the lower leg and did not radiate. In addition to pain, he had a tense swelling of the lower extremity. No temperature changes were associated. This was his first episode. The patient was admitted and appropriately evaluated for DVT, including Doppler ultrasound and blood work. He was started on anticoagulation therapy with oral rivaroxaban. The patient tolerated the treatment well, and his prothrombin time and activated partial thromboplastin time were monitored. Five days after admission and receiving an anticoagulant, he developed dyspnea and hyperventilation in the morning. His arterial blood gas test showed respiratory alkalosis. Because the probability of PE was high, he was given a heparin infusion and was taken for a pulmonary angiogram, which showed a thrombus in the right pulmonary artery, involving the right upper middle and lower lobar arteries. Since sudden onset DVT and subsequent PE in a young male patient, despite being on anticoagulation, is rare, it raised a suspicion of underlying thrombophilia. A panel was ordered that came back positive for high levels of homocysteine. After the patient stabilized, he was again prescribed oral rivaroxaban. Vitamin B12, folate, and vitamin B6 levels were evaluated and found to be surprisingly normal because homocysteinemia is usually associated with vitamin B12 deficiency. He was also started on vitamin B6, vitamin B12, and folate.\nPhysical exam\nThe measurements of his legs before and after anticoagulation therapy are presented in Table .\nNotable results from the laboratory workup and coagulation profile are presented in Table and Table , respectively. His homocysteine level was greater than 65 μmol/L. No other findings were remarkable.\nHis dilated RV diameter was 27.9 mm. The Doppler ultrasound revealed thrombotic plaques in the superficial femoral vein at the midthigh level, involving the popliteal, posterior tibial, and peroneal veins. The veins were dilated and noncompressible. His perforator veins were dilated in the calf region. An electrocardiogram showed an S1Q3 pattern. The pulmonary angiogram showed thrombus in the distal right pulmonary artery, as shown in Figure . We also noted mild lymph node enlargement, the largest approximately 5 mm to 9 mm, in the aortopulmonary window. The anticardiolipin antibody test result was negative. D dimers were 1290 ng/mL (i.e., positive).
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A 76-year-old woman who threw herself in front of a train arrived at our hospital by ambulance. She had landed between the rails and evaluation in the emergency room found no injuries except a small subcutaneous hematoma in the left temporal region. When chest X-ray examination and brain computed tomography (CT) revealed she had lung cancer with brain metastasis, the emergency room staff referred her to psycho-oncology. Following a diagnosis of depression, she was moved to the psychiatric ward.\nThe patient was the daughter of a farmer. In the chaotic times after World War II, she unwillingly got married, divorced a year later, and worked in various jobs before eventually opening a small bar. She did not have family history or past history of suicide or depression. After running the bar for more than 20 years, in 2002 at the age of 70, she handed running the bar over to her employee. The next year, Mr. A, a customer of the bar and her friend for 30 years who was a widower and 4 years older than her, began to make advance towards her, stating his wish to live with her and to guarantee her an adequate income. Issues of money and marriage were of no importance to her, but she began to dream of life with a reliable partner in her golden years.\nWhen she was admitted to hospital with severe hypertension in 2004, Mr. A was unexpectedly cold towards her and she became suspicious of his sincerity towards her. After discharge, repeated episodes of hypertension led to emergency admissions. In 2005, tired of a single life, anxious about the future, and led on by Mr. A's ardent desire to be with her, she decided to live with him. However, until she moved into Mr. A's house she did not know that his socially withdrawn son, who was in his fifties, would be living with them. She frequently witnessed family quarrels and Mr. A used to go out early in the morning to avoid quarreling, leaving her with his son. The son followed what she did closely all day, became extremely angry when he did not get his way, and was sometimes violent towards her. She endured the situation for about a year until she developed insomnia, avolition, and deteriorated hypertension. She moved in with her nephew for 6 months to escape the situation and her health improved. As she felt recovered and Mr. A demanded she return because her absence was an “inconvenience,” she decided to move back in with them again.\nHowever, the son treated her ever more unkindly, claiming she had designs on his father's assets. With this and having an unreliable partner, she started to feel uncertain about the future and again developed insomnia and avolition as well as loss of appetite in 2008. In March that year, a routine chest X-ray examination revealed a large coin lesion in the right upper lung field () and she was referred to a general hospital. When she told Mr. A of the shadow on her lung, he told her to move out. She managed to get him to let her stay until a detailed examination was carried out. At this time she began to have suicidal ideation.\nAfter the detailed examination was performed in April, she was diagnosed with squamous cell carcinoma of the lung with metastasis to the supraclavicular lymph nodes, right adrenal gland, and liver. She wanted to be informed of the actual nature of her illness and said she did not need relatives present when the doctor explained it to her. She was informed she had advanced lung cancer that was considered nonoperable and not treatable by chemotherapy or radiation therapy. The physician recommended she visit a local hospital, because he had no therapeutic options. The next day, she moved to her nephew's house with 50,000 yen “palimony” from Mr. A. She suffered insomnia and had suicidal ideation.\nThree days after receiving the bad news, she got on a local train headed south to find a distant place to die. However, she could not find a suitable place before reaching the end of the line, so she traveled north by Shinkansen. She got off at a spa town with a suspension bridge nearby and took a taxi to the suspension bridge. However, she abandoned the idea as it was already dusk and returned to the Shinkansen station by bus. From there, she took a local train to the closest station to her nephew's house. She suddenly thought to throw herself in front of a train there. She was brought to our hospital after this suicide attempt.\nThe psycho-oncologist started her on fluvoxamine (50 mg) and zolpidem (5 mg). Upon admission to the psychiatric ward, she did not seem so depressed although she talked much about her disillusionment and disappointment with Mr. A. Brain CT performed during emergency care had revealed a low density area with a nodular structure in the lower part of the right temporal lobe and a smaller low density area in the left paraventricular subcortical area which suggested brain metastasis and brain edema (). However, her responses were natural and prompt, she talked logically, and her behavior was polite and appropriate. There seemed to be no manifestations of the brain metastasis. Psychometric tests such as the Wechsler Adult Intelligence Scale were not performed as it seemed ungracious to perform further evaluation of a dying patient who had survived suicide. While on the ward she was informed of her illness once again with her sister present and she expressed the wish to spend the rest of her life in hospital. We planned on transferring her to a hospital near her sister's house when her mental stability was confirmed.\nAround 4 weeks later she came to talk much, especially in the morning, and appeared to be hypomanic. She was started on sodium valproate 200 mg, which resolved the hypomania. However, she was still euphoric and said repeatedly how happy she was to live in such a nice place. Around 6 weeks later her responses were incoherent and circumstantial. She laughed inappropriately and sometimes fell to the floor. Brain CT revealed enlargement of brain edema. She was transferred to a hospital near her sister's house on hospital day 69. She died about 8 weeks after transfer.
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A 2-month-old female child presented to the neurosurgery outpatient department with complaints of large swelling over the back of head and difficulty in feeding. The swelling was small at the time of birth, but it gradually increased in size. The child was born by normal vaginal delivery at home, had 4 siblings who were all normal. Folic acid supplementation was not taken by mother in any pregnancy. The weight of the child was 6.5 kg. On examination, patient large spherical swelling was present over occipital region and there was no head control []. The patient was active, conscious with no focal neurological deficit. Systemic examination was unremarkable. The head circumference was 30 cm and circumference of occipital swelling was 63 cm. The overlying skin was tense and without any CSF leak. Swelling was cystic and its size increased on crying. Fluctuation could be elicited and transillumination test was also positive. There was no any bruit or murmur over the swelling. Anterior fontanelle and posterior fontanelle were both open.\nA computed tomography (CT) scan was done [Figures and ], which showed a bony defect of size 22 mm × 15 mm in occipital bone in the midline. There was herniation of CSF-filled sac through the defect into the extracalvarial soft tissue layer and herniation of bilateral cerebellar hemisphere into CSF filled sac. Features favored the diagnosis of giant occipital meningoencephalocele.\nThe patient routine laboratory investigation was normal. After arrangement of adequate blood, the patient was posted for surgery. The patient was operated in lateral position. A circumferential incision was given on the swelling with meticulous dissection, and hemostasis sac was opened and gradual decompression of sac done, clear fluid (CSF) came out from the sac. The protruded portion of cerebellum was excised and the dura closure was done. Scalp closure was done in layers. The patient was extubated without any difficulty and shifted to postoperative room. Preoperative weight of the patient was 6.5 kg and the postoperative weight of 3 kg. On the 3rd postoperative day, the patient developed bulging of wound. CT scan showed a mild communicating hydrocephalus which was managed by repeated lumber puncture and CSF drainage. Stitches were removed and the patient was discharged on the 10th day.
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A 16-year-old female was referred with pain involving the upper left incisors region. Patient history revealed endodontic treatment of the maxillary upper left incisors with necrotic pulp and periapical radiolucency six months earlier. A few months after the treatment, she experienced discomfort pain. Extraoral examination revealed an integrate mucosa with normal appearance, whereas, intraorally, the upper left lateral incisor presented chromatic alterations and mobility in the region. A periapical radiograph showed the presence of a defined radiolucency lesion between the upper left incisors of the endodontically treated teeth with a size of 2.5 × 1.0 cm in a high diameter (). An incisional biopsy was made using local anesthesia and sent to the Oral Pathology Laboratory. The specimen was fixed in 10% neutral formalin and routinely prepared for light microscopy; the sections were stained with hematoxylin and eosin. Histological examination showed malignant neoplasm fragments consisting of fusiform cells with comma-shaped nuclei, originating from cell bundles exhibiting one of two forms: a round shape with large nuclei (occasionally palisading) or hyalinized strands and/or islets (Figures and ). Immunohistochemistry analysis was performed using streptavidin-biotin technique with monoclonal antibodies; the cells were positive for both the S-100 protein and the glial fibrillary acidic protein (GFAP) (Figures and ). The immunohistochemical expression of protein S-100 was weak at less than 50% of the tumor cells (), and a diagnosis of MPNST of the maxilla was made. The patient was referred to the Oncology Department and was subjected to surgical excision of the upper left lateral incisor as well as the total removal of the remaining lesion and adjuvant chemotherapy. The examination of the surgical part had not exhibited banks committed and it was staged as low grade of malignancy. The research of metastasis through the exams for images revealed no secondary tumors. The conduct of not using radiotherapy was a decision of the Clinical Oncology team. The patient was rehabilitated with an adhesive prosthesis in the region of the removal tooth (). In the last exam, cone beam computerized tomography (CBCT) imaging examination revealed the absence of the upper left lateral incisor, a loss of bone matter, and the absence of vestibular and lingual cortices in the inferior and central thirds of the alveolar ridge (vide reconstructions: panoramic in and axial in ). The tomography revealed normal trabeculation of adjacent bone tissue and preservation of the upper third of the alveolar ridge. The upper left central incisor exhibited a filled canal and a hypodense periapical area, suggestive of an inflammatory periapical lesion or a bone repair lesion after endodontic treatment. The absence of alveolar lamina dura and the loss of radicular matter in the mesiobuccal face were consistent with external root resorption and/or surgical resection (vide reconstructions: coronal in and upper left lateral incisor tooth in (sagittal)). The patient was tumor-free at the nine-year follow-up consultation.
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A 39-years-old Caucasian woman with a three-year history of recurrent swellings of both pinnae presented to our hospital's ENT department. Two weeks before presenting to the hospital, she suffered acute exacerbations that led to the obstruction of her left external auditory meatus. The swelling was painless and her main problem was diminished hearing as a result of the sudden occlusion of her external auditory canal. Although no positive family history could be found, the patient's personal medical history revealed that she suffered from generalized eczema and asthma during childhood. Her hearing was also impaired and she used hearing aids between the ages of one and 16 years.\nHer clinical records revealed that she first presented to a dermatologist due to intertrigal dermatitis when she was only 26 days old. By the time she was four months old, her whole body was covered with inflammation. She developed asthma at the age of four years and was diagnosed to have an eczema-asthma syndrome (ichthyosis and eczema). At the age of 11, she developed polyarthritis that affected her large and small joints. Rheumatoid arthritis was ruled out after due investigations, but she continued to receive treatment for seronegative polyarthritis.\nWhen the patient was 14 years old she presented to ENT with nasal obstruction and a large septal perforation. An audiogram examination showed that the patient had a bilateral conductive loss of hearing with an average of 35 decibels of air-bone gap across the 0.5, 1, 2 and 4KHz speech frequencies (Figure ). Tympanograms were peaked and showed a normal pressure range. Ossicular chain malformation was suspected and so her right ear was explored. A fixed stapes was discovered and a partial stapedectomy was carried out, which restored her normal hearing (Figure ).\nTen years later, she was offered surgical stapedectomy to improve hearing in her left ear but the patient declined this, as she was content with the normal hearing in one ear. The patient has maintained normal hearing in her right ear until she was 39-years-old (Figure ).\nA clinical examination of the patient revealed that she had thick, dry, scaly skin and scalp. Serous discharge from the skin folds and the scalp was also discovered. There was also a marked generalized telangiectasia (Figure ). Both auricles of the patient were chronically inflamed with the loss of normal contours but her earlobes bore no such inflammation (Figure ). A cystic swelling measuring about 3 × 4 cm in diameter filled the patient's left concha, which obstructed the external meatus. Her tympanic membranes were not visible. The patient had rhinolalia and her nose had a large septal perforation of both the cartilaginous and bony nasal septum (Figure ). The lateral walls of the nasal cavity were crusty and both middle and superior turbinates were atrophic and unidentifiable.\nBiochemical analysis and microbiological study of aspirate from the cystic swelling were unremarkable. Full blood count, erythrocyte sedimentation rate, urea, and electrolyte were all normal. Anti-neutrophil cytoplasmic antibody (c-ANCA), antinuclear antibodies, smooth muscles antibodies, and Venereal Disease Research Laboratory (VDRL) and treponema palladium haemagglutination (TPHA) tests for syphilis were all negative. Rheumatoid arthritis screen and autoantibody screen were also negative. Biopsies of the patient's left auricular cartilage, nasal septal cartilage and the lateral walls of the nose revealed a chronic non-specific inflammation.\nBased on her clinical features at presentation and her medical history, a clinical diagnosis of relapsing polychondritis was made, the patient having exhibited the following features: 1) recurrent bilateral auricular chondritis; 2) non-erosive seronegative polyarthritis; 3) chondritis of nasal cartilage; and 4) cutaneous inflammation. She was subsequently started on treatment. Seven years later, the activity of the patient's disease is under control although there is a significant irreversible damage to the affected organs. She was initially treated with high dose prednisolone and cyclophosphamide and is now on maintenance doses of prednisolone and azathioprine.
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A nine-year-old girl with HME and a strong family history presented with a limping gait and right drop foot. Plain radiography demonstrated exostosis in the right proximal tibia. The exostosis was excised, mostly from the posterior medial aspect of proximal tibia, and the peroneal nerve was explored one year later. There was no postoperative clinical recovery of the peroneal nerve. Nerve conduction studies performed one year later showed no evidence of sensory or motor abnormality within the right peroneal nerve. At the age of 12 years, the patient was referred to the senior author’s clinic and the clinical examination revealed a hemiplegic gait and brisk reflexes on the right side. The neurological examination revealed numbness below the neck, in both hands, and in both legs, which worsened when the neck was flexed or extended. The findings of examinations of the central nervous system and higher mental functions were normal, as was cranial nerve function. Examination of the motor system revealed spasticity and wasting on the right side, which was more proximal than distal. Muscle power was +4/5 in the right upper limb and +4/5 in the right lower limb with the exception of dorsiflexion of her ankle. Strength on the left side was normal.\nC-spine radiography did not show any obvious bony deformity. The MRI showed C1 exostosis arising from the left lamina causing cord compression. She underwent a C1 laminectomy and complete removal of the exostosis under general anaesthesia. There were no complications and no adverse events. The results of the neurology examination at discharge were the same as before surgery. The final pathologic diagnosis revealed a 2.5 cm exostosis.\nAt the 10-year postoperative follow up, her physical examination revealed a stable residual right hemiparesis, recurrent intermittent anisocoria, exaggerated reflexes, and clonus on the right side. Cervical magnetic resonance imaging (MRI) follow-up studies showed no recurrence of the lesion. The last MRI at age 19 years demonstrated an attenuated upper cervical cord with associated myelomalacia ().
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A 19-year-old male patient presented to us with NYHA class two dyspnea. He had previously been diagnosed with rheumatic heart disease and was put on penicillin prophylaxis. His physical examination showed regular pulse and his blood pressure was 120/86 mm Hg cardiac palpation and percussion was unremarkable; auscultation showed an accentuated first heart sound, and diastolic rumbling murmur. Chest X-ray showed evidence of pulmonary venous congestion. Transthoracic and transesophageal 2-dimensional echocardiography () revealed a double-orifice mitral valve of incomplete type at the leaflet level. Both orifice sizes were unequal in our patient, with the anterolateral orifice being much smaller than its counterpart. Surprisingly in our patient there was moderate subvalvular fusion and both commisures were fused contrary to other case reports mentioned in literature. Color doppler examination showed 2 separate mitral diastolic flows with mean gradients of 11 and 13 mm of Hg, respectively. There was no left atrial clot seen by transesophageal echocardiography.\nAfter informed written consent, BMV was performed using the Inoue-balloon technique. Initially, PA pressure recording was done and LV angiography recorded in RAO view for assessment of mitral regurgitation. Transseptal catheterization and left atrial placement of the balloon catheter were performed in the usual manner []. As balloon crossing of the anterolateral orifice proved difficult in the previous cases mentioned in literature, we crossed balloon through posteromedial orifice which was readily accomplished []. The posteromedial orifices were dilated using the stepwise dilation technique. Balloon catheter selection was based on the balloon reference size derived from the usual height-based formula and 4 mm less size was taken for first dilation. Following each dilation procedure and after confirming no significant mitral regurgitation or leaflet tears by echocardiography, the balloon size was increased by one mm. The procedure was terminated when the waist of the inflated balloon suddenly disappeared, and echocardiography confirmed separation of the mitral valve septation, resulting in a single enlarged orifice (). At the end of the procedure, the mean left atrial pressure, transmitral pressure gradient, and mean pulmonary artery pressure decreased as shown in . Repeat left ventriculography showed no increase in mitral regurgitation. Patient remained asymptomatic at the latest follow-up visits at one month after BMV. Follow-up echocardiography showed no mitral valve restenosis as defined by 50% reduction in the mitral valve area.
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The patient is a 29-year-old female with a history of diabetes mellitus type 1 who presented to the clinic for evaluation of recurrent symptoms of sinusitis and a persistent nasopharyngeal mass. Her symptoms first started at the age of 12 with chronic nasal congestion, repetitive sinus infections and chronic cough. Her tonsils and adenoids were removed at the time, but her symptoms persisted. Between the ages of 13 to 15 she was found to have a recurrent adenoid mass and tonsillar regrowth. She underwent another adenoidectomy and tonsillectomy. Microscopic description of the specimen showed overall preservation of the architecture with follicular hyperplasia and mildly expanded paracortex with scattered immunoblasts. The follicles show polarized germinal centers and contain numerous tangible body macrophages. Immunohistochemistry showed that the interfollicular paracortical cells are positive for CD3, CD5, CD10, CD43, BCL-2, CD1a, CD7, CD4, CD8, and TdT. The tumor was also negative for clonally rearranged immunoglobulin heavy chain gene and negative for clonal T-cell receptor gamma chain gene rearrangement. Additionally, the patient was noted to have an enlarged right cervical lymph node. Due to concerns about malignancy she was hospitalized for a bone marrow biopsy that was deemed negative.\nOver the following years the patient developed progressively worsening severe thick nasal drainage, rhinorrhea, frontal pressure and headaches, for which she presented to the clinic again at the age of 25. Her neck and sinus CT scan revealed maxillary sinus disease and significant lymphoid hyperplasia in the adenoid and tongue base region as well as a right cervical lymph node. She underwent a revision endoscopic sinus surgery and an adenoidectomy. Biopsy of the right-sided inflammatory process demonstrated an atypical T-cell lymphoid infiltrate, with a Ki-67 of 50–60%. She was then given a month of methylprednisolone (2 mg) taper and her cervical adenopathy diminished in size for a few weeks before it grew back along with fullness of the adenoid region, right posterolateral tongue asymmetry and lingual tonsil hypertrophy. She was given glycopyrrolate and saline nasal spray for her mucous secretions and was operated on again with removal of right lingual tonsillary tissue. Pathology of the tongue tissue demonstrated a predominantly atypical immature T-cell proliferation comprised of CD3-positive cells that co-express CD5, CD7, CD99, TdT, and CD117 with nodules of CD20 positive B-cells and scattered plasma cells. The atypical T-cells were also positive for CD4 and focal CD8. Immunostains for kappa and lambda showed no light chain restriction revealing that the plasma cells were polyclonal. Based on the clinical and pathological findings she was diagnosed with indolent T-lymphoblastic proliferation.\nUpon follow up she was noted to have regrowth of the lymphoid tissue within the nasopharynx and oropharynx leading to new symptoms of dysphagia and an intermittent choking sensation due to fullness in the back of the nose and throat. Due to this regrowth, decision was made to treat her involved pharynx and larynx with 12 days of radiotherapy to a total dose of 2400 cGy as shown in . Radiotherapy showed only partial improvement for 6 months and then symptoms progressed again and she was referred for an immunologic evaluation.\nPrior to the initiation of immunotherapy, a full immunologic workup was done. This showed normal serum immunoglobulins and IgG subclasses, negative HIV and 16/23 protective post-immunization titers to Pneumovax. Tetanus and diphtheria IgG were low protective. Serum EBV, CMV and HBV viral loads were all negative. Decision was made to start her on 50 mg of cyclosporine BID which was later increased to 100 mg BID due to persistent symptoms. She was also asked to rate her symptoms in severity from 1 to 10 prior to the initiation of the drug (), in order to assess her response to the steroid-sparing immunosuppressants.\nWhile on cyclosporine she reported episodes of recurrent sinus infections, progressive hoarseness and worsening dyspnea with increased work of breathing. On physical exam she had a regrowth of lymphoid tissue behind the left soft palate, increased lingual tonsil tissue which was partially obstructing her pharynx, and progressive airway distress with stridor. Laryngeal exam revealed fullness of the bilateral false vocal folds, fullness of the medial/inferior true vocal folds narrowing her airway, and irregular pink tissue of the proximal trachea all consistent with her proliferative T-cell process. The decision was made to provide definitive airway management through an awake tracheostomy with debridement of the excess laryngeal tissue.\nWith her airway safely secured, attention was returned to attempted medical management of her lymphoproliferative disorder. Due to lack of improvement on cyclosporine, a trial of 6 rituximab (100 mg) injections were administered. CT scan of the neck was performed following the 6 injections and showed no change. She was then started on Sirolimus, 2 mg daily.\nAfter 2 months on Sirolimus the patient started to report improvement. She tolerated Sirolimus well with no side effects, had improved airflow through the nose and mouth, and denied any exercise limitations. Her symptoms scores have all improved (). There was also improvement noted on laryngoscopy in the subcordal/subglottic area, with stable disease in the nasopharyngeal and tongue base. She was thus downsized to a Montgomery cannula. 10 months following the initiation of Sirolimus, her nasopharynx was less obstructed and she was no longer dyspneic with exercise. The globus stopped bothering her as much as it previously did, and her sleeping improved. She had an MRI to delineate the oropharyngeal component and it showed some base of the tongue and right lateral pharyngeal wall involvement but none were obstructing. Laryngoscopy showed stable nasopharyngeal and tongue fullness and reduced burden of the subcordal/subglottic disease on the true vocal cords. Due to the remarkable improvement, decision was made for decannulation with close follow up at 3 months' intervals.
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A 57-year-old, previously healthy woman working in the Department of Clinical Pathology of our hospital volunteered to participate as “healthy control” in a study to validate the accuracy of a new PCT assay. She reported to be in good general health condition without signs of ongoing infection or disease. The patient did not smoke or consume large amounts of alcohol and had no signs of malignancy on physical examination or routine blood analysis. Yet, a markedly increased level of circulating PCT of 0.35 μg/L (normal range < 0.03 μg/L) was detected, which remained elevated on follow-up measurements for the next 2 mo.\nSubsequently, calcitonin levels were found to be elevated as well (33 ng/L, normal range < 5 ng/L). A thyroid ultrasound revealed a goiter with small nodules in both thyroid lobes. There were two suspicious thyroid nodules, a small one lateral in the right thyroid lobe (7 mm × 5 mm × 6 mm) and a larger one (10 mm × 10 mm × 13 mm) in the left lobe. A fine needle aspiration (FNA) of the bigger node on the left side was done but neither reveal any malignant cells nor was it positive for calcitonin staining, making the existence of a MTC unlikely. To exclude a gastrointestinal neuroendocrine tumor or a small cell lung cancer, both of which have been reported to ectopically produce PCT as well, we decided to perform a 18F-FDG positron emission tomography-computed tomography (PET-CT), in which the left thyroid nodule detected on ultrasound showed an increased 18F-FDG uptake. There were no other suspicious lesions in the whole body PET-CT scan (Figure ).\nA previously healthy woman willing to support a scientific study was found to have an elevated level of PCT and calcitonin, a goiter, 2 suspicious nodes in the sonography of the thyroid gland with one of them showing metabolic activity in PET-CT scan.\nThe case was discussed at our internal tumor board, which recommended total thyroidectomy to exclude MTC despite the negative fine needle aspiration as no other cause of elevations in calcitonin and PCT could be found (Figure ).\nThe patient agreed to have surgery which went without complications. The histological evaluation of the thyroid gland showed an (incidental) 3 mm papillary microcarcinoma in the left lobe and a 6 mm medullary carcinoma in the right lobe, inconsistent with the active nodule in the left thyroid lobe in PET-CT. No further neck dissection was done due to the relatively low preoperative calcitonin levels.\nTwo weeks after surgery the patient came back to the endocrine office. Her PCT and calcitonin levels were now undetectable. We recommended close clinical and biochemical monitoring over the next years. Her prognosis is favorable due to the early recognition of the medullary cancer with small tumor volume, in total resection and no signs of metastasis.
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A 66-year-old male with comorbidity of diabetes mellitus and polyneuropathy underwent a living donor renal transplantation in 2013. A left-sided kidney was placed in the right iliac fossa. There was primary renal function and baseline creatinine was 83 mmol/L.\nThe patient presented with a one-day history of accidentally tripping and sustaining a fall on his way home from a football match. Though the impact of the fall was on the same side as his renal allograft, his presenting complaint was pain over the right chest wall. On examination, his pulse rate was 90/min and blood pressure was 164/72 mmHg. There was tenderness over the right chest wall but the abdomen was soft and the transplanted kidney was non-tender. A urine dipstick test was negative for red blood cells. There was no decrease in hemoglobin levels (Hb 11.9 gm/dL, WCC 10.3). Serum creatinine increased to 302 mmol/L. An ultrasound scan of the abdomen revealed an increased echogenicity of the kidney with a high resistive index of 0.96 and a perinephric hematoma which was 2.5 cm deep. A CT scan confirmed the presence of hematoma limited to the subcapsular space over the anteromedial surface of the kidney (). The patient was managed conservatively for 2 days as there was no decrease in hemoglobin levels. Creatinine levels deteriorated over the next 48 hours to 453 mmol/L and the patient’s blood pressure continued to increase to 196/90 mmHg. On the 3rd day of admission, he developed mild tenderness over the transplanted kidney and an ultrasound was repeated. This showed an increase in the size of the subcapsular hematoma to 11 × 4 cm mainly anterior to the kidney and compression of the kidney parenchyma and vasculature (). The resistive index increased further with a reversal of diastolic flow but no direct compression of the renal blood vessels (). There was no associated hydronephrosis.\nThe transplanted kidney was explored immediately and a large perinephric hematoma was evacuated. There was a small laceration on the anterior surface of the transplanted kidney which was not actively bleeding. A drain was inserted, topical hemostatic agents were applied, and the wound was closed. The patient recovered and creatinine levels returned to baseline (99 mmol/L) within 3 days.
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A 14-year-old girl, presented to our clinic with left knee pain, especially on full extension of the knee, for duration of 6 months. There was no trauma involved. Examination showed lateral joint line tenderness without any ligamentous laxity. Plain radiographs of the knee were normal. Further imaging with magnetic resonance imaging (MRI) scan revealed discoid lateral meniscus with a horizontal tear (\n). Diagnostic scope was done and we found an incomplete discoid lateral meniscus with complex vertical tear involving anterior horn with horizontal extension into the midbody (\n). Arthroscopic all-inside repair was done without any implant. Postoperatively, the patient's knee was protected with a brace. Postsurgery, 6 weeks, the brace was discontinued and the patient started full weight bearing without pain. At 6 months postsurgery, the patient was pain free and without any mechanical symptoms.\nThe position was supine, with the leg hung freely at the end of the table. A tourniquet was used to secure hemostasis. A standard anterolateral portal was used for diagnostic arthroscopy. The finding was an incomplete discoid lateral meniscus with peripheral vertical tear of the anterior horn and partial horizontal tear involving the mid body but not breaching the inner peripheries (\n). A standard anteromedial portal was made and the tear was further assessed using a probe. The tear site was prepared for repair. An additional far medial portal was made to allow arthroscopic instrumentation. A suture passer loaded with synthetic monofilament absorbable suture, introduced through far medial portal, while viewing through anteromedial portal (\n). The torn central fragment and the peripheral rim of the meniscus were penetrated and the tip of suture was pulled through using an arthroscopic grasper through anterolateral portal. The suture passer was reversed out of the far medial portal, leaving the suture inside. Then, a suture retriever was introduced through anterolateral portal and used to retrieve the suture tip bringing both suture-ends out through one portal. Both the suture ends were tied using a sliding knot technique. This whole process was repeated for a second suture repair (\n). The stability of the repair was assessed using a probe. Initially, we planned to saucerize the discoid meniscus together with meniscus repair. However, intraoperatively we decided not to saucerize the meniscus in view of the tear configuration. Due to the complex nature of the tear pattern (peripheral vertical tear with extensive horizontal tear through the meniscus body), saucerization would have made the articular surface of the meniscus a loose fragment or created a flap tear, which is more difficult to repair.
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A previously healthy one-year old Saudi boy presented to emergency ophthalmic room accompanied by his family with history of rapidly progressive proptosis of the left globe over the course of two weeks. There was no associated night sweat, fever, or weight loss and the patient had no previous illnesses. Systemic review showed that the patient was born at full term, of SVD, developmentally and vaccination is up to age. The patient had no known allergies, and no surgical history. The patient had stable vital signs, was active and alert. Ophthalmic examination revealed upper and lower lid edema, proptosis with mild downward and outward displacement of the eye without any signs of inflammation or chemosis of the left eye. Vision was central, steady, and maintained. EOM was mildly restricted with normal intraocular pressure. He had normal anterior segment and round, regular, reactive pupil and normal lens and fundus. Right eye examination was within normal limit. A complete physical examination was unremarkable, no signs of acute infection, and no palpable lymph nodes. The investigations ordered for the patient were full blood count (CBC), peripheral blood film, bone marrow aspiration, and CT and MRI imaging of orbits to determine the exact location and size of tumor.\nComplete blood count and peripheral blood smears showed elevated, unexpected, and abnormal high level of white blood cell count of 84.01 × 109/L with few atypical and blast cells which pointed toward acute leukemia. Chemistry was normal.\nComputed tomography (CT) of the head and orbit disclosed about 2.5 × 1 × 0.6 cm ill-defined focal lesion seen at the left orbital extra-conal region at the superomedial aspect causing inferolateral displacement of the left eye globe with mass effect also on the superior bony orbital roof. The mass showed mild homogenous enhancement after IV contrast (–). Orbital magnetic resonance imaging (MRI) showed left orbital mass of superomedial aspect of left orbit causing inferolateral displacement of left globe and medial orbital wall erosion with periosteal reaction, and opacification of left ethmoid and both maxillary sinuses (–). Based on the clinical, lab, and imaging study results, the differential diagnosis included: leukemia, lymphoma, rhabdomyosarcoma, eosinophilic granuloma, and idiopathic orbital inflammation (inflammatory pseudotumor). The patient was referred to a tertiary center where the patient was cared for by pediatric oncology team for diagnosis and treatment. The patient underwent thorough investigations in which bone marrow biopsy demonstrated leukemic cells and a diagnosis of acute myeloid leukemia (AML) with orbital granulocytic sarcoma was made.\nThe patient underwent systemic antileukemic chemotherapy, where the standard regimen for AML was given in the pediatric oncology unit. The regimen was two cycles of highly intensive chemotherapy. The first cycle of chemotherapy consisted of allopurinol, high doses of vitamin A, together with intrathecal methotrexate and dexamethasone, daunorubicin hydrochloride, and intrathecal vidarabine for central nervous system prophylaxis. No side effects or complications of chemotherapy were noted during the follow up period. Two weeks after chemotherapy, remarkable improvement and decrease of proptosis were observed, and the patient was scheduled for further follow up and a second cycle of chemotherapy in the coming weeks.\nThe parent of the patient provided written informed consent for the case details to be published, and no institutional approval was required to publish the case details.
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A 78-year-old woman underwent computed tomography (CT) because of a follow-up observation 1 year after right breast cancer surgery, and CT revealed a tumor in the colon. The patient was referred to our hospital for detailed examinations in November 2015. She had had recurrent right lower abdominal pain for about 1 year. She had no previous medical history other than the right breast cancer, and her family history was unremarkable. Physical examination revealed tenderness of the right lower abdomen, and the initial laboratory data were within normal limits. An abdominal CT showed a low-density tumor measuring approximately 30 mm in its largest dimension in the ascending colon (fig ). The tumor was well circumscribed and had a smooth demarcation. The CT density inside the tumor was the same as that of fatty tissues, and the CT density of the tumor circumference was same as that of the mucosal layer of the small intestine (fig ). An air contrast barium enema revealed an elevated lesion of approximately 40 mm in diameter with a smooth surface (fig ). A colonoscopy showed an SMT in the proximal ascending colon developing from the terminal ileum (fig ). The tumor was pedunculated, and the cushion sign associated with tumor was present (fig ). A colonoscopic ultrasonography revealed that the SMT was a high-echoic mass mainly localized in the submucosal layer (fig ). Based on the above findings, the SMT was diagnosed as a pedunculated lipoma originating from the terminal ileum and treated with ESD because of recurrent abdominal pain.\nA physiological saline with indigo carmine dye was injected into the basal portion of the tumor (fig ). This portion of the tumor was incised using an SB knife (Sumitomo Bakelite, Tokyo, Japan), and the submucosal layer of the basal portion was dissected (fig ). The 40-mm tumor was resected en bloc, and the resected SMT showed a yellowish inner substance, which coincides with the lipoma finding. No complications occurred during or after ESD. The patient was discharged 4 days after the surgery without complications and was relieved of symptoms afterwards.
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A 32-year-old man presented with colicky abdominal pain in the left lower quadrant for 2 weeks duration. He had a significant weight loss of approximately 30 kg over 2 months associated with decreased appetite. He also has a history of chronic alcoholism and smoking. There was no associated nausea, vomiting, hematemesis, melena, or hematochezia. Review of symptoms was negative for fever, arthritis, skin rash, jaundice, and pruritus. Two months prior, the patient was discharged from another hospital following a 6-week hospitalization for alcohol-induced necrotizing acute pancreatitis, which was treated successfully by conservative measures. Admission vitals revealed an afebrile and normotensive patient with a heart rate of 92 beats per minute and oxygen saturation of 98% on room air. On physical examination, the abdomen was soft with mild tenderness to deep palpation in the left iliac fossa and lumbar region. There were no signs of peritonitis. Laboratory results and abdominal sonogram showed no significant findings. Abdominal CT scan from the episode of acute pancreatitis 2 months ago showed findings consistent with necrotizing acute pancreatitis ().\nA colonoscopy was done because of the abdominal pain and significant weight loss. The scope revealed ulceration with a partial stricture at the descending colon approximately 30 cm from the anal verge (). However, the scope could not be navigated beyond the stricture. Controlled radial expansion balloon dilatation was tried without success in dilating the stricture.\nDue to tuberculosis (TB) being a possible differential diagnosis, a workup for TB was warranted. This included sputum for acid-fast bacillus, chest X-ray, purified protein derivative test, erythrocyte sedimentation rate, and pathological examination, all of which were negative for TB. Biopsy of the lesion revealed active focal colitis with ulceration, but no granulomas were seen. Barium enema and CT colonoscopy were done to assess the length of the stricture to plan an appropriate treatment strategy as shown in and , respectively. Barium enema findings were consistent with inflammatory bowel disease, as a benign stricture was seen with no evidence of malignancy.\nBased on the clinical presentation and barium enema, Crohn’s disease was high in the differential diagnosis. ASCA immunoglobulin G antibodies to saccharomyces cerevisiae was ordered with a result of 22.2 U/mL (>10 U/mL; ELISA [enzyme-linked immune sorbent assay]). The patient was thought to have had a CD at this point and was subsequently initiated on sulfasalazine. Despite treatment for CD, the abdominal pain persisted over the next month with worsening weight loss. Repeat colonoscopy was performed, which revealed further strictures requiring a segmentectomy with single layer extra mucosal end-to-end anastomosis. Anatomically, the left colonic segment was observed to be adherent to the pancreas. A surgical biopsy specimen revealed active focal colitis, and negative for TB and CD. A final diagnosis of colonic stricture due to acute necrotizing pancreatitis was made. Abdominal pain decreased postoperatively, and the patient was discharged on postoperative day 7. A follow-up colonoscopy 2 months later revealed healed anastomotic sites.
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A 42-year-old Caucasian male with ALS was admitted to the hospital with complaints of progressive swallowing and speech difficulties. Three years ago, this patient was diagnosed with limb-onset ALS and presented with other symptoms typical of ALS, including dysphagia, dysarthria, difficulty with coordination, and muscle wasting. The patient had no history of syphilis or other systemic infection, and the diagnosis of ALS was confirmed by the Netherlands National ALS Center.\nUpon admission to the hospital, the patient was only able to take a few steps and had been wheelchair-bound for the past four months. In addition, his upper extremities had been paralyzed for over twelve months (see\n). In the preceding months, the patient’s speech had degenerated, and the patient had difficulty swallowing both solid food and liquids, including saliva.\nshows the progression of symptoms and the effect of treatment. Dysphagia was confirmed at the time of admission by performing a fiber-optic endoscopic evaluation of swallowing (FEES) examination\n (\n). Physical examination and laboratory blood analysis revealed no other clinical pathology, and renal function was normal. The patient was not taking any prescription medications.\nThe patient had no history of seizures and was therefore eligible to receive high doses of penicillin G. After confirming that the patient was not allergic to penicillin (by administering a daily dose of amoxicillin for six days), the patient was started on a 21-day course of penicillin G and hydrocortisone (\n) delivered via midline catheter infusion. This treatment course was recently postulated to be efficacious for treating dysphagia, dysarthria, and other ALS-related symptoms\n.\nOn the 2\nnd and 3\nrd treatment days, the patient reported that he was able to lie in bed without experiencing muscle pain in the neck, shoulders, or back. On day 4, the patient was able to stand from a sitting position. On day 5, the patient was able to walk unaided a distance of approximately 100 meters (see\n). In addition, the patient’s speech and swallowing improved.\nAt the end of the first week, the patient’s dysphagia and dysarthria symptoms had resolved fully, and his walking had improved further. On day 9, the patient was able to move the fourth and fifth fingers on his right hand for the first time in a year, and by day 11 he had regained control of these two fingers (\n). On day 11, a repeat FEES examination confirmed that the patient’s dysphagia had resolved. On day 12, the patient was able to move all of the fingers on his right hand (\n) and grasp objects with his left hand, and he could once again operate the mouse attached to his computer. Furthermore, the patient’s voice recognition software was able to interpret the speech of the patient for the first time in months. On day 14, it was possible to sample venous blood from the patient’s forearm for the first time since he was admitted to the hospital. On day 18, the patient’s motor function further improved (\n).\nAt the end of day 21, physiological and FEES examinations revealed that swallowing function remained intact (\n), and the patient reported that his breathing and sleep quality had improved markedly during the treatment course. Therefore, in accordance with the defined treatment protocol, the midline catheter was removed and the patient was discharged. Upon discharge, the patient’s speech was restored to nearly pre-ALS levels, and he had regained the ability to stand from his wheelchair and walk unaided. The patient had also regained control over his fingers and had regained the ability to grasp light objects. Overall muscle function and strength were also improved as evidenced by increased power in his arms and legs and his renewed ability to stand, walk, and bend at the waist. Furthermore, his respiratory function had improved. Lastly, the patient reported that his general muscle pain had regressed, and the pain in his shoulder muscles had resolved completely.\nAfter returning home, the patient continued to improve. On day 22 (the first day following the end of the treatment course), the patient was able to lie in a dentist’s chair for 40 minutes without muscle pain, which had not been possible prior to receiving the treatment, and the patient was able to complete the dental procedure. On day 25, the patient was able to walk unaided a distance of approximately 650 meters. During the follow-up period from day 25 through day 75, the patient had generally stabilized. During days 76 to 91 the patient experienced increasing muscle pain in the neck, shoulders, or back, he no longer could operate the mouse attached to his computer, his voice recognition software no longer was able to interpret his speech, his walking ability regressed to the point that he not even take a few steps, and the patient became wheelchair-bound again. His swallowing and speech remained functional.\nOn day 92, the patient was readmitted to the hospital and started on a second 21-day course of penicillin G and hydrocortisone (\n) delivered via midline catheter infusion. Physiological and FEES examination on day 92 revealed that swallowing function had remained stable relative to day 21. During the 2\nnd 21-day course (days 92 to 113), the patient reported that he was able to lie in bed without experiencing muscle pain in the neck, shoulders, or back, and that his walking ability had slightly improved. Furthermore, his speech and swallowing function had improved. During days 114 to 150 the patient remained wheelchair-bound. His regained finger movement, swallowing and speech remained functional.
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Fifty-nine years old, Male.
Severe impairments in neurocognitive functions were identified during the treatment of his depressive disorder.
He was diagnosed with substance-induced depressive disorder in the mental health clinic of our hospital and was hospitalized for treatment. During this hospitalization, broad cognitive impairments were identified in the neuropsychological tests performed in January 2017. He visited the occupational environmental medicine clinic of Kosin University Gospel Hospital as an outpatient for the evaluation of the association with work.
The patient did not have a notable medical history except being hospitalized for herniated lumbar disc in 1997 and noise induced deafness in 1988. He did not have a family history of nervous disease or mental disease. He received worker’s compensation due to substance-induced depressive disorder in 2001.
He was married. With regard to the smoking history, the patient began smoking about a pack of cigarettes per week at age 20 and quit smoking after age 40. As for the alcohol history, he said that he drank about a bottle of soju per week from age 20 to 40.
The patient worked in the restaurant business for four years from age 23, and began working as a shipyard painter at age 27 in 1984. He was employed at the large shipyard D in July 1985. Since then he performed outdoor touch-up painting and spray painting ratio of 50 to 50. According to his statement, in his early working period, he had used inappropriate protection gear such as cotton cloth instead of gas mask. He also mentioned that he often worked overtime (until 10 p.m.), although the regular working hours were from 8 a.m. to 5 p.m. He was diagnosed with depressive disorder resulting from organic solvent intoxication, and it was approved as an industrial accident in 2001. He returned to work in 2006 and worked as a shipyard painter for about four years. Later, he repeatedly alternated between a leave of absence and return
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The patient is a 43-year-old female who developed end stage renal disease following an ANCA positive rapid progressive glomerulonephritis, for which she received a living donor renal transplant six years ago. The donor tissue was negative for Epstein Barr Virus (EBV serologies, while the recipient was positive for EBV IgG Antibodies only. She was managed on chronic immunosuppression with a combination of azathioprine and prednisone.\nThe patient presented initially after an exacerbation of chronic lower back pain following a non-traumatic injury while dancing. Radiographs and MRI of the lumbar spine were performed as part of the initial work-up. Radiographs were negative for acute injury. MRI of her L-spine incompletely captured irregular marrow signal at her left ischium and right sacral ala. This raised the concern for a primary or metastatic marrow replacing process and prompted further imaging work-up. MRI of the pelvis and sacrum performed at this time demonstrated multiple T\n2-hyperintense and enhancing osseous lesions involving the lumbar spine, sacrum, pelvis, and proximal left femur. Several lesions demonstrated aggressive features, including periosteal reaction and large extra osseous soft tissue components (). The multifocal nature of the bone involvement and the presence of lytic and aggressive features raised concern for osseous metastatic disease from a distant primary.\nCT of the chest, abdomen, and pelvis was performed at this time in attempt to locate a primary site of disease. The CT scan again demonstrated multiple bone lesions with areas of marked cortical destruction (). Numerous round pulmonary nodules measuring up to 1.8 cm, as well as a few enlarged axillary lymph nodes, the largest measuring 2.1 cm in the short axis, were also noted. However, there was no conclusive primary site of malignancy. Fluo-D-glucose positron emission tomography revealed markedly fludeoxyglucose (FDG) avid bone lesions with maximum standardized uptake value up to 35.8 (). Additionally, the rounded pulmonary nodules and prominent thoracic lymph nodes were found to be FDG avid as well, with the SUVmax of the nodules and lymph nodes measuring 23.6 and 30.9, respectively ().\nCT guidance was utilized in the biopsy of the large destructive sacral bone lesion. Pathological analysis revealed an EBV negative, diffuse large b-cell lymphoma with a high proliferation rate. confirming the diagnosis of PTLD. The additional thoracic findings were then presumed to be from PTLD given their rounded, mass-like appearance and marked FDG, and therefore biopsy of these lesions was not pursued.
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A 13-year old boy born in Albany was admitted to Santa Maria Hospital of Terni on 19 July 2017 for left renal colic. He had been an orphan at the age of three years and was entrusted and adopted to his uncles in Italy at the age of four years. His clinical history indicates no relevant medical problems until the age of nine when he underwent appendectomy for acute appendicitis. In the following two years, no disease occurred, and neuromotor and psychiatric development was normal as stated by the primary care paediatrician who visited him during annual health check-ups.\nApproximately one year before admission to our hospital at 12 years of age, the boy began to suffer from severe pains in the left lumbar region. These painful crises were characterized by monthly cadence, sudden onset, extremely high intensity and spontaneous remission within a few tens of minutes. To assess whether the pain depended on the kidney and the urinary tract, renal ultrasonography and renal scintigraphy with technetium-m99 mercaptoacetyltriglycerine (MAG 3) were performed. Echography revealed a grade 3 hydronephrosis (20 mm) in the left kidney. Almost all calyces were observed, and a large renal pelvis without parenchymal thinning was noted. MAG3 revealed good renal function balanced between the two kidneys with only slight reduction of the ureteropelvic drainage on the left side. A ureteropelvic junction obstruction caused by abnormal polar vessels was suspected. A JJ stent was positioned. A few weeks later, laparoscopic robotic pyeloplasty was performed. However, no polar vessels were found.\nDespite this procedure, two months later, he was admitted to a second hospital for left renal colic. Here, radiographic evaluation of the abdomen revealed that the stent was correctly positioned, and renal ultrasonography revealed reduction of the known left pelvic dilation to 17 mm. The abdominal pain was attributed to the prolonged stay of the JJ stent with a supposed coexistence of vesicoureteral reflux caused by the stent itself. No complication of the pyeloplasty was noted. The JJ stent was removed, and this procedure was associated with the apparent remission of pain.\nHowever, new hospitalization in a third hospital was necessary on July 2017 for a new episode of renal colic. During this hospitalization, a further reduction of the pelvic dilation to 10 mm was noted through renal ultrasonography and abdominal magnetic resonance. Paradoxically, repeated urinalyses never evidenced blood or increased mineral excretion suggesting urolithiasis. Tests for the evaluation of renal function were in a normal range. The boy was discharged without any therapy but with the recommendation to return within two weeks for further assessments.\nOne day after discharge, symptoms of renal colic occurred, and he was admitted to our hospital. Physical examination did not reveal significant abnormalities. Only some small scars were noted on the mucous side of the prepuce. When asked, the boy could not provide an answer regarding the origin of these scars and how long they were present. All the laboratory tests already performed, including urinalysis, were repeated. In the repeated analysis, no abnormal results were observed. In particular, no blood was detected, whereas Mg, Ca, P, oxalate, citrate, sulfate and ammonia excretion levels were in the normal range. Radiopaque concretions were not noted in direct abdomen radiography. Ultrasonography was negative for calculi, and the previously observed slight pielectasia in the left renal pelvis was confirmed. The bladder was distended without appreciable endoluminal images. Despite these findings, on the morning of the second day of hospitalization, the boy indicated he expelled multiple stones from the urinary tract during the night. The stones were greyish-whitish with irregular margins and seven to eight millimetres in diameter (). Laboratory evaluation revealed that the examined stone material was not related to lithiasis of the urinary tract.\nThus, the patient was observed during his following urinations by the nursing staff to monitor the possible expulsion of additional stones. After three days of close observation and surveillance of each urination event, the patient did not expel any additional stones.\nDespite this, he continued to claim he experienced severe pains in his left flank. Suspicions about the factitious nature of his symptoms were raised. A placebo was administered, which led to the resolution of renal colic. Consequently, a psychological and psychiatric evaluation of the boy was performed. Regarding the neuropsychiatric evaluation, several specific tests and interviews were performed. The Wechsler Intelligence Scale for Children: Fourth Edition (WISC: IV) was used to assess intelligence and cognitive function. From the evaluation, a cognitive level in the standard (QI of 80) emerged with a Verbal Comprehension Index (VCI) of 108, a Perceptual Reasoning Index (PRI) of 93, a Working Memory Index (WMI) of 103, and a Processing Speed Index (PSI) of 53. To examine the presence of anxious symptoms, Multidimensional Anxiety Scale for Children (MASC) was used. Clinically significant scores were noted in areas related to Performance Fears (T80) and Physical Symptoms (T72). To analyse the presence of depressive symptoms, Children’s Depression Inventory (CDI) was used, and clinically positive scores were found in areas related to Negative Self Esteem (T75), Interpersonal Problems (T80) and Anhedonia (T71). Overall, based on tests and interviews, socio-relational difficulties and a marked tendency for isolation emerged that was associated with relevant aspects of emotional and behavioural inhibition. Therefore, individual psychotherapy intervention was recommended. The paediatric psychiatrist confirmed the diagnosis of Munchausen syndrome according to the DSM 5 diagnostic criteria for this condition [].\nThe patient’s uncle was not convinced of the diagnosis and pretended to demonstrate the real nature of the patient’s symptoms by showing some videos in which the patient expelled the stones from his urethra during urination. However, upon closer observation of the videos, it appeared clear that the boy was actually handling his prepuce to excrete the stones. This evidence explained the scars that were found on the mucous face of his prepuce. Despite this information, the patient’s uncles continued to refuse the diagnosis. Fortunately, a therapeutic plan with psychiatrist support was later accepted with a positive outcome. No further signs and symptoms of renal colic were reported.
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A 54 year old male, with no comorbidities or significant social history presented to the emergency department with a three day history of intermittent generalized abdominal pain radiating to the back. He did not endorse a history of constitutional symptoms. Upon presentation to the emergency department he was hemodynamically stable. Physical examination revealed a soft abdomen with generalized tenderness particularly in the epigastric region. Initial lab results showed a WBC 6.77 × 109/L, serum amylase 79IU/L, urinary amylase 738IU/L, CRP 73.88 mg/L, D-dimer 13.66ug/ml, and a Lactate of 1.87 mmol/L. The patient was subsequently admitted under the gastroenterology service with the diagnosis of pancreatitis.\nPreliminary CT Abdomen with oral and IV contrast showed acute pancreatitis with superior mesenteric and portal vein thrombosis and no evidence of mesenteric small bowel involvement (). He was managed conservatively on the ward by means of heparin Infusion and thereafter switched to LMWH and warfarin. A week later he developed sustained tachycardia and sudden drop in WBC with associated increase in lactate to 5.31IU/L. A follow up CT abdomen with IV contrast revealed diffuse wall thickening involving multiple loops of jejunum highly suspicious of bowel ischemia (). A decision was made to proceed with an exploratory laparotomy which revealed no evidence of full thickness necrosis but characteristics of small bowel edema secondary to SMV thrombosis. Additionally, the pancreas appeared inflamed and edematous with evidence of intraperitoneal calcification within the lesser sac. An ABthera vacuum dressing was applied in anticipation of a second look laparotomy. The patient was shifted to the ICU where he showed evidence of progressive acute hepatic failure with rising INR, bilirubin, and serum ammonia level. On re-evaluation of the bowel within 48 h, we noted viable but dusky appearing jejunum. An access sheath was inserted retrograde from the middle colic vein into the superior mesenteric vein and portal vein where a catheter was placed for the direct thrombolysis (). A bolus of Heparin 1000 IU followed by 500 IU/hr infusion was delivered through the sheath along with Altepase 1 mg/hr for a 24 h period.\nFollowing the 24 h period, a third look exploratory laparotomy was performed where the vascular catheter placed was removed. An Intraoperative venography showed patent portal veins (). However, 100 cm segment of proximal bowel was found ischemic and therefore a resection and side to side anastomosis was done.\nThe patient had an uneventful post-operative course. A week after his final laparotomy, an ultrasound abdomen was performed showing resolved portal and superior mesenteric vein thrombosis. The patient was discharged in a satisfactory condition on Warfarin 3 mg PO OD.
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A nineteen-year-old female patient had been referred to the orthodontist by a general practitioner, and her major complaint was unsatisfactory facial and dental aesthetics in addition to remaining dental spaces due to early loss of the permanent first lower molars. Clinical records indicated no step back for orthodontic treatment. The extraoral examination pointed out to slight facial asymmetry, convex profile, and absence of passive lip sealing (). No signs and symptoms of TMJ dysfunction were indicated.\nThe intraoral clinical examination and casts evaluation revealed that the patient was in permanent dentition phase, with the absence of teeth 36 and 46, Class I canine relationship, and biprotrusion (). The early loss of the first lower molars had occurred due to extensive cavities. The edentulous spaces presented 6 mm on the left side and 9 mm on the right side. The bucco-lingual width of the alveolar crest was 5 mm on the left side and 4 mm on the right side. The curve of Spee was moderate ().\nThe panoramic radiograph examination showed absence of the first lower molars, tipping of the second molars towards the edentulous space, and presence of the left third lower molar and right third lower molar in the eruption process, with 2/3 of the root formed. No significant indication of bone loss in the edentulous region was indicated ().\nThe lateral cephalometric analysis indicated maxillary protrusion and minimum mandibular retrusion (). In addition, the dolichocephalic skeletal pattern was observed, proclined upper and lower incisors, which leads to biprotrusion diagnosis and protrusion of lower lip turning soft tissue profile not suitable ().\nThe objectives of this treatment were to improve facial aesthetics, correct dental biprotrusion, and close edentulous spaces.\nThe patient's complaint regarding her facial aesthetics could have been solved through the extraction of the upper and lower first bicuspids as well as anterior retraction if conventional orthodontics were to be applied. The space of the lower molars could have been maintained with further prosthetic rehabilitation using implants and/or fixed prosthesis. After discussing the treatment options with the patient, it was decided to close the edentulous lower spaces instead of extraction of first lower bicuspids and extract the upper first bicuspids in order to maintain canine Class I and provide anterior retraction on upper and lower arches.\nA Roth prescription bracket, slot 0.022″ (Abzil, 3M), was installed, and bands were placed on the upper first molars and lower second molars and also on third lower molars. The initial alignment and leveling were carried out using 0.012″ NiTi, 0.014″ NiTi, and 0.016″ NiTi and 0.018″ and 0.020″ stainless steel wires until reaching 0.019 × 0.025″ ss. At this stage, the upper arch was segmented in three parts: (1) between canine-canine, (2) second bicuspid to first right molar, and (3) second bicuspid to first left molar. The lower arch was also segmented in three parts: (1) between second bicuspids; (2) second molar to third right molar, and (3) second molar to third left molar. This segmentation was done in order to prepare for installation of T-loops, and because a segmented arch technique was planned, this needed to be done.\nT-loops were then constructed with 0.017 × 0.025 TMA wire and positioned on the upper and lower arches for space closure. The springs were positioned between the cross tube (lateral incisor and canine) and the accessory tube of the bands. The upper arch received a T-loop symmetrically activated, type B, to provide anterior retraction and anchorage loss at the same time. The lower arch, on the other hand, had a T-loop displaced to the anterior, type A, enabling anterior retraction () without or with minimum anchorage loss of second molars. The preactivations of the T spring were conducted according to Kuhlberg and Burstone [].\nAfter the full closure of spaces, details of the occlusion were taken into consideration with continuous 0.019 × 0.025″ stainless steel arches. After 32 months of active treatment, the fixed appliance was removed.\nBy the final stage of the orthodontic treatment, we observed more pleasant facial aesthetics with improvement of the lip protrusion and passive lip sealing (). The intraoral examination pointed out to a satisfactory occlusion with coincidental mid-lines, Class I canine relationship, Class II molar relationship, and correction of upper and lower incisor excessive inclination occurred. The spaces of teeth 36 and 46 were fully closed. The major alterations were the retraction of the anterior teeth and space closure (Figures and ). The panoramic radiograph pointed out average control of posterior lower teeth axial positioning and the presence of tooth 28 (). Lateral radiograph showed better inclination of upper and lower incisors, along with better lip sealing and improvement of soft tissue profile ().\nInformation shown in shows the gradual increase of nasolabial angle through debonding and follow-up; decrease of IMPA, demonstrating the retraction of inferior incisors; and an improvement of interincisal angle and upper and lower aesthetic line.\nThe facial characteristics obtained after the treatment were maintained throughout a six-year follow-up (). Extraction spaces remained closed, and little alteration occurred in the positioning of the incisors (Figures and ); panoramic and lateral radiographs demonstrated that the characteristics were maintained (Figures and ). The superimposition of cephalometric tracings can show dental and profile modifications during orthodontic treatment through a 6-year follow-up ().
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A 15-year-old female with a past medical history of obesity presented to the emergency department with a marked 90-degree flexion at the thoracolumbar region. She was able to walk only by using a walker in an unusual manner; she placed her axillae on the hand grips. The patient described constant back pain almost daily for which she took ibuprofen with moderate relief. These symptoms began three years ago following a sexual assault and have progressed significantly. As per the patient's mother, the only time the patient's spine straightened out was during deep sleep. She had no neurologic complaints, specifically denying any sensory or motor deficits, fatigue, ptosis, or any complaints consistent with any form of endocrinopathy. Her family history included siblings with epilepsy, ADHD, and mood disorders.\nThe patient denied any substance abuse, including use of alcohol or cigarettes, as well as being sexually active. She reported no history of mood or psychotic symptoms and no suicide attempts.\nDespite the pain, however, the patient was not concerned with her condition. The patient herself was not interested in physical therapy or additional diagnostic testing or counseling despite her mother's encouragement. She refused a gynecological examination due to anxiety following having been a victim of sexual assault; it was unclear the extent of counseling, if any, she received following the assault.\nThe patient was a seventh grader at a local school where she participated in extracurricular activities. She reported being well accepted by her peers. She stated having a good social support network including friends and family. Her parents were separated and she lived with her mother and brother.\nPhysical exam revealed an obese (BMI 39.2) Caucasian female, leaning forward with the spine nearly ninety degrees at the waist. Extremities showed normal strength, sensation, and range of motion. The patient was unwilling to attempt spinal extension. Tenderness to palpation of the paraspinal muscles was present. The rest of the physical examination was unremarkable.\nUpon Pediatric Neurology consultation, no evidence of neuromuscular disease was found. Plain radiography of the cervical, thoracic, and lumbar spine was limited due to her deformity, but no abnormalities were noted. Magnetic resonance imaging of the same was unrevealing. Psychiatric consultation was obtained; they concluded that the patient's symptoms were likely manifestations of Conversion Disorder, following exclusion of organic causes.\nWhile she is currently receiving social services support and physical therapy; she declines psychiatric outpatient care at this time.
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The patient was a 73-year-old Chinese woman with osteoarthritis in both knees. In the recent half year, she had been suffering from intractable right knee pain with failed conservative treatment and prepared for right side TKA. She had a 27-year history of hypertension and her blood pressure was controlled well by medication. She had no other medical history, including smoking history. Her BMI was 24. The physical examination showed a limited range of motion (ROM) of 0°–120° without varus or valgus deformity. Preoperative X-ray showed narrow medial knee joint space and osteophyte formation without vascular calcification (Fig. ). The peripheral pulses and capillary refill were normal, although the preoperative Doppler ultrasound showed arteriosclerosis with plaque formation in the arteries in both legs.\nThe right side TKA with a posterior stabilized design (LPS, NexGen, Zimmer, Warsaw, USA) was performed under general anesthesia. A tourniquet was applied for 70 min at a pressure of 250 mmHg. The whole surgery was completed without any complications and there was normal intraoperative bleeding at the surgical site. The postoperative X-ray showed successful implantation for the right knee (Fig. ).\nHowever, immediately after the surgery, routine peripheral pulse check in the operating room found absent dorsalis pedis artery pulse in the right foot. The patient was closely monitored in the recovery room. After approximately 2 h, there was no improvement in peripheral pulses, capillary refill, and oxygen saturation. In consideration of the high possibility of arterial occlusion, the vascular consultant recommended using 1000 U heparin for anticoagulation and immediate evaluation by arteriography for diagnosis. An emergency arteriography under local anesthesia showed that there was a short segmental occlusion of the popliteal artery (Fig. ). Then the angioplasty was performed with a balloon with a diameter of 5 mm for 3 min. Follow-up imaging showed excellent blood flow although vascular stenosis was still observed in popliteal artery (Fig. ). There was a return of palpable pulses and a normal capillary refill and oxygen saturation.\nAfter the patient returned to the ward, 12 500 U heparin in 50 mL saline was pumped 1 mL/h and activated partial thromboplastin time (APTT) was controlled around 40 s. The peripheral pulses were closely monitored. On postoperative day 2, the patient was allowed to walk with aids. On postoperative day 6, the anticoagulation plan was changed to rivaroxaban 10 mg two times a day and aspirin 100 mg one time a day for 3 weeks orally. The patient was discharged home 2 weeks after surgery without any complaints.\nAt the most recent follow-up in the orthopaedic clinic (3 months after surgery), there were no orthopaedic or vascular complaints. The patient had an ROM of 0° to 125° with excellent muscle strength and could walk without aids for 1 km.
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An 18-year-old male visited the medicine outpatient department with the primary complaint of pain in the neck, weakness in the right upper and lower limb, increased sensations on bilateral upper and lower limbs and pain in both the upper and lower limbs along with tingling sensations for the last three months. There was no history of bladder and bowel involvement. There was no history of trauma, fever, or loose stools. The patient had no prior co-morbidities and there was no family history of any congenital disorder.\nOn examination, pulse was 88 beats per minute, regular, blood pressure was 110/70 mm Hg in right arm supine position,spo2 was 97 percent on room air, pallor was absent and there was no cyanosis. The patient had tall and thin stature with the ratio of the distance from head to pubic symphysis divided by the distance of pubic symphysis to the sole calculated to be 0.80( less than a normal ratio of 0.85) and a raised ratio of arm span length to the height calculated to be 1.09 (more than the threshold of 1.05) as shown in Figure . The wrist sign and thumb sign were positive. There was no low-lying hairline. The patient was conscious and oriented to, time place and person with normal higher functions. Cranial nerves were normal. On motor examination, the bulk of the muscles was bilaterally equal, the tone was normal in all four limbs, power was 4/5 in the right upper and lower limb and 5/5 in the left upper and lower limb, gait was normal and there were no involuntary movements. On sensory examination, the sensation of pain and temperature were raised bilaterally, vibration and pressure sensation were intact. Joint position and stereognosis were intact. Deep tendon reflexes were exaggerated bilaterally and were 3+ on the right upper and lower limb and 2+ on the left upper and lower limb; there was no inversion of biceps reflex and plantar was bilateral extensor. Coordination was normal. The patient had a clear chest on auscultation,s1 and s2 were heard and abdomen was soft and non-tender. MRI of the cervical spine was done, which revealed evidence of fusion of the anterior arch of the atlas with clivus along with the fusion of the posterior arch of C1 with occipital bone (Figure ). There was hypoplasia of the occipital condyles with narrowing of the foramen magnum (8mm in anteroposterior diameter) with kinking and compression over T2 signals which were approximately 17 mm long. These features were suggestive of craniovertebral junction anomaly in the form of atlantooccipital assimilation with basilar invagination along with compression myelopathy of the adjacent cervical medullary junction and proximal cord. Routine lab investigations were carried out which were within the normal limit (Table ). 2D echo was done, which revealed floppy mitral valve, normal chambers, good biventricular systolic function, no pericardial effusion, no signs of infective endocarditis, no mitral or aortic regurgitation and no evidence of aortic root dilatation. The patient was taken for Decompression to relieve compression along with cervical arthrodesis at C1-C2 level to provide spinal stability, as shown in Figure . A midline incision was made below C2 level and it was deepened, leading to exposure of subocciput, foramen magnum and C2. C2 was found to be in approximation with foramen magnum. Facet joints C1C2 were found distorted and the facet of C2 was placed superficially on the right side and the facet of C1 was deeper and had lost its normal alignment. Under C arm guidance C1C2 fixation was done and foramen magnum decompression was performed by excision of about 2.5 cm rim. The patient was given physiotherapy post-operatively. He recovered and was discharged after 23 days of surgery and is currently doing well on follow-up.
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The patient in this case was a 24-year-old male. According to his parents, the patient was a healthy individual with no past medical history or social history. He had been traveling with his family in the back seat of the car when he became unresponsive and “started shaking” per his parents. The emergency medicine personnel who were on scene indicated that the patient had experienced a witnessed generalized seizure and was unresponsive until arrival to the ED.\nIn the ED, the patient appeared to be postictal but slowly became more arousible, capable of answering questions for himself. As the patient's mental status improved, he became combative, requiring an initial dose of 2mg of lorazapam then a second dose of 6mg of lorazapam. The labs for this patient showed an elevated ammonia level at 86, lactic acid of 8.1 and an anion gap of 18. Urinary drug screen, alcohol, and CT of the head were also negative.\nAfter discussion with the family, the patient was then admitted to the hospital due to the possibility of a first seizure. An MRI of the brain and EEG were both performed and returned with normal results. Patient was seen by neurology and was discharged home on phenytoin with a discharge diagnosis of generalized seizures.\nTable 1 highlights the lab work that was performed for each of these patients and the specific times that the initial and subsequent labs were drawn. Please note that abnormal values are listed in bold font. As this was a retrospective case series, there were no criteria for timing of initial or repeat lab draws followed. Labs were drawn upon evaluation of the patients and repeated as indicated by clinicians’ judgments.\nAs shown in Table 1, each of the patients had initially elevated ammonia levels. Even though repeat labs were drawn at various times, each showed decreased patient ammonia levels. Of note, Cases 2, 4, 5 showed ammonia levels of 290, 277, 96 respectfully, with each of these patients’ repeat labs performed around 3 hours later and showing normal ammonia lab values (i.e., 19, 22, 47, respectively). Also of interest, Case 6, with an initial ammonia of 86, showed a repeat normal ammonia level approximately two hours later.
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A 61-year-old man experienced upper abdominal and lower left back pain 1 month and 1 week prior to examination, respectively. He was referred to our hospital after the pain had worsened. The patient experienced spontaneous lumbar and epigastric pain with muscular defense of the epigastrium and accompanying tenderness. Blood test results indicated a white blood cell count of 12,430 /μL, a C-reactive protein level of 0.6 mg/dL, and mild but increasing inflammation. No abnormal findings were reported from the other blood counts, biochemical examinations, and coagulation tests.\nAbdominal contrast-enhanced computed tomography (CT) revealed disruption and thickening of the anterior wall of the gastric antrum. CT also revealed the presence of ascites and free air at the ventral side of the stomach and on the surface of the liver (Fig. ). Several enlarged LNs (maximum diameter, 30 mm) were identified along the greater gastric curve and a low enhanced lesion (measuring 30 × 25 mm) was detected on the lateral segment of the liver (Fig. ). A diagnosis of advanced-stage GC resulting in a spontaneous gastric perforation, with perforative peritonitis, multiple LN metastases, and a solitary liver metastasis was made and an emergency laparotomy was performed on the same day. A moderate amount of turbid ascites was observed in the abdominal cavity during laparotomy. A 7-mm perforation of the gastric antrum was detected, along with marked thickening of the gastric wall and coarse neoplastic tumors that were attached to the gastric wall (Fig. ). The tumors were exposed on the serosal surface along the gastric perforation. The patient was diagnosed with advanced-stage GC resulting in a spontaneous gastric perforation. No peritoneal dissemination was observed. Preoperative CT also revealed the presence of metastases in several enlarged LNs along the greater gastric curve, as well as, a number of hardened regions in the lateral segment of the liver. A distal gastrectomy with radical lymphadenectomy and cholecystectomy was performed. Reconstructive surgery was achieved using Billroth II anastomosis. No postoperative complications occurred and the patient was discharged.\nGross findings of the resected specimen included an ulcerative and infiltrative (type 3) tumor (approximately 100 × 50 mm) with an infiltrative serosal surface and 7-mm puncture sites (Fig. ). Microscopic findings revealed that the tumor was comprised of a homogeneous proliferation of polygonal tumor cells with abundant, eosinophilic, and clear cytoplasm. Numerous mitoses were also detected. The tumor cells exhibited solid or thick-trabecular patterns with scanty stroma containing blood vessels that resembled HCC and expansive invasion into the gastric wall (Fig. ). Features of enteroblastic differentiation and Schiller-Duval bodies were absent.\nImmunohistochemical staining was performed to characterize the tumor cells (Table ). The tumor cells stained positive for AFP and Sal-like protein 4 (SALL4), but were negative for carcinoembryonic antigen, synaptophysin, chromogranin A, and neural cell adhesion molecule (Fig. –). According to these findings, the patient was diagnosed with GHAC. No tumor cells were observed during the cytological examination of ascites. LN metastases were detected in 6 LNs (20%) and a solitary metastasis was detected on the lateral segment of the liver. Subsequently, the patient was classified as having a Stage IV (T4aN2M1) GHAC. Moderate venous and lymphatic infiltration was observed. Postoperative blood biochemical analysis revealed an elevated AFP level (487.4 ng/mL), which supported a diagnosis of GHAC.\nThe patient was followed-up for 11 weeks post-gastrectomy to monitor the occurrence of new LN or liver metastases. Because no new lesions were detected, resection of the lateral segment of the liver was performed, at another hospital, 13 weeks after the initial operation. The patient was confirmed from histopathological examinations as having GHAC with a solitary liver metastasis. An elevated serum AFP level (1214.9 ng/mL) was recorded 6 weeks after hepatic resection and recurrence of LN metastasis was detected on CT. Combination chemotherapy with tegafur/gimeracil/oteracil (S-1) was administered at a dose of 120 mg/day for 2 weeks with a 1-week rest. Three months later, serum AFP levels had normalized and shrinkage of the resected LN was observed. Elevated serum AFP levels were not detected 15 months post-recurrence and complete response of the LN metastasis was achieved.
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A 35-year-old Caucasian female patient presented to her local emergency department in November 2016 with a chief complaint of neck pain. The patient had a past medical history significant for Hodgkin lymphoma diagnosed in 1998 following excision of a neck mass at age 16. She underwent chemotherapy and mantle field radiation in 1998. The radiation targeted lymph nodes in the neck, axilla, and behind the sternum in order to encompass the nodal basin of her cancer and the common lymph node drainage areas. The patient denied any history of radiation to her face. She reported remission at the time of presentation for this complaint of neck pain and was not following with anyone for her history of HL. She had no notable past surgical history. Menarche was at age 13 and she gave birth to one child at age 18. The patient’s family history was unremarkable with the exception of ovarian cancer in her maternal great aunt. There was no family history of breast or thyroid cancer. The patient was a previous smoker, quitting after about 10 years of use. No drug or alcohol use was recorded.\nIn the emergency department, a neck CT revealed a subcutaneous mass over the mid-clavicle, a breast mass, and multiple nodules in the thyroid gland with the largest nodule measuring 1.5 × 1.6 × 2.0 cm. The breast mass had dimensions of 2.6 × 4.0 × 4.9 cm by ultrasound. The patient was instructed to follow-up in breast and thyroid clinics for these findings.\nThe patient followed the emergency department’s recommendations and was examined by a surgical oncologist. In the breast clinic, she stated that the large right upper-outer quadrant breast mass had been present for 1 year. She was unsure how long the mass overlying the clavicle had been present, as it had been asymptomatic. On physical examination, the patient appeared well developed and well nourished. Respiratory, abdominal, musculoskeletal, and cardiovascular systems were normal. An 8.0 cm mass was located in the upper-outer quadrant of the right breast centered at the 10:00 axis about two fingerbreadths on the nipple border. Nipples were normal bilaterally. There was no cervical, supraclavicular, or axillary lymphadenopathy. Directly overlying the clavicle about two fingerbreadths medial to the mid-clavicular line was a 0.6 cm mobile mass within the skin. It was not associated with any regional lymphadenopathy. Laboratory workup was negative and unremarkable.\nThe patient underwent a bilateral mammogram in December 2016, followed by ultrasound-guided core biopsy of the breast mass. Initial core biopsy performed at an outside institution of the right breast mass came back as fibrocystic change. The outside biopsy was not reviewed at our institution. Based on a high level of clinical suspicion, additional imaging and a repeat biopsy were performed at our institution in January 2017. The repeat biopsy of the right upper-outer quadrant breast mass showed a phyllodes tumor. Pathology results described a fibroepithelial lesion with hypercellular stroma, mild-moderate stromal cytologic atypia, increased stromal mitotic activity (4-5/10 HPF), and focal areas suggestive of phyllodes architecture. The nature of the margins (pushing or infiltrative) could not be determined from the biopsy material. MRI showed the phyllodes tumor in the right breast measuring 4.7 cm. An excisional biopsy of the clavicular mass was done in a separate operation. The biopsy result was a cutaneous adnexal adenocarcinoma with eccrine differentiation. Surgical excision was recommended for both the breast and clavicular masses (Figures and ).\nThe patient also followed up in thyroid clinic for the multinodular goiter seen on her CT scan of the neck in the emergency department. Review of systems in the thyroid clinic was negative for change in voice or positional dyspnea but was significant for difficulty swallowing that started roughly 3 months prior. The patient also had pain in the right lower neck. She described the pain as constant, with an intensity of 5/10, and alleviated by acetaminophen. Ultrasound revealed three complex nodules with the largest in the left lobe measuring 1.3 × 1.8 × 2.5 cm, and other smaller nodules. The patient was diagnosed with multinodular goiter at this time. Two nodules met criteria for FNA. Cytology for both nodules was benign. The patient elected to defer any intervention and did not continue to follow-up.\nIn early March 2017, the patient underwent wide local excision of the phyllodes tumor, wide local excision of the cutaneous adnexal adenocarcinoma and right axillary sentinel lymph node biopsy, and concurrent post-reduction bilateral oncoplastic reconstruction. Surgery entailed intra-dermal injections of Tc99m-filtered sulfur colloid 1-2 cm from the margins of the lesion located over the right clavicle. Lymphoscintigraphy revealed uptake in two right axillary nodes. Once in the operating room, a standard axillary incision was made and 2 “hot” and blue lymph nodes were identified and removed. The cutaneous adnexal adenocarcinoma was then resected with a 1.5 cm margin which created a 4 × 10 cm ellipse. A lumpectomy was performed through predesigned incisions to ensure a cosmetically favorable closure for the phyllodes tumor in the right upper-outer breast. After removal, the plastic surgery team completed a bilateral breast tissue rearrangement and left breast reduction for symmetry. All aspects of the operation went smoothly, and the patient recovered uneventfully.\nPathology confirmed a phyllodes tumor measuring 4.1 cm in greatest diameter and clear margins. The phyllodes tumor pathology showed a circumscribed border, mild to moderate stromal cellularity, mild stromal cytologic atypia, and a mitotic rate of 4-5/10 HPF. Necrosis and malignant heterologous elements or stromal overgrowth were not identified. Overall, features were consistent with a benign phyllodes tumor (Figure ).\nThe adnexal neoplasm in the right chest was resected with negative surgical margins, and 0 of 2 nodes were positive for metastatic disease. The pathology report noted the presence of mitotic figures and rare atypical mitotic figures, favoring the diagnosis of a malignant adnexal neoplasm. The report adds that since the breast is a modified sweat gland, it is impossible to distinguish a primary cutaneous adnexal neoplasm from a primary breast neoplasm based on histologic features and that no immunoperoxidase stains can distinguish these two entities.\nOn her first postoperative clinic visit, the patient was recovering well. Her incisions were clean, dry and intact without erythema, drainage, hematoma or seroma. The patient has since continued to follow-up and has not experienced any complication or recurrence. She is recommended to follow-up annually.
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A 71-year-old woman visited our hospital on September 2, 2020 due to shortness of breath and palpitation after exercise 1 day ago. The symptoms occurred once only and were inactive on admission. shows the timeline of this case. She was diagnosed with sick sinus syndrome with normal atrioventricular conduction and had a single-chamber AAI pacemaker implanted in 2004. The pacemaker was implanted on the right side because of left-handedness. The battery ran out 10 years later and she was admitted to our hospital in 2014. Similar single-chamber pacemakers were not available and not covered by the patient’s medical care program anymore. Moreover, her atrioventricular node function had shown to be slightly reduced with age. Thus, the pacemaker was upgraded to a dual-chamber one back then. The atrial lead was kept, while a new ventricular lead was implanted. The patient did not routinely go to follow-up visits in the following 5 years. A chest X-ray image from December 2019 showed that both leads were intact (). Eight months prior to this admission (January 2020), she fell off from a running bicycle, causing blunt force trauma to her right subclavicular region. She went to a community hospital and underwent a chest X-ray screening. It showed a complete right-ventricular pacemaker lead fracture (). The fractured lead was seen at the level of the right clavicle, while the proximal end of the lead was still attached to the pacemaker. The atrial lead was still intact. The patient was suggested to go to a superior hospital for further evaluation and treatment. However, she refused to do so, thinking that it was unnecessary due to the lack of any specific symptoms back then. She was then discharged and did not have any medical visits or hospitalization until this time. Her comorbidities included stable angina and hypertension.\nPhysical and laboratory examinations on this admission showed no significant findings. Myocardial enzyme test had negative results. Her electrocardiography (ECG) showed atrial pacemaker rhythm and no specific ST-T changes. Chest X-ray scanning had similar findings as compared with 8 months ago, showing a complete ventricular lead fracture (). The results of chest fluoroscopy confirmed that the free end of the fractured ventricular lead was in a fixed position and did not move with heartbeats or change of body position (). The patient then underwent a 24 h Holter monitor to further examine the status of her pacemaker. The results showed satisfying atrial sensing and pacing with an AAI pacing mode. Further examinations including coronary angiography and coronary CT angiography were refused by the patient. After symptomatic treatment and observation, the patient was discharged 7 days after admission. The patient had paid follow-up visits routinely after discharge and there were no symptoms up to her latest visit on January 12, 2021.
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A 45-year-old female patient reported in August 2017 to the department of Oral Medicine and Radiology, with a chief complaint of pain and swelling on right side of her face since 1 year and numbness of her lip on the affected side. She gives a previous history of similar swelling on the same site 8 years back for which she was operated (enucleation) under general anesthesia. However, she noticed recurrence of the swelling since 1 year and complains of paresthesia, and difficulty in mouth opening and swallowing in the same since 1 year. There was no significant medical and family history. On extra oral examination, there was difference in relationship of two sides of face due to swelling noted on right side, which was measuring approximately 4 cm × 9 cm in diameter, extending superiorly from zygomatic arch and infra orbital margin inferiorly to lower border of mandible (). The skin over swelling was stretched with no signs of inflammation. Inspectory findings were confirmed on palpation. Swelling was tender, firm in nature, with diffuse margins, and there is no rise of temperature. On intraoral examination, entire mandibular teeth were missing, soft tissue swelling was seen on the right buccal vestibule, obliterating the vestibule, and no signs of pus discharge and inflammatory component were noted. Buccal and lingual cortical plates were expanded on palpation with perforation of lingual cortical plate in lower first molar region (region 46). Based on patient’s history, and on general examination, a provisional diagnosis of recurrent ameloblastoma was given with a differential diagnosis of ameloblastic carcinoma, calcifying epithelial odontogenic tumor an odontogenic keratocyst. The patient was advised for further investigations like panoramic radiograph, computed tomography (CT), and biopsy. A multilocular pattern was seen on panoramic radiograph extending from right mandibular symphysis to the right condylar region, and there was a loss of continuity in lower border of mandible suggestive of pathological fracture (). Axial CT section showed opacification of entire mandible on right side with destruction of condyle and lower border of mandible (). An incisional biopsy of section showed islands of ameloblastic epithelial cells with long columnar and stellate reticulum cells with reversal polarity in the nest suggestive of follicular ameloblastoma (). Treatment was scheduled for surgical resection under general anesthesia with right hemimandibulectomy (). Final histopathological examination reports of excised tumor mass confirmed to be follicular ameloblastoma (). Further investigation revealed involvement of cervical and lung lymph nodes suggestive of metastasis.
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A 60-year old female underwent a phase III Oxford UKA [Biomet UK Ltd, Bridgend, United Kingdom] in 2006 for antero-medial osteoarthritis. A minimally invasive medial para-patellar approach was used and medium sized femur, 44 X 28mm tibia and 3mm meniscal bearing insert were implanted. She had an uneventful post-operative recovery. She was completely asymptomatic and was discharged from the follow-up at two years following the surgery with no symptoms and a range of motion of 0 to 130 degrees.\nShe presented to the Accident and Emergency (A&E) department in April, 2013 with history of a sudden onset of pain and swelling in the same knee. She heard a ‘pop’ in the knee while standing and did not report any obvious injury to the knee. On clinical examination, she was haemodynamically stable and afebrile and there was moderate effusion in the knee. The range of motion was from 30 to 60 degrees and she was unable to weight bear through the knee due to pain. The radiographs of her knee in the A&E department raised a suspicion of posterior dislocation of the polyethylene insert (). There was no evidence of loosening of femoral or tibial components.\nThe white cell count and CRP were normal, excluding an acute infection. She was admitted to the ward and surgical exploration was planned for the following day, with the view of changing the polyethylene insert or to revise the components if they were loose or damaged. The knee was opened through the previous scar of medial para-patellar approach. Intraoperatively, both the femoral and the tibial components were found to be well fixed with no scratches and rest of the knee did not show any evidence of osteoarthritis. The polyethylene insert was found to be fractured through the middle (). The anterior half was sitting on the tibial component and the posterior half was dislodged into the posterior compartment of the knee, stuck to the posterior capsule. It was not possible to retrieve that fragment from the front.\nThe operating surgeon had two options; either to remove both the components and then retrieve the fragment from the front or to retrieve it through a posterior incision. Eventually, rather than making a separate skin incision, the previous skin incision was extended and medial skin flap was raised to expose the postero-medial aspect of the knee. Deep fascia was incised to expose the pes anserinus. An interval was created between the pes anserinus and the medial collateral ligament anteriorly and medial head of Gastronemius posterioly (). Capsulotomy was performed through this\ninterval and the dislodged part of the polyethylene insert was retrieved through the opening. The polyethylene insert showed some pitting and whitening and it seemed to have fractured cleanly through the thinnest part (). A new polyethylene of the same size insert was implanted. The patient made uneventful recovery following the surgery. At two year follow-up she was completely asymptomatic with the range of knee movement from 0 to 125 degrees.
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A 32-year-old Saudi male patient who is a known case of Multiple Endocrine Neoplasia type 1 (MEN1) status post parathyroidectomy, distal panreatectomy and spleenectomy in 2006 was found, on CT screening, to have extra luminal midesophageal mass about five cm in greatest dimension at the level of the carina, compatible with leiomyoma []. Further review of symptoms revealed mild intermittent dysphagia for solids. Based on these findings the decision was to proceed with thoracoscopic enucleation for which the patient agreed and was consented.\nUnder general anesthesia utilizing a double lumen tube and in left lateral position, right thoracoscopy was performed after right lung isolation using four ports: 11-mm port is inserted through the sixth intercostal space by blunt dissection at the midaxillary line to provide access for a 10-mm thoracoscope. Three more ports are placed bluntly to provide access for surgery: Five mm port is placed in the posterior axillary line at the fifth intercostal space, 10 mm scope 30 degree is placed in the posterior axillary line at the eighth intercostals space, and a five-mm trocar is placed in the anterior axillary line at the ninth intercostals space for lung retraction.\nThe mediastinal pleura over the esophagus were divided to expose the tumor and the adjacent esophagus. About five-cm of the esophagus below the azygus vein was mobilized and the tumor was located. A four-cm myotomy was performed using combination of hook and endoscopic scissor avoiding injury to the mucosa. After that blunt dissection was performed separating the tumor from the mucosa, followed by applying traction suture to the tumor to aid in tumor elevation as well as in the dissection which was done mostly by blunt dissection and occasionally using sharp dissection. After tumor enucleation, the specimen was placed in a retrieval bag introduced through anterior 10-mm trocar and was delivered through this trocar wound [].\nTo ensure that the underlying mucosa is intact, the right thoracic cavity was instilled with normal saline. Size 14F nasogastric tube was inserted proximal to the area of the myotomy and 50-cc of air injected by the anesthetist gently which did not show any leak. The esophageal muscle fibers were approximated using interrupted 2-0 absorbable suture. Size 24F chest tube was introduced through the anterior 10-mm port and directed towards the apex, the trocars were removed under vision, the intercostal muscle fibers were approximated with 2-0 absorbable suture and the skin closed in subcuticular pattern.\nThe patient was kept nil by mouth till next day when contrast swallow confirmed mucosal integrity, after which he was started on oral fluid sand his drain was removed. On the second postoperative day he was on a soft diet and discharged on the same day. He was to be on soft diet for two weeks. Final histology confirmed the diagnosis of leiomyoma.
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The first case involved a 15-year-old female patient with replacement root resorption secondary to an intrusion of the maxillary left lateral incisor (2.2) () after a traumatic injury to the 4 upper incisors when she was eight years old, which included soft-tissue laceration. In accordance with the IADT protocol informed consent was obtained and we waited for two weeks, in order to assess whether there had been any tooth movement, indicating the onset of spontaneous reeruption of 2.2 (). This did not happen and orthodontic extrusion of the affected tooth was carried out. ().\nClinical and radiographic monitoring was performed after 1 week, 15 days, 1 month, 6 months, and 1 year and then annually up to 5 years. After 6 years, it was observed that the root had stopped growing and that there was bone-like tissue growth in the root canal (). After 7 years of clinical and radiological monitoring, it was confirmed that root development had stopped and that resorption had spread from the cervical area to practically the entire root (). The clinical appearance of the tooth was completely normal ().\nWhen we saw these clinical and radiographic complications, we considered the best treatment option. Since the patient was still growing, it was decided to decoronate the tooth and then fit an adhesive bridge.\nAfter local anesthesia, the decoronation procedure began with the raising of a full-thickness flap to gain direct access to the ankylosed tooth. Then, using a diamond bur, odontosection of the crown was performed above the cementoenamel junction, taking particular care not to leave any enamel residue in the root of the decoronated tooth (). After removing the crown, a K-file was used to extract the filling from the root, which was then washed with a saline solution, allowing the canal to fill with blood (if there is no bleeding, it should be stimulated by inserting a K-file through the canal into the apical bone). Finally primary closure was obtained by coronal repositioning of the flap () [, , ].\nWe subsequently carried out esthetic rehabilitation using an adhesive bridge with 0.9 mm wire and a composite pontic, taking special care to leave a space of at least 1 mm between the mucous membrane and the pontic to avoid interfering with later alveolar bone remodeling (). This gave the patient satisfactory functional and esthetic integrity (). Rehabilitation will continue until the patient is fully grown and the necessary conditions for inserting an implant are fulfilled.
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A 55-year-old male who underwent right L4-5 and L5-S1 laminectomy was re-admitted two days after this surgery for mild headache, neck pain, and significant swelling at the lower back surgical incision site. His lumbar spine MRI revealed a large CSF collection at L4-5 level extending from the spinal canal into the laminectomy bed, paravertebral regions and subcutaneous tissues (). He was evaluated by neurosurgery and he was recommended to have a lumbar EBP with drainage of this fluid collection. Given the large size of CSF collection revealed by MRI, the decision was made to proceed with this intervention on an urgent basis.\nThis EBP was performed under fluoroscopic guidance. According to the postoperative MRI, the site of CSF leak was in the right L4-5 laminectomy area and the left side L4 and L5 lamina remained intact. In order to access the epidural space close to the site of CSF leak with loss of resistance technique, we used a left paramedian approach to target the left L5 lamina. During the procedure, the left L5 lamina was first identified by fluoroscopy, an 18-gauge epidural needle was placed on the skin and advanced toward the left L5 lamina. We were able to aspirate about 100 mL of the fluid collection while this needle was in the subcutaneous level. This needle was then further advanced under fluoroscopic guidance to the left side L5 lamina. After the needle reached the lamina, it was redirected superiorly and medially into the ligamentum flavum. The loss of resistance was accomplished when needle reached the midline of interlaminar space. There was no fluid return after the needle entered the epidural space. Subsequently, 2 mL of contrast was injected and contrast was visualized in the right side of the epidural space at L4-5 level. Fourteen milliliters of autologous blood was injected through the needle. This patient tolerated the procedure well with no apparent immediate complications. However, he reported no improvement of headache immediately after the blood patch. Unfortunately, one day after the epidural blood patch, he was found to have re-accumulation of CSF in the lower back. The patient underwent a surgical dural repair two days after the EBP. The dural repair was successful and the patient was discharged three days later.
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A 68-year-old Caucasian male with a history of hypertension, hypercholesterolemia, coronary artery disease status post five vessel coronary artery bypass grafting presented to the emergency room with chest pain for four days which radiated to his jaw and along the left arm (Figure ).\nElectrocardiogram (EKG) showed old Q waves in inferior leads and new ST depression in leads I, AVL, V5 and V6 and troponin peaked up to 15.8. At the time of presentation, the patient was also short of breath with initial chest plain, a radiograph (X-ray) showing pulmonary edema is depicted (Figures and 3).\nThe patient was electively intubated before urgent cardiac catheterization, which was performed within 12 hours of patient’s arrival, and revealed 100% occlusion in right coronary, left main coronary, and the proximal portion of the circumflex artery as well as diffuse disease of the grafted vessels to circumflex. Furthermore, during catheterization, the patient was also noted to have hemodynamic compromise with blood pressure observed to be 86/63 mmHg and a heart rate of 115 beats per minute, which prompted emergency echocardiography (ECHO) showing partial disruption of medial papillary muscle with severely flail posterior MV leaflet and severe MR. He subsequently underwent venoarterial extracorporeal membrane oxygenation (ECMO) pump placement by cardiothoracic surgery for hemodynamic support accessing through the right common femoral artery and right femoral vein (Figure ).\nHeart team specialists thus discussed the possibility of performing an MV clipping, and it was decided in favor of proceeding with the transcatheter procedure as the patient had a history of median sternotomy and previous bypass surgery. The patient remained intubated and was taken to cath lab on the fifth day of hospitalization. The femoral vein was accessed using ultrasound guidance, and the transseptal puncture was performed using intraoperative transesophageal echocardiography. This was then followed by prepping the MitraClip using standard technique and positioning it across the interatrial septum and above the atrial valve. For this procedure, two clips were used, one was on the posterior segment P2 and just beside it to cinch up P2 and A2, and the second one for P2 and P1 laterally. Once the resulting MR reduction was regarded as adequate, clips were deployed (Figures and 6).\nThe only complication noted was the transient Wenckebach heart block for which the patient subsequently received a pacemaker later in the hospital course. Thus, the patient underwent two successful MitraClip placements, and the severity of MR went down from 4+ to no more than 1+. The patient’s left ventricular function improved postprocedure and ECMO was subsequently followed by extubation later on. Repeat ECHO on third postprocedure day showed mild MR and normal left ventricular ejection fraction. At the 30th day, the patient was followed up in the clinic and repeat ECHO at that time showed mild MR only.
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A 82-year-old man with the diagnosis of unstable angina was transferred for possible PCI. His past medical history included hypertension, hyperlipidemia, chronic renal insufficiency (baseline creatinine 2 mg/dl), and previous myocardial infarction with five vessel CABG for coronary artery disease 10 years ago. He did have a remote smoking history of four years but quit 65 years ago and had no known history of lung disease.\nUpon arrival to our facility, he was pain free and his blood pressure was 120/75 mmHg with heart rate of 74 beats per minute. ECG showed normal sinus rhythm, left axis deviation, and ST segment depression in the inferior leads. The patients’ prothrombin time was 14 seconds with a corresponding INR of 1.2 and a normal platelet count. CXR did not reveal any infiltrates or other acute processes ().\nThe patient was treated with full dose aspirin, started on heparin by standard weight based protocol, and taken to the cardiac catheterization laboratory for coronary angiography. The coronary angiogram showed severe native three vessel disease, widely patent RIMA and LIMA, and 80% focal stenosis in the mid portion of the patients saphenous vein graft to the obtuse marginal branch of the left circumflex artery. These findings correlated with the patients ECG findings and therefore he underwent percutaneous coronary intervention of his saphenous vein graft. A bolus of 180 mcg/kg of intravenous eptifibatide was given followed by a continuous intravenous infusion at 1 mcg/kg/min for 18 hours. Balloon angioplasty and stenting was performed using standard technique and reduced the stenosis to 0% restoring TIMI-3 coronary flow to the vessel. Following the procedure, the patient was transferred to the coronary care unit in stable condition.\nFour hours following the procedure the patient developed severe dyspnea and hypoxemia. Electrocardiography revealed sinus tachycardia and arterial blood gas measurements on 100% non re-breather mask showed a pH of 7.44, Po2 of 50 mmHg a Pco2 of 32 mmHg, and oxygen saturation of 85%. Chest examination revealed diffuse rales over both the lung fields, and bed side CXR revealed bilateral diffuse alveolar infiltrates. ().\nBased on the clinical picture, the patient was diagnosed with respiratory insufficiency secondary to acute cardiogenic pulmonary edema related to his recent myocardial infarction and was treated with intravenous diuretics for 48 hours. During this time, the patients clinically picture did not improve leading to a right heart catheterization revealing a right atrial pressure of 6 mmHg, a pulmonary capillary wedge pressure of 9 mmHg, cardiac output of 5.45 litres/min, and a cardiac index of 2.74 litres/min/sqm. These findings were suggestive of non-cardiogenic pulmonary edema and resulted in an alternative workup for the patients’ unexplained respiratory insufficiency and pulmonary infiltrates. The possibility of pulmonary embolus was first investigated, but negative lower extremity Doppler’s and a low probability ventilation perfusion scan made this diagnosis unlikely.\nHigh resolution chest computed tomography was performed without contrast and showed bilateral ground glass opacities with interstitial infiltrates involving the upper and lower lobes consistent with pulmonary edema ().\nWhen the patients’ haemoglobin subsequently fell two gram over 24 hours, the diagnosis of DAH was suspected. The patient underwent bronchoscopy which revealed diffused blood throughout the bronchial tree with increased hemorrhagic return on serial bronchiolar lavages confirming the diagnosis of DAH. Subsequently, the patient was treated with methylprednisolone 125 mg IV × 3 days followed by a 9 day taper. The patients oxygenation steadily improved over the next 7 days and the patient was eventually discharged from the hospital on day 17 days with no further complications.
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Mr. SH, A 35-year-old male patient presented to us with a history of fall from a height of 15 feet after which he was unable to bear weight on right lower limb. He was treated by a local quack in his village. He continued to experience pain for the next 6 months after which he presented to our emergency department with an antalgic gait. On clinical examination, he had a right lower limb abduction and external rotation deformity with painful restricted movements. Radiological imaging confirmed the clinical suspicion of anterior hip dislocation of obturator variety ( and ).\nNo associated fractures and intact distal neurovascular status were observed. An open reduction and internal fixation of the joint through an anterolateral approach was planned. After opening the hip joint, the head was visualized in the obturator foramen with findings of a dent and irregularity on the surface at the posterosuperior margin, absence of cartilage was noted, but intact vascularity confirmed by drill hole blood oozing ().\nAt this point reduction was successful with Murphy’s skid technique alone, post-reduction radiographs showed concentric and congruent reduction and stabilization achieved with two Steinman pins across the hip joint ().\nSteinman pins and sutures removed after 15 days, but the hip joint continued to be kept immobilized in Thomas Splint for 3 weeks postoperative after which gradual mobilization started ().\nPatient went discharge thereafter and returned back to his village but failed to follow-up at 6 weeks due to financial issues in addition to the restrictive travel conditions in the lockdown, now at 3 months postoperative the patient has painfree ambulation with stick support with early signs avascular necrosis (AVN) of the femoral head as seen on the X-ray and computed tomography scan (-).\nPatient has been planned for a total hip replacement (THR) at a later date as currently patient can ambulate to his satisfaction and there is no hindrance in his daily routine activities.
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A 63-year-old man came to the clinical observation because of a rapid onset of dyspnea and dysphonia along with the development of a bulky node in the left side of the neck. He had been working as an interventional cardiologist in an angiographic room for 15 years at the local Hospital. Family history was negative with regard to malignancies and thyroid disease.\nThe relevant medical history included hypertension treated with valsartan and hydrochlorothiazide and non-insulin-dependent diabetes mellitus treated with metformin. There was no previous history of thyroid disease. Two years before the admission, he was treated with warfarin because of a deep venous thrombosis of the left leg occurred after a short bed rest for prostatitis. He was a heavy smoker.\nThe iodine status of the patient was not known; however, he was from a non-Alpine region and he was still living in the same area which is considered as a mildly iodine insufficient [].\nOn physical examination, the patient had a 8 × 10-cm firm left-sided neck mass with a right-sided shift of the larynx. On ultrasound examination, a nodule of the left thyroid lobe was found measuring 5 and 6-cm in its antero-posterior (AP) and transverse (T) diameters, respectively. The nodule was hypoechoic but inhomogeneous, with no vascularization; at the strain elastography, the nodule ranged from a medium elasticity to a hard pattern. The volume of the right thyroid lobe was reduced with a small hypoechoic nodule. No enlarged lymphnodes were found at the neck ultrasound. Computed tomography (CT) of the neck confirmed a 7 × 5 × 13-cm (T × AP × Long diameters) large, inhomogeneous neck mass originating from the left lobe that caused displacement of the trachea, the left common carotid artery and the left internal jugular vein. No evidence of primary malignancies or suspicious for secondary lesions was found at the CT of the head, abdomen, and pelvis. The chest CT showed a 6-mm round-shaped nodule not suspicious for malignancy close to the parietal pleura at the lower lobe of the right lung.\nA fine needle aspiration cytology (FNAC) of the mass was performed which yielded hemorrhagic smears with few groups of large, epithelioid cells, with vesicular, severely atypical nuclei and eosinophilic dense cytoplasms. A diagnosis of malignancy was given (Category 6 according to Bethesda 2010) with a suggestion for an anaplastic carcinoma (Figure ).\nThe patient underwent a total thyroidectomy and lymphadenectomy of central and left lateral cervical nodes. At the gross pathology examination, the tumor measured 6 × 6 × 12 cm (T × AP × Long diameters) and was partially circumscribed by a fibrous pseudocapsule. The mass had a gray, tan and red cut surface, with areas of hemorrhagic necrosis. Histology showed a vasoformative high grade neoplasia characterized by large epithelioid cells growing in sheets and lining abnormal vascular spaces; some cells showed intracytoplasmic lumina. There were areas of spontaneous necrosis and hemorrhage and a brisk mitotic activity; angioinvasion was noted. The tumor immunostained for vascular markers (CD31, ERG, CD34, factor VIII and vimentin), whereas epithelial differentiation markers were negative (cytokeratins, thyroid transcription factor 1, thyroglobulin, and EMA). The final histologic diagnosis was primary epithelioid angiosarcoma of the thyroid, grade 3 according to FFCCS (Figures ). This diagnosis was confirmed at a second opinion from a different institution. The tumor was restricted to the thyroid with free surgical margins. The mass had substernal extension and displaced the surrounding structures but it did not infiltrate the thyroid capsule, the strap muscles, or other neck tissues. The remaining thyroid tissue had nodular colloid goiter. No lymphnode metastases were detected.\nFifteen days after the thyroidectomy, the patient was operated to prevent rupture of an aneurysm of the abdominal aorta. One month after thyroidectomy, the chest CT showed multiple pulmonary nodular lesions some of them with a solid pattern surrounded by a ground-glass halo, 12 mm in maximum diameter. There was no consensus as to the oncologic relevance of these lesions, therefore, no biopsy was performed. A bone scintigraphy yielded negative results.\nChemotherapy with Epirubicin, Ifosfamide, and Mesna was administered but it was discontinued after 4 cycles because of pancytopenia and infection by Klebsiella Pneumoniae, treated with piperacillin/tazobactam, and by Clostridium difficile, treated with vancomycin. The patient recovered from the infections and, at a 6-month follow-up, the chest CT showed a reduction of the number and volume of the lung lesions with only three of them remaining in the medial lobe of the right lung.\nAt a further 18-month control, the chest CT was unchanged. The 6 mm round-shaped nodule close to the parietal pleura at the lower lobe of the right lung was also found to be stable. One year later, the patient developed pneumonitis and recovered after antibiotic therapy. At that time, he was investigated by neck, chest, abdomen and pelvis CT as well as with FDG-PET without any evidence of disease recurrence.\nAfterward, a 6-month CT follow-up program was started which is still ongoing. At present, the patient is alive with no evidence of disease after 62 months from initial diagnosis.
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A 75-year-old woman presented at our emergency department with a complaint of progressive epistaxis. The patient had a 3-year history of nasal obstruction and intermittent epistaxis and absence of specific underlying systemic disease or trauma in her medical history. In the nasal endoscopic examination at the time of visit to our hospital, a hemorrhagic mass filling up the left nasal cavity without any ulceration was observed (Fig. A). In the laboratory tests, unremarkable findings were noted, which did not suggest a diagnosis of the nasal mass. A 3.7 × 2.5-cm bulging mass with heterogeneous enhancement in the left nasal cavity, and blurred boundary of the paranasal sinus was observed in the computed tomography (CT) scans (Fig. B and C). Destruction of the bone of the nasal floor or medial wall of the maxillary sinus was not evident.\nA presumptive diagnosis of malignancy was made based on the aggressive appearance, despite the lack of significant cervical adenopathy. Due to active bleeding caused by the mass in the nasal cavity, diagnosis through biopsy of the mass preoperatively was not possible. Therefore, excisional biopsy and surgical resection via endonasal endoscopic approach were performed in the patient under general anesthesia. Intraoperatively, the nasal floor and lateral nasal wall were free from attachment to the tumor, but the inferior turbinate was remodeled by the tumor (Fig. A); possible origin of the tumor at the nasal septum without infiltration of the septal cartilage was observed (Fig. B). Mitotic figures in the tumor cells were observed in the intraoperative frozen section biopsy; however, differentiating between the presence of benign or malignant tumor was difficult. Subsequently, continuous peeling of the affected septal mucosa and finally, complete extirpation of the lesion was performed by the surgeon.\nIn the final pathology report, two components of the tumor cells including the luminal ductal inner epithelial cells with nuclear polymorphism and peripheral outer myoepithelial cells were revealed (Fig. A). The results of biphasic differentiation were confirmed by immunohistochemical staining: positive for p63 and S-100 in the surrounding myoepithelial cells, and intense positive for epithelial markers, such as cytokeratin-7 in the luminal tumor cells (Fig. B and C, respectively). Based on these results, the mass was diagnosed as an epithelial-myoepithelial carcinoma of the nasal septum. The Ki-67 labeling index (proliferation index) of 3.5% was obtained. No evidence of regional or distant metastases through 2-Deoxy-2-(18F)-fluoro-D-glucose (FDG) positron emission tomography (PET)/CT was found postoperatively. The surgical specimens were fragmented such that the margins could not be properly evaluated; thus, radiotherapy for the locoregional area was recommended as adjuvant therapy. However, additional therapy could not be performed due to patient refusal. In the follow-up of the patient for 18 months after surgery, no recurrence was observed, and ongoing follow-up is being conducted (Fig. ). This study was approved by the institutional review board of the Yonsei University Wonju College of Medicine. Informed consent was given by the patient.
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A 58 year-old male with end stage renal disease due to IgA nephropathy who had previously undergone a renal transplant which had failed was declined for redo renal transplantation. He had progressive dyspnoea and a history of syncope on exertion. The transthoracic echocardiogram confirmed severe stenosis of a BAV with a peak velocity of 3.9 m/s (peak gradient 61 mmHg, mean gradient of 39 mmHg and area of 0.89 cm2). There was also the presence of moderate aortic regurgitation. Coronary angiography revealed non-flow limiting coronary artery disease. MSCT confirmed a Sievers Type 1 bicuspid valve with a partial raphe between the right and left cusps. The aortic annulus was large with a perimeter measuring 98 mm, mean Sinus of Valsalva diameter of 40 mm and an inter-commisural distance of 29 mm (Figure ). Both common femoral arteries were of large caliber and measured 8 mm on the left and 9 mm on the right. Following discussion by the Heart team and careful analysis of the MSCT it was felt that TAVI was technically possible if deployed at the inter-commisural space.\nTAVI was performed under local anesthetic and the right femoral artery was cannulated and a 20 Fr sheath was inserted. The left femoral artery was cannulated and a 7 Fr sheath was inserted. The left femoral vein was used for insertion of a temporary pacemaker lead. The bicuspid aortic valve was crossed retrogradely using a Amplatz Left 1 diagnostic catheter and a hydrophilic coated straight tipped Glidewire. This was exchanged for a pre-shaped Safari wire and placed in the left ventricular apex. A balloon valvuloplasty was performed using a 25 mm balloon and a simultaneous aortogram was performed. The aortogram revealed a leak of contrast into the left ventricular cavity during balloon aortic valvuloplasty and felt to be an inadequate seal. A 34 mm Evolut CoreValve was deployed at the level of the leaflet tips, with hemodynamics and echocardiography confirming a good result with no significant PVL. The peak velocity across the TAVI valve was 1.8 m/s, peak gradient of 14 mmHg and area of 1.11 cm2.
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A previously healthy five year old girl was admitted with severe respiratory distress due to pneumonia of the upper and middle right lobe. Her past medical history was clear. Shortly after admission she went on hypercapnic respiratory failure, required intubation and Paediatric Intensive Care Unit (PICU) transfer. Laboratory testing identified Adenovirus type 3. Supportive treatment with mechanical ventilation was continued for a total of 2 months, with subsequent non-invasive support (BiPAP) for one more month, because of co-existing generalized hypotonia due to adenovirus encephalopathy. As a complication of the prolonged immobilization she developed left femoral vein thrombosis.\nAfter a total of 3 months of PICU stay, she was transferred to the pediatric ward, alert and fully orientated, on BiPAP support for 10 additional days. During her admission her respiratory status gradually improved. Her muscle tone and power quickly normalized, but when she attempted to walk, she had a limp and complained of a worsening hip pain. On clinical examination both hips had restricted movements. There was marked reduction of internal and external rotation and abduction of the hips. Hip flexion was less affected. There was no previous history of trauma and infection indices were negative. Radiographs of the pelvis revealed ossifying masses in the soft tissues projecting over the acetabulum, head and neck of both femurs. The lesions were more extensive on the right side. They were mainly affecting the gluteus medius with normal bone trabeculae formation and well separated from the neck of the femur on the AP x-ray. The periphery of the ossifying masses was denser than the center. There was absent periosteal reaction of the pelvic bones that appeared normal, (). No other joints were clinically found to have restriction of movements. Combining the symmetrical involvement of heterotopic formation with prolonged immobilization, we proceeded with the diagnosis of non traumatic myositis ossificans. No biopsy was performed.\nThe patient was started on NSAISs (ibuprofen) and physiotherapy. The patient was regularly followed up, with no signs of worsening. Eleven months later she could walk freely with subsequent radiographical improvement regarding the size of the ossified masses.
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The patient was a Colombian 2-year-old female infant who was a product of non-consanguineous pregnancy and the first and only child of the family. She was born when her father was 34 years old and her mother was 30 years old. She had a family history of seizure syndrome and febrile crisis from the maternal lineage without other important family histories, such as genetic or neurological disorders. No complications were reported during the perinatal care and prenatal studies. She was born through vaginal delivery at 39.5 weeks gesta tion without any complications, weighed 3.170 g (50th–75th percentile), had a height of 51 cm (50th–75th percentile), with an Apgar score of 9–10. She was born with multiple CDSL and bilateral phocomelia, shortening of the left arm mainly, syndactyly of the second and third fingers of the left hand, and agenesis of both thumbs (). She underwent a period of hospitalization for these multiple malformations.\nThe patient presented with ostium secundum-type atrial septal defect, muscular ventricular septal defect, and pulmonary hypertension that worsened when she was 6 months old. Due to this worsening, she was placed under pediatric critical care again. The computerized tomography scan showed diffuse cerebral edema with a partial collapse of the ventricular system without other focal lesions such as embolism and bleeding. Magnetic resonance imaging of the brain revealed restriction of generalized diffusion predominantly in the posterior and right areas without ventricular collapse and subdural efflux without compressive effect associated with adjacent cortical changes ascribable to necrosis. The electroencephalogram showed the absence of deep rhythms, severe slowing of the wave registers, and high-voltage bursts. Surgical intervention was provided to close the aortopulmonary and the pulmonary cerclage. After the first surgery, she presented with cerebral edema with encephalopathy due to axonal sprouting after the cortical lesion and generalized hypertonia as a consequence of the motor descending tract lesion, which was treated with clonazepam and phenobarbital without new episodes.\nAt 14 months of age, she presented with oropharyngeal dysphagia with moderate oral motor skills. For that reason, she received enteral feeding by gastrostomy. An intestinal transit study showed a duodenal corkscrew sign in the second intestinal portion at the Treitz angle level on the right side close to the right pedicle (L1). The image showed that the first jejunal handles were at the right center. All of these findings were related to intestinal malrotation changes. These changes included normal cecum position and gastroesophageal reflux grade III, which reached the barium column up to the proximal region of the esophagus. The follow-up electrocardiogram showed increased signs of sinus rhythm and right ventricular function. In addition, there was evidence of successful modification of the aortopulmonary window and pulmonary cerclage, muscular restrictive interventricular communication with a few left to right shunts, properly biventricular function without overflow, and pulmonary hypertension signs without clots and vegetations.\nRadiological studies of the upper limbs revealed absence of bilateral metacarpal bones and phalanges of the first finger, bilateral radioulnar hypoplasia, absence of the ulna in the left arm (), hip dysplasia, and femoral–tibial varum angle (genu varum). No radiological changes in the spinal column X-ray were detected.\nShe was referred for genetic consultation at 2 years of age with a weight of 11.8 kg (50th–75th percentile), height 88 cm (75th–90th percentile). She presented with forehead hemangioma and hypoplasia of the nasal bones without appropriate visual follow-up, cephalic support was not successful, trunk and upper limbs were hypotonic, superior limbs with spasticity were more notable on the left side, and nipple hypertelorism.\nA complete sequence of the TBX5 gene was generated and compared to the NG_007373.1 (GeneBank) reference sequence which identified a novel potentially pathogenic variant in the heterozygous status NM_181486.2:c.243-1G>C. This splice-site mutation alters the acceptor site of the third intron, which is predicted to affect the splicing and lead to a nonfunctional protein. Using Sanger sequencing, this novel variant was confirmed using an ABI 3500 sequencer (Applied Biosystems, Thermo Fisher Scientific, Waltham, MA, USA). A carrier study in the parents was negative for this mutation (). For that reason, this mutation was considered to be a novel de novo mutation, which has not been previously reported.
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A 78-year-old woman was involved in a motor vehicle collision while traveling approximately six weeks before presenting to our institution. She initially had high cervical neck pain at the time of the event but no other neurologic symptoms. She was brought to a local trauma center at the time of the event, and a computed tomographic angiography (CTA) of the neck revealed a Levine and Edwards Type II fracture with bilateral C2 pars and pedicle fractures extending into the vertebral body with anterolisthesis of C2 on C3 (see Figure ). Also seen was a tortuous right dominant vertebral artery that filled a large C2 transverse foramen with a congenitally small pedicle (see Figure ). Her vertebral artery on the left appeared to contribute very little to her posterior circulation. There was no evidence of radiographic vascular injury. She was advised to undergo surgical fixation at the time of her injury, however, she elected to wait until she returned home. She was discharged from the outside hospital with a hard cervical collar and presented to our institution for further evaluation over a month later. After discussing the possible treatment options, including continued conservative treatment with continued external orthosis vs. surgical intervention, the patient elected for surgical intervention. The risks and benefits of the surgical options were discussed with her in detail, including an anterior approach at C2-3, or a posterior C1-3 fusion. The patient elected to have a posterior fusion to avoid the possible swallowing complications of a high cervical exposure and other possible risks of an anterior approach..\nInformed consent was obtained and the patient was brought to the operating room. Neurophysiologic monitoring was utilized to establish baseline motor and somatosensory evoked potentials. After application of cranial pinions, the patient’s neck was brought into a neutral and slightly flexed position under live fluoroscopy. A post-positioning film showed the patient’s anterolisthesis had reduced and the fractured pedicle showed improved alignment (see Figure ). Motor-evoked potentials and somatosensory-evoked potentials showed no change from baseline. A cranial reference frame was attached to the head clamp for CT-guided intraoperative navigation (see Figure ). Attachment of the cranial reference frame to the head clamp was a key step to ensure maximal accuracy of the optical system during instrumentation, as the posterior elements of C2 would not be stable enough to accept the spinous process clamp after exposure.\nAfter exposure of the posterior elements from C1-3 and the C1 lateral masses, an O-arm spin was performed for navigation registration. The left C2 pedicle was accessed using a navigated drill. The fracture line in the middle of the pedicle was crossed with the drill bit into the vertebral body. Careful palpation of the drill track with a ball-tipped probe did not show any breaches. The hole was tapped with a navigated 3.5-mm tapered tap. A 4.0 mm x 24 mm screw was slowly advanced across the fracture into the C2 vertebral body. Care was taken during screw placement to ensure purchase across the fracture so that the tip of the pedicle screw did not push the vertebral body anteriorly. Bilateral C1 and C3 lateral mass screws were then placed. The right C2 pedicle was skipped due to her congenital abnormality and the risk of vertebral artery injury. An intraoperative CT scan showed excellent hardware placement (see Figure ). A cortico-cancellous piece of iliac crest was harvested and contoured to an appropriate dimension for placement between the C1 and C2 lamina. The laminae were decorticated and a piece of iliac crest graft was placed in between. Bilateral titanium rods were cut and placed. The wound was closed in layers and the patient awoke with no complications. She was placed in a hard cervical collar post-operatively. Postoperative X-ray images were obtained after the patient mobilized and showed stability of the construct (see Figure ).
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A 59-year-old female patient presented to her local family doctor with chronic generalized intermittent colicky abdominal pain and altered bowel habit for a few months. She has no other associated symptoms. She previously had laparoscopic adjustable gastric band (LAGB) insertion 8 years prior with good result (BMI pre-procedure was 56 kg/m2, and now 36 kg/m2). Her other comorbidities include hypertension and colonic diverticular disease with previous acute diverticulitis. She was organized to have an elective colonoscopy. Colonoscopy revealed tubular foreign body embedded in the wall of colon, with an entry and exit point, ~55 cm from anal verge (Fig. ). There was also significant sigmoid and descending colon diverticular disease.\nCT abdomen with oral and intravenous contrast was organized to further investigate the tubular foreign body. It revealed concurrent gastric band erosion into gastric lumen and connection tubing eroding into the posterior wall of transverse colon and exiting inferiorly (Figs –). There was no evidence of any oral contrast leak from the stomach.\nThis patient has previously been admitted for acute diverticulitis 4 years prior. Reviewing prior imaging did not reveal any gastric or colonic erosion. The gastric band tubing is noted to be running along the inflamed colon. Since the initial admission for acute diverticulitis, she has had multiple further acute diverticulitis episodes, which were treated with oral antibiotics. We suspect recurrent diverticulitis lead to the erosion of the gastric band into the colon and stomach.\nAs part of the surgical management, both colorectal and upper GI surgeon were involved in the operation. Patient underwent laparoscopic removal of gastric band and laparoscopic assisted wedge resection of transverse colon. The gastric band was removed following adhesiolysis and the gastric defect was repaired with intracorporeal suturing. The gastric band port was subsequently removed. Gastroscopy was done to ensure the repair was airtight. For the colectomy, transverse colon and splenic flexure was mobilized laparoscopically and the transverse colon was extracted through the gastric band port site for external inspection. A tract was identified passing from the antimesenteric border to colonic lumen and then along the colonic mesentery. A wedge resection performed with stapler end to side anastomosis. Flexible sigmoidoscopy was performed to confirm the anastomosis was airtight. Her post-operative recovery was uneventful, and she continued to be well on post-operative follow up in clinic. She remains well on subsequent phone follow up 12 months post operatively.
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A 9-year-old boy complained of malaise, just a few minutes after his first summer swim in the sea; soon after, he presented generalized urticaria, dyspnea, conjunctival hyperemia, blurred vision and faintness. When first aid arrived, since anaphylactic shock was suspected, intramuscular steroids, intravenous antihistamine and nebulized salbutamol were administered, with rapid improvement on the part of the patient. The only thing of note in the child’s medical history was allergy to dust mite, and no other allergies were reported. There was no evidence of any insect bite or drug ingestion; an hour before the swim, the child had eaten his usual breakfast, with hot chocolate. Apparently, there was not contact with fish during the swim. The child had never complained of similar symptoms before and had never had urticaria after contact with water, be it seawater or tap water. No familiarity for allergic disease or chronic urticaria was reported. The child was referred to the local Allergy Department and in order to identify the offender, skin tests and specific IgE assays were performed. In detail, they tested allergy to milk, due the history of milk intake before the appearance of symptoms, and to insect venom and fish, because of the possibility of contact with insects and fish during the bath; all the tests were negative. Although the patient developed no symptoms on contact with tap water, an aquagenic urticaria was suspected, but the specific test was negative. Finally, a cold urticaria was suspected but the cold stimulation test (CST) was negative too. Given the severity of the reaction, prophylactic antihistamine therapy was commenced, but in spite of this, throughout the summer the patient continued to develop wheals all over his body after every swim in the sea (Fig. ), even in places where there had been no direct contact between the skin and the water. The child then came to our attention, at the Burlo Garofalo Institute for Maternal and Child Health in Trieste (Italy), the referral centre for allergic diseases in the north-east of Italy. There, based on the child’s clinical history, a diagnosis of an atypical form of cold urticaria (ACU) was formulated. The specific diagnostic test of ACU involves keeping the lightly clothed patient in a cold room (at a temperature of 4 °C) for 30 min; in our case, it was avoided because of the past patient’s severe systemic reaction. In any case, the boy’s history was fairly characteristic enough to confirm the diagnosis of this rare and often unrecognised chronic physical urticaria: typical diagnostic features of ACU are in fact the appearance of wheals after exposure to various sources of cold (such as seawater at the beginning of summer), also in areas not directly in contact with water and the negativity of the CST. Antihistamine therapy was continued for the whole summer with fair control of symptoms and self-injectable epinephrine was prescribed but the child has never used it.
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A 64-year-old female patient was admitted to our institute with mild right hemiparesis, numbness on the right upper extremity, nausea, vomiting, and dizziness. Neurologic examination revealed grade IV+ right-side motor weakness. A magnetic resonance image (MRI) scan of the brain showed multiple small, round and tubular low-signal intensity regions on the left frontal lobe, a finding suggestive of vascular malformation. Initial digital subtraction angiography (DSA) identified a hypervascular lesion and arteriovenous shunting lesion on both external carotid artery (ECA) angiograms (). Both lesions suggestive of DAVF showed abnormal retrograde flow from the middle meningeal artery (MMA) and the superficial temporal artery into the superior sagittal sinus, including cortical venous reflux via the arteriovenous shunt (Borden classification II). We planned to treat the lesions with an endovascular approach because they were correlated with the patient's symptoms and showed cortical venous reflux. However, the patient and her family refused further treatment and requested hospital discharge.\nAt 4 months after hospital discharge, the patient was readmitted with repeated seizure that had been occurring for 3 weeks. The most recent seizure was a generalized tonic-clonic seizure with head turning and eyeball deviation to the right side; postictal confusion was also shown for 10 minutes. Brain MRI revealed subacute focal cerebral infarction with minimal hemorrhagic transformation on the left frontal lobe (). Antiepileptic drugs were initially loaded, and follow-up DSA was performed after 5 days when the patient's seizures were controlled by medication. DSA revealed a change of venous drainage pattern of the original lesions (). Abnormal venous reflux into the superior sagittal sinus was not present in the right ECA angiogram. Unexpectedly, only venous drainage directly into the subarachnoid cortical vein was observed, without contrast filling in the venous sinus in the left ECA angiogram (Borden classification III). Mild stenosis between the cortical vein and superior saggital sinus remained. We hypothesized that the hemiparesis and seizure arose from venous infarction with congestion of the left frontal lobe due to progression and rerouting of the cortical venous reflux after venous sinus thrombosis. We planned to treat the lesions with trans-arterial endovascular embolization with Onyx® (a nonadhesive liquid embolic agent; eV3 Neurovascular, Irvine, CA, USA).\nOnyx® embolization was performed with successful obliteration of the arteriovenous shunt through the superselected left MMA in a single session (). Abnormal vascular structures, including cortical venous reflux, did not appear on any follow-up magnetic resonance angiography scans. The Glasgow outcome scale score was 2 when the patient was discharged, an improvement over the hemiparesis from her status at admission. Over a clinical follow-up period of 3 years, the patient did not experience any major problems.
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A 65-year-old Caucasian man had a recent hospital admission where he was diagnosed with an NSTEMI. At the time of admission, his past medical history was significant for hyperlipidemia and smoking and he had a family history of coronary artery disease. He received a stent to the LAD and PTCA to a diagonal vessel. During hospitalization, he experienced a cardiac arrest and developed a right bundle branch block requiring temporary pacing with subsequently placement of a permanent dual-chamber pacemaker. On discharge, the patient was started on multiple new medications including clopidogrel and atorvastatin.\nThree and a half weeks after discharge, he presented to the Emergency Department (ED) with swelling, redness, and pain in his hands, feet, and elbow that began about one week prior. The symptoms began with swelling in his right index finger and this became painful and spread to the rest of his right hand over the preceding 3 days. On the day of presentation, he also noticed left anterior malleolar and midfoot pain that had been increasing throughout the day. The patient denied a history of gout, previous arthritic pain, or rheumatologic disorders. The patient's home medications were aspirin 81 mg daily, atorvastatin 80 mg daily, clopidogrel 75 mg daily, and metoprolol 25 mg PO BID and he reported compliance with his home regimen. He reported taking a statin about a year previously but could not confirm which statin or dosing and had not been taking any cholesterol medication prior to his hospitalization.\nThe patient reported subjective fevers and chills; however, on arrival he was afebrile and normotensive with a heart rate of 91 and pulse oximetry of 96% on room air. Physical exam findings were right hand swelling > left hand swelling; erythema overlying MCPs of right hand; decreased range of motion bilaterally due to swelling; sensation in tact; good capillary refill. Notable labs were WBC 17.64 × 109/L, ESR 35 mm/hr, CRP 2.60 mg/dL. The patient's presentation was not consistent with an infectious etiology and he was discharged with watchful waiting, instructed to discontinue atorvastatin, and given follow-up with rheumatology.\nHe was seen by rheumatology a week later and there was concern for a new inflammatory arthritis triggered by the stress of his MI. His uric acid level was normal and he was started on prednisone. He initially responded well to prednisone but 2 days later his symptoms returned. He had a cardiology follow-up 2 weeks after ED presentation. Patient continued to experience the polyarthralgias at that time despite withdrawal of atorvastatin and addition of prednisone. Clopidogrel was discontinued and patient was switched to ticagrelor 60 mg bid. On follow-up one month later his symptoms of joint and muscle aches had completely resolved.
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A 27-year-old female was referred to Gil Medical Center due to a painful and edematous left lower extremity of 4 days’ duration after varicose vein surgery at a local clinic. Both saphenous veins were ablated by an endovenous laser procedure. In addition to the edematous left lower extremity, there were bruises on the left thigh and around the operation wound site. Since deep vein thrombosis was suspected, computed tomography (CT) was performed, and the left common femoral vein above the proximal superficial femoral vein was not visualized (). Iatrogenic femoral vein division, rather than deep vein thrombosis, was then suspected. Subsequent venography depicted a divided left femoral vein and thrombosis around its stump ().\nThe patient suffered from severe pain in her leg. She was a flight attendant, and the edematous, painful leg caused inconvenience both professionally and cosmetically; thus, we decided on femoral vein repair. The patient had undergone saphenous vein ablation in both legs, which meant that no autologous saphenous vein was available for femoral vein repair. Accordingly, left femoral vein repair with a polytetrafluoroethylene (PTFE) graft and an arteriovenous (AV) fistula (to improve PTFE graft patency) was chosen. During surgery, the previous surgical wound on the left inguinal area was extended and the hematoma around the left femoral vein was removed (). Thrombectomy was performed in the left iliac and femoral veins (), the left cephalic vein was harvested for the AV graft, and the divided left femoral vein was repaired using a 14-mm ringed PTFE graft (). The AV fistula was constructed between the left common femoral artery and the PTFE graft using the harvested cephalic vein. The patency of the left femoral vein and AV fistula was confirmed by CT at 7 days after surgery (), and edema of the lower extremity had improved. The fistula was removed at 6 months after surgery by coil embolization (). The patient took warfarin (initial dosage: 4 mg, target international normalized ratio: 2) immediately after surgery in order to keep the graft patent, and the international normalized ratio level was maintained around 2. At 18 months postoperatively, there was no evidence of edema and Doppler ultrasonography confirmed the patiency of the left femoral vein (). This study was reviewed by the institutional review board of Gil Hospital (IRB No. GAIRB2016-091).
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A 43-year-old woman with DS was admitted to hospital with a 3-week history of cough, shortness of breath after activities and dyspnea. The patient's motor and sensory status were grossly intact. However, her mental capacity and verbal response to commands were deemed consistent with those of a 5-year-old child. She was a non-smoker and didn't expose to tobacco smoke in her family or known chemical carcinogens for the lung, such as asbestos. And she had no known family history of cancer.\nClinical examination revealed pulmonary alveolar respiratory sounds were weakened in right lower lung. Pulmonary mass in right central lung, multiple irregular nodules scattered in bilateral lung and right pleural effusion were observed on chest X-ray. Contrast CT scan showed enlarged bilateral mediastinal lymph nodes, metastases of liver segment 4 and eighth thoracic vertebrae, third and forth lumbar vertebrae (Figure ). Subsequently, the patient underwent CT-guided percutaneous lung biopsy of the right lung mass. After the procedure, the CT scan showed right side hydropneumothorax, but the chest tube drainage did not needed. Pathologic evaluation confirmed the diagnosis of infiltrating lung adenocarcinoma. EGFR mutation status evaluated by allele specific PCR assays (SNaPshot) and PCR-based direct sequencing both showed exon 21 L858R mutation.\nAfter a detailed discussion with the family and consent of the mother and sister, the patient was administrated with EGFR TKI- gefitinib at a dose of 250 mg once a day for the first-line treatment. The symptom, such as cough and short of breath both relieved after one week. Two months later, CT scan showed shrinked all of the primary and metastatic tumors and decreased pleural effusion. The principal complications of this regimen were 1 grade diarrhea and rash. A repeat CT scan after six months of therapy was performed due to worsening short of breath. The radiological findings consisted of increase in size of both of the primary tumor as well as liver mass and pleural effusion but not new metastases (Figure ). The best response of the first-line treatment is stable disease according to Response Evaluation Criteria In Solid Tumors (RECIST version 1.0), and the progression-free survival was six months.\nWe tried to repeat lung biopsy for analyzing mechanisms of acquired EGFR-TKIs resistance, such as T790M, MET amplification or mutations in BRAF, PIK3CA, but her caregivers declined. Following the discovery that T790M is the dominant resistance mechanism to erlotinib and gefitinib [], therefore the chosen treatment option was the third generation of EGFR inhibitors-osimertinib (at a dose of 80 mg once daily). After one month of second-line treatment, CT scan showed same size all of primary and metastatic tumors and decreased pleural effusion (Figure ), but new liver metastasis. And short of breath relieved lightly. Unfortunately, two month later she died in respiratory failure at home. No autopsy was performed.
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The first proband is a female, the firstborn child of a 19-year-old mother at 38 weeks’ gestation via vaginal vertex delivery. She is the daughter of African American, nonconsanguineous parents. The mother had a normal anatomic scan of the fetus, and prenatal screening was positive for the mother being a carrier of sickle cell anemia and of spinal muscular atrophy (SMA). The patient tested negative, with the presence of 2 copies of the survival motor neuron (SMN1) gene. Growth parameters at birth are detailed in Table .\nThe parents first noticed developmental delay at 6 months of age. The child did not transfer objects at 18 months and could not roll over at 3 years. While she started sitting with support at 12 months, at 3 years of age she is still unable to sit alone. At the age of 3 years, she can pull herself to standing with someone supporting her from behind, but she is still unable to crawl or walk with help. She said her first words at age 12 months and was able to use some 2-word phrases. Her mom was able to understand her limited speech, and the patient was able to follow simple commands. Feeding issues began to arise, and she now gags on some solid foods. Growth parameters at 3 years of age can be found in Table .\nAt the age of 7 months she was seen by a neurologist, initially for hypotonia, developmental delays, and intermittent episodes of decreased tone and eye crossing. During these episodes she was usually tired but continued to be interactive. She had to sleep 30 min to an hour to come out of a spell, and when she woke up she was back to her baseline. Her spells lasted for hours at a time, but there was never any loss of consciousness.\nOn physical exam, she had oculogyric crisis, dystonia, and hypokinesia. Otherwise, she had a normal physical and vision exam.\nThere have been no concerns with her sleep. She has a history of some nasal congestion as an infant. She also has a history of some autonomic symptoms, such as abnormal sweating.\nAt the age of 17 months, magnetic resonance imaging (MRI) of her brain demonstrated a subtle area of chronic tissue loss in the subependymal white matter in the posterior left frontal area. The lateral and third ventricles were borderline in size, indicating mild ventriculomegaly. Seizure disorders were considered due to abnormal eye movements, but multiple electroencephalograms (EEGs) showed no seizure activity. However, there was abnormal activity that was suggestive of a metabolic and structural etiology.\nPlasma amino acids and total and free carnitine levels were within normal limits. Urine organic acids revealed moderate elevations of vanillactic and vanilpyruvic acids with slight elevation of N-acetylvanilalanine, a pattern suggestive of AADC deficiency [].\nNext-generation sequencing of the proband revealed 2 variants in the DDC gene: NM_000790.3: c.48C > A (p.Tyr16Ter) and NM_000790.3: c.116G > C (p.Arg39Pro). Analysis of amino acid conservation indicates that the wild-type amino acid, Arg39, is completely conserved in all 98 vertebrates examined, increasing the likelihood that a change at this position would not be tolerated and could adversely affect the function of the protein. As far as we are aware, these variants have not been previously reported in association with AADC deficiency. Sanger sequencing confirmed the results. Additional evidence for pathogenicity was provided by a finding of low AADC activity (2.13 pmol/min/mL [normal range = 36–129 pmol/min/mL]) and elevated 3-OMD (3733.0 nmol/L [normal range = 64–280 nmol/L]) in plasma.\nA chromosome microarray revealed a 677 kb copy gain in chromosome 4q27 (122,570,932 – 123,248,135) that contained OMIM genes ANXA5, EXOSC9, CCNA2, BBS7, TRPC3, and KIAA1109 as well as the genes TMEM155 and PP12613 with unknown clinical significance. However, fluorescence in situ hybridization analysis using an oligonucleotide clone (RP11-184P16) from the duplicated region was inconclusive and could not confirm the microarray result in the metaphase analysis. The interphase analysis identified two RP11-184P16 signals in 86% of the nuclei.\nFollowing diagnosis of AADC deficiency, the proband started receiving vitamin B6 with no clinical improvement. She also initiated physical, speech, feeding, and occupational therapies.
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A 32-year-old man with a history of drug abuse presented to the emergency department with deterioration of paresthesia and limited movement of the left neck for 7 d.\nThe patient had slight paresthesia of the neck for 5 years. Seven days before this admission, the symptom became intolerable and was accompanied by a limited movement of the neck after an acute upper respiratory tract infection. He perceived a foreign body existing on the left side of the neck and the feeling was severe while coughing or swallowing.\nThe patient had no history of neck trauma, cervical spondylosis, or contagious diseases.\nThe patient was a heroin abuser 5 years ago and achieved successful detoxification for 2 years. He had no family history of hereditary diseases.\nThere was no abnormality in vital signs. Physical examination revealed only mild pain during the palpation of the left neck, and a rod-shaped solid substance was touched. Its location was parallel with the long axis of the left cervical artery.\nA blood test revealed a slightly elevated C-reactive protein level (1.53 mg/dL) and white blood cell count (10.94 × 109/L). Other blood test results were normal.\nThe radiological examination showed that a rod-shaped foreign body was diagonally located in the anterior region of the neck and the lower end of the rod extended to the thorax (Figure ) and computed tomography revealed a high density extending from the cervical region to the upper mediastinal area (Figure ).\nBecause of the unexpected imaging findings, further medical history was acquired. He finally admitted that he deliberately swallowed a segment of mercury thermometer after he broke a mercury thermometer and poured out the mercury 5 years ago under the influence of drugs when he was alone. He was sent to the emergency department immediately to undergo an endoscopy after he told his family about the accident. But neither a foreign body nor trauma or perforation was found. He did not receive further examinations or treatments because the clinician thought that he was talking nonsense under the influence of drugs, and the patient’s symptoms were tolerable until 7 d before this admission.
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An 84 year-old woman with LC and hepatocellular carcinoma had a MELD score of 11 and was classified as Child Pugh C. She also suffered from hepatopulmonar syndrome and choledocolitiasis with several cholangitis episodes.\nIn June 2013, she had a first episode of CDI that was treated with metronidazole. She had six recurrences; three were treated with vancomycin standard dose, the fourth with fidaxomicin, the fifth with vancomycin tapering and in the last one treated with vancomycin followed by FMT by nasogastric tube. Seven days later, the patient died due to a new episode of cholangitis but blood cultures had not been obtained.\nAdvanced liver cirrhosis (LC) was present as an underlying condition in approximately 25% of our patients who received a FMT.\nOut of our four cases with advanced LC that were treated with FMT, in our report, two patients had severe complications post procedure and one of them died.\nThere is no question that the severity of the previous underlying conditions of our four candidates can explain episodes of superinfection at any time which may endanger their lives.\nBacterial translocation and bacteremia is relatively common in advanced LC without the contribution of FMT but the coincidence of FMT in our second patient is a cause of concern. We were surprised by the very low number of LC patients that appear in large series of patients with FMT. We speculate that the risk aversion towards some complications seen in some of our patients may have accounted for a reluctance of some physicians to perform the FMT.\nOur literature research highlights one clinical trial that used FMT in LC patients to treat hepatic encephalopathy. However, it is not applicable to our possible future patients, as the methodology was not designed to treat CDI, used a small quantity of stool and an antibiotic prophylaxis prior to FMT [].\nBacteremia, as a complication of FMT has been reported only anecdotally [].\nCholangitis after FMT in the fourth patient, it is quite possible that it was a mere coincidence. However, focusing in the second case, a proven episode of superinfection out of our four cases appears to be striking.\nAs a contrast to our concerns, the three cases who survived the FMT, were free of recurrent CDI episodes in the ongoing follow up periods of eleven, five and one months.\nDespite the fact that the advanced LC is not a formal contraindication of FMT, this report is advisory in its intent and recommends the need for a careful follow up with a systematic review of complications of FMT in cirrhotic patients.
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A 24-year-old right-handed male reported to our emergency department with the history of trauma to his left forearm and hand while working on a wood-cutting machine. There was no associated injuries or comorbidities. There was near-total amputation of the left upper limb at two levels: at the junction of middle and lower one-third of forearm and at the level of metacarpal shafts. All the forearm structures were transected except preserved skin tag of 2 cm width on the ulnar side of the forearm []. The left thumb was also amputated at the level of mid distal phalynx. After the bony fixation, revascularisation of the limb was undertaken by repair of ulnar and radial arteries. Venous flow was established by repair of cephalic and basilic veins. Perineural repair of the ulnar nerve, the median nerve, superficial branch of radial nerve. and the lateral cutaneous nerve of forearm was carried out in an end-to-end fashion. Similarly, the first, second and third common digital arteries and nerves were repaired after the fixation of metacarpals. Thumb stump was closed primarily. Injury to reperfusion time was 7 h and total operating time was 13 h.\nIn the post-operative period, the patient developed vascular insufficiency of the distal part of the hand which could not be salvaged. We performed trans-metacarpal amputation of the left hand and covered the stump with a pedicled groin flap. Small raw area on the dorsum of the forearm was skin grafted. Complete healing of the wounds occurred after 1 month, at which time the patient was discharged from the hospital []. The patient was referred to the physiotherapy unit for rehabilitation and was followed up in our outpatient department monthly for sensory and motor evaluation.\nFour months after the discharge, the patient reported with acute-onset skin lesions over the revascularised part of the forearm and hand. The physical examination revealed weeping and crusting exudative lesions suggestive of of eczematous dermatitis. The revascularised part of an extremity developed irregular erythematous plaques covered with yellowish thick crust. There were multiple erosions at places along with serous discharge. These lesions were strictly limited to the revascularised part of the limb; rest of the limb was normal []. The patient did not have any allergy and other reactive skin lesions in the past. Negative Patch test with standard series ruled out contact dermatitis. Skin biopsy revealed the findings of acute eczematous dermatitis.\nSeveral studies in the past have reported the association between autonomic dysfunction and skin lesions like atopic dermatitis, psoriasis and CRPS.[] As the patient had suffered traumatic neuropathy, investigations were done to rule out autonomic dysfunction in the revascularised part. We performed Ninhydrin sweat test and Sympathetic Skin Response (SSR) test. Negative Ninhydrin sweat test indicated disturbance of sweating function.\nSSR test was performed using a four-channel electromyography machine as described by Cicek et al.[] The affected hand did not show any waveform indicating sudomotor dysfunction.\nSympathetic dysfunction in the revascularised part of the limb was confirmed by above investigations. Sympathetic dysfunction led to abnormal sudomotor and vasomotor functions and eczematous dermatitis in the revascularised part of the limb. Therefore, we coined the term sympathetic dysfunction dermatitis to describe the skin lesions developing in the revascularised or replanted part of an extremity.\nThe patient responded well to a topical cream of 2% fusidic acid and 0.1% betamethasone along with oral prednisolone for 1 week. All the skin lesions subsided with appearance of a normal skin texture []. However, there was one episode of recurrence 3 weeks after the resolution of the skin lesions which was treated as before. There was no further episode of dermatitis. The patient is presently on emollients to prevent recurrence.\nTo evaluate the sensory recovery, Semmes–Weinstein monofilament test and 2-point discrimination test (2PD) were performed at the 4th, 5th, 6th and 8th months postoperatively. On evaluation at the 6th month, the patient was free of skin lesions and his sensory recovery improved.
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A 2-year old girl was referred to the Jos University Teaching Hospital in north central Nigeria, with complains of progressive cough and difficulty in breathing in the preceding six months. She was treated at several health facilities for pneumonia and asthma without resolution of symptoms. Patient had no fever or features suggestive of tuberculosis. Pregnancy, delivery, neonatal and infant periods were uneventful and patient had received all immunization appropriate for her age. Examination at presentation showed a child in severe respiratory difficulty necessitating oxygen administration, with Spo2 89–90% at room air and 96% on oxygen by nasal prongs. There was bulging of the right side of her anterior chest wall and markedly reduced breath sounds on the right hemithorax. No features suggestive of congenital heart disease. Chest X-ray showed homogenous opacity continuous with the cardiac silhouette, involving almost the entire right thoracic cavity with a shift of the mediastinum to the left (Fig. ). Echocardiography confirmed a very large well defined mediastinal cyst compressing the right atrium, left atrium and right ventricle (Fig. ). Contrast-enhanced computed tomography scan of the chest showed a well defined large cyst of the anterior mediastinum compressing the right main bronchus (Fig. ). Blood investigations were all normal. A diagnosis of anterior mediastinal cyst was made and the patient had right posterolateral thoracotomy through the fifth intercostals space. Intraoperatively a large tense cyst measuring 20 × 16 × 3.5 cm was noted adjacent to the pericardium and attached loosely to the thymus compressing but not attached to the bronchus. The cyst was unilocular with a thick wall and contained serous fluid (Figs. & ); the cyst was excised en bloc. There was moderate pericardial fluid which was drained by a pericardiostomy. Histopathological sections showed ectopic pancreatic tissues in the wall of the cyst (Figs. , and ). The post operative course was uneventful; the patient has been asymptomatic after a followed-up period of twenty four months.
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In 1976, a 23-year-old male with tuberculous kyphosis presented with incomplete bilateral paraplegia of his legs of twenty days duration. He was not able to stand or walk without any assistance due to motor weakness and sensory disturbances in both lower extremities. He had disabling back pain, and muscle weakness of his lower extremities had gradually been getting worse ().\nHe remembered that his kyphotic deformity started about 20 years ago. The patient's past medical history included tuberculous meningitis seven years ago. He took anti-tuberculous medications. A fistula was formed in the posterior lower back area six years ago, but it healed spontaneously. On admission, preoperative radiographs demonstrated a T12-L4 kyphotic Cobb's angle of 100° with severe destruction of the vertebral body from L1-L4. A lumbar myeolgram demonstrated a complete block of CSF flow at L4-5. The patient's height and weight on admission were, respectively, 142 cm and 50.0 kg.\nOne week before spinal surgery, we fit a halo pelvic apparatus onto the patient so that he could adapt to it and develop confidence with his breathing (). The patient underwent anterior correctional osteotomy and release. After surgery, the apparatus was re-fit onto the patient, and distraction was begun. The bars were wound down, on average, 2 mm each day. Daily calculation of the force applied to the spine was made from measurements of the springs incorporated into the halo hoop device and recorded. We carefully monitored whether the neurological deficit got worsening.\nDuring distraction for 2 months, he had no neurologic deterioration and no back pain. After distraction, posterior osteotomy and release were performed to achieve final correction because flexibility of the kyphosis was not sufficient. At the posterior surgery, autologous rib bone grafting was also performed simultaneously. After a second operation, distraction was maintained at the same rate for another three weeks. Total correction took eleven weeks.\nAfter distraction for 11 weeks, the kyphotic deformity was corrected to a Cobb's angle of 62° from T12 to L4. After correction, the patient's height increased to 150 cm from 142 cm. In order to maintain the correction, supplementary anterior fusion was done using an autologous iliac bone graft. The apparatus was removed when the grafts had consolidated.\nDuring these procedures, there was no specific complication related to the halo pelvic distraction, and the patient's previous paralyzed lower extremities recovered gradually so that the patient could stand and walk without any assistance 6 months after the operation. He could look straight ahead without knee flexion after the 3rd operation ().\nThe patient had been followed for 20 years after correction of the tuberculous kyphosis using osteotomy and halopelvic traction. The patients had no neurological deterioration, and could walk without use of a walking device. He had no back pain or leg pain and no limitation to his daily activity. He stated that he could work as a farmer using agricultural machines. Correction angle and good sagittal balance were well maintained (). At a follow up MRI (magnetic resonance image) taken twenty years after treatment, there was no compression of the dural sac ().
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A now 76-year-old male underwent buried PD catheter insertion in 1998 at the Ottawa Hospital. He had membranous glomerulopathy and stage 5 chronic kidney disease (CKD) with an estimated glomerular filtration rate (eGFR) of 13 mL/min/1.73m2. Over the ensuing years, he continued to have subnephrotic proteinuria and was managed with perindopril. The renal function remained relatively stable and only began to decline in late 2017. He consented to initiation of PD in February 2018 after his eGFR dropped to 7 mL/min/1.73m2. A plain radiograph of the abdomen showed the PD catheter optimally positioned in the true pelvis ().\nThe exteriorization procedure was performed in the Home Dialysis Unit. A 0.5 cm skin incision was made 2 cm distal to the superficial cuff and a loop of the catheter was mobilized and the fibrin was cleared off the catheter. The distal catheter did not glide out easily. With the assistance of a surgeon, a second incision was made over the distal end of the catheter and it was separated from the subcutaneous tissue by dissection and the end of the catheter was cut off (). A large fibrin plug was removed from the lumen of the catheter with push and pull syringe aspiration. The flow remained very sluggish. Tissue plasminogen activator (tPA) was instilled into the catheter and by the following day the inflow significantly improved but outflow was still slow.\nTwo days later, a cathetergram and guide wire manipulation of the catheter was then arranged through interventional radiology. The initial contrast injection showed the PD catheter localized within a pocket of fibrous tissue communicating with the greater peritoneal cavity along the right pelvic wall. Two angled glide-wires were utilized to clear fibrin out of the lumen of the catheter and a torque cable was then used to flip the draining loop out of the fibrous pocket into the greater peritoneal cavity. Following this, outflow improved and the patient was able to successfully initiate continuous ambulatory PD (CAPD). We have documented a filling time of 6 minutes and drain time of 9 minutes. His clinical course has otherwise been uneventful.
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A 32-year-old woman in her first pregnancy presented at 37 weeks gestation to the obstetric review centre in the late evening with a two-hour history of new onset right-sided leg pain and numbness. She was able to mobilise short distances and was otherwise well. Initially her symptoms were most suggestive of sciatica, a common complaint during pregnancy.\nHer symptoms progressed rapidly over the next two hours and she reported bilateral lower limb numbness and severe shooting midthoracic back pain and was unable to move her legs. Initially she had no urinary retention or faecal incontinence. She also reported no history of trauma or any similar symptoms in the past.\nShe had an otherwise low risk pregnancy and there were no signs of fetal distress on arrival. Her past medical history included asthma, allergic rhinoconjunctivitis, and depression. She was a smoker and migrated to Australia from England several years earlier.\nOn initial examination, vital signs were normal. She was afebrile. Cardiotocograph revealed no concerns for fetal wellbeing. Her neurological examination was inconsistent but nevertheless concerning. She was found to have patchy bilateral sensory loss up to a sensory level of T10. Lower limb examination revealed reduced power bilaterally (1-2/5) across all myotomes with hyperreflexia, clonus, and upgoing plantar reflexes. Upper limb neurological examination was normal. There was no bony tenderness on palpation of her spine. Insertion of a urinary catheter five hours after presentation drained 700 ml of urine. This was suggestive of urinary retention, particularly in the context of her advanced gestation. However, she reported normal perineal sensation on catheter insertion, again inconsistent with her other symptoms and examination findings.\nDue to her pregnant state, an urgent CT was not performed. An after hours MRI was not considered necessary as it was felt an acute surgical cause for the presenting signs and symptoms was unlikely. A kidney ultrasound ruled out renal stones as a cause for severe back pain.\nThe next morning an MRI spine was performed. This revealed a previously undiagnosed mixed intra- and perimedullary spinal cord AVM at T8 with surrounding spinal cord oedema from T6-T11 (see ). Her case was discussed with the neurosurgical team who felt she was not amenable to urgent surgical decompression or intervention based on MRI findings. A decision was made for urgent delivery to facilitate further investigation. A healthy baby girl was delivered that afternoon via caesarean under general anaesthetic. This was performed without complications.\nSubsequent angiography showed a predominantly perimedullary slow flow spinal cord AVM with intramedullary extension at T8 to a compact nidus (see ). The AVM received arterial supply from the radicular branches of the right T9 intercostal artery with a branch to the anterior spinal artery from the same level. The venous drainage of the AVM was via a single caudal draining vein that extended to the left internal iliac vein with attenuation at L5/S1.\nIn discussion between the radiology and neurosurgical teams, it was concluded the most likely aetiology for the patient's presentation was acute rupture of the AVM at T8 secondary to venous outflow compression from the enlarged uterus onto the draining vein at the level of L5 causing high pressure within the AVM and subsequent rupture. Given the lesion was partially within the spinal cord, treatment with surgical resection would risk potential permanent paraplegia. Additionally, she was considered not a good candidate for embolisation. As such, the patient was managed conservatively in the hope that she might have at least partial recovery of her neurological function. An inferior vena cava (IVC) filter was inserted at the time of initial angiography to prevent pulmonary emboli given the relative risk of anticoagulation in the setting of recent caesarean section and recent AVM rupture.\nOne month after admission, the patient developed left leg swelling and was diagnosed with a left leg extensive occlusive deep vein thrombosis extending to left external and common iliac vein as far as the IVC filter. There was concern about potential obstruction of venous outflow from the AVM precipitating further rupture as well as potential clot propagation above the IVC filter, so a decision was made for mechanical thrombectomy and removal of IVC filter. She was therapeutically anticoagulated on warfarin with clexane bridging and clot progression was monitored on weekly ultrasound scans.\nGiven the difficulties in finding a suitable discharge destination with a newborn baby, the patient's first few months of rehabilitation were as an inpatient in a private room on the neurosurgery ward. At the time of writing this article (six months after delivery), the patient remains paraplegic to the level of T8 with urinary and bowel incontinence. At this stage, she has a guarded prognosis for recovery.
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A 38-year-old female with no past medical history came to the hospital with complaints of episodic chest discomfort, mild dyspnea, and occasional non-productive cough. On physical examination, she was hemodynamically stable without any pathological finding. A chest x-ray was done and it showed mass-like opacities abutting the right heart (Figure ).\nTo have a better idea of the cause of opacity, a further assessment with computed tomography (CT) chest with contrast was ordered and it showed a large, well-circumscribed, heterogeneously enhancing mass of 10 cm with peripheral calcification in the right mediastinum. Also, there was a dilated vessel along the posteromedial and inferior of the mass (Figure ).\nAfter the chest CT findings, the patient was admitted to the hospital for further evaluation and cardiac consult was called. In order to differentiate if the mass was due to some tumor or some anomaly of the coronary vessel, coronary CT angiography with contrast was ordered. A subsequent coronary CT angiography (CCTA) showed a 9.7 cm aneurysm and an anomalous vessel emanating from the left coronary artery and the proximal circumflex, fistulizing into the right atrial appendage. CCTA also showed a dilated right atrium likely due to fistula formation (Figures -).\nWhen the right heart catheterization was performed, a rise in saturation was noted in the right side of the heart due to shunting of blood from the left side to the right side of the heart as a result of coronary cameral fistula formation between the right heart and the anomalous vessel originating from the left coronary artery and proximal circumflex artery. On transesophageal echocardiogram (TEE), an enlarged right atrial chamber was noted due to the fistulous tract draining into the right atrium. The cardiothoracic department then scheduled the patient for surgery. Sternotomy was performed to repair the coronary artery aneurysm with ligation and resection of the coronary cameral fistula and repair of the right atrium. Surgery went well and no intra-operative and postoperative complications were noted.
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A 29-year-old woman was referred to our hospital with a mass shadow in her left mid-lung field detected by chest X-ray during a routine health screen. Chest computed tomography (CT) revealed a slightly attenuating 3 × 3 cm mass in the interlobar fissure, in contact with the interlobar pulmonary artery (Fig a,b). The mass exhibited mild heterogeneous enhancement (Fig c). We considered the possibility of primary lung cancer because the patient was young, female, with no relevant family history. No abnormality was evident on gross bronchoscopic and cytological examinations. Blood test data and tumor marker levels were normal. We considered percutaneous needle biopsy, but decided that such a procedure would be dangerous as the tumor was located centrally. Although chest CT radiologic findings suggested sclerosing hemangioma or carcinoid tumors, we planned surgical resection because we could not rule out malignancy. During surgery, a mass was evident in the interlobar fissure above the interlobar pulmonary artery. The mass was covered by visceral pleura and was well encapsulated; no invasion of the adjacent lung parenchyma was evident. Internally, the mass was composed of myxoid materials that were easily removed by surgical suction. The internal surface of the capsule was smooth, but vascularity was well developed and the bleeding tendency was high. We completely enucleated the mass via video-assisted thoracoscopic surgery. There was no need for pulmonary parenchymal resection. The postoperative course was uneventful.\nMicroscopically, the tumor was composed of short spindle-shaped to ovoid and stellate cells embedded in the reticular network of a myxoid stroma. Lymphoplasmacytic cell infiltration was also evident. The extent of cellular atypia was mild and mitosis was uncommon. Alveolar cells of normal appearance were observed in the peripheral region of the tumor (Fig a–d). Although the pathologic findings did not reveal mesothelial cells, we concluded that the tumor did not originate from the pleura because the tumor was well encapsulated, covered by visceral pleura and was located in the interlobar fissure, as previously described. On immunohistochemical staining, the tumor cells were positive for vimentin and epithelial membrane antigen (EMA), but negative for rhabdoid cells (Fig e), smooth muscle actin, smooth muscle myosin heavy chain (SM-MHC), calretinin, thyroid transcription factor-1 (TTF-1), cytokeratin 7 (CK7), p63, S-100, CD34, and CD56. The Ki-67 labeling index was ca. 1–2%. The overall histological profile suggested PPMS with an EWSR1-CREB1 translocation, as described in the 4th edition of the World Health Organization lung tumor classification. We performed fluorescence in situ hybridization on formalin-fixed, paraffin-embedded tumor tissue. The EWSR1 break-apart probe revealed split red and green signals suggestive of an EWSR1 translocation (Fig f). During 17 months of follow-up, the patient has remained well and has not reported any medical issues.
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A 66-year-old male patient, with a history of smoking (30 pack-years) and no known medical or surgical history, was admitted in our department for a spontaneously resolved inferior ST elevation myocardial infarction (STEMI). The intra-hospital treatment included enoxaparin 0.6 ml twice a day, clopidogrel 75 mg once a day, aspirin 100 mg once a day, bisoprolol 2.5 mg once a day and atorvastatin 40 mg once a day. The coronary angiogram (performed at day 3 through the right radial artery) showed a severe thrombotic lesion of the distal circumflex. The patient underwent an ad-hoc successful angioplasty of the circumflex with a drug eluting (everolimus) stent. Initial laboratory tests at admission were normal except elevated troponin. Echocardiography showed a 65% left ventricular ejection fraction. The patient was discharged after 5 days of anticoagulation by low molecular weight heparin (enoxaparin). Laboratory tests were not controlled during the hospitalization. The discharge treatment included clopidogrel 75 mg once a day, aspirin 100 mg once a day, bisoprolol 2.5 mg once a day and atorvastatin 40 mg once a day.\nOne week later, the patient was referred again to our department for both chest and right lower limb pain. The electrocardiogram showed an inferior STEMI and the physical exam of the right lower limb found ischemic signs with absence of the femoral pulse. There was no history of aspirin or clopidogrel discontinuation. An urgent coronary angiogram (performed through the left femoral artery) showed total thrombosis of the circumflex stent (\n). The patient underwent a successful primary angioplasty of the circumflex by simple balloon (\n). Urgent lower limb contrast-enhanced computed tomography was performed immediately after the angioplasty, revealing total acute thrombosis of the right common femoral artery (\n). The patient underwent an urgent successful thrombectomy with Fogarty catheter. Immediate evolution was favorable with total regression of coronary and right lower limb ischemic signs. Laboratory tests showed a marked fall in the platelet count (68,000/L) which was normal (364,000/L) in the previous hospitalization. A diagnosis of concomitant coronary stent and femoral artery thrombosis due to HIT was strongly suspected (4T score = 8). Our therapeutic strategy was immediate discontinuation of low molecular weight heparin (enoxaparin), aspirin and clopidogrel with strict daily control of platelet count. During this period, no alternative anticoagulation was initiated because of the unavailability of direct thrombin inhibitors in our center. Anticoagulation with a vitamin K antagonist (acenocoumarol 4 mg once a day) and dual antiplatelet therapy with aspirin 100 mg once a day and clopidogrel 75 mg once a day were initiated at day 3 once platelet count had recovered. The in-hospital outcome was favorable and the patient was discharged after 15 days on acenocoumarol 4 mg once a day, aspirin 100 mg once a day and clopidogrel 75 mg once a day. The 3-month follow-up, with controlled blood tests and lower limb contrast-enhanced computed tomography showing total reperfusion of the right femoral artery (\n), was unremarkable.
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A 61-year-old female patient with past history of hypertension, diabetes mellitus, hyperlipidemia, and a coronary artery bypass surgery 8 years ago was admitted to the emergency department with complaints of sudden onset of a severe blunt pain in the right lower quadrant. She had no episodes of vomiting or nausea, but had a chronic constipation complaint. On her general and physical examination, she was moderately obese, had right lower quadrant tenderness, and guarding and rebound was positive. The blood tests revealed leukocytosis around 13.5 K/µL, an elevated C-reactive protein value around 124 mg/L, and an elevated glucose value around 340 mg/dL. Other biochemical values were at within normal limits. The abdominal ultrasonography detected a 113 × 44 × 55 mm-sized, hypoanechoic encapsulated lesion with distinct contours located in the right lower quadrant adjacent to anterior wall of the abdomen. A planned abdominal CT to evaluate the differential diagnosis and the presence of additional pathologies revealed a tubular-shaped cystic mass without any solid components, superiorly extending to anterior abdominal wall from the level of right ileocecal valve, about 14 × 5 cm in size, with a thin wall, having a density of about 20 HU (). Due to patient’s discomfort, assuming a perforation of appendicitis or the cystic mass, she underwent an emergency operation in which McBurney’s incision was performed where an enlarged unperforated appendix was observed, which was clearly a mucocele (). Considering the risk of perforation and consequences, we resected the base of appendix with linear stapler involving some of the cecum for robust surgical margins ( and ). Histopathological examination of the specimen showed a cystically dilated appendix measuring 14 × 5 × 4 cm in size. The luminal content of the cyst measuring 9 × 4.5 cm in size consisted of mucinous fluid and was green fecaloid in the appendiceal lumen. Microscopically, the specimen had features of mucinous cystadenoma placed in the diagnosis (). After monitoring in intensive care and service 2 and 3 days respectively, the patient was discharged, and control colonoscopy and abdominal CT was planned after 6 months following the discharge.
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A 52-year-old man presented with gradually increasing pain in his neck and left upper arm over a 3 month period. When he had visited our hospital, he could not move his neck as a result of the pain. The plain radiographs demonstrated a collapsed vertebral body at C-6 (). The CT scan findings of the lung revealed a solitary round tumor with an irregular margin in the left upper lobe. The size was 2 cm in diameter. Technetium-99 bone scintigraphy demonstrated multiple spinal bone metastases, which were diagnosed as a stage IV (T1N0M1).\nThe patient underwent posterior decompression and spinal fusion as palliative surgery. The visual analog scale (VAS) improved to 2 cm from 10 cm. The pathological diagnosis was adenocarcinoma. Although platinum-based chemotherapy was administered, the tumor marker and size did not improve. The patient rejected additional therapy. Four months after the first operation, the C3-6 vertebral body collapsed and he could sit up (). Therefore, the patient underwent C2-7 anterior body fusion as palliative surgery again. After surgery, the neck pain was reduced, and the VAS was improved to 4 cm from 10 cm. However, two months after the second operation, he presented with intolerable neck pain. The performance status deteriorated to 3. Since the radiograph showed the progress of osteolysis () and the primary focus progressed, the oral administration of gefitinib 250 mg/day was started as a second-line chemotherapy with informed consent. After administration for one month, the pain was reduced to allow walking. The performance status improved to. The VAS improved to 4 cm from 10 cm. At three months after administration, the cervical metastatic lesions showed remarkable increasing bone formation (). The CT scan findings of the cervical vertebrae confirmed osteosclerosis matched with the metastatic bone tumor lesion (). The patient survived for a further two years after having a recognized bone metastasis. The activity of daily living (ADL) continued during the term of gefitinib administration.
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