A 44-year-old non-smoking athletic Caucasian man with unremarkable medical history presented in the emergency room with unilateral right pressure-like headache. The pain had a rapid onset over 30 s and was rated 10/10 on a visual analogue scale. It was accompanied by nausea and right hemifacial hypoesthesia but not by vomiting, phonophobia, photophobia, tearing, rhinorrhea, nasal congestion, eye redness, visual impairment or motor deficit. Pain subsided within about 1 h after initiating analgesic treatment. The patient had suffered two similar headache episodes 3 and 6 days ago, rated 8/10 with spontaneous remission after 30 min. Right after the first episode, he felt a constant dull retrosternal pain rated 2/10, radiating to the back and aggravated by deep inspiration. He noticed that the subsequent episodes of hemicrania were preceded by exacerbation of the thoracic pain with radiation to the right side of the neck. A few hours after the second episode and for about 30 min, he saw flashing lights move slowly toward the midline in the right visual field, without fortification spectra and without ensuing headache. He denied any family history of migraine.
Upon admission, the patient was in good general health with normal and symmetrical values of blood pressure on both arms and bradycardia (54 beats per minute). Neurological examination was unremarkable as was cardiovascular examination, including careful search for murmurs from large neck, thoracic and abdominal vessels. An electrocardiogram showed a normal sinus rhythm without signs of myocardial ischemia or infarction. Brain magnetic resonance imaging did not disclose any abnormality that could be related to the headache episodes. The concomitant presence of dull chest pain paved the way for suspecting aortic dissection. Contrast-enhanced cervico-thoraco-abdominal computerized tomography revealed type A aortic dissection sparing coronary arteries and supra-aortic vessels (Figure ). Heart ultrasound showed an intact aortic valve. Testing for Marfan syndrome was negative. The patient underwent surgical replacement of the ascending aorta. No further episode of headache was reported after the intervention.


An 11-years-old female German Shepherd was admitted to the Veterinary Teaching Hospital of the Universidade Federal de Minas Gerais, Brazil with a history of prostration one month ago. According to the owner, the animal had multiple normal deliveries, never exposed to contraceptives and experienced estrus regularly twice a year. Clinical examination showed mild dehydration, prostration and intensely pale mucosa. However, no other changes were observed as the dog suddenly died during the clinical examination, before laboratory testing was possible.
Necropsy revealed intensely pale mucous membranes, generalized atrophy of the skeletal muscles and absence of subcutaneous and visceral adipose tissue. In the abdominal cavity, there were approximately 600 ml of reddish and translucent fluid. Adjacent to the left ovary and uterus and adherent to the retroperitoneum, there was a well-demarcated reddish mass, measuring 25.0 × 20.0 cm (Fig. ) with a mixture of soft and firm areas. Upon incision, the mass was found to be solid with variable sized cystic cavities filled with coagulated blood (Fig. ). The lungs showed moderate congestion. The other organs showed no significant lesions.
The entire genital tract and specimens of the mass and other abdominal and thoracic organs were fixed in 10 % neutral phosphate-buffered formalin, sectioned, processed, embedded in paraffin, and stained with hematoxylin-eosin for histopathological examination. To better characterize the mass, staining with Masson trichrome, Periodic Acid Schiff (PAS) and immunohistochemistry were performed. Antibodies used for immunohistochemistry and their dilutions were as follows: anti-Factor VIII (1:300) (A0082, DAKO, St. Louis, MO, USA), anti-vimentin (1:200) (Sigma Chemical Co. St. Louis, MO USA), anti-cytokeratin (1:200) (AE1, AE3, Dako, St. Louis, MO, USA), anti-VEGF (1:100) (sc-152, Santa Cruz Biotechnology, CA, USA), anti-COX2 (1:40) (M3617, Dako, St Louis, MO, US), anti-estrogen receptor (ER) β (1:25) (Novocastra Laboratories, Newcastle, UK), and anti-androgen receptor (AR) (1:500) (PG21, Upstate, Lake Place, NY). The streptavidin-biotin-peroxidase technique was used and antigen retrieval was performed in a water bath at 98 °C using Retrieval solution for anti-Factor VIII, anti-cytokeratin and anti-vimentin antibodies. For anti-ERβ and anti-androgen receptor (AR), antigen retrieval was achieved by microwave. The slides were incubated overnight in a humid chamber with the primary antibody and for 30 min for each of the following steps: blocking endogenous peroxidase, blocking serum (Ultra Vision Block; Fremont, CA, USA) and streptavidin peroxidase (Vectastain Elite ABC Kit, Vector Laboratories, Burlingame, USA for anti-ERβ and anti-androgen receptor and LSAB kit, Dako, St. Louis, MO, USA for others antibodies). Incubation with the secondary antibody (Dako, St. Louis, MO, USA) was performed for 45 min. The chromogen used was diaminobenzidine (DAB Substrate System, Dako, St. Louis, MO, USA). Sections were counterstained with Harris hematoxylin. As a positive control for each antibody, the ovary of the animal was used because it expresses all the markers assessed. A negative control was performed by replacing the primary antibodies by IgG.
Microscopically, the mass was composed of cuboidal or prismatic epithelial cells arranged in tubules, acini or cystic structures, which were sometimes filled with erythrocytes. The epithelium had a round basal nucleus with loose chromatin and the apex of the cell had a finely particulate PAS-positive material (Fig. and). The epithelium of the mass had similar characteristics to that of a normal endometrium. No mitotic figures or cellular atypia were observed. The stroma surrounding the epithelial tissue was prominent and formed by loose connective tissue and smooth muscle fibers stained red with Masson trichrome staining (Fig. ). Extensive multifocal areas of hemorrhage were also observed in the stroma of the mass and blood was present in the lumen of some cystic structures lined with endometrial epithelium (Fig. ).
Epithelial cells, especially prismatic cells, formed structures such as endometrial glands and demonstrated strong and diffuse cytokeratin expression (Fig. ) although some cuboidal and flattened epithelial cells demonstrated weaker cytokeratin expression. The stroma possessed areas with strong vimentin expression between areas with weaker expression (Fig. and). Some epithelial cells also displayed vimentin expression. The majority of the epithelial cells and some stromal cells also possessed cytoplasmic and nuclear ERβ and AR expression (Fig. and). VEGF expression was cytoplasmic, strong and diffuse in epithelial cells, the endothelium of blood vessels, and in some stromal cells (Fig. ), whereas COX2 expression was moderate in some epithelial cells and strong in some stromal cells (Fig. ). Factor VIII expression was observed in only the blood vessels of the stroma.
Moderate cystic endometrial hyperplasia with the presence of endometrial glands in the myometrium was observed in the uterus (adenomyosis). The right and left ovaries showed corpus luteum in regression and some follicles at different stages of development. The other organs showed no significant microscopic changes.
Clinical and macroscopic findings of anemia may have been derived from extensive bleeding in the endometrial tissue. Cases of ascites associated with endometriosis have also been reported. It is suggested that the occurrence of ascites may be due to the rupture of cysts in the endometrial tissue with extravasation of fluid and red blood cells into the abdominal cavity. Moreover, when the formation of large masses occurs, as in this dog, lymphatic drainage may be impaired with extravasation of fluid from the endometrial tissue or from adjacent organs and tissue [, –]. Although rare, endometriosis in women may cause ascites, anemia and circulatory shock [].
Despite the endometrioma, the dog had showed no disturbance of the estrous cycle or fertility as it had delivered normal viable full-term offspring previously. Unlike endometrioma, deep endometriosis is the main presentation that causes pelvic pain and infertility in women [, ]. In women, there are also reports of large endometriomas during pregnancy [, ].
The occurrence of endometriosis caused by cell implantation is unlikely in dogs because dogs lack the endometrial desquamation observed in women during menses and in non-human primates in the diestrus phase. In dogs, endometrial shedding does not occur and the bleeding during estrus comes from red cell diapedesis from blood vessels. In addition, female dogs have 3–10 months of anestrus characterized by the permanence of serum sex hormones at basal levels. Therefore, we suggest that these differences might favor, at least in part, the occurrence of endometriosis in women []. However, the coelomic mesothelium is a pluripotent tissue with high transformation capacity. In bitches, morphological changes of the coelomic mesothelium as cysts and tumors are relatively common compared to other species. Therefore, the coelomic metaplasia theory of the parietal peritoneum better supports the development of the ectopic endometrial tissue in this case [, , ]. This theory has also been suggested to explain the genesis of endometriosis in men and women outside of reproductive age [, , ] as well as endometriosis in distant extra-pelvic organs [].
Studies have demonstrated that estradiol plays an important role in the appearance, perpetuation and proliferative potential of the endometrial tissue [, , ]. In humans, some cases of endometriosis are associated with prolonged use of estradiol for the treatment of prostate cancer []. However, the bitch in this case did not receive hormonal treatment or had been exposed to contraceptives. In addition, no hormonally active ovarian alteration was observed. However, we cannot rule out the involvement of estradiol in the pathogenesis of the endometrioma in this bitch, mostly because the ectopic endometrial tissue showed immunohistochemical expression of the β receptor for estradiol.
Despite the macroscopic characteristics of the mass described in some cases of endometrioma in women [, ], based solely on the macroscopic mass, especially the red color and the presence of cavities filled with coagulated blood, an initial diagnosis of hemangiosarcoma was made in this dog. However, microscopic and immunohistochemical features belied this suspicion. The histomorphology was slightly similar to cystadenoma of the rete ovarii because such tumors have cysts averaged 8.7 cm, a flat, cuboidal, or columnar, usually nonciliated-lining epithelium and can sometimes present a fibromuscular wall [, ]. However, the cysts are not filled with blood and there is not extensive bleeding in the stroma as seen in this case [, ]. The extra-ovarian location and the microscopic characteristics of the mass also ruled out the possibility of a granulosa cell tumor or ovarian germ cell tumor [, ]. The differential diagnosis of cystic abdominal mesothelioma or others celomic epithelium tumors such as ovary papillary cystadenoma and cystadenocarcinoma were also ruled out. Abdominal mesothelioma in dogs generally presents by dissemination to the parietal and visceral peritoneum []. However, the human peritoneal mesothelioma may also be present as a major pelvic mass []. Moreover, mesothelioma cysts are characterized by the presence of bright and clear yellow fluid, contrary to what was observed in the present dog. The epithelial tissue of the mass was also positive for PAS secretion, and the stroma had smooth muscle cells, which are not found in mesothelioma and ovary papillary cystadenoma [–].
The endometrial tissue found in this bitch was restricted to a mass located adjacent to the uterus and ovary and fixed to the retroperitoneum. The association of the epithelium with a richly vascularized fibrous stroma observed in the present dog has also been described in endometrioma in women [, , ]. However, the presence of bundles of smooth muscle in the stroma of the lesion, as was observed in this case, is unusual. This feature makes the lesion more of a uterus-like mass or endomiometrioma [].
The immunohistochemical characteristics of endometriosis have been widely studied. Similar to what was observed herein, ectopic endometrial cells are positive for cytokeratin [] and may also express receptors for estradiol and androgen [, ]. In this case, some endometrial cells also expressed vimentin. The endometrium is derived from intermediate mesoderm through the transition from the epithelium to mesenchyme during development of the urogenital system. Although vimentin is a mesenchymal marker, it is expressed in epithelial tissues derived from mesoderm, such as endometrium []. Cytokeratin expression in epithelial cells was diffuse, as opposed to vimentin expression, which was multifocal and less intense. This difference can be attributed to the degree of cell differentiation of the epithelium, as cytokeratin and vimentin expression varies with the composition of the cell filaments and, consequently, the degree of histological differentiation [, ].
Immunohistochemical expression of COX2 and VEGF by endometrial epithelium and stromal cells was also observed in cases of endometriosis in women [, ]. It is believed that the expression of COX2 and VEGF, stimulated by estradiol, promote the growth and maintenance of endometrial tissue to stimulate angiogenesis and, consequently, the blood supply [, –]. Inhibition of COX2 in rats with experimental endometriosis causes regression of endometrial tissue by inhibiting VEGF expression and angiogenesis [, ]. The endometrioma observed in this dog was highly vascularized, which was important to maintain tissue viability as areas of necrosis were not observed despite the large size of the mass.


A 27 years-old female presented at the emergency department with complaints of nausea, vomiting and inability to move all extremities which lasted for six hours. She had sore throat seven days ago and used amoxycillin-clavulanate tablet (tab) 2×1000 mg for five days. Her past medical history revealed quadryparesis attacks for the last 5 months. These attacks mostly came at night with cramps and weakness, which lasted about 2-3 hours. The frequency of the attacks was about every two weeks. She was diagnosed hyperthyroidism two months ago and she was put on propylthiouracil tab. 75 mg/day and propranolol tab. 40 mg/day.
Physical examination revealed that she was fully conscious, well oriented. Her blood pressure was 95/50 mmHg, heart rate was 110/min rhythmic and body temperature was 37ºC. Her muscle strength was 2/5 in lower and 3/5 upper extremities. The deep tendon reflexes were decreased.
Her laboratory results are presented in . The levels of hemoglobin, hematocrit, thrombocytes, bilirubins, creatinine, uric acid, calcium, magnesium, sodium, chloride and urinalysis were within normal limits. Thyroid function tests showed TSH as 0.005 uU/mL, free T4 as 4.98 ng/dL and free T3 as 15.54 pg/ml () Electrocardiography showed sinusal tachycardia, abdominal ultrasonography showed a gallstone of 0.5 cm in diameter, and normal gallbladder wall. Chest X-ray was normal.
She was admitted to the intensive care unit. She was administered potassium chloride with the infusion rate of 10 mEq/h, followed by oral potassium supplement on day two. Therapy for hyperthyroidism was rearranged as propylthiouracil 3X100 mg and propranolol 2X40 mg/day. On the second day, her pulse was 80/min regular and potassium level was 2,6mmol/L. On the third day her muscle strength was 3/5 lower and 4/5 upper extremities, and potassium level was 3.1 mmol/L. Fifth day her muscle strength was 5/5 lower and upper extremities. Her liver enzymes and hs-CRP returned back to normal values in four days. She was discharged six days later with normal muscle strength and potassium level of 3.8 mmol/L.


A 29-year-old Japanese woman presented with paroxysmal palpitation and headache. She had no history of hypertension. Blood catecholamine analysis during the palpitation revealed epinephrine, norepinephrine, and dopamine levels of 417 pg/ml (reference range, 0–100 pg/ml), 2,665 pg/ml (reference range, 100–450 pg/ml), and 16 pg/ml (reference range, 0–60 pg/ml), respectively. Magnetic resonance imaging revealed a heterogeneous left adrenal mass with slightly high intensity on T2-weighted images (Figure a). 123I-meta-iodobenzylguanidine (MIBG) scintigraphy showed a high level of accumulation in the left adrenal tumor. After diagnosis of left adrenal pheochromocytoma, the patient underwent laparoscopic left adrenalectomy. Pathological findings showed a composite pheochromocytoma-ganglioneuroma in which 4.3% of cells were Ki67-positive (Figure a, d, g). She was followed closely after surgery. Despite the high number of Ki67-positive cells, no recurrence was observed for 2 years.


A 59-year-old Japanese man presented with asymptomatic macrohematuria. He had a history of angina pectoris and took a daily dose of aspirin. Abdominal ultrasonography showed no evidence of a renal or bladder tumor, and cystoscopy showed no evidence of a bladder tumor. Computed tomography revealed a 5.5-cm left adrenal mass (Figure b). Blood catecholamine analysis revealed epinephrine, norepinephrine, and dopamine levels of 136 pg/ml (reference range, 0–100 pg/ml), 458 pg/ml (reference range, 100–450 pg/ml), and 15 pg/ml (reference range, 0–60 pg/ml), respectively. 123I-MIBG scintigraphy showed a high level of accumulation in the left adrenal gland. After diagnosis of a left adrenal pheochromocytoma, the patient underwent laparoscopic left adrenalectomy. Pathological examination revealed a composite pheochromocytoma–ganglioneuroma with focal Ki67-positive cells (1%) (Figure b, e, h).


A 53-year-old Japanese man presented with asymptomatic macrohematuria. He had undergone hemodialysis for 17 years and had a history of hypertension. Cystoscopy showed no evidence of a bladder tumor. Abdominal magnetic resonance imaging showed acquired cystic kidney disease and a 3-cm right adrenal mass (Figure c). Serum catecholamine analysis revealed an epinephrine level of 50 pg/ml (reference range, 0–100 pg/ml), norepinephrine level of 3,801 pg/ml (reference range, 100–450 pg/ml), and dopamine level of 90 pg/ml (reference range, 0–60 pg/ml). 123I-MIBG scintigraphy revealed strong accumulation in the right adrenal gland. After diagnosis of a right adrenal pheochromocytoma, the patient underwent laparoscopic right adrenalectomy. Pathological examination revealed a composite pheochromocytoma–ganglioneuroblastoma with a 6.2% rate of Ki67-positive cells (Figure c, f, i). Despite the unfavorable tumor histology, he remained tumor-free for 6 years after the surgery.
In the present report, two patients showed asymptomatic hematuria. However, cystoscopy showed no evidence of a bladder tumor. The ratio of eventual coexistence of hematuria and composite pheochromocytoma was unknown, although we reviewed previous reports.


A previously healthy 9-year-old boy presented to the emergency department with a 6 h history of left chest pain and increasing respiratory distress. His respiratory rate was 40/min and heart rate was 105/min, cardiac auscultation was unremarkable, auscultation of lung fields revealed diminished breath sound over the left side. A chest x-ray (Fig. ) showing a large air-fluid level in the left hemithorax with shift of the mediastinum to the right was interpreted as tension gastrothorax. Prompt insertion of a nasogastric tube with evacuation of air and 800 ml of gastric content led to immediate relief of symptoms. Subsequent chest x-ray showed normalization of the mediastinal shift and the nasogastric tube was found to curve back into the left hemithorax (Fig. ). On the same day, the patient underwent repair of a 5 × 5 cm posterolateral defect in the left diaphragm after the stomach and spleen were repositioned in the abdominal cavity. The postoperative course was uneventful and he was discharged home 7 days after surgery. He remained well at follow-up 2 and 8 months later and chest x-ray was normal (Fig. ).


The patient, a 30-year-old man with a past history of mental deficiency and repeated pneumonia, was referred to our hospital for further evaluation of PS which was identified when he received a health diagnosis. He had no history of smoking. A physical examination and laboratory investigation showed no specific findings. Three-dimensional enhanced computed tomography of the chest and aorta revealed intra lobar PS with an aberrant systemic artery originating from the abdominal aorta, and flowing into a consolidation lying in the posterior basal segment of the right lower lobe (Fig. ). The bronchus, pulmonary artery, and pulmonary vein of the right lower lobe appeared normal on the computed tomographic scan. On the basis of these findings, the patient was diagnosed with intra lobar PS, which was of type 1 according to Pryce’s classification, and treatment using video-assisted thoracic surgery (VATS) was planned.
The patient was administered general anesthesia using one-lung ventilation and was placed in a full left lateral decubitus position. A 10-mm 30-degree thoracoscope was inserted into the right pleural cavity through a 3-cm incision in the 7th intercostal space along the midaxillary line, at which time several capillaries meandering on the visceral pleura of the lower lobe were found. Running parallel to the inferior vena cava, the aberrant artery (7 mm in diameter) flowing into the lower lobe was identified (Fig. ). A 4-cm incision in the 5th intercostal space along the anterior axillary line and a 3-cm incision in the 7th intercostal space along the posterior axillary line were made. The aberrant artery was transected using a 45-mm stapling device at a distance of 2 cm from the diaphragm toward the head (Fig. ) and a standard VATS lobectomy was performed The patient had no postoperative complications and was discharged on postoperative day 10.


A 60-year-old African American female with no known prior medical history presented to the emergency department with complaint of intermittent fever, nausea, and vomiting for 2-week duration, in addition to a dry cough for five days. Also notable in her history was a recent travel to Dallas and Las Vegas from Michigan 1 week prior to presentation. Initially, she had a septic presentation with a blood pressure of 82/45 mm Hg, fever of 101 degrees Fahrenheit, leukopenia with a white blood cell count (WBC) of 3.5 k/mcl, a respiratory rate of 22 breaths per minute, and a rapid heart rate of 150 bpm. After hemodynamic stabilization with intravenous fluids, a computed tomography (CT) of abdomen and pelvis with contrast was performed and it demonstrated a septic deep venous thrombosis of the ovarian vein with extension into the inferior vena cava (IVC), seen in . Anticoagulation with intravenous heparin and broad-spectrum antibiotics (ceftriaxone, gentamicin, and metronidazole) were initiated. Blood cultures from two bottles collected prior to antibiotic administration grew Streptococcus constellatus, and the initial antibiotics were changed to ampicillin-sulbactam. The pelvic and transvaginal ultrasound tests were unremarkable. Urine and cervical cultures were negative. Chest X-ray findings included right upper lobe infiltrates concerning pneumonia. CT-thorax demonstrated a 1.1-centimeter nodule in the right lung and airspace disease in the right middle lobe suspicious for pneumonia superimposed on emphysema, but it was negative for acute pulmonary embolism. Echocardiogram was normal with no vegetation visualized. The patient remained free of fever for more than 24 hours prior to discharge. She was also bridged after 24 hours to warfarin for continued anticoagulation therapy and remained hemodynamically stable and asymptomatic. She was discharged home in stable condition after a 5-day hospitalization; she was continued on oral antibiotics (amoxicillin and clindamycin) for 10 days, as well as oral anticoagulation (warfarin) for 3 months. The patient was followed up as an outpatient and was clinically doing well with no complaints and had remained persistently afebrile; her international normalized ratio (INR) remained therapeutic. A repeated CT two and a half months later showed a complete resolution of the septic thrombophlebitis of the right ovarian vein and IVC, . Also there has been a complete resolution of the pulmonary nodule which may suggest septic emboli to the lung versus upper respiratory infection at presentation.


A 10-year-old Afro-American boy (36 kg), diagnosed with idiopathic nephrotic syndrome for 3 years, was treated initially with prednisolone (1.5 mg/kg/day) and then for a shorter time with mycophenolate mofetil (MMF) partly in combination with cyclosporine. His caretaker refused to continue the advised cyclosporine + MMF treatment or to switch to tacrolimus and only gave him high-dose prednisolone for more than 1 year. In this year he developed steroid resistance. A kidney biopsy—taken shortly before treatment with RTX—showed minimal change nephropathy.
On admission the patient was Cushingoid and had proteinuria with significant peripheral edema, pleural and pericardial effusion, and ascites. Following drainage of the pleural, pericardial, and peritoneal fluid he showed clinical improvement. Laboratory results demonstrated elevated serum creatinine [91 μmol/L; estimated glomerular filtration rate 60 mL/min/1.73 m2; normal range 80–120 mL/min/1.73 m2 (Schwarz formula)], elevated blood urea nitrogen (8.2 mmol/L; normal range 1.8–6.4 mmol/L), and severe hypoalbuminemia (≤15 g/L; normal range 35–55 g/L). Serum immunoglobulin G (IgG) was extremely low (0.25 g/L; normal range 5.2–15.6 g/L), probably due to non-selective proteinuria. Urinalysis showed severe proteinuria (21.5 g/L; >2220 mg albumin/mmol creatinine), with a low selectivity index of 0.33 [(urine IgG/serum IgG) × (serum albumin/urine albumin)]. The clinical decision to treat the patient with RTX was made in order to achieve quick clinical improvement.
RTX was started at a dose of 375 mg/m2, and serum concentrations of RTX and B lymphocyte counts were measured. The concentration of RTX in serum samples was determined using a direct enzyme-linked immunosorbent assay [see (ESM)]. RTX concentrations fell very quickly (Fig. a), and at 14 days after the initiation of RTX therapy, complete CD20+ B cell depletion was documented (<10 CD20+ B cells/μL) (Fig. b); however, as quickly as 1 week later CD20+ B lymphocytes reappeared. The next three RTX doses were given at shorter intervals, with a target serum RTX concentration of >10 μg/L (20, 24 and 31 days after the first dose, respectively). This therapeutic strategy achieved CD20+ B lymphocyte depletion from day 19 to day 39. A few circulating CD19+ B lymphocytes were still present at day 39, but after day 39 B lymphocytes were not tested anymore. The elimination serum half-life of RTX in our patient was <1 day, compared to 20 days in a group of patients receiving RTX post-stem cell transplantation. These latter patients had no urinary protein loss, normal kidney function, and no ascites (C.M. Jol–van der Zijde; unpublished observations). High concentrations of RTX were found in our patient’s urine and pleural fluid (Fig. a).
The population pharmacokinetics of RTX was simulated in a two-compartment structure [, ], with additional simulations for urinary and pleural fluid loss, using the software package R 2.12 (see Table 2). Urinary clearance, as derived from the measurements of RTX concentrations in the urine and urine production, was at least 25 % of the total clearance, whereas in stem cell transplantation patients without proteinuria, urinary clearance was nil. Pleural clearance, as derived from RTX concentrations in pleural fluid and the drained amount of pleural fluid, was around 2 % of the total clearance (data not shown). However, these losses explained only part of the rapid drop in serum RTX concentration. Antibodies against RTX could not be detected [].
Because of ongoing proteinuria and ascites, pleural and pericardial effusions after the four doses of RTX, and severe hypertension, an angiotensin-converting enzyme-inhibitor (enalapril), diuretics, and tacrolimus were added to the therapeutic regimen. Four months after the first dose of RTX, prednisolone was tapered and could be stopped. Six months after RTX treatment, the patient still had proteinuria (1000 mg albumin/mmol creatinine), but he was in a stable situation, without edema and with normal blood pressure, under treatment with tacrolimus, ramipril, and hydrochlorothiazide.


The patient was a 62-year-old nonparous woman with no history of a gynecological disease. She had an enlarged abdomen during the 2 months preceding her visit to our hospital, and she had lower abdominal pain 2 days before her visit. She was transported to our hospital by ambulance and complained of disabling back pain. An abdominal examination revealed a palpable mass in the right lateral region of her abdomen. Transabdominal echography and computed tomography revealed a multilocular-solid tumor (>20 cm in diameter) in her pelvis, and massive ascites extended into the liver and spleen (). Blood analysis showed hyperuricemia, hyperkalemia, hyperphosphatemia, and increased levels of plasma creatinine (). These findings fulfilled the diagnostic criteria of TLS.
Following admission, the patient had anuria that responded poorly to aggressive fluid administration. We thought that her presentation could not be explained only by fluid shifts. Two days after admission, laboratory data indicated that her condition had worsened. Her respiratory status declined, and she was placed on a respirator. She also received a vasopressor to maintain her blood pressure. We decided to surgically reduce the amount of the tumor mass and to drain her abdomen in order to improve her condition. Abdominal bilateral salpingo-oophorectomy, hysterectomy, and abdominal drainage were performed ().
We made a midline skin excision extending from the symphysis pubis to the right side of the umbilicus. The abdominal cavity was adequately exteriorized, and 3,300 mL of bloody, viscous fluid was suctioned. The large mass in the right ovary was extracted with the uterus and left ovary, which were macroscopically normal. The abdominal cavity was washed with saline to remove tumor tissue that adhered to the thickened, hyperemic peritonea. A drainage tube was placed in the upper abdomen, and the abdomen was closed. The patient received intensive care postoperatively, and her condition improved. The expression levels of biochemical markers returned to normal.
Pathologic examination of the neoplasm from the right ovary showed a well-differentiated (grade 1) endometrioid adenocarcinoma with extensive necrosis and capsular rupture (). Cytology of the ascitic fluid showed no malignant cells. There were no remarkable changes in the macroscopic appearance of the left ovary or uterus. The final surgical pathologic diagnosis was stage IC ovarian endometrioid adenocarcinoma.
Postoperatively, the patient received six cycles of combination chemotherapy, which consisted of docetaxel and carboplatin. No signs of recurrence were observed at the 8-month follow-up.


A 41-year-old man was admitted for acute rehabilitation after a right middle cerebral artery ischemic stroke which was not treated with a thrombolytic agent. His past medical history included poorly controlled hypertension, type 2 diabetes mellitus (DM), and prior transient ischemic attacks. He had no known allergies to medications and denied having had surgeries.
Eight days after the stroke, he complained of a cold sensation and excessive perspiration on the right side of his face and body. He also began having daily fevers (max 101.5°F) associated with tachycardia (max 119 beats per minute). He had no significant tachypnea (range 18–20 breaths per minute) or hypertension (max systolic blood pressure 132 mm Hg, max diastolic 83 mm Hg), although he was taking fosinopril. Extensive workup revealed no infectious source, and his fever did not abate with repeated doses of acetaminophen.
He was fully conscious, alert, and oriented at each examination and fully participating in physical therapy. On inspection, excessive sweating was noted along the right side of his body and lower right side of his face. On palpation, his right arm was cool to the touch. Neurologic examination revealed normal mental status and cranial nerves II–XII were intact. Strength testing revealed right upper extremity strength of 4/5 for shoulder abduction, elbow flexion, elbow extension, and handgrip. The right lower extremity exhibited 3/5 strength for hip flexion, 4/5 for knee flexion, and 2/5 for ankle dorsiflexion. Tone was diffusely increased on the right, rated 1/4 on the modified Ashworth scale. Reflexes were 2+ and symmetrical in the biceps brachioradialis, triceps, and gastrocnemius-soleus complex; however, the right great toe was upgoing. Sensation was impaired to temperature and light touch along the right side of his body and face.
Magnetic resonance imaging (MRI) revealed a large area of infarction in the left periventricular white matter, left internal capsule posterior limb, and dorsal aspect of left lateral basal ganglia extending into white matter adjacent to the left occipital horn.
With a presumptive diagnosis of PSH, propranolol 10 mg twice daily was started. After demonstrating tolerance and persistent breakthrough symptoms, dosing was increased to three times daily. The patient's symptoms of unilateral cold sensations, hyperhidrosis, tachycardia, and fever resolved within one day. As a trial, propranolol was discontinued, and, although no fever or tachycardia was documented, symptoms of unilateral hyperhidrosis, cold sensations, and subjective fever returned. Propranolol was then restarted, and the patient continued to have symptomatic relief at follow-up.
Using the PSH Assessment Measure [], our patient scored 4/18 on the Clinical Features Scale and 9/11 on the diagnosis Likelihood Tool. The total score of 13 suggests the diagnosis of PSH is “possible” (range 8–16). He had no identifiable triggers for his symptoms, such as an allodynic reaction, and only the fevers and tachycardia were paroxysmal; the hyperhidrosis and cold sensation on the right side were constant. Aside from the spasticity attributed to his stroke, he experienced no dystonic posturing associated with paroxysms. Unlike many patients with traumatic brain injury, our patient had a focal unilateral ischemic stroke, which likely tempered the severity of his symptoms in comparison to those with more severe or bilateral injuries.


52-year-old man, plumber by profession, presented at the emergency department with one day history of having sudden onset spontaneous pain and functional impairment of left knee while he was walking. The patient had history of hypertension. He had no history of taking medications such as corticosteroids or fluoroquinolones and did not remember having suffered any knee pain previously. On clinical examination effusion was present in knee. It was possible to palpate a gap between the distal patellar tendon and the tibial tuberosity and patient was not able to extend the leg. X-ray of the left knee showed a high patella and presence of calcification in the distal part of the patellar tendon (). Ultrasound later confirmed the diagnosis of distal avulsion of the patellar tendon. Although CT scan and MRI are superior modalities for confirmation of the diagnosis but based on our clinical examination, typical radiographic finding and ultrasound imaging, we considered these expensive investigations unnecessary in this case. On the second day, patient was taken to the operating room. Under tourniquet control, patellar tendon was exposed through anterior approach to the knee. Distal insertion of the tendon was found to be completely avulsed from the tibial tuberosity with some flakes of sclerotic bone (). The torn tendon was found to have degenerative changes at the injury site. The tendon stump was debrided and refashioned. Locking double Krackow stitch was taken with FiberWire number 5, and then it was anchored to tibial tuberosity after drilling four 2.0 mm transverse holes in tuberosity. Full range of motion of the knee was performed to evaluate the repair and we found it satisfactory. Repair of paratenon was performed and wound was closed. Postoperatively, knee was locked in a brace at 0 degrees of extension and the patient was encouraged to do isometric quadriceps strengthening exercises. Patient was allowed weight bearing as tolerated. A range of motion exercises were progressively started after 5-week follow-up. The patient achieved full active range of motion by third month of follow-up, complaining only of a slight tenderness on pressure at the level of the tibial tuberosity. X-rays were taken in the last follow-up at 5 months showing normal position of the patella (), while clinical examination revealed full recovery.


Twenty three year-old female was complained of mouth opening limitation, TMJ pain and sound. The mouth opening at initial examination was 32 mm (Fig. ). The patient has suffered from this problem, and experienced arthrocentesis before. Under diagnosing to chronic closed lock on both TMJ and anterior disk displacement without reduction in MRI (Fig. ), ultra-thin arthroscopic diagnosis and arthrocentesis was performed, and the adhesion was removed with trocar through the portal of Chung's needle (Figs. , ). After arthrocentesis, range of mouth opening was 45 mm, and symptom was disappeared (Fig. ).


Twenty two year-old female was complained of habitual dislocation, articular sound and pain. The patient had prior history of TMJ dislocation 3 to 4 times in a week, and reduced by herself. Chung’s needle introduced to the superior joint space of the TMJ, inserted the unltra-thin arthroscopy and RF surgery tip (Fig. ) and retrodiscal tissue was injured with RF surgery instrument through the Chung’s needle and irrigated the joint space (Fig. ). The patient had no pain during mouth opening and no episodes of dislocation after treatment.


The proposita is a 10.5 year-old girl, second born of non-consanguineous healthy parents. Her elder brother is referred to be healthy and his stature is 150 cm at 14 years (5th centile for age) (National Center for Health Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion (2000) []), with pubertal development of PH3 G3 following Tanner stage. A third pregnancy hesitated in a spontaneous abortion. Her father is 169 cm whereas her mother is 150 cm high.
She was born at 39 gestational weeks, after normal pregnancy, by Caesarian section. Intrauterine growth retardation was detected during last weeks of gestation and her neonatal weight was 2.400 Kg, with a stature of 48 cm and an occipito-frontal circumference of 33 cm. In neonatal period, because of heart murmur, she underwent echocardiographic evaluation that evidenced an ostium secundum interatrial defect, spontaneously closed at 2 years. At 7 years slight hairs covered her back and arms, and overweigh was noted. Her parents reported slowdown in growth curve in the last 6 months despite a rapid increase in body weight.
Anthropometric values and clinical findings at 7 years were: stature 114.6 cm (3-10th centile), weight 25 kg (75th centile), BMI 19 (90-95th centile). Pubertal development was PH1 B1 following Tanner stage; genetic target was cm 153.5 + 6. At a further observation at 8 years, she presented with healthy condition, short stature (height cm 116 – below 3rd centile), overweight (weight kg 29 – 75th centile, BMI 21.55 – above 95th centile), hypertrichosis with slightly hairy legs and back, mild short neck, very mild valgus elbow, and small joint hyperlaxity, shortening of the fifth metacarpal with syndactyly of 2th and 3th of the toes.
At a first examination, laboratory tests evidenced: FSH: 12.3 mIU/ml; LH: 0.8 mIU/ml; Estradiol 10.2 pg/ml. Adrenal and thyroid profiles were within the normal range for age. Abdominal ultrasound revealed normal kidney, and pelvic echography showed reduced ovarian size range for age (right ovary 15 mm × 8 mm × 12 mm; left 13 mm × 7.4 mm × 10 mm). Because of hairiness increase, a new serum hormonal evaluation was performed at 7.5 years: laboratory tests showed elevated FSH values (31.3 mUI/ml) with normal prepuberal values of LH (0,7 mUI/ml) and Estradiol (13.2 pg/ml); a further pelvic ultrasound revealed infantile uterus and confirmed size reduced ovaries.
Analysis of FMR1 triplet repeat sizes in the proband by repeat primed PCR [] revealed sizes in the normal range (20 to 33 CGG repeats) (data not shown).
During 1-year follow-up period, a POI was suspected according to high FSH and LH levels and low Estradiol, inhibin B and AMH levels. Serum FSH and LH values increased to 179.90 mlU/ml and 40.30 mlU/ml respectively, while Estradiol decreased to 10 pg/ml. Inhibin B showed a level <20 pg/ml and AMH serum levels were 0.4 ng/ml, well below the normal range.
Bone age of 6 years was assessed by radiological examination of the left-hand wrist (Tanner e Whitehouse (TW2) method), despite a chronological age of 8 years. Stimulation tests for growth hormone (GH) reserve were performed because of deceleration of growth curve, increased gap from the stature target, and retardation of bone age. Testing for GH revealed a 1.4 ng/ml peak after arginine injection (0.5 g Arginina/kg in vein infusion in 30 minutes) and a 4.5 ng/ml peak after clonidine administration (100 mcg/m2 per os). Replacement therapy with rh-GH at standard dose for GHD patient was started (0.23 mg/kg/week). During GH-replacement therapy follow-up a gain of growth rate (25-50th centile) with achievement of target height in the first 6 months of therapy was observed. Any side effect was reported.
Pubertal induction with estroprogestin hormones was considered in long-term follow-up to prevent the ovarian failure that often occurs in majority cases before puberty and leads to infertility.


A fifty-nine year old male presented with a 4 × 2 cm lump in the right neck at level II. He had noticed the swelling for less than one week but reported a three year history of sore throat, fatigue, reduced exercise tolerance and shortness of breath. He had never smoked and consumed 18 international units of alcohol per week. There was no other lymphadenopathy and no intra-oral abnormality. Fine needle aspiration cytology was inconclusive and the patient underwent a diagnostic lymph node excision for histological evaluation, which showed metastatic squamous cell carcinoma. Computed tomography (CT) and 15fluoro-deoxyglucose positron emission tomography-computed tomography (FDG-PET/CT) were undertaken to identify the primary site and revealed a 2 cm mass involving the right tonsil with a right sided level II lymph node mass extending into the deep lobe of the right parotid gland. He was treated with radical chemoradiation comprising image-guided intensity modulated radiotherapy (IMRT) delivering 65Gy in 30 fractions to the oropharynx and right neck level II with 54Gy in 30 fractions to right neck levels III to V and left neck levels II to V. Concomitant cisplatin 100 mg/m2 was given on days 1 and 29 of radiotherapy. A FDG-PET/CT scan performed at 3 months post-treatment confirmed a complete metabolic response. The patient remains disease free after 15 months.
Histological evaluation of the excised lymph showed complete effacement by carcinoma comprising two clearly demarcated and morphologically distinct subpopulations of cells. In most areas, the two subpopulations were separated by fibrous tissue bands. Where the two phenotypes were not separated by fibrous tissue, there was abrupt delineation of the subpopulations without any intermediate transition. One component was composed of broad interconnecting strands of tumour cells with obvious squamous maturation but with minimal keratinisation typical of conventional HPV-associated OpSCC, designated the ‘differentiated’ component. The second component, referred to as the ‘undifferentiated’ component, was arranged as syncytial sheets of cells with comparatively large vesicular nuclei (Fig. and ). Immunohistochemically, both components demonstrated strong nuclear positivity for p63 (1:50, Clone 4A4, Santa Cruz) and strong nuclear and cytoplasmic staining for p16 (pre-diluted, CINTec, MTM Laboratories) in greater than 70 % of tumour cells (Fig. and ). While the differentiated component demonstrated strong and moderate staining for CK5/6 (1:25, Clone D5/16 B4, Dako; Fig. ) and Vimentin (1:500, Clone V9, Dako; Fig. ), respectively, expression of these proteins were weak to absent in the undifferentiated component. Similarly, while there was moderate protein expression of CK8/18 (1:2, Clone Cam5.2, Dako) and CK19 (1:50, Clone RCK108, Dako) in the differentiated areas, there was no staining for these cytokeratins in the undifferentiated component (data not shown). Both components were negative for CK7 (1:200, Clone OV-TL 12/30, Dako) and CK20 (1:25, Clone Ks 20.8, Dako; data not shown). A modified quick score was used for semi-quantification of immunohistochemical staining. Briefly, the proportion and intensity of staining was quantified from 0–5 and 0–3, respectively. The quick score is the sum of the proportion and intensity giving a range of 0–8 []. There was also a greater proliferation index (Ki-67; 1:50, Clone MIB-1, Dako; data not shown) and a denser population of tumour infiltrating lymphocytes (TILs; CD45, 1:100, Dako; Fig. ) in the differentiated component in this case. By contrast, the undifferentiated cells showed strong diffuse nuclear staining for high-risk HPV DNA (Inform HPV III Family 16 probe, Ventana Medical Systems) suggestive of episomal viral DNA while the differentiated cells only showed punctate nuclear staining in a pattern consistent with viral integration (Fig. ).


A fifty-four year old male presented with an eight month history of right-sided level II neck lump. He had a life-long history of smoking 10 cigarettes a day and heavy alcohol use of 40 international units per week. Examination revealed a 2 cm right sided tonsillar mass extending to the tonsillar pillar and the soft palate with a 6 × 4 cm right sided neck mass spanning levels II and III. Tonsil biopsy confirmed squamous cell carcinoma. The patient was treated with two 3-weekly cycles of induction chemotherapy comprising cisplatin 80 mg/m2 on day 1 and continuous infusional 5-fluorouracil 1000 mg/m2 on days 1–4, followed by radical chemoradiation. IMRT consisted of 65Gy in 30 fractions to the oropharynx and right neck levels Ib, II and the upper part of level III and 54Gy in 30 fractions to the right neck lower level III, IV and V and left neck levels II to V. Concomitant cisplatin 100 mg/m2 was delivered on days 1 and 29 of radiotherapy. A 3 month post-treatment FDG-PET-CT scan showed an equivocal FDG uptake of 4.5 maximum Standardised Uptake Variable (SUV) noted at the original site but with no mass lesion correlated on CT imaging and only low-grade FDG uptake in minimally enlarged right sided level II neck nodes. A multidisciplinary review recommended surveillance with repeat FDG-PET/CT scanning after three months.
Incisional biopsy of the right tonsil showed a biphenotypic carcinoma with features similar to those of Case 1. In addition, the differentiated component demonstrated a focal papillary architecture lacking keratinisation and centred on the tonsillar crypts (Fig. and ). Both components demonstrated strong nuclear positivity for p63 and strong nuclear and cytoplasmic staining for p16 in greater than 70 % of tumour cells (Fig. and ). By contrast to Case 1, the differentiated component showed greater percentage and intensity of staining for CK7 (Fig. ) and CK19. Furthermore, unlike Case 1, both components showed similar percentage and intensity for CK8/18 and similar percentage of cells in cycle (data not shown). Also by contrast to Case 1, high-risk HPV ISH showed diffuse nuclear staining in the differentiated compartment and a punctate pattern in the undifferentated areas (Fig. ). A slightly lower density of TILs was present in the former component (Fig. ). The relative expression of Vimentin in the two components was similar to that of Case 1 (Fig. ). The immunohistochemical profiles for cases 1 and 2 are summarised in Table .


A 62-year-old male presented with progressive dyspnoea for 10 days. He had a background of stage IV metastatic non-small lung carcinoma treated for 6 months with non-cardiotoxic chemotherapy (carboplatin and gemcitabine), and recently commenced on target therapy (Erlotinib). Clinical examination revealed signs consistent with cardiac tamponade, including significant pulsus paradoxus, tachycardia (heart rate 101), tachypnea (respiratory rate 25), elevated jugular venous pressure and muffled heart sounds. He was normotensive at 130/90mmHg. The patient was extremely anxious and spontaneously expressed concern about his imminent death.
His electrocardiogram (ECG) (Fig. ) demonstrated electrical alternans and bedside transthoracic echocardiography (TTE) revealed a large pericardial effusion with features of cardiac tamponade, including diastolic compression of both right atrium and ventricle (Fig. , Additional file : Video 1 and Additional file : Video 2) and large mitral inflow variation (Fig. ). Urgent pericardiocentesis was performed with a restricted aspiration of only 600 ml drained initially over the first hour, and a total drainage of 1.8 l of heavily blood-stained pericardial fluid over 36 h. During initial aspiration of pericardial fluid there was immediate symptomatic relief and haemodynamic improvement (heart rate [HR] decreased to 80/min, respiratory rate [RR] decreased to 15 breaths/min and BP increased to 150/70 mmHg).
Overnight (9 h post procedure) the patient developed chest discomfort, dyspnea, tachycardia (HR 110) and tachypnoea (RR 24). TTE the next morning showed no re-accumulation of pericardial fluid, but detected new severe impairment in function of both ventricles, with akinesis of the apex and peri-apical region (Figs. and , Additional file : Video 3 and Additional file : Video 4). Biomarkers demonstrated a rise in highly sensitive troponin from 8 to 224ng/L, but creatinine kinase did not rise significantly (107 to 116U/L). ECG after chest pain demonstrated resolution of the electrical alternans, with new loss of R waves in the anterior leads (Fig. ).
Based on a presumptive diagnosis of SCM, angiotensin converting enzyme inhibitor and long acting beta-blocker were commenced, chemotherapy withheld and the patient discharged for early clinical and echocardiographic review. Serial follow up TTEs showed normalization of bi-ventricular function after two weeks (Figs. and , Additional file : Video 5 and Additional file : Video 6), and restoration of R waves on subsequent ECGs (Fig. ). Subsequent computed tomography examination showed normal coronary arteries with a calcium score of zero and no evidence of LAD laceration or dissection.
The patient presented three months later with re-accumulation of pericardial effusion and tamponade. Therapeutic pericardiocentesis was performed with 500 ml of blood stained pericardial fluid drained immediately, with 1.9 L in total over 36 h. On this presentation he was relaxed and well adjusted in regards to his diagnosis. No LV dysfunction was detected on serial follow-up echocardiograms after the second pericardiocentesis (Fig. ).


A 19-year-old man with no markedly past medical history was found lying on the floor, unresponsive, by his colleagues at 09:40 AM of October 28, 2014. One colleague immediately called the emergency medical services (EMSs) by mobile phone, while another performed bystander cardiopulmonary resuscitation (CPR). The ambulance with 2 EMS providers arrived within 5 minutes. They found the patient pulseless, with no signs of breathing and nonreacting pupils. The first electrocardiogram detected pulseless electrical activity (PEA). The patient was transported to the emergency department under continuous manual chest compression. The patient did not receive any medications before admission.
The patient arrived at the Emergency Department of Nanjing Drum Tower Hospital 15 minutes after cardiac arrest. He had poor general conditions with Glasgow Coma Scale score 3; he had no spontaneous respirations and heart rhythm, no response to verbal stimuli, and had fixed and dilated pupils. The advanced life support protocol was immediately started by emergency physicians in our department. The patient was intubated and mechanically ventilated, while CPR was continuously performed using a gas-driven mechanical chest compression (Grand Rapids, Michigan Instruments; Hirtz, Koln, Germany) with compression rate 100/min and deepness of chest compression 5 cm). Ventricular fibrillation was first detected 35 minutes after cardiac arrest by the defibrillator, and 4 defibrillations (ventricular fibrillation or pulseless ventricular tachycardia) were performed in all, following injections of adrenaline (5 mg in all), as well as amiodarone and dopamine infusions. One hundred and twenty minutes after cardiac arrest, he presented successful return of spontaneous circulation (ROSC) with blood pressure 85/42 mm Hg and heart rate 103 bpm. The patient showed hypoxaemia (pulse oxygen saturation <90%; positive end-expiratory pressure 12 mm Hg, Fio2 100%, 1 hour after ROSC), although invasive mechanical ventilation was given. The arterial blood gas was pH 7.309, partial arterial CO2 pressure 40.3 mm Hg, PO2 52.8 mm Hg, Fio2 100%, and Po2/Fio2 52.8, and the chest x-ray showed pulmonary edema (Figure ).
Then the patient was moved to the emergency intensive care unit 3.5 hour after the onset, and his vital signs were as follows: temperature 39°C, heart rate 110 bpm, blood pressure 83/55 mm Hg (dopamine infusion 12 mcg/kg · min), and oxygen saturation 95% (mechanical ventilation, Fio2 50%), and the serum neuron-specific enolase (NSE) was significantly elevated (75.05 ng/mL, reference 0–16.3 ng/mL). Neurological examination was notable for the following: disappeared spontaneous respiration, fixed and dilated pupils, absent corneal reflexes, and absent motor responses to painful stimuli in all extremities. The repeat electrocardiogram showed a right bundle branch block and ST segment elevation in leads V1–V2 (Figure ). The patient's uncle had experienced the same event and had received implantable cardioverter defibrillator (ICD) treatment 1 year earlier. Therefore, the patient was diagnosed with Brugada syndrome.
A mild therapeutic hypothermia (MTH) was started (∼5 hours after cardiac arrest) by infusing a cold (4°C) saline solution (1.8 L in all). The body temperature decreased to 35.9°C (24 hours after cardiac arrest), and the core temperature was maintained between 34°C and 36°C for 24 hours in combination with an external cooling mattress (HICO-Hypotherm 680 of Hirtz and HICO-Polyurethan water mat; Hirtz, Koln, Germany). Shivering appeared in MTH; the shivering was suppressed with lytic cocktail therapy (chlorpromazine, promethazine, and pethidine) and high doses of sedatives (midazolam, fentanyl, and propofol). No other complications occurred during the cooling procedure. Bedside echocardiography showed left heart insufficiency and an ejection fraction of 33%. Because of heart dysfunction and unstable circulation (systolic blood pressure 76–83 mm Hg), the patient received dopamine and an intraaortic balloon pump (IABP), and pulse index continuous cardiac output (PiCCO) monitoring system was introduced (Table ). Active rewarming was initiated at 0.2°C/hour 48 hours after cardiac arrest. The rewarming goal temperature of 37.0°C was reached within 6 hours. Dopamine infusion and IABP were then discontinued because circulatory condition and heart function had improved.
The patient's consciousness improved 58 hours after cardiac arrest; he was able to open his eyes to command and respond to painful stimuli. He was awake and intermittently moved his extremities 71 hours after cardiac arrest. The patient was extubated after a successful spontaneous breathing trial on day 4 after cardiac arrest. Then he spoke in full sentences, was fully aware of person, place, and time, and accurately exhibited full strength in all his extremities. The repeat NSE was 13.77 ng/mL. A noncontrast head computed tomography scan was performed, which showed no evidence of intracranial hemorrhage, mass infarction, or cerebral edema. He was able to ambulate with a walker and independently perform activities of daily life on day 5 after the cardiac arrest. Magnetic resonance imaging and an electroencephalogram were performed, showing nothing abnormal. He completely recovered with 1 point based on the criteria of cerebral performance category on day 8 after cardiac arrest and was then transferred to the cardiology department. He was implanted an ICD on day 10 after the cardiac arrest. The patient was followed up at 1 and 4 months after discharge and he had no noticeable neurological or intellectual deficits (Figure ).


Informed patient consent was obtained prior to all treatments.
A 51-year-old male with a previous history of metastatic papillary thyroid carcinoma presented with lower facial numbness and a fullness sensation on the left ear for four months. The patient’s medical history includes a total thyroidectomy and radiotherapy with Iodine-131 six years prior. Three years later, he developed metastatic disease to the left neck and internal jugular vein that was treated with a left neck dissection, including jugular vein resection followed by postoperative radiotherapy to 6600 cGy. Three more years later, he subsequently developed a left serous effusion and marked numbness in the left V3 territory. A myringotomy with fluid evacuation as well as magnetic resonance imaging (MRI) with gadolinium of the head and neck were performed. The MRI revealed a 4 x 3.3 cm highly vascularized tumor in the left pre-styloid PS with foramen ovale invasion (Figure ). A fine needle biopsy confirmed a papillary thyroid carcinoma metastasis. A preoperative endovascular embolization of the tumor feeders, including the left distal internal maxillary, accessory meningeal, and pharyngeal branch of the ascending pharyngeal artery, was performed two days prior to surgery.
Bearing in mind the prior treatment given to neck and the close relationship of the tumor with the foramen ovale, and considering the complexity of approaching this location only by a TC access, a combined TC and EEA approach was considered.
A simultaneous, transmaxillary-transpterygoid endoscopic EEA and TC approach was performed on the left side of the neck. The standard transcervical approach was performed first as described in the literature []. The styloid process was resected and the retro-styloid compartment was identified. The carotid artery and lower cranial nerves were identified and dissected to the skull base away from the tumor (Figure ). The vessel was protected with cottonoid pledgets. The tumor was dissected free along its anterior, inferior, and lateral margins and detached from the pterygoid muscle and medial constrictor muscle.
Subsequently, the superior and medial margins were approached through the EEA. The left nasal cavity was accessed through the left nostril and the middle turbinate was removed. The medial maxillary wall was removed, along with the piriform process and 5 mm of the anterior maxillary wall to access the maxillary sinus []. Next, the posterior and lateral walls of the maxillary sinus were removed to expose the pterygopalatine fossa. The internal maxillary artery was identified laterally and ligated with endoscopic clips. The transpterygoid approach was carried out to dissect the tumor from the Eustachian tube [], expose the foramen ovale, and delineate the tumor involvement at the skull base (Figure ). At this point, the foramen ovale and rotundum were dissected preserving V2 and V3. The dura exposed was in direct contact to the tumor, but no signs of an invasion were observed. The combined approach provided a 360-degree access to the tumor, allowing the direct control of the neurovascular structures and a safe PS dissection.
The wound defect was closed using vascularized buccal fat and a pedicled mucosal flap harvested from the floor of the nasal fossa (Figure ). Postoperative MRI revealed a gross total resection of the mass. The patient was discharged from the hospital on postoperative day five without significant cranial nerve dysfunction or wound complication. An abbreviated CyberKnife radiation treatment was given to the dura at the foramen ovale. One year after the operation, the patient recovered sensation over the face and had no left ear symptoms.


A 37-year-old female, postlaminectomy status for the treatment of lumbar back pain, presented with unrelenting abdominal pain 10 hours after the procedure. The patient denied any nausea, vomiting, diarrhea, fevers, or chills at that time, but due to the acute nature of the pain it was evident to her that she had either developed some type of postoperative complication or was experiencing a nascent abdominal pathology that would require immediate medical attention. The patient's past medical history was significant for chronic back pain and lumbar disc disease, with no significant surgical history prior to the laminectomy. Vital signs upon admission and consultation were stable and the patient was afebrile. Physical exam revealed a well-nourished, well-developed female that was alert and oriented albeit in obvious discomfort. The patient's physical exam was unremarkable except that her abdomen was exquisitely tender to palpation without any distension and there was significant tympany upon percussion. The electrolyte profile was essentially normal, but total bilirubin was elevated at 2.1 mg/dL. Urine pregnancy test was negative and the complete blood count showed an elevated white blood cell count of 15.4 × 103/μL, with a hemoglobin and hematocrit of 12 g/dL and 34%, respectively.
Computed tomography (CT) of the abdomen and pelvis showed evidence of retroperitoneal air, which seemingly tracked back into the spinal canal (). In addition, there was free air seen intraperitoneally without an obvious source or evidence of an inflammatory process in her abdomen at that time (). It was suspected that the retroperitoneal air may be secondary to deep surgical penetration into the small bowel during the laminectomy and the patient was initially treated expectantly with intravenous antibiotics and observation. On hospital course days two and three the patient began to spike and maintain fevers, with air continuing to appear in the psoas muscles and significant air within the peritoneal cavity. The follow-up CT showed that the patient had developed ascites suggesting a small bowel perforation until proven otherwise (). The patient was taken to the operating room for emergent laparoscopic exploration.
After dissecting through the subcutaneous tissue and the anterior rectus fascia in a standard fashion, the Hassan trocar was inserted and a laparoscopic view of the abdomen was undertaken. There was a marked amount of seropurulent fluid extending from the right and left colic gutters down to the Pouch of Douglas. The appendix was visualized and appeared normal; however, while running the small bowel, beginning at the terminal ileum, a significant amount of inflammatory and fibrinous exudate was discovered (). Upon approaching the proximal ileum and jejunum, an area of perforation was identified as evidenced by where the omentum had adhered to the small bowel (). With very light manipulation, enteric contents exuded from the small bowel and the procedure was converted to an open exploratory laparotomy. After repairing the enterotomy with interrupted Vicryl sutures and reinforcing it with silk suture in a Lembert fashion, the abdomen was irrigated copiously. Other than the jejunal-ileal perforation, no other intra-abdominal pathologies were noted during exploration. The patient's postoperative hospital course was unremarkable and she tolerated the small bowel repair without complication.


The patient was a 49-year-old male who came to our hospital due to “sudden severe headache accompanied by nausea and vomiting for three hours.” The patient had a medical history of a space-occupying lesion in the sellar region, which was regarded as a pituitary adenoma and had not been treated. The patient had no history of hypertension or diabetes mellitus. The examination of neurological system revealed the following: the patient was conscious and could answer questions correctly, the left eye vision was 0.2, the right eye vision was 0.5, there was bilateral temporal hemianopsia, and optic nerve atrophy was observed in the fundus. The patient had flexible limbs, normal muscle tension, grade V muscle strength, positive Kernig signs, and a grade III Hunt-Hess classification. The routine physical examination revealed that the skin was delicate, the pubic hair was sparse, and the breasts were developed. The laboratory tests showed that prolactin (PRL) was 1020 mIU/L (normal range, 70.81–566.46 mIU/L), growth hormone (GH) was 0.60 ng/mL (normal range, 1–5 ng/mL), and other indicators did not show any abnormalities.
Emergency cranial computed tomography (CT) revealed space-occupying lesions in the sellar region with suprasellar expansion, local bone mass destruction, increased density in and around tumors, patchy hemorrhage, and high-density cord-like images in the bilateral sylvian cisterns. The findings were considered to indicate subarachnoid hemorrhage (Fig. , ). Further cranial CT angiography (CTA) examination showed an anterior communicating artery aneurysm; the neck of the aneurysm was shifted toward the left anterior cerebral artery, and the Willis Circle was compressed and pushed to the lateral side (Fig. , ). In addition, cranial magnetic resonance imaging (MRI) revealed that the tumor in the sellar region was significantly enhanced, the boundary was clear, the shape was irregular, and the bilateral carotid arteries were encased by the tumor; the tumor size was approximately 5 cm × 4 cm × 3 cm (Fig. , ). Given the combination of the patient’s medical history, MRI scans, and laboratory examinations, the confirmed diagnosis of the patient was pituitary adenoma apoplexy and a ruptured anterior communicating artery aneurysm.
Anterior communicating artery aneurysm clipping and tumor resection were scheduled. The surgery used the left pterional approach. The tumor was observed in the optic chiasm space; after the tumor was partially resected, the sample was immediately sent for a pathological examination. The pathological hematoxylin-eosin (HE) stain demonstrated a diffuse distribution of cells; the shape was constant, there were few interstitia, and sinusoid capillaries were observed. The immunohistochemistry was PRL positive and confirmed the lesion to be a PRL-type pituitary adenoma (Fig. , ). The anterior communicating artery aneurysm was observed after separation was conducted along the A1 segment of the anterior cerebral artery to the anterior communicating artery. A hematoma was observed in the surroundings, indicating the ruptured aneurysm. The aneurysm pointed to the contralateral side. After the neck of the aneurysm was exposed, the aneurysm was clipped, and the surroundings were explored. The aneurysm was found to be encased by the tumor. The tumor portion was resected (Fig. –). After the surgery, the patient recovered well, and his vision was significantly improved. Cranial CTA was conducted again after 1 week of surgery; the results showed that the aneurysm was well closured, there was no residual neck in the aneurysm, and the morphology and course of the Willis Circle were normal (Fig. , ). The patient recovered well and was discharged. After discharge, the patient received gamma knife radiotherapy. After a half year of follow-up, the patient experienced no clinical complications.
Pituitary adenoma combined with intracranial aneurysm is not rare. The studies of Pant et al. demonstrated that approximately 7.4 % of pituitary adenomas were combined with an aneurysm; 97 % of these aneurysms were located in the anterior circulation []. Because both pituitary adenomas and cerebral aneurysms are common intracranial lesions, these two lesions sometimes coincide and occur concurrently; however, to date, no exact incidence of pituitary adenoma associated with intracranial aneurysm has been determined; nonetheless, there is a general consensus that intracranial aneurysms occur more frequently in association with pituitary adenomas than among the general patient population. In addition, associations with intracranial aneurysms are generally thought to be stronger for patients with pituitary adenomas than for patients with other brain tumors, although the manner in which a pituitary adenoma contributes to the formation of an intracranial aneurysm remains unclear []. Thus, in addition to speculation of an accidental encounter between a pituitary adenoma and an intracranial aneurysm, there exist other hypotheses to explain the manifestations in the described case.
Because the pituitary adenoma is a hormone-secreting tumor, the secreted hormones can induce aneurysm occurrence and growth. The study of Jakubowski et al. showed that in the cases of pituitary adenoma associated with an aneurysm, the pituitary adenomas were mostly of the GH type; by contrast, among the PRL-type pituitary adenomas that had the highest incidence, the probability of association with an aneurysm was very low. Therefore, it was speculated that although GH might induce aneurysm development and growth, PRL may have only weak capabilities in this regard [, ]. Despite these weak capabilities, among 5 cases of pituitary adenoma apoplexy or subarachnoid hemorrhage that we reviewed, at least 4 of the cases involved PRL-type adenomas (Table ). Oh et al. examined 800 cases of pituitary adenoma associated with aneurysm and demonstrated that older age and the existence of a cavernous sinus invasion were correlated with an increased incidence of intracranial aneurysm among patients with pituitary adenomas []. Numerous hypotheses to explain this phenomenon have been proposed, including a direct mechanical effect of the pituitary adenoma on the vasculature, direct infiltration by the tumor, and GH production leading to arteriosclerotic and degenerative changes in the arterial walls of the circle of Willis, thereby, predisposing patients to the formation of aneurysms [–]. Therefore, the underlying reasons for the association between pituitary adenomas and aneurysms require continued exploration and study.
Among the pituitary adenomas associated with aneurysms, aneurysms at the cavernous sinus segment are the most common. This type of aneurysm is mostly embedded inside the pituitary adenoma below the sellar diaphragm []. In cases involving pituitary adenoma combined with an aneurysm, most of the aneurysms are inactive and unruptured. The clinical symptoms are mainly caused by hormones secreted by pituitary adenomas or by compression on the surrounding brain tissues and optic nerve []. However, pituitary adenomas have a rare hemorrhagic clinical presentation, namely, tumor apoplexy; thus, the combined aneurysm factor should be considered. A simple pituitary apoplexy is mainly caused by the rupture and hemorrhage of blood-supplying arteries within tumors; the major presentations are a hemorrhage confined within the tumor, a rapid increase in the tumor volume caused by this hemorrhage, and severe headache and vision loss caused by compression of the optic nerve and surrounding dura []. When a pituitary adenoma is combined with an aneurysm under the sellar diaphragm, if the aneurysm is ruptured, it may also cause the typical pituitary adenoma apoplexy symptoms. For example, in 2001, Suzuki et al. reported one case of an intracavernous carotid artery aneurysm embedded in a pituitary adenoma. The hemorrhage after rupture was confined inside the tumor, and the presentation included the typical pituitary adenoma apoplexy symptoms and imaging results [].
At times, hemorrhage caused by aneurysm rupture is not limited to the tumor; for instance, in 2007, Okawara et al. reported a case (similar to the case described in this report) that involved an intracavernous carotid artery aneurysm located in a pituitary adenoma. The manifestations of the hemorrhage that occurred after aneurysm rupture included intratumoral hemorrhage, intraventricular hemorrhage, subdural hemorrhage, pituitary adenoma apoplexy, and other hemorrhages []. In addition to aneurysms in the cavernous sinus segment, other aneurysms can also cause pituitary adenoma apoplexy; for instance, in 2014, Song et al. reported a case in which a posterior communicating aneurysm caused pituitary adenoma apoplexy and in which invasive growth had caused the pituitary adenoma to wrap around the aneurysm [].
When the aneurysm that is combined with a pituitary adenoma is not inside the cavernous sinus, the aneurysm may be wrapped by the invasive pituitary adenoma that grows through the sellar diaphragm. Once rupture and hemorrhage occur, the aneurysm may not be confined inside the tumor and may enter into the subarachnoid space to combine with subarachnoid hemorrhage. The presentation is pituitary adenoma apoplexy combined with subarachnoid hemorrhage. This disease is very rare. The case reported in this article falls into this category. The rupture of the anterior communicating artery aneurysm caused hemorrhage inside the pituitary adenoma and extensive subarachnoid hemorrhage. During the surgery, the aneurysm was confirmed to be ruptured; there were blood clots in the surroundings, and the aneurysm was inside the pituitary adenoma. The patient successfully underwent tumor removal and aneurysm clipping. Because of his ignorance of medicine and his difficult living conditions, the patient did not accept a dopamine agonist to treat his prolactinoma; instead, he chose to adopt a wait-and-see approach to his disease even though he lost a portion of his eyesight. If the prolactinoma had been dissolved with medication, the treatment of the aneurysm would have been less complex.
A case involving mechanisms similar to those of the case discussed in this article was reported in 2006 by Shahlaie et al., who described how the rupture of an anterior communicating artery aneurysm caused pituitary gland apoplexy and subarachnoid hemorrhage []. Because the anterior communicating artery is higher, not all pituitary adenomas can grow upward to encase it. For example, in 2014, Almeida et al. reported a case of pituitary adenoma associated with an anterior communicating artery aneurysm and demonstrated that a hemorrhage after aneurysm rupture could not enter the pituitary adenoma due to the elevated location of the aneurysm; therefore, the only observed presentations of this hemorrhage were an interhemispheric hematoma and a subarachnoid hemorrhage []. Overall, in pituitary adenoma apoplexy combined with aneurysm rupture, based on the aneurysm’s location and relationship with the sellar diaphragm, the presentation may (or may not) be combined with subarachnoid hemorrhage.
Therefore, when hemorrhagic apoplexy occurs in a pituitary adenoma and is combined with subarachnoid hemorrhage, the possibility of an associated aneurysm should be considered. However, the literature reports that simple pituitary adenoma apoplexy might also present subarachnoid hemorrhage. For example, Nakahara et al. reported one case showing that subarachnoid hemorrhage occurred when the pituitary adenoma was not associated with an aneurysm. This condition was considered to result from arterial laceration caused by stretching of the adjacent arteries (such as the superior hypophyseal artery) by tumor expansion and invasive growth []. Currently, transsphenoidal resection is the main treatment method for pituitary adenomas []. If the aneurysm diagnosis is missed before surgery, surgical resection of the tumor can easily cause aneurysm rupture and hemorrhage; the tumor-loading artery cannot be found in the narrow and small surgical space to control the bleeding, thus, causing disastrous consequences. However, for pituitary adenoma apoplexies caused by intracranial aneurysms, if the aneurysms could be found, aneurysm coiling combined with transsphenoidal pituitary adenoma resection remains a good treatment option [, ].


An 18-year-old young woman presented with 6 months amenorrhea. Menarche had occurred at age 11 years. She suffered from mild cerebral palsy (possibly due to low birth weight of 1.88 kg at 38 weeks’ gestation), mild asthma, Asperger’s syndrome, anxiety, and epileptic events from age 14 to 15 years, considered secondary to cerebral palsy. She had a ruptured appendix at age 12 years. There was no other significant past history; no drug usage; she did not smoke or drink alcohol, and had not become sexually active. Sertraline was used for treatment of anxiety from 2009 to 2010 followed by fluoxetine. There was a family history of osteoarthritis and osteopenia and of pancreatic cancer; no family history of premature menopause. The OCP was commenced at age 12 years. The attending gynecologist recorded “although her periods were reasonably normal, she was put on the pill (20 µg ethinyloestradiol and 100 µg levonorgestrol) the next year because coping with her periods made her anxiety and depression symptoms worse.” Her first HPV4 vaccination was administered at age 12 years and 9 months; the second vaccination near her 13th birthday, and the third vaccination at age 13 years and 5 months. The first HPV4 vaccination was given concomitantly with hepatitis B vaccination in the other arm. OCP usage continued for 2 years to age 14 years. It was briefly ceased at age 14 and this was followed by 3 months amenorrhea. OCP was then resumed without further investigation. At age 18 years, the OCP was again ceased and amenorrhea again ensued.
Follicle-stimulating hormone 1 month later was elevated at 44.5 IU/L (menopausal range is 25-130 IU/L). Luteinizing hormone was 29.2 IU/L (basal range 2.0-12, midcycle peak range 8.0-90, postmenopausal range 5.0-62 IU/L). Estradiol was 157 pmol/L. She continued amenorrheic and presented again for investigation 6 months later. At this time, follicle-stimulating hormone remained elevated at 34 IU/L. Luteinizing hormone was elevated at 46 IU/L. Estrodiol (Oest2) was 413 pmol/L and progesterone 2 nmol/L. Anti-Müllerian hormone was 1.5 pmol/L (14.0-30.0 pmol/L normal; levels <14 pmol/L suggest diminished ovulatory reserve) tested by Beckman Coulter Gen II ELISA assay. Anti-Müllerian hormone repeated 6 months later was <1 pmol/L and estradiol was <37 pmol/L. At this time and at age 18 years POI was diagnosed.
Full blood count, iron levels, liver function, blood glucose, and renal function were normal. Thyroid-stimulating hormone was normal 0.4 mIU/L (normal 0.3-3.5 mIU/L) and thyroid antibodies were normal. Prolactin was normal 294 mIU/L. Testosterone 0.9 nmol/L (normal 0.2-1.8 nmol/L); free androgen index 2.6 (normal 0.3-4.0); iron studies were normal. There were no antiadrenal or antiovarian antibodies detected. Morning cortisol was 218 nmol/L (normal range 160-650) nmol/L, ACTH 14 ng/L (normal range 9-51 ng/L), growth factor-1 27 nmol/L (normal range 21-76 nmol/L). Pelvic ultrasound performed at the time when the anti-Müllerian hormone level was 1.5 showed a normal uterus with an endometrial echo of 8.2 mm. Transvaginal ultrasound was declined and the left ovary was not visualized. The right ovary was 3.1 cm3 in size and there was a 9-mm follicle within it. Brief menstrual bleeds then occurred for 4 months before amenorrhea resumed.
Testing for Fragile X revealed 2 normal-sized triplet alleles 23 and 37 cytosine–guanine–guanine n repeats (the normal zone is <44). Testing for galactosemia showed a normal Gal-1-P uridyl transferase-RC at 0.31 U/g hemoglobin (normal range 0.26-0.52 U/g). Records reported a vitamin B12 deficiency at age 16 years, but levels of vitamin B12 were within normal limits at 275 pmol/L (normal range 135-650 pmol/L). Karyotype was established as 46XX.
This young woman elected to undergo right ovary cryopreservation through Monash IVF in the hope that future developments, such as stimulation of ovarian stem cells, may be of later benefit. She was not deemed a suitable candidate for gonadotropin stimulation for oocyte preservation due to the undetectable anti-Müllerian hormone level. The pathologist described the macroscopic appearance of the ovary as “cystic and disrupted.” Microscopic histology of three right ovarian biopsies reported fibrovascular connective tissue with no primordial follicles in the ovarian cortex of sample one. Ovarian sample 2 reported a cystic follicle and a cystic corpus luteum but no primordial follicles within surrounding parenchyma. Ovarian sample 3 reported “fibrofatty connective tissue only. No ovarian parenchyma is identified.” Summary: “Levels through all tissue containing ovarian parenchyma show a single primordial follicle. No other follicular structures are identified.” No samples contained evidence of atypia or malignancy (Sullivan Nicolaides Pathology. Brisbane, Queensland, Australia). Personal communication with the reporting pathologist confirmed no lymphoid or granulomatous inflammation and suggested the ovarian appearance was “consistent with that of a woman in her late forties.”
She has been counseled about bone density preservation and the need for hormone replacement therapy. This case was notified to the Therapeutic Goods Administration (TGA) of Australia in January 2014 (reference number 333136) as diagnosed POI. Its listing as “amenorrhoea” on the TGA database in May 2014 was later altered to POF (July 2014).


A 24-year-old male with no significant prior medical history was brought to the emergency department (ED) after sustaining nine gunshot wounds (GSWs), inflicted by two assailants wielding handguns from 4–6 meters away.
Upon arrival to the ED, the patient was alert and oriented. Breath sounds were symmetric and clear, and pulse oximetry was 100%. Central and peripheral pulses were strong and symmetric. One GSW was sustained to the left buttock posteriorly. Another penetrated the right lower quadrant of the abdomen, but the rest of the abdomen was otherwise soft, non-tender, and non-distended. No deformity or bullet wound was noted in the neck, thoracic, axillary, or upper abdominal areas. Exposure of the extremities revealed GSWs to the right thigh and left arm.
During the log roll examination of the back, SpO2 dropped to 80–90% while the patient breathed spontaneously on nasal cannula with oxygen at 2 liters per minute. The patient was positioned supine and the nasal cannula was replaced with 15 liters per minute of oxygen delivered via non-rebreather mask. After 2 minutes, his SpO2 corrected to 100% with resolution of his shortness of breath. The patient remained hemodynamically stable and the quality of the pulse oximetry waveform signal was confirmed throughout the episode. Bedside eFAST (Extended Focused Assessment with Sonography for Trauma) was negative for pneumothorax, pericardial and intra-abdominal fluid. Chest radiograph demonstrated a radiopaque foreign body measuring approximately 9×19mm, overlying the cardiac silhouette (). The patient denied ever being shot in the past, and a preliminary concern for a bullet embolus was raised.
Computed tomograph (CT) of the chest confirmed a bullet in the right ventricle (). CT of the abdomen and pelvis along with cystogram revealed a moderate amount of acute pelvic hemorrhage with evidence of right common iliac vein injury.
Cardiothoracic surgery and cardiology were then consulted for removal of the bullet. Intraoperative transesophageal echocardiogram (TEE) was performed to confirm the location of the bullet within the right ventricle, adjacent to the ventricular septum ( and attached .mp4 at 0.5× speed [Supplemental Digital Content]SDC-1). The right ventricular transverse view on TEE showed a comet tail artifact, commonly seen with metal foreign bodies (). TEE further revealed normal right ventricular function, normal left ventricular function, no pericardial effusion, and no valvular abnormalities. It was uncertain after TEE whether the bullet was free floating within the ventricle at the time. Given the lack of direct damage to cardiac structures, an attempt at endovascular retrieval was made. Right internal jugular venous access was obtained by surgical cutdown, and an 11 French sheath was placed under direct visualization through the right internal jugular vein. With guided fluoroscopy, multiple attempts were made to retrieve the bullet with both Amplatz GooseNeck® (Coviden, Plymouth, MN) and ensnare devices (). The cardiothoracic surgeons then performed a median sternotomy, and approached the right ventricle via right atriotomy with cardiopulmonary bypass and cardioplegic arrest. Exploration of the right ventricle through the tricuspid valve revealed the bullet was embedded within the right ventricular trabeculations. Extraction of the bullet required minor dissection of some trabeculations with Metzenbaum scissors. The intact bullet was discovered to be a minimally deformed .38 caliber pistol round, specifically 9×19mm Parabellum full metal jacket. The atriotomy and sternotomy were closed with no complication. The patient was transferred to intensive care in stable condition, and extubated later that day.
On POD #6, the patient developed a fever. A CT chest/abdomen/pelvis showed a large pericardial effusion, and moderate right pleural effusion with right lower lobe collapse. Echocardiogram demonstrated low-normal left ventricular ejection fraction at 50%, and furthermore confirmed the large pericardial effusion without any tamponade criteria. Clinically, the patient experienced intermittent drops in pulse oximetry and concurrent shortness of breath, but remained hemodynamically stable. Pericardiocentesis removed 650mL of hemorrhagic effusion immediately, and a drain left in place evacuated 320mL over the next three days. Follow-up echocardiogram showed a very small pericardial effusion. The 340mL of serosanginous fluid was then drained from the right pleural effusion, with no residual fluid on repeat ultrasound. There were no further acute events, and the patient was determined to be stable for transfer to the comprehensive rehabilitation center on POD #15.


The patient is a 47-year-old black male, with no medical history reported, diagnosed with a giant, cavitated, and unresectable gastric stromal tumor (GIST) (Figures and ) with high mitotic index and c-kit gene exon 11 mutations, fistulized to the stomach lumen (Figures and ), and liver metastases. The patient was started to be treated in March 2013 with imatinib 400 mg daily for a month. In May 2013, he was admitted to the Emergency Department due to melena. At the time of his admission the hemoglobin was 5 g/dL, blood pressure was 80/40 mmHg, and heart rate was 90 lpm.
Once hemodynamically stable, a gastroscopy was performed, with findings of a stomach full of blood clots and heavy bleeding coming from the tumor cavity, which was also full of clotted blood and its irregular walls were oozing blood that was not controllable with argon beam; therefore, an urgent laparotomy was carried out to achieve hemostasis. Intraoperatively, a huge intra-abdominal mass was found blocking nearly three-quarters of the abdominal cavity with strong fibrotic adhesions to the diaphragm, abdominal viscera, and abdominal wall, which made it inadvisable to resect. A gastrotomy was performed through anterior gastric wall to remove all blood clots and the intragastric fistula hole was closed with interrupted absorbable suture. The tumor cavity was opened through the softer tumor area and complete hemostasis was achieved using diathermia and homeostatic biological sheets (Tachosil, Surgicel). A closed drainage was left in the tumor cavity. Patient recovered uneventfully and was discharged on postop day 14, in order to continue his treatment in the outpatient clinics. In August 2013, he started suffering from vomiting and imatinib was reduced to a dose of 300 mg daily, being well tolerated.
The patient was readmitted to the Emergency Department four months later, with fever (37.8°C), weight loss, persistent cough, pus leaking through the old drainage scar, and left pleural effusion. A sample of sputum was obtained. CT imaging showed persistence of liver metastases without relevant changes, but the primary tumor had experienced a very impressive shrinkage. The CT scan also showed a left pleural effusion with atelectasis and a left subphrenic abscess that was not suitable for percutaneous drainage; therefore, a surgical debridement and drainage were indicated.
Intraoperatively, a complete blockage of the supramesocolic abdomen was found. Several biopsies were taken (all of which were negative for GIST). Following the old drain tract, a collection with chronic appearance was debrided and sent for culture. A double closed drainage was left in the abscess cavity and a feeding jejunostomy was placed. Microbiological culture of the sputum and collection samples were positive for MRSA and Candida. The patient was treated with appropriate antibiotics and antifungals.
Postoperatively, after an early clinical improvement, we realized that performing flushes through the double drain tube caused intense cough. A left bronchial fistula () and a gastric fistula were confirmed. Both were connected with the abscess cavity and skin through the abscess drainage. The attempt to close twice a small gastric hole using over-the-scope clips (OTSC) not only was unsuccessful but also made the gastric fistula bigger, worsening the bronchial symptoms.
As the performance status was inappropriate for a left thoracotomy and taking into account the complete frozen upper abdomen, it was decided to isolate the bronchial fistula organizing a controlled gastrocutaneous fistula tract. Using a pediatric gastroscope, a transgastric abscess cavity examination was performed. Once in the abscess cavity, the tip of the drain was identified, and as it was being removed, it was followed by the pediatric endoscope until the skin was reached. A nylon guide was introduced and a 20 Fr percutaneous gastrostomy (PEG) tube was placed from stomach to skin ().
Progressive hyperproteic enteral feeding was given up to 5,25 kcal/kg/hour. Two weeks later, the cough, pleural effusion, and atelectasis had disappeared. In 2 months, the patient had gained 12 kg (to reach 54 kg), and a regular 18 cm long gastrocutaneous fistulous tract had been achieved (). Gastrografin transit showed no leakage () and once the PEG tube was removed, the fistula tract closed completely in 6 days and the patient was discharged with oral intake and imatinib treatment. Although liver metastases are still in regression, the abdominal mass has not recurred and the patient is having a good quality of life sixteen months later.


A 52 year old previously healthy Sri Lankan male was admitted to our facility with a history of fever for 4 days associated with headache, abdominal pain, generalized myalgia and reduced urine output. On admission he was febrile, rational and nonicteric, with a blood pressure of 90/60 mmHg, pulse of 118 beats/min, breathing frequency of 22/min and oxygen saturation of 97 % on room air. The liver was tender and palpable 3 cm below the right costal margin. He did not have clinical evidence of pneumonitis, pleural effusion, ascites. Laboratory investigations on admission showed thrombocytopenia with normal white cell count and increased levels of blood urea, serum creatinine, liver transaminases, prothombin time, creatinine phosphokinase and trophonin I. Both IgG and IgM dengue antibody tests were positive indicating recent dengue infection. Serological tests for leptospirosis (microscopic agglutination test) was negative. The investigation results are summarized in Table . Despite adequate fluid resuscitation, the patient remained hypotensive and he was started on inotropes and vasopressors. He was started on ceftriaxone and transferred to an intensive care unit where haemodialysis was started due to worsening acidaemia and fluid overload. On the second day, he developed haemoptysis and chest X ray showed evidence of diffuse bilateral alveolar haemorrhages. Arterial blood gas analysis showed type 1 respiratory failure. As the patient was in severe respiratory distress, he was placed on mechanical ventilation. Later his condition was further complicated by disseminated intravascular coagulation. Leptospirosis serology was repeated on day 7 and it showed a rising titre of 3,600, indicating recent leptospirosis infection. Despite aggressive management of septic shock, oliguric acute renal failure, acute respiratory distress syndrome and disseminated intravascular coagulation, the patient succumbed to his illness on the eighth day of admission.


A 40-year-old female complaining of dysphagia came to our gastroenterology outpatient clinic. In her upper endoscopy, an ulcerative mass was found between 25 and 38 cm from the incisors (). After initial work-up and also after the pathology report of an endoscopic biopsy (which was squamous cell cancer), the case was discussed in the oncologic committee. All blood tests (biochemistry, complete blood count) were in the normal range. Pretreatment computed tomography (CT) was as seen in . Positron emission tomography (PET) was performed for occult distant metastases and there were no metastases. The patient's performance status was good and she had no comorbidities. Unfortunately, there is no endoscopic ultrasound unit (EUS) in our hospital so this modality was not performed.
After our case was discussed in the oncologic committee that gathered every week on Thursday, it was decided to characterize the clinical stage of the tumour as T3 or T4a, NX, M0 according to the 7th AJCC Staging System. As expected, for this advanced esophageal tumor, a neoadjuvant CRT decision was taken. In our oncology clinic, chemotherapy and simultaneous radiotherapy were given as follows: Paclitaxel (50 mg/m2), Carboplatin (target AUC = 2 mg/Ml·min) plus radiotherapy (41.4 Gy in 23 fractions for 5 days per week). This chemotherapy protocol was given on the first day of radiotherapy and once a week until reaching 5 weeks. After the patient had completed the whole CRT protocol, a control CT was performed (). According to the CT report, there was more than 50% response.
Six weeks after CRT, with a curative intention, minimal invasive surgery (MIS) was performed (thoracoscopic esophageal mobilization done first and then gastric mobilization and tube formation performed with laparotomy and cervical anastomosis). There was no tumour or any other lesion when the specimen was examined intraoperatively. No intraoperative complications occurred. However, on the 5th postoperative day, elevated temperature (38.7°C) and tachycardia (145 beats/min) developed. In radiological examination and with methylene blue test, we found a leak in the stapler line on the gastric wall that was formed while creating a gastric tube. Subsequently, despite all interventions and reoperation she was still in the intensive care unit and was intubated at the time of this writing.
The pathology report was as follows. “There were no neoplastic cells in the suspected area of the esophageal mucosa upon examination with HMWCK, P63, PAS, and dPAS staining. There were areas of ulceration and severe chronic inflammation and fibrosis in the esophageal lumen: perineural invasion (−), lymphovascular invasion (−). There was no cancer at resection margins. Four metastatic lymph nodes (Figures and ) were infiltrated with squamous cell cancer. The other 21 harvested lymph nodes were reactive.” We then consulted with the pathologist and requested reevaluation of the specimen and of course the lymph nodes. Nevertheless, the pathological reevaluation was the same.