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An 83-year-old woman abruptly presented one morning with the belief that her husband had been replaced by a nearly identical substitute. She repeatedly asked him who he was and where she could find her real husband, to the point of showing around a picture of him and calling his work office for help. During that day, the patient was able to manage her daily activities as usual, she prepared lunch and dinner, but she seemed often confused. She believed that her dead father was still alive and looked for him, she did not recognize some objects in her home, and she thought that a third person lived with them. She did not experience hallucinations or prosopagnosia. These symptoms gradually disappeared during the following day, when she was able to correctly recognize her husband. Although she was initially unable to recall what happened, the patient regained her memories of that day in the following weeks.\nHer past medical history revealed hypertension, rheumatic polymyalgia, hysterectomy to remove a fibroma, and an oncological history. Three years before, she was diagnosed with non-small cell lung carcinoma and pancreatic carcinoma with liver and diaphragmatic metastasis. She underwent radiation therapy first and then chemotherapy treatments with gemcitabine (8 cycles) with good response. The follow-up visits showed no disease progression. Since few months before the focal seizure, the patient also complained of right frontal headache.\nThe patient was evaluated at our outpatient neurology clinic 3 days after the event and hospitalized 1 week later. When the patient was admitted to our Department, the neurological examination was normal. Neuropsychologic evaluation revealed a mild cognitive impairment characterized by selective frontal dysfunction with dysexecutive deficits and a minor involvement of language skills. The test showed no prosopagnosia or visuoperceptive impairment. A deflection of mood was also reported. EEG revealed focal theta activity on right frontal regions, and brain MRI showed the presence of a large right frontobasal meningioma with marked perilesional edema and mild compressive effect on adjacent structures (shown in Fig. ). Surgical treatment was postponed because of age, comorbidities, and patient decision. During the hospitalization, the patient was started on levetiracetam 500 mg b.i.d. and dexamethasone without seizure recurrence. In the following months after the discharge, the patient did not complain of confusion or delusional beliefs anymore, and regular follow-up visits (last in July 2020) showed a stable clinical condition. |
A 30-year-old male presented with diplopia in left eye for 20 days following occupational accident over the left side of his nose. The chief complaint of the patient was binocular diplopia in primary gaze. He being a carpenter by profession, sustained the injury while working with a nail gun, as one of the nails had been wrongly placed and bounced off the concrete wall and hit the left lateral aspect of his nose, leaving a small laceration, which had healed by the time he presented. The left eye was congested with hyperglobus and the extra-ocular movements were restricted and painful []. Patient had normal vision. Injury to the left eye was ruled out by the ophthalmologist. A provisional diagnosis of orbital floor fracture with entrapment of orbital tissue, with or without a retained foreign body was made. Occipito-mental view 10o and 30o radiographs were taken, revealing the presence of a metallic foreign body [].\nThe exact site and position of the foreign body was confirmed by a computed tomography (CT) scan, a metallic foreign body lodged in the left orbit without any bone injury and settled in the posterior part of the orbit [Fig. and ]. Retrospectively, the patient was examined for the wound of entry. There was a faint scar over the left lateral aspect of the nose [].\nThe high velocity sharp projectile had pierced the skin of left lateral side of the nose and into the supporting tissues of the eye and lodged in the posterior aspect of the orbit. Patient was informed about the foreign body present in his left eye and the treatment options. A decision was made to remove the foreign body. Under general anesthesia, Left lateral eyebrow incision was given exposing the supra-orbital margin and orbital roof []. Blunt dissection was done through the orbital fat and other soft tissues and the nail head was detected using an image intensifier [] which was removed along the axis of curvature of the nail without damaging the eye globe and adjacent tissues []. Post surgery, the patient recovered with complete resolution of diplopia with normal extra ocular movements of the left eye. |
A 51-year-old Iranian woman presented with 2-month history of progressive unremitting back pain, exacerbated at night, superimposed on a creeping paraparesis. She also suffered from episodes of urinary retention for which she had undergone thorough clinical examination and a series of investigation including neuroimaging, cerebrospinal fluid analysis and also serologic surveys to find the aetiology. MR imaging of the brain and spine revealed one non-enhancing cystic lesion without surrounding enhancement located within the left cerebral hemisphere and another one at the level of conus medullaris in the spine (). No infectious aetiology had been found despite performing detailed investigation to detect any sign of cysticercosis, brucellosis and/or HTLV infection. The tissue biopsy of the involved area was not obtained as she had not consented to it. An extremely painful induration with indistinct border was found over the dorsum of the left hand. X-Ray imaging showed osteolysis of the second metacarpal bone (). The other sites of body skeleton were normal on examination despite her complaint about the agonizing pain over most parts of her body. 99 m Tc-DTPA revealed increased uptake of radiotracer in axial skeleton and left hand area and, also a photon-deficient area adjacent to the lower pole of the left kidney suggestive of a space occupying lesion originating from that kidney ().\nComplex cystic renal mass lesion was revealed on ultrasonography which was found to be hypervascular on contrast-enhanced CT scan. The result of imaging investigations was compatible with renal cell carcinoma diagnosis, till otherwise proved. In the meantime, the patient was hospitalized for nutritional supplementation and other supportive care. Radical nephrectomy was done afterwards and the histology confirmed renal cell carcinoma with sarcomatous component. Early in postoperative period she developed .thromboses in proximal veins of left lower extremity for which she received enoxaparin 60 mg twice daily subcutaneousely. She also had severe hypercalcemia probably due to paraneoplastic effect of the tumour producing PTHrP, and widespread bony metastases as the intact PTH assay was undetectable. She received appropriate treatment for her hypercalcemia. The patient and her family refused to accept further treatment when they were informed regarding the natural course and poor prognosis of the illness and the limitations of the currently available treatment, and she was lost for further follow up. |
A 19-year-old male patient presented to our hospital in July 2019, with complaints of abdominal pain and vomiting for the last 15 days.\nThe patient had a history of recurrent abdominal pain for the last two years. Each episode was characteristic of severe central abdominal pain along with vomiting. He had multiple admissions as a result of these episodes. Detailed inquiry and checking of previous records revealed that these episodes were a result of recurrent attacks of acute pancreatitis. Each episode was characterized by markedly elevated levels of serum amylase and lipase, and imaging studies in the form of ultrasound and contrast-enhanced CT of the abdomen revealed a swollen pancreas and peripancreatic fluid collection. His imaging two years back revealed gallstones as well. Last year, he underwent endoscopic retrograde cholangiopancreaticography (ERCP) which showed gallstones and common bile duct (CBD) stones. Biliary stone removal and sphincterotomy were performed during the ERCP procedure. It was followed a few weeks later by laparoscopic cholecystectomy. He remained symptom-free for a few months. However, he again suffered from two further attacks of pancreatitis and underwent ERCP again which did not reveal any bile duct stones.\nNow, the patient presented to our department with complaints of severe central abdominal pain and vomiting for the last two weeks. The pain was of moderate intensity with radiation to the back. The pain was only relieved by taking narcotic painkillers. He also had multiple episodes of vomiting associated with food intake. There was no blood in his vomitus. The patient denied intake of alcohol, illicit drugs, or any type of alternative form of medicine. There was no history of trauma, insect bite, other procedures (apart from those mentioned above), headaches, altered level of consciousness, fever, cough, altered bowel habits, jaundice, skin rashes, or abdominal distension. He had lost around 10-kg weight in the last two years. Both of his parents had type 2 diabetes mellitus (DM). He did not smoke and belonged to a middle-class family. Due to these problems, he had left his studies about two years ago.\nOn examination, the patient was clearly malnourished. He was in obvious distress. His vitals were as follows: blood pressure 130/80 mmHg, pulse 100 beats per minute, respiratory rate 22 breaths per minute, and temperature of 100°F. His abdomen was sunken with tenderness in the central part of his abdomen. His initial laboratory investigations are shown in Table . His serum calcium levels and lipid profile (including the triglyceride levels) were in the normal range. His contrast-enhanced CT of the abdomen showed diffusely enlarged pancreas with internal low-density foci, intrapancreatic calcification, and significant peripancreatic fat stranding. Based on his clinical presentation, laboratory investigations (raised amylase and lipase), and imaging, he was diagnosed as a case of acute pancreatitis. He was managed with intravenous fluids, painkillers, antiemetics, and proton pump inhibitors. Oral feeding was started as soon as the patient was able to tolerate it. Due to the repeated episodes of pancreatitis, the patient's blood was tested for serum IgG4 which was markedly elevated (Table ), pointing toward the diagnosis of AIP.\nThe patient was then referred to a specialized center for endoscopic ultrasound (EUS) and biopsy. EUS showed a sausage-shaped pancreas with hyper- and hypoechoic strands. The pancreatic duct was of normal size, 4 mm in the head and 1.7 mm in the body. Multiple peripancreatic lymph nodes in the celiac region and in the subhepatic region were seen. The largest one was 2.4 x 1.8 cm. CBD size was normal, and there was no evidence of CBD stone. There was no evidence of pancreatic divisum. Fine needle aspiration cytology (FNAC) of the lymph nodes was performed in the celiac region. Histopathology showed a mixed population of lymphoid cells. The pancreatic biopsy was not performed by the specialized center, and the reason they explained to us was that according to the diagnostic criteria, the patient had specific CT findings so only one more diagnostic test was required to confirm it and it was raised IgG4 levels. They performed FNAC of the lymph nodes to rule out any malignancy. Also due to a young age, the patient was not willing for more invasive tests.\nBased on all the work-up, our patient was diagnosed as type 1 AIP. He was started on steroids (tab prednisone 40 mg per day). His condition improved on steroids, and he was gradually tapered off of steroids in 12 to 16 weeks. |
A thirty-two-year-old female patient presented with progressive abdominal swelling of two-year duration. The swelling started from the left side of the abdomen and progressed to involve the whole abdomen. The swelling became prominent since one year (), with associated dull aching left flank pain. She had no hematuria or any other urinary symptoms. On physical examination, her vital signs were within the normal range with a pulse of 83 beats per minute and blood pressure of 100/80 mmHg. On abdominal examination, she had visible abdominal swelling, which was prominent on the left side of the abdomen. The swelling was cystic with no attachment to the surrounding structure.\nLaboratory findings of the patient, including urine analysis, serum electrolyte, and hematology profile, were all in the normal range (). During the initial evaluation, the ultrasound index of the left kidney showed a huge hydronephrosis passing the midline and filling almost the whole abdomen. Computerized tomography (CT) scan of the abdomen without contrast showed massive left kidney pelvicalyceal dilatation with a maximum cortical thickness of 3 mm. The dilatation spans seven vertebral lengths with the inferior border reaching the pelvis (). The left ureter and left renal arteries are not visible, and significant mass effects on other abdominal organs were also noted.\nA diagnosis of giant left hydronephrosis was made and the patient was prepared for laparotomy. The abdomen was opened with a subcostal flank incision under general anesthesia. Upon entry, 9.5 liters of urine was drained, and a left nephrectomy was performed, which was sent for histopathology. The left ureter was explored and showed severe stenosis at the level of ureteropelvic junction (). An intra-abdominal drain was left in situ, and the abdominal wall closed in layers.\nShe had a smooth postoperative course following the surgery. Her postoperative hematocrit was 21.7%, for which she was transfused with one unit of crossmatched whole blood. Her postoperative serum electrolyte and renal function test were also in the normal range. The intra-abdominal drainage was removed on the 5th postoperative day, and the patient was discharged a day later with satisfactory clinical condition. Histopathologic examination of the biopsy showed a hydronephrotic kidney with no feature of malignant growth (). |
A 24-year-old male with history of congenital membranous ventricular septal defect (VSD) developed tricuspid valve endocarditis following a dental procedure in 2007 and subsequently underwent VSD closure and bioprosthetic tricuspid valve replacement. His left ventricular (LV) ejection fraction prior to surgery was normal. In 2009, he presented with heart failure symptoms and was found to have severe LV systolic dysfunction. Since LV dysfunction persisted despite optimal medical therapy, he was referred to electrophysiology for consideration of a primary prevention ICD in 2010.\nHis 12-lead electrocardiogram at baseline () showed sinus rhythm with a QRS pattern consistent with ventricular pre-excitation over a right free wall accessory pathway (AP). The QRS duration was 193 msec. A transthoracic echocardiogram showed normal LV size with evidence of abnormal septal wall motion and an LV ejection fraction of 35%. The bioprosthetic tricuspid valve showed normal function and there was no evidence of residual VSD. A cardiac CT revealed normal coronary arteries and a cardiac MRI showed no evidence of delayed enhancement. We felt that the ventricular preexcitation pattern mimicking left bundle branch block could potentially contribute to his cardiomyopathy by causing dyssynchrony [,]. Therefore, the patient underwent electrophysiology study with a plan for catheter ablation of the AP.\nBaseline rhythm was sinus with a preexcited QRS complex of 193 msec. The HV interval was negative. The antegrade and retrograde AP block cycle length were 270 and 280 msec, respectively. Retrograde atrial activation was entirely eccentric with the earliest local activation in the area of the antero-lateral tricuspid annulus. The antegrade AP effective refractory period (ERP) was 320/600 msec. No significant changes in QRS duration or pattern were noted during atrial programmed stimulation and decremental pacing (). The retrograde AP ERP was ≤ ventricular ERP (240/600 msec). No arrhythmia could be induced with aggressive atrial and ventricular stimulation protocol (with or without isoproterenol).\nMapping along the atrial aspect of the tricuspid annulus was performed using a 4 mm solid tip ablation catheter (St. Jude Medical, Minneapolis, MN). This revealed earliest endocardial ventricular and atrial activation to be at the anterolateral tricuspid annulus. A pre-formed sheath (SR2, St. Jude Medical, Minneapolis, MN) was employed to improve catheter stability in this area. During mapping, mechanical block of pathway conduction was noted. RF lesions deployed at this location resulted in permanent abolition of accessory pathway conduction.\nPost-ablation, complete AV block with a junctional escape rhythm of 60-65 beats/min was noted (). Damage to the AV node probably occurred during prior cardiac surgery and was masked by antegrade preexcitation until now.\nIn view of significant LV dysfunction with heart failure symptoms and complete AV block, the patient underwent implantation of a biventricular ICD the following day. A 12-lead electrocardiogram showing sinus rhythm with biventricular pacing is shown in . At a 2-week follow up visit, significant improvement in heart failure symptoms and exercise tolerance was seen. The underlying intrinsic rhythm was complete AV block. Serial echocardiograms done at 3-month and 1-year follow up visits showed complete normalization of LV systolic function and wall motion with an estimated LV ejection fraction of 55%. |
A 68-year-old female underwent a partial left-sided chest wall resection, with partial removal of the 6th and 7th ribs and of the scapula angle for elastofibroma (). The chest wall defect was reconstructed by using a Mersilene mesh, secured by interrupted pericostal stitches, and covered by a sufficient volume of viable muscles. The postoperative course was uneventful; the radiographic aspect at discharge was normal (). The first symptoms in the form of pains in the region of the incision appeared five months after the operation, and computer tomography (CT) of the thorax showed a lung hernia in the region of the mesh covering the chest wall defect (Figures and ). The patient refused the proposed surgical correction, being only slightly limited in usual daily activities. During the next several months, the symptoms persisted with variable intensity under analgesic therapy, till the moment when pains significantly limited patient's daily activities, 22 months after the operation. The repeated chest CT showed a slight increase in hernia size, with no signs of tumour recurrence (), so that reoperation was planned.\nAfter the excision of the previous skin scar and the incision of the muscular layer, the mesh region was exposed, showing a lung protrusion (4 × 3 cm) along the anterolateral edge of the mesh (). The local situation is schematically presented on . The mesh suture line in the hernia region was completely disrupted, with a small piece of the herniated lung being completely detached from the mesh, the remaining lung surface under the mesh area being fully adherent to the mesh. By careful dissection, the mesh was separated from a firmly adherent lung and removed (). After adhaesiolysis and complete lung liberation, a wedge resection of the afunctional lung tissue of the superior segment of the lingula was done, just in the region of contact with the mesh. After the chest tube insertion, the chest wall defect was reconstructed by suturing a Mersilene mesh in two layers—single pericostal sutures for initial fixation and running suture for additional reinforcement (). A final chest wall stabilization was done by the fixation of two Synthes plates (DePuy Synthes J&J) over the 5th and 6th ribs (). The postoperative course was uneventful. The chest X-ray on discharge, on postoperative day 5, is presented in .\nAt the last contact with the patient, one year after the operation, the general condition was good, without the need for analgesics. |
A 24-year-old Chinese female undergoing orthodontic treatment was referred to the National Dental Center Singapore for orthognathic surgery. She presented with a Class III skeletal profile with an asymmetry of the mandible and a maxillary cant. The right side of her mandible appeared broader than the left side although her chin point was coincidental with her facial midline. She had a Class III malocclusion with a left posterior open bite and a right crossbite. The inter-incisal opening was 32 mm. An orthopantomogram taken showed an incidental finding of a large bony growth at the left temporomandibular joint. The only symptom she had was an occasional left earache.\nComputed tomography scans showed a bony mass 2 × 2 cm arising from the lateral part of the left condyle, resulting in a downward displacement of the left condyle and facial asymmetry from a clockwise rotation of mandible when viewed from the superior and anterior aspect. The diagnosis based on the clinical presentation and radiographic appearance was an osteochondroma of the mandibular condyle. The patient was planned for a conservative excision of the lesion with simultaneous orthognathic surgery. The surgery was planned using the SimPlant Pro 2011 from Materialise Dental program and the lesion was removed digitally. The surgery was simulated achieving good occlusal relationship with correction of the facial deformity. Together with the 3dMD system simulation of soft tissue contours, 3D facial profile prediction was made of the surgical outcome.\nThe patient was operated on under general anesthesia through nasoendotracheal intubation. A Le Fort 1 osteotomy was first performed through a circumvestibular incision. The maxilla was advanced and the cant was corrected, as guided by an intermediate wafer. The maxilla was then fixed with 4 miniplates (Medicon 2.0 miniplates, Germany). After that, an endaural incision was made, followed by an anterograde blunt dissection to access the bony lesion at the left temporomandibular joint. Care was taken to preserve the neurovascular structures at the region. The mandible was retracted inferiorly, and the mass superior and lateral to the condyle was excised in pieces together with a margin of healthy bone, but preserving the medial pole of the condyle. Bilateral sagittal split osteotomies were then carried out through vestibular incisions at the posterior mandible. The mandible was setback and the asymmetry corrected, as guided by the final wafer. The remnant condylar head was repositioned into the glenoid fossa of the temporal bone. The mandible was fixed with 1 miniplate bilaterally (Medicon 2.0 miniplates, Germany) and she was placed into intermaxillary fixation. The recovery postoperation was uneventful and the patient was discharged on the second postoperative day. The intermaxillary fixation was maintained for 14 days and subsequently converted to light training elastics for one more week. Jaw exercise was implemented after 3 weeks. Histology of the lesion confirmed the diagnosis of an osteochondroma.\nAt 7 months postoperation, mouth opening of 29 mm was achieved with no signs of recurrence. The decrease in mouth opening might be due to fibrosis at the operated condyle site as the patient was not very compliant with her jaw exercises [Figures –]. |
A 50-year-old Caucasian male with autism presented with 1week of abdominal pain and vomiting progressing to obstipation. The patient’s limited communication skills led to a delayed diagnosis of a complete bowel obstruction. The patient underwent exploratory laparotomy which revealed extremely dilated loops of small bowel secondary to cecal volvulus, leading to a right hemicolectomy. He was discharged with instruction to return to the wound clinic for midline abdominal wound care. On return to the wound clinic, the patient’s abdominal wound was found to have dehiscence with bowel evisceration. This complication arose as the patient had difficulty understanding postoperative instruction to refrain from using his abdominal muscles. The subsequent OR trip consisted of component separation along with mesh implantation to allow for decreased tension on the wound hoping for complete closure and healing. A full timeline of his hospital course is referenced in .\nThe patient was a 50-year-old intellectually disabled male who arrived at the hospital as a transfer from an outside facility for a diagnosed small bowel obstruction. Prior to his transfer, the patient had nonoperative management of suspected partial bowel obstruction with gastric decompression, analgesia, nausea control and bowel rest. This yielded a resolution of his symptoms for 1 day, but the patient faced a rapid return of his symptoms, after which he was transferred to a higher level of care for operative management. While his disability significantly limited his communication with those involved, he was able to relay the presence of periumbilical abdominal pain with failure to pass flatus or stool.\nThe patient was autistic and legally blind. His past medical history consists of gout and hypertension. Past surgical history was significant for fracture repair of the right upper and lower extremities leading to gross deformity and negative for any abdominal surgeries. Family history consisted of hypertension and diabetes mellitus. The patient denied alcohol, tobacco, or illicit drug use. He was taking Thorazine, Lopressor and Allopurinol and had no known drug allergies.\nThe patient was an obese male in mild distress. He presented with a blood pressure of 121/72 mmHg, heart rate of 109 bpm, respiratory rate of 18 breaths/min, the temperature of 97.9 F and oxygen saturation of 96% on room air. Examination showed moist mucous membranes, no jugular venous distension and no peripheral edema. No rashes or abnormal bruising were noted. Heart sounds were regular in rate and rhythm. Lungs were clear to auscultation bilaterally. The abdomen was soft and distended with faint bowel sounds. Palpation elicited tenderness in the periumbilical region with no rebound or guarding. |
We present a case of a 67-year-old female who was recently treated with a decompression and 10th thoracic to second lumbar fusion secondary to formation of an epidural hematoma from a 12th thoracic vertebra fracture (type unknown). While in a physical therapy session the patient suffered a fall forward, trying to break her fall with her arms outstretched above her head. After the fall the patient’s arms were stuck in full abduction and pronation and she was in significant pain. The patient’s presenting position is displayed in . She arrived in the emergency department where X-rays were taken and demonstrated bilateral inferior shoulder dislocations, LEH ().\nOrthopedics was consulted to evaluate and treat. Upon evaluation, the patient was distally neurovascularly intact with 2/4 radial pulses bilaterally, sensation intact to light touch about the fifth cervical to first thoracic dermatomes, and motor function was intact in all peripheral motor groups of the upper extremities. The emergency physician provided sedation with closed reduction performed by the orthopedic service. The right shoulder was reduced using traction through the humerus through a flexed elbow to control the limb, and the opposite hand was used to place superior pressure on the humeral head through the axilla to guide the head into the glenoid. Slight external rotation and adduction was added as the head cleared the glenoid. Attention was then turned to the left shoulder, which was reduced, in a similar fashion; however, this shoulder was converted from an inferior to anterior dislocation using pressure in the axilla and slight external rotation.\nFollowing this, traction through the humerus external rotation, and lateral pressure on the humeral head yielded a successful relocation of the glenohumeral joint. After reduction the patient remained neurovascularly intact bilaterally. The patient was placed into bilateral shoulder slings, advised to avoid active shoulder range of motion, and admitted to the hospital for placement. Three days after the patient’s admission she adjusted a continuous positive airway pressure (CPAP) mask with her right arm dislocating anteroinferiorly ().\nShe was again noted to be distally neurovascularly intact. Sedation was performed by the anesthesia department, and the orthopedic service then performed closed reduction. The patient remained neurovascularly intact after reduction. She has not had another instability event to date. |
A 52-year-old male patient presented with the complaint of sudden vision loss in his left eye 3 days earlier. Past medical history was significant for chronic kidney disease, secondary hypertension, chronic hepatitis C virus infection and arrhythmia. Ophthalmologic examination revealed best corrected visual acuity of 10/10 in the right eye and 4/10 in the left eye from the temporal field. Confrontation test revealed inferonasal visual field loss in the left eye. Direct and indirect light reflexes were normal in both eyes and there was no relative afferent pupillary defect. Anterior segment examination was normal and intraocular pressure was 13 mmHg in both eyes. Dilated fundus exam demonstrated soft exudates consistent with hypertensive retinopathy in the right eye. Fundoscopy of the left eye revealed an area of pallor in the superotemporal quadrant and the macula with macular cherry red spot, which were consistent with occlusion of the superotemporal branch of the left retinal artery (). On OCT, peripapillary retinal nerve fiber layer (RNFL) thickness was within normal limits (). In the patient’s visual field, there was an inferonasal defect in the left eye corresponding to the occluded region (). The patient was treated with a single dose of 500 cc intravenous dextran-40 and 200 mg intravenous pentoxifylline. In etiologic studies, Doppler ultrasonography revealed an atherosclerotic stenosis in the right and left main carotid arteries and a calcified plaque causing luminal narrowing in the left internal carotid artery. Transthoracic echocardiography revealed second- to third-degree aortic valve regurgitation and first-degree tricuspid valve regurgitation. There was no improvement in visual acuity or visual field despite treatment. At follow-up 7 months later, OCT showed thinning of the superior, inferior and temporal peripapillary RNFL (). On the thickness map, ganglion cell layer was thinner in the superior and temporal areas (). Decreased vascular density in the superficial and deep capillary plexus consistent with ischemia in the regions supplied by the superotemporal branch of the retinal artery was observed in a 6x6 mm macular field on OCTA (). The borders of the ischemic area were more clearly seen in en face images (). In optic disc OCTA, capillary density was reduced in the superotemporal region and collateral vessels were present in the area (). When compared to the fellow eye, there was a decrease in the macular deep and superficial capillary density in the superior and temporal quadrants () and a decrease in peripapillary capillary density in the superior quadrant (). Visual field loss persisted in post-treatment threshold perimetry (). |
A 27 years old Iranian male was referred to the clinic as a candidate for septorhinoplasty surgery. After initial examinations and X-ray imaging, the following tests were requested for the patient including PT, PTT, INR, BT, CT CBC and platelet count. All results were reported as normal. Surgery was carried out by open approach and septal harvest and external osteotomy. The patient was discharged after removal of the nasal pouch of antibiotic as well as pain killer prescription a day after surgery. At the end of the first week, the splint was removed; the patient’s general condition was fine and had no major complaints, so his next visit was scheduled for two weeks later.\nOn the second visit, the patient had complaint of headache and he was asked to return if it continued despite the medications. During the next two days, his headache worsened and the patient was hospitalized. The patient was afebrile and conscious but neck rigidity was found in physical examination. Funduscopy was normal and there was no diplopia or eye movement impairment. Neurologic consultation was done with brain CT scan and MR angiography ( and ) that revealed diffuse brain edema, cavernous and sigmoid sinus thrombosis.\nThen anticoagulant therapy was initiated. Then he developed seizure which was controlled by diazepam and dilantin. Three days after admission, his seizure was fully controlled; however he developed pain and edema in both lower extremities. Doppler sonography revealed extensive thrombosis in both ileofemoral venous systems ().\nConsultation with cardiologic, hematologic and vascular surgery services were performed. Considering his condition, a filter was placed in his inferior vena cava in one step, while in at the same time; laboratory studies including proteins C and S deficiency assay were done which were reported normal. The studies on gene mutation demonstrated the heterozygote type of MTHFR C677T mutation. His signs and symptoms improved gradually and he was discharged after administration of coumadin and PT control tests after 8 days. |
A 69-year-old man was admitted to the Department of Gastroenterology for evaluation of an incidental hepatic mass in August 2013. In 2005, he had been admitted to the Department of Endocrinology because of cold sweating, facial flushing, and uncontrolled blood pressure. A ~7 cm right adrenal mass had been observed on computed tomography (CT) and there had been no distant metastasis on an MIBG scan. The patient had undergone laparoscopic right adrenalectomy due to PCC. After surgery, he had been followed up in the outpatient clinic until 2007. During that period, there was no evidence of metastasis in abdominal CT. The patient had also been treated for hypertension and type 2 diabetes mellitus for 3 years and had a history of coronary stent insertion for non-ST-elevation myocardial infarction in March 2012. At admission to the Department of Gastroenterology, he experienced dizziness, diaphoresis, general weakness, and poor oral intake; his blood pressure was 130/80 mm Hg and his heart rate was 78 bpm. Contrast-enhanced abdominal CT and magnetic resonance imaging (MRI) were performed. They revealed a ~10 cm hepatic mass in the right lobe of the liver that had a high signal intensity on T2-weighted images and early arterial enhancement and delayed washout on dynamic contrast-enhanced images. Also, it had a low signal intensity on the hepatobiliary phase and high cellularity on the diffusion phase (). The hepatic mass was considered to be hepatocellular carcinoma rather than malignant PCC. For these reasons, liver biopsy was performed to evaluate the incidental hepatic mass. The patient was given the α-adrenergic antagonist phenoxybenzamine to prevent a hypertensive crisis before biopsy because we could not completely rule out the possibility of metastatic PCC. However, during and after the liver biopsy, his vital signs were stable. PCC was finally confirmed on the basis of morphological and immunohistochemical findings, with the specimens staining positive for chromogranin A and synaptophysin. Laboratory tests revealed the following serum metabolite levels on the day of admission: aspartate aminotransferase, 29 IU/L (normal, 10 to 40); alanine aminotransferase, 24 IU/L (normal, 6 to 40); alkaline phosphatase, 97 IU/L (normal, 40 to 129); total bilirubin, 0.42 mg/dL (normal, 0.1 to 1.2); direct bilirubin, 0.16 mg/dL (normal, 0.09 to 0.30); and γ-glutamyltranspeptidase (GGT), 150 IU/L (normal, 11 to 73). These levels, obtained by performing a liver function test, were all in the normal ranges, except for the mild elevation of GGT. Hepatitis virus markers were negative and tumor markers for hepatocellular carcinoma (α-fetoprotein and protein induced by vitamin K absence or antagonist II) were in the normal ranges. Furthermore, at admission we measured the patient's serum/urine levels of catecholamines, which were as follows: serum epinephrine, 0.078 pg/mL (normal, <50); serum norepinephrine, 1.473 pg/mL (normal, 110 to 410); serum metanephrine, 2.47 nmol/L (normal, <0.5); serum normetanephrine, 44.97 nmol/L (normal, <0.5); 24-hour urine epinephrine, 43.8 µg (normal, 0 to 20 µg/day); 24-hour urine norepinephrine, 339 µg (normal, 12.1 to 85.5 µg/day); 24-hour urine metanephrine, 35.931 mg (normal, 0.0 to 1.3 mg/day); and 24-hour urine vanillylmandelic acid, 120 mg (normal, 1.20 to 6.52 mg/day). The total urine volume collected in one day was 1,900 mL, and contained 1,171.16 mg of creatinine. The serum and 24-hour urine catecholamine levels were high. An 131I-MIBG scan revealed increased uptake of 131I-MIBG in the right adrenal gland bed and adjacent liver parenchyma (). Surgical resection was impossible because the tumor had invaded the portal vein and the adjacent lymph nodes. Therefore, we planned radionuclide therapy. However, the isolated ward needed for that was not available for at least 6 weeks. Finally, TACE was performed for the liver metastasis. Celiac angiography showed a large mass in the right lobe of the liver. An emulsion of 10 mL of lipiodol and 50 mg of doxorubicin (an anticancer drug) was injected (). The tumor was well lipiodolized, as observed by post-TACE imaging ().\nBefore the procedure, the patient continued to receive phenoxybenzamine. After TACE, he was transferred to the intensive care unit for 6 days for management of a hypertensive crisis and postembolization syndrome. His high blood pressure and tachycardia were strictly controlled by infusion of nitroprusside, nifedipine, and labetalol (). Abdominal CT was performed 2 weeks after TACE. Although the size of the metastatic hepatic mass had not decreased, it showed lipiodol uptake (). However, follow-up abdominal CT 7 months after TACE showed that the diameter of the hepatic mass had decreased from 10 to 8.3 cm (). Although the response was that of stable disease on the basis of modified RECIST criteria, the tumor seemed to have responded to TACE because of its decreased size. The patient's symptoms at admission, including dizziness and diaphoresis, improved substantially. The serum catecholamine levels were followed up 2 months after TACE and were as follows: serum epinephrine, 0.091 pg/mL; serum norepinephrine, 0.842 pg/mL; serum metanephrine, 4.26 nmol/L; and serum normetanephrine, 22.27 nmol/L. The serum norepinephrine and normetanephrine levels had decreased significantly (). The patient continues to be followed up and has shown no significant problems. |
A 25-year-old male presented with paroxysmal left upper limb tics and weakness that had been ongoing for two years. The involuntary limb tics exhibited a sudden onset and lasted for seconds, but were not accompanied by consciousness disturbance. The patient had approximately 10 attacks per day, which were accompanied by limb weakness. A magnetic resonance imaging (MRI) scan was performed initially and was found to be normal. The patient had received irregular diazepam administration from the onset of the disease; however, the symptoms became increasingly more serious. The patient was prescribed 600 mg per day valproate sodium on admission to hospital to control the seizures, but experienced one or two attacks per month subsequent to the administration of valproate sodium. The past medical history of the patient was unremarkable. On examination, the patient was alert and his pupils adjusted to light. Neurological examination revealed intact cranial nerves, but decreased deep tendon reflexes and a decreased sensation of touch, pain and vibration. The gait of the patient was broad and he was unable to walk in a straight line. Full strength was observed in all the muscle groups. The results of the Romberg, heel-knee-shin and finger-to-nose tests were normal. An electroencephalogram (EEG) revealed diffuse spikes and slow waves, predominantly in the frontal and temporal lobes (). A further MRI scan was performed and revealed increased signal density on T2-weighted imaging and decreased signal density on T1-weighted imaging in the right temporal occipital cortical lesions. Local cortical atrophy was also observed in the left temporal-occipital cortex. In addition, the lactic acid concentration (5.2 mmol/l) had markedly increased. The results of the carotid ultrasound and electromyography were normal. A biopsy of the biceps muscle demonstrated a variation in fiber size and the presence of ragged-red fibers (). In addition to the prescribed 600 mg per day valproate sodium, the patient was administered 10 mg per day coenzyme Q10 for approximately 2 years. Two years later his symptoms relieved and an EEG showed less spikes and slow waves than it had previously shown. |
The patient was a 40-year-old, gravida 0 woman with a history of ureteral stones and was receiving treatment for Behcet's disease prior to entering our hospital. She expressed a desire to become pregnant to her primary physician and subsequently stopped receiving prednisone. A year prior, at 39 years old, the patient was diagnosed with multiple myoma by transvaginal ultrasound. Her primary physician referred the patient to our hospital for infertility treatment, which included a myomectomy followed by timed intercourse after monitoring her ovarian cycle via vaginal ultrasound. Laparoscopic-assisted myomectomy was performed in our department, and infertility treatment was started 3 months postoperatively. Serum LH and FSH hormone levels were found to be within the normal range (Table ). The patient indicated in her interview that she had regular menstrual cycles, but upon further investigation, this was found not to be the case. The results from the ultrasound monitoring showed an irregular cycle and that the patient met some of the criteria for PCOS, most notably a high AMH level.\nFollowing standard treatment guidelines in Japan, the patient underwent timed intercourse with cyclofenil administered at a dose of 600 mg/d for 5 days, starting on cycle day 5 until cycle day 9. However, no follicular development was observed, even on the 25th day of the menstrual cycle. At this time, a mass was not observed in the right ovary on the ultrasonogram and a follicle width diameter of 8.6 mm was confirmed (Figure A). Starting on the 25th day of the menstrual cycle, 4 mg/d of chlormadinone acetate was administered for 10 days after which the patient experienced withdrawal bleeding. Following this, the patient underwent timed intercourse with clomiphene citrate, which was administered at a dose of 50 mg/day for 5 days starting on cycle day 5 until cycle day 9. On the 11th day of the menstrual cycle, a 48 × 41 mm anechoic mass was observed in the right ovary on the ultrasonogram (Figure B). We considered it a follicle and monitored its progress after obtaining informed consent from the patient. The mass changed to a 40 × 28 mm anechoic mass with a small follicle (Figure C). On the 16th day of the menstrual cycle, the mass size increased to 61 × 40 mm, showing a mixed pattern with a solid component (Figure D). We obtained a blood sample to identify tumor markers and serum E2 and P4 levels because the mass contained a solid component. Carbohydrate antigen 19-9 (CA19-9), carbohydrate antigen 125 (CA125), and human epididymis protein 4 (HE4) had normal values (Table ). E2 and P4 levels were 595 pg/mL and 1.21 ng/mL, respectively. We judged that the mass was a follicle before ovulation. These results suggest that in Figure B the anechoic ovarian structure was a functional ovarian cyst or a persistent follicle. In Figure D, 5000 IU of human chorionic gonadotropin (hCG) was administered along with timed intercourse. On the 6th day of the next menstrual cycle, mass size increased to 90 × 68 mm, showing a mixed pattern with a solid component (Figure E). The patient had no symptoms. She received a followed up without any medication for infertility treatment. On the 14th day of the next menstrual cycle, the size slightly reduced to 73 × 72 mm with the solid part increasing in size (Figure F). Then, the mass became a 55 × 37 mm mixed mass with dense echo and echo-free spaces on the 21st day of the menstrual cycle (Figure G). On the 28th day of the menstrual cycle, the mass changed to a 38 × 39 mm sponge-like mass (Figure H). On the 5th day of the next menstrual cycle, it decreased to 34 × 22 mm (Figure ) and continued to gradually decrease in size (Figure J). At 62 days since detection (19th day of the menstrual cycle), the mass disappeared (Figure K), and we ultimately diagnosed the mass as a HOC according to its clinical course. Vaginal sonography was performed using a Mochida SONOVISTA FX, PE (7.5 MHz transvaginal probe) at an angle of 220° (Mochida Co.). |
A 46-year-old man was referred from local clinic for the dental implant and bone graft. For the initial evaluation we took a panoramagraphy. This showed a very thin remaining alveolar ridge after tooth loss (#26) with severe alveolar bone destruction due to periodontal problem and slight pneumatization of maxillary sinus cavity. For the precise evaluation of the residual alveolar bone and left maxillary sinus cavity, we took a dental computed tomography (CT) scan. The CT scan confirmed the panoramagraphic finding of severe alveolar bone damage, especially the buccal area, resulting from the periodontitis at the maxillary left first molar, #26. The residual alveolar ridge was very thin with mild pneumatization of the left maxillary sinus cavity ().\nWe did a vestibular incision on the movable mucosal area horizontally and parallel with a residual alveolar ridge, instead of a crestal incision, for the simultaneous installation of the dental implant with sinus graft. We did a careful dissection of the mucoperiosteal flap elevation under the sinus floor to prepare the recipient site for vertical augmentation of maxillary alveolar ridge. The mucoperiosteal flap elevation extended to the palatal side to allow room for vertical augmentation without damage or perforation of the flap. We then made a lateral window opening with a round bur using ordinary methods and created a lateral bony window for sinus graft. The maxillary sinus membrane was elevated for the maxillary sinus graft. An allogenic block bone was hydrated sufficiently with normal saline ().\nAfter evaluation of the recipient site shape and size for vertical augmentation of the maxillary posterior alveolar ridge, we trimmed the allogenic block bone with a bur and bone rongeur following the shape and size of recipient site. We put the trimmed allogenic block into the recipient site, taking care not to damage or perforate the mucoperiosteal flap. The preformed recipient site, shaped into a pocket, was surrounded by thick keratinized attached gingival and palatal mucosa. The allogenic block bone was put into the recipient site surrounded by a thick mucoperiosteal flap as a wedge, so there was no need for fixation with screws. After the allogenic block bone graft, small allogenic bone chips and heterogenic bone chips were put in a dead space between the allogenic block bone and overlying mucoperiosteal flap. Simultaneous maxillary sinus graft was performed with allogenic bone chips and heterogenic bone chips by the layered graft technique described in our previous report []. After sinus graft, the lateral bony window was opened on the lateral side of the allogenic block bone graft area. We wanted the lateral bony window rolled as a cortical autogenous bone wall for maintenance of volume and a more favorable result of vertical augmentation. We applied a tissue adhesive (fibrin sealant, Beriplast®; Behring GmbH, Marburg, Germany) to fix the grafted materials in the sinus cavity and vertical augmentation area. We closed the wound with 3-0 black silk. After operation, we took a panoramagraphy to evaluate the results ().\nAfter six months, we installed a dental implant on the previous vertical augmentation of maxillary posterior alveolar ridge and sinus graft site. During drilling for placement of a dental implant, we took a specimen from the allogenic block bone graft area. We made slides (H&E stain and M&T stain) for light microscopic evaluation of new bone formation on the allogenic block bone graft site. These slides show new bone formation beside a slightly resorbed allogenic block bone particle for remodeling. We drilled very carefully to prevent separating the allogenic block bone and host maxillary alveolar ridge ().\nWe made a final prosthodontic appliance on the dental implant fixture after five months. We expect a good prognosis of the final prosthodontic appliance, because the crown to implant fixture ratio was good due to vertical augmentation of maxillary posterior alveolar ridge (). |
A 17-year-old boy was referred to the Department of Conservative Dentistry and Endodontics because of swelling in his upper front region. His medical status was noncontributory. According to his questionnaire, 4 years earlier he was hit by a ball and had broken his maxillary right lateral incisors. It was left untreated for many years. Three years later, the patient developed swelling in the upper front region for which he consulted a general dentist. The dentist extracted the right fractured lateral incisor. After 11 months, he again developed swelling and pain in the same region. He again consulted the same dentist. A root canal treatment was performed in the upper right central incisor and the dressing of calcium hydroxide was given. The patient was told to return after 2 weeks. The symptoms did not subside; hence, the patient came to our department for consultation.\nA panoramic radiograph showed a well-circumscribed radiolucent lesion extending from the apices of teeth 13 to 11 []. The lesion was approximately 14 mm in diameter.\nThermal and electronic pulp testing was negative for tooth 13. After evaluating all the data, nonsurgical endodontic root canal treatment of teeth 13 and 11 was planned. Teeth were isolated with a rubber dam and access opening was done. Upon access, a thick purulent discharge exuded from the orifices of the canals. After ensuring the presence of a clean root canal, a working length radiograph was taken. The teeth were instrumented to ISO size 60 for the central incisor and 70 for the canine tooth by using the step-back technique. During the instrumentation, the canal was irrigated copiously with a 3% sodium hypochlorite solution. The canals were dried and the calcium hydroxide dressing was given. The calcium hydroxide dressing was changed every 1 week for four times. As the discharge did not cease completely and the symptoms still persisted, the treatment procedure was changed. The canals were irrigated and dried, a triple antibiotic paste was placed, and the teeth were temporized.\nThe patient was called after a 1-month interval for refreshing the triple antibiotic paste in the canals. After 3 months, the canals were irrigated with 2.5% sodium hypochlorite and obturated with gutta-percha and AH plus. The restoration was accomplished with composite resin. The patient returned to the department for the 10-month follow-up examination and was asymptomatic. Radiographic examination [] showed progressive healing of lesions associated with each tooth. |
A 17-year-old adolescent boy with significant psychiatric history and prior history of self-insertion of foreign bodies per urethra first presented to our institution after inserting a nail per urethra in an act of self-harm. This was identified on plain film X-ray (). The patient was brought to the operating room and placed under general anesthesia, and the foreign body was removed using a 19fr cystoscope and flexible grasper.\nSince his initial encounter, he had a total of 20 emergency department visits for urethral foreign body, and nine of these encounters required endoscopic removal. He did place several foreign bodies per urethra during one admission. In total, he was able to expel a urethral foreign body 13 times, thereby preventing surgical intervention or external manipulation at bedside. He also never required admission for trial of passage.\nSeveral months later, he presented with self-insertion of a metal screw into his urethra in addition to hydroxyzine ingestion. During this presentation, a foreign body was palpable in the distal penile urethra, and a plain film X-ray () identified the location of the screw. His symptoms primarily consisted of urinary retention and penile pain.\nIn review of his history of foreign bodies per urethra, he has been able to void a piece of plastic coffee lid, small construction nails, metal wire from hospital face mask (), and a plastic fork tong. Objects that required endoscopic removal included staples (), assorted pieces of plastic, and larger nails. If the object appeared sharp and/or proximally placed in the urethra, we favored endoscopic removal to prevent damage to the urethra. After several trips to the OR for endoscopic removal, we started to identify urethral scarring from repeated trauma.\nWe are aware that he has a higher than normal bladder capacity for his age group. After several of his prior trips to the emergency department, he would typically present retaining up to 1 L of urine without showing signs of discomfort. The screw was located in the distal urethra and positioned so the blunt end would be expelled first. We continued conservative observational management with trial of void for the patient to expel the foreign body. Our indications to take him to the operating room included urinary retention with 1.0–1.5 L on bladder scan and/or severe uncontrolled pain. Eventually, he voided 1 L of urine with the foreign body without complication. He had no complaints of abdominal pain during this period of observation. Once he was able to demonstrate a second spontaneous void, there was no further urological intervention indicated other than a 5-day course of oral antibiotics. We have attempted to arrange follow-up for each visit. Unfortunately, his situation is particularly difficult given the fact that he is frequently admitted to the inpatient psychiatric facility and overall non-compliant with our recommendations. On each occasion, we had warned him of the expected long-term trauma to his urethra. It would be ideal to follow him in an office-based setting to evaluate his voiding habits, monitor his behavior, and perform a videourodynamic study. |
A 57-year-old gentleman, volunteer community driver, with a history of ethanol abuse, presented to the emergency department 2 days following a mechanical fall, with left shoulder pain and reduced function. He slipped on the pavement, fell backward, outstretching his left arm to break the fall, sustaining an isolated injury to the left shoulder. The only significant past medical history was recurrent deep venous thrombosis and pulmonary emboli for which he takes long-term oral anticoagulation (warfarin). On clinical examination, the patient had reduced range of motion and there was no neurovascular deficit in the left upper limb. Initial radiographs confirmed a primary glenohumeral dislocation with a possible Bankart lesion. Based on the plain radiographs [], the patient underwent two unsuccessful left shoulder manipulations under sedation in the emergency department. Subsequently, manipulation under general anesthetic was performed the following day by the orthopedic team and was similarly unsuccessful. At this point operative intervention was considered, but given the long-term warfarin use and history of chronic alcohol abuse, it was felt on balance the case should be managed non-surgically, if at all possible.\nCT of the left shoulder was performed, which identified a 2-cm, >20% Hill–Sachs lesion with significant impaction of the humeral head and anterior dislocation. There were small bony fragments around inferior glenoid; these little flecks of bone might have been produced during attempted reduction under anesthesia. demonstrates significant undermining of the humeral articular surface. After review of the image, it was appreciated that an incorrect reduction may cause further soft tissue injury or humeral fractures. Following this, a planned sequence of movements was generated in an attempt to reduce the shoulder. The patient underwent a second manipulation under anesthetic; the arm was externally rotated by 40° with the arm in extension, after which direct lateral traction was applied and the shoulder was successfully disimpacted and reduced without causing any iatrogenic injury. Examination under anesthesia demonstrated shoulder joint stability. Patient was discharged with a shoulder immobilizer for 4 weeks and sling thereafter for 2 weeks with physiotherapy. Patient suffered initial stiffness due to immobilization, but was responding well to physiotherapy with good rotations and range of motion. At 6-month follow-up, there were no further episodes of re-dislocation reported. He has returned to work as a driver and reports no functional deficit in comparison to pre-operative levels or effect on the quality of life. On examination, the patient can abduct to 140°, has forward flexion to 170° and normal rotations. |
The patient was a 24-year-old male with a past psychiatric history of schizophrenia who was seen in the outpatient clinic due to hypersexuality after starting aripiprazole. The patient had no known health problems. He had no history of head trauma, seizures, sexually transmitted disease, or significant substance abuse problems. He was first diagnosed with schizophrenia at the age of 19 years and was started on olanzapine, which he responded well to for years. The patient was living with his mother and had completed 11th grade level education. He did not have any history of developmental or intellectual difficulties. He was working part time in a fast food restaurant when he started to have the decline. He was single, never married, and had no significant other. The patient did not have very many acquaintances and led a quiet life. He has no known legal issues so far. The patient used cannabis occasionally when he was 17, but denied any use now. He did not have any problems with alcohol and or other illicit substances. He did not have any history of tobacco use. There was no known family history of mental illness.\nThe patient was previously stable on olanzapine 20 mg/day for four years and then became noncompliant due to unclear reasons, leading to worsening of psychotic symptoms. He was switched to oral aripiprazole 15 mg/day with a plan to switch to a long-acting injectable due to possible nonadherence. During the initial oral one-week trial, the patient became increasingly unstable, with physical and verbal altercations with his mother. The patient also ran away from home and lost his job due to public masturbation at his workplace. His mother also noticed that the patient was increasingly flirtatious and inappropriate in public with females, which were behaviors he had never displayed previously. Given his worsening behaviors, the patient was admitted to the inpatient unit and was switched to intramuscular injection (IM) of aripiprazole 400 mg, assuming that he would benefit from a long-acting injectable and that he could be non-adherent with the oral medication. He became increasingly sexually aroused and was acting inappropriate in the days following. During the hospital stay, there was an instance where he had sex with a female peer and had to be placed on 1 : 1 observation, i.e., one staff was assigned to continuously observe the patient. After discharge from the hospital, the patient needed constant reminders in his group home to keep his hands out of his pants. Despite these attempts to reduce the inappropriate behavior, the patient endorsed that his sexual arousal was more than normal after starting the aripiprazole. At this point in time, the patient had received two doses of aripiprazole 400 mg IM. While on aripiprazole, he did not show any gambling urges and or other impulsivity other than the sexual preoccupations. The sexual preoccupations started within a week of starting with aripiprazole. Further aripiprazole injections were discontinued, and the patient was again prescribed olanzapine 20 mg/day given his previous good response. In the group home, the patient continued to remain occasionally agitated with outbursts and required constant redirection about appropriate sexual behaviors in public. He also continued to display sexually inappropriate behaviors towards females in a day program and was banned from attending the program until he was able to behave appropriately. Although he had reduction in the intense sexual behaviors four weeks after stopping the aripiprazole injections, he did not completely return to baseline. Given his ongoing sexually inappropriateness and possible reports of being internally stimulated, he was started on paliperidone 6 mg/day for augmentation and with plan to taper and stop olanzapine. The patient started to have fewer outbursts and was noted to be in much better mood after three to four weeks of starting the paliperidone. He was noted to be less sexually preoccupied and with reduction in inappropriate behaviors in public. When writing this report, the patient was on both olanzapine 20 mg/day and paliperidone 6 mg/day, with the goal of attaining paliperidone monotherapy, initially oral and subsequently long-acting injections. The patient continued to live in the group home to learn social skills before moving into independent housing. After 12 weeks of paliperidone use, the patient was completely free from hypersexual thoughts and behaviors. |
A 36-year-old male patient with a 6-year history of chronic kidney disease of unknown etiology was brought to the emergency department due to neurological impairment that started during the previous hour characterized by altered mental status while he was walking down the street. On examination he was stuporous, with poor response to external stimuli. The patient was admitted to the hospital and vital signs and capillary glucose were determined. Glucose levels were 20 mg/dl and increased to 42 mg/dl after a 50 ml infusion of 50% dextrose. During his stay his mental status recovered after glucose levels were returned to normal parameters, requiring high doses of intravenous glucose. After his stabilization he was transferred to the internal medicine department. We confirmed that the patient was not taking medications that would cause hypoglycemia. On physical examination he was somnolent and pale, with slight oedema in both legs. A new episode of symptomatic hypoglycemia was observed while he was receiving an infusion of 20% dextrose. The infusion rate at that moment was 10.416 ml/hr. The infusion was not being weaned off or was an acute disruption. It caught our attention that although the patient was on a 20% dextrose infusion, he continued with hypoglycemia. Blood samples were taken and the results were abnormal ().\nAlthough hypoglycemia could be explained by chronic kidney disease, the diagnosis of insulinoma was considered, so a computed axial tomography with double contrast was taken but unfortunately there were no abnormal findings. During the patient's hospital stay he received several treatments that failed to achieve proper glucose control. We used ascending doses of diazoxide up to 600 mg/day with a poor response. In order to reduce episodes of hypoglycemia, we started with low doses of octreotide and found a good response that created tolerance quickly, so we decided to increase the dose by 0.1 mcg/kg/h always observing the same phenomenon. We decided to suspend this treatment when we reached 0.4. mcg/kg/h. Finally, we decided to maintain a continuous infusion of 50% dextrose with which we achieved serum glucose levels between 120 and 160 mg/dl. Magnetic resonance imaging and an endoscopic ultrasonography were performed but no conclusive data on any structural pancreatic disorder were obtained. In order to locate the tumor, we performed selective intra-arterial pancreatic stimulation with hepatic venous sampling at 0, 20, 40, and 60 seconds. High insulin levels were obtained after a selective injection of 0.025mEq/Kg calcium gluconate in the proximal splenic and gastroduodenal arteries () (). With these results, the patient was scheduled for surgery. During the procedure, bimanual palpation of the pancreas was performed, as well as a pancreatic ultrasound in which no tumor could be identified. The body and tail of the pancreas were resected. For two days the patient had an adequate glycemic control but after a couple of days, he presented with hypoglycemia again. The macroscopic pathology report did not show any tumor compatible with insulinoma; however, on microscopic examination pancreatic islets with elongated cells and clear cytoplasm compatible with nesidioblastosis were seen (). Unfortunately, during his stay at the intensive care unit, the patient developed late-onset hospital-acquired pneumonia and, in spite of treatment, he developed sepsis followed by septic shock which ultimately caused his death. |
A 12 year-old female patient suffering from persistent hearing loss after birth visited the outpatient clinic for evaluation and treatment of the hearing loss. The patient showed typical features of achondroplasia, such as short limbs, especially the proximal segment, with a long trunk, narrow thorax, large head with frontal bossing, and midfacial hypoplasia at birth. Although there was no one with achondroplasia in the family, and a genetic study of FGFR3 was not performed, the typical features of achondroplasia in the patient and the short statue were enough to diagnose the achondroplasia. The patient had suffered from frequent otitis media since childhood, and had a history of bilateral tympanostomy tube insertion 7 years ago. Both tympanostomy tubes were extruded 2 years after insertion. Because she showed a feature of sensorineural hearing loss, she was referred to our hospital for consultation for hearing rehabilitation, such as the use of a hearing aid.\nThe right tympanic membrane was intact and there was a large perforation in the left tympanic membrane. Pure tone audiometry (PTA) was performed and the hearing threshold averaged from 0.5 kHz, 1 kHz, 2 kHz, and 4 kHz. The air conduction hearing threshold was 82 dB HL on the right and 52 dB HL on the right, and the bone conduction hearing threshold was 46 dB HL on the left, and 44 dB HL on the left. The type of hearing loss was mixed hearing loss (). Speech recognition threshold and the speech discrimination score were 70 dB HL and 96% on the right, and 50 dB HL and 100% on the left, respectively. On auditory brainstem response testing, there was prolonged interlatency of the right side, while the left side was normal (). The patient was recommended to use a hearing aid on the right side and have tympanoplasty for the left side. But the patient denied further treatment and was lost.\nThe patient re-visited the outpatient clinic 5 years later after the first visit. The right ear had been operated at another hospital but she still complained of hearing loss on the right side, and she suffered from intermittent otorrhea and otalgia of the left ear. There were no specific findings of the right ear. The tympanic membrane of the left ear was perforated and the margin of the perforation was attached to the mucosa of the middle ear. Air conduction and bone conduction hearing threshold were 65 dB HL and 17 dB HL for the right ear, and 30 dB HL and 12 dB HL for the left ear, respectively (). Temporal bone computed tomography was performed. The right ear was well pneumatized, and was in a canal-wall-up mastoidectomized state. There was no incus and malleus head at the epitympanum, and foreign material, estimated to be material of the implanted prosthesis, was visible in the mesotympanum. There was no abnormal lesion in the middle ear cavity. Although the left ear was well pneumatized, a lesion with soft tissue attenuation partially filled the mastoid air cells. The incus and malleus were normal in appearance ().\nRight exploratory tympanotomy was planned first because the air-bone gap was larger and the state of the tympanic membrane was better than in the left ear. A previously inserted total ossicular replacement prosthesis (TORP) was found during the operation, and the TORP was displaced from the stapes footplate. Curetting of the posterior-superior portion of the bony tympanic ring was done and a stapedial superstructure was observed. All stapedial superstructures were intact and located at the posterior-superior side of the middle ear cavity. A round window reflex during stapes palpation was observed. A partial ossicular replacement prosthesis (PORP) made of titanium was inserted on the stapes head and the conchal cartilage was interpositioned between the tympanic membrane and prosthesis head (). Gelfoam was packed into the external auditory canal, but not in the middle ear cavity. The whole of the gelfoam was removed two weeks after the operation, and postoperative PTA was performed four weeks after the operation: the hearing threshold was 22 dB HL on the right, and 38 dB HL on the left (). A second PTA was performed three months after the operation, and the hearing threshold was 21 dB HL on the right, and 36 dB HL on the left ().\nAfter confirmation of correction of hearing in the right ear, an operation on the left ear was planned. During the operation on the left ear, a large sized central perforation with adhesion of the perforation margin to the middle ear mucosa was observed. Although all ossicles were normal and their continuity was intact, the mobility of the ossicles was decreased during palpation. The incudostapedial joint was separated and the distal portion of the long process of the incus was removed because of decreased motility. The PORP was interpositioned between the stapes head and the handle of the malleus, and the conchal cartilage was also interpositioned on the prosthesis head to avoid contact of the prosthesis with the tympanic membrane. The temporalis muscle fascia was inserted via the underlay method, and gelfoam was packed into the middle ear cavity and external auditory canal. The gelfoam was removed on the postoperative 14th day. PTA was performed three months after the second operation, and the hearing threshold was 16 dB HL on the right, and 26 dB HL on the left (). The patient was observed at the outpatient clinic. |
A 14-year-old boy, who was initially examined for continuous coughing, was referred to our hospital owing to an anterior mediastinal mass identified on chest X-ray (). Systematic examination revealed a 20 × 10 cm sized mass at the right anterior mediastinum that involved the right pulmonary vein and elevated levels of alpha fetoprotein (AFP), a tumor marker, at 3825 ng/ml. Needle aspiration was performed, but only necrotic tissue could be collected. We did not analyze the karyotype since the symptoms suggesting the Klinefelter syndrome were not observed. Therefore, a clinical diagnosis of malignant teratoma was made, and three courses of cisplatin-based chemotherapy were administered because AFP levels continuously increased. After chemotherapy, AFP levels decreased, although the size of the tumor did not change, as evident in a computed tomography (CT) scan. Next, tumorectomy and total right lung extraction were performed. The pathological diagnosis of the extracted tumor was malignant teratoma with areas of yolk sac tumor (). No cancer cells were found at the edges of the area where the tumor was removed. Two courses of cisplatin-based postoperative chemotherapy were administered until AFP levels were normal.\nAfter 3 months of follow-up, the patient experienced pain in his right hip joint while AFP was still normal. The 99mTc-methylene diphosphonate bone scan showed increased tracer uptake at the left forehead and right hip joint (). Head and pelvic MRI also revealed signs of metastasis at the left forehead and right hip joint. Abdominal CT showed a metastatic region in the liver. Bone biopsy was performed at the left forehead. The pathological diagnosis was metastatic malignant melanoma originating from an immature teratoma of mediastinum (). Large heteromorphic cells with melanin were found in the original mediastinal malignant teratoma by retrospective re-examination. This suggested that a section of the malignant melanoma in the original malignant teratoma, which was composed of various components, metastasized. Because of the very fast disease progression, after consultation with the family, aggressive treatment was discontinued, and palliative therapy was provided. He died 15 months after diagnosis of the original malignant teratoma. |
A 68-year-old female presented with sudden onset posterior neck and right shoulder pain with progressive right side weakness while falling asleep. During consult, she had reported taking anti-hypertensive medication for 20 years and was followed regularly for hepatitis C. She reported no trauma history or physical exertion for the past few weeks. Neurological examination resulted in alert mental status and the detection of right hemiparesis. Motor power of her right upper limb was grade III and ipsilateral hand grasping power was grade II. In her right lower extremity, motor power was grade IV, and her left whole extremities were intact. Right side hypoesthesia was also observed. Based on her medical history and clinical symptoms, the physician working at the emergency department ordered brain CT to rule out intracranial hemorrhage. However, brain CT did not show any positive findings (). Subsequent brain diffuse MRI was taken to rule out cerebral infarction, but it was also negative (). Cervical MRI was performed to rule out a cervical lesion based on the patient's report of posterior neck pain and revealed a mass like lesion in the right posterior epidural space at the C3-6 level compressing the right side of the spinal cord. The mass was isointensive to the spinal cord on T1WI and heterogeneously hyperintensive with central high signal foci on T2WI. At the C5 level, the MRI showed an ovoid, enhancing, nodular lesion, which was a suspected tumorous condition such as hemangioma or hemangiopericytoma (). Initial laboratory tests showed only severe thrombocytopenia (45,000/mm3). As her neurologic signs were getting worse with time, we decided to perform surgical intervention. Under general endotracheal anesthesia via light wand intubation, right C5 unilateral total laminectomy and C6 partial hemilaminectomy were performed. The mass lesion was pure hematoma and was removed (). We could find neither vascular malformation or an active bleeding point. She went into rehabilitation after her operation and finally achieved complete neurologic recovery and relief of neck and shoulder pain. |
A 28-year-old female presented to an outside hospital in 2007 with fainting spells that were suspicious for seizures by family's report. A magnetic resonance imaging (MRI) was obtained and revealed a right occipital tumor. The patient underwent a right occipital craniotomy and image-guided resection of the lesion. It was noted that there were three areas which were concerning for tumor invasion of the surrounding parenchyma due to its general discoloration. Frozen biopsies were sent for evaluation. The pathology report came back negative for marginal tumor infiltration. The patient was incorrectly told that the tumor was meningioma due to an incorrect preliminary read and that no further treatment was necessary; however, the final pathological diagnosis revealed a WHO grade III anaplastic ependymoma. Unfortunately, the revised diagnosis was not made known to the patient, nor her future physicians. She did not undergo chemotherapy or radiation at that time.\nIn 2012, the patient presented to our hospital with severe (8/10) headaches, nausea, and photophobia. Computed tomography (CT) and MRI of the brain did not show any acute pathology or evidence of tumor recurrence. The patient was given a diagnosis of migraine headaches and treated medically.\nThe patient re-presented in 2014 with relapse of her headaches and fainting spells. An MRI of the brain was obtained, revealing a recurrent 4.1 cm enhancing mass in the right occipital lobe with surrounding edema (without evidence of drop metastasis or other enhancing lesions on spinal MRI []). In light of the rather rapid interval growth of the lesion, despite no new onset focal deficits, and concern for malignant transformation to a WHO grade IV glioma, the neurosurgical team recommended re-resection of the tumor. The patient underwent subsequently re-do craniotomy, and did well clinically postoperatively as she remained neurologically intact and showed improvement in her headaches. The postoperative MRI demonstrated a gross total resection and she subsequently underwent adjuvant radiotherapy.\nTwo years after her second resection, the patient presented to her primary care physician with a cough lasting for several weeks. A chest X-ray was performed, which revealed multiple, bilateral pulmonary nodules. The largest lesion was seen in the left lower lobe, measuring 4.5 × 3.4 × 3.9 cm []. The second largest lesion was in the left upper lobe, in close proximity to the major fissure. Additional pleural-based masses were seen. A CT-guided biopsy of the mass was performed, confirming the diagnosis of grade III anaplastic ependymoma.\nAn MRI of the brain was obtained at the same time, which revealed the interval development of several new right-sided intracranial frontal extraaxial masses side, but without any evidence of tumor recurrence in the right occipital lobe tumor resection bed [Figure –]. The largest mass measured at 4.7 × 4.4 × 3.0 cm and was located along the right temporal–frontal convexity. Imaging displayed heterogeneous hyper-intense T2- and hypo-intense T1-signal characteristics and some foci of restricted diffusion. There was diffuse heterogeneous enhancement on postcontrast imaging. The lesion exerted significant mass effect upon the adjacent right temporal lobe gyri, uncus, and cerebral peduncle and a second mass (measuring 2.1 × 2.1 × 1.7 cm) and was located along the right posterior frontal convexity, also causing mass effect. Two additional masses were detected immediately anterior to the second largest mass along the right posterior frontal lobe, measuring 1.3 cm each in the greatest dimension. There was no evidence of recurrent disease at the initial occipital site of presentation, nor evidence of drop metastasis or other enhancing lesions on spinal MRI [Figure , ].\nThe patient once again underwent respective surgery and all cranial tumors were removed successfully as seen on postoperative imaging [].\nThe patient is currently under close follow-up, with adjuvant radiotherapy and chemotherapy for her lung metastases without evidence of intracranial recurrence 12 months following her most recent resection seen on imaging. |
A 61-year-old African American woman presented with right periorbital fullness and a perforated cornea with expulsed intraocular contents. She reported a 4 month history of progressive orbital fullness with worsening vision and eye pain over the preceding 3 weeks. She denied a history of infectious keratitis, contact lens use, ocular trauma, melanoma, lymphoma, or any other malignancy.\nThe patient originally presented for evaluation by an outside provider 3 months prior, after noticing blurry vision of the right eye with associated periorbital fullness and swelling for 1 month. Orbital MRI was obtained revealing an area of hyperintensity in the right orbit and an 8mm fluid collection contiguous with the superior aspect of the optic nerve sheath. The imaging findings were interpreted as being consistent with orbital cellulitis and a retrobulbar abscess and the patient was admitted for IV broad spectrum antibiotic treatment with ceftazidime, clindamycin, and vancomycin. Her visual acuity in the right eye at the time of admission was 20/200 and the globe was intact. Treatment with antibiotics was deemed ineffective and she was subsequently diagnosed with orbital inflammatory syndrome and started on systemic oral corticosteroids. A biopsy of the mass lesion was recommended but the patient was lost to follow-up.\nThree weeks later, a total of 4 months since the onset of eye symptoms, the patient presented to Bascom Palmer Eye Institute for management of presumed panophthalmitis. The vision in the right eye was no light perception and extraocular motility was restricted in all directions of gaze. Examination revealed an inflamed and tense right orbit with palpable firmness in both the upper and lower eyelids. The cornea was perforated with expulsion of the intraocular contents ( A&B). Examination of the left eye was unremarkable. Imaging ( A & B) showed a large ill-defined orbital mass that enhanced heterogeneously with contrast. The mass encased the globe and was compressing it with severe tenting of the posterior pole. After a thorough discussion with the patient of the findings of her case she agreed to undergo evisceration of the right eye with simultaneous biopsy of the orbital mass. During surgery it was noted that the sclera was almost completely collapsed and nearly all of the intraocular contents had been expulsed. The orbital mass was dense and white without much vascularity.\nMicroscopic examination of the evisceration specimen disclosed acute and chronic inflammatory cell infiltrates in the cornea, uveal tissue, vitreous, and neural retina. A cytokeratin stain for carcinoma within the intraocular contents was negative. Histopathologic examination of the orbital mass revealed a tumor comprised of atypical basophilic cells in a linear configuration with pleomorphic nuclei and an increased nucleocytoplasmic ratio (A). Cytokeratin and estrogen receptor stains were positive (B&C). These findings were consistent with an orbital metastatic lesion from a yet undetected primary breast carcinoma.\nThe patient suffered no intraoperative or immediate postoperative complications and the patient returned to her home country 1 week after surgery. The diagnosis was relayed to the patient and her primary care physician who arranged further evaluation with a local oncologist. Breast biopsy confirmed the diagnosis of breast carcinoma. Three months after surgery the patient was feeling well and reported an uneventful recovery period. At that time, the patient had not yet begun oncological treatment. |
A 66-year-old male patient presented with an enlarging mass in the left maxilla (Fig. ). The mass had been present for a few weeks. An incisional biopsy revealed squamous cell carcinoma. Staging scans were undertaken (Fig. ) which demonstrated a T4N0M0 maxillary alveolus tumour in close proximity to the left orbital floor with obliteration of the maxillary antrum and destruction of the lateral maxillary wall (Fig. ). The patient was partially dentate in both jaws with no significant dental pathology (Fig. ).\nThe findings were discussed with the patient together with the treatment options for this malignant tumour requiring a low-level Brown class 2b maxillectomy []. The patient preference was not to have prosthodontic obturation but rather reconstruction using microvascular free tissue transfer. In view of the unilateral low-level nature of the tumour, a soft tissue reconstruction combined with primary insertion of zygomatic implants to support a subsequent fixed dental prosthesis on a shortened dental arch concept was considered the best option. The remaining molar teeth were planned for extraction based on the potential need for post-operative radiotherapy and likelihood of trismus post-operatively. The remaining maxillary teeth on the non-defect right-hand side were planned for extraction to allow either the placement of immediate dental implants or the placement of conventional zygomatic implants depending on the state of the socket anatomy post-extraction.\nDental impressions were taken to allow construction of a maxillary complete denture template to both aid the placement of the zygomatic implants on the defect side and to act as an occlusal registration device during surgery. The occlusal vertical dimension was also measured between nasal tip and chin point to allow subsequent registration to occur at the correct level during surgery.\nThe patient underwent tracheostomy, a limited left-sided selective neck dissection for node sampling and vessels preparation. The maxillary tumour was excised in a standard manner via an intra-oral approach with preservation of the left orbital floor (Fig. ). The resection extended to the maxillary alveolar midline in the incisor region with extension posteriorly just into the soft palate. The defect was measured to allow the harvesting of a slightly oversized left fascio-cutaneous radial forearm flap which was carried out in parallel to the implant procedures. Following resection, the amount of bone remaining in the left zygoma was assessed and deemed satisfactory for the placement of two zygomatic oncology implants [] (Southern Implants Ltd., South Africa) which were subsequently inserted with excellent primary stability (Fig. ). The remaining maxillary teeth were then carefully extracted although it was not possible to preserve all the labial socket bone which was fused to several of the teeth. It was therefore decided to proceed with an alveoloplasty and insertion of two conventional zygomatic implants (Southern Implants Ltd., South Africa) on the right side which were inserted into the canine and second premolar sites with high primary stability (Fig. ). Standard implant bridge abutments (AMCZ abutments, Southern Implants, South Africa) were then torqued into place onto all four zygomatic implants with longer 5 mm versions being used on the defect side to facilitate the later flap perforation. The soft tissues of the right maxilla were then closed with multiple resorbable sutures.\nThe implant positions were then accurately registered by utilising light-cured resin tray material (Individo® Lux, Voco Gmbh, Germany) and abutment level impression copings. The resin material was applied in sections around the impression copings and cured incrementally to ensure a rigid splinting of the impression copings (Fig. ). Abutment protection caps were then placed over all four abutments prior to the jaw registration procedure which was undertaken using the pre-fabricated denture appliance relined with silicone putty material (Provil soft putty, Heraeus Kulzer GmbH) (Fig. ).\nThe radial forearm free flap (RFFF) was then disconnected from the arm and inset into the maxillary defect after creating a tunnel down into the left neck for the pedicle. The flap was carefully perforated over the zygomatic implant abutment protection caps using a short incision just through the skin layer followed by blunt dissection to allow the abutment and cap to perforate the flap ensuring a tight adaptation of the flap around the abutment (Fig. ). The flap anastomosis was then completed utilising the operating microscope and the neck and arm wounds closed. The patient recovered well from the surgery and was subsequently discharged at 8 days post-operatively. The tumour and neck dissection specimens were examined and reported as pT4a NO M0 squamous cell carcinoma of the left maxilla with a 7.2 mm depth of invasion. There was a close anterior mucosal margin of 1.3 mm and the decision was therefore taken for post-operative adjuvant radiotherapy.\nThree weeks post-surgery, the patient was seen for review and to try-in the provisional prosthesis. Unfortunately, in the interim, the RFFF had overgrown the zygomatic implants (Fig. .) and so, under local anaesthesia, the implants were re-exposed to allow the provisional prosthesis to be tried in. The incisal level of the prosthesis was modified, and the prosthesis was then finalised in the laboratory and fitted 1 week later, 1 month following surgery (Fig. ). A post-fitting radiograph demonstrated good positioning of the implants and seating of the initial prosthesis (Fig. ). The patient then completed 6 weeks of radiotherapy (63 Gy in 30 fractions). He subsequently attended with a fracture of the provisional prosthesis 3 weeks after completion of radiotherapy when the bridge was removed for repair. All implants were firmly integrated, the initial oral ulceration was now settling and the flap reconstruction was performing well with no evidence of breakdown or dehiscence (Fig. ). The bridge was repaired and re-fitted the same day, and arrangements were made for the construction of a new definitive acrylic bridge with a cobalt-chrome framework which was subsequently fitted for the patient. The patient continued to be followed up, and 12 months following surgery completed a quality of life feedback questionnaire [] where he rated his overall quality of life as “very good” and scored maximally in most domains with the exception of speech and fear of recurrence (Table ). At 18 months post-surgery, the patient was still disease free with no further incidents of prosthodontic related complications since the definitive bridge was fitted. His facial appearance (Fig. ) was symmetrical with no significant distortion despite his previous maxillary resective surgery.\nIn order to address some of the issues highlighted in this early case, the technique was modified slightly to try and prevent flap overgrowth and prosthesis fracture in the early stages. In order to prevent flap overgrowth over the zygomatic oncology implant abutments, the use of a polythene washer was instituted on subsequent cases treated in the unit. Once the flap was perforated, a 2-mm thick polythene sheet (Centriform Soft Mouthguard material, WHW Plastics Ltd., Hull, UK) was taken and a small disc cut out corresponding to an area of 1–2 cm2 surrounding the zygomatic oncology implants. Using a 5-mm tissue biopsy punch, holes were cut into the sheet corresponding to the positions of the abutments and the perforated polythene sheet was then placed over the abutments to keep the flap in a superior position during the initial healing phase prior to restoration. The polythene washer was then kept in place using conical abutment protection caps (Fig. ), and this enabled the prevention of flap tissue overgrowth and retained access to the oncology implants for subsequent restoration (Fig. ). In view of the fracture of the interim prosthesis reported in this case, the technique was modified with a definitive cobalt chrome framework being constructed within the first 2 weeks post-surgery with one visit for try-in of the framework and tooth set-up being scheduled to allow any modifications required to either incisal level, occlusion and overall soft tissue fit to be completed. This try in visit occurred at 2–3 weeks post-surgery with the final fit occurring 1 week later. This has prevented further issues for all subsequent patients.\nIn order to reduce intra-operative time, the soft tissue free flap is harvested at the same time as the implant placement and prosthodontic procedures. On raising a skin island, it is appropriate to make it a little over-sized for the required defect to ensure that tension and possible dehiscence at the surgical margins during healing is reduced.\nIn low-level maxillectomy (Brown class II), the need for bony reconstruction is questionable depending on the horizontal component. With the preservation of the orbital floor, zygomatic prominence and some bony support for the nose, facial appearance, in the experience of the authors and, as demonstrated by this case, is not significantly worsened despite low-level removal of the maxilla. The key issues in these low level defects are adequate clearance of tumour, dealing with the oro-nasal communication and reconstruction of the dentition. Whilst prosthodontic obturation can deal with these aspects in a simple manner, the stability of the obturator prosthesis and its ability to completely seal the oro-nasal defect has limitations. In addition, these prostheses require a significant amount of adjustments, clinic visits and on-going maintenance. The soft lining materials perish, discolour and harbour surface biofilm often resulting in some mal-odour and the need for regular replacement. For many patients, there is a psychological impact of retaining the maxillectomy defect and high anxiety related to the insertion and removal of the prosthesis as well as concerns relating to the handicap they would experience to speech, and eating should their prosthesis fracture or fail in some way. The use of implants to retain maxillary obturators certainly improves their stability and retention, but efficacy of the oro-nasal seal still requires regular maintenance and patients still often dislike the hygiene aspects of looking after the defect and their implant supra-structure within the defect.\nThe use of soft tissue flaps to close a typical hemi-maxillectomy defect is an effective way of dealing with the oro-nasal communication, but in isolation, this technique works against dental rehabilitation as the bulk of the flap provides a very poor moveable foundation for a subsequent removable prosthesis. The move towards the use of composite reconstruction (especially the fibula flap) has been facilitated by the use of digital planning in which dental implants can be inserted into the fibula flap at the time of harvest and inset facilitated by the use of stereolithographic guides. However, this procedure is not widely applicable for all patients due to financial, technological and medical restrictions and is not currently able to provide patients with an early loaded fixed dental prosthesis especially when post-operative radiotherapy is being utilised. Many older patients presenting with maxillary malignant tumours also have significant peripheral vascular disease and other significant medical co-morbidities which may prevent the harvest of a vascularised composite flap.\nIn contrast, the use of a soft tissue flap such as the RFFF or antero-lateral thigh flap can often be safely employed in elderly patients with peripheral vascular disease without unduly lengthening the operation too significantly with two-team operating. In addition, the predictability of these flaps with their excellent pedicle lengths is ideal for closure of the resulting oro-nasal surgical defect. The use of a slightly oversized graft is recommended to ensure that any tension on the wound peripheries is kept to a minimum during the healing phase. In addition, for those patients undergoing post-operative radiotherapy, a degree of shrinkage and tightening of the flap tissues is to be expected.\nImmediate/early loading of zygomatic [] and dental implants [] have been well demonstrated already within the literature with very high implant survival rates. In the oncology setting, Boyes-Varley et al. [] lost no zygomatic/oncology implants in their series of 20 patients restored with implant-retained obturators, 6 of whom received radiotherapy post-operatively. The case reported has been followed up for 18 months so far without evidence of zygomatic implant failure despite the use of radiotherapy. A recent review of conventional zygomatic implant surgery demonstrated that the incidence of failure after the 6-month stage was extremely low [] although for zygomatic oncology implants, this data is not yet fully reported in the literature with the only data available on zygomatic oncology implants being limited to the work of Boyes-Valey [], Pellegrino [] and the authors themselves []. The removal of teeth at primary cancer surgery to facilitate placement of implants on the non-defect side requires careful consideration; where teeth are of poor prognosis with poor bone support, it is easier to extract, perform localised osteoplasty prior to the insertion of a conventional zygomatic implant with its inherent excellent stability and ability to be loaded early in the post-operative period. Where teeth have excellent bone support but additional implants are required to facilitate the construction of a fixed prosthesis, then careful extraction of selected teeth with the immediate installation of a root form implant can be utilised with good success as long as high primary stability is achieved at these sites.\nWhilst technically, it would be possible to construct and fit the prosthesis on the same day or even a week later, the need for microvascular flap monitoring in the immediate post-operative period, together with the significant recovery period required by the patient following surgery has lead the authors to delay the fitting of the prosthesis at the 4 to 6-week period post-operatively. In terms of ongoing clinical implant follow-up, no attempt was made at peri-implant probing for the oncology zygomatic implants perforating the soft-tissue flap as it was deemed important not to disturb the soft tissue seal of the skin flap around the implant abutments. No discharge or suppuration was noted during follow-up in this case. Periodontal probing around the conventionally placed zygomatic implants was undertaken periodically during follow up and remained within normal limits.\nThe use of a soft tissue rather than composite reconstruction may also facilitate a shorter hospital stay and allow adjuvant radiotherapy to be delivered in a more rapid timescale with possible impact on overall cure rates of this very debilitating tumour. The initial experiences with this procedure in over ten cases have been extremely positive with excellent appreciation by patients who value being provided with a fixed dental prosthesis so quickly after major surgery. |
A 21-year-old female patient reported to us with the chief compliant of swelling in gums in the upper and lower anterior tooth region. These swellings were increasing in size for the past 15 days and were associated with bleeding gums, purulent discharge, and intermittent pain that were increased on chewing food. She had also noticed increase in gaps between her front upper teeth with slight mobility with the same. The patient was concerned for her compromised esthetics. Her medical history was suggestive of abnormal menstrual cycles and her drug history revealed that she was on hormonal supplements for reducing her body weight. She had a waist circumference of 102 cm and weighed 91 kg. All her vitals were within normal limits.\nThe patient was cooperative and had no reported tissue abuse habits. No abnormality was detected during her extraoral examination. Her intraoral clinical examination revealed soft and edematous gingiva which bled spontaneously on probing. It was associated with purulent discharge with a marked halitosis. There were multiple reddish granulomatous swellings in relation to tooth no. 12, 11, and 21 in the upper arch and 31, 41, and 42 in the lower arch []. There was an associated localized gingival overgrowth covering at least one-third of the clinical crown height on the labial surfaces of teeth. Lesions had pedunculated base, varying from 4 mm × 3.5 mm in 11 and 21 regions to 5 mm × 4 mm in 12 region. A provisional diagnosis of PG was made. The differential diagnosis of the lesion included fibroma, irritational fibroma, peripheral ossifying fibroma, peripheral giant cell granuloma, and hemangioma.\nThe gingiva was painful to touch and the associated teeth were tender on percussion. Periodontal probing was done after administration of local anesthesia. Anterior teeth revealed deeper probing depth measuring around 9–10 mm []. Grade I mobility was also seen with 11 and 21. Radiograph showed presence of angular bone loss in all anterior teeth []. The hematological findings were observed to be within the normal range.\nAn immediate drainage of abscess under local anesthesia was done and suitable antimicrobial and analgesic agents were prescribed. Phase 1 therapy was carried out after a week and was followed for 8 weeks. A significant reduction in gingival inflammation was observed after 8 weeks []. However, there was persistence of localized gingival overgrowth and periodontal pockets. Therefore, an excisional biopsy of the lesion along with surgical pocket therapy was planned and explained to the patient, and written consent was obtained.\nComplete excision of the gingival overgrowth was done with scalpel under local anesthesia and the tissue was sent to the department of oral and maxillofacial pathology for histopathology. Histopathological report revealed hyperplastic, parakeratotic, stratified squamous epithelium with an underlying fibrovascular stroma that consisted of large number of dilated and budding capillaries, plump fibroblasts, and areas of extravasated blood and mixed modified inflammatory cell infiltrate []. The observed features confirmed the diagnosis of PG. Postexcisional biopsy healing was uneventful [].\nSurgical pocket therapy included elevation of full-thickness flap for access []. A papilla preservation flap was planned in relation to 21 and 11 and extended to 16. Surgical sites were thoroughly debrided. An autologous platelet-rich fibrin (PRF) membrane was prepared according to the following protocol: 10 ml of intravenous blood was withdrawn by venipuncture from antecubital fossa into a sterile tube. The tube was immediately centrifuged at 3000 rpm for 10 min. It yielded a fibrin clot in between the top layer of acellular plasma and bottom layer of erythrocytes. PRF membrane was used along with osseous grafts in sites with two or three walled angular osseous defects. Primary closure was achieved with 4-0 nonabsorbable black silk sutures (Ethicon, Johnson and Johnson, Somerville, NJ, USA) and periodontal dressings (Coe-Pak, GC America, Alsip, IL, USA) were placed.\nPostoperatively, the patient was prescribed with antimicrobials and analgesics. Verbal oral hygiene instructions were given in detail. No complaints were reported at 48 h postoperative visit and progress of healing was satisfactory. She was recalled after 7 days, sutures were removed, and postoperative maintenance care was continued at regular interval.\nClinical re-evaluation after 1 year revealed an improvement in clinical parameters [], reduced mobility, and significant bone fill in relation to 11 and 12 []. |
In 1998, a 47-year-old man developed vague symptoms of shortness of breath and fever while on military service in Kuwait. He was diagnosed with and treated for bronchitis at the time. When he returned to the United States, he was evaluated with a transthoracic echocardiogram, which revealed mild aortic regurgitation. He was presumed to have had endocarditis and he was treated and followed up. In 2000, his symptoms worsened and he underwent aortic valve replacement with a St. Jude Toronto stentless porcine valve (Fig.). Despite his young age, he refused a mechanical valve prosthesis since he wished to avoid anticoagulation so he could continue active military duty. Shortly after the procedure, his symptoms resolved and then he was lost to follow-up.\nHe presented twelve years later in the Fall of 2012, at the age of 59, complaining of progressive exertional dyspnea and chest pain. Despite these symptoms, he was still able to exercise about two hours daily, but he noted that this was a substantial decline from his baseline. In December of 2012, he underwent repeat transthoracic echocardiogram, which showed a moderately thickened and calcified bioprosthetic aortic valve with severe regurgitation. He was scheduled for reoperation within a few months. Over the ensuing months, he developed worsening symptoms with orthopnea and lower extremity edema. Repeat transthoracic echocardiogram in April of 2013 showed a markedly dilated left ventricle with severe global hypokinesis and a left ventricular ejection fraction of 20%. He was admitted to the hospital for IV diuresis and inotropic support. He was gradually transitioned to his oral regimen of lisinopril, furosemide, and carvedilol. However, his severe physical decline and cardiomyopathy prompted consideration of heart transplant rather than redo aortic valve replacement.\nHe was transferred to our institution and evaluated by the heart transplant team, who deemed him an appropriate candidate for transplant. However, before listing, they consulted the interventional cardiology and cardiac surgery team regarding other possible options. Although it was unclear whether his left ventricular function would recover even after successful valve-in-valve TAVR, the interventional cardiology and cardiac surgery team counseled the patient regarding the possible risks and benefits. With the patient's consent, he was scheduled urgently for TAVR under a compassionate use protocol.\nPre-TAVR evaluation included a coronary angiogram, right heart catheterization, and CT of the Chest/Abdomen/Pelvis. The angiogram showed normal coronary arteries. Right heart catheterization showed a right atrial pressure of 6 mmHg, right ventricular pressure of 50/6 mmHg, and pulmonary arterial pressure of 50/26 mmHg with a mean of 34 mmHg. The Pulmonary Capillary Wedge Pressure (PCWP) was 27 mmHg, with a blood pressure of 90/50 mmHg, the cardiac output was 3.2 L/min and the cardiac index was 1.9. The pulmonary vascular resistance was 2.2 woods units and the systemic vascular resistance was 1700 dyn-s/cm5.\nCT showed an aortic annulus of 20.4 × 29.2 mm with a perimeter of 76.6 mm and an angle of 35.5° (Fig.). The sinuses of Valsalva measured 32.5, 33.5, and 35.3 mm at the noncoronary, left, and right coronary cusps, respectively. The ascending aorta measured 36.8 × 38.8 mm at a level 40 mm above the valve. The inner diameter of the previous stentless valve was 18.2 × 24.1 mm with an inner circumference of 67.4 mm. The distance from the valve to the right coronary ostium was 16 mm, and the distance from the valve to the left coronary ostium was 14.7 mm. The right coronary cusp was somewhat dilated and the left coronary cusp was asymmetric. Ilio-femoral arterial dimensions bilaterally were all greater than 8.3 mm, without significant calcification or tortuosity. Based on these measurements, a femoral approach was planned with the anticipated use of either a 26 or 29 mm CoreValve prosthesis.\nFor the procedure, an 18F sheath was inserted via surgical cut down in the right femoral artery and the aortic valve was crossed with a 0.35 mm straight wire. A pigtail was advanced over the wire into the left ventricle and baseline hemodynamic measurements were performed. An exchange length pre-shaped Lunderquist wire was advanced against the left ventricular apex. After removal of the pigtail catheter, a 26 mm CoreValve prosthesis was passed and partially deployed (Fig.). Even with partial deployment, we found that the annulus of the previous stentless valve gripped the CoreValve device. Any attempt to position the device by pulling back encountered considerable resistance. During this process of repositioning, the partially deployed CoreValve, the valve abruptly popped back across the stentless valve. We resheathed the device and removed it.\nWe next attempted to deploy a 29 mm CoreValve prosthesis with the plan to deploy the valve at a greater depth because of the asymmetry of the coronary cusps due to the previously described left cusp. Again when trying to adjust the depth of the device by pulling back on the valve, we encountered considerable resistance, with subsequent popout of the valve again. As with the first attempt, the bioprosthetic annulus gripped the CoreValve precluding adjustment. We resheathed the valve and removed it.\nFinally, a third Corevalve prosthesis (26 mm) was attempted and successful deployment was obtained through a different strategy. Instead of allowing the valve to advance across the annulus with subsequent withdrawal to an optimal position, we pushed the wire against the LV apex, and oriented the device using the left coronary cusp as the reference. Pushing on the wire resulted in its being oriented against the greater curvature of the aorta (Fig.). Following partial deployment, we noted that the device was relatively deep with respect to the non- and right coronary cusps, but was ideally oriented to the deformed left coronary cusp. As opposed to the first two attempts, this time we simply pushed on the wire and did not pull back on the valve with our usual counter-traction. This maneuver resulted in a more optimal angle across the aortic valve, which better matched the orientation of the stentless valve and allowed for successful deployment (Figs. and ). Postprocedure TEE showed negligible aortic regurgitation. The postprocedure transvalvular gradient was 8 mmHg. The patient had a rapid postprocedure recovery and reported much improved symptoms by the time of discharge. Discharge TTE showed mild-moderate perivalvular aortic regurgitation (Fig.) and follow-up transthoracic echocardiogram at five months showed a well-seated valve with mild perivalvular aortic regurgitation and complete resolution of his LV function to normal. |
A 30-years old woman visited at our hospital, complaining of pain in her lower back, left inguinal area, and left leg. Two months before this visit, she was found to have a mass growing in her left thigh, which was causing her pain (). The tumor in her thigh was removed surgically. Her excisional biopsy revealed fibromatosis of the rectus femoris muscle. Following the procedure, she continued to experience pain at the operated site, as well as pain in her left inguinal region. Starting from day 3 after the surgery, the previously mentioned pains were accompanied by pain in her lower back and in the medial side of her left knee. She was asked to rate her pain using a visual analogue scale (VAS) and her rating, on average, was 100/100. She was admitted to the hospital due to the high severity of her pain. She complained of more severe pain when sitting or lying down on her back.\nPhysical examination found hyperesthesia and static allodynia in the left medial side of her affected leg. Both her left hip flexion (G 4/5) and left knee flexion (G 4/5) were diminished. The results of her straight leg raise test and trendelenburg test were normal. Her blood test results revealed an elevated erythrocyte sedimentation rate and C-reactive protein concentration of 56 and 4.49, respectively.\nOn her first day at the hospital, motor nerve conduction studies were performed. The results showed that the compound motor action potential amplitudes in her left femoral nerve were within the normal range but were reduced as compared with her right femoral nerve. Sensory nerve conduction tests revealed that sensory nerve action potentials were not obtained in her left saphenous nerve or in her medial femoral cutaneous nerve. Electromyography (EMG) results showed increased insertional activity in the left vastus lateralis, fibrillation, positive sharp waves (2+), and diminished recruitment. Based on the results, femoral neuropathy was suspected and pregabalin 150 mg and duloxetine 60 mg were, accordingly, administered.\nTwenty-one days into her hospitalization, the pain in her left lower leg diminished slightly, to 30/100 on her VAS rating. However, the pain in her left inguinal area and in the medial side of her left knee continued. Thus, a femoral nerve block was performed and the dosage of pregabalin was increased to 300 mg and administered along with duloxetine 60 mg. On the patient's thirty-five days of hospitalization, the pain in her left inguinal area improved. In contrast, the pain in the medial side of her left knee worsened to 100/100 on her VAS rating. Significantly reduced sensory reflex responses to cold (2/10), touch (0/10), and pinprick (0/1) were found in the medial side of her left knee. No allodynia was found. After a left L3 transforaminal epidural steroid injection, the pain in the medial side of her left knee showed an improvement based on her VAS rating of 40/100. She was, therefore, discharged from the hospital. On the thirty-six days after her first visit to the hospital, her leg pain diminished. Nevertheless, she experienced abdominal pain, nausea, and vomiting and came to the ER at the hospital to have those symptoms treated. Her abdominal X-rays revealed an ileus and abdominal computer tomography tests showed a huge retroperitoneal mass. These findings led to performing lumbar spine magnetic resonance imaging (MRI) (), which found disc degeneration accompanied by an annular tear in L5-S1 as well as a mass in her left iliopsoas muscle. In addition, her torso PET scans () revealed a suprarenal mass in her right side, as well as tumors seeded in her left psoas muscle, in both lungs, and in her pleura and peritoneum.\nA needle aspiration biopsy was performed on the mass in her left psoas muscle. The results showed a well-differentiated liposarcoma. With this diagnosis, the patient was transferred to the department of internal medicine at the hospital to receive treatment for her metastatic retroperitoneal liposarcoma. |
A 52-year-old male patient presented with the complaint of sudden vision loss in his left eye 3 days earlier. Past medical history was significant for chronic kidney disease, secondary hypertension, chronic hepatitis C virus infection and arrhythmia. Ophthalmologic examination revealed best corrected visual acuity of 10/10 in the right eye and 4/10 in the left eye from the temporal field. Confrontation test revealed inferonasal visual field loss in the left eye. Direct and indirect light reflexes were normal in both eyes and there was no relative afferent pupillary defect. Anterior segment examination was normal and intraocular pressure was 13 mmHg in both eyes. Dilated fundus exam demonstrated soft exudates consistent with hypertensive retinopathy in the right eye. Fundoscopy of the left eye revealed an area of pallor in the superotemporal quadrant and the macula with macular cherry red spot, which were consistent with occlusion of the superotemporal branch of the left retinal artery (). On OCT, peripapillary retinal nerve fiber layer (RNFL) thickness was within normal limits (). In the patient’s visual field, there was an inferonasal defect in the left eye corresponding to the occluded region (). The patient was treated with a single dose of 500 cc intravenous dextran-40 and 200 mg intravenous pentoxifylline. In etiologic studies, Doppler ultrasonography revealed an atherosclerotic stenosis in the right and left main carotid arteries and a calcified plaque causing luminal narrowing in the left internal carotid artery. Transthoracic echocardiography revealed second- to third-degree aortic valve regurgitation and first-degree tricuspid valve regurgitation. There was no improvement in visual acuity or visual field despite treatment. At follow-up 7 months later, OCT showed thinning of the superior, inferior and temporal peripapillary RNFL (). On the thickness map, ganglion cell layer was thinner in the superior and temporal areas (). Decreased vascular density in the superficial and deep capillary plexus consistent with ischemia in the regions supplied by the superotemporal branch of the retinal artery was observed in a 6x6 mm macular field on OCTA (). The borders of the ischemic area were more clearly seen in en face images (). In optic disc OCTA, capillary density was reduced in the superotemporal region and collateral vessels were present in the area (). When compared to the fellow eye, there was a decrease in the macular deep and superficial capillary density in the superior and temporal quadrants () and a decrease in peripapillary capillary density in the superior quadrant (). Visual field loss persisted in post-treatment threshold perimetry (). |
A 55-year-old, Caucasian woman was referred to our tertiary women’s heart center for persistent chest pain, palpitations, and dyspnea. Her medical history included hypertension, dyslipidemia, chronic anxiety, and bilateral non-obstructive carotid atherosclerosis. She had no prior history of diabetes mellitus, tobacco smoking, alcohol or substance abuse, or adverse pregnancy outcomes. Her family history was significant for premature coronary artery disease. Her father had a history of hypertension and had a myocardial infarction (MI) and coronary artery bypass grafting at the age of 39. Her brother had a history of coronary artery disease and also had a MI at the age of 40. Her occupational history indicated that she had been working in the field of psychology and was still an employee in the same job at the time of the hospital visit and follow-up care.\nTable summarizes the general symptoms and characteristic signs of our patient for the onset of CMD and her progression to HFpEF. She had undergone an exercise treadmill test which revealed ischemic ECG changes and dyspnea. Her initial echocardiogram demonstrated a LVEF of 67%, mild diastolic dysfunction, mild left ventricular (LV) hypertrophy, no significant valvular heart disease, and no pulmonary hypertension. Subsequent invasive left heart catheterization was performed and it showed normal epicardial coronary arteries without angiographic evidence of atherosclerotic plaque. She continued to have exertional symptoms and angina-like chest pain and was subsequently referred to our center for further evaluation of suspected INOCA. During her evaluation and treatment she continued to experience stable angina and exertional dyspnea despite initial management with atorvastatin 20 mg daily, lisinopril 20 mg daily, aspirin 81 mg daily, and sublingual nitroglycerin as needed. She had a poor clinical response to sublingual nitroglycerin. Due to her persistent symptoms and abnormal stress testing, she was referred for coronary reactivity testing (CRT) to establish the diagnosis of CMD.\nOur patient underwent invasive CRT, as previously published []. Testing demonstrated normal coronary flow reserve (CFR) in response to intra-coronary adenosine (CFR 3.1; normal ≥ 2.5), abnormal macrovascular endothelial function to intra-coronary acetylcholine (− 6% change in coronary diameter, constriction; normal, dilation), abnormal microvascular endothelial function (coronary blood flow change 48%; normal ≥ 50%), and abnormal non-endothelial function to intra-coronary nitroglycerin (coronary diameter change + 0%; normal dilation) (Table ). She also underwent cardiac magnetic resonance imaging (CMRI) with perfusion imaging at rest and with adenosine stress (140 μg/kg per minute) which showed circumferential subendocardial perfusion defect at stress, normal LV end-diastolic volume indexed to body surface area (EDVi) of 56.4 mL/m2, LV mass index 42.3 grams/m2, and no LV hypertrophy (septum 7.2 mm and lateral wall 6.0 mm). The myocardial perfusion reserve index (MPRI) was 1.8 which was considered borderline abnormal [] (Table ). There was no evidence of myocardial scar.\nThe diagnosis of CMD was established by the coronary endothelial dysfunction observed with invasive CRT, and carvedilol and eplerenone 25 mg daily were added to her regimen. She was followed regularly in clinic with good control of her blood pressure and serum lipid levels. She reported improvement of her angina and dyspnea along with reduction in the duration and frequency of these episodes.\nTen years after her initial diagnosis of CMD, our patient was hospitalized due to symptoms of dyspnea. She was found to have elevated brain natriuretic peptide (BNP) levels of 406 pg/mL and normal LVEF. She had a computed tomography (CT) angiogram of her chest to evaluate for pulmonary embolism, which was negative but revealed bilateral pulmonary edema. She was treated with intravenously administered furosemide for pulmonary edema and diagnosed as having HFpEF. Subsequently, she was discharged with instructions to increase her eplerenone.\nShe continued to experience worsening dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. A repeat echocardiogram demonstrated normal LV systolic function with an LVEF of 64%, and diastolic dysfunction as evidenced by decreased lateral E′ velocity (4.2 cm/s, indicating impaired myocardial relaxation) and elevated E/E′ ratio 12.9 (suggestive of increased LV filling pressure). She underwent coronary CT angiography which showed absence of coronary atherosclerotic plaque and a coronary calcium score of 0. She was diagnosed as having HFpEF based on clinical symptoms, preserved ejection fraction of 64%, elevated BNP, and evidence of diastolic dysfunction.\nAs part of the WISE – Coronary Vascular Dysfunction (WISE-CVD) Continuation Study (NCT00832702), she underwent a repeat rest-stress CMRI to assess myocardial structure, function, perfusion, and scar, and 13C magnetic resonance (CMR) spectroscopy. Compared to her prior CMRI 7 years ago, she had an increase in LV wall thickness in both the septum and lateral wall (Table ). On CMR spectroscopy, the myocardial triglyceride content was elevated (0.83%) compared to normal control women (mean 0.43%), suggesting myocardial steatosis which is consistent with an ischemia-induced metabolic shift and HFpEF phenotype []. Adenosine stress first pass-perfusion CMRI again showed circumferential subendocardial hypoperfusion (Fig. ) and her MPRI worsened from 1.8 to 1.1, consistent with severe CMD []. There was no evidence of scar on late gadolinium enhancement imaging. |
A 35-year-old male attended the orthopedic outpatient department with complaints of displacement of the left patella as he moves his knee into flexion. He first noticed this symptom 3 months before, when he started mobilization exercise of his left knee following a surgical procedure. He had a history of a twisting injury to his left knee during a road traffic accident 9 months back. He experienced buckling of his left knee following that accident, and a magnetic resonance imaging (MRI) showed a torn anterior cruciate ligament (ACL) at the mid-substance level. After 2 months, he underwent an arthroscopic ACLR using the ipsilateral semitendinosus autograft in a local hospital.\nThe patient developed discharge from the surgical wound site associated with fever on the seventh postoperative day. The inflammatory markers, including the erythrocyte sedimentation rate, C-reactive protein, and the total leukocyte count, were elevated. Finally, he got diagnosed with septic arthritis, and arthroscopic debridement of the knee was done in the same hospital, preserving the graft. The condition got resolved initially, and the patient began the mobilization exercises with gradual improvement. However, the features of septic arthritis reappeared 3 months later. The patient underwent a repeat arthroscopic debridement with removal of the graft after 2 weeks of the onset of this second episode of infection. The patient began the range of motion exercise on the second day of this surgery and noticed the patella is dislocating every time he flexes his knee.\nOn clinical examination, we found dislocation of the patella on each cycle of flexion of the knee, which reduces spontaneously on the extension (). Since, unlike recurrent dislocation, the patella was relocating on the extension without any pain and swelling, we termed it a habitual dislocation of the patella. However, there were no signs of active infection. The surgical scar marks of previous procedures were observed, including scars of superomedial, and superolateral, portals. Furthermore, there was no generalized hyperlaxity or exaggeration of anteversion of the femur. The Q-angle was 15°. The skyline view radiograph of both the knees did not indicate trochlear dysplasia considering the sulcus angle on the left side, which was 130° (). The Insall Salvati ratio measured by dividing patellar tendon length to patellar height was 0.8.\nOn further evaluation, we found the tibial tuberosity-trochlear groove (TT-TG) distance to be 18.4 mm (), which indicates a mild distal malalignment that predisposes the patient to dislocation of the patella. We performed an MRI of the left knee and noticed a medial patellofemoral ligament (MPFL) tear ( and ). The MPFL must have been injured during the surgery, as the patient experienced his first dislocation immediately after the second arthroscopic debridement procedure and as the initial MRI performed before the ACL reconstruction suggested an intact MPFL. Therefore, we made a diagnosis of iatrogenic MPFL tear.\nFor the habitual dislocation of the patella, we planned an MPFL reconstruction using the contralateral semitendinosus autograft. Despite explaining the need for surgical intervention, the patient denied any surgical procedure and preferred non-operative management. At 2 years of follow-up, the patient does not have any pain in his left knee and complaints of only mild buckling while walking on uneven ground. However, the habitual dislocation of the patella persists. Nevertheless, the patient performs his daily pursuits, including walking, squatting, and climbing stairs without much difficulty. There are no features suggestive of any active infection. The recent radiograph shows signs of early osteoarthritic changes (). The patient is still unwilling for any surgery and is under our regular follow-up. |
Mr P was a married man in his 40s with one child. He had served in the UK army and was deployed to the Bosnian conflict in the mid-1990s. During his deployment he was stationed at a morgue that had been set up to aid the identification of bodies recovered from a mass burial site. He described how the morgue contained a large number of bodies in various states of decomposition, with varying degrees of physical trauma. He reported re-experiencing fragmented intrusive images of the morgue and daily emotionally distressing nightmares of which he could not recall the content. He experienced high levels of anxiety that triggered his dissociative symptoms. These appeared to function as a coping strategy to avoid distressing emotions connected to his memory of the morgue. Other avoidance symptoms included feeling detached from people around him and feeling emotionally numb. Mr P avoided family occasions and busy places which could trigger his hyper-arousal symptoms and had never spoken to anyone about his experiences. He reported coping historically through the use of alcohol to block out his emotions. His avoidance behaviours had maintained his PTSD symptoms.\nAt the start of therapy sessions, Mr P was reluctant to talk about his past experiences stating he only felt able to discuss vague details about his intrusive memories. Mr P attempted to use physical objects such as stones and leaves, or his e-cigarette, as grounding strategies in the clinic room. However, he also reported feeling unable to tolerate any emotions connected to the events and found it difficult to identify peri-traumatic cognitions. Mr P appeared to experience intrusions of one particular fragmented image and could not recall any other contextual information from before or after this moment.\nIn both cases Mr C and Mr P experienced difficulties in engaging with traditional methods of imaginal reliving and prolonged exposure, due to high levels of avoidance and low thresholds for dissociation, and subsequently had difficulties accessing their cognitions for updating. For both clients the prior use of multiple grounding methods in the therapy room were unsuccessful. They experienced their traumatic memories as fragmented images with a sense of ‘nowness’ (), which indicated a distinct lack of contextualization.\nAn adaptive approach was then trialled to address these hindering factors. This involved three stages: (1) walking the client through the imaginal scene outdoors to address dissociation, (2) viewing the imaginal scene from multiple perspectives to facilitate contextualization of the memory and (3) identifying and reappraising the cognitions with frequently used approaches in trauma-focused therapy. |
A 50-year-old Caucasian female visited the regional dental office due to uncertain pain in the right mandibular region. No significant diseases were mentioned in the anamnesis. The patient was diagnosed with gingivitis, and treated with a non-steroid anti-inflammatory drug and oral rinsing with chlorhexidine. The condition of the patient did not improve significantly. When she returned a week later, she had no alleviation, but labial paresthesia on the right side of her lip. As the cause of the new symptom remained unidentified, she was referred to the oral surgery group. Initially, the paraesthesia affected only the right side of the lower lip, but by this time it had spread to the skin of the right side of her chin. The oral surgeons decided to extract the lower right wisdom tooth, but the labial paraesthesia still persisted. Since there was an extended composite restoration in the lower right first molar, and translucency around its apical region was visible, the lesion was diagnosed as periapical granuloma. The lesion on tooth 46 was not close to the mandibular canal; this can be seen on Fig. . Therefore, root canal treatment was carried out, despite the uncertain result of the percussion, palpation and sensibility test. The transparent lesion around the apex and the negative sensibility test lead to the decision of endodontic treatment. Diagnosis was made by a dentist who is not a staff member of our Department. The treatment revealed that the pulp was vital. Our oral diagnostic team examined the patient, and we diagnosed the case as cemento-osseous dysplasia based on the panoramic radiograph showing apical translucency lesions around the anterior teeth with vital pulp (Fig. ). The paraesthesia has been continually present ever since. Because the lesion around the lower right canine had already involved the cortical bone by CBCT scan (Fig. ), a root canal filling and removal of the apical lesion were performed. On the CBCT image the involvement of the entire periapical region can be seen including the lingual region and the buccal cortical (Fig. ). It became clear during the planning of the surgery that the blood vessels and nerves of tooth 43 would be injured.\nThe root canal treatment was carried out on the lower right canine in a single-visit treatment using local anaesthaesia. We explored the entire root canal length using a size #15 hand instrument. The working length was determined using an apex locator, (Woodpex III, Guilin,China), then the length was also confirmed with radiographic imaging. Following the length determination, the root canal was shaped using Wave One (Densply Maillefer, York, USA) rotary instrument. The root canal was obturated using guttapercha and AH Plus sealer (Dentsply DeTrey GmbH, Konstanz, Germany) with lateral condensation technique. Glass ionomer cement (Fuji IX GP, GC Co., Tokyo, Japan) was then applied to seal off the access cavity, while the permanent restoration was done.\nWe prepared an intraoral mucoperiostal flap using an L-shaped incision and the surgery was carried out by using a surgical microscope (Aspheron, Schmidt and Bender Hungaria, Budapest, Hungary).\nWe opened up the buccal cortical bone using a surgical bur, thereafter we removed the lesion surrounding the apex of the root. The root apex was resected and a retrograde root canal filling was placed using mineral trioxid aggregate (MTA+, Cerkamed, Stalowa Wola, Poland).\nThe area of the lesion was augmented using gentamicin impregnated BoneAlbumin (OrthoSera Dental Zrt., Gyor, Hungary). We seeked to lower the chance of osteomyelitis occuring with the use of gentamicin. Sutures were then carefully placed to achieve tensionfree closure of the flap for optimal healing.\nThe 19-year-old Caucasian woman is the daughter of the first patient. CBCT showed a radiolucent lesion around the root of the lower right incisor (Fig. ). She is presently asymptomatic after a one-year follow-up, but she occasionally felt tension and moderate pain in the right side of the mandibular region eradiating to her ear, approximately 2 years earlier. The symptoms had no dental background, and ceased gradually.\nPulp tests and periapical pathology diagnoses were made by authors on teeth 33,32,41,43 with the use of percussion, palpation and sensibility test.\nPanoramic radiograph and CBCT scans of the first patient showed radiolucent lesions located in the periapical bone, specifically on lower incisors and canines – in the premandibular, and in the right molar region of the mandible with radiopaque parts showing the lesions inside (Figs. and ). The affected teeth were asymptomatic, CBCT proved the presence of apical pathology. The buccal cortical involvement was discovered with the aid of CBCT, which also affected the treatment plan because 2D imaging methods provide no information on bucco-lingual dimension. Prior to the surgical intervention the use of CBCT was motivated by the fact that only 3D imaging could ascertain the precise shape, location and involvement of surrounding anatomical landmarks of the lesion.\nFigure shows the postoperative condition (Fig. ). At the 6-months periapical follow-up, the bone healing is being processed (Fig. ). 18 months later it can be seen on the CT image that the buccal cortical bone surrounding the root of tooth 43 has regenerated (Fig. ). In the case of the second patient, there were no notable changes in the radiographic status 1 year later, and she has no complaint at present.\nThe removed tissue pieces contained both connective tissue and calcified areas. In the calcified area, beside the irregular trabecular – lamellar bony formations, oval and globular cementum-like structures were present. In the non-calcified area connective tissue was found and connective tissue filled out the centre of another bony sample as well. No elements or remnants of a capsule were visible. The histological diagnosis was cemento-osseous dysplasia (Fig. ). |
A 66-year-old male with known history of hypertension and hypothyroidism presented to the emergency department (ED) with sudden, painless loss of vision in his left eye of two hours duration. The patient reported that he had sneezed four times in rapid succession and then stated he lost vision in his left eye, but experienced no eye pain. The patient then drove himself to the ED. He denied any other accompanying symptoms on extensive review of systems. Examination revealed 20/30 vision in his right eye with corrective lenses (eyeglasses), but no light perception in his left. The left pupil did not have any direct light response but had preserved consensual response. Consensual light response was absent in the right pupil, but direct response was preserved. Point-of-care ocular ultrasound was performed but did not reveal any apparent abnormality. The patient had no other focal neurological deficits and was found to be in normal sinus rhythm on electrocardiogram. Tonometry was not available at this facility nor were ophthalmologic services. A head computed tomography (CT) without contrast showed no acute hemorrhage or apparent infarct and he was sent emergently to the ophthalmology clinic at the tertiary care hospital several miles away in consultation with the receiving ophthalmologist.\nIn the ophthalmology clinic, the patient was confirmed to have multiple arterial thrombi with characteristic cherry-red spot on exam consistent with CRAO. He was then transferred directly from the ophthalmology clinic to the hyperbaric chamber for hyperbaric oxygen therapy. Upon the initial dive at 33 feet of therapy he began seeing letters and his vision continued to improve after one hour at 60 feet. Vision in the affected eye improved from solely light perception to 20/50 at 24 hours, with subsequent resolution of symptoms. Shortly thereafter, while inpatient he received CT angiography of the neck and head (), which revealed complete left internal carotid artery (ICA) occlusion at its origin with retrograde filling of the distal cervical and intracranial portions. The right ICA showed regions concerning for dissection with associated pseudoaneurysm formation, with another region just distal with critical narrowing of the cervical internal carotid artery to approximately one millimeter.\nSeveral days later the patient underwent successful transcarotid artery revascularization in the operating room. |
A 64-year-old heavy smoker male patient was admitted for the first time to our urology department for hematuria and dysuria. His past medical history was unremarkable. He had a transurethral resection of the prostate 5 years ago. He did not have any familial history of urothelial or bladder cancer. Physical examination and blood tests were normal. In the emergency room, an abdominal and pelvic ultrasound showed a thickening of the right lateral wall of the bladder with mild right side hydronephrosis (). On cystoscopy, a large tumor was found on the anterior and right lateral walls of the bladder, with invasion of the bladder neck and the prostate. The anatomopathological study of the tumor showed a neoplastic proliferation of large malignant polygonal cells with dark, irregular nuclei and frequent mitosis. A second component made of cylindrical cells was also present. Muscular invasion was documented with multiple necrotic areas (). Immunohistochemistry showed high positivity for CD56 marker and synaptophysin, minor and heterogenic positivity for cytokeratin 7, and negativity for cytokeratin 20 and CDX2 (Figures –). Overall, the histopathological study corresponded to LCNC with minor adenocarcinomatous component. Disease extension was assessed using computed tomography (CT) scan of the thorax, abdomen, and pelvis. A 6 × 3.5 cm mass of the anterior and right lateral walls of the bladder was identified, with diffuse infiltration of the perivesical fat and multiple necrotic iliac lymph nodes bilaterally (). Neither visceral nor bone metastasis was identified. Initially, the patient refused the treatment and was lost to follow-up. Two months later, he was readmitted to the hospital for similar complaints and additional pelvic pain. Blood tests were normal. A new CT scan revealed an increase in the size of the tumor, occupying now the majority of the bladder lumen, a persistent right hydronephrosis, and no new secondary lesions. The tumor was resected again, until the appearance of the muscular layer of the bladder, and the patient was discharged after stabilization. A later PET CT confirmed the previous findings of locoregional disease (tumor of the bladder base with infiltration of the prostate gland and a diffuse metastatic bilateral iliac chain and retroperitoneal lymph nodes) and denied secondary lesions. The multidisciplinary team meeting decided for radiotherapy and chemotherapy using cisplatin and etoposide every 21 days. Four months later, after the completion of four cycles of chemotherapy, the patient underwent new assessment for disease extension (). CT scan showed progression of the disease with the tumor occupying now the totality of the bladder lumen, infiltration of the anterior abdominal wall, and subcutaneous liquid collection measuring 33 × 36 mm. A similar left retrovesical mass of 60 × 38 mm along with multiple para-aortic and mediastinal lymphadenopathies with central necrosis was also found. A few months later, the patient died in the oncology department after recurrent admissions for different complications. |
A 63-year-old woman, with arterial hypertension as the only relevant medical history, presented with a sudden binocular diplopia. Right 6th nerve palsy was evidenced on physical examination at admission. AngioCT revealed a right ICCA aneurysm with signs of partial thrombosis without evidence of rupture []. Patient’s symptoms worsened to complete cavernous syndrome 5-days later, and a new AngioCT showed progression of the thrombosis with discrete mass effect [], so steroids and antiplatelet therapy were initiated. Angiography on admission confirmed the presence of a giant aneurysm of the anterior portion of the right ICCA [-]. Since endovascular techniques seemed inappropriate due to the partially intraluminal thrombosis and very wide neck, PAO was considered as the optimal treatment choice. A balloon test occlusion (BTO) was performed to evaluate the preoperative risk of ischemia without relevant findings and no evidence of retrograde filling of the aneurysm by anterior or posterior communicating arteries [ and ]. Then, the patient underwent surgical ligation of the cervical CCA at the level of C6 with a 3/0-silk, and anticoagulation was started 3 days after surgery. Symptoms of cavernous sinus syndrome resolved with the exception of 6th nerve palsy during postoperative recovery. A cerebral magnetic resonance angiography (MRA) revealed decrease of the size of the aneurysm lumen and no ischemic lesions were detected [].\nNine months later, and without new neurological symptoms, signs of aneurysm growth were detected in a serial MRA [], and a new angiography was planned. Right CCA angiogram showed the therapeutic occlusion of the right ICA, but the right vertebral angiogram demonstrated proximal partial recanalization of the ICCA aneurysm. Collateral supply was explained from the external carotid artery (ECA) through the occipital artery with an inverse flow to the ICA []. Therefore, surgical occlusion of the cervical ICA at the level of the ansa cervicalis of the hypoglossal nerve with a 0-silk was performed, and intraoperative Doppler ultrasound revealed no efferent flow in ICA. Postoperative new angiography confirmed the total occlusion of the aneurysm []. After 6 years of follow-up, we have not detected refilling or thromboembolic events []. |
A 63-year-old female was admitted to Tokyo Rosai Hospital with discomfort in the right lower quadrant, which the patient had being experiencing since approximately January 2011. Physical examination revealed no tenderness; however, a palpable, fist-sized mass in the right lower quadrant prompted abdominal CT, which revealed a 60-mm cystic mass at the site corresponding to the appendix with calcification in its wall on the appendicular tip. With no thickening or contrast enhancement in the entire wall of the mass, cystadenoma, as opposed to carcinoma was suspected (). Since the possibility of carcinoma could not be ruled out, surgical removal of the mass was recommended; however, the patient refused surgery and was placed on a careful outpatient follow-up program.\nThree months later, the patient returned to the hospital. Abdominal CT revealed no changes compared with the previous examination. The patient was advised to return to the outpatient clinic in 3 months; however, the patient did not return. Later, the patient presented with persistent pain in the right lower quadrant, which the patient had experienced since August 2012. On examination, a mass was felt in the right lower quadrant that resembled the one felt previously and tenderness was experienced at the same site. The patient was then admitted for workup. The patient had no history of alcohol or smoking and the prior medical history included surgery for internal hemorrhoids at the age of 59 years. No signifant family history was reported and no oral medication was being used. On admission, the patient had clear sensorium and a blood pressure of 123/73 mmHg, a pulse rate of 60 beats/min (non-arrhythmic) and a body temperature of 37.5°C. The palpebral conjunctiva was not anemic and no yellow discoloration of the bulbar conjunctiva was observed. Heart and breath sounds were noted to be clear. The abdomen was flat and soft with a palpable fist-sized mass present in the right lower quadrant. The mass was slightly hard and minimally movable with tenderness; however, no rebound tenderness or muscular rigidity was apparent. The liver and spleen were impalpable. Hematological examination on admission revealed mild anemia (hemoglobin, 11.4 g/dl) and increased inflammatory reaction (C-reactive protein, 6.5 mg/dl). No increase in the levels of tumor markers was observed ().\nAbdominal CT on day 2 revealed no change in the size of the existing cystic mass from the previous CT scan performed in January 2011; however, it revealed thickening of the mass wall on the appendicular ostium and contrast enhancement at the corresponding site. No projection was observed in the mass cavity (). On abdominal US on day 2, the mass was anechoic overall and demonstrated a partly layered echo pattern. The mass wall on the appendicular ostium was thickened with a 13-mm projection protruding toward the cavity from part of the wall. Another 9-mm projection was also observed in the appendicular tip ().\nCEUS was then performed to assess blood flow using a Toshiba SSA-790A US system (Aplio XG; Toshiba Medical Systems, Otawara, Japan) with a 3.75-MHz convex probe (PVT-375BT). Imaging was performed with a mechanical index of 0.21 and the focus was adjusted to the depth of the mass. After imaging conditions were set, Sonazoid (perfluorobutane; GE Healthcare, Oslo, Norway) was infused at the recommended dose of 0.015 ml/kg via the cubital vein. Contrast enhancement was observed in the thickened wall of the mass on the appendicular ostium and in the projection on the same side; however, not in the projection on the appendicular tip ().\nBased on the thickened and contrast-enhanced wall of the mass on the appendicular ostium on abdominal CT and US, as well as contrast enhancement of the projection on the appendicular ostium on US, the mass was diagnosed as mucinous cystadenocarcinoma of the appendix and ileocecal resection was performed on day 10. The mass was excised with surrounding connective tissue with care taken not to break the mass.\nThe appendix was swollen with a 60-mm cyst with a glossy white surface. No rupture of the mass was observed ().\nThe mass wall was thickened on the appendicular ostium and accompanied by enlarged nuclei and pseudostratified cells, leading to the diagnosis of adenocarcinoma. The protrusion on the appendicular ostium was located inside the thickened wall and composed of granulation tissue with proliferating capillaries. The protrusion on the appendicular tip was composed of mucus, and part of the wall was calcified (). |
A 59-year-old woman presented for evaluation of hoarseness which had persisted for 1 month. She was diagnosed with asthma at the age of 28 and fluticasone propionate had been administered in a daily dose of 500 mcg for many years via the use of a large volume spacer device. She previously experienced two to three asthma exacerbations annually which responded to pulse doses of oral corticosteroids. Ten years prior to the development of hoarseness, immunoglobulin E (IgE) specific antibodies to aspergillus and aspergillus precipitins were negative and a serum IgE level was 135. Previous attempts at discontinuation of inhaled corticosteroids resulted in more frequent exacerbations of her asthma symptoms and a methacholine challenge test had demonstrated significant bronchial hyperresponsiveness. At the age of 51, she was diagnosed with focal bronchiectasis in the right middle lobe which had been associated with recurrent Pseudomonas aeruginosa infection treated with courses of anti-Pseudomonal antibiotics. Her medical history also included cigarette smoking, 15 sticks/day for 7 years until the age of 26. There was no history of immunodeficiency, malignancy, or diabetes mellitus. Lung function testing at the time of presentation was normal with a forced expiratory volume in one second of 2.72 L (111% predicted). A referral was made for an ear, nose, and throat opinion and she underwent microlaryngoscopy which demonstrated a cystic lesion of the left vocal cord (Fig. ). This was excised and the histopathology demonstrated a laryngoma with fungal colonies containing branching hyphae, consistent with aspergillus (Fig. ). Unfortunately, the excised tissue was not sent for culture or polymerase chain reaction analysis. Recent measurements of aspergillus precipitins were negative and a serum IgE level was normal. She was treated with itraconazole as the treatment of choice, and inhaled corticosteroids were ceased. She remained on inhaled salbutamol as required, and her asthma symptoms were infrequent. Repeat laryngoscopy at 3 months demonstrated complete resolution of the lesion. Fiberoptic bronchoscopy and bronchial washings after the diagnosis of laryngoma did not demonstrate fungal elements on cytologic examination and fungal cultures were negative. Investigations for underlying B or T cell-associated immunodeficiency were normal. The patient has been followed for 18 months since the onset of vocal cord aspergillosis and there has been no recurrence of the fungal infection. |
A 31-year-old male was injured by baamboo and was admitted to Fuding People’s Hospital (Fuding, China) for wound debridement and suturing. However, the patient was transferred to The Affiliated Hospital of Wenzhou Medical College (Wenzhou, China) due to progressive swelling and numbness of the right chest wall and absence of pulses in the right upper limb. Physical examination showed that the patient was anemic, with a reduced level of consciousness, clear breath sounds bilaterally and blood pressure <70/40 mmHg in the left upper limb following volume expansion. Oxygen saturation of the right upper limb was 0% and the pulse rate was 110 bpm. There were two right thoracic wounds; a 2-cm wound located 1.5 cm below the medial end of the clavicle, and a 3-cm wound located below the lateral end of the clavicle in the anterior axillary fossa. The wounds were sutured, with evident capillary hemorrhage in the wound at the lateral end of the clavicle. The right chest wall and the right upper limb were swollen. The right axillary, brachial and ulnar pulses were absent, and there was no capillary return in the fingers. Traction on the limb produced pain and increased numbness. Muscle strength was grade II and muscle tone was normal. Thoracic CT scan images are shown in . The patient was diagnosed with hemorrhagic shock, right axillary artery injury, right brachial plexus injury, right scapular fracture, damage to the right shoulder muscles and a large right shoulder hematoma. This study was approved by the ethics committee of First Affiliated Hospital of Wenzhou Medical College. The informed consent was obtained from the patient.\nColor ultrasonography showed an injury at the junction of the right subclavian artery and the axillary artery. Emergency repair of the injury was performed under general anesthesia with tracheal intubation. A longitudinal incision was made on the medial aspect of the right upper arm and an endovascular stent delivery catheter system was inserted into the brachial artery. C-arm fluoroscopy-guided arteriography showed leakage of contrast medium from the proximal segment of the axillary artery and the distal vessels were not visualized (). A 5-cm Wallgraft artificial coated endovascular stent with Unistep Plus propulsion system (Boston Scientific Ireland Ltd., Galway, Ireland) was placed in the injured vessel. Arteriography following stent placement showed contrast medium passing normally through the proximal axillary artery, with distal and collateral vessels clearly visualized (). Radial and ulnar pulses were palpable following the procedure, but limb swelling increased following the intervention, possibly due to ischemia/reperfusion injury and venous injury. Considering the signs of brachial plexus injury, an exploratory surgery was performed immediately. During the surgery, exploration revealed a false aneurysm in the proximal segment of the axillary artery. Following removal of the hematoma, a 1.5-cm U-shaped wound was covered with a coated endovascular stent. Gauze was used to stop bleeding and the ruptured accompanying vein was ligated. There was no disruption of the brachial plexus and the surrounding hematoma was removed. Clopidogrel was administrated orally for 2 weeks to inhibit platelet aggregation postoperatively.\nOne week after injury, a CT scan of the right clavicular region showed that the stent was correctly positioned and patent, with no surrounding false aneurysm. A second-look surgery was performed to remove the gauze and the organized blood clot surrounding the stent. Doppler ultrasonography () and CT arteriography (CTA; ) were performed at 1, 3 and 6 months after the second-look surgery, and showed a patent coated endovascular stent, normal blood flow wave pattern, and the right upper limb with 97–100% oxygen saturation on finger pulse oximetry.\nAfter injury, traction on the right upper limb produced pain and increased numbness, and muscle strength was grade II. During the first surgery, a false aneurysm was found in the proximal segment of the axillary artery, with surrounding hematoma causing brachial plexus compression. The hematoma was removed to decompress the brachial plexus. One week after the initial surgery, a second-look surgery was performed to examine the brachial plexus and remove the organized blood clot. At 1 month after the initial operation, the patient had developed atrophy of the pectoralis major, pectoralis minor, deltoid and infraspinatus muscles (). Right upper limb function was examined () and evaluated using various clinical scales; the Gilbert score () for shoulder joint function was stage I, the Gilbert and Raimondi score () for elbow function was 3 points (Grade II), the Raimondi score () for hand and wrist function was stage II and the disabilities of the arm, shoulder and hand (DASH) score () was 53.33 (). After 3 months of oral neurotrophic medication, the Gilbert score for shoulder function had increased to stage II and the DASH score had decreased to 48.33, indicating partial recovery of shoulder function. However, the elbow, hand and wrist function scores had not improved, and the region innervated by the ulnar nerve had not recovered. Electromyography (EMG) showed injury to the right cord of the brachial plexus, including severe injury to the median, ulnar and axillary nerves and mild injury to the radial and musculocutaneous nerves. The second brachial plexus neurolysis was performed at 3.5 months after injury. The right upper limb function was re-evaluated following the second brachial plexus neurolysis, and the shoulder, elbow, wrist and hand function and DASH scores are shown in and .\nThe patient was followed up until 13 months postoperatively. Color B-mode Doppler ultrasonography showed that the stent at the junction of the right axillary artery and the subclavian artery had a 5.3–8.7 mm internal diameter, with intimal thickening of ≤2.7 mm, and slower blood flow than that on the contralateral side. Part of the right axillary vein was reversed and used to form a collateral branch. CT angiography (CTA) showed the stent and the normal size and appearance of the right subclavian and axillary arteries, with no evidence of stenosis. These results indicate that the endovascular stent was stable and remained patent in vivo, and may be used to repair injured great vessels in the clavicular region. Notably, stent distortion or deformation due to the large range of motion of the shoulder joint did not cause stenosis during the follow-up period. However, the possibility of stenosis resulting from the large range of motion should be considered when repairing vessels close to the shoulder joint. All parameters of EMG at 13 months were significantly improved compared with the results at 3 months. The right upper limb function was almost restored to normal, with the exception of hypothenar muscle atrophy, limited interphalangeal joint extension, limited intrinsic muscle function and numbness of the fourth and fifth fingers and ulnar palm. The DASH score at 13 months was 7.5, indicating minimal influence on the life and work of the patient. |
A 50 year old Caucasian male was referred to the thoracic surgery department for evaluation of an intramural esophageal mass. The patient complained of atypical chest pain of gradual onset over the previous 6 months. He denied weight loss, dysphagia, upper GI bleeding, reflux, or other symptoms. The patient's medical history included hypertension and a 30-pack-year smoking history. After a chest radiograph failed to show any pathology, a computed tomography (CT) scan was ordered which revealed showed a 5 cm mass on the midesophagus at the junction of the azygos vein with the superior vena cava (). Endoscopy showed a normal esophageal mucosa and endoscopic ultrasound a smooth, submucosal mass. A CT scan of the abdomen did not show any evidence of distant metastases.\nThe mass was approached via a right posterolateral thoracotomy (). The subcarinal lymph nodes were found to be enlarged and were sent for frozen section, which was negative for malignancy. The mass was enucleated from the esophageal wall by gently detaching it from the mucosa. No adhesions with the mucosa or muscularis were noted, and the mass was excised with its capsule intact. A frozen section of the mass indicated the mesenchymal origin, with a possible diagnosis of leiomyoma. The muscular layer of the esophagus was repaired with vicryl 4-0 interrupted sutures and covered with parietal pleura. Integrity of the esophageal mucosa was established by intraoperative endoscopy. An upper gastrointestinal series on postoperative day 1 showed no evidence of a leak, and the patient was uneventfully discharged on the 6th postoperative day.\nOn macroscopic examination, the mass was 5.5 × 3.5 × 1.5 cm in size and grayish in color with a fasciated texture (). Histologically the mass corresponded to an encapsulated mesenchymatous neoplasm, consisting of fibrous and muscle fascicles with sparse round and spindle cells (). No neoplastic cells were found to infiltrate the margins of the capsule. There was no evidence of necrosis and <2 mitoses per 50 high-power fields. Less than 1% of cells stained positive for Ki67. The diagnosis of a GIST was established by immunohistochemistry, which revealed a positive immunoreaction to c-kit and CD34 (Figures and ). There was also an unusual positive reaction to smooth muscle actin (SMA) () [, ]. All excised lymph nodes were negative.\nAfter a multidisciplinary meeting the patient received adjuvant therapy (imatinib mesylate 400 mg/d for 1 year). He is closely followedup with endoscopy and CT scans every 3 months and is currently free of disease one year after surgery. |
A 64-year old white English male was presented to the vascular outpatient clinic with history of a lump behind his right ankle on inner aspect over a year. Apart from the presence of a lump, he denied any other complaints including any violent or repeated trauma. He also suffered from diet controlled Type II diabetes mallitus and gout and had tonsillectomy and manipulation of colles’ fracture in childhood. He was not taking any antiplatelet or anti-coagulation medications and denied any use of tobacco. On examination, there was 3 × 3 cm size lump just behind the right medial malleous which was non-tender and non-pulsatile. The peripheral pulses were easily palpable on either side. There was no evidence of aneurysm anywhere else in the body on clinical examination. He underwent Doppler ultrasound which confirmed 1.4 cm size aneurysm of posterior tibial artery with presence of mural thrombus. The distal and proximal parts of posterior tibial artery, anterior tibial artery and popliteal artery were reported normal. He underwent an elective operation in the form of excision of aneurysm (Figure ) followed by reversed vein graft from the same leg (Figure ). Histology confirmed the true aneurysm of posterior tibial artery with mural thrombus attached to the intima of the vessel with normal arterial wall pattern without any evidence of connective tissue disorders, arteritis, necrotizing vasculitis, infection or inflammation (Figures , , and ). The bacteriology examination neither revealed any organisms nor grown any organisms in the culture media. He recovered well postoperatively and was discharged the next day. At follow up at one year, he did not develop any complications and colour Doppler revealed patent posterior tibial artery.\nFalse aneurysms are more common in comparison to the true aneurysms of infrapatellar blood vessels. There have been only very few case reports of true aneurysms of posterior tibial artery published [,]. The precise aetiological factors are not identified, but trauma, collagen vascular pathology, fibromuscular dysplasia, inflammation, infection and atherosclerosis were suggested.\nThe most common clinical presentations include asysmptomatic lump, distal embolism and aneurysm thrombosis. Paraesthesia secondary to such aneurysm is rare but reported in literature []. Tshomba et al. reported 9% of cases presented with distal critical ischaemia of which two third ended up having midfood amputation, while only 3% of cases presented with rupture that resulted in acute compartment syndrome []. Differential diagnoses of this aneurysm include tendon cyst, neurinoma, soft tissue tumour or pulsatile masses [].\nIn our case, we could not find any aetiological factor for the aneurysm development. Out of eleven published case reports of true posterior tibial artery aneurysms, in four of them, aetiology was unknown [,,,]. Two cases were reported secondary to degenerative changes [,] and another three cases were secondary to mycotic infection [,]. In one case, polyarteritis nodosa was responsible for such aneurysm [] while in another case, histology was suggestive of syphilitic infection but immunostaining and culture isolation did not confirm the diagnosis [].\nThe management options vary from conservative approach to surgical excision followed by reconstitution of posterior tibial artery. Due to very limited number of published cases, a standard treatment has not been defined. Therefore, the indications for treating these lesions are still a matter of debate, but symptomatic aneurysms, asymptomatic large aneurysms and those with laminated thrombus should be offered treatment []. Yao and McCarthy observed asymptomatic aneurysm for seven years without any enlargement of aneurysm or any development of symptoms []. Borozan also reported and suggested conservative approach in asymptomatic aneurysms []. Although ligation of posterior tibial artery may be performed, especially in emergency settings, surgical excision with posterior tibial artery reconstitution either by primary repair or by interposition vein graft is the preferred treatment. Endovascular embolisation and percutaneous occlusion of aneurysm with various modalities are more commonly used in pseudo-aneurysms and are associated with risk of limb ischaemia.\nIn this case, patient underwent surgical excision followed by interposition vein graft. Out of eleven published case reports, six patients had undergone surgical excision of posterior tibial artery aneurysm with interposition vein graft [,,,,], while four patients had ligation of posterior tibial artery [,,,]. One patient had surgical excision with primary end to end anastomosis of posterior tibial artery []. In our patient, anterior tibial artery was intact and one might question the need for operation in this report, however we believe that infrapopliteal aneurysms should be treated irrespective of symptomatology due to the risk of embolization, thrombosis and rupture leading to potential ischaemia and amputation. |
In the present case study, authors observed variations in course and branching pattern of the brachial artery in the left upper extremity of 82-year-old male cadaver during routine dissection.\nBrachial artery was seen medial to the median nerve in the proximal arm region. At the level of the middle one-third of the arm, bifurcation of brachial artery into medial and lateral branches was observed. Medial branch crossed median nerve to become SBA at lower one-third of the arm, whereas lateral branch which was located on the deeper plane in relation to median nerve continued as deep brachial artery (DBA). At the level of apex of cubital fossa, SBA was seen dividing into SUA and SRA [].\nIn the region of lower two-third of the arm, DBA was the main source of vascular supply to all the surrounding muscles. At the level of insertion of biceps brachii tendon, DBA was trifurcated into common interosseous, medial and lateral branch. Common interosseous artery after a short course of about 1 cm, divided into anterior and posterior interosseous artery which followed their normal course. The anterior interosseous artery was seen supplying the majority of superficial as well as deep muscles in the flexor compartment of the forearm. Posterior interosseous artery passed through an opening between oblique cord and interosseous membrane to enter the posterior compartment and supplied the muscles of back of forearm. Medial branch was a comparative smaller branch supplying pronator teres muscle. Lateral branch supplied brachioradialis muscle and extensor carpi radialis longus muscle [].\nIn the forearm, SUA was seen first lying in relation to pronator teres muscle and then, flexor carpi ulnaris muscle and was not accompanied by ulnar nerve as nerve was lying on the deeper plane. However, at the level of wrist both structures came to lie adjacent to each other and thereafter followed normal course as that followed by normal ulnar artery in the palm. SRA coursed first in the middle of forearm, then proceeding laterally at the level of the middle of forearm where it came to lie superficial to the tendon of flexor carpi radialis and brachioradialis muscle. Then, SRA accompanied by superficial radial nerve entered the snuff box and thereafter, followed normal course as that of normal radial artery in the palm [Figures and ]. |
A 54-year-old male presented with proptosis of the right eye that had been slowly progressing over 15 years. This was associated with blurred vision for the 3 months prior to presentation. The patient denied pain or double vision, and there was no history of trauma at any time. The patient had had type 2 diabetes mellitus for more than 20 years. On examination, his best corrected visual acuity in the right eye was count fingers at 3 feet and 20/25 in the left eye, with no relative afferent pupillary defect. Color vision and confrontation visual fields were normal bilaterally. Mild restriction of ocular motility in superior gaze, as well as 4 mm of proptosis and 4 mm of hypoglobus were present. A palpable mass was present above the globe []. The fundus exam showed severe bilateral nonproliferative diabetic retinopathy, with greater macular edema in the right eye compared to the left eye. Fundus fluorescein angiography revealed evidence of an ischemic macula in the right eye. Macular edema was responsible for his decreased vision and this was managed with laser photocoagulation by the retina service. An orbital computed tomography (CT) scan indicated a large intra-orbital cyst in the superotemporal aspect of the right orbit, which was associated with an irregular bony erosion of the orbital roof and inferior displacement of the globe []. Magnetic resonance imaging (MRI) of the orbit was not performed.\nThe patient underwent a right lateral orbitotomy and the entire cyst was removed intact. The cyst was filled with a dark yellowish material. A large defect in the orbital roof (2.5 × 2.0 cm) was noticed intraoperatively; however, the dura over the defect was intact. Histopathology of the specimen showed a benign fibrous-walled cyst containing areas of calcification, birefringent and crystalline foreign particles with giant cell reaction and numerous cholesterol clefts []. The cyst lacked an epithelial lining. These histopathological findings are consistent with CG. The postoperative course was unremarkable and there is no sign of recurrence at 6 months []. |
A 37 year old woman presented to the Athens Naval Hospital with a slight impairment of gaze. She denied having any other focal symptoms, such as nausea and vomiting or any previous relevant history. Neurological examination failed to reveal any other signs apart from upward diplopia. All laboratory findings were within normal limits. She underwent an MRI of the brain, which disclosed a cystic pineal/posterior third ventricular region mass. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journalOn radiological grounds, the tumour mass seemed to be sharply demarcated and had a homogenous peripheral enhancement. (Figure ).\nThe patient underwent a total excision of this cystic lesion, through an midline infratentorial supracerebellar approach to the pineal region. After a slight transposition of the Galenic venous system a cystic mass with a yellowish content was revealed, that was removed by gradually detaching the wall of the cyst from the surrounding neurovascular structures, down to the compressed tectal plate. Intra-operative inspection revealed a well demarcated cystic lesion, without showing any infiltration of adjacent structures. There was slight haemorrhage in this area, which was controlled with haemostatic agents.\nThe resected lesion was fixed in formalin solution and routinely processed in paraffin for light microscopy and immunohistochemistry.\nMicroscopic examination of hematoxylin and eosin stained sections showed that the cystic lesion wall was composed of white matter partially covered by cuboidal cells. Within the cyst wall there were aggregates of uniformly round neoplastic cells with characteristic perinuclear haloes and a centrally located round nucleus with open chromatin and without any pleomorphism (Figure ). Between these cells there was a dense network of branching capillaries. Moreover, detailed examination did not reveal the presence of any Rosenthal fibers, granular bodies or necrosis. Immunohistochemical analysis showed that the neoplastic cells were positive for CD57 and negative for EMA, Ker 18, Ker 7, synaptophysin, neurofilaments, CD99 and CD10, as well as glial fibrillary acidic protein (GFAP) (Figure ). The Ki67 proliferation index was very low (approximately 1% of neoplastic cells). We tried to perform FISH analysis for chromosome arms 1p and 19q. Given that the neoplastic tissue was almost exhausted during immunohistochemistry, we were able to analyze only a small number of neoplastic cells, which did not show 1p and 19q deletion. Therefore, on the basis only of morphology and immunophenotype a diagnosis of oligodendroglioma, Grade II was assigned.\nPost-operativeMRI performed one day after surgery did not demonstrate the presence of any residual pathologic tissue. The patient was also examined monthly after the surgery and was always free of any symptoms. In the 6 months follow-up in MRI there was still no evidence of recurrence. |
Patient 3 was a 21-year-old Caucasian woman with an end-stage obstructive and restrictive ventilation disorder (Table ), who presented to our facility with severe lower back pain, left-sided ischialgia and paresis of the feet and toe extensor muscles as well as paresthesia of the dorsum pedis and toes corresponding to dermatome L5 for one week. A lumbar NMR scan showed a paramedian LDH at L4/5 with compression of nerve root L5 and a paramedian LDH at L5/S1 touching nerve root S1. A decompression operation was not performed despite the neurosurgeons' recommendations as our patient refused because of the fear of prolonged ventilation and respirator dependency after operation in the light of her severely impaired lung function. In spite of intensive physiotherapy, full mobilization took several weeks and inspiration was impaired by the pain, so that it was not possible to perform respiratory physiotherapy to its full extent. The paresis disappeared under physiotherapy but the pain did not fully disappear, needing NSAIDs and opioids. A course of intravenous antibiotic therapy was necessary at one, four and five months later. Her lung function parameters declined further and home oxygen therapy was started three months after LDH diagnosis, with 3 to 6L of O2 per minute. From six months after LDH diagnosis onwards she was hospitalized in an intensive care unit. A sternal fracture occurred seven months after LDH due to coughing and osteoporosis. Finally, our patient died eight months after LDH diagnosis while on the high urgency waiting list for lung transplantation because of an unmanageable pulmonary infection with massive pulmonary bleeding. She had spent three weeks on extracorporeal membrane oxygenation (ECMO) before she died. The fact that she temporarily fell from the high urgency list a month before her death because of improving partial CO2 values on blood gas analysis may have also played a role in the disease process, as it tremendously destabilized her mood and raised fears she may not get a transplant organ. |
A 27-year-old male presented with a functional and cosmetic concerns regarding his nose. His cosmetic concerns included a prominent dorsal hump and overprojection. He had a history of traumatic rugby impact on the nose but had never sought treatment. Functionally, he noticed nasal obstruction, worse at night. After confirming septal deviation with nasopharyngoscopy and proceeding to preliminary photographic visual planning, both the patient and the surgeon noted that a balanced facial aesthetic would require a specific correction of the patients microgenia to the mid facial plane (see ). Chin augmentation with an Implantech Conform extended anatomical chin implant was agreed as a simultaneous procedure to overcome his chin recession (see ). Septorhinoplasty proceeded uneventfully and the chin augmentation via a transoral approach was undertaken successfully with care to identify and preserve mental nerves. Fixation for the implant was achieved by creating a snug pocket for the implant and two-layered closure. The patient recovered well in the immediate postoperative period. He represented ten months postoperatively with dysesthesia over the right lower lip, a burning shooting pain, and had noticed a small lump intraorally along the right lower gingivobuccal sulcus. One month prior to this representation, the patient had undergone wisdom teeth extraction and the ensuing dysesthesia over the mental nerve distribution was thought by the surgeon to be temporally related to the dental procedure. The intraoral lesion was planned for biopsy under general anaesthetic. Intraoperatively, the right mandibular submucosal lesion planned for biopsy was confirmed to be the migrated chin implant impinging on the mental nerve (see Figures and ). Superior displacement of the chin implant was causing mental nerve irritation by elevating the mental nerve shortly after exiting the mental foramen. Shortening of the implant was undertaken by one centimetre and a steroid injection also administered intraoperatively to relieve nerve compression. The patient recovered well postoperatively and experienced complete resolution of his symptoms. Only postoperatively did the patient recall a history of trauma to the area approximately one month earlier: his daughter's head contacted the right mandibular region. This impact was posited to be the time of the implant migration. |
Case reports are exempt from institutional review board approval at our institution.
A 75-year-old woman was evaluated for long standing right-sided nasal obstruction, dependent mouth breathing, clear rhinorrhea, congestion, and hyposmia not relieved by intranasal steroids or nasal irrigations. She initially presented with a history of previous endoscopic sinus surgery in Russia more than 20 years ago followed by nasal polyposis treated with ambulatory cauterization. She was also noted to have a history of nonmelanotic skin cancers of the nose treated with radiation in Russia.
Physical exam findings included a fleshy intranasal lesion that, in the setting of previous nasal skin cancer treated with radiation, raised a concern for possible secondary carcinoma. Computed tomography showed complete opacification of the right maxillary sinus, obstruction of the right ostiomeatal complex, and soft tissue density in the right nasal passage ().
Initial biopsy revealed a nasal mass that originated in the right inferior meatus. Pathology showed multiple polypoid fragments lined by a respiratory type epithelium with underlying edematous stroma with mild chronic inflammation. There was invagination of the surface epithelium into the underlying stroma resulting in nested aggregates of bland glandular and mucinous cells and focally benign squamous epithelium (). These features were found to be consistent with a benign inverted papilloma.
The patient presented with continued nasal obstruction and was evaluated for definitive treatment. Given her diagnosis of inverted papilloma and chronic rhinosinusitis, complete excision and revision endoscopic sinus surgery was recommended. During endoscopic sinus surgery, an exophytic mass with abnormal maxillary mucosa was seen emanating from the left inferior meatus that was thought to originate from the right maxillary sinus, given that it was protruding through a bony dehiscence into the inferior meatus and nasal cavity. Right partial inferior turbinectomy was performed, along with right extended maxillary antrostomy and stripping of maxillary mucosa to remove the entirety of the presumed inverted papilloma base within the maxillary sinus. Intraoperative and postoperative pathology again showed inverted papilloma.
Given |
A 47-year-old obese woman, who had a history of smoking, presented with untreated hypertension and diabetes mellitus. She was found to have developed acute type-B aortic dissection (type IIIb) consisting of entry at the descending aorta and re-entry of the bilateral common carotid arteries, left renal artery, and left common iliac artery, causing cerebral infarction that further resulted in left hemiplegia. At that time, she had rehabilitation therapy. There was no occlusion of the carotid arteries, even with false lumen patency; thus, no additional intervention was required. She was referred to our hospital and underwent follow-up computed tomography (CT) once a year until the diameter of the descending aorta was observed to have enlarged to 50 mm; thereafter, her visits for follow-up CT were shortened to every 6 months. These CT results, however, now revealed a gradual increase in the diameter of the descending aorta to more than 60 mm with a patent false lumen. Although we have strongly recommended treatment for the dissecting aortic aneurysm, she declined. At 69 years of age, the diameter of the dissecting aortic aneurysm had increased to more than 70 mm, presenting a high probability of aneurysmal rupture, and was already compressing the left atrium. We again explained the necessity of treatment by surgical or endovascular intervention (). Finally, she opted for endovascular intervention of the chronic type-B aortic dissection and dissecting aortic aneurysm. We then planned to perform endovascular interventions with occlusion of the entry of the descending aorta and the distal false lumen. At that time, we did not consider occlusion of the re-entry in the carotid artery because of the risk of cerebral arterial emboli. CT angiography revealed sufficient visceral arterial connection between the celiac artery and the superior mesenteric artery, allowing occlusion of the celiac artery. The arteria radicularis magna (Adamkiewicz artery) received its blood supply from the collateral arterial network, including the intercostal artery, which had been occluded via endovascular intervention. Therefore, if she experienced spinal cord injury during the endovascular intervention owing to extensive covering of the aorta, we were prepared to perform immediate spinal fluid drainage. Patient consent for this study was obtained simultaneously with that for the endovascular intervention.\nAfter induction of general anesthesia in a hybrid operating room, we then performed endovascular intervention using a Zenith® Dissection Endovascular Stent (Cook Medical, Inc., LLC, Bloomington, IN, USA). The choice was made to close the entry of the descending aorta and to further embolize the distal false lumen. First, we performed coil embolization of the celiac artery and cannulated the superior mesenteric artery. This was done because the deployment of a stent graft at the level of the superior mesenteric artery was necessitated by substantial covering of the entry of the descending aorta and appropriate embolization of the false lumen in the thoracoabdominal aorta. Because of the difference in terms of the diameter between the true lumen of the aortic arch and the thoracoabdominal aorta, we deployed a stent graft (24-mm diameter, 80-mm length, 5% oversizing of true lumen) in the thoracoabdominal aorta above the superior mesenteric artery, followed by the placement of two stent grafts (both 28-mm diameter, 200-mm length, 5% oversizing of the true lumen) from distal to the left subclavian artery to the thoracoabdominal aorta via the right common femoral artery. We then performed angioplasty of the superior mesenteric artery with a covered stent graft and coil embolization of the false lumen at the level of the branching of the celiac and superior mesenteric arteries. Additionally, we have closed the false lumen of the infrarenal abdominal aorta using the candy-plug technique with a GORE® EXCLUDER® AAA Endoprosthesis aortic extender (26-mm diameter; W. L. Gore & Associates, Inc., Newark, DE, USA) and an AMPLATZER™ Vascular Plug II (16-mm diameter; Abbott Laboratories, Abbott Park, IL, USA) through the left femoral artery. This procedure aims to decrease the flow in the false lumen from the left common iliac artery. The surgery allowed her to maintain her mean blood pressure at ≥90 mmHg and hemoglobin at ≥10 g/dL. The surgery was completed with no complications, and CT angiography showed decreased blood flow in the false lumen with apparent partial thrombosis.\nHowever, follow-up CT angiography revealed further dilation of the false lumen of the descending aorta to more than 80 mm, without complete false lumen thrombosis, due to flow from the re-entry of the carotid artery (). Although she rejected open surgical intervention, she did agree to re-intervention in order to prevent this flow. Coil and plug embolization of the aortic arch was thus carried out using an AMPLATZER™ Vascular Plug II (20- and 22-mm diameters) via the false lumen of the right common carotid artery through open puncture of the right common carotid artery, under general anesthesia. Postoperative CT angiography showed complete occlusion of the false lumen at the descending aorta. She then subsequently returned for follow-up visits, with no complications reported. One year after the surgeries, follow-up CT angiography detected appreciable shrinkage of the false lumen of the descending aorta to less than 60 mm with relief of the left atrial compression and no endoleakage (). |
A 35-year-old, para 2, Afro-Caribbean woman, with no significant past medical history, presented on several occasions with abdominal pain during early pregnancy. An ultrasound (USS) scan was performed at 11 weeks gestation to exclude an ectopic pregnancy, which demonstrated a singleton viable intrauterine pregnancy with 2 small cervical fibroids (<4 cm) and a small amount of free fluid in the pouch of Douglas (). A diagnosis of fibroid red cell degeneration was determined as an explanation for the abdominal pain. A routine anomaly USS was performed at 20 weeks which was unremarkable ().\nDue to ongoing episodes of abdominal pain, an abdominal USS was performed at 21 + 4 weeks gestation which demonstrated normal abdominal and pelvic organs and an intrauterine gestation with anhydramnios. On referral to the obstetric team, a bedside USS performed was unable to identify the fetus.\nA subsequent USS was performed in the fetal medicine unit, which proved challenging due to severe oligohydramnios and uterine fibroids. The fetus could be identified and was noted to be lying laterally in the pelvis.\nInitial management for preterm rupture of membranes was implemented; however, an USS 2 days later demonstrated an empty uterus with the fetus situated near the liver.\nThe patient was referred for an urgent MRI which confirmed the diagnosis of suspected abdominal pregnancy ().\nThe patient was transferred to a tertiary center for specialist multidisciplinary management at 22 + 1 weeks gestation, with access to interventional radiology services. She was extensively counselled regarding her options for conservative management or surgical termination of the pregnancy. This included discussions with the neonatal team regarding fetal outcomes at extreme prematurity as well as obstetric and anesthetic input regarding maternal risk of major hemorrhage. The patient remained committed to the pregnancy and was admitted for observation.\nAt 24 + 4 weeks gestation, the patient collapsed with clinical signs of acute intraabdominal bleeding. A laparotomy performed revealed 2 liters of hemoperitoneum. The placenta was embedded at the left cornua, continuous with the left fallopian tube and ovary, and adherent to the omentum.\nThe baby was identified extrauterine and delivered alive but in poor condition. Placental tissue continued within the myometrium; therefore, the left cornua were excised and the uterus repaired, with a blood loss of 4000 ml. Postnatally, the woman was managed in ICU and discharged on day 12. Sadly, the baby died at 24 hours of age. |
A 31-year-old female patient presented with cough and mild dyspnea to the outpatient department. She had a history of being diagnosed with pulmonary tuberculosis 7 years ago, which she had completely recovered after 6 months of antituberculosis drug regimen. There was no other notable history. Dullness and decreased breathing sound at the left side was noted after auscultation. Complete blood count revealed no abnormal finding, and no acid-fast bacilli was discovered on the sputum culture test. Plain chest radiography showed giant bulla in the left lung and subsegmental consolidation in the left lower lung field. Chest computed tomography (CT) scan revealed the left upper lobe of the lung being replaced by bullae of various sizes, and subsegmental consolidation had broad contacted with bullae at the lingular segment of the left upper lobe (). The right lung showed no abnormality. The patient's pulmonary function test signified moderate obstructive respiratory failure. Wedge resection of the left lung using video-assisted thoracoscopy was performed under the preoperative diagnoses of giant bullae and pulmonary emphysema. During operation, the left lower lobe was found to be severely compressed by the bullae. Gross examination of the wedge resected lung was 15 × 9 × 4 cm in size with dilated giant bullae (). Spongiform emphysema was observed at the cut surface, and there were partial solid changes and fibrotic progression. Examination of the solidified sites by light microscope indicated general emphysematous changes with destruction of the alveolar wall in addition to numerous tissues replaced by structures similar to the chorionic villi. The villous structure was adjacent to, or in some cases adhered to, the destroyed alveolar wall and interlobular septa. Immunohistochemical staining of the epithelium lining the villous structure was partly positive for thyroid transcription factor-1, and the interstitial cells at the core was positive for CD-10, D2-40 and vimentin (). There was no human chorionic gonadotropin positive cell.\nThe chest tube was removed 8 days after surgery. Pathologic examination of the surgical specimen reported placental transmogrification of the lung. Chest CT scan was taken to rule out the possibility of remnant bullae or transmogrified tissue. The giant bullae at the left upper lobe were removed, but some fibrotic tissue still remained. Additional left upper lobectomy was planned to remove the remaining tissue in order to minimize recurrence. However, the patient did not complain of any symptoms and refused further operation. She was explained about the possibility of recurrence and scheduled visits to the outpatient clinic on a regular basis for follow-ups. |
A 55-year-old, Caucasian woman was referred to our tertiary women’s heart center for persistent chest pain, palpitations, and dyspnea. Her medical history included hypertension, dyslipidemia, chronic anxiety, and bilateral non-obstructive carotid atherosclerosis. She had no prior history of diabetes mellitus, tobacco smoking, alcohol or substance abuse, or adverse pregnancy outcomes. Her family history was significant for premature coronary artery disease. Her father had a history of hypertension and had a myocardial infarction (MI) and coronary artery bypass grafting at the age of 39. Her brother had a history of coronary artery disease and also had a MI at the age of 40. Her occupational history indicated that she had been working in the field of psychology and was still an employee in the same job at the time of the hospital visit and follow-up care.\nTable summarizes the general symptoms and characteristic signs of our patient for the onset of CMD and her progression to HFpEF. She had undergone an exercise treadmill test which revealed ischemic ECG changes and dyspnea. Her initial echocardiogram demonstrated a LVEF of 67%, mild diastolic dysfunction, mild left ventricular (LV) hypertrophy, no significant valvular heart disease, and no pulmonary hypertension. Subsequent invasive left heart catheterization was performed and it showed normal epicardial coronary arteries without angiographic evidence of atherosclerotic plaque. She continued to have exertional symptoms and angina-like chest pain and was subsequently referred to our center for further evaluation of suspected INOCA. During her evaluation and treatment she continued to experience stable angina and exertional dyspnea despite initial management with atorvastatin 20 mg daily, lisinopril 20 mg daily, aspirin 81 mg daily, and sublingual nitroglycerin as needed. She had a poor clinical response to sublingual nitroglycerin. Due to her persistent symptoms and abnormal stress testing, she was referred for coronary reactivity testing (CRT) to establish the diagnosis of CMD.\nOur patient underwent invasive CRT, as previously published []. Testing demonstrated normal coronary flow reserve (CFR) in response to intra-coronary adenosine (CFR 3.1; normal ≥ 2.5), abnormal macrovascular endothelial function to intra-coronary acetylcholine (− 6% change in coronary diameter, constriction; normal, dilation), abnormal microvascular endothelial function (coronary blood flow change 48%; normal ≥ 50%), and abnormal non-endothelial function to intra-coronary nitroglycerin (coronary diameter change + 0%; normal dilation) (Table ). She also underwent cardiac magnetic resonance imaging (CMRI) with perfusion imaging at rest and with adenosine stress (140 μg/kg per minute) which showed circumferential subendocardial perfusion defect at stress, normal LV end-diastolic volume indexed to body surface area (EDVi) of 56.4 mL/m2, LV mass index 42.3 grams/m2, and no LV hypertrophy (septum 7.2 mm and lateral wall 6.0 mm). The myocardial perfusion reserve index (MPRI) was 1.8 which was considered borderline abnormal [] (Table ). There was no evidence of myocardial scar.\nThe diagnosis of CMD was established by the coronary endothelial dysfunction observed with invasive CRT, and carvedilol and eplerenone 25 mg daily were added to her regimen. She was followed regularly in clinic with good control of her blood pressure and serum lipid levels. She reported improvement of her angina and dyspnea along with reduction in the duration and frequency of these episodes.\nTen years after her initial diagnosis of CMD, our patient was hospitalized due to symptoms of dyspnea. She was found to have elevated brain natriuretic peptide (BNP) levels of 406 pg/mL and normal LVEF. She had a computed tomography (CT) angiogram of her chest to evaluate for pulmonary embolism, which was negative but revealed bilateral pulmonary edema. She was treated with intravenously administered furosemide for pulmonary edema and diagnosed as having HFpEF. Subsequently, she was discharged with instructions to increase her eplerenone.\nShe continued to experience worsening dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. A repeat echocardiogram demonstrated normal LV systolic function with an LVEF of 64%, and diastolic dysfunction as evidenced by decreased lateral E′ velocity (4.2 cm/s, indicating impaired myocardial relaxation) and elevated E/E′ ratio 12.9 (suggestive of increased LV filling pressure). She underwent coronary CT angiography which showed absence of coronary atherosclerotic plaque and a coronary calcium score of 0. She was diagnosed as having HFpEF based on clinical symptoms, preserved ejection fraction of 64%, elevated BNP, and evidence of diastolic dysfunction.\nAs part of the WISE – Coronary Vascular Dysfunction (WISE-CVD) Continuation Study (NCT00832702), she underwent a repeat rest-stress CMRI to assess myocardial structure, function, perfusion, and scar, and 13C magnetic resonance (CMR) spectroscopy. Compared to her prior CMRI 7 years ago, she had an increase in LV wall thickness in both the septum and lateral wall (Table ). On CMR spectroscopy, the myocardial triglyceride content was elevated (0.83%) compared to normal control women (mean 0.43%), suggesting myocardial steatosis which is consistent with an ischemia-induced metabolic shift and HFpEF phenotype []. Adenosine stress first pass-perfusion CMRI again showed circumferential subendocardial hypoperfusion (Fig. ) and her MPRI worsened from 1.8 to 1.1, consistent with severe CMD []. There was no evidence of scar on late gadolinium enhancement imaging. |
A 47 years old Moroccan woman with a familial history of a father dead from a colorectal cancer, and a maternal aunt dead from a breast cancer, presented to our institute with complaints of nasal obstruction, headache, and ear fullness for three months, and skin changes on the right breast for two months. She did not breastfeed her four children, had a regular menstrual cycle, and took oral contraception.\nOn physical examination, the right breast had a 6 × 5 cm lump on retroareolar area fixed to the skin with thickening of the whole breast and nipple retraction. The axillae and the cervical regions were free of any adenopathy. Mammogram showed an increase in density on the right breast with abnormal skin thickening in the periareolar area and associated microcalcifications (Figure ), the complement of ultrasound revealed a nodular lesion measuring 4 × 4 cm. On the fine needle aspiration cytology there were signs of malignancy confirmed with core biopsy of the lump suggesting a ductal infiltrating carcinoma with micropapillary component (Figure ).\nAt presentation our patient had developed a unilateral conductive hearing loss associated with recurrent otitis media and numbness of the face. A computed tomography (CT) of the face and the skull showed an asymmetric mass in the posterior nasopharynx extended into the adjacent parapharyngeal spaces and infiltrating the sphenoid bone, no regional adenopathies were revealed, and the nasopharyngeal biopsy confirmed the diagnosis of an undifferentiated nasopharyngeal carcinoma (Figure ). There were no distant metastases and we conclude the diagnosis of a locally advanced breast cancer with a synchronous stage III undifferentiated nasopharyngeal carcinoma.\nThe patient received induction chemotherapy combination of drugs sharing an activity on breast and nasopharyngeal carcinomas, association of taxanes and anthracyclines drugs was used (weekly Paclitaxel 80 mg/m2 for 12 weeks associated to Doxorubicine 50 mg/m2 every 3 weeks) for a total of 4 cycles. The treatment was generally well tolerated; the patient had 3 episodes of grade III-IV non febrile neutropenia, grade II mucositis, total alopecia, and grade II neuropathy reversible after several months thereafter. After the four cycles of chemotherapy there were a remarkable improvement on the breast and a relief in the symptoms of the nasopharyngeal tumour.\nThe induction therapy was followed by external beam radiation for the nasopharynx (70Gy in 35 fractions) with concurrent chemotherapy (weekly Cisplatine 40 mg/m2 for four weeks) and a prophylactic radiation to cervical lymph nodes. Evolution was marked by the improvement of the symptoms and a radiological reduction volume of the nasopharyngeal mucosa thickening which biopsy confirmed the absence of malignancy. This sequelar lesion has persisted until the last control without trend to progression.\nBreast intervention was delayed until after the local control of the nasopharyngeal tumour. A right-sided modified radical mastectomy with axillary nodes dissection was carried out. Histological analysis of the mastectomy specimen revealed a 2 mm residual infiltrating ductal carcinoma grade II, neither insitu component nor lymphovascular emboli were found, hormonal receptors were positives (90% on estrogens receptor, and 30% on progesterone receptor), Her2 status was negative, and from the 11 lymph nodes dissected 4 were involved. Surgery was followed by chest wall irradiation, and the patient undergoes now an antihormonal therapy; she has accomplished 12 months of Tamoxifene. The latest medical controls show no signs of locoregional relapse for both tumours and our patient remains disease-free 27 months after beginning therapy. |
A 54-year-old woman with diabetes mellitus (DM) type 2 and hyperlipidemia controlled on long-acting insulin, metformin and atorvastatin was admitted to the neurology ward with symptoms of acute headache, diplopia, vertigo and vomiting. In physical examination she had left-sided peripheral facial nerve palsy, and right homonymous hemianopia.\nAttention was paid to accelerated ESR – 68/hour. The MRI study of the brain revealed tiny subacute ischemic spot in the right frontal lobe, intracranial right internal carotid artery (ICA) stenosis, mild pan-sinusitis () and right side mastoiditis. Color Doppler sonography of both carotid arteries also showed total occlusion of the right internal carotid artery. Sinus CT scan showed mild mucosal thickening in all paranasal sinuses suggestive for pan-sinusitis. Due to headache lumbar puncture was done and showed 40 leucocytes, 97% lymphocytes and normal picture of cytology, and negative culture. A temporal artery biopsy was also performed and no abnormalities were observed. The patient was discharged with antibiotics with the diagnosis of impression of sinusitis, facial nerve palsy, meningitis and right internal carotid artery thrombosis. The patient gradually developed left cheek swelling and protrusion without any fever and after 5 months needed aspiration of the left maxillary sinus and histopathological assessment showed necrotizing granulomatous inflammation of the sinus. So the patient was admitted to the rheumatology ward. On admission the patient interview revealed 5 months history of bilateral hearing loss, mild left side peripheral facial nerve palsy and a protruded left cheek mass, non-tender and hard on examination. Other examinations were unremarkable. Still high ESR was observed (lab tests in ). MRI of the left maxillary sinus showed destruction of the anterior wall of the left maxillary sinus accompanied by a large soft tissue component showing enhancement following contrast administration suggesting osteomyelitis. On the right side also osteomyelitis was noted with smaller bone destruction and soft tissue component. Mucosal thickening of sphenoid and ethmoid air cells was also noted (). An open sinus biopsy also showed ulceration with granulomatous tissue formation, thrombosed vessels and some eosinophilic infiltrations suggesting granulomatosis with polyangiitis (GPA). The PCR screening for tuberculosis was negative. The patient had negative ANCA, no eosinophilia and normal lung CT scan and also no kidney involvement. Due to severe involvement of sinuses and hearing loss treatment with prednisolone and oral cyclophosphamide was started and in the follow-up after 2.5 months showed complete resolution of the cheek mass. |
A 21-year-old male patient presented to the Department of Periodontics for treatment, with a chief complaint of bleeding from gums. Intra-oral clinical examination of the patient revealed generalized pale pink gingiva with reddish pink interdental papilla and marginal gingiva in mandibular central incisors []. Notably, significant deposits of plaque and calculus were also present on the lingual surface of mandibular incisors. Bleeding on probing was noted. Grade II and grade I mobility was present in mandibular right and left central incisor respectively. A sinus opening was also seen at the apex of mandibular right central incisor []. Radiographic examination of mandibular anterior teeth showed severe bone loss in mandibular central incisors along with involvement of peri-apex in mandibular right central incisor. The sinus tract on the facial surface of mandibular right central incisor could be traced up to the apex of the tooth with gutta percha point []. Vitality testing of mandibular right central incisor showed the tooth to be non-vital. Patient gave no history of trauma to mandibular right central incisor and trauma from occlusion was absent. A diagnosis of chronic localized periodontitis was made on the basis of history, clinical, and radiographic examination.\nInitial periodontal treatment consisted of oral hygiene instructions and generalized scaling. Completion of phase I therapy led to an incidental finding of enamel pearl on the lingual surface of mandibular right central incisor at a distance of approx. 2.5 mm from the CEJ and about 2 mm × 3 mm in diameter []. Subsequently, root canal treatment was done in mandibular right central incisor [] and the flap was raised in mandibular incisor region []. The area was completely debrided and odontoplasty was performed in mandibular right central incisor to remove the enamel pearl []. The flap was re-approximated and sutured []. The patient was recalled after 1 week for suture removal and showed uneventful healing []. Six month recall of the patient showed complete resolution of gingival inflammation [], reduction in mobility and significant resolution of periapical lesion []. |
A 56 year old Caucasian male with history of non insulin dependent diabetes presented with lower abdominal pain with increasing frequency of bowel movements for 3 months, rectal pain for a month and acute onset urinary retention. He also reported sporadic night sweats and subjective fever for 5 months. Earlier work up by his primary physician failed to elucidate a cause for his symptoms. On presentation, he was afebrile and remained hemodynamically stable. His physical examination showed right lower quadrant tenderness with no signs of peritonitis. Digital rectal examination showed tender, firm nodular mass along the anterior wall of rectum. Laboratory results revealed leukocytosis with neutrophilia and eosinophilia. Radiological examination included Computed Tomography (CT) scan and Magnetic Resonance Imaging (MRI) scan of abdomen and pelvis. They demonstrated circumferential thickening of recto sigmoid region measuring 16 cm in length with significant luminal narrowing (Figure ). There was an extrinsic component to the lesion with extension anteriorly into seminal vesicles and prostate and posteriorly into the presacral region.\nHe had another inflammatory lesion involving the cecum circumferentially and measuring 6 cm in length was also noted. There were secondary inflammatory changes in the appendix and the mesentery. He had significant retroperitoneal lymphadenopathy involving the external iliac, common iliac and para-aortic nodes.\nPatient’s social history was significant for his residence in southern Arizona for the last 28 years.\nHe is a professor of archaeology and geography with extensive travel history to the Middle East including Jordan and Israel. Incidentally he had installed a sprinkler system at his property a month prior to the onset of his symptoms. He had an earlier screening colonoscopy showing sigmoid diverticulosis 2 years ago. Differential diagnosis considered at this point included colorectal cancer and lymphoma.\nEndoscopic examination showed congested circumferential lesion from anal verge to up to 27 cm proximal to anus (Figure ). Histopathological examination of biopsies showed marked mucosal eosinophilia without an associated increase in mast cells and failed to reveal a specific diagnosis. Endoscopic examination and biopsies were repeated with no additional benefit. CT guided biopsy of the lesion was performed to obtain additional specimens from extrinsic component of the lesion over the cecum and recto-sigmoid lesion. Histopathological examination of CT guided biopsy showed granulation tissue with extensive acute inflammation and fibrosis along with fungal organisms which were confirmed by Grocott's methenamine silver (GMS) stain. The morphology of the fungal organisms on the staining within the clinical context were consistent with basidiobolomycosis (Figure ). No associated malignancy was identified.\nThe patient was treated for basidiobolomycosis with oral itraconazole therapy (100 mg oral twice daily) with significant improvement in pain, frequency of stools and urinary retention within 4 days. His anti fungal treatment was continued over the next 12 months with periodic clinical and radiological examinations. Although no specific guidelines are available on the duration of the treatment and surveillance for treatment response, we chose to evaluate him with MRI scans at 3 month intervals to evaluate the response to antifungal treatment. He continue to improve symptomatically with near resolution of the lesion on the MRI scan of pelvis after 12 months of treatment (Figure ). |
A 56-year-old male patient was referred to our clinic for nausea, vomiting, and a swelling on the anterior abdominal wall. He had undergone surgery for a perforated peptic ulcer 15 years ago. A physical examination revealed hyperemia around the abdominal wall incision and a fascial defect at the abdominal midline. Abdominal US showed that a few of the lesions were consistent with HCs in both lobes of the liver and the spleen. The patient was examined with a panendoscope to differentially diagnose the dyspeptic complaints. The endoscopic examination revealed external compression of the gastric wall. The echinococcal indirect hemagglutination test was positive at a titer of 1:256. A contrast-enhanced abdominal CT scan showed 2 calcifying lesions consistent with HCs, the largest of which had a diameter of 5 cm, in the anterior and posterior segments of the right lobe of the liver. The other HC lesion was 11 × 10 cm and almost completely filled the left lobe of the liver. This HC was compressing the stomach, and was close to the anterior abdominal wall. Additionally, 2 more lesions resembling HCs, of which the larger had a 10-cm diameter, were detected in the spleen (Figs. and ). Surgery was scheduled, so the patient was administered two 400-mg doses of albendazole p.o. and a pneumococcal vaccine. Five days after the initial examination the patient presented to our emergency department with marked redness and discharge from the abdominal wall. A physical examination revealed a clear fluid discharge from a 1.5-cm opening. After local anesthesia, the orifice was dilated and daughter vesicles and a large volume of HC fluid were drained (Fig. ). The patient underwent surgery the next day. The cyst that almost completely filled the left lobe of the liver and fistulized to the epigastrium was excised completely. Then, the cyst in the right lobe was drained with a partial cystectomy + omentopexy, and a splenectomy was performed. The fascia was closed, the incision was debrided, and the wound was allowed to heal. Albendazole was started 3 days after surgery; the patient received 4 cycles. No recurrences were detected at the 6-month follow-up visit. |
A 72-year-old woman admitted to emergency unit with acute abdominal pain. She had a history of open heart surgery (valvuloplasty), and she was taking warfarin regularly. There was no trauma history. Her blood pressure, pulse, and respiratory rates were 78/42 mmHg, 112/min, and 28/min, respectively. There was a generalized abdominal pain that was more apparent on the right upper quadrant. Ultrasound demonstrated free abdominal fluid and an irregular lesion at the right liver lobe. Computed tomography revealed abdominal free fluid and a liver lesion on segments V, VI, and VII (). Liver pathology was not clearly diagnosed, but it was reported as a possibly ruptured hemangioma. Her hemoglobin, hematocrit, and INR values were 5.2 g/dL, 14.9%, and 6,7, respectively. Her general condition was deteriorated during examinations despite intravenous fluid supports, blood transfusions, and inotropic infusions. Emergency laparotomy was required and 1500 mL blood was aspirated from the abdomen. At the first sight, there was large subcapsular liver hematoma, which was still bleeding from a 4 cm length tear on segment V of the liver (). We packed the liver and waited for cessation of the bleeding, but it was still going on particularly from the posterior part of the liver. Right liver was mobilized from the posterior attachments, and there was a large subcapsular hematoma on the right posterior sector of the liver. Blood was coming out from a tear of the liver capsule. The liver capsule was removed to see the origin of bleeding. Active hemorrhage was coming from the liver parenchyma through the two deep lacerations at segment VI and VII (), and there was a palpable focal lesion in the liver at the same location. By Pringle maneuver, we blocked the blood inflow of the liver and packed the liver again, but prolonged INR failed the success of packing. We decided an urgent resection of the bleeding part of the liver including the mass. Under total hepatic vascular occlusion, segments V, VI, and VII were resected with endoscopic staplers (Covidien endostaplers, US). We used 10 nonvascular (blue-cartilage) staplers because there was no vascular stapler at that time in the operating room. Before applying staplers, we created tunnels in the liver parenchyma by a long clamp. Hepatectomy time took almost six minutes, and the cut surface of the liver was coagulated with bipolar cautery and covered with a hemostatic material (TachoSil, Takeda Company, Zurich). Total vascular clamping was released, and the cut surface of the liver was pressed with moisturized gauzes for a few minutes. There was no bleeding (), and surgery was ended within total 80 minutes. During surgery, total six packs of erythrocyte and four packs of fresh frozen plasma were transfused. Postoperative period was uneventful, and the patient did not require any extra blood transfusion. There was no complication, and the patient was discharged on day eight. Pathological result was a surprise for us that the mass was belonged to Fasciola hepatica. After surgery the patient was consulted with the infectious diseases unit, and Triclabendazol was recommended. |
A 28-year-old single nulligravida Eritrean patient presented in 2013 to the emergency department with right lower quadrant pain for 3 weeks. Her pain started gradually; it was colicky and throbbing in nature and radiated to her right leg. The pain was aggravated by fatty and spicy food, occurred on and off, and was partially alleviated by painkillers. The pain was associated with nausea, vomiting, bloating, alternating diarrhea and constipation, and episodes of bleeding per rectum. The patient had her first menstrual period when she was 11; she had regular cycles for 7 days until recently, as her period lasted only for 3 days in the two cycles preceding her presentation, with increased premenstruation pain. She reported that she had no weight loss, no loss of appetite, no night sweats, but had palpitations while her other systems were unremarkable. She only complained of eczema and her past surgical history was of an anal fistula in 2010; she had no blood transfusion and no known food or drug allergies, and she is a nonsmoker. Her younger sister was known to have ileal Crohn's disease.\nShe was diagnosed in the ER with appendicitis and underwent emergency appendectomy. After appendectomy, she continued to complain of continuous abdominal discomfort. In March of 2017, the patient returned to the hospital due to recurrence of pain associated with loss of appetite. A CT scan of the abdomen revealed a right adnexal mass inseparable from a thickened and stenosed distal ileum. An exploratory lower midline laparotomy was done that revealed an abscess in the right side of the abdomen in the vicinity of the distal part of the small intestines along with ovarian swelling. She underwent abscess drainage and right ovarian cystectomy only, as the ileum itself was inflamed but with no fat creeping and was not fibrotic, indicating that it itself was not diseased but showed signs of inflammation due to proximity to the diseased ovary. The patient tolerated the procedure well, had an uneventful hospital stay, and was discharged from the hospital three days later.\nThe histopathological examination of the right ovarian mass revealed infiltration of the ovarian stroma by a mixture of inflammatory cells composed of lymphocytes, plasma cells, neutrophils, and histiocytes, with formation of multiple microabscesses. Collections of epithelioid histiocytes with formation of granulomas were also noted. Some of these granulomas showed central suppuration. There was no evidence of malignancy. Ziehl-Neelsen and Grocott's methenamine silver stains were performed and found to be negative for acid-fast Bacilli and fungal organisms. The final pathological impression was of a diffuse multifocal necrotizing granulomatous inflammation that was consistent with CD (see ). |
The patient is a 56-year-old woman with a previous history of a major depressive episode 10 years ago. The first episode was precipitated by the diagnosis of renal cancer which required simple nephrectomy. After a failing trial with escitalopram, this first episode was treated with venlafaxine up to 300 mg/day during 16 weeks to obtain a sustained remission. All psychotropics were discontinued one year later and the patient maintained complete stability the next nine years. On January 2014 she was admitted to the psychiatric ward due to a relapse in severe depressive symptoms with continuous suicidal thoughts. The current episode might be triggered by a back pain that reminded the onset of the cancer. Imaging methods ruled out a cancer relapse and additional blood tests, including thyroid status, showed no significant abnormalities. The patient had a negative record for any substance use, but additional medical history included properly corrected hypothyroidism, intrinsic asthma, and hypercholesterolemia. Nevertheless, the initial anxiety symptoms generated by the fear of a cancer relapse gradually became a major depressive episode with extreme fear for everything, including any new physical or mental disease that kept her from going out of the house, restlessness, fragmented sleep, and lack of energy that caused total impairment of daily activities. Venlafaxine titrated to 300 mg/day had been initiated two weeks before admission with no relief. Quetiapine 400 mg/day was added and the patient showed an improvement in anxiety and insomnia but core depressive symptoms remained unmodified. After two more weeks without any improvement venlafaxine was switched to imipramine up to 300 mg/day and lithium at doses to obtain therapeutic levels. Three weeks later no improvement was observed and bilateral ECT was initiated three times per week until obtaining a slight improvement in mood that allowed discharge. The patient was complaining of moderate retrograde amnesia and subjective perception of mild cognitive deficit. During ECT sessions the medication regimen was switched to desvenlafaxine 100 mg/day, bupropion 300 mg/day, quetiapine 300 mg/day, and lamotrigine (100 mg/day). After a few days of staying at home the feelings of inability to cope with daily tasks were growing and provoked a new relapse in depression with a similar severity to the previous admission. Once in the psychiatric ward, lithium was added to her medication regimen while the institutional review board of the hospital approved the compassionate use of ketamine. Even with optimal serum lithium levels (0.7 mmol/L) the symptomatology remained unmodified and ketamine infusions were started two weeks later. The patient received six i.v. infusions of ketamine (0.5 mg/kg) during 40 min on a Monday-Thursday schedule over an 18-day period. This treatment was administered at the Post Anaesthesia Care Unit (PACU) under the supervision of a staff anaesthesiologist. Ketamine was very well tolerated and no changes in vital signs, including heart rate or blood pressure, were observed. Furthermore, no psychotomimetic or dissociative symptoms were experienced during all the infusions and cognitive complaints related to ECT did not get worse. All the psychotropic regimen was maintained with similar doses and there was no adverse effect associated with them. A robust improvement in mood was gradually observed after the third infusion allowing her to be discharged and gradually resuming her daily life activities. Six months later she is still in clinical remission and on the same medication regimen. |
A 7 year old girl was seen at our clinic for pain at the right calf with limping and weakness during plantar flexion of the right foot. Her mother stated that she had started to limp about 8 weeks before after a swinging door hit her on the back of the leg while she was running. At that time she complained of a small cut on the skin that was over her Achilles mid-tendon. She was then taken to the emergency department of the closest hospital, where the skin was sutured. She was allowed to walk but she started to limp on her right lower limb and to feel a kind of weakness during plantar flexion. She was seen again by a pediatrician after 6 weeks, who then referred her to us.\nPhysical examination showed an Achilles tendon gap under the skin at inspection and upon palpation of the area (Fig. ) and an inability to raise her heel off the ground on the right side. A swollen mass was also present during palpation at the proximal part of the calf muscle, and a positive Thompson squeezing test was noted. Magnetic resonance imaging (MRI) showed a chronic full-thickness tear of the right Achilles tendon with a gap of 5 cm (Fig. ).\nShe was then taken to the operating room. Under general anesthesia and in the prone position, the right foot showed slight dorsiflexion due to the prevalence of the extensor muscles (Fig. ). After the right lower limb was exanguinated, a medial para-Achilles tendon incision was made just over the gap. The proximal part of the tendon appeared to be severely proximally retracted, while a small stump of the distal insertion was present over the posterior calcaneal tuberosity. The proximal part of the tendon was released from all of the scar tissue and the plantaris gracilis tendon was found to be intact (Fig. ). A termino-terminal tenorrhaphy was then possible, but only with the foot flexed in the full equinus position, utilizing the plantaris gracilis tendon as an augmentation (Fig. ). The skin was then closed under extreme tension with reabsorbable sutures. A non-weight-bearing short leg cast in the equinus position was then used for 2 weeks, followed by a new short leg cast in a less equinus position to recover the plantigrade position for three weeks. After the cast was removed, a physical therapy program was prescribed for 3 weeks to recover the correct plantigrade position as well as tip-toed walking. She was able to return to normal activities within a month after cast removal.\nThe patient was completely asymptomatic at 3 years follow-up.\nThe parents of the young patient gave informed consent prior to their daughter being included in the study. |
A 30-year-old woman known case of seasonal bronchial asthma on Ventolin as needed presented with a history of palpitation, bilateral upper and lower limbs numbness, nausea, diarrhea, and generalized fatigue for three days. The palpitation started suddenly while she was sitting, and it continued throughout the day and was not associated with dizziness, syncope, chest pain, or sweating. For the numbness of the limbs, it started first in the upper limbs then it progressed to involve the lower limbs as well and it was associated with generalized fatigue. She had watery diarrhea four times per day, small in amount with no blood, associated with nausea. The patient did not complain of abnormal movement, abdominal pain, or vomiting. There was no history of diuretic use or unusual eating habits. The family history was unremarkable with no kidney or endocrine diseases. She had similar complaints of limbs numbness, and generalized fatigue for the past eight years and she followed up with different hospitals and several investigations were done on her; however, she was never diagnosed or managed appropriately before. On physical examination, the patient was laying on bed conscious, alert and oriented, looks pale, dehydrated, not in respiratory distress. She had intact cranial nerves; the power was five out of five bilaterally in both upper and lower limbs with intact sensation, gait, and coordination. Her vital signs are shown in Table . Chest x-ray showed no abnormality, and the electrocardiogram (ECG) showed sinus rhythm with prolonged QT interval, prominent U-wave (Figure ). Serum electrolytes including, potassium, sodium, magnesium, and chloride were done and showed low serum levels of potassium and magnesium (Table ). The patient was diagnosed with enteritis and the primary team thought the low potassium and magnesium levels were secondary to the gastrointestinal loss. Therefore, she was given potassium chloride and magnesium sulfate orally but she did not improve so she was placed on potassium chloride 40 mmol twice a day for few days but the serum level of potassium was still on the lower side. For that reason, the nephrology team was consulted for the case and they ordered urine electrolytes and blood gas analysis. The patient was found to have high spot urine potassium and chloride levels. So, 24-hour urine potassium and calcium levels were done and showed high potassium levels along with decreased calcium levels (Table ). In addition, blood gas analysis showed high pH along with a high bicarbonate level, and the patient was diagnosed with metabolic alkalosis (Table ). Through these biochemical investigations, we diagnosed the patient with GS after making sure the patient had no reach to thiazide diuretic through a negative thiazide assay. The patient was placed on potassium chloride (80-120 mmol/day) and magnesium sulfate (2-4 g/day) intravenously for few days and was advised to consume foods rich in potassium and magnesium like bananas, dates, dark chocolate, avocados, nuts, and seeds. The patient’s complaints resolved and her electrolyte improved post-treatment (Table ). The patient did not have any further complaints and she was discharged home in stable condition on magnesium oxide 800 mg and potassium chloride 1,200 mg orally three times per day in addition to spironolactone 50 mg once daily. |
A 29-year-old man presented at a emergency room in a stupor.
The patient had started psychiatric treatment after being diagnosed with personality disorder and hypochondriasis by the department of psychiatry in our hospital 4 years ago. After about 1 year of treatment, olanzapine was administered due to the patient's symptoms of social withdrawal and distrust of people. After the initiation of olanzapine, the patient's body weight increased by ≥30 kg, and hyperthermia occurred together with nausea and vomiting 1 week prior to the visit to our hospital. The patient received a prescription from a neighboring hospital and had taken antipyretics, but did not show any improvement. Then the patient showed mental deterioration and was admitted to our hospital via the emergency room.
Both parents were moderately built, and none of the family members, including siblings, had a metabolic disease such as diabetes.
The patient was on medication due to incidences of personality disorder, hypochondriasis, and psychotic tendency, taking olanzapine 10 mg, valproic acid 500 mg, clonazepam 0.5 mg, and lorazepam 1 mg on a daily basis. The aforementioned medication regimen was maintained for over 1 year without any dosage change, and the intake period of olanzapine was 32 months. There was no other underlying disease than the aforementioned, and there were no abnormal test results based on blood assay, including an assay for fasting plasma glucose, which was performed prior to administration of antipsychotics.
The patient had no history of smoking or alcohol drinking and was unemployed since completion of military service as social service personnel.
In physical examination, the patient showed acute signs of illness and was in a coma. His vital signs measured at the time of visit to our hospital were 110/70 mm Hg for blood pressure (BP), 120 beats per minute for pulse rate, 24 times per minute for respiratory rate, and 37.2℃ for body temperature. The patient's height was 181 cm, weight was 104 kg and body mass index (BMI |
A 67-year-old female with past medical history of congenital deafness presented to the emergency room with complaints of right-sided facial droop and right upper extremity weakness, tingling, and numbness. These symptoms were sudden in onset and lasted for a few minutes. Symptoms had completely resolved at the time of presentation. She did not have a history of any atherosclerotic risk factor including hypertension, diabetes, or hypercholesterolemia. The initial set of vital signs were normal; routine laboratory tests including complete blood count and basic metabolic panel were unremarkable. A computed tomography (CT) of the head without contrast as well as a magnetic resonance imaging (MRI) of the brain with and without contrast did not show any acute intracranial hemorrhage or infarction.\nThe patient was diagnosed with TIA, and further investigations were planned to determine the etiology. A magnetic resonance angiogram (MRA) of the head and neck with and without contrast did not show any arterial flow limiting stenosis or occlusion. A transthoracic echocardiogram (TTE) with bubble study using agitated normal saline contrast was performed and was found to be normal. Patient's heart rhythm was monitored with continuous cardiac monitoring, and no arrhythmias were noted during her stay at the hospital. At this point, the patient was identified as having cryptogenic TIA, having failed to determine the precise etiology from routine workup. Patient was started on aspirin therapy and discharged from the hospital on day 3 with further outpatient workup planned. Outpatient workup for hypercoagulability showed a high factor VIII activity of 153%, which potentially put her at increased risk of venous thromboembolism. However, this test was performed just one week after the thrombotic event and was hence difficult to interpret. Subsequently, a transesophageal echocardiogram (TEE) was performed that revealed a patent foramen ovale with right-to-left shunt. This raised the concern for paradoxical embolism as the cause of patient's TIA. Lower extremity duplex venous ultrasound showed no evidence of deep vein thrombosis. However, magnetic resonance venogram (MRV) of pelvis showed compression of the left common iliac vein just after its origin, which was suggestive of May-Thurner syndrome (). There was no evidence of venous thrombosis on the MRV. May-Thurner syndrome was recognized as the probable source of paradoxical embolism causing TIA in the patient. The patient was eventually referred for percutaneous PFO repair, which was performed without any complications. The patient had been regularly followed yearly at the cardiology clinic for 5 years now. She remains in good health with no further episodes of TIA. |
A 50-year-old Caucasian female visited the regional dental office due to uncertain pain in the right mandibular region. No significant diseases were mentioned in the anamnesis. The patient was diagnosed with gingivitis, and treated with a non-steroid anti-inflammatory drug and oral rinsing with chlorhexidine. The condition of the patient did not improve significantly. When she returned a week later, she had no alleviation, but labial paresthesia on the right side of her lip. As the cause of the new symptom remained unidentified, she was referred to the oral surgery group. Initially, the paraesthesia affected only the right side of the lower lip, but by this time it had spread to the skin of the right side of her chin. The oral surgeons decided to extract the lower right wisdom tooth, but the labial paraesthesia still persisted. Since there was an extended composite restoration in the lower right first molar, and translucency around its apical region was visible, the lesion was diagnosed as periapical granuloma. The lesion on tooth 46 was not close to the mandibular canal; this can be seen on Fig. . Therefore, root canal treatment was carried out, despite the uncertain result of the percussion, palpation and sensibility test. The transparent lesion around the apex and the negative sensibility test lead to the decision of endodontic treatment. Diagnosis was made by a dentist who is not a staff member of our Department. The treatment revealed that the pulp was vital. Our oral diagnostic team examined the patient, and we diagnosed the case as cemento-osseous dysplasia based on the panoramic radiograph showing apical translucency lesions around the anterior teeth with vital pulp (Fig. ). The paraesthesia has been continually present ever since. Because the lesion around the lower right canine had already involved the cortical bone by CBCT scan (Fig. ), a root canal filling and removal of the apical lesion were performed. On the CBCT image the involvement of the entire periapical region can be seen including the lingual region and the buccal cortical (Fig. ). It became clear during the planning of the surgery that the blood vessels and nerves of tooth 43 would be injured.\nThe root canal treatment was carried out on the lower right canine in a single-visit treatment using local anaesthaesia. We explored the entire root canal length using a size #15 hand instrument. The working length was determined using an apex locator, (Woodpex III, Guilin,China), then the length was also confirmed with radiographic imaging. Following the length determination, the root canal was shaped using Wave One (Densply Maillefer, York, USA) rotary instrument. The root canal was obturated using guttapercha and AH Plus sealer (Dentsply DeTrey GmbH, Konstanz, Germany) with lateral condensation technique. Glass ionomer cement (Fuji IX GP, GC Co., Tokyo, Japan) was then applied to seal off the access cavity, while the permanent restoration was done.\nWe prepared an intraoral mucoperiostal flap using an L-shaped incision and the surgery was carried out by using a surgical microscope (Aspheron, Schmidt and Bender Hungaria, Budapest, Hungary).\nWe opened up the buccal cortical bone using a surgical bur, thereafter we removed the lesion surrounding the apex of the root. The root apex was resected and a retrograde root canal filling was placed using mineral trioxid aggregate (MTA+, Cerkamed, Stalowa Wola, Poland).\nThe area of the lesion was augmented using gentamicin impregnated BoneAlbumin (OrthoSera Dental Zrt., Gyor, Hungary). We seeked to lower the chance of osteomyelitis occuring with the use of gentamicin. Sutures were then carefully placed to achieve tensionfree closure of the flap for optimal healing.\nThe 19-year-old Caucasian woman is the daughter of the first patient. CBCT showed a radiolucent lesion around the root of the lower right incisor (Fig. ). She is presently asymptomatic after a one-year follow-up, but she occasionally felt tension and moderate pain in the right side of the mandibular region eradiating to her ear, approximately 2 years earlier. The symptoms had no dental background, and ceased gradually.\nPulp tests and periapical pathology diagnoses were made by authors on teeth 33,32,41,43 with the use of percussion, palpation and sensibility test.\nPanoramic radiograph and CBCT scans of the first patient showed radiolucent lesions located in the periapical bone, specifically on lower incisors and canines – in the premandibular, and in the right molar region of the mandible with radiopaque parts showing the lesions inside (Figs. and ). The affected teeth were asymptomatic, CBCT proved the presence of apical pathology. The buccal cortical involvement was discovered with the aid of CBCT, which also affected the treatment plan because 2D imaging methods provide no information on bucco-lingual dimension. Prior to the surgical intervention the use of CBCT was motivated by the fact that only 3D imaging could ascertain the precise shape, location and involvement of surrounding anatomical landmarks of the lesion.\nFigure shows the postoperative condition (Fig. ). At the 6-months periapical follow-up, the bone healing is being processed (Fig. ). 18 months later it can be seen on the CT image that the buccal cortical bone surrounding the root of tooth 43 has regenerated (Fig. ). In the case of the second patient, there were no notable changes in the radiographic status 1 year later, and she has no complaint at present.\nThe removed tissue pieces contained both connective tissue and calcified areas. In the calcified area, beside the irregular trabecular – lamellar bony formations, oval and globular cementum-like structures were present. In the non-calcified area connective tissue was found and connective tissue filled out the centre of another bony sample as well. No elements or remnants of a capsule were visible. The histological diagnosis was cemento-osseous dysplasia (Fig. ). |
A 72-year-old male, who has been in generally good health for 50 years, presented to an outside hospital with symptoms of hoarseness, dysphagia, headaches, dizziness and chronic diarrhea for a few weeks. His head computed tomography (CT) scan revealed multiple intraventricular lesions (), and he was transferred to our hospital for evaluation. A magnetic resonance imaging (MRI) of his brain confirmed the previously noted enhanced intraventricular lesions within the right lateral ventricle, the fourth ventricle and bilateral foramen of Luschka (). An oncologic workup ensued and a CT of the chest, abdomen, and pelvis revealed thickening of the rectum with surrounding fat stranding and a heterogeneous mass in the right cardiophrenic region (). The patient underwent a flexible sigmoidoscopy with rectal biopsies showing a moderately differentiated invasive adenocarcinoma. He also underwent a CT-guided biopsy of the anterior mediastinal mass, which was diagnosed as a World Health Organization (WHO) grade AB thymoma and was thought to be an incidental diagnosis unrelated to his metastatic rectal adenocarcinoma. The patient's neurological functions were assessed intact with no deficits, but he continued to have progressive dysphagia possibly due to the thymoma impinging on his vocal cords. As opposed to performing an invasive craniotomy for resection of the patient's intraventricular lesions, we decided to proceed with a less invasive intraventricular Ommaya reservoir placement. This decision was predicated by the fact that the patient had multiple ventricular involvement, a potential need for intrathecal chemotherapy and the possibility of developing hydrocephalus. Typically, the Ommaya reservoir placement would be performed under general anesthesia, but the anesthesia team had concerns about intubating the patient in the setting of vocal cord compression from his thymoma. Due to these concerns, the procedure was performed under local anesthesia and monitored airway care rather than general anesthesia.\nThe patient was slightly sedated under monitored anesthesia care. A total of 0.5 mg remifentanil was administered intravenously at 0.05 to 0.075 μg/kg/minute, 100 μg of fentanyl was used intravenously for sedation, and 6 mL of 1% lidocaine with 1:100 000 epinephrine was injected subcutaneously for local anesthesia. The patient was then positioned supine on a donut head-fixator and the AxiEM electromagnetic neuronavigation system (Medtronic, Louisville, USA) was registered with great accuracy. A trajectory was planned to encompass all the catheter holes in the ventricular system, to avoid affecting the parenchyma. Incision was made at the right frontal Kocher's point and the Ommaya reservoir was placed under navigation with no complications. The reservoir was noted to fill with clear CSF and pumped easily. CSF was sent for cytology and carcinoembryonic antigen (CEA). The patient remained neurologically and hemodynamically stable throughout the procedure.\nMicroscopic examination of the rectal mass demonstrated a moderately differentiated invasive adenocarcinoma arising in tubular adenoma with high grade-dysplasia (). The tumor was negative for BRAF V600E mutation and KRAS codon 12/13 mutation. Immunohistochemical staining of the tumor showed abnormal loss of expression of MSH2/MSH6 proteins with retained expression of MLH1/PMS2 proteins, suggestive of Lynch syndrome.\nCSF cytology was positive for malignancy and consistent with adenocarcinoma ( and ). CSF CEA was also positive, with a level of 2 355.4 ng/mL, while the serum CEA was 13.4 ng/mL, thereby ruling out passive transfer from serum. The results of CSF cytology and CEA tests confirmed the intra-ventricular lesions to be distant metastases of a primary rectal adenocarcinoma.\nThe patient was neurologically intact postoperatively, only complaining of mild incisional pain. CT scan of the head demonstrated adequate placement of the catheter in the body of the lateral ventricle and small expected intraventricular air. Two weeks postoperatively, the patient underwent whole brain radiation and received 3000 cGy in 10 fractions. Two weeks after that, he was also treated with palliative radiation to the rectum, 3000 cGy in 10 fractions. His clinical course was complicated by aspiration pneumonia, treated with two separate courses of antibiotics, and pulmonary embolism, treated with prophylactic anticoagulation with a consideration of the risk of intracranial hemorrhage from therapeutic anticoagulation. The initial nasogastric tube feeding was replaced by total parenteral nutrition because a jejunostomy tube was unable to be placed surgically due to site obstruction by colon distention from stool and air. Due to poor performance status, he was not a candidate for systemic chemotherapy, rectal surgery or stenting. Given all this, family decided to pursue hospice care. Six weeks postoperatively, he was discharged to a hospice facility where he expired 3 days later. |
In August of 2012 a 16-year-old male presented complaining of rest and activity pain worsening for the past year. He denied any history of trauma. The patient reported is worsening left knee pain and decreased range of motion were limiting his daily activities. Radiographs from an outside facility (not available for publication) showed a lobulated well-defined epiphyseal lesion with sclerotic margins and without stippled calcifications. Computerized tomography (CT) further defined a low-attenuation lesion in the medial femoral condyle measuring 13 mm by 16 mm with well-defined sclerotic margins and depression of the subchondral bone at the lesion border (). Differential diagnosis at this time included chondroblastoma, giant cell tumor, clear cell chondrosarcoma, and osteomyelitis. Given the patient's delayed presentation and our increased concern for metastatic disease we elected to proceed with a CT chest, in place of a routine screening chest radiograph. This CT showed no evidence of metastatic disease. Core needle biopsy () showed mononuclear neoplastic cells with intermixed multinucleated giant cells, tumor cells surrounded by dark blue “chicken wire” calcifications, and fibrochondroid islands all consistent with a chondroblastoma. At this point an MRI of the left knee was obtained to evaluate the extent of articular cartilage involvement and to determine reconstruction options after recommended intralesional curettage. MRI demonstrated a lytic lesion with sclerotic borders involving the posterior aspect of the medial femoral condyle and abutting the posterior articular surface with a 3 mm collapse of the subchondral bone and breach of the chondral surface (). Also the significant enhancing of marrow edema in the medial femoral condyle and adjacent soft tissue edema with associated joint effusion is well demonstrated on the T2 STIR images (). The imaging and pathology were reviewed at multidisciplinary tumor board and the surgical approach and reconstructive options were discussed at the weekly orthopaedic departmental preoperative planning meeting. It was determined that no medical therapy was indicated as there is no role for chemotherapy in the management of chondroblastoma and radiation therapy is not recommended given an increase in risk of malignant transformation [, ]. Surgical plans were then made for curettage and osteochondral allograft reconstruction using a direct approach.\nThe patient underwent resection and allograft reconstruction in January of 2013. The posterior aspect of the medial femoral condyle was approached through a posterior medial approach to the knee using an extensile skin incision dissecting down through the interval between the medial head of the gastrocnemius and the semimembranosus tendon as described by Burks and Schaffer []. The lesion was identified and a high-speed burr and curette were used to achieve intralesional curettage and the tissue was sent to pathology. Then using a K-wire in the center of the lesion a 20 mm trephine was used to the depth of 25 mm in preparation for the allograft. Hydrogen peroxide irrigation and a high-speed burr were used as adjuvant therapy. A 20 mm trephine was then used to the depth of 25 mm in the articular surface of the fresh frozen distal femur allograft (obtained from the Musculoskeletal Transplant Foundation) to prepare the osteochondral plug. The graft was then inserted in a press fit fashion using clock face markings for orientation (). Stability of the allograft was then assessed and confirmed. The wound was irrigated and closed in standard fashion.\nThe patient tolerated the procedure well without complication and was instructed to remain touch down weight bearing in a hinged knee brace locked in full extension for two weeks. He was seen two weeks postoperatively with minimal pain and swelling noted on exam. At this point the Bledsoe brace was unlocked and he was allowed to weight bear as tolerated. He then completed a full course of physical therapy and was seen in follow-up at the three- and five-month marks. At the five-month postoperative visit he denied any pain and reported ability to run and jump without pain or limitation. He demonstrated full active flexion and extension compared to the contralateral extremity (). At his one-year anniversary appointment he again denied pain and demonstrated full painless range of motion, similar to the contralateral knee. He had no effusion and no tenderness to palpation over the medial femoral condyle. MRI and CT imaging of the left knee were obtained which demonstrated incorporation of the osteochondral allograft (Figures and ) and resolution of the previously associated medial condyle marrow edema. MRI and CT scan of the knee and CT chest also revealed no evidence of local recurrence or distant metastasis, respectively. |
A 42-year-old male patient underwent right parietal lobe tumorectomy for a meningioma at Beijing Tiantan Hospital in 2005 (Figure ). He was discharged 8 days after the surgery with a normal temperature and normal muscle strength but an abnormal hemogram. Three months later, he presented to a local hospital with pus at the surgical incision site and was diagnosed with a surgical site infection. One month later, he underwent a decompressive craniotomy for increased intracranial pressure at the local hospital. He was then transferred to our hospital for better symptomatic management, pus evacuation and treatment for occasional epilepsy. On admission, he was oriented but had white exudates posterior to the incision site. He could move his limbs, and his muscle strength was normal. Computed tomography (CT) revealed enhancement of the dura with the surgical area surrounded by cerebral edema.\nThe patient was treated with a third generation cephalosporin for 10 days after the evacuation of the yellow-white pus posterior to the incision site via an arche-cut was performed. Three weeks later, he experienced weakness of his left extremities and hyperspasticity of his right extremities. Routine blood tests showed an intermediate cell percentage of 11.8%. CT and magnetic resonance imaging (MRI) revealed an enhanced cavity wall with an apparent brain tissue hydrocephalus.\nThree months after the last surgery, the patient underwent another procedure to treat the intracranial infection. The thick abscess wall taken during the operation was identified as an Aspergillus granuloma. After the surgery, he was treated with an anti-epileptic and intravenous administration of fluconazole for 1 week. Three weeks later, a broken pustule was found on the incision site and was treated with drainage and flushing with penicillin, gentamicin, and cephalosporin.\nAfter another 2 months, he developed walking dysfunction, along with a diminished muscle strength of 4/5 in his left upper limb and 3/5 in his left lower limb. MRI demonstrated an irregular lesion on the apical lobe, and there was massive hydrocephalus (Figure ). He then underwent his third and fourth operations for the intracranial infection. The wound was drained and flushed with fluconazole and attenuated iodophors. The presence of A. fumigatus was confirmed in the specimens and secretions tested by the Skin & Fungus Lab of Peking University First Hospital (Figure ). Intravenous administration of voriconazole was started according to the susceptibility test, with 400 mg bid on the first day and 200 mg bid from the second day on. Secretions from the wound decreased.\nSixteen days later, a new open abscessed cavity was found at the front of the wound. A cranial CT scan revealed obvious hydrocephalus that involved the motion area. He underwent a procedure for the intracranial infection with an expansion of the original incision site to resect the hypodermis, the abnormal aponeurosis of the occipitofrontalis muscle and the abnormal brain tissue. During the postsurgical physical examination, his muscle strength of the right limb was 4/5 compared with the 0/5 muscle strength in his left limb. His body temperature was elevated at 38.8°C, and a lumbar puncture was performed that revealed leukocytosis in the collected sample of yellow CSF. Intravenous voriconzole was started, resulting in the cessation of pus secretion from the wound. However, the patient started exhibiting some psychiatric symptoms, such as absentmindedness, apathy, and depression, after 2 weeks of oral voriconazole treatment. He was then treated with intravenous itraconazole. One month later, another CT demonstrated that there was no hydrops in the hypodermis layer. He was discharged when he was afebrile and had a normal tension on the operation area. The muscle strength of his proximal left upper limb was 3/5. His distal left upper limb and left lower limb showed a 0/5 muscle strength. His right upper and lower limbs were 4/5.\nThis patient died from recurrent infection 1.5 years later. The FBS of this patient was continuously normal during the admission, indicating that the patient was not diabetic. The WBC of this patient was normal and the bacterial culture was negative during the admission. |
A 8-year-old male patient reported to our department with a complaint of multiple decayed teeth and swelling in relation to lower left back teeth.\nDental history revealed that the patient had a similar swelling about 2 weeks ago. An OPG was taken and abscess drainage was carried out after antibiotic coverage.\nThe medical history revealed the patient was a known case of obstructive hydrocephalus and attention deficit hyperactivity disorder (ADHD) and was under medication. He had a history of seizures.\nIntraoral examination revealed infected root stumps in relation to 75 with intraoral swelling 1.5 cm wide extending from the gingival margin to the sulcus, soft in consistency and tender on palpation. Root stumps were seen in relation to 54, 64, 74 and 84 deep dentinal caries in relation to 85 and caries in relation to 55 and 83.\nDue to the hyperactive nature of the patient, taking radiographs was difficult and it was decided to evaluate the OPG taken 2 weeks ago. The OPG showed a large diffuse radiolucency in relation to 75 approximately 2 cm × 2 cm, extending inferiorly to involve the entire tooth bud of 35, involving both the roots of 75 and mesial root of 36. A provisional diagnosis of radicular cyst was made. Since the radiolucency also involved the crown of 34, a differential diagnosis of dentigerous cyst was suggested.\nOn careful examination of the OPG, a circular radiopacity was observed in the right nasal cavity and a foreign body was suspected (). The patient did not give any history of foreign body insertion. On further questioning , the mother gave a history of snoring.\nThe patient was referred to ENT department. On examination, a button was visualized in the right nasal cavity and successfully removed using a Killian’s nasal speculum. Another gritty object was felt but it could not be removed. The same was scheduled for removal under GA during dental treatment.\nInformed written consent was obtained from the parent for dental treatment and foreign body removal under general anesthesia.\nDental treatment undertaken included cyst enucleation in relation to 75, extractions of 54, 64, 74, 36, 84 and 85, restoration of 55 and 83. Pit and fissure sealants were placed in relation to 16, 26 and 36. Histopathological examination confirmed a diagnosis of dentigerous cyst.\nForeign body retrieved under GA included 2 beads, 1 tack and piece of eraser from right nostril. A plastic piece was recovered from the left nostril (). Examination of the ear canal was also undertaken as a precautionary measure. |
A 47-year-old female was referred to the hospital due to gradual abdominal enlargement accompanied by leg swelling lasting for 2 weeks. There was also a decrease in body weight about 10 kg in the last 8 months. The starting weight of the patient was 67 kg and reduced to 57 kg in the past 8 months. General weakness, pruritus, and decreased pubic and axillary hair were also noticeable. Eight months earlier, she had profound jaundice without abdominal pain. At that time, she got ursodeoxycholic acid and got better. After 2 months of treatment, the patient was lost to follow-up and never visited again to the hospital. She had no noteworthy medical or family history, including gastrointestinal bleeding or liver disease. On physical examination, the patient was alert, fully oriented, and the vital sign was stable. There were pale conjunctiva and icteric of the sclera. Her abdomen was round and soft with severe ascites. There was no abdominal tenderness. Mass or organomegaly was difficult to assess due to massive ascites. Bilateral pitting edema was present on both ankles.\nInitial laboratory data are shown in Table ; it revealed that she had macrocytic anemia, thrombocytopenia, and leukocytosis. The liver function test showed an increase in bilirubin level with mainly direct hyperbilirubinemia with an increase in AST and ALT with AST/ALT ratio >1. ALP and γ-GT levels were normal. Hemostatic functions showed an increase in both INR and APTT. Albumin levels were decreased with an increase in globulin levels. Renal function tests were still normal, and the results of hepatitis B and C were negative. Compared to the laboratory results from 8 months ago, the AST and ALT levels were higher and also the levels of bilirubin more severe compared to the present admission. However, there was no anemia nor thrombocytopenia documented 8 months ago. Ascites fluid analysis showed that the fluid was clear and yellow colored with low levels of protein, LDH, leukocyte, and erythrocyte. SAAG was <1.1 mg/dL. Cytology of ascetic fluid analysis found some polymorphonuclear and mononuclear cells without malignant cells. The results of ascites fluid analysis are also shown in Table .\nThe urinalysis result showed that there was moderate bilirubinuria, but no proteinuria was found. We also found mild urobilinogen in the urine. We already excluded the cause of hypoalbuminemia was due to nephrotic syndrome because no nephrotic-range proteinuria was found based on the examination of protein-creatinine ratio or albumin-creatinine ratio. Compared to the results from 8 months ago, the bilirubin and urobilinogen in the urine were milder in this admission with the other results similar. The urinalysis results are shown in Table .\nAbdominal ultrasound examination (shown in Fig. ) showed ascites fluid in perivesical, perihepatic, perisplenic, hepatorenal fossa, and peri-intestine regions. No mass or organomegaly was found. Previous abdominal ultrasound from 8 months ago showed no ascites, but there was a thickening of the wall of the gall bladder without a sign of biliary obstruction. Because of the high level of globulin in this patient, we performed plasma protein electrophoresis in this patient. It showed a monoclonal gammopathy with an M spike in the gamma region with an increased level of γ-globulin. The result of plasma protein electrophoresis examination is shown in Figure .\nWhile it is unfortunate that there was a lack of data regarding the bone marrow analysis in this patient, we found no sign of organ damage related to suspicion of multiple myeloma regarding the hypergammaglobulinemia in this patient. There were no lytic lesion from bone survey, hypercalcemia, or renal dysfunction from this patient. Because we suspected the possibility of autoimmunity in this patient, we found that there was an increased level of serum anti-nuclear antibody (ANA) by ELISA.\nBased on the current data, the ascites was thought due to portal hypertension that might be caused by AIH. The patient was restricted for sodium intake and was given spironolactone 100 mg QD, furosemide 40 mg QD, ursodeoxycholic acid 250 mg b.i.d., and prednisone 60 mg/day. She also underwent large-volume paracentesis for the ascites followed by albumin transfusion. We also administered vitamin K injection and transfusion of fresh frozen plasma to correct the hemostasis function; however, there was no improvement regarding prolongation of INR and APTT.\nClinical improvements were found for the ascites and the laboratory results after 1-week treatment. She visited the Gastroenterohepatology outpatient clinic 1 week later, and there was a clinical improvement for the ascites showed by the decrease in abdominal circumference with a decrease in body weight of 2 kg in 1 week. The monitoring of laboratory results is shown in Figure .\nThe patient was planned to do magnetic resonance cholangiopancreatography and liver biopsy afterward. However, 1 week later, she visited the outpatient Gastroenterohepatology clinic. She had a sudden decrease of consciousness in the morning with the suspicion of stroke with intracranial hemorrhage. She died because of brain herniation due to the intracranial hemorrhage. |
The patient was a 69-year-old woman with intermittent chest tightness and chest pain over the previous five years. She was hospitalised for severe chest tightness and chest pain persisting for three days. She had a history of hypertension and hyperlipidaemia; the admission examination showed no other abnormalities. Routine blood, urine and stool tests, liver and kidney function, clotting time, electrocardiogram, chest radiography and echocardiography were normal. A diagnosis of coronary artery disease was considered.\nCoronary angiography showed a right coronary arterydominant circulation. The left main coronary artery was normal, 80% of the middle segment of the left anterior descending (LAD) coronary artery showed stenosis, and the diagonal branch issuing from the site of the stenosis was thicker than the LAD artery. Plaques, but no obvious stenosis, were found in the circumflex and right coronary arteries ().\nAfter discussing treatment with the patient, it was decided to perform PCI of the LAD artery. Because of the narrow opening of the diagonal branch, and because the diagonal branch was thicker than the LAD artery, we planned to implant a stent at the juncture of the diagonal branch and the LAD artery, and to position a guide wire in the artery to protect it ().\nAfter stent implantation, the guide wire was set for expansion (). After expansion, angiography showed no mezzanine, side branch occlusion or residual stenosis at the implantation site, and forward blood flow was TIMI grade 3. However, contrast agent overflow was seen at the distal left LAD artery (). The patient did not experience discomfort and had normal blood pressure with a steady heart rate. As the guide wire did not reach the distal vessel through the perforation site even after several attempts, it was positioned proximal to the perforation site, and a balloon was used for compression (). Because this did not successfully close the perforation (), a coil was used to achieve successful closure (), after obtaining the consent of family members. |
A 49-year-old caucasian female patient with a previous medical history significant for von Willebrand type one disease presented to a hand surgeon at our department of orthopedic surgery after sustaining a crush injury to her left fifth digit following a motor vehicle accident. Physical examination was notable for 30-degree flexion contractures of both the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints of the left fifth digit, associated with a substantial decrease in active and passive range of motion (ROM). The patient underwent an uneventful capsulectomy of the MCP and PIP joints with tenolysis of the flexor tendons of the left fifth digit. Given her adequate tolerance to the procedure, she was later discharged with an implanted infraclavicular PNC and a prescription for daily occupational therapy (OT), with the PNC being removed on the fifth day postoperatively.\nAt the sixth-week postoperative follow-up consultation, the patient described intense pain in her left fifth digit, which she characterized as often burning, sometimes aching and throbbing, with an average intensity of 7 out of 10 on the numeric rating scale (NRS). Additionally, she presented with diffuse edema of the whole fifth digit, did not show any improvements in passive ROM, and reported being unable to tolerate most exercises during OT sessions. At this time, passive ROM of her left fifth digit was still severely limited, being restricted to 30 degrees of flexion on the both the MCP and PIP joints. Additionally, she was unable to initiate active flexion of the MCP, while being able to perform an active flexion of 20 degrees of the PIP\nAfter consulting with the regional anesthesia medical staff, a determination was made to submit the patient to a trial with an ulnar PNC, so as to assist with targeted pain relief and OT goals, as well as to ascertain for a possible CRPS type 1 diagnosis. The PNC was implanted under ultrasound guidance and was left in place for seven days. During the trial, the patient reported a decrease in the pain intensity score from 7 out of 10 to 0-1 out of 10 on the NRS.\nGiven the result of the trial, the patient was then submitted to a nuclear bone scan, which revealed increased radioactive tracer activity in the entire left fifth digit on blood pool and delayed imaging, which, in the context of her medical history, was consistent with a diagnosis of active CRPS type 1.\nGiven the patient’s medical history (symptoms and signs fulfilling the 2010 revised CRPS clinical diagnostic criteria proposed by the International Association for the Study of Pain), the successful trial with an implanted ulnar PNC, the anatomical region of radioactive tracer caption on the nuclear bone scan, and after consulting with the medical staff of our department of pain medicine, the patient was submitted to an uneventful ultrasound-guided implantation of a percutaneous PNS (Bioness StimRouter®, Valencia, CA) (Figure ) parallel with the trajectory of the left ulnar nerve just distal to the ulnar tunnel, with intraoperative stimulation of the nerve obtained at 1.0 milliamps [] (Figure ).\nTwo weeks after implantation of the PNS, the patient experienced a reduction in the pain intensity score from 7 out of 10 to 0-1 out of 10 on the NRS and was able to initiate pain-free active motion of her left fifth digit. At the 3-month follow-up consultation, the patient reported maintenance of the reduction of pain in her left upper extremity with the implanted percutaneous PNS, as well as improved performance in her daily activities. |
A 46-year-old man also reported exercise/activity-related pain and fatigue from early childhood. As patient 1, he was always considered to be “a lazy child”. He was not able to run and physical activities such as walking or swimming were challenging. As a child he reported trying to build a good relationship with his physical education teachers, so they would feel pity for him and he could avoid any strenuous physical activities (PA). He experienced three severe episodes of rhabdomyolyses in his life. The first one happened during childhood, which followed vigorous physical activities. The second rhabdomyolysis episode was at the age of 18 following multiple squats, which he performed during a physical test for military service. Not qualifying for the military service, instead he had to complete a civilian service at the university hospital at the age of 22. As he was clearly weaker than his colleagues, a diagnostic investigation took place, which included a skeletal muscle biopsy. At that time, doctors advised him to avoid excessive physical effort. He was told about the second wind phenomenon; however, it was not explained how to reach it. Additionally, he was recommended to eat a maximum of 20% of his daily food intake in carbohydrates. However, the rest of the macronutrients recommendations were not specified. In the following years, his physical activity level decreased, leading to physical deconditioning, loss of muscle mass, and increase in fatty adipose tissue and body weight.\nThe third rhabdomyolysis episode was experienced one year ago and was nearly fatal. He was undergoing physical assessment for the insurance company and pushed himself too hard, resulting in a severe contracture of his lower back muscles. He was admitted to hospital. During the hospital stay he was also diagnosed with myocarditis. Following this episode, he decided to learn more about the condition to manage it better.\nHe began doing gentle aerobic exercises, which improved his ability to attain a second wind. He attended a conference where he met a Spanish team from whom he learnt about the strength training trial performed in Madrid and decided to try it himself in a local gym []. Initially he approached a personal trainer. However, he did not feel the trainer understood his condition and was pushing him too hard. He decided to write his own programme based on strength training principles and exercises he learnt at the conferences and meetings.\nWhen in the gym he reports always doing an aerobic “warm up” by cycling on a stationary bike for 20 minutes, he then exercises on resistance machines (chest press, seated row, butterfly, chest horizontal adduction, reversed butterfly, rare deltoids and trapezius, lat pulldown, leg press, leg adductors, and leg abductors). He finishes his sessions with more aerobic exercise by walking on a treadmill and/or cycling on a stationary bike. and illustrate his progress during the first three months of training (based on personal records). He completes between 5 and 15 repetitions of each exercise with one-minute rest in between sets. He stops a set of exercise earlier if he feels any discomfort in the muscle.\nHe did not report Delayed Onset Muscle Soreness (DOMS) or McArdle symptoms following initial sessions. After three months of resistance training, he found his sleep pattern, overall stamina and McArdle symptoms improved. He is now able to walk two kilometres stopping only once, as opposed to previously when he would have to stop multiple times. He has also found it easier to perform everyday tasks such as changing a car tyre. He has been eating a balanced diet. He autonomously chose not to take any supplements containing glucose pre- or intratraining session. |
A 31-year-old gravida 4 para 0 African American woman at 22-weeks gestation presented with vaginal bleeding to an outside hospital. Her obstetric history was significant for 2 therapeutic abortions and 1 spontaneous abortion. During prenatal care, the fetus was noted to have a unilateral dysplastic kidney. The patient’s family history was significant for two family members with cervical cancer and two family members with endometrial cancer. She was placed on bedrest with inpatient admission. 48 h after admission she developed pelvic pain and uterine contractions. She expelled a mass vaginally measuring 11 × 9 × 5 cm with no fetal contents. The pathology from the outside facility showed a showed a highly cellular tumor composed of spindle-shaped cells and bizarre multinucleated giant cells with focal myxomatous change with mitotic count is greater than 50 per 10 high power field (Positive for CD10, SMA, ER, PR, EMA) with the differential diagnosis including endometrial stromal sarcoma and undifferentiated uterine sarcoma. The patient underwent examination under anesthesia, demonstrating a 3 × 3 cm defect of the posterior vaginal wall with active bleeding, which was sutured for hemostasis. The cervix was long, closed, and high with no evidence of bleeding and the fetus was intact with normal heart tones. She was discharged in stable condition.\nAt 27-weeks, the patient was referred to our institution for maternal-fetal medicine, and gynecology oncology consultation. On initial evaluation, she reported no prior abnormal gynecology history and no history of infertility issues. She denied dyspareunia and bulk symptoms prior to or during pregnancy, and her periods before pregnancy were normal. A pap smear at 27-weeks gestation was normal and negative for human papilloma virus. Her intake physical exam at our institution revealed a normal pelvic exam with no evidence of residual vaginal mass, and an ultrasound revealed no intrauterine myomas.\nGiven the differential diagnosis included an endometrial stromal sarcoma, an undifferentiated uterine sarcoma, and a primary vaginal sarcoma, the patient underwent magnetic resonance imaging (MRI) without contrast of the chest, abdomen, and pelvis at 27 weeks. MRI findings were notable for a peri-centimeter cyst in the cervix consistent with a Nabothian cyst, a multiloculated cystic structure in the fetal abdomen consistent with dysplastic kidney, and an anterior placenta. There was no evidence of metastatic disease.\nDue to the inability to ascertain whether the cancer had originated in the uterus, cervix or vagina, the patient desired definitive management for possible uterine sarcoma. In consultation with maternal fetal medicine and gynecology oncology specialists, the decision was made to proceed with a cesarean hysterectomy at 36 weeks. Betamethasone 12 mg intramuscularly was given for two doses 24 h apart with the first dose at 35 weeks and 6 days gestational age.\nAt 36 weeks and 1 day, she underwent planned exam under anesthesia of the vaginal canal with cesarean hysterectomy, bilateral salpingectomy, and peritoneal biopsies. She delivered a male infant weighing 2520 g with Apgars of 9 and 9. Operative findings were notable for normal appearing pelvic organs. There were no palpable or visibly enlarged pelvic/periaortic lymph nodes or evidence of metastatic disease throughout the peritoneal cavity. The neonate was admitted to the NICU post-delivery for prematurity. Neonatal US confirmed a right multi-cystic dysplastic kidney. He was transferred out of NICU on day 2 of life, and discharged home with his mother.\nThe final surgical pathology report was benign: no malignant or neoplastic cells were seen. The patient was seen at her 6-week postpartum visit and was doing well with a normal pelvic exam. At a follow-up surveillance visit 3 months postpartum, she was noted to have a 1 cm posterior vaginal wall lesion; biopsy results showed a high-grade sarcoma. The tumor was estrogen receptor and progesterone receptor positive. Computer tomography (CT) with contrast of the chest, abdomen, and pelvis showed no evidence of metastatic disease. The patient underwent an upper vaginectomy and proctoscopy. Operative findings were notable for 1.5 cm polypoid lesion in the posterior vagina wall 5 cm distal to the posterior vaginal apex. A 1 cm surgical margin was obtained circumferentially around this lesion where feasible, and surgical pathology showed high-grade sarcoma () of the polyp lesion with negative surgical margins. The tissue removed from this excision showed residual sarcoma, morphologically similar to the original pathology from the outside hospital pathology. All other vaginal biopsies were also negative for malignancy. Marker seeds were placed in the proximal and distal margins of the areas where the sarcoma was excised. She was treated adjuvant high dose rate vaginal brachytherapy using a multi-channel vaginal cylinder. She received a biologically equivalent 2 Gy dose (EQD2) of 45 Gy to the whole length of the vagina and 60 Gy to the post-operative bed (). A CT scan 36 months after surgery continue to show no evidence of disease. She remains disease free 58 months after completion of vaginal brachytherapy. |
A 40-year-old man with no significant past medical history presented to his primary care physician with worsening intermittent right lower quadrant abdominal pain radiating to his right flank. This pain was described as a constant dull ache with intermittent sharp pains. For the last three days, he had feelings of being bloated with progressive abdominal discomfort. His medical history was unremarkable aside from asthma, hypertension, and obesity with BMI of 35.7, while family history was significant for ovarian cancer in his mother. Of note, within the past week, he was treated with a course of high dose steroids for asthma exacerbation. His social history consisted of being a father to four biological children. Upon presentation, the patient denied dysuria, diarrhea, and blood or pain with bowel movements. On physical exam, he had a distended abdomen with right lower quadrant tenderness but no costovertebral angle tenderness, rebound tenderness, or guarding. A CT scan of the abdomen and pelvis revealed a large midline pelvic complex cystic lesion that appeared to arise from the right vas deferens (Figures and ). Radiology recommended an MRI for clearer visualization and location of the mass based on results of the CT scan (Figures and ). The MRI displayed intensity of the mass on T2-weighted imaging (). The distal portion of the right vas deferens was also dilated near the ejaculatory duct junction. The patient had followup appointments with general surgery and urology for surgical evaluation. A joint procedure between general surgery and urology was planned for cystourethroscopy, diagnostic laparoscopy, and excision of the pelvic mass.\nA cystourethroscopy was performed to visualize the urethra and prostate. Diagnostic laparoscopy confirmed the presence of a mass anterior to the rectum and under the parietal peritoneum covering the dome of the bladder. The remainder of the procedure was converted to exploratory laparotomy for safer removal of the mass. The mass was palpated and found to be separate from the bladder and prostate and attached to the right vas deferens near the junction of the bladder and prostate. The right vas deferens was surgically divided proximal to the mass. A 9.0 × 5.6 × 5.3 cm, 125 g mass was successfully excised without evidence of invasion into surrounding structures or vasculature.\nGross exam of the mass in the operating room revealed a central cystic cavity with cloudy brown fluid. Further, the results from immunological stains performed by pathology revealed a highly unexpected diagnosis with an immunoprofile consistent with endometriosis. The H&E stain () displayed a layer of endometrial epithelium with underlying stroma. The cells lining the cystic mass stained strongly positive for CK7 () and estrogen receptors (). CD10 stains were positive () and CD15 staining was focally positive () in the underlying stromal-like tissue. GATA-3 stain was negative. The patient was discharged on postoperative day two. In a two-week followup appointment, he had complete resolution of abdominal pain. |
A 66-year-old man was referred to our hospital with the diagnosis of a left ventricular mass detected incidentally during transthoracic echocardiography that was performed prior to a cholecystectomy. He had no cardiac symptoms or history of embolism. On physical examination, he had normal heart sounds without any cardiac murmurs. The results on chest radiography, electrocardiography, and blood examinations were normal. Transthoracic echocardiography revealed a mobile mass, 16 mm in diameter, originating from the anterolateral wall of the left ventricle. Its stalk was short, and the tumor was directly attached to the ventricular wall. The diameter of the left ventricle was 52 mm in the diastolic phase and 30 mm in the systolic phase. The ejection fraction (EF) of the left ventricle was estimated as 80 %. Computed tomography showed a homogeneous 20-mm-diameter tumor that originated from the anterolateral wall of the left ventricle with an extremely short stalk.\nUnder general anesthesia, the heart was exposed through a median thoracotomy. The pericardium was retracted by Lima suture []. The tumor was observed in detail via transesophageal echocardiography (TEE). Tumor location, its relation to the coronary arteries in particular, was estimated by gentle pressure placed on the left ventricular wall by the surgeon’s finger. The origin of the tumor was detected to be on the free wall of the left ventricle between the first diagonal and obtuse marginal branches (Fig. ). The incision line was carefully planned under echo-guidance and then cardiopulmonary bypass through bicaval and aortic cannulation was instituted. The heart was arrested with antegrade tepid blood cardioplegia. The final location of the incision was determined by epicardial echocardiography focused on the surgical margin. A 3-cm-long ventriculotomy was placed between the first diagonal and obtuse marginal branches along the planned incision line. A gelatinous 18-mm mass was directly visualized and found to originate from the trabecular muscle. The distance from the incision line to the edge of the stalk was 5 mm. The tumor was completely resected with a >5-mm margin of attached trabecular muscle (Fig. ).\nOn a subsequent histopathological examination, typical features of myxoma were demonstrated, a good surgical margin >5 mm was achieved, and there was no evidence of invasion in the cross-section of the resected myocardium. The ventriculotomy was closed by four mattress sutures and a running 4-0 polyvinylidenefluoride suture (Asflex; CrownJun Kono Corp., Tokyo) with underlying Teflon felt strips (CrownJun Kono Corp., Tokyo). The postoperative course was uneventful, and no evidence of recurrence or arrhythmia has been seen in the 24 months since the operation. Postoperative cardiac function was estimated by echocardiography prior to discharge from the hospital and at 6 months after the operation. The diastolic and systolic diameters of the left ventricle were 50 and 26 mm, respectively, at discharge, and 51 and 30 mm, respectively, at 6 months after the surgery. The EF of the left ventricle at discharge and 6 months after the surgery was 85 and 75 %, respectively.\nPrimary cardiac tumors are rare. Nearly 75 % are benign, and most of these benign heart tumors are myxomas. Approximately 75 % of cardiac myxomas originate from the left atrium; only 3–4 % are found in the left ventricle []. Myxomas are histopathologically benign; however, they tend to recur. The major surgical concern is preventing recurrence. Complete extirpation with precise removal of the base under a clear surgical view is required. In the case of myxomas originating from the left ventricle, the surgical approach is important. A transaortic or transmitral approach is generally employed for their removal [, ]. A transaortic approach would be useful for myxomas located in the left ventricular outflow tract versus the transmitral approach for those in posterior locations. Many of the myxomas originating from the left ventricle can be removed by those approaches. However, in cases of myxomas with a short stalk, or myxomas located at the apical region or subvalvular region, surgical manipulation by the approaches mentioned above should be performed under an inadequate surgical view.\nGreco et al. reported an approach combined with video-assisted cardioscopy for myxoma at the apex region []. For subvalvular myxomas, Talwalker et al. reported an approach using mobilization of the anterior leaflet of the mitral valve []. These alternatives may have advantages in certain limited cases, but are too complicated to be standard approaches. Even though a transventricular approach has potential complications, such as dysfunction of the left ventricle or postoperative ventricular arrhythmia, this approach provides a good surgical view that enables excision of both the tumor and its stalk in an en bloc fashion.\nIn our patient, the approach route was planned preoperatively. Because the tumor was located on the anterolateral wall of the left ventricle and had a short and wide stalk and the diameter of the aortic annulus (estimated as 21 mm) was relatively small, we concluded that the transaortic and transmitral approaches were inadequate. We estimated that the transaortic view via a relatively small aortic annulus might be insufficient to achieve complete resection. We also examined the transmitral approaches including superior septal and Dubost incision. We concluded that a competent surgical field except beyond the tumor might be provided by these approaches. The incidence of incomplete surgical margin at the apical edge might be considered. Since our highest priority should be to achieve complete tumor resection, we decided to select a transventricular approach. To minimize the incidence of complications associated with a left ventriculotomy, the length of the ventriculotomy was designed to be as short as possible. A proper ventriculotomy was planned according to measurement by the combined use of TEE [] from the inside and epicardial direct echocardiography from the outside. This method provided a good guide without being complicated. The tumor and its attachment were exposed under good visualization and completely resected in an en bloc fashion. No recurrence has occurred to date. |
A 65-year-old male was scheduled for clipping of right superior cerebellar artery aneurysm in left lateral position. The patient was intubated with 8.5-mm polyvinylchloride cuffed tube which was examined for any cuff leaks before intubation. The procedure was uneventful and the patient was positioned for surgery in the left lateral position. Anaesthesia was maintained with sevoflurane in air–oxygen mixture with intermittent doses of intravenous opioids and vecuronium bromide for skeletal muscle relaxation. After an hour of surgery, it was noticed that the exhaled tidal volume was low and the bellows were collapsing in spite of increasing the fresh gas flows to 5 L/min. The surgical team was informed and a thorough check for leaks in the machine and circuits was conducted which did not reveal any issue. On examining the ETT pilot balloon under the drapes, we found the pilot balloon was deflated. On inflating with 3 mL of air, the tidal volume was increased back to normal, and the bellows were filling even with fresh gas flows of <1 L/min. However, the issue recurred after 5 min and the cuff pressure monitor showed a pressure of 5 cm water. As at this stage the surgeons had applied temporary clip to the aneurysm and there was intraoperative brain bulge, it was decided not to change the ETT.\nThere was an immediate need to find the source of leak, as to whether it was at the level of the inflation valve, pilot balloon, pilot tubing, or a cuff defect. A mixture of 5 mL saline and 5 mL lignocaine jelly was injected with the intent to seal any small rent in the inflation system. To make up for possible defective inflation valve, and at the same time to provide means to inflate the cuff when required, one end of a 100-cm arterial extension line was attached to the inflation valve and the other end was attached to the ETT cuff pressure monitor (Portex, Smiths Medical, Inc).\nHowever, the cuff continued to deflate every 5 min with recurring ventilatory leak indicating that the seal caused by lignocaine jelly was not effective. An attempt was made to find a solution to keep the pilot cuff in an inflated state. To the three-way end of the arterial extension, in one port ET cuff pressure monitor was connected and to the other port a 50-mL syringe filled with air in an infusion pump was connected. This formed an inflation system which was attached to the inflation valve of the pilot balloon of the ETT []. The rate of infusion of air through the syringe pump was started at 10 mL/h increasing it stepwise by 10 mL till the rate at which there was no leak. At this stage, optimal ventilation was possible through the ETT without any leak. This was achieved at a rate of 50 mL/h which was sufficient to keep the cuff inflated making up for the loss. The surgery was successfully completed with no untoward complication. The patient was extubated and a thorough inspection of the tube revealed a rent in the cuff []. |
A 74-year-old male patient presented with a 1.5 cm ulcerated swelling over the skin of his left pinna in October 2008. Biopsy revealed an invasive moderately differentiated squamous cell carcinoma (MDSCC) which was excised with wide margins. In April 2009, he developed recurrent disease posterior to the angle of the mandible with regional metastasis to the parotid and suspicious involvement of ipsilateral level II neck nodes. A total parotidectomy with modified radical neck dissection was performed in May 2009. Pathology confirmed MDSCC in the parotid with positive margins. All dissected lymph nodes were negative. He received a hypofractionated course of adjuvant RT to the parotid region: 60 Gy/25 fractions (2.4 Gy per fraction, one fraction per day, five days per week). RT was planned with 6 MV photons using a 5-field 3D conformal technique. He tolerated treatment reasonably well and completed treatment in September 2009 without interruptions.\nAt 18 months post-RT, a small patch of osteoradionecrosis was noted in the left external auditory canal. This was treated conservatively and it healed well. A follow-up head and neck computed tomography (CT) scan was done in June 2013 (Figure ), when his care was transferred to a new physician. This reported an incidental finding of an irregular enhancing focus involving the left temporal lobe and extending to left parietal lobe measuring about 8 x 3.3 cm in size. It was associated with moderate white matter edema extending up to the periventricular location of the posterior horn of the lateral ventricle. The differential diagnoses were brain metastasis and subacute cerebral infarct. There was no evidence of recurrence in the post-op or irradiated region. The patient denied development of any new symptoms. However, his wife had noted some short term memory loss and occasional word-finding difficulty over the last few months. A clinical examination revealed a stable lower motor neuron facial palsy, which he had developed postoperatively in 2009. Neurological examination was otherwise unremarkable.\nA magnetic resonance imaging scan (MRI) of the brain (Figures -) revealed a heterogeneous mass with peripheral nodular enhancement and some areas of T2-weighted-fluid-attenuated inversion recovery (T2/ FLAIR) signal hyperintensity. The surrounding vasogenic edema was seen reaching high parietal lobe superiorly and left hippocampus medially.\nThere was no evidence of abnormal restricted diffusion (Figures -). The differential diagnoses were revised to exclude subacute infarction and include radionecrosis or infection.\nThe radiation treatment plan was reviewed to rule out radionecrosis of the temporal lobe. The extent of the lesion in the temporo-parietal lobes correlated with the shape of the isodose curves on the treatment planning system, and hence, radionecrosis of the temporal lobe was established as the working diagnosis (Figure ). As the patient was asymptomatic, it was decided to observe the natural evolution of this lesion with serial imaging and intervene early if any new signs or symptoms developed. Subsequent MRI at three months (Figure ) showed reduction in edema and mass effect; however, the enhancement remained unchanged. At nine months, the MRI showed a new well-defined sub-centimeter enhancing nodule in the contralateral para hippocampal cortex reported as progression of metastatic disease (Figure ). A neuroradiology consultation suggested that the lesion could be a part of the evolving radionecrosis; however, there remained a distinct possibility of it being metastasis. In view of the lack of new clinical signs or symptoms, we decided to continue observation. An imaging at 12 months revealed no change in the size or characteristics of either lesion.\nAn MRI scan done in September 2014 reported that there was regression in the edema and T2/FLAIR changes but there was no change in the contralateral enhancing nodule (Figure ). An MRI scan at two years reported significant encephalomalacia with ex-vacuo dilatation of the temporal horn with loss of volume of the temporal lobe cortex and white matter (Figure ). The contralateral enhancing lesion had resolved. Throughout this follow-up period, the patient remained healthy and his clinical condition remained stable without any intervention. The patient remains well 30 months after the first suspicious CT. |
An 18-year-old girl admitted with history of weakness of all four limbs for 6 weeks. The weakness started in right upper limb, followed by involvement of right lower limb, left lower limb and finally the left upper limb within 3 weeks. She subsequently developed burning sensation of limbs and trunk. There was no history of sphincter involvement. She had past history of few episodes of generalized tonic–clonic seizures in 1 year preceding her admission. There was no history of headache, vomiting or visual impairment. She was born at home at full term, and according to her father, she had delayed milestones. She relinquished her study at Class I because of poor performance as well as financial constraints. She had her menarche at the age of 14 years. On enquiry, she disclosed that she had multiple nodular swellings all over her body since her childhood, which increased in number with increasing age. Similar swellings were also noticed by her father and one of her younger sisters.\nHer general examination revealed normal vital functions, multiple rubbery nodular swellings all over her body and multiple areas of skin pigmentation of varying sizes all over the body, more than six of which were measuring 1.5 cm or more. Both pupils were eccentric, with features of hypertelorism (distance between inner canthus of both eyes is more than half of inter-pupillary distance). She also had pes cavus deformities in both feet.\nThe neurological examination revealed grossly normal higher mental function and cranial nerves. She had wasting of both legs with normal tone in lower limbs and spasticity in upper limbs. The upper limbs had MRC grade 3 power and lower limbs had MRC grade 4 power. All deep tendon reflexes were exaggerated except ankle jerks which were depressed on the left side and absent on the right. The Babinski sign was positive on both sides. There was no abnormal movement and co-ordination was normal. The sensory examination revealed absent joint and position senses in toes with impaired vibration senses up to C5 spinous process with normal pain and temperature senses. The examination of cranium and spine did not reveal any abnormality.\nThe ophthalmological examination revealed eccentric pupils with slightly thin limbal area and elevated limbal curvature, the presence of two Lisch nodules and changed corneal curvature in the left eye, and normal cornea and five to seven Lisch nodules in the right eye. The cardiovascular examination revealed normal 1st heart sound with single 2nd heart sound and a systolic click followed by a crescendo–decresendo murmur over the pulmonary area. The respiratory and gastrointestinal (GI) systemic examinations were unremarkable.\nHer investigations revealed Hb of 10 g/dl with normal total and differential counts, erythrocyte sedimentation rate (ESR) of 26 mm/hour, normal liver and renal functions and serum electrolytes. ECG showed features of right ventricular hypertrophy with strain pattern. Echocardiography showed situs solitus, congenital pulmonary stenosis (both infundibular and valvular) with right ventricular outflow tract gradient of 37 mmHg []. Ultrasonography of the whole abdomen was normal. Cranial computed tomography (CT) scan was also unremarkable. Magnetic resonance imaging (MRI) of the cervical spine showed a rounded enhancing intradural extramedullary mass on the left side at C1 –C2 level, compressing the cord from outside with extension through the intervertebral foramen on the left side suggesting “dumbbell”-shaped schwannoma [Figures and ]. Nerve conduction study revealed prolonged distal latencies, slow conduction velocities with preserved Compound Muscle Action Potential amplitude of lower limbs, suggesting demyelinating type of neuropathy with absent sural Sensory nerve Action Potential on both the sides []. |
A 32-year-old white woman, who was undergoing transgender body modifications and no previous medical history, presented to our emergency department (ED) with a chief complaint of right forearm pain, associated with redness and blistering. The patient was a tattoo fanatic who underwent solar branding on her right forearm approximately 2 weeks before presentation. The patient first noticed the blistering of the branded area 3 days after her body modification. Over the next few days, the entire branded area became very warm, swollen, painful to touch, and developed cellulitis with weeping blisters. Given her dire situation, the patient finally sought medical care in the local urgent care center. The patient was diagnosed with a superficial infection of her right forearm full thickness burn and prescribed oral clindamycin. The patient continued to develop painful blisters for the next week and did not notice any improvements in her cellulitis despite the antibiotic treatment, prompting her to come to our ED for a second medical opinion.\nDuring her physical examination, the patient was noted to have painful blisters, redness, and swelling of the right forearm and hand (Figure ). She did have a full range of motion of the hand; however, there was mild pain noted on the flexion of the hand. There were no signs of sepsis, and her vital signs and her laboratory panel which included white blood cell count were all within normal limits. The rest of the physical examination was also unremarkable. The patient was admitted to the Burn Surgery Service for intravenous (IV) antibiotics and possible operative interventions.\nThe patient was started on IV clindamycin 600 mg every 8 hours, and once adequate pain control was achieved, a bedside debridement was performed in the Burn Unit. The following day, the patient was taken to the operating room for tangential excision of her wound and split-thickness skin autograft (STSG) placement onto her right forearm. The left anterolateral thigh was chosen as the donor site. The grafted site was dressed with xeroform, followed by a layer of bacitracin ointment and then wrapped with Kerlex and Coban dressings. A right forearm elbow splint was fitted and placed by the occupational therapy service for further graft protection. Postoperatively, the patient was transferred back to the floors without complications, and antibiotics were stopped. The right forearm dressing was taken down on postoperative day 4 to evaluate the STSG. The entire graft was viable and taken. Subsequently, the graft staples were removed on postoperative day 5.\nThe patient recovered exceptionally well and was discharged home a few days later. Two weeks later, the patient returned to the burn clinic for a follow-up appointment. The skin graft and the donor site healed remarkably well (Figure ). The patient reported no pain and had a full range of motion of the hand and wrist. The patient was discharged from the burn service and advised to use over-the-counter moisturizer or lotion as needed. |
A 68 year old lady was referred to oncology outpatients in January 2010, with a month history of severe abdominal pain. Her past clinical history included no tubal ligation or hormone replacement therapy. She had previously given birth to a female child at her age of 21. The patient was fit and well with no significant past medical history apart from hypertension and diabetes. There was no family history of breast or ovarian carcinoma.\nPhysical examination revealed an abdominal pelvic mass with ascites and omental deposits. Blood analysis showed haemoglobin concentration of 11.3 g/dl while the rest of the analysis were normal including the carcinoembryonic antigen (CEA), alphafetoprotein and Cancer Antigen-125 (CA-125) (1.25 U/ml). The cytological examination of the ascitic fluid showed cellular smear composing of mixed inflammatory cells admixed with papillary and acinar clusters of eosinophilic cells with pleomorphic hyperchromatic nuclei thus suggesting a metastatic carcinoma.\nPelvic sonogram revealed a large tumour mass with solid and cystic components. Minimal ascites was noted. A subsequent computerized tomography (CT) scan of the abdomen and pelvis revealed heterogeneously enhancing mass lesion measuring 9 × 7.1 cm with solid and cystic areas and calcification in the retrovesical region (Figure ). The mass was found to be compressing on the right lower ureter leading to right hydrodeuteronephrosis. Multiple enlarged peritoneal nodules with a largest one measuring 10 × 6.3 cm were observed. Moderate free fluid in abdomen and pelvis with moderate right pleural effusion was observed. The diagnosis of the malignant transformation was suggested by the invasive growth of soft tissue components through the teratoma wall by CT scan images. Finally based on the clinical manifestations she was diagnosed as having FIGO stage IIIC of immature teratoma.\nDue to unresectable bulky tumours and poor performance status the patient underwent neoadjuvant chemotherapy (NAC) followed by Interval Cytoreductive Surgery (ICS). Four cycles of combination of paclitaxel and carboplatin were administered every 3 weeks. ICS was performed in the 5th week after administration of the 4th cycle of NAC. Standard procedures of ICS consisting of total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy and maximal debulking of metastatic tumour was adopted. Following the procedure there was no residual macroscopic disease and she was transferred to high dependency.\nThe surface of the tumour appeared rough and congested. On cutting, the ovarian mass was full of sebaceous material and hair densely adherent to surrounding structures. Histopathological examination confirmed bilateral teratoma complicated with carcinosarcoma (Figure ) with heterogeneous rhabdoid elements (Figure ) Microscopically the left ovarian tumour displayed variable size cyst lined by multilayered malignant squamous cells (Figure ) with rhabdoid spindle cells, cytoplasmic clearing, mature atypical cartilage (Figure ), malignant tubules, small round cells with rosettes, bone marrow and neural bundle. In addition the focal area showed atypical giant bizarre cells. The observation of the right ovarian tumour displayed admixture of malignant, epithelial and mesenchymal elements. The epithelial layers showed variable sized islands of squamoid and polygonal spindle cells and rarely showed tubular papillary structure. The stroma appeared to be a mixture of rhabdoid spindle cells, primitive mesenchymal cells, neural elements, adipocytic elements. Focal area showed pigmented cells.\nThe patient recovered well from surgery and was referred for oncological follow up and post- surgical chemotherapy (same regime as NAC). Given her age and performance status a surveillance approach was taken with regular clinical examinations, serial tumour markers and routine CT scans. The follow up studies showed no evidence of recurrence, regional or distant metastasis. |
A 55-year-old, Caucasian woman was referred to our tertiary women’s heart center for persistent chest pain, palpitations, and dyspnea. Her medical history included hypertension, dyslipidemia, chronic anxiety, and bilateral non-obstructive carotid atherosclerosis. She had no prior history of diabetes mellitus, tobacco smoking, alcohol or substance abuse, or adverse pregnancy outcomes. Her family history was significant for premature coronary artery disease. Her father had a history of hypertension and had a myocardial infarction (MI) and coronary artery bypass grafting at the age of 39. Her brother had a history of coronary artery disease and also had a MI at the age of 40. Her occupational history indicated that she had been working in the field of psychology and was still an employee in the same job at the time of the hospital visit and follow-up care.\nTable summarizes the general symptoms and characteristic signs of our patient for the onset of CMD and her progression to HFpEF. She had undergone an exercise treadmill test which revealed ischemic ECG changes and dyspnea. Her initial echocardiogram demonstrated a LVEF of 67%, mild diastolic dysfunction, mild left ventricular (LV) hypertrophy, no significant valvular heart disease, and no pulmonary hypertension. Subsequent invasive left heart catheterization was performed and it showed normal epicardial coronary arteries without angiographic evidence of atherosclerotic plaque. She continued to have exertional symptoms and angina-like chest pain and was subsequently referred to our center for further evaluation of suspected INOCA. During her evaluation and treatment she continued to experience stable angina and exertional dyspnea despite initial management with atorvastatin 20 mg daily, lisinopril 20 mg daily, aspirin 81 mg daily, and sublingual nitroglycerin as needed. She had a poor clinical response to sublingual nitroglycerin. Due to her persistent symptoms and abnormal stress testing, she was referred for coronary reactivity testing (CRT) to establish the diagnosis of CMD.\nOur patient underwent invasive CRT, as previously published []. Testing demonstrated normal coronary flow reserve (CFR) in response to intra-coronary adenosine (CFR 3.1; normal ≥ 2.5), abnormal macrovascular endothelial function to intra-coronary acetylcholine (− 6% change in coronary diameter, constriction; normal, dilation), abnormal microvascular endothelial function (coronary blood flow change 48%; normal ≥ 50%), and abnormal non-endothelial function to intra-coronary nitroglycerin (coronary diameter change + 0%; normal dilation) (Table ). She also underwent cardiac magnetic resonance imaging (CMRI) with perfusion imaging at rest and with adenosine stress (140 μg/kg per minute) which showed circumferential subendocardial perfusion defect at stress, normal LV end-diastolic volume indexed to body surface area (EDVi) of 56.4 mL/m2, LV mass index 42.3 grams/m2, and no LV hypertrophy (septum 7.2 mm and lateral wall 6.0 mm). The myocardial perfusion reserve index (MPRI) was 1.8 which was considered borderline abnormal [] (Table ). There was no evidence of myocardial scar.\nThe diagnosis of CMD was established by the coronary endothelial dysfunction observed with invasive CRT, and carvedilol and eplerenone 25 mg daily were added to her regimen. She was followed regularly in clinic with good control of her blood pressure and serum lipid levels. She reported improvement of her angina and dyspnea along with reduction in the duration and frequency of these episodes.\nTen years after her initial diagnosis of CMD, our patient was hospitalized due to symptoms of dyspnea. She was found to have elevated brain natriuretic peptide (BNP) levels of 406 pg/mL and normal LVEF. She had a computed tomography (CT) angiogram of her chest to evaluate for pulmonary embolism, which was negative but revealed bilateral pulmonary edema. She was treated with intravenously administered furosemide for pulmonary edema and diagnosed as having HFpEF. Subsequently, she was discharged with instructions to increase her eplerenone.\nShe continued to experience worsening dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. A repeat echocardiogram demonstrated normal LV systolic function with an LVEF of 64%, and diastolic dysfunction as evidenced by decreased lateral E′ velocity (4.2 cm/s, indicating impaired myocardial relaxation) and elevated E/E′ ratio 12.9 (suggestive of increased LV filling pressure). She underwent coronary CT angiography which showed absence of coronary atherosclerotic plaque and a coronary calcium score of 0. She was diagnosed as having HFpEF based on clinical symptoms, preserved ejection fraction of 64%, elevated BNP, and evidence of diastolic dysfunction.\nAs part of the WISE – Coronary Vascular Dysfunction (WISE-CVD) Continuation Study (NCT00832702), she underwent a repeat rest-stress CMRI to assess myocardial structure, function, perfusion, and scar, and 13C magnetic resonance (CMR) spectroscopy. Compared to her prior CMRI 7 years ago, she had an increase in LV wall thickness in both the septum and lateral wall (Table ). On CMR spectroscopy, the myocardial triglyceride content was elevated (0.83%) compared to normal control women (mean 0.43%), suggesting myocardial steatosis which is consistent with an ischemia-induced metabolic shift and HFpEF phenotype []. Adenosine stress first pass-perfusion CMRI again showed circumferential subendocardial hypoperfusion (Fig. ) and her MPRI worsened from 1.8 to 1.1, consistent with severe CMD []. There was no evidence of scar on late gadolinium enhancement imaging. |
A 73-year-old woman, who started dialysis because of chronic renal failure secondary to chronic glomerulonephritis 13 years previously, consulted us for vascular surgery to correct a continuously worsening cardiothoracic ratio and echocardiographic preload that were detected by her dialysis physicians. A radial artery–cephalic vein shunt was constructed in the left forearm 13 years before. On preoperative examination, chest radiography revealed heart enlargement with a cardiothoracic ratio of 57.2%, and echocardiography showed mild tricuspid regurgitation (TR), mitral regurgitation (MR), and a TR pressure gradient of 25 mm Hg. Vascular echo-Doppler indicated that the preoperative flow rate in the brachial artery was 2336 mL/min. The absence of ischemic findings in her fingers suggested that steal syndrome was not present.\nOn visual inspection of the left upper limb, the radial artery made a hairpin turn at the AV fistula. The AV fistula was 9 mm in diameter, and no stenosis was observed. The diameters of the radial artery proximal and distal to the AV fistula were 5.4 and 3.7 mm, respectively (). For initial restoration treatment, she requested the utilization of the current vascular access route without intentional occlusion and wished to avoid surgery using vascular prostheses. Following a thorough discussion with the vascular surgeon and colleagues, the patient provided consent for treatment with the RAHT technique.\nThe operation was performed with the patient under local anesthesia using a total volume of 110 mg of 1% lidocaine with a 2.5-cm longitudinal skin incision just above the radial artery that made a hairpin turn near the AV fistula. We controlled the radial artery at the proximal and distal ends of the AV fistula. Following intravenous administration of heparin (1500 units), the radial artery was dissected just above the AV fistula. We ligated and divided the juxta-anastomosis proximal radial artery and subsequently created an end-to-side anastomosis between the proximal and the distal radial artery using a single 6-0 polypropylene suture. The anastomosis ostium in the distal radial artery (the recipient) was formed with a 4-mm longitudinal gently curved incision. The radial artery between the former AV fistula and the new arterial end-to-side anastomosis was 15.1 mm in length (). Intraoperative vascular echo-Doppler showed that the flow rate in the brachial artery after revision was 500 mL/min. The operation lasted 93 min, and the volume of blood lost was 10 mL.\nTwo months after the operation, vascular echo-Doppler showed that the flow rate in the brachial artery was 560 mL/min and the diameter of the radial artery between previous AV fistula and new anastomosis was 4.0 mm (). The cardiothoracic ratio decreased to 52%, and echocardiography showed an improvement in TR and MR and a decrease in TR pressure gradient to 18 mm Hg, suggesting a decrease in the cardiac preload. |
A 14-year-old boy, who was initially examined for continuous coughing, was referred to our hospital owing to an anterior mediastinal mass identified on chest X-ray (). Systematic examination revealed a 20 × 10 cm sized mass at the right anterior mediastinum that involved the right pulmonary vein and elevated levels of alpha fetoprotein (AFP), a tumor marker, at 3825 ng/ml. Needle aspiration was performed, but only necrotic tissue could be collected. We did not analyze the karyotype since the symptoms suggesting the Klinefelter syndrome were not observed. Therefore, a clinical diagnosis of malignant teratoma was made, and three courses of cisplatin-based chemotherapy were administered because AFP levels continuously increased. After chemotherapy, AFP levels decreased, although the size of the tumor did not change, as evident in a computed tomography (CT) scan. Next, tumorectomy and total right lung extraction were performed. The pathological diagnosis of the extracted tumor was malignant teratoma with areas of yolk sac tumor (). No cancer cells were found at the edges of the area where the tumor was removed. Two courses of cisplatin-based postoperative chemotherapy were administered until AFP levels were normal.\nAfter 3 months of follow-up, the patient experienced pain in his right hip joint while AFP was still normal. The 99mTc-methylene diphosphonate bone scan showed increased tracer uptake at the left forehead and right hip joint (). Head and pelvic MRI also revealed signs of metastasis at the left forehead and right hip joint. Abdominal CT showed a metastatic region in the liver. Bone biopsy was performed at the left forehead. The pathological diagnosis was metastatic malignant melanoma originating from an immature teratoma of mediastinum (). Large heteromorphic cells with melanin were found in the original mediastinal malignant teratoma by retrospective re-examination. This suggested that a section of the malignant melanoma in the original malignant teratoma, which was composed of various components, metastasized. Because of the very fast disease progression, after consultation with the family, aggressive treatment was discontinued, and palliative therapy was provided. He died 15 months after diagnosis of the original malignant teratoma. |
A 39-year-old female with pelvic congestion syndrome had undergone coil embolization of the left internal iliac and ovarian veins three months earlier. For the prior month, the patient endorsed right-sided pleuritic chest pain and dyspnea with orthopnea. Differential diagnosis included a viral or bacterial pulmonary infection, pulmonary embolism, acute coronary syndrome, pericarditis, and less likely pneumothorax, aortic dissection, or congestive heart failure. Outpatient chest radiograph (CXR) demonstrated an ectopic coil in the right pulmonary vasculature, with a second coil still in place in the left ovarian vein on subsequent abdominal radiograph.\nOn emergency department evaluation, the patient had normal vitals including 100% oxygen saturation on room air with a respiratory rate of 18 breaths per minute, clear breath sounds, and no leg edema. Labs were unremarkable. Electrocardiogram demonstrated normal sinus rhythm at 84 beats per minute. CXR and computed tomography (CT) imaging revealed an ectopic pelvic coil in the right main pulmonary artery extending into multiple upper and lower lobe segmental branches ().\nCoil artifact somewhat limited the identification of thrombus, but there were peripheral wedge-shaped opacities in the right middle and lower lobes concerning for infarcts and a small right pleural effusion (). There was no evidence of right heart strain on CT.\nFollowing consultation with vascular surgery, it was decided that vascular interventional radiology (VIR) would be the least invasive yet most likely successful method for coil retrieval when compared to an open surgical approach. The patient was consented and transported directly to VIR, where the groin was prepped in standard fashion. The right common femoral vein was accessed with a micropuncture kit using ultrasound guidance. A pulmonary angiography catheter was advanced over a guidewire into the right main pulmonary artery via a 7 French sheath. Contrast phase did not show significant clot within the artery.\nThe sheath was exchanged for a long 7 French sheath with the tip in the right pulmonary artery. Multiple snares were passed through the sheath to engage the 20-millimeter (mm) Nester coil pack (Cook Medical, Bloomington, IN); however, the coil unraveled into small pieces, until eventually a large piece was snared and retracted to the right femoral vein. Interventional radiology then performed en bloc removal through the right groin access site given the coil was too large to pass through the sheath; however, a piece of coil remained in the right femoral vein (). Multiple attempts to snare the coil via an upsized 11 French sheath were still unsuccessful.\nSimilarly, the left femoral vein was accessed and upsized to a 9 French sheath, which finally allowed for successful snare removal of the remaining coil. Repeat imaging showed a small residual coil fragment in the right mid-lung that was deemed not to cause increased injury, thus was left in situ. An intact, 16mm Nester coil pack was noted in the left gonadal vein.\nThe patient was observed in the hospital overnight and went home the following day without anticoagulation or other acute complications. The patient followed up with vascular surgery clinic several months later for recommendations on her remaining gonadal vein coil with no additional interventions. |
Case reports are exempt from institutional review board approval at our institution.
A 75-year-old woman was evaluated for long standing right-sided nasal obstruction, dependent mouth breathing, clear rhinorrhea, congestion, and hyposmia not relieved by intranasal steroids or nasal irrigations. She initially presented with a history of previous endoscopic sinus surgery in Russia more than 20 years ago followed by nasal polyposis treated with ambulatory cauterization. She was also noted to have a history of nonmelanotic skin cancers of the nose treated with radiation in Russia.
Physical exam findings included a fleshy intranasal lesion that, in the setting of previous nasal skin cancer treated with radiation, raised a concern for possible secondary carcinoma. Computed tomography showed complete opacification of the right maxillary sinus, obstruction of the right ostiomeatal complex, and soft tissue density in the right nasal passage ().
Initial biopsy revealed a nasal mass that originated in the right inferior meatus. Pathology showed multiple polypoid fragments lined by a respiratory type epithelium with underlying edematous stroma with mild chronic inflammation. There was invagination of the surface epithelium into the underlying stroma resulting in nested aggregates of bland glandular and mucinous cells and focally benign squamous epithelium (). These features were found to be consistent with a benign inverted papilloma.
The patient presented with continued nasal obstruction and was evaluated for definitive treatment. Given her diagnosis of inverted papilloma and chronic rhinosinusitis, complete excision and revision endoscopic sinus surgery was recommended. During endoscopic sinus surgery, an exophytic mass with abnormal maxillary mucosa was seen emanating from the left inferior meatus that was thought to originate from the right maxillary sinus, given that it was protruding through a bony dehiscence into the inferior meatus and nasal cavity. Right partial inferior turbinectomy was performed, along with right extended maxillary antrostomy and stripping of maxillary mucosa to remove the entirety of the presumed inverted papilloma base within the maxillary sinus. Intraoperative and postoperative pathology again showed inverted papilloma.
Given |
M is a 15years old male who was delivered at home. Pregnancy and immediate post-partum period were uneventful. It was noted soon after birth that the right lower limb was progressively increasing in size when compared with the rest of the upper and lower limbs. He had an uneventful childhood except that he spent a lot of time at home and was withdrawn from other children. He was healthy but soon the limb began to be too heavy for him to move around with and he could no longer afford proper foot wears. His mother who raised him abandoned him which led him to the streets. He was soon recognized by a friend of his father and was rescued from the street. He presented at the University of Calabar Teaching Hospital for the first time at the age of 15 years. He was initially managed at the pediatric dermatologic clinic as a case of suspected elephantiasis and later referred to the Pediatric Surgery Unit where an initial diagnosis of congenital gigantism was made. He was referred for x-rays and Doppler studies of both lower limbs. The diagnosis of typical KTWS was made on the basis of clinical and radiological findings which included the following:\nSkin: Port wine stains on both hands and feet ().\nMusculo-skeletal system: Marfan like hands and feet, no significant limb length discrepancy. There were marked differences in the circumferential dimensions of the lower limbs (). The right lower limb showed significant enlargement of the soft tissues of the leg and foot, worse distally, odematous right leg and foot as well as significant sclerosis of right foot with numerous hemangiomas ( and ). There were no differences in circumferences of the upper limbs (mid-upper arm circumference 18.5 cm, mid-forearm circumference 18 cm.\nCardiovascular system: Significant right lower limb varicosities, multiple sinuses in which clear but foul smelling lymph was noted to be draining ().\nGenitourinary System: enlarged peni-scrotal organ with subcutaneous oedema ().\nAll other systems were essentially normal. Patient in addition was asked to carry out multi detector computerized angiography which has not been done due to financial constraint.\nFirm bandaging of the affected limb was applied in order to reduce lymphatic flow and prevention of infection. Antibiotics and pain relief were also prescribed. Patient is still being awaited as the managing team have decided to bear the cost of the rest of his investigations and treatment. Surgical debulking of the right foot is being envisaged at the moment. |
A 3 years old boy presented with history of recurrent fever, episodes of painful urination, increased frequency and haematuria for one year. He had been treated with several courses of antibiotics for urinary tract infections with temporary relief of symptoms before recurrence. At initial presentations several urine analysis using dipstics were performed at the local dispensary and reported to show features of urinary tract infections but no further work up such as urine culture, voiding cyctourethrogram or abdominal ultrasound was performed. Three months before admission to our unit, his mother had felt a mass on his left flank and an abdominal ultrasound done at the nearby District Hospital suspected Wilms’ tumor and the patient was referred to our unit for further evaluation. The patient had otherwise attained his developmental mile stones as per age and had no any dysmorphic features.\nOn examination; the child was febrile with body temperature of 38.8 °C with tenderness on the left lumber region and had a palpable mass on the same side. Laboratory investigations performed are summarised in the concise table below; Table .\nA repeat abdominal ultrasound showed a left renal mass 7.4X7.1X5 cm with multiple cystic lesions. The renal pelvis was destroyed with some calcific changes but no extension to the neighboring structures were noted. The right kidney was normal in size and echogenicity.\nAbdominal CT Scan (Figs. and ) showed an enlarged left kidney measuring 7.9X6.7 cm in size with thinning of the cortices and loss of corticomedullary differentiation, foci of calcifications were also seen and the renal parenchyma was replaced with multiple septations (A). Contrast enhanced CT scans showed areas of peripheral enhancement surrounding non-enhancing cystic foci within the mass. There was no obvious filling defect seen in the renal vein or inferior vena cava. The right kidney was normal in size and shape, urinary bladder displayed normal outline and other abdominal organs were all normal.\nBased on the clinical presentation and abdominal CT scan, a clinical diagnosis of Xanthogranulomatous pyelonephritis was made and the patient underwent left radical nephrectomy. Intra-operatively an enlarged yellowish grey left kidney with multiple mesenteric and hilar lymph nodes was seen, radical left nephroureterectomy and hilar lymphnode resection was performed, the right kidney was normal on inspection. The resected tissues were sampled and sent for culture and sensitivity but there was no bacterial growth after 7 days. Histological studies reported macroscopically gross yellowish renal tissues microscopically showing a renal histology infiltrated with foamy lipid laden macrophages in a mixture of chronic inflammatory cells and fibrosis confirming a diagnosis of Xanthogralomatous pyelophritis (Fig. ).\nThe patient faired well postoperatively and was kept on a 7 days course of intravenous Tazobactam/piperacillin and discharged home 10 days post nephrectomy. |
A 52 year old man received a pre-emptive renal transplant from his wife for the treatment of end stage renal disease due to autosomal dominant polycystic kidney disease (HLA mismatch 1–1-1, CMV mismatch D+/R-, EBV IgG not detected). He received alemtuzumab at induction (30 mg subcutanously on day 0 and day 1) followed by maintenance immunosuppression with tacrolimus, mycophenylate mofetil (MMF) and prednisolone. As he was enrolled in a clinical trial, the use of alemtuzumab for induction was determined by the arm he was randomised to. He continued on tacrolimus before being randomised at 6 months to switch to sirolimus as part of the clinical trial []. A year later he had to leave the study as he was undergoing incisional hernia repair so returned to tacrolimus-based immunosuppression.\nThree years after transplantation renal function started to decline. Chronic antibody mediated rejection (CAMR) was found on transplant renal biopsy and new donor specific antibodies against HLA class II were detected. Tacrolimus and MMF doses were increased and he restarted on 5 mg prednisolone. The daily total tacrolimus dose was increased from 3 mg to 5 mg with levels rising from 5.4 μg/L to 7.0 μg/L and MMF daily dose was doubled from 1000 mg to 2000 mg. A month after this change he presented to primary care having passed frank blood in his stool and with a one week history of abdominal pain and faecal urgency. In response to these symptoms MMF was switched to mycophenolic acid, but the diarrhoea continued and he was admitted on two occasions due to worsening renal function.\nFive months after biopsy confirmed CAMR, rituximab was started at a dose of 200 mg with a planned frequency of every 6–8 months and mycophenolic acid was withdrawn. Although rectal bleeding resolved the diarrhoea continued and he experienced 4 kg of weight loss over 2 months with an overall weight loss of around 14 kg over a year.\nInvestigations for the cause of his diarrhoea included CMV and EBV PCR and stool culture which were all negative at initial presentation. Faecal elastase was also normal and gastric parietal cell and enterocyte antibody testing was negative. Flexisigmoidoscopy showed non-bleeding haemorrhoids and colonoscopy was normal. Radionucleotide SeHCAT bile study to assess for bile acid malabsorption was also normal. Imaging studies including PET, CT thorax-abdomen-pelvis, CT enterography and MRI small bowel showed no evidence of malignancy or other bowel pathology.\nEBV DNA was not detectable in serum by PCR at the onset of diarrhoea and EBV IgG remained negative. However, 6 weeks after the onset of diarrhoea EBV DNA was detected at titres of 1612 IU/ml and then fluctuated between not detected and 6770 IU/ml for the duration of his diarrhoea. EBV DNA was detected at low levels (< 1000 IU/ml) when tacrolimus dose was further reduced (levels in the region of 3.8 μg/L). Given symptomatic improvement EBV DNA PCR was not repeated on complete withdrawal of immunosuppression.\nCreon was started under gastroenterology advice and loperamide was prescribed for symptomatic relief. Oesophagogastroduodenoscopy (OGD) was performed to investigate loss of appetite and further weight loss. Biopsies from the duodenum identified moderate lymphocytic duodenitis with mucosal damage as evidenced by shortening villi, in keeping with coeliac disease (Fig. ). However, diarrhoea was unresponsive to a gluten free diet and he was negative for antibodies to tissue transglutaminase and HLA DQ2 and DQ8.\nRepeat OGD after 6 months of gluten free diet identified a clonal T-cell population. The intra-epithelial T-cells had normal immunohistochemistry, in that they expressed the antigens CD3 and CD8, but reproducible clonal T-cell receptor (TCR) beta and TCR gamma rearrangements were detected using a multiplex PCR assay []. Immunoglobulin heavy chain gene rearrangements were polyclonal, excluding clonal B cell proliferation. There was no evidence of lymphoma either on biopsy or CT enterography and no FDG avid disease on PET.\nAfter further reductions in tacrolimus repeat duodenal biopsies found a persistence of a clonal T cell population and mucosal damage with subtotal villous atrophy and a suggestion of crypt hyperplasia. Almost 3 years since the episode of CAMR and onset of diarrhoea all immunosuppression was withdrawn and peritoneal dialysis was commenced. The diarrhoea improved within days of stopping immunosuppression and the patient remains well on dialysis with no diarrhoea and he has successfully regained the weight he lost when unwell. |
A 21-year-old, gravid 1 woman with term pregnancy attended an academic hospital with labor pain. She had two prenatal care visits in the first and second trimester with normal appearance and did not have any appointment with obstetricians in the third trimester due to COVID-19 pandemics. She experienced mild episodes of dyspnea during the third trimester of pregnancy that did not consider important for her to seek consultation. Her pulse rate was 88 beats per minute with a respiratory rate of 14 per minute, blood pressure 132/88 mmHg, and oral temperature 37.5° centigrade. She had no dyspnea. In cardiovascular exam, the heart sound was normal and the lung was clear. The O2 saturation was 97%. On vaginal examination, cervical dilatation was 3 cm with effacement 50%; cephalic presentation, and intact amniotic membrane. The fetal heart rate was 140 beats per minute. The patient was admitted to the labor unit due to the regular uterine contractions. In general appearance, she looked good with no apparent distress.\nAccording to the patient's biography, this was her first pregnancy. She denied a history of any disease or surgery except a subtle common cold about 2 weeks ago. Her family history was non-significant. She did not take any medications other than iron and multivitamin supplements. Labor progressed without any problems and after about 8 h she delivered a full‑term girl with the Apgar score of 9 and 10 in the first and the fifth minute, respectively.\nThe third stage of the labor between deliveries of the newborn until the placenta last about 10 min without abnormal hemorrhage. For PPH prophylaxis 30 IU of IV Oxytocin in 500 ml NaCl 0.9% was administered in this stage. After delivering the placenta, she experienced an onset of uterine atonia and postpartum hemorrhage (about 700 ml) that was controlled with intravenous oxytocin and uterine massage. After the second episode of bleeding (about 550 ml) in 15 min, because of deteriorating hemodynamics despite intravenous fluid, she was transferred to the operating room for invasive resuscitation and uterine and vaginal examination under anesthesia to investigate the potential source of bleeding. The total estimated blood loss was 1200 ml.\nShe was pale but alert with tachycardia of about 125 beats per minute with an O2 saturation of 93% and systolic blood pressure of 73/49 mm Hg. After 2 large bores peripheral lines, 2500 cc crystalloid fluids besides 500 ml of colloid were infused. Shortly after, cardiac monitoring in the operating room showed ventricular tachycardia at a rate of 180 beats per minute and then PSVT (Paroxysmal Supraventricular Tachycardia), which was controlled by injecting lidocaine with an initial dose of 100 mg intravenously and then 4 mg/min as the maintenance dose. After that, the heart rhythm was converted to sinus tachycardia at a rate of 120 beats per minute and the patient's blood pressure reaches 110/60. Two pack cells (cross match) were transfused by jugular vein.\nAfter being stable, the physical examination by two obstetricians in the operation room revealed no evidence of uterine atonia, laceration, or detectable hematoma. The hemorrhage was stopped with a contracted and global uterus. Abdominal and pelvic ultrasound was performed with no evidence of intra-abdominal bleeding, but the patient was got deteriorated and progressed to pulmonary edema. Furosemide was administered with an initial dose of 300 mg and then 2 to 4 mg per hour as a maintenance dose. The patient's urinary output was 300 cc. A 12 lead electrocardiography showed ventricular tachycardia with a wide QRS complex. Cardiac echocardiography was performed by a cardiologist that showed ejection fraction about 10% to 15% and moderate mitral valve regurgitation.\nAfter two cardiac resuscitations, she was intubated and fentanyl and midazolam were started as a drip, and the patient was transferred to the intensive care unit with an oxygen saturation rate of 95–98%. After three hours, she experienced a high-grade fever (40.5° centigrade) that was resistant to intravenous Apotel. Therefore, broad-spectrum antibiotics besides epinephrine drip started and COVID-19 test by polymerase chain reaction (PCR) was performed for her with negative results.\nChest X-ray showed bilateral patchy infiltration without cardiomegaly (Figure ). Despite all supportive and therapeutic proceedings, the patient experienced ventricular tachycardia, which returned with cardiac shock and administration of epinephrine and atropine; and unfortunately, in the second attack, she deceased due to not responding to cardiac resuscitation 12 h after delivery. The autopsy revealed cardiomyopathy with diffuse inflammatory cell infiltration with a small heart size and fibrotic tissue as well as the aortic stenosis. Thin layers of pus in the bases of the lungs were observed either.\nThis paper was conducted according to the principles of the Helsinki Declaration. The principles of confidentiality were observed, and the identity of the individual was not disclosed. |
Mr. A is a 19-year-old single engineering student, from a middle socioeconomic background. Over the previous year and a half, he firmly believed that every time he assumed an upright posture, he attained penile erection. He believed that others were able to identify his physiological state by the appearance of his groin and therefore were laughing at him and making derogatory comments. He had made attempts to mask these perceived bodily changes by changing the way he dressed. Secondary to these beliefs he had also become socially withdrawn, was frequently absent from class and had had significant academic decline. The patient had even shifted colleges because of the perceived ridicule by others. He also avoided situations, which required him to stand upright, such as crowded buses, elevators, and shops. He had attempted self-harm a year earlier by slashing his wrist due to the distress related to his beliefs. These beliefs persisted though several attempts were made to persuade him otherwise. There were no other unusual beliefs or abnormalities of perception reported by the patient. There were no first rank symptoms of schizophrenia or obsessive compulsive symptoms. There was no history suggestive of seizures, other organic illness or substance abuse. The patient had been on fluvoxamine and risperidone for about 7 months at the time of presentation.\nPhysical examination, including a detailed neurological and genital examination did not reveal any abnormalities. He was evaluated in the Department of Andrology where physical abnormalities were ruled out. Blood investigations including hormonal assays were within the normal limits. Mental status examination revealed a well groomed young man with normal psychomotor activity and speech. He was distressed by the sexual problems that he perceived he had, but denied suicidal ideation. He had a fixed belief that he attained penile erection whenever in an erect posture. This belief persisted despite evidence to the contrary. There were no other delusions or perceptual abnormalities. There were no obsessive compulsive symptoms or volitional abnormalities. He was alert and oriented with normal attention and concentration. His intelligence was estimated to be average; insight and judgment were poor.\nThe degree of conviction with which the patient held his belief despite evidence to the contrary suggested it to be a delusion, upon which he was acting. A diagnosis of delusional disorder was considered in view of the single delusional theme in the absence of first rank symptoms or affective features.\nThe management focused on establishing rapport with the patient along with eliciting and understanding the explanatory model for his beliefs. Supportive therapy was provided to reduce anxiety and reassure the patient. Cognitive and behavioral techniques were employed to modify the beliefs. Socratic questioning was used to identify negative thoughts and dysfunctional assumptions, which were reflected to the patient. A hierarchy of situations based on distress and avoidance were charted down and he was asked to expose himself to the least anxiety provoking situation. The patient was also encouraged to do some behavioral experiments in these situations to confirm or disprove his assumptions. The antidepressant medication was tapered and stopped, while the dose of risperidone was gradually increased to 4 mg/day. There was a gradual improvement in his symptoms with the above interventions. |
A male aged 9 years and 9 months presented to the Emergency Department for evaluation of a one-week history of increased urinary frequency and thirst. He also complained of decreased appetite and was noted to have a 7 lbs unintentional weight loss over the past week. Given his constellation of symptoms in the setting of a strong family history of diabetes mellitus, he was seen by his primary care physician earlier that day where a blood glucose finger stick was found to be elevated at 138 mg/dL and urinalysis showed glucosuria with 100 mg/dL. He was then referred to the Emergency Department for further care.\nHis birth history was remarkable for prematurity as his mother was induced at 36 weeks for intrauterine growth restriction. He was born via Cesarean section secondary to fetal distress. His birth weight was 2690 grams and his birth length was 48.3 cm. He was monitored in the neonatal intensive care unit for 24 hours for concerns of hypoglycemia given maternal gestational diabetes but his blood glucose levels remained within normal range. He was noted to have jaundice but did not require phototherapy. He passed his newborn hearing screen prior to discharge.\nHis past medical history was significant for an endocrine evaluation at 4 years and 3 months of age for polyuria, polydipsia, and weight gain. His weight was stable in the 50th percentile until approximately 2 years of age when it increased to the 90th percentile. His weight was in the 99th percentile at the time of his endocrinology clinic visit. His height had decreased from the 25th percentile at 3 years of age to approximately the 15th percentile at the time of his endocrinology visit. He underwent evaluation which was remarkable for an elevated fasting blood glucose level of 113 mg/dL and mildly elevated thyroid stimulating hormone at 5.3 mIU/L (normal range 0.5–4.3 mIU/L). His serum creatinine was 0.41 mg/dL and electrolytes were unremarkable. Further studies were recommended for evaluation of thyroid function and Cushing's syndrome but not completed at that time.\nHe also had a history of multiple sinus and ear infections requiring adenoidectomy and four sets of myringotomy tubes being placed over his lifetime. He had speech delay as sequela of his frequent ear infections and was receiving speech therapy twice weekly and hearing therapy three times weekly. He had received physical and occupational therapy services until he was in kindergarten for delayed milestones including walking at 16 months of age. He receives additional support for reading. Formal academic testing was recommended by his school which has not yet been completed. He had undergone an immunologic evaluation at an outside hospital due to his frequent infections which was unremarkable. He was diagnosed with asthma starting at 1 year of age and was prescribed fluticasone and cetirizine.\nHis family history was notable for maternal renal injury secondary to diabetes occurring during pregnancy but not requiring renal replacement therapy and photophobia in his mother, nephrolithiasis in the maternal grandfather and maternal aunt, hypertension in the maternal grandfather, and hearing loss and photophobia in a first cousin on the maternal side. There was no family history of consanguinity.\nReview of systems revealed subjective chills and constipation. He also admitted to waking at night to drink and to void. He denied fever, abdominal pain, daytime or nighttime enuresis, urgency, dysuria, inability to empty his bladder, or hematuria.\nIn the Emergency Department his blood pressure was 123/71 mmHg, weight was 37 kg (82nd percentile), and height was 127.5 cm (3rd percentile). His physical examination was remarkable for a grade 2/6 systolic ejection murmur and hypogonadism. There were concerns for photophobia during his eye exam. There were no other dysmorphic features noted. His initial laboratory work-up was significant for elevated serum creatinine of 4.4 mg/dL, low serum calcium of 7.7 mg/dL (8.8–10.1 mg/dL), and slightly elevated serum phosphorus of 6.1 mg/dL (3.7–5.6 mg/dL). His serum intact parathyroid hormone level was elevated at 340 pg/mL (9–52 pg/mL). His complete blood count revealed normocytic anemia with serum hemoglobin of 8.1 g/dL (11.5–15.5 g/dL). His urinalysis showed moderate blood, no proteinuria, no leukocyte esterase, and a specific gravity of ≤1.005. His renal/bladder ultrasound showed small kidneys with right kidney 6.6 cm and left kidney 7.8 cm with increased echogenicity bilaterally and no evidence of cystic disease. He had an echocardiogram given his finding of a murmur which was unremarkable. An ophthalmology exam was performed with concern for cystinosis but cystine crystals were not visualized. He was diagnosed with bilateral retinal dystrophy with 20/50 OD and 20/30 OS. A bone age was obtained secondary to concerns of short stature which was greater than 2 standard deviations above his chronological age.\nGiven his constellation of symptoms and results of his evaluation, the suspicion for a ciliopathy, specifically juvenile nephronophthisis or Bardet-Biedl, was high. ALMS1 gene testing for Alström syndrome and a commercial Ciliopathy Panel (from Prevention Genetics) were sent. The Ciliopathy Panel included 73 genes for disorders such as Joubert Syndrome, nephronophthisis, Bardet-Biedl, and Meckel syndrome. He had a computed tomography chest which was negative for bronchiectasis which was performed given his history of asthma and pulmonary system involvement with Alström syndrome. ALMS1 gene testing was negative.\nGenome-wide array analysis revealed a 3–12 Kb pathogenic hemizygous deletion within chromosome Xp22.2 that includes several exons of the OFD1 gene (OMIM # 300170, NM_003611). His Ciliopathy Panel showed a likely pathogenic deletion, approximately 7.9 kb, in the OFD1 gene encompassing exons 16, 17, and 19 (c.1654+833_2599+423del) which is a novel mutation. His mother underwent genetic testing and was found to have the same deletion. She lacks any characteristic features of OFD1.\nHe had a brain MRI which showed mild T2/fluid attenuation inversion recovery (FLAIR) hyperintensities in the medial temporal lobes bilaterally as well as a mildly thickened corpus callosum but no findings more typical of OFD1, such as intracerebral cysts, hydrocephalus, malformations of cortical development, agenesis of the corpus callosum, brainstem malformation, or Dandy-Walker malformation [].\nHis renal function has continued to decline rapidly. Given symptomatic uremia, he has started on chronic hemodialysis. He is currently awaiting transplant from a living donor. |
A 25-year-old right-handed woman was admitted to our hospital with a 3-week history of intermittent non-throbbing bilateral headache involving frontal and temporal lobes, accompanied by nausea, vomiting, left upper extremity numbness and weakness, left-sided tongue and perioral numbness, and involuntary movements of the left upper extremity. There were five episodes with complete recovery in the last 3 weeks, of which two episodes were without any neurologic deficit and three episodes were preceded by transient symptoms. The numbness and weakness lasted for about 10 to 20 mins and were ensued by headache and involuntary movements of the left upper extremity. The headache lasted approximately 2–9 hrs and was graded as 8/10 in the VAS (with 0 indicating no headache and 10 the most severe headache). The involuntary movements of the left upper extremity occurred in two episodes and lasted for about 1 to 2 hrs. The involuntary movements of the left upper extremity and headache occurred simultaneously after numbness and weakness of the left upper extremity, and the duration of involuntary movement was shorter than that of the headache. She was conscious during the episodes. The involuntary movements were chorea of the left upper extremity, which presented as irregular, arrhythmic and brief movements of the left hand and forearm. The chorea of the left hand was more obvious than the forearm, and the movement was remarkable during the voluntary movements. Cough, yellow sputum and snot were also reported, but no fever. She had no history or relevant family history of migraine. She had a regular menstrual cycle and no history of previous pregnancy. She did not take oral contraceptives or any other medication before the headache. She was Han Chinese and worked as an office clerk.\nUpon admission, she had no symptom and the neurological examinations were unremarkable. Fundus examination revealed no papilledema or any other abnormalities. The routine blood tests and autoimmune tests were both normal. Also, the cerebral magnetic resonance imaging (with contrast medium) and angiography did not show any abnormality ().\nThe first lumbar puncture at an external hospital showed intrathecal cerebrospinal fluid (CSF) opening pressure of 20cmH2O and prominent lymphocytic (90%) pleocytosis with the cell count of 114/µL.\nThe second lumbar puncture conducted in our hospital revealed slightly increased CSF opening pressure of 30cmH2O, and confirmed the pleocytosis with cell count of 54/µL (lymphocytes 81%). There was also increased level of protein with 5.04 g/L, but normal glucose level. Serological tests were positive for lgG coxsackie virus and lgG varicella-zoster, and CSF tests of IgM/G virus were negative. Mycobacterium tuberculosis and parasites were not detected in CSF, and oligoclonal bands were not detected as well. Electroencephalogram of asymptomatic period showed no abnormality.\nInitial treatment with non-steroidal anti-inflammatory drugs, ganciclovir, mannitol and anti-epileptic medications at an external hospital did not halt the recurrence of the symptoms. During admission at our hospital, she was given ganciclovir initially, but she developed two new episodes of headache (VAS 7/10) with focal neurological symptoms, including numbness, weakness and involuntary movements of the left upper extremity. Chorea of the left hand lasted for 30–45 mins and headache for about 2 hrs. The left upper extremity weakness was graded as 4/5 using the Medical Research Council grading system. The characteristics of the episodes were similar to that described above. Meningeal irritation sign was absent during the attack.\nThe third lumbar puncture showed 30cmH2O of CSF opening pressure and lymphocytosis (74%). She was treated with intravenous methylprednisolone with initial dose of 120 mg/day which was tapered to 40 mg/day within 7 days. The fourth CSF examination after the administration of methylprednisolone for 7 days showed CSF opening pressure of 23cmH2O and cell number of 24/µL with 74% of lymphocytes. She did not experience any recurrence of the symptoms, and the oral methylprednisolone was discontinued gradually within 1 month. After about 1 month, she was discharged from our hospital. The final and fifth CSF examination showed CSF opening pressure of 17cmH2O and cell count of 12/µL with 79% of lymphocytes. The five CSF examinations are summarized in . At 1-year follow-up, she denied any recurrence of the symptoms. Written informed consent from the patient was obtained to perform invasive procedures and publish data. The ethics committee of our institute approved the publication of the case details. |
An 80-year-old man with a history of en bloc resection of squamous cell carcinoma of the hard palate (T4aN0M0) complained of mastication difficulties due to the maxillary defect, and water and air leakage into the maxillary sinus. Maxillary segmentectomy included resection of the alveolar ridge from the left central incisor to the right pterygoid process of the sphenoid bone (Fig. ). The resection site was reconstructed with a forearm flap, and the maxillary sinus was completely closed.\nThe patient used a jaw prosthesis with clasps over the remaining left maxillary teeth. However, these teeth were not strong enough to support a large jaw prosthesis that would cover the right maxillary defect, and residual teeth were missing. The patient sought implant treatment in the left maxillary molar region. However, computed tomography (CT) revealed that the bone mass of the left molar region was inadequate for implantation of these fixtures (Fig. ). We performed the sinus-lift procedure under local anesthesia. The soft tissue from the canine region to the molar tooth region was incised and elevated to expose the underlying lateral wall of the left maxillary sinus. A 12 × 5 mm window was created in the bone of the maxillary sinus anterior wall with a piezoelectric instrument to expose the underlying Schneiderian membrane, which is the lining of the maxillary sinus cavity. Through careful instrumentation, the membrane was carefully peeled from the inner aspect of the sinus cavity (Fig. a). No damage to the membrane of the maxillary sinus was present. The newly formed space within the bony cavity of the sinus inferior to the intact membrane was grafted with artificial bone, and artificial bone was placed on the alveolar crest to raise the alveolar crest (Fig. b). The gingival flap was replaced and sutured to complete the sinus-lift procedure. There was minimal hemorrhage during the operation, and hemostasis was adequate. There was insignificant facial swelling immediately after the operation.\nTwo hours after the surgery, the patient complained of sudden malar swelling (Fig. ). Marked swelling was present from the left infraorbital region to the buccal region, and we suspected postoperative bleeding. Thus, we considered hemostasis treatment necessary and reopened the wound under local anesthesia. There were a few hematomas in the wound, but an apparent bleeding point was absent. We removed a hematoma and closed the wound. The CT images revealed that the artificial bone grafted inferior to the membrane had not leaked into the maxillary sinus, and there was no apparent damage of the maxillary sinus membrane. However, the marked malar swelling was associated with air pockets at the alar base and in the angulus oculi medialis region and subcutaneous malar tissue, and no hematoma was evident (Fig. a and b). We made a diagnosis of subcutaneous emphysema and administered an intravenous drip containing antibiotics to the patient for 3 days. The swelling improved day by day. We confirmed emphysematous improvement and the graft situation of the artificial bone on the CT images at 12 days postoperatively. |
A 69-year-old female patient attended for examination in need of dental prosthesis in the upper left maxilla. The patient refers that a few years ago she had an implant-supported dental prosthesis in the mandible without complications. As interesting aspects of her medical history, she only refers osteopenia and the use of bisphosphonates, discontinued in the last 6 months. During the physical examination, the upper right and left premolars appeared fractured and infected with a bilateral abscess formation. Simple X-rays shows a well-delimited radiopaque mass of 4 mm × 8 mm in the left maxilla [].\nAfter additional interrogation, the patient refers the finding of an anomaly in a previous X-ray of 10 years ago, which was reviewed, finding a small radiopaque mass of 4 mm × 7 mm similar to the one recently found. Nevertheless, she denies any previous symptoms or history of trauma at the site of injury. Further investigation with computed tomography identified a bone mass of 5 mm × 8 mm with clear edges and neither invasion of the cortical nor the tissue surround, there was no ganglionar reactivity [].\nDue to the lack of growth, small size, delimited borders and absence of locoregional compromise (no ganglionar reactivity in physical examination or imaging), surgical removal of the lesion was performed considering a benign bone growth and dental implants were implanted during the same surgical time. A full-thickness flap was developed with a light osteotomy for easy liberation of the lesion using surgical burs; complete liberation was performed in a conservative way. The complete specimen was sent to pathology in 10% neutral-buffered formalin, the report described a benign differentiated bone lesion close to the cortical, inside presents thick trabeculae of mature bone with laminar and sclerotic formations such as Haversian system, there is a dense bone mass with medullar activity without osteoblastic or osteoclastic activity; suggesting an OO [].\nAfter 12 months of follow-up, the patient has proper healing without clinical or radiographic evidence of recurrence. |
A 41-year-old Korean woman visited the ophthalmic clinic because of visual disturbance. She was determined to be a hepatitis B antigen carrier seven months prior to visiting the clinic and was treated for a mental disorder with psychiatric medication one year prior to visiting the clinic. In addition, she underwent a neck mass excision at a private clinic six months previously. A history of herpes zoster infection in the skin or elsewhere was not found. Visual acuity was 20/100 in the right eye and 20/200 in left eye. Ophthalmoscopic examination detected a deep, white outer retinal lesion in the mid-peripheral retina and posterior pole. Also, some retinal hemorrhages were noted around the major vascular arcade in the left eye (). Fluorescence angiography showed no active vascular leakage, but there was diffuse leakage from the subretinal area. The patient would have been referred to retinal service, but she was unreachable for one week for private reasons. When she returned to the eye clinics on June 12, 2000, her retina finding had markedly changed. The previous deep, white retinal lesions had coalesced and progressively expanded in a circumferential manner, with sparing of the perivascular retina. Retinal and vitreous hemorrhages could be noted around the optic nerve. Retinal detachment was noted at the inferior mid-periphery of the left eye. Visual acuity was 20/200 in the right eye and hand motion in the left eye (). Typical progressive outer retinal necrosis was considered, but would not explain the moderate retinal and vitreous hemorrhage around optic nerve. Thus, necrotizing herpetic retinopathy was considered. Intravenous treatment with acyclovir for presumed VZV or HSV retinitis was administered. A systemic work-up was evaluated, and anti-HIV antibodies and HBs Ag were detected in the serum. Anterior chamber paracentesis was taken for the identification of a specific causative agent. A 0.1 cc sample of aqueous humor was acquired for polymerase chain reaction. The PCR-RFLP analysis of the aqueous humor specimen was positive for VZV, HSV-1, HSV-2, and CMV DNA. At the same time, the patient was diagnosed with AIDS at the C3 stage (CDC classification) because of the decreased CD4+ cell count of 18 /ul and the presence of encephalopathy caused by AIDS. Because of the association between HIV infection and suspiciously combined CMV retinitis, intravenous treatment with ganciclovir was added. Forscarnet is not available in Korea. The patient was referred to Yonsei University Hospital for management of her HIV infection. After the diagnosis, she was treated with zidovudine, lamivudine, and indinavir. On June 16, in spite of medical therapy, the retinal necrosis had progressed (). Total retinal detachment and extensive full-thickness necrosis were found in the left eye, and inferior partial retinal and choroidal detachment were noted in the right eye. The patient's visual acuity was hand motion for both eyes. |
We present a case of a 50-year-old male previously a healthy recreational powerlifter who presented to a clinic several days after sustaining an injury to his left thigh while dead lifting approximately 400 pounds. He was a nonsmoker and otherwise healthy prior to the injury. He described a sudden pop in his left knee with immediate swelling. Examination revealed tenderness to palpation with palpable defect over the lateral quadriceps muscle as well as 3/5 weakness with knee extension and limited knee flexion to approximately 50 degrees. No patellar instability was noted. An MRI was obtained which showed an isolated rupture of the vastus lateralis, and the decision was made to move forward with surgical fixation.\nMRI was performed which showed a full-thickness tear of the vastus lateralis component of the quadriceps tendon from the patellar attachment, retracted by approximately 3 cm. The torn tendon end was diffusely thickened. The vastus medialis, rectus femoris, and vastus intermedius components of the quadriceps tendon were noted to be intact (). Operative and nonoperative options along with informed consent were provided. The decision was made to move forward with surgical repair of the tendon as the patient wished to return to preinjury activity level with no weakness.\nIn the operating room, midline incision was placed centered laterally over the palpable defect in the quadriceps tendon. The vastus lateralis was isolated and noted be torn off the lateral third of the patella. This was noted to be a full-thickness tear extending into the knee joint (). Of note, the bulk of the quadriceps tendon was still noted to be intact which correlated to the MRI findings. The lateral border of the patella was then prepped for repair. Soft tissue was removed and a bleeding bony bed was prepared. A pilot hole was treated for a 5.5 mm Bio-Corkscrew Suture Anchor (Arthrex Inc., Naples, FL) in the lateral patella. The sutures were then passed through the tendon in the locking Krakow fashion. The knee was placed in hyperextension and the sutures were tied. The split between the quadriceps tendon, and the vastus lateralis were repaired using interrupted figure of eight #2 FiberWire (Arthrex Inc., Naples, FL). The lateral retinaculum was noted to be torn and this was repaired using interrupted #2 FiberWire (Arthrex, Naples, FL). The knee was flexed and was stable to about 80 degrees. Fascia was closed with 0 Vicryl. The skin was closed with 2-0 Monocryl and a running 3-0 Monocryl.\nPostoperatively, the patient was made to perform full weight bearing with hinged knee brace initially locked in extension during ambulation. He was gradually advanced to an unrestricted range of motion at 6 weeks with continued physical therapy for strength and range of motion exercises. At approximately 10 weeks after his injury, the patient exhibited 5/5 strength in knee extension and near normal knee range of motion. No palpable gap was detected. He was allowed to gradually return to full activity starting at 3 months with full activity achieved without restrictions at 4 months postinjury. |
A 72-year-old male presented with a complaint of swelling on both sides of the groin for the past 40 years and left groin pain for 1 month. The pain reduced when the patient was in the supine position. The patient had undergone bilateral inguinal hernia suture repair 50 years ago. He had no sexual dysfunction and was fertile; he was married with three sons. On physical examination, a swelling of approximately 10 cm in diameter was found in the left groin extending into the left scrotum and a swelling of approximately 3 cm in diameter was found in the right groin. The swelling was reducible on both sides. Laboratory data were normal. Computed tomography showed a herniation in the left groin, but not in the right. The hernia contents seemed to be the intestinal tract and solid tissue considered the omentum (Fig. ).\nAfter confirming the patient's fitness to undergo anesthesia, surgery was planned. TAPP was performed. There was a fibrous structure linking the left and right hernia orifice and a muscular structure in the hernia sac on the left (Fig. A). It was difficult to separate the peritoneal cavity and the structure of the fiber and muscle. The muscular structure was continuous in the pelvic cavity and adherent (Fig. B). We consulted a pediatric urologist and noticed that the muscular structure was a vagina and fibrous structure was a salpinx, and we diagnosed the patient with PMDS (Fig. C). We explained it to patient family and it was decided to resect a vagina and a salpinx for hernia repair. After dissection of the uterus, right salpinx, and the upper part of the vagina, supravaginal hysterectomy and right salpingectomy were performed. We divided the vagina with a linear stapler after dissecting the vagina as much as possible. Following which a preperitoneal mesh repair was performed for bilateral inguinal hernia. The mass comprised of Müllerian duct derivatives with a rudimentary uterus and right salpinx (Fig. D). The operative time was 545 min, and the amount of bleeding was 50 mL. The patient had an uneventful recovery, with 7 postoperative days. Histologically, the tissue was accompanied by a salpinx-like structure, thick muscle tissues, and endometrial membranes, and the diagnosis was confirmed as PMDS (Fig. ). There was no postoperative recurrence for 1 year and 10 months. |
A 61-year-old Korean woman was admitted to the Department of Vascular Surgery, presenting with a tingling sensation on both lower legs and vague chest discomfort for one month. She was a never smoker and had dyspnea (3 on Medical Research Council scale) for two weeks but no fever. She had undergone surgical excision of a benign mass of the left breast and hysterectomy due to uterine prolapse, 15 and five years ago, respectively; denied any postoperative complications and history of renal or hepatic disease. Computed tomogram (CT) angiography of the chest did not show evidence of pulmonary thromboembolism. However, 2×1.2-cm-sized nodular lesion in left lingular division abutting to mediastinal pleura and lymphadenopathies on the left paraaortic and supraclavicular area and both prevascular and subaortic area were noted (). Clots in the popliteal and calf vein of the right leg were noted on a CT angiogram for the pelvis and legs (). The patient was immediately started on treatment with continuous administration of intravenous heparin. An extensive laboratory work-up was performed in search of underlying hypercoagulability disorders (). On the fourth day, she was transferred to Department of Center for Lung Cancer for further evaluation of lung cancer. No endobronchial lesion was observed on bronchoscopic examination. Adenocarcinoma was diagnosed pathologically on a biopsy specimen of supraclavicular lymph node. Thyroid transcription factor-1 was positive on immunohistochemistry and activating mutation of epidermal growth factor receptor gene was not demonstrated. On the fifth day, palsy of the lateral gaze of both eyes and double vision was developed suddenly. She underwent brain magnetic resonance angiogram, which demonstrated subacute stage of embolic infarctions on territories of both the middle and posterior cerebral arteries and the right cerebellar hemisphere (). Neither stenotic flow nor visible plaque was demonstrated in Doppler ultrasound examination for both carotid arteries. No evidence of distant metastasis was observed on brain magnetic resonance image (MRI), bone scan, and positron emission tomography. Finally, her disease was staged as IIIB; however, she did not want to receive any treatment for her lung cancer. On Transthoracic echocardiogram, vegetation measuring 9 mm in size was observed on the posterior mitral leaflet with moderate mitral regurgitation and the basal inferior wall was akinetic with 50% of left ventricular ejection fraction (). Blood culture of the patient revealed no evidence of bacteremia. Diffuse irregular stenosis (30% of diameter) of the distal portion of the left anterior descending artery and diffuse irregular stenosis (80% of diameter) of the posterolateral branch of the right coronary artery were observed on coronary angiogram (). Intracoronary injection was administered with ReoPro (Abciximab, Eli-Lilly, Indianapolis, IN, USA) and thrombus was aspirated from the right coronary artery. On the eighth day, heparin was switched to warfarin. On the 15th day, follow-up transthoracic echocardiogram showed a decrease in size of the vegetation (4 mm), improvement of mitral regurgitation (mild degree), and normalization of left ventricular ejection fraction. She was discharged on the 17th day. Three weeks later, she visited to the emergency room with sudden development of dysarthria, aphasia, and right hemiplegia. A newly demonstrated hyperacute embolic infarction in the operculum area of the left frontal-parietal junction was observed on her brain MRI. She is receiving rehabilitation treatment for her hemiplegia. |
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