A 33-year-old woman and her 30-year-old husband presented with history of primary infertility over a period of 4 years. Although she did not report a history of pelvic inflammatory disease or sexually transmitted infection in the past, she had ultrasound confirmed bilateral hydrosalpinges, and both of her fallopian tubes had been removed laparoscopically. Thereafter, she required fertility assistance by in vitro fertilization (IVF).
After confirmation of a pregnancy in the 1st attempt of IVF in February 2005 she was admitted to the local hospital with abdominal pain during the first trimester. Following an ultrasound suspicion of an interstitial pregnancy, she underwent a laparoscopy, which confirmed a right cornual ectopic pregnancy. The operation was then graduated to a laparotomy, and the cornual ectopic was removed by a longitudinal incision on the right cornu. After evacuating the products, the bleeding was minimised by diathermy coagulation. Postoperatively, she received supplementary treatment with intramuscular methotrexate to resolve any remnant trophoblastic tissue. Trophoblastic tissue, however, remained viable for up to 3 months after the first dose of methotrexate, and serum hCG was detectable albeit at low concentrations (27–45 iu/L). She opted for a conservative management as opposed to a repeat dose of methotrexate, and it was finally 8 months before all evidence of trophoblastic activity disappeared completely.
She conceived again after the 2nd attempt of IVF performed in February 2006. This time she presented with an acute abdomen at 6-week gestation at her local hospital and underwent an emergency laparoscopy. She was then found to have 1200 mL of haemoperitoneum. Active bleeding at the right cornu was seen, but trophoblastic tissue attached to the uterine cornu was not seen. Subsequently tissue found amongst the blood clots was histologically confirmed to be the “product of conception.” Due to this very early rupture, the exact location of this pregnancy and muscular integrity of the uterine cornua could not be assessed by scan prior to the rupture. The surgeon used a laparoscopic approach to achieve haemostasis. A blunt diathermy probe was inserted into the cornu, and the cornual bleeding site was coagulated from outside to inside. It was hoped that the diathermy coagulation would also lead to occlusion of the interstitium.
Upon recovery the patient returned to the tertiary centre for assisted conception. She then had a detailed discussion with regards to the possible causes and consequences of recurrent cornual ectopic pregnancies. The patient was advised of the high risk of recurrent uterine rupture in another pregnancy with potentially lifethreatening consequences. Since she was strongly motivated to give birth to a child, a couple of options were discussed with her as below.Hysteroscopic occlusion of the intramural part of the fallopian tubes was considered. At that time, this method was being practiced only for sterilisation by a single surgeon at our hospital. It had not gained popularity due to its high failure rate. There was no evidence for its value in preventing an interstitial pregnancy, and there could have been the risk of an adverse impact on pregnancy and uterine perforation with the ring coils. Recurrent uterine dehiscence due to primary weakness in the myometrium at this cornual site remained a concern, and hence this was not considered a sufficiently safe option. Assessment of uterine integrity as a first step followed by uterine repair if deemed necessary without any intervening myometrium in between the serosa and the uterine cavity. She was made aware that the proposed operation was novel to the author's knowledge and had not been done before. Therefore no information could be given regarding the likelihood of its success and the risk of uterine rupture in a future pregnancy. She consented to this strategy after receiving ample opportunity to reconsider and reflect.
A preliminary ultrasound scan of her pelvis showed a normally appearing uterine fundus without any evidence of asymmetry of either cornu. A further assessment of myometrial integrity at the site of uterine rupture was deemed necessary. After appraisal of the available investigative techniques a saline sonohysterography as a real time assessment of the myometrial thickness was chosen as the method of choice. A saline sonohysterography was performed, whereby the uterine cavity was sealed at the cervix with a sonography balloon catheter (H/S catheter set with ingrated stylet, Cooper Surgical, CT 61-3005 5F), and the uterus was subjected to gradual distension with warmed normal saline. This was carefully and slowly injected to avoid myometrial spasm until the patient experienced discomfort. At this point the scan frame was frozen, and the distension reduced. This process was slowly repeated several times in the same episode to enable multiple measurement opportunities and to minimise intraobserver variation. The minimum myometrial thickness was measured in the transverse plane at the uterine fundus on both sides, and this revealed an asymmetry of muscle thickness in the cornual regions. The myometrial thickness in the left cornual region was 5-6 mm whilst, it was less than half of this thickness at 1.6 cm on the contralateral side. Additionally with saline distension, during real time scanning, a track of endometrial cavity on the right side with suspected fluid was seen leaking through the track into the peritoneal cavity suggesting thereby the possibility of an endometrial-peritoneal fistula.
A further detailed outpatient discussion with the patient and partner occurred in April 2006 and increased risk of another acute uterine rupture during pregnancy at this cornual site or a slow rupture leading to abdominal pregnancy was discussed. The couple were advised to consider the alternatives of surrogacy and/or adoption. However, the patient remained strongly motivated to try an elective uterine reconstruction. Therefore an elective laparotomy was performed.
At surgery in July 2006, a hysteroscopy was performed in the first instance, and this showed a normal uterine cavity. No abnormalities were noted in the cornual regions. A unique surgical method to identify areas of myometrial weakness was then devised. A 10 mL balloon Foley's catheter, size 10, was inserted into the uterine cavity, the balloon was gently distended with warm methylene blue, and the catheter was left in situ. A laparotomy was performed immediately, and uterus carefully inspected. The uterus externally appeared normal. Although both uterine cornua were found to be thin, in the right cornual region, there were two sites at which only peritoneum separated the intrauterine balloon and the serosal surface of the uterus, and methylene blue was seen through the peritoneum without any intervening myometrium between the layers (). Adjacent to this site was a vesicular blue lesion that resembled an endometriotic nodule with neovascularisation that radiated like spider nevi. At this site also the uterine muscle layer was extremely thin, and upon incision around the nodule the intrauterine catheter was reached at the depth of 2.5 mm (). It was evident that these sites of weakness would have been the site of previous cornual ectopic and uterine rupture and the endometrial-peritoneal fistula formation.
The uterine cornu was incised, and the endometrial cavity was immediately entered. The blue nodule was excised, and on inspection of the endometrial cavity it was noted that subsequent to the previous ruptures the deeper muscle layers had retracted into the endometrial cavity. These were brought into the incision site with U-shaped continuous sutures. The cornu was gradually reconstructed in several layers (at least 3), and cornual musculature was artificially thickened by bringing the laterally retracted myometrial superficial fibres from the fundus also onto and above the incision site (). Once again U-shaped continuous sutures in several layers with intramural vicryl (polyglactin 910) suture material were used. Inverting superficial prolene (polypropylene) sutures were applied to the uterine muscle on the serosal surface for haemostasis and to prevent fibrosis or adhesion formation on the peritoneal surface (). Similar strengthening of the cornu was performed on the left side but without a uterine incision or exposure of endometrium. For this, U-shaped continuous sutures in several layers were placed in the seromuscular part of the thinned-out left cornual region before placing a final inverted superficial prolene suture on the peritoneal surface. She recovered well from the surgery.
At approximately 3 months after the surgery the outpatient saline sonohysterography was repeated in the same manner as described above. On this occasion, myometrial thickness in the transverse plane was assessed; a 3-4 cm symmetrical all round myometrial thickness was noted, particularly at both cornual ends.
After appropriate discussion and consenting process a fresh cycle of IVF was performed in July 2007. A single embryo was transferred electively on day 3 of embryonic development. Supernumerary embryos were cryopreserved on this day. The pregnancy test was positive, and a scan confirmed a viable intrauterine pregnancy at 7-week gestation. The pregnancy sac was very much at the centre of the uterine cavity without any evidence of asymmetric thinning of the myometrium at the cornua or at any site. The muscle thickness was 4 cm. A further scan at 10 weeks was similarly reassuring with regards to the uterine muscle thickness all around the pregnancy and especially in the cornual areas. The patient was thereafter discharged to the care of her local obstetrician who monitored her closely throughout the pregnancy. She remained well and was delivered by an elective caesarean section at term in 2008 at which time the cornual regions were inspected and found to be normal and intact as in a normal uterus.
The patient subsequently attended our centre again in 2009 for a frozen embryo transfer cycle to use the spare embryos from the previous attempt. As per patient request, all frozen embryos from her previous IVF attempt were thawed and cultured for 48 hours. A single blastocyst was transferred, but on this occasion a pregnancy was not achieved. This patient has not returned for further treatment.


An 8-month-old Egyptian boy with BNH was referred to our institution from the Dermatology department for evaluation of poor activity and developmental delay. He was the second child of consanguineous parents; he was delivered at term by Caesarean section following an uncomplicated pregnancy and cried immediately after delivery with a birth weight of 3.5kg. There was no family history of hemangiomas or congenital malformation. Neonatal screening tests were normal. His mother observed the appearance of multiple pinpoint erythematous lesions all over his body at the age of 35 days that increased rapidly in number and size. She reported that her baby remained well until the age of three months. At the age of six months, he was unable to roll over prone to supine or vice versa. An examination revealed a quiet baby who was able to sit only with support but unable to orient to voice. His height and weight were 25th percentile. Vital signs on admission were recorded as follows: temperature, 36°C; blood pressure, 80/60mmHg; and heart rate, regular at 66 beats/minute. A physical examination found generalized hypotonia, a wide anterior fontanelle, puffy eyes, cold extremities, and mild abdominal distension. There were no signs of rickets or thyroid enlargement. An examination of his skin revealed more than 100 dome-shaped red-purple cutaneous hemangiomas that varied in size from 5 to 10mm on the back, the abdomen and the extremities with no mucus membranes involvement (Figure
). Other systematic examinations were unremarkable. Thyroid ultrasonography and scan, ophthalmic examination, laryngoscopy, bone screening and computed tomography (CT) scan of the brain were normal. Repeated chest radiography, echocardiography, and abdominal ultrasonography with a Doppler study were normal which ruled out respiratory system, cardiovascular and hepatic involvement. Laboratory studies revealed that serum electrolytes, hemogram, blood glucose and aminotransferase levels were normal. A hormonal assay revealed a serum thyroid-stimulating hormone (TSH) of 176μIU/mL (normal 0.3 to 5.0μIU/mL), serum free thyroxine (FT4) of 0.4ng/dL (normal 1.0 to 2.5ng/dL), and serum triiodothyronine (T3) of 65ng/dL (normal 85 to 250ng/dL). Serum reverse-T3 (rT3) level was 865ng/dL (normal 10 to 50ng/dL). The mother's thyroid function tests were normal and no thyroid autoantibodies were found in the mother or in the baby. Based on these findings, a diagnosis of consumptive hypothyroidism due to BNH was made. He was started on oral thyroid medication which was gradually increased to 90μg L-thyroxine daily (15μg/kg/day). After one month of treatment, blood hormone levels were: TSH 45mIU/mL, FT4 0.99ng/dL, T3 80ng/dL and rT3 70ng/dL. Blood hormone levels were completely normal two months later (TSH 1.99mIU/mL, FT4 1.44ng/dL and T3 40.23ng/dL) with spontaneous involution of some of his cutaneous hemangiomas. He was able to sit without support at that time. He is still seen at three-month intervals for out-patient follow-up visits.


A 65-year-old diabetic woman presented with one-week history of abdominal pain and repeated vomiting. She admitted to a history of long standing recurrent abdominal pain. Significant examination findings were in the abdomen with right upper quadrant pain and a palpable mass. The initial clinical diagnosis was acute on chronic cholelithiasis, and she was admitted for laparoscopic cholecystectomy. The abdominal ultrasonography showed heterogeneous gallbladder lesion with calcification. Computed tomography scan revealed heterogeneous mass (8 × 7.6 × 7.4 cm) at the gallbladder bed and two satellite lesions in the right hepatic lobe (). There was no paraaortic lymph node. The chest X-ray and CT scan were normal. The clinical diagnosis was reviewed to gallbladder cancer with hepatic metastasis. Complete blood count was normal except for leukocytosis (WBC 11, 800/mm3). Serum alkaline phosphatase was elevated (ALP −166 u/L). At laparotomy, the gallbladder tumour was adherent to the liver and omentum. The gallbladder-omental mass was excised together with biopsy from the liver nodule.
The gallbladder mass with omental attachment was irregular, measured 8 × 5 × 4 cm with areas of haemorrhages. The liver biopsy measured 1 cm in diameter. Microscopic sections showed replacement of the gallbladder tissue as well as omental fat by malignant spindle-shaped tumour cells arranged in fascicles and storiform patterns with few clusters of malignant epithelioid cells (). Similar malignant spindle cells were seen infiltrating the liver tissues. Numerous tumour giant cells, mitoses of more than 5–7 per HPF, and necrosis were seen. There were numerous vascular channels and areas of haemorrhages. The initial histopathological diagnosis of undifferentiated pleomorphic sarcoma, stage IV (T3, Nx, M1) disease was made because the epithelioid clusters were only apparent after deeper sections were cut. Immunohistochemistry staining showed focal positivity for vimentin () but negative for desmin, smooth muscle actin, S-100, CAM 5.2, EMA, and cytokeratin 20. The clusters of malignant epithelioid cells were positive for CEA and focally for CK7 (Figures and ). Further immunostaining showed Hep Par 1 negativity and CD 68 focally positive in the spindle-cell components of the tumour. A final pathological diagnosis of undifferentiated spindle-cell carcinoma was concluded. The patient was referred for adjuvant radio-chemotherapy, but she demanded to be discharged against medical advice. The patient was lost to follow up and died 1 year after surgery of disease progression.


A 50-year-old female presented to our observation with epigastric pain. Her past surgical history was uneventful except for appendectomy. A 30-mm gastric solid mass, suggestive of mesenchimal tumor, was documented by endoscopy. Due to its high vascularization and the risk of gastrointestinal bleeding, a biopsy was not indicated. The CT scan of the abdomen confirmed the presence of the gastric lesion, and incidentally showed a pelvic mass of 65×45×60 mm in the right adnexa (Figure ). The patient was asymptomatic. The pelvic finding was confirmed by US scan: the right ovarian mass had a prevalent solid component with a rich supply of blood vessels. No signs or symptoms of hyperthyroidism were observed. The patient underwent right oophorectomy, and after intraoperative histological diagnosis of ovarian carcinoma, a total abdominal hysterectomy with bilateral salpingo-oophorectomy, retroperitoneal lymph node dissection, and omentectomy were finally performed. The gastric lesion was resected and the digestive continuity was restored by Billroth’s II anastomosis. At surgery, no abnormal lymph nodes and ascites were noted. Histology did not reveal signs of peritoneal carcinomatosis in the pelvis. Macroscopically the right ovary mass measured 62x45 mm and cut sections showed a solid white-yellowish tissue with focally hemorrhagic areas.
The follicular thyroid-type carcinoma was characterized by the proliferation of cells arranged in follicular and trabecular pattern (Figure ). In the contest of ovarian teratoma, the follicular component showed an infiltrative growth as observed in thyroid carcinoma with moderate differentiation. The mitotic index was not elevated and any necrotic tissue areas have been documented. The follicular tumor border was infiltrated but the cellular growth was restricted within the capsule. Vascular invasion was reported in pericapsular capillary structures (Figure ). Together with the focal follicular thyroid-type carcinoma, the mature ovarian teratoma showed a well-differentiated neuroendocrine component with cells arranged in cordonal-alveolar structures (Figure ).
For immunohistochemistry, sections of formalin-fixed paraffin-embedded samples were treated with H2O2/3% for 5 minutes to inhibit endogenous peroxidase and then washed in H2O. Antigen was unmasked by treatment with EDTA at pH 9, or with citrate buffer at pH 6 in a microwave oven (two 5-minutes courses). The slices were then held for 20 minutes at room temperature. After washing in PBS/Tween-20, sections were incubated for 30 minutes with the primary antibodies. Then, they were washed and stained with BondTM Polymer Refine/HRP Detection Kit according to the manufacturer’s protocol (Leica, Wetzlar, Germany) or BondTM Polymer Refine Red Detection Kit (Leica) for PgR, ER, TTF1, Chromogranin A, Calcitonin, CD56, CDX2, CEA, CK20. For negative controls, we substituted non-immune sera for the primary antibodies. The immunohistochemistry analysis demonstrated positivity for PgR, TTF1, Chromogranin A, CD56, CDX2, CEA, and CK20. It was negative for ER and calcitonin. Based on these specific immunophenotype profile, diagnosis of follicular thyroid-type carcinoma arising in SO was made (Figures and ). The multiple peritoneal biopsies and the lymph nodes were free from metastatic cancer cells. In addition, peritoneal washing revealed mesothelial cells, leukocytes but not tumor cells on cytological examination. The definitive diagnosis of gastric neoplasm was cavernous hemangioma involving submucosa (Figure ).
The immediate postoperative course was characterized by anemia treated by medical supporting therapy and blood transfusions. Postoperative thyroid scan and thyroid function were normal. She was referred for thyroidectomy but she refused the operation. Thyroglobulin levels were monitored in the postoperative period. Nine months after treatment, laboratory evaluation revealed normal serum TSH (0.95 mU/L) and thyroglobulin (6.17 ng/mL) levels. Local and distant recurrences were not observed at the CT scan evaluation after a follow-up period of 1-year and the patients was scheduled for further follow-up. During this period the US of the neck revealed a normal thyroid gland.


A 63-year-old man who had suffered from esophageal achalasia for more than 20 years complained of acute respiratory distress due to stenosis of the trachea resulting from advanced esophageal cancer with tracheal invasion. He was admitted as an emergency to the referral hospital and computed tomography revealed a huge esophageal tumor significantly compressing the trachea (Fig. ). The patient underwent placement of a Dumon Y-shaped tracheobronchial stent (T M Y stent:φcon) to avoid suffocation. He was diagnosed as having esophageal cancer with tracheal invasion, and then underwent chemoradiation therapy (CRT). Following 18 Gy of irradiation and a course of chemotherapy using docetaxel, cisplatin, and 5-fluorouracil, a large TEF developed despite significant tumor shrinkage (Fig. a, b). The physician decided to cease the CRT and treat him with the best supportive care. Oral intake was prevented due to aspiration through the TEF, and a gastrostomy was performed under endoscopy.
The patient was referred to our hospital as he was unable to eat. At the time of admission, he had a good performance status and no comorbidities. We initially considered the possibility of esophageal stenting to close the TEF. However, as CRT significantly decreased the size of the esophageal tumor, and there had been an esophageal dilatation due to pre-existing achalasia, an esophageal stent seemed unlikely to be able to close the TEF. Therefore, we decided to perform an esophageal bypass using a gastric conduit after obtaining informed consent.
We prepared a percutaneous cardiopulmonary support (PCPS) system that could be used whenever needed, and both arterial and venous catheter sheaths were inserted from the femoral vessels prior to an endotracheal intubation. We then intubated a 6.0 mm spiral tube under the guidance of both bronchoscopy and X-ray guidance. A cuff of the tracheal tube effectively sealed the space between the stent and tracheal tube and enabled positive pressure ventilation. We were then able to perform esophageal bypass without using PCPS. Esophageal bypass surgery was performed through upper abdominal and collar neck incisions. Bypass was made using a gastric conduit through the subcutaneous route, and esophagogastrostomy was performed using a circular stapler. A decompression tube was inserted into the esophagus through the distal stump covered with the greater omentum. After the surgery was completed, the tracheal tube was safely removed under bronchoscopy. The patient was able to start oral intake on postoperative day 9, and was discharged on postoperative day 23. Though he died of respiratory failure three months after the operation, he was able to take in sustenance orally and to live at home after the operation.


A 65-year-old male with past history of anti-phospholipid (APL) syndrome on coumadin was admitted for acute right sided pleuritic chest pain. He was recently bridged with low molecular weight heparin after a right knee replacement. The CT-angiogram of the chest revealed a pulmonary infarct and a 5 cm right adrenal mass. A dedicated CT of his adrenals confirmed a right adrenal mass of 5.2 × 3.1 cm with pre-contrast attenuation of 53 Hounsfield units (HU) () with evidence of fat stranding, a sign of blood infiltrating fat containing retroperitoneal soft tissue, surrounding it. The left adrenal gland was thickened. A review of the patient's imaging studies was notable for normal adrenal glands on a CT scan two years ago. Lab work-up revealed a cortisol level of 4.4 mcg/dL after 1 mg dexamethasone suppression test, a normal plasma ACTH 28 pg/mL (8–42), and a slightly elevated plasma normetanephrine 1.2 nmol/L (<0.9). Given the clinical circumstances of APL syndrome, history of anticoagulation and radiological features, a close monitoring of the adrenal mass was planned. A repeat CT scan at 2 months showed a decrease in right adrenal mass and noncontrast CT attenuation value to 4.5 × 2.6 cm and 32 HU, respectively. Another CT scan done at 4 months showed 50% reduction in size (2.6 × 1.4 cm) and attenuation reduced to 21 HU (). The CT washout showed no significant enhancement or de-enhancement (). Left adrenal gland appeared normal. What is the diagnosis?


A 47-year-old housewife presented with 2 days history of foreign body sensation and reduced vision over the left eye (). There was no history of trauma. She has never used glasses or contact lens in the past as she claimed that her visual acuity on each eye was equally good. On examination, her visual acuity was 6/9 in the right eye and counting finger in the left eye. The conjunctiva of the left eye was injected. There was no foreign body. There was a stromal abscess at the centre of the cornea measuring 2.8 mm × 2.5 mm with overlying cornea epithelial defect of 2.0 mm size in diameter. The edge of the abscess was well defined. There was no endothelial plaque or satellite lesion to suggest fungal keratitis. The left eye anterior chamber filled with inflammatory cells and a level of hypopyon (0.8 mm). Cornea sensation on the left eye was slightly reduced compared to the right eye. The left eye posterior segment was hazy in view. Both eyes have similar intraocular pressure ranging from 14 mmHg to 16 mmHg. The right eye was entirely normal.
Topical Ceftazidime 1% and Gentamicin 0.3% eye drops were commenced after cornea scrapping. She was admitted the same day for intensive treatment of the left cornea ulcer. Later that day, fungal hyphae were seen on cornea sample under the microscope. Gram stain for bacteria was negative. She was started on eye drop of Amphotericin B 0.15% while Gentamicin eye drop was changed to Ciprofloxacin eye drop. On the day of admission, her random capillary blood sugar was found out to be 30.6 mmol/L. She is only known to suffer from hypertension for the past 4 years. Her blood sugar was subsequently well controlled with two types of oral hypoglycaemic agent and comanagement with dietician. The hypopyon in the left eye has completely disappeared after 3 days on treatment.
However, the next day, we noticed that the abscess started to have more obvious endothelial plaque. There was a new level of hypopyon on the following day. As the abscess progressively become thicker over a week, she underwent deep cornea debridement under local anaesthesia. Another cornea sample was sent for gram stain and cultures. No fungal element was seen this time and bacteria gram stain was also negative. The following day, the first cornea scraping was reported to isolate Scedosporium apiospermum. Oral Fluconazole 200 mg daily and hourly Fluconazole eye drop were initiated while the frequency of topical Ciprofloxacin eye drop was reduced. The oral Fluconazole was increased to twice a day on the next day as her left eye worsens. The left eye progressively worsens over the next five days despite combinations of systemic antifungal, two types of antifungal eye drop and tight control of capillary blood sugar (ranging from 4 to 6 mmol/L). At this stage, we stopped the Fluconazole and put her on daily dose of 200 mg oral Voriconazole and hourly Voriconazole 1% eye drop which was prepared extemporaneously.
The left eye showed slow improvement with the combination of Amphotericin B and Voriconazole. Two days later, the second scraping has isolated Scedosporium apiospermum. After a week, she was discharged against medical advice due to family problem. She remains compliant to her treatment and was self-admitted 4 days later. The left eye slowly improved where the hypopyon resolved after 5 weeks on the combination of Amphotericin B and Voriconazole. Oral Voriconazole was administered till 6 weeks. Topical Amphotericin B was used for 4 months while the topical Voriconazole was used for 8 months. She developed no adverse reaction throughout the treatment. Her best corrected vision upon completion of medication was 6/12. She remains asymptomatic with visual acuity of 6/9 in each eye on a year followup ().


A 40 year old male had a history of single chamber permanent pacemaker implantation (VVIR) in 2001 for complete heart block. As the patient was young, basic investigations were done at that time to exclude auto - immune and infiltrative diseases. Tests for Anti nuclear antibody (ANA), anti phosoholipid antibodies (APLA) and Rheumatoid factor were negative. In 2008, he was detected to have ERI (Emergency Replacement Indicated) and re-implantation was done with the change of pulse generator and pacing lead as lead impedance was high. The old lead was left in situ. After 4 years, he presented in our department with gradually progressive dyspnoea, bilateral pedal oedema and abdominal distension. At the time of presentation, he was in NYHA II functional class. On examination, the patient had pulse rate of 90/ min, blood pressure of 100/60 and normal heart sounds. General physical examination showed bilateral pedal oedema and icterus. The chest examination was normal. Abdominal examination showed distended superficial abdominal veins flowing centrifugally from umbilicus, tender hepatomegaly and shifting dullness, which was indicative of ascites. ECG showed paced rhythum. Chest radiograph revealed pacemaker in situ with its lead at right ventricular (RV) apex and another functionless lead, also at RV apex. 2D trans-thoracic echocardiography showed normal biventricular functions with paradoxical inter ventricular septal motion. Pacemaker lead was seen across tricuspid valve, positioned at RV apex along with another functionless lead at RV apex. This functionless lead had a small loop in right atrium (RA) close to the opening of inferior vena cava (IVC) into RA. A small mass was seen at this site over the lead with an accompanying thrombus at the mouth of IVC which was completely obliterating it (). Similar findings were confirmed with three dimensional echocardiography (). Colour Doppler also showed no flow from IVC to RA, instead increased flow was seen from superior vena cava to RA. A huge conglomeration of veins was seen around IVC which were collaterals, diverting blood from IVC to RA. Ultrasonography (USG) of abdomen showed hepatomegaly with dilated hepatic veins, dilated portal vein with a diameter of 12 mm, and moderate ascites. IVC venography showed no flow from IVC to RA, with flow diverting from IVC along collaterals to RA (). So, a diagnosis of 'thrombus over the functionless lead along with IVC thrombosis, leading to portal hypertension' was made. Basic laboratory investigations were done for excluding thrombophillic disorders. Levels of Protein C, protein S and antithrombin III were normal; reports for Factor V Leiden mutation and Prothrombin gene mutation were negative. USG abdomen and pelvis did not show any abnormality favouring intra-abdominal malignancy leading to increased thrombogenicity. After this, the patient was put on anti-coagulation. There was no improvement with anti-coagulation and patient was thereafter referred to surgeon for retrieval of thrombus and functionless pacemaker lead.


A 70-year-old Japanese woman was admitted to another hospital for paralytic ileus. An abdominal computed tomography (CT) scan showed widespread thickening of the small intestinal wall and ascites. The soluble interleukin-2 receptor level was increased to 2930 U/ml (normal, 220–530 U/ml). She was transferred to our hospital for close examination of the small intestine because intestinal malignant lymphoma was suspected. Her blood pressure and pulse were normal. Her body temperature was 37.4°C. Her weight decreased from 54 to 41 kg in 1.5 years. She had a 2-year history of lower-extremity paresthesia, and lumbar spinal canal stenosis was diagnosed at another hospital. A physical examination revealed signs of anemia. Superficial lymph nodes were not palpable. Livedo reticularis appeared occasionally on the extremities. She was not taking any non-steroidal anti-inflammatory drugs or antibiotics. Peripheral blood analysis showed normocytic normochromic anemia (red blood cell count, 297 × 104/μl [normal, 350–510 × 104/μl], hemoglobin, 8.2 g/dl [normal, 11.1–15.1 g/dl], and hematocrit, 26.0% [normal, 33.5%–45.1%]). Her white blood cell count was 12600/μl (normal, 3900–9800/μl) with 1% eosinophils (normal, 0.0%–8.0%). She demonstrated hypoproteinemia at 6.0 g/dl (normal, 6.5–8.5 g/dl) and hypoalbuminemia at 2.3 g/dl (normal, 3.9–4.9 g/dl). The C-reactive protein level was 6.07 mg/dl (normal, 0.00–0.50 mg/dl). Blood urea nitrogen and creatinine levels were in the normal range. Slight proteinuria (1+) was observed. Hematuria was not observed. Chest and abdominal CT scans showed honeycomb changes and ground-glass opacities in the lung and dilatation and wall thickening of the small intestine (Figure ).
Retrograde DBE showed irregular ulcers in the ileum, which took various forms such as spiral and longitudinal (Figure A, B). The most distal ulcer was about 20 cm proximal to the ileocecal valve. Redness and edema were observed around the ulcers, and the borders of the ulcers were unclear. Some of the mucosa between the ulcers was reddish and edematous. A stenosis was also present in the ileum (Figure C), and the scope could not pass through the stenosis. No abnormality was detected in the colon. Pathological examination revealed inflammatory cell infiltration (including lymphocytes, neutrophils and eosinophils), intestinal edema and crypt destruction (Figure A). Although the interstitial edema and crypt destruction were conspicuous, the inflammatory cell infiltration was relatively mild. These features were suggestive of ischemic changes. It is not known if there was transmural inflammation, because the biopsy specimens did not show the full thickness of the intestinal wall. Lymphoma cells, granuloma formation, and vasculitis were not detected. Retrograde DBE was performed again 1 week later, and the result was similar. Biopsy culture and polymerase chain reaction of tuberculosis were negative. The tuberculin reaction was also negative. The cause of the small intestinal involvement was unknown at that time.
Upper-extremity paresthesia and a fever spike appeared several days after the second DBE. Neurological examination revealed sensory and motor disturbances of the extremities. Mononeuritis multiplex, including lower-extremity paresthesia, was diagnosed. Anti-myeloperoxidase ANCA increased to 42.5 U/ml (normal, <9.0 U/ml). Anti-proteinase 3 ANCA, IgG, IgA, IgM, and IgE were within their normal ranges. Sural nerve biopsy was carried out. It did not reveal necrotizing vasculitis; however, it suggested small-vessel vasculitis (Figure A). Axonopathy was revealed. Renal biopsy revealed pauci-immune tubulointestinal nephritis (Figure B). Esophagogastroduodenoscopy showed no abnormality. Anti-nuclear antibody titers were weakly positive at 1:80. C1q immune complex, lupus anticoagulant, and anti-cardiolipin-β2-glycoprotein I complex antibody were negative. From these findings, the diagnosis of MPA was made. It was suggested that the cause of the intestinal involvement was MPA. Intravenous pulse cyclophosphamide (10 mg/kg, every 2 weeks for the first three treatments and every 3 weeks thereafter) and oral predonisolone (1 mg/kg/day) were started. Six treatment cycles of intravenous pulse cyclophosphamide were performed. Her white blood cell count, C-reactive protein level, and anti-myeloperoxidase ANCA level decreased to their normal ranges. Retrograde DBE about 10 months after the last DBE showed ulcer scars, but ulcers were not detected (Figure D). The stenosis was observed in the ileum (Figure E); however, she had no gastrointestinal complaints. Pathological examination of the biopsy specimens revealed fibrosis, suggestive of scarring resulting from the previous ulceration (Figure B). Paresthesia has remained, but has not deteriorated. Muscle weakness has been recovering gradually.


We present a case of a 72 year-old woman with a rapidly growing neck mass over a period of two months. Her past medical history includes a multinodular goiter diagnosed two years ago with no follow-up.
At the physical exam we found a painful mass of the left neck with fistulae to the skin. She is clinically euthyroid with normal plasma level of thyroid stimulating hormones. A total body scan didn’t show any other mass.
The patient underwent a surgical exploration. There was a hard, irregular tumor of the whole left lobe of the thyroid gland, which was attached to the sterno-thyroidian muscle and the left cervical pedicle. A left lobectomy was realized. As the tumor largely invaded the surrounding tissues, a curative operation seemed impossible.
The resected lobe measured 8.5 cm in the largest dimension; there is a multinodular appearance with a yellowish nodule measuring 5 cm in diameter. On histology, the lesion was focally well defined, but unencapsulated and was composed of interlacing fascicles of atypical spindle and epithelioid cells (Figure ). These cells had an abundant eosinophilic cytoplasm and a hyperchromatic blunt-ended and cigar shaped nuclei with marked anisocaryosis and high mitotic ratio (Figure ). The stroma was scant, essentially composed of capillaries with rare lymphocytes. Some areas of necrosis were found.
The tumor invaded the surrounding thyroidian parenchyma with some non tumoral thyroid follicles trapped into the tumor (Figure ).
Undifferentiated thyroid carcinoma was suspected. The immunohistochemical study with cytokeratin was negative (Figure ). Secondary immunohistochemical stains showed positive diffusion for Hcaldesmone (Figure ), and focal positivity for desmine ( Figure ) in the spindle cells all the other stains performed (chromogranine, synaptophysine, TTF1, estrogen receptor) were negative (Figure , Figure , Figure ).


A 44-year-old man without notable previous medical history presented with severe headache, nausea, and vomiting that had persisted for a few days. He was admitted to a local hospital, and computed tomography (CT) and magnetic resonance imaging revealed a large tumor with intratumoral hemorrhage in the right frontal lobe. For the management of intracranial hypertension, osmotic diuretics were administrated, leading to dehydration. The third day after admission, he was transferred to our hospital due to neurological deterioration including progressive disturbance of consciousness and left hemiparesis.
Magnetic resonance imaging performed at our hospital showed a rapid increase in mass effect, resulting in subfalcial and transtentorial herniation (). The commonly measured coagulation parameters, including prothrombin time, activated partial thromboplastin time, international normalized ratio, and thrombocyte count, were within the normal range. The patient underwent an emergency right frontal craniotomy performed in the supine position without excessive head rotation. The tumor was removed en bloc using the navigation-guided fence-post procedure without opening the ventricle or cistern. Accordingly, excessive CSF leakage did not occur during the operation. In addition, postoperative CSF loss through closed subgaleal drain did not occur.
Postoperatively, the level of consciousness remained unchanged from the preoperative level and no new neurological deficits were detected. A routine postoperative CT scan on the day after surgery revealed a bilateral cerebellar hemorrhage along with the cerebellar sulci facing the tentorium (). Magnetic resonance imaging showed bilateral anterior cerebral artery infarction due to subfalcial herniation and right posterior cerebral artery infarction due to transtentorial herniation that reflected the preoperative intracranial hypertension, and no evidence of residual tumor at the surgical site was found (Figures –). The cerebellar hemorrhage was carefully treated conservatively with osmotic diuretics. A follow-up CT scan demonstrated no further progression of hemorrhage and no occurrence of obstructive hydrocephalus due to compression of the fourth ventricle by the associated edema (). The level of consciousness recovered gradually and no neurological deterioration occurred during the course. The histological diagnosis was anaplastic oligoastrocytoma. Conventional radiotherapy of 60 Gy concurrent with PAV combination chemotherapy of procarbazine, nimustine hydrochloride (ACNU), and vincristine was performed. The patient did not have any cerebellar deficits and was transferred to a rehabilitation center for rehabilitation of paraparesis that occurred due to anterior cerebral artery infarction.


An 82-year-old male with concomitant chronic obstructive pulmonary disease (COPD) was referred to our institution for further evaluation and treatment of a protruded lesion in the stomach. His physical examination on admission was unremarkable. Laboratory data, including CEA and CA19-9, were almost normal. EGD showed a small protruding lesion on the lesser curvature of the lower gastric body, and also a large superficial elevated lesion on the lesser curvature of the stomach which spread from the upper to the lower gastric body (). Biopsy specimens taken from the lesions showed moderately differentiated tubular adenocarcinoma (tub2) and well-differentiated tubular adenocarcinoma (tub1), respectively. EUS and CT visualized a small round LN 11 mm in size located near the lesser curvature side of the stomach, although submucosal invasion was not evident. The patient chose to undergo ESD first under detailed informed consent.
ESD was performed with a hook knife, and the two lesions were resected en bloc. The resected specimen included a small protruded lesion (0-I) 13 × 10 mm in size and a large superficial elevated lesion (0-IIa) 89 × 33 mm in size.
Histological examination of the two lesions showed tub2 and tub1, respectively. The intervening mucosa between the two lesions was nonneoplastic (). The depth of tumor invasion was limited to the mucosal layer, and lymphatic-vascular involvement was not evident by HE staining in either lesions. Based on these findings, additional gastrectomy was not performed.
He underwent follow-up EGD/EUS and CT 2 months after ESD. No residual cancerous lesion was observed in the stomach. On the other hand, the LN became enlarged from 11 mm to 16 mm in size as measured by EUS. EUS-FNA with the cell block method revealed LN metastasis of poorly differentiated adenocarcinoma (por). Subsequently, total gastrectomy with LN dissection was performed 4 months after ESD. Histological examination of the surgically resected specimen revealed metastasis to the No. 3 LN. No residual cancer was detected in the stomach. His postoperative course was uneventful. After discharge, he has been followed up at the outpatient department without any sign of recurrence for 5 years.
Reexamination of the specimen obtained by ESD was carried out with special staining and immunohistochemistry. Smooth muscle actin (SMA) staining revealed that submucosal invasion was not present in either lesions. However, tumor cells became poorly differentiated at the front of the mucosal invasion in the 0-I lesion (Figures and ), and D2-40 staining revealed lymphatic invasion in the lamina propria (). Vascular involvement was not detected by either factor-VIII staining or Elastica-Masson (EM) staining. The mucin expression pattern of the 0-I lesion was MUC1(−), MUC2(−), MUC 5AC(+), and MUC6(−), suggesting a gastric-type mucin phenotype. On the other hand, lymphatic-vascular involvement was not proven by D2-40, factor-VIII, or EM staining in the large 0-IIa lesion. Finally, the lesions were pathologically diagnosed as 0-I, tub2 > por, 13 × 10 mm, pT1(M), ly2, v0, INF β, VM(−), LM(−); and 0-IIa, tub1, 89 × 33 mm, pT1(M), ly0, v0, VM(−), LM(−), respectively ().


A 36-year-old female without any medical problems presented to our institution for normal vaginal delivery. On the day of admission, she had hemoglobin (Hb) of 11 g/dl and a hematocrit (Hct) of 35%. Her puerperal course was complicated by excessive vaginal bleeding and a drop in the hemoglobin from 11 to 6.8 g/dl. She refused blood transfusions. She returned to Mexico and continued to have bleeding and sought medical attention in Mexico. Chorioamnionitis was diagnosed by hysteroscopy and received intravenous antibiotics. Hysterectomy was performed for persistent vaginal bleeding that was complicated by intraabdominal hemorrhage, intraabdominal abscess, and two subsequent wash outs. Her condition continued to deteriorate and was referred back to our institution with a diagnosis of disseminated intravascular coagulation (DIC).
She was intubated for hemodynamic instability. Her initial lab work revealed white blood cell count of 19.4/microliter, Hb 6.9 g/dl, Hct 19.5%, platelet count of 136/microliter, PTT of 71.7 sec, PT of 15.9 sec, international normalized ratio (INR) 1.3, fibrinogen 369 mg/dl (234–500), and fibrin degradation products (FDP) greater than 5 micrograms/ml (<20 normal). DIC was considered. CT scan of the abdomen revealed probable retained sponges and exploratory laparotomy was performed after transfusing packed red blood cells (PRBCs), fresh frozen plasma (FFP), and cryoprecipitate. Hemostasis was initially achieved with FFP. However, postoperatively, intraabdominal hemorrhage reoccurred and could not be controlled with multiple FFP and cryoprecipitate transfusions.
Medical services were consulted for coagulopathy evaluation. PAH was suspected because of isolated elevation of PTT, normal PT, INR, fibrinogen, and FDP. Mixing studies, factor assays, and inhibitor levels were performed. Hemostasis was achieved with recombinant factor VII concentrates and desmopressin. The factor VIII activity level was less than 1 with a factor VIII inhibitor at a concentration of 54.3 Bethesda units (very high), thus confirming the diagnosis of PAH. Methylprednisolone, Cytoxan, and plasmapheresis were prescribed. The patient responded with an appropriate decline in PTT, but her hospital course was complicated by the vesico-vaginal fistula, recto-vaginal fistula, and C diff colitis and bacteremia. We discontinued the immunosuppressive therapy and discharged after inhibitor levels were undetectable. Unfortunately, one month later she was readmitted to the hospital with severe sepsis and subsequently died.


A 36-year-old man presented to the Gastroenterology Outpatients Department with a four-month history of weight loss and iron-deficiency anaemia. He denied abdominal pain and described no change in bowel habit or rectal bleeding. He had previously been diagnosed with UC approximately 20 years ago and had undergone a colectomy with ileostomy two years later. 15 years ago, he had an ileoanal pouch formed.
Oesophagoduodenogastroscopy (OGD) and flexible pouchoscopy were unremarkable. VCE was performed; however the capsule was not passed (). Pouchoscopy/retrograde ileoscopy with a paediatric colonoscope showed a normal pouch with scattered aphthous ulcers in the ileum (). Two strictures were identified, the more significant 100 cm proximal to the pouch, which could not be traversed by the scope. Small bowel barium follow-through confirmed the endoscopy findings and showed the capsule was impacted but freely mobile proximal to this stricture.
The capsule was retained proximal to an ileal stricture. The findings of small bowel ulceration led to a diagnosis of small bowel CD being made. There was no history of nonsteroidal anti-inflammatory drug (NSAID) consumption, vasculitis, or connective tissue disease.
A course of budesonide was given to resolve the inflammatory component of the stricture and the patient was followed up for two months with serial abdominal radiographs, but the capsule did not pass. At repeat ileoscopy, the dominant ileal stricture could not be traversed by a paediatric colonoscope even after gentle balloon dilatation. An attempt to insert a biodegradable stent was unsuccessful.
Azathioprine and a tapering course of prednisolone were commenced but unfortunately the capsule was still retained. After eight weeks of immunosuppression therapy, colonoscopy showed that the ileal ulceration and inflammation had markedly improved. The dominant stricture was gently dilated to 12 mm using a controlled radial expansion balloon under fluoroscopy (), allowing passage of the scope passage and retrieval of the capsule with a Roth net ().


A 40-year-old woman presented to doctor with a history of a painless left breast lump without associated nipple discharge. She was otherwise healthy with no other relevant history. Physical examination revealed a nontender, freely movable mass in the left breast. Breast ultrasonography and mammography revealed a 20 × 15 mm periareolar mass with irregular speculated borders without microcalcifications and multiple left axillary hypoechoic malignant lymph nodes with loss of fatty hilum. Fine-needle aspiration cytology was reported as malignant epithelial tumor. She was then referred for staging with 18F-FDG PET CT that was acquired from the base of skull to upper thigh with the arms raised on a Siemens Biograph TruePoint 2008A. CT data was acquired without contrast enhancement and using the following parameters: 130 kV; 60 mAs; pitch 1.5; and slice thickness, 5 mm. The PET CT scan revealed a left breast mass with a size of 27 × 17 mm with a maximum standard uptake value (SUV) of 10,13 and six left axillary lymph nodes measuring up to 17 × 12 mm in size showed intense FDG avidity with SUV value of 8,10 (). In addition, right paratracheal, prevascular, aorticopulmonary, precarinal, subcarinal, hilar, and subhilar multiple conglomerated mediastinal lymph nodes with SUV value of 8,16 were revealed (). A trucut biopsy was done and reported as invasive carcinoma, estrogen and progesterone receptor status was strongly positive, and HER-2/neu was negative (score 0) with no membrane staining of malignant cells by immunohistochemistry. She was referred to thoracic surgery department, mediastinoscopy was performed under general anaesthesia using a cervical approach, and suspicious lymph nodes were biopsied. Pathology was reported as granulomatous lymphadenitis, auramine-rhodamine (A-R) and Ehrlich-Ziehl-Neelsen (EZN) stainings were negative, no Schaumann or asteroid bodies were observed, and examination of histological sections revealed epithelioid histiocytes, lymphocytes, and a few Langhans-type giant cells with noncaseating granulomas (Figures and ). Microbiological studies (sputum cultures, tissue staining for acid fast bacilli, and serology) were negative. The patient received 6 cycles of neoadjuvant chemotherapy consisting of taxotere, Adriamycin, and cyclophosphamide (TAC) every 3 weeks. One month after the completion of last cycle of neoadjuvant chemotherapy, PET CT scan revealed right paratracheal, prevascular, aorticopulmonary, precarinal, subcarinal, hilar, and subhilar multiple conglomerated mediastinal lymph nodes with SUV value of 13,13. When compared with the pretreatment PET CT scan, the mass lesion in left breast and left axillary lymph nodes cannot be visualized. The patient was referred for surgery.


A 27-year-old male with history of CML on remission since treatment with imatinib, chemoradiation, and allogenic bone marrow transplantation 1 year prior to consultation and with active and recurrent acyclovir-resistant herpes simplex stomatosis presented with a 2-day history of floaters in his right eye. Patient’s medications included several immunosuppressive agents such as tacrolimus, sirolimus, and mycophenolate along with the prophylactic medications, atovaquone, valacyclovir, and ciprofloxacin. Visual acuity was 20/30 +3 and 20/100 in the right and left eyes, respectively. Fundus examination of the right eye revealed irregular, fluffy, white subretinal and intraretinal lesions with pigmentary changes in the superotemporal arcade (Figure a). In the left eye, a smaller similar lesion was noted just inferotemporally to the optic nerve with adjacent retinal edema involving the macula. No vitritis was noted bilaterally. Differential diagnosis included viral retinochoroiditis (cytomegalovirus (CMV), herpes simplex virus (HSV), and varicella zoster virus (VZV)) vs. CML relapse vs. atypical toxoplasmosis (Figure b).
Serum IgM and IgG titers for CMV and toxoplasmosis were negative in addition to syphilis screening being negative. Cerebrospinal fluid (CSF) analysis was negative for CMV, HSV, toxoplasmosis via PCR, and bacterial growth. CSF analysis also showed atypical cells with no blasts indicating no evidence of CML relapse. MRI brain/orbits showed no abnormalities. Intravenous cidofovir had recently been started for HSV stomatitis, and the patient was initially observed on this treatment.
Two weeks after presentation, visual acuity decreased to 20/70 OD and 20/400 OS. Examination revealed progression of the retinal lesions with a mild vitritis (Figure ). The clinical picture was highly suspicious for CMV retinitis; however, the negative serum CMV PCR and progression of lesions on cidofovir raised serious doubt. An anterior chamber paracentesis was performed, and the aqueous humor was sent for PCR for CMV, HSV, VZV, Epstein-Barr virus (EBV), and toxoplasmosis. A more aggressive treatment of the CMV retinitis was also pursued with bilateral intravitreal injections of foscarnet in addition to intravenous route.
Five days later, quantitative PCR analysis revealed 3,400 DNA copies/ml OD and 2,800 DNA copies/ml OS of Toxoplasma gondii and negative PCR for HSV, VZV, EBV, and CMV OU. A diagnosis of Toxoplasma retinochorioditis was made. Clindamycin (1.0 mg/0.1 mL) was injected intravitreally OU twice at 4 days apart. Over the next month, the active areas of retinochoroiditis regressed followed by gliosis of the lesions with pigmentary changes (Figure a,b). The vision subsequently improved to 20/50 OD and 20/100 OS. Patient was also started on trimethoprim-sulfamethoxazole to prevent future reactivation of the disease.


A 45-year-old woman with a known history of rheumatic mitral stenosis presented with a 9 months history of progressive shortness of breath and bilateral peripheral oedema.
The patient had a successful closed mitral valvotomy in 1987, from which she completely recovered and was maintained on digoxin and warfarin.
Few months before admission her activity became limited due to increase shortness of breath, repeated coughing and recurrent paroxysmal nocturnal dyspnea. She was treated with aggressive diuretic regimen, digoxin, cordarone, beta-blockers and warfarin.
Physical examination revealed signs of right sided heart failure with decrease air entry along both lung bases. A mid-diastolic murmur was heard at the apex together with pansystolic murmur at left lower parasternal region.
Electrocardiography showed atrial fibrillation with enlarged right ventricle. Marked cardiomegaly was seen on chest radiography (Figure ). A hugely enlarged left atrium (11 × 10 cm) occupied by a thrombus was demonstrated by transthoracic echocardiography (Figure ). Evidence of mitral restenosis (MVA 0.9 cm2) with mild regurgitation was seen. Tricuspid valve was severely incompetent with an estimated PAP of 75 mmHg.
Laboratory investigations revealed a low hemoglobin level (9.5 g/dL), low platelets count (135,000/cmm), mildly elevated liver enzymes with positive hepatitis C antibodies.
Abdominal ultrasound showed hepatomegaly with mild cirrhosis as well as mild splenomegaly.
Surgery was performed using standard CPB with moderate hypothermia and antegrade blood cardioplegia. The stenosed mitral valve was exposed through an inverted T-shaped biatrial incision. A huge organized thrombus measuring 11 × 10 × 5 cm was removed (Figure ). Mitral valve was replaced with St. Jude Medical valve 31-mm. Tricuspid valve was repaired using Devag’s annuloplasty. Minimal inotropic support was used during weaning from bypass.
Postoperatively, the patient remained hemodynamically stable. She was ventilated for 17 hours and had minimal blood loss. She stayed in ICU for 3 days, during which intensive chest physiotherapy was performed. The patient was discharged after 12 days.
Follow-up by TTE and chest X-ray two weeks after surgery showed a well functioning prosthetic valve, clear left atrium with an estimated size of 9 × 9.8 cm (Figure ). Both lung fields were clear with reduced cardiothoracic ratio (Figure ).


Twenty-four-year-old G1P1001 single Caucasian female, who had been on DMPA for seven years, presented with complaints of dyspareunia and urinary urgency with nocturia. She stated that the dyspareunia had been present and worsening for 4 years. Dyspareunia occurred throughout intercourse, worse with rear entry, and had caused her to limit sexual activity. Her urinary complaints included burning with urination, urgency, and nocturia greater than three times per night for the last 2 years. She had previously seen a urologist and had urodynamics and cystoscopy which was negative. At that time, she received treatment with 6-dimethyl sulfoxide which showed improvement in her nocturia to one void per night. However, all other symptoms persisted unchanged. Past medical and surgical history was negative. On physical exam, vaginal atrophy was noted. Pap smear, urodynamics, urine culture, and cystoscopy were performed in the office, and all were within normal limits except for filling cystometrography values that were low. Patient was unable to tolerate potassium sensitivity testing and developed urethral bleeding after initial bladder distention. Vaginal maturation index was performed and found to be 5% in the superficial layer and 95% in intermediate and 0% in parabasal layers. Patient was informed of diagnosis of atrophic vaginitis likely secondary to long-term depo-provera use. Patient was instructed to discontinue depo-provera, given prescription to start combined oral contraceptive pills and vaginal estrogen cream. At 5-month followup, the patient reported improvement in dyspareunia, and she has some pain only with penetration. Urinary complaints were only present for first 1-2 voids after intercourse. Pelvic exam was within normal limits with no signs of vaginal atrophy. Vaginal maturation index was scheduled to be completed at 6-month follow-up visit; however, patient did not return for continued follow-up care.


A 2-week-old baby girl born to nonconsanguineous Japanese parents was referred to us because of skin lesions. The family history and personal history were unremarkable, and the pregnancy and labor had been uneventful. The baby's weight and height at birth were in the 50th percentile. On physical examination, we noted erythematous macules and plaques over her right chest, abdomen, and arm. We diagnosed these lesions as a port-wine stain (PWS). We also noted extensive areas of reddish-blue reticulated, marble-like lesions over her back and buttocks, consistent with a diagnosis of cutis marmorata telangiectatica congenita (CMTC). CMTC with hemihypertrophy was present on her lower right leg. Bilateral, demarcated greyish-blue hyperpigmentation on the buttocks and thighs, partly intermingled with the vascular lesions, was diagnosed as aberrant Mongolian spots. The rest of the physical examination was normal. Blood biochemistry, complete blood cell count, chest radiography, electrocardiography, and echocardiography were all within normal limits.
The physical findings indicated a diagnosis of PPV type IIb and Klippel–Trénaunay syndrome. Laser therapy was started when the patient was one-year-old. We used a QAL (ALEXLASER; Candela Corporation, Wayland, MA, USA) with an energy density of 6.0J/cm2 to treat the dermal melanosis of her buttocks and thighs. An LPDL (Vbeam®; Candela Corporation) with an energy density of 10J/cm2 and 1.5ms was used simultaneously to treat the PWS and CMTC lesions. Where the lesions were intermingled, we treated the dermal melanosis before the PWS and CMTC. The patient underwent five laser therapy sessions under general anesthesia. In each session, approximately 30% of the lesion area was treated; however, her back has yet to be treated.
The patient is now 3-years-old and shows normal mental and physical development. Although the hemihypertrophy remains, there is no leg length discrepancy. The aberrant Mongolian spots have faded. The four authors of this paper evaluated the amount of fading and agreed that although the lesions are still visible their color has decreased by about 80%. The PWS on the patient's trunk and arm has also decreased by about 80%, but the CMTC on her leg is mostly unchanged. We plan to change the laser power and pulse width for this patient's future treatment. Of interest, the CMTC on the patient's back has faded by about 90%, without laser therapy (Figure ).


A 4-month-old baby boy born to nonconsanguineous Japanese parents was referred to us because of skin lesions. The family history and personal history were unremarkable, and the pregnancy and labor had been uneventful. The boy's weight and height at birth were in the 50th percentile, and his postnatal development was normal. On physical examination, we noted a PWS on his right cheek and CMTC on his right side on his back, buttock, and arm. We found aberrant Mongolian spots, partly intermingled with the vascular lesions, on his chest and arms. We also noted ocular pigmentation of his right eye. Ophthalmologic examination revealed no other findings. No atrophy or hypertrophy of the soft tissues was observed. The rest of the physical examination was normal. Blood biochemistry, complete blood cell count, chest radiography, and electrocardiography were within normal limits.
PPV type IIa was diagnosed, and laser therapy began when the patient reached one year of age. We used a QAL with an energy density of 6.0J/cm2 to treat the dermal melanosis of his chest and upper limbs. We used an LPDL with an energy density of 10J/cm2 and 1.5ms to treat his PWS lesions simultaneously. Where the lesions were intermingled, we treated the dermal melanosis before the PWS. The patient underwent three laser therapy sessions under general anesthesia. We did not treat the CMTC in any of the sessions.
The boy is now 2-years-old and shows normal mental and physical development. Both the aberrant Mongolian spots on his trunk and upper limb and the PWS on his cheek have decreased by about 60%, although they are still visible. We plan to treat this patient with another session of combined laser therapy. The CMTC on the child's back, buttocks, and arms has faded by about 90% without laser therapy (Figure ).


A 58-year-old male patient was admitted to Su Bei People’s Hospital of Jiangsu Province on 13 March 2012, with a major complaint of ‘lower left quadrant abdominal discomfort with bloody stools.’ His symptoms began about a month prior to the abdominal discomfort in the lower left quadrant and he experienced two to three bloody bowel movements a day without an obvious etiology. These symptoms became more severe in the next three days. Blood appeared purple and red on the surface of soft stools combined with mucus. He also experienced occasional abdominal pain and tenesmus. Colonoscopy (Figure
) at an outside hospital on 5 March 2012 had revealed a large pedunculated, cauliflower shaped lump with superficial ulceration and necrosis at approximately 40 cm from the anal verge. The mass appeared hard and friable. The rest of the colon and rectum appeared normal. Biopsy of the lesion showed non-specific chronic mucosal inflammation with necrosis and exudate. The patient’s past medical history and family history were unremarkable. At his physical examination on arrival at our hospital, the abdomen was soft, non-distended and without visible peristalsis. There was mild tenderness on palpation without rebound tenderness. No lumps were spotted. Rectal examination was unremarkable and blood was present. Laboratory tests showed a white blood cell count of 7.4 × 109/L, a red blood cell count of 3.08 × 1012/L, a neutrophil count of 5.78 × 109/L (78.1%), and a hemoglobin level of 90 g/L. Tumor markers were as follows: alpha fetoprotein (AFP) 3.87, CA 199, and carcinoembryonic antigen (CEA) 2.29. An abdominal CT scan with contrast showed a 5-cm diameter lump-like lesion at the junction of the descending and sigmoid colon with significantly thickened walls with dilated lumen (Figure
). There were multiple rings within the lump with smooth rims suggesting colon intussusception. Colon cancer could not be ruled out. The patient was urgently taken to the operating room to probe with a preoperative diagnosis of colon intussusception and possible colon cancer. Intraoperatively, the mass was located at the splenic flexure measuring 10 × 7 cm. Colon intussusception was present with dilatation of the proximal colon. No other lesions were identified. Once the intussusception was reduced, an 8 × 5 cm colon lesion was revealed and a partial colectomy was performed. Frozen section revealed an angiolipoma. No further resection was indicated. The patient recovered from surgery well and was taken back to the ward. Final pathology showed an 8 × 6 × 6 cm exophytic colon lesion consisting mainly of fatty tissue with ulceration. Seven lymph nodes ranging from 2 mm to 10 mm were identified outside the colon. Histologic examination (Figure
) revealed a mass consisting of mature adipose tissue with vascular structures. Intralesional fat necrosis and mucosal ulcerations were present with a large amount of neutrophil and lymphocyte infiltration. Lymph nodes showed reactive proliferation with no evidence of tumor. The final pathologic diagnosis was angiolipoma of the descending colon. During follow-up, this patient showed no recurrence.


In June 2012, a 71-year-old man has been admitted to our Emergency Department with low back pain, dyspnea, and fever.
The patient entered menopause at the age of 54, and osteoporosis was diagnosed in 2006 using DXA-scan (lumbar spine BMD 0.690 g/cm2, T-score 2.6 DS, femoral neck BMD 0.547 g/cm2, T-score 2.5 DS).
The patient referred posttraumatic subarachnoid haemorrhage in 2007 that resulted in right upper limb plegia and paraplegia and immobilization syndrome complicated by a sacral decubitus ulcer (stage IV).
Approximately 20 hours after arrival, the patient was transferred to the Department of Internal Medicine.
During the hospitalization, the analgesic therapy was administered without achieving a complete resolution of the clinical picture, with persistence of low back pain at rest, exacerbated by the mobilization, limiting the performance of the physiological functions and the personal care.
A radiograph of the lumbar spine revealed morphological and structural alteration of D12 body, right-convex scoliosis of the thoracic spine, and marked reduction in calcium tone.
Magnetic resonance (MR) of the lumbar spine with administration of intravenous gadolinium showed recent vertebral collapses at the level of L1 and L4 bodies and confirmed previous fractures in D12 body ().
After the evaluation of the case by the interventional radiologist, the PVP of vertebrae D12, L1, and L4 was performed.
PVP is not routinely performed in immobilized patients; in fact, while it is commonly used for the treatment of osteoporotic thoracolumbar vertebral compression fractures, its role in vertebral stabilization in patient with immobilization syndrome has not been reported in the literature [].
Anyway, we decided to proceed to improve quality life of the patient treating the intense pain.
The preoperative and postoperative pain perceptions were compared using (Visual Analogue Scale) VAS. The latter is nothing but a simple graphical representation of the pain, recorded on a 10 cm numerical scale ranging from zero (no pain) to 10 (maximum pain ever felt). This method allows the patient to bypass the cognitive level of his brain and give a truer representation of pain.
For assessing the quality of life questionnaire, (Psychological General Well Being Index) PGWBI was administered [].
The patient was informed on the technique, the benefits, and the potential complications of the intervention as well as postprocedure care, and a written informed consent was obtained.
The hematological examinations including blood coagulation were obtained, and all the values were within the normal range.
The segment to be treated was identified under fluoroscopic guidance (Allura, Phillips, The Netherlands) on the angiography table with the patient in prone position.
Local anesthesia consisting of lidocaine 2% (10 mL) and naropine 7.5% (10 mL) and drugs for sedation in spontaneous breathing were administered, and a 13 G needle with left transpedicular approach at the level of D12, L1, and L4 bodies was introduced.
About 3 mL of polymethylmethacrylate (PMMA) were injected in every vertebral body with uniform distribution of cementing material without intra- and postprocedural complications ().
After a few hours from the end of the procedure, pain relief was significant.
Duration of the procedure was about 25 minutes.
The efficacy of a PVP was demonstrated by a decrease from 9/10 to 4/10 on static VAS score.
For the evaluation of psychophysical well-being, PGWBI [] questionnaire was used, including 22 items, each of which presents a series of six possible answers, whose score is proportional to the positivity and well-being over the last four weeks.
The scale consists of six domains or dimensions: anxiety, depression, positivity and well-being, self-control, general health, and vitality.
During hospitalization, the patient obtained a score of 54, equal to serious illness. At one month after PVP, the patient has scored 65, equivalent to moderate discomfort.
After the procedure, the patient did not need any antalgic therapy, and there was a significant improvement on passive mobilization, performance of physiological functions, daily management of personal care, and maintaining skin integrity for the treatment of decubitus ulcers, with a significant increase of life quality and psychological well-being.


A 48 year old cattle rearer in a village in northern part of Nigeria presented with 3 hr history of an arrow shot in anterior part of the neck which he sustained the while trying to prevent some armed robbers from stealing his cow. There was scanty bleeding from the site with the arrow insitu sealing the wound. At presentation, there was no associated heamatemesis, cough, difficulty in breathing nor loss of speech. However, there was a small swelling around the entrance point of the arrow with moderate pain.
The physical examination revealed a middle aged man conscious not pale, with temperature of 37°C, respiratory rate of 21/min, pulse rate of 86/min and BP of 130/80 mm Hg.
There was an obvious distal end, 13 cm in length, of a metallic arrow in the anterior neck of the patient. The entrance point of the arrow, about 1 cm in diameter, was just at the anterior border of the right sternocleidomastoid muscle, about 4 cm above the medial end of the right clavicle. There was a small skin bruise with slight swelling and tenderness around the opening but no active bleeding and no crepitus (Fig. & ). Ear, Nose and Throat Examination were normal so were other systemic examinations. An urgent PCV done was 36%. X-rays of the neck were done which revealed the barbed arrow tip in right tracheo-esophageal groove. The barbed end lay vertical (Fig. ).
He was commenced on intravenous fluid, cefuroxime and metronidazole. 2 units of blood was cross matched for him and he was planned for urgent anterior neck exploration and foreign body removal under general anesthesia.
At surgery, a 6 cm para-sternocleidomastoid incision was made on the skin with the entrance point of the arrow at the mid-point. The incision was deepened down and dissections done to reach the barbed end. The arrow lied in the right trachea-esophageal grove with the pointed end slightly buried in the wall of the esophagus. There was a 2 cm laceration on esophageal wall into the muscle but the mucosa was intact. Also the pre-tracheal fascia was bruised. The esophageal wall laceration was repaired in layers. No injuries to the great vessels of the neck. The wound was thoroughly irrigated with normal saline and closed in layers. A nasogastric tube (NG tube) was inserted intra-operatively.
N-G tube feeding was commenced 12 hrs after surgery for 1 week followed by peri-nasogastric tube feeding for another 5 days during which there was no evidence of mediastinitis. The tube was finally removed on the 14th day. Skin suture was removed on the 5th day post-op. The patient had post-operative antibiotics for 2 weeks. He was discharged on 15th day post-op and had been followed up in the clinic for 2 months without complications.


In the ultrasonography of a 54-year-old male patient with renal colic pain, we detected a renal stone and hydronephrosis and an incidental solid mass 88 × 67 × 100 mm in size right of the midline. It had heterogeneous echogenicity, lobulated contour and calcification foci, and was distinctly separated from the kidneys and liver, suggesting a pancreatic mass (). In MRI, a retroperitoneal mass lesion was detected in the anteromedial adjacency of the upper-middle part of the right kidney. It had a calcification foci and was distinctly separated from the liver and kidneys, but not from the pancreas and inferior vena cava (IVC). It was isointense on T1-weighted images compared to the skeletal muscle () and hyperintense on T2-weighted fat suppressed sequences compared to the surrounding muscle tissue showing heterogeneous signal intensity (). It was remarkable that the defined mass lesion gradually showed a moderate level of heterogeneous contrast enhancement when compared to surrounding muscle planes following IV injection of contrast material ().
The retroperitoneal mass was excised and pathologically examined. It was an encapsulated, cream-colored 10 × 6 × 4cm sized mass. An immunohistochemical examination showed positive results of smooth muscle actin (SMA) staining and negative results with p53 and S-100. The Ki-67 proliferation index was up to 10%. Accordingly, the histopathological diagnosis was considered as symplastic leiomyoma. One month after operation, MR imaging was performed and no residual mass was determined around the IVC (). IVC was patent and healing in the hydronephrosis of the right kidney was noticed.


A 41-year-old Taiwanese male with a previous history of hypertension and major depressive disorder under control with medication came to the outpatient clinic of the Division of Gastroenterology complaining of recent anal bleeding. Physical examination and colon fiberoscopy revealed a subepithelial tumor at anal verge (Figure ), for which he received a papillectomy.


A 30-year-old female came to the emergency department of our institute with difficulty in swallowing since one day. The patient was not even able to have water. An assessment of the nervous system was made because neuromuscular disorders may present with dysphagia as an initial symptom. Proper history revealed that the patient was a known case of rheumatoid arthritis and was taking routine anti-inflammatory drugs. The prior day, the patient was advised to take ayurvedic tablets by relatives for immediate relief. The tablet was about I cm in diameter and was spherical in shape. The moment the patient took the first tablet with water, she started having discomfort in the throat. She took more water but was not relieved. She visited local doctors and was referred to our institute.
On arrival she had drooling of saliva; the oxygen saturation was between 70%-80% and the patient was not able to take anything orally since 12-14 hours. While performing an indirect laryngoscopy, we found pooling of saliva in both pyriform fossae. Taking history into account rigid oesophagoscopy under general anaesthesia was planned. All routine blood tests were in normal limits. The X-ray of the neck lateral view revealed a radiopaque spherical shadow at the lower level of cricopharynx, which was a surprise to us, as routinely tablets are not radiopaque. There was also a slight prevertebral widening in front of C6 and C7 ().
To understand what we were going to encounter, the patient’s husband was asked to provide another ayurvedic pill of the same kind. The tablet’s colour was black, it was spherical, stony hard and its approximate size was of 1 cm. Not knowing the contents of the pill, it was decided that it should be removed immediately because a long-standing tablet may cause erosion/obstruction of the wall of the oesophagus. The patient was shifted to operation theatre for rigid hypopharyngoscopy under general anaesthesia. On rigid hypopharyngoscopy, the tablet was visualised in lower border of the cricopharynx. The surrounding area was extremely congested and oedematous. With the help of a foreign body removal forceps, the tablet was grasped but some part of it broke, which made the removal action easier. The rest of the tablet affected the wall of the cricopharynx and was eventually removed (). On gross appearance, the pill’s colour was black; it was hard in consistency and of approximately 1.25 cm in size.
The postoperative X-ray of the neck confirmed the complete removal of the contents ().
As there was an erosion of the wall of the oesophagus, the patient was kept nil orally along with routine intravenous antibiotics and steroids. After two days, liquids were started, followed by semisolids and a normal diet. The patient was discharged on the 4th day postoperatively, being totally relieved of symptoms.


A 43-year-old gravida 2 para 2 Caucasian female with a past medical history of anemia, uterine fibroids, and hyperthyroidism treated with radiation six years earlier presented to the emergency room with complaints of painless spontaneous gum bleeding and vaginal bleeding. There was no history of trauma or bleeding from any other site. The patient had no history of unusual or excessive bleeding, although she had a history of anemia secondary to prolonged menstrual bleeding from uterine fibroids, for which she previously received two units of packed red blood cells (PRBC). Her family history was noncontributory.
Her blood pressure, heart rate, and respiratory rate were 118/65, 72, and 18, respectively. On examination, she was noted to have buccal purpura and scattered petechiae on her anterior abdominal wall and lower extremities. The rest of the exam was unremarkable.
Blood work revealed a hemoglobin (Hgb) of 9.2 g/dL (normal range—12.0–15.5), mean corpuscular volume (MCV) of 69.8 (normal range—80–100), platelets of 6,000 (normal range—150,000–450,000), and WBC of 9.2 k/mm cu (4.2–11.0). Three days prior to this presentation, her Hgb was 8.6 g/dL, MCV 68.3 fl, platelets of 330,000/uL, and WBC of 8.6 k/mm cu, following PRBC transfusion of two units for severe symptomatic anemia (Hgb 5.4) one week earlier. Further laboratory studies revealed a negative direct antiglobulin test and antinuclear antibody, normal levels of fibrinogen, prothrombin time, INR, D-dimer, and haptoglobin, with an elevated reticulocyte count. Peripheral blood smear showed no platelet clumping. The platelet morphology was normal, with markedly decreased number of platelets. The patient was started on intravenous methylprednisolone and IVIG. Repeat complete blood count showed a gradual trend towards an improvement in platelet count with normalization on day 7. Laboratory studies demonstrated a homozygous platelet genotype of HPA-Ib/1b with antibodies against HLA class I and platelet glycoproteins (GP IIb/IIIa and GPIa/IIa), which was consistent with PTP. This transfusion complication was reported to the blood bank.


A 31-year-old woman (origin: Algeria) was referred to our academic gynecological institute for unexplained primary infertility. The patient presented with no complaint. Hysteroscopy showed a 10 mm sized endometrial polyp located on the left lateral wall of the uterine isthmus. Neither adhesion (synechia) nor other abnormality was noted during hysteroscopy. Hysteroscopic view of superficial blood vessels showed regular vascular pattern, with a classic benign appearance. No other infertility etiology was discovered. The polyp was removed using hysteroscopic bipolar loop (24 French). Pathology () showed lymphocytic and plasmacytic chronic inflammatory modification, granulomatous modification, and gigantocellular modification, which lead to the diagnosis of tuberculosis. No acid fast organism was seen on Ziehl-Neelsen staining. A chest thorax X-ray revealed no sign of pulmonary tuberculosis. The patient underwent antituberculosis therapy (rifampicin, isoniazid, pyrazinamide, and ethambutol) during one year. Posttreatment hysteroscopy revealed no abnormality. Followup of the patient was 18 months. She did not start trying to get pregnant since the treatment (marital problems).


A 5 years old male Testudo graeca (Leo), of 500 gr weight was brought to our attention in May with skin and muscle injuries localized in particular in the dorsal front limbs caused by rat bites 2 days before (Figure A). The tortoise, which had come out of hibernation in March, live in a garden near a landfill. These severe injuries, localized in particular in the dorsal left front limb, (Figure B) showed a considerable loss of substance and humeral-radioulnar joint and bone exposure. The wounds were lightly contaminated with soil and showed a small tissue necrosis. After debridement of all necrotic and non-viable tissues, a local disinfection with a mixed solution of sodium chloride, hydrogen peroxide and iodopovidone for 2 weeks, enrofloxacin IM 5 mg/kg once for day (Baytril 2, 5%, Bayer) for 2 weeks, and ceftazidime IM 20 mg/kg once for day (Glazidim, GlaxoSmithKline) for 5 weeks were administered; moreover chloramphenicol and collagenase based cream (Iruxol cream 1%, Smith+Nephew) for 3 weeks after systemic antibiotics was locally dispensed. During this period the reptile was kept in an acclimatized terrarium with the temperature ranging from 24 to 32°C, and artificial sun light (UVB 10% for 6 hours for day). After 60 days, because no significant improvements in wound repair were observed, (Figure C) we decided to expose the reptile to REAC TO-B treatment. Therefore all the other therapies were stopped one day before the beginning of this innovative therapy. The animal was submitted to 12 sessions of REAC TO-B along 17 days. This treatment required the use of anesthesia, only during the first 4 sessions (alphaxalone IM 20 mg/Kg), afterword anesthesia was no more necessary, because the animal was calm, and during the last session it was asleep. During the time of treatment the tortoise eats regularly its usual diet. After 12 sessions of REAC TO-B tissue growth was evident in injuries localized in both front limbs (Figure A-B-C-D-E-F). Considering the tissue damages occurring during the first 2 months of traditional treatments, after 17 days of REAC TO-B treatment there was an evident increase in recovery of both legs’ lesions. This tissue recovery, growth and remodeling, was confirmed by histological analysis obtained evaluating cutaneous biopsies taken at the level of the lesions, before (T0), 3, 7 (Figure A-B-C-D-E) and 14 days after the first REAC TO-B treatment. Before REAC TO-B treatment underlying dermis of moderate cutaneous excoriation appeared infiltrated by mixed mononuclear inflammatory cells and some eosinophilic granular cells. Noteworthy just three days after the first REAC TO-B session the upper dermis presented numerous fibroblasts surrounded by extracellular matrix and few mononuclear inflammatory cells, whereas the epidermis appeared hyperplasic. Four days later skin biopsy showed mature connective tissue and tissue remodeling. After 17 days there was a complete healing. Considering the success obtained in the case of tortoise Leo we treated with REAC TO-B therapy also other turtles which presented lesions in soft tissue and in the carapace. In particular: a Trachemys scripta elegans (female, 25 years old, Ice) which exhibited a shell wound due to partial freezing (Figure ), a Trachemys scripta scripta (female 2.5 years old, Penelope), with a small infected wound of the shell (Figure ), a Testudo hermanni (female 15 years old, Juta) with a traumatic lesion of right front limb (Figure ), a Testudo Graeca (male 50 years old, Margherito) with a jaw fracture (Figure ) caused by a dog bite as well as a Trachemys scripta scripta (male 5 years old, Mir) with a necrosis of the mouth, caused by a hook (Figure ). Margherito has been subjected to surgery and was treated with ceftazidime IM 20 mg/kg once (Glazidim, GlaxoSmithKline) for 2 weeks before REAC-TO treatment. Ice and Mir exposed to REAC TO-B were not previously treated with other pharmacological therapies except wounds debridement, while Penelope, after debridement, was subjected to local disinfection of the infected shell with a mixed solution of sodium chloride and iodopovidone for four days. Juta didn’t receive any treatment before REAC-TO. Before starting REAC TO-B treatment all the previously administered therapies were stopped.
The REAC is an innovative-patented technology (WO2002004069) for bio-stimulation and/or bio-enhancement techniques that induces weak radio-electric currents in the tissues, to induce a cell reprogramming activity. The model used in this study (ASMED, Florence, Italy) is specific for regenerative treatments. The REAC-TO protocol consisted of 100 radio frequency bursts, each of 2.4 GHz for 0.5 seconds, with a specific absorption rate of 7 μW/kg, spaced with 4.5-second pauses, applied to the skin by a special laminar aluminum electrode (Figure ). Each therapy session lasted about 10 minutes, with 18 sessions constituting a REAC TO-B treatment cycle. A REAC model (ASMED, Florence, Italy), was used in this study. During therapy the patients were completely wrapped in a special laminar aluminum electrode, specific for REAC TO-B treatments, in a way that the ends of the aluminum electrode were not touching each other. The conveyors electrodes were placed in this way: 4 in the cranial part of the aluminum foil and 4 in the caudal part (Figure ). The distribution of daily sessions was organized according to the eventual administration of anesthesia [] and to the response of the animal to handling: when the patient was calm and showed no signs of discomfort, more sessions for day were performed for a maximum of 6 sessions for day (the animals were more calm if we covered them with a dark cloth).
As previously described for Leo all the other turtles were exposed to 12 or more sessions of REAC TO-B treatment, by the aid of anesthesia or not along different period of time. The ameliorations of the shell of the animal after REAC TO-B treatments are reported in Figure . In particular the case of the animal showing a loss of the shell (Ice) was particularly evident because of the possibility of verifying the scarring and hardening of the tissue underlying the lesion. In fact, after 2.5 REAC TO-B treatment cycle, corresponding to 60 days, the animal showed a marked narrowing of the area of exposure of the peritoneal membrane. This resulted in a significant reduction in visibility of raising and lowering related to breathing, that were highly visible before treatment. Penelope (Figure ) began REAC TO-B treatment after local disinfection was applied for four days. For this reason 18 sessions of REAC TO-B, corresponding to 7 days were enough to see evident wound healing (Figure B).
After 18 sessions of REAC TO-B, corresponding to 20 days, Mir showed wound reepithelization and necrosis disappearance, and a complete healing over the next 7 days (Figure D).
All the animals were monitored after REAC TO-B treatments; 2 of them for 18 months and 4 for 12 months and we didn’t see any long term disorder or problem.
Macroscopic and histological results underline a significant tissue repair based on clinical observation in Leo and other reptiles. Thereby wound healing also in tortoises proceeds by a process of granulation, epithelialization and wound contraction, [,] which generally takes several weeks to heal, and has been shown to be temperature dependent.
In the present work we evidenced that Testudo graeca Leo, and 3 turtles with different injuries of soft and hard tissues treated with REAC-TO showed an evident amelioration of healing wounds. It is known that the reptilian epidermis is composed of a beta-keratin layer, the mesos layer and the alpha-keratin layer, [] which is supported by the underlying stratum germinativum, whereas the chelonian shell is composed of a thick epithelium and contains layers of keratin []. The deeper dermis, derived from embryonic mesoderm contains connective tissues, vascular tissues, sensory structures and dermal bone (osteodermis). We have previously demonstrated that REAC TO-B treatment induces cell proliferation and differentiation toward different lineages in vitro [,]. In particular REAC-TO was found to have the ability to modulate the expression of genes and proteins involved in the differentiation of embryonic mouse cells in vitro []. Moreover we recently observed that REAC-TO influenced the plasticity and differentiation capability of human skin derived fibroblasts toward different cellular lineages, [] thus further demonstrating the modulatory effect of this device on cell fate and tissue regeneration. Therefore we can argue that the amelioration of wound healing and bone fracture of reptiles observed here may be due to a proliferation of the germinativum stratum of the epidermis and of the embryonic mesoderm responsible for the formation of connective tissues, vascular tissues, sensory structures and osteodermis. Osteodermis is composed of a mixture of spongy and compact bone and, in tortoises, is fused with the ribcage and spine, expanding to form the plates of bone that make up the chelonian carapace and plastron [-]. Our patients were subjected to different sessions of REAC-TO treatment, ranging from 12 (Leo) to 42 (Ice), considering the site and seriousness of injury. Therefore as supposed the number of REAC-TO sessions was higher in the patient exhibiting lesions of shell (Ice). The REAC-TO treatment, applied after the complete debridement of the necrotic tissues, did not cause a severe stress to patient and required only few anesthetic treatments (Leo). The positive action of REAC-TO treatment is further inferred by clinical results obtained by us in healthy human subjects, improving circulation, hydration, and the tropism of facial skin [].
Since REAC-TO is able to activate the process of tissue repair by inducing cellular organization and a vascular network, activating and accelerating tissue recovery may represent a powerful approach that could pave new ways in veterinary and human healing, besides other physical and chemical treatments [,].


A 64-year-old male patient was admitted to the emergency ward for severe occipital headache, visual disturbances and new-onset severe hypertension. The symptoms were initially noted three days before admission. His medical history was notable for hypercholesterolemia with atorvastatin therapy. Thirteen months before admission, an EVAR operation was performed to repair a rapidly expanding AAA with a diameter of 53 mm. EVAR with Endurant endograft (Medtronic, Minneapolis, MN) was combined with a Chimney procedure into the left renal artery, using a balloon expandable covered stent-graft (7 × 38 mm Advanta V12; Atrium Medical Corp). The Chimney technique was used due to irregular aortic neck with posterior ulceration and high difference of right renal artery origin, 10 mm above the left renal artery origin. Antiplatelet therapy with clopidrogel (75 mg/day) was initiated after the surgery. During the 6th month follow-up an abdominal computed-tomography angiography (CTA) revealed a well functioning aortic stent and a patent CG (Figure
A-B). One month before presentation with hypertension, clopidrogel therapy was temporarily stopped for six days, in order to undergo an elective laparoscopic bilateral inguinal hernia repair (IHR) surgery. The immediate-post operative follow-up after the IHR was uneventful with normal blood pressure measuring.
At admission, the patient was without abdominal or flank pain. Blood pressure was 224/113 mmHg, heart rate 91 beats per minute. Ophthalmology examination including optical coherence tomography (OCT) revealed retinal detachment and a large accumulation of subretinal fluid in the right eye. There were no murmurs or bruits over the renal arteries. Laboratory results at admission with comparison to values taken five weeks before admission are summarized in Table
.
Renal duplex ultrasound failed to detect blood flow into the left renal artery. CTA demonstrated an abdominal endograft that was patent without a leak, dissection or migration. However, a total occlusion of the CG to the left renal artery was noted without stent kinking (Figure
C-D). The left renal parenchyma was smaller compared to the previous CTA, with decreased contrast media uptake and hypodense wedge areas, indicative of multiple infract (Figure
E).
Medical therapy to reduce blood pressure was initiated with intravenous nitroglycerine and subsequently with maximal dosage of oral ramipril, amlodipine and hydrochlorothiazide. Blood pressure was lowered gradually and the patient was discharged with improvement of ophthalmological findings and serum creatinine levels of 1.5 mg/dL. Eight months after discharge, the patient was asymptomatic with only ramipril 2.5 mg/day as antihypertensive medication. At that point of time, office blood pressure was measured 128/81 mmHg and serum creatinine levels were of 1.3 mg/dL. The protein excretion in urine was of 280 mg/day.


A 21-year-old 37-week primigravida was referred to our hospital with a femoral pathological fracture following a minor fall event at home. The patient was known to have goiter for three years. The goiter was predominately left-sided and stable with neither significant increase in size nor obstructive symptoms. Exposure to ionizing radiation and family history for thyroid malignancy were negative. Systemic review was remarkable for a one-week history of on/off back pain. The course of pregnancy was uneventful.
Upon admission, laboratory work-up was significant for serum thyroglobulin (TG) of 1,368.0 μg/L (normal range: 1.4–78.0 μg/L). Neck ultrasound (US) was done and showed a unifocal 11.7 × 7.1 × 8.2 cm left-sided heteroechoic lesion involving the left thyroid lobe with moderately increased vascularity, foci of calcifications, and areas of necrosis. The neck US was highly suggestive of primary thyroid malignancy with no suspicious lymph nodes. Fine needle aspiration of the suspicious neck lesion confirmed the diagnosis of PTC. The patient was admitted for pregnancy delivery and further tumor work-up after delivery.
Day-7 after admission, the patient delivered her baby at 38 weeks of gestation by an uneventful lower segment cesarean section. The baby was otherwise healthy and placenta was not examined histologically for search of metastasis. After delivery, the patient was worked up for her femoral pathological fracture and query of metastatic PTC. Computed tomography (CT) scan showed no evidence of lung metastasis or lymphadenopathy. Magnetic resonance imaging (MRI) scan showed destructive expansile osteolytic lesions involving the left proximal femur, the vertebral body of L2, and the right transverse process of T10. A multidisciplinary team was involved in the management of the patient.
Patient underwent total thyroidectomy with left and central neck dissection. Grossly, the tumor was well circumscribed measuring 9.5 cm in the maximum diameter showing vascular invasion and without signs of invading surrounding tissues. Histopathological examination of the left thyroid lobe was consistent with primary PTC (). All the twenty-nine reactive lymph nodes identified in the neck dissection specimen were negative for metastasis. Moreover, during the same surgery, the patient underwent left proximal femur resection with endoprosthesis. Histopathological examination of the resected proximal femur was consistent with metastatic PTC (). Three months after left femur implantation, patient developed severe chronic prosthetic infection for 4 months which was managed aggressively with antibiotics. Two weeks after surgery, the patient underwent L2 vertebral body resection with posterior decompression (foraminotomy), interbody fusion, stabilization, and instrumentation. Histopathological examination of the resected L2 vertebral body was consistent with metastatic PTC. The surgical resection of the T10 mass was not a favorable option for three reasons: first, positive history of chronic left femur prosthetic infection; second, increased risk of metal chronic infection; third, the bloody nature of T10 tumor with possible life-threatening operative complications. Instead, the plan was to consider the patient for ten in-patient spine external beam radiation therapy (EBRT) sessions spread over two weeks without any further surgical intervention.
Postoperatively, patient had a single session of radioactive iodine (I-131) therapy (dose: 190 mCi). A follow-up US of neck soft tissue showed a clear right thyroid bed and a hypoechoic nodule in the left thyroid bed measuring 0.4 cm in the maximum diameter with no vascularity and no suspicious lymph nodes. Postoperative thyroid function tests (TFTs) showed normal values and TG dropped to 51.6 μg/L (normal range: 1.4–78.0 μg/L). Whole body positron emission tomography/computed tomography (PET/CT) scan showed interval resolution of neck findings with postoperative changes and multiple metastatic minimal fluorodeoxyglucose (FDG) avid bony lesions around the left total hip replacement prosthesis, L2 and T10. The patient was scheduled to be seen after 3 months.


A 42-year-old G4P1 with hypertrophic cardiomyopathy (HCM) presented to the emergency department seven days after uneventful cesarean delivery with severe shortness of breath. Physical exam revealed elevated jugular venous pressure, bilateral leg edema, and bibasilar lung crackles. Chest radiographs demonstrated bilateral pleural effusions and perihilar airspace opacities (Figures and ). Thoracic computed tomography (CT) pulmonary angiography ruled out pulmonary embolus and confirmed pulmonary edema (). Asymmetric interventricular septal thickening measuring up to 22 mm was noted, despite the fact that the patient's diagnosis of HCM was not known at the time of reporting (Figures , , and ).
Subsequent transthoracic echocardiography demonstrated normal systolic function (see videos A and B in Supplementary Material available online at ). Diastolic parameters were abnormal with an E/E′ of 19 mmHg indicating elevated left atrial pressure and a mild provocable left ventricular outflow tract gradient of 33 mmHg with amyl nitrate.
The patient was admitted to hospital and improved rapidly following administration of intravenous diuretics. Peripartum intravascular fluid shifts and diastolic impairment likely contributed to heart failure in this patient.
The patient was discharged home the following day and has remained well with no further complications at followup six months later.