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Our patient is a 49-year-old male of Afro-Caribbean descent with a known diagnosis of B cell lymphoma and acral lentigous melanoma. He presented with a pigmented lesion found to be melanoma on his right plantar lateral sole of foot as well as widespread lymphadenopathy.\nAn incision biopsy revealed a breslow thickness (BT) of 3.4 mm, clark level 4 and he was referred to a plastic surgery department in a tertiary skin cancer network for a wide local excision. As our patient had clinical lymphadenopathy in the right groin and widespread palpable lymph nodes secondary to his concurrent diagnosis of B cell lymphoma, SLNB was discussed within the skin cancer MDT rather than proceeding directly to lypmph node clearance.\nMeanwhile a subsequent narrow margin wide local excision found a BT of 1.1 mm and the surgical defect was reconstructed with double stage integra and split thickness skin graft application. A combination of clinical examination and CT imaging identified widespread lymphadenopathy involving bilateral groins, axillae, cervical and intra-abdominal regions. SLNB confirmed a diagnosis of metastatic melanoma in a 8 mm sentinel node. Figure shows the presence of intracytoplasmic melanin pigment seen on histological analysis\nIn accordance to national guidelines the patient underwent a complete right inguinal block dissection and histological analysis identified a further four melanoma positive lymph nodes. Affected lymph nodes were also reported to have background features of low grade lymphoma. Figure is a histological image illustrating features of metastatic melanoma and lymphoma coexisting in lymphatic tissue.\nSpecimens were tested for PDL 1 and BRAF mutations and found to be negative. These findings were discussed within the skin cancer MDT and a course of adjuvant radiotherapy treatment was recommended. The patient has since been diagnosed with further cutaneous metastases, indicating disease progression to Stage 4 metastatic melanoma. Unfortunately, our patient experienced a further gradual decline over a 3-month period and received a palliative approach to care in the terminal stages of his illness.
A 72-year-old Japanese man underwent an abdominoperineal resection for rectal cancer. At 5 and 12 months after his operation, a perineal hernia and an incisional hernia in the midline were repaired with prosthesis using a transabdominal approach, respectively. Three years after his rectal surgery, a parastomal hernia developed lateral to the stoma. A CT scan confirmed a hernia sac on the lateral side of the stoma, which was a protruding redundant sigmoid colon (Figure ). A parastomal hernia was diagnosed and an operation was scheduled, but as with case 1, the patient had previously undergone mesh repair for an incisional hernia as well as abdominal polysurgery, which meant that access to the abdominal cavity was judged as difficult, and a modified CSM was employed.\nThe surgical field was prepared in the same fashion as in case 1, and a semicircular incision was made on the skin 5cm lateral to the stoma. The hernia sac was located on the stoma’s lateral aspect, and palpation confirmed that the inside was adhered to the intestine (Figure ). The hernia sac was opened to enter the peritoneal cavity, where the sigmoid colon continuing from the stoma limb was found to be adhered to the hernia sac. The adhesion was dissected, the sigmoid colon was reduced to the peritoneal cavity, and the hernia sac was closed. Then, in order to close the fascial defect, a 10cm incision was made longitudinally on the aponeurosis of the external abdominal oblique muscle (Figure ), and a repair was done without tension using the modified CSM (Figure ). The fascia closure was the same as for case 1: a balloon was inserted into the stoma, and the fascia was tightly closed around the stoma. In this case, it was clear that the patient’s abdominal wall was weakened due to abdominal polysurgery, and a lightweight polyester mesh was used in the onlay method to provide further reinforcement. His postoperative recovery was uneventful and the patient was discharged on postoperative day 9, and as of 8 months after the repair, he remains well and without any recurrence.
The patient was a 64-year-old man with destructive injury of both lower extremities due to a machine accident. His left ankle and heel bone, along with the soft tissue, were torn off, and the peripheral blood supply and sensation to the toes of the left foot were lost. We amputated his left leg below the knee. The left fibular head was retained after the left foot operation. Two months later, the patient came to our hospital for additional treatment after debridement of necrotic tissue operations twice. There was still approximately a 20 ×10-cm area on the right foot and right external ankle exposing the distal fibula fractures. X-ray showed that the right external ankle bony defect and the right medial ankle mortise widened; fortunately, the left fibular head was retained after left foot amputation (Fig. ). We reconstructed the right ankle using vascular anastomosis of the fibular head and a flap taken from the left stump. The Ethics Committee of the Second Affiliated Hospital of Soochow University approved the study.\nWe used an ultrasonic Doppler instrument (Model: ES-1000SPM Hayashi Denki Co., Ltd, Hong Kong China) to find the perforating branch of the peroneal artery before surgery, and near that location we created a flap approximately 20 × 10 cm in size according to the right foot wound (Fig. ). Surgery was performed with the patient under general anesthesia. The patient was placed in the supine position on the operating table with the left knee joint slightly bent and the left lower limb stump in internal torsion. The incision began in the popliteal space, swept down to the fibular head, and continued along the lateral peroneus muscles to the stump extremity. We cut the skin and subcutaneous tissue, then separated the peroneus longus and soleus muscles. We found the nervus peroneus communis on the inner posterior margin of the biceps femoris tendon and dissociated it for protection. The peroneal perforator was located in the intermuscular space between the peroneus longus and triceps surae muscles, then we freed the peroneal artery and 2 accompanying veins. We cut off the biceps femoris tendon, fibular collateral ligament and other muscle tissue attached to the fibula, extracted the fibular head, and then divided the superior tibiofibular joint. On release of the tourniquet, bleeding spots on the fibula and residual muscle tissue showed that the blood supply was satisfied. Therefore, we could then cut off the vessels and take the fibular head (Fig. ). We sewed the biceps femoris tendon and fibular collateral ligament with deep fascia around the lateral tibial plateau to avoid instability of the knee joint. We completely debrided bone splinters and necrotic soft tissue from the lower right limb and smoothed the edges. The free fibular head was fixated to the distal fibula with a fibular plate. The reconstructed inferior tibiofibular joint was reinforced with 3 lag screws before anastomosis of the vessels in the transplanted fibular head with the recipient area. Lastly, we made a suture flap in the wound and inserted rubber drainages (Fig. ).\nDue to necrosis of the skin and soft tissue of the distal flap 7 days after the operation, part of the reconstructed external ankle bone was exposed, so we transferred the sural neurocutaneous vascular flap to repair the skin and soft tissue defects of the lateral malleolus. X-ray examination 3 months after the operation showed that the fracture had a bony union and the shape of the transplanted fibular head was similar to the normal external ankle. At 12-month follow-up, walking function had been recovered with the help of a left artificial limb (Fig. ). According to the Baird–Jackson scoring system, the curative effect was satisfied.
A 63-year-old female with a history of long-term tobacco use, COPD, and stable disease of stage 4 lung adenocarcinoma for three years after short-term nivolumab treatment, developed a pulmonary nodule in the right upper lobe during the interval of her three-year surveillance for primary lung adenocarcinoma.\nThe patient was originally diagnosed with a stage IIIb adenocarcinoma nearly four years previously after initial presentation with left-sided neck lymphadenopathy. She had a left upper lobe mass with diffuse lymphadenopathies in the hilum and mediastinum visible on CT scan. She was treated with paclitaxel and carboplatin, but the disease progressed with brain metastasis and bulky lymphadenopathies over eight months. Her lung adenocarcinoma was restaged to stage IV. She received stereotactic radiation for brain metastasis and received nivolumab every three weeks, in total eight doses, until she refused further treatment. She underwent imaging surveillance every six months. Her scan revealed a partial response to immunotherapy with resolution of lymphadenopathy. Her primary lung cancer remained stable without any new nodules, progression, or metastasis for three years until a new nodule was found. The patient also remained asymptomatic other than her chronic shortness of breath and cough due to her underlying COPD.\nAt her three-year surveillance, the newly developed right upper lobe nodule measured 1.5 cm × 0.8 cm (shown in Fig ). The patient missed her follow-up appointment, so PET- CT scan was delayed for two months. Following PET-CT scan, there were no other signs of increased metabolic activity other than the new nodule (as shown in Fig ). At around the same time, the patient was seen at the emergency department due to exacerbation of her COPD symptoms. A CT pulmonary angiogram was carried out as part of her COPD exacerbation work-up at the emergency department visit. The study revealed an increase in the size of the mass to 2.8 cm × 2.1 cm, which was eight times larger in volume compared to that initially detected (shown in Fig ).\nHistopathology from imaging-guided biopsy of the mass showed high grade neoplasm with malignant glandular and mesenchymal elements, consistent with biphasic pulmonary blastoma. Histologic characteristics were distinctly different from the patient's previously diagnosed adenocarcinoma. Immunohistochemistry stains revealed wild-type beta-catenin, diffuse p53 expression, positive AE1/AE3 in the glandular component, and negative TTF-1 and chromogranin. Her previous adenocarcinoma exhibited a glandular pattern and TTF-1 expression was positive (Fig ). Next-generation sequencing (NGS) revealed a genetic profile distinctly different from the primary lung adenocarcinoma. The secondary tumor expressed a high tumor burden with 23 mutations per megabase. Extensive mutations were found in NF1, FGFR3, MBN1, ATRX, KDMGA, PARK2, PBRM1, amplifications in MCL1, MDM4, NKX2 and PIK3CB with low expression of PD-L1 (Table ). The primary adenocarcinoma was found to have a high PD-L1 expression in the primary tumor without high mutational burden.\nShortly after her diagnosis, the patient underwent right upper lobectomy and mediastinal lymph node dissection. Surgical margins and mediastinal lymph node dissection were negative for tumor involvement. The surgical pathology confirmed the biopsy pathological findings. The follow-up CT scan of her chest after recent surgery revealed only postsurgical changes. To date, the patient has remained clinically well at her follow-up appointments.
A 6-hour-old female neonate born from a 22-year-old Para 1 mother after term pregnancy. The newborn had protrusion of mass per vagina since birth; she also has a defect at the lower back with no discharge since the time of birth. Additionally the mother has noticed deformity on both legs and feet which barely move. The baby was active since the time of delivery and is sucking well and she passed meconium. The mother had two ANC visits and was vaccinated according to the national schedule and she reported the whole course of the pregnancy as uneventful. She did not have any known medical illness and has never taken any medication during the entire course of the index pregnancy except iron folate which was prescribed during the ANC visit.\nShe had spontaneous onset of labor and the membrane was ruptured spontaneously intrapartum. She gave birth to a 2330-gram female neonate after 5 hours of labor at a local health center. Baby had good APGAR score. Health care providers at the health center noticed defect at the back of the baby and referred her to Hawassa University Comprehensive Specialized Hospital (HUCSH) with the diagnosis of spinal bifida.\nDuring the initial evaluation at HUCSH the baby was active, vital signs were in the normal limits, and all neonatal reflexes were intact. There was 4x4 cm pink mass protruding through the introitus, cervical os is noted at the tip of the mass, the external genitalia appears normal, no discharge or bleeding from the mass, and the mass was reducible digitally and increases in size when the baby cries (see ). There was also 4x4 cm defect at the lumbosacral region the major portion of which is covered with skin while the lower edge is open, no discharge from the mass (see ). Additionally the newborn had bilateral club foot deformity (see ).\nOn investigation, the complete blood count was normal, creatinine level was 0.4mg/dl, and transfontanelle ultrasound scan shows mild dilatation of the lateral and third ventricles with an index of “mild hydrocephalus” and abdominal ultrasound was normal.\nAfter obtaining consent from the parents, under aseptic technique, the baby was catheterized, the vaginal mass was reduced digitally, and bandage was applied from the lower abdomen, both buttocks and legs were strapped in the bandage to the level of the mid-thigh leaving an opening at the anal orifice for passage of stool (see ). The bandage was removed after 72 hours at which time the mass was completely reduced and there was no recurrence of the prolapse afterwards (see ). Unfortunately one day after the removal of the bandage the baby started to shoot fever and had difficulty of sucking, on examination she had tachycardia and tachypnea and was febrile, she had depressed reflexes, the lower border of the meningocele got ruptured, her fontanels were bulged, and she was diagnosed with ruptured myelomeningocele and meningitis. The plan was to start her on antimeningitis drugs and repair the spinal cord defect after improvement but the parents insisted and went home against medical advice frustrated by her multiple anomalies. We communicated with the parents after her discharge and were informed that the baby died 7 days after she went home, but there was no recurrence of the prolapse throughout her stay.
A 32-year-old male presented with a painful subconjunctival horseshoe shaped swelling around the limbus in the superior part of the bulbar conjunctiva with surrounding chemosis and congestion []. Other ocular examination findings of both the eyes were within normal limits including fundi and visual acuity. The swelling initially started in the lower part of the eye, in the infero-lateral part of the bulbar conjunctiva 2½ years back; for which he went to a private eye hospital. Computed tomography scan report at that time was suggestive of orbital pseudotumor. Blood examination findings including blood sugar and cell count were within normal limits. The patient was treated with topical as well as oral corticosteroid (60 mg daily, which was tapered off within a period of 6 weeks). But the lesion did not resolve; for which he consulted several ophthalmologists. As the patient did not get relief, he started taking oral prednisolone 10 mg on his own whenever symptoms like pain, redness and swelling aggravated. This went on for 26 months after which he developed pain, swelling and redness in his left leg in October 2011. He consulted a physician and was diagnosed with steroid induced type 2 diabetes mellitus with cellulitis of the left leg. At the time of diagnosis, his postprandial blood sugar was 378 mg%, and fasting blood sugar was 153 mg %. He was hospitalized for 10 days and treated with metformin at a dose of 500 mg twice daily and injectable piperacillin and tazobactam. After treatment, his blood sugar came down to normal limit and cellulitis resolved. During this time, the nodular mass in the superior bulbar conjunctiva decreased in size to 3 cm × 2.5 cm and appeared fixed to sclera []. Ultra-sonography of the eye showed a hazy mass without any fluid in the episcleral area with no intra-ocular extension []. The patient was advised surgical excision, but he refused surgery. After 6 weeks, he again reported with increased pain and swelling. On examination, the lesion was found to be covering almost the whole of the upper part of the limbus as in . Patient agreed for surgical excision this time and on opening the cystic wall a little fluid came out with a white ribbon like worm (cestode larvae) with a yellow coiled area around the broadened head []. The cyst was removed and sent for histopathological examination, and the worm was sent to Department of Microbiology for identification in formalin. The patient was given moxifloxacin 0.5% eye drop 8 hourly for 4 weeks and prednisolone acetate 1% eye drop initially 2 hourly for 7 days and then tapered as 4 hourly for 7 days, 6 hourly for 7 days and 8 hourly for 7 days. Tablet ciprofloxacin 500 mg 12 hourly and tablet ibuprofen and paracetamol were given orally both for 5 days. The inflammation and other symptoms resolved after 2 days, and he was discharged from hospital. The patient was lost to follow-up after his discharge from hospital.\nThe worm was a cestode larva, about 40 mm × 1 mm in size, flat with a broadened anterior end which appeared as pseudoscolex, without any mature proglottids and showed presence of bothria [Figures –]. There were no suckers. The larva was identified as sparganum, the plerocercoid larvae of the genus Spirometra.
A 75-year-old man presented at the emergency room shortly after he sustained an injury from a horse fall. When he fell, the horse lost balance and fell on him, crushing his groin. His past history showed he was diabetic. His heart rate (HR) was 90 beats/min and blood pressure (BP) was 50/0 mmHg. Bruising, swelling, and distention were seen in the right groin on inspection. A large pulsatile hematoma in the right groin was palpated. There was a right lower quadrant tenderness, and no rebound tenderness or guarding (). The ankle pulses were palpable and there were no edema and ischemic changes in the lower extremities. His hemoglobin level was 10.2 g/dL on admission but decreased 1 hour later to 6.7 g/dL. After rapid transfusion of five units of packed red blood cells (RBCs) and five units of fresh frozen plasma (FFP) through a central venous catheter, his vital signs stabilized. His BP was 95/50 mmHg and his HR was 90 beats/min. An emergency computed tomography angiogram showed a hematoma in the right inguinal and femoral region, and active bleeding of the iliac or femoral artery was confirmed. There were no accompanying fractures of the pelvis or lower extremities ().\nWe determined that it would be difficult to access the injury site and secure the field during open surgery due to severe swelling and hematoma. If it took a lot of time to access the surgical site, the patient’s chances of resuscitation would be expected low. Therefore, we decided to perform an emergent endovascular procedure for rapid hemostasis under general anesthesia with C-arm. We directly punctured the left CFA and inserted a catheter to the right external iliac artery in a crossover approach. Active bleeding of the iliac artery was not seen on the intraoperative angiogram, but extravasation of the contrast media was confirmed in the femoral artery. The rupture site was the EPA, below the inguinal ligament, and quite above the bifurcation of superficial femoral artery and deep femoral artery. The rupture site was covered with an 8×50 mm Viabahn® stent-graft (W.L. Gore & Associates, Inc., Flagstaff, AZ, USA) (). The final angiography confirmed that there was no more bleeding from the artery, and blood flow to the right lower extremity was not disrupted.\nAfter removing of the endovascular device and compressing the puncture site for hemostasis, BP decreased to 70/35 mmHg and did not rise thereafter. After rapid transfusion of 3 units of RBCs and 1 unit of FFP through the Fluid Management System (Model 2516 universal 3-Spike disposable set; Belmont Inst., Billerica, MA, USA), BP rose to 110/50 mmHg. Bleeding from other sites was suspected; therefore, we performed a longitudinal incision and explored the right inguinal area. A 3-mm defect was found on the anterior wall of EIV above the right inguinal ligament. And a primary repair was performed with a prolene suture 5-0 (). Minor bleeding was controlled, a 200 mL Jackson-Pratt drain was inserted, and the incision was closed. The patient was then moved to the intensive care unit. Dual antiplatelet therapy (aspirin and clopidogrel) were started on the 10th day postoperatively, when the bleeding tendency decreased and disseminate intravascular coagulation improved.\nDuring the second postoperative month, pulmonary edema developed, and a non-ST-elevation myocardial infarction was diagnosed. A percutaneous coronary intervention was done, and a coronary stent was placed. There was repeated surgical site infection by staphylococcus epidermidis, a skin flora at the groin, and it was improved by intravenous administration of vancomycin. Wound debridement and skin grafts were performed twice (). As the inguinal wound improved, the patient was discharged 94 days after surgery. He has been continually monitored through the outpatient clinic, and 71 months after the deployment of the Viabahn® stent-graft, it is still patent ().
A 57-year-old female was referred for evaluation of pain on #26, the upper left first molar. She complained dull pain on #26 when chewing. The patient reported a history of pain on #26 five months ago. To resolve her discomfort, she visited her general dental practitioner and root canal therapy was performed on this tooth. The patient had some relief of pain for approximately 2 weeks after root canal treatment of #26 was completed, but the pain returned. The patient was subsequently referred when the pain did not abate.\nClinical examination revealed that tooth #26 was restored with gold crown. Percussion and bite testing of #26 were positive and periodontal probing depths of #26 were less than 3 mm. All adjacent teeth responded within normal limits for percussion, palpation, bite test and vitality when tested with cold and electronic pulp tester. Radiographic examination revealed tooth #26 had root canal treatment and no noticeable pathologies were observed (). On the basis of clinical findings and history of pain, a diagnosis of acute apical periodontitis was suspected. Root canal retreatment was performed on this tooth. During the treatment, missing canal MB2 of #26 was found. After canal enlargement and canal dressing with calcium hydroxide on MB2 canal of #26, the pain was relieved and root canal retreatment was completed () on assumption that acute apical periodontitis because of untreated canal, MB2 of #26 was the source of her pain.\nThe patient visited again 9 months later complaining that the pain returned to the area of tooth #26. The patient reported spontaneous dull pain and gingival pain of #26. The patient also wanted removal of gold crown on #26 because she felt odd taste of crown. Percussion, palpation and bite testing of #26 were negative. A Radiograph was taken, which revealed no noticeable pathologies () As well, all adjacent teeth responded within normal limits for percussion, palpation, bite test and vitality when tested with cold and electronic pulp tester. Intraligamental injection on this area was not effective in reducing the pain. A definitive diagnosis could not be made from the clinical findings, the following treatment options were discussed with the patient: (1) no treatment and follow-up check for monthly, (2) apical surgery, or (3) extraction. The patient was told that the pain may be referred from another source or from another tooth. The patient elected to have no treatment and follow-up check for monthly.\nOn follow-up 1 month later, the patient reported continued pain in the area of the treated tooth. The dull pain on #26 was exacerbated and tingling on the right maxillary posterior area and burning sensation of left lateral side of tongue were appeared. The patient insisted that treated tooth #26 was the source of the pain. Radiographic examination revealed that no noticeable pathologies were observed on #26 (). There were no mucosal abnormalities and the patient is a postmenopausal woman. A possible diagnosis of burning mouth syndrome was suspected. The patient was referred to the Department of Oral Medicine, Kyungpook National Dental Hospital. Further questioning revealed that the onset of pain was spontaneous and the burning sensation often occurred in more than one oral site, those were the left posterior palate, buccal gingiva and left lateral side of tongue. Alterations in taste also occurred. The presenting complaint was diagnosed as burning mouth syndrome. 10 mg of benzodiazepine (Rivotril, a chlonazepam, Roche, Basal, Switzerland) taken twice daily, was prescribed. This provided a reduction in pain from 8 of VAS scale to 4 after four weeks and to 1 after ten weeks, this was effective in controlling the symptoms.
A 44-year-old male presented to the emergency with the chief complaints of recurrent postprandial epigastric pain for three days. On scrutiny of previous records, it was discovered that this was his third hospitalization for the same complaint. On all three occasions, the patient reported that his complaints were triggered after fasting for religious reasons. He had also undergone a gastroduodenoscopy three months back revealing gastric erosions for which he had been prescribed omeprazole. At the time of the admission, this was the only drug he had been taking. No history of previous abdominal surgery was noted. On examination, apart from tachycardia, other vitals were stable. The abdomen was distended but tenderness could not be elicited. On digital rectal examination, there was rectal ballooning without any soiling of the examining finger. All hematological investigations were within normal limits and an ultrasound of the abdomen was also normal. The abdominal radiograph showed multiple air fluid levels suggestive of intestinal obstruction. A computed tomography of the abdomen was also suggestive of subacute intestinal obstruction. The patient was started on intravenous fluids and a nasogastric tube was inserted. Twelve hours later, the patient underwent an exploratory laparotomy for worsening abdominal pain, signs of peritonitis and non-resolving small bowel obstruction. On opening the abdomen, the ileum had twisted along its mesenteric axis in the clockwise direction (Figure ).\nMild distention of the stomach and proximal ileal loops was noted. The large bowel distal to the site of twisting was collapsed. No perforation or band was found. The volvulus was untwisted, and a line of rotation was seen. No fixation of the twisted segemnt was done. The bowel was slightly discoloured, but viable and started to return to its normal colour and shine (Figure ).\nThe patient was given 100% oxygen and the bowel was covered with warm moist sponges till the serosa returned to its normal color. Further examination revealed no other abnormalities like internal hernias or malrotation. The post-operative period was uneventful and the patient was discharged on the fourth postoperative day.
The patient involved provided written consent for reporting of this case. A 63-year-old woman with medical history of super morbid obesity (BMI 54) and atrial fibrillation for which she was anticoagulated with apixaban presented for an open reduction internal fixation (ORIF) of an ankle fracture. Significant medical history included diabetes mellitus type 2, obstructive sleep apnea, chronic obstructive pulmonary disease, and diastolic heart failure. The patient's last dose of apixaban was 48 hours prior to surgery. Other than moderate anemia (hemoglobin 8.8 g/dL), all laboratory studies, including a coagulation profile, were normal. Prior to surgery, the patient was offered a sciatic nerve catheter and an adductor canal block as part of a multimodal postoperative analgesia strategy. Because of her many, serious medical conditions, we concluded that a peripheral nerve block offered the best opportunity to provide satisfactory postoperative analgesia. Specifically, we were concerned that the postoperative pain management primarily with opioid medications would pose increased cardiopulmonary risk to the patient. We were careful to explain the risks associated with peripheral nerve blocks, including the risk of bleeding and hematoma formation, and verbal consent was obtained. The surgery was performed under general anesthesia and her intraoperative course was uncomplicated. Upon arrival to the recovery room, our acute pain service was contacted to evaluate her for peripheral nerve blockade. We positioned the patient in the lateral decubitus position and placed a sciatic nerve catheter. Though technically challenging due to body habitus, this sciatic nerve block was performed successfully and without any complication. The patient was then positioned supine for the adductor canal block. The leg was externally rotated and the knee slightly flexed for optimal positioning. A high-frequency linear array ultrasound transducer was applied to the mid-thigh in short-axis and the adductor canal was identified. Imaging was again challenging given the patient's habitus, but with firm compression of the ultrasound transducer, the important anatomical structures were clearly identified. The superficial femoral artery (SFA) was visualized
A 58-year-old male with a distant history of inguinal hernia repair presented to the emergency department with severe, sudden onset left groin pain after swinging a golf club. The pain was aggravated by lying or sitting, and not alleviated by over the counter strength acetaminophen. Vital signs on presentation were within normal limits except for a systolic blood pressure that remained in the 170s until midway through his hospital stay. On physical exam, the patient was positive for tenderness in the left lower quadrant, but negative for rebound pain. His bowel sounds were of normal quantity and quality, and clearly auscultated throughout the abdomen. Initial laboratory results, which are detailed in , were grossly normal. Ultrasound imaging was negative for testicular torsion or mass. A computed tomography (CT) scan of the abdomen and pelvis with intravenous (IV) and oral contrast revealed the presence of a pelvic kidney. Acute and chronic infarctions were noted in distant locations within that kidney.\nThe etiology of the infarction remained unknown. A full hypercoagulability panel, renal doppler ultrasound, and computed tomography angiography (CTA) were ordered along with initiation of a heparin drip for a presumed acute embolic event. The hypercoagulability panel () and renal artery dopplers did not identify a cause for the infarction. The CTA showed three arterial supplies from the following locations: (1) the bifurcation of the aorta (implicated in the infarction); (2) the proximal portion of the right common iliac; and (3) the left internal iliac artery. A dissection was identified in the aortic branch supplying the anterior pole of the pelvic kidney and its associated necrosis (–).\nConversations with vascular surgery, interventional radiology and cardiology led to a decision to treat the infarction medically with dual antiplatelet therapy (Plavix 75 mg and aspirin 325 mg) along with continuation of his heparin drip while hospitalized. An endovascular attempt to stent the dissected area was not plausible for several reasons. The size and location of the vessel made it difficult to access and may have caused more trauma to the area without overall benefit. In addition, the IV contrast needed to perform the procedure may have damaged the remaining healthy nephrotic tissue. After three hospital days, the patient was discharged in a hemodynamically stable condition, with instructions to continue the dual antiplatelet therapy medications for 6 months. Follow-up CT scan and labs showed a stable infarct and normal creatinine level indicating there was no lasting damage from the incident.
The patient was an 86-year-old man suffering from a long lasting myelodysplastic syndrome (MDS) transformed to an acute myeloid leukemia (AML). In order to avoid a useless hospital admission for a chronic and unrecoverable condition, he was followed up at his home, given the need of transfusion and his severe state of disability,[] due to which he was unable to attend our day hospital unit. The patient was unsuitable for intensive chemotherapy and was treated with hydroxyurea, with a palliative intent. He suffered from multiple comorbidities, such as diabetes mellitus, hypertension, severe cognitive impairment due to progressive cerebrovascular illness, and chronic renal failure (CRF), which progressed to ESRD after one month of beginning of the home care program. Therefore, he was evaluated for HD; however, his clinical conditions and functional status precluded the possibility to attend a regular HD program as outpatient for which domiciliary CPD was offered. Therefore, the patient was admitted in the hospital for placement of peritoneal catheter. No complications were found in the postoperative period. During the recovery, given that he was unsuitable for learning or performing CPD, a patient's caregiver was trained in the catheter exit site medications, in the process and support system related to the technique to achieve the best practise for peritoneal dialysis state. Moreover, the caregiver was educated on the importance of infection control and an appropriate medical regimen to ensure adequate dialysis and improvment in the patient's general condition and well-being. The patient was discharged 10 days later, and caregiver training continued at the patient's home for another two weeks. The treatment plan were prescribed and supervised by our team, which included a skilled nephrologist, seven hematologists, 10 nurses, one psychologist and social worker, and several other care providers trained in hematology, palliative care, and rehabilitation medicine. A trained caregiver was present at home; moreover, written guidelines for the rapid admission of patients in case of clinical complications unmanageable at home were predisposed. Oral palliative chemotherapy with hydroxyurea, regular red blood cell transfusion and other medications were given as required. The CPD program was safely and effectively carried out for entire course of the domiciliary assistance without any complications. However, the patient died because of disease progression and pneumonia in his home, sustained during the end-life by the closeness and good feeling of his loved ones.
A 44-year-old previously healthy Asian female reported to the neurology clinic with complaints of episodic, persistent, uncomfortable needle-like sensations in her genitalia extending to the anal area and the tip of the coccyx. She had been suffering from these symptoms for approximately 11 years. She had difficulty describing the actual nature of this phenomenon, which, according to her, was more of an irritation and discomfort than actual pain. The discomfort was aggravated during rest and periods of inactivity, particularly at night. It responded briefly to mefenamic acid tablets for four to five hours. She also reported the pain was worse before her monthly menstrual cycle but that sexual activity did not affect her discomfort. Sometimes, the discomfort was intense and would wake her from sleep causing severe discomfort and resulting in difficulty sitting; walking would relieve her symptoms partially. She was better in the morning, but the symptoms appeared again at end of the day. She had multiple gynecology and dermatology consults with no relief or clear diagnosis. She was prescribed antifungal creams, including fluconazole and ketoconazole, topical steroids (betamethasone and hydrocortisone), and mefenamic acid for pain relief. All failed to bring relief. She also consulted a homeopathy practitioner, who labeled her as suffering from a chronic skin disease and prescribed oral and topical medication. She took it for a few months but stopped it due to lack of relief. Ultimately, due to the distress and anguish associated with the condition, lack of response to various treatments, and social embarrassment, she stopped visiting doctors for some time. However, during a recent visit, the consulting gynecologist suspected it was not a dermatological or gynecological problem and referred her for a neurology consult.\nThere was no history of back pain, sensory symptoms in the legs, urinary incontinence, or neurological disorder, such as Parkinsonism or restless leg disorder. She had a stable and happy marital life of 22 years and had three children. She has used no substance of abuse or recreational drugs. Her neurological and gynecological examinations, as well as magnetic resonance imaging (MRI) of the spine, were normal (Figure ). Similarly, her biochemical profile (including complete blood count, urine analysis, serum urea, and creatinine) and an ultrasound examination of abdomen and pelvis were normal.\nConsidering her history of circadian rhythm variations in symptoms and aggravation on rest, RGS was considered the most likely cause of her symptoms. After a detailed discussion with the patient, she was prescribed 0.5 mg of ropinirole once at night. It was increased to twice daily after seven days, to which she responded well and reported a dramatic relief of symptoms after 14 days. The dose was increased to 1 mg in the morning and 0.5 mg at night, which led to further improvement. On her third follow-up after two months, she reported taking her medication regularly, which led to almost no episodes of discomfort, with exception of one or two times. The dose of ropinirole was maintained for one month. At the three-month follow-up, she reported only one episode of pain and itching, when she missed one dose of her medicine for a few days; otherwise, she had no complaints and reported no side effects of the medication.
A 70-year-old female presented to our department with a 3 cm irregular left auxiliary mass. Diagnostic ultrasound, computer tomography, and magnetic resonance imaging revealed direct contact with the auxiliary vessels and the auxiliary nerves (Figs. 5(a) and (b)). The patient's medical history included invasive ductal cancer of the left breast nine years earlier (initially cT2 cN0 M0) treated with neoadjuvant chemotherapy (6x DAC), breast conserving surgery, auxiliary lymph node dissection , adjuvant radiotherapy to the left breast and lower axilla (without the auxiliary apex or the supraclavicular region) up to 50 Gy, followed by adjuvant hormonal treatment. The current auxiliary mass was located at the upper edge of the previously irradiated volume. An ultrasound-guided auxiliary biopsy revealed a malignant sarcomatous growth, which based its location at the inner edge of the old radiation field used to treat the patient for breast cancer, and the latency period of nine years fits the pattern of a radiation-induced secondary cancer., , , Surgical dissection of the auxiliary mass was planned. Given the expected difficulty to achieve wide resection margins close to the auxiliary vessels and the added difficulty of postoperatively reirradiating the axilla to an adequate dose, intraoperative irradiation of the tumor bed, including the vascular sheath, was proposed in case inadequate resection margins were found. Patient's consent was obtained. Macroscopically removed, the attachment of the mass to the sheath of the auxiliary vessels prevented the surgeon from reaching clear resection margins. The decision to use IORT was made intraoperatively, based on the judgment of the experienced surgeon and the radiation oncologist. To reduce the risk of local auxiliary recurrence, intraoperative irradiation of the vascular sheath and the surrounding auxiliary fat at the resection bed was performed using the 4 cm flat applicator, which was optimal in regard to shape and size to cover the area to be treated. The thoracodorsal nerve was dissected and displaced temporarily outside of the radiation field (Figs. 5(c) and (d)). The brachial plexus was located 1.5-2 cm deep to the applicator and required no special protection measures. A dose of 5 Gy was delivered in 5 mm depth (corresponds to 6.5 Gy at 3 mm (dhmax), 10.5 Gy at the applicator surface and 1.7 Gy in 15 mm depth (location of the brachial plexus)) over 21 minutes. The IORT dose was chosen to be used as an early boost within the total concept of adjuvant radiotherapy that included a planned postoperative external beam radiotherapy (EBRT) to the axilla and, after considering the previous exposure of the brachial plexus nine years ago, estimated to be equivalent to 24 Gy in 2 Gy fractions. Histopathological and immunohistochemical examinations of the removed mass revealed a pT2b pN0 M0 G3 angiosarcoma. The patient was discharged from hospital on the third day after surgery to regular outpatient postoperative follow-up. No treatment-related side effects were observed five months after radiotherapy.
5-year-old Hispanic female with history of Bardet Biedl syndrome (BBS) presented with concern for early onset weight gain in the setting of hyperphagia. She was born full term, via normal spontaneous vaginal delivery. Prenatal ultrasound at 36 weeks gestational age revealed enlarged kidney and extra digit. Delivery was uncomplicated. At 8 months of age, she was noted to have horizontal nystagmus followed by delayed speech noted at 24 months of age. Subsequent evaluation and testing revealed a heterozygous mutation of c. 273 c>G of BBS10 gene with predicted pCys91Trp mutation consistent with diagnosis of BBS. Shortly after diagnosis, she was enrolled in therapy services including physical, occupational and speech therapy. She was referred to endocrinology for assistance with weight management at the age of 4 due to parental concerns of worsening hyperphagia type symptoms and rapid weight gain over the past 9 months. Prior to the initial evaluation, the family had not implemented any form of structured eating plan for the patient and she was consistently eating frequently from 7 AM to 9 PM.\nInitial evaluation revealed that the child did exhibit hyperphagia behaviors with significant behavioral responses to be refused food. The Family elected to implement a TLE approach for the whole family and limit eating to between 8 AM-5 PM, 5 days per week. The remaining two days the parents allowed for eating until 7 PM, which was the child’s bedtime. At the one month follow up visit, the parents reported that the child took very well to the TLE approach. They reported that the structured time of eating provided a guideline for the whole family and ensured all caregivers were consistent.\nAdditionally, the parents described that they were able to decrease the amount of food focused behavioral rewards they were administering for good behaviors during the fasting periods, especially in the evenings. The parents, older brother (age 9) and patient all were implementing the TLE approach together in the home. At the one month follow up, her zBMI has trended down by −0.1 SD. The family returned to all scheduled follow up visits and the zBMI continued to decrease with a −0.39 SD reduction at 4 months compared to baseline (See ). Overall, the child adapted very well to the intervention and per parents did not demonstrate any distress of behavioral concerns in relationship to the eating periods. Parents reported high levels of satisfaction with this approach and have continued it past the 4 months follow up.
A 17-year-old female patient attended the neurosurgery department complaining of a palpable mass in the left frontal bone as well as headaches and seizures since the age of 8 years. She was born after a normal labor. Nine years later, when she attended the clinic, a physical exam was undertaken that revealed a firm and rounded palpable mass at the left frontal bone ().\nOn neurological exam, the patient had no focal signs. She had normal mental status and vital signs. She was conscious, and her pupillary reflex to light was normal, as were the muscular force, the deep tendon reflexes, and her sensibility. The computed tomography (CT) scan of her head showed a left frontal bone a protrusion ().\nThe CT scan also showed an underlying hypoattenuating, supratentorial lesion in the left frontal lobe and interhemispheric space, which was oval in shape with regular and well-defined borders, suggesting an arachnoid cyst that did not cause a shift in the midline structures when the left frontal lobe was compressed ().\nThe patient was operated on under general anesthesia in the supine position with her head in a neutral position. After the cranium was shaved and cleaned of hair, a bi-temporal incision was made. The underlying tissues were cut in a normal fashion until the left frontal bone deformity was revealed, which had a lilac color (). Six burr holes were made surrounding the deformity (). The bone dust was collected and the bridges between the holes were eliminated with a Gigli saw. A concave–convex bone flap was lifted, which revealed the arachnoid cyst (). The cyst membrane and 20 mL of the intracystic fluid (collected with a syringe) were sent for histological examination. After exeresis of the membrane, it was evident that the cerebral sulci at the level of the interhemispheric fissure and the adjacent areas of the left frontal lobe were flat and depressed due to compression by the cyst. The duramater was closed in a watertight fashion with polyester 5-0 ().\nAn exeresis of the concave–convex and protruding surface of the bone flap was made using an electric saw, which created a free, smaller concave–convex fragment (). Three small holes were made in this free fragment as well as in the surrounding bone flap using a 2 mm low-speed drill. The free concave–convex fragment was placed after being turned inside out and upside down. This fragment was fixed to the surrounding bone using polyester 2-0 sutures ().\nThe resulting bone flap was returned to the skull, and the burr holes were filled with the bone dust that had been collected earlier during the burr placements. The closure was in the normal fashion using polyester 2-0 sutures.\nThe histological exam of the lesion confirmed the diagnosis of an arachnoid cyst. The patient was prescribed antibiotics, an anticonvulsant, and an analgesic during the postoperative period. A CT scan performed 1 week after surgery demonstrated the absence of the cyst and adequate surgical reconstruction ( and ).\nTen days after surgery the patient was discharged. Currently, she is asymptomatic and her physical exam is normal.
A healthy 18-year-old man presented with a 2-week history of chickenpox, and was treated with oral acyclovir for 5 days. Ten days after onset of the cutaneous vesicular eruptions, he experienced blurring of vision in his right eye that descended to the level of hand motion (HM) in 6 hours. At presentation, 4 days after blurred vision, visual acuity in his right eye was hand movement. Examination of the anterior segments was unremarkable except for an obvious relative afferent pupillary defect. His extraocular muscle examination was normal. Fundus examinations revealed an edematous disc, retinal whitening and edema along the posterior pole, and the presence of a cherry red spot; no retinal infiltration or vitreous opacity was observed (). His left eye was normal with 20/20 vision. Optical coherence tomography showed increased thickness and hyperreflectivity in the inner retina layer, consistent with inner retina infarction. The early phase of fundus fluorescein angiography demonstrated delayed filling of the optic disc with minimal leakage from the small retinal arteriole, which was more prominent in the macular and optic disc regions. Minimal capillary dropout in the macular area was also noted. Staining of small vessels was observed in the late phase of the angiogram (–). A multifocal electroretinogram (ERG) showed diminished waveform in the entire macular area (). A full field ERG showed decreased b-wave amplitude of both rod and cone response and oscillatory potential wave. Electronegative ERG pattern was evidenced in maximal combined ERG that represented a generalized ischemic process, which involved mainly the inner retina layer (). The patient demonstrated decreased amplitude and increased latency in flash visual evoked potential (VEP), which is consistent with generalized involvement of the entire retina, not limited only to the posterior pole ().\nMinimal increased signal in T2-weighted magnetic resonance imaging and enhancing with contrast limited to the anterior part of the optic nerve could represent an inflammatory response to the ischemic process of the optic nerve head (). Serologic tests were positive for both immunoglobulin (Ig)M and IgG anti-VZV antibodies, confirming recent primary VZV infection. The diagnosis of ischemic vasculitis of the small retinal vessels associated with chickenpox was made. Since this process could either be caused by infection or an immunological response to VZV infection, and there is no consensus on the optimal treatment regimen for this VZV-associated vasculopathy, either treated with antiviral alone or combined with corticosteroid, we decided to treat the patient with antiviral agent according to the acute retinal necrosis treatment guideline published by the American Uveitis Society, ie, with intravenous Acyclovir 10 mg/kg every 8 hours for 2 weeks in conjunction with intravenous methylprednisolone 1 g daily for 3 days, then with oral prednisolone tapering over 1 month and oral Acyclovir 800 mg 5 times daily for 1 month. Despite the treatment, a pale optic disc and attenuated retinal artery resulted. His final best-corrected visual acuity was counting fingers at 1 foot at 6 months’ follow-up.
A 56-year-old female with a history of uncontrolled biopsy-proven bullous pemphigoid began treatment with cyclosporine 100 mg three times a day for a total daily dose of 300 mg. After five weeks of therapy, the patient complained of nervousness and shakiness, and the cyclosporine dose was decreased to 100 mg twice daily for a total daily dose of 200 mg. After an additional five weeks of cyclosporine therapy at 200 mg daily, the patient returned with complaints of the gradual onset of redness, swelling, and pain of her left hand over the past six weeks (Figure ). On examination, erythema and violaceous swelling were present on the patient’s left hand, most predominant over the dorsal and palmar aspects of the left second and third metacarpals, and left proximal and mid phalanges. There was tenderness to palpation and pain with movement of the left hand and phalanges. The patient described the associated pain as a burning sensation. Although erythromelalgia was considered, this was believed to be a local reaction, and the cyclosporine was continued as treatment for the patient’s bullous pemphigoid.\nSeven weeks later, the patient returned complaining of significantly worsened redness, swelling, and pain of the left hand with progression of involvement of the right hand. On examination, the erythema and edema involved the dorsal and palmar aspects of the left hand and phalanges, most severely affecting the left proximal phalanges. The right hand was also visibly erythematous with edema most prominently involving the right second proximal phalanx. The patient complained of worsened pain, described as “burning similar to a sunburn” that significantly worsened upon exposure to the sun or heat. The pain also worsened with passive and active movement of the hand or digits, as well as palpation of the affected areas. The patient endorsed improvement with exposure of the hands to cold temperatures, particularly describing relief of the pain while running the hands under cold water. At this time, the cyclosporine dose was decreased to 100 mg once daily with a diagnosis of erythromelalgia secondary to cyclosporine. It was hoped that a lower dose of cyclosporine could be used to treat the bullous pemphigoid, with resolution of the symptoms of erythromelalgia.\nSix weeks later, the patient returned for a follow-up to evaluate the erythromelalgia. The erythema and edema had significantly improved, with only minor swelling of the second and third phalanges of the left hand and the second phalanx of the right hand. The patient's symptoms improved following the transition to low-dose cyclosporine therapy (100 mg once daily). At an additional follow-up eight weeks later, the patient’s symptoms of erythromelalgia had completely resolved.
A 64-year-old Asian woman was referred to our department with a 1-month history of DHS. She also suffered from severe right foot pain because of limb ischemia related to systemic sclerosis. She had a history of systemic sclerosis that was diagnosed 30 years earlier and was classified as having limited cutaneous systemic sclerosis. Cutaneous fibrosis was limited to her hands without involvement of her head or neck. There was no family history of any neuromuscular disease. One month before visiting our hospital she developed right foot gangrene. Although she had Raynaud’s phenomenon and ulcerations in her fingers, she had had no symptom in her foot before she had gangrene. Pain in her right foot was so severe that she used tramadol and NSAIDs as painkillers. She began to complain of DHS as her foot pain worsened. She had difficulty in keeping her head straight and her gaze forward. Clinical examination revealed severe weakness of her neck extensor muscles. Her neck deformity was flexible and easily corrected passively (Fig. a). There were no neurological abnormalities including sensory disturbance or muscle weakness in her extremities. Plain radiographs of her cervical spine revealed only mild degenerative changes and severe cervical kyphosis (Fig. ). Cervical magnetic resonance imaging showed no spinal canal stenosis and no abnormal signal change in the cervical paraspinal muscles. Computed tomographic angiography showed occlusion of bilateral anterior tibial arteries and peroneal arteries, and development of collaterals. Despite intensive conservative therapy including alprostadil, argatroban, and sarpogrelate, lower extremity ischemia progressed. Therefore, we decided to amputate her leg below the knee under general anesthesia. Her postoperative course was uneventful. Her severe foot pain was markedly resolved after the surgery. At the postoperative follow-up visit 3 weeks after surgery, her DHS was significantly attenuated (Fig. b). Her forward vision and neck pain were markedly improved.\nThe feature of the present patient was attenuation of her DHS after pain relief by amputation of her severely ischemic limb. The clinical course of the present case suggests that severe pain from her ischemic limb caused the DHS.\nThe patient had a medical history of systemic sclerosis which is also known as scleroderma. There is one case report of a patient with systemic sclerosis who developed DHS, but showed no improvement in a 2-year follow up []. Considering the DHS in our patient resolved within 2 months from onset regardless of the state of the systemic sclerosis, her DHS was unrelated to either systemic sclerosis or other neuromuscular disease. The vast majority of cases of isolated neck extensor myopathy never resolve spontaneously, so it is less likely that she had isolated neck extensor myopathy []. We also found no clinical or laboratory evidence of myositis []. The onset of her DHS coincided with worsening of foot pain and improvement of DHS coincided with pain relief. The cause and the pathogenesis of the DHS remain unclear, but there is a possibility that severe pain caused the DHS. The indirect lines of evidence suggest that severe pain can be a cause of DHS. Although it may be rare, if a patient with DHS has severe pain, we recommend considering the possibility that severe pain is a cause of the DHS after excluding neuromuscular disease. The underlying mechanism by which pain causes DHS is unclear and warrants investigation.
A 30 year old non- smoker woman was admitted to our centre with a 10 year history of asthma like symptoms which did not respond to bronchodilators anymore.\nHer chest radiograph showed bullous lesions, widespread infiltrates and volume reduction in the right lung. Computed tomography of the thorax demonstrated a mass lesion in the right main bronchus extending to the trachea as well as unilateral bullous emphysema with relatively thick septa, pleural thickness and reduced volume of the right hemi thorax ().\nFiberoptic bronchoscopy detected a pink large mass completely obstructing the lumen of right main bronchus and extending to a point close to carina \n(). Due to vascularised appearance of the mass and presumptive diagnosis of carcinoid tumor, biopsy was not attempted. Rigid bronchoscopy was performed under general anaesthesia and biopsy specimens were obtained.\nHistopathologic examination revealed that immediately beneath the intact pseudostratified ciliated columnar epithelium with some focal squamous metaplesia, the neoplasm composed of bundles and whorls of spindle shaped cells with monomorphous fusiform nuclei and acidophilic cytoplasms without cytonuclear atypia, mitotic figures or necrosis (). Also, sections of small blood vessels were observable. Immunohistochemically the tumor showed diffuse cytoplasmic reactivity for desmin while myogenin reactivity was negative (). Ultrasonography of the uterus did not find any abnormality. On the basis of morphological and immunohistochemical findings the lesion was diagnosed as bronchial leiomyoma.\nThe patient was treated by endoscopic resection. However, the tumor was firm and large (3 centimeters in diameter) to remove through the rigid broncoscope despite great effort. In order to avoid tracheotomy and resection of a large portion of lung, a small cut was made in the neck area and the trachea was incised horizontally (tracheostomy). With cooperation of the anesthetics the tumor was brought to the incised region and removed by surgical forceps (). Then the incisions were repaired. The patient was discharged after receiving medical treatment for her lung infection and showed remarkable improvement both clinically and on her control chest radiograph which was performed two weeks after surgery.
A 90-year-old male patient was admitted to the emergency room by his family doctor with suspicion of sepsis due to an infection of his lower limb, of which he was suffering for several days. Clinically he showed a hyperemic, hyper thermic and swollen lower leg with an extensive hematoma in the ventral lower medial limb ( and ).\nAdditionally, the patient was suffering from hypertensive and valvular heart disease, diabetes mellitus type II, cerebrovascular disease and atrial fibrillation. Due to the infection, he had a derailment of his anticoagulation with an INR of 7.8 at admission, requiring an initial conservative treatment.\nAs he showed no improvement of the local status of the ventral lower leg under anti-microbial medication and immobilization, an operative debridement was performed after correction of the coagulation, where there was seen an extensive subcutaneous abscess at the lower leg extending from the medial malleolus upwards to the ventro-medial lower leg ( and ). Wound conditioning was performed with several debridements and vacuum therapy (). As a defect in the region of the medial malleolus persisted, a wound closure with a free flap was indicated.\nA CT angiography showed a relevant stenosis of the arteriae fibularis and tibialis posterior. A percutaneous transluminal angioplasty (PTA) was successfully performed.\nAfter 5 days a wound closure with a free ALT-flap of the ipsilateral leg was done. The A. tibialis posterior was chosen for the anastomosis ( and ).\nPostoperatively the patient developed a wound healing disorder first at the proximal and then at the distal part of the flap. Debridement and VAC therapy was performed, and a secondary wound closure could be done some days later. Additionally, the patient developed a severe postoperative delirium and recurrent episodes of gastrointestinal bleedings. After 5 weeks of hospital stay the patient was discharged back to the nursing home.\nThe further follow up was uneventful and the patient was very satisfied with the functional and aesthetic result ().
An 86-year-old woman who had been living with her elderly husband was admitted to our hospital with the complaints of nausea, anorexia, and epigastric discomfort. When she was 73 years old, the patient had undergone laparotomy and right hemicolectomy for resection of colon cancer. Five years after hemicolectomy, she had received hernia repair surgery using mesh for an abdominal incisional hernia. There was no history of abdominal or thoracic trauma. Laboratory tests were all within the normal range. Her electrocardiogram showed no ischemic changes. Although chest X-ray revealed an abnormal gas-filled mass in the left thoracic cavity, the patient had no symptom of dyspnea. Contrast-enhanced computed tomography (CT) scan confirmed herniation of the gastric corpus through the left posterior part of the diaphragm (). We diagnosed adult Bochdalek hernia and planned its surgical treatment. As mesh had been placed under the previous upper abdominal midline incision more than 10 years earlier, dense adhesions between the mesh and abdominal tissues were expected. Therefore, we decided to perform diaphragmatic hernia repair by HALS, considering the patient’s safety. After induction of general anesthesia, the patient was placed in the supine position with her legs apart. The previous midline incision was opened carefully to insert a LAP DISC® (Hakko, Nagano, Japan) for a hand port. Dense adhesions, which had to be divided, were found between the mesh used to repair her incisional hernia and loops of the small intestine. The disk for HALS was placed after complete removal of the mesh. Subsequently, a 12 mm trocar was inserted into the inferior umbilical region for the laparoscope. A 5 mm trocar was also inserted into the left upper abdominal region. Herniation of the gastric corpus into the left thoracic cavity through a hernial orifice in the left posterior diaphragm was confirmed. The gastric corpus could not be pulled back into the abdominal cavity because of adhesions around the hernial orifice. After these adhesions were carefully removed by HALS using Harmonic ACE shears (Ethicon, NJ, USA) (a), the stomach was completely freed and could be returned to the abdominal cavity. A 5 × 3 cm hernial defect with sac was observed (b). We decided to perform simple closure of the defect without mesh reinforcement because the rim of the hernial orifice was relatively strong. Accordingly, the defect was repaired with interrupted nonabsorbable sutures (2-0 Nesporen; Alfresa Pharma Corporation, Osaka, Japan) using a 5 mm port on the left upper abdomen and the surgeon’s left hand via the hand port (c). The midline incision for the hand port was closed without mesh reinforcement. A drain tube was placed under the left hemidiaphragm. The operating time was 244 min and there was no significant bleeding. Her postoperative course was uneventful. The patient was discharged on postoperative day 20. There was no evidence of recurrence at 1-year follow-up.
A 64-year-old male presented with acute on chronic backache and short distance claudication. He had a background history of hypertension, diabetes, and severe chronic obstructive pulmonary disease (COPD). He also had a history of previous stroke with mild right hemiparesis, slurred speech, and history of epilepsy unrelated to stroke, which was well controlled with antiepileptic medications. A computerized tomography angiogram (CTA) scan demonstrated a 6.5 cm Crawford type III TAAA extending from the midthoracic aorta to the aortic bifurcation with no evidence of any leak. The celiac, superior mesenteric, and right renal arteries were patent, whereas the origin of the left renal artery was occluded with an atrophic left kidney (Figures , , , and ) and normal serum creatinine. The infrarenal component of the aneurysm and both common iliac arteries were thrombosed (Figures and ). A plain chest radiograph revealed a left-sided pleural effusion. Doppler ultrasound of the carotid arteries showed intimal hyperplasia with few calcified plaques in the right common carotid artery but no significant stenosis.\nGeneral anesthesia was induced and a spinal drainage was placed to keep the cerebrospinal fluid (CSF) pressure below 10 mmHg throughout the procedure. A midline laparotomy was performed and repair was carried out in three steps as a one-stage procedure. First, the thrombosed infrarenal component of the TAAA was exposed. In all, 5,000 international units of unfractionated heparin were administered intravenously and a 3 cm vertical incision was made at the anterior wall of the thrombosed infrarenal part of the aneurysm without aortic clamping as the aorta was thrombosed at this level with no blood flow. A 20 × 10 mm bifurcated Dacron graft was anastomosed in an end-to-side fashion to the anterior wall of the thrombosed infrarenal aorta. Once the anastomosis was completed, the thrombus in the infrarenal aorta adjacent and proximal to the aortic anastomosis was retrieved via the limbs of the bifurcated aortic graft. A pulsatile blood flow was achieved in both limbs of the graft. In the second step of the procedure, a second bifurcated graft measuring 14 × 7 mm was oriented in an upside-down direction and anastomosed to the main body of the previously sutured bifurcated graft in an end-to-side fashion for visceral perfusion. The first limb of the new graft was anastomosed to the right renal artery in an end-to-side fashion, while the second limb was sutured to the superior mesenteric artery (side-to-side) and the celiac artery (end-to-side), (). The left renal artery was not bypassed as it was occluded with the atrophic left kidney. During the third and the final step of the hybrid procedure, two tapered Medtronic, Inc. (Minneapolis, MN), stent grafts sized 28 × 24 × 15 mm and 36 × 32 × 15 mm were deployed via the left limb of the first aortic bifurcated graft in a reversed fashion, starting from inside the bifurcated aortic graft and extending upward toward the midthoracic aorta. The two endovascular grafts covered the aorta from the midthoracic level to the main bifurcated Dacron graft with a 5 cm overlap. The endovascular grafts were balloon-molded and all debranched vessels were ligated to prevent a type II endoleak. The right and left limbs of bifurcated aortic graft were finally anastomosed to the respective common femoral arteries in an end-to-side fashion. A good pulsatile blood flow was established in both common femoral arteries and the debranching limbs of the bypass graft. Completion angiogram revealed the complete exclusion of the TAAA without any endoleak and good flow to all the debranched vessels (Figures and ). The retroperitoneum was closed covering all the grafts. The patient tolerated the procedure very well. He was hemodynamically stable during the entire procedure and was transferred to the intensive care unit in a stable condition with a spinal drain in place.\nThe patient was placed on a prophylactic dose of subcutaneous low molecular weight heparin and the CSF pressure was kept below 10 mmHg for 48 hours. He remained hemodynamically stable with no neurological deficit. Renal function deteriorated in the first 48 hours but recovered without the need for renal replacement therapy. He remained on ventilatory support in view of the severe COPD. On the fifth postoperative day, while slowly weaning off the ventilator, he became tachypneic, with signs of progressive hypoxia and right heart failure. A presumptive clinical diagnosis of pulmonary embolism (PE) was made and he was switched to intravenous heparin. While a CTA was being arranged to confirm the diagnosis of a PE, he became hemodynamically unstable with signs of worsening right heart failure and suffered cardiopulmonary arrest, which did not respond to resuscitation. The autopsy was requested but refused by the family.
I present the case of a 62-year-old female nurse with morbid obesity (BMI 52) and a large ventral hernia (Figure ).\nShe had undergone previous gastric bypass surgery and lost over 100 lbs and still weighed 320 lbs with a current BMI of 52. Despite her obesity, she was non-diabetic with no known cardiac disease. She presented to me as a referral from general surgery as she had a large recurrent ventral hernia as well as an excessive pannus. She had undergone previous open ventral hernia repairs with synthetic mesh twice. The pannus was not addressed during the hernia repairs or after her gastric bypass procedure. The weight of the pannus may have contributed to the hernia recurrence after repair, and ultimately compromised her functional status rendering her essentially unable to exercise and barely able to ambulate.\nPreoperatively, the patient was optimized by her primary care physician. Following a lengthy discussion with the patient as well as her general surgeon, we all agreed that the best option was to proceed with one surgery to include both abdominal wall reconstruction with biologic mesh ventral hernia repair and panniculectomy to allow one anesthesia and one recovery. While we anticipated postoperative incisional wound healing complications and prepared the patient to expect such, we planned to utilize negative pressure incisional management with Prevena™ to reduce the risk.\nOperatively, she underwent combined procedures including abdominal wall reconstruction with biologic mesh hernia repair and panniculectomy (Figure ).\nThe large pannus was addressed first. An incision was made hip to hip measuring 90 cm. The excision included approximately 45 lbs of tissue (Figures , ).\nThe large hernia was then addressed and approached from the lower abdominal tranverse incision. An additional midline incision was avoided. The skin flap was raised, similar to an abdominoplasty flap. This allowed entrance to the hernia defect from a "new" tissue plane that enhanced our ability to address the hernia. Additionally, this avoided the midline T-shaped incision that historically is known to result in high rates of dehiscence. The hernia defect was identified, and biologic mesh was placed as an underlay and secured with a #0 polydioxanone monofilament absorbable suture. A layered closure was performed to include epidermal closure with skin staples. There was little to no tension along the incision, and the skin flaps appeared well perfused (Figure ).\nImmediately following closure, Prevena Plus™ 125 was placed (Figure ). The customizable dressing allowed for complete coverage of the incision (90 cm length).\nBecause of the excess tissue removal (pannus) as well as the extensive undermining, six 10-mm Jackson-Pratt (JP) drains were placed (Figure ).\nThe Ulta™ hospital VAC® unit (3M + KCI) was connected to the Prevena™ and utilized as the pump while the patient was hospitalized.\nPostoperatively, the patient remained in the hospital for 72 hr. Once she was ambulating, an abdominal binder was placed, the portable Prevena™ unit replaced the Ulta system, and she was discharged to home. On Day 10, the Prevena™ dressing was removed. The incision was intact. The dermal edges were well approximated and there was no drainage from the incision or evidence of infection (Figures -).\nThe JP drains were draining serosanguinous fluid and were left in place and removed when each JP output was less than 24 cc in 24 hr (1 cc/hr). At the end of six weeks, all the JP drains had been removed. The incision healed without incident (Figures , ).\nThis was life changing for her, as she was finally able to walk and exercise (Figure ).\nThe patient was followed up for one year with no evidence of incisional breakdown, seroma, or hernia recurrence. One year after her procedure, she had lost an additional 75 lbs, and resumed daily exercise.
A 66-year-old male patient was admitted to the our department in May 2014 with pain of the abdomen accompanied with nausea. Laboratory blood tests performed at admission revealed increased levels of pancreatic enzymes (amylase 765 U/l; lipase 1436 U/l) as well as increased inflammatory markers (C-reactive protein (CRP) level 145 mg/l; leucocytosis 14 G/l). Severe acute pancreatitis of alcoholic etiology was diagnosed and conservative treatment was administered. An intensive liquid therapy was applied together with analgesic treatment and starvation diet. After 5 days enteral nutrition was initiated and continued for 15 days. Deterioration of general condition took place on the 7th day of hospitalization and was manifested by symptoms of multiorgan failure. Furthermore, fever up to 39°C appeared together with increased levels of inflammatory markers profiled in laboratory blood tests (CRP level 217 mg/l, leucocytosis 21 G/l). The blood culture proved negative. The features of acute pancreatitis with necrosis of the pancreatic body and tail were recognized in contrast-enhanced computed tomography of the abdomen. The same examination also confirmed necrosis of peripancreatic tissues running down the abdominal cavity up to the minor pelvis. Intravenous broad-spectrum antibiotic therapy (piperacillin with tazobactam) was included empirically and continued for the next 14 days. The conservative treatment was continued with good clinical effect. Gradual improvement of the patient’s general condition was observed during the next days of hospitalization. Not only gradual liquidation, but also encapsulation of peripancreatic and pancreatic necrosis were proved by the next imaging examinations performed during hospitalization. Significantly, the mentioned examinations did not prove features of infection of the necrosis. Considering the improvement of general condition and the results of laboratory blood tests as well as observation of partial regression of necrotic areas in imaging examination the patient was discharged home after 4 weeks of hospitalization. The patient was left for further ambulatory observation. Due to the lack of symptoms from the presence of necrotic collections the patient was also left without interventional treatment of walled-off pancreatic necrosis (‘watchful waiting’ strategy).\nThe patient was admitted to our department for an emergency procedure again in June 2014 due to symptoms of infected walled-off pancreatic necrosis. The patient complained of abdominal pain, which had lasted for a month, a fever of 38°C and loss of body weight (10 kg per month). Leukocytosis (18 G/l) together with a raised level of CRP (182 mg/l) was present in the laboratory blood tests. The performed blood culture was negative. The presence of three well-defined, pancreatic fluid collections with necrotic contents was revealed in contrast-enhanced computed tomography (CECT) of the abdomen performed at admission (). The first collection had a size of 74 × 64 × 36 mm and was positioned on the border of the body and tail of the pancreas. The second and third collections, which communicated with each other, were of size 110 × 98 × 86 mm and 89 × 74 × 68 mm and were located in the peripancreatic area.\nEndoscopic transmural drainage was performed during the time spent in the department. A stoma between the gastric lumen and the collection positioned at the border of the body and tail of the pancreas was created using a cystotome (Cystotome CST-10, Wilson-Cook, Ireland) and under control of endoscopic ultrasonography (EUS) (Pentax EG3870UTK, Japan). After execution of gastrocystostomy on the posterior wall of the gastric corpus an outflow of necrotic content through the stoma was observed. The gastrocystostomy was widened using a high-pressure balloon (Boston Scientific, USA) to the diameter of 15 mm (). Thereafter two 7 Fr endoprostheses (Wilson-Cook, Ireland) and a 7 Fr nasal drain (Wilson-Cook, Ireland) were guided through the stoma into the lumen of the collection for irrigation purposes (active drainage – 200 ml saline solution per every 4 h).\nPerformed culture of necrotic content revealed presence of Enterococcus faecalis as well as Enterococcus faecium. A targeted antibiotherapy (piperacillin with tazobactam) was applied for the period of 21 days.\nThe second endoscopic procedure was performed after 7 days of active drainage. Contrast applied through the nasal drain demonstrated partial regression of the drained necrotic collection. The fact that the remaining two walled-off collections held on despite the use of drainage was revealed on the endosonography image. The next gastropancreatic fistula was performed during the same procedure under EUS control in the antrum of the stomach (). The outflow of dense, necrotic content was visible then. The fistula was widened using a high-pressure balloon (Boston Scientific, USA) of 20 mm diameter. Thereafter two 7 Fr endoprostheses were guided through the fistula (). Their distal endings were left in the lumen of the necrotic collection (passive drainage).\nImprovement of the patient’s clinical condition occurred after 2 weeks of drainage. The fever retreated and the parameters of inflammation became normal. Regression of necrotic collections was revealed in CECT of the abdomen, which was performed after two weeks. The next (third) endoscopic procedure was performed after 17 days of active drainage. During this procedure an endoscopic retrograde pancreatography was executed in order to evaluate the morphology of the main pancreatic duct. The contrast applied through the major duodenal papilla filled the pancreatic duct, where in the area of the pancreatic body and tail the contrast leaked to the necrotic collection (). Two pancreatic stents (Wilson-Cook, Ireland) were inserted transpapillary. The distal ends of the endoprostheses were left in the tail of the pancreas, bridging numerous partial disruptions of the main pancreatic duct ().\nAfter 21 days of active drainage and observation of gradual regression of collections of WOPN it was decided to remove the nasal drain, leaving four transmural endoprostheses and two transpapillary pancreatic stents.\nThe control CECT was done in January 2015, which was 6 months after the end of the active drainage. The complete regression of WOPN (the diameter of collections did not exceed 30 mm) was confirmed then (). During the performed endoscopic examination it was decided to remove transmural stents, due to the clinical condition and the results of radiological examination. The previously guided transpapillary pancreatic endoprostheses were also removed. What is more, the main pancreatic duct was contrasted and no leak into the peripancreatic area was observed. No new stents were inserted.\nAfter 2 years of observation the patient is said to be in good general condition, without any symptoms. No new recurrence of collections was observed later on, during the next imaging examinations.
A 44-year-old previously healthy Asian female reported to the neurology clinic with complaints of episodic, persistent, uncomfortable needle-like sensations in her genitalia extending to the anal area and the tip of the coccyx. She had been suffering from these symptoms for approximately 11 years. She had difficulty describing the actual nature of this phenomenon, which, according to her, was more of an irritation and discomfort than actual pain. The discomfort was aggravated during rest and periods of inactivity, particularly at night. It responded briefly to mefenamic acid tablets for four to five hours. She also reported the pain was worse before her monthly menstrual cycle but that sexual activity did not affect her discomfort. Sometimes, the discomfort was intense and would wake her from sleep causing severe discomfort and resulting in difficulty sitting; walking would relieve her symptoms partially. She was better in the morning, but the symptoms appeared again at end of the day. She had multiple gynecology and dermatology consults with no relief or clear diagnosis. She was prescribed antifungal creams, including fluconazole and ketoconazole, topical steroids (betamethasone and hydrocortisone), and mefenamic acid for pain relief. All failed to bring relief. She also consulted a homeopathy practitioner, who labeled her as suffering from a chronic skin disease and prescribed oral and topical medication. She took it for a few months but stopped it due to lack of relief. Ultimately, due to the distress and anguish associated with the condition, lack of response to various treatments, and social embarrassment, she stopped visiting doctors for some time. However, during a recent visit, the consulting gynecologist suspected it was not a dermatological or gynecological problem and referred her for a neurology consult.\nThere was no history of back pain, sensory symptoms in the legs, urinary incontinence, or neurological disorder, such as Parkinsonism or restless leg disorder. She had a stable and happy marital life of 22 years and had three children. She has used no substance of abuse or recreational drugs. Her neurological and gynecological examinations, as well as magnetic resonance imaging (MRI) of the spine, were normal (Figure ). Similarly, her biochemical profile (including complete blood count, urine analysis, serum urea, and creatinine) and an ultrasound examination of abdomen and pelvis were normal.\nConsidering her history of circadian rhythm variations in symptoms and aggravation on rest, RGS was considered the most likely cause of her symptoms. After a detailed discussion with the patient, she was prescribed 0.5 mg of ropinirole once at night. It was increased to twice daily after seven days, to which she responded well and reported a dramatic relief of symptoms after 14 days. The dose was increased to 1 mg in the morning and 0.5 mg at night, which led to further improvement. On her third follow-up after two months, she reported taking her medication regularly, which led to almost no episodes of discomfort, with exception of one or two times. The dose of ropinirole was maintained for one month. At the three-month follow-up, she reported only one episode of pain and itching, when she missed one dose of her medicine for a few days; otherwise, she had no complaints and reported no side effects of the medication.
A 60-year-old male with a background of NF1 (diagnosed around 30 years previously) was referred by his general practitioner with a history of intermittent left lower limb claudication at 100–200 yards. Magnetic resonance angiography (MRA) revealed mild atheromatous disease of both lower limbs, with a 6.5 cm occlusion of the left external iliac artery attributed as being the likely cause of his symptoms (). He was admitted for elective angioplasty and stenting of the left external iliac artery.\nPercutaneous access was obtained using ultrasound guidance at the right groin, and pump aortic angiography was performed using a pigtail catheter, confirming the MRA findings. A 7F destination sheath was placed from the right side across the aortic bifurcation, and a 0.018′′ wire was placed within the internal iliac system in order to protect it during the subsequent procedure. The left external iliac artery occlusion was then successfully crossed antegradely using a 4 French Cobra catheter and hydrophilic wire, although this proved difficult due to the firm nature of the occlusion. Predilatation was performed with 3 mm and 5 mm balloons, with no evidence of rupture on subsequent angiography, before placement of a 8 mm × 60 mm self-expanding bare metal stent (ev3 Inc, MN, USA). Postdilatation was performed with a 7 mm balloon.\nUnfortunately, subsequent angiography demonstrated rupture of the stented segment of the left external iliac artery at two separate sites, with a very large amount of contrast extravasation, indicative of a large retroperitoneal haemorrhage (). This was tamponaded immediately with a 7 mm balloon, before deployment of two Advanta V12 7 mm × 38 mm covered stents (Atrium, NH, USA). A good result was achieved with wide patency of the external iliac artery and coverage of the ruptured segments with no evidence of ongoing haemorrhage (). The proximal end of the covered stents was deployed across the left internal iliac artery origin. A small nonocclusive filling defect was noted in the tibioperoneal trunk but otherwise patent runoff. A 6F Angioseal VIP device (St Jude Medical, MN, USA) was deployed for haemostasis at the right groin under ultrasound guidance.\nThe patient was symptomatic with pain and hypotension (BP 70/55 mmHg) at the time of rupture; however, symptoms improved following deployment of the covered stents. Wide bore intravenous access was obtained, and intravenous saline and gelofusine infusions commenced. Analgesia was given in the form of 5 mg of intravenous morphine. He remained stable following the procedure and was transferred to the ward for close observation. Six hours postprocedure, the patient developed left iliac fossa pain and was found to be hypotensive and tachycardic. Fluid resuscitation was commenced and an urgent CT scan was ordered. The precontrast scan confirmed a large retroperitoneal haematoma in the left iliac fossa, extending from the level of the iliac bifurcation to the splenic flexure and measuring approximately 11 cm × 7 cm in the coronal plane. This had areas of high attenuation, suggestive of acute blood but there was no active contrast extravasation or pseudoaneurysm seen either at the stented segment or at the right common femoral artery access site.\nThe patient remained well overnight; however, the next evening he developed right-sided groin pain and a large pulsatile swelling, which had developed acutely over the course of an hour. An ultrasound scan revealed a bilobed right common femoral artery pseudoaneurysm, approximately 10 cm × 8 cm in diameter. Two hundred units of thrombin (Tisseel, Baxter Healthcare Ltd, UK) were injected, causing thrombosis of the pseudoaneurysm. Repeat ultrasound the next day showed that it had remained thrombosed, with no evidence of persisting leak. A full blood count confirmed that the patient's haemoglobin level was stable and he did not require a blood transfusion.\nAt three days postprocedure, the patient experienced some vomiting with an episode of headache and anxiety, which he felt was similar to the symptoms he had had when he suffered a small lacunar infarct the previous year. Neurological examination showed no new focal neurological deficit, and his symptoms were attributed to the stress and anxiety of his current admission. The patient remained well for the rest of his hospital admission and was discharged at four days postangioplasty. At the time of discharge, it was noted that his blood pressure had been particularly labile, even accounting for the events during and postangioplasty. Intraoperatively (ignoring the period of hypotension at the time of stent rupture), his blood pressure varied between 98/60 mmHg and 218/118 mmHg. In the stable postoperative period, it varied between 88/50 mmHg and 174/100 mmHg. In light of the patient's background of NF1, a diagnosis of phaeochromocytoma was considered. He was discharged with a 24-hour urine collection bottle for catecholamine and metanephrine analysis.\nThe CT scan taken postangioplasty () for diagnosis of retroperitoneal haemorrhage was re-reviewed at the regional vascular multidisciplinary team meeting. This showed bilateral adrenal masses, measuring 36 × 19 mm axially on the right and 32 × 20 mm axially on the left. The right-sided lesion had a low attenuation centre, whilst the left sided lesion contained foci of high density, suggestive of calcification.\nThe subsequent 24-hour urinary collection analysis showed significantly raised levels of all catecholamines and metanephrines except the dopamine metabolite 3-methoxytyramine which was within normal range: adrenaline 720 nmol/24 hrs (normal range 0–70 nmol/24 hrs), noradrenaline 1944 nmol/24 hrs (normal range 0–430 nmol/24 hrs), dopamine 3999 nmol/24 hrs (normal range 0–2700 nmol/24 hrs), metadrenaline 5719 nmol/24 hrs (0–1000 nmol/24 hrs), normetadrenaline 8105 nmol/24 hrs (0–3000 nmol/24 hrs), 3-methoxytyramine 1664 nmol/24 hrs (normal range 0–2300 nmol/24 hrs). These results and the findings of the CT scan were discussed with the hospital's biochemistry laboratory; they advised that although bilateral phaeochromocytomas would be rare, in light of this patient's high clinical probability, repeat 24-hour urine collection analysis plus a chromogranin A test should be performed. The levels of three separate chromogranin A assays were mildly raised: 6.9 nmol/L, 6.4 nmol/L, and 6.2 nmol/L (normal range 0–6 nmol/L). Once again, all urinary catecholamines and metanephrines other than 3-methoxytyramine were significantly raised: adrenaline 522 nmol/24 hrs, noradrenaline 1456 nmol/24 hrs, dopamine 3109 nmol/24 hrs, metadrenaline 4547 nmol/24 hrs, normetadrenaline 6355 nmol/24 hrs, and 3-methoxytyramine 1379 nmol/24 hrs. The latter 24-hour urinary collection was performed at exactly 1 month postangioplasty. The fact that the catecholamine and metanephrine levels remained significantly elevated by this point in time would suggest that they were not simply raised as part of the acute stress response of the hospital admission but rather supports the evidence for there being an underlying phaeochromocytoma.\nThe patient has now been reviewed by a consultant endocrinologist. I-131 MIBG (iodine-131-metaiodobenzylguanidine) scintigraphy demonstrated moderate to high-grade uptake in the enlarged adrenal glands consistent with bilateral phaeochromocytomas. His cutaneous neurofibromas did not exhibit I-131 MIBG uptake; however, low grade uptake was noted in the right paracolic gutter and within the proximal small bowel loops, suggestive of plexiform neurofibromas. He has been commenced on the alpha adrenoreceptor blocker Phenoxybenzamine and is tolerating a dose of 20 mg twice daily with only minor nasal congestion and occasional dizziness. He has been referred to an endocrine surgeon for consideration for bilateral adrenalectomy.
A 38-year-old Indian woman reported to the Department of Periodontics, Government Dental College and Hospital, Hyderabad, India in July 2011 with a chief complaint of burning sensation and itching in relation to mandibular anterior lingual gingiva for past 1 month. Patient had provided informed consent to be profiled. Past dental history revealed that the patient had visited a couple of private general dental practitioners where the lesion was misdiagnosed as an aphthous ulcer and palliative care was provided for the same. As there was no improvement in her complaint, she decided to come to the dental school for an additional opinion. She was referred for diagnosis and treatment in post-graduate periodontics clinic. There was no contributing medical or family history except that the patient had undergone hysterectomy and appendectomy 10 years back. Patient was in good health and denied any deleterious habits like smoking, alcohol consumption or recreational drug use. No lymph nodes were palpable or tender in a head and neck examination.\nIntraoral examination revealed a clean mouth with good gingival health and minimal deposits with the full complement of teeth. Clinical examination of the lingual gingiva revealed a 1 cm × 1 cm ulcer extending mesiodistally from mid lingual surface of 41 to mesiolingual surface of 43 and corono-apically from the gingival margin to the floor of the mouth, not extending beyond the anterior part of lingual frenum. The surface of the lesion appeared to be ulcerated and pebbly with isolated areas of erythema and had well-defined borders that were found to be in level with the adjacent tissue. The ulcerated part of the lesion had rhomboid appearance. The surface of lesion toward the lingual frenum appeared to have a shaggy base covered with slough and there was no exudation []. Intraoral periapical X-ray showed bone loss extending up to the apical 3rd in relation to 41, 42 []. Since the clinical findings of the existing lesion didn’t correlate with any of the features of periodontal lesions and the fact that it has been present for the past 1 month was enough to suspect a malignant ulcer. At this stage, a provisional diagnosis of GSCC was made and after obtaining the patient's consent, an incisional biopsy was taken immediately. The specimen was then sent for histopathological examination.\nThe histological examination of the soft-tissue specimen revealed severe dysplastic changes of the epithelium. There were many sheets and clusters of cells, which were polygonal in shape and contained moderate to abundant pale acidophilic cytoplasm and sharp cellular margins. The nucleus was round to oval in shape and showed moderate pleomorphism, disorganization, coarse chromatin clumping and prominent nucleoli. Mitotic activity was high. There were patchy dense infiltrates of lymphocytes, plasma cells and neutrophils []. A clear and prominent feature was the presence of multiple, keratin pearls in connective tissue []. The above clinical and histological features are conclusive of invasive keratinizing GSCC.\nThe patient was immediately referred to a specialty hospital for cancer (Indo-American Cancer Institute, Hyderabad, India) where a computed tomography scan was taken to evaluate any alveolar bone invasion. Subsequently, the lesion was staged as T1N0M0. The involved teeth 41, 42 were extracted and the lesion was treated with radiation therapy alone (intensity modulated radiation therapy, 6600 U/33 fractions using ×6 photons). Six months follow-up revealed uneventful healing and no recurrence.
We report a case of a 62-year-old male who developed DRESS syndrome after seven weeks of antibiotic treatment with vancomycin. He initially underwent instrumented thoracic spinal fusion (T1–7) due to cord compression from a metastatic T4 lesion from renal cell carcinoma and developed a postoperative deep spinal infection. He underwent multiple washouts and vacuum-assisted closure over a period of twelve weeks, with various antimicrobial regimes, initially receiving seven weeks of vancomycin as well as a shorter duration of ciprofloxacin. He developed a maculopapular morbilliform rash, () initially on the right arm and scalp, before spreading to cover the entire head, trunk, and upper legs () which progressed to become exfoliative and was intensely pruritic and painful (). This was accompanied by a fever and eosinophil count of 9.77 × 10−9/L at the highest, occurring simultaneously with the development of the rash, and which remained elevated over the course of a month of regular blood tests. Other haematological abnormalities were also present, with a rise in both lymphocytes and neutrophils. Vancomycin was discontinued immediately, and other causes for these results were excluded, with negative blood cultures, CMV, EBV, ANA, and hepatitis B, hepatitis C, and HIV titres. There was no clinically apparent lymphadenopathy; however, a CT scan performed after the onset of symptoms showed new prominent right hilar lymph nodes, although this may have been due to metastatic cancer and not DRESS syndrome. Skin biopsy showed superficial perivascular lymphocytic infiltrate and rare eosinophils, consistent with a morbilliform drug rash. Ciprofloxacin was felt to be unlikely to be the cause of his DRESS, as he had been prescribed the drug several times in the past, as well as having a shorter duration of treatment which would not fit with the typical timeframe for DRESS, so this was continued to treat his infection.\nThe patient initially received a single dose of intravenous high-dose hydrocortisone, but due to the severity of infection and the risk of immunosuppression, he was subsequently treated exclusively with topical steroids, emollients, and antihistamines (). No liver or renal function abnormalities were noted during this time; however his eosinophils remained raised as described. He developed acute chest pain and shortness of breath four weeks after the initial rash, with new onset fast atrial fibrillation and negative troponin and creatinine kinase. A CT scan demonstrated bilateral pleural effusions, as well as progression of lung and rib metastases. An echocardiogram showed mild left ventricular and right ventricular impairment and a rim of pericardial fluid. Unfortunately, within three months of initial surgery, the metastatic spinal load increased causing further cord injury and paraplegia. Further surgical intervention was deemed inappropriate at this point, and the patient was discharged to the community palliative care team.
A 20 year old Sri Lankan male who was employed as a helper in a grocery, admitted to our unit with weakness of both hands of 1 month’s duration. He was treated for serologically confirmed (Dengue NS1 antigen positive) dengue fever approximately 5 weeks ago at the local hospital and had made an uneventful recovery. He has been given 5 days of inward treatment and the records from the local hospital revealed that he had simple dengue fever with no evidence of fluid leakage.\nFive days after discharge from the hospital he has first noticed the weakness of his right hand when he dropped a glass of water due to poor grip. Weakness was more in the right hand which was his dominant hand and it was slowly progressive over 1 month. At the time of presentation to us he could not write or button on his shirt due the weakness of the hands. Weakness of the left hand was milder than that of the right. The weakness was confined to hands and did not involve forearms or arms. He denied any accompanying numbness, parasthesia or pain.\nOn inquiry he admitted that there was slight weakness of both feet which did not significantly interfere with walking. There was no associated neck/back pain or bladder/bowel incontinence. He did not complain of difficulty in breathing, diplopia, dysphagia, nasal regurgitation, dysarthria or fatigability. He did not give a recent history of trauma to the spine/neck or any preceding diarrheal illness or skin rash.\nHe had no previously diagnosed long term medical ailments and has not undergone any surgical procedures in the past. He was not on any long term medications and he denied smoking, use of alcohol or illicit drugs. He did not give a family history of any progressive neurological conditions.\nOn general examination he had an average built with no pallor, lymphadenopathy or any signs of malnutrition. No skin rashes or hypopigmented patches were noted. There was minimal small muscle wasting of bilateral hands and feet. No muscle fasciculations were noted. Distal upper limb (hand) power was diminished asymmetrically, right hand demonstrating a power of 3 out of 5 and left hand demonstrating a power of 4 out of 5. All fine finger movements including flexion, extension, abduction and adduction were affected with some degree of weakness in wrist extension as well. Bilateral supinator and biceps reflexes were diminished.\nDistal lower limb (feet) power was also diminished but was less pronounced (power grade 4) when compared to the degree of hand weakness. Bilateral foot dorsiflexion was weak. Ankle jerks were elicited with reinforcement whereas the knee jerks were elicited without reinforcement. There was no objective sensory impairment of touch, pain, temperature, vibration and joint position sensations in both upper and lower limbs. Bilateral plantar responses were down going. No palpable nerve thickening identified. No cerebellar signs were demonstrated and his gait showed a minor degree of high stepping due to weak dorsiflexion. Examination of higher functions and cranial nerves including the fundal examination revealed no abnormality.\nExamination of the cardiovascular, respiratory systems and the abdomen was essentially normal.\nFull blood count revealed white blood cell count: 8.5 × 109/L, platelet count: 274 × 109/L, hemoglobin 12 g/dl with normal red cell indices. Blood picture showed normochromic normocytic cells with some reactive lymphocytes suggestive of a recent viral infection. Serum creatinine 80 μmol/l (60 - 110 μmol/l), serum sodium 138 mmol/l (135 - 145 mmol/l), serum potassium 3.8 mmol/l (3.5 - 5 mmol/l), serum magnesium 0.9 mmol/l (0.8–1.1 mmol/l), serum ionized calcium 1.2 mmol/l (1.05–1.30 mmol/l). Liver profile: AST 21u/l (10 - 40u/l), ALT 13u/l (7–56 u/l), ALP 67u/l (100–360 u/l), serum total bilirubin 0.7 mg/dl (0.1–1.2 mg/dl), serum albumin 36 g/l (35 - 50 g/l), serum globulin 32 g/l (20 - 35 g/l). CPK levels were normal. Inflammatory markers: ESR 25 mm/hour and CRP < 6 mg/dl.\nNerve conduction study revealed findings in keeping with multifocal motor neuropathy with conduction blocks involving the distal upper and lower limb peripheral nerves without any conduction abnormalities in the sensory nerves (Fig. ).\nCSF analysis did not show any increase in proteins or cells and the values were within the normal limits. Anti-GM1 IgM antibody test was not carried out due to the high cost of the test and the patient’s unstable financial background. A sural nerve biopsy (a sensory nerve) was carried out and revealed histologically unremarkable nerve fibres and blood vessels with no evidence of inflammation, atrophy or granulomata formation. Recent dengue infection was confirmed with positive dengue IgM and IgG antibodies with enzyme-linked immunosorbent assay (ELISA).\nAs the patient fulfilled criteria, the diagnosis of multifocal motor neuropathy with conduction blocks was confirmed. He was then referred to the neurologist and was started on intravenous immunoglobulin (IVIg) therapy (2 g/kg/day) which was given for 5 days. He showed a mild improvement of his neurological weakness with the treatment and outpatient physiotherapy was arranged. The next immunoglobulin dose was planned to be given after 2 weeks.
A 41-year-old man presented with a tender mass in the upper outer quadrant of the left breast. He reported having this mass since he was 26 years old and noted that it had been increasing in size over the past several months. His past medical history is significant for coronary atherosclerotic disease and depression. The patient denied any known family history of breast cancer. He previously smoked cigarettes, quantified to eight pack-years, but denied alcohol and illicit drug use. On physical examination of the right breast, no mass was palpated. On physical examination of the left breast, there was a solid mass at one o’clock at a distance of 10 cm from the left nipple. The normal right breast and the left breast mass can be visualized on diagnostic mammography (Figure , ). Diagnostic mammogram spot compression was performed on the area of interest in the upper outer quadrant of the left breast, revealing a high-density oval mass with microlobulated margins and associated grouped coarse heterogeneous calcifications (Figures ).\nTargeted ultrasound of the left breast showed a solid mass measuring 34 x 34 x 6 mm at the site of the mammographic and clinically palpable mass in the upper outer quadrant at one o’clock at a distance of 10 cm from the nipple (Figure ). The characteristics of the imaging included an orientation parallel to the skin line and an oval shape. Increased vascularity was present.\nIn consideration of the enlarging left breast mass and the abnormal imaging findings, an ultrasound-guided core needle biopsy of the left breast was performed for tissue diagnosis (Figure ).\nHistology of the biopsy revealed smooth muscle bundles, accompanied by fibrous stromal and adipose tissue, which is consistent with hamartoma (Figure ). Pseudoangiomatous stromal hyperplasia was also present (Figure ).\nWith the imaging and histology findings, a diagnosis of benign breast hamartoma was made without further clinical investigation. Reassurance and education were provided. The patient remained asymptomatic without any new breast masses at his follow-up health check a year later.
Our patient was a two-month-old male referred for evaluation of a left postauricular mass, present since birth. Workup by the patient's pediatrician including an ultrasound suggested a cystic mass prompting referral for surgical excision. The parents endorsed noticing the lesion at birth and that it had been painless and slowly progressive. Physical exam demonstrated a firm 2 × 2 cm subcutaneous lesion of the postauricular region. An MRI was obtained demonstrating a 2.3 × 1.4 × 2.2 cm well-defined solid mass involving the outer table of the right temporal bone and temporoparietal suture with intense peripheral enhancement and without restricted diffusion (). Initial resection in the operating room was undertaken, and a deep plane between the mass and skull was identified and followed reflecting the lesion off of the skull. Unfortunately, pathology demonstrated focal presence of tumor cells at the peripheral margin. The patient underwent a repeat resection, with a canal wall up mastoidectomy. The lesion was again resected en bloc, and the underlying cortical bone was drilled down to the inner table of the temporal bone with healthy appearing bone stock. Despite clinically normal-appearing bone, the pathology again demonstrated presence of tumor cells at the soft tissue margins, and clinically the patient demonstrated significant regrowth of the lesion. The patient returned to the operating room once more, with a fairly impressive progression of gross tumor, nearly 2.5 × 2.0 cm (). A revision mastoidectomy was performed, and neurosurgical consultation was obtained. The mass was excised en bloc resulting in a full-thickness craniectomy. The dura appeared healthy and unaffected by the tumor (). The wound was closed primarily, and the patient was observed overnight in the PICU before being discharged home postoperative day one in stable condition. The patient developed purulence at his incision site one month postoperatively requiring intra-washout with neurosurgery. The infection resolved without further complication or treatment requirement. He was seen at six months postoperatively with no evidence of disease in good condition.
A two-year-old male child presented with abdominal pain of 15 days duration. There was no history of vomiting or constipation. He had a slightly distended abdomen. A vaguely palpable lump could be felt on abdominal examination. It occupied almost the entire abdomen. The child weighed 10 kg. His haematologic investigations were normal.\nAn erect radiograph of the abdomen showed a well-defined, huge, soft tissue lesion in upper abdomen. There was paucity of gas in the abdomen and pelvis. Two to three different cysts were noted within the abdomen on ultrasonography. Computed tomogram (CT) scan of the abdomen showed a 10×5 cm large, cystic, lesion in the lower abdomen, continuous with the bowel wall [].\nAt laparotomy, cystic duplication of the jejunum was seen. A cyst measuring 12×10 cm in size was connected by a small stalk to a larger cyst of about 28×12 cm in size. There was no communication with the native jejunum. The blood vessels of the involved bowel passed both anterior and posterior to the cyst. Enucleation of the cysts was done by opening one leaf of the jejunal mesentery and preserving the vascularity of the bowel, through the posterior arcade. After near complete enucleation of the cystic duplication, another 70 cm long tubular duplication was found in continuity [], invading up to the proximal ileum. Thus, only 30 cm of the terminal ileum and initial 20–25 cm of the proximal jejunum were uninvolved. This segment of duplication, however, shared the muscularis with the native small bowel. By gradual dissection through the anterior mesenteric leaf and division of the common muscularis between the native bowel and the tubular duplication, the involved jejunoileal segment of bowel could also be dissected free.\nThe tubular duplication was entering the terminal ileum at its distal end. There were a lot of hypertrophic mucosal folds at the entry point into the ileum. This portion (about 8 cm of bowel) was excised and local end-to-end anastomosis was done. The operative time was five hours. Blood loss of 60 cc was replaced. The dissection was aided by use of bipolar diathermy and operating loupes with 2.5×magnification.\nThe excised mass weighed 750 g and contained viscid mucous. The histopathology showed the intestinal type lining mucosa. The patient had an uneventful post-operative recovery. At 1-year follow-up, the child is healthy and asymptomatic.
A 69-year-old male patient, with a three months history of abdominal pain asthenia and macroscopic hematuria, was admitted to the outpatient clinic. Abdominal CT revealed an 8 cm left renal growth suggestive of neoplasia, with the involvement of the tail of the pancreas, tumor thrombus in the left renal vein and multiple left para-aortic adenopathies (). A biopsy was performed and showed to be inconclusive regarding the possibility of renal cell carcinoma. Radical left nephrectomy with distal pancreatectomy and splenectomy was proposed.\nThe procedure (Video 1 in Supplementary data) started with an extensive Cattel-Braasch Maneuver, allowing exposure of the inferior vena cava and the aorta, and thus isolation of the left renal vessels. The tail of the pancreas and spleen were freed, and a no-touch approach [] was adopted to minimize the spread of tumor cells with proximal splenic vein ligation. Caudal splenopancreatectomy was performed with section of the pancreas with a GIA 80 (vascular load), followed by proximal ligation and section of the splenic artery and what was thought to be the left renal artery (). The junction of the left renal vein with the vena cava was opened, and the tumor thrombus was resected, followed by caval suture. The renal vessels were, at this point, presumably controlled. The nephrectomy was continued with the release of the kidney and para-aortic lymphadenectomy, during which only the stump of the left renal vein could be identified, lacking the previously ligated renal artery stump. The renal artery was located inside the mass of lymph node tissue in the left para-aortic space, and the stump belonged to the superior mesenteric artery, ligated flush with the aorta. There was no arterial pulse in the mesentery confirming the injury. After removing the specimen, the distal stump of the superior mesenteric artery was exposed, and a repair with a terminoterminal anastomosis was performed from the proximal stump of the splenic artery (). The viability of the gut was assessed by palpation of an arterial pulse in the superior mesenteric artery.\nThe postoperative period went uneventfully. Histological examination showed a renal sarcomatoid carcinoma pT4N1M0G3. Control imaging at three months showed permeability of the celiac trunk and the superior mesenteric artery ().
A 59-year-old man presented to our hospital with a varicose vein on right tibia, a varicose ulcer, and bone exposure. The patient underwent bone drilling to allow granulation followed by a successful free skin graft.\nThe patient noticed a varicose vein had developed in his right leg 10 years before presentation to our hospital. However, 5 years before this, the patient reported occasional right leg pain, which worsened when he stood for prolonged periods and was relieved when he elevated the leg. At this time, the patient refused analgesia. The patient noticed swelling in the lower two-thirds of the right leg in the mornings 4 years before presentation. He experienced stasis dermatitis, with symptoms, including hyperpigmentation and lipodermatosclerosis 2 years before presentation. The patient also complained of itching and nocturnal leg cramps but experienced no palpitations, dyspnea, fatigue, or dizziness. The patient was accidentally knocked by a sharp object 1 year before presentation. He developed a varicose ulcer 1 cm in diameter above the medial malleolus. The patient visited a traditional Chinese medicine clinic and was treated with unidentified plasters, which exacerbated the condition leading to involvement of the tibia 40 days before presentation ().\nThe patient had a 40-year history of hypertension without any intervention. He had suffered a cerebral infarction 6 years ago with no lasting symptoms. The patient had not been diagnosed with diabetes mellitus or a rheumatic disease. Physical examination revealed a temperature of 36.5°C, blood pressure of 118/83 mmHg, a pulse of 70 beats per minute, and a respiratory rate of 18 breaths per minute. Pedal pulses were easily palpable, and there were no crackles in the lungs. The patient had right lower extremity superficial varicose veins, especially on the inner side of the calf. A section of a superficial vein of the lower two-thirds of calf was hard, there was an ulcer exuding pus on the anterior surface of the tibia, the middle third of the tibia was exposed, and the right lower leg was swollen and tender to palpitation above the ankle. Clinical examination showed Trendelenburg test (+), Perthes test (−), Pratt test (−), and a VCSS of 21. Routine blood, urine, liver function, and renal function tests, and coagulation were normal. Culture on pus from the ulcer demonstrated Klebsiella pneumoniae that was sensitive to piperacillin, cefepime, and meropenem. Duplex ultrasonography indicated a varicose vein in the right calf. Deep vein thrombosis was not observed.\nThe patient was diagnosed with a varicose vein on right tibia, a varicose ulcer, and bone exposure. He was administered an anti-infective agent (flucloxacillin sodium 2 g tid sc), therapy for reducing edema (torasemide 20 mg qd iv, mucopolysaccharide polysulfate cream 3 cm bid topical), vasodilators (alprostadil 10 μg qd iv, troxerutin10 ml qd iv), an antihypertensive agent (nifedipine controlled-release tablets 30 mg qd po), and an analgesic (propaptam 2 g qd iv). On the 14th day (11 November 2016) of hospitalization, the patient was treated by high ligation and stripping of the great saphenous vein and segmental endovenous laser ablation. After surgery, he was administered an anticoagulant (rivaroxaban 10 mg qd po).\nAs a granulation tissue bed had not developed over the exposed bone, on 26 December 2016, the patient underwent a second surgery that involved drilling the tibia. Under general anesthetic, the patient was placed in the supine position, and the right lower limb was routinely disinfected. The wound was debrided and washed repeatedly, and a 1.5 mm Kirschner wire was used to drill multiple pores in the exposed tibia until blood was seen (). Hemostasis was established, and the wound was flushed and covered with a vacuum sealing drainage (VSD) dressing. On 23 January 2017, a healthy, uniform granulation tissue bed had developed over the exposed bone (). To prevent osteomyelitis, we gave the patient antibiotics both locally and systemically.\nOn 20 February 2017, the patient underwent reconstructive surgery with a free full thickness skin graft to replace skin loss on the right calf. A 9 × 8 cm graft obtained from the right groin was fixed with suturing (). The wound was dried and covered with VSD dressings. After surgery, the patient was administered rivaroxaban and mucopolysaccharide polysulfate cream. Compression stockings were used to prevent the recurrence of varicose veins when the wound had been fully healed. The model of the compression stockings is AD, 5 (Cizeta Surgical, Bologna, Italy), and the pressure was 30 mmHg. However, 2 years after discharge, outcomes remain satisfactory ().
A 45-year-old woman presented to medical attention for abdominal pain, episodic diarrhea, and a mild weight loss (<10% body weight). Informed consent was obtained from patients included in the study. All procedures performed were in accordance with the ethical standards of our institutional research committee. She underwent a colonoscopy that showed a 4 cm stenosis of the sigmoid colon, covered with pale mucosa that could not be passed by a conventional colonscope (13.2 mm) but could be passed with an enteroscope (9.2 mm) with which the cecum could be reached; the mucosa of the other colonic tract, as well as the mucosa of the terminal ileum, were unremarkable. Random ileal and colonic biopsies were obtained, which were unremarkable as well. Histology of the stenosis showed mild inflammation, mild stromal fibrosis, and architectural disruption. Subsequently, she underwent a computed tomography scan, which showed a mild thickening of the terminal ileum and sigmoid colon. The finding of thickened terminal ileum was further confirmed by a subsequent magnetic resonance imaging enterography, suggestive for Crohn disease (CD) localized at the terminal ileum. Due to the discrepancy of the radiological findings with the initial endoscopic examination, a further colonscopy with retrograde ileoscopy was performed, showing no visible endoscopic signs of inflammation and confirming the sigmoid stenosis. The repeated ileal and colonic biopsy sampling was again not diagnostic, showing a nonspecific pattern of inflammation affecting the sigmoid colonic specimens.\nThe physician in charge of the patient, in view of her clinical history and the radiologic finding of intestinal thickening, reckoned that the patient was affected by CD with terminal ileum and sigmoid colon localization and proposed a therapy immunomodulators: corticosteroids 1 mg/kg for 12 weeks together with antitumor necrosis factor (TNF) infliximab 5 mg at weeks 0, 2, and 6, followed by infliximab alone. After 6 months of treatment with infliximab (5 mg/kg every 8 weeks as maintenance), an endoscopic reevaluation was scheduled, showing a resolution of the stenosis in the sigmoid colon and a normal-appearing terminal ileum. The marked improvement of the sigmoid inflammation together with the finding of fibrosis on the corresponding histology further convinced the physician in charge of the patient in favor of a diagnosis of CD, and the anti-TNF treatment with infliximab 5 mg/kg was continued. After 3 months (9 months after the beginning of anti-TNF), the patient was admitted for obstructive symptoms. A computed tomography suspected neoplasia of ileocecal region. The patient underwent an uneventful ileocecal surgical resection. The surgical specimen consisted of a portion of 8 cm of terminal ileum with the cecum and the vermiform appendix. The ileal wall showed an increased consistency and a diffuse thickening, with cystic-hemorrhagic foci in the perivisceral fat. The ileal mucosa was corrugated and showed a polypoid structure with a wide base (1.5 cm maximum diameter) originating from the submucosa and determining ulceration of the mucosal layer. The ileocecal valve, the cecum, and the appendix were normal, except for a mild lipomatous filling of the submucosa.
A 35-year-old lady presented to the craniofacial surgeons looking for a permanent fixture to the bony defect in her lower-right mandible. In 1991 she had her first operation to remove the ameloblastoma and then had it further excised 6 years later due to a reoccurrence. This resulted in an absence of teeth from the canines back and removal of bone down to the inferior alveolar nerve. The patient has since been clear of any further reoccurrences and wears lower dentures for aesthetic reasons.\nShe has no significant past medical history nor family history, nor does she have any known drug allergies. She does not smoke or drink alcohol.\nOn clinical examination, the patient experiences mild parasthesia in the distribution of her right inferior dental nerve, particularly the lateral aspect of the lower lip.\nOn examination, there is clear absence of teeth on the lower-right side from the canines back (to include the premolar, molar and wisdom teeth) and presence of healthy oral mucosa with laxity to move the submucosa medially. There is a loss of the vertical height of the posterior body of the mandible of about 50% and the vestigial remnants of the lingual plate are just palpable and visible on plain radiograph and CT. Scans show that the superior margin of the resection is well corticated under the inferior dental nerve (Fig. a and b). No functional problems exist. As a long-term solution to her defect, the patient wishes to get dental implants. The surgical approach taken, prior to the implants, shall be discussed.\nThe patient was initially given the option between a bone graft or vascularized tissue (free fibular flap) and informed of the complications—a bone graft carries a risk of rejection and vascularized tissue needs an increased amount of post-operative care to ensure that the tissue remains vascularized. The patient was not keen on a free flap and given the fact that the bony deformity was <5 cm, non-vascularized iliac bone graft was deemed to be sufficient to carry out this operation [].\nThe surgery occurred in several steps. The first step was achieving significant tissue expansion (>2 cm) using Osmed pellets, guided into the submucosa and kept over the alveolar ridge for several months (Fig. a–c).\nTwo months later, the patient underwent the main bulk of her operation. The Osmed pellets were removed from the subperiosteum (Fig. a and b) and the iliac bone graft was taken, made up of cortical and cancellous bone and placed to one side (Fig. a–c). An epidural catheter was placed inside the soft tissue of the graft site and left overnight. It had a continuous fusion of a local anaesthetic to improve post-operative pain and encourage early mobilization.\nPreviously, using CT scans, a titanium construct was made to guide the outline of the bone graft and complete the missing height and width of the mandible []. Once fitted to the patients jaw, it was packed with the bone graft and screwed down into position (Fig. ). A slight groove was made on the mandible to allow space for the inferior dental nerve to lay, so that the construct did not compact the nerve and cause functional problems.\nTo complete the surgery, the periosteum was sutured over the construct and then the buccal muscosa was sutured over again to form a double-layered closure (Fig. a–c).The purpose of this was to prevent infection and rejection, by ensuring that there was an increased distance between the foreign object (titanium construct) and the outside environment. The dental implants are scheduled to be inserted several months after this operation.
A 4-month-old baby Ibibio tribe girl was referred in August 2019 to our Radiology Department, UUTH, Uyo, Nigeria from the Orthopedic Unit for plain radiography of her lower limbs; this was on account of her short left lower limb noticed from birth. Her parents said that her left lower limb was getting progressively shorter but she had no other abnormalities. Antenatal history, past medical history, and family history were not remarkable. There was no history of trauma to the mother during pregnancy or perinatal exposure to radiation. Developmental milestones had been normal so far.\nOn physical examination, she appeared otherwise normal and well nourished. Both her lower limbs were actively mobile. Her left lower limb was shortened and in external rotation (see Fig. ). Her right lower limb measured 27 cm from the anterior superior iliac spine to the tip of medial malleolus, whereas her left lower limb measured 23 cm on similar landmarks. Normal range of motion of both knee joints and hip joints were observed. Hip abduction was full and back examination was normal. Her upper limbs showed no anomaly with full range of movement. Aside from umbilical hernia, no other congenital abnormalities were seen on abdominopelvic ultrasonography. A diagnosis of PFFD was made and she was referred for radiographic examinations.\nPlain radiographs of her thigh and lower limbs showed shortened and hypoplastic left femur with preserved left femoral capital epiphysis. Her left femur had normal configuration but had a shorter shaft than the contralateral femur. The shaft of her left femur measured 9.41 cm whereas the shaft of her right femur measured 11.88 cm (see Fig. ).\nOn receipt of the radiographs, the possible plans of management were discussed with her parents. Unfortunately, they have not kept any further appointments. Recent telephone communications in December 2019 with the parents revealed that the child has been left to her fate. This is because of the parents’ belief of spontaneous limb lengthening.
We report a case of a 62-year-old male who developed DRESS syndrome after seven weeks of antibiotic treatment with vancomycin. He initially underwent instrumented thoracic spinal fusion (T1–7) due to cord compression from a metastatic T4 lesion from renal cell carcinoma and developed a postoperative deep spinal infection. He underwent multiple washouts and vacuum-assisted closure over a period of twelve weeks, with various antimicrobial regimes, initially receiving seven weeks of vancomycin as well as a shorter duration of ciprofloxacin. He developed a maculopapular morbilliform rash, () initially on the right arm and scalp, before spreading to cover the entire head, trunk, and upper legs () which progressed to become exfoliative and was intensely pruritic and painful (). This was accompanied by a fever and eosinophil count of 9.77 × 10−9/L at the highest, occurring simultaneously with the development of the rash, and which remained elevated over the course of a month of regular blood tests. Other haematological abnormalities were also present, with a rise in both lymphocytes and neutrophils. Vancomycin was discontinued immediately, and other causes for these results were excluded, with negative blood cultures, CMV, EBV, ANA, and hepatitis B, hepatitis C, and HIV titres. There was no clinically apparent lymphadenopathy; however, a CT scan performed after the onset of symptoms showed new prominent right hilar lymph nodes, although this may have been due to metastatic cancer and not DRESS syndrome. Skin biopsy showed superficial perivascular lymphocytic infiltrate and rare eosinophils, consistent with a morbilliform drug rash. Ciprofloxacin was felt to be unlikely to be the cause of his DRESS, as he had been prescribed the drug several times in the past, as well as having a shorter duration of treatment which would not fit with the typical timeframe for DRESS, so this was continued to treat his infection.\nThe patient initially received a single dose of intravenous high-dose hydrocortisone, but due to the severity of infection and the risk of immunosuppression, he was subsequently treated exclusively with topical steroids, emollients, and antihistamines (). No liver or renal function abnormalities were noted during this time; however his eosinophils remained raised as described. He developed acute chest pain and shortness of breath four weeks after the initial rash, with new onset fast atrial fibrillation and negative troponin and creatinine kinase. A CT scan demonstrated bilateral pleural effusions, as well as progression of lung and rib metastases. An echocardiogram showed mild left ventricular and right ventricular impairment and a rim of pericardial fluid. Unfortunately, within three months of initial surgery, the metastatic spinal load increased causing further cord injury and paraplegia. Further surgical intervention was deemed inappropriate at this point, and the patient was discharged to the community palliative care team.
A 77-year-old male with a past medical history of coronary artery disease status post coronary artery bypass grafting, hypertension, chronic obstructive pulmonary disease, diabetes mellitus type 2, and cerebrovascular accident presented to a local hospital with acute abdominal pain and bloating. A computed tomography (CT) scan of the patient's abdomen and pelvis was performed and showed intraabdominal bleed and multifocal liver lesions. Initial complete blood count (CBC) revealed a hemoglobin of 7 g/dL and he was transfused one unit of packed red blood cells prior to transfer to our institution. On arrival, CT angiogram of the abdomen and pelvis showed multiple dense, heterogeneous masses throughout the liver with associated perihepatic and intraperitoneal hemorrhage and areas of tumor blush were noted but no extravasation was seen to suggest active hemorrhage. There was also multiple enlarged periportal and upper mesenteric lymph nodes, likely representing metastatic adenopathy. There were no lesions present on the pancreas. CT chest was obtained and showed no evidence of intrathoracic metastatic disease. Initial blood work revealed normal liver function tests, appropriate response in hemoglobin to transfusion and negative viral hepatitis panel. Tumor markers revealed AFP elevation to 8705 ng/mL, normal Carcinoembryonic Antigen and Cancer Antigen 19-9. Magnetic Resonance Imaging (MRI) of the abdomen and pelvis showed multiple lesions throughout the liver with targetoid appearance. There was no evidence of cirrhosis and these lesions did not have imaging characteristics of typical HCC (Figure ). It was suspected the multifocal liver lesions were HCC given the elevated AFP. However, the MRI was not consistent with HCC and a liver biopsy was obtained. Pathology results were consistent with poorly differentiated, large cell-type neuroendocrine carcinoma with metastatic disease to the liver (Figure ). The patient had an unremarkable colonoscopy and esophagogastroduodenoscopy six months prior to presentation therefore, it was suspected the primary origin of NET was in the small bowel. Regarding the intraabdominal bleed noted on initial CT scan, this remained stable on repeat scans and surgery recommended conservative management. The planned chemotherapy regimen will be Carboplatin and Etoposide.
A 55-year-old right handed male with a past medical history of diabetes, hypertension, and a greater than 10 pack-year history of cigarette smoking, presented with headache, nausea, vomiting, and worsening double vision. On physical examination, the patient was alert and oriented. His cranial nerves were intact. He was noted to have facial asymmetry and slight mass over the right forehead. Further on examination it was noted that he had a lesion on his right breast and nipple that he reported had been present for approximately one year, with occasional enlargement, bleeding, and purulent discharge. He had no lymphadenopathy on examination. Noncontrast computed tomography (CT) head indicated a 4.3 × 2.2 × 1.7 cm right frontal calvarial lesion, with internal trabeculated bone mixed with fatty components, and no associated involvement of overlying soft tissue or brain parenchyma []. Magnetic resonance imaging (MRI) of the brain confirmed the presence of a right sided heterogeneously enhancing calvarial lesion with mild mass effect on the adjacent frontal lobe []. A CT of the chest, abdomen, and pelvis showed a soft tissue density in the right retroareolar space, corresponding to the location of the painful breast lesion, and associated with enlarged right hilar and subcarinal lymph nodes.\nThe patient initially underwent a punch biopsy of the breast lesion and subsequent histopathologic analysis revealed the lesion to be invasive ductal carcinoma. In order to obtain a tissue diagnosis and relieve symptoms caused by the calvarial lesion, the patient underwent a right frontal image-guided craniectomy. A modified bicoronal incision was carried out with exposure of the mass. Using image guidance, a craniectomy was carried out with en-bloc calvarial tumor resection. There was no dural involvement. A titanium mesh cranioplasty was performed. Postoperative imaging showed no residual tumor and the patient was discharged on postoperative day 2 with improvement in his headaches. The patient later underwent a modified radical mastectomy and biopsy of an axillary sentinel node. Pathology and staging demonstrated a T4aN1aM0 Stage IIIB infiltrating ductal carcinoma.\nThe pathologic calvarial specimen consisted of a 5.5 × 5.5 × 0.8 cm portion of calvarium involved by an expansile lesion measuring 3.5 × 3.5 × 1.5 cm. The lesion was well-circumscribed and showed mixed areas of firm-to-soft tan and red lobulated tissue. Histopathologic analysis performed on the specimen proved the tumor to be an angiolipoma. Microscopically, the lesion consisted of mature trabecular bone intermixed with mature adipocytes and variably sized dilated vascular channels []. The adipose component was mature and composed of normal appearing lobules separated by thin, fibrous septa. No cytologicalatypia, hyperchromasia, mitoses, or lipoblasts were present. No increased cellularity or epithelioid cells were noted, and immunohistochemical stains for pankeratin were negative.
A 72-year-old man with no significant history of liver disease, neurologic disorder, or prior relevant surgical intervention presented with the acute onset of lower extremity weakness and confusion. A full neurological workup was performed which included a normal electro encephalogram (EEG) and an unremarkable MRI of the brain. An ammonia level of 145 mmol/L (normal range 11-32 mmol/L) was measured which suggested hepatic encephalopathy as the cause of the patient's altered mental status. A contrast-enhanced CT of the abdomen and pelvis was then performed which demonstrated an intrahepatic portosystemic shunt between the left portal vein and the left hepatic vein with multiple venous connections (Figure A). After consultation with the interventional radiology service, angiography with endovascular embolization of the shunt was planned and began with transhepatic access of the right portal vein from a transjugular approach using a Colapinto needle; however, the right portal vein was small in caliber due to retrograde flow across the existing portosystemic shunt. Left hepatic to left portal venous access was subsequently obtained utilizing a transjugular approach via manipulation of the catheter across the left hepatic vein. The main portal vein was then catheterized with an MPA catheter followed by a direct portal venogram which demonstrated three separate communicating branches. The pressure of the main portal vein was measured before the procedure and corresponds to 6 mm Hg before balloon inflation. Another transjugular access was obtained to catheterize the second more prominent branch. A balloon-occlusion test was then performed simultaneously occluding the two more prominent shunts as a safety measure to mimic any potential hemodynamic changes following embolization obtaining a sustained increase in the main portal vein pressure up to 14 mm Hg interpreted as low risk for embolization. Next, the three communicating branches were embolized using Amplatzer Vascular Plugs II (St. Jude Medical). Each plug was oversized by approximately 30% relative to the shunt caliber. There were no complications following completion of the procedure. A postembolization triple-phase contrast-enhanced CT of the abdomen and pelvis was performed which demonstrated successful occlusion of the shunt (Figure ). Shortly following embolization, the patient's ammonia level returned to normal and his encephalopathy resolved. Follow-up 6 months later, a liver Doppler ultrasound showed no recurrence of shunts and the ammonia levels remained within normal limits.
The patient is a 62-year-old male with a recent history of left frontal ICH (Fig. , ), hypertension, and atrial fibrillation (not anticoagulated) who presented to the emergency department after a fall due to suspected seizure while in rehabilitation. There was no other history of risk factors related to ischemic or hemorrhagic stroke. At presentation, the patient was unconscious and intubated with pupils that remained reactive to light. Computed tomography (CT) scan of the brain showed a right cerebellar hemorrhage with surrounding edema and mass effect on the fourth ventricle (Figure , ). The patient’s family was counseled and, after review of the potential risks and benefits, consented to the surgical evacuation of the cerebellar ICH.\nA suboccipital craniotomy was completed without complication. His hospital course was complicated by Klebsiella pneumoniae pneumonia, and despite treatment for this, he required re-intubation and subsequent tracheostomy and gastrostomy placement due to failure to progress. He was later discharged back to rehabilitation in improved condition.\nRadiological assessment regarding the etiology of this patient’s stroke included multiple CT scans, magnetic resonance imaging (MRI) of the brain, including MR angiography of the head and neck, and cerebral angiography. The CT scans demonstrated his prior left frontal ICH and his new right cerebellar ICH at this presentation. His MRI scan did not show any acute ischemic stroke in the cerebellum associated with the new ICH. His cerebral angiography was unremarkable and did not reveal any evidence of vascular pathology or mycotic aneurysms to explain his recurrent intracranial hemorrhages. His blood workup at presentation showed normal coagulation studies and his platelet count was low normal at 119 x 109/L. Post-resection pathology report showed acute intracranial hemorrhage but special stains did not reveal any evidence of amyloid angiopathy or vasculitis (Figure ). Through persistent patient and family interviews, it came to light that a few weeks prior to the patient’s first ICH, he was diagnosed with a bloodstream infection by S. mutans.
An 82-year-old female patient presented to our clinics following progressive right hip nontender erythema, warmth, and swelling, with no functional impotence worsening progressively during the last month. She has no fever and no general weakness or loss of weight or any sign of infection or systemic disease.\nShe has a past medical history significant for hypertension and well controlled diabetes with bilateral total hip arthroplasty for osteoarthritis. On the left asymptomatic side, she underwent a total hip arthroplasty at the age of 60 which was complicated, at age of 78, of periprosthetic infection and was treated with a two-stage revision of total hip arthroplasty. On the right symptomatic side, she underwent total hip arthroplasty at age of 67 which was complicated of nonunion of greater trochanter treated surgically with wiring at age of 74 and posterior dislocation at age of 77 that was treated surgically with a one-stage revision of the acetabulum due to instability. She was completely asymptomatic back then until the last month when she noted erythema, warmth, and swelling of the right hip. There was no history of rheumatoid arthritis, general systemic disease, or chronic infection conditions such as tuberculosis.\nLaboratory investigations were unremarkable with a normal WBC count, except for a CRP of 10 ng/mL and an ESR of 45 mm/hr. Radiographs of the pelvis showed bilateral noncemented total hip arthroplasty (metal on polyethylene) with no significant soft tissue changes (). No cyst or mass was visualized. A magnetic resonance imaging (MRI) of the pelvis demonstrated a large well-circumscribed hematoma collection with inflammatory changes and cystic areas facing superficially the right hip prosthetic material but not surrounding it with an intermediate signal on T1- and T2-weighted images (). The yield of this imaging technique was extremely limited by the artifacts coming from the prosthesis. A tentative of percutaneous puncture under X-ray guidance failed to yield any liquid.\nSurgical exploration was performed through an excision of the old lateral wound and by adopting the classic lateral approach of the hip. After cutting the gluteus medius, a large cystic mass formation was noted, overlying the hip joint and extending into it. This well contoured mass is opened revealing a collection of 250 mL of “rice-like” bodies measuring 1 cm each bathing in a clear fluid (). It was completely excised and sent to culture and anatomopathological studies. Cultures were sent to look for aerobic, anaerobic, fungal, and acid fast bacilli. There was no evidence of necrotizing or infected or malignant tissue. The hip prosthesis was in place with no evidence of loosening. The wound was copiously irrigated and closed in layers using absorbable suture over drain and stapler on the skin.\nAll the taken cultures came back negative. The PPD was nonreactive. The RF and the anti-CCP serology were also negative. The microscopic study of the cystic collection and its content revealed a fibrotic synovial nature of cystic wall with fibrinous projections in the cystic cavity similar to the foreign objects qualified as “rice-like” bodies (). In fact, they appeared to be fibrinous formation with a collagenous fibrosis. There was no evidence of granulomatosis formation or amyloid deposition. The patient had an uncomplicated postoperative course, the wound healed, and she was asymptomatic at two months of follow-up.
A 33-year old woman with CML CP and low Sokal score had received imatinib treatment before pregnancy for nearly 9 years. A first attempt to conceive was made after 1 year of imatinib 400 mg, when no MMR was achieved and only BCR-ABL level<1% was observed. The patient stopped taking imatinib and was switched to interferon alpha (IFN). No pregnancy took place, the BCR-ABL level increased to 35%, and the patient restarted treatment with imatinib. The dose of imatinib was increased to 600 mg and the patient continued this treatment for 6 years. A DMR was reached but it was not stable and long-lasting. Two more attempts to conceive with imatinib interruption for 3–7 months were made by the patient. The DMR was lost, the BCR-ABL level raised to 3%, and again no pregnancy occurred. The patient restarted treatment with imatinib at a dose of 400 mg ().\nThe last attempt to stop taking imatinib and to conceive with the help of in vitro fertilization was successful. The off-treatment period for conception lasted for 1 month and it was prolonged after pregnancy confirmation. The molecular test which was done at the 10th week of gestation (2.5 months after treatment was stopped) showed a BCR-ABL level of 65%. The haematological relapse of CML which was reflected by the loss of CHR was observed after 1 month. The whole treatment-free period during conception/pregnancy lasted for 5 months. Imatinib at 400 mg was resumed in the second trimester after the 16th week of gestation as imatinib was a drug with a high efficacy in this patient and has a low placental transfer. The CHR was restored in 3 weeks. The next molecular test during pregnancy was done 3 months after the administration of imatinib. The level of BCR-ABL was 5,16%. It was strongly recommended to the patient that she should continue imatinib after labour. However, the patient interrupted treatment to breastfeed and resumed imatinib at a dose of 600 mg after 1 month. She maintained CHR, but nearly 3 months after delivery the level of BCR-ABL increased to 10%. No BCR-ABL mutations were found. The patient was switched to nilotinib at a dose of 800 mg and the MMR was achieved in 3 months. (). The MMR remained stable during further observation. The recommended frequency of molecular monitoring every 3 months was not followed properly by the patent. The follow-up of the child for nearly 3 years showed no developmental delay and no growth retardation.
A 47-year old female presented in our emergency room with a confused mentality, left side weakness, and left forearm pain. She had no relevant medical history; however, upon questioning, she revealed that she had been prescribed medication at another orthopedic clinic for left shoulder pain 2 weeks previously. Swelling and tenderness of the left forearm was noted, and blood pressure was not measurable, and no pulse was detected in the left upper limb. On the right side, blood pressure was 130/80 mmHg with a regular radial pulse of 80 beats per minute. Disorientation with respect to time and place, a slightly lethargic mental status, and left side hemiparesis with hyperreflexia and Babinski's sign were observed during neurologic examination. The routine battery of blood tests, which included electrolyte analysis, complete blood count, thyroid function test, coagulation factors, and erythrocyte sedimentation rate, did not indicate any abnormalities, except a decrease in protein S activity (48%) and an elevated erythrocyte sedimentation rate (51 cm/hr). Brain magnetic resonance imaging (MRI) with angiography showed acute infarctions in the left posterior cerebral artery (PCA) territory, right thalamus, right medial temporal lobe, and right superior cerebellar artery territory of the cerebellum with mild stenosis of the right PCA and the carotid portion of the right internal carotid artery, suggestive of an embolic source proximal to the origins of common carotid and vertebral arteries bilaterally. Normal transesophageal echocardiography and 24-hour holter monitoring were performed in order to exclude possible explanations for cerebral thromboembolism from the heart. Brachial computed tomography (CT) angiography showed occlusion of the left axillary and brachial arteries. Based on suspicion of a cerebral thromboembolism originating from the occluded subclavian artery, intravenous infusion of non-fractionated heparin was administered daily at 1000 units/h with careful monitoring of activated partial thromboplastin.\nOn day 3, the patient complained of aggravated left arm pain; her left hand was found to be cold to the touch and pale in appearance. Emergent thrombectomy was performed, resulting in rapid subsidence of the left arm pain and recovery of the left radial pulse. Pathologic examination of the thrombus revealed that it contained fibrin, blood clots, and arterial tissue, suggesting organizing thrombi. Anti-coagulant therapy with warfarin was continued postoperatively. The patient was discharged with mild left arm weakness and a left side tingling sensation. Repeat testing for protein S activity after 3 months showed a 2-fold decrease in protein S activity (20%), which was also compatible with protein S type I deficiency.
A 15-year-old male patient with the right side congenital microtia was referred to our department. The patient was examined, and the presence of rudimentary cartilage was seen on right side with missing malformed ear []. The left side ear was normal, and there was no other congenital anomaly present except microtia. The patient was further evaluated for hearing sensation, and there was the presence of hearing loss on the right side.\nPreliminary impressions of both the sides were taken, and the models were fabricated. Prototype of wax mimicking the left side ear was fabricated. A computed tomography (CT) scan of the middle third face in the mastoid region showed sufficient bone for the implant placement []. Tentative sites for implants were marked on the patient's face and transferred to diagnostic impressions. The landmarks used for selection of the implant sites were superior horizontal line through superior tarsal plate and nasion, inferior horizontal line through base of nose, anterior vertical line through outer rim of orbit and perpendicular to horizontal lines and posterior vertical line through angle of mandible and perpendicular to horizontal.\nCorrelating the clinical findings, the CT diagnosis and patient expectations, it was decided to place 6-mm diameter and 6.25-mm length, internal hex implants (Adin Dental Implant System, Afula, Israel) at the 3 sites, respectively. The surgery was planned under necessary anesthesia after fitness of the patient and written informed consent. Implant sites were marked tentatively by drilling osteotomy in the prospective implant site location (transferred from the diagnostic cast at the time of diagnosis and using CT scan guide), and implants were placed in these positions [Figures and ]. Rudimentary cartilage was removed and thinning of subcutaneous tissue was done. In the second stage, uncovering of implants by removal of soft tissue and placement of secondary healing caps, 4 months after first stage surgery was carried out. Abutment placement with ball and socket attachment was done at the next stage []. Postoperative phase after second stage surgery was uneventful and healing was satisfactory around the abutments [].\nFabrication of ear prosthesis using ball and socket attachment was done 3 weeks after the second stage surgery. The next step was making impression of implant positions and soft tissues together. For this, the guidelines to assist in wax-up of prosthesis were drawn on left side of face. Irreversible hydrocolloid, silicone impression material was used for making impressions.\nThe next prosthetic step was fabrication of an acrylic resin substructure. The acrylic resin substructure is an acrylic plate fabricated in clear resin that provides a backing for silicone and carries retentive component in its tissue surface. Its superior surface priming was done to create adhesion of acrylic with silicone. Wax up of the prosthesis was then done followed by trial on the patient. This was followed by three-part flasking of the wax up with formation of the channels for silicone escape followed by curing at room temperature overnight. Shade matching was done according to surrounding anatomic regions on patients face. Final prosthesis was retrieved and then placed on patient's face []. Maintenance of the peri-implant tissue was explained to the patient as it is imperative for the long-term success of prosthesis. Mechanical cleaning with interdental brush around abutments and with gauze soaked in peroxide 3% solution and saline in (1:1) ratio or soap water is advised to the patient. As it is a removable appliance, the soft-tissue cuff around the implant needs to be maintained, and for this purpose, the patient was demonstrated for the regular cleaning and maintenance of the implantation site.
A 75-year-old male was referred to M M College of Dental Sciences and Research for a swelling on left side of the mandible. The patient first noticed the swelling five years back when he underwent uneventful extraction of 33, 34. Initially the swelling was minimal, but it had grown slowly with time to the present size. The swelling was painless throughout its course.\nClinical examination disclosed a 4 × 2 cm, ovoid firm swelling on the residual ridge in the region of 32 to 34 []. The swelling was noncompressible and immobile with an intact overlying mucosa. There was no associated lymphadenopathy. Radiographically a poorly demarcated unilocular radiolucency with radiopaque foci in the region of 33, 34 was seen []. Expansion of the cortical plates in relation to the lesional site was evident.\nThe lesion was excised under local anesthesia. After fixation in buffered formalin the tissue was processed and stained with H and E stain.\nThe H and E stained section showed a cystic cavity lined by odontogenic epithelium of varying thickness (1–3 cell layers). The basal cells were cuboidal to columnar in shape with their nuclei pushed away from the basement membrane resembling ameloblasts. The outer layers of the cells were composed of loosely arranged angular cells resembling stellate reticulum, which in some areas were eosinophilic, ballooned, and keratinized forming ghost cells []. The nuclei of these cells were pushed to the periphery and eventually disappeared as the cells enlarged. Individual cells became confluent with the adjacent ballooning cells and gradually lost their cell boundaries, making large sheets of amorphous, acellular eosinophilic material, filling the cystic lumen. Some ghost cells were also seen in the underlying connective tissue, which was loose and vascular, with hemorrhagic areas along with some variable-sized islands of odontogenic epithelium. Irregular masses of hyalinized acellular calcified material (dentinoid) were also observed in the connective tissue, in relation to both epithelial lining and masses of ghost cells [, ].\nBased on these features the lesion was diagnosed intraosseous calcifying cyst odontogenic tumor. Healing was uneventful and in the six-month follow-up there were no signs of recurrence.
A 26-year-old woman (gravida 1, para 0) at 24 weeks of pregnancy with placenta previa was referred to our hospital for intrauterine fetal death in March 2019. MRI on March 15, 2019 showed that the lower edge of the placenta completely covered the cervical os, with no obvious infiltration of placenta in uterine wall or cervix. The estimated thickness of the placenta at the os was 3 centimeters. After an intra amniotic injection of 100 mg ethacridine lactate solution, 50 mg mifepristone was administered orally once every 12 hours 3 times. At 18:45 on March 16, uterine contractions were normal at 3-min intervals and lasting for 25 seconds. The cervix opening was dilated to 1.5 cm. The total volume of intermittent vaginal bleeding was 200 mL (by weight) in 40 minutes. The patient's hemoglobin level was 127 g/L. Under the ultrasound guidance, a cervical ripening balloon was inserted through the placenta and placed between the fetus and the placenta using toothless oval forceps. Saline (150 mL) was injected into the cervical ripening balloon. At the time of cervix expansion, an external traction force was applied to the balloon; vaginal bleeding was immediately reduced due to the cervical ripening balloon compressing against the placenta. At 21:09, when the cervical ripening balloon was slipped out of the vagina, the cervix opening was dilated to 3 cm, with fetal presentation at S-1 cm (the lowest point of fetal skull is 1 cm above the ischial spine plane) and fetal head close to the cervix; contractions were normal. Six minutes later, the fetus was delivered via the vagina; there was total 50 mL of bleeding during the delivery. Placenta and fetal membranes were naturally delivered afterward without placental defect. The total time from the balloon placement to the end of the delivery was 2 hours and 30 minutes. The patient recovered in the hospital for 3 days with no complications. The hypersensitive C-reactive protein level was 22.2 mg/L and the hemoglobin level was 115 g/L post-delivery. The patient was discharged from the hospital on day 3 post-delivery. After 10 days, the follow-up transabdominal ultrasound showed normal endometrial thickness of 0.2 cm (single layer) and endometrial cavity width of 0.4 cm.
A 69-year-old male was admitted to a hospital in June 2016 because of right arm asthenia and dysarthria and was diagnosed as having cerebral infarction in the left middle cerebral artery area along with deep vein thrombosis. ECG demonstrated normal sinus rhythm and echocardiography revealed no intra-cardiac thrombus or vegetation. The patient was discharged from the hospital following administration of apixaban.\nIn August 2016, the patient was readmitted to the hospital because of recurrent right arm asthenia and dysarthria. MRI revealed multiple cerebral infarctions in not only the bilateral cerebral hemispheres but also the cerebellum. Trousseau’s syndrome was suspected at this time. Apixaban administration was stopped and an intravenous drip of heparin was started. Echocardiography revealed mild mitral regurgitation with vegetation on the mitral valve. Although the laboratory data suggested no evidence of infection, ceftriaxone and gentamicin were added as a precaution against infective endocarditis. The patient was then referred to our hospital for surgery.\nA CT scan revealed a left renal infarction and multiple swollen lymph nodes around both the abdominal aorta and stomach with antral hypertrophy, suggesting an advanced gastric cancer or lymphoma. As the vegetation showed no change despite the heparin and antibiotics therapy, cardiac surgery was performed on day 5 after referral. Extracorporeal circulation was instituted employing aortic and bicaval cannulation. After aortic cross-clamping, the mitral valve was exposed via a left atriotomy. Both mitral leaflets had vegetation on the surface, and major vegetation 15 mm in width was evident on the anterior leaflet (Fig. ). These were resected in their entirety and replaced with a 25-mm Epic bioprosthesis (Abbott). Continuous intravenous heparin administration was resumed on the following day, aiming for an activated partial thromboplastin time of between 40 and 50 s. Histologic analysis revealed that the vegetations were thrombi covered with vascular endothelium and that the mitral leaflet tissue was not damaged (Fig. ). On the basis of these findings, the patient was diagnosed as having NBTE.\nAn endoscopic stomach biopsy was performed on the seventh postoperative day, and histologic analysis revealed non-solid poorly differentiated adenocarcinoma with components of signet-ring cell carcinoma and moderately differentiated tubular adenocarcinoma. The patient was definitively diagnosed as having Trousseau’s syndrome and, subsequently, transferred to the department of surgery. A Billroth I distal gastrectomy was performed, and a continuous intravenous heparin drip was employed during the operation. Histologic analysis revealed poorly differentiated adenocarcinoma with a component of moderately differentiated tubular adenocarcinoma and metastatic tumor cells in the dissected lymph nodes (T4aN3bM0; stage IIIb). Further histologic analysis using alcian blue staining confirmed the presence of mucin in the tumor.\nSubcutaneous heparin injection was introduced on day 8 after the gastric surgery, and the patient was discharged from our hospital in October after acquisition of the self-injection technique. During this long hospitalization, no thromboembolic events were observed. Chemotherapy was started in November. The patient has survived for 18 months after the diagnosis of Trousseau’s syndrome without any recurrence of thromboembolism.
A 22-year-old African gentleman presented with left nasal obstruction and epistaxis for 2 years. Examination revealed a nasopharyngeal mass which upon biopsy revealed an undifferentiated nasopharyngeal carcinoma stage III. He had radiotherapy but in view of persistent symptoms and poor response to radiotherapy, endoscopic tumour excision was planned. Prior to that, he underwent embolotherapy of the maxillary branch of the left ECA under sedation and local anaesthesia. The indication for embolization was intractable epistaxis and to reduce intraoperative bleeding during tumour excision. Intermittent Embozene® Microspheres 250 μm injection under fluoroscopy guidance was done before deployment of a 2 mm × 5 mm coil. He was not given heparin or anticoagulant during or after the procedure.\nApproximately 2 h after the procedure, the patient complained of sudden painless profound visual loss in the left eye (LE). Visual acuity in the LE was no light perception with a dense afferent pupillary defect. Funduscopy examination showed a pale retina without cherry red spot; and generalized arterial attenuation (Fig. ). The other eye was completely normal. He did not have neurological deficit.\nA diagnosis of left central retinal artery occlusion was made but the absence of a cherry red spot further suggests the absence of choroidal circulation indicating a possible occlusion of the ophthalmic artery as well. Ocular massage and immediate lowering of intraocular pressure with intravenous acetazolamide 500 mg stat and topical antiglaucomas failed to restore the retinal circulation, with visual acuity remaining no light perception after 24 h. We did not do AC paracentesis as the patient was drowsy from the sedation. MRI of the brain and orbit showed high signal intensity foci on diffusion weighted image (DWI) involving the left caudate nucleus and basal ganglia (Fig. ), suggestive of small infarctions. The patent however did not show any clinically apparent neuro-deficits from these infarcts. Cerebral angiogram revealed collaterals between branches of the ECA and lacrimal artery (a branch of the internal carotid artery (ICA) (Fig. ). The patient however declined fundus fluoresecence angiography and other ocular investigations. His vision remained no light perception on the last follow-up three months later.
Miss S, 20-year-old female presented to us with a history of psychiatric illness of 5-year duration. It started after the excessive worries related to her health. She started reporting that her neighbors were trying to harm her. Over a span of few months, she would remain fearful most of the day. On being asked, she reported camera being fitted in her room to spy on her. She also reported hearing voices of her neighbor abusing her and making plans to harm her. She could hear these voices clearly during awaken state. Though her family members could not hear such voices and reassured her frequently stating that it is not possible, she continued to believe so to an extent that she complained to police about the same. After about a year, she would mutter even when no one was around. She tried to run away from home repeatedly, and hence family members had to keep a constant watch on her. Her predominant mood was irritable during this time. As she did not improve even after treatment with multiple antipsychotics (including olanzapine, haloperidol, risperidone, valproate, etc.), the patient was referred to us for further management.\nOn elaborating the past medical history, it was found that she suffered from multiple respiratory tract infections during her infancy and childhood leading to multiple hospital admissions. Over the years, she developed progressively decreased exercise tolerance. Investigations were performed after a consultation with chest medicine department. Her hematological and biochemical parameters were normal. Pulmonary function tests revealed an obstructive pattern along with air-trapping. X-ray chest revealed hyperlucency in the left lung field []. Computed tomography (CT) scan of the chest showed emphysematous changes with central bronchiectatic changes in the left lung. Magnetic resonance (MR) angiography was also performed which suggested hypoplasia of left pulmonary artery with oligemic lung fields on the left side along with decreased left lung volume, ipsilateral mediastinal shift, and compensatory herniation of the right lung. Echocardiogram (ECHO) suggested congenital hypoplasia of left pulmonary artery with no cardiac abnormalities. Her electrocardiogram was normal, and bronchoscopy revealed no airway obstruction.\nBased on these findings, the patient was diagnosed as a case of paranoid schizophrenia (treatment resistant) with SJMS. She was prescribed tablet clozapine, started with 25 mg, very slowly builds up to 300 mg over 6 weeks and was managed conservatively for the SJMS. The patient showed sedation and constipation while building up dose to 300 mg, but her blood parameters were within normal range. The patient started showing a response on positive symptom on similar 300 mg doses of clozapine. We had decided to continue similar dose of clozapine. Side effect of medication was managed conservatively, and dose was adjusted accordingly. The patient followed up regularly for a period of 10-month during which her positive symptoms improved substantially. However, she continued suffering from intermittent productive cough, dyspnea, and shortness of breath. Frequent complete blood counts and other routine investigations were done owing to patient's proneness to infections and clozapine treatment.
A 6-year-old boy with no pathological history accidentally fell from the top of an approximately 3 m climbing pole and injured his right extended elbow and wrist joint. Due to pain and deformity in the right elbow and wrist joints, he visited our hospital. Swelling and a dinner fork deformity of the right wrist joint and pronounced swelling of the right elbow joint were observed. No skin damage was observed. No findings of nerve injury or arterial injury were obtained in the right upper limb. Radiography revealed lateral dislocation of the radial head, a fracture of the proximal ulnar metaphysis, and mild bending deformation at the fracture site. In addition, fractures of the distal radius and ulna, as well as dorsal displacement of the distal fragment, were seen (). Thus, the patient was diagnosed with Bado type III Monteggia injury with ipsilateral fracture of the distal radius and ulna.\nManual reduction under nerve block was attempted on the day of injury. However, because it was difficult to maintain the reduction of the radial head, as shown in , open reduction and percutaneous procedures were performed under general anesthesia. A Kirschner wire was inserted, percutaneously, from the olecranon into the ulnar diaphysis. When the Kirschner wire was in place, the dislocation of the radial head immediately showed good reduction. Further, open reduction and fixation of the fractured distal radius and ulna were performed with Kirschner wires (). A long-arm cast was used for external fixation with the elbow in 90° flexion and the forearm in an intermediate position.\nTwo weeks after surgery, callus formation at the fractured bone was observed. Therefore, the cast was removed, and range of motion (ROM) exercises of the elbow and wrist joints were initiated. Since bone union was achieved at 6 weeks postsurgery, the Kirschner wires were removed. Pain, ROM limitation, and lateral instability were not observed in the elbow or wrist joints at 3 months after surgery. Additionally, plain radiographs taken at the same time showed a radially convex curvature at the proximal portion of the ulna and lateral subluxation of the radial head (). However, a gradual correction in the outward displacement of the radial head was observed during the 3-year follow-up.\nTwenty-one years after surgery, the patient returned to our hospital for another disorder. At that time, we obtained informed consent to perform an examination and take radiographs of the previous Monteggia injury. Neither spontaneous pain, pain during exercise, tenderness, nor ROM asymmetry were observed (). The biocompatibility of the radiocapitellar joint was good, and no malunion was found in the distal radius and ulna (). The patient reports that he has been working as a computer programmer and performs weight training as a hobby without limitations.
A 46-year-old Asian woman was referred to our department for a renal angiogram following 8 months of uncontrolled hypertension despite receiving medications. Initially, the patient presented with severe headache and fatigue. She had no history of smoking or drinking alcohol, was not diabetic, and had no history of diabetes in her family. She had no history of atherosclerosis. Apart from high blood pressure, the result of her physical examination was unremarkable; her general, cardiovascular system, respiratory system, and abdominal examinations were unremarkable. Neurological examination on admission showed that the patient was alert, attentive, and oriented. Her speech was clear and fluent with good repetition, comprehension, and naming. She recalled 3/3 objects at 5 min. All of her cranial nerves were intact. Motor examination revealed no pronator drift of outstretched arms. Her muscle bulk and tone were normal. Her strength was full bilaterally. Her reflexes and sensory were both intact. Her coordination and gait were normal. Laboratory investigations revealed normal complete blood count, serum cholesterol, lipid profile, and renal function (serum creatinine 119 μmol/L). Her left kidney size was normal with measurement of 9.6 cm by 4.8 cm. Renal Doppler ultrasound confirmed renal artery stenosis with renal resistive index of 0.58. The percentage of renal artery stenosis in the two branches of the left renal artery was 70% and 75%, respectively , before the first balloon angioplasty; after the first balloon angioplasty, these percentages remained the same. After the second ballooning and stenting procedure, revascularization was achieved. The patient had been attending a hypertension clinic and receiving antihypertensive drugs for the past 8 months on a regular basis under close observation. Despite this treatment and care, her blood pressure remained high at 175/110 mmHg, which the attending doctor concluded to be uncontrolled blood pressure. Initial imaging indicated left renal artery stenosis, and the patient was referred to our department (Fig. ). Prior to the diagnosis of renal artery stenosis, the patient had been receiving amlodipine 10 mg twice daily, bisoprolol 10 mg twice daily, and indapamide 2.5 mg every morning.\nThe procedure was performed under the guidance of digital subtraction angiography (floor-mounted Artis zee; Siemens Medical Solutions, Munich, Germany) using the Seldinger technique. With the patient under local anesthesia, the right femoral artery was punctured by a 21-gauge vascular access needle with an angled tip 0.035-inch guidewire, then catheterized with a 5-French introducer sheath (Terumo Interventional Systems, Tokyo, Japan). The first aortogram was obtained using a pigtail catheter (Fig. a), then an 8-French guiding catheter (Cook Medical, Bloomington, IN, USA; Cordis, Hialeah, FL, USA) was used to obtain selective renal angiograms whereby the proximal main flow and the stenosis of both branches and their respective distal flow on the left renal side were revealed. The right renal artery was normal in appearance. The left renal artery angiogram then was used as a reference for further guided interventional procedures in which the individual length and diameter of stenosis were measured. The decision was reached to perform percutaneous transluminal renal angioplasty, and the length and diameter of balloon needed were calibrated. With two balloons of 4 mm × 18 mm (Biotronik, Berlin, Germany), both were was dilated at the same time. Despite expert effort in dilatation, the stenosis was observed to persist (Fig. c). Stent placement was considered, and the procedure was continued. A preprocedure intravenous bolus of 5000 IU of heparin was administered. By using two 0.014-inch guidewires (V14; Boston Scientific, Natick, MA, USA), the interventional radiologist guided the stent to cross the upper and lower branches, respectively, through the same vascular sheath (Fig. b). Two balloon expandable stents measuring 4 mm × 18 mm and 5 mm × 18 mm (Biotronik) were placed in parallel (kissing) and simultaneously inflated both branches. A good angiographic result was revealed (Fig. d) with no need for further ballooning. Angiography contrast media (Omnipaque 350; GE Healthcare, Shanghai, China) were used. Volumes of 25 ml of contrast agent were injected at a flow rate of 5 ml/s. The final angiogram was obtained to confirm the position of the stent, the patency of the lumen, and distal blood flow. Finally, the femoral access site was closed with Perclose ProGlide (Abbott Vascular, Chicago, IL, USA). After the procedure, the patient was admitted in the ambulatory room for further observation. Her blood pressure was monitored and recorded, it showed a significant reduction of blood pressure to 128/87 mmHg. After 24 h of observation, the patient was discharged to home with aspirin (100 mg/day) and clopidogrel (75 mg/day for 3 months). During 12 months of follow-up, the patient remained well with blood pressure of 126/87 mmHg. Renal ultrasound showed bilateral kidneys of normal size and shape with good cortical medullary differentiation. A bilateral renal Doppler study appeared normal.
The patient is a 60-year-old married Caucasian female who presented in the emergency room of a local community hospital with a chief complaint of acute memory loss. She reported being confused for the past two days. She had no recollection about what has transpired the past two days but she remembered the details of her identity and that of her family. She could not recall the circumstances that brought her to the hospital, the name and dosages of her medications, her work history, or her medical history. The patient denied abusing any illicit drugs. She could not identify neighbors who visited her. She reported to her husband that she was not anxious about the memory loss. Her husband was worried that she was having a stroke, so they rushed to the hospital emergency room. Patient struggled to remember details of her morning routine, including her jogging at the neighborhood park, despite the husband's insistence that they ran together. Further inquiry revealed that the patient had attended a recent psychiatric appointment. She had an appointment with her outpatient psychotherapist three days before the acute onset of the memory loss. During that appointment, they discussed the person who physically assaulted her five years ago. She was a teacher in a special education residential program where one of her students with autism spectrum disorder punched her repeatedly on the head until she lost consciousness. Since the assault, the patient has been complaining of nightmares and flashbacks about the attack. She became socially withdrawn.\nAfter the psychotherapist appointment, there was an exacerbation of the patient's anxiety symptoms leading up to the memory loss. There was no loss of consciousness during this period. During the psychiatric evaluation, the patient became tearful when discussing the details of the beating she endured. She described vivid memories of the assault as well as unpleasant dreams related to it. She gets particularly anxious whenever she sees a person that resembles her attacker. She could not perform the task of immediate retention and recall. The patient only identified one out of three words after five minutes. She could not complete her other cognitive examinations because she became tearful and requested to end it. The patient's husband reported that she was diagnosed with post-traumatic stress disorder (PTSD) three years ago and has since been treated with sertraline 100 mg per day. She is also being treated with cognitive-behavioral therapy.\nThis is reportedly the first time she has experienced memory loss. She denied any symptoms of depression, suicidal thoughts, mania, delusions, or hallucinations. There was no family psychiatric history. Mental status examination described a patient who looked appropriate to her stated age, dressed in a hospital gown, and was calm and cooperative with good eye contact during the psychiatric evaluation. There was no agitation observed. Her speech was coherent and goal-directed. She appeared anxious and restless; her mood was "stressed" and her affect was anxious. The patient was ambulating with good muscle strength. There was no aphasia or apraxia. Preliminary work-up showed a complete blood count with a white blood cell count of 5,900 cells per cubic millimeter of blood. Her basic metabolic panel showed serum sodium of 144 mEq/L. The urine toxicology screen was negative for illicit drugs. Magnetic resonance imaging (MRI) of the brain without contrast, magnetic resonance angiography of the circle of Willis, and a computed tomography (CT) scan of the head without contrast showed no acute intracranial pathology. After 48 hours, her cognitive symptoms improved. There was no anti-coagulation treatment. Her vital signs were stable and her 24-hour electroencephalogram monitoring showed no abnormalities. She was discharged home after 48 hours of observation with no cognitive problems.
The patient was a 55-year-old woman with history of hypertension that was under medical control. The patient presented at this facility complaining of recurrent infection, tenderness and swelling in the lower left second premolar tooth. When the patient was examined clinically, a badly carious tooth with a 5-mm swelling buccally Fig. () and grade I tooth mobility was found with mild tenderness to percussion. A periodontal probe was used to examine the pocket depth, revealing a depth of greater than 7 mm on the buccal side. A radiograph showed that the lower left second premolar tooth had periodontal widening, periapical radiolucency and proximal bone resorption. Plaque control and motivation start before implant placement, for mal alignment teeth the patient needed to instruct about interdental plaque control through the periodontal aid. The patient was briefed regarding her situation and the treatment plan. After discussing the options with the patient, she agreed to remove the tooth with socket preservation and a healing period of 6 months before an implant would be placed to replace the missing tooth. Under local anesthesia, a periotome was used to first cut the periodontium and then luxate the tooth Fig. (). Finally, a lower forceps was used to remove the tooth without trauma. After tooth extraction, the socket was examined with a periodontal probe to estimate the width and depth of the buccal bone defect. The defect was 9 mm in depth and 5 mm in width at the crestal bone. Curettage was performed in the socket with a spoon excavator, and the remaining soft tissue with inflammation was removed. Using a scalpel, a small pouch was created between the bone and the gingiva, which will allow the periosteal elevator to reflect the gingiva around the defect for placement of the collagen membrane Fig. (). The collagen membrane was shaped to cover the buccal bone defect with at least 1-mm spacing from the bone margin defect to ensure the membrane would not collapse inside the socket. The membrane was shaped according to the shape of the bone defect; in this case, it was shaped like an “Ice Man” Fig. (). The membrane was placed above the bone and below the gingiva, and the membrane was confirmed to be resting on the remaining buccal bone plate Fig. (). One difficulty of this technique occurs when the membrane becomes wet with blood, resulting in the membrane becoming soft and thus not rigid enough to be pushed underneath the gingiva. Another difficulty is the limited access space and view in this procedure due to the delicate tissue. All these factors make this technique difficult, requiring more time and microsurgery instruments to perform atraumatic surgery. After collagen membrane insertion, part of the collagen membrane should remain outside the socket to cover the socket after bone graft placement. Bovine bone (Cerabone, Botiss, Berlin, Germany) was mixed with saline and applied in layers inside the socket without packing until reaching the bone level Fig. (). Next, the exposed part of the collagen membrane was flipped to cover the grafted socket, with a margin of the membrane tag underneath the gingival margin. Vicryal suture 4/0 was used to secure the membrane in place with a Fig. () suture Fig. (). Postoperative instruction was given to the patient, with special care to clean the exposed membrane. The patient was advised to use a 0.12% chlorhexidine mouthwash after each meal, using an irrigation syringe. A combined antibiotic was prescribed (amoxicillin 500 mg tds for 5 days and metronidazole 200 mg tds for 5 days). Paracetamol was also prescribed to control the pain. After two weeks, the sutures were removed, the wound healed uneventfully, and the membrane remained exposed. After one month, the wound was completely closed with healthy gingival tissue.\nAfter 6 months, the patient returned for a review and augmented site evaluation. There was mild buccal plate resorption and shallowing of the buccal vestibule Fig. (). Under local anesthesia, a crestal incision was performed to expose the crestal bone. An implant with a 3.6 mm diameter and 10 mm length (Dentium, superline) was selected for the missing tooth (no. 34). Bone drilling and an osteotomy were performed according to the manufacturer’s recommendations. The implant was placed with more than 45 Ncm torque with high primary stability Fig. (). A non-submerged implant was selected due to its high primary stability, and flap closure was performed with cut gut suture 3/0. Postoperative instructions were given to the patient. The sutures were removed after one week. The wound healed uneventfully, and the implant was loaded after 3 months.
A 46-year-old Asian woman was referred to our department for a renal angiogram following 8 months of uncontrolled hypertension despite receiving medications. Initially, the patient presented with severe headache and fatigue. She had no history of smoking or drinking alcohol, was not diabetic, and had no history of diabetes in her family. She had no history of atherosclerosis. Apart from high blood pressure, the result of her physical examination was unremarkable; her general, cardiovascular system, respiratory system, and abdominal examinations were unremarkable. Neurological examination on admission showed that the patient was alert, attentive, and oriented. Her speech was clear and fluent with good repetition, comprehension, and naming. She recalled 3/3 objects at 5 min. All of her cranial nerves were intact. Motor examination revealed no pronator drift of outstretched arms. Her muscle bulk and tone were normal. Her strength was full bilaterally. Her reflexes and sensory were both intact. Her coordination and gait were normal. Laboratory investigations revealed normal complete blood count, serum cholesterol, lipid profile, and renal function (serum creatinine 119 μmol/L). Her left kidney size was normal with measurement of 9.6 cm by 4.8 cm. Renal Doppler ultrasound confirmed renal artery stenosis with renal resistive index of 0.58. The percentage of renal artery stenosis in the two branches of the left renal artery was 70% and 75%, respectively , before the first balloon angioplasty; after the first balloon angioplasty, these percentages remained the same. After the second ballooning and stenting procedure, revascularization was achieved. The patient had been attending a hypertension clinic and receiving antihypertensive drugs for the past 8 months on a regular basis under close observation. Despite this treatment and care, her blood pressure remained high at 175/110 mmHg, which the attending doctor concluded to be uncontrolled blood pressure. Initial imaging indicated left renal artery stenosis, and the patient was referred to our department (Fig. ). Prior to the diagnosis of renal artery stenosis, the patient had been receiving amlodipine 10 mg twice daily, bisoprolol 10 mg twice daily, and indapamide 2.5 mg every morning.\nThe procedure was performed under the guidance of digital subtraction angiography (floor-mounted Artis zee; Siemens Medical Solutions, Munich, Germany) using the Seldinger technique. With the patient under local anesthesia, the right femoral artery was punctured by a 21-gauge vascular access needle with an angled tip 0.035-inch guidewire, then catheterized with a 5-French introducer sheath (Terumo Interventional Systems, Tokyo, Japan). The first aortogram was obtained using a pigtail catheter (Fig. a), then an 8-French guiding catheter (Cook Medical, Bloomington, IN, USA; Cordis, Hialeah, FL, USA) was used to obtain selective renal angiograms whereby the proximal main flow and the stenosis of both branches and their respective distal flow on the left renal side were revealed. The right renal artery was normal in appearance. The left renal artery angiogram then was used as a reference for further guided interventional procedures in which the individual length and diameter of stenosis were measured. The decision was reached to perform percutaneous transluminal renal angioplasty, and the length and diameter of balloon needed were calibrated. With two balloons of 4 mm × 18 mm (Biotronik, Berlin, Germany), both were was dilated at the same time. Despite expert effort in dilatation, the stenosis was observed to persist (Fig. c). Stent placement was considered, and the procedure was continued. A preprocedure intravenous bolus of 5000 IU of heparin was administered. By using two 0.014-inch guidewires (V14; Boston Scientific, Natick, MA, USA), the interventional radiologist guided the stent to cross the upper and lower branches, respectively, through the same vascular sheath (Fig. b). Two balloon expandable stents measuring 4 mm × 18 mm and 5 mm × 18 mm (Biotronik) were placed in parallel (kissing) and simultaneously inflated both branches. A good angiographic result was revealed (Fig. d) with no need for further ballooning. Angiography contrast media (Omnipaque 350; GE Healthcare, Shanghai, China) were used. Volumes of 25 ml of contrast agent were injected at a flow rate of 5 ml/s. The final angiogram was obtained to confirm the position of the stent, the patency of the lumen, and distal blood flow. Finally, the femoral access site was closed with Perclose ProGlide (Abbott Vascular, Chicago, IL, USA). After the procedure, the patient was admitted in the ambulatory room for further observation. Her blood pressure was monitored and recorded, it showed a significant reduction of blood pressure to 128/87 mmHg. After 24 h of observation, the patient was discharged to home with aspirin (100 mg/day) and clopidogrel (75 mg/day for 3 months). During 12 months of follow-up, the patient remained well with blood pressure of 126/87 mmHg. Renal ultrasound showed bilateral kidneys of normal size and shape with good cortical medullary differentiation. A bilateral renal Doppler study appeared normal.
A 43-year-old man presented to the hospital with a history of progressive memory loss. He would get lost frequently, had trouble recalling recent events, and had been sent home from his job on several occasions due to the inability to perform his duties. Eight months prior to his presentation, he had been admitted to the hospital for a hyperosmolar hyperglycemic state and found to have a small subacute infarct involving the left posterior cerebral artery distribution. He was started on 80 mg of atorvastatin and dual antiplatelet therapy with aspirin and clopidogrel as well as insulin for diabetes. He was discharged home, yet soon after, his fiancé started noticing further progression of memory loss, and he was readmitted to the hospital for further evaluation. CT imaging showed an evolving acute to subacute right occipital lobe infarct with an acute to subacute left anterior thalamic lacunar infarct, which were new compared to prior scan. Given that his infarcts were in multiple territories, an echocardiogram was done which ruled out thrombus. He was diagnosed with early vascular dementia and continued on medical therapy for aggressive risk factor modification. He was discharged home to the care of his mother-in-law and fiancé for approximately 5 months. However, due to difficulties in taking care of him by his fiancé and mother-in-law, he was referred for a third admission to better define his condition and needs while the court assigned a conservator for him as psychiatric evaluation deemed him to lack capacity for medical decision-making.\nHis past medical history was significant for heart failure, diabetes mellitus, hypertension, hyperlipidemia, obesity, and obstructive sleep apnea. There was no history of early stroke or dementia in his parents, and he has a healthy sister without any known medical conditions. Examination revealed BP: 168/91, HR: 110, and RR: 18. Initial neurologic exam showed correct orientation to place and person and a GCS of 15. However, he was unable to state the current month, subtract serial 7s without prompting, or to tell the months of the year backwards, yet no aphasia or neglect was noted. He also failed the 3-word recall test.\nCTA of the head showed multifocal moderate to severe stenosis and irregularities including bilateral distal ICA (moderate) R M1 (mild to moderate) and nearly occluded bilateral PCAs. MRI showed bilateral subcortical infarcts (as shown by a white arrow in Fig. ) which were more pronounced compared to a previous MRI 8 months ago. There was also a new subacute posterior corpus callosum hyperintensity (as shown by a white arrow in Fig. ) and a right cortical occipital and left pontine stroke, all of which were not seen on previous MRI. The patient was believed to have accelerated intracranial atherosclerosis, but given his age and the dramatic clinical and MRI progression over the course of only 8 months, alternative diagnoses such as vasculitis, intravascular lymphoma, sarcoidosis, and infectious etiologies were considered. Cerebrospinal fluid (CSF) studies showed clear fluid with a white cell count of 5/µL, red cell count of 2,000/µL, glucose of 74 mg/dL, and protein of 65.4 mg/dL. CSF VDRL was negative. ESR was 24 mm/h, and hsCRP was 4.4 mg/L. RF, ANA, and ANCA were negative. ACE level was <5 (units). His lipid panels before and after initiation of 80 mg of daily atorvastatin revealed a total cholesterol of 219 and 101, HDL 36 and 29, and LDL 160 and 63, in milligrams per deciliter, respectively. Homocysteine and MMA levels were normal. Lipoprotein little a (Lpa) was checked on 2 occasions while on statin therapy when his total cholesterol levels were 101 and 107 mg/dL and was found to be 267 and 287 nM (<75 nM). Ezetimibe had been added at a dose of 10 mg a day in between measures of Lp(a).\nGenetic testing was performed to look for variants in Lp(a) and other genes associated with early-onset dementia and revealed a heterogeneous variant in DNAJC5 NM_025219:exon3:c.C188T:p.A63V (chr20:62560745 [hg19]), a gene commonly associated with ceroid lipofuscinosis (neuronal, 4, parry type). The variant was identified using exome sequencing where paired end sequence reads were converted to FASTQ format and were aligned to the reference human genome assembly GRCh37/hg19. Following variant annotation using a Genome Analysis Toolkit (GATK) and AnnoVar, filtering was applied against allele frequencies and disease citations using databases including the Genome Aggregation Database, an internal database of Yale DNA Diagnostics Laboratory, ClinVAR, OMIM, and other in silico predictors of functional consequences. Variants with allele frequency above 3% were excluded from further analysis. Genes of variants with an allele frequency <3% were cross-compared with panel(s) of lab-curated genes associated with condition(s) including cerebrovascular disease, hyperlipidemia, and dementia that can explain the patient's phenotype (refer to the gene list in online suppl. Section; for all online suppl. material, see ).
A 65-year-old female presented with a 2 months history of progressive intermittent claudication of the right calf. She had no history of limb trauma but exhibited hypertension, hyperlipidemia, and paroxysmal atrial fibrillation that were well controlled. Her maximum walking distance was approximately 500 meters, but she did not experience rest pain at the time she presented to our hospital. On physical examination, the right posterior tibial or dorsalis pedis arteries were not palpable. The ankle-brachial index on the right leg was 0.70. Her vital signs were stable, with no significant laboratory findings. Enhanced computed tomography showed an occlusion of the right popliteal artery with a 60-mm-long circular cystic arterial lesion but preservation of arterial flow below the knee by collateral circulation (). The left popliteal artery and aortoiliac region showed no signs of arteriosclerosis. She was diagnosed as having ACDPA. Because she was symptomatic, with a 500-m intermittent claudication caused by the occlusive lesion, we decided upon surgical treatment. Under general anesthesia, in the prone position and through a posterior approach, a 60-mm-long intramural cyst of the right popliteal artery was exposed. No popliteal arterial pulse was noted below the knee. The cyst was punctured to reveal tenacious mucoid material, although there was no improvement in arterial flow. We then incised the cyst for drainage and decompression (), but the right popliteal arterial flow remained diminished on intraoperative angiography. Finally, we resected the affected popliteal artery with interposition using a right great saphenous vein graft. The operative time was 3 h 56 min, and blood loss was 170 mL. The ankle-brachial index after revascularization improved to 1.10 in the right leg, and the right posterior tibial and dorsalis pedis pulses became palpable. On the 13th postoperative day, she was discharged from our hospital. Histopathological examination revealed that the mucoid materials were located only in the media of the popliteal artery, in contrast to our preoperative expectation. There was no evidence of communication between the cyst and the knee joint capsule (). The patient has had no walking difficulties for 2 years since the operation.
A six-month-old female infant was referred to cardiology due to progressively increasing oxygen requirements and cardiomegaly on chest X-ray. She was born at 25 weeks of gestation and had multiple medical problems in the early neonatal period including retinopathy of prematurity, hyaline membrane disease, gastroesophageal reflux, severe liver dysfunction, and suspected necrotizing enterocolitis. She had a history of ligation of her patent arterial duct on the 16th day of life. On physical exam her respiratory rate was 65, her heart rate was 153, and blood pressure was 130/80 mmHg. Her oxygen saturation was in the low 90s on 30% FiO2 (fraction of inspired oxygen). Her lung sounds were coarse. Her heart had regular rate and rhythm, with no murmurs. Her abdomen showed a liver edge that was palpable three centimeters below the right subcostal margin. She had a palpable bruit at the left antecubital fossa. Pulses were normal and equal on all extremities, and there were no obvious discrepancies in limb lengths. An echocardiogram showed severe pulmonary artery hypertension with mild right ventricular and atrial dilatation, with a patent foramen ovale shunting right to left. Biventricular systolic function was normal, with no evidence of left ventricular hypertrophy or dilatation. A duplex ultrasound of the left upper extremity showed presence of an AVF between the left brachial artery and vein as evidenced by increased flow obtained from the left brachial artery with dilated, tortuous brachial veins demonstrating arterialized flow along the length of the veins. Velocity measurements of up to 692 cm/second were obtained at the level of the AVF (Figures and ).\nThe calculated blood flow in the fistula was estimated to be about 450–500 mL/min, which is equivalent to up to twice the estimated total cardiac output for this patient. The fistula was not ligated because its location was high risk for limb-loss. She was managed with diuresis and blood pressure control. One month later, she was reevaluated for recurrent and progressive episodes of desaturations and respiratory distress. On physical exam her vital signs showed a respiratory rate of 60 per minute, and oxygen saturations were between 90–95% on oxygen supplementation by nasal cannula. Her blood pressure was 52/32 mmHg, and the heart rate was 134–148 beats per minute. Cardiac exam demonstrated normal S1 and S2, no murmurs, and an intermittent gallop. Electrocardiogram showed normal sinus rhythm with right atrial enlargement and right axis deviation and T-wave inversion in the lateral leads, suggesting right ventricular strain. The echocardiogram suggested elevated pulmonary artery systolic pressures, which were 2/3 of the systemic pressure. The right ventricle showed mildly depressed systolic function.\nThe patient was started on sildenafil for management of the pulmonary hypertension, but this did not alter the measured pulmonary pressures upon echocardiographic reevaluation one week later. On careful assessment of the left antecubital fossa, with temporary manual occlusion of the affected area, there was a decrease in the heart rate from 128 bpm to 102 bpm, and an increase in the blood pressure from 76/55 to 92/57 mmHg (positive Nicoladoni-Branham sign [, ]). An echocardiogram that was done simultaneously showed a decrease in the flow through the right ventricle. The fistula was subsequently surgically ligated without complications. Repeat physical exam showed normalization of the patient's blood pressure and heart rate readings. She was quickly weaned to room air. A repeat echocardiogram done thirteen days after the repair showed no evidence of pulmonary artery hypertension.
A 76-year-old woman presented to our hospital with a mass occurring on the skin of her right chest wall. She had been diagnosed with right breast cancer (T1N0M0, stage I) 9 years previously and had received breast-conserving surgery, sentinel lymph node biopsy, and adjuvant chemotherapy and radiation therapy for the residual whole right breast at a previous hospital. She then developed pigmented skin on her right breast 6 years after surgery, and this lesion was diagnosed as an angiosarcoma. The patient underwent a breast mastectomy to treat for RAAS. Following this, however, the angiosarcoma on her chest wall recurred three times within 2 years. The angiosarcoma was resected each time, and she received radiation therapy to her chest wall after the third operation. Four years after the first occurrence of RAAS, we observed light pigmentation and a dark red tumor (gross diameter of 5 mm) on her right chest wall (Fig. ). Clinically, recurrence of RAAS was suspected, and recurrence of angiosarcoma was diagnosed by biopsy. We considered that it was necessary to remove the irradiated skin as much as possible in order to cure the RAAS. After extensive resection of the irradiated skin and tumor, new skin collected from her right thigh was grafted to the site (Fig. ). Pathologically, the tumor size was 6 mm and the surgical margin was negative. Histologically, there were many spindle cells and dilated vascular channels. Immunostaining showed that the tumor was CD31-positive and mildly positive for CD34 (Fig. ). Ki-67 index was also high. It was revealed that there is no inconsistency as recurrence of RAAS is pathological. After the operation, the patient was hospitalized for 30 days and did not experience any complications. Although some reports suggest chemotherapy can be used to treat RAAS, we considered that this option would offer little benefit in this case, because the patient was elderly and had a history of cerebral infarction. Indeed, the patient has remained angiosarcoma-free for the last 3 years following our intervention, even without chemotherapy (Fig. ).
A 70-year-old man with history of unstable angina, hypertension, and impaired glucose tolerance was referred for coronary artery bypass grafting. Preoperative coronary angiogram showed double vessel disease with 90% ostial left anterior descending stenosis and 75% stenosis of the left circumflex bifurcation. Echocardiogram, preoperatively, showed left ventricular ejection fraction of 55% with preserved LV function. CABG was performed with left internal thoracic artery to left anterior descending artery and saphenous vein to the second obtuse marginal artery. The vein was harvested from the right lower leg. Crepe bandage with minimal compression was applied to the leg after surgery. There were no intraoperative complications.\nPostoperatively he was successfully extubated and was transferred to ward on day 1 postoperatively from intensive care unit. He developed fast atrial fibrillation while on ward, managed with intravenous followed by oral amiodarone. The atrial fibrillation lasted for a few hours on day 2 postoperatively. On day three postoperatively, he complained of severe pain in right leg. On assessment the right leg was tense, tender, and swollen with minimal pain on passive flexion. Power in the foot was 1/5 on dorsiflexion and 5/5 on plantar flexion with loss of sensations over the dorsum of foot. He had foot drop on clinical exam with steppage gait. Foot pulses were not palpable with capillary refill time of more than 4 seconds. Nothing abnormal was found on neurovascular exam on the opposite side.\nDoppler ultrasound scan of right leg excluded deep venous thrombosis. CTA lower limbs showed bilateral diffuse anterior tibial artery disease with no evidence of embolus (preoperative history and clinical examination were negative for peripheral vascular disease). Compartment pressures were measured in right leg which were elevated and he was diagnosed with the anterolateral compartment syndrome. Urgent fasciotomy was done. Muscles in the anterior compartment (tibialis anterior and external hallucis longus) were pale and were not contracting to diathermy stimulation. The wound was left open and a delayed closure was done by which time the muscles appeared to be pink. Pain resolved markedly after surgery; however, there was residual foot drop with impaired sensation over the dorsum of the foot. Once comfortable, he was transferred to the rehabilitation ward.
An 84-year-old man accidentally fell at home and was admitted to our hospital. The patient was hospitalized with several problems such as multiple metastases of prostate cancer, chronic heart failure, emphysema, impaired renal function, and biliary stent placement due to idiopathic biliary stenosis. While no fracture was identified, the patient complained of lower back pain and was unable to move. As a consequence, he was hospitalized for the purpose of pain management. On the third day of hospitalization, the patient developed a fever of 38.2°C, and his laboratory data showed high levels of WBC count and CRP. While the source of infection was not identified, a urinary tract infection was suspected because he had purulent urine from previous examination and no symptom of respiratory tract infection. The patient underwent treatment with CMZ 1 g every 12 hrs. Three days after therapy initiation, the fever declined and the laboratory data of the inflammatory response normalized. Although blood culture was negative, we decided to treat according to sepsis because he was frail. We, therefore, planned to administer CMZ for 14 days. During the treatment course, the patient did not develop fever and had a healthy appetite.\nOn the morning of the 14th day of hospitalization, the patient complained of a sudden difficulty in breathing. His peripheral artery oxygen saturation decreased to 74%. No fever, coughing, or sputum was identified. A chest computed tomography (CT) scan was performed, showing the presence of ground glass shadows bilaterally (). While the blood work demonstrated the absence of an inflammatory response, Hb decreased by 1.5 g/dL from the previous day. The BNP value was 103 pg/dL, similar to that at initial hospitalization. Because hemostasis of the blood sampling site was difficult, additional laboratory tests were performed. These showed a marked prolongation of PT-INR (). In the evening, his value of Hb dropped from 6.8 to 5.5 g/dl in six hours. We doubted gastrointestinal bleeding, but there was no black stool. Additionally, he began to spit bloody sputum. We considered bronchoscopy but could not carry out because of his poor respiration. Since the patient had an acute respiratory failure accompanied by blood sputum and progressive anemia without exacerbation of heart failure, he was diagnosed with pulmonary alveolar hemorrhage due to coagulation abnormality. Two units of red blood cell concentrates stored in mannitol adenine phosphate and six units of fresh frozen plasma were immediately administered to the patient.\nWe believe that the pulmonary alveolar hemorrhage was caused by disseminated intravascular coagulation (DIC) due to the prostate cancer. However, the patient did not meet the DIC's diagnostic criteria because each level was fibrinogen 393.8 mg/dL, fibrinogen degradation products (FDPs) 23.0 ug/dl, and platelet count 15.3 × 104/uL, even though PT-INR indicated extremely abnormal value (). We took into consideration the possibility of Vit K deficiency. To overcome this issue, we administered 10 mg menatetrenone per day. Three days later, all coagulation systems had recovered to their normal values (). Protein induced by vitamin K absence-II (PIVKAII) reached 8,884 mAU/mL (normal range below 40 mAU/mL) by the 23rd day of hospitalization.\nBased on these observations, we investigated the cause behind the Vit K deficiency. The prescription drugs had not been changed before and after hospitalization, and antiplatelet and anticoagulant agents had not been used. The only additional drug used during hospitalization was CMZ. Furthermore, the patient's food intake remained unchanged in the course of the hospitalization as well as his hepatobiliary system's laboratory tests. No diarrhea developed during the patient's illness. Based on these observations, the patient was diagnosed with hypoprothrombinemia due to CMZ inhibition of Vit K epoxide reductase. Despite discontinuation of Vit K (menatetrenone) administration, the coagulation activity did not decrease. The pulmonary alveolar hemorrhage gradually improved, and the patient was discharged after one month.\nOne month after discharge, the patient was rehospitalized with pneumonia. He was treated with sulbactam/ampicillin 3 g quaque 12 hrs for 7 days, but hypoprothrombinemia was not observed.
In May 15 2013 a 34-year-old healthy woman was treated by her general dental practitioner and a non-surgical endodontic treatment was performed on her maxillary left first premolar tooth. During canal irrigation patient complained intense pain. She didn’t know what kind of liquid was used but she reported to smell bleach.\nAt home, pain increased and patient had tense and warm swelling extending from the mandibular border to left eyelid with initial reduction in visual acuity. Patient tried to contact her general dentist but he didn’t answer. The woman, worried for increasing symptoms, the same evening went to the Dental Clinic of the local Hospital and immediately transferred to the Emergency Department in the same Hospital.\nOn examination there was a firm left facial swelling and ecchymosis from below the border of the mandible up to the left eye. Doctors gave her antibiotic therapy and they quit on her with indication to return the next morning.\nThe next day, patient went again at the Civil Hospital of Brescia, where she submitted to maxillofacial visit. Doctors and patient contacted the dentist for information on the treatment performed. The dentist stated to used hydrogen peroxide at 10%. Doctor prescribed to the woman antibiotics and anti-inflammatory.\nTwo days later patient went back to the emergency department of the Hospital complaining alteration of vision of the eye left, an increased edema of the left cheek and an hemorrhagic episode of the oral cavity. Therefore, given the clinical, she was hospitalized at the Department of Maxillofacial Surgery of the same hospital.\nExtra oral examination revealed significant soft tissue swelling extend from left intraorbital region to the mandibular border. Infraorbitally and in the region of the upper left lip, there was altered sensation. This is the area of the left infraorbital nerve. In addition the buccal branch of the facial nerve was affected. This resulted in a distinct loss of upper lip and cheek function (the corner of the mouth could not be pulled up by the mimic musculature). Eye examination revealed blepharospasm and a TC examination revealed areas of bone resorption. NaOCl accident was suspected. To prevent risk of infection orally antibiotic therapy was administered for 7 days and ibuprofen was prescribed for pain management.\nBoth swelling and ecchymosis kept progressively decreasing during the follow up period but neurological symptoms didn’t resolved.\nOn neurological review one month later was found a deficit on left of the second branch of the fifth cranial nerve, of the seventh cranial nerve, of the ninth and the tenth cranial nerve. There were anesthesia and paraesthesia of the left side of the face, a detour to the left of the tongue (to the right during protrusion), deficit of left orbicularis muscle of the mouth, eye spasms during fixation and deficit of the sternocleidomastoid in the rotation of the head to the left.\nOne year later neurological symptoms resolved only partially. On examination it was confirmed nerve deficits on II branch of the fifth cranial nerve left, a slight deficit in the upper territory of the seventh cranial nerve left and a definite weakness in the lower area of the seventh cranial nerve left ().\nThe patient filed legal claims against the dentist and the case was kept to the attention of the Penal Court.
We report the case of a 60-year-old woman admitted to the emergency department following a minor road traffic accident. The patient had a medical history of breast infiltrating ductal carcinoma (HER2+) under trastuzumab monotherapy for seven months and had been submitted to chemotherapy with FEC regimen (5-fluorouracil, epidoxorubicin and cyclophosphamide) four years before trastuzumab initiation. The patient had recently been diagnosed (six weeks before) with hypertension and started treatment with an angiotensin-converting enzyme inhibitor (enalapril 10 mg once daily) together with a calcium channel blocker (amlodipine 5 mg once daily). Despite treatment, it was still poorly controlled.\nOn examination in the emergency room, there was no evidence of traumatic lesions in keeping with the paramedics' initial report, the patient was hypertensive (196/97 mmHg), with a Glasgow Coma Scale score of 14 (E4V4M6), following verbal commands but with a new onset left hemiplegia with a National Institutes of Health Stroke Scale (NIHSS) score of 6 (4 points on left arm motor drift and 2 points on left leg motor drift). A non-enhanced computed tomography of the head revealed a right intracerebral haemorrhage of 70 x 40 mm with associated midline shift of 4 mm to the left side (Figure ).\nShe was diagnosed with a spontaneous haemorrhagic stroke secondary to uncontrolled blood pressure. Other investigations, such as electrocardiogram and blood analysis, did not show any significant abnormalities. With regards to the transthoracic echocardiogram, it was found to have a segmental wall motion abnormality with a left ventricular mid inferior and basal inferior wall hypokinesia with no compromise of ventricular systolic function. We did not have access to previous echocardiograms for comparison but according to patient’s verbal information, there were no abnormalities on the echocardiography examination performed prior to trastuzumab initiation. Despite information provided by the patient with regards to her medical history, we were unable to safely exclude that the left ventricular regional wall motion abnormality was secondary to the previous chemotherapy regimen or due to a different etiology.\nEven though the patient presented with an intracerebral haemorrhage which could lead to a poor outcome, recovery was favourable with minor neurological deficits (NIHSS score of 1 on left arm motor drift) after 10 days of hospitalization. Short follow-up appointment with her oncologist was set up and antihypertensive therapy optimized before discharge (enalapril 20 mg once daily, amlodipine 10 mg once daily and indapamide 2.5 mg once daily).
A 47 year-old, 42-kg man with 1-year history of localised scleroderma referred to Trauma Department in our hospital because of acetabular fracture due to a car accident. After a series of pre-operation examinations, he was scheduled for a selective operation of inner fixation 6 days after his trauma. During the preanesthesia assessment, we found him not on any drugs but some kind of Chinese medication occasionally for scleroderma for about a year because of the side effects of the Chinese medications. There was no history of any surgery or anesthesia. Examination of his airway revealed microstomia with mouth opening of 2.5 cm and a Mallampati class III airway. However, there was no problem with motion of his head and neck, as the skin on his neck was not affected by scleroderma. On general physical examination, vital signs were stable, heart sounds were normal and breath sounds were clear bilaterally. His face was smooth and wrinkleless, his forearms had non-pitting edema, and his fingers were shortened and sausage-like, with flexion contractures on both wrists and fingers. Laboratory tests of total blood cell count, arterial blood gas analysis, pulmonary, liver and kidney function, ECG, echocardiography and X-ray were taken, all of which were normal except for mild anemia (Hb 90 g/L), which could be inferred that his viscera were not badly affected by scleroderma. For the reason of his anemia and predicted volume of blood loss he might have during the surgery, 2 U of packed red blood cell was prepared and ready for use on the surgery day.\nIn the operating room, standard monitors were attached, showing heart rate of 72 bpm and blood pressure of 112/65 mmHg. However, SpO2 could not be read on any of his fingers. We assumed it may because of skin thickening and vasospasm on his hands and fingers, so we moved the probe to his toes and finally got the value of 95 % while he was breathing room air. Peripheral intravenous access was obtained with difficulty hence awake right internal jugular venous insertion was achieved under regional anesthesia. Ranitidine 50 mg and tropisetron 3 mg were given intravenously. An ENT surgeon for tracheostomy was kept ready. After pre-oxygenation, anesthesia was induced with penehyclidine hydrocloride 0.2 mg, midazolam 2 mg, sufentanyl 25 μg, propofol 40 mg. After ensuring optimal bag and mask ventilation, neuromuscular blockade was administered with 60 mg succinylcholine to facilitate tracheal intubation. With epiglottis, glottis and tracheal cartilage clearly seen under Shikani Optical Stylet (SOS), endotracheal tube of ID (internal diameter) 7 mm was achieved and confirmed by symmetrical breath sounds and capnography. Before changing to lateral position, radial artery cannulation was preformed with difficulty. Anesthesia was maintained with 1 % sevoflurane, 4–6 mg/kg of propofol and 0.1–0.2 μg/kg/min of remifentanil. Guided by neuromuscular monitor, non-depolarization muscle reluxant atracurium was administered intermittently. Surgery lasted for 1 h and 40 min, with the blood loss of 300 ml. At the end of surgery and before he was transferred to post-anesthesia care unit (PACU), neuromuscular block was reversed and trachea was extubated. Intra-operative and postoperative course was uneventful.
A 26 year old male patient was changing his car tyre on the roadside when he was hit by another car from the side. On arrival to the emergency department (ED), he was hemodynamically stable with heart rate of 100/minute, BP 100/70 mm of Hg and respiratory rate of 18/minute. He was managed as per Advanced Trauma Life Support (ATLS) protocol. The patient was oriented with negative focused assessment with sonography for trauma (FAST) and inability to lift left leg with pain in the pelvic region. On examination, pelvic compression test was positive. He was having foot drop on the left side. After initial clinical assessment plain anteroposterior radiograph of the pelvis suggested a pelvic fracture. Subsequent computed tomography (CT) scans and radiographs revealed a fracture of the left posterior ilium with anterior dislocation of the SIJ []. There was associated symphyseal disruption with marked widening and high oblique fracture of the left superior ramus.\nThe patient was operated for his pelvic injuries on the 5th day following trauma. Pfannenstiel incision and lateral window of the ilioinguinal approach were used to access the fractures. The fractured ilium was found to be lying anterior to the sacrum. A Schanz pin was placed onto the iliac crest to get a proper hold of the iliac blade, which was then levered anteriorly, laterally to its anatomical position. Proper care was taken to avoid further damage to the intact yet contused L5 nerve root while reducing the anteriorly placed fractured iliac blade. The fractured fragment was reduced anatomically and fixed with a reconstruction plate (4 hole) across the SIJ in the standard fashion. The symphysis was also stabilized with a 3.5 mm plate and screws []. The total operative time was 2 hrs with a blood loss of 300 ml. Patient was allowed full weight bearing after 8 weeks. At the end of 18 months, patient was back to his pretrauma activities. The functional outcome of the patient was good with recovery of the peroneal nerve function at the last followup at 2 years.
A 46-year-old Chinese woman from a low-income family, living with her mother and two sons in the suburb of Taichung City, had a history of recurrent abdominal pain. Within two years, she visited the gastroenterology clinic many times with the same complaint. There was no remarkable family history. Likewise, results of her abdominal ultrasound, endoscopy, and colonoscopy were within normal limits. The patient reported intermittent episodes of anxiety and general weakness that became progressively worse over time. Blood tests from previous visits revealed slightly abnormal liver and renal function. Chronic hepatitis C infection was diagnosed on the basis of these findings. One month before this admission, the patient presented with acute abdominal pain and progressive bilateral weakness and pain in the limbs. She also experienced significant muscle atrophy and decreased strength. During admission, the patient reported moderate, sharp pain (pain score: 5) in extremities, back, chest, and neck. She also experienced episodes of sinus tachycardia and acute urinary retention, suggesting autonomic neuropathy. The patient also reported an unusual “floating sensation” in the trunk and extremities, which was suggestive of a proprioceptive defect. In addition to anxiety, minor behavioral changes, including confusion and signs of depression, were observed. Results of a nerve conduction potential study revealed motor-sensory polyneuropathy. A motor conduction study revealed a reduced compound muscle action potential amplitude, slowed nerve conduction velocity, delayed distal latency, and prolonged F latency over the median, ulnar, tibial, and peroneal nerves.\nA sensory conduction study of the median, ulnar, and sural nerves revealed reduced sensory nerve action potential amplitude and delayed onset latency. Computed tomography of the brain was normal, and examination of cerebrospinal fluid showed no remarkable findings. Initial differential diagnoses included acute porphyria, lead toxicity, and vasculitis. Serum lead levels and autoimmune titers were normal, thus ruling out lead poisoning or vasculitis. A simple urine test was performed in which the urine sample of the patient was exposed to sunlight for 3 days. The urine changed from a normal yellow to port wine color after 3 days because of the accumulation of increased concentrations of porphyrin intermediates (). Hoesch and Watson–Schwartz urine tests were also performed. These tests revealed increased levels of coproporhyrin and porphyrin precursors such as porphobilinogen (PBG) and aminolevulinic acid. A diagnosis of acute porphyria was thereby confirmed. Furthermore, PBG deaminase activity was within the normal range, suggesting a specific diagnosis of HCP, since patients with AIP have low PBG deaminase activity, those with ADP have normal PBG levels, and those with VP often exhibit cutaneous manifestations. The patient was initially treated with intravenous glucose 200 mg/day and cimetidine 300 mg twice daily. Abdominal pain and polyneuropathy showed mild improvement after initiating therapy. Soon after, she received intravenous hemin therapy, and the duration and severity of her abdominal pain decreased. The patient then continued to receive regular rehabilitation therapy for motor and speech deficits. After two months, the patient had no recurrence of symptoms, and her muscle strength improved significantly. She was instructed to avoid predisposing factors such as sunlight and nonsteroidal anti-inflammatory drugs.
A 49-year-old Nigerian female presented to her local hospital with a 1-year history of recurrent chest infections. She had non-insulin dependent diabetes but no other significant past medical history. She took metformin twice daily and had no known drug allergies. She had no past surgical history and was a lifelong non-smoker. She had no relevant past family history of any genetic disorders, in addition to no recent foreign travel or contact exposure to tuberculosis. When she initially presented, plain chest radiographs were performed and demonstrated multiple lung lesions suggestive of an infective/inflammatory process. She grew pseudomonas on sputum culture, but despite treatment for atypical pneumonia with multiple courses of antibiotics, she failed to adequately improve. Chest CT was consequently performed and demonstrated multiple cavitating lung lesions (fig ). During this time, she had intermittent vomiting with an associated 15-kg weight loss over a 12-month period. These symptoms were initially attributed to her recurrent chest infections and were not further investigated.\nThe lung lesions were sampled and were found to be negative for tuberculosis. A working diagnosis of aspergillus infection was established, and the patient remained under the care of the respiratory physicians. At the time of chest CT, however, an incidental finding was noted in the second to the fourth part of the duodenum. Concurrently, she developed subacute bowel obstruction with persistent vomiting and was unable to tolerate oral intake. A dedicated CT scan of the abdomen and pelvis was therefore performed, demonstrating an obstructing polypoid mass at D2 (fig ).\nThis lesion was confirmed on upper gastrointestinal endoscopy, and a biopsy demonstrated a tubulovillous adenoma with high-grade dysplasia. Nasojejunal tube insertion was attempted at her local hospital; however, this failed to bypass the obstructing lesion. Her case was discussed at the regional hepatopancreaticobiliary multidisciplinary team meeting at the Royal London Hospital. As her biopsy demonstrated high-grade dysplasia, in addition to her symptomatic presentation, it was felt that a resection was required. Based upon her cross-sectional and endoscopic imaging, it was deemed that this would not be amenable to an endoscopic excision, and she was likely to require surgical resection and should be transferred to the HPB unit at The Royal London Hospital. Interestingly, despite this large lesion, she never became jaundiced and maintained a normal bilirubin level.\nOn arrival at the hospital, she was admitted to the surgical ward, and although she had persistent vomiting and was cachectic, she was haemodynamically stable. She was nutritionally deplete with a moderate hypokalaemia at 2.7 mmol/l (normal range 3.5–5.0) and an albumin level of 30 g/l (normal range 35–50) due to the failed nasojejunal tube insertion. Consequently, a PICC line was inserted by interventional radiology, and in an attempt to optimise her for major abdominal surgery, total parenteral nutrition was administered. However, due to these ongoing nutritional problems and a failure to adequately improve, she underwent a semi-urgent conventional pancreaticoduodenectomy. The procedure was successful without any intraoperative complications.\nIntraoperatively, a large mass at D2 with a duodeno-duodenal intussusception and distal duodenal ischaemia was identified (fig ). Histological analysis reported a polypoid tumour at the Ampulla of Vater, 75 × 28 × 30 mm in size, with a reduced intussusception and an ischaemic distal duodenum (fig ). These findings were in keeping with a duodenal ampullary low-grade tubular adenoma, with intussusception and complete resection margins. There was no evidence of any high-grade dysplasia, in contrast to her previous diagnostic biopsy, or invasive malignancy. The patient was admitted to the high-dependency unit postoperatively and was stepped down to the surgical ward on postoperative day 2. She progressed well with early mobilisation, and her nutritional status greatly improved during this time, with due care not to induce a refeeding syndrome. She was medically stable and deemed fit for discharge on postoperative day 10. She resumed work 4 weeks postoperatively, with no evidence of recurrent chest infections. She did not develop any exocrine pancreatic insufficiency or any derangement from her baseline glycaemic control. To date, the patient has not suffered any long-term complications, and remains clinically well on follow-up.
A 60-year-old male presented to hospital with left flank pain and burning micturition since 2 months. Pain was colicky in nature and was relieved by medication. The patient had no history of weight loss or fever. There was no significant past or family history.\nPhysical examination and routine investigations were done including blood pressure and complete blood count all were within normal limits except for urine examination which revealed trace of blood.\nContrast-enhanced computed tomography (CT) scan of abdomen was performed which revealed two fat density lesions of size (12 × 11 × 11) cm and (5.8 × 5 × 4.7) cm in left adrenal gland. Larger one showed few heterogeneously hyperdense internal contents and bone like calcification with cortical and medullary differentiation. Smaller one also had internal hyperdense content and showed internal as well as peripheral rim like calcification [Figures and ]. Lesions showed acute angle with left kidney. Left adrenal gland was not distinctly visualised on imaging. There were few stones in left renal pelvis and left pelvi-ureteric junction [] with left moderate hydronephrosis which explained colicky left flank pain and burning micturition. X-ray abdomen was performed, which showed peripheral and bone like calcification []. On imaging possibility of adrenal teratoma with second possibility of retroperitoneal teratoma was given.\nSurgical resection of tumor was done along with left adrenalectomy without any intraoperative or postoperative complications. The specimen was sent for histopathological examination. On gross examination cystic mass with tooth and bone like areas and hair tuft was seen. On microscopic examination cells from all three germ layers were seen, residual compressed adrenal cortical tissue was evident in the wall of cyst. Final diagnosis of mature cystic teratoma of adrenal gland was made.\nWe did an extensive search for recent literature—from 2000 to 2018—on the internet about adrenal teratomas in adults and children.\nCases of primary adrenal lesions were included where histopathological lesion origin was proven to be of adrenal gland. Primary retroperitoneal teratomas which involved the adrenal gland were also included. Cases where adrenal gland was found only to be compressed by the lesion or was completely uninvolved were not included in this review.\nAdrenal teratomas were more common in adults than in children (26 vs 6).\nAdult patients: 26 cases of adrenal teratomas were found. Majority of them were female accounting to 82.7% cases. Only 5 of them were male. 15 cases involved the left adrenal gland whereas 14 involved the right adrenal gland. All cases were surgically resected. Only 3 cases were of size less than 5 cm. Rest all were more than 5 cm Modalities used were CT, USG and MRI. CT was used in majority of cases. Typical imaging features of adrenal teratoma which include heterogeneous lesion, internal fat component and calcifications were evaluated in this review. All three features were present in 19 out of 26 cases. Histopathological confirmation was mentioned in all cases except one [; case no - 18]. 7 cases were diagnosed as primary retroperitoneal adrenal teratomas, where their origin was not definitely identified to be from adrenal gland but adrenal gland involvement was affirmative. Among all these cases, one case of malignant transformation of teratoma and one case of rupture of adrenal teratoma in the hemi-thorax was noted. Paediatric patients: 6 cases of adrenal teratomas were found. 4 cases were female and 2 male. 5 cases were noted involving right adrenal gland. Modalities used were USG, CT and MRI. Typical imaging features of teratoma were noted in 3 out of 6 cases All of them were surgically resected and histological proven cases. Follow-up of minimum of 6 months was noted in 3 cases, with no recurrence in any case [].
We report a case of transmesocolic herniation of jejunal loops into supracolic compartment with intestinal obstruction which was diagnosed intraoperatively.\nA 48-year-old female was admitted to casualty with a history of abdominal distension and vomiting of 3 days duration. She had no past history of any gastrointestinal surgery but had undergone lower segment caesarean section 21 years earlier. The caesarean section was uneventful without any iatrogenic injury. On admission, she had bilious vomiting. Physical examination revealed tachycardia, generalized abdominal distension, rebound tenderness and rigidity over left upper quadrant. There was no evidence of organomegaly or free fluid and her external hernia orifices were normal. Her bowel sounds were sluggish. Digital rectal examination revealed an empty rectum. Laboratory investigation on admission revealed a normal full blood count with a white blood cell count of 5000/mm3 and normal renal and liver functions. Her serum potassium on admission was 3.5 mmol/l and she was started in intravenous potassium supplements. An abdominal X-ray supine film showed multiple small bowel loops with air fluid levels without free air under the dome of the diaphragm (Fig. ). Surgical exploration revealed significant amount of free fluid in the peritoneal cavity and ischemic small intestine. On further exploration, we found the DJ flexure in the supracolic compartment and almost all the jejunum and proximal ileum herniating through a small defect about 5 × 6 cm in the transverse mesocolon. Jejunal loops were contained inside a thick walled hernial sac (Fig. ) which was extending in to the supracolic compartment. The hernia sac with contents was extending into the lesser sac. The contents were reduced and the sac was opened and repaired (Fig. ). Paraduodenal fossae were found to be normal during the surgery (Fig. ). The defect in the transverse mesocolon was repaired. Small bowel showed features of viability and therefore, was not resected. The patient was discharged on post operative day 14. Her post operative period was uneventful. She also underwent a contrast study of the small bowel at post op day 10 which showed normal small intestine (Fig. ).
A 68-year-old man with a history of abdominal pain of unknown cause despite numerous radiological and endoscopic investigations by a gastroenterologist underwent a laparotomy in 2008. This revealed dilatation of the entire small bowel up to 12 cm until two feet from the ileocaecal valve with the collapsed large bowel; no mechanical cause was found to explain the small bowel distension. He subsequently developed an incisional hernia which was repaired laparoscopically with a large intraperitoneal mesh the following year.\nHe was readmitted in 2016 and underwent a laparoscopy which showed small bowel distension. Laparoscopic division of adhesions was performed for presumed adhesional small bowel obstruction. After a few days, he developed abdominal pain and distension, and clinical examination showed gross distension of the abdomen with features of peritonitis. CT scan of the abdomen revealed gross distension of the small bowel with pneumatosis intestinalis and free intraperitoneal air (Figure ). A laparotomy was performed, but it did not show any perforation of the grossly distended (up to 15 cm) entire small bowel; instead gas bubble/sacs were seen in the small bowel wall and the mesentery. Without access to his old notes, the diagnosis was not clear. To decompress the bowel, a double-barrelled ileostomy was fashioned as a venting enterotomy. Over the next few weeks, the abdominal distension reduced, and the stoma started functioning. He was fed enterally. Unfortunately, small bowel stasis and repeated episodes of small bowel pseudo-obstruction resulted in intermittent high output ileostomy and repeated admissions with dehydration and progressive malnutrition. His care proved to be challenging not only to the surgeons but also to the nutrition team. He was referred to the National Intestinal Failure Unit at Salford.\nInvestigations at Salford Royal Hospital provided further insight. Small bowel manometry showed low amplitude wave for phase III activity in the stomach and duodenum. Barium studies displayed slow propagation of contrast. Large bowel studies were normal, as were investigations for gut hormones, autoantibodies, faecal elastase, amyloid and onconeural antibody screen. The final diagnosis was chronic small bowel pseudo-obstruction. The patient was managed with home parenteral nutrition and after several months, his ileostomy was reversed. He subsequently developed two further episodes of small bowel pseudo-obstruction which were managed conservatively in our hospital over the last two years.
A twenty-seven-year-old male patient who had been involved in a motor vehicle accident was brought to the emergency room with multiple injuries in October 2008. The patient was not examined on arrival due to the fact that he was intubated shortly after admission for airway protection and hemodynamic instability; however, he was reported to be moving all 4 extremities at the scene. Neutral cervical spine radiographs performed under general anaesthesia revealed no fracture or dislocation. The patient was estubated after a few days and he was found to have a severe torticollis with his head rotated to the left side and tilted toward the right side in a “cock-robin” position, muscles spasms, painful limitation of motion, and inability to turn the head to the right side. However, the neurological examination was normal. At this time, a computed tomography (CT) of the cervical spine with a bone window was performed showing an atlanto-dental interval (ADI) greater than 5 mm (), 45 degrees of axial rotation (), and no bone fracture. Additionally, an asymmetry of the lateral masses of C1 with respect to the odontoid process was seen on the anteroposterior CT bone scan image and a loss of normal articular apposition at C1-C2 was documented (). Furthermore, a magnetic angioresonance was performed to rule out the risk of injury to the vertebral arteries. A manual manipulation was then attempted under general anaesthesia and a quite complete reduction was confirmed with CT bone scan. At this time, a new cervical spine magnetic resonance imaging was performed to determine the disruption of ligaments revealing soft tissues swelling, a Type IA injury of transverse ligament, a complete rupture of the right alar ligament, and a partial injury of the left one (Figures , , and ). No spinal cord compression or signal changes were identified.\nFinally, the patient was placed in a Philadelphia collar and he was transported directly to the operating room. An early posterior stabilisation from the occiput to C3 was performed by using a Hartshill U-shaped rod and Songer sublaminar wires. Moreover, an autologous bone graft, a porcine xenograft, and a biocompatible graft substitute like hydroxyapatite were placed in the decorticated areas. In addition, initial and intraoperative motor and somatosensory evoked potentials suggested no neurological modifications. The postoperative neurological examination did not reveal any deficit and the torticollis was completely resolved. After surgery, the patient was placed in a Philadelphia collar for 60 days. Immediate postoperative radiographs showed a proper implant placement (). CT bone scans at 60-day and 3-year followup demonstrated an occipitocervical stable fusion (); furthermore, the patient was free of pain and torticollis and returned to his normal daily activities.
A 55-year-old Caucasian woman with a 5-month history of abdominal pain and vomiting was diagnosed as having a probable high-grade ovarian malignancy with a large volume of peritoneal disease. She had a prior ultrasound of her pelvis which demonstrated a 17 cm large irregular solid vascularized mass in her right ovary. Her comorbidities included obesity (body mass index of 33), asthma, and she had previously undergone a laparoscopic cholecystectomy. There was no significant family history. She did not smoke tobacco and she drank alcohol occasionally. She was scheduled for debulking surgery; however, she presented to our emergency department with worsening abdominal pain, vomiting, and diarrhea. A physical examination showed dry mucous membranes, capillary refill < 3 seconds, and jugular venous pressure of 4 cm. Her chest was clear on auscultation with dual heart sounds. Her abdomen was distended with generalized tenderness but no guarding or signs of peritonism. Bowel sounds were present. A computed tomography (CT) scan of her abdomen and pelvis was performed which demonstrated the large right ovarian tumor, peritoneal tumor deposits, and ascites. There was extrinsic compression of her sigmoid colon due to the tumor without radiological signs of large bowel obstruction. There were no other abnormalities of her bowel. She received intravenously administered fluids for rehydration, anti-emetics for nausea, and intravenously administered morphine for abdominal pain. She remained overnight in our emergency department for treatment. She was reassessed the following morning after resolution of her symptoms and was found to be hemodynamically stable and subsequently discharged home.\nShe re-presented 1 week later with similar symptoms and was admitted to hospital for further management. Following multidisciplinary discussion, she was recommended for neoadjuvant chemotherapy prior to surgical debulking. An urgent core biopsy of the mass confirmed the likely diagnosis of ovarian malignancy. This biopsy indicated a high-grade serous adenocarcinoma. The histology and CT findings were consistent with an International Federation of Gynaecology and Obstetrics (FIGO) stage III ovarian cancer. She was appropriately counselled as to the benefits and risks of chemotherapy prior to commencing treatment.\nShe was commenced on a first cycle of the commonly used platinum-based two-drug chemotherapy regime of paclitaxel and carboplatin []. The dose prescribed was a three weekly cycle of paclitaxel 100 mg/m2 and carboplatin 385 mg/body to achieve area under the curve (AUC) of 5 using the Calvert formula. The results of her pre-chemotherapy blood tests were within acceptable ranges. Specifically, her white cell count (WCC) was 10.1 × 109/L (normal 4–11 × 109/L) and neutrophils were 8.5 × 109/L (normal 1.5–8 × 109/L). She reported feeling better 1 day after chemotherapy. However, 3 days following the commencement of chemotherapy, persistent diarrhea developed. Stool cultures were negative for stool pathogens including Clostridium difficile. On the sixth day post-chemotherapy, she became febrile and acutely unwell with severe abdominal pain. Blood tests at the time revealed a WCC of 0.6 × 109/L and neutropenia of 0.1 × 109/L. A repeat CT of her abdomen and pelvis showed a thickened descending colon and rectal pneumatosis with perforation into the mesorectum (Figs. and ). Blood cultures were positive for Escherichia coli and meropenem was commenced. She was transferred to our intensive care unit for hemodynamic support due to septic shock. A surgical assessment was conducted but immediate surgical intervention was deemed inappropriate due to high predicted mortality. She was administered granulocyte colony-stimulating factor but her white blood cell counts did not improve and her respiratory function deteriorated. She died 9 days after the administration of the first dose of chemotherapy. An autopsy was not performed due to the wishes of our patient’s family.
A 35-year-old man presented with a painless mass at the right side of the chest wall. One month prior to admission, the patient presented with a raised and painless mass in the right infraclavicular fossa. The patient was diagnosed with a gastric GIST in April 2016. A computed tomography (CT) scan showed a huge inhomogeneous soft tissue mass (approximately 18.1 cm × 11.9 cm) with central necrosis, occupying the entire left upper abdomen, along with two nodular enhancing liver lesions (the largest lesion was approximately 2.5 cm) suspicious of a metastatic malignancy in the right lobe (Figure and ). In light of the pathologic diagnosis and the CT scan, the tumor was classified as an advanced GIST. The patient was administered imatinib 400 mg orally daily on a neoadjuvant basis before surgery. After 10 mo of imatinib therapy, the tumor showed a marked reduction in size (approximately 8.6 cm × 6.7 cm), tumor enhancement at arterial phase CT decreased substantially and hepatic metastatic lesions showed no enhancement (Figure and ). Surgery was requested by the patient. At laparotomy, the tumor was located at the gastric fundus and invaded the nearby organs including the spleen, the tail of the pancreas and the left adrenal gland. The tumor was resected en bloc with the spleen, a portion of the stomach and the left adrenal gland, and the tail of the pancreas, and the hepatic metastatic tumors were also removed according to the findings of intraoperative ultrasonography, achieving an R0 resection. The pathological report of the resected specimen showed a tumor mass with diffuse hyalinization, fibrosis and focal hemorrhage and necrosis. Only a few spindle cells were distributed in the tumor lesion and the cells were positive for CD117 and DOG-1 (Figure ). Unfortunately, the patient developed a gastric fistula postoperatively, and a single lumen 16 G TIVAP was inserted into the right subclavian vein via the Seldinger technique, with the aim of prolonged parenteral nutrition
A 28-year-old female was diagnosed in Tunisia with stage IV synovial sarcoma originating from the soft tissue of the left trapezius with lung metastases, after complaining of shoulder swelling and pain back in July 2018. Written reports of the CT imaging obtained in Tunisia revealed that she had a 4 x 2 cm left paravertebral pleural formation, 1 cm left pleural nodule and 10 x 9 x 3.5 cm left posterior dorsal wall mass of muscular origin presumed to be the trapezius, at the time of diagnosis. Outside reports of the biopsy of the intramuscular mass revealed that she was diagnosed with a grade 2 monophasic synovial cell sarcoma. She had no family history of malignancy. She received 6 cycles of adriamycin and ifosfamide with mesna. The size of tumor decreased after the third cycle and continued to be stable afterwards. The plan was to start radiation after completion of chemotherapy, but she relocated to the United States before starting radiation therapy.\nShe established care in our institution in February 2019. A repeat CT revealed a left pleural nodule measuring 3.9 cm, left lower lobe nodule measuring 1.5 cm, and a right upper lobe nodule measuring 3.5 cm (Figures , ). The CT scan also revealed a trapezius mass measuring 8 x 4 cm (Figures , ). She was not a candidate for resection of chest wall tumor due to the extensive nature of the required surgery. Pazopanib 800 mg daily was started due to disease progression, in addition to palliative radiation to the left scapula for pain control. Radiation was completed in May 2019. Clinically, her symptoms improved, and she had stable disease on imaging. She developed leukopenia during radiation therapy, which was attributed to medication side effects, so pazopanib was held in May and was resumed after completion of radiation therapy. A fluctuating thyroid-stimulating hormone level was observed and was attributed to drug-induced thyroiditis, with transient subclinical hyperthyroidism followed by hypothyroidism. This was treated with levothyroxine 75mcg.\nAfter a few months of treatment with pazopanib, she presented with acute shortness of breath and was diagnosed with spontaneous right-sided tension pneumothorax in October 2019, secondary to necrosis of metastatic lung lesions. This was possibly caused by pazopanib therapy, and therefore, pazopanib was stopped and pneumothorax was treated with chest tube placement followed by chemical pleurodesis for management of the hydrothorax that developed later. A few weeks later, she was readmitted to the hospital due to uncontrolled left upper extremity pain and acute shortness of breath secondary to a large recurrent left-sided pleural effusion, which was treated with a pleurx catheter. Dyspnea continued to worsen despite treatment. CT-thorax obtained at this time revealed widespread bilateral hemi-thoracic loculated malignant pleural effusion compressing most of the left lung and right lung base (Figure ). The remaining functional aerated lung included the right apex and a segment of left lung apex. Scattered lobular sarcomatous masses were noted on the CT scan, throughout the lower right lung base (Figure ). The malignant pericardial effusion was comparable to prior exams. Due to the poor prognosis and substantial clinical deterioration, the patient was transferred out of the intensive care unit (ICU) to pursue comfort measures. Unfortunately, our patient passed away a few days later due to respiratory failure secondary to malignant disease progression.
A 76-year-old man was admitted to the Department of Pulmonology due to dyspnea and respiratory distress. Chest radiography revealed infiltration in both lower lung fields, compatible with aspiration pneumonia. The patient was intubated and received antibiotics. He had been on a full feeding tube for five weeks after being diagnosed, with an infarction in the right middle cerebral artery territory. One day before readmission, he had aspirated vomit into his lungs. After two weeks of antibiotic treatment, he showed improvement on chest radiography. A fiberoptic endoscopic evaluation of swallowing (FEES) performed prior to discharge confirmed neurogenic dysphagia and showed aspiration in liquid form; otherwise, he showed tolerable swallowing of puree forms with a functional oral intake scale (FOIS) level of 2 [], which allowed only minimal bolus training during therapy, and he was mainly dependent on tube feeding. Otherwise, he showed no accumulation of saliva. He was discharged to a rehabilitation facility with instructions for swallowing training. A recording of his cough sound confirmed strong sounds and suggested that he could clear his secretions (, cough A).\nTwo days after discharge, he was readmitted because of cyanosis and dyspnea related to recurrent aspiration pneumonia. The patient had inadvertently ingested large amounts of liquid. Subsequently, a chest radiograph showed increased haziness in the right lung field relative to that on the previous image collected at discharge. Bronchoscopy was performed for toileting, and bacterial culture was conducted to direct targeted antibiotic therapy. At the point of aggravation, he could not clear his secretions, and a cough recording (cough B) demonstrated markedly weaker sounds than those present in the recording obtained days before his discharge.\nA follow-up FEES at this time showed increased collection of pulmonary secretion around the arytenoids, which the patient was unable to clear despite attempts. A strict nil per mouth status, with total dependency on tube feeding, was prescribed. The patient started to receive swallowing training along with respiratory physiotherapy to help improve his voluntary coughing.\nAfter 10 days of antibiotic therapy, his chest radiograph revealed improvement. In addition, a follow-up recording of his cough sounds (cough C) included more robust cough sounds. A subsequent FEES examination suggested improvement in both secretion management and swallowing, and he was able to commence oral bolus training. After a few weeks, his swallowing and cough levels improved to a level that allowed nasogastric tube removal and tolerance to an oral diet. Two months after discharge, the patient was fully ambulant, with no significant recurrence of aspiration events.
A 51-years-old Pakistani male, without any known medical co-morbidity, presented to the emergency department at our institution with a 1 day history of sudden-onset and severe abdominal pain along with abdominal distension. The pain had started after a long drive of 12 - 14 hours. It was initially localized to the right upper quadrant and right lumbar region but had evolved to a more generalized distribution over time. The pain was aggravated on movement and relieved by rest. There were no other associated symptoms. His past surgical history was significant for a repaired left sided inguinal hernia 10 years back.\nThe patient was in obvious anxiety and distress when first encountered in the emergency room. His vital signs were stable except for an increased pulse of 105 beats per minute. Examination of his respiratory system revealed vesicular breathing with decreased intensity of breath sounds in the right lung base as well as dullness on percussion on the right side of the chest. His abdomen was distended with generalized tenderness on palpation and minimal movement with respiration. No organomegaly was appreciated on the physical examination. His bowel sounds were sluggish.\nThe laboratory tests done at the time of admission are shown in table . The patient had mild anemia, mildly reduced hematocrit, leukocytosis with neutrophilia and hyponatremia. His serum amylase, lipase and random blood sugar levels were all within normal limits. His abdominal x-ray showed sub-optimal inspiration with minimal right sided pleural effusion. However, there were no signs of intestinal obstruction or pneumoperitoneum noted. Subsequently, computed tomography (CT) scan of the abdomen was done. Gallbladder margins were not very clearly identifiable; there was significant pericholecystic fat stranding with pericholecystic fluid. A circular high density focus in the proximity of gallbladder was identified which was thought to be representing a gallstone. Mild ascites was also present. These features were collectively suggestive f gallbladder perforation. (Figures and )\nThe patient's emergent management included nothing per oral status, regular vitals and input/output charting, insertion of nasogastric tube, administration of intravenous fluids, narcotic analgesics, proton pump inhibitors, metochlopramide, ceftriaxone, metronidazole, and ampicillin.\nThe patient was then taken to the operating room and a diagnostic laparoscopy was performed. It revealed free yellowish green fluid, most likely bilious, in the peritoneum. As the triangle of Calot could not be identified on laparoscopy, the procedure was converted to an open laparotomy. Intra-operative findings included presence of frank bile in the abdomen and a thick walled gall bladder. Dense adhesions of the gall bladder with surrounding structures were observed. A small perforation was visible near the neck of gall bladder in association with a large gall stone. The anatomy of the Calot's triangle was still obscure. A near-total or partial cholecystectomy including the perforated area was performed and a single large gall stone measuring around 2 × 1 cm was retrieved. The peritoneal cavity was washed with copious amounts of normal saline and a drain was placed. The rectus sheath was closed with loop polydioxanon (PDS) but the wound was kept open for healing by delayed primary closure.\nHistopathology of the specimen showed full thickness gallbladder wall lined by mucosa with focal ulceration. Rokitansky aschoff sinuses were also seen. A pathological diagnosis of acute on chronic cholecystitis was made.\nThe patient's hospital course was uneventful. His symptoms significantly improved and he was discharged from the hospital on the third post-operative day. He returned to the clinic after one week when his drain was removed and his wound closed.
A 51 year old man presented to the ED for the third time in 2 weeks with complaints of flank pain and hematuria. He had complained of left sided flank pain during the initial 2 visits. During the first visit, the patient was diagnosed to have renal colic. X-ray KUB did not show any renal stone. He was treated symptomatically with analgesia and discharged. During the second visit with complaints of persistent left flank pain despite taking analgesia given at discharge, he was admitted to the emergency observation ward for pain management. Bedside ultrasound done then was noted to have mild left sided hydronephrosis. He was pain free at the end of the observation and was then discharged with analgesia and an outpatient follow-up with the urology department. He was also scheduled to have an outpatient computed tomography scan of the kidneys, ureters, and bladder (CT KUB). However, 2 days before the scheduled CT, he represented to the ED with right sided flank pain since morning on the day of his visit. The pain radiated to the right groin and was associated with hematuria. He was not passing blood clots. He denied any other complaints of fever, weight loss, vomiting, diarrhea, or constipation. He had a past medical history of hypertension, diabetes mellitus, and hyperlipidemia. He had previous surgeries for appendicectomy and cholecystectomy.\nHis vital signs were stable. There was tenderness over the right flank on physical examination. There was also a palpable tender mass measuring about 5x5cm over the right lumbar region. There was no renal angel tenderness. Bedside ultrasound in the ED showed an appearance of a 6 cm cystic lesion around the inferior pole of the right kidney with internal echogenicity within the cyst. The provisional diagnosis was a bleeding renal cyst versus a tumor. Blood tests done in the ED showed a mildly elevated white cell count 12.64 × 10(9), hemoglobin of 14 gm/dL, and creatinine of 109 Umol/L.\nPatient was seen by the urology on-call in the ED and his bedside ultrasound done by the urologist revealed a 10 cms cystic lesion anterior to the lower pole of the right kidney with irregular internal echogenicity. Patient was admitted to urology department for further evaluation and management.\nInpatient CT Intravenous Pyelography (IVP) was done and the left kidney showed relative hypoenhancement and reduced excretion of contrast, associated with diffuse ureteric thickening and periureteric fat stranding which could be related to a passed left renal calculus or a differential diagnosis of ureteropyelonephritis which was less likely due to diffuse involvement of left kidney. There was a tubular cystic structure in the right flank with inferior tip at the same site of previously inflamed appendix stump base which could represent mucocele of the appendix stump ().\nPatient was then transferred under the care of the general surgery department, where he underwent a colonoscopy which demonstrated an extrinsic compression at the caecum and appendiceal orifice and a smooth pedunculated polyp measuring 10 mm in the sigmoid colon (). Exploratory laparotomy was done, the mucocele was resected, and patient recovered well. Histopathology revealed a benign mucinous cystadenoma. The patient was discharged well with an outpatient surgical follow-up.
A 29-year-old gravida 1 woman presented at 6 weeks and 2 days of gestational age for prenatal care. She had a history of liver toxicity that occurred in 2009 and again in 2014, which was thought to be related to drug-induced liver injury caused by oral contraceptive pills. At the time of her liver toxicity episodes, she had had an extensive infectious and autoimmune workup, which included testing for acute and chronic hepatitis A, hepatitis E, hepatitis B, hepatitis C, Epstein-Barr virus, cytomegalovirus, and human herpesvirus, all of which were negative. A liver biopsy was taken in 2014 which was consistent with possible drug-induced cholestasis. At the beginning of her pregnancy, she started having symptoms of pruritus, dark urine, and pale stool. She was followed by the hospital's monthly maternal critical care conference meetings from the beginning of her pregnancy because of her cholestasis diagnosis, elevated liver enzymes, and initial elevated TSBA levels of 215 μmol/L at 8 weeks and 3 days of gestation.\nShe was being followed by hepatology experts and was initially started on ursodeoxycholic acid (UDCA) 300 mg 3 times a day, which was subsequently increased to 600 mg 2 times a day in her first trimester. She reported mild improvement in her symptoms after she was started on ursodiol. Her liver enzymes, which had been in a mixed hepatocellular and cholestatic pattern, improved after starting the UDCA. An underlying genetic cause within the differential diagnosis was suspected as the culprit of her clinical presentation, especially because of the patient's previous recurrent cholestatic episodes before her pregnancy. The follow-up plan during her pregnancy included liver profile and bile acid monitoring every 2 to 4 weeks (Figures and ), weekly bilirubin checks (), serial growth ultrasounds every 4 weeks, nonstress tests twice weekly starting at 32 weeks of gestation, and ultimately delivery via induction of labor at 36 to 37 weeks and pending maternal and fetal status. Her growth ultrasounds were within normal limits with the last growth done at 32 weeks of gestation. Because of her increasing TSBA levels, the patient's UDCA dose was increased to 600 mg 3 times daily (15 mg/kg/day) (). The plan was then to schedule induction of labor at 36 weeks with administration of 2 doses of betamethasone before her scheduled induction. When she presented for her betamethasone, she had a reactive nonstress test and received her first dose of betamethasone followed by a second dose the next day.\nShe arrived at 36 weeks and 0 days for induction of labor. She reported having contractions and leakage of yellow-brown fluid, with decreased fetal movement. The patient's cervix was 4 cm dilated with no evidence of prelabor preterm rupture of the membrane. No fetal heart tones were noted, and fetal death was confirmed upon evaluation by 2 healthcare providers. The patient was induced at that time with oxytocin and vaginally delivered a male newborn a few hours after the start of her induction. The newborn had normal anatomy. The patient had fetal death laboratory workup that included assessment of Kleihauer-Betke fetal hemoglobin, complete blood count, thyroid-stimulating hormone, and lactate dehydrogenase levels, in which all were within the reference range, as well as testing for the presence of toxoplasmosis, parvovirus, and antiphospholipid syndrome, all of which were negative. Her liver enzymes remained elevated (). A karyotype was performed on the newborn and showed a normal male karyotype. The patient underwent genetic testing after delivery, and her result showed a heterozygous variant of ABCB11, which is one of several recessive alleles associated with BRIC.
The patient was a 36-year-old gravida 0 woman. At the age of 7, she underwent ventricular septal defect closure for the right ventricular outflow tract. At the age of 11, she received a mechanical aortic valve replacement. Since after the replacement, she has been receiving warfarin orally at a dosage of 4.5 mg/day. She conceived naturally and she was referred to our hospital for perinatal management. Oral administration of warfarin was discontinued at 5 weeks of gestation and she began self-injection of heparin. At 21 weeks and 5 days of gestation, she was admitted to our hospital with a high risk of spontaneous abortion and was put on intravenous ritodrine. This successfully prevented a miscarriage. At 21 weeks and 6 days of gestation, we started a continuous infusion of 25,000 units of heparin daily. On the 22nd week, transesophageal echocardiography showed a movable thrombus in the aortic valve. The size of the biggest thrombus was 26 × 8 mm (). We increased the dosage of heparin to 28,000 units daily and restarted the administration of warfarin. Following this, the thrombus reduced in size, and at 23 weeks and 5 days transesophageal echocardiography showed no signs of thrombosis in the patient. At 32 weeks and 2 days of gestation, a routine cardiotocography showed a decreased fetal heart rate; thus, an emergency Cesarean section was performed under general anesthesia because of the presence of warfarin in the blood. The baby was delivered, weighing 1,702 g, with an Apgar Score of l at l minute, and 4 at 5 minutes. The total amount of blood loss during the surgery was 1,410 ml. During the surgery, 16 units of fresh frozen plasma (FFP) was transfused; and after surgery, we continued to infuse 20,000 units of heparin daily. On the 11th day after surgery, owing to continuous genital bleeding, heparin administration was discontinued and uterine artery embolization was performed. This treatment stopped the bleeding and on the 21st postsurgical day; we started warfarin administration at 5 mg/day. She was discharged on the 34th postoperative day due to the stable PT-INR levels ().\nThe newly born infant was intubated and admitted to the newborn intensive care unit. At the time of admission, activated partial thromboplastin time was 180 seconds or more and bilateral intracerebral ventricular hemorrhage was detected using ultrasonography. On the first day of life, anemia was observed in the infant and red cell concentrate and FFP were transfused (). We attempted to reduce the infant's dependence on the ventilator and at 8 days of age the infant was extubated. On the postnatal 10th day, a cranial CT scan showed bilateral intraventricular hemorrhage with ventricular dilation and midline shift (). Although convulsions accompanying the intracranial hemorrhage were observed, the infant's general condition was stable and oral feeding was started on postnatal day 10. The newborn was discharged on postnatal day 54. However, the infant later developed cerebral palsy and is currently receiving treatment at our hospital.
A 57 year old man born in Egypt started chronic HD treatment in 2011 in Belgium for ESRD due to chronic pyelonephritis and kidney stones. The patient came to live in Belgium in 1997 but he often travelled to Egypt. The medical history included ischemic cardiomyopathy, type 2 diabetes mellitus, and urinary shistosomiasis. An arterio-venous graft was placed due to the irreversible occlusion of the fistulae, and the patient had undergone surgery for urethral stenosis. His home medication consisted of aspirin, bisoprolol, simvastatine, furosemide, oral antidiabetic medication and a phosphate-binder, whereas erythropoietin, iron substitution and vitamin B complex were administrated during HD sessions.\nBetween February 2012 and July 2015, the patient presented with several episodes of recurrent fever with myalgia after coming back from his journeys in Egypt. He had no diarrhea, nor any urinary symptoms or respiratory complaints, and reported no insect or dog bites. His physical examination was normal, but each episode of fever and myalgia was accompanied by high C-reactive protein (CRP) blood levels (Fig. ), while liver enzyme concentrations remained normal. At each episode, both the inflammatory syndrome and the clinical complaints decreased partially or completely within less than 1 month, as illustrated in Fig. , without any explanation or specific treatment. The patient was hospitalized at each episode for exhaustive infectious evaluations, and blood cultures were sampled at each HD session, as well as during chills and/or peaks of temperature. All bacteriological blood cultures remained negative, as well as viral serologies for HIV, hepatitis A, B and C. Chest radiography did not show any infiltrate, cavity or calcification, whereas a Computed Tomography (CT) scan demonstrated a pulmonary infiltrate in the left lower lobe, and a mediastinal adenopathy. Ultrasounds of the arterio-venous graft excluded a collection near the prosthetic material. Given the impaired immunity related to the ESRD, the frequent travels to Egypt and the past history of schistosomiasis, a recurrence of parasitic infection was suspected and the patient received an empirical treatment based on praziquantel, despite the absence of parasitological proof of Shistosomiasis. A second CT scan performed 3 months later confirmed the presence of a pulmonary infiltrate in the left lower lobe and demonstrated several mediastinal lymphadenopathies. A multitude of differential diagnoses were evoked, including infectious diseases (M. tuberculosis or atypical mycobacteria, herpes virus, histoplasmosis, toxoplasmosis, leishmaniosis, trypanosomiasis, filariasis, rickettsiosis), systemic diseases (sarcoidosis, systemic lupus erythematosus, dermatomyositis, Sjogren, Sharp, Castelman syndrome, histiocytosis, anthraco-silicosis) and neoplastic diseases (Hodgkin disease or other lymphoma, leukemia, metastasis of a solid cancer). Viral, parasitic and auto-immune serologies were all negative as were several searches for parasites in the feces. An endobronchial ultrasound-guided trans-bronchial needle aspiration (EBUS) of a mediastinal lymph node was performed, but provided no element in favor of any infectious or neoplastic disease, although sinus histiocytosis was demonstrated. To exclude M. tuberculosis infection, PCR and cultures were performed on broncho-alveolar lavage fluid and on the mediastinal lymph node aspiration, and they were negative. A TST was not performed because of its poor negative predictive value in HD patients [, ]. Instead, we performed two well-standardized home-made IGRA on peripheral blood mononuclear cells (PBMC) and compared the IFN-γ secretion induced by ESAT-6 with that induced by HBHA. The secretion of IFN-γ upon stimulation with purified protein derivative (PPD or tuberculin) was used as a positive control of mycobacterial infection [–]. In addition, staphylococcal enterotoxin B (SEB) was used as a positive control for T cell reactivity, while the negative control contained no added stimulant. These IGRA performed in October 2012 resulted in a very high level of IFN-γ secretion in response to ESAT-6 and a low level in response to HBHA (Table ). Combined with the clinical presentation, these results were highly suggestive of aTB, but this diagnosis was at that time not retained because of the negative microbiological results. In October 2012, after the same recurrent complaints, a 18F-fluorodeoxyglucose Positron Emission Tomography/Computed Tomography (18FDG PET-CT) was performed with the hope to identify a lesion accessible for biopsy. It only confirmed the existence of several FDG-active mediastinal lymphadenopathies accompanied by a small subpleural infiltrate in the left lower lobe. Several lymph nodes were removed by mediastinoscopy but Ziehl-Neelsen acid-fast stain was negative as were M. tuberculosis cultures and PCR.\nIn April 2013, fever and myalgia reappeared and a second PET-CT was performed, which demonstrated de novo FDG-positive pulmonary nodules, in addition to the preexisting and stable mediastinal lymphadenopathies. Thoracoscopic resection of an apical pulmonary nodule was performed, which showed several granulomas, a few of which with central non-caseating necrosis. However, due to persistent negativity of the M. tuberculosis cultures and PCR, the clinicians did not prescribe anti-TB treatment.\nIn July 2015, a new PET-CT was performed following a recurrent fever episode, and it highlighted now cervical, mediastinal, retroperitoneal and hepatic hilar FDG-active lymph nodes (Fig. ). The patient underwent a resection of a retro-clavicular lymphadenopathy for further search of M. tuberculosis, and the Ziehl-Neelsen acid-fast stain was positive. After 2 weeks, the culture was positive for M. tuberculosis, confirming the diagnosis of TBLA, and quadritherapy was started. Adherence and tolerability to the treatment were assessed twice weekly during the HD session. Since the patient did not have a family doctor, all the prescriptions were given at regular basis by the nephrologists. The treatment shifted after 2 weeks to a tritherapy (tebrazid, rifadine and myambutol) for 14 months, as isoniazid had to be stopped because of encephalopathy. The inflammatory syndrome disappeared completely under treatment (Fig. ), as well as the patient’s symptoms. The IGRA performed after 6 months of treatment indicated an increased IFN-γ response to HBHA and a decreased response to ESAT-6 compared to the first IGRA, suggesting a favorable response to treatment []. The patient gained 8 kg during his treatment and could successfully undergo kidney transplantation in February 2018. Three months after the transplantation, the IGRA results were doubtful in response to PPD, negative in response to HBHA, but still slightly positive in response to ESAT-6 (Table ). The patient was at that time under immunosuppressive treatment. However, since he nevertheless secreted measurable levels of IFN-γ secretion in response to SEB, we considered him as cured from the M. tuberculosis infection.
A 24-year-old male with HA was admitted to our department with pain in multiple joints on May 23, 2011. The patient had a medical history of hemophilia A since the age of 3 and was intermittently treated with factor VIII. During these years, he sequentially developed left knee, left elbow, left hip, and right knee joint pain and swelling with limited activity and was soon diagnosed as HA. Initially, the joint manifestations could be largely relieved by factor VIII replacement therapy. Factor VIII inhibitor screening remained negative. Later, factor replacement therapy failed to achieve satisfactory effects, so in 2002 and 2006, he received left elbow synovectomy and left total hip arthroplasty, separately. In the subsequent years, the patient still suffered from the recurrent episodes of left elbow and bilateral knee joints hemorrhage, pain, and swelling. In recent 2 years, the frequency of joint hemorrhage had increased to approximately 2 times a week and only slightly relieved after factor VIII replacement therapy. Currently, the activity of those joints was limited to various degrees. Other medical history involved 2 cerebral hemorrhages 18 and 15 years ago, separately.\nOn physical examination, significant tenderness was noted in the left elbow joint with limited pronation and decreased grip strength. The preoperative Mayo elbow performance score (MEPS)[ was 55 for the left elbow. Moreover, knee valgus (left 20° and right 15°) was noted, and hyperextension, hyperflexion, and positive grinding test results were noted in both knee joints with a swollen and warm right knee. The preoperative Hospital for Special Surgery (HSS) knee scores[ were 58 for the left knee and 65 for the right knee.\nBilateral knee joints and left elbow joint exhibit advanced arthropathy on radiographs (Figs. A and 2A). These joints present narrowing of joint space, erosions of the articular facets, and bone deformation to various degrees.\nOur diagnosis was hemophilia A and HA of the left elbow joint, both knee joints, and left hip joint. The patient received left elbow synovectomy and left total hip arthroplasty, but the condition continued to deteriorate over time with worsening of the left elbow and both knee joints. Taking all of these factors into account, surgical methods were our top priority, and simultaneous total multi-joint replacement was indicated. Due to the complicated joint lesions and medical conditions, our preparations for this arthroplasty were far more sufficient than usual. Given that arthroplasty for patients with hemophilia A, particularly the simultaneous replacement of multiple joints, is challenging, the patient and his family were informed in detail of the possible benefits and risks of the surgery. We performed a full musculoskeletal assessment and thorough medical evaluation beforehand. Blood products were prepared for possible bleeding events. Then, our team performed bilateral total knee arthroplasty (Zimmer NexGen) and left total elbow arthroplasty (Zimmer) under tightly regulated factor VIII replacement therapy. Antibiotic prophylaxis was administered 30 minutes prior to surgery, and an additional dose was administered once during the operation. Local hemorrhage was carefully controlled to prevent secondary joint damage. Approximately 1800 mL blood was lost during the entire surgery. The patient received 900 mL blood by autotransfusion and 4 units of red blood cells plus 800 mL fresh frozen plasma by intraoperative infusion. During surgery, we observed hemarthrosis and villous synovial hypertrophy at the joints, and severe erosion of the articular surface and various degrees of bone deformation were noted. These findings confirmed the preoperative diagnosis and preoperative assessments. After surgery, hemostasis management, such as compressive bandage, factor VIII infusion, and rigorous monitoring of coagulation indicators, was performed. An early rehabilitation program was applied to achieve improved regain of function.\nWe managed factor VIII replacement therapy during perioperative period under the guidance of hematologists. On the day of surgery, 3000 U/12 h (the body weight of this patient is 63 kg) factor VIII (ADVATE) was administered intravenously followed by 2000 U/12 h on postoperative days 1 to 3 (POD 1–3). Then, on POD 4 to 6, a dose of 1500 U/12 h was administered followed by 1000 U/12 h over the following 6 weeks. Factor VIII inhibitor remained negative in perioperative tests.\nAt the follow-up, the patient's joints functioned well. The MEPS of the left elbow was 85, and the HSS score of knee joints were 71 (left) and 81 (right). On radiographs (3 months and 5 years after operation), the arthropathy of bilateral knee joints and left elbow joint was significantly relieved (Figs. B,C and 2B,C).
The patient is a 61-year-old Korean male with a significant past medical history of rheumatoid arthritis, hypertension, and diabetes mellitus who presented to the hospital with sudden onset of blurry vision in his left eye three days prior. A head CT had been performed at an outside facility, which was negative for acute ischemia, hemorrhage, midline shift, or extra-axial fluid collection. The patient denied visual complaints in his right eye and had no history of similar events.\nOphthalmologic and Neurologic consultations initially revealed visual acuity was 20/40 on right eye; however, on the left eye, there was an apparent left-sided visual loss. Patient's intraocular pressure was normal in both eyes, pupils were equally round and reactive to light, and no afferent pupillary defect was observed. Moreover, the extraocular muscles were intact and with full range of motion. In the right eye, visual fields were full to finger count. In the left eye, the acuity in the nasal visual field was greater than that in the temporal visual field. In the nasal visual field, the patient was able to count fingers; however, in the temporal visual field, the patient could barely detect gross hand movement at one foot out. External examination was within normal limits, and pen light examination was only remarkable for nuclear sclerotic cataracts bilaterally. Dilated fundus examination demonstrated no evidence of pathology to the vitreous, optic nerve, or retina that might explain the vision loss. Four days later, repeat examination by Ophthalmology demonstrated a stable right eye; nonetheless, the left eye temporal visual field was 20/25 and patient was able to count fingers without mistake on left visual field. Pupil and retina examination were unchanged from previous examination. However, visual field mapping could not be done as this patient was seen in the inpatient setting.\nConsequently, an initial head MRI with and without contrast was performed, which showed focal areas of restricted diffusion in the right medial temporal lobe, inferior right basal ganglia with possible involvement of the right lateral geniculate nucleus. The head MRI did not show any other pathology such as masses or hemorrhages (Figure ). The subsequent head MR angiogram done demonstrated no focal occlusion or stenosis, and the MRI of the orbits showed no focal defects bilaterally. At this point, it was evident that the patient was suffering from a left temporal monocular hemianopia and that there must be a correlation with the subtle but definitely present right LGN ischemic lesion. An infarct affecting the right lateral geniculate nucleus would most likely cause bilateral left homonymous hemianopia. Nevertheless, a lesion at the vicinity of right LGN that had taken out the inputs going to layers 1, 4, and 6 became generally accepted among all physicians involved at this point in the care of this patient as the only possible explanation. Patient's left visual symptoms slowly started to improve, and after four days of hospitalization and monitoring, patient's left monocular temporal hemianopia had almost resolved and his vision had almost returned to his normal baseline.
A 34-year-old male presented as a trauma after he was assaulted with an ice pick. On presentation, he was an American Spinal Injury Association (ASIA) score C; the motor exam of the lower extremities demonstrated full strength in the right leg and weakness in the left leg; based on the MRC scale, the patient was 2/5 in the proximal and 3/5 in the distal muscle groups. His bowel and bladder function and sensation to light touch and pinprick remained intact. There was a small skin puncture site slightly asymmetric to the right in the lower thoracic spine that was identified as the entry point. A computed tomography (CT) scan demonstrated an 8 cm hyperdense foreign body, consistent with an ice pick fragment, entering the right T10 lamina with an upward and medial trajectory []. The foreign body then traversed the spinal canal and thoracic spinal cord, penetrated the T9 thoracic vertebral, entered the left chest cavity, and perforated the descending thoracic aorta [].\nGiven the patient’s neurologic status and concern for worsening vascular injury, a decision was made to take the patient to the operating room to repair the breach in the aorta and remove the retained ice pick. A multidisciplinary team consisting of neurosurgery, vascular surgery, and cardiothoracic surgery was formed, and the treatment plan consisted of endovascular repair of the aortic injury and removal of the ice pick from the aorta. The patient was positioned in a “lazy” left lateral decubitus position to allow access to the groins and the back. Although the foreign body was eccentric to the right, placing the position on the left would allow the cardiothoracic surgeons access to the aorta, in the event an endovascular solution was unsuccessful. Vascular surgery first gained bilateral access to the common femoral arteries under ultrasound guidance. A thoracic pigtail catheter was placed from the right side to image the descending thoracic aorta. A 12-French sheath was placed in the left common femoral artery in preparation for occlusion of the thoracic aorta with a Coda balloon if the patient became hemodynamically unstable. The aorta was measured and sized using the previous CT of the chest and a Cook TX2 28 × 80 mm graft was deemed appropriate for the repair of the aorta. First, an aortogram was performed via the pigtail catheter that showed no active extravasation of contrast from the entry site. The endograft was then advanced from the left side and positioned at T9. Once the endograft was in place, neurosurgery began exposing the foreign body. A paramedian incision that incorporated the entry site was made and the tract of the foreign body was followed to the spinous process of T10. A subperiosteal dissection was done and the foreign body was localized at its entry point in to the lamina medial to the spinous process. A circumferential exposure required drilling of the surrounding bone structures to optimize access to the foreign body. The distal end of the ice pick was then removed with a large thoracic sternal needle driver []. As the foreign body was removed, the vascular surgery team deployed the thoracic stent graft. A completion angiogram of the descending thoracic aorta was performed which showed no evidence of extravasation or endoleak.\nAfter securing the aortic injury, we examined the entry point of the ice pick. CSF was leaking posteriorly through the lamina with Valsalva maneuvers. A fat graft and fibrin sealant were placed over the defect. Special care was taken to minimize the dead space during the closure of the muscle and fascial layers. A lumbar drain was placed at the L4/L5 interspace with caution not to engage the level of the spinal cord injury with the catheter. A chest tube was placed by CT surgery to address the hemothorax; however, the chest tube was purposefully left closed for a few hours before the drainage was started to avoid creating an anterior CSF fistula. The patient was extubated on postoperative day 1, with improvement of his neurological examination (4/5 in all muscle groups of the left lower extremity). The lumbar drain was clamped 48 hours postoperatively and was removed after verifying that there was no leak from the incision site posteriorly. The patient had an uncomplicated hospital stay and was discharged on postoperative day 6 with a normal motor exam except for the left extensor hallucis longus and dorsiflexion at 5-/5.
A 30-year-old woman was admitted to our hospital to further evaluate her hepatic nodules. She had experienced dyspnea on exertion since the time of attending middle school. She had been diagnosed as having pulmonary hypertension and multiple liver nodules ten years earlier. She has been treated with diuretics, calcium channel blockers and sildenafil. She had experienced transient aggravation of her dyspnea one week before her recent delivery. Her platelet count was 99,000/mm3. Blood chemistry tests showed normal levels of transaminases, alkaline phosphatase and bilirubin. The serologic markers for hepatitis B and C virus were negative. Chest radiography () showed enlarged pulmonary arteries and cardiomegaly.\nUltrasonography showed numerous hyperechoic and isoechoic nodules of various sizes in the liver. On CT, the liver showed heterogeneous contrast enhancement due to the numerous nodules (). These nodules were heterogeneously hyperattenuating during hepatic arterial phase, and they showed contrast material washout during the portal venous phase. Persistent central scar-like enhancement was found in some of the nodules. The hepatic arteries were hypertrophied. The portal vein was not visualized; however, splenic varix and splenorenal shunt were present.\nThe hepatic nodules had high signal intensity with central portions of low signal intensity on the T1 weighted magnetic resonance images, and the hepatic nodules were of low signal intensity with central portions of high signal intensity on the T2 weighted images (). On the gadolinium enhanced dynamic MR scans, the central hypointense portions of the nodules were filled with contrast media for a length of time and they showed persistent intense enhancement (). On the gradient echo sequence images obtained after superparamagnetic iron oxide enhancement, the nodules showed a drop in signal intensity except at their central portions ().\nThe patient underwent percutaneous ultrasound-guided needle biopsy. The biopsied tissue core demonstrated a dense fibrous septum containing numerous vascular structures at low power (). Higher power magnification of the portal tracts revealed thick-walled vessels, and some had eccentric thickening. The surrounding hepatic parenchyma had slightly increased cellularity, with increased liver cell plate thickness. These findings were consistent with FNH.\nAdditional abdominal angiographies were obtained during the diagnostic cardiography to evaluate her cardiac function. Hepatic arteriography showed numerous stained nodules in the liver with hypertrophied hepatic arteries. The delayed phase of the superior mesenteric arteriography showed the absence of the main portal vein flow, and the portosystemic collaterals drained into the inferior vena cava ().
A 39-year-old female with no medical history presented to a referring hospital with complaints of worsening dyspnea. Chest computed tomography (CT) revealed a large tumor primarily in the middle mediastinum invading the tracheal carina (Fig ). Furthermore, the left main bronchus and right main pulmonary artery showed severe stenosis from the tumor, restricting pulmonary blood flow to the right lung (Fig ). Due to persistent hypoxemia, the patient was intubated and transferred to the ICU of our hospital (day 1). Upon arrival, the patient's condition continued to deteriorate because of the obstructing malignancy. Since high-pressure ventilation did not improve the patient's respiratory condition, a decision was made to initiate veno-venous ECMO. Under ECMO support, the patient safely underwent bronchoscopic examination. The tumor was observed to be mainly on the tracheal carina, completely occluding the left main bronchus (Fig ). The patient underwent interventional therapy through flexible bronchoscopy using an endoscopic electrocautery device to cut down the tumor (Fig ). The stenosis was temporarily relieved after bronchial intervention but the left main bronchus was easily reoccluded due to necrotic tumor tissue. Therefore, stent implantation was deemed necessary to maintain bronchial patency. This procedure was performed on day 11 under general anesthesia via rigid bronchoscopy. The left main bronchus was dilated with a balloon catheter and the trimmed silicon Y-stent was then inserted (Fig ). After stent implantation, the patient was successfully weaned off ECMO on day 12 and extubated on day 14. The tumor was histologically diagnosed as poorly differentiated adenocarcinoma (Fig ). Immunohistochemical staining revealed that tumor cells were positive for thyroid transcription factor-1 and diffusely positive for ALK (Fig ). Moreover, ALK gene rearrangement was detected by fluorescence in situ hybridization analysis. The patient received a tyrosine kinase inhibitor (TKI), alectinib, via nasogastric tube from day 16, recovered well and was discharged from the ICU without any adverse events related to the targeted therapy. Six months later, a chest CT scan showed a marked reduction of the tumor (Fig ). Since the stent had migrated proximally causing slight dyspnea, it was removed under rigid bronchoscopy. The patient remains alive a year after diagnosis without any respiratory symptoms and alectinib treatment is continuing.
A 52-year-old male was admitted to the outpatient clinic of the department of internal medicine with the complaints of progressively increasing dyspnea and swelling of the body during the last three months. The patient had variceal enlargements of the veins from the time of birth and his left leg was thicker than the right one, but he did not have a certain diagnosis. The family history was negative. The pathological findings on physical examination at the time of diagnosis were diffuse edema in the body, decreased lung sounds at the right basal site, increased diameter and decreased length of the left leg compared with the right one, diffuse variceal enlargements, and a few hemangiomatosis lesions on the left leg (). The pathological laboratory findings were as follows: serum albumin: 2.2 g/dL, total cholesterol: 216 mg/dL, LDL cholesterol: 152 mg/dL, creatinine: 1.23 mg/dL, and proteinuria: 7.6 g/day. Urine sediment was inactive. The abdominal ultrasonography revealed a cystic lesion of 7 × 4.5 cm diameters in the liver with thin septations and dense content in some areas; splenomegaly (133 mm), a solid lesion resembling hemangioma measured 3 × 2.5 cm at the lower pole of the spleen; and multiple anechoic cysts measured at most 2 cm at the upper pole of the spleen. The sizes of the kidneys were normal, while the echogenicity was increased. There were one cortical cyst (2.5 cm) in the upper pole of the right kidney and two cysts (the bigger one measured 6 cm in diameter) in the upper pole of the left kidney. Dynamic magnetic resonance imaging of the abdomen with intravenous contrast material showed a cystic lesion measured 53 × 47 mm with peripheral capsular contrast involvement in the segment 4a-7 of the liver and nodular lesions consistent with hemangiomas in segments 7-8 and 4A of the liver. There were also splenomegaly (136 mm), heterogeneity of the splenic parenchyma, and multiple lesions resembling hemangiomas measuring 25 mm at most in the spleen. There were simple cortical cysts in the kidneys, one in the upper pole of the right kidney (27 mm) and two in the upper pole of the left kidney (the bigger one measuring 6 mm). The radiologists reported bilateral pleural effusion reaching 15 mm of thickness on the right side and AV malformation on the left posterolateral thigh that fills the mesorectum and hypertrophy of the soft tissues of the proximal left lower extremity.\nHe was diagnosed to have KTWS putting together the hemihypertrophy, diffuse variceal enlargements of the veins, and AV malformations detected radiologically. Gastroscopic examination was normal, while colonoscopy revealed diffuse blue-purple variceal enlargements on the rectal mucosa (hemangioma) and a polyp in the rectum with a diameter of 1 cm. The rectal mucosa was bluish purple from the 10th cm to 20th cm (hemangioma) ().\nHe was transferred to the nephrology clinic for evaluation of the cause of nephrotic syndrome. Paleness of the temporal regions and increased deepness of the optic hollow were detected at eye examination. Hepatitis serology, antineutrophil cytoplasmic antibody, and antinuclear antibody were negative. Complement levels were within normal limits. Renal biopsy was performed to determine the cause of nephrotic syndrome. Of the 13 glomeruli detected, five were globally sclerotic while another five had segmental sclerosis. There was prominent mesangial enlargement in other glomeruli together with patchy atrophy of tubuli, interstitial fibrosis, mild mononuclear cellular infiltration, and thickened arteriolar walls (). No accumulation was detected with examination by immune fluorescence techniques. Electron microscopic examination was not available. With these findings, he was diagnosed as focal segmental sclerosis (FSGS). He was started on oral methylprednisolone at the dosage of 1 mg/kg and began to be followed up in the nephrology outpatient clinic. It was learned that he was admitted to the emergency clinic of another hospital due to profuse rectal bleeding at the end of the third week of steroid treatment. The steroid treatment was terminated at that time. Proteinuria was measured as 5.2 g/day and serum creatinine was 2.1 mg/dL. He is still under follow-up with conservative treatment.
A 34-year-old Caucasian male with past medical history notable for intravenous drug abuse was admitted to the general medicine service with chief complaint of rash, pain, and edema in his heels for the past 1 to 2 days concerning for cellulitis. The patient reported he had been unable to find veins in his upper extremities, and so had been injecting buprenorphine into his posterior tibial veins. The rash had started on his left heel and shortly thereafter appeared on his right heel in a symmetric distribution. The exam on admission was notable for a slightly purpuric mottled erythema that blanched with residual petechiae on his heels and plantar arches. The patient had a history 1 month prior of gangrenous infection of the penis that grew methicillin-resistant Staphylococcus aureus following similar injection into the dorsal vein of his penis. He was therefore started on empiric clindamycin. The rash continued to evolve with increased pain and swelling, with the development of a reticular, nonblanching border (). The patient had remained afebrile, with no leukocytosis, no increased warmth of the eruption, and negative blood cultures. At this time, it was felt this was not a cellulitis, but rather livedoid dermatitis secondary to injection of buprenorphine due to the clinical appearance and history. Labs drawn during the patient’s previous admission 1 month prior were negative for coagulopathy or vasculitis, including HIV, hepatitis B and C serologies, as were repeat viral serologies. A full vasculitis workup was not repeated during this admission. On hospital day 3 there was further increased erythema, edema, and pain with concern for impending ulceration. One hypothesis for the underlying mechanism of livedoid dermatitis is local vasospasm. Because of its utility in treating Raynaud’s phenomenon, which is also thought to be caused by local vasospasm, a trial of nifedipine was started. The patient’s clinical presentation slowly improved over the following 2 days and was discharged home with follow-up appointments made with psychiatry and his primary care physician. Despite these efforts, he has been lost to follow-up.
A 46-year-old female was referred to the Department of Dentistry and Oral Surgery of Hakujikai Memorial General Hospital for clinical examination of the left maxilla with spontaneous pain. The patient had sustained an injury to the lower face 12 days earlier. She promptly consulted a neighboring emergency hospital because of laceration of the lower lip and gingiva of the maxilla. Thereafter, she was treated with suture of the lower lip under local anesthesia by a general surgeon and was instructed to put pressure on the bleeding gingiva with gauze. In addition, she lost the left maxillary lateral incisor and canine due to trauma. She could confirm the existence of one of the teeth, but the existence of the other tooth was unclear. No treatment or examination was provided for the missing teeth. She received prescriptions for antibiotics and analgesics and returned home. The bleeding easily stopped afterwards. However, because of swelling and pain of the left maxilla, the patient consulted our hospital.\nHer chief complaint at the time of the first medical examination was swelling and oppressive pain of the left maxilla (). Intraoral view confirmed swelling of the oral vestibule mucosa in the first premolar region (). Panoramic radiography showed a horizontal embedded canine (). CT scan showed fracture of the alveolar bone in parts of the lateral incisor and canine (). Based on these findings, replantation of the canine was not an option. Furthermore, CT scan showed that the canine was embedded in the vestibule soft tissue (). We decided to perform surgical excision of the embedded canine under local anesthesia (3.6 cc lidocaine in 2% solution with 1 : 80,000 adrenaline) together with intravenous sedation with midazolam (3 mg/body). An incision was then made in the lacerated gingiva, and the embedded canine was removed surgically. Fibrous tissue and fragments of alveolar bone surrounding the embedded canine were also curetted (Figures and ). The incision was sutured with 4.0 silk suture threads. Systemic antibiotic (1 g flomoxef sodium, twice a day for three days) was intravenously administered to the patient. Analgesic (tramadol hydrochloride/acetaminophen, 2 tablets for pain) was also prescribed to the patient. The wound healed favorably and sutures were removed on the seventh postoperative day, and the patient was discharged from the hospital.
A 67-year-old female patient with a locally advanced distal rectal adenocarcinoma (cT3N+) underwent laparoscopic abdominoperineal resection after short-term radiotherapy. A vaginal resection or repair was not required for the patient as she did not have any intraoperative problems. The patient with the pathology test result of pT2N0 received adjuvant chemotherapy. No complication was observed in the third and sixth month controls; however, the perineal hernia was detected at the ninth month. The abdominal computed tomography (CT) imaging taken without valsalva maneuver revealed no pathological findings except perineal hernia (). The patient was, then, scheduled for follow-up, since she had no complaints. However, surgery was decided for the perineal hernia in the first postoperative year upon the growth of hernia and the restriction of daily activities due to the hernia.\nThe patient was placed on a Jackknife position. The perineal defect was revealed by dissecting the hernia vesicle through posterior approach. After the hernia content was reduced into the abdomen, the double-sided synthetic patch was placed over the defect and fixed to the levator ani muscle laterally, the vagina anteriorly, and the coccyx posteriorly with the 2/0 polyprolene sutures. The patient was discharged without any complication.\nThe patient had no complaints related to the perineal hernia during the follow-up using CT imaging (). The patient who was followed in the oncology clinic without problem was admitted to the emergency department with the complaint of prolapsed intestines from the vagina 12 months after the repair of the perineal hernia. During the examination, the small intestines were observed to be freely prolapsed from the vagina and several local ischemic changes were detected (). In the emergency laparotomy, the terminal ileum revealed a herniation out of the posterior vaginal wall of the 110 cm ileum segment from the 10th cm of caecum. The ischemic areas were observed to be developed locally in the ileum. Following the withdrawal of the small intestine into the abdomen, a functional side-by-side ileocolic anastomosis was performed by resecting the ischemic segment with the caecum. The formerly placed mesh material was explored and seen as intact (no folding or detachment) and well placed below the levator ani muscle. As the formerly placed mesh material was located below levator ani muscle level, it was not covering the posterior vaginal wall. Instead, the previous mesh was only anchored to vagina anteriorly below the levator level. The vaginal defect was reconstructed with interrupted sutures by using the 3/0 polydioxanone (). A new double-sided mesh material with antiadhesion barrier site facing the viscera was placed over the pelvic brim and fixed to the pubic bone anteriorly, the sacral promontory posteriorly, and the pelvic wall laterally by using the 2/0 polypropylene sutures. The patient was uneventfully discharged on the postoperative day 4; the wound sites were observed to be healed at three months, and no herniation finding was observed.
A 48-year-old female patient visited the hospital due to a left hip pain, radiating to the lower extremity with a hip snapping sensation for 2 months, especially on walking. There was no symptom on the right side. She was able to walk independently and bear weight on the affected side, but complained of more pain on the weight bearing status. She had no history of lower extremity trauma or surgery except hypertension due to primary aldosteronoma. In physical examination, a range of motion of the hip internal and external rotation was decreased slightly without pain. She had strong palpable deep peroneal artery and audible digital artery flow bilaterally. There was no motor weakness, but there was a sensory change on the lateral aspect of the leg and dorsum of foot, compatible with the L5 dermatomal area. She had normal deep tendon reflex bilaterally on knee jerk and ankle jerk. Babinski sign and ankle clonus were absent. Straight leg raising test was decreased to 30 degrees only on the left side. Lasegue test and Patrick sign were positive on the left side, but negative on the right side.\nWe requested radiographs and MRI of the lumbar spine for further evaluation. MRI of the spine showed no abnormality except diffuse and mild bulging disc without cord compression at the lumbosacral area. The radiographs of pelvis in anteroposterior and frog lateral projection showed no abnormal finding. Electrophysiologic study showed normal findings. There were no abnormal results compatible to the lumbosacral radiculopathy or spinal stenosis. At last, MRI of the hip was performed. Hip MRI revealed bilaterally increased signal intensity of the quadratus femoris muscle with concurrent narrowing of the ischiofemoral space. On axial T2-weighted fat-suppressed magnetic resonance images (), there were diffuse edema and increased signal intensity within the quadratus femoris muscle bilaterally. The distance of ischiofemoral space was 12.96 mm on the right side and 10.24 mm on the left side. The distance of quadratus femoris space was 6.17 mm on the right side and 4.31 mm on the left side (). There were no abnormal findings, such as degenerative arthritis, femoroacetabular impingement, or osteonecrosis, as possible causes of other hip pain origins. It was compatible with ischiofemoral impingement syndrome bilaterally. She complained the hip pain only on the left side, not the right side.\nAfter being diagnosed with the ischiofemoral impingement syndrome, the patient was hospitalized for a treatment over four weeks. Nonsteroidal anti-inflammatory drugs and gabapentin were prescribed for pain relief. Hot pack, ultrasound, and interferential current therapies were applied around the hip area. She received an exercise program for stretching of the hip muscle and connective tissues. The exercise program was targeted to the quadriceps femoris, piriformis, and other hip muscles, in order to adequately reduce pain and increase the range of motion in the hip joint. After discharge, the patient maintained the drug regimen and exercise program. The initial visual analogue scale (VAS) was 7 to 8. After six weeks of treatment, pain of the left hip was decreased gradually to VAS 2 to 3. The range of motion in the hip joint was normalized, and the hip snapping sensation was resolved.
Presenting concerns This is a case of a 22-year-old white female who presented at 34 weeks with preterm premature rupture of membranes. She had a history of two prior cesarean deliveries. A left ovarian tumor, not noted during the course of her current pregnancy, was noted on cesarean delivery. Current pregnancy When she presented with preterm premature rupture of membranes, repeat cesarean section was performed again. At the time of surgery, another 8 cm mass on her left ovary was diagnosed intraoperatively. This mass was not diagnosed prior to surgery. A second trimester ultrasound was performed that did not show any ovarian cyst. During the surgery, the mass appeared tan with punctate focal hemorrhage. The mass was unable to be separated from her left fallopian tube, so the mass, the left fallopian tube and part of the left ovary were all removed. We were able to leave a small amount of residual ovarian tissue. Pathologic description noted a multiloculated and cystic mass with clear mucinous fluid consistent with mature cystic teratoma (Figure ). Her postoperative course was uncomplicated. Previous pregnancy Her antecedent pregnancy was complicated by right ovarian torsion at 13 weeks secondary to an ovarian tumor. A right salpingo-oophorectomy was performed. The right ovary was sent to pathology and noted to be infarcted with no viable tissue from the mass to make a definitive diagnosis (Figure ). During that same surgery, an 8 cm, irregularly shaped mass with a focally hemorrhagic surface was noted on the left ovary. A left ovarian cystectomy was performed, and final pathology showed a benign mucinous cystadenoma (Figure ). At the time of cesarean in the same pregnancy, a metachronous mucinous cystadenoma was noted on her left ovary; cystectomy and partial left oophorectomy were performed. Follow-up and outcomes Following her third cesarean delivery, this patient was surprised to learn that she had developed another ovarian cyst in pregnancy necessitating removal. She was concerned about the function of
The patient was a 34-year-old woman, G4 L2 Ab1 who had married her cousin 7 years ago. She had a history of two normal vaginal deliveries and one abortion in the 1st trimester. The first pregnancy in the age of 28 had terminated with a normal vaginal delivery (NVD) resulting in a term baby girl who weighed 3150 gr. The second pregnancy had occurred two years later; curettage was done at week 6 due to spontaneous abortion. Her 3rd pregnancy was in the age 32 resulting in a healthy term baby girl weighing 3400gr with NVD. Due to her unwillingness for becoming pregnant she had withdrawal contraception, whereas because of the non-occurrence of menstruation during breastfeeding and 6 months after her last pregnancy, a pregnancy test was requested. Due to the positive pregnancy result, ultrasound study was done which revealed a 10-week spontaneous gestation with 4 gestational sacs and 4 fetuses. There was no case of multiple pregnancies in her or her husband's family.\nShe received prenatal care during her pregnancy but there was no need for prophylactic cerclage. At week 24 of gestation she was hospitalized due to premature contractions. The contractions were controlled with the prescription of pethidine and hydration and she was discharged 3 days later. She was once again admitted at 28 weeks of gestation due to similar contractions; this time she was treated with indomethacin and pethidine and discharged 3 days after the contractions suppression. She also received two doses of betamethasone during hospitalization.\nShe was admitted a week later due to labour contractions. In vaginal examination 2 finger dilatation with no effacement was detected. Serum test results were reported all in the normal range and the vital signs during hospitalization were normal. At this stage she was treated with tocolytics (adalat). The fetuses' health was monitored by Doppler ultrasound imaging, biophysical profile and fetal non stress test (NST). After the labour contractions' suppression and due to the presence of sporadic contractions she was monitored while being hospitalized up to the time of delivery.\nAt 32 weeks and 4 days of gestation, due to the resumption of labour contractions and dilatation progression, after receiving the rescue dose of betamethasone, cesarean section and tubectomy (upon the request of the patient and her husband) was performed. The outcome of cesarean section was 4 fetuses, 3 girls and a boy, quadriamniotic and quadrichorionic. Quadruplet A weighed 1820 gram with an Apgar score of 9 to 10; quadruplet B weighed 1810 gram with an Apgar score of 6-7. Quadruplets C and D weighed 2100 and 1980 gram with an Apgar score of 7-8 and 9-10, respectively. Among the 4 neonates, only quadruplet B was transferred to the NICU; she was discharged after 2 days in good health. and show the quadruplets after birth.\nBecause of atonic uterus during the cesarean section, after the administration of the appropriate dosage of oxytocin and methylergonovine and 800µgr of rectal misoprostol, the uterine arteries were blocked and the B-Lynch suture was done. No blood transfusion was required for the mother and her hemoglobin (Hb) level 6 hours after the operation was 9 g/dl; her pre-operational Hb level was 10g/dl. The mother was discharged 3 days after delivery with no complications.\nFor close follow up, the mother and her newborns were visited two weeks after delivery; they were all healthy and had no problem. The infants were visited once again 6 months later revealing normal physical and mental development in all four. shows the babies at 6 months of age.\nThis project has been approved by Ethical Committee and Vice Chancellor for Research of Mashhad University of Medical Sciences (97/429008).
An 84-year-old female was independent one year ago without past medical history. Two months before admission, the patient had developed a short memory span and difficulties walking. About two weeks before admission, she developed visual hallucination, complaining repeatedly that she could see a thief entering her house every day at midnight. In contrast, the patient spent her daytime calmly and never complained of such sightings. Her family doctor clinically diagnosed her with probable DLB with fluctuating cognition, recurrent visual hallucinations and spontaneous motor parkinsonism. She received 5 mg per day of donepezil around the same time. About one week before admission, her psychiatric symptoms deteriorated and she started calling the police almost every night. She was admitted to our psychiatric ward due to worsening of visual hallucination and insomnia.\nAfter admission, she continued to complain repeatedly of seeing a thief entering her room in addition to dizziness and sweat deregulation, which were thought to be DLB-related autonomic dysfunctions. Single-photon emission tomography (SPECT) scan detected a significant decrease in cerebral blood flow in the occipital area and this finding supported the diagnosis of DLB. We prescribed 4 mg of the antipsychotic perospirone with a relatively short half-life in order to manage her psychiatric symptoms, paying close attention to hypersensitivity for antipsychotics. However, the symptoms did not get better and her insomnia persisted. On day 20 after admission, she suddenly developed a loss of consciousness while sitting, which triggered us to perform an electrocardiogram (ECG) examination (Figure ).\nThe findings revealed severe bradycardia, prompting us to consult cardiologists. Subsequently, the patient was immediately subjected to Holter monitoring in order to detect the origins of syncope. The findings disclosed the cardiac arrest of approximately 7 seconds, and the patient was diagnosed with sick sinus syndrome. Finally, she was transferred to the cardiac ward and had pacemaker implantation. After she was transferred again to our psychiatric ward on day 29 after admission, dizziness and loss of consciousness perfectly disappeared. However, visual hallucination, insomnia, and sweat deregulation persisted. Thus, we again prescribed 4 mg of perospirone, not donepezil. From day 50 onwards after admission, her visual hallucinations and insomnia gradually decreased and she spent her time more calmly without any side effects of antipsychotics.
A 37-year-old woman was admitted to our hospital for the treatment of a tracheoesophageal fistula. Medical history revealed that she had epilepsy and took anticonvulsant medication continuously from the age of 10 years. When the patient was 29 years old, she had an epileptic seizure when a fire occurred, and she suffered from smoke inhalation. Chronic coughing and breathing difficulties appeared a few months after the fire. The symptoms gradually worsened, and hospital consultation was obtained two years afterward. As a result of a thorough examination, she was diagnosed as having breathing difficulty due to tracheal strangulation. A noncovered, metallic Ultraflex Tracheobronchial Stent (Boston Scientific Corporation, Natick, MA) was inserted approximately 2 years after the fire. Since there was no evidence of congenital disease, the cause of tracheal stenosis was attributed to smoke inhalation based on her history. Although her condition improved after stent insertion, repeated bronchoscopic medical treatment was carried out for modification of the stent and granulation formation.\nOne year after stent insertion, the patient experienced postprandial obstruction. Since the airway narrowing had worsened, she returned to the hospital. An attempt was made to remove the stent completely. However, it was possible to extract only part of the stent due to adhesion of the stent and the trachea. The stent had been inserted in the trachea on the proximal side while the tracheotomy was performed. Subsequently, food was discharged from the tracheotomy, and a tracheoesophageal fistula was diagnosed. For this reason, nutrition was provided primarily via the gastrostoma.\nWhen the patient was 37 years old, she was admitted to our hospital for a procedure to remove the stent and close the tracheoesophageal fistula. Computed tomographic (CT) scans showed strangulation of the stent on the proximal side from the tracheotomy. The part of the stent distal from the tracheotomy was not a circular form. The deepest part of the stent was inferior to the left innominate vein (). Based on the reconstruction picture of the CT, the stent was fractured, and one section was positioned posteriorly and to the left of the trachea ().\nEsophagoscopy revealed the following: stenosis in the cervical esophagus, granulation in the distal side, and the tracheal tube in the distal side (). When the tracheal tube was removed, bronchoscopy revealed the covered stent. Granulation was present directly under the tracheal hole, and food emerged from the side of the granulation. Abnormalities did not extend to the peripheral trachea from the stent (). When esophagography was performed, leakage into the trachea was apparent.\nWe diagnosed it as a tracheoesophageal fistula due to the fact that the damaged tracheal stent collapsed to the esophageal side, and we decided to operate. The patient was intubated from the tracheotomy and underwent right thoracotomy at the fifth intercostal space. We planned to observe the length of the damaged trachea through the intercostal thoracotomy incision. The operation was due to be stopped when the remaining trachea was shortened. The thickening of pleural membranes and adhesions were observed in the upper mediastinum. First, the upper esophagus was peeled away from the trachea. Adhesions were intense, so that they went to the proximal side. We could peel the esophagus only to the lower end of the stent but no further. At this point, we judged that the respiratory tract reconstruction would require an anterior mediastinal tracheostomy [].\nA U-shaped incision was made just above the isthmus of the thyroid, and a vertical midline incision was made from the bottom of the U incision to the level of the third rib. The sternocleidomastoid muscles were divided at their origins. The pectoralis muscles were reflected off the chest wall bilaterally to expose the ribs and their costal cartilage. With a sternal saw, the anterior thoracic breastplate was resected, including the medial third of the clavicles, the medial segments of the first and second costal cartilages, and the upper third of the sternum to the upper edge of the third rib. The ample removal of the anterior thoracic wall allowed excellent exposure of the thoracic inlet and access to the cervicothoracic esophagus. The trachea was divided gently from the esophagus, and the trachea and the damaged stent were extracted (). The length of the distal trachea was 5 cm. The damaged esophageal wall was sutured by about 1/2 rounds layer to layer. The trachea was transposed inferiorly and between the superior vena cava and aortic arch. The end of the trachea was sutured to the skin overlying the resected sternum (). The patient's postoperative progress has been good, and her hospital stay lasted for 45 days after the operation. After leaving the hospital, the patient was seen in follow-up at 6 months after discharge, and she has been able to take meals sufficiently.
A 69-year-old male patient, with a three months history of abdominal pain asthenia and macroscopic hematuria, was admitted to the outpatient clinic. Abdominal CT revealed an 8 cm left renal growth suggestive of neoplasia, with the involvement of the tail of the pancreas, tumor thrombus in the left renal vein and multiple left para-aortic adenopathies (). A biopsy was performed and showed to be inconclusive regarding the possibility of renal cell carcinoma. Radical left nephrectomy with distal pancreatectomy and splenectomy was proposed.\nThe procedure (Video 1 in Supplementary data) started with an extensive Cattel-Braasch Maneuver, allowing exposure of the inferior vena cava and the aorta, and thus isolation of the left renal vessels. The tail of the pancreas and spleen were freed, and a no-touch approach [] was adopted to minimize the spread of tumor cells with proximal splenic vein ligation. Caudal splenopancreatectomy was performed with section of the pancreas with a GIA 80 (vascular load), followed by proximal ligation and section of the splenic artery and what was thought to be the left renal artery (). The junction of the left renal vein with the vena cava was opened, and the tumor thrombus was resected, followed by caval suture. The renal vessels were, at this point, presumably controlled. The nephrectomy was continued with the release of the kidney and para-aortic lymphadenectomy, during which only the stump of the left renal vein could be identified, lacking the previously ligated renal artery stump. The renal artery was located inside the mass of lymph node tissue in the left para-aortic space, and the stump belonged to the superior mesenteric artery, ligated flush with the aorta. There was no arterial pulse in the mesentery confirming the injury. After removing the specimen, the distal stump of the superior mesenteric artery was exposed, and a repair with a terminoterminal anastomosis was performed from the proximal stump of the splenic artery (). The viability of the gut was assessed by palpation of an arterial pulse in the superior mesenteric artery.\nThe postoperative period went uneventfully. Histological examination showed a renal sarcomatoid carcinoma pT4N1M0G3. Control imaging at three months showed permeability of the celiac trunk and the superior mesenteric artery ().
Case A, a 36-year-old man whose initial cause of end stage renal disease was Hemolytic uremic syndrome. His history is significant for receiving a deceased donor kidney transplant in 1991. In 1992 he underwent bilateral native nephrectomy and in 2007 a transplant nephrectomy was performed for chronic allograft nephropathy. Significant comorbidities include infection with hepatitis C virus (grade 1, stage 0).\nHe received zero mismatch, cross match negative, a standard criteria deceased donor kidney transplant after 21 hours of cold preservation. Induction immunosuppression included antithymocyte globulin (rabbit, 1.5 mg/kg) and glucocorticoids. The kidney was implanted into a left lower quadrant retroperitoneal pocket. Due to a short donor ureter an ureteroureterostomy with internal stent provided drainage. After reperfusion the transplanted kidney was pink with firm turgor.\nOn posttransplant (PT) day 1 there was scant urine output and the patient required hemodialysis. Urine output increased until postoperative day 4 when a decrease in urine output was associated with pain over the left lower quadrant and left groin. On PT 8, ultrasound was obtained due to a rising creatinine, which showed a migrated ureteral stent with hydronephrosis and he underwent cystoscopy with ureteral stent removal. Ultrasound on PT 9 showed persistent hydronephrosis and a nephrostomy tube was placed on PT 10. Nephrostogram on PT 11 showed the nephrostomy tube in proper position, but obstruction of the kidney. He had a persistent leukocytosis and fevers, but blood and urine cultures were negative for growth of aerobes and anaerobes. Due to concerns for rejection, he underwent allograft biopsy which showed mucormycosis and necrosis (). He underwent an emergent total transplant nephrectomy including the ureter on PT 11 and was started on a course of amphotericin B. Histology of the explanted graft showed invasive mucormycosis of the transplanted kidney parenchyma and both donor and recipient ureter with an invasion pattern advancing from the luminal surface. There was no invasion of the graft renal vein or artery (). This was suggestive of the recipient's urinary tract as the primary source for the mucormycosis. Rhizomucor was isolated from the specimen (speciation not identified).\nCystoscopy done 4 days after nephrectomy showed normal appearing bladder with no evidence of necrosis. Due to the known predilection for pulmonary and rhinocerebral manifestations of mucormycosis, CT imaging of the lungs, sinuses, and brain were done which showed no evidence of mucormycosis. The patient was discharged home on PT 21.\nReturn to clinic on postnephrectomy day 25 revealed drainage from the incision. The patient underwent surgical debridement and wound exploration. Pathology showed no evidence of cutaneous mucormycosis in the wound. The organ procurement organization was promptly notified of this case of renal mucormycosis at the time of initial discovery. Neither the recipient of the partner kidney graft nor liver graft has demonstrated any evidence of mucormycosis.
A 15-year-old female patient reported to the Department of Oral Medicine and Radiology with the chief complaint of fractured and discolored tooth in the upper front teeth region of the jaw for 8 years []. The patient revealed no contributory medical and dental history but reported a minor trauma to the upper jaw 8 years back. The patient never had any symptoms related to the region. Previously, she had visited a private dental practitioner with the same complaint. She was advised extraction of the tooth, followed by implant placement for which the patient had undergone cone-beam computed tomography (CBCT) scanning of the maxillary anterior region (5 mA, 90 kV, and 360°) for implant planning. In that scan, the dentist encountered a large cystic lesion in the upper right posterior region. For further evaluation of the lesion, the dentist referred the patient to our department.\nOn clinical examination, maxillary right central incisors, right lateral incisor, left central incisor, and left lateral incisor were vital and they responded normally to both thermal and electrical pulp testing. No swelling or draining sinuses were noticed, and the overlying mucosa was normal on the buccal as well as palatal aspect in the maxillary right posterior region [Figure and ]. Apart from this, there was Ellis Class III fracture with maxillary left central incisor.\nOn radiographic examination, panoramic view showed a 2 cm × 1.5 cm well-defined unilocular radiolucent lesion with sclerotic border extending from the apical region of the upper right second premolar to the second molar. Radiolucency between the teeth showed scalloping with intact lamina dura of all involved teeth. Mild root resorption was evident with the upper right second premolar, upper right first molar, and upper right second molar, and altered root morphology was seen with the upper right second premolar. In addition, there was a fracture of 21 along with external and internal resorption []. CBCT of maxilla (5 mA, 90 kV, and 360°) also revealed single, large, well-defined, expansile radiolucent lesion of size 2.8 cm × 2.1 cm on the right side of the maxilla. The lesion showed scalloped borders along with the displacement of the floor of maxillary sinus [Figure –]. There was no evidence of expansion of the buccal or lingual cortical plates in the CBCT of maxilla. Based on the location of the lesion, differential diagnoses included were keratocystic odontogenic tumor, ameloblastoma, and solitary (traumatic) bone cyst.\nFine-needle aspiration was carried out which showed clear, thin, red-colored aspirate with few epithelial remnants. [] Incisional biopsy was also done under local anesthesia and the incised tissue was sent for histopathological examination. Microscopic section revealed hemorrhagic areas, scanty fibrous tissue, and bony fragments. There was no evidence of epithelial lining in the present sections [Figure and ]. Thus, the diagnosis of solitary or traumatic bone cyst was obtained after correlating clinical, radiological, and histopathological features. The patient was advised to undergo for conservative surgical treatment, but she did not turn up for further follow-up.
We present the case of a 51-year-old Caucasian woman with a four-year history of recurrent, right-sided facial pain, in the distribution of all three branches of the trigeminal nerve. These episodes occurred on average two to three times per week and were characterised by brief episodes of unilateral right-sided sharp lancinating pain, lasting on average less than one minute and predominantly affecting the maxillary and mandibular divisions of the trigeminal nerve, although occasionally involving all three branches. Attacks were typically triggered by such actions as washing her face or smiling. There were no other features associated with these attacks; in particular there were no associated headaches or visual disturbance. She had no prior history of headache and there was no family history of trigeminal neuralgia. Her neurological and dental examinations, a computed axial tomography scan of brain and sinuses, and routine blood tests were all normal.\nThe patient initially commenced on gabapentin (up to 1200 mg daily) to which carbamazepine (up to 800 mg daily) was later added without any significant benefit. Following a neurosurgical assessment, she underwent decompression of her right trigeminal nerve, nine months after the initial onset of her symptoms. Unfortunately, her symptoms worsened following this and she was referred for radiofrequency ablation 14 months after the decompressive surgery. This resulted in some permanent numbness in her right infra-orbital area but no pain relief. She was then referred to a specialist pain clinic and initially treated with a combination of dothiepin (75 mg daily), pregabalin (600 mg daily) and numesulide (200 mg daily). This regime resulted in a transient improvement in her symptoms. At this stage, oxycodone 10 mg daily was added; a treatment escalation that her general practitioner (GP) had reservations about. Based on previous experience using sumatriptan for abdominal pain [], a trial of oral sumatriptan 50 mg was suggested, to be taken at the onset of facial pain. This resulted in effective pain relief, and propranolol to a dose of 160 mg daily was added. This reduced the frequency of her facial pain from two to three episodes per week to one every two weeks. Numesulide, dothiepin and pregabalin were safely withdrawn.

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