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A 66-year-old African American female with a past medical history of refractory immunoglobulin G (IgG) lambda MM, essential hypertension, and chronic kidney disease presented to the emergency department with five days of right upper quadrant pain.\nHer MM was diagnosed one year prior when she presented with altered mental status, uremia, hypercalcemia, hypoalbuminemia, and paraproteinemia. A skeletal survey at that time revealed multiple thoracic spinal lytic lesions and an eroding soft tissue mass at the level of T10. Further evaluation revealed a very high IgG level, elevated M protein band, and a kappa/lambda ratio <0.01 (normal 0.26-1.65). A biopsy from the soft tissue mass revealed a plasmacytoma. Radiation therapy was initiated for 10 days. She received three cycles of bortezomib and dexamethasone followed by two cycles of bortezomib, dexamethasone, and lenalidomide. Her disease progressed, and a subsequent bone marrow biopsy revealed hypercellular bone marrow with 70% atypical plasma cells. The patient subsequently received seven cycles of carfilzomib, lenalidomide, and dexamethasone. She was not a candidate for bone marrow transplantation given the high plasma cell burden.\nOn her current presentation, the pain was sudden in onset, intermittent, worse with eating, and without radiation. The pain was associated with nausea and anorexia, but she was without any change in bowel habits. She denied any previous similar episodes. Upon physical exam, the patient was in distress but remained alert and oriented. Her vital signs were all stable. She exhibited right upper quadrant abdominal tenderness without rebound or guarding. Her initial labs are presented in Table . The patient was admitted to the hospital for further evaluation of her abnormal labs and supportive treatment.\nThe patient was started on intravenous hydration and was made nil per os. An abdominal ultrasound revealed a distended GB with sludge (Figure ). The GB wall was thickened up to 9.5 mm, and the sonographic Murphy sign was positive. The common bile duct and common hepatic duct measured 6.3 mm and 3 mm, respectively. The liver measured 18.3 cm and exhibited normal echogenicity. There were no intraparenchymal masses or fluid collections. The portal and hepatic veins were patent.\nThe patient was diagnosed with acute cholecystitis. Intravenous piperacillin-tazobactam 3.37 g every eight hours was initiated, and the patient was referred for open cholecystectomy given her overall condition and lactic acidosis. Intra-operatively, the GB was thickened and firm but not overly distended or perforated. The GB was dissected from the liver edge, and a liver biopsy was performed successfully.\nThe pathology report from the cholecystectomy revealed chronic cholecystitis with involvement of the GB submucosa and serosa by abnormal plasma cells with lambda light chain restriction (Figure ). Subsequently, Congo red stain of the GB sections revealed apple-green birefringence throughout the submucosal areas consistent with amyloid deposits. The liver biopsy exhibited abnormal plasma cells in periportal locations with lambda light chain restriction as well; Congo red stain was not done on the liver sample.\nThe patient declined any further treatment for MM and decided to proceed with hospice care. She was discharged home with comfort measures.
A 22-year-old female patient came to our clinic with a complaint of pain in her left wrist. Her clinical history revealed that she fell on this wrist approximately 2 months before and the pain started afterwards. Her physical examination showed mildly painful wrist movements with minimal limitation. Anatomically there were mild tenderness and swelling in fossa radialis. There was no other systemic complaint. Her personal and family histories were unrevealing. Wrist and scaphoid X-rays were performed. The radiographic examination revealed a well demarcated cystic structure at proximal pole of the scaphoid (Figure ). Magnetic resonance imaging confirmed a 0.5-cm diameter bony cyst at proximal pole of the scaphoid (Figure ). Laboratory evaluations including complete blood count, C-reactive protein, erythrocyte sedimentation rate, and urine analysis were within normal limits except eosinophilia. Cyst hydatic indirect hemagglutination (IHA) test and indirect immunofluorescence antibody test were reported to be negative. We planned surgical treatment with an initial diagnosis of wrist pain due to simple bone cyst. After a tourniquet was applied to forearm, scaphoid was reached by volar approach. A light colored liquid and a white membrane resembling germinative membrane of hydatic cyst were observed. Curettage was applied to cystic area and it was flashed with abundant hypertonic solution and povidone iodine solution. No mechanical bone damage was seen. After curettage the formed cavity was filled with spongious allograft. Two weeks after the surgery short-arm splint with thumb support was applied. Histopathological evaluation revealed cyst hydatic scolexes in cystic spaces inside fibrous tissue and inflammatory cellular infiltrates inside surrounding fibrous tissue (Figures and ).\nThe patient was consulted by an infectious diseases specialist and a general surgeon. To exclude involvement of another organ, chest X-ray and abdominal ultrasonography were ordered. No cystic mass was observed in thorax or abdomen. The patient took daily 2 × 400 mg albendazol oral for 3 months. After 2 months, the splint was removed and wrist exercises were started. Two months after the surgery, swelling in fossa radialis terminated. Wrist movements were painless and complete. The patient was evaluated by clinical examination, serological tests, and radiological imaging at 3rd, 6th, and 12th month follow-up visits. No finding related with local or systemic hydatic cyst was detected at 12th month follow-up. Recurrence was not observed at 12th month follow-up visit and serological tests were negative.
We report the case of an otherwise healthy 13-year-old female lacrosse player who had a remote history of intermittent foot drop associated with pain several years prior. She had undergone extensive workup at that time with X-ray of the knee, which was only significant for osteochondritis dissecans of the lateral femoral condyle, and magnetic resonance imaging (MRI) of the brain, leg, knee and ankle. The MRI revealed no significant findings, including no visible abnormality of the peroneal nerve but did show mild tenosynovitis of the flexor hallucis longus and flexor digitorum longus. It was believed that she suffered from CECS, and she was treated conservatively with foot orthotics and physical therapy.\nSeveral years later, she experienced foot drop twice in 6 months which brought her back to the orthopedic office for reevaluation. Physical examination at that time was significant for 3/5 strength with dorsiflexion and 4+/5 strength in her extensor hallucis longus (EHL). In addition, she exhibited hyperesthesia in her deep peroneal nerve distribution and tenderness to palpation throughout her anterior leg musculature. A right lower extremity MRI was performed, which showed no evidence of neuropathy or compressive lesion. She re-presented 2 days later with complaints of severe pain, persistent foot drop and a cool leg in the absence of a clear etiology.\nAt that time, she was sent to the emergency room for evaluation of acute compartment syndrome. In the emergency department, compartment pressures were measured with a Hand-Held Stryker compartment monitor (Stryker, Kalamazoo, Michigan). Compartment pressures were 51 mm Hg in the anterior compartment and 45 mm Hg in the lateral compartment. She was promptly taken to the operating room for an anterior and lateral compartment fasciotomy and a muscle biopsy of the anterior compartment. Intraoperatively, she was found to have thick fascia, but no other abnormalities were noted. In the post-anesthesia care unit, she had improvement in her foot dorsiflexion and EHL strength. The muscle biopsy returned as normal and she had complete resolution of her symptoms on her post-operative visit 8 days later.\nAt a 5-month post-operative follow-up, she complained of recent onset of numbness and tingling in her superficial and deep peroneal nerve distributions. On physical exam, she had a positive Tinel’s sign over her common peroneal nerve at the fibular head. MRI was negative for pathology, but electromyography revealed slowed conduction velocity of the peroneal nerve across the fibular head. It was decided to proceed with neurolysis and exploration of her peroneal nerve.\nIntraoperatively, fibrous constricting bands and a vascular leash were discovered around her peroneal nerve in the popliteal fossa (). The nerve was freed from any points of tethering in a 12 cm window from the fibular head to the popliteal fossa. Immediately postoperatively, the patient showed no evidence of peroneal nerve palsy with full dorsiflexion and eversion of the foot. She has been recently seen for follow-up 5 years postoperatively, and she is symptom-free with full strength and no neurologic symptoms. She has experienced excellent recovery and she is playing Division I varsity collegiate lacrosse as a senior in college.
A 69-year-old Italian man came to our hospital for treatment of a 5-mm fistula at the proximal third of the anterior region of the tibia. He was affected by chronic osteomyelitis because of an exposed fracture that had occurred 40 years ago. Plain x-rays showed an osteolytic area above the wound (Fig. ). In the first years following the trauma, he had undergone many osteosynthesis surgical interventions and antibiotic regimens. The patient was self-sufficient, in good clinical condition, and had no comorbidities. The neurovascular status of his affected leg was intact. In 1994, he had undergone a bilateral inguinal herniotomy, and in 2000 he had had a hemorrhoidectomy. He contracted hepatitis C virus during his first hospitalization after the trauma.\nScintigraphy confirmed the presence of an intraosseous infective process in the involved region (Fig. ). A swab culture of the fistula was positive for Bacteroides fragilis and Corynebacterium striatum, so the patient underwent therapy with metronidazole (500 mg by mouth every 6 h). After 30 days, the fistula had increased in size, and fibrotic tissue, perilesional erythema, and malodor were present. We recommended to the patient that he undergo amputation of the knee, a treatment that he refused. Therefore, he underwent a surgical toilet of the osteomyelitic hotbed, and inflammatory tissue and macerated bone were removed. The bone defect was treated with bioglass (Fig. ). The surgical wound was closed without any skin grafting. The result of an intrasurgical swab culture was positive for Pseudomonas aeruginosa. We started the patient on a multiple-antibiotic regimen with amikacin (500 mg intravenously every 12 h), meropenem (2 g intravenously every 8 h), and ciprofloxacin (500 mg by mouth every 12 h). After 2 months of inpatient care, a fulminating budding formation was observed on the wound margins. A biopsy revealed that it was a squamous cell carcinoma (Fig. ). The patient underwent whole-body computed tomography (CT), which revealed bone lesions and soft tissue masses. His neoplasia turned out to be T3N0M0; according to the American Cancer Society guidelines, it was at stage III []. He underwent a wide-margin surgical debridement and bioglass removal (Figs. and ). After 2 months, the malignant lesion recurred locally (Fig. ), and we performed a below-the-knee amputation.
An asymptomatic 58 year-old woman was referred to this institution for a liver mass detected by abdominal ultrasonography (US) during a routine examination. The US showed a hypoechoic mass with calcifications and multiple non-homogeneous areas in the right hepatic lobe. Her past medical history was unremarkable. The menarche was at the age of 13, menstrual periods were regular. Physiologic menopause occurred when she was 49 years old. She had no history of drug or alcohol abuse. Physical examination was unremarkable.\nLiver function tests and urine analysis were within normal limits. Hepatitis B surface antigen, anti-HBs antibody and anti-hepatitis C virus antibody were negative. Serum tumor markers (CEA, CA 19–9 and α-fetoprotein) were also negative. Moreover, laboratory and serology data ruled out liver abscess, amebae or hydatid cyst.\nAbdominal computer tomography (CT) showed a voluminous lesion measuring 142 × 126 × 132 mm and localized in the IV, VII, and VIII hepatic segments Figure ); it also showed the presence of multicystic areas with calcifications (Figure ). The lesion was well defined, hypodense and with a hyperdense rim. The arterial phase exhibited significant enhancement during the arterial phase, decreasing during the portal phase, until becoming isodense relative to the liver in delayed scans. CT findings were characteristic for a giant hepatic adenoma. Since the diagnostic work-up supported the hypothesis of a hepatic adenoma, the surgical treatment was advocated. In this case surgery was the only therapeutic option. In fact, hepatic adenomas larger than 5 cm should be surgically removed due to the risk of hemorrhage and/or malignant transformation. No pre-operative biopsy was performed since its outcome would not have influenced the surgical treatment.\nThe patient was brought to the OR and a bilateral subcostal incision was performed. A voluminous hepatic lesion involving IV, VII and IVb segments was found. There was a first attempt to enucleate the mass from the surrounding liver parenchyma. However, since the mass was closely adherent to the right and middle hepatic veins, a liver resection was carried out. After performing the Pringle maneuver, parenchymal dissection was accomplished using the cavitational ultrasonic surgical aspirator. Hemostasis was achieved using argon beam coagulator, bipolar forceps and suture ligatures.\nThe specimen measured 19 × 15 × 7 cm. The mass appeared as a well circumscribed green-brown colored tumour with hemorrhagic areas and a cyst of 6 cm in diameter, with macroscopic calcification within. The surrounding liver tissue was normal.\nMicroscopically, the lesion was composed of mature hepatocytes organized in sheets, mainly 2 cells thick. The cells had large cytoplasms and round nuclei with inconspicuous nucleoli. Some bi-nucleated cells were present. Gomori's staining showed that reticulin production was preserved within the proliferation. No vascular invasion was present. Large areas of hemorrhage and focal dilatation of peliosis-like sinusoid were present. A cystic formation with fibrotic and focally calcified wall was found within the lesion. Histologically, in the context of the wall, lamellar bone forming trabeculae intermingled with fat tissue containing myeloid and erythroid cells (bone marrow metaplasia) were found (Figure and ). CD 34 immunostaining was negative. Therefore, a diagnosis of hepatocellular adenoma was established.\nThe patient started oral intake on 4th postoperative day, with a carbohydrate-based diet. No signs of liver failure were recorded and the patient was discharged on day 13 post-op, after removing the J-P drains.
A 33-year-old female presented at the outpatient clinic with painful diminution of vision in the left eye developing over a period of 10 days. The pain persisted beyond the onset of visual loss. The patient provided a background history of 5 similar attacks over the previous 5 years involv-ing a single eye but never both simultaneously or sequential bilateral involvement. Each episode began with local pain, which increased with eye movement and visual loss progressed over the next 7 to 10 days. During these episodes, the patient’s visual acuity varied between the percep-tion of light to finger counting at 1 m. The interval between episodes varied between 2 and 6 months. Each episode remitted after the administration of intravenous steroids (methylpredniso-lone, 1 g) for 3 days and oral methylprednisolone at 1 mg/kg for the following 11 days. Partial recovery of vision occurred upon remittance.\nThe patient did not have any temporal artery tenderness, and temporal pulses were palpable bi-laterally. There was no history suggestive of any other cranial nerve, motor, sensory, or auto-nomic system involvement. No relevant symptoms suggestive of connective tissue disease or autoimmune illness were noted historically. An examination revealed a relative afferent pupillary defect in the left eye. There was reduced visual acuity in the left eye, with finger counting at 1 m, as well as 6/6 visual acuity in the right eye according to the Snellen chart.\nFundoscopy revealed a pale optic disc in the left eye and normal retinas (). There was re-duced color vision in the left eye (2/12 of Ishihara plates), and a left relative afferent papillary defect was present. Visual field mapping revealed complete left visual field loss and a normal right-sided visual field (). The remainder of the neuroophthalmological examination was unremarkable. There was nothing in the patient’s history or physical examination that was sug-gestive of connective tissue disease or sarcoidosis. Initial blood tests showed a normal full blood count, normal levels of urea and electrolytes, normal liver function tests, and normal C-reactive protein (CRP: <1 mg/L), plasma viscosity, and glycated hemoglobin values. A chest X-ray was also normal. A lumbar puncture was performed, which yielded cerebrospinal fluid with normal white and red blood cell counts, a normal angiotension-converting enzyme (ACE) level, and no oligoclonal bands. A magnetic resonance imaging (MRI) scan of the patient’s brain and spinal cord was normal. The Mantoux test and a collagen workup (antinuclear antibody, an-tiphospholipid antibody, and rheumatoid factor) were negative. The serum ACE level was nor-mal. Hepatitis B antigen and HIV serology were non-reactive. A test for serum immunoglobulin G (IgG) neuromyelitis optica (NMO) antibody was negative. A visually evoked response test revealed prolonged P100 latency in both eyes. Optical coherence tomography (OCT) demon-strated reduced retinal nerve fiber layer (RNFL) thickness (). Due to acute and painful vision loss, a diagnosis of unilateral acute retrobulbar ON was made. Visual acuity improved to 6/10 (Snellen chart) following administration of intravenous steroids (methylprednisolone, 1 g) for 3 days and oral methylprednisolone at 1 mg/kg for the following 11 days.
A 68-year-old male presented with left mandibular area pain due to third trigeminal neuralgia. He had underdone conventional radiofrequency lesioning in the left third branch of the trigeminal nerve for trigeminal neuralgia one year previously. Following the procedure he had been without pain until quite recently. However, at the time of his presentation, he was reporting pain in the same area of 40/100 using the VAS (Visual Analogue Scale) score. We decided to proceed with medical treatment including carbamazepine 200 mg three times a day, tramadol (37.5 mg)/acetaminophen (325 mg) combination three times a day, and nortriptyline 10 mg one time a day because his pain was mild. On his second day of medication, a mild fever and general weakness had occurred. On his fourth day after beginning the medication, an oral rash and bullae on the cheek, neck, forearm and leg were found. On the fifth day, the patient visited the emergency room and was admitted with a presumptive diagnosis of SJS. Further history revealed that he had discontinued medication including carbamazepine 200 mg one year previously on his own due to pruritus after taking the medication once. The medical history was otherwise unremarkable. On physical examination, the patient displayed pruritic and stinging erythema and painful crursted erosions on both lips, with several flaccid and ruptured bullae on the left cheek, neck, forearm, and leg (). Pharyngitis was present but he was able to swallow some food. Eye discomfort and genital mucosa involvement were not present. Nikolsky's sign was positive. Laboratory examination revealed mild leukocytosis, and alanine aminotransferase, C-reactive protein, and potassium were mildly elevated. Carbamazepine was withdrawn and prednisolone 125 mg/day was started. A skin biopsy performed on the third day after admission, demonstrated subepidermal bullae formation with epidermal necrosis and minimal perivascular lymphohistocytic infiltration in the upper dermis and the correct diagnosis of SJS was established. Steroid treatment was given for 5 days and gradually withdrawn. On the eighth day the patient was discharged in good condition, with generalized desquamation and incomplete peeling of the skin on the neck, forearm, and face. Two weeks after discharge, he underwent conventional radiofrequency lesioning of the left third branch of the trigeminal nerve. Two weeks later, his pain was nearly gone.
A 56-year-old Caucasian male farmer sought the Oral Diagnosis Clinic complaining of a pricking pain in the lower lip where he had an unhealed wound for about six years. His medical history included hypertension and diabetes and there was no history of drinking or smoking. However, the patient reported being exposed daily to the sun without UV protection. The examination showed a 3-cm ulcerated and crusted area on the lower lip ( and ). There were no clinical changes in the intraoral examination. The clinical findings and the patient’s occupation led to the diagnosis of lip squamous cell carcinoma or actinic cheilitis.\nAn incisional biopsy could not be performed at the first appointment due to the patient’s high blood pressure (200/120 mmHg). The topical use of 0.1% triamcinolone acetonide cream was prescribed until the next appointment. After seven days, the patient returned to the clinic with significant clinical improvement. The incisional biopsy was performed under local anesthesia and the tissue specimen was sent to histopathological analysis. The tissue sections showed parakeratotic stratum corneum with ulcerated areas, showing in the lamina propria a dense sheet-like infiltrate predominantly of mature plasma cells, some lymphocytes, few eosinophils, and sparse Russell bodies (). The plasma cells infiltrated the entire connective tissue up to the minor salivary glands. It is worth noting the absence of cellular atypia, pleomorphic figures, and mitotic activity. Immunohistochemistry to kappa and lambda immunoglobulin light chains showed polyclonal plasma cells, with a predominance of lambda ( and ).\nConsidering the clinical and histopathological findings and a negative serological test for syphilis, PCC was diagnosed. The topical corticosteroid was suspended after 10 days of use. Lip balm cream and sunscreen were prescribed and the lesion completely regressed 35 days after the biopsy ().\nThere was no recurrence after six months of follow-up and the administration of lip balm and sunscreen was maintained.
A morbidly obese 66yr old white female with history of hypertension, diabetes, ischemic cardiomyopathy eventually leading to cardiac transplantation 11 years earlier and end stage dialysis-dependent renal disease, required admission to Intensive care unit for worsening respiratory failure and hypotension. She had formerly been a smoker, and was morbidly obese with obstructive sleep apnea. In addition she had been maintained on chronic immunosuppressant therapy following cardiac transplantation. She was intubated and started on mechanical ventilation. Hypotension and peripheral edema worsened and laboratory values revealed marked anemia, with initial hemoglobin of 8.8gm/dl and a creatinine of 4.8mg/dl. She was treated on the lines of septic shock and hemodialysis was started for renal failure. Eventual blood cultures showed gram negative septicemia. Chest X-ray showed pulmonary vascular congestion and a probable left pleural effusion. Although she slowly improved hemodynamically; she could not be weaned off the ventilator. Given the suspicion of a significant left pleural effusion, consultation was obtained for chest tube drainage. A 28 French trocar tube was inserted, and immediately yielded massive drainage of frank blood. Her hemoglobin dropped from 8.8 to 5gm/dl. The chest tube was clamped promptly and she was resuscitated with multiple units of blood transfusion, blood pressure was stabilized. A Chest x-ray [] showed a chest tube near the midline. Breath sounds were still audible over both hemithoraces. CT scan of the chest [Figures and ] showed presence of the chest tube in left main pulmonary artery. Atelectasis and consolidation of the left lung were also evident. Contrast injection through the chest tube confirmed its presence in the left main pulmonary artery []. Plans were made for surgical removal of the tube, possibly requiring cardiopulmonary bypass. It was noteworthy that each attempt to unclamp the chest tube resulted in frank hemorrhage through the tube. Preparations were made and the patient was taken to the operating room. Pump standby was used. The patient was then prepared, with multiple monitoring lines placed, and was placed in semi-right lateral decubitus position. A left lateral thoracotomy was performed, with the chest tube still in place. Dense adhesions of the left lung to the chest wall were encountered. Although initially consideration was given to dissection around the lung to obtain vascular control of the hilum, this did not seem feasible, given dense adhesions and consolidation of the left lung. Therefore, purse string sutures of Prolene were placed around the entrance of the tube into the lateral portion of the lower lobe of the left lung. The tube was then quickly withdrawn while the purse string sutures, placed on the lung tissue were tied, and hemorrhage controlled. Bleeding from the orotracheal tube, which had been positioned in the right main stem bronchus, was noted and required suctioning. This seemed to be controlled with limited suctioning. Postoperatively the patient was followed in the Intensive care unit with continued intubation of the right main stem bronchus so as to facilitate the healing of traumatized and eventually repaired left lung. Chest X-rays initially showed consolidation and atelectasis of the left lung; however no further bleeding was noted. Gradually the orotracheal airway was pulled with slow reaeration of left lung. Eventually, the patient was weaned from the ventilator, and was successfully extubated without further evidence of bleeding.
The patient was a 66-year-old man who presented with dyspnea and cough and was referred to the Second Hospital of Jilin University 5 years ago. The patient was a retired worker with a 40 pack-year history of smoking and no history of other diseases. HRCT scan of the chest revealed that the patient had masses in both lungs, with fibrous stripes and diffuse subpleural reticular pattern, which were indicative of IPF (Fig. a, b). Lung function tests showed a substantial decrease in the diffusing capacity of the lungs for carbon monoxide (DLCO; < 60%), while blood gas analysis showed reduced levels of partial pressure of oxygen (PaO2). Treatment with glucocorticoids and pirfenidone led to improvement of the symptoms. With regular treatment, the patient’s condition continued to remain stable, as confirmed by a follow-up chest HRCT performed 5 years later. However, the follow-up scan revealed a newly developed, irregular mass in the right upper lobe and enlargement of the anterior trachea and posterior vena caval groups of lymph nodes; the lower lobes did not show any changes on either side (Fig. c, d). The patient then underwent fiberoptic bronchoscopy for retrieval of a tissue sample. Pathological examination of the sample revealed SCLC in the superior lobe of the right lung (Fig. e, f).\nA chemotherapeutic regimen comprising nedaplatin (80 mg/m2) and etoposide (100 mg for 5 days) was then initiated. However, during the chemotherapy, the administration of antifibrotic agents was continued. After 4 courses of treatment, marked reduction of the tumor was observed. A repeat thoracic CT scan revealed reduction in the size of the shadow in the upper right lung and significant decrease in the size of the metastatic lymph nodes in the anterior tracheal and posterior vena caval groups of lymph nodes; however, there was no visible decrease in the severity of IPF (Fig. g, h). Thus, we concluded that the treatment was effective and safe, and we recommend that chemotherapy be continued, depending on whether the patient can tolerate and afford it. We followed up the patient three months later. The patient’s vital signs were stable, and there were no instances of subsequent infections or other complications. Therefore, we concluded that chemotherapy was relatively safe and the patient could benefit from chemotherapy.
A 49-year-old-man visited our outpatient clinic on October 1, 2007 with atypical chest pain that had started 2 months before. He complained of crushing chest pain that lasted for 5 to 10 seconds. The pain usually occurred early in the morning and was not related to exercise. The pain would disappear without any specific treatment. ECG showed no definite ST-segment changes. Echocardiography also showed normal left ventricular systolic function and there were no regional wall motion abnormalities. He was not taking any medication except for a budesonide inhaler and mometasone (topical corticosteroid) for treatment of asthma.\nThe patient underwent coronary angiography and ergonovine provocation test. Ergonovine 0.2 mg was injected twice intravenously at a 5-minute interval. We achieved cineangiogram at 90 seconds after each ergonovine injection. Coronary angiography showed no significant lesions in the coronary arteries and the intravenous ergonovine provocation test was negative (). There was no chest pain, ST-segment changes, or coronary artery vasospasm noted during the ergonovine provocation test. We did not prescribe any antianginal medication such as nitroglycerine before the ergonovine provocation test, which would have affected the results of the test. Esophagogastroduodenoscopy showed hemorrhagic gastritis and erosive duodenitis. The gastrointestinal tract was thought to be the source of the pain and he was prescribed a proton pump inhibitor and prokinetics for pain relief.\nAfter 5 years, on January 15, 2012, he visited the ER with sudden onset of chest pain while sleeping. The characteristics of the chest pain were very similar to the pain that occurred in 2007. In the ER, the chest pain was relieved by sublingual nitroglycerin and he was admitted to the coronary care unit. After several hours, the chest pain recurred and the patient complained of dizziness, nausea, and vomiting. His blood pressure dropped to 76/41 mm Hg, and he had symptomatic sinus bradycardia. ECG showed no definite ST-segment changes (), but troponin I was elevated to 90.3 ng/mL. Suspicious of non ST-segment elevation myocardial infarction combined with cardiogenic shock, we performed coronary angiography. Coronary angiography showed no significant stenosis of the left main, left anterior descending, or left circumflex coronary arteries (), but total occlusion with distal Thrombolysis in Myocardial Infarction flow grade 2 in the distal right coronary artery, posterior descending artery, and posterolateral branch bifurcation segment was observed (). After intra-coronary nitroglycerin injection, the occluded segment was dilated () and chest pain was slowly relieved. Blood pressure and heart rate were also stabilized. Echocardiography showed akinesia of the apical anterior, septal, and inferior walls. Chest pain did not recur after taking diltiazem and nicorandil. The patient is now under outpatient clinic follow up without any further event.
The second patient died was a 39-year-old female with univentricular heart (tricuspid atresia), who had had previously two cardiac surgeries (the last was atrio-pulmonary Fontan, 33 years earlier). The patient suffered from a serious right atriomegaly with frequent episodes of atrial tachycardia, so she was a candidate for Fontan conversion surgery. Pre-operative ventricular function was mildly reduced (50%). In the post-operative, the patient suffered from severe single ventricle dysfunction resulting in LCOS and the need for ECMO implantation. Both patients could not be weaned from ECMO due to multi-organ failure.\nSeven patients required pace-maker implantation due to post-operative sinus node dysfunction or atrioventricular conduction abnormalities. All patients were discharged on oral antiarrhythmic for 3–6 months and anticoagulants for 6 months. At discharge, 15 patients were in sinus rhythm, 5 had a stable pacemaker rhythm, 2 had atrial fibrillation, and 1 atrial flutter. One patient discharged in sinus rhythm had a pacemaker implant 5 months after the operation due to the presence of sinus node dysfunction.\nDuring a median follow-up of 14 months (IQR 7–27), there was no late mortality and 17/23 patients had an improvement of NYHA functional class. Five patients in NYHA III progressed to class II and 4 to class I; eight patients progressed from class II to class I.\nAt follow up electrocardiogram, 16 patients were in sinus rhythm, 6 with stable pacemaker rhythm, and 1 with permanent atrial fibrillation.\nRecurrence of arrhythmia occurred in 2/23 (8.6%) patients, more than 3 months after surgery. These patients presented at surgical ablation with history of atrial fibrillation lasting 4 and 19 years, respectively, and both had atrial fibrillation, which was treated with right-sided Maze rather than Cox maze III due to technical issues. Sixteen (69%) patients are in stable sinus rhythm, 12 without any anti-arrhythmic therapy. At median follow up of 14 months (IQR 7–27), freedom from recurrence of arrhythmia was 90.9% and cumulative risk of recurrence was 9.6% ().
A 76-year-old female patient who underwent bipolar hemiarthroplasty due to right femoral neck fracture six years ago, presented with increasing pain in her right hip. Her complaints had started approximately three years ago. Implant loosening and malposition were detected in the right hip prosthesis; therefore, revision surgery was indicated (Figure ).\nThe patient underwent hip arthroplasty revision surgery with a posterior approach (Figure ).\nAcetabular cup no. 48, CoCr femoral head no. 32 (+4 mm) and lateralized offset neck (+4 mm) (Lima Corporate, Italy) were used. The femoral head was impacted on the neck with an appropriate force and the hip was reduced.\nWeight-bearing was allowed at the end of sixth week. At third-month follow-up, the patient was able to mobilize pain-free. However, a few days after her third-month follow-up, she was admitted to the outpatient clinic with complaints of severe pain and limitation of motion in the right hip without any history of obvious trauma. The patient reported that the pain and limitation emerged following a sound she heard while getting up from her seat. Disassociation of femoral head and neck components and accompanying hip dislocation was detected in the right hip (Figure ).\nThe femoral head was in the acetabular cup. There were no signs of osteolysis or loosening of the components on the radiographs.\nA same-sized femoral head, liner, and proximal modular part of femoral stem replacement were performed via the same anatomic approach (Figure ).\nBoth distal part of the femoral stem and acetabular shell were in a good position as observed intraoperatively, thus were not revised. No apparent corrosion was detected on the removed components. There were no signs of metallosis in the surrounding tissues, nor any sign of an impingement that could potentially affect femoral head or neck. The retrieved parts of the prosthesis revealed that the head-neck interface was not matching appropriately although no visible damage was detected on the implants and the taper sizes (12/14) were appropriate for both neck and head components. The disassociation was attributed to a possible manufacturing error of either head or neck component. The hip joint was stable after revision. No problems were encountered during the patient’s three years of follow-up.
Owing to the inability to swallow and severe odynophagia after swallowing a large piece of meat, a 68-year-old man underwent flexible esophagoscopy, which revealed the swallowed meat stuck in the distal part of the esophagus. All attempts in another hospital to remove the foreign body by using rigid esophagoscopy were unsuccessful, and the patient was then referred to our center. He was ill and toxic on arrival, and rupture of the esophagus was subsequently confirmed based on computed tomography findings (). The patient was prepared for urgent thoracotomy. Preoperative esophagoscopy revealed a full-thickness esophageal wall perforation approximately 37 cm from the incisor teeth just above the foreign body. The stuck swallowed meat was completely removed with grasping forceps, and reassessment of the esophagus did not show any abnormality. A right-sided posterolateral thoracotomy through the sixth intercostal space was performed and revealed a 5-cm longitudinal perforation in the distal part of the esophagus just above the esophageal hiatus and severe mediastinal inflammation around the perforation site. Despite the presence of signs of sepsis, including fever, tachypnea, tachycardia and loss of consciousness, and severe mediastinal inflammation, because of the relatively short interval between the onset of the primary injury and the operation, which was approximately 24 hours, a decision for primary repair was made. Vertical esophagomyotomy was performed to fully expose the damaged mucosa. After trimming the edges of the perforation, a secure two-layer interrupted closure was performed by using fine 4-0 Vicryl sutures. The repair site was buttressed by a 9.5- × 4.8-cm collagen patch coated with human fibrinogen and thrombin (TachoSil, Nycomed, Austria, Vienna).\nThe postoperative course was uneventful except for sputum retention, which was managed with flexible bronchoscopy on the third postoperative day. Gastrografin swallow radiographs obtained on postoperative day 9 did not demonstrate any leakage, and liquid diet was started and advanced gradually. The patient was discharged in a good condition on the 15th postoperative day. Owing to the history of esophageal foreign body in an elderly patient, he underwent flexible esophagoscopy and esophageal manometry 2 months later for detection of any undiagnosed esophageal disorder, but no abnormalities were found. The follow-up examination and chest radiography results were also normal ().
A 30-year-old woman patient visited our outpatient clinic after experiencing headache and blurred vision for 1 month. Her neurological examination was within the normal limits, except that bilateral congested papillae were identified. Her family history was unavailable because she was adopted. MRI revealed a solid tumor with a maximum diameter of 3.5 cm accompanying an internal cyst in the left cerebellar hemisphere. In addition, extensive cerebral edema and ventricular dilation were noted. On presurgical brain MRI, the solid region showed uniform contrast enhancement. On cerebral angiography, feeding arteries were noted to arise from the left anterior inferior cerebellar artery (AICA) and left posterior inferior cerebellar artery (PICA), and both the draining veins to the petrosal vein and the inferior vermian vein were identified [].\nWe performed 200 ml of 10% glycerol (twice a day) with dexamethasone (8 mg/day) for 6 days before the operation. Because the symptoms improved, we did not perform external ventricular drainage prior to the operation. Surgery was performed via the midline suboccipital approach with the patient in the prone position. The dura mater was dissected and ICG fluorescence angiography was performed. We observed the feeding artery coming off the PICA arose from the cerebellar hemisphere and drained via the horizontal fissure, additionally feeding vessels from the AICA were confirmed on the outside. The lesional veins drained into the inferior vermian vein []. Intraoperatively, the feeding artery from the PICA was coagulated first and then cut. Because there was a clear cleavage plane from the surrounding tissue, which was not swollen, detachment was performed, leaving the thick draining veins intact. The most significant draining veins, which converged onto the petrosal vein, were positioned anteriorly on the outside. Finally, these veins were coagulated and cut, and the tumor was removed en bloc. The estimated blood loss was 500 ml. Pathological examination of the specimen confirmed hemangioblastoma WHO I.
The images presented in Figs. , , and the related Additional file : Video 4 and Additional file : Video 5 were acquired after left lobe liver resection surgery in a 67-year-old woman with a giant hepatic angioma. During the surgical dissection of the tissues, an accidental laceration of the inferior vena cava occurred, which required almost complete clamping. To re-establish blood flow, the surgeons used an Edwards® Bovine Pericardial Patch. After declamping, the surgeon requested that the patency of the inferior vena cava and blood flow in the suprahepatic veins were checked using TEE. A comparison of TEE for visualization of the main hepatic veins with the acquisition of Doppler ultrasound curves using the transabdominal approach was first described by Meierhenrich et al. [] in their study of 34 patients scheduled for abdominal surgery. Using a multiplane TEE, they were able to identify the three main hepatic veins in all of the patients, and they reported that adequate Doppler tracings of the right and middle hepatic veins could be obtained in 100 and 97% of the patients, respectively, by TEE and in 91 and 50% of the patients by transabdominal sonography (TAS). Doppler tracing of the left hepatic vein could only be acquired in 18% of the patients by TEE, but in 47% of the patients by TAS. Doppler ultrasound and Pulse Wave Doppler (PW) analysis, which measure blood flow velocity (using a correct insonation angle, <60°), play an important role in the assessment of liver vessel patency, resistivity, and flow direction (as already shown in Figs. , , and Additional file : Video 4 and Additional file : Video 5).\nUsually, the normal hepatic vein waveform has four components: a retrograde A wave (right atrial contraction), an anterograde S wave (right ventricular systolic), a transitional V wave (pulmonary vein closure), and an anterograde D wave (right ventricular diastole)—see Fig. . The Doppler waveform of left hepatic vein blood flow resembles that of the pulmonary vein. It is important for the anesthesiologist to know that flow above the baseline indicates flow toward the transducer and flow below the baseline indicates flow away from the transducer. At least four questions need to be answered: Is there flow? Where it is directed (forward vs. backward)? What is the relationship of magnitude between the S and D waves (normal S>D vs. abnormal S<D)? What is the magnitude of the A wave (normal vs. abnormal)? A detailed explanation has been provided elsewhere [].
During home sequestration enacted due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic in March of 2020, an otherwise healthy 12-year-old boy developed a unilateral asymptomatic rash limited to his left lower extremity. Household contacts lacked a similar rash. Because of the pandemic and unseasonably cold weather, he had not traveled nor left his house in several days. The boy had no history of fever, malaise, insect exposure, nor prolonged compression or trauma to the affected extremity. Since this occurred during the upswing of the pandemic, the child could not be seen in-person in the clinic, and he was examined via a telemedicine visit. The child appeared well on the computer screen with clear conjunctiva and mucus membranes. No skin lesions were seen, except for an area of reticulated erythema on his left shin (Figure ).\nDue to the reticular pattern of the rash, a diagnosis of parvovirus infection was initially considered, even though there were no systemic symptoms, prior “slapped cheek” appearance, or generalized distribution of the rash. Since the diagnosis was in doubt and further in-person evaluation could not be performed, such as obtaining parvovirus titers, a pediatric dermatologist was consulted. An additional historical question was posed about the child’s potential chronic exposure to a heater. The mother verified that since the boy had been sequestered in his home for several days due to the pandemic, he was spending approximately two hours per day sitting on a couch playing video games in the cold basement of his house, with a space heater positioned close to his left leg (Figure ).\nDue to the history of exposure to a portable heater and the classic appearance of the rash, the clinical diagnosis of erythema ab igne was made. The patient was advised to avoid direct exposure to the portable heater, and reassurance was provided that no other intervention was required except for follow-up examination to ensure resolution of the rash. After approximately four weeks of avoidance of the direct heating source, the skin erythema was much reduced. The child remained otherwise asymptomatic.
We present the case of a 42-year-old man who presented to the emergency department with a complaint of abdominal pain and diarrhea for 3 days. The abdominal pain started in the periumbilical region and was shifted to the right lower quadrant of the abdomen. The pain started gradually and had been progressing in severity. He described the pain as a stabbing in nature. It was exacerbated by movement and food intake. The pain was partially relieved by oral analgesic medications like paracetamol. The pain was associated with low-grade fever and decreased appetite. The patient also complained of diarrhea with five bowel motions/day. The stools were watery with no mucus or blood. He reported that diarrhea developed after he received an oral antibiotic therapy (cefuroxime) for a recent upper respiratory tract infection.\nThe past medical history of the patient was remarkable for diabetes mellitus that was well-controlled with oral antidiabetic agents. He did not undergo any previous abdominal surgeries. He had a smoking history of 15 pack-years. He had never drunk alcohol before. He worked as a taxi driver. The family history was unremarkable for any inherited gastrointestinal disorders.\nUpon examination, the patient appeared sick. He was not pale, jaundiced, or cyanosed. Vital signs revealed tachycardia (115 bpm), low-grade fever (37.5℃), normal respiratory rate (14 bpm), and maintained blood pressure (122/80 mmHg). The oxygen saturation was 99% on room air. Abdominal examination revealed a soft abdomen with diffuse tenderness. However, the tenderness was more pronounced in the right iliac fossa with a positive rebound sign. Further, the Rovsing sign was positive. Initial laboratory investigation revealed elevated leukocyte count and elevated inflammatory markers, including erythrocyte sedimentation rate and C-reactive protein. The renal and hepatic profiles were within the normal limits (Table ).\nIn light of the aforementioned clinical information, the patient was diagnosed as having acute appendicitis. A CT scan with intravenous contrast was performed to confirm the diagnosis. The scan demonstrated colonic wall thickening with edematous haustral folds suggestive of pseudomembranous colitis. Further, an endoluminal lesion was observed in the cecum with an average size of 6 cm. The lesion was well-defined and had a homogenous fat density with no solid component. The mass was causing a partial colonic obstruction. Such findings conferred the diagnosis of cecal lipoma (Figure ).\nThe patient was prepared for an emergency laparoscopy for further evaluation and management. The operation was done under general anesthesia and the patient was placed in the supine position. Limited segmental rection of the cecum with appendectomy was performed. The estimated blood loss was 10 mL and the total operative time was 100 minutes. The patient tolerated the operation with no complications. He had an uneventful recovery. Histopathological examination of the resected sample revealed the diagnosis of cecal lipoma and the associated acute appendicitis. The patient was discharged on the fifth postoperative day. After 3 months of follow-up, the patient remained asymptomatic with no active issues.
A 62-year-old man with a past medical history significant for iron deficiency anemia, coronary artery disease, benign essential hypertension, gastroesophageal reflux disease, treated hepatitis C, alcoholic liver cirrhosis with history of esophageal varices, and internal hemorrhoids was a well-known patient for our hepatology team for history of liver cirrhosis in the past. Four months prior to establishing care in our clinic, he had presented with epigastric pain to the emergency department. During that emergency department visit, he underwent a CT of the abdomen and pelvis with intravenous contrast, which was notable for peri-pancreatic stranding and multiple small fluid collections around the entire pancreas, the largest of which was along the superior aspect of the pancreatic tail measuring 4.7 x 3.4 cm (Figure ).\nEvaluation done at an other center showed a hemoglobin level of 5.9 and was admitted to the emergency department for workup. The patient gave a history of having intermittent melena and one episode of emesis of blood clot. The patient had a full evaluation with esophagogastroduodenoscopy (EGD) and colonoscopy to rule out common causes or expected causes of GI bleed. EGD showed small isolated gastric varices (IGV 1 in the fundus) without bleeding, and otherwise normal stomach mucosa and no esophageal varices. On colonoscopy, the patient had medium-sized non-bleeding external and internal hemorrhoids but the entire colonic mucosa was unremarkable. The terminal ileum was intubated and showed old coffee-ground appearing contents. His video capsule endoscopic examination was unremarkable. The patient was conservatively managed but the exact source of bleeding was not identified, and his bleeding stopped. Two weeks later, the patient underwent endoscopic ultrasound (EUS) to evaluate for chronic pancreatitis, and also follow up of pancreatic tail cyst found on imaging four months prior. EUS demonstrated an overall atrophic appearance of pancreas with diffuse hypoechogenicity with lobularity and honeycombing, and shadowing calcifications, with areas of hyperechogenic stranding, most prominent in the distal body and tail of the pancreas. Additionally was seen a round peripancreatic complex collection measuring about 27.3 x 23.7 mm, with some anechoic areas along with hyperechogenic contents, which was suspected to be old blood (Figure ). The pancreatic duct (PD) appeared normal, without any disruption or stricture, and no obvious communication with the cyst was identified, and the common bile duct (CBD) was unremarkable. Given complex nature of the collection, fine needle aspiration (FNA) was deferred.\nFor further evaluation of the complex pancreatic collection containing hyperchogenic blood-like material, with the background presentation of recurrent melena and persistent anemia, a duodenoscope was used to evaluate the ampulla, and small amount of blood was seen extruding, raising differentials for HP or hemobilia (Figure ). The upper enteroscopic examination to proximal jejunum was otherwise unremarkable. CT angiography (CTA) of the abdomen did not show any mass in the liver or biliary system, but was notable for pancreatic pseudocyst with no evidence of active arterial extravasation, findings suggestive of chronic pancreatitis, thrombosis of distal splenic vein (associated perisplenic and upper abdominal collaterals).\nAfter multi-disciplinary discussion, IR approach was preferred over endoscopic approach, and through ultrasound-guide access of the left radial artery, selective catheterization of the celiac trunk, with subselective catheterization of the left gastric artery/splenic artery/gastroepiploic artery branch of the gastroduodenal artery with angiogram was performed. Superselective gastroepiploic angiogram demonstrated abnormal area of contrast pooling at the level of the midportion of the gastroepiploic artery corresponding with site of pancreatic complex collection abutting the stomach (Figure , ), and finally coil embolization of the gastroepiploic artery (bleeding source), and splenic artery (to decrease flow to the area of bleeding) was achieved with "back and front door" technique (Figure , ). The patient did well post-procedure, and did not have further bleeding, and hemoglobin remained stable on two-month follow-up.
A 46-year-old white woman presented to our emergency department with facial pain, eyelid swelling, and proptosis with ophthalmoplegia in her left eye (LE), suggesting unilateral OC, and normal vital signs parameters. These signs had been present for 6 hours and started with ophthalmoplegia by eye movements. She had a history of dyslipidemia and hypertension and was receiving drug therapy; she had no fever, sinusitis, or facial skin infections in the previous days.\nGiven the absence of other associated issues an ophthalmologic evaluation was initially requested. Her best corrected visual acuity in both eyes was 20/20 with intraocular pressure 15 mmHg, and there was no detectable afferent pupillary defect. Her right eye was normal. Her LE had substantial chemosis and hyperemia of the conjunctiva, with exacerbation of the ophthalmoplegia by eye movements. A fundus examination of her LE was normal. Palpation of her left orbital area generated significant crackles but also revealed major pulsation in the scanned region. An urgent non-contrast-enhanced computed axial tomography (NCCAT) of her brain and orbits showed a dense and distended superior ophthalmic vein on the left side, with periorbital swelling. Contrast-enhanced computed tomography (CECT) confirmed the presence of a thrombus in her superior ophthalmic vein, as a filling defect in the late phase, and also showed a non-fat density filling defect in the ipsilateral part of the cavernous sinus (Fig. ). Finally, contrast-enhanced magnetic resonance imaging (CEMRI) confirmed the distended cavernous sinus and superior ophthalmic vein with the non-fat density filling defect (Fig. ).\nThe day after she started to develop dyspnea an arterial blood gas test was done. The findings of hypocapnia and hypoxemia suggested PE, so CECT with the PE protocol was done, showing massive bilateral pulmonary artery thrombosis and a lung infarct in the superior segment of the basal lobe of her right lung (Fig. ).\nShe had neutrophilia, with a total white cell count of 18.1 × 109/liter and elevated C-reactive protein of 341 mg/liter. Blood culture was positive for Streptococcus constellatus, a member of the Peptostreptococcus family, a saprophyte of the oral mucosa that can be pathogenic in immunocompromised persons, but human immunodeficiency virus (HIV) testing was negative. Dental panoramic images confirmed a maxillary abscess.\nShe was prescribed a cycle of intravenously administered antibiotics (piperacillin/tazobactam) and anticoagulation therapy with heparin for 10 days, after which she no longer had ophthalmoplegia and periorbital edema. A radiological orbit CECT showed that the diameter of her superior ophthalmic vein on the left and the signal of the fatty periorbital tissue were both normal (Fig. ). Her white blood cell count normalized. She was discharged from hospital after 15 days with orally administered antibiotic therapy to be taken for 1 month. The affected teeth were extracted after 3 weeks from the onset of ocular symptoms.\nAt 1-month follow-up she no longer had shortness of breath. A chest CECT check with the PE protocol confirmed there was no evidence of thrombosis in her main pulmonary arteries.
A 27-year-old woman with unexplained infertility was referred to the reproductive endocrinology clinic. Her medical history was significant for polycystic ovary syndrome. She reported menstrual cycles every 30 to 37 days with menses lasting five to seven days. She was a nonsmoker and denied a history of sexually transmitted infections. Her past surgical history was significant for a laparoscopic appendectomy and right salpingectomy for ruptured appendicitis at age 13.\nAs part of the infertility workup, a saline infusion sonohysterogram was ordered but not completed due to a positive pregnancy test and pelvic cramping upon presentation to radiology. The following day, she reported that her symptoms became worse to include passing large clots. She then presented to the emergency department, and her quantitative human chorionic gonadotropin (HCG) was 98 mIU/ml. A transvaginal ultrasound was performed, which showed no intrauterine pregnancy and normal adnexa. She was diagnosed with a pregnancy of unknown location and referred to the acute gynecology clinic.\nThree days later, she presented to the clinic and reported vaginal spotting and that her pelvic pain had resolved. Her quantitative HCG was 449 mIU/ml. She was given return precautions and a follow-up appointment. Seven days later, she presented to the clinic for her scheduled follow-up assessment. Her quantitative HCG was now 3798 mIU/ml, and a bedside transvaginal ultrasound showed an ectopic pregnancy within her left adnexa with fetal cardiac activity. She was counseled, admitted to the hospital, and underwent an uncomplicated left salpingectomy.\nHer final pathology evaluation results were consistent with ectopic pregnancy. Chorionic villi were identified within the fimbria and the wall of the fallopian tube. Proximal to the ectopic pregnancy, a single metal staple was found. The staple was embedded within the fallopian tube wall and believed to be from the prior appendectomy (Figures , ). At the time of surgery, a few surgical staples were noted within the posterior cul-de-sac.
A 35-year-old male was admitted with chief complaints of bloody diarrhea and mild fever for 3 days. The patient had been suffering from watery diarrhea and general weakness for 2 months. The patient was not on any medication nor had any other medical history in the past. Laboratory findings showed an elevated white blood cell counts (14,600/µL), ESR (42 mm/hr), CRP level (2.82 mg/dL), and D-dimer (7.8 µg/mL), and a decreased hemoglobin level (8.6 g/dL), and platelet count (100,000/µL). All other biochemical, electrolyte tests were within the normal limits. Sigmoidoscopic findings showed hyperemic and edematous mucosa, friability, and shallow ulcers from the sigmoid colon to the rectum (). With suspicion of UC, he was provided supportive care and intravenous antibiotics while waiting for serologic and pathologic results. Three days later, the patient started complaining of a headache and gradually developed a decreased level of consciousness and intermittent dystonic posture of the right arm. On neurologic examination, slight motor weakness in the right upper and lower limbs was detected. There were no obvious pathologic reflexes. A CT scan of the head showed hemorrhagic infarction in the left basal ganglia and infarctions in the right anterior frontal and left parietal lobe, which are outside the boundaries for an arterial territory (). With suspicion of venous thrombosis, MRI of the brain with venogram was obtained, and diffuse dural venous thrombosis with multiple hemorrhagic infarctions was identified (). Doppler ultrasonography of lower extremities showed no deep venous thrombosis. The patient was immediately transferred to the intensive care unit, and anticoagulation therapy was initiated with intravenous heparin infusion. An angiogram was obtained to evaluate the extent of CVT, but invasive endovascular therapy was not performed due to concerns of complications (). Sigmoidoscopic biopsies showed chronic active colitis with ulcer, crypt distortion, and cryptitis, which was consistent with UC. Perinuclear antineutrophil cytoplasmic antibody was positive and fecal calprotectin was highly elevated (6,545 µg/g). UC was diagnosed based on clinical history, laboratory studies, and biopsies of the colon. The patient was treated with a combination of oral and rectal 5-aminosalicylic acid. A prothrombotic workup that assessed for protein C, protein S, and antithrombin III deficiencies, anticardiolipin antibody, and fasting homocysteine was negative, except for lupus anticoagulant (LA). His initial Mayo score was 11, but symptoms of UC and CVT were gradually improved during hospitalization. When he was discharged 4 weeks later, the score improved to partial Mayo score 1. After discharge, the patient was recovered without neurologic deficit, and remission of UC (Mayo score 0) was also obtained (). Anticoagulation was continued with warfarin, and follow-up imaging after 8 weeks showed a decreased extent of CVT (). Persistently positive LA was detected 12 weeks apart, and mild to moderate thrombocytopenia (platelet count, 50,000–100,000/µL) persisted without bone marrow abnormalities.
A 15-year-old teenage boy initially presented in a district hospital, with a swelling at the right side of his neck, without any significant clinical symptoms. Although full details of the work-up performed at the time are not available, he was diagnosed with a branchial cleft cyst and was offered surveillance with follow-up imaging. Eight years later, he visited our unit. Physical examination revealed a painless palpable well-defined mass () within the right carotid triangle with positive Fontaine and Kocher I signs []. There was no palpable lymphadenopathy. An ultrasound scan was performed depicting a solid mass of mixed echogenicity in the right carotid triangle echogenicity in the left carotid triangle. This was suspected to be neurogenic in origin because of its location. A digital subtraction angiography (DSA) () followed, which revealed a 60x35mm protruding mass in the right carotid bifurcation, causing local compressive effects and posterior displacement of the vessels. The patient was admitted in our unit in order to be treated surgically. During the operation a large CBP was identified as seen in . The tumor was classified as Shamblin II and was completely excised. Histopathology study showed a 3 cm carotid body paraganglioma with characteristic “zellballen” growth pattern and cell nests surrounded by prominent fibrovascular stroma, with no evidence of malignancy (). The patient had an unremarkable recovery and was discharged home on the second POD.\nThe surgical technique adopted in both patients consisted of an oblique incision along the sternal head of the left sternocleidomastoid muscle under general anesthesia. Our strategy was to expose, dissect, and isolate the proximal common carotid artery using a vascular tape. The ansa cervicalis was also exposed early in the operation. The carotid bifurcation was exposed in a caudocranial approach. The proximal external and the proximal internal carotid arteries were isolated and controlled with vessel loops. Dissection was extended to the level of the digastor muscle in order to expose and control the distal internal carotid artery. During this process, the hypoglossal nerve was identified and preserved, by following the ansa cervicalis. The external carotid artery was cross-clamped temporarily. Finally, the tumor was removed with sharp dissection from the bifurcation with meticulous technique in order to avoid injury to the internal carotid artery and the cranial nerves. The reported plane of dissection reported as a white interface plane between the tumor and the vessels was not identified in the first patient as the tumor was severely adhering to the vessel wall and was typically found in the second patient. Following the removal of the CBP, the carotid sheath and platysma were approximated and the skin closed with a continuous subcuticular suture, after performing meticulous hemostasis (Figures and ).\nBoth patients had an annual postoperative follow-up with cervical ultrasound and carotid duplex ultrasonography with no evidence of local recurrence. Familial disease was excluded clinically, by screening the patient's first degree relatives with ultrasound imaging.
A 40-year-old male not known to have any chronic medical illness, presented complaining of epigastric and left upper quadrant pain for 1 month, associated with intermittent nausea and vomiting, and aggravated by fatty meals, with no other associated symptoms. He had frequent visits to the emergency department where he was managed with analgesia and antacids with mild symptomatic improvement. Clinical examination was unremarkable with no evidence of jaundice or abdominal tenderness. His blood test results showed a normal complete blood count, kidney function, and liver function. Chest X Ray revealed dextrocardia with stomach fundic gas shadow on Right side (). Abdominal ultrasonography revealed transpositioning of the solid organs with a left sided liver and gallbladder with a solitary stone and mild wall thickening. We elected to perform a Magnetic Resonance Cholangiopancreatography to delineate the anatomy and to rule out any anomalies within the biliary tree. It confirmed the previously noted findings, showed no evident anomaly within the biliary tree, and confirmed the diagnosis of situs inversus totalis (, ). The patient was Scheduled for an elective laparoscopic cholecystectomy.\nThe Operating room equipment arrangement was adjusted as Mirror Image of Routine Laparoscopic cholecystectomy (). The Monitor was placed on left side of the patient. The surgeon with the camera assistant were on right side of the patient and the first assistant was on left side of the patient. The abdomen was scrubbed and draped in the standard aseptic technique. The first infraumbilical 11 mm trocar introduced and pneumoperitoneum induced using the open technique. Three 5 mm trocars were placed, at the xiphisternum which was used for the surgeon’s left hand, at the left midclavicular line 2 cm below the costal margin which was used as working port for the surgeon’s right hand and at left anterior axillary line 5 cm from the costal margin which was used for retraction of the gallbladder fundus by the second assistant, respectively. Inspection of the abdominal cavity confirmed the presence of situs inversus totalis, with the liver and the gallbladder positioned in the left side (). The Calot’s triangle was identified. The peritoneum overlying the gallbladder infundibulum was then incised and the cystic duct and cystic artery identified and circumferentially dissected, till the critical view was obtained. The cystic duct and cystic artery were then doubly clipped and divided, through the subcostal port using the right hand. The gallbladder was dissected from its peritoneal attachments using electrocautery and was retrieved using Endoscopic bag through the infraumbilical port. The total operative duration was 80 min, which was longer than the conventional laparoscopic cholecystectomy performed in patient without underlying anatomical variation. It can be attributed to the modification in the technique required to adjust to the mirror image anatomy.\nThe patient had an uneventful postoperative course and was discharged on postoperative day 1. Pathological examination of the gallbladder confirmed the presence of gallstones with chronic cholecystitis. No postoperative complications were noted during his follow up in the outpatient department.
A 24-year-old woman presented at our department with complaint of low-grade intermittent fever and dry cough for 2 months that were not responding to antibiotics. She had no history of diabetes, hypertension or any other significant disease. Her routine investigations were within normal range. Chest radiograph taken at OPD was suggestive of miliary opacities []. She had a positive tuberculin test (an induration of 18 × 18 mm) with 1 TU of PPD RT 23. She was diagnosed to have miliary tuberculosis and was admitted in the ward to evaluate other systems and to observe the response to antitubercular chemotherapy. She was prescribed WHO category I antitubercular chemotherapy (2H3R3Z3E3/4H3R3) along with other supportive treatment. After a few days, the fever subsided and there was clinical improvement seen in the patient. She was being planned for discharge from the ward, when her breathlessness increased. She had decreased breath sound over left lung. The chest radiograph confirmed the presence of pneumothorax []. An intercostal drain under water seal was placed. By 48 h, the pneumothorax was reduced, the affected lung expanded and there was no water column movement at ‘under water seal’ drain. After having a stable course for over 2 days, the intercostal drain was withdrawn and she was discharged with advice to continue her antitubercular treatment and to avoid exertion. She remained clinically stable for 10 days, when she developed pain in the chest and her dyspnea increased. Her chest radiograph confirmed the recurrence of pneumothorax. Patient was readmitted and managed with intercostal drain under water seal for pneumothorax. Pleurodesis was done with tetracycline after her lung expanded. She was evaluated by high-resolution computed tomographic study, which showed miliary opacities [] and the presence of blebs over left lung apex []. Her antitubercular chemotherapy was continued for 6 months. She had a stable course, with no recurrence of the pneumothorax.
An 81-year-old male presented for consideration of vertebral augmentation due to diagnosis of stage IV, metastatic prostate adenocarcinoma, and worsening back pain. Lupron therapy was initiated at diagnosis four months prior. Docetaxel treatment was planned for six cycles but was subsequently stopped after the first cycle secondary to side effects. No radiation therapy was previously given. PSA level was 120.73 at diagnosis and 0.6 before radiofrequency ablation.\nAt the first appointment, the patient reported mild back pain and required a walker but was able to ambulate without difficulty. He did have pain upon palpation of the thoracolumbar junctional level. He did not have any neurologic deficit at presentation. Computed tomography (CT) scans showed 40% compression deformity of T12. Magnetic resonance imaging (MRI) showed pathologic involvement of T12 and L1 and metastatic involvement of the epidural component, resulting in 40% spinal canal stenosis (Figure ). At this time, vertebral augmentation was recommended although it was believed the epidural component would not be addressed and Radiation Oncology would need to be consulted. In a short period of two months, the patient’s condition deteriorated where he was wheelchair bound due to severe pain, not controlled with NSAIDS or opioids. In addition, repeat studies showed further tumor infiltration involving T11, prompting augmentation of T11, in addition to T12 and L1.\nThe procedure was performed under monitored anesthesia care (MAC) and fluoroscopic guided imaging. Under this image guidance, 10-gauge introducer needles were advanced into the T11, T12, and L1 vertebral levels using a bilateral transpedicular approach (Figure ). A drill and osteotome were used to create cavities at the anterior aspect of the vertebral bodies. Bilateral 17-gauge bipolar radiofrequency probes were advanced into the vertebral cavities and simultaneous application of radiofrequency energy was performed as part of the protocol for volumetric ablation of the vertebral bodies. These were done in serial at T11, T12, and L1 vertebral bodies for approximately 15 minutes for each level. Lastly, methylmethacrylate was injected into the vertebral bodies of T11, T12, and L1 (Figure ) for vertebral stability. No complications occurred during the surgery and the patient was discharged the same day.\nThe patient reported no pain at the three-week follow-up and he was able to ambulate without assistance and continued to increase daily activities. He also no longer required any pain medication. He continued to be pain-free at the eight-week follow-up and repeat MRI showed stable vertebral changes and complete resolution of epidural disease at the T12 and L1 level (Figure ). At nine-months post-op, the patient still had no pain and returned back to his normal activities.
After a 75-year-old male, who pursued gardening as a hobby, noticed decreased vision in his left eye, he visited an ophthalmologist in September of 2015. He had a history of hypertension, colon cancer and metastatic hepatic tumor. As an ophthalmologic examination revealed macular edema in his left retina resulting from branch retinal vein occlusion (BRVO), he underwent a posterior STTA injection in his left eye to treat the macular edema. After routine disinfection of the lid margins and conjunctival sac with 10% and 0.625% (16-fold dilution) povidone iodine, respectively, the procedure was performed uneventfully. The patient once again visited his ophthalmologist in November due to complaints of ocular pain and hyperemia in his left eye. The symptoms did not improve even though he received oral and topical antibiotic treatment for 3 days. Computed tomography of the orbit was performed and revealed a peribulbar high density lesion of the left eyeball. Due to a suspected peribulbar infection, he was subsequently referred to our hospital in the middle of November.\nAt his first visit, best corrected visual acuity (BCVA) (decimal) was 1.2 in the right eye and 0.15 in the left eye. Intraocular pressures were normal. Although the upper and lower eyelids of his left eye were swollen, we observed no restrictions of his eye movement. Slit lamp examination of the left eye showed ciliary injection, cells in the anterior chamber and a subtenon abscess in the superotemporal quadrant, which corresponded to the site of the posterior STTA (Fig. ). While our fundus examination did not reveal any intravitreal involvement, it did find macular edema and BRVO, which had been reported by his previous doctor. The right eye exhibited no abnormal findings, including both the anterior and posterior segments. The patient had no fever. The orbital magnetic resonance imaging (MRI) revealed the presence of a peribulbar high intensity lesion that corresponded to the subtenon abscess (Fig. ). The MRI did not detect any paranasal sinus or intracranial invasion. The serologic test, which included white blood cells, C-reactive protein and beta-D-glucan, only revealed a slight elevation of C-reactive protein (1.11 mg/dL). To determine the causative pathogen, incision and drainage of the subtenon abscess were performed, with the obtained purulent fluid submitted for bacterial and fungal cultures. While the smears revealed polymorphonuclear leukocytes and a large number of round or oval conidia-like structures, a fungal filamentous appearance was not observed (Fig. ). Based on these results, we suspected fungal infectious scleritis induced by STTA. Therefore, the patient was initially started on 1% voriconazole (VRCZ) and 1.5% levofloxacin (LVFX) eye drops that were each administered six times per day in an outpatient department. Inflammation of the anterior chamber of the left eye worsened after 4 days, with choroidal detachment observed in the temporal region of the fundus. The fungal culture found an early colony of a filamentous fungus. Based on the definitive diagnosis of infectious scleritis by filamentous fungi, we then performed debridement of the infected sclera and Tenon’s capsule. The resected scleral tissue was submitted for further pathological examination. The conjunctival sac of the left eye was irrigated with 0.625% povidone iodine, followed by hospitalization for treatments with 1% natamycin ointment, 1% atropine eye drops and intravenous VRCZ. Ten days after the initial visit, we noted improvement in both his ocular pain and inflammation of the anterior chamber. As a result, we switched the voriconazole from an intravenous to an oral administration. Histopathological examination using Grocott staining revealed infiltration of branching hyphae into the sclera (Fig. ). Due to a novel subtenon abscess of the adjacent upper region of the left eyeball that developed at 18 days after the initial visit, we once again performed scleral debridement. The fungal species, Scedosporium apiospermum, was identified by DNA sequencing of the internal transcribed spacer (ITS) region of ribosomal DNA amplified by polymerase chain reaction (PCR) with ITS1F and ITS1R primers []. The strain was sent to Teikyo University for complete species identification. The susceptibility testing of the antifungal agents was performed using the broth microdilution method based on CLSI M38-A2 []. Results indicated low minimum inhibitory concentrations against micafungin, VRCZ and miconazole (Table ). Based on the antifungal susceptibility test findings, the natamycin ointment was discontinued. Topical and systemic voriconazole administrations were continued for 2 and 1 months, respectively, and then stopped once the ciliary injection subsided. However, 1 month after the discontinuation of topical VRCZ, the subtenon abscess recurred at the same place (superotemporal quadrant). Incision and drainage of the abscess was performed three times. Light microscopic examination of the smears of the subtenon abscess revealed that septate hyphae were still present. As a result, we resumed the 1% VRCZ and 1.5% LVFX eye drops for 2 weeks and then stopped the administration. No recurrence was observed after the final treatment. Due to the prolonged macular edema, however, the final BCVA (decimal) of the left eye was 0.2 as of April 2016 (Fig. ).\nCharacteristics of the colonies found on the potato dextrose agar incubated at 28 °C for 21 days included a grayish white and cottony appearance with an umbonate center on the surface, and a reverse side showing a brownish dark wrinkle appearance in the center and a yellow-white appearance on the margin (Fig. ). Microscopic features observed when using the slide culture technique on potato dextrose agar at 10 days included septate hyphae that were 2 μm in diameter and branching irregularly, along with the production of lateral and terminal conidia, which were round or oval (3 to 5 by 5 to 10 μm) (Fig. ). We also observed a Graphium synanamorph that produced a brush of cylindrical conidia (3 by 12 μm) (Fig. ).\nIn order to confirm the species identification using a molecular approach, the BUT locus of the β tubulin gene was also amplified by PCR using Bt1a/Bt1b primers [, ] and then applied to DNA sequencing [, ]. The obtained DNA sequencing was compared by using the Basic Local Alignment Search Tool. Both the ITS and the BUT exhibited 100% homology with that reported by Zouhair et al. for Scedosporium apiospermum (GenBank accession no. JQ690950 and JQ691056) []. Based on the current and previous results, we were finally able to identify the causative fungal strain as Scedosporium apiospermum sensu stricto.
A 54-year-old Japanese woman presented to our hospital with a 10-month history of bilateral finger extension weakness and clumsiness. The chief complaint at her first visit was bilateral ulnar side numbness of her forearm and middle finger, ring finger, and little finger. There was atrophy of intrinsic muscles. She had no decline in her balance or ambulatory abilities. Magnetic resonance imaging (MRI) showed displacement of her cerebellar tonsils below the foramen magnum level, with syringomyelia presenting from the C4 to T8 level (Fig. ). A surgical procedure was planned due to the progressiveness of her neurological conditions.\nSuboccipital craniectomy and C1 laminectomy with duraplasty were performed under general anesthesia. The craniotomy was 3 cm in size and rectangular. After opening the dura in a Y-shaped fashion, a pinhole unexpectedly opened in the arachnoid membrane. The dural graft used an absorbable artificial dural substitute (Seamdura, Gunze Limited Medical Division, Tokyo, Japan), which was carefully sewn into place using a running 5-0 nylon suture. After placement of an absorbable suture reinforcement felt sheet made of polyglycolic acid (Neoveil, Gunze Limited) for use as an absorbable artificial dural substitute interface, the surface was covered by fibrin glue. The total operative time was 3 hours 27 minutes, and there was little estimated blood loss.\nPostoperative bleeding was 80 ml while under a zero vacuum pressure drain, which was removed at 2 days after surgery. Although our patient exhibited no new neurological deficits, she had a prolonged headache. At the time of her release at 1 month after the operation, she still had a slight headache. At 1 month after discharge, she again presented to our hospital due to severe headache and nausea. On examination, her wound was well healed and there was no evidence of CSF leakage or infection. There were also no cranial neurological symptoms observed. MRI of her cervical spine showed pseudomeningocele compressing her cerebellum and spinal cord. MRI of her brain also showed ventriculomegaly (Fig. ). Pseudomeningocele aspiration with a 22-gauge hypodermic needle was performed, with 25 ml of fluid removed under X-ray control (Fig. ). Immediately after aspiration, her headache and nausea decreased, and she was subsequently discharged at 3 weeks after aspiration. At 4 months after the operation, cervical spine MRI showed shrinkage of spinal syringomyelia and resolution of the stenosis at the level of the cerebellar tonsils (Fig. ), although the pseudomeningocele remained. At her 1-year follow-up, she reported improvement in her symptoms with increasing bilateral finger extension strength and decreasing bilateral upper extremity numbness.\nInstitutional Review Board approval was obtained for this case report, and our patient gave written informed consent to publish this case and any accompanying images.
A 53-year-old man presented with a gradually increasing mass located in the soft tissue of the oral cavity. The lesion was biopsied, and the pathology report showed increased infiltration of the buccal mucosa with monoclonal plasma cells. Immunochemistry demonstrated positivity for CD138, CIgA, and negativity for CD56, Cyclin D1 and CD20. Therefore, the diagnosis of soft tissue plasmacytoma was confirmed, for which he received localized radiotherapy with a total dose of 40 Gy, due to the absence of systemic disease as the bone marrow biopsy revealed the absence of neoplastic infiltration and serum and urine immunofixation were all negative.\nAfter five years, the patient noticed a painless swelling in his right testis. An ultrasound of the scrotum was performed that showed a hypoechoic mass in the right testicle with increased vascularization, and a normal-appearing left testis (Figure ). The patient subsequently underwent a right radical orchiectomy and the histopathology report showed testicular infiltration by a plasma cell neoplasm with identical immunophenotype (CD138+, CIgA+, CD56-, CD20-, Cyclin D1-) to the primary site in the oral cavity. Subsequently, the patient underwent a bone marrow biopsy that showed the absence of monoclonal plasma cell infiltration, and a PET/CT scan that was negative for reactive lesions suspicious of malignancy. In addition, serum and urine protein electrophoresis, as well as serum-free light chain assay were all within normal range, thus, excluding the presence of systemic disease, while complete blood count and full biochemical profile were normal.\nHowever, after one year, the patient presented again with painless swelling of his left testis that was attributed to disease relapse based on the imaging findings (Figure ). He refused to undergo left orchiectomy, thus he proceeded with systemic treatment based on lenalidomide, bortezomib and dexamethasone. Following 4 cycles of treatment, the patient underwent high dose melphalan with autologous stem cell transplantation. The blood tests of the patient revealed an increase in serum creatinine (1.3 mg/dl with 1mg/dl baseline level), normal calcium levels and normal complete blood count. Complete response was achieved with negative PET/CT scan and negative marrow minimal residual disease assessment. The patient continued on lenalidomide maintenance; however, six months later he was diagnosed with disease relapse in his left testicle (Figure ). A PET/CT scan was then performed, and showed a reactive lesion with an increased SUV max of 7 in the left testis, with no other loci suspicious of disease relapse. The blood analysis of the patient revealed no abnormal values. Since the patient refused surgery, he was initiated with next-line therapy, with bortezomib, cyclophosphamide and dexamethasone, he responded partially and still remains in remission (Figure ), while serum protein electrophoresis, immunofixation and serum-free light chain assay, all remain within normal levels.
A 23-year-old man sought emergency care complaining of a 2-month history of a burning mesogastric pain irradiating to the lumbar region that worsened on the palpation of the right flank. On the tenth postoperative day of an elective right inguinal hernioplasty, an abdominal pulsatile mass was detected. The hernioplasty was indicated before the abdominal symptoms started and preoperative lab work-up did not reveal abnormalities such as leukocytosis. The patient was advised to proceed with further investigation, but he refused.\nDue to the worsening of his abdominal pain, he sought medical assistance in a hospital emergency department on the 10th post-operative day. On admission, the physical examination revealed a well-looking patient, slightly pale with normal vital signs, emaciated (the patient mentioned a weight loss of 10 kg over the past 2 months), and was afebrile. The abdominal palpation depicted a painful pulsatile mass in the mesogastrium, and on auscultation there was a bruit in the same region. No signs of peritoneal irritation were found. The patient denied drug addiction and did not recall any infections over recent months. The search for Koch's bacillus in sputum and urine was negative, and the patient's epidemiology was not conducive to tuberculosis. VDRL and ELISA tests were negative and excluded syphilis and HIV infection, respectively.\nThe aortic angiogram computed tomography (CT) revealed an infrarenal aortic saccular aneurysm measuring 6.7 × 5.2 cm ().\nThe aneurysm presented irregular contours and ulcerations, and was surrounded in its entire extension by an irregular dense tissue with fat tissue obliteration (). The aneurysm anteriorly displaced the duodenum and laterally the inferior vena cava and the iliac veins (). The CT findings were consistent with a mycotic aneurysm (MA). The patient was hospitalized and submitted to an endovascular treatment which consisted of the implantation of an aorto-bi-iliac endovascular stent associated with long-lasting empiric antibiotic therapy, which comprised oxacillin and ceftriaxone. A blood culture was sampled before the procedure, but the result was negative. An abdominal CT was undertaken and the patient was discharged clinically well and afebrile, four days after the procedure.\nOver the next 3 months, the patient was hospitalized two more times. At each admission, he was in poor clinical condition, febrile, and presented abdominal pain. He was prescribed vancomycin, meropenem, and micafungin. Blood cultures were repeatedly negative (including anaerobic cultures) and continuing transthoracic and transesophageal echocardiograms were normal.\nDuring his third hospitalization, the patient received 35 days of antimicrobial therapy, ran out of fever and refused to remain longer in the hospital. After 2 months he returned to the emergency facility complaining of severe and diffuse abdominal pain followed by upper digestive hemorrhage and hypovolemic shock. The abdominal CT revealed the presence of thrombi throughout the entire aorta and gaseous foci within the endoprosthesis indicating the presence of an aortoenteric fistula (). Unfortunately, the patient died 1 day after hospital admission. An autopsy was performed with an informed consent signed by the family.
A 51-year-old Greek male patient was admitted to our clinic, referring to intense headaches and hip pain lasting for 12 hours. His medical history was significant for an episode of incomplete cauda equina syndrome of unknown etiology, with additional corrosion of the sacrum, dura mater disruption, and cerebrospinal fluid leak. This resulted in a productive sinus ending posteriorly to the right greater trochanter nine years ago. After that, he was treated with a lumboperitoneal valve implantation, but two years later, he developed a soft tissue infection at the sinus outfall. The radiological evaluation revealed multiple abscesses of the lower lumbar spine and the S1-S2 vertebrae. The physicians performed a superficial surgical debridement of the soft tissue around the buttock without bony intervention. Despite being an ineffective treatment option, the reason for not proceeding with bone lesion debridement remains unclear. In those cultures, Staphylococcus aureus was isolated. Interestingly, at that time, specific cultures for Salmonella spp were negative. We suppose that the doctors tried to connect the infection recurrence with specific bacteria causing sacroiliitis, like Salmonella spp. However, no tests for brucellosis were found in the patient’s medical report at that period. Oral medication with moxifloxacin did not manage to control the infection in the long term, with the patient having multiple surgical soft tissue debridements in the past. Meanwhile, no episodes of meningitis were noticed.\nThe patient also reported the last hospital visit six months before his current admission with exacerbating hip pain and excessive sinus fluid production. The right hip joint was typical on plain roentgenography, with multiple sclerotic and osteolytic lesions noted on the right sacroiliac joint (Figure ).\nThe magnetic resonance imaging (MRI) with intravenous contrast agent (gadoteric acid) revealed multiple osteolytic lesions of the right sacroiliac joint and the L4 vertebra (Figure ).\nEvaluating the former MRI imaging from the patient's medical file, the epidural sinus was notably expanded around the right hip joint affecting the piriformis muscle belly and tendon, and finally communicating with the joint capsule (Figures , , )\nDespite the alteration of the imaging findings, the patient was treated conservatively with blinded intravenous administration of ciprofloxacin and clindamycin and oral celecoxib. This conservative treatment scheme six months ago managed to improve his symptoms until today.\nOn our clinical examination, a posterior thigh scar and a sinus just posteriorly to the greater trochanter were noted.\nLumbar spine range of motion (ROM), leg muscle strength, reflexes, and sensation of both limbs were normal. The patient had significant gait difficulty with intolerable weight-bearing, a positive Trendelenburg sign on the right hip, and a painful log-roll test. Hip flexion was relatively comfortable at 20°, extension 10°, and abduction/adduction of 20°. At that time, the sacroiliac joint's clinical evaluation was misleading as the FABER test could not be performed, and distraction/compression tests were controversial.\nOn our radiological evaluation, brain computed tomography (CT) was standard, while anterior hip soft tissue ultrasound revealed a newly formed cavity communicating with the regional sinus. The CT of the lumbar spine and hip confirmed the former findings revealing additional intramuscular multiple abscesses of the psoas (Figures , )\nCerebrospinal fluid (colorless, glucose=60-80% of serum glucose, lactate dehydrogenase (LDH)=10% of serum LDH) and abscess fluid cultures were negative for common bacteria, where no fungal cultures were obtained. Due to radiological imaging characteristics with multiple abscess cavities affecting non-continuous vertebras, in addition to the sacroiliac joint and psoas involvement and culture-negative abscesses, chronic brucellosis was highly suspected. The serum agglutination test (SAT-Wright) was positive, with an SAT titer of 320 (>1/160, prozone phenomenon). We thereafter proposed a surgical debridement and lumboperitoneal valve removal, but the patient denied any further operation. By rejecting every surgical recommendation, we could not obtain different cultures but from the local sinus, which were positive for Staphylococcus aureus and Streptococcus mutans and negative for Brucella species, results that are indicative for sinus contamination. Thus, we proceeded with oral administration of doxycycline (200 mg/day), ciprofloxacin (800 mg/day), and rifampicin (900 mg/day). Additional administration of celecoxib (200 mg/day) was prescribed. The patient was discharged with instructions for tactical follow-up for clinical examination and inflammatory markers (white blood cells [WBC], erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) evaluation. After six months of antibiotics administration, his blood laboratory markers remained slightly high with ESR=30 mm/1st h, WBC=12300/uL, and CRP=3,3 mg/dl, but the patient is asymptomatic regarding pain and reports unimportant gait abnormalities. Although the indices remained borderline, the antibiotic scheme reached a maximum duration of six months. Our infectious disease specialist consultation proposed against treatment continuation, under the high possibility of side effects due to the prolonged treatment period. In addition, the patient was informed that in case of a major relapse, radical debridement would be unavoidable. Eventually, subsequent MRI on six-month evaluation revealed improved sinuses tract imaging (Figures , ).\nNonetheless, they remainclinically productive with a fluid quantity of less than 10ml/day. To date, 14 months after the final admission, the patient has no prominent sinus, while the laboratory examination, including ESR and CRP, is regular. He reports significant pain control and gait improvement, and spine and pelvic roentgenography do not show notable alterations. He is instructed for periodic blood test evaluation and is strongly advised to proceed to radical surgical debridement in future disease relapse.\nThe authors have obtained informed consent about data publication, including photographs, clinical history, and radiological images.
A 45 year old male presented to us with complaints of redness, discharge and foreign body sensation in his right eye since one month. He had undergone a scleral buckling procedure elsewhere 14 years back of which he had no records. There was no visual gain post-operatively. He had no history of trauma and is a healthy patient without any systemic diseases. On examination, he had no perception of light in the right eye. Mucopurulent discharge was present and conjunctival congestion was noted. A circumferentially placed and anteriorly displaced exposed solid scleral buckle explant was noted with black coloured deposit over the buckle in the superior quadrant (Fig. (), ()). Anterior chamber was deep and quiet and lens was clear. Fundus examination revealed a visible buckle indentation superiorly and an inferior retinal detachment with disc pallor. No visible inflammatory reaction was noted internally. The left eye had a best corrected visual acuity of 6/6, N6 with a normal anterior segment and fundus picture. A diagnosis of exposed and anteriorly displaced infected scleral buckle was made. Removal of the infected buckle was planned. The conjunctiva was dissected and the buckle along with sutures was removed and sent for microbiological evaluation. The eye was cleared of the necrotic debris and discharge. A thorough subconjunctival wash was done with antibiotic (gentamycin) and antifungal agents (voriconazole) and the conjunctival peritomy was closed. The patient was started on empirical treatment with oral ciprofloxacin 750 mg twice a day, oral fluconazone 150 mg twice a day, eye drop moxifloxacin hourly, eye drop voriconazole hourly, eye drop atropine 3 times a day and eye drop carboxymethylcelluose 0.5% 6 times a day in the right eye. Both blood agar and Sabouraud’s dextrose agar grew blackish colonies with irregular boundaries. On microbiological evaluation of the growth, pigmented hyphae were noted along with the presence of conidiophores and conidia and a diagnosis of Curvularia species was made (Fig. ). The patient received oral ciprofloxacin for one week and fluconazole for three weeks. The patient was followed up closely and at 1 month after buckle removal he had no conjunctival congestion, the superotemporal sclera appeared thinned out (Fig. (), ()). Topical medications were stopped. We presume that the inferior retinal detachment was exudative in nature as on subsequent follow-up at 2 months it was seen to have settled and no break was found.
The patient is a 28-year-old male with prior history of a grade 3 astrocytoma, who presented to our emergency department (ED) after having a general tonic-clonic seizure (GTC). Initially, his disease was appreciated four years prior when he presented with a GTC and was found to have a grade 3 astrocytoma of the left occipital lobe (Figure ). He underwent maximal safe resection followed by adjuvant EBRT to 45 Gy in 25 fractions at an outside institution. Due to reasons outside the patient’s control, he received only two cycles of adjuvant temozolomide following EBRT. He developed disease recurrence, presenting as a GTC six months prior to this ED presentation, where imaging demonstrated tumor progression with increased extension into the parietal lobe (Figure ). He subsequently underwent a second maximal safe resection later that month. Final pathology returned as GB. Follow-up imaging four months afterward demonstrated disease progression and he was started on bevacizumab as well as a tumor treatment field (TTF) device. He unfortunately only tolerated TTFs for one month, ending one month prior to the ED presentation.\nUpon admission to our hospital from the ED, MRI demonstrated progression of disease in the left occipital-parietal lobes with extension into the splenium and anterior-inferior extension into the left thalamus and basal ganglia (Figure ). His physical exam was notable for mild right-hand weakness, but he was otherwise neurologically intact. Despite changes to his antiepileptic medication, he had seizure recurrence a few weeks following admission. Presuming that the area of tumor recurrence received a definitive dose in the past, the consensus decision was to proceed with repeat maximal safe resection with GammaTile placement. A dose of 60 Gy was prescribed to a 5 mm depth using a total of eight tiles, each containing four Cesium-131 3.5U seeds, to line the post-operative cavity volume of 17.6 cc. A significant portion of the occipital-parietal disease was debulked, with final pathology again demonstrating a grade 4 astrocytoma with molecular studies indicating an IDH-mutated, ATRX mutated, and MGMT promoter methylated phenotype with hypermutation. Postoperatively he was noted to have right upper and lower extremity weakness/spasticity with right foot drop and mild right face weakness. He required a cane to assist with ambulation and reported word-finding difficulties and decreased short-term memory. He was planning to start adjuvant temozolomide; however, he developed a severe GTC with increased muscle weakness and altered mental status two months later. MRI following this episode demonstrated mildly increased enhancement to the tissue surrounding the surgical bed with the progression of disease in the splenium and left thalamus/basal ganglia (Figure ).\nGiven this symptomatic disease progression, a treatment plan was made to take the progressive regions of disease outside the irradiated GammaTile volume to 35 Gy in 10 fractions. As shown in Figure , an initial planning target volume (PTV) was delineated consisting of the T1 post-contrast-enhancing disease with a 5 mm margin. The volume that received greater than 35 Gy from the GammaTile treatment was excluded from the PTV. The PTV was then separated into two portions by subdividing the remaining volume between tissue that received less than 17.5 Gy (PTV1), and that which received 17.5-35 Gy (PTV2). Using a volumetric modulated arc therapy plan with five arcs, one non-co-planar, a homogeneous dose of 35 Gy in 10 fractions was delivered to PTV1. This dose was calculated to have a biologically equivalent dose in 2 Gy fractions (EQD2) of 45 Gy. Dose painting gradually decreased the dose from 35 Gy to as low a dose as achievable approaching the resection bed border of PTV2 (Figure ). A composite of the GammaTile dose volume (Figure ) with a dose delivered from PTV1 and PTV2 resulted in a homogeneous dose of approximately 50 Gy EQD2 to the residual disease extending into the splenium and the left thalamus/basal ganglia (Figure ). Digital imaging and communications in medicine (DICOM)-RT data from the initial 45 Gy delivered from the outside institution were obtained, and cumulative dose to critical organs at risk (OARs), including the brainstem, ocular structures, and cochlea, were within established constraints.\nDue to the hypermutation phenotype of his tumor, the patient was started on CCNU (100 mg/m2) and completed his EBRT with no issue or progression of his current neurological symptoms. He was last seen in follow-up by our team three months after his most recent EBRT, at which point he reported significant improvement in the right leg tremors/spasms and improved headache. He demonstrated decreased right foot drop but continued to have word-finding difficulties and short-term memory deficits. He has not developed any new areas of muscle weakness or paresthesia, visual loss, or other forms of altered sensoria. The current plan is to complete six cycles of CCNU with alternative systemic therapy thereafter upon disease progression. While temozolomide could be used to this effect, the high mutational burden found in his most recently resected disease would permit entry into currently available trials of immunotherapy.
A 40-year-old, North African man working as a plumber came presenting with diffuse hair loss for 4 months. It started by the falling of the beard, followed by scalp hair () then progressed to loss of pubic hair and the extremities. Finally, it was followed by the loss of eyebrows (). He also reported nail changes in the form of discoloration and nail dystrophy affecting fingers and toenails (). On questioning, the patient admitted intermittent diarrhea of 6 years duration, which in the last 4 months reached a frequency of 6 motions per day. The attacks of watery diarrhea lasted for 2 days and were characterized by tenesmus, not associated with hematochezia, pus, or worms. Stool analysis was insignificant. The patient denied the intake of any drugs known to cause hair loss or receiving treatment for any other medical conditions except for over-the-counter anti-diarrheal medications. His history was significant for surgery for hemorrhoids. He had a 30 pack-year history of smoking. He was married and had two offspring. His sister was diagnosed as having Behcet’s disease. Possibly related to his condition, he reported low back pain associated with limitation of movement and inability to walk with stiffness increased by rest and decreased by movement. This pain was relieved by non-steroidal anti-inflammatory drugs (NSAIDs) and well tolerated by the patient. On physical examination he was of average built with generalized alopecia with sparse grey hair on his scalp and his genitals associated with dystrophy of all nails. System review was unremarkable for any other abnormality. Total colonoscopy with ileoscopy was done and multiple biopsy samples were taken from the terminal ileum and rectum. The histopathological examination confirmed a picture of UC with mild to moderate activity (). Capilloroscopy revealed scanty capillaries and veiling of the capillary nail bed. His laboratory examination was remarkable for elevated ESR. The virology screening included Epstein Barr virus (EBV) and Cytomegalovirus (CMV) was negative. Anticardiolipin IgM, anti-nuclear (ANA), anti-dsDNA, and anti-neutrophil cytoplasmic antibodies were negative. The micronutrient levels including iron and zinc were assessed to exclude nutritional causes of hair loss. The patient received the following regimen; Azathioprine 2mg/kg/day, prednisone 40 mg/day, mesalamine 500mg/8hrs with good compliance. On follow-up, there is improvement in the bowel condition as well as observed re-growth of scalp, beard, and other body hair.
In January 2021, a 2-year-old boy of white Caucasian origin presented to his local ophthalmologist for acute unilateral sixth nerve palsy and was subsequently transferred to our pediatric emergency department for further evaluation. The patient, generally being fit and well, had developed a sudden dysfunction in lateral movement of his left eye, resulting in a continuous abduction deficit with consecutive fixated turn of the head to the left side. His medical history was unremarkable for trauma, headache, vomiting or fever. He had not received any vaccinations within the last few weeks. Apart from a mild gait instability, there were no concomitant symptoms or other focal neurological deficits on clinical examination. The patient did not suffer from any chronic diseases and did not take any regular medication; his vaccination status was complete according to national recommendations.\nThree weeks prior to onset of symptoms the patient had experienced a respiratory tract infection resulting in an increased respiratory rate, dry cough, intermittent fever and loss of appetite, lasting for 2 weeks. Symptomatic treatment was initiated by his local pediatrician, who attributed the patient's symptoms to a common cold rather than COVID-19. Thus, no oropharyngeal swab for SARS-CoV-2 or other viruses was obtained. At the same time, the patient's father and his uncle developed cough, dyspnea, sore throat and muscle aches; the uncle tested positive for SARS-CoV-2 on PCR from oropharyngeal swab (). The child's uncle does not live in the same household but had been in close contact to the patient 4 days prior to his positive test for several hours due to an indoor-birthday party. The patient's relatives were unvaccinated as at that time the COVID-19 vaccines were still unavailable for the general public.\nOn admission, laboratory inflammatory markers including C-reactive protein were negative. Full blood count showed mild thrombocytopenia (186 109/) but was unremarkable otherwise. Cranial contrast-enhanced magnetic resonance imaging (MRI) showed an hypoplastic left abducens nerve and atrophy of the corresponding left lateral rectus muscle compared to the contralateral side (). There were no signs suggesting any inflammatory intracranial process or elevated intracranial pressure, no papilledema. A lumbar puncture was performed. The cerebrospinal fluid (CSF) opening pressure was 24 cmH2O corresponding to the upper limit of normal range () thus diagnostic lumbar puncture was followed by therapeutic drainage of 8 ml CSF. Routine CSF laboratory parameters yielded a normal result; no oligoclonal bands were detected on CSF/serum. Multiplex-PCR (Filmarray, BioFire, Biomerieux Lyon, France) from CSF was negative for cytomegalovirus (CMV), enterovirus, herpes simplex viruses 1 and 2, human herpesvirus 6, human parechovirus, varicella zoster virus, Cryptococcus neoformans and gattii, E. coli K1, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitides as well as Streptococcus agalactiae and pneumoniae. An additional multiplex-PCR performed on an oropharyngeal swab sample yielded a negative result for adenovirus, coronaviruses 229E, HKU1, NL63 and OC43, human metapneumovirus, human rhino-/ enterovirus, influenza virus A and B, Middle East Respiratory Syndrome Coronavirus (MERS-CoV), SARS-CoV-2, parainfluenza virus 1–4, respiratory syncytial virus, Bordetella pertussis, Bordetella parapertusssis, Chlamydophila pneumonia and Mycoplasma pneumoniae. Testing for Borrelia burgdorferi showed no antibodies in neither serum nor CSF. An EEG was unremarkable. Repeated ophthalmologic examinations revealed incomitant squint angles due to left-sided sixth nerve palsy and a significant abduction deficit of the left eye, consistent with the diagnosis of left abducens nerve palsy. An underlying retraction syndrome was considered unlikely due to the sudden onset of symptoms and absent globe retraction. Optic nerve examination was unremarkable.\nReal-time reverse transcriptase PCR (rRT-PCR) test for SARS-CoV-2 (oropharyngeal swab sample) was negative on admission, while serology turned out to be positive for SARS-CoV-2 anti-spike IgG (Euroimmune, Germany). Of particular note in this context, SARS-CoV-2 specific IgG was also detected in CSF. Pathogen-specific antibody index as an indicator for potential intrathecal antibody production was negative, suggesting involvement of central nervous system being secondary to systemic infection rather than direct viral infection (). An rRT-PCR for SARS-CoV-2 from CSF was negative.\nGiven the boy's history of recent respiratory tract infection, COVID-19 very likely in his father and proven in his uncle, and detection of SARS-CoV-2-IgG antibodies in the patient's serum and CSF, post-infectious abducens nerve palsy appeared to be the most likely diagnosis. During inpatient stay, symptoms already showed spontaneous mild improvement without therapeutic measures. Following discharge, the boy was regularly seen for ophthalmologic follow-ups. Three months following onset of abducens nerve palsy, the family noticed a distinct improvement in eye movement and the child eventually made a full recovery 2 weeks later.
A healthy looking, 50-year-old Nepali man came to our clinic with a complaint of multiple growths on his scrotum for 15 years. The growths started as a single lesion on the right side of his scrotum, with the gradual appearance of similar lesions on other parts. Several of these lesions coalesced at various places to form large-sized nodules. The condition was mostly asymptomatic with an occasional complaint of itching. There was no history of pain, burning sensation, trauma, ulceration, or discharge. The lesions did not interfere with urination or sexual activities. He was worried because of the increasing size of the growth and hence came to us for advice. He did not give a history of any systemic illness including metabolic, autoimmune, or malignant disorders. There was also no history of a similar complaint in his family.\nOn physical examination, multiple pink to brown nodules ranging in size from 0.5 × 0.5 × 0.5 cm to 3 × 3 × 1 cm involving almost half of his scrotum were noticed (Fig. ). The skin over the nodules was shiny with several yellowish points indicative of underlying calcium deposition. The skin surrounding the nodules, testis, and penis was normal on palpation. The nodules were painless and firm in consistency. On laboratory examinations the following were found to be within normal limits: serum calcium, phosphorus, parathyroid hormone, and vitamin D hormone levels; uric acid; alkaline phosphatase; and lipid profile. Based on clinical features and laboratory reports, a diagnosis of ICCS was made.\nHe was advised a scrotectomy under spinal anesthesia, which he refused. The nodules were excised under local anesthesia in several sittings. The skin was sutured using chromic catgut (4–0). His postoperative period was unremarkable with good cosmetic result and no evidence of recurrence in a 1-year follow-up period. The cut section of nodules showed solid white to yellow homogenous areas. Histopathological examination revealed skin tissue lined by keratinized stratified squamous epithelium. The underlying dermis had areas of fibrosis and calcification (Fig. ). Numerous multinucleated giant cells were also seen (Fig. a and b). An obvious cystic structure was absent.
A 51-year-old woman presented with fatigue, nausea, and vomiting for three days. She was diagnosed with metastatic melanoma to pelvic nodes in July 2014 and was treated with ipilimumab (anti-CTLA-4) in combination with nivolumab (PD-1 inhibitor) between September 2014 and April 2015, receiving a total of 4 cycles of combination therapy and 9 cycles of nivolumab monotherapy with an initial mixed response followed by slow progression of disease. In April 2015 she was enrolled on a study of radiation (to pelvic mass) in combination with pembrolizumab (PD-1 inhibitor), receiving a total of 9 cycles of pembrolizumab with no toxicities. In December 2016 she was found to have new brain metastases and in January 2017 pembrolizumab was added. The day following her second dose of pembrolizumab, she developed fatigue and nausea and began having intermittent vomiting and diarrhea. Abdominal CT scan demonstrated diffuse colitis. Infectious studies including C. difficile antigen, stool culture, viral PCR, and ova and parasites exam were all negative. She was started on methylprednisolone 2m/kg/day. Over four days of hospitalization, her abdominal pain worsened and she developed melena, which progressed to bright red blood per rectum. She was given infliximab at 10mg/kg. Repeat imaging performed 48 hours later due to severe abdominal distension showed large amounts of free air with gaseous distention of large and small bowel loops, consistent with perforation in the context of colitis with ileus. She was taken to the operating room for emergent bowel resection and a perforation site was identified at the transverse colon. The resected transverse colon serosa was congested and dusky with site of perforation identified (). The colonic mucosa revealed diffusely edematous folds as well as confluent areas of yellowish exudate and multifocal ulcers (). Histologic sections confirmed the presence of transmural necroinflammation and multifocal ulceration (Figures and ). The findings were of a fulminant colitis with multifocal ulceration and perforation. No evidence of metastatic melanoma to the bowel was identified.
A 69-year-old male was admitted because of a continually worsening abdominal cramping pain, which had started two days before his admission. The pain was radiating to his back and it was associated with nausea and appetite loss. The patient had previously undergone a total gastrectomy for advanced gastric cancer two years earlier.\nThereafter, peritoneal relapse occurred and chemotherapy with paclitaxel and S-1 was administered by the outpatient department for six months with uneventfully. At admission, he was fully alert and his vital signs were normal, although he had mild grade fever (37.5°C). On examination, his abdomen was soft and flat with abdominal tenderness at the epigastrium, with diminished bowel sounds. Biochemical results and coagulation studies were within the normal limits. However, his symptoms were getting worse and opioid titillation was thus initiated. He underwent abdominal ultrasonography (US), which showed evidence of thrombosis or tumor thrombosis in the portal vein. A contrast-enhanced CT scan showed evidence of superior mesenteric venous thrombosis associated with thrombosis of the portal vein without cavernous formation(Figure ). There was no thrombosis in the splenic vein (Figure ). The dehydration was corrected by the fluid therapy. Anticoagulant therapy was started, because the thrombosis had formed recently and the risk of bleeding was low. The patient was given low-molecular-weight heparin (Dalteparin sodium, Fragmin) at a dosage of 10,000 U per day. Three days after the administration of heparin, he had a complete recovery from abdominal pain without opioid use and was thus able to start eating. He was discharged after 14 days of admission with a shift of the anticoagulant therapy to warfarin with a targeted international normalized ratio (PT-INR) of 1.5-2.0. Three months later, he was doing well and the thrombosis of the superior mesenteric vein and portal vein had completely disappeared on a follow-up CT. Six months later, he died from gastric cancer and the autopsy showed no thrombosis in the superior mesenteric vein and portal vein.
A 15 year old middle eastern female patient from Gaza strip with free past medical and allergic history who was admitted at our internal medicine department on July 20. 2016. At time of admission, she had intermittent high grade fever and sore throat for 1 week duration. Additionally, a non-itchy skin eruption was noticed for 2 weeks duration. As well as she started to have yellowish eye discoloration 5 days after the onset of fever. The patient was taking phenytoin 200 mg QD PO as a seizure prophylaxis since she had significant head trauma 4 weeks prior to her presentation.\nShe denied any history of red eye, digital swelling, seizures, photophobia or any weight changes. Family history was unremarkable. She was sexually inactive and started to have irregular menstruation 1 year before the time of admission. In addition to phenytoin, her only medication at the time of admission was acetaminophen 500 mg twice daily.\nOn physical examination, she was alert, oriented and conscious. Her hemodynamics were stable. Temperature 39.9 C and her tonsils were erythematous. Generally, she looked deeply jaundiced as well as fatigued. Systemic examination was normal except maculopapular rash on her limbs, abdomen, chest and back (Figs. , ) besides peeling on both palms (Figs. , ). On abdominal examination, the spleen was palpable 2 cm below costal margin and her liver was palpable and tender as well. She also had left axillary and inguinal lymphadenopathy around 1 × 1 cm in diameter each.\nAbdominal ultrasound was done and showed moderate hepatosplenomegaly, in addition to that, there was enlarged retroperitoneal, portahepatis and mesenteric lymph nodes. She also underwent brain MRI which did not show any intracranial pathology. Liver Doppler and cardiac echocardiography were both normal. Chest x-ray and EKG were normal as well. Laboratory work up was summarized in Table .\nBeside AHS, autoimmune hepatitis and infectious mononucleosis were suspected at that time. Phenytoin was stopped as well as acetaminophen due to elevated liver enzymes. The patient was given IV hydrocortisone. Over 10 days of admission, her condition significantly improved then she was sent home. The patient was seen 1 month after her discharge, at that time, the fever was gone, the rash was resolved and her liver enzymes were normalized.
Our patient is a 49-year-old male with a history of high-grade T1 urothelial cell carcinoma of the bladder who underwent induction Bacillus Calmette–Guerin (BCG) immunotherapy, and repeat biopsies of the bladder which were negative. Surveillance with a computed tomography (CT) urogram demonstrated a suspicious nodular focus along the right lateral wall of the bladder. Subsequent two office cystoscopies demonstrated no evidence of tumor recurrence or abnormalities. The patient, however, later underwent partial cystectomy 2 months later where the pathology was negative for malignancy. Repeat bladder biopsies 8 months after surgery revealed urothelial CIS. The patient elected to undergo a second induction course of BCG. After completing 4 of the 6 treatments, the patient developed low-grade fever/chills and low back pain and was seen in the emergency department. Contrast-enhanced CT (CECT) scan of the abdomen which was performed as part of the workup showed a roughly 2 cm mass-like area in the lower pole of the right kidney with moderate perinephric inflammatory changes [Figures and ]. Smaller subcentimeter ill-defined hypodense foci were also seen. A primary renal mass was suspected, and a repeat CECT scan performed 3 weeks later demonstrated a persistent mass-like hypodense lesion in the right kidney with significantly improved perinephric inflammatory changes [Figures and ]. The differential included infection or inflammation. Primary renal malignancies such as renal cell carcinoma and urothelial cell carcinoma and infiltrative masses such as lymphoma continued to be the main suspicions, and a CT-guided biopsy was recommended for histological confirmation []. Histopathology confirmed marked chronic inflammation and necrotizing granulomas without evidence for malignancy []. The primary clinical team decided to manage the patient conservatively with close follow-up due to resolution of the symptoms. Although antituberculous therapies are instituted in some cases, there continues to be a lack of consensus regarding appropriate management of renal granulomatosis. The patient then finished his fifth instillation of BCG. Eight months later, a CECT scan showed interval resolution of the right renal lesions with mild residual cortical scarring [Figures and ]. On repeat cystoscopy and biopsy 8 months later, the patient was noted to have recurrent non-invasive high-grade papillary urothelial cell carcinoma. The patient has since had a radical cystectomy with ileal conduit urinary diversion.
A 26-year-old man presented with complaints of blurred vision in his right eye of 1-week duration following blunt ocular trauma. He gave a history of injury sustained to the right side of the face near the cheek and right forehead 10 days before presentation. He was a pillion rider in the motorcycle and due to sudden break application; his face collided with a protruding log loaded in the vehicle which was moving in front of his motorbike. He had two lacerations one near the corner of right eyebrow near the forehead, and one on the skin over the right zygomatic region and they were sutured as first aid measure in local hospital after ruling out other faciomaxillary injuries by specialists there. He gave a history of swelling and inability to open his right eyelid for initial 3 days following injury and history of noticing defective vision in RE on the 4th day on opening the eyelid once the swelling subsided.\nOn examination, the uncorrected visual acuity (UCVA) in his right eye was 20/120 improving to 20/60 with +2DS/−2DC at 40° correction. K reading as measured by autokeratometer and refractometer did not show significant corneal astigmatism. The intraocular pressure in the right eye was 14 mmhg. Cornea showed few pigment deposits on the endothelium, and the rest of the layers were within normal limits. Anterior chamber (AC) was deep and showed cellular reaction of 1+ grade with few pigment dispersions. Lens showed a dense posterior subcapsular cataract [] with an oval defect in the posterior capsule which was confirmed with the help of an anterior segment optical coherence tomography (Visante, Carl Zeiss) []. Gonioscopy and detailed peripheral retinal examination with scleral indentation were done as it was a case of trauma and were within normal limits. Examination of the left eye was within normal limits, and the unaided visual acuity was 20/20.\nThe occupation of the patient, visual expectations, and motivation to remain spectacle free in the future were discussed and considered and after all the risks duly explained to him, the patient was taken up for cataract removal with extended focal length IOL implantation [] after control of inflammation and after waiting for a period of 4 weeks from the time of injury for better fibrosis of PCR edges so that fear of extension of PCR is lesser and In the bag IOL placement can be achieved after a good biometry. Axial length was measured by immersion biometry (24.07 mm) and optical biometry, and K reading was obtained from optical biometer (K1 41.77D/8.08 mm at 55°, K2 42.03D/8.03 mm at 145°, ACD 4.33 mm) and manual keratometer. IOL power calculation was done using SRK T formula, and the appropriate IOL power (SYMFONY +22.0 D) was selected for implantation. A superotemporal triplanar clear corneal incision measuring 2.8 mm was made using a keratome. The side port was made 2 clock hours anticlockwise from the main port, and the AC was entered. The anterior capsule was stained using trypan blue and a 5.5 mm continuous curvilinear capsulorhexis was made using a cystotome. The lens material was removed using high vacuum low flow rate when preexisting PC rupture was clearly viewed, viscoelastic, 2% hydroxypropyl methylcellulose was injected through the side port, and the irrigation-aspiration probe was removed from main port. A trocar AC maintainer was fixed in the AC. Trocar AC maintainer was not placed in the beginning on purpose as it could interfere with rhexis and if turned on, saline flow through it into AC could increase the hydrostatic pressure in AC which could cause further damage to the weak posterior capsule. It was placed as a measure to maintain AC when anterior vitrectomy was commenced. At 0.5 mm from the limbus, an obliquely angled sclerotomy incision was framed; after conjunctival displacement, the trocar was introduced at a 45° angle to the sclera, parallel to the limbus. The trocar was then turned 90° perpendicular to the limbus and directed toward the AC, so the trocar enters the AC in front of the iris tissue. The cannula was flushed to the surface of the sclera, and the trocar was withdrawn, leaving the cannula in place. The infusion line was then attached to the hub of the cannula, and the infusion turned on. The remaining cortex and lens material were removed after anterior vitrectomy using a vitrectomy cutter [].[] As the vitreous disturbance was minimal and the operating surgeon was sure of no residual vitreous in AC after vitrectomy by observing a round pupil and air bubble test in AC, intracameral triamcinolone injection was not done at the end of anterior vitrectomy.\nA single piece extended focal length IOL (Symfony IOL, AMO) was implanted in the bag and centered. Care was taken to place the haptic perpendicular to the PCR. After the removal of the AC maintainer, the main wound and the side port were closed with a single 10-0 nylon suture. The eye had minimal AC reaction and well-secured wound on postoperative day 1 and day 3, the sutures at the main and side port were removed under sterile aseptic precautions. On postoperative day 7, UCVA was 20/20, with near visual acuity of N8 and a well-centered IOL was in situ. The patient remained comfortable throughout the postoperative period. At 6 months of follow-up, the patient visual axis clarity was maintained, no IOL deposits were present which would hamper vision, no evidence of posterior synechiae formation was observed. On follow-up at 12 months, the patient was comfortable with all daily activities including driving with no significant glare or haloes, with normal binocular single vision, the unaided visual acuity was 20/20, and N8 [] and no IOL decentration [] or pseudophakodonesis.
A healthy looking, 50-year-old Nepali man came to our clinic with a complaint of multiple growths on his scrotum for 15 years. The growths started as a single lesion on the right side of his scrotum, with the gradual appearance of similar lesions on other parts. Several of these lesions coalesced at various places to form large-sized nodules. The condition was mostly asymptomatic with an occasional complaint of itching. There was no history of pain, burning sensation, trauma, ulceration, or discharge. The lesions did not interfere with urination or sexual activities. He was worried because of the increasing size of the growth and hence came to us for advice. He did not give a history of any systemic illness including metabolic, autoimmune, or malignant disorders. There was also no history of a similar complaint in his family.\nOn physical examination, multiple pink to brown nodules ranging in size from 0.5 × 0.5 × 0.5 cm to 3 × 3 × 1 cm involving almost half of his scrotum were noticed (Fig. ). The skin over the nodules was shiny with several yellowish points indicative of underlying calcium deposition. The skin surrounding the nodules, testis, and penis was normal on palpation. The nodules were painless and firm in consistency. On laboratory examinations the following were found to be within normal limits: serum calcium, phosphorus, parathyroid hormone, and vitamin D hormone levels; uric acid; alkaline phosphatase; and lipid profile. Based on clinical features and laboratory reports, a diagnosis of ICCS was made.\nHe was advised a scrotectomy under spinal anesthesia, which he refused. The nodules were excised under local anesthesia in several sittings. The skin was sutured using chromic catgut (4–0). His postoperative period was unremarkable with good cosmetic result and no evidence of recurrence in a 1-year follow-up period. The cut section of nodules showed solid white to yellow homogenous areas. Histopathological examination revealed skin tissue lined by keratinized stratified squamous epithelium. The underlying dermis had areas of fibrosis and calcification (Fig. ). Numerous multinucleated giant cells were also seen (Fig. a and b). An obvious cystic structure was absent.
This is a case of a 59-year-old morbidly obese female with situs inversus totalis who presented for a laparoscopic sleeve gastrectomy. Her BMI was 38 (height 4 ft 11.5 inches, weight 188.2 pounds), and she had a lifelong history of morbid obesity and obesity-related comorbidities, including obstructive sleep apnea requiring a continuous positive airway pressure machine, an elevated hemoglobin A1c (5.8) and a fasting blood glucose increasing her risk of developing diabetes mellitus, and degenerative joint disease which significantly impacted her ability to exercise. The main challenges she identified in losing weight involved eating carbohydrate rich foods, overeating during meals and limited activity due to musculoskeletal pain. The patient had made multiple attempts to lose weight through commercial dieting programs but had been unsuccessful. The patient also completed a six-month medically supervised diet through her primary care provider, which also included working closely with a bariatric registered dietician, following a strict diet of about 1800 calories/day and performing modified exercise, about 120 minutes/week. Despite these intense medical weight loss efforts, she was unable to maintain a healthy weight. The patient was motivated to try bariatric surgery after she witnessed the significant weight loss success her daughters had from this intervention. Her greatest hope from the bariatric surgery was to be healthier and to alleviate her obesity-related comorbidities.\nThe patient’s surgical history included cesarean section and evacuation of an ectopic pregnancy. She was a former smoker, quitting over 25 years ago, and has no other history of substance or alcohol use. Family history is positive for obesity, diabetes, hypertension, coronary artery disease and hypercholesterolemia. She did not take any medications, including supplements, except for Ibuprofen 800 mg 1–3/daily for musculoskeletal pain.\nThe patient underwent a comprehensive evaluation and treatment plan prior to the surgery including: psychiatric evaluation and clearance, nutritional consultation with a registered dietician, education about bariatric surgery and pre/post op expectations, routine preoperative labs, UGI, esophagogastroduodenoscopy (EGD), pulmonary function analysis, and a cardiovascular exam. Situs inversus totalis was confirmed with abdominal X-ray and CT, and echocardiogram. Pre-procedural evaluation with UGI revealed mild gastroesophageal reflux observed to the level of the distal one-third esophagus and small sliding-type hiatal hernia. EGD revealed normal esophagus and duodenum. Stomach biopsy was obtained for antral gastritis, and no helicobacter organism was identified. Abdominal ultrasound confirmed fatty liver disease. Pulmonary function analysis including spirometry, lung volumes and diffusion was normal. A pre-procedural cardiovascular exam was performed due to dextrocardia to exclude other structural cardiac abnormalities. 2-D echocardiography with M-mode demonstrated a left ventricular ejection fraction of 60%, no structural abnormalities in the aortic, pulmonic, tricuspid and mitral valve, or right and left atrium and ventricles. Color Doppler and continuous and pulse wave Doppler demonstrated mild pulmonic regurgitation and mild tricuspid regurgitation.\nThe patient discontinued the Ibuprofen more than one month before her surgery and began a low-calorie liquid diet two weeks prior to surgery. On the day of surgery, preoperative antibiotics, Cefazolin, were given within 60 minutes before the first incision. Prior to induction, the patient received 5000 units of heparin subcutaneously and sequential compression device (SCD) boots were placed for deep vein thrombosis (DVT) prophylaxis. No beta-blockers were administered. The patient was placed in the supine position and general anesthesia was induced. A Foley catheter was placed and the patient was supported with positioning devices including: arms on padded arm boards, gel pad under left axilla, footboard with gel pads, hover mat and a bariatric safety belt over patient’s thighs. The abdomen was then prepped and draped in the standard surgical fashion.\nA Veress needle was used in the right upper quadrant to access the abdomen and insufflation was created to 15 mmHg. Veress was removed and replaced with a 5 mm trocar and the scope was placed. Additional trocars were placed in the following position: right and left 5 mm lateral trocars, right and left 12 and 15 mm supra-umbilical trocars. The placement of all retractors and graspers was adjusted accordingly to the mirror image anatomy of the intraabdominal organs. The primary surgeon was positioned on the left side of the patient and the assisting surgeon on right side of the patient. Situs inversus totalis was confirmed with the majority of the liver oriented to the patient’s right, spleen on the right, greater curvature of the stomach on the right and gallbladder on the left.\nThe operating table was placed in the reverse Trendelenburg position. The patient’s right-sided half of the liver was retracted cephalically using a Nathanson retractor to expose the vicinity of the esophageal hiatus. The peritoneum over the cardia was incised using the Ethicon Harmonic scalpel, and the plane between the cardia and the left crus of the diaphragm was opened to expose the right diaphragmatic crus. No hiatal hernia was present. A point 5 cm proximal to the pylorus along the greater curvature of the stomach was marked corresponding to the incisura angularis just proximal to the crow’s foot of Latarjet’s nerve. The vessels along the greater curvature and all the short gastric vessels were sealed and divided using the Ethicon Harmonic scalpel, freeing the greater curvature and the fundus of the stomach. A 42-French bougie was placed and oriented towards the antrum along the lesser curvature (Figure ). The stomach was stapled and divided alongside the tube in a vertical fashion towards the angle of His (Figures -).\nAn Ethicon Echelon Flex triple staple line power stapler with a total of one black, three green, and one gold staple loads was used. All staple loads were 60 millimeters in length with staple line bio-absorbable reinforcement. Hemostasis at the external staple line was achieved (Figure ). The stomach was removed from the abdomen via the left-sided 15 mm trocar (Figures , ). Intraoperative endoscopy was performed using a 5 mm Olympus Ultrathin gastroscope revealing no areas of stenosis, internal staple line bleeding, nor staple malformation or leak seen. Total operation time was 108 minutes. There were no post-operative complications.\nPost-operative care included pain management and DVT prophylaxis with SCD, heparin and early ambulation four hours post-surgery. A UGI was performed on post-op day 2 with normal findings for a post-bariatric surgery evaluation and clear fluids were started. The patient was discharged on post-op day 3 without any complications. Upon discharge, the patient had a treatment plan that was previously discussed that included instructions for diet and medications, including vitamin supplementation and antacids. At her three-month follow-up, the patient was still without complications and very pleased with her weight loss of 46.2 lbs, weighing 142 lbs (BMI 29).
A 49-year-old Caucasian man presented at our institution with SLE that had been diagnosed originally in August 1996. Manifestations of his disease included arthritis, a rash on sun-exposed skin, and skin lesions resembling urticaria. Laboratory findings are shown in Table . A skin biopsy revealed urticarial vasculitis. There was no evidence of cerebral or renal involevement. His therapy for SLE required long-term plaquenil and prednisone. In September 1997 the patient was admitted with progressive exertional dyspnoea, cardiac decompensation, and a blowing systolic murmur at the apex radiating to the left axilla. Transthoracic (TTE) and transesophageal echocardiography (TEE) revealed severe MR with thickened mitral valve leaflets and a small vegetation on the posterior mitral valve leaflet. Repeated blood cultures were negative and there was no other evidence of infective endocarditis. The patient was recompensated with diuretics and discharged. Echocardiographic follow-up over the following months revealed a rapid increase in left ventricular diameters and normal left ventricular (LV) function. Results of cardiac catherization are shown in Table . The patient underwent mitral valve repair in March 1998. Intraoperative inspection showed slightly thickened, but otherwise surprisingly normal leaflets. A small perforation was found in the P2 section of the posterior leaflet. Preoperatively a small vegetation was found near this location. Although rare and more often seen in infectious endocarditis, leaflet perforation in LS endocarditis has been reported before []. This patient's history did not reveal any documented thromboembolic events. A quadrangular resection of the P2 section of the posterior mitral valve leaflet was performed, followed by implantation of a 32 mm Carpentier-Edwards Classic annuloplasty ring. Microscopic examination of the excised mitral valve segment revealed myxoid degeneration and no evident signs of inflammation. Although evidence of LS endocarditis could not be found microscopically, the diagnosis was made based on the clinical features, laboratory findings, and echocardiographic appearance. The patient's recovery from surgery was uneventful, and he was discharged on the seventh postoperative day. Echocardiographic follow-up revealed stable slight MR from April 1998 through January 2009. When last seen in March 2009, the patient was doing well, except for a mild degree of dyspnoea.
A 38-year-old, gravida 0, para 0 woman presented with severe pain in both hip joints. In terms of past history, she had developed an eating disorder at 18 years old and amenorrhea at 20 years old. She consulted a gynecologist and psychiatrist, both of whom diagnosed AN, but she only continued follow-up with these doctors for two years. The patient was 157 cm tall, and her weight and body mass index (BMI) were 33 kg and 13.4 kg/m2, respectively. Several years after the onset of AN, her appetite spontaneously recovered and she gradually regained weight. Menstruation resumed at 31 years old, at a weight of 40 kg, and her menstrual cycles had thereafter remained regular. She married at 34 and became pregnant spontaneously at 37 (weight 40 kg, BMI 16.2 kg/m2).\nThe patient had no preceding history of trauma, fever, disease other than AN, smoking or alcohol abuse. Family history revealed that her mother had developed vertebral compression fractures resulting from osteoporosis at 60 years of age.\nPain localized over the left hip joint began at 28 weeks of gestation, of unknown cause. This pain progressively increased to involve both hip joints.\nIn consultation with an orthopedician at 32 weeks of gestation after hip pain continued to increase, left hip range of motion was 0–90° for flexion and 20° for external rotation, limited by pain, whereas rotation of the right hip showed no limitation. The Patrick test showed positive results in the left leg and negative results in the right. No imaging was performed because of the potential risk to the unborn child. Osteoarthritis of the hip and probable acetabular dysplasia were suspected, and conservative treatment was followed.\nAt 35 weeks and five days of gestation, she was admitted to our hospital with difficulty walking. At this point, she weighed 48.2 kg. Serum 1,25(OH)2D3 and parathyroid hormone levels were not measured, but other laboratory investigations revealed no abnormalities. MRI of the hips showed a fracture of the left femoral neck as well as diffuse BME involving both femoral heads. T1-weighted imaging revealed decreased intensity of the bone marrow (Fig. a), while short-tau inversion recovery T2-weighted imaging revealed a matching increase in intensity (Fig. b). Epiphyseal stress fracture, which is associated with avascular necrosis of the femoral head, was not observed. Cesarean section was performed two days after admission and a healthy 2720 g girl was delivered. Surgical intervention for the fracture was scheduled for a week after cesarean section, but the right hip pain worsened on the third day. On post-partum day 5, dual-energy X-ray absorptiometry of lumbar vertebrae 2–4 showed a T score of −3.5, a Z score of −3.5 and a BMD of 0.696 g/cm2, representing osteoporosis according to World Health Organization guidelines. Radiography of the pelvis performed the same day showed bilateral femoral neck fractures (Fig. ).\nThe patient immediately underwent open reduction and cannulated screw fixation of both fractures, followed by administration of teriparatide at 20 μg/day and calcium lactate at 2 g/day, considering that she was still of reproductive age. The neonate was bottle-fed. At five months post-operatively, the patient was able to walk without pain.
A previously healthy 45-year-old male developed sharp left lower quadrant and groin pain. He was evaluated by his primary physician and his symptoms were thought to be related to diverticulitis. He was treated conservatively with an antibiotic, though there was no resolution of his symptoms.\nA computed tomography (CT) scan of the pelvis revealed a 5.6×5.1 cm heterogeneously enhancing mass involving the left lobe of the seminal vesicle and minimally the right lobe across the midline. The mass was invading the left bladder base and ureterovesicular junction (UVJ), and a few cm of left distal ureter (). This was accompanied by left-sided hydronephrosis. The mass also invaded the left obturator internus muscle, and potentially the base of prostate gland as well as into the perirectal space abutting the rectum. There was no pelvic lymphadenopathy. A transrectal biopsy of the mass was performed which was reviewed at several different institutions, though it was considered indeterminate. A second transrectal biopsy of the periprostatic/seminal vesicle soft tissue mass was performed, which was reviewed at our institution and found to be a grade 4 (of 4) epithelioid angiosarcoma. Immunohistochemical stains showed the tumor cells reacted strongly and diffusely with antibodies to CD31 and vimentin, but did not react to antibodies to keratin (Cam 5.2, 7, 20 and wide spectrum), prostate specific antigen, actin, desmin, melanin A, S-100, CD117 (C-kit), synaptophysin, and chromogranin, supporting the diagnosis.\nThe patient was referred to our institution for further evaluation and management. Digital rectal examination revealed a normal anal sphincter tone and a large, firm, fixed mass in the left lateral rectal area without apparent rectal mucosal involvement. Magnetic resonance imaging (MRI) was performed, which showed an infiltrating soft tissue mass in the left lower pelvis involving the left seminal vesicle, the base of the prostate and the left bladder wall (). The mass extended laterally resulting in effacement of the left obturator internus muscle. A fatty soft tissue plane separated the mass from the adjacent left anterior rectal wall. A chest CT showed a few small indeterminate pulmonary nodules and a small calcified granuloma within the left lower lobe. A colonoscopy showed no evidence of rectal invasion. Given the presence of locally advanced tumor and the high risk for micrometastatic disease, the multidisciplinary team consisting of urology, medical oncology, and radiation oncology physicians recommended multimodality therapy consisting of neoadjuvant chemotherapy and radiotherapy followed by potential surgical resection.\nThe patient received two cycles of neoadjuvant IMAP chemotherapy, consisting of ifosfamide (2500 mg/m2 IV days 1-2), Adriamycin (40 mg/m2 IV day 2), mitomycin (4 mg/m2 IV day 2), cisplatin (60 mg/m2 IV day 2), and mesna (1500 mg/m2 IV and 2500 mg/m2 per days 1-2.) Repeat imaging following IMAP showed that the soft tissue mass in the left pelvis slightly decreased in size from 5.6×5.1 cm to 4.3×4.0 cm. The patient then received external beam radiation therapy () consisting of 50 Gray in 25 fractions delivered daily over 5 weeks with 2 cycles of concomitant MAP chemotherapy, consisting of mitomycin (8 mg/m2 IV), adriamycin (40 mg/m2 IV) and cisplatin (60 mg/m2 IV).\nFollowing a six-week recovery from preoperative chemoradiation, repeat imaging studies showed no significant change in the pelvic mass and no evidence of distant metastatic disease. He then proceeded to surgical resection with a radical prostatectomy, partial cystectomy, distal ureterectomy, bilateral pelvic lymph node dissection, and ureteroneocystostomy. Frozen section margins at the bladder and left pelvic sidewall were positive. Additional resection was performed and the margins were negative. An intraoperative electron radiation therapy boost (9 Gy) was given to the left pelvic sidewall as there was a concern for residual microscopic disease. Review of the surgical pathology demonstrated grade 4 (of 4) epithelioid angiosarcoma forming a 3.5×2.6×1.8 cm mass in soft tissue in the region of the left seminal vesicle (). The tumor involved the left seminal vesicle, infiltrated adjacent skeletal muscle, and extensively involved regional nerves and ganglia, but tumor did not extend into prostatic parenchyma. The final surgical margins were negative for tumor. Multiple left and right pelvic lymph nodes (external iliac, internal iliac, common iliac and obturator regions) were negative for tumor involvement.\nPost-operatively he had left thigh numbness that subsequently resolved. He developed a vesicourethral anastomotic leak which required prolonged (3 months) Foley catheter use; however, this completely resolved. He developed an abscess that was drained and resolved. The patient was then seen in regular follow up with serial imaging studies over the subsequent six years following surgery and he has not developed evidence of cancer recurrence.
An otherwise healthy 75-year-old man had a spontaneous collapse on a golf course, witnessed by other club members. He had no pulse and was not breathing and received cardiopulmonary resuscitation (CPR) from a bystander. After 15 minutes of CPR, a public automated external defibrillator (AED) was appropriately deployed, and he received one shock, following which he appeared to regain some consciousness.\nDue to the rural location, the fastest prehospital transport to the scene was by air ambulance. A crew of two Critical Care Paramedics (CCPs) arrived to find the patient placed in the recovery position, spontaneously ventilating, with a palpable pulse, adequate blood pressure, normal oxygen saturation readings, and normal blood glucose. A 12-lead ECG showed no acute abnormalities.\nThe patient had a reduced Glasgow Coma Scale (GCS) and a unilateral fixed, dilated pupil. He exhibited trismus and occasional decorticate posturing. History from the patient's wife (via telephone) was that earlier in the morning he had slipped on some ice and fallen over, hitting his head, but had decided that he was well enough to play golf. Raised intracranial pressure was considered a possibility due to these signs. The patient was given high flow oxygen via a nonrebreathing mask and the airway was managed to good effect using basic manual techniques and a nasal pharyngeal airway.\nDetermining the aetiology of cardiac arrest in the prehospital environment can be difficult, and some of the differential diagnoses in this case included traumatic brain injury, acute myocardial infarction, or cerebrovascular accident. The CCPs made a decision to convey the patient to a Major Trauma Centre that had neurosurgical and cardiology specialist expertise, rather than the nearest hospital. When he arrived at the Emergency Department, he was anaesthetised and underwent rapid sequence induction. A head CT was performed, and this was reported as normal. He then proceeded to undergo coronary angiography, which demonstrated an occlusion of two coronary arteries. He underwent percutaneous coronary intervention (PCI) via the right radial artery, with angioplasty and stenting of the right coronary artery, left main stem, and proximal left anterior descending coronary artery.\nDuring his inpatient stay, he informed medical staff that his left pupil has been permanently dilated since he was a boy, following a traumatic ocular injury whilst playing football (shown in ).
A 13-year-old boy was referred to our hospital for the evaluation of mental retardation due to poor performance at school. The parents gave a history of delayed milestones as compared to siblings and multiple respiratory tract infections. There was no history of visual disturbances, trauma, or central venous catheterization. The patient had two elder sisters, both of whom had no known medical issues. There was no history of mental retardation or sudden cardiac death in the first degree relatives of the mother or father. Physical examination revealed a weight for age and height for age below 3rd centile with a high arched palate, slender extremities, and long thin fingers. “Thumb sign” was positive. No kyphosis or scoliosis was present. Ophthalmological examination revealed bilateral ectopia lentis. Chest examination revealed bilateral basal crepts. Chest radiograph showed a calcified mass in the right hilar region and prominent bilateral bronchovascular markings. The patient underwent contrast-enhanced computed tomography for the evaluation of the hilar mass which was found to be a densely calcified mass in the right atrium with a calcified tail extending into superior vena cava (SVC) and the right subclavian vein. Bronchiectasis was seen in both lungs [Figures and ]. Echocardiography performed subsequently showed a nonmobile right atrial mass adherent to the endocardium with dense posterior acoustic shadowing. The lack of mobility, the absence of myocardial continuity, no relation to foramen ovale, and morphology of the mass, especially the extension into the SVC suggested that the mass represented a calcified thrombus. Coagulation studies showed prolongation of PT and aPTT with elevation of fasting plasma homocysteine (235 μmol/l) and elevated methionine (139.3 μmol/l). Radiographs of his hands showed diffuse osteopenia with long fingers []. Elevated levels of homocysteine may be found in deficiencies of vitamin B12 or folic acid and in other disorders of methionine metabolism; however, the severity of homocysteinemia with coexisting methioninemia, Marfanoid features, and mental retardation suggest the diagnosis of homocystinuria. The patient was then started on pyridoxine, folic acid, and vitamin B12, and then referred to a higher center for the surgical management of the right atrial mass.
A 4-year-old boy presented to our outpatient department with a history of recurrent lower respiratory tract infection since childhood. He had no history of cyanosis, and the examination was significant for an ejection systolic murmur at the pulmonary area. His blood O2 saturation on room air was within normal limits.\nTransthoracic echocardiography suggested a 2-cm ostium secundum atrial septal defect (OS ASD) (left-to-right shunt) with deficient superior vena cava (SVC) margins. There was normal systemic and pulmonary venous drainage, and no other associated cardiac lesions were noted.\nThe patient was taken up for surgical patch closure after due informed consent. Cardiopulmonary bypass (CPB) was established using aorto-bicaval cannulation and mild hypothermia (32°C). Aorta was clamped and antegrade cardioplegia was perfused. After right atriotomy, a solitary OS-ASD was found. There was normal pulmonary venous drainage. However, there was a slightly aneurysmal outpouching on the right side of the left atrium (LA), and right pulmonary veins were opening into this aneurysmal sac. A small additional opening in the aneurysmal sac where right pulmonary veins were opening was noted and this was probed. The distal end seemed to be directed into the right lung. No intervention was done for it as it was thought to be an abnormal opening of a right lobar pulmonary vein into LA. Pericardial patch closure of ASD was done. However, on weaning the patient off, CPB blood SpO2 dropped down to 72%.\nA transthoracic echocardiogram with saline contrast was performed which demonstrated intact ASD patch. SVC and inferior vena cava were seen draining into the right atrium (RA). This ruled out patch dehiscence or routing of caval blood into LA. However, there was delayed appearance of contrast in LA after a couple of cardiac cycles without any identifiable source.\nDecision was taken to shift the patient to the catheterization laboratory for an emergent catheterization study. Cardiac catheterization revealed a large RPA-to-left atrial fistula [].\nThe fistula was closed with a 12-mm Amplatzer ventricular septal defect closure device using a trans-RPA approach [Figures and ]. Post procedure, the patient's saturation improved immediately to 100% and the patient had uneventful postoperative course. The patient was discharged on postoperative day 5 on aspirin and anticoagulant. He is healthy on 1-year follow-up.
A 39-year-old female with a history of obesity and tobacco use presented to the emergency department with a 10-day history of increased swelling, redness, drainage, and pain of the right breast and upper abdomen. The patient reported associated fever, chills, nausea, and emesis. There was no history of trauma or previous surgery. She also stated she was reluctant to visit her primary care physician or any emergency department when her symptoms began due to anxiety related to COVID-19 viral exposure.\nOn clinical examination, the right breast was noted to have a 12 × 14 cm area of skin sloughing along the inferior inner aspect of the breast. A necrotic open wound was also seen within the lower outer quadrant with foul-smelling drainage surrounded by edema, erythema, and crepitus extending onto the right anterior abdominal wall (Figures and ) The patient was noted to be hypotensive with mild tachycardia.\nPertinent laboratory findings revealed a leukocytosis of 16.9 × 109/L with neutrophilia, thrombocytosis of 608 × 109/L, and mild hyponatremia of 133 meq/L. Mild anemia was present, but renal function and lactic acid were found to be within normal limits.\nA chest computer tomography (CT) ordered by the emergency room physician revealed the right breast wound with several locules of gas within the superficial subcutaneous tissues of the right lateral and posterior breast with minimally increased attenuation of the subcutaneous tissues. (Figures –) These findings were consistent with a necrotizing soft tissue infection, and general surgery was consulted. After surgical evaluation, a decision was made to proceed with emergent surgical intervention to provide source control. Prior to surgery, resuscitative intravenous fluids were administered in addition to vancomycin, clindamycin, and aztreonam, due to an unknown reported allergy to cephalexin.\nThe patient was taken to the operating room for an emergent wide excision and debridement of the infected tissue within the inferior right breast and the upper portion of the abdominal wall including the fascia overlying the pectoralis major muscle and external oblique. An attempt was made to obtain adequate source control while preserving as much breast tissue as possible, leaving the nipple areola complex intact. Cultures were obtained intraoperatively approximately 90 minutes after antibiotics had been administered. The wound was packed with wet-to-dry gauze and managed with daily dressing changes. An infectious disease consultation was performed, and the decision was made to replace aztreonam with piperacillin-tazobactam.\nDuring the second operative debridement approximately 36 hours later, findings of advancing cellulitis extending superiorly on the right breast, encompassing the entire areolar complex, were identified. A completion mastectomy was performed in order to obtain adequate source control. Again, the wound was packed with planned daily local wound care and a return to the operating room for potential delayed primary closure. A third operation with minimal debridement of the lateral aspect of the right breast was performed and the wound, measuring 25 × 15 × 8 cm, underwent delayed primary closure in a multilayer fashion over closed suction drains.\nHistopathologic evaluation of all tissue excised during all three operations was noted to be negative for malignancy and showed extensive acute suppurative inflammation, multiple abscesses, and tissue necrosis. The final tissue cultures grew Corynebacterium with negative blood cultures. The patient was discharged home 12 days after presentation on a 5-day course of ertapenem and daptomycin via a PICC line. Drains were removed during outpatient follow-up visit (). The patient was offered plastic surgery consultation for possible reconstruction, but refused. The case underwent a multidisciplinary breast conference review two weeks after discharge, and no further recommendations were made.
The patient was a 45-year-old man who presented with a headache for 3 months which was progressive and had been intolerable for 2 weeks. However, the patient was a football player with good health. There was no such family history and family members were perfectly well. There were no other clinical symptoms reported by the patient.\nThe patient was advised to do CT-scan and MRI. Interestingly both CT-scan and MRI revealed brilliantly enhancing left lateral ventricular lesion with unilateral hydrocephalus (). T1 Image axial view postcontrast () and precontrast film () were also examined. T1 image of coronal view in postcontrast film was also evaluated (). T2 image in sagittal view () also found the SOL.\nFlare image () was examined as well. All other investigations were within normal limit. Then the patient was advised for surgery for removal of the lesion. In this context, left parietal craniotomy was performed with total removal of the lesion through intraparietal approach. Reversal from GA and the postoperative period was uneventful and the patient had got rid of clinical symptom completely after surgery.\nThe tumor was well defined preoperatively and was removed under microscopic surgery meticulously. The patient was very poor to bear the cost of postoperative CT-scan and hence it was not done. The biopsy was sent for histopathological examination. The lesion was nearly spherical measuring 3.0 cm + 2.5 cm, whitish, and firm.\nThere was no evidence of necrosis. Microscopy revealed multicystic appearance with cyst lined by columnar epithelium with apical mucin. Few goblet cells were seen. Few areas had shown pseudostratified lining epithelium with nuclear hyperchromasia, nuclear enlargement, and increased mitosis.\nThere was no evidence of stromal invasion. The mucinous material was seen within the lumen. Hemosiderin laden macrophages were present in the stroma. It was confirmed as a lateral ventricular enterogenous cyst. Then the patient was well in around one year. After about one year of the surgical removal of the lesion, there was a recurrence of a headache whose intensity was more than the previous one.\nThen the patient was advised to do a CT-scan which revealed lesion of the same pattern in the same location as before (). The patient was reexplored surgically and the tumor was removed completely through the same route and histopathology was again revealed it as a case of the enterogenous cyst. Again the total removal of the lesion from the brain was confirmed by postoperative CT-scan. Then the patient was advised for radiotherapy. After completion of radiotherapy, the patient was perfectly well at 13th postoperative month ().
A 40-year-old Somali man presented to our hospital with a large midfacial defect, inability to open his mouth, oral incompetence and incoherent speech. Eight years prior to his presentation, he had noted a small blister in his left maxillary buccal mucosa, which had ruptured and a few weeks later had left a small ulcer that progressively increased in size with time. He eventually lost both his upper and lower lips, parts of the maxilla and some teeth, as well as the ability to open his mouth. Concurrently, he had developed difficulties with eating and speech.\nOn examination, he had a hideously deformed face - an extensive ulcer covered what used to be his mouth and midface. A deep ulcer cavity with a foul-smelling purulent discharge covered what used to be his left maxilla. Most of what remained of his left upper and lower dentition was visible through the soft tissue defect. On the right side, the esion was less extensive but also had no lip tissue (Figure ). An orthopantogram revealed bilateral chronic osteomyelitis of his midfacial skeleton with bilateral maxilla-mandibular ankylosis. He did not have diabetes mellitus, HIV/AIDS, or any other co-morbidity.\nA feeding gastrostomy and a tracheostomy preceded the midfacial reconstruction, which initially involved bilateral excision of the bony block between the mandible and maxillae, mobilization of the temporomandibular joint and soft tissue coverage achieved by use of bilateral pectoralis major muscle myocutaneous flaps.\nUnfortunately, poor communication, misunderstanding and significant differences in surgeon and patient expectation led to the patient destroying this initial reconstruction on the first 3 postoperative days. He had expected to look his "normal old self" immediately postoperatively, and such was his disappointment with the results, that he stoically tore through his flaps, destroying the entire reconstruction.\nAfter discussion with the patient and his relatives, a staged reconstruction was agreed upon. Bilateral platysma flaps and a left deltopectoral flap were used for intra-oral lining, with the deltopectoral flap providing the lower lip lining, along with additional bulk needed to fill the defect over the left maxilla (Figures and ). A scalp visor flap was designed and prefabricated with a skin graft, and subsequently raised a week later. This was used to cover the midfacial defect, reconstruct his lips, and provide a moustache and beard, all as a single unit. The scalp defect was skin grafted.\nAlthough continence to solids was gained, he remained incontinent to liquids. Non-adherence to postoperative rehabilitation led to significant loss of mouth opening, from 35 mm immediately postoperatively to about 10 mm at 2 years.
A 17-year-old boy with history of fall from height of approximately 15 meters presented to our institution after receiving primary care at another hospital. At presentation, he was conscious, hemodynamically stable maintaining oxygen saturation at 98% on room air with no visible signs of respiratory distress. His Glasgow coma scale (GCS) was 15, and was able to move all four limbs. The patient had sustained open fracture both bone left leg along with fracture right ankle.\nChest radiograph showed no intrathoracic injury with normal lung parenchyma. Computed Tomography showed burst fracture of fifth lumbar vertebra with canal compromise () and ruled out any injury to head, cervical spine, thorax and abdomen. After primary care, patient was admitted to the orthopedic ward for spine stabilization surgery and surgery for lower limb fracture.\nOn day four post-admission, an emergency consultation call was sent to our intensive care unit (ICU) in view of patient’s deteriorating status. When seen, he was grossly pale and febrile at 101 F, pulse rate of 140 per minute, systolic blood pressure of 80 mmHg and respiratory rate of 32 per minute maintaining oxygen saturation around 90% on oxygen face-mask. Patient’s GCS was 15. Chest auscultation revealed bilateral diffuse coarse crepitation and he was immediately transferred to the ICU. Initial arterial blood gas (ABG) showed partial pressure oxygen (pO2) of 49mm Hg on oxygen by face mask. Patient was intubated, sedated, paralyzed and put on mechanical ventilation with initial settings of volume assist control and high positive end expiratory pressure (PEEP). Central venous catheter was secured in right internal jugular vein under ultrasound guidance. An arterial line was secured in right radial artery for invasive blood pressure and arterial blood gas analysis. Chest radiograph showed bilateral fluffy opacities (). Preliminary blood investigations were mostly unremarkable except for hemoglobin of 6.8 mg/dl and raised ESR of 44. Fundus exam specific for FES was normal and there was no petechial rash on general examination. Urine for fat globules was positive. Over the next few hours, patient’s hypoxemia worsened requiring higher fraction inhaled oxygen (FiO2) of up to 0.8 and PEEP of 16 cm water. A decision was made to turn the patient into prone position after discussion with the orthopedic surgery team in view of unstable lumbar spine fracture. Patient’s family were informed about the specific risks and benefits of prone positioning, particularly in a patient with pre-existing unstable lumbar spine fracture and a written consent for the same was obtained. Positioning was done with the help of 5 trained ICU staff, using logrolling technique for turning the patient lateral followed by a 6th member placing the spinal board under the patient. After securing the patient on the spinal board, he was then shifted to one edge of the bed while the head gel support, chest and pelvic roll were placed in position. Patient was then shifted to prone position and spinal board was removed. Patient’s hands were abducted and placed next to the head and all the pressure points were padded using pillows and cotton rolls.\nOver the next 16 hours, we kept our patient sedated and paralyzed in prone position during which he received targeted fluid therapy and remained hemodynamically stable. Wake up test and pupil examination were done at regular intervals. Serial ABG’s showed dramatic improvement with Fio2 requirement decreasing to 0.4 and PEEP of 8 following which patient was repositioned supine. Two units packed red cells were transfused while the patient was prone. Chest radiograph showed resolving lung infiltrates and we decided to electively mechanically ventilate our patient for next 24 hours in supine position. Weaning was started next day and patient was extubated a day after and transferred back to ward 24 hours later.\nThe patient later on went on to have multiple surgical procedures for injuries to spine and bilateral lower limbs. He was then followed for 8 weeks in the out-patient department following discharge during which he recovered well without any neurovascular deficit.
A 69-year-old Caucasian man presented with intermittent upper abdominal pain, nausea and bloating for the previous 12 months. There was no history of fever, jaundice, pale stools or dark urine. His past medical history included a Billroth II gastrectomy and Roux-en-Y reconstruction for peptic ulcer disease 11 years earlier. On examination, he was haemodynamically stable and afebrile. Abdominal examination was unremarkable. Laboratory tests, including liver function tests and inflammatory markers were all normal. Transabdominal ultrasound examination revealed gallstones and intra- and extrahepatic biliary dilatation. Endoscopic retrograde cholangiopancreatography (ERCP) was unsuccessful. Magnetic resonance cholangiopancreatogram (MRCP) and computed tomography (CT) confirmed gallstones within the gallbladder and biliary dilatation to the level of the ampulla, and demonstrated a 4 × 3 cm low density filling defect in the second part of the duodenum (Figure ).\nAfter he was admitted to a specialist centre, endoscopic ultrasonography and repeat ERCP were attempted but failed due to inability to cannulate the duodenal limb of the Roux-en-Y. Two hours after the procedure he developed severe, generalized abdominal pain and hypotension. This raised the possibility of iatrogenic intestinal perforation. However, it was decided to proceed directly to laparotomy rather than repeat imaging, since it was apparent that surgical exploration would be required in the event of unsuccessful ERCP. During the operation, there was no evidence of intestinal perforation. A 3.5 cm gallstone was found proximal to a stricture in the second part of the duodenum. There was no evidence of a cholecystoduodenal fistula. The duodenal papilla and pancreas were normal. The common bile duct, which was dilated due to extrinsic compression by the intraduodenal gallstone, was explored and found to be normal, and contained no stones. The gallstone in the duodenum was extracted via a duodenotomy, the duodenal stricture was dilated digitally and a cholecystectomy was performed. A t-tube was placed in the common bile duct. He made an uneventful postoperative recovery and was discharged 10 days later after a normal t-tube cholangiogram. The t-tube was removed six weeks post-operatively.
An 82-year-old woman underwent emergent aortic repair for acute type A aortic dissection. Intraoperative TEE showed aortic dissection in ascending to abdominal aorta with moderate aortic valve (AV) regurgitation. Neither regional wall motion abnormalities nor tricuspid and mitral valve abnormalities were shown on TEE. Under cardiopulmonary bypass (CPB), the aortic valve was replaced with a biological valve. After that, under circulatory arrest with selective brain perfusion, the ascending aorta was replaced with a vascular graft. The TEE after weaning from CPB showed no unusual findings. Tracheal extubation was performed on postoperative day (POD) 1. The postoperative course was comparatively stable and inflammatory reaction was not remarkable. We administrated an antibacterial drug, cefazolin of 2 g intraoperatively and 1 g/day postoperatively. On POD 9, however, she suddenly complained of both dyspnea and fever. C-reactive protein (CRP) was remarkably increased at 22 mg/dl. To prevent infection of the artificial vascular graft, we changed the antibacterial drug, vancomycin of 1.5 g/day and imipenem of 0.5 g/day. She was transferred to the intensive care unit (ICU) immediately. After emergency tracheal intubation, we inserted the pulmonary artery catheter (PAC) from the right internal jugular vein to evaluate cardiac function. Mixed venous blood oxygen saturation obtained from the PAC was revealed to be 90 %. As we suspected an intra-cardiac shunt, we firstly performed a transthoracic echocardiography (TTE). The two-dimensional TTE in the apical four-chamber view showed that a large vegetation seemed to be attached on the septal leaflet of the tricuspid valve (Fig. ). Furthermore, TTE with color Doppler from a parasternal aortic valve short axis view showed abnormal flow in the RA (Fig. ). To evaluate intra-cardiac appearance in detail, we performed a TEE examination, suspicious of an intra-cardiac shunt. The two-dimensional TEE from the modified four-chamber view clearly showed a large vegetation on the annulus of the aortic valve which protruded into the RA chamber (Fig. ). Furthermore, the color Doppler TEE from the modified five-chamber view showed an intra-cardiac shunt from the LV to the RA through a subaortic ventricular septal fistula (Fig. ). The three-dimensional TEE showed a structural connection between the aortic valve annulus and the attachment site of the vegetation (Fig. ). After the intraoperative TEE found the abnormalities coincidently, we decided to perform an emergency surgical repair. We performed aortic annuloplasty with re-AVR and closure of the subaortic ventricular septal fistula using bio-pericardium. After repairing, the patient was somehow weaned from CPB with a high-dose inotrope. We confirmed by TEE that there was no pathologic flow associated with the fistula. Pathogenic bacteria were gram-positive coccus. In spite of all our medical efforts, on 30 POD, the patient died of multiple organ failure due to IE at the hospital.\nAn acquired ventricle-atrium shunt has various etiologies: (1) after aortic and/or mitral valve replacement surgery, (2) infective endocarditis, and (3) chest trauma []. A schematic transverse section of a heart of the case is shown in Fig. ; a membranous ventricular septum divides the LV chamber from the RA chamber []. Because a membranous ventricular septum is structured by thin connective tissue of the fibrous ring, an acquired LV-RA and/or RV shunt is likely to generate a membranous ventricular septum. The authors thought that the membranous ventricular septum was included in the aortic prosthetic valve structure line because of its proximity to the aortic root, resulting in IE and subsequently resulting in intra-cardiac shunt.\nAfter the patient complained of the abnormality, the authors firstly inserted the PAC to evaluate the cardiac function. This revealed abnormal increased mixed venous blood oxygen saturation. Among many causes of increased mixed venous blood oxygen saturation, an intra-cardiac left to right shunt is one of the possible causes because of acute appearance of dyspnea. Although the patient unfortunately died of acute heart failure due to IE, decisive diagnosis without delay was required for performing adequate treatment. Although TTE revealed both the vegetation on the peri-aortic root and abnormal flow in the RA, the detailed site of the intra-cardiac shunt was difficult to detect. Because TEE depicts the subaortic structures clearly using an acoustic window from both of the LA and the RA, TEE depicts the structures better than TTE []. One of the tips for clearly depicting the detailed site of the LV-RA shunt is to adjust the aliasing velocity appropriately []. The authors adjusted the aliasing velocity at 30.8 cm/ms. Because pressure gradient between the LV and the RA decreases due to pressure overload at the RA, a relative slow velocity of shunt flow was predicted. Furthermore, three-dimensional TEE revealed the exact location of the vegetation attached to the aortic root structures. In this aspect, TEE examination in the ICU was a crucial diagnostic method to decide emergent surgical revision.
A 41-year-old pregnant woman referred to our hospital in the 22nd week of gestational age with right upper abdominal pain and jaundice. She had mild abdominal pain six weeks before presentation which was aggravated one week before admission. Abdominal pain was not related to food intake and referred to her right shoulder. Four days before admission, she had icter, tea colored urine and edema in her lower extremities. She had nausea and vomiting but no headache, blurred vision or bleeding was mentioned. She mentioned fatigue and hypertension from the eighth week of pregnancy. A past history was remarkable for two abortions and one live birth prior to this pregnancy. She took only ferrous sulfate and aspirin in this pregnancy and no other drugs, herbal medicines or oral contraceptives (OCPs).\nThere was no history of blood transfusion, hepatitis or exposure to aflatoxin in her past history however her father died from HCC due to hepatitis B virus (HBV). Laboratory investigations showed features of microangiopathic hemolytic anemia that included schistocytes, elevated prothrombin time and erythrocyte sedimentation rate (ESR), and negative viral markers(negative HBsAg and HBcAb). Differential diagnoses of HELLP syndrome, thrombotic thrombocytopenic purpura (TTP) or acute fatty liver of pregnancy (AFLP) were made for further evaluation and management.\nShe seemed ill and icteric at admission but not toxic. Her blood pressure was 110/70 mmHg with a pulse rate of 110 beats/min, respiratory rate about 18/min and oral temperature of 370C. Conjuctivae was pale and sclera was icteric. Jugular venous pressure was normal. Pulmonary sounds were diminished in the basal parts but cardiac examination showed no abnormalities. Her abdomen was tender, particularly in the right upper quadrant, but without rebound and guarding. Lower extremities had 3+ pitting edema and there were ecchymotic lesions at previous injection sites.\nLaboratory examination showed leukocytosis, anemia and lower limit platelet counts. Blood electrolytes were normal but there was direct hyperbilirubinemia and liver enzymes showed a cholestatic pattern. Lactate dehydrogenase (LDH) was elevated and haptoglobin was low. Peripheral blood smear showed features of microangiopathic hemolytic anemia that included target cells, tear drop and nucleated RBCs, and numerous schistocytes. Urine analysis was positive for microscopic hematuria and proteinuria.A 24-hour urine collection showed 226 milligrams of protein.\nViral markers of HBV and HCV, autoantibodies and Adisintegrin-like and metalloproteinase with thrombospondin type 1 motif (Adamts)-13 antigen and antibody (markers for Thrombotic Thrombocytopenic pupura=TTP) were all negative. AFP level was 90.7 and cancer antigen 125 (CA125) titer was >1000.\nTransabdominalsonography showed a normal fetus with a gestational age of about 23 weeks and normal amniotic fluid in the breech position. The liver showed a coarse echopattern with a diameter of 20 cm. The biliary ducts were normal and the gallbladder was contracted. No lesion was noted in the portal vein, which had a diameter of 10 mm. The inferior vena cava and suprahepatic vessels were normal. The pancreas, spleen and kidneys were all normal. There were no ascites, however bilateral pleural effusion was detected.\nA possible diagnosis of HELLP was made and supportive care for correction of coagulation disorder with fresh frozen plasma (FFP) and corticosteroids were administrated. Because of deterioration in her mental state in conjunction with an increased bilirubin level and international normalized ratio (INR), the pregnancy was terminated. Vaginal delivery was not possible because of the patient’s decreased mental state so a cesarean section was performed. The fetus was delivered and transferred to NICU but expired because of immaturity. At laparotomy, approximately one liter of ascitic fluid was noted in the abdomen and the liver had multiple malignant appearing mass lesions, which were biopsied with wedge resection. Pathologic evaluation showed sheaths of malignant hepatocytes typical of HCC ( ).\nAfter delivery the patient experienced progressive loss of conscious along with multi-organ failure and unfortunately died after a few days.
A 62-year-old man was admitted to our hospital for the removal of a suspected metastatic brain tumor. He had suffered from gait disturbance and visual field defects for 3 months. He has recently developed left hemiplegia due to multiple brain lesions. He had no specific past history aside from being a heavy smoker. The main brain tumor was located in the right occipital lobe, and the imaging study suggested that it was a metastatic tumor from lung cancer. A subsequent chest CT revealed a large solid tumor (maximum diameter, 72.25 mm) in the mediastinum (Fig. ). As for the main bronchus, the maximum reduction in the cross-sectional area was estimated to be 50 % in the side just rostral to the bifurcation (Fig. ), and the length of the stenosis was approximately 35 mm. In addition, the bilateral innominate veins were completely obstructed before merging into SVC, and SVC was involved in the mass and was completely compressed. Despite the imaging findings, he did not show any cardiopulmonary symptoms or upper body edema. Initially, we intended to consult a pulmonologist for further examination before craniotomy; however, the removal of the tumor was prioritized because of progressive neurological symptoms.\nPeripheral 20-G and 22-G intravenous lines were secured at the right forearm and the right back of the hand. General anesthesia was induced with 100 mg of propofol plus 100 μg of fentanyl, and neuromuscular blockade was achieved with 50 mg of rocuronium. Manual ventilation with a mask was easily performed. Tracheal intubation with a 7.5 mm silicone reinforced tracheal tube was performed uneventfully. Before tube fixation, we confirmed that the distal tube end was positioned to avoid injury to the stenotic part of the trachea using a fiberoptic bronchoscope. General anesthesia was maintained with 1–1.5 % of sevoflurane, 0.05–0.1 μg/kg/min of remifentanil, and 10–15 mg/h of rocuronium. Transient hypotension was observed during induction of the anesthesia; however, it was treated using 8 mg of ephedrine. Craniotomy and removal of the brain tumor was performed in the left park-bench position. During the surgery, hemodynamic status fluctuated and was unstable, which became particularly apparent after an increase in urine output by mannitol administration. To maintain systolic blood pressure at 80–90 mmHg through the procedures, continuous, massive infusion of noradrenaline (0.05–0.07 μg/kg/min) was required. The operation time for the procedures was prolonged to 4 h and 25 min probably because of poor brain relaxation. Fluid balance including crystalloids and colloids infusion (5600 ml), blood products transfusion (560 ml), urine output (2650 ml), and blood loss (625 ml) was 2885 ml.\nAfter the surgery, the patient was turned to the supine position. Massive facial edema was apparent, and the bilateral upper extremities were significantly swollen. Immediately, a bronchoscopic examination was performed to evaluate the patency of the trachea, which revealed a worsened stenotic lesion. Contrary to our expectation, the respiratory condition of the patient was not impaired. Although tracheal stenting may have been a therapeutic option for this condition, we hesitated to select this option because of lack of detailed information regarding the mediastinal tumor. After the administration of 200 mg of sugamadex, the patient’s spontaneous breathing was sufficient; however, he did not regain consciousness. The tracheal tube was then removed. Critical strider accompanied with tachycardia and hypertension was observed. It did not seem likely that the patient’s respiratory condition would rapidly improve. Consequently, reintubation was performed to maintain patency of the trachea, which was confirmed by a subsequent bronchoscopic examination. The tracheal wall was supported by the tracheal tube although the tracheal tube did not pass the stenotic lesion. A head and chest CT was performed before the patient was transferred to the intensive care unit (ICU). Head CT revealed remaining brain edema with mild midline shift despite removal of the main lesion (Fig. ). Chest CT showed that the maximum reduction in the cross-sectional area of the trachea was estimated to be >90 % (Fig. ). Compared with the size of the tumor before the surgery, the tumor at the almost same CT slice level appeared to increase in size (Fig. and Fig. ).\nAfter admission to ICU, the patient remained sedated under mechanical ventilation. He was placed in the Fowler’s position to facilitate blood flow from the upper body. Simultaneously, diuretics (mannitol and furosemide) were used for edema treatment. Owing to the intensive care, the stenotic lesion improved dramatically. On the day following craniotomy, considering the progressive nature of the mediastinal tumor, tracheal stenting using a covered metal stent 60 mm long (Ultraflex™, Boston Scientific Japan, Tokyo) was performed (Fig. ). Following the successful tracheal stenting, the patient regained consciousness immediately after cessation of sedatives. His trachea was extubated, and his respiratory condition did not deteriorate. Finally, he was discharged from ICU and underwent chemotherapy and radiotherapy. He was discharged from the hospital 3 months after the surgery. Although the patient did not develop SVC syndrome, he died from asphyxiation after coughing up blood at home 2 months after being discharged.
A 26-year-old man was brought to the emergency department of our hospital following a stab injury on the left posterolateral aspect of the neck. The patient developed a progressively enlarging swelling in the left posterolateral aspect of the neck within two days following the penetrating injury. The patient also complained of headache and giddiness following the injury. There was no neurological deficit. The patient was conscious and oriented to time, place and person. His vitals were stable. On visual inspection, a gaping wound was noted at the entry site of the penetrating injury. However, there was no active bleeding through the wound. On palpation, the swelling was pulsatile and a thrill could be felt. He did not have any comorbid illness. He did not give any history of substance abuse. His social and family history was unremarkable.\nCT angiogram was performed which showed an enhancing sac-like structure on the left paravertebral region with apparent communication with the V2 segment of the left vertebral artery (Figure ). The epidural venous plexus appeared engorged. A diagnosis of left vertebral artery pseudoaneurysm with arteriovenous fistula was suspected on the basis of the clinical and CT angiogram findings.\nOn digital subtraction angiogram, there was evidence of extravasation of the contrast through the V2 segment of left vertebral artery at the level of C2 vertebral body which was then seen to be draining into vertebral venous plexus (Figure ). There was no anterograde flow distal to the site of fistula.\nA covered stent was deployed across the site of fistula to exclude the pseudoaneurysm from the main left vertebral artery which would also close the direct arteriovenous communication. We used a 6F guide catheter (Envoy, Codman Neurovascular, Raynham, MA) over a 0.035" guide wire (Terumo) and navigated it into the V2 segment of left vertebral artery using roadmap guidance. Following this, a 0.014” microwire (Traxcess, Microvention) was advanced through guide catheter and the site of fistula was crossed. A covered stent (Graftmaster, Abbott Vascular) of size 3.5 mm x 19 mm was taken over microwire. The stent was then deployed covering V2 and V3 segments of the left vertebral artery. A check angiogram after the deployment of stent showed residual filling of the pseudoaneurysm and the fistula (Figure ). This was probably due to the fact that the vessel calibre was slightly larger than the size of the stent.\nThen, we dilated the stent with a balloon. A 5 mm x 20 mm, 135 cm size balloon (Viatrac 14 plus, Abbott Vascular) was taken over the 0.014" wire, and the stent was dilated to approximate the vessel walls. Check angiogram showed no residual filling of the fistula with good anterograde flow in the left vertebral artery (Figure ).\nThe patient was started on IV tirofiban at 28 ml/hr infusion for 30 minutes followed by 7 ml/hr for 18 hours post-procedure. A bridging dose of aspirin 300 mg orally and clopidogrel 300 mg orally was given six hours before stopping tirofiban. The patient was discharged in stable condition 24 hours after the intervention on aspirin 150 mg once a day orally and clopidogrel 75 mg once a day orally for three months.\nFollowing the procedure, the patient reported a gradual reduction in the size of the swelling with healing of the stab wound. At one month after the intervention, check angiogram showed patency of the stent with normal anterograde flow through the stent on selective left vertebral artery injection (Figure ).
A 68-year-old male who had owned a bicycle shop for several decades visited our institute in March 2004 with a one-month history of swelling and pain of the right distal forearm. His dominant hand was right. On physical examination, an elastic soft mass, measuring 6 cm×4 cm, was observed on the palmar side of the right forearm. Motion of each finger was normal, but the range of motion of the wrist joint was slightly restricted. Skin color change and local heat were not observed around the mass. Laboratory data, including rheumatoid factor and C-reactive protein, were not contributory. He had no history of tuberculosis, and his tuberculin reaction on admission to the hospital was weakly positive. No hilar lymphoadenopathy was observed on a chest radiogram.\nPlain radiograms of the right wrist and hand showed degenerative changes and Heberden's nodes in the distal interphalangeal joints, but no apparent calcification was observed in the mass (). On magnetic resonance (MR) imaging, T1-weighted images showed a low-intensity mass surrounding the flexor tendons (A). On T2-weighed images, the mass partially showed high-signal intensity (B). Sagittal T2-weighed images demonstrated an effusion in the sheaths of the flexor tendons and many small low-intensity bodies in the mass (C). The mass was moderately enhanced by administration of intravenous gadolinium (D), but the small bodies were not enhanced.\nAn incisional biopsy was performed in June 2004. The mass existed adjacent to the flexor tendons and was encapsulated by a yellow fibrous wall. Many rice bodies had erupted from a small hole in the wall of the mass (). Histological findings revealed hyperplastic tenosynovitis with fibrinous loose bodies (). During the surgery, we confirmed that the flexor tendons were intact. In July 2004, he complained of disability to flex in his ring and little fingers. After physical examinations, we made a diagnosis of spontaneous rupture of the flexor tendons. An open repair was performed in August 2004. During the surgery, we observed granulation tissues proliferating around the flexor tendons () and a rupture of the flexor tendons of the ring and little fingers. The granulation tissues were removed, and the superficial flexor tendon was transferred to the ring finger. Tendon graft of the palmaris longus to the little finger was also performed. Histologically, the granulation tissues showed chronic synovitis (), and acid-fast bacilli were negative. There was no apparent granuloma suggesting of sarcoidosis. The patient regained good function of the operated ring and little fingers with no evidence of recurrence at the latest follow-up in March 2009.
A 24-year-old woman of African descent with prior normal vision was referred to us from a specialized ophthalmic center for a preoperative cardiovascular assessment. She had chief complaints of gradual decline in visual acuity in both eyes for 3 years and unintentional weight loss (17 kg) within the past 1 year. Her past medical history was unremarkable except for a self-reported history of pulmonary tuberculosis at the age of 4 years. Her progressive loss of vision which initially started in her left eye and later involved her right eye was associated with intermittent pain, redness, tearing, and headaches. Within the first year, she completely lost vision in her left eye. She denied any history of arthralgias, claudication, skin lesions, chest pain, convulsions, or syncope. She had several out-patient visits in the past 3 years all due to her ongoing visual impairment. She was prescribed gentamycin eye drops, carbimazole, propranolol, furosemide, and multivitamin capsules at different points in time with no relief of her deteriorating vision.\nHer physical examination revealed feeble brachial and radial arterial pulses on her left side, whereas pulses on her right side and in both lower limbs were normal. Her blood pressure was 85/59 mmHg on her left and 134/82 mmHg on her right side. She had a pulse rate of 136 beats/minute which was regular and of good volume, body temperature of 37.0 °C, and a body mass index (BMI) of 19.6 kg/m2. On ophthalmic examination, she had no light perception in her left eye but she could count fingers at a 2-meter distance using her right eye. Bilateral microaneurysms, dot and blot hemorrhages, and multiple ischemic areas of retina together with neovascularization in her right eye were noted during a funduscopic examination. These ophthalmic findings are in line with a bilateral ocular ischemic syndrome.\nLaboratory results revealed an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) of 56 mm/hour and 25.4 mg/L respectively. Electrolytes, liver, renal, and thyroid function tests were normal. Serology for human immunodeficiency virus (HIV), hepatitis B and C, Venereal Disease Research Laboratory (VDRL) test for syphilis, rheumatoid factor, anti-double-stranded DNA (dsDNA), and antineutrophil cytoplasmic antibody (ANCA) were negative, however, antinuclear antibody (ANA) was positive. A tuberculin test was negative. There were no aneurysmal formations, bruits, ventricular hypertrophy, or any other cardiac abnormalities apart from a sinus tachycardia and trace aortic regurgitation. We did not perform coronary angiography or computed tomography (CT) angiography of her head and neck due to her financial constraints. A CT angiogram of her thoracic and abdominal aorta revealed irregular narrowing with variable degrees of stenosis, tapering, and corrugated appearance (Figs. , , and ). Based on the clinical presentation, physical findings, and angiographic features, she fulfilled the American College of Rheumatology criteria [] for Takayasu’s arteritis. However, we could not rule out temporal arteritis in this case as our patient refused a temporal artery biopsy procedure. Nevertheless, based on the age of onset (that is, <40 years) and the clinicoradiographic picture (decreased pulsation of brachial artery, difference of over 10 mmHg in systolic blood pressure between arms, and arteriographic narrowing of aorta) we entertained a diagnosis of TA. She was counseled and treated with dexamethasone (60 mg per day), methotrexate (10 mg per day), and low-dose aspirin (75 mg once daily). She was discharged home on self-request after 9 days of hospitalization. We reviewed her as an out-patient after 3 months but there was neither improvement nor further deterioration in her visual acuity despite self-reported good adherence.
A 65-year-old African man presented to our emergency department 5 hours after severe chest pain onset. He is a tobacco smoker, diabetes status unknown, neither hypertensive nor dyslipidemic, and had no history of stroke. He had no personal or family medical history, including heart disease or heart rhythm disorder, and he was not under any treatment prior to diagnosis. He was from a low socio-economic level. An EKG showed a sinus rhythm with ST-segment elevation in inferior and posterior leads (Fig. ). At admission he was conscious, GCS of 15/15, without motor deficit or sensory disorder; his chest pain was constrictive irradiating to his two upper limbs without syncope. BP on admission was at 190/120 mmHg symmetrical, pulse rate at 122 bpm, heart sounds clearly auscultated, no heart or carotid murmur, there was no murmur of mitral insufficiency or ventricular septal defect, no signs of heart failure including no crackles, and he was without edema of his lower limbs or turgor of his jugular veins leading to a right ventricular infarction. His peripheral pulses were perceived symmetrically. The rest of the examination was strictly normal. Acute inferior and posterior STEMI was diagnosed and intravenously administered TT using tenecteplase (intravenous bolus of 35 mg considering a weight of 65 kg) was performed after lowering BP at 150/90 mmHg, associated with aspirin 300 mg administered orally and clopidogrel 300 mg administered orally. It is important to note that the first dose of heparin was missed. Echocardiographic examination (Vivid 6S) was performed following the therapy. It revealed segmental wall motion abnormalities, LVEF at 50%, no mitral valve insufficiency, pulmonary artery pressure at 29 mmHg, and no thrombus or any mechanical complication was detected. One hour after TT, his chest pain and more than 50% of ST-segment elevation resolved with no hemorrhagic complications. The laboratory findings were as follows: troponin Ic, 9 ng/ml; normal liver function tests; serum creatinine level, 14.9 mg/l; estimating a GFR at 50.5 ml/1.73 m2 BSA per minute using MDRD; hemoglobin, 16.3 g/dL; hematocrit, 49.5%; platelets count, 281,000/mm3; plasmatic fibrinogen level, 7.4 g/l; WBC, 14,900/mm3; and CRP, 62 mg/l.\nTen hours later, he developed a left hemiparesis with motor aphasia without sensory disturbance and drowsiness: GCS of 14/15. The first cerebral CT performed 3 hours later was normal and the one performed 24 hours later showed right internal capsule ischemic stroke without hemorrhagic infarct (Fig. ). An echo-Doppler of the supra-aortic trunks was normal. The case was discussed with neurologists and aspirin 75 mg administered orally once daily, clopidogrel 75 mg administered orally once daily, and unfractionated heparin, which was monitored by partial thromboplastin time (PTT), were continued. His neurological condition improved (level of consciousness and motor deficit). He was discharged after 12 days of hospitalization; physiotherapy and neurological follow-up were planned. One month after discharge, PCI using a bare-metal stent (BMS) was performed on a circumflex coronary artery lesion.\nHe was followed-up regularly after discharge every 2 months. At 1 year of follow-up, clinically he no longer presents a deficit, he is without recurrence of chest pain, and the ischemic image at a cerebral control scan disappeared. No hemorrhagic complications were developed under dual antiplatelet therapies (DAPT). Clopidogrel was stopped after 6 months.
A 10 year old white girl with severe (class 3: BMI ≥140% of the 95th percentile for age and sex) obesity and otherwise normal development presented to the Pediatric Weight Management Clinic with her mother. The mother reported that the patient had been at the 75th percentile for height and weight for most of the patient's life but she experienced a “20 to 30 pound” weight gain over the past year. The mother further explained that this recent weight gain coincided with treatment of seasonal allergies with montelukast and she wondered if this may have been the cause of the weight increase. The patient had no prior weight loss attempts.\nThe patient was born full term, weighing 3.18 kg. The mother's pregnancy was uncomplicated, as was the patient's newborn course. Aside from seasonal allergies, the patient was healthy. She had no history of hospitalizations, surgeries, or mental health concerns. She was not taking any medications.\nThe patient was eating regularly-spaced meals consisting primarily of highly processed foods and simple carbohydrates (e.g., pastries for breakfast, potatoes with cheese for dinner). The family was eating fast food three times per week on average. The patient endorsed having a big appetite and feeling hungry all the time. She was eating while watching TV and when bored. She denied binge eating, loss of control eating, emotional eating, sneaking/hiding food, or eating during the night. Her physical activity was limited to gym class at school three times per week.\nThe patient was living with her mother and her mother's partner. The patient's parents divorced when she was very young and the mother's partner had been living with them since the patient was a toddler. The patient saw her biological father rarely. She had no siblings. She was attending fourth grade and enjoyed reading and writing. The mother and her partner worked full-time and the patient was cared for by a baby sitter after school a few times per week. They had no food insecurity. The family history was notable for obesity in both biological parents and type 2 diabetes in the maternal grandmother.\nThe patient's review of systems was negative. She reached menarche several months prior to presentation. On physical examination, her weight was 70.31 kg (155 lbs.), height was 142 cm (4'8”), and BMI was 34 kg/m2 (145% of the 95th percentile). Her blood pressure was 105/65 mmHg and pulse was 74 beats per minute. Her physical examination was normal. The results of her fasting labs were: total cholesterol 176 mg/dL (normal: < 170 mg/dL), HDL-c 49 mg/dL (>45 mg/dL), LDL-c 96 mg/dL (< 110 mg/dL), triglycerides 157 mg/dL (< 90 mg/dL), ALT 27 (< 50 U/L), AST 29 (< 50 U/L), glucose 98 mg/dL (70-99 mg/dL), and HbA1c 5.5% (0-5.6%). Her Pediatric Symptom Checklist (routinely obtained in the Pediatric Weight Management Clinic) score was 8 (> 28 is considered abnormal).\nThe patient and family were started on a program of lifestyle modification therapy and responded particularly well with decreasing fast food consumption and liquid calories. Further, the patient started bringing her lunch to school instead of eating the school fare and was able to keep a food log almost daily. The patient's physical activity, however, continued to be limited. Over the course of 5 months, the patient's BMI decreased 5 units (15%), from 34 kg/m2 to 29 kg/m2 (145% of the 95th percentile to 125% of the 95th percentile).\nAt the end of the 5 month period, coinciding with the end of the school year and beginning of summer vacation, the patient's sleep/wake cycle became irregular. Because she did not like the hot weather, she chose to stay inside all day. Her mother left prepared meals for the patient to encourage healthy eating while mom was at work. Despite this, the patient's BMI began to trend upward from 29 kg/m2 to 31 kg/m2 over the summer months. Upon school resuming in the fall, the patient's sleep/wake cycle normalized and eating behaviors and patterns improved, returning to those of the previous school year. The patient's BMI stabilized for a few months but then increased further. The patient expressed frustration because she believed that she was eating well, which was indeed reflected in her daily food logs. She continued to attend monthly visits with the Pediatric Weight Management Clinic dietician, psychologist, and pediatrician with specialized training in obesity medicine. Yet, the patient's BMI continued to increase such that by 2 years after her initial appointment, the patient's BMI returned to baseline (135% of the 95th percentile) (see Figure ).\nSuspecting that metabolic adaptation was causing the patient's weight rebound, adjunct pharmacotherapy was recommended. Orlistat was considered but not started because of concern about gastrointestinal side effects and lack of insurance coverage. Metformin may have been another reasonable option but the patient's fasting glucose and HbA1c were in the normal range and she did not have acanthosis nigricans on physical examination which would have suggested insulin resistance. She was ultimately started on topiramate 75 mg daily in addition to ongoing LSMT. She and her mother were cautioned that although topiramate is not FDA-approved for the indication of obesity (in children or adults), multiple studies have demonstrated clinically-meaningful weight loss efficacy in adults. Additionally, it was explained that the side effect profile in children is well established stemming from its use for epilepsy treatment.\nAfter 4 months of treatment with topiramate, the patient's BMI trajectory plateaued yet was not decreasing as was desired. Recognizing that the combination of topiramate and phentermine is the most effective weight loss medication currently available for adult obesity, phentermine 15 mg daily was added to the topiramate 75 mg daily. The patient and mother were informed that phentermine is FDA-approved only for individuals older than 16 years and for “short-term use.” With combination treatment for ~22 months, the patient experienced good BMI reduction, from 34.1 to 25.7 kg/m2. Her blood pressure and heart rate were monitored regularly and though her blood pressure did not increase, her heart rate increased slightly from 60 to 70 s, in line with the mechanisms of action of phentermine (stimulant-like effects). Later, the patient reported that she was experiencing some “memory” issues but noted no change in her academic performance. Although it seemed unusual for this type of symptom to emerge 10 months after starting topiramate, the topiramate dose was decreased from 75 to 50 mg daily and the memory issues resolved. Written informed consent was obtained from the parent of the patient for the publication of this case report.
An 82-year-old man was admitted to our hospital because of appetite loss and anemia. His medical history included chronic obstructive pulmonary disease and dementia. On physical examination, he was 150 cm tall and weighed 45 kg. His abdomen was soft and flat and showed no palpable masses. Laboratory tests revealed hypohemoglobinemia (Hb 7.5 g/dl) and hypoproteinemia (albumin 2.5 g/dl); all other results were normal. Upper gastrointestinal endoscopy showed a type 1 hemorrhagic tumor located in the middle body of the stomach, although observation of the entire stomach was impossible because of extreme transformation. An upper gastrointestinal series showed organoaxial rotation of the body of the stomach with the entire stomach located in the mediastinum, which is indicative of upside-down stomach. The tumor was present in the upside-down stomach through a PEH (fig. ). Pathological analysis of biopsy specimens revealed moderately differentiated tubular adenocarcinoma. Coronal computed tomography images showed an organoaxial gastric volvulus and sliding up through a PEH (fig. ). A gastric tumor was detected in the upside-down stomach through the PEH and lymph node metastases were observed surrounding the stomach; however, liver metastases and peritoneal dissemination were not observed. Preoperative staging according to the TNM classification of gastric cancer was T3N2M0, stage IIIA. On the basis of the preoperative diagnosis of gastric cancer arising from an upside-down stomach through a PEH, the patient underwent surgical treatment.\nSurgery was performed via a median laparotomy incision. The entire stomach was found to be herniated through the enormously dilated hiatus into the left thorax together with the greater omentum (fig. ). The hernial orifice was approximately 5 cm in diameter (fig. ). After the incarcerated stomach had been untwisted and reduced back into the abdomen, the tumor was found to be located in the middle body of the stomach; however, the short esophagus was not found in the state of esophagus. After reduction of the abdominal contents from the thoracic cavity, a total gastrectomy with a Roux-en-Y reconstruction and dissection of the lymph nodes surrounding the stomach was performed. The crura of the diaphragm were approximated with interrupted nonabsorbable sutures for closure of the hernial orifice. The jejunum just under the anastomosis was sutured to the crus to permanently fix the esophagojejunal anastomosis in an abdominal position (fig. ). In consideration of the patient's age and preoperative performance status, a jejunostomy was constructed as a route of enteral nutrition after surgery.\nThe resected specimen revealed a type 1 hemorrhagic tumor measuring approximately 7.7 × 7.4 cm (fig. ). Histopathological examination revealed a moderate tubular adenocarcinoma with vascular invasion and metastasis in three lymph nodes surrounding the stomach, and the final clinical stage was IIIA (T3N2M0) according to the TNM classification.\nThe postoperative course was uneventful. Roentgenography showed good passage without leakage of the anastomosis, and oral intake was initiated on postoperative day 7, although no increase in food intake was achieved. Therefore, the energy deficit was supported by enteral nutrition through the jejunostomy. The patient was discharged 35 days after surgery, and there was no recurrence of cancer or hernia during 1-year follow-up.
A 45-year-old male was referred to our department for an unexplained onset of cervical discomfort and painful swelling in the left anterior area of the neck. The patients complained of acute febrile episode (39–40°C) two weeks before our evaluation, treated by ceftriaxone (2 grams daily). Physical examination showed the presence of goitre, predominantly in the left lobe, characterised by the presence of very firm tissue. The laboratory findings are reported in .\nNeck ultrasound showed an enlarged thyroid left lobe characterised by the presence of a dishomogeneous marked hypoechoic tissue surrounding a hyperechoic nodular lesion with antero-posterior diameter of 15 mm and transverse of 16 mm. Both areas were promptly submitted to fine needle aspiration cytology (FNAC). During FNAC, the hypoechoic tissue felt remarkably harder than the hyperechoic nodule.\nThe cytology of the hypoechoic tissue showed blood and histiocytes whereas that of the nodule showed necrotic material and polymorphonuclear leukocytes.\nTaking in account the cytological result, and moreover, the increasing symptoms of mechanical complaints such as dysphagia and dyspnea reported to the patient, he was submitted to total thyroidectomy.\nThe surgeon found an extremely firm thyroid tissue adhered to adjacent structures including parathyroid glands, trachea, neck vessels, and perithyroid muscles, making dissection very difficult.\nOn gross examination, the gland was found to be asymmetrically enlarged with adherent fibroadipose and muscular tissue on the left. The cut surface was pale grey to white, firm, and fibrotic, with a cystic area containing purulent exudate ().\nHistopathologic examination showed that the left lobe, the isthmus, and roughly the right lobe were destroyed and extensively replaced by a dense, inflamed fibrous tissue, which involved blood vessels, and extended into the perithyroidal soft tissue (Figures and ), encasing one lymph node and one parathyroid gland.\nIn the right lobe, thyroid follicles were almost completely replaced by a dense nodular chronic inflammatory infiltrate with germinal centers. Residual follicular epithelium was atrophic with extensive oncocytic metaplasia (). Finally, the cystic area was an abscess with cellular debris, neutrophils, occasional eosinophils and histiocytes.\nMicroabscesses were seldom seen in the close parenchyma ().\nImmunostains for CD20, CD3, and immunoglobulin light chain showed a mixed and polyclonal pattern of B-cell and T-cell phenotype which excluded extranodal marginal zone B-cell lymphoma. The absence in the dense fibrous stroma of cytokeratin stains for AE1, AE3, CAM5.2, Ck7, panCk (Ck5,6,8, and 17), and Ck19 excluded paucicellular variant of anaplastic thyroid carcinoma or a diffuse sclerosing variant of papillary carcinoma. A solitary fibrous tumour was excluded by the absence of reactivity for CD34 and bcl-2.\nOur diagnosis was combined Riedel's disease and fibrosing Hashimoto's thyroiditis showing coexisting suppurative thyroiditis.\nHe was submitted to a whole body tomography with contrast enhancement that excluded a multifocal fibrosis involvement.\nNow the patient is in good health, undergoing thyroid replacement therapy (levothyroxine 100 mcg/daily).
A 74-year-old woman visited our station with squamous cell carcinoma (SCC) on the right buccal mucosa. Her past medical history included chronic obstructive airways disease, hypertension, and diabetes mellitus. The patient is a current smoker, with a history of 20 pack-years. Preoperative chest radiography, electrocardiogram, full blood count, and serum biochemistry were within the normal range. After being diagnosed with SCC as a result of incisional biopsy, the patient underwent the resection of SCC on the right buccal mucosa of the mandible, modified radical neck dissection, and primary reconstruction with a fibula-free flap. Tourniquet pressure was 300 mm/Hg, and its application time was 60 min. Total on-table time was approximately 7 h. Upon admission to the SICU after the 7-h operation, hypothermia and hypotension were noted. On the first postoperative day, the patient exhibited oliguria and proteinuria and elevation of CK, AST, ALT, and LDH. Together with the nephrology and neurology staff, we tried to figure out our patient’s symptoms and clinical findings. We thought that her clinical picture was based on an impression in which acute renal failure was diagnosed as secondary to rhabdomyolysis. Thus, she was managed with high-dose loop diuretic therapy. Additionally, we gave her hepatotonic to recover her liver function. The patient was supplemented with 150 to 250 mL/h of lactated Ringer’s solution and 0.9% NaCl. When the volume was full, urine output of above 100 mL/h was maintained by 20 mg intravenous injection with furosemide.\nHer urine output for the first hour is at 20 mL/hour, but after the medication, her urine output began to improve on day 4 with a corresponding reversal in the serum creatinine. After postoperative day 4, the muscular enzyme showed a downward trend. We treated the patient with medication and hydration, and then the result became favorable. In the end, she was able to recover fully from the symptoms. Figures and show the change in serum enzyme levels during hospitalization (Figs. and ).
A 71-year-old woman underwent PEG using a 20-Fr introducer PEG kit at the age of 65 years, due to severe dysphagia caused by disuse syndrome after an emergent surgery for necrotic ischemic colitis. She had a bipolar disorder and was severely frail. She gradually resumed her oral intake due to the effects of continuous rehabilitation, and finally the PEG tube was removed at six years after PEG. However, the gastrostomy site did not close spontaneously over a period of one month despite conservative medical management using a proton pump inhibitor. She was admitted to our hospital for the persistent gastrocutaneous fistula.\nOn admission to our hospital, her height and weight were 155 cm and 35 kg, respectively. Body mass index (BMI) was 14.6. Severe dermatitis was observed around the gastrostomy site. Esophagogastroduodenoscopy (EGD) on day 1 revealed a gastrocutaneous fistula on the anterior antral wall (Figure ).\nThe size of the fistula measured by endoscopy was 6 mm. OTSC closure was chosen over surgical closure considering the patient’s general condition. On day 4, OTSC closure (size 9 mm, t-type) using the suction method was performed (Figure ).\nA GIF-Q260J endoscope (Olympus, Tokyo, Japan) was used for this procedure. Following the OTSC closure, leakage of gastric juice from the fistula stopped after the OTSC closure but started again two days later. EGD on day 8 revealed the OTSC dropping off from the fistula, which was endoscopically removed (Figure ).\nA second attempt for OTSC or surgical closure of the fistula was not performed considering the invasiveness of the procedure and further increase in the medical cost. Instead, PEG was performed through the same fistula as the patient still had mild dysphagia and was concerned about the exacerbation of the symptom due to the underlying condition. No skin problems were observed after the PEG procedure. On day 18, the patient was discharged and transferred to the long-term care hospital where she was originally hospitalized.
A 41-year-old woman was admitted to the hospital with mild abdominal pain, discomfort, and bloating on the abdomen. In recent years, the patient had mildly suffered from these symptoms. The patient did not complain of weight loss, nausea, vomiting, weakness, or anorexia, but she was worried about increasing waist circumference and some dyspeptic symptoms. Physical examination revealed a big, relatively mobile, nontender, smooth solid mass occupying almost the entire abdomen. There was no evidence of mechanical bowel obstruction. There was no history of any abnormalities of the digestive system, liver or renal failure, gynecological malignancy, or any other reason to cause abdominal ascites. All hematological and biochemical parameters were within normal range. Also, tumor markers (please be specific) were normal. A solid, well-defined mass lesion measuring approximately 40 cm in greatest diameter was reported on ultrasound (USG). On magnetic resonance imaging (MRI), T1-weighted axial and coronal MR images showed a hyperintense giant mass filling most of the abdomen and displacing the bowels. The lesion was also compressing the liver. In fat-saturated T1-weighted MR images, the signal of the mass was suppressed similarly to fat. The mass did not enhance with contrast. The lesion measured approximately 34 cm × 26 cm in size (Figures –). Given the symptomatic nature of the mass, surgical resection was recommended. A laparotomy was performed by midline abdominal incision. Operative exploration revealed a giant mass with a smooth surface, encapsulated and lobulated that was originating from the greater omentum.\nIt was extending along the falciform ligament to the posterior liver and filled the entire abdomen and pelvis caudad without strong adhesion to adjoining tissues and organs. The mass displaced the intestines posteriorly but did not cause obstruction. Also, the entire colon was intact. The mass was completely extracted without any violation of lipoma capsule. The final specimen measured 40 × 26 × 8 cm and weighed 11,520 g (). Macroscopically, the specimen was a soft, encapsulated yellow fatty mass, and the cut surface consisted of homogenous fatty tissue. Pathological examination with hematoxylin-eosin staining revealed fine-encapsulated mature adipose tissue without atypia or malignant degeneration or necrotic tissue, consistent with a mature benign lipoma. In postoperative follow-up, liquid food was tolerated on the first postoperative day and solid food on the second day. She was discharged without any complications on postoperative day 3. No recurrence was observed during the 4-year follow-up.
A 59-year-old male, known diabetic and hypertensive for the past 5 years and on medications, presented with a history of breathlessness on exertion for the past 2 months. There was no history of chest pain, cough, palpitations or syncope. On examination no significant findings could be elicited. Laboratory investigations and complete haematological profile was within normal limits (no features of hypercoagulable disorders). Echocardiography showed dilated right atrium and right ventricle with impaired right ventricular systolic function. The pulmonary valve appeared thickened with possible mass attached to it, with turbulence and gradient in the main pulmonary artery. A contrast enhanced CT was performed which revealed a hypodense filling defect in the main and bilateral pulmonary arteries which did not exhibit any significant post contrast enhancement (Fig. ). Based on the clinical and radiological findings a diagnosis of pulmonary thromboembolism was made and pulmonary thromboendarterectomy was planned. Under GA, midline sternotomy was performed and main pulmonary artery was opened. Grey white organised mass with thrombosed areas was removed by separating it from the main pulmonary artery, bilateral pulmonary artery branches and pulmonary valves. On histopathology the tumor was composed of spindle to epithelioid cells exhibiting moderate to marked pleomorphism with vascular growth pattern and prominent areas of intratumoral haemorrhage and fibrinoid necrosis. Interspersed were mitotic figures and areas of focal myxoid change showed features of high grade sarcoma involving the media and intima and the lumen of the pulmonary artery with epithelioid morphology (Fig. a, b). On Immunohistochemistry, tumor cells were diffusely positive for Fli1 (Fig. c), which is a surrogate vascular marker; focally weakly positive for CD31, while were negative for CD34. Tumor cells were negative for SMA, desmin and H-caldesmon (myogenic/myofibroblastic markers). The final diagnosis was primary pulmonary artery high grade sarcoma and the suggestive histogenesis was vascular (angiosarcoma).\nThe immediate post-operative period was uneventful. Two-month post-surgery patient present with on and off pleuritic type of chest pain and was referred to our tertiary care centre for further management. As a part of the work up, Cine-cardiac MRI was performed which showed non-enhancing altered signal intensity lobulated mass in the left pulmonary artery with both exophytic and endophytic intravascular component (Fig. a–d). CT was performed to rule out pulmonary metastatic disease however CT thorax revealed ill-defined focal patchy pneumonic areas in bilateral lung parenchyma that were in favour of pulmonary changes as a sequel to chronic thromboembolic phenomenon (Fig. e, f). In view of the progressive residual disease patient was treated with definitive external beam radiotherapy (60 Gy in 30 fractions; dose per fraction: 200 cGy). During the course of treatment patient had occasional haemoptysis which resolved spontaneously. Follow-up imaging after 12 cycles of radiotherapy revealed significant progression of the primary disease with new development of pulmonary parenchymal metastasis (Fig. ). In view of the disease progression with short disease free interval period the patient is currently treated with metronomic therapy.
A 42 years old male presented to the emergency room with the alleged history of suicidal ingestion of an unknown poison 2 hours back following a family dispute. The patient immediately had two episodes of nonbilious nonprojectile vomiting followed by excessive lacrimation, bowel and bladder incontinence, and dizziness within 2 hours of ingestion of the poison. There was no history of shortness of breath, chest pain, loss of consciousness, or seizures. He did not have any past medical or psychiatric history or similar suicidal attempts in the past. On examination in the emergency room, the patient was drowsy but followed verbal commands. He had a radial pulse of 50 beats per minute, blood pressure of 90/50 mm Hg, respiratory rate of 16 breaths/minute, temperature of 98.6 degrees Fahrenheit, and oxygen saturation of 94% in room air. His pupils were three millimeters in size bilaterally and reacting to light. Furthermore, the peculiar garlicky smell of organophosphate was not detected from his breath. His chest auscultation was clear, abdomen was soft and nontender, and the remaining systemic examination did not reveal any abnormality.\nWith the provisional diagnosis of a possible organophosphorus poisoning, the patient was managed initially by administering an intravenous dose of atropine 0.6 mg following which his heart rate increased to 100 beats per minute showing a normal sinus rhythm in the 12-lead electrocardiogram. Dermal decontamination was done by removing the patient's vomitus soaked clothing. The skin was cleaned thoroughly with soap water, and gastric lavage was performed simultaneously. A bolus dose of 500 mL of 0.9% normal saline and an intravenous dose of pralidoxime 2 grams over 30 minutes were administered. His investigations comprising a full blood count, arterial blood gas, renal function tests, a random blood sugar level, liver function tests, a coagulation profile, and a serum cholinesterase level were all within normal limits. A chest radiograph and an ultrasonogram of the abdomen and pelvis did not reveal any abnormalities.\nA bottle of the herbicide pretilachlor 50% emulsifiable concentrate (EC) was retrieved from his room and was brought to the emergency room by his son after 2 hours. The patient confirmed to have consumed the full bottle containing 250 mL of the herbicide. Close monitoring with continuous supportive management was done for 24 hours with intravenous fluids and antiemetics following which he gradually became asymptomatic. His heart rate remained within the normal range, his blood pressure normalized, and a normal urine output was maintained throughout the hospital stay. Symptoms of lacrimation and incontinence subsided. Repeat blood counts, renal, and liver functions were within normal ranges. He was kept under observation with strict hemodynamic monitoring for the next 2 days which was uneventful. He was discharged from the hospital on the third day after a behavioral counseling session. He was in good health during a 1-week follow-up in the outpatient department.
A 2-year-old healthy boy underwent an office-based surgical circumcision by his physician. During the procedure, profound bleeding was observed that was not controlled by applying direct pressure. The physician attempted to control the bleeding by multiple deep suturing; the bleeding was stopped successfully and the patient was discharged home. During the postoperative period, the child had progressive painful and difficult voiding with only few drops of urine after straining. During this period the child was prescribed painkillers for his discomfort and no additional evaluation was done. After about a week he was referred to a district hospital with fever (temperature=38.1C), agitation, vomiting, urinary retention, and significant abdominal distension. Abdominal examination showed decreased bowel sounds, dull percussion, and severe guarding. Urgent abdominopelvic ultrasound revealed large volume of free fluid in the abdomen and pelvis, with small amount of urine in the bladder. The initial lab tests also showed leukocytosis with left shift and increased blood creatinine and blood urea nitrogen. Catheterization with a 6-Fr feeding tube failed because it did not pass beyond the subcoronal urethra. The patient underwent emergency midline laparotomy with the diagnosis of acute abdomen and the fluid was drained. A small intraperitoneal bladder rupture was noticed at the dome of bladder. The gastrointestinal tract was inspected precisely and was intact. The diagnosis of intraperitoneal bladder rupture with urinary ascites was made probably due to near-total urethral obstruction. The rupture site was repaired in two layers and a suprapubic cystostomy catheter was fixed.\nTwo months later, the patient was referred to our center for further evaluation and treatment. Antegrade voiding cystourethrography (VCUG) was performed via the suprapubic catheter that showed terminal urethral obstruction (). Urethroscopy was attempted under general anesthesia that failed due to complete obstruction at 1 cm from the meatus.\nDecision was made to explore the area and to repair the urethra. Through a circumferential incision, distal urethra was elevated from the corpus spongiosum. A 3-Fr ureteric catheter also did not pass the obstructed part (). A 5-mm fibrotic tissue was encountered at the site of obstruction (). The corpus spongiosum was dissected free from the corpora cavernosa to prevent iatrogenic chordee after end-to-end urethral anastomosis. The obstructed fibrotic part of urethra was completely resected and an end-to-end urethral anastomosis was performed along with spongioplasty over an 8-Fr silicon catheter in two layers; dartos pedicled flap was used to cover the site of anastomosis. The postoperative period was uneventful and the patient was discharged home with suprapubic and urethral catheter. The urethral catheter was removed seven days following the surgery. The suprapubic catheter was removed four weeks after the surgery following normal urethral voiding and normal ultrasound. A VCUG was performed six weeks after the surgery that showed normal bladder and urethra with acceptable voiding per urethra (). During a 2.5-year follow-up period, the patient was asymptomatic with normal renal function, ultrasound, and voiding pattern. He had a maximum flow rate of 15.3 ml/sec in uroflowmetry study.
A 26-year-old Thai woman presented with a foreign body in her left orbit that had been retained for 8 months. Eight months previously, she had sustained a gunshot injury to her left eye. There was only a small wound on her left eyelid (Fig. ); she had normal eye movement, a normal visual field, and no pain. A plain radiograph was performed at that time; it detected a round-shaped metallic foreign body located medially in her left eye globe. She was then diagnosed as having a retained foreign body in her left orbit and she was advised to have clinical observation. However, 8 months later, she developed pain in her left eye without any sinonasal symptoms. After discussion about the risk of surgery and retention of an orbital foreign body, an ophthalmologist referred her to our department for the minimally invasive procedure option of removal of the foreign body using an endoscopic transnasal approach. On examination, the movements of her left orbit were not restricted and there was normal visual acuity (20/20) with no proptosis or chemosis. A computed tomography (CT) scan of her left orbit revealed a round-shaped metallic foreign body in the medial intraconal space, and lateral attachment of posterior ethmoid sinus, measuring 6 mm (Fig. ). A transnasal endoscopic approach, with navigator assistance (Brainlab), was used to remove the bullet. Uncinectomy and anterior-posterior ethmoidectomy were performed. The location of the intraconal metallic foreign body was confirmed with a navigator system, then part of the lamina papyracea was removed and the periorbita incision was done. The defect was enlarged and the fibrotically encapsulated bullet was found lying in the orbital fat (Fig. ). The fibrotic capsule was dissected, and the bullet was delivered through her left nostril with probes and curetted (Fig. ). No intraorbital bleeding or damage to any soft ocular structures was noted. A relative afferent pupillary defect was found in her left eye during removal of the foreign body, but it resolved and no postoperative complications were observed.
This is a case of a 59-year-old morbidly obese female with situs inversus totalis who presented for a laparoscopic sleeve gastrectomy. Her BMI was 38 (height 4 ft 11.5 inches, weight 188.2 pounds), and she had a lifelong history of morbid obesity and obesity-related comorbidities, including obstructive sleep apnea requiring a continuous positive airway pressure machine, an elevated hemoglobin A1c (5.8) and a fasting blood glucose increasing her risk of developing diabetes mellitus, and degenerative joint disease which significantly impacted her ability to exercise. The main challenges she identified in losing weight involved eating carbohydrate rich foods, overeating during meals and limited activity due to musculoskeletal pain. The patient had made multiple attempts to lose weight through commercial dieting programs but had been unsuccessful. The patient also completed a six-month medically supervised diet through her primary care provider, which also included working closely with a bariatric registered dietician, following a strict diet of about 1800 calories/day and performing modified exercise, about 120 minutes/week. Despite these intense medical weight loss efforts, she was unable to maintain a healthy weight. The patient was motivated to try bariatric surgery after she witnessed the significant weight loss success her daughters had from this intervention. Her greatest hope from the bariatric surgery was to be healthier and to alleviate her obesity-related comorbidities.\nThe patient’s surgical history included cesarean section and evacuation of an ectopic pregnancy. She was a former smoker, quitting over 25 years ago, and has no other history of substance or alcohol use. Family history is positive for obesity, diabetes, hypertension, coronary artery disease and hypercholesterolemia. She did not take any medications, including supplements, except for Ibuprofen 800 mg 1–3/daily for musculoskeletal pain.\nThe patient underwent a comprehensive evaluation and treatment plan prior to the surgery including: psychiatric evaluation and clearance, nutritional consultation with a registered dietician, education about bariatric surgery and pre/post op expectations, routine preoperative labs, UGI, esophagogastroduodenoscopy (EGD), pulmonary function analysis, and a cardiovascular exam. Situs inversus totalis was confirmed with abdominal X-ray and CT, and echocardiogram. Pre-procedural evaluation with UGI revealed mild gastroesophageal reflux observed to the level of the distal one-third esophagus and small sliding-type hiatal hernia. EGD revealed normal esophagus and duodenum. Stomach biopsy was obtained for antral gastritis, and no helicobacter organism was identified. Abdominal ultrasound confirmed fatty liver disease. Pulmonary function analysis including spirometry, lung volumes and diffusion was normal. A pre-procedural cardiovascular exam was performed due to dextrocardia to exclude other structural cardiac abnormalities. 2-D echocardiography with M-mode demonstrated a left ventricular ejection fraction of 60%, no structural abnormalities in the aortic, pulmonic, tricuspid and mitral valve, or right and left atrium and ventricles. Color Doppler and continuous and pulse wave Doppler demonstrated mild pulmonic regurgitation and mild tricuspid regurgitation.\nThe patient discontinued the Ibuprofen more than one month before her surgery and began a low-calorie liquid diet two weeks prior to surgery. On the day of surgery, preoperative antibiotics, Cefazolin, were given within 60 minutes before the first incision. Prior to induction, the patient received 5000 units of heparin subcutaneously and sequential compression device (SCD) boots were placed for deep vein thrombosis (DVT) prophylaxis. No beta-blockers were administered. The patient was placed in the supine position and general anesthesia was induced. A Foley catheter was placed and the patient was supported with positioning devices including: arms on padded arm boards, gel pad under left axilla, footboard with gel pads, hover mat and a bariatric safety belt over patient’s thighs. The abdomen was then prepped and draped in the standard surgical fashion.\nA Veress needle was used in the right upper quadrant to access the abdomen and insufflation was created to 15 mmHg. Veress was removed and replaced with a 5 mm trocar and the scope was placed. Additional trocars were placed in the following position: right and left 5 mm lateral trocars, right and left 12 and 15 mm supra-umbilical trocars. The placement of all retractors and graspers was adjusted accordingly to the mirror image anatomy of the intraabdominal organs. The primary surgeon was positioned on the left side of the patient and the assisting surgeon on right side of the patient. Situs inversus totalis was confirmed with the majority of the liver oriented to the patient’s right, spleen on the right, greater curvature of the stomach on the right and gallbladder on the left.\nThe operating table was placed in the reverse Trendelenburg position. The patient’s right-sided half of the liver was retracted cephalically using a Nathanson retractor to expose the vicinity of the esophageal hiatus. The peritoneum over the cardia was incised using the Ethicon Harmonic scalpel, and the plane between the cardia and the left crus of the diaphragm was opened to expose the right diaphragmatic crus. No hiatal hernia was present. A point 5 cm proximal to the pylorus along the greater curvature of the stomach was marked corresponding to the incisura angularis just proximal to the crow’s foot of Latarjet’s nerve. The vessels along the greater curvature and all the short gastric vessels were sealed and divided using the Ethicon Harmonic scalpel, freeing the greater curvature and the fundus of the stomach. A 42-French bougie was placed and oriented towards the antrum along the lesser curvature (Figure ). The stomach was stapled and divided alongside the tube in a vertical fashion towards the angle of His (Figures -).\nAn Ethicon Echelon Flex triple staple line power stapler with a total of one black, three green, and one gold staple loads was used. All staple loads were 60 millimeters in length with staple line bio-absorbable reinforcement. Hemostasis at the external staple line was achieved (Figure ). The stomach was removed from the abdomen via the left-sided 15 mm trocar (Figures , ). Intraoperative endoscopy was performed using a 5 mm Olympus Ultrathin gastroscope revealing no areas of stenosis, internal staple line bleeding, nor staple malformation or leak seen. Total operation time was 108 minutes. There were no post-operative complications.\nPost-operative care included pain management and DVT prophylaxis with SCD, heparin and early ambulation four hours post-surgery. A UGI was performed on post-op day 2 with normal findings for a post-bariatric surgery evaluation and clear fluids were started. The patient was discharged on post-op day 3 without any complications. Upon discharge, the patient had a treatment plan that was previously discussed that included instructions for diet and medications, including vitamin supplementation and antacids. At her three-month follow-up, the patient was still without complications and very pleased with her weight loss of 46.2 lbs, weighing 142 lbs (BMI 29).
A 30-year-old female presented to us with swelling of the right shoulder since 1 year, along with the complaints of restricted mobility of the right arm. On local examination, a globular swelling was present at the right shoulder, measuring 6 × 4.5 cm and having a cystic to firm consistency. There were dilated veins over the swelling and the local temperature was raised. X-ray of the right shoulder showed an expansile lytic lesion with soap bubble appearance of the lateral part of the acromion of the right scapula; there was destruction of periosteum and a prominent overlying soft tissue shadow []. Magnetic resonance imaging showed a large heterogeneous mass in the acromion. Serum chemistry, including serum calcium level, phosphorus, alkaline phosphatase, and parathormone level, was within the normal range. Renal and liver function tests were also within the normal range\nThe patient underwent a partial scapulectomy with removal of the acromion and spine of scapula []. The tissue was submitted for histopathological examination.\nGross examination revealed irregular tissue pieces, with firm to hard areas measuring 6 × 4.5 × 4 cm. It had a heterogeneous appearance, with creamy areas mixed with hemorrhagic areas. The cut surface had a variegated appearance, with cystic, hemorrhagic, and necrotic areas.\nMicroscopic examination showed features consistent with the diagnosis of GCT, with polygonal to elongated mononuclear cells mixed with numerous osteoclast-like giant cells []. In some areas, morphology consistent with aneurysmal bone cyst was noted []. A peripheral shell of reactive bone was present. No evidence of malignant change was seen.\nFive months post surgery the patient is doing well. Early active exercises were started for the elbow and hand and passive and active movements of the right shoulder were encouraged. Following this, the patient was able to use his elbow and hand normally and the abduction is now 100° at the operated shoulder joint.
A 15-year-old boy presented with profound painless progressive diminution of vision of right eye since 3 months. Suddenly, in the left eye, he developed a painful red eye during the last 15 days. On ocular examination, best-corrected visual acuity in the right eye was hand movement close to face with an inaccurate projection of rays and in the left eye was 6/60. The right eye pupil was 8 mm in size, dilated, and nonreacting (), and the retina had exudative retinal detachment around the disc with macular edema (). The left eye was congested and the cornea was edematous. The anterior chamber was filled with fibrinous exudates and hyphema (). Hemorrhagic iris nodules were noted in the iris stroma without iris neovascularization. The pupil was 5 mm in size, irregular with multiple posterior synechiae, and sluggishly reacting and covered with fibrinous exudates. The lens appeared clear, but the details of vitreous and retina of the left eye could not be appreciated. An ultrasonography of right eye showed hyperechoic shadow in vitreous and areas of retinal detachment with subretinal fluid collection, but left eye ultrasonography was normal. Intraocular pressures in right and left eye were 12 and 31 mmHg.\nThe episode was preceded by high-grade fever with chills/rigor and multiple skin rashes involving the face and trunks for the past 4 months. It was also associated with painful subcutaneous nodules over the scalp, trunk, and arms followed by painless enlargement of axillary and cervical lymph nodes.\nOn systemic examination, there were multiple papulonodular rashes over the face () and trunk with a subcutaneous ulcerated nodule in the scalp, arm, and back of trunk (). The cervical and axillary lymph nodes were enlarged, firm, nontender, and not matted. Histopathological examination of skin and axillary lymph nodes revealed dense infiltrate of cells composed of histiocytes, lymphocytes, and occasional eosinophils. The histiocytes have scanty cytoplasm, a nucleus with coffee bean appearance and prominent nucleoli with mitosis () and were positive for histiocytic S 100, suggestive of LCH. MRI of the brain showed a well-defined enhancing lesion measuring 2×0.8 cm in the right scalp of superior temporal fossa which was isodense in T1 but hyperdense in T2 and fluid-attenuated inversion recovery with no obvious bony lesion. With the diagnosis of multifocal LCH, chemotherapy in form of injection of vinblastine 6 mg was started by an oncologist.\nFor eyes, the patient was treated with prednisolone acetate 1% eye drop 6 hourly in the right eye and 1 hourly in left eye along with atropine 1% eye drop thrice and brimonidine tartrate 0.2% + timolol maleate 0.5% eye drop twice in the left eye. After consultation with an oncologist, a tapering dose of prednisolone 40 mg tablet once daily along with proton pump inhibitor therapy was started.\nAfter 1 week, vision in right eye improved to counting finger at 1 foot with an inaccurate projection of rays and 6/24 in the left eye. No other significant changes were noticed in the right eye. In the left eye, the conjunctival congestion decreased, cornea became clear, and hypopyon and hyphaema were resolved and fundus glow became visible. The intraocular pressure was 16 and 13 mmHg in each eye. The dose of oral steroids was tapered, and the patient was kept under regular follow-up, but was lost to follow-up after 2 months. Later, the death of the patient due to multiple organ failure was confirmed by the patient’s guardian.
An ex 35 weeker, dichorionic-diamniotic twin A, was born to a 26-year-old G1P2 via caesarean section for pregnancy induced hypertension. His birthweight was 2.06 kg and Apgars were 9,9 at one and five minutes of life. At 3 days of life, patient had a murmur and echocardiogram performed showed a mildly dilated left atrium (LA) without any intracardiac lesions. Two weeks later, a follow-up echo showed progression of the LA dilation, left ventricle dilation, and significant pulmonary venous return from the left lower pulmonary vein, without evidence of a PDA. A Computer Tomography Angiogram was performed to look for vascular anomalies. The imaging showed a large anomalous systemic artery arising from the descending thoracic aorta supplying the left lower lobe. Because he was stable on room air and gaining weight appropriately, we deemed it reasonable to intervene in the APC when he was older, to decrease the vascular injury risks of a cardiac catheterization procedure. However, when he was seen as an outpatient, it was reported that the patient was becoming more tachypneic and not gaining weight as well. Thus, he was taken to the cardiac catheterization laboratory for possible closure of the APC.\nData from cardiac catheterization showed normal baseline cardiac index (5.79 L/min/m2) with normal intracardiac pressures and no intracardiac shunting. The pulmonary artery pressure (15/10 mmHg, mean 13 mmHg) and transpulmonary gradient (5 mmHg) were normal. Aortic cineangiogram showed a large aortopulmonary collateral supplying the entire left lower lung (). A digital subtraction cineangiography performed in the left pulmonary artery (LPA) showed flow only to the left upper lobe (). Since the APC was the only source of left lower lung perfusion, it was not closed at this time.\nHe then underwent surgical unifocalization of the left major aortopulmonary collateral artery onto the left pulmonary artery. The APC itself would not reach the left pulmonary artery and required a segment of the aorta for unifocalization. With that, the aorta was reconstructed with an end to end anastomosis of the descending aorta. Routine postoperative care was taken and he was discharged home safely after 5 days.
A 15-year-old boy presented to the pediatric outpatient clinic with excruciating back pain, mainly localized in the lumbar region for 1 week. He was tossing on bed due to backache. He was unable to bear weight on his lower limbs. There were symptoms of bladder and bowel dysfunction for the last 3 days.\nHe was a resident of an ongoing dengue-outbreak area. He had a recent history of high-grade fever 28 days back with chills, generalized myalgia, arthralgia, headache, and petechial rash, which was diagnosed as dengue fever by serological tests. His previous records included blood investigation reports positive for nonstructural protein 1 (NS1) antigen test of dengue virus as well as decreased platelet counts documented on serial complete blood counts. HIV test was performed, which turned out to be negative.\nThe patient was fully conscious and oriented with preserved higher mental functions. On neurological examination, there was flaccid paralysis involving bilateral lower limbs. Muscle power in the lower limbs was 3/5 (distal more prominently involved than proximal), and generalized areflexia was evident on motor examination. Bilateral plantar reflexes were not elicitable. Abdominal reflexes were absent. There were no signs of meningeal irritation. Neurologic examination of the upper limbs and the cranial nerves was normal. Tingling sensation was present in the bilateral lower limbs.\nThere was no respiratory distress at the time of presentation. Other systems were completely normal. There was persistent tachycardia with a heart rate of 140–150 beats/min. Laboratory parameters showed normal complete blood picture, blood sugars, electrolytes, and kidney function test. Immunoglobulin G and M antibody test were positive for dengue.\nMagnetic resonance imaging (MRI) of the spine was done on the 2nd day of admission to exclude compressive or inflammatory disease of the spinal cord. MRI revealed continuous intramedullary T2 hyperintense signal intensity in the long segment of the dorsal and lumbar cords extending from T5 to the conus medullaris []. Screening MRI brain was normal.\nA provisional diagnosis of LETM was made after considering the patient's symptoms and correlating the clinical examination findings. Cerebrospinal fluid analysis was not possible because the patient did not give consent for the lumbar puncture.\nThe patient was treated with analgesics and intravenous (IV) pulse therapy with methylprednisolone at a dosage of 1 g/day for 7 days and then was shifted to a regimen of oral prednisolone. The oral prednisolone dosage was started at 60 mg/day and then was tapered gradually over 6 weeks. The patient's bladder was catheterized for the first 3 days. Physical rehabilitation therapy exercises were done simultaneously with medical treatment. The weakness dramatically improved with corticosteroids, and the patient was able to walk by the 2nd week of treatment. He was discharged after 17 days of inpatient treatment, with some residual neurologic deficits. In the follow-up after 1 month, the patient had some difficulty in climbing stairs but no difficulty in walking on the floor.\nOur patient had a recent history of dengue fever with rash, thrombocytopenia, and positive NS1 antigen for dengue virus. With all these features and the lack of any other important physical findings, LETM in this patient was probably the result of dengue infection. The patient responded dramatically to corticosteroid treatment with very minimal residual neurological deficit. In our patient, LETM developed in the postinfectious phase of dengue illness. The pathogenesis of myelitis in our case was likely an immune-mediated phenomenon in response to dengue virus infection.
A 17-year-old female patient with no significant medical history presented with a 2-year history of night pain in the lateral aspect of the hindfoot and ankle. She denied any history of trauma. Her symptoms could be partially relieved with aspirin. A plain radiograph showed a sclerotic area in the left calcaneus just inferior to the subtalar joint (). She underwent a needle biopsy of the calcaneus in a local hospital. The pathological report described a small amount of bone tissue with a poor blood supply and no signs of tumors or tuberculosis. She was diagnosed with chronic osteomyelitis and received conservative treatments including analgesic drugs and physiotherapy. One month later, the patient presented to our medical center because the pain had become severe. On physical examination, we found severe swelling of the left hindfoot () with mild tenderness, and the motion of the subtalar joint was limited. A computed tomography (CT) scan revealed a lesion with a sclerotic rim in the anterolateral aspect of the left calcaneus adjacent to the posterior talocalcaneal joint (). Magnetic resonance images showed a well-circumscribed area of low-signal intensity in the anterolateral aspect of the left calcaneus with surrounding edema (). The erythrocyte sedimentation rate and C-reactive protein concentration were within their reference ranges. The tuberculosis antibody titer was negative. A clinical diagnosis of osteoid osteoma was made.\nThe CT images were processed with MIMICS software (Materialise, Ann Arbor, MI). A 3D model of the left calcaneus was created, and the volume (cm3) and position of the osteoid osteoma was determined (, ). A surgical guiding plate was designed to guide a trephine to make a bone window on the lateral aspect of the calcaneus (, ). Both the 3D model of the calcaneus and surgical guiding plate were fabricated by a 3D printer (ZPrinter 450; Z Corporation, Burlington, MA) in our medical center (). After administration of epidural anesthesia, the patient was placed in the supine position, and a suitably sized sandbag was placed under the ipsilateral buttock to maintain the position of the limb. A tourniquet was positioned around the left thigh. A lateral approach was used to expose the subtalar joint. We found effusion in the peroneus tendon sheath, and the cartilage of the calcaneus had been eroded by the tumor. With the aid of the surgical guiding plate, we made a bone window on the lateral aspect of the calcaneus using a trephine. The tumor lesion was easily reached, and complete resection was achieved. The bone defect in the calcaneus was repaired with an autogenous bone graft. The subtalar arthrodesis was completed as planned. The postoperative pathological diagnosis was an osteoid osteoma (). At the 2-year follow-up examination, the patient remained asymptomatic with no recurrence of the osteoid osteoma (, ).
The patient is a 73-year-old man with a history of three previous open right inguinal hernia repairs at other institutions as well as a robotic prostatectomy who presented with a recurrent right and symptomatic left inguinal hernia. Given the patient's history of multiple prior open hernia surgeries, we initially favoured a laparoscopic approach. Given the history of robotic prostatectomy with a post-operative pelvic haematoma and the likelihood of adhesions, we decided on a robotic TAPP approach, which would allow for easier lysis of adhesions, reduction of the hernia sac and sutured closure of the peritoneal pocket.\nOn insufflation of the abdomen, placement of robotic trocars and docking of the da Vinci Si system, a large right indirect inguinal hernia defect containing small bowel was visualised lateral to the inferior epigastric vessels. The peritoneum was incised and the hernia sac reduced into the peritoneal cavity with subsequent development of a pre-peritoneal pocket. An extra-large Bard 3DMax polypropylene mesh (12.4 cm × 17.3 cm) was tacked into place to the pubic tubercle and onto the anterior pubic ramus at Cooper's ligament. The peritoneal defect was then closed using 2-0 absorbable V-Loc (barbed) suture in a running fashion. The left-sided hernia was repaired in the same manner.\nThe patient was discharged home on the same day after surgery but returned to the emergency room on the 2nd post-operative day with complaints of significant abdominal pain, nausea, vomiting and obstipation. He was diffusely tender on abdominal examination and a computed tomography (CT) scan [] was performed demonstrating a high grade closed-loop small bowel obstruction with a transition point in the right lower quadrant. The patient was urgently taken to the operating room where he underwent a diagnostic laparoscopy. The peritoneal closure on the right had dehisced, and a loop of small bowel had incarcerated within it [] which upon reduction appeared bruised but viable. The peritoneum was attenuated and did not hold sutures well, so the peritoneal pocket was packed with Surgicel Nu-Knit to obliterate the dead space and prevent re-incarceration and then repaired using 0-silk figure-of-eight sutures using the Endo Stitch device. The patient's hospital course thereafter was significant for a 10-day ileus which eventually resolved. At 12-month follow-up, there was no evidence of recurrent inguinal hernia, no chronic pain and no recurrent intestinal obstruction.
Our patient, a 12-day-old Asian male infant, weighed 1025 grams and was the second twin born of in-vitro fertilized donor eggs to a 47-year-old nulliparous woman at 301/7 weeks gestation. The pregnancy was complicated by hypertension requiring 10 days of hospitalization prior to delivery for administration of labetolol. Her condition was associated with normal liver function tests and a platelet count of 150,000/ mcl. Prior to delivery, the mother received dexamethasone and ampicillin therapy because of the unknown status of her group B streptococcus cervical cultures. Premature spontaneous vaginal delivery (ascribed to hypertension and mild toxemia) was complicated with breech presentation and poor respiratory effort requiring 30 seconds of positive-pressure ventilation. Apgar scores were 5 at one minute and 7 at five minutes. The infant was intubated for worsening respiratory distress at 20 minutes of life. Initial arterial blood gas demonstrated a pH of 7.35, carbon dioxide of 44 mmHg, PaO2 of 66 mmHg with a bicarbonate level of 23 mg/dl and a base deficit of -1.6. Beractant was delivered via endotracheal tube at 1.5 hours of life. Echocardiography revealed a 2 mm patent ductus arteriosis on the first day of life treated with 72 hours of indomethicin. Repeat echocardiography demonstrated closure of the ductus. Feeds were begun, via naso-gastric tube, on the third day of life. Antibiotic therapy with ampicillin and gentamicin were continued for a total of seven days for presumed bacteremia. Complete blood count at birth was not significantly abnormal revealing a WBC count of 7,500 /mcl, a hematocrit of 53%, however platelets were low at 132,000 and were attributed to the low maternal platelet count. Initial immature to total neutrophil ratio on admission was 0.2. Initial cranial ultrasound was normal for gestational age.\nThe patient weaned from conventional mechanical ventilation and was extubated to nasal continuous positive airway pressure of 5 cm H2O on the second day of life. He required only nasal cannula supplementation by his seventh day of life. On the twelfth day of life, at a weight of 1045 grams, the infant presented with increasing nasal secretions and oxygen desaturation episodes. Within 45 minutes the patient's work of breathing increased and his respiratory rate rose to 100 breaths/minute requiring intubation. Large amounts of fresh blood were noted upon laryngoscopy prior to intubation. Extensive bleeding was noted after endotracheal tube placement with worsening respiratory function requiring increased ventilatory settings in 100% Fio2 to maintain pulse oximetry saturations of 87%. Arterial blood gas and complete blood count sampling at this time were significant for a pH of 6.99, carbon dioxide of 74 mmHg, paO2 of 48 mmHg with a base deficit of -15. The infant's hematocrit decreased from 30.1% the previous day to 19% with a platelet count of 252,000. Mean arterial pressure decreased from a baseline of 33 mmHg to 27 mmHg with associated tachycardia to 220 beats per minute. Partial thromboplastin time and prothrombin time at this time were normal for gestational age. Chest X-Ray () was consistent with acute pulmonary hemorrhage.\nAfter placement on high frequency oscillatory ventilation (HFOV) as well as three rapid infusions of packed red blood cells, the infant stabilized. Treatment with vancomycin, cefotaxime and acyclovir were initiated. Blood culture and surface cultures for herpes simplex virus were negative. The possibility of RSV was entertained upon discussion with the nurse caring for the infant. She noted the patient's father engaged in kangaroo care with the infant and his twin while exhibiting clear rhinorrhea and sneezing. Rapid RSV and influenza studies were sent from both nasal secretions and tracheal aspirates. Rapid RSV was positive in both specimens and RSV was also demonstrated from the father's secretions via rapid assay. Antibiotics were discontinued after 48-hours of blood cultures demonstrating no growth. Infectious disease consultation did not recommend use of ribavirin [,]. Nasal viral cultures and viral electron microscopy were positive for RSV but negative for the presence of other viruses.\nThe patient remained on HFOV for three additional days prior to weaning to conventional ventilation for 15 additional days. Head ultrasonography on day of life 19 demonstrated increased echogenicity in the left periventricular white matter consistent with cerebral ischemia as compared to a normal initial study obtained at seven days of age. The patient was discharged on hospital day 147.
A 60-year-old man with AF was admitted to our hospital after experiencing dyspnea, orthopnea, and a non-productive cough for 2 weeks. The patient had a 10-year history of longstanding persistent AF, four previous radiofrequency catheter ablation procedures (10, 9, and 2 years, and 5 months prior to admission), and a strong family history of AF with ischemic stroke. His CHA2DS2-VASc score was 0 (male, age <60 years old, and no congestive heart failure, hypertension, diabetes, stroke/transient ischemic attack/thromboembolism, or vascular disease), and highly symptomatic paroxysmal AF remained after multiple procedures. Although this patient had undergone his 1st and 2nd procedures at another institute and we have limited information based on the medical record, he did show arrhythmogenic PV triggers from the left upper PV. At the 3rd procedure, we had found reconnected PV potentials at the left superior PV and right inferior PV and noted persistence of AF triggers from the left superior PV. Therefore, we had conducted complete circumferential PV isolation and added linear ablations. However, AF recurred as paroxysmal type. At the 4th procedure, all PV isolations and bidirectional blocks of linear ablation were maintained well, and a complex fractionated atrial electrogram-guided ablation was added (). Although a left upper PV trigger occurred during the first three procedures, we did not confirm the exit block by inside PV pacing at the last procedure. To exclude potential epicardial conduction after circumferential PV isolation, inside PV pacing with maximal electrode contact might be important, especially during repeat procedures. There was no evidence of non-PV triggers after electrical cardioversion under isoproterenol infusion. At that time, 75% luminal narrowing of the left superior PV was noticed, but there were no respiratory symptoms. However, the patient became symptomatic with AF recurrence 5 months later, and 3-dimensional-computed tomography (CT) revealed progression of PV stenosis with a significantly atrophied left atrium (). An increased left superior PV systolic peak flow velocity (251 cm/s) with turbulent flow at the PV ostium was observed on the transesophageal echocardiogram (). Based on the diagnosis of clinically significant left superior PV stenosis (), balloon-expandable stent deployment (10×19 mm, OMNILINK, Abbott Inc., Chicago, IL, USA) after balloon angioplasty (8×20 mm, POWERFLEX, Cordis Inc., Hialeah, FL, USA) () was performed. Sinus rhythm was restored, and the patient exhibited no apparent symptoms related to PV stenosis or AF recurrence 1 day after PV stenting. A follow-up CT performed 12 months after the procedure showed a patent left superior PV (). There was no recurrence of AF based on 24-hour Holter electrocardiogram monitoring based on 2012 ACC/AHA/ESC guidelines during regular follow-ups for 2 years ().
A 49-year-old woman presented with a 3-month history of repeated ptosis of both eyelids and oral ulcers and erosions. Physical examinations revealed scattered ulcers and erosions in the mouth (Fig. ). Laboratory examinations showed that CA 125 was elevated (51.6 U/ml), while other tumor markers, including CA199, 153, CEA, and AFP, were normal. Autoimmune antibodies, including anti-CENP-B antibody, ANCA, anti-AchR antibody, and ANA, were all positive.\nThe patient was first diagnosed with an oral aphthous ulcer and ocular myopathy myasthenia gravis. She was treated with gentamycin and dexamethasone spray inhalation to improve her oral lesions and pyridostigmine to cure muscle weakness. However, the oral ulcers improved slightly and the myasthenia gravis persisted. An abdominal ultrasound showed a hypoechoic mass in the left adrenal gland. A further CT examination showed a 6 × 5 cm, well-defined round solid mass with central necrosis in the pancreatic tail. There was no calcification detected in the mass. The solid part of the mass had slight enhancement in the arterial phase with many serpentine feeding arteries, moderate enhancement with a draining vein around the tumor in the portal venous phase and persistent enhancement in the delayed phase (Fig. a-e). The fundus of the stomach was compressed by the mass. The boundary between the mass and the splenic artery and vein was not clear, and swollen lymph nodes were not observed in the posterior peritoneum. The mass was initially considered to be a neuroendocrine tumor in the pancreatic tail.\nAt the same time, the patient’s symptoms worsened. She could not swallow, and she felt severe pain in her mouth. She also developed a cough and expectoration. A chest CT revealed infection in the lower lobes of both lungs. Streptococcus was detected from a throat swab. Levofloxacin was administered to fight the infection, methylprednisolone to fight the inflammation, and thalidomide to alleviate the vascular inflammatory reaction in addition to pyridostigmine and immunomodulatory therapy. However, 3 days later, the patient progressed to severe dyspnea, wheezing and difficulty with expectoration. Emergency intubation and mechanical ventilation were administered. Aspergillus was detected after bronchoalveolar lavage. Immunoglobin and voriconazole were given. Four days later, the symptoms resolved and the intubation was detached. Most of the infections in the lungs were resolved according to a chest CT. The pain in the mouth was also alleviated.\nAfter a multidisciplinary discussion, the patient’s tentative diagnosis was paraneoplastic pemphigus and the myasthenia symptoms caused by the pancreatic tumor. Myasthenia gravis, in turn, led to the patient’s inability to excrete sputum. If the pancreatic tumor could not be removed, the symptoms would not completely remit, and the symptoms due to myasthenia gravis would also continue to aggravate, finally leading to the occlusion of the respiratory tract. Therefore, the patient was transferred to general surgery. During the surgery, a 4 × 5 cm dark-red tumor with medium texture and clear boundaries was detected in the pancreatic tail (Fig. ). The tumor was close to the splenic artery and vein, and the spleen was normal. Postoperative pathology confirmed the tumor was a follicular dendritic cell sarcoma with immunohistochemistry showing CD21(+), CD23(+), CD138(+), SMA(+), Des(+), CD117(−), DOG-1(−), S-100(−), CD34(−), CK(−), EBER and EBV(−)(Fig. a-c).\nThe patient continued to be treated with antifungal and anti-infection therapy. Twelve days after surgery, the patient developed sudden heart palpitation, discomfort and difficulty in breathing. Mechanical ventilation was again administered. However, the patient died of inability to excrete sputum and occlusion of the respiratory tract.
An 86-year-old female with a history of metastatic ovarian cancer presented to the ED with painful bilateral lower extremity edema and a left lateral leg ulceration. Her metastatic ovarian cancer had been diagnosed by malignant pleural effusion five months earlier, and she had completed neoadjuvant chemotherapy with carboplatin and Taxol approximately one week prior to this presentation. She was admitted to the hospital and started on cefazolin for left lower extremity cellulitis on hospital day one.\nOn admission, plain films and ultrasound did not reveal any evidence of osteomyelitis, fracture, DVT, or abscess to the left lower extremity. On exam, she had 3+ pitting edema below the knee bilaterally as well as chronic venous stasis changes. The patient also had a venous ulcer (approximately 2 cm in diameter) on the anterolateral aspect of the distal third of her left lower leg. At the time of admission, this venous ulcer had some serous weeping but no purulent drainage or fluctuance on examination. Her initial Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score was 4, suggesting a low risk for necrotizing fasciitis; however, on hospital day 3, her CRP began to uptrend and she became febrile. At this point, her antibiotics were switched from cefazolin to vancomycin to cover MRSA.\nOn hospital day five, the patient was noted to have a new erythematous area over the anterior left knee, inferior to the patella (). Ultrasound revealed a small fluid collection superficial to the patellar tendon in the infrapatellar region measuring 3.3 × 2.5 × 0.4 cm (). The infrapatellar bursa was aspirated and sent for culture. The patient was started on piperacillin-tazobactam, given the patient's immunocompromised status and subsequent risk for atypical and gram-negative organisms.\nAn MRI was performed on hospital day seven (this was delayed due to the patient's pacemaker) but did not reveal any evidence of osteomyelitis. The patient was clinically improved after starting piperacillin-tazobactam, and vancomycin was discontinued on hospital day seven. On hospital day eight, aspirate cultures returned with Pseudomonas aeruginosa; she was stable for discharge at that time and was sent out with a ten-day course of levofloxacin (culture was pan-sensitive) and close follow-up with infectious disease.
A 27-year old Dutch Caucasian primigravida was referred to our hospital at 30 3/7 weeks gestation because of preterm premature rupture of the membranes. There was a history of polyhydramnion. Fetal ultrasonography had revealed no abnormalities such as abnormal lung development or absent gastric filling. A course of antenatal steroids was given to induce lung maturation. At 31 weeks gestation delivery was imminent and a boy was born. Despite the fact that there were no signs of fetal distress during labour the newborn baby had a poor start: there were signs of severe respiratory distress and there was no audible cry. Positive pressure ventilation with a mask was initiated, which not resulted in thoracic excursions and lead to further deterioration of the newborn. Apgar score was 1 after 1 minute and tracheal intubation was attempted with an endotracheal tube size 3.0. Despite good visualisation of the epiglottis and vocal cords, the tube could not pass any further than the vocal cords. Subsequent attempts with a tube 2.5 and tube 2.0 failed in a similar way. While breathing spontaneous with CPAP and 100% oxygen there were periods of visible chest excursions and brief improvement of the condition of the patient. Flexible tracheoscopy showed a blind ending larynx. Based on this finding combined with profound hypoxia and bradycardia resuscitation attempts were ceased. Post mortem analysis showed a normal larynx, complete absence of the trachea, a normal developed carina and main bronchi and a small fistula (diameter 1 mm) between the distal oesophagus to the right main bronchus ( and ). Thus classifying this case as a type II tracheal agenesis according to Floyd. Furthermore, the post mortem analysis revealed a lobation defect of the right lung. The right lung consisted of one singular lobe. Post mortem radiology studies revealed a hemivertebra of the 11th thoracic vertebra. No further congenital abnormalities were found.
A 36-year-old male, a seasoned cyclist with no past medical history, presents to the emergency department with complaints of lightheadedness and diaphoresis after a bicycle fall. Patient was participating in a bicycle race when another rider ahead of him fell causing the patient to swerve to avoid him. Patient states that he fell on his left side and hit a tree with his right leg. Patient was wearing a helmet and did not suffer any chest or head trauma. After the fall, he felt lightheaded and diaphoretic and complained of mid back pain. Patient denied any chest pains or shortness of breath. Patient was subsequently brought to the hospital directly following the accident by ambulance.\nIn the emergency department, patient was noted to be in no acute distress; initial blood pressure was 128/69 mmHg with pulse of 65 beats per minute. He was afebrile, not tachypneic, and well appearing with marked right thigh swelling and tenderness to his medial thigh. Given the dizziness and diaphoresis initially, patient had an ECG performed which showed lateral ST segment elevation () and had a subsequent troponin I that was positive, 0.49ng/mL, with a Creatine Phosphokinase (CPK) of 617 U/L.\nThere was initial concern for a possible cardiac contusion, although the patient had no chest wall trauma and thus was admitted for further evaluation. As an inpatient, an echocardiogram was performed demonstrating normal right and left ventricular function and trace pericardial effusion while the patients troponin continued to trend upwards towards a maximum of 21ng/mL. He was loaded with Aspirin and Clopidogrel as well as initiation of a heparin infusion, Lisinopril, and a Beta Blocker. Coronary angiography was subsequently performed demonstrating a spontaneous coronary artery dissection of left anterior descending coronary artery. No further diagnostic study was performed at that time. Further history revealed that he took multiple caffeine Jello shots and drank a large cup of coffee prior to participation in the race. He denied cocaine, amphetamine, or other performance enhancing drug use ().\nThe patient's CPK and troponin trended downwards on conservative medical management and his back pain resolved; therefore a stent was not placed. The patient was visiting from outside the area; discharge planning included repeat coronary angiography in 6 weeks and instructions that he will not be able to perform competitive cycling again. Should his dissection extend at that period of time or patient become symptomatic, stent placement would be considered. Patient was to continue the Aspirin and Clopidogrel until the repeat angiography was performed. Patient was discharged with plans to follow up with a cardiologist in his home state. Multiple follow-up phone calls made us unable to reach the patient and he was subsequently lost to follow-up.
A 33-year-old man with MPS IS presented neck and radicular pain with an onset of symptoms of 3 months, along with a recent onset of insecure gait, of about 2 weeks. The patient was of below-average stature, and regarding his metabolic disease he claimed that he had never received any treatment. In addition, he maintained a rather athletic lifestyle, which was significantly affected by the presenting symptomatology. Conservative treatment had not been able to relieve him from his symptoms, and clinical examination showed sensorimotor deficits corresponding to C6 and C7 dermatomes bilateral with the left upper extremity being slightly more affected. Bilateral paresthesias were also present over the plantar sides of the feet, along with hyperreflexia of the left leg. Bilateral upper extremity weakness [4/5] in three muscle groups was noticed, and the electrophysiological study that was performed was indicative of myelopathy. Plain radiographs were consistent with the characteristic abnormal vertebral formation that occurs in MPS, without evidence of atlantoaxial instability whatsoever (). Magnetic resonance imaging (MRI) revealed spinal stenosis at C2-5 levels with concomitant myelopathy hyperintense signs, secondary to a marked soft tissue thickening that was lying mainly posterior to the dens (). Surgical management was deemed necessary for reversing the patients incipient myelopathy symptomsor at least forpreventing them from deteriorating. During the preoperative planning, serious doubts existed with respect to the bone healing properties of the patient, and considerations were made regarding whether a revision surgery would be necessary in the future. This led us to the decision, to perform posterior decompression and fixation, with the minimum instrumentation possible, nonetheless, to preserve sufficient bone stock. Under a rather difficult and challenging general anesthesia, the patient underwent posterior decompression with C2-C3 laminectomies, and C4-C6 hemilaminectomies. Intraoperatively, a gluey soft tissue thickening covering the spinal cord was discovered; this tissue formation was strongly adherent to the dura and itscomplete resectionwas not feasible, due to great risk of dural tear. We noticed also a hypertrophic ligamentumflavum, which was rather underestimated in the MRI. A posterior C1-C7 fixation was performed with Cl/2 transarticular and C7 pedicle screws(Neon™, Ulrich Medical, Ulm, Germany), under navigation (Brainlab AG, Munich, Germany). At day2 after surgery, the patient was ambulatory and pain free, with mild paraesthesias remaining over the feet. He was discharged home 5 days later, and was strongly advised to return gradually to his athletic activities (at least after 3 months). Due to his great improvement though, the patient returned to sports rather sooner than advised (4-6 weeks), and 6 months after surgery a relapse of severe neck pain occurred. Plain radiographs showed that both C7 pedicle screws had failed; a cutout of the right and breakage of the left screw had occurred (). The patient was readmitted and a reoperation was scheduled. The initial instrumentation was revised and extended to a C1-T2 posterior fusion, with screws at Cl/2, C5, Tl, and T2 levels (). Patient s post-operative course was uneventful without pain or motor deficits, and 4 days later he was discharged.\nFour months later, the patient had a motor vehicle accident and sustained a severe head injury, for which he underwent brain surgery at another institution. Surprisingly enough, the spinal instrumentation remained intact, and the patient fully recoveredó months after his latter injury. At the last follow-up (24 months postoperatively) the patient remained pain free with no motor deficits, and no gait disturbances. A mild discomfort resulting from the limited neck range of motion was present throughout the follow-up period. Mild paresthesias of the left foot with ipsilateral leg hyperreflexia remained, not creating any severe discomfort whatsoever.
A 67-year-old male with a past medical history of congestive heart failure, non-ischemic dilated cardiomyopathy, atrial fibrillation, and pacer-dependent heart block, presented to the University of Miami emergency department with refractory complex partial seizures. Due to the fact that the patient was pacemaker-dependent, he was unable to undergo MRI. Therefore, a contrasted CT scan of the brain was performed, which demonstrated a heterogeneously enhancing left frontal mass just anterior to the left motor cortex thought to be either a primary central nervous system tumor or a metastatic lesion (Figure ).\nA full metastatic workup was conducted with no primary lesion detected. Given the location of the lesion, further imaging was thought to be necessary for two reasons: 1) to further elucidate the differential diagnosis of the lesion and 2) to help safely guide resection or biopsy of a lesion in close proximity to eloquent brain tissue. As a result, cardiothoracic surgery was consulted for the possible replacement of the patient’s current pacemaker with an MRI-compatible alternative. The patient subsequently underwent the removal of their pacemaker and replacement with a Surescan Medtronic DDD Pacemaker RVDR01 (Minneapolis, MN, US). Following this procedure, an MRI was performed and demonstrated a multi-lobulated, relatively uniformly enhancing left frontal lesion (Figure ). Due to the lack of a definitive diagnosis, the decision was made to perform an awake craniotomy with MRI-assisted stereotactic guidance and intraoperative electrocorticoraphy for a definitive diagnosis. The lesion was able to be resected with the initial pathology suggestive of Mycobacterium tuberculosae brain abscess. The patient was placed on anti-tuberculosis medication and intravenous (IV) antibiotics and discharged home. Approximately one year later, he returned to the hospital after suffering a partial seizure with subsequent right upper extremity weakness. He was found to have a recurrence of his left frontal lesion and was again taken to the operating room for surgical resection. Repeat imaging at one year did not demonstrate any further recurrence of his previously seen lesion.
A 68-year-old man presented with computerized tomography (CT) scan results showing a 5-cm solid cystic mass in the tail of the pancreas (Figures and ), with no signs of vascular or visceral invasion. There was no evidence of metastatic disease. The patient was completely asymptomatic; the CT scan was performed as part of a routine follow-up of angiographic aortic endoprosthesis placement 3 years prior for treatment of an abdominal aortic aneurysm. In addition, the patient's history included well-compensated pulmonary emphysema and a pulmonary lobectomy for a pT2N0M0 adenocarcinoma of the lung (lower left lobe) 5 years prior. There was no history of abdominal trauma or previous abdominal surgery and no family history to suggest genetic disease.\nNo clinical signs were found on physical examination. Magnetic resonance imaging failed, owing to the generation of artifacts associated with the aortic prosthesis. Levels of serum tumor markers (carcinoembryonic antigen [CEA] and CA 19.9) were in the normal range. Surgery was performed on the suspicion of cystadenocarcinoma. During the surgical exploration, the mass appeared to be localized completely to the tail of the pancreas, with no invasion of adjacent structures. There were no enlarged nodes surrounding the tumor. A left pancreatectomy was performed with spleen preservation and lymphadenectomy of the celiac axis and peripancreatic nodes. The transection margin was tumor-free. The gross appearance of the mass was of a dense grayish tumor containing a cystic cavity, with no signs of a capsule and no evidence of necrosis.\nHistologic sections showed proliferation of spindle-shaped or stellate cells, with a fasciculate and storiform growth pattern within a background of myxoid intercellular matrix (). Glassy, hyalinized, and keloid-like collagen fibers were also present focally. The cystic area was the result of dilatation of entrapped excretory pancreatic ducts. Immunohistochemical staining showed cytoplasmic positivity for smooth muscle actin and focal nuclear positivity for beta-catenin (). Immunohistochemistry for desmin, CD117 (c-kit), and CD34 was negative, and the proliferation marker Ki67 stained 2% of the cells. The features were those of intraabdominal fibromatosis.\nThe tumor infiltrated the pancreas and surrounding adipose tissue. The patient developed an abscess of the pancreatic stump, which was treated by CT-guided percutaneous drainage and resolved on postoperative day 28. Oral intake was initiated on postoperative day 5, and patient was discharged on postoperative day 16. The patient is doing well and remained disease-free according to 60-month follow-up CT ().
A 37-year-old man presented to the emergency department at our hospital on October 2012 with a 4-month history of worsening lower back pain. There was no history of trauma or falls. He was unemployed and lived with his mother. He took no medications or supplements, did not smoke, consume excessive alcohol, or use illegal drugs, and had never been treated with corticosteroids. He had no history of prior fractures. Family history was negative for gonadal, endocrine, or bone diseases. Review of systems was remarkable for markedly delayed puberty for which he had received testosterone injections starting at 16 years of age. Three years later, testosterone replacement therapy was terminated by the treating physician, after he responded well in terms of growth and development of secondary male sexual characteristics. He remarked decreased libido for several years and absence of morning erections.\nOn examination, he was a well-nourished gentleman in obvious distress due to pain at the level of the lower thoracic/lumbar spine. He had an eunuchoidal body habitus with the arm span (181 cm) exceeding the height (174 cm). The pupils were round, equal, and reactive to light. Visual fields were normal to confrontation. The skin turgor was normal, the mucous membranes were moist and the teeth were in good condition with no decay. Examination of the head and neck was remarkable for hyposmia to a number of odorants. The cardiovascular, respiratory, and abdominal exams were within normal limits. There was no edema in the extremities and neurological assessment was normal. Examination of the integument was remarkable for sparsity of pubic hair. The penile length was normal but testicular volume was decreased (approximately 5 cm3 as determined using the Prader orchidometer).\nOn biochemistry, serum levels for luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol were extremely low while baseline values for serum creatinine, electrolytes, thyroid function tests [thyroid-stimulating hormone (TSH) and free T4], prolactin, cortisol, parathyroid hormone (PTH), and alkaline phosphatase activity were all within normal limits. Osteocalcin levels were increased while serum 25(OH) vitamin D levels were insufficient (). Complete blood count showed a normochromic normocytic anemia. Serum protein electrophoresis was unremarkable.\nRadiographic examination of the spine disclosed diffuse osteopenia with moderate wedging of several mid-thoracic vertebrae along with severe compression fractures of T11, T12, and L1 (80%–90% vertebral height loss). There was a 10% superior endplate collapse at L5. Dual-energy X-ray absorptiometry (DXA) scan of the skeleton reported a Z-score of −6.9 at the lumbar vertebrae (L2–L4), −3.3 at the femoral neck, and −4.1 at the total hip ().\nMagnetic resonance imaging (MRI) of the brain with particular attention to the hypophysis was carried out. The pituitary gland was normal except for a 2.4 × 2.6 mm left anterior pituitary cyst with no evidence of a mass effect.\nBased on the aforementioned history, physical examination, radiographic evaluation, and biochemical data indicative of hypogonadotropic hypogonadism with hyposmia, the patient was diagnosed with Kallmann syndrome with severe osteoporosis due to hypogonadism. He was given analgesia and was started on calcium (500 mg/day), vitamin D (2000 IU/day), and testosterone replacement therapy (Androgel™ 1% 2.5 g daily) while awaiting for government approval for teriparatide (Forteo™) use.\nThree weeks later, he presented again to the emergency department with a 4-day history of being unable to ambulate due to severe low back pain following a fall from standing height. A CT scan of the spine disclosed a new L3 compression fracture, with 75% loss of height, along with an interval progression of the L5 superior endplate collapse (from 10% to 40% loss of height). The T11-L1 fractures remained unchanged (, left panel). Given that the area of maximal pain was at the L5 level, the patient underwent L5 vertebroplasty with good analgesic response and near complete ambulatory recovery (, right panel).\nWhile convalescing, his application for teriparatide use was approved and treatment was initiated. Skeletal response to the drug was monitored using osteocalcin and procollagen type 1 N-terminal propeptide (P1NP) serum levels as surrogate markers of bone formation (). Concurrently, the dose of Androgel was gradually increased to 10 g daily. While on this dose, serum testosterone levels normalized and the anemia resolved. On December 2014, after completing 24 months of teriparatide treatment, he was switched over to sequential treatment with denosumab (Prolia™) 60 mg s/c q6 months. A repeat DXA scan performed on May 2015 (following two doses of denosumab) showed improvement of the bone mineral density at the lumbosacral spine, femoral neck, and total hip [Z score of −5 (from −6.9), −3.3 (from −3.3), and −3.9 (from −4.1)] (). He has been doing well since then, and while continuing with calcium, vitamin D, testosterone, and denosumab therapy, he has remained pain-free and has not sustained further fractures.
A 40 year old female presented with a 4 months history of recurrent right sided lower thoracic pain during sports. Medical history consisted of a hysterectomy for symptomatic uterine myomatosis four years previously, after giving birth to her second child. This was a non-radical non-oncological resection. The original pathology report revealed a 15 cm low grade ESS. Now, four years after the hysterectomy, a CT scan showed a large mediastinal mass with expansion in the upper abdomen and compression of the left atrium and multiple lesions in both lungs. A bronchoscopic biopsy showed cells similar to the earlier diagnosed ESS. Treatment with six courses of doxorubicin resulted in a very good partial response. Maintenance therapy with megestrol acetate 160 mg was started hoping to prolong the time to progression. Two years later, an increase in size and number of the lung metastases was observed, so megestrol acetate was stopped and anastrozole 1 mg started. Further disease progression was noticed 4 months later (Fig. ). Pazopanib 800 mg orally once daily was started in the named patient program in collaboration with the Leiden University Medical Centre, one of the Dutch sarcoma reference centres. At the same time, pathology review was performed, confirming the diagnosis of low grade ESS, but also noticing a CyclinD1 positive and CD10 negative higher grade component suggesting a YWHAE-FAM22 translocated ESS. (Fig. -) Fluorescent in situ hybridisation confirmed the diagnosis. The tumour showed high expression of KIT in the high grade component of the tumour.\nSix weeks after start of pazopanib 800 mg once daily an increase in ALAT to > 10 times the upper limit of normal (ULN) was observed. (Figure ) Hepatitis serology, liver ultrasound and liver biopsy were not performed because of the clear relationship of the increased liver enzymes with the start of pazopanib. She had no history of liver disease, no liver metastases and no liver function abnormalities before start of pazopanib. During the previous treatment with doxorubicin, y-glutamyl transferase increased to 20× ULN and ALAT to 6× ULN, no other liver function abnormalities occurred. The CT scan showed a decrease in the sum of the largest diameters of the target lesions of 23%. Pazopanib was put on hold immediately until the liver enzymes returned to normal. (Figure ) After six weeks without pazopanib the CT scan showed a further decrease of the target lesions of 38% compared to baseline (19% compared to the previous CT scan) indicating a partial response. Figure ) At the time the liver toxicity had almost recovered, a re-challenge with pazopanib 200 mg once daily was performed, but after one week liver function abnormalities recurred and pazopanib was stopped again. After liver function recoverage, pazopanib 200 mg once every other day was initiated, but again after 2 weeks liver enzymes increased to > 3× ULN. Another week later pazopanib 200 mg every third day was given for 2 weeks, until a CT scan showed progression (six months after the start of pazopanib). She was still in very good clinical condition and besides the remarkable inclination of liver enzymes at the beginning of treatment and lesser rises thereafter she had had little other toxicity with pazopanib. She consented to another challenge with pazopanib 200 mg every day under further strict surveillance of liver enzymes. The liver enzymes remained < 3 times ULN, but 3 weeks later she was admitted with a bilateral pneumothorax and pazopanib was stopped. On the right side a pleurodesis was performed and on the left side it was drained. Anastrozole and leuproreline were prescribed, hoping to slow down progression. Two months later, a CT scan again showed progressive disease, and ifosfamide chemotherapy (5 g/m2 in a 24-h continuous infusion every 3 weeks) was initiated. CT scans after 3 and 6 cycles showed stable disease. During ifosfamide treatment only a slight increase in y-glutamyl transferase was noticed (increase to < 2× ULN). Two months after the last ifosfamide administration, radiological progression was observed again and pazopanib 400 mg daily was prescribed again under strict weekly surveillance of the liver enzymes. This dose was chosen because patient had a pleural effusion due to the progression and thereby a lot of complaints. To be sure of a therapeutic dose of pazopanib we started with 400 mg daily. Two weeks after reinitiating pazopanib the pneumothorax on the left side recurred and persisted. Pazopanib was held for two weeks, but was then reinitiated after discussion of the risks with the patient. CT scans 6 weeks and 3.5 months after the restart of pazopanib showed stable disease. Pazopanib was stopped permanently 6 months after the restart because of progressive disease, and she died 2 weeks later. In the second period of pazopanib treatment, no liver toxicity occurred. No differences between co-medication were found between the first period of pazopanib treatment and the second. A summary of the patients’ history is given in Fig. .\nThe DNA of the patient was analyzed for single nucleotide polymorphisms (SNPs) in enzymes known to be involved in the absorption, distribution, metabolism and elimination of pazopanib []. The genes analyzed were CYP3A4, CYP1A2, CYP2C8, ABCB1 and SLCO1B1. The main metabolizing enzyme for pazopanib, CYP3A4 did not have SNPs associated with a decreased metabolic function. Two SNP variants in CYP1A2 (rs762551 and rs2470890) and one in SLCO1B1 (rs4149057) were detected, but no evidence exists that these polymorphisms cause elevated levels of pazopanib. So, this analysis did not result in the elucidation of a cause for the liver toxicity in this patient.
A 74-year-old gentleman presented to the Accident and Emergency Department following a 3-month stay in India. Four weeks into his return, he started developing daily episodes of fever and night sweats. Whilst in India, he was asymptomatic although he did not take any malaria prophylaxis or salmonella vaccine during his travel.\nThe patient had no comorbidities except for a renal calculi detected in 2004. He was also known to have a simple cyst measuring 5 cm in diameter in the right lobe of the liver, incidentally found on routine abdominal ultrasonography (USG). He did not take any regular medication, and was otherwise in good health.\nOn examination, he had a temperature of 38.2°C, pulse 90 beats per minute regular, and blood pressure of 116/60 mmHg. Systemic examinations of cardiovascular, respiratory, abdominal, and neurological systems were unremarkable.\nHis initial blood biochemical examination showed normal liver and kidney functions but a raised c-reactive protein (CRP) of 129 mg/dL. His haematological parameters showed a raised white cell count of 12 000/cumm with predominant neutrophilia. No malarial parasites were detected. Chest X-ray did not show any signs of underlying infection.\nRepeated blood and urine cultures were obtained and abdominal USG requested to find any abdominal collection as a source of sepsis. Our differential diagnosis at this stage was malaria, salmonellosis, or amoebiasis. The delayed start of his symptoms vis a vis his travel history made viral aetiology, namely, dengue fever unlikely.\nHis blood culture grew Salmonella paratyphi A. Serologies for amoeba and hydatid disease were negative. Abdominal USG showed a collection in the right liver lobe, the same site as the simple cyst noted on the previous scans. The area was significantly larger than previously noted with an underlying abscess. Abdominal and pelvic CT scan did not reveal any further abscesses.\nThe liver abscess was drained under ultrasound guidance using a pigtail catheter and the aspirate cultures also grew Salmonella paratyphi A. The patient received systemic antibiotic, Ceftriaxone 2 gm intravenously once daily for 10 days based on the sensitivity report and made an uneventful recovery. On followup, he remains asymptomatic.\nWe present a case of liver abscess caused by Salmonella paratyphi A, in a previously known simple cyst of the liver. Such a case has been reported only once previously.
A 55-year-old Caucasian man from Germany presented in our tinnitus clinic with complaints of severe disabling right-sided tinnitus. The tinnitus resulted from sudden right-sided deafness, which occurred about one year before. In spite of different therapies such as intravenous steroids, infusion of rheological agents and tympanoscopy with grafting of the round window, the affected ear remained deaf. Subsequently, a pre-exisiting mild bilateral tinnitus exacerbated in the right ear (narrow band noise, 5 kHz). Due to the tinnitus the patient complained of insomnia and concentration problems resulting in severe disability of leading a normal life. Pure tone audiometry testing revealed right-sided deafness and moderate hearing impairment on the contralateral side (pure tone average of 500, 1000 and 2000 Hz: 37 dB HL). Electrical promontory stimulation via needle electrode demonstrated normal function of the auditory nerve. Tinnitus masking was impossible due to the right-sided deafness even when sounds were presented to the left ear. Tinnitus severity has been assessed with questionnaires [,] and visual analogue scales (VAS) (). Using a ten-point VAS the tinnitus was rated by the patient according to loudness and annoyance. Analysis of the scores showed severe impairment in consequence of the unilateral tinnitus. Magnetic resonance imaging (MRI) resulted in regular anatomical structures of the cochlea and the cranial nerves. No pathologic processes affecting the brain, the brainstem or the cerebellum were detected.\nThe deaf right ear was successfully implanted with a MedEL SONATAti 100 Cochlear Implant (MedEL, Innsbruck, Austria). Post-operative X-Ray revealed a correct position of the electrode in relation to the basal turn of the cochlea. Shortly after activation of the cochlear implant in the context of a standard fitting procedure the patient reported a reduction of his tinnitus, which completely disappeared during electrical stimulation within the following 3 months. With a deactivated implant the tinnitus only reoccurred after presentation to loud noise. The clinical improvement was also reflected by a distinct decrease in the scores of the questionnaires and the VAS (). Speech reception of monosyllables at 65 dB SPL improved from 0% preoperatively to 60% 3 months after first fitting and the patient reported no conflict of hearing between the implanted and the contralateral ear.
The patient is a 26-year-old single gravida 3 para 0+2 Nigerian trader. She was admitted into the gynaecology ward through the accident and emergency unit of our hospital. She was pregnant with an estimated gestational age of 20 weeks.\nHer presenting complaints were abdominal pain of 4 days duration and vomiting of a day's duration. Abdominal pain started after she had gone for her regular abdominal massage in a traditional birth attendant's home. It was moderately severe and relieved mildly by analgesics. She vomited twice before presentation. Vomiting was non-projectile and not provoked by oral intake. Bowel opening was normal. There was associated dizziness and she felt faint. However, there was no bleeding per vagina.\nShe had attempted terminating this pregnancy thrice at a gestational age of 6, 8 and 11 weeks respectively by dilatation and curettage without success in a private medical clinic. She had not done any previous ultrasound scan.\nAt presentation, she looked pale and had a tinge of jaundiced. Her height and weight was not recorded. Her pulse was 120 beats per minute and of low volume. The blood pressure was 100/50 mmHg. The abdomen was enlarged with generalised tenderness. There was a suprapubic mass corresponding to a 22 weeks size uterus. There was no bleeding per vagina. A diagnosis of an acute abdomen with heamoperitoneum from a possible extra uterine pregnancy was made.\nThe packed cell volume was 19% and immediate blood transfusion was commenced, urgent ultrasound scan was requested and laparotomy planned.\nAbdominal ultrasound scan done was reported as follows:\n“A single viable intrauterine fetus with normal cardiac activity is noted. The BPD is 48mm corresponding to a gestational age of 19 weeks and 6 days. There is also a contracted liver with increased echogenicity and surrounded by ascitic fluid.\nConclusion:\nA single viable intrauterine pregnancy of about 20 weeks.\nChronic liver disease? Cirrhosis.”\nLaparotomy was withheld and the medical team invited to evaluate the patient. Liver enzymes were elevated and total protein was reduced. A diagnosis of Septicaemia to rule out Malaria and Hepatitis was made by the medical team.\nShe was given parenteral antibiotics, anti-malarial, fluids and analgesics. There was a marginal transient improvement in her condition. A subsequent repeat abdominal ultrasound scan was requested which showed:\n“Marked ascites with a contracted liver. There is a non-viable intra-abdominal fetus. There is a bulky non-gravid anteverted uterus.\nConclusion:\nNon-viable intra-abdominal pregnancy of about 20 weeks.\nCirrhosis of the liver.”\nShe subsequently had Laparotomy. Findings at Laparotomy were a haemoperitoneum of about 1.5 litres, and a dead fetus floating in the peritoneal cavity. The fetus weighed 350 grams. There was a left rudimentary horn of the uterus with a 5 cm rupture on the superior margin. The placenta was still within the uterine horn. The cavity of the horn did not communicate with the uterine cavity. The left fallopian tube was of normal length and attached to the rudimentary horn. Left ovary was normal and attached by its ligament to the rudimentary horn. The uterus was of normal size with the right fallopian tube and right ovary attached to it ().\nExcision of the rudimentary horn and the left fallopian tube was done. The left ovary was conserved. She was transfused with 2 pints of blood intraoperatively. Her post operative recovery was normal. She was discharged on the 7th post operative day and given a 6 weeks follow-up appointment when she will do an intravenous urogram. She however did not turn up for her appointment.
A 63-year-old white female was diagnosed with stage 1 infiltrating ductal carcinoma at an outside hospital in August 2005. Her tumor was 1 cm in size and was ER/PR/Her2Neu positive with an oncotype score of 29. Axillary lymph node sampling revealed 0/6 positive lymph nodes. She underwent adjuvant treatment with epirubicin, cyclophosphamide, and trastuzumab later that year. At that time she had no clinical signs of congestive heart failure (CHF). In January 2007, she developed pain in her sternum and back, and X-rays revealed multiple small lytic lesions. The diagnosis of metastatic breast cancer was made and she underwent radiation therapy to the symptomatic lesions as well as further trastuzumab treatment for metastatic disease. She did not receive hormones at the time of diagnosis of presumed relapse. Soon after start of adjuvant therapy, she developed symptomatic CHF and was found to have a left ventricular ejection fraction of 15%. The patient was diagnosed empirically with trastuzumab-induced cardiomyopathy at an outside hospital and was started on diuretics. After a time in rehab, she improved and went back home.\nIn February 2008, she presented to our institution for a second opinion regarding metastatic breast cancer treatment. Because she was dehydrated and lightheaded she was admitted. The patient was diagnosed with renal failure with a creatinine above 3 mg/dL. Her work-up also included serum and urine protein electrophoresis. Both demonstrated a monoclonal gammopathy. She was noted to have 3.5 gm of protein on a 24-hour urine collection and both the urine and serum immunofixation demonstrated an IgG kappa monoclonal protein with a serum M-spike of.88 gm/dL. Her serum free light chains revealed a serum free kappa of 8300 mg/L with a kappa/lambda ratio of 418. Quantitative immunoglobulins were normal, Beta-2 microglobulin was 15.6 mg/L and calcium was normal.\nThe inpatient hematology service was asked to comment on the seemingly unusual constellation of diagnoses: metastatic breast cancer, trastuzumab-induced cardiotoxicity, and a new diagnosis of multiple myeloma. She was noted to have bilateral pleural effusions, pedal edema, and nausea. Complaints of back pain led to the discovery of multiple thoracic compression fractures. Because of back pain and concern for cord instability, she underwent T5, T6, and T7 corpectomy with reconstruction. Pathologic evaluation of the resected bony fragments revealed no breast tumor cells, while some plasma cells were detected. There was not enough tissue to adequately evaluate for plasma cell clonality by immunohistochemistry. A bone marrow biopsy revealed clonal kappa light chain restricted cells comprising 30% of the total cells consistent with a diagnosis of multiple myeloma. Cytogenetics revealed monosomy 13. A bone survey showed progressing lytic lesions and a CT guided biopsy of a sacral lesion was performed that revealed numerous atypical plasma cells that stained positive for CD138 and negative for pankeratin consistent with a plasma cell neoplasm. She was therefore staged III in the International staging system (ISS), and stage IIIB in the Durie-Salmon staging system with extensive bone disease and was started on thalidomide, dexamethasone, and bortezomib with consideration for autologous hematopoietic stem cell transplant in the future depending on improvement of her performance status. After receiving her first dose of thalidomide, dexamethasone, and bortezomib, she required admission to the hospital for shortness of breath and was noted to have worsening bilateral pleural effusions. While admitted she also complained of persistent nausea. A gastric emptying scan revealed emptying of 138 minutes (normal less than 110). An echocardiogram revealed both left ventricular wall and septal wall thickness. Her septal thickness measured 1.5 cm (normal 0.7–1.2 cm). Additional findings included multiple areas of hypokineses, dilated inferior vena cava and right atrium felt by the echo-cardiographer to be consistent with amyloid heart disease. While hospitalized she had persistent pedal edema, pleural effusions, anasarca, and subsequent hypotension with diuretic use. She was treated for a time with milrinone without appreciable change. Eventually the decision was made to change the direction of her care to comfort. She was discharged to a hospice closer to her home.
The patient is a 7-year-old Asian girl who was diagnosed with nephrotic syndrome in June 2017 in a local primary care clinic before transferring care to our department 9 months later. Prior to diagnosis, patient was healthy, with no significant birth history and no history of surgery, trauma, or blood transfusion. The patient visited the local clinic due to cold/flu-like symptoms, swelling eyelids and lower limbs, and abdominal pain that was eventually diagnosed as nephrotic syndrome. No family history was reported. Based on the records provided by the patient's parents, the patient underwent a course of oral corticosteroid, and subsequently, urine protein was negative, indicating corticosteroid-sensitive response. However, patient's urine protein increased once again after tapering corticosteroid, and her steroid dosage was increased. Subsequently, her urinalysis was once again negative for protein, but each time steroid taper was attempted, patient relapsed with significant proteinuria. Although her disease was progressively steroid dependent, corticosteroid was discontinued per the request of the patient's parents after several courses due to concern for adverse effects of long-term therapy. Instead, the patient was switched to traditional Chinese medicine (ingredients unknown) for nearly 4 months (). During the treatment with traditional Chinese medicine alone, the patient visited her local primary care clinic for several urinalyses that consistently demonstrated 3+ proteinuria and occult blood. Meanwhile, the patient showed progressive clinical decline with severe complications including urinary tract infections, systemic edema, shortness of breath, frequent urination, and dysuria. Due to significant disease progression, patient was referred to our hospital in March 2018.\nOn presentation to our hospital, the patient was admitted to the Pediatric Intensive Care Unit (PICU) and found to have a fungal infection, heart failure, hypertension, ascites, and persistent oliguria. Routine examination and laboratory tests showed body weight of 33 kg, body surface area of 1.11 m2, serum albumin of 14.3 g/L, total cholesterol of 20.78 mol/L, and triglyceride of 11.13 mmol/L, indicating hypoproteinemia and hyperlipidemia. Renal function tests showed serum uric acid of 545 μmol/L, creatinine of 121.0 μmol/L, blood urea nitrogen (BUN) of 22.4 mmol/L, and glomerular filtration rate (GFR) of 37.86 ml/min, indicating azotemia and renal dysfunction. Initial treatment included correcting electrolyte disorder, diuresis, anticoaglutant therapy, and fluconazole (3.6 mg/kg) for fungal treatment. During this time, she was also treated with methylprednisolone (2 mg/kg daily) and aldehyde oxystarch, without significant efficacy (). Therefore, the patient underwent continuous renal replacement therapy (CRRT) with significant improvement of disease. Laboratory tests showed blood creatinine of 46 μmol/L, BUN of 10 mmol/L, and GFR of 99.59 ml/min. Patient was then transferred from PICU to our department for subsequent therapy. Autoimmune antibody panel was ordered, and all resulted negative. These included antinuclear antibody (ANA), antidouble-stranded DNA (anti-dsDNA), anti-Smith, antihistone antibody (AHA), anti-Sjögren's-syndrome-related antigen A (anti-SSA), anti-SSB, rheumatoid factor, ANCA, cardiolipin autoantibody, antimitochondrial antibody (AMA), smooth muscle antibody (SMA), anticentromere antibody, and antibasement membrane antibody. With negative immunological workup, we recommended a renal biopsy, but this was declined by her parents at that time with concerns regarding invasiveness of biopsy. During that admission, patient experienced repeated hypertension that was difficult to control on nifedipine and, subsequently, developed convulsions accompanied by right hemiplegia concerning for hypertensive encephalopathy. She subsequently underwent aggressive sodium nitroprusside (1–5 μg/kg/min), diuretic (spironolactone 20 mg and hydrochlorothiazide 10 mg daily), and steroid therapy (methylprednisolone 40 mg, q.o.d). Following these, her blood pressure returned to normal, neurological symptoms resolved, and systemic edema also improved. Laboratory tests showed that urine protein and occult blood decreased to 2+, blood creatinine was 42.0 μmol/L, and hypoproteinemia was corrected. Patient was discharged with continuation on methylprednisolone (40 mg daily in divided doses), losartan potassium (20 mg daily), and spironolactone (20 mg daily).\nDuring her outpatient follow-up, patient's urine protein consistently returned 2–3+, suggesting steroid resistance. The need for tissue diagnosis via biopsy was reiterated, but patient's family continued to refuse at that time. Therefore, cyclosporine 5 mg/kg PO was added to her regimen. Subsequent labs showed improved proteinuria without significant decrease in serum creatinine despite the addition of cyclosporine. Due to frequency of relapses, renal biopsy was discussed again with the patient's parents for which consent was given in May 2018, and microscopy results were consistent with C1q nephropathy ().\nBased on the pathological findings, a trial of rituximab was initiated after lymphocyte subset analysis showed B lymphocyte ratio of 43.2%. The patient received a single intravenous dose of 100 mg rituximab (93 mg/m2). During infusion, patient experienced facial flushing but no other significant discomfort. B lymphocyte subset fell to 6.1% after 1 day. After 2 weeks of rituximab treatment, B cells were completely depleted, and renal function was significantly improved with a GFR of 93 ml/min (). Patient was then given prednisone starting at 30 mg every other day and gradually tapered at a rate of 5 mg/month. At 1-year follow-up in August 2019, patient presented with symptoms of urinary tract infection. Urinalysis at that time showed 4+ white blood cells (WBCs) but was negative for protein and blood. Serum tests showed normal kidney function and 3.30% of total B lymphocyte subset. At present, patient has maintained normal kidney function off steroid therapy and has had no relapses since rituximab therapy. The treatment courses and selected laboratory results are shown in .
Sixty-three-year-old woman presented with multicentric left breast cancer requiring mastectomy. She is 69 inches tall with a weight of 215 pounds and a corresponding BMI of 31.8 kg/m2. She has a history of inferior pedicle breast reduction surgery performed 20 years ago (Fig. 1). Despite her previous reduction, she has a very large breast volume and footprint that will be difficult to replicate on the reconstructed left side. She desires nipple preservation and wants to keep her native right breast. We proceed with a left nipple-sparing mastectomy through her previous vertical limb and immediate prepectoral reconstruction using a full-height variable-projection tissue expander (width = 16 cm, height = 16.5 cm, projection = 6.8 cm, and volume = 850 ml) with anterior coverage using an acellular dermal matrix. Twelve weeks later, we exchange her tissue expander for the largest anatomical implant available, a full-height extra-projection 775 ml implant (width = 15.5 cm, height = 16 cm, and projection = 7.1 cm). She also undergoes a contralateral reduction of 300 g to achieve better symmetry. The final result is shown in Figure . Despite using the largest and tallest implant available and reducing the right breast by an additional 300 g, the entire upper pole of the left breast was depleted with significant size asymmetry between the breasts. We discussed multiple sessions of lipofilling to fill this defect but felt that an autologous flap would be more definitive. The LICAP flap was chosen to reconstruct the upper pole of the left breast. An intraoperative photograph is shown in Figure , where an extended flap is dissected based off the known perforators that arise anterior to the latissimus muscle at the level of the inframammary fold as previously described. This flap is rotated on its pivot point and used to reconstruct the upper pole of the breast by suturing it to the underlying pectoralis muscle. The final result 6 months after surgery is shown in Figure , where we have reconstructed the upper pole of her breast with the LICAP flap and have acceptable symmetry between the 2 sides. The patient is discharged the same day, and drains are removed on postoperative day 4.
The third case is of a 68-year-old Irish woman who presented to the MMUH in April 2016 with acute laryngitis. She had a background of bipolar affective disorder which had been stable for the past 30 years on monotherapy with lithium. There had been a recent history of lithium toxicity secondary to a deterioration of her renal function, which had been managed at her local psychiatric hospital. After the episode, she had been restarted on a low dose of lithium as well as a low dose of valproate.\nOn presentation to the MMUH she was initially treated jointly by the ear, nose, and throat (ENT) team and medical team and was managed in an ICU environment due to respiratory compromise. She had no oral intake for multiple days. Once stabilized she was transferred to an acute medical ward but an acute onset confusional state with bizarre behavior was noted over a period of 2 days. Due to her psychiatric history the Liaison Psychiatry service was consulted. On review she was severely thought disordered and confused. She was only able to produce a word salad and showed echolalia. She had motor retardation, increased tone, negativism, and posturing on examination. The impression was that she was suffering from acute catatonia. Brain imaging did not reveal acute abnormalities. She was diagnosed as having bipolar I disorder with catatonia as per DSM-5 (Table ).\nAdvice was given to treat her with paliperidone. Her mental state improved slightly as a result, but she remained severely thought disordered and confused for 2 weeks. Eventually, lithium was cautiously reintroduced under close monitoring of her renal function. The reintroduction of lithium was well tolerated and she improved significantly over a 2-week period. At discharge she was no longer thought disordered, she was well orientated, and back to her fully independent baseline. She continues to live independently to date.
A five-year-old previously healthy bilingual (English and Spanish) boy presented to the ED with his parents due to insomnia for the previous two nights. The family history was negative for neurologic or psychiatric illness. The patient was a typically developing child born after a full term uncomplicated gestation and delivery. He had no prior history of injury, ingestion, psychosocial stressors, change in appetite, involuntary movements, or seizures. One week prior to presentation to the ED, he had been evaluated by his primary care physician after a three-day febrile illness and was diagnosed with a viral infection. Since that time, he had become more irritable and fussy, frequently having outbursts of crying without being able to articulate why he was crying. His father was concerned that he seemed scared during these episodes and was concerned about eye pain.\nThe patients' initial physical examination revealed normal vital signs, cardiovascular, pulmonary, and abdominal findings. He did not have dysmorphic features or a rash. Neuropsychiatric examination revealed an emotionally labile child with periods of calm and seemingly appropriate bilingual language development and behavior for age with episodes of extreme distress during which he would burst into tears and require physical restraint by family members against combativeness. Examination of the cranial nerves, motor tone, strength, coordination, and gait were normal and there was no sign of meningismus on physical examination.\nInitial differential for this clinical presentation was broad including insomnia secondary to pain from corneal abrasion or other unidentified traumatic or infectious source, traumatic brain injury, thyrotoxicosis, developmental disorder with regression, encephalopathy due to acute intoxication, acute psychosis, postinfectious or parainfectious encephalitis, and autoimmune encephalopathy. Screening in the ED with urine drug screen, serum acetaminophen and salicylate levels, complete blood count, complete metabolic panel, thyroid function tests, inflammatory markers, urinalysis, head CT scan, and EKG all revealed normal results. PCR respiratory panel (nasal swab) was negative for frequently tested viral and bacterial pathogens including negative for mycoplasma pneumoniae. The patient was admitted to the general pediatrics service with support from consulting services for further evaluation and management given his altered mental status and concern for acute encephalopathy.
An 18-year-old male patient reported to our ED following a road traffic accident with severe pain in the right hip and right thigh. The patient had a deformity of the right hip and thigh, and was unable to walk. On clinical examination, we found that he had ﬂexion-adduction deformity of the right hip. His leg and foot showed external rotation and abduction. There was tenderness and abnormal mobility at the right thigh. In addition, there was tenderness at the right hip joint and the femoral head was palpable in the gluteal region. The range of movements at the right hip was grossly restricted and painful. There was no distal neurovascular deﬁcit noted.\nAfter providing the advanced trauma life support in causality, the patient was sent for radiography. X-rays of the pelvis with both hips and of the right thigh with hip and knee were taken (Figure ).\nCT scan of the hip and pelvis was also taken to exclude acetabulum fractures (Figure ).\nFrom the radiograph, we conﬁrmed that there was a fracture in the shaft of femur and a posterior dislocation in the hip. The patient was taken to an emergency OT and subjected to closed manipulation of the hip joint. As there was a fracture in the shaft of femur, the force was not transmitted to the hip joint and we are unable to reduce the hip dislocation. At that moment, we had two options: open reduction and external ﬁxation, and closed manipulation of the dislocation of the hip joint. We placed a temporary external ﬁxator in the femur under anesthesia, and performed closed manipulation and reduction of dislocation of the hip using the Allis method (Figure ).\nThe patient was subjected to ﬁnal ﬁxation of the femur shaft fracture after one day in elective OT. Femur shaft fracture was ﬁxed with a closed reduction and an internal ﬁxation with an intramedullary femur interlocking nail (Figure ).\nThe operation was done on a traction table under the guidance of ﬂuoroscopy.\nPostoperatively, the patient’s legs were placed on an abduction pillow and physiotherapy was started. Low-molecular-weight heparin was given as deep vein thrombosis (DVT) prophylaxis. The patient was not allowed weight-bearing for two weeks. Gradually, he was allowed partial weight-bearing based on his tolerance.
A 69-year-old female (weight 41 kg, height 142 cm) with degenerative spinal stenosis was scheduled for transforaminal lumbar interbody fusion surgery under general anesthesia in prone position. She was not taking any medication and had no known previous cardiovascular disease, as well as no family history of sudden cardiac death. In addition, the patient had no cardiovascular symptoms, including syncope, tachycardia, or chest pain, under at least 4 METs of daily activity. However, routine preoperative resting 12-lead electrocardiogram (ECG) revealed a second-degree 2:1 AV block with a narrow QRS complex (0.102 s), heart rate (HR) of 46 bpm, normal axis, and with no ischemic change (Fig. ). The patient was sent to the cardiology department in our hospital for detailed cardiac examinations. Holter’s ECG recording for 24 h indicated the constant fixed 2:1 AV block. Echocardiography demonstrated a normal left ventricular systolic function with ejection of 80.2% with no segmental anomaly. At that time, exercise stress testing and cardiac artery computed tomography were not conducted due to the symptom of lumbar spinal canal stenosis and patient’s denial, respectively. After discussion with the consulting cardiologists, we concluded that she was at a low risk of progression to high grade AV block as she was asymptomatic, had a stable heart rhythm, had no established underlying cardiac disease, and a narrow QRS interval. Therefore, we decided that a temporary (or permanent) pacemaker would not be implanted before surgery in this case. In addition to the general preoperative explanation, the attending anesthesiologist informed the patient about the potential risks associated with her AV block, as well as our recommendations including relevant alternatives, obtaining the consent for the management of anesthesia.\nOn the day of surgery, no premedication was administered before surgery. Standard monitoring systems, including ECG, pulse-oximetry, and non-invasive blood pressure, as well as a radial arterial line, were placed in the operating room. An external transcutaneous pacemaker was ready to use in case it was needed. Just before induction of anesthesia, the patient’s ECG pattern remained similar to preoperative examinations, i.e., second-degree 2:1 AV block, at a rate of 46 bpm, and blood pressure was 121/74 mmHg, SpO2 was 97% at room air. After administration of 100% oxygen, general anesthesia was induced with 150 mg of intravenous thiamylal and 25 μg of fentanyl followed by intravenous administration of 50 mg of rocuronium to facilitate endotracheal intubation. Sevoflurane (1.0–2.0%) was used to maintain anesthesia. A few minutes after induction, the HR gradually decreased to <40 bpm. Atropine was then given intravenously as a bolus of 0.5 mg, but showed ineffective. Conversely, the 2:1 AV block progressively converted to complete AV block (Fig. ). During the third-degree AV block, the hemodynamic collapse did not occur, i.e., the patient’s hemodynamic status was relatively stable with a HR of 38–46 bpm and BP of up to 80/50 mmHg. Arterial blood gas analysis revealed no pathological data. Therefore, the pacing or pharmacological interventions were not considered at that time. After discussion with the surgeons and cardiologists, surgery was postponed in order to implant prophylactic transvenous pacemaker leads and to obtain an additional patient’s informed consent. Subsequently, sevoflurane inhalation was interrupted and 200 mg of sugammadex was given for reversal of neuromuscular block. During emergence from anesthesia, the third-degree AV block recovered to 2:1 AV block, similar to the preoperative pattern. The patient emerged smoothly and was extubated in the operating room. The vital signs remained stable with HR in the range of 48–61 bpm and BP in the range of systolic 100 to 138 and diastolic 68 to 80 mmHg. She was monitored in the intensive care unit for 2 days and then transferred to the normal orthopedic ward uneventfully.\nThe patient’s surgery was rescheduled for 1 month later. This time, implantation of a preoperative transvenous temporary pacemaker was performed for the emergent treatment of bradyarrhythmias, with the patient agreement. On arrival to the operating room, the patient’s ECG showed 2:1 AV block, same as the previous time, at a rate of 52 bpm, and blood pressure was 119/67 mmHg. A slow mask induction using sevoflurane with oxygen was started. Upon loss of consciousness during the inhalation of the initial 2% sevoflurane, HR decreased to <40 bpm just as it did during the first anesthesia. Temporary pacing was immediately initiated with 60 bpm in VVI mode (output 5 mA, sensitivity 1 mV), after that it worked well. Subsequent anesthesia and surgery were uneventful. The emergence from anesthesia was smooth, and she was extubated without difficulty in the operating room. The patient made an uncomplicated recovery from surgery with stable hemodynamics. Since the temporary pacemaker was no longer required, the catheter was removed 1 day after surgery. The patient was discharged 14 days postoperatively and has been in periodical follow-up at the department of cardiology. Approximately 6 months after surgery, the patient experienced bradycardia-related symptoms such as dizziness and weakness and underwent permanent pacemaker implantation. Her symptoms completely disappeared after the implantation.
An 18-year-old otherwise healthy female patient presented to a local community hospital emergency department with a 3-day history of non-specific abdominal pain. While at the referring facility, the patients’ pain progressed rapidly to peritonitis. Initial evaluation at the referring facility included a CT scan, which demonstrated herniated large bowel into her thoracic cavity through a suspected anterior/retrosternal hernia (Fig. ). The patient was transferred to our institution for further management.\nUpon arrival to our emergency department, the patient was febrile, obtunded and with a heart rate of 200 beats per minute. Her abdominal exam was consistent with peritonitis and her laboratory studies were consistent with shock and lactic acidosis. During evaluation by the surgical team, the patient required emergent intubation for progressive respiratory distress with ongoing fluid resuscitation for the treatment of shock. En route to the operating suite, the patient demonstrated rapid escalation in airway pressures, and cardiac arrest. After return of spontaneous circulation, a post-intubation chest radiograph demonstrated opacification of her left thoracic cavity and a coiled nasogastric tube within her stomach above her diaphragm (Fig. ). Her abdomen became progressively more distended, concerning for abdominal compartment syndrome. With ongoing bag-mask ventilation, the patient was rushed to the operating room for emergent laparotomy.\nLaparotomy revealed intra-abdominal contents under pressure with turbid fluid. Manual reduction of the retrosternal diaphragmatic hernia contents revealed strangulated ascending and transverse colon with full thickness necrosis and an incarcerated yet viable stomach. The contents of the hernia (stomach, ascending and transverse colon) were carefully reduced and a 3 × 3 cm2 hernia defect was noted in the retrosternal position which was repaired primarily. The hernia sac was reduced and excised. An extended right hemicolectomy was performed in damage control fashion, leaving the bowel in discontinuity with a plan for re-exploration after further resuscitation.\nThereafter, the patient was admitted to the ICU for further resuscitation. She was gradually weaned off vasopressors, and sedation was weaned revealing intact neurologic function. After normalization of her physiologic parameters, the patient was taken back to the operating room for planned re-exploration at which time a gastrostomy tube was placed, and further necrotic bowel margins were resected. She subsequently underwent two additional planned abdominal re-explorations resulting in restoration of intestinal continuity with an ileo-descending colon anastomosis and reconstruction of her abdominal wall utilizing a biologic mesh. Due to prolonged ventilator dependency and respiratory failure, a tracheostomy was performed on hospital Day 10. Her post-operative course was unremarkable and she was downgraded from the ICU on hospital Day 23, decannulated on Day 30, and was discharged on hospital Day 33 after tolerating a regular diet. She suffered no neurologic sequelae and has since resumed full activities of daily living.

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