text
stringlengths 746
31k
|
|---|
A 57-year-old asymptomatic man with no significant past medical history was found to have an enlarged cardiac silhouette on a routine chest radiograph (). Magnetic resonance imaging (MRI) revealed a 9 cm pericardial cyst in the right cardiophrenic angle that was associated with right atrial compression (Figures , , and ). Although the pericardial cyst wall showed contrast uptake, no uptake within the cyst was observed on first-pass or delayed images. There was no compression of the airway or superior vena cava (SVC) and the pericardial cyst had not eroded into the heart. The patient was not at high risk for hydatid cysts and he did not have any history of fever, suggesting that an infectious cause for his pericardial cyst is unlikely. He did not have any history of chest trauma or intrathoracic surgery. The absence of hypertension, hematuria, and a positive family history made a diagnosis of autosomal dominant polycystic kidney disease (ADPKD) unlikely. The patient was scheduled for resection of the pericardial cyst using VATS. Preoperative electrocardiographic findings, complete blood count results, serum creatinine levels, liver function tests, and serum electrolyte levels were normal.\nOn the day of surgery, the physical exam, including heart and lung auscultation, was unremarkable and the vital signs were within normal limits (blood pressure of 119/75 mmHg, heart rate of 83 beats per minute, respiratory rate of 14 per minute, blood oxygen saturation of 97% on room air, and temperature of 36.9°C). A left radial arterial line and two large-bore intravenous catheters were placed. The patient was adequately hydrated with intravenous administration of normal saline. He was transferred to the operating room and placed in the supine position on the operating table. The standard American Society of Anesthesiologists monitors were placed on the patient. The pericardial cyst did not compress the patient's right bronchus or the SVC, and therefore, he was able to tolerate the supine position with no shortness of breath or hemodynamic instability. The patient was preoxygenated and general anesthesia was induced by slow intravenous administration of etomidate 0.2 mg/kg and fentanyl 1 μg/kg. Neuromuscular blockade was achieved by intravenous administration of succinylcholine 1.5 mg/kg. Ephedrine 0.1 mg/kg was administered following induction to minimize the hemodynamic effects of the induction agents and positive pressure ventilation. A 37-French left-sided double-lumen endobronchial tube (DLT) was placed. The patient was placed in the left lateral decubitus position. Anesthesia was maintained with oxygen (fraction of inspired oxygen of 0.6), air, and sevoflurane (1 minimum alveolar concentration). The right lung was collapsed and neuromuscular blockade was induced with rocuronium 0.6 mg/kg. A 1-cm incision was made in the posterior axillary line at the fifth intercostal space. A metal port was placed and a 10-mm, 30° thoracoscope was placed through the incision. A 2-cm incision was made above the fifth intercostal space at the mid axillary line to access the cyst. The pericardial cyst was found to be firm, and had some calcifications on the surface (Figures , , and ). The cyst was easily separated from the pericardial fat. However, it was attached to the anterior chest wall. Following separation of the cyst from the anterior chest wall some bleeding occurred from the distal right internal mammary artery. The bleeding was controlled with Enseal and clips. The cyst was large, and hence, access to the superior aspect of the cyst was difficult. Therefore, an 18-gauge needle was used to aspirate the cyst fluid. Approximately 300 ml of brown, murky, nonodorous fluid was aspirated from the cyst before it was completely resected (). The patient remained hemodynamically stable throughout the procedure and the DLT was removed in the operating room at the end of the procedure. Postoperative pain was managed with an intercostal nerve block using 10 ml of 0.5% bupivacaine and patient controlled analgesia pump using hydromorphone (intravenously, 0.2 mg every 10 minutes). The patient's postoperative course was uneventful, and he was discharged on postoperative day 1 in a stable condition. Cyst fluid cultures were negative. |
A 46-year-old woman with morbid obesity, hypertension, hyperlipidemia, active smoking, and bipolar disorder was evaluated for paroxysmal atrial fibrillation as an outpatient. A transthoracic echocardiogram showed a right atrial mass close to the RA-IVC junction. A transesophageal echocardiogram confirmed the presence of a pedunculated right atrial mobile bilobular mass measuring 2.1 × 1.8 cm, not arising from the interatrial septum with extension into the inferior vena cava (Figures –). A secundum atrial septal defect was also identified. The patient was referred to cardiac surgery for resection of a presumed right atrial myxoma given the possibility of embolization. The intraoperative TEE suggested the presence of one bilobulated mass arising low in the right atrium.\nUsing aortic and bicaval cannulation, a right atriotomy was performed and a discrete 2 × 3 cm mass was removed from the IVC-RA junction near the Eustachian valve. The right atrium was closed and the patient weaned from bypass. The specimen did not appear to be a myxoma, so it was sent for frozen section and interpreted as being ectopic liver tissue. In the interim, a repeat TEE showed an additional discrete 2 × 2 cm mass in the IVC near the hepatic veins. Femoral venous cannulation was then performed to allow for visualization of the IVC below the pericardial reflection. Through the same right atriotomy and using additional suction directly in the IVC, the IVC mass was visualized and resected. Both specimens were interpreted as showing partially encapsulated liver parenchyma with mild steatosis, fibrosis, ductal proliferation, and periductal chronic inflammation, consistent with ectopic hepatic tissue ().\nDespite a brief period of cardiopulmonary bypass, the patient had persistent hypoxemic respiratory failure ascribed to her morbid obesity and underlying lung disease. She also developed extensive left lower extremity deep venous thrombosis from a presumed heparin-induced thrombocytopenia for which she was treated with argatroban and placement of an IVC filter. Because of chronic respiratory failure, she underwent tracheostomy and feeding tube placement, and she was placed on warfarin for intermittent atrial fibrillation due to her CHA2DS2-VASc score of 4. She gradually improved and was transferred to rehab where her tracheostomy tube and PEG tube were removed. A few months later, she looked quite well during an office visit. |
We present the case of a 45-year-old Caucasian man suffering from psoriasis for more than 20 years at the time of the first visit. No relevant comorbidities were found at history collection, apart from benign prostatic hyperplasia, for which he is treated with tamsulosine. He was initially diagnosed and followed-up by dermatologists, who treated him with topical corticosteroids and salicylic acid for skin involvement and systemic corticosteroids for resistant lesions as needed ().\nThe skin component had always been <30% of the total body surface area (BSA). The patient reported distress in personal and social relationships with consequently reduced HRQoL. After ten years, he started experiencing dactylitis of feet and recurrent arthritis of the small joints of hands, shoulders and knees, together with inflammatory morning stiffness lasting around one hour, with negative rheumatoid factor (RF); thus fulfilling ClASsification criteria for Psoriatic ARthritis CASPAR criteria for PsA []. He was referred to the rheumatology outpatient clinic of another hospital and treated with indomethacine and systemic corticosteroids as needed for about five years, and then achieved complete remission of joint symptoms. Three years later, because of a flare of joint involvement (episodes of peripheral arthritis and dactylitis of the small joints of hands and feet once per week) and skin involvement, he was started on methotrexate 10 mg weekly with folate supplementation, in combination with cyclosporine 200 mg daily, with reduced extension and severity of skin lesions and decreased frequency of arthritis flares to once per month. However, he did not reach complete remission. Shortly after initiation, due to a 2-fold increase of liver enzymes (hepatitis excluded based on abdomen ultrasound and hepatitis B and C viral profile), methotrexate was reduced to 7.5 mg weekly []. The reduced methotrexate regimen led to normalization of the liver enzymes but was ineffective in controlling both skin and joint involvement. Two years later, due to elevated arterial pressure values (up to 150/90 mmHg) and serum creatinine increase >30% of baseline value (up to 1.4 g/L), cyclosporine was stopped.\nThe following year, he referred to our outpatient clinic for skin and joint flare. At referral, physical examination demonstrated mild psoriasis of trunk, arms and legs, with a psoriasis area severity index (PASI) score of 5.1 (), dactylitis of the third digit of the left foot and arthritis of the third interphalangeal joint of the left hand, which, together with a normal C reactive protein (CRP), activity visual analogue scale (VAS) and pain VAS of 4 and 4.5 respectively, accounted for a disease activity in psoriatic arthritis (DAPSA) score of 12 (low disease activity) [].\nLaboratory tests showed no relevant alterations. Radiographic assessment of hands and feet showed no erosions and no signs of axial involvement were found at magnetic resonance imaging (MRI). Ultrasound imaging of the third metacarpophalangeal (MCP) joint showed inflammation of the joint and of the peritendon of the extensor tendon (a).\nConsidering that the patient failed to respond to two DMARDs (cyclosporine and methotrexate), that he refused a parenteral drug, that he presented mild skin and joint involvement, no bone erosions, dactylitis and no axial involvement, apremilast was chosen [,,]. At baseline, the EQ-5D questionnaire reported altered HRQoL, with some difficulties in motility, no difficulties in self-care and some difficulties in usual activities, moderate pain/discomfort and moderately anxious/depressed mood. Patient’s global health (GH) VAS was 60 and pain VAS was 45 (). Furthermore, the patient was screened at baseline for CV risk; carotid arterial doppler ultrasound demonstrated only intimal thickening of the left bulb and 24 h blood pressure monitoring demonstrated mild systolic and diastolic daily hypertension for which he started lercanidipine 10 mg/daily. At baseline, total cholesterol (TC) and triglyceride (TG) serum levels were 173 mg/dL and 113 mg/dL respectively, and TC/high density lipoprotein (HDL) ratio was 4.94 (). After 4 weeks, the extension and severity of erythema and infiltration of psoriatic plaques were substantially reduced (PASI 2.5, ). Furthermore, the patient reported a marked improvement of joint involvement with no further episodes of arthritis or dactylitis, although inflammatory morning stiffness persisted (DAPSA 6.0). At the 2-month follow-up, the patient reported several side effects such as mild headache, dizziness and hypotension and, due to further amelioration of the skin and joint involvement he stopped apremilast, which was restarted shortly after, due to worsening of psoriasis (PASI 3.0) and occurrence of a new joint flare (DAPSA 10). At the time he was still taking methotrexate 7.5 mg weekly. At the 6-month follow-up he reported no arthritis flares and no inflammatory morning stiffness. At physical examination, the third MCP joint was swollen but not tender (DAPSA 3), and ultrasound imaging showed reduction of joint and soft tissue inflammation (b). A further improvement of skin involvement was observed and reported by the patient (PASI 1.2, ). During the follow-up, we observed an amelioration of the serum lipid profile already after 4 weeks, with a 5.8% reduction of TC and a reduction of TC/HDL ratio, and after 12 months, a further reduction of TC, LDL and TG values of 15.6%, 25.7% and 17.7% respectively, and a 20% increase of HDL levels compared to baseline values. TC/HDL ratio reached the favorable value of 3.48, as shown in . We even observed a 5% weight loss—although our patient already had a normal baseline weight and body mass index (BMI)—reaching a final normal weight with a normal body mass index (BMI 21.5). After 12 months, the clinical manifestations were stable. We therefore decided to stop methotrexate, but the patient experienced a slight relapse of both skin and arthritis (PASI 2.5, DAPSA 6), shortly after. Therefore, although dosage was low (7.5 mg), we reintroduced methotrexate, leading at the 18-month follow-up to stable minimal disease activity with PASI 75 and joint remission (PASI 1.2, DAPSA 2) [,] and a dramatic improvement in HRQoL (). |
Male patient, 40 years old, dyslipidemic, presented with a right carotid territory transient ischemic attack 7 months prior. At the time, he underwent diagnostic investigation during which there was found evidence of moderate stenosis (about 60%) in the right carotid bulb associated with an ulcerated plaque. Double antiplatelet aggregation therapy was then prescribed with aspirin and clopidogrel and the use of statins, in addition to angioplasty with a 7 × 40 mm carotid wall stent. He progressed without complications and was discharged after 3 days without sequelae.\nThe patient had been involved in an automobile accident (a collision between a car and a pole) and was referred to the emergency room, with no neurological deficit at the time of admission. Tomography and angiotomography scans of both the neck and skull were performed and revealed signs of thrombosis/occlusion of the bifurcation of the right internal carotid artery, close to the origin of the middle cerebral artery.\nSubsequently, he underwent cerebral angiography that showed multiple fractures in the stent and a small metallic image in the topography of a branch of the right lingual artery, which is suggestive of a fragment thereof []. The study of intracranial vessels showed the presence of a negative image in the bifurcation of the right internal carotid artery, which was compatible with a thrombus and thus determined a subocclusive stenosis (about 95%) at the site. That observation was also associated with an increasing slowing down in the opacification process of the right middle cerebral artery []. This artery was rechanneled from pial anastomoses originating from the right anterior and posterior cerebral arteries. Two small metallic images were evident in the topography of branches of the right middle cerebral artery as well, which was also suggestive of stent fragments [].\nAs he was an asymptomatic patient (NIHSS 0, Rankin zero), we opted for a conservative treatment with oral anticoagulant and a target international normalized ratio (INR) between 2.0 and 3.0. |
A 42 year old female presented with a 6 months history of progressively worsening pain over the right shoulder and chest wall, aggravated by movement and with associated right arm oedema and paraesthesia. She believed mild symptoms began 2 years prior to presentation.\nOn physical examination she had a tender mass over the 2nd–5th intercostals spaces with over lying visibly engorged veins. The blood pressure was BP 130/70 mmHg and pulse rate (PR) was 62 bpm and regular.\nA chest xray showed a vague shadow over the 3rd intercostals space mid clavicular line, (Fig. ), a CT scan showed clearly a mass extending to a butting the pleural cavity pleura, see Fig. .\nAn echocardiogram and ECG were normal; cardiac enzymes panel was normal too.\nThe patient was consented for an exploration under general anesthesia, in supine position under general anaesthesia (GA), a 6–8 cm incision was made over the mass and a combination of blunt and sharp dissection the mass was wholly excised without opening into the pleura.\nThe patient was discharged on the 3rd post operation day, pain had significantly reduced and the limb oedema nearly resolved.\nThe histopathological examination revealed a benign lesion; a schwannoma with degenerative changes. The section revealed a benign nerve sheath tumor characterized by a proliferation of band spindle cells arranged in fascicles and variable cellularity and associated with dilated and think walled blood vessels. There was no evidence of malignancy.\nSchwannoma is a benign neurogenic tumour and is usually founded as a solitary lesion. Chest wall schwannoma is rare and usually asymptomatic (Moon et al. ). In this patient it was symptomatic and mimicked a metastatic lesion even though no primary lesion was detected prior to the exploratory surgery. The lesion was completely excised under general anaesthesia and endotracheal intubation in supine position. The procedure lasted 45 min with minimal blood loss. The immediate post operative period was unremarkable. A review at 8 weeks after surgery was unremarkable too. Treatment is complete surgical excision, however long term follow up is required in case of recurrence (Chen et al. ).\nDifferential diagnosis includes neurofibroma and leiomyoma. Neurofibromas are not encapsulated and lack the biphasic pattern of schwannomas. Leiomyomas have spindle cells with tapering cytoplasm and elongated blunt ended nuclei (Sawas et al. ). This lesion had proliferation of band spindle cells with no evidence of malignancy. |
A 40-year-old woman with an amenorrhea of 5.5 weeks was admitted to the Department of Obstetrics and Gynecology of Foggia Hospital with acute onset of poor vaginal bleeding and mild cramping lower abdominal pain. Regarding her obstetric history, she had a normal vaginal delivery and two cesarean sections. The physical examination was remarkable only for the mild lower abdominal tenderness to deep palpation, a small amount of bleeding from the external cervical os, and a mild pain of the uterus. Laboratory data revealed a quantitative serum human chorionic gonadotropin level of 53,539 mIU/mL. A transvaginal ultrasound showed a gestational sac containing a yolk sac and an embryonic pole with cardiac activity (), located in the anterior lower uterine wall near a previous cesarean scar. We repeated an ultrasound scan the day after the initial examination and confirmed a persistent gestational sac within the anterior uterine isthmus, close to the anatomic location of the previous cesarean scar (type 1, with preferential development of the pregnancy toward the uterine cavity). There was neither uterine bleeding nor any amount of blood in the abdominal cavity.\nThe patient was informed about the details of the procedure and signed an informed consent to allow anonymized data collection for research purposes. All procedures performed in the study were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Approval for the procedure was obtained from the local Ethics and Research Committee. This report follows the Consensus-based Clinical Case Reporting (CARE) guidelines, available through the Enhancing the QUAlity and Transparency Of health Research (EQUATOR) network ( accessed on 15 January 2021).\nThe patient underwent UAE as the first step of treatment. The right femoral artery was cannulated using a flexible angiographic catheter through which the uterine arteries were reached. After selective arteriography, the left uterine artery was totally embolized with a gelatin hemostatic sponge (SPONGOSTANTM). The procedure was repeated on the right uterine artery. The following day we performed a hysteroscopic resection of the ectopic pregnancy. The patient was placed in a dorsal lithotomy position, and a 4-mm continuous-flow office hysteroscope (Bettocchi Office Hysteroscope ‘‘size 4” Karl Storz, Tuttlingen, Germany) with a 2.9-mm rod lens optic was introduced into the cervical canal using the vaginoscopic approach, with no speculum and tenaculum, in an office setting, with no anesthesia or sedation.\nWe used a new Dual wavelengths Laser System (Leonardo® Dual 45, Biolitec, Jena, Germany). This highly compact diode laser features the combination of two wavelengths, 980nm and 1470 nm, giving a contemporary absorption in H2O and in hemoglobin (Hb) with an excellent ability of hemostasis, cutting, and vaporization, as was previously shown in hysteroscopic and laparoscopic surgery [,,].\nThe gestational sac and the umbilical cord were identified, and the implantation site as the extent of placentation was determined. A conical angled fiber (MyoFiber® CA, IC) with a wider cutting surface was introduced through the operative channel of the hysteroscope, and a laser excision of the ectopic pregnancy near to the implantation site was performed ( and ). The trophoblastic tissue was also removed with the use of the laser and 5 Fr mechanical instruments (crocodile forceps) with excellent control of hemostasis.\nThe histological examination confirmed the presence in the endometrium of massive decidual proliferation with necrotic-inflammatory-hemorrhagic phenomena and glandular modifications (Arias Stella phenomenon) and with chorionic villus regression. The patient had an uneventful postoperative recovery and was discharged after three days. Confirmation of the procedure success was obtained from the laboratory data, that showed a negative quantitative serum human chorionic gonadotropin level on the tenth day after the operation. At four weeks follow-up the patient was asymptomatic and under combined oral hormonal contraception. |
A 30-year-old male patient presented to the Department of Maxillofacial Surgery with swelling in the right facial region. His anamnesis revealed that the patient had his right first molar tooth extracted owing to infection a year ago and that painless swelling in that region had been present ever since. Clinical examination of the swelling demonstrated a painless, hard, mobile, localized elastic lesion on palpation in the subcutaneous tissues extending in line with mandibular border. The lesion was located approximately between the angle of the mandible and the anterior aspect of the sternocleidomastoid muscle (2–3 cm below the inferior border of the mandible) [].\nThere was no lymphadenopathy in the region. No specific finding was detected on radiological examination. The lesion was explored at the level of the subplatismal plane via extraoral approach under local anesthesia through an incision made parallel to the mandibular border. The lesion, which appeared of vascular origin because of red-brown color, was capsulated and associated with a small artery on both the anterior and posterior borders [].\nThe borders of the lesion were ligated with polyglycolic acid suture to control bleeding. After total enucleation, subcutaneous tissues were sutured with 3/0 polyglycolic acid and the skin was sutured with 4/0 polyprolene. The excised specimen measuring 1.5 cm was sent to the laboratory for histopathological examination [].\nHistopathological examination revealed a restricted tumoral lesion consisting of vascular configurations of various diameters. Vascular configurations were rich with capillary vessels arranged in a lobular pattern. There was a large blood vessel with patent lumen and thick wall in the middle of the lesion [].\nVascular configurations were lined by epithelioid endothelial cells. Endothelial cells showed no atypia. Edematous connective tissue with lymphocyte and eosinophilic leukocyte infiltration were detected among vascular configurations [].\nUnder the light of these findings, the patient was diagnosed with epithelioid hemangioma. No esthetic problem or complaint or recurrence was encountered over the course of the 3-year follow-up period []. |
A 24-year-old male presented with diffuse skin lesions on the chest and abdominal walls from the age of 8, accompanied by pigmentation and epidermal nodular hyperplasia. Because of sudden spontaneous swelling and pain in the left upper abdomen that could not be relieved by rest or changing body position, he went to the emergency department of our hospital. The main vital signs of the patient were body temperature of 37.8℃, blood pressure of 140/93 mmHg, respiration of 24 beats/min, heart rate of 115 beats/min, and oxygen saturation of 96%. The emergency chest and abdominal enhanced CT scan showed the following: possible left diaphragmatic hernia; partially inflated left lung; massive left abdominal mass with hemorrhage, with the left 9th/11th ribs partially absorbed; left chest and back subcutaneous soft tissue thickened with an abnormal density; and bleeding nodules (shadow) on the chest and back skin (Fig. ).\nPhysical examination showed that the breathing sound in the left lung was not clear, very large diffuse skin lesions with brown pigment spots in the left chest and abdomen, a large number of fibromatous hyperplasias on the epidermis, very large skin masses protruding outward, left abdominal compression pain (+), and abdominal muscle tension.\nBased on the patient's condition and CT findings, the possibility of a diaphragmatic hernia caused by spontaneous diaphragmatic rupture was not ruled out. After communicating with the patient's family members, we decided to perform thoracotomy. We selected the left 7th intercostal incision site, from the skin to the subcutaneous tissue there were a lot of neurofibroma tissue, brittle tissue and easy to bleed. The tumor covered a wide area, including the lateral chest wall, the back, and the whole abdomen. Because large areas of tumor tissue cannot be completely removed, only the thorax and abdominal problems can be dealt with. The left pleura and diaphragm were found to be invaded by tumor during the operation. The left diaphragm appears dark green with thinning tissue and reduced elasticity. The left diaphragm is significantly elevated, but not ruptured. Compression atelectasis was observed in the left lung. A small amount of bloody effusion was found in the abdominal cavity, and a portion of the bowel was embedded in the very large, twisted subcutaneous neurofibroma without necrosis. The bloody effusion was considered to be bloody exudation caused by intestinal cantun, and there is no obvious active bleeding in abdominal cavity. We found no obvious bleeding and necrosis in the abdominal cavity, and then a drainage tube was been placed. Diaphragmatic folding was performed. A portion of subcutaneous tissue and various diaphragmatic muscle tissues were removed during the operation and sent for rapid pathology. The diagnosis was neurofibroma (Fig. ). The patient was admitted to the surgical ICU for care and treatment after surgery. The endotracheal intubation was removed 1 day after surgery, and the patient returned to the general ward 3 days after surgery. The patient had fever in the first 5 days, the highest temperature was 38.6 °C, other vital signs were stable, and then the temperature gradually dropped to normal. The postoperative abdominal pain disappeared and the incision healed well, and the patient was discharged 10 days after surgery. |
The patient was a 49-year-old man diagnosed with familial adenomatous polyposis (FAP) caused by a defect in the adenomatous polyposis coli (APC) gene. In March 1998 (aged 36), he underwent total proctocolectomy and ileostomy for polyps involving the entire colon, and the stoma was closed 9 months later. Pathological findings showed that the polyps were adenomas. In August 2001 (aged 39) and August 2003 (aged 41), multiple mesenteric tumors were removed, which were pathologically diagnosed as desmoid tumors characterized by invasive growth of fibroblasts into the surrounding muscle layer. He subsequently experienced repeated episodes of ileus symptoms attributable to intestinal adhesion as a postoperative complication and to recurrent mesenteric desmoid tumors; thus, duodenojejunostomy was performed in March 2011 (aged 49). Around December 2011, 9 months after the operation, a desmoid tumor of the abdominal wall was found immediately above the peritoneum just below the previous operative wound, which grew to 7.3 cm in the longest diameter in 3 months (Fig. ). It was considered surgically unresectable partly because tumor adhesion to the intestinal tract and peritoneum was severe and partly because tumor removal would have resulted in a large defect in the abdominal wall. Among the available treatment options for desmoid tumor of the abdominal wall, chemotherapy, carbon ion radiotherapy, etc. were proposed. After a thorough discussion about informed consent, the patient selected carbon ion radiotherapy, which is a type of radiotherapy that can deliver high-dose radiation to a tumor while minimizing the dose delivered to the organs at risk. From May to July 2012, he received carbon ion beam irradiation at a total dose of 50 Gy (relative biological effectiveness [RBE]) in 25 fractions at the Hyogo Ion Beam Medical Center (HIBMC). Figure shows the carbon ion treatment plan for this patient. The solid abdominal wall tumor continued to grow until 2 months after treatment, reaching 12 cm in diameter, and then gradually shrank to 7.8 cm at 5 months. One year after treatment, the contents of the tumor had liquefied, and the tumor had shrunk to 4.3 cm in diameter. The liquid components consisted primarily of fibrin, with no malignant cells. Currently, 3 years after the operation, the abdominal wall tumor remains stable, with a diameter of 3.3 cm, and is being followed up (Fig. ).\nDesmoid tumor is a rare with 2.4~4.3 cases occurring per one million individuals each year []. It has been correlated with the FAP [], and the overall incidence of desmoid tumor in patients with FAP is 10–20 %, which equates to relative risk of 852 compared to the general population []. Desmoid tumor is a benign fibromatosis that originate from fascia and muscular aponeuroses, with an infiltrating growth pattern. As indicated by its name, aggressive fibromatosis, a desmoid tumor is characterized by a clinically malignant course, with a reported recurrence rate up to 45 % after surgical resection [].\nTreatment of desmoid tumor is a complex condition with many recognized treatments including active observation, hormonal therapy, nonsteroidal anti-inflammatory drugs (NSAIDs), chemotherapy, radiotherapy, and surgical resection []. As desmoid tumors sometimes exhibit characteristics of stable or regress, the conservative approach is recommended []. In this case, the tumor grew more than 7 cm in just 3 months and the patient complained the tumor pain, so it was necessary to provide the aggressive treatments. Radiotherapy has been adopted as a primary treatment in patients who undergo progression during observation. Mounting literature supports this approach, with several groups reporting long term local control in 70–93 % of patients at doses of 50–60 Gy (1.8–2 Gy/fraction) [, ]. It is also reported that the radiotherapy combined with surgical resection results in better progression-free survival time (PFS) than surgery alone []. But simultaneously, radiotherapy has a risk to cause damage to the neighboring intestine and organ such as perforation or abscess formation, and potential late radiation effects, including second malignancies []. It was reported a partial response of hormone therapy (tamoxifen) for desmoid tumor in male patients, 24~54 months after treatment initiation as well as female patients []. And, there is some evidence that the treatments are most effective when NSAIDs and hormonal therapies are given together []. Various chemotherapy regimes were reported and most of them were used as combination, included methotrexate with vinblastine or vinorelbine, doxorubicin with dacarbazine, doxorubicin with cyclophosphamide and vincristine, and actinomycin-D-based chemotherapy. The average response rate of them was 50 % (range 17~100 %) []. Although hormonal therapies, nonsteroidal anti-inflammatory drugs (NSAIDs), interferon, or chemotherapy are options for unresectable or recurrent disease, the appropriate therapeutic approach has not yet been fully elucidated [].\nCarbon ion radiotherapy can precisely irradiate the target lesion, thereby reducing its adverse effects on the adjacent intestinal tracts. Photon beam sensitivity varies with the type of tumor, whereas carbon ion radiotherapy, which uses carbon (C) molecules, can be expected to have potent effects on all types of tumor, irrespective of sensitivity []. The finding that carbon ion radiotherapy was effective for recurrent desmoid tumor of the abdominal wall in this patient will lead to an increase in treatment options and thus have important implications for patients suffering from this disease and for the physicians treating them. In addition, this is the first report of a case of desmoid tumor successfully treated with carbon ion radiotherapy. We hope that our report will be of some help in determining the treatment strategy for this disease. |
A 47-year-old male visited the hospital with the complaint of right lower quadrant pain that had started 3 days prior. He had a family history of his mother dying of colon cancer, but no other medical history. At the time of the visit, the physical examination results showed right lower abdominal tenderness, but no rebound tenderness. The peripheral blood examination showed that leucocytes had increased to 11,900/mm3 and the CRP to 12.31 mg/dL; no specific findings were observed on plain abdominal X-ray. The abdominal CT findings suggested 4 cm × 1 cm fluid retention in the proximal ascending colon and abscess formation due to diverticulitis perforation towards the outer wall of the ascending colon. In addition, the centripetal focal wall thickening was concurrent; therefore, colon cancer could not be excluded (). Ultrasound-guided percutaneous abscess drainage was performed, and conservative treatment with intravenous antibiotics (ciprofloxacin, metronidazole) was initiated. Three days later, tubography was performed, and because no residual abscess was found, the patient was discharged seven days after admission. After removal of the drainage catheter in the outpatient clinic, a colonoscopy was recommended due to the possibility of colon cancer. However, the patient did not revisit. Approximately two years later, the patient was readmitted with the main complaint of right lower quadrant pain that had started 1 month prior. The abdominal CT suggested diverticulitis-induced bowel perforation in the middle of the ascending colon, accompanied by a thickening of the wall of the ascending colon of ~7 to 8 cm in length (). A colonoscopy was performed to verify the lesion; the results showed an inflammatory mass surrounding the lumen in the proximal ascending colon accompanied by edema ().\nThe CEA level was 2.8 ng/mL, and the biopsy result was high-grade dysplasia; however, the abdominal CT and colonoscopy findings suggested colon cancer. Therefore, a right hemicolectomy was performed. Based on the surgical specimen, the patient was finally diagnosed with an adenocarcinoma, moderately differentiated, at the T3N2M0 stage. The patient is receiving palliative chemotherapy and has been followed up for 19 months to date. |
A 40-year-old woman was referred to us for salvage treatment. She was diagnosed in February 2005 with a 6.5 cm right occipital tumor with small millimetric parenchymal metastases and drop metastases throughout the neuraxis. She presented with clinical evidence of increased intra-crania pressure (ICP), mass effect with extensive vasogenic edema requiring urgent surgery. She underwent gross tumor resection and pathology reported an atypical choroid plexus papilloma. Her staging work up was obtained following her recovery including brain and full spine contrast enhanced magnetic resonance imaging (MRI) scans. This revealed small drop metastases in the posterior fossa and along the spinal cord. The patient received radiation therapy to the neuraxis (the CSI dose was 36 Gy and the total dose to the primary tumor bed or surgical cavity was 54 Gy). She remained clinically stable for two years, and was able to perform activities of daily living. Repeated contrast enhanced MRI scans of the brain and full spine reported stable appearance in size and enhancement of all drop metastases in the posterior fossa and the spinal canal.\nAt relapse, she presented with continuous headaches, neck stiffness, altered mental status, and severe ataxia. Imaging revealed metastasis to bilateral cerebello-pontine (CP) angles and intraparenchymal supratentorial lesions (left frontal, right thalamic, and right temporal). She received 2 cycles of nitrosourea without response and worsening symptoms. Hence this was changed to ifosfamide, carboplatin and etoposide based combination. Radiological and clinical stabilization were attained following three cycles, but second progression was documented after the fifth cycle. Further surgeries and performed for rapidly growing and symptomatic right CP angle metastasis and dorsal brain stem metastasis. Post-operative imaging revealed decrease size of the tumor. With remaining residual disease, the patient was referred to us for salvage treatment.\nIn this setting of previous craniospinal irradiation, significant chemotherapy toxicity, and only short-lived stabilization of the disease, bevacizumab was offered as single agent treatment in an attempt to spare the patient further toxicities. The first treatment was injected after 8 weeks from last surgery.\nThe patient received bevacizumab, 5 mg/kg on day 1 and day 15 of each cycle. Cycles were repeated every 4 weeks. Contrast enhanced MRI scans were obtained after the initial two treatments and every 2 cycles thereafter or sooner if required to assess new or worsening symptoms.\nThe patient was taken off steroids, which was started at first relapse, shortly after starting bevacizumab and did not receive steroids later during the course of her disease. Her symptoms immediately stabilized following the first cycle of bevacizumab and progressively improved. The headaches resolved, the mental status returned to normal, and the ataxia improved very slowly but her cervical pain and stiffness did not. She achieved radiological stabilization with significant decrease of the vasogenic edema, and minimal decrease in the size and enhancement of all metastatic lesions ( and ). This response continued for over 5 months of therapy. A total of five cycles of bevacizumab were administered (10 treatments). An elective cerebello-pontine angle metastasis resection was opted to relieve her debilitating neck stiffness.\nThe postoperative course was complicated by respiratory failure requiring tracheostomy, although there was no evidence of disease progression. The patient died form pulmonary infection, in turn complicated by severe sepsis. |
The patient was a 64-year-old man with destructive injury of both lower extremities due to a machine accident. His left ankle and heel bone, along with the soft tissue, were torn off, and the peripheral blood supply and sensation to the toes of the left foot were lost. We amputated his left leg below the knee. The left fibular head was retained after the left foot operation. Two months later, the patient came to our hospital for additional treatment after debridement of necrotic tissue operations twice. There was still approximately a 20 ×10-cm area on the right foot and right external ankle exposing the distal fibula fractures. X-ray showed that the right external ankle bony defect and the right medial ankle mortise widened; fortunately, the left fibular head was retained after left foot amputation (Fig. ). We reconstructed the right ankle using vascular anastomosis of the fibular head and a flap taken from the left stump. The Ethics Committee of the Second Affiliated Hospital of Soochow University approved the study.\nWe used an ultrasonic Doppler instrument (Model: ES-1000SPM Hayashi Denki Co., Ltd, Hong Kong China) to find the perforating branch of the peroneal artery before surgery, and near that location we created a flap approximately 20 × 10 cm in size according to the right foot wound (Fig. ). Surgery was performed with the patient under general anesthesia. The patient was placed in the supine position on the operating table with the left knee joint slightly bent and the left lower limb stump in internal torsion. The incision began in the popliteal space, swept down to the fibular head, and continued along the lateral peroneus muscles to the stump extremity. We cut the skin and subcutaneous tissue, then separated the peroneus longus and soleus muscles. We found the nervus peroneus communis on the inner posterior margin of the biceps femoris tendon and dissociated it for protection. The peroneal perforator was located in the intermuscular space between the peroneus longus and triceps surae muscles, then we freed the peroneal artery and 2 accompanying veins. We cut off the biceps femoris tendon, fibular collateral ligament and other muscle tissue attached to the fibula, extracted the fibular head, and then divided the superior tibiofibular joint. On release of the tourniquet, bleeding spots on the fibula and residual muscle tissue showed that the blood supply was satisfied. Therefore, we could then cut off the vessels and take the fibular head (Fig. ). We sewed the biceps femoris tendon and fibular collateral ligament with deep fascia around the lateral tibial plateau to avoid instability of the knee joint. We completely debrided bone splinters and necrotic soft tissue from the lower right limb and smoothed the edges. The free fibular head was fixated to the distal fibula with a fibular plate. The reconstructed inferior tibiofibular joint was reinforced with 3 lag screws before anastomosis of the vessels in the transplanted fibular head with the recipient area. Lastly, we made a suture flap in the wound and inserted rubber drainages (Fig. ).\nDue to necrosis of the skin and soft tissue of the distal flap 7 days after the operation, part of the reconstructed external ankle bone was exposed, so we transferred the sural neurocutaneous vascular flap to repair the skin and soft tissue defects of the lateral malleolus. X-ray examination 3 months after the operation showed that the fracture had a bony union and the shape of the transplanted fibular head was similar to the normal external ankle. At 12-month follow-up, walking function had been recovered with the help of a left artificial limb (Fig. ). According to the Baird–Jackson scoring system, the curative effect was satisfied. |
A 65-yr-old male presented to the emergency department with acute mental changes after a traffic accident on September 16, 2006. He was hit by a car while riding a motorcycle. On physical examination, he exhibited a stuporous mental state. There were positive light reflexes on both sides, but no spontaneous nystagmus. He had bilateral ear bleeding and multiple contusions on his body. An otologic examination revealed a bilateral hemotympanum. The function of the other cranial nerves was impossible to check due to his stuporous mental state.\nAn emergency brain CT scan revealed a hemorrhage in the left temporal subarachnoid space with a pneumocephalus. A high resolution CT scan of the temporal bone revealed bilateral transverse temporal bone fractures involving the otic capsules with evidence of a bilateral pneumolabyrinth (). The fracture line extended to the internal auditory canal on the left side and was associated with a pneumocephalus in the internal auditory canal.\nHe was admitted to the neurosurgical department for conservative treatment. Two days after the trauma, he exhibited an alert mental state with a complete bilateral hearing loss. No facial asymmetry or weakness was observed.\nAudiometry was performed 25 days after the trauma. There was no reliable response to the application of a pure tone or speech stimuli at the maximum limits of the audiometer. Immitance audiometry revealed a type A tympanometry on both sides. Vestibular function testing revealed the absence of any caloric responses bilaterally with ice water.\nThe patient was offered a cochlear implant soon after the trauma. However, he accepted the fact that his deafness was permanent near three months after the trauma and decided to get an operation of cochlear implantation. Follow-up audiometry revealed similar to the previous one, except residual hearing response at 500, 1,000, and 2,000 Hz on the right side. A repeated high-resolution CT scan of the temporal bones was obtained which showed no evidence of labyrinthitis ossificans or obliteration of the mastoid cavity, facial recess, or middle ear space. However, T2-weighted MR image showed a focal low-intensity lesion suggesting fibrosis in the lumen of the left cochlea (). The right ear was selected as the side for the implantation.\nHe then underwent a right cochlear implant procedure through a transmastoid facial recess approach. A HiRes 90K Cochlear Implant (Advanced Bionics, Boston Scientific) was implanted. The cochlear implant procedure was successful with no evidence of infection and other complications after the cochlear implantation. However, 14 of 16 electrodes were inserted due to the resistance.\nFollowing the mapping, programming, and aural rehabilitation, the patient's listening skills to speech and environmental sounds improved. An implant-aided audiogram three months after the operation revealed responses in the region of 30 dB HL. Still about one and half year after the operation, he always wears the implant and understands 70% of the usual conversation with his family. |
A 45-year-old Asian-Indian female presented to her physician with the symptoms of constant fatigue, pain, inability to focus, and heavy vaginal bleeding every two weeks that would last 8-10 days and remit. The patient reported that this pattern occurred for a year before it became constant light bleeding that did not cease. She was found to have an iron deficiency anemia, not corrected by oral iron supplementation. She had no history of smoking and only drank a couple of times a month. There was no known family history of leiomyomas or RCC. Upon completion of pelvic ultrasound, two uterine leiomyomas were detected with possible endometrial cavity involvement. The largest leiomyoma was observed to be 3.4 cm in the greatest dimension on ultrasound. The patient then underwent a laparoscopic complete hysterectomy about a year and a half after the onset of symptoms. Gross observation of the removed uterus revealed an 11 x 9 x 7 cm uterus with two fibroids, an endometrial polyp, and unremarkable tubes and ovaries. Histologically, the leiomyomas demonstrated classic benign histologic findings (Figure ). The patient had no symptomology or complications until eight months later when the patient presented with hematuria.\nX-ray, computed tomography (CT), and magnetic resonance imaging (MRI) were performed and revealed a left enhancing, exophytic renal mass measuring 14 x 11 x 9.3 cm (Figure ). Positron emission tomography (PET) CT revealed no focus of increased metabolism concerning for metastatic disease. The patient underwent a transabdominal open left radical left nephrectomy with the removal of the left adrenal gland and hilar and periaortic lymph node dissection. The mass removed measured 12 x 12 x 8 cm. Gross examination of the kidney specimen revealed multiple sites of necrosis with extension of the tumor to the renal sinus, ureter, and segmental branches of the renal vein without invasion. The tumor did not invade the Gerota’s fascia. Histological examination revealed chromophobe RCC due to the presence of cells with eosinophilic cytoplasm and a halo around the nucleus (Figure ). All 12 lymph nodes histologically assessed were benign. Staining for FH was negative (Figure ). The patient was staged with a pT3aMxN0 disease. Five years post nephrectomy, the patient reports no worrisome symptoms and shows no signs of metastatic disease (Figure ). |
This is a case of 71-year-old Caucasian male with past medical history significant for choroideremia who presented to the emergency department (ED) with complaints of left sided temporoparietal headache upon waking up on the day of admission.\nPatient in his thirties had progressive vision loss and was diagnosed as choroideremia with the deletion of REP 1. He became completely blind by the age of 50. The other significant past medical history includes ablation for supraventricular tachycardia around 20 years ago, coronary artery disease with percutaneous coronary intervention in the left anterior descending artery around 10 years ago, hypertension, and hyperlipidemia. His social history is significant for no history of smoking, alcohol consumption, and drug abuse. His family history is significant for choroideremia in his brother (complete blindness) and carrier state in his sister (asymptomatic). His medications included aspirin, clopidogrel, losartan, and pravastatin.\nOn the day of admission, the patient woke up with a severe left sided temporoparietal headache with no numbness or weakness. Concerning this symptom, the patient contacted his primary care physician who advised the patient to go to the emergency department. His initial vitals in the ED were significant for blood pressure of 107/49 mm of hg and a heart rate of 38 beats per minute. The lab work was unremarkable with negative troponins; an ECG () that was done was significant for sinus bradycardia with some T wave abnormalities in lead V3 to V6 and the initial chest X-ray () was significant for prominence of the thoracic aorta. His physical examination was unremarkable except for his vision where the patient was able to perceive only shadows and otherwise he was completely blind. He had no focal neurological deficits. The differential at this time due to his symptoms and physical exam was possibly a pulmonary embolism versus any intracranial hemorrhage versus acute coronary syndrome. The repeat blood pressure bilaterally showed 134/61 mm of hg on the right arm and 123/53 mm of hg on the left arm with a heart rate of around 49 beats per minute.\nConcerning the persistent nature of the headache and prominent thoracic aorta on the X-ray, a CT head without contrast was done which was unremarkable and a CT of the chest with contrast (Figures –) was also done which was significant for a thoracic aortic dissection involving the ascending aorta and descending aorta, with an intramural hematoma in the descending aorta. The dissection extended superiorly to the brachiocephalic/left common carotid trunk. Concerning the life-threatening emergency of the situation it was decided that the patient needed surgical intervention. His vitals continued to be unchanged with no worsening of symptoms. Patient was emergently transferred to a tertiary care center. The patient underwent an ascending aortic replacement and hemiarch replacement as well as a suspension of the aortic valve. Patient was subsequently discharged with a stable follow-up course. |
A 57-year-old woman with an extensive medical history was diagnosed with angiosarcoma of the spleen. In 1991, she was diagnosed with breast ductal carcinoma (T2pN0p) and received a right quadrantectomy and radiotherapy (5,500 cGy total dose). In 2004, a partial thyroidectomy was carried out due to a papillary carcinoma. She was a carrier of polycystic kidney disease type 1, asthma, dyslipidemia and hiatal hernia.\nIn November 2012, she sought medical help for gastrointestinal discomfort that had become more intense a few months earlier. A high digestive endoscopy was performed showing short Barrett esophagus without dysplasia and hiatal hernia. She was treated with prokinetic and proton pump inhibitor drugs and dietary advice. In addition, abdominal ultrasound was performed showing splenic complex cysts; for better evaluation, magnetic resonance imaging (MRI) was requested.\nThree months later, the MRI showed a single 2-cm cystic nodule, presenting a homogeneous content. An imaging monitoring was proposed for 6 months and gastric drugs were maintained for gastroesophageal reflux disease (GERD) control. On April 19, 2013, she went to the emergency service after 1 week of diffuse and nonstop abdominal pain, without peritonitis. A tomography scan showed splenic cysts that had increased in number and size. The CA 125 level was analyzed and presented a slight increase. The patient underwent a diagnostic laparoscopy splenectomy and the spleen was sent to pathological analysis.\nThe patient was discharged 2 days after surgery with no peri- or postoperative complications. The pathologic analysis described a spleen of 200 mg weight, size 14 × 10 × 6 cm, capsule smooth, gray, with interruption areas measuring 4 cm in length. The cut surface had a fine granular appearance of brownish color with wine-dotted areas. Microscopically, irregular nodular areas could be seen with areas of proliferation with elongated cells, arranged in bundles or around large vascular spaces with poorly defined cytoplasm and elongated nuclei and sometimes hyperstained. The mitotic index was low with large areas of bleeding. The diagnosis was vascular neoplasm found by immunohistochemical evaluation, which suggests angiosarcoma of the spleen.\nPostoperative treatment was initiated 1 month after the procedure: 4 cycles divided into 12 infusions of paclitaxel chemotherapy and pazopanib were performed. A prior CT was performed showing no evidence of disease.\nAfter 7 months of medical follow-up, the patient presented earlier gastrointestinal symptoms, and abdominal and thoracic imaging examinations showed no signs of disease. One year and 2 months after the surgery, in the following examination, the patient complained about neck pain and cervical imaging was performed. An MRI showed secondary bone lesion with contrast enhancement in the vertebral body of C7, with soft-tissue components projecting into the spinal canal (size 1.7 × 1.5 × 1.1 cm). The diagnosis was metastatic angiosarcoma. Three months later, the C7 lesion was resected, replaced by a titanium implant followed by 10 radiotherapy sessions (total dose of 3,000 cGy).\nDuring 1 year and 1 month, the patient presented few symptoms, basically gastrointestinal symptoms due to GERD. However, although there was no evidence of local recurrence, the patient presented weight loss, immunodeficiency signs and hypoalbuminemia, suggesting a consumptive syndrome. The consumptive syndrome further evolved followed by impairment of the immunologic system. The patient was diagnosed with bronchopneumonia and developed sepsis. She died in February 2016, more than 3 years after the diagnosis. |
A 42-year-old Caucasian female was admitted to the inpatient psychiatry unit due to a severe depressive episode in the course of BD. Before admission, she had quarreled with her husband, and under the influence of ethanol, she had tried to commit suicide by cutting her wrist. She had never been hospitalized in a psychiatric unit before. During hospitalization, she was treated with venlafaxine 375 mg, lamotrigine 200 mg, and quetiapine 200 mg with a small improvement of her depressive symptoms but no effect on her suicidal ideations. The patient stayed at the hospital for 10 days, subsequently withdrawing consent for further hospitalization—claiming her mental state had much improved. The next day, she came to our outpatient clinic still presenting active suicidal thoughts and depressive symptoms. She refused to be hospitalized but agreed to take medication at home with the close supervision of her family and frequent ambulatory visits (three times a week). The patient had been diagnosed with BD type I 21 years ago. During her illness, she had three episodes of major depression, two manic episodes, and one mixed episode. The current depressive episode lasted 2 months before admission and was related to a relationship crisis due to her marital relations. She had a low mood and anhedonia, psychomotor retardation, reduced sleep, and active, persistent suicidal thoughts that were the leading cause of her concern at the moment.\nShe agreed to be treated with clozapine up to 100 mg as an add-on treatment to previous drugs. During the next two weeks, the patient improved significantly, with the most prominent anti-suicidal effect after 10 days of clozapine treatment. Although she was still depressed, she did not express any suicidal thoughts, and this effect was present as long as the clozapine was subscribed. Two months later, due to sedation, she tried to decrease the dose of clozapine to 25 mg/day, but suicidal thoughts returned. Since then (2 years), she has been taking clozapine as an add-on treatment with a good clinical effect.\nThe previously discussed cases constitute the part of the clozapine registry approved by the independent ethics committee of the Medical University of Gdansk (approval number NKEBN/355/2016). The previously mentioned cases are presented according to guidelines for disguising case material. |
An 83-year-old man who underwent a right carotid endarterectomy (CEA) with a Dacron patch in 2011 following an ipsilateral right hemispherical transient ischaemic attack, presented 4 years later in 2015, with bleeding and pus discharging from a sinus tracking down to the wound. His background included a 3-year history of left internal carotid artery (ICA) occlusion with bilateral high-grade vertebral artery stenosis of more than 70%. He had a left hemispherical stroke in 2008 and a long-standing history of hypertension for which he takes two antihypertensive medications.\nIn September 2015, the patient reported a 12-month history of discharge from his CEA scar, initially managed by his general practitioner with local dressings and oral antibiotics. Examination revealed a sinus at the distal end of his scar that was expressing haemoserous fluid. No underlying fluctuant collection was palpable, but the overlying region was mildly tender with no surrounding erythema. The patient was haemodynamically stable and did not exhibit any fevers or rigours. A CT angiogram (CTA) demonstrated a mural atheroma at the right proximal ICA with no pseudoaneurysm or collection noted. A whole body labelled white cell study with positron emission tomography (PECT)/CT (technetium colloid) was normal with no objective evidence of graft infection related to the previous CEA. Surgical management was offered, but the patient declined. Consequently, the wound was monitored closely in the outpatient clinic, and he was managed on broad-spectrum antibiotics for 12 weeks.\nThe patient presented again to the vascular department in June 2016 after he noted approximately 500 mL of haemoserous liquid discharging from the inferior portion of his CEA wound. He was subsequently admitted and investigated with another CTA scan. The CTA demonstrated some irregularity of the proximal right ICA at the region of surgical interest, with mild enhancement of the surrounding soft tissue. But there was no definite evidence of a pseudoaneurysm formation or dissection. The left ICA remained completely occluded with a complete circle of Willis. However, the carotid duplex scan demonstrated a sinus tract extending down to the anterior inferior margin of the Dacron carotid patch (). There was a focal outpouching in the contour of the inferior aspect of the lumen covered by the patch. A Tc-99m labelled leucocyte scan supplemented with localised planar single photon emission computed tomography (SPECT)-CT of the neck demonstrated active infection in the soft tissue of the sinus track at the right upper neck with involvement of the anterior aspect of the right CEA patch just superior to the hyoid bone (). |
A 46-year-old man presented to the emergency medical assessment unit with an 8-day history of visual hallucinations and paranoid delusions. He had a past medical history of essential tremor that was being treated with topiramate. In the past he had tried propranolol and labetalol with little benefit. There was no past history of psychiatric symptoms. He had consumed no alcohol in the previous 3 months but had in the past been drinking eight units of alcohol per day to help control his tremor. No cause for the altered mental state was apparent on clinical examination and initial investigations. The following blood tests were performed and were all normal: full blood count, urea, creatinine, electrolytes, liver function tests, vitamin B12 level, thyroid function tests, autoimmune screen, syphilis serology and blood cultures. On the mini-mental state examination he scored 26/30. A computer tomography scan of the brain and a lumbar puncture were performed and both were normal. There was no evidence of delirium tremens or Wernicke's encephalopathy.\nAfter a discussion with his father on day five of the admission we were told that the onset of the symptoms occurred 2 days after an increase in the dose of topiramate. The patient had commenced topiramate 3 months previously and reached a dose of 75 mg twice a day. The dose had been increased in 25 mg increments. Since the increase in the dose of topiramate and while in the ward he was disorientated as to time and place, had visual and auditory hallucinations and his short-term registration and recall were impaired. He was unable to remember any events occurring after the day the dose of topiramate was increased. The topiramate was stopped and over the following few days he gradually improved. A week after discontinuing the topiramate he was back to his normal self and was discharged. Unfortunately his tremor returned.\nAfter discussing the diagnosis of topiramate-induced psychosis with the patient he told us that his sister had developed visual hallucinations when commenced on topiramate 25 mg twice a day for migraine prophylaxis, and that these had resolved on discontinuing the treatment. She also had no past history of psychiatric symptoms. |
A 13-year-old male patient presented to the hospital with a complaint of swelling and discomfort in maxillary anterior region since 10–12 days. On medical examination, the patient was found to be mentally retarded. The patient was from low socioeconomic background and residing in a rural area. On extra oral examination, the upper lip was swollen causing slight protrusion on the left side (). Systemic examination of the patient was normal with normal body temperature and the regional lymph nodes were not palpable. Intraoral examination revealed an ulcerated area in the maxillary left labial vestibular region at 21 and 22. It was of 1.8 × 1.0 cm in size and a number of maggots were seen in the ulcerated area. The surrounding area of the ulcer was erythematous and swollen (). On instrumentation, the teeth in the involved area had no mobility and his oral hygiene was poor. Based on the clinical findings, the case was provisionally diagnosed as oral myiasis. His hematological analysis was within normal limits.\nThe most common protocol followed for the myiasis was given for this patient. It consists of flushing affected area with turpentine oil, followed by administration of local anesthesia and removal of maggots by simple tweezers. Around 11–13 maggots were removed from the affected site (). Ivermectin 6 mg OD for 3 days, along with metronidazole 400 mg for 5 days and analgesic, and ibuprofen with paracetamol were given to the patient. The area was then washed with saline and irrigation was done with Betadine. The procedure was repeated for 3 consecutive days until all the maggots were removed and the area was completely cleaned. On the fourth day, the site was examined for any remaining larvae and control of the infection. Then, it was sutured with 3–0 silk. Personal hygiene instructions were given to the parents of the patient.\nThe maggots were preserved in 10% formalin and sent to a parasitology department of medical college for identification, where they were identified as larvae of Musca domestica (common housefly). The larvae of the housefly were of cylindrical shape but tapering towards the head, were typical creamy white in color, and had 13 segments, of which 12 were apparent, as the first 2 were partly fused. The head was containing one pair of dark hooks.\nAfter 1 month, the lesional site was found to be healed properly. On the follow-up of the patient, after 6 months, he was absolutely alright and no parasitic infestation was found in oral cavity. |
A 55-year-old lady, a college professor, presented to us with a history of persistent itching, erythema, oozing and crusting over the nipple, areola and periareolar region on the left breast of more than 6 months duration. The lesions had been localized to the nipple and immediate periareolar region initially but had started extending recently. She had been using various topical medications for the same including steroids of varying potency. The patient had good response to topical steroids initially but on further use the lesion appeared to be getting worse. The patient had no other significant co-morbidity and was in otherwise good health. On examination we found an ill-defined area of scaling, erythema and minimal crusting over the over the nipple, areola and peri-areolar region on the left breast (). There was minimal induration over the nipple and immediate peri-areolar area and no significant tenderness or bleeding on touch. Patient had no significant lymphadenopathy. The unilateral nature of the central lesions and the apparent lack of response to topical steroids made us consider a possibility of mammary Paget's disease, for which the patient was evaluated. Routine blood and urine investigation were within normal limits. Potassium hydroxide smears and cytology findings were normal. Mammography showed no evidence of any micro calcification or significant breast tissue involvement suggestive of malignancy. A skin biopsy was taken form two sites and both the specimens showed features of a dermatitis with spongiosis and moderate lymphocytic infiltration. Based on the investigation results we ruled out the possibility of Paget's disease and considered an alternative possibility of a primary non-specific dermatitis with a persistent contact dermatitis to topical applications. We initially patch tested the patient with the commercial products she was using, including brands of fluticasone and betamethasone. Interestingly all the products showed a strong positive reaction after 48h. We then patch-tested the patient with multiple antigens including topical antibiotics, preservatives and bases. The patch tests showed a strongly positive reaction to propylene glycol, parabens and chlorocresol and a moderate reaction to both neomycin and gentamycin. We also carried out an intradermal test with hydrocortisone and betamethasone solutions in saline, which gave a negative result. Based on the patch test findings we asked the patient to stop all topical preparations and started the patient on saline compresses and plain Vaseline along with a short course of systemic steroids. The lesions improved and by the end of two weeks had subsided almost entirely with only a mild residual hyperpigmentation (). |
A healthy 28-year-old woman restrained driver presented to the trauma unit post-MVC with significant vehicular intrusion. Examination demonstrated a 15-cm transverse wound over the medial malleolus and anterior ankle with exposed muscle, tendon, and bone without gross contamination. Her physical examination was otherwise unremarkable. Distal to the wound, there was no Doppler signal in either dorsalis pedis or posterior tibial arteries and the foot appeared cold with delayed cap refill. She was taken to the operating room urgently for debridement and irrigation, open reduction internal fixation of both distal tibia and fibular fractures, and supplemental external fixation application. The foot regained a normal color and capillary refill upon reduction, and biphasic Doppler signals returned.\nThe patient did well postoperatively and was discharged home on postoperative day 6. At her 6-week postoperative visit, the external fixation was removed and she was placed in a well-padded short leg cast. At postoperative week 9, the patient returned to clinic after having fevers and when the cast was removed and a 1.5 × 2.5 cm area of superficial central wound dehiscence was observed without surrounding erythema or fluctuance. She was prescribed Bactrim and placed in another short leg cast. At postoperative week 10, the cast was removed demonstrating exposed bone and hardware in the central aspect of the wound and the patient was admitted to the hospital for debridement and removal of implants with antibiotic spacer placement. At this time, there was a 10 × 14 cm wound over the medial malleolus (Fig. ).\nAs part of routine flap planning for open fractures, a formal angiogram was obtained. This demonstrated congenital absence of the posterior tibial artery. A large peroneal artery and a normal anterior tibial artery were noted. This anatomic variation is found in 5% of the normal population. A perforator supplying the medial skin, well proximal to the zone of injury, was identified via the CTA, completed upon presentation weeks earlier (Fig. ). The perforator to the medial skin, proximal to the defect and arising from the peroneal artery, was again visualized emanating from the peroneal artery, coursing between the deep and superficial compartments to the medial skin.\nIn this case, free tissue was deemed a relative contraindication because the patient demonstrated a single vessel supplying the foot. A propeller flap, based on the perforator from the peroneal artery, was chosen to provide medial soft tissue coverage. As noted, preoperative CTA and angiography demonstrated a suitable peroneal perforator providing flow to medial skin, in the absence of the PT artery.\nIntraoperatively, after the perforator was localized with pencil Doppler, laser-assisted endocyanin green angiography was used to confirm the location of perforator.\nAn anterior exploratory incision was made, just posterior to the tibial border. The fascia was elevated off deep posterior compartment, and upon reaching septa between the deep and superficial compartments of the leg, the perforator was easily visualized superficial to the flexor digitorum longus muscle. The perforator was found and dissected in the typical plane of the medial perforators, that being between the superficial and deep compartments. As expected from preoperative imaging, this perforator had its origin from the peroneal artery, found lateral to the tibial nerve, as opposed to the posterior tibial artery, typically found medial to the nerve. A lengthy perforator was isolated as the pedicle to the skin island, totaling slightly more than 4 cm in length, substantially longer than most perforators in those location. After the pedicle was isolated, the flap was rotated on its long axis approximately 160 degrees. The proximal skin defect was covered with split thickness skin graft harvested from the ipsilateral thigh (Figs. , ). The patient underwent routine flap care with strict elevation and a Bair hugger over the affected extremity. The patient was discharged to home on postoperative day 4. |
A 59-year-old male presented to the emergency department with complaints of diffuse abdominal pain, vomiting, and abdominal distension for five days. He reported not passing stools for two days. He had an elective laparotomy done 15 years back for peptic ulcer disease in our institute, the details of which were not known. On examination, he was conscious, oriented, and his vitals were stable. His abdomen was soft and distended with exaggerated bowel sounds. On digital rectal examination, the rectum was empty. Plain x-ray of the abdomen did not show any evidence of acute intestinal obstruction. An ultrasound of the abdomen was done which showed dilated hyper-peristaltic small bowel loops of maximum caliber 3.5 cm. There was no free-fluid in the peritoneal cavity and the gall bladder was normal. A clinical diagnosis of the adhesive intestinal obstruction was made, and the patient was managed conservatively with intravenous fluids and nasogastric drainage. Following 48 hours of conservative treatment, the patient had clinical improvement and was started on oral fluids. After two days of starting oral feeds, the patient again developed abdominal distension with bilious vomiting. A water-soluble contrast study was done which revealed dilated jejunal loops with multiple air-fluid levels and slow filling of the contrast till the ileum [Figure ].\nIn view of the persistent high nasogastric drainage of more than one litre a day and diffuse abdominal pain with guarding, the patient was planned for an exploratory laparotomy. Intraoperatively, there were no adhesions. A 6 × 5 cm well-defined firm intraluminal mass was palpable in the ileum about 45 cm proximal to the ileocaecal junction. The bowel loops proximal to the mass were dilated and the loops distal to it were collapsed [Figures -]. The mass, which was firm but mouldable with pressure, was found impacted at the transition area in the bowel. There was no structural abnormality identified in the bowel or the gall bladder. The mass, probably a stool bolus or fecal mass, was crushed and milked into the caecum.\nThe postoperative period was uneventful. The patient was started on oral feeds on postoperative day two and was discharged on postoperative day six. On follow-up, an oral contrast study was done, which showed normal study of the bowel. |
A 70-year old woman was admitted from a dermatologist to the Department of Plastic and Breast Surgery, Roskilde, Denmark. A biopsy verified well-differentiated full-thickness squamous cell cancer was found at the right side of the lower lip. The tumour had been present for three years. The patient had a history of ischemic heart disease with a percutanous coronary intervention and implantation of a stent in 2002. She was a heavy smoker. No alcohol overconsumption was reported. By clinical examination, a 15 × 15 mm sore, firm, central ulcerating tumour was seen located at the vermillion border (). At the mucosal side of the lip, leukoplakia was observed.\nNo enlarged lymph nodes in the cervical region was found at the clinical examination.\nSurgical intervention would remove approximately 50% of the lower lip. The patient was offered radiotherapy as an alternative to surgery and chose the former. She underwent a series of radiotherapy for a period of two months.\nFive weeks after the initial clinical examination at our clinic, the patient was readmitted to our department from the Department of Oncology at Copenhagen University Hospital due to recurrence of the squamous cell cancer located to the lower lip. At this point, the patient presented a monstrous, ulcerating tumour, involving most of the lower lip (). No clinical signs of systemic spread to lymph nodes in area was found by thorough clinical examination and palpation of the head and neck. Furthermore, a 18FDG-PET-CT was performed and ruled out further local or systemic spread.\nFirst, a total excision of the lower lip including the commisures during which free resection borders of 1 cm were confirmed by intraoperative frozen section diagnosis. 8 days after primary excision, histopathology confirmed free resection borders, and reconstruction of the lower lip by bilateral Fujimori technique was performed (, , ). Due to paucity of mucosal tissue between the orifice of the parotid duct and commisures of the mouth besides a relatively narrow labial sulcus, the remaining lack of mucosal lining was reconstructed by use of split skin harvested from the right thigh.\nAt a clinical follow-up three months after surgery, palpable enlarged, firm lymph node was found located to the lower jaw. Biopsy confirmed the histological diagnosis of metastasis from squamous cell carcinoma. Position Emission Tomography Scan (PET) confirmed the localisation of metastasis from a squamous cell carcinoma on the left side of the jaw, but as well on the right side. No distant metastases were found. Clinical presentation 5 months after surgery is seen in .\n5 ½ months after the initial admission to our department, bilateral neck dissection was performed. Several metastases with extensive perinodular growth was found on the right side, and infiltrating underlying musculature on the left side. The patient was referred to the Department of Oncology, Herlev Hospital, Denmark, where radiotherapy was given.\nOne months after completed radiotherapy, the patient presented in our clinic a very sore, ulcerated tumour at the jaw line on the left side. The tumour was adherent and dripping with what appeared to be saliva. Punch biopsies were not representative. A computer tomography (CT) scan confirmed local recurrence of aggressive squamous cell cancer. The patient was referred for more extensive surgery and further treatment, which is why eventual defatting of the lip was postponed. |
A 67-year-old man experienced repeated pneumonia during his childhood and often had hemoptysis and bloody phlegm since the age of 38. He always had a cough and sputum during food or liquid intake. During examinations that were conducted before surgery for atrial fibrillation and valvular disease in another hospital, computed tomography (CT) showed severe bronchiectasis in the right middle and lower lung lobes. Due to concerns about the risk of pulmonary bleeding during heart surgery using an artificial cardiopulmonary device with systemic heparinization, the patient was introduced to our hospital for lung resection. The presence of a fistula between the esophagus and the right lower lung lobe was suspected after CT (Fig. ), and consequently, esophagoscopy (Fig. ) and esophagography (Fig. ) through the fistula were performed, which revealed the flow of contrast medium from the esophagus to the right lower lobe and finally to the right main bronchus. CT angiography (Fig. ) and catheter angiography (Fig. ) revealed an abnormal artery branching from the inferior phrenic artery into the right lower lobe. Endovascular embolization of a few bronchial arteries and the abnormal artery was carried out to reduce bleeding during surgery.\nThe patient was placed in the left decubitus position. He underwent thoracotomy through the fifth intercostal space with a posterolateral skin incision. The middle and lower lobes strongly adhered to the chest wall and the diaphragm. We carefully cut the adhesion on the diaphragm using ligation, an energy device, and an automatic stapler because the abnormal artery could have been situated behind it. After that, we located the fistula easily without adhesion to the surroundings, severed it using an automatic stapler, and resected the middle and lower lobes. There was a defect in the pleura around the fistula, and we stitched the surrounding tissue including the pleura and cover it with collagen patches coated with human fibrinogen and thrombin (TachoSil, Nycomed, Vienna, Austria) to strengthen the surface of the esophagus (shown in Fig. ). Furthermore, we attached the fifth intercostal muscle to the middle and lower bronchus for protection. This surgery took 12 h with bleeding of 4000 ml.\nThe diagnosis of congenital EBF to pulmonary sequestration was established with intraoperative and pathological findings (Fig. ). The symptoms disappeared immediately following the operation, and the patient was discharged on the 12th day after surgery.\nTracheo/bronchoesophageal fistula may be congenital, traumatic, inflammatory, or neoplastic. Most patients with congenital tracheoesophageal fistulas (TEF) are diagnosed immediately following birth or during infancy, because more than 98 % are associated with atresia of the esophagus []. Congenital TEF without esophagus atresia H type TEF is rare but reportedly detected in adults because of long-standing respiratory symptoms [–]. The distribution of this disease is equal between males and females. It is three times more common on the right than the left and is seen more in the right lower lobe [, ]. According to the classification of Braimbridge and Keith [], type I is a fistula associated with a wide-necked congenital diverticulum of the esophagus with inflammation at the tip. Type II, which is the most common, consists of a short tract running directly from the esophagus to the lobar or segmental bronchi. In type III, the fistulous tract connects the esophagus to a cystic pulmonary change. In type IV, a fistula runs into a sequestered pulmonary segment. The patient described here may come under the definition of type IV because the existence of sequestered lung was suspected on the ground of an abnormal artery from an abdominal artery running into the right lower lung lobe, and a septum was clearly detected in the lobe by microscope.\nSymptoms sometimes present during childhood or adulthood but are seldom seen at birth [, –]. Theories on the cause of this delay have been discussed: a membrane existing on the fistula subsequently ruptures, the fistulous track runs upward and may close during swallowing (the track in this case appeared to run downward), or a fold of esophageal mucosa overlaps the orifice but subsequently becomes less mobile. Symptoms are usually due to chronic bronchopulmonary suppuration, cough (almost universal), hemoptysis, pneumonia, and choking when swallowing liquids (or the appearance of food in the sputum). Although digestive symptoms are relatively uncommon, it was reported that the stomach filled with air on expiration and caused reflux, and dysphagia was sometimes present, 13 and 4 %, respectively []. The patient discussed in this paper suffered several episodes of pneumonia during childhood but had not experienced any apparent pulmonary infection in adulthood before the age of 38. Apart from the aforementioned reasons, the silent period could have existed because the tract from the esophagus opened into the sequestered lung, not the bronchus. The reason for the later symptoms that occurred from the age of 38 could be that the continuous inflammation of the sequestered lung led to a connection between the damaged area and the right lower bronchus, and the inflammation was spread over the whole right lower and middle lobes. This theory may support the existence of the sequestered lung, but no image data before the lung got destroyed existed and the theory cannot be established.\nThe diagnosis is usually made by barium swallow. Bronchoscopy and esophagoscopy sometimes demonstrate the orifices of the fistula, which are usually small and only recognized when the exact site is known [–]. In this case, EBF was first suspected by computed tomography, which showed the tract between the esophagus and the right lower lobe, and the heavily damaged right middle and lower lobes.\nCriteria for congenital EBF are suggested pathologically by the absence of surrounding inflammation and adherent lymph nodes, along with the presence of mucosa and definitive muscularis mucosa within the fistulous tract. Surgically, uncomplicated and easy dissection of the fistula and absence of inflammation suggests a congenital fistula [, ]. In this patient, there was strong adhesion around the destroyed lung, but no adhesion was apparent around the EBF.\nIn terms of treatment, the division of the fistula and excision of the permanently diseased lung segment have been performed. There was no operative mortality reported, and symptoms rapidly improved [–]. |
A 38-year-old male referred with the complaint of partial edentulousness in the lower jaw and intended to get it replaced. The patient gave history of mobility of lower teeth, which gradually became exfoliated in the span of the last 10 years. He had previously consulted multiple dental surgeons for the same issue, where the remaining mobile teeth were extracted. The patient noticed that his lower jaw was becoming thinner progressively after extraction. There was negative history of pain, blood or purulent discharge from the associated region. Medical, family, and personal history were found to be inconspicuous.\nOn extraoral examination, retrognathic profile, decreased vertical height of lower one-third of the face was noted (). Intraoral examination revealed the presence of only third molars in completely resorbed mandibular arch. All the teeth were present in maxillary arch and were periodontally weak (). Based on history and clinical features, a provisional diagnosis of osteolytic lesion of mandible was considered.\nThe patient was subjected to radiological, laboratory, and histopathological investigations. Orthopantomograph showed resorption of the mandibular arch with decreased vertical height of the mandibular body leaving a thin rim and discontinuation in the right lower border of mandible suggestive of pathological fracture (). Axial section of computed tomographic image revealed almost completely resorbed lower arch along with hypodense areas in right upper maxilla (). Coronal and sagittal sections of the cone beam computerized tomographic (3D-CBCT) image showed hypodense areas in right posterior maxillary region and thin rim of alveolar ridge, observed throughout the length of the mandible. There was loss of integrity of right lower border of mandible, indicating pathological fracture ( and ). Laboratory investigations revealed normal blood picture except for elevated acid phosphatase and decreased alkaline phosphatase levels. Incisonal biopsy was performed from the left mandibular region and the photomicrograph revealed thinned out bony matrix, vascular spaces, and fibrous connective tissue stroma with dense collagenous bundles (). Based on the history, clinical findings, and investigations, a final diagnosis of Gorham’s disease was confirmed.\nThe patient was explicated about the rapidly progressive nature of the disease and recieved counselling and support as there is currently no definitive treatment. |
Patient is a 45-year-old female patient, with past medical history of gastritis. Six months before she sought medical attention, she was complaining of mild upper abdominal pain, however, due to her previous condition she was medicated with proton pump inhibitors assuming that the pain was due to her gastritis. In the last 3 months, she noticed a mass in her upper abdomen and the pain became more severe and started to affect her daily activities, thus she presented to a routine physical exam. No weight loss or other constitutional symptoms were noticed. Also no history of malignancy in her family was mentioned. On clinical examination, a 12 × 15 cm2 mass was discovered on her upper abdomen, mild pain was found on palpation but no tenderness was present. An abdominal ultrasonography revealed a 15 × 15 cm2 septate thin-walled giant cystic mass, it was anechoic and had a volume of ~735 ml. The cyst occupied most of the hepatorenal space and it was in intimate contact with the liver, right kidney and pancreas (Fig. A). Due to the size of the mass, CT was requested, it revealed well-defined 19.7 × 15 × 10 cm3 giant cyst, the cyst was located within the small bowel mesentery and it was in intimate contact with the liver, gallbladder, pancreas and right kidney (Fig. A). Nevertheless, the tomography could not rule out that the mass had some sort of communication with the bile duct or the pancreas. This is why a magnetic resonance cholangiopancreatography found that the cyst was attached but had no communication with the bile duct or the pancreas (Fig. A). CBC and blood work was normal.\nDue to the size of the cyst and clinical condition surgery was planned. At laparotomy, a 19 × 15 × 10 cm3 mesenteric cyst was discovered (Fig. B), the cyst was near the root of the small bowel mesentery but did not compromise its main vessels, it had a yellowish appearance (Fig. B), and clear fluid was found within the cyst. Multiple adhesion were identified between the cyst wall and the transverse colon, liver, third portion of the duodenum and gallbladder. With these findings surgery was straightforward, complete resection of the cystic mass was performed, however, the cyst wall was completely attached to the body of the gallbladder and could not be resected without compromising it (Fig. B), so a cholecystectomy was performed as well. After this, the remainder of the procedure continued without any complication.\nPathology reported a giant primary mesenteric cyst, it was lined with a single layer of cuboidal epithelial cells and partially covered by adipose tissue and prominent vasculature, it had a yellowish wall and its thickness varied between 0.1 and 0.3 cm (Fig. C). Its interior had a white trabecular internal surface with brown patches it did not have any communication with other organs, and no areas of malignancy were found (Fig. C).\nIn the early postoperative period, a tachycardic patient with severe abdominal pain and tenderness was encountered, she became hypotensive an oliguric, thus an emergency re-laparotomy was performed. The 1000 ml of hemoperitoneum was encountered and after extensive washing of the abdominal cavity, an arterial vessel from the resected gallbladder was discovered and successfully managed. After this surgery patient fully recovered. Sips of liquids were initiated on the third postoperative day, and full diet was initiated a day after. She was discharged without any complications and, on follow up controls patient is doing well. |
A 33-year-old African American woman with a history of omphalocele repair as an infant presented to the general surgery clinic with left upper and lower quadrant abdominal pain that radiates to the back, nausea related to fatty food ingestion, bloating, diarrhea, and subjective fevers. She had undergone an extensive workup with her gastroenterologist and was found to have cholelithiasis. Her past medical history included gastroesophageal reflux disease, anxiety, depression, and kidney stones. Past surgical history was significant for repair of an omphalocele shortly after birth. Her social history was negative for smoking or alcohol use.\nOn physical examination, she was hemodynamically normal, and the only pertinent finding was tenderness to palpation in her midabdomen. All blood tests were within normal limits including a white blood cell count and liver function tests. Abdominal ultrasound demonstrated cholelithiasis and sludge in an intrahepatic gallbladder located in her ectopic liver, but no evidence of gallbladder wall thickening or pericholecystic fluid (). Previous computed tomography (CT) scans demonstrated an ectopic liver located in the pelvis as well as an intrahepatic gallbladder and interval contracture of the gallbladder in subsequent scans (Figures and ). Magnetic resonance cholangiopancreatography (MRCP) demonstrated a relatively decompressed intrahepatic gallbladder in the pelvis joining the hepatic duct more superiorly with the common bile duct emptying into the duodenum, which has its usual right upper quadrant location (). As the patient had been symptomatic for several months and her clinical status did not improve during a period of observation and trial of ursodiol, cholecystectomy was recommended. The patient was consented for open cholecystectomy due to her unusual anatomy and likely need for hepatotomy to access the gallbladder.\nAt laparotomy, the liver was encountered just beneath the fascia in the lower abdomen and was adhesed to the anterior abdominal wall and into the pelvis. A small portion of the gallbladder infundibulum was identified in a cleft on the underside of the liver once it was rotated right to left and cranially. The cleft was extended to the edge of the liver and down to the gallbladder with a recently introduced microwave ablation technology for hepatic parenchymal pretransection coagulation, to expose the gallbladder, which was then separated from the surrounding liver parenchyma (). The cystic artery was identified, ligated, and divided. The cystic duct was identified, and a stone was found to be lodged in the cystic duct, which was then manipulated up into the fundus. The cystic duct was then ligated and divided, and a cholangiogram was performed via the cystic duct stump. The right and left hepatic ducts were visualized, as well as a long common bile duct, which traveled cranially to the right upper quadrant, where contrast was visualized within the duodenum (). Ultrasound of the whole liver was then performed. There were no abnormal lesions noted. The patient recovered without major events and was discharged to home on postoperative day three. Final pathology revealed chronic cholecystitis with cholelithiasis. |
A 19 year old nulliparous, British Caucasian woman was admitted with a sudden onset of right iliac fossa pain. Urine pregnancy test was negative. This pain was sharp and stabbing in nature with no radiation. There was no associated vomiting or fever. She denied any urinary urgency, frequency or dysuria and her bowels were normal. On examination there was minimal guarding and no rebound tenderness. No distension was seen and bowel sounds were heard. Transvaginal pelvic ultrasound demonstrated two small simple cysts within the right ovary. She was managed conservatively with analgesics only and the pain resolved within 24 hours. Following this acute episode she developed intermittent pelvic pain. Her subsequent scan showed 9.8 × 4.5 cm complex cystic mass in right adnexa with features suggestive of a dermoid cyst with no colour flow on Doppler examination. Interestingly her CA 125 was markedly elevated at 657; CEA, ∝ FP, HCG, white cell count (WCC) and CRP were all within normal limits. Her periods were regular and she was using condoms for contraception. She was in a new relationship and they had been together for the last 4 months.\nPast medical history included well controlled asthma, a negative laparotomy at the age of seven for abdominal pain but no previous pelvic infections. Pelvic examination revealed a normal size uterus with a right adnexal mass which appeared fixed to the pelvic side wall.\nA subsequent CT scan one week later suggested a right adnexal dermoid cyst 5.4 × 4.8 cm with abnormal soft tissue 3.0 × 2.6 cm deep to right rectus muscle and abnormal irregular soft tissue along pelvic side wall extending from left common iliac bifurcation to left adnexa and an enlarged 10 mm precaval lymph node was also seen. These features were thought to be highly suspicious of malignancy during the case review at the Gynaecology oncology Multidisciplinary Team (MDT) meeting.\nA further CA 125 level was measured pre-operatively and had fallen to 342. A provisional diagnosis of either pelvic inflammatory disease, endometriotic cyst or an ovarian malignancy was made. She underwent a midline laparotomy that revealed right ovarian cyst (7 × 6 × 6 cm), with associated hydrosalpinx. The tubo-ovarian mass was adherent to the terminal ileum, caecum and omentum with appendix buried in the mass. The left ovary was normal, although there was evidence of a left pyosalpinx, which was drained to conserve left tube. A right salpingo-opherectomy, appendicectomy and omental biopsy was performed and an intraoperative swab from the mass was sent for culture and sensitivity. She had high vaginal, endocervical and Chlamydia swabs postoperatively and her recovery was uneventful.\nHistology revealed a benign cystic ovarian teratoma, the fallopian tube showed acute on chronic salpingitis and the appendix was normal. The post operative endocervical swab was positive for Chlamydia. Both the partners were then subsequently referred to Genito- urinary clinic for ongoing treatment and contact tracing. |
A 24-year-old female presented to our outpatient department with complaints of foreign body sensation of the throat for the last 1 year. She also complained of change in voice for the past 4 months. She had no associated history of dysphagia or difficulty in breathing. On examination there was a 3 × 3 cm smooth, grayish-white, firm, nontender swelling in the right side of base of tongue occupying the oropharynx (). No cervical lymph nodes were palpable in the neck. Rest of examination of the ear, nose, and neck, as well as general physical examination, was unremarkable.\nContrast-enhanced computed tomography of the neck revealed a well-defined moderately enhancing soft tissue lesion involving the right side of base of tongue nearly 2.34 × 2.29 cm in size which was compromising the oropharyngeal airway. The thyroid gland was normally located in the anterior neck (). Transoral fine needle aspiration cytology from the swelling was done which showed scattered cohesive clusters of epithelial cells surrounded by hyaline material. There was mild hyperchromasia and scattered squamous cells in background. Overall features suggested the possibility of pleomorphic adenoma.\nThe patient was taken up for surgical excision. Tracheostomy was done prior to the procedure. A midline glossotomy was performed and deepened until the tumor was palpable. The lateral surface of the tumor was palpated and dissected using electrocautery. This approach provided an end on view to the lateral and inferior aspects of the tumor. The tumor was removed in toto with a cuff of normal tissue. The wound was sutured vertically in the midline from vallecula to tip of tongue (). Patient was started on oral feeding on the first postoperative day and was decannulated on the 5th day.\nPostoperative histopathology confirmed the diagnosis of pleomorphic adenoma with focal area of skeletal muscle involvement ().\nA postoperative computed tomography was done after 2 months of the operation which showed complete removal of the tumor. There has been neither functional disturbance nor any signs of recurrence to date (). |
This patient is a 29-year-old white woman from the USA with a medical history significant for severe IBS-D (diagnosed at age 12) and anxiety disorder. In July 2015, she presented with severe bleeding hemorrhoids secondary to IBS, which required hemorrhoidectomy and anal sphincterotomy in August 2015. The week before the surgery she developed pharyngitis and was treated with azithromycin, which resulted in mucousy diarrhea and abdominal discomfort. She tested negative for C. difficile antigen and toxins at that time.\nA week after surgery, she developed a perirectal abscess that had formed at the site of the sphincterotomy and was prescribed orally administered ciprofloxacin. Despite moderate symptom improvement, in September 2015 she required an abscess incision and drainage procedure and Penrose drain insertion. Prior to the surgery she was given a single dose of clindamycin. An additional 2-week course of ciprofloxacin and metronidazole was then prescribed. In late September 2015 she was admitted to the hospital for two nights due to further complications related to the abscess and was then diagnosed as having a perianal fistula.\nIn November 2015, she was prescribed clindamycin for an episode of group C streptococcal-positive pharyngitis. In late November 2015, she was also diagnosed as having Ehlers–Danlos syndrome, which according to her medical record may partially explain the poor wound healing from the perirectal abscess. In December 2015, her fistula required an anus seton placement. She was treated with multiple courses of ciprofloxacin and metronidazole off and on from December 2015 to January 2016.\nIn January 2016, following up on her recurrent pharyngitis, she was diagnosed as having chronic tonsillitis which led to tonsillectomy. In February 2016, 2 weeks after the surgery she was prescribed clindamycin. At the beginning of March 2016, she was diagnosed as having bacterial vaginosis and was prescribed orally administered metronidazole. A week later she was diagnosed as having vaginal candidiasis and was prescribed orally administered fluconazole. In April 2016, she complained of dysuria and was prescribed ciprofloxacin. After 2 days, when urine analysis results came back negative, she was asked by her physician to stop the treatment.\nIn June 2016, she presented for follow-up with ongoing diarrhea and abdominal pain. She was diagnosed as having C. difficile diarrhea, her antigen and toxins laboratory results were indeterminate, and a toxigenic strain was confirmed by polymerase chain reaction (PCR). She was prescribed a 6-week course of orally administered vancomycin. After a week of treatment her symptoms worsened, and following discussion with her gastroenterologist her treatment was switched to a 2-week course of metronidazole. Hours later, she was admitted to the hospital for a 4-day period for colitis. Her C. difficile antigen and toxin test returned negative during her admission. She received intravenously administered metronidazole treatment during her hospitalization. Her symptoms improved during her hospital stay, with 1–2 soft bowel movements a day. At discharge her metronidazole course was stopped and she was again prescribed vancomycin, which she took for over a month. She continued to experience GI irregularity (3–5 bowel movements a day) beyond what she had experienced secondary to her IBS prior to her surgeries. In March 2017, she was prescribed rifaximin for 2 weeks to treat chronic diarrhea.\nIn November 2017, she was prescribed a series of clinical intestinal tests (SmartGut™, uBiome Inc., San Francisco, USA) with the instructions to administer the test at home whenever she was experiencing a noticeable change of GI symptoms, then follow-up with her health care provider to discuss the results. This sequencing-based test requires that patients use a sterile swab to transfer a small amount of fecal material from toilet paper into a vial containing a lysis and stabilization buffer that preserves the microbial DNA for transport by mail back to the laboratory for processing, which involves DNA extraction, 16S ribosomal RNA (rRNA) gene amplification, and sequencing []. She first used this test in November 2017, about a month after completing a 2-week course of rifaximin. The results revealed a number of microbial organisms that were outside the healthy reference ranges, but she was negative for all pathogenic organisms included in the test, including C. difficile (Fig. ).\nBetween November and December 2017, her GI symptoms worsened considerably; her daily bowel movements increased from 3–4 to 6–10, stool consistency became more mucous-like and gelatinous, and she was experiencing more pain with defecation. She re-tested with SmartGut™ test again in January 2018. Her results continued to reveal a number of microbial organisms outside the healthy range and, this time, her sample also indicated the presence of C. difficile (Fig. ). She immediately contacted her primary care provider, who re-tested her for C. difficile and confirmed indeterminate CDI by antigen and toxins A and B. Additional PCR testing at a regional laboratory confirmed the sample was positive for a toxigenic C. difficile strain. As a result of testing, her clinician started her on fidaxomicin; her symptoms improved rapidly. By April 2018, she had returned to her baseline in regard to her IBS-related GI symptoms with no blood in her stools.\nIn addition, the second SmartGut™ sample was tested for toxins A and B by sequencing at uBiome Inc. laboratory in San Francisco, USA, which resulted positive for both and confirmed the toxigenic nature of the C. difficile strain. |
A 78-year-old Caucasian man was referred to our stroke unit because of the sudden onset of a headache associated with speech and visual disturbances during early morning sexual intercourse. He had been lying in a supine position with his head hanging off the bed in a slightly downwards position. The patient was brought to the hospital few hours later. On admission, neurological examination showed a right hemianopia with alexia. His systolic blood pressure was 115 mmHg and the diastolic pressure was 60 mmHg.\nA thorough review of familial and personal clinical histories suggested no other possible cause for this condition. In particular, there were no signs of arterial hypertension or hematological disorders and our patient was not taking anti-coagulants or anti-platelet drugs. He had not experienced any head trauma and had no other risk factors for cerebrovascular disease. He had also not taken sildenafil citrate or any other cyclic guanosine monophosphate (cGMP) inhibitors.\nA cerebral CT scan showed a small left cortical temporo-occipital hemorrhage with mild mass effect and hypodense halo (Figure ). A carotid and vertebral duplex scan was normal, as was an arterial trans-cranial Doppler. Neuropsychological testing and a neuropsychiatric interview showed no cognitive impairment (Mini-Mental State Examination (MMSE) was 29 out of 30). Routine blood tests, including a platelet count and the plasma level of coagulation factors gave results within normal ranges. A peri-umbilical biopsy for systemic amyloidosis was normal. A cerebral MRI was not carried out because of the presence of abdominal vascular clips. Therefore, a contrast-enhanced CT scan and a traditional digital subtraction angiography (DSA) were performed the following day to rule out the possibility of cerebral venous thrombosis or arteriovenous malformations. These tests provided no evidence of venous thrombosis or vascular malformations, whereas an air contrast ultrasound venography (ACUV) of the jugular veins showed a severe bilateral jugular valve incompetence, with a huge reflow to the brain during a Valsalva maneuver [,].\nOur patient was discharged a week after presentation, with mild left hemianopia and alexia. The control CT scan showed a partial regression of the cerebral hemorrhage. He was advised to be careful during physical activity and to frequently measure his blood pressure. |
The patient is a 61-year-old Korean male with a significant past medical history of rheumatoid arthritis, hypertension, and diabetes mellitus who presented to the hospital with sudden onset of blurry vision in his left eye three days prior. A head CT had been performed at an outside facility, which was negative for acute ischemia, hemorrhage, midline shift, or extra-axial fluid collection. The patient denied visual complaints in his right eye and had no history of similar events.\nOphthalmologic and Neurologic consultations initially revealed visual acuity was 20/40 on right eye; however, on the left eye, there was an apparent left-sided visual loss. Patient's intraocular pressure was normal in both eyes, pupils were equally round and reactive to light, and no afferent pupillary defect was observed. Moreover, the extraocular muscles were intact and with full range of motion. In the right eye, visual fields were full to finger count. In the left eye, the acuity in the nasal visual field was greater than that in the temporal visual field. In the nasal visual field, the patient was able to count fingers; however, in the temporal visual field, the patient could barely detect gross hand movement at one foot out. External examination was within normal limits, and pen light examination was only remarkable for nuclear sclerotic cataracts bilaterally. Dilated fundus examination demonstrated no evidence of pathology to the vitreous, optic nerve, or retina that might explain the vision loss. Four days later, repeat examination by Ophthalmology demonstrated a stable right eye; nonetheless, the left eye temporal visual field was 20/25 and patient was able to count fingers without mistake on left visual field. Pupil and retina examination were unchanged from previous examination. However, visual field mapping could not be done as this patient was seen in the inpatient setting.\nConsequently, an initial head MRI with and without contrast was performed, which showed focal areas of restricted diffusion in the right medial temporal lobe, inferior right basal ganglia with possible involvement of the right lateral geniculate nucleus. The head MRI did not show any other pathology such as masses or hemorrhages (Figure ). The subsequent head MR angiogram done demonstrated no focal occlusion or stenosis, and the MRI of the orbits showed no focal defects bilaterally. At this point, it was evident that the patient was suffering from a left temporal monocular hemianopia and that there must be a correlation with the subtle but definitely present right LGN ischemic lesion. An infarct affecting the right lateral geniculate nucleus would most likely cause bilateral left homonymous hemianopia. Nevertheless, a lesion at the vicinity of right LGN that had taken out the inputs going to layers 1, 4, and 6 became generally accepted among all physicians involved at this point in the care of this patient as the only possible explanation. Patient's left visual symptoms slowly started to improve, and after four days of hospitalization and monitoring, patient's left monocular temporal hemianopia had almost resolved and his vision had almost returned to his normal baseline. |
A 69-year-old African American man sees his podiatrist because he was experiencing rapidly progressing pain in his right leg and inability to either stand or walk. He had paresthesia, pallor, and cold skin with black discoloration of his toes bilaterally. On physical examination, the podiatrist noticed bilateral absent pulses, dry skin, and ischemic appearing toes, worse on the right than the left. The podiatrist referred him to the cardiovascular clinic urgently. Based on the symptomatology and physical findings, he was diagnosed with critical limb ischemia bilaterally and an AARO was performed the next day via left radial artery access.\nThe AARO revealed a totally occluded distal aorta right after the origin of the inferior mesenteric artery (IMA) which had a 95% ostial lesion; however, it still supplied perfusion to most of the collaterals in lower extremities (). A CT angiography of the aorta and lower extremities was ordered to better evaluate the distal circulation. The CT findings were consistent with aortoiliac occlusion. The origin of celiac trunk and superior mesenteric artery (SMA) showed mild disease. The ostium of the IMA had severe stenosis of 95%, and the aorta distal to IMA was completely occluded ( and ). There were extensive collaterals to both iliac arteries. The superior rectal artery, which originates from IMA, had anastomosis to the middle rectal artery, which originates from internal iliac artery. In addition, the CT scan noted a prominent inferior epigastric and lumbar collaterals that reconstituted the left external iliac artery at the origin of the common femoral artery and the right distal common iliac artery. There was evidence of moderate calcific atherosclerotic disease in the right lower extremity at the level of mid-popliteal artery and distal anterior tibial artery with three-vessel runoff to the foot. The left lower extremity has two-vessel runoff to the foot because of severe disease in the left tibioperoneal trunk and peroneal artery. Based on these findings, the patient was referred to vascular surgery for bilateral aortoiliac bypass graft surgery. |
A 54-year-old female without prior thoraco-abdominal trauma presented to the office with two right lower lobe lung nodules. The nodules were initially noted incidentally on a computerized tomography (CT) scan in August 2009 and measured 1.5 cm × 2.8 cm and 0.9 cm × 1.3 cm ( and ). A follow-up CT scan and positron emission tomography (PET) performed in 2010 demonstrated that the nodules were stable in size. The patient was lost to follow-up until March 2019 when she had a CT scan for concern for pneumonia. On these images, the lung nodules had increased in size to 2.8 cm × 4.1 cm and 1.1 cm × 1.4 cm. The patient was otherwise asymptomatic. A PET scan was obtained which showed hypermetabolic nodules with maximum SUV of 3.29 and 1.4, for the larger and smaller nodule, respectively ( and ). Radiographic appearance as well as the growth pattern was consistent with low-grade malignancy suspicious for carcinoid tumor. CT-guided biopsy was not feasible because of location of the tumor.\nWe performed a robotic thoracoscopy with plan for wedge resection and possible completion lobectomy. Gross inspection of the thoracic cavity revealed an abnormal mass on the dome of the diaphragm with the appearance similar to liver ( and ). The mass was noted to be positioned in the oblique fissure and correlated with the location of the larger nodule seen on CT scan. There was a second area of thinned-out diaphragm where a small nodule was noted to be protruding under the diaphragm. This second mass also had the appearance of liver and was consistent with location of smaller lesion on CT scan. A core needle biopsy was performed which was consistent with benign liver tissue. The decision was made not to proceed with any diaphragmatic repair or reinforcement with mesh. This was diagnosed as an asymptomatic herniation through the diaphragm, and the liver was fused to the diaphragm therefore preventing future intestinal herniation. |
A 72-year-old man was referred to our hospital because of progressive cognitive impairment noticed for a few weeks and a sudden right-sided haemiparesis after falling from his bicycle. His medical history revealed a deceased donor kidney transplantation 15 years previously, a mitral valve replacement and a mild aortic valve stenosis. Maintenance immunosuppression was stable in dose and consisted of prednisolone 7.5 mg once daily and mycophenolate 1000 mg twice daily with normal plasma levels.\nIn the referring hospital, CT and brain MRI demonstrated one solitary cerebral mass near the nuclei basales with a questionable ring contrast enhancement and a midline shift of 5 mm, described as probable metastasis of a tumour with unknown origin (). Because of the possible malignant aspect, he had been on a course of dexamethasone but his symptoms did not improve at all. He did not complain about fever, skin lesions or signs suggesting infection. Before this cognitive impairment started, his condition was normal without any episodes of flu-like illnesses. Blood cultures in the referring hospital remained negative. Physical examination showed only neurological symptoms of which a haemiparesis, impaired cognitive function and slurred speech were the most prominent. No signs of meningitis were found. There was no lymphadenopathy nor enlarged liver or spleen. Laboratory revealed no abnormal findings except for slightly elevated C-reactive protein of 13 mL/L (normal value < 5 mL/L). Chest radiography was normal. Further blood cultures and cytomegalovirus viral load in whole blood remained negative. Yet, up to 40 700 copies/mL EBV DNA were detected by reverse transcription–polymerase chain reaction (RT–PCR) in whole blood. In the CSF besides a white blood count of 22 × 106/L (mainly lymphocytes with a few monocytes), no protein and a glucose 3.5 mmol/L, also 7160 copies/mL EBV DNA could be detected. These positive EBV viral loads provided a high suspicion of EBV-driven CNS lymphoma, mainly because of the clinical symptoms and radiological symptoms, which made an infectious origin less likely.\nHowever, immunophenotyping of the CSF showed mainly T cells, without markers of bone marrow diseases or CD20-positive B cells. Doubt was cast and a stereotactic brain biopsy was performed after a PET scan, which did not answer our differential diagnosis between malignant or infectious cause. However, the biopsy showed T.\n gondii tachyzoites and bradyzoites, without any signs of malignancy and PTLD (). Unfortunately, T.\n gondii serology at time of transplantation had not been performed, but subsequently, high antibodies against T.\n gondii (negative IgM, IgG > 300) and T.\n gondii DNA in CSF using RT–PCR could be detected. The patient was treated with oral trimethoprim-sulfamethoxazole (co-trimoxazol) 960 mg three times daily for 6 weeks, improving the neurological symptoms.\nUnfortunately, in the course of his disease, he developed massive gastrointestinal bleeding because of stomach ulcers twice, which necessitated admission to the intensive care unit.\nHe had not regained his prior condition when he was referred to a nursing home and was re-admitted for pneumonia within a few weeks. His condition detoriated quickly and he died within 3 months after diagnosis of cerebral mass lesions due to toxoplasmosis. Unfortunately, no CT cerebrums were done after we started treatment and autopsy was refused. |
A 60-year-old African American female with a past medical history of hypertension, chronic obstructive pulmonary disease (COPD), hyperlipidemia, sickle cell trait, class III obesity, presented to the hospital with shortness of breath two days ago, associated with a progressively worsening tongue and neck swelling that developed for five days. She was referred to the emergency room from her Primary Care Physician (PCP) office for high clinical suspicion of angioedema. Earlier that day the patient had presented to her PCP office with a progressively worsening, asymmetric (right greater than left) tongue swelling for five days. The tongue swelling had disrupted the patient's sleep and made it difficult for her to swallow solid food. She also endorsed associated painful neck swelling and shortness of breath. She did not notice any rash on her body and denied itching. She also reported having a dry cough for two months, which was persistent despite trying all cough remedies. Her home lisinopril was discontinued four weeks ago with some improvement of cough. She had previously tolerated ACE inhibitor for months without any issue. Upon arrival at the hospital, on physical examination, her vital signs included a temperature of 37.1ºC, blood pressure of 164/89 mmHg, heart rate of 102 beats per minute, respiratory rate of 22 breaths per minute, and oxygen saturation of 93% on room air. She was alert and oriented, speech and voice with wet quality, without stridor, head and neck exam was significant for lower lip swelling, diffuse neck swelling with tenderness, palpable cervical, and retro auricular lymph nodes. A heart exam revealed regular rate and rhythm. Lung examination was notable for decreased air entry bilaterally without any added sounds. Skin exam was without evidence of any erythema, swelling, or rash. The remainder of the examination was unremarkable. Her initial lab work including a comprehensive metabolic panel and complete blood count were within normal limits. Her erythrocyte sedimentation rate was elevated at 59 mm/hr. An initial chest x-ray and x-ray of the soft tissues of the neck were unremarkable. A clinical diagnosis of angioedema related to either ACE inhibitor use or other etiology was made. The patient immediately received steroids, histamine 2 (H2) receptor blockers, Icatibant, and fresh frozen plasma. The patient was evaluated by an otolaryngologist with transnasal flexible fiberoptic laryngoscopy (FFL), which revealed symmetric bilateral watery edema on the lateral edges of the lingual surface of epiglottis without evidence of laryngeal involvement. She was transferred to the Intensive care unit for closer monitoring and anticipated intubation. Further lab testing revealed normal C-1 esterase levels, complement C3 levels, complement C4 levels, and C-reactive protein. The patient’s symptoms persisted on the next day and a repeat FFL evaluation remained unchanged from prior. A computed tomography scan with intravenous contrast of the soft tissues of the neck was obtained which revealed an unremarkable exam of pharyngeal mucosal spaces, larynx, and neck spaces. She was started on antihistamines, H2 receptor blockers, and steroids. The patient received a total five-day course of steroids and had resolution of swelling without requiring intubation. In the absence of associated itching, hives, and normal C-1esterase levels; bradykinin mediated angioedema in the setting of prior ACE inhibitor use was deemed the cause of her angioedema. ACE inhibitor-induced angioedema was permanently added to the list of her allergies. She was transferred to a regular medicine floor within three days and discharged home after a seven-day hospital course with an outpatient follow-up with PCP. |
A 58 year old woman from central Nepal presented to our outpatient clinic with a history of painful swelling around her right eye for two months. The patient also complained of diminishing vision in the same eye. The vision in the patient’s left eye had been previously lost following an injury during childhood. There was no other relevant family information or any significant past medical or surgical illnesses of the patient. Local examination revealed presence of peri-orbital swelling in the right eye with restricted eye movements (\n). The patient’s visual acuity in the same eye was restricted to only perception to light. Funduscopy revealed the presence of papilledema. Remaining physical examinations were normal.\nRadio-imaging of the patient’s orbits revealed the presence of hyperostotic changes in theright orbit, with presence of enhancing lesions on the right globe with extension to the para-nasal sinuses and also invasion along the dural base in the anterior cranial fossa (\n and\n). The initial differential diagnosis was an infective pathology. However, the patient was not immuno-compromised.\nA chest X-ray was performed as a routine work up, which inadvertently revealed the presence of an elevated right hemi-diaphragm with presence of right para-hilar mass (\n). Further evaluation through chest computed tomography confirmed the finding of a right para-hilar mass (\n).\nWe discussed with the patient and her relatives the possibility of the eye findings to be related to the lung lesion and recommended approaches to obtain a definitive diagnosis. Ultrasound guided fine needle aspiration cytology (FNAC) from the lung lesion revealed findings suggestive of a malignant lung disease (\n). Diagnostic biopsy from the nasal endoscope confirmed the metastatic nature of the disease from the lung (\n). Therefore, a diagnosis of metastatic lung disease to the orbit was finally confirmed.\nThe patient was started on a steroid therapy (injection dexamethasone at 8mg stat followed by 4 mg every eight hours), which decreased the swelling on the patient’s eye and improved visual acuity to finger counting within a period of 1 week. This further hinted at compressive rather than infiltrative effect on the optic nerve by the lesion. The patient was counseled and then immediately referred to the National Cancer Centre, Kathmandu, Nepal for further management with systemic chemo-radiation therapy after evaluation. Since the patient had a single and minimally functioning eye left, the decision was taken not to surgically decompress the lesion from the orbit. The patients was initially started on chemotherapy with a further plan of management to be tailored as per the clinical response seen in the patient.\nInitially, metastatic deposits causing eye swelling in the patient was not suspected. It was serendipity that the routine chest X-ray gave a clue to the presence of a lung mass. Even a small delay may have had a disastrous impact on the outcome of the vision in the patient. |
A 4-year-old girl with unexplained hypergastrinemia was referred to our department after abdominal ultrasonography detected a cystic lesion at her prepyloric antrum. When she first presented with a duodenal ulcer at 2 years of age, her serum gastrin levels had ranged between 700 and 1000 pg/ml. The imaging studies with a contrast-enhanced computed tomography (CT) scan had repeatedly revealed no tumor around the pancreas or duodenum suggestive of gastrinoma but revealed only a thickened wall of the duodenum potentially due to the initially severe duodenal ulcer. She had continuously taken a proton pump inhibitor (PPI) until the referral since the first presentation of the duodenal ulcer, which had relieved its symptoms such as epigastric pain.\nAt the referral, the patient’s physical and mental development were normal for her age. She was afebrile, and other vital signs were also within the normal ranges. A physical examination revealed no particular symptoms. Her blood tests were unremarkable except for elevated serum gastrin (877 pg/ml, normal range 37–172 pg/ml). Upper gastrointestinal series revealed a 2.5 × 5 cm cystic lesion on the anterior wall of the antrum, communicating with the gastric lumen (Fig. ), which was also detected as a solid mass with slight enhancement on abdominal contrast-enhanced CT (Fig. ). Upper endoscopy showed a scar at the duodenal bulb, but no erosion or ulcers in the stomach or the duodenum, and we could not detect the opening of the lesion. A gastric tissue biopsy did not demonstrate Helicobacter pylori. According to these findings, we suspected gastric duplication. As we speculated that the lesion might have caused the duodenal ulcer in this patient, we proceeded with operative treatment for the lesion. The operation was performed with the umbilical approach. A 2 × 3 cm protruded lesion was observed on the anterior wall of the gastric antrum (Fig. a) and resected with the common muscular layer with the opening to the gastric lumen (Fig. b). A pathological examination was consistent with gastric duplication with antral mucosa, which strongly stained positive for gastrin (Fig. ) and also contained heterotopic pancreas tissue. The postoperative course was uneventful, and the patient was discharged on the eleventh postoperative day (POD). Her serum gastrin level remained elevated after the operation (755 pg/ml on POD 7 and 727 pg/ml on POD 98) but started to decrease after PPI was switched to famotidine 3 months after the operation (228 pg/ml on POD 148 and 235 pg/ml on POD 291) and finally normalized after famotidine was stopped 10 months after the operation (151 pg/ml on POD 365 and 77 pg/ml on POD 461). She has remained entirely asymptomatic during a follow-up of 20 months.\nEnteric duplications are ectopic cystic or tubular structures composed of smooth muscle surrounding the mucosa of the gastrointestinal tract and occur most commonly along the ileum, esophagus, or colon []. Gastric duplications are relatively rare in children, accounting for only 4–8 % of all enteral tract duplications []. They are usually spherical or tubular cysts in the greater curvature of the stomach and may not communicate with the gastric lumen []. Their presentations range from asymptomatic to an acute abdomen and include gastric outlet obstructions, pancreatitis, hemoptysis, gastrointestinal bleeding, and an ulcerated antral mass []; hypergastrinemia has been rarely reported [] as one of the complications associated with a gastric duplication.\nNormally, acid in the gastric lumen acts directly on the somatostatin cells (D cells) to stimulate the release of somatostatin, thereby preventing gastrin release from gastrin cells (G cells) by a paracrine mechanism. When gastric antral mucosa is isolated from its usual acidic environment, such as in cases of a retained gastric antrum following partial gastrectomy with Billroth II reconstruction, there is no hydrogen ion feedback inhibition of gastrin release, leading to hypergastrinemia followed by increased gastric acid production, recurrent ulceration, and bleeding []. We speculate that this same mechanism caused hypergastrinemia and the resultant peptic ulcer at the initial presentation in our case whose ectopic antral mucosa in the duplication barely communicated with her gastric lumen. If more gastric acidic juice comes into the duplication lumen through a larger opening and/or the amount of the G cells is less than that in our case, hypergastrinemia may not happen. A literature review revealed only one case of a gastric duplication [] and another of a pancreatic duplication [] presenting with hypergastrinemia. Stephen et al. [] reported a female who presented with hematemesis and melena at 2 weeks of age. The possibility of gastrinoma was excluded using a secretin stimulation test and imaging studies; however, exploratory laparotomy could not detect any pathology, and thus, antrectomy and Billroth II reconstruction were performed. The pathological findings revealed gastroduodenal erosions and an antral duplication cyst with deep glands at the intracystic mucosa that stained positive for gastrin. Siddiqui et al. [] reported the case of a 2-year-old girl who presented with failure to thrive and gastroesophageal reflux with continued low gastric pH levels. Portal and pancreatic venous sampling in that patient during the operation revealed elevated levels of gastrin to the pancreatic venous cascade, and CT demonstrated a cystic lesion in the head of the pancreas. The patient underwent local resection of the lesion, and a pathological study confirmed the duplication with gastric mucosa (immunostaining of gastrin was not performed).\nAlthough the time course of the serum gastrin level of the latter patient was not described, that of the former patient normalized promptly after the operation. In contrast, the reason why hypergastrinemia in our case did not improve until PPI and famotidine were stopped may be explained by another mechanism related to the preoperative long-term use of PPI. A modest increase in the serum gastrin level in adult patients under a long-term treatment with acid-lowering compounds, especially PPI, has been reported []. PPI causes potent suppression of gastric acid secretion and leads to persistently high intragastric pH, and long-term PPI therapy has been reported to be associated with a significant increase in the G cell numbers and the ratio of G to D cells in the gastric antrum in children [].\nAccording to previous reports [, ], we speculate that the pathophysiology of our case was as follows: (1) the antral mucosa in the duplication was isolated from its typically acidic environment, which led to the lack of hydrogen ion feedback inhibition of gastrin release, and therefore, resultant hypergastrinemia caused the duodenal ulcer; (2) PPI suppressed gastric acid secretion and improved the duodenal ulcer, but the secretion of gastrin continued from the duplication for 2 years until it was removed, with an increase in the antral G cell numbers and the G to D cell ratio caused by the long-term use of PPI, thus additionally leading to hypergastrinemia; and (3) even after the removal of the duplication, hypergastrinemia continued until PPI and famotidine were stopped by the same mechanism. |
A 70-year-old Asian woman from Karachi presented with a history of pain in the right iliac fossa (RIF) for 15 days. The pain was pricking in nature, moderate in intensity and non-radiating. She also had a six-month history of a dragging sensation in her lower abdomen. There was no history of bleeding per rectum or documented weight loss. She was hemodynamically stable at the time of presentation. A physical examination showed tenderness and a firm, mobile mass of 5 × 2 cm in the RIF. Bowel sounds were audible and rebound tenderness could not be elicited. Her laboratory work-up including complete blood count, serum creatinine and liver function tests were all within normal limits.\nShe next underwent upper and lower gastrointestinal endoscopies which revealed an esophageal diverticulum, hiatal hernia, mild chronic Helicobacter pylori gastritis and evidence of external compression of the cecum. The mucosal biopsies from her cecum were reported as benign. A computed tomography (CT) scan of the abdomen and pelvis was subsequently obtained which showed a calcified mucocele of the appendix along with multiple calcified mesenteric lymph nodes. Minimal periappendiceal fat infiltration was also seen (Figure ).\nShe was electively admitted and an informed consent for appendectomy or possible right hemicolectomy was obtained. She underwent an initial diagnostic laparoscopy to evaluate any mucin spillage or seeding of the peritoneal cavity before surgical intervention, because any such finding could mandate a more extensive procedure. Once no spillage was identified, we proceeded with open surgery using a limited transverse muscle cutting incision. The appendix was carefully dissected and removed. Intra-operative findings included an appendicular mass which was most likely a previously perforated appendix along the lateral abdominal wall. The lateral abdominal wall peritoneum was excised with the appendix to prevent any spillage of appendiceal contents into the abdominal cavity. The base of the appendix was fixed using absorbable transfixation sutures.\nThe frozen section of this mass showed extensive foci of dystrophic calcification and non-specific acute and chronic inflammation. A detailed histopathology report of the appendix along with the attached mesoappendix showed a 1.5 cm perforation in the lumen of the appendix with mucopurulent exudate in the surrounding area. Mucinous material was observed in the dilated appendicular lumen. Tall columnar, hyperplastic mucosa with focal papillary architecture lining the appendix was identified. Foci of dystrophic calcification, extensive areas of fibrosis and patchy acute and chronic non-specific inflammation were also seen in the wall of the appendix. No significant cytological atypia or invasion of the appendiceal wall by atypical glands was noted (Figures and ). A final histopathological diagnosis of mucinous cystadenoma was made. The patient remained well post-operatively and was discharged after an uneventful hospital stay. At one-year follow-up, the patient was symptom-free. |
A 60-year-old man was presented to the medical unit in July 2020 with symptoms of respiratory problems, severe headache, cough, dizziness, and frequent vomiting. Initial physical and clinical examinations of the patient were normal and there was no underlying disease. The patient had no history of alcohol or tobacco use and was not taking any specific medications at the time. His blood pressure was 120/80 mmHg with a regular pulse rate of 112 beats/min, a respiratory rate of 22 cycles/min, and a temperature of 36 °C. While the patient had no symptoms of arrhythmia, he had mild hypoxemia with an oxygen level of 85–92% (Table ). Important laboratory findings of the patient are listed in Table . PCR on the nasopharyngeal swab sample was performed on the day of hospitalization, which confirmed the diagnosis of COVID-19. The patient was discharged from the hospital after 2 days because his symptoms were relatively mild and there were no other serious symptoms. He was admitted to the hospital 5 days later with respiratory problems, and initial examinations revealed that his oxygen saturation was then 82% on room air. The patient underwent high-resolution computed tomography (CT) scans of the lungs and CT pulmonary angiography. CT scans of the lungs (Fig. ) showed several diffuse areas of opacity in both right and left lungs, which could indicate viral pneumonia. In addition, on CT angiography of the lungs (Fig. ), several filling defects were visible in the branch of the pulmonary artery leading to the lower lobe of the right lung, which may indicate acute pulmonary embolism. The patient was started on medications including naproxen to control the muscle pain, hydroxychloroquine and famotidine with antiviral effects, zinc to boost the immune system and repair lung tissue, and neurobion to strengthen the immune system. Some anticoagulant including injected heparin and acetylsalicylic acid tablets, and high-flow oxygen were also used. The severity of COVID-19 in this patient was moderate and he did not require mechanical ventilation or intensive care unit (ICU) management and was released from the hospital 15 days after partial recovery. |
Case 2. A 30-month-old boy was transferred to our institution due to up left-sided neck swelling for 10 days. Presenting symptoms like case 1, presented with a rapidly neck swelling and enlarging but without fever. Past history did not reveal any trauma to the head, nor any bleeding disorder or pertinent family history. He was not on any anticoagulants or antiplatelet drugs. The patient was afebrile, and the neurological examination showed normal. A 5 × 4 cm spherical swelling was seen on up left-sided neck.\nThe laboratory tests indicated high inflammatory reactions in case 1. The haematological and biochemical investigations were normal in case 2. All the patients coagulation function and bleeding times were both normal. Taken together, acute bleeding of the neck was suspected.\nA computed tomography (CT) scan with contrast of the neck was reported as resolving haematoma 4.3 cm deep to the left occipitalia at the level of lobulus auriculae in case 1 (Figure ), and magnetic resonance imaging (MRI) of the head with contrast demonstrated a posterior, lobulated mass extending to the left occipitalia (Figure ). All the CT and MRI did not show any evidence of destructive change or fracture of the vertebral body and neural arch.\nA CT scan of the neck was reported as resolving haematoma 4.9 cm deep to the left sternocleidomastoid at the level of above the hyoid bone in case 2 (Figure ). The CT scan did not show any evidence of destructive change or fracture of the vertebral body and neural arch.\nA definite diagnosis of acute spontaneous neck haematoma was made by hematoma puncture in the two children. During this procedure, the aspiration was performed with 5 ml syringe, and the diagnosis was achieved by the successful aspiration of bleeding liquid.\nIn case 1, the patient was treated with analgesics. No hemostatic was used. Both patient received treatment of fine needle aspiration of bleeding liquid form, but the hematoma expanded rapidly in a few hours. Thus, we decided to wait for a time for spontaneous resolution. The lesion resolved spontaneously two weeks later, without any complications or sequelae. |
A 58-year-old female underwent bilateral breast lift and augmentation with silicone implants in September 2012. In August 2014, she presented with right breast swelling and heaviness in the inferior aspect of the breast. The patient denied weight loss, night sweats, fevers, chills, or systemic complaints. Imaging including mammogram and bilateral breast ultrasound noted presence of fluid surrounding the entire visible right breast implant. Presence of a 2 cm mass in the lower inner quadrant of the right breast and an enlarged 3 cm right axillary lymph node was also confirmed on MRI (). Staging PET/CT showed multiple lesions in the right breast, the largest measuring up to 5 cm with SUV ranging from 10 to 52.4 () and two hypermetabolic lymph nodes in the right axilla measuring 1.7 and 3.7 cm with SUV of 6.0 and 15.8, respectively (). There was also a hypermetabolic band posterior to the implant involving the pectoralis minor muscle measuring 5 × 1 cm with an SUV of 33.7 (). Bone marrow biopsy was not performed. The biopsies of the breast, right axillary lymph nodes, and fluid cytology surrounding the breast capsule confirmed CD30+/ALK− anaplastic large cell lymphoma ().\nMultidisciplinary treatment plan included bilateral capsulectomy and right partial mastectomy with excision of the right breast mass and no axillary surgery. The right axillary node was intentionally left in place to serve as a correlate to the response to systemic chemotherapy during the postoperative period. At the time of surgery, all gross disease was removed; however, there was disease adherent to the chest wall in the area posterior to the dominant lesion of lower inner quadrant of the right breast. It was assumed that there would be residual microscopic disease in this area and that postoperative RT to the chest wall would be indicated, regardless of the results of a postoperative PET/CT scan. Surgical pathology noted residual lymphoma in the fibroconnective tissue of the right breast chest wall. In addition, surgical pathology confirmed areas of disease found on the pretreatment imaging (Figures , , , and ), including the right breast capsule, right breast extracapsular tissue, right medial breast glandular tissue, and right breast chest wall. Postoperatively, the patient received 6 cycles of adjuvant CHOP chemotherapy, which she tolerated well. PET/CT after 3 cycles of chemotherapy showed complete resolution of the previously noted hypermetabolic areas in the right breast () and chest wall (), as well as a decrease in size of the right axillary lymph nodes to 0.5 cm (from 1.7 to 3.7 cm) (). Subsequent to completing chemotherapy, the patient received radiation to the right breast and regional nodes. A total dose of 3600 cGy in 20 fractions using 180 cGy per fraction was delivered over 4 weeks. The patient tolerated the therapy well.\nSince completing treatments, the patient has been followed by the multidisciplinary team at regular intervals and has not required subsequent therapy. At present follow-up 2.5 years from diagnosis, the patient remains without evidence of disease on physical exam and PET/CT scans. |
A 19-year-old female patient visited the outpatient wing of the department of periodontics with a complaint of spacing in the upper front tooth region associated with loosening of teeth for 3 months. She was otherwise healthy and had no significant medical issues. The patient provided a dental history of spacing between the left lateral incisor and the canine from childhood. She narrated that the lateral incisor and canine had become mobile because of the increased spacing with a preoperative probing depth of 9 mm around the involved teeth. To manage the condition, orthodontic treatment was initiated and suitable periodontal treatment was also planned.\nThe patient was prepared for surgery with the infiltration of local anesthesia on the labial and palatal aspects of the anterior maxilla. Full-thickness mucoperiosteal advancement flaps along the gingival sulcus on the labial side extending into the cleft were elevated [] as the incision would go all the way into the cleft. A similar process was done for the palatal aspect too. Careful elevation was performed by placing sharp periosteal elevators along the labial and palatal surfaces of the alveolus into the cleft, and two separate labial and palatal flaps were hence obtained. The epithelial attachment present inside the cleft was removed by debridement, and the cleft alveolus was exposed []. With the use of round and tapered fissure burs, holes of 0.5–1.0 mm diameter were driven adjacent to the cleft, both labially and palatally, from the coronal to the apical parts to ensure regional accelerated phenomenon.[] Ten milliliters of fresh autologous blood was obtained from the patient, and the PRF membrane was prepared according to the conventional Choukroun protocol[] []. To avoid a second site for the procurement of autologous bone graft, a demineralized freeze-dried bone allograft (DFDBA) was placed in the cleft area. The PRF membrane was mixed with the graft and the amnion membrane was placed over it and stabilized with sling sutures [Figures and ]. The two separate edges of the full-thickness flap were closed with interrupted sutures in the labial and palatal areas []. Subsequently, a pack was placed, proper postoperative instructions were given, and medications such as antibiotic amoxicillin 500 mg for 6 days and analgesics such as Imol and acecloren-p possessing both anti-inflammatory and painkiller properties along with chlorhexidine mouthwash for 15 days were prescribed. The case was followed up for a period of 2 weeks, 3 months, and 6 months [Figures -]. |
A 29-year-old military male basic trainee (71 inches, 200 pounds, BMI 27.89) presented with a one-month history of atraumatic bilateral leg pain. He reported pain within the first week of initiating running at basic training. He was diagnosed with bilateral proximal tibia stress fractures at three weeks with instructions to stop impact activities. After failure of his symptoms to improve, he was referred to our facility. On presentation, he had tenderness about the medial aspect of each proximal tibia. Radiographs obtained at that time demonstrated bilateral proximal tibia stress fractures with varus alignment about each knee and articular collapse of the left tibial plateau. Metabolic labs were obtained and significant for a low vitamin D (15), but the remainders of labs including calcium, thyroid-stimulating hormone (TSH), and testosterone were unremarkable. MRI of the left knee demonstrated a medial tibial plateau fracture with two millimeters of articular depression and extension of the fracture to the tibial spine (). MRI of the right knee demonstrated a hypointense linear T2 signal surrounded by diffuse hyperintense signal suggesting a medial tibial plateau stress fracture with surrounding bone edema, without articular collapse or extension (). These fractures were at the level of the physis, and there was surrounding sclerosis on plain radiographs. Given the collapse of the articular surface in his left knee, the patient was indicated for open reduction internal fixation with allograft bone. The patient underwent the aforementioned procedure without complication, and the patient remained nonweight bearing to his bilateral lower extremities (). At the time of surgery, the bone at the fracture distal to the articular surface was softer and more friable in composition than expected for the stress fracture. It was easily debrided back to stable, healthy bone edges, and we were interested in analyzing its composition, so a biopsy was obtained and sent to the lab for analysis. Histology demonstrated nonossifying hyaline cartilage with admixed fibroconnective tissue consistent with a persistent physis ().\nAt the six-week follow-up visit after the procedure on his left knee, the patient was still having significant pain in his right lower extremity and, after extensive counseling, elected to undergo the same procedure on the contralateral limb in an effort to return to running and continue his military career (). We suspected that a similar pathology of a persistent physis was present in the right proximal tibia and that this was contributing to his slow healing progression. Similar intraoperative pathology specimens were again obtained at the fracture site distal to the articular surface (), and these demonstrated fragments of purple to purple-gray staining matrix with chondroid metaplasia. This presence of cartilage distal to the articular surface was consistent with a persistent physis.\nAt four-and-a-half months from the index procedure (three months from the staged procedure), the patient was ambulating without assisted devices and had painless range of motion from 0 to 120° in each knee with well-healed incisions, maintained hardware and alignment, but had not returned to impact activities. Due to his status as a basic trainee, he was released from active duty at six months' time postoperatively and was lost to follow-up. |
An 84-year-old man accidentally fell at home and was admitted to our hospital. The patient was hospitalized with several problems such as multiple metastases of prostate cancer, chronic heart failure, emphysema, impaired renal function, and biliary stent placement due to idiopathic biliary stenosis. While no fracture was identified, the patient complained of lower back pain and was unable to move. As a consequence, he was hospitalized for the purpose of pain management. On the third day of hospitalization, the patient developed a fever of 38.2°C, and his laboratory data showed high levels of WBC count and CRP. While the source of infection was not identified, a urinary tract infection was suspected because he had purulent urine from previous examination and no symptom of respiratory tract infection. The patient underwent treatment with CMZ 1 g every 12 hrs. Three days after therapy initiation, the fever declined and the laboratory data of the inflammatory response normalized. Although blood culture was negative, we decided to treat according to sepsis because he was frail. We, therefore, planned to administer CMZ for 14 days. During the treatment course, the patient did not develop fever and had a healthy appetite.\nOn the morning of the 14th day of hospitalization, the patient complained of a sudden difficulty in breathing. His peripheral artery oxygen saturation decreased to 74%. No fever, coughing, or sputum was identified. A chest computed tomography (CT) scan was performed, showing the presence of ground glass shadows bilaterally (). While the blood work demonstrated the absence of an inflammatory response, Hb decreased by 1.5 g/dL from the previous day. The BNP value was 103 pg/dL, similar to that at initial hospitalization. Because hemostasis of the blood sampling site was difficult, additional laboratory tests were performed. These showed a marked prolongation of PT-INR (). In the evening, his value of Hb dropped from 6.8 to 5.5 g/dl in six hours. We doubted gastrointestinal bleeding, but there was no black stool. Additionally, he began to spit bloody sputum. We considered bronchoscopy but could not carry out because of his poor respiration. Since the patient had an acute respiratory failure accompanied by blood sputum and progressive anemia without exacerbation of heart failure, he was diagnosed with pulmonary alveolar hemorrhage due to coagulation abnormality. Two units of red blood cell concentrates stored in mannitol adenine phosphate and six units of fresh frozen plasma were immediately administered to the patient.\nWe believe that the pulmonary alveolar hemorrhage was caused by disseminated intravascular coagulation (DIC) due to the prostate cancer. However, the patient did not meet the DIC's diagnostic criteria because each level was fibrinogen 393.8 mg/dL, fibrinogen degradation products (FDPs) 23.0 ug/dl, and platelet count 15.3 × 104/uL, even though PT-INR indicated extremely abnormal value (). We took into consideration the possibility of Vit K deficiency. To overcome this issue, we administered 10 mg menatetrenone per day. Three days later, all coagulation systems had recovered to their normal values (). Protein induced by vitamin K absence-II (PIVKAII) reached 8,884 mAU/mL (normal range below 40 mAU/mL) by the 23rd day of hospitalization.\nBased on these observations, we investigated the cause behind the Vit K deficiency. The prescription drugs had not been changed before and after hospitalization, and antiplatelet and anticoagulant agents had not been used. The only additional drug used during hospitalization was CMZ. Furthermore, the patient's food intake remained unchanged in the course of the hospitalization as well as his hepatobiliary system's laboratory tests. No diarrhea developed during the patient's illness. Based on these observations, the patient was diagnosed with hypoprothrombinemia due to CMZ inhibition of Vit K epoxide reductase. Despite discontinuation of Vit K (menatetrenone) administration, the coagulation activity did not decrease. The pulmonary alveolar hemorrhage gradually improved, and the patient was discharged after one month.\nOne month after discharge, the patient was rehospitalized with pneumonia. He was treated with sulbactam/ampicillin 3 g quaque 12 hrs for 7 days, but hypoprothrombinemia was not observed. |
A 36-year-old female patient with end-stage renal disease due to chronic nephritic syndrome had been treated with various dialysis accesses for over 8 years. She complained of dyspnea and had a thrombosed autogenous radial artery-cephalic fistula for 1 day. Significant medical history included failed tunneled cuffed hemodialysis catheter in both internal jugular vein and dialysis grafts in both upper extremities over 8 years, along with severe secondary hyperparathyroidism leading to bilateral femoral neck fracture and lack of movement of the lower extremities for 6 months. On physical examination, swelling of the face and lower extremities, along with tenderness and limited motion of both hip joints, No other significant findings were detected. The results of laboratory tests as following: parathyroid hormone 1396.8pg/mL, albumin 37.8 g/L, serum creatinine 1125umol/L, and hemoglobin 109 g/L. Liver function and coagulation function were within the normal range. A Doppler cardiac ultrasound revealed total cardiac enlargement with decreased left ventricular contractile function. A radiograph of the pelvis found bilateral femoral neck fracture.\nJugular vein venograms demonstrated superior vena cava occlusion, is not treatable using a smart stent. Upper extremity venograms demonstrated occlusion of the left internal jugular, and right cephalic vein. Placement of a left femoral vein catheter established temporary hemodialysis access. Due to bilateral upper extremities failed to find an adequate outflow vein and the patient's history of central venous occlusion, we decided to perform a left femoral artery to right femoral vein dialysis access utilizing a prosthetic graft and autologous cephalic vein.\nThe patient was placed in the supine position. Using a longitudinal incision on the right arm, the thrombosed cephalic vein was harvested. The thrombosed cephalic vein was cut open and its inner hyperplasia was removed. We reconstructed the cephalic vein preparing for anastomosis with the left femoral artery and prosthetic graft. The left femoral artery and right femoral vein on both sides were dissected through small groin incisions. Then, the left femoral artery and right femoral vein were exposed. The graft was then tunneled through the hypogastric region below the umbilicus. An end-to-side anastomosis was performed between the left femoral artery and reconstructed cephalic vein. Then, end-to-end anastomosis was performed between the reconstructed cephalic vein and prosthetic graft (Figs. and ). The bottom anastomosis was carried out with the same suture, end-to-side with the common femoral vein. Ultimately, a drainage tube was placed and all the wounds closed in layers. The patient experienced bleeding (750 mL) and received an autologous blood transfusion (600 mL).\nPost-operatively, the patient received aspirin 100 mg daily. The graft was used for hemodialysis 3 weeks after the operation. There was no edema of the lower extremity through the immediate postoperative period as well as at follow up. On follow up, the patient has been using the access for 9 months with no complication of thrombosis, infection, or bleeding. |
A 57-year-old asymptomatic man with no significant past medical history was found to have an enlarged cardiac silhouette on a routine chest radiograph (). Magnetic resonance imaging (MRI) revealed a 9 cm pericardial cyst in the right cardiophrenic angle that was associated with right atrial compression (Figures , , and ). Although the pericardial cyst wall showed contrast uptake, no uptake within the cyst was observed on first-pass or delayed images. There was no compression of the airway or superior vena cava (SVC) and the pericardial cyst had not eroded into the heart. The patient was not at high risk for hydatid cysts and he did not have any history of fever, suggesting that an infectious cause for his pericardial cyst is unlikely. He did not have any history of chest trauma or intrathoracic surgery. The absence of hypertension, hematuria, and a positive family history made a diagnosis of autosomal dominant polycystic kidney disease (ADPKD) unlikely. The patient was scheduled for resection of the pericardial cyst using VATS. Preoperative electrocardiographic findings, complete blood count results, serum creatinine levels, liver function tests, and serum electrolyte levels were normal.\nOn the day of surgery, the physical exam, including heart and lung auscultation, was unremarkable and the vital signs were within normal limits (blood pressure of 119/75 mmHg, heart rate of 83 beats per minute, respiratory rate of 14 per minute, blood oxygen saturation of 97% on room air, and temperature of 36.9°C). A left radial arterial line and two large-bore intravenous catheters were placed. The patient was adequately hydrated with intravenous administration of normal saline. He was transferred to the operating room and placed in the supine position on the operating table. The standard American Society of Anesthesiologists monitors were placed on the patient. The pericardial cyst did not compress the patient's right bronchus or the SVC, and therefore, he was able to tolerate the supine position with no shortness of breath or hemodynamic instability. The patient was preoxygenated and general anesthesia was induced by slow intravenous administration of etomidate 0.2 mg/kg and fentanyl 1 μg/kg. Neuromuscular blockade was achieved by intravenous administration of succinylcholine 1.5 mg/kg. Ephedrine 0.1 mg/kg was administered following induction to minimize the hemodynamic effects of the induction agents and positive pressure ventilation. A 37-French left-sided double-lumen endobronchial tube (DLT) was placed. The patient was placed in the left lateral decubitus position. Anesthesia was maintained with oxygen (fraction of inspired oxygen of 0.6), air, and sevoflurane (1 minimum alveolar concentration). The right lung was collapsed and neuromuscular blockade was induced with rocuronium 0.6 mg/kg. A 1-cm incision was made in the posterior axillary line at the fifth intercostal space. A metal port was placed and a 10-mm, 30° thoracoscope was placed through the incision. A 2-cm incision was made above the fifth intercostal space at the mid axillary line to access the cyst. The pericardial cyst was found to be firm, and had some calcifications on the surface (Figures , , and ). The cyst was easily separated from the pericardial fat. However, it was attached to the anterior chest wall. Following separation of the cyst from the anterior chest wall some bleeding occurred from the distal right internal mammary artery. The bleeding was controlled with Enseal and clips. The cyst was large, and hence, access to the superior aspect of the cyst was difficult. Therefore, an 18-gauge needle was used to aspirate the cyst fluid. Approximately 300 ml of brown, murky, nonodorous fluid was aspirated from the cyst before it was completely resected (). The patient remained hemodynamically stable throughout the procedure and the DLT was removed in the operating room at the end of the procedure. Postoperative pain was managed with an intercostal nerve block using 10 ml of 0.5% bupivacaine and patient controlled analgesia pump using hydromorphone (intravenously, 0.2 mg every 10 minutes). The patient's postoperative course was uneventful, and he was discharged on postoperative day 1 in a stable condition. Cyst fluid cultures were negative. |
An 87-year-old man with a past medical history significant for chronic obstructive pulmonary disease (COPD), myelodysplastic syndrome (MDS) and subsequent anemia of chronic disease, pulmonary nodule, obstructive sleep apnea (OSA), coronary artery bypass grafting (CABG), and percutaneous coronary interventions (PCI) for coronary artery disease presented with over a year history of exertional dyspnea that had progressed in the last few weeks before his presentation.\nOur patient had been a one pack-per-day smoker for 50 years with a remote past history of occupational asbestos exposure. The first CABG was complicated by disruption of the left phrenic nerve and left-sided diaphragmatic paralysis leading to severe dyspnea. The patient followed in cardiology clinic for his numerous cardiovascular comorbidities. Over a year before the patient’s presentation, he was admitted for dyspnea that was diagnosed as secondary to acute on chronic symptomatic anemia in the setting of recurrent epistaxis with a background of MDS. History of a recent prior admission with symptoms of angina but an unremarkable nuclear stress test prompted the primary team to perform an exercise stress echocardiogram to investigate his dyspnea. The stress test was limited by dyspnea with pulse-oxygen saturation ranging 92%-96% on room air and was negative for both electrocardiographic and echocardiographic evidence of ischemia at the achieved workload. On the echocardiographic imaging part of the test, it was noted that the inter-atrial septum was aneurysmal. A subsequent complete transthoracic echocardiogram (TTE) confirmed that the inter-atrial septum was aneurysmal with no color Doppler evidence of an ASD. The estimated ejection fraction on both these investigations was recorded to be 60%-65%. Over the course of time following this admission, the patient underwent multiple hospitalizations for diverse complaints such as weakness, rectal bleeding, hematuria, urosepsis, syncope, and fever. During this period of time, he also underwent multiple follow-up echocardiograms that showed no significant changes when compared to prior studies. It was only until a month prior to his current presentation that a transesophageal echocardiogram (TEE) with agitated saline contrast revealed a large PFO with a substantial right-to-left inter-atrial shunt and a hypermobile inter-atrial septum (Figure ).\nOn his current presentation, the patient stated that his dyspnea was worse whenever he would be up and moving. He had received two units of packed red blood cells two weeks prior to his admission to the hospital. In the emergency department, his vital signs were noted to be stable, and there was no hypoxia at rest. Laboratory studies were remarkable for a hemoglobin level of 8.2 g/dL, a decrease from approximately two months’ prior hemoglobin level of 9.6 g/dL. Chest x-ray showed no acute cardiopulmonary process at play. Electrocardiogram (EKG) showed no acute ST-T wave changes. The patient was transfused one unit of packed red blood cells and admitted to the hospital medicine floor for further management. Anemia work-up confirmed anemia of chronic disease in the setting of MDS with mild folate deficiency, and he was started on folic acid replacement therapy.\nDuring the course of his admission with multiple episodes of arterial desaturation on ambulation, pulmonology was consulted. On bedside evaluation of the patient by pulmonology, he was noted to have an abrupt oxygen desaturation as checked on a pulse oximeter upon standing to 86% on room air. Significant shunting was evidenced on a bedside shunt study using supplemental oxygen at 100% FiO2, and hypoxemia was noted upon sitting from a supine position. This observation along with the recent TTE findings of a large PFO made the patient a good candidate for further exploration and a possible eventual closure of the PFO. He was subsequently scheduled for a TEE for a better view of his heart and the great vessels. The TEE showed estimated ejection fraction (EF) of 65% and a large PFO with right-to-left inter-atrial shunt (Figure ).\nBased on these developments the primary team decided to perform right heart catheterization and PFO closure. He had a 25-mm Amplatzer PFO occluder device placed with intracardiac echocardiographic guidance without any immediate complications. The implanted PFO occluder device was noted to be in stable position with trivial residual inter-atrial shunting on the morning after the procedure (Figure ). Patient was instructed to follow up with his cardiologist within two weeks of discharge. His symptom of positional dyspnea improved dramatically, and he stopped having any changes in his blood oxygen saturation with different positions of the body. And on multiple occasions post-PFO closure, his pulse oximeter reading was never noted to be below 96%. |
A 62-year-old woman (Figure , II-3) was admitted to the hospital for recurrent partial headache with weakness of one side and aphasia for about 45 years. In her first attack, the patient suddenly experienced an aura with visual disturbances which she described as increasing scotomata in the bilateral visual field. After a few seconds, the patient developed a serious headache, mainly located on the left side. After a few minutes, she presented a paralysis of the right side and speech difficulties accompanied by dizziness and vomiting. These symptoms resolved after about 2 h. After this initial onset, she had an attack nearly every 4–5 years, and the clinical presentations of her attacks were always similar to the first one. The duration of the aura symptoms and the migraine was typically 1–2 h but sometimes the migraine could last up to 4 days. Sometimes headaches occurred before the hemiplegia and aphasia. Each headache was accompanied by dizziness and vomiting but without loss of consciousness. In most attacks, this patient experienced additionally a flushing of the neck and face and felt that the skin temperature of this affected area was increased, but the temperature was never measured. These symptoms may be related to an extracranial vasodilation when a migraine attack occurred. She did not undergo regular treatment except for simple analgesics as a symptomatic therapy. Recently, her condition aggravated as the frequency of attacks increased from once every 4–5 years to once every 1–2 weeks which had a serious impact on her everyday life. Therefore, during a severe migraine attack, she visited our hospital. We reviewed her family history, and we found that three other subjects, her mother, brother, and nephew, had similar clinical symptoms (Figure ). Their presentations are as follows:\nThe proband's mother (Figure , I-2) died of uremia at the age of 72. According to her husband and children, she reported typical hemiplegic migraines since an age of 14 years with five attacks per year on average. The aura symptoms were similar to those in the proband, including bilateral visual symptoms (scotomata), speech difficulties, and hemiparesis.\nThe proband's 55-year-old brother (Figure , II-1) had first at the age of 15 headache attacks with nausea, vomiting, visual field defects, and one-sided motor weakness. Usually, these attacks last 5 h. The disease presentation was progressive with age.\nThe proband's nephew (Figure , III-1), a 25-year-old fitness coach, had first headache attacks with visual symptoms (scotomata) and lateralized motor weakness at the age of 13. Each attack lasts about 20 min.\nAfter admission, her neurological examinations were unremarkable and brain magnetic resonance imaging (MRI) and Magnetic Resonance Angiography (MRA) showed no meaningful abnormalities (Figure ). Thus, the suspected diagnosis was transient ischemic attack (TIA). During her hospitalization, the patient had several migraine attacks that were characterized first by visual symptoms, then aphasia and right limb paralysis 10 min later, and finally severe headaches after 20 min. At that time, the neurological examination revealed: no loss of consciousness, motor aphasia, muscle strength 2 in the right limb, and normal findings in the examination of the residual nervous system. After about 1 h, the symptoms of the aura were relieved, while the headache lasted for about 1 day. However, the symptoms were not relieved after dual antiplatelet aggregation treatment, and transthoracic echocardiography and carotid ultrasound failed to identify any underlying cerebrovascular etiology. After careful consideration of all aspects, she was diagnosed with hemiplegic migraine. So, we conducted a genetic test on the patient and found a heterozygous point mutation (c.4495T>C) in exon 26 of the SCN1A gene. This mutation caused amino acid 1499 to change from phenylalanine to leucine (p. Phe1499Leu), which may cause the disease by affecting the SCN1A protein function.\nTo establish the diagnosis, we performed a genetic test on those family members to analyze for the presence of mutations in genes including CACNA1A, ATP1A2, and SCN1A related to FHM. We only found a gene mutation in SCN1A, but this mutation was detected in all affected subjects in this family (Figure ). Therefore, this patient was diagnosed with FHM3. She was discharged after receiving a health education on migraine attacks, which suggested her staying away from stress, bright lights, sleep disturbances, physical exertion, and alcohol consumption because these have all been reported as trigger factors in FHM (). Upon being discharged from the hospital, she had intermittently taken flunarizine capsules and rizatriptan benzoate tablets to prevent and control migraine attacks. After 6 months of follow-up, the efficacy of the drug was uncertain, because the frequency of headache attacks was not adequately reduced. After the low efficacy of her medication became clear, we consulted again the literature and consider now a trial with lamotrigine or acetazolamide (). |
In May 2014, a 48-year-old male, working as bus driver, underwent occupational evaluation. He was asymptomatic for chest pain and dyspnea and declared smoking habits and no history of other cardiovascular risk factors. He was HIV positive. He referred to a previous access for a twenty-minute-long chest pain episode at emergency department two months before; nevertheless he was discharged after six hours on the basis of a normal ECG () and negative serum cardiac markers, with indication for ambulatory exercise stress test and invitation to stop smoking. Yet in the subsequent period he felt well and decided to hold over any other examination.\nDuring the occupational evaluation the routine ECG showed sinus rhythm, 60 bpm, and normal R-wave progression in peripheral and precordial leads, with biphasic T wave in V2-V3 and deeply inverted T wave in V4-V5; negative T wave was also present in aVL (). Therefore he was advised with early cardiological assessment. These findings were suggestive of Wellens ECG pattern [], strongly associated with critical stenosis of proximal left anterior descending artery, meaning a very large amount of myocardial tissue at risk of necrosis and subsequent sudden death.\nIn this case a rest echocardiography showed no regional contractility anomaly without evidence of valvular and pericardial disease. Thus the patient was admitted to cardiovascular department with indication for coronary angiography. The exam revealed critical stenosis of proximal left anterior descending (LAD) artery, first and second diagonal branch, and subcritical stenosis of intermediate branch (); at same time ventriculography confirmed normal ventricular contractility (). He underwent successful percutaneous coronary angioplasty with placement of multiple drug eluting stent at critical lesions levels and discharged safely two days after with indication of best drug therapy, strong advice in smoke cessation, and regular cardiovascular follow-up.\nWellens' syndrome is characterized by previous history of angina, minimal or no elevation of serum cardiac markers, biphasic or deeply inverted T wave in leads V2-V3, sometimes extended in leads V1 and V4–V6, no pathological Q wave, no loss of precordial R-wave progression, and minimal or no ST-segment elevation during pain-free presentation and it is recurrently associated with pseudonormalization of the described pattern during angina. As underlined by Movahed [], this electrocardiographic cluster, associated with critical LAD stenosis, was first described in patients undergoing exercise stress test by Gerston in 1979, who named it “exercise induced U-wave inversion,” although the ECG alterations only interest the latter phase of T wave; Wellens [] described the same pattern at rest two years later in a more extensive population affected by angina, obtaining the world wide eponym for the syndrome, still described in both terminologies by different authors. The pathophysiology of this ECG genesis is likely due to repetitive and uneventful episode of transmural myocardial ischemia-reperfusion in the large territory of left anterior descending artery, associated with edema of myocardial wall [], while the described T wave pseudonormalization during angina is the expression of the ongoing large transmural myocardial ischemia []. The prompt recognition of this ECG pattern has paramount implication for the correct management of the patient, as it likely underlines the presence of proximal LAD critical stenosis [], avoiding both acute complication and chronic coronary disease progression. This consideration implies both early coronary angiography in pain-free patient presenting at outpatient clinic with this ECG characteristics (after careful exclusion of other myocardial and pericardial cause by echocardiography) and prolonged and mindful observation of ECG pattern variation in chest pain patient with normal ECG presenting at emergency department in the close period following angina. An inappropriate discharge in this setting will easily translate into a very high risk of myocardial infarction and sudden death; at same time the indication for exercise test would represent the double hazard of delayed diagnosis and lethal ischemia-related ventricular arrhythmias. |
A 29-year-old military male basic trainee (71 inches, 200 pounds, BMI 27.89) presented with a one-month history of atraumatic bilateral leg pain. He reported pain within the first week of initiating running at basic training. He was diagnosed with bilateral proximal tibia stress fractures at three weeks with instructions to stop impact activities. After failure of his symptoms to improve, he was referred to our facility. On presentation, he had tenderness about the medial aspect of each proximal tibia. Radiographs obtained at that time demonstrated bilateral proximal tibia stress fractures with varus alignment about each knee and articular collapse of the left tibial plateau. Metabolic labs were obtained and significant for a low vitamin D (15), but the remainders of labs including calcium, thyroid-stimulating hormone (TSH), and testosterone were unremarkable. MRI of the left knee demonstrated a medial tibial plateau fracture with two millimeters of articular depression and extension of the fracture to the tibial spine (). MRI of the right knee demonstrated a hypointense linear T2 signal surrounded by diffuse hyperintense signal suggesting a medial tibial plateau stress fracture with surrounding bone edema, without articular collapse or extension (). These fractures were at the level of the physis, and there was surrounding sclerosis on plain radiographs. Given the collapse of the articular surface in his left knee, the patient was indicated for open reduction internal fixation with allograft bone. The patient underwent the aforementioned procedure without complication, and the patient remained nonweight bearing to his bilateral lower extremities (). At the time of surgery, the bone at the fracture distal to the articular surface was softer and more friable in composition than expected for the stress fracture. It was easily debrided back to stable, healthy bone edges, and we were interested in analyzing its composition, so a biopsy was obtained and sent to the lab for analysis. Histology demonstrated nonossifying hyaline cartilage with admixed fibroconnective tissue consistent with a persistent physis ().\nAt the six-week follow-up visit after the procedure on his left knee, the patient was still having significant pain in his right lower extremity and, after extensive counseling, elected to undergo the same procedure on the contralateral limb in an effort to return to running and continue his military career (). We suspected that a similar pathology of a persistent physis was present in the right proximal tibia and that this was contributing to his slow healing progression. Similar intraoperative pathology specimens were again obtained at the fracture site distal to the articular surface (), and these demonstrated fragments of purple to purple-gray staining matrix with chondroid metaplasia. This presence of cartilage distal to the articular surface was consistent with a persistent physis.\nAt four-and-a-half months from the index procedure (three months from the staged procedure), the patient was ambulating without assisted devices and had painless range of motion from 0 to 120° in each knee with well-healed incisions, maintained hardware and alignment, but had not returned to impact activities. Due to his status as a basic trainee, he was released from active duty at six months' time postoperatively and was lost to follow-up. |
A 22-year-old woman with a known history of giant cell tumor of the left first metatarsal was evaluated for worsening left medial midfoot pain. She had previously undergone curettage and polymethylmethacrylate (PMMA) cementation of a biopsy-proven giant cell tumor of the first metatarsal two and a half years prior at a different institution. Six months following the index surgery, she had a recurrence treated with repeat curettage, liquid nitrogen local adjuvant, and placement of bone substitute graft. After the second procedure, she was ambulatory, but occasionally used a boot for comfort and avoided high-impact activities. Physical examination demonstrated a prominent first metatarsal base and a well-healed dorsal incision. She exhibited tenderness to palpation throughout the area of the scar.\nRadiographs of the left foot showed an expansile, radiolucent lesion of the first metatarsal base surrounding the known cement implantation of the first metatarsal (). Magnetic resonance imaging showed a large soft-tissue mass surrounding the first metatarsal circumferentially and abutting the second metatarsal (). There was high T2 signal with no T1 signal changes at the base of the second metatarsal. Computed tomography (CT) scan demonstrated an expansile lucency at the proximal aspect of the first metatarsal base toward the dorsal lateral side (). There were some areas of cortical breach, and the bone was expanded and abutting the base of the second metatarsal. There was no evidence of direct extension into the second metatarsal or areas of osteolysis within the second metatarsal base. She was diagnosed with a second recurrence of giant cell tumor of bone of the first metatarsal base. As the tumor was recurrent, with destruction of the articular surface and little residual bone of the first metatarsal base, a wide resection of the tumor was recommended.\nThe procedure began by harvesting iliac crest bone graft (5 cm in length, 2 cm in depth). The prior dorsal incision was extended along the entire first metatarsal and proximally across the tarsometatarsal (TMT) joint. A wide resection was performed by disarticulating the TMT joint, maintaining periosteal coverage surrounding the metatarsal, and osteotomizing the metatarsal about 4.5 cm from the TMT joint. The damaged cuneiform articular surface (from articulation with cement) was resected with a wafer osteotomy. The resection bed was treated with adjuvant thermal necrosis. Margins were extended further with 10% hydrogen peroxide. The first toe was held in appropriate length and rotation and pinned to the second metatarsal. The iliac crest graft was fashioned to fit appropriately, contouring the angles for an appropriate junction. The graft was secured with an anatomic plate and screw construct (Figures and ).\nNonweight bearing was maintained until the three month postoperative visit, at which time she began weight bearing as tolerated through the heel and 50% weight bearing through the forefoot with a removable boot. Four months following her operation, she was advanced to full weight bearing as tolerated in the boot. Five months after surgery, she began weight bearing as tolerated in a regular shoe and nonimpact exercises. Nine months after surgery, plain radiographs and CT demonstrated osseous bridging at both the proximal and distal graft sites with no signs of tumor recurrence (). At one year following surgery, she denied pain in the left foot and was able to complete all activities of daily living without difficulty. Eighteen months following surgery, the patient had no left foot pain, was exercising without difficulty, and there was no radiographic evidence of recurrence. The patient was informed that data concerning the case would be submitted for publication, and she agreed. |
A 56-year-old female never-smoker initially developed persistent cough, sputum and progressive dyspnea approximately 1 month before the diagnose NSCLC stage IV. The radiograph and computed tomography (CT) of the chest showed a 2.2-cm soft tissue mass in the right upper lobe with multiple small nodules in the bilateral lungs. A case of lung adenocarcinoma with bilateral intrapulmonary metastases was diagnosed. The patient received two courses of systemic chemotherapy with paclitaxel and cisplatin. However, the chemotherapy had to be discontinued due to paclitaxel-induced hypersensitivity reaction. Thereafter the patient refused further chemotherapy. One year later, after receiving two cycles of first-line chemotherapy, the patient visited the emergency room with an abrupt onset of stuttering, quadriparesis and dyspnea. A spontaneous pneumothorax in the left lung and multiple brain metastases were noted. After a chest tube insertion in the left lung and a 30-Gy whole brain irradiation for brain metastases, the treatment with gefitinib was started with a 250-mg daily dosage and continued for the following 15 months because the patient showed an improvement of symptoms and pulmonary function. Although the primary mass in the right upper lobe with multiple metastatic nodules slightly decreased in size after one month gefitinib treatment, the development of new multiple cystic changes was detected on the follow-up high-resolution CT (HRCT) scan. The pulmonary function 9 months after the initiation of gefitinib therapy showed combined severe obstructive and restrictive ventilatory disturbances (predicted forced expiratory volume at timed interval of 1 second [FEV1] 36%, predicted forced vital capacity [FVC] 31%). Due to a poor performance status neither bronchoalveolar lavages nor histological evaluations were available. In contrast to the gradual progression of parenchymal cystic changes in both lungs were on the follow-up chest CT scan a radiographic regression of the main lesion of NSCLC and metastatic nodules noted (). Simple chest radiographs showed diffuse multiple various sized thin walled cysts and illdefined nodules in bilateral hemi-thorax after the gefitinib therapy. A fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography scan taken 7 months after the use of gefitinib demonstrated a significant increased FDG uptake in the primary lesion only. No uptake was seen in other areas of both lungs, suggesting an interval improvement of metastatic lesions (). Because the patient's condition was tolerable with improved respiratory symptoms, the therapy with gefitinib was continued for 15 months with the patient's approval, despite of the air cystic changes in both lungs. During the follow-up period, neurologic recovery was noted and the patient underwent pulmonary and physical rehabilitation therapies. A follow-up pulmonary function was performed 13 months after the initiation of gefitinib therapy and more improvement was shown than after 9 months (FEV1, 56%; FVC, 53% vs. FEV1, 36%; FVC, 31%) respectively. |
Our patient was a two-month-old male referred for evaluation of a left postauricular mass, present since birth. Workup by the patient's pediatrician including an ultrasound suggested a cystic mass prompting referral for surgical excision. The parents endorsed noticing the lesion at birth and that it had been painless and slowly progressive. Physical exam demonstrated a firm 2 × 2 cm subcutaneous lesion of the postauricular region. An MRI was obtained demonstrating a 2.3 × 1.4 × 2.2 cm well-defined solid mass involving the outer table of the right temporal bone and temporoparietal suture with intense peripheral enhancement and without restricted diffusion (). Initial resection in the operating room was undertaken, and a deep plane between the mass and skull was identified and followed reflecting the lesion off of the skull. Unfortunately, pathology demonstrated focal presence of tumor cells at the peripheral margin. The patient underwent a repeat resection, with a canal wall up mastoidectomy. The lesion was again resected en bloc, and the underlying cortical bone was drilled down to the inner table of the temporal bone with healthy appearing bone stock. Despite clinically normal-appearing bone, the pathology again demonstrated presence of tumor cells at the soft tissue margins, and clinically the patient demonstrated significant regrowth of the lesion. The patient returned to the operating room once more, with a fairly impressive progression of gross tumor, nearly 2.5 × 2.0 cm (). A revision mastoidectomy was performed, and neurosurgical consultation was obtained. The mass was excised en bloc resulting in a full-thickness craniectomy. The dura appeared healthy and unaffected by the tumor (). The wound was closed primarily, and the patient was observed overnight in the PICU before being discharged home postoperative day one in stable condition. The patient developed purulence at his incision site one month postoperatively requiring intra-washout with neurosurgery. The infection resolved without further complication or treatment requirement. He was seen at six months postoperatively with no evidence of disease in good condition. |
A 48-year-old male was diagnosed with a Stanford A aortic dissection when he presented to an emergency department with hemodynamic instability and a history of sudden-onset severe chest pain. A computed tomography aortogram (CTA) revealed an acute type A aortic dissection involving the aortic root, arch, and the rest of the aorta down to the left external iliac artery. The dissection flap also extended into the brachiocephalic trunk, left common carotid, and proximal left subclavian artery (LSA). There was complete occlusion of the left internal carotid artery while the right carotid artery supplied the entire anterior circulation through the intact circle of Willis; the posterior circulation was supplied by both vertebral arteries. Swiftly after diagnosis, he underwent emergency ascending aortic replacement and re-suspension of the aortic valve as a first step.\nPostoperative surveillance CTA showed progression of the dissection in the left common carotid and LSA and coeliac artery dissection and re-entry into the false lumen of the thoracic aorta from the abdominal aorta []. Magnetic resonance angiography confirmed the findings on the CTA. The initial plan was to replace the aortic arch, however intra-operative assessment prompted deferring the patient to a staged procedure using endovascular technology in conjunction with surgical debranching of the innominate artery and the left common carotid artery using a Y-graft attached to the ascending aorta interposition graft.\nPostdebranching CTA showed good results of the debranching procedure, but subsequent studies showed progressive dilatation of the descending thoracic aorta, and at 6 months, there was an increase in the dimension of the arch of aorta from 44 cm × 47 mm to 44 cm × 52 mm [].\nIn light of these findings, a consensus was made to use a customized stent-graft for reconstructing the dissected and expanding arch segment. There were also concerns that it would be difficult to transpose or bypass the dissected LSA []. A fenestrated aortic stent-graft was custom-made with a side hole to accommodate a side branch stent-graft at the level of the offspring of the LSA. This configuration was chosen to provide both successful sealing and firm lasting aortic reconstruction.\nPoststenting of the aorta, the patient had an uneventful postoperative period and was discharged from hospital within 4 days. There was surveillance computed tomography scans up to 4 months after the operation, confirming flow in the LSA and sealing of the entry point in the aorta.\nIn a staged fashion after surgical repair of the proximal aorta, endovascular reconstruction was performed of the aortic arch and descending aorta. A customized 250 mm × 28/26 mm Bolton Medical RELAY stent-graft and a Fluency 12 mm × 40 mm stent-graft were utilized.\nUnder fluoroscopic control, the fenestrated stent-graft was navigated toward the orifice of the left subclavian; its position was double checked by virtue of metallic markers before deployment. After deployment, the fenestration was then cannulated through the left brachial access using a 0.035 Terumo wire before a Fluency graft was placed through the fenestration into the LSA. For this procedure, access was obtained through the right common femoral artery and the left brachial artery. The right femoral artery was accessed through a cut down, as this was thought to be safer than the percutaneous approach in a patient with an aortopathy and dissection. Since the LSA was also dissected, the true lumen was confirmed using transesophageal echocardiography (TOE) in conjunction with fluoroscopy and injection of contrast.\nThe patient was heparinized to obtain an activating clotting time of ~ 350. The LSA orifice was confirmed using a balloon catheter [] which also served as a marker for positioning of the aortic stent before deployment. Ensuring that the orifice was aligned with the LSA lumen, the aortic stent-graft was deployed under rapid ventricular pacing to decrease blood pressure and avoid a wind-sock effect.\nGuide wires were passed from the lumen of the aorta into the LSA before a covered Fluency stent was placed into the LSA and deployed under fluoroscopy and TOE. Postdeployment of the LSA stent, there was no leakage of contrast from the true to the false lumen in the LSA. |
The patient “ES” was a 71-year-old white female diagnosed with cervical disc herniation at the levels of C5-6 and C6-7. MRI results confirmed this diagnosis. She presented to physical therapy with complaints of left upper extremity tingling and achy feeling with symptoms radiating to the 5th digit of the left hand. The patient reports the upper extremity achy feeling has been present for around three months along with cervical soreness. ES’s past medical history includes a left mastectomy in 1991 which led to adhesive capsulitis in the left shoulder, and a history of neck pain for about 2 years. She reports using an over the door traction unit at home for a total of 15 minutes twice a day with 10 pounds for about a week now. She reports that the home traction has helped maintain her symptoms, where her symptoms have not become worse, yet have not resolved.\nES presented to physical therapy with a pain level of 3/10 on the VAS pain scale in her neck, she had an achy feeling in her left upper extremity and some tingling in her 5th digit of the left hand. She reported her pain increases with sleeping and computer work and her pain decreases with traction. The patient presented with tenderness to palpation on the right upper trapezius. All upper extremity dermatomes were equal and symmetrical bilaterally within normal limits. Active ROM of the shoulders was taken in supine (see ). Goniometric measurements were taking for shoulder flexion, abduction, internal rotation, and external rotation. Range of motion measures were performed using standard techniques.\nCervical active ROM was obtained seated (see ). Range of motion measures were performed using standard techniques. Other cervical ROM was within normal limits.\nUpper extremity strength was assessed in a seated position graded on a 0–5 scale and grip strength was obtained using a hand dynamometer (see ).\nSpecial tests assessed included: empty can which was positive on left upper extremity, Hawkins Kennedy test also positive on left upper extremity, cervical compression test with an increase in distal symptoms, and cervical distraction which centralized her symptoms. Lastly ulnar neural tension tested in supine was found to be negative, indicating no adhesion of the ulnar nerve along the path through the upper extremity.\nEvaluation of the results of ES’s initial examination shows decreased ROM of cervical spine and upper extremity, decreased strength in left upper extremity, and pain and tingling in left upper extremity all consistent with cervical disc herniation of C5-6 and C6-7. The results also show a possible impingement at the brachial plexus. It was felt that the patient had a good potential for rehabilitation due to prior level of functional, uncomplicated past medical history, early onset of diagnosis, and good motivation in participating in therapy.\nES received outpatient therapy in a clinic for 7 treatments over a 4 week period. Her intervention began at the end of the initial evaluation where she received intermittent mechanical cervical traction in supine for 15 minutes with cervical flexion of 25 degrees and traction was applied for 45 seconds at 14 pounds and released to 10 pounds for 15 seconds. ES was also given a home exercise program of cervical lateral flexion stretch, unilateral wall stretch for the pectoralis muscles that could be the cause of the impingement at the brachial plexus, and to continue with her home traction unit. Throughout her therapy, ES continued to receive mechanical cervical traction increasing the degree of cervical flexion to 30 degrees, increasing the weight of intermittent traction to 10–16 pounds, and increasing the amount of time to 20 minutes. Chin tucks, standing rows with thera-band, and scapular stabilization exercises were also added in the progression of therapy.\nAfter 4 weeks of outpatient physical therapy treatment, ES was able to return to her premorbid lifestyle. Her pain level decreased to 0/10 on the VAS scale for the neck and upper extremity. The achy feeling and tingling of the left upper extremity and hand had resolved. ES’s shoulder and cervical active ROM both increased to achieve normal functional limits with no pain. Left upper extremity strength also increased to be comparable to the right upper extremity. Lastly grip strength also increased (see ). ES was able to return to all functional activities that were giving her difficulty prior to treatment such as: sleeping without pain, fastening her bra, performing yard work/gardening, and she was also able to lift using her left upper extremity. The patient was discharged with a home exercise program of all the exercises given during treatment and with instructions to continue cervical traction with her home traction unit. |
In February 1996, a 40-year-old Caucasian woman consulted an orthopaedic surgeon because of persistent pain in the right foot. On radiograms, a lytic tumoral process was discovered in the right os naviculare. Curettage was performed, and anatomopathological revision of the obtained tissue at the Mayo Clinic Rochester (Dr. Unni) confirmed the diagnosis of a clear cell chondrosarcoma (). In June 1996, local progression of the disease was discovered and an amputation of the right lower leg was performed. Subsequently, she was followed with annual chest X-ray examination and clinical examination by her treating orthopaedic surgeon.\nIn April 2016, her chest radiogram showed a new dense opacity in the left upper lung lobe. On CT scan, two opacities in the left upper lobe were detected, with a diameter of 6 mm and 3 mm, respectively (). After multidisciplinary consultation, close follow-up was advised given the aspecific and small diameter of the lesions. Three months later, only one lesion remained on CT scan. Further follow-up with annual radiograms was organised. In December 2019, a slight increase in diameter in the nodule in the left upper lobe was seen. Subsequently, a new CT scan was performed, which showed a single nodule of 13.5 mm. Apart from a dry cough, the patient was asymptomatic at the time of this finding. A lung function examination was performed and showed no abnormalities. Further staging with an abdominal CT showed no other lesions suspected for metastases. There was no history of smoking. A CT-guided lung biopsy was performed, and the patient was referred to our tertiary sarcoma centre for further diagnostic examination and treatment because of the probable diagnosis of a chondrosarcoma metastasis.\nAt the time of referral, the patient was in good health and had no symptoms other than a transient dry cough. She did not have complaints of weight loss or exhaustion. Clinical examination showed no abnormalities besides the lower right leg amputation after surgery for the chondrosarcoma.\nHistopathological examination of the lung biopsy showed the presence of an atypical chondroid tumoral proliferation composed of atypical spindled to rounded chondroid cells embedded in a chondroid matrix (). No obvious clear cell morphology, high-grade cytonuclear atypia, or mitotic activity was observed in this biopsy. Immunohistochemically, the atypical cells showed a diffuse expression of S100 and Podoplanin (D2-40). These morphological and immunohistochemical findings were suspected for a metastasis of a chondrosarcoma.\nAfter discussion in our multidisciplinary bone and soft tissue sarcoma board, a video-assisted thoracoscopic wedge resection was performed. Histopathological examination of the resected lung nodule showed a 15 mm large, well-circumscribed chondroid tumoral proliferation composed of atypical rounded cells with a centrally placed, large round nucleus and abundant clear to slightly eosinophilic cytoplasm. Intermingled within these atypical clear cells, osteoclast-like giant cells, a chondroid matrix, and calcifications were observed. The atypical cells stained strongly with antibodies against S100 and Podoplanin (D2-40), further confirming the diagnosis of a lung metastasis of the known clear cell chondrosarcoma ().\nShe recovered well from surgery. Given the extended time frame between the primary tumor and the development of this single lung metastasis (20 years) and the insensitivity of clear cell chondrosarcomas to chemotherapy, a conservative approach was held with regular imaging as follow-up, meaning a chest CT every six months during the first year. |
An 84-year-old man accidentally fell at home and was admitted to our hospital. The patient was hospitalized with several problems such as multiple metastases of prostate cancer, chronic heart failure, emphysema, impaired renal function, and biliary stent placement due to idiopathic biliary stenosis. While no fracture was identified, the patient complained of lower back pain and was unable to move. As a consequence, he was hospitalized for the purpose of pain management. On the third day of hospitalization, the patient developed a fever of 38.2°C, and his laboratory data showed high levels of WBC count and CRP. While the source of infection was not identified, a urinary tract infection was suspected because he had purulent urine from previous examination and no symptom of respiratory tract infection. The patient underwent treatment with CMZ 1 g every 12 hrs. Three days after therapy initiation, the fever declined and the laboratory data of the inflammatory response normalized. Although blood culture was negative, we decided to treat according to sepsis because he was frail. We, therefore, planned to administer CMZ for 14 days. During the treatment course, the patient did not develop fever and had a healthy appetite.\nOn the morning of the 14th day of hospitalization, the patient complained of a sudden difficulty in breathing. His peripheral artery oxygen saturation decreased to 74%. No fever, coughing, or sputum was identified. A chest computed tomography (CT) scan was performed, showing the presence of ground glass shadows bilaterally (). While the blood work demonstrated the absence of an inflammatory response, Hb decreased by 1.5 g/dL from the previous day. The BNP value was 103 pg/dL, similar to that at initial hospitalization. Because hemostasis of the blood sampling site was difficult, additional laboratory tests were performed. These showed a marked prolongation of PT-INR (). In the evening, his value of Hb dropped from 6.8 to 5.5 g/dl in six hours. We doubted gastrointestinal bleeding, but there was no black stool. Additionally, he began to spit bloody sputum. We considered bronchoscopy but could not carry out because of his poor respiration. Since the patient had an acute respiratory failure accompanied by blood sputum and progressive anemia without exacerbation of heart failure, he was diagnosed with pulmonary alveolar hemorrhage due to coagulation abnormality. Two units of red blood cell concentrates stored in mannitol adenine phosphate and six units of fresh frozen plasma were immediately administered to the patient.\nWe believe that the pulmonary alveolar hemorrhage was caused by disseminated intravascular coagulation (DIC) due to the prostate cancer. However, the patient did not meet the DIC's diagnostic criteria because each level was fibrinogen 393.8 mg/dL, fibrinogen degradation products (FDPs) 23.0 ug/dl, and platelet count 15.3 × 104/uL, even though PT-INR indicated extremely abnormal value (). We took into consideration the possibility of Vit K deficiency. To overcome this issue, we administered 10 mg menatetrenone per day. Three days later, all coagulation systems had recovered to their normal values (). Protein induced by vitamin K absence-II (PIVKAII) reached 8,884 mAU/mL (normal range below 40 mAU/mL) by the 23rd day of hospitalization.\nBased on these observations, we investigated the cause behind the Vit K deficiency. The prescription drugs had not been changed before and after hospitalization, and antiplatelet and anticoagulant agents had not been used. The only additional drug used during hospitalization was CMZ. Furthermore, the patient's food intake remained unchanged in the course of the hospitalization as well as his hepatobiliary system's laboratory tests. No diarrhea developed during the patient's illness. Based on these observations, the patient was diagnosed with hypoprothrombinemia due to CMZ inhibition of Vit K epoxide reductase. Despite discontinuation of Vit K (menatetrenone) administration, the coagulation activity did not decrease. The pulmonary alveolar hemorrhage gradually improved, and the patient was discharged after one month.\nOne month after discharge, the patient was rehospitalized with pneumonia. He was treated with sulbactam/ampicillin 3 g quaque 12 hrs for 7 days, but hypoprothrombinemia was not observed. |
The patient was a 16-year-old male with a past medical history significant for severe factor VII deficiency who presented with a several months' history of iron deficiency anemia requiring multiple blood transfusions and positive Hemoccult stool tests. His history extends back to when he was around 10 years of age and was found to have severe iron deficiency anemia also with Hemoccult-positive stool, so that he was referred to pediatric gastroenterology for evaluation. An extensive workup was done at the time that included upper endoscopy, colonoscopy, Meckel's scintigraphy, a nuclear medicine bleeding scan, and capsule endoscopy. The nuclear medicine bleeding scan showed some increased uptake in the second portion of the duodenum, but his upper endoscopy was visually normal and the remainder of his workup all came back within normal limits. Throughout this time, he was treated with multiple, repeat blood transfusions and was managed by pediatric hematology.\nAt the time of presentation, he was receiving approximately 2–3 blood transfusions per week as well as iron transfusions, but his blood work continued to worsen. His hemoglobin level had dropped to 8.6 g/dL with a hematocrit level of 27.7%. His ferritin level had also reached a low of 12.7 ng/mL with a reticulocyte count elevated at 4.5%. His Hemoccult stool tests continued to remain positive. He underwent an upper gastrointestinal barium contrast study with small bowel follow-through in anticipation of a repeat capsule endoscopy for further evaluation that was ultimately read as normal. During capsule endoscopy evaluation, it was discovered that he had a large polypoid growth in approximately the third portion of the duodenum, just proximal to the ligament of Treitz, that was actively bleeding (Fig. ). At that point, it was decided that a repeat upper endoscopy would be performed with possible enteroscopy and polypectomy. The patient was admitted to the hospital the day prior to the procedure with pediatric hematology consulted for administration of NovoSeven RT to help with bleeding control due to his factor VII deficiency. During the upper endoscopy, a large polypoid lesion was noted near the ligament of Treitz that had a notable clot from a prior bleed but no other abnormal surrounding mucosa (Fig. ). The tissue was extremely friable, and based on the size of the lesion as well as its position in the duodenum, combined with the patient's bleeding disorder, it was felt that it would be safer to remove the polyp via surgery with partial bowel resection rather than endoscopic polypectomy. The lesion was biopsied once with cold forceps and was then tattooed and the patient was given several doses of factor VII for hemostasis. The next day, surgery was consulted, and the child was taken back to the operating room for robotic resection. A small 2- to 3-cm section of jejunum near the ligament of Treitz was ultimately resected and a primary end-to-end anastomosis was created with no significant bleeding or any other complications. The bowel section was sent to pathology and the patient recovered without concerns. He was started on high-dose proton pump inhibitor therapy and discharged home on postoperative day 4. The patient had a pediatric gastroenterology follow-up appointment approximately 2 months after surgery where he was found to be asymptomatic and was eventually weaned off his proton pump inhibitor with no further follow-up recommended. His intestinal pathology came back showing duodenal mucosa with gastric heterotopia that was negative for dysplasia or carcinoma. He continues to be followed by pediatric hematology but is no longer receiving frequent blood transfusions and no longer having any significant gastrointestinal symptoms. |
A 13-year-old female Dachshund was presented to the veterinary clinic at the University of Life Sciences in Lublin, Poland with a history of a soft painless oval-shaped swelling over the left side of the submandibular area that had gradually increased in size over time (Fig. a). The overlying skin was normal and there was no history of trauma or previous surgery in this region. Regional lymphadenopathy was not detected by palpation. According to the owner, the dog had suffered from persistent halitosis due to chronic periodontitis for several years. The dog had been treated with antibiotics or received enhanced treatment for periodontitis such as instrumental debridement and ultrasonic scaling several times during this period. An intraoral examination confirmed the existence of numerous lesions of the oral mucosa and advanced periodontal disease (Fig. b).\nAn ultrasound examination of the neck region was performed with the use of a linear 7.5 MHz transducer. The examination revealed the presence of an anechogenic cystic lesion in the left mandibular salivary gland measuring approximately 2.5 × 1.3 cm. Normal mandibular tissue was only partially visible. Changes were not observed in the right mandibular gland or in other neck tissues, including the lymph nodes, which were oval in shape and hypoechoic to the adjacent tissue.\nNext, abdominal and thorax radiography was performed in dorsoventral and lateral recumbency, as well as abdominal ultrasonographic examination. These examinations did not reveal any significant changes. Based on the history and the physical and ultrasound examinations, a preliminary diagnosis of a mandibular gland cyst was established.\nTranscutaneous needle aspiration of the left mandibular gland was carried out and a saliva-like fluid obtained. Microscopic evaluation of fluid revealed numerous, mobile trophozoites of trichomonads, mucus and aggregation of eosinophils. Swabs were also taken from gingival pockets and revealed the presence of trichomonads and a mixed bacterial flora.\nThe aspirated fluid was examined bacteriologically for aerobic and anaerobic growth and for yeast cultures but was found to be without growth.\nThe aspirated cystic content as well as swabs from gingival pockets were inoculated on a diphasic medium for cultivation of trichomonads: solid phase composition: 9 ml heat-inactivated horse serum, 1 ml 3 % beef extract, and 0.2 g glucose; liquid phase composition: 0.59 g Na2HPO4, 0.45 g KH2PO4, 8.0 g NaCl, dissolved in 1000 ml distilled water. The complete medium was allocated in sterile 10 ml tubes, supplemented with rice starch and 0.5 ml heat-inactivated horse serum. The media were cultivated at 37 °C and examined under light microscope every 24 h. Positive cultures were used for morphological characterization based on scanning electron microscopy. Trophozoites were prepared according to standard procedure for protozoa cells modified according to Szczepaniak []. In brief, trichomonads were isolated by centrifugation 2500×g for 5 min and fixed with 2.5 % glutaraldehyde in 0.1 M cacodylate buffer pH 7.2 for 2.5 h. Afterwards, the trichomonads were washed in phosphate-buffer saline and allowed to adhere to glass coverslips precoated with 0.1 % poly-l-lysine and post-fixed for 2 h with 1 % OsO4. Fixed samples were dehydrated in ethanol and acetone, dried in a critical point using a Polaron CPD 7501 critical-point dryer and coated with gold/palladium (Au/Pd) in a Polaron Range SC7620 sputter coater. Examinations were carried out using a ZEISS Ultra Plus scanning electron microscope.\nPeriodontal pocket swabs showed significant growth of trichomonads in the xenic culture in contrast to the cyst aspirate, which showed slow and poor growth. Undoubtedly, there are factors, which may influence the growth of trichomonads in vitro, such as low numbers of cells in the inoculum; but in the present study many trophozoites were found by direct microscopy of the aspirate. Because the aspirate was negative for bacteria and fungi, we hypothesise that the growth of trichomonads from the aspirate was compromised by the lack of bacteria. While some trichomonads such a T. vaginalis can be established directly into axenic cultures, others species (especially from alimentary track) require adaptation in monoxenic or polyxenic cultures, which is usually time consuming and laborious process [, ].\nObservation of trichomonads from a positive culture (5 days after inoculation) by light microscopy and scanning electron microscopy revealed numerous trophozoites and a single spherical, non-flagellated pseudocyst. The trophozoites varied in shape from piriform to spherical with four anterior flagella and a fifth recurrent undulating membrane and axostyle (Fig. ). Accurate assessment of flagella size was difficult due to the large number of starch granules and bacteria. The major morphological features were typical for genera trichomonas or tetratrichomonas []. As detection and identification of trichomonads by conventional techniques are noticeably less reliable than PCR [, ], we chose to use molecular methods for taxonomical identification. The analyses were performed on the aspirate and the classification was based on the analysis of the partial sequence of the gene encoding in the SSU rDNA and the ITS region (ITS1, 5.8S rDNA, ITS2), after performing PCR with the primers TFR1 (5′-TGC TTC AGT TCA GCG GGT CTT CC-3′) and TFR2 (5′-CGG TAG GTG AAC CTG CCG TTG G-3′) according to the protocol described by Felleisen []. PCR products of approximately 370 bp were obtained from both samples (cystic content and gingival packet).\nThe DNA sequence was determined directly from the PCR products on both strands using the same primers employed for PCR at a DNA sequencing core facility (Genomed S.A., Warsaw, Poland). The obtained sequences were analysed using the Basic Local Alignment Search Tool program (BLASTn) and compared with those deposited at GenBank. The 368 bp fragment showed complete shared identity (100 %) with a sequence of T. tenax (strain—Hs-4:NIH,USA; ATCC 30207) with accession No. U86615.1\nThe owner decided not to bear the costs of treatment and the dog was euthanized by the wish of the owner. The dog was not necropsied. |
A 55-year-old gentleman, ex-smoker, presented to our hospital complaining of mild epigastric pain, regurgitation, and heartburn. On top of that, he has a long-standing history of gastroesophageal reflux disease (GERD), which was managed by proton pump inhibitors. His past medical history was significant for hypertension. He was previously diagnosed with a liver hemangioma based on abdominal ultrasound two years before the presentation. He had no relevant family history. Physical examination revealed mild epigastric tenderness with no palpable abdominal mass. Laboratory data showed no anemia but positive stool occult blood test. Tumor markers including AFP, CEA, and CA 19-9 were all within normal range. Upper GI endoscopy revealed mild esophagitis, Los Angles grade A along with Barrett's esophagus without dysplasia and a 1 cm polyp at the GEJ. A sample was sent for histopathology; the rest of the stomach and duodenum were normal. The patient did not have a previous endoscopy prior to this one.\nInfused computed tomography (CT) of the abdomen and chest showed mild GEJ thickness with no evidence of mediastinal or celiac lymphadenopathy and no signs of metastasis. It also demonstrated a large heterogeneously enhancing mass about 6 × 9.5 cm with central necrosis in the upper abdomen that appears to be originating from the gastric antrum (greater curve). The mass was highly suggestive of GIST based on CT; it was the same mass that was previously misdiagnosed as a liver hemangioma (). Endoscopic ultrasound confirmed the previous findings. However, no biopsy was attempted due to the risk of bleeding.\nHistopathological examination of the GEJ polyp revealed tubulovillous adenoma with elements of adenocarcinoma in situ. The patient was admitted with a provisional diagnosis of early-stage adenocarcinoma of GEJ along with the incidental finding of enlarging gastric GIST. A trial of endoscopic mucosal resection of GEJ polyp was attempted but failed because of the polyp location that created a technical difficulty. Therefore, the patient was taken to the operating room with a plan to perform a wedge resection of the gastric mass and a submucosal resection of GEJ polyp through the same gastric opening. We planned to use frozen section (FS) to document negative margin resection and determine the need for a formal esophagectomy. Intraoperatively; a large (10 × 7 × 6 cm), extraluminal pedunculated mass was found at the posterior wall of the greater curvature of the stomach (). Wedge resection of the gastric mass with negative margins was achieved along with a transgastric submucosal resection of the GEJ polyp. Fortunately, the FS examination of the polyp showed negative margins as well with no evidence of deep invasion. Postoperatively, the patient had a smooth course and was discharged home in a stable condition. The final pathological examination revealed a GEJ polyp around 1.7 × 1.4 × 0.6 cm. Microscopically, there was a focus of invasive adenocarcinoma involving the superficial submucosa of the polypoid lesion, negative margins, and no lymphovascular invasion (T1a NxM0). Furthermore, the gastric wall mass measured around 10 × 7 × 6 cm with a 2 × 1.5 cm stalk. Histopathology revealed encapsulated high-grade epithelioid GIST tumor with negative margins (pT3). The mitotic rate of 6/50 HPF and immunohistochemical stains were positive for DOG1 and CD34 but negative for CD117 (c-Kit) ().\nThe final diagnosis was synchronous early-stage GEJ adenocarcinoma and a high-grade gastric GIST. Therefore, the patient was started on adjuvant imatinib treatment, along with endoscopic surveillance every six months and proton pump inhibitors. |
A 78-year-old lady presented to our service in February 2013 with a 12-month history of a mass over the right eye. The mass had been gradually enlarging but was not associated with any pain or change in periocular sensation. She denied any vision loss, double vision, epiphora, or xerophthalmia. The patient suffered from hypertrophic cardiomyopathy with an implantable defibrillator inserted to maintain cardiac function but was otherwise fit and well.\nOn examination, a firm mass was arising from the palpebral lobe of the right lacrimal gland, underneath the supraorbital rim. Visual field testing and ophthalmoscopy examination were normal. Visual acuity testing using a Snellen chart revealed 20/70 vision in both eyes, which was in a normal range for a person of this age. Cranial nerve, ear, nose, and throat examinations were all normal. A computed tomography (CT) scan reported that the mass was a soft tissue tumour arising from the palpebral lobe of the lacrimal gland but that the orbits and globes were otherwise normal with no tissue compression or invasion ().\nThe entire right lacrimal gland was removed in our hospital under general anaesthetic through an orbitotomy. The expectation was that the tumour would be a pleomorphic adenoma and that removal would prevent future carcinoma development requiring more aggressive surgery with loss of vision. Following surgery the patient made a good recovery and was discharged from hospital the day after surgery. Hypromellose 0.3% eye drops were provided for the right eye to compensate for the reduced lacrimation that would now affect that eye.\nHistopathological assessment of the removed gland revealed that the soft tissue mass within the lacrimal gland was a PCV-ACC (Figures , , and ). Analysis of the specimen did reveal that the carcinoma had been excised in its entirety with sufficient margins of normal tissue surrounding the carcinoma.\nThe patient's case was discussed at our local head and neck cancer multidisciplinary team meeting. When the histological subtype was considered, the meeting advised that a chest X-ray and ultrasound scan of the liver should be performed to assess pulmonary or liver metastases, respectively. Both these investigations were normal and the patient remains under review by our service. No further complications of surgery developed and to date no recurrence or new tumour has developed. |
A 78 year-old woman was consulted to our department because of abrupt onset dysarthria and involuntary movements of her left toes without any accompanying pain two days ago. These symptoms appeared abruptly and simultaneously as like the initial symptoms of stroke. The patient had a past history of hypertension and diabetes mellitus for 20 years, and the medications for these disorders were not changed currently. Her social history was unremarkable and her family history was negative for any other neurological disorders.\nOn neurological examination, she was alert and well oriented. Cranial nerve examination revealed severe dysarthria. Her muscle strength, sensations and reflexes were symmetrically intact in all 4 extremities. There were no pathologic plantar responses. She had an involuntary movement of her left toes which appeared irregularly with various frequencies and intensities. The pattern of involuntary movements was mainly continuous sinuous, wriggling dorsiflexion of the left big toe in combination with intermittent abducting contraction of second toe. The frequency of this involuntary movement was about 2 Hz (Video, Segment 1). She could suppress the movements voluntarily only for a few seconds. However, the patient did not experience any accompanying pain at left leg. There was no “inner” desire to move the limbs. The pattern of this movement was reminiscent of painless legs and moving toes syndrome. These involuntary movements were accompanied by intermittent internal rotation of the ankle and were aggravated by brain activations such as drawing, speaking or thinking (Video, Segment 1). Her initial routine blood tests and cerebrospinal fluid (CSF) studies were unremarkable.\nBrain magnetic resonance imaging (MRI) showed a newly developed cortical infarction in the right superior frontal cortex in comparison with brain MRI which had checked two months before the onset of symptom (). Because she had already been taking an oral antiplatelet agent along with hypertensive medication, she was only treated with conservative management by intravenous hydration for 3 weeks. After two weeks of conservative management, her dysarthria and involuntary movements of the left toes were markedly improved, and then these involuntary movements of the left toes only appeared in the case of brain activation due to such activities as speaking or thinking (Video, Segment 2). Both of her symptoms nearly disappeared one month after conservative management by intravenous normal saline infusion. However, at that time, no electromyography, electroencephalography or follow-up brain MRI were performed because of the rapid improvement and patient’s refusal. |
A 62-year-old man presented to our emergency department due to acute onset chest pain. He originally presented three days earlier with similar symptoms but was released from the emergency department when the cardiovascular workup was negative. His current chest pains were localized to the midsubsternal area. Morphine and nitrate treatment were not effective in relieving his pain.\nThe patient has a history of seizure disorder, high blood pressure, reflux disease, gastritis, hiatal hernia, osteoporosis, and osteoarthritis. He had encephalitis at approximately 18 months of age and a subsequent head injury. At 3 years old, the patient had a large benign brain tumor which was removed. These early incidents resulted in developmental and physical disabilities.\nOn admission his troponin I level was minimally elevated, and D-dimer was elevated. The patient was anemic and an upper endoscopy was scheduled to rule out a gastrointestinal bleed.\nThe endoscopy findings showed evidence of Grade IV esophagitis. The ulcerations extended in the esophagus from 25 cm to 32 cm. A 15 mm linear ulcer was also seen on a hiatal hernia (). The stomach and duodenum appeared normal.\nThe biopsy results of the esophagus showed esophageal squamous mucosa with marked acute and chronic inflammation, granulation tissue, and overlying necroinflammatory exudate. In addition, there were abundant sheets of plasma cells, seen in all biopsy fragments (). The atypical plasma cells demonstrated abundant cytoplasm with eccentrically placed nuclei, some with prominent nucleoli ().\nImmunohistochemical analysis revealed that the plasma cells expressed CD138 and MUM1 and were IgG kappa restricted ().\nA whole body PET/CT scan was subsequently performed. The findings showed a focal area of increased metabolic activity in the midesophagus which may correspond to the biopsy site. An enlarged and abnormally metabolically active lymph node was identified in the left paratracheal position measuring 1.3 cm. There was also an enlarged lymph node identified in the left submental location measuring 1.1 cm.\nA bone marrow biopsy was performed which showed a normocellular marrow with maturing trilineage hematopoiesis. There was no histologic, flow cytometric, or immunophenotypic evidence of clonal plasma cell disorder or significant plasma cell infiltrate.\nThe submental lymph node was removed two months later for histopathologic examination. The histologic evaluation revealed preserved architecture, patent subcapsular sinuses, lymphoid follicles with germinal center formation, and slight expansion of the T-zones (). Focal areas of Castleman disease-like changes were noted ().\nImmunohistochemical stains demonstrated normal distribution of B cell and T cells. Focal plasma cell aggregates were seen and highlighted with CD138 immunostain. There was an excess of kappa-expressing cells with cluster and aggregate formation, therefore low level involvement by a plasma cell process could not be excluded. |
A 28 year-old male was found to have a slightly increased serum creatinine (1.7 mg/dl) during the admission to ER because of abdominal pain. Since both his past medical history and an abdominal ultrasound performed on admission were unremarkable he was discharged with the indication to see a Nephrologist. At the Nephrology outpatient clinic, because of the reduced eGFR and of the presence of proteinuria (300 mg/24 h), an hospitalization for further investigations was planned.\nWhile waiting for the admission, a couple of weeks later, the patient was admitted to the emergency room in another hospital for abdominal pain and dyspnea. On admittance the ECG tracing performed showed sinus rhythm with diffuse repolarization abnormalities. Further exams revealed an increase of troponin (54 ng/ml) and transaminases levels (GOT 50 U/L; GPT 125 U/L) and a cardiac ultrasound showed a severe left ventricular dysfunction with right heart failure. Patient was thus admitted to the coronary intensive care unit. During his hospital stay the possibility of acute myocarditis was excluded because of the absence of a recent viral syndrome and the negativity of IgM antibodies against the viruses most commonly affecting the cardiovascular system and because of the low inflammatory indexes. An abdominal ultrasound demonstrated abdominal and pleural effusions, regular size and morphology of spleen and liver, no pancreatic changes; both kidneys had normal size but showed irregular margins and a reduced thickness of the cortex, no hydronephrosis nor stones were observed. A magnetic resonance demonstrated an increased volume of the cardiac chambers with a severe reduction of the function of both ventricles (EF20%), however no signs of reduced myocardial perfusion, valvular defects or other tissue changes such as inflammation, fibrosis or edema could be demonstrated. A chest CT scan confirmed the presence of pleural effusion and showed parenchymal atelectasias mainly involving the lower lobes of the lungs. The patient was discharged after 11 days on diuretics (furosemide 100 mg/daily), B-blocker (carvedilol 37.5 mg/daily), acetyl salicylic acid (Aspirin 100 mg/day) and an Ace inhibitor (Ramipril 5 mg/day) with a diagnosis of dilated cardiomyopathy and severe left ventricular dysfunction complicated with cardiogenic shock and anasarca. Few days later an EKG ergometric test revealed no areas of inducible ischemia. A further admission to the Cardiology Unit to define the effect of treatment was performed a week later. Cardiac ultrasound confirmed the left ventricular dysfunction (EF 23%), a coronary angiography was negative and a right chamber catheterism and endomyocardic biopsy demonstrated no specific lesion nor inflammatory infiltrate. The patient was then admitted to our Nephrology Unit, as planned, to evaluate the cause of the chronic kidney disease. On admission the patient appeared healthy and well oriented, his blood pressure was 110/60 mmHg, heart rate 56 bpm, physical examination was unremarkable except for a 1/6 intensity systolic heart murmur better audible on mitral valve area. ECG tracing showed sinus bradycardia. Laboratory studies revealed an increased serum creatinine (1.87 mg/dl), eGFR 48 ml/min/1.73 m2, hypercalcemia (serum calcium 11.5 mg/dl), hemoglobin 15.1 g/dl, sodium 135 mEq/L, potassium 4.37 mEq/L, phosphate 3.1 mg/dl, serum albumin 4.07 g/dl. The patient denied use of vitamin D analogs thus in consideration of the unexplained hypercalcemia other exams were performed. Thyroid hormones, calcitonin, vitamin D, serum ACE, phosphate and calcium urinary excretion rate were all within the normal range. PTH was lower than 3 pg/ml. To rule out multiple myeloma serum protein electrophoresis, serum and urine immunofixation, and spine and skull x-ray were performed and did not show any pathological changes.\nRenal biopsy was finally performed without complications and the patient was discharged after 24 h. While waiting for the renal biopsy pathology report, medications were not modified, but for an increase of the dose of furosemide because of the hypercalcemia. The renal biopsy contained eight glomeruli none of which was globally or partially sclerotic and no pathological changes were observed at glomerular level, vessels were also unremarkable. Tubulointerstitium was the only affected compartment with a moderate to severe inflammatory infiltrate, some calcium crystals in the tubular lumen and two granulomas with multinucleated giant cells (Figs. and ). No necrosis could be observed within the granulomas. A diagnosis of granulomatous interstitial nephritis due to sarcoidosis was made.\nWhen the patient was called to discuss his kidney biopsy, his serum creatinine had further increased (3.5 mg /dl), eGFR 22 ml/min/1.73 m2 and so had his serum calcium (13.3 mg/dl), serum albumin 4.06 g/dl. For this reason, he was hospitalized again and treated with pulse methylprednisolone (250 mg/day for three days) and then with maintenance dose prednisone (50 mg/day). Serum creatinine decreased in a few days and so did his serum calcium. Since the episode of acute kidney injury the patient has been followed at our unit and at the unit of Cardiology. Renal function returned to normal (serum creatinine 1.1 mg/dl, eGFR 91 ml/min/1.73 m2) and heart function markedly improved over the following two years (EF 49% vs 37% vs 32% vs 23%). The diuretic and cardiologic therapy was significantly reduced to only 25 mg of furosemide and a small dose of beta blocker. The steroid was gradually tapered to 5 mg/day of prednisone for one year and then stopped. |
A 27-year-old woman was discovered to have a giant retroperitoneal tumor incidentally during her routine obstetric examination at 16 weeks of gestation. Ultrasonographies demonstrated a giant left retroperitoneal tumor measuring 21 × 8 cm that extended from the lower border of the left kidney to the left pelvis. An abdominal routine MRI revealed the giant left retroperitoneal tumor, measuring 16 × 9 cm that extended from the hilum of the left kidney to the left pelvis, the lesion had a close relation with the psoas and iliopsoas, and the left kidney and uterus were compressed laterally. There was no liver metastasis and urinary system and major vessel involvement (Figures and ). All tumor markers were within normal range.\nCore needle aspiration was not performed because the lesion was so consistent with liposarcoma in MRI. The patient was a young woman with firm willing for preserving the fetus. After thorough consultation with radiologist, obstetrician, urologist, and anesthesiologist, considering the MRI revealed no clear evidence of major organ and vessel involvement, and the patient was in her second trimester, we decided to perform the en bloc resection with an attempt for fetus preservation.\nThe laparotomy was performed with left paramedian incision under general anesthesia at 20 weeks of gestation. The giant retroperitoneal tumor located in the left retroperitoneal space extended from the hilum of the left kidney to the left pelvis, without involvement of adjacent muscle, kidney, intestine, and major vessels. The en bloc resection was accomplished with negative surgical margin. The operation lasts 3 h, and intraoperative hemorrhage was 450 ml, with transfusion of 2 u of packed red blood cell. Fetal heart rate under perioperative ultrasonography monitoring ranged from 130 to 150 bpm. Retodrine was administered until 1 week postoperatively. The patient had an uneventful recovery. The final pathology demonstrated a low-grade myxoid liposarcoma with negative surgical margin, mitotic index 5/50 HPF. IHC results showed the following: desmin (−), Ki-67 (<15%), NF (−), vimentin (+), S-100 (−), SMA (−), MyoD1 (−), CD34 (−), CD117 (−), NeuN (−), P16 (−), HMB45 (−), CD68 (−), CD31 (−), calretinin (−), calponin (−) (Figure ). The patient had a planned cesarean section at 37 weeks of gestation and delivered a healthy baby. The patient was under regular follow-up, a CT was taken 6 months following the surgery, and no recurrence was detected (Figure ). |
A 44-year-old Japanese male, an office worker, was transported to our emergency department with a complaint of temporary loss of consciousness. He had experienced fatigue for 3 years and had fallen easily in his daily life starting 2 months before admission. He was feverish and had a cough and phlegm for several days before admission. On the way to work, he felt drowsy and fell down the stairs of the train station, necessitating transport to our hospital by ambulance. The peripheral blood analysis noted mild elevation of white blood cells. The blood chemistry test disclosed mild elevation of C-reactive protein and mild liver dysfunction (). He was thin, i.e., his height was 174 cm and he weighed 52 kg (). Chest computed tomography (CT) showed severe infiltration in the upper posterior fields of both lungs as well as food debris in the esophagus. He was diagnosed as having aspiration pneumonia. His past medical history included diabetes mellitus that had been treated by a local doctor; glycated hemoglobin was approximately 7%. He had experienced ileus six times since age 30 years. He was not married. His father had died of dilated cardiomyopathy at the age of 70 and had also been thin. On the other hand, his mother was healthy but his maternal uncle was diabetic. His younger sister (Case 2) also had mild muscle weakness of the four extremities. Aspiration pneumonia was treated by intravenous administration of antibiotics under conditions of food-take restriction combined with temporary insulin infusion, and the respiratory symptoms subsided. On the neurological examinations after improvement of pneumonia, he presented with typical clinical manifestations of DM1 (), such as forehead balding, hatchet face with bilateral ptosis, nasal speech, mild muscle weakness of the four extremities, handgrip myotonia, and diffuse muscle atrophy. Electromyography performed to test the biceps brachii muscle and femoral quadriceps muscle on the left side revealed frequent myotonic discharges. Because DM1 was strongly suspected, we recommended that, after providing informed consent during genetic counseling, he undergo genetic testing for DM1 together with his younger sister. The number of CTG repeats in the DMPK gene was abnormally expanded to about 600 repeats in the elder brother and about 900 repeats in the younger sister, in contrast to those of healthy individuals who have 5 to 37 repeats (), thereby confirming the diagnosis of DM1 in these siblings (). |
A 32-year-old male was diagnosed with metastatic IMT involving his left lung and chest wall, medial right thigh, right gluteal muscle and omentum ∼1 year after he presented with dyspnea. He was initially treated with prednisone with improvement of his dyspnea for possible eosinophilic pneumonia because of a prominent eosinophil component identified in a bronchioloalveolar lavage specimen. He was then lost to follow-up. Approximately 1 year later, his dyspnea worsened and was accompanied by a palpable mass in his medial right thigh. A biopsy of this lesion was pursued. Multiple pathologists reviewed the specimen and agreed on the diagnosis of IMT. Immunohistochemistry was carried out and identified intense, extensive expression of ALK. Treatment was initiated with crizotinib and resulted in a partial response. Eight months later, he experienced worsening chest pain and dyspnea and imaging studies confirmed disease progression. He was placed on celecoxib, and over the course of 1 month, he experienced significant worsening of his symptoms and performance status decline. He then presented to our center for further management. This patient did not qualify for available clinical trials (NCT01742286, NCT01283516) at the time of his presentation based on his performance status.\nDue to this patient's previous response to crizotinib and ALK expression, arrangements were made with Novartis, the Mayo Clinic Institutional Review Board and the United States Food and Drug Administration to administer ceritinib 750 mg daily on a compassionate use basis. His symptoms of dyspnea and pain significantly improved within 2 weeks of therapy. He developed mild nausea (grade 1) that was controlled with ondansetron and a dose reduction in ceritinib to 600 mg daily. Imaging studies after 8 weeks of treatment demonstrated a significant partial response to treatment that was confirmed 8 weeks later (Figure ). Given the minimal residual disease burden after 6 months of therapy with ceritinib, surgical resection of his pulmonary lesion and ablation of his gluteal lesion were recommended by a multi-institutional Sarcoma Tumor Board to consolidate his significant response. This patient continued with ceritinib in an adjuvant fashion for 18 additional months after its initiation until a left-sided, 18F-fluorodeoxyglucose-avid pleural lesion was identified and confirmed to be recurrent IMT by biopsy. |
The patient, a 59-year-old Chinese woman, was treated at our centre in 1994 for a T3N0M0 nasopharyngeal carcinoma. She was treated with external beam radiotherapy to 60 Gy in 30 fractions over 6 weeks in accordance to ICRU-50. Two lateral parallel opposed fields were used to treat the nasopharynx and upper neck. The lower neck was irradiated with a direct anterior field with a central cord shield and a lower border just below clavicular heads. The junction of the upper and lower field was at the level of hyoid bone. It was followed by a 10 Gy Iridium-192 brachytherapy boost to the nasopharynx. Treatment was completed in May 1994. She remained well with no further recurrence of the nasopharyngeal carcinoma but developed xerostomia and mild fibrosis of the lower neck.\nShe re-presented in December 1999 with a mass in the left supraclavicular fossa and numbness in the arm, but no motor weakness. The mass was located within the area previously irradiated to 60 Gy. Her disease was staged with our standard protocol at the time with MRI of the neck and shoulder, CT of the chest and functional imaging using thallium-201 scintigraphy []. MRI showed a 3 cm × 5 cm mass involving the brachial plexus (Figure ). Open biopsy confirmed pleomorphic spindle cell sarcoma.\nThe management of her case was discussed in our multi-disciplinary meeting. The agreed treatment plan was preoperative radiotherapy followed by en bloc resection. She received an accelerated hyperfractionated course of radiotherapy 48 Gy in 40 fractions (ICRU-50), treating twice a day over four weeks. The radiation field incorporated the brachial plexus and used 6 MV photons in an anterior-weighted, opposed oblique arrangement avoiding the spinal cord. Radiotherapy was completed in February 2000. Restaging investigations showed that the lesion had become more cystic on MRI, but its size had not changed. The degree of thallium-201 scintigraphy uptake had not changed significantly either. The patient proceeded on to surgery four weeks later.\nSurgery in March 2000 consisted of en bloc resection of the tumor along with the left sternomastoid and superior and middle trunks of the brachial plexus. Clavicular osteotomy was necessary to allow dissection of the tumor from the subclavian vessels. Sural nerve grafts were used to restore continuity of nerve supply from C5 and C6 to the suprascapular, musculocutaneous and axillary nerves. A latissimus dorsi myocutaneous flap was raised to close the defect in the neck. The middle third of the clavicle that had been reflected downwards was replaced and secured with a plate and screws.\nHistological examination of the surgical specimen showed evidence of radiotherapy, with large areas of necrosis and hemorrhage seen both macroscopically and microscopically. Comparison was made between the operative specimen and the pre-irradiation biopsy; necrosis was not seen in the pre-irradiation specimen (Figures and ). Surgical excision appeared complete.\nImmediate postoperative recovery was uncomplicated. The patient retained good function in her hand but was left with a flail shoulder and no power in elbow flexion. She thus underwent cable grafting of the musculocutaneous nerve in October 2000, with gradual return of elbow function following this procedure.\nThe patient presented again in December 2001 with pain in the shoulder. X-ray confirmed that there had been non-union of the osteopaenic clavicle, the plate having detached from the lateral end of the clavicle. She returned to theatre and had a bone graft and internal fixation (Figure ). Following this procedure, pain settled and she continues to have good use of her arm, although shoulder movement remains minimal.\nThe patient remains well five years after combined therapy for the PRS, with no evidence of recurrence of either her nasopharyngeal carcinoma or the PRS. The patient had no lymphoedema, neurovascular, severe fibrosis or other significant late effect as a result of re-irradiation. |
The patient was a 34-year-old woman, G4 L2 Ab1 who had married her cousin 7 years ago. She had a history of two normal vaginal deliveries and one abortion in the 1st trimester. The first pregnancy in the age of 28 had terminated with a normal vaginal delivery (NVD) resulting in a term baby girl who weighed 3150 gr. The second pregnancy had occurred two years later; curettage was done at week 6 due to spontaneous abortion. Her 3rd pregnancy was in the age 32 resulting in a healthy term baby girl weighing 3400gr with NVD. Due to her unwillingness for becoming pregnant she had withdrawal contraception, whereas because of the non-occurrence of menstruation during breastfeeding and 6 months after her last pregnancy, a pregnancy test was requested. Due to the positive pregnancy result, ultrasound study was done which revealed a 10-week spontaneous gestation with 4 gestational sacs and 4 fetuses. There was no case of multiple pregnancies in her or her husband's family.\nShe received prenatal care during her pregnancy but there was no need for prophylactic cerclage. At week 24 of gestation she was hospitalized due to premature contractions. The contractions were controlled with the prescription of pethidine and hydration and she was discharged 3 days later. She was once again admitted at 28 weeks of gestation due to similar contractions; this time she was treated with indomethacin and pethidine and discharged 3 days after the contractions suppression. She also received two doses of betamethasone during hospitalization.\nShe was admitted a week later due to labour contractions. In vaginal examination 2 finger dilatation with no effacement was detected. Serum test results were reported all in the normal range and the vital signs during hospitalization were normal. At this stage she was treated with tocolytics (adalat). The fetuses' health was monitored by Doppler ultrasound imaging, biophysical profile and fetal non stress test (NST). After the labour contractions' suppression and due to the presence of sporadic contractions she was monitored while being hospitalized up to the time of delivery.\nAt 32 weeks and 4 days of gestation, due to the resumption of labour contractions and dilatation progression, after receiving the rescue dose of betamethasone, cesarean section and tubectomy (upon the request of the patient and her husband) was performed. The outcome of cesarean section was 4 fetuses, 3 girls and a boy, quadriamniotic and quadrichorionic. Quadruplet A weighed 1820 gram with an Apgar score of 9 to 10; quadruplet B weighed 1810 gram with an Apgar score of 6-7. Quadruplets C and D weighed 2100 and 1980 gram with an Apgar score of 7-8 and 9-10, respectively. Among the 4 neonates, only quadruplet B was transferred to the NICU; she was discharged after 2 days in good health. and show the quadruplets after birth.\nBecause of atonic uterus during the cesarean section, after the administration of the appropriate dosage of oxytocin and methylergonovine and 800µgr of rectal misoprostol, the uterine arteries were blocked and the B-Lynch suture was done. No blood transfusion was required for the mother and her hemoglobin (Hb) level 6 hours after the operation was 9 g/dl; her pre-operational Hb level was 10g/dl. The mother was discharged 3 days after delivery with no complications.\nFor close follow up, the mother and her newborns were visited two weeks after delivery; they were all healthy and had no problem. The infants were visited once again 6 months later revealing normal physical and mental development in all four. shows the babies at 6 months of age.\nThis project has been approved by Ethical Committee and Vice Chancellor for Research of Mashhad University of Medical Sciences (97/429008). |
An 86-year-old woman who had been living with her elderly husband was admitted to our hospital with the complaints of nausea, anorexia, and epigastric discomfort. When she was 73 years old, the patient had undergone laparotomy and right hemicolectomy for resection of colon cancer. Five years after hemicolectomy, she had received hernia repair surgery using mesh for an abdominal incisional hernia. There was no history of abdominal or thoracic trauma. Laboratory tests were all within the normal range. Her electrocardiogram showed no ischemic changes. Although chest X-ray revealed an abnormal gas-filled mass in the left thoracic cavity, the patient had no symptom of dyspnea. Contrast-enhanced computed tomography (CT) scan confirmed herniation of the gastric corpus through the left posterior part of the diaphragm (). We diagnosed adult Bochdalek hernia and planned its surgical treatment. As mesh had been placed under the previous upper abdominal midline incision more than 10 years earlier, dense adhesions between the mesh and abdominal tissues were expected. Therefore, we decided to perform diaphragmatic hernia repair by HALS, considering the patient’s safety. After induction of general anesthesia, the patient was placed in the supine position with her legs apart. The previous midline incision was opened carefully to insert a LAP DISC® (Hakko, Nagano, Japan) for a hand port. Dense adhesions, which had to be divided, were found between the mesh used to repair her incisional hernia and loops of the small intestine. The disk for HALS was placed after complete removal of the mesh. Subsequently, a 12 mm trocar was inserted into the inferior umbilical region for the laparoscope. A 5 mm trocar was also inserted into the left upper abdominal region. Herniation of the gastric corpus into the left thoracic cavity through a hernial orifice in the left posterior diaphragm was confirmed. The gastric corpus could not be pulled back into the abdominal cavity because of adhesions around the hernial orifice. After these adhesions were carefully removed by HALS using Harmonic ACE shears (Ethicon, NJ, USA) (a), the stomach was completely freed and could be returned to the abdominal cavity. A 5 × 3 cm hernial defect with sac was observed (b). We decided to perform simple closure of the defect without mesh reinforcement because the rim of the hernial orifice was relatively strong. Accordingly, the defect was repaired with interrupted nonabsorbable sutures (2-0 Nesporen; Alfresa Pharma Corporation, Osaka, Japan) using a 5 mm port on the left upper abdomen and the surgeon’s left hand via the hand port (c). The midline incision for the hand port was closed without mesh reinforcement. A drain tube was placed under the left hemidiaphragm. The operating time was 244 min and there was no significant bleeding. Her postoperative course was uneventful. The patient was discharged on postoperative day 20. There was no evidence of recurrence at 1-year follow-up. |
A 22-year-old woman with a known history of giant cell tumor of the left first metatarsal was evaluated for worsening left medial midfoot pain. She had previously undergone curettage and polymethylmethacrylate (PMMA) cementation of a biopsy-proven giant cell tumor of the first metatarsal two and a half years prior at a different institution. Six months following the index surgery, she had a recurrence treated with repeat curettage, liquid nitrogen local adjuvant, and placement of bone substitute graft. After the second procedure, she was ambulatory, but occasionally used a boot for comfort and avoided high-impact activities. Physical examination demonstrated a prominent first metatarsal base and a well-healed dorsal incision. She exhibited tenderness to palpation throughout the area of the scar.\nRadiographs of the left foot showed an expansile, radiolucent lesion of the first metatarsal base surrounding the known cement implantation of the first metatarsal (). Magnetic resonance imaging showed a large soft-tissue mass surrounding the first metatarsal circumferentially and abutting the second metatarsal (). There was high T2 signal with no T1 signal changes at the base of the second metatarsal. Computed tomography (CT) scan demonstrated an expansile lucency at the proximal aspect of the first metatarsal base toward the dorsal lateral side (). There were some areas of cortical breach, and the bone was expanded and abutting the base of the second metatarsal. There was no evidence of direct extension into the second metatarsal or areas of osteolysis within the second metatarsal base. She was diagnosed with a second recurrence of giant cell tumor of bone of the first metatarsal base. As the tumor was recurrent, with destruction of the articular surface and little residual bone of the first metatarsal base, a wide resection of the tumor was recommended.\nThe procedure began by harvesting iliac crest bone graft (5 cm in length, 2 cm in depth). The prior dorsal incision was extended along the entire first metatarsal and proximally across the tarsometatarsal (TMT) joint. A wide resection was performed by disarticulating the TMT joint, maintaining periosteal coverage surrounding the metatarsal, and osteotomizing the metatarsal about 4.5 cm from the TMT joint. The damaged cuneiform articular surface (from articulation with cement) was resected with a wafer osteotomy. The resection bed was treated with adjuvant thermal necrosis. Margins were extended further with 10% hydrogen peroxide. The first toe was held in appropriate length and rotation and pinned to the second metatarsal. The iliac crest graft was fashioned to fit appropriately, contouring the angles for an appropriate junction. The graft was secured with an anatomic plate and screw construct (Figures and ).\nNonweight bearing was maintained until the three month postoperative visit, at which time she began weight bearing as tolerated through the heel and 50% weight bearing through the forefoot with a removable boot. Four months following her operation, she was advanced to full weight bearing as tolerated in the boot. Five months after surgery, she began weight bearing as tolerated in a regular shoe and nonimpact exercises. Nine months after surgery, plain radiographs and CT demonstrated osseous bridging at both the proximal and distal graft sites with no signs of tumor recurrence (). At one year following surgery, she denied pain in the left foot and was able to complete all activities of daily living without difficulty. Eighteen months following surgery, the patient had no left foot pain, was exercising without difficulty, and there was no radiographic evidence of recurrence. The patient was informed that data concerning the case would be submitted for publication, and she agreed. |
A 56-year-old man was admitted to Asan Medical Center with a gastric submucosal lesion that was detected by esophagogastroduodenoscopy during a regular check-up (). The overlying gastric mucosa was normal except for a slight elevation, and no associated symptoms were present. His medical and family histories were unremarkable. A complete blood count and serum chemistry tests were normal. A computerized tomography (CT) scan revealed a 5.5-cm low attenuating cystic mass located in the submucosal layer along the greater curvature of the body (). The radiologic differential diagnoses were cystic degeneration of the neurogenic tumor, gastrointestinal stromal tumor (GIST), and gastric duplication cyst. The patient underwent a wedge resection to remove the lesion, and an unilocular cystic mass measuring 5.5×3.5×2.5 cm was identified in the proper muscle layer with smooth and intact overlying gastric mucosa. Thick, yellowish fluid filled the cyst and there were no connections between the cyst and the lumen of the stomach. The cystic wall had a regionally thickened portion (0.6 cm) and its cut surface was firm and granular (). Microscopically, the cystic wall was comprised of all of the layers of the stomach wall (from the mucosa to the muscularis propria). The proper muscle layer of the cyst merged into the proper muscle layer of the stomach, sharing a common wall (). The lining epithelial cells of the cyst were columnar and mucus-secreting cells resembling foveolar cells (). There were multiple foci of high grade dysplasia () and adenocarcinoma showing invasion to the proper muscle layer of the cyst was observed (). The histological features of the carcinoma resembled conventional adenocarcinomas commonly observed in the gastrointestinal tract. The carcinoma did not extend beyond the cyst wall, and neither the proper muscle nor the subserosal layer of the surrounding normal stomach harbored any tumor cells. The overlying gastric mucosa was normal and the resection margins were clear. Three regional lymph nodes were harvested during the wedge resection, which showed no metastasis. |
The patient was a 36-year-old gravida 0 woman. At the age of 7, she underwent ventricular septal defect closure for the right ventricular outflow tract. At the age of 11, she received a mechanical aortic valve replacement. Since after the replacement, she has been receiving warfarin orally at a dosage of 4.5 mg/day. She conceived naturally and she was referred to our hospital for perinatal management. Oral administration of warfarin was discontinued at 5 weeks of gestation and she began self-injection of heparin. At 21 weeks and 5 days of gestation, she was admitted to our hospital with a high risk of spontaneous abortion and was put on intravenous ritodrine. This successfully prevented a miscarriage. At 21 weeks and 6 days of gestation, we started a continuous infusion of 25,000 units of heparin daily. On the 22nd week, transesophageal echocardiography showed a movable thrombus in the aortic valve. The size of the biggest thrombus was 26 × 8 mm (). We increased the dosage of heparin to 28,000 units daily and restarted the administration of warfarin. Following this, the thrombus reduced in size, and at 23 weeks and 5 days transesophageal echocardiography showed no signs of thrombosis in the patient. At 32 weeks and 2 days of gestation, a routine cardiotocography showed a decreased fetal heart rate; thus, an emergency Cesarean section was performed under general anesthesia because of the presence of warfarin in the blood. The baby was delivered, weighing 1,702 g, with an Apgar Score of l at l minute, and 4 at 5 minutes. The total amount of blood loss during the surgery was 1,410 ml. During the surgery, 16 units of fresh frozen plasma (FFP) was transfused; and after surgery, we continued to infuse 20,000 units of heparin daily. On the 11th day after surgery, owing to continuous genital bleeding, heparin administration was discontinued and uterine artery embolization was performed. This treatment stopped the bleeding and on the 21st postsurgical day; we started warfarin administration at 5 mg/day. She was discharged on the 34th postoperative day due to the stable PT-INR levels ().\nThe newly born infant was intubated and admitted to the newborn intensive care unit. At the time of admission, activated partial thromboplastin time was 180 seconds or more and bilateral intracerebral ventricular hemorrhage was detected using ultrasonography. On the first day of life, anemia was observed in the infant and red cell concentrate and FFP were transfused (). We attempted to reduce the infant's dependence on the ventilator and at 8 days of age the infant was extubated. On the postnatal 10th day, a cranial CT scan showed bilateral intraventricular hemorrhage with ventricular dilation and midline shift (). Although convulsions accompanying the intracranial hemorrhage were observed, the infant's general condition was stable and oral feeding was started on postnatal day 10. The newborn was discharged on postnatal day 54. However, the infant later developed cerebral palsy and is currently receiving treatment at our hospital. |
A 40 years old man, was injured in a car accident as a front passenger, occurred during a frontal collision with another vehicle passing illegally in continuous white line down the center of a national road, the impact speed was 100 km per hour. Unfortunately, the patient was not restrained by seatbelt and sustained lower extremity and head impacts without loss of consciousness, he experienced a severe pain in his hips. On presentation to the emergency department, patient was hemodynamically stable and conscious, examination of the chest and abdomen was normal. However, both hips were deformed in flexion, internal rotation and adduction (), without neurovascular deficit or skin lesions of the lower limbs. Radiographs displayed bilateral posterior hip dislocation combined with right femoral head fracture, and small posterior wall fracture of the left acetabulum. () Prompt hips reduction was performed within one hour of presentation through closed manipulation below general anesthesia, curarisation and controlled by fluoroscopy, patient was maintained in supine position on the ground and the aide applied a hand pression on the iliac wings of the pelvis, while the operator exerted a traction on the leg then flexed the hip with adduction and external rotation, the same technique was applied successfully to the second hip. The Left hip was stable up to 100° flexion and 45° internal and external rotation after reduction. However, the right hip was unstable, for this reason, we have positioned a posterior knee splint for temporary stabilization. Reduction of each hip was checked by antero-posterior pelvic radiograph () and CT-scan (). X-ray showed an irreducible right femoral head fracture, but in the other side it showed a concentric reduction of the left hip joint. CT scan showed in the right side a one-third of femoral head suprafoveal fracture Pipkin type II that was anterior, rotated and incarcerated associated with two small fragments; one was superior and the second inferior. In the left side we have detected a minor posterior wall fracture of the left acetabulum without any intra-articular fragments. Surgical treatment was planned next day to accomplish anatomic open reduction of the right femoral head fracture and its internal fixation (ORIF) using a modified Hardinge approach that was chosen because the Pipkin II fragment was switched, therefore its reduction need surgical dislocation of the hip and a wide access to the femoral head. Moreover, this approach is known to have less risk of sciatic nerve injury, preserve the pelvitrochanteric muscles and have less risk of limping in comparison with the conventional Hardinge approach, because we spread the fibers of the gluteus medius just at its anterior middle one-third, preserving a great portion of this muscle insertions and function []. In the operational room, under general anesthesia the patient was placed in the full lateral position with pubic and sacral support, left leg was maintained in extension to stabilize ipsilateral hip, then a modified external approach of Hardinge was performed exposing the fascia lata that was incised in line with skin incision and retracted anteriorly while the gluteus maximus was retracted posteriorly to expose the common tendon of vastus lateralis and the gluteus medius, it was split longitudinally at the anterior third and sharply separated from the greater trochanter. Without extension more than 3 cm proximally to the insertion of the great trochanter to avoid inferior branch of the superior gluteal nerve injury. An anterior flap was formed by the anterior portion of the gluteus medius, the underlying gluteus minimus, and the anterior portion of the vastus lateralis. A T-shaped capsulotomy was performed to release the anterior capsule. The hip joint was then dislocated, and the femoral head fracture was exposed, we have explored a rotated pipkin II fragment and extracted two small parts that had footprints in the not weight bearing area in the distal part of the femoral head (). After cleaning and washing hip joint, we have reduced the Pipkin fragment and fixed them by two small pins that was over-drilled with a cannulated drill bit, followed by osteosynthesis with two Herbert screws, then hip was reduced and the flaps was repaired by transosseuses sutures to the great trochanter layer by layer using a vicryl number 2. Postoperative examination revealed no neurological deficit and the postoperative imaging of the pelvis showed an anatomic reduction of the femoral head fracture and a good position of the two Herbert screws (). The patient was kept on bed rest for three weeks, followed by a further six weeks of right non-weight bearing. At 6 months there was a good fracture healing, the patient had no limited hip motion, without limping and normal return to his daily activity (). Then at one and two years follow up there was no signs of osteoarthritis or avascular necrosis detected on the pelvic X-rays. However, a right hip non-bridging Brooker type I heterotopic ossification was noticed (). |
A 69-year-old male patient, with a three months history of abdominal pain asthenia and macroscopic hematuria, was admitted to the outpatient clinic. Abdominal CT revealed an 8 cm left renal growth suggestive of neoplasia, with the involvement of the tail of the pancreas, tumor thrombus in the left renal vein and multiple left para-aortic adenopathies (). A biopsy was performed and showed to be inconclusive regarding the possibility of renal cell carcinoma. Radical left nephrectomy with distal pancreatectomy and splenectomy was proposed.\nThe procedure (Video 1 in Supplementary data) started with an extensive Cattel-Braasch Maneuver, allowing exposure of the inferior vena cava and the aorta, and thus isolation of the left renal vessels. The tail of the pancreas and spleen were freed, and a no-touch approach [] was adopted to minimize the spread of tumor cells with proximal splenic vein ligation. Caudal splenopancreatectomy was performed with section of the pancreas with a GIA 80 (vascular load), followed by proximal ligation and section of the splenic artery and what was thought to be the left renal artery (). The junction of the left renal vein with the vena cava was opened, and the tumor thrombus was resected, followed by caval suture. The renal vessels were, at this point, presumably controlled. The nephrectomy was continued with the release of the kidney and para-aortic lymphadenectomy, during which only the stump of the left renal vein could be identified, lacking the previously ligated renal artery stump. The renal artery was located inside the mass of lymph node tissue in the left para-aortic space, and the stump belonged to the superior mesenteric artery, ligated flush with the aorta. There was no arterial pulse in the mesentery confirming the injury. After removing the specimen, the distal stump of the superior mesenteric artery was exposed, and a repair with a terminoterminal anastomosis was performed from the proximal stump of the splenic artery (). The viability of the gut was assessed by palpation of an arterial pulse in the superior mesenteric artery.\nThe postoperative period went uneventfully. Histological examination showed a renal sarcomatoid carcinoma pT4N1M0G3. Control imaging at three months showed permeability of the celiac trunk and the superior mesenteric artery (). |
A previously healthy 42 years old male presented to our institute with history of gradually progressive and painless swelling over left calf since two months. He was a non-smoker, laborer by occupation. The patient noticed a firm swelling in calf region of left leg 5 years ago. No history of trauma or infection prior to the appearance of the mass was reported. No family history of any such swelling in the past. Patient was operated for swelling over calf region 20 years back but no records were available. There was a history of gradual increase in deformity of left foot since 3 years and the patient had started walking on toes on left side with no dorsiflexion at ankle joint.\nOn examination, there was a single, non-tender, hyperpigmented scar of size 8×3 cm over mid-calf region fixed to underlying structures. A large, well defined non-tender, firm, swelling was palpable in posterior aspect of left leg measuring about 28×8 cm extending from tendoachilles region up to 5 cm distal to popliteal fossa and medially and laterally up to border of tibia and fibula respectively. The overlying skin was normal with no discoloration and local raise of temperature. Movement of knee joint was normal. There was fixed equinus deformity of left foot (). No inflammatory signs, skin changes or adenopathies were present. No bruits were heard on auscultation. Neurovascular examination of left leg and foot was normal. Laboratory findings were within normal limits. Radiological examination revealed large soft tissue mass with linear and streak-like ossification around the left tibia. MR Angiography () showed arteriovenous malformation in left calf with multiple feeding arteries arising from popliteal, peroneal and anterior tibial artery and large draining veins draining deep into venous system of leg. The tibia and fibula marrow showed normal signal intensity.\nBecause of patient symptoms and with clinical diagnosis of a vascular malformation, a wide surgical excision of the lesion was done. Through a 25 cm longitudinal incision across the calf, posterior compartment muscles were exposed. The mass was found completely involving superficial group of posterior compartment muscles sparing the deep compartment with no attachment to periosteum or bone (). Peroneal artery and vein were found to be embedded in the lesion and thus sacrificed. Plane of dissection was between superficial and deep muscles.\nThe lesion was completely removed along with overlying cutaneous scar with wide surgical margins leaving posterior tibial artery in continuity. Intraoperative, complete dorsiflexion of foot was achieved with intact vascularity of leg. The excised specimen was very hard like bone and had to be cut longitudinally with saw (). Grossly the resected specimen showed ossified tissue covered with skin and soft tissues including muscle, tendons and adipose tissue measuring 15×7×5 cm. The cut surface of the ossified area was grey white, gritty and congested (). Microscopically, it revealed features of a vascular malformation with numerous blood vessels of variable size and shape composed of arteries and veins which were dissecting soft tissues and interstitial planes of skeletal muscle.\nMany of the vessels were thin walled with anastomosing and a sinusoidal appearance. Some of them showed fresh and organized thrombi within this vascular background, extensive osseous metaplasia characterized by mature lamellar bone formation was seen. (). The diagnosis was consistent with arterio-venous malformation with extensive osseous metaplasia. At the time of recent follow up after one year from the operation, no local recurrence of the tumor was demonstrated clinically and radiologically. No restriction of motion of ankle joint was found. Patient is presently walking with a normal gait. |
A 22-year-old female, a case of thalassemia major, was undergoing treatment at our thalassemia day care center. She was on oral iron chelator deferiprone 3000 mg/day in three divided doses for the past 8–9 years and was diagnosed as a case of deferiprone-induced arthropathy of the right knee and hip joint as other causes of arthropathy were ruled out. Rheumatoid factor and ANA were negative. The findings were further confirmed on magnetic resonance imaging. As a result of the pain due to arthropathy, she used to come limping all the way into the thalassemia day care ward and was advised to start with the alternative, oral iron chelator deferasirox. Despite this adverse effect, she was continuing on deferiprone because of nonaffordability of the drug. It was only after the availability of the drug at our pharmacy that she was started on deferasirox at a dose of 750 mg once a day. On day 6 of initiation of therapy, she started with pruritic skin rash that started from the neck and spread downwards to involve the whole body. She reported to us on day 11. On history taking, the patient reported that there was an increase in the number and severity of lesions since then. There was no history of breathlessness, difficulty in breathing or any episode of loss of consciousness. There was no family history of any allergic disease or bronchial asthma. On examination, she was having diffuse erythematous and palpable urticarial lesions all over the body. The lesions were more prominent on the dorsal surfaces. On physical examination, except for mild splenomegaly, the rest of the examination was normal. Laboratory investigations revealed low Hb (10.6 g/dL), normal leukocyte count and platelets. Liver function and renal functions were within normal limits. Oral deferasirox was stopped and the patient was started on oral antihistaminics. The rashes subsided gradually and the patient recovered completely by the 9th day after the discontinuation of deferasirox and initiation of antihistaminic therapy. In order to confirm the cause and type of hypersensitivity, we approached the patient for the skin prick and patch tests, for which she refused to give consent. |
A 61-year-old Caucasian male with a history of T2 N1 M0 squamous cell carcinoma of the tonsil (), curatively treated with surgery and adjuvant radiation therapy six years earlier and with a history of continued smoking and insulin-dependent diabetes mellitus was admitted to the hospital for chest pain. After excluding acute cardiac changes, diagnostic work-up revealed a large mass in the upper lobe of the left lung as well as multiple small nodules in both lungs and multiple osteolytic bone changes, with no evidence of locoregional recurrence in the head and neck region or of enlarged intrathoracic lymph nodes. Histology of the lung mass derived from bronchoscopy showed poorly differentiated squamous cell carcinoma (). No clear differentiation between metastases from the previous head and neck cancer and a second primary tumor could be made. Given the long time interval between the diagnosis of cancer the first time and the new findings with the evidence of tumor cells in the bronchial tree, a therapeutic approach for metastatic non-small cell lung cancer was chosen.\nTreatment consisted of three courses of carboplatin/vinorelbine and monthly zoledronic acid. In the following period of stable disease (no reduction in lesion size), the patient developed three consecutive episodes of pneumonia, each accompanied by elevated C-reactive protein (CRP) levels, and resulting in hospitalisation. During the third episode, almost one year after initial presentation of chest pain, detection of liver and adrenal gland metastases indicated disease progression. Therefore, second line treatment with pemetrexed was initiated. After eight treatments, restaging computed tomography showed stable disease, but was indicative of abscess formation around the right hip (). Distinctly elevated CRP levels were also present. Following drainage, systemic treatment with antibiotics was initiated, yet microbiological examination of the fluid revealed sterile cultures. Six weeks later, the patient developed impaired vision, eventually leading to magnetic resonance imaging (MRI) of the brain. Different sequences were performed: T1-weighted with and without iv contrast, T2-weighted, fluid attenuated inversion recovery (FLAIR) and diffusion-weighted. Two non-contiguous lesions were detected—a large cystic lesion in the right occipital lobe () and a solid lesion in the subcutis (). The low apparent diffusion coefficient (ADC) ratio, peripheral contrast enhancement and T2 hypointensity rim prompted the radiologist to state in his report that occipital lobe abscess was at least as likely as metastasis. The other lesion in the subcutis corresponded to a non-ulcerated 2 cm large nodule by physical examination. During this period, CRP was normal. Given the patient’s history and diagnostic uncertainty, invasive characterisation of the occipital mass and excision of the subcutaneous lesion was attempted in order to differentiate between new metastases and non-malignant causes. The subcutaneous lesion was histologically confirmed as poorly differentiated squamous cell carcinoma (). During stereotactic biopsy, the other lesion was found to be a brain abscess and 15 ml of puriform fluid were drained. Local and systemic antibiotic treatment was initiated. Moreover, this time, the Gram’s stain showed inflammatory cells, but no bacterial or fungal source of infection could be determined. Further fluid evaluations, e.g. for mycobacteria as potentially causative organisms were also negative. Two months later, imaging follow-up showed resolution of the occipital mass, consistent with the diagnosis of brain abscess. |
A 77-year-old male with a past medical history of coronary artery disease status post coronary artery bypass grafting, hypertension, chronic obstructive pulmonary disease, diabetes mellitus type 2, and cerebrovascular accident presented to a local hospital with acute abdominal pain and bloating. A computed tomography (CT) scan of the patient's abdomen and pelvis was performed and showed intraabdominal bleed and multifocal liver lesions. Initial complete blood count (CBC) revealed a hemoglobin of 7 g/dL and he was transfused one unit of packed red blood cells prior to transfer to our institution. On arrival, CT angiogram of the abdomen and pelvis showed multiple dense, heterogeneous masses throughout the liver with associated perihepatic and intraperitoneal hemorrhage and areas of tumor blush were noted but no extravasation was seen to suggest active hemorrhage. There was also multiple enlarged periportal and upper mesenteric lymph nodes, likely representing metastatic adenopathy. There were no lesions present on the pancreas. CT chest was obtained and showed no evidence of intrathoracic metastatic disease. Initial blood work revealed normal liver function tests, appropriate response in hemoglobin to transfusion and negative viral hepatitis panel. Tumor markers revealed AFP elevation to 8705 ng/mL, normal Carcinoembryonic Antigen and Cancer Antigen 19-9. Magnetic Resonance Imaging (MRI) of the abdomen and pelvis showed multiple lesions throughout the liver with targetoid appearance. There was no evidence of cirrhosis and these lesions did not have imaging characteristics of typical HCC (Figure ). It was suspected the multifocal liver lesions were HCC given the elevated AFP. However, the MRI was not consistent with HCC and a liver biopsy was obtained. Pathology results were consistent with poorly differentiated, large cell-type neuroendocrine carcinoma with metastatic disease to the liver (Figure ). The patient had an unremarkable colonoscopy and esophagogastroduodenoscopy six months prior to presentation therefore, it was suspected the primary origin of NET was in the small bowel. Regarding the intraabdominal bleed noted on initial CT scan, this remained stable on repeat scans and surgery recommended conservative management. The planned chemotherapy regimen will be Carboplatin and Etoposide. |
A 44-year old male presented with a visible mass over the dorsal aspect of his right dominant hand. The mass was enlarging gradually for the past 3 months and was painless. No mass was found elsewhere. The patient sought treatment due to his inability to fully flex his right long finger. There was no significant previous history of trauma or similar condition found in the family.\nOn physical examination, we found a visible mass over the dorsal aspect of right hand (over the third metacarpal), which was visibly moving as the long finger was flexed and extended. There was limited flexion as the mass reached the metacarpophalangeal joint region. There were no skin color changes or local change in skin temperature. The mass itself was felt solid-hard with irregular surface and clear border, sized 4 cm × 3 cm and fixed to the extensor digitorum tendon of the long finger. There was no tenderness.\nLaboratory results were insignificant except for the serum uric acid (8.4 mg/dL) and decreased eGFR (81 mL/min/1.73 m2; mildly decreased renal function according to the Chronic Kidney Disease Epidemiology Collaboration calculation). Radiograph examination of the hand region showed a soft tissue mass over the dorsal aspect of the right hand with no calcification.\nWe decided to perform an open exploration to restore the motion of the long finger. The incision was made longitudinally along the dorsal aspect of right hand. Dissection of the tendon sheath of the long finger extensor digitorum revealed a white chalky mass adhering and infiltrating the tendon. We could not completely excise the mass, but we managed to reduce the mass volume so that it does not disrupt the movement of the long finger anymore.\nPost-operatively, active motion of the finger was encouraged and a prescription of allopurinol was given. On 2 months follow-up, the wound healed uneventfully and the lesion did not recur elsewhere. The range of motion of the right long finger was excellent (). |
A 45-year-old woman presented to medical attention for abdominal pain, episodic diarrhea, and a mild weight loss (<10% body weight). Informed consent was obtained from patients included in the study. All procedures performed were in accordance with the ethical standards of our institutional research committee. She underwent a colonoscopy that showed a 4 cm stenosis of the sigmoid colon, covered with pale mucosa that could not be passed by a conventional colonscope (13.2 mm) but could be passed with an enteroscope (9.2 mm) with which the cecum could be reached; the mucosa of the other colonic tract, as well as the mucosa of the terminal ileum, were unremarkable. Random ileal and colonic biopsies were obtained, which were unremarkable as well. Histology of the stenosis showed mild inflammation, mild stromal fibrosis, and architectural disruption. Subsequently, she underwent a computed tomography scan, which showed a mild thickening of the terminal ileum and sigmoid colon. The finding of thickened terminal ileum was further confirmed by a subsequent magnetic resonance imaging enterography, suggestive for Crohn disease (CD) localized at the terminal ileum. Due to the discrepancy of the radiological findings with the initial endoscopic examination, a further colonscopy with retrograde ileoscopy was performed, showing no visible endoscopic signs of inflammation and confirming the sigmoid stenosis. The repeated ileal and colonic biopsy sampling was again not diagnostic, showing a nonspecific pattern of inflammation affecting the sigmoid colonic specimens.\nThe physician in charge of the patient, in view of her clinical history and the radiologic finding of intestinal thickening, reckoned that the patient was affected by CD with terminal ileum and sigmoid colon localization and proposed a therapy immunomodulators: corticosteroids 1 mg/kg for 12 weeks together with antitumor necrosis factor (TNF) infliximab 5 mg at weeks 0, 2, and 6, followed by infliximab alone. After 6 months of treatment with infliximab (5 mg/kg every 8 weeks as maintenance), an endoscopic reevaluation was scheduled, showing a resolution of the stenosis in the sigmoid colon and a normal-appearing terminal ileum. The marked improvement of the sigmoid inflammation together with the finding of fibrosis on the corresponding histology further convinced the physician in charge of the patient in favor of a diagnosis of CD, and the anti-TNF treatment with infliximab 5 mg/kg was continued. After 3 months (9 months after the beginning of anti-TNF), the patient was admitted for obstructive symptoms. A computed tomography suspected neoplasia of ileocecal region. The patient underwent an uneventful ileocecal surgical resection. The surgical specimen consisted of a portion of 8 cm of terminal ileum with the cecum and the vermiform appendix. The ileal wall showed an increased consistency and a diffuse thickening, with cystic-hemorrhagic foci in the perivisceral fat. The ileal mucosa was corrugated and showed a polypoid structure with a wide base (1.5 cm maximum diameter) originating from the submucosa and determining ulceration of the mucosal layer. The ileocecal valve, the cecum, and the appendix were normal, except for a mild lipomatous filling of the submucosa. |
A 59-year-old man with a history of type 2 diabetes mellitus, hypertension, and dyslipidemia was referred to cardiology clinic for evaluation of atypical chest pain. The patient denied any family history of coronary artery disease and had a history of 60 pack years of smoking. Physical examination was normal as was the 12-lead electrocardiogram. He had a recent workup, including transthoracic echocardiography that showed a left ventricular ejection fraction of 60%, stage II diastolic dysfunction and mild biatrial enlargement, and a radionuclear myocardial perfusion imaging stress test that showed no evidence of inducible ischemia or previous myocardial infarction. Patient underwent cardiac catheterization for definite evaluation of coronary artery disease. Selective right coronary angiography with a 6 F right coronary Judkins 4 catheter revealed a common blood vessel from which the right coronary artery (RCA) and the LMCA were arising. The RCA followed its normal course around the atrioventricular groove and the LMCA traveled to the left side of the heart and divided at the level of the interventricular septum giving off a long LADCA and the LCXCA (). Selective left coronary angiography with a 6F left Judkins 3.5 catheter revealed a second short hypoplastic LADCA that ended at the distal end of the proximal third of the interventricular sulcus without giving any branches of significant size (). An aortogram was done to demonstrate the origins of the coronary blood vessels. Four coronary arteries were identified, one arising from the left coronary sinus and the other three originating from a main blood vessel from the right sinus of Valsalva. Left ventriculography showed normal chamber size and wall motion. There was significant calcification of the proximal segments of the RCA, LMCA, the longer LADCA, and the LCXCA without significant diameter stenoses. A coronary computed tomography angiography (CTA) was ordered to further delineate the course of the longer LADCA. Images were acquired with prospective gating on a 64-Multislice detector computed tomography scanner (Somatom Definition, Siemens, Forchheim, Germany) in the craniocaudal direction during suspended respiration at 0.75 mm slice thickness and reconstruction interval, 0.33 second gantry rotation speed, tube voltage 120 kVp, and a peak tube current of 390 mA. Cumulative dose-length product was 651 mGy × cm. Iso-osmolar nonionic contrast material (Omnipaque, GE Healthcare, Princeton, NJ) was used. Premedication with nitroglycerin 0.6 mg SL was administered. No beta blocker was given since heart rate was <70 per minute. CTA demonstrated the LMCA traveling to the left side of the heart behind the right ventricular outflow tract and through the interventricular septum (Figures and ). No angiographically significant stenoses or high-degree calcifications were noted. |
This is a 50-year-old right-handed male, with 33-year history of T6 AIS A SCI from a gunshot wound complicated by chronic pain, left hip and knee heterotophic ossification, and a chronic dislocation of his right hip, who initially presented to the emergency room with a right shoulder mass in September 2014. While he initially noticed the mass about 2 months earlier, he presented for evaluation now because of acute onset of pain, weakness and paresthesias in the right arm. He was admitted to the general medicine service for pain management and underwent an initial work up for his right shoulder mass, including advanced imaging and a core biopsy. Physiatry was consulted due to his functional deterioration that precluded him from returning to his previous independent living arrangement. He demonstrated diffuse, mild weakness throughout the right arm that was variable and seemed to be correlated with his reported pain level, but his most consistent and weakest movement patterns were his grade 4/5 weakness in finger abduction and distal interphalangeal joint flexion. He had reduced pin prick sensation over the volar surface of digits 3–5, palm and forearm of the right arm and hand. He was not able to perform transfers to or from his manual wheelchair due to his level of pain. The magnetic resonance imaging (MRI) revealed a heterogeneously enhancing mass with a maximum diameter of 6.9 cm (Fig. ) that involved the right deltoid and pectoralis major muscles. His core biopsy demonstrated a STS that was classified as a high grade (III) spindle cell sarcoma.\nOncology recommended treatment for his STS with a course of outpatient neo-adjuvant radiation therapy followed by gross total resection with wide margins. Physiatry pre-operative consult focused heavily on functional prognostication. The patient expressed multiple times that he placed the highest priority on return to his previous modified independent living arrangement and not only survival after his STS treatment course. The patient’s personal values combined with the physiatric assessment informed the pre-surgical planning. In particular a decision was made to take a narrower surgical margin around key muscle group (pectoralis major and deltoids) in order to help maintain the man’s manual wheelchair mobility and his ability to independently transfer himself.\nHe completed neo-adjuvant radiation therapy in November of 2014 and underwent radical excision of his right shoulder mass with flap closure that December. He began intensive inpatient rehabilitation after he was given clearance to weight bear through his arm about 8 weeks later. Initially he required total assistance for most ADL’s, including transfers, manual wheelchair propulsion, dressing and toileting. Despite the extensive surgery and radiation treatments, the gentleman was able to return to a functional level, approaching his pre-morbid status (modified independence). He was successfully discharged home to live alone in his accessible apartment complex. |
A 20-year-old right-handed woman presented with pain on her left elbow radiating along the radial side of the forearm since the age of 14. At that time, our young patient had undergone surgical decompression of ulnar nerve at the cubital tunnel for the first time due to ulnar neuritis confirmed by nerve conduction studies. One year later, medial epicondylectomy was performed additionally. Because of poor results, nerve conduction studies were repeated and concluded that there was no ulnar nerve lesion.\nThe young patient presented at our department four years later and she was methodically examined to investigate her chronic pain. At first, a thorough history was taken. Apart from two surgical decompression procedures of the ulnar nerve, she reported no previous elbow trauma and no previous medical history. Physical examination was carried out and revealed full range of motion of the elbow. She had negative Tinel's sign and Phalen's test and no tenderness at the epicondyles.\nSince there were no significant clinical findings; a radiographic examination of her left elbow was undertaken. Radiographs showed an area of dense mineralization along with surrounding reactive sclerosis at the bicipital tuberosity of the radius ().\nTo confirm the diagnosis, further imaging with a three-phase bone scan () and an MRI control of the region was made. The bone scan showed a high tracer uptake during all phases in the proximal end of the radius. The MRI scan revealed an intraosseous lesion that had no expansion at the surrounding tissues.\nSurgical removal of the tumor was decided. The lesion was excised en bloc, under general anesthesia and tourniquet application. We used demineralized bone matrix graft to fill in the gap of the radius. There was no need to transpose the bicipital insertion in the radius.\nPostoperatively, no evidence of elbow instability was observed. The diagnosis of the osteoid osteoma was confirmed histologically.\nSince then, our patient has been pain-free and reports no need for painkillers. There was no need for physiotherapy to obtain full motion of the elbow. The normal follow-up visits for the patient were one after 6 weeks and a second after one year. Eight years after the operation, the patient visited again our outpatient department, had a full range of motion, and reported not consuming any painkillers for her elbow. She was fully satisfied by the operation and the final outcome (). |
A 32-year-old woman, gravida 2, para 0, was admitted to Seoul National University Bundang Hospital at 35 weeks and 5 days gestational age with symptoms of vaginal bleeding in October 2011. Trans-vaginal ultrasonography revealed that the placenta completely covered the internal os. Approximately two thirds of the placenta was located in the posterior wall of the uterus and the remaining portion was located in the anterior lower segment of uterus. When the patient and her husband were counseled about the risk of hysterectomy, they strongly requested preservation of the uterus for future fertility. Therefore, a Cesarean section with prophylactic intraoperative UAE was planned. Under spinal anesthesia, a uterine incision was made transversely at the lower uterine segment. The surgeon could not avoid tearing the placenta before the female newborn weighing 2,465 g was delivered. The torn placental margins and the cut edges of the uterus were clamped by Allis forceps. During the interventional radiologist tried to insert an angiographic catheter into the right femoral artery for four minutes, the surgeon found a diffuse hemorrhage from the torn placental margin and cut edges of the uterus. At this point, the surgeon abandoned the plan of a prophylactic UAE. The surgeon removed the placenta manually and profuse hemorrhage from the placental bed sites developed. Although the implantation site was repeatedly over-sewn with 0-monofilament absorbable suture, bleeding was quite severe, thus a Cesarean hysterectomy was indicated. However, it was decided that intraoperative UAE would be attempted once more before the Cesarean hysterectomy since massive transfusion was successful. The interventional radiologist inserted an angiographic catheter into the right femoral artery and approached both uterine arteries. Embolization with gelfoam was performed under fluoroscopic guidance for bilateral enlarged tortuous uterine arteries (). Fortunately, blood flow decreased on angiography and bleeding through the vagina decreased. At this point it seemed possible to avoid a hysterectomy. The uterine wall was repaired after an additional intraoperative UAE. Estimated blood loss was 5,000 mL and massive transfusion (9 packs of RBC and 3 packs of FFP) was performed during the operation. Although bleeding decreased markedly after two attempts of intraoperative UAE, the patient was transferred to the angiography room for another attempt at UAE. Embolization of the uterine artery was performed with a coil in the angiography room () and then the patient was transferred to the intensive care unit (ICU) for close observation. While in the ICU, the patient received three more packs of RBC and six more packs of FFP as well as cryoprecipitate and platelet. The next day, her hemoglobin level was 10.2 g/dL and vital signs were stable. She was transferred to the general ward for further postoperative care. On the second day after surgery, the patient presented with a fever of 39.1℃ and after a full fever study, her antibiotic regimen was changed. The fever resolved on the fourth day and the patient was discharged from the hospital 10 days after surgery with no other complications. |
A 55-year-old Caucasian male with cirrhosis secondary to hemochromatosis and heavy alcohol use presented with dyspnea on exertion and a resting oxygen saturation of 87%. ABG revealed a PaO2 of 55 mm Hg on room air with a shunt fraction of 20% while on 100% oxygen. A transthoracic echocardiogram with contrast demonstrated an extracardiac shunt consistent with HPS. A CT scan of the chest with contrast demonstrated mild interstitial lung disease, distributed primarily in the periphery and lower lung bases without evidence of arteriovenous malformations. PFTs revealed a mild restrictive ventilatory defect with severe diffusion impairment. A work-up for secondary causes of interstitial lung disease was negative.\nThe patient was placed on home oxygen and listed for OLT with a MELD exception for HPS. Six months after his initial evaluation, his PaO2 had declined to 46 mm Hg on room air and his oxygen requirement increased to 4 L of oxygen. He was treated with garlic 2 grams daily and N-acetylcysteine for HPS and pulmonary fibrosis, respectively. His hypoxemia continued to worsen with a PaO2 of 34 mm Hg on room air, requiring 10 L of supplemental oxygen with exertion. PFTs also demonstrated worsening restriction and diffusion impairment (DLCO 27% of predicted). A repeat CT scan () showed worsening of his basilar and subpleural pulmonary fibrosis. Given his profound orthodeoxia and the observation that his oxygen requirements remained significantly out of proportion to his mild to moderate pulmonary fibrosis, it was felt that the majority of his hypoxemia was still related to his HPS. Nine months later, the patient underwent an OLT. On POD 1, his oxygenation worsened with a PaO2 of 30 mm Hg while on FiO2 1.0 on the mechanical ventilator. A trial of increased positive-end expiratory pressure (PEEP) worsened his hypoxemia. The patient was initiated on inhaled NO at 20 ppm and within one hour, his PaO2 rose from 50 to 154 mm Hg while on a FiO2 of 1.0. In the ensuing 24 hours, his PaO2 improved to 93 mm Hg on FiO2 of 0.45. The NO was weaned off on POD 4 and he was subsequently extubated to 4 L of oxygen via nasal cannula. By POD 16, he was on room air at rest and eventually discharged home on POD 25 with 1 L of oxygen to use as needed with exertion.\nFour weeks after discharge, he was seen in pulmonary clinic and reported dramatic improvement in his symptoms of dyspnea. His PaO2 improved to 79 mm Hg on room air, and he continues to do well with improvement of his PFTs and stability of his CT imaging findings. |
A 51-year-old woman with established renal failure due to diabetic nephropathy had been receiving regular haemodialysis three times per week at her regular outpatient haemodialysis unit for 7 years. A policy of routine three-monthly blood sampling for the presence of hepatitis B surface antigen and hepatitis C antibodies was in place, and this patient demonstrated consistently negative results throughout their time on renal replacement therapy.\nIn early September 2009, an HCV antibody titre for the patient was reported as ‘equivocal’. Repeat testing 9 days later demonstrated an HCV antibody titre of 10.23 IU with a corresponding HCV polymerase chain reaction (PCR) titre of 8195 IU/mL (3.9 log copies). Retrospective analysis of the preceding sample taken in June 2009 confirmed HCV PCR positivity and thus suggested acute infection. Serum alanine transaminase titres were noted to be consistently < 30 IU/mL, while hepatitis A, hepatitis B, HIV and autoantibody screening were negative.\nThe patient had no history of other risk factors for HCV transmission. She had never injected drugs nor undergone tattooing and had not received blood products during the 12 months prior to the first positive HCV PCR result. All patients who attended the same outpatient haemodialysis facility during the time of the possible transmission were HCV antibody negative. The index patient had however been admitted to a renal inpatient unit for a period of 10 days in late March/early April 2009 during treatment for an infected diabetic foot ulcer. At this time, she received four separate haemodialysis sessions at the hospital’s inpatient dialysis facility. On one occasion, the patient underwent haemodialysis using a machine immediately following a known HCV-positive patient. Subsequent viral genotyping demonstrated HCV 3A genotype in both patients. Consensus full-length E1E2 sequencing/phylogenetic analysis on samples from the recipient and suspected source, together with nine Nottingham and eight Glasgow epidemiologically unrelated genotype 3A control samples, were conducted. Bootstrapped replicate trees for hepatitis C nucleic acid and amino acid sequencing () were generated for the suspected source, recipient, and the nine Nottingham and eight Glasgow HCV genotype 3A controls. This demonstrated a clustering of the source and recipient viruses. These findings indicate infection with the same strain of virus.\nThe index case was known to be of low infectivity and dialysed at a different time from the affected patient. Neither had ever undergone haemodialysis in the same facility at the same time. On the date of transmission, there was a time period of over 1 h between the index case leaving the unit and the recipient arriving with both patients supervised by different members of nursing staff. Standard infection control policies were adhered to and were observed to be complied with. The haemodialysis machine in question had undergone a standard single cycle of chemical decontamination between patients and functioned without evidence of a fault. Despite these practices, transmission of HCV via the haemodialysis circuit is the most plausible explanation of this event. |
A 72-year-old male presented to emergency department with tender mass on lower back and posterior aspect of neck. Apparently, he had noticed it on his lower back 6 months ago and had grown in size with another similar swelling appearing on his neck, also they were increasingly painful and sore to touch. He had a history of ongoing sore throat for 3 years for which he was extensively investigated by ENT services. His CT neck and mediastinum did not show any abnormalities at that time. This was followed by laryngoscopy which showed a white patch on the right vocal cord, biopsy of which showed non-specific chronic inflammatory changes and cultures grew candida. Background history included COPD; he was heavy current smoker and smoked about 60 cigarettes per day. His medications included salmeterol/fluticasone propionate and ipratropium bromide inhalers. Vitals were within normal range. On examination, 4 cm nodular, firm, tender, immobile mass on lower back and 3 cm mass on posterior aspect of lower cervical spine were noted.\nHis laboratory investigation including renal and liver function, full blood count and coagulation profile were normal. A CT of thorax, abdomen and pelvis was arranged which showed 2 × 2 cm mass in right lung lower lobe likely malignant with no hilar or mediastinal lymphadenopathy, also 3 × 3 cm soft tissue mass at C6-C7 level posteriorly and 4 × 2 cm mass was noted on lumbar region with multiple prominent inguinal lymph nodes ().\nA referral for bronchoscopy was sent and biopsy of the nodule was planned. While awaiting bronchoscopy appointment, biopsy was taken from mass in lower back and send for histopathology. Histology showed poorly differentiated tumour cells in cohesive groups and sheets with moderate pleomorphism and eosinophilic cytoplasm; immunohistochemistry was positive for AE1/3, cytokeratin 7 and carcinoembryonic antigen antibody stain and periodic-acid schiff. Weak nuclear positivity for TTF-1 was also seen. Overall features were consistent with poorly differentiated adenocarcinoma likely of lung origin.\nHe was then referred to oncology services and unfortunately passed away within 5 months of diagnosis. |
A 28-year-old male patient presented to our surgical emergency with a history of pus discharge per urethra and recurrent episodes of urinary tract infection (UTI) for 1 year. The patient had a history of cystolithotomy done 1 year ago for which he was seeking treatment outside; the operation details were not available with the patient. There was no associated fever, hematurea, loss of appetite or constipation. The urine stream was normal. On examination, we found the patient was of average build and all the vitals were stable. Abdominal examination showed a horizontal scar in the lower abdomen at the previous cystolithotomy site and external genitalia were normal. Gross examination of urine showed turbid urine with pus flakes. The patient’s blood parameters were within normal limits. On initial presentation, urine culture was done, yielding Klebsiella spp. for which appropriate antibiotics were started. The patient presented again after 2 weeks with same symptoms and was investigated for the cause of recurrent UTI. An ultrasonography of the urinary bladder was done in view of recurrent episodes of UTI, revealing an echogenic mass in the urinary bladder, 30.8 mm in size and suspected to be vesical calculus. However, an X-ray of the kidney and urinary bladder did not show any radiopaque shadow. A CT scan was done which showed a diffusely thickened wall of the urinary bladder, predominantly the right lateral wall with multiple vesical calculi and the possibility of a foreign body in the bladder (). A cystoscopy was performed showing organised white colour sediments adhering to the anterior wall of the urinary bladder, possibly a retained gauze piece with organised pus flakes (). The mass was big and fragile and not amenable for cystoscopy removal. The patient underwent an exploration of the urinary bladder which revealed a gauze piece adhering to the anterior wall with organised pus flakes (). The rest of the bladder wall was found to be normal. The patient was discharged on the 4th day post-operation. The patient has been asymptomatic and healthy during 8 months of follow-up and free from recurrent UTI. |
A 24-year-old male with HA was admitted to our department with pain in multiple joints on May 23, 2011. The patient had a medical history of hemophilia A since the age of 3 and was intermittently treated with factor VIII. During these years, he sequentially developed left knee, left elbow, left hip, and right knee joint pain and swelling with limited activity and was soon diagnosed as HA. Initially, the joint manifestations could be largely relieved by factor VIII replacement therapy. Factor VIII inhibitor screening remained negative. Later, factor replacement therapy failed to achieve satisfactory effects, so in 2002 and 2006, he received left elbow synovectomy and left total hip arthroplasty, separately. In the subsequent years, the patient still suffered from the recurrent episodes of left elbow and bilateral knee joints hemorrhage, pain, and swelling. In recent 2 years, the frequency of joint hemorrhage had increased to approximately 2 times a week and only slightly relieved after factor VIII replacement therapy. Currently, the activity of those joints was limited to various degrees. Other medical history involved 2 cerebral hemorrhages 18 and 15 years ago, separately.\nOn physical examination, significant tenderness was noted in the left elbow joint with limited pronation and decreased grip strength. The preoperative Mayo elbow performance score (MEPS)[ was 55 for the left elbow. Moreover, knee valgus (left 20° and right 15°) was noted, and hyperextension, hyperflexion, and positive grinding test results were noted in both knee joints with a swollen and warm right knee. The preoperative Hospital for Special Surgery (HSS) knee scores[ were 58 for the left knee and 65 for the right knee.\nBilateral knee joints and left elbow joint exhibit advanced arthropathy on radiographs (Figs. A and 2A). These joints present narrowing of joint space, erosions of the articular facets, and bone deformation to various degrees.\nOur diagnosis was hemophilia A and HA of the left elbow joint, both knee joints, and left hip joint. The patient received left elbow synovectomy and left total hip arthroplasty, but the condition continued to deteriorate over time with worsening of the left elbow and both knee joints. Taking all of these factors into account, surgical methods were our top priority, and simultaneous total multi-joint replacement was indicated. Due to the complicated joint lesions and medical conditions, our preparations for this arthroplasty were far more sufficient than usual. Given that arthroplasty for patients with hemophilia A, particularly the simultaneous replacement of multiple joints, is challenging, the patient and his family were informed in detail of the possible benefits and risks of the surgery. We performed a full musculoskeletal assessment and thorough medical evaluation beforehand. Blood products were prepared for possible bleeding events. Then, our team performed bilateral total knee arthroplasty (Zimmer NexGen) and left total elbow arthroplasty (Zimmer) under tightly regulated factor VIII replacement therapy. Antibiotic prophylaxis was administered 30 minutes prior to surgery, and an additional dose was administered once during the operation. Local hemorrhage was carefully controlled to prevent secondary joint damage. Approximately 1800 mL blood was lost during the entire surgery. The patient received 900 mL blood by autotransfusion and 4 units of red blood cells plus 800 mL fresh frozen plasma by intraoperative infusion. During surgery, we observed hemarthrosis and villous synovial hypertrophy at the joints, and severe erosion of the articular surface and various degrees of bone deformation were noted. These findings confirmed the preoperative diagnosis and preoperative assessments. After surgery, hemostasis management, such as compressive bandage, factor VIII infusion, and rigorous monitoring of coagulation indicators, was performed. An early rehabilitation program was applied to achieve improved regain of function.\nWe managed factor VIII replacement therapy during perioperative period under the guidance of hematologists. On the day of surgery, 3000 U/12 h (the body weight of this patient is 63 kg) factor VIII (ADVATE) was administered intravenously followed by 2000 U/12 h on postoperative days 1 to 3 (POD 1–3). Then, on POD 4 to 6, a dose of 1500 U/12 h was administered followed by 1000 U/12 h over the following 6 weeks. Factor VIII inhibitor remained negative in perioperative tests.\nAt the follow-up, the patient's joints functioned well. The MEPS of the left elbow was 85, and the HSS score of knee joints were 71 (left) and 81 (right). On radiographs (3 months and 5 years after operation), the arthropathy of bilateral knee joints and left elbow joint was significantly relieved (Figs. B,C and 2B,C). |
An 8-year-old boy was admitted in the burn unit of our hospital with the history of electrical burn injury to both of his knees when his lower limbs were entangled in a live electric wire. On examination, there was third-degree burn on both knees anteriorly with near full-thickness destruction of patellar ligament on both sides. The patient was initially managed conservatively. After multiple debridements over next 4 weeks, resultant defects on left side consisted of complete loss of patellar ligament, loss of some part of the upper end of tibia due to osteomyelitis and exposure of the joint space. On the right side also, patellar ligament was destroyed, tubercle of tibia and lower pole of patella were exposed, but the joint cavity seemed to be intact [].\nAt this point of time, as both patellar ligaments were destroyed, the young boy was unable to extend his knees actively, thus he became wheelchair bound for locomotion. Hence, to give the boy an opportunity to walk, reconstruction of patellar ligament, at least on one side, became essential. For the right knee, reconstruction of patellar tendon was done with an ipsilateral and looped semitendinosus tendon graft, and for the grossly destroyed left knee joint, arthrodesis was done.\nBoth the joints were operated in the same sitting by two teams simultaneously. The patient was operated in supine position under general anaesthesia. On the left-sided knee joint, infected and necrotic cartilages and bone of the articular surfaces of tibia and femur were removed; the bone ends were made raw and the exposed bones were covered with ipsilateral pedicled medial gastrocnemius muscle flap with skin graft over it.\nOn the right side, patellar tendon was reconstructed. Incision was made at pes anserinus. Semitendinosus tendon was identified and divided at musculotendinous junction. Proximal end of the divided distal part was delivered distally at incision site keeping the insertion intact. Mid pole of the patella and the tibial tuberosity were drilled separately to make a tunnel with a cannulated burr over a K-wire. Great care was taken so as not to damage the articular surface of the patella. Thereafter, the semitendinosus tendon was passed through patella from medial to lateral side and then passed in reverse direction through the tibial tunnel and fixed to distal intact insertion of semitendinosus, thus forming a loop; the tension of the reconstructed tendon was adjusted by sutured in 30° of flexion of knee joint [Figure and ]. The whole reconstruction was covered with medial gastrocnemius musculocutaneous flap.\nOn the left side, physiotherapy for hip and ankle joint was started on the 4th post-operative day. On the right side, knee joint was subjected to physiotherapy from 2nd week onwards; he was given passive motion training, gradually increasing the range of motion and later active movements from second post-operative week to subsequent 12 weeks. For both sides, gradual weightbearing such as standing with help was started after 6 weeks postoperatively and walking with assistance started on 8th post-operative week.\nOn follow-up after 10 months, the functional outcome was evaluated using Insall modification of Knee scoring (1993) system on the right side where the patellar tendon reconstruction was done. We found no flexion contracture, no pain, no extension lag, normal alignment (no varus or valgus deformity) of knee and total range of motion was 120°; with no anteroposterior or mediolateral instability. Thus, total Knee Society score was 72 out of 100. The patient thus achieved a good range of motion of the right knee joint [Figure and ] and walking without any assistance []. |
The patient is a 61-year-old Korean male with a significant past medical history of rheumatoid arthritis, hypertension, and diabetes mellitus who presented to the hospital with sudden onset of blurry vision in his left eye three days prior. A head CT had been performed at an outside facility, which was negative for acute ischemia, hemorrhage, midline shift, or extra-axial fluid collection. The patient denied visual complaints in his right eye and had no history of similar events.\nOphthalmologic and Neurologic consultations initially revealed visual acuity was 20/40 on right eye; however, on the left eye, there was an apparent left-sided visual loss. Patient's intraocular pressure was normal in both eyes, pupils were equally round and reactive to light, and no afferent pupillary defect was observed. Moreover, the extraocular muscles were intact and with full range of motion. In the right eye, visual fields were full to finger count. In the left eye, the acuity in the nasal visual field was greater than that in the temporal visual field. In the nasal visual field, the patient was able to count fingers; however, in the temporal visual field, the patient could barely detect gross hand movement at one foot out. External examination was within normal limits, and pen light examination was only remarkable for nuclear sclerotic cataracts bilaterally. Dilated fundus examination demonstrated no evidence of pathology to the vitreous, optic nerve, or retina that might explain the vision loss. Four days later, repeat examination by Ophthalmology demonstrated a stable right eye; nonetheless, the left eye temporal visual field was 20/25 and patient was able to count fingers without mistake on left visual field. Pupil and retina examination were unchanged from previous examination. However, visual field mapping could not be done as this patient was seen in the inpatient setting.\nConsequently, an initial head MRI with and without contrast was performed, which showed focal areas of restricted diffusion in the right medial temporal lobe, inferior right basal ganglia with possible involvement of the right lateral geniculate nucleus. The head MRI did not show any other pathology such as masses or hemorrhages (Figure ). The subsequent head MR angiogram done demonstrated no focal occlusion or stenosis, and the MRI of the orbits showed no focal defects bilaterally. At this point, it was evident that the patient was suffering from a left temporal monocular hemianopia and that there must be a correlation with the subtle but definitely present right LGN ischemic lesion. An infarct affecting the right lateral geniculate nucleus would most likely cause bilateral left homonymous hemianopia. Nevertheless, a lesion at the vicinity of right LGN that had taken out the inputs going to layers 1, 4, and 6 became generally accepted among all physicians involved at this point in the care of this patient as the only possible explanation. Patient's left visual symptoms slowly started to improve, and after four days of hospitalization and monitoring, patient's left monocular temporal hemianopia had almost resolved and his vision had almost returned to his normal baseline. |
A 38-year-old male presented to the surgery outpatient department with complaints of odynophagia and chest pain for two weeks. The symptoms had started after a meal when the patient felt the sensation of a foreign body in the throat, which he reportedly swallowed with a bolus of food. As the initial evaluation with neck and chest X-rays was reported as normal, he did not receive any specific intervention. However, in the third week after ingestion, he developed chest pain and fever. On evaluation with a contrast-enhanced thorax, chest, and abdomen scan, he was diagnosed with a right-sided pleural effusion and a suspected foreign body in the periesophageal region of the lower thoracic esophagus close to the inferior vena cava (Figures , ).\nFrom the hiatus region, the foreign body was located at approximately 5 cm cephalad. An intercostal drain was placed under image guidance and approximately 750 mL of serosanguinous pleural effusion was drained. An upper gastrointestinal contrast study did not show any contrast extravasation from the esophageal lumen. Upper gastrointestinal endoscopy also did not show any signs of recent perforation or a foreign body in the esophagus. An after adequate chest optimization, he underwent laparoscopic foreign body removal.\nThe procedure was done under general anesthesia in the supine split leg position. After initial access and the creation of a pneumoperitoneum through the left paramedian 12 mm port using an open method, five additional 5 mm ports were placed, including two midclavicular line ports on either side, a left subcostal port for assistance, and an epigastric port for liver retraction. The gastrohepatic ligament was divided to reach the right crus. The phrenoesophageal membrane was then opened to enter the mediastinum. The esophagus was then looped with an umbilical tape at the level of the hiatus and used for subsequent retraction. The right side of the esophagus was dissected meticulously, preserving the vagus nerves. At about 6 cm from the gastro esophageal junction, there was a fibrotic tract along the lateral aspect, which was then cut with scissors exposing the 2.7 cm long metallic foreign body (Figure ).\nRight pleura were thickened and were not opened. The foreign body was then extracted and removed under vision (Figure ).\nThe tract, which was seen extending to the esophagus, was clipped on the esophageal side using a hemolock. A thorough mediastinal lavage was given and a 16 Fr suction drain was placed in the paraesophageal region. An upper gastrointestinal oral contrast study that was done on the second postoperative day did not reveal any contrast leak, and the patient was started on an oral diet. He had an uneventful postoperative course and was discharged on the fifth postoperative day. |
A 20-year-old collegiate football lineman was blocking during practice, when he was forced from his left side over an extended right leg, creating an internal rotation and adduction moment of the hip. He felt a ‘sliding and crunching sensation’ as he was driven over his right hip. He fell to the ground, and immediately had pain in his right hip. Initial evaluation on the field by the training staff and physician revealed that the hip had full motion, but there was pain with rotation of hip and inability of the athlete to bear weight. The patient was transferred to the emergency room for radiographs and further evaluation.\nIn the emergency room, the athlete complained of further pain in the hip which was increased with hip rotation. Initial radiographs consisted of pelvis anteroposterior view and lateral view of right hip []. The radiographs did not reveal any fracture or dislocation. With his persistent symptoms and continued pain with rotation, magnetic resonance imaging (MRI) was obtained to rule out an occult fracture within three hours of the initial injury. The MRI revealed a small hemarthrosis and a posterior labral tear, but there was no iliofemoral ligament tear or bone edema in the acetabulum or femoral head []. The patient was discharged with instructions to not bear weight on the right hip, and use crutches.\nThe athlete was re-evaluated the next day and found to have continued tenderness with internal rotation and with stressing of the posterior capsule and labrum. He continued to feel a ‘sliding sensation as if (his) hip was popping out,’ although this was not reproducible on examination. A diagnosis of traumatic hip subluxation was made based on his original injury, continued feelings of slipping, and his examination findings. The athlete was placed on hip precautions (patient was instructed to limit internal rotation of the hip, limit adduction of hip, sleeping on back with pillows between the leg) and continued on non-weight bearing, with crutches, for six weeks.\nOver the course of this time, the athlete’s symptoms and capsular signs resolved. Radiographs (AP pelvis, AP and lateral hip films) at six weeks were unremarkable. An MRI was obtained to search for signs of avascular necrosis (AVN) and to determine the safety of a possible clearance for return-to-play. An increased signal was observed in a well-localized area in the superior anterior aspect of the femoral head near the fovea on the T2-weighted images []. The location was atypical for AVN, but the lack of edema in the same area immediately post injury made these changes worrisome. The differential diagnosis was atypical AVN (by location) or an atypical femoral head bone bruise (by the lack of edema on the initial MRI). On account of the uncertainty of diagnosis the patient was continued on toe touch weight bearing for a further six weeks, but allowed gentle range of motion exercises with the trainers. The patient reported compliance with all physician instructions.\nAn MRI was obtained three months after injury []. The lesion on T2 weighted images was still present in the same location and had increased in size and signal intensity. A CT scan was performed to better delineate this lesion and revealed a posterior lip acetabular fracture [].\nThe patient remained on restricted activities, but was allowed to start range of motion activities and non-impact conditioning under the supervision of the athletic trainers.\nSubsequent MRIs at five and 10 months post injury revealed progressive improvement with almost complete resolution of the abnormal signal intensity []. The athlete progressed with training under supervision after his five month MR, and continued, within two months, to unsupervised training for football without any episodes of instability, clicking or pain. He returned to competitive football the following season, 12 months after injury without incident. The final diagnosis was hip subluxation with bone bruise of the femoral head that was not seen on the acute MRI. The subject was informed that data concerning the case would be submitted for publication. |
A 46-year-old woman with morbid obesity, hypertension, hyperlipidemia, active smoking, and bipolar disorder was evaluated for paroxysmal atrial fibrillation as an outpatient. A transthoracic echocardiogram showed a right atrial mass close to the RA-IVC junction. A transesophageal echocardiogram confirmed the presence of a pedunculated right atrial mobile bilobular mass measuring 2.1 × 1.8 cm, not arising from the interatrial septum with extension into the inferior vena cava (Figures –). A secundum atrial septal defect was also identified. The patient was referred to cardiac surgery for resection of a presumed right atrial myxoma given the possibility of embolization. The intraoperative TEE suggested the presence of one bilobulated mass arising low in the right atrium.\nUsing aortic and bicaval cannulation, a right atriotomy was performed and a discrete 2 × 3 cm mass was removed from the IVC-RA junction near the Eustachian valve. The right atrium was closed and the patient weaned from bypass. The specimen did not appear to be a myxoma, so it was sent for frozen section and interpreted as being ectopic liver tissue. In the interim, a repeat TEE showed an additional discrete 2 × 2 cm mass in the IVC near the hepatic veins. Femoral venous cannulation was then performed to allow for visualization of the IVC below the pericardial reflection. Through the same right atriotomy and using additional suction directly in the IVC, the IVC mass was visualized and resected. Both specimens were interpreted as showing partially encapsulated liver parenchyma with mild steatosis, fibrosis, ductal proliferation, and periductal chronic inflammation, consistent with ectopic hepatic tissue ().\nDespite a brief period of cardiopulmonary bypass, the patient had persistent hypoxemic respiratory failure ascribed to her morbid obesity and underlying lung disease. She also developed extensive left lower extremity deep venous thrombosis from a presumed heparin-induced thrombocytopenia for which she was treated with argatroban and placement of an IVC filter. Because of chronic respiratory failure, she underwent tracheostomy and feeding tube placement, and she was placed on warfarin for intermittent atrial fibrillation due to her CHA2DS2-VASc score of 4. She gradually improved and was transferred to rehab where her tracheostomy tube and PEG tube were removed. A few months later, she looked quite well during an office visit. |
A 30-year-old female presented to our hospital with trivial injury to her right thigh, following which she had pain over right thigh and unable to weight bear on the involved lower limb. Other associated injuries were ruled out at the time of admission in the emergency room. Physical examination revealed swelling, tenderness, and deformity over the middle-third of her right thigh region without neurovascular deficit. Patient was stabilized initially in our emergency department, and radiograph of right femur showed displaced transverse fracture in the femoral shaft (). The other radiographic findings were diffuse osteosclerosis and narrow medullary canal. The patient gave a history of earlier episodes of fracture for which conservative treatment in form of native splinting had been done. Thus, a diagnosis of pathological fracture was made. On general examination, the patient had short stature and dysmorphic facies with radiological signs of generalized osteosclerosis and narrow medullary canal. A detailed history, clinical, and radiological examination was carried out. She was second child of four siblings. The first child died days after delivery, of unknown cause, and other two younger siblings had similar clinical features ().\nParents had a first-degree consanguinity. The antenatal history was not significant. Milestone and intelligence attainted appropriate for age. There was a history of frequent episodes of upper respiratory tract infection, snoring during sleep since childhood. The patient also gave a history of hard of hearing on the right side. The patient went through regular general medical checkups, and there was no significant treatment history.\nOn general physical examination, weight of patient was 63 kg; her standing height was 126 cm; her upper segment and lower segment length were 64 and 62 cm, chest expansion of 3 cm, respectively, with a head circumference of 49 cm. Other clinical features include dysmorphic facies, frontal and parietal bossing, beaked nose, midfacial hypoplasia, short hands and feet with dysplastic nail (), grooved palate (), dental caries, impacted and malposed tooth, and sandal gap deformity of the foot (). Radiograph of the skull was found to be widely open anterior and posterior fontanelle, with obtuse mandibular angle and separated cranial sutures (). Radiograph of the hand showed aplastic terminal phalanges with acroosteolysis. Abovementioned clinical and radiographic findings suggested pyknodysostosis as the most likely diagnosis. The patient was taken up for surgery within a week from injury. An intramedullary interlocking nailing was contemplated initially for fracture fixation.\nHowever, for this case, we preferred plate osteosynthesis because of the altered anatomy of the bone with a narrow medullary canal and severe osteosclerosis. Under Spinal anaesthesia, through lateral approach to the middle third of femur, a 12 cm incision was made. After deep dissection, fracture site was identified and exposed. After reducing fractures fragments an “8 holed broad dynamic compression plate with 3 proximal and 3 distal screws in compression mode was used for fracture fixation ().”\nThe difficulty encountered in the intra-operative period include, a difficulty in drilling the cortices and excess blood loss. The wound was closed in layers after adequate hemostasis. The immediate post-operative period was uneventful, and the patient discharged on the 14th post-operative day. The patient was discharged with advice of non-weight bearing walking with the help of walker support for minimum of 2 months and advised to review in the out-patient department for follow up every fortnight. At 10-week post-operative, after patient has been started on partial weight bearing walking, the patient reported with the complaints of pain over surgical site. On radiological examination, patient was found to have no signs of union at the fracture. Patient was immobilized for one month, but even after that, there were no signs of union. Hence, an additional stabilization procedure was done in the form of plating with autogenous cancellous bone grafting. Bone graft harvested from ipsilateral iliac crest was inadequate, and there was heavy bleeding from donor site so that an additional synthetic bone graft substitute was used. In the immediate post-operative period, patient developed deep seated infection which showed organism grown was staphylococcus aureus for which wound debridement was done. Patient was started on Intravenous antibiotics of Linezolid 600 mg twice a day after obtaining culture and sentivity report for period of 2 weeks, followed by oral antibiotics for 4 weeks. Patient was discharged 4 weeks later after complete subsidence of infection. Patient was advised physiotherapy in form of static and dynamic Quadriceps strengthening exercises, followed by hip and knee mobilization exercises and strict non weight bearing for 2 months.. At 3-month post-operative follow-up, there were signs of union clinically and radiologically ( and ). The patient at present in the 6-month post-operative period with fracture united and on full weight bearing carrying out her daily activities without difficulty (). |
A 21-year-old male soldier visited the division of cardiology of our medical center with the complaint of effort angina. He had no history of smoking and no family history of heart disease. His vital signs were stable, his electrocardiogram showed a normal sinus rhythm, and the results of baseline laboratory findings were nonspecific. However, owing to the typical nature of his chest pain, which suggested an ischemic origin, we decided to perform cardiac computed tomography angiography (CTA) to rule out coronary artery diseases. The cardiac CTA images showed normal left coronary arteries but an RCA anomalously originating from the left sinus of Valsalva. Also, the proximal RCA had an interarterial course, which meant that the RCA was trapped between the aorta and the pulmonary artery ().\nWe performed coronary angiography (CAG) to verify the anomaly. CAG from the left sinus of Valsalva showed all 3 coronary arteries, suggesting the anomalously originating RCA (). CAG from the right coronary sinus showed no significant stenosis in the left anterior oblique view. In the right anterior oblique view, however, significant stenosis was noted in the proximal RCA as the result of external compression (). Also during CAG, an intravascular ultrasonography (IVUS) study of the RCA showed that the minimum lumen area in the proximal RCA was 3.8 mm2, which suggested significant stenosis. After CAG, we could not proceed to additional diagnostic tests to verify the evidence of ischemia in the RCA territory, such as myocardial single photon emission computed tomography (M-SPECT) or fractional flow reserve (FFR), because the patient was on a mandatory military service and did not have enough time for many diagnostic tests. However, given the findings from the CAG and IVUS, we regarded the chest pain to be originating from ischemia of the RCA territory. We therefore decided to perform surgical intervention. Owing to a slit-like stenosis of the RCA ostium, we could not choose reimplantation of the RCA ostium, and surgical unroofing was not favored because of a concern for persistent myocardial ischemia in such cases. Finally, CABG [right internal mammary artery (RIMA) to RCA] was selected as the surgical intervention. After the CABG, the patient's symptom was relieved, which suggested that the effort angina was caused by myocardial ischemia. A follow-up CAG done 1 week after the operation showed a patent RIMA to RCA graft (). The patient was discharged from our hospital with medications including aspirin.\nThe patient had no chest pain for more than 10 months after the operation. However, nearly 1 year after the operation, he visited our center and reported suffering from chest pain for about 2 weeks. We recommended that he undergo CAG again. The follow-up CAG revealed no interval changes of the 3 native coronary arteries, but the RIMA to RCA graft was totally occluded (). The right subclavian artery was intact and the patient had no other risk factors for atherosclerosis. Thus, the total occlusion seemed to have developed as the result of complete inhibition by good antegrade flow of the RCA. At this point, we decided to control the patient's symptom with medical treatment, and we recommended that he undergo reimplantation of the right coronary ostium if his symptom persisted after optimal medical treatment. |
A 79-year-old Thai woman presented with hoarseness and neck mass. She had been diagnosed with a 3-cm PTC in right side of the thyroid gland 2 months earlier. Her medical conditions included hypertension and heart failure with preserved ejection fraction. The patient underwent a total thyroidectomy at the initial hospital and received a high dose radioactive iodine treatment (150 mCi) at our hospital 1 month following the surgery and then was lost to follow-up. Preoperative serum thyroid hormone levels were within normal range and thyroid auto-antibodies were negative. No details on initial thyroid surgery and pathological report had been obtained.\nTwo years later, she came back again with new development of a 3-cm right solid-cystic neck mass which was found to be recurrent PTC based on aspiration cytology. There was no evidence of distant metastases and there were no other obvious lymph node metastases in the neck. Radical neck dissection was done at our hospital and the second high dose radioactive iodine treatment was given (a total accumulative dose of 300 mCi). Pathological report revealed classical type of PTC without angiolymphatic invasion in excised tumor. However, she developed recurrent mass with tenderness at the site above previous solid cystic mass 6 months later. Additional work-up by neck ultrasound showed heterogeneous echogenicity of solid lesion with multiple internal calcifications at right thyroid bed (size 2.1 × 1.6 × 2.8 cm) with adjacent complex multilocular cystic lesion with septations and enlarged cervical lymph node with absent fat hilum (Fig. ).\nRe-exploration of neck mass revealed inflamed midline mass 2 cm with enlarged right lateral cervical lymph nodes. A pathological examination of midline neck mass showed poorly differentiated SCC with lymphatic invasion. The intermingling of 2 morphologically distinct tumors, a classical PTC and a poorly differentiated SCC, had been identified in 1 out of 14 excised cervical lymph nodes as shown in Figure . Immunohistochemistry revealed P63 (a well-known marker of squamous differentiation), and paired-box gene 8 positivity in both PTC and SCC components suggesting a transformation process, not a collision tumor. While thyroglobulin was positive in PTC component only, diffuse cytokeratin 5/6 showed positive staining in only SCC component. Results of various immunohistochemical staining in a dissected lymph node are summarized in Figure . No molecular studies (BRAF and TERT mutation) were done.\nPostoperative course was unremarkable and the patient was treated with a course of external beam radiation (40 Gray in 2 Gray per fraction) without chemotherapy because of her advanced age and co-morbidities. Concerned over airway protection, a prophylactic tracheostomy was done. The latest surveillance imaging done at 18 months after the last surgery revealed evidence of recurrent disease in the neck but the patient decided on watchful waiting without further treatments. She is still in stable condition at 18 months after the last operation. |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.