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A 46-year-old woman (gravida 2, para 2) was referred to our hospital complaining of a lower abdominal mass and pain. Her medical history was unremarkable. She was initially diagnosed with a uterine leiomyoma by transcervical needle biopsy. CT revealed a large heterogeneous tumor occupying the pelvic cavity and an intravascular tumor within the dilated left internal iliac and ovarian veins (Figures and ). Her preoperative cervical cytology results were negative for intraepithelial lesions and malignancy. The endometrial cytology and needle biopsy results were also negative. Thus, the preoperative diagnosis was IVL, with extension of the tumor into the left internal iliac and ovarian veins.\nIntraoperatively, multiple myomas were found within the uterine corpus and cervix, and the tumor extended to the parametrium and paracolpium. Detachment of the tumor from the left ureter and vaginal wall was very difficult. Intravenous tumors in the left internal iliac and ovarian veins could be palpated. The left internal iliac vein forming the common iliac vein was transected at the bifurcation region. In addition, TAH and bilateral salpingo-oophorectomy (BSO) were performed, resulting in the complete surgical resection of the tumor (operative time, 11 hours; blood loss, 8462 g). The resected uterus and adnexa weighed 897 g (Figures and ). There was no residual tumor detected in the venous resection stump.\nThe nodule resected from the uterus and the internal iliac and ovarian veins consisted of a proliferation of spindle cells. There was no nuclear atypia and the mitotic index was low. In addition, vessel endothelium cells and a vascular smooth muscle layer covered the IVL (Figures and ). The tumor cells stained positive for Alcian blue (pH = 2.5) and the staining disappeared after hyaluronidase digestion. However, compared to that in Case 1, the intensity of the staining was weaker and less diffuse (Figures and ). Similar findings for hyaluronan expression were obtained using the sample retrieved from the preoperative needle biopsy.\nThe histopathological diagnosis of the uterine and intravascular tumors was IVL. There has been no evidence of IVL recurrence, with the most recent follow-up at 38 months postoperatively. |
A 25-year-old nulliparous lady, presented to the gynecology OPD with complaints of inability to conceive. She was married for 7 years, cohabiting since 5 years. At 16 years of age, she consulted a local doctor in her village for primary amenorrhea and cyclical pain in abdomen, where some operative procedure was done. Since then the patient has passage of blood mixed urine periodically every month for 2 to 3 days with suprapubic abdominal pain. She had thelarche at 13 years and pubarche at 15 years of age. There was no urinary incontinence or dysparunia.\nOn general physical examination, secondary sexual characters were present. On local examination, external urethral meatus appeared dilated, and there was blindly ending vagina approximately 3 cm in length. On per rectum examination, uterus appeared normal in size and there was no bulge felt below it to suggest any collection. On investigations, the ultrasound showed normal uterus with endometrial thickness 9.5 mm, ovaries were normal, and bilateral kidneys were also normal. MRI of abdomen showed normal uterine body and cervix with small amount of fluid in endometrial cavity, endocervical cavity, and in upper part of vagina; below that there was a transverse vaginal septum of about 3.5 cm in thickness. No fistulous tract or communication was visualized between the genital and urinary tract. [] On cystoscopy, a fistulous opening of approximately 2 mm was seen below the internal sphincter of urethra through which menstrual blood was seen coming out; the bladder and ureteric orifices were normal. Micturating cystourethrography also failed to provide any idea about the fistulous tract. Vaginoplasty and repair of fistulous communication between the genital tract and the urethra was planned for the patient.\nThe woman was subjected to operation using abdominoperineal approach. On laparotomy, uterus was normal in size, bilateral tubes were present, and ovaries were normal. The methylene blue dye was injected into the fundus of the uterus; dye was visualized coming out of urethra by the side of the indwelling catheter. From the perineal approach, a transverse incision was made through the vault of the short vagina, the dissection was done upward in the connective tissue between the bladder above and rectum below and vaginal space was created. After sharp and blunt dissection, cervix was visualized as dye was coming through it. The cervical os was dilated with Hegar's dilator. The urethrovaginal fistulous tract was identified and repair was done in two layers. Over the raw area of vagina, the amnion graft was employed over a sponge mould with condom. An indwelling catheter was applied. The mould change was done after a week; the amnion graft had successfully taken up. Dentine moulds were made and applied. Patient was taught how to change the mould daily. The patient was found to be fine at follow-up after a month, with no hematuria and normal menstruation. She was advised to have regular intercourse. She was explained about the fertility period and asked to come at 3 monthly follow-up. |
A 40-year-old woman (gravida 0, para 0, 153.8 cm, 66.9 kg) with placenta previa totalis and multiple myomas was admitted to our hospital at 36+6 weeks gestation for a cesarean delivery. She had no history of medical illness or trauma. Due to the possibility of massive bleeding during removal of the placenta, multidisciplinary management was considered. We discussed the delivery with the obstetrician and radiologist, and the decision was made to attempt preventive UAE before placental expulsion. Initially, the plan was to transfer the patient from the maternity ward on the 4th floor to the angiography room on the first basement level after fetal delivery, and, after finishing the intervention, to transfer her back to the operating theater. However, we strongly recommended intraoperative radiologic intervention to avoid both possible infection and difficult and unnecessary patient monitoring and management, as well as to reduce additional blood loss during transfer of the patient in such an emergent situation. In the end, we all agreed to perform the embolization intraoperatively immediately after delivery of the fetus and before removal of the placenta during cesarean delivery under spinal anesthesia. All equipment, including a C-arm fluoroscope for the interventional radiologist, was prepared in the operating room before the delivery. The patient's vital signs were stable on the day of operation. Preoperative blood pressure was 107/52 mmHg, heart rate was 80 beats/min, hemoglobin was 9.8 g/dl, and other laboratory findings were normal.\nAfter arrival of the patient in the operating room, standard monitoring (electrocardiogram, pulse oximetry, and noninvasive blood pressure) was begun. Initial blood pressure was 100/49 mmHg, heart rate was 98 beats/min with normal sinus rhythm, SpO2 was 95% on room air, and 100% O2 was administered via face mask at a flow rate of 5 L/min. She had two 18-gauge intravenous lines in both arms, and an arterial catheter was placed in the right radial artery with a 20 G angiocatheter to monitor arterial blood pressure.\nUnder strict aseptic conditions, a combined spinal-epidural block was performed at the 2nd-3rd lumbar interspace in the right lateral position with a needle-through-needle technique using an 18 G Tuohy and 27 G pencil point spinal needle by the median approach without difficulty. After that, 8 mg of heavy bupivacaine and 20 µg of fentanyl was administered intrathecally. The epidural catheter tip was threaded 5 cm into the epidural space and 3 ml of 1% lidocaine with 1:200,000 epinephrine was then slowly administered into the epidural space. No changes were observed in cardiac rhythm, heart rate, or blood pressure. We subsequently assessed the extent of bilateral sensory blockade by observing the loss of cold sense to alcohol sponges and the loss of pain sense to pinpricks. At that time, the sensory level was located at T4. At 25 minutes after administration of the initial dose, block was established up to T1, and the obstetricians proceeded with the surgery. Before skin incision, 350 ml of crystalloid solution and 150 ml of colloid solution were infused.\nAt 9 minutes after skin incision, a 2.815 kg male baby (Apgar scores of 7 and 8 at 1 and 5 min, respectively) was delivered. At that time, the patient's blood pressure was 114/60 mmHg, heart rate was 79 beats/min, and SpO2 was 97%. The arterial blood gas analysis performed immediately before the embolization revealed the following: pH 7.35, PCO2 39 mmHg, PO2 81.5 mmHg, HCO3 - 21.2 mEq/L, SaO2 96.4%, Hct 24%.\nAt 25 minutes after skin incision, UAE of both arteries using gel foam particles was performed for 30 minutes without incident. During the embolization procedure, vital signs were as follows: blood pressure 110-115/48-55 mmHg, respiratory rate 18 breaths/min, heart rate 69-79 beats/min. Midazolam 3 mg was administered to reduce the patient's anxiety. After confirming successful complete embolization, placental expulsion was performed without complications. Three units of packed RBCs were transfused with a rapid blood infuser (Level-1®, Smiths Medical, Ashford, UK). The arterial blood gas analysis performed immediately after the placental expulsion and transfusion revealed the following: pH 7.33, PCO2 37.9 mmHg, PO2 149.7 mmHg, HCO3 - 19.5 mEq/L, Hb 7.1 g/dl, Hct 21%. Forty minutes after placental expulsion, 3 ml of 1% lidocaine with fentanyl 80 µg was administered via epidural catheter and midazolam 3 mg was intravenously injected. An additional forty minutes after that, 10 ml of 0.75% ropivacaine with fentanyl 50 µg was administered via epidural catheter. Two additional units of packed RBCs were also transfused.\nThe total operation time was 175 minutes, and anesthesia time was 225 minutes. Total infused amounts of crystalloid, colloid, and RBCs were 1,950 ml, 1,500 ml, and 5 U, respectively. Estimated blood loss and urine output were 2,500 ml and 300 ml. During the operation, the patient's hemodynamics were as follows: blood pressure 90-120/45-70 mmHg, heart rate 60-103 beats/min. The patient's postoperative pain was managed with an epidural patient-controlled analgesia device (0.15% ropivacaine 250 ml with fentanyl 1,500 µg, basal rate 4 ml, bolus 2 ml, and lockout time 30 min) for 3 days after the operation with numeric rating scale 3 points pain. She was discharged without complications on postoperative day 4. |
A 42-year-old Caucasian woman was admitted to our institution with a four-week history of gradually worsening headache after she had attended a ‘pilates reformer’ class. She described the sudden feeling of a ‘pop’ in the left side of her neck during a certain pilates reformer maneuver but there was no head injury. Our patient developed a headache after one hour, which improved when lying flat. She initially presented to primary care where she received treatment (opiate analgesic and muscle relaxant) for suspected trapezius muscle injury and referred head pain. Over a four-week period, our patient underwent a series of physiotherapy sessions with intensive neck manipulation. During this time, our patient had a number of interactions with primary care, in addition to one emergency department attendance after two-and-a-half weeks. There was no relief with simple or opiate analgesics. The severity of the headache had a profound impact on her ability to perform her activities of daily living. There was no prior history of migraine, head or spine trauma, recent travel or the use of any anticoagulants. She had a history of medically refractory ulcerative colitis treated with subtotal colectomy and subsequent ileo-anal pouch anastomosis. Our patient reported some relief of symptoms in response to a nonsteroidal anti-inflammatory drug (NSAID) but experienced an episode of pouchitis and NSAID treatment was terminated.\nOn admission to our institution she was afebrile with normal blood pressure and pulse. There were no meningitic signs. An examination of the cranial nerves, peripheral nervous system and spine was unremarkable. Basic hematological and biochemical blood tests were unremarkable. A computed tomography (CT) scan of her head demonstrated bilateral chronic subdural hematomas and cerebellar descent (Figure \n). Magnetic resonance imaging (MRI) of her spine revealed the presence of extensive extradural CSF collections (Figure \n) but was unable to identify the exact location of the dural tear. Initially, we opted for conservative management with bed rest and caffeinated drinks rather than use an epidural blood patch. Our patient responded well to the conservative management with a significant improvement in her headaches. She was discharged two weeks after admission and one month after discharge repeat neuroimaging revealed normal intracranial appearances (Figure \n). Our patient was reviewed following this repeat neuroimaging: she remained asymptomatic and, therefore, no further routine follow-up was arranged. |
A 29-year-old man presented with eight-year history of vague pain in the right knee that aggravated when squatting. He was a sedentary worker. He stated that there had been no prior trauma to the knee. There was no catching, swelling or sense of giving way. On physical examination, there were negative findings on the Lachman and pivot-shift tests and no swelling or tenderness along the joint line. The range of motion was full, with no loss of extension, but painful in extreme range of flexion. Patellar movements were normal and negative on patellar compression test. The findings on radiographs of the knee were interpreted as normal. Magnetic resonance imaging revealed that meniscus and posterior cruciate ligament were normal. Coronal and sagittal T1-weighted images demonstrated that the soft tissue mass was isointense to muscle and obscured the ACL. T2-weighted sagittal magnetic resonance images showed heterogenous, intermediate to low signal intensity, which was slightly higher than that of skeletal muscle (). There were no palpable mass-like lesions on his whole body and no family history of hyperlipidemia or xanthomatosis. Laboratory examinations, including platelet count, prothrombin time, bleeding time and total cholesterol, were all within normal limits. Other blood parameters showed normal range. Arthroscopic examination showed normal findings of both meniscus, posterior cruciate ligament and articular cartilage.\nThe ACL appeared to be diffusely bulging, but maintained normal tension. Posteromedial and posterolateral portals were made to visualize the mass more clearly. We were able to access the lesions by switching the posterolateral and posteromedial portal alternatively. The mass was located behind the ACL, close to the femoral attachment site. It was round in shape, measuring about 20 mm × 11 mm in diameter with a reddish-brown color (). It was excised using a motorized instrument and basket forceps by piecemeal (). A repeat performance of the Lachman test and pivot-shift test showed a stable knee.\nMicroscopic features varied on different parts of the tumor. The basic cellular composition of the tumor was well-defined polygonal mononuclear cells with a scanty, faintly eosinophilic cytoplasm. In some areas, there were bands or sheets of amorphous collagen (). Foci of xanthoma cells with foamy cytoplasm and vacuoles were present, accompanied by branching capillaries. Multinucleated giant cells had abundant eosinophilic cytoplasm and contained eight or more nuclei (). The patient had no further complaints following the operation, and there was no recurrence on 55-months of follow-up. |
A 45-year-old-woman presented with a history of sudden onset of right-sided lower abdominal pain since five hours and was associated with vomiting. She gave a history of recurrent episodes of right-sided lower abdominal pain since the past 2 years and several imaging studies done over this time period, including ultrasonography and computed tomography scans, failed to reveal the etiology of her symptoms. She had no previous surgical history, but was recently detected to have type 2 Diabetes Mellitus. Clinical examination revealed an obese abdomen with maximal focal tenderness in the right lower quadrant. However, a vague fullness was palpable in the lower right quadrant which corresponded to the site of maximal tenderness. She was afebrile, the heart rate was 90/minute, blood pressure was 140/90 mm of Hg, and the bowel sounds were hyperperistaltic. Laboratory investigations were unremarkable except for neutrophilic leucocytosis. Plain abdominal radiograph and ultrasonography were inconclusive. Hence, with a provisional clinical diagnosis of an appendicular pathology, the patient was taken-up for laparoscopic surgery.\nPrior to the induction of anaesthesia, the patient's abdomen was palpated and the area of maximal focal tenderness and the fullness was outlined with a marking pen (). Pneumoperitoneum was created by an open technique and a 30-degree 10 mm telescope was used for the procedure. Immediately upon entry, a loop of small bowel was seen herniating through a defect in the anterior abdominal wall and this coincided with the area that was marked over the skin (). This site was in the territory of the “Spigelian hernia belt” and hence consistent with a Spigelian hernia. An additional 5 mm port was placed in the left iliac fossa for the grasper tool. Laparoscopic reduction of bowel was done and a slit-like Spigelian defect about 3 cm by 2 cm was clearly seen (Figures and ). The incarcerated bowel which was the mid ileum appeared viable and peristalsis was noted. Now as the diagnosis was certain and as the patient could not afford a composite dual mesh, we decided to do a conventional hernia repair using a regular polypropylene mesh instead of a totally laparoscopic repair. Thus, a transverse incision was made over the site of the hernia on the anterior abdominal wall. The sac was identified below the arcuate line which illuminated well with the light transmitted from the laparoscope (Figures and ). The sac was excised and defect was repaired using an onlay polypropylene mesh as for an open hernioplasty. The repair was then inspected from within with the help of the laparoscope and found to be adequate, and there was no bulge at the repaired site even on air-insufflation of the peritoneal cavity. Postoperatively, the patient made good progress and was discharged on the seventh postoperative day. The patient is on regular follow-up since 6 months and is doing well. |
A 22-year-old multiparous woman with a history of primary sclerosing cholangitis complicated by portal hypertension, esophageal varices, and thrombocytopenia was admitted at 29 0/7 weeks for evaluation and management of shortness of breath and lower extremity edema. Her obstetric history was significant for prior spontaneous preterm birth with placement of an ultrasound-indicated McDonald cerclage at 20 1/7 weeks of gestation in the index pregnancy. At the time of cerclage placement, the 5 mm Mersilene (polyester) tape was noted to be suboptimally placed along the posterior rim, distal to the internal os, so a second McDonald cerclage of 0-polyester suture was placed cephalad to the tape. She was admitted at 28 0/7 weeks for preterm labor and the cerclages were removed with no remarkable anatomic irregularities. She received antenatal corticosteroids and magnesium sulfate during her admission for preterm labor and was discharged on hospital day #3 with a cervical exam of 1cm dilation and 70% effacement. During her readmission at 29 0/7 weeks for shortness of breath, she began to have contractions and moderate vaginal bleeding on hospital day #3. Her cervical exam was 4 cm and 90% effaced. She was transferred to labor and delivery, where she continued to have a rapid cervical change to 6 cm. A brief fetal heart rate bradycardia occurred with spontaneous recovery to a normal baseline. At this time, findings were concerning for placental abruption or possible coagulopathy from decompensated liver failure with a total estimated blood loss of 500 mL. Amniotomy was performed to expedite vaginal delivery. However, cervical dilation did not continue and complete cessation of vaginal bleeding was noted. Careful visualization of the cervix revealed that the posterior rim of cervix was detached and traversing the presenting fetal head creating a tension band that prevented further dilation or descent. This band of cervical tissue was clamped and suture-ligated followed by rapid delivery. She delivered a male infant with a weight of 1325 g and Apgar scores of 5 and 7 at 1 and 5 minutes, respectively; arterial cord pH was 7.33. Following delivery of the placenta, vaginal exam revealed a partial posterior cervical detachment from 2 to 9 o'clock. The avulsed portion of the cervix did not appear necrotic and was bleeding briskly. Hemostasis was achieved with a single running locked suture. Her postpartum course was otherwise unremarkable, and she was discharged on postpartum day #2. At her six-week postpartum visit her cervical exam was remarkable for a normal appearing anterior lip; however the posterior lip was not visible and not palpable on digital exam (). Pathology was not available for the fragments of cervix that were excised and the placenta was remarkable for acute chorioamnionitis. |
A male infant, who was term appropriate for gestational age, was born via repeat caesarean section to a healthy 26-year-old woman. No family history of bleeding disorders was reported by the mother. Pregnancy was unremarkable, and Apgar scores were 9 and 9 at 1 and 5 minutes, respectively. On initial physical examination, a localized hematoma to the left parietotemporal region was identified. A routine complete blood count (CBC) displayed normal counts. It was decided to repeat the CBC in 12 hours and, in the interim, to observe for dissemination of the blood collection. Prior to the next blood test, the physician was called to the bedside because the infant now had a change in his clinical examination: pale and tachycardic. His examination now revealed a large palpable fluid wave that extended behind the neck and left ear. Given the infant’s change in clinical status and concern for a subgaleal hematoma, the infant was transferred to the neonatal intensive care unit (NICU). The repeat CBC showed a hemoglobin level of 7.6 g/dL, with a hematocrit of 22% and platelets of 169 × 109/L. In the NICU, the patient received a transfusion of 20 cc/kg of O Rh-negative packed red cells. His coagulation profile disclosed a normal prothrombin time but an activated partial thromboplastin time (PTT) of 101 seconds (normal = 25-30 seconds).\nSubsequently, a FVIII level was ordered, which was very low at <0.01 U/mL. He was diagnosed with severe HA and was initially treated with 50 U/kg of recombinant FVIII. His repeat doses were adjusted to bring his FVIII level to 100%. A computed tomography (CT) scan of the head revealed a large subgaleal hematoma, beginning in the left parietal area, extending to the occiput and down the nape of the neck. The infant was discharged at 1 week of age following a repeat head imaging confirming complete resolution of the extracranial hemorrhage (ECH) without any evidence of intracranial bleeding. |
A 62-year-old man with a vertical crushing injury in his left facial area caused by a grinder visited our emergency department. His left upper eyelid was cut and showed a partial levator aponeurotic rupture (). Debridement and wound closure were performed with a levator aponeurotic repair the day after the onset of trauma. The wound healing was unremarkable. Approximately 45 days later, he developed a severe upper eyelid scar contracture that resulted in lagophthalmos, with exposure of 5 mm of his left eyeball when both eyes were fully closed (). As the patient was also followed up by the ophthalmology department, keratitis was identified right after its initial development and had been treated conservatively. However, his compliance to the ophthalmic conservative treatments was poor because the therapeutic contact lens kept dropping out of his eye continuously owing to the severe lagophthalmos. Hence, early lagophthalmos release was inevitable, and scar release with pentagonal wedge resection, fat redistribution, and fullthickness skin grafting (FTSG) were performed under general anesthesia. Pentagonal wedge resection was performed, and the scar tissue was dissected just anterior to the tarsus. After scar release, we observed a skin defect measuring 3× 1 cm in size. The eyelid margin was approximated first with minimal tension and without any eyelid deformity, followed by repair of the conjunctiva. Then, subcutaneous fat tissue redistribution was performed to prevent readhesion of the thin upper eyelid skin or orbicularis oculi muscle to the levator complex at an undesirable level, and to prepare the nutritional bed for skin tissue. The aponeurotic fat was advanced and anchored on the tarsal plate and carefully handled to cover the whole levator complex. Then, the skin flaps around the redistributed fat were mobilized to achieve maximal coverage of the pentagonally excised defect. Skin flaps on the medial (glabella) and lateral sides were advanced for bilateral coverage using 5-0 PDS and 6-0 nylon sutures. After the advancement flap placement, a defect measuring 1.5 × 1.0 cm persisted and required skin grafting. Fullthickness skin (2.0× 1.0 cm) harvested from the left posterior auricular area was defatted and grafted onto the upper eyelid and fixed with 6-0 nylon sutures with a tie-over dressing using 6-0 silk to secure the graft (). At the 10-day follow-up, we observed an excellent postoperative outcome, and he was able to fully close his upper eyelid. He had regained his ability to completely close the injured eyelid at the 18-month postoperative follow-up (), and no readhesion has been observed since then. |
A 61-year-old female with medical history of hypertension, diabetes mellitus type 2, and chronic kidney disease stage V was transferred to our institution from an outside hospital for further evaluation and definitive management of a migrated intracardiac stent.\nShe initially presented to the outside facility with progressive dyspnea on exertion, orthopnea, and bilateral lower extremity edema. She was initially diagnosed with acute heart failure and pneumonia and treated with diuretics and antibiotics. Subsequently, a transthoracic echocardiogram was performed, which revealed a foreign body within the right ventricle. On transfer to our facility, a transesophageal echocardiogram revealed a long stent straddling the tricuspid valve from the right atrium with the other end lodged in the trabeculation of the right ventricle with severe tricuspid regurgitation ().\nOn further investigation, we learned that the patient had undergone peripheral endovascular intervention for May-Thurner syndrome with placement of a self-expanding Nitinol Protege (14 mm × 60 mm) stent to the left iliac vein 6 months prior to presentation.\nA percutaneous endovascular approach with a 35- mm Medtronic-Covidien Amplatzer Gooseneck Snare was initially attempted to retrieve the migrated stent. However, the snared proximal segment fractured, leaving behind 2 stent fragments. After ensuring there was no myocardial perforation or pericardial effusion with intracardiac ultrasound, the patient was referred for surgical extraction via median sternotomy with use of cardiopulmonary bypass.\nDuring the operative procedure, the stent was found to be densely adherent to the tricuspid leaflets and the subvalvular apparatus, with majority of the primary chords to the anterior and posterior leaflets ruptured (). After successful extraction of the stent and native tricuspid valve, she underwent valve replacement with a 29-mm Carpentier-Edwards bioprosthetic valve. Her postoperative course was complicated by hemopericardium secondary to anticoagulation resulting in cardiac tamponade that was drained percutaneously, and small thromboembolic cerebellar stroke from atrial fibrillation. She was discharged to an inpatient rehabilitation facility and did well on 8-month follow-up. |
A 30-year-old woman was referred to our hospital with a history of pain and an increased volume in her right elbow which had been for 5 months. On physical examination, a 6-cm firm mass was detected in the lateral face of the elbow. The mass was painful, non-mobile, and attached to the deep planes corresponding to the proximal radial head. There was hypoesthesia and the flexion/extension and prono-supination movements of the patient’s right arm were limited.\nX-ray revealed a lytic lesion localized in the proximal meta-epiphysis of the radius with ill-defined borders and a permeative pattern of bone destruction. The lesion destroyed the lateral aspect of the radius’s cortical. However, the humerus and the ulna the joint surface of the radius were uninvolved ().\nSagittal magnetic resonance imaging showed a proximal radius lesion with periosteal reaction, destruction of the anterior cortical, and spreading to the adjacent soft tissues. The humerus, the ulna and the joint surface of the radius were uninvolved ().\nAfter the clinical diagnosis of a primary bone tumor of the radius was confirmed, an en bloc resection was performed. The resected portion was a bone tumor of the distal radius with an extension to soft tissues. Macroscopically it consisted of two components: the first component was epiphyseal and didn’t affect the joint cartilage of the radius and was located next to the bone with no extension to soft tissues. This component was solid and white in color with focal areas of yellowish discoloration. The second component of the tumor was more metadiaphyseal, had an extension to soft tissues, and a fleshy appearance with areas of hemorrhage and necrosis (). On histological examination, the epiphyseal tumor was subchondral, did not affect the articular cartilage and showed a GCT composed of mononuclear stromal cells alternating with giant multinucleated cells. The stromal cells were spindle-shaped with no nuclear atypia or hyperchromatism. In this stromal component, mitotic figures were not observed. The giant multinucleated cells were similar to osteoclasts, but with more nuclei arranged towards the center of the cell (). The remainder of the radial tumor was composed of a monotonous proliferation of small cells with rounded and basophilic nuclei and scant cytoplasm. The nuclei exhibited a finely-dispersed chromatin pattern. There were multiple areas of necrosis and the cells localized around vessels were generally preserved (). Scattered mitotic figures were identified, Homer-Wright- or Flexner-type rosettes were absent, and the periodic acid-Schiff preparation was negative in the cytoplasm of these cells. There was an interface, which consisted of spindle cells and necrotic tissue, between the GCT and the small, rounded, and basophilic component. Immunohistochemistry was negative for CD99, cytokeratin, and leukocyte common antigen, and was only positive for Vimentin. Due to the unusual histology, we consulted two bone tumor experts to discuss about this case. Their opinion was that this case was a dedifferentiated GCT with an undifferentiated, round cell, mesenchymal component. In the gammagraphic follow-up at 3 months after the en bloc resection, the patient presented multiple lesions in pelvis, sternum, right femur, and left supraclavicular. |
62-year-old woman with medical history significant for aortic stenosis and chronic atrial fibrillation presented to the emergency department with fatigue and progressively worsening shortness of breath with minimal exertion. She was asymptomatic at rest and denied chest pain, orthopnea, paroxysmal nocturnal dyspnea, leg swelling, presyncope, or syncope. She was incidentally found to have a systolic murmur during her pregnancy 20 years prior to this presentation. Notably, she had been offered aortic valve replacement in the past but declined.\nVital signs were normal with blood pressure of 110/60 mmHg, pulse rate of 79/min, temperature of 97.2°F, and respiratory rate of 16 breaths/min with normal oxygen saturation of 100% on ambient air. Physical examination was significant for irregularly irregular heart rhythm, and ejection systolic murmur was loudest in the aortic area with radiation to the carotids. Her lungs were clear to auscultation, and no pedal edema was noted. Electrocardiogram revealed atrial fibrillation with voltage criteria for left ventricular hypertrophy. Her most recent transthoracic echocardiogram revealed a thickened calcified aortic valve with decreased excursion with 4.6 m/s velocity suggesting a peak of 86 mmHg and mean of 36 mmHg suggestive of severe aortic stenosis. No other significant valvular abnormalities noted. Cardiac catheterization revealed widely patent coronary arteries.\nBased on the presence of worsening symptoms and the risk of sudden cardiac death, the decision was made to proceed with surgical aortic valve replacement. Given her history of chronic atrial fibrillation, she was also planned for left atrial appendage exclusion and Cox Maze IV procedure simultaneously with the aortic valve replacement. Intraoperative transesophageal echocardiogram revealed quadricuspid aortic valves confirmed during surgical exploration (). The native stenotic quadricuspid aortic valve leaflets were excised, and a 21 mm Saint Jude Medical Trifecta valve was implanted. The left atrial appendage was excised, and Cox Maze IV procedure was performed. Postoperatively, she remained in junctional rhythm and underwent uneventful placement of the dual chamber pacemaker on postoperative day 3. She recovered without further complications and was discharged on the eight postoperative day. |
The patient was a 49-year-old woman with no family history of note. She had worked at a child welfare facility where she sustained a wound to the left side of her upper eyelid after it was scratched by a child facility resident's finger. She was conscious and had a stable general condition without nausea or vomiting when she was transported to a local hospital by an ambulance. Immediately on arrival, only the skin tissue was sutured by a general surgeon.\nFive weeks after the injury, she showed upper eyelid drooping and complete left-sided ptosis, so she was referred to our department. Locally, left-side eye-opening dysfunction associated with the fissure and swelling of the left upper eyelid was observed []. Nine weeks after the injury, surgery was performed to restore the eye-opening function.\nThe surgical procedure was performed under local anesthesia, and the left side of the upper eyelid area was infiltrated with 0.5% lidocaine with 1:100,000 epinephrine. After the removal of the scar on the inner side of the eyelid, which was the previous sutured part, it was peeled off to expose the front surface of the aponeurotic and levator muscles []. As the medial canthal band was torn, scar tissue was removed as much as possible []. Subsequently, the band was sutured with periosteum inside the orbit and 5-0 nylon to return to the original position. Attempts were made to separate the conjunctiva from the Muller muscle, but the scar contracture was so severe that the levator and Muller muscles could not be identified. These two muscles were combined into a lump, with the tissue in front of the levator muscle fixed firmly at approximately half the height of the tarsus with a single 6-0 nylon horizontal mattress suture []. Fixation for a double fold was made, and the skin was closed with 6-0 nylon interrupted sutures. Six months after the operation, the upper eyelids showed symmetrically appropriate heights. The patient did not demonstrate exposure keratitis, wound infection, lagophthalmos, eye movement disorders, or ptosis in the 6 months following the operation []. |
A 5-year-old boy with ECC was referred to the Department of Pediatric Dentistry, School of Dentistry, in Isfahan University of Medical Sciences. The child was medically fit and well. Clinical and radiographic examinations were conducted to establish a treatment plan.\nOn explaining the restoration technique for the subject and his parents, they accepted the suggested treatment and signed an informed consent form before the treatment began. Following treatment of all posterior decayed teeth, the maxillary canines were considered to be restored with composite resin restoration []. Due to the extensive damage that had occurred in the maxillary right canine structure, this tooth was considered for treatment with the novel technique described as follows.\nThe patient was anesthetized, rubber dam isolation was performed, caries removal was done and pulp tissue was extirpated [Figures –]. The canal was prepared using a sequence of three consecutive endodontic files #30-45 (Maillefere, Kerr, Orange, CA, USA) under constant irrigation with physiologic saline, dried with paper points, and obturated with zinc oxide eugenol paste (ZOE BP, BDH Ltd., Germany). Three millimeters of the coronal part of the canal was prepared for future replacement of post. This part of the canal was then prepared to be almost rectangular with semi-rounded line angles in order to match with the quadrangle core of a prefabricated metal post (Dentatus, Switzerland) that was planned to be placed reversely into the prepared canal. Generally, the core length of prefabricated metal posts is 3 mm and suitable for this purpose.\nThe No. 1 short post was chosen because the length of the post (5 mm) was long enough to build up the coronal length of the destroyed canine and the bulk of composite resin around it was enough to ensure that it did not show the metal shadow and also there was less possibility for interference with the occlusion. The sharp four line angles of quadrangle core of the post were then semi-beveled to not exert stress to the root and the post was examined in the prepared canal [Figures and ].\nSubsequent to occlusion evaluation, 1 mm end of the post which interfered with the occlusion was cut []. The post was then cemented into the canal using zinc phosphate cement (Harvard, Richer and Hoff-man, Berlin, Germany). After initial setting of the cement, etching with 37% phosphoric acid and rinsing, the screws of the post were covered with one layer of flowable composite resin (Aelite flow, Kuraray Co., Osaka, Japan) and the coronal restoration was reconstructed incrementally using A2 shade composite resin (APX, Kuraray Co., Osaka, Japan) [Figures and ].\nFinally, the occlusion was adjusted using articulating paper; finishing and polishing was carried out using fine diamond burs (Teezkavan, Tehran, Iran) and Soft Lex Pop On Disks (3M ESPE, St. Paul, MN, USA) [].\nThe patient and his parents were instructed on proper dietary and hygiene habits and advised to come for regular check-up. In intervals of 6, 12, and 18 months, the subject was examined for regular evaluations of his orodental situation and the restored canine [Figures and ]. |
A 53-year old female was admitted to the Intensive Care Unit of Kingston General Hospital in Kingston, Ontario, Canada with diabetic ketoacidosis (DKA). She had a past medical history of type 1 diabetes with recurrent DKA and end stage renal disease secondary to diabetic nephropathy on intermittent hemodialysis. Prior to admission, she was being dialyzed through a left arm arteriovenous fistula.\nShortly after admission, her left arm fistula thrombosed, and a right internal jugular (IJ) tunneled double-lumen catheter was inserted for dialysis along with a peripherally inserted central catheter (PICC) via right basilic vein for intravenous access. The patient had a previous failed right arm AV fistula so the left arm was avoided in hopes of future recovery of the left AV fistula.\nTwo weeks later during the course of her admission, she continued to have episodes of DKA, and inadvertently her PICC line was dislodged, requiring removal. The patient had poor peripheral intravenous (IV) access and multiple attempts to insert peripheral IVs under ultrasound guidance were unsuccessful. Ultrasound examination of the patient's left internal jugular showed significant narrowing. The patient declined an attempt femoral venous access because she had previous lower extremity venous grafting for her AV fistula and she was told to avoid cannulization of any of those vessels. A 7 French, 16cm triple-lumen CVC was placed into the right internal jugular vein with sonographic guidance without difficulty. The puncture site for the CVC insertion was significantly distal to the tunneled dialysis catheter. Post-procedure, all three lumens were able to draw blood and flush saline. A chest X-ray confirmed placement of the catheter adjacent to the tunneled dialysis catheter () close to the cavoatrial junction. The patient did not have any immediate complaints or discomfort. Approximately six hours later, the on-call resident was called by nursing staff to assess the patient for new neck discomfort and jaw pain which had begun two hours prior.\nAt the time of assessment, the patient's heart rate was 95 beats per minute and regular. Her blood pressure was 188/84, respiratory rate was 18 and oxygen saturation was 99% on room air. She was afebrile. On examination, the patient had distended neck veins, pronounced facial edema and plethora (). She also had bilateral upper-extremity edema primarily manifesting in her digits. The rest of her cardiorespiratory examination was unremarkable.\nAll three lumens of the CVC were withdrawing blood and flushing without difficulty.\nPoint of care ultrasound of the right internal jugular vein revealed no thrombus at the site of CVC entry or distal to it. The SVC was not visualized directly. The CVC was removed promptly. There was no visible clot on the catheter, and no clot was pulled along with the catheter. Within an hour, the patient's facial swelling and plethora began to resolve, and her neck pain began to improve. The next morning, pain and swelling had resolved completely ().\nA retrospective chart review revealed a fistulogram performed months prior that showed significant stenosis at the left subclavian vein and mild narrowing at the junction where the two brachiocephalic veins merge to form the SVC (). At that time, angiography was attempted to alleviate the stenosis. However, the patient did not tolerate this, and the procedure did not lead to a significant change in the degree of stenosis.\nThe events surrounding the SVC syndrome and the previously identified SVC stenosis were disclosed to the patient. In order to prevent a similar event from occurring in the future, a note was made in the chart that would be more visible should the need for further CVCs arise. |
A 45-year-old man, right lower limb being wedged in the rear wheel of a roller when walking across the street, was transferred to our hospital with his right lower limb unable to move for 12 h. Physical examination showing that the patient’s blood pressure was 85/57 mmHg and the pulse rate was 150 per minute. He was confusion and his right chest and rib area displayed extensive skin ecchymosis, with a wound area of 10 × 10 cm2 in the right hip that extended to the pelvis. There was a 3 cm laceration in his anal sphincter, and rigor mortis in the right lower extremity with cold skin and a loss of sensory and motor function. X-ray imaging showed that the right sacroiliac joint and pubic symphysis were separated, and the ilium was fractured. The patient was diagnosed with hemorrhagic shock, traumatic hemipelvectomy on the right side and laceration of the anal sphincter. Active resuscitation was performed. The blood pressure became stable and general condition was improved. But 8 hours later, the systolic pressure dropped persistently, and sustained hemorrhage in pelvis was suspected. The pelvic angiography was performed 12 hours after admission. It showed a wide range of small arterial bleeding in the pelvic cavity and a thrombosis in the right common iliac artery. The pelvic hemorrhage was significantly decreased following embolization of the left internal iliac artery. Due to the dead right lower extremity at the initial admission, hemipelvectomy was performed and the wound was covered with a gluteus maximus flap 33 h after admission. In view of the partial injury of anal sphincter, the mucosal eversion suture rather than a colostomy was performed. Following once debridement and twice skin grafting, the wound was healed. At the seven-year follow-up, the wound was in stable condition, his rectal mucosa was mildly prolapsed and the patient could walk with crutches (Figure \n). |
A 39-year-old man presented to a local dermatologist, with symptoms of multiple subcutaneous nodules over the anterior chest wall and forehead for 3 months (). The patient also had history of significant weight loss and loss of appetite since last 3 months. He also had history of intermittent constipation lasting for 3-4 days since last 2 months. Fine needle aspiration cytology from skin nodules showed malignant cells with hyperchromatic nuclei, prominent nucleoli, and scanty cytoplasm, with some cells showing intracellular mucin collection suggestive of metastatic mucinous adenocarcinoma (). For expert opinion this patient came to our Cancer Care Centre.\nOn examination his vital signs were stable with performance status of 1. His weight was 40 kgs, with emaciated, cachectic look and there was marked pallor. There was no associated lympadenopathy, icterus, or pedal edema. Multiple subcutaneous nodules were noted over the anterior abdominal wall, anterior chest wall, and forehead with size of 1-2 cm, firm too hard in consistency and non-tender (). There was no history of any bleeding per rectum, but the patient used to have altered bowel habits in the form of intermittent constipation.\nComplete blood count showed hemoglobin of 8 gr/dL, with normal leukocyte count of 5300 per cumm and platelet count of 350,000 per cumm. Carcinoembryonic antigen was 480 IU/mL. Peripheral smear was suggestive of dimorphic anemia with MCV of 97 pg/mL. Contrast enhanced computed tomography (CT) of the abdomen showed asymmetrical circumferential thickening with luminal narrowing of caecum and ascending colon, extending to involve luminal narrowing of ascending colon near hepatic flexure with mild ascites without any evidence of liver metastasis (). Colonoscopy was done and biopsy samples were taken from the right sided ascending colonic mass. Histopathological image showed malignant cells with abundant mucinous cytoplasm and vesicular nuclei with hyperchromatism and prominent nucleoli. Tumor cells were arranged in glandular pattern with intraglandular mucin collection (). The patient was managed with blood transfusion, hematinics, and palliative right sided hemicolectomy in view of intermittent constipation. Postoperative chemotherapy with 5- fluorouracil, leucovorin, and oxiliplatin (FOLFOX) regimen was started and the patient is under regular treatment at our centre until date. Total 16 cycles of FOLFOX chemotherapy was completed without any major side effects except for the mild grade peripheral neuropathy. All the subcutaneous lesions have been regressed after 3 months of treatment and the current CEA(Carcinoembryonic antigen) is 56 IU/mL. |
A 56-year-old, black, male patient was brought to hospital by the emergency services and admitted to the thoracic service after presenting with acute respiratory failure of unknown cause. He complained of discomfort in the left hemithorax, dry coughing and dyspnea.\nHe had a history of more than 20 years of alcoholism (spirits) and smoking (1 pack a day for 30 years).\nHe reported arterial hypertension under control and no other comorbidities.\nPhysical examination revealed that the patient was in good general health, with good color, good oxygenation, and free from fever. Cardiac auscultation was unremarkable. Pulmonary auscultation revealed rales in the left hemithorax and vesicular murmur was reduced at the ipsilateral base. Extremities exhibited good perfusion and pulses were strong and symmetrical in all limbs.\nThoracentesis was performed, followed by thoracostomy with closed left pleural drainage via underwater seal, because of high volume hemothorax.\nThe chest drain was removed after 5 days under observation and on the eleventh day in hospital the patient underwent pleuroscopy, which showed residual fluid with traces of blood. On the 12th day he was discharged from hospital with instructions to return for outpatients follow-up at the thoracic surgery service.\nThirty days after hospital discharge, the patient was referred for investigation by the vascular surgery team because of a pulsating swelling in the upper abdomen, with clinical suspicion of a thoracoabdominal aneurysm.\nAngiotomography of the chest, abdomen, and pelvis was conducted, ruling out thoracoabdominal aneurysm and raising a diagnostic hypothesis of pseudoaneurysm of the splenic artery, as shown in . Tumoral markers ruled out a diagnosis of pancreatic cancer and high lipase levels confirmed the diagnosis of pancreatitis.\nIn view of the suspected pseudoaneurysm of the splenic artery, the decision was taken to conduct digital subtraction angiography with selective catheterization of the celiac trunk, which confirmed the diagnosis of pseudoaneurysm of the splenic artery.\nHaving made this diagnosis, it was decided to treat the lesion using endovascular techniques. Under local anesthesia and venous sedation, femoral access was obtained via the right lower limb, a 0.035 guidewire was advanced via the celiac trunk and splenic artery, and three 8 × 50 mm controlled detachment coils were released, followed by placement of a 6 × 50 mm balloon-expandable covered stent, with coverage from the celiac trunk to the common hepatic artery, with the objective of excluding the splenic artery. This procedure was executed with no intercurrent conditions, and the final angiographic image can be seen in .\nOn the fifth day after the operation, the patient was vaccinated against encapsulated bacteria and discharged from hospital for outpatients follow-up. |
A 20-year-old male patient presented to P. M. Nadagouda Memorial Dental College with the chief complaint of painless soft tissue swelling in the lower lip []. The history of present illness consisted of the development of a swelling on the lower lip 6 months ago, which had gradually increased to the present size of 2 cm. The patient gave a history of associated trauma at the same region 1 year ago. On clinical examination, a well-circumscribed, single, oval, sessile, soft to firm and nontender swelling was observed on the left side of labial mucosa of lower lip. There was no associated pain and paraesthesia and the color of the overlying mucosa was normal. The clinical diagnosis of mucocele was rendered. The treatment plan consisted of the surgical removal of the lesion by placing a vertical incision, then splitting the overlying mucosa and resecting the lesion from the base to decrease the chances of reoccurrence. Sutures were placed and the excised lesion was sent for histopathologic examination. The differential diagnoses included lymphangioma, hemangioma, AH, benign lymphoepithelial lesion and minor salivary gland neoplasms.\nAt low power of OLYMPUS CX41 light microscope, hematoxylin and eosin stained tissue section of 5 mm thickness showed two large, well-circumscribed lobules of normal appearing mucinous acini and ducts with intervening connective tissue septae [Figures and ]. Mucinous acini were larger than normal and distended. The filled mucin showed a bubbly appearance. Myoepithelial cells surrounding the acini were also evident. No dysplastic features were observed. Mild chronic inflammatory infiltration was also noticed which consisted of plasma cells and lymphocytes primarily. Mucicarmine stained histopathologic section of the lesion showed distended mucinous acini filled with mucin []. Mucicarmine stain helps in precise localization of accumulated intracellular and extracellular mucin content. The lesion healed without any complication, and the patient was recalled after 6 months and checked for recurrence of the lesion. |
A healthy 9-year-old Japanese girl presented to a clinic with left hip joint pain without apparent cause for 1 month. She was diagnosed as having coxitis simplex. Although she had taken anti-inflammatory drugs, her pain did not change for 1 year. She was then sent to another hospital, where OO in her left acetabulum was suspected. As a result, she was referred to our hospital approximately 1 year after her first symptom presentation, where she presented with severe left hip pain and was completely unable to walk. Radiographs of her left hip showed no obvious osseous abnormality (Fig. ). In contrast, CT examinations revealed a well-demarcated 5 mm mass with limited bone sclerosis in her left acetabulum (Fig. ). The mass was characterized by low intensity on T1 and high intensity on T2 magnetic resonance imaging (MRI) images. MRI also revealed joint effusion (Fig. ). Clinical and radiological findings were consistent with OO of the left acetabulum. She underwent CT-guided resection of the nidus and ablation using a standard electrosurgical generator at a power output of 15 W for 60-seconds duration (Fig. ). This procedure was performed under total anesthesia and in the prone position. We identified the positional relationship between the nidus, triradiate cartilage, and sciatic nerve using a CT marker. After making a small 3-cm long incision while avoiding her sciatic nerve, a guide pin was inserted. A 5.0 mm cannulated drill was inserted over the guide pin to remove the nidus, which was then sent for histological examination. Next, ablation using a standard electrosurgical generator was performed to completely destroy any residual tumors. To preserve her triradiate cartilage, the position of the electrode tip was confirmed on intraoperative images during each step. The technical tips and pearls of CT-guided resection are summarized in Table . A histological examination confirmed the characteristic appearance of OO (Fig. ). Complete pain relief was achieved beginning on the first postoperative day. Our patient could walk without any pain at the final follow-up 1 year post-treatment, and no local recurrence was observed. |
A 31-year-old female reported with a history of developing a progressing mass 7 years ago on the left lateral wall of the nose with the symptoms of epistaxis, which further lead to the unilateral nasal obstruction which was not relieved with medication. She underwent four surgical interventions in a span of 6 years in various hospitals at Bengal, Bhopal, and Kolkata due to the recurrence of the tumor to a huge size of almost resembling an elephant trunk [Figure and ]. Under histopathological examination, the tumor was diagnosed as “HEMANGIOPERICYTOMA.” The lesion was surgically removed, and subsequently, the patient was made to undergo radiotherapy and chemotherapy. The extensive surgery left her with huge embarrassment and humiliation whenever she interacted.\nDuring the examination, the patient-related dissatisfaction with her appearance and was especially concerned about her facial disfigurement []. There were a large septal perforation and the bilateral absence of mucous blanket, which lead to mucosal atrophy []. Thus, there was a postoperative nasal breathing dysfunction. The only provision of breathing for the patient was through the large defect after excision of the tumor.\nThis defect was elliptical with obliterated edges measuring about 6 cm long and 2 cm wide with a depth of more than that 3 cm along the left side of the face []. The exposed structures of the defect were conchae and meatus with an intact nasal bone, lateral part of the septal cartilage, frontal process of maxilla, and medial wall of the orbit and the cribriform plate of the ethmoidal bone []. With the existing situation, the patient was extremely depressed psychologically, and hence, it was important to treat with an interdisciplinary approach of psychiatry, and ENT. Once the patient was got to a confidence level, a prosthodontic approach was made.\nVarious prosthetic treatment modalities ranging from acrylic resin partial facial mask to an implant-retained silicone prosthesis[] were explained and discussed with the patient. Due to economic constraints and remoteness of her area of residence, the patient denied to come for repeated recalls and reviews. Hence, the prosthesis made of polymethyl methacrylate (PMMA) resin was chosen to be made. There was absolutely no viable bone left over to plan for implant-supported Maxillofacialprosthesis (MFP). Hence, it was decided to use a spectacle glass frame for retaining the prosthesis.\nThe patient was draped, and the petroleum jelly was applied to the patient's eyebrows and eyelashes. Moist gauze was packed to prevent the flow of material into the undesired areas of the defect, and an impression was made of the defect and adjacent tissues using an alginate in a semi-upright position to minimize tissue bed distortion [] The impression was then poured with the type III dental stone (Kala Stone; Kala Bhai Pvt Ltd., Mumbai, India) to achieve a cast []. A model of the prosthesis was sculpted on the facial cast with No. 2 dental modeling wax (MDM Corporation; Delhi, India). Taking into account the patient's general appearance, the esthetic contours were developed. With repeated surgeries, the patient was suffering from nasal stenosis due to which she was unable to breathe through her nares instead the only possible way she could breathe was through the defect. Hence, closing the defect with the prosthesis would make her inconvenient to breathe. Therefore, it was planned to incorporate two slits on the facial prosthesis, to facilitate the passage of air to make her comfortable to breathe [Figure and ] In the wax pattern, two longitudinal vents were then provided on the patient's left lateral wall resembling part of the wax pattern as a provision for breathing for the patient [] The wax pattern adaptation on the patient's face was checked, especially in the border areas for the close adaptation [] Spectacles with a thicker frame with the power of the patient were chosen and adapted at the nasal bridge area of the wax pattern to increase the surface area and close adaptation of the spectacles to the prosthesis [] Once the fitting and approximation have been confirmed, further laboratory procedures of dewaxing and acrylization have been followed Care should be taken, that the vents should be blocked out with an elastomeric putty material. As the wax pattern to be processed had made contours and undercuts, a three-part mold pouring (multisectional mold)[] was necessary to achieve easy placement of acrylic. Investing the wax pattern in the lower half of a large flask was the first pour. Apply separating medium to the stone surface. Invest the posterior undercut surface of the wax pattern with dental stone. The walls of this section must cover toward the center of the flask and are considered as a second pour. The dental stone should be at least 0.5 cm thick in all areas. Apply separating medium to the stone surfaces. Invest the lower half of the wax pattern with the third pour of dental stone and close the lid, and further acrylization was carried out by short curing cycles Heat cure polymethyl-methacrylate material of three shades, namely tooth colored, pink, and clear acrylics were chosen. Shade matching was done by intrinsically staining the material with acrylic stains crylization of the prosthesis was carried out by short curing cycles. The final prosthesis was been tried on the patient, and shade matching was done by extrinsic staining The placement of the prosthesis was demonstrated to the patient and was then delivered. Detailed instructions regarding care and use were provided to the patient [].\nThe patient was scheduled for the first postinsertion adjustments, 1 day after the insertion to ensure the health of the tissues and to relieve the prosthesis for pressure areas on the tissues.\nAt the follow-up evaluation after 2 weeks, the prosthesis appeared to be functioning within normal limits. The patient was then asked to come for recall visit once in every 3 months for the evaluation of prosthesis and observation of any recurrence. |
An 80-year-old Japanese female presented with a 1-month history of progressive dyspnea and dry cough. On admission, she had tachycardia (102 beats per minute), tachypnea (32 respirations per minute), and normotensive blood pressure (123/75 mm Hg). Initial oxygen saturation was 83% with the patient breathing room air. Blood tests revealed a high C-reactive protein level (201.4 mg/l) and a white blood cell count of 18,700/µl. A chest radiograph showed bilateral opacities (fig. ), and a chest high-resolution computed tomography (HRCT) scan revealed ground glass opacity (GGO) of bilateral peripheral lung field predominance (fig. ). Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. A copy of the written consent is available for review from the editor of this journal.\nThe patient was first treated with intravenous antibiotics based on an initial diagnosis of bacterial pneumonia. Despite this treatment, her condition worsened dramatically over the following days. A transthoracic echocardiogram showed a normal ejection fraction with an extremely elevated estimated systolic pulmonary artery pressure of 114 mm Hg. Plasma coagulation tests indicated activation of coagulation systems with D-dimers elevated to 9,700 mg/l (compared to a normal level of <1,000 mg/l). Although pulmonary thromboembolic disease was suspected, CT pulmonary angiography showed no evidence of pulmonary emboli but revealed a left ureteral nodule involving the left common iliac vein suggestive of ureteral carcinoma (fig. ). We then considered the diagnosis of PTTM induced by ureteral carcinoma. The patient refused chemotherapy and selected palliative care for the suspected ureteral carcinoma. She died of respiratory failure on the eighth day of hospitalization.\nPostmortem examination revealed tumor cells in the ureter of the left kidney positive for cytokeratin 7 and cytokeratin 20 upon immunohistochemical analysis, which led to the pathological diagnosis of urothelial carcinoma (fig. ). Tumor cells morphologically similar to the carcinoma of the ureter were identified in the pulmonary arterioles. Marked intimal fibrocellular proliferation and fibrin thrombi were also observed in the pulmonary arterioles (fig. ). In some arterioles, recanalization of organized thrombi was identified. Extravasation of tumor cells and carcinomatous lymphangitis were not seen. These findings are consistent with the histopathologic features of PTTM. The final diagnosis was PTTM induced by ureteral carcinoma. |
A 62-year-old female patient was referred by her oncologist for a routine dental evaluation. The patient’s medical history revealed a cutaneous melanoma of the left dorsum diagnosed six years before she was referred to our dental service. The tumor was primarily treated by surgery and developed two local recurrences (one and three years following surgery, respectively), which were also managed by surgical resection. Disease progression was identified five years after the first treatment and confirmed by a computed tomography (CT), which revealed multiple organ involvement including the lungs, skin (subcutaneous nodules on the dorsum) and bone (osteolytic lesions in the iliac and femur bones, ribs, vertebrae, sternum and scapula).\nThe patient was undergoing a palliative treatment protocol based on dacarbazine, zoledronic acid and radiotherapy in the lumbar region (total dose of 20 Gy) and in the left supraclavicular fossa (total dose of 36 Gy) when she was referred to our dental facility. An extraoral clinical examination identified a pigmented subcutaneous nodule on the patient’s dorsum, measuring 5 cm in diameter, and scarring from the previous surgical resections.\nThe patient’s chief complaint was the loss of the dental crown of her upper left incisor. She denied oral pain or the existence of any relevant oral soft tissue lesion. Intraoral soft tissue examination revealed a nodule with an ulcerated surface and areas of telangiectasia, on the posterior left lateral border of the tongue, measuring approximately 1 cm in diameter, adjacent to a partial edentulous mandibular area (Fig. A). Based on the clinical features of the tongue lesion and on the patient’s medical background, the diagnostic hypothesis included metastatic melanoma, squamous cell carcinoma and fibrous hyperplasia.\nAn incisional biopsy was performed under local anesthesia. The histopathological analysis showed nests and solid sheets of non-pigmented atypical cells with an epithelioid phenotype infiltrating the sub-epithelial connective tissue. A high mitotic index was observed (Fig. B). Tumor cells displayed diffuse immustaining for S100 protein. Other melanocytic markers such as HMB-45 and Melan-A were negative. (Fig. C).\nAfter the diagnosis of a metastatic lesion on the tongue, the patient was referred back to the clinical oncologist who maintained her in a palliative protocol of chemotherapy with cisplatin, dacarbazine and vinblastine (CVD). Unfortunately, the patient died due to disease progression four and a half months after the diagnosis of tongue metastasis. |
A 63-year-old male with a past medical history of non-ischemic cardiomyopathy (ejection fraction 10%-15%), hypertension, chronic kidney disease stage G3A, and severe mitral valve regurgitation status post valve repair initially presented for an upgradation of his biventricular pacemaker to biventricular implantable cardioverter defibrillator (BIV-ICD) and replacement of non-functional right atrial lead. The pacemaker pocket was exposed and identified and the atrial and ventricular leads were pulled back under fluoroscopic guidance. A new left coronary sinus lead was placed. Next, right atrial (RA) and right ventricular (RV) leads were placed and access was obtained via the left coronary sinus as the left subclavian vein was found to be occluded with formation of collaterals. The leads were sutured in fascial planes via silk suture. The pacing and sensing parameters were confirmed. BIV-ICD was placed in the pocket, and the pouch was closed via vicryl sutures. The patient had electrocardiogram (EKG) (Figure ) and chest X-ray (Figure ) performed after the procedure. He had developed small pneumothorax from the procedure, which resolved on its own.\nThe patient was asymptomatic for the next seven months and then he developed increasing shortness of breath. At that point, the EKG (Figure ) revealed loss of appropriate pacing function. It was discovered that the patient kept massaging his pacemaker pocket site in the last seven months but he denied manipulating the device itself. He had also been moving his arm up and down frequently, which would have led all his device leads to be pulled up towards the device in a ratchet-like fashion. The patient was scheduled again for revision of BIV-ICD and on incision of the generator pocket, the left ventricular lead was found coiled up in the pocket beside the generator (Figure ). A new left ventricular lead was placed in the coronary sinus and then access was obtained via the right subclavian vein for right-sided leads. His right atrial and right ventricular leads were also found pulled up. A decision was made to place new right atrial and right ventricular leads. It is to be noted that all his device leads were undamaged and his device was found to be in the pocket in normal orientation. After securing the leads via sutures, the pacing and sensing function was analyzed. The pocket was revised and closed with vicryl sutures and the device was sewn to the pectoral fascia. A chest X-ray (Figure ) and EKG (Figure ) were obtained after the procedure to ensure the absence of pneumothorax and to document the appropriate functioning of the device, respectively. |
Two swellings had rapidly developed in the upper lip of a 17-year-old female, 3 months prior to presentation at the oral surgery department with a possible history of trauma. On examination there were two firms, smooth masses in the upper lip; one present in the midline and the other on the left side () measuring 1 and 1.5 cm, respectively. The patient was asymptomatic with no history of pain or paraesthesia.\nThe results of ultrasound-guided aspiration were inconclusive with a report showing a scanty sample composed of bland spindle cells. The radiologist suggested provisional diagnoses of a peripheral nerve sheath tumour, NF or other spindle cell tumours and a core biopsy was recommended. Based on this information, an excisional biopsy of the larger lesion in the left side of the lip was undertaken ().\nThe samples showed fragments of a cellular tumour composed of fascicles of uniform myofibroblastic spindle cells set in a fibrous stroma (). The tumour exhibited infiltrative growth into skeletal muscle entrapping lobules of fat and small neurovascular bundles. Mitotic activity was 2/10 HPF and there was no necrosis, haemorrhage nor prominent blood vessels within the lesion. Immunohistochemistry showed that tumour cells were positive for smooth muscle actin (SMA) and calponin (). The samples were negative for H-caldesmon, CD34, S100, beta-catenin, desmin, myogenin and MyoD1. Studies have shown that the USP6 gene\nis a recurrent and specific finding in NF. However, molecular genetics showed that the USP6 gene rearrangement was not detected in this case. The histopathological opinion was that this was an infiltrative myofibroblastic tumour, which is difficult to classify. Molecular genetics and histopathological assessment stated that a low-grade, myofibroblastic sarcoma could not be excluded. Specialist soft tissue opinion was sought which corroborated the diagnosis.\nThe case was taken to a multidisciplinary team meeting where differential diagnoses and treatment options including surgery were discussed. Upon clinical review, however, the lesions reduced in size over the course of 1 month and were monitored with no further intervention required. With the clinical and histopathological information gathered, a probable diagnosis of NF was made. |
A 24-year-old systemically healthy female subject came with the complaint of mobile upper right central incisor []. Clinical examination revealed an endodontic-periodontic lesion in relation to 11 and the tooth was Grade II mobile. Since it was an esthetic region, extraction with an appropriate technique to achieve soft tissue augmentation over a grafted maxillary anterior extraction site was planned.\nAfter premedication, local anesthesia was secured and an atraumatic extraction was performed carefully preserving the remaining hard and soft periodontal tissues []. Following extraction, intraoral measurements were taken to harvest a pediculated CTG to cover the extraction socket. The length of the required pediculated connective tissue was calculated by the sum of three pre-recorded measurements 1. The buccolingual width of the extraction site 2. The distance between the palatal edge of the extraction site and the base of the pedicle (usually 4mm), and 3. An extra 3 mm to “tuck” the flap into the buccal gingival tissue. The width of the pedicle was determined by measuring the mesiodistal dimension of the extraction site and adding 1 mm to account for graft shrinkage. An “L-”shaped incision was given distal to the lateral incisor that extended to the mesial side of first molar. The margin of the incision was maintained at a distance of 4–5 mm from the free gingival margin to prevent marginal tissue recession at the donor site. The base of the incision was maintained at a distance of 3–4 mm from the extraction socket. A partial thickness dissection was done to facilitate harvesting the underlying connective tissue. The connective tissue was elevated with the underlying periosteum and was attached at the base close to the socket []. The isthmus between the socket and the base of the pedicle was undermined using an Orban's knife. The extraction socket was packed with bone graft (Sil-Oss®, AzureBio, Spain) and the pediculated connective tissue was tucked into the buccal pouch [] and secured with the help of sutures []. Primary closure was obtained at the donor site as well []. Appropriate postsurgical protocols were followed.\nThe patient reported to the clinic after 1 month with a complaint of dysphagia and intermittent bleeding. On examination, a 15 mm × 20 mm exophytic growth extending from the palatal donor site to distance of 3–4 mm from the extraction socket was observed []. While it appeared sessile, on manipulation, the growth was pediculated at the palatal donor site and resulted in the displacement of the “epithelial door” that essentially covers the surgical site in CTG procedures []. The growth was creamish-brown and soft and exhibited a slightly nodular surface that bled easily on slight touch. The recipient site appeared normal and no extravasation or exposure of the graft material was seen.\nAfter obtaining the subject's consent, surgical excision of the growth was planned and scheduled. Local anesthesia was administered and the growth was excised from the base []. The growth appeared to have originated mostly from the donor site and from an isthmus of CTG near the extraction socket []. Necrotized epithelial tags were excised, debris were flushed out under irrigation, and the flaps were loosely closed []. Two weeks post-excision, the sites exhibited uneventful healing []. On histopathological examination [], thin parakeratinized stratified squamous epithelium and underlying connective tissue with haphazardly arranged dense collagen fibers with numerous blood vessels lined by endothelial cell proliferation wer seen. In deeper sections, glands are evident in focal areas. Chronic inflammatory cells were also noted. These findings were suggestive of pyogenic granuloma. |
The patient is a 55-year-old right-handed female with a past medical history of previous diagnosis of chronic lymphocytic leukemia, and recurrent TB exposure presenting with new-onset daily frontal headaches. She originally presented to her primary care physician with intermittent burning left frontal headaches that were worse with exertion and without associated focal neurologic deficit. Initial neurological examination was unremarkable. MRI of the brain revealed an 11-mm left frontal lobe enhancing lesion with surrounding vasogenic edema, as well as multiple punctate bilateral cortical/subcortical enhancing lesions (Fig. ). Her headaches began to worsen in intensity and frequency and were associated with new-onset right facial tingling and intermittent bilateral upper and lower extremity pain. Extensive infectious, autoimmune, and neoplastic workup was completed and was unremarkable. Malignancy workup included CT of the chest, abdomen, and pelvis, followed by a whole-body bone scan, PET-CT, and flow cytometry which were all negative for malignancy. A summary of the infectious and autoimmune workup can be found in Table .\nThe patient was referred to neurosurgery for open brain biopsy targeting the left frontal enhancing lesion. Postoperative neurologic examination demonstrated a mild expressive aphasia with word finding difficulties. Neuropathology revealed chronic granulomatous inflammation of the brain and meninges. The granulomas noted within the meninges showed central necrosis surrounded by a rim of lymphocytes, plasma cells, and epithelioid histiocytes in addition to eosinophils and giant cells. Marked fibrosis and burnt-out granulomas were seen within both the meninges and brain tissue with dense perivascular lymphoplasmacytic infiltrate along with reactive gliosis within the cerebral cortex. These findings were consistent with chronic necrotizing granulomatous meningoencephalitis. There were no findings on biopsy consistent with mycobacterial infection.\nThe patient was treated with intravenous 1,000 mg Solumedrol for 3 days followed by a 6-week prednisone taper. Over the next 6 months, the patient remained clinically stable with mild expressive aphasia. Six months after treatment, she began having staring spells that started with a strange feeling. No EEG correlate was noted on long-term EEG monitoring; however, she was started on Lamictal for high suspicion of focal seizures, with complete resolution of symptoms. She remained clinically and radiographically stable without additional treatment for 4 years until the most recent MRI in 2018 suggesting recurrence (Fig. ). |
A 29-year-old male with a history of right tibial shaft and lateral malleolus fractures following a fall injury underwent open reduction and internal fixation with a locking plate for the fibula fracture and minimally invasive percutaneous osteosynthesis for the tibial shaft fracture at another hospital. Postoperatively, the patient was followed up at our hospital for 1 year due to residential issues, and the removal of the plate was scheduled after confirmation of bone union. According to the previous hospital’s medical records, a 9-hole locking plate (APIS®, Gwangju, Republic of Korea) was used for the distal tibia, with three 5.0-mm locking screws for proximal fixation and six 3.5-mm locking screws for distal fixation. Under spinal anesthesia, a plate removal surgery was performed, following which the fibular plate was easily removed. However, five of the six distal locking screws were damaged, and they could not be removed with a screwdriver. This situation was explained to the patient during the operation, and we could confirm that the patient wanted to remove the plate irrespective of the amount of time required. At the time, a tourniquet was used for approximately 1 h, and screw removal was attempted using a conical extraction screw, but only one of the six screws could be removed. Previously proposed techniques requiring additional skin incisions were not considered because there were multiple damaged screws that could not be removed, these techniques would require extended amount of time for removal, and the surrounding soft tissues could be damaged. Hence, we decided to use a screw extractor (IRWIN®, Huntersville, NC, USA), a non-medical instrument, following sterilization with ethylene oxide. In brief, 6-mm drill bit of the extractor was used, four screw heads were drilled, the locking screws and locking plate were separated, and the plate was removed. Of the remaining four screws, one was removed using a vice grip; the remaining three screws could not be removed with the vice grip owing to a short extruded portion. A hollow reamer could not be used because the three screws were adjacent to each other and the reamer could cause a large bone defect; hence, we created sufficient space around the screws by forming small holes around them with a 1.8-mm K-wire, following which all screws could be removed using the vice grip. After saline irrigation, debridement of the soft tissues contaminated with metal debris was performed. The sizes of the metal debris were found to be relatively large, which facilitated easier debris removal. With 2-h use of a tourniquet, all implants could be removed and the skin could be closed (). Postoperatively, no complications were noted during physical and radiological examinations. Remarkably, no problems were noted at the final outpatient visit at 3 months after discharge; therefore, follow-up was terminated. The patient had not visited an outpatient clinic for more than a year since the last follow-up, thus we thought that he had no specific complications including infection and re-fracture. |
A 39-year-old man, taxi driver, known to have hypothyroidism (being treated with levothyroxine) presented to the emergency ward with dyspnea and coughing after exposure to detergents in a closed environment. The patient was smoker (3 pack/year). The only in clinical examinations except for wheezing in the right side of chest. The patient's chest radiography identified a mass. For further investigation, a spiral computerized tomography (CT) scan was performed. Lymph nodes were enlarged on the right side of the trachea, measuring about 23 mm with a mass of 70 × 77 mm, in the vicinity of the right lung hilum. A hypodense nodule in the posterior part of the liver, suspected to be malignant, was also reported (\n). The lesions were suspected to be metastatic tumors, therefore, a biopsy of the mass was performed via bronchoscopy. The biopsy results were reported as chronic inflammation and mucosal hyperplasia without malignancy (\n), which did not conform to the CT report. The CT has repeated again, and confirmed the previous CT report. A CT guided mass biopsy was performed for pathological evaluation. The result showed chronic granulomatous inflammation, the two most likely causes being tuberculosis (TB) and sarcoidosis. Sputum smear, culture, and PCR were performed to test for TB, and angiotensin-converting enzyme (ACE) levels were measured for sarcoidosis. The results ruled out TB and showed high levels of ACE (ACE = 88 IU/L (normal 8-53)). In report of bronchoscopy, Vocal cord, trachea was normal. Carina was edematous that lead to narrowing of lumen of right bronchus. Two months after the first visit, sarcoidosis was diagnosed and treatment started with prednisolone. Ophthalmology test for eye evaluation, echocardiography for cardiac evaluation and EMG/NCV (Electromyogram test and nerve conduction study) for evaluation of the nervous system were also performed to determine if there was any extra-pulmonary sarcoidosis, however, no lesions were found. After treatment by corticosteroid the symptoms of the patient subsided. Now the patient is on follow-up.\n show the CT scan of patient after treatment. |
A 55-year-old male who had been diagnosed with HIV 1 year previously presented with a 2-week history of intermittent right abdominal pain and gross hematuria. The patient had a 2-year history of sexual intercourse with prostitutes. His medical history included hepatitis B and HIV infections. The HIV infection was well controlled with drugs. He had no significant family, allergic, or smoking history. He had not received any blood transfusions. The physical examination was unremarkable, except for a soft, non-tender mass palpated in his right upper abdomen. A chest X-ray was normal. Ultrasonography detected a mass occupying the upper half of the right kidney. A contrast enhanced computed tomography (CT) scan (Fig. ) of the abdomen revealed a large heterogeneously enhancing mass measuring ∼14 × 10 cm involving the upper right aspect of the right kidney. A microscopic urinalysis revealed red blood cells, but no white cells, and urine cytology findings were negative for urothelial carcinoma. The complete blood count and electrolyte profile were normal. No abnormalities were detected on a renal function test. No bladder tumor was observed on cystoscopy. We diagnosed the renal tumor as a renal cell carcinoma because of the hematuria, the right renal tumor, and the CT scan findings. A retroperitoneal radical nephrectomy was performed. The surgical margins were clean on histology. A microscopic examination of the tumor section revealed that the tumor was composed of round monomorphic cells with vesicular and eccentric nuclei and immature plasma cells (hematoxylin and eosin [H&E] ×200) (Fig. A). A high power view (H&E ×400) revealed plasma cells with basophilic cytoplasm, eccentric nuclei, and typical peripheral condensation of the chromatin (Fig. B). Invasion of tumor cells was observed in the pelvic mucosa, renal parenchyma, and perirenal soft tissue of the kidney. Immunohistochemical studies confirmed that the tumor was composed of plasma cells, as evidenced by their reactivity with antibodies to CD138, CD45, vimentin, Lambda light chain, CD79a, and EMA (Fig. C). The tumor was negative for Kappa light chain, CD20, CD3, CD56, CD10, smooth muscle actin, and creatine kinase. Further postoperative investigations were performed. No high levels of monoclonal protein were found in the blood or urine. The bone marrow aspiration findings were normal, and a skeletal X-ray revealed no lytic lesions. Eventually, the patient met all of the required clinical and laboratory criteria for a solitary EMP. Adjuvant radiation therapy was given at doses of 50 Gy in 20 fractions. He is alive and disease free 7 months postoperatively. |
An 81-year-old white man experienced decreased vision and redness in his right eye that worsened over 3 weeks. Past medical history was significant for multiple sclerosis in 1950 with bilateral optic neuritis in remission, cerebrovascular accident in 2000, hyperlipidemia, and diabetes. Granulomatous anterior segment inflammation and a central retinal artery occlusion of the right eye were noted by an outside ophthalmologist. Serum CMV IgG antibody and varicella zoster antibody were positive. CMV IgM antibody, HSV I and II IgG antibodies, and syphilis antibody were negative. Carotid artery stenosis was 70% to 80% on the right and 50% on the left on carotid Doppler ultrasound. Varicella-related necrotizing retinitis was suspected, and famciclovir 500 mg three times daily was initiated.\nOn referral 2 months after onset, vision was counting fingers at 6 feet in the right eye and 20/20 in the left eye with a 2+ relative afferent pupillary defect in the right eye. There were large white keratic precipitates on the right corneal endothelium, 2+ anterior chamber cell, and 1+ flare. On dilated examination of the right eye, the optic nerve was pale, with sclerotic, attenuated arterioles, segmentation of the venous blood columns, and no evidence of recanalization (Figure ). There was a patchy, granular retinitis in the inferotemporal quadrant. The diagnosis of necrotizing retinitis with central retinal artery occlusion was made. The left eye was free of inflammation.\nDiagnostic AC paracentesis for PCR for CMV, varicella zoster virus, and herpes simplex virus was positive for CMV DNA only. HIV serology was negative. An intravitreal injection of foscarnet was given and oral valganciclovir was started. Three months later, there was florid neovascularization of the iris. The retinitis was inactive. Bevacizumab was injected intracamerally, and PRP was performed with regression of the NVI. Vision remained stable at hand motions. Valganciclovir was continued at 450 mg daily adjusted for renal function to complete 3 months of treatment. |
A 75-year old healthy female presented with a 2-week history of a paracentral scotoma in the right eye without symptoms in the left eye. On initial examination, funduscopic examination showed cream-colored deep lesions in the posterior pole in the right eye and several plaque-like deep choroidal lesions in the left eye. FAF demonstrated hyperautofluorescent lesions surrounded by a hypoautofluorescent ring in the right eye and no abnormal hyperfluorescence in the left eye (). She underwent a negative infectious work-up and was started on prednisone 50 mg daily with a slow taper.\nOne month later, fundus photos revealed complete resolution of the previously noted cream-colored lesions in both eyes. Following disease resolution, FAF showed hypoautofluorescent lesions with fewer reticulated areas of hyperautofluoresence in the right eye and no abnormal autofluorescence in the asymptomatic left eye. The absence of FAF findings in the left eye despite fundus photo and ICG evidence of disease suggested that the disease process was choroidal in nature, with secondary involvement of the outer retina and RPE, as evidenced by changes in the FA and FAF of the right eye. Specifically, FA demonstrated staining of the lesions in the right eye, while the angiogram was normal in the left eye. ICG showed areas of choroidal vascular dilation with irregular borders in the right eye without hypocyanescent lesions.\nThis patient was atypical in her older age at onset of the disease and absence of symptoms in the left eye at presentation. Given that the left eye did not have overlying RPE or photoreceptor disruption, this slightly asymmetric presentation at onset suggested that her disease was still evolving in the left eye at the time, and improved following corticosteroid treatment. Coxsackievirus B titers (CVB2 1:320; CVB4 1:80) were elevated during the course of her disease. She was tapered off prednisone over the next four months and maintained inactive disease without recurrence. |
A 3-month-old male was seen in our pediatric oncology department because of a growing parotid gland mass. The mass was congenital and was followed by the pediatric oncology team with a prediagnosis of hemangioma. The patient’s magnetic resonance imaging (MRI) scan showed an infantile hemangioma in the proliferative phase filling the parapharyngeal space ().\nThe child then received propranolol therapy, but despite this treatment the mass continued to grow, and the child was referred to our department at the age of 10 months. The otorhinolaryngological examination revealed an 8×7-cm mass filling the left parotid region, with normal facial nerve motor functions (). Histopathological diagnosis of the mass was provided by an incisional biopsy as sialolipoma.\nWe planned to perform total excision of the mass with a transparotid approach. The facial nerve was monitored intra-operatively, and surgery was performed under magnification using surgical loops. A standard modified Blair incision was used, flaps were raised (), then the facial nerve was identified in a standard fashion using a tragal pointer and posterior belly of the digastric muscle as landmarks.\nThe main trunk of the facial nerve was found to be unusually elongated before pes anserinus. A soft lobular mass was encountered. A tumor involving the superficial parotid lobe was first dissected, then the deep lobe of the parotid gland and portion of the tumor filling the parapharyngeal space were gently dissected under the facial nerve (). A Jackson-Pratt drain was inserted into the wound after the excision of the tumor.\nOn macroscopic examination, the mass was found to be a lipomatous specimen, 9×8×4 cm in size. The cut surface was consistent with the appearance of a lipoma. Histopathologic examination confirmed the diagnosis of a sialolipoma. The lesion was composed of mature adipose tissue mixed with acinar, ductal structures of a normal salivary gland ().\nThe postoperative period was uneventful. The patient’s facial nerve motor functions were well preserved, and he was discharged on the third postoperative day. The patient is still followed, and has no signs of recurrence in his 24th postoperative month. |
A twenty-seven-year-old male presented to the Emergency Room (ER) with the alleged history of ingestion of an unknown poison, amount unknown, ten hours back following a family dispute. The patient immediately had two episodes of vomiting and then gradually developed altered sensorium in the form of drowsiness within two hours of ingestion of the poison. On examination in the ER, the patient had a Glasgow coma scale score of 9/15 (E2V2M5). Vital signs revealed a radial pulse of 50 beats per minute, blood pressure 90/50mm Hg, respiratory rate 16 breaths/minute, the temperature of 97.2 degrees F and oxygen saturation of 86% in room air. His pupils were constricted bilaterally and sluggishly reacting to light. His chest auscultation revealed bilateral vesicular breath sounds, the abdomen was soft with normal bowel sounds on auscultation. Deep tendon reflexes were present with down going plantars.\nThe patient was provided oxygen at two litres per minute via nasal cannula, his oxygen saturation improved to 96%. He was managed by administering immediately a bolus dose of 500ml of 0.9% of normal saline and an intravenous dose of atropine 0.6mg following which his heart rate increased to 96 beats per minute showing a normal sinus rhythm in the 12 lead electrocardiogram and was normotensive. His investigations comprising a full blood count, renal function tests, a random blood sugar level, liver function tests, and a coagulation profile were all within normal limits. Arterial blood gas (ABG) analysis did not reveal any abnormalities and a serum cholinesterase level was within normal limit.\nSix hours of close monitoring with continuous supportive management resulted in the patient opening his eyes spontaneously with a purposeful response to verbal stimuli. His Glasgow coma score improved to 15/15 and his symptoms resolved over the next 12 hours. During his stay, he did not develop any convulsions, respiratory depression or hypothermia. His bowels moved on the second day of admission and his urine output was normal throughout his stay. His blood glucose, measured every six hours for 24 hours and then every 12 hours, did not reveal hyperglycemia. An empty bottle of the pesticide amitraz 12.5% recovered from the patient’s room was brought along by the patient’s relative to which the patient agreed having ingested two teaspoonful of it. He was kept under observation with strict hemodynamic monitoring for the next three days which was uneventful. He was finally discharged from the hospital on the fourth day in good health. |
Our patient was a 17-year-old adolescent girl with an extensive past medical history that included aortic atresia with a ventricular septal defect (VSD), atrial septal defect (ASD), an interrupted inferior vena cava with drainage to the left superior vena cava, heterotaxy with dextrocardia, ventricular ectopy, pulmonary hypertension and polysplenia. She had an equally extensive surgical history that included Norwood arch reconstruction, VSD closure and conduit revision, Rastelli repair of unroofed coronary sinus, pacemaker implantation for sick sinus syndrome and lastly a cardiac catheterization with a placement of a pulmonary artery stent. Her last cardiac procedure (placement of the pulmonary stent) was 20 months prior to this episode. Socially, she is an active well developed adolescent school girl, who has met all her developmental milestones at the appropriate times and is looking forward to graduating from high school to start college in a few months’ time. She initially presented to her cardiologist with 2 weeks of intermittent fevers. The cardiologist confirmed that she was pale and had dusky nail beds. No new murmurs were heard and a transthoracic echocardiogram showed no vegetation. She later presented to her primary care physician for continuing fever and associated fatigue. Urine and blood cultures were negative for bacterial growth. Co-incidentally she had dysmenorrhea with menorrhagia for which her gynecologist started her on oral contraceptive therapy along with iron supplements for iron deficiency anemia that was confirmed by laboratory studies. Since she was still febrile and fatigued, now with a 4 kg weight loss in 4 weeks, she was hospitalized for further evaluation. She appeared pale, had night sweats, myalgia, and chest pain. Her last dental cleaning was 4 months prior, and was done with appropriate antibiotic prophylaxis. She did not have a history of excessive intake of dairy products, nor was she on any probiotics. Physical examination revealed a tired looking pale teenager who was hemodynamically stable without any respiratory problems. Laboratory studies showed a normal total white blood cell count with mild predominance of neutrophils without any immature forms. She was anemic, with iron deficiency and had normal electrolytes, renal function and hepatic function. A cardiac CT scan showed non-occlusive vegetation in the pulmonary artery (at the root of the conduit) and a pulmonary septic embolus in the left lower lobe. Subsequent transthoracic echocardiogram confirmed the vegetation in the pulmonary artery. Two peripheral blood cultures were drawn upon admission to the hospital, one of which grew gram-positive rod like bacteria after 76 hours (3.2 days). The blood culture on the second day since admission also grew gram-positive rod like bacteria after 107 hours (4.5 days). All subsequent blood cultures were reported as no growth. She was started on empiric antimicrobial therapy with ceftriaxone and vancomycin dosed appropriately for endocarditis; and gentamicin for synergy at 1 mg/kg every eight hours. She also received a 5 day course of azithromycin for positive Mycoplasma serology (IgG and IgM). On day 6 the microbiology laboratory reported a preliminary identification of the gram positive rod like bacterium as Arcanobacterium haemolyticum, and therefore gentamicin and vancomycin were discontinued, and she was continued on ceftriaxone.\nHowever, she was re-hospitalized after 7 days, for persistent and now almost continuous low grade fever with occasional high grade spikes and associated night sweats. A transthoracic echocardiogram now showed the vegetation to be of the same size and the ESR and CRP had increased. At that time, which was about two weeks since antibiotics inception; the final identification of the gram positive rod like bacterium was reported to be Lactobacillus by Matrix-Assisted Laser Desorption and Ionization method. The organism could not be further speciated and the susceptibility studies revealed the organism to be susceptible to ceftriaxone, clindamycin, daptomycin, erythromycin, gentamicin, linezolid, penicillin and vancomycin (). Due to high risk for morbidity and mortality with repeat cardiac surgery in our patient, aggressive antimicrobial therapy was pursued with full dose gentamicin 2.5 mg/kg every 8 hours, clindamycin 10 mg/kg every 6 hours and penicillin 24 million units (adult dose) as continuous infusion daily. Our patient improved clinically with her fever trending down. She was later discharged, and continued on the aforementioned regimen for 4 weeks. She became afebrile after week 4 of therapy, after which gentamicin and clindamycin were discontinued. Penicillin infusion was continued until the end of week 6. The transthoracic echocardiogram 11 months after the onset of her illness shows the vegetation to be less than half its original size. One year later, our patient has remained asymptomatic, anemia has resolved, she has gained weight and is back to school. |
A 23-year-old female was admitted to our department with dull pain and feeling of weight in the left upper abdomen which increases in the upright and prone position and after meals. Her medical history began about 2 years ago when she was admitted to a different surgical Department with the same symptoms; the CT scan revealed a large well-defined cystic mass of 15 × 12 cm in size in the upper pole of the spleen. Elective laparoscopic decapsulation was performed along with puncture of the cyst in order to reduce its size. At histological examination, the cyst was composed of a thick fibrous tissue wall lined by a stratified squamous epithelium. After 5 months of follow-up, a CT scan demonstrated a recurrent cystic lesion; subsequently, the patient turned to another surgical team who performed further laparoscopic decapsulation with drainage of the lesion. In this case, the microscopic examination of the removed wall fragment showed a coating of squamous epithelial cells. Eight months later, the patient complained again of pain and sense of weight in the same location, and a CT examination revealed the second recurrence of the cyst. She came to our attention 10 months later. On the clinical examination, pre-existing surgical scars were noted, and deep palpation of the left hypochondrium evoked an intense pain. After preliminary tests, an abdominal CT scan with intravenous contrast was performed that confirmed the recurrent splenic mass (7.7 × 8.5 cm), disclosing absence of calcifications, no contrast uptake, no involvement of splenic vessels, and the presence of satellite nodules, without compression of the spleen, pancreas, and left kidney (Fig. ). Serological examinations allowed us to rule out parasitic and viral etiology (Echinococcus granulosus, Epstein Barr Virus, Human Herpes Virus 1/2, Cytomegalovirus), and showed slight anemia (HGB 10.80 g/dL, HCT 32.40 %, MCV 62.50 fl) and a normal white blood cell count (5.7 × 103/uL). For the first time, compared to the previous blood findings, the level of the CA19-9 was raised to 54 UI/ml (normal range 0–37 UI/ml). In agreement with the hematologists, we decided to undergo the patient to open splenectomy (elective laparotomy and splenectomy) due to the size and site of the cyst, after a vaccine prophylaxis of 1-month duration with administration of Pneumo23, Mencevax, and Acthib. Macroscopically, the fully resected spleen weighed 770 g, with dimension of 18 × 13 × 7 cm, and was almost totally replaced by the large cyst. Histological examination disclosed a large multilocular cyst with fibrous walls lined on their inner surface by squamous epithelial cells with no nuclear atypia, which were immunohistochemically positive for epithelial membrane antigen (EMA), carcinoembryonic antigen (CEA), and CA19-9 (Fig. ). The final pathological diagnosis was an epidermoid cyst of the spleen. No perioperative and postoperative complications occurred. The patient was discharged on the fifth postoperative day with all the blood parameters within the normal range, including CA19-9. |
In 2002, a 54 year old man presented with mild heart-burn. Incidental "hepatomegaly" was found on examination accompanied by a slightly elevated bilirubin but otherwise normal liver function. A computerized tomography (CT) scan reported a well defined cyst arising from the right lower pole of the liver, measuring 14 × 12 × 10 cm (figure ). Hydatid was excluded and the cyst was thought to be simple and benign, due to the absence of calcification. It was decided to treat this conservatively and the patient was discharged.\nFour years later, he re-presented with a 5-month history of intermittent dull right sided abdominal pain and a right sided palpable abdominal mass was palpated. Liver function tests revealed a bilirubin of 29 but no other abnormalities. His α-feto-protein was 3 and CA 19.9 was 22129.\nThe repeat CT scan concurred with the previous scan, reporting a large benign cyst, with a maximum diameter of 16 cm. Figure demonstrates the CT with the cyst, and the marker is the measure of the maximum diameter. Endoscopic ultrasound demonstrated a frond-like mucosal prominence within the cyst wall lining.\nAt laparotomy, the cyst was found to be retroperitoneal lateral to the right psoas muscle, displacing the pancreas and duodenum medially, the liver superiorly and the right kidney and ureter inferiorly. It did not appear to be arising from any particular organ. An attempt at complete excision was successful but there was some spillage of viscous cyst fluid. The abdominal cavity was thoroughly lavaged with water, followed by saline.\nHistology reported an invasive mucinous cystadenocarcinoma with clear circumferential margins and due to the nature of stratified columnar epithelium (figure ) and high CA 19.9, it was considered to be of pancreatic or biliary origin.\nThis conclusion was not entirely satisfactory due to the lack of specificity of CA 19-9 as a mucinous tumour marker. Also, the CT scans and operative findings were reviewed retrospectively and it was confirmed that the cyst was not involved with the pancreatic or biliary tree. It was thus concluded that this was adenocarcinomatous change within an enterogenous cyst as there was smooth muscle lining the walls with cytokeratins CK20 and CK7 both positive, suggesting a fore-gut origin. Figure is a picture of the histological slide. Also, there was clear carcinomatous change in a plaque within the cyst wall with no penetration from the outer lining described, suggesting no external origin of the malignancy. The patient was to be given Fluoropyrimidine and oxaliplatin following recovery from surgery.\nWith such a rare condition there is no evidence base for the role of adjuvant chemotherapy. A discussion was had with the patient regarding the possible benefits and risks of adjuvant chemotherapy. In view of the immunohistochemical findings the use of a regimen containing a fluoropyrimidine and oxaliplatin was recommended. Within 3 weeks of surgical excision, the patient developed back pain radiating down the right lower limb. He also had an intermittent fever. He was admitted to hospital and commenced on intravenous antibiotic therapy with a working diagnosis of an infected psoas abscess. However, serial blood cultures grew no organisms. A CT scan demonstrated multiple lesions in the right psoas muscle (Figure ). Two sequential CT guided fine needle aspirations of these lesions were performed and both revealed cellular appearances suspicious of metastatic adenocarcinoma. The immunohistochemical profile performed on these aspirates was not conclusive. Consequently a laparotomy and open biopsy of these lesions was performed. Unfortunately, multiple peritoneal deposits were apparent at laparotomy. The biopsy demonstrated metastatic adenocarcinoma similar to the original enterogenous cyst with the same differential cytokeratin profile. The Ki67 proliferation fraction was over 80%. His performance status deteriorated greatly, thus preventing the administration of palliative chemotherapy. He died of metastatic disease, 6 weeks following resection of the cyst. |
A 53-year-old male, chronic smoker, presented with history of left-sided dull aching chest pain for 1 month and significant weight loss of 5 kg in 1 month. There were no symptoms of breathing difficulty, hemoptysis, bony pains, or lumps noticed anywhere in body. Evaluation included a contrast-enhanced computed tomography (CT) of thorax which revealed a left upper lobe peripherally situated mass of size 2 × 2 cm involving chest wall, enlarged pretracheal, prevascular, and aortopulmonary window nodes, and mild left pleural effusion.\nThe common differential diagnoses for weight loss and lung mass with lymphadenopathy in a male smoker in our country are chronic obstructive lung disease, chronic bronchitis, tuberculosis, pneumonia, and lung cancer. Clinical history and thorough examination should be made with careful palpation of the neck for lymphadenopathy and chest auscultation. A chest radiograph is the basis of imaging and is complemented by a contrast-enhanced CT scan of the chest, which should include the liver and the adrenal glands. Tissue diagnosis is mandatory if the clinicoradiological suspicion of malignancy is high and a biopsy should be performed either by bronchoscopy or with CT guidance. If confirmed to be malignant, further staging workup would be required if the chest CT scan shows non-metastatic disease. A metastatic workup would include a positron emission tomography (PET)-CT scan and a magnetic resonance imaging (MRI) scan of the brain.\nOur patient presented to us with a CT scan showing a left upper lobe mass with ipsilateral mediastinal lymphadenopathy and a small pleural effusion. His vitals were normal, physical examination was unremarkable, and ECOG performance status was 1. Fiber optic bronchoscopy showed no endobronchial growth. Diagnostic thoracentesis was performed. Pleural fluid cytology was positive for metastatic squamous cell carcinoma.\nConventional cytologies such as sputum examination, bronchial lavage, bronchial brushings, fine-needle aspiration biopsy have played an important role in the diagnosis of primary and metastatic lung cancers. Immunohistochemical stains can be applied on cytological material. The immunohistochemical markers such as TTF-1, CK7, CK20, 4A4, 34 E12, and p63 help to classify further subtypes in Non-small cell lung cancer (NSCLC). In addition, epidermal growth factor receptor (EGFR) gene mutation studies can also be done on the blocks prepared from cytological material, which helps in choosing appropriate targeted therapy. Thus, cytology plays an important role not only to subclassify tumors but also to individualize treatment strategy with the advantage of easy availability and minimum invasiveness.[]\nThus, the patient was diagnosed with squamous cell carcinoma of the lung, T3N2M1a, stage IV. |
A 44-year-old female had been suffering from dry cough, myalgia, and arthralgia since 2013 and was diagnosed as DM (Table ). Her symptoms were abated by combination treatment using prednisolone and tacrolimus. However, the cough, pyrexia, and arthralgia recurred due to the exacerbation of DM. The patient was admitted to our hospital for further checkup and treatment. Laboratory data showed that her white blood cell count and C-reactive protein levels were elevated. Her serum carcinoembryonic antigen and carbohydrate antigen 19-9 were not elevated (Table ). Enhanced computed tomography showed a 20-mm low-density tumor with a gradual enhancement in segment 4 of the liver (Fig. ). Ultrasonography showed a 20-mm tumor in segment 4 of the liver (Fig. ). In magnetic resonance imaging (MRI), the tumor had a weak signal intensity on T1-weighted images and a strong signal intensity on T2-weighted and diffusion-weighted images. In the dynamic study of MRI, enhancement of the edge of the tumor was gradually increased from the early to the late phase (Fig. ). Following the diagnosis of ICC in segment 4 of the liver, hepatic medial segmentectomy and cholecystectomy were performed. In the resected specimen, macroscopic findings consisted of a solid hepatic tumor with the diameter of 35 × 25 × 21 mm (Fig. ). The pathological diagnosis was moderately differentiated adenocarcinoma with vascular invasions and without lymph node metastasis (pStage III). The tumor consists of cells with coarse chromatin (Fig. ). Many of the tumors have tube formation and immunohistological findings of intrahepatic ICC and moderately differentiated adenocarcinoma with CK7 (+), CK 19 (+), and CK 20 (–) (Fig. ). The patient made a satisfactory recovery with no postoperative complications and was transferred to the Department of the Internal Medicine to treat DM with tacrolimus 5 mg/day and prednisone 20 mg/day. The patient was discharged on postoperative day 23. Since this case was a high-risk case of stage III with vascular invasion, adjuvant chemotherapy using S-1 for 6 months was performed. The patient has remained well without recurrence of ICC or relapse of DM after hepatic resection. |
A 13-year 8-month-old female presented to our orthodontic clinic, with a chief complaint of “a labially positioned upper right canine”. The patient had a nonrelevant medical history, her dental history showed extraction of upper right first permanent molar and remaining roots of upper left first permanent molar.\nExtraoral examination revealed that the patient had a fairly symmetrical face; her upper midline was shifted to the right 2 mm in relation to the facial midline. She had normal incisor show during smiling. The patient showed a convex profile with a retruded chin, decreased lower face height, protrusive and incompetent lips.\nIntraoral examination revealed that the patient had a poor oral hygiene, with some carious teeth. All permanent teeth were present through second molars except for the extracted upper right first molar and the upper left first molar which was in a nonrestorable status. Upper right canine was labially positioned, upper right second premolar was rotated, and upper left second premolar was in a crossbite. Canine was in Class II relationship on the left side. Right molar relationship could not be determined because of the missing upper right and left first molars. Canine relationship could not be determined on the right side due to the labially positioned upper canine. The overjet was 4 mm with 20-40% overbite. The lower midline was shifted 1 mm to the right in relation to facial midline. There was 3-mm crowding in the lower arch. There was no crowding in the upper with most of the space of extracted upper right first molar lost before starting treatment. Bolton analysis revealed 1.5-mm anterior mandibular excess [Figures and ].\nThe Panoramic radiograph revealed normal morphology of the condyles, no bone pathologies. All permanent teeth are present, including the four wisdom teeth, except for the extracted upper right first permanent molar and the nonrestorable upper left first permanent molar [].\nCephalometric analysis showed a skeletal Class II relationship, hyperdivergent mandibular plane, slightly decreased lower facial height. Upper and lower incisors were proclined and protruded. Upper and lower lips were protrusive in relation to E line of Ricketts[] with a normal nasolabial angle [ and ].\nThe problem list included: skeletal Class II, left side Class II canine relationship, bimaxillary dentoalveolar protrusion, increased overjet (4 mm), crowding in lower anterior teeth (3 mm), deviated upper midline to the right (2 mm) and lower midline to the right of facial midline (1 mm), lower left second premolar is in crossbite, anterior Bolton excess in lower anterior teeth, protrusive and incompetent lips.\nThe treatment was aiming at correcting the inclination and position of upper and lower anterior teeth to resolve the bimaxillary dentoalveolar and lip protrusion, resolving mandibular crowding , achieving minimum overbite and overjet, correcting tooth mass discrepancy, achieving Class I buccal segment relationships, and correcting crossbite of lower left second premolar.\nExtraction of lower first molars, distalization of the maxillary and mandibular premolars, the use of miniscrews for en-masse retraction of the upper and lower anterior teeth, finishing and detailing followed by retention.\nExtraction option was important to resolve the bimaxillary dentoalveolar protrusion and crowding. The option of extracting the lower first molars and distalization in the upper arch will achieve better posterior interdigitation over extracting first premolars in the lower arch which will lead to lower molar opposing upper premolars.\nThe mandibular first molars were extracted. The patient received 0.018-inch Roth preadjusted edgewise appliance. Initial leveling was accomplished with 0.016- inch nickel-titanium (Ni-Ti) arch wires. After leveling and alignment, two orthodontic miniscrews (Dual Top; Rocky Mountain Orthodontics Inc, Denver, CO), 1.6 mm in diameter and 6 mm in length, were placed in the interdental space between the maxillary canines and the first premolars buccally. Active open Niti coil spring (3M Unitek, Monrovia, CA) inserted between the canines and the first premolars, the two canines where then ligated to the miniscrews using 0.010-inch stainless steel ligature wire. In the lower arch a “V” bend was done in the 0.016 × 0.016-inch stainless steel arch wire just mesial to the lower second molars (tip back) for anchorage. A power chain was extended from the first and second premolars to the second molar on both sides [Figures and ].\nAfter completion of distalization of upper and lower premolars, the miniscrews were removed and new miniscrews with the same specifications were inserted mesial to the second molars in the upper and lower arches.\nEn masse retraction was started in the upper and lower arches using 0.016 × 0.022- inch stainless steel arch wire, with a medium size Niti closed coil spring (3M Unitek, Monrovia.).\nThe minscrews in the lower arch failed. New ones were inserted between the first and second premolars []. After the completion of retraction, 0.017 × 0.025-inch stainless steel finishing arch wires were used. During the finishing stage, the patient was instructed to use ¼-inch, 3.5-oz box elastics bilaterally to improve interdigitation.\nThe case was finished with normal overbite and overjet. The arches were well coordinated. The maxillary and mandibular dental midlines were coincident with the facial midline. The bimaxillary dentoalveolar protrusion was resolved [Figures -]. Retention was done using upper wrap-around retainer and lower fixed 3-3 retainer.\nPre- and post-treatment cephalometric tracings superimposition showed retraction of maxillary incisors (6 mm). The mandibular incisors were retracted (5 mm) with 10° retroclination. Maxillary superimposition shows retraction of upper incisors 5 mm. The upper second molar moved backward 5 mm. Mandibular superimposition showed 5 mm retraction of the lower incisors. The lower second molar moved forward 5 mm [Figures and ].\nThe ANB angle changed from 5° to 4°, as shown in . |
A 31-year-old female, gravida 2, para 2 (G2 P2), referred to the gynecologic clinic with a main complaint of secondary infertility during the last twelve months. Written informed consent was obtained from the patient for publication of this case report and any accompanying images. The patient had two previous C-sections. Her menstrual cycles were ovulatory. Spermogram was unremarkable and hormonal assay did not show any abnormality. HSG was performed and revealed a migrated copper IUD with its long tail out of the uterine cavity (Fig. ). Plain abdominopelvic radiography also indicated a rotated T-shaped IUD in the pelvis (Fig. ). A transvaginal ultrasound was also performed by a skilled radiologist who reported a copper IUD in the bladder lumen with a small portion of it within the bladder musculature. The patient had taken multiple courses of antibiotics for urinary tract infection (UTI), but her symptoms never disappeared. The patient also underwent cystoscopy for recurrent infection last year, but no pathological finding was detected. Eventually, the patient said that her symptoms were related to the possible adhesions following two previous operations. The patient had a history of IUD insertion following her last C-section about eight years ago. After three years, however, the patient decided to remove it due to recurrent vaginal secretions. Three years later, her IUD was expelled, and another copper IUD was inserted. The patient removed the other copper IUD for becoming pregnant about two years ago. The patient was very confident of its removal, but her recent HSG, interestingly, demonstrated a rotated copper IUD in the pelvic cavity. Physical examination was essentially normal. A baseline complete blood count, urea, and creatinine levels were normal. The patient was candidate for a hysteroscopic cystoscopy. Hysteroscopy was normal except for a small fibrotic defect at the lower segment of the uterus. During cystoscopy, the long tail of the copper IUD was found on the posterolateral border of the bladder far from ureteral offices (Fig. ). The two short arms adhered to each other were embedded in the mucosal and muscular layer (Fig. ). No calculus was observed within the bladder cavity. Using glycine as the media, a mono-polar loop entered the bladder. A gentle and brief cautery was applied on the mucosa where the shadow of a short arm of the device was observed. The copper IUD was safely removed through the urethra using a special grasper. There was no major defect in the place of the copper IUD in the bladder. The bleeding points were effectively cauterized (Fig. ). The patient was discharged the next day with an indwelling catheter. After catheter removal, the patient did not complain of any urinary symptoms. |
A 49-year-old woman consulted our hospital because of sudden onset of headache and vomiting. Physical examination found the World Federation of Neurosurgical Societies grade II with systolic blood pressure of 152 mm Hg. No morphological features were identified suggesting congenital structural vascular disease such as Ehlers–Danlos syndrome or Marfan's syndrome. Her past history and family history were unremarkable, and systemic evaluation demonstrated no abnormality. Most laboratory data on admission were unremarkable including white blood cell count of 11.3 × 103/mm3, C-reactive protein level of 0.3 mg/dL, and negative findings for human immunodeficiency virus and syphilis. She smoked 10 cigarettes per day and occasionally consumed alcohol. Computed tomography (CT) of the head revealed SAH [] and cerebral angiography showed a saccular aneurysm at the C1 portion of the left internal carotid artery (ICA) [].\nThe patient underwent emergent clipping of the typical saccular aneurysm which had no features of dissection []. Norepinephrine was continuously administered intravenously between 1.8 to 4.8 μg/min during the operation under general anesthesia to prevent any decrease in blood pressure caused by increased remifentanil hydrochloride dose. The postoperative course was uneventful without neurological deficits. Postoperative natural hypertension was permitted and systolic blood pressure was controlled between 130 to 160 mm Hg without continuous intravenous administration of norepinephrine. However, 4 days after the SAH, the patient suddenly developed shock after severe abdominal pain. CT of the abdomen revealed massive hematoma in the abdominal cavity around a splenic artery aneurysm, suggestive of the origin of bleeding []. In addition to this lesion, three-dimensional CT angiography of the abdomen showed multiple aneurysms involving the gastroduodenal artery, common hepatic artery, and superior mesenteric artery []. Blood transfusion for shock and coil embolization of the splenic artery to prevent bleeding were performed immediately. Extensive laboratory analysis was performed with negative myeloperoxidase-anti-neutrophil cytoplasmic antibody, proteinase 3-anti-neutrophil cytoplasmic antibody, and anti-nuclear antibody. The diagnosis of abdominal lesions was compatible with SAM based on the combination of clinical and imaging findings and absence of laboratory findings indicating infection or inflammatory etiology.\nTreatment for cerebral vasospasm following SAH was performed with prevention of hypertension, which might be contraindicated in the presence of abdominal lesions. She was given oral and continuous intravenous administration of calcium antagonist to maintain a systolic blood pressure of 100–140 mm Hg. Left temporal lobe infarction was detected, but the patient was discharged after 1 month hospitalization with mild aphasia which recovered completely afterward. The patient remained asymptomatic for 34 months after SAH and CT angiography of the head and abdomen demonstrated no recurrence of the aneurysms in both visceral and intracranial arteries. |
A 33 year-old woman presented with abdominal pain in 2018. Computed tomography (CT) imaging revealed a 3.9 × 3.7 cm heterogenous soft tissue mass in the ascending colon near the hepatic flexure with invasion of the right anterior pararenal fascia and the second/third portion of the duodenum. There were associated enlarged and necrotic portacaval and mesenteric lymph nodes and a 1 cm hypodense lesion in the right hepatic lobe. Colonoscopy with biopsy confirmed a diagnosis of adenocarcinoma, and subsequent immunohistochemistry (IHC) showed loss of MLH1 and PMS2 gene expression consistent with MSI-H/dMMR. The patient was started on 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX), but continued experiencing symptoms of partial bowel obstruction including severe nausea, emesis, abdominal pain and dizziness from hypovolemia. CT imaging at this time is shown in . Given no evidence of response to chemotherapy for 2 months, she was transitioned to pembrolizumab (anti-PD-1). Shortly after initiation of pembrolizumab, she developed a partial large bowel obstruction secondary to the tumor. This was relieved by placement of a percutaneous gastrostomy tube and she was started on total parenteral nutrition (TPN) and resumed immunotherapy. Following three cycles of immunotherapy, imaging was consistent with partial response in the primary tumor and associated lymph nodes and the patient was also able to transition to an oral diet. However, after 8 months on immunotherapy she developed complete bowel obstruction, though imaging showed continued response in the primary tumor and metastases. The bowel obstruction was thought to be from adhesions and inflammatory changes and not progression of the patient's primary disease. Following multidisciplinary discussions between the patient and her treatment team including Medical Oncology, Surgical Oncology, and Palliative Care, the decision was made to proceed with surgical intervention. She underwent an internal colonic bypass with anastomosis of the cecum to the transverse colon bypassing the inflamed segment. She recovered without complications and was able to resume oral alimentation with resumption of pembrolizumab monotherapy. At the time of this report, 14 months since initiating pembrolizumab, imaging demonstrates continued partial response on immunotherapy (). |
A 51-year-old African American female with a medical history significant for diabetes mellitus and NHL presented to the medical emergency room with complaints of dizziness for nearly 12 hours. The patient stated that she noticed the abrupt onset of dizziness while at rest, which she described as persistent and not related to changes in position. She denied any nausea, vomiting, headaches, fevers, chills, abdominal pain, and fatigue. She denied the use of any medications at home as her diabetes mellitus was diet controlled. She was recently diagnosed with NHL 2 months before, and was currently being evaluated by her oncologist for varying therapeutic options. She denied the use of any illicit drugs, tobacco, and alcohol. Family history was noncontributory, including the absence of any malignancy.\nIn the emergency room, the patient was lethargic, pale, and appeared to be in moderate distress. Vital signs recorded on initial examination revealed the presence of hypotension and tachycardia, with fluid resuscitation only modestly increasing the patient's systolic blood pressure to 80 mm Hg. Physical examination was remarkable for moderate abdominal distention with marked hepatosplenomegaly. There was no abdominal tenderness noted.\nComplete blood count (CBC) was significant for hemoglobin of 6.1 g/dL, hematocrit of 19 percent, and a platelet count of 41,000/mm3. An emergent chest radiograph revealed the presence of an elevated right diaphragm, likely secondary to marked hepatosplenomegaly. Prior to the initiation of further diagnostic and therapeutic interventions, the patient was again noted to be hypotensive with a systolic blood pressure of 60 mm Hg. The patient was now minimally responsive with absent peripheral pulses, thus cardiopulmonary resuscitation was initiated. Despite numerous therapeutic interventions such as the administration of vasopressors, mechanical intubation, and other measures outlined in Advanced Cardiac Life Saving (ACLS) protocols, the patient expired.\nAn autopsy performed revealed a markedly enlarged spleen measuring 30 cm × 20 cm × 10 cm, weighing 6400 grams, with multiple foci of capsular lacerations noted (). Hemoperitoneum of fresh and clotted blood amounting to approximately 1000 mL was also noted. Histopathologic examination of splenic tissue showed massive nodular infiltration of the spleen by small cleaved lymphocytes (Figures and ). Immunohistochemistry results supported the diagnosis of NHL of mantle cell type (Figures and ; ). |
Patient 10 (Tables and ), a 76-year-old female, was referred to the department of neurology in July 2012 because of progressing cognitive decline over the last 12 months, loss of weight, nausea, gait disturbance and tremor. She was seen on May 2011 for the first time by a neurologist with a 3-month history of dull holocephalic headache who ordered a cranial magnetic resonance imaging (MRI) and diagnosed a tension-type headache and a depressive disorder. Treatment with an antidepressant (duloxetine) was started. The patient experienced no improvement and a second examination by another neurologist was undertaken 2 months later. Again no focal neurological signs could be detected. Due to the weight loss, an occult neoplasm was suspected but not detected during an extensive inpatient investigation at a medical department during February 2012; however, the MRI showed bilateral white matter lesions (WML) and an old lacunar lesion located at the left striatum, the latter was not seen in the previous MRI from May 2011. Since the patient also suffered from mild hypertension, vascular encephalopathy was thought to be the cause of the progressive cognitive decline. Extensive neurocognitive testing was carried out in a rehabilitation centre in May 2012 and disclosed a severe decline of attention, memory and executive functions corresponding to subcortical dementia (Fig. ). When the patient was seen for a further diagnostic work-up at the SMZ-Ost-Donauspital in July 2012, the weight was 47 kg and a weight loss of 20 kg was reported over the past year. The gait was insecure with postural instability and with a tendency to fall when turning around. Frontal signs were positive, the voice was quiet, the tonus was mildly elevated and showed a slight hesitancy (“Gegenhalten”), tendon reflexes were brisk, paresis and pyramidal signs missing. There were no signs of ataxia, but a mild bradykinesia. Action tremor was more distinct than a mild resting tremor. Again, neurocognitive testing and gait disturbances were consistent with subcortical dementia (Figs. and ). Regarding the mild signs of parkinsonism, dementia with Lewy bodies (DLB) was also suspected but excluded by a dopamine transporter (DAT) scan. Fluorodeoxyglucose positron emission tomography (FDG-PET) demonstrated hypometabolism in the left striatum and in the left frontotemporal cortex (Fig. ). Cerebrospinal fluid (CSF) showed signs of a chronic lymphocytic inflammation. The CSF markers for dementia, total tau protein and phosphor-tau were within the normal range, while beta-amyloid 1-42 and the Innotest-amyloid-tau index (IATI) were found to be below the reference values (beta-amyloid 1-42: 290 pg/ml, reference value > 500 pg/ml; IATI 0.6, reference values > 1). Finally, LNB was diagnosed when further CSF examinations disclosed a highly elevated Bb-specific-AI indicating local intrathecal Bb-specific antibody synthesis (Table ). The patient was treated with 2 g ceftriaxone daily for 3 weeks.\nNeurological symptoms and impaired cognitive functions, although persistent for a year, recovered rapidly within a few weeks (Figs. , and ) and so did the pathological CSF findings (Table ). A follow-up FDG-PET examination showed the left frontotemporal hypometabolism in remission, while this was not the case for the cystic lacunar lesion in the left striatum. A new and clinically silent small right thalamic lesion was detected that was not present in the pretreatment MRI (Fig. ). The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) test battery at the last follow-up in April 2014 scored within the age-dependent normal range with the exception of verbal learning and semantic verbal fluency (Fig. ). In a telephone call in February 2018 at the age of 82 years, the patient reported no gait problems or cognitive impairment and had just returned from a trip to Cuba. |
A 51-year-old Caucasian woman was admitted to our department in April 2011 for a third kidney transplantation. Focal segmental glomerulosclerosis (FSGS) has been diagnosed in 1973, and the patient reached end-stage renal failure in 1982. He received two kidney allografts, in 1983 and 1993, which both failed as a consequence of early recurrence of FSGS. Since 2002, hemodialysis was performed on a left femorofemoral fistula, because it was impossible to create new upper arm fistula after multiple episodes of thrombosis.\nThe third kidney transplantation was performed in April 2011 on the right iliac fossa. The patient was not immunized, and cold ischemia time was 23 hours. The patient received thymoglobulin as an induction therapy, with mycophenolate mofetil daily, and tacrolimus and corticosteroids as maintenance therapy. After an initial delayed graft function, renal function improved, and on day 10 serum creatinine was 155 µmol/L.\nA rise of serum creatinine at 180 µmol/L on day 10 led to the initial diagnosis of moderate acute humoral rejection (g1, cpt1, C4d 3, and acute tubular necrosis), despite the absence of donor specific antibodies. Serum creatinine improved after an increase of corticosteroids doses and plasma exchange therapy.\nThe patient was discharged 3 weeks after transplantation with serum creatinine at 124 µmol/L.\nA phlebography with carbon dioxide followed by an angioplasty of the femorofemoral fistula was performed 3 weeks after discharge because of a stenosis diagnosed before the transplantation, leading to decreased blood flow and difficulties in cannulation.\nThree days after angioplasty, the patient was readmitted for volume overload syndrome with peripheral oedema and shortness of breath.\nOn admission, the patient was afebrile, its blood pressure was 118/66 mmHg, and its pulse rate 83/min. A weight gain of 4 kg was noticed. His respiratory rate was 27/min, and oxygen saturation was 96% on ambient air. Physical examination revealed crackles in the two lung fields, jugular venous distension, and pitting peripheral oedema.\nMedications included prednisone, mycophenolate mofetil, tacrolimus, esomeprazole, trimethoprim/sulfamethoxazole, and furosemide.\nBlood urea nitrogen was 18 mmol/L, serum creatinine 200 µmol/L, sodium 135 mmol/L, troponin < 0,01 ng/mL, brain natriuretic peptide 500 ng/L (normal < 100 ng/L), hemoglobin 10 g/dL, natriuresis 10 mmol/L, and kaliuresis 55 mmol/L. There was no significant proteinuria. Liver enzymes were slightly elevated. Electrocardiogram was not modified, and chest radiography showed bilateral alveolointerstitial syndrome.\nIntravenous diuretics therapy with high dose of furosemide, hydrochlorothiazide, and spironolactone was administered, but did not lead to a clinical improvement.\nEchocardiograms showed a moderate left ventricular hypertrophy with normal function and no sign for right heart failure with normal pulmonary arterial pressure.\nA duplex ultrasound revealed an increased blood flow of the AVF, estimated at 1400 mL/min. Allograft vascularisation was not influenced by the AVF. There was no evidence for a renal artery stenosis or iliac artery stenosis, which was confirmed by a nuclear magnetic resonance imaging.\nA kidney allograft biopsy was performed which showed that there was no sign of antibody mediated rejection (g0, cpt0, and C4d score = 1).\nDespite normal echocardiogram, a right heart catheterization was performed. The mean pulmonary arterial pressure was 44 mmHg, cardiac index was 3,1 L/min/m2, and pulmonary capillary wedge pressure was 30 mmHg. Systemic arterial resistance was decreased. The diagnosis was heart failure triggered by high blood flow arteriovenous fistula.\nThis was confirmed by AVF ligature, which led to an increase of urine output and natriuresis, kidney allograft function improvement (), and loss of weight and peripheral oedema. |
A 54-year-old woman was admitted to the ENT outpatient clinic with tinnitus, humming, fullness, and hearing loss in her right ear. The patient did not have any problems with her right ear until an ache, followed by complaints like fullness, increasing hearing loss, tinnitus emerged abruptly. In the first clinical examination, a pouch hanging on the anterior upper quadrant was detected in the tympanic membrane of the right ear. The pouch was a 5x4 mm cystic bag filled with fluid in constant motion ().\nThe patient’s medical history revealed that she was diagnosed with glomus jugulare in her left ear and was treated with radiotherapy. Deafness was found in the left ear after radiotherapy and the patient had not been followed-up in the past two years. The left EAC and tympanic membrane were found normal in otoscopic examination.\nIn addition to the constantly moving fluid in the pouch, there was an increase in the vascularization of the rest of the tympanic membrane, and its color was matte. Minimal fluid (air-fluid level) existed behind the tympanic membrane. Audiometric analysis revealed a conductive hearing loss in the right ear, audiogram, air 46 dB, and bone 16 dB. In the left ear, air 97 dB and bone 74 dB were found (sensorineural hearing loss associated with the glomus tumor and radiotherapy). In the tympanometric assessment, there were type B and A tympanograms respectively for the right and left ears.\nThe patient was hospitalized with otitis media and a preliminary diagnosis of tumor of vascular origin attached to the eardrum in the middle ear or epidermoid cyst of the tympanic membrane. The patient was given antibiotic (ampicillin/sulbactam) and topical nasal decongestant (oxymetazoline hydrochloride) as treatment. The temporal bone was scanned with computed tomography to evaluate the middle ear structures and the examination revealed no pathology. The complaints of the patients did not decrease but increased in the 48 hours after the treatment was started. In examination, the sac was enlarged and pronounced. On the third day of hospitalization, severe tinnitus and ear pain emerged in the patient’s right ear. Otoscopic examination revealed that the cystic pouch on the tympanic membrane had burst, and an arthropod was moving in the EAC. The arthropod was carefully removed from the EAC and placed in a glass jar (). The patient’s tympanic membrane was intact, and all complaints, tinnitus, humming, and hearing loss regressed.\nThe tympanic membrane was normal two days after the arthropod was removed. New audiometric analysis revealed normal hearing in the right ear with type A tympanogram. The patient was referred to the department of infectious diseases for Crimean-Congo hemorrhagic fever. All the hematologic and biochemical examinations were normal.\nThe arthropod was sent to the departments of parasitology and medical microbiology of the Veterinary Faculty for parasitological analysis. Parasitological analysis defined the arthropod as a tick due to its specular formation and four pairs of legs (). The tick was in the latest stage of the first nymph (the juvenile stages of life) and nearly past the second nymph stage without bloodsucking. After its subtype was defined, the tick was released to the natural environment and no more examinations were performed. |
A 70-year-old male with history of amyotrophic lateral sclerosis (ALS), dysphagia status post gastrostomy tube placement, chronic respiratory failure status post tracheostomy, and gastroesophageal reflux disease presents with six-day duration of melanotic stools. The patient was mechanically ventilated with gastrostomy tube and tracheostomy in place. His physical exam otherwise was benign. He was found to have acute onset anemia with hemoglobin of 7.1 g/dl. He was suspected of having peptic ulcer disease secondary to NSAIDs given the history of chronic musculoskeletal pain with NSAID use. Due to continual decrease in hemoglobin requiring daily blood transfusions despite conservative management, upper endoscopy was performed. It demonstrated a bleeding ulcer distal to pylorus in the duodenal bulb. Endoscopic technique was used to remove the clot, but the procedure resulted in bleeding that could not be stopped leading to poor visualization despite epinephrine injections. Due to his multiple comorbidities, he was deemed to be a poor surgical candidate. The patient was referred to interventional radiology for embolization of gastroduodenal artery (GDA).\nDuring the embolization of GDA, the celiac angiogram demonstrated no evidence of active extravasation, but contour irregularity at the level of the mid-GDA was noted. Prophylactic coil embolization of GDA was performed achieving GDA stasis. Post-embolization angiography of the SMA demonstrated no evidence of bleeding from IPDA branches. Incidentally noted was a replaced right hepatic artery arising from the SMA.\nDespite embolization of GDA, patient’s hemoglobin continued to decrease to 6.8 g/dl and the patient continued to have melena and hematemesis resulting in hypotension. The patient required an additional nine units of packed red blood cells (pRBCs), six units of platelets, and five units of fresh frozen plasma. Computed tomographic angiography (CTA) showed a large bleed from IPDA off the SMA immediately posterior to the origin of the replaced RHA (Figure ).\nThe patient was referred for urgent embolization by interventional radiology.\nDuring angiography, no active extravasation was identified and given that the GDA was already embolized, the most reasonable source vessel in the suspected territory would be the IPDA. The replaced RHA was selected and IPDA was identified as its first branch (Figures , ).\nWhile the branch arising directly from the replaced RHA represented the posterior IPDA, the anterior IPDA was seen as collateral vessel going back to the middle colic artery (Figure ).\nHowever, no focus of active bleeding could be identified from digital subtraction angiography from the posterior IPDA or the anterior IPDA. Cone beam computed tomography (CBCT) catheter angiography of the posterior IPDA was performed to identify the region of the duodenal bleed analogous to the region of active extravasation seen on abdominal CTA. The same location on the posterior wall of the duodenum seen on abdominal CTA was matched on CBCT angiography (Figure ).\nSubsequently, the posterior IPDA was embolized using n-butyl cyanoacrylate (NBCA) (Trufill n-BCA Liquid Embolic, Codman Neurovascular, Raynham, Massachusetts, USA) mixed with ethiodol 1:4 dilution ratio administered via the microcatheter (Figure ).\nPost-embolization angiography of the SMA demonstrated successful embolization of the posterior IPDA with sparing of the anterior IPDA. The patient became hemodynamically stable post procedure and no longer required blood products transfusion. His hemoglobin stabilized at 8.6 g/dl. The patient was successfully discharged to a skilled nursing facility to continue his recovery. At eight weeks follow-up the patient remained asymptomatic and he agreed to participate in this case report. |
A 55-year-old lady underwent an elective laparoscopic Nissen fundoplication. On the second postoperative day she deteriorated with persistent vomiting, pyrexia, and low oxygen saturations and was promptly admitted to the intensive care unit (ICU). Oesophago-gastro-duodenoscopy (OGD) was performed with dilatation of a tight gastro-oesophageal junction (GOJ).\nShe then continued to be hypoxic and hypotensive and a chest X-ray revealed a right sided pneumothorax which was managed with a right chest drain. Serial arterial blood gas samples did not reveal any acid-base disturbances at this stage. A gastrografin swallow ruled out any perforation in the oesophagus and was otherwise nonspecific. After a short period of noninvasive ventilation, she remained hypoxic and was consequently intubated. A second chest drain was inserted on the left side due to worsening bilateral pleural effusions on a subsequent chest X-ray.\nA repeat OGD revealed a normal GOJ with a rotated and distended stomach but there was no evidence of gastric outlet obstruction. As the patient continued to deteriorate, a computerised tomography (CT) scan was done () which confirmed herniation of the stomach into a congenital postdiaphragmatic space. At exploratory laparotomy, the anterior wall of the stomach was noted to be herniating into a congenital space behind the diaphragm pushing the liver and the inferior vena cava anteriorly. There was no evidence of a gastric volvulus. Following the retrieval of the herniating segment, the wrap was noted to be congested with an area of ischaemia which recovered promptly following reduction and no resection was necessary. The wrap was undone revealing a defect in the anterior wall of the stomach. The margins of the defect, which were of doubtful viability, were trimmed and the defect was closed with nonabsorbable sutures and covered with omentum. The stomach was then fixed to the anterior abdominal wall with nonabsorbable sutures. No defect was noted in the diaphragm where three hiatal interrupted nonabsorbable sutures, which were placed during the previous fundoplication and were noted with a normal length of abdominal oesophagus.\nThe patient made a swift recovery and was discharged from the ICU. Both drains were eventually removed prior to her discharge from the hospital on the seventh postoperative day. The patient remained asymptomatic with no reflux symptoms after a period of 2 years of followup leading to her discharge from our care. |
The patient is a 28-year old male final year medical student from the South-Eastern region of Nigeria in sub-Saharan Africa. He was declared missing for 10 days prior to presentation because his whereabouts was unknown. He was later seen in a city in South-Western Nigeria, a distance of about 634km from South-Eastern Nigeria where he lived and schooled. Ten days before presentation, while studying in his room alone at night, the patient suddenly saw a full human skeleton reading at the same table with him, sitting at the opposite side. At the same time, the patient claimed he felt unease and quite uncomfortable. He saw the whole room turning with everything inside becoming unstable and unreal. After this he had overwhelming fears and did not know when he left the room. Two days later, he discovered he was with his younger sibling in South-Western Nigeria. The patient had no knowledge of how he made the journey that takes approximately 8 hours by road. He equally could not remember where he slept the night he left his room, how he raised money for the journey or the buses and routes he took. The patient denied all memory of events for the 2 days from when he left his room at the university to the time he suddenly realized he was at his brother’s house, 634km away. The brother, however, reported that the patient appeared unkempt, looked exhausted but was fully conscious and alert on arrival at his house without any assistance.\nPrior to this episode, the patient had been under severe economic and academic pressures. The younger brother who paid the patient’s bills had threatened to withdraw his sponsorship because of the patient’s prolonged stay in school beyond the stipulated duration of training occasioned by his repeats of examinations and classes. The patient had been worried that he might also fail in his final qualifying examinations scheduled to be held in 3 months. He subsequently became involved in several religious activities to obviate his perception of impending doom.\nThe patient admitted to having low mood, loss of interest in usually pleasurable activities and poor appetite. He had lost weight and most often preferred being alone. He had also been feeling weak especially in the morning hours but had managed to grudgingly carry on with the day’s activities. He had suicidal ideation but never attempted suicide. The patient slept poorly at night. His sleep had been marked by early morning wakefulness and waking up not feeling refreshed.\nThere were no symptoms suggestive of seizure, manic episode, schizophrenia, anxiety or organic disorders. He never drank alcohol or abused any psychoactive substances. The patient denied a history of head trauma or loss of consciousness in the past.\nPast medical, psychiatric, family and personal histories revealed no significant findings.\nExamination of his mental state revealed a young man who was clean, appropriately dressed and mildly emaciated with poor eye contact. His mood was depressed. He had preceding visual and derealization perceptual disorders. He had no thought disorders. The patient was oriented in time, place and person but had impaired attention and concentration at the time of the examination. Immediate recall, short- and long-term memory were intact. However, there was amnesia for the 2 days he wandered away from school. Judgment and insight were not impaired.\nHis physical examination was unremarkable. Neurological assessment and basic laboratory testing revealed no significant abnormalities.\nAn electroencephalogram reported no seizure activity. A computed axial tomography of the brain was not done because the patient lacked resources to pay for it. Also, a test for blood alcohol level and urine drug screening were not done because the hospital had no facilities for the tests.\nThe Dissociative Experiences Scale (DES) was administered to the patient and he had a score of 50%. The DES is an effective screening instrument for dissociative disorders\n[,].\nA diagnosis of dissociative fugue-like syndrome was made with comorbid major depressive episode. He was engaged in psychotherapy by the departmental clinical psychologists and his depression was treated with paroxetine. He responded very well and was able to write his final qualifying examinations 3 months later. He, however, did not pass either of the two subjects examined.\nAt 6-month follow up, the patient could still not recall events for the 2 days from when he left school to the time he was seen in his brother’s house, 634km away. He reported no further periods of amnesia or wandering away from his place of residence. |
A 70-year-old male known with hypothyroidism and hypercholesterolemia presented to his general practitioner (GP) with a painful wound on the pulp of the right middle finger with suppuration for several days. On physical examination, an erythematous finger was seen with pus secretion and blisters. The patient was not aware of how he had acquired the wound. As a professional taxidermist, he regularly came into contact with a wide range of deceased animals ranging from wild swans to horses. His most recent project prior to the incident was preparing a horse. The GP started a short antibiotic regimen and the infection settled quickly.\nThree weeks later, he suddenly developed fever combined with sharp back pain. The patient was admitted to a local hospital. The initial diagnosis was pyelonephritis. The urine culture, however, turned out to be negative, while the blood cultures were positive for group C streptococcus. The patient was treated with intravenous amoxicillin/clavulanic acid for 5 days and was discharged in a stable clinical condition.\nThe back pain, however, did not subside after discharge and gradually increased. The patient became septic and was readmitted with high suspicion of endocarditis.\nDuring the workup, endocarditis was ruled out using transesophageal echocardiography. Duplex ultrasound examination (DUS) of the abdomen revealed an aneurysm of the abdominal aorta with wall-mounted thrombus formation. Further, magnetic resonance imaging (MRI) of the spine illustrated another isolated aneurysm in the right common iliac artery. Computed tomography angiography (CTA) confirmed the presence of the aneurysms in the distal abdominal aorta and in the right common iliac artery (\n).\nSESZ was isolated from the blood. Urine and fecal cultures were negative for bacterial growth.\nThe patient was then transferred to our tertiary referral center for further treatment. Upon arrival, a septic patient with excruciating back pain was seen. Blood analysis showed a white blood cell (WBC) count of 11.9 10E9/L (4–10 10E9/L), hemoglobin was 5.5 mmol/L (8.5–11 mmol/L), platelet count was 223 10E9/L (150–400 10E9/L), and C-reactive protein (CRP) was 77 mg/L (<5 mg/L).\nThe treatment plan consisted of a combined medical and surgical approach. Penicillin was given for a total duration of 6 weeks.\nSurgically, the infected tissue was debrided, followed by direct autologous vein reconstruction of the abdominal aorta and iliac artery using both superficial femoral veins. For this purpose the superficial femoral veins from both legs were harvested. For the aortic reconstruction, one vein was cut in half and the two halves were anastomosed to each other to form a tube with a larger diameter (\n). For the iliac reconstruction, the other femoral vein was used. Both venous grafts were anastomosed in an end-to-end reconstruction.\nThe patient was readmitted to the hospital shortly after discharge with fever, shivering, malaise, and increased infection parameters, regardless of being treated with oral antibiotics. CTA demonstrated collections of fluid adjacent to the venous reconstruction. Serous fluid was percutaneously drained and cultured. The cultures were negative and the clinical condition dramatically improved directly after drainage. The patient was discharged and penicillin was continued orally at home.\nThe patient came back for follow-up 3 weeks after discharge and a new CTA showed a dramatic reduction of the fluid collections. Infection parameters, as follows, had decreased as well: WBC count of 4.5 10E9/L (4–10 10E9/L) and a CRP of 1.6 mg/L (<5 mg/L). During the last follow-up, 1 year after discharge, DUS of the abdomen showed an open venous reconstruction with no fluid collections and a CRP of 0.5 mg/L (<5 mg/L). |
A 54-year-old, Hispanic male with no known past medical history presented to the emergency room with a chief complaint of sudden-onset right-sided weakness over the past 24 hours. The patient denied any associated dizziness, visual disturbance, or reduced level of consciousness. He had not seen a physician in over 20 years. His social history was significant for chronic alcohol abuse with consumption of at least one pint of tequila or beer per day for at least 35 years. The patient was tachycardic to 101/min with a physical exam that was remarkable for right-sided facial droop as well as 1/5 strength in the right upper and lower extremities. He was noted to have a National Institutes of Health stroke scale of 17.\nA stat computed tomography (CT) of the head without contrast as well as magnetic resonance imaging (MRI) without contrast were negative for acute stroke. The patient's urine drug screen and alcohol level was unremarkable. His labs were significant for an ALT of 70, AST 251, direct bilirubin 0.4, INR 1.1, platelets 79 x 10^3 (Table ). All of his other labs were normal. Further investigation with right upper quadrant ultrasound suggested possible liver cirrhosis. Computed tomography of the abdomen and pelvis revealed a micronodular appearance of the liver with numerous scattered hypodensities (Figure ). A hepatitis A, B, C panel, autoimmune panel, alpha-1 antitrypsin deficiency panel and iron panel were all negative. Our patient was suspected to have alcohol-induced cirrhosis due to his extensive alcohol history.\nA lipid panel and Doppler of the neck were obtained which were found to be normal. Once an ammonia level was found to be 140 micro mol/L, the patient was started on lactulose and rifaximin. The patient opted out of physical therapy the first two days of admission; however, his neurological symptoms resolved without residual neurological deficits about 36 hours after treatment of lactulose and rifaximin. We discharged our patient with close follow-up at a GI clinic and repeat labs one month after discharge (Table ). |
An 84-year-old female was referred for cardiac catheterization for evaluation of a suspected significant coronary artery disease and mitral valve regurgitation. The patient complained of worsening of dyspnea symptoms during exercise, New York Heart Association (NYHA) class II–III for several months without angina. The resting electrocardiogram (ECG) showed atrial fibrillation with a heart rate of 90/min (see supplemental figure 1). The N‑terminal pro B‑type natriuretic peptide (NT-proBNP) level was moderately elevated (2274 ng/l) with normal renal and thyroid function and borderline anemia (hemoglobin 116 g/l). Transthoracic and transesophageal 3D echocardiography (see Fig. , upper panels, supplemental video 1) revealed a rare cause of heart failure in octogenarians, i. e. a partially calcified but patent ductus arteriosus 6 mm in diameter, which was confirmed by 3D-VRT computed tomography (see Fig. , lower panels, supplemental video 2). All 4 heart chambers were dilated (echocardiography: left ventricular end-diastolic diameter 67 mm, right ventricle 35 mm, left atrium 59 mm and right atrium 48 mm), the pulmonary arteries (right 40 mm and left 30 mm) and the pulmonary trunk (55 mm) were severely dilated. Left ventricular systolic function was slightly decreased (left ventricular ejection fraction 45 %) and the right ventricular systolic function was normal. There was only mild to moderate mitral valve regurgitation and moderate pulmonary valve and tricuspid valve regurgitation. Cardiac catheterization revealed a significant left to right shunt of 0.56 (arterial, right atrial and pulmonary artery oxygen saturation was and 93 %, 27 % and 65 %, respectively) and severe pulmonary arterial hypertension (systolic 62 mm Hg and diastolic 28 mm Hg, mean 42 mm Hg, the pulmonary artery occlusion pressure was at maximum 14 mm Hg, mean 10 mm Hg; transpulmonary gradient 32 mmHg, diastolic pulmonary pressure gradient 18 mmHg). Significant coronary artery disease was ruled out by coronary angiography.\nThe subsequent detailed medical history revealed that the patient was first informed of the presence of a cardiac murmur at the age of 23 years and a holosystolic 3/6 systolic murmur (best heard right second intercostal space) could be heard at presentation to our department. At this young age the patient was asymptomatic but over the subsequent decades the substantial left to right shunt led to left ventricular dysfunction and severe pulmonary arterial hypertension. |
A 39-year-old woman, gravida 1, para 0, was diagnosed with invasive squamous cell carcinoma of the cervix following conization. Pathological findings showed carcinoma consistent with FIGO stage IA1 with lymphovascular invasion. She was referred to Keio University Hospital. The patient and her husband were informed of the treatment options, including AmRT and pelvic lymphadenectomy. The patient was told that the outcome of this procedure could not be guaranteed because an insufficient number of these procedures have been performed worldwide to yield reliable conclusions. The patient wished to preserve fertility, and she and her husband signed a written consent form agreeing to this treatment. Pathological findings after AmRT and pelvic lymphadenectomy showed no residual tumor and no lymph node metastasis. There was no finding of an ovarian tumor before surgery. A left ovarian cyst of 4 cm was identified during postoperative follow-up.\nAt 3 years and 6 months after surgery, the patient underwent IUI and then had fever and pain in her left lower abdomen 10 days later. At her first visit, her temperature was mildly elevated to 37.5°C. The patient's pregnancy was denied because a qualitative urine human chorionic gonadotropin (hCG) test was negative. A tumor with tenderness was palpated in the left adnexal area. A cystic tumor of 64x 41 mm was found by transvaginal ultrasonography (). Blood tests showed increases in white blood cell (WBC) count to 11900/μL and C-reactive protein (CRP) to 22.80 mg/dL. The patient was diagnosed with PID with ovarian cyst infection and hospitalized for treatment. Conservative treatment with antibiotics was initially used, but her symptoms did not improve. On hospital day 8, blood tests showed a further increase in WBC count to 23900/μL and CRP to 28.17 mg/dL, and pelvic CT showed that the ovarian cyst had grown to 10 cm in size ().\nWe decided to perform laparoscopic left ovarian cystectomy on day 8. Since the patient had a history of open surgery, adhesion was likely in the abdominal cavity. Before surgery, we asked the urologist to insert bilateral 6 Fr ureteral catheters because of possible difficulty identifying the ureters. The catheters were fixed to the thigh with tape (). The uterine manipulator was not inserted before surgery to avoid the risk of uterine perforation.\nCO2 pneumoperitoneum was established at 10 mmHg. Laparoscopic left ovarian cystectomy was performed using typical trocar placement. The left ovary was swollen to 10 cm and the fluid contents were purulent (). The left adnexa, posterior uterine wall, and retroperitoneum were firmly adhered (). The bilateral fallopian tubes were firmly adhered to the surrounding tissue and were unable to be identified. During surgery, by moving the catheter manually back and forth from outside the body, we were able to identify the ureters visually (). The 7 cm uterine manipulator was inserted during surgery under a laparoscopic view. The left ovarian cyst was excised, leaving the normal part of the ovary (). The operation time was 2 h and 58 min, and blood loss was 550 mL. No complications occurred during or after surgery. After the operation, symptoms improved rapidly and the patient was discharged 8 days after surgery. The excised specimen was pathologically an endometriotic cyst. A bacterial culture of the cyst fluid was positive for Prevotella bivia, Prevotella species, and Finegoldia magna. |
A 16-year-old male patient was referred by his orthodontist with main chief complaint being a dull pain sensation in the upper maxillary region. According to his parents, his upper left central incisor (i.e., tooth no. 21) had been slightly discolored after a trauma during bicycle riding at the age of nine. His orthodontic treatment had started 2 months before referral and he had been experiencing this dull pain for the last 2 weeks.\nOn clinical evaluation, the periradicular region of the upper left central incisor was tender on palpation. An orthoradial periapical radiograph revealed a periapical lesion with its epicenter being the apical foramen of the tooth no. 21 []. The extent of the lesion was ~10 × 13 mm. The tooth was nonresponsive to vitality tests using cold as well as electric pulp testing (Vitality Scanner, Model 2006, Analytic Technology, Redmond, WA).\nAccording to patients medical and dental history a presumptive diagnosis of pulp necrosis of traumatic origin associated with extensive AP was established. Considering the history of trauma and the apical size of the canal in tooth no. 21, which was assessed to be ~1 mm and taking into account the fact that for a tooth to be labeled as mature, the size of apical foramen needs to be less than 1 mm wide in direct periapical radiographs,[] it was assumed that the process of apical closure had ceased prior to tooth maturation, due to pulp necrosis. In other words, the necrotic pulp was a consequence of previous traumatic injury. This phenomenon was independent of orthodontic treatment and could be cured without having to unload the tooth. The treatment plan consisted of single-visit orthograde endodontic intervention and placement of an apical plug. The patient's parents signed an informed consent regarding the treatment strategy.\nOn a subsequent visit, after local anesthesia with 2% lidocaine containing epinephrine 1:80000 (DarouPakhsh, Teharn, Iran), the root canal therapy was done using the RaCe rotary files (RaCe, FKG Dentaire SA, Switzerland) to # 50/0.04 with simultaneous 5.25% NaOCl irrigation. Then the canal was dried using paper points (Ariadent, Tehran, Iran). CEM cement powder and liquid (BioniqueDent, Tehran, Iran) were mixed according to the manufacturer's instructions and a ~5 mm plug was placed in the apical area of the canal. The opacity and length of the plug was confirmed with a periapical radiograph, a prefabricated metal post was cemented in the canal and the tooth was restored using composite resin (Herculite Ultra Flow and OptiBond Solo, Kerr, Orange, CA) []. The patient was put on a regular follow-up plan. By the end of the 1st week all the symptoms faded away; the 4 month postoperative radiograph revealed the incomplete bone replacement process starting from the periphery of the lesion, as the sign of healing [] and progressed to the 7th month []. [], shows the 2-year follow-up radiograph which shows the complete bone healing. An outstanding finding beyond the apical end of the CEM plug was the increase in root length, which was radiographically visible from the 3th month; and was also surrounded by PDL in the final cliché []. |
An 11-month-old female infant presented to our Paediatric Emergency Department (PED) with a 10-day history of metallic cough and intermittent fever. These symptoms were complicated by progressive dysphagia and episodes of mucus regurgitation accompanied by choking and dyspnoea in the last few days before admission. The symptoms started at the end of the flu epidemic season. Therefore, she was initially diagnosed by a general practitioner with a respiratory tract infection and treated with a 7-day course of antibiotics and a short-course of corticosteroids without any relief. During this course, she developed progressive dysphagia, initially for solid food, and then also for liquid food. In the last few days before admission, her parents reported nocturnal regurgitation of thick mucus followed by choking and dyspnoea. At the moment of admission to the PED, the patient was in a fair general condition, apyretic, and without any apparent signs of respiratory distress, but she had drooling and refused food intake. During a physical examination, she suddenly presented with an abrupt onset of coughing with a metallic sound and regurgitation of thick saliva and mucus. Pulse and oxygen saturation levels were within the normal range, while a thoracic examination showed bilateral rhonchi.\nTherefore, chest radiography was performed and it showed a radiopaque OFB (). To better characterize the location of the OFB and its anatomical relationship with adjacent tissues, a chest computed tomography (CT) study was performed (). The CT scan confirmed a radiopaque OFB, which was a 2.5- x 1.5-cm spring with five helixes, and two of them were embedded in the oesophageal mucosa. The OFB appeared to be dislocated in the proximal oesophagus, and projected at the level of the thoracic vertebrae T2–T3 and leaned on the aortic arch. Cranially, the oesophagus appeared to be patent. No active parenchymal lesion or pleural effusion was found. Unfortunately, the presence of many artefacts did not allow study of the tracheal wall.\nThe patient was then referred to the Paediatric Anaesthesiology and Surgery Unit of a tertiary level PED. She underwent a rigid and then flexible oesophagoscopy, which showed considerable granulation tissue inside the spring (). Because of proximity of the spring to the aorta, consultation of a vascular and heart surgeon was requested during the procedure. The first attempt of endoscopic removal failed. With the aim of preserving the oesophagus and removing the OFB endoscopically, a laparoscopic plier was anchored to the spring and was rotated in the opposite direction of the spiral. This technique enabled successful endoscopic removal at the second attempt (). As expected, the oesophageal mucosa was seriously damaged by the caustic effect of rust. This resulted in oedema and surrounding granulating tissues, as well as almost complete erosion of the oesophageal wall ().\nTotal parenteral nutrition was provided for 2 weeks. The infant was then fed with enteral nutrition through nasogastric tubes and treated with a long-term course of antacids. Because of subsequent oesophageal stenosis, she underwent several endoscopic oesophageal dilations with Savary nasogastric tubes ((Savary-Gilliard dilator; Cook Medical, Bloomington, IN, USA) of increasing size (5-7-9 Ch). She was discharged after 2 months of hospitalization. Currently, after 19 endoscopic oesophageal dilations, she is in good general condition and has obtained acceptable food transit. The patient’s parents provided written informed consent to publish. |
The patient is a 51-year-old man with a 13-year history of UC, who experienced frequent exacerbations of his disease proven by colonoscopies () and subsequent biopsies. Some of the flares were severe and some of them were mild to moderate. Early in the course of the disease, the patient was treated with three doses of infliximab; however, this treatment was terminated based on the patient's decision. He did not tolerate aminosalicylic acid derivatives due to an allergic reaction; therefore, azathioprine was used chronically to suppress the UC in addition to episodic oral or rectal steroids to treat the breakthrough flares. The azathioprine dose ranged mainly between 100–125 mg daily.\nMost exacerbations were related to CDI, which was diagnosed by testing the stool for Clostridium difficile toxin (PCR was used once to establish the diagnosis). CDI recurred 4 times in the last few years, which made it more difficult to control the UC. The patient was complaining of continuous weakness and fatigue along with the diarrhea. CDI episodes were treated with oral vancomycin. The eradication of CDI allowed better control of his UC; therefore, he was committed to long-term suppressive therapy with oral once-daily vancomycin.\nFecal transplantation was considered in this patient despite the uniqueness of this case. The risks and benefits were discussed with the patient. His blood work prior to the procedure revealed: white blood count of 5.7 k/uL, hemoglobin of 15.5 mg/dL, platelets of 258 k/uL, Albumin of 4.2 mg/dL, and creatinine of 1.1 mg/dL. The donor's stool specimen was obtained from the wife who tested negative for Clostridium difficile PCR in the stool. Also, the wife serology was negative for HIV and hepatitis (hepatitis A antibodies, hepatitis B surface antigen, hepatitis B core antibodies, and hepatitis C antibodies). Oral vancomycin was discontinued 24 hours before the transplantation. The stool suspension was prepared according to standard protocols []. Warm water was added to 300 mL of the donor's stool, and the sample was instilled via colonoscope without complications. Afterwards, the patient remained symptom-free for 8 months and was able to stop oral vancomycin without CDI recurrence to date. The procedure was not associated with side effects despite the fact that it was done while the patient was on an immunomodulator. The patient was aware of the unusual nature of his circumstance and was anxious to have this information available for other patients with similar problem. |
A 55-year-old male presented to the emergency department of a regional hospital with scrotal oedema of 2 weeks’ duration. He had a history of hypertension and type 2 diabetes mellitus with associated nephropathy and peripheral vascular disease. Physical examination revealed bilateral leg oedema as well as generalized scrotal swelling with associated erythema and tenderness. The patient was admitted into the surgical unit and treated with intravenous (IV) antibiotics for scrotal cellulitis.\nOn day 2 of admission, he had a witnessed cardiac arrest whilst getting out of bed. A rhythm check during resuscitation revealed asystole. The patient had return of spontaneous circulation after 15 minutes of cardiopulmonary resuscitation (CPR) and 2 mg of IV adrenaline. He was intubated and subsequently transferred to a tertiary hospital intensive care unit (ICU) for further care.\nOn arrival at the ICU, physical examination revealed dual heart sounds with a pansystolic murmur consistent with mitral regurgitation, bilateral inspiratory crepitations at the lung bases and moderate bilateral pitting oedema to the thighs and scrotum. An electrocardiogram (ECG) showed sinus rhythm, normal QRS morphology, a prolonged QTc interval at 470 ms and no features of ischaemia ().\nSerum creatinine was 402 μmol/l, and troponin T was 266 ng/l (normal <14). Chest x-ray revealed cardiomegaly and pulmonary congestion. A transthoracic echocardiogram showed a mildly dilated left ventricle (LV) with moderate impairment of ejection fraction (EF) at 35%, a moderately dilated right ventricle (RV) with moderate impairment of systolic function, moderate mitral regurgitation, mild tricuspid regurgitation and a right ventricular systolic pressure of 49 mmHg. The provisional diagnosis for the patient’s presentation was congestive cardiac failure (CCF) and an arrhythmia secondary to underlying cardiomyopathy, and a decision was made to delay coronary angiography due to the lack of ECG changes and the risks of contrast-induced nephropathy. He was treated with frusemide, hydralazine, and glyceryl trinitrate. He was also given subcutaneous heparin for venous thromboembolism (VTE) prophylaxis.\nThe patient was mildly delirious after extubation on day 3, but subsequently made a full neurological recovery by day 5. Ventilatory status was stable after extubation with oxygen saturation at 98% on room air. He was transferred to the coronary care unit and subsequently had a second cardiac arrest the same night. The initial rhythm was asystole, followed by ventricular fibrillation (defibrillated at 200 J), and intermittent asystole and pulseless electrical activity. After administration of multiple doses of IV adrenaline, intubation and 16 minutes of CPR, a weak carotid pulse was felt, along with a systolic blood pressure of 70 mmHg. An ECG showed sinus rhythm with a PR interval of 260, a normal QTc interval and no ST segment changes suggestive of ischaemia. The on-call cardiology team was contacted to perform emergent bedside echocardiography, which revealed complete occlusion of the RV and right atrium (RA) by thrombus, and severe LV systolic impairment with spontaneous echo contrast in the LV and left atrium (LA) (, and ). Thrombolysis was immediately initiated using IV alteplase, leading to prompt restoration of haemodynamic stability. Repeat TTE performed 15 minutes post-thrombolysis demonstrated complete resolution of the RHT, as well as improvement in both RV and LV systolic function (, and ).\nA bilateral venous duplex study was performed to investigate a potential source of the RHT. This showed hypoechoic acute and occlusive thrombus in the posterior tibial and soleal veins of the right leg, and hypoechoic acute thrombus in the peroneal and soleal veins of the left leg. The proximal leg veins and the inferior vena cava were free of thrombus. Unfortunately, the second cardiac arrest resulted in brain death, which was confirmed by clinical examination and cerebral scintigraphy with single photon emission computed tomography. After discussion with the patient’s family, the decision was made to withdraw ongoing invasive ventilatory and inotropic support. The patient died shortly thereafter. |
A 14-year-old male patient reported to the Department of Periodontology with the chief complaint of swollen gums and deafness for the past 1 year. The patient also complained of poor esthetics due to a “gummy smile” and inability to close the mouth completely. The medical history was non-contributory for systemic diseases or drug intake. No history of ear trauma or exposure to loud noises was reported. Family history revealed that the patient was the only one to be affected over three generations.\nOn intraoral examination, there was a generalized gingival overgrowth. It was firm, nodular and fibrotic involving the marginal, attached gingiva and interdental papillae of all the teeth with no associated inflammation [Figures and ]. The gingiva was dark in color due to heavy melanin pigmentation. The lower anterior teeth were barely visible as the enlargement extended upto the incisal-third of the crowns. Examination of the teeth revealed that the patient was still in the mixed dentition stage though he was 14 years old. Orthopantamograph revealed all the missing permanent teeth to be present radiographically []. There was no evidence of alveolar bone loss. Periodontal examination with a periodontal probe (UNC-15 periodontal probe, Hu-Friedy, Chicago, IL) revealed no associated clinical attachment loss or mobility.\nThe patient was referred to an ENT surgeon for management of hearing loss. Pure tone audiogram, impedance audiometry and Tone decay test and brainstem evoked response audiometry tests were conducted. It was concluded there was severe to profound right and moderately severe to severe left sensorineural hearing loss. The case was provisionally diagnosed to be a case of idiopathic gingival fibromatosis with progressive hearing loss. The patient was recommended high occlusion computer generated hearing aids.\nManagement of the gingival overgrowth was done with phase I therapy and surgical excision. Under local anesthesia, quadrant by quadrant gingivectomy was carried out. A biopsy sample of the excised tissues was presented for histological evaluation. The histopathological picture showed parakeratinized stratified squamous epithelium with underlying dense fibrous connective tissue stroma []. The overlying epithelium was characteristically hyperplastic and showed prominent, elongated rete ridges []. Periodic review was carried out every 3 months. The patient was followed-up for a period of 24 months. There was a slight recurrence in the overgrowth, though lip competence was maintained []. The auditory tests, repeated after 1 year, revealed the hearing loss to be at the same level. The etiology was unknown, though an immunological influence could not be ruled out. Periodic review and audiometry once a year were suggested to monitor the progression of the hearing loss. |
A 35-year-old male with a history of hyperlipidemia and seizure disorder presented to an outside hospital following a breakthrough seizure, where he was incidentally also found to have punctate areas of acute cerebral infarcts in multiple vascular territories. Additional workup revealed the presence of a left atrial thrombus and newly diagnosed atrial fibrillation. He was ultimately discharged to home on apixaban. The patient then re-presented a month later for evaluation of transient diplopia, expressive aphasia, daily right temporal headaches, and right facial and left leg weakness. MRI of the brain showed new areas of diffusion restriction in the left cerebellar hemisphere and left medial occipital lobe (Figure ). CTA showed no signs of carotid occlusion or stenosis. The etiology of his multifocal strokes was thought to be related to his newly diagnosed atrial fibrillation and left atrial thrombus.\nThe patient was then transferred to our hospital for further evaluation. His initial NIH stroke scale was 8 (primary deficits were including unilateral facial palsy, bilateral lower extremity pronator drift and ataxia). Stroke labs, including lipid panel and hemoglobin A1C, were unremarkable. MRI of the brain with contrast showed a new infarct in the splenium of the corpus callosum in addition to prominent generalized meningeal enhancement (Figure ). MRI of the spine with contrast showed possible meningeal enhancement as well as punctate areas of encephalomalacia in the C3-4, C7, and T3 spinal levels. A bedside LP revealed a mildly elevated opening pressure of 24 cm H20, lymphocytic pleocytosis (WBC 150 K/cumm, 61% lymphocytes), protein 170 mg/dl, hypoglycorrhachia of 15 mg/dl, and presence of cryptococcal antigen. Other notable CSF labs included the presence of 11 oligoclonal bands. He was diagnosed with cryptococcal meningoencephalitis and started on a four-week course of amphotericin B and flucytosine. A repeat LP after several days of treatment showed a normal opening pressure of 14 cm H20, mildly improved pleocytosis (WBC 130 K/cumm, 84% lymphocytes), protein 172 mg/dl, and glucose 14 mg/dl. He did not require any additional lumbar punctures, and his symptoms (including headaches and left lower extremity weakness) gradually improved. The patient was discharged to an inpatient rehabilitation facility prior to returning home.\nThough our patient in Case 1 had a history of an unknown autoimmune disease, our patient in Case 2 had no history of autoimmune disease or other existing immunodeficiency. Both patients developed multiple cerebral infarcts in multiple vascular territories in the setting of cryptococcal meningoencephalitis, though our patient in Case 2 also had recently diagnosed with atrial fibrillation which further confounds the underlying etiology of his strokes. |
A 25-year-old female patient was referred to the Department of Orthodontics, Dental School, Shahed University of Medical Sciences, Tehran, Iran. Past medical history revealed a kidney cyst, but the patient did not suffer from any systemic disease. Clinical examinations eliminated the possibilities of any developmental disorders and syndromes. Extra-oral examination did not reveal any abnormality. In intraoral examination, mild spacing in both of dental arches was noted. Her upper left lateral incisor, second premolar and first molar were in dental crossbite without any functional shift. She had class III occlusal relationships and cephalometric evaluation revealed a class III skeletal pattern (). In her panoramic radiograph, four impacted third molars were present (Figure 2). Significant root dilaceration of maxillary lateral incisors and right first premolar was evident. Surprisingly, an impacted supernumerary canine was noted on the right side of the mandible and a primary canine accompanied by two impacted teeth, both resembling a canine, was present on the left side of the mandible. All of the three impacted teeth had fully-developed roots, and showed the configuration, size and root length of a permanent canine (Figures & ). Occlusal radiograph revealed the impacted tooth on the right was lingual and both of impacted teeth on the left were buccal (). According to the patient, there was no history of tooth extraction. The parents did not have supernumerary teeth; the patient had no siblings.\nFixed orthodontic treatment started for the patient. After six months of treatment including leveling and aligning, the right canine and first premolar were not properly aligned because of the impacted supernumerary canine; therefore, surgical removal of the supernumerary tooth was carried out.\nAnother surgical session was planned for the left side, in which the distal impacted canine was removed after extraction of the ankylosed primary canine, and a bracket was placed on the mesial canine for forced eruption because of its longer root. Both of the extracted teeth had the size and anatomy of a normal canine (). |
A 71-year-old female presented with 70-mm left breast invasive ductal carcinoma. Her medical history included early dementia, hypothyroidism and rheumatoid arthritis, with World Health Organization performance status 2. She initially underwent a left mastectomy and sentinel node biopsy. There were no intra-operative complications and post-operatively she recoveredwell.\nHistopathology confirmed 77 mm, grade III invasive ductal carcinoma with one involved sentinel lymph node biopsy (SLN). Subsequent staging computed tomography scan was clear. The patient proceeded to uneventful axillary clearance to level III, 7 weeks later, a Redivac suction drain was left in the axilla. All of the remaining 18 lymph nodes excised showed no evidence of malignancy on subsequent histology.\nPost-operative day (POD) 1 on examination 800 ml of a milky fluid was present in the drain, indicative of a chyle leak. Other imaging modalities such as lymphoscintigraphy and biochemical studies were not considered as it was felt that these would not alter management. In view of the high output, the decision was made for a re-exploration of the axilla on POD 2. Intra-operatively, the source of the leak was localized to posterior to the axillary vein next to the chest wall, although the specific vessel could not be identified within the residual tissue edge. Ligaclips and suture ligation of the area appeared to control the leak intra-operatively. The Redivac was changed to a Blake low-pressure suction drain and a pressure bandage was applied.\nPost-operatively, however, the chylous leakage continued but at a reduced rate. The drain remained in situ initially and the patient progressed well post-operatively, albeit with some oozing from around the Blake drain site, which was managed by removal of the suction and stoma bag placement, prior to discharge on POD 5 with nursing input in the community (–).\nFrom POD 10, the patient developed an axillary chyloma despite flushing the drain and continued leakage into the stoma bag. On POD 11 the drain was removed and the pressure dressing re-applied. After 2 days, 120 ml of chylous fluid aspirated from the axilla, and a further 170 ml of chylous fluid was aspirated from the axilla on POD 15. On POD 18, a further 90 ml of chylous fluid aspirated and the collection was noted to be more loculated than before.\nThe patient re-attended the breast clinic on POD 20 and no further evidence of chyle leak was noted. She was subsequently referred to the clinical oncology team for consideration of chemotherapy and radiotherapy. |
A 57-year-old male patient with no specific medical history was admitted to University Hospital for paraparesis and sensory disturbances in both lower extremities, caused by a fall 3 months prior to admission. He was diagnosed with CES, due to a L3 burst facture and spinal canal compression. Thus, posterior lumbar interbody fusion was performed (). After surgery, paraparesis improved progressively and no specific symptoms were reported, except neuropathic pain. The patient was transferred to a rehabilitation hospital for conservative treatment of the neurogenic pain and gait training; no specific complication was found during treatment.\nThe patient was transferred to our emergency department with fever and general weakness for 7 days. A complete blood count indicated leukocytosis, and Klebsiella pneumoniae was isolated from blood and urine culture tests. By abdominal ultrasonography, edema was observed in the bilateral renal parenchyma with hyperechogenicity, indicating renal failure, caused by acute pyelonephritis. No local lesion in the renal parenchyma, decreased blood perfusion, or extension of the renal pelvis or renal calyx was observed. After diagnosing sepsis, caused by acute pyelonephritis, meropenem was administered intravenously. After antibiotic treatment for 13 days, vital signs were stable and laboratory findings returned to normal. Antibiotics were stopped on the 15th day.\nThe patient was transferred to the rehabilitation medicine department for comprehensive management of his CES on the 16th day of hospitalization. In the Medical Research Council Manual Muscle Test, muscular weakness was observed in both lower limbs, with hip flexor 4/4 (right/left), knee extensor 3/3, ankle dorsiflexor 3/3, hallucis extensor 3/3, and ankle plantar flexor 2/2 grades. The patient complained of tingling sensations, allodynia, hyperalgesia, and decreased sensations below the third lumbar segment.\nSitting and standing up could be performed independently according to the functional evaluation, but moderate assistance was necessary for balanced-level walking and the Modified Barthel Index was 76 points. The deep tendon reflex was decreased in both lower limbs, though no pathological reflex was observed. Anal sphincter tone and the bulbocavernosus reflex were decreased. An electrodiagnostic study revealed normal sensory nerve conduction in both lower limbs, but the conduction velocity for bilateral peroneal and tibial nerves was slow and the amplitude of the compound muscle action potential was decreased. The H-reflex showed delayed latency in the bilateral tibial nerves. Somatosensory evoked potential stimulating of the bilateral tibial nerves and the bulbocavernosus reflex, stimulating the pudendal nerves, revealed delayed latencies. In needle electromyography, increased insertional activity and abnormal spontaneous activity were observed in muscles innervated from L2 to S2. From these findings, bilateral lumbosacral polyradiculopathy, accompanied by a sacral reflex arc lesion, was diagnosed, and was clinically compatible with CES.\nAt the time of transfer to our department, the patient was voided with an indwelling catheter. The amount of self-voiding after removing the indwelling catheter was 100-200 mL and the residual urine volume was measured to be about 200-300 mL. Voiding sense and desire were normal, and no incontinence, feeling of residual urine or hesitancy was reported. However, timed intermittent catheterization was used for removal of residual urine after self-voiding.\nThe patient had sufficient improvements with walking independently on an even surface level through comprehensive rehabilitative managements, including drug therapy (tramadol 150 mg, gabapentin 900 mg) for neuropathic pains, muscle strengthening exercises, functional electrical stimulation for bilateral lower limbs, and gait training. On the 13th day after transfer, the patient was presented with chills and fever (38.5℃). In a complete blood count, leukocytes revealed 26,110/µL, hemoglobin was 9.3 g/dL, and platelets were 168,000/µL. Creactive protein and the erythrocyte sedimentation rate increased to 34.32 mg/L and 120 mm/h, respectively. In serum biochemical tests, the blood urea nitrogen (BUN)/creatinine ratio increased slightly, to 30.9/1.6 mg/dL, and no other specific finding was observed. A routine urinalysis showed a specific gravity of 1.016, pH 6.0, albumin (2+), glucose (3+), ketones (-), hemoglobin (1+), leukocyte (3+), nitrate (-), and red blood cell 1-4/high power field (HPF), and a white blood cell in excess of 5/HPF by high-resolution microscopy. After diagnosis of recurrent acute pyelonephritis, tazobactam, an empirical antibiotic drug, was administered intravenously. However, Klebsiella pneumoniae was isolated from blood and urine cultures, so the antibiotic was changed to meropenem.\nAfter 3 days, the patient suddenly complained of pain and tenderness on the left flank during voiding and a 10×20 cm-sized mass was palpated in the left abdomen. Vital signs at that time showed a blood pressure of 100/60 mmHg, a heart rate of 115 beats/min, a respiratory rate of 20 breaths/min, and an axillary temperature of 36.5℃. In a complete blood count, leukocytes were 28,900/µL, hemoglobin was 7.1 g/dL, and platelets were 158,000/µL, indicating a sharp decrease in hemoglobin; thus, an acute hemorrhage was suspected. In a coagulation profile test, the prothrombin time was 13.7 seconds, the international normalized ratio was 1.21, and the activated partial thromboplastin time was 35.7 seconds, indicating normal findings. In a serum biochemical test, the BUN/creatinine ratio had increased, to 43.1/3.5 mg/dL, but no other specific finding was observed. In contrast-enhanced abdominal computed tomography (CT), pyelonephritis with multifocal low-density lesions was observed in the left kidney and a perirenal hemorrhage of low density was found in the perinephric space. From the arterial to the delayed phase, active extravasation of contrast media was observed near the perinephric space and was thought to be a hemorrhage in a capsular artery outside the renal capsule.\nThe mass palpated in the left abdomen was found to be a retroperitoneal hematoma with low density in the left iliac fossa (). Systolic blood pressure had decreased by 90 mmHg with declined hemoglobin, thus, emergent transfusion and angiography were performed. No tumor or vascular malformation was found, but coil embolization was carried out due to suspicion of progressive hemorrhage in the left capsular artery (). After transferring the patient to the intensive care unit, conservative treatment for acute renal failure with acute pyelonephritis was performed. No more active bleeding was observed in a follow-up abdominal CT, and the embolized capsular artery was found around the anterior cortex of the left kidney, at the site of the acute pyelonephritis ().\nAfter coil embolization, the hemorrhage stopped, so, nephrectomy was not being considered. However, surgical hematoma removal was conducted, because of persistent abdominal pains. In voiding cystourethrography, the vesicoureteral reflux was not observed, and no voiding images were obtained because the patient failed to void after filling 450 mL of contrast medium even though he had voiding desire. In an urodynamic study, the patient had strong voiding desire when infused with 500 mL of saline, but failed to void due to detrusor areflexia.\nThe patient was administered oral medications, including an alpha blocker and a choline agonist, but intermittent self-catheterization was carried out five times per day due to urinary retention in excess of 500 mL. No additional UTIs or other complications occurred, so he was transferred to a rehabilitation hospital. |
A 66-year-old male patient developed upper digestive hemorrhage, with two episodes of hematemesis, 2 days prior to hospital admission, and several episodes of melena thereafter. Fifteen years previously, he had undergone open surgery to perform right aortofemoral and left external iliac bypass with a Dacron graft. He also had a history of systemic arterial hypertension and chronic obstructive pulmonary disease.\nAbdominal angiotomography showed saccular dilation of the infrarenal abdominal aorta proximal of the bypass, communicating with the fourth portion of the duodenum and measuring 51x41 mm, suggestive of pseudoaneurysm of the anastomosis proximal of the graft, associated with an aortoenteric fistula ( and ).\nSince this was a secondary aortoenteric fistula, linked to a prior abdominal intervention in a patient with very poor clinical status, the decision was taken to use an endovascular approach to repair the injury. However, while using angiotomography reconstruction to take measurements to plan endovascular repair, it was found that the patient’s anatomic parameters were unsuitable, for two main reasons:\nThe proximal neck diameter was 36 mm, preventing use of bifurcated endografts. It should be remembered that the largest diameters available are of the order of 36 mm;\nThe distance between the lower renal artery and the bifurcation in the Dacron graft used for the right aortofemoral and left external iliac bypass was 89 mm, ruling out use of a thoracic aorta stent graft, since the shortest devices have a length of 100 mm.\nFaced with these anatomic conditions, there was therefore no comercially available endovascular device that could be used immediately.\nGiven the urgency and severity of the case, combined with the impossibility of ordering a customized endovascular device, the decision was taken to perform intraoperative customization of a 40x167 mm Medtronic Valiant Captivia thoracic stent graft (Medtronic, Minnesota, United States).\nFirst, the device was released on a surgical back table (). Next, the first stage of the Medtronic Valiant Captivia stent graft was released, maintaining its open proximal ring fixed. Then measurements were taken of the device and the excess distal portion was resected with a scalpel blade ().\nThe stent graft was then re-sheathed, with the aid of cardiac tape, slowly and progressively, until the entire length of the device was completely covered by the delivery and release system (). For the procedure, the right femoral artery was dissected for insertion of a 7F introducer and a 5F introducer was inserted into the left femoral artery via an ultrasound-guided puncture. The stent graft was introduced via the right common femoral artery, over a Lunderquist guidewire (Cook Group Inc., Indiana, United States), and positioned infrarenally, covering the pseudoaneurysm of the proximal anastomosis of the previous aortic bypass. There were no complications during deployment of the stent graft and the final angiographic control demonstrated complete exclusion of the pseudoaneurysm and resolution of the aortoenteric fistula ().\nThe patient recovered well during the postoperative period, was discharged from hospital after 72h, adapting well to oral feeding, with no intercurrent conditions, and with no further bleeding episodes. |
A 36-year-old man who denied previous systemic disease had a history of drug abuse with ketamine for 6 to 7 years (at a frequency of 2–3 times per week, by nasal inhalation, and hence the dosage could not be measured), and had then ceased use for approximately 4 years.\nHe had suffered from dysuria, bladder pain, and a mild burning sensation during urination, especially over the urethral meatus and the perineal region, for approximately 1 month prior to admission. He ignored these symptoms initially, but the burning pain worsened, with concomitant urinary frequency and urgency. He visited another hospital for help, at which routine urine analysis revealed pyuria. Under the impression of acute prostatitis, oral antibiotic treatment with ciprofloxacin was initiated during an outpatient visit; however, his symptoms remained, with no improvement. Two days before admission to our hospital, the symptoms worsened, with a newly-developed decreased voiding amount (approximately 50 mL per void) and urgency with urge incontinence, accompanied by painful hematuria and blood clot formation, especially at the first urine void of the morning. The patient then presented to our Emergency Department. Urine analysis showed pyuria, over 100 white blood cells (WBCs)/high-power field (HPF), and significant tenderness and swelling of the prostate was noted upon digital rectal examination, but no pus-like urethral discharge was seen. Under the impression of acute prostatitis, for which oral antibiotic treatment had failed, the patient was then advised to undergo hospital admission for advanced antibiotic treatment.\nAfter admission, we consulted an infectious disease specialist for evaluation, and antibiotic treatment with ceftriaxone was started immediately. A blood test revealed WBC 4870/μL without predominance of neutrophils or eosinophils. No marked elevation of serum C-reactive protein (CRP) (0.25 mg/dL) was noted. The patient's temperature after admission had remained within the normal range, and there were no accompanying signs or symptoms of toxicity. Several blood and urine cultures were performed, including tuberculosis, but all results were negative. The symptoms of pyuria (which remained over 100 WBCs/HPF), urgency, and painful hematuria persisted with no improvement after one week of intravenous antibiotic treatment. However, a sonogram performed upon admission revealed suspected bladder wall thickening. Due to the persistent symptoms that failed to respond to advanced intravenous antibiotic treatment for 1 week, abdominal computed tomography (CT) with contrast was then arranged. The CT scan showed asymmetrical wall thickening (thickness of up to 1.2 cm) of the anterior aspect of the urinary bladder with a mural nodule, and mucosal enhancement with perivesical fatty stranding (Fig. ). According to the above findings and the clinical symptoms, bladder cancer was highly suspected, and we discussed cystoscopy with bladder biopsy with the patient and his wife, which was then performed the next day. Prior to hydrodistension, the bladder mucosa presented with hypervascularity, but there was no tumor over the anterior wall of the bladder as seen on the CT scan. The bladder mucosa of the anterior wall was erythematous, with multiple hump-like changes, and several biopsies were performed. After hydrodistension at a pressure of 90 cm H2O for 8 minutes, the bladder capacity was approximately 150 mL, and bleeding over multiple aspects of the bladder was seen, with glomerulation and ulcerative changes (Fig. A and B). Pathologic analysis of the bladder biopsies showed erosive cystitis, characterized by denuded urothelial cells, with prominent infiltration by eosinophils, lymphocytes, neutrophils, and plasma cells over the mucosa and submucosal layer. In addition, hypervascularity and submucosal granulation formation with fibrosis were observed (Fig. A and B).\nAfter the operation, the bladder capacity increased a little, to approximately 70 to 80 mL per urination, but the urgency, frequency, nocturia, and hematuria still persisted. We also prescribed an anticholinergic agent, a beta-3 agonist and a nonsteroidal anti-inflammatory drug (NSAID), and the patient was then discharged. During 2 weeks of outpatient treatment, his symptoms did not improve with medication. Thus, we discontinued medical treatment and performed hyaluronic acid (HA) instillation, once a week for a total of 10 times. After the treatment, the symptoms of urgency, frequency and nocturia improved, and the bladder capacity increased to 350 mL per urination according to the patient's own voiding diary; in addition, no morning hematuria or hematuria after holding back urine occurred. After the patient's symptoms had improved, we arranged follow-up MRI of the bladder and cystoscopy; on the images, no thickening of the bladder wall nor nodules were observed (Fig. ). Cystoscopy showed marked improvement of the previously-noted erythematous bladder mucosa, and there was neither active bleeding nor glomerulation seen during the whole procedure. Bladder biopsy near the previous biopsy site was performed, and the final pathologic analysis showed decreased inflammatory cell infiltration, regeneration of the urothelium, and less vascularity (Fig. A and B).\nWritten informed consent to publish this case report was provided by the patient, and the consent procedure was approved by the Ethics Committee of Tri-Service General Hospital. |
A 22-year-old multiparous woman with a history of primary sclerosing cholangitis complicated by portal hypertension, esophageal varices, and thrombocytopenia was admitted at 29 0/7 weeks for evaluation and management of shortness of breath and lower extremity edema. Her obstetric history was significant for prior spontaneous preterm birth with placement of an ultrasound-indicated McDonald cerclage at 20 1/7 weeks of gestation in the index pregnancy. At the time of cerclage placement, the 5 mm Mersilene (polyester) tape was noted to be suboptimally placed along the posterior rim, distal to the internal os, so a second McDonald cerclage of 0-polyester suture was placed cephalad to the tape. She was admitted at 28 0/7 weeks for preterm labor and the cerclages were removed with no remarkable anatomic irregularities. She received antenatal corticosteroids and magnesium sulfate during her admission for preterm labor and was discharged on hospital day #3 with a cervical exam of 1cm dilation and 70% effacement. During her readmission at 29 0/7 weeks for shortness of breath, she began to have contractions and moderate vaginal bleeding on hospital day #3. Her cervical exam was 4 cm and 90% effaced. She was transferred to labor and delivery, where she continued to have a rapid cervical change to 6 cm. A brief fetal heart rate bradycardia occurred with spontaneous recovery to a normal baseline. At this time, findings were concerning for placental abruption or possible coagulopathy from decompensated liver failure with a total estimated blood loss of 500 mL. Amniotomy was performed to expedite vaginal delivery. However, cervical dilation did not continue and complete cessation of vaginal bleeding was noted. Careful visualization of the cervix revealed that the posterior rim of cervix was detached and traversing the presenting fetal head creating a tension band that prevented further dilation or descent. This band of cervical tissue was clamped and suture-ligated followed by rapid delivery. She delivered a male infant with a weight of 1325 g and Apgar scores of 5 and 7 at 1 and 5 minutes, respectively; arterial cord pH was 7.33. Following delivery of the placenta, vaginal exam revealed a partial posterior cervical detachment from 2 to 9 o'clock. The avulsed portion of the cervix did not appear necrotic and was bleeding briskly. Hemostasis was achieved with a single running locked suture. Her postpartum course was otherwise unremarkable, and she was discharged on postpartum day #2. At her six-week postpartum visit her cervical exam was remarkable for a normal appearing anterior lip; however the posterior lip was not visible and not palpable on digital exam (). Pathology was not available for the fragments of cervix that were excised and the placenta was remarkable for acute chorioamnionitis. |
A 71-year-old female smoker presented with stage IV lung adenocarcinoma harboring the EGFR exon 21 L858R mutation. She had no history of drug allergies or autoimmune disease. She was started on erlotinib at 150 mg/day for the treatment. Although she had been taking medications over many years, including calcium-channel blocker for hypertension and statin for hyperlipidemia, erlotinib was her only new medication. Then, by 28 days after the start of erlotinib therapy, she presented with severe pruritus of grade 3 according to the National Cancer Institute's Common Toxicity Criteria. The pruritus was resistant to local application of steroid ointment and to standard systemic therapies, including oral steroids and antihistamines. Furthermore, the pruritus was also linked to acneiform skin rush, leading to the interruption of erlotinib therapy for a period of 2 weeks.\nAfter recovering from these skin side-effects, she was restarted on erlotinib at a reduced dose of 100 mg/day. Oral steroids and antihistamines were continued to prevent recurrence of the pruritus and skin rush. However, within 2 weeks after restarting erlotinib, severe pruritus of grade 3 developed again, followed by acneiform skin rush especially on her face (Fig. ). An evaluation of the pruritus by means of a visual analogue scale (VAS), in which a score of 0 indicates no pruritus and a score of 10 indicates the worst pruritus imaginable, resulted in a score of 8. Therefore, erlotinib was again discontinued, and she was started on aprepitant at 125 mg on day 1 after discontinuation, 80 mg on day 3, and 80 mg on day 5 with the aim of treating the pruritus and skin rush. This treatment schedule for aprepitant administration was decided after studying the various treatment schedules on the basis of the scientific reports of aprepitant administration [, , , , , , , , , , , , ]. Then, the prompt improvement was observed within 5 days after starting the first dose of aprepitant, leading to a score of 2 for the pruritus on the VAS (Fig. ).\nAfter this recovery, she was restarted on erlotinib at 100 mg/day. However, the pruritus and skin rush gradually exacerbated thereafter, leading to scores of 4 and 8 for the pruritus on the VAS within 2 and 4 weeks, respectively (Fig. ). Then, by starting the second dose of aprepitant, the prompt improvement was again observed within 5 days, leading to a score of 2 for the pruritus on the VAS. However, the pruritus and skin rush eventually exacerbated within 4 weeks. At this point, bi-weekly schedule for aprepitant administration (125 mg on day 1, 80 mg on day 3, and 80 mg on day 5, every 2 weeks) was considered and, then, adopted. As the results, throughout the subsequent treatment with erlotinib, the pruritus and skin rush remained well-controlled within the scores of 2 and 4 for the pruritus on the VAS (Fig. ). |
A 59-year-old man developed sudden respiratory distress, tachycardia, hypotonia, and coma about one minute after flexible endoscopy with dilatation and irrigation of a perineal abscess under sedation with propofol. Two years ago he had undergone pelvic exenteration because of advanced prostate cancer with intraoperative (15 Gy) and adjuvant radiotherapy (63 Gy). Wound healing was complicated by a perineal wound infection and development of a perineal abscess. Afterwards, periodical bouginage by flexible endoscopy (Hegar bouginage) of the abscess fistula had been necessary in order to drain pus and to keep the fistula open.\nAfter a few seconds tachycardia ceased spontaneously but neurologic examination revealed a comatose patient with ping-pong gaze, decerebrate rigidity and positive Babinski response bilaterally. Mechanical ventilation was initiated with 100% oxygen since vascular air embolism was suspected. Furthermore, the patient was placed in partial left lateral decubitus position in order to entrap possible air in the right ventricle. Head CT showed massive air entrapment in cortical branches of both middle cerebral arteries, predominantly on the right side, and in the cavernous sinus (Figure ). Since the patient was in need of critical care medicine we were not able to administer hyperbaric therapy. Thus, in order to reduce brain injury we decided to apply moderate hypothermia with a target bladder temperature of 33°C for 24 hours. Hypothermia was immediately induced with rapid free floating ice cold saline infusions (4°C, 25 ml/kg body weight) and after the diagnostic procedures by an external cooling system. Transthoracic echocardiography detected no intraventricular air. One hour and fifteen minutes after the first imaging, CT angiography showed normal cerebral blood vessels and complete resolution of the intracranial air. During rewarming the patient developed generalized myoclonus which did not respond to intravenous valproic acid, phenytoin and levetiracetam. Only propofol resulted in a discontinuation of myoclonus. The following days the patient increasingly regained consciousness and could be extubated on day ten. At that time MRI of the brain demonstrated multiple bihemispheric and cortially localized areas of restricted diffusion along the gyri (Figure ). Sixteen days after the event the patient was discharged to a rehabilitation facility with a multimodal neglect and a moderate hemiparesis of the left extremities. Three months later his Rankin scale score remained 4. |
A 16-year-old male complained of inability to flex his left elbow since 1 year prior to admission. One and a half year before, he fell down and hit his elbow during football practice. He felt pain and there was swelling on his elbow. However, he didn't seek for medical treatment. He had his elbow massaged every week for 5 months but there was no improvement. His elbow became fixed in extended position. A month later, he went to an orthopaedic surgeon and underwent x-ray examination which revealed a fracture and dislocation on his left elbow. He was then referred to our institution for further treatment.\nFrom clinical examination, range of flexion-extension of the elbow was 300-00 with normal pronation-supination. There was no neurological deficit (). From radiological examination, there was a malunion of medial epicondyle with subluxation of left proximal ulna (). From 3D CT reconstruction, there was a deformity and malunion fracture in humeral capitellum with radial and ulnar postero-superior dislocation (). The patient was diagnosed with extension contracture of the left elbow due to malunion of left capitellum, neglected dislocation of the radiohumeral joint, and neglected dislocation of the ulnohumeral joint. The patient was scheduled to have a contracture release, open reduction and internal fixation, and ulnar interposition.\nIntraoperatively, we did a posterior approach to the elbow. The ulnar nerve was identified and preserved. The fibrotic tissues and heterotopic ossification were excised. We did a contracture release and open reduction and internal fixation using K-Wire. The flexion and extension of the elbow were evaluated and we managed to get 300 - 130° of flexion-extension ROM. Afterwards, ulnar interposition was performed to prevent ulnar impingement. The wound was closed and a single drain was placed. The elbow was immobilized with back-slab in 900 flexion position for two weeks.\nAfter 1 week, the patient went back to our hospital for follow-up examination. In the 1st evaluation, we tried to remove the back slab and moved the elbow passively. The movement is restricted due to pain and the patient went back home with the back slab on. In the 2nd week follow-up, we permanently remove the back slab and the stitches. At that time, the pain still persisted and the patient was planned to have physical rehabilitation.\nOn the 4th week after surgery, the surgical wound was infected. We performed debridement, implant removal, and manipulation under general anesthesia. Two weeks later, patient came back to our hospital. We removed the stitches and started rehabilitation. Later on, he continued his rehabilitation in his previous hospital.\nAfter 6 months, he visited our outpatient clinic for medical checkup. From physical examination, the elbow flexion-extension ROM was 1100 - 300 (). The patient is able to do normal daily activities (). |
The patient is a 71-year-old white male who was found to have a 3.5 cm right kidney mass and had been followed by the urology team closely at VA Pittsburgh Healthcare System. Urine cytology was suspicious for malignant cells. He underwent a radical right nephrectomy on February 3, 2014. Pathology showed clear cell RCC. The tumor was located at the lower pole with a size of 4.5 cm (pT1b) and Fuhrman nuclear grade 2. All margins were not involved by carcinoma, and there was no vascular invasion. He had been followed with a regular CT scan every year. He was found to have small bilateral lung metastasis and lymphadenopathy in 2016. The PET scan on April 26, 2016, revealed FDG activity in the lung and hilar and mediastinal lymph nodes. He underwent endobronchial ultrasound biopsy of the mediastinal lymph node which confirmed to be metastatic from clear cell RCC. Due to his comorbidities and mild thrombocytopenia, we started him on lower dose sunitinib at 37.5 mg per oral daily ×4 weeks every 6 weeks in May 2016. In total, he received 7 cycles of sunitinib. He had been followed every 6 weeks in the clinic. He only developed fatigue due to mild hypothyroidism for which he received levothyroxine. During the follow-up, he was found to have worsening thrombocytopenia with platelet counts in the range of 60,000 to 90,000. A follow-up CT scan and PET scan in October 2016 showed improvement of the lung metastasis and lymphadenopathy. He was last seen in the clinic on March 13, 2017.\nHe was admitted on March 29, 2017, due to muscle weakness, fatigue, poor oral intake, and difficulty swallowing for 2 weeks. During admission, his platelet count was found to be 13,000, serum creatinine 2.3, total bilirubin 4, AST/ALT > 2000, INR 2.9, calcium 7.5, creatine phosphokinase (CPK) > 5000, and uric acid 12 (see ). Sunitinib was discontinued on the first day of admission. CT head revealed no evidence of metastatic disease. Chest X-ray did not show evidence of infiltration or effusion. Echocardiogram showed severe global hypokinesia with LVEF of 30–35%. His LVEF was 55% prior to starting on sunitinib. He quickly developed lactic acidosis and acute respiratory failure. In the intensive care unit, he received bicarbonate, high-dose oxygen, furosemide, and treatment for hyperkalemia. Despite all treatment support, he continued to decline. His family chose to deescalate care, and he died on April 1, 2017. |
A 90-year-old man was seen in consultation for complaints of acute onset of gross hematuria. The patient reported that for roughly one month he had intermittent “tomato juice” colored urine. He had no previous reports of urologic malignancy or hematuria and denied any weight loss, lower urinary tract symptoms, or irritative voiding symptoms. Upon consultation, urinalysis was positive for blood, and a review of urine labs performed in the previous three months demonstrated microscopic hematuria. Physical examination revealed bilateral inguinal hernias, the right larger than the left, but neither causing symptoms. All pertinent biochemical labs were within normal limits.\nCT urogram revealed a number of bladder masses suspicious for malignancy. A large right-sided bladder herniation extended down into the right inguinal canal and scrotal sac, consistent with physical exam findings. Due to patient positioning, this herniated portion did not contain any contrast on delayed phases of CT; however, wall thickening was observed and a mass was noted in the neck portion of the diverticulum that extended through the inguinal canal (Figures , , and ). Additionally, a left-sided hernia was noted to contain descending and proximal sigmoid colon. Cystoscopy revealed a number of large masses within the bladder, one of which emanated from the entrance into the herniation. Due to the acute angle necessary to enter the herniation, the inside was not visualized. Bladder washings obtained during cystoscopy revealed high-grade carcinoma. Two weeks later, the patient underwent a transurethral resection of bladder tumor. During the surgery, the herniation was reduced; however, the tumor burden was too large to be resected completely. Notably, the bladder was mobile on bimanual exam at the end of the case. Pathology returned as T1 high-grade transitional cell carcinoma. Muscle was present in the specimen. The patient was counseled on possible surgical, chemotherapy, and radiotherapy options and declined all. He is currently doing well and remains asymptomatic. |
A 16-year-old, previously healthy, male patient presented initially to a general practitioner with neck pain and torticollis, which was interpreted as a benign condition, and he was sent home with paracetamol. The patient was then admitted to Karolinska University Hospital the day after when he presented again to the Emergency Department with sore throat, severe neck pain, and right-sided Horner´s syndrome. A computed tomography (CT) scan of the brain showed a thrombosed internal carotid artery, a large abscess on the neck, and suspected multiple abscesses in the right hemisphere of the brain. A magnetic resonance imaging (MRI) scan the day after admission confirmed the suspected findings (Figures and ). The patient was started on intravenous antibiotics in the form of cefotaxime 2 g three times daily (TID) intravenously (4) in combination with clindamycin 600 mg TID iv plus metronidazole 1,500 mg once followed by 1,000 mg once daily (OD) iv, while the abscess on the neck was surgically drained. Furthermore, the patient was put on low-molecular weight heparin 10.000 IU OD subcutaneously (sc) to prevent further thrombotic events.\nThe patient had multiple revisions of the neck abscess over the next few days, while the blood cultures came back positive for F. necrophorum, and antibiotics were changed to meropenem 2 g TID iv in combination with clindamycin 600 mg TID iv. A surgical intervention to drain the patient's multiple intracranial abscesses was deemed futile as: (1) diagnosis was already known and relevant antibiotic treatment initiated, and (2) the multiple abscesses were small in nature, without the possibility of significant volumetric reduction by drainage. Instead, based on previous experience, HBOT was suggested as a treatment adjunct, but not initiated since the patient showed slow improvement with reduced C-reactive protein over the following 5 days. Nevertheless, no radiological decrease in the abscess formation was seen on an MRI performed at day 6. On Days 6–15, the patient gradually experienced a clinical decline with increasing pain; he was treated with high doses of opioids, clonidine, and eventually methadone (50 mg oxycodone, 17.4 mg methadone, and 300 µg clonidine daily). An MRI day 10 demonstrated increasing size of abscesses, increased edema (still moderate), and minimal midline shift. Betamethasone 4 mg daily was started on Day 13 (3 days before HBOT), and the dose was increased to 8 mg the day after the first HBO treatment. On Day 16, the patient's clinical condition worsened further with a decrease in consciousness to a Glascow Coma Scale (GCS) score of 13, a progressive left-sided hemiparesis and severe pain. An MRI demonstrated increased edema, midline shift, and uncus herniation. The abscesses were mostly stationary in size, with some decreases or increases in comparison with an earlier (1 week previously) MRI exam. Once again surgery was deemed futile without the possibility of significant volumetric reduction by drainage. The patient was referred for HBOT treatment.\nAt HBOT initiation, the patient was afebrile and had a GCS of 11, severe pain, right fascial paresis, and paresis in the left arm. HBOT (280 kPa, 113 min in a multi-place chamber) was initiated immediately upon referral, with the GCS increasing to 14–15 after the first HBOT session. Complete remission of the hemiparesis occurred after three HBOTs. All opioids were weaned after ten HBOTs. The patient was discharged to an out-patients rehabilitation clinic after 15 HBOTs (received 37 HBOTs in total, no adverse events reported) and was continued on iv ceftriaxone 4 g OD iv for 2 months and long-term oral clindamycin 300 mg TID po. He returned to school 2 months after presentation, feeling perfectly fine, why he did not want to complete the planned 40 HBO treatments. He went through neurorehabilitation and follow-up as an out-patient; neuro-psychological assessment at 4 months after initial presentation was normal. MRI at 7 months showed complete remission of abscesses but a persistently occluded carotid artery and collateral flow to the right hemisphere (Figure ). Antibiotics were discontinued at 8 months. The case timeline, including GCS, important diagnostic and medical interventions, and drug doses, is summarized in (Figure ). |
A 29-year-old Asian female presented to the emergency department for a progressively worsening rash over the prior week. The eruption originated as a solitary pruritic plaque on her left arm, which over the next two days spread to her trunk and legs. Her family physician initially prescribed a course of valacyclovir for presumed varicella zoster virus infection. She returned to the same provider three days later and the rash was noted to now involve the interdigital aspects of her hands and feet. Permethrin cream was prescribed due to concern for scabies. The lesions continued to worsen and the patient developed a fever and sore throat eight days after the eruption onset. She was subsequently instructed by her primary care provider to go to the emergency department for further evaluation.\nIn the emergency department, she complained of severe pruritis and painful oral lesions but denied having any painful skin lesions, skin sloughing, or any anogenital lesions. On exam, she was tachycardic to 131 bpm but was afebrile, normotensive, and in no acute distress. Cardiovascular and pulmonary examinations were unremarkable. Cutaneous examination revealed numerous erythematous discrete papules and minimal blanching on the bilaterally distal extremities, face, and neck (). There were also discrete papules coalescing into nonblanching, erythematous plaques on her trunk and proximal extremities (Figures and ). The soft palate did exhibit petechiae, without any erosions or ulcerations. Cervical lymphadenopathy was also appreciated.\nThe patient had a history of Hodgkin lymphoma diagnosed, in 2007, at the age of 25, which was treated with chemotherapy and electron beam radiotherapy, and has been in remission since then. Medications included venlafaxine for depression and oxcarbazepine for mood stabilization which was started approximately 2 months before. She endorsed allergies to latex and shellfish and admitted smoking less than one pack of cigarettes per day.\nA cell blood count was notable for atypical lymphocytes at 9% (1.1 × 109/L) and elevated eosinophils of 7% (0.68 × 109/L). Liver enzymes were also elevated, with alanine aminotransferase at 130 units/L (15–46 units/L), aspartate aminotransferase at 108 units/L (13–69 units/L), and alkaline phosphatase of 267 units/L (38–126 units/L). Chemistry and coagulation studies were unremarkable. Despite a thorough discussion regarding the necessity of a skin biopsy, the patient declined.\nThe patient was diagnosed with DRESS based on a “definite” RegiSCAR score and subsequently admitted to the hospital. Oxcarbazepine was discontinued and prednisone was initiated at 1.5 mg/kg daily. During the hospitalization, liver enzymes downtrended, while the eosinophilia increased from 7% to 12% (1.55 × 109/L). An HHV-6 IgG level was checked 1 week after admission and was elevated at 7.96 IV (>1.11 indicates current or past infection).\nThe patient was discharged on hospital day three and was continued on prednisone 1.5 mg/kg daily, given the stabilization of her eruption. She was educated on the importance of avoiding aromatic epileptic drugs and to follow up with her psychiatrist for medication reevaluation.\nOne week after discharge, her eruption continued to improve and her lymphadenopathy had resolved. The lesions became blanchable on the trunk; however, her eosinophilia increased from 12% to 23% (4.68 × 109/L). On postdischarge day fifteen, there was a decrease in her edema with truncal desquamation. Prednisone dose was decreased to 1 mg/kg. On postdischarge day 27, the lesions had almost completely resolved, with residual postinflammatory hyperpigmentation observed on bilateral ankles. The prednisone was tapered off over the next month with total resolution of the rash and normalization of eosinophils (0.23 × 109/L). |
A 72-yr old male patient was diagnosed with stage IV non-small-cell lung cancer (NSCLC) in March 2012. He was treated with weekly docetaxel-cisplatin (DP) chemotherapy: docetaxel 35 mg/m2 and cisplatin 30 mg/m2 on day 1 and 8 every 3 weeks. During the 1st cycle, grade 3 nausea and vomiting developed from day 3 of chemotherapy. Thus fasting, parenteral nutritional support, and hydration with intravenous administration of metoclopramide and lorazepam were given. During the 2nd cycle, neither nausea nor vomiting but grade 3 diarrhea (8-10 stools per day) developed from day 4 and he was admitted to hospital on day 6. Diarrhea was profuse and watery without blood or pus. Grade 3 dehydration was combined while there was no abdominal pain, tenderness or fever. Stool studies including culture revealed neither pathogen nor white/red blood cells. Laboratory examinations including white blood cell count, erythrocyte sedimentation rate, and C-reactive protein were within normal limits. Fasting, parenteral nutritional support and hydration with oral loperamide, starting with 4mg followed by 2 mg every 2 hr, were done. Despite of the management, diarrhea continued until day 9 of chemotherapy. On day 10 of his 2nd cycle, diarrhea was resolved and he started diet on day 12, but diarrhea redeveloped. The same management with loperamide was done and the diarrhea was resolved on day 15. Chemotherapy at day 8 of the 2nd cycle was delayed to day 16 and given with 20% reduced dose. After 3 days, grade 3 diarrhea developed again and he visited emergency room. The same management with loperamide was done for 3 days and diarrhea was resolved.\nWe concluded that docetaxel induced his diarrhea because of several reasons: no signs of infection, no use of antibiotics, repeated diarrhea after chemotherapy and little probability of diarrhea with other medications including dexamethasone, palonosetron and cisplatin. Chest computed tomography after 2 cycles of DP showed near complete response according to RECIST v 1.1 (). Thus we decided to continue DP chemotherapy despite of the severe repeated docetaxel induced diarrhea.\nOn day 1 of the 3rd DP chemotherapy with 20% reduced dose, prophylactic loperamide (2 mg every 8 hr) and fasting was started before administration of chemotherapy. Diarrhea did not develop with 4 days of fasting and 7 days of loperamide. Day 8 DP of 3rd cycle was delayed due to grade 2 asthenia and started on day 15. On day 15, prophylactic loperamide was started before chemotherapy and fasting was started after administration of chemotherapy. The duration of fasting and administration of loperamide were shortened to 2 and 5 days, respectively. The 3rd cycle was completed without diarrhea. Subsequent cycles of DP chemotherapy with 20% reduced dose could be given without diarrhea by virtue of loperamide. Now he finished 6 cycles of DP and which resulted near CR. |
Our patient was an 18-year-old male university student who was diagnosed with SLE at the age of 10 by a pediatric rheumatologist based on clinical and laboratory findings; however, the patient had no records of the initial diagnosis at the time of presentation. He had continuously active disease due to poor compliance with his regular medication and poor follow-up. During the 8 years since diagnosis of SLE, he had had SJS three times with similar presentations each time. Each attack of SJS was preceded by febrile illness, for which the patient had visited local health centers and was given antibiotics or antimalarial drugs, which are considered a triggering factor for SJS. He presented to Omdurman Military Hospital (Khartoum, Sudan) on 25 April 2018 with a skin rash that was preceded by symptoms of a short febrile illness. The rash was minimally painful. He had no other symptoms related to SLE. His mother reported that he had developed convulsions with the last attack and underwent magnetic resonance imaging of the brain, which showed viral encephalitis. On examination, the patient had a maculopapular rash involving the trunk, palms, soles, and mucous membranes, affecting less than 10% of his body surface area. Examination of the lesions on his back and chest showed purpuric macules and papules, as well as well-defined violaceous annular plaques on the back and upper chest. He had erythematous macules and patches with some overlying erosions and hemorrhagic crusts on his hands. Chilblain-like lesions on the tips of some digits and skin peeling were noted. Mouth lesions showed mucosal erosions and hemorrhagic mucositis involving all of the mouth and lips (–). There was no ocular involvement, no target lesions, and no other SLE-related manifestations. All vital signs were normal. On the basis of this presentation, the differential diagnoses included skin infection, SLE-related mucocutaneous manifestation, SJS, acute cutaneous lupus erythematous (ACLE), toxic epidermal necrolysis (TEN), and drug-induced lesions. The patient had no family history of similar conditions. Laboratory evaluations revealed hemoglobin of 85%, a white blood cell (WBC) count of 4.8 × 109/L (normal range: 4–11 × 109/L), erythrocyte sedimentation rate of 40 mm/hour (normal range: <20 mm/hour), blood urea nitrogen of 36 mg/dL (normal range: 7–20 mg/dL), serum creatinine of 1.1 mg/dL (normal range: 0.5–1.1 mg/dL), total immunoglobulin (Ig) E level of 101.8 IU/mL (normal range: 150–1000 IU/mL), IgM of 0.90 g/L (normal range: 0.4–2.5 g/L), IgG of 15.0 g/L (normal range: 6.0–16.0 g/L), anti-double strand DNA antibodies of 31 (positive: ≥25 U/mL), and anti-nuclear antibody (ANA) titer by ELISA of 2.3 (positive: >1.2 index value). The patient had negative or normal results for anti-histone antibodies and viral screening, a complement C3 level of 30 mg/dL (normal range: 80–178 mg/dL), and C4 level of 6 mg/dL (normal range: 12–42 mg/dL). Skin biopsies were taken from the affected areas and sent for histological study. Sections showed a small skin biopsy exhibiting alterations in the vacuolar epidermal interface with lymphocytic infiltration and pigment incontinence (). The skin lesions were consistent with early changes of SJS. There were no facilities for immune fluorescence; therefore, it was not performed.\nThe patient was admitted, and supportive care, intravenous (IV) fluids, and IV proton pump inhibitor were initiated. The patient first received IV hydrocortisone, followed by oral prednisolone. Because he had a possible history of herpes encephalitis, he was also treated with IV acyclovir (750 mg/8 hours) for 3 weeks, followed by a prophylaxis dose of oral acyclovir 250 mg/day. Intravenous immunoglobulin was considered but was not needed. The patient’s condition improved markedly, and the rash had completely resolved after 3 weeks (). For continuous management of his condition, he was started the immunosuppressant medication CellCept 500 mg twice a day (Genentech, San Francisco, CA, USA). |
A 20-year-old male patient was consulted to the emergency service, nearly 6 hours after a firearm injury directed at his left infraclavicular region. Arterial blood pressure was 100/60 mm Hg, and heart rate was 105/min. Presumed bullet entrance hole was located nearly 3 cm above the left scapula, and its exit hole was approximately 12 cm above the left nipple. On the anterior aspect of the left hemithorax, a marked swelling when compared with the right hemithorax, hematoma, and subcutaneous emphysema which caused respiratory distress were noted. Presumably venous blood was oozing from the exit hole on this site. Arterial pulses were palpable, and any sign of ischemia was not detected on the upper extremity. Radiograms obtained did not show any evidence of pneumothorax, hemothorax, or bone fracture. Computed tomograms revealed a widespread subcutaneous hematoma, emphysema covering all over the anterior aspect of the left hemithorax, diffuse contusion of the left lung, and mediastinal air. The patient was taken into the angiography unit. Selective left subclavian artery imaging demonstrated intact subclavian artery. Venographic examination disclosed extravasation in the subclavian vein extending from just proximal to the axillary vein (). The patient was urgently operated with a severely decreased hematocrit (18%). Through a 5 cm long incision, axillary artery and vein were explored. Still through a nearly 15 cm long incision extending from one-third medial of the clavicula in the left infraclavicular region and encompassing the wounded area, pectoralis major muscle was partially excised, and on the medial side, subclavian artery and vein were explored. Distally, at the shoulder level a nearly 5 cm defect created by axillary vein rupture extending up to its insertion into the subclavian vein which roughly corresponds to the midpoint of clavicula was observed. Abundant venous bleeding was noted oozing through this site. Proximal and distal explorations revealed terminal ends of veins; then vascular clamps were placed, so as to stop bleeding. The patient was heparinized. Through a right femoral incision, saphenous vein was brought out and interposed between axillary and subclavian veins (). Subclavian artery and brachial plexus were observedly intact. Muscular structures were repaired, and adequate debridement was ensured. A total of 2100 cc blood and blood product were replaced intraoperatively. At the start of the operation, before hemostatic control, and at the end of the operation, following anastomosis, cardiac arrest occurred and heart rhythm was corrected with medical therapy. |
A 32-year-old female with a history of hyperthyroidism status after radiation resulting in hypothyroidism and no history of seizures presented with an acute onset of behavioral changes and witnessed seizure activity. Family history is remarkable for thyroid disease in multiple relatives, but negative for seizure or psychiatric disorders. Behavioral changes included uncontrolled laughter, screaming, signs of agitation, spitting on the floor, complete lack of appetite, and speaking in a British accent. A further history revealed that the patient is of Caucasian descent, was born in Germany, moved to the United States when she was a baby, and has no ties to Britain.\nShe had two seizures both involving tongue biting and postictal confusion with combative behavior. Her workups for seizures, including but not limited to head CT, urine drug screen, and electrolyte levels, were all within normal limits. She, as well as her family, refused MRI and subsequently was discharged on levetiracetam for new onset seizures. On the fourth day of illness (DOI), the patient was admitted to a local community hospital with continued behavioral changes, where an MRI and lumbar puncture (LP) were found to be unremarkable, with a WBC count of 1 cell per mm3. Other CSF parameters include a RBC count of 10 cells per mm3, glucose of 53 mg per dL, and protein of 26 mg per dL. She was subsequently transferred to our hospital care on the fourteenth day of illness because of persisting and worsening behavioral changes. Upon revisiting the initially unremarkable impression of the MRI, abnormal T2 flair hyperintensity in the mesial temporal lobes was noted, with left lobe hyperintensity greater than that of the right lobe (). These features raised suspicion for limbic encephalitis.\nTiters for serum anti-NMDAR and paraneoplastic antibody panel were sent on clinical suspicion. Video EEG () showed frequent focal onset electrographic seizures from the left frontocentral and left frontotemporal region. Some of these electroclinical seizures showed delta brushes (). With strong clinical suspicion for an anti-NMDAR or paraneoplastic antibody related encephalitis, before even receiving antibody titer results, the patient was started on five-day IV steroids on the fourteenth DOI, and IVIG course started on the fifteenth DOI.\nAt this point, multiple differential diagnoses were being considered including autoimmune encephalitides. During hospital admission, the patient continued to remain afebrile. Repeat LP showed lymphocytic pleocytosis, with a quantitative value of 54 cells per mm3 with 98% lymphocytes, after which she was started on empiric acyclovir until HSV PCR was later confirmed to be negative. All other CSF findings were insignificant, with a normal protein level of 16.8 mg per dL, no RBCs, and an elevated glucose level of 95 mg per dL. She continued to have seizures requiring Lacosamide followed by an addition of Lamotrigine. On the fifth day of IVIG course and twentieth DOI, NMDAR antibody was found to be positive in the serum. CT of the chest, abdomen, and pelvis showed no evidence for neoplasms and a transvaginal ultrasound was negative for ovarian teratoma. CSF was positive for NMDAR antibody with a titer of 1:64. After completion of IV steroids and IVIG, there was no significant clinical improvement. She was started on rituximab on DOI 27 for a total of 4 weeks given weekly, with subsequent clinical improvement in addition to no clinical seizures on EEG and resolution of her new onset British accent.\nThe patient continued to have subclinical focal seizures, catatonia, and orofacial dyskinesias with subsequent gradual improvement in her behavior at discharge. When seen for follow-up as an outpatient, she still was found to have some residual memory and cognitive processing deficits. The patient continues to follow up in the hospital for rituximab infusions which is controlling her anti-NMDAR encephalitis and she has now returned back to baseline health. |
A 15-year-old right-handed boy, accompanied by his mother, arrived at the Pediatric Dentistry Department, Rural Dental College, Loni after seeking treatment without success in a private dental clinic. His chief complaint was pain in the upper front region of jaw associated with front teeth.\nDuring history taking, the mother reported that the patient's “crises” began at 6 years of age. Since then, there have been frequent episodes in which he turned his eyes up, shook, stiffened, contorted his body, and clenched his fists. She could not ascertain if there was any loss of consciousness, during these episodes. She had consulted a pediatrician and a neurologist for evaluation of his general and neurological evaluation. Neurological examination reports revealed that, the patient presented with some spontaneous myoclonic jerks of right and left arms. The diagnosis of right and left focal epileptic fits, which were secondarily generalized was made. Language and learning difficulties were diagnosed as the patient had been repeating his fifth grade for 5 years. Medical reports also revealed that the patient was initially on carbamazepine 200 mg twice/day and risperidone 1 mg/day for 6 years. The drug therapy was changed at the age of 12 years by discarding the risperidone and increasing the carbamazepine dosage to 600 mg/day. The mother did not understand that a diagnosis of epilepsy had been made because of her lack of education. Patient's routine hematological investigations were within the normal limits.\nAt first dental visit patient was extremely anxious about the dental clinical environment. The patient was relaxed by the dental staff and nurses. He was introduced to the dental equipment's in a stepwise manner. Tell-show-do approach was very helpful in this patient. The oral examination revealed numerous grossly decayed teeth with poor oral hygiene []. Root stumps were present for 31, 32, 41, and 42. Endodontic treatment was carried out for 21 and 22 by the previous dentist with iatrogenic mishaps. Intraoral periapical radiographs revealed extruding gutta-percha point beyond the apical foramen in association with 21 and a broken endodontic file at the apical 3rd of 22 []. The patient had underwent extractions of first permanent molars in 3rd and 4th quadrants by the previous dentist at the age of 14 years. The patient's dental occlusion was entirely deranged. The case was diagnosed as adolescent dental caries with special health-care needs. Treatment plan was formulated for the patient with following goals in mind:\nEducation and motivation of the parent for improvement of patient's oral hygiene Minimizing the pain in maxillary anterior region Reducing and treating other carious teeth Stabilizing the occlusion Improving the masticatory efficiency Improving the salivary flow rate Improving the overall oral health. Patient's parent was informed about the diagnosis, were explained about the treatment plan and the need for endodontic, surgical, and prosthetic rehabilitation. After the motivation of the parent, they were willing for the treatment and were ready to keep up the appointments. In the initial appointments, a thorough oral prophylaxis was carried out, and 0.12% chlorhexidine oral rinses twice daily were prescribed at home. A salivary substitute like mouthkote solution was prescribed to minimize the oral dryness.\nAfter obtaining the neurologist's consent, the blood reports, and under an antiepileptic drug regime, endodontic surgery was planned for 21 and 22 along with endodontic retreatment for the same. Following oral prophylaxis and administration of a local anesthetic (lignocaine and adrenaline injection I.P. (Harson Laboratories, Baroda, Gujarath, India) a semilunar incision was placed with no. 15 blade on the attached gingiva extending from mesial aspect of 21 and until the distal aspect of 22. A bony window was made with surgical round carbide bur (no. 8R, SS White Company, Dental Avenue India, Pvt. Ltd., Mumbai, India) mounted on a slow speed handpiece (NSK, PANA AIR; Nakanishi Inc., Shimohinata, Tochigi-Ken, Japan) under copious normal saline irrigation []. The extruded gutta-percha was excised from the apical 3rd of 21. Furthermore, the broken endodontic file was removed from the apical 3rd of 22. A complete curettage of the area was carried out followed by suturing of the flap with 3-0 non-resorbable black surgical silk suture (Ethicon, Johnson and Johnson Ltd., Mumbai, India) []. The endodontic treatment was repeated with 21 and 22 followed by treatment with 11 and 12. Postoperatively antibiotics and analgesics were prescribed for 5 days. Patient's pain was relieved completely after the endodontic surgery, and endodontic treatment and the healing of the surgical area was uneventful.\nThe clinical crowns of maxillary incisors were compromised as a result of caries, hence prior to planning for extracoronal fixed restorations on these teeth, and it was mandatory to restore them with custom made the post and core. The 2/3rd of gutta-percha was removed from the endodontically treated maxillary incisors root canals with the help of no. 2 Peeso reamer (Prime Dental Products, Mumbai, India) for post-space preparation. Post-space impression was made using blue inlay wax (Inlay Wax Medium, GC Corporation, Tokyo, Japan) along with the fabrication of core with the blue inlay wax for the four maxillary incisors. The casting was carried for the impressions of post and core. The custom made the post and core were trail fitted on the four maxillary incisors and then were cemented with Type 1 Glass Ionomer cement (GC Corporation, Tokyo, Japan) []. Extra-coronal porcelain fused metal (PFM) restorations were given on the four maxillary incisors after []. Meanwhile, extractions of the anterior root stumps in the lower arch were carried out. All the procedures were carried out under antiepileptic medication, with Neurologist's and Parental consent. The extraction sockets were allowed to heal till a period of 4-6 weeks.\nAfter the complete healing of the extraction sockets, diagnostic impressions were made for the arches using irreversible hydrocolloid (Alginate) impression material (Imprint Alginate Impression Material, Mumbai, India). Special tray was fabricated on the diagnostic cast for the dual impression technique. After border molding and final impression of mandibular edentulous region under physiological loading, using non-eugenol impression paste (IMAGE, Eugenol Free Impression Paste, Prime Dental Products, Mumbai, India) and the anatomical (dentulous) region was recorded using alginate pick up impression []. The master casts were obtained, and a surveying of the master casts revealed larger amount of lingual undercuts, so a labial flange flexible denture was planned. After blocking out of all the undercut areas and the diagnostic wax up, Face bow transfer was carried out, and centric jaw relation was recorded. The jaw relation record was quite difficult for this patient and required repeated training at home by the parent as well as in the dental operatory by the dentist. Try-in was carried out after the teeth arrangement. A flexible Valplast partial denture (Katara Dental Laboratories, Mumbai, India) was fabricated and was inserted in the lower arch []. Patient's comfort, speech, and acceptance for the treatment were assessed. The patient and his parent were happy and satisfied with the treatment being carried out. There was a significant improvement in the speech as well. The entire treatment was completed in 8 months due to intellectual deterioration of the adolescent. After the insertion of removable prosthesis to the patient, it needs to be changed after a period of 6-8 months until the age of 17-18 years unless the maxillo-mandibular growth of the patient is ceased. The patient was regularly followed-up every month. |
A 14-year-old female patient reported to the Department of Periodontology, Jaipur with a complaint of swollen gums on both the arches for 3 years, which was slow at the outset, and then the swelling started to dilate for 4 months. Due to swollen gums, she was facing a hurdle in speech, while chewing food, and during the cleaning of teeth with the brush and also complaint of bleeding gums and bad breath since last 4 months. The patient had also gone for surgical intervention for similar swollen gums 3 years ago.\nThe patient had no signs of mental retardation, hypertrichosis, or epilepsy and had no history of any medication that can be the reason for the occurrence of the overgrowth of the gingiva. The history of the family was noncontributory.\nExtraoral examination of the patient revealed a convex profile and prominent lips. Intraoral examination exhibiting generalized overgrowth of the gingiva in both the arches. More than half of the crown was covered with gingival tissue (). The gingiva color was normal with dense consistency. Maxillary anterior teeth were proclined. There was spacing between the teeth and a deep bite was also present. Orthopantomogram (OPG) showed localized vertical bone loss with respect to 46 and horizontal bone loss 16 and 47 and except for the third molars, all the permanent teeth were present. The treatment plan was followed by phase 1 therapy (scaling and root planing) and after completion of phase 1 therapy, the labial tissue from the mandibular anterior region was excised and sent for histopathological examination. Histopathological appearance revealed idiopathic gingival fibromatosis which showed parakeratinized stratified squamous cell epithelium with elongated rete pegs. The connective tissue showed densely packed collagen bundles (). After the result of the biopsy, the external bevel gingivectomy in association with gingivoplasty was planned and performed under local anesthesia quadrant-wise (). And after the required crown lengthening was attained () then the excised site was thoroughly irrigated and the periodontal dressing was applied for 7 days and the chlorhexidine mouthwash (0.2%) was instructed to the patient, to rinse it twice a day and to maintain proper oral hygiene.\nAfter 1-week dressing was removed and postoperative healing was uneventful. And after 1 week next quadrant was excised similarly. After 1 month of the recall, it was observed that there was no recurrence of the enlargement ( and ). |
A 54-year-old Japanese man presented to a Department of Internal Medicine with chief complaints of dry mouth and weight loss that he had been experiencing for two months. He had type 1 diabetes mellitus, which was being treated with insulin. Computed tomography (CT) scans showed the presence of bilateral renal and pulmonary masses, and swelling of his pancreatic parenchyma. He was referred to our hospital with suspected bilateral renal cancer, multiple lung metastases and autoimmune pancreatitis. He had bronchial asthma, but no habitual contributory factors. Blood tests revealed high IgG (1775 mg/dL) and IgG4 levels (351 mg/dL). Lactate dehydrogenase and C-reactive protein levels, which are prognostic factors for renal cancer, were normal (162U/L and 0. mg/dL, respectively). No other abnormal values were noted, including urine analysis results. Contrast-enhanced CT scans showed multiple nodular opacities of various sizes with irregular margins in both lung fields. In his abdomen, there were slight poorly enhanced mass lesions (left, 10 × 10 mm; right, 18 × 14 mm) in the upper pole of both kidneys (Figure ). Magnetic resonance imaging showed a mass in each kidney with a low signal intensity on the T1- and T2-weighted images, and poorly enhanced areas inside each mass. Magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography were performed, and our patient was diagnosed with autoimmune pancreatitis. The bilateral renal and pulmonary masses were suspected of being multiple lung metastases stemming from bilateral renal cancer, but inflammatory pseudotumors associated with autoimmune pancreatitis could not be ruled out. Based on these findings, a CT-guided biopsy was performed on the right pulmonary mass and right renal mass. Histopathological examination of the biopsy specimens showed extensive fibrous tissue around the glomeruli in his kidney and alveoli in his lung. Infiltration of lymphocytes and plasma cells was also observed. A malignant tumor was considered unlikely because no atypical cells were observed. However, immunohistochemical staining revealed the presence of IgG- and IgG4-positive plasma cells; the number of IgG4-positive plasma cells was 44 cells per high power field (HPF) as shown in Figure . Based on these findings, we diagnosed the tumor as IgG4-related bilateral renal and multiple pulmonary masses.\nFollowing diagnosis, treatment with oral prednisolone (40 mg/day) was initiated. A CT scan performed on the ninth day of treatment showed a reduction in the size of the masses, so the dose was decreased to 30 mg. Subsequent CT scans showed a further reduction in the size of the masses so treatment with prednisolone was tapered. After one month of treatment, contrast-enhanced CT revealed new, small pulmonary lesions, but also demonstrated a general improvement, with a reduction in size of the right renal mass, and disappearance of the left renal mass (Figure ). Serum IgG levels decreased to values within the normal range after initiation of treatment with prednisolone. Our patient continued receiving 10 mg prednisolone per day to prevent a recurrence, which to date, has not occurred. |
The patient was an 83-year-old postmenopausal woman with a paternal family history of gastric cancer. The patient had a history of colon cancer and Hashimoto’s disease. She underwent breast augmentation with silicone injection approximately 60 years ago and underwent surgery for colon cancer approximately 1 year ago. A PET/CT was done to detect colon cancer recurrence. During this time, a lesion showing FDG uptake was incidentally detected in her right breast and was suspected to be breast cancer (). Diffuse undulations were palpated on both sides of the breast, which is consistent with the influence of breast augmentation with silicone injection; however, no apparent mass was palpated near the FDG uptake area. MMG was not performed considering breast augmentation surgery. US did not show a clear hypoechoic mass lesion at the site corresponding to the FDG uptake site, but careful observation using CD revealed a slight hypoechoic area with hypervascularity (yellow lesion in the schematic) (). An US-guided core needle biopsy was performed (), and invasive ductal carcinoma (IDC) was diagnosed based on the histological findings. Two punctures were made at the 12 o’clock position of the right breast, and cancer tissue was detected in both needle biopsy specimens. Immunohistochemical staining revealed positive expressions of oestrogen receptor and progesterone receptor. The human epidermal growth factor receptor-2 (HER-2) expression score was 2+, but in situ hybridisation showed no amplification of the HER2 gene. US also revealed multiple hypoechoic masses with no vascularity in her right breast, near the FDG uptake site based on PET/CT images (red lesions in the schematic) (). Silicone granulomas were suspected; thus, additional core needle biopsies were performed on one of the mass lesions (red lesions in the schematic) to rule out breast cancer. As expected, the diagnosis was silicone granuloma. PET/CT revealed the absence of axillary metastasis and distant metastasis, and revealed the maximum lesion diameter to be 25 mm. Thus, the diagnosis was classified as stage IIA IDC (cT2N0M0) based on the eighth edition of the Union for International Cancer Control tumour–node–metastasis classification of malignant tumours. Right mastectomy and sentinel lymph node biopsy were performed. Postoperative pathological findings confirmed that the tumour was IDC with an infiltration diameter of 29 mm. Therefore, the final diagnosis was stage IIA IDC (pT2N0M0). Macroscopic findings of the resected specimen revealed multiple silicone granulomas on the dorsal side of breast cancer mass (). Histological findings showed that extensive granulomas were present in the mammary tissue surrounding or within the tumour, consistent with postsilicone injection findings. No axillary lymph node metastases were observed, but macrophage aggregation was prominent; this may have been due to the silicone injection. |
The patient was a 69-year-old female with a past medical history of atrial fibrillation, hypertension, hyperlipidemia, and hypothyroidism. She denied any family history of neurovascular disease, AVM, or aneurysm. A right cerebellar hemispheric AVM was discovered incidentally during workup for dizziness. She had undergone neurologic work-up for intermittent vertigo 2 years before the admission, which in turn had resulted in the discovery, on brain MRI, of a right cerebellar hemispheric lesion, thought to represent a cavernous malformation (CM). At that time, she did not have any complaints of headache, motor or sensory disturbances, or loss of bladder or bowel control. Her neurologic evaluation was intact. Thus, she was being followed up by brain MRI and neurologic examination annually. The repeat MRI brain during her second year of follow up was interpreted as demonstrating an AVM rather than a CM, and she was scheduled for cerebral angiography to confirm the diagnosis.\nAngiography revealed a 2.5 cm pial AVM in the superomedial right cerebellar hemisphere, abutting the tentorium. The AVM was supplied primarily through branches of a hypertrophied right superior cerebellar artery (SCA), with lesser arterial supply provided by distal branches of the right posterior inferior cerebellar artery (PICA) (). A single short superficial cerebellar vein drained the AVM into a right cerebellar tentorial vein, and then into the right transverse sinus. Two small nidal aneurysms were also identified, the largest of which measured 1.8 mm in maximal dimension. Magnetic Resonance T2 gradient echo imaging demonstrated small foci of susceptibility in the region of the AVM, presumably reflecting small areas of chronic hemosiderin deposition, but there was no evidence of recent hemorrhage. The vertebral arteries were relatively co-dominant.\nAfter neurosurgical consultation, surgical resection of the AVM was recommended, and pre-surgical embolization was requested to minimize the risk of intraoperative bleeding.\nEmbolization was performed under general anesthesia. Blood pressure, heart rate, and oxygen saturation were monitored intra-procedurally. The mean arterial pressure (MAP) averaged 94.5 mmHg (range 76–117 mmHg) and no hypoxia or hypotension occurred throughout the procedure. Using ultrasound guidance, a five French shuttle guide sheath was placed into the right common femoral artery. Heparin was administered intravenously with intermittent bolus administration to maintain therapeutic anticoagulation. Activated Clotting Time was monitored, with an average value of 201 and a baseline of 135.\nThe sheath was advanced over a four French angled vertebral catheter into the proximal cervical left vertebral artery (VA). As noted on the diagnostic angiogram, the left VA had a variant origin, arising directly from the aortic arch, and was chosen for access due to marked tortuosity at the origin of the right VA. Five micrograms of intra-arterial verapamil was administered to prevent vasospasm, and the five French guide sheath was advanced to the mid-cervical left VA, beyond the origin of the artery of cervical enlargement, which was visualized on roadmap digital subtraction angiograms (DSA). The vertebral catheter was removed and DSA was performed through the sheath. There was good flow around the five French sheath without evidence of any contrast stagnation to suggest flow compromise or occlusion of the VA (). The AVM was unchanged compared to the angiogram 2 months earlier.\nNext, a Phenom Plus delivery catheter and Apollo microcatheter were advanced coaxially over a microwire through the five French sheath, with the Phenom Plus catheter terminating in the distal cervical left VA. An Apollo microcatheter was first taken distally into the dominant SCA branch supplying the AVM, and Onyx 34 was used to embolize a portion of the AVM nidus. The Apollo microcatheter was slowly removed, and the tip detached, remaining in the right SCA. Next, a new Apollo microcatheter was taken into a second SCA branch supplying the AVM, and additional Onyx was administered. This microcatheter was removed, without tip detachment. Finally, an SL-10 microcatheter was advanced into an inferior branch of the right SCA supplying the AVM, and a small amount of Onyx was administered before removing the microcatheter.\nThe remaining branches of the right SCA supplying the AVM were not easily catheterized. Embolization had resulted in an approximately 50% reduction in the size of the AVM nidus, so a decision was made to terminate the exam. Post-embolization intracranial and cervical angiography demonstrated patency of the arteries of the posterior circulation and the extracranial and intracranial segments of the left VA. The artery of cervical enlargement and the ASA remained patent at completion of the procedure. The sheath was removed, and hemostasis achieved. A Cone beam CT demonstrated expected post-procedural changes.\nThe patient was extubated and transferred to the intensive care unit. She was slow to awaken from general anesthesia, but was oriented, following commands, and moving all extremities antigravity immediately post-extubation.\nOn evaluation 3 h post-procedure, she was sleepy but easily aroused by voice, and could follow simple commands. Her neurologic examination at that time was intact. Additionally, she had bilateral upper extremity strength of at least 4/5 and intact light touch sensation throughout. Over the next 2 h, her condition mostly remained unchanged, with mild weakness of bilateral upper extremities on examination that was suspected to be limited by the element of effort and of position, given otherwise normal findings. She was reported to have general weakness at approximately 8 h after the procedure. Her situation did not improve after 2 h and required a repeat of examination and further evaluation.\nHer examination, approximately 10 h post-embolization, revealed strength of 3–4/5 in both upper extremities. Her lower extremities strength remained 5/5, with normal pinprick and vibration sensory exam throughout. Her vital signs were within normal limits and stable, and her examination was otherwise unremarkable. However, concern for ischemia prompted a Magnetic Resonance Imaging (MRI) brain, which suggested diffusion restriction in the upper cervical spinal cord, although this was sub-optimally evaluated due to motion artifact. A cervical spine MRI was obtained next and demonstrated T2/STIR hyperintense signal at the C1 level, corresponding to the region of restricted diffusion reported on MRI of the brain, raising suspicion for possible cord infarction. The patient's upper extremity weakness continued to progress over the subsequent 8 h despite maintaining MAP >75 mmHg, and stable vital signs, and she developed new intermittent lower extremity weakness, but light touch sensation remained intact in all extremities. Clinical examination at this point was consistent with acute SCI. A second cervical MRI revealed more extensive abnormal signal centered at the C2 and C3 levels with associated cord expansion. Additionally, new signal abnormality had developed at the C5–C6 level, without associated cord expansion (). Her limb weakness continued to progress. On evaluation 1 day post-procedure, she had a strength of 1/5 and 2/5 in proximal and distal muscle groups of both upper extremities, respectively, with a strength of 2/5 in both lower extremities. Pinprick and temperature sensation were decreased at the approximate level of C2–C4 throughout the lateral torso and both upper extremities, while vibration and proprioception remained intact in all extremities. These findings reinforced the diagnosis of acute SCI. demonstrates the timeline of the events within 24 h after the procedure. A second brain MRIat this time showed evidence of T2/FLAIR hyperintense signal and increased diffusion restriction in the right cerebellar hemisphere at the site of Onyx embolization. As a result of the SCI, she developed hypercapnic respiratory failure requiring urgent endotracheal intubation and mechanical ventilation. She eventually required tracheostomy placement for anticipated prolonged ventilator weaning along with percutaneous gastrostomy placement. She was successfully weaned off the ventilator and resumed oral intake by 3 weeks, and underwent acute inpatient rehabilitation for a total 4 months, and is now residing at home with significant assistance. |
The patient was a 20-year-old right handed, healthy man presented to our emergency department due to acute diplopia since 2 days before admission following a powerful sneeze. He had always been well except for a history of slight unsteadiness since a month before admission. Additionally, he reported a daily dull, non-incapacitating generalized pain aggravated by coughing or sneezing. On examination, the patient was alert and conscious with normal verbal communication. Examination of the head and neck revealed inward deviation of both eyes and the inability to move outwards. Noting taken, no papilledema was observed on fundoscopic examination. No other abnormal neurologic signs were observed.\nThe patient had been under brain and cervical magnetic resonance imaging (MRI) which revealed a descent of the cerebellar tonsils and part of the brainstem in the foramen magnum (10 mm), which was not accompanied by cervical syringomyelia (). Subsequently, the patient had been under posterior fossa decompression with suboccipital craniotomy and duraplasty which resulted to complete resolution of the chirai. The surgery was followed by partial remission of the diplopia. However, the unsteadiness had gradually worsened in a way that the patient got severely ataxic over 6 months. The neurological examination was characterized by slurred speech, gait ataxia without a tilt, bilateral dysmetria at the index-nose and heel to shin test. The cranial examination revealed right 6th nerve palsy which was the remainder of the recent diplopia (), nystagmus in all gaze direction, more evident on the right side. Other neurologic examination was remarkable.\nIn a more précised history, the family history was negative for any neurological disorder and the patient did not make biographies of any problem except for ataxia. Consequently, the patient underwent a complete screening for acquired ataxia including vitamin B1 deficiency due to alcohol abuse, autoimmune and paraneoplastic ataxia, ataxia associated with celiac disease, demyelinating disorder and autoimmune thyroiditis, nutritional deficiency and infections which were all unrevealing. Again the patient had been under brain MRI which showed a significant bilateral cerebellar hemispheres atrophy.\nAccording to the new findings, the inherited atatxia was strongly suggested aside the underlying chari malformation. At this time the patient had been under genetic test. Ataxia repeat expansion panel test was checked which revealed a pathogenic (full penetrance) CAG repeats (64 repeats) in the ATX3 gene. Eventually the patient was diagnosed with SCA-3 (Machado-Joseph-Disease). |
A 56-year-old male welder presented to a hospital with sudden onset of left foot drop. He underwent lumbar magnetic resonance imaging (MRI) and mild disc protrusions of L3-4 and L4-5 were observed (Fig. ). The initial diagnosis was L5 radiculopathy with profound ankle dorsiflexor weakness. Spine operation was planned and electrodiagnosis (EDX) was conducted to determine the exact location of lesion and to differentiate peripheral nerve lesions before surgery in another clinic (Table ).\nThe patient had been experiencing foot drop for 9 days and initial EDX results revealed abnormal spontaneous activity (ASA) in the left tibialis anterior (TA), peroneus longus (PL), and extensor hallucis longus (EHL). These findings suggested that the patient's foot drop was more likely due to peroneal nerve injury than lumbar radiculopathy. ASA, such as fibrillation, usually appears within 5 to 6 weeks after the onset of the lesion in radiculopathy.[ Consequently, the surgery was cancelled.\nThe next day, the patient was referred to our outpatient clinic for peroneal neuropathy. He complained of numbness in the area below the knee and especially in the dorsal aspect of his foot. These symptoms began 10 days prior and he did not recall any history of trauma. On physical examination, muscle manual testing (MMT) of the TA and EHL revealed a trace grade, while the peroneus muscle showed poor plus grade. There were no signs of TA or peroneal muscle atrophy. Soft tissue swelling was not palpable around the fibular head and popliteal fossa. The palpation of the lateral aspect of the knee showed no degree of tenderness. The Tinel sign over the fibular head was negative. The patient's ankle and knee jerks were normal.\nEDX, performed on the day of the patient's visit to our outpatient clinic, showed common peroneal neuropathy around the left knee with significant axonal denervation in the TA and PL. Compared with the contralateral limb, the compound muscle action potential (CMAP) amplitude was reduced by greater than 70% in the left lower limb distal muscles, which are innervated by the common peroneal nerve. However, because a conduction block across fibular head was not observed, we considered that the lesion was proximal to the stimulation site. Consequently, a diagnostic ultrasonography (USG) was performed to identify the lesion, which was compressing the peroneal nerve. However, we did not find any lesion around the fibular neck and proximal tibiofibular joint, where compression of peroneal nerve is most commonly found.\nAt the 1-week follow-up, the patient's symptoms did not improve. As compression of the peroneal nerve can occur anywhere along its axonal tract, we investigated whether the compression site was located proximally to the knee. A follow-up USG revealed an approximately 19 × 16 × 40 mm sized cystic mass located in the upper lateral component of the popliteal fossa (Fig. ). Surgical excision was planned and MRI was evaluated to find the anatomical relation between mass and peroneal nerve. The images revealed the presence of an approximately 18 × 17 × 41 mm sized multilobulated cystic lesion, which was located anteromedial to the common peroneal nerve and between the common peroneal and tibial nerves on the left side of the supracondylar area of the femur (Fig. ).\nSurgical excision was performed using a direct posterior approach of popliteal fossa using curvelinear incision under general anesthesia. We found the cystic mass after traction of hamstring muscle. The cystic mass was compressing the common peroneal nerve from the medial side of the supracondylar region on the femur resulting the swelling of the nerve. The mass was carefully and completely removed ensuring that all nerve branches were protected with neurolysis (Fig. ). The mass was not connected to the knee joint. A histopathologic evaluation confirmed the diagnosis of a ganglion cyst. There were no postoperative complications.\nTwo months after the surgery, follow-up USG revealed no evidence of cyst recurrence or residual lesions (Fig. ). Moreover, the amplitude of left peroneal nerve CMAP improved mildly on follow-up EDX. Six months after surgery, the patient's pain and hypoesthesia resolved. MMT of the TA and EHL improved to a fair grade. |
A 47-year-old otherwise healthy Caucasian male was evaluated for traumatic subdural hematoma and facial fractures following an altercation. The patient was visually asymptomatic, denying any change in visual acuity, loss of peripheral vision, or diplopia. Past ocular history was notable for a BB gun injury to the left eye at the age of twelve, for which he had never sought medical evaluation. Without any ocular conditions, he had never had an ophthalmological examination. Another medical history included occasional alcohol and tobacco use.\nA noncontrast head CT showed left orbital floor and lateral wall fractures with associated soft tissue swelling. No evidence of globe injury or muscle entrapment was present; however, a small round metallic foreign body was noted in the left orbital apex abutting the superior aspect of the optic nerve (). There were also small posterolateral intraocular calcifications in the left eye.\nThe patient's visual acuity with a reading card was 20/25 in the right and left eyes. Visual fields were full to confrontation in the right eye, but a significant nasal field deficit was present in the left eye. Pupils were equal and reactive without an afferent pupillary defect (APD). Intraocular pressure was 14 mmHg in the right eye and 19 mmHg in the left eye. Elevation of the left eye was mildly restricted, but all other positions of gaze were full bilaterally. Left adnexal edema and ecchymosis as well as temporal subconjunctival hemorrhage of the left eye were present. The remainder of his anterior examination was normal. Fundus examination showed healthy discs, vessels, and maculae bilaterally; however, a large elongated peripheral temporal chorioretinal scar consistent with sclopetaria was noted in the left eye ().\nGiven his lack of symptomatology and uneventful ocular history, a conservative therapeutic approach with periodic observation was recommended. He was referred for outpatient surgical management of his facial fractures following resolution of adnexal edema. |
A previously healthy 10-year-old Asian girl presented to the emergency department with headache, vomiting, and one week of mild nonproductive cough. Her headache started the evening prior to presentation, was gradual in onset and frontotemporal in location, and improved with acetaminophen but subsequently woke her from sleep. It was accompanied by two episodes of emesis. On presentation to the ED, the patient described her headache pain as 3 out of 10 in severity. She denied photophobia, had no further nausea, and denied abdominal pain. She reported that the headache worsened with standing and improved with lying down. Review of systems was significant only for pallor.\nThe patient was otherwise healthy with no prior medical issues and taking no regular medications. She was fully vaccinated and had no known allergies. Her family history was significant for frequent headaches in her mother and maternal aunt. She was living with her parents and brother and attending 4th grade.\nVital signs demonstrated blood pressure 111/56, pulse 104, temperature 37.1°C, respiratory rate 22, and oxygen saturation 100% on room air. Initial exam revealed a well-appearing female and was unremarkable including a normal fundoscopic exam and a normal complete neurologic exam.\nThe patient received ibuprofen and oral rehydration and her headache further improved. A presumptive diagnosis of migraine headache was made and was discharged with primary care follow-up the following day.\nTwo days after her initial emergency department visit, the patient returned to the ED with worsening headache, myalgia, subjective fever, and diffuse weakness. The patient's mother reported that the patient was unable to stand or walk and as a result her mother had been carrying her, including to and from the bathroom. The patient endorsed nausea but no further vomiting.\nVital signs demonstrated blood pressure 105/49, pulse 123, temperature 36.9°C, respiratory rate 30, and oxygenation saturation of 97% on room air. On exam, the patient was moderately ill appearing, lying in bed responding slowly to questions. Her lips were noted to be cracked and with some oozing blood. No oral lesions were noted in the mouth. Pupils were equal, round, and sluggishly reactive bilaterally. Neck was supple with no adenopathy noted. Cardiovascularly, she was noted to be tachycardic with a regular rhythm and II/VI flow murmur. Her respiratory exam was normal. Her abdominal exam was benign with no organomegaly. Neurologically the patient was noted to be slow to respond to questions and moving slowly but without focal deficits. She was, however, unable to walk without assistance. Skin exam revealed diffuse ecchymoses on the lower extremities bilaterally.\nLaboratory studies were ordered along with a rapid brain MRI, and pediatric neurology was consulted.\nLaboratory results were as follows: hemoglobin 2.6 g/dL, hematocrit 8.3%, platelets 10K/uL, and WBC 60.5K/uL with 83% blasts in the differential. CRP was 15.7 mg/L, and ESR was 125 mm/h. Electrolytes showed sodium 139 mmol/L, potassium 4.0 mmol/L, chloride 100 mmol/L, carbon dioxide 24 mmol/L, BUN 11mg/dL, creatinine 0.56 mg/dL, glucose 129, magnesium 2.5mg/dL, and phosphorus 3.6 mg/dL. LDH was 359 U/L, uric acid was 2.3mg/dL. PTT was 29.4 seconds, PT was 19.5 seconds, and INR was 1.7. Fibrinogen was 117 mg/dL and D-dimer was >10,000 ng/mL. Review of peripheral blood smear () demonstrated many primitive cells with round and lobated nuclei, numerous cytoplasmic granules with Auer rods readily identified, and some cells with multiple Auer rods.\nRapid MRI Brain () was obtained which demonstrated leptomeningeal enhancement in the supratentorial parenchyma suggestive of leptomeningeal carcinomatosis, a hemorrhagic lesion in the corpus callosum, multiple subdural hematomas with mild mass effect, and petechial hemorrhages throughout the brain.\nPediatric Oncology was consulted and treatment initiated emergently with ATRA, dexamethasone, allopurinol, cefepime, and blood products including packed red blood cells, platelets, and cryoprecipitate. The patient was subsequently admitted to the pediatric intensive care unit.\nIn the pediatric ICU the patient received several transfusions with platelets, cryoprecipitate, and fresh frozen plasma to manage DIC. She was continued on an induction course of chemotherapy including ATRA, dexamethasone, idarubicin, and arsenic trioxide. Molecular analysis of the peripheral blood was positive for PML-RARA, confirming the diagnosis of APL. After the coagulopathy improved and the patient stabilized, lumbar puncture was performed with administration of intrathecal chemotherapy. The cerebrospinal fluid was notable for the presence of leukemia cells, confirming the involvement of the central nervous system. The patient's encephalopathy gradually improved and she returned to her baseline mental status by day 7 of treatment. The patient was noted to have elevated opening pressure on lumbar punctures, which worsened over the course of induction, attributed to pseudotumor cerebri secondary to ATRA.\nUpon completion of the first 28 days of induction therapy, repeat lumbar puncture and bone marrow studies demonstrated no morphologic evidence of acute promyelocytic leukemia, consistent with remission. |
A 55-year-old female was referred to our institution with a diagnosis of juxtarenal abdominal aortic aneurysm. She had complaints of severe abdominal pain over the past 10 days, which was radiating to the back and was also associated with heaviness over the entire abdomen. On examination, tachycardia was present and she was hypertensive with blood pressure of around 150/96mmhg, with mild pallor. Abdominal examination revealed fullness over the epigastric region, which was pulsatile. We avoided palpation.\nOn CT Angiography ( and ) a large fusiform saccular aneurysm was present in the abdominal aorta, measuring 17.7 cm in length and extending from D12 to L5 vertebral bodies, to the bifurcation, and eccentric, irregular, and largely non-calcified thrombi were seen along the right lateral walls of the aneurysm, which had a neck diameter of 2.5 cm. We scheduled her for open transperitoneal aneurysmorrhaphy. She was started on anti-hypertensive metoprolol 100 mg which was later reduced to 50 mg and telmisartan 40 mg was also started, targeting systolic pressure of <130 mmHg. Preoperative CT images did not reveal duplication of the IVC, probably due to IVC compression because of the large aortic aneurysm. EVAR was not feasible due to technical issues.\nA standard midline approach was used and a large saccular juxtarenal aortic aneurysm with dimensions of 18 cm x 7cm was noted. The transverse colon was retracted cephalad, and the small bowel loops were wrapped in a wet sheet and retracted to the left side, as opposed to the conventional approach. We carefully dissected the neck of the aneurysm, retracing the left renal vein to take proximal control just above the insertion of the renal artery. During dissection, we identified a large diameter vein coursing along the left side of the aneurysm sac () which we then followed to find a preaortic trunk continuing to the right-side IVC. Thus, an intraoperative finding of type 1 IVC duplication was made, which was very much essential, since if we would have missed it then injury to the preaortic trunk during opening of aneurysm sac could have led to torrential bleeding. Suprarenal clamping space was created and bilateral renal arteries were looped. After heparinization, the clamp was applied above the bilateral renal arteries and we packed the kidneys on both sides with cold saline solution for renal hypothermia. A 22 x 11 mm knitted graft was used for aneurysm repair, the proximal anastomosis was completed in 20 minutes, and renal reperfusion was maintained. Distal anastomosis was done to common iliac arteries bilaterally. Postoperatively, the patient did well. She developed ileus, which was resolved medically, and is in follow up.\nFor case report publication we don’t require approval from Institutions ethic committee. Only consent from the patient for his discussion in the case report. |
A 15-year-old female patient accompanied by her uncle was referred to the Department of Periodontics, ACPM Dental Collage and Hospital, Dhule, (Maharashtra) for the complaint of progressively enlarging gums. According to her, gums started growing about 1 year back beginning in the upper left back tooth region and gradually progressively involved all the teeth on that side. Similar enlargement of gums was also noticed with the lower back tooth region of that side. As the patient had difficulty in chewing from that side she continued to chew from the opposite side. Over a period of time, as the enlargement took a massive form and caused difficulty in mastication and compromised her esthetics, the school authorities brought it to the notice of her parents and they approached for treatment for it.\nOn further communication, the patient's past medical history and dental history was non-significant and was reporting for the first time to dental hospital.\nExtraoral examination revealed a slight asymmetry of the face on the left side []. Intra-orally massive gingival enlargement was noted in the maxillary as well as mandibular gingiva, but only on the left side whereas the right side gingiva appeared normal. The gingival enlargement extended from distal aspect of maxillary left lateral incisor to second molar []. The mandibular gingiva enlargement extended from distal aspect of lower lateral incisor up to the second molar and almost encroached the occlusal surface leaving a small view of it. The degree of enlargement was categorized as grade 3 (Angelopoulos 1971) [].\nThe color of the gingiva appeared pink with consistency being firm and fibrous with no evidence of stippling on the affected side. Traces of plaque, food debris and calculus were noted on the affected side. Bleeding on probing was minimal/evident/present. Periodontal examination revealed deep periodontal pockets in relation to 25, 26, 27, 35, 36 and 37. Mobility of grade 3 degree was found with 26 and 27 and grade 1 degree mobility with 25 and 35. An orthopantomograph was advised to rule out bony changes. Along with this a complete blood examination along with hormonal analysis of estrogen and progesterone were advised.\nBlood examination reports revealed all parameters to be within the normal limits including hormones (estrogen and progesterone). Radiographic examination revealed severe angular bone loss localized around maxillary first and second molars and moderate bone loss around mandibular first and second molars, but of the left side only []. Based on onset of age, presence of minimal local factors, clinical, radiographic and non-significant medical history and a diagnosis of IGF with localized aggressive periodontitis was made.\nA biopsy was advised and sent for histopathological examination, which confirmed the features of fibrous gingival overgrowth. The section was stained with hematoxylin and eosin, which revealed thickened epithelium with elongated retepegs that penetrated deep into the connective tissue. Dense collagenous tissue bundles arranged in parallel were found scattered throughout the connective tissue. Few fibroblasts, inflammatory cells, blood capillaries were also found [].\nThe usual treatment for IGF consists of surgical excision of gingiva the treatment for aggressive periodontitis initially consists of Phase 1 therapy that comprises of scaling and root planing, advise on oral hygiene instructions, administration of antibiotics, drugs amoxicillin (500 mg) and metronidazole (400 mg) for 5 days, along with anti-inflammatory drugs (ibuprofen and paracetamol) and use of chlorhexidine mouthrinses The same was carried out for the patient. The patient was discharged with oral hygiene instructions and recalled after 4 weeks.\nAt the end of 4 weeks, internal bevel gingivectomy quadrant wise along with open flap debridement was carried out. This procedure eliminates the pocket reduces the bulk of tissue and makes plaque control much easier. External bevel gingivectomy remains the method of choice if no bony involvement exists. Maxillary first and second molars were extracted as their prognosis was hopeless. Interrupted sutures were placed and periodontal dressing given []. Healing after 2 weeks at suture removal was satisfactory. Patient was recalled again at the end of 3 months, during which time there were no signs of recurrence. The clinical picture of the jaws at the end of 3 months []. The patient was advised to get the missing teeth replaced. Follow-up at the end of 1 year showed no recurrence of gingival overgrowth []. |
A 28-year-old woman, gravida 3 para 1, had a medical termination of a miscarriage at seven weeks, with no dilation and curettage, in 2008. In 2015, a baby was delivered by caesarean section in the breech position, weighing 3900 g. She had no significant past medical history, and her antenatal care had been uneventful. On August 9, 2018, at 19:15, she was admitted to our hospital due to a pregnancy of 9+ months and irregular contractions for 4+ hours. Periodic uterine contractions occurred every 6–8 min. The patient was not accompanied by abdominal pain or vaginal bleeding and had intermittent term after contractions. Clinical examination showed that her body temperature was 36.7 °C, blood pressure was 102/65 mmHg, pulse rate was 100 bpm, and oxygen saturation was 100%. Blood tests showed mild leucocytosis (16.61 × 109/L), normal platelet count, normal coagulation test, and haemoglobin of 102 g/L. Vaginal examination showed the cervix was tightly closed; no vaginal bleeding or fluid was found. The ultrasonography indicated that the foetal head was located above the uterine cavity, the foetal size was consistent with the gestational age, the placental position was normal, and the scar thickness of the previous caesarean section was approximately 0.2 cm. Uterine contractions declined after admission. During admission, the patient was clinically and biochemically stable, and daily cardiotocograms showed a reassuring foetal heart rate pattern. Because of the patient’s progressive anaemia (blood tests revealed a slow decline in haemoglobin to 93 g/L, 87 g/L) and sudden increasing abdominal pain, ultrasound was used but did not show ruptured abdominal fluid. An urgent laparotomy was performed and revealed a massive haemoperitoneum caused by the rupture of the uterine posterior wall. A haemoperitoneum with approximately 1 liter of blood was recovered. The lower uterine segment was intact and not ruptured. A boy with a body weight of 2900 g was delivered. Apgar scores were 9 at 1 min and 10 at 5 min. The amniotic fluid was clear, the placental was completely delivered, and no placental abruption occurred. The patient’s uterus was closed in two layers. After removing the blood and clots, a 12 cm-long tear in the posterior wall and active bleeding from the uterine rupture were found. Uterine tissue adhered to the bowel (see Fig. ). After separation of the adhesions between the bowel and the uterine wall, two layer of uninterrupted stitches restored the uterine integrity, and interrupted stitches closed the mesentery defect (see Fig. ). It was suspected that future conceptions would be dangerous, so bilateral tubal ligation was performed at the same time, under the permission of the patient and the patient’s family member. Our patient’s uterine and pelvis showed no abnormalities and, particularly, no evidence of endometriosis. Inspection of her liver showed no rupture. The placenta was sent for pathological examination. Syntocinon (oxytocin) (Ma an Mountain Company, China, SFDA approval number: H34020474) was administered intravenously. The operation was uncomplicated, and the estimated total blood loss was 2500 ml. Ten units of blood and 400 ml of blood plasma were transfused. The patient’s postoperative course was regular, and she was discharged 6 days later. |
An 8-year-old boy was referred to the Pediatric unit of the Oral Health Sciences Center by a private practitioner with chief complaint of “soft tissue growth” on right cheek mucosa, which did not heal with local application of ointment and was gradually increasing in size over a period of 4 months. An intraoral examination of the patient showed hypertrophic, soft, roughened, non-pedunculated growth of about 2 mm × 2 mm on right mucosa of cheek. The growth was opaque white, non tender, without any ulceration []. The patient gave the history of traumatic injury to cheek while eating after which the tissue started growing in size and had resulted in a habit of cheek biting. The growth was evident along the masticatory surfaces of the primary molars. The patient was aware of the habit of cheek biting during the day and occasionally during his sleep. No lymphadenopathy or other constitutional signs/symptoms were detected. As the history and clinical findings were suggestive of cheek biting, surgical excision of the soft tissue growth was done using cautery [], after which the patient presented with uneventful healing. The excised tissue was sent for histopathological examination which showed evidence of hypertrophic tissue. After 2 months, however, patient again reported with a growing tissue of almost similar dimensions as the previous one and present at the same site due to persistence of habit, as revealed by the parents []. Fabrication of mouth guard was planned to prevent any further trauma to cheek mucosa and to promote healing. Maxillary and mandibular impressions were made using irreversible hydrocolloid. Mouth guard was fabricated from soft polyvinyl sheet of thick resilient material (Bioplast® Scheu Dental GmbH Iserlohn Germany) of 2 mm thickness after occluding the dental casts and placing sheet in a vacuum formed pressure molding device (Biostar® Scheu Scheu Dental GmbH Iserlohn Germany) with a thermally controlled infrared heater []. The sheet extended laterally from first molar region on the left side to first molar region on right side []. The patient was directed to wear the appliance during daytime after school hours and at night during his sleep. Patient was reviewed every 2 months till 6 months and he presented with uneventful healing, with no recurrence. After 6 months, the appliance was discontinued. The patient was again recalled and reviewed 6 months after the discontinuation of appliance; the tissue remained healed with no sign of recurrence of any traumatic lesions on the cheek mucosa [Figure and ]. |
A 20-year-old African American man was admitted to a psychiatric facility for psychosis. On initial presentation, the patient had an antalgic gait, which he attributed to his history of dopa-responsive dystonia. His mood was depressed and his affect was restricted. He had disorganized thought process and was slow to recall. He endorsed auditory hallucinations, paranoid delusions, depressive symptoms, frequent night awakenings, and persecutory nightmares. Per the ambulance report, the patient was wandering the streets in a confused state, so bystanders called 911. The patient stated that he had been homeless for the past 3 weeks. During this 3-week period, he admitted to not being complaint with his medications. Urine toxicology screen was negative.\nPer medical records, he was diagnosed with dopa-responsive dystonia at age 11 after a 2.5-year history of progressive abnormal gait. He was initially misdiagnosed with tight heel cords at age 10 and treated with serial casting that resulted in good improvement on the right but marginal improvement on the left. His toe walking became more pronounced overtime accompanied by worsening left calf pain and stiffness, increasingly frequent falls, and new onset of intermittent torticollis. These symptoms worsened over the course of the day. He was eventually taken to an urban teaching hospital, where he was diagnosed with dopa-responsive dystonia based on clinical presentation and marked improvement on a levodopa trial. Magnetic resonance imaging of the brain and spine was unremarkable at the time.\nAt age 15, he was diagnosed with schizoaffective disorder bipolar type. His psychiatric history is also significant for multiple psychiatric hospitalizations, history of previous suicide attempts with medication overdose, and history of trauma. He also endorsed marijuana use since age 15 and daily tobacco use since age 18. He denies using any other illicit drugs. Per collateral information from his mother, his schizoaffective disorder has never been well controlled given the conflicting effects of his medications. She also mentioned that he was placed in individualized education programs as a child due to learning disabilities. His family history is significant for bipolar disorder on his maternal side. His family history on his paternal side is unknown. In addition to carbidopa-levodopa, his outpatient medications included sertraline, divalproex sodium, aripiprazole, and benztropine.\nOn hospital day 1, he was started on carbidopa-levodopa 25/100 mg tablet three times daily for dopa-responsive dystonia. On day 2 of his hospital course, sertraline 50 mg once daily, benztropine 2 mg twice daily, divalproex sodium 500 mg twice daily, and risperidone 0.5 mg twice daily were added to his medication regimen. We started him on a low-dose risperidone to avoid exacerbating his dopa-responsive dystonia symptoms. Physical exams were also performed daily to assess for dystonia and parkinsonian symptoms. His initial physical exam revealed an antalgic gait secondary to left lower extremity dystonia, which improved by hospital day 2 and resolved by hospital day 3. On hospital day 3, he became agitated and aggressive with staff members, which led to intramuscular administrations of haloperidol 10 mg, diphenhydramine 50 mg, and lorazepam 2 mg. He continued to endorse auditory hallucinations, so risperidone was increased to 0.5 mg in the morning and 1 mg at bedtime. His auditory hallucinations resolved and then returned on day 6. He reported hearing “good” voices and “bad” voices. He also continued to endorse depressive symptoms, multiple night awakenings, and persecutory nightmares. As a result, his risperidone dosage was increased to 1 mg twice daily. On hospital day 7, the patient reported hearing “mumbling” voices only and improvement in his sleep and depressive symptoms. On hospital day 8, his auditory hallucinations fully abated. By hospital day 10, he slept throughout the night, no longer had depressive symptoms, and had normal spontaneous speech. His thought process was linear, logical, and goal-oriented. His mood and affect was euthymic and full range. No psychotic symptoms were noted. The patient was compliant with his medications throughout the whole hospital course and his daily physical exams were negative for dystonia or parkinsonian symptoms since day 3 of his hospitalization. He was subsequently discharged on hospital day 14 with appropriate outpatient follow-up. |
A 76-year-old Japanese man previously underwent a right direct inguinal hernia repair using the plug-and-patch technique in our department. The PerFix™ Light Plug, size XL (C.R. Bard, Inc., Murray Hill, NJ), was fixed to the fascia transversalis using 4 absorbable sutures. The onlay patch was not sutured in place. The patient experienced severe groin pain after surgery, but this improved with administration of tramadol hydrochloride. Two years later, the patient again began to experience groin pain, for which he was prescribed pain medication at a nearby clinic.\nFour years after the initial surgery, he visited our department with the complaint of right groin pain. A solid mass was palpable in the right inguinal region; we presumed this was attributable to the mesh. Palpation of the mass caused severe pain, but there was no pain at any other location. Abdominal computed tomography revealed a meshoma (). The patient was offered mesh extraction, but he declined. We consulted an anesthesiologist about the possibility of a nerve block and trigger point injections, but they advised that the effect would be temporary.\nFive years after surgery, the patient expressed a desire for mesh removal, as his pain rated 8 out of 10 on a numeric rating scale. We determined that the likely etiology of his pain was nociceptive, caused by a plug meshoma. Computed tomography findings indicated that the plug would be easy to extract by a transabdominal surgical approach. We thought there was a high possibility of improving the patient’s pain by removing the plug, and laparoscopic surgery would be an easy way to accomplish this. However, the International Guidelines for Groin Hernia Management (IGGHM) recommend mesh removal with triple neurectomy for patients with CPIP []. In addition to laparoscopic plug removal, we also considered removing the onlay patch and performing triple neurectomy at the same time, but in our patient with mainly nociceptive pain caused by the plug, we felt the more extensive procedure would be overly invasive and would carry the risk of causing new pain by adding a groin incision. We offered the patient laparoscopic plug extraction with simultaneous resection of the genital branch of the genitofemoral nerve. If this procedure did not improve his pain, the plan was to later remove the onlay patch and perform iliohypogastric and ilioinguinal nerve resection by an anterior approach. The above explanation was given to the patient and consent was obtained.\nLaparoscopy revealed that the plug projected into the abdominal cavity (a). The plug was excised using an ultrasonically activated device (b, c). In addition, the genital branch of the genitofemoral nerve was exposed, ligated using an ENDLOOP® Ligature (Ethicon, USA), and dissected (d). Finally, the peritoneum was closed using continuous suturing technique.\nThe patient reported that his inguinal pain improved to 2 out of 10 on the second postoperative day, and he was discharged from the hospital. He still required pain medication for low back pain, but he stopped taking this by 10 months after surgery. There has been no recurrence of the inguinal hernia. |
A 55-year-old male patient was presented to a general hospital with fever, myalgia, and persistent cough. Polymerase chain reaction testing for COVID-19 was positive and he was admitted to the hospital due to severe respiratory symptoms. The patient is a known diabetic and hypertensive with a history of a nonfunctioning pituitary macroadenoma for which he underwent an endoscopic endonasal transsphenoidal resection 11 years ago in another hospital. Pituitary tumor recurrence was documented in the available two postoperative magnetic resonance imaging (MRI) studies []. After surgery, the patient was kept on maintenance levothyroxine and hydrocortisone for panhypopituitarism.\nSix days after admission, the patient complained of severe headache and acute onset of ptosis and diminution of vision in the left eye. Ophthalmological evaluation revealed complete visual loss in the left eye, a visual acuity of 20/60 in the right eye, left oculomotor nerve palsy with ptosis, and dilated nonreactive pupil. Fundus examination revealed a pale left optic nerve head. Neurological examination was otherwise normal. Computed tomography revealed hyperdensity of the sellar and suprasellar areas. MRI was consistent with PA in a recurrent large pituitary adenoma [ and ].\nThe patient was transferred to our center and underwent an urgent endoscopic endonasal transsphenoidal surgery through which a near total excision of the tumor was achieved [ and ].\nThe procedure was performed under strict COVID-19 precautions including use of powered air purifying respirators and limited OR personnel. Intraoperative findings were similar to those usually seen in cases of PA and included dark blood mixed with purple-red adenoma tissues of variable consistencies []. It was our observation that the nasal mucosa was pale and separated easily from the underlying bone. We have previously observed such features in two patients who previously tested positive for COVID-19. Histopathological examination demonstrated classic features of PA.\nWithin the first 3 postoperative days, the patient had some improvement of vision of the left eye so that he was able to perceive hand movement. Ptosis also improved partially. However, his chest condition progressed and he had to be transferred to COVID-19 intensive care unit in the referring hospital where he was intubated and put on mechanical ventilation. One week later, the patient unfortunately passed away due to complications of severe COVID-19 pneumonia. |
An 8-month-old Caucasian baby boy with heterotaxy syndrome was admitted to our general pediatric ward after presenting to a scheduled clinic visit with fever, hypoxemia and cyanosis. His history was significant for dextrocardia, polysplenia, interrupted inferior vena cava, biliary atresia status post-Kasai procedure, and malrotation status post-Ladd’s procedure. He was febrile on presentation, and was started on oxygen via nasal cannula for oxyhemoglobin saturations as low as 70%. His chest radiograph on admission showed a patchy right lower lobe opacity, and he was started on antibiotics out of concern for pneumonia. He was subsequently transferred to our pediatric intensive care unit (PICU) for refractory hypoxemia requiring high flow oxygen therapy.\nThroughout his PICU admission, he continued to require high flow oxygen up to 9L per minute and fraction of inspired oxygen (FiO2) of 1 to maintain oxyhemoglobin saturation greater than 75%, with persistent desaturations while upset. Early in his admission, he developed increased work of breathing requiring positive pressure ventilation with bilevel positive airway pressure. A chest radiograph revealed pulmonary edema, and brain natriuretic peptide (BNP) at that time was elevated at 1130pg/mL. His pulmonary edema improved with diuresis, resulting in de-escalation of therapy with return to standard nasal cannula. He required blood pressure support with a dopamine infusion during aggressive diuresis, which was subsequently weaned off without complication. Multiple echocardiograms revealed no clear cardiac etiology of his hypoxemia.\nA chest CT angiogram with high resolution reconstruction of the lung parenchyma was performed on the recommendation of our Radiology department to further evaluate the pulmonary vasculature and lung parenchyma. CT imaging showed dilatation of the pulmonary vasculature bilaterally without significant abnormalities of the lung parenchyma (Figure ). Pulmonary arterial hypertension was felt to be an unlikely cause of his dilated pulmonary vasculature as right ventricular pressures were measured as less than half of systemic pressures on echocardiogram. Given his history of biliary atresia and constellation of symptoms, HPS was included on the differential diagnosis. He underwent agitated saline contrast study, which showed bubbles entering the right-sided atrium (systemic atrium in the setting of dextrocardia) through a right pulmonary vein approximately 3 cardiac beats after opacification of the left-sided chambers (Figure ), consistent with clinically significant intrapulmonary shunting.\nAbdominal magnetic resonance imaging (MRI) was performed to evaluate for the presence of a congenital portosystemic shunt given the strong association of Abernethy malformation and heterotaxy syndrome and the possibility of reversal of HPS with shunt occlusion. MRI did not reveal portosystemic shunting. The patient subsequently underwent evaluation for liver transplantation. His liver enzymes and coagulation studies were normal. His bilirubin levels were also normal and given normal bile ducts on abdominal ultrasound, a hepatobiliary iminodiacetic acid scan was not performed. Abdominal ultrasound also demonstrated diffuse liver disease, patent portal vein with hepatopetal flow, and no ascites. He did have polysplenia with splenomegaly. He had no signs of collateral circulation on examination. No abnormalities were noted in his stools. His partial pressure of oxygen in arterial blood (PaO2) was measured at 29mmHg while on FiO2 of 0.5. He was listed for transplant with a pediatric end-stage liver disease score of 28, which was further increased to 35 following petition to UNOS for worsening clinical status.\nPrior to diagnosis of HPS, the patient was initiated on a milrinone infusion for suspicion of diastolic heart failure. Following the diagnosis, he was trialed off milrinone with the rationale that further pulmonary vasodilation actually may be deleterious given the diagnosis of HPS. However, he responded poorly with subsequent oxyhemoglobin desaturations requiring reinitiation of the infusion. His oxygenation stabilized on a milrinone infusion of 0.5μg/kg/minute. Inhaled nitric oxide was also trialed without significant improvement in oxygen requirement and was subsequently weaned off. Oxygen requirements ultimately stabilized on a diuretic regimen including spironolactone and furosemide.\nHe underwent OLT 2 months after initial presentation. His postoperative period was complicated by hypercarbic and hypoxemic respiratory failure requiring mechanical ventilation. He underwent tracheostomy for chronic ventilator-dependent respiratory failure. He was transferred out of the PICU 2 months after OLT and subsequently weaned off mechanical ventilation during the daytime. He was discharged home 4 months following OLT on FiO2 of 0.21 through a tracheostomy mask with nighttime ventilator support. He continues to do well. Please see Figure for a timeline of the patient’s clinical course. |
A 32-year-old female known case of rheumatoid arthritis affecting both knees presented to our clinic complaining of severe right knee stiffness post TKA 4-years-ago done in an outside facility ( and ). She lives in a rural community and was on hydroxychloroquine, but her disease was active as she was not compliant to her medication. On physical examinations, the right knee was larger in size compared to the left knee without joint effusion. Range of motion was zero on flexion, −10° in extension. Standing knee X-ray showed HO around the prosthesis (). Computed tomography (CT) demonstrated extensive HO with implants fixed in place (). Revision surgery and replacement of the prostheses was considered to restore function.\nThe old medial parapatellar approach was utilized. The medial and lateral gutters were completely released up to the posteromedial corner. When the knee was too stiff to be mobilized further, the patellar tendon was found to be severely contracted and shortened with patella baja deformity. A tibial tubercle osteotomy was needed for adequate exposure. Osteotomy fragment measured 6 cm with 1.5 cm thickness, after which we became able to flex the knee. The components were completely engulfed by capsular heterotopic bone (). Using osteotomes and burrs, the tibial and the femoral components were slowly visualized. Both components were found to be well fixed. Carful removal of the posterior heterotopic bone was done with a bone curette, which finally allowed for component removal. Intraoperative culture samples were taken as routine measure for revision surgeries. RT-Plus modular rotating hinge knee system (Smith & Nephew, Memphis, TN, USA) was used. The procedure was started with reaming the tibia up to size 12 mm. It was sized to be size four. Proximal drilling and rasping were done, and posterior offset stem was used.\nAfter that, reaming of the femur was carried out reaching size 14 mm, giving a good fixation. Distal resection was done followed by posterior resection and box preparation. Afterward, the implants were cemented into place. The knee was in full extension with excellent stability. Attention was then taken to realign the patella. Osteotomy fragment was moved proximally 1 cm and fixed with 3.5 cortical screws achieving bicortical fixation. Bone graft was used for the remaining osteotomy site.\nOn the table, range of motion was 0–90°. Intraoperative image intensifier was used and demonstrated excellent position of the implant and the osteotomy site ().\nPostoperatively, she could flex her knee up to 90° in bed. Cultures were negative and upon discharge, she was referred to rheumatology department for review. She was started on disease-modifying antirheumatic drugs DMARDs. She was also put on indomethacin for 6 weeks for HO prophylaxis. In the immediate post-operative period, she was able to maintain 90° of flexion and full extension using continuous passive motion machine only.\nThe patient lost some of her range of motion (ROM) in the post-operative period even with extensive physiotherapy. On her 4-month follow up appointment; ROM was 10–80°, which she sustained afterward. Plain radiographs continued to show no new HO formation at 4 months (). |
A 34-year-old male patient presented with paroxysmal headaches and progressive vision loss for 10 months and blindness for 2 weeks. Physical examination revealed loss of bilateral direct and indirect light reflexes. No other neurologic deficits and laboratory abnormalities were noted. CT imaging showed an irregular isodense mass with a cerebriform appearance and extensive peritumoral edema in the parietal-occipital-temporal region of the right hemisphere (). MR imaging demonstrated a cerebriform, irregular but well-defined mass in the parietal-occipital-temporal region of the right hemisphere. It was isointense on T1-weighted images and slightly hyperintense on T2-weighted images. There was intense homogeneous enhancement after contrast administration. The mass measured 46 cm × 80 cm × 51 cm and demonstrated significant mass effect, resulting in a 13 mm midline shift, compression of brainstem, and effacement of the occipital horn of the right lateral ventricle and ambient cistern (). Unfortunately, advanced MRI imaging such as perfusion weighted imaging (PWI) and MR spectroscopy (MRS) was not performed on the initial MRI examination and the patient denied the suggestion of further imaging. Intraoperatively, the tumor was completely buried in a sulcus in the parietal-occipital-temporal region. The tumor was completely resected with careful dissection from the surrounding brain tissues. Macroscopically, the tumor showed rich blood supplies but without a dominant feeding artery. Histopathologically, the tumor showed a large number of spindle cells. There was no distinct karyokinesis. On immunohistochemical staining, the pathology specimen of this tumor was positive for epithelial membrane antigen () but negative for glial fibrillary acidic protein. Ki-67 was 1-2%. Based on the pathological findings, the tumor was diagnosed as a grade II intracranial meningioma according to classification criteria of World Health Organization (WHO). Postoperative radiotherapy was offered to the patient. However, the patient and his family denied the treatment. Twelve months after surgery, the patient returned to the hospital with progressive headaches and a CT examination () revealed recurrence. After surgical resection, the recurrent tumor was determined to be meningioma (WHO grade III). |
A 33-year-old man came for evaluation of pain in his right thigh. His symptoms started approximately three years ago. He suffered from two kinds of pain, one was deep-seated right hip pain, which was insidious in onset and got gradually progressive and was diagnosed as femoral acetabular impingement syndrome. The second kind of pain was described by him as burning pain on the anterior and lateral aspect of his thigh. The skin of his right thigh was hypersensitive to touch. The burning pain started within a month of the deep seated hip pain. He denied any weakness. However, he was limited in his activity due to the pain. He had no back pain. He denied any bowel or bladder incontinence. His past medical and family history were unremarkable. He is a truck driver by profession and denied smoking, drinking and use of illicit drugs. He recently was started on Cymbalta 30 mg daily for the burning pain. On exam his vitals were stable. He was of normal body habitus and reported no recent weight changes. He weighed 200 pounds and his height was 6 feet. Heart sounds were audible and chest was clear to auscultation. His cranial nerve exam was unremarkable. Motor examination showed full strength for neck flexion and extension as well as the upper and lower extremity muscles proximally and distally. No fasciculation or atrophy were noted anywhere. No trophic skin changes were noted. His tone was normal throughout. His reflexes were 2+ in the upper and lower limbs bilaterally. Babinski sign was mute bilaterally. No Hoffman sign was noted. Sensory examination showed hyperesthesia in L2, L3 and L4 distribution of the right thigh, otherwise normal pinprick elsewhere. Vibration and position were intact symmetrically. He was able to get up from a seated position with his arm folded across his chest. He had no dysmetria. His casual gait was normal. He could stand on his heels and on his tiptoes. He was able to maintain his stance on Romberg test. Work-up that was done includes magnetic resonance imaging (MRI) on right thigh which showed a well defined fluid collection between the femoral condyle and iliotibial band and was suggested to be responsible for mild iliotibial band friction syndrome. Lumbosacral spine MRI was unremarkable. Right hip MRI showed labral cartilage being 'pinched' between the rim of the socket and the anterior femoral head-neck junction with superior and laterally torn labrum. Medial femoral head osteophyte was also noted. Based on the imaging studies, he was diagnosed with femoral acetabular impingement syndrome. Two weeks prior to the presentation at our clinic, he had arthroscopic debridement of the torn labrum, arthroscopic osteochondroplasty of pincer, and cam lesion. Subsequent to surgery he noted improvement in his deep seated hip pain up to 90%. However, the burning pain had remained unchanged. A right lateral femoral cutaneous neuropathy was suspected and an electrodiagnostic study was performed (). There was electrophysiologic evidence suggestive of a right lateral femoral cutaneous neuropathy as no response was seen on the right side compared to normal response on the left side. Lumbar paraspinal and femoral nerve innervated muscles were normal on the needle exam. Patient was referred to pain clinic for nerve block. |
A 40-year-old Caucasian man was referred to our intensive care unit for further diagnostic work-up because of gastrointestinal bleeding of unknown location. After blood transfusions in the referring hospital, he presented with a hemoglobin level of 12.3 mg/dL at 3:45 pm.\nIn March 1997, he received a simultaneous pancreatic-duodenal transplantation connected to the right iliac artery and renal transplantation connected to the left iliac artery on the basis of long-standing diabetes mellitus type I. The transplantation procedure was more difficult due to abdominal adhesions caused by peritoneal dialysis over five years with recurrent bacterial peritonitis. Two episodes of hemoglobin-relevant bleeding occurred; the first five days after the transplantation and the second 14 days after. These were followed by surgical revisions of the severe adhesive abdomen without finding the bleeding site. In April 1998, July 1998, February 1999, and August 1999 acute and hemoglobin-relevant gastrointestinal bleeding episodes occurred. Repeated gastroscopy and colonoscopy, in addition to conventional and magnetic resonance (MR)-angiographies, and repeat exploratory surgeries with intra-operative endoscopies in cooperation with skilled endoscopists and Tc-erythrocyte scintigraphies, could not reveal the location of the bleeding. The renal graft lost function due to rejection in August 1998. In June 1999, he received a second renal graft on his left side, leaving the first kidney graft in place. The second renal graft also lost function due to rejection in April 2003 and hemodialysis was started in October 2003. The pancreas graft lost function in 2002 due to rejection.\nAt about 10 pm on the day of his admission to our unit, he complained of severe, colic-like diffuse abdominal pain. An ultrasound did not show cholelithiasis, kidney or bladder problems and an X-ray of the chest and abdomen did not show any air-fluid levels. Administration of butyl-scopalamine relieved the colic-like pain completely. At 2 am, in a routine blood-gas check, his hemoglobin was down to 7.9 mg/dL and two units of blood were transfused with adequate rise to 9.4 mg/dL after one unit of blood. At 5 am, he again complained of severe colic-like diffuse abdominal pain with nausea, tachycardia, and hypotension. His hemoglobin levels dropped to 5.7 mg/dL without showing bloody stools. Intravenous fluids, blood transfusions and catecholamines were administered immediately. Suddenly, he vomited massive amounts of blood mixed with large blood clots, making intubation impossible. He died of hemorrhagic shock.\nAutopsy revealed extensive intra-abdominal adhesions. Meticulous exploration by the pathologist finally revealed an arterio-enteric fistula between his left common iliac artery, where the initial kidney was engrafted, and the adjacent ileum (Figure ). In addition, large blood clots were found distal to the fistula in his small intestine which led to intestinal obstruction; explaining the eruptive vomiting of blood instead of showing bloody stools. The obstruction with intestinal distension might also explain the colic-like pain [] which was alleviated after administration of butyl-scopalamine. |
A 12-year-old girl presented with progressive hearing loss in the right ear and was referred to our hospital. The patient complained of progressive hearing impairment and fullness of the right ear. She had no history of otitis media or previous trauma to the ear. On physical examination, the right tympanic membrane was not visible because of a mass that was completely obstructing the EAC. Right-sided hearing measured using pure tone audiometry was 55 dB hearing level, with an air-bone gap of 45 dB, demonstrating moderate, conductive hearing loss (). The patient had a normal hearing threshold in the left ear. High-resolution computed tomography (CT) revealed a large, soft-tissue mass located in the right temporal bone measuring 4.0×3.3 cm in size with clearly defined boundaries. The mass filled the right EAC and had eroded the lateral part of the EAC and the mastoid cortex. The mass did not involve the tympanic membrane, middle ear, ossicles, or mastoid antrum (). In order to better characterize the lesion, magnetic resonance imaging (MRI) was performed. MRI revealed a mass with high signal intensity in T1- and T2-weighted images. Contrast-enhanced, T1-weighted images revealed a non-enhanced mass with high signal intensity ().\nBased on the diagnosis of a cholesterol granuloma from the results of medical imaging, surgery under general anesthesia was performed via a postauricular approach. A cystic mass containing a sticky, brown-colored liquid was located just below the subcutaneous tissue and was discovered to have eroded the mastoid cortex at the posterior and superior portions of the lateral EAC (). The mass had extended near to the tympanic membrane and superficial mastoid air cell but not into the mastoid antrum or middle ear. After the mass was completely excised (), the widened EAC and exposed mastoid air cells were covered with a posterior-based periosteal flap, and the skin of the EAC was repositioned. There were no post-operative complications such as infection, bleeding, or facial palsy. Histopathological analysis of the mass revealed a typical cholesterol granuloma with numerous cholesterol clefts surrounded by immature, fibrous tissue. The mass was also described as having an abundance of polynuclear cells, giant cells, and round cells ().\nPost-operatively, the child's hearing was restored to the threshold of 10 dB in the right ear (). At 2 years after surgery, there were no postoperative complications, nor was there recurrence or EAC stenosis (). |
A 69-year-old Japanese woman was referred to our department in August 2015, complaining of swelling in the right preauricular region. She had shown a mass lesion of the right lung on a chest x-ray and was referred to the university hospital. Fluorodeoxyglucose-positron emission tomography (FDG-PET) examination showed accumulation indicative of a pulmonary lesion and a temporomandibular joint lesion. The temporomandibular joint lesion had been enlarging but was otherwise asymptomatic. Her medical history included treatment for pulmonary tuberculosis at the age of 13 and surgery to remove breast cancer at the age of 53.\nOn examination, a tender mass in the right preauricular region was palpable. The chin of the mandible was deviated to the right side during mouth opening (mandibular maximum mouth opening, 41 mm). Facial nerve function and mandibular nerve were intact. There was no indication of cervical lymphadenopathy.\nA panoramic radiographic examination showed resorption of the right mandibular condyle to the ramus (Fig. ). Computed tomography (CT) showed destruction of the right mandibular condyle and a large mass lesion with enhanced margin in the masticator space; a cystic lesion was present inside the tumor mass. Three-dimensional CT was useful to understand the bone resorption findings of the mandibular condyle. There was no finding of metastatic cervical lymph node (Fig. ). T1-weighted magnetic resonance imaging showed an enhanced mass lesion in the right masticator space. Because some portions of the mass lesion showed high intensity in T2-weighted images, cystic lesions were suspected to exhibit changes of blood flow or retention of high-protein liquid. Tumor development was not observed in the articular disk of the temporomandibular joint (Fig. ). FDG-PET revealed abnormal FDG uptake in the right submandibular condyle and masticator space.\nA malignant tumor was suspected after analysis by various modalities. Therefore, we performed an incisional biopsy via preauricular incision. Histopathologically, the tumor was largely composed of proliferative, atypical, spindle-shaped cells. Some tumor cells showed increasing mitotic change and extreme atypia (Fig. ). The histopathological findings of biopsy suggested spindle-cell sarcoma. Tumor resection was performed with the patient under general anesthesia via a combined preauricular and transmandibular approach to the masticator space and infratemporal fossa.\nAfter preauricular temporomandibular incision, the superficial temporal fascia and temporal fascia were elevated. The facial nerve (temporal and zygomatic branches) was protected by the fascia (Fig. a).\nThe facial nerve trunk was identified, and its branch was traced according to the conventional method.\nA midline lip-splitting incision was connected to the submandibular incision and accessed the anterior mandibular ramus. The lip-split incision traversed to the periosteum of the mandible; the periosteum dissector was used to elevate the soft tissues of the mandible, and the lateral mandible was exposed. The branch of the facial nerve was traced continuously with the skin flap, and the masseter muscle and deep parotid gland were dissected on the tumor side (Fig. c). The mandible was resected to within ≥ 20 mm from the primary tumor on the anterior of the mandibular ramus. The masseter muscle was divided at the lower edge of the zygomatic arch; further, the temporal muscle was divided horizontally at the height of the zygomatic arch to reach the side of the temporal bone. Excision was performed on the temporal bone to the base of the pterygoid process, and an osteotomy was performed continuously from the maxilla to the pterygoid process. Osteotomy was performed via ultrasonic scalpel. Then, deep excision was performed on the skull base until the foramen ovale was reached. The mandibular branch (VIII) of the trigeminal nerve was resected at the foramen ovale, and bone wax was used to fill the foramen ovale when hemostasis was achieved. The tumor was excised in bulk with the surrounding tissue (Fig. d). Especially, the glenoid fossa was close to the primary tumor site; however, it was excised including the joint disc, and the glenoid and infratemporal fossa were excised, including the periosteum of the skull base. For that reason, the margin was considered complete, and we did not perform the histopathological evaluation intraoperatively.\nThe surgical defect was reconstructed with a free vascularized fibula with skin paddle (Fig. e). The occlusion was performed with intermaxillary wire fixation for 1 week postoperatively. There were no abnormal findings during the postoperative course with complete healing. Right-sided facial nerve dysfunction appeared immediately after surgery.\nThe resected specimen exhibited nearly identical histological findings as observed in the biopsy. Because it involved a periosteal reaction corresponding partially to Codman’s triangle, the tumor was thought to have derived from bone (Fig. ). Immunohistochemical analysis showed positive staining for vimentin, MIB-1 index (40–80%), desmin, α-smooth muscle actin, Bcl-2, neuron-specific enolase, and S-100; it showed negative staining for AE1/AE3, caldesmon, and CD34. Thus, the final diagnosis was osteosarcoma (fibroblastic). The resection margin was negative for tumor. After excision of the mandibular tumor, excision of lung cancer was performed under thoracoscopy by a respiratory surgeon in our hospital. Although we recommended adjuvant treatment after surgery, the patient refused this treatment.\nThere has been no evidence of local recurrence or distant metastasis through 30 months of follow-up. The chin of the mandible deviates to the right side during opening (maximum mouth opening, 40 mm). Centric occlusion has not changed. Facial nerve dysfunction gradually improved and became mild according to House-Brackmann Scale evaluation (Figs. and ). |
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