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163,900 |
3810585-1
| 24,174,956 |
noncomm/PMC003xxxxxx/PMC3810585.xml
|
Bilateral internal laryngoceles mimicking asthma
|
A 43-year-old male admitted to the pulmonology clinic of Acibadem Healthw Care Group, Acibadem Masalk Hospital, Istanbul, Turkey, in 2011, with dyspnea, cough, and excessive phlegm for a month and a late onset stridor. The patient had a history of asthma and he had been treated as asthma for 4 years. The response of the patient to antiasthmatic drugs was not sufficient and asthmatic attacks were frequent. A bronchoscopy was performed and upper airway obstruction was detected. Atalectatic bronchial segments were found. Sixth bronchi of the right inferior lung lobe was totally obstructed. The patient was referred to the Ear Nose and Throat (ENT) Clinic for upper airway evaluation. Flexible nasopharyngolaryngoscopy showed bilateral cystic enlargements of the false vocal folds and true vocal folds could not be visualized properly [Figures -]. Supraglottic area was narrow. Laryngeal CT without contrast enhancement showed bilateral internal laryngoceles. Hypodense areas causing expansion at the level of aryepiglottic folds were detected [Figures and ]. Endolaryngeal laser surgery was done under general anesthesia. Submucosal total excision of bilateral cystic masses including parts of false vocal folds was performed. The symptoms resolved immediately after surgery. Airway was open and true vocal folds were visible during the postoperative endoscopic laryngeal examinations of the patient [Figures -, ]. The patient did not experience any respiratory event during the follow-up period after surgery. His last visit, free of symptoms, was at the sixth postoperative month.
|
[[43.0, 'year']]
|
M
|
{'19410402': 1, '17357676': 1, '17129390': 2, '18392516': 1, '20430574': 1, '24729979': 1, '11593174': 1, '10718436': 1, '17275541': 1, '31360929': 1, '9450842': 1, '12172256': 1, '24174956': 2}
|
{'1676021-1': 1}
|
163,901 |
3811690-1
| 24,396,684 |
noncomm/PMC003xxxxxx/PMC3811690.xml
|
Delayed Surgery for Parathyroid Adenoma Misdiagnosed as a Thyroid Nodule and Treated with Radiofrequency Ablation
|
A 53-year-old female presented to our hospital complaining of a 6-month history of backache. Judging from the blood testing results, she had hypercalcemia, and alkaline phosphatase (ALP) was increased to 1,253 U/L (normal range, 35 to 130); the patient was sent to the endocrinology department. Her past history was significant for a surgical procedure for fibrocystoma of her right humerus 20 years ago, and she had donated one of her kidneys to a relative 7 years previously. She had taken atorvastatin 10 mg, amlodipine 5 mg, and omega-3 fatty acid 1,000 mg daily for the past 3 years to treat high blood pressure and dyslipidemia. The patient had been misdiagnosed with a thyroid nodule and hypothyroidism at another hospital 4 years previously and had immediately been prescribed levothyroxine 50 µg/day. At that time, the thyroid ultrasonography revealed two nodules that were 0.3 and 0.5 cm in diameter on her right lobe and another nodule that was 2.3×1.3 cm in size that was projected backwards. She had fine needle aspiration cytology for the nodule on the left lobe, and this had revealed a benign nodule. She had been followed up every 6 months by neck ultrasonography. Two years later, when the nodule on the left lobe of the thyroid had increased in size to 2.9×1.7 cm, they carried out radiofrequency ablation. However, the thyroid nodule remained the same size even after the radiofrequency ablation, so they monitored its size every 6 months for 2 more years (). During that time, the patient began experiencing backache and visited the orthopedics department of our hospital where she was suspected of having metabolic bone disease due to the high serum ALP value.\nThe patient presented with generalized weakness and fatigue without other hypercalcemic symptoms. The peripheral blood examination was as follows: leukocyte count, 7,020/mm3; hemoglobin, 9.3 g/dL; platelet count, 249,000/mm3; prothrombin time (PT), 14.4 seconds (normal range, 11.9 to 14.3); activated partial thromboplastin time (aPTT), 31.3 seconds (normal range, 29.1 to 43.5); serum iron, 65 µg/dL (normal range, 40 to 160); total iron binding capacity (TIBC), 258 µg/dL (normal range, 230 to 430); transferrin saturation, 25%; and ferritin, 158.6 ng/mL (normal range, 13 to 150). Serum chemistry values were also obtained: blood urea nitrogen, 26.9 mg/dL; creatinine, 1.98 mg/dL; glucose, 110 mg/dL; ALP, 1,011 U/L; aspartate aminotransferase, 23 U/L; and alanine aminotransferase, 11 U/L. Serum calcium was 14.6 mg/dL, phosphate was 3.5 mg/dL, and ionized calcium was 7.2 mg/dL. Serum protein and serum albumin were 6.9 and 3.7 g/dL, respectively. The results of the serum electrolyte test revealed that sodium was 135.7 mmol/L, potassium was 4.3 mmol/L, chloride was 104.0 mmol/L, and serum osmotic pressure was 286 mOsm/kg. According to the serum lipid examination, the total cholesterol was 146 mg/dL, triglyceride was 95 mg/dL, high density lipoprotein was 33 mg/dL, and low density lipoprotein was 79 mg/dL. A thyroid function test found T3 was 108.9 ng/dL (normal range, 80 to 200), thyroid stimulating hormone was 0.40 mIU/L (normal range, 0.27 to 4.2), and free T4 was 0.74 ng/dL (normal range, 0.93 to 1.70). Under dual energy X-ray absorptiometry-based bone density examination, the T-score of the lumbar region was -1.4, while the T-scores of the neck were -1.2 on the left and -1.8 on the right. Except for the fifth lumbar vertebra, which had spondylolisthesis, nothing remarkable was found on magnetic resonance imaging.\nAccording to further blood tests, 25-hydroxyvitamin D3 was 9.6 ng/mL (normal range, 4.8 to 52.8), and 1,25-dihydroxyvitamin D3 was 10.5 pg/mL (normal range, 19.6 to 54.3), while the intact parathyroid hormone (iPTH) was 1,911 pg/mL (normal range, 15 to 65). When we performed bone scanning with 99mTc, the amount of cortical bone radioactive isotope uptake increased very high (). Because we suspected hyperparathyroidism, we carried out a 99mTc sestamibi scan and suspected the lesion that had been previously diagnosed as a left thyroid nodule was likely a parathyroid adenoma (). Using thyroid Doppler ultrasonography, we discovered a hypervascular adenoma that was 5-cm-sized solid mass with similar echo of surrounding thyroid tissue in the center, and slightly low echo in outer part in the inferior site of left thyroid gland (), while on the right thyroid parenchyma we discovered two thyroid nodules, 0.3 and 0.5 cm each in diameter, that the patient had had 4 years before. We performed neck computed tomography and found there was no neck lymph node metastastasis and local invasion of other organs ().\nThe patient received both hydration and diuretic treatments until she underwent a surgical operation to control the hypercalcemia; she also had pamidronate 90 mg intravenous injections twice a week. On the 11th day after hydration and diuretic treatment, her condition had improved; serum calcium was reduced to 11.6 mg/dL, and creatinine improved to 1.11 mg/dL. On the 12th day, the patient had left parathyroid excision and was diagnosed with a parathyroid adenoma (). Following the surgical procedure, iPTH normalized to 42.5 pg/mL, but calcium and vitamin D were prescribed for 9 months to cure the hypocalcemia that had developed due to hungry bone syndrome. It has been a year since the surgical operation, and her calcium, phosphate, ALP, and iPTH all remain at normal levels.
|
[[53.0, 'year']]
|
F
|
{'21998044': 1, '18085636': 1, '11193726': 1, '19593861': 1, '17669707': 1, '34095487': 1, '25309783': 1, '26350418': 2, '22187986': 1, '19845029': 1, '8777906': 1, '14730259': 1, '21841482': 1, '18483228': 1, '27734796': 1, '24396684': 2}
|
{'4563849-1': 1}
|
163,902 |
3811692-1
| 24,396,685 |
noncomm/PMC003xxxxxx/PMC3811692.xml
|
Polyglandular Autoimmune Syndrome Type III with Primary Hypoparathyroidism
|
32-year-old female.\nGeneral weakness.\nShe was receiving insulin injections for type 1 diabetes, but her symptoms had not been improved at all, which prompted her decision to come to our hospital.\nShe had been using 32 U insulin every day for type 1 diabetes for 11 years before her visit to our hospital.\nAll family members, including both parents and all siblings, had diabetes.\nWhen she appeared, her blood pressure was 130/80 mm Hg, pulse rate was 74 beats per minute, and body temperature was 36.6℃. She had no other symptoms, except for general weakness and central obesity (body mass index 23.4 kg/m2). No tumor-like mass was checked at her head and neck, nothing was discovered in chest auscultation. When we checked her abdomen, neither any pain nor hepatosplenomegaly was observed. No skin or oral mucosa pigmentation was found. There was no edema in lower leg. The neurological examination results were also normal. She weighed 51.5 kg and was 148.2 cm tall, and she was somewhat short woman with a short neck and round face, similar to a clinical features of AHO, but there was no pathognomonic brachydactyly.\nThe result of complete blood count was the hemoglobin 9.3 g/dL, the erythrocyte average volume 96 fL, leukocyte 5,720/mm3, and platelets 310,000/mm. The results of anemia work up were the total iron binding capacity 447.5 µg/dL, serum ferritin 35.11 ng/mL, reticulocyte count 2.89%, average erythrocyte hemoglobin density 32.6 g/dL, and vitamin B12 839.65 pg/mL. Her blood glucose level was 212 mg/dL, the level of hemoglobin A1c was 7.3%, and the simultaneous measurement of serum level of C-peptide showed decreased level of 0.13 ng/mL. Serum concentration of total calcium were 5.5 mg/dL (range, 8.7 to 1.4); ionized Ca 1.56 mg/dL (range, 2.3 to 2.58); phosphorus 6.7 mg/dL (range, 2.5 to 4.5); total protein 6.7 g/dL; albumin 3.3 g/dL; alkaline phosphatase 329 IU/L; aspartate aminotransferase 119 IU; alanine aminotransferase 65 IU/L. Intact PTH level was 13.32 pg/mL (range, 13 to 54). Serum adrenocorticotropic hormone (ACTH) and cortisol levels were 11.92 pg/mL (range, 10 to 60) and 0.94 (range, 9.4 to 26.1). The results of rapid ACTH stimulation test for adrenal function were normal. The results of thyroid function test were T3 99.01 ng/mL, free T4 0.85 µg/dL, and thyroid stimulating hormone 7.99 µIU/mL. The results for antimicrosomal and antithyroglobulin antibody were positive (52.91 IU/mL, 132.57 IU/mL), and, both islet cell antibody and antiglutamic acid decarboxylase antibody tested negative. In the Ellsworth-Howard examination, urinary phosphoric acid was slightly increased (12.3 mg/dL) and the increase of cyclic adenosine monophosphate (cAMP) was sufficient (4,400 µmol/mL). There was no GNAS mutation. Serum levels of sodium, potassium, blood urea nitrogen, and creatinine were within normal limits at 144 mmol/L, 5.3 mmol/L, 8.2 mg/dL, and 1.0 mg/dL.\nThe chest X-ray showed no abnormal lesion. An brain computed tomography scan showed prominent calcifications in both basal ganglion and hypothalamus (). The thyroid sonogram discovered several nodules, sized 4.5×3.7 mm and 3.9×2.9 mm on each side that were suspected to be thyroid papillary cancer.\nThe patient came to the hospital experiencing general weakness, and she was diagnosed with hypocalcaemia on laboratory examination. At that time, both the levels of PTH and vitamin D were within normal range, but she had previously experienced spasm symptoms and the levels of previous intact PTH were low (4.38 to 10.66 pg/mL) 7 years ago. She has taken oral calcium medicine for treatment of idiopathic hypoparathyroidism because she had no underlying secondary disorders for hypocalcemia and low PTH level. Although she has no pathognomonic brachydactyly, her appearance was similar to AHO in clinical features including short stature, intelligence decline, round face, calcification on basal ganglion and hypothalamus, or obesity. Furthermore, she had a lower normal PTH level and hypocalemia on admission, and we decided to investigate the PTH resistance to identify PHP Ia or PPHP with AHO. In the Ellsworth-Howard examination for investigation of the PTH resistance, it was confirmed that there was no PTH resistance at the kidney and there was no sign of GNAS mutation. We diagnosed this case as hypocalcemia due to idiopathic hypoparathyroidism for lower serum calcium and traced intact PTH levels and began calcium and calcitriol medicine to treat the hypocalcaemia. Subsequently, her symptoms were improved with normalization of ionized Ca at 2.32 mg/dL (range, 2.3 to 2.53). The results of fine needle aspiration on two nodules of thyroid were suggestive malignancy and she underwent a total thyroidectomy. The biopsy results were papillary microcarcinoma with lymphocytic thyroiditis for two suspicious nodules (sized 1.5×1.0 cm on the left and 2.0×1.0 cm on the right). Among the four parathyroid glands, the left inferior parathyroid gland was not discovered, and the remaining three parathyroid glands were remained during surgery. We used levothyroxine 0.05 mg medication for Hashimoto thyroiditis and insulin determir 12 U and aspart 16 U for glucose control.
|
[[32.0, 'year']]
|
F
|
{'32049851': 2, '9860993': 1, '6096181': 1, '25309783': 1, '2333733': 1, '9398840': 1, '9398839': 1, '11588148': 1, '6990358': 1, '14671404': 1, '3003142': 1, '13362295': 1, '24396685': 2}
|
{'7035075-1': 1}
|
163,903 |
3811697-1
| 24,396,682 |
noncomm/PMC003xxxxxx/PMC3811697.xml
|
Thyroid Dysfunction Associated with Administration of the Long-Acting Gonadotropin-Releasing Hormone Agonist
|
A 30-year-old female came to the Department of Obstetrics and Gynecology at Cheil General Hospital & Women's Healthcare Center with dysmenorrhea 3 months ago. She received subcutaneous injections of leuprorelin acetate 3.75 mg per month, three times in all, with a diagnosis of uterine myoma and endometriosis. She was examined for thyroid function prior to laparoscopic surgery 1 week ago and she was sent to the Department of Internal Medicine because of thyroid dysfunction. Her blood pressure was 116/76 mm Hg, pulse was 60 per minute, and body mass index (BMI) was 21.9 kg/m2 160 cm, 56 kg. She had no past medical history, but her mother had previously taken medication for hypothyroidism.\nShe had no special symptoms, such as fatigue, weight fluctuation, edema, and gastrointestinal problems. However, she complained of recently occurred sweating and facial flushing. On physical examination, she had slightly diffuse thyroid enlargement and the electrocardiography (ECG) was normal.\nSerum free T4 (fT4, 6.9 pmol/L) was decreased and thyroid stimulating hormone (TSH, 154.4 µU/mL) was elevated. Antithyroglobulin antibody (anti-TG Ab, 100 U/mL) and anti thyroid peroxidase antibody (anti-TPO Ab, 58 U/mL) were both positive, whereas TSH binding inhibitory immunoglobulin (TBII, 4%) was negative. Thus, she started thyroid hormone replacement therapy (levothyroxine 0.1 mg) with a diagnosis of hypothyroidism.\nOne month later, her thyroid function was normalized (fT4, 21.9 pmol/L; TSH, 2.91 µU/mL) and 2 months later, she underwent laparoscopic myomectomy. After the operation, she received injections of leuprorelin acetate three more times; thereafter, her thyroid function was maintained within the normal range. She is currently maintaining levothyroxine 0.1 mg under serial assessment by the Department of Internal Medicine ().
|
[[30.0, 'year']]
|
F
|
{'19307103': 1, '14558924': 1, '29877268': 1, '10447018': 1, '20446435': 1, '10818434': 1, '11407303': 1, '25309783': 1, '15001954': 1, '31391696': 1, '11228038': 1, '9269652': 1, '18689910': 1, '11228054': 1, '33202820': 1, '24396682': 2}
|
{'3811697-2': 2, '3811697-3': 2}
|
163,904 |
3811697-2
| 24,396,682 |
noncomm/PMC003xxxxxx/PMC3811697.xml
|
Thyroid Dysfunction Associated with Administration of the Long-Acting Gonadotropin-Releasing Hormone Agonist
|
A 35-year-old female came to the Department of Obstetrics and Gynecology at Cheil General Hospital & Women's Healthcare Center with sterility 6 months ago. In the past medical history, she had been treated with medication for hyperthyroidism and had underwent surgery for endometriosis. She had received subcutaneous injections of leuprorelin acetate of 3.75 mg per month, three times in all, as a pretreatment for in vitro fertilization from 2 months ago. Since she had a past history of hyperthyroidism, she was refered to the Department of Internal Medicine for further evaluation.\nHer blood pressure was 118/79 mm Hg, pulse was 79 per minute, and BMI was 18.6 kg/m2 (159 cm/47 kg). She had been diagnosed with hyperthyroidism a decade ago and had taken methimazole 10 to 2.5 mg until 3 months before she came to our hospital because her thyroid function was normalized. She also underwent surgery for endometriosis at another hospital 1 year ago. Nothing was noteworthy in her family history.\nShe complained of sweating, heat sensation intolerance, and facial flushing. On physical examination, she had slightly diffuse thyroid enlargement and the ECG was normal.\nSerum T3 (120.6 ng/dL), fT4 (21.8 pmol/L), and TSH (0.51 µU/mL) were all whinin the normal range, but anti-TG Ab (13 U/mL), anti-TPO Ab (>100 U/mL), and TBII (22%) were all positive. Thus, further observation was required.\nOne month later, she complained of palpitation and fatigue, while T3 (259.5 ng/dL) and fT4 (60.6 pmol/L) were elevated, TSH (<0.01 µU/mL) was suppressed, and anti-TG Ab (17 U/mL), anti-TPO Ab (>100 U/mL), and TBII was elevated to 27%. Thus, she was diagnosed with hyperthyroidism and started taking methimazole 10 mg. Two months later, T3 (304.0 ng/dL), fT4 (57.0 pmol/L), TSH (<0.01 µU/mL), and TBII was elevated to 37% and medication was changed to propylthiouracil 200 mg. Three months later, she is currently maintaining propylthiouracil 100 mg under serial assessment by the Department of Internal Medicine ().
|
[[35.0, 'year']]
|
F
|
{'19307103': 1, '14558924': 1, '29877268': 1, '10447018': 1, '20446435': 1, '10818434': 1, '11407303': 1, '25309783': 1, '15001954': 1, '31391696': 1, '11228038': 1, '9269652': 1, '18689910': 1, '11228054': 1, '33202820': 1, '24396682': 2}
|
{'3811697-1': 2, '3811697-3': 2}
|
163,905 |
3811697-3
| 24,396,682 |
noncomm/PMC003xxxxxx/PMC3811697.xml
|
Thyroid Dysfunction Associated with Administration of the Long-Acting Gonadotropin-Releasing Hormone Agonist
|
A 24-year-old female came to the Department of Obstetrics and Gynecology at Cheil General Hospital & Women's Healthcare Center with right lower abdominal pain 2 months ago and she underwent laparoscopic ovarian cystectomy. Subsequently, she had received subcutaneous injections of leuprorelin acetate of 3.75 mg per month, twice in all. It was accidentally found by another hospital that she had thyroid dysfunction and thyroid enlargement verified by a sonogram 2 days ago. Thus, she was referred to the Department of Internal Medicine.\nHer blood pressure was 111/67 mm Hg, pulse was 80 per minute, and BMI was 18.4 kg/m2 (165 cm/50 kg). Nothing was noteworthy in her medical histoy or family history.\nShe complained of weight loss of 4 kg over 1 year, cold sensation intolerance, and facial flushing. On physical examination, she had diffuse thyroid enlargement and the ECG was normal.\nBoth serum T3 (211.6 ng/dL) and fT4 (38.6 pmol/L) were elevated and TSH (<0.01 µU/mL) was suppressed. Anti-TG Ab (17 U/mL) and anti-TPO Ab (>100 U/mL) were all positive and TBII was 4%. Meanwhile, the reduction of thyroid uptake was discovered on technetium-99m thyroid scan. She was diagnosed with transient thyrotoxicosis and observed without treatment.\nOne month later, TSH (0.01 µU/mL) still had been suppressed, but both T3 (112.3 ng/dL) and fT4 (14.3 pmol/L) were normalized; thereafter, leuprorelin acetate was injected subcutaneously four more times. Two months later, fT4 (9.1 pmol/L) was decreased and TSH (9.81 µU/mL) was elevated without symptoms of hypothyroidism, and observation was continued. Four months later, both fT4 (11.5 pmol/L) and TSH (2.33 µU/mL) were normalized and she is currently under serial assessment ().
|
[[24.0, 'year']]
|
F
|
{'19307103': 1, '14558924': 1, '29877268': 1, '10447018': 1, '20446435': 1, '10818434': 1, '11407303': 1, '25309783': 1, '15001954': 1, '31391696': 1, '11228038': 1, '9269652': 1, '18689910': 1, '11228054': 1, '33202820': 1, '24396682': 2}
|
{'3811697-1': 2, '3811697-2': 2}
|
163,906 |
3811703-1
| 24,396,683 |
noncomm/PMC003xxxxxx/PMC3811703.xml
|
Graves' Disease that Developed Shortly after Surgery for Thyroid Cancer
|
A 41-year-old female.\nPalpitations, heat intolerance, perspiration.\nIn November 2010, 0.5×0.6 cm hypoechoic nodules were found in the right thyroid of a female patient. Fine needle aspiration biopsy was performed. Through the pathology examination, she was diagnosed with papillary thyroid cancer and had robot thyroidectomy on the right thyroid in January 2011. During the postsurgery recovery period, she was found to have clinical features of Graves' disease, and the surgery department sent her to our department for investigation and treatment.\nShe had been taking antituberculous drugs since September as she had been treated for tuberculosis.\nShe drank two to three times a week (one bottle of Soju each time), but never smoked.\nNothing noteworthy was seen.\nHer initial blood pressure was 133/78 mm Hg, pulse 95 beats per minute, respirations 20 breaths per minute, and body temperature 36.4℃. She had a clear level of consciousness without acute signs of disease, but She looked rather sick. The thyroid was not swollen and was painless, and there were no palpable nodules. Also, retraction of the palpebral fissures, proptosis, hyperemia of the conjunctivae, and edema were not observed.\nPeripheral blood was examined and the blood results were white blood cells 7,220/mm3, hemoglobin 13.6 g/dL, hematocrit 41.2%, and platelets 353,000/mm3, while the blood sedimentation rate was 7 mm/hr; therefore, all of the test results were normal. According to the serum biochemical examination, blood urea nitrogen was 13 mg/dL, serum creatinine 0.6 mg/dL, calcium 8.8 mg/dL, phosphorus 4.0 mg/dL, gross protein 7.0 g/dL, albumin 4.0 g/dL, aspartate aminotransferase 25 IU/L, alanine aminotransferase 34 IU/L, and gross bilirubin 0.4 mg/dL; therefore, all of the biochemical results were normal. Meanwhile, the alkaline phosphatase density was elevated (111 IU/L). According to the serum electrolyte examination, sodium density was 144 mEq/L and potassium 4.4 mEq/L.\nBefore the operation, triiodothyronine (T3) was 80 ng/dL (normal range, 65 to 150), free thyroxine (free T4) 1.07 ng/dL (normal range, 0.89 to 1.76), and TSH 1.80 µIU/mL (normal range, 0.35 to 5.50), all of which were in the normal range, but 9 months after the operation, the patient was diagnosed with thyrotoxicosis with T3 363 ng/dL, free T4 2.33 ng/dL, and TSH 0.02 µIU/mL. Meanwhile, there was an increase in thyroglobulin (Tg) 16.6 ng/mL (normally, 1.4 to 78.0), antithyroperoxidase antibody 39.6 IU/mL (normally, 0 to 34), antithyroglobulin antibody (anti-Tg Ab) 335.8 IU/mL (normally, 0 to 60.0), and TSHR Ab 5.44 IU/L (normally, 0 to 1.75).\nIn the thyroid sonogram before the operation, 0.5×0.6-cm sized hypoechoic nodules were found in the right lobe of the thyroid which was a normal size, and there was no sign of increased blood flow (). On thyroid ultrasound after the operation, we could not find any tumor or nodule in the remaining thyroid, but the left thyroid was a little increased in size, the overall phosphorus shade reduced, and the blood flow increased (). However, there was no sign of enlarged cervical lymph nodes in the sonogram either before or after the operation.\nThe patient's thyroid activity examination was normal 1 year before she was diagnosed with thyroid cancer and remained normal just before the thyroid cancer operation. On the preoperative thyroid ultrasound, nothing was noteworthy except for hypoechoic nodules in the right thyroid. However, she was diagnosed with thyrotoxicosis during an examination performed 3 months after the right thyroidectomy. When she was transferred to the surgery department for the operation, her T3 was 226 ng/dL, free T4 2.39 ng/dL, and TSH 0.03 µIU/mL. The surgery department decided to reduce the amount of her levothyroxine from 100 to 50 µg (). Since her condition had not improved at all, she stopped taking the drug, but her condition worsened 3 months later (9 months after the operation) and a blood test was performed, and eventually she was sent to the endocrinology department.\nWhen we considered the clinical features, blood examination results, and ultrasound result, we came to the conclusion that the patient had Graves' disease resulting from the thyroid cancer operation, and we began observing the development of her disease while treating her with carbimazole 20 mg/day and propranolol 30 mg/day. After a month, follow-up tests were performed and we found that her results had greatly improved, with T3 at 177 ng/dL, free T4 1.21 ng/dL, and TSH 0.02 µIU/mL. After 6 months of drug treatment, all the values stabilized: T3 was 102 ng/dL, Free T4 1.14 ng/dL, TSH 2.02 µIU/mL, and TSHR Ab, and she currently comes to the hospital for checkups while taking carbimazole 10 mg/day.
|
[[41.0, 'year']]
|
F
|
{'3168323': 1, '1351465': 1, '1983330': 1, '4134013': 1, '3361079': 1, '12192541': 1, '9737358': 1, '8822326': 1, '18166819': 1, '9870090': 1, '12412748': 1, '29071241': 1, '9447291': 1, '20195406': 1, '25309783': 1, '34966209': 2, '26256985': 2, '9830373': 1, '6103007': 1, '10943744': 1, '24396683': 2}
|
{'8666488-1': 1, '4541672-1': 1, '4541672-2': 1, '4541672-3': 1, '4541672-4': 1, '4541672-5': 1, '4541672-6': 1, '4541672-7': 1}
|
163,907 |
3811707-1
| 24,396,670 |
noncomm/PMC003xxxxxx/PMC3811707.xml
|
Transformation of Nonfunctioning Pancreatic Neuroendocrine Carcinoma Cells into Insulin Producing Cells after Treatment with Sunitinib
|
A 46-year-old woman was carried to the emergency room with sudden loss of consciousness before breakfast. During transfer in the ambulance, her blood glucose level was measured as 20 mg/dL. After intravenous infusion of dextrose solution, she regained consciousness.\nHer medical history included a 7-mm size neuroendocrine carcinoma in the pancreas (), with metastases to retroperitoneal lymph nodes, left supraclavicular lymph nodes and liver (). The patient had received this diagnosis 4 months prior, after presenting with right flank pain. Needle biopsy and immunohistochemical (IHC) staining of the supraclavicular lymph node had been positive for CD56, chromogranin, and synaptophysin, and negative for glucagon and insulin. One month later, she started taking sunitinib 37.5 mg per day because the disease progressed and the right flank pain increased. After 2 months of sunitinib treatment she felt severe fatigue from which she was diagnosed with hypothyroidism, a common adverse event of sunitinib. She began levothyroxine, but even after normalization of thyroid hormone levels, she experienced intermittent weakness, dizziness, and hunger. To relieve fatigue and hunger, she increased oral intake and experienced weight gain of 10 kg over a month. Her medications included oxycodone to relieve flank pain and famotidine for epigastric soreness. She reported having no personal or family history of thyroid disease or diabetes mellitus.\nOn physical examination, she appeared well. Her vital signs were within the normal range, height 156.5 cm and body weight 53 kg. There were two palpable, hard, and nontender lymph nodes of less than 1 cm each in the left supraclavicular area. Goiter was not found. She had tenderness in the right flank on percussion, but hepatosplenomegaly was not noted. Grade 1 hand-foot syndrome (mild erythema), a skin-related side effect of sunitinib was observed. The blood cell count, urinalysis, and serum chemistry and electrolytes were within normal range. A1c at admission was 5.6%. An electrocardiogram revealed a normal sinus rhythm and chest X-ray showed no abnormality. Computed tomography of the abdomen demonstrated an increase in the size of the liver mass from 1.8 to 2.8 cm.\nOvernight fasting plasma glucose was 16 mg/dL with C-peptide and insulin levels of 6.1 ng/mL and 27.2 µIU/mL, respectively. These inappropriately elevated fasting insulin and C-peptide levels compared to the glucose level confirmed that the patient's hypoglycemia resulted from endogenous hyperinsulinemia. Differential diagnosis of endogenous hyperinsulinemia was based on negative titers for insulin antibody and insulin receptor antibody. We performed a liver biopsy to obtain metastatic tissue, and the histologic examination revealed diffuse infiltration of the cancer cells in the liver. IHC staining positive for CD56, chromogranin, and synaptophysin confirmed metastatic neuroendocrine carcinoma. In addition, the metastatic lesion in the liver which had been negative at the initial diagnosis () was strongly positive for insulin (). We concluded that the nonfunctional neuroendocrine carcinoma that metastasized to the liver changed into an insulin-producing tumor after 2 months of administration of sunitinib.\nSince sunitinib may have played a role in the transformation, it was discontinued. However, even with frequent dietary intake, the patient required more than 500 g of glucose per day via the central vein to prevent hypoglycemia. High-dose glucocorticoid and glucagon administration were not effective in relieving the severe hypoglycemia. Eighteen days after discontinuation of sunitinib, severe hypoglycemia persisted and she underwent transarterial chemoembolization (TACE) for the metastatic lesions in the left lobe of her liver. TACE showed extensive and multiple staining of liver nodules, which suggested successful embolization. Intravenous glucose infusion was slowly tapered to 200 g per day during the 2 weeks after TACE. Then a β-cell toxin, streptozotocin (500 mg/m2), and adriamycin (50 mg/m2) were administrated intravenously. Intravenous glucose infusion was stopped 1 week after this infusion. The patient underwent another round of TACE for the right lobe of the liver and intravenous streptozotocin/adriamycin, and she was successfully discharged. One month after the final treatment, her fasting blood glucose was 101 mg/dL. Local control of metastatic carcinoma and systemic administration of β-cell toxin had reversed her severe hypoglycemia.
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[[46.0, 'year']]
|
F
|
{'17868036': 1, '33434180': 1, '19015530': 1, '21993628': 1, '21673539': 1, '19171749': 1, '25309783': 1, '18326519': 1, '17135364': 1, '17020808': 1, '19886867': 1, '27981444': 1, '21565416': 1, '33102220': 2, '18841151': 1, '26113980': 1, '24396670': 2}
|
{'7544986-1': 1, '7544986-2': 1}
|
163,908 |
3811708-1
| 24,396,669 |
noncomm/PMC003xxxxxx/PMC3811708.xml
|
Benign Teratoma of the Thyroid Gland
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A 54-year-old woman.\nA growing thyroid mass found during a routine check-up.\nA thyroid mass was detected by ultrasound during a routine medical check-up 4 years ago. Since then her doctor took a wait and see approach. However, the mass became larger. She had a repeat thyroid ultrasound examination, which revealed that the mass had extended substernally, and she was subsequently transferred to our hospital.\nShe underwent a laparoscopic hysterectomy for the treatment of a uterine myoma 7 years ago. There was no medical history of diseases, particularly thyroid-associated diseases, in her family. She had no drinking and smoking history.\nShe had a blood pressure of 132/65 mm Hg, pulse of 59 beats per minute, respiration rate of 20 breaths per minute, and temperature of 36.0℃. She was conscious without acute distress. A solid and fixed mass was identified on the left side of the neck, but the cervical lymph nodes were not affected.\nComplete blood count revealed a white blood cell count of 8,300/mm3, hemoglobin of 12.8 g/dL, hematocrit of 36.7%, and platelet count of 18,100/mm3. Biochemical examination of serum revealed blood urea nitrogen/creatinine of 13.2/0.4 mg/dL, total protein/albumin of 6.5/4.0 g/dL, aspartate aminotransferase/alanine aminotransferase of 22/16 IU/L, alkaline phophatase of 68 IU/L, and Ca of 8.2 mEq/L. Measurement of electrolytes showed Na/K of 143/3.6 mEq/L.\nThyroid hormone tests revealed thyroid stimulation hormone of 1.88 µIU/mL (normal range, 0.4 to 4.8), free thyroxine of 1.48 ng/dL (normal range, 0.8 to 1.71), and triiodothyronine (T3) of 1.44 ng/mL (normal range, 0.6 to 1.6), showing normal thyroid function. Results of antithyroid peroxidase antibody and antithyroglobulin antibody tests were negative.\nThyroid ultrasonography (US) revealed a hypoechoic and heterogeneous nodule measuring 4.7 cm in diameter, with substernal extension of the inferior portion of the left thyroid lobe. Hyperechoic internal lesions were also observed (). The posteriosr boundary of the nodule was not clearly visualized due to deep attenuation of ultrasound. Ultrasound-guided fine needle aspiration cytology (FNAC) was performed. Based on the cytological examination, thyroid follicular cells were not detected, but cystic liquid was mainly observed, leading to a suspicion of cystic tumor. Computed tomography (CT) scan, which was performed to evaluate the mass due to its substernal extension, exhibited a mass (6.1×5.0×3.6 cm in size) that extended from the left thyroid lobe to the anterior mediastinum, with irregular enhancement, and clear margins that contained fat (). The mass caused deviation of the airway to the right, but there was neither a change in shape nor adhesion. Abnormal enlargement of lymph nodes was not observed in the neck.\nResults of FNAC and CT scan of the neck revealed a low possibility for a malignant tumor. However, the large size of the mass was concerning, and a lobectomy was performed to remove the left lobe. In histological examination, the removed mass was soft, but extended to the anterior mediastinum from the left thyroid lobe. The cut surface was dark yellow. There were multiple cystic masses, which were encapsulated in a wall of fibrotic capsule (). A microscopic examination revealed cystoma multiplex in which pilosebaceous structures, ciliated respiratory epithelium, intestinal columnar epithelium with goblet cells, and muscular structures were mixed (). Since there was no infiltration into surrounding tissues, benign thyroid teratoma was diagnosed. The patient is currently taking 50 µg of levothyroxine daily and attending outpatient clinic.
|
[[54.0, 'year']]
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F
|
{'15832097': 1, '8166978': 1, '17322585': 1, '5314525': 1, '2105009': 1, '17596674': 2, '2664866': 1, '10758996': 1, '9537215': 1, '34295469': 1, '3293377': 1, '21569901': 1, '9308448': 1, '17223853': 1, '2982716': 1, '10699906': 1, '352506': 1, '25309783': 1, '16009816': 1, '2091821': 1, '26664704': 2, '24396669': 2}
|
{'4654446-1': 1, '2693658-1': 1}
|
163,909 |
3811709-1
| 24,396,668 |
noncomm/PMC003xxxxxx/PMC3811709.xml
|
Riedel Thyroiditis in a Patient with Graves Disease
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Mrs. Kim, age 57.\nRecently enlarging neck mass and hoarseness that started 5 days before admission to the hospital.\nA 57-year-old woman visited the outpatient clinic with a very hard, fixed lump that had been present on the right side of her neck for months and hoarseness, which started 5 days previous. The patient had previously taken antithyroid agents prescribed by a private hospital but did not undergo additional tests or follow-up related to her hyperthyroidism. She did not show any symptoms associated with thyrotoxicosis on admission.\nShe underwent intermittent treatment for hyperthyroidism over the last three decades. She has had no other symptoms.\nNo medical problems.\nThe patient was conscious and in no acute distress. She was medically stable with a blood pressure of 130/90 mm Hg, pulse of 76 beats per minute, respiration rate of 20 breaths per minute, and a temperature of 36.5℃. Globe protrusion, scleral icterus, and conjunctival anemia were not observed. Enlarged cervical lymph nodes and jugular vein engorgement were also not present. A hard and fixed thyroid nodule that measured approximately 5×4 cm was palpated, but no neck tenderness was appreciated (). On auscultation, normal heart and breath sounds were observed. Physical examination revealed no pitting edema in her extremities.\nComplete blood count revealed a white blood cell count of 6,460/mm3 (neutrophil 57.4%, lymphocyte 36.6%, monocyte 7.7%, eosinophil 0.6%), hemoglobin of 11.6 g/dL, hematocrit of 35.2%, and platelet count of 295×103/mm3. Urine test was normal. Serum biochemical examination revealed a blood urea nitrogen/creatinine of 25/0.6 mg/dL, total protein/albumin of 7.4/4.3 g/dL, aspartate aminotransferase/alanine aminotransferase of 22/20 IU/L, Na/K/Cl of 142/5.1/105 mEq/L, Ca of 4.6 mEq/L (normal range, 4.5 to 5.2), erythrocyte sedimentation rate of 19 mm/hr, and C-reactive protein <0.2 mg/day. Thyroid function tests revealed thyroid stimulation hormone of 0.07 µIU/mL (normal range, 0.4 to 4.5), free T4 of 3.86 ng/dL (normal range, 0.7 to 2), TBII of 51% (normal range, 0 to 15), thyroglobulin of 493 ng/dL (normal range, 2 to 60), antithyroid microsomal antibody of 3.1 U/mL (normal range, 0 to 8), and negative thyroglobulin antibody of 22 U/mL (normal range, 0 to 55), consistent with Graves disease.\nNormal sinus rhythm.\nSigns of emphysema and right to left shift of the trachea as a consequence of the thyroid nodule.\nA well-defined irregular and hypoechoic nodule measuring 4 cm in diameter, along with large scattered dense calcifications, was observed in the right thyroid lobe (). However, enlarged cervical lymph nodes and invasion into the parathyroid glands were not present.\nSince repeated nonaspiration technique failed to obtain a specimen, we employed an aspiration technique which yielded a very small amount of cytologic specimen. In cytopathologic examination, no malignant cells were detected, but adenomatous goiter was suspected. Although thyroid cancer was not diagnosed by FNA, the large, solid mass and paralyzed vocal cords on the right side suggested the possibility of thyroid cancer. Therefore, a surgical approach was determined for histological diagnosis and treatment.\nThere was a 4.3×4.0 cm nodular lesion occupying most of the right lobe of the thyroid. A peripheral calcified lesion was also identified. Very severe marginal calcification was detected in the inferior portion of the nodule, which was barely observable in ultrasonography (). Unilateral fixed vocal cords were revealed in a paramedian position. Vocal cord paralysis was suspected on the right side ().\nA total thyroidectomy was performed. A 4.5-cm solid mass of the right thyroid lobe was closely adhered to the surrounding airway and recurrent laryngeal nerve. It was impossible to completely dissect the mass from the nerve.\nThe resected mass was covered by a thin capsule, and its cut surface showed mixed strips of white, yellowish-brown, and pink colors. Peripheral dense calcification was also seen. Microscopic examination revealed that thyroid follicles were replaced by extensive inflammatory and fibrous tissue. Inflammation was also noticed in the vein, which was encased in fibrous tissue, but no malignant cells were found. Based on these pathologic characteristics, RT was diagnosed ().\nThe patient recovered from RT, and there were no signs of complications. She is currently taking 100 µg levothyroxine while undergoing postsurgical outpatient follow-up. She has not yet recovered from her vocal cord paralysis.
|
[[57.0, 'year']]
|
F
|
{'20525902': 1, '11155216': 1, '15298150': 1, '8604680': 1, '8120524': 1, '21568724': 1, '12906372': 1, '25309783': 1, '22187229': 1, '20506114': 1, '3057862': 1, '6195075': 1, '12161472': 1, '8957485': 1, '7865983': 1, '16033720': 1, '3906289': 1, '22563540': 2, '8454764': 1, '14986301': 1, '24396668': 2}
|
{'3341482-1': 1}
|
163,910 |
3811713-1
| 24,396,667 |
noncomm/PMC003xxxxxx/PMC3811713.xml
|
Adrenocorticotropic Hormone-Independent Cushing Syndrome with Bilateral Cortisol-Secreting Adenomas
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A 48-year-old woman.\nIncidentally found bilateral adrenal masses.\nThe patient had been diagnosed with hypertension 3 years prior, and had been receiving carvedilol 25 mg as prescribed by a private clinic. However, the patient's blood pressure (BP) had not been under control for about 3 months prior to the visit at our hospital. A year prior, the patient's menstrual cycle had become irregular and her weight had increased by 5 kg in the last year. The patient had visited our hospital due to the identification of bilateral adrenal masses from abdominal CT during a routine health examination.\nNothing specific except hypertension.\nNothing specific.\nAt the time of the visit to our hospital, the patient's height was 150 cm, weight was 53.8 kg, BP was 145/95 mm Hg, pulse rate was 72 beats per minute, respiratory rate was 20 times per minute, and body temperature was 37.1℃. She had an alert mental state, no visible signs for acute or chronic illness and no abnormal findings for skin, sclera and conjunctiva. Examination of the head and neck revealed a moon face, while a buffalo hump deformity was observed upon thoracic examination. There was no specific finding on the abdominal examination and no edema of extremities was identified. The patient had no accompanying muscle weakness or sensory deterioration.\nThe peripheral blood test performed at the time of visit to the hospital showed the following; white blood cell, 6,450/mm3; hemoglobin, 12.9 g/dL; hematocrit, 41.6%; and platelet, 289,000/mm3. The serum biochemical assay showed the following; calcium, 9.4 mg/dL; phosphorus, 3.3 mg/dL; total protein, 7.0 g/dL; albumin, 4.2 g/dL; aspartate aminotransferase, 21 IU/L; alanine aminotransferase, 19 IU/L; alkaline phosphatase, 43 IU/L; blood urea nitrogen, 10 mg/dL; creatinine, 0.7 mg/dL; sodium, 144 mEq/L; potassium, 3.4 mEq/L; and chlorine, 102 mEq/L.\nThe hormone test indicated that the morning baseline blood cortisol was 15.7 µg/dL and ACTH was less than 5 pg/mL. The 24-hour urine free cortisol excretion increased to 198.7 µg/day (normal range, 23 to 135). In addition, the following were in the normal range; metanephrine, 63 µg/day (normal range, 52 to 341); normetanephrine, 176 µg/day (normal range, 88 to 444); epinephrine, 3.1 µg/day (normal range, 0 to 20); norepinephrine, 28.9 µg/day (normal range, 15 to 80); and vanillylmandelic acid, 5.4 mg/day (normal range, 0 to 8). The 24-hour urine creatinine was 0.5 g/day (normal range, 0.8 to 1.8) and the creatinine clearance was calculated to be 122.4 mL/min (normal range, 75 to 125), indicating that the urine sampling was done relatively well. The plasma aldosterone concentration was 7.5 ng/dL and plasma renin activity was 0.4 ng/mL/hr, indicating that the aldosterone/renin activity ratio was 18.7 and there was no finding of primary aldosteronism.\nThe serum cortisol after an overnight 1 mg dexamethasone suppression test was 14.5 µg/dL, which was not suppressed. The low-dose dexamethasone suppression test demonstrated that the 24-hour urine free cortisol excretion increased to 397.8 µg/day and the blood cortisol concentration increased to 21.1 µg/dL, so we diagnosed the patient's condition as Cushing Syndrome. In the high-dose dexamethasone suppression test, the urine free cortisol excretion and blood cortisol concentration were not suppressed ().\nBilateral adrenal tumors were identified on adrenal CT, with one sized 2.8×2.0 cm on the right side and the others sized 2×2.3 cm and 1.7×1.4 cm, respectively, on the left side (). There were no abnormal findings from the Sella MRI.\nAdrenal vein sampling (AVS) was done in order to identify the location of a functional tumor secreting cortisol in between the bilateral adrenal tumors. AVS was conducted without an ACTH stimulus on the day after the high-dose dexamethasone suppression test. The blood cortisol concentration was measured by sampling the blood twice from catheterization to the femoral vein and bilateral adrenal veins ().\nWhen the bone density was measured by dual energy X-ray absorptiometry, osteopenia was found based on the finding that the T score of lumber spine was -2.1, T score of femoral neck was -1.0 and T score of the total hip was -0.7.\nAs the adrenal vein cortisol measured from AVS was eight times higher than that of the inferior vena cava, it was determined that the AVS was done selectively. The blood cortisol concentration was measured as high from the bilateral adrenal veins with AVS. Therefore, we diagnosed the patient with Cushing Syndrome induced by bilateral cortisol-secreting adenomas. To treat the patient, we removed all of the bilateral adrenal tumors by laparoscopic bilateral adrenalectomy. Immediately after the surgery, the patient was discharged because there was no specific complication while implementing supplementary therapy with prednisolone and fludrocortisone, and we had discontinued the antihypertensive agent as the BP had improved to 120/80 mm Hg at the 2-month follow-up observation. At 5 months postoperatively, the blood cortisol concentration was 5.0 µg/dL, ACTH was 19.0 pg/mL, the plasma aldosterone concentration was 15.0 ng/dL, and the plasma renin activity was 3.0 ng/mL/hr, indicating no evidence of recurrence. The patient is currently under follow-up study as an outpatient while receiving prednisolone 5 to 2.5 mg and fludrocortisone 0.1 mg.\nA single mass was found on each of the adrenal glands and their sizes were 2.6×2.3×1.7 cm for the left side mass and 2.6×2.5×1.6 cm for the right side mass. Based on the visual findings, the left mass was in the shape of a dumbbell with a narrowed mid-part, showing a light brown cross-section, and the right mass had a brown cross-section ().\nFrom the optical microscopic findings, the bilateral adenomas were composed of large round vacuolar cells of consistent shape and size, and with good differentiation, whereas the normal tissues of the adrenal cortex around the adenoma were atrophic. As an atypical nucleus and necrosis, hemorrhage, or reverse differentiation were not found, the findings were appropriate for adrenal adenoma ().
|
[[48.0, 'year']]
|
F
|
{'27252858': 1, '31467526': 1, '18334580': 1, '25309783': 1, '26248855': 2, '18074172': 1, '29685132': 2, '31440949': 1, '16698415': 1, '24396667': 2}
|
{'4722418-1': 1, '5913873-1': 1}
|
163,911 |
3811790-1
| 24,396,654 |
noncomm/PMC003xxxxxx/PMC3811790.xml
|
Steroid Responsive Xanthomatous Hypophysitis Associated with Autoimmune Thyroiditis: A Case Report
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A 36-year-old woman was referred for the evaluation of a pituitary mass detected by brain magnetic resonance image (MRI). She had a 4-month history of amenorrhea and had suffered from headache for 2 months. One month prior to admission, she visited a different hospital emergency room for headache, fever, and vomiting. She was noted to be febrile with a body temperature of 38.5℃. A cerebrospinal fluid (CSF) examination was performed given concerns for meningitis and the CSF findings displayed an elevated white cell count of 350/mm3 (48% lymphocyte), a glucose level of 2.39 mmol/L (normal range, 2.77 to 4.99), and protein 112.7 g/L (normal range, 200 to 400), suggestive of aseptic meningitis. No bacteria or fungi were grown from culture. There was no leukocytosis (white blood count, 7,200/mm3). Her fever resolved after several days of conservative therapies and supportive care. However, her headache still persisted, prompting further imaging. Brain MRI scans showed a cystic pituitary mass prompting her transfer to our hospital.\nOn admission, she also had complaints of general weakness, polydipsia, and polyuria. Her urine volume was more than 5 L per day (specific gravity, 1.006). There was no family history of endocrine disease except for her brother who has hyperthyroidism. She was dehydrated and appeared clinically unwell. She had no visual disturbance and no neurologic deficits such as an abnormal extraocular movement. Her body temperature was 36.4℃ with stable vital signs (blood pressure, 102/77 mm Hg; pulse rate, 96 beats/min). Laboratory investigation showed mild hypernatremia (sodium of 147 mmol/L; normal range, 136 to 145). The patient's serum and urinary osmolarity were 304 and 111 mmol/kg, respectively. Morning serum levels of cortisol (38.64 nmol/L; normal range, 49.66 to 717.34) and estradiol (11.01 pmol/L; normal range, 36.7 to 1,618.4) were low. A mildly elevated level of prolactin (2,756.50 pmol/L; normal range, 156.52 to 821.73) was also noted. Her thyroid function test revealed hyperthyroidism with a high free T4 (34.75 pmol/L; normal range, 8.24 to 22.14) and low thyroid stimulating hormone (0.01 mIU/L; normal range, 0.3 to 6.50). While antithyroglobulin antibody (1,457 kIU/L; normal range, <60) and antimicrosomal antibody (1,720 kIU/L; normal range, <60) were high, anti-TSH receptor antibody (0.1 kIU/L; normal range, 0.1 to 1.0) levels were normal (). Thyroid gland ultrasonography showed a normal volume with diffuse heterogeneous background echotexture of both thyroid glands. Stimulation test with gonadotropin releasing hormone (GnRH) and insulin revealed poor responsiveness to gonadotroph, somatotroph, and corticotrophs. Other routine laboratory findings were all unremarkable. A MRI disclosed a 1.0×0.9 cm sized cystic mass enlarging the sella turcica. The mass had heterogeneous signal intensity and mainly peripheral enhancement was observed after administration of contrast material. There was no extension of the mass into the suprasellar cistern or cavernous sinus (). After 0.2 mg of desmopressin was given orally twice a day, urine volume, serum sodium, and osmolarity normalized. Glucocorticoids were administrated before neurosurgical exploration was performed. Surgical resection via the endoscopic transsphenoidal route was performed. On the pituitary gland, a friable, encapsulated mass with moderate vascularity was found. Histological examination of the resected lesion showed that the pituitary gland was destroyed by infiltration of lymphoplasma cells and foamy histiocytes, fibrosis, and focal necrosis. Foamy histiocytes were positive for CD68 and negative for CD1a and S-100 protein. There was no evidence of an associated adenoma or granuloma (). A postoperative Gadolinium-enhanced MRI was performed on day one postoperatively and showed a residual soft tissue lesion in the superior aspect of pituitary fossa and pituitary stalk (). The patient continued to take desmopressin 0.2 mg twice daily and prednisolone 5 mg once daily after surgery. Two months later, the patient underwent an endocrine work-up. Poor responsiveness to gonadotroph, somatotroph, and corticotrophs was still shown on the anterior pituitary stimulation test with GnRH and insulin. Desmopressin was also not able to be withdrawn. In comparison to her previous study, the level of TSH was still under the normal range (0.02 mIU/L), but her free T4 had decreased (5.53 pmol/L) significantly, which is consistent with secondary hypothyroidism, prompting thyroxin replacement (). At 5 months after operation, the patient still had amenorrhea with low estradiol (11.01 pmol/L) and normal serum follicle stimulating hormone/luteinizing hormone (0.3/1.3 IU/L), and she started estrogen replacement.\nAt the 10-month postoperative visit, the patient complained of progressive visual impairment and headaches. An MRI performed immediately showed that the residual mass seen on the previous MRI had increased in size and infiltrated the suprasellar lesion (). The patient refused to undergo surgery again, prompting a trial of high dose steroid therapy. High dose (500 mg intravenous) methylprednisolone was administered for 3 days. During the methyprednisolone pulse therapy, the patient's visual acuity became clear and her headache resolved. An MRI taken 4 days after methyprednisolone initiation revealed a decreased mass size (). After confirmation of steroid effect on the lesion, high doses of prednisolone (50 mg) were given orally and tapered gradually by 5 to 10 mg per week until her dose reached 10 mg a day. Three months later, a MRI was performed after maintaining prednisolone treatment at 10 mg a day, which demonstrated a marked mass reduction at the sella and suprasellar area ().
|
[[36.0, 'year']]
|
F
|
{'25325267': 1, '27500004': 2, '16793955': 1, '14971740': 1, '34095493': 1, '31863360': 1, '28120170': 1, '15309917': 1, '15634713': 1, '1791874': 1, '12446917': 1, '25309783': 1, '28236350': 1, '22682648': 1, '34659121': 2, '11238484': 1, '20671950': 1, '10449568': 1, '24396654': 2}
|
{'8518622-1': 1, '4960922-1': 1}
|
163,912 |
3811791-1
| 24,396,651 |
noncomm/PMC003xxxxxx/PMC3811791.xml
|
A Case of Acute Suppurative Thyroiditis with Thyrotoxicosis in an Elderly Patient
|
A 70-year-old female.\nFever and systemic debilitation.\nThe patient was transferred to our hospital due to the finding of thyrotoxicosis during an in-patient stay at another hospital where she was being treated for a 2-week fever and systemic debilitation.\nThe patient had hypertension and had taken antihypertensive medication for 20 years.\nThere was nothing specific.\nThe patient was quite alert, but showed signs of acute illness. Her blood pressure measured 120/80 mm Hg, pulse rate was 110 bpm, respiratory rate was 20 times per minutes and axillary temperature was 38.4℃. Based on examinations of her head and neck, a lump was detected and palpitation of the lump was accompanied by local heatness and minor tenderness. The lump was fixated and soft. There was no finding of tenderness of the paranasal sinus or pharyngolaryngeal flare, tonsillar hypertrophy, or enlargements of lymph node.\nThe blood assay revealed that white blood cell (WBC) count was 13,500/mm3 (neutrophils, 80.9%), hemoglobin was 9.3 g/dL, and platelet was 456,000/µL. The erythrocyte sedimentation rate (ESR) increased to 151 mm/hr, and C-reactive protein increased to 24.7 mg/dL. The endocrinology report showed that T3 was 228.0 ng/dL (normal range, 80 to 200), free T4 (FT4) was >7.77 ng/dL (normal range, 0.93 to 1.7), thyroid stimulating hormone (TSH) was 0.02 µIU/mL (normal range, 0.27 to 4.2), and thyroglobulin was >5,000 ng/mL (normal range, 1.4 to 78). Antimicrosome antibody (Ab), antithyroglobulin Ab, and thyroid stimulating Ab were in the normal ranges. Serum calcitonin was in the normal range of less than 1.0 pg/mL, and the HIV Ab test was negative.\nThe 99mTc thyroid scan showed that the radioactive isotope intake of the thyroid was reduced and irregular ().\nThe margin of the right side of the thyroid was unclear and a multilobulated lump with poor contrast was observed. Multiple lymph nodes were observed from the IV, V, and VI areas of the right side of the neck ().\nNeck sonography revealed that there were no abnormal structures found in the homogeneous image of the left lobe of the thyroid, but in the right lobe, there was a mass that was about 4.5×2.5×4.6 cm in size with heterogeneous echogenicity (). Using fine needle aspiration biopsy, we obtained chocolate-colored abscess fluid that was chocolate in color (), and a cytopathogenic test revealed no atypical cells or malignant cells, but many neutrophil cells and histiocytes were observed.\nImmediately, we commenced with treatment by administration of amoxicillin/clavulanate 1 g/200 mg three times a day and prescribed 40 mg propranolol four times a day for relieving the symptoms of thyrotoxicosis. No microbes were identified from the culture test of aspirated samples from blood or thyroid gland. Hyperpyrexia gradually disappeared within 3 days after administration of antibiotics, but the feeling of local fever, neck swelling and tenderness continued for up to 10 days after administration of antibiotics. We performed a thyroid lobectomy and found that the abscess was accompanied by fibrosis in the right lobe of the thyroid. The pathological findings revealed inflammation accompanied by necrotic tissue and abscess.\nAfter the surgery, the patient showed symptomatic recovery from neck pain and swelling, and was discharged from the hospital. We performed outpatient follow-up with esophagography and neck computed tomography (CT) and we could not find any anatomical defect such as fistula. A thyroid function test in the outpatient department at 2 months after surgery revealed that FT4 was 1.02 ng/dL and TSH was 2.40 µIU/mL, indicating that thyroid function had been restored to normal.
|
[[70.0, 'year']]
|
F
|
{'9640421': 1, '12697345': 1, '16279853': 1, '10750960': 1, '9457253': 1, '1987447': 1, '34966206': 2, '9827283': 1, '17471585': 1, '25309783': 1, '16571095': 1, '17071148': 1, '11916288': 1, '20144025': 1, '17674951': 1, '24396651': 2}
|
{'8666487-1': 1}
|
163,913 |
3811799-1
| 24,396,655 |
noncomm/PMC003xxxxxx/PMC3811799.xml
|
Olanzapine-Induced Diabetic Ketoacidosis and Neuroleptic Malignant Syndrome with Rhabdomyolysis: A Case Report
|
A 29-year-old man presented at a emergency room in a stupor.\nThe patient had started psychiatric treatment after being diagnosed with personality disorder and hypochondriasis by the department of psychiatry in our hospital 4 years ago. After about 1 year of treatment, olanzapine was administered due to the patient's symptoms of social withdrawal and distrust of people. After the initiation of olanzapine, the patient's body weight increased by ≥30 kg, and hyperthermia occurred together with nausea and vomiting 1 week prior to the visit to our hospital. The patient received a prescription from a neighboring hospital and had taken antipyretics, but did not show any improvement. Then the patient showed mental deterioration and was admitted to our hospital via the emergency room.\nBoth parents were moderately built, and none of the family members, including siblings, had a metabolic disease such as diabetes.\nThe patient was on medication due to incidences of personality disorder, hypochondriasis, and psychotic tendency, taking olanzapine 10 mg, valproic acid 500 mg, clonazepam 0.5 mg, and lorazepam 1 mg on a daily basis. The aforementioned medication regimen was maintained for over 1 year without any dosage change, and the intake period of olanzapine was 32 months. There was no other underlying disease than the aforementioned, and there were no abnormal test results based on blood assay, including an assay for fasting plasma glucose, which was performed prior to administration of antipsychotics.\nThe patient had no history of smoking or alcohol drinking and was unemployed since completion of military service as social service personnel.\nIn physical examination, the patient showed acute signs of illness and was in a coma. His vital signs measured at the time of visit to our hospital were 110/70 mm Hg for blood pressure (BP), 120 beats per minute for pulse rate, 24 times per minute for respiratory rate, and 37.2℃ for body temperature. The patient's height was 181 cm, weight was 104 kg and body mass index (BMI) was 31.7 kg/m2. His consciousness state was stupor with normal light reflexes, and senses as well as spontaneous motions of extremities were maintained. Chest auscultation revealed that the heart rate was fast, but there was no murmur, and the patient had tachypnea, but had no crackles or wheezing sound auscultated. There was neither notable tenderness nor rebound tenderness from the abdomen. The patient's skin was dry overall.\nPeripheral blood assay showed the following results: white blood cell 6,560/mm3 (neutrophil 72%), hemoglobin 20.2 g/dL, hematocrit 60.8%, and platelets 228,000/mm3. Taking the findings of physical examination into account, dehydration-induced hemoconcentration was suspected. The results of serum biochemical assay revealed that the plasma glucose level had increased to 1,216 mg/dL, the blood urea nitrogen level was 31 mg/dL, and creatinine level was 2.4 mg/dL. The result also showed the following: sodium, 149 mEq/L; potassium, 4.5 mEq/L; chloride, 96 mEq/L; total protein, 8.7 g/dL; albumin, 5.0 mg/dL; aspartate aminotransferase, 28 IU/L; alanine aminotransferase, 44 IU/L; total bilirubin, 0.6 mg/dL; calcium, 11.5 mg/dL; phosphate, 6.1 mg/dL; and creatine phosphokinase (CPK), 80 U/L (reference range, 30 to 170). Dipstick-utilized urine assay showed a positive reaction to ketone, and increases in amylase and lipase to 545 IU/L (reference range, 28 to 100) and 1,435 U/L (reference range, 13 to 60), respectively. Arterial blood gas analysis (ABGA) showed that the pH was 7.25, pCO2 was 18.9 mm Hg, pO2 was 86.1 mm Hg, HCO3- was 8.2 mEq/L, and oxygen saturation was 95.7%, presenting metabolic acidosis with 44.8 mEq/L of anion gap. The glycosylated hemoglobin level was 13.8%, while the serum C-peptide level tested during the administration of insulin were 0.38 ng/mL. So the patient was presumed to be in DKA and acute renal failure.\nElectrocardiography findings showed sinus tachycardia with rate of 150 beats per minute.\nThere were no specific findings from the chest X-ray examination, and there was no evidence of ileus other than fecal impaction shown on abdominal X-ray examination. An abdominal computed tomography scan showed no findings of edema or necrosis or fluid retention in the pancreatic parenchyme and its periphery ().\nAlthough there was no sign of BP reduction, the patient showed severe dehydration induced by extreme hyperglycemia and metabolic acidosis. We administered ≥4 L per day of fluid through intravenous infusion and immediately began insulin pump therapy. Within 24 hours of insulin therapy, the plasma glucose level was reduced to less than 300 mg/dL (), the anion gap level was reduced to normal range and ABGA showed that the patient was out of metabolic acidosis. But, in spite of fluid infusion of ≥2 L per day, hyperthermia occurred and the levels of CPK and creatinine began to increase rapidly to 16,161 U/L and 4.1 mg/dL, respectively, on the 3rd day of hospitalization. Also, the urinary myoglobin level was 1,879 ng/mL. In addition, the patient was in a confused mental state with severe muscle stiffness and rigidity, and increased uptake at upper and lower proximal limb was shown on bone scan (). Even with fluid treatment for acute renal failure, the level of creatinine continued to increase, so we started continuous renal replacement therapy (CRRT) on the 5th day of hospitalization (). After initiation of CRRT, the patient showed remarkable improvement in fever and consciousness, so we converted dialysis modality to intermittent hemodialysis 3 days later and maintained the treatment until the 12th day of hospitalization. The urine output was normalized and there was no additional elevation in creatinine and CPK concentrations, so we discontinued hemodialysis (). The patient presented consciousness deterioration, muscle stiffness, and high fever that did not respond to antipyretics and fluid infusion with history of taking antipsychotics, so we determined that the patient had NMS, and implemented supportive therapy including discontinuation of causative medication. We used the insulin pump for glycemic control in the early stage, and changed to multiple daily injections of insulin to manage the patient's condition. We could discontinue the administration of insulin on the 41st day after the first visit to our hospital as the insulin demand had gradually decreased. And we changed to metformin monotherapy. We stopped the administration of oral hypoglycemic agents on the 52nd day. On follow-up examination, we confirmed a notable reduction in glycosylated hemoglobin and a remarkable restoration of the serum C-peptide level (). Currently, the patient is maintaining very good glycemic control only by life style modification and is under prognostic observation as an outpatient.
|
[[29.0, 'year']]
|
M
|
{'6824251': 1, '15096088': 1, '9825080': 1, '17192353': 1, '9921705': 1, '12413635': 1, '8093494': 1, '8935797': 1, '19081460': 1, '12050274': 1, '6132930': 1, '15734866': 1, '27034860': 2, '33936704': 1, '25309783': 1, '30558060': 1, '15706465': 1, '19067992': 1, '28816925': 1, '14638600': 1, '24396655': 2}
|
{'4806275-1': 1}
|
163,914 |
3811800-1
| 24,396,653 |
noncomm/PMC003xxxxxx/PMC3811800.xml
|
Anaplastic Thyroid Carcinoma Following Radioactive Iodine Therapy for Graves' Disease
|
A 42-year-old woman was referred to our clinic in 1998, because of palpitations, hand tremor, and laboratory findings of hyperthyroidism (serum thyrotropin [thyroid-stimulating hormone, TSH] 0.05 µIU/mL [reference range, 0.17 to 4.05], free thyroxine 4.01 ng/dL [reference range, 0.79 to 1.86], and positive TSH receptor antibody at 201.7% [percent binding inhibition index, radioreceptor assay, reference range; ±15.0%]), and had been diagnosed as Graves' disease. A technetium-99m thyroid scan showed enlarged and homogeneously increased uptake, and ultrasonography revealed a diffuse goiter without nodules. The patient received 200 mg/day of propylthiouracil and β-adrenergic blocking agents for 1 year. However, due to recurrent hyperthyroidism, she received RAI therapy twice with an administered dose 370 MBq (10 mCi), 296 MBq (8 mCi), each. Two years later, she received thyroid hormone replacement due to subsequent hypothyroidism at a local clinic.\nIn September 2010, over 10 years later, she revisited us with complaints of hoarseness, dysphagia, and dyspnea, which had been presented for 2 months. An anterior neck mass, which was hard and fixed, and some lymph nodes (LNs) around the mass were palpable. Her chest radiography showed a tracheal narrowing and deviation to the right without active lung lesion. On computed tomography (CT) of the neck, the thyroidal mass invaded the tracheal cartilage and the right tracheoesophageal groove (). In fludeoxyglucose positron emission tomography-CT, an intense hypermetabolic lesion was noted in the thyroid gland and LNs on her left neck without distant metastasis. LN biopsy was performed and microscopically showed metastatic papillary carcinoma (). In September 2010, a total thyroidectomy with selective neck dissection, tracheal sleeve resection, and end-to-end anastomosis were performed. The surgical specimen from the thyroid was diagnosed as anaplastic carcinoma (). The final pathologic staging was T4bN1bM0. Subsequently, she had concurrent cisplatin-based chemoradiotherapy for her neck and superior mediastinum (total 6,600 cGy/33 fractions).\nAfter 4 months of follow-up, despite the aggressive treatment, the disease progressed. She developed shortness of breath, dyspnea, and pain in her left arm. On neck CT, a new focal necrotic mass on the left side of her neck was noted, suggesting local recurrence. The mass extended up to the tracheal lumen and the patient died of sudden uncontrolled bleeding in the airway.
|
[[42.0, 'year']]
|
F
|
{'4134013': 1, '15770642': 1, '30854863': 1, '11895209': 1, '10450109': 1, '17341574': 1, '25309783': 1, '10382695': 1, '6700935': 1, '16284432': 1, '15579770': 1, '17665195': 1, '9492154': 1, '5818522': 1, '9133697': 1, '24396653': 2}
|
{}
|
163,915 |
3811804-1
| 24,396,650 |
noncomm/PMC003xxxxxx/PMC3811804.xml
|
Long-Term Survival of a Patient with Pulmonary Artery Intimal Sarcoma after Sequential Metastasectomies of the Thyroid and Adrenal Glands
|
A 62-year-old woman presented with a 4-week history of dyspnea on exertion and facial edema in November 1999. Her past medical history was unremarkable. Electrocardiography showed T wave inversion at leads V1-5, III, and aVF, right axis deviation, and right ventricular hypertrophy. Initial echocardiography revealed an echogenic mass in the main pulmonary artery with significant flow obstruction and right ventricular dysfunction suggesting pulmonary embolism. Chest computed tomography (CT) revealed an embolism-like mass in the pulmonary trunk and in both sides of the main pulmonary arteries (). Pulmonary artery endarterectomy with pulmonary valve replacement and pulmonary artery reconstruction were performed. The surgical specimen showed an ill-defined, protruding polypoid mass that was 4.8 cm in the greatest dimension. The pathology revealed pulmonary artery intimal sarcoma, which was supported by positive smooth muscle actin and negative desmin in immunohistochemical staining (). Involvement of the resection margin by the tumor was noted. She received radiation therapy (4,500 cGy fractionated) and chemotherapy (cyclophosphamide, doxorubicin, and dacarbazine) as adjuvant treatments. During follow-up, she was regularly checked by echocardiography and chest CT. There was no evidence of local recurrence on echocardiography. On initial follow-up chest CT (November 2001, 2 years after initial surgery), mild diffuse enlargement of the thyroid gland with multiple small low density lesions was discovered. It is hard to know if these findings existed before the initial operation, because the preoperative chest CT did not include the neck. She showed normal thyroid function tests. This lesion was just followed up with chest CT yearly and showed no change for 3 years.\nIn August 2004 (4.7 years after initial surgery), she was referred to an endocrinologist for abnormal thyroid function tests. There was a palpable nodule in the left thyroid gland. Cervical lymphadenopathy was not present. The serum thyroid stimulating hormone level was 0.12 mIU/L (normal, 0.4 to 5.0), and total T4 was 166 nmol/L (normal, 76 to 178). CT of the neck showed two low density nodules of 2.0×2.5 cm and 0.9×0.9 cm in both lobes of the thyroid glands, which was no different from previous studies (). Fine needle aspiration cytology was done and revealed atypical spindle cells, suggestive of metastatic intimal sarcoma (). She had no other metastatic sites in the chest and abdomen-pelvic CT. She underwent total thyroidectomy, and histology confirmed metastatic intimal sarcoma with clear resection margins. She was followed by neck and chest CT (covering the adrenal gland), and there was no evidence of local recurrence or distant metastasis until August 2005.\nA 10.0×8.5 cm sized round, heterogeneous mass replacing the whole adrenal gland superior to the right kidney was newly detected by chest CT in March 2006 (6.3 years after initial surgery), suggesting a metastatic lesion in the right adrenal gland (). An 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET)/CT scan showed a large hypermetabolic mass (max standardized uptake value, 6.8) with internal necrosis (). The lesion was suspected as a recurrence of intimal sarcoma. Right adrenalectomy was done without preoperative biopsy. The histopathologic diagnosis was metastatic intimal sarcoma. The tumor cells were positive for smooth muscle actin and were negative for inhibin, cytokeratin, chromogranin, and desmin, supporting the above diagnosis.\nDuring follow-up after right adrenalectomy, abdomen-pelvic CT and 18F-FDG PET/CT showed no evidence of recurrences or metastases, including the anastomosis site of the main pulmonary trunk, thyroid bed, and adrenalectomy site. She has been alive and well without any evidence of disease as of May 2012 (12.5 years after initial surgery).
|
[[62.0, 'year']]
|
F
|
{'15670202': 1, '18594450': 1, '18467425': 1, '4051119': 1, '9315827': 1, '25510635': 1, '8665251': 1, '9448014': 1, '17287480': 1, '12392639': 1, '25628857': 1, '7898109': 1, '27709853': 1, '22041929': 1, '9445197': 1, '28848704': 2, '7230827': 1, '19500766': 1, '9028370': 1, '11849252': 1, '16547618': 1, '21440106': 1, '19231448': 1, '31966739': 1, '25309783': 1, '7641022': 1, '24396650': 2}
|
{'5554881-1': 1}
|
163,916 |
3811805-1
| 24,396,652 |
noncomm/PMC003xxxxxx/PMC3811805.xml
|
Two Cases of Methimazole-Induced Insulin Autoimmune Syndrome in Graves' Disease
|
A 52-year-old woman presented at our hospital with heat intolerance, palpitation, and chest discomfort persisting for 2 months. Physical examination revealed thyroid gland enlargement but no exophthalmos. Thyroid function test indicated hyperthyroidism with thyroid stimulating hormone (TSH) <0.05 µIU/mL (normal range, 0.4 to 4.1), free thyroxine (free T4) 5.71 ng/dL (normal range, 0.70 to 1.80), and triiodothyronine (T3) 375 ng/dL (normal range, 87 to 184). The level of thyroid stimulating immunoglobulin was 60.8% (normal range, 0 to 15). A thyroid scan demonstrated an increase of 20-minute thyroid uptake of 99mTc. A diagnosis of Graves' disease was made and the patient was started on methimazole 30 mg/day. Four weeks after beginning methimazole treatment, she suffered general weakness and sweating that disappeared with food intake. The patient visited the emergency room because of confusion, irritability, and inappropriate verbal responses. She had no history of diabetes mellitus or exposure to insulin or oral antidiabetic agents. The patient's younger brother had a medical history of hyperthyroidism; however, there was no family history of diabetes mellitus. The patient's initial serum glucose level was 34 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. Thyroid function study revealed TSH <0.05 µIU/mL, free T4 0.77 ng/dL, and T3 146 ng/dL. Hemoglobin A1c (HbA1c) was 5.8%. The total serum insulin concentration was 119 µIU/mL (normal range, 2 to 25) and serum C-peptide was 14.7 ng/mL (normal range, 0.8 to 4.0). Insulin autoantibody was measured by radioimmunoassay at 84.7% (normal range, 0 to 7). Percent 125I-insulin binding was not measured. A computed tomography (CT) scan revealed a small cyst of the pancreas tail, which had no contrast enhancement. There was no evidence of insulinoma or extrapancreatic neoplasm. The result of 75-g oral glucose tolerance test showed an abnormal increase of total serum insulin levels with delayed hypoglycemia developing after 240 minutes with symptoms of sweating and dizziness (). A diagnosis of methimazole-induced insulin autoimmune syndrome was made based on the high serum concentration of total insulin, fasting hypoglycemia, and the presence of insulin autoantibodies. Methimazole was discontinued, and consumption of six or more small meals throughout the day with low carbohydrate was recommended. Hypoglycemic attacks subsided within 1 week and there were no further hypoglycemic episodes after discharge. Total serum insulin, titer of insulin autoantibody, and level of serum C-peptide decreased gradually after 5 months (). Treatment with 131I 20 mCi was performed to address Graves' disease in the patient.
|
[[52.0, 'year']]
|
F
|
{'3595431': 1, '4407888': 1, '15251622': 1, '8325948': 1, '7578855': 1, '30515677': 1, '10717808': 1, '27933175': 1, '1346661': 1, '856650': 1, '17329919': 1, '30306074': 1, '25309783': 1, '15993720': 1, '8228261': 1, '31883520': 2, '6138590': 1, '30085133': 1, '21831969': 1, '8200300': 1, '24396652': 2}
|
{'3811805-2': 2, '6935495-1': 1, '6935495-2': 1, '6935495-3': 1, '6935495-4': 1}
|
163,917 |
3811805-2
| 24,396,652 |
noncomm/PMC003xxxxxx/PMC3811805.xml
|
Two Cases of Methimazole-Induced Insulin Autoimmune Syndrome in Graves' Disease
|
A 53-year-old woman visited the emergency room of our hospital complaining of headache, palpitation, and chest discomfort. She was diagnosed with Graves' disease at a different hospital 1 month prior to being admitted at our hospital and had been taking both methimazole 40 mg/day and β-blocker since her diagnosis. Prior to visiting our emergency room, she consumed breakfast and was measured with a serum glucose level of 294 mg/dL. Laboratory studies including complete blood cell count with differential, chemistry profile, and electrolytes were all within normal limits. The result of thyroid function tests were TSH <0.01 µIU/mL, free T4 2.74 ng/dL, and T3 184.8 ng/dL. The patient's symptoms were initially attributed to hyperthyroidism due to the lack of abnormal findings on neurologic exam and brain magnetic resonance imaging. However, 6 hours after discharge, the patient revisited our emergency room due to sweating and altered mental state, where it was noted that she had neither a history of diabetes mellitus nor previous exposure to insulin or oral antidiabetic agents. Furthermore, there was no family history of thyroid disease and diabetes mellitus. The patient's initial serum glucose level was 27 mg/dL, HbA1c was 5.8%, serum total insulin was 600 µIU/mL, and serum C-peptide was 15.3 ng/mL. The titer of insulin autoantibody was 84.8%, while detection of both insulin receptor antibody and islet cell antibody were negative. The percent of 125I-insulin binding was not measured. The titers of serum thyroid autoantibodies were high. Specifically, antithyroid peroxidase antibody was 2,876 U/mL (normal range, 0 to 100), antithyroglobulin antibody was 330 IU/mL (normal range, 0 to 115), and TSH receptor antibody was 2.95 IU/L (normal range, <1.22). A CT scan revealed no evidence of insulinoma or extrapancreatic neoplasm. The patient's fasting insulin level was more than 3,000 µIU/mL and C-peptide was 25.9 ng/mL on hospital day 7. A 75-g oral glucose tolerance test showed marked increase of total insulin level and subsequent hypoglycemia developed after 240 minutes (). HLA genotyping was performed by sequence based typing and the result was HLA-DRB1*0406 and *1501. Continuous intravenous glucose injection was needed due to recurrent fasting hypoglycemia. Methimazole-induced insulin autoimmune syndrome was diagnosed, and methimazole was subsequently discontinued. Hypoglycemic episodes disappeared after 1 month, with the patient consuming small frequent meals and a low carbohydrate diet. The concentration of serum total insulin, titer of insulin autoantibody, and serum C-peptide level decreased gradually after 5 months (). Radioactive iodine therapy with 131I 15 mCi was performed to address Graves' disease in the patient.
|
[[53.0, 'year']]
|
F
|
{'3595431': 1, '4407888': 1, '15251622': 1, '8325948': 1, '7578855': 1, '30515677': 1, '10717808': 1, '27933175': 1, '1346661': 1, '856650': 1, '17329919': 1, '30306074': 1, '25309783': 1, '15993720': 1, '8228261': 1, '31883520': 2, '6138590': 1, '30085133': 1, '21831969': 1, '8200300': 1, '24396652': 2}
|
{'3811805-1': 2, '6935495-1': 1, '6935495-2': 1, '6935495-3': 1, '6935495-4': 1}
|
163,918 |
3811850-1
| 24,179,699 |
noncomm/PMC003xxxxxx/PMC3811850.xml
|
Anterior cerebral artery aneurysm associated with multiple intracranial aneurysms and abdominal aorta aneurysm
|
During a routine dissection at Jeju National University Medical School in 2012, multiple aneurysms were observed in the intracranial arteries and abdominal aorta of an 87-year-old female Korean cadaver, whose cause of death was listed as "cholangiocarcinoma." The protocol for the current report did not include any specific issue that required the approval of the ethics committee of our institution, and it conformed to the provisions of the Declaration of Helsinki in 1995.\nGross dissection was performed in the customary fashion. During dissection, an aneurysm was observed in the infrarenal aorta, 19.1 mm superior to its bifurcation into the common iliac arteries. The size of the AAA was 46.5×40.6×36.7 mm where the inferior mesenteric artery arose (). In longitudinal section, atherosclerotic thickening was observed.\nAfter removal of the brain, we found multiple aneurysms in the intracranial arteries (); one aneurysm was located in the A3 segment of the ACA and another at the bifurcation of the MCA. A distal ACA aneurysm was located on the central part of the A3 segment, anterior to the genu of corpus callosum, 18.0 mm distal to the anterior communicating artery. The aneurysm was a small berry-type aneurysm, with a size of 6.8×5.5×3.7 mm. The aneurysm at the bifurcation of the MCA was located 13.5 mm distal to the bifurcation of the internal carotid artery (ICA) into the ACA and MCA. The aneurysm was a small saccular-type aneurysm with a size of 4.3×2.8×3.2 mm.
|
[[87.0, 'year']]
|
F
|
{'18948608': 1, '18797351': 1, '18585678': 1, '18647115': 1, '12511744': 1, '22036120': 1, '17316419': 1, '17273890': 1, '11354403': 1, '21841346': 1, '20053631': 1, '21641282': 1, '15866312': 1, '22700728': 1, '18928355': 1, '3673680': 1, '24179699': 2}
|
{}
|
163,919 |
3811973-1
| 24,175,084 |
noncomm/PMC003xxxxxx/PMC3811973.xml
|
Contrast-induced acute kidney injury following iodine opacification other than by intravascular injection
|
A 57-year-old woman having two stomies due to a long history of intestinal resections was admitted to the intensive care unit (ICU) because of an acute rise in serum creatinine level (from 67 to 134 µmol/L in 24 h) with oliguria and drowsiness. Three days before, she developed fever with C-reactive protein elevation attributed to a digestive bacterial translocation and was treated by Imipenem 500 mg t.i.d without any other change in her current medication. On the same day, looking for a peritoneal fistula, a trans-jejunostomy enteroclysis was performed with 300 mL of Iopamiro 300 (low-osmolar CM; 90 g iodine load), which showed no intestinal leak. Since ICU admission, the patient remained haemodynamically stable and after rehydration a normal diuresis resumed. To note, the urine sediment was normal, in particular without leukocyturia nor eosinophiluria, while the urinary βNAG and lysozyme were markedly increased. Thereafter, the serum creatinine level continued to increase rapidly up to 481 µmol/L on Day 6 after enteroclysis and then slowly returned to baseline within a month ().\nIn the attempt to find the reason for this acute renal failure, it turned out that the radiologist had noticed the presence of CM in the urinary tracts already during the enteroclysis. For this reason, he had performed a native abdominal computed tomography (CT)-scan 1 h later, which confirmed the unexpected presence of CM in both renal pelvis and ureters, without evidence for any peritoneal resorption of CM (). Therefore, although no intravascular-iodinated CM had been administered to this patient, we considered the diagnosis of CI-AKI on the basis of the presence of CM in both urinary tracts associated with a typical clinical evolution. As no leak of CM into the peritoneal space was detected on the CT-scan, we assumed that the rapid absorption of CM occurred through the intestinal mucosa, the permeability of which was apparently increased by the local inflammatory state. Moreover, in our patient, the transmucosal resorption of CM could have been sustained, as suggested by the persistence of CM in the caecum on a native CT-scan made 7 days after the enteroclysis.
|
[[57.0, 'year']]
|
F
|
{'16462667': 1, '5344013': 1, '17449491': 1, '10030741': 1, '12612997': 1, '30291466': 1, '2246887': 1, '3417739': 1, '10622659': 1, '6732387': 1, '25788754': 1, '5784785': 1, '12738023': 1, '7354494': 1, '16723348': 1, '28766491': 2, '20863346': 1, '18333096': 1, '14053348': 1, '21680134': 1, '17544177': 1, '3994451': 1, '3718137': 1, '55590': 1, '24175084': 2}
|
{'5642467-1': 1}
|
163,920 |
3811979-1
| 24,175,086 |
noncomm/PMC003xxxxxx/PMC3811979.xml
|
Medullary nephrocalcinosis in an adult patient with idiopathic infantile hypercalcaemia and a novel CYP24A1 mutation
|
A 29-year-old man was admitted for evaluation of an elevated serum creatinine of 1.40 mg/dL (estimated glomerular filtration rate, eGFR, 70 mL/min/1.73 m2). He suffered from mild hypertension treated with 8 mg of candesartan. Urine analysis revealed microalbuminuria (albumin/creatinine 36 mg/g). A renal sonogram demonstrated medullary nephrocalcinosis (). The patient also suffered from mild nephrogenic diabetes insipidus with isosthenuria and 3 to 4 L of urine per day.\nMedical history revealed that the patient had suffered from IIH, manifesting in his third month of life, when he was admitted for failure to thrive. He was noted to have total serum calcium of 4.2 mmol/L, hypercalciuria and nephrocalcinosis. He had received 800 IU of vitamin D3 supplementation per day at that time. His serum 25(OH)D3 level was seen to be elevated to 123 ng/mL, and vitamin D was stopped. The child was treated with prednisolone and put on a calcium-free formula. Serum calcium normalized quickly. Further development under low calcium alimentation was normal. Total serum calcium levels remained in the upper range of normal or slightly elevated (2.4–2.6 mmol/L), but hypercalciuria (0.35–0.45 g calcium/g creatinine) persisted. Intact PTH levels measured on multiple occasions were always suppressed. The 25(OH)D3 levels were elevated during the first 4 years of life (range 110–609 ng/mL) and then returned to normal. The 1,25(OH)D3 was first determined at 13 years of age and was in the upper range of normal (65 pg/mL). The current results of calcium and vitamin D metabolism are shown in . Bone density determined by DEXA was normal (lumbar spine 1.247 g/cm2, T score 0.2; femoral neck 1.175 g/cm2, T score 0.7).\nSequence analysis of the CYP24A1 gene was performed in the patient. For this purpose, all exons including intron–exon boundaries of the CYP24A1 gene were amplified by the polymerase chain reaction (PCR) according to a previously published protocol (PMID: 22337913). PCR products were directly sequenced using an ABI 3130 DNA Analyser (Applied Biosystems).\nSequencing analysis revealed that the patient was homozygous for three common DNA polymorphisms (rs2296241, rs2762934 and rs6022987) and additionally for a yet undescribed nonsynonymous mutation in exon 4 (c.628T>C), causing tryptophan to be replaced with arginine in codon 210 (W210R) (). In silico analysis of the W210R mutation using the SIFT tool (; PMID: 19561590) and the PolyPhen-2 tool (; PMID: 20354512) consistently showed a probably damaging effect on the protein, reaching highest possible scores of the two algorithms (SIFT score: 0.00; PolyPhen-2 score: 1.000).\nBoth parents and the two siblings of the patient were genotyped for the presence of the W210R variant by sequence analysis of exon 4. All family members carried the heterozygous genotype of mutation c.628T>C (.\nTo assess the frequency of the W210R variant in the local population, 514 DNA samples of patients previously recruited for study purposes at Feldkirch Academic Teaching Hospital (PMID: 19135198) were genotyped for the mutation. Genotyping was carried out with the 5′ nuclease assay on a LightCycler® 480 Real-Time PCR System (F. Hoffmann-La Roche Ltd., Basel, Switzerland) using TaqMan® MGB probes and PCR primers obtained from the Assay-by-design™ service (Applied Biosystems, Forster City, CA, USA). Genotyping was successful in all patients. None of the patients were found to carry the W210R mutation.\nshows laboratory parameters of the patient's parents and his younger brother and sister. No major abnormalities in calcium metabolism were evident. However, the younger brother had a borderline total serum calcium level and elevated 1,25(OH)D3. A renal sonogram of the family members showed no nephrocalcinosis or renal calculi.\nSerum levels of fibroblast growth factor 23 (FGF23) were measured by enzyme-linked immunosorbent assay in all family members (C-terminal FGF23 assay, Immunotopics, San Clemente, CA). Whereas serum levels in the heterozygous family members were normal, the patient's FGF23 was considerably elevated (3- to 4-fold compared with patients with a similar eGFR as measured using the same assay) () []. Consequently, the patient also had moderate renal phosphate wasting with a reduced tubular reabsorption of phosphate and tubular maximum reabsorption of phosphate per litre of GFR ().
|
[[29.0, 'year']]
|
M
|
{'15998839': 1, '27639704': 1, '1606583': 1, '25375986': 1, '24670084': 1, '8844545': 1, '15498883': 1, '12671131': 1, '11698670': 1, '34959915': 1, '22100522': 1, '19961857': 1, '16932902': 1, '22047572': 1, '30591926': 1, '20541252': 1, '3360901': 1, '21675912': 1, '27588937': 1, '20394945': 1, '11019830': 1, '10423037': 1, '21389978': 1, '23001465': 1, '22112808': 1, '34721296': 1, '13333114': 1, '20418485': 1, '33099630': 1, '25618772': 1, '34337279': 1, '13070618': 1, '22337913': 1, '17699549': 1, '24175086': 2}
|
{}
|
163,921 |
3812785-1
| 24,179,557 |
noncomm/PMC003xxxxxx/PMC3812785.xml
|
Case Report: Meningioma with Intra-tumoural Haemorrhage Secondary to Ruptured Distal Anterior Cerebral Artery Aneurysm
|
A 34-year-old male was suffering from a mild headache and had difficulty sleeping for a month prior to his admission to hospital. In addition, he complained of difficulty in focusing his thoughts. Early in the morning of the day he came to the hospital, he said that he woke up with the worst headache of his life. He had no other neurological symptoms, and his past medical history was unremarkable.\nIn the emergency department at the University of Alberta Hospital, the patient was in pain, but he was otherwise haemodynamically stable with a Glasgow Coma Score of 15 and no neurological deficits.\nA computed tomography (CT) scan revealed a rounded mass of 3.3 cm within the intra-hemispheric region, and it was associated with acute haemorrhage, which was predominantly in the right postero-medial frontal area (Fig. ). Therefore, the patient was admitted to the neurosurgery step-down unit for monitoring. A cerebral angiography revealed displaced peri-callosal arteries on both sides with mild opacification of the midline lesion from a distal branch of the left middle meningeal artery. No associated vascular abnormalities were observed (Fig. ).\nBrain magnetic resonance imaging (MRI) with and without contrast revealed an intra-hemispheric falcine enhancing extra-axial mass that measured 3.8 × 3.2 × 3.6 cm. The most likely diagnosis was a meningioma. The mass itself was composed of 2 components. One enhancing component was present in the middle and left portions of the tumour, which was iso-intense to grey matter in all sequences. Along the right lateral margin, there was a nonenhancing component, which was dark on T2-weighted sequences and contained multiple foci of increased T1 signal. This was in line with a haemorrhage (Fig. ).\nDuring his stay in the hospital, the patient’s clinical condition remained stable, and second conventional angiogram was obtained, which revealed no vascular abnormalities that differed from those in the previous study.\nBecause MRI revealed significant swelling around the haemorrhage, a delayed elective surgery was planned. The patient was then discharged home with steroids and anticonvulsants. Four weeks later, a pre-operative cerebral angiogram, which was conducted for the purpose of tumour embolisation, did not reveal any appropriate targets for embolisation; rather, a 3-mm saccular aneurysm was noticed with a left internal artery injection from the distal left pericallosal artery (Fig. ).\nOn the next day, with the patient’s consent, an endovascular embolisation of the aneurysm was performed with N-butyl-2-cyanoacrylate, and no complications were encountered. On the following day, the patient underwent a surgery for resection of the tumour. The craniotomy was performed through a bifrontal incision. The tumour was midline attached to the falx. Normally we would prefer a midline approach from the nondominant side (right side). However, there were two large bridging veins on the right side and a clear corridor on the left. We approached the tumour from the left. The tumour was evident within one centimeter of the cortical surface. There was obvious hemosiderin staining around the tumour posteriorly, however the tumour was easily dissected from the surrounding brain without significant adherence. At the deepest margin of the tumour the pericallosal arteries were embedded within the tumour base. As a result a small rim of tumour was left attached to the preserved pericallosal vessels.\nThe patient was discharged home 3 days after the procedure, and a follow-up cerebral angiogram showed no recurrence of the aneurysm. The final pathology confirmed the diagnosis of a World Health Organization grade-I meningioma with embolisation material within the tumour (Fig. ).
|
[[34.0, 'year']]
|
M
|
{'10541248': 1, '10070475': 1, '32113168': 2, '3728094': 1, '4669242': 1, '19576683': 1, '24179557': 2}
|
{'7044651-1': 1}
|
163,922 |
3812853-1
| 22,993,245 |
noncomm/PMC003xxxxxx/PMC3812853.xml
|
Double-barrel extracranial–intracranial bypass surgery followed by endovascular carotid artery occlusion in a patient with an extracranial giant internal carotid artery aneurysm due to Ehlers–Danlos syndrome
|
A 42-year-old man with EDS type IV was admitted to our department with a rapidly progressive cervical pulsatile and painful swelling on the right side (). Apart from the swelling, a neurological examination also showed right-sided palsy of the hypoglossal nerve. The patient's history indicated that, in 1999, direct revascularization using a vessel graft to treat an extracranial giant aneurysm of the left ICA had failed due to technical problems in performing an adequate anastomosis causing left hemispheric ischemia. Neurological impairment such as right-sided hemiparesis or aphasia was not seen at the current presentation.\nCerebral digital subtraction angiography (DSA) showed a giant aneurysm of the right ICA (C1 segment) measuring 10×7×7 cm, extending from the carotid bifurcation to the base of the skull (). A largely dilated basal artery and left posterior communicating branch indicating compensatory supply to the left hemisphere was also demonstrated. A Doppler-controlled balloon occlusion test of the right ICA revealed a moderate insufficiency of the middle cerebral artery (MCA) territory and additional collateralization of the right hemisphere via the ophthalmic branches. MRI demonstrated ischemic lesions of the left hemisphere as a result of the previous occlusion of the left ICA.\nThe radiological findings were then thoroughly discussed in an interdisciplinary conference including neuroradiological, neurological and neurosurgical colleagues in order to achieve a low-risk and adequate treatment of the growing aneurysm of the right ICA. The agreed strategy consisted of securing right cerebral perfusion via flow redirection through a double-barrel extracranial–intracranial bypass followed by surgical trapping of the aneurysm. The double-barrel bypass was successfully placed from the superficial temporal artery to two M4 cortical branches of the right MCA (). Both branches showed sufficient flow in postoperative angiographic studies. Prior to definite occlusion, a temporary ICA occlusion test was conducted using an eclipse balloon in order to confirm sufficient contrast perfusion of the right hemisphere through the previously placed tandem bypass (). The occlusion test showed good flow through the bypass and additional ophthalmic collateral filling, so we were able to proceed with the permanent elimination of the aneurysm from the circulation. Surgical trapping of the aneurysm failed due to the risk of sacrificing the external carotid artery. A decision was therefore made to occlude the aneurysm by means of endovascular coiling. Two separate sessions were needed to occlude both the distal and proximal segments of the giant aneurysm. The distal segment was successfully occluded with platinum spiral coils (). A stent was then placed in the right external carotid artery to secure its patency and, from there, stent-supported coiling was performed to occlude the proximal segment (). Secure proximal placement of the coils was not possible in a single-catheter technique owing to the high flow turbulence within the aneurysm sac. By using a double-catheter method, two coils could be placed simultaneously directly outside the stent wall facing the proximal segment of the extracranial ICA. Immediately after the procedure the patient had a transient ischemic attack with latent left-sided hemiparesis which regressed within 48 h. Ischemic lesions were excluded in post-procedural non-enhancement CT scans. Minor surgery was later performed to drain the residual hematoma in the aneurysm sac. The bulging skin collapsed instantly, reducing the large visible swelling on the patient's neck. The patient recovered rapidly from the individual procedures without any additional impairment and was discharged in an unaltered clinical/neurological condition.\nFollow-up at 2 months revealed a good clinical result without any deficits with slight recurrence of the swelling on the right side of the neck. CT and CT angiography showed a hypodense non-enhancing filling of the remaining aneurysm sac. Density measurements indicated the filling to be serous fluid which was safely drained via CT-assisted puncture. Again the swelling collapsed immediately, leaving the patient with a good cosmetic result (). The patient died a year later due to a ruptured aneurysm of the splenic artery.
|
[[42.0, 'year']]
|
M
|
{'18212690': 1, '7350266': 1, '7411205': 1, '10753278': 1, '544122': 1, '7811577': 1, '16338669': 1, '501417': 1, '20140961': 1, '3670572': 1, '2352023': 1, '22993245': 2}
|
{}
|
163,923 |
3813457-1
| 24,963,905 |
noncomm/PMC003xxxxxx/PMC3813457.xml
|
Delayed presentation of an aspirated capsule endoscope
|
A 56-year-old gentleman presented with a 2-week history of progressive shortness of breath following a coughing fit whilst having a meal. He is a reformed smoker, with mild chronic airway disease, hypertension, gout and a left-sided cerebrovascular accident (CVA) in 2006 with complete neurological recovery. He had been investigated 6 weeks previously for iron deficiency anaemia with a capsule endoscopy, which was reportedly ‘lost’ during the procedure. An esophagogastroscopy performed immediately failed to locate the capsule. The patient refused any further investigations to locate the capsule.\nChest X-ray (Fig. ) and computed tomography (CT) scan (Fig. ) revealed a foreign body in the right bronchus intermedius with collapse and consolidation of the distal bronchial tree. The gentleman was transferred to the cardiothoracic unit. An adult Negus rigid bronchoscope introduced under general anaesthesia revealed a metallic foreign body with smooth rounded contours wedged in the bronchus intermedius. This was removed using a Wolfe lighted grabber. The foreign body was a capsule endoscope (Given Imaging Limited, Israel) (Fig. ).\nThe patient received post-operative antibiotics and intensive physiotherapy. Chest X-ray prior to discharge revealed complete resolution of the atelectasis and consolidation. The patient continues to do well on follow-up. On retrospective questioning the patient denied any problems in swallowing the capsule endoscope.
|
[[56.0, 'year']]
|
M
|
{'18036432': 1, '18273788': 1, '19246497': 1, '12612537': 1, '12929075': 1, '17397783': 1, '15557975': 1, '24963905': 2}
|
{}
|
163,924 |
3813458-1
| 24,964,454 |
noncomm/PMC003xxxxxx/PMC3813458.xml
|
Orthotopic neobladder perforation: an unusual presentation of small bowel obstruction
|
A 71-year-old male had undergone a radical cystectomy and orthotopic neobladder formation 5 years previously, and was self-catheterising. He presented to the emergency department with a 24-h history of abdominal pain and distension. There was associated nausea and a reported decrease in urine production. Examination revealed a distended abdomen with some lower abdominal tenderness but no evidence of peritonism. Bowel sounds were absent. Relevant blood analysis revealed creatinine 354 µmol/l, WCC 15.9 × 109/l and CRP > 380. An abdominal X-ray revealed dilated small bowel loops, and a CT showed moderate volume ascites and distal small bowel obstruction with the transition being a thickened small bowel loop lying next to the neobladder (Fig. ).\nConservative management was instituted (catheter, nasogastric tube) for presumed adhesional obstruction, and the patient was admitted under the care of the general surgical team. The urology team were contacted in light of the CT findings, and as the patient had not improved over a 24-h period, a decision was made to proceed with an exploratory laparotomy.\nAt surgery, there was a large amount of turbid urinary ascites, and the offending loop of small bowel seen on the CT was found to be stuck to a 5 mm perforation in the neobladder, at the junction of the afferent limb and the pouch. This was oversewn with an omental patch. The patient made a good recovery, creatinine normalized to 95 µmol/l, bowel function returned to normal and a cystogram at 10 days did not show any evidence of a leak.
|
[[71.0, 'year']]
|
M
|
{'12444295': 1, '11956437': 1, '17658158': 1, '19076133': 1, '12050514': 1, '11257680': 1, '24964454': 2}
|
{}
|
163,925 |
3813460-1
| 24,964,448 |
noncomm/PMC003xxxxxx/PMC3813460.xml
|
Atypical mycobacterial infection mimicking metastatic cholangiocarcinoma
|
A previously fit and healthy 45-year-old Caucasian female presented to our unit with history of jaundice, mild upper abdominal discomfort and weight loss. She had undergone a laparoscopic cholecystectomy 5 years ago followed by an endoscopic retrograde cholangiopancreatography (ERCP) to extract a common bile duct (CBD) calculus. There was no history of overseas travel or contact with patients with tuberculosis.\nThe liver function tests revealed an obstructive picture. Bilirubin level was 86 µmol/l (normal 2–24 µmol/l). Gamma glutamyl transferase (GGT) and alkaline phosphatase were 347 and 340 U/l, respectively. In view of prior history of choledocolithiasis, an ERCP was undertaken. An eccentric stricture at the level of the junction of cystic duct and CBD was seen along with a dilatation of proximal the bile duct. There were no ductal calculi. A plastic stent was inserted to relieve the jaundice (Fig. ). These findings raised the suspicion of a malignant process, and a computerized tomography (CT) scan of the chest, abdomen and pelvis was consequently performed.\nThe CT scan revealed multiple hypodense liver lesions predominantly in the right lobe of the liver (Segment 6 and 8) highly suspicious of metastatic deposits (Fig. ). A preliminary diagnosis of metastatic cholangiocarcinoma was made on this basis.\nThe case was discussed in the multidisciplinary meeting and decision was taken to attempt a percutaneous biopsy of the liver lesions to confirm the diagnosis and plan for palliative chemotherapy.\nAn ultrasound-guided core biopsy was attempted, but failed due to technical reasons. A CT-guided core biopsy of Segment 6 lesion was successful, but an interval reduction in the size of the liver lesions was noted. A magnetic resonance cholangiopancreatography (MRCP) to reassess the liver and biliary tree was therefore planned. MRCP revealed a persistent stricture at the cystic duct CBD junction (Fig. ). The histology from the core biopsies of the liver revealed a granulomatous process with Langhans giant cells (Fig. ). The pathologists opined that although rare, mycobacterial involvement should be considered as a differential diagnosis. This coupled with the spontaneous reduction in the size of the liver lesions led to a consensus opinion for a surgical exploration to resect the biliary stricture and re-biopsy the liver lesions.\nAt surgery multiple liver lesions were evident and two of these were biopsied. A fibrotic stricture was evident in the mid-portion of the CBD with proximal dilatation.\nSurgical resection of the stricture was undertaken with a Roux-en-Y hepaticojejunostomy. Since the possibility of Mycobacterial granulomas had been raised, a sample of tissue from the resected specimen was sent for mycobacterial culture.\nLiver biopsies confirmed granulomatous inflammation. Histology of the resected biliary stricture showed granulomas causing wall thickening and structuring of the bile duct. The mucosa was uninvolved (Fig. ). No malignancy was evident. Tissue sent for culture grew Mycobacterium abcessus sensitive only to Amikacin. There was no suggestion of immunodeficiency and HIV testing was negative. The patient was commenced on therapy and is currently progressing very well.
|
[[45.0, 'year']]
|
F
|
{'16725007': 1, '12481730': 1, '22093291': 1, '21055685': 1, '18312287': 1, '21198529': 1, '22010508': 1, '21378550': 1, '18603675': 1, '24964448': 2}
|
{}
|
163,926 |
3813461-1
| 24,964,467 |
noncomm/PMC003xxxxxx/PMC3813461.xml
|
Young male survivor of a spontaneous left main coronary artery dissection treated with surgery
|
A 31-year-old male, airline pilot, with no clinical history or cardiovascular risk factors, was admitted to the emergency room with 12 h history of retrosternal chest pain radiating to the jaw and upper extremities, during a trans-Atlantic flight, which did not improve with analgesia. Because of persistent pain, he came to our hospital. Upon arrival to the emergency room, his vital signs were stable and he had a normal physical examination but complained of precordial pain. The cardiac enzymes were elevated and the EKG detected S-T changes consistent with MI (Fig. ). A multidetector CT coronary angiography was performed showing left main trunk dissection with 50% stenosis (Fig. ).\nThe patient underwent emergent coronary revascularization with saphenous vein grafts to the first obtuse marginal and the left anterior descending artery (LAD). His postoperative course was uneventful and the patient was discharged home 7 days later. Control CT coronary angiography was performed 2 months later revealing patent aorto-coronary grafts (Fig. ).
|
[[31.0, 'year']]
|
M
|
{'3300585': 1, '20776438': 1, '12215191': 1, '17992314': 1, '20448134': 1, '19697798': 1, '19156232': 1, '24964467': 2}
|
{}
|
163,927 |
3813486-1
| 24,964,457 |
noncomm/PMC003xxxxxx/PMC3813486.xml
|
Atraumatic splenic rupture secondary to metastatic non-small-cell lung cancer
|
A 61-year-old male presented with a 2-week history of worsening posterior neck and bilateral shoulder pain, and a several hour history of severe, left-sided abdominal tenderness. The patient reported no recent history of trauma. The patient had been diagnosed with poorly differentiated, left lung adenocarcinoma 5 months prior; he was status-post left upper lobectomy. PET scan, at that time (Fig. ), showed no evidence of metastatic disease and the pathologic staging was determined to be T2aN0M0 (Stage 1B).\nIn the emergency department on current presentation, the patient was hypotensive with a blood pressure of 76/40. Physical examination revealed a soft, distended abdomen that was tender in the left upper quadrant. The patient demonstrated no rebound tenderness or guarding. CT scan of the chest, abdomen and pelvis revealed hemoperitoneum and a possible splenic laceration (Fig. ). Laboratory work showed hemoglobin of 10.9 g/dl and a hematocrit of 30.4%. The patient was optimized for emergent exploratory laparotomy.\nSurgery revealed gross, metastatic lesions in the spleen and mesentery. A splenectomy with en bloc resection of the involved mesentery was preformed. The resected specimens all revealed metastatic, poorly differentiated non-small-cell carcinoma; consistent on immunoperoxide staining with the previously known primary lung cancer diagnosed and treated 4 months prior.\nFurther workup on this patient revealed a final diagnosis of stage IV non-small-cell lung cancer with metastases to the liver, mesentery, spleen and cervical spine. The patient was started on radiation therapy, but eventually refused more treatment due to the pain he was experiencing. The patient died <1 month later.
|
[[61.0, 'year']]
|
M
|
{'17550328': 1, '11230502': 1, '19787754': 1, '22284605': 2, '21899758': 2, '28784910': 1, '10747308': 1, '24964457': 2}
|
{'3178521-1': 1, '3296588-1': 1}
|
163,928 |
3813488-1
| 24,964,453 |
noncomm/PMC003xxxxxx/PMC3813488.xml
|
Aggressive osseous commitment result by keratocyst odontogenic tumour: case report, radiographic and clinical standpoints
|
A 40-year-old male Caucasian patient coming to the Department of Biosciences and Diagnosis of Sao Paulo State University–UNESP to evaluate an increase of volume in a left side of the face and neck with pain, dysphonia and dysphagia symptoms. The extra oral clinical exam showed an extensive oedema in region of mandible, relatively hard to palpation, with no committal of the skin and no lymphadenopathy. The intra oral examination showed a large mass in the vestibular region that extended to the middle of the mandible until the ascendant ramous, tender to palpation, oedema and mobility of the present teeth. A punch with a needle in a hypodermic syringe showed a viscous liquid with yellowish colour and high internal pressure. Immediately after the decompression, the skin diminished considerably.\nThree-dimensional images allowed for the visualization of the lesion in relation to relevant anatomical structures providing depiction of bone destruction in the body of the mandible. Preoperative 3D CT reconstruction indicated destruction of the buccal cortex of the mandible (left side) caused by the lesion and projection of osseous spiculae (Fig. A and B).\nThe panoramic radiography shows a large radiolucent and well-defined lesion with a radiopaque corticates margin involving the left mandibular premolar and molar (Fig. ).\nThe clinical, radiolological and tomography signs (Fig. ) evoke the hypothesis of a KCOT or ameloblastoma. An incisional biopsy and cytological smears were done and the results showed thin epithelial layer, composed of from 8 to 10 cell. The basal layer shows palisade organized cells with a uniform nucleus. In the direction of the cyst lumen, there is parakeratosis with a focal zone created of orthokeratins. The palisading appearance of the basal cells was evident and confirms the diagnosis of KCOT.\nThe patient was sent to a Maxillofacial Surgery Department and after the clinical and laboratorial routine examinations, a vigorous curettage washed with Carnoy solution as well as an ostectomy and removal of all the osseous spiculae before the marsupialization was done. A resin obturator was made and was fixed in the mucosa by suture in order to not allow the closure of the mucosa and to permit the patient to clean the lumen with 9% NaCl solution in a hypodermic syringe through the marsupialization aperture and return each 3 months to follow up and makes new radiographic examinations. After 6 months, the radiographic examinations show an initial osseous organization and the clinical appearance have no signal of infection or recurrence.
|
[[40.0, 'year']]
|
M
|
{'28388515': 1, '12167890': 1, '9690244': 1, '264648': 1, '11250631': 1, '1451083': 1, '2579223': 1, '12892445': 1, '2187964': 1, '11429726': 1, '24964453': 2}
|
{}
|
163,929 |
3813490-1
| 24,963,900 |
noncomm/PMC003xxxxxx/PMC3813490.xml
|
A unique presentation, and management, of acute urinary retention in a young boy with underlying vesicoureteral reflux
|
A 7-year-old boy who had no relevant past medical history (UTIs or other) presented with acute urinary retention. He was systemically well but had mild suprapubic discomfort and a palpable bladder. Examination of the penile shaft revealed a palpable hard swelling. The urethral meatus was patent. Following failure of conservative management of urinary retention (placing the boy in a warm-bath, adequate analgesia), a cysto-urethroscopy was performed under general anaesthetic. Due to lack of paediatric instruments on site, a 6.6-Fr adult ureteroscope was used. This revealed an obstructing urethral calculus impacted in the navicular fossa. The stone was fragmented using a HoYag laser and extracted. Cystoscopy with the same instrument then revealed multiple bladder calculi with a patulous right ureteric orifice. These stones were washed out and the patient was catheterized (6-Fr urethral catheter). Serum calcium, urate and renal function were normal. Post-operative ultrasound revealed a small, scarred right kidney and large (hypertrophied) left kidney. Micturating cystourethrogram demonstrated grade 1 and 2 VUR in the right and left ureters, respectively, and an opacification in the upper right ureter suspicious of a calculus. CT KUB confirmed a 4 cm (cranio-caudal) by 0.8cm (transverse) right ureteric calculus (Fig. ). DMSA scan revealed 4% (right) split renal function. The patient subsequently underwent a right laparoscopic nephroureterectomy (Fig. ).
|
[[7.0, 'year']]
|
M
|
{'16716788': 1, '22698573': 1, '9112544': 1, '1433584': 1, '21369387': 1, '22264440': 1, '21814729': 1, '24963900': 2}
|
{}
|
163,930 |
3813507-1
| 24,964,474 |
noncomm/PMC003xxxxxx/PMC3813507.xml
|
Spontaneous idiopathic recurrent pneumoperitoneum
|
In 2011, a 46-year-old man presented with an acute abdomen. Patient had a 3 day history of abdominal pain with dyspepsia, initially epigastric with pain radiating to his shoulder. He had no associated symptoms of nausea, vomiting or change in bowel habit. There was no history of peptic ulcer disease, inflammatory bowel disease, diverticular disease or malignancy. His pain was refractory to standard analgesics and exacerbated by movement and palpation of the abdomen. There was no past medical or family history of note, and the patient had never experienced these symptoms before. Routine observations were normal, except for tachycardia. On examination, there were no peripheral stigmata of inflammatory bowel disease, abdomen was diffusely tender and tympanic, but soft with normal bowel sounds. Blood tests showed no significant abnormalities, and C-reactive protein (CRP) levels were not measured. Plain abdominal and erect chest radiographs showed pneumoperitoneum (Fig. ) with Rigler's sign present around small bowel loops lower in the abdomen (Fig. ).\nHe was taken for urgent laparotomy to evacuate the free gas and aid diagnosis. The bowel was extensively examined and no evidence of perforation was found. The abdominal wall was closed and he returned to the ward. Subsequent X-rays showed that the pneumoperitoneum had resolved. Post-operatively his CRP level was 226 and he went into ileus requiring nasogastric tube placement (Fig. ). With recurrence of normal bowel activity and with settling of his symptoms, he was discharged.\nOver a year later, the same gentlemen presented to the surgical admissions unit once again with a history of acute abdominal pain. The duration and nature of symptoms were very similar to his previous admission. He again underwent plain film abdomen and erect chest radiographs that showed a large volume of free air under the diaphragm (Figs. and ).\nThe patient was apyrexial and cardiovascularly stable, other than his acute abdominal pain, he was healthy. We managed his pain with analgesia, stepping up as required. A water soluble contrast study was arranged, this demonstrated no leak or diverticular in the oesophagus, stomach or duodenum.\nHe underwent a computed tomography (CT) scan of his chest/abdomen and pelvis, and this showed some upper abdominal fluid, some small sigmoid diverticulae but nil else. The scan was discussed at a regional radiology meeting to look for any diaphragmatic defects or any other cause of pneumoperitoneum, but none were found.\nThis man demonstrated clear pneumoperitoneum, he was extensively investigated; all blood tests were normal except for a raised postoperative CRP, his laparotomy showed no evidence of perforation, the contrast study showed no leak and a CT scan showed mild sigmoid diverticulae only. In light of all this, we reached a diagnosis of ‘Recurrent spontaneous idiopathic pneumoperitoneum’.
|
[[46.0, 'year']]
|
M
|
{'2059801': 1, '26366365': 2, '28674585': 1, '1863299': 1, '9373590': 1, '31499325': 2, '27229749': 1, '27058151': 1, '21352588': 2, '25603306': 1, '24964474': 2}
|
{'6734534-1': 1, '4560205-1': 1, '3052194-1': 1}
|
163,931 |
3813509-1
| 24,964,444 |
noncomm/PMC003xxxxxx/PMC3813509.xml
|
Cortical blindness as a rare presentation of cerebral venous thrombosis
|
An 18-year-old female with a three-week history of headaches presented with an acute onset of blindness in both eyes after her afternoon nap. Physical examination demonstrated normal pupils and funduscopic exam, but without light perception in either eye. Cranial nerve examinations were otherwise unremarkable. Speech was intact with no naming or repetition deficits. Although alert, she was mildly confused. No isolated motor or sensory deficits were identified in the extremities. Deep tendon reflexes were 3+ in the upper extremities and 4+ in the lower extremities. No ankle clonus was noted, and plantar reflexes were equivocal.\nCranial computed tomography (CT) demonstrated subtle hypodensity mainly in the left occipital lobe, with a characteristic empty delta sign (Fig. ). Computed tomography angiography demonstrated normal filling of the posterior cerebral arteries (PCA). Cranial magnetic resonance imaging (MRI) evaluations demonstrated bilateral ischemic changes involving the occipital and parietal lobes, more extensively on the left (Fig. ). Magnetic resonance venography (MRV) demonstrated complete occlusion of the left transverse and sigmoid sinuses, as well as near occlusion of the posterior superior sagittal sinus (Fig. C).\nThe patient was treated emergently with endovascular mechanical thrombolysis with technical success (Fig. A and B), followed by systemic anticoagulation therapy. Post-intervention MRV demonstrated persistent recanalization of the left transverse and sigmoid sinuses, along with much improved flow in the posterior superior sagittal sinus (Fig. D).\nShe was subsequently diagnosed with mixed connective tissue disease. Clinically, she recovered the left visual field but continued to have a dense right homonymous hemianopsia at discharge. She returned to her home state and was unfortunately lost to further follow-up.
|
[[18.0, 'year']]
|
F
|
{'28904465': 2, '4827505': 1, '20538479': 1, '15644627': 1, '29441008': 1, '20103505': 1, '7196529': 1, '24964444': 2}
|
{'5586128-1': 1, '5586128-2': 1, '5586128-3': 1, '5586128-4': 1, '5586128-5': 1}
|
163,932 |
3813510-1
| 24,964,461 |
noncomm/PMC003xxxxxx/PMC3813510.xml
|
Abdominal wall haematoma in the obese: a dangerous phenomenon
|
A 59-year-old obese female was admitted to the hospital with fever on the background of poorly controlled Type 2 diabetes (Hba1c 9.5%). The patient's background included ischaemic heart disease, chronic kidney disease, peripheral vascular disease and a right-side, below-knee amputation. On examination, the patient's weight was 125 kg, height 154 cm and body mass index was 53. A diabetic foot ulcer was identified at the base of the left heel.\nTwo weeks later, the patient remained hospitalized for the management of an infected diabetic foot ulcer and awoke one morning with acute abdominal pain and shortness of breath. The patient was haemodynamically compromised with a pulse rate of 120 and blood pressure 90/60 lying. The haemoglobin fell overnight from 126 to 90 g/l and a few hours later there was a further fall to 79 g/l. The medical emergency team were called. Platelet count was 242, international normalized ratio (INR) 1.0, activated partial thromboplastin time (APTT) 33 and anti-factor Xa level 0.41 in keeping with prophylactic clexane administration. A CT scan was performed, which demonstrated a large abdominal wall haematoma (see Fig. ).
|
[[59.0, 'year']]
|
F
|
{'27738545': 2, '18770005': 1, '19358089': 1, '15795543': 1, '21848819': 1, '8602241': 1, '29764885': 1, '19562421': 1, '21994960': 1, '10966044': 1, '18295690': 1, '20591405': 1, '24964461': 2}
|
{'5050346-1': 1}
|
163,933 |
3813514-1
| 24,964,472 |
noncomm/PMC003xxxxxx/PMC3813514.xml
|
Popliteal schwannoma mimicking baker cyst: an unusual case
|
Fifty-eight-year-old man presented to the outpatient clinic of orthopaedics department with the complaints of slowly growing mass on his right popliteal region and mild pain and intermittent paresthesia of right leg and right foot. The patient emphasized that the mass existed for 2 years but has grown in the last 6 months. On physical examination, 4 × 2 cm mobile, solid mass was palpable at the posterior of the knee. There was no erythema, warmth or ulceration and Tinel's sign was positive. Sensory and motor examinations of lower extremity were normal. Ultrasound imaging showed that the mass was solid and separate from the adjacent muscles and tendons. MRI showed well-defined solid, heterogenous, dense mass originating from the tibial nerve (Fig. ). Surgical exploration and excisional biopsy was performed. At prone position with longitudinal incision, popliteal region was explorated and tumoural mass originating from tibial nerve was dissected. Sheath of the nerve was incised longitudinally to minimize damage to the nerve fascicles and the mass was resected in en-bloc form by sharp dissection using the microscope with no complication. The patient was discharged at the post-op third day. At the third week of the operation, the patient was free of all complaints. Histopathological examination of the mass revealed hypocellular Antoni B and spindle-shaped Schwann cells containing Antoni A areas with nuclear palisading. Also immunohistochemical staining (S100+) confirmed the diagnosis of schwannoma.
|
[[58.0, 'year']]
|
M
|
{'17613510': 1, '34169007': 2, '15275682': 1, '16185011': 1, '28217572': 1, '14665342': 1, '24964472': 2}
|
{'8046459-1': 1}
|
163,934 |
3813551-1
| 24,964,469 |
noncomm/PMC003xxxxxx/PMC3813551.xml
|
Obstructive jaundice: a rare complication of laparoscopic greater curvature plication
|
A 24-year-old female, who had undergone laparoscopic greater curvature plication (LGCP) 6 months earlier, presented to the emergency room with 1 day history of severe epigastric pain, associated with nausea. She also complained of yellow discoloration of skin and dark urine.\nOn examination, she was jaundiced. Vital signs were as follows: temperature 38°C, heart rate 120 bpm, blood pressure 140/87. Abdominal examination revealed marked tenderness at the epigastric and peri-umbilical areas, with guarding. White blood cells count was 12.8 × 109/l and haemoglobin count was 109 g/l. Renal profile was within normal. Total bilirubin was elevated at 74.1 mmol/l, and the reminder of liver function test was within normal.\nAn ultrasound of abdomen showed distended gallbladder with no calculi, dilated CBD and mild intra-hepatic biliary radicles dilatation. Stomach and duodenum were shown to be grossly dilated. The CT scan of the abdomen showed gastric outlet obstruction with an abnormal position of gastro-duodenal junction. Gastric mucosal prolapsed with mass effect on duodenum (and ampulla of Vater) and secondary dilatation of the biliary and pancreatic ducts.\nUpper GI endoscopy showed the status post gastric plication with herniation of gastric fold into the duodenum. An attempt was made to manipulate the fold but was not successful (Fig. ).\nThe patient underwent exploratory laparotomy, and anterior gastrotomy. The mucosal fold was delivered relieving the obstruction. The redundant mucosa was transacted by a linear cutter stapler (Fig. ) and the gastrotomy closed primarily.\nThe post-operative course was unremarkable, with gradual normalization of total bilirubin.
|
[[24.0, 'year']]
|
F
|
{'18158812': 1, '22960951': 1, '21144804': 1, '21898042': 1, '21621164': 1, '22913751': 1, '33215360': 1, '12448398': 1, '7235951': 1, '21295846': 1, '22811900': 1, '20678969': 1, '24964469': 2}
|
{}
|
163,935 |
3813552-1
| 24,964,441 |
noncomm/PMC003xxxxxx/PMC3813552.xml
|
Intraluminal migration of retained surgical sponge as a cause of intestinal obstruction
|
29-year-old woman was referred by her gynecologist with a history of diffuse colicky abdominal pain, nausea, repeated vomiting, constipation and progressive abdominal distention for 7 days prior to hospitalization. She had undergone an emergency cesarean section 9 months previously at a private hospital and since that time she had been complaining of recurrent attacks of nonspecific abdominal pain and occasional episodes of vomiting especially after heavy meals from which she had lost 10 kg since delivery. The patient had attended emergency departments at different institutions with similar complaints and had been discharged home after each occassion, but her symptoms passed undiagnosed. Five days prior to admission, abdominal roentography was done at an emergency department for her abdominal complaint, which showed radio-opaque density in the pelvis (Fig. ), but it was mistakenly overlooked and she was discharged home with a diagnosis of nonspecific abdominal pain.\nUpon admission, she was afebrile, vitally stable, and her abdomen was distended and tympanic. Bowel sounds were increased in frequency and pitch. Digital rectal examination showed normal-colored stool. Laboratory investigations showed a white blood cell count of 10 700 cells/ml and a sodium level of 123 mmol/l, while other biochemical parameters were within normal limits. Abdominal roentography revealed dilated small intestinal loops with a finding of a radio-opaque density in the abdomen (Fig. ). A diagnosis of small intestinal obstruction most likely caused by retained surgical sponge was made. On abdominal exploration, the small intestine was dilated down to the ileum with an intraluminal mobile mass felt in the distal ileum (Fig. ). Before proceeding for mass removal, at around 80 cm from the duodenojejunal junction, there were two adjacent segments of the jejunum adherent to each other and both were adherent to the peritoneal wall by fibrous adhesions. Consequently, adhenolysis, enterotomy and removal of the mass, which was manually pushed there (Fig. ), followed by resection and anastomosis of the compromised jejunal segment, were achieved. The foreign body was found to be retained surgical sponge (Fig. ). However, apart from the isolated area of adhesion, exploration of the rest of the abdominal cavity did not show any lesions in the peritoneal cavity or perforation or fistula or pelvic collection. The authors concluded that the transluminal migration of the sponge most likely occurred from that adherent part of the jejunum. The postoperative period was uneventful and the patient was discharged on the seventh day of her hospitalization in good condition.
|
[[29.0, 'year']]
|
F
|
{'31435093': 1, '19447736': 1, '20616421': 2, '8855619': 1, '12529464': 1, '16097075': 1, '23070411': 1, '18559122': 1, '18589366': 1, '11409471': 1, '18656641': 1, '24964441': 2}
|
{'3003212-1': 1}
|
163,936 |
3813553-1
| 24,964,466 |
noncomm/PMC003xxxxxx/PMC3813553.xml
|
Management of a complex recurrent perineal hernia
|
A 79-year-old gentleman who initially underwent a laparoscopic assisted extralevator abdomino-perineal excision (ELAPE) of the rectum for extensive circumferential low rectal cancer after neo-adjuvant long course chemoradiotherapy developed a symptomatic perineal hernia. Initial closure of the perineal wound was performed using a double layer of interrupted mattress sutures with a 2/0 absorbable braided suture. The patient's only co-morbidity was intermittent asthma, for which he was prescribed a Salbutamol inhaler.\nGiven the nature of the disease, it was felt that he would benefit from adjuvant chemotherapy. Subsequent radiological surveillance did not show any evidence of recurrence and CEA levels remained low. However, magnetic resonance imaging (MRI) carried out at 19 months demonstrated that the small bowel had herniated through the levator sling and the patient had started to experience severe discomfort in the perineal region.\nRepair of the defect was carried out in conjunction with the Plastic surgery team, using a pedicled gracilis flap. Again, despite an uneventful recovery, 5 months later the patient experienced lower abdominal pain and nausea and noted a distinct swelling of his left upper thigh.\nA repeat MRI confirmed a further recurrence of the perineal hernia in the form of uncompromised bowel, which extended beneath the gracilis flap, which then continued into the adductor compartment of the left thigh (Fig. a and b).\nGiven the recurrent nature of the hernia, a rectus flap repair was performed and after 15 months he remains hernia free.
|
[[79.0, 'year']]
|
M
|
{'28508281': 1, '22308975': 1, '16361623': 1, '17587090': 1, '22006494': 1, '16946992': 1, '21116669': 1, '20186891': 1, '9269813': 1, '21660417': 1, '22762519': 1, '24964466': 2}
|
{}
|
163,937 |
3813558-1
| 24,964,439 |
noncomm/PMC003xxxxxx/PMC3813558.xml
|
Clavicular osteomyelitis: a rare presentation of extra pulmonary tuberculosis
|
A 35-year-old male presented to us with ulcerative lesion over the right shoulder region for 2 years. The lesion was gradually progressive, which later developed a foul-smelling discharge. For this complain, he visited various physicians and was prescribed various antibiotics but there was no relief of complain. There was no history of trauma, cough, pain chest, dyspnoea or fever. Past history was insignificant. There was no history of TB and no one in the family had a history of TB.\nClinical examination revealed an ulcerative lesion 3 × 2.5 × 2.5 cm in the right clavicle at the junction of medial two-third and lateral one-third of the clavicle, with irregular margins, firm base and foul-smelling discharge. Bone was seen exposed with sequestrum present (Fig. ). There was no evidence of cervical or axillary lymphadenopathy and the lung fields were essentially clear. Routine investigations showed moderate hypochromic microcytic anaemia, haemoglobin 9 g/dl, total leukocyte count of 7900 with polymorphs 42%, lymphocytes 54% and eosinophil 4%. Renal and hepatic panels were within normal limit. ESR was 35 mm. The gram staining of the discharge from the ulcer revealed gram-positive cocci, and the Ziehl Nielsen staining for acid-fast bacilli was negative. Culture of the discharge revealed growth of Staphylococcus aureus. ELISA IgG/IgM for TB was negative. HIV-I and II were negative. Chest X-ray was grossly normal (Fig. ). Sequestrectomy was done and the bone along with the excised tissue was sent for biopsy. Histopathology showed it to be either foreign body granuloma or rare possibility of tubercular pathology.\nPatient put on Category I ATT. Patient responded to treatment. The ulcer over shoulder healed in 6 weeks (Fig. ) with formation of granulation tissue. Patient completed full course of ATT and is doing well on regular follow-ups.
|
[[35.0, 'year']]
|
M
|
{'3721650': 1, '33575360': 1, '24960138': 1, '27299003': 2, '26768706': 1, '28630838': 2, '11026712': 1, '12437243': 1, '8672048': 1, '10815746': 1, '34141650': 1, '19398810': 1, '24964439': 2}
|
{'5458696-1': 1, '4719272-1': 1}
|
163,938 |
3813587-1
| 24,964,447 |
noncomm/PMC003xxxxxx/PMC3813587.xml
|
Penetration of a divided cystoperitoneal shunt catheter into the transverse colon inducing acute mastitis
|
The patient is a 56-year-old woman who underwent a surgical treatment of a lateral ventricle meningioma at the age of 29. A month later, she underwent CP shunt placement for cyst formation after resection. The postoperative course was uneventful and she was well without shunt-related problems for 26 years. She developed a brain abscess related to the shunt catheter at the age of 55. A surgical removal of the catheter was attempted, but was not technically possible, and only the segment from the clavicle to the breast was removed with ligation of the two remaining ends. The two disconnected catheter segments remained in situ and were not retrieved. A year later, she was taken to a local hospital with continuous right-breast pain. The diagnosis of acute mastitis was made and she was referred to our institution for further examination. On presentation, her right breast was swollen with erythema (Fig. ). There was no abdominal pain and change in bowel habits. Funduscopic evaluation was normal with no signs of increased intracranial pressure. Her temperature was 36.7°C, and laboratory tests revealed a decreased platelet count of 103 000/μl, elevated AST of 97 U/l, ALT of 72 U/l and C-reactive protein level of 1.4 mg/dl. The breast abscess was drained under local anesthesia. Cultures taken from the abscess showed enteric organisms including Enterococcus avium, Klebsiella oxytoca and Bacillus. Abdominal CT showed that the shunt catheter was in the splenic flexure of the transverse colon with no other abnormalities (Fig. ). Colonoscopy was performed to survey the colon and the shunt catheter was found inside the lumen at the splenic flexure (Fig. ). Acute mastitis caused by enteric organisms which had migrated through the shunt catheter after penetration into the transverse colon was the presumptive diagnosis, and the catheter removed under general anesthesia. The breast to the abdomen segment of the catheter was exteriorized through the right-anterior chest wall without laparotomy. The postoperative course was uneventful. She was transferred to local hospital 15 days later.
|
[[56.0, 'year']]
|
F
|
{'22882605': 1, '11165622': 1, '3941987': 1, '12838246': 1, '17387494': 1, '22026307': 1, '24964447': 2}
|
{}
|
163,939 |
3813589-1
| 24,963,903 |
noncomm/PMC003xxxxxx/PMC3813589.xml
|
Surgical options for the retrieval of a migrated intrauterine contraceptive device
|
A 27-year-old woman with a previous history of two uneventful vaginal deliveries opted for an IUCD (copper coil) as form of contraception. The coil was fitted easily by an experienced family planning physician. During a routine check 6 weeks later the threads of the coil were not visible on speculum examination. An abdominal X-ray confirmed the presence of the coil in the pelvis. To further specify its location, transvaginal ultrasound scan was performed, which showed an IUCD perforating through the uterine serosa. The patient reported no abdominal pain or irregular vaginal bleeding. After a consultation with the gynaecologist she agreed to proceed for the retrieval of the coil by either hysteroscopy or laparoscopy.\nDuring the hysteroscopy 4 weeks later there was no evidence of an IUCD into the uterine cavity and no evidence of a perforation site in the uterus (Fig. ). A laparoscopy followed, locating the coil threads deep in the Pouch of Douglas, with the IUCD perforating through the sigmoid colon into the lumen (Fig. ). The IUCD was retrieved laparoscopically and the defect in the sigmoid colon was repaired by stapling the tear (Fig. ).\nThe patient made a non-eventful postoperative recovery and was discharged after 72 h of observation.
|
[[27.0, 'year']]
|
F
|
{'20716271': 1, '21973139': 1, '16448954': 1, '21333209': 1, '18402749': 1, '28572893': 2, '24963903': 2}
|
{'5451451-1': 1}
|
163,940 |
3813590-1
| 24,963,907 |
noncomm/PMC003xxxxxx/PMC3813590.xml
|
A novel approach: chest wall cyst excised by MIS
|
A 62-year-old Caucasian male presented with swelling and fullness in the left posterior chest. Mild discomfort of the chest wall had worsened over the preceding 6 months. Pain was associated with sitting or leaning against a wall. His range of motion was normal, and he performed daily activities well. Physical examination revealed a morbidly obese white male with a non-tender fluctuant mass on the left side of the upper back. It extended above and below the left scapula. The right side was without abnormality. There were no surgical scars in the thoracic region. The fluctuant mass was the size of a deflated football. An upper midline scar of the neck was noted. The past surgical history included previous cervical spine surgery. The patient had two motor vehicle accidents that caused a lower right-sided lumbar injury. His past medical history was significant for hypertension, hyperlipidemia, sleep apnea, osteoarthritis, gastroesophageal reflux disease and chronic mild asthma.\nComputed tomography (CT) scan of the chest demonstrated a large cystic mass between the posterior aspect of the thoracic ribs and deep to the muscles of the left back and scapula. There was no obvious connection with the spinal cord or pleural space. No solid or enhancing component was identified.\nChest magnetic resonance imaging delineated a large cystic mass extending from the level of the lower neck to just above the level of the diaphragm measuring 11 cm transversely, 4.5 cm anteroposteriorly and 23 cm craniocaudally (Fig. ).\nThe primary care physician aspirated clear fluid under sterile conditions providing symptomatic relief. Cytologic studies were unremarkable. When the mass returned 2 weeks later, he was referred to our institution for further treatment. Due to symptoms referred to the cyst and the lack of response to aspiration, the decision was made to excise the lesion.\nThe patient underwent general endotracheal anesthesia and was placed in the right lateral decubitus position. A 2.5-cm longitudinal incision was made at a paramedian position on the left mid-back and it was carried through the level of the fascia by cautery. The paraspinous muscle fibers were separated and the bottom of the cyst was bluntly dissected free and the cyst was aspirated of its serous contents. A balloon dissector was inserted ventral to the cyst for additional blunt dissection. The balloon was inflated to grapefruit size and left inflated for 2 min for hemostasis. The balloon dissector created a larger space beneath the cyst and along its lateral margins. The balloon was then replaced with a Hasson trocar, and two additional 5-mm trocars were placed under direct vision to allow access to the CO2-filled cavity (Fig. ). Using a combination of blunt and electrocautery dissection, the cystic lesion was circumferentially freed from the trapezius muscle and cervical structures. Several feeding vessels were clipped and divided. Once freed, the cystic mass was removed in its entirety through the Hasson trocar site. Two 15-French round JP drains were inserted through the 5-mm trocar sites and placed to grenade suction.\nIntraoperatively, the aspirated cystic fluid was clear and devoid of malignant cells. Histologic analysis of the unilocular cyst revealed a primarily fibrous wall with some adipose tissue and associated vasculature. The cyst lacked a true epithelial lining and any malignant features such as hypercellularity, hyperchromasia, cellular pleomorphism or increased mitoses (Fig. ). The final pathologic diagnosis was that of a benign, fibrous-walled cyst.
|
[[62.0, 'year']]
|
M
|
{'17693287': 1, '10697186': 1, '17646896': 1, '11893141': 1, '24963907': 2}
|
{}
|
163,941 |
3813601-1
| 24,964,452 |
noncomm/PMC003xxxxxx/PMC3813601.xml
|
Colonic perforation associated with neostigmine administration
|
The patient, a 34-year-old female, developed symptoms consistent with pseudo-obstruction on Day 3 post-emergency Caesarean section, which was performed for foetal distress and possible placenta abruption. An abdominal X-ray was performed which showed a significantly dilated colon (Fig. ), and the diagnosis of pseudo-obstruction was again confirmed on computer tomography (CT) scan of the abdomen which showed a caecum measuring 9.8 cm transversely (Fig. ). Emergency colonoscopic decompression with the insertion of a flatus tube was performed and medical management, including cessation of opioids, anticholinergics and correction of electrolyte abnormalities, was commenced.\nThe patient failed to have a return of normal bowel function post-decompression and after 3 days was administered 500 µg of neostigmine via subcutaneous injection in an attempt to improve bowel motility. That evening she developed fever, and abdominal pain and erect chest X-ray confirmed free gas under her diaphragms (Fig. ). She was taken to theatre for emergency laparotomy. At operation she was found to have two sites of caecal perforation with a moderate faecal contamination in the right paracolic gutter. A right hemicolectomy with primary anastomosis was performed. She was discharged home on post-operative Day 7 without further complication. It is possible that the serosal tears of the caecum had occurred secondary to either administration of neostigmine or dilatation in the post-Caesarean period.
|
[[34.0, 'year']]
|
F
|
{'11270887': 1, '14985959': 1, '9177149': 1, '10403850': 1, '1416711': 1, '34741961': 1, '3753674': 1, '10826417': 1, '23186058': 1, '24964452': 2}
|
{}
|
163,942 |
3813620-1
| 24,964,446 |
noncomm/PMC003xxxxxx/PMC3813620.xml
|
Internal hernia due to mesenteric defect
|
An 18-year-old woman was brought to our emergency department with sudden onset lower abdominal pain. She had no remarkable past medical history and took no medications.\nOn physical examination, her abdomen was firm and an ∼15 cm fullness was palpable in the mid-to-lower abdomen, with severe tenderness.\nAbdominal computed tomography (CT) revealed loops of edematous small intestines which possible gangrenous changes ().\nAn emergency laparotomy was performed. On exploring the abdominal cavity, small intestine was necrotic. The mesenteric defect is detected in the jejunal region, 3 cm in size (Fig. ). Loops of small intestine had gone through the defect three times in a complex manner and strangulated. The mesenterium needed to be incised to complete resection of necrotic small intestines. The gangrenous intestines were resected and a primary anastomosis was performed.\nThe patient's postoperative course was uneventful and she was discharged on postoperative day 6 without any complications.
|
[[18.0, 'year']]
|
F
|
{'17211617': 1, '32577528': 2, '31492915': 1, '25553528': 1, '19994806': 1, '20616422': 2, '18205527': 1, '22288064': 1, '27134943': 1, '22075661': 1, '30487968': 2, '20091075': 1, '27656502': 1, '24964446': 2}
|
{'3003213-1': 1, '6250910-1': 1, '7305018-1': 1}
|
163,943 |
3813623-1
| 24,964,460 |
noncomm/PMC003xxxxxx/PMC3813623.xml
|
Resolution of diplopia after 33 years
|
A 54-year-old male presented to our department with a right-sided chemosis, periorbital swelling and was systemically unwell. Clinically, his visual acuity was 6/12 in his right eye and 6/6 in his left eye. He had an obvious right enopthalmos. He reported that he had surgery on a fractured right orbit 33 years ago and had had persistent diplopia since. He had never had any infective episode previously.\nHe was treated with systemic and topical antibiotics. On review he reported that his diplopia had worsened, but clinically his eye and swelling was much improved. A CT scan (Fig. ) showed: ‘A 17 mm defect in his right orbital floor. A (silastic) implant was displaced, lying vertically in the saggital plane. It protrudes through the orbital defect into the medial orbit. The inferior rectus is prolapsed through the orbital floor. Inferior and medial recti are both trapped by the implant’.\nA decision was made to remove the implant surgically via a Caldwell–Luc approach. This was performed successfully.\nWithin 4 weeks of surgery, the patient reported that his diplopia had resolved, for the first time, in 33 years. His visual acuity was 6/6 in both eyes.\nThe treatment of orbital floor fractures with silastic sheet is well documented and there are large case series published []. However, there is a high complication rate when using silastic as a material to repair orbital floor fractures. Complications include: implant migration to the skin and the maxillary sinus, skin fistula, persistent diplopia, communication between the orbit and the sinus, periorbital cellulitis []. 13.8% of patients required surgery to remove the silastic at 20 years [].
|
[[54.0, 'year']]
|
M
|
{'22132260': 1, '7699495': 1, '18569817': 1, '9471710': 1, '24964460': 2}
|
{}
|
163,944 |
3813666-1
| 24,963,909 |
noncomm/PMC003xxxxxx/PMC3813666.xml
|
Cerebral metastasis from malignant pleural mesothelioma
|
We report a case of a 62-year-old gentleman who presented with shortness of breath and right-sided chest pain over the period of 12 months. A chest X-ray showed a right pleural plaque that subsequently caused a right pleural effusion (Fig. ). Decortication, pleurodesis and pleural biopsy were performed with histopathology confirmation of mesothelioma. He declined chemotherapy or radiotherapy, although he was having regular follow-up by the oncologist.\nHe confirmed being exposed to asbestos, having worked for 20 years in aluminum and margarine factories.\nEighteen months after his initial presentation, he experienced progressive left-sided weakness and left-sided homonymous hemianopia. An MRI scan of his brain showed extra-axial right occipitoparietal enhancing mass (43 × 43 × 47 mm) with surrounding vasogenic oedema. It was isointense to grey matter on T2 and abutting the falx cerebri with midline shift and effacement of the right lateral ventricle (Fig. ). The lesion was approached through a right occipital craniotomy and entirely removed in a piecemeal fashion. At surgery, it appeared as a greyish-white firm vascular mass with a clear cleavage plane with the surrounding brain. He recovered well after surgery. His left-sided weakness improved significantly with some improvement in the hemianopia. Histopathology revealed metastatic malignant mesothelioma (Fig. ). The patient had good recovery and was discharged home. On 6-week follow-up, the patient continued to improve with significant improvement in his quality of life.\nSection from the intraoperative specimen showed a large cell-epithelioid malignancy composed of markedly pleomorphic epithelial cells with large hyperchromatic nuclei. Other characteristics included large and multiple nucleoli and abundant acidophilic cytoplasm. Necrosis was also abundant and so were atypical mitoses. Immunohistochemistry is essential to differentiate methastatic mesothelioma from adenocarcinoma. Immunoperioxidase stains demonstrated in fact that the cells expressed vimentin, calretinine, AE1/AE3 and Cam 5.2 as in the previously biopsied pleural lesion. The CK5/6 marker that was previously only lightly positive was now well expressed. EMA and thrombomodulin were also moderately positive. Important negative markers included CEA, CDI5, S100 and TTR-1.
|
[[62.0, 'year']]
|
M
|
{'10741777': 1, '8120568': 1, '34041868': 1, '1710103': 1, '10476113': 1, '13782506': 1, '15519879': 1, '16054941': 1, '34317932': 1, '9181361': 1, '24963909': 2}
|
{}
|
163,945 |
3813678-1
| 24,964,471 |
noncomm/PMC003xxxxxx/PMC3813678.xml
|
A case report of a rare adnexal tumour: aggressive digital papillary adenocarcinoma
|
A 78-year-old Caucasian gentleman presented with a painful 2 cm irregular swelling in the nail bed of the distal phalanx of the right middle finger, with brown discolouration of the nail bed. The swelling in the digit had been present for ∼30 years, which had begun following a fracture of the terminal phalanx and had gradually increased in size over the preceding 6 months. There was no axillary or cervical lymphadenopathy and the patient was fit and well.\nClinically a differential diagnosis of an aggressive adenocarcinoma was suspected, but this was not supported by multiple radiological investigations. CT and MRI of the lesion showed a vascular destructive lesion that was causing severe erosion of the distal interphalangeal bone (Figs and , respectively). A plain chest radiograph at that time showed no pulmonary metastasis.\nAs the radiological investigations had shown that the distal phalanx was not viable and a lack of proximal invasion, it was felt appropriate to perform an amputation at the level of middle to distal third of the middle phalanx. Such an amputation was aimed at being curative, in addition to providing a definite diagnosis, maintaining function and allowing for primary closure.\nThe patient underwent an amputation of the middle phalanx of the right middle finger. Histopathology of the specimen showed a high mitotic grade lesion with a small focus of lymphovascular invasion, diagnostic of ADPA (Fig. ). The tumour was 0.7 mm from the nearest resection margin. The high rates of recurrence and metastasis were explained to the patient, who declined further surgical treatment.\nSeventeen months following initial presentation, the patient developed a mass in the right axilla. In addition, subsequent plain chest radiograph (Fig. ) and CT of the thorax showed multiple pulmonary metastasis. An axillary clearance was performed and one of the ten nodes confirmed metastatic disease. Shortly after this, the patient suffered an intracranial haemorrhage into the right internal capsule. Over the last 2 years the patient has remained only mildly short of breath due to his pulmonary metastasis and was improving neurologically. At a recent review, the patient showed features of deterioration due to the pulmonary metastasis.
|
[[78.0, 'year']]
|
M
|
{'30792586': 1, '16055244': 1, '16048414': 1, '11285414': 1, '10843279': 1, '17645380': 1, '10848941': 1, '24964471': 2}
|
{}
|
163,946 |
3813680-1
| 24,964,456 |
noncomm/PMC003xxxxxx/PMC3813680.xml
|
Successful laparoscopic management of an incarcerated obturator hernia
|
An 85-year-old female with a background of trans-abdominal hysterectomy, hypertension and a previous thyroid lobectomy, presented acutely with a 1-day history of upper abdominal pain radiating down her left leg associated with numerous episodes of emesis. Her bowels had opened three times in the previous 24 h. She was anorexic for the previous 24 h. She reported a similar episode requiring hospitalization 3 weeks before, which was treated non-operatively in another institution.\nOn examination, her vitals were stable. She displayed mild upper abdominal tenderness without signs of peritonism. Bowel sounds were present. Her haematological investigations were unremarkable. A plain film of abdomen was unremarkable. She was treated presumptively as a small bowel obstruction and non-operative measures were employed and the patient proceeded to have a computed tomography (CT) scan of the abdomen and pelvis, which indicated proximal small bowel obstruction secondary to a left obturator hernia (Fig. ). She proceeded to emergent laparoscopy and subsequent mesh repair of left obturator hernia, containing an obstructed loop of small bowel. There was a concomitant femoral hernia that was repaired separately.\nUnder general anaesthetic, the optical technique for access was utilized at the umbilicus with a 5 mm port. Two further working ports, a 5 and 10 mm, were placed in the right lower quadrant and right hypochondrium, under direct vision. Findings included visualization of small bowel dilatation down to small bowel in a left obturator hernia with an incidental left femoral hernia containing omentum (Fig. ). The incarcerated small bowel was reduced using a pair of non-traumatic forceps and deemed viable. The omentum was reduced from the femoral hernia.\nThe obturator hernia was repaired with Proceed™ Ventral patch (Ethicon, Inc., Sommerville, NJ, USA) tacked with AbsorbaTack™ (Covidien, Mansfield, Inc., MA, USA) fixation device. The initial fixation was performed onto Cooper's ligament. This then allowed the mesh to be spread laterally and fixed to the transversalis fascia. The femoral hernia was repaired with 2 × 2/0 Vicryl (Ethicon, Inc., Sommerville, NJ, USA) sutures placed laparoscopically. Port sites were closed in a routine manner. The patient did suffer a post-operative pneumonia but was treated appropriately, made a good recovery and was discharged home well.
|
[[85.0, 'year']]
|
F
|
{'19554389': 1, '8304319': 1, '9876738': 1, '27113790': 1, '4808720': 1, '21858557': 1, '27287915': 1, '30154915': 2, '7793500': 1, '27780090': 1, '31927400': 1, '15041510': 1, '32772276': 1, '9880435': 1, '18188503': 1, '32623327': 1, '8239189': 1, '24964456': 2}
|
{'6108096-1': 1}
|
163,947 |
3813682-1
| 24,963,906 |
noncomm/PMC003xxxxxx/PMC3813682.xml
|
Giant mesenteric lymphatic malformation presenting as small bowel volvulus
|
A 4-year-old previously healthy male presented to an outside hospital with 2 days of nausea and bilious emesis. An abdominal plain film (Fig. a) revealed small bowel obstruction and an abdominal ultrasound was nondiagnostic. Upon transfer to our institution, he had persistent bilious emesis with periumbilical abdominal pain. His medical and surgical history was unremarkable, with no history of antecedent trauma. His mother noted an increasing abdominal girth over the prior several months, but did not seek medical attention. On physical examination, the child's abdomen was soft, mildly distended and with periumbilical tenderness. He had no rebound tenderness or guarding, and no hernias were present. Review of the ultrasound revealed extensive intra-abdominal fluid. An abdominal computed tomography (CT) scan was obtained and revealed a large intraperitoneal cystic mass measuring 13 × 21 × 9 cm in the left abdomen (Fig. b). A small bowel obstruction was also present with concern for volvulus due to mesenteric swirl seen on axial imaging. There was no evidence of compromised intestine on CT (Fig. c). The patient was taken to the operating room for laparoscopy. The cyst, which arose from the mesentery of the small intestine, resulted in a segmental volvulus with congestion of the involved segment (Fig. a–c). A short vertical midline incision was made to allow the giant cyst to be delivered and the volvulus reduced. After reduction, the congested small bowel returned to a normal appearance. The cyst was excised by removing the 8 cm segment of small bowel from whose mesentery it arose (Fig. c). The abdomen was closed and the patient was discharged in excellent condition.\nPathologic inspection of the mass revealed a thin-walled cyst containing milky fluid. Immunohistochemistry showed that the cyst lining expressed D2–40 (a marker of lymphatic endothelium), but was negative for keratin, WT-1 and calretinin, confirming the diagnosis of lymphatic malformation (Fig. ).\nThe patient continues to do well with no postoperative complications at 7-month follow-up.
|
[[4.0, 'year']]
|
M
|
{'18753753': 1, '18558209': 1, '20062588': 2, '19503641': 1, '8414761': 1, '19853765': 1, '22005353': 1, '12691938': 1, '15149994': 1, '22358782': 1, '24963906': 2}
|
{'2803988-1': 1}
|
163,948 |
3813689-1
| 24,964,459 |
noncomm/PMC003xxxxxx/PMC3813689.xml
|
The white-eyed blowout fracture in the child: beware of distractions
|
A 14-year-old boy was playing soccer, when he sustained a blow from a knee to his left orbit. He sustained no loss of consciousness. He presented to his nearest emergency department. He was assessed and, as he was nauseous and vomited once, a decision was made to admit him under the paediatric services to monitor his head injury.\nHe had minimal periorbital bruising, and his visual acuity was 6/6; however, his ability to move his eye was reduced over the next 24h, and his diplopia worsened. His nausea and vomiting continued, and he had a head CT scan performed. This showed no brain injury; however, the scan discovered a left orbital floor fracture with entrapment of the inferior rectus muscle (Fig. ).\nHe was subsequently transferred to our unit, and when he arrived 60h after his initial injury, his left eye showed no vertical movement and very limited downward gaze and some preserved lateral and medial movement. Movements were painful. There was no subconjunctival haemorrhage; 6/6 visual acuity; his pupils were equal and reactive to light and he had marked diplopia in upward gaze. The patient kept the eye habitually closed to avoid diplopia.\nHe was urgently taken to theatre, where an open exploration of his left orbit was performed. This was performed via a second crease incision, and his Inferior rectus was successfully released.\nAt 1 month following surgery, his diplopia and range of ocular movement has improved significantly but has not completely returned to normal. He continues to be monitored under review.
|
[[14.0, 'year']]
|
M
|
{'21596296': 1, '30289909': 1, '19386870': 1, '33584039': 1, '31245200': 1, '12882507': 1, '24964459': 2}
|
{}
|
163,949 |
3813704-1
| 24,964,465 |
noncomm/PMC003xxxxxx/PMC3813704.xml
|
Successful liver resection for the unusual case of peripheral intra bile duct growth of liver metastasis from colorectal carcinoma
|
A 67-year-old male patient underwent emergency left hemi-colectomy due to ileus caused by descending colon cancer. The pathological examination was consistent with adenocarcinoma (T3N1M0). Sixteen months following resection, there was a significant increase in routine follow-up carcinoembryonic antigen 19-9 (CA19-9): 607.7 U/ml.\nComputed tomography (CT) demonstrated two solitary lesions in segment (S) eight. Furthermore, S3 hepatic duct dilatation was clearly detected on CT scanning (Fig. ).\nMagnetic resonance imaging (MRI) of the lateral segment lesion showed an irregular line shape lesion: hyper-intensity in T2-weighted; hypo-isointense in T1-weighted image (Fig. ). These CT and MRI findings supported the identification of a fulfilment of tumour in B3. Endoscopic retrograde cholangiopancretography (ERCP) demonstrated a stricture involving the B2 and B3 hepatic ducts but not involving the left hepatic duct. Considering the patient's medical history along with the clinical features, the final diagnosis was secondary liver metastases due to primary descending colon adenocarcinoma, with the possibility of peripheral cholangiocarcinoma.\nIn order to obtain efficient bile duct tumour clearance as well as to maintain liver function (15-min retention rate of Indocyanine green: 19%), the patient underwent anatomic S8 resection and lateral segmentectomy (Fig. ). The metastasis in the lateral segment demonstrated intra bile duct tumour growth.\nAlthough there was B3 intra bile duct growth, there was no pathological evidence of malignancy in the left main bile duct. For the S8 metastases, systemic S8 resection with indigo carmine S5 counter strain had also been performed. Subsequently, normal anatomic lateral segmentectomy was performed without extra hepatic bile duct resection or cholecystectomy. His clinical course was stable without complications, and he was discharged after 7-days of hospitalisation. The patient is currently suffering from amyotrophic lateral sclerosis, without any sign of local metastatic tumour recurrence 14 months post-operatively.\nPathological examination for the descending colon carcinoma revealed an adenocarcinoma which was well differentiated, with one out of ten lymph node metastasis identified (Dukes' C). Macroscopically, the surgical specimen of the liver demonstrated a papillary tumour with clear margin intra and extra hepatic duct growth. On microscopic examination, the histological differentiation of the three metastatic tumours was identical to that of the descending colon cancer. The lateral segment tumour was located in the intrahepatic duct which demonstrated cytokeratin (CK) 7(+), CK20(−) and caudal-type homeobox (CDX2) (−). These findings are consistent with liver metastases due to colorectal adenocarcinoma []. The S8 metastases did not reveal intra biliary tumour growth. Following this histological finding, the tumour invaded into hepatic duct, followed by the hepatic duct being filled with metastatic tumour at S3.
|
[[67.0, 'year']]
|
M
|
{'30658608': 2, '10568181': 1, '11937308': 1, '22370732': 1, '20947473': 1, '30367665': 2, '12366810': 1, '8756838': 1, '12397294': 1, '9298879': 1, '22864889': 1, '12093342': 1, '24964465': 2}
|
{'6339384-1': 1, '6204027-1': 1}
|
163,950 |
3813706-1
| 24,964,443 |
noncomm/PMC003xxxxxx/PMC3813706.xml
|
Intrathyroidal parathyroid hyperplasia in tertiary hyperparathyroidism
|
A 41-year-old female with a 13-year history of hemodialysis for chronic renal failure underwent a kidney transplant in May 2011 without complications or rejection reactions. Blood tests performed prior to the kidney transplantation indicated that serum total calcium (Ca) and intact parathyroid hormone (iPTH) level were 9.9 mg/dl (normal, 8.2–10.4 mg/dl) and 453.3 pg/ml (normal, 14–72 pg/ml), respectively. Postoperative laboratory tests performed three months later revealed elevated serum Ca (10.4 mg/dl), which lasted for 15 months. Her iPTH level did not return to normal after kidney transplantation (Fig. ). The patient was diagnosed with tertiary hyperparathyroidism and was recommended for surgery.\nIn the preoperative evaluation, two-hour-delayed 99mTc-sestamibi scintigraphy showed increased uptake in both inferior parathyroid glands (Fig. ). Computed tomography (CT) of the neck showed a calcified nodule posterior to the right superior thyroid gland, a solid nodule in the right lower thyroid gland and an enlarged parathyroid gland posterior to the left inferior thyroid (Fig. ). Sonography (SONO) showed a benign-looking nodule in the right lower thyroid and two adjoining enlarged parathyroid glands posterior to the left lower thyroid (Fig. ). The right mid-thyroid nodule appeared benign, and a fine-needle aspiration biopsy was not performed. The right inferior parathyroid gland could not be identified in the CT or SONO findings. During neck exploration, four oval masses similar to parathyroid glands were observed (right superior: 1.7 × 1.0 cm, right inferior: 0.5 × 0.3 cm, left superior: 1.0 × 0.7 cm, left inferior: 0.8 × 0.6 cm). The left inferior parathyroid gland was partially preserved, while the other lesions were completely removed. Intraoperative frozen biopsy of the four masses revealed two cases of parathyroid hyperplasia, a parathyroid hyperplasia with a calcified nodule in the right superior area and a lymph node in the right inferior area. The right inferior parathyroid was not found during right neck exploration.\nIntraoperative iPTH levels 20 min after the parathyroidectomy were still elevated (102.6 pg/ml). A small and soft nodule (12 mm diameter) was palpable in the lower pole of the right thyroid lobe. A partial resection of thyroid including the nodule was performed (Fig. ). Intraoperative frozen biopsy of the intrathyroidal nodule revealed parathyroid hyperplasia (Fig. ). Intraoperative iPTH levels decreased 20 min after the thyrotomy (30 pg/dL). After surgery, the patient's serum Ca and iPTH levels returned to normal, and renal function was well maintained.
|
[[41.0, 'year']]
|
F
|
{'8813259': 1, '22921681': 1, '22968537': 1, '22748545': 1, '19566521': 1, '18238745': 1, '12398239': 1, '22792527': 1, '19355835': 1, '24964443': 2}
|
{}
|
163,951 |
3813725-1
| 24,963,904 |
noncomm/PMC003xxxxxx/PMC3813725.xml
|
Isolated inferior rectus muscle rupture after blunt orbital trauma
|
A 44-year-old man was referred to our department with a monocular hematoma, swelling and diplopia. He was punched in the area of the left orbit the day prior during a violent conflict.\nThe clinical examination revealed a left-side periorbital swelling and monocular hematoma with significant subconjunctival haemorrhage. A vertical diplopia with restriction of infraduction was also observed (Fig. . Additionally, he presented with hyperopia. The palpation of the underlying bone showed no bony step-off of the orbital rim. A preoperative ophthalmological evaluation confirmed the vertical diplopia, and showed an isolated IR muscle underaction with deficiency of depression in abduction, as well as a vertical deviation in primary position.\nComputed tomography (CT 1 mm slices) presented a large, left-orbital floor fracture with caudal dislocation of the bone fragment and prolapse of the IR muscle and orbital fat into the maxillary sinus (Fig. a). Transection or disinsertion of the IR was not described.\nPreoperative forced-duction testing indicated mild restriction in the vertical upward direction, suggesting an entrapment of the IR muscle. Uneventful surgery via a transconjunctival incision was performed under general anaesthesia. The intraoperative finding showed a huge defect of the bone. Therefore, the entrapped orbital tissues were lifted out of the fracture, repositioned and a titanium mesh was inserted for repair of the orbital floor (Fig. b).\nFour days after surgery, despite good resolution of swelling, there had been essentially no change in the clinical–functional deficit and vertical diplopia persisted due to restriction of infraduction.\nA postoperative CT scan showed a good position of the titanium mesh, as well as repositioning of herniated tissues, but highlighted a tear of the IR muscle in its middle part.\nAccordingly, the preoperative CT scan was re-evaluated in 0.5 mm slices and the pre-existence of the ruptured IR was shown (Fig. . After ophthalmological consultation and treatment of the patient with a combination of orthoptics and prismatic glasses, satisfactory functional recovery was achieved after 6 months without need of surgical repair of the ruptured muscle.
|
[[44.0, 'year']]
|
M
|
{'937429': 1, '22551369': 1, '9630302': 1, '10849393': 1, '17286186': 1, '12439059': 1, '20159478': 1, '22824489': 1, '33456689': 1, '11797320': 1, '16555047': 1, '24963904': 2}
|
{}
|
163,952 |
3813727-1
| 24,963,901 |
noncomm/PMC003xxxxxx/PMC3813727.xml
|
Revision hip arthroplasty following recurrence of a phosphaturic mesenchymal tumor
|
In March 2003, a 47-year-old man was referred from the endocrine clinic to the outpatient center of our department with diffuse hip pain on the right side. In 1997, he had severe osteomalacia and was treated symptomatically with phosphate and calcitriol. There was no family history of any disease inducing osteomalacia, such as inborn errors of metabolism or chronic renal disease.\nAt the time of our investigation, laboratory tests revealed hypophosphatemia with 0.44 mmol/l of phosphate (normal range: 0.81–1.6 mmol/l), normal serum calcium (under substitution with calcitriol) with 2.6 mmol/l (normal range: 2.0–2.6 mmol/l), and low urinary inorganic phosphorus excretion with 15 mmol/24 h (normal range: 21–85 mmol/24 h).\nMagnetic resonance imaging (MRI) and computed tomography (CT) scanning showed a destructive lesion, 5 cm in diameter, in the right os ilium and obturator internus muscle (Fig. ). FGF-23 levels were significantly high and an octreotide scan was positive for radionuclide uptake in the right acetabulum. CT-observed biopsy of the right acetabulum was performed, and histological analysis revealed a benign phosphaturic tumor (PHT) of mixed connective tissue type.\nAfter tumor resection through an ilioinguinal approach, serum phosphate levels normalized. To address persistent hip pain, a total hip arthroplasty was performed, and complete remission of clinical symptoms accomplished.\nEight years later, the patient presented with hip pain on the same side over a longer period. CT scan and MRI revealed tumor recurrence (Fig. ) on the dorsomedial circumference of the acetabulum with a bone defect 2 cm in diameter. Signs of loosening of the cup of the hip arthroplasty were considered secondary. Biochemical evaluation revealed hypophosphatemia with 0.69 mmol/l of phosphate, normal serum calcium of 2.42 mmol/l and a secondary hyperparathyroidism with parathyroid hormone of 85.7 ng/l (normal range: 15–65 ng/l). An octreotide scan of the right hip showed massive enhancement of the acetabulum. Assessment of FGF-23 was inconclusive.\nIn revision surgery, the stem was fixed but the socket was easily removed and the center of the acetabulum exhibited massive destruction. There was no clear demarcation between the tumor mass, consisting of soft tissue, and its surroundings. After wide resection of the tumor, the bone defect was filled with homologous bone and a 52-mm roof reinforcement ring (Mathys), with a cemented 50-mm low-profile cup (Mathys), was implanted (Fig. ).\nHistological analysis of the removed tissue showed the same benign PHT as previously excised in 2003. Re-evaluation 1 year after revision arthroplasty revealed normal phosphate levels, and the patient reported no symptoms or complaints.
|
[[47.0, 'year']]
|
M
|
{'17014386': 1, '3545439': 1, '11318793': 1, '20059333': 1, '12970268': 1, '29552133': 1, '22029985': 1, '3584490': 1, '21611969': 1, '22035861': 2, '14707860': 1, '24963901': 2}
|
{'4013303-1': 1}
|
163,953 |
3813728-1
| 24,964,440 |
noncomm/PMC003xxxxxx/PMC3813728.xml
|
Simultaneous double ileoileal intussusception due to Burkitt's lymphoma in a young male
|
A 26-year-old male patient, previously healthy, presented to our ER complaining of diffuse colicky abdominal pain of one week duration. He also reported nausea, two episodes of non-bilious vomiting and a two-day history of constipation and obstipation. No fever or chills. He denied any past surgical history. His vital signs were all within normal limits. On physical examination, his abdomen was tender, distended and tympanic on percussion. Bowel sounds were hyperactive. DRE showed empty rectum. All his lab tests were normal except for mild leukocytosis. Plain abdominal film showed two air-fluid levels. A follow-up CT scan of the abdomen and pelvis showed small bowel obstruction and a 5 × 5 cm mesenteric mass (Fig. ). Another mass of 3 × 3 cm was also noted. The patient was referred for surgical management.\nUnder general anesthesia, patient in supine position, a midline laparotomy was performed. A large amount of abdominal fluid was aspirated and sent for culture and cytology. During running of the bowel at the level of 20 cm from the ligament of Treitz, an intussusception with a palpable intraluminal mass was found. Another intussusception 120 cm distal to the first was also noted (Fig. ). No other pathologies were found. Double enterectomies with end-to-end anastamoses were performed. The patient was discharged home on Day 5 post op. Pathological analysis revealed polypoid and infiltrating intraluminal lymphoid proliferation (Fig. ), extending to serosa and exhibiting diffuse aspect composed of medium-sized B-cells: pattern of Burkitt's Lymphoma. Abdominal fluid cytology analysis showed the presence of atypical lymphoid cells.
|
[[26.0, 'year']]
|
M
|
{'21461167': 1, '17560209': 1, '21910876': 2, '18716102': 1, '17348303': 1, '10195723': 1, '21390139': 1, '9296505': 1, '4306129': 1, '24964440': 2}
|
{'3178522-1': 1}
|
163,954 |
3813747-1
| 24,964,458 |
noncomm/PMC003xxxxxx/PMC3813747.xml
|
Diagnosis and management of retroareolar cysts in adolescents: a case report
|
A healthy 15-year-old girl presented to her GP with mastalgia and periareolar cellulitis of her right breast. She was initially treated with a course of oral flucloxacillin but after 2 days there was no improvement and an emergency hospital referral was organized. Physical examination identified periareolar erythema in the presence of a tender subareolar inflammatory mass and a mild pyrexia. A provisional diagnosis of retroareolar abscess was made and an ultrasound scan (USS) was requested. The USS revealed three focal fluid collections or cysts located behind the nipple which were in direct communication with each other. The cysts contained echogenic fluid with surrounding hyperaemia and subcutaneous oedema. After conversation with a consultant breast surgeon, it was decided not to aspirate the mass but to discharge the patient on an additional course of amoxicillin and follow her up 3 days later with consultant review.\nSubsequent review revealed a mild improvement in symptoms and an alternative diagnosis of retroareolar cyst established. Follow-up with repeat USS 2 days later revealed a well-defined anechoic lesion cystic in nature rather than abscess. The lesion had decreased in size, and clinical examination revealed no existing erythema and decreased tenderness on palpation of the inflammatory mass.
|
[[15.0, 'year']]
|
F
|
{'17174833': 1, '7738735': 1, '3171840': 1, '32831561': 1, '34012369': 1, '12604147': 1, '16179617': 1, '31152211': 1, '28845840': 1, '32757082': 1, '11112814': 1, '24964458': 2}
|
{}
|
163,955 |
3813751-1
| 24,964,462 |
noncomm/PMC003xxxxxx/PMC3813751.xml
|
The use of bone anchors for autologous flap fixation in perineal reconstruction: a case report
|
A 64-year-old female presented to our office with a perineal hernia (Fig. ) 1.5 years after abdominoperineal resection (APR). She had a history of recurrent low-lying rectal cancer for which she received neoadjuvent external beam radiation and chemotherapy, followed by APR. Physical examination showed the hernia was reducible and tender to palpation. Radiation skin changes were also noted in the perineum. The patient reported not being able to sit due to pain related to the hernia. She also did have a large ventral hernia related to her previous abdominal surgeries.\nDue to her history of perineal radiation, we decided to treat her with a VRAM (Fig. ) via trans-abdominal approach. There was concern about securing the flap in the perineum due to the size of the defect and previous radiation making the tissues friable. In light of this, we decided to use bone anchor fixation to secure the autologous flap. She also underwent abdominal wall reconstruction with separation of components and mesh placement during the same operation.\nA standard VRAM was harvested from the abdominal wall. The bowel and abdominal contents were then returned to the abdominal cavity. Several Fastin Mitek brand (Raynham, MA) bone anchors were placed in the bones surrounding the pelvic outlet, including the fecal promintory, pubic tubercle and pelvic rim (Fig. ). Holes were pre-drilled after the bone had been exposed. The anchors were then screwed into place with suture attached. Care was taken not to injure the ureters, sacral venous plexus, surrounding nerves and blood vessesl. The skin of the flap of the VRAM was de-epithelialized. The bone-anchored suture was then passed through the dermis of the flap. The flap was parachuted down into the pelvis and the sutures were tied to secure the flap in place. This created a pelvic sling to close off the pelvic inlet from the abdominal cavity.\nPost-operatively the patient did well. She did however present with infected abdominal mesh 3 months after surgery. She was returned to the OR for removal of the abdominal mesh. The perineal repair at that time was intact. At 18 month follow-up, there was good healing of all the wounds and no recurrence of either hernia (Fig. ).
|
[[64.0, 'year']]
|
F
|
{'21659846': 1, '19495919': 1, '28508281': 1, '17587090': 1, '20490587': 1, '18985271': 1, '16946992': 1, '19560944': 1, '3803102': 1, '19296976': 1, '22108954': 1, '24964462': 2}
|
{}
|
163,956 |
3813753-1
| 24,964,455 |
noncomm/PMC003xxxxxx/PMC3813753.xml
|
A case of small bowel obstruction due to phytobezoars
|
A 63-year-old Syrian male presented to the emergency department with a 2-day history of generalized colicky abdominal pain associated with repeated vomiting and absolute constipation. There was no associated history of alteration of bowel habit, rectal bleeding, fever or dysuria.\nHis past medical history was significant for a laparotomy in 1979 due to a peptic ulcer-related complication, but he was unaware of the details. He was also recently diagnosed with diabetes mellitus for which he was using herbal treatment consisting of boiled olive tree leaves (Olea europaea).\nOn physical examination, the patient looked unwell but was hemodynamically stable and apyrexial. His abdomen was distended. There was a midline laparotomy scar with a reducible incisional hernia in the epigastric area. He had mild lower abdominal tenderness with no muscle guarding and his bowel sounds were exaggerated. Rectal examination revealed no abnormalities and there was a small amount of stool in the rectum.\nThe rest of the physical examination was unremarkable. Routine blood investigation and abdominal X-rays were obtained. Apart from leukocytosis, they were unremarkable.\nA contrast-enhanced CT scan was arranged and it showed features of SBO with collapse of the terminal ileum. There was evidence of a previous gastrojejunostomy with suspected foreign bodies in the stomach and proximal ileum. (Figs and )\n.\nAt laparotomy, a previous gastrojejunostomy with dense adhesions in the upper abdomen was found. An obstructing hard foreign body was palpable in the ileum with dilatation of the proximal small bowel loops. A larger similar foreign body was mobile and palpable within the stomach. (Fig. ) Both foreign bodies were removed through an enterotomy and gastrotomy, respectively, and the bowel was decompressed. After limited adhesiolysis, the abdomen was closed en mass repairing the midline hernia defect.\nPostoperative recovery was unremarkable except for a short duration of ileus, after which the patient made a steady recovery. He was referred to the diabetology department and dietician during admission and was discharged with outpatient clinic follow-up.\nA follow-up upper GI endoscopy was done and it showed evidence of a hiatus hernia with gastrooesophageal reflux disease. The patient was well controlled on Proton pump inhibitors and remained largely symptom free.
|
[[63.0, 'year']]
|
M
|
{'25437689': 1, '22040770': 1, '21038126': 1, '32141815': 1, '29756104': 1, '23252775': 1, '27403434': 1, '22408356': 1, '23336647': 1, '21605530': 1, '24964455': 2}
|
{}
|
163,957 |
3813768-1
| 24,963,902 |
noncomm/PMC003xxxxxx/PMC3813768.xml
|
Branchial cleft cyst encircling the hypoglossal nerve
|
A 10-year-old African boy presented with complaints of left-sided anterior neck swelling for 1year. The swelling was non-tender, not associated with any prior trauma and had no drainage or sinus tract. The patient reported occasional shortness of breath and a history of snoring, but was otherwise in good health. He had no prior medical or surgical history, no allergies and took no medications. He was the fifth born in a family of seven children. On physical examination, the patient was alert and in no distress. He had a prominent non-tender swelling in the left anterior neck, measuring 8 cm by 5 cm. The remainder of his physical examination was unremarkable, as were vital signs and basic laboratory values.\nAfter obtaining informed consent from the parents, the patient was taken to the operating room with a diagnosis of a branchial cleft cyst. After incision, a large cystic mass was easily identified. During dissection of the cyst, it was noted that a structure appeared to pass through the cyst (Fig. A). This was identified as the hypoglossal nerve. The cyst was found to completely encircle the hypoglossal nerve. With careful dissection and eventual transection of the cyst anterior to the nerve, the cyst was removed and the hypoglossal nerve remained intact (Fig. B). Rupture of the cyst was necessary to release the nerve at the time of excision. The completion of the procedure was uneventful and the patient recovered from general anesthetic without incident. On postoperative day 1, he was noted to have mild left-sided tongue deviation, suggesting hypoglossal nerve palsy. No hypoglossal nerve palsy was present preoperatively. He remained otherwise asymptomatic and was discharged home in stable condition.
|
[[10.0, 'year']]
|
M
|
{'18273506': 1, '23120450': 1, '21680029': 1, '20236623': 1, '2037480': 1, '24963902': 2}
|
{}
|
163,958 |
3813769-1
| 24,964,470 |
noncomm/PMC003xxxxxx/PMC3813769.xml
|
Intrapericardial parathyroid adenoma
|
A 32-year-old male was referred to the endocrine surgery team with hypercalcemia and a history of several years of kidney stones. He had first been diagnosed with elevated serum calcium ∼6months prior to his visit in the endocrine surgery clinic but had experienced recurrent problems with nephrolithiasis for several years prior to this. He underwent three lithotripsy procedures and multiple urologic stent placements during this time. Additional symptoms included severe fatigue, weakness and joint pain. Aside from his nephrolithiasis and subsequent renal failure, the patient was otherwise healthy, with no medication use, no allergies, and no history of tobacco or alcohol use.\nSix months prior to our evaluation, at another hospital, the patient underwent failed neck exploration for primary hyperparathyroidism. Pre-operative imaging suggested a right inferior parathyroid adenoma, but bilateral neck exploration including a right thyroid lobectomy was unsuccessful. The initial operation was complicated by transient bilateral vocal cord palsies. The patient was evaluated by an otolaryngologist, and his weak voice and vocal cord palsies resolved without any further intervention.\nHis hypercalcemia persisted and the patient continued to suffer from nephrolithiasis. Despite his multiple urologic interventions, he developed renal failure with a creatinine peaking at 13.5 and requiring temporary dialysis. Parathyroid imaging, including sestamibi/SPECT scan as well as MRI/MRA of the neck and chest suggested an ectopic parathyroid adenoma in the aortopulmonary window (Fig. ). Following consultation with cardiothoracic surgery, the patient underwent a minimally invasive thoracic approach to the mediastinum, followed by conversion to a left posterolateral thoracotomy. Neither approach located the suspected mediastinal adenoma. A median sternotomy was then performed. The entire thymus and all mediastinal fatty tissues were removed without evidence of any abnormality. Finally, the pericardium was opened and a 0.610 g starfish-shaped parathyroid adenoma removed without complication (Figs and ). The patient's intraoperative PTH levels dropped precipitously from 400 to 53 pg/ml. The patient recovered uneventfully and was discharged home on calcium supplementation. At 6-month follow-up, no further evidence of renal stone disease was noted on imaging.
|
[[32.0, 'year']]
|
M
|
{'20523997': 1, '19944253': 1, '18503371': 1, '21646371': 1, '19836493': 1, '16490559': 1, '22431655': 1, '24964470': 2}
|
{}
|
163,959 |
3813775-1
| 24,963,908 |
noncomm/PMC003xxxxxx/PMC3813775.xml
|
A rare splenic pseudocyst
|
A 47-year-old female presented with complaints of a small lump (Figs –) in left upper abdomen and a past history of fall on ladders a year back. On examination, there was a small lump confined to the left hypochondrium, firm in consistency with rounded borders suggesting origin from the spleen. The patient underwent CT scan of the abdomen after abdomen sonography and CECT suggested the presence of a cystic lesion originating from the lower margin of spleen ∼12 × 8 cm in size. The patient underwent a surgery and cystic lesion was removed preserving the spleen (Figs –). The cyst on histopathological examination was a pseudocyst.
|
[[47.0, 'year']]
|
F
|
{'16647350': 1, '25246475': 1, '20184691': 2, '12680182': 1, '29435376': 2, '31492728': 1, '30416137': 1, '19547686': 2, '11318135': 1, '6024340': 1, '2754580': 1, '13034324': 1, '24963908': 2}
|
{'2699073-1': 1, '5757091-1': 1, '2827097-1': 1}
|
163,960 |
3813776-1
| 24,964,449 |
noncomm/PMC003xxxxxx/PMC3813776.xml
|
The space between: a supralevator abscess caused by perforated diverticulitis
|
A 60-year-old male presented to our institution with a 4–6-week history of progressive constipation, painful defecation, urinary retention and increasing lower abdominal pain and pressure. He described some associated nausea, chills and tenesmus after small, frequent movements. Additionally, this patient relayed ∼8-lb weight loss over a 2-month period secondary to decreased oral intake and fear of painful and incomplete evacuation, and had begun experiencing pelvic and sacral pain when sitting. His past medical history included hypothyroidism, anxiety, hypercholesterolemia and smoking. On physical exam the patient demonstrated tenderness to palpation across the lower abdomen without evidence of peritonitis. Digital rectal examination revealed an enlarged prostate, good sphincter tone; significant tenderness upon palpation of the rectum was elicited, with no purulent drainage expressed.\nContrast-enhanced computed tomography (CT) scan revealed the presence of diverticulosis and perirectal mesenteric stranding concerning for diverticulitis (Fig. ); therefore, the patient was admitted and treated empirically for the same with i.v. antibiotics. He was discharged several days later with a 2-week course of amoxicillin clavulanate.\nIn the 6-week follow-up, repeat CT demonstrated eccentric thickening of the rectosigmoid with interval development of an adjacent complex pelvic fluid collection with supralevator extension measuring 3.5 × 2.5 cm (Fig. a and b). Percutaneous needle biopsy revealed pus, and a drainage catheter was left in place (Fig. a and b). The patient did not improve, was reimaged and was found to have collection extending into the ischiorectal fossa and supralevator space (Fig. ). Owing to refractory pain and persistent leukocytosis, the patient was taken to the operating room for examination under anesthesia. No fistulous tract or internal drainage was noted within the rectal vault; however, consistent with the imaging, external induration was observed along the right ischiorectal fossa, where, upon incision, a large purulent cavity was evacuated. On evening rounds, the patient was noted to have a marked leukocytosis and frank stool coming from the ischial wound, and he was taken emergently to the operating room for diagnostic laparotomy where a perforated diverticulum adherent to the pelvic sidewall was identified (Fig. ). Therefore, a Hartmann procedure, drainage of supralevator abscess, irrigation and debridement of the right ischiorectal wound, was performed.
|
[[60.0, 'year']]
|
M
|
{'8273946': 1, '19863596': 1, '9106694': 1, '11089598': 1, '1267867': 1, '7273983': 1, '22649747': 2, '24964449': 2}
|
{'3357932-1': 1}
|
163,961 |
3813789-1
| 24,964,437 |
noncomm/PMC003xxxxxx/PMC3813789.xml
|
A delayed presentation of Boerhaave's syndrome with mediastinitis managed using the over-the-scope clip
|
A 69-year-old gentleman presented to hospital following an episode of forceful vomiting and chest discomfort. An initial chest radiograph revealed a left-sided pleural effusion. After several days with no improvement in the patient's condition, it was decided to perform a CT chest, which showed a suspected oesophageal perforation with mediastinitis. Two water-soluble contrast swallows were performed, which showed no leak and thus it was decided to continue to treat the patient conservatively.\nHowever, a subsequent contrast CT scan showed a persistence of the perforation with ongoing mediastinitis (Fig. ). In consideration of the size of the defect and the delay in presentation, it was decided not to perform surgery. An endoscopy revealed a persistent perforation at the lower oesophagus. This was closed successfully using the OTSC. This is demonstrated by a subsequent contrast swallow, showing no leak of contrast with the clip in place (Fig. ). A naso-jejunal tube was inserted at the same time to facilitate post-pyloric feeding. The patient was initially managed with total parenteral nutrition post procedure for 3 days before being fed via an NJ tube. Furthermore, the patient was treated with intravenous antibiotics and bilateral chest drains were inserted. These measures resulted in a successful closure of the defect and resolving mediastinitis. The patient was later discharged from hospital with no further complications. At 6-month follow up, he was clinically well apart from a left-sided small chronic empyema, which was drained.
|
[[69.0, 'year']]
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M
|
{'20226056': 2, '16567897': 1, '19863642': 1, '27633439': 1, '21811949': 1, '21120779': 1, '26788259': 1, '31178585': 1, '28116696': 1, '21424197': 1, '15180177': 1, '27259548': 1, '28750314': 1, '11677490': 1, '17220586': 1, '24964437': 2}
|
{'2847967-1': 1}
|
163,962 |
3813790-1
| 24,964,442 |
noncomm/PMC003xxxxxx/PMC3813790.xml
|
Unicystic ameloblastoma metastasizing to multiple cervical lymph nodes
|
In 2009, a 26-year-old Japanese female patient was referred to our clinic, presenting with radiolucent cystic lesion in the left mandibular region. On oral examination, no swelling appeared to gingiva of the lower left second molar region. Neither paresthesia of the mental region nor palpable lymphadenopathy was observed. Panoramic radiography showed a radiolucent cystic lesion measuring 15 mm in diameter with impacted wisdom tooth (Fig. A). CT revealed a cystic lesion surrounding the crown of the wisdom tooth (Fig. B). Under clinical diagnosis of a dentigerous cyst, enucleation of the cystic lesion and removal of the wisdom tooth were performed (Fig. C). Histopathogical diagnosis was unicystic ameloblastoma (Fig. A and B). The postoperative course was uneventful.\nIn May 2012, this patient complained of a swelling at the left submandibular region of 2 months' duration (Fig. A). Physical examination showed a soft, mobile mass 30 mm in diameter in the submandibular area, and there was no clinical and radiographic sign of recurrence in the left mandibular lesion in the follow-up period (Fig. B). A CT scan with contrast medium showed a bilobed mass-like mucocele compressing the submandibular gland (Fig. C). MRI revealed that the contents of this mass were fluidic. A chest X-ray showed no abnormal finding. The patient underwent extirpation of a cystic mass with the submandibular gland and the associated lymph nodes (Fig. D). The submandibular mass showed a smooth surface covered with this capsule, and its contents was yellowish, transparent, mucinous liquid. The final histopathological diagnosis was consistent with ameloblastoma encapsulated in the mass and encapsulated with two metastatic lymph nodes. The patient had an uneventful postoperative course. In July 2012, the patient received CT scan of the mandible, neck and chest, and all regions were disease-free. The patient was placed on a strict follow-up schedule, with annual CT and chest X-ray. At the follow-up, the patient maintained disease-free.\nMacro- and microscopically, the primary lesion was a typical cystic lesion including an unerupted wisdom tooth. Cyst wall consisted of ameloblastomatous epithelium which was laminated by palisading and nuclear polarized cells without any mitotic features (Fig. A and B). The lesion was diagnosed as a unicystic ameloblastoma, intraluminal type. The submandibular mass was cystic and lymph follicles were seen in the cyst-like wall (Fig. D). The laminated epithelium of cyst wall was ameloblastomatous epithelium similar to that of primary tumor, and presented no atypia and mitotic figures (Fig. E). The ameloblastomatous tumors also were found in the cervical lymph nodes. Cell proliferative analysis of submandibular lesion by Ki-67 immunohistochemical staining, however, indicated obviously high index compared with primary lesion, and the index ratio is <5% in primary lesion but >10% in palisading and nuclear polarized cells of metastatic lesion (Fig. C and F). Therefore, final diagnosis of tumor was metastasizing unicystic ameloblastoma.
|
[[26.0, 'year']]
|
F
|
{'25409848': 1, '4080638': 1, '10468461': 1, '17275258': 1, '8410456': 1, '33394372': 1, '21459020': 1, '19446199': 1, '24964442': 2}
|
{}
|
163,963 |
3813791-1
| 24,964,450 |
noncomm/PMC003xxxxxx/PMC3813791.xml
|
An atypical case of large bowel obstruction
|
A 63-year-old woman self-presented to the emergency department with a week's history of worsening abdominal pain, distension, faeculent vomiting and two days of absolute constipation. She denied any urinary symptoms or previous urinary tract infections. There were no red flag symptoms for colonic malignancy.\nExamination revealed a soft distended abdomen, which was generally tender but more so in the left upper quadrant, with no palpable masses. Obstructive tinkling bowel sounds were heard on auscultation. Rectal examination and other system examinations were unremarkable.\nRoutine bloods were all within normal parameters, including white cells of 8.9, except for a marginally raised CRP of 28. Urinalysis on admission had a trace of protein and one plus of blood. Urine culture revealed no growth.\nAbdominal X-ray confirmed large bowel obstruction with a cut-off point in the proximal descending colon. A large staghorn calculus was evident in the left kidney with a second smaller well-defined area of calcification just lateral to the renal parenchyma. (Fig. )\nConservative management of bowel obstruction was initiated, a nasogastric tube was inserted and the patient was made nil by mouth while intravenous fluids were started.\nA subsequent CT scan confirmed the presence of xanthogranulomatous pyelonephritis and established that the second area of calcification was a 1.5 × 1.0 × 2.5 cm perforated extra-renal fragment of calculus positioned adjacent to the proximal descending colon.\nThis stimulated a diffuse inflammatory response in the left upper quadrant, resulting in a prominent thick-walled proximal descending colon with an abrupt calibre change in the mid descending colon, mesenteric fat stranding, a thickened ileo-psoas muscle with fragments of calculi in the left iliac fossa, gross lymphadenopathy and inflammatory changes around the spleen. (Fig. )\nThe patient's symptoms did not settle with conservative management, and as a result, she underwent an emergency left hemi-colectomy, left nephrectomy and extraction of the fragmented calculi. Recovery was uneventful. Histology confirmed an inflammatory stricture with hypertrophy and fibrosis but no malignancy. Stone analysis interestingly showed a struvite stone. Kidney histology revealed end-stage kidney disease with nephrosclerosis and chronic pyelonephritis. The parenchyma had been replaced with extensive fibro-fatty tissue and chronic inflammatory cell infiltrate with small areas of calcification. It contained thick-walled blood vessels and a few atrophic completely hyalinized renal glomeruli and various-size tubules with cast-like esosinophilic amorphous material. Many non-caseating granulomas were present in the hilar area with most containing a central calcification.
|
[[63.0, 'year']]
|
F
|
{'17324312': 1, '7960533': 1, '22014820': 1, '2354308': 1, '24964450': 2}
|
{}
|
163,964 |
3813796-1
| 24,964,451 |
noncomm/PMC003xxxxxx/PMC3813796.xml
|
Osteoma with cholesteatoma of the external auditory canal: neck manifestation of this rare association
|
A 24-year-old female with Rett syndrome developed recurrent unilateral neck abscesses over a 6-month period.\nRett syndrome is a severe neurodevelopmental disorder characterized by the progressive loss of intellectual functioning, fine and gross motor skills and communicative abilities, deceleration of head growth and the development of stereotypic hand movements, occurring after a period of normal development [].\nAt initial consult, a 2 cm abcess overlying the left mastoid tip and a bony swelling arising from the EAC with overlying normal skin (Fig. ) obstructing the view of the left ear canal and tympanic membrane was noted. Following incision and drainage of the abscess in theatre, the patient returned 2 weeks later with a self-draining left neck wound. As she was otherwise systemically well, the patient was treated as an outpatient with a course of oral antibiotics and listed for excision of the EAC osteoma and exploration of her left mastoid cavity. Due to the patient's global learning disabilities, audiological assessment and imaging of her ears were only possible under general anaesthesia. A combined decision was taken to proceed to surgical exploration, as it was felt that these adjunctive tests will not impact on her immediate management and would subject the patient to an additional anaesthetic challenge.\nAt surgery, transmeatal exicision of the EAC osteoma revealed an underlying cholesteatoma that has caused bony erosion of the inferior canal wall (Fig. ) and formed a fistulous connection to the overlying neck skin (Fig. ). The post-aural sinus and fistula were excised through a post-auricular incision. A cortical mastoidectomy was performed to explore the mastoid cavity, which was found to be disease free. The temporalis fascia was harvested and used to reconstruct the inferior canal wall defect. Histopathologic examination of the excised tissues confirmed the synchronous dual pathology involving the EAC (Figs and ).\nThe patient's symptoms settled after surgery and the neck abscess healed completely. There was no clinically detectable neck disease or cholesteatoma formation in the left ear canal at her 12-month clinic review.
|
[[24.0, 'year']]
|
F
|
{'22115754': 1, '15744157': 1, '30745589': 2, '6717225': 1, '1376388': 1, '8163908': 1, '6638958': 1, '24964451': 2}
|
{'6843583-1': 1}
|
163,965 |
3813797-1
| 24,964,463 |
noncomm/PMC003xxxxxx/PMC3813797.xml
|
Stable construction of the sternum after broad radical resection of malignant tumours
|
A 60-year-old male patient presented himself to the outpatient clinic of our department with a progressive sternal mass. An MRI scan indicated a tumour involving the manubrium extending to the first and second ribs and involving the right clavicle and sternoclavicular joint (Figs and ). Based on radiological evaluation, a core biopsy was obtained and a low-grade chondrosarcoma was characterized. Radiological evaluation indicated primary tumour resection to be the treatment of choice. Radical excision of the tumour was performed and resulted in resection of the manubrium, as well as the medial third of the right clavicle and the right first and second ribs. Steel wires through the sternum and left sternoclavicular joint spanned the 6.5 cm sternal defect (Figs and ) and a polypropylene mesh filled with methyl methacrylate composite (Surgical Simplex®), Howmedica Osteonics, Limerick, Ireland, was placed, yielding a stable reconstruction of the sternal defect (Figs –). The sternocleidomatoideus muscle was re-inserted to the polypropylene mesh. Pathological examination showed complete excision of the tumour. The patient recovered uneventfully and was discharged 7 days post-operatively. At seven year follow-up, the patient displayed excellent functional and aesthetic results. Optimal function of his shoulders allowed a complete return to work and other activities without disabilities.
|
[[60.0, 'year']]
|
M
|
{'3713261': 1, '11343936': 1, '17670403': 1, '21243569': 1, '16368380': 1, '17656168': 1, '9240298': 1, '12052759': 1, '14566281': 1, '23440949': 2, '24964463': 2}
|
{'3573561-1': 1}
|
163,966 |
3813824-1
| 24,963,899 |
noncomm/PMC003xxxxxx/PMC3813824.xml
|
Amyand's hernia: a rare inguinal hernia
|
A 61-year-old African-American male was seen in the surgery clinic with a 6-year history of an umbilical and enlarging right inguinal hernia. The umbilical hernia was symptomatic causing intermittent discomfort. The right inguinal hernia was also symptomatic and had progressively enlarged over time. He denied any changes in bowel habits or history of intestinal obstruction.\nOn physical examination, his abdomen was soft, non-tender and non-distended. A small supra-umbilical tender bulge was present and incarcerated. An inguinal examination was significant for a right-sided, tender, reducible mass without scrotal involvement.\nOn the day of surgery, the patient was prepped, and draped in an aseptic technique. Initially, the umbilical hernia was repaired primarily without complication. The right inguinal hernia repair was approached with a 5 cm right-sided oblique incision parallel to the inguinal ligament. Subcutaneous tissue through Scarpa's fascia was divided until aponeurotic fibers of the external oblique were visualized. After dividing the external oblique to the superficial inguinal ring, the contents of the inguinal canal were then circumscribed using blunt dissection. The hernia sac lateral to the inferior epigastric pedicle was dissected away from the spermatic cord to the deep inguinal ring. The sac was opened illustrating the cecum and vermiform appendix (Fig. ). There were no inflammatory changes of the appendix or cecum. The sac contents were reduced into the peritoneal cavity. The hernia sac was excised and the peritoneum was suture ligated. We performed a tension-free polypropylene mesh repair. The patient was discharged the same day. He returned to clinic 1 month later with no complications and no recurrence of his hernias.
|
[[61.0, 'year']]
|
M
|
{'21929777': 2, '18186392': 1, '30131920': 2, '19918306': 1, '18214637': 1, '34234944': 2, '28432931': 1, '25941568': 1, '32934789': 2, '30886693': 2, '21292218': 1, '24963899': 2}
|
{'6101460-1': 1, '8257258-1': 1, '3185278-1': 1, '3185278-2': 1, '3185278-3': 1, '3185278-4': 1, '6413376-1': 1, '7479644-1': 1}
|
163,967 |
3814545-1
| 24,228,207 |
noncomm/PMC003xxxxxx/PMC3814545.xml
|
Acquired Arteriovenous Fistula of the Breast Following Ultrasound Guided Biopsy of Invasive Ductal Carcinoma
|
A 58-year-old female presented for her annual screening mammogram. At that time, a new mass was identified in the right breast at 9 o’clock, middle depth region. Targeted ultrasound showed a 1.7 cm × 1.4 cm × 1.3 cm irregular hypoechoic mass to correlate with the mammographic abnormality. Ultrasound guided biopsy of the right breast mass was subsequently performed with a 14 gauge vacuum assisted biopsy device. At the time of biopsy, a significant amount of bleeding was noted after the final core biopsy. Bleeding was controlled with manual compression. A marker clip was placed. Post-procedure mammograms demonstrated a large hematoma at the biopsy site with the marker clip associated with the mass. Pathology results showed this mass represented invasive ductal carcinoma. Subsequent magnetic resonance imaging (MRI) demonstrated a new round enhancing mass with rapid wash-in and rapid wash-out characteristics. The mass measuring 0.8 cm × 0.8 cm was seen at the site of biopsy adjacent to the enhancing known cancer that measured up to 2.1 cm []. Large vessels were seen coursing to and from the new arterially enhancing mass []. Clinical examination revealed a new pulsatile mass within the right breast.\nUltrasound examination of the breast was performed to evaluate the new suspected vascular mass. A vascular mass was seen adjacent to the known carcinoma within a region of hematoma and measured 0.9 cm × 0.8 cm × 0.6 cm []. Two large vessels were seen in continuity with this vascular mass. A high velocity flow, low resistance Doppler wave form was seen in the mass consistent with an AVF []. Arterialization of the draining vein was also noted []. The vascular mass and adjacent known neoplasm were excised using intraoperative ultrasound. The pathology demonstrated invasive ductal carcinoma adjacent to a vascular lesion.
|
[[58.0, 'year']]
|
F
|
{'19277831': 1, '15009046': 1, '10976242': 1, '19843763': 1, '15326053': 1, '24228207': 2}
|
{}
|
163,968 |
3814568-1
| 24,223,389 |
noncomm/PMC003xxxxxx/PMC3814568.xml
|
A rare case of laryngotracheal chondrosarcoma in a patient with past history of radioiodine therapy for thyroid cancer
|
A 74-year-old male patient suffered from progressive dyspnea, hoarseness, and stridor over a period of a few months prior to preoperative assessment. He had a total thyroidectomy and was treated with 3,700 MBq (100 mCi) of radioactive iodine following thyroidectomy due to thyroid papillary carcinoma. Computed tomography (CT) scan and fiberoptic bronchoscopy were performed with suspicion of recurrent papillary carcinoma in cricoid cartilage and trachea. There was a mass in the left side of the subglotic area with intact mucosa []. After exploration of the neck via a collar incision, a mass on the left side proximal to the trachea and cricoid cartilage with involvement of left recurrent nerve was discovered. Proximal trachea, in addition to the left half of cricoid cartilage, was resected.\nIn order to reconstruct the airway, the trachea was cut in the shape of the letter L. So, the left and longer side of the trachea was sutured to the thyroid cartilage and the short right side to right half of the cricoid cartilage. Fiberoptic bronchoscopy was used for airway assessment and the patient was put on orotracheal intubation for 48 h. After extubation 48 h later, good phonation was observed in the patient without any respiratory problems. The patient was discharged from the hospital without any complications. In gross pathologic examination, the specimen consisted of a fragment of trachea measuring 4 × 3 × 2 cm that in cut section showed a polypoid mass in the inner wall with chondroid consistency and gray color. Microscopically, the sections revealed neoplastic proliferation of chondrocytes in a pale, basophilic, hyaline chondroid matrix. The chondrocytes showed increased nuclear-to-cytoplasmic ratios, irregular nuclear membranes, and nucleoli. Mitotic activity was scant, but cellularity was markedly increased and several chondrocytes were seen on a single lacuna, indicating low-grade chondrosarcoma [].
|
[[74.0, 'year']]
|
M
|
{'11302261': 1, '704818': 1, '20709656': 1, '19729547': 1, '3893893': 1, '25510635': 1, '14688730': 1, '27402094': 2, '1120013': 1, '9702546': 1, '3059736': 1, '15998893': 1, '28756568': 2, '24223389': 2}
|
{'4939552-1': 1, '5599471-1': 1}
|
163,969 |
3814656-1
| 24,228,067 |
noncomm/PMC003xxxxxx/PMC3814656.xml
|
Bone marrow elements in cerebrospinal fluid: Review of literature with a case study
|
A 16-year-old female patient presented with a sudden onset headache, photophobia, left lower leg weakness and jerking movements of upper and lower limbs. Meningitis was queried clinically. She had no past medical history and both chest X-ray and computed topography scan were normal. A lumbar puncture (LP) was performed and CSF for cytology was collected into two tubes. The first tube had 0.5 ml of clear colorless fluid and the second tube had 0.3 ml of slightly blood-tinged fluid. Two cytospin slides were prepared from each of the tubes and stained with both Papanicolaou stain and a Romanowsky-based stain for examination.\nBoth specimens show similar findings, with the second specimen more cellular than the first specimen. The specimen contains myeloid and erythroid precursors at various stages of maturation together with occasional lymphocytes and monocytes []. Myeloid precursors such as promyelocyte, myelocyte and metamyelocyte are seen in . No megakaryocytes are seen. On review by the cytopathologist, the diagnosis of bone marrow elements as contaminants in the CSF was suggested.\nThe CSF was reported as non-diagnostic as it contains predominantly bone marrow elements, which are indicative of sampling error and as such, an unsuitable specimen for accurate assessment. Correlation with microbiology and hematology studies was recommended. Subsequent microbiology studies showed decreased leucocyte count (<1 × 106/l) and no growth in blood culture. Hematology studies were within normal limits despite the slight increase in neutrophils and a slight decrease in lymphocytes, red blood cell count and hemoglobin and hematocrit value. Patient was discharged subsequently.\nMost CSF specimens are obtained from the subarachnoid space by LP.[] The cutting Quincke needle remains the most commonly used needle for LP despite the introduction of the non-cutting atraumatic needle that decreases the incidences of post LP headache.[] Wright et al.,[] details the stepwise procedure for CSF collection, from the preferable lateral recumbent position that the patient assumes, the use of the L4 vertebra to locate the L3-L4 or L4-L5 intervertebral spaces,[] insertion of an LP needle, indication of successful needle entry into the subarachnoid space and assessment of CSF flow. Needle repositioning is indicated if the attempt is unsuccessful such as when the needle strikes bone or when the patient experiences a shooting leg pain, which indicates overly lateral needle placement touching the lateral nerve root. The needle is withdrawn slightly, re-angled and advanced gently until a gap is found.[] Multiple attempts at different sites during the procedure are discouraged, but when needed, the use of muscle relaxants such as a low dose benzodiazepine may aid in minimizing risk of muscle spasms.[] CSF collected from a traumatic LP will be tinged with blood, which should disappear with serial collections.[]\nNormal CSF, collected from an adult who does not have a neurologic disorder, seizures or undergoing myelography, has low cellularity containing less than 5 cells/mm3.[] These cells consist of small numbers of mature lymphocytes, monocytes and occasional neutrophils. Other non-neoplastic cellular elements that may be seen in CSF include squamous cells, chondrocytes, meningothelial cells, brain fragments, choroidal cells, ependymal cells and hemopoietic elements from bone marrow or peripheral blood.[] Germinal matrix cells and notochord remnants may also be seen in newborns.[] Most of the above mentioned cells are easily recognizable. Bone marrow and peripheral blood elements however require discernment when deciding if a specimen is representative of the area sampled. Bone marrow contamination in particular is rare and may be misinterpreted or overlooked due to inexperience.\nThe sole cytological diagnostic criterion for bone marrow elements in CSF is the presence of erthyroid precursors, for example a normoblast, together with myeloid precursors.[] Megakaryocytes may be helpful and have been seen in some cases.[] When unnoticed, bone marrow elements may become a pitfall for CNS infection such as bacterial or viral meningitis or hematological malignancies including acute leukemia or lymphoma.[]\nIncreased cellularity of CSF due to bone marrow elements presents an abnormal CSF picture and has many differential diagnoses. It is important to identify these cases and not over diagnose them as lymphomas or leukemia. Bone marrow elements in CSF should not be misdiagnosed as inflammatory infection caused by CNS infection to prevent the unnecessary antibiotic administration. A cytological picture of predominantly polymorphonuclear leukocytes may indicate non-specific mixed inflammation [], bacterial meningitis [], cerebral abscess and empyema, CNS hemorrhage and infarction or occasionally the early stages of viral and fungal infection.[] Immune response caused by malignant processes may present a similar picture [].[] Other infective differential diagnoses include mycobacterial tuberculosis and viral meningoencephalitis in which the CSF contains predominantly lymphocytes and monocytes [].[] The presence of myeloid and lymphoid precursors may suggest CNS involvement by acute leukemia [], lymphoma [] or contamination by peripheral blood with abnormal blasts [].[] Increased numbers of red blood cells may also result in misdiagnosis of a traumatic tap [].\nBone marrow-contaminated CSF submitted for hematological review may result in abnormal white cell counts, unusual differential counts and occasional erroneous diagnosis.[] Therefore, correlation with microbiological, biochemical and cytological results is important for the assessment of CSF. Negative cultures for virus, fungal, tuberculosis and bacteria exclude the possibility of an infection. The lack of malignant cells together with a combination of low total protein (<45 mg/dl), high glucose (above 45 mg/dl) and normal total cell count has a high negative predictive value, eliminating the possibility of a malignant process.[] The presence of bone marrow elements cytologically highlights the possibility that the abnormal white blood cell population could be benign hemopoietic elements.\nThe common explanation for having bone marrow elements in a CSF is when the LP needle is pushed too far anteriorly into the marrow cavity of a vertebral body sampling bone marrow elements. The cells adhere to the needle barrel and are subsequently flushed out together with the flow of CSF after the needle is successfully repositioned.[] McIntyre[] suggested an alternate situation where the tip of the needle gets embedded in the bone marrow and cells are aspirated into the needle by very high vacuum forces generated when the stylet is withdrawn rapidly. CSF specimen containing bone marrow elements previously reported were most often from elderly or infant and young patients whereby decreased bone density resulting from geriatric conditions, metastatic diseases or developing bones may have allowed easier penetration of vertebral bone by the LP needle.[]\nIt is rare to see bone marrow elements in CSF because the vertebral body is avoided during the LP to reduce patient discomfort and ensure good CSF collection flow.[] Experienced neurologists and imaging aids play a great role in improving accuracy and efficiency of CSF collection.[] Improved knowledge of nutrition and ideal dietary habits aid in prevention and treatment of bone conditions such as osteoporosis, reducing the likelihood of needle penetration of the vertebral body. There may also be cases that have been overlooked or misinterpreted by cytotechnologists and pathologists.
|
[[16.0, 'year']]
|
F
|
{'6828109': 1, '19131853': 1, '22278331': 1, '6694022': 1, '11039963': 1, '17349909': 1, '17952285': 1, '2014779': 1, '6877306': 1, '22205758': 1, '24228067': 2}
|
{}
|
163,970 |
3814668-1
| 24,205,479 |
noncomm/PMC003xxxxxx/PMC3814668.xml
|
The use of mandibular body distraction in hemifacial microsomia
|
A 12-year-old girl presented with grade IIb right-sided hemifacial microsomia. She had already undergone right ear reconstruction for microtia and maxillary driven simultaneous maxillomandibular distraction[] [].\nWe initially performed a computer-simulated surgery using image processing software (Mimics, Materialise NV, Leuven, Belgium) and a substance model (Kezulex, Ono and Co., Ltd, Tokyo, Japan) as a preoperative simulation. We planned the osteotomy lines to avoid damaging the nerve pathway. The simulation of surgery indicated that mandibular body on the affected side should be distracted 15 mm to the anterior and 10 mm inferiorly to improve facial symmetry. We proceeded with the surgery based on simulation [].\nThe procedure was performed under general anesthesia with nasotracheal intubation. Incisions were made along the mandibular rim and at the base of gingivolabial groove of canine tooth on right side to canine tooth on left side. Mucoperiosteal detachment was performed from the chin region to mandibular body while avoiding damage to mentonian nerve. The muscle insertion on the mandible's internal cortical bone was preserved to ensure vascularization of osteotomized segment, thus retaining effective traction of genioglossus muscle.\nFollowing these incisions, an osteotomy was performed according to preoperative simulation. Thereafter, two sets of the three-dimensional NAVID system were fixed to ramus and free mandible on the affected side. The front of the system was equipped with a distraction vector in inferior direction, and the rear of the system was equipped with a distraction vector in anterior direction []. The rods of the system were inserted through a small skin incision at the mentum, and hinge plate was attached on unaffected side and served as a pivot point for rotation. The wound was then closed.\nAfter 7 days, the distraction was initiated at a rate of 1 mm per day. This process was continued until desired clinical endpoints were achieved; the process is summarized in . As the distraction continued, there was a change in the angle at which two devices crossed and free mandible extended towards the anterior direction and inferiorly because neck of NAVID system could move in three dimensions. Towards the end of distraction period, we performed a 15 mm distraction with frontal device and a 22 mm distraction with rear device.\nWhen the distraction was completed, externally exposed rods were cut in very close proximity to the skin. After a 3-month consolidation period, the devices were removed under general anesthesia. Both the intraoperative view and preoperative computed tomography (CT) image indicated presence of osteogenesis, and showed a symmetrical improvement of mandibular contour compared with preoperative profile [].
|
[[12.0, 'year']]
|
F
|
{'16256360': 1, '21195627': 1, '27104097': 1, '17448668': 1, '16641721': 1, '19447635': 1, '24205479': 2}
|
{}
|
163,971 |
3814669-1
| 24,205,480 |
noncomm/PMC003xxxxxx/PMC3814669.xml
|
Parotid fistula from transparotid approach for mandibular subcondylar fracture reduction
|
A 24-year-old otherwise healthy male patient reported with the chief complaint of watery discharge from a swelling on the right side of the face for the past 1 month. Patient had a history of mandibular condylar fracture from a road traffic accident, for which he was treated elsewhere with direct open reduction and internal fixation of the condyle. The surgical scar was observed on the post-ramus swelling, and there was fistula in one end of the scar that was about 0.5 cm in diameter [Figures and ]. The wound was 2 cm deep and had a healthy granulating margin with no obvious clinical signs of infection, but the wound continued to have a drain of a copious amount of clear, watery, and odorless fluid.\nOn examination of parotid papillae, intraorally, active secretion was present on the left side, but not on the right side. Neurological examination revealed no motor loss due to severance of any branch of facial nerve in the affected side. Location of the fistula and nature of the discharge suggested a laceration of the right parotid gland substance resulting in a sialocele and a right parotid fistula formation. Siaologram confirmed the clinical suspicion [Figures –].\nIn the present case, trauma in the parotid glandular substance lead to formation of sialocele by accumulation of extravasated saliva into glandular parenchyma. It was decided to create a controlled internal fistula with drainage intraorally under local anesthesia. After standard preparation, intraorally, a 1-cm long incision was placed on external oblique ridge behind the third molar. A small artery forceps was forced through the superficial fascia of masseter reaching the sialocele. With the help of this forceps, approximately 5-cm long, slender, sterile, punched plastic tube of diameter 4 mm was positioned with one end in the glandular substance and the other end in the mouth, seated along the vestibule, ensuring complete convenience. The tube was secured by suturing it to the mucosal surface of the cheek []. Extraorally, the wound was sutured primarily in layers, followed by compression dressing on the cheek. The patient was covered with Ciprofloxacin and Metronidazole for 5 days to prevent superadded infections. Saliva stopped draining by 10th postoperative day of surgery. The tube was subsequently removed to enable the internal fistula to close and salivary secretions to drain through the right Stenson's duct normally. The patient's recovery was uncomplicated and follow-up was done for 5 months and lost to follow-up.
|
[[24.0, 'year']]
|
M
|
{'21346080': 1, '2910210': 1, '28356695': 2, '22639509': 2, '29925226': 2, '15620776': 1, '32855935': 1, '19147260': 1, '24205480': 2}
|
{'5357935-1': 1, '3343397-1': 1, '3343397-2': 1, '6057129-1': 1}
|
163,972 |
3814671-1
| 24,205,482 |
noncomm/PMC003xxxxxx/PMC3814671.xml
|
Primary peripheral primitive neuroectodermal tumor of the mandible
|
A 22-year-old female presented with a complaint of insidious onset painless swelling in the left side of the face which had increased in size over 4 months. Clinical examination revealed a firm, well-circumscribed swelling measuring 7 × 7 cm in the left parotid region with numbness in the chin region []. The angle of the mandible was widened by the tumor resulting in a left-sided intraoral bulge. Otorhinolaryngological findings were otherwise normal; there was no evidence of cervical lymphadenopathy or any systemic symptoms.\nComputed tomography (CT) revealed a heterodense mass lesion measuring 8 × 7 cm at its greatest dimension causing bony destruction of the ascending mandibular ramus and with extension into the skull base. The tumor caused effacement of the fat and muscle planes of the infratemporal fossa and the masticator spaces. It was seen pushing the parotid space laterally and the parapharyngeal space medially. The left temporomandibular joint was obliterated by the tumor [–]. A bone scintigram showed an increased abnormal activity in the left side of mandible corresponding to the tumor []. A bone marrow aspiration and a bone marrow biopsy were within normal limits. An extraoral trucut biopsy from the tumor on histopathologic examination revealed a diffused collection of small malignant round to oval cells with hyperchromatic nuclei, inconspicuous nucleoli, with vacuolated to pale cytoplasm and high mitotic activity, and scattered blood vessels with peritheliomatous arrangements of the tumor cells. The tumor cells on immunohistochemistry were positive for vimentin, CD99, Bcl2, chromogranin, and S-100. It was negative for keratin, LCA, CD3, CD 20, CD56, and Alk 1. Fifty percentage of the tumor cells showed strong nuclear positivity to Ki-67. The histopathology along with immunohistochemistry correlation favored a diagnosis of PNET of the mandible [–].\nThe patient was planned for a multimodality treatment. She initially received four cycles of vincristine, adriamycin, cyclophosphamide alternating with ifosfamide and etoposide (VAC/IE) based chemotherapy. In view of the extensive soft tissue involvement, she was initially considered for external beam radiotherapy as a part of her local therapy. A static response was noted after 54 Grey (Gy) of radiotherapy, which was confirmed on a subsequent CT of the mandible which showed a necrotic residue with patchy contrast uptake. She was subsequently taken for a definitive surgery after the sixth cycle of chemotherapy. En bloc excision of the tumor along with a posterior segmental mandibulectomy from the level of left first molar to left condyle and left temporomandibular joint was done [–]. An ‘L’ shaped reconstruction plate was anchored to the zygoma and the remnant mandible to bridge the bony defect, soft tissue cover was achieved by an anterolateral thigh free flap. [Figures and ] The postoperative histopathology revealed no viable tumor and a 100% tumor necrosis. She further went on to complete her further courses of chemotherapy and is presently disease free.
|
[[22.0, 'year']]
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F
|
{'11904342': 1, '16094594': 1, '12696243': 1, '28438883': 1, '16243245': 1, '17711755': 1, '12242143': 1, '11679946': 1, '12594313': 1, '12784241': 1, '24205482': 2}
|
{}
|
163,973 |
3814672-1
| 24,205,483 |
noncomm/PMC003xxxxxx/PMC3814672.xml
|
Pleomorphic adenoma palate: Major tumor in a minor gland
|
A 45-year-old female presented with a slow growing swelling, of approximately 20 years duration involving her hard and soft palate junction on the left side, which was peanut sized when she first observed. The lesion always had been asymptomatic, with no associated pain or paresthesia. The patient's medical history was noncontributory. She had no known allergies and had not undergone any surgeries of head and neck. She had no complaints of pharyngeal or airway obstruction. General physical examination revealed a well oriented and moderately built individual with no signs of any systemic illness. The patient presented a typical ‘hot potato in mouth’ speech. The clinical examination revealed nonulcerated, dome-shaped, palatal swelling on her hard and soft palate junction, crossing the midline []. The mass had a bosselated surface and overlying mucosa was cherry red and stretched. The lesion was multinodular, firm, and nontender on palpation. Magnetic resonance imaging (MRI) report revealed a well-defined, multilobulated mass measuring 3.2 × 5.5 × 6.3 cm Antero-Posterior × Transverse × Cranio-Caudal (AP × TR × CC) and is hypointense on T1W1 and heterogeneously hyperintense on T2W1 with multiple well-defined areas of low cellularity within. The mass had well-enhanced soft tissue density without any invasion to adjacent tissues, displacing posterior third of the tongue downward [].\nFNA biopsy was performed, which was suggestive of PA. All preoperative blood and urine investigations were done, which were within normal limits. The patient was intubated through endotracheal tube by fiber-optic guidance and was operated for wide local excision of the mass and primary closure of adjacent mucosa. The excised mass was 7 × 6 cm []. Following excision of tumor, surgical wound [] was closed in layers in a tension-free water tight fashion []. The excised mass was sent for histopathological examination, which revealed stratified squamous epithelium covering connective tissue and underlying connective tissue showed the cells arranged in sheets and duct-like pattern with a mucoid background []. This was confirmatory of PA. The specimen was weighed 95g []. The patient's postoperative course was uneventful. The healing was satisfactory. No recurrence was observed after a follow-up period of 1 year [].
|
[[45.0, 'year']]
|
F
|
{'22754859': 1, '22484885': 1, '15968569': 1, '15787647': 1, '29963438': 2, '31183288': 2, '29808148': 2, '29038635': 1, '22532914': 1, '19926180': 1, '16540285': 1, '11127155': 1, '17577550': 1, '24205483': 2}
|
{'6018296-1': 1, '6538108-1': 1, '5902113-1': 1}
|
163,974 |
3814812-1
| 24,223,378 |
noncomm/PMC003xxxxxx/PMC3814812.xml
|
Awake craniotomy for tumor resection
|
A 56-year-old female patient with weighing 46 kg with left-sided body hyposthesia since last 3 months was operated under craniotomy for brain tumor resection. Anatomical location was in the right parietal lobe. On perioperative evaluation, airway was normal, mallampati was class I, and neck movement was within normal limits and didn’t have any abnormal anatomical picture and no movement restriction in jaw joints. Heart and lung examination were normal. Patient GCS (Glasgow Coma Scale) was 15/15 and examination of cranial nerves was normal. Laboratory studies, including CBC (complete blood count), BUN (Blood Urea Nitrogen), Cr, Na, K, BS, PT (Prothrombin time), PTT (Partial thromboplastin time), INR (International Normalized. Ratio), were normal and her blood group was A+. Any abnormality couldn’t be seen on the chest radiography.
|
[[56.0, 'year']]
|
F
|
{'20977126': 1, '16368836': 1, '10413153': 1, '17620841': 1, '20118799': 1, '17549277': 1, '11133607': 1, '17303322': 1, '19560738': 1, '10671844': 1, '11426102': 1, '16374563': 1, '9632190': 1, '10830329': 1, '12538371': 1, '17549278': 1, '18289443': 1, '24223378': 2}
|
{'3814812-2': 2}
|
163,975 |
3814812-2
| 24,223,378 |
noncomm/PMC003xxxxxx/PMC3814812.xml
|
Awake craniotomy for tumor resection
|
A 25-year-old female patient weighing 49 kg had severe headache of 1 month duration. Examination of cranial nerves and sensorimotor function of the limbs were normal. On perioperative evaluation, the airway was normal, mallampati was class I, and neck movement was within normal limits. She didn’t have any abnormal anatomical picture or no restriction in jaw joints’ movement. Heart and lung examination were normal. Patient's GCS was 15/15 and cranial nerves examinations were normal. Laboratory studies, including CBC, BUN, Cr, Na, K, BS, PT, PTT, INR, were normal and her blood group A+. Any abnormality couldn’t be seen on the chest radiography.\nWhen the patients were visited in preoperative anesthesia clinic being awake during surgery, type of anesthesia, surgery and the need of patient cooperation was described for them even if it was hard for them. Without prescription of premedication, we got electrocardiogram, pulse oximetery, non-invasive blood pressure NIBP. Under regional anesthesia, we got arterial line for continuous checking of blood pressure. Then we started invasive blood pressure IBP monitoring, and catheterized their bladder. Before starting sensory nerve block, first 1 micg/kg fentanyl and then 25 mg propofol was injected. Scalp nerves block include supraorbital, supra-auricular, lesser and greater occipital with 0.5% marcaine plus epinephrine 1/200,000 was done. The area that pins fixed head separately was infiltrated by lidocaine 2%. Continuous CO2 sampling via nasal canola was done. Oxygen 6 L/min was established through a face mask. To avoid fatigue and discomfort, shoulders, arms, and lower extremities were supported through pillows. Then, continuous intravenous infusion of remifentanil 0.3 micg/kg was started. For sedation, a bolus dose of propofol 1 mg/kg was infused and continued by infusion at 30 micg/kg/min. We didn’t carry out monitoring of bispecteral index due to proximity to the surgical side and the need to sterilize skin on the forehead. During the surgery, systolic BP of 56-year-old patient at 110-150 mmHg and 25-year-old patient at 100-130 mmHg was retained. Respiration in 56-year-old patient at 10-15/min and 25-year-old patient at 9-15/min was retained. In both the patients, ET CO2 was maintained at 32-40 mmHg and during surgery, pulse oximetery was maintained at 97-100%. During surgery, for removing lesion, the patients were awake and obeyed the surgeon's commands and moved their limbs and fingers. After removal of the lesion, the patient was asleep, dura matter was sutured. The bone of head was placed and scalp was sutured. The patients, after removing the fixative pin of head slowly woke up, without any unexpected problem.
|
[[25.0, 'year']]
|
F
|
{'20977126': 1, '16368836': 1, '10413153': 1, '17620841': 1, '20118799': 1, '17549277': 1, '11133607': 1, '17303322': 1, '19560738': 1, '10671844': 1, '11426102': 1, '16374563': 1, '9632190': 1, '10830329': 1, '12538371': 1, '17549278': 1, '18289443': 1, '24223378': 2}
|
{'3814812-1': 2}
|
163,976 |
3814902-1
| 24,228,208 |
noncomm/PMC003xxxxxx/PMC3814902.xml
|
Adenoid Cystic Carcinoma of the Upper Trachea: A Rare Neoplasm
|
A 42-year-old male patient presents with a 6-month history of dyspnea. General physical examination did not reveal any significant abnormality. He had no history of smoking. The hematological and biochemical profile were essentially normal. Chest radiograph was within normal limits. Plain lateral radiograph of the neck revealed a broad-based polypoidal mass arising from the posterior wall of the proximal trachea []. Bronchoscopy confirmed the neoplasm. Histopatholgical examination of the mass confirmed it to be an ACC []. Patient suddenly developed severe respiratory distress and change of voice for which emergency tracheostomy was performed. CT and MRI were advised for treatment planning. MDCT [Figures and ] revealed a broad-based polypoidal soft tissue mass arising from the posterior wall of the proximal end of the trachea just below the cricoid cartilage and extending to involve the subglottis resulting in near total luminal obstruction. The tracheal mass eroded the tracheal cartilage and was abutting the right lobe of the thyroid. MRI [Figures and ] confirmed almost similar findings like CT. Metastatic work up which included CT thorax, abdominal ultrasound, and bone scan were normal. Surgical resection of the tumor was planned. Because of laryngeal extension, total laryngectomy and end-tracheostomy was performed in addition to resection of the tracheal segment. Histopathological examination of the surgical specimen confirmed the diagnosis of ACC. The patient also received external beam radiation therapy following surgery. The patient was on regular follow-up after the treatment. Follow-up of the patient after 18 months post-treatment did not reveal local recurrence or distant metastases.
|
[[42.0, 'year']]
|
M
|
{'15269011': 1, '34703477': 1, '27890995': 2, '19357541': 1, '26677161': 1, '21907453': 1, '8975844': 1, '25589527': 1, '16086551': 1, '2153371': 1, '25550788': 1, '33415039': 2, '29456738': 1, '27386036': 1, '18594327': 1, '12797606': 1, '10388015': 1, '24228208': 2}
|
{'5112823-1': 1, '5112823-2': 1, '7781776-1': 1}
|
163,977 |
3814994-1
| 24,232,072 |
noncomm/PMC003xxxxxx/PMC3814994.xml
|
Intracranial bleeding following induction of anesthesia in a patient undergoing elective surgery for refractory epilepsy
|
The patient was a 47-year-old male with hypertension who was diagnosed with multi drug-resistant Left (L) temporal lobe seizures secondary to (L) mesial temporal sclerosis. His seizure had started at the age of 35 years. The seizure semiology was that of a complex partial seizure with secondary generalization. Electroencephalography (EEG) revealed the seizures to be originating from the (L) temporal lobe. A Video EEG further confirmed the (L) temporal seizure focus and was concordant with the previous EEG and imaging features. He was investigated with a magnetic resonance image of the brain, which revealed evidence of mesial temporal sclerosis of the (L) temporal lobe. Patient was then submitted for neuropsychological evaluation and found to be suitable for epilepsy surgery. He was admitted for an elective anterior temporal lobectomy with amygdalo-hippocampectomy. The preoperative imaging done did not reveal evidence of any other underlying abnormality in the brain besides the mesial temporal sclerosis.\nPatient was admitted electively for his surgery. During the preoperative evaluation he was found to be well with a controlled blood pressure of 130/80 on a single oral antihypertensive medication. Just prior to induction, his blood pressure was noted to be 150/100. Patient was subsequently induced using intravenous propofol, fentanyl, and rocuronium. Intubation was then done using an appropriately sized tube. No difficulty was encountered during this procedure. Patient was then maintained on total intravenous anesthesia (TIVA). Blood pressure monitoring revealed that the initial postinduction blood pressure was 180/100, which subsequently was controlled and maintained so throughout the surgery at a range of systolic 170-120 and diastolic 90-60. Patient was subsequently handed over to the neurosurgical team.\nFollowing craniotomy, it was noted that the dura and underlying brain was very tense. Upon durotomy, the brain bulged out and there was evidence of subarachnoid hemorrhage seen over the cortical surface. A transcortical approach was attempted via the medial temporal gyrus. During corticectomy, an intraparenchymal clot was encountered. The clot was evacuated and subsequently a left selective amygdalo-hippocampectomy was performed [Figure -].\nIn the immediate postoperative patient was kept ventilated and sedated. A computed tomographic (CT) scan of his brain revealed the presence of a small residual temporoparietal intraparenchymal clot as well as bleeding with the subarachnoid space especially in the region of the left sylvian fissure []. CT Angiography as well as digital subtraction angiography was done and revealed no evidence of any underlying vascular lesion that might be the source of intraparenchymal bleeding that was noted intraoperatively. This patient's postoperative course was complicated with hydrocephalus with ventriculitis as well as nosocomial pneumonia. Despite aggressive therapy he succumbed to widespread infection about one month postoperatively.
|
[[47.0, 'year']]
|
M
|
{'29379392': 1, '5453244': 1, '5550843': 1, '24232072': 2}
|
{}
|
163,978 |
3814995-1
| 24,232,171 |
noncomm/PMC003xxxxxx/PMC3814995.xml
|
Posterior reversible encephalopathy syndrome in a patient with a Chiari I malformation
|
A 25-year-old right handed female initially presented with complaints of left upper and lower extremity paresthesias and gait disturbance as well as nausea and vomiting. Her symptoms had progressed for a few months prior to admission. Her initial workup included an MRI of the brain and cervical spine, which showed a Chiari I malformation with tonsillar descent beyond the level of the C1 lamina and syringomyelia and syringobulbia with dilation throughout the cervical spinal cord and no evidence of hydrocephalus []. On physical exam she was noted to be weak in bilateral upper extremities with 4+/5 motor strength in the right upper extremity and 4-/5 motor strength in the left upper extremity. Bilateral lower extremities were 5/5 strength with the exception of bilateral extensor hallucis longus, which were 4/5. She had brisk patellar reflexes bilaterally and impaired tandem gait.\nShe underwent a suboccipital craniectomy, C1 laminectomy, cerebellar tonsillar cauterization using bipolar cautery, and duraplasty with Gore-Tex dural substitute. Intraoperative somatosensory evoked potentials (SSEP) and motor evoked potentials (MEP) monitoring demonstrated impaired amplitude in the right lower extremity, with no change following positioning or throughout the operation other than gradual improvement in the right lower extremity MEP during the surgery. Postoperatively she improved to full strength in the right upper extremity and 4+/5 throughout the left upper extremity. She was started on a dexamethasone taper postoperatively as prophylaxis against an inflammatory response given the cerebellar manipulation. Postoperative MRI revealed a suggestion of an acute infarct of the right inferior vermis and otherwise normal postoperative changes []. The MRI findings were attributed to the bipolar cautery of the cerebellar tonsils. She remained in the hospital for 4 days postoperatively for pain control and monitoring of slight postoperative dysphagia and was subsequently discharged to a rehabilitation facility.\nShe was readmitted to the hospital from rehab 6 days after discharge with complaints of worsening of her swallowing. She also noted left sided pain and worsening weakness. At this point her exam had declined from her postoperative exam and motor exam now revealed 3/5 strength in left dorsiflexion and extensor hallucis longus. At the time of readmission, she was normotensive with a blood pressure of 130/70. A swallow evaluation revealed significant aspiration. She underwent an MRI that showed bilateral acute infarcts of the cerebellar vermis []. We did not have a clear explanation for this increase from her postoperative scan. Given the evolution of the infarct she was started on pressors to increase her systolic parameters to 160-180 mmHg and optimize perfusion in the setting of ischemia. Two days after initiating pressors, the patient had a generalized tonic–clonic seizure. A CT of the head at that time demonstrated diffuse loss of sulci with effacement of the suprasellar and quadrigeminal cisterns. She was subsequently intubated for worsening mental status and lethargy. A follow-up MRI revealed diffuse bifrontal and parietal gray matter hyperintensity on FLAIR without changes on diffusion-weighted imaging consistent with PRES and suggestive of edema from hypoxic ischemic changes secondary to prior seizure []. An electroencephalography (EEG) showed no further seizure activity and CSF cultures were negative. She underwent an angiogram to evaluate for vasospasm as a possible etiology of her evolving infarcts, which showed no evidence of vasospasm or vasculitis. Following those results, the pressors were weaned off. A repeat CT of the head was obtained, which showed increasing cerebral edema. As a result of the increasing edema and her compromised neurologic exam, an intracranial pressure (ICP) monitor was placed and maintained for 2 days, which showed low opening pressure, and ICPs ranging from 1 to 7. Follow-up MRIs demonstrated progressive resolution of the cerebral edema and FLAIR signal [] with complete resolution at 2 years postoperative [].\nShe had progressive improvement in her mental status and was extubated. She continued to have swallowing difficulties and underwent serial swallow evaluations, ultimately requiring placement of a percutaneous endogastric tube (PEG). She ultimately improved and had only residual left hand weakness with motor strength 4/5. She was ultimately transferred to rehab. She continued to have significant left upper extremity dysesthesia. At 9-month follow-up, she was noted to have worsening of her syrinx and further descent of her cerebellar tonsils and so she underwent placement of a ventriculoperitoneal shunt.\nAt her latest follow up 4 years postoperatively, her motor exam was 5/5 throughout her right upper extremity, 5/5 in her left deltoid, biceps and triceps and 4/5 left opponens and 3/5 interossei. Both lower extremities were 5/5 strength throughout with a steady gait and impaired tandem gait, significantly improved from prior, though she has a stiff and wide-based spastic gait. She was no longer having any dysphagia, had no bulbar symptoms and her PEG had been removed. Her left upper extremity dysesthesia has significantly improved. Her 4 year follow-up MRI demonstrates resolution of her syringomyelia [].
|
[[25.0, 'year']]
|
F
|
{'26858804': 1, '18356474': 1, '10954269': 1, '7969828': 1, '21732118': 1, '9350407': 1, '22044364': 1, '15290193': 1, '19684634': 1, '11123390': 1, '9536483': 1, '8559202': 1, '7645483': 1, '7968030': 1, '17786004': 1, '6848674': 1, '18854692': 1, '11303661': 1, '9808255': 1, '21492735': 1, '21318395': 1, '11170913': 1, '21806360': 1, '18403560': 1, '9165512': 1, '1882738': 1, '11883849': 1, '7596521': 1, '1632361': 1, '20572911': 1, '6856062': 1, '21590625': 1, '9378600': 1, '2133406': 1, '17110690': 1, '18268188': 1, '17119920': 1, '20890606': 1, '16617001': 1, '9606593': 1, '10232534': 1, '10522914': 1, '24232171': 2}
|
{}
|
163,979 |
3815013-1
| 24,232,309 |
noncomm/PMC003xxxxxx/PMC3815013.xml
|
Intraoperative assessment of spinal vascular flow in the surgery of spinal intramedullary tumors using indocyanine green videoangiography
|
Patient 3: A 42-year-old female was admitted with back pain, gait disturbance, and moderate dysesthesia of right upper extremity. Symptoms were more apparent in the upper extremities than in the lower extremities. Assessment of neurological condition before surgery suggested Grade 3 on the modified McCormick functional schema and Grade 3 on the sensory pain scale. T2-weighted magnetic resonance images (MRIs) of the cervical spine showed local enlargement and intramedullary mixed signal of the spinal cord at C6 []. T2*-weighted gradient-echo MRIs showed mixed low signal within the spinal cord [], which was consistent with blood degradation products. Imaging diagnosis before surgery was intramedullary hemorrhage associated with cavernous malformation.\nThe patient underwent C5 to C7 osteoplastic laminotomy for evacuation of the intramedullary hemorrhage and total resection of the tumor. The spinal cord appeared slightly swollen []. Posterior spinal arteries on both sides were well differentiated from posterior spinal veins and the pial venous plexus []. Venous circulation of posterior spinal veins and the pial venous plexus appeared stagnant []. Crossing veins on the PMS were coagulated with a microbipolar coagulator at very low power levels under continuous saline irrigation. A PMS approach to the spinal cord revealed the intramedullary hemorrhage. Careful dissection within the spinal cord revealed the tumor–cord interface with the surrounding hemosiderin-stained tissue. The tumor was removed segmentally. The surrounding hemosiderin-stained tissue was not resected to avoid the damage of spinal tissue []. Posterior sulcal central veins were well visualized []. The pial edges were sutured together as much as possible to restore the shape of the spinal cord []. Supplemental digital content of surgical was provided.\nT2-weighted MRIs obtained 3 months after surgery showed satisfactory recovery of the intramedullary signal of the spinal cord []. Assessment of neurological condition at 3 months after surgery suggested Grade 2 on the modified McCormick functional schema and Grade 2 on the sensory pain scale.
|
[[42.0, 'year']]
|
F
|
{'12408386': 1, '12956461': 1, '12493110': 1, '15069240': 1, '4294586': 1, '11045198': 1, '986698': 1, '25797779': 1, '20881574': 1, '19687689': 1, '13222169': 1, '26692694': 2, '21590519': 1, '2319309': 1, '847637': 1, '568531': 1, '24172592': 1, '28477043': 1, '26143269': 1, '21841520': 1, '11950409': 1, '20679920': 1, '22914702': 1, '25289155': 1, '10352743': 1, '9932879': 1, '24232309': 2}
|
{'3815013-2': 2, '3815013-3': 2, '4660493-1': 1, '4660493-2': 1}
|
163,980 |
3815013-2
| 24,232,309 |
noncomm/PMC003xxxxxx/PMC3815013.xml
|
Intraoperative assessment of spinal vascular flow in the surgery of spinal intramedullary tumors using indocyanine green videoangiography
|
Patient 12: A 46-year-old female was admitted with severe dysesthetic pain radiating from the posterior neck to the right upper extremity. Assessment of neurological condition before surgery suggested Grade 2 on the modified McCormick functional schema and Grade 3 on the sensory pain scale. T2-weighted MRIs of the cervical spine showed an intramedullary tumor with syrinx formation at C6 []. The tumor was well enhanced on T1-weighted images []. Imaging diagnosis before surgery was intramedullary ependymoma.\nThe patient underwent C5 to C7 osteoplastic laminotomy for evacuation of the intramedullary hemorrhage and total resection of the tumor. The spinal cord appeared slightly swollen []. Posterior spinal arteries on both sides were well differentiated from posterior spinal veins and the pial venous plexus []. Venous circulation of posterior spinal veins and the pial venous plexus was stagnant []. Crossing veins on the PMS were coagulated with a microbipolar coagulator at very low power levels under continuous saline irrigation. A PMS approach to the spinal cord revealed the tumor surface. Careful dissection within the spinal cord revealed the tumor–cord interface with the surrounding gliotic tissue. The tumor was removed in an en bloc fashion. Sulcal central branches of the anterior spinal artery were well preserved [Figure and ]. The surrounding gliotic tissue was not resected to avoid the damage of spinal tissue []. The pial edges were sutured together as much as possible to restore the shape of the spinal cord.\nT2-weighted MRIs obtained 3 months after surgery showed satisfactory recovery of the intramedullary signal of the spinal cord []. Assessment of neurological condition at 3 months after surgery suggested Grade 2 on the modified McCormick functional schema and Grade 2 on the sensory pain scale.
|
[[46.0, 'year']]
|
F
|
{'12408386': 1, '12956461': 1, '12493110': 1, '15069240': 1, '4294586': 1, '11045198': 1, '986698': 1, '25797779': 1, '20881574': 1, '19687689': 1, '13222169': 1, '26692694': 2, '21590519': 1, '2319309': 1, '847637': 1, '568531': 1, '24172592': 1, '28477043': 1, '26143269': 1, '21841520': 1, '11950409': 1, '20679920': 1, '22914702': 1, '25289155': 1, '10352743': 1, '9932879': 1, '24232309': 2}
|
{'3815013-1': 2, '3815013-3': 2, '4660493-1': 1, '4660493-2': 1}
|
163,981 |
3815013-3
| 24,232,309 |
noncomm/PMC003xxxxxx/PMC3815013.xml
|
Intraoperative assessment of spinal vascular flow in the surgery of spinal intramedullary tumors using indocyanine green videoangiography
|
Patient 4: A 17-year-old male was admitted with moderate dysesthetic pain radiating from the posterior neck to the right upper extremity. Assessment of neurological condition before surgery suggested Grade 1 on the modified McCormick functional schema and Grade 3 on the sensory pain scale. T2-weighted MRIs of the cervical spine showed an intramedullary tumor formation at C6/7 accompanying extensive syrinx []. The tumor was enhanced on T1-weighted MRIs []. Imaging diagnosis before surgery was intramedullary hemangioblastoma.\nThe patient underwent C5 to C7 osteoplastic laminotomy for total resection of the tumor. The spinal cord appeared slightly swollen []. Feeding arteries to the tumor were well differentiated from draining veins [], and were intercepted just proximal to the tumor. Blood flow to the tumor decreased during occlusion of feeding arteries []. Thick and cloudy pia mater encircling the tumor was cut sharply to reveal the clear gliosis layer of tumor–cord interface []. The tumor was completely removed in an en bloc fashion under the microscope []. When tumor removal was complete, there was little or no need for further hemostasis. ICG-VA after en bloc complete removal of the tumor revealed no sign of residual tumor and well preserved posterior spinal artery []. The pial edges were sutured together as much as possible to restore the shape of the spinal cord. Supplemental digital content of surgical was provided.\nT2-weighted MRIs obtained 3 months after surgery showed complete resection of the tumor []. Assessment of neurological condition at 3 months after surgery suggested Grade 1 on the modified McCormick functional schema and Grade 1 on the sensory pain scale.
|
[[17.0, 'year']]
|
M
|
{'12408386': 1, '12956461': 1, '12493110': 1, '15069240': 1, '4294586': 1, '11045198': 1, '986698': 1, '25797779': 1, '20881574': 1, '19687689': 1, '13222169': 1, '26692694': 2, '21590519': 1, '2319309': 1, '847637': 1, '568531': 1, '24172592': 1, '28477043': 1, '26143269': 1, '21841520': 1, '11950409': 1, '20679920': 1, '22914702': 1, '25289155': 1, '10352743': 1, '9932879': 1, '24232309': 2}
|
{'3815013-1': 2, '3815013-2': 2, '4660493-1': 1, '4660493-2': 1}
|
163,982 |
3815018-1
| 24,232,386 |
noncomm/PMC003xxxxxx/PMC3815018.xml
|
Bilateral iliopsoas hematoma: Case report and literature review
|
A 63-year-old female presented to the emergency room with acute chest pain, discomfort, and breathing difficulties. A computed tomography (CT) angiogram of the chest revealed a sub-segmental pulmonary embolism in the right lower lung lobe. The patient was subsequently admitted and started on intravenous heparin. She also received a single dose of clopidogrel (Plavix®) at the time of admission. The next day, she was started on warfarin (Coumadin®) 7.5 mg at bedtime with heparin bridging. Partial thromboplastin time was monitored but poorly controlled, showing variations from 29 to 180 seconds over the next several days. Five days later, the patient's International Normalized Ratio reached a therapeutic range at 2.0 and heparin was discontinued. That same day, she began complaining of abdominal and flank pain.\nOn day 7 of hospitalization, the patient developed moderate weakness in the proximal lower extremities. A CT scan of the abdomen was performed and demonstrated large, bilateral iliopsoas muscle hematomas. Magnetic resonance imaging (MRI) of the lumbar spine demonstrated acute hematoma formation in the iliopsoas bilaterally [Figure -]. Neurosurgery was consulted on day 8. On physical examination, the patient was in no apparent distress and stable hemodynamically. She had normal tone, but moderate bilateral proximal lower extremity weakness with 3/5 strength in bilateral iliopsoas and 2/5 strength in quadriceps. Extension of the hip elicited pain in the back and groin. The patient also exhibited hyperalgesia and numbness over the L2-L4 dermatomes, bilaterally.\nConservative management using vitamin K and fresh frozen plasma for Coumadin® reversal was recommended, with the intention of monitoring and following the patient's clinical examination. Over the next 2 days, the patient reported symptomatic improvement of her abdominal pain and thigh numbness, but persistent weakness. On day 11 of hospitalization, it was noted that the patient's strength had deteriorated further with iliopsoas and quadriceps strength of 1/5, bilaterally. Based on this neurological deterioration, she was taken for surgical decompression of the hematomas through bilateral flank incisions. The external oblique muscle and external oblique fascia were transected. The incision was carried down to the internal oblique muscle and preperitoneal space. A longitudinal incision was made over the psoas major muscles and hematoma material of 240 and 220 ml was drained from the right and left compartments, respectively. The femoral nerves were identified and separated from clot material. Despite bipolar stimulation of 1-4 μV to the femoral nerve, no significant electromyography response was elicited.\nBy the third postoperative day, the patient demonstrated marked improvement in strength and near complete resolution of her thigh numbness; both iliopsoas muscles had 4/5 power. The left quadriceps showed 4/5 strength while her right quadriceps remained 0/5. She was then discharged to a rehabilitation facility. Iliopsoas strength remained 4/5 bilaterally at 6-week follow-up. Her left quadriceps improved to 5/5 and her right quadriceps improved to 1/5. At 3- and 6-month follow-up visits, the patient was noted to have full strength in her lower extremities, but experienced continued mild dysesthesias in anterolateral thighs bilaterally.
|
[[63.0, 'year']]
|
F
|
{'4338821': 1, '28536664': 2, '33061676': 2, '1651940': 1, '12904147': 1, '11779099': 1, '25750219': 1, '20012044': 1, '4289644': 1, '4286456': 1, '8358198': 1, '31720283': 2, '17336570': 1, '25572538': 1, '28811743': 2, '30889163': 2, '9000371': 1, '1660685': 1, '32995155': 1, '17342281': 1, '19934129': 1, '24232386': 2}
|
{'6502161-1': 1, '5425841-1': 1, '5425841-2': 1, '6826083-1': 1, '6826083-2': 1, '5542073-1': 1, '7519345-1': 1}
|
163,983 |
3815032-1
| 24,232,572 |
noncomm/PMC003xxxxxx/PMC3815032.xml
|
Regression of cerebellar tonsillar descent and hydrocephalus after endoscopic third ventriculostomy in a patient with a quadrigeminal arachnoid cyst
|
A 28-year-old female presented at our hospital with a 2-year history of headaches. Her headaches, located at occipital and temporal regions, became progressively worse after the delivery of her first child 5 months ago. Her neurological status was intact except for numbness in her left arm, a symptom that appeared after the delivery. Ophthalmoscopy revealed bilateral papilledema. Her medical and family history was unremarkable.\nMagnetic resonance imaging (MRI) revealed marked dilatation of the lateral and third ventricles with downward bowing of the latter's floor; the fourth ventricle was normal. The cyst, which was considered as congenital arachnoid cyst, was located at the quadrigeminal cistern extending caudally into the supracerebellar cistern [Figure and ]. The cyst compressed downward into both the cerebellar vermis and the hemispheres, leading to cerebellar tonsillar descent and Sylvian aqueductal stenosis. However, heavily T2-weighted images revealed a definite discontinuity between the anterior part of the cyst wall and the third ventricle []. Moreover, no syringomyelia in the cervical spinal cord was observed.\nHydrocephalus was believed to have developed as follows: the QCAC extending to the supracerebellar cistern compressed on the cerebellar tonsils, forcing them to move downward and plug the foramen magnum. This in turn blocked the flow of cerebrospinal fluid (CSF) at the fourth ventricle outlet resulting in the accumulation of CSF and hypertensive hydrocephalus.\nAfter induction of general anesthesia, the patient underwent ETV with the use of a fiberscope (VEF-V, Olympus Co.). Endoscopically, the floor of the third ventricle looked very thin, suggesting the existence of a long-standing hypertensive dilatation of the third ventricle. The endoscope was then advanced towards the quadrigeminal cistern, which revealed the cistern was surrounded entirely by a membrane consistent with the membrane of an arachnoid cyst. As shown on the heavily T2-weighted MRI image [], the cyst wall facing the posterior part of the third ventricle was opened widely []. The aqueduct stenosis was easily apparent []. ETV was successfully performed enabling communication between the third ventricle and prepontine cistern.\nHer postoperative course was uneventful, and her headaches, left arm numbness, and bilateral papilledema were completely resolved. A postoperative MRI of the brain at the 12-month follow-up displayed marked reductions in size of the lateral and third ventricles and the quadrigeminal cyst; it also revealed normalization of the cerebellar tonsillar descent, and patency of the stoma was clearly indicated by the flow artifact, which is depicted on the postoperative T2-weighted image in .
|
[[28.0, 'year']]
|
F
|
{'17622461': 1, '21039175': 1, '16724812': 1, '12865864': 1, '10350261': 1, '3715700': 1, '4762818': 1, '19494562': 1, '3748264': 1, '20737274': 1, '20480382': 1, '24232572': 2}
|
{}
|
163,984 |
3815034-1
| 24,232,934 |
noncomm/PMC003xxxxxx/PMC3815034.xml
|
Intraoperative dynamic assessment of the posterior communicating artery and its branches by indocyanine green videoangiography
|
A 42-year-old female presented with Hunt and Hess grade IV subarachnoid hemorrhage (SAH), which improved to grade III after placement of a ventriculostomy. Computed tomography (CT) and CT angiography revealed a diffuse SAH and ruptured basilar tip aneurysm []. Digital subtraction angiography (DSA) confirmed the diagnosis of a basilar bifurcation aneurysm with a wide neck and shallow dome []. Due to its unfavorable neck/dome ratio, endovascular obliteration of this aneurysm was thought to be high risk. The basilar bifurcation was noted to be quite high in relation to the dorsum sella []. A right cranio-orbital approach was used for the clipping of the aneurysm in this patient. After wide opening of the Sylvian fissure and arachnoid cisterns, the PComA, and the P1 and P2 segments of the PCA were isolated. Due to the high riding basilar bifurcation, dissection of the basilar bifurcation was restricted by the PComA, which was tethering the PCA. Because the PComA was not a fetal type, the decision was made to divide the PComA. However, before dividing it in its perforator-free segment, we performed ICG-VA with a temporary clip on the perforator-free segment, and demonstrated that both perforators were filling from both the PCA and the internal carotid artery (ICA). The PComA was divided between the proximal and distal perforators. Another ICG-VA was performed and this showed that the perforators were still filling. The aneurysm was then clipped (see video, , which demonstrates the surgery, 3 min 18 s, and 71.8 MB). Postoperatively the patient's clinical status improved and she was extubated on the 7th postoperative day with intact speech and was able to follow verbal commands. A postoperative angiogram showed the total obliteration of the aneurysm []. Two days after the removal of the external ventricular drainage, the patient suffered a rapid decline because of right intraventricular hemorrhage. Emergency evacuation of the hematoma was performed. She eventually made a good recovery and was discharged to a rehabilitation center. On postoperative 3rd month follow-up she was neurologically intact.
|
[[42.0, 'year']]
|
F
|
{'19066012': 1, '16381184': 1, '27136915': 1, '12434177': 1, '18695550': 1, '2222241': 1, '5858437': 1, '8177246': 1, '3561728': 1, '22959212': 1, '23157184': 1, '20881574': 1, '501400': 1, '2011233': 1, '21164372': 1, '845644': 1, '8869714': 1, '24232934': 2}
|
{'3815034-2': 2}
|
163,985 |
3815034-2
| 24,232,934 |
noncomm/PMC003xxxxxx/PMC3815034.xml
|
Intraoperative dynamic assessment of the posterior communicating artery and its branches by indocyanine green videoangiography
|
A 47-year-old female presented with headache. CT angiography and a four-vessel angiogram revealed a PComA–PCA junction aneurysm on the right hemisphere and P1 segment aneurysm on the left side [Figure and ]. The patient elected to undergo coil embolization of both aneurysms. Although the right-sided P1–PComA junction aneurysm was successfully coiled the left-sided P1 aneurysm was not amenable to safe coiling due to its broad neck involving the P1 posterior thalamoperforating artery. Therefore, the patient underwent a cranio-orbital approach for the clipping of the left P1 aneurysm. After wide splitting of the arachnoid cisterns, the ICA, PComA, PCA and basilar bifurcation were all exposed. The aneurysm was originating from the P1 segment of the PCA in relation to the P1 perforating artery. The tethered PComA was obstructing the view of the aneurysm neck and origin of the P1 perforator. Preclipping ICG-VA was performed to lay out the vasculature. Although few clip options were exercised, it was felt that without dividing the PComA, safe clipping would not be possible. As such, a temporary clip was placed along the distal P1 vessel and then ICG-VA performed to ensure that there was flow through the PComA perforators. After this was confirmed, the distal portion of the PComA was divided. The aneurysm was then dissected free and good clip purchase was provided. Postclipping ICG-VA revealed no flow through the aneurysm dome and persistent flow in the P1 perforator and rest of the P1 (see video, , which demonstrates the surgery, 3 min 18 s, and 97.5 MB). The patient refused to undergo postoperative arterial DSA, so intravenous-DSA was performed and revealed the total obliteration of the aneurysm [Figure and ]. The postoperative course was uneventful and the patient was discharged home in stable and neurologically intact condition.
|
[[47.0, 'year']]
|
F
|
{'19066012': 1, '16381184': 1, '27136915': 1, '12434177': 1, '18695550': 1, '2222241': 1, '5858437': 1, '8177246': 1, '3561728': 1, '22959212': 1, '23157184': 1, '20881574': 1, '501400': 1, '2011233': 1, '21164372': 1, '845644': 1, '8869714': 1, '24232934': 2}
|
{'3815034-1': 2}
|
163,986 |
3815043-1
| 24,233,058 |
noncomm/PMC003xxxxxx/PMC3815043.xml
|
Contralateral delayed epidural hematoma following intracerebral hematoma surgery
|
A 28-year-old right-handed male with trauma signs on his head (a wound in his occipital region, nasal hemoliquorrhea, right-sided otohemoliquorrhea) was admitted to Yalta City Hospital after he felt down while riding a skateboard. On admission, he was Glasgow coma scale (GCS) 5 with left dilated pupil.\nCT scans showed intracerebral traumatic hematoma in the left frontal lobe, 6 mm midline shift, right temporal bone fracture and a small pneumocephalus in sellar region [].\nPerformed operation: left-sided hemicraniectomy through “trauma-flap” incision, evacuation of traumatic intracerebral hematoma in left frontal lobe. Intraoperatively an acute brain swelling occurred. Patient was transferred to ICU after the operation. One day after the operation, right-sided anisocoria occurred and a contralateral EDH with 10 mm of midline shifting was found at the control CT scans [].\nPatient underwent decompressive craniectomy in the right temporo-parietal region and evacuation of EDH about 100 cc in volume.\nOne day later there were no signs of residual hematoma on CT scans [].\nAt the fifth day after the operation, percutaneous tracheostomy was performed. Patient was comatose 19 days after admitting to the hospital. He underwent conservative treatment of brain edema. After that control CT scans were performed [].\nNext day patient became apallic and 7 days later akinetic mutism was found.\nAt the 32nd day in the hospital, he was transferred from the intensive care unit (ICU) into the neurosurgical department.\nOne month later patient was awake and spoke with single separated words.\nOn 76th day in the hospital the CT scans were performed with 1 mm collimation for the titanium mesh implants and stereolithographic models development [].\nAt his 2 month follow-up, he had neurological deficit of left-sided spastic hemiparesis, anosognosia, right-sided convergent strabismus.\nBilateral cranioplasty of two huge bone defects [Figures and ] with individually constructed titanium mesh was performed.\nPostoperative period was uneventful and in 15 days patient was sent to rehabilitation.\nCT scans in a month after the cranioplasty showed brain expansion to its original shape [].
|
[[28.0, 'year']]
|
M
|
{'23238942': 1, '15558204': 1, '19918570': 2, '24991470': 1, '3687495': 1, '16574562': 1, '3548224': 1, '24872919': 1, '1726254': 1, '19077617': 1, '29202748': 2, '21247768': 1, '19005615': 1, '24233058': 2}
|
{'2769280-1': 1, '5715532-1': 1}
|
163,987 |
3815044-1
| 24,233,130 |
noncomm/PMC003xxxxxx/PMC3815044.xml
|
Trigeminocardiac reflex in neurosurgical practice: Report of two new cases
|
A 71-year-old male presented with remarkable decrease of vision during the previous 6 months (down to 2/10). The pituitary function tests were compatible with hypo-functioning pituitary gland. The magnetic resonance imaging (MRI) revealed a large pituitary adenoma with remarkable supra-sellar extension []. The basic cardiac evaluations were reported to be in the average normal range. He was on aspirin for long period of time, which was discontinued 10 days prior to operation, and mild antihypertensive Thiazide type medication. It was decided to approach the tumor transsphenoidally. The patient fasted for morning hours prior to surgery. The peroperative antibiotic was given as usual, Cephalexin Lupin Pharmaceuticals, Inc. 2 g IV. Routine monitoring during surgery included electrocardiography (ECG), noninvasive blood pressure (NIBP) end-tidal (ET) concentration of CO2, and pulse oximetry.\nAnesthesia was induced with midazolam (2 mg total dosage), fentanyl (150 μg total dosage) and propofol (2.5 mg/kg), and followed by atracurium (0.5 mg/kg). After intubation, the lungs were ventilated on volume controlled ventilation mode (S/5Aespire Config; Datex-Ohmeda Inc., Madison, WI, USA) with a mixture of medical air and O2 (50-50%). Anesthesia was maintained using isoflurane (1-1.5%). An additional dosage of 50 μg fentanyl was applied every one hour during the intervention. The sella was approached via sub-mucosal transseptal dissection entering the sphenoid sinus by the rhinologist. The soft, pinkish gray tumor evacuated gross totally applying microscopic illumination (KA). Considering leakage of cerebrospinal fluid (CSF) in this stage, it was decided to pack the sella by autologous fat taken from the wall of his abdomen. While packing the sella, his BP dropped to 50/20 mmHg and HR to 38/min. Removing more than two-thirds of the implanted fat, the BP raised to 95/65 mmHg and HR to 88/min. It was preferred to apply surgical absorbable hemostat, Ethicon Inc., and cover it with mucosal flap. Since the bradycardia and hypotension were normalized gradually no excess medications were administered. The postoperative course was uneventful except for CSF leakage, which could be managed with repeated lumbar punctures.
|
[[71.0, 'year']]
|
M
|
{'23147445': 1, '18514393': 1, '22240287': 1, '33253333': 1, '19787294': 1, '23045405': 1, '27217962': 2, '21118536': 2, '3475443': 1, '8946342': 1, '17592354': 1, '2124598': 1, '12022304': 1, '12069514': 1, '3137840': 1, '26376385': 1, '17885228': 1, '10721197': 1, '29245296': 1, '15680656': 1, '16547089': 1, '19921355': 1, '15311339': 1, '12420088': 1, '22152579': 1, '20377980': 1, '19770535': 1, '15623488': 1, '16202819': 1, '18524784': 1, '4838186': 1, '9950491': 1, '24233130': 2}
|
{'3815044-2': 2, '4863081-1': 1, '3002900-1': 1}
|
163,988 |
3815044-2
| 24,233,130 |
noncomm/PMC003xxxxxx/PMC3815044.xml
|
Trigeminocardiac reflex in neurosurgical practice: Report of two new cases
|
A 52-year-old female was admitted because of decreased vision of about 8 months duration. She had no preoperative comorbidity. She was operated for a right clinoidal meningioma [Figure and ]. General anesthesia was given in usual standard manner (using medications as in the previous case). A right standard pterional craniotomy was performed and tumor could be resected totally using micro-dissection technique. Hemostasis was achieved and bone flap fixed and skin closed in routine fashion. Bandage was applied while the patient was still intubated. Attaching the subgaleal drain to the suction bottle, her HR dropped from 86/min to 45/min and BP from 110/85 to 75/43 mmHg. The suction was disconnected and the patient was taken to the recovery room and extubated. All the vital signs were normal in the recovery room but when connecting the drain to the vacuum bag, HR and BP dropped again. Lastly, she could not tolerate the vacuum drain and we had to attach it to the bag without negative pressure. No extra medications were administered and drain was removed the day after operation. The postoperative course was otherwise uncomplicated.
|
[[52.0, 'year']]
|
F
|
{'23147445': 1, '18514393': 1, '22240287': 1, '33253333': 1, '19787294': 1, '23045405': 1, '27217962': 2, '21118536': 2, '3475443': 1, '8946342': 1, '17592354': 1, '2124598': 1, '12022304': 1, '12069514': 1, '3137840': 1, '26376385': 1, '17885228': 1, '10721197': 1, '29245296': 1, '15680656': 1, '16547089': 1, '19921355': 1, '15311339': 1, '12420088': 1, '22152579': 1, '20377980': 1, '19770535': 1, '15623488': 1, '16202819': 1, '18524784': 1, '4838186': 1, '9950491': 1, '24233130': 2}
|
{'3815044-1': 2, '4863081-1': 1, '3002900-1': 1}
|
163,989 |
3815051-1
| 24,233,184 |
noncomm/PMC003xxxxxx/PMC3815051.xml
|
Primary human chorionic gonadotropin secreting germinoma of the corpus callosum
|
A 15-year-old Malay boy with no significant past medical history was referred to our institution with a 2-month history of intermittent fever, recurrent headaches, vomiting, significant weight loss, and deterioration in school performance. He did not have any significant drug, family, or developmental history.\nOn examination, he was found to be disorientated to time, place, and person. He also demonstrated terminal past-pointing bilaterally and left-sided dysdiadochokinesia.\nInitial blood investigations revealed a white blood cell count of 6.92×109/L and a C-reactive protein level of <5.0 mg/L. Serum alphafetoprotein (AFP) and human chorionic gonadotropin (b-HCG) were not elevated. Other abnormal serum biochemical parameters included free thyroxine (FT4) of 9.4 pmol/L, thyroid stimulating hormone (TSH) of 3.92 mIU/L, follicular stimulating hormone of <0.1 IU/L, luteinizing hormone of <0.07 IU/L, sodium of 155 mmol/L and serum osmolality of 323 mOSm/kg. Cerebrospinal fluid (CSF) AFP levels were normal but CSF b-HCG levels, however, were markedly elevated at 1837.01 IU/L. Contrasted computer tomographic (CT) imaging revealed a heterogenous 4 cm mass centered in the genu of the corpus callosum, filling the anterior aspect of the third ventricle and spreading along the margins of both frontal horns, causing obstruction of the Foramina of Monro and hydrocephalus. Thickening and enhancement was also noted along the margins of both lateral ventricles and a 1.3×0.9 cm enhancing nodule visualised in the 4th ventricle []. Further workup also revealed that the patient was suffering from central diabetes insipidus as well as panhypopituitarism. After neurosurgical team review, the diagnosis of GCT with extensive intraventricular CSF seeding was considered. Subsequent magnetic resonance imaging (MRI) brain reported multiple intraventricular contiguous and noncontiguous cystic masses with extension superiorly into the frontal horns, the genu of the corpus callosum and the septum pellucidum, inferiorly into the suprasellar region, as well as laterally into the right temporal horn []. Small cystic foci were also noted in the vicinity of the pineal gland. MRI attempted at this juncture was not augmented with contrasted medium due to acute kidney injury from excessive diuresis precipitated by central diabetes insipidus. No spinal drop metastases were visualized on MRI.\nThe patient underwent open craniotomy and biopsy of the intraventricular portion of the tumor. Histology revealed a germinoma composed of sheets of large primitive cells with round nuclei bearing prominent nucleoli, and ample clear cytoplasm with discrete cell membranes, interrupted by fibrous septa containing smaller reactive lymphocytes []. Immunohistochemical staining showed positive reactivity for CD117 (c-kit) and placental alkaline phosphatase, confirming the diagnosis of germinoma. Although CSF b-HCG was found to be elevated at 1837.01 IU/L, immunohistochemical staining for the same was negative.\nThe patient underwent four cycles of carboplatin, etoposide, and ifosfamide as per International Society of Pediatric Oncology Central Nervous System Germ Cell Tumor (SIOP CNS GCT) 96 protocol and subsequent craniospinal irradiation (CSI) of 54 Gray (Gy) in 32 fractions, which he tolerated well. Radiologically, his lesions remained stable despite completing treatment [] but he demonstrated good biochemical response with CSF b-HCG falling from 1837.01 IU/L to less than 2.0 IU/L. The patient had to be on permanent hormonal replacement therapy for panhypopituitarism. His last CSF b-HCG reading taken 12 months after completion of treatment remains stable at <1.2 IU/L and most recent MRI brain done 15 months after completion of treatment shows no evidence of recurrence.
|
[[15.0, 'year']]
|
M
|
{'22869621': 1, '18304618': 1, '2178773': 1, '18590442': 1, '18287340': 1, '12777087': 1, '11936056': 1, '7432586': 1, '12076946': 1, '16768139': 1, '25674279': 1, '26012485': 1, '23460321': 1, '23432481': 1, '17609967': 1, '15914969': 1, '18355878': 1, '12012121': 1, '11821471': 1, '22246339': 1, '20671388': 1, '9950496': 1, '9112445': 1, '10209181': 1, '18586924': 1, '891304': 1, '10964999': 1, '2569683': 1, '9307195': 1, '2039390': 1, '24233184': 2}
|
{}
|
163,990 |
3815079-1
| 24,231,690 |
noncomm/PMC003xxxxxx/PMC3815079.xml
|
Undifferentiated uterine sarcoma metastatic to the brain
|
A 65-year-old gravida 3, para 3-0-0-3, female presented with postmenopausal bleeding in July 2008. The patient sought medical attention from her gynecologist who performed a D and C, which revealed high-grade sarcoma of the uterus. Subsequent computed tomography (CT) scan of the chest, abdomen, and pelvis noted 9.5 × 6 cm irregular low density mass in the uterus with no extrauterine disease. She underwent a total abdominal hysterectomy, bilateral salpingo-oophorectomy, and omentectomy. The tumor measured 10 × 8 cm and demonstrated extensive necrosis. The margins were negative although the posterior wall of the myometrium was extensively involved. The final pathologic evaluation was consistent with undifferentiated endometrial sarcoma. She subsequently underwent pelvic radiation receiving 45 Gy in 25 fractions.\nOne year follow up imaging revealed multiple lung metastases for which she underwent a needle biopsy, consistent with metastatic undifferentiated uterine endometrial sarcoma. She completed six doses of a single chemotherapy agent, Adriamycin, with good radiographic response on interval CT and positron emission tomography (PET) scan. Three months later she began complaining of headaches and visual complaints. Magnetic resonance imaging (MRI) of the brain showed a homogenous enhancing occipital dural-based mass measuring 1.6 × 1.8 × 1.7 cm with a small amount of surrounding edema []. Due to the rarity of uterine sarcoma metastasizing to the brain, this was believed to represent a meningioma. Interval MRI scan revealed a significant increase in size of the right occipital mass to 2.3 cm with increased edema and mass effect. She underwent right occipital image guided craniotomy for resection of the mass. Postoperative imaging revealed complete resection of the dural-based mass []. Histopathology confirmed UUS metastases [Figures and ]. The patient was discharged on postoperative day one and started on taxol and carboplatin chemotherapy, as well as Gamma Knife stereotactic radiosurgery to the tumor bed.
|
[[65.0, 'year']]
|
F
|
{'8690287': 1, '14766270': 1, '6243247': 1, '7969824': 1, '8063254': 1, '19356236': 1, '2914299': 1, '6489828': 1, '12173340': 1, '2405271': 1, '10344114': 1, '13871981': 1, '30200635': 1, '8349151': 1, '1507253': 1, '8741380': 1, '2614515': 1, '698911': 1, '24231690': 2}
|
{}
|
163,991 |
3815080-1
| 24,231,754 |
noncomm/PMC003xxxxxx/PMC3815080.xml
|
Endoglin (CD105) is a more appropriate marker than CD31 for detecting microvessels in carotid artery plaques
|
A 61-year-old male was incidentally found to have left internal carotid artery stenosis. He had hypertension, hyperlipidemia, and diabetes mellitus. Angiography revealed 80% stenosis. He underwent carotid endarterectomy, and the results of pathology are shown in . Compared with CD31, CD105 was more strongly expressed in microvessels.
|
[[61.0, 'year']]
|
M
|
{'11987155': 1, '14761253': 1, '11705856': 1, '19812043': 1, '26919112': 1, '10029075': 1, '29364596': 1, '33946583': 1, '9842001': 1, '10539840': 1, '8667496': 1, '16037567': 1, '9872992': 1, '14530185': 1, '10225446': 1, '11549570': 1, '10815930': 1, '11382917': 1, '18559597': 1, '14668457': 1, '11442525': 1, '21099723': 1, '1674060': 1, '10436445': 1, '10078489': 1, '22463585': 1, '9830054': 1, '1852179': 1, '24231754': 2}
|
{'3815080-2': 2}
|
163,992 |
3815080-2
| 24,231,754 |
noncomm/PMC003xxxxxx/PMC3815080.xml
|
Endoglin (CD105) is a more appropriate marker than CD31 for detecting microvessels in carotid artery plaques
|
A 78-year-old male presented left hemiparesis and magnetic resonance imaging (MRI) demonstrated cerebral infarction in the right hemisphere. He had hypertension and diabetes mellitus, and angiography revealed 65% right carotid artery stenosis. He underwent carotid endarterectomy, and the results of pathology are shown in . The microvessels were faintly stained with CD31, but strongly expressed CD105 in the whole circumference.
|
[[78.0, 'year']]
|
M
|
{'11987155': 1, '14761253': 1, '11705856': 1, '19812043': 1, '26919112': 1, '10029075': 1, '29364596': 1, '33946583': 1, '9842001': 1, '10539840': 1, '8667496': 1, '16037567': 1, '9872992': 1, '14530185': 1, '10225446': 1, '11549570': 1, '10815930': 1, '11382917': 1, '18559597': 1, '14668457': 1, '11442525': 1, '21099723': 1, '1674060': 1, '10436445': 1, '10078489': 1, '22463585': 1, '9830054': 1, '1852179': 1, '24231754': 2}
|
{'3815080-1': 2}
|
163,993 |
3815085-1
| 24,231,802 |
noncomm/PMC003xxxxxx/PMC3815085.xml
|
Giant cell angiofibroma of the scalp: A benign rare neoplasm with bone destruction
|
A 30-year-old female presented with a bony swelling over her left parietal region that had increased in size over the past 2 years. She had no history of trauma, bone pain, systemic disease, or neurological symptoms. Physical examination found a swelling that was 6 × 5 cm in size, soft, and without any tenderness []. The skin over the swelling area was loosely attached to the underlying soft tissue. There was no venous dilatation, scars, sinuses, or any bruit heard over the swelling. Neurological examination was unremarkable and fundoscopy examination revealed no papilledema.\nRadiological examination of a skull x-ray showed a lytic lesion that involving the left temporoparietal bone, and computed tomography (CT) scan confirmed the presence of extensive bone destruction [], with a well-defined soft tissue lesion expanding into the temporal muscle. We were unable to obtain a magnetic resonance imaging (MRI) scan for this patient. On clinical grounds, the decision was made to operate immediately.\nThe tumor mass was approached through a horseshoe scalp incision [Figure and ]. During the operation, the mass appeared to be eroding through the internal tabule of the bone and infiltrating the muscle, but no mass transversed or invaded the dura mater. Temporal muscle that been infiltrated by the GCA (size 2 × 1 cm) was removed []. The bone surrounding the tumor mass appeared rarefied and was removed with rongeurs until a normal border was identified [Figure and ]. The postoperative bone defect was 7 × 6 cm in size and was closed using titanium mesh. The patient's neurological status was intact postoperatively.\nThe histopathological examination showed both cellular areas with especially oval and round- to spindle-shaped cells intermixed with floret-like giant cells in no particular pattern and hypocellular areas. Giant cells often lined the pseudovascular spaces [Figure and ]. The pathologic exam also showed bone erosion without any signs of reformation [] and hypervascularization demonstrated by varying calibers of blood vessels. Immunohistochemistry staining showed positive CD34 staining []. Mitotic activity was inconspicuous. On the basis of these findings, a diagnosis of GCA of the scalp was made.\nShe was discharged from the hospital uneventfully, and no recurrence of the mass was detected at her one-year follow-up.
|
[[30.0, 'year']]
|
F
|
{'11683940': 1, '18758395': 1, '15313722': 1, '22934216': 2, '16359538': 1, '10616532': 1, '7573691': 1, '16767212': 1, '10440068': 1, '16527610': 1, '12325476': 1, '13664723': 1, '10895819': 1, '24231802': 2}
|
{'3420791-1': 1}
|
163,994 |
3816164-1
| 24,198,920 |
noncomm/PMC003xxxxxx/PMC3816164.xml
|
A Case of Persistent Apical Ballooning Complicated by Apical Thrombus in Takotsubo Cardiomyopathy of Systemic Lupus Erythematosus Patient
|
A 63-year-old Korean woman with a past medical history of hypertension and a 25-year history of SLE presented with a 3-week history of shortness of breath. She had been treated with hydroxychloroquine 400 mg/day and varying doses of prednisone between 5 and 15 mg/day for the SLE. Additionally, the hypertension was under control with carvedilol 25 mg/day. On examination, her blood pressure was 110/70 mmHg, pulse rate was 112 beats/min, respiratory rate was 24 breaths/min, and body temperature was 36.5℃. Jugular venous distention was noted on inspection. On cardiac auscultation, her rhythm was noted to be tachycardic but regular, weak summation gallops were heard at the cardiac apex, and no pericardial friction rubs were appreciated. Blood tests showed a white blood cell count of 4000/mm3 (normal, 4300-9400/mm3), hemoglobin of 11.5 g/dL (normal, 12-14.3 g/dL) and platelet count of 67000/mm3 (normal, 169-365/mm3). The C-reactive protein level was found to be 0.29 mg/L (normal, 0-0.75 mg/L). A blood chemistry panel revealed a blood urea nitrogen level of 25.0 mg/dL (normal, 7-20 mg/dL), creatinine of 1.3 mg/dL (normal, 0.5-1.5 mg/dL), total protein of 6.7 g/dL (normal, 6.0-8.3 gm/dL), and albumin of 3.2 g/dL (normal, 3.5-4.5 mg/dL). Analysis of the urinary sediment revealed 1-4 white blood cells/high power field (hpf), many red blood cells/hpf, and trace levels of proteinuria. Cardiac enzymelabs were drawn and found to be elevated: CK-MB of 8.7 U/L (normal, 0.6-6.3 U/L), troponin-I of 0.35 ng/mL (normal, 0.0-0.2 ng/mL), and pro-brain natriuretic peptide of 8110 pg/mL (normal, 0-125 pg/mL). Chest X-ray revealed an enlarged cardiac silhouette and an electrocardiogram revealed ST elevation in leads V1-6 (). Immunofluorescence tests were negative for double-stranded DNA antibodies and anti-extractable nuclear antigen antibodies (anti-Ro and anti-La). Complement levels were found to be low (C3 0.39 g/L, normal 0.8-1.7 g/L; C4 0.04 g/L, normal 0.12-0.36 g/L). Viral markers for cytomegalovirus, Coxsackie virus B type 2, herpes simplex virus, and Epstein-Barr virus were all negative. Echocardiography demonstrated moderate left ventricular systolic dysfunction [left ventricular ejection fraction (LVEF) was 42%] with apical akinesia but no evidence of pericardial effusion (). Echocardiography performed 2 years earlier showed mild concentric left ventricular hypertrophy with a LVEF of 70%. A coronary angiography showed normal coronary arteries.\nWe suspected takotsubo cardiomyopathy. However there was no trigger event as physical and emotional stress. The patient was treated with angiotensin converting enzyme inhibitor, furosemide, and intravenous nitrates. The dose of glucocorticoids was between 0.5 to 1 mg/kg for the control of SLE activity. Her dyspnea gradually improved, however, a three-week follow-up echocardiography test revealed persistent apical ballooning and a newly developed apical thrombus (size, 1.10 × 2.12 cm) () with no significant improvement in LVEF. Heparin was then administered followed by oral anticoagulation therapy with warfarin. There were no embolic events during the patient's hospital stay. On the 35th day of hospital admission, follow-up echocardiography showed slightly improved wall motion of the left ventricular apex with a partially resolved thrombus and a LVEF of 50%. Although cardiac enzymes remained elevated (CK-MB 12.80 U/L and troponin-I 0.64 ng/mL), the patient was discharged on oral anticoagulation therapy.\nThree months later, she was readmitted to the hospital due to a severe herpes zoster outbreak on her left shoulder. Cardiac enzymes were again found to be elevated (CK-MB 8.8 U/L and troponin-I 0.98 ng/mL). Electrocardiography revealed persistent ST segment elevation () and echocardiography revealed mild apical hypokinesia with a LVEF 50%, but no apical thrombus (). During her hospital stay she developed a mild fever and candidemia which was treated with an intravenous antifungal agent. Unfortunately, she developed septic shock and expired on day 54 of hospital re-admission.
|
[[63.0, 'year']]
|
F
|
{'22205847': 2, '22056476': 1, '12714146': 1, '18662833': 1, '28673245': 2, '25114700': 2, '19237215': 1, '19438699': 1, '16583180': 1, '18063149': 1, '30328054': 1, '19375185': 1, '18053952': 1, '24198920': 2}
|
{'3245395-1': 1, '5496147-1': 1, '4127409-1': 1}
|
163,995 |
3816165-1
| 24,198,921 |
noncomm/PMC003xxxxxx/PMC3816165.xml
|
Device Closure of a Large Atrial Septal Defect in a Patient with Severe Pulmonary Arterial Hypertension after 1 Year Use of an Oral Endothelin Receptor Antagonist
|
A 20-year-old woman presented with progressively worsening dyspnea for 6 months. She had no history of evaluation or treatment for her symptoms, although the symptoms started at the age of high school. Her symptoms became worse with time, and she presented with NYHA class III exertional dyspnea and orthopnea. Her height, weight, and body surface area were 156 cm, 49 kg, and 1.45 m2 respectively. Her vital signs were blood pressure 104/68 mmHg, heart rate 104/min, and respiratory rate 22/min. A regular heart beat was detected with wide fixed splitting of S2 at the pulmonary valve area, and no clubbing of the fingers or nails was observed. A simple chest X-ray showed cardiomegaly and a dilated pulmonary trunk with cephalization of pulmonary vascular marking. Electrocardiography revealed normal sinus rhythm with compatible findings of RV hypertrophy. A transthoracic echocardiogram revealed a large tissue defect of 29 mm with a bi-directional shunt through the interatrial septum (). The RV was prominently dilated and revealed significantly decreased contractility with a D-shaped left ventricle (LV) showing normal contractility (). There was no significant RV hypertrophy. The systolic pulmonary arterial pressure measured by maximal tricuspid regurgitation velocity (TR Vmax) was estimated at 95 mmHg (TR Vmax = 4.6 m/sec), which was roughly equal to systemic systolic blood pressure (). Her walking distance was 362 m on the 6-minute walking test with slightly decreased oxygen saturation from 98% to 92%. Further evaluations to identify the etiology of the pulmonary hypertension included a pulmonary function test, chest computed tomography angiogram and autoimmune panel, but all were negative.\nCardiac catheterization confirmed severe pulmonary hypertension with a mean pulmonary arterial pressure of 48 mmHg (76/36 mmHg absolute) and pulmonary vascular resistance (Rp) of 9.6 Wood units (WU) on room air. The mean systemic arterial pressure was 84 mmHg (97/73 mmHg absolute). After administering oxygen (10 L/min for 10 minutes via a nasal prong) and inhaling iloprost, her mean pulmonary arterial pressure was 50 and 46 mmHg respectively, and had not changed significantly. We failed to identify the pulmonary arterial responsibility after pulmonary vasodilator administration. Based on these findings, closure of the ASD was not performed. Instead, medical treatment including oral bosentan was started to improve patient's symptom.\nHer symptoms and exercise tolerance improved from NYHA class III to NYHA class I to II after 1 year of using bosentan. She was able to walk 426 m during the 6-min walk test without desaturation. A follow-up echocardiogram showed no significant interval change except slight improvement in RV contractility compared to the initial echocardiogram, even though her symptoms were much improved. TR Vmax was 4.3 m/sec by continuous wave Doppler test, but there was no significant improvement in comparison with the initial test. Although the follow-up echocardiogram result was very disappointing, we decided to perform a cardiac catheterization and balloon occlusion test to confirm the change in Rp and possibly correct the ASD. We expected some favorable changes in pulmonary vascular physiology, because her exercise tolerance had much improved.\nA follow-up cardiac catheterization revealed severe pulmonary hypertension with mean pulmonary arterial pressure of 45 mmHg (75/29 mmHg absolute). The mean aortic pressure was 74 mmHg (95/60 mmHg absolute). Although the patient still had severe pulmonary hypertension, Rp had decreased markedly from 9.6 to 4.2 WU and calculated pulmonary to systemic flow ratio (Qp/Qs) increased from 1.9 to 2.6 in comparison with the initial data. We performed the transient balloon occlusion test using a 34 mm sizing balloon for 10 minutes. As a result, mean pulmonary arterial pressure decreased to 36 mmHg (48/25 mmHg absolute), and mean aortic pressure increased to 85 mmHg (118/70 mmHg absolute). We decided to close the ASD with a transcatheter occluder device considering her young age and the high perioperative risk. We performed percutaneous closure of the defect with a 34 mm Amplatzer® septal occluder (AGA Medical Corp., Minneapolis, MN, USA).\nNo residual leak was observed on the follow-up transthoracic echocardiography. The patient was given antiplatelet therapy and was maintained on 62.5 mg bosentan bid with diuretics and an angiotensin receptor blocker for 1 year. Finally, her physical activity and symptoms were much improved as she could walk 554 m on the walk test 1 year after the device was deployed. A chest X-ray showed remarkably decreased pulmonary vascularity, but cardiomegaly remained. Follow-up transthoracic echocardiography showed increased left atrial size from 37 to 42 mm and LV chamber size of end-diastole/end-systole from 40/23 to 46/28 mm. RV size had decreased significantly, and RV contractility was much improved in comparison with the initial study, but a compressed LV still remained on the parasternal short axis view (). TR Vmax also decreased markedly from 4.6 m/sec to 3.0 m/sec ().
|
[[20.0, 'year']]
|
F
|
{'29124030': 2, '15992947': 1, '18367267': 1, '32313642': 1, '17932093': 1, '17325254': 1, '16801459': 1, '20417794': 1, '22073329': 2, '18610164': 1, '11565678': 1, '7623878': 1, '11694894': 1, '24198921': 2}
|
{'3209598-1': 1, '5628966-1': 1}
|
163,996 |
3816166-1
| 24,198,922 |
noncomm/PMC003xxxxxx/PMC3816166.xml
|
Left Atrial Wall Dissection after Mitral Valve Replacement
|
A 68-year-old Korean female presented with moderate mitral stenosis, mild mitral regurgitation, moderate tricuspid regurgitation and mild aortic regurgitation. She had no past medical history other than valve diseases and was scheduled for mitral valve replacement and tricuspid annuloplasty. Standard monitors were placed, and right radial arterial cannulation was done for continuous blood pressure monitoring. After preoxygenation, general anesthesia was induced with propofol and remifentanil, infused with a target-site concentration-control infusion device (Base Prima Orchestra, Fresenius Vial, Brezins, France). Tracheal intubation was done with a 7.0 mm tube and a triple lumen central catheter (via left subclavian vein) and Swan-Ganz catheter (PAC: Swan-Ganz CCOmbo V Model 774HF75w: Edwards Lifesciences LLC, Irvine, CA, USA) (via right internal jugular vein) were placed. Continuous cardiac output monitoring and mixed venous oxygen saturation monitoring was done by CCO/Oxymetry/volumetric monitor (Vigilance Monitor: Edwards Lifesciences LLC, Irvine, CA, USA). Transesophageal echocardiography (TEE) findings were consistent with previous transthoracic echocardiography (TTE). During surgery, radiofrequency ablation was done around the coronary sinus and pulmonary vein box lesion, and right side Maze procedure was done. The mitral valve was replaced with a St. Jude Medical (St. Jude Medical Inc., St. Paul, MN, USA) supra-epic 29 mm tissue valve. The LA auricle was externally obliterated with a 5-0 prolene continuous suture and a tricuspid annuloplasty was done with a Duran ring (Medtronic, Minneapolis, MN, USA) 27 mm. After closing the atrium, the patient was weaned off cardiopulmonary bypass with inotropic support of 5 µg/kg/min of dobutamine. The TEE exam during weaning showed a well-seated prosthetic valve and no paravalvular leakage; however, the patient developed posterolateral atrial wall dissection. A false chamber formed in the LA wall and was 2 × 2.5 cm in size (). A surgeon explored the heart externally but could not find any engorgement. The TEE showed small blood flow pouring into the false chamber but it decreased and disappeared in 30 minutes. The false chamber did not seem to increase in size and showed spontaneous echogenic contrast, that is, no communication with the true atrial space. Additionally, the pulmonary venous flow was not hindered by that chamber (). We had a discussion with the surgeon and concluded the risk of re-exploring and repairing the dissection exceeded that of the dissection itself. The patient was uneventfully weaned off CPB. Total CPB time was 4 hours 47 minutes; the aortic cross clamp time was 3 hours 45 minutes. Follow-up TTE taken 6 days after surgery showed normal pulmonary vein flow, and the false chamber was not visible (). The patient agreed to have her case presented to the public for academic purposes.
|
[[68.0, 'year']]
|
F
|
{'11916586': 1, '19447803': 1, '21493092': 1, '24198922': 2}
|
{}
|
163,997 |
3816167-1
| 24,198,923 |
noncomm/PMC003xxxxxx/PMC3816167.xml
|
Recurrent Syncope Episodes and Exercise Intolerance in Hypertrophic Cardiomyopathy Combined with Atrioventricular Conduction Disturbance
|
A 30-year-old female was referred to the cardiology center due to recurrent syncope episodes and aggravated shortness of breath for a month. She was diagnosed as HCMP 7 years ago, and had been taken atenolol irregularly since then. There was no previous medical history and no family history of any cardiac disease. The first syncope occurred in 2007, during discontinuation of medication. After experienced recurrent syncope episodes, she visited another medical center for evaluation of loss of consciousness. Cardiac evaluation, including conventional echocardiography and 24-hour ambulatory electrocardiogram (ECG) monitoring, couldn't reveal the cause of repeated syncope. The neurologic exams for differential diagnosis showed no evidence of seizure disorder or any other diseases, inducing loss of consciousness. She restarted atenolol for HCMP. However, despite medication, symptoms developed more frequently, combined with shortness of breath and exercise intolerance. In 2012, she visited our cardiology clinic for further evaluation and management of worsening symptoms under medical treatment.\nInitial ECG showed 2 : 1 AV block with 36 beats/min of the ventricular rate (). The baseline two-dimensional echocardiography showed HCMP with asymmetric septal hypertrophy (septal wall thickness during diastole 16 mm) and systolic anterior motion of mitral valve (). After discontinuation of the previous medication (atenolol), follow-up ECG showed normal sinus rhythm (). To evaluate the cause of recurrent syncope, additional studies including stress echocardiography, 24-hour ambulatory ECG and treadmill test were performed. During the stress echocardiography with bicycle exercise, when reached 50 watts of workload stage, mitral inflow pattern showed multiple spikes during a late filling phase by atrial contraction accompanied with high grade AV block on ECG monitoring (). Patient suffered from exhaustion and shortness of breath. The baseline blood pressure was 91/59 mmHg (systole/diastole blood pressure) and 46 beats/min of the heart rate, but there was no hypotensive response representing dynamic left ventricular outflow tract obstruction. Simultaneous 24-hour ECG also showed conduction disturbance (including 3 : 1 and 4 : 1 AV block) during the exercise and additionally disclosed 1 episode of non-sustained ventricular tachycardia (NSVT) (). Subsequent treadmill test also revealed high grade AV block with dyspnea and exhaustion at 7.0 METS of exercise under Bruce protocol ().\nAlthough there was no syncope event when ECG monitoring records high grade AV block or NSVT in both 24-hour ECG and stress test, we thought this conduction disturbance and arrhythmia could play a role in repeated loss of consciousness and exercise intolerance. According to the guideline for risk stratification of sudden cardiac death in HCMP, based on her unexplained syncope episodes, it is reasonable to treat this patient with implantable cardioverter/defibrillator (ICD). Patient underwent elective ICD with dual-chamber pacemaker implantation. After that, patient showed no more conduction disturbance at high stage of workload and improved exercise capacity of 12.8 METS under Bruce protocol without any distress in repeated stress test ().
|
[[30.0, 'year']]
|
F
|
{'6542253': 1, '9456495': 1, '3547135': 1, '22093723': 1, '1816229': 1, '10853000': 1, '11714644': 1, '12651046': 1, '17522079': 1, '8546514': 1, '2312980': 1, '1765747': 1, '2329232': 1, '3335690': 1, '7193406': 1, '11127463': 1, '24198923': 2}
|
{}
|
163,998 |
3816295-1
| 24,231,945 |
noncomm/PMC003xxxxxx/PMC3816295.xml
|
Large cerebellar mass lesion: A rare intracranial manifestation of blastomycosis
|
The patient is a 63-year-old man with a history of non-Hodgkin's lymphoma 9 years prior; he had sustained remission after treatment with chemotherapy and radiation. He had presented with persistent nausea and vomiting for 2 months prior to his transfer to our institution. The patient underwent multiple gastrointestinal studies, which did not reveal a clear etiology of his symptoms. Routine chest X-ray demonstrated nonspecific left upper lobe opacities that were further evaluated with computed tomography (CT) and determined to be consistent with pneumonia. Head CT demonstrated a hypodense right cerebellar lesion that minimally enhanced with contrast [Figure and ], prompting further investigation with magnetic resonance imaging (MRI). This revealed an enhancing right cerebellar mass with surrounding cystic lesions causing compression of the 4th ventricle and dorsal medulla resulting in obstructive hydrocephalus [Figure –].\nThe patient underwent a suboccipital craniotomy, finding an intradural lesion that was adherent to the surrounding meninges. Dissection around the lesion revealed a firm, avascular mass with surrounding cystic structures that were filled with yellow fluid. Gross total resection of the mass lesion and surrounding cystic structures was achieved.\nThe patient recovered from surgery well and his nausea and vomiting slowly resolved. Pathology and microbiologic analysis revealed fungal elements and budding yeast consistent with blastomycosis [Figure –]. There was no evidence of CNS dissemination. The patient was started on antifungal therapy with amphotericin B. He was able to tolerate 1 week of amphotericin B before he developed acute hepatitis, prompting its discontinuation. At that time, he was switched to voriconazole. Treatment with voriconazole was planned to last for 1 year.\nAt last follow up, the patient had mild ataxia. His MRI performed 1 month after surgery demonstrated expected postoperative changes and improvement in ventricular dilation seen preoperatively; there was no evidence of recurrent infection [].
|
[[63.0, 'year']]
|
M
|
{'25870142': 1, '10761497': 1, '20717513': 1, '6023515': 1, '5053356': 1, '10547020': 1, '20166817': 1, '7792710': 1, '17502562': 1, '2277199': 1, '12942409': 1, '18306569': 1, '7282737': 1, '27081235': 2, '8311954': 1, '12751259': 1, '17921653': 1, '450231': 1, '18462107': 1, '655652': 1, '24231945': 2}
|
{'4813061-1': 1, '4813061-2': 1, '4813061-3': 1}
|
163,999 |
3817031-1
| 24,204,152 |
noncomm/PMC003xxxxxx/PMC3817031.xml
|
Sodium valproate-induced enuresis in a pediatric bipolar patient
|
“Z,” a 14-year-old girl, was referred to our child psychiatry clinic because she was experiencing a mania episode. Both a magnetic resonance imaging scan and an electroencephalography revealed no hint of an organic cause of her manic symptoms. Since her history also revealed a depressive episode, she was diagnosed as having bipolar disorder type 1 using the Kiddie-Sads-Present and Lifetime Version. Then, the Young Mania Rating Scale was used to measure the severity of her manic symptoms; her score was 45.\nWe started treatment with SV 250 mg/day for the first 4 days. We also administered risperidone 1 mg/day to resolve the ideas of reference symptom throughout the course of treatment. At the 15th day, the dose of SV was titrated to 750 mg/day (250 mg at noon and 500 mg at night). Since the SV dose reached 750mg/day Z began bedwetting. About 4 weeks later, when the dose of SV was titrated up to 500mg twice a day (a blood level of 75μg/ml), Z developed diurnal and nocturnal enuresis every day at the fifth week, she even had urinary incontinence in the classroom at school.\nZ had not taken SV before, and her personal history revealed that she achieved urinary bladder control at 4 years old; since then, she had had no urinary incontinence. The family history was negative for enuresis, and urological and neurological evaluations were normal. Because of the enuresis, the SV dose was reduced to 500 mg/day (a blood level of 38.3 μg/mL), and her bedwetting disappeared completely 2 days later. At her follow-up visit half a year later, she appeared to be well adjusted to the treatment, which consisted of SV at 500 mg/night and risperidone 1 mg/day.
|
[[14.0, 'year']]
|
F
|
{'8768340': 1, '6790086': 1, '2860475': 1, '6420147': 1, '9204677': 1, '30854975': 1, '22694920': 1, '2859433': 1, '728692': 1, '23543036': 2, '22215862': 1, '3142761': 1, '24204152': 2}
|
{'3608303-1': 1}
|
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