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The second case is a 68-year-old female diagnosed with a cT4aN2cM0 laryngeal carcinoma located around the epiglottis. The interval with surgery was six and eight days for CT and MRI, respectively.\nOn the b800 diffusion-weighted image, a clear and homogeneous contrast with high diffusion restriction between tumor and surrounding tissue was visible. The ADC map shows corresponding low ADC values in the tumor and increased ADC values directly adjacent to the tumor. This was in correspondence with the T1-weighted MRI, which showed a homogeneous contrast uptake within the tumor and an increased uptake adjacent to the tumor. The T2-weighted MRI cranially showed an increased homogeneous signal compared with the surrounding tissue, whereas more caudally, the contrast between the tumor and the surrounding tissue was low.\nIn the images, a large ulcerative mass on the right side of the larynx was visible, probably originating from the laryngeal side of the aryepiglottic fold. The maximum diameter measured in the coronal plane is 4.6 cm. There is an extension around the right side of the epiglottis. Caudally, extension into the false and true vocal cord is found, while a subglottic extension is not observed. There is an obliteration of the paralaryngeal fat with a broad contact with the thyroid cartilage. The thyroid cartilage shows some signal enhancement but no invasion was visible. Anteriorly, an extension across the midline at the level of the false vocal cord is evident. Cranially to the thyroid cartilage on the right, some extension beyond the larynx without invasion of the strap muscles was present. In addition, the tumor extended minimally through the laryngeal incisura. No tumor invasion of the arytenoid or cricoid cartilage was apparent. The clinical tumor staging was T4. The patient was offered a total laryngectomy.\nOn histopathology, a poorly differentiated supraglottic squamous cell carcinoma of the basaloid type was visible. The growth pattern was mainly cohesive, with a diameter of 3.6 cm and bilateral extension. The tumor extended between the hyoid and the ventral part of the thyroid cartilage. The hyoid cartilage was slightly invaded by the tumor, resulting in a pathological T4 stage.\nThe volume of this tumor measured on histopathology was 10.9 ml, which was largely overestimated by GTVclinical with a volume of 21.6 ml, and comparable to the GTVDWI of 11.5 ml (Figure ). The clinical delineation showed more overestimation than the DWI segmentation (37% and 70% of the GTVclinical and GTVDWI-contained tumor, respectively), while a comparable region of the tumor was included in both GTV delineations (72% and 74% for GTVclinical and GTVDWI, respectively). The underestimation of the tumor extent by the GTVclinical was 2.1 mm and for the GTVDWI, it was 2.7 mm (Figure ).
A 45-year-old man came to our outpatient clinic because of blood pressure level abnormality (200/100 mm Hg), which had persisted for >30 years. The patient was found with abnormal blood pressure when he was 10 years old. Maximal blood pressure level at 260/110 mm Hg was recorded during the physical examination for several years. The patient had a smoking history of 20 years and no similar family medical history was reported, but suffers no other significant clinical symptoms. In recent weeks, he suffered dizziness and was treated with oral antihypertensive medications. The treatment regime was nifedipine (controlled release tablets 30 mg Bid), irbesartan and hydrochlorothiazide (tablets 150 mg qd), and irbesartan (150 mg qd). The curative effect is limited and his blood pressure remains at elevated level. On physical examination, the patient had a pulse rate of 68 bpm, a respiratory rate of 18 bmp, a body temperature of 36.7°C, and a body mass index of 23 kg/m2. The first medical evaluation in our hospital revealed a regular heart rate of 68 bpm and a grade 4/6 systolic murmur at the position of T1-T3 on back. The murmur conducted to neck. His blood pressure was measured as 183/92 mm Hg in the left arm and 175/95 mm Hg in the right arm, 96/64 mm Hg in the left ankle, and 101/60 mm Hg in the right ankle (left ankle brachial index: 0.54, right ankle brachial index: 0.56). It indicated a significant differential blood pressure between the upper and lower limbs. Echocardiography showed the left ventricle did not present severe abnormal dimensions and impaired systolic function, the descending aortic arch could not be observed, and aortic valve regurgitated moderately. Computed tomography angiogram (CTA) revealed a type A interrupted aortic arch with complete discontinuity of the aortic lumen distal to the origin of the left subclavian artery, and a massive aorta arch which included 2 full-fledged collaterals network ensuring blood circulation to distal aorta (Fig. ). Angiography showed absence of anatomical continuity between the ascending aorta distal to the left subclavian artery and the descending aorta. There was no patent ductus arteriosus (PDA) and associated endocardial fibroelastosis. The descending aorta was fed exclusively by massive systemic collateral circulation (Fig. ). Cardiac magnetic resonance (CMR) found nothing abnormal. Carotid artery ultrasonography indicated bilateral carotid plaques. Lower limbs (right) ultrasonography indicated plaques on the arterial wall. Based on the available evidences, we have concluded that the patient suffered from secondary hypertension due to isolated interrupted aortic arch (IAA). We had discussed the advantages and disadvantages of the surgery option with the patient, but he refused. Therefore, we had prescribed antihypertensive medications: nifedipine controlled release tablets (Adalat) 30 mg bid; irbesartan and hydrochlorothiazide tablets (Coaprovel) 150 mg qd; irbesartan (Aprovel) 150 mg qd; doxazosin mesylate extended release tablets (Cardura) 4 mg qn; spironolactone tablets (Antisterone) 20 mg qd; carvedilol tablets 5 mg bid.\nAfter 10-day medication, 24-hour ambulatory blood pressure monitoring showed a mean of 24-hour blood pressure at 129/68 mm Hg. The day and night mean blood pressure was 139/79 and 103/54 mm Hg, respectively (Fig. ). The mean office blood pressure fluctuated between 140 to 160 and 90 to 100 mm Hg. The significant discrepancy between ambulatory and office blood pressure should be attributed to the white coat effect.
A 54-year-old man came to the private dental clinic with complaint of difficulty in mastication and esthetical concern for his upper anterior teeth. He was a nonsmoker and was diagnosed with IgG-kappa type MM in November 2011. In the physical examination, he was diagnosed with MM. Bony metastasis was present at the time of diagnosis of the disease. A full radiographic skeletal survey showed multiple bony lesions at the ribs, femurs, and hip (Figures and ).\nPanoramic view revealed bony lytic and punch out lesions at the right side of the mandible. This patient had no history of surgery. His weight had decreased by 7 kg, following 22 months of acute intravenous injection (IV) BP treatment after the last chemotherapy treatment session. His blood pressure was 130/80, and he had a normal breathing and pulse rate. Preoperative examination of his oral mucosa revealed no evidence of pathological lesions, and overall oral hygiene was good. The patient was felt healthy and was well nourished, alert, and cooperative. After thorough clinical examination, maxillary right first premolar was found missing.\nAfter meticulous consulting sessions with the patient and discussing the advantages and disadvantages of all treatment options, he accepted to receive dental implant.\nAccording to the patient's physician, the appropriate time for the surgery relied upon the patient's regular blood cell counts. This patient did not undergo any radiotherapy phases in the entire duration of his active IV BP treatment. He underwent chemotherapy for two separate sessions. After the last session of chemotherapy, the patient received monthly infusion of 3.5 mg of the IV BP drug zoledronate (Zometa; Novartis Pharmaceuticals Corporation) for a period of 22 months (from May 2014 to March 2016). As per the physician's recommendation, C-terminal cross-linking telopeptide (CTX) examination was carried out 6 months after stopping IV BP therapy. The CTX above of more than 150 was considered to be safe, in that the CTX was 289 pg/mL.\nBefore surgery, the patient was premeditated with 2 g of amoxicillin/clavulanic acid and 50 mg of diclofenac. A root form titanium dental implant (Superline; Dentium) of 3.6 mm in diameter and 10 mm in length was inserted under local anesthesia (Figure ). The patient well-tolerated the procedure and his vital signs were regularly monitored. Postoperative medications including antibiotics (1000 mg amoxicillin/clavulanic acid twice daily for 7 days, starting on the day of surgery), an analgesic (600 mg ibuprofen as required every 6 hours), and mouthwash (0.2% chlorhexidine twice daily for 2 weeks, starting on the day after surgery) were prescribed to the patient. Postoperative course and healing were unremarkable and typical. He was instructed to resume normal oral hygiene and chewing by week six. Postsurgical cleaning protocols, including oral hygiene instructions, were implemented at weeks 1, 2, 6, and 12.\nFour months after the implant insertion, the patient returned for punch removal of the gingiva overlying the implants. After 1 week, the appropriate impression copings were connected to the fixture. Polyether (Permadyne light and regular body; ESPE, Plymouth Meeting) was injected around the transfer copings and placed inside the custom tray using the dispenser. After laboratory procedure, abutment were positioned and torqued according to the manufacture's guidelines at 30 Ncm. After the surgical and prosthetic treatments were completed on February 2017, the patient was placed on a regular follow-up for peri-implant maintenance. The patient resumed IV BP therapy on May 2017. The oral hygiene regimen was implemented for this patient in a 6-month recall. The last follow-up (12 months after prosthetic delivery) showed minimum bone loss, as compared with the X-rays taken immediately after the prosthetic delivery and the implant, and its restoration was successful. The patient was satisfied with the treatment (Figure ).
A 40-year-old gravida 4 para 4 was referred to our centre for an abdominal and perineal mass that gradually enlarged over the past 3 years. She complained of abdominal distension, slow transit with 1–2 stools per week, and difficulty in voiding. There was no abdominal pain. She lost 8 kg over the past 3 years. On physical examination, the patient had a large, firm and indolent abdominal mass that emerged through an incisional hernia of the abdominal wall. We also noted a second mass, measuring 40 cm and occupying the internal part of the gluteal region. Its pedicle extended into the pelvis through the right ischiorectal fossa (). Perineal examination revealed a grade IV hysterocele. Computed tomography (CT) showed a huge, well-demarcated solid, homogeneous mass with moderate enhancement occupying the abdomen and pelvis herniating through the perineum (). The core needle biopsy findings were consistent with myxoid neurofibroma. Exploratory laparotomy showed a firm multilobed mass () that contracted intimate adhesions with the pelvic colon, right ureter and rectum. Resection was performed without organ involvement through a combined perineal approach. Tumour resection was macroscopically completed except in the perineum, where the tumour was left (R2 resection) to avoid anal sphincter injury. The operative specimen weighed 5.842 kg. Histological analysis showed a spindle cell tumour with a myxoid matrix without atypia or mitosis. On immunochemistry, the tumour was negative for PS 100 and CD 117 and positive for nuclear β-catenin and smooth muscle actin. It was diagnosed as a desmoid tumour. During the immediate postoperative period, wound infection and partial dehiscence were noted. Flatus and liquid stool incontinence were also observed. The incontinence completely improved during the 12th postoperative week. Adjuvant treatment with tamoxifen at an initial dose of 150 mg/day and indomethacin (100 mg per day) was given for the incomplete excision (R2). Tamoxifen was tolerated by the patient and continued for 24 months. A follow-up examination 12 months postoperatively documented a complete response. Indomethacin was discontinued after 4 months due to gastralgia. Colonoscopy was performed in the third postoperative month, and there was no polyadenomatosis, confirming the sporadic character of the desmoid tumour. After 36 months of follow-up, no recurrence was observed.
The present case report is about a 51-year-old female patient reported to our department with complaints of non-resolving swelling over right side of the face and a dull, continuous, aching pain in the mandibular right posterior region radiating to the right ear.\nShe gave a history of loss of appetite, weight loss and persistent non-productive cough over a period of past 6-8 weeks. Her mouth opening had progressively worsened over the past 2-3 months affecting her nutritional status.\nShe was a chronic smoker since past 30 years with a 5 bidis/day history of tobacco use. Her past medical history was not significant.\nThe patient gave no history of trauma. The patient had been seeking treatment from a general practitioner who had carried out incision and drainage suspecting the swelling to be a massetric space infection and had planned for extraction of her posterior teeth at a later date on improvement of mouth opening. The patient also gave a history of altered sensation on the right side of her lower lip.\nGeneral examination revealed Grade III clubbing with a characteristic parrot beak appearance of her nails.\nOn local examination, there was gross facial asymmetry with a single diffuse swelling over right preauricular region extending up to the lower border of the mandible. The skin overlying the swelling had a taut and shiny appearance [].\nOn palpation, the swelling was firm, non-tender and fluctuant. There was no lymphadenopathy.\nIntra oral examination revealed poor oral hygiene and carious teeth present in all four quadrants.\nThe only relevant finding on routine blood examination was an elevated erythrocyte sedimentation rate of 40 mm.\nThe orthopantomogram revealed multiple carious teeth suspected to be the possible cause of infection []. The clinical differential diagnosis at this stage included massetric space infection, salivary gland tumor, primary carcinoma of oral cavity, chronic non-suppurative osteomyelitis.\nThe non-resolving nature of the swelling even after extraction of foci of infection and the patient's history made us investigate the general status of the patient. Following which chest X-ray and contrast enhanced computed tomography (CECT) of thorax was advised.\nThe chest X-ray (posteroanterior view) revealed a nodular opacity in right M2, L2 measuring approximately 6 cm × 4 cm with right hilar prominence strongly suggestive of bronchogenic carcinoma [].\nDiagnosis of pulmonary carcinoma was considered when CECT of thorax was suggestive of bronchogenic carcinoma with mediastinal lymphadenopathy and adjacent lymphangitis carcinomatosis [].\nOn further investigating, fine-needle aspiration cytology (FNAC) of the swelling over the right massetric region showed malignant squamous cells arranged singly and in groups conclusive of metastasis from a poorly differentiated squamous cell carcinoma [].\nA FNAC was selected over conventional incisional biopsy as it had several advantages as a diagnostic modality of being quick, reliable and safe. Elimination of tissue embedding or sectioning with this technique allowed for a more rapid diagnosis than with surgical biopsy.\nA computed tomographic scan of the mandible was carried out to see for the extent of bony involvement which revealed an oval shaped osteolytic lesion over the right side of the ramus of the mandible with thinning out of posterior border of the ramus measuring approximately 8 cm × 4 cm in greatest diameter [].\nThe axial and coronal slices of the computed tomographic scan revealed perforation of buccal and lingual cortices of ramus of the mandible on the right side with minimal expansion of buccal and lingual cortex [Figures and ].\nA definitive diagnosis of pulmonary squamous cell carcinoma was arrived at following CT guided FNAC of tumor mass in the right lung [] which was consistent with the cytopathologic findings of the metastatic lesion.\nThe patient upon definitive diagnosis of pulmonary squamous cell carcinoma was started on Cisplatin based palliative chemotherapy. Although, partial regression of primary tumor was present, relapse with worsening of symptoms was observed 6 months after diagnosis was established. Unfortunately, the patient was lost to follow-up following 6 months after chemotherapy after being discharged from our unit.
A 27-year-old female patient with a known case of triple-negative breast cancer admitted to the emergency room complaining of documented fever 40°C at home which was relieved with an antipyretic. She was status post 4 cycles of neoadjuvant dose-dense AC regimen which consists of doxorubicin 60 mg/m2 and cyclophosphamide 600 mg/m2 administered every 14 days. She was prescribed primary prophylaxis filgrastim after all cycles. Physical examination was unremarkable apart from her fever. The patient was admitted to the hospital having febrile neutropenia with no focus of infection and started on empiric antibiotics and filgrastim. She had a low white blood cell (WBC) count with an absolute neutrophil count (ANC) of 1100 cells/microlitre on day 11 after cycle 4 despite being on appropriate filgrastim dose at 300 μg per day for 9 days. On the second day of her admission, she recovered from neutropenia but continued to have persistent high-grade fever for almost two weeks despite escalation of the antibiotics and addition of an antifungal agent. She underwent series of investigations to identify the cause of her unexplained fever. She had extensive blood and urine cultures after each spike of fever, which all came back negative. Computed tomography (CT) scan ruled out infectious focus and showed hepatosplenomegaly with multiple splenic hypodensities and minimal perisplenic fluid which did not appear in the baseline scan (Figures and ). Infectious disease team advised for a splenic biopsy which showed splenic infarction only with no evidence of bacterial, fungal, viral, or malignant involvement (). She also underwent an echocardiogram study, sinoscopy, and series of rheumatologic investigations that were normal. General surgery team was consulted and did not recommend any surgical intervention since the follow-up CT scan turned out negative for splenic abscesses with interval improvement in the previous splenic wedge-shaped hypodensities (). Eventually, the patient was discharged on oral antibiotics with infectious disease and oncology clinic follow-up after being afebrile and asymptomatic for more than 72 hours.
A 14-year-old male presented with expressed concern about the abnormal shape of the right maxillary central incisor crown (). His main complaint was abnormal tooth shape and impaired\naesthetics. There was no particular medical history. No similar dental abnormalities were seen in other members of the family. An intra-oral examination revealed good dental health.\nThe occlusion was a class I molar relationship but there was a severe lack of space.\nThe right maxillary central incisor had a lesion that was first looked like calculus. The consult with periodontists revealed that it was not calculus. The lesion was extended to\nthe cervical part of crown and root.\nThe size of lesion was about 8 mm. The patient had no pain and no clinical symptom. It was not associated with caries and vitality tests revealed normal pulp response.\nNo association with other dental anomalies was established. A periapical radiograph was provided (). On radiological examination, the lesion presented a combination of radiolucent\nand radiopaque appearance and no periapical changes were noticed.\nInitially, it was attempted to remove the lesion with an ultrasonic scaler; but it was not possible. So finally, therapeutic procedure included complete removal of the lesion\n() with fine diamond burr in a high speed handpiece and aesthetic correction was performed with composite material immediately after removal of the lesion and managing the bleeding\n(). The resected material was put in formalin and sent for histopathological evaluation.\nThe microscopic data showed the lesion was composed of tubular dentin and enamel matrix in an unorganized manner as we see in a complex odontoma ( and ).\nPatient was followed up for six months and no recurrence was reported. Informed consent was read and signed by the patient for publishing his images and data anonymously.\nThis report was confirmed by Research Ethic Committee of Shiraz University of Medical Sciences, Shiraz, Iran (code: IR.SUMS.DENTAL. REC.1399.109).
A 66-year-old female with a past medical history of nonalcoholic steatohepatitis, complicated by ascites, hepatorenal syndrome, and spontaneous bacterial peritonitis, with a MELD (Model for End-Stage Liver Disease) score of 31, was admitted for an orthotopic liver transplant.\nGeneral anesthesia was induced with fentanyl, propofol, and succinylcholine. An 8.0 Endotracheal tube was placed in the trachea. A vecuronium drip at 4 mg/hr was started. Invasive monitoring consisted of a 20 gauge, 10 cmin length arterial catheter placed in left radial artery. A right internal jugular 7-French 16 cm in length triple lumen central venous catheter and a 16-French SVC catheter were inserted under ultrasonographic guidance using Seldinger technique.\nA chest X-ray performed after line placement () demonstrated satisfactory right internal jugular placement with the tip of the catheter positioned in the superior vena cava and without any evidence of pneumothorax. The liver transplant was performed uneventfully. Cold ischemic time was 7 hours and 3 minutes, warm ischemic time was 32 minutes, and portosystemic bypass time was 1 hours and 9 minutes.\nA routine postoperative chest X-ray () displayed a linear density, representing a catheter fragment, at the level of the right ventricle. The patient remained intubated and hemodynamically stable, with no evidence of jugular venous distension. Cardiac monitoring demonstrated sinus tachycardia and cardiac enzymes were negative. A Chest CT () was performed and demonstrated a fragment of distal portion of the catheter projecting at the apical wall of the right ventricle. The internal jugular central line catheter placed by anesthesiologist was removed and careful examination found the catheter to be complete and intact. The intracardiac catheter remnant was successfully retrieved by interventional radiology team under fluoroscopy, using 5 mm trilobed snare device through the right femoral vein (). Examination of the foreign body revealed an 8 cm portion of a triple lumen catheter with a clean 45-degree cut at its distal end.\nFurther investigation determined that the foreign central line catheter placed in the donor was inadvertently transected, with embolization to the donor hepatic vein through donor IVC, by the cardiac transplant team during procurement of the donor's heart and lungs. The liver transplant with subsequent reperfusion resulted in the dislodgement and embolization of the remnant into the right ventricle of the recipient.\nThe patient continued to recover well and was extubated on postoperative day 1. Following continued recovery, on postoperative day 5, patient was discharged to rehabilitation center.
A 77-year-old man admitted to our hospital with 1-month history of cough and dyspnea. He had personal history of pulmonary tuberculosis 1 year ago. On physical examination of the thorax, inspiratory dry crackles were heard on both lower lung fields. In observation of oral cavity, a large oval mass composed of soft tissue was detected in his throat. The mass was arising from the right palatine tonsil and extending across the midline of the oropharynx (Figure A).\nHigh-resolution computed tomography of chest showed 2 masses in the left lower lobe, 1 mass in the right upper lobe, and multiple enlarged mediastinal lymph nodes of the lung (Figure ). One of the left lower lobe masses was 4.4 × 4.0 cm sized in superior and lateral segments, and the other was 5.7 × 3.7 cm sized with fibrosis in subpleural region. A right upper lobe mass was 2.1 × 1.5 cm sized. Also, there was typical honeycomb appearance with traction bronchiectasis and ground-glass opacity pattern, predominantly in subpleural areas of both lower lobes. Under suspicion of lung cancer and usual interstitial pneumonia that is pathological equivalent to IPF, further workup was started to confirm the diagnosis.\nPercutaneous transthoracic needle biopsy for lung mass and punch biopsy for tonsillar lesion were performed. Both tumors were composed of nests of small, round, or oval cells with little cytoplasm and hyperchromatic nuclei. They also showed molding and crushing artifact. In immunohistochemical staining, the cells from both tumors were positive for CD56, a glycoprotein expressed on the surface of neurons and neuroendocrine tumors as well known that it is the neural cell adhesion molecule (NCAM). In addition, the cells showed positive staining for synaptophysin and chromogranin A, although the intensity was weaker than CD56, and it was more distinct in lung mass than that in tonsillar mass. Based on these pathologic findings and the known fact that SCLC belongs to the neuroendocrine lineage of lung cancer, the masses were diagnosed as SCLC and tonsillar metastasis (Figure ).\nWe performed systemic evaluation using whole-body magnetic resonance imaging, which showed a mass indicating brain metastasis in body portion of the right corpus callosum and a 2 × 2.8 cm-sized, intraluminal protruding mass in the right peritonsillar region with heterogeneous enhancement, suggesting malignancy of palatine tonsil (Figure B).\nWe suspected that the patient has IPF based on the clinical findings and radiological patterns. There was no history of exposure to any toxic materials and no clinical symptoms of connective tissue diseases. Bronchioloalveolar lavage fluid analysis exhibited the percentage of alveolar macrophage, lymphocytes, neutrophil, and eosinophil was 77%, 3%, 15%, and 5%, respectively. T-cell helper/suppressor ratio was 0.97. The analysis of bronchioalveolar lavage did not show any other abnormal cells or components. Pulmonary function test revealed restrictive pattern of ventilation. With all these findings, we diagnosed that the patient had IPF.\nChemotherapy with irinotecan and carboplatin for SCLC and a standard medication of steroid and acetylcysteine for IPF were applied. He received gamma-knife surgery for metastatic brain cancer 2 weeks later. However, in following-up, he expired due to respiratory failure by an acute exacerbation of IPF 3 months after the diagnosis.
A previously healthy 16-year-old Danish boy presented to our emergency department with diffuse chest pain. Ten days prior to hospitalization he had suffered a blunt trauma to the chest while playing soccer. Closer inspection revealed accentuated vein drawing on the front of the chest and slight direct and indirect tenderness of the thorax. During lung auscultation, ceased respiration sounds on the right side and normal vesicular respiration on the left side were found. A chest X-ray revealed a collapsed right lung and pleural effusion (Figure ). He was clinically unaffected and the vital parameters were normal.\nA pleural drain was established and 2.5L of clear yellow fluid was drained. During the following few hours he went into respiratory distress (saturation 85% on 15L of oxygen), became hypotensive (blood pressure 64mmHg over 40mmHg) and tachypneic (respiratory frequency 24 breaths/minute). We administered 2L of saline solution and continuous positive airway pressure, which briefly stabilized the patient. On suspicion of lung embolism, an acute echocardiography was performed. This revealed pericardial effusion and dilatation of the right atrium. His respiratory and circulatory function became increasingly unstable. He was intubated and transferred to a level 1 trauma centre.\nThe trauma computed tomography (CT) scan revealed multiple enlarged lymph nodes anteriorly in the mediastinum, bilaterally in the axillae, the throat, and along the aorta down to retroperitoneum. Furthermore, an almost collapsed superior vena cava was revealed (Figure ). The following day we performed a positron emission tomography computed tomography scan. This revealed increased activity in the area equaling the lymphoid mass (Figure ). On the suspicion of malignant lymphoma causing superior vena cava syndrome, the patient was transferred from the intensive care unit to the hematological service after 2 days, after he was stabilized and extubated. Excision of a cervical lymph node, a bone marrow biopsy, and analysis of pleural fluid for cytological examination were conducted. Biochemically, a lactate dehydrogenase of 350U/L and leukocytosis of 21.7×109/L was found. His peripheral blood showed normal composition and his bone marrow showed no significant blast accumulation indicating no sign of T-cell lymphoblastic leukemia.\nCytological examination of his lymph node revealed an altered architecture and diffuse infiltration of tumor cells, with cell markers positive for CD3, CD5, CD2, CD7, CD4, Bcl-2, and TDT, and negative for CD23, Bcl-6, cyclin D1, CD34, CD8 CD56, tia-1, granzymB, and CD30, consistent with T–cell lymphoblastic lymphoma.\nHe started treatment immediately with vincristine and dexamethasone to reduce the tumor burden prior to the initiation of the chemotherapeutic regimen.
An 18-year-old female with a history of quadriplegic cerebral palsy (GMFCS-V) was admitted to our orthopaedic department following a peri-prosthetic fracture of the right femur. She is well known to our department, as her non-ambulatory status has resulted in a number of surgeries including a right adductor tenotomy, aged 11, femoral derotation osteotomy and dega acetabular osteotomy, aged 13 and right distal hamstring and knee capsule release, aged 14. She presented to the emergency department with a painful right thigh after getting her leg caught in doorway while being mobilized in a wheelchair. The trauma resulted in lateral bending of the leg, with examination revealing a significant deformity of the thigh with audible crepitus. Radiographs revealed a peri-prosthetic fracture of the right femoral shaft extending distal to the AO blade plate (Fig. ). The blade was also seen to be encroaching on the inferior cortex of the femoral neck leading to concerns about creating a stress riser or femoral neck fracture in the event of revision blade plate fixation. There was also concern that the longest replacement blade plate available would not be of sufficient length to stabilize the fracture distally. The complexity of this case along with the patients low body weight (26 kg), small skeletal morphology and underlying neurological disorder deemed revision with a long-blade plate, or standard adult femoral fixation devices unsuitable. Therefore, we proposed a long PHILOS™ proximal humeral locking plate (Synthes, UK) as a suitable device for internal fixation of the fracture to provide adequate plate osteosynthesis, with secure proximal and distal fixation, bridging the fracture and the femoral neck defect.\nUnder general anaesthesia, open reduction and internal fixation using a 10 hole philos plate was performed with the patient in a supine position on the traction table utilizing a lateral approach. Using C-arm image intensification, the height of the plate was judged, then applied to the bone and secured both proximally and distally to the fracture with proximal locking screws inserted where possible (Fig. a–c). Securing the cephalic segment of the philos plate to the proximal femur proved challenging due to the femoral neck defect left by the removal of the blade plate. Final reduction was judged to be near anatomical with the wound thoroughly irrigated with saline before closure. Post-operative treatment included IV antibiotics with mobility instructions unnecessary due to the patient's non-ambulatory status. The patient was discharged after 5 days with a follow-up period over 11 months. There were no post-operative complications during this time and radiographs showed an anatomically healed fracture (Fig. ).
A 43-year-old male patient attended a dental clinic with the prosthetic crown of tooth 24 in hand, with the remaining fractured root core, part of which was inside the root canal (Figures and ).\nClinical and radiographic examination revealed the absence of a root fracture, which might preclude maintenance of the tooth (). It was also observed that the root canal had not been submitted to removal of sealing material up to the adequate length of 2/3 of the dental remnant to the root apex [, ]; the cast metallic core was short, which impaired the intraradicular retention.\nDuring clinical examination, it was observed that the dental remnant presented satisfactory conditions for a new rehabilitation with placement of an intraradicular core and a total prosthetic crown. It was proposed to remove the portion of the cast core that was inside the root canal for later accomplishment of a new intraradicular cast core, using the existing metal-ceramic crown as a reverse template for the coronal portion of this future core.\nThis alternative was possible because there was no need for additional preparation (wear) of the dental remnant at the cervical level, which would impair the adaptation and reuse of the original prosthetic crown. Initially, root canal preparation (buccal and palatal) was performed by instrumentation with Gates Glidden drills at the appropriate length (2/3 of the dental remnant in the largest (palatal root canal), 1/2 of the dental remnant in the other canal (buccal)) [, ].\nThen, the prosthetic crown was internally ground with carbide drills to allow coronal adaptation of the new cast core. For that purpose, the prepared root canals were previously isolated with petroleum jelly and filled with fluid acrylic resin, supported by prefabricated resin rods (Pincanal®) in each canal. Polymerization of the acrylic resin was properly controlled to avoid adhesion of the resin pin inside the root canal ().\nFor preparation of the coronal portion of the core, the prosthetic crown was fitted on the coronal remnant and was internally isolated with petroleum jelly, filled with acrylic resin, and repositioned on the dental remnant with the core in place, thus serving as a reverse template for reconstruction of the coronal portion of this new core (Figures –).\nAfter completion of polymerization, the finished resin core was sent to the prosthesis laboratory for alloy casting (Figures and ).\nThis new core was properly adjusted to the remaining root, and the adaptation of the metal-ceramic crown on it was also verified (Figures –).\nFinally, both pieces (core and crown) were cemented with definitive zinc phosphate cement (Figures and ), and the occlusal contacts were adjusted ().
A 41-year-old man presented to our Neurology Department with pain at the level of the right shoulder and right interscapular–vertebral region, with onset for about 6 months. In the last 30 days, the pain exacerbated and radiated in the anteromedial part of the arm and clavicular area. The patient also reported pain in the joints of the distal part of upper and lower limbs, especially in the small joints, which afterward became swollen.\nThe patient presented with a medical history of arterial hypertension for the last 10 years, treated with beta-blockers and sartans, and he was a heavy smoker (in the last period he used only electronic cigarettes).\nThe neurologic examination was normal, except for slightly diminished deep tendon reflexes of the lower limbs. The patient reported pain that did not correspond to any radicular or nerve territory, which was exacerbated by pressure on the distal third of radius and ulna, but was not related to active or passive movements of the cervical spine. The general examination showed clubbing of the fingers and toes (not mentioned initially by the patient, but present for about 1 year) with an increase of the shoe size of more than 1.5 sizes, enlargement of the large joints, swollen extremities with a tubular appearance (Figs. and ), a right lateral cervical mobile, painless adenopathy of 1 cm diameter, and pachydermia with thickening of the skin of the scalp, forehead, and fingers, with cranial skin folds.\nCervical magnetic resonance imaging performed in another clinic before the admission to our department showed the presence of disc protrusions from C2 to C7, with concomitant C2, C4, and C5 root compressions. The electrophysiological study revealed an active denervation in the territory of the right C5, C6, and C7 roots.\nThe radiographic examinations of the upper and lower limbs depicted symmetric osseous abnormalities, typical for periostosis, and linear halving of the diaphysis with an increase in the bone circumference. There were no fractures or cortical destruction (Figs. and ). Transthoracic echocardiography and electrocardiography were normal.\nThe computed tomography (CT) of the thorax, abdomen, and pelvis revealed the presence of a 23/19 mm (transverse) and 20 mm (cranial–caudal) mass lesion, respectively, having speculated margins, contrast enhancement, and areas of necrosis at the level of the dorsal segment of the right upper pulmonary lobe. The mass presented several extensions to the pleura and determined pleural invasion (Figs. and ). In addition, multiple mediastinal adenopathy were noticed, and some of them presented central necrosis. No oncologic abnormalities were found at the examination of the abdomen and pelvis. Also, the cerebral CT scan did not show any pathological findings.\nLaboratory findings were normal, except for the presence of inflammatory syndrome, slight anemia, and high values of vascular endothelial growth factor (VEGF) (1291 pg/mL, with normal values less than 100 pg/mL).\nThe patient was admitted to the Pneumology Clinic, where biopsy from the lateral cervical adenopathy was performed (tumor excision was not an option, due to the presence of multiple adenopathy). The anatomopathological examination of multiple fragments from the lymph node revealed multiple neoplastic infiltrates, suggestive of adenocarcinoma metastasis.\nPositron emission tomography with 2-deoxy-2-[fluorine-18]fluoro-D-glucose confirmed the presence of the pulmonary malignant tumor with multiple active adenopathy.\nBased on the clinical examination that revealed signs and symptoms suggestive of Pierre Marie–Bamberger syndrome, the X-ray examination that showed abnormalities compatible with the same pathology mentioned earlier, and on the positron emission tomography and histologic findings, the diagnosis of pulmonary adenocarcinoma with lymph nodes metastases and paraneoplastic hypertrophic osteoarthropathy was established.\nThe patient received treatment with nonsteroidal antiinflammatory drugs and opiate analgesics, which relieved the pain without any adverse event; he was then referred to the Oncology Department for further treatment of the primary pathology. The patient was treated with different types of chemotherapeutics, immunotherapy, and gamma-knife radiotherapy for cerebral metastases. Unfortunately, the disease progressed despite all of these therapeutic measures and the patient died 9 months later.
A cardiologist calls as they are planning a coronary angiogram for a 68-year-old trans woman and are concerned because the estimated glomerular filtration rate (eGFR) is unknown. They are uncertain how to risk stratify her for potential contrast-induced nephropathy. She has a history of longstanding hypertension and hypercholesterolemia, vaginoplasty, and has been on various formulations of estradiol therapy for over 20 years. On review of her investigations, her serum creatinine is 109 umol/L (1.23 mg/dL) but her eGFR has not been reported for the last 18 months. Laboratory providers cannot report eGFR if a male or female marker is not provided on the request form, as this is required along with age to estimate eGFR. Using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula, if classified as female, the eGFR would be 45 mL/min/1.73m\nclassed as Stage 3 chronic kidney disease and would meet the guidelines for intravenous hydration prior to procedure. However, if classified male, the patient would have an eGFR of 60 mL/min/1.73m\nwhich would be classed as Stage 2 chronic kidney disease and would not require prehydration. Which is the most appropriate eGFR to use?\nAccurately assessing renal function is essential for not only assessment of renal diseases, but also clinical situations that may potentially affect renal function (such as diabetes or radioiodine contrast administration) as well as considerations for medication dosing of renally cleared drugs. The most commonly used marker of renal function in clinical pathology laboratories is eGFR, which is calculated based upon an individual’s serum creatinine level, age, and sex (). Typically, people presumed male at birth have a higher eGFR than people presumed female at birth at the same level of serum creatinine because the formula assumes a higher muscle mass in men contributing to the serum creatinine independent of renal function. The difference between these groups (given the same age and weight) is more marked at higher levels (with a difference of approximately 30 when eGFR >90 mL/min/1.73m2), becoming much more similar as eGFR declines (difference of approximately 4 when eGFR <30 mL/min/1.73m2). In clinical situations where accurate assessment of renal function is necessary, such as in the transplant setting, it may be more appropriate to use 24-hour urine creatinine clearance, urinary inulin clearance (), or serum cystatin c levels, which are less affected by sex and not affected by muscle mass in contrast to serum creatinine (). Inulin clearance and cystatin c are more expensive and less readily available. Creatinine clearance can be calculated on paired 24-hour urine and serum creatinine concentration and is independent of muscle mass and sex steroids. This can provide a baseline estimation for renal function and cumulative serum creatinine results can then be used to monitor decline in renal function with aging.\nFrom a practical perspective, laboratory reports will need to make an assessment on how to report the eGFR for trans individuals. For individuals receiving masculinizing or feminizing hormone therapy, changes in body composition appear to be maximal in the early period after commencement, evident within the first 3 months of treatment (, ). For those receiving masculinizing hormone therapy with testosterone, given higher muscle mass and lower fat mass compared to females, the male CKD-EPI formula would be more appropriate. Conversely if a person has been on feminizing hormone therapy, which typically induces gain in fat and decrease in muscle mass from 3 months of use, then the female equations should be used. It would be a challenging task to expect pathology laboratories to provide the “right” eGFR given limited access to clinical information.\nWe recommend that the treating clinician specify the sex-specific reference interval desired for reporting on the laboratory request (ie, female for a trans person using feminizing hormone therapy). Using current laboratory information systems, the gender marker can be used as a field to specify the reference range desired for reporting. While the binary female or male gender may not necessarily reflect the individual’s gender, this will allow for the appropriate reference range to be reported and the trans patient informed so they can prepare to be misgendered. For laboratory providers, if the gender marker is unknown, then treating clinicians should be contacted to specify the sex-specific reference interval desired.\nFor the trans woman described in Case 2 who was on longstanding feminizing hormone therapy with female body composition, the female reference range for renal function would be most appropriate triggering appropriate renoprotection prior to administration of radioiodine contrast for her angiogram. From a harm reduction approach, given the absence of data in the field, if either the male or female calculated eGFR suggests renoprotective strategies, then this can be implemented. A 24-hour urine creatinine clearance can also be performed to more accurately assess renal function.
A 49-year-old trans man who had been on testosterone therapy for 10 years presented to the emergency department with central chest pain. His high-sensitivity cardiac troponin was 24 ng/L (female reference range <16 ng/L, male reference range <26 ng/L). How should he be managed?\nCardiac troponin is released from damaged cardiomyocytes and is one of the most common biomarkers used in the prediction of myocardial infarction. There is considerable debate regarding the use of sex-specific reference ranges for high-sensitivity cardiac troponin (hs-cTn), as there is uncertainty whether the use of sex-specific reference limits impact upon clinical management or outcome prediction (). However, as upper reference limits based on sex-specific 99th percentiles for hs-cTn are subtly higher for people recorded as males than those recorded females in population studies (), use of sex-specific cutoffs for hs-cTn assays have been endorsed by the International Federation of Clinical Chemistry and Laboratory Medicine (). The difference has been attributed to people presumed male at birth having a larger cardiac mass as well as subclinical coronary artery disease (). No studies have been performed to examine cardiac mass changes that may occur with masculinizing hormone therapy in people presumed female at birth. There are however data in polycystic ovary syndrome in which high testosterone concentrations are a clinical feature (albeit far lower than testosterone concentrations seen in transgender men). Polycystic ovary syndrome has been associated with higher left ventricular mass index and larger left atrial diameter over 5 years of follow-up, even after adjustment for blood pressure, body mass index, glucose, and lipids (). Large population-based studies have also shown that left ventricular mass correlates with body weight, lean body mass, and fat mass (). There is currently insufficient data to draw an inference regarding the appropriate reference range in people using gender-affirming hormone therapy, and emphasis must be placed on clinical history, electrocardiogram (ECG) changes, and serial trajectory of hs-cTn levels if the hs-cTn falls in between the male and female-specific reference ranges.\nDespite the fact that Case 4 had been on established testosterone therapy for 10 years with resultant male body composition, there is insufficient data to suggest that cardiac remodeling or change in cardiac size occurs\nwith high (or low) testosterone concentrations. Despite the risk of being oversensitive, in order to minimize the risk of missing an acute coronary event, we suggest that the reference range of the sex presumed at birth (female) should be used to interpret hs-cTn, provided the patient is informed of this rationale in addition to monitoring with serial troponin to ensure there is no rise. Case 3’s subsequent hs-cTn was elevated above the male reference range and his ECG revealed anterior ST-segment depression consistent with acute coronary syndrome.
Mr. S is a 31-year-old, single, unemployed gentleman from a low socioeconomic Tamil-speaking background, who first came to psychiatric hospital in 2003 at the age of 17 years within 10 days of onset of symptoms of psychosis and mania. He was treated with tablet risperidone up to 4 mg/day. He responded well and even went back to school. After 9 months of regular treatment, he stopped medicines. Two months after stopping of medicines he had relapse of psychotic symptoms including Schniderian first rank symptoms without any mood symptoms. His diagnosis was revised to paranoid schizophrenia. He failed trials of tablet risperidone 8 mg/day, tablet olanzepine 25 mg/day, a course of 10 sittings of electroconvulsive therapy, and injection fluphenazine decanoate depot 100 mg intramuscular every month. He did not show significant improvement. He was started on tablet clozapine and the dose was gradually built up to 450 mg/day by 2007. He was on regular follow-up for 9 years during which he had fluctuations in psychiatric symptoms but was managing well without any physical health issues.\nIn 2016, he developed pain in the left lumbar region following trivial trauma (while using a crowbar) and later developed a swelling in the region for which incision and drainage were done at a primary health center. When the ulcer did not heal for about 3 months, he was referred to a surgical department of a teaching hospital for further management. The non-healing ulcer in the incision site of left lumbar gradually had increased in size and was associated with passage of air through the ulcer while defecating or straining. There was no history of abdominal distension, vomiting, obstipation, hematemeis, malena, or fever. Physical examination revealed a soft non-tender abdomen.\nRoentgenogram of abdomen and ultrasonography investigations revealed a foreign body in the abdominal cavity just below the diaphragm without any other features of obstruction or perforation. Contrast-enhanced computer tomography and magnetic resonance imaging revealed a linear foreign body forming a fistula communicating with splenic flexure of the colon [].\nThe patient was posted for elective exploratory laparotomy. On laparotomy, an intact ball point pen of size about 11 cm in length was found to be the foreign body with its tip inside the lumen of splenic flexure and its rear end facing the external ulcer []. The pen was carefully delivered through the external wound and the sealed perforation of size 1 × 1 cm was closed primarily []. Postoperative period was uneventful and the patient was discharged on the 11th postoperative day.\nThe patient recollected that he had swallowed the very same pen in 2004 when he had been very psychotic []. He reported that he had vague abdomen pain on and off, which he did not feel serious enough to report. There was no record of abdomen pain in the patient's case notes over the previous 13 years.\nHe is doing physically well and is on regular follow-up. He is not regularly employed but helps his family in household chores. He is currently on clozapine 450 mg/day, on which he has a serum level was 933 ng/mL.
A 31-year-old gravida 2 para 1 with a gestational age of 37 weeks 6 days presented with the diagnosis of placenta percreta, which had invaded the bladder. Her past obstetric history included a previous caesarean section for placenta praevia. In order to avoid obstetric hysterectomy, which would have led to sacrificing a part of the bladder, a staged procedure that involved bilateral internal artery balloon catheterisation, caesarean section delivery, and embolisation was planned.\nAn informed written consent was obtained after explaining the risks and benefits involved in the procedure. Adequate blood was reserved, and the blood bank was informed about the possibility of massive blood transfusion. Keeping the possibility of conducting a caesarean section in the interventional radiology suite, arrangements were made with the required anaesthesia equipment to deal with the airway, operating instruments, neonatal resuscitation, and portable lights for such an emergency.\nIn the interventional radiology suite monitoring along with invasive arterial blood pressure was established. Two wide bore 18 gauge cannulae were secured. Under local anaesthesia, bilateral internal iliac artery balloons were placed through right femoral artery []. Injection heparin 3000 units was given intravenous (I.V.) Accompanied by the anaesthesiologist and trained staff, the patient was transported to the operation theatre with adequate monitoring. During the procedure, and during the transportation, a wedge under the patient's right hip to facilitate left uterine displacement and also protect the femoral artery sheath. In the operation theatre, general anaesthesia was instituted. Post-delivery oxytocics were avoided to prevent placental separation. The balloons in the internal iliac arteries were inflated intra-operatively to control the haemorrhage. The total blood loss during surgery was 800 ml. A healthy baby of 3.2 kg was delivered. Crystalloids were used during the procedure.\nIn order to embolise the internal iliac artery [], the patient was once again transported to the interventional radiology suite with monitoring and ventilation. At the end of the procedure in the radiology suite, patient was reversed and extubated. The placenta was left in situ, and she received 4 doses of methotrexate 1 mg/kg I.V. along with leucovorin rescue 0.1 mg/kg in the post-operative period. Serial ultrasonography and beta human chorionic gonadotropin showed a downwards trend. The patient was discharged on 7th post-operative day without any complications. Complete resorption of the placenta with the absence in the Doppler flow took 14 weeks.
A 55-year-old female with one-sided nasal obstruction and rhinorrhea in her nose for more than five months referred to our center in the ENT department of Khalili Hospital (Shiraz, Iran) in 2014. She was a known case of papillary thyroid carcinoma with metastases to the pelvic and lung. She had a history of severe bone pain and haemoptysis (more than a year) and was a candidate for total laryngectomy and thyroidectomy due to her advanced thyroid cancer. However, due to the dissatisfaction of her visitors, she only underwent total thyroidectomy. Examination of the patient revealed an ulcer mass covered with crust in the anterior and inferior part of the right-sided nasal cavity.\nPatient’s PNS CT with contrast revealed an irregular border mild enhancing tumoral solid mass measuring 30×30 mm at the anteroinferior of the right nasal cavity without calcification or lytic osseous lesion at adjacent bone and PNS were clear (). Based on the roll out of vascular lesion, a biopsy was done. The biopsy result indicated high suspicious to carcinoma. Thus, the patient was scheduled for mass excision with functional endoscopic sinus surgery (FESS). After a general and local anesthesia, bilateral endoscopic sinus was done. The left nasal cavity was normal for mucosal lesion, but a mass measuring approximately 3×3 cm was seen in the anteroinferior part of the right nasal cavity that involved uncinate posteriorly and inferior turbinate inferiorly. The mass was removed with inferior turbinate. Right uncinectomy, right antrostomy and right anterior ethmoidectomy were done. Right maxillary sinus was viewed with endoscope and showed no mass involvement. Septum showed neither mass nor involvement. The mass was sent for pathology and the report revealed metastatic papillary cell carcinoma (figures -). The patient was symptoms free at 6-month and 1-year follow-up after the surgery.\nWritten informed consent was obtained from the patient for the publication of this case report and any accompanying images according to ethical consideration of Shiraz University of Medical Sciences.
A 45 year old Caucasian woman had a long history of falls due to progressive ataxia since the age of 10. Her birth history and early developmental milestones were unremarkable. She completed secondary school and achieved basic qualification in education but was never good in sport. At age 17, she developed poor night vision and bilateral hearing deficit. She had bilateral cataract surgeries and used hearing aids at age 31. She experienced fatigue but did not complain of overt muscle weakness. She developed moderately heavy proteinuria (Albumin to creatinine ratio 152) but with normal serum albumin level since age 43.\nHer mother has glucose intolerance and her father has sensorineural deafness. There was no family history of neurological disorder, eye problem, or cardiomyopathy. All her siblings are fit and well, and as such did not request molecular genetic testing.\nHer resting blood lactate level was normal and creatine kinase (CK) level was 276 U/L. There was no glucose intolerance. Her renal function declined gradually and the current urea and creatinine levels were 11 mmol/L and 97 µmol/L, respectively (compared to 5 mmol/L and 88 µmol/L 8 years ago). Renal ultrasound demonstrated loss of cortico-medullary differentiation, increased echogenicity and asymmetrical kidney size (left kidney measured 7.9 cm, right kidney 10.2 cm). Nerve conduction studies were normal at age 28. Her initial CT head and cranial MRI showed bilateral basal ganglia calcification, periventricular white matter changes and cerebral and cerebellar atrophy ().\nClinical examination (at age 43) revealed pigmentary retinopathy, deafness, bilateral pes cavus, areflexia in the lower limbs, mild myopathy with MRC grade 4+/5, cerebellar signs, loss of proprioception sense and vibration sense in the lower limbs and broad-based gait.\nShe was admitted to hospital with left sided weakness and loss of mobility at age 44. The neurological deficit evolved over 12 hours. There was no associated speech disturbance or visual field defect. Her ECG showed sinus rhythm and she had hypertension. Cranial MRI revealed acute changes involving the right internal capsule and lentiform nucleus (). She was treated with antiplatelet, angiotensin converting enzyme inhibitor, oral L-arginine and co-enzyme Q10. Further cardiac assessment including 48 hour ambulatory ECG and transthoracic echocardiogram was unremarkable. Despite a period of rehabilitation, she only made partial recovery and required walking aid for mobility. In addition, the cerebellar syndrome has progressed with worsening dysarthria and ataxia on the last clinic review.
A 31-year-old male was admitted to our hospital with an open fracture, classified as Gustilo IIIa, of the tibia and fibula on the right leg 2 weeks after a road traffic accident (A). The patient had no comorbidities, no history of musculoskeletal disease, and no notable medical history and reported not smoking or consuming alcohol.\nPreviously, in a tertiary hospital, the patient underwent debridement and was later referred to our hospital, where we performed open reduction internal fixation (ORIF) surgery (B). The patient had otherwise remained healthy, and the surgical wound healed flawlessly without any active infection in any system. Nevertheless, on Day 2 postoperatively, he received 3 units of blood via transfusion and began mobilization.\nUpon being admitted to the hospital, the patient was administered 1 g of antibiotic cefuroxime intravenously 3 times per day until receiving none on Day 8 postoperatively. Although discharged to his home 8 days after the operation, he returned 20 weeks after surgery with complaints of implant exposure at the wound site and a fever of 101.3 °F for 4 days. From the outside, the wound appeared tenderness to palpation, although exposed implants measured 2 cm long and 1 cm wide ().\nThe patient underwent radiological examination, and the results showed new bone thickening that formed a sheath, or involucrum, covering the sequestrum and infected tissue (A). Considering the symptoms, physical examination, and radiological examination, the most likely preoperative diagnosis was stage 4 chronic osteomyelitis, according to the Cierny–Mader staging system ().\nWhen the elevated temperature persisted, debridement was performed, and when pus was observed, the internal fixation was replaced (B). Cultures taken from bone lesion revealed Staphylococcus epidermidis and Enterococcus faecalis. Except for S. epidermidis, the other infection agents are rarely found in our department and hospitals.\nWhen the patient's body temperature rises to 103.2 °F, treatment proceeded with the intravenous antibiotic cefazolin due to the patient's allergy to penicillin and surgical debridement () in an effort to control the infection and maintain internal fixation until the fracture fused. As a postoperative outcome, the patient showed satisfactory progress at 6- and 12-month follow-up.
Our patient was a 47-year-old male with past medical history including aorto-occlusive disease status post femoral-popliteal bypass, with peripheral artery disease, coronary artery disease, and tobacco dependence. He initially presented with right groin and lower-extremity numbness with an otherwise unremarkable review of systems. The patient was diagnosed with right limb occlusion with critical limb ischemia of the right lower extremity due to an aorto-femoral bypass graft occlusion. Initial workup included a computed tomography (CT) angiogram of the chest, prior to treatment of the occlusion with a femoral-femoral bypass.\nComputed tomography angiography (CTA) of the chest revealed a 1.4 cm nodule at the left lung apex, slightly cavitary in nature together with a left paratracheal soft tissue density that was suspected to be adenopathy related to pneumonia that was being treated. The lesion was considered to be incidental with the recommendation of short-term follow-up with another chest CT in three months. There was no prior imaging for comparison.\nTwo months later, the patient presented to the emergency room with bilateral chest pain and associated shortness of breath and dyspnea. He was admitted to the intensive care unit (ICU) for respiratory instability and treated for multiple bilateral pulmonary embolisms. The diagnosing CTA of the chest showed an increase in the left upper lobe mass density with 2.5 cm x 2.4 cm dimensions including marked interval increase in diffuse mediastinal and bilateral hilar adenopathy involving levels T5, T10, and T11, suggesting a primary neoplasm with metastatic disease. The primary lesion was pleural based and thought to be invading the pleura. Once the patient stabilized, a CT-guided left upper lobe biopsy was obtained.\nBiopsy revealed a poorly differentiated non-small cell carcinoma consistent with squamous cell carcinoma. Sections showed nests and individual large cells with brisk mitotic activity with medium to large nuclei. There was considerable tumor necrosis. Immunohistochemical stains showed positive staining for p63 and negative for TTF1. Morphology and stains were consistent with squamous cell carcinoma of the lung. It was suggested that the pulmonary embolisms the patient experienced were attributed to a hypercoagulable state related to malignancy.\nOncologic positron emission tomography (PET)/CT scan suggested invasion of the pleura with perivascular and lymphatic metastatic involvement, confirming a hypermetabolic left upper lobe mass of 2.5 cm x 2.8 cm with SUV of 10.7 (Figures -) and hypermetabolic left hilar adenopathy (Figures -). Subsequently, a magnetic resonance imaging (MRI) of the brain was completed for evaluation of metastasis. A 6 mm ring-enhancing metastatic lesion was noted in the left frontal lobe with surrounding edema (Figures -). The imaging was otherwise unremarkable.\nThe initial treatment plan included a radiosurgery approach to the solitary brain lesion. The lesion was treated with five volumetric arc therapy (VMAT) beams with the isocenter located in the center of the lesion, which was contoured on the MRI images. A total peripheral dose of 2500 cGy delivered in five fractions was prescribed to the planning target volume (PTV). Dose-volume histogram (DVH) analysis of the target lesions showed dose statistics (minimum, maximum, and mean) of 2396.0 cGy, 2941.2 cGy, and 2759.3 cGy to the PTV, respectively. The total volume of the gross lesion and margins was 0.4 cc. The total volume of tissue receiving 100% of the total prescribed dose (V100%) was 0.5 cc. The patient did not receive any form of systemic therapy, such as chemotherapy or immunotherapy.\nPost-treatment MRI of the brain at one-month follow-up after the initial brain lesion diagnosis showed a reduction in size from the original 6 mm nodule (Figures -) on the stealth protocol study. Remarkably, repeat PET/CT four weeks post-treatment stereotactic radiosurgery treatment (SRS) revealed no appreciable mass in the left upper lobe (Figures -) with resolution of hypermetabolism. Fluorodeoxyglucose (FDG) activity in the left hilum gave SUV level 2.2-2.7, an improvement from the previous SUV of 9.3 (Figures -). Chest CT confirmed that there was no longer an appreciable left upper lobe mass. An additional follow-up chest CT was completed two months later (three months post-treatment) confirming complete resolution of the original left upper lobe pleural-based mass.\nThe most recent imaging at seven months post-treatment continued to remain free of residual left upper lobe and mediastinal masses on chest CT. Brain MRI showed complete resolution of the solitary metastatic focus in the left frontal region. There was no evidence of new metastatic disease.
Written informed consent was obtained from the patient for publication of this report. A 54-year-old man visited our clinic with a sudden onset of dizziness and left-sided hearing loss a day before. The patient was diagnosed with hypertension and diabetes for six months and was on medication. The dizziness was rotatory and persisted for several minutes, but the symptoms of nausea and vomiting were not severe. The left-side ear was accompanied by earfullness and tinnitus similar to a “wing” sound, and no sensory abnormality of the face, headache, diplopia, swallowing disorder, consciousness disorder, or movement disorder was observed. The otoscopic examination was normal on both sides of the ear. In the pure-tone hearing test, the left side showed sensorineural hearing loss localized to the lowfrequency region () and the right side was normal. No prolongation of the latency period was found in the auditory brainstem response test, and no nystagmus was observed in the spontaneous nystagmus test, gaze nystagmus test, and positioning nystagmus test. Although the patient was recommended hospitalization for the sudden onset of hearing loss with dizziness, he decided to proceed with steroid therapy on the outpatient basis for personal reasons. Five days later, hearing was restored to normal range () and dizziness improved, but the left low-frequency hearing was reduced again after one week (). Temporal bone magnetic resonance imaging revealed no evidence of abnormal lesions in bilateral internal auditory canal and brain parenchyma. The patient was diagnosed with a possible Meniere’s disease and started conservative treatment at the outpatient clinic. After one year of follow-up, left-sided hearing loss and dizziness did not worsen, but the follow-up was lost afterward. Seven years later, he visited the emergency room with dizziness, vomiting, and headache. The symptoms subsided after intravenous hydration and medication. Three days later, a non-rotatory dizziness occurred and left tinnitus became severe. According to the pure-tone audiometry, left
A 10-year-old girl first noted a swollen left knee and underwent repeated arthrocentesis. At age 13, she underwent arthroscopic surgery and was diagnosed with benign TGCT. She subsequently underwent numerous synovectomies to treat local recurrences and radiation therapy to her left knee joint at age 15. Ultimately, her disease spread to her upper calf and posterior thigh. At age 32, her upper calf lesion was resected, and the tumor in her posterior thigh was treated with radiation. At age 34, swelling of an inguinal lymph node was noted and fine needle aspiration was consistent with malignant TGCT. Other staging scans revealed a pelvic mass and a sub-centimeter pulmonary nodule. Her disease remained stable after four cycles of doxorubicin/ifosfamide and she subsequently received gemcitabine/docetaxel as well as radiation therapy to her pelvis with stable disease for three months. She underwent left-sided above the knee amputation and excision of the intrapelvic masses. Eight months later, enlarging pulmonary nodules were resected. She was treated with sirolimus (rapamycin) and remained disease-free for eight months until a pulmonary nodule and two inguinal masses were noted. In 2007, at age 37, she was referred to our hospital and treated with sorafenib for four months with mixed response. She subsequently began on sunitinib 37.5 mg daily. Interval restaging scans showed no evidence of progressive disease for 15 months. She had significant interval progression of a right-sided pelvic mass while she temporarily stopped sunitinib in the perioperative setting of resection of painful metastatic nodules near the amputation stump (Fig. a, b, and c). Given that the drug had a significant role of controlling the disease, her sunitinib was restarted in combination with sirolimus (rapamycin). Her disease was under good control for eight additional months until she had progressive disease in the pelvis and underwent hemipelvectomy. She died of the disease at age of 39, six years after the malignant transformation.
The present case is about ES a 4-year-old male, an only child of his parents. He first presented to our children's out-patient department at the University of Nigeria Teaching Hospital Enugu in January 2008, on self-referral but had been previously seen at the University of Port Harcourt Teaching Hospital Port Harcourt, Nigeria. The complaints were swelling at the back, first noted at 2 weeks of age as a bony protuberance over the mid-spine. Other complaints were poor growth, especially of height, that parents had noted when ES was 1 year old. There were associated skeletal deformities: Chest wall, wrists, knees and ankle joints that were progressive over the next 3 years. The back swelling was non-tender and was not increasing in size; however parents had noted the head increased in size in relation to the rest of the body.\nOf note in prenatal and post natal history of ES is that mother's pregnancy was properly supervised in a tertiary hospital and the index pregnancy was said to have lasted 11 months and culminated in an emergency caesarian section. ES cried at birth and weighed 4.2 kg. He was exclusively breast-fed for 6 months, after which appropriate and adequate complementary feeding was started. He was also exposed appropriately to outdoor sunshine. Motor mile-stones were noted to be delayed. The child achieved head control at 6 months and walked at 17 months. Other milestones were within normal range. The child was fully immunized.\nFor the current illness, medical attention was first sought at a tertiary hospital where he was assessed and the diagnosis of rickets was made. He was started on high dose oral vitamin D and calcium for 1 year with regular follow-up visits. There was however no obvious improvement and the patient presented to our hospital.\nGeneral examination revealed [] a child who appeared short for his age with caput quadratum, craniofacial disproportion, coarse facial features, saddle shaped nose and thick lips with bilateral corneal clouding/opacity. ES was fully conscious, well-oriented but apprehensive with limited language skills. The anterior fontanel was closed. The cranial nerve examination revealed no abnormality and the deep tendon reflexes were not exaggerated. He had a normally erupted set of teeth that were stained dark yellow. His abdomen was protuberant with an enlarged smooth non-tender liver, 5 cm below the right costal margin but without splenomegaly. Hearing was not impaired. The cardio-respiratory examination was normal.\nThe musculoskeletal system revealed a severely stunted child with an apparent large head. The weight was 13.2 kg which was above the 50th centile with a height of 80 cm, which was below 3rd centile. The occipito-frontal circumference of 56 cm was at the upper limit of normal.\nThe upper to lower body segment ratio [US/LS] was 1.3. He had pectus-carinatum [] with Harrison sulcus but no costo-chondral beading. Other deformities noted included bilateral swelling of wrists and ankle joints [Figures -], a thoracolumbar gibbus [], bilateral genu valgum []. He walked with a waddling gait.\nA diagnosis of short stature of uncertain etiology was made with the following possible differentials: Vitamin D- resistant rickets, achondroplasia and MPS (probably Hurler syndrome due to the corneal clouding). An endocrine abnormality involving the thyroid gland was also considered.\nAlkaline phosphatase assay done was at a level of 59 mmol, which was normal. Serial serum electrolytes, calcium and phosphate levels as well as complete blood count were also done and were within normal ranges as well.\nThe 24-hr urine protein and uric acid was performed and were normal. The erythrocyte sedimentation rate was 14 mm in 1st hr westergreen; the thyroid function tests revealed a high normal T3, moderately elevated T4 and very low TSH titer. The growth hormone (hGH) was elevated at 2.3 ng (0.02-1). The mucopolysachariduria analysis and urinary electrophoresis for GAGs were however not done due to lack of facilities\nA full skeletal radiologic survey of all affected bones (skull, cervical, thoro-columbar spines and limbs) was done and X-ray images sent for expert radiological interpretation. This revealed the following: Osteoporotic spatulate shaped ribs which were pinched and constricted at the vertebral ends and flexed at the sternal ends []. The iliac bones were flared at the upper end and constricted at the acetabular ends. The acetabular angles were widened and the Menano-Sheriton lines undisturbed. The proximal femoral epiphyses were flattened. Femoral necks were flayed and the shaft angles widened causing significant valgus deformity.\nX-ray of the radius and ulna bones revealed an acute angle, substended by the axis of both bones tilting toward each other. The 2-5th metacarpal bones were noted to be constricted, pointing proximally with distal phalangeal hypoplasia. The spine showed localized kyphosis, hypoplasia of L1 body and vertebra. These findings were noted to be in keeping with dysostosis multiplex of MPS.\nHe was referred to the orthopedic surgeons for bone tissue biopsy and assay and discharged to outpatient follow-up. He was however lost to subsequent follow-up.
On August 1, 2017, a 38-year-old American woman with a negative past medical history presented to our Emergency Department (ED) with chest pain. Our patient stated that pain started on the morning of July 31 around 11:00 am, while participating in outdoor physical activities (Zumba) at a fundraising event. After 2 h into the workout, she began to feel chest pain, that was substernal, pressure-like, and throbbing in nature. The pain was non-radiating, six out of ten in intensity, and associated with diaphoresis and shortness of breath. Pain was alleviated in the ED when she was given sublingual nitroglycerin and intravenous morphine. She also stated episodes of a “fluttery feeling” and at times feeling lightheaded. She denied any previous history of a similar episode. She has no known cardiac history. Our patient did state that she never did any kind of exercise except for the activities of daily living. On review of her medical history, she stated that she was taking spironolactone for hirsutism, from August to January 2016 and then May 2017–present, with initial dosing of 125 mg titrated up to 150 mg and then back down to 125 mg due to muscle fatigue. Our patient had intentional weight loss of 30 lbs from March to July 2017. She follows a healthy diet and has a normal body mass index (BMI) of 24. Our patient denied any family history of cardiac disease or heart failure. She admitted to being a former occasional smoker and to drinking alcohol socially. She denied any illicit drug use. She works as a social worker, and reported that she does not experience much stress in her life and denied any “one big life-changing event” or any major stressful news. She reported a history of anxiety and was medicated approximately 4 years ago with alprazolam that was later discontinued as our patient was comfortable with her stress levels at that time.\nWhile in the ED, patient was hemodynamically stable with a heart rate of 60s–70s beats/min, respiratory rate of 12–20 breaths/min, blood pressure of 90s/60s mmHg, O2 saturation of > 95% on room air, and afebrile. On physical examination, our patient was awake, alert, oriented to self, others, time, and place. Her skin was warm, dry, with no apparent rashes. Her neck was supple and non-tender with no jugular venous distension or apparent masses. A cardiovascular examination showed a regular rate and rhythm, with no murmurs or gallops. Our patient did not demonstrate any lower extremity edema and pulses were intact bilaterally. Her lungs were clear with equal breath sounds. Her abdomen was soft and non-tender with no hepatosplenomegaly. No lymphadenopathy was appreciated. A neurological examination showed grossly intact cranial nerves 2–12, normal sensation, strength was full bilaterally, normal reflexes, intact coordination and normal gait. An electrocardiogram (EKG) was performed and showed sinus rhythm with no ST elevation/depression but noted T-wave inversion in leads I and aVL, and T wave flattening in leads V1 and V2. Her troponin levels were 0.294 and 0.231 consecutively. A chest X-ray showed mild atelectasis at the left lung base, prominent pectus excavatum deformity of the anterior chest wall, bilateral small pleural effusions or pleural scarring, and no evidence of pulmonary vascular congestion.\nAn echocardiogram was done and showed hypokinetic apical and mid-distal walls and hyperdynamic basal walls of the left ventricle (LV) with ejection fraction (EF) of 35–40%, consistent with apical ballooning syndrome (Fig. ).\nCardiac catheterization was subsequently done and showed depressed LV systolic function, ejection fraction of 30–35% with anteroapical dyskinesia and no evidence of coronary artery disease (CAD) (Fig. ).\nOur patient was subsequently treated with a beta blocker, and angiotensin-converting enzyme inhibitor. Our patient was discharged with a LifeVest (a wearable cardiac defibrillator) and instructed to follow up in 1 month with the cardiologist to have a repeat echocardiogram. One month later, during her follow-up with the cardiologist, she denied any episodes of chest pain, palpitations, or shortness of breath. At that visit, a repeat echocardiogram was done and showed normal findings with an EF of 60–65%, thus the LifeVest was discontinued. After that visit, patient was lost to follow-up. We followed CARE reporting guidelines in publishing our case report with important information from our case presented as a timeline (Table ).
A 25-year-old woman visited our hospital for left mandibular third molar extraction. She had no notable medical history. Before surgery, she complained of gastrointestinal discomfort after taking prophylactic antibiotics and anti-inflammatory drugs, but her symptoms had improved. To extract the third molar, IANBA was performed on the left side. For local anesthesia, 1.8 cm3 of lidocaine with epinephrine in a 1:80000 ratio (Huons Lidocaine HCL and Epinephrine Inj. [1:80,000], Huons co. LTD, Sungnam, Republic of Korea) was used. Immediately after anesthetic injection in the left mandibular foramen area, the left side of the patient's face turned pale white, and she complained of pain and discomfort in the left facial area (). Aspiration was not performed during injection.\nThereafter, she complained of pain and discomfort extending from the middle left facial region to the left orbital region, including the eye. After evaluating facial nerve function, we confirmed that the symptoms were not related to any complication caused by anesthetic injection into the facial nerve. Although the patient chiefly complained of eye discomfort, she showed no signs such as the inability to close the eye or weakness of the frontalis associated with facial nerve paralysis (). The patient was observed in a supine position. Signs indicating blanching were observed from the outside of the nose, upper lip, central facial region, and the left zygomatic area. The patient complained of discomfort accompanying pain in the region with blanching, especially around the eye. The symptoms had occurred immediately after anesthetic injection and became severe within 1–2 min. The symptoms remained stable, but they improved after more than 10 min (). The patient's pain symptoms also improved, but the ischemic sign in the left facial region did not improve completely, especially in the lateral nasal area.\nAs the patient did not complain of severe symptoms and showed improvement, her current condition was explained to her, and surgical extraction of the left mandibular third molar was performed. After extraction, her progress was monitored until her symptoms completely improved approximately 40 min after the initial facial blanching sign. She was informed again that it was a complication of anesthesia. We decided to conduct additional examinations and treatment if the symptoms reappeared after discharge. No notable additional symptoms were observed.
A 51-year-old woman presented with a 1-month history of recurrent abdominal discomfort and a 7-day history of pericardial effusion managed at her local hospital. After the removal of 200 ml of bloody pericardial effusion by pericardiocentesis, she experienced remarkable symptomatic improvement. She went to our outpatient department for follow-up treatment. She had no significant medical history. An electrocardiogram was unremarkable. Echocardiography revealed a heterogeneous mass in her right atrium and a small pericardial effusion. A computed tomography (CT) scan confirmed the findings of a large mass (7.0x8.3 cm) in the right atrium, with irregular enhancement on enhanced CT scan (Fig. ) and involvement of a coronary artery as well (Fig. ). Coronary arteriography revealed more than 60 % stenosis of the middle segment of the right coronary artery. Computed tomography of the chest and abdomen were unremarkable.\nAt surgery, the patient was placed on cardiopulmonary bypass using bicaval cannulation through a median sternotomy approach. A large mass was observed arising from the right atrioventricular groove and extending to the anterior of the right atrium. By opening her right atrium, the surgeons observed that the main body of the tumour was located in the wall of the right atrium, involving the right ventricle as well as the anterior leaflets of the tricuspid valve and encompassing the stem of the right coronary artery. The surgeons were diligent in removing the tumour; they also resected some tricuspid valve and involved the right ventricle wall, after which coronary artery bypass grafting was performed.\nGross examination showed the tumour to be generally grey-white tissue with a total size of 8x8x5 cm, with partial surface encapsulation (Fig. ); the cut surface was grey-pink, solid and firm with a few haemorrhagic areas (Fig. ). The size of the largest tissue fragment was 6.5x5.5x5 cm. Microscopically, the tumour displayed a mixture of spindle cell and epithelioid components in most areas, which mimicked carcinosarcoma (Fig. ) with a few slit-like structures (Fig. ) and necrosis. Only a small number of tumour areas were composed of pure spindle cell elements, which exhibited eosinophilic cytoplasm and round to oval nuclei with nuclear pleomorphism. Mitoses were readily observed (8-10/10 high-powered fields) (Fig. ). The epithelioid element was the main component in most mixed areas, comprising well-differentiated glandular structures with lighter cytoplasm and intraluminal eosinophilic material, and was observed to be blended with less voluminous spindled components (Fig. ). In very few areas close to the tumour border, there were solely obvious glandular structures mimicking adenocarcinoma (Fig. ). The right coronary artery was involved by the tumour and thrombus could be observed within the lumen (Fig. ). A small tumour embolus could be seen in the blood vessel. Immunohistochemical staining showed that the epithelioid components were positive for cytokeratin, CK19 (Fig. ) and S-100(focally). The spindle cell components were positive for calponin (Fig. ) and vimentin. Both components were positive for BCL-2 and CD99 (Fig. ). The Ki-67 index was 25 % in both components. Desmin, WT-1, calretinin and SMA were negative in both components. Details regarding the antibodies used are given in Table . Fluorescence in situ hybridization (FISH) showed the rearrangement of SS18 (Vysis SS18 Break Apart FISH Probe Kit, Abbott Molecular Inc., USA) in the tumour cells (Fig. ). Based on the above-mentioned findings, the final diagnosis was primary synovial sarcoma of the right heart involving the tricuspid valve. This study was approved by the Ethics Committee of the Peking Union Medical College Hospital, and informed consent was obtained from the patient.
A late preterm infant of 36 weeks gestation, product of spontaneous vaginal delivery with Apgar Score of 5 and 7 at 1 and 5 minutes respectively and admitted initially, was admitted initially as a case of multiple congenital anomalies with genital anomalies.\nThe infant was born to a 23-year-old Saudi female, G3 P1 + 1, who was not known to have any chronic medical illnesses, but with a history of a previous infant that had died of complicated surgically-corrected diaphragmatic hernia. She was on regular antenatal care follow-up in a private hospital. She had no history of pregnancy-related illnesses or exposure to radiation. There was a history of desogestrel/ethinyl estradiol oral contraceptive pills intake of 3 months duration that was discontinued by the mother who was 1 month pregnant. Regarding the family, there is the first-degree consanguinity between the parents (i.e., cousins), with no similar conditions being reported in the family.\nAt 28 weeks gestation, an ultrasound study revealed the presence of fetal omphalocele and accordingly she was referred to our hospital for feto-maternal services. The repeated ultrasound scan was of a limited anomaly. Amniocentesis was tried but failed due to advanced gestation.\nThe delivery went smoothly with the cephalic presentation of the infant and complete placental appearance with three umbilical cord vessels (two arteries/one vein). On examination, the infant looked pale but not cyanosed or jaundiced, with no apparent dysmorphic features. Central nervous system examination revealed an active infant moving upper and lower limbs freely, with myelomeningocele at the lumbosacral area (2 cm × 2 cm) that was covered by intact skin. The cardiovascular and respiratory examination was normal. Gastrointestinal and urinary systems examination revealed omphalocele minor below the umbilicus with an intact sac containing only the bowel. The central area of defect was identified as the caecal plate with a dilated prolapsed terminal ileum with the length of 4–5 cm presenting as characteristic “elephant trunk deformity.” There was a small pinhole-sized opening in the proximal ventral aspect of the prolapsed terminal ileum, which noted to be passing the meconium. On lateral aspects, there were exstrophy bladder plates with two hemispheric bladders, each of which contained a visible ureteric orifice. An imperforate anus with an anal dimple was noticed. The genital system examination revealed multiple genital anomalies in the form of asymmetrical widely bifid sacrolabial folds that were hyperpigmented. The gonad was palpable in the left side only with absent phallus and absent urethral opening [].\nInvestigations were performed, including radiographic studies and chromosomal analysis. Echocardiography showed a normal study. The chromosomal study revealed a normal male karyotype of 46, XY with no numerical or structural abnormalities discernible. A computed tomography (CT) scan revealed mildly balanced congenital scoliosis, widening of symphysis pubis indicating an open book pelvic deformity and evidence of congenital bilateral hip dislocation. A multilevel vertebral failure of formation and segmentation with hemivertebra were noted at the mid-thoracic and lower lumbosacral regions. A posterior spinal dysraphism at the lower lumbosacral region was noted that was associated with a low-lying spinal cord that herniates dorsally with skin coverage representing a tethered cord with myelomeningocele [].\nA multidisciplinary approach had been discussed with a multispecialty surgical team at our center. Due to the absence of a pediatric urology specialty in our hospital, the infant was transferred to a specialized center where the patient underwent a multi-staged surgical intervention to correct the complicated defect.
In May 2014, a 51-year-old morbidly obese woman (BMI 48), suffering from non-insulin-dependent diabetes, presented at the emergency department with a 20-year-old incisional hernia that had become incarcerated. At admittance, the abdomen was described with horizontal and vertical scars from former surgery and a discolored midline hernia measuring 30 × 50 cm. Acute CT of the abdomen demonstrated small bowel obstruction, and an immediate explorative laparotomy was performed via the vertical scar. Perioperatively, the abdominal wall defect measured 15 × 10 cm, and the ventricle, colon, and small intestine were encapsulated in a subcutaneous cavity. The lower 150 cm of the small intestine was cyanotic and torqued around the mesentery; detorquing resulted in revitalization. The intra-abdominal cavity was found shrunken and too small to contain the intestinal organs. Consequently, the fascia was split proximally and distally of the hernia port; however, the abdominal wall could not be closed without the use of three pieces of nonabsorbable mesh each measuring 35 × 35 cm (Fig. ). The intra-abdominal organs were enclosed in the new cavity, and the skin was closed above the cavity.\nIn the following days, the patient gradually developed necrosis of the skin covering the mesh. The wound was revised and necrotized tissue excised leaving a 40 × 50 cm defect with the underlying mesh being intact. Thereafter, the patient was treated with NPWT and surgically revised or cleansed and dressed every other or third day for a period of 8 months, aiming for granulation tissue formation upon the mesh. General anesthesia was used for the first 3 months, and thereafter, wound care was provided with the use of intravenous sedatives and pain medication, but no anesthesia. After another 2 months, wound dressings were performed in the ward without medication, and 5.5 months after the hernia operation, the patient was discharged and wound dressings were performed in the outpatient clinic. One specific nurse was dedicated to the task. After a total of 8 months, the mesh was covered with granulation tissue without infection (Fig. ) and split-skin grafts were harvested from both thighs and transplanted to the defect. The patient afterwards developed a low-output fistula from the small intestine, treated conservatively (Fig. ). The fistula sealed 6 months postoperatively. After immediate take of the transplanted skin, the mesh started to erode the overlying vital transplant and this problem worsened as the patient was mobilized (Fig. ). The mesh was very stiff, and wrinkles damaged the overlying skin. A long period of careful and meticulous removal of the exposed mesh was performed bedside or later in the outpatient clinic with tiny bits or threads being removed successively. Now, two years after, a thread can occasionally be removed, but more and more seldom.\nToday, our patient has begun her everyday life working 14 h per week. She has a small skin defect in the right lateral area where the native skin meets the transplanted area (Fig. ). The lateral skin area especially in the right side is very heavy, and this in combination with the strong elastic belt she must use to keep the hernia in place creates friction in the wound area. Unfortunately, the patient has gained about 20 kg since discharge from the hospital, which has been counterproductive for this problem. If massive weight loss can be accomplished, reduction of the excess skin and perhaps even hernia repair could be pursued, although the latter would entail considerable risk of intestinal damage.
An 85-year-old woman with a history of smoking presented with an abnormal shadow on chest X-ray, which was performed as part of a pre-operative evaluation for osteoarthritis of the knee in December 2012. A chest computed tomography (CT) scan revealed a 2.8 cm nodule in the right upper lung lobe (Fig ) and fluorodeoxyglucose–positron emission tomography (FDG-PET) showed uptake only within the nodule. Although transbronchial lung biopsy (TBLB) was negative, cytology of bronchoalveolar lavage fluid from the right upper bronchi showed atypical cells suspicious for malignancy.\nThe patient was referred to our hospital for curative pulmonary resection in March 2013. Her physical examination was unremarkable, and her blood examination, including tumor markers, showed anemia with a hemoglobin value of 10.2 mg/dL. The cause of the anemia was not clear despite scrutiny. In April 2013, the size of the tumor shadow decreased from 2.8 to 1.8 cm (Fig ). We strongly suspected the tumor was benign rather than malignant and planned to perform a follow-up imaging examination. The tumor shadow remained unchanged for the next three months (Fig ). In July 2013, the patient was diagnosed with rheumatoid arthritis and began to receive glucocorticoid treatment. In January 2014, the tumor increased from 1.8 to 4.8 cm (Fig ) and a TBLB of the tumor was performed with suspicions of inflammatory disease or malignancy; however results of the TBLB were inconclusive. A chest CT scan was repeated in June 2014 and showed that the tumor shadow had further enlarged to 8.6 cm, with swelling of the mediastinal lymph nodes and suspected invasion of the superior vena cava and chest wall (Fig ). FDG-PET showed uptake within the tumor with a maximal standard uptake value of 23.6, but did not show uptake within the mediastinal lymph nodes. An ultrasound-guided biopsy of the tumor revealed a proliferation of tumor cells with large and irregular nuclei (Fig ). We diagnosed primary lung cancer, cT4N0M0, stage IIIA, according to the TNM (tumor node metastasis) Classification of Malignant Tumors (7th edition).\nA right upper lobectomy with lymph node dissection in the hilum and right upper mediastinum was performed. Although the tumor had invaded the mediastinal fat tissue and parietal pleura, it did not invade the superior vena cava. The patient experienced a good postoperative course with no complications. On pathologic examination, the tumor was 7.5 cm in diameter and invaded the mediastinal fat tissue, but the lymph nodes did not show any evidence of metastasis. The histopathological results were similar to those from the biopsied tissue, and we diagnosed lung LCNEC, pathological stage IIIA (T4N0M0), based on immunohistochemical studies. The tumor was positive for synaptophysin, thyroid transcription factor-1, and cytokeratin 7, and was negative for chromogranin, CD56, and p63 (Fig –). The patient did not receive postoperative cytotoxic chemotherapy because of her own request and her advanced age.
A 73-year-old male with edentulous maxilla was referred to the University Department of Oral and Maxillofacial Surgery of the “Evaggelismοs” general hospital due to a migrated implant into the right maxillary sinus. The patient suffered from chronic obstructive pulmonary disease and therefore he had quitted smoking. Five years ago he underwent dental rehabilitation with the placement of six implants in the maxilla and four in the mandible. In less than 2 months after initial placement, all implants had failed to osseointegrate. A year and a half later the patient underwent guided bone regeneration with bovine-derived xenograft and 7 months after this point, another 10 implants were inserted into both the maxilla and mandible. Two months later, all implants had once again failed to osseointegrate. During the attempt of removal by the dentist, one of the implants was displaced into the maxillary sinus, without the dentist being able to retrieve it. The patient then visited another dentist, who could not either remove the migrated implant.\nUpon arrival to our clinic, a full medical and dental record was retrieved from the patient, and he was scheduled for surgical removal of the implant. Prior to operation, the patient underwent a radiographic examination with water’s X-ray (Fig. ), as well as CBCT examination (Fig. ) which confirmed implant migration and revealed its exact position inside the maxillary sinus.\nSurgical procedure initiated with local anesthesia by injecting xylocaine 1% andepinephrine 1:100,000 solution in the soft tissues involving the right half of the maxilla. After a crestal incision, a full-thickness mucoperiosteal flap was raised, exposing the anterior-lateral wall of the maxilla in an area extending from canine to molar region. Using a high-speed rotary instrument under sterile saline solution irrigation, a rectangular window was created in the anterior-lateral maxillary wall. The implant was detected through the bony window and captured by a mosquito forceps (Fig. ). The mucoperiosteal flap was then placed back at its initial position and was anchored with 4.0 resorbable sutures (Fig. ). Amoxicillin (1 g twice daily) was prescribed for 1 week with analgesic treatment. Sutures were removed 2 weeks after surgery. The patient was advised to follow a soft diet plan for 4 weeks and was provided with proper oral hygiene instructions. He underwent scheduled visits on a monthly basis to check the course of healing for the following 6 months.
A 42-year-old female patient was admitted to our outpatient clinics with hypertension. She presented with long-standing essential hypertension that was resistant to pharmacological therapy with five different antihypertensive drugs, namely irbesartan 300 mg/day, Triazide 25 mg/day, amlodipine 10 mg/day, spironolactone 100 mg/day and nebivolol 5 mg/day. Her office blood pressure was 175/100 mmHg. All causes of secondary hypertension were excluded. She did not have diabetes mellitus, coronary artery disease or renal failure. Transthoracic echocardiography showed normal left ventricular systolic function and mild mitral regurgitation. Fundoscopy revealed grade 2 hypertensive retinopathy. Due to the uncontrolled nature of the resistant hypertension and progression of target organ damage, the patient was eligible for percutaneous renal denervation treatment.\nUnder local anesthesia, the femoral artery was accessed in standard technique, 5000 IU UF heparin was given intravenously and fluoroscopic angiography was performed to visualize the renal artery. Angiography showed normal configuration of the right renal artery (diameter >4 mm, length >20 mm, no stenosis; ). While there was a well developed accessory renal artery on the left side []. The diameter of both left renal artery and left accessory renal artery were greater than 4 mm and their length was greater than 20 mm [].\nTo prevent renal artery spasm IV nitrate was injected directly to renal artery. Midazolam was used for sedation. Then the specially designed and commercially available radiofrequency ablation catheter (Symplicity, Ardian, Medtronic) was inserted into both renal arteries, and accessory left renal artery.\nDenervation was performed with application of 6 low-power radiofrequency treatments along the proximal portion of the vessels. Mean temperature was 50°C during 2 min of ablation at each point. Radiofrequency ablation was applied to both renal arteries and accessory left renal arteries without apparent procedural complications. There were no vascular complications.\nAfter the procedure, the patient was followed in the coronary care unit for one day. Immediately after the procedure, the patient's blood pressure was reduced to 110/60 mmHg. No change was observed in renal functions of the patient. The patient was discharged at the third day with nebivolol 5 mg/day and amlodipine 10 mg/day. Her blood pressure was 120/80 mmHg at office and ambulatory blood pressure monitoring was repeated which revealed an average systolic and diastolic blood pressure of 119/63 mmHg one month later. The patient was prescribed only amlodipine 10 mg/day.
A 69-year-old male with known hypertension and poor dentition presented to the hospital with 5 months of dry cough, night sweats, and weight loss. Physical exam revealed a new 2/6 diastolic murmur. Investigative TEE showed a left aortic perivalvular abscess with vegetations and severe aortic insufficiency. The diagnosis of native valve subacute endocarditis was made, with blood cultures positive for Streptococcus anginosus. The patient was discharged on a 1-month course of IV Ceftriaxone and scheduled for a minimally invasive aortic valve replacement with possible aortic root reconstruction on completion of antibiotic therapy. On day 26/28 of antibiotic therapy, the patient presented to his local emergency room after having experienced a first-time seizure and loss of consciousness. He had no personal history or known family history of seizures or seizure disorders.\nOn admission, physical exam showed elevated blood pressure at 151/61 with a regular heart rate of 68, a faint diastolic murmur at the base, and obvious favoring of the right upper and lower extremities without pronator drift. Physical exam was otherwise unremarkable. The patient was given Levetiracetam 1000 mg and Dexamethasone 6 mg for seizure management.\nAt the patient’s local ED, initial contrast CT of the head showed a 1.5 cm rim enhancing lesion with no reported hydrocephalus. He was transferred to our center for further care. On the morning following transfer, the patient suffered a second left-sided seizure at which point an MRI with and without contrast was performed. The MRI revealed a 1.4 × 1.4 × 1.6 cm rim-enhancing lesion in the right middle frontal gyrus with surrounding vasogenic edema suggestive of a pyogenic abscess []. Further, both cerebral hemispheres showed focal areas of abnormal leptomeningeal and patchy cortical enhancement suggestive of early cerebritis.\nAfter visualization of the suspected abscess on MRI [], a repeat CTA was performed revealing a 1 mm aneurysmal dilation in the M4 frontal branch of the right distal middle cerebral artery (MCA) [ and ]. Imaging was highly suggestive of a mycotic aneurysmal rupture with bleed and active inflammation. A cerebral angiogram with embolization was scheduled and performed shortly thereafter. Such cases are typically treated with surgical ligation and removal but due to this patient’s poor condition, a minimally invasive endovascular approach was favored.\nVascular access was first gained through the right femoral artery. An Envoy guide catheter was advanced to the right internal carotid artery through roadmap assistance at which point a 3D angiogram was taken to better visualize the right MCA. Due to the tortuosity of the patient’s right iliac system, the guide catheter was unable to be advanced any further. Instead, left femoral artery access was gained and the vascular catheter was advanced in a similar fashion. The guide catheter was advanced to the M2 branch of the right MCA where it was exchanged for an intermediate catheter over a microcatheter over a Synchro microwire. A superselective M3 and M4 angiogram were then performed, allowing for visualization of the 1 mm infectious aneurysm in the cortical M4 frontal MCA branch [-]. On visualizing the feeding vessels, Onyx 18 material was advanced through the Synchro microwire into the M4 pedicle, filling the aneurysm []. The Envoy catheter was removed and 3-mm J-wires were advanced into the vascular sheaths. The patient remained stable for the duration of the 1-h procedure and was then transported to the neurointensive care unit (NICU) as planned.\nOne day following surgery, the patient developed seizures with partial status epilepticus. CT of the brain showed a hyperdensity in the subarachnoid space with subtle ventriculomegaly due to rupture of the IIA with subarachnoid hemorrhage (Modified Fisher Scale grade 2/Hunt and Hess grade 3) status post embolization. The patient was closely monitored for deterioration of symptoms. Two days later, follow-up CT of the brain revealed stable subarachnoid and intraventricular hemorrhage with no hydrocephalus. It was ultimately decided no external ventricular drain would be placed given the lack of hydrocephalus and stability of bleed. The patient remained in the NICU for 22 days where he was placed on Levetiracetam, Clobazam, and Lacosamide for seizure control. During this time, the patient was followed closely by neurology with daily electroencephalograms and by pulmonary/critical care as he remained intubated on mechanical ventilation post procedure. Infectious disease also followed the patient for infective endocarditis and later began triple antibiotic treatment with Vancomycin, Cefepime, and Metronidazole for ventilator associated pneumonia and right middle frontal gyrus abscess.\nOn leaving the NICU, the patient was evaluated by physical medicine and rehabilitation who initiated aggressive physical therapy, occupational therapy, and speech therapy. The patient was discharged to a hospital-adjacent rehabilitation center 1 week later where he continued to undergo physical, occupational, and speech therapy for 1 month.\nFour months after the patient’s initial hospital discharge, he was deemed a suitable candidate to undergo cardiothoracic surgery. The patient underwent an aortic and mitral valve replacement without complication and was discharged home after 4 days of hospital care.\nFor 6 months, the patient remained out of the hospital with mild lifestyle modifications and changes to mood (including some confusion) which improved on cessation of steroid therapy.\nThe patient was readmitted to the hospital 6 months after cardiac surgery when he suffered a left sided seizure with associated Todd’s paralysis attributed to possible nonadherence. During the admission, he suffered a pulmonary embolism for which an IVC filter was placed. He was discharged home again with daily speech, occupational, and physical therapy. Since the episode, the patient had no major hospital admission and has been adherent to his antiseizure regimen of Levetiracetam, Lacosamide, Topiramate, and Clobazam.\nAt present, the patient is 1½ years status post initial rupture of the IIA. The patient is currently alive, and his mood has significantly improved per both his family and healthcare team. He has suffered several minor seizures in the interim due to medication titrations. However, he has reached the point where he is again confident enough and possibly eligible to begin driving school.
A 63-year-old Caucasian female with squamous cell carcinoma of the vocal cords developed a small grayish lesion on the ventral surface of her tongue one month after local external radiation therapy (XRT). It gradually increased in size and the patient noticed 2 new lesions (3 × 2 cm and 4 × 2 cm), one on either side of the tongue (Figures and ). The lesions had well-demarcated margins with slightly raised and rolled edges, without bleeding or discharge, and were initially painless, but later became extremely painful. Biopsy did not reveal any malignancy. Symptoms progressed and she developed shortness of breath, stridor, and hoarseness of voice that prompted evaluation by an otolaryngologist. Laryngoscopy revealed grayish exudates on both vocal cords that were similar in appearance to the oral lesions. No oropharyngeal mucositis was seen. Complete blood cell count at the time of presentation did not reveal any abnormalities. Information regarding mucositis or leukopenia immediately following XRT was not available. The patient was started empirically on oral fluconazole 400 mg/day for presumed candidal infection. There was no improvement despite 2 weeks of therapy, and she presented to the emergency room with severe difficulty in breathing. Repeat laryngoscopy revealed worsening of the grayish exudates on the vocal cords, vocal cord edema, and narrowing of the airway that required tracheostomy.\nRight vocal cord biopsy showed ulcerated squamous mucosa with polymorphonuclear leukocytes, and monocytes and macrophages indicating acute and chronic inflammation. No stromal fibrosis to indicate effects of radiation therapy was noted. Abundant extracellular oval budding yeast forms were seen on hematoxylin and eosin and Grocott's methenamine silver stains (). Tissue culture on Sabouraud dextrose agar at 30°C grew a creamy moist colony that was evident after 72 hours. This was then placed on Cornmeal agar, and a Vitek card identified it as Saccharomyces cerevisiae. Microscopic examination revealed multilateral ellipsoidal budding yeasts without a capsule with a largest diameter of 7–9 μm and occasional pseudohyphae. Kinyoun stain revealed oval asci with 1–4 ascospores inside, a characteristic finding of Saccharomyces genus (). Using the broth microdilution method of the Clinical and Laboratory Standards Institute [], the isolate was found to have fluconazole MIC ≤ 8 μg/mL.\nGiven lack of response to oral fluconazole 400 mg/day after 2 weeks despite low fluconazole MIC, the dose was increased to 800 mg/day. Significant improvement in the tongue lesions was seen within 1 week with 50% reduction in the size of the lesions. After 4 weeks, one of the tongue lesions had resolved completely, and the other showed 90% clearance. Repeat laryngoscopy also showed significant improvement, and fluconazole was continued for 6 weeks until the oral lesions had resolved completely.
A 68-year-old man presented to the emergency department (ED) complaining of feeling lightheaded, confused, and dizzy and subsequently called for emergency medical service. En route to the ED via ambulance, the patient was noted to have a pulse in the thirties and a systolic blood pressure of 50 mmHg. Upon arrival, the patient vitals were as follows: blood pressure of 79/35, pulse of 47, oral temperature of 35.3°C, and respiratory rate of 18 with an oxygen saturation of 100 percent. His body weight was 87.3 kg, nearly 10 kg above his baseline weight. The patient was alert and oriented with a GCS of 15 but had difficulty communicating his symptoms secondary to his dizziness and feeling profoundly ill; however, he was able to clearly state that he felt he “was going to die.”\nThe patient's past medical history was significant for primary hypertension, type-2 diabetes mellitus, coronary artery disease, and end-stage renal disease resulting in a renal transplant five years ago. A review of the records revealed that the patient was recently hospitalized for a hypertensive emergency and pulmonary edema resultant from declining renal function. The patient's blood pressure was labile during his admission and uncontrolled during this last hospitalization. Upon discharge, the patient was told to follow up with his nephrologist to redress his hypertension.\nThe patient indeed followed up as instructed with his nephrologist, which was the morning of the described ED visit. At the office visit his blood pressure was noted to be 154/62. His doctor added nifedipine to his current regimen of doxazosin, hydralazine, metoprolol, and metolazone. The patient filled his new prescription and took all of the medications that afternoon except for metoprolol which he believed he was supposed to discontinue. Approximately one hour after ingesting his medications the patient became acutely ill and presented to the ED as described.\nDuring this ED visit, in addition to the patient's abnormal vital signs and altered mental status, he was also found to be moderately hyperkalemic with potassium of 6.3 mEq/L and had an elevated BUN (40.0 mg/dL) and creatinine (2.20 mg/dL) which were both above his baseline renal function. The patient's chest X-ray was consistent with pulmonary edema and his electrocardiogram (EKG) was significant for bradycardia without hyperacute T wave or ischemic changes.\nThroughout his stay in the ED, the patient received fluids, insulin and glucose, calcium gluconate, glucagon, and aerosolized albuterol in an effort to reverse his antihypertensive medications and hyperkalemia. While the patient's hyperkalemia and hypotension were corrected with treatment, he remained bradycardia while being in the ED. The patient was also warmed with warm fluids and blankets given his hypothermia. The patient was admitted for further evaluation and treatment of his fluid overload, pulmonary edema, hypotension, hyperkalemia, and bradycardia. The following diagnoses were considered: medication reaction/overdose, renal failure, endocrinopathy, and sepsis. The patient was hospitalized for almost two weeks during which he was diuresed and his blood pressure regimen was adjusted to include only doxazosin and nifedipine. Followup since discharge demonstrated the patient's hypertension to be within normal ranges.
We report an 80-year-old gentleman with a background history of chronic obstructive pulmonary disease (Global Initiative for Chronic Obstructive Lung Disease (GOLD) Grade D; Modified Medical Research Council Dyspnoea Scale (mMRC) class III) who was admitted for a right spontaneous secondary pneumothorax. He unfortunately developed extensive SE one day after right chest tube insertion leading to hoarseness of voice, tense palpebral fissures, and tense neck swellings. Computed tomography (CT) of the thorax demonstrated extensive SE together with the presence of pneumomediastinum (Fig. ). CT images also revealed that the tip of the chest tube was seen penetrating through part of his lung parenchyma which is the most likely cause of extensive SE. An urgent cardiothoracic surgery consult was made but unfortunately our patient was deemed unfit for surgery in view of his advanced underlying lung condition with poor lung reserve. He was intubated for airway protection on the fourth day of stay in view of development of stridor (Fig. A). Our patient continued to develop worsening SE despite adequate thoracic drainage via a new chest tube. Earlier attempts of subcutaneous cannula insertions for cutaneous tension release were not successful.\nA multidisciplinary team discussion involving physicians, nurses, surgeons, physiotherapists, intensive care doctors, and patient's family members was conducted on the fifth day of hospitalization. It was then decided to insert two NPWTD in patient's subcutaneous tissue via incisions made at left and right anterior chest wall, 5 cm below the clavicle level. Extra precautions were made to ensure that the incisions were made at superior borders of the rib below and approximately 5 cm from the midline to avoid injuries to the intercostal and internal mammary vessels, respectively. The NPWTDs were created by using trimmed sterile sponge to fit the wound shape. The sponge was then wrapped around a modified nasogastric tube containing self-created fenestrations on one end to aid in suction. Sutures were used to secure the sponge on the nasogastric tube. The other non-fenestrated end of the nasogastric tube was connected onto a suction machine. After achieving wound haemostasis, the sponges were carefully inserted into the two subcutaneous incisions and secured by using sterile transparent drapes (Fig. B). Continuous negative pressure of 10 mmHg with sequential increment up to 50 mmHg was used.\nPrompt regression of SE was noticed within the first 24 h followed by successful extubation after four days of NPWTD (Fig. B). External pressure and massage were done intermittently to enhance exit of trapped gas. In view of significant improvements, the drains were removed after four days from the date of insertion with no recurrence of SE following removal.
A 60-year-old female with osteoarthritis of the right knee underwent Mako/Stryker robotic-assisted total knee arthroplasty. The patient's past medical history consisted of hypertension. No medical conditions predisposing the patient to a fracture were noted. A midvastus approach was used, and trackers were placed with unicortically inserted pins in the tibial shaft and femoral shaft for the robotic tracking system. The operation was performed without complication, and the tracking pins were removed manually at the conclusion of the case. Postoperative radiology reports noted proper positioning of prosthesis with no acute fracture.\nPhysical therapy was begun on postoperative day 1 with partial weight bearing with a front wheel walker with PT assistance and was able to walk the entire hospital corridor two times. Patient was discharged on postoperative day 2 with outpatient physical therapy arrangements. Patient had a satisfactory postoperative course.\nThe patient had an uncomplicated recovery until 6 weeks postoperatively when she was at work and sustained a ground level fall due to acute pain of the right thigh and her leg “giving out.” Patient was unable to bear weight on the extremity. She presented to the emergency department where she was found to have a complete, oblique fracture through the midshaft of the right femur (). On radiography, the femoral tracking pin site is clearly visible at the location of the fracture in the distal segment (). The patient was taken to the OR and underwent intramedullary nailing of the right femur with retention of right knee prosthesis hardware (). CT scan of right lower extremity confirmed evidence of a fracture through the prior surgery pin tracks. Following intramedullary nail placement, the patient had a normal postoperative course. Final films at 6 months showed a healed fracture with stable orthopedic hardware (). At this time, the patient was pain free, ambulating without issue, and elected to proceed with an as needed follow-up.
A 70-year-old Japanese man was admitted to our emergency room because of high fever and left shoulder pain in May, 2013. His medical history was unremarkable and he was taking no medications. He had not undergone any regular medical check-up. About 1 week before admission, he suddenly developed a fever of more than 38 degrees. About 4 days later, he developed pain and swelling of the skin around the left scapula, and he had difficulty in lifting his left upper limb. His symptoms persisted; thus, he was admitted to our hospital. He did not have any recent trauma nor did he travel to any tropical countries.\nOn admission, he was in good condition, without abnormalities of vital signs except for a body temperature of 38.4 degrees and a heart rate of 111/min. On physical examination, the flaring and swelling of the skin just below his left scapula were observed. The affected skin area was over 8 cm in its major axis. He also felt tenderness in this area. He had normal heart and respiratory sounds and no abnormalities in the abdominal region. No superficial lymph nodes were palpable, and no rashes or scars were observed in his entire skin. Laboratory examination results indicated severe inflammation: white blood cell count, 17200/μL; C-reactive protein (CRP) level, 13.3 mg/dL. None of the myogenic enzymes showed elevated levels. He did not have diabetes nor did he have human immunodeficiency virus (HIV). Computed tomography (CT) revealed swelling of the left rhomboideus muscle and a solitary low-density area (LDA) around a contrast enhancement in this muscle (Figures and ). No other abnormalities were detected in the thorax or abdomen. From these findings, we suspected the presence of intramuscular abscess; thus, we punctured the affected area. However, the puncture fluid was bloody with no gross pus. After the puncture, we started empiric therapy using intravenous administration of ceftriaxone (CTRX, 2 g b.i.d.). On Day 7 of hospitalization, his condition did not improve and CT showed the enlargement of LDA in the left rhomboideus muscle. No organisms were isolated by the cultures of blood sampled several times. No vegetation was detected by transthoracic echocardiography. On Day 9 of hospitalization, we decided to perform incision and drainage of the left rhomboideus muscle. S. anginosus and S. intermedius were isolated by the culture of drainage fluid. On oral examination, multiple treated dental caries and periodontitis with pus were found. At that time, he was diagnosed as having solitary pyomyositis of the left rhomboideus muscle. We considered that the source of pyomyositis was periodontitis, although we did not detect a bacterial growth in the pus collected from the dental caries.\nAfter the drainage, we empirically switched the antibiotics to intravenous meropenem (1.5 g t.i.d.) for 14 days; then his symptoms gradually improved. His carious teeth were extracted during meropenem administration. At that time, CT showed residual LDA in the left rhomboideus muscle (Figures and ), and his laboratory examinations showed the persistence of CRP positivity (0.8; normal range, 0 to 0.5 mg/dL). Therefore, we switched to oral amoxicillin (AMPC, 750 mg t.i.d.) on the basis of results of the antimicrobial susceptibility test and continued it for two months. After finishing the AMPC treatment, magnetic resonance imaging (MRI) showed no abnormalities in the left rhomboideus muscle (Figures and ). No relapse occurred more than one year after his discharge from the hospital.
A 43-year-old adult male patient reported with complaint of a black space between the upper front teeth and the gum region since 6 months. On examination, the patient presented with class 1 gingival recession and class 1 papilla []. The patient was diagnosed as chronic generalised marginal gingivitis with papillary gingival recession type 2 with 11 and 21 () [, ]. As the interdental bone was more than 5 mm from the contact point, the pouch and tunnel technique with interposed connective tissue graft using microsurgical instruments was planned. Scaling and root planning was performed for the patient on the first visit. After 1 week, surgical procedure was carried by anesthetising the interdental area by local infiltration using 0.2% lignocaine with 1 : 80000 epinephrine. Next, under magnification of 2.5x, a sulcular incision was given around the facial and proximal surfaces; next, using microsurgical tunnelling instruments, a subperiosteal pouch was created by raising a partial thickness flap using sharp dissection (). The pouch was extended towards the interdental gingiva, detaching it from the palatal aspect partially. The tunnel was extended beyond the mucogingival junction to allow coronal movement of the interdental gingival unit. Once the interdental gingiva was coronally advanced passively, the amount of connective tissue graft required was estimated by using a tin foil and measuring the amount of space present in the subperiosteal tunnel. The tin foil was used as a guide to harvest the connective tissue graft from the hard palate using the trap door technique. After harvesting the connective tissue graft, the donor site was sutured using 3-0 silk suture with the horizontal mattress suturing technique (). The connective tissue graft was then tied at one end with 5-0 resorbable suture as a lasso suture and was inserted into the tunnel created by pulling the suture and tying it to stabilize its position []. Similarly, the other end of graft was also stabilized by suturing. Next, 3-0 silk suture was allowed to pass through the labial interdental gingiva, connective tissue graft, and palatal gingiva to bind the graft together and was tied as a sling suture with a composite stop in the middle of the two incisors (). Periodontal dressing (Coe-Pak) was given to provide mechanical protection, and the patient was instructed to take analgesics twice a day to avoid postoperative pain. Suture removal was done after 10 days, and there was almost complete fill of the interdental papilla, and after 1 month (), the interdental papilla completely filled the interdental area. After approximately 2 years, the interdental papillary fill showed a relapse of about 0.5 mm (). In all the three cases, the papilla presence score decreased, quantifying the gain in the papilla as shown in .
A 55-year-old female patient, taking once-daily dosage of Cilnidipine – 5 mg, was referred by her physician to the Periodontics division of our Dental College, for improving her oral hygiene [-]. She was under antihypertensive treatment for 6 years. She gave a history of slowly progressing enlargements on her gums for 1 year. She also reported discomfort while brushing the teeth due to bleeding from gums in the last 6 months after which the size of the swelling enlarged rapidly.\nIntraorally, the gingiva was enlarged in relation to maxillary and mandibular teeth, and it was firm, diffuse, and lobulated and characteristically appears to project from beneath the gingival margin, with Grade II to Grade III gingival overgrowth according to Buchner et al.'s grading criteria. In the maxillary arch, the overgrowth extended labially from 22 to 27; it was localized around 12. In the mandibular arch, the overgrowth extended labially from the distal aspect of 33–43 regions and localized around 46. There was minimal involvement of the palatal or lingual areas. Few areas showed signs of secondary inflammatory changes. Teeth in the involved area had plaque and calculus. The Oral Hygiene Index score was 2 (fair oral hygiene). The presence of the enlargement made plaque control difficult, resulting in secondary inflammatory changes especially in the mandibular teeth, which complicated the gingival overgrowth caused by the drug. Since she was undergoing antihypertensive therapy and no other known drugs which could induce gingival overgrowth were prescribed, the case was clinically diagnosed as drug-induced (Cilnidipine) gingival overgrowth with secondary inflammatory changes which was confirmed histologically.\nHistologically, there was pronounced hyperplasia of the connective tissue and epithelium. There was acanthosis of the epithelium and elongated rete pegs were extending into the connective tissue, along with densely arranged collagen bundles, many fibroblasts and new blood vessels, and few inflammatory cell infiltrates [].\nShe was advised to undergo a full-mouth periodontal rehabilitation along with drug modification after consulting her physician. Unfortunately, 1 week later, we lost the patient as she succumbed to massive cardiac arrest. A limitation of this case report is that radiographs could not be obtained, and importantly, we could not deliver dental treatment for her.
A 44-year-old man from Southeast Asia presented to our hospital complaining of a severe episode of central chest pain on a background of on and off chest pain with moderate exertion that started 3 days before admission. He was known to have suffered a non-ST elevation myocardial infarction 2 months prior with subsequent coronary angiography revealing nonobstructive coronary artery disease. He was for medical treatment with a nonculprit incidental finding of a CTO of the left anterior descending (LAD) artery.\nHe had an ejection fraction (EF) of 49% at the time and was discharged on optimal anti-ischemic therapy with a plan to evaluate the need of further intervention based on a myocardial perfusion imaging study.\nHowever, the patient presented again to our hospital with unstable angina. Repeat electrocardiography (ECG) and echocardiography revealed the same findings as previous admission. Based on his recurrent anginal symptoms, he was sent for PCI for his CTO of the LAD.\nDual femoral access was obtained with 7F XB 3.5 and AL1 guides in the femoral arteries bilaterally. The antegrade approach was used initially to cross the lesion using the accelerated wire technique that failed. Then we switched to retrograde approach through the collateral septal branches that were being supplied by the posterior descending artery and posterior left ventricular, respectively. Retrograde approach from the right coronary artery-septal used with corsair then finecross microcatheter support. Sion wire was used to sail through septal collaterals. Eventually, the lesion was successfully crossed with pilot 200. The final result of TIMI 3 flow was achieved with 3 overlapping drug-eluting stents from the ostial left main coronary artery to mid-LAD that were postdilated with noncompliant balloon to high pressure. Guidewire perforation of septal collateral was noticed. There was a myocardial blush but no extravasation []. Immediate echocardiogram did not show any evidence of pericardial effusion. The patient was transferred to the coronary intensive care unit for observation with serial echocardiography. Two hours after the transfer, echocardiogram did not reveal any pericardial effusion; however, there was a 2 cm × 1.4 cm mid anterior and posterior IVSH [].\nThe patient then started to complain of mild chest pain but remained hemodynamically stable without any new ECG changes. However, repeat echocardiogram showed mild increase in the size of the IVSH with partial rupture into the right ventricle []. He was taken for relook coronary angiogram which showed perforation of two septal arteries communicating with the hematoma site with partial rupture of the ventricular septum into the right ventricle [].\nMultiple prolonged balloon inflations strategy at low atmospheric pressure was used first to seal the perforation. However, the blush persisted. Then, it was decided to go for covered stenting using a Graftmaster 2.8 mm × 16 mm stent to the mid distal LAD segment. Postdilation was performed using a Quantum Apex compliant balloon. The main culprit which was the distal septal perforation was successfully sealed, yet there was one septal perforation remaining. Subsequently, intracoronary injection of autologous fat obtained from the groin was considered. The perforated vessel was embolized by the fat particles through corsair microcatheter.\nUnfortunately, this method did not work as well mainly due to its very small lumen. The export catheter was then used but it failed as well, due to the inability to track it further down to the perforated vessel due to its bulkiness. Hence, we decided to cover it using a second covered stent. Covered stenting was performed, using a Graftmaster 3.5 mm × 16 mm stent to the mid LAD segment. The end result was achieved by successfully sealing the septal perforator [].\nImmediate post-PCI echocardiography showed no increment in the size of the IVSH and absence of any significant pericardial effusion. Serial echocardiograms over the next few days demonstrated an EF of 51%, and the IVSH seem to be decreasing in size, but there was the persistence of turbulence on the right ventricle suggestive of partial rupture of the IVSH with a peak gradient of 45 mmHg.\nThe patient, however, remained free of chest pain and hemodynamically stable with no new ECG changes. He was discharged after a week of observation and the final echocardiogram showing partial rupture of IVSH with peak gradient of 22 mmHg and decreasing size of IVSH. Follow-up cardiac magnetic resonance imaging (MRI) showed complete resolution of IVSH and normal LV volumes with normal systolic function (EF 69%). The maximum wall thickness at the mid interventricular septal wall measured 11 mm indicative of a very small interventricular serpiginous track/defect. Neither demonstrable communication to the right ventricular cavity nor significant LV to RV shunts could be further seen [].
A 43-year-old male patient came to surgery OPD with complaints of dull and intermittent right side flank pain for several months. The patient also complained of decreased urine output. The patient did not give any other significant history. The X-ray and ultrasound of the abdomen revealed multiple stones in the right kidney and hydronephrosis. Blood urea and serum creatinine were also raised. A clinical diagnosis of non-functioning right kidney secondary to nephrolithiasis was made and a nephrectomy was performed.\nA total of 53 nephrectomy specimens were received in our department in the last four years for chronic kidney disease, of which only one showed renal pelvic SCC. A nephrectomy specimen in 10% formalin was received in the Department of Pathology, Dr. Baba Saheb Ambedkar Hospital with an attached ureter measuring 10 × 6 × 3 cm3. The outer surface was nodular covered with adherent perinephric fat. On serial slicing, it was observed that the kidney had converted into a multilocular cystic structure with thinned out cortex and cortico-medullary junction could not be appreciated. A solid, greyish white growth in the renal pelvis measuring 3 × 2.5 cm2 was also seen which was infiltrating the perirenal adipose tissue. Multiple stones were seen in the pelvis and in the dilated calyceal spaces. Sections from the growth revealed histomorphology consistent with well-differentiated SCC with areas of necrosis and hemorrhage (Figure ).\nThe tumor was seen infiltrating the perinephric fat. Sections from adjacent renal parenchyma showed features of chronic pyelonephritis (Figure ).\nThe ureteric end was free of tumor, however, the vessels could not be identified due to the location of the tumor. Taking note of all the findings, a final diagnosis of SCC, renal pelvis, pT3NxMx, and right kidney was made. The patient returned to the hospital one year after, with complaints of vomiting, weight loss, and right side abdominal pain. CT scan of the abdomen revealed a mass involving the right retroperitoneal area extending up to the right lobe of the liver. The whole mass along with the right lobe of the liver (partial) was resected and sent for histopathological examination. A globular soft tissue mass with a skin flap was received measuring 15 × 14 × 10 cm3. The mass measured 12 × 11 × 9 cm3. It was 1 cm away from the skin. Resected liver sent separately showed a growth measuring 5 × 3 × 2 cm3. On the cut section, the tumor had a variegated appearance with necrotic and hemorrhagic areas. Multiple sections from the tumor showed features of moderately differentiated SCC (Figure ).\nThe overlying skin was free from any tumor. Sections from the liver showed infiltration by a similar tumor. The patient was lost to follow up after discharge from the hospital.
Clinical history A 69-year-old male with a history of hypertension presented to the emergency department with complaints of urinary frequency, urgency, and hesitation to pass urine. Physical examination was unremarkable. Laboratory tests showed high leukocytes in urine (19 WBC/hpf) and elevated prostate-specific antigen (PSA) of 14 ng/mL. Radiological features Ultrasound examination of the urinary tract showed an enlarged prostate with an estimated volume of 67 mL. In addition to this, two solid mass lesions were found incidentally in the right kidney. The first lesion was a well-defined hypoechoic mass lesion in the middle pole region, measuring 25 x 22 mm. A second hypoechoic lesion was identified in the lower pole measuring 10 cm and had calcifications as well. The left kidney also showed a small hypoechoic lesion in the lower pole (Figure ). The patient had undergone treatment for urinary tract infection and benign prostatic hypertrophy. On follow-up, repeated PSA showed a significant decrease in level to 6 ng/mL as compared with the previous reading of 14 ng/mL. Thus, the patient did not undergo prostatic biopsy. The patient underwent a contrast-enhanced CT scan for further characterization of the renal masses. CT scan confirmed three renal mass lesions, two in the right kidney and one in the left kidney (Figure ). There was an exophytic mass lesion in the middle pole of the right kidney, measuring 27 mm in diameter, and showed enhancement similar to the renal cortex on post-contrast images with a central non-enhancing area. This lesion showed contrast washout in the delayed phase (Figure ). The lesion in the lower pole of the right kidney was a large (77 x 61 mm) exophytic heterogeneous lesion with foci of macrocalcifications. It showed heterogeneous contrast enhancement and multiple areas of fatty components. In the lower pole of the left kidney, there was a small lesion measuring 14 mm in diameter, showing heterogeneous contrast
The patient was a 24-year-old nulliparous female without sexual experience. She had undergone the surgeries of the maxillary cyst at the age of 18 and 20 years. With reference to the diagnosis criteria of this syndrome, she was given the definitive diagnosis as BCNS with the odontogenic keratinocytes of the jaw, the three of more palmar or plantar pits as the major criteria, in addition, with the ovarian fibroma as the minor criteria, whereas she did not have the bilamellar calcification of the falx cerebri, the bifid, fused or markedly splayed ribs, and the first, degree relative with this syndrome. First, she visited a gynecologic clinic for uterine cervical cancer screening. A fist-size pelvic mass was found by transrectal ultrasonography, and then, she was referred to our hospital. The magnetic resonance imaging (MRI) of the pelvis indicated an 8-cm suspected subserosal myoma that showed the iso-intensity to the myometrium on T1-weighted images and exhibited uneven signals on T2-weighted images of the ventral uterine side. Furthermore, a 4-cm tumor was suspected to be an ovarian fibroma because of the hypo-intensity on T1- and T2-weighted images of the right ovary []. We decided the patient be indicated for the surgery. Although the GnRH agonist was preoperatively administered for 3 months to decrease the size of the myoma, the tumor did not shrink. Before re-evaluation by MRI scans, we had planned to perform the tumorectomy and myomectomy for the right ovarian tumor and uterine myoma. Re-evaluation by MRI indicated that both pelvic masses were originated from the right ovary and that the interstitial of the right ovary was edematous, the massive ovarian edema []. Therefore, we decided to perform the right ovarian tumorectomy.\nIntraoperative findings on laparoscopic surgery showed that there was no uterine myoma, and white and smooth superficial masses of 8 and 5 cm in diameter were found in the right ovary []. Both tumors were extremely rigid and could not be morcellated with surgical scalpels or Cooper's scissors. We made a 2.5-cm incision in the lower abdomen and then fitted the Smart retractor® (TOP Corporation, Tokyo, Japan) and the Free access® (TOP Corporation) to the abdominal wall [Figure and ]. From this space, the tumors were excised little by little using the Luer Bone Rongeurs (ISO Medical Systems, Tokyo, Japan) and removed them [Figure and ]. The histopathological diagnosis was the ovarian fibroma with marked calcification and no malignancy.\nWe recommended the patient to receive genetic counseling. She had no relatives of BCNS, and sporadic occurrence was suspected. The patient has not shown any findings of recurrence until 1 year after the surgery.
A 38-year-old male with a history of chronic pain secondary to idiopathic retroperitoneal fibrosis (RPF) was referred to our tertiary cancer pain clinic for pain management. The pain started in his low back and primarily radiated across his abdomen and into his lower extremities. His abdominal and pelvic MRI showed an enhancing retroperitoneal mass surrounding the aorta with compression of the ureters and inferior vena cava.\nAfter a complete evaluation, the patient was placed on oral opioids, including methadone and hydromorphone, as well as adjuvant medication therapy, including baclofen and gabapentin. Despite this treatment, he continued to have intractable pain and a decision was made to offer an IDDS trial after a few months. The trial was successful, and he subsequently had a permanent IDDS implantation with morphine infusion. After about two years, his pain symptoms progressed and he was offered a spinal cord stimulator (SCS) as an off-label use for the intractable abdominal, pelvic, and back pain. SCS was implanted after the completion of a successful trial.\nOver the course of treatment, his intrathecal medications were escalated to morphine 33.08 mg/day, clonidine 661 mcg/day, and baclofen 248 mcg/day. Initially, his pain was managed well, but he eventually showed declining functional status with progressive weakness in his lower extremities and increasing pain. At this point, it remained unclear whether his pain and neurological symptoms were due to catheter-tip granuloma, worsening RPF, or a non-functioning SCS. Therefore, a CT myelogram was ordered. The risks of paralysis were explained to the patient; however, he deferred imaging at that time. Later, the patient also reported that his SCS was causing pain at the implantation site and he wanted it removed. Since he began developing progressive neurological deficits, a decision was made to explant his non-MRI compatible SCS. After this surgery, the patient refused to obtain imaging studies as ordered. For unknown reasons, the patient deferred his MRI appointments as ordered.\nAfter 10 months of non-compliance, the patient presented with profound weakness of the lower extremities and was confined to wheelchair. Emergent MRI revealed an intradural lesion at T11-T12 with impingement upon, and compression of, the thoracic cord, spinal cord edema, and associated mass effect (Figures -).\nNeurosurgery performed an emergent thoracic laminectomy at T11-12 with intradural exploration. The pathology report confirmed an intradural malignant epithelial round/spindle cell neoplasm with abundant myxoid matrix. The patient was discharged to a neurosurgical rehabilitation facility. He later received radiation therapy for possible residual tumor. Fortunately for this patient, there was a gradual improvement in his neurological status as well as pain control.
A 72-year-old male presented with a two-day history of right upper quadrant pain on a background of a metastatic, small bowel, well-differentiated NET diagnosed 5 years previously. The tumour was a low-grade mesenteric NET with a ki67 of 8% at diagnosis. He had multiple liver metastasis, which were stable. Carcinoid syndrome was well controlled on a long-acting, monthly dose of a somatostatin analogue with last dose being 28 days prior to presentation and due in three days. His comorbidities included hypertension, an infrarenal aortic aneurysm and chronic obstructive pulmonary disease. He presented with right upper quadrant tenderness and the liver edge was palpable 4 cm below the costal margin. Initial blood tests showed a white cell count of 18.9 × 109/L, C-reactive protein 212 mg/L and liver function tests within normal limits. Vital signs were reassuring, and an abdominal ultrasound described a thickened gallbladder wall, mobile sludge and an 8.5-mm common bile duct suggestive of cholecystitis (). Computerised tomography (CT) of the abdomen was noted to show multiple segment V liver masses with capsular deformity suggestive of central necrosis. He was initially managed with analgesia and intravenous piperacillin-tazobactam. After a discussion with the patient and consultation with his treating oncologist regarding his relatively stable disease burden and reasonable prognosis, a laparoscopic cholecystectomy was performed.\nDuring cholecystectomy, extensive carcinoid metastases were encountered (). To perform the operation laparoscopically required retraction of the left liver lobe. However, the liver was stiff and inflamed making exposure of the biliary tree difficult. The gallbladder was mobilized, a critical view of safety and an unremarkable intraoperative cholangiogram was obtained. The length of the operation was 1 h and 35 min. Histopathology of the gallbladder showed benign, chronic outlet obstruction, patchy serosal mixed inflammation and one lymph node containing metastatic disease.\nDuring the procedure, the patient developed a persistent tachycardia and an octreotide infusion was initiated. He developed hypotension, wheeze, sweating, bronchospasm and flushing. Venous pH was 7.14. Electrocardiogram showed pronounced ST-segment elevation in leads V3 and V4, multiple ventricular ectopic beats, bigeminy and bundle branch block. Troponin levels rose to >50 000 ng/L. A bedside echocardiogram showed hyperdynamic left ventricular function and septal regional wall abnormality. Profound vasodilatory and cardiogenic shock resulted requiring vasopressin at 6 mL/h (0.04 IU/min) titrated over 7 hours and noradrenaline at 5 mL/h (5ug/min) titrated over 6 h. Later, cardiac angiography showed minor coronary disease and within 24 h, he was extubated, his pain resolved, and inflammatory markers had normalised within 48 h.
A 29-year-old woman who had undergone surgical removal of the ovaries at the age of three years for malignancy presented after failing four egg donor transfer cycles. She believed that the malignancy was lymphoma of the ovaries but was not entirely sure, and pathology reports were unavailable since this had occurred in Lebanon. The male partner was 41 years old without medical issues and had a semen analysis of 3.2 mL, with 49.2 million sperm per mL, 72% forward motility, and 1% normal forms, according to strict morphology. After the third failed transfer, she underwent an estrogen and progesterone mock cycle and two biopsies for Adhesio. As per the Adhesio protocol, biopsies were performed at six and eight days of progesterone administration. This test determined a delayed WOI, which was receptive after eight days of progesterone treatment. Adhesio presented the levels of messenger RNA expression at the time of each biopsy, which was about 90% of the control level on day 8 and less than 40% of the control level on day 6, in this patient’s case. She underwent embryo transfer subsequent to the biopsy, with transfer on the 8th day of progesterone, and it failed. The patient was then transferred to our clinic. Upon presentation, she was recommended to undergo her first ERA test. This test was performed at 100 hours of progesterone in an estrogen-primed mock cycle, giving a WOI of 124±3 hours. Not feeling comfortable transferring at 124-hours of progesterone, given the conflicting results between the two tests, she requested that we repeat the ERA test with biopsies at both 124±3 hours and 192 hours (8 days×24-hours) to coincide with the WOI timing suggested by both the previous ERA and Adhesio tests. Performing the ERA tests at the time of the suggested WOI and not at 120 hours, as suggested by the company, should confirm the previously recommended WOI. This second ERA included a biopsy performed at 126 hours of progesterone treatment and demonstrated a WOI of 126±3 hours in July 2018. The third ERA biopsy performed in the same mock cycles as the second ERA was read as post-receptive based on a biopsy at 195 hours of progesterone. For the three ERA tests and Adhesio, the patient received the same dose and type of progesterone. Blastocyst transfer was subsequently performed at 126 hours of progesterone and it also failed.
A 58-year-old woman was admitted to our hospital with hemorrhagic shock due to suicidal cervical stab wounds. On admission, her blood pressure was 69/46 mmHg, which recovered and remained stable after resuscitation. No active bleeding was observed from the two stab wounds, which were observed at zone II with surrounding hematoma to the right of the midline (Fig. A). No extravasation was noted on cervical post-enhanced computed tomography (CT). We undertook local wound exploration under general anesthesia, and found lacerations of the right internal jugular vein and the facial vein, which were repaired with sutures. Intubation care under sedation was continued until the following day. On the next day, 80-row 3-D CT angiogram (CTA) showed occlusion of the right VA at the C3 level (Fig. B). No arteriovenous fistula was noted. A retrospective review of the reconstructed CT the day before also showed occlusion of the right VA. The patient immediately underwent conventional angiography. The right VA angiogram revealed termination of the right VA at the C3 level after muscular branching, and the left VA angiogram revealed anterograde flow in the basilar artery, and retrograde flow across the VA union down to the right VA and posterior inferior cerebellar artery (Fig. A). A high-flow single AVF communicating with the right distal VA and paravertebral veins at the C2–3 level was also observed (Fig. B). The right internal carotid artery angiogram revealed no congestion of the intracranial venous drainage. Although the patient had no symptoms, we carried out elective endovascular obliteration within a week, but the patient’s consent for the treatment could not be obtained due to psychological anxiety. Magnetic resonance (MR) angiogram 3 days later showed no apparent VVF (Fig. C). Eventually, after 10 days, the patient agreed to the treatment. A follow-up angiogram 10 days later revealed an enlarged fistula with a venous drainage route from the fistula through the paravertebral veins, pterygoid plexus, and posterior cervical veins (Fig. A). Successive percutaneous coil embolization of the fistula was carried out. Briefly, using a guiding catheter (7 Fr Roadmaster; Goodman, Nagoya, Japan) at the left VA, a balloon occlusion catheter (Scepter HC 4 × 11 mm; Terumo Corporation, Tokyo, Japan) was settled at the C1 level of the right VA across the VA union to control shunt flow. Following this, a microcatheter (Excelsior SL-10; Stryker, Kalamazoo, MI, USA) was positioned at the fistula point, which was occluded with seven detachable coils (Target coils, Stryker; and Hydrosoft coils, Terumo Corporation) (Fig. B). Immediately after the embolization, the bilateral posterior cerebral arteries became clearly visible on the left VA angiogram (Fig. C), compared with the preoperative angiogram where each posterior cerebral artery was visualized through the posterior communicating artery. This suggested an improvement in circulation of posterior cerebral arteries. The patient was transferred to psychological care at a different hospital 2 weeks after the surgery with slight dysphagia due to right recurrent nerve injury. Follow-up CTA after 8 months showed no detectable recanalization of the fistula. Follow-up conventional angiogram has not been obtained due to continued psychological care.
A 72-year-old male presented to our emergency department with distal right leg pain. He has a past medical history of uncontrolled type 2 diabetes, medication noncompliance, and coronary artery disease. His surgical history was also significant for a right distal fibular open fracture nine years ago requiring a combination of washout, open reduction with internal fixation. His postoperative course was uncomplicated and he had since returned to full and normal function. He had no history of infection or problems with his leg in the years thereafter. The patient presented to us with a seven-day history of worsening right ankle pain. He works barefoot for a significant amount of time in a golf course but did not recall any fall, trauma, animal or bug bites, skin laceration, or accidents. His vital signs were normal and his examination was remarkable only for tenderness in his right ankle. His ankle X-ray showed the hardware in proper position with only minor degenerative changes. The patient was discharged home without a definitive diagnosis and provided with pain medications. The patient presented to his primary care doctor for follow-up three days later with increased ankle pain, swelling, inability to bear weight, fevers, chills, and lightheadedness. He was found to be hypotensive with exam findings suspicious for septic arthritis. He was sent immediately to the hospital, where he was found to be in severe sepsis. He was hypotensive with blood pressure of 70/40, tachycardic at 112, and febrile at 39.0 degree Celsius. On labs, he had elevated creatinine from baseline, blood glucose of 400 mg/dL, and lactate of 4.2 mmol/L. He had no leukocytosis. His hemoglobin A1c was 12%. Blood cultures and urinalysis were obtained and the patient was started on early goal directed therapy with quick stabilization of his vital signs. Joint aspiration was performed revealing grossly blood-tinged thick fluid with 8600 WBC, with 97% neutrophils. His aspirate and blood cultures returned positive for Serratia marcescens. Broad-spectrum antibiotics were deescalated to Ertapenem. On hospital day 2, the patient was taken to the operating room for incision and washout. He was found to have significant purulent fluid in the tibiotalar joint. A drain was placed to aid in drainage. MRI was obtained at this time and showed findings consistent with osteomyelitis involving the distal tibia. There was also suspected sinus tract at the medial cortex just above the medial malleolus. On day 4, the patient underwent hardware removal with further washout performed. The implanted hardware in the distal fibula, although appeared uninfected, was removed. His tibia was incised with significant noted purulence and liquefaction of the bone extending proximally, requiring extensive washout and debridement. Despite the antibiotics and drainage, his joint remained purulent and appeared to have significant residual infection and inflammation requiring successive washouts on hospital days 6, 11, and 13. On hospital day 13, he also had antibiotic-impregnated beads placed. All of the cultures obtained from the joint remained positive. All repeat blood cultures remained negative. Since the most common source of Serratia is the urine and to rule out secondary sources leading to hematogenous spread, kidney and prostate ultrasounds were performed and were negative. Urinalysis was also noted to be negative on admission. The source of infection was believed to be inoculation through the skin from the golf-course soil. The patient's creatinine and vital signs recovered and the patient was discharged to subacute rehabilitation on day 14 on a six-week course of Ertapenem. On his 5-week follow-up, he was doing well on his antibiotics therapy with no systemic or localized signs of ongoing infection.
An 88-year-old male was admitted to our clinic with complaint of effort dyspnea. Transthoracic echocardiography revealed severe aortic stenosis. The Society of Thoracic Surgery (STS) risk score was calculated to determine the risk of surgery, and then the patient with 6 STS point had decided to undergo TAVR operation by the heart team. In the preoperative preparation phase, valvular annulus and aortic–iliac vessels could not be evaluated using computed tomography (CT) due to high creatinine levels. Therefore, the diameter of the aortic annulus measured using transesophageal echocardiography (TEE) was found to be 26 mm. The Edwards Sapien S3 valve (Edwards Lifesciences Inc., Irvine California, USA) was selected for implantation, because the main femoral arteries were observed to be 6 mm in diameter and calcified by iliac digital subtraction angiography. Additionally, aortic root angiography was performed prior to the procedure; the ascending aorta was found to be horizontal, whereas the descending aorta was distinctly tortuous and locally calcified. With the standard TAVR procedure, a Safari-2 guidewire was placed in the left ventricle. Predilatation was performed with a 25×40 mm balloon by the Safari-2 guidewire. Then, the 29 mm valve was loaded into the delivery system, and the valve started to move from the right femoral artery. The valve was difficult to load into the vessel due to the lack of complete coaxiality after the sheath was removed. After seeing that the valve was brought to the proper position (), the balloon with valve was tried to inflate for implantation but we could not, so the valve could not be opened, at that moment some blood came out from the system when negative pressure was applied. After this, we thought that the balloon exploded, and the valve was taken back into the delivery system. The Safari-2 guidewire was just left in the ventricle, but the entire system was pulled back together with the sheath. The valve that was pulled back with the other system was checked; no structural or functional problem was found (). Then the same valve was loaded into a new delivery system from the same femoral artery but at another puncture place. Fortunately, the valve system was successfully implanted (). Paravalvular insufficiency was not observed during the control aortography ().
A 31-year-old male patient presented to our clinic with symptoms of neck pain, back pain (pain in the lower cervical and upper thoracic region), and numbness in both arms for the last 3 months. His physical examination revealed hypoesthesia at the C4 and C5 dermatomes in both arms with no loss of strength. Cervical computed tomography (CT) showed a destructive and compressive lesion in the C4 vertebra corpus (Fig. ). The retropulsion caused by compression had narrowed the canal. The lesion was also seen to be completely wrapped around the vertebral foramen at the right C4 level and to extend to the lateral mass posteriorly in the axial sections on CT (Fig. ). Weinstein, Boriani, Biagini (WBB) classification was used for the classification of the tumor (Fig. ) []. In this case, the tumor was located at the regions 5, 6, 7, 8, and 9 and invaded all the layers except the dura mater. Corpectomy was performed to the C4 vertebra with an anterior approach together with discectomy to the upper and lower disc spaces during surgery. The lesion was seen to extend to the right C4 vertebral foramen in the surgical observation after corpectomy, and the tumor was carefully dissected 360° around the vertebral artery at this level. Once the vertebral artery was revealed, we entered between the mass extending posteriorly to the lateral mass, the spinal cord, and the vertebral artery and performed meticulous intracavitary curettage. In order to ensure stability after tumor excision, the upper and lower corpus endplates were decorticated with the curette. A corpectomy cage was placed into the C4 space, and the system was fixed by placing a plate screw on the upper and lower vertebra from the anterior (Fig. ). There was no additional neurological deficit postoperatively. The patient’s neurological complaints improved during the postoperative period. There was no residual or remaining tumor after resection. The pathological microscopical evaluation revealed a tumor rich in osteoclastic multinuclear giant cells interspersed in a stroma composed of cells with oval-fusiform nuclei. The pathological diagnosis was giant cell tumor of the bone (Fig. a, b). No recurrence was seen during 3 years of follow-up (Fig. ).
A 59-year-old woman presented for evaluation of scalp alopecia. Her past medical history was significant for PT1cN1mi estrogen receptor (ER)+, progesterone receptor (PR)+, human epidermal growth factor receptor (HER)2+ g3 invasive ductal carcinoma of the right breast diagnosed 15 months earlier. She had been treated with bilateral lumpectomy with right-sided sentinel lymph node biopsy and started chemotherapy nine months earlier; she received pertuzumab, docetaxel, carboplatin, and trastuzumab every three weeks for six cycles and was maintained on trastuzumab 6 mg/kg every three weeks for one year. Three weeks after completing taxane chemotherapy, she began treatment with anastrozole 1 mg daily (which was switched to tamoxifen 20 mg daily due to joint pain). She was also treated with radiation therapy and is currently on neratinib 240 mg daily; neratinib is a tyrosine kinase inhibitor anticancer drug used to prevent recurrence in patients with early-stage HER2+ breast cancer who have finished at least one year of post-surgery trastuzumab therapy.\nShe noted hair loss beginning after her first course of systemic chemotherapy. It became more extensive throughout the remainder of her treatment. She had not experienced any regrowth of scalp hair since the completion of chemotherapy nor during her current hormonal therapy.\nCutaneous examination revealed alopecia of the scalp. The clinical presentation was most consistent with female pattern alopecia with diffuse and nearly complete hair loss on the central and vertex region with retention of hair on the occipital scalp. There was partial, diffuse hair loss – to a lesser degree – on the parietal scalp bilaterally (Figure ). There was also loss of hair on the eyebrows, axillae, pubic region, and upper lip. However, these areas had already slowly started to show regrowth.\nBiopsies from the right and left sides of her parietal scalp, in areas of alopecia with some preservation of follicles, were performed for horizontal and vertical sectioning. Both showed similar pathologic changes of a non-scarring alopecia. The predominant feature noted was extensive miniaturization of the hair follicles; this change was most suggestive of androgenetic alopecia. However, other findings – present to a lesser extent – included pigment casts in hair follicles, increased catagen to telogen ratio, and empty fibrous tracks; these changes may be observed in alopecia areata.\nCorrelation of the patient’s history, clinical presentation, and pathologic findings supported a diagnosis of antineoplastic (chemotherapy and hormonal) treatment-associated alopecia. Specifically, her features were consistent with those previously reported in patients with breast cancer after taxane chemotherapy and adjuvant hormonal therapy who developed permanent alopecia []. Treatment was initiated with minoxidil 5% foam to be topically applied to the scalp twice daily.\nThe patient returned for follow up four months later. She was pleased with the clinical outcome and had noticed increased scalp hair growth; however, she commented that she always used minoxidil once daily and occasionally twice daily. In addition, hair growth on the eyebrows, axillae, and pubic area continued to demonstrate clinical improvement. She decided to continue treating her scalp in a similar manner.\nHer subsequent follow-up visit, six months later (after ten months of topical minoxidil therapy), showed additional hair regrowth. Specifically, the central and vertex area of her scalp had thickening of her hair; in addition, there was new hair growth on the parietal regions bilaterally (Figure ). She continues to use 5% minoxidil foam once daily.
A 22-year-old male, who worked at a hardware store, presented to the outpatient department with history of fever up to 102° F with night sweats, abdominal pain, anorexia, and weight loss of 4 kg over the previous month. He had progressively increasing fatigue and had to be brought in on a wheel chair. The abdominal pain was non-colicky and present diffusely over the upper abdomen. It had no association with meals, and was not exacerbated or relieved with changes in body posture. There was no history of cough, breathlessness, hemoptysis, chest pain, headache, altered bowel habits, dysuria or rash. He did not smoke and had no health problems in the past. There was no history of any substance abuse or intake of any immunosuppressive medication.\nHe lived in the outskirts of the city with his parents and sister in a two-room house with poor ventilation. His parents were apparently healthy, but his sister had suffered from pulmonary TB a year earlier, for which she was treated with anti-tubercular therapy (ATT) for six months. There was no significant history of travel and they owned no pets.\nOn examination, he appeared dehydrated and pale with blood pressure of 110/70 mm of Hg, and pulse of 90 beats per minute with regular rhythm. There was no evidence of respiratory distress or cyanosis, and the respiratory rate was 14 breaths per minute with peripheral capillary oxygen saturation of 99%. There was no jaundice, edema or palpable lymphadenopathy. The abdominal examination revealed tender hepatomegaly, so a detailed examination was deferred. The breath sounds were vesicular in character and no added sounds were present. Cardiovascular examination did not reveal any abnormality.\nThe laboratory investigations revealed mild anemia, raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and deranged liver functions with disproportionately elevated alkaline phosphatase (ALP) (Table ). Blood and urine cultures were sterile. Human immunodeficiency virus (HIV), hepatitis B surface antigen (HBsAg) and anti-hepatitis C antibody (anti-HCV) were negative. Mantoux test was positive with an induration of 24 mm after 72 hours (Figure ).\nA plain radiograph of the chest did not show any abnormality. Ultrasound of the abdomen revealed an enlarged liver (20 cm) and spleen (15 cm) with tiny hypoechoic foci. This was followed by a contrast-enhanced computed tomographic (CT) scan of the abdomen. The findings are illustrated in Figures -.\nUltrasound guided fine needle aspiration was performed from a hepatic lesion. It displayed necrotic hepatocytes within inflammatory infiltrate. Acid fast bacilli (AFB) staining did not reveal any organisms. Bodyweight based multi-drug regimen for TB was started, consisting of isoniazid 300 mg, rifampicin 600 mg, pyrazinamide 1500 mg and ethambutol 1200 mg a day. It was supplemented with pyridoxine 10 mg a day. The treatment was well tolerated, and was followed by defervescence within two weeks. His appetite increased and he started gaining weight. The culture of the hepatic aspirate did not grow tubercle bacilli at the end of six weeks. The liver function tests normalized within two months, and the liver and spleen size deceased on ultrasound with no visible parenchymal lesions.
A 25-year-old male patient, victim of torsional trauma in the right knee during a soccer match, was brought to the emergency department with a locked knee. At the time of the injury, the patient felt a pop and immediately after, he could not move his knee. Plain radiographs of the knee showed no signs of acute osteoarticular lesions. Subsequently, magnetic resonance imaging identified a bucket handle tear in the medial meniscus (). The patient was referred to the orthopedic trauma service for emergency surgical treatment.\nOne week after the injury, the patient sought our service. Physical examination revealed the following findings: joint effusion, 30 degrees of flexion, and an inability to actively contract the quadriceps. In the prone position, an important contracture of the hamstring muscle group was observed when compared to the contralateral side (). Based on the patient's history and physical examination, we suspected that the extension deficit resulted from arthrogenic muscle inhibition. A set of exercises was performed, using the technique described by Delaloye et al. [], which usually results in full restoration of the knee extension: the patient was initially placed in prone position, with the feet off the stretcher, and asked to perform active contraction of the hamstrings. The contraction should be held for 2 to 3 seconds. Between contractions, the patient was asked to completely relax the hamstrings. This sequence of exercises was performed repeatedly until fatigue was observed, at which point, a complete hamstring relaxation had occurred. Once full passive extension was recovered, the patient was placed in dorsal decubitus, with the trunk elevated to 90 degrees and with the lower limb in extension. In this position, the patient was instructed to perform isometric contractions of the quadriceps (vastus medialis) until he succeeded in performing an adequate contraction. The patient in our report presented complete extension after approximately 7 min of the resisted exercises ().
A 17-year-old girl with no disease history initially presented to a local community hospital for the acute onset of intense cephalagia, emesis, and left hemiplegia with normal mental state with bilateral pupils equal and reacting.\nComputed tomography (CT) scan of the brain showed the right frontal parietal lobe intracerebral hemorrhage of the patient at the local hospital, and the patient underwent evacuation of hematoma by emergency craniotomy. Nine days after the first surgery, the patient complaint of severe headache, accompanied by jet vomiting, and the vomit was gastric contents. The patient underwent another evacuation of hematoma by craniotomy. Five days after the second operation, a third attack of headache and vomiting began, and the patient underwent the third evacuation of hematoma by craniotomy to control the hemorrhage. Postoperative pathological examination showed foam-like histiocyte proliferation, and tumor cells were found in the hemorrhagic and necrotic tissues (Figure ). Immunohistochemical results: pan-cytokeratin (+), epithelial membrane antigen (+), human chorionic gonadotropin (HCG) (+), granulocyte chemotactic protein-3 (+, focal area), Sal-like protein 4 (+), octamer binding transcription factor 3/4 (-), and placental alkaline phosphatase (-), supporting metastatic choriocarcinoma. After confrontation, the patient admitted to having a sexual history and having had an abortion 2 years ago. She hid her medical history for fear that her parents would find out. Laboratory findings revealed that serum β-HCG level was more than 200000 U/mL. Based on all these findings, choriocarcinoma was strongly indicated. She received mannitol dehydration and brain protective treatment, and was then transferred to a general hospital for further treatment, at which time she was transferred to our center.\nThe patient’s menstrual cycle was regular and she declared no history of sexual intercourse or abortion. No history of hypertension could be identified.\nNo personal and family history available.\nOn presentation in our hospital, the patient was in a normal mental state with bilateral pupils equal and reacting. The muscle strength of left limb was grade III, the right limb grade V. The physical examination showed there was a bluish violet nodule with a diameter of about 6 cm at the cervix.\nThe blood level of β-HCG was 766510.0 mIU/mL (normal value, < 2.0 mIU/mL).\nBrain CT with contrast enhancement showed the right parietal lobe in the area of the previous operations had obvious edema, and local softening foci were formed. The adjacent meninges and brain were swollen, indicating residual tumor at the surgical area. Chest CT showed multiple round nodules and masses of variable sizes in both lungs, with scanty amounts of right pleural effusion, compatible with lung metastasis. Abdomen CT showed an abnormal, high and low mixed density in the spleen and kidneys, and the cervical was enlarged with uneven and enhancement CT value.
We present the case of a 28-year-old male who suffered a high-energy motorcycle accident. At admission, the patient was conscious, Glasgow coma scale (GCS) 15, hemodynamically stable, and presenting superficial excoriations on the trunk and lower limbs. However, there was a wound of approximately 20 cm on the lateral aspect of the right hip at the level of the greater trochanter, exposing the entire proximal end of the femur (Figure ).\nAfter a clinical evaluation and imaging tests that excluded cranial or abdominal disorders, we prioritized the neurovascular examination of the affected limb, which did not present complications, and the protection of the femoral head with the use of moistened gauze and saline solution. Radiographs in the anteroposterior view of the right hip showed a hip dislocation with a greater trochanter fracture (Figure ).\nAn exhaustive irrigation of the acetabular cavity and the exposed femur was performed, using 10 liters of saline solution at 9% when the patient was in the surgical room. The procedure happened under sedation and spinal anesthesia. A large debridement of muscle, fascia, and bone tissues was required to remove all the devitalized tissue, considered viable only when active bleeding and the clean appearance of the open wound was observed through direct vision by the surgeons.\nThe fractured fragment of the greater trochanter was fixed with two 6.5 mm cancellous screws and washers at the proximal end of the femur (Figure ). After a revision of the debridement sites and radioscopic control of the hip reduction and fixation, the wound was closed (Figure ).\nAfter the first 48 hours of surgery, the wound was releasing a significant amount of secretion, bloody and serum like, and a strong odor was observed, with no laboratory exams indicating infection. At this time, a new surgical procedure (second look) with greater aggressiveness was obtained, removing all devitalized tissue and bad-in-appearance cutaneous cover, which was not necrotic but had an unhealthy appearance (Figure ). A vacuum-assisted closure was used (Figure ).\nThe vacuum-assisted closure was changed every week for four weeks until the appearance of granulation tissue at the surface of the surgical wound (Figure ). During this period, the patient's laboratory exams showed a drop in the hemoglobin level, resulting in a 7.1 g/dl result, which was corrected with a transfusion of 600 ml of red blood cell (RBC) concentrate. As a rehabilitation procedure, we started daily physiotherapy with passive limb mobility and activity, within pain limits, with no load on the right hip.\nIn the fifth week, a new surgical procedure was performed for skin grafting. It was performed with no major occurrences and implantation of the graft was successful. Shortly after the removal of the stitches from the graft surgery, in about eight weeks, partial weight bearing on the affected limb was initiated with the use of two crutches.\nAfter a one-year follow-up, the patient had good mobility of the affected limb (Figure ) without significant pain during mobilization and examination of the joint, with a Harris Hip Score of 93 points. The radiograph showed a decrease of the articular space in the right hip (Figure ) but the magnetic resonance imaging (MRI) showed no necrosis of the femoral head. (Figure ). He was able to ride a bicycle, run, and do squats.
A 19-year-old healthy Korean male (93 kg; 175 cm; BMI, 30.36) experienced rapid onset of acute back pain with gradual sensory loss and ongoing weakness in the lower extremities when returning to shore from his first surfing lesson. Though he had fallen off the board into the water once, there was no impact trauma. First, he developed acute, severe pain in his back with a tingling sensation in his lower extremities and progressive weakness within half an hour. He was taken to the local emergency room, where he presented with complete paraplegia with absence of bladder function. He decided to transfer to our hospital. Physical evaluation showed that his lower extremity strength was 3/3. Both paresthesia and hypoesthesia below the level of the umbilicus were noted. Proprioception of the big toes was intact. Perianal sensation was decreased and urinary retention was present. Bulbocavernosus reflex was intact. He underwent MRI of the thoracic and lumbar spine without contrast, which showed increased T2 signal intensity in the gray matter of the central spinal cord from T10 to the conus (); otherwise, MRI was negative for structural lesions including disc herniation, fractures, spondylosis, or vascular lesions. Laboratory tests were within normal limits. Considering his clinical history as a first time surfer, the patient was suspected of having surfer’s myelopathy. He was admitted to the department of neurosurgery, and we focused on maintaining the degree of hypertension (average mean arterial blood pressure >85 mmHg) and did not administer steroids. His motor grade of the lower extremities recovered to 4+/4+, and he was able to ambulate with assistance the day after admission; however, there was little improvement in paresthesia and hypoesthesia. The next day, he transferred to his hometown hospital to be close to his parents. One month after the event, he recovered his strength to almost normal levels with intact bladder function and improved sensory deficit.
A 57-year-old female with rectal cancer successfully treated with chemotherapy and radiation over a year ago, renal cell cancer with subsequent nephrectomy and ESRD from lupus nephritis, and on PD since 2014 presented to an outside hospital with melena. She underwent colonoscopy and endoscopy that revealed a clean-based duodenal ulcer that was treated with twice daily intravenous pantoprazole. Several days later, she presented with another gastrointestinal bleed requiring repeat upper endoscopy and subsequently angiogram and coil embolization of the gastroduodenal artery. PD treatments were withheld and she received hemodialysis treatments via her arteriovenous fistula during this hospitalization. She had not received prophylactic antibiotics to prevent peritonitis prior to these procedures. In the interim, she was diagnosed with Clostridium difficile diarrhea, which was treated with oral vancomycin.\nFollowing her second endoscopy, she developed diffuse abdominal pain and became febrile to 100.6°F. Her abdomen was soft but diffusely tender. Peritonitis was suspected and her peritoneal fluid effluent was drawn for analysis (Table ). Gram stain of the peritoneal fluid revealed gram-positive cocci, and cultures grew gram-positive micrococcus and Candida tropicalis. Intravenous vancomycin and oral fluconazole were initiated. Final culture growth revealed the CDC group EO-4 organism, which was susceptible to levofloxacin. She was switched to levofloxacin to complete a total of 2 weeks of antibiotics. She was discharged home on PD and was readmitted 1 day later for hematochezia. She continued to have abdominal cramps unchanged in severity from before, but bleeding scan followed by a third endoscopy remained negative.\nShe was then transferred to our institution for further evaluation and consideration for double-balloon enteroscopy. Upon arrival, her vital signs were stable: blood pressure 122/75 mm Hg, heart rate 85, temperature 97.6°F. Cardiac examination was benign and lungs were clear to auscultation. Her abdominal examination revealed an intact PD catheter exit site without erythema or exudate, a diffusely tender abdomen without rebound or guarding, no lower extremity edema, and the left upper extremity revealed a brachiocephalic arteriovenous fistula with bruit. Laboratory values were as follows: hemoglobin 10.8 g/dL, white blood cell count 4.2 × 109/L, platelet count 110 × 109/L, normal transaminases, alkaline phosphatase 245 IU/L, total bilirubin 0.3 mg/dL, serum albumin 1.3 g/dL, and serum lactate level 0.8 mmol/L. Serum coagulation studies were normal. Serum electrolytes revealed a bicarbonate level of 25 mmol/L, potassium 3.4 mmol/L, BUN 15 mg/dL, and creatinine 6.9 mg/dL. Urinalysis was benign with only 4 white cells/HPF and negative leukocyte esterase and nitrite. Clostridium difficile toxin was negative. Serum lipase was normal at 6 U/L. Peritoneal fluid cell count and culture was repeated at our institution (Table ). Abdominal CT with oral and intravenous contrast revealed wall thickening in the right colon extending to the proximal portion of the transverse colon compatible with regional colitis. There was a moderate amount of ascites related to PD. The PD catheter entered the right lower quadrant and coiled in the right lower quadrant. There was an abdominal wall fluid collection around the insertion of the PD catheter. Capsule endoscopy was unrevealing.\nGiven multiple gastrointestinal procedures, recent C. difficile infection which had been adequately treated, and incomplete treatment for a recent fungal peritonitis, her persistent abdominal pain was attributed to intractable catheter-related fungal peritonitis. Surgical catheter removal was performed and she was switched to hemodialysis. Catheter tip culture grew C. tropicalis. The fungal peritonitis was treated with oral fluconazole for 2 months. Her abdominal pain improved and she was discharged home.
A 64-year-old male came to our observation complaining of pain localized in the posterior side of his right inferior limb since at least 2 years. Over the last 6 months, he progressively developed numbness in the same dermatome. There was neither obvious relief nor precipitating factors.\nAt the admission, the neurological examination was unremarkable. Physical examination revealed no palpable mass within the abdomen.\nSpinal CT scan without contrast medium () revealed a 44 mm × 55 mm inhomogeneous soft-tissue mass arising from the right L5-S1 neural foramen and its most anterior portion had a clear colliquative aspect. The mass extended along the lumbar column up to the sacrum and to the ipsilateral sacroiliac joint and eroded the right posterolateral portion of the L5 vertebral body. It developed as well in the retroperitoneal space, posteriorly to the iliac vein, up to the psoas muscle with wide erosion of the omolateral conjugate foramen.\nMagnetic resonance image (MRI) showed () a neoplastic lesion with homogeneous low signal in T1WI, heterogeneous signal in T2WI, and strong enhancement in postgadolinium examination. The mass extended along the right side of the L5-S1 intervertebral foramen with erosion of the L5 body without injuring its stability. Besides, displacement of the right psoas muscle was also noted.\nElectroneurography and electromyography at the lower extremities showed neurogenic damage with denervation signs of the right L5 nerve.\nWe decided to perform a one-step combined approach with the vascular surgeon because the lesion was too huge to allow a complete resection via a posterior approach and furthermore its tight relationship with the psoas muscle and the iliac vessels in the retroperitoneal space should be more safely managed via a retroperitoneal approach.\nFirst we dissected free the nerve root from the tumor's capsule debulking the lesion and decompressing the spinal canal and then removed the residual portion after the control of the psoas muscle and the iliac vessels.\nDuring the first step, we performed an L5-S1 hemilaminectomy, a facetectomy, and a resection of L5 transverse process. The tumor clearly originated from the L5 nerve root and invaded the vertebral foramen. We debulked the lesion using the ultrasonic surgical aspirator clearly maintaining the capsular surface to keep the correct margins of resection allowing a complete removal of the tumor.\nSuch approach allowed us not to sacrifice completely the nerve root, and after debulking, the mass was removed from the vertebral foramen up to the psoas muscle and the bony resection was minimal.\nImmediately after the neurosurgical procedure, the vascular surgeon excised the residual retroperitoneal portion of the tumor by a right semilunar, subumbilical approach. He exposed the common iliac artery and the common iliac vein as well as the major part of the external iliac vein and of the hypogastric vein. The distal segment of the inferior vena cava and the aorta were also accurately visualized. Resection of the lesion medially to the psoas muscle was impossible because of its firm adherence to the muscle itself and the risk of vascular injury.\nThe mass was firmly impinged to the bone and to the posterior aspect of the common iliac vein in its passage to extern iliac vein ().\nIn order not to damage the iliac veins and to save the hypogastric vein, the last lumbar vein was tied and the vena cava was raised and moved laterally. The iliac vein was pulled upwards and medially with a widening of the operative field and the mass was finally removed, without traction, laterally ().\nThe spine was considered stable and no additional fixation was performed because of a standard unilateral posterior approach and of the small portions of eroded vertebral body.\nFive days after the operation, the patient was discharged and neurological examination revealed mild numbness in the right L5 dermatome that recovered 3 months later. There were no walking difficulties or back pain. The postoperative magnetic resonance image (MRI) confirmed () the complete resection of the tumor and a dynamic X-ray exam demonstrated the stability of the spine.\nClinical follow-up at 3, 6, and 12 months demonstrated the complete recovery of the patient.\nMicroscope examination revealed a mesenchymal spindle-cells tumor with rare mitotic activity. Tumor cells strongly and diffusely express S-100 protein, providing the diagnosis of benign schwannoma (WHO I).
A gravida 2 and live 0, 28-year-old female patient was admitted in our institute at 34 weeks of period of gestation (POG) for safe confinement. During her previous pregnancy 2 years back, she had suffered from pyrexia due to pyonephritis, severe hyperglycemia, metabolic acidosis, pyrexia, acute kidney injury, septicemic shock, bilateral pleural effusion, and respiratory distress leading to loss of the fetus. During previous hospitalization, she was managed with drainage of pus, broad-spectrum antibiotics, and even required two cycles of hemodialysis.\nLater, she underwent complete hormonal workup for the inability to conceive and was diagnosed to have hypothyroidism with serum cortisol levels in equivocal range. Magnetic resonance imaging (MRI) of the brain was suggestive of pituitary apoplexy and diagnosis of SS was established. She was started on tablet hydrocortisone 10 mg/day along with tablet thyroxine 88 mcg once a day. After few months, she conceived via intrauterine insemination (IUI) and had diamniotic monochorionic twins. She also had gestational diabetes mellitus (GDM) during this pregnancy in addition to SS. In view of multiple metabolic derangements and intrauterine growth retardation of fetuses, an elective LSCS was planned at 36th week of gestation. The patient was co-operative, conscious, and her vitals were stable. Her height was 152 cm and she weighed 65 kg.\nAs the patient had twin pregnancy with multiple metabolic and endocrinological issues, subarachnoid block with adjuvant, added to a local anesthetic drug with invasive blood pressure monitoring and perioperative intravenous hydrocortisone supplementation was planned for her and she was counseled for the same. She was kept nil per oral 8 h prior to surgery, advised to take tablet thyroxine, tablet ranitidine 150 mg and tablet metoclopramide 10 mg on the morning of surgery, 2 h prior to shifting to the operating room with sips of water. Her fasting blood sugar was 124 mg/dL and the morning dose of insulin was withheld. She was shifted to the operating room in the left lateral position.\nInjection hydrocortisone 100 mg intravenously (i/v) was administered in the operating room followed by an infusion of 4 mg/h till oral intake started postoperatively. Though the surgery was planned under the subarachnoid block, a backup for general anesthesia in case of any emergency of block failure was also kept ready with appropriate preparations to manage the airway in a term pregnant patient. After applying electrocardiogram, pulse oximetry, and noninvasive blood pressure monitoring; two wide bores i/v cannulae were inserted. A 20-gauge arterial cannula was placed in the left radial artery under local anesthesia (0.5 mL of 2% lignocaine) for invasive blood pressure monitoring. Supplemental oxygen was given via venturi mask with FiO2 of 0.4% and oxygen flow of 8 L/min. Subarachnoid block was administered at L4-L5 intervertebral disc space using 26-gauge Quincke spinal needle with the patient in the left lateral position and drug 1.5 mL (7.5 mg) of hyperbaric, 0.5% bupivacaine, and 20 mcg fentanyl (0.4 mL) was placed intrathecally. The patient was made supine and a wedge was placed for left lateral tilt. The surgery commenced when the level of the block was achieved until T4. A lower segment cesarean section was conducted with adequate hemostasis achieved at the end of the surgery. Intraoperatively, three episodes of hypotension (defined as a 20% decrease from baseline) about 6 min after subarachnoid block were managed with bolus dosing of injection phenylephrine 50 mcg. Patient delivered two live male babies with APGAR scores of 7/10 and 8/10 at 1 min, weighing 1.8 kg and 2.0 kg. The babies had no major complication nor required supplemental oxygen. They were shifted to the neonatal intensive care unit and kept under observation. Injection oxytocin infusion was started after delivery of the second baby. The intraoperative blood loss was about 800 mL and the duration of surgery was 60 min. Intraoperative arterial blood gas analysis (ABG) and blood sugar levels were within normal limits.\nThe level of sensory block regressed to T10 within 2 h of the subarachnoid block. In the postoperative period, the patient was managed in high dependency unit for first 48 h and she received injection paracetamol 1 g i/v sixth hourly for postoperative pain relief. The patient and the babies were followed for 7 days and the postoperative period remained uneventful.
A 14-year-old Caucasian girl with JIA diagnosed at 2 years of age returned to our pediatric rheumatology clinic with complaints of increased morning stiffness of both knees and a mass of the left knee. Three weeks prior to the onset of knee stiffness, she noticed a mass on the lateral side of her left knee. She had decreased knee flexion and pain with walking that was greater on her left side. She reported a painful snap when she moved her left knee from a flexed to extended position, but no instability or locking. There was no warmth, erythema, interval growth, or fluctuance of the mass. She also did not have any systemic symptoms including fever, chills, or recent weight loss.\nHer past medical history was significant for extended oligoarticular JIA with 5 joint involvement and a positive Anti-nuclear antibody (ANA at 1:80), HLA-B27 negative, and rheumatoid factor (RF) negative. Over the first two years of her illness, she required only NSAIDs until she developed a photosensitive rash with Naproxen. Over the next 6 years, she needed methotrexate and ibuprofen intermittently for flare ups and was maintained on these medications for 1 to 2 year intervals and then tapered off. She had been disease free for three years when she presented with this new knee mass. She had a brief episode of mild iritis earlier in the course of her disease with full resolution while on methotrexate. Our patient lived on a neighboring island far from pediatric rheumatology services. When we were informed about the patient’s knee mass, we were extremely concerned because of her strong family history of cancer and her earlier treatment with methotrexate. Her family had a range of cancers including liver, pancreatic, stomach, throat, lymphoma, melanoma, non-Hodgkin's lymphoma, and glioblastoma in different members of the family.\nOn examination, there was a 1.5 × 2.0 cm well-circumscribed, and non-tender mass. The mass was on the lateral superior aspect of the left patella/quadriceps tendon just above the kneecap and crossed over the top of the femur. As the knee was moved from flexion to extension, there was a palpable and painful snap when the muscles moved past this mass over the tendon. The knee had full range of motion, was stable to varus/valgus stress, and had no medial or lateral joint line tenderness. There was also swelling in both knees. McMurrays and Lachmans test were negative, and capillary refill was brisk in all digits.\nDiagnostic imaging included a normal knee radiograph. Magnetic resonance imaging (MRI) of the left knee showed a moderate joint effusion with an approximately 1.5 cm diameter loculation slightly offset laterally which corresponded to the patient’s knee mass (Figure ). Orthopedics diagnosed an IAGC and aspirated 0.5 ml of off-white, translucent thick material from the left knee mass. Cytology of the fluid revealed lymphocytes and macrophages without malignant cells. The combination of methotrexate and the IAGC aspiration resolved the patient’s knee pain, swelling, stiffness, and snapping symptoms she had experienced with the IAGC.
A 58-year-old male patient presented with left knee lateral pain after a slip down injury a month ago. He had a history of ligamentous injury that occurred 20 years ago, for which no further diagnosis or treatment was done. He had been experiencing mild ‘giving way’ symptoms since then, but the symptom aggravated after the recent trauma. On the physical examination, we found that the range of motion of the patient’s left knee was normal. Medial joint line tenderness was present. The result of the posterior drawer test was grade 2 positive, and McMurray test was also positive-knee pain in external rotation. Plain X-ray showed unremarkable findings.\nOn magnetic resonance imaging (MRI), a longitudinal tear of the medial meniscus () and a horizontal tear of the lateral meniscus () were shown with high-intensity signal on the proton density spectral presaturation inversion recovery coronal image. There was also a slightly high-intensity signal shown in the posterior cruciate ligament (PCL), indicating a probable acute partial tear of the ligament or evidence of an old injury.\nFor diagnostic arthroscopy, we made an anterolateral portal for visualization and an anteromedial portal for performing surgery. By examining the intercondylar notch and articular surfaces of the femur and tibia through these portals, we arthroscopically confirmed a longitudinal tear of the medial meniscus but the lateral meniscus was intact without tear. Instead, we confirmed a cord-like structure, originating from the posterior 1/3 portion of the lateral meniscus and passing obliquely toward the medial femoral condyle in front of the PCL-anterior meniscofemoral ligament (ligament of Humphrey) (). There was no sign of a tear of the anterior cruciate ligament and PCL structures. The main cause of the knee pain was finally proven to be due to the medial meniscus tear because there was neither a lateral meniscus tear nor a PCL injury in this patient.\nArthroscopic partial medial meniscectomy was performed, and at the 1-year follow-up, the patient could perform daily activities without any discomfort.
A 70-year-old otherwise healthy woman presented with a 1-month history of a left upper arm mass that started small and grew over the past several weeks. She denied having any heavy lifting, history of overuse or injury to the area. She was not on any blood thinners, noticed that the mass was tender to the touch and had occasional tingling into the left hand. There was no weakness of the left arm or hand.\nOn examination, there was a visible and palpable mass near the posterolateral distal humerus, which was firm and somewhat mobile within the triceps muscle. The mass measured approximately 4.5×2.4 cm and was sensitive to the touch; however, there was no warmth or skin discolouration noted. Full range of motion at the left shoulder and elbow was demonstrated without pain, and sensation was grossly intact for the left upper extremity. Radial pulse was 2+ on the left side, with capillary refill less than 1 s, and no epicondylar, axillary, cervical or supraclavicular lymphadenopathy was noted on the left side.\nThe patient underwent an MRI with and without contrast of the left upper arm, revealing a fusiform-shaped, enhancing mass that was in direct contact with the lateral cortex of the mid humerus, followed the course of the radial nerve. The patient also had a preoperative evaluation by neurology whose examination demonstrated cranial nerves 2–12 to be intact with 5/5 motor strength throughout. Sensory examination was normal to pinprick, touch and position. The patient demonstrated generalised hyporeflexia. There was no clonus, Babinski sign or Hoffmann sign. Cerebellar examination and gait was normal. There was also a normal range of movement. Based on the normal clinical examination findings, nerve conduction study was not performed. After consultation with an orthopaedic oncologist, the patient decided to have surgery to remove what appeared to be a nerve sheath tumour, such as a schwannoma, based on clinical presentation and imaging findings. During surgery, it was noted that the tumour was located just under the brachioradialis muscle, had displaced the majority of the radial nerve and was also adherent to the humerus.
A 35-year-old male presented to our out-patient department with complaints of recurrent abdominal pain and general weakness for 1 week. No history of prior surgery, trauma, or any other comorbidity existed. He had no alcohol abuse habit or familial history of pancreatic disease. The initial computed tomography (CT) scan demonstrated a large cystic lesion in the upper abdomen and the origin of the lesion could not be identified.\nAt physical examination, an immovable abdominal mass was detected in the upper quadrant was found and the tenderness and rebound-tenderness of the whole abdomen were obvious. Initial laboratory findings revealed mild leukocytosis (10.7 × 109/L), elevated neutrophil granulocytes (89% of the leukocytes) and elevated C reactive protein (CRP) (373.2 mg/L). The measured tumor markers were within the normal range. These results decreased the likelihood of a diagnosis of malignancy. His other laboratory investigations were within the normal reference ranges. Subsequently, he was admitted to the general surgery department. During his hospitalization, a CT scan and ultrasound (US) were performed again to assess the properties of abdominal lesions. The US showed that a large cystic lesion occupied the abdomen (Fig. ). The review result of the CT scan showed a large cystic lesion of the abdominal cavity, which was considered a lymphatic cyst combined with purulent inflammation (Fig. A). Under the direction of the B-ultrasonic scan, we obtained 20 mL liquid from the cystic lesion through fine needle aspiration. Cell morphological examination showed a large number of lymphocytes and fewer monocytes in the cystic fluid. Then we gathered the cast-off cells, and identified the cells by immunohistochemical (IHC) staining. We observed the positivity of CD31 and D2-40 in the cast-off cells.\nDue to the volume of tumor occupied most of abdominal cavity interspace, laparoscopic exploration was hard to perform. Therefore, the patient underwent excision laparotomy of the cyst based on clinical and radiological findings. Abdominal exploration was performed and a cystic lesion measuring approximately 40.0 cm × 30.0 cm originated from the body of pancreas and extended into the mesocolon (Fig. ). The tumor invaded to the spleen and no invasion into vascular structures. In order to retain the pancreatic secretion function and achieve radical resection effect of the patient, distal pancreatectomy (including the cyst, the body, and tail of pancreas) and splenectomy were performed. The pathologic reports showed that, the cyst measured 22.0 cm × 15.0 cm × 5.0 cm (the out-flowing lymphatic fluid in the surgery caused decreased volume of the specimen), and the cyst had a thin membranous appearance. Histological analysis revealed the variable sizes of multiple cysts with thin walls and ectasia of the lymphatic vessels (Fig. ). IHC stains for SMA, CD31, and D2-40 showed positivity, but CD34 staining was negative. The final pathological diagnosis was pancreatic cystic lymphangioma. After 19 days, the patient was discharged without any complications.
Patient 3 is a 45-year-old Jordanian female with an itchy eruption of 3 months' duration. This affected the nape of the neck and the upper back. No triggers were identified and the patient was otherwise healthy.\nThe patients' demographics and their clinical features are outlined in . Clinically, all patients were noted to have erythematous papules that coalesced to form plaques. These were arranged in a reticular pattern that was more prominent peripherally. In addition, patient 1 had associated vesicles and minimal erosions (Figures and ). In all patients, the lesions were symmetrically distributed and had a predilection for the trunk. Other involved areas included the lateral and posterior aspects of the neck (patients 1 and 3), the lateral chest wall (patient 1), and the lumbosacral area (patient 1). Different types of lesions coexisted in all patients including papules, patches, and plaques, in addition to vesicles and erosions in patient 1. A clinical diagnosis of PP was suspected clinically in patients 1 and 2.\nThe main histological findings are summarized in and . The histopathological features were similar in all cases, showing features consistent with early lesions according to Boer's criteria []. The major histological differential diagnoses were impetiginized spongiotic dermatitis, pityriasis lichenoides, and viral exanthem. Periodic acid-Schiff stain was negative in all specimens. Direct immunofluorescence was performed for patients 1 and 2 only and was negative.\nThe clinical course varied, but all three patients had eventual complete resolution of all lesions. Patient 1 was treated with superpotent topical corticosteroids prior to presentation to our department. However, there was no improvement and new lesions continued to emerge. The patient subsequently reported gradual spontaneous resolution 10 weeks after onset of the eruption, leaving postinflammatory hyperpigmentation. Patient 2 was previously treated with moderately potent topical corticosteroids and antihistamines without any improvement. New lesions continued to emerge. On initiation of doxycycline, the lesions cleared within 1 week. No recurrence was reported during a 10-month follow-up period throughout which the patient avoided strict dieting. Patient 3 reported spontaneous resolution of some lesions before presentation to our department. Doxycycline was subsequently initiated with complete resolution.
A 66-year-old woman with WPW syndrome was admitted to the hospital because of frequent paroxysmal tachycardia attacks occasionally accompanied by dizziness, which started when she was 58 years old. She suffered repeated chest distress and palpitations for eight years without treatment. An electrocardiogram from the emergency department showed atrial fibrillation with type A pre-excitation syndrome (Fig. ). The serum troponin I level was 0.415 ng/mL, the creatine kinase isoenzyme level was 5.9 ng/mL, and the myohemoglobin level was 288.3 ng/mL. Physical examination showed a blood pressure of 128/70 mmHg, normal breath sound, normal heart borders, a heart rate of 200 bpm, irregular cardiac rhythm, pulse deficit, and no audible murmur or pericardial friction sound. The patient converted to a sinus rhythm under external direct current cardioversion after unsuccessful drug cardioversion with amiodarone. The echocardiogram after the conversion to sinus rhythm revealed no organic heart disease, an estimated left ventricular ejection fraction (LVEF) of 62%, and mild tricuspid valve regurgitation.\nBecause of the possibility of recurrence of atrial fibrillation with the complication of pre-excitation, the patient underwent RF catheter ablation the following day. A ten-polar coronary sinus (CS) catheter was placed into the CS and an electrophysiological examination catheter was positioned in the right ventricular apex through the left femoral vein. During the sinus rhythm, the earliest anterograde ventricular activation was recorded at the site of CS 34 (the third and fourth poles of the coronary sinus catheter, Fig. a). This site was also the earliest retrograde atrial activation site during ventricular pacing (Fig. b). Therefore, an accessory pathway (AP) was thought to connect the posterior wall of the left ventricle. The medium curved temperature-controlled bipolar ablation catheter was then inserted into the right femoral vein and advanced to the mitral annulus via the atrial septal puncture. An atrioventricular (AV) fusion wave was identified in the electrogram of the distal end of the ablation catheter (ABLd) when ablation was performed over the left atrial endocardium near CS34 and CS56 (Fig. c,d). However, AP conduction remained present after multiple RF applications with power settings ranging between 30 and 40 W. The bipolar ablation catheter was then pulled into the CS and RF applications were administered near CS34 and CS56. Before ablation within the CS, angiography was performed to estimate the CS size. The diameter of the CS proximal end was 7.7 mm while the middle portion was 6.1 mm. With a power setting of 20 W, a prolonged AV interval (Fig. e,f) and smaller delta wave (Fig. g) were identified in the local electrograms. Concentric decremental retrograde conduction of the V-A wave phenomenon was observed via repeated right ventricular apex extra-stimuli with overdrive pacing mode (RVA S1S1, Fig. h). This finding indicated that retrograde conduction of the AP was blocked. Anterograde conduction of the AP could not be completely blocked even after multiple irrigated ablations, because the delta wave did not completely disappear. The total amount of RF application energy in the CS was 6800 J. When the bipolar ablation catheter was again sent to the mitral annulus, an AV fusion wave was identified in the electrogram of ABLd when the catheter was at the 5 o’clock position in the left anterior oblique position of the mitral annulus near CS34 (Fig. i). The anterograde conduction of the AP disappeared 4 s later with an RF application power setting of 30 W (Fig. j). Anterograde and retrograde conduction of the AP could not be induced by the high-frequency atrial and ventricular stimuli. The patient was free of palpitation attacks, and the electrocardiogram was normal immediately after ablation (Fig. j).\nAnother electrocardiogram was performed the following day, revealing a sinus rhythm with frequent atrial premature beats, paroxysmal atrial tachycardia, widespread concave ST-segment elevation, T-wave changes, and left ventricular high voltage (Fig. a). The serum troponin I level was 8.700 ng/mL, the creatine kinase isoenzyme level was 23.2 ng/mL, and the myohemoglobin level was 325.0 ng/mL. Repeated electrocardiograms showed sustained widespread concave ST-segment elevation without dynamic changes in QRS and with ST-T morphology. Echocardiograms revealed mild pericardial effusion with an estimated LVEF of 59% and mild tricuspid valve regurgitation. The patient did not show any symptoms such as chest pain or chest distress, thus leading to a suspicion of myocardial injury and pericarditis caused by ablation-related injury. The patient was not scheduled for any specific treatment for pericarditis but was instead monitored, asked to rest and take aspirin 100 mg orally daily for a month which was used to prevent postoperative embolic events. The patient was discharged five days after the procedure with significantly decreased levels of troponin I (0.036 ng/mL) and myohemoglobin (94.7 ng/mL). A repeated electrocardiogram after three weeks revealed normal findngs (Fig. b).
A 45-year-old man discovered bulging of the right side of his abdomen 10 days before visiting our hospital. He had no pain, eruption, or paresthesia on the trunk or extremities, and he had no digestive symptoms. Although he had a history of HZ in the same area of the bulge 20 years previously, he had noticed no abdominal wall abnormalities since then. He was in good health except for mild hypertension, for which he took a calcium antagonist. He had no history of diabetes mellitus, immunodeficiency disorders, or surgery. He had never traveled abroad and had engaged in no outdoor activities in mountainous areas during the previous few years.\nUpon his first visit to our outpatient clinic, the patient was awake and alert. His body temperature was 36.7°C, and his blood pressure was 146/108 mm Hg. A marked bulge was observed on the right side of his abdomen in the area innervated by the 10th to 11th thoracic nerves (Figure ). The bulge became more pronounced with increased abdominal pressure. Spontaneous pain or tenderness on palpation was absent in the area of the bulge. Although a vesicular rash typical for HZ was not present, there were five eschars on the right abdominal skin of the 11th thoracic dermatome. Neurologic abnormalities other than abdominal muscle weakness, which presented as the above-described bulging, were absent below the 11th thoracic nerve. Additionally, no abnormalities in the cranial nerves or deep tendon reflexes were found, and pathological reflexes and nuchal rigidity were absent. Laboratory examination showed a white blood cell count of 8570/μL, C-reactive protein level of 0.04 mg/dL, creatinine kinase level of 330 IU/L, and blood glucose level of 94 mg/dL. Abdominal computed tomography without contrast enhancement showed right lateral abdominal bulging without prolapse of the intestine or a subcutaneous mass through the abdominal wall. No mass lesion was detected in or around the spinal canal (Figure ).\nThe patient was treated with famciclovir for 1 week without steroid therapy. Although the abdominal muscle paralysis showed no signs of improvement for about 3 weeks, it completely resolved 3 months after its onset.
This patient was a generally healthy 62-year-old male with a left lobe complex nodule within a nontoxic multinodular goiter that had been enlarging for approximately 3 years. In 2015, the patient had a FNAB reported as benign, BC II. Because of continued growth, he had a second FNA biopsy approximately six months later reported as a Hürthle cell neoplasm or suspicious for a Hürthle cell neoplasm, BC IV with Oncocytic / Hürthle cells dispersed mostly singly and in small fragments in a background of lysed blood. CKAE1/AE3, TTF-1, and thyroglobulin immunostains were positive (). Molecular testing with ThyroSeq® v2 revealed an absence of gene mutations or fusions but overexpression of the MET gene with an uncertain increased risk of malignancy. After repeat ultrasound imaging, the nodule had grown from 4.9 to 6.0 cm over the course of 1 year. He was euthyroid with negative anti-thyroid antibodies. There was no family history of thyroid cancer or known radiation exposures in his youth. He had no obstructive symptoms despite the size of the mass and denied shortness of breath, dysphagia, neck pain, neck pressure, or recent voice changes. His weight had been stable and appetite good. His past medical history was significant for a retinal detachment, hypertension, and inguinal hernia with a surgical history limited to eye surgery and hernia repair. He denied tobacco or alcohol use. On exam, the patient had an enlarged, firm thyroid gland with the left thyroid lobe causing significant tracheal deviation to the right. A neck CT scan demonstrated a markedly enlarged left thyroid lobe (7.2 cm in sagittal height) causing significant rightward tracheal deviation, minimal tracheal compression, and slight early substernal extension (). He had multiple opinions from both endocrinologists and surgeons with various recommendations from left thyroid lobectomy to total thyroidectomy. The patient had initially contemplated a hemithyroidectomy due to concerns for voice impairment that could impact his occupation as an attorney.\nAfter a second surgical consultation, he elected to have another, more advanced molecular test performed on the same FNAB specimen. The ThyroSeq® v3 test has been designed to improve the performance of its previous version, ThyroSeq v2, specifically with respect to Hürthle cell tumors. This has been achieved by expanding the number of gene markers analyzed for mutations and gene fusions and particularly by incorporating the analysis of copy number alterations (CNAs), which are common in Hürthle cell cancers. ThyroSeq® v3 test results in this case showed CNAs involving multiple chromosomes with the pattern of genome haploidization which predicted a much greater probability that the left lobe nodule represented a Hürthle cell malignancy rather than Hürthle cell metaplasia or an adenoma. Based on the additional information provided by ThyroSeq® v3, in July, 2017, the patient elected a total thyroidectomy. At surgery, the overlying strap muscles were superficially adherent to the thyroid capsule on the left with a suspicion of minimal extrathyroidal extension of the tumor and a layer of muscle was left attached to the specimen. There were no paratracheal lymph nodes. He did require single gland parathyroid autotransplantation. Postoperatively, his parathyroid hormone and calcium levels were within normal limits. On final surgical pathology, an encapsulated 7 cm Hürthle cell carcinoma with 5 foci of angioinvasion was found along with foci of capsular invasion, without extrathyroidal extension (). A second opinion was sought and the reviewing pathologist reported 4 foci of capsular invasion and 3 foci of vascular invasion. The number of foci of vascular invasion was prognostically important and prompted more aggressive treatment and follow-up.\nOne month postoperatively, thyroglobulin was 308 ng/mL. A small thyroid remnant with 2.4% uptake in the surgical bed was found on I-131 whole body scan. An FDG-PET scan was negative for any activity in the thyroidectomy bed or for distant metastatic disease; therefore he was given 30 mCi of radioactive iodine to ablate the remnant. At this time, his thyroglobulin had decreased from 308 to 8.71 ng/mL. His postablation, I-131 whole body scan showed ablation of the thyroid remnant and no evidence of metastatic disease. By 10/27/2017, the thyroglobulin had decreased further to 0.2 ng/mL with no detectable thyroglobulin antibodies and a TSH of 0.09 uIU/ml indicating a favorable early response to initial treatment.
This case involves a 60-year-old male with a history significant for benign prostatic hyperplasia, hypertension, and insulin-dependent diabetes who presented in July 2017 with diabetic ketoacidosis and Fournier’s gangrene. The patient’s treatment course for Fournier’s gangrene subsequently consisted of multiple operative debridements, an intensive care unit (ICU) admission, and ultimately a penectomy in July 2017 (Figure ). He continued his post-discharge follow-up at an outside hospital for recuperative care as he became homeless during this time. He received wound care with home healthcare and continued to undergo a follow-up in the outpatient clinic at the urology and plastic and reconstructive surgery departments, where he discussed his desire to undergo penile reconstruction. After discussing all treatment options as well as the risks and benefits of the surgery, the patient agreed to move forward with surgical reconstruction. The patient obtained consent for a free flap procedure, and plans were discussed to proceed with a radial forearm reconstruction of his penis.\nThis procedure involved phallus and neourethra construction utilizing a single radial forearm free flap. First, a 12-cm circumferential circle was marked and dissected out at the planned penis insertion site. Next, two branches of the dorsal penile nerve were carefully isolated and dissected out along with the left deep inferior epigastric and vena comitans that provided approximately 8 cm of pedicle length. An 8-cm segment of the great saphenous vein was also dissected out and transposed to the inferior epigastric vessels to assist with the flap anastomosis. The recipient vessels and nerves were now defined and attention was turned to harvesting the radial forearm free flap. The radial forearm free flap was lifted in the subfascial plane, while special attention was given to preserving the cephalic vein, the basilic vein, and the radial sensory nerve. The medial and lateral antebrachial cutaneous nerves were then isolated, and the flap was fashioned into a neophallus and urethra prior to vessel and nerve ligation. Once completed, the nerves and vessels were ligated, the flap was transferred to the groin for microsurgery, and the radial forearm donor site was covered with Integra (Integra LifeSciences, Plainsboro, NJ). The radial artery was anastomosed with the left deep inferior epigastric artery, two vena comitans were coupled to the greater saphenous vein, and two nerves were coapted to the dorsal penile nerve stump. The procedure was concluded and the patient was transferred to the ICU in stable condition. Postoperatively, the patient developed a 1 x 1.5-cm2 area of distal flap tip necrosis that resolved following conservative treatment with daily topical Silvadene. The patients remained in the ICU postoperatively for close flap monitoring and nutritional optimization, and he was discharged 14 days following the procedure. The postoperative course was complicated by a flap and donor-site infection requiring debridement of both sites with subsequent resolution of the infection. The patient is pending anastomosis of his neourethra to his native urethral stump by the urology department. The patient currently has a catheter in place for a urinary function that will be removed only after the neourethral anastomosis is complete. Should the patient desire the ability to maintain an erection for sexual activity, he would require an additional surgery for penile prosthesis placement. The patient has reported preserved sensation in the phallus and expressed satisfaction with his result.
A 30-year-old female presented to our hospital complaining of shortness of breath on exertion for approximately three years and exacerbation for three months. Her medical history revealed that she was diagnosed with Gardner’s syndrome eight years earlier. This diagnosis was confirmed by specific genetic tests for APC mutation performed at Peking University Shenzhen Hospital. There was no relevant family history for adenomatous polyposis. Multiple swelling was found on her occipital, face, neck, right side of the back, and buttock when she was 13 years old, gradually enlarging since then. She underwent a biopsy 10 years ago and histopathologic evaluation of the biopsy specimen confirmed a diagnosis of neurofibroma. All tumors were completely excised in the following years.\nOn physical examination, the right lung field was dull to percussion with decreased breath sounds on auscultation. In addition, multiple lipomas were found in her back, buttock and legs. The remainder of the physical examination was unremarkable. No relevant abnormalities were noted on the hematologic or biochemical studies. Microbiologic analysis of the sputum was negative. A gastroscopy and colonoscopy were performed and revealed normal findings. A thorax roentgenogram showed a large mass in the anterior mediastinum with small lung volumes. Pulmonary function tests showed a decrease in forced vital capacity (24% predicted) and forced expiratory volume (22% predicted) with a total lung capacity of only 37%. Chest computed tomography (CT) revealed a large fat containing mass occupying almost the entire right hemithorax and extending anteriorly into the left hemithorax with a clear boundary, which resulted in lung collapse and mediastinal shift (Fig ). The patient confirmed that the mass had been present for a period of more than six years. An evaluation for distant metastases using positron-emission tomography–CT was negative.\nSurgical exploration was performed via a bilateral posterolateral thoracotomy and revealed a large, smooth, yellow, non-infiltrating encapsulated mass. The mass occupied approximately 80% of the right and 50% of the left pleural cavity, resulting in marked compression of both lungs. The mass was removed in two parts because of its large size. A 20 × 17 × 15 cm mass was first excised by a left chest posterolateral incision, followed by the remaining mass measuring 28 × 25 × 17 cm by a right chest posterolateral incision (Fig ). The two masses weighed 4150 g. Histological examination showed that the tumor was predominantly composed of mature adipose tissue intermixed with septa of thymus tissue containing lymphocytes and Hassall’s corpuscles (Fig ). The final diagnosis was thymolipoma. The patient was discharged 15 days later in excellent condition (Fig ). There was no recurrence after 20 months of follow-up.
After a multidisciplinary evaluation, at the end of November 2019, a 13-year-old girl attended the Pain Therapy Clinic of the Ospedale Pediatrico Bambino Gesù in Rome, where acupuncture is also practiced as an analgesic technique. She reported pain in the left wrist and hand, with intensity 10 on the Numeric Pain Rating Scale (NRS), pulsating, and always present, thus preventing any movement. Marked hypersensitivity and allodynia were present at the level of the left fingers, wrist and hand. Pain was present in both flexion and extension of the wrist and caused a marked reduction in strength in the left wrist and hand, making a handshake impossible for the girl. There was no redness but swelling and sweating at the level of the fingers of the left hand. The pain was so intense that it interfered with her regular attendance at school, generating social withdrawal phenomena, which are unfortunately very frequent in patients with chronic pain.\nPain began three months before the consultation, after an accidental fall with trauma to the left wrist. It gradually increased and did not respond to either NSAIDs or limb immobilization. The diagnostic tests performed at the time (X-ray, Doppler ultrasound and magnetic resonance imaging) were negative, as were the blood chemistry tests ( and ).\nFrom the age of 8, the girl was followed by a pediatrician in our hospital for a history of cramps and pain in the lower limbs, especially in the ankle and left knee, both in the absence of trauma or caused by frequent falls. In the following years, clinicians found bilateral flatfoot (with subsequent surgery), mild ligamentous hyperlaxity and vitamin D deficiency. In addition, borderline cognitive level with motor coordination disorder and executive function deficit, as well as stuttering, were then diagnosed. Elements of anxiety emerged from the administration of Self Administered Psychiatric Scales for Children and Adolescents (SAFA-A, D and S) questionnaires, as highlighted in particular by the subscales “Separation anxiety” and “Generalized anxiety” [,]. Concern for one’s own health was observed, with experiences of herself as being ill; the scores indicate a propensity to somatize. There was a tone of mood oriented in a deflected sense, and insecurity. The results of the Lie scale were: 8; T: 65 [,]. In addition to pulsating headache with phono and photophobia, frontal epilepsy was also diagnosed, which could explain the frequent falls, and moreover had excluded hyperbaric oxygen therapy as a feasible regimen in this case (due to a cost/benefit evaluation, and increased exposure to oxygen toxicity during the treatment itself). Episodes of dizziness with difficulty in maintaining an upright position lasting a few hours were also observed, and on two occasions she also had an episode of unconsciousness lasting about 2 min.\nDuring the first visit, as a consequence of the mother’s need to have time to convince the recalcitrant daughter, in the meantime it was recommended to administer oral tramadol (100 mg/mL), 5 gtt in the morning and 5 gtt in order to reduce musculoskeletal pain. The reason for choosing a drug such as tramadol rather than any other pharmacological option lies in the fact that the pain was so intense that it affected the patient’s relationships []. We therefore opted for a drug that would have an immediate effect, so as to be able to undertake the acupuncture course. Subsequently, in the first two sessions, after careful disinfection of the skin with 2% chlorhexidine, and using the appropriate needles for length and diameter based on the type of acupuncture and the selected points, we used the following acupoints: TE 4 (Yang Pool), TE 5 (Waiguan), LI 5 (Yang Xi) and SI 4 (Wan Gu), all on the left side. These points were chosen on the basis of a pathology which, according to traditional Chinese medicine, was caused by cold wind. These points produced heat and dissipated the wind []. The needles were kept for 30′, with stimulation every 10′. In the third session, the girl reported a slight improvement in the painful symptoms but at the same time unbearable pain in the affected limb during the previous sessions due to the insertion and maintenance of the needles in the affected area. We decided to change strategy and to use abdominal acupuncture and stimulation of the points CV 4 (Guan Yuan), CV 12 (Zhong Wan), CV 16 (Zhong Ting), CV 17 (Shan Zong), ST 24 bilateral (Huaroumen) and KI 17 bilateral (Shang Qu), with appropriate needles and maintaining the same interspeed and time of stimulation. The needles were inserted to a depth of 0.2 cun. These new points (CV 4, CV 12, CV 16, CV 17 and KI 17), in addition to heating and dissipating the wind, re-established the correct circulation of qi []. In fact, used in combination, their purpose was to move the qi from the kidney to the extremity of the upper limb passing through the shoulder [,]. ST 24 was used to calm the patient and increase her compliance with acupuncture [].\nAuriculotherapy was also associated with Vaccaria seeds on the Wrist, Hand and Shenmen points, with the recommendation to stimulate them at home for 10 min, 4 times a day until the next session. Vaccaria seeds are used to stimulate certain points in auriculotherapy due to their almost spherical shape, and the absence of pharmacological properties []. The Shenmen point was chosen for its anxiolytic effect, given the patient’s psychological difficulties [].\nAfter eight sessions (two months) of abdominal acupuncture the pain completely disappeared (Numeric Pain Rating Scale value 0) and the girl regained full functional capacity of the arm and a normal life. Follow-up at three months, six months and one year demonstrated complete remission of symptoms, with constant values of NRS equal to 0. The reduction in pain, and subsequently its total disappearance, allowed the patient to resume normal school attendance, and therefore to resume a life of normal, balanced relationships.
A 45-year-old woman was first diagnosed in 2006 with ACC showing typical signs of Cushing’s syndrome with consecutive increase of weight and body hair, acne, therapy-refractory arterial hypertension and decrease of physical working capacity. Hormonal work-up revealed elevated cortisol levels basal and after dexamethasone suppression, as well as elevated dehydroepiandrosterone sulphate (DHEA-S) and androgen levels. CT scan showed a 4.7 × 5.2 × 4.5 cm sized mass of the left adrenal gland with venous contrast enhancement suspicious for adrenocortical carcinoma (Fig. ).\nThe patient underwent conventional resection of the left adrenal gland and lymphadenectomy. Pathological study of the resected tissue was performed by two independent pathologists. The tumor presented a solid growth pattern with some fibrous bands and small areas of necrosis. Tumor cells appeared monomorphic with small nuclei and condensated chromatin. The rate of mitosis was under 1 in 10 high power fields. Interestingly there were large amounts of myelolipomatosis metaplastic areas. All three classic scoring systems showed results still within the value range for benign lesions. However, a high Ki-67 expression of 20 % led to the diagnosis of an adrenocortical carcinoma (ENSAT stage II). Due to a good differentiation, no adjuvant mitotane therapy has been performed. Though the patient underwent follow-up examinations periodically, including hormonal work-up and CT or MR imaging performed initially every 3 months and eventually every 6 months after a 2-year-recurrence-free survival.\nSixty-six months after surgical treatment MR imaging showed a new hyperperfused mass in the head of the pancreas with progression of size in the following studies as well as a high FDG-uptake in positron emission tomography (Fig. ). Thus, the mass was highly suspicious of malignancy and resection was recommended by interdisciplinary consensus.\nThe patient underwent pylorus preserving partial pancreaticoduodenectomy. Postoperatively the patient developed a pancreatic fistula with an intraabdominal abscess formation, which had to be drained interventionally on day 10 after surgery. The drain could be removed on day 24 after surgery.\nHistological and immunohistochemical examination of the resected tissue showed a 1.5 cm sized well differentiated tumor with solid growth pattern (Fig. ). Tumor cells presented monomorphic with eosinophilic cytoplasm and unremarkable nuclei. The metastasis stained positive for synapthophysin, Melan A and steroidogenic factor 1 (SF-1) in consistency with the diagnosis as a metastasis of the adrenocortical carcinoma (Fig. ) with a Ki-67 expression in 10 % of tumor cells. There where no signs of a primary pancreatic carcinoma as the tumor cells stained negative for pan cytokeratine (pan-ck) (Fig. ). In addition, pathological examination by the reference pathologist of the German ACC study group was performed and confirmed the correlation between the ACC primary tumor and the unusual site of metastasis.\nAccording to interdisciplinary consensus an adjuvant mitotane therapy was initiated after the tumor resection and is still ongoing. During follow-up, including endocrine and imaging work-up every 3 months now for more than 3 years, there is no evidence of recurrence (Time axis see Table ).\nA literature review has been performed to identify the distribution of different tumor entities of solitary metastases inside the pancreas. A PubMed search for studies or case reports dealing with “metastases to pancreas” was performed. Articles were included in this review if 10 or more patients were investigated retrospectively or prospectively, patients suffered of metastases to pancreas (no infiltrative involvement) and only the pancreas was affected by metastases, patients received resection of pancreas metastases in curative intension and different tumor entities were included in each study. Four retrospective studies [–] summerized in Table met the inclusion criteria with a total of 92 patients. Median age of patients ranged from 59 to 64 years. Most frequent origin of pancreatic metastases was the kidney in 46 % of the cases followed by melanoma in about 10 % of the cases. Rectal and Colon carcinomas were involved in only 5 cases. One “non-pancreatic endocrine tumor” was reported but not specified in more detail []. Here, the distribution of metastatic origin is different to other literature reviews, where the proportion of renal cell carcinomas range between 60 and 70 % []. This is caused by the exclusion of studies intending to investigate a single tumor entity metastatic to the pancreas (mostly renal cell carcinomas). Median survival after curative resection of pancreatic metastases was 2.2 to 4.3 years. 5-year-survival ranged between 36 % and 61 %.
A 31-year-old male presented for evaluation of right knee pain, muscle spasms, and mechanical snapping. The symptoms had been present for 2 years with no antecedent trauma or injury. The knee pain was associated with a snapping sensation with extension of the right knee joint notably in the posteromedial region. Initial work up at the onset of symptoms included magnetic resonance imaging at an outside facility that revealed mild chondromalacia of the lateral facet of the patella, bone contusions of the femoral condyles, as well medial and lateral tibial plateau consistent with hyperextension injury. An electromyogram was normal. He ultimately underwent arthroscopic lateral retinaculum release, which did not improve his symptoms.\nPhysical examination revealed an antalgic gait with mild atrophy of the right quadriceps and calf musculature compared to the left. The pain was noted with palpation of the medial thigh and pes anserine region. With repetitive flexion and extension, there was visible and audible snapping of the medial, distal hamstring region, reproducing his discomfort. Manipulation of the patella did not cause pain, and there was no joint line tenderness. Hyperextension was not noticeable on examination at full extension. McMurray test was negative. There was no obvious effusion.\nAn updated magnetic resonance imaging revealed mild edema-like signal along the confluence of the pes anserine tendons and a small tear of the medial meniscus. Dynamic ultrasound over the posterior and medial thigh and knee was performed with the patient lying lateral recumbent on the right side. Static sonographic examination revealed no abnormal character or quality to the hamstring muscles and tendons, no osseous abnormality, no meniscal pathology, and no abnormal fluid collections. However, with repetitive flexion and extension of the knee, dramatic snapping of the gracilis tendon between the sartorius muscle and the medial femoral condyle was encountered [Figures , and ]. Sonopalpation with the pressure of the ultrasound probe over this region reproduced the patient's pain, and the patient was diagnosed with snapping pes anserinus syndrome. A corresponding magnetic resonance imaging of the region where the snapping occurred is shown in for correlation, and an ultrasound of the normal contralateral knee is shown in . shows the normal knee with a fixed gracilis tendon without snapping. A subsequent ultrasound-guided triamcinolone and lidocaine injection of the gracilis tendon at the level of the medial femoral condyle performed to assist with diagnosis provided immediate pain relief despite the persistence of tendon snapping.\nDue to long standing pain and dysfunction, the patient subsequently elected for resection of the gracilis and semitendinosus tendons along with arthroscopic partial medial meniscectomy followed by physical therapy. The soft tissue snapping resolved postoperatively [] as did his knee pain. A follow-up diagnostic ultrasound revealed resolution of tendon snapping on dynamic examination [].
A 26-year-old woman noted pain and swelling in her proximal right arm. Imaging revealed a mass in the posterior compartment of the arm as well as innumerable lung lesions consistent with metastases. MRI showed no brain lesions. Biopsy revealed ASPS and she began sunitinib at 37.5 mg daily. Toxicity included hand-foot syndrome (ultimately requiring dose reduction to 25 mg daily), but imaging showed both primary tumor and metastases to have decreased in size on imaging 3 months after initiation. She continued on sunitinib for the ensuing 33 months with stable disease on imaging. At 33 months, because of worsening neuropathic arm pain, sunitinib was held and palliative radiation (50 Gy/20 fractions) to the arm was administered, with sunitinib resumed afterwards. Arm pain and swelling initially worsened over several months before finally improving above baseline.\nFollowing the treatment break for radiation, imaging showed lung nodules to have grown slightly. It was hoped that this was due to interruption of treatment, but over the ensuing year, the lung metastases continued to grow despite ongoing sunitinib. Forty-seven months from her initial presentation, sunitinib was discontinued and she began bevacizumab 7.5 mg/m2/14 days. With this, she enjoyed a decrease in swelling in her right arm and consequent improvement in strength; we had not realized that sunitinib had been worsening the edema in her arm. CT of the chest 2 months later confirmed continuing progression and bevacizumab was discontinued. She embarked on cyclophosphamide and sirolimus, but tolerated this for only 2 months before discontinuing for worsened fatigue, anxiety, and shortness of breath.\nImaging confirmed progression of lung nodules, and 53 months after her initial presentation, she began pazopanib at 800 mg daily. This too proved difficult to tolerate. She was admitted to the hospital for hypoxia and found to have a pulmonary embolism, which in retrospect was probably responsible for her earlier clinical decline. She began low-molecular-weight heparin, and with this, her dyspnea improved over the subsequent weeks. After 4 days off, she resumed pazopanib at 400 mg daily. Imaging 2 months later showed response in most lung nodules and subsequent follow-up imaging shows stable disease (fig ). At the time of this writing, she has been on pazopanib for 8 months with stable metastatic disease in the lung and improvement in arm pain. Her arm edema has not recurred.
A 41-year-old Japanese woman presented to our clinic with a 4 month history of bilateral groin pain and right buttock pain. Her right hip was more painful than her left hip. There was no history of trauma, alcohol abuse, or steroid use. Her medical history included iron-deficiency anemia diagnosed 2 years earlier, after which she had been on iron supplements. She had no fracture episodes, including fragility fractures.\nHer height, body weight, and body mass index were 155 cm, 42 kg, and 18.7 kg/m2, respectively. She was able to walk for approximately 10 minutes without a stick, albeit at a slow speed. Limitations in the passive motion of her bilateral hip joint were observed thus: flexion, 100°, internal rotation 5°, external rotation 15°, and abduction 20°, on both sides. She was able to perform a straight-leg raise of the right limb with substantial pain. The neurovascular status of both lower extremities was intact. The Japanese Orthopaedic Association scoring system for the evaluation of hip-joint function (JOA hip score) was 46 points for her right hip and 56 points for her left hip. The score was based on a total of 100 points, comprising 40 for pain, 20 for range of motion, 20 for the ability to walk, and 20 for activities of daily living [].\nStandard radiographs of both hips (Fig. a–c) demonstrated no characteristic findings such as the crescent sign, sclerotic band pattern, and collapse of the femoral head, and no joint space narrowing was seen in either femoral head. MRI of both hips (Fig. d, e) presented a low signal line in the subchondral region of the femoral head in the T1 weighted image and high signal region in almost all of the femoral head in the short tau inversion recovery (STIR). The oblique axial views of the proton density-weighted image showed a low-signal sinuous line in the anteromedial region of the femoral head (Fig. ). Dual-energy X-ray absorptiometry (DEXA) values were low in both femoral necks. Bone mineral density was 0.909 g/cm2 (T-score –0.9, Z-score −0.8) in the lumbar spine, 0.594 g/cm2 (T-score −1.8, Z-score −1.4) in the right femoral neck, and 0.529 g/cm2 (T-score −2.4, Z-score −2.0) in the left femoral neck. Laboratory findings were as follows: C-reactive protein (CRP) 0.03 mg/dl (normal range: 0–0.5 mg/dl); alkaline phosphatase 608 IU/l (40–150 IU/l); calcium 9.0 mg/dl (8.4–10.2 mg/dl); albumin 4.4 g/d (3.9–4.9 g/d); and hemoglobin 9.7 g/dl (12–16 g/dl). Bone turnover markers were as follows: tartrate-resistant acid phosphatase 5b (TRACP-5b) 463 mU/dl (premenopausal normal range: 120–420 mU/dl) and total procollagen type 1 N-terminal propeptide (Total P1NP) 72.7 ng/ml (26.4–98.2 ng/ml). We diagnosed bilateral osteonecrosis of the femoral head and classified it as stage 1 in both femoral heads, according to the Association Research Circulation Osseous (ARCO) classification [].\nThe patient was instructed not to take as much weight as possible using sticks on the right side. Her symptoms improved immediately. However, 6 months later, her symptoms increased slightly without any traumatic episodes. Radiographic findings indicated almost no change (Fig. a–c). However, a slight signal change in the medial subcapital region was observed in the MRI scan (Fig. d, e). Her pain gradually increased thereafter, and 10 months after her first visit, walking became difficult. The JOA hip score decreased to 34 points in both hips; still, no changes could be observed in the radiograph (Fig. a–c). MRI of both hips showed a nondisplaced subcapital fracture on the medial side of both femoral necks, with bone marrow edema around the fracture (Fig. d, e). Because the cause of the fractures was not identified, the DEXA and bone turnover markers were measured again, and 25-hydroxy (OH) vitamin D was measured for the first time. All DEXA values decreased. The bone mineral density was 0.849 g/cm2 (T-score −1.5, Z-score −1.2) in the lumbar spine, 0.527 g/ cm2 (T-score −2.4, Z-score −2.1) in the right femoral neck, and 0.490 g/cm2 (T-score −2.7, Z-score −2.4) in the left femoral neck. TRACP-5b level increased to 607 mU/dl, and total P1NP decreased to 52.7 ng/ml. Her 25(OH) vitamin D level was 11.1 ng/dL and she was diagnosed with vitamin D deficiency. Based on the above results, our diagnosis was bilateral stress fracture of the femoral neck secondary to osteonecrosis of the femoral head. The patient underwent internal fixation of both hips with sliding hip screws (Dual SC screw system; Kisco, Kobe, Japan) to stabilize the stress fractures. In addition, the reaming performed before inserting of the sliding hip screw served as core decompression for the femoral heads [, ]. The specimens obtained from the reaming were examined histologically. Definitive findings of osteonecrosis such as bone marrow necrosis and loss of osteocyte nuclei in the femoral heads were observed (Fig. ). Postoperative radiographs showed no evidence of displacement of the fractures (Fig. ). We administered eldecalcitol 0.75 μg per day orally for vitamin D deficiency, and daily subcutaneous injections of teriparatide acetate. In the immediate postoperative period, the patient began to bear weight as tolerated with the use of an assistive device bilaterally. One month postoperatively, she was able to walk without pain and used a cane part time. She eventually regained full walking ability without a cane 3 months after surgery. Furthermore, her JOA hip score improved to 90 points in both hip joints at 5 months after surgery. Radiographs showed no evidence of recurrent stress fracture in the femoral neck or progression of osteonecrosis (Fig. ). Sequential oblique axial MRI showed that the necrotic region of the femoral head had decreased 5 months after surgery (Fig. ).
A 69-year old Caucasian lady presented to the emergency department with a two day history of haemoptysis, pleuritic chest pain and dyspnoea. She had a productive cough with thick, yellowish sputum, associated with intermittent low-grade pyrexia and mild weight loss over the past few weeks. There were no significant comorbidities, history of recent travel or positive family history. She was a non-smoker.\nPhysical examination revealed a septic patient, in apparent distress and extremely short of breath. Observations revealed pyrexia, tachycardia, tachypnoea and hypoxia with oxygen saturations of 93 % on air. Blood tests revealed a raised C-reactive protein of 347.2 mg/L along with a raised white cell count of 28.2 × 109 /L. Differential counts revealed neutrophilia 61.7 %, raised lymphocytes 33.2 % and eosinophilia 7 %. All other biochemical tests including urea and electrolytes, liver function tests and clotting profile were within normal range. She was started on broad-spectrum antibiotic therapy and her sputum sample was then cultured which revealed no significant bacterial growth including absence of acid fast bacilli for tuberculosis, however multiple cysts were seen on microscopy. A suspicion of hydatid disease was confirmed by a positive hydatid complement fixation test of the sputum.\nBaseline investigations such as an electrocardiogram and echocardiography were unremarkable.\nA plain chest radiograph showed a hydropneumothorax on the right side with the pneumothorax component measuring 16 mm. The left lung was clear. There was a near-complete whiteout of the right hemithorax with sparing of the apex, which was most likely to be a persistent pneumothorax with possible rupture of the hydatid cyst (Fig. ). In order to obtain more clear details of the disease process, a magnetic resonance imaging (MRI) scan of the thorax and liver revealed a complex pulmonary mass, which extended from the right lower lobe of the lung, through the hemidiaphragm and into the posterior aspect of the right lobe of the liver. The intrahepatic component appeared thicker walled and well encapsulated. The thoracic component measured 9.5 cm, the intrahepatic component was 9.6 cm and the overall craniocaudal length was 13.2 cm (Fig. ). There was extensive involvement and rupture of the right posterior diaphragm by the hydatid cyst as it passed into the chest. The mass appeared heterogeneous with a serpiginous internal structure. The chest component appeared more irregular and tubular and was occupying a greater proportion of the lower lobe of the lung, with likely airway involvement. There were further ‘simple’ cysts within the liver and both kidneys. There was a small right pleural effusion, and significantly increased atelectasis in the lower lobe posterior to the hydatid mass.\nThe patient was then commenced on the anti-helminthics albendezole and praziquantel. A multidisciplinary team consensus determined that the patient required complex surgical intervention to eradicate the fistula and prevent further deterioration. A computed tomography (CT) scan was performed for accurate surgical planning, delineating the margins to ensure complete division (Fig. ). The patient underwent a right-sided thoracotomy and a lower lobectomy. There was extensive evidence of thickened pleura with empyema intraoperatively. The fistulous tract was then identified and over sewn. All remaining cystic lesions were removed and curetted and all defects were closed aseptically. Drains were placed post operatively. Following surgery, the patient’s inflammatory markers for sepsis steadily improved. A CT scan post-operatively demonstrated complete resection of the fistula. She continued on the anti-helminthic medications and remained well at six months post discharge.
A 57-year-old male with a remote history of a two-stage fasciocutaneous urethroplasty presented with a new penetrating injury to his perineum after falling on a crowbar at work. He was reluctant to see a physician immediately and has delayed his visit by 3 months. By the time of his first visit he had a large perineal abscess and a fistula through which he was voiding since the injury. The patient was immediately admitted to the hospital and underwent incision, drainage, and conservative debridement of the perineal abscess and a suprapubic tube placement. On urethroscopy the urethral lumen could not be visualized beyond proximal pendulous urethra. The patient was managed with wet to dry dressing changes as outpatient until complete closure of the perineal wound.\nThree months later he presented for reevaluation with a voiding retrograde urethrogram and attempted voiding cystourethrogram (). The study demonstrated a 5 cm stricture involving most of the bulbous urethra and a persistent urethrocutaneous fistula draining into the perineum. Patient was counseled on available reconstruction and diversion techniques, and had chosen reconstruction. In view of his prior extensive reconstruction with local flaps and subsequent significant trauma to the perineum followed by abscess a reliable local tissue was not available for reconstruction. The plan was to excise the devastated urethral segment and reconstruct it by augmenting the defect with buccal mucosal graft dorsally and composite buccal mucosa-gracilis flap ventrally. The procedure was planned to be performed in two stages to monitor graft survival and contracture before committing to “tubularization.”\nStage 1. After appropriate informed consent was obtained, the patient underwent a general anesthesia, administered IV Cefazolin and Gentamycin, placed in a low lithotomy position, prepped, and draped in a manner allowing access to the perineum and the left inner leg (). The suprapubic tube was removed and a suprapubic cystoscopy was performed with an attempt to pass a guide wire antegrade through the bladder neck into the urethra. The wire had preferentially passed into the urethrocutaneous fistula.\n(a) Augmented Perineal Urethrostomy. An inverted Y-incision was carried through the perineum and through the abundant scar. The fistula and the affected urethra were dissected and removed leading to a 6 cm defect (). The proximal and distal urethral stumps were spatulated both ventrally and dorsally and their lumens measured at 24 French. Two 6 × 2.5 cm buccal mucosal grafts were harvested, defatted, and fenestrated (). One graft was quilted on the corpora cavernosa and anastomosed to the spatulated urethral stumps dorsally using 4-0 polydioxanone suture. A perineal urethrostomy was matured by approximating edges of skin to the edges of neourethral plate (). A catheter was placed in the urethrostomy and a tie-over dressing applied over the graft.\n(b) Gracilis Prelamination. During the same operation, the left gracilis tendon was identified and a 6 × 2.5 cm elliptical skin defect was created just proximal to the tendon (). The exposed muscle was sutured to the skin edges as previously described by Zinman []. The second harvested buccal graft was quilted on the exposed muscle with 4-0 polydioxanone sutures and a tie-over dressing and an elastic bandage around the leg were applied for one week (). The patient had returned home on postoperative day one and was seen in the clinic at 1-2-week intervals for the graft assessments. Both the urethral catheter and the tie-over dressings were removed at one-week follow-up.\nStage 2. Eight weeks after the first stage, both grafts appeared to have taken well with no signs of a contracture or stenosis of the urethrostomy (). Again, the patient was placed in a low lithotomy position and prepped with access to the perineum and the left inner thigh. The perineal urethrostomy was freed by incising the skin just around the edges of the buccal graft (new dorsal hemi-plate) and dissecting laterally away from the graft (). Both proximal and distal urethral stumps were again calibrated with a bougie at 24 French.\nThe second incision was made around the buccal mucosa engrafted on gracilis and extended distally and proximally 3–5 cm along the axis of the muscle. The muscle was circumferentially dissected proximally and distally and its tendon transected (). The minor distal vascular pedicles to gracilis were tied and severed. To facilitate the gracilis harvest and its tunneling, another 5 cm incision was made along the course of the muscle equidistant between the perineal incision and the distal gracilis incision. The major proximal vascular pedicle located approximately 10 cm distal to the pubic ramus was preserved. The muscle-graft composite was passed through a wide tunnel into the perineal incision and the BMG edges on the flap (new ventral plate) were approximated apex-to-apex to the edges of the dorsal graft with running 4-0 polydioxanone sutures (Figures –). A 16-French silicone catheter was left in place. The gracilis muscle was sutured to corpora cavernosa as a second layer over the first suture line with a 3-0 polyglactin suture. Both the perineal and the leg incisions were closed in layers and a Jackson-Pratt drain was left in the gracilis harvest bed for one week. The patient returned home one day after the operation and was followed in the office at 1-2-week intervals. He had retrograde and antegrade imaging studies in the office at 3 weeks demonstrating a small contrast extravasation which had resolved by 5 weeks at which point his urethral catheter was removed (). The suprapubic catheter was removed 6 weeks later after a period of successful voiding with tube clamped.\nAt 8-month follow-up patient was voiding with a maximum flow of 53 cc/sec and a postvoid residual of 51 cc. He has reported no urinary incontinence and no fistulous connection to the perineum itself. He has demonstrated a relatively preserved erectile function with SHIM score decreasing from 21 preoperatively to 18 postoperatively. Through his follow-up patient reported having neither chordee nor pain with erections. As expected, he admitted diminished force of ejaculation (since before his trauma) and minimal postvoid dribbling. On the office cystoscopy at 8-month follow-up the patient demonstrated patent anastomotic sites and a patulous neourethral segment circumferentially lined with healthy appearing buccal mucosa (). The patient has reported working without limitations and has not been having any functional disability or changes in his gate.
A 73-year-old male with edentulous maxilla was referred to the University Department of Oral and Maxillofacial Surgery of the “Evaggelismοs” general hospital due to a migrated implant into the right maxillary sinus. The patient suffered from chronic obstructive pulmonary disease and therefore he had quitted smoking. Five years ago he underwent dental rehabilitation with the placement of six implants in the maxilla and four in the mandible. In less than 2 months after initial placement, all implants had failed to osseointegrate. A year and a half later the patient underwent guided bone regeneration with bovine-derived xenograft and 7 months after this point, another 10 implants were inserted into both the maxilla and mandible. Two months later, all implants had once again failed to osseointegrate. During the attempt of removal by the dentist, one of the implants was displaced into the maxillary sinus, without the dentist being able to retrieve it. The patient then visited another dentist, who could not either remove the migrated implant.\nUpon arrival to our clinic, a full medical and dental record was retrieved from the patient, and he was scheduled for surgical removal of the implant. Prior to operation, the patient underwent a radiographic examination with water’s X-ray (Fig. ), as well as CBCT examination (Fig. ) which confirmed implant migration and revealed its exact position inside the maxillary sinus.\nSurgical procedure initiated with local anesthesia by injecting xylocaine 1% andepinephrine 1:100,000 solution in the soft tissues involving the right half of the maxilla. After a crestal incision, a full-thickness mucoperiosteal flap was raised, exposing the anterior-lateral wall of the maxilla in an area extending from canine to molar region. Using a high-speed rotary instrument under sterile saline solution irrigation, a rectangular window was created in the anterior-lateral maxillary wall. The implant was detected through the bony window and captured by a mosquito forceps (Fig. ). The mucoperiosteal flap was then placed back at its initial position and was anchored with 4.0 resorbable sutures (Fig. ). Amoxicillin (1 g twice daily) was prescribed for 1 week with analgesic treatment. Sutures were removed 2 weeks after surgery. The patient was advised to follow a soft diet plan for 4 weeks and was provided with proper oral hygiene instructions. He underwent scheduled visits on a monthly basis to check the course of healing for the following 6 months.
An asymptomatic 3-year-old male was referred for murmur evaluation. Transthoracic echocardiography revealed a bicuspid aortic valve (BAV) with moderate valvar stenosis and regurgitation; the left coronary artery was difficult to visualize. Left ventricular (LV) function was normal. At age 4, he experienced exertional syncope with spontaneous return of consciousness. He was evaluated in a local emergency room and had returned to his baseline with no additional symptoms. He was observed and discharged with no additional testing and instructed to follow up with his cardiologist. Repeat echocardiogram demonstrated stable BAV function, normal biventricular function, and newly appreciated diastolic flow signals in the interventricular septum by color Doppler with continued inability to visualize the left coronary ostium (, and ). The RCA was dilated with normal origin. There were no abnormalities of the mitral valve papillary muscles. Ambulatory rhythm monitor demonstrated no arrhythmias. Cardiac magnetic resonance imaging confirmed RCA dilation with normal origin. The left coronary origin and proximal LMCA were not visualized, although the left anterior descending (LAD) and circumflex arteries were seen in their normal position. Perfusion imaging demonstrated an endocardial perfusion defect in the distribution of the LMCA with no late gadolinium enhancement, consistent with hibernating myocardium (). Cardiac catheterization was performed with angiography, demonstrating atresia of the left coronary ostia and long-segment LMCA atresia with retrograde filling of the LAD and circumflex through collaterals from a dilated RCA (, and ). Hemodynamics demonstrated mild aortic valve stenosis (peak gradient, 15 mm Hg), mild LV diastolic dysfunction (LV end-diastolic pressure, 14 mm Hg), and a normal cardiac index of 3.74 L/min/m2.\nHe was referred for surgical coronary revascularization in combination with a Ross-Konno procedure to provide aortic valve competence to prevent coronary hypoperfusion related to aortic regurgitation. Intraoperatively, LMCA atresia was confirmed, which extended beyond the bifurcation of the LAD and circumflex. Given the discontinuity of the circumflex and LAD with a comparably small circumflex artery, a left internal mammary artery (LIMA) to LAD bypass graft was performed.\nThe postoperative course was uneventful without arrhythmias. Postoperative catheterization demonstrated a patent LIMA supplying the LAD (, ). Metoprolol was started for cardioprotection and aspirin for antiplatelet effect. He remains without arrhythmias or syncopal episodes and with good activity tolerance on outpatient follow-up. Computed tomography imaging performed 6 months postoperatively demonstrated continued LIMA graft patency ().
A young male patient aged 17 years reported with the complaint of broken upper front tooth as a consequence of sports injury 1-h back. He was carrying the fractured fragment with him in dehydrated condition. On thorough clinical examination, an oblique fracture of maxillary right central incisor with pulp exposure was noticed []. A diagnosis of Ellis class III fracture (fracture exposing enamel, dentin, and pulp) was made. Radiographic imaging suggested oblique fracture of the tooth with fracture line uncovering the pulp with normal periapical status. A multitude of treatment alternatives were considered: Simple reattachment procedure using dual cure composites; vital pulp therapy using mineral trioxide aggregate (MTA), followed by fractured fragment reattachment using fiber reinforced composites; endodontic treatment, followed by post and core and extraction as the last resort.\nAll the viable treatment alternatives were explained in depth to the patient and his legal guardians. Considering the young age of the patient and his desire to maintain his natural tooth structure, he and his guardians chose fractured fragment reattachment. As there was minute pulp exposure following trauma, Simple reattachment procedure using dual cure composites would not have offered predictable success. Hence, instead of a simple reattachment, vital pulp therapy using MTA, followed by fractured fragment reattachment, functionally strengthened by fiber reinforced composites was planned.\nThe fractured fragment was cleaned, verified for its fit on the fractured tooth and stored in normal physiologic saline to prevent further dehydration.\nInformed consent was taken by the patient and the legal guardians and the fractured site was debrided using normal saline, followed by irrigation with 0.5% sodium hypochlorite solution for disinfection of exposed pulp tissue. A cavity was prepared in to the tooth using a round diamond point (Mani, Japan) and direct pulp capping was performed by placing 1-1.5 mm of freshly mixed MTA Plus (Prevest DenPro Limited, India) directly over the pulp. Following this, a flap was raised and apical extent of fracture site exposed to allow optimal bonding in subgingival area []. Hemostasis was achieved using a 20% ferric sulfate solution in the form of ViscoStat (Ultradent, USA) and Gelfoam (Pfizer, Newyork, USA). The fragment and the tooth were etched using Scotchbond Universal Etchant (3M ESPE, SP, Brazil) and bonding agent (Fusion Bond DC, Prevest DenPro, India) applied and cured. This was followed by cementation of fractured fragment to the retained tooth structure using ultra DC dual cure cement (Prevest DenPro, India) and cured. A Coe Pak Automix NDS (GC America Inc., Alsip, IL, USA) was formed into a rope and packed at the surgical site and the patient was recalled after 1-week for further treatment []. At recall visit after 1-week, patient was clinically reevaluated for pulpal and periodontal health and was found asymptomatic. To ensure the complete and effective reattachment of the fragment, a vertical groove of depth 2 mm was created using Tapered Fissure bur (Mani, Japan) on the palatal aspect, half on the reattached fragment and half on the tooth structure. A 2 mm segment of Ribbond (Ribbond Inc., Seattle, WA, USA) was approximated into the groove. The groove was then etched and Ribbond bonded and cured using ultra DC dual cure cement (Prevest DenPro, India) [].\nExcess cement was then removed using bard parker blade and cured. The restoration was kept slightly overcontoured. Finishing and polishing using Soflex contouring and polishing discs (3M ESPE, USA) was done to simulate the natural appearance of a tooth. The fracture line was indiscernible, and the patient was satisfied with the esthetic outcome of the procedure []. Occlusion was checked under all positions and patient was cautioned to avoid excessive biting forces on reattached tooth. A custom made mouth guard was delivered to the patient to prevent further dental injury. A 6 months follow-up period revealed positive tooth vitality on cold testing using ethyl Chloride Spray (Endo Ice, Coltene Whaledent, USA). Clinically, the restoration was intact and esthetically and functionally acceptable. Follow-up radiographs were normal without any evidence of periapical pathology [].
A 30-year-old lactating female presented to the breast surgery clinic with a complaint of left breast heaviness and gradual enlargement since one year. Physical examination revealed gross asymmetric left breast enlargement with an ill-defined palpable lump measuring approximately 12 x 4.6 cm. There was overlying skin thickening with induration, although no redness and a palpable left axillary lymph node. As the patient was lactating, she initially underwent bilateral breast ultrasound, which showed a large circumscribed mass, wider than tall without any posterior acoustic shadowing predominantly in upper outer quadrant of the left breast with few intralesional cystic spaces showing mild vascularity on color Doppler and an abnormal left axillary lymph node (Figure ).\nThe short axis of the lymph node measured 12 mm and the cortical thickness 8 mm with compressed fatty hilum. A breast imaging-reporting and data system (BI-RADS) category 4 assessment was given, and biopsy of the lesion and the axillary lymph node was recommended.\nThe patient was electively admitted for ultrasound-guided core biopsy, blood workup, CT chest, abdomen and pelvis scan, and bone scintigraphy for metastatic disease. Contrast-enhanced CT of the chest, abdomen and pelvis showed edematous left breast parenchyma with a large well-defined solid enhancing lesion associated with overlying skin thickening (Figure ).\nMultiple enlarged left axillary lymph nodes were also noted associated with perinodal fuzziness. There was no visceral metastasis on CT scan. Whole-body skeletal scintigraphy was also negative for bony metastasis. On histopathology, the core specimen from left breast lesion revealed benign breast tissue exhibiting adenosis, stromal sclerosis and pseudovascular proliferation of mammary stroma delineated by endothelial cells without atypia, features representing PASH (Figure ).\nThere was no evidence of ductal carcinoma in situ (DCIS) or malignancy. Core specimen from the left axillary lymph node showed benign lymphoid tissue exhibiting sinus histiocytosis and acute on chronic inflammation.\nThe patient received lactation suppression drug (bromocriptine) and anti-hormonal therapy comprising tamoxifen, and she showed significant clinical improvement.
A 58-year-old Caucasian male with past medical history of hypertension, hypertriglyceridemia, chronic atrial fibrillation, coronary artery disease (CAD) s/p coronary artery bypass graft (CABG), ischemic cardiomyopathy and past surgical history of pacemaker/defibrillator placement presented to our institution with complaint of shortness of breath for about a week prior to admission. In the emergency room, the patient was noted to be febrile. His heart rate and blood pressure, however, were acceptable. On the chest X-ray, he was noted to have bilateral infiltrates. He was hypoxemic on room air. Lab reports were notable for thrombocytopenia and leukopenia as well as marked elevation of his liver transaminases and an elevated CPK level. Values are trended in . The patient was started on non-invasive ventilation with BiPAP. The initial presumed diagnosis was diffuse bacterial pneumonia. He was started on broad spectrum antibiotic therapy.\nThe patient's respiratory status continued to deteriorate and he was intubated. Throughout the course of hospitalization, spontaneous breathing and pupillary responses were intact; however, his gag and cough reflexes were absent. The patient was started on broad spectrum antibiotics. He developed acute renal failure early during hospitalization and hemodialysis was started. He later developed hypotension requiring the use of pressor medications. The patient remained thrombocytopenic and although he had no evidence of bleeding, platelets were transfused. He subsequently developed gastrointestinal bleeding secondary to stress ulceration as well as prior use of anti-platelet drugs and thrombocytopenia. The patient received multiple units of packed cells. Ferritin level was markedly elevated at over 12,000 and viral-associated hemophagocytic syndrome was suspected. Bone marrow biopsy was performed, which showed mildly hypocellular bone marrow showing mild increase in histiocytes with hemophagocytosis.\nThe patient's condition continued to deteriorate. In the second week, the patient developed massive hemoptysis as well as bleeding from IV sites suggestive of disseminated intravascular coagulation (DIC). Cardiac arrest soon followed. Cardiopulmonary resuscitation efforts were unsuccessful. The patient soon after expired.
A 52-year-old man sustained a gunshot wound to the left upper quadrant of the abdomen. He had peritonitis and was taken for emergent exploratory laparotomy. He was found to have injuries to the small bowel, transverse colon, and the right colon. He underwent small bowel resection and extended right colectomy without anastomoses, and he was packed open with a temporary abdominal closure. He was taken back to the operating room 2 days later, the packs were removed, and two anastomoses were performed. His abdominal wall was closed at this time.\nOn postoperative day 10, the patient eviscerated. Closure of the fascia was not possible, and he underwent split-thickness skin grafting to his abdominal wall on postoperative day 14. The soft tissue defect measured 24 cm × 10 cm at that time. His hospital course was further complicated by a low-output enterocutaneous fistula, and this never closed.\nThe patient was then lost to follow-up until he was admitted with acute cholecystitis 9 months later. At that time, the fistula was still present, but the output was only a few cubic centimeters per day, and contamination was minimal. Ultrasound showed gallstones with mild gall bladder wall thickening and pericholecystic fluid, consistent with acute cholecystitis. Along with demonstrating the enterocutaneous fistula, CT scan showed a wide abdominal wall defect, with the rectus muscles separated by about 12 cm (). The patient was thus scheduled for cholecystectomy, reversal of the enterocutaneous fistula, and reconstruction of the abdominal wall.\nAt operation, the skin graft was first removed from the underlying viscera. This was not difficult. Extensive adhesiolysis was then performed. Cholecystectomy followed this, and the gall bladder was found to be chronically inflamed. Next, resection of the ileocolonic anastomosis was performed, as the fistula was found to originate from the old ileocolonic staple line. A stapled ileocolonic reanastomosis was fashioned. A retrorectus dissection along with release of the transversus abdominis muscle was performed. A 28 cm × 15 cm piece of polypropylene mesh was cut to shape and placed as a sublay into the retrorectus/preperitoneal space.\nThe patient had no in-hospital complications and was discharged on postoperative day 8. He was later readmitted on postoperative day 20 with an early postoperative small bowel obstruction along with a 3 cm × 18 cm × 18 cm seroma in the retrorectus space. Both resolved spontaneously. A CT scan which was performed at that time showed that the hernia had been repaired and demonstrated apposition of the rectus muscles in the midline (). He was last seen 2 months postoperatively and was feeling well, tolerating a diet, had no pain and no evidence of infection, and was able to do a sit-up in the office without evidence of recurrent hernia.
A 77-year-old Caucasian gentleman was admitted with acute kidney injury discovered on blood tests. He was known to have high-grade prostate intraepithelial neoplasia and atypical small acinar proliferation from prostate biopsies performed for a raised prostate-specific antigen (PSA), with a bone scan negative for potential metastases and was on PSA surveillance with the latest reading of 43 pre-admission. Prior to admission, he had lower urinary tract symptoms in the form of frequency, nocturia, intermittent urinary stream, terminal dribbling and a feeling of incomplete emptying. There was no significant past medical history. On examination, he was haemodynamically stable and afebrile. There was a palpable non-tender bladder with dullness to percussion and no renal angle tenderness.\nBlood tests revealed a Stage 3 acute kidney injury (baseline renal function was normal) with raised inflammatory markers and elevated PSA compared with baseline (Table ). A mid-stream urine specimen sent for microscopy, cultures and sensitivities yielded no growth of organisms. A bedside bladder scan revealed a bladder volume of >999 ml, necessitating the insertion of a urethral catheter with a residual volume of 2.4 l, and intravenous antibiotics were commenced. An ultrasound scan (USS) of the urinary tract was performed to evaluate for the presence of hydronephrosis; but while this demonstrated a minor dilatation of the left renal pelvis, it also found a shallow fluid collection around the left kidney extending into the left lateral retroperitoneum, separate from the left psoas muscle (Fig. ). In the urinary bladder, there was an irregular 4 cm mass on the left posterolateral aspect. In view of the findings, an urgent flexible cystoscopy was performed, revealing a massive median lobe of the prostate protruding up and back into the bladder; the ureteric orifices were not visualized because of this, and the bladder mucosa was normal. The patient subsequently underwent a computed tomography (CT) urogram, which showed bilateral fullness in the pelvicalyceal systems and confirmed a 4.8 × 4.4 × 2.8 cm fluid collection adjacent to the lower pole of the left kidney as detected on the USS, with perinephric stranding. The fluid collection was demonstrated to be extravasated urine on the delayed post-contrast images arising from a defect in the left proximal ureter, and extending down the left paracolic gutter (Figs and ). The massive prostate was also demonstrable (Fig. ).\nManagement options were discussed with the patient in the form of conservative treatment with antibiotics and catheterization, or insertion of a nephrostomy as retrograde ureteral stenting would have not been possible due to prostatic size. He opted for the conservative approach which was successful with resolution of renal function and inflammatory markers to normal parameters. He was offered a Millins' prostatectomy but declined and was happy to be managed with a long-term catheter and repeat PSA measurement in 3 months' time.
A 71-year-old woman with performance status 2 had right chest and left lumbar pain and was referred to our hospital for treatment. The computed tomography (CT) findings in the previous hospital showed some recurrent masses and metastatic tumors: 144 × 137 × 120 mm3 mass in the left abdomen to the pelvic cavity, a 50 × 43 mm2 mass on the right pelvic wall, a 52 × 47 mm2 mass on the ascending colon, and small metastatic masses on the diaphragm and bilateral lungs (). Serum carbohydrate antigen (CA)19-9 and CA125 levels were 3128 and 96.1 ng/mL, respectively. She had a previous history of 4 years’ treatment with paclitaxel and carboplatin, docetaxel and carboplatin, doxorubicin and cisplatin, medroxyprogesterone acetate, and paclitaxel-alone chemotherapies, as well as immunotherapy for the present recurrent tumors found 5 years after standard surgery for endometrioid adenocarcinoma G1 (Stage IB). Although she and her husband were informed by the former doctor and by us that palliative care would be appropriate, they desired another anti-cancer therapy. They were therefore told about daily oral administration of half-dose etoposide (25 mg/day) that had been reported in the 1990s in Japan. They provided written, informed consent to its administration, and the therapy was then started. Treatment for 4 months reduced serum tumor marker levels and relieved her pain; however, the therapy was discontinued at the end of the fourth month at her request because of mild to moderate stomachache, and serum tumor marker levels increased again. Therefore, the same treatment was quickly restarted. Serum CA19-9 and CA125 levels decreased dramatically to around 110 ng/mL and the normal range, respectively (), and CT showed shrinkage of the recurrent tumors (). She became cheerful with a good appetite and bowel habit, with slight lumbar pain. However, the tumor marker levels gradually increased in the 22nd month of treatment, and she again complained of lumbar pain. The CT findings indicated tumor growth (). Her recurrent tumor had become refractory again. They asked for another chemotherapy regimen, and weekly paclitaxel and carboplatin chemotherapy was tried. However, it was ineffective. She developed genital bleeding, her serum tumor marker levels further increased, and she died suddenly from pulmonary embolism.
A 38-year-old white male who is an avid skier presented with left calf pain described as sharp on the medial aspect that started after he fell while skiing about two weeks prior. During the fall, his left ankle was forced into extreme dorsiflexion. He had immediate onset of severe pain and had to stop skiing that day. He noticed swelling in the medial calf along with bruising of the area over the next few days. After about a week, he was able to ski again but had pain aggravated by active plantar flexion.\nOn physical examination of his left leg, his knee and ankle both appeared normal and had normal strength and range of motion with no tenderness. Sensation and pulses were normal. There was tenderness over the medial head of his gastrocnemius with a palpable, firm, four-centimeter ovoid mass. Pain was elicited during resisted plantar flexion. His right leg was completely normal.\nRadiographs of the lower leg obtained in the ED were normal. A POCUS was then performed in the ED with specific focus over the mass in the medial head of the gastrocnemius, revealing a swollen, heterogeneous, disorganized mass in the medial head of the gastrocnemius, as demonstrated in –. Comparison views to the unaffected extremity, as seen in , further clarified the findings. We made a diagnosis of muscle tear in the medial head of the gastrocnemius.\nThe patient was instructed on exercises for strengthening and range of motion of the calf and ankle and specifically eccentric exercises that he should complete after an initial rest period of two weeks. On follow-up two months after the initial visit, his symptoms had nearly completely resolved. He reported mountain biking several times per week with only minimal pain after a long ride. The mass in the calf resolved, and he relayed no concerns about his leg for the upcoming ski season.
A 24-year-old Hispanic female with diabetes mellitus type 1, anemia, hypertension, chronic pancreatitis with partial pancreatectomy, cholecystectomy, and splenectomy presented to the emergency department (ED) with abdominal pain not relieved by oral pain medications. She recalled her home medications to be mirtazapine 30 mg orally nightly, fluoxetine unknown dose orally three times a day, carbamazepine 200 mg orally twice daily, insulin glargine 15–20 units subcutaneously nightly, morphine sulfate 30 mg orally twice daily, tramadol 50 mg orally four times a day, hydromorphone 4 mg orally six times a day as needed for pain, and hydrocodone/acetaminophen 325/10 mg orally six times a day as needed for pain, and she had been taking them to relieve her pain. She was discharged from the ED but returned on the same day with worsening abdominal pain, loss of sensation in lower extremities, lips, and hands, and ascending paralysis. The patient was noted to have a leukocytosis with bandemia, fever, and tachycardia suspicious for sepsis. Computed tomography (CT) of the abdomen was significant for small bowel edema and ascites. The patient continued to deteriorate with worsening ascending paralysis, bilateral hearing loss, hypotension, and respiratory failure with subsequent endotracheal intubation. She underwent two rounds of cardiopulmonary resuscitation (CPR) for a total of approximately 109 minutes but ultimately expired.\nAn autopsy was performed and documented a well-developed woman with no evidence of traumatic injuries. Postmortem serum analysis revealed fatal levels of heart blood fluoxetine concentration of 2.3 mcg/mL.\nThe cause of death was thought to be multiple medication intoxication with fatal levels of fluoxetine. A neuropathologist was consulted who agreed with the diagnosis and thought that her symptoms were primarily due to overmedication with fluoxetine. She had no known history of suicidal ideation or attempt but did have chronic pain. Thus, the favored mode of death was accident. Contributory factors to death included acute on chronic, culture negative pancreatitis with abscess formation, and likely sepsis.
A 50-year-old previously well Sri Lankan woman presented to a local hospital following a bite on her right foot by a snake. The snake was killed and brought to the hospital by members of her family and was confirmed as a hump-nosed viper by the attending doctors. Species identification was not performed. She only had features of local envenoming including pain, local swelling, and blistering. She did not have any bleeding manifestations, maintained good urine output, and there were no neurological deficits. Her full blood count, serum creatinine, and 20-minute whole blood clotting test were normal on the first day. She was given paracetamol, orally administered antibiotics, and observed in the local hospital and was discharged on the second day of admission.\nFive days after the snakebite she was readmitted to the local hospital due to worsening swelling and pain of her right foot and leg. She was afebrile on admission and did not complain of any reduction in urine output or bleeding manifestation. However, by the next day her urine output was found to be low and she was transferred to the National Hospital of Sri Lanka (NHSL) for further management. On admission to NHSL she was fully conscious and only complained of pain and swelling of right lower limb, reduced urine output, and mild shortness of breath at rest. She was pale, not icteric and there was generalized edema. There was right lower limb cellulitis with hemorrhagic blisters. There was bruising on puncture sites. She was dyspneic with a respiratory rate of 24 breaths/minute; her heart rate was 100 beats/minute and blood pressure was 120/80 mmHg. Oxygen saturation on air was 96%. Her jugular venous pressure was raised. A precordial examination was normal. A respiratory examination revealed bibasal crackles suggestive of pulmonary edema. An abdominal examination was normal. She had a urethral catheter with no urine.\nLaboratory investigations on admission revealed a hemoglobin of 7 g/dl, mean corpuscular volume of (MCV) 82.6 fl, and red cell count of 2.36 × 1012/l. Her white cell count (WCC) was 10.96 × 109/l with 75% neutrophils and 17% lymphocytes. Her platelet count was 92 × 109/l. Her blood picture revealed fragmented red cells suggestive of microangiopathic hemolytic anemia (MAHA) and toxic neutrophils suggestive of bacterial infection. Her serum lactate dehydrogenase (LDH) level was 2300 U/L. Her prothrombin time was 12.6 seconds and activated partial thromboplastin time (APTT) was 24 seconds. Serum creatinine was 888 μmol/l, while potassium was 7 mmol/l and sodium was 126 mmol/l. Venous blood gas revealed a pH of 7.29 with bicarbonate of 11 mmol/l. A clinical diagnosis of a hump-nosed viper bite leading to cellulitis, acute kidney injury, and TMA was made. Her ECG on admission was normal.\nShe was started on intravenously administered meropenem and metronidazole and urgent hemodialysis was arranged via a femoral catheter. In the absence of evidence for the benefit of therapeutic plasma exchange or fresh frozen plasma in MAHA following hump-nosed viper bites it was decided to manage her without these therapeutic modalities. She underwent regular hemodialysis with adequate ultrafiltration on the sixth, seventh and ninth days after the snakebite. She remained anuric throughout. Her thrombocytopenia improved within the next 2 days with her platelet count rising to 160 × 109/l and some fragmented red cells remained in the blood picture. She was given two packs of red cell concentrates over the next 2 days.\nOn day 10 she developed acute onset shortness of breath and retrosternal chest pain with bibasal crackles on lung auscultation despite adequate ultrafiltration the previous night and adherence to a strict fluid restriction. Her oxygen saturation on air was 89% and improved to 97% with 5% oxygen via facemask. An ECG showed T wave inversion in V3 to V6 and aVL leads (Fig. ). Serum troponin I titer was 0.433 ng/ml (normal < 0.03) 12 hours after the onset of chest pain. A diagnosis of non-ST elevation myocardial infarction was made. At that time her hemoglobin was 8 g/dl, platelet count was 205 × 109/l, and serum LDH was 2100 U/l (Fig. ). Her serum electrolytes were within normal range. She was started on subcutaneous enoxaparin 60 mg/day, aspirin 75 mg/day, clopidogrel 75 mg/day, and atorvastatin 20 mg/day. Any existing coagulopathy was excluded by thromboelastography before initiating the antiplatelet drugs and anticoagulation. She was given a few more packed cell transfusions during hemodialysis. An echocardiogram done 3 days later revealed anterior and lateral wall hypokinesia in the left ventricle and her ejection fraction was at 45 to 50%.\nOn day 15 she developed an upper gastrointestinal bleed confirmed by an esophagogastroduodenoscopy. Antiplatelet drugs and anticoagulation were withheld and she was transfused with blood.\nOn day 18 she developed worsening shortness of breath associated with reduced oxygen saturation and fever. A repeat ECG did not show any new changes. A chest radiograph revealed bilateral diffuse opacification (Fig. ) which persisted even after adequate ultrafiltration. A presumptive diagnosis of hospital-acquired bronchopneumonia was made and her antibiotics were changed to piperacillin-tazobactam and teicoplanin. Subsequently she developed respiratory failure and was intubated and transferred to our Medical Intensive Care Unit (MICU) for ventilator support. Bronchoscopy revealed absence of pulmonary hemorrhage and both bronchoalveolar lavage fluid and tracheal aspirate grew coliforms resistant to all available antibiotics in the hospital setting and sensitive only to colistin which was not available. Her stay in MICU was further complicated with a deep vein thrombosis involving her right ileofemoral vein which was treated with unfractionated heparin while maintaining APTT within the therapeutic range. She progressively deteriorated and developed a cardiac arrest and died on day 33 of the snakebite (Table ).
A 51-year-old woman presented with a massive painless lump on both of her thighs that had been enlarging for the past 6 months. The patient denied any history of trauma, manipulation, or injection around the lump before. She was otherwise healthy despite her lumps. However, she had a history of lymph node tuberculosis on her neck about 25 years before and underwent tuberculosis chemotherapy regiment for about six months.\nOn the local physical examination, we found a painless non-mobile distention on her gluteal and upper femoral region bilaterally with some fluctuation and cystic consistency on palpation of the mass. The initial largest diameter of her thigh was 60 cm on the left and 45 cm on the right. There was no signs of inflammation, sinus or fistula around her thighs and buttock, or any remarkable signs on physical examinations (). Laboratory examinations however, showed elevated level of ESR and CRP. Mantoux test were inconclusive due to previous infection of tuberculosis. Radiological examination showed no signs of abnormality besides the expanding soft tissue shadow especially on her left femur region.\nMRI examinations were then performed over the lumbosacral and pelvis region. Sagittal T2 weighted MR images of the sacrum showed destruction on anterior lower sacral segments, with hyperintense anterior lesion and presacral abscess. Axial T2 weighted images confirmed sacral body destruction and extension of the hyperintense lesion that involved the insertion of piriformis muscle (a and b).\nPelvic axial fat-suppressed (FS) T2 weighted images gave another extended view of the lesion, showing lateral extension of the lesion over the posterior ilium that also extended to superior and inferior filling the gluteal compartment beneath the gluteus maximus and tensor fascia lata (c). Involvement of the piriformis muscle and gluteus medius were confirmed at the coronal FS-T2 images of proximal femur, in which there was a hyperintese bony lesion at the tip of greater trochanter.\nThe abscess also extended distally through the space around the greater trochanter between the vastus lateralis and tensor fascia lata without any intracapsular involvement of the hip joint (a). Distal extension of the abscess reached the level of midshaft femur beneath the hamstring and tensor fascia lata muscle (c).\nDue to the previous history of tuberculosis and the endemic nature of the disease, we started anti-tuberculosis treatment (ATT) initially for about 2 weeks. Serial laboratory examination of ESR and CRP showed remarkable decrease, which substantiates our working diagnosis. Surgical debridement and biopsy was performed. A curved incision centered on the left greater trochanter was used since it was the convergence point of the abscess on MRI images (b). Superficial dissection of posterior approach of the hip were used and after dissecting the gluteus maximus muscle, sero-purulent liquid discharged from the plane. Further debridement was performed and about 2.7 liters of pus were evacuated. There was intact muscular structure around the greater trochanter as well as the short external rotator thus the debridement were not extended to the hip joint (). An additional debridement through posterior midline incision through the multifidus muscle around the sacral region were also performed but turned out negative. During the wound closure, a submuscular drain was put and minimal production was found during the first two days. The patient was discharged and started her antituberculosis drug regime due to high suspicion of tuberculosis.\nOn the two weeks follow up, the surgical wound healed without any complication and there were no signs of recurrent fluid collection. Despite negative result on the culture result, the histopathological examination showed a necrotic tissue with appearance of epitheloid cells, lymphocytes, histiocytes, and Langhans multinucleated giant cells which was in accordance with chronic inflammation due to tuberculosis. Neither recurrence nor complication was found after 6 months follow up.
A 45-year-old male reported with seizure. The patient's neurologic examination was normal. However, brain magnetic resonance imaging (MRI) showed findings suggestive of eDAVF, with a large nidus located near the left gyrus rectus (). Digital subtraction angiography showed a DAVF, arterialized by the left anterior and posterior ethmoidal arteries, by anastomosis of the right ophthalmic artery, and by both the left and right external carotid arteries. The DAVF was drained by a large vein originating from the cribriform plate, which drained into the cortical draining veins and then into the superior sagittal sinus (). MRI also showed that the large, ectatic left frontal cortical vein (19 mm × 15 mm) was being compressed, thus causing brain edema of the corresponding area (). Surgical management was chosen instead of an endovascular approach. The patient was placed in a supine position with a lumbar drain and the head was laid straight but slightly elevated. A bicoronal incision was made, revealing the periosteum. The skin flap was wrapped with gauze and then retracted as much as possible in order to reveal the supraorbital notch. A neuronavigation system was used to confirm and outline the location of the frontal sinus, and a 3.6 cm × 2.7 cm craniotomy was then performed over the marked frontal sinus ().\nOpening of the dura, after removal of the frontal sinus, revealed a small feeding artery flowing from both ophthalmic arteries. The main arterialized vein was connected to the dura near the cribriform plate of the ethmoid bone. This portion of the dura was cauterized along with all of the main arterialized veins, as revealed in the surgical field.\nBrain retraction was restricted in order to avoid frontal lobe injury. The craniotomy was closed with the patient's original sinus wall and Poly-bone cement. Post-operative CT scan showed no abnormalities, and the postoperative angiography showed clearance of the fistula ().\nImmediately after the operation, severe visual disturbances were detected in both eyes, with a central blind spot in the left visual field. Fluorescein angiography showed a slight filling delay in the choroidal arteries without apparent vascular occlusions or ischemic disease. The patient's vision in the right eye was completely restored to preoperative status but a thick central scotoma remained in the left eye.
An 83 year-old man presented with a pain in the right knee of 8 in VAS (visual analogue scale). The symptoms were worsening over the last few years. He had a history of arterial hypertension, glaucoma and cataract. Forty years ago he had right femur fracture, and underwent surgical intervention. Plate and screws after osteosynthesis were not removed, and no documentation on the details of the intervention were available. He also underwent prostatectomy, appendectomy and hemorrhoidectomy in the past. The patient signed an informed consent for publishing his case.\nOn admission the patient was stable, BP 125/85 mmHg, HR 72/min. Initial laboratory results were within normal values. Pre-procedurally the patient was administered ananticoagulant according to local standards (enoxaparin, 40 mg) and a prophylactic dose of antibiotic (cefazoline) along with his regular drug regime. Based on the radiological features of right lower limb joints the patient was qualified for total knee arthroplasty with a cemented knee prosthesis - NexGen (LPS-Flex) implant (Fig. ).\nDue to long time interval between past surgery and current intervention and concomitant diseases, the patient was not found eligible for hardware removal. Extensive surgery including simultaneous hardware removal and TKA could put the patient at unacceptably high risk of complications (such as infection, perioperative fracture, and significant blood loss), because of his advanced age and comorbidities (Fig. ).\nPlacement of femoral guide intramedullary (which is preferred by most surgeons because, as it makes fitting of the prosthetic material easier, because the rod goes along anatomical axis of the limb) was not possible due to the presence of retained hardware. Its presence would not allow passage of intramedullary rod. Therefore, a decision to use an extramedullary guide was made preoperatively. Correct insertion of extramedullary guide is found challenging, because visual assessment of reference points used to determine the correct positioning is difficult intraoperatively. However, because confirmation of guide’s correct position is vital in order to achieve a good long-term outcome, ultrasound was chosen to inspect its position along the mechanical axis, being an accessible, inexpensive and a non-invasive imaging modality that could be performed intraoperatively by a trained member of the surgical team.\nSeveral other imaging methods were considered. Fluoroscopy was not found to be optimal, because it requires a specific position of the limb (flexion in the hip and knee joint (of 90 degrees). It is also linked with an exposure to radiation, which forms its disadvantage in comparison with ultrasound. Using a patient specific instrument (PSI) was also not applicable to this case. It imposes performing an MRI of the limb, which was contraindicated. There was no available documentation of the previous surgery, therefore the metal alloy of the retained hardware was unknown.\nTKA was performed in supine position. The right knee joint was approached with anterior incision. Numerous degenerative changes were present in both medial and lateral compartment, dominating in the medial compartment. Anterior compartment presented normally. Hardware retained after previous intervention, in the form of screws and an ostheosyntesis plate were present. After examining local conditions, a femoral guide was introduced extramedullary. Ultrasonography was used to pinpoint the center of the femur’s head. Distal cut in femur was performed. Tibial guide was than introduced intramedullary followed by a standard cut of the proximal part. The initial fit of implants was assessed. The patella’s osteophytes were removed. It was followed by ZIMMER NEXGEN prosthesis embedment on cement (vacuum mixed). Size of the tibial part was 5, femoral part F and polyethylene insertion – 9 mm. Layered closure was applied with the introduction of ATS reciprocal drainageto reduce oedema at the surgical site.\nOn the 2nd day after surgery the drainage was removed (it collected 200 ml of bloody excretion, which was within normal volumes expected after TKA). The postoperative period was uneventful. The correct position of the implants along the mechanical axis was confirmed on X-ray. On the 4th postoperative day the patient was able to walk using crutches and he was discharged from the hospital and he was advised to continue rehabilitation, use of analgesics (paracetamol 3x500mg, dexketoprofen 2x25mg taken as needed) and anticoagulant (enoxaparin 40 mg) administered daily in the first 6 weeks after discharge.\nAt a follow-up visit 6 months after surgery the patient was generally satisfied with the results of TKA, The patient recovered full range of motion (in comparison with the contralateral side). Pain decreased significantly to 1–2 in VAS (before surgery – up to 8 in VAS). On physical examination knee joint had normal appearance, with no signs of edema (Fig. ).
A previously healthy 51-year-old man was admitted to our critical care unit after a bicycle accident. On arrival, the patient was hemodynamically stable but sedated and on mechanical ventilation.\nBefore intubation, at the scene, he had flaccid paralysis of both legs and left arm, with minimal movements of the right arm.\nCT demonstrated bilateral small pneumothoraxes, bilateral pulmonary contusions, and dislocated fractures of the vertebral spine at C4-C5.\nAn MRI demonstrated a significant narrowing of the cervical spinal canal with myelomalacia signs, edema, and hemorrhagic contusion at the level of C3–C6. The spinal cord was also compressed at the level of D5 due to vertebral fractures at D7.\nAn emergency cervical discectomy of C4-5 followed by fusion of D2-3 and D6–8 was performed and the patient was transferred to the ICU.\nDuring his ICU stay the patient developed several events of extreme bradycardia which occasionally deteriorated to asystole.\nSome of these events resolved spontaneously within a few seconds, while some events required pharmacological treatment or CPR.\nInitially, these events were attributed to neurological disturbances which have been well described in high spinal cord injuries [] and it was hoped that they will either resolve with time or if not, a pacemaker will be required.\nAfter a few weeks of observation the nursing staff reported that these events always occurred when the patient was in the left lateral decubitus position. This observation suggested an anatomical problem.\nA second CT scan demonstrated that one of the screws used in the process of ORIF at the level of C5 abutted on the esophagus and was compressing the vagus nerve when the patient was in the left lateral decubitus position ().\nFollowing these findings, the patient was taken to the operating theater and the offending screw was repositioned. The postoperative course was uneventful: soon after surgery, the temporary pacemaker placed before the operation was removed and the patient was transferred to a rehabilitation ward. Over three years of follow-up no episodes of dysrhythmia occurred.
A 19-year-old female presented with facial asymmetry and canting of an occlusal plane due to right-sided condylar hyperplasia that starts developing at her puberty. Preoperative workup included a detailed clinical examination, photography, dental impressions, and cephalometric analysis (Figure ).\nThe MMS started with the face bow registration and transfer followed by upper dental cast mounting on the adjustable platform of the surgical articulator MT, reflecting the orientation of the patient's maxilla in the 3D space of the articulator. The lower cast then mounted according to the registered patient's occlusion in the centric relation (Figure ).\nThe planned correction of the maxillary cant was carried out by rotation of the upper dental cast around the coronal plane, through increasing the posterior height of the upper frame on the right side to the planned extent, while maintaining the anterior height at the incisal pin. That was performed by rotating the height adjustment pulley that controls the extrusion of a side rod with a millimeter scale. Fabrication of surgical wafer then followed. Upon occlusal plane correction, a shift in the upper midline created toward the right side and subsequently addressed by transverse relocation of the upper cast on the adjustable platform toward the planned position to coincide with the marked facial midline (Figure ).\nThe magnitude of the planned correction in the vertical direction was determined by measuring the change in the distance between the buccal cusps of the upper and lower first molars before and after the height adjustment of the upper frame.\nAt surgery, Lefort I osteotomy was performed first to seat the maxilla in the planned position guided by the surgical wafer (Figure ), followed by bilateral sagittal split osteotomy (BSSO) of the mandible which followed the maxilla.\nThe postoperative view (Figure ) demonstrates the improvement of facial appearance and correction of both facial asymmetry and the cant of the occlusal plane.
A 67-year-old woman was referred from primary care to gynaecology outpatients’ due to post-menopausal bleeding and a clinically suspicious cervix. The patient reported no history of post-coital bleeding or abdominal pain and had a normal smear history. She had two normal vaginal deliveries and had received hormone-replacement therapy following her menopause for a brief time period. There was no significant past medical or family history.\nOn clinical examination, a 2 cm friable mass that bled on contact was found protruding through the uterine cervix. Cervical punch biopsies and an endometrial sampling biopsy were taken. Imaging investigations of the uterine cervix were arranged and the case was referred to the local tumour board for further management.\nThe cervical punch biopsies showed flat sheets of an epithelioid tumour with minimal pleomorphism, cytoplasmic pigmentation and a low mitotic index (<1/50 high power fields). Immunohistochemistry showed that the tumour was strongly positive for HMB-45, weakly positive for Melan-A, and negative for S100. The differential diagnosis of the cervical punch biopsies based on the cytological and immunohistochemical characteristics was between primary or secondary cervical melanoma and cervical PEComa. However, the low degree of pleomorphism and the low mitotic count favoured PEComa over melanoma (Fig. ). The endometrial tissue specimen was negative for any endometrial pathology.\nOn ultrasound scanning of the cervix, a 3.4 × 2.1 cm2 hypoechoic mass was noted in the proximal endocervical region with some internal colour flow Doppler signals. The MRI imaging of the pelvis showed a 3 cm endocervical mass with an intermediate signal intensity. PET-CT scan imaging of the pelvis demonstrated a 4.5 × 2.5 cm2 soft tissue mass located at the centre of the uterine cervix with a marked uptake (max SUV 14.8) indicative of a malignant tumour. The mass was in close proximity to the posterior wall of the bladder but there was no definite direct invasion. No evidence of metastatic disease or abnormal lymph nodes was shown (Fig. ).\nThe patient underwent radical hysterectomy with bilateral salpingo-oophorectomy and pelvic lymphadenectomy. Histopathology showed a residual benign PEComa and a moderately differentiated MNA. The MNA was composed of small glands with mild nuclear pleomorphism, scanty mitoses and no cytoplasmic vacuolation. Many of the glands contained dense eosinophilic luminal material. The MNA of the cervix was 4 cm in size, and was extending into the isthmic region and the myometrium of the uterine corpus. The vaginal resection margins and the paracervical fat were also involved (R1 resection). The 17 lymph nodes in total from the pelvis were identified and they were all free of the malignant tumour.\nThe patient was finally diagnosed with a tumour of the uterine cervix comprising a completely excised residual benign PEComa and a moderately differentiated MNA of the cervix FIGO stage IIB with positive excision margins and positive parametrial involvement. After radical surgery, the patient received chemo-radiotherapy and brachytherapy treatment. There is no disease recurrence 12 months after the surgery. The patient is being monitored closely.
A 57-year-old male patient with a smoking history of more than 40 years and extensive stage SCLC was brought to The Emergency Department at the Tartu University Hospital due to acute neurological symptoms: the patient had suddenly become disoriented and did not recognize his family members and relatives. Severe hyponatremia was diagnosed at his admission, with the sodium level of 104 mmol/L.\nThe patient had first been admitted to the Tartu University Hospital approximately 7 months earlier with extensive stage SCLC (lymph node and liver metastases). Patient's serum sodium level at diagnosis was normal. Patient's initial treatment had consisted of 6 cycles of chemotherapy with cisplatin and etoposide that had resulted in stable disease. Afterwards, the patient had been followed up for 2 months. Subsequently, a progressive disease had been diagnosed in primary site and liver and second-line chemotherapy with topotecan started. First cycle of topotecan had ended 2 days prior to the patient's admittance to the emergency department with acute neurological symptoms (mainly disorientation) described above.\nIn parallel with the hyponatremia referred to above, other abnormal blood tests included slight increases in the levels of serum bilirubin (43 μmol/L) and liver enzymes (alanine aminotransferase 145 U/L, aspartate aminotransferase 107 U/L), as well as increased levels of alkaline phosphatase (460 U/L) and lactate dehydrogenase (798 U/L). Serum levels of potassium, glucose, creatinine, urea, and ammonia were normal. Serum osmolality was decreased (218 mOsm/L), which is a frequent finding in patients with hyponatremia. For unknown reasons, urine sodium and osmolality analyses were not ordered by first physicians taking care of the patient. Definitely, these latter analyses would have added valuable information in the management of this case. Patient was euvolemic.\nThe computed tomography with contrast media showed no brain metastases.\nIn the emergency department, treatment of hyponatremia was initiated according to the current guidelines by administration of hypertonic saline via continuous infusion that resulted in improvement of patient's general condition and neurological status [, ]. This treatment was continued for several days at the department of oncology. However, with hypertonic saline infusion, only minor correction of hyponatremia was achieved with an increase of the serum sodium level up to only 119 mmol/L. After this slight increase in blood sodium level, an aggravation of hyponatremia evolved (115 mmol/L) with a new episode of disorientation and mental confusedness that was compared to the first episode (at admission to the emergency department) much slighter and shorter. Subsequently, the saline infusion therapy was discontinued and treatment with fludrocortisone (Florinef 0.1 mg b.i.d.) started. The treatment with fludrocortisone resulted in a quick increase in the serum sodium levels from 115 to 121 mmol/L within 3 days and subsequent persistent increase up to 131 mmol/L within the following 11 days. Changes in the serum sodium levels during the treatment of hyponatremia are illustrated in .\nThe patient continued treatment with fludrocortisone (Florinef 0.1 mg b.i.d.) with no more episodes of severe hyponatremia and neurological symptoms. Eventually, due to pneumonia, second-line chemotherapy was postponed and terminated later on because of treatment brake that was long enough to allow the tumour to progress. The patient died of progressive SCLC approximately 2 months later.
We report a 60-year-old white man with a history of AML in the first complete remission after allergenic stem cell transplantation. Four years later, he developed a mass of soft tissues in the lower third of the posterior compartment of his left thigh, gradually increasing, as well as stiffness of the left knee.\nClinical examination found a 10-cm mass in the left popliteal mass with bending limitation. No abnormality was seen in the complete blood count parameters. MRI showed a bulky mass syndrome of 12 × 7 × 4 cm in the lower part of the posterior ledge of the left thigh in contact with the posterior cortex of the lower metaphysis femur. This appeared in hypodensity in T1 and in heterogeneous hyperdensity in T2 on the MRI. At diagnosis, the positron emission tomography-CT (PET-CT) revealed metabolic tumor syndrome in the popliteal muscle, with a standardized uptake value (SUVmax) of 11.8 (fig ). As part of the workup, bone marrow analyses revealed normal cellular marrow with no excess of immature cells, but with some atypia and signs of dysmyelopoiesis.\nBiopsy of the mass found a subcutaneous location of myeloblastic acute leukemia with transdifferentiation to plasmacytoid dendritic phenotype blasts. Immunohistochemical study showed expression of CD34+, CD33+, and 50% of CD117. The proliferation index was evaluated at 60%.\nThe participants of the multidisciplinary board meeting recommended combined chemotherapy [using Azacitidine (Vidaza)] and RT to the tumor bed. Radiation CT scan simulation was performed in the treatment position using personalized means for immobilization. 3D conformal RT planning target volume (PTV) was defined as the gross tumor volume plus 1 cm of margin surrounding the tumor. This resulted in a total PTV of 560 cm3. The prescribed dose to the PTV was 30.6 Gy given in 17 fractions, i.e. 5 fractions a week delivered using 6 MV lateral photon beams. Due to the well-known radiosensitivity of this type of tumor, a limited dose of 1.8 Gy per fraction was chosen.\nART was planned after administration of two-thirds of the prescribed dose, namely 19.8 Gy, using the second CT scan simulations with the same conditions. After this dose, the PTV decreased to a residual volume of 157 cm3 (fig ). Thus, ART allowed delivering the rest of the dose (as a boost) of 10.8 Gy to only 28% of the initial PTV with significant sparing of healthy tissue of the knee joint and the cartilage.\nThe first evaluation after RT showed complete clinical response without skin toxicity. The patient, who had significant functional deterioration of the knee at diagnosis, recovered normal knee function and mobility at 2 months after RT. In terms of imaging response, the PET-CT showed a significant metabolic response of the left popliteal mass at 2 months, and the SUVmax was 2.4 versus 11.8 (–80%) prior to RT (fig ).
We report a case of a 35 year old female who had mitral valve (MV) commissurotomy and ring annuloplasty (32 mm Carperntier) on July 28, 1987 for rheumatic valvular disease. Fifteen months after this surgery, she presented with an embolic event to posterior cerebellar artery. Her blood cultures were positive for Candida tropicalis. Echocardiography showed moderate mitral stenosis with 0.5 × 0.4 cm density on the anterior portion of the ring behind the mitral valve consistent with fungal vegetation. She did not improve clinically after treatment with amphotericin B and required a 31 mm Medtronic Hall mechanical prosthesis on 10/17/88 which was followed by chronic outpatient suppressive treatment with fluconazole.\nIn August 1989, she presented to the hospital with pancytopenia, splenomegaly and renal failure. A large fungal vegetation was noted on the MV annulus and blood cultures were positive for a different species of candida (C. parapsilosis) leading to her third mitral valve procedure (second replacement) on 8/14/1989. She was discharged home and enjoyed a period of seven years with good functionality while being on 200 mg per day of fluconazole suppressive therapy.\nIn December 1996, she presented with three weeks of fever, marked splenomegaly and hemorrhagic infarct of the left optic disc. Her blood cultures grew C. parapsilosis prompting the initiation of amphotericin B and fluconazole therapy and surgical consultation at University of Virginia (UVa) for the third episode of CPE. The fourth mitral valve procedure (third replacement) was performed on 1/22/1997 at UVa followed by increased dose of fluconazole (400 mg per day).\nIn November 1998, she presented with continued fever, heart failure and overt pulmonary edema secondary to C. tropicalis prosthetic MV endocarditis with positive blood cultures. TEE showed dilated and hypokinetic right ventricle, severe tricuspid and mitral valve regurgitation with an LV ejection fraction of 35 %, and severely elevated pulmonary artery pressure (80–90 mmHg). The fifth, and last, mitral valve procedure [fourth replacement (St Jude Valve)] was performed on 11/23/1998 at UVa due to worsening heart failure and pulmonary edema. Due to recurrent CPE, she was also considered for heart transplant but repeat MVR along with ongoing antifungal treatment was thought to be better. She was discharged on liposomal amphotericin B three times a week to correspond with her visits for erythropoietin infusion secondary to pancytopenia before resuming fluconazole. She was closely followed on oral fluconazole at 800 mg daily from January 1999 until 2006. She consistently denied using any intravenous drug or medication noncompliance. During this 7 year period, she enjoyed an active lifestyle including camping and fishing.\nWorsening pancytopenia and splenomegaly developed in the second half of 2006 secondary to recurrent C. parapsilosis MV vegetation with positive blood cultures which led to biventricular heart failure, multiorgan failure, pancytopenia and acute kidney injury requiring hemodialysis. The candida species was still sensitive to fluconazole, voriconazole, itraconazole, amphotericin B and 5-flucytosine. The patient was felt not to be a candidate for redo surgery and subsequently died in November 2006.
A 71-year old woman presented with a history of type 2 diabetes and osteoarthritis in both knees. The temperature of the bath was approximately 44°C, so she tried to cool down the water. However, it was difficult for her to move because of knee osteoarthritis. She called out for help to her neighboring family, but they did not take notice of her. She sat there for 2 hours and eventually suffered scald second-degree burns on both buttocks and plantar regions of the feet. After the emergency call, the family cooled the patient with cold water for 30 minutes. At the time of transport to a treatment facility, erythema was the only clinical sign; therefore, she was diagnosed with a superficial dermal burn (Figure , B). The patient was treated with dimethyl isopropyl azulene ointment every day until she was referred to our hospital. However, on the 7th day after the injury, the burn wound deepened, and she was referred for further medical treatment. The burn surface at the time of consultation was deep with 6% total burn surface area (Figure -E). On the 12th day after the injury, debridement and split-thickness skin grafting were performed under general anesthesia. First, bilateral buttocks and heels were debrided by sequential excision, and dermal bleeding was observed in a small area of the heel; however, adipose tissue was exposed beyond the dermis in most areas (Figure -H). Except for both heels, epithelialization had already occurred at the time of surgery. Skin grafts were subsequently taken from the left thigh at 12/1000 inches, processed into a triple mesh, and split-thickness skin grafting was performed on both buttocks and both heels. She was transferred to the primary care hospital on the 20th-day post-injury. Skin grafts were engrafted on the heel and 80% engrafted on the buttocks (photographs of the wound at the time of transfer were not taken).
A 19-year-old man was brought to the emergency department following a road traffic accident after his motorcycle skidded and hit the road divider. His Glasgow Coma Scale (GSC) on initial examination was 12/15. He sustained laceration of his upper lip and tongue, comminuted fracture of the right mandible parasymphysis, and avulsed teeth 11, 12, 41, 42, 43, and 44 (). He was intubated immediately for airway protection. An emergency head CT scan showed that he also sustained depressed fracture of the frontal bone with subdural and epidural hemorrhage. CT scan also showed right parasymphysis mandible fracture and dislocated left condyle (). The left condyle was dislocated anteriorly and superiorly into the infratemporal fossa medial to the zygomatic arch. There were no fractures of the condyle and zygomatic arch.\nHe underwent emergency craniotomy with evacuation of blood clot by the neurosurgical team. In the same setting, the facial laceration injury was sutured and an arch bar with intraosseous wiring was placed to stabilize the fractured mandible. Condyle dislocation reduction was also attempted. Due to the orotracheal intubation tube, the occlusion was not assessed following reduction. The patient was then transferred to the intensive care unit (ICU) subsequently with the orotracheal intubation kept in place. Following extubation 5 days later, it was noted that the patient kept his mouth open without any closure movement. There was also excessive drooling of saliva due to the inability to close his mouth. On examination, his mandible movement appeared restricted and the mandible was unable to move in any direction. He was not obeying instruction well. Multiple manual reduction attempts at bedside were unsuccessful.\nAn open reduction and internal fixation was planned for the right parasymphysis of mandible fracture, and it was planned to perform reduction of the dislocated condyle on the left side. Owing to the patient's neurological injury, the surgery could only be done 2 weeks after the injuries were sustained. In view of the ASD condyle and the prolonged period of dislocation, we anticipated difficult reduction. This was discussed with the patient and his family, and it was decided if the need for open or surgical reduction arises, they prefer surgical approach to be done intraorally. During the surgery under general anesthesia with muscle relaxation, initial attempts were made to reduce the left condylar dislocation by using manual traction by Hippocratic method and then with the assistance of a mouth gag but proved to be unsuccessful. Our next attempt was to release the intraosseous wiring at the parasymphysis fracture site effectively rendering the mandible in two separate pieces to simulate mandibulotomy-assisted reduction as described by previous clinicians [, ]. Once this was not successful, we went ahead with an intraoral condylotomy on the left side by piezoelectric surgery. First, a coronoidectomy was done to get access to the condyle. Then, the condylar neck was osteotomized using the piezosurgery, and the mandible was then able to be pushed back into occlusion. Finally, open reduction and fixation of the right parasymphysis fracture was performed and stable occlusion was achieved.\nPostoperative CT scan confirmed the reduction of the dislocation (). There was a slight deviation of the jaw to the left and mouth opening was 19 mm. Occlusion was acceptable and elastics were placed for 6 weeks. Jaw exercises were encouraged, and review after 2 months postoperatively showed improvement in mouth opening at 40 mm with stable occlusion. The patient was then referred to a prosthodontist for further rehabilitation and treatment of the missing teeth.\nOn 1-year follow-up, the patient presented with no complaint. Clinically, there was no tenderness at the joint or muscle of mastication on palpation or during movement. However, there was mild asymmetry of the jaw with the chin deviated 2 mm to the left (). Mouth opening was maintained at 40 mm with deviation to the left on opening (). Occlusion was good with upper and lower dentures in place. CT scan shows union between the condyle head and the condylar process stump (). Its position remains as seen immediately after surgery. The stump of the condylar process meanwhile has remodeled to form a neocondyle.
The first patient was a 71-year-old male with LHON 4917, a mutation of mitochondrial DNA at position 4917. In March, 1982, he awoke with sudden painless visual loss in the left eye. The family medical history was remarkable for a brother who had lost the vision in one eye and had been diagnosed with optic neuritis. The patient's neurology work up was negative for infections and lupus erythematosus. Visual evoked potential was normal in the right eye and “profoundly abnormal” in the left eye with prolongation. The brainstem auditory evoked responses were normal. He received intravenous steroids followed by a 14 day taper of oral decadron. In July, 1983, he had a second attack in the left eye reducing his vision to 20/200 with pain. It was treated as acute optic neuritis with intravenous methylprednisolone for 3 days at the Cleveland Clinic. On August 4, 1983, he experienced the loss of vision in the opposite eye with visual acuity 20/50 in the right eye and 20/200 in the left eye. The diagnosis of Leber's hereditary optic neuropathy was considered. In 1984, the patient suffered additional visual loss in the right eye. Blood testing was negative for 11778 (mitochondrial DNA position 11778) Leber's mutation.\nIn 1994, the patient's blood and that of his mother, were tested positive for the newly recognized LHON4917 mutation (The patient's mother was blind with a combination of glaucoma, Graves’ orbitopathy and a stepwise optic neuropathy in both eyes by 90 years of age).\nThe patient was referred for SCOTS evaluation. The past ocular history was significant for argon laser trabeculoplasty, followed by trabeculectomy for glaucoma in the right eye in 1990 and an uneventful cataract surgery in 2004. The left eye had no light perception (NLP) in 1984 after a central retinal artery occlusion. A conjunctival biopsy in 1989 showed numerous plasma cells and histiocytes with periodic acid-Schiff (PAS)-positive inclusion bodies.\nThe best-corrected visual acuity was counting fingers (CF) at 1 foot in the right eye, and NLP in the right eye. The visual field in the right eye was almost extinguished. Both optic nerves were atrophic and surrounded by peripapillary retinal pigment epithelial scars. The left eye had atretic arteries following the central retinal artery occlusion 29 years ago. On intravenous fluorescein angiography the right eye had spotty microaneurysms consistent with background diabetic retinopathy and non-leaking telangiectatic microangiopathy consistent with Leber's optic neuropathies.\nOn October 15, 2013, the patient underwent the SCOTS procedure in both eyes (Arm 3 in the left eye, Arm 2 in the right eye) without complications. At 6 months after treatment, the visual acuity was CF at 2 feet in the right eye and NLP in the left eye. His eye pressures at 6 months were 10 mm Hg in the right eye and 11 mm Hg in the left eye and he used Istalol twice daily.